STANDARD TREATMENT GUIDELINE

FOR GENERAL HOSPITALS IN

ETHIOPIA
4th Edition

Ethiopian Federal Ministry of Health

2021
STG 4th Edition, draft 2020

MINISTRY OF HEALTH ETHIOPIA

STANDARD TREATMENT GUIDELINES FOR

GENERAL HOSPITALS

FOURTH EDITION, 2021

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ACKNOWLEDGMENTS
The ministry of health is gratefully to acknowledge the following individuals and institutions
for their efforts through the development of this Standard treatment guideline (STG).

I. Central core team

s.no Name (Alphabetically) Specialty Institution

1 Addisu Melkie (MD) Internal Medicine and TASH/CHS/AAU
Nephrology
2 Desalew Mekonnen (MD) Internal Medicine and TASH/CHS/AAU
Cardiology
3 Getachew Alemkere Clinical Pharmacy TASH/CHS/AAU
4 Getachew Asfaw Clinical Pharmacy PMED/MOH
5 Mahdi Abdella Public Health PMED/MOH
6 Regassa Bayisa Public health PMED/MOH
7 Wondwossen shewerega Pharmacy PMED/MOH
8 Workineh Getahun Social Pharmacy and MTAPS/USAIDS
Pharmacoepidemiology
9 Yakob Semaneh Public Health MSDG/ MOH
10 Yidnekachew Degefaw Pharmacy PMED/MOH
11 Yohannis Demissew (MD) Medical Doctor MTAPS/USAIDS

II. Technical working Group

S.no Name (Alphabetically) Specialty Institution

Abera Mulatu Clinical Pharmacy ASMH

1
Addisu Melkie (MD) Internal Medicine and TASH/CHS/AAU
2
Nephrology

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Debela Gemeda Pharmacology SPMMC

3
Desalew Mekonnen (MD) Internal Medicine and TASH/CHS/AAU
4
Cardiology

Getachew Alemkere Clinical Pharmacy TASH/CHS/AAU

5
Getachew Asfaw Clinical Pharmacy PMED/MOH
6
Martha Fekadu (MD) Internal medicine St. Peter Specialized
7
Hospital

Workineh Getahun Social Pharmacy and MTAPS/USAID

8
Pharmacoepidemiology
Worku Bedada (PhD) Pharmacology AHMC
9
Yidnekachew Degefaw Pharmacy PMED/MOH
10
Yohannis Demissew (MD) Medical Doctor MTAPS/USAID
11

III. Reviewers of the first drafted Standard Treatment Guideline

S.no Name (Alphabetically) Specialty Institution

1 Clinical Pharmacy ASMH
Abera Mulatu
2 Abraham Barana Medical Parasitology Wolaita Soddo University
Teaching Hospital
3 Addisu Melkie (MD) Internal Medicine and TASH/CHS/AAU
Nephrology
4 Adnan Abdulkedir (MD) Surgery Hiwot Fana Hospital
5 Amsalu Bekele (MD) Internal Medicine, TASH/CHS/AAU
Pulmonology

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6 Aynalem Abraha (MD) Oncology TASH/CHS/AAU

7 Belay Yadeta (DDM) Dentistry Jimma Medical Center
8 Birhanu Demelash (MD) Internal Medicine, TASH/CHS/AAU
Rheumatology
9 Dawit Bacha (MD) Internal Medicine, St.Paul Hospital Millenium
Cardiology Medical College
10 Dawit Kebede (MD) Internal Medicine, TASH/CHS/AAU
Pulmonology
11 Pharmacology SPMMC
Debela Gemeda
12 Desalew Mekonnen (MD) Internal Medicine and TASH/CHS/AAU
Cardiology
13 Eskinder Tesfaye (MD) Internal Medicine, Washington Clinic
Gastroenterology
14 Clinical Pharmacy TASH/CHS/AAU
Getachew Alemkere
15 Clinical Pharmacy PMED/MOH
Getachew Asfaw
16 Getachew Yilma (MD) Pediatrics Debrebirhan Referral
Hospital
17 Getamesay Abayneh (MD) Pathology Dilchora Hospital
18 Hamere Tesfaye (MD) Ear, Nose and Throat Yekatit 12 Medical College
19 Kibrom Haile (MD) Psychiatry Amanuel Mnetal
Specialized Hospital
20 Lina Mohammed (MD) Internal Medicine, St.Paul Hospital Millenium
Nephrology Medical College
21 Mamo Dessalegn (MD) Neurology Myasung Christian Medical
Center
22 Mariamawit Solomon (MD) Emergency Medicine Aabet Hospital/ St.Paul
and Critical Care Hospital Millennium
Medical College
23 Internal medicine St. Peter Specialized
Martha Fekadu (MD)
Hospital

24 Misgina Ayele Nurse Hawasa University college

of health Science
25 Seifu Kebede (MD) Internal Medicine, TASH/CHS/AAU

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Hematology
26 Selamawit Tilahun (MD) Pulmonary and Critical St.Paul Hospital Millenium
care Medical College
27 Shimelis Nigusse (MD) Dermatology and ALERT Hospital
Vernology
28 Sisay Sirgu (MD) Endocrinology SPMMC
29 Sofanit Haile (MD) Gynecology TASH/CHS/AAU
30 Tajudin Hassen (MD) Neurosurgery St.Paul Hospital Millenium
Medical College
31 Tesfaye Tadesse (MD) Ophthalmology Menillik II hospital
32 Tolossa Gishle (MD) Gynecology Ambo University Hospital
33 Wondowossen Amogne (MD,PhD) Internal Medicine, TASH/CHS/AAU
Infectious Disease
34 Workeabeba Abebe (MD) Internal medicine, TASH/CHS/AAU
Infectious Disease
35 Social Pharmacy and MTAPS/USAID
Workineh Getahun
Pharmacoepidemiology
36 Pharmacology AHMC
Worku Bedada (PhD)
37 Pharmacy PMED/MOH
Yidnekachew Degefaw
38 Medical Doctor MTAPS/USAID
Yohannis Demissew (MD)
39 Yonas Lakew (MD) Psychiatry Amanuel Mental
Specialized Hospital

IV. Contributors during draft document preparation

S.no Name (Alphabetically) Specialty Institutions
1 Adamu Addissie (MD) Public Health AAU/CHS
2 Adane Petros (MD) Internal Medicine AAU/CHS
3 Ayele Belachew (MD) Public Health AAU/CHS
4 Jilcha Diribi (MD) Oncology AAU/CHS
5 Meskerem Aleka (MD) ENT AAU/CHS

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6 Muluken Goshime (MD) Ophthalmology AAU/CHS

7 Negussie Deyessa (MD) Public Health AAU/CHS
8 Solomon M.Abay (PhD) Pharmacology AAU/CHS
9 Workeabeba Abebe (MD) Infectious Disease AAU/CHS
10 Workie Temesgen (MD) Dermato-venerology AAU/CHS

V. Consultants
S.no Name (Alphabetically) Specialty Institutions

Addisu Melkie (MD) Internal medicine and TASH/CHS/AAU

1
Nephrology
Desalew Mekonnen (MD) Internal Medicine and TASH/CHS/AAU
2
Cardiology
Getachew Alemkere Clinical Pharmacy TASH/CHS/AAU
3

ACRONYMS
ACD: Allergic contact dermatitis
ACEIs:Angiotensin converting enzyme inhibitors
ACS: Acute Coronary Syndrome
ADL: Acute adenolymphangitis
ADRs: Adverse Drug Reactions
AFB: Acid fast Bacilli
AIVR: Accelerated Idioventricular Rhythm
AKI: Acute kidney Injury
ALF: Acute liver failure
ARBs: Angiotensin receptor blockers
ART: anti-retroviral therapy
AV: Atrio ventricular
BID: Twice a day
BMI: body mass index

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C/Is: Contraindications
CBC: Complete blood count
CDAD: Clostridium Difficille Associated Disease
CKD: Chronic kidney Injury
CL: Cutaneous leishmaniasis
CLL: Chronic lymphocytic leukemia
CML: Chronic Myelogenous Leukemia
CNS: Central nervous system
COPD: Chronic Obstructive Pulmonary Disease
CPR: Cardiopulmonary resuscitation
CRP: C-reactive protein
CSF: Cerebrospinal fluid
D/Is: Drug interactions
D/S: Dextrose in Saline solution
D/W: Dextrose in water solution
DBS: Dry Blood Spot
DEC: Diethylcarbamazine citrate
DKA Diabetic Ketoacidosis
DLA Dermatolymphangioadenitis
DMARD: Disease-modifying anti-rheumatic medicines
DST: Medicine Susceptibility Testing deep vein thrombosis,
DVT: deep venous thrombosis
ECG: electrocardiogram
ENL: Erythema Nodosum Leprosum
ENT: Ear, Nose and Throat
ESR erythrocyte sedimentation rate
ESRD: End Stage Renal Disease
FH: Fulminant hepatitis
FPG: Fasting plasma glucose
GDM: Gestational Diabetes Mellitus
GERD:Gastro Esophageal Reflux Disease
GFR: Glomerular Filtration rate
GI: Gastrointestinal
GTD: Gestational Trophblastic diseases
GTN: Gestational Trophoblastic Neoplasia
HDL: high-density lipoprotein cholesterol
HHS: Hyp: rglycemic Hyperosmolar State
Hrs: Hours

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ICD: Irritant Contact Dermatitis

IDU: Intravenous medicine use
IHCP: Intra-hepatic cholestasis pregnancy
IM: Intramuascular
IMU: Intravenous Medicine Use
IOP: Intra-ocular pressure
IRIS: Immune Reconstitution Immune Syndrome
ITP: Immune Thrombocytopenic Purpura
IU: International Unit
IUGR: Intrauterine growth restriction
IV: Intravenous
IVDA: intravenous medicine abuse endocarditic
LDL:low-density lipoprotein cholesterol
MAT: Multifocal Atrial Tachycardia
MDR: Multi Drug Resistance
MDT: Multi- Drug therapy
mL: Milliliter
MNT: Medical Nutrition Therapy
MOH: Ministry of Health
MOH: Ministry of Health of Ethiopia
MSH: Management Sciences for Health
N/S: Normal saline solution
NNRTI: Nucleoside Reverse Transcriptase Inhibitors
NRTIs: Nucleoside Reverse Transcriptase Inhibitors
NSVT: Non sustained ventricular tachycardia
NVE: native valve endocarditic
OGTT: Oral Glucose Tolerance Test
P.O : Per Os (mouth)
P/Cs: Precautions
PCP: Pneumocystis Carinni Pneumonia
PEP: Post-exposure prophylaxis
PI: Protease Inhibitors
PKDL: Post kala-azar Dermal Leishmaniasis
PMTCT: Prevention of mother-to-child transmission
PPH: Post-Partum Haemorrhage
PrEP:Pre-exposure prophylaxis
PRN: As required
PROM: Premature Rupture Of Membranes

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PSVT: Paroxysmal supra-ventricular tachycardia

PTE: Pulmonary thrombo-embolism
PTT: Placental trophoblastic tumour
PVE: Prosthetic Valve Endocarditits
QD: Once a day
QID: Four times a day
RA: Rheumatoid Arthritis
RBC: Reduction in red blood cell
RDT: Rapid Diagnostic Tests
RUTF: Ready to use therapeutic feeding
SBGM: Self-blood glucose monitoring
SBP: Prophylaxis for spontaneous bacterial peritonitis
SSIs: Surgical site infections
STG: Standard Treatment Guideline
STI: Sexually transmitted infections
TID: Three times a day
VT: Ventricular Tachycardia
VTE: Venous thromboembolism
WBC: White blood cell count
WPW: Wolff-Parkinson-White

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FORWARD
The Ethiopian Standard Treatment Guideline (STG) was first published in 2004 which is
recognized as the first edition. There were subsequent revisions then after. The current edition
is the fourth one. The reasons behind the revision of the STG are the dynamic nature of
medicine, change in diagnostic and therapeutic modalities, updates in health strategies and
policies as well as the advancement in Technology.
The current edition of the STG has 23 chapters. Four new chapters are added which was not
partially or completely addressed by the previous editions. These four chapters include
Antimicrobial resistance and its containment, Care of patients in Ambulatory and Hospitalized
settings, Oral and dental conditions, and Palliative care.
The antimicrobial resistance and its containment chapter is designed to address the alarmingly
increasing burden of antimicrobial resistance. It is enriched with national data revealing the
higher prevalence of antimicrobial resistance. The chapter is designed to introduce the WHO
AWaRe strategy of saving antimicrobial agents which are aligned with the Ethiopian Essential
Medicines List. The Ethiopian antimicrobial stewardship guideline is considered and
incorporated.
The care delivered to patients at the out-patient or hospitalized setting is not well structured in
Ethiopia. Such care ultimately has an impact on the quality of care delivered and treatment
outcome. The current edition of the STG addressed this new concept clearly and
understandably to the Ethiopian health workforce.
Dental and Oral Health in Ethiopia is at its infancy stage of integration to the other services. It
has been considered as a separate disciple and health care delivery settings were delivered
separately though patient needs are not designed in such a way. The current STG incorporated
this new concept to ensure continuity of service and better health care delivery.
As we move forward through evidence-based medicine with the support of science and
technology; early diagnosis and early treatment will improve survival. Early diagnosis might
bring non-curable health conditions as well as treatment-related survival will bring new health
related conditions which can not be avoided completely. Ultimately the quality of life will be
compromised with pain, hypoxia, insomnia, mental conditions, and other health needs that
palliative care can bring a difference. Through palliative care and the disciplines around, care
and treatment services will be complete. The current guideline included a chapter on palliative
care with is aligned with the national palliative care guideline as well as context.
The STG preparation process is well documented as a separate chapter to reveal the due
process that the revision process went though. Trust and credibility will be ensured as the
users of the guideline are plenty much behind.
The current fourth edition of STG is designed to be user-friendly that health care workers
(physicians, nurses, and pharmacists) can utilize in their work discipline to provide
comprehensive care to their patients. The guideline is also aligned with other program-related

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guidelines as well as clinical management guidelines in the country. Users of the guideline are
also forward their practical challenges to be included in the STG and were done accordingly.
Several stakeholders from different health-related disciplines (Policy makers, health leaders,
program leads, clinicians, health educators, professional societies, support staffs and partners)
are engaged in the due process of the preparation of the guideline. Several sessions of
consultation and discussion forums were conducted. Ideas, opinions, challenges,
opportunities, threats, possible solutions were forwarded. There is no conflict of interest.
The Federal Ministry of health and agencies in it (EFDA, EPSA, Ethiopian Health Insurance
agency) are working to consider the STG as a binding document for health service delivery in
Ethiopia. Patients will receive at least the minimum care at the STG. The STG will help to
secure the drugs and supplies in the health facilities to implement it which ultimately improve
health care delivery.
Proper implementation of the STG will induce accountability as well as trust to the health
facilities. It will help to implement health care financing, data quality, task sharing and
shifting as well as many more components of the WHO building blocks in health care.
Periodic monitoring and evaluation of STG implementation is mandatory for further
enrichment as health care is a dynamic process and change is always imminent. Further
revision should be based on the outputs of the monitoring and evaluation data.

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Table of Contents
ACKNOWLEDGMENTS _______________________________________________________ II
ACRONYMS _______________________________________________________________ VI
FORWARD _________________________________________________________________ X
THE STG REVISION PROCESS _________________________________________________ 32
CHAPTER 1: GOOD PRESCRIBING AND DISPENSING PRACTICES ______________________ 36
CHAPTER 2: ANTIMICROBIAL RESISTANCE AND ITS CONTAINMENT _____ 48
CHAPTER 3: CARE OF PATIENTS IN AMBULATORY AND HOSPITALIZED SETTING _________ 76

1. CLINICAL EVALUATION AND COMMUNICATION IN THE OUTPATIENT SETTING ______76

2. CHRONIC CARE MODEL: PROVISION OF CARE FOR CHRONIC DISEASES AND THE CHRONIC
CARE MODEL ____________________________________________________80

3. GENERAL CARE FOR HOSPITALIZED PATIENTS ___________________________82

3.1 Intravenous (IV) fluid therapy in adults ..................................................................................................82

3.2 Intravenous lines: Care and Complications ..............................................................................................91

3.3 Pressure (Bed sore) prevention and management ..................................................................................97

3.4 Stress ulcer prophylaxis and treatment ................................................................................................103

3.5 Hospital acquired infection prevention ..................................................................................................105

3.6 Surgical wound infection: prevention and management .......................................................................106

3.7 Urinary bladder catheter care ...............................................................................................................111

4. VENOUS THROMBOEMBOLIC DISEASE PREVENTION ______________________116

CHAPTER 4: CARDIOVASCULAR DISORDERS_____________________________________ 116

4.1. ARRHYTHMIAS _____________________________________________116

4.2. HEART FAILURE ____________________________________________125

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4.3. HYPERTENSION __________________________________________138

4.4. ATHEROSCLEROTIC CARDIOVASCULAR DISEASES ________________________148

4.5. RHEUMATIC HEART DISEASE ____________________________________158

4.6. VALVULAR HEART DISEASE _____________________________________160

4.7. INFECTIVE ENDOCARDITIS ______________________________________164

CHAPTER 5: ENDOCRINE DISORDERS __________________________________________ 169

1. DIABETES MELLITUS __________________________________________169

1.1 Treatment of Type-2 Diabetes Mellitus .................................................................................................172

1.2 Treatment of Type 1 Diabetes Mellitus..................................................................................................178

1.3 Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) ..........................................179

1.4 Hypoglycemia in Diabetes .....................................................................................................................182

1.5 Chronic complications of diabetes .........................................................................................................185

2. DYSLIPIDEMIA AND METABOLIC SYNDROME __________________________188

3. THYROID DISORDERS _________________________________________192

3.1 Goiter .....................................................................................................................................................192

3.2 Thyrotoxicosis ........................................................................................................................................195

3.3 Hypothyroidism......................................................................................................................................198

4. ADRENAL DISORDERS _________________________________________200

4.1 ADRENAL INSUFFICIENCY ________________________________________200

4.2 CUSHING'S SYNDROME _________________________________________203

5. MINERAL AND BONE DISORDERS__________________________________205

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5.1 Vitamin D deficiency in adults ...............................................................................................................205

5.2 Osteoporosis ..........................................................................................................................................207

CHAPTER 6: GASTROINTESTINAL TRACT AND HEPATOBILIARY DISEASES ______________ 211

1. DYSPEPSIA AND PEPTIC ULCER DISEASE _____________________________211

2. GASTROESOPHAGEAL REFLUX DISEASE (GERD) ________________________213

3. GASTROINTESTINAL BLEEDING ___________________________________216

3.1 Upper Gastrointestinal (GI) Bleeding .....................................................................................................216

3.2 Lower Gastrointestinal (GI) Bleeding .....................................................................................................221

4. NAUSEA AND VOMITING_______________________________________224

5. CHRONIC DIARRHEA IN ADULTS __________________________________229

6. CONSTIPATION _____________________________________________234

7. ANORECTAL DISORDERS _______________________________________235

7.1 Hemorrhoids ..........................................................................................................................................235

7.2 Anal fissure ............................................................................................................................................237

7.3 Perianal (Anorectal) abscess ..................................................................................................................239

8. HEPATITIS ________________________________________________241
8.1 Hepatitis B Virus infection .....................................................................................................................241

8.2 Hepatitis C virus infection ......................................................................................................................249

9. ACUTE LIVER FAILURE AND FULMINANT HEPATITIS _____________________251

10. LIVER CIRRHOSIS AND PORTAL HYPERTENSION _________________________252

11. CHOLELITHIASIS (GALL STONES) AND CHOLECYSTITIS ____________________254

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11. 1 Cholelithiasis (Gall stones) ..................................................................................................................254

11.2 Acute cholecystitis ...............................................................................................................................257

12. LIVER ABSCESS _____________________________________________260

12.1 Pyogenic liver abscess ..........................................................................................................................260

12.2 Amebic liver abscesses .........................................................................................................................262

13. ACUTE PANCREATITIS_________________________________________264

CHAPTER 7: HEMATOLOGIC DISORDERS _______________________________________ 266

1. ANEMIA ____________________________________________________266
1.1 Approach to adults with anemia ...........................................................................................................266

1.2 Iron deficiency anemia ...........................................................................................................................269

1.3 Megaloblastic anemia ...........................................................................................................................271

2. ERYTHROCYTOSIS (POLYCYTHEMIA) _______________________________274

3. THROMBOCYTOPENIA ________________________________________278
3.1 Thrombocytopenia in hospitalized patients...........................................................................................278

3.2 Immune Thrombocytopenia (ITP) ..........................................................................................................281

4. BLOOD TRANSFUSION AND TRANSFUSION REACTIONS ____________________284

FURTHER READING _______________________________________________285

5. VENOUS THROMBOEMBOLIC DISEASE (VTE) __________________________285

5.1 Venous thromboembolic disease (VTE) prophylaxis ..............................................................................285

5.2 Venous Thromboembolism (VTE) Disease: Deep vein thrombosis and pulmonary embolism ...............289

6. HEMATOLOGIC MALIGNANCIES __________________________________292

6.1 Acute Leukemia .....................................................................................................................................292

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6.2 CHRONIC LEUKEMIAS ___________________________________________294

6.2.1 Chronic Lymphatic Leukemia (CLL) .....................................................................................................294

6.2.2 Chronic Myelogenous Leukemia (CML) ...............................................................................................297

6.3 LYMPHOMAS ________________________________________________300

CHAPTER 8: INFECTIOUS DISEASE ____________________________________________ 304

1. ANTIMICROBIAL PROPHYLAXIS IN SURGERY ___________________________304

2. PRINCIPLES OF ANTIMICROBIAL REGIMEN SELECTION_____________________310

3. ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) ____________________317

a. Diagnosis and management of ARV nave patients .............................................................................317

b. Diagnosis and management of ARV failure ........................................................................................321

c. Monitoring ARV Treatment.................................................................................................................328

d. Post-exposure prophylaxis (PEP) and care ..........................................................................................337

e. Pre-Exposure prophylaxis (PrEP) .........................................................................................................340

f. Management of common co-infections of HIV ...................................................................................341

g. Screening for co-morbidities among HIV patients ..............................................................................373

4. ACUTE FEBRILE ILLNESSES ______________________________________374

4.1 Over view on acute febrile illnesses .......................................................................................................375

4.1 Malaria ..................................................................................................................................................377

4.2 Typhoid fever (Enteric fever) .................................................................................................................391

4.3 Typhus ...................................................................................................................................................394

4.4 Relapsing Fever .....................................................................................................................................397

4.5 Viral febrile illnesses ..............................................................................................................................399

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5. PULMONARY INFECTIONS ______________________________________410

5.1 Community Acquired Pneumonia (CAP) ................................................................................................410

5.2 Hospital-acquired and ventilator-associated Pneumonia......................................................................415

5.3 Empyema and complicated parapneumonic effusions ........................................................................419

5.4 Aspiration pneumonia and lung abscess ..............................................................................................422

6. MENINGITIS (ACUTE BACTERIAL MENINGITIS) ________________________426

7. INFECTIOUS DIARRHEAL DISEASE _________________________________432

7.1 Bloody diarrhea ..............................................................................................................................432

7.2 Watery diarrhea .............................................................................................................................434

8. PYOGENIC OSTEOMYELITIS _____________________________________441

9. SEPTIC ARTHRITIS ___________________________________________443

10. NEUTROPENIC FEVER ________________________________________445

11. SEPSIS AND SEPTIC SHOCK _____________________________________449

12. URINARY TRACT INFECTION _____________________________________454

13. INTESTINAL HELMINTHIC INFESTATIONS _____________________________458

14. BRUCELLOSIS ______________________________________________460

15. ANTHRAX ________________________________________________464

16. LEISHMANIASIS _____________________________________________467

16.1 Visceral Leishmaniasis (Kala azar).................................................................................................468

16.2 Cutaneous Leishmaniasis (Oriental leishmaniasis, Oriental Sore, Leishmaniasis Tropica) .............471

17. SCHISTSOMIASIS ____________________________________________474

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18. FILARIASIS, LYMPHATIC (ELEPHANTIASIS) ____________________________477

19. ONCHOCERCIASIS ___________________________________________480

20. RABIES __________________________________________________482

21. TETANUS _________________________________________________486

22. TUBERCULOSIS _____________________________________________489

22.1 Drug susceptible Tuberculosis ........................................................................................................489

22.2 Drug resistant TB ............................................................................................................................498

23. LEPROSY (HANSEN’S DISEASE) __________________________________506

CHAPTER 9: KIDNEY AND URINARY TRACT DISORDERS ____________________________ 513
CHAPTER 10: RHEUMATOLOGIC DISORDERS ____________________________________ 576

1. OVERVIEW ON CONNECTIVE TISSUE DISEASES _________________________576

2. GOUT ___________________________________________________578

3. OSTEOARTHRITIS ______________________________________________584

4. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) (LUPUS) ______________________588

5. RAYNAUD’S PHENOMENON _____________________________________591

6. RHEUMATOID ARTHRITIS (RA) __________________________________594

CHAPTER 11: NEUROLOGICAL DISORDERS______________________________________ 599

1. DEMENTIA ______________________________________________599

2. HEADACHE _____________________________________________603
2.1 Migraine Headache ..............................................................................................................................606

2.2 Tension type headache .........................................................................................................................610

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2.3 Medication overuse headache .......................................................................................................612

2.4 Cluster Headaches .........................................................................................................................614

3. MOVEMENT DISORDERS ___________________________________616

3.1 Overview of movement disorders ................................................................................................616

3.2 Essential Tremor ...........................................................................................................................618

3.2 Parkinson Disease ................................................................................................................................619

4. SEIZURE DISORDER AND EPILEPSY ___________________________622

4.1 Status epilepticus .................................................................................................................................627

5. CEREBROVASCULAR DISEASE (STROKE) ______________________627

5.1 Ischemic Stroke.....................................................................................................................................627

5.2 Hemorrhagic Stroke .............................................................................................................................632

5.3 Subarachnoid Hemorrhage ...............................................................................................................634

6. VERTIGO _______________________________________________635

7. GUILLAIN–BARRÉ SYNDROME (GBS) ________________________637

8. BELL‘S PALSY ___________________________________________638

9. LOW BACK PAIN ____________________________________________639

CHAPTER 12: ONCOLOGY ___________________________________________________ 641

1. Breast cancer ......................................................................................................................................641

2. Cervical cancer ....................................................................................................................................647

3. Colorectal cancer ................................................................................................................................650

4. Hepatocellular carcinoma ...................................................................................................................653

5. Prostate cancer ...................................................................................................................................656

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6. Ovarian cancer ....................................................................................................................................660

7. Head and neck cancer .........................................................................................................................664

CHAPTER 13: PSYCHIATRIC DISORDERS ________________________________________ 667

13.1. ANXIETY DISORDERS, PTSD AND OCD ____________________________667

13.2. DEPRESSIVE DISORDERS AND BIPOLAR SPECTRUM DISORDERS _______________669

I. Depressive disorders .................................................................................................................................669

II. Bipolar spectrum disorders ......................................................................................................................673

13.3. SCHIZOPHRENIA ____________________________________________676

13.4. SUICIDE/SELF-HARM _________________________________________682

13.5. DELIRIUM ________________________________________________684

13.6. SUBSTANCE RELATED DISORDERS _________________________________684

CHAPTER 14: RESPIRATORY DISORDERS _______________________________________ 688

14.1. COUGH __________________________________________________688

14.2. OBSTRUCTIVE LUNG DISEASES ___________________________________689

14.3. PNEUMONIA ______________________________________________709

14.4. BRONCHIECTASIS ___________________________________________709

CHAPTER 15: EMERGENCY CONDITIONS _______________________________________ 710

1. TRIAGE IN THE EMERGENCY DEPARTMENT ______________________________710

2. GENERAL APPROACHES TO EMERGENCIES ______________________________713

3. ACUTE RESPIRATORY FAILURE ______________________________________717

4. ALTERED MENTAL STATUS AND COMA _________________________________718

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5. ANAPHYLAXIS_________________________________________________720

6. SUDDEN CARDIAC ARREST _________________________________________722

7. HYPOGLYCEMIA _______________________________________________723

9. SHOCK _____________________________________________________724
9.1. Approach to shock ................................................................................................................................724

9.2. Cardiogenic shock (pump failure) .........................................................................................................725

9.3. Hypovolemic shock ...............................................................................................................................726

9.4. Septic shock. .........................................................................................................................................726

10. TRAUMA: GENERAL APPROACH TO TRAUMA PATIENTS _____________________727

11.POISONING AND OVERDOSE ______________________________________731

11.1 Approach to a patient with poisoning and toxidromes .......................................................................731

11.2 Specific poisons and overdoses ............................................................................................................736

12. ENVIRONMENTAL EMERGENCIES ___________________________________738

12.1. Burn ....................................................................................................................................................738

12.2. Mammalian and Human Bites ............................................................................................................742

3. Snake Bites...............................................................................................................................................744

12.4. Near Drowning ...................................................................................................................................747

CHAPTER 16: PEDIATRIC DISORDERS __________________________________________ 749

TREATMENT _________________________________________________768

OBJECTIVE __________________________________________________768

NON-PHARMACOLOGIC ________________________________________768

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PHARMACOLOGIC _____________________________________________768

CLINICAL FEATURES ___________________________________________773

DIAGNOSIS __________________________________________________773

TREATMENT _________________________________________________773
Etiology .......................................................................................................................................................776

Risk factors .................................................................................................................................................776

LABORATORY STUDIES _________________________________________776

MILD OR MODERATE __________________________________________807

SEVERE _____________________________________________________807

DIAGNOSIS: GUIDED BY HISTORY, PHYSICAL EXAMINATION FINDINGS AND THE

LIKELY DIFFERENTIAL DIAGNOSIS CONSIDERED ACCORDINGLY ___________822

TYPES ______________________________________________________823
Risk of iron deficiency ................................................................................................................................824

CLINICAL FEATURES ___________________________________________825

Pharmacologic ............................................................................................................................................828

- Early and ample hydration with intravenous isotonic saline is associated with a lower risk of
progression to oligoanuric hemolytic-uremic syndrome in patients with diarrhea .....................................828

CAUSE ______________________________________________________828

INDICATION OF BLOOD TRANSFUSION _____________________________830

COMPLICATIONS OF TRANSFUSION _______________________________830

Clinical features ..........................................................................................................................................831

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STG 4th Edition, draft 2020

Diagnosis.....................................................................................................................................................832

Laboratory tests...........................................................................................................................................834

No single laboratory test can confirm Henoch-Schonlein purpura, but certain tests can help rule out other
diseases and make a diagnosis of Henoch-Schonlein seem likely. They may include: ................................834

Imaging tests: rule out other causes of abdominal pain and to check for possible complications, such as a
bowel obstruction. .......................................................................................................................................834

DIAGNOSIS __________________________________________________835
O REPEAT GLUCOSE AND ELECTROLYTES ONE HOUR AFTER INSULIN AND IV FLUIDS
INITIATED. CONTINUE HOURLY GLUCOSE AND ELECTROLYTES UNTIL PATIENT IS READY FOR
DISCHARGE OR ADMISSION. ________________________________________________ 848
O FLUID/INSULIN _______________________________________________________ 848

Cautions and contraindications to physical restraint and emergency sedation: ......................................864

Emergency chemical restraint ....................................................................................................................864

Procedure ....................................................................................................................................................864

Complications of emergency restraint .......................................................................................................865

Complications of mechanical restraints .....................................................................................................865

Ongoing care ..............................................................................................................................................865

MAJOR DEPRESSIVE DISORDER __________________________________868

Causes and Risk Factors ............................................................................................................................872

Clinical features ..........................................................................................................................................873

References ...................................................................................................................................................873

Clinical features ..........................................................................................................................................892

Clinical features ..........................................................................................................................................892

COMPLICATIONS ______________________________________________898

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REFERENCES _________________________________________________898
CHAPTER 17: SEXUALLY TRANSMITTED INFECTIONS (STI): SYNDROMIC MANAGEMENT OF STI
_______________________________________________________________________ 907

URETHRAL DISCHARGE SYNDROME ____________________________________908

PERSISTENT/RECURRENT URETHRAL DISCHARGE ___________________________910

GENITAL ULCER SYNDROME (GUS) ____________________________________911

VAGINAL DISCHARGE _____________________________________________915

LOWER ABDOMINAL PAIN __________________________________________917

SCROTAL SWELLING ______________________________________________919

INGUINAL BUBO _________________________________________________921

BALANITIS/ BALANOPOSTHITIS (BAL) ___________________________________923

SYPHILIS SCREENING AND MANAGEMENT _________________________________927

GENITAL WARTS ________________________________________________932

GENITAL SCABIES ________________________________________________933

PEDICULOSIS PUBIS _______________________________________________934

PREVENTION OF STIS _____________________________________________935

FURTHER READING _______________________________________________936

CHAPTER 18: SKIN DISEASES ________________________________________________ 936

 GENERAL GUIDELINE FOR USE OF TOPICAL STEROIDS _____________________937

 DRY SKIN _________________________________________________938

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 DIAGNOSIS IS CLINICAL. ____________________________________________ 938

 TO HELP HEAL DRY SKIN, PREVENT ITS RETURN AND REDUCE
DISCOMFORT __________________________________________________________ 938
 AVOID EXCESSIVE BATHING ________________________________________ 938
 AVOID STRONG ALKALINE HARSH SOAPS ____________________________ 938
 LIBERAL APPLICATION OF EMOLLIENTS _____________________________ 938
 TOPICAL STEROIDS ARE NOT HELPFUL UNLESS THERE IS SEVERE
PRURITUS AND SEVERE INFLAMMATION. ________________________________ 938

 ITCHING _________________________________________________938

 ACNE VULGARIS ____________________________________________939

BACTERIAL INFECTIONS OF THE SKIN AND SOFT TISSUE ________________________940

Cellulitis and erysipelas ................................................................................................................................940

Carbuncles and Furuncles ............................................................................................................................941

CLINICAL FEATURES __________________________________________________ 942

Impetigo ......................................................................................................................................................942

Chronic lower limb ulcers .............................................................................................................................943

Necrotizing fasciitis and pyomyositis ...........................................................................................................944

 FUNGAL INFECTIONS OF THE SKIN _________________________________945

Candidiasis (Mucocutaneous Candidiasis) ...................................................................................................945

 CLINICAL FEATURES AND INVESTIGATIONS DEPEND ON EACH SPECIFIC

SITE. __________________________________________________________________ 945

Balanoposthitis ............................................................................................................................................945

Candidal Intertrigo.......................................................................................................................................946

Candidal paronychia ....................................................................................................................................946

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STG 4th Edition, draft 2020

Genital Candidiasis (Vulvovaginitis) ............................................................................................................947

Oral candidiasis (thrush) ..............................................................................................................................947

Dermatophytoses (ring wom) ......................................................................................................................947

Pityriasis Versicolor (PV) ..............................................................................................................................950

 EXO-PARASITIC INFESTATION ____________________________________951

lice: body and head lice ...............................................................................................................................951

scabies .........................................................................................................................................................952

 VIRAL SKIN DISORDERS ________________________________________953

Herpes Simplex (HS) .....................................................................................................................................953

herpes zoster ...............................................................................................................................................954

INVESTIGATIONS _____________________________________________________ 954

Molluscum Contagiosum .............................................................................................................................955

PHARMACOLOGIC ____________________________________________________ 955

Pityriasis rosea .............................................................................................................................................955

DRUG REACTIONS AND ALLERGIES ______________________________________956

Steven Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) ........................................................956

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) .............................................................958

SIGNS: _________________________________________________________________ 958

Erythema multiforme ..................................................................................................................................959

Urticaria and angioedema ...........................................................................................................................960

 ECZEMA _________________________________________________961
Atopic Dermatitis (AD) .................................................................................................................................961

INFANT ________________________________________________________________ 962

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CHILDREN: ____________________________________________________________ 962

Contact dermatitis .......................................................................................................................................963

Seborrhoeic dermatitis ................................................................................................................................965

 PSORIASIS ________________________________________________966

 VITILIGO _________________________________________________967
GOAL OF TREATMENT _________________________________________________ 968
CHAPTER 19: EYE DISEASES _________________________________________________ 968

MAJOR BLINDING EYE DISEASES ______________________________________968

Cataract .......................................................................................................................................................968

Glaucoma ....................................................................................................................................................969

Trachoma .....................................................................................................................................................971

RED EYES _____________________________________________________972

Red Eye with Significant/Severe Pain ..........................................................................................................973

Red eye without significant pain .................................................................................................................978

3. BLEPHARITIS _________________________________________________984
Staphylococcal (Ulcerative) Blepharitis .......................................................................................................984

CELLULITIS ____________________________________________________986
Preseptal Cellulitis .......................................................................................................................................986

Orbital Cellulitis ...........................................................................................................................................988

DACRYOADENITIS AND DACRYOCYSTITIS _________________________________989

Dacryoadenitis .............................................................................................................................................989

Dacryocystitis...............................................................................................................................................990

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SWELLING ON AND AROUND THE EYEBALL ________________________________991

Hordeolum ...................................................................................................................................................991

Meibomian cyst (Chalazion) ........................................................................................................................992

Pinguecula and Pterygium ...........................................................................................................................993

REFRACTIVE ERROR AND LOW VISION ___________________________________994

ANNEX: FORTIFICATION OF ANTIBIOTICS _________________________________996

CHAPTER 20: EAR, NOSE AND THROAT DISEASE _________________________________ 997

1. EAR CONDITIONS ______________________________________________997

1. 1. Acute Otitis Media ...............................................................................................................................997

1.2. Chronic Suppurative Otitis Media .......................................................................................................1000

1.3 Otitis Externa .......................................................................................................................................1001

1. 4 Cerumen (wax) impaction ...................................................................................................................1003

1.5. Foreign Bodies in The Ear ...................................................................................................................1003

1.6. Tinnitus ...............................................................................................................................................1004

2. NOSE AND PARA-NASAL SINUSES __________________________________ 1005

2.1 RhinoSinusitis .......................................................................................................................................1005

2.2. Epistaxis ..............................................................................................................................................1009

2.3. Foreign bodies in the nose ..................................................................................................................1010

2.4. Nasal bone fracture ............................................................................................................................1011

3. THROAT CONDITIONS _________________________________________ 1011

3.1 Acute Tonsillitis ....................................................................................................................................1011

3.2. Adenoid tonsillar hypertrophy ............................................................................................................1013

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STG 4th Edition, draft 2020

3.3. Acute Laryngitis ..................................................................................................................................1014

3.4. Foreign body in the throat ..................................................................................................................1014

4. SALIVARY GLAND CONDITIONS ____________________________________ 1015

4.1. Mumps (Epidemic Parotitis)................................................................................................................1015

4.2 Acute and non-chronic non-obstructive suppurative Sialadenitis .......................................................1016

Upper airway obstruction ..........................................................................................................................1016

CHAPTER 21: ORALFACIAL AND DENTAL CONDITIONS ___________________________ 1017

1. PERIODENTAL CONDITIONS ___________________________________ 1017

1.1 Gingivitis ..............................................................................................................................................1017

1.2 Periodontitis.........................................................................................................................................1019

1.3 Necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) ......................1020

2. DENTAL CARIES ___________________________________________ 1023

3. ODONTOGENIC AND NON-ODONTOGENIC OROFACIAL INFECTIONS__________ 1025

3.1 Periapical abscess ................................................................................................................................1025

3.2 Periodontal Abscess .............................................................................................................................1027

3.3 Pericoronitis .........................................................................................................................................1029

3.4 Ludwig’s Angina ...................................................................................................................................1031

3.5 Osteomyelitis of the jaw ......................................................................................................................1033

4. DENTINE HYPERSENSITIVITIES _________________________________ 1035

5. POST TOOTH EXTRACTION COMPLICATIONS_________________________ 1036

5.1 Post extraction bleeding ......................................................................................................................1036

5.2 Infected Socket ....................................................................................................................................1038

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5.3 Dry socket (Alveolar Osteitis) (AO).......................................................................................................1039

6. TOOTH ERUPTION, SHEDDING AND EDENTULOUSNESS _________________ 1040

6.1 Teeth Eruption disorders ......................................................................................................................1040

6.2 Shedding of Deciduous/Primary (Milk) Teeth ......................................................................................1040

6.3 Edentulousness ....................................................................................................................................1041

6.4 Malocclusions ......................................................................................................................................1041

7. ORAL MUCOSAL CONDITIONS _________________________________ 1041

7.1 Aphthous ulcers (Recurrent aphthous stomatitis, RAS) .......................................................................1041

7.2 Candidiasis, oropharyngeal (Thrush) ..................................................................................................1043

7.3 Herpes simplex gingivostomatitis ........................................................................................................1045

8. TRAUMATIC DENTAL INJURIES _________________________________ 1047

CHAPTER 22: OBSTETRICS, GYNAECOLOGY AND FAMILY PLANNING ________________ 1049
CHAPTER 23: PALLIATIVE CARE _____________________________________________ 1132

 ANTI-HISTAMINES ______________________________________ 1156

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The STG Revision process

The availability of multiple treatment options will put a great pressure on the healthcare
practitioners and increase healthcare costs and compromise the quality of care. The development,
on time revision and implementation of standard treatment guidelines (STGs) thus is a crucial
strategy for prioritizing and tailoring care to the local context, ensuring effective and safe use of
medicines, containing health care costs, and preventing antimicrobial resistance.
By providing specific and clear recommendations for each clinical condition management, STGs
promote an effective and economic use of medicines at different levels of health facilities.
Therefore, a given treatment guidelines should provide up-to-date information relevant to the
prevention, diagnosis and treatment of common health care problems in Ethiopia for the
provision of quality care to patients.
Based on this understanding the guideline was revised with the consideration of the following
basic components:
i) The disease/conditions to be covered to the Ethiopian context.
ii) Guideline category and level of application: health center, primary hospital and general
hospital level as per the Ethiopian healthcare system and pharmaceutical delivery context.
iii) Intended users of the guideline: the physicians, health officers, nurses, clinical pharmacists,
and other allied health personals.
iv) Guideline objective(s): focus on the inclusion of specific and tailored recommendations to
the particular level of the health care system.
v) Interventions and practice considerations: the following key practice areas were
specifically considered as a guiding scopes of the revision process for every healthcare problem
to be addressed:

Topic
Subtopics
Brief  Definition or simple description and/or classification and/or epidemiology
description and/or causes and/or risk factors
 Present based on relevance
 Incorporating local epidemiologic data (if available EDHS, meta-analysis,
national level (large scale) studies, Ethiopian WHO reports etc…are
preferred)
 Tailoring (for broader topics) to the points that will be addressed in the
consecutive diagnosis and treatment is required.
Clinical  Symptoms and/or
features:  Signs
Investigations  Most appropriate and practical investigations
and diagnosis  Diagrammatic illustrations if likely (if possible extend to include treatments

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for each algorithm point)

 Not to miss popular/confirmatory methods
Treatment  Goals of treatment
 Pharmacologic (most appropriate and practical once)
o Not to miss specific dose and administration points
o Not to miss discussing clinically significant side effects and there
management
o Will be good if special population considerations forwarded
o Based on AWaRe classification (only for antibiotics) and indicate
stewardship considerations as necessary (for infectious cases)
 Non pharmacologic (most appropriate and practical once)
 Additional considerations,
o Special population considerations
o Perioperative considerations
Prevention  As necessary
References  Relevant and/or most-up-to-date once
 Focus on local studies and resource
 Please do not hesitate to included important points if no reference

The STG The revision process passed through the following steps:
 Appointing a consultant by USAID MTaPS program
 Establishing of STG technical working group by MOH
 Establishing of STG steering committee by MOH,
 kickoff and successive supportive meetings among the MOH, MTaPS and consultants
 Preparing zero draft list by consultants
 Participating in the EEML consultative meetings and aligning with the EEML
 Refining and submitting the first draft to MTaPS and MOH
 Reviewing of final STG by specialists, experts and service delivery units. Subject area
experts from specialized centers across all corners of the country underwent a 16 days
extensive review of the document. The central core team selected by MOH with the
consultants facilitated the review process, collect comments forwarded and revise the
document.
 Finalization of the document and editorial work will be undertaken to produce a print ready
form for approval by the MoH leadership.
The STG was revised based on evidence-based approach with efforts of contextualization to the
local contexts. Accordingly, four new chapters were added upon consultant suggestion and
consensus to increase the total chapters‘ from 19 to 21 in the current version. In addition, new
addition, deletion, or change/modifications was made to the previous editions.

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The following four new chapters were included based on the current health care demand and
associated national strategic directions. Except the basics of AMR have been presented under the
first chapter of the previous revision, the rest three new chapters were not considered in the
previous revision.
1) Antimicrobial al resistance and containment (Included as Chapter 2 in the revised
content): The inclusion of containment strategies tailored to the health system level may help the
overall containment effort of the country and is in line with the current global demand.
2) Care of patients in ambulatory and hospitalized setting (Included as Chapter 3 in the
revised content): Despite the routine care issues are always there, it is largely overlooked in
terms of having shared modeling and provision of consistent standard and safe care.
3) Oral and dental conditions (Included as Chapter 20 in the revised content): Given the high
demand of dental care and the expansion of dental clinics in the country, it is indispensable to
include in the current revision.
4) Palliative care (Included as Chapter 23 in the revised content): The MOH had developed a
national palliative guideline (2016) to address increasing demand for the inclusion of the service
to the Ethiopian healthcare system and to meet the needs of people suffering from cancer and
other non-communicable conditions that require this specialized care. In line to this we included
it to acknowledge the demand.
Although major changes were made across all chapters, some topics were almost completely
rewritten as in the case of the pediatric disorders. Multiple new topics were introduced under the
Emergency conditions and neurologic disorders too. The modifications made can be stated in to
the following three themes 1) Introducing new topics (across almost all chapters), 2) removing
topics (done extremely rarely) and 3) moving topics form on chapter to the other mainly based
on consensus.
Despite different relevant and up-to-date scientific evidence were cited as indicated in each
specific section, the following national materials have been used as a source document while
revising the STG.
 Ethiopian Essential Medicine List (EEML-2020); Ministry of Health/Ethiopian Food and
Drug Administration, Addis Ababa, September 2020.
 Guideline for Diagnosis, Treatment and Prevention of Leishmaniasis in Ethiopia, 2nd edition
(June, 2013)
 National Comprehensive Guidelines for Clinical and Programmatic Management of Major
Non-Communicable Diseases (February, 2016)
 National palliative care Guideline, 2016
 National consolidated Guideline for comprehensive HIV prevention, care and treatment
(August, 2018)
 National Essential Medicine List (5th edition, 2020)
 National guideline for prevention and control of viral hepatitis (2016-2020)
 National guideline for TB, DR-TB and Leprosy in Ethiopia, 6th edition (August, 2018)

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 National Malaria Guideline (March, 2018)

 National viral hepatitis management guideline for Hepatitis C Virus (November, 2019)
 Standard Treatment Guidelines for General Hospitals, 3rd ed. Food, Medicine and Health
Care Administration and Control Authority, Addis Ababa, 2014
The support from FMOH and MSH, consultants working at academic institution with different
networks, different expert forums, and availability of program related diseases guidelines (HIV,
TB, Malaria, STI etc.) were the opportunities for the STG development. Coronavirus (COVID-
19) pandemic, internet interruption (in the month of July) and shortcomings for wider expert
engagement were some of the limitations in the revision process.
To this end, we want to highlight that this latest version of the STG will have paramount worth
to support the medical practice. Hence, shall be widely accessible in both electronic and printed
forms.
Note: The information presented in these guidelines conforms to the current medical,
nursing and pharmaceutical practice. Contributors and editors cannot be held responsible
for errors, individual responses to medicines and other consequences.

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Chapter 1: GOOD PRESCRIBING AND DISPENSING

PRACTICES
Prescription is the link between the prescriber, the pharmacist (or dispenser) and the patient.
It is important for the successful management of the presenting medical condition.
Prescribers fill the diagnosis or ICD code for proper communication with the dispenser and
choice of the medicine among the available generic options. Readers are kindly requested to
refer ―Ethiopian Medicines Good Prescribing Practices (GPP)‖ and Medicines Good
Dispensing Practice guideline/manual.

Rational use of medicines is a mechanism through which safe, effective and economic
medication is provided. It is promoted through the collaborative efforts of prescribers,
dispensers, patient and policymakers. Rational prescribing ensures adherence to treatment
and protects medicine consumers from unnecessary adverse medicine reactions. The
prescriber could be a physician, a nurse or health officer Or any health professional
authorized to prescribe. Rational dispensing, on the other hand, promotes the safe,
effective and economic use of medicines. The dispenser could be a pharmacist, and
pharmacy technician. Prior to prescribing or dispensing any Medicines, the prescriber or
dispenser should make sure that it is within his/her scope of practice.

Medicines should only be prescribed when necessary, and the benefit-risk ratio of
administering the medicine should always be considered prior to prescribing. Irrational
prescribing leads to ineffective, unsafe and uneconomical treatment. Thus it is very
important that steps are taken to promote rational medicine use in order to effectively
promote the health of the public especially given limited resources. One way of promoting
rational medicine use is through the development and use of standard treatment
guidelines.

Rational approaches to therapeutics requires careful evaluation of health problems and

selecting appropriate therapeutic strategies. Making the right diagnosis is the cornerstone for
choosing the right kinds of therapy. Based on the diagnosis, health workers may select more
than one treatment and the patient should agree with the selected treatment. The treatment
could be non-pharmacologic or pharmacologic. It is important to consider the total cost of
treatment in the selection process. The process should also consider efficacy, safety,
suitability and availability. Medicine treatment should be individualized to the needs of each
patient as much as possible. The concept of good clinical practice has to be incorporated
within rational prescribing.

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A major step towards rational use of medicines was taken in 1977, when WHO established the
first Model List of Essential Medicines to assist countries in formulating their own national lists.
Essential medicines are those that satisfy the priority health care needs of the population. Using
an essential medicine list (EML) makes medicine management easy; and prescribing and
dispensing are easier for professionals if they have to know about fewer essential items. This
current standard treatment guideline is used as a resource to prepare the updated national EML of
the country. EML should be regularly updated to consider the changes in need of the public at
different time. Public sector procurement and distribution of medicines should be limited
primarily to those medicines on the EML, and it must be ensured that only those health workers
approved to use certain medicines are supplied with them. Healthcare professionals are
recommended to refer the annexed EML for Ethiopia for further.
Prescription writing
A prescription is electronic or paper based therapeutic transaction between the
prescriber and dispenser. It is a written order by the prescriber to the dispenser on
how the medicine should be dispensed. It serves as a means of communication
among the prescriber, dispenser and medicine consumer, pertaining to treatment or
prophylaxis.
A prescription should be written on a blank standard prescription legibly and clearly
in ink and using generic names of the medicine(s). Some facilities may use electronic
system.

A prescription should contain:

Name, address, age, body weight of the medicine consumer and date of the
prescription;
 Diagnosis; Generic name, dosage form and strength and directions for use of the
medicines. The pharmaceutical form (for example ‗tablet‘, ‗oral solution‘, ‗eye
ointment‘, ‗cream‘) should also be stated.
 The strength of the drug should be stated in standard units using abbreviations that are
consistent with the Systéme Internationale (SI). ‗Microgram‘ and ‗nanogram‘ should
not, however, be abbreviated. Also, ‗units‘ should not be abbreviated. Avoid decimals
whenever possible. If unavoidable, a zero should be written in front of the decimal
point.
 Prescriber‘s name, signature and address.
 See Annex……. for Standard Prescription form Directions for medicine use

Directions specifying the route, dose and frequency should be clear and explicit; use of
phrases such as ‗take as directed‘ or ‗take as before‘ should be avoided. For preparations
which are to be taken on an ‗as required‘ basis, the minimum dose interval should be stated
together with, where relevant, the maximum daily dose. It is good practice to qualify such

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prescriptions with the purpose of the medication (for example ‗every 6 hours as required for
pain‘, ‗at night as required to sleep‘). It is good practice to explain the directions to the
patient; these directions will then be reinforced by the label on the medicinal product and
possibly by appropriate counseling by the dispenser. It may be worthwhile giving a written
note for complicated regimens although it must be borne in mind that the patient may lose
the separate note.

Good Dispensing Practice

Good dispensing practices ensure that the correct medicine is delivered to the right patient, in
the required dosage and quantities, with clear information, and in package that maintains an
acceptable potency and quality of the medicine. Dispensing includes all the activities that occur
between the times the prescription or oral request of the patient or care provider is presented
and the medicine is issued. This process may take place in health institutions or community
drug retail outlets. It is often carried out by pharmacy professionals. No matter where
dispensing takes place or who does it, any error or failure in the dispensing process can
seriously affect the care of the patient mainly with health and economic consequences.
Therefore, the dispenser plays a crucial role in the therapeutic process. The quality of
dispensing may be determined by the training and supervision the dispenser has received.
During medicines dispensing and counseling the information mentioned under prescribing
above, the ―Medicines Good Dispensing Practices‖ manual 2012 edition and also medicines
dispensing and counseling guides including the Ethiopian Hospital Services Transformation
Guideline (Pharmacy Service) 2017are good resources to use. Finally, an application of the
professional code of ethics by pharmacy professionals is an important issue that needs due
consideration particularly with respect to confidentiality of patient data, withholding therapeutic
interventions and varying cost of drug.

Patient adherence

Patient compliance is the extent to which the patient follows the prescribed medicine
regime, while adherence is participation of patients in their care plan resulting in
understanding, consent and partnership with the provider. There are different factors
which contribute to patients‘ non-adherence. These factors include:
 Nature of treatment, which in turn depends on:
o the complexity of the regime (increases with the frequency of administration and number
of medicines prescribed)
o adverse effects
 Characteristics of the patient, such as:
o forgetfulness about taking the medication

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o inability to finish as they feel better

o lack of understanding the prescription
o fear of dependence
o social or physical problems to go to pharmacies
o inability to pay prescription charges
o inconvenience of taking medicines everyday
 Type of illness, like schizophrenia
 The health care system (long waiting times, uncaring staff, uncomfortable
environment, exhausted medicine supply, inaccessibility of health institutions)
 Behaviour of prescribers and dispensers:
o not able to gain confidence from patients
o irrational prescribing and dispensing
o giving inadequate information on the treatment
o poor attitude towards patients
o negligence
o poor perception to teamwork
o absence or ineffective care plan
Patient adherence can be improved by supervising medicine administration; simplifying the
therapeutic regime; educating patients on the importance of adhering to the prescribed
medication and improving the attitudes of prescribers.

Adverse drugs/ medicine reactions

Adverse drugs/ medicine reactions (ADRs) are unwanted effects that occur at certain
therapeutic doses. ADRs is a response to a medicine which is noxious and unintended,
and which occurs at doses normally used in man for the prophylaxis, diagnosis, or
therapy of disease, or for the modification of physiological functions. They could be
mild (where no intervention is required), moderate (where switching to another medicine is
necessary), severe (where an antidote should be employed to alleviate the situation), or lethal.
They could also be predictable (extensions of pharmacological effects) or unpredictable
(bizarre reactions which are not expected in all patients taking the medicine, such as
hypersensitivity and idiosyncratic reactions). ADRs are different from toxic reactions for the
latter occur at doses higher than therapeutics. They are also different from side effects as this
is a broader concept, i.e., including both beneficial and all unwanted effects which may not
necessarily be noxious. The two extreme age groups, i.e., pediatric and geriatric patients, are
more susceptible to ADRs due to physiological and pathological factors. Special precaution
should be taken for coexisting illnesses, such as kidney and liver diseases, as they could
contribute to ADRs. Readers are recommended to refer Ethiopian Guideline for Adverse Drug
Events Monitoring (2014).

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Monitoring ADRs
Pre-marketing clinical trials cannot be exhaustive as far as detection of all ADRs is concerned
due to:
 Recruitment of small populations (often < 2500 patients)
 Low chance of low incidence reactions being picked up before marketing
 Shorter duration of assessment
 Exclusion of patients who may take the medicine post-marketing

Only the most common ADRs could be detected during pre-marketing trials. It is therefore,
important to devise methods for quickly detecting ADRs. This could be carried out by post-
marketing surveillance, i.e., ADR monitoring. All health professionals have the responsibility
to report any observed unique adverse reactions from drugs, vaccines or traditional herbal
medicine products to Ethiopian Food and Drug Authority (EFDA).
e-Reporting system available at EFDA website (https://primaryreporting.who-
umc.org/Reporting/Reporter?OrganizationID=ET).
Drug/ Medicine Interactions

Drug/medicines interaction is alteration of the response to drugs upon the concurrent

administration of other drugs. The interaction includes a reaction between two (or more) drugs
or between a drug and a food, drinks, or supplement/herbs. Taking a drug while having certain
medical conditions can also cause a drug interaction. Although some medicine interactions
could be beneficial, most are harmful. Hence, it is always important to note the possible
medicine interactions prior to concomitant medicine/food or drink administration.
Drug/ Medicine interactions could occur at different levels, including:
 Pharmaceutics, which are physicochemical interactions in an IV infusion or in the same
solution;
 Pharmacokinetics, which may take place at the level of absorption, distribution,
biotransformation or excretion;
 Pharmacodynamics, which could occur directly at receptor level, or indirectly, where a
medicine alters the response to another medicine for example by eliciting opposite
physiological effect.
Drug/Medicine interactions could be additive (the effect is simple algebraic sum), synergism
(the total effect is more than the algebraic sum), potentiation (the effect of one medicine
increases by the presence of another medicine or food), or antagonism (the effect of the
agonist is blocked by the antagonist when given together). Medicine interactions are some of
the most common causes of adverse reactions. As medicine reactions could also occur
between a medicine and food or a medicine and drink. The healthcare provider should
always inform patients the type of food or drink which they have to avoid or are
recommended to have while taking the medicine.

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Medicines should not be added to blood, amino acid solutions or fat emulsions. Some
medicines, when added to IV fluids, may be inactivated due to changes in pH, precipitate
formation or chemical reactions. For example, benzylepenicillin and ampicillin lose potency
after 6-8 hours if added to dextrose solutions, due to the acidity of the solutions. Some
medicines, such as diazepam and insulin, bind to plastic containers and tubing.
Aminoglycosides are incompatible with penicillins and heparin. Hydrocortisone is incompatible
with heparin, tetracycline and chloramphenicol.
Prescribing for special populations:
Pharmacotherapy of special groups like pregnant women, children, the elderly and others
require consideration of the differences in pharmacokinetics and pharmacodynamics that can
significantly affect the safety and efficacy of drugs used in these special populations. Moreover,
most randomized controlled clinical trials exclude these groups, which makes it difficult for the
health professional to make evidence-based decisions regarding appropriate drugs and dosing
regimens to use in these patients. Health professionals are recommended to consider the
physiological and pathological conditions that affect treatment outcomes in special populations.

Prescribing for pregnant women

Pharmacokinetics of a medicine is altered during pregnancy: the rate of absorption
decreases, while volume of distribution, metabolism and glomerular filtration rate increase.
These phenomena may alter the serum drug level and seen by changes on required response.
The embryonic period, where, organogesis takes place, is the most susceptible period to
medicine effects. Administration of medicines, except those proved safe, in the first trimester,
is therefore not generally recommended. It is advisable not to prescribe any medicine
during any stage of pregnancy if possible. This, however, should not preclude the
importance of prescribing in life-threatening conditions of the mother. Prior to prescribing any
medicine for pregnant women, the benefit risk ratio of prescribing should be considered.
Readers are recommended to refer the National Medicines Formulary and Pregnancy
Category Guides to select appropriate medicines during pregnancy.

Prescribing for breast feeding women

Most medicines administered are detectable in breast milk. The concentration, however, is
low. If the woman has to take a relatively safe medicine, she should do so optimally 30-60
minutes after breast feeding and 3-4 hours before the next feeding in order to allow time for
medicines to be cleared from the blood, and concentration in the breast milk is relatively low.
Medicines for which no safety data are available during lactation should be avoided, or breast
feeding discontinued while they are administered. Most antibiotics taken by breast feeding
mothers can be detected in breast milk. e.g., tetracycline and chloramphenichol. Similarly,
isoniazid, sedative hypnotics and opioids enter breast milk sufficient to produce a
pharmacologic effect in infants.. Antineoplastic medicines are contraindicated in breast

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feeding.

Prescribing for infants/children

Physiologic processes that influence medicine kinetics in infants change significantly in the
first year of life, especially the first few months, while there is not much difference in the
dynamics. All the four processes of pharmacokinetics are, therefore, affect infants/children.
Gastric acid secretion begins soon after birth and increases gradually over several hours in full
term infants. In premature infants, however, secretion is slower, with the highest
concentration occurring on the fourth day. So medicines, which are partially or totally
inactivated by the low pH of gastric content should not be administered orally. Gastrointestinal
enzymes are lower in neonates than in adults. Neonates have less bile acids such that lipid
soluble medicines is absorbed less. Gastric emptying time is prolonged in the first day.
Thus, medicines that are absorbed primarily in the stomach may be more fully absorbed.
For medicines absorbed in the small intestine, therapeutic effects may be delayed. Peristalsis
in neonates is slow. More medicines, therefore, will get absorbed from the small intestine. The
volume of distribution is low in children, and medicine metabolizing enzymes are not well
developed. The glomerular filtration rate is slower than in adults (30-40%), such that the
clearance of medicines is slower in children than in adults. This definitely demands dose
adjustment for these age groups.

Dose adjustment in pediatrics

The most reliable pediatric doses are those given by the manufacturer. If no such information
is given, the dose can be calculated using formulae based on age, weight or surface area.
Calculations of doses based on age or weight are conservative and tend to underestimate the
required dose. Doses based on surface area are more likely to be correct, which makes it the
common approach used for dose estimation of cytotoxic chemotherapeutic agents. Pediatric
doses can be calculated as follows:
Dose calculations based on age:

Dose = adult dose*(age in years/(age+12)) Dose calculations based on weight:Dose = adult

dose*(weight in kg/70)
Dose calculations based on surface area:
[ ] [ ]
[ ]

Prescribing for elderly patients

There is no major alteration in medicine absorption in elderly patients. However, conditions
associated with age may alter the rate of absorption of some medicines. Such conditions
include altered nutritional habits; alteration in gastric emptying (which is often slower); and

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the concurrent administration of other medicines affecting pH and motility of the gut. Aged
people have reduced lean body mass, reduced body water and an increase in fat as a
percentage of body mass. There is a decrease in serum albumin, and the ratio of bound to free
medicine is significantly changed. Capacity of liver to metabolize drugs declines with age for
some drugs. Phase I reactions carried out by microsomal P450 systems are affected more in
elderly patients than phase II reactions. There is a decline with age of the liver‘s ability to
recover from injury. Diseases that affect hepatic function like congestive cardiac failure and
nutritional deficiencies are more common in the elderly. Creatinine clearance declines in the
elderly leading to marked prolongation of the half life of medicines excreted by kidney. The
increased incidence of active pulmonary disease in the elderly could compromise medicine
elimination through exhalation.
There is also a change in the sensitivities of receptors to medicines in elderly people. The
quality and quantity of life for elderly patients can be improved through the careful use of
medicines. Adherence to the doses is absolutely required in these patients. Unfortunately
patient nonadherence in the elderly is common because of forgetfulness, confusion, deliberate
underdosing or overdosing and physical disabilities.

Prescribing in renal failure

Many medicines are excreted through the kidneys and impairment of renal function alters the
excretion of these medicines, resulting in renal as well as non-renal toxicity unless doses are
adjusted accordingly. There are two principal pathways for medicine excretion by the kidneys;
glomerular filtration and tubular excretion. Glomerular filtration plays a major role in the
excretion of small, non-protein bound molecules whereas protein bound molecules that are
excreted in urine are eliminated by secretion into the proximal tubules.
For dose adjustment in renal failure it may occasionally be necessary to measure medicine
levels and adjust doses accordingly, but generally, doses are adjusted on the basis of the
estimated glomerular filtration rate (GFR). Among the various formulae used to estimate the
GFR from the serum creatinine, the Cockcroft- Gault (CG) formula is the easiest to use
(although not the most accurate) to adjust doses of medications that are eliminated by the
kidneys. The GFR in the CG formula is calculated as follows:
[ ] [ ]
[ ]
The value is multiplied by 0.85 in women to account for smaller muscle mass.

Factors that potentiate renal dysfunction and contribute to the nephrotoxic potential of renally
excreted medicines include: i) intravascular volume depletion either due to external losses or
fluid sequestration (as in ascites or edema) and ii)concomitant use of 2 or more nephrotoxic
agents e.g. Nonsteroidal anti-inflammatory agents, aminoglycosides, radio contrast agents. To
avoid worsening renal dysfunction in the presence of renal impairment:

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 Avoid potentially nephrotoxic medicines and use alternative medicines that are excreted
through other routes (Medicine formularies and text books tabulate drugs to be avoided or
used with caution in patients with renal failure);
 If there are no alternatives, calculate the GFR and adjust the dose on the basis of the
estimated GFR (many textbooks, formularies have tables showing dose adjustment on the
basis of estimated GFR). Dose adjustment may be accomplished in three different ways: i)
decreasing each individual dose and maintaining the same dose frequency; ii) maintaining
the same individual dose but administering each dose less frequently; and iii) modifying
both individual doses and the frequency of administration, which is a combination method;
 Avoid concomitant use of two or more potentially nephrotoxic agents;
 Insure that the patient is adequately hydrated;
 If the patient is on dialysis check if the medicine is eliminated by the specific dialysis
modality and consider administering a supplemental dose at the end of the dialysis session;
 Serially monitor kidney function.
Prescribing in liver disease

The liver is a site for the metabolism and elimination of many medicines but it is only with
severe liver disease that changes in medicine metabolism occur. Unfortunately, routine
determination of liver enzymes and other tests of liver function cannot predict the extent to
which the metabolism of a certain medicine may be impaired in an individual patient.
In general terms medicine prescription should be kept to a minimum in all patients with
severe liver disease as it may alter the response to medicines in several ways. Major problems
occur in patients with advanced liver disease who have ascites, jaundice or hepatic
encephalopathy:
 The hypoproteinemia in patients with severe liver disease is associated with reduced
protein binding and increased toxicity when highly protein bound medicines are used.
 One must exercise caution in the use of some medicines like sedatives, opioids and
diuretics which may precipitate hepatic encephalopathy in patients with advanced liver
disease.
It is always advisable to consult tables in standard textbooks or medicine formularies before
prescribing medicines for patients with severe liver disease.

Prescribing and Pain Management in Palliative Care

Palliative care is the active total care of patients whose disease is not responsive to curative
treatment. Focus lies in four main domains: 1) control of pain and other physical symptoms;
2) mental or psychological symptoms; 3) social needs; and 4) spiritual needs. This requires
careful assessment of the symptoms and needs of the patient by a multidisciplinary team. The
family should be included in the care of terminally ill patients.
The number of medicines should be as few as possible. Oral medications are usually

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satisfactory unless there is severe nausea and vomiting, dysphagia, weakness, or coma, in
which case parenteral medications may be necessary. The most common medicine classes
used in palliative care are strong opioids, nonopioids, corticosteroids, laxatives, antiemetics,
gastric protection agents, neuroleptics, sedatives/anxiolytics, antidepressants and diuretics.
Interventions for pain must be tailored to each individual with the goal of preempting chronic
pain and relieving breakthrough pain. Pain relief in palliative care may require
nonpharmacologic interventions such as radiotherapy or neurosurgical procedures such as
peripheral nerve blocks. Pharmacologic interventions follow the World Health Organization
three-step approach involving nonopiod analgesics, mild opioids and strong opioids with or
without adjuvants. The pain management ladder guide suggests pain management based on
pain severity. The concept of a ladder easily explains the need for pain assessment and for
appropriate management of pain based on a pain severity assessment.
Analgesics are more effective in preventing pain than in relieving established pain; it is
important that they are given regularly. Nonopioid analgesics, especially nonsteroidal anti-
inflammatory medicines, are the initial management for mild pain. Ibuprofen, up to
1600mg/day, has minimal risk of gastrointestinal bleeding and renal impairment and is a good
initial choice. If nonopioid analgesics are insufficient, then weak opioids such as c odeine
should be used. However, if weak opioids are escalated but fail to relieve pain, then strong
opioids such as morphine should be used. When using opioids, start with short acting
formulations and once pain relief is obtained, switch to extended release preparations. Opioids
have no ceiling dose. The appropriate dose is one required to achieve pain relief and
tolerated by the patient. When using opioids, side effects like constipation, nausea and
vomiting have to be anticipated and treated preemptively.
Constipation is another physical symptom that may require pharmacologic management and
one may use stimulant laxatives such as bisacodyl or osmotic laxatives, such as lactulose or
magnesium hydroxide. Similarly, patients may need to be treated with antiemtic medicines to
control the nausea and vomiting due to opioids.

General guidelines for use of topical steroids

 Absorption steroids from the skin depends on the sites (high at axilla, face and scalp;
medium at limbs and trunk; and low at palm, elbow and knee) and nature of lesion (high in
exfoliative dermatitis and low in hyperkeratinised skin)
 Potent preparations should be avoided at highly absorption sites and on acute lesions.
They may, however, be used for chronic lesions.
 Lotions/creams are better for exudative lesions as they allow evaporation, have cooling,
drying and antipruritic effects
 Sprays and gels are good for hairy regions
 Ointments from occlusive film and are good for chronic scaly conditions
 Occlusive dressing enhances steroid absorption, retains moisture and results in maceration

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of horny layer
 Absorption is greater in pediatric patients, hence milder preparations should be used
 Do not use potent and high strength steroids routinely
 Potent and high strength preparations should be restricted for short term use only
 Sudden withdrawal should be avoided
 Upon improvement, milder preparations should be substituted
 Twice a day application is enough: do not exceed three times a day

Narcotic and psychotropic drugs: controlled substances

Prescribing a medicine that is liable to abuse requires special attention and may be subject
to specific legal requirements. Authorized health workers must use these medicines
responsibly. The strength, directions and quantity of the controlled substance to be dispensed
should be stated clearly. Required details must be filled in the special prescription form
carefully to avoid alteration and abuse. Readers are recommended to refer the National List of
Psychotropic Substances and Narcotic drugs (2017) that contains the list of psychotropic
substance and narcotic drugs under national control to assist health professional in promoting
rational drug use of psychotropic substance and narcotic drugs.

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Annex: Standard prescription form

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STG 4th Edition, draft 2020

Chapter 2: ANTIMICROBIAL RESISTANCE AND ITS

CONTAINMENT
Overview of antimicrobial resistance (AMR)
Infectious diseases are those which are caused by microorganisms like bacteria, protozoa,
viruses and fungi. These diseases are threats to all societies irrespective of age, gender,
ethnicity, education and socioeconomic status. Unexpected outbreaks of infectious disease can
occur at any time and at any place resulting in high morbidity and mortality. Their treatment
imposes a huge financial burden to societies, especially developing ones. On top of these
problems, antimicrobial resistance (AMR) can easily emerge through microorganisms in
medicines used for the treatment of infectious diseases, known as antimicrobials. AMR is the
ability of microorganisms to survive and/or multiply in the presence of tolerable doses of
antimicrobial medicines. AMR may be natural when it occurs spontaneously as a result of gene
mutation, or may be acquired due to inappropriate exposure to antimicrobials.
There are different definitions used to describe various forms of AMR. These include:
 Multidrug resistant (MDR) was defined as acquired non-susceptibility to at least one agent in
three or more antimicrobial categories,
 Extensively drug resistant (XDR) was defined as non-susceptibility to at least one agent in all
but two or fewer antimicrobial categories (i.e. bacterial isolates remain susceptible to only
one or two categories)
 Pan-drug resistant (PDR) was defined as non-susceptibility to all agents in all antimicrobial
categories,
 Cross-resistance refers occurs of resistance among other (different) antimicrobials as a
result of exposure to a similarly acting antimicrobial
 Co-resistance refers to resistance to more than one class of antibiotics in the same bacterial
strain as might occur on a plasmid.

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Factors which contribute to antimicrobial resistance

Antimicrobials are the most misused medicines in many developing countries like Ethiopia.
They are available not only over the counter (OTC) in pharmacies but also in open markets.
Studies indicate the most common medicines used for self-medication are antibacterials. There
are a number of factors responsible for resistance to emergence. Some of them include:
 Poor infection prevention and control; poor waste management (environment contamination
with antimicrobials)
 Irrational prescribing, Irrational dispensing and irrational use (non-compliance, self-
medication, sharing)
 Irrational use of antimicrobials in agriculture (animal feeds, crop production). Currently,
antimicrobials are irrationally used for the treatment of zoonosis, prophylaxis and growth
promotion of food for animals.

Mechanisms for antimicrobial resistance

There are several mechanisms by which microorganisms develop AMR. These include:
1. Inability of antimicrobials to concentrate on their targets by a) Denying access to their sites of
action, e.g., Resistance to cephalosporins; b) Increasing their efflux e.g., Resistance to
tetracycline.
2. Inactivation of antimicrobials through a) Production of degrading enzymes like β lactamases
which hydrolyze β lactams, e.g. resistance to penicillins; and medicine biotransforming
enzymes, e.g., resistance to chloramphenicol; b) Inducing bacterial failure to convert a pro-
medicine to active metabolites, e.g., resistance to INH.
3. Alteration of targets, due to: a) Target modification, e.g., macrolide resistance; b) Substitution
with a resistant target to the native agent e.g., methicillin resistance; c) Use of alternate
metabolic pathways, e.g., sulfonamides resistance; d) Mutation of the natural target, e.g.,
fluoroquinolone resistance.

Threats of antimicrobial resistance

Many important medicine options for the treatment of common infectious diseases are becoming
limited, expensive or cease to exist. Today, nearly all Staphylococcus aureus strains are resistant
to penicillin. Resistance to methicillin and also vancomycin is also increasingly observed. If it is
not possible to limit emergence and/or spread of AMR, infections may become untreatable.
AMR has several economic and health impacts. They cause prolonged illness, absence from
work and reduced productivity. AMR can also contribute towards longer hospital stay which
increases cost. AMR prolongs the period of infectiousness resulting in spread of infection,
ultimately impacting mortality rates.
AMR in Ethiopia
Ethiopia published the first AMR baseline surveillance in 2009 (http://www.fmhaca.gov.et/wp-

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content/uploads/2019/03/AMR_Baseline_Survey.pdf). The data was generated form routine

surveillance of public hospitals carried from 1996 to 2000. A total of 52, 682 culture records
were retrospectively reviewed, of which 18, 466 have growth and sensitivity tests done and were
included in the analysis. Although, the collected data suffer from a small number of isolate in
majority of case, considerable degree of resistance to commonly used first line antibacterials
over the five year period was observed as shown below.
Pathogen Increase in resistance from 1996 to 200 Resistance data from
systematic reviews discussed
below
Coagulase Erythromycin resistance 21.6% in 1996 Erythromycin: 37% (95% CI:
negative to 51.9% in 2000 21, 55%)
staphylococcus
Streptococcus Erythromycin resistance from 0% in 1996
pneumonia to 18.2% in 2000
chloramphenicol resistance 0% in 1996 to
17.4 % in 2000
Salmonella Cotrimoxazole resistance 33.3% in 1997 Cotrimoxazole: 68.01%
species to 62.5% in 2000
Staphylococcus methicillin resistance 87.5% in 1996 to
aureus 100% in 2000
Shigella spp. Over all chloramphenicol resistance Chloramphenicol; 47.6 (39.9–
31.8% 55.5)
Over all cotrimoxazole resistance 43.8% Cotrimoxazole: 59.4 (49.3–
68.8)
Over all ampicillin resistance 81% Ampicillin: 83.1 (75.7–88.6)
Over all Tetracycline resistance 89.5% Tetracycline:86.1 (82.5–89.6)
Coagulase negative staphylococcus (CoNS)
Based on 2018 systematic review, Coagulase negative staphylococcus (CoNS) resistance to
vancomycin (9.11%[95% CI: 0, 35%]), clindamycin (11% [95% CI: 2, 27%]) and ciprofloxacin
(14%[95% CI: 6, 22%]) relatively lower than all other agents like penicillin‘s (including amino
and anti-staphylococcus penicillin‘s), cephalosporin‘s, tetracycline‘s, macrolides,
chloramphenicol, and cotrimoxazole (https://pubmed.ncbi.nlm.nih.gov/29801462/).
Salmonella species
The 2014 Salmonella systematic review reported a progressive increase in the odds of multi-drug
resistant isolates in the early 2000s as compared to the late 1990s (OR =18.86, 95% CI = 13.08,
27.19). Among the tested drugs, resistance was low for ciprofloxacin (3.61%). The pooled
proportions of ampicillin, co-trimoxazole, chloramphenicol, and multi-drug resistant isolates in
the 2000s were 86.01%, 68.01%, 62.08%, and 79.56% respectively.
(https://pubmed.ncbi.nlm.nih.gov/25213011/).

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Shigella species
A systematic review and meta-analysis of 25 studies (published form 1999 to 2018) that assessed
stool samples of 8521 patients (including community cases) was published in 2019. The pooled
prevalence of Shigella species was 6.6% (95% CI 4.7-8.8)
(https://pubmed.ncbi.nlm.nih.gov/31288806/), i.e 8.5%, 95% CI (6.2-11.5) among patients in
Health facility and 1.6%, (95% CI 0.8-3.4) in Community based studies. Shigella species were
highly resistant (>80% for each) for Tetracycline, ampicillin, amoxicillin and erythromycin (see
some of the figures in the right column of above table). The MDR rate is 83.2% (95% CI 77.1-
87.9). On the other hand, <10% resistance was reported for each ciprofloxacin, ceftriaxone, and
norfloxacin. Resistance to aminoglycosides is between 10 to 20%. Subgroup analyses indicated
that study years were associated with a decreasing Shigella prevalence over time (p = 0.002).
Escherichia coli
Based on 2018 systematic review of 35 studies (most of the studies utilized specimens for
screening particularly with multisite swabbing), E. coli antibacterial resistance was 45.38% (95%
CI: 33.50 to 57.27). Greater than 50% resistance was noted for aminopencillins (>80% R),
cotrimoxazole, tetracycline, Erythromycin and cephalexin. Resistance to fluoroquinolones, third
generation cephalosporin‘s and aminoglycosides was less than 50% (but >20%). The only agent
showed < 20% was nitrofurantoin (https://pubmed.ncbi.nlm.nih.gov/29854757/). Similarly,
24.3% fluoroquinolone resistance was observed for E.coli in a review published in 2018
(https://pubmed.ncbi.nlm.nih.gov/30541613/). This study also reported high fluoroquinolone
resistance for Neisseria gonorrhea (48.1%) and Klebsiella pneumonia (23.2%). All these are an
alarmingly report that loom out the traditional empiric decision. Hence, infection prevention
measures will be crucial (see additional details about ESBL-producing grave pathogens like
E.coli below).
Magnitude of multidrug resistant infections in Ethiopia
Recent systematic review and meta-analysis were conducted for different grave infections like
Extended-spectrum beta-lactamase (ESBL)-producing gram negative bacteria, Vancomycin
resistance enterococci (VRE), Methicillin resistant Staphylococcus aureus (MRSA) and
multidrug resistant tuberculosis (MDR TB). All the pooled estimates were based on highly
heterogeneous data. The data of the majority of these reviews were generated form in-patients
and high level hospitals and research laboratories (See table below) and need to be interpreted
cautiously for the settings where this guideline is intended to be used. In addition, data from
emerging regions were largely missed. Hospital with microbiology laboratories should better
relay on their setting specific surveillance data. Future national or regional (especially
community based is lacking) surveillance should be carried for a better decision.
Extended-spectrum beta-lactamase-producing gram-negative organisms
A 2020 systematic review and meta-analysis of 14 studies assessed 1649 Gram-negative bacteria
isolated from 5191 clinical samples for ESBL-producing pathogens
(https://aricjournal.biomedcentral.com/articles/10.1186/s13756-020-00782-x). Despite high level

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of data heterogeneity (I2 = 95%, P < 0.01), the pooled proportion of ESBL-producing Gram-
negative bacteria was 50% (95% CI: 47.7–52.5%. Specifically, 65.7% (n = 263)
for Klebsiella spp., 62.2% (n = 33) for Enterobacter spp., 48.4% (n = 90) for Salmonella spp.,
47.0% (n = 383) for E. coli, 46.8% (n = 22) for Citrobacter spp., 43.8% (n = 7)
for Providencia spp., 28.3% (n = 15) for Proteus spp., 17.4% (n = 4) for Pseudomonas
aeruginosa, 9.4% (n = 3) for Acinetobacter spp., and 20.8% (n = 5) for other Gram-negative
bacteria, respectively. ESBL-encoding genes were found in 81 isolates: 67 isolates harbored the
CTX-M-1 group and 14 isolates TEM. The mortality associated with infections by bacteria
resistant to third generation cephalosporins has reported only in two included studies, reaching
33.3% (1/3) and 100% (11/11)1. (See table below)
Vancomycin resistance enterococci (VRE)
A recent systematic review and meta-analysis included 20 studies. In this study among
831 enterococci, 71 VRE isolates were identified. The pooled VRE estimate accounts 14.8%
(95% CI; 8.7–24.3; I2 = 74.05%; P < 0.001)
2
(https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-020-4833-2) . (See table
below)
Methicillin resistant Staphylococcus aureus (MRSA)
MRSA accounts 32.5% (95% CI, 24.1 to 40.9%; I2 = 96%, P < 0.001). MRSA strains were
>97% resistant to penicillin, ampicillin, erythromycin, and amoxicillin. On the other hand, have
low resistance (5.3%) to vancomycin
3
(https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-016-2014-0) . (See table
below)
MDR TB in Ethiopia
The prevalence of MDR TB among newly diagnosed patients was 2.7% as per the first national
prevalence survey of Ethiopia (https://pubmed.ncbi.nlm.nih.gov/24903931/). Recent meta-
analysis in 2017 and 2018 reported 2% (95% CI 1% - 2%)
(https://pubmed.ncbi.nlm.nih.gov/28320336/) and 2.18% (95% CI 1.44–2.92%)

1
Tufa TB, Fuchs A, Tufa TB, et al. High rate of extended-spectrum beta-lactamase-producing
gram-negative infections and associated mortality in Ethiopia: a systematic review and meta-
analysis. Antimicrob Resist Infect Control. 2020;9(1):128. Published 2020 Aug 8.
doi:10.1186/s13756-020-00782-x
2
Melese A, Genet C, Andualem T. Prevalence of Vancomycin resistant enterococci (VRE) in
Ethiopia: a systematic review and meta-analysis. BMC Infect Dis. 2020;20(1):124. Published
2020 Feb 11. doi:10.1186/s12879-020-4833-2
3
Eshetie S, Tarekegn F, Moges F, Amsalu A, Birhan W, Huruy K. Methicillin resistant
Staphylococcus aureus in Ethiopia: a meta-analysis. BMC Infect Dis. 2016;16(1):689. Published
2016 Nov 21. doi:10.1186/s12879-016-2014-0

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(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000958/), respectively. These same meta-

analysis reported a prevalence of 15% (95% CI 12% - 17%) and 21.07% (95% CI 11.47–
30.67%) among previously treated patients. MDR-TB is mainly associated with history of
previous treatment and to a lesser extent with contact history. As per the 2018 systematic review
MDR TB accounted for the pooled death computed among 5 articles showed that 12.25% (95%
CI 9.39–15.11%) death. Complication, drug side effects and HIV infection were the main
determinants for the death. (See table below)
Resistant Prevalence of Settings and period Methods Specimen
Pathogens resistance
ESBL-RE 50% (95% CI: 0.48– In-patient and/or Double Disk urine &
2
0.52, I = 95%, p < outpatient departments Synergy Test multisite (stool,
0.01); of tertiary hospitals; & both DDST swabs, sputum,
2003 to 2017. and PCR blood & fluids)
Enterococcus 14.8% (95% CI; 8.7– Hospital patients, except Disc diffusion Stool and
2
(VRE) 24.3; I = 74.05%; P < one; Amhara, Oromia, or multisite (stool
0.001), High in AA AA and SNNP; 2013 to Dilution/MIC urine, blood &
and Amhara 2018 swab)
Staphylococcu 32.5% (95% CI, 24.1 Mixed (in- and Not Available multisite
s (MRSA) to 40.9%; I2 = 96%, P outpatients) studies, swab
< 0.001); except 13.8% for school
Vanco resistance = children, 2004 to 2014
5.3% (0–10.6)
MDR-TB 7.24% (95% CI 6.11- Except one, all are -- --
8.37); I2=98.4%, institution based studies;
p=0.000; 2.18% (95% 1997 and 2017
CI 1.44–2.92%) of
newly diagnosed and
21.07% (95% CI
11.47–30.67%) of
previously treated

National response to antimicrobial resistance

In response to the alarming rise in AMR, Ethiopia under took the following progressive and key
steps to combat AMR:
 Synthesized the first AMR surveillance data in 2009. http://www.fmhaca.gov.et/wp-
content/uploads/2019/03/AMR_Baseline_Survey.pdf
 Developed the national strategy for prevention and containment of AMR.
http://www.fmhaca.gov.et/wp-content/uploads/2019/03/Strategy-for-the-Prevention-and-

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Containment-of-AMR-in-Ethiopia-Oct-2015.pdf. This national framework does have five

strategic objectives in line with the international directions of AMR containment. These are:
o Raise awareness and understanding and improve education on antimicrobial use,
resistance prevention, and containment through effective communication and training.
o Strengthen the knowledge and evidence on antimicrobial use and resistance through one-
health surveillance and research.
o Improve infection prevention and contain the spread of resistant microorganisms across
human and animal communities and health care settings through individual and
environmental sanitation, hygiene, and infection prevention measures.
o Optimize the use of antimicrobials in human and animal health through effective
stewardship practices.
o Strengthen and establish national alliances and partnerships, management and governance
arrangements, and resource mobilizations for the prevention and containment of AMR at
all levels.
 Developed a Practical Guide to Antimicrobial Stewardship implementation in Ethiopian
Hospitals, MOH, 2018. https://www.ghsupplychain.org/practical-guide-antimicrobial-
stewardship-ethiopian-hospitals
 Ethiopian public health institute (EPHI) started to coordinate, perform and report an annual
AMR surveillance across the country, since 2017 (16 sentinel sites). This surveillance so far
produced two reports. (NB: Those surveillance reports did not reflect data of lower level
hospitals and should not be used for decisions in hospitals where this STG is applicable).

Containment strategies of AMR

Key strategies for antimicrobial containment include:
 Optimizing prescribing, dispensing and use of antimicrobials through stewardship (All
healthcare settings in Ethiopia should have customized stewardship interventions in place)
 Strong infection prevention and control strategies and practices (All healthcare settings in
Ethiopia must have national IPC polices in practice)
 Surveillance: Keeping track of a resistance profile (antibiogram data) in the healthcare
institution to help identify the most prevalent pathogens, status of resistance, and appropriate
choices of treatment (All healthcare settings in Ethiopia where microbiologic laboratories are
available should have a regularly updated antibiogram data)
 Research: conducting and reporting antimicrobial consumption pattern (proper prescribing,
dispensing and utilization practices) of the healthcare setting or ward (All healthcare settings
in Ethiopia should encourage their staffs and students to carry antimicrobial utilization
studies in their healthcare context for an appropriate action).
 Raising awareness (All healthcare settings in Ethiopia should prepare AMR and containment
awareness operations to the management, clinicians, students, patients and the larger public)

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STG 4th Edition, draft 2020

 Through collaborative/multidisciplinary engagement (physicians, nurses, pharmacists,

microbiologists, infection prevention and control team, healthcare management, bureau and
ministry)

Antimicrobial Stewardship program (ASP)

Objectives;

 Establish ASP team in health facilities

 Describe the role and responsibilities of health professionals in ASP

Definition
Antimicrobial stewardship (AMS) is defined as an organizational or healthcare system-wide
approach for promoting and monitoring judicious use of antimicrobials to preserve their
future effectiveness. ASP is recognized globally as a key strategy to manage inappropriate
use of antibiotics.
Core Elements for ASP
For effective implementation of ASP, the core elements listed below are important,

 Leadership Commitment: Dedicating necessary human, financial and information

technology resources

 Accountability: Head of clinical or appropriately appointed clinician and other health

professionals responsible for program outcomes.

 Appropriate Expertise: Appointing a single pharmacist or microbiologist or infection

prevention expert, leader responsible for working to improve antibiotic use.

 Action: Implementing at least one recommended action, such as systemic evaluation of

ongoing treatment need after a set period of initial treatment (i.e. ―antibiotic time out‖ after
48-72 hours)

 Tracking: Monitoring antimicrobial rational use and resistance patterns

 Reporting: Regularly reporting information on antimicrobial use and resistance to health

professional and other relevant staff as well as appropriate regional and federal organization

 Education: Educating clinicians, other health care professional, hospital communities,

patients and societies at large about resistance and optimal use of antimicrobials
Formation of ASP Team in Health Facilities

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The hospital management should give due emphasis for the establishment and functionality of
ASP in the hospital. The organizational structure of ASP in any hospital may look like as follow:

Drug and Therapeutic Committee

Antimicrobial Stewardship Team

 Infectious Diseases specialist (trained

physician) (Director)
 Clinical Pharmacist (Trained in infectious
disease) (Co-director)
Infection Prevention and Quality improvement
 Clinical Microbiologist (member)
team
Patient Safety committee  Infection Control and Patient Safety
representatives (member)
 Hospital epidemiologist (or quality
office representative) (member)
 Nursing department representative
(member)

Refer; Practical Guide of ASP for Hospitals, EFMHACA, 2018 for the major duties and
responsibilities of ASP team members in general and individual members in particular

Strategies of Antimicrobial Stewardship Program

The problem is critical, and it is high time to prevent and contain AMR using different strategies.
In order to attain the goals of ASP, several strategies can be designed considering local
antimicrobial use, AMR problems, availability of resource, and collaboration with an
effective infection control program to minimize secondary spread of resistance.
The following core and supplemental antimicrobial stewardship strategies are recommended to
be implemented in Ethiopian hospitals
 Facility specific guidelines and clinical pathways
Local antibiotics guidelines or clinical pathways should be formulated based on the national
antibiotic guideline, evidence in the literature and local microbiology and resistance patterns.
Clinical pathways such as common infections can be produced to bring about uniformity in
prescribers approaches in local setting.
 Surveillance and Feedback
Antimicrobial use surveillance is the collection of information concerning prescribing,
dispensing, antimicrobial consumption, adherence to antimicrobial treatment and compliance
to different practice guidelines in a regular time period to assess the rationality of

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antimicrobial use. Surveillance of antimicrobial use can show us how and why antimicrobial
are being used and misused by patients and healthcare providers. Monitoring antimicrobial
prescription and consumption behavior provides insights and tools needed to inform therapy
decisions, to assess the public health consequences of antimicrobial misuse, and to evaluate
the impact of resistance containment interventions.
Access to information on antimicrobial consumption can be an important source for healthcare
professionals and policy makers to monitor progress towards a more prudent use of
antimicrobials.

 Collection and analysis of local antimicrobial consumption and expenditure

o Data collection and analysis of antimicrobial use and expenditure should be undertaken
regularly (at least every 6 months).

o The results of antimicrobial use and expenditure should be forwarded to prescribing clinician
and discuss the results in relevant meeting.

 Indicators for reporting antibiotic consumption (https://extranet.who.int/glass/portal/):

o Daily Defined Dose (DDD) per 100 patient admissions and DDD per 1000 Patient Days or
other indicators are used to determine the antibiotic consumption.

o Proportion of consumed antibiotics in AWaRe Access category (target is 60 %)

o Proportion of AWaRe Reserve category antibiotics inappropriately prescribed and used

 Provision of data to regional /national surveillance programs

o The data should be reported and presented at local and zone level. It also has to be submitted
to national/regional pharmacy service directorate

Prospective Audit and Feedback

A prospective audit and feedback system involves a multidisciplinary team who regularly
reviews patients.

Process of prospective audit: Audit is achieved by conducting a systematic review of care set
against pre‐ determined criteria; suitable changes implemented and the effect of those
changes re‐ evaluated. It comprises:

 Prior to initiation of audit, selected antibiotics will be chosen based on the AWaRe
recommendations or data on susceptibility of organisms against selected antimicrobials.

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 A predetermined criterion has to be set and agreed which includes approved indications and
utilization patterns.

 Any deviations based on agreed predetermined criteria has to be communicated and

discussed with the doctors and other health care team who are involved with the patients.

 Any reasons for deviations from the predetermined criteria have to be documented.

Elements of audit

 Guideline/Protocol: For any selected antimicrobial to be audited, an established antimicrobial

guideline or protocol either from local hospitals or national guidelines (STG) should be
available and practiced by prescribers.

 Predetermined audit criteria: Any predetermined audit criteria will be discussed, its
suitability and practicality, prior to implementation. It consists of:

o Approved indications based on available guidelines/protocol. The antimicrobial audit may be

conducted for:
 Surgical prophylaxis
 Empirical therapy where patient‘s clinical conditions, supported by laboratory findings
suggest an infection
 Definitive therapy, whereby antimicrobial is prescribed following the availability of
microbiological and sensitivity test results

o Utilization patterns derived from process indicators which measures one or all the following:
 Time and date of administration of antimicrobials
 Appropriate dose or frequency in special populations, pediatrics, renal compromise, etc.
 Available cultures and their antimicrobial susceptibilities (If facility is available)
 Duration of antimicrobial treatment

o Intervention and Outcome of the therapy

 Audit on antimicrobial should be extended until it is stopped or switched. The reasons for
changes in therapy shall be documented. All data must be documented and reviewed
periodically. Any deviations from agreed criteria has to be communicated, discussed and
documented.

Feedback

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STG 4th Edition, draft 2020

In order to ensure the success of the program, a two‐ way system of communication has to be
established within the institution. Feedback on antimicrobial prescribing should be provided
regularly to prescribers in the critical care setting, and areas of high and/or poor quality
antimicrobial use through a direct way, including peer review and discussion groups.
Feedback in the form of report may also be forwarded to the healthcare
administration/management team.

Formulary Restriction and Pre-authorization

Preauthorization is a strategy to improve antibiotic use by requiring clinicians to get approval for
certain antibiotics before they are prescribed. A list of restricted antimicrobials (Watch and
Reserve) would need to be included in the hospital antimicrobial policy which will be
reviewed on regular basis.
Restriction can be implemented through a number of ways:

 pre‐ approval (can only be prescribed after getting a specific approval from an authorized
senior or team)

 Temporary approval (can be started but would need approval for continued usage and this
can be done via antimicrobial order tools)
Methods to acquire approval:

 Antimicrobial order tools

 Telephone

Antimicrobial Streamlining
The use of empirical broad-spectrum antimicrobial treatment may increase the risk of AMR. The
de-escalation strategy has the potential to improve patient outcomes without compromising
patient safety. Studies show that de-escalation was associated with reduced mortality, shorter
length of stay and lower costs.
Streamlining can be typically conducted in:

 Broad empirical to narrow spectrum agents once cultures and sensitivities are available.

 Initially high dose can be deescalated to a standard dosage for a susceptible organism.

 Discontinuing empiric therapy if testing subsequently fails to demonstrate infection.

 Discontinuing dual antimicrobial therapy if there is overlapping in the spectrum of activity

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STG 4th Edition, draft 2020

 Advising on the optimal choice of antimicrobials for the specific clinical setting (e.g. through
the AWaRe process)

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STG 4th Edition, draft 2020

Sample Chart sticker for Antibiotic discontinuation after recommended treatment

duration
Treatment duration reminder
Date_________ Time________ Patient Name ______________________
This patient currently has orders for:____________________________
The Antimicrobial Stewardship Team identified that your patient received the recommended
duration of antimicrobial therapy. This is to kindly remind to stop the antimicrobial therapy.
Completed by: ______________________________

Antimicrobial Selection and Dose Optimization

It will help to tailor therapy to the patient‘s characteristics, causative organism, site of infection,
and pharmacokinetic and pharmacodynamic characteristics of the antimicrobial agent.
Strategies that may be considered for dose optimization include:

 Extended or continuous infusion of beta‐ lactams (e.g. for serious infections)

 Once‐ daily dosing of aminoglycosides (e.g. for most infections)

 appropriate dosing of antimicrobials (e.g.; vancomycin, polymyxins, cefepime)

 Weight‐ based dosing based on patient type or certain antimicrobial types.

 Dose adjustments for patients with renal dysfunction

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STG 4th Edition, draft 2020

Sample Chart sticker for Organ Dysfunction Regimen and/or Dose adjustment Reminder
Organ Dysfunction based Regimen and/or Dose Adjustment reminder
Date_________ Time________ Patient Name ______________________
This patient currently has orders for:____________________________
The Antimicrobial Stewardship Team identified Renal/liver dysfunction demanding clinical
criteria for regimen and Dose adjustment. You are kindly reminded to adjust the treatment
dose based on the clinical guideline recommendations.
Completed by: ______________________________

Intravenous (IV) to Oral (PO) Antibiotics Conversion

This describes the practice of converting intravenous antimicrobials therapy to an effective
alternative oral formulation. Several clinical trials have been conducted that demonstrate the
efficacy and safety of IV to PO antimicrobials conversion, and several studies have also
addressed the economic impact of this conversion.
Cost savings are achieved through lowering direct acquisition costs, eliminating the need for
ancillary supplies, reducing pharmacy and nursing time, and shortening the length of hospital
stay. IV to oral antimicrobials conversion also benefits the patient by eliminating adverse events
associated with IV therapy, increasing patient comfort and mobility and earlier discharge.

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Sample Chart Stickers for Intravenous to Oral Antimicrobial Switch Reminder

IV to Oral Antimicrobial Interchange Program
Date_________ Time________ Patient Name ______________________
This patient currently has orders for:_______________________________________
Responsible or authorized person from the ASP team has approved an IV to oral conversion for
patients meeting specific clinical criteria.
Your patient‘s therapy has been changed to:__________________________
Completed by: ______________________________

Education
Antimicrobial Stewardship team would prepare a program of ongoing education for pharmacists,
doctors and nurses to influence prescribing behavior and to provide knowledge that will enhance
and increase the acceptance of Antimicrobial Stewardship strategies. This program should
ideally be included in the induction training for all newly reporting medical, nursing and
pharmacy staff.
AWaRe classification of antibiotics
AWaRe stands for ACCESS, WATCH and RESERVE. It is an antibiotic classification
system introduced in 2017 by The World health Organization (WHO) Essential medicine list
(EML). It was first introduced in 2020 in the Ethiopian Essential Medicine List (EEML-
2020). The classification is aimed to promote rational antibiotic use and provide a tool for
antimicrobial stewardship (AMS) activities and monitoring of antimicrobial consumption.
The AWaRe classification implementation aims to enhance the health facility‘s ability to
contribute to the national antibiotic consumption goal, i.e. increasing the proportion of Access
group antibiotics consumption to at least 60%, and to reduce use of the antibiotics most at risk
of resistance from the Watch and Reserve groups. Hence this will help to contain
antimicrobial resistant by:
 Strengthening the capacity of the health-care facility‘s ASP to implement AMS
 Aligning empirical antibiotic treatment with ACCESS antibiotics;
 Targeting WATCH and RESERVE groups for AMS;
 Reviewing antimicrobial consumption and use surveillance data with AWaRe approach;
ACCESS group antibiotics
 Have activity against a wide range of commonly encountered susceptible pathogens while
showing lower resistance potential than antibiotics in Watch and Reserve groups.
 Widely used as first- or second -choice empiric treatment options for specified infectious
syndromes.
 Should be widely available, affordable and quality-assured to improve access and promote
appropriate use.

WATCH group antibiotics

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STG 4th Edition, draft 2020

 Have higher resistance potential and includes most of the highest priority agents among the
Critically Important Antimicrobials (CIA) for Human Medicine and/or antibiotics that are at
relatively high risk of selection of bacterial resistance.
 Widely used as first- or second -choice empiric treatment options for specified infectious
syndromes.
 Should be prioritized as key targets of hospital stewardship programmes and monitoring.
 Use in animal health and food production must be highly regulated
RESERVE group antibiotics
 Should be reserved for treatment of confirmed or suspected infections due to multi drug-
resistant organisms, and treated as ―last-resort‖ options.
 They should be accessible, but their use should be tailored to highly specific patients and
settings, when all alternatives have failed or are not suitable.
 They must be protected and prioritized as key targets of hospital stewardship programmes,
involving monitoring and utilization reporting, to preserve their effectiveness.
 Used when they have a favorable risk-benefit profile and proven activity against ―Critical
Priority‖ or ―High Priority‖ pathogens identified by the WHO Priority Pathogens List,
notably carbapenem resistant Enterobacteriaceae.
Table 1: AWaRe classification of antibiotics in the EEML-2020
Group
Access Watch Reserve
1. Amoxicillin 1. Ampicillin + 1. Piperacillin +
2. Amoxicillin + Sulbactam tazobactam
Clavulanic Acid 2. Cefuroxime 2. Meropenem
3. Ampicillin 3. Cefixime 3. Meropenem +
4. Penicillin G, Benzanthin 4. Cefpodoxime Vaborbactam
5. Penicillin G, Sodium Cefotaxime Sodium 4. Ceftazidime +
Crystalline 5. Ceftriaxone Avibactam
6. Cloxacillin 6. Ceftazidime 5. Colistin
7. Cephalexin 7. Cefepime 6. Polymyxin B
8. Cefazolin 8. Ceftriaxone + Vancmycin
9. Azithromycin sulbactam
10. Clarithromycin 9. Ciprofloxacin
11. Sulphamethoxazole + 10. Clindamycin
Trimethoprim
12. Nitrofurantoin
13. Norfloxacin
14. Gentamicin
15. Metronidazole

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16. Doxycycline

References
1. Ethiopian Essential Medicines List, 6th edition; Addis Ababa, Ministry of Health/Ethiopian
Food and Drug Administration; 2020
2. Global antimicrobial resistance surveillance system (GLASS) report: early implementation
2020. Geneva: World Health Organization; 2020. Licence: CC BY-NC-SA 3.0 IGO
(https://apps.who.int/iris/bitstream/handle/10665/332081/9789240005587-eng.pdf?ua=1)
3. The selection and use of essential medicines: World Health Organization technical report
series. Geneva: World Health Organization; 2017.
(https://www.who.int/medicines/publications/essentialmedicines/EML_2017_EC21_Unedite
d_Full_Report.pdf)
4. Executive summary: the selection and use of essential medicines 2019. Geneva: World
Health Organization; 2019.
5. https://adoptaware.org/

Hospital acquired infection (HAI) prevention measures

The goal of infection control is to prevent and reduce rates of resistant hospital acquired
(nosocomial) infections. Please visit Ethiopian infection prevention guideline for healthcare
facilities: https://agris.fao.org/agris-search/search.do?recordID=US2012413697. The CDC also
has infection prevention toolkits that can be adapted to our settings
(https://www.cdc.gov/hai/prevent/prevention_tools.html)
Measures at the each healthcare level
Every health setting should have 1) infection prevention and control team. 2) Provide ongoing
training and retraining of staff with responsibility for cleaning and disinfection, 3) standardized
cleaning process/IPC protocol, monitoring and feedback strategies to decrease the risk of
infection. It would be good if the protocol is based on the surveillance of the health settings
infection volume or potential. As well, Health Care Waste Management (including
pharmaceutical waste management) should be one core quality indicator for IPC
(http://www.fmhaca.gov.et/wp-content/uploads/2019/03/Healtcare-Waste-management.pdf).
Core Infection Control Measures in Health Care Settings
 Early recognition and reporting
 Infection control precautions (Standard precautions, Transmission-based precautions)
 Cleaning, disinfection and sterilization of medical equipment-according to equipment type.
 Hand hygiene: alcohol-based hand rub, hand washing with soap and water
 Personal Protecting Equipment (PPE): gloves, gowns, masks/respirators, eye protection
 Patient accommodations and care (bed spacing)

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 Environmental cleaning, disinfection and waste disposal: removal of organic material on

soiled surfaces followed by disinfection, which eliminates microorganisms and proper
disposal. Better performed by public health or environmental science professionals
 Occupational health management
Precautions to infection prevention
Precautions for preventing transmission of infection include standard precautions and
additional precautions which include isolation (contact, airborn) precautions. Standard
Precautions are guidelines designed to create a physical, mechanical, or chemical barrier
between microorganisms and a person (patients and health care workers) to prevent the spread
(break the chain) of infection and reduce the risk of pathogen transmission in hospitals.
Examples of Barriers:
 Physical: PPE (gloves, face masks, goggles, gowns, plastic or rubber aprons, and drapes)
 Mechanical: HLD by boiling or steaming and sterilization by autoclaving or dry heat ovens
 Chemical: Antiseptics (alcohol-based antiseptic agents) and high-level disinfectants
(chlorine and glutaraldehydes)

Standard precautions
The following standard precautions should be performed for the care of all patients:
 Hand hygiene before and after every patient contact with soap and water (preferred for
norovirus and C. difficile infection over ABHR) or alcohol-based hand rub (ABHR)… single
most important measure to reduce transmission.
 Use of gloves, gowns, and eye protection (for situations in which exposure to body fluids is
possible); glove use should never be a replacement for hand washing.
 Use of respiratory hygiene/cough etiquette: Patients and caretakers should cover their nose or
mouth when coughing, dispose used tissues immediately, and exercise hand hygiene after
contact with respiratory secretions.
 Safe disposal of sharp instruments in impermeable containers.
 Safe disposal or cleaning of instruments and linen.
 Routinely cleaning and disinfecting equipment and furniture in patient care areas
 Using safe work practices
Isolating patients only if secretions or excretions cannot be contained
Isolation precautions: Must be practiced in addition to the standard precautions above.
Carried based on main modes of microorganism transmission in healthcare settings: contact,
droplet, and airborne spread
Contact precautions
 Contact precautions are recommended for Colonization of any bodily site with multidrug-
resistant bacteria (MRSA, VRE, ESBL producing), Enteric infections (Norovirus,
Clostridioides difficile, Escherichia coli), Viral infections (HSV, VZV, RSV, parainfluenza,

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STG 4th Edition, draft 2020

rhinovirus, enterovirus, certain coronaviruses [eg, COVID-19, MERS-CoV]), Scabies,

Impetigo, Noncontained abcesses or decubitus ulcers (especially for Staphylococcus aureus
and group A Streptococcus).
 The following contact precautions should be performed in addition to standard precautions:
o Were gloves upon entering room. Change gloves after contact with contaminated secretions.
o Gown required if anticipated contact with the patient or environmental surfaces or if the
patient has diarrhea/abdominal secretions.
o minimize risk of environmental contamination during patient transport (eg, patient can be
placed in a gown).
o Noncritical items should be dedicated to use for a single patient if possible.
o Health care workers should implement hand hygiene, wear gloves and Gowns upon room
entry, even if no direct patient contact is anticipated.

Droplet precautions
 Droplet precautions are suggested for known or suspected bacterial infections (Neisseria
meningitides, Haemophilus influenzae type B, Mycoplasma pneumonia, Bordetella pertussis,
Group A Streptococcus, Diphtheria, Pneumonic plague), viruses (Influenza, Rubella,
Mumps, Adenovirus, Parvovirus B19, Rhinovirus, Certain coronaviruses).
 The following droplet precautions should be performed in addition to standard precautions
o Private room preferred; cohorting required if necessary. If no private room, place patient in
room with patient having active infection with the same disease, but with no other infection.
If neither option is available, maintain separation of at least 3 feet between patients
o Wear (healthcare workers and attendants) a mask when within 3 to 6 feet of the patient. No
special air handling or higher level respirator masks required, and door may remain open.
o Mask the patient during transport (use surgical mask).
o Cough etiquette: Patients and visitors should cover their nose or mouth when coughing,
promptly dispose used tissues, and practice hand hygiene after contact with respiratory
secretions.

Airborne precautions
 Airborne precaution are recommended for known or suspected Tuberculosis, Varicella,
Measles, Smallpox, Certain coronaviruses and Ebola:
 The following droplet precautions should be performed in addition to standard precautions
o Place the patient in an airborne infection isolation room (AIIR), (a private, monitored
negative pressure room with at least 6 to 12 air exchanges per hour).
o The door must remain closed, and all individuals who enter must wear a respirator with a
filtering capacity of 95 percent that allows a tight seal over the nose and mouth.
o Susceptible individuals should not enter the room of patients with confirmed or suspected
measles or chickenpox.

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o Room exhaust must be appropriately discharged outdoors or passed through a HEPA filter
before recirculation within the hospital.
o Transport of the patient should be minimized; the patient should be masked if transport
within the hospital is unavoidable.
o Cough etiquette: Patients and visitors should cover their nose or mouth when coughing,
promptly dispose used tissues, and practice hand hygiene after contact with respiratory
secretions.
Discontinuation of precautions for several common organisms is variable. For some, it will be
after 24 to 72 hours. For other majority cases it is after duration of illness finished (with wound
lesions, until wounds stop draining or until lesions dry and crusted) or until off antimicrobial
treatment and culture-negativity ensured. Congenital rubella may need contact precautions until
1 year of age. Please visit case specific updated evidences.
Specific IPC recommendations for hospitalized patients
The most important nosocomial infections that can be prevented include:

o Urinary tract infections, pneumonia and diarrhea

o Infections following surgery or invasive medical procedures

o Maternal and newborn infections Most of the nosocomial infections

Prevention of surgical site infection (SSI)

o Appropriate administration of effective preoperative antibiotics – most important (see
‗Antimicrobial prophylaxis in surgery‘ section)
o Other perioperative control measures. Use alcohol-containing (with chlorhexidine
gluconate or an iodophor) preoperative skin preparatory agents if no contraindication
exists. Avoid alcohol in areas that pool or not dry (eg, involving hair) due to fire risk,
procedures involving mucosa, cornea, or ear. In absence of alcohol, chlorhexidine
gluconate have advantages over povidone-iodine, for longer residual activity and activity
in the presence of blood or serum
o Careful infection control is essential; hand hygiene and use of gloves and other barrier
devices (masks, caps, gowns, drapes, and shoe covers) by all operating room personnel.
Antiseptics to the skin to reduce burden of skin flora.
o Patients with evidence of active infection prior to elective surgical procedures should
complete treatment for the infection prior to surgery, particularly in circumstances when
placement of prosthetic material is anticipated. For circumstances in which urgent
surgery is required, the Weight risk of infection with the timing of surgical intervention
on an individual basis.

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o Staphylococcus aureus screening and decolonization may be reasonable for surgical

patients known to be nasal carriers of S. aureus with a high risk of undesirable outcomes
if S. aureus SSI develop (eg, cardiothoracic surgery, orthopedic procedures with
hardware implantation, immunocompromised patients).
o Wound protectors (impervious plastic sheath) are required for clean-contaminated,
contaminated, and dirty abdominal procedures (GI and biliary tract surgeries).
o If hair removal is essential, remove it outside the operating room using clippers or a
depilatory agent. Do not use razors as possible.
o Controling blood glucose (180 mg/dL or lower) during immediate postoperative period
for cardiac surgery patients is critical. Non-cardiac surgery patients may also benefit.
o Maintaining peri-operative normothermia (temperature of 35.5°C or more) decreases
SSI.
o Perioperative high-inspired (supplemental) oxygen during and immediately following
surgical procedures reduces the risk of SSI. Supplemental oxygen is recognized in
patients undergoing surgery with general anesthesia using mechanical ventilation. It is
most effective if combined with additional schemes to improve oxygenation, like
normothermia and appropriate volume replacement.
Prevention of infection in the intensive care units (ICUs)
In ICU, Comorbid conditions, long hospital courses, frequent contact with health care personnel,
indwelling catheterization, and receipt of antimicrobial therapy all increase the risk of
colonization and infection with multidrug-resistant pathogens (e.g. MRSA, VRE). Infections
with such organisms are associated with increased mortality, length of stay, and hospital costs.
Measures to prevent spread of resistant organisms in the ICU include:
 Infection control measures such as good hand hygiene compliance,
 contact precautions for patients for drug-resistant organisms, and
 Minimizing unnecessary hospitalization and interventions.
 Adequate and standardized environmental cleaning and disinfection.
 Antimicrobial stewardship program can decrease selective pressure that promotes
emergence of resistant bacterial strains
 More intensive infection control interventions to reduce colonization pressure include:

o Dedicated staffing,

o Daily chlorhexidine bathing (decrease risk of colonization and infection including MDR),

o Selective decontamination,

o Active surveillance for certain pathogens,

o Reduction of catheterization utilization.

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The most common infections in the ICU are those associated with indwelling devices, namely
catheter-associated UTI, VAP, and intravascular catheter-related bloodstream infection. In
addition to minimizing their use, proper placement and care of indwelling devices can decrease
the risk of infection (see below).

Prevention of catheter-associated urinary tract infections (UTI)

 Avoid unnecessary urinary catheterization. Limiting use to appropriate indications is
important in minimizing catheter-related complications like infection. Catheters are not
indicated for determining the residual volume of urine, or in the management of most
patients with urinary incontinence. Urinary catheters are used selectively for operative
patients based upon the nature (ie, pelvic surgery) and duration of the procedure, or need
for perioperative fluid monitoring.

 use sterile technique (e.g. avoid touching the tip) when placing the catheter,

 Remove catheters as soon as possible (preferably in the recovery area or when no longer
indicated). However, catheters inserted for surgery on the urinary tract need approval of the
surgeon (urologist) to remove.
 Considering alternatives to indwelling urethral catheters. For bladder emptying
dysfunction, intermittent catheterization can be used over chronic indwelling catheters.
External catheters are preferred over urethral catheters whenever possible for male patients
with no evidence of urinary retention or bladder outlet obstruction.

 Not routinely replace urethral catheters: Indwelling urethral catheters and drainage systems
are changed only for a specific clinical indication such as infection, obstruction, or
compromise of closed system integrity.

 Adequate training of healthcare staff, patients, and caregivers on catheter placement and
management is important.

 No clear benefit of using antibiotic-coated urinary catheters or prophylactic antibiotics to

reduce the risk of catheter associated urinary tract infection. So not recommended.
Specific measures to prevent catheter-associated urinary tract infection include:
 Using a continuously closed drainage system. Following aseptic placement of indwelling
catheters, a closed drainage system should be carried. Breaks in the integrity of the closed
system should prompt replacement of the drainage system.
 Not routinely irrigating catheters or irrigate only under select circumstances. Do not irrigate
urinary catheters for patients who do not have gross hematuria associated with clots.
 Routine maintenance of urinary catheters includes:

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o proper hygiene of the pericatheter region,

o maintenance of unobstructed urine flow,

o frequent and proper emptying of the closed catheter drainage system, and

o proper specimen collection.

Preventing ventilator-associated pneumonia (VAP)
Practices that are recommended for preventing VAP include (i.e. decreases average duration of
mechanical ventilation, length of stay, mortality, and/or costs; benefits likely outweigh risks):

 Use noninvasive positive pressure ventilation in selected populations

 Manage patients without sedation whenever possible

 Interrupt sedation daily

 Assess readiness to extubate daily

 Perform spontaneous breathing trials with sedatives turned off

 Facilitate early mobility

 Utilize endotracheal tubes with subglottic secretion drainage ports for expected greater than
48 or 72 hours of mechanical ventilation

 minimizing pooling of secretions above the endotracheal tube cuff,

 Change the ventilator circuit only if visibly soiled or malfunctioning

 Elevate the head of the bed to 30 to 45°

Prevention of intravascular catheters associated infection
All types of intravascular catheters are associated with a risk of both local infection and catheter-
related bloodstream infection (CRBSI). General measures for prevention of infections associated
with any intravascular catheter include:
The site chosen for catheter placement can influence the infection risk.

 Placing peripheral intravenous catheter in the upper extremity rather than the lower extremity
is strongly preferred.

 Avoid femoral site for insertion of central venous or pulmonary artery catheters in adults, if
possible due to high risk of infection. Internal jugular vein or subclavian veins are preferred.

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Replacement of intravascular catheters

 Remove any intravascular catheter that is no longer essential. The risk of infection increases
with the duration, increasing after more than three to six days at all catheter sites.

 Peripheral intravenous catheters be removed or replaced as clinically indicated, rather than

routine removal or replacement after a designated time period.

 Always ensure aseptic technique. If adherence to aseptic technique cannot be assured (such
as in emergent catheter placement requirement), replace catheter as soon as possible (and no
longer than 48 hours after insertion).

 Central venous catheters, pulmonary artery catheters, and peripheral arterial catheters should
be removed as soon as clinically feasible. Routine replacement of these catheters is not
praised.

 When central venous catheters are replaced, use of guidewire exchange techniques is not
recommended as the approach increases the risk of bloodstream infection.

 Use of antimicrobial-impregnated catheters is good, especially useful in ICUs with high

bloodstream infection rates than other comparable units.
Replacement of administration sets

 Replace administration sets, including secondary sets and add-on devices, no more frequently
than at 72-hour intervals, unless clinically indicated.

o Replace tubing used to administer blood, blood products, or lipid emulsions within 24 hours
of initiating the infusion.

o Replace tubing used to administer propofol infusions every 6 to 12 hours, depending on its
use, per the manufacturer's direction.
Catheter and site care measures can minimize incidence of catheter-related infections.

The best recommend procedures are:

 Hand washing with antiseptic-containing soap or ABHR; the use of gloves should not
obviate hand hygiene.

 Maintain aseptic technique for the insertion and care of intravascular catheters. Use
maximal barrier precautions when inserting arterial or central venous catheters. Full barrier

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precautions during insertion of CVCs, including sterile gloves, long-sleeved surgical gown, a
surgical mask, and a large sterile sheet drape.

 Catheter site care

o Disinfect clean skin with an appropriate antiseptic before catheter insertion and at the time of
dressing changes. The antiseptic should air dry before catheter insertion. A 2%
chlorhexidine-based preparation is preferred, but there is no recommendation for its use in
infants less than two months of age.

o Use sterile gauze or sterile transparent semipermeable dressing to cover the catheter site.

o Do not use topical antibiotic ointment or creams on insertion sites (except for dialysis
catheters).

o Avoid femoral insertion site.

o Prompt removal of catheters when no longer indicated.

o Complications must be watched by examine the catheter site at least once each day. Check
every 8-12 hours for phlebitis or evidence of infection.

 Intravenous injection ports

o Clean injection ports with 70% alcohol or an iodophor before accessing the system.

 Parenteral fluids

o Complete the infusion of lipid-containing solutions within 24 hours of hanging the solution.

o Complete the infusion of lipid emulsions alone within 12 hours of hanging the solution.

o Complete infusions of blood or other blood products within 4 hours of hanging the blood.

 Health care worker education and training

o Educate regarding indication for intravascular catheter use, proper procedures for insertion
and maintenance, and infection control measures to prevent intravascular catheter-associated
infections.
Antibiotic lock therapy may be applied for patients with long-term catheters and a history of
recurrent CRBSI despite adherence to other routine infection prevention measures.
Preventing Maternal and Newborn Infections

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The following prevention efforts are being recommended to successfully reduce the risk of fetal
and newborn infections (more details are available in the 2005 guideline):

 Maternal immunization (Tetanus Toxoid)

 Antenatal treatment of maternal syphilis, gonorrhea and Chlamydia infections.

 Prophylactic use of postnatal eye drops to prevent chlamydia, gonorrhea and candida eye
infections

 Prophylactic treatment of pregnant women at risk of group B streptococcal disease and

 Maternal and newborn treatment with antiretroviral to prevent mother-to-child transmission

of HIV.
References
1. Ethiopian Ministry of Health, Infection Prevention Guidelines for Healthcare Facilities in
Ethiopia. MOH Disease Prevention and Control Department, 2005.
2. Guidelines on core components of infection prevention and control programmes at the national
and acute health care facility level. Geneva: World Health Organization; 2016. Licence: CC BY-
NC-SA 3.0 IGO
3. Anderson DJ, Podgorny K, Berríos-Torres SI, et al. Strategies to prevent surgical site
infections in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol. 2014;35(6):605-
627. doi:10.1086/676022
4. Lo, E., Nicolle, L., Coffin, S., Gould, C., Maragakis, L., Meddings, J., Yokoe, D. (2014).
Strategies to Prevent Catheter-Associated Urinary Tract Infections in Acute Care Hospitals: 2014
Update. Infection Control & Hospital Epidemiology, 35(5), 464-479. doi:10.1086/675718
5. Marschall J, Mermel LA, Fakih M, et al. Strategies to prevent central line-associated
bloodstream infections in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol.
2014;35(7):753-771. doi:10.1086/676533

Antimicrobial Surveillance and Research

Surveillance is a systematic collection of data that can identify baseline rates of infection and
alert out breaks to concerned health professional and bodies so as to focus on intervention and
resource mobilization. Surveillance data also can be used to identify risk factors for infection,
compare rates between institutions, and evaluate process and outcome measures. Moreover,
prevention and early intervention through surveillance improves patient safety and helps control
costs.
If microbiologic facilities are available in the health facility:
Researchers can best address most common and critical bacterial profile and susceptibility
patterns in the health facility and even can generate antibiogram data.

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 Cases will be analyzed and reported among routine clinical samples by Antimicrobial
sensitivity test (AST) of defined specimen types from patients selected for sampling at
surveillance sites according to local practice. This might be carried on the priority pathogens
or specimens based on the Global Antimicrobial Resistance Surveillance System (GLASS) or
the health facility requirement. AST results will thus be combined with the patient data that
accompany every request for AST and related to population data from the surveillance site.
Facility based formats can be developed. AST results will be classified as susceptible (S),
intermediate (I), resistant (R), or not tested or not applicable.
Other Researches in in the absence or presence of microbiologic facilities
In addition to the research elaborated above, applied/operational researches should be performed
so as to preserve/properly utilize the existing antimicrobials as well as to monitor and evaluate
the implementation of antimicrobial stewardship programs. Priority thematic areas for
operational research are including but not limited to the following:
 Knowledge attitude and/or practice of health care providers and supportive staff on infection
prevention (IP)
 Availability of essential antimicrobials in the hospital
 Pattern of antimicrobial prescribing (for example prophylaxis in surgery patients, dental,
etc.)
 Prescription pattern of antimicrobials based on WHO guideline
 Examination of the effectiveness of antimicrobial stewardship strategies
 The long-term impact of formulary restriction and preauthorization requirements on
antimicrobial use and resistance.
 Prescribing Adherence pattern as per STG/formulary
 Hospital‘s expenditure on antimicrobials as percentage of total hospital medicines cost (in
line morbidity pattern)
 Studies trial on appropriate dose, interval and duration
 Economic impact of AMR (direct and indirect)
 Antimicrobial treatment outcome and associated factors (Socio-economic, demographic,
Clinician interaction, etc.)

Health facility level implementation of AMR containment strategies

 All health facilities must have functioning infection prevention and control team (at least a
focal person)
 All hospitals should have an antimicrobial stewardship program customized to their human
and capital resources.
 In hospitals with a microbiologic laboratory, development and updating of antibiogram data
should be considered on a regular base.

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 All health facilities are encouraged to undertake an antimicrobial prescription monitoring

and antimicrobial consumption studies on annual basis.

References

 Ethiopian Essential Medicine List (EEML-2020); Ministry of Health/Ethiopian Food and

Drug Administration, Addis Ababa, 2020.

 CDC, 2014. The Core Elements of Hospital Antibiotic Stewardship Programs

 EFMHACA, 2018. A Practical Guide to Antimicrobial Stewardship Program in Ethiopian

Hospitals

 Dellite et al, 2007. Infectious Diseases Society of America and the Society for Healthcare
Epidemiology of America Guidelines for Developing an Institutional Program to Enhance
Antimicrobial Stewardship.

CHAPTER 3: CARE OF PATIENTS IN AMBULATORY

AND HOSPITALIZED SETTING

1. Clinical evaluation and communication in the outpatient setting

 The over goal of clinical care is to reach to accurate diagnosis, cure or improve the condition,
address the concerns of the clients (patients and families), improve the functional status and
sense of wellbeing of the patient.
 Clinicians envisage seeing a satisfied patient and family, improved or cured patient, and
trustful continued relationships.
 Accomplishing the above goal requires a strong patient-clinician partnership. The key
element for establishing this relationship is good communication.

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 The practice of medicine is much more than ordering a set of tests, reaching to a diagnosis
and prescribing the ―best‖ medicine. It encompasses a good humanely interaction. Patients
and family members deserve a humanely interaction.
 Effective communication has been shown to improve not only patient satisfaction rates but
also other health outcomes.
 Communication varies based on the gender, age, literacy, culture, and clinical settings
 Clinicians should identify potential barriers to communication in every encounter. The
following are common barriers;
A. Language or dialect
B. Mental status or cognitive capacity
C. Emotional/psychological distress
D. Cultural differences
E. Gender differences
F. The environment: the examination room

 Steps to follow during clinical evaluation and communicating the client.

1. Observe
o Observe the patient as he/she enters the room for severity of illness and
danger clinical signs to act accordingly.
2. Greet appropriately and establish rapport
o Stand from your chair, call the patient by her or his name with appropriate
title and give culturally appropriate greetings.
o Establish a rapport: e.g. ― please sit down…..you like tired‖ ― Please take a
sit…. Let me help you with your stick‖
3. Give attention
o Sit facing the patient, lean forward, establish eye contact and relax.
4. Listen
o The golden ―first minute‖ allows you to listen to the patient without
interrupting, whatsoever.
o Just give opening questions and listen:
E.g. ―How have you been feeling?‖ ―What is bothering you?.....tell me
about it‖ ―Have you been feeling unwell?...tell me about it‖
5. Open ended questions initially
o Ask about their chief complaints and their durations
o Then ask more open ended questions like ―tell me more about that‖ to
explore about their complaints without interrupting.
6. Close ended questions when necessary
o If needed ask guiding questions? E.g. did you have a travel history to such
places? Have you ever experienced such symptoms?
o Ask past history, drugs being taken, recent treatments and allergies
7. Do a complete physical examination:
o Focused but not limited to the complaints
8. Document your findings

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9. Formulate a differential diagnosis and diagnosis: Give a brief explanation about

the possible diagnosis.
10. Do relevant tests and imaging: Explain about the tests,

 Communicating once the diagnosis is made, treatment planned and prognosis

understood

A. Briefly assess what the patient already knows…….. But don‘t push it hard, if
they don‘t want to tell. See the examples below
o Example for educated urban dweller
―These days we get a lot of information from the media, the internet or
communicating with health care workers, tell me what you know about
this… and what really concerns you‖
o For uneducated a rural patient
―When we are sick, we discuss it with relatives, neighbors, other people with
similar illnesses or elders. What have you heard about this…. tell me what
you heard and what really concerns you‖
o Individuals vary on what they want to know
B. Be empathic
o Empathy needs to be developed in every clinicians practice.
o Without empathy one cannot understand the emotions of patients and
communicate effectively.
o Do not ignore or minimize patient‘s feelings.
C. Try to assess what the patient wants to know
o Patients vary with the amount of information they want to receive.
o Use direct and indirect cues to understand what the patient wants to know.
o Encourage them to ask questions. There questions would give you clues to
the level of understanding.
o Ask questions: Do you like to know more about this? Anything else you want
to know or ask?
D. Slow down
o Speak slowly and deliberately.
o Give pauses. It helps the client to think and understand.
E. Keep it simple
o Use simple language and short sentences
F. Avoid medical jargon
G. Tell the truth
o Be truthful.
o Do not minimize or soften the impact of a diagnosis or treatment. This type
of information can be extremely misleading and create confusion, delay
treatment and affect outcomes.
o Inform the truth with all the potential solutions and words of support and
partnership. ―It is not something good that you have this….. but we will do
everything possible and I hope things will improve …..‖

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H. Be hopeful
o While telling the truth in situations like advanced cancer, covey some hope.
o The therapeutic options available.
o Therapies that alleviate symptoms and give comfort.
I. Watch the patient‘s body language
J. Be prepared for a reaction
o Individuals vary in the way they react to stressful information.
o Some could be non-emotional. This should not be taken as lack of worry or
not understanding the severity of the problem.
o Some could cry or show denial: let them express it, don‘t interrupt but your
body language should show signs of support.
o Some could develop distrust and blame: do not react, do not let your
emotions control you. It could be difficult to establish a good partnership
with such patients.

 Don‘t dos during clinical communication

1. False reassurance
o Clients get discouraged if most symptoms and feelings they tell are answered
by reassuring them e.g. by saying ―that is okay‖ ―that is simple‖ ―we all fell
like that‖.
o They can feel their feelings are down-played or sometimes ridiculed.
2. Rejecting
o Avoid refusing patients ideas or belief without adequate explanation
3. Probing
o Do not probe patients on issues they don‘t want to discuss
4. Asking ―Why‖
o Asking ―why‖ means the patient has to defend himself or herself. Rather, ask
―how?‖.
5. Belittling patient‘s feelings or complaints
6. Judging patients or making stereotype comments
7. Interrupting conversation
o Phone calls are the most common reasons.
o Don‘t interrupt conversations to respond voice calls or distract your attention
to watch your phone for texts or alerts.
o If there are urgent issues, ask permission from the patient, tell the caller that
you are with a patient while the patient listening and ask the caller ― is there
anything urgent‖ while the patient is listening.
o You must show that the priority for you at that time is the patient.
8. Writing while having active discussion

Further reading
1. Carol Teutsch. Patient–doctor communication. Med Clin N Am 87 (2003) 1115–1145.

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2. John M. Travaline, Robert Ruchinskas, Gilbert E. D‘Alonzo. Patient-Physician

Communication: Why and How. JAOA • Vol 105 • No 1 • January 2005.
3. Iedema, R. and Manidis, M. (2013) Patient‐ Clinician Communication: An Overview of
Relevant Research and Policy Literatures. Sydney: Australian Commission on Safety and
Quality in Health Care and UTS Centre for Health Communication.ISBN: ISBN‐ 10:
0988669501.

2. Chronic Care model: Provision of care for chronic diseases and the
Chronic care model
 Chronic diseases such as diabetes, hypertension, heat failure, cancer, chronic respiratory
diseases, chronic kidney disease, and mental illnesses are major global public health
problems.
 Some communicable diseases such as HIV and hepatitis B are chronic diseases that require
follow up and treatment as in the non-communicable chronic diseases.
 The prevalence of chronic non-communicable diseases is rising in Ethiopia. The 2015
Ethiopian STEPS report on risk factors and prevalence of selected non-communicable
diseases indicated that prevalence of hypertension is 16 % and impaired fasting blood sugar
to be 5.4%.
 The management of chronic diseases is becoming a major component of primary care.
 In addition to clinical skills provision of chronic care requires a great deal of coordination,
leadership and practice improvement.
 Most primary health care systems are designed for provision of acute care, which mainly
involves evaluating and treating the disease once or a few times.
 Quality chronic care cannot be provided by a 15-minute or less interaction with health care
provider which significantly varies from provider to provider.
 The care of patients with chronic diseases entails achieving certain targets, based on
evidences. However, most patients with these diseases are either not getting the treatment at
all or they are not treated to the recommended targets. This gap occurs due to several reasons
but the most important ones are related to systems.
 Patients and their family members play important role in the care. Hence, they need to be
educated about their illnesses and actively participate in their care. They are important in
improving adherence to medications, follow up and life style changes.
 The following are basic organizations that need to be in place for providing chronic care.
1. Identify the chronic illnesses that can be followed in your institution.
2. Select a team of health care workers that will be involved in this work.
3. Identify an existing space which will be used for chronic illness follow up.

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4. Based on the standard treatment guidelines summarize the diagnostic and

treatment protocol for each disease. Focus the following areas.
I. How diagnosis is conformed? What additional clinical information is needed?
II. The treatment protocol: Pharmacologic and non-pharmacologic.
III. Follow up: Clinical &laboratory parameters to be followed and their frequency.
IV. Clearly define optimal care: what are the targets to be achieved?
V. The role of the patients and family members
VI. Patient and family education materials
5. Develop a recording keeping system
- Do not allow every health care provider to record the way they like.
- The format for follow up should be simple but includes the required relevant
information.
6. Create an appointment system
7. Keep contact addresses of patients and families and have a tracing mechanism.
8. Use the HIV care model as a template
 Once there is a chronic disease care provision service in your institution continuous
improvement in the quality of care is needed.
 There are different models used to improve the quality of chronic illness care provided in
primary care.
 One of the most widely used models is the chronic care model (CCM). The chronic care
model is a frame work of improving the quality of care. It has care six basic components.
1. Organizational support 2. Clinical information system
3. Delivery system design 4. Decision support
5. Self-management support 6. Community resources
Table. Components of the chronic care model

Components of the What is the component about and what we do?

No. chronic care model
1. Organizational Engagement and support from the leadership
support -The leadership plays important role in supporting changes,
motivating staff, securing resources and removing barriers.
role in providing motivation,
2. Clinical information Have a registry
systems  Have a system or technology that provides clinicians with a
comprehensive list and important details of patients with a
given chronic illness, called registry.
 It helps clinicians to track their patients‘ status and make
decisions.
3. Delivery system design Organizing visits and follow-ups
 Use clear appointment plans
 Have evidenced based recommendation for treatment

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 Ensure that there is a system that all patients receive the

recommended treatment
 Design an active follow up program as well : telephone
visits
4. Decision support Primary care providers need support and professional
development
 Guidelines will only be effectively implemented when
provider get professional support.
 Organize education for the staff
 Create important in reminders in their rooms
 Incorporate the summary of the guidelines in to flow
charts, patient assessment tools
 Get professional support from specialists.
5. Self-management
support Active patient and family involvement
 Patient empowerment
 Educate patients on self-management skills, setting their
goals, have their own action plans and achieve their targets
6. Community resources
The patient and the health care institutions are not enough
 Supporting organizations small or big, charity, non-
governmental, faith based, societies can provide useful
support.
 Create linkage to these organizations

Further reading
1. Ashoo Grover & Ashish Joshi. An Overview of Chronic Disease Models: A Systematic
Literature Review. Global Journal of Health Science; Vol. 7, No. 2; 2015. Published by
Canadian Center of Science and Education.
2. Katie Coleman, Brian T. Austin, Cindy Brach, and Edward H. Wagner.Evidence On The
Chronic CareModel In The NewMillennium
3. Curing the system: Stories of Change in Chronic Illness Care. Accelerating change today
(A.C.T) for America‘s health, May 2002 National Coalition on Health Care and the Institute
for Healthcare Improvement.
4. Ethiopia STEPS Report on Risk Factors for Non-Communicable Diseases and Prevalence of
Selected NCDS. Ethiopian Public Health Institute Addis Ababa; December 2016.

3. General care for hospitalized patients

3.1 Intravenous (IV) fluid therapy in adults

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Brief description
 Intravenous (IV) fluids are one of the commonly prescribed interventions in clinical practice.
They have been used for over a century
 Many clinicians take the decision of prescribing IV fluids very lightly or carelessly.
However, IV fluids are drugs with benefits and risks.
 Inappropriate IV fluid prescription is associated with increased morbidity, mortality, and
prolonged hospital stay.
 Understanding fluid-electrolyte homeostasis, conditions associated with fluid-electrolyte
disturbance, the constituents of IV fluids , assessment of volume status of patients is
important for clinicians who prescribe IV fluids.
 Total body water constitutes 60% of body weight in men and 50% in women. It is distributed
in to the intracellular fluid (ICF) compartment (40% of body weight) and extracellular fluid
(ECF) compartment (20% of body weight).
 The extracellular fluid is again divided in to interstitial (3/4 of ECF) and intravascular fluid
(1/4 of ECF) compartment
A 70kg male adult will have the following
o Total body water = 70kg x 60% = 42liters
o ICF= 70kg x 40%= 28liter
o ECF= 70Kg x 20%= 14liter
o Interstitial fluid = 14 x 3/4= 10.5
o Intravascular (plasma) volume= 3.5 liter
 Under normal conditions the body maintains fluid (water) and electrolyte balance. The fluid
input and output are balanced (equal) and the same for electrolytes.

1. Fluid balance and assessment of volume status

 Clinically fluid balance is defined as the difference between fluid intake (input) and fluid
excreted (output). See the table below for components of fluid balance.
Table. Fluid balance components for adults under normal circumstances
Normal input Volume in Variability in healthy
24hour individuals
Water from oral fluid intake (average) 1500ml highly variable
Water contained in solid foods (average) 800ml Variable
Water generated from metabolism 300ml No significant variation

Normal output Volume in 24 Variability in healthy

hours individuals
Urine 1500ml Highly variable
(minimum
500ml)
Stool 200ml Slightly variable

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Sweating and respiratory loss 900ml Highly variable

o Loss from sweat can vary
enormously from100ml to
2000ml)
o Hyperventilation also
increases fluid loss.
Insensible loss in adults for clinical purposes = 700ml/day (30 -40ml/hour) (ranges 600-
900ml)

*In febrile patients for every degree celsius increase above 37, increase the insensible loss
by 100 -150ml/day

Fluid balance = Input# (oral + IV) – Output (Urine output + Insensible loss + Other
losses*)
*Other losses :
 Drains/taps
 Diarrhea, vomiting, discharge
 Bleeding
 Loss from burn ( depends on the surface area)
#Usually forgotten input: Fluid used to dilute IV medications or keep lines patent
1. Negative fluid balance = LOSS OF FLUID
2. Positive fluid balance = GAIN OF FLUID
3. Zero fluid balance = NO LOSS OR NO GAIN (BALANCED)

 Fluid balance is not easy to measure due to significant variations in the insensible loss, water
gain from solid foods, and other factors.
 For hospitalized patients daily weight monitoring is reliable measure for fluid status.
 Incorporate daily weight monitoring as part of vital signs.
 In addition to fluid balance and weight monitoring volume status should be evaluated using
clinical assessment tools.
 Good fluid status assessment = Daily Fluid balance + Daily weight monitoring + clinical
assessment.
 Clinical tools used for assessing volume status are summarized as follows:
I. History indicating volume depletion
o History of loss: Diarrhea, vomiting, polyuria, bleeding, burn
o History of poor oral intake: Not able to take enough drinks or food.
o Thirst: usually excessive thirst
o Decreased urine volume
o Postural dizziness and palpitation
II. Physical examination indicating volume depletion
o Vital signs: Low BP, postural drop in BP, tachycardia and tachypnea

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o Weight: daily weight monitoring is a very sensitive measurement.

o Delayed capillary refill time: Press the pad (soft part) of the finger tips
until it gets pale and watch how long it takes to return back. It is delayed if
it is >2seconds
o Skin and mucosa: dried oral mucosa, decreased skin turgor
o Extremities: cold in state of shock
III. Physical examination indicating volume overload states
o Weight gain: Daily weight measurement
o Lungs: Lower lung zone crackles (also called crepitation or rales)
o JVP and neck vessels: raised JVP and full neck veins
o Liver: enlarged liver
o Lower extremities: edema
IV. Investigation useful to make IV fluid therapy decision.
o BUN and creatinine :
o Be cautious with IV fluids in patients with impaired kidney
function as they might easily develop pulmonary edema
o BUN to creatinine ration > 20 might suggest volume depletion but it
Never be used in obviously fluid overloaded (edematous patients)
o Serum electrolytes
o Sodium: crucial to decide the type of IV fluid
o Potassium: important to decide on the addition of potassium.
2. Indications for IV fluid therapy
 IV fluids are indicated when the fluid needs of an individual cannot be met with oral
intake.
 The three main indications for IV fluid therapy are resuscitation, replacement, routine
maintenance (simply called maintenance) 3R‘s. A 4th R is added in the IV fluid therapy to
encourage removal when there is evidence of fluid overload in a patient.
Indications for IV fluid therapy : 4R‘s

1. Resuscitation  Rapid correction of shock using rapid boluses of

IV fluids
2. Replacement  Replace lost fluid until signs of hypovolemia
improve
 Continue replacement if there is ongoing loss
3. Routine maintenance  Providing the daily fluid and electrolyte needs
using IV fluid, when a patient cannot or is not
allowed to take orally.
4. Removal  When there are signs of fluid overload or
excessive positive fluid balance, allow removal
by stopping IV fluids or IV furosemide.

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3. Composition and availability of IV fluids in Ethiopia

 Ideal IV fluid does not exist. It should also be known that the available IV fluids have
significantly different composition.
 IV fluid prescription and administration requires understanding the compositions of the IV
fluids.
 The commonly available IV fluids in Ethiopia are the following.
1. 0.9% saline (Normal saline or NS)
2. Ringer‘s lactate (RL),
3. 5%Dextrose in water (5%DW or D5W)
4. 5%dextrose in normal saline (DNS or D5NS).
 Unfortunately all the available IV fluids come with similar 1000ml package. Other smaller
packages like 500ml and 100ml are not available.
 Some important IV fluids and additives are not available in the Ethiopian market. This
compromises choices and can result in using the wrong IV fluids or mixing existing fluids at
the bedside, increasing the risk of infection and wrong volume proportions.
 We recommend having the following IV fluids and additives for clinical use in addition to
the available ones.
1. 0.45% saline (Half-strength normal saline, 1/2NS): for common use
2. 0.45% saline with 5% dextrose: for common use
3. 5% dextrose in Ringers lactate: for common use
3. Sodium bicarbonate: for common use
4. 3% Saline (hypertonic saline): for specialized hospitals
 To improve ease and safety, we recommend availing at least: 500ml and 100ml volume
packages.
Table. Compositions of common IV fluids

Na Cl K Glucos Ca Buffer Volume Comment

Fluid (mmol/l) (mmol/l) (mmol/l) e (mmol/l) increas
type e by 1L
135-145 95-105 3.5-5.5 70-140 2.2-2.6 24-32 - -
Plasma (mg/dl)
(serum)
154 154 0 0 0 0 250 Too much chlorine.
NS Causes hyperchloremic
metabolic acidosis
130 109 4 0 1.35 28 250ml A balanced
RL lactate crystalloid.
Lactate is
metabolized to

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bicarbonate.

0 0 0 50 g/l 0 0 84 Electrolyte free

5%DW water.
Risk of
hyponatremia.

154 154 0 50 g/l 0 0 300ml

DNS
77 77 0 0 0 0 125ml Less chloride than
½ NS NS

77 77 0 50g/l 0 0 200ml
1/2NS
with 5%
dextrose

5. Prescription and administration of IV fluids: based on indications

A. Indication: Resuscitation for hypovolemia

 Who needs IV fluid resuscitation, in state of hypovolemia?
1. Patients with severe hypovolemia
Severe hypovolemia = Cold extremities and delayed capillary refill >2seconds +/-
other signs of hypovolemia (tachycardia, oliguria, dry buccal mucosa, dizziness)
2. Patients with Hypovolemic shock
Hypovolemic shock = severe hypovolemia (as above) + systolic BP (SBP)
<90mmHg or mean arterial BP (Map) <65mg +/- change in mental status

 Which IV fluids to use for resuscitation?

o Use either Ringer‘s lactate(RL) or Normal Saline(NS)
o RL is preferred over NS, particularly if larger volumes continue to be
required.
o Never use 5%DW for resuscitation.
o In case of hemorrhage blood transfusion is preferred but as it takes time
resuscitation should start with RL or NS.

 How much and how fast?

o For adults: Give the first 1000ml (01liter) fast. Then reassess.
o Assessment: BP, PR, mental status, capillary refill and extremities, urine
output.
o If the shock or signs of severe hypovolemia continue: Give 500ml bolus
(over15 minutes) and reassess. If needed give another 500ml bolus.

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o After giving a total of 2000ml, revaluate. Look for ongoing loss and
other causes of shock (sepsis, cardiogenic shock, cardiac tamponade,
adrenal insufficiency).
o If severe hypovolemia continues, give 200-300ml bolus 3-4 times;
assess also for signs of fluid overload(particularly pulmonary crackles)

 When do we say resuscitation is completed and proceed to next step?

o Minimum requirement: SBP >90mmHg or MAP>65mmHg, improved
mental status, good urine output (>50ml/hour), improved capillary refill.
o Shock might recur: with ongoing losses severe hypovolemia or shock
might recur, hence, re-evaluation is needed

B. Indication: Replacement

 What is replacement fluid?

o IV fluid given to correct non-severe hypovolemia and ongoing losses.
o It is given when there is hypovolemia but no need for renunciation or after
resuscitation is completed.

 Which fluid is the preferred?

o The preferred fluid depends on the fluid lost and electrolyte abnormalities.
o One must bear in mind that there is no ideal fluid; hence, monitoring of
electrolytes is important.
o The following serves as a guide for the preferred initial IV for common
losses. Subsequent fluid should be decided based on serum electrolytes.
Loss/clinical disorder Initial preferred fluid

1. Hemorrhage Blood products

2. Diarrhea RL

3. Vomiting NS

4. Burn RL

5. Intraoperative RL

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6. DKA/HHS NS

7. Head injury/stroke NS(do not add dextrose)

 How much replacement fluid is given?

o The volume of replacement fluid needed is variable depending on the degree
of volume depletion, ongoing loss and urine output.
o Give = estimated ongoing loss + urine output + 100ml/hour
o If estimation is difficult give 150-200ml/hour (1liter over 06 hours for the
first 12 -24hour) to achieve a urine output > 50ml/hr.
o If there is any sign of fluid overload stop fluid. If there is worsening of
hypotension give 200-300ml bolus and increase the rate of fluid
administration.
 When to stop replacement?
o When signs of hypovolemia are corrected and ongoing loss either stopped or
can be corrected by oral fluid.
o Do not leave IV fluid replacement order unrevised over 24 hours.

C. Routine maintenance IV fluid

o Maintenance fluid therapy is needed when a patient is not able to or expected to
eat or drink for a prolonged period of time e.g. Patient ordered to be NPO
perioperatively, NPO ordered for resting the bowel, severe dysphagia, refractory
vomiting).
o The goal of maintenance fluid therapy is to preserve water and electrolyte
balance and to prevent starvation ketosis.

 What is the average fluid and electrolyte requirement for an adult, not taking
oral fluids and food? Although it is variable, the following gives a good estimate
o Water ~ 2000ml/day
o Sodium ~ 1-2mmol/Kg/day
o Potassium ~ 0.5-1mmol/kg/day(Half of the sodium)
Hence for an average adult man (~70kg) the needs will the following in 24hr
o Water ~2000ml (25-30ml/kg/day)
o Sodium ~ 70 -140mmol
o Potassium ~ 35-70mmol

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o Glucose ~ 50-100g of glucose. This amount of glucose is just to prevent

starvation ketosis and catabolism. This will not address the nutritional
needs of an adult at all.

 What is the preferred IV fluid type for routine maintenance in adults?

o The preferred fluid type: ½ strength (0.45%) NS with 5% dextrose +
20meq (01amouple of KCl) added in each liter. One liter(01bag) running
for 12 hours.

o The practical fluid type for maintenance: Because of the 0.45% NS is

not available we recommend DNS (NS with 5% dextrose) + 20eq of KCl
(01 ampoule added to it).
DNS 1000ml + 20mmol of KCl (01ampoule) run 12 hourly
- Potential side effects: hyperchloremia, worsening of hypernatremia,
hyperchloremic metabolic acidosis but as the volume of the
maintenance fluid is low the risk is also low.

o Alternative maintenance fluid:

- If DNS is not available, use the following as alternatives. We do not
recommend routine use of the following as repeated puncture of the
IV fluid bag for adding dextrose increases the risk of infection and
increases cost significantly.
RL 1000ml + 20mmol of KCl (01ampoule) + 32g of glucose (80ml
or 04 vials of 40% dextrose, each 20ml) run 12hrly
OR
NS 1000ml + 20mmol of KCl (01ampoule) + 32g of glucose (80ml
or 04 vials of 40% dextrose, each 20ml) run 12hrly

 When to stop maintenance IV fluid?

o As soon as the patient starts to take oral fluids or liquid diet.

D. Complex medical problems where IV fluid therapy should be used cautiously. See
the relevant topic in this guideline.
1. Heart failure, impaired kidney function (AKI or CKD), nephritic or nephrotic
syndrome: IV fluids should generally be avoided unless absolutely needed. When
used use low volumes with close monitoring.
2. Cirrhosis and hepatic encephalopathy: Avoid RL and DW. Be cautious with NS or
DNS.
3. Poorly controlled diabetes: Avoid dextrose containing fluids
4. Hyponatremia: Avoid D5W, RL. NS or DNS might be used.

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5. Hypernatremia: Avoid NS and DNS. Use D5W.

Reminder: The four D‘s of IV fluid therapy.

1. Drug: IV fluids are drugs. They have indications, contraindications, benefits as

well as adverse effects.
2. Dosing: Different indications (resuscitation, replacement or routine maintenance)
have different dosing. Dose also varies depending on other factors.
3. Duration: Stop IV fluids when there are no more indications. Always ask‖ does
this patient need IV fluids at this point in time)
4. De-escalation: When there are signs of fluid overload decrease or stop the IV fluid
and consider IV diuretics if the fluid overload is severe.

Further reading
1. Intravenous fluid therapy in adults in hospital: NICE (National Institute for Health and Care
Excellence, UK) Clinical guideline [CG174]. Published date: 10 December 2013 last
updated: 05 May 2017. https://www.nice.org.uk/guidance/cg174.
2. Michael L. Moritz, M.D., and Juan C. Ayus, M.D. Maintenance Intravenous Fluids in
Acutely Ill Patients. N Engl J Med 2015;373:1350-60.DOI: 10.1056/NEJMra1412877
3. Richard Leach. Fluid management on hospital medical wards. Clinical Medicine 2010, Vol
10, No 6: 611–15. Royal College of Physicians, 2010.
4. Manu L. N. G. Malbrain, Thomas Langer, Djillali Annane, Luciano Gattinoni et al.
Intravenous fluid therapy in the perioperative and critical care setting: Executive summary of
the International Fluid Academy (IFA). Ann. Intensive Care (2020) 10:64
https://doi.org/10.1186/s13613-020-00679-3.

3.2 Intravenous lines: Care and Complications

 Intravenous (IV) lines or cannuale are one of the most commonly used devices in clinical
practice.
 IV lines are commonly inserted to peripheral veins; however, in certain situation big IV lines
might be needed to be inserted in to big central veins, these lines are called central lines.
 Peripheral IV lines are generally safe devices but if they are not inserted or cared
appropriately they can be associated with significant complications.
 Here, we give guidance on the care and complications of peripheral IV lines. Discussion on
central lines is beyond the scope of this guideline.

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1. Insertion of peripheral IV lines (Cannulae)

A. Site selection
 Upper extremity
o Upper extremity veins are preferred.
o Try to avoid lower extremity veins due to high risk of thrombosis and
thrombophlebitis.
 Non-dominant forearm
o Give preference to the non-dominant side (the left side in right handed individuals
and the vice versa).
 Start distally
o The distal posterior forearm veins are preferred; followed by veins of the dorsum
of the hand.
o If the distal veins have been used repeatedly or fail, go to more proximal veins.
o Using proximal veins initially might result in extravasation and hematomas when
distal veins are used later.

 Areas to avoid
o Infected skin
o Joints: in emergency situations (resuscitation) veins in the antecubital fossa
(anterior elbow) can be used for about 24 hour.
o Recently attempted site
o Burnt skin or severe edema
o Evidence of thrombophlebitis or repeatedly used veins
o Arms in which there is hemodialysis arteriovenous (AV)fistula
o In patients with CKD avoid the anterior forearm for future need of AV fistula

B. Insertion
 Consent
o A verbal consent with appropriate explanation is adequate.
 Aseptic precautions
o Hand hygiene
- Don‘t start insertion without having an alcohol based hand rub with
you.
- The initial hand hygiene can be done using soap and water or alcohol
based hand rubs.
- In between the procedure use alcohol based hand rubs
- After gloving, hand rubs should be applied on gloves as well.

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o Skin disinfection
- Wash the insertion site with soap and water if dirty before using
antiseptics.
- Preferred disinfectant: alcohol-chlorhexidine solution, 1-2% in ≥ 70%
alcohol.
- If not available: use either a 10% iodine in ≥ 70% alcohol solution or
≥ 70% alcohol solution
- Apply the disinfectant in a circular motion to a wide area (~10cm long
X 5cm wide)
- Allow the antiseptic to dry.
o Non-touch technique
- Do not touch part of the cannula to be inside the vein and the tip of the
IV set.
o Don‘t shave ( Clipping hair is preferred)
o Have a colleague to assist you: Only if possible

 The insertion procedure

o Prepare equipment
- Prepare all the necessary equipment, including normal saline for
flushing.
o Select vein
- Select vein, apply tourniquet to visualize it better and palpate it. Then,
loosen or release the tourniquet.
o Disinfect the skin
- Perform hand hygiene with alcohol based hand rub, irrespective of
gloving
- Disinfect the insertion site as detailed above.
o Insert
- Tighten the loosened tourniquet or reapply it.
- Perform hand hygiene with alcohol based hand rub.
- Put on clean (non-sterile) gloves, if not applied at the beginning.
- Insert the device: Using the direct or indirect method
Direct: Enter the skin over the vein directly at 30-40 degree.
Indirect: Enter the skin adjacent to the vein and direct it again to enter
the side of the vein.
- .Advance the device slowly and steadily until you meet resistance.
- Lower the needle to a 15 to 20 degree and slowly pierce the vein.
- Observe flashback of blood. If you fail to see flashback, pull the
catheter slightly back and observe.

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-If there no is flash back remove the catheter and try again
-Tilt the needle lightly upward or pull back the needle slightly to
advance the cannula. Push the cannula until fully inserted or you feel
a resistance.
- Withdraw the needle while applying a gentle pressure over the cannula
to prevent bleeding.
- Release tourniquet and remove the stylet.
o Flush with saline
- Give saline push 2-4ml with a 10cc syringe or attach IV fluids.
- A 10cc syringe is preferred as it produces lower pressure.
- If the there is a resistance or there is a swelling remove the cannula
immediately.
o Call a colleague
- After three to four unsuccessful attempts at inform another colleague
to attempts.
- If there is any breach of aseptic technique, use a new cannula.
o Secure the cannula
- Use sterile tape.
Table: Color coding of cannulae base on size
Color Size(gauge ) Flow rate (mL/min)
Orange 14 290
Gray 16 176
Green 18 76
Pink 20 54
Blue 22 31
Yellow 24 14

C. Complication during IV line insertion

o Hematoma: When veins rupture or rarely when an artery is injured
o Arterial puncture or cannulation of an artery:
- This serious complication tends to occur more in neonates and infants when the
cannula is inserted in the antecubital fossa (elbow).
- Suspect it when there is a bright red blood, pulsatile flow (comes-pause-comes-
pause) with high pressure (pushing the syringe plunger).

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-When you suspect an arterial puncture/cannulation or when you have any doubt
remove the cannula immediately, apply localized pressure with a single finger
for 5-10 minutes and observe.
o Damage to nerves
o Vasovagal syncope (fainting): some patients are afraid of the sight of a needle or
blood. It mainly occurs when the patient is in sitting position. If the patient is
anxious or has previous history of syncope, do the insertion in supine position

2. Care of the IV line(cannula)

I. Observation ( review)
o During each shift (at the end of each shift) and every time when injections
are given and infusion are changed
o Observe for signs of phlebitis (see below)
o Position
o Infiltration
o Bleeding
o Soiling
II. Inform and encourage patients or care givers to report when there is one of
the followings:
o Pain
o Bleeding
o Dislodgement
o Flushing Intravenous fluid is completed
III. Flushing
o Before giving any injection or infusion
o If not used, every 24 hour. Consider removing if not used for 48 hours.
o During flushing use 10cc syringe to decrease pressure
o Flush with normal saline 3-5 ml in pulsatile way ( push-stop-push)
IV. Resite (remove and change to another site)
o When there are signs of phlebitis
o The IV site is not functional
o If there is infiltration or extravasation
o If the IV site stayed for more than 4 days and it is still necessary. Needed
and functional IV lines without signs of phlebitis may be kept for more
than 5 days, if the patient has difficult vein or in children.
o IV line inserted at referring health institutions need to be changed (re-
sited) if there is no clear indication when they were inserted.
o IV lines inserted on the neck (external jugular) should be changed as soon
as other peripheral veins are accessed.

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V. Removal
o Remove any IV line which is not needed.
VI. Changing IV set (administration set)
o Change immediately: after giving chemotherapy or blood products
(blood products need a different set provided by the blood bank service)
o Change in 24hour: continuous infusion of heparin or lipid containing
parenteral nutrition
o Change when IV site is changed: Change the IV set every time there a
new cannula inserted.
o Do not change when not indicated: Frequent changes in IV sets without
indications increases the risk of infection
VII. Medication labeling
o All bags or bottles of intravenous fluids or medications should be labeled,
containing the following information
- Name of the patient
- Date and time of start
- Rate of infusion
- Nurse‘s (any other any care professional doing it) name and sign
VIII. Hand hygiene
 All health care workers should perform hand hygiene using alcohol based hand
rubs (>70% alcohol) or wash with soap and water in the following circumstance.

o Insertion or removal (before putting gloves), dressing change, drawing

blood, or before
o Before manipulation or changing dressing
o Before opening the IV set (administration set)
o During preparation of medications for IV administration

3. Complication associated with peripheral IV lines

 Phlebitis: Inflammation of the vein due to either infection, chemical irritation
caused by the medications given or mechanically induced by the cannula itself.
 IV line (catheter) associated blood stream infection: when microorganisms
enter in to the blood stream via the IV line.
 Infiltration: when a non-vesicant solution ruptures in to the tissue surrounding
the vein. This occurs when tip of catheter slips out of the vein or passes through
the wall of the vein, or as the vein stretches it allows fluid to pass into the
surrounding tissue
 Extravasation: occurs when a vesicant drug or fluid infiltrates into the tissue
surrounding the venipuncture site.

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 Thrombosis: When a clot forms in with within the lumen of the cannula or the
vein where the cannula is inserted
 Dislodgement: a cannula can dislodge if it is not properly fixed.

Signs of phlebitis
Early signs
o Swelling
o Redness
o Hotness
o Pain: along the path of the cannula
Late signs
o Fever
o Cord like vein( hard to palpate)
o Pussy discharge

Further reading
1. Australia, Queensland Government Department of Health Centre for Healthcare Related
Infection Surveillance and Prevention & Tuberculosis Control Guideline for Peripheral
Intravenous Catheters [PIVC] Version 2 – March 2013.
https://www.health.qld.gov.au/__data/assets/pdf_file/0025/444490/icare-pivc-guideline
2. Eoin Harty. Inserting peripheral intravenous cannulae –tips and tricks. Update in Anaesthesia
| www.anaesthesiologists.org.
3. Gabriel B. Beecham; Gary Tackling.Peripheral Line Placement. StatPearls [Internet].

3.3 Pressure (Bed sore) prevention and management

 A pressure sore/ulcer (bed sore) is a localized injury to the skin and the underlying tissue
resulting from unrelieved pressure.
 The sore arises as a result of the soft tissue compression between a bony prominence and
external structures (e.g. bed, stretcher or wheelchair).
 Pressure sores pose a huge burden on patients, families, and health care systems.
 The rate of development of pressures sores in hospital wards is one of the key indicators of
the quality of nursing care.
 Prevention and management of pressure sores is a fundamental aspect of the care of
hospitalized patients.
I. Who is at high risk for pressure sore?
 The risk factors for pressure sore can be related to the patient (intrinsic) or the external
environment. See the table below.

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Table. Risk factors for pressure sore

I. Patient related (Intrinsic) risk factors

Risk factors Typical examples
No.
1. Decreased mobility Paralysis form any cause, coma or prolonged sedation,
fracture

2. Comorbidities Peripheral arterial disease, decreased pain sensation,

malignancy, diabetes mellitus, dementia, heart failure

3. Poor nutritional status Anorexia or cachexia from chronic illness, catabolism

from acute illnesses, dehydration

4. Ageing skin

II. External (Extrinsic risk factors )

Risk factors Typical examples
No.
5. Pressure form hard Beds, wheelchair or stretcher
surfaces
6. Moisture Urinary or fecal incontinence, excessive sweating,
discharges

7. Friction or shear From patient inability to move and involuntary muscle

movements

II. Assessing the risk of pressure sore in individual patients

 There are a few validated score (scales) to assess the risk of pressure sores in individual
patients.
 None of the scoring tools completely replace clinical evaluation; however, they provide
objective, reproducible and comprehensive guide.
 One of the commonly used scales, BRADEN SCALE is provide in the table below.
 The BRADEN scale needs to be completed at the time of admission and reassessment
needs to be depending on the patient‘s clinical condition. In patients who are clinically
deteriorating, the score should be revised more frequently.

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BRADEN SCALE: For predicating pressure sore risk

Name of the patient: _________________________ Hospital no. _________

Date of assessment:__________________________ Name of the HCW: ____________

SCORE
RISK FACTOR
1 2 3 4 Patient‘s
score

1. Sensory perception Completely very Slightly No

(Ability to respond to absent limited limited impairment _______
pressure related discomfort)
2. Moisture Constantly Often occasionally Rarely
(Degree to which the skin is moist moist moist moist _______
exposed to moisture)
3. Activity Bed Chair Walks Walks
(Degree to which patient bound bound occasionally frequently _______
moves)
4. Nutrition Probably Adequate Excellent _______
(Usual food intake pattern) Very poor inadequate
5. Friction and shear Moves but Moves -
(Ability to move on bed or Requires with independent _______
chair) moderate to minimum ly
maximum assistance
assistance
_______
TOTAL SCORE OF THE PATIENT

Interpretation: the lower the total score, the higher the risk of pressure sore.
Total score < 12 = high risk 13 – 14 = Moderate risk 15 – 18 = Low risk

III. Evaluating the patient for the presence of pressure sores

 Inspect the skin every time the patient is repositioned
 All skin areas from head to toe need to inspected quickly, focusing on bony
prominences: Sacrum, Ischial tuberosity, greater trochanters of the femurs, heels
 Look for the presence of visible ulcer, erythema, swelling, induration (hardness),
hotness or coldness.
 If there is visible change or ulcer, describe and categorize the lesion.

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 Ulcer: Location, size (width X length in cm), stage, discharge (exudate)

Table. NPUAP/EPUAP PRESSURE ULCER CLASSIFICATION SYSTEM

Description
Stage / category
I: Non-blanchable  Intact skin with non-blanchable redness of a localized area
Erythema usually over a bony prominence
 The area may be painful, firm, soft, warmer or cooler.
 .It may be difficult to detect

II: Partial Thickness Skin  Shallow, open ulcer with a red/pink wound bed.
Loss  May also present as an intact or ruptured blister.

 Full thickness skin loss, subcutaneous fat may be visible.

III: Full Thickness Skin  Bone, tendon or muscle are not exposed.
Loss

 Full thickness tissue loss with exposed bone, tendon or

IV: Full Thickness muscle. The exposed tendon/bone is visible or palpable.
Tissue Loss  Slough or eschar may be present on some parts of the
wound bed.
Unstageable: Depth  Full thickness tissue loss in which the base of the ulcer is
Unknown covered by slough (yellow, gray, green or brown) and/or
eschar (tan, brown or black) in the wound bed.
 Stable (dry, adherent, intact without erythema or fluctuance)
eschar on the heels should not be removed.

IV. Preventive care for pressure sores

 All high risk patients should be provided with preventive care.
A. Skin care
o Keeping the skin clean.
o Cleanse the skin promptly after episodes of incontinence.
o Use high absorbency incontinence products.
o Avoid vigorously massaging or rubbing the skin.
o Use emollients (e.g. paraffin, vaseline, petrolatum) in dry skin and old
individuals
B. Positioning and repositioning
o Reposition frequency depends on the individual conditions. It should be
prescribed clearly.

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o Determine repositioning frequency based on the individual‘s level of

mobility, general condition, comfort, and pain.
o For patients who can‘t move at all, repositioning is typically needed every 2
hours.
o Have a reminder strategy to adhere to the repositioning schedule.
o Use 300 tilt position (Tilt the pelvis with pillow under the buttock and a pillow
in between the legs). See the picture below.
o Position in the right, back, left side +/- prone alternatively. Use prone position
if the patient condition allows.
o In hemodynamically unstable patients repositioning should be down slowly
and with close observation.
o Avoid positioning on bony prominences, erythematous skin, an already formed
ulcer or medical devices (tubes, drains or foreign bodies).
o Avoid dragging; rather use lifting e.g. using bed sheets.
o To decrease sliding down avoid positioning patients in semi-recumbent
positions; unless medically contraindicated e.g.in patients with heart failure.
o In patients with heart failure or other fluid overload states, keeping patients in
semi-recumbent or sitting (900) is absolutely needed.
o Ensure the heels are off the surface. Elevate the heels using a pillow or other
cushions.
o Offload the heel completely and distribute the weight of the leg along the calf
without placing pressure on the Achilles tendon.
o Do not leave a patient on a bed pan for a long period of time.

300 tilt positioning

C. Nutrition and hydration

o Evaluate the nutritional and hydration status of patients. Treat malnutrition
o Most hospitalized patients need high calories and high protein diet.

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o Encourage patients to take foods rich in vitamins and minerals; if not possible,
provide multivitamin and mineral supplements.
o Make sure patients are well hydrated.
D. Keep sleeping and sitting surfaces clean and dry
o Keep bed sheets clean and dry. Change bed sheets promptly when they get wet
or soiled.
o Make sure mattresses are comfortable and distribute weight evenly.
E. Regularly inspect the skin(see above on evaluating for the presence of pressure
sores)

V. Managing a pressures sore.

 Management of a pressure sore depends on the stage, the presence or absence of
necrotic tissue, and the presence or absence of infection.
A. Pain control
B. Cleansing the wound: stage II and above
o Cleanse the wound every time dressing is done
o Use normal saline for cleansing.
o Do not use hydrogen peroxide for any degree of pressures sore. Hydrogen
peroxide is too toxic for tissue even at low concentrations.
C. Dressing; Stage II and above
o Apply dressing to open pressure sores (stage II and above).
o Moist dressing is preferable. The most practical one in the Ethiopian setting
is saline moist gauze dressing.
o Use a single gauze to cover deep ulcer.
o The frequency of changing the dressing depends on the amount exudate.
Initially more frequent (twice daily to daily), subsequently the frequency of
dressing might be reduced, depending on the healing.
D. Debridement: Stage III and IV
o Devitalized (dead or necrotic tissue) should be debrided.
o There are two types of debridement: Sharp (surgical) or non-sharp (non-
surgical).
o Sharp (surgical debridement): stage III or IV ulcer with necrotic tissue and
features of cellulitis, abscess, crepitus or sepsis needs urgent sharp
debridement.
o Non-sharp debridement: Stage III or IV ulcer with non-adherent necrotic
tissue and no urgent indication. The most practical approach in Ethiopian
setting is mechanical debridement before each dressing session.
o Do not debride dry eschar (dark or brown) on the heel or ischemic limbs.
E. Systemic antibiotics

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o Use of systemic antibiotics is indicated when there is evidence of spreading

infection. The following the indications
- Sepsis suspected to originate from infected wound
- Cellulitis : hot, red, swollen, and tender surrounding tissue
- Osteomyelitis: clinical and radiologic evidence
o Infections of pressure ulcers are typically polymicrobial. The most
commonly isolated organisms include staphylococci and streptococci as
well as enterococci, Enterobacter, Proteus, and anaerobes
o Antibiotics choice should be driven by local sensitivity data of these
organisms when there are indications (see the relevant chapter for antibiotic
choices)
F. Topical antibiotics
o Topical antibiotics are not indicated in the routine care of pressure sores.
o Topical antibiotics might be considered when there in non-healing ulcers
with no overt infection but a possibility of bio-film is considered.
G. Evaluation of healing
o Assess pressure sore for healing: decreasing wound size, decreasing
exudate, clean wound bed, and granulation.
o If the wound does not show evidence of healing in two weeks‘ time with
wound care, alleviation of pressure and nutritional support, look for
evidence of infection (superficial or deep) or non-debrided necrotic tissue.
H. Surgical consultation: Consult surgical team when the following are evident
o Sepsis suspected form the wound
o Cellulitis advancing from the pressure ulcer
o Crepitus
o Persistent malodor
o Fluctuant lesion
o Crepitus

Further reading
1. Prevention and Treatment of Pressure Ulcers/Injuries: Quick Reference Guide. Emily
Haesler (Ed.). EPUAP/NPIAP/PPPIA: 2019.
2. Daniel Bluestein, Ashkan Javaheri. Pressure Ulcers: Prevention, Evaluation, and
Management Am Fam Physician. 2008;78(10):1186-1194, 1195-1196.
3. NICE (National Institute for Healthcare and excellence) UK Clinical guideline:
Pressure ulcers: prevention and management. Published: 23 April 2014.
www.nice.org.uk/guidance/cg179

3.4 Stress ulcer prophylaxis and treatment

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 Stress ulcers area gastric ulcers which occur in critically sick patients in ICUs or patients with
burn, and sever trauma.
 Stress ulcer commonly occurs in the fundus and body of the stomach but can also occur in
other parts of the stomach the duodenum or esophagus.
 A clinically important stress ulcer bleeding is defined us an upper GI bleeding in critically
sick patients resulting hemodynamic deterioration or requiring blood transfusion.
 The two major risk factors for clinically important stress ulcer bleeding are being on a
mechanical ventilator for more than 48 hours and the presence of coagulopathy.
 Overt stress ulcer bleeding in ICU patients is associated with increased mortality.
 The clinical manifestations of a bleeding stress ulcer are: hematemesis (coffee ground or frank
red blood in the NG tube aspiration or vomiting), melena, progressive drop in hemoglobin.
 All patients admitted to ICU, patients with severe burn and, trauma need evaluation for
possible stress ulcer prophylaxis.

A. Indication for providing stress ulcer prophylaxis

1. Mechanical ventilation for >48 hours.
2. Coagulopathy: platelet count <50,000 per m3 or INR >1.5, or PTT >2 times the
upper limit of normal.
3. History of upper GI bleeding or confirmed peptic ulcer disease in the past year.
4. Traumatic brain or spinal cord injury
5. Severe burn
6. Two or more of the following minor criteria: severe sepsis/septic shock, ICU stay
> 1week, or glucocorticoid therapy (>250 mg hydrocortisone or the equivalent)
B. Which agents to use for prophylaxis?
o Either a proton pump inhibitor (PPI) or a histamine-2 (H2) blocker can be used.
o Route: oral (NG tube) or IV route can be used.
o Dose:
Omeprazole 20 - 40mg, PO (via NG tube) or IV once daily
OR
Cimetidine 400mg, PO (via NG tube) BID to TID or 200mg IV, BID to TID
o Duration: the prophylaxis should only be given as long as the risk factors are
there. It should be discontinued when there are no risk factors.
C. Potential harms of providing stress ulcer prophylaxis
o Suppression of gastric acid secretion in critically ill patients is associated with
increased risk of nosocomial pneumonia and Clostridium difficile infection (CDI).
o Prophylaxis should only be provided for high risk patients (see above).
Stress ulcer prophylaxis is not indicated in non-ICU hospitalized patients and ICU
patients without risks.

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D. Management of a bleeding stress ulcer

1. Resuscitation
o Patients with hemodynamic compromise should be resuscitated with crystalloids
promptly. It is good to warm the crystalloids to avoid hypothermic coagulopathy.
o Whole blood should be prepared in the meantime and transfusion should be the
main stay of resuscitation once it is made available
2. Correction of coagulopathy
o If INR > 1.5: Give fresh frozen plasma (10-15ml/kg) which is 3 -4 bags, then
follow if the coagulopathy is corrected or not.
o If platelet is <50,000 or the patient has been on Aspirin or Clopidogrel: 06 units
of platelets and check if the bleeding is corrected
3. Nasogastric(NG) tube placement
o NG tube should be inserted in all patients with stress ulcer bleeding for
decompression +/- lavage.
4. Proton pump inhibitor, intravenous route
o Omeprazole 80mg IV loading followed by 40mg IV BID: preferred for cost
effectiveness.
OR
o Esomeprazole 80mg IV loading followed by 40mg IV BID
OR
o Pantoprazole 80mg IV loading followed by 40mg IV BID
o Alternative: If Intravenous PPIs are not available use oral PPI‘s with similar
doses as in the IV.
5. Endoscopy
o Endoscopy is indicated for all patients with suspected stress ulcer bleeding for
both diagnostic and therapeutic purposes.
6. Surgery
o Surgery is indicated in patients with refractory bleeding despite conservative
therapy or if there is evidence of perforation

Further reading
1. Deborah Cook and Gordon Guyatt. Prophylaxis against Upper Gastrointestinal Bleeding in
Hospitalized Patients. N Engl J Med 2018;378:2506-16. DOI: 10.1056/NEJMra1605507
2. Toews I, George AT, Peter JV et. al. Interventions for preventing upper gastrointestinal
bleeding in people admitted to intensive care units (Review). Cochrane Database of
Systematic Reviews 2018, Issue 6. DOI:10.1002/14651858.CD008687.pub2.

3.5 Hospital acquired infection prevention

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 See chapter II on antimicrobial resistance and its containment, topic 2.3 hospital acquired
infection prevention.

3.6 Surgical wound infection: prevention and management

 Surgical site infections (SSIs) are infections which occur at or near a surgical incision site or
the organ operated or the space left after surgery, within 30 days of the procedure or 90 days
if a prosthetic material is implanted.
 SSIs can be superficial, deep, organ/space specific.
1. Superficial infection: involving the skin or subcutaneous tissue of the incision.
2. Deep infection: involving the deep soft tissue of the incision (fascial & muscle layers)
3. Organ/space infection: involving any part of the organs or spaces that was
manipulated during surgery.
 SSIs are common sources of hospital acquired infection with an associated increase in
morbidity and mortality, hospital stay, and increased cost of care.
 Nearly half of SSIs are preventable by applying good clinical practice.
 SSIs arise from interaction of several risk factors; including the degree of contamination of
the site at the time of the surgery, overall health of the patient, use of appropriate
antimicrobial prophylaxis, and the technique of the surgeon.
 Some of the patient related risk factors are smoking, obesity, diabetes, malnutrition, use of
steroids and other immunosuppressive medications, old age, and anemia.
 Surgical wounds are classified based the degree of contamination of the surgical wound at
the time of the operation. (See the table below)

Table. Wound class as it applies to surgical wound

Wound class Description
1. Clean  An incision in which no inflammation is encountered during the
procedure, without a break in sterile technique.
and
 The respiratory, alimentary, genital, or urinary tracts are not
entered.
2. Clean-contaminated  An incision through which the respiratory, alimentary, or
genitourinary tract is entered under controlled conditions but with
no contamination encountered.
3. Contaminated  An operation in which there is a major break in sterile technique
or gross spillage from the gastrointestinal tract.
or

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 An incision in which acute, non-purulent inflammation is

encountered.
or
 Open traumatic wounds that are >12 - 24 hours old.
4. Dirty or infected  An operation in which the viscera are perforated or when acute
inflammation with pus is encountered.
or
 Traumatic wounds in which treatment is delayed, there is fecal
contamination, or devitalized tissue.

 Wound healing can occur with either primary or as secondary intention.

o Healing by primary intention occurs when a wound has been sutured after an
operation and heals leaving a minimal, cosmetically acceptable scar.
o Healing by secondary intention occurs when a wound is deliberately left open at the
end of an operation because of excessive bacterial contamination or when there is a
devitalized tissue.
o Wound healing by secondary intention may be sutured within a few days (delayed
primary closure), or much later when the wound is clean and granulating
(secondary closure), or left to complete healing naturally without suturing.

I. Prevention of surgical site infections

 Several interventions in perioperative period have been shown to reduce the risk of
surgical site infections; they are summarized in the table below.

Table: Preventive interventions to decrease surgical site infection rates

Preoperative interventions

Additional information Responsible

Intervention body

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Patient and
Patients baths or showers before surgery surgical ward
team

Surgical ward
Mechanical bowel preparation for elective team
colorectal surgeries
Surgical team
Do not remove hair. If absolutely necessary,
do not shave, rather use clippers
Indications Anesthetist or
Give prophylactic IV antibiotics 60-120 o Clean-contaminated surgical team
minutes before incision when there is o Contaminated
indication. procedures.
o Consider the half-life of the antibiotic and o Dirty or infected wounds
the time needed for infusion to achieve the require therapeutic, not
high tissue concentration during incision prophylactic, antibiotics
o In cesarean delivery give the prophylactic
antibiotic before skin incision.
Surgical team
Scrubbing ( proper hand hygiene)
>>
Do not discontinue immunosuppressives

Intraoperative

Surgeons
Use sterile drapes and surgical gloves
o Alcohol based Surgeons +
Use alcohol based solutions for skin chlorhexidine solutions pharmacy
preparation are preferred. (procurement)
o If chlorhexidine solutions
are not, use alcohol-based
povidone-iodine solution.
If it is not also available
aqueous povidone-iodine
solution
Anesthetist
Maintain adequate tissue perfusion and
oxygenation.
Administer 80% Fio2 and keep SPO2 >95%
Use available warming Surgical team
Avoid hypothermia mechanisms

Maintain asepsis and discipline in the

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operating room

Post operatively

Anesthetist
Administer 80% FiO2 in the first 2-4 hours and surgical
postoperatively ward team

Surgical team
Do not administer additional prophylactic
antibiotics in the postoperative period, in
clean and clean-contaminated wounds, even
with the presence of a drain
Evaluate the wound using Surgical ward
Wound care non-touch technique team
Cleanse and dress the wound
Ward team
Glycemic targets: keep blood sugar < and medical
200mg/dl all the time in both diabetic and department
non-diabetic patients

II. How to select antibiotics for prophylaxis?

 The commonest organisms causing surgical site infection in clean procedures are
streptococcal species, Staphylococcus aureus, and coagulase negative staphylococci.
 In clean-contaminated procedures in addition to the above, gram negative rods and
enterococci predominate.
 In a surgical procedure involving a viscus, the organisms involved reflect the flora and
it is polymicrobial.
 The prophylactic antibiotic choice depends on the procedure type as mentioned above
and the local antimicrobial sensitivity.
 Intravenous route is preferred.
III. Evaluation of surgical wounds
 Surgical wounds need to be evaluated regularly using a non-touch technique, assess the
bed, edge, size, presence of exudate, presence of dead tissue(eschar or slough),
tunneling and categorize the wound condition as follows:
A. New epithelialized: wound completely covered with epithelium, no exudate, and
no signs of infection.
B. Fully granulating: wound bed filled with granulation tissue to the level of the
surrounding skin, no dead space or devitalized tissue, no signs of infection.

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C. Early/partial granulation: > 25% of wound bed covered with granulation tissue,
< 25% covered with devitalized tissue (eschar and/or slough), no signs or
symptoms of infection and wound edges open.
D. Not healing: wound with > 25% avascular tissue (eschar and/or slough) or the
presence of sign of infection or clean but non-granulating wound bed or
closed/hyperkeratotic wound edges.
IV. Wound cleaning and dressing
 Clean wounds healing primary intention need little intervention other than protection by
clean dressing and regular observation.
o Cleansing will be required if any foreign material, debris, exudate or devitalized
tissue is observed.
o Clean with normal saline.
o Showering can be allowed after 48 hours, unless the surgeon has a specific
recommendation.
 Wounds healing by secondary intention or with dehiscence:
o Need cleansing with normal saline with the aim of removing foreign materials,
debris, and lose dead tissue.
o Debridement: the need and the type (sharp vs. non-sharp) should be decided by
the surgeon depending on the extent of adherent devitalized tissue.
o Loculated abscess should be opened and drained
V. Treatment of surgical wound infections
 Localized infection with no signs of cellulitis or systemic symptoms like fever need
wound cleansing and debridement (if needed) only. No need for antibiotics.
 Fever: fever < 48 hours from surgery is unlikely from wound infection, >96 hours
(04days) it is likely to be wound infection among other causes, in between 48-96hours
it is a possibility.
o Explore the wound: examine the wound, remove sutures, drain any collection
and take samples for culture.
o Start systemic antibiotics depending on sensitivity data
 Infections above the waste (the diaphragm):
1. Coverage of Staphylococcus aureus with either cloxacillin or a first or
second generation cephalosporin or Clindamycin.
2. If high rates of methicillin resistant Staphylococcus aureus: cover
methicillin resistant staphylococcus with vancomycin.
3. If the patient has other features of sepsis: start vancomycin.
 Infections below the waist (the diaphragm): coverage of gram negatives,
anaerobes, and gram positives needed.

Further reading

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1. Connie L. Harris RN; Janet Kuhnke; Jennifer Haley BMSc et. al. BEST PRACTICE
RECOMMENDATIONS FOR THE Prevention and Management of Surgical Wound
Complications. 2018 Canadian Association of Wound Care.
woundscanada.ca [email protected]
2. Preventing surgical site infections: implementation approaches for evidence-based
recommendations. World Health Organization 2018.
3. Sandra I. Berríos-Torres ; Craig A. Umscheid ; DaleW. Bratzler et. al. Centers for Disease
Control and Prevention Guideline for the Prevention of Surgical Site Infection, 2017. JAMA
Surg. 2017;152(8):784-791. doi:10.1001/jamasurg.2017.0904.
4. Surgical site infections: prevention and treatment. National Institute for Health and Care
Excellence (NICE) guideline(NG125). 11 April 2019. www.nice.org.uk/guidance/ng125

3.7 Urinary bladder catheter care

 Urinary bladder catheterization is a common procedure done in both in-patient and out-
patient settings.
 Although it appears to be a simple and straightforward procedure, it is associated with
significant complications.
 The most common complication associated with indwelling urinary is urinary tract infection
called catheter associated urinary tract infection (CAUTI) and the sepsis associated with it.
 Other complications include urethral trauma/erosion/perforation, bladder perforation and
fistula, retention of balloon fragments, encrustation (deposition of mineral salts resulting in
obstruction) and bladder stone formation.
 External (―condom‖) catheters in males can cause pressure associated ulceration of the skin,
pigment changes, and in prolonged applications the ring of the catheter can cause ischemia
and necrosis of the penis.
 Rate of CAUTI is considered one quality measure of hospitals.

I. Principles of urinary bladder care

1. Catheterize when only absolutely needed.
2. Keep the catheter if and only if the patient still needs it.
3. Apply aseptic precautions and rigorous infection prevention practice.
4. Provision of consent, ensuring privacy, dignity to the patient.

II. Appropriate indications for indwelling urinary catheter (Foley) insertion

(Modified from The Ann Arbor Criteria for Appropriate Urinary Catheter Use. Ann Intern Med. 2015;162:S1-
S34. Reference number 2.)

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1. Acute urinary retention due to non-traumatic causes. E.g. BPH and medications
which cause bladder outlet obstruction.
2. Chronic urinary retention with bladder outlet obstruction.
3. Stage III or IV pressure ulcers that cannot be kept clear of urinary incontinence
other urinary management strategies.
4. Urinary incontinence in patients for whom it is found difficult to provide skin care
despite other urinary management strategies.
5. Hourly monitoring of urine volume needed for fluid/vasopressor decision or as part
of close hemodynamic follow up in critically ill patients.
6. During surgery: to follow volume status and prevent bladder over-distention.
7. After specific surgeries of the genitourinary tract or adjacent structures (i.e.
urologic, gynecologic, colorectal surgery).
8. For preventing severe pain caused by movement to urinate e.g. acute fracture
9. In the management of gross hematuria with clots for the purpose of irrigation.
10. Improving the comfort of a patient receiving end of life care, if catheter insertion
addresses the patient‘s and family‘s goals.

III. Contraindications to indwelling urinary catheter

 The only absolute contraindication to insert a Foley catheter is urethral injury,
commonly associated with pelvic trauma.
 Gross hematuria or the presence of blood at the urethral meatus in a patient with
pelvic trauma should be considered as possible urethral trauma.
 Relative contraindication includes systemic bleeding, urethral surgery, the presence
of false passages, and urethral surgery.

IV. Inappropriate use of indwelling urinary catheters

1. Urinary incontinence when skin care and other cares can keep the patient dry;
including patients with dermatitis or grade I-II pressure ulcers.
2. Routine use in ICU without the above mentioned indication.
3. Urine sample collection for sterile or non-sterile specimens, if possible by other
collection strategies.

V. Appropriate indications for condom (external) catheter use

 Indications for external catheter use are similar to indwelling catheter except the fact
that it should not be used for patients with urinary retention or management of gross
hematuria with clots.

VI. Indwelling urinary catheter selection, preparation, and insertion

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 Clinician‘s order
o Urinary catheterization should be performed up on the order of a clinician.
 Consent
o Verbal consent should be received.
o During consent adequate explanation on the need to catheterize, about the
insertion procedure, expected duration, the potential discomfort, and possible
complications.
 Privacy and dignity
o The procedure should be done in private procedure rooms or using appropriate
shield.
o The procedure should be done in a dignifying manner.
 Catheter size
o Length: The standard length Foley catheter (40-44 cm) can be used in
hospitalized women and women.
o In ambulatory women shorter length catheters (23-26cm) are preferred, if
available.
o Short length catheter should never be used in men as it causes damage to the
prostatic urethra.
o Charriere (Fr) Size: The smallest size that provides adequate drainage should be
used.
- Females= 14 or 16
- Male = 16 or 18
o Balloon size: A 5cm balloon size should be used for routine catheterization.
Check the manufacturer‘s recommendation on the balloon size.

 The procedure
o Needed materials: appropriate size catheter, 2 pairs of sterile gloves, cleansing
agent (normal saline), lubricating gel (sterile, closed), syringe filled with water
for injection, drainage bag, bed protection(disposable pad), and alcohol based
hand rub.
o See the table below for detailed description of the procedure.

VII. Urinary catheter and drainage system care

1. Avoid kinking of the catheter or collecting tube.
2. Keep the urine collecting bag below the level of the bladder at all times.
3. Do not rest the bag on the floor.
4. Empty the urine bag regularly. Do not keep it until it is full, empty when it about
two-third fill. Avoid contact of the drainage plug with the collecting container.

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5. Unless obstruction is anticipated as in bleeding after prostatic or bladder surgery

irrigation should be avoided.
6. Do not clean the periurethral area with antiseptics in an attempt to prevent
infection (CAUTI). Routine hygiene such as cleansing the meatus area during bathing is
appropriate.
7. Do not use topical or systemic antibiotics in an attempt to prevent CAUTI
8. Do not change catheter at fixed regular intervals. It should be when clinical
indications such as, obstruction, infection, or when the closed system is compromised.
9. Urine sample collection: For urinalysis and culture, aspirate urine using sterile
adaptor or after clamping collect the urine directly in to test tube. For large volumes of
urine (e.g. 24 hour urine for protein or electrolytes) can be obtained from the urine bag.

Table. Indwelling urinary catheter insertion procedure

(Adapted from Adult Catheterisation and Catheter Care Guidelines. NHS Grampian Corporate.
NHSG/ACCCG/GUI/001)
1. Positioning , preparation of equipment and sterile filed
o Explain & discuss procedure with patient. Receive verbal consent.
o Ensure good light source is available
o Perform hand hygiene (water and soap or alcohol-based hand rub)
o Inform or assist or remove patient‘s lower garments in respectful manner.
o Assist into supine position with legs bent and hips flexed.
o Place protection pad on the bed. Cover patient‘s body.
o Prepare work area with required equipment.
o Open out sterile dressing pack using an aseptic technique.
o Pour normal saline into container. Open gloves, gel, catheter
o Create a sterile field. Arrange the sterile drape under patient‘s buttocks and thighs.
o Perform hand hygiene again and put on sterile gloves
2. Insertion of the catheter
Female Male

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o Using sterile swabs, separate the labia o Hold the penis with a sterile swab, retract
minora so that the urethral meatus is the Foreskin (if present)
visible. o Clean the glans and urethral orifice with
o Using sterile swabs, cleanse around the saline.
urethral orifice with saline using single o Hold the penis with a sterile swab below
downward strokes. the glans, raise it until it is almost totally
o Apply lubricating gel to the urethral office extended.
or at the tip of the catheter o Maintain this position until the catheter is
o Remove and dispose of the first pair of inserted and urine flows.
gloves o Insert catheter gently into the urethral
o Perform hand hygiene orifice, slowly advance the catheter up the
o Apply 2nd pair of sterile gloves urethra for 15-25cm.
o Position a sterile container to catch urine o If resistance is felt at the external sphincter
o Open the inner cover of the catheter and slightly increase the traction on the penis
expose 10cm of catheter and apply gentle steady pressure on the
o Introduce the tip of the catheter into the catheter. Ask the patient to strain slightly
urethral orifice in an upward (superiorly) or cough.
then backward (posteriorly) direction. o Once urine flows, advance the catheter
o Advance the catheter until 5 - 6 cm has almost to its bifurcation.
been inserted. When urine is present o Reduce or replace the foreskin
advance the catheter 6–8 cm.
3. Fixing and connecting the catheter
o Inflate the catheter balloon slowly with sterile water 5cm or as per the manufacturer‘s
recommendation.
o Observe patient for signs of pain and distress.
o Withdraw catheter gently until resistance is felt to ensure the catheter balloon is inflated.
o Attach the catheter to a sterile closed drainage system
o Ensure vulva area or the glans is clean and dry
o Measure amount of urine drained

Further reading
.
1. Carolyn V. Gould; Craig A. Umscheid; Rajender K. Agarwal et al. GUIDELINE FOR
PREVENTION OF CATHETER-ASSOCIATED URINARY TRACT INFECTIONS 2009.
Last update June 06 2019. https://www.cdc.gov/infectioncontrol/guidelines/cauti/
2. Jennifer Meddings; Sanjay Saint; Karen E. Fowler et al. The Ann Arbor Criteria for
Appropriate Urinary Catheter Use in Hospitalized Medical Patients: Results Obtained by
Using the RAND/UCLA Appropriateness Method. Ann Intern Med. 2015;162:S1-S34.
doi:10.7326/M14-1304.
3. NHSG/ACCCG/GUI/001. Adult Catheterisation and Catheter Care Guidelines December
2017 Version 1. NHS Grampian.
4. Urinary Catheter Care Guidelines Version: 6 June 2020. NHS Southern health. NHS trust.

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4. Venous thromboembolic disease prevention

 See chapter VII. Hematologic disorders, topic 5 venous thromboembolic disease, sub
topic 5.1 prevention of venous thromboembolic disease

Chapter 4: CARDIOVASCULAR DISORDERS

4.1. Arrhythmias
Brief description
 Arrhythmias are disorders of cardiac rate, rhythm and conduction.
 Bradyarrhythmias include sinus bradycardia, sinus pauses and atrioventricular blocks.
 The tachyarrhythmias can further be classified into supraventricular and ventricular
arrhythmias, based on their site of origin.
o Supraventricular tachyarrhythmias includes atrial fibrillation, atrial flutter,
paroxysmal supraventricular tachycardia and multifocal atrial tachycardia.
o Ventricular tachyarrhythmias include ventricular tachycardia and ventricular
fibrillation.
 The etiologies for arrhythmias are:
o structural heart disease (valvular heart disease, cardiomyopathies, coronary artery
disease)
o Thyrotoxicosis
o electrolyte abnormalities
o ingestion of stimulants
o side effects of some medicines (digoxin, antiarrhythmic medicines
 Clinical features of arrythmias in general include:
o Palpitation
o Shortness of breath
o Dizziness/syncope
o Sensation of a pause in the heart beat
o Chest discomfort that mimics symptoms of myocardial ischemia(angina)
o Development of Heart Failure or decompensation of previously existing Heart
Failure
o Sudden death
 ECG is the main stay of diagnosis.
o Other investigations like Echocardiography, Chest X-ray, Thyroid function test,
blood count, electrolytes should be guided by clinical data.

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o Prior to treatment of any suspected arrhythmia the diagnosis should be confirmed

with ECG.
- It is dangerous to give any antiarrhythmic medicine without doing ECG!

Figure 1.1: Clinical approach to arrhythmias (adopted from STG 3rd edition, 2014)

1.1 Tachyarrhythmias
1.1.1 Supraventricular tachyarrhythmias
1.1.1.1 Paroxysmal supraventricular tachycardia
Brief description
 Paroxysmal supra-ventricular tachycardia (PSVT) is an intermittent narrow complex
tachyarrhythmia other than AF, atrial flutter, and MAT (Multifocal Atrial Tachycardia).
 PSVT usually occurs in individuals without underlying structural heart disease.
 ECG shows regular narrow QRS tachycardia. P wave may be seen preceding or following
or superimposed on QRS complex or may not be seen.
Treatment
Objectives of therapy include:
 Control ventricular rate
 Identify and treat the cause
 Identify, prevent and treat precipitating factors

Non pharmacologic
 Vagal maneuvers: maneuvers which increase vagal activity can terminate episodes of
PSVT. ECG and blood pressure monitoring is required during the procedure.
o Carotid sinus massage: supine position with the neck extended. The carotid sinus
is located inferior to the angle of the jaw at the level of the thyroid cartilage.

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Steady pressure is applied to one carotid sinus for 5 to 10 seconds. If no response,

repeat it in the contralateral side after 1-2 minutes.
Note: Carotid massage should not be attempted in patients with carotid bruit/stenosis or
ischemic stroke. Both carotid sinuses should never be massaged simultaneously.
o Valsalva maneuver: while in the supine position the patient is instructed to exhale
forcefully against a closed glottis with closed mouth and nose for 10 seconds.
Adequacy indicated by neck vein distension, and increased tone in the abdominal
wall muscles.
 Synchronized electrical Cardioversion: required rarely for hemodynamically unstable
patients. The energy needed is 150 to 200 joules for monophasic defibrillators.
Pharmacologic
 Termination of acute episode
First line
Adenosine, I.V, very rapidly (over 1-2 seconds): Initial: 6mg; if not effective within 1-2 minutes,
12mg may be given; may repeat 12mg bolus if needed. Follow each dose with 20mL very rapid
Normal saline flush.
Alternatives
Metoprolol, IV, 2.5-5mg every 2-5 minutes (maximum total dose: 15mg over a 10-15minute
period).
or
Verapamil, I.V, 2.5-5mg over 2 minutes; second dose of 5-10mg may be given after 15-30
minutes; maximum total dose: 20-30mg
or
Digoxin, 0.5 to 1mg IV over a period of 10 to 15 min followed by 0.25mg every 2-4 hours with a
total dose less than 1.5mg with in 24-hour period
 Prevention of recurrence (chronic therapy)
First line: beta blockers
Metoprolol succinate (Extended release): 25-200mg/day, P.O.
or
Atenolol, 25-100mg/day, P.O. or Propranolol 10-40mg P.O. 3-4 times daily
Alternatives
Verapamil, immediate release 40-120mg, P.O.TID or extended release 180-360mg/day
1.1.1.2 Atrial fibrillation and flutter
Brief description
Atrial fibrillation is marked by disorganized, rapid, and irregular atrial activation which results
in irregular ventricular response. The ventricular rate is usually rapid. The ECG in Atrial
Fibrillation is characterized by the lack of P-waves, irregularly irregular ventricular response and
narrow QRS.

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Atrial flutter is characterized by regular rapid atrial rate of 260–300 beats per minute, which
usually results in a regular ventricular response in a 2:1 ratio resulting in a heart rate of 130– 150
beats per minute. The ventricular response can sometimes be in 3:1, 4:1, irregular or rarely 1:1
ratio. The typical ECG finding is of saw-tooth appearance of the baseline mainly on inferior
leads (II,III,AVF) with rapid, regular and narrow QRS.

Treatment
Note: The management of atrial fibrillation and atrial flutter are the same.
Objectives of treatment
 Controlling ventricular rate
 Prevention of thromboembolic events
 Identification and treatment of the cause
 Identification, prevention and treatment of precipitating factors
Non pharmacologic
 Avoid stimulants (e.g. Caffeine, Khat) and alcohol intake.
 Immediate electrical cardio-version-associated with hemodynamic instability
(cardiogenic shock) due to a rapid ventricular rate. If hypotension occurs at
ventricular rate <130 beats/min, other causes of hypotension should be investigated.
The energy requirement is usually 100 to 200 joules; it should be synchronized.

Pharmacologic
 Acute ventricular rate control
First line
Metoprolol, 2.5-5mg, IV, over 3–5 min, to maximum total dose 15mg over 10-15 minutes
Alternative
Digoxin, 0.25mg, IV, q2h until 1 mg total (digoxin is the first line medicine if atrial
fibrillation is associated with severe left Ventricular dysfunction)
 Chronic ventricular rate control
First line: Beta blockers
Metoprolol, preferred beta blocker in patients with Heart Failure with depressed LV (left
ventricle) systolic function.
Immediate release: 25-100 mg twice daily
Extended release: 25-200mg/day
or
Atenolol, 25-100mg P.O., daily
Alternatives
Digoxin, 0.125 – 0.25mg P.O., daily. Digoxin can be added to beta blocker when the
ventricular rate control is suboptimal. It is the preferred agent when Heart Failure due to LV
systolic dysfunction is not well controlled.

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or
Verapamil, 40-80mg P.O., 2-3 times daily.

 Anticoagulation to prevent cardioembolic cerebrovascular accident (CVA)

Risk stratify patients for thrombotic complications with the CHA2DS2-VASc score.
This is a scoring calculator used to estimate annual stroke risk in a patient with AFib or atrial
flutter. It assigns 1 point each to presence of heart failure, HTN, age 65 to 74, diabetes, female
sex, vascular disease, and 2 points each to age >75, and history of CVA. The higher the score,
the higher the annual stroke risk. For patients with CHADSVASC score >1, anticoagulation is
generally indicated unless high bleeding risk.

Scoring systems for assessing the risk of stroke (CHA2DS2-VASc) and bleeding (HAS-BLED)
in patients with atrial fibrillation

CHA2DS2-VASc Score HAS-BLED Score

Congestive heart failure 1 Hypertension (systolic blood pressure 1
>160 mm Hg)
Hypertension 1 Abnormal renal and liver function 1 or 2
(1 point each)
2 Stroke 1
Diabetes mellitus 1 Bleeding tendency/predisposition 1
Stroke/transient ischaemic 2 Labile INRs (if on warfarin) 1
attack/thromboembolism
Vascular disease (prior myocardial 1 Elderly (e.g. age >65 years old) 1
infarction, peripheral artery disease, or
aortic plaque)
Age 65–74 years old 1 Drugs or alcohol (1 point each) 1 or 2
Sex category (i.e. female sex) 1
Maximum score 9 Maximum score 9

Choice of anticoagulant: depends on etiology of AFib or atrial flutter.

 For patients with mechanical valves, mitral valvular disease, or ventricular assist devices,
warfarin is the only oral anticoagulant available. For other patients, direct oral
anticoagulants (DOACs) can be used.
 DOACs approved for AFib include factor Xa inhibitors (apixaban, rivaroxaban,
edoxaban) and direct thrombin inhibitors (dabigatran). These agents do not require lab
monitoring. Cost is the limiting factor for wider use in resource limited settings like
Ethiopia.
 Rivaroxaban is the available direct oral anticoagulant in Ethiopia.

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o The dose is Rivaroxaban 20 mg Po daily.

o Dose adjustment is required for patients with renal failure, elderly, low body
weight and those with high risk of bleeding.

Warfarin: widely available and affordable anticoagulant

Warfarin has a narrow therapeutic range and during therapy monitoring using INR is mandatory.
An INR of 2 to 3 is the anticoagulation goal range for warfarin.
Warfarin, starting dose, 2.5-5mg/day, dose titrated to achieve INR of 2.0-3.0. The goal is to
maintain time in therapeutic (TTR) range above 70 %.

Warfarin dosing and monitoring

Suggested dose changes for maintaining INR within a target range of 2–3

INR Dose change

<1.5 Increase by 20%
1.6–1.9 Increase by 10%
3.1–3.4 Decrease by 10%, adjustment may not be necessary
3.5–3.9 Decrease by 20%, consider holding one dose
4.0–4.9 Hold dose until INR returns to range then decrease by 20–30%

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Management of supratherapeutic INR values

INR Patient situation Action
3.1–5.0 No bleeding or need for rapid Omit next few warfarin doses and/or restart at lower dose
reversal when INR approaches desired range. If INR is only
minimally above range, no dose reduction may be needed.
(i.e., no need for surgery)

5.1–9.0 No bleeding or need for rapid Omit next 1–2 doses, monitor INR more frequently, and
reversal restart at lower dose when INR approaches target range or
omit dose and give 1-2.5 mg vitamin K orally (use this if
patient has risk factor for bleeding).

No bleeding but reversal needed Vitamin K1 2–4 mg orally (expected reversal within 24
for surgery or dental extraction hours); give additional 1–2 mg if INR remains high at 24
within 24 hours hours.
9.1–20.0 No bleeding Stop warfarin; give vitamin K1 3–5 mg orally; follow INR
closely; repeat vitamin K1 if needed. Reassess need and
dose of warfarin when INR approaches desirable range.
Rapid Serious bleeding or major Stop warfarin; give vitamin K1 10 mg by slow IV
reversal warfarin overdose infusion. May repeat vitamin K1 every 12 hours and give
required fresh plasma transfusion or prothrombin complex
(>20.0) concentrate as needed. When appropriate, heparin can be
given until the patient becomes responsive to warfarin.

Life Replace with prothrombin complex concentrate and give

Threatening 10 mg of vitamin K1 by infusion. May repeat if needed.
bleeding Give fresh frozen plasma if prothrombin complex
concentrate not available.

In addition to stroke risk assessment, a discussion regarding anticoagulation should include an

assessment of bleeding risk and involve shared decision making to take into account patient
preferences. The HAS-BLED (Hypertension, Abnormal renal/liver function, Stroke, Bleeding

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history or predisposition, Labile international normalized ratio, Elderly, Drugs/alcohol

concomitantly) score uses several common risk factors and provides an estimate of bleeding risk.
The selection of an anticoagulant agent (warfarin or rivaroxaban) for should be individualized
on the basis of risk factors, cost, tolerability, patient preference, potential for drug interactions,
and other clinical characteristics, including time in the international normalized ratio (INR)
therapeutic range (TTR) if the patient has been taking warfarin.

1.1.1.2. Ventricular tachycardia

Brief description
Ventricular tachycardias are wide QRS tachychyarrhythmias that originate in the myocardium.
They are commonly associated with some form of structural heart disease. Based on their clinical
significance, they can be divided in to two:
1. Malignant (potentially lethal) arrhythmias: sustained ventricular tachycardia (VT) and
Ventricular fibrillation.
2. Non sustained (hemodynamically tolerated) arrhythmias: premature ventricular contractions
(PVCs), non sustained ventricular tachycardia (NSVT), and accelerated idioventricular rhythm
(AIVR).
A ventricular tachycardia which stays for more than 30 seconds is labeled sustained.
All Wide QRS (> 120 ms) tachycardias are considered and treated as ventricular
tachyarrhythmias until proved otherwise.
Treatment
Objectives of treatment include:
 Prevent degeneration of ventricular tachycardia to ventricular fibrillation.
 Reverse cardiac arrest
Non pharmacologic
 CPR should be provided to patients with sustained VT with cardiac arrest (the victim is
unresponsive, pulseless and not breathing).
 O2 via face mask or nasal catheter.
 Continuous ECG monitor.
 Suction device and endotracheal intubation set should be ready.
 Correct electrolyte disorders.
 Reassure patients with non sustained ventricular tachycardia.
Defibrillation:
 Sustained polymorphic VT, ventricular flutter, or ventricular fibrillation
Emergency defibrillation (without synchronization), with >200 Joules (monophasic),
increase the energy to the maximum if arrhythmia persists.
 Sustained monomorphic VT: synchronized with >200 Joules (monophasic).
Note:

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 If the hemodynamic status allows conscious sedation should be provided.

 DC cardioversion is first line therapy for sustained wide QRS tachycardias.
 Pharmacologic treatment may be an acceptable option in hemodynamically stable
monomorphic VT with no Heart Failure.
Pharmacologic
First line: Intravenous Amiodarone
Stable VT regimen:
Step 1: 150mg over first 10 minutes (dilute in 100mL D5W)
Step 2: 360mg over next 6 hours (dilute 500mL D5W): 1 mg/minute
Step 3: 540mg (dilute in 500 to 1000ml D5W) over next 18 hours: 0.5mg/minute

Pulseless VT (cardiac arrest) regimen: If unresponsive to defibrillation attempts and CPR

Amiodarone, I.V push, 300mg (undiluted), if VT or VF recurs, administer supplemental dose of
150mg and continue CPR.
Alternative: Intravenous lidocaine
Both stable VT and Pulseless VT (cardiac arrest) regimen:
Lidocaine, I.V, 1-1.5mg/kg; repeat with 0.5-0.75mg/kg every 5-10 minutes if no response.
(maximum cumulative dose: 3mg/kg).
- Follow with continuous infusion of 1-4mg/minute
- Preparation for continuous infusion: 2g of lidocaine/250mL D5W
- Rate of infusion: 1mg/min = 7.5ml/hour, 2mg/min =15ml/hour, 3mg/min= 22.5ml/hr,
4mg/min= 30ml/min

Prevention of recurrence
Non-pharmacologic
 Standard treatment of the underlying cause is the main stay of treatment for preventing
recurrent VT. (e.g. treatment of acute coronary syndrome)
 Correct precipitating causes (e.g. hypoxia, hypo/hyperkalemia, acidosis, pulmonary
embolism).
 Discontinue arrhythmogenic medicines-digoxin, antiarrhythmic medicines.
Pharmacologic
First line
Amiodarone, P.O., 800-1600mg/day in 2 divided doses for 1-3 weeks, when adequate arrhythmia
control is achieved, decrease to 600-800mg/day in 1-2 doses for 1 month. Maintenance:
400mg/day
Alternative or additional to Amiodarone
Beta blockers: Metoprolol, extended release: P.O.,25-200mg/day or Atenolol, 25-100mg daily

Refer the patient to next care delivery after stabilization is strongly recommended.

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1.2 Bradycardia (Bradyarrhythmia)

Brief description
AV block describes a delay/block of atrial impulses at the atrioventricular node of varying
severity. When severe it results in symptomatic bradycardia which can manifest as easy
fatigability, Heart Failure, syncope, seizures and bradycardia associated ventricular tachycardias.
It is caused by structural heart diseases (mainly ischemic heart disease, cardiomyopathies,
congenital heart disease), medicines (beta blockers, verapamil, digoxin), electrolyte
abnormalities, hypothyroidism and cardiac surgery.
ECG is the diagnostic of AV block.
Treatment
 Look for reversible causes and act accordingly
 Symptomatic bradycardia should be referred to the next health care facility for
cardiologist evaluation.

4.2. Heart Failure

Brief description
Heart Failure is an abnormality of cardiac structure or function leading to failure of the cardiac
output to meet the body's metabolic requirements despite normal filling pressures. Clinically it is
a syndrome consisting of typical symptoms (shortness of breath, fatigue, orthopnea, ankle
swelling) and signs (raised JVP, pulmonary crackles, displaced apex beat, edema). Identification
of the underlying cause of the Heart Failure is central to diagnosis. It could result from valvular
disease, ischemic heart disease, hypertension, cardiomyopathies, thyrotoxicosis, congenital heart
disease, etc.
2.1 Acute Heart Failure

Definition: The new onset or recurrence of gradually or rapidly developing symptoms and signs
of HF requiring urgent or emergent therapy and resulting in hospitalization. It can be worsening
of symptoms in known cardiac patients (the majority) or a new onset heart failure (Denovo).
Acute heart failure syndromes are classified based on the relative absence and/or presence of
congestion and hemodynamic compromise.
Key Questions

 Does the patient have heart failure?

 If so which syndrome among the acute heart failure syndromes?
 Is it a new onset or worsening of a previously known cardiac disease?
 Is there a treatable precipitating factor?
 Does the patient require admission to the ICU or a general medical ward?

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Two-minute hemodynamic profile

assessment: Patients presentation can be
fitted in either of these syndromes.

Warm=good systemic perfusion

Cold=hypoperfusion (Cardiogenic shock

CS=Cardiogenic shock

Dry=No lung congestion

No PE or CS (only Predominant PE Wet= Lung congestion (Pulmonary Edema
worsened congestion) (PE=Pulmonary Edema

Predominant CS Both PE and CS

PE:Pulmonaryedema CS=Cardiogenic
shock

The following management approach works for all acute heart failure syndromes. Additional
Specific management recommendations for pulmonary edema and cardiogenic shock are given
separately.

Clinical features:

Symptoms: dyspnea, orthopnea, PND, cough, leg swelling, RUQ pain, abdominal distension
Signs: tachycardia, tachypnea, high/normal/low BP, basal crepitations, pleural effusion,
distended neck veins, raised JVP or Positive hepatojugular reflex, displaced AI, active/quite
precordium, S3/S4 gallop, +/- murmurs, tender hepatomegaly, ascites, leg edema

Factors leading to less rapid deterioration

Non adherence to drugs/diet or under dosage

Infections (pneumonia, IE)
Anemia
Thyroid disorders
Pregnancy
Renal failure
Drugs (BB, CCB, NSAIDS)

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Factors leading to rapid deterioration

Tachy/brady arrhythmia
Acute Coronary Syndrome
(ACS)
Acute pulmonary embolism
Hypertensive crisis
Cardiac tamponade
Aortic dissection
Also look for precipitating factors through history and P/E

Indications for admission

Indications for admission to the ICU Indications for admission to General ward

 Cardiogenic shock  Worsened congestion

 Dyspnea at rest (SO2 < 90% which doesn‘t  Dyspnea at rest (tachypnea or SO2<
improve with intranasal O2) 90%) which improves with intranasal O2

 Hemodynamically significant arrhythmia

 Acute Coronary Syndrome (ACS)

 Hypertensive emergency

 Altered mental status

Diagnosis
Diagnosis of heart failure is clinical. But investigations are necessary to identify the underlying
cause, precipitating factor, and to guide and monitor management.

To identify the underlying cause: Echocardiography, ECG, CXR

To identify precipitating factors based on clinical evaluation (in addition to the above
investigations): CBC, ESR, U/A, blood culture, TFTs, Urine HCG, Cr, BUN, etc..
To guide and monitor management: K+, Na+, Cr, BUN, ALT, AST

New York Heart Association (NYHA) Classification of Severity /Functional Capacity

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Class I Patients with cardiac disease but without resulting limitation of physical
activity. Ordinary physical activity does not cause undue fatigue, palpitations,
dyspnea, or anginal pain.
Class II Patients with cardiac disease resulting in slight limitation of physical activity. They
are comfortable at rest. Ordinary physical activity results in fatigue,
palpitation, dyspnea, or anginal pain.
Class III Patients with cardiac disease resulting in marked limitation of physical activity.
They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation,
dyspnea, or angina.
Class IV Patients with cardiac disease resulting in inability to carry on any physical activity
without discomfort. Symptoms of heart failure or the anginal syndrome may be
present even at rest. If any physical activity is undertaken,
discomfort is increased.

Stage of Heart Failure

Stage A High risk for HF, without structural heart disease or symptoms
Stage B Heart disease with asymptomatic left ventricular dysfunction
Stage C Prior or current symptoms of HF
Stage D Advanced heart disease and severely symptomatic or refractory HF
Treatment
Goals of management
 Improve symptoms (congestion and low output symptoms)
 Restore normal oxygenation
 Optimize volume status
 Identify and manage precipitating factor
 Identify etiology and manage if possible (eg. ACS, arrhythmias)
 Optimize chronic oral therapy when needed
NB. Management should be instituted early in parallel with the diagnostic work up.
If patient has pulmonary edema or cardiogenic shock (see the respective sections for
initial management approach)
Non-Pharmacologic
 Salt restriction (< 2gm or added salt), fluid restriction (< 1.5-2l/day) for
hyponatremic patients
 Administer O2 if SO2< 90%.
Pharmacologic
Diuresis:

 Send sample for Cr, BUN, K+ and Na+ initially and proceed with diuresis.

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 For diuretic naive patients start furosemide 40 mg IV if BP>90/60 mmHg and double the
dose every 2-4 hour until the urine output is >1 ml/kg/hr (40-70ml/hr). Response to IV dose
occurs 2-4 hours later.
 For those already on oral furosemide, start with equal dose of IV furosemide.
 Maintain the dose of furosemide which gave adequate response on a TID basis.
 Start spironolactone 25-50 mg/day unless K+> 5.0 meq/l or Cr> 1.6 mg/dl or GFR<30
ml/min (main reason is to prevent hypokalemia due to furosemide).
 If patients were already talking ACEIs and BBs, they can continue to take them during
hospitalization as long as they are not severely congested, are hemodynamically stable and
have normal renal function.
 Temporary discontinuation or dose reduction of BB may be necessary if BP is low or
borderline and patient is severely congested (pulmonary edema).
 Temporary discontinuation or dose reduction of ACEIs/ARBs may be necessary if BP is low
or borderline and recent renal function derangement.
 Manage the identified precipitating factors.
Follow up
 Use the standard heart failure management follow up sheet posted by the bedside.
 V/S including orthostatic hypotension and SO2 every 1hr until patient stabilizes and
then every 4-6 hrs.
 24 hrs urine output and fluid balance documented every 6hrs together with V/S.
 Weight every 24hrs (morning prior to eating and voiding, same scale).
o goal is 1kg/day weight loss
 Signs of heart failure every 12hrs (JVP, basal crackles, S3 gallop, hepatomegaly,
edema).
 Symptoms (dyspnea, orthopnea).
 Cr, BUN, K+, Na+ every 24hrs until patient stabilizes and then every 3-5 days and
manage accordingly

Table: Sample heart failure follow up form

Date time PR RR BP T Wt SO2 UOP Creps Hepato JVP Edema Cr Na+ K+ sign

megaly

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Goal of diuresis Signs of excess diuresis

 Negative fluid balance  Signs of dehydration

 Weight loss (0.5-1kg/day)  Hypotension(overt/orthostatic)
 Clearance of crepitations in the lungs  Elevated RFTs despite improvement of congestion
 Decrement in edema, hepatomegaly,  Severe hypokalemia
JVP
 Improvement of dyspnea, orthopnea
Improvement in renal function (Cr,
BUN)

Patient not responding

 Make sure that
o Patient is taking medications as prescribed and is on salt free diet.
o Precipitating factors is managed.
o Patient is not getting drugs like NSAIDS, CCBs, BBs.
NB: Patients with deranged renal function and hypoalbuminemia require higher doses of frusemide from
the outset.
 Adjust the diuresis.
o Increase the dose of furosemide (max. 400-600mg/day) and increase spironolactone
to 50-100mg/day.
o Increase the frequency of administration of furosemide 4-6 x per day. Repeated IV
bolus doses are recommended that continuous infusion.
o In ICU continuous furosemide infusion by perfuser according to protocol: ( 10-
80mg/hr) can be used if still refractory to the above measures.
o If patient not responding with the above approaches, add hydrochlorthiazide 12.5
mg/day in the morning 30 minutes before frusemide administration.
 Digoxin 0.125-0.25 mg/day for positive inotropy and rate control in patients with atrial
fibrillation.
 For patients with hypertension and severe Acute MR intravenous nitroglycerin infusion can be
considered in addition to diuretics. (see pulmonary edema section)

Patient improving
 Decrease the dose of diuretics every day depending on patient condition.
o goal is to use the lowest possible dose and frequency to keep patient dry.
 For patients in whom previous BB and ACEIs/ARBs have been discontinued consider
reinitiating the drugs as soon as possible sequentially(ACEIs/ARBs followed by B
blockers)

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 For HFrEF previously not taking ACEIs/ARBs or BB.

o Start one of the ACEIs/ARBs as soon as BP and RFTs permit and escalate until
discharge (see chronic heart failure section)
o Start one of the BB following ACEIs/ARBs when BP and PR permit and escalate
until discharge (see chronic heart failure section)
o Start Spironolactone 25mg/d.
 Change IV furosemide to PO and observe the patient with ambulation for a day or two.
o Patients requiring higher dose of furosemide may require a double dose.
 Institute further management for the underlying heart disease (see specific topic and
comorbidities
Before Discharge
 Proper advise: salt consumption, activity, adherence to medications and follow up.
 Prescribe adequate medications and give requests for further planned outpatient investigations.
1
 Document medications with dose and further plans clearly on the discharge note. 1
 Early appointment preferably in one week time to follow up clinic.

Pulmonary edema
Brief description
 Principles of management and follow up is similar but more frequent than other AHF
syndromes.
 Early oxygenation and ventilation support is life saving.
 Treatable precipitating causes (eg. Arrhythmia, hypertensive crisis, ACS) should be
looked for and managed promptly
Clinical features
 Rapid development of dyspnea at rest,
 cardiorespiratory distress,
 tachypnea,
 SO2< 90%,
 high/normal BP,
 crepitations and wheeze in the lung,
 raised JVP, S3 gallop

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Treatable causes of pulmonary edema (eg. Hypertensive emergency, ACS, arrhythmia like AF)
should be seriously looked for and managed according to the respective protocol together with
management of pulmonary edema.

Treatment
Non pharmacologic
 Oxygenation
o Sitting position
o If SO2< 90%, administer O2 by nasal canula at 4-6 l/min.
o If SO2 doesn‘t improve in 10 min, administer high flow O2(10-12 l/min) by face
mask.
o If SO2 is still low, give ventilator support by CPAP in conscious cooperative
patients or intubate if patient cannot protect his /her airways and put on MV with
low PEEP.
o If SO2 is persistently higher than 90% and cardiorespiratory distress improves with
treatment, revert O2 administration to nasal canula and progressively decrease O2
flow and discontinue
Pharmacologic
 Administer morphine 2-4 mg IV bolus every 2-4 hr.
 Furosemide 40mg IV for naïve (intravenous dose which is equal to their previous oral dose
for those already taking oral furosemide) and double the dose every 1hr until adequate
urine output AND crackles in the chest start to decrease and maintain the dose of
furosemide that gave adequate response every 4hrs for the first 24 hr and decrease
frequency in subsequent days.

Follow up of response and other management principles are similar to management of other
acute heart failure syndromes (see acute heart failure section)

For patients not responding adequately to diuretics with systolic BP >110mmHg, the following
vasodilator therapies can be used:
 Intravenous nitroglycerine infusion started with 10-20ug/min and escalated to 200ug/min
depending on response and development of hypotension can be used.
 If nitroglycerine not available, either of the following can be tried.
o Isosorbide dinitrite 10mg po TID (8AM, 1PM and 6PM) escalated to 40mg po TID
or
o Captopril 12.5 mg or enalapril 2.5 mg and increase dose every 6hrs depending on
response.

Cardiogenic Shock

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Definition: systemic hypoperfusion secondary to decreased cardiac output and sustained systolic
BP less than 90 mmHg despite an elevated filling pressure with evidence of organ
hypoperfusion.
Clinical features
 apprehensive and diaphoretic,
 cold extremity,
 poor capillary refill,
 change in mentation,
 systolic BP< 90mmhg,
 decreased Urine output,
 symptoms and signs of heart failure

Inquire for history of fluid loss (vomiting, diarrhea, bleeding)

Treatment
Non pharmacologic
 Administer O2 if SO2<90%
Pharmacologic
 Administer NS 250ml over 30 min and see the change in BP, UOP and worsening of HF.
o If BP improves then consider hypovolemic shock and continue slowly replacing the
fluid with NS.
o No response to fluid or worsening heart failure, use either of the following
vasopressor therapies:
- Norepinephrine 0.2 ug/kg/min escalated to 1ug/kg/min by doubling the dose
q20 min until BP> 90/60 mmHg. Maintain the dose that maintained the BP>
90/60 mmHg
Alternative
- Dopamine infusion at 5ug/kg/min and escalate to 40ug/kg/min by doubling
the dose q20 min until BP> 90/60 mmHg. Maintain the dose that maintained
the BP> 90/60 mmHg.
If patient has concomitant pulmonary edema resulting in hypoxia
 Continuous infusion of frusemide started at 5-10 mg/hr should be started through another IV
line (escalate dose based on Blood Pressure).
 Taper the dose of vasopressor in the same way as it was escalated if BP is maintained.

More frequent follow up of V/S, SO2 and UOP q 20-30min until patient stabilizes

Further follow up and management is similar to other heart failure syndromes.

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2.2 Chronic Heart Failure

This guideline focuses on the management and follow up of non-rheumatic chronic heart failure
in those with depressed LV function (EF<40%). Management of chronic rheumatic valvular
heart disease is given separately.

At First Encounter:

History:

 Low output: fatigue, weakness, exercise intolerance, change in mental status, anorexia

 Congestive: left sided: dyspnea, orthopnea, PND

 Right sided: peripheral edema, RUQ discomfort, bloating, satiety

 Functional classification: using NYHA classification

 Stage the disease: see below

Diagnostic work up:

 Basic: CXR, ECG, Echocardiography

 Lab tests: BUN, Cr, electrolyte, urinalysis, FBS, lipid profile

 Evaluate for possible risk factor and treat.

Steps in the management of Heart Failure with Reduced Left Ventricular Systolic Function

Objectives: relieve symptoms, reduce hospitalization, improve survival, reduce complications

 Step 1: Start low dose ACEs
 Step 2: review after two weeks: Check tolerance and side effects
o BP, symptoms
o Side effects ACEs
 Step 3: Increase dose of ACEs
o If there is troubling cough related to the ACEs (not because of heart failure),
switch therapy to ARBs
 Step 4: review after one month and assess for Beta blocker therapy
o If a candidate; start low dose Betablocker

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 Step 5: Review after two weeks for assessment

o If tolerated, increase dose
 Step 6: Review heart failure status (symptom, NYHA class, congestion)
o Optimize therapy as per evidences
 Step 7: Monitor therapy at each visit (RFT, Electrolytes, optimize risk factors)
 Step 8: Early referral for refractory cases for cardiologist evaluation

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Treatment of chronic heart failure with reduced EF (LVEF<40%) (non-rheumatic)
STG 4th Edition, draft 2020
Diet, exercise Avoid table salt intake, alcohol and smoking
Avoid stimulant caffeine other like khat, marijuana
Avoid excess free water consumption
Exercise training in ambulating patients
ACEI Escalate every 1-2 week

 Optimal doses are more efficacious Enalapril dose 2.5mg/day - 20mg BID

 Watch for azotemia, increased K+, Alternative

cough, angioedema
Lisinopril dose 10-40mg/day
 Contraindicated; pregnancy, renal artery
stenosis, hyperkalemia

ARBs (ATII receptor blockers) Candesartan 8-32 mg/day in 1-2 divided doses
Alternative
 Alternative to ACEI (cough, Valsartan 40 -80 mg PO BID
angioedema) but not a substitute

Others same with ACEI

ARNI (Angiotensin-Neprolysin Inhibitors Sacubutril/Valsarthan combination starting with 50 mg
(24/26) PO BID to increase to the most tolerable dose
of 200 mg (97/103) PO BID

Beta- blockers Preferred: (long releasing and escalate every 2 week)

 High dose are more efficacious Metoprolol dose 6.75 - 200mg per day

 Caution: severe COPD/asthma, AV Carvedilol dose 3.125-25mg BID

block(bradycardia),
hypotension(shock) Bisoprolol 1.25 mg Po-10 mg Po daily

Nebivolol 1.25 mg PO-10 mg Po daily

Aldosterone antagonist Spironolactone 25mg po per day
NB: 50mg/day patients with high dose furosemide
 Consider in severe HF or post MI and hypokalemia

 Caution: renal function, Increased K

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Diuretics Loop diuretics

 Patients with congestion (ie. Not only Lasix(furosemide) 20mg/day up to 100- 120mg
right sided but also orthopnea, PND, TID/QID (preferred to keep low dose)
nocturnal cough) Thiazide:
HCT 12.5-25mg per day (congestion not improved with
 Watch electrolyte (Na, K, Cl) and high dose lasix) see diuretic resistance
BUN, Cr
Digoxin Dose 0.125-0.25mg per day

 Caution: renal failure, hypokalemia,

Rheumatic heart disease(MS)

 Use: rate control in AFFVR and added

on therapy

In every follow up visit:

Assess Manage:
 Symptoms  Escalate dose of ACEIs and BBs if no problem
 Functional status  Consider add on therapies like spironolactone,
 Adherence digoxin if patient not improving after optimal
 Medication tolerance diuretic, ACEI and BB therapy
 P/E : V/S, signs of heart failure,  on adherence to treatment and life style
precordial exam modifications
 Investigations: Cr, BUN, K+,
Na+ as appropriate

Further Reading
2. ACC/AHA Guideline for the management of Heart Failure, 2016
3. ESC Guideline for the management of Heart Failure, 2016

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4.3. HYPERTENSION
Brief description

Hypertension is a serious medical condition that significantly increases the risks of heart, brain,
kidney and other diseases. According to the WHO STEPS survey the prevalence of hypertension
in Ethiopia is 16%.

In Ethiopia and other low- and middle-income countries, there is a wide gap between evidence-
based recommendations and current practice. Treatment of major CVD risk factors remains
suboptimal, and only a minority of patients who are treated reach their target levels for blood
pressure, blood sugar and blood cholesterol.

Hypertension Detection and Treatment

When to measure blood pressure

Measuring blood pressure is the only way to diagnose hypertension, as most people with raised
blood pressure have no symptoms.

Blood pressure measurements should be conducted on all patients during health facility visits as
part of the vital sign. Every patient with elevated blood pressure readings requires immediate
follow-up, according to the protocol. More frequent blood pressure measurements and control is
particularly important in adults who:

 Have had a prior heart attack or stroke

 Have diabetes

 Have chronic kidney disease (CKD)

 Are obese

 Use tobacco

 Have a family history of heart attack or stroke

How to measure blood pressure

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Effective treatment algorithms for hypertension are dependent on accurate blood pressure
measurement. The following advice should be followed for measuring blood pressure:

 Use the appropriate cuff size, noting the lines on the cuff to ensure that it is positioned
correctly on the arm. (If the arm circumference is >32 cm, use large cuff.)

 On initial evaluation it is preferable to measure blood pressure on both arms and use the arm
with the higher reading thereafter

 The patient should be sitting with back supported, legs uncrossed, empty bladder, relaxed for
5 minutes and not talking.

 It is preferable to take at least two readings at each occasion of measurement and to use the
second reading.

 Blood pressure can be measured either by a conventional sphygmomanometer, using a

stethoscope, or by an automated electronic device. The WHO recommended calibrated
electronic device, if available, is preferred because it provides more reproducible results and
is not influenced by variations in technique or by the bias of the observers.

Diagnosing hypertension

The diagnosis of hypertension should be confirmed at an additional patient visit, usually 1 to 4

weeks after the first measurement depending on the measured values and other circumstances. In
general, hypertension is diagnosed if, on two visits, on different days:

 Systolic blood pressure on both days is ≥140 mmHg and/or diastolic blood pressure on both

Clinical Condition Office Blood Pressure Measurement

< 140/90 140-159/90-99 160-179/100-109 >180/110
If there is no evidence Re- Confirm in one Confirm as soon as Diagnose HTN and
of end-organ damages measure Month possible within one refer to specialist
after 1year week
If there is evidence of Confirm HTN and refer to specialist
end-organ damages
Hypertensive Crises
(BP> 180/110 mmHg)
with or without target
organ damage
days is ≥90 mmHg.

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Once diagnosis of hypertension is made:

 Look for end-organ damage based on:

o History: Symptoms of heart failure (SOB, unusual fatigue and body swelling),
history of sudden onset body weakness (stroke), intermittent claudication or previous
diagnosis of the above problems on previous evaluation at other health institutions,
severe headache and blurring of vision.

o Physical Examination: Pulse rate and rhythm, signs of heart failure (edema, elevated
JVP, crackles on the lungs), Focal neurologic deficit, eye signs. The physical
examination should be done to the maximum capacity of the health work force
including fundoscopic retinal examination if possible.

o Laboratory and other diagnostic tests:

Health facilities should thrive to avail at east mandatory tests. Please note that
waiting for laboratory tests shouldn‘t delay the intervention of hypertension as the
disease do much harm than the extra benefit obtained from the tests. The tests are
categorized as follows:

 Mandatory tests at diagnosis (urine dipstick to check for protein,

Creatinine to check for renal function)

 Optional tests at diagnosis (ECG to look for effect of blood pressure

on the heart, Serum electrolytes mainly potassium, Thyroid function
test to assess a secondary cause of hypertension)

 Indication based tests (Echocardiography for heart failure patients,

brain imaging for suspicion of stroke)

 Comorbidity and risk factor assessment tests (Blood sugar and

cholesterol)

 Look for risk factors:

o History: Smoking, excess salt intake, sedentary life, low fruit and vegetable intake,
excess alcohol consumption

o Physical Measurement: Weight, height, abdominal circumference,

Calculate BMI: wt in kg / square root of height in meter

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 Cardiovascular Risk assessment; For all patients found to have raised BP, their future
10-year cardiovascular risk should be assessed by using WHO CV risk score (Refer
WHO CV risk assessment manual). In a setting where serum cholesterol and fasting
blood glucose can be determined use the laboratory-based risk assessment. If
laboratory assessment service is not available, the non-laboratory-based risk chart.

Hypertension Treatment

Who should receive hypertension treatment?

Hypertension treatment is indicated for adults diagnosed with hypertension, as defined above
(SBP ≥140 mmHg and/or DBP ≥90 mmHg). Patients with SBP ≥180 mmHg or DBP ≥110
mmHg may be indicated for immediate treatment based on one assessment.

Lifestyle counseling (healthy diet, physical activity, tobacco use, and harmful use of alcohol) is a
critical component of good hypertension management and is often recommended as a first step
for patients with blood pressure of SBP 130–139 mmHg and/or DBP 80–89 mmHg who do not
have other CVD risk factors. However, in settings where people do not regularly visit the doctor,
people who are recommended only lifestyle modification may not return for re-evaluation and
needed treatment, resulting in uncontrolled hypertension and associated complications.

 Non pharmacologic (Life Style interventions)

All patients diagnosed to have hypertension should be given lifestyle interventions which
include:

o Consume healthy diet:

o Engage in physical activity,
o Avoid smoking
o Limit use of alcohol
 Pharmacologic (Drug Treatment)
Indications:
o Patient who couldn‘t achieve target blood pressure with life style
interventions.
o At initial presentation in those with:
 End-organ damage or high WHO cardiovascular risk (>20%)
 Hypertensive Crises (see below)
Treatment targets

For most patients, blood pressure is considered controlled when SBP <140 mmHg and DBP <90
mmHg.

Life style intervention

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Life style intervention should be implemented in all grades of hypertension. For uncomplicated
grade 1 hypertension life style intervention can be tried for three months before initiation of
medications. If failed to achieve a blood pressure of less than 140/90 mmHg, then initiation of
antihypertensive medication is recommended.

What medications should be used to treat hypertension?

Initial monotherapy in uncomplicated hypertension:

Long-acting dihydropyridine calcium channel blocker such as amlodipine as first line drug for
the treatment of uncomplicated essential hypertension in our country at General Hospital level as
it is the most extensively studied drug with evidence. It is probably effective for all races;
reduces need for monitoring of electrolytes and renal function; avoids need for different
treatment for women of childbearing age who may become pregnant.

Dose: Amlodipine 5 mg daily, escalate to 10 mg if BP is uncontrolled.

Thiazide diuretics such as hydrochlorothiazide to be used as add on when target BP not achieved
on long-acting dihydropyridine calcium channel blocker such as amlodipine it is less expensive
than other hypertension medications in our setting and are probably effective for all races.
Because of the lack of evidence with the readily available thiazide diuretics such as
hydrochlorothiazide as monotherapy with regards to CVD event reduction, the risk of
hypokalemia and the unfavorable effects on lipid and glucose associated with the drug which
necessitates laboratory monitoring, we suggest to be used as add on.

Dose: Hydrochlorothiazide 25 mg Po daily

If a third agent is needed, the alternative class of medication is ACE inhibitors considering cost
of the drug and availability at the General Hospitals in Ethiopia. Lisinopril is the preferred drug
in this class due to its ease of administration. The alternative is Enalapril.

Dose: Lisinopril 5 mg daily, escalate dose to 40 mg Po daily if BP is uncontrolled

Enalapril 5 mg Po BID, escalate to 20 mg Po BID if BP is uncontrolled

Notes on specific hypertension medications

 Pregnant women and women of childbearing age not on effective contraception should not be
given ACE inhibitors, ARBs, or thiazide/thiazide-like diuretics; CCBs should be used. If not
controlled with intensification dose of medication, refer to specialist. Please refer to the
Hypertension and Pregnancy module for the management of such cases.

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 Beta blockers are not recommended as first-line therapy. If a heart attack has been diagnosed
within the previous three years, or there is atrial fibrillation or heart failure, then a beta
blocker should be added to the starting dose of antihypertensive medication. Patients with
angina may also benefit from treatment with a beta blocker.

Treatment adherence

Adherence to treatment is critical for blood pressure control. If antihypertensive medication is

being prescribed, the following are critical to ensuring adherence:

 Teach the patient how to take the medications at home.

 Explain the difference between medicines for long-term control (for example, of blood
pressure) and medicines for quick relief (such as for headaches).
 Explain the reason for prescribing the medicine(s).
o Explain the diagnosis of hypertension.
o Discuss the asymptomatic nature of hypertension and explain that medications
must be taken even if there are no symptoms.
o Inform patient of the complications of untreated hypertension, including stroke,
heart attack, and kidney failure.
o Explain the disability and economic and family burden these preventable
complications cause.
o Show the patient the appropriate dose.
o Explain how many times a day the patient should take the medication and at what
time, and adopt the following simple steps to help them to adhere to the
guidelines:
o Label and package the tablets.
o Check the patient‘s understanding before the patient leaves the hospital.
o Wherever possible, use once-daily dosages of all medications, to be given at the
same time each day.
 Explain how important it is for the patient to:
o Keep an adequate supply of medications safely at home.
o Take the medicines regularly as advised, even if there are no symptoms.
 Explain potential adverse effects of the medications and what to do if the patient experiences
them.

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Common and Other Comorbidities and Complications of Hypertension

(adopted from the ISH 2020 guideline in alignment with the Ethiopian context)

This intervention is intended to be done at a General hospital level where basic infrastructure,
equipment, drugs and man power is available. Unanticipated complications might happen
when trying to manage complicated patients in a primary health care facility.

Brief description

 Hypertensive patients have several common and other comorbidities that can affect
cardiovascular risk and treatment strategies.
 The number of comorbidities increases with age, with the prevalence of hypertension and
other diseases.
 Common comorbidities include coronary artery disease (CAD), stroke, CKD, HF, and
COPD.
 Uncommon comorbidities include rheumatic diseases and psychiatric diseases.
 Common and uncommon comorbidities should be identified and managed according to
available evidence.

Common Comorbidities and Complications

1. Hypertension and Coronary Artery Disease (CAD)

o A strong epidemiological interaction exists between CAD and hypertension that accounts
for 25%–30% of acute myocardial infarctions.
o Lifestyle changes are recommended (smoking cessation, diet and exercise).
o BP should be lowered if ≥140/90 mm Hg and treated to a target <130/80 mm Hg (<140/80
in elderly patients).
o Refer coronary artery disease protocol

2. Hypertension and Previous Stroke

o Hypertension is the most important risk factor for ischemic or hemorrhagic stroke
o Stroke can be largely prevented by BP control.
o BP should be lowered if ≥140/90 mm Hg and treated to a target <130/80 mm Hg (<140/80
in elderly patients).
Refer stroke protocol

3. Hypertension and Heart Failure (HF)

o Hypertension is a risk factor for the development of HF with reduced ejection fraction
(HFrEF), and with preserved ejection fraction (HFpEF). Clinical outcome is worse and

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mortality is increased in hypertensive patients with HF.

o Lifestyle changes are recommended (diet and exercise).
o Treating hypertension has a major impact on reducing the risk of incident HF and HF
hospitalization. BP should be lowered if ≥140/90 mm Hg and treated to a target <130/80
mm Hg but >120/70 mm Hg.
Refer to the Heart failure protocol

4. Hypertension and Chronic Kidney Disease (CKD)

o Hypertension is a major risk factor for the development and progression of albuminuria
and any form of CKD.
o A lower eGFR is associated with resistant hypertension, masked hypertension, and
elevated nighttime BP values.
o The effects of BP lowering on renal function (and albuminuria) are dissociated from
cardiovascular benefit.
o BP should be lowered if ≥140/90 mm Hg and treated to a target <130/80 mm Hg (<140/80
in elderly patients).
Refer the CKD protocol

5. Hypertension and Chronic Obstructive Pulmonary Disease (COPD)

o Hypertension is the most frequent comorbidity in patients with COPD.

o BP should be lowered if ≥140/90 mm Hg and treat- ed to a target <130/80 mm Hg

(<140/80 in elderly patients).
o Lifestyle changes (smoking cessation) are mandatory.
o Environmental (air) pollution should be considered and avoided if possible.
Refer the COPD Protocol

6. Diabetes
o BP should be lowered if ≥140/90 mm Hg and treated to a target <130/80 mm Hg
(<140/80 in elderly patients).
o The treatment should include glucose and lipid lowering as per current guidelines.
Refer Diabetes protocol

7. Metabolic Syndrome (MS)

o Patients with hypertension and MS have a high-risk profile.
o The diagnosis of MS should be made by separate evaluation of single components.
o The treatment of MS is based on changes in lifestyle (diet and exercise).
o The treatment of hypertension and MS should include BP control as in the general
population and treatment of additional risk factors based on level and overall cardio-
vascular risk.
Refer WHO cardiovascular risk prediction chart and accompanied protocol

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Hypertensive Emergencies
Definition of Hypertensive Emergencies and Their Clinical Presentation
A hypertensive emergency is the association of substantially elevated BP with acute
Hypertension Mediated Organ Damage (acute HMOD). Target organs include the retina, brain,
heart, large arteries, and the kidneys. This situation requires rapid diagnostic workup and
immediate BP reduction to avoid progressive organ failure. Intravenous therapy is usually
required. The choice of antihypertensive treatment is predominantly determined by the type of
organ damage. Specific clinical presentations of hypertensive emergencies include:
 Malignant hypertension: Severe BP elevation (commonly >200/120 mm Hg) associated
with advanced bilateral retinopathy (hemorrhages, cotton wool spots, papilledema).
 Hypertensive encephalopathy: Severe BP elevation associated with lethargy, seizures,
cortical blindness and coma in the absence of other explanations.
 Hypertensive thrombotic microangiopathy: Severe BP elevation associated with
hemolysis and thrombocytopenia in the absence of other causes and improvement with
BP-lowering therapy.
 Other presentations of hypertensive emergencies include severe BP elevation associated
with cerebral hemorrhage, acute stroke, acute coronary syndrome, cardio- genic
pulmonary edema, aortic aneurysm/dissection, and severe preeclampsia and eclampsia.
Patients with substantially elevated BP who lack acute HMOD are not considered a
hypertensive emergency and can typically be treated with oral antihypertensive therapy

Clinical Presentation and Diagnostic Workup

The clinical presentation of a hypertensive emergency can vary and is mainly determined by the
organ(s) acutely affected. There is no specific BP threshold to define a hypertensive emergency.
Symptoms include headaches, visual disturbances, chest pain, dyspnea, neurologic symptoms,
dizziness, and more unspecific presentations.
Medical history: preexisting hypertension, onset and duration of symptoms, potential causes
(nonadherence with prescribed antihypertensive drugs, lifestyle changes, concomitant use of BP
elevating drugs [NSAIDS, steroids, immunosuppressants, sympathomimetics, cocaine,
antiangiogenic therapy]).

Diagnostic Tests and Acute Therapeutic Management

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The overall therapeutic goal in patients presenting with hypertensive emergencies is a

controlled BP reduction to safer levels to prevent or limit further hypertensive damage while
avoiding hypotension and related complications. There is a lack of randomized controlled trial
data to provide clear cut guidance on BP targets and times within which these should be
achieved. Most recommendations are based on expert consensus. The type of acute HMOD is
the main determinant of the preferred treatment choice. The timeline and magnitude of BP
reduction is strongly dependent on the clinical context. For example, acute pulmonary edema and
aortic dissection require rapid BP reduction, whereas BP levels not exceeding 220/120 mm Hg
are generally tolerated in acute ischemic stroke for certain periods. The table below provides a
general overview of timelines and BP targets as well as preferred antihypertensive drug choices
with most common clinical presentations. Availability of drugs and local experience with
individual drugs are likely to influence the choice of drugs.
See Table below for locally adopted agents for BP lowering during Hypertensive Emergency

Follow-Up
Patients who experienced a hypertensive emergency are at increased risk of cardiovascular
and renal disease. Thorough investigation of potential underlying causes and assessment of
HMOD is mandatory to avoid recurrent presentations with hypertensive emergencies.
Regular and frequent follow-up (monthly) is recommended until target BP and ideally
regression of HMOD has been achieved.

Hypertensive Emergencies Requiring Immediate BP Lowering

Clinical Presentation Timeline and Target BP First Line Treatment Alternative

Malignant hypertension with or Several hours, MAP −20% to Labetalol Hydralazine
without thrombotic −25%
microangiopathy or acute renal
failure
Hypertensive encephalopathy Immediate, MAP −20% to Labetalol Hydralazine
−25%
Acute ischaemic stroke and SBP 1 h, MAP −15% Labetalol Hydralazine
>220 mm Hg or DBP >120 mm
Hg
Acute ischaemic stroke with 1 h, MAP −15% Labetalol Hydralazine
indication for thrombolytic therapy
and SBP >185 mm Hg or DBP >110
mm Hg

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Acute hemorrhagic stroke and SBP Immediate, 130<SBP<180 Labetalol Hydralazine

>180 mm Hg mm Hg
Acute coronary event Immediate, SBP Nitroglycerine
<140 mm Hg
Acute cardiogenic pulmonary Immediate, SBP Nitroglycerine (with loop diuretic
edema <140 mm Hg loop diuretic)
Acute aortic disease Immediate, SBP <120 mm nitroglycerine and Labetalol or
Hg and heart rate metoprolol metoprolol
<60 bpm
Eclampsia and severe preeclampsia/ Immediate, SBP <160 Labetalol and Hydralazine or
HELLP mm Hg and DBP magnesium short acting
<105 mm Hg sulphate nifedipine

4.4. Atherosclerotic cardiovascular diseases

Ischemic Heart Disease

Chest Pain (Approach and work up)

Chest pain is one of the cardinal symptoms of cardiovascular disease, but it may also be present
in many non-cardiovascular diseases.
Differential Diagnosis
1. Heart, pericardium, vascular causes:
o Stable angina, variant angina
o Acute Coronary Syndrome (ACS)
o Pericarditis
o Aortic dissection
2. Pulmonary:
o Pulmonary embolism
o Pneumothorax
o Pleuritis (pleural pain)
o Pneumonia
o Status asthmaticus
3. Gastrointestinal:
o Gastroesophageal reflux disease (GERD)
o Diffuse esophageal spasm, Peptic ulcer disease
o Esophageal rupture
4. Chest wall:
o Costochondritis

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o Muscle strain
o Rib fracture
o Herpes zoster
5. Psychiatric:
o Panic attacks
o Anxiety
o Somatization
Approach to Treating a Patient with Chest Pain
 Rule out any life-threatening causes. These include ACS, aortic dissection, pericarditis with
cardiac tamponade, pulmonary embolus, tension pneumothorax, and esophageal rupture
 Assess vital signs
 Develop a focused history
o Character of the pain (pressure, squeezing, tearing, sharp, stabbing, etc.)
o Location of pain
o Severity of pain
o Duration of pain
o Setting in which pain occurred (during exertion, at rest, after meal)
o Radiation of pain
o Aggravating or alleviating factors (e.g., meal, exertion, rest, respiration)
o Does the patient have a cardiac history? Ask about results of previous stress
tests, echocardiograms, cardiac catheterization, or of any procedures (PCI or
CABG)
o If the patient has a history of angina, ask how this episode differs from previous
ones (more severe? longer duration?)
 Perform a focused physical examination, with attention to cardiopulmonary, abdominal, and
musculoskeletal examination
 Investigation: focused
o Obtain ECG in almost all cases
o Cardiac enzymes (CK, CK-MB, troponin) depending on clinical suspicion
o Obtain chest radiograph (CXR) in a supportive clinical data
o Under appropriate clinical setting, work up the patient for pulmonary embolism
(PE) (see Pulmonary section)
Chronic Coronary Syndrome
 Chronic Coronary Syndrome is due to usually due to atherosclerotic lesions that narrow the
major coronary arteries. Coronary ischemia is due to an imbalance between blood supply and
oxygen demand, leading to inadequate perfusion. Stable angina occurs when oxygen demand
exceeds available blood supply.
 Major risk factors
 Diabetes mellitus (DM)—worst risk factor

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 Hyperlipidemia—elevated low-density lipoprotein (LDL)

 Hypertension (HTN)—most common risk factor
 Cigarette smoking
 Age (men >45 years; women >55 years)
 Family history of premature coronary artery disease (CAD) or myocardial infarction (MI)
in first-degree relative: Men <55 years; women <65 years
 Low levels of high-density lipoprotein (HDL)
 Less common risk factors include:
o end-stage renal disease (ESRD) on hemodialysis,
o human immunodeficiency virus (HIV) infection,
o history of mediastinal radiation.
 Minor risk factors (less clear significance) include:
o obesity
o sedentary lifestyle (lack of physical activity)
o stress
o excess alcohol use
Clinical Features
 Chest pain or substernal pressure sensation
o Lasts less than 10 to 15 minutes (usually 1 to 5 minutes).
o Frightening chest discomfort, usually described as heaviness, pressure. squeezing,
tightness; rarely described as sharp or stabbing pain.
o Pain is often gradual in onset.
o Brought on by factors that increase myocardial oxygen demand, such as exertion,
stress, or drugs.
o Relieved with rest or nitroglycerin
Diagnosis and investigation
 Note that physical examination in most patients with CCS is normal.
 Resting ECG:
o Usually normal in patients with chronic coronary syndrome
o Q waves are consistent with a prior MI
o If ST-segment or T-wave abnormalities are present during an episode
of chest pain, then treat as unstable angina.
 Stress test: useful for patients with an intermediate pretest probability of
CAD based upon age, gender, and symptoms. Stress testing is used in the
following situations:
o To confirm diagnosis of angina
o To evaluate response to therapy in patients with documented CCS
o To identify patients with CCS who may have a high risk of acute

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coronary events
 Confirmatory tests are not routinely available at General Hospitals.
o Refer patients who need further work up
Treatment
 Risk factor modification
o Smoking cessation
o Blood pressure control: Refer Hypertension protocol
o Dyslipidemia management: Refer Dyslipidemia protocol
o Obesity: weight loss modifies other risk factors (diabetes, HTN, and
hyperlipidemia) and provides other health benefits.
o Exercise: it minimizes emotional stress, promotes weight loss, and helps
reduce other risk factors.
o Diet: Reduce intake of saturated fat and cholesterol
Standard of care for patients with CCS
 Antiplatelet therapy
o ASA 75-100 mg PO daily
o Alternative: Clopidogrel 75 mg Po daily
 Beta blocker: chest pain, heart rate and blood pressure control
o Metoprolol succinate 50-200 mg PO daily
o Alternative: Bisoprolol 2.5-10 mg PO daily
 Statin: target LDL< 70 mg/dl, dose of statin titrated as per the response
o Atorvastatin 20-80 mg PO daily
o Alternative: Rosuvastatin 5-20 mg PO daily
 Angina management
o Betablockers: see above
o Calcium channel blockers
 Amlodipine 2.5-10 mg PO daily for those with
hypertension
o Nitrates
 Nitroglycerine 0.4 mg sublingual tablets for acute relief
 Isosorbid di nitrate 2.5-20 mg PO single dose or divided
doses as needed
o Trimetazidine 35 mg Po daily
 Review risk factor, symptoms and indication for revascularization
o Refractory cases: Refer patients for Cardiologist evaluation

Acute Coronary Syndrome (ACS)

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Brief description
ACS describes a group of clinical entities that are characterized by severe, acute myocardial
ischemia or infarction resulting from thrombotic occlusion of coronary artery/ies as a result
atherosclerotic plaque erosion/rupture. Rarely, the ischemia could be due to coronary artery
spasm. ACS is a medical emergency and should be managed in the intensive care unit.

ACS comprises the following three clinical entities:

1. Unstable angina: symptoms of myocardial ischemia (typical or atypical) but no

elevation in cardiac enzymes, with or without ECG changes indicative of ischemia.
Unstable angina is considered to be present in the following circumstances:
 Rest angina >20 minutes in duration
 New onset angina
 Increasing angina- more frequent or longer in duration, or occurs with less exertion
than previous angina

2. ST-segment elevation myocardial infarction (STEMI): Significant ST elevation or

new left bundle branch block (LBBB) on ECG, elevated cardiac enzymes (Troponin
and/or CKMB) and symptoms of myocardial ischemia (typical or atypical).

3. Non-ST-segment elevation myocardial infarction (NSTEMI): No ST elevation

on ECG (other ECG evidence of ischemia may or may not be present), elevated
cardiac enzymes and symptoms of myocardial ischemia (typical or atypical).

1. Unstable Angina

 The following patients may be said to have unstable angina:

o Patients with chronic angina with increasing frequency, duration, or intensity of
chest pain.
o Patients with new-onset angina that is severe and worsening.
o Patients with angina at rest
 The distinction between unstable angina and NSTEMI is based entirely on cardiac
enzymes. The latter has elevation of troponin or creatine kinase-MB (CK-MB). Both
unstable angina and NSTEMI lack ST-segment elevations and pathologic Q waves.
 Unstable angina has a higher risk of MI and death than stable angina, and patients with
this diagnosis should be hospitalized. Its management is encompassed in Acute
Coronary Syndrome.
Diagnosis
 Perform a diagnostic workup to exclude MI in all patients.
 Patients with unstable angina have a higher risk of adverse events during stress

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testing. These patients should be stabilized with medical management before referral
for stress testing.
Treatment
 Hospital admission with continuous cardiac monitoring.
 Establish IV access.
 Give supplemental oxygen if patients are hypoxic (Spo2 <90 %).
 Provide pain control:
o Nitroglycerin: short acting (sublingual or spray): don‘t give nitrates for
patients who took phosphodiesterase inhibitors (sildenafil)
o Morphine 4 mg IV if pain refractory to nitrate therapy alone.
 Aggressive medical management is indicated: treat as in MI
o Dual antiplatelet therapy:
 ASA 300 mg loading followed by 81-100 mg Po daily
AND
 Clopidogrel 300 mg loading followed by 75 mg Po daily
o β-Blockers:
 Metoprolol 12.5 mg Po BID and titrate as needed
o Anticoagulation using Heparin for the first five days until ambulation starts
 Enoxaparin 1 mg/kg SC BID
 Alternative: Unfractionated Heparin 5000 IU IV loading
followed by 17,500 IU SC BID
o High intensity statin therapy
 Atorvastatin 80 mg PO daily

After the acute treatment

 Refer to the next referral facility for further evaluation and treatment optimization.

Acute Myocardial Infarction (STEMI and NSTEMI)

Brief description
 MI is due to necrosis of myocardium as a result of an interruption of blood
supply (after a thrombotic occlusion of a coronary artery previously
narrowed by atherosclerosis).
 Most cases are due to acute coronary thrombosis: Atheromatous plaque
ruptures into the vessel lumen, and thrombus forms on top of this lesion,
which causes occlusion of the vessel.

Clinical Features

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 Chest pain
o Intense substernal pressure sensation; often described as ―crushing‖ and ―an
elephant standing on my chest.‖
o Radiation to neck, jaw, arms, or back, commonly to the left side.
o Pain is more severe and lasts longer.
 Some patients may have epigastric discomfort.
 Can be asymptomatic in up to one-third of patients; painless infarcts or atypical
presentations more likely in postoperative patients, the elderly, diabetic patients, and
women.
 Other symptoms
o Dyspnea
o Diaphoresis
o Weakness, fatigue
o Nausea and vomiting
o Sense of impending doom
o Syncope
o Sudden cardiac death—usually due to ventricular fibrillation (VFib)

The combination of substernal chest pain persisting for longer than 30 minutes and
diaphoresis strongly suggests acute MI.
Right ventricular infarct will present with inferior ECG changes, hypotension, elevated jugular
venous pressure, hepatomegaly, and clear lungs.

Diagnosis
 ECG: Markers for ischemia/infarction include:
o Peaked T waves: Occur very early and may be missed
o ST-segment elevation: indicates transmural injury and can be diagnostic of an
acute infarct.
o Q waves: Evidence for necrosis (specific).
o T-wave inversion is sensitive but not specific
o ST-segment depression: Subendocardial injury
 Cardiac enzymes: currently the diagnostic gold standard for myocardial injury
o Troponins (Troponin I and T): most important enzyme test to order
o CK-MB: less commonly used
o Cardiac enzymes are drawn serially: once on admission and every 6 hours until
three samples are obtained. The higher the peak and the longer enzyme levels
remain elevated, the more severe the myocardial injury and the worse the
prognosis.

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Cardiac Monitoring for a Patient with an Acute MI

 BP and HR
 Rhythm strip with continuous cardiac monitor: Watch for arrhythmias.
 Auscultate the heart (third and fourth heart sounds, friction rub, and so on) and
lungs (crackles may indicate LV failure, pulmonary edema).

Treatment
 Early referral to the next level facility OR urgent specialist consultation
 Give ASA 300 mg PO: Advice to chew the tablet

Peripheral Arterial Disease (Chronic Arterial Insufficiency)

Brief description
 Peripheral arterial disease (PAD) is an occlusive atherosclerotic disease of the
lower extremities.
 Patients with PAD usually have coexisting CAD (with CHF, history of MI, and so
on) and other chronic medical problems (e.g., diabetes, lung disease)
 Sites of occlusion/stenosis:
o Superficial femoral artery (in Hunter canal) is the most common site
o Popliteal artery
o Aortoiliac occlusive disease

Risk factors
 Smoking is by far the most important risk factor
 Chronic Coronary Syndrome
 Dyslipidemia
 Hypertension
 Diabetes: prevalence is markedly increased in these patients

Clinical Features
 Symptoms:
o Intermittent claudication: Cramping leg pain that is reliably reproduced by same
walking distance (distance is very constant and reproducible). Pain is
completely relieved by rest.
o Rest pain (continuous): Usually felt over the distal metatarsals, where the
arteries are the smallest. Often prominent at night (awakens patient from
sleep). Hanging the foot over side of the bed or standing relieves pain (extra

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perfusion to ischemic areas due to gravity)

 Rest pain is always worrisome: suggests severe ischemia such that frank
gangrene of involved limb may occur in the absence of intervention.
 Signs:
o Diminished or absent pulses, muscular atrophy, decreased hair growth, thick
toenails, and decreased skin temperature
o Ischemic ulceration (usually on the toes)
o Localized skin necrosis: Secondary to local trauma that does not heal (due to
ischemic limb)
o Tissue infarction/gangrene in end-stage disease
o Pallor of elevation and rubor of dependency (in advanced disease)

Femoral or popliteal disease causes calf claudication.

Aortoiliac occlusive disease causes buttock and hip claudication (in addition to the
calves).

Diagnosis
 Clinical suspicion based on symptoms, signs and risk factors
 Ankle-to-brachial index (ABI): Ratio of the systolic BP at the ankle to the systolic
BP at the arm.
o Normal ABI is between 0.9 and 1.3
o ABI >1.3 is due to noncompressible vessels and indicates severe disease
o Claudication usually when ABI <0.7
o Rest pain usually when ABI <0.4
 Doppler study of the peripheral vessels
 Arteriography (contrast in vessels and radiographs)
o Gold standard for diagnosing and locating PAD

Treatment
Non pharmacologic

Conservative management for intermittent claudication.

 Smoking cessation (the importance of this cannot be overemphasized).
Smoking is linked to progression of atherosclerosis and causes
vasoconstriction (further decreasing blood flow).
 Graduated exercise program: Walk to point of claudication, rest, and then
continue walking for another cycle.
 Foot care (especially important in diabetic patients).
 Avoid extremes of temperature (especially extreme cold).

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Pharmacologic
 Atherosclerotic risk factor reduction (control of hyperlipidemia,
Hypertension, Diabetes): see specific protocols
 Antiplatelets
o ASA 81-100 mg Po daily
o Alternative: Clopidogrel 75 mg Po daily
 Statin
o Atorvastatin 20-80 mg Po daily
o Alternative: Rosuvastatin 5-20 mg Po daily

Consult specialist or refer patient to the next level facility for further evaluation

Acute Arterial Occlusion

Brief description
Acute occlusion of an artery, usually caused by embolization. The common femoral
artery is the most common site of occlusion. Less commonly, in situ thrombosis is
the cause.

Sources of emboli:
 Heart (85%)
o Atrial fibrillation is the most common cause of embolus from the heart
o Post-MI
o Post arterial procedure (i.e., coronary angiogram, peripheral angiogram)
o Endocarditis
o Myxoma
 Aneurysms
 Atheromatous plaque

Clinical Features of Acute Limb Ischemia (Remember the Six Ps)

 Pain: acute onset. The patient can tell you precisely when and where it happened.
The pain is very severe, and the patient may have to sit down or may fall to the ground.
 Pallor
 Polar (cold)
 Paralysis
 Paresthesias
 Pulselessness

Diagnosis

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 Clinical: high index of suspicion with supportive clinical data.

 Doppler study of the vessels.
 ECG to look for MI, AFib
 Echocardiogram for evaluation of cardiac source of emboli—valves, thrombus, shunt

Treatment
 Main goal: Assess viability of tissues to salvage the limb.
 Skeletal muscle can tolerate 6 hours of ischemia; perfusion should be reestablished
within this time frame.
 Immediately anticoagulate with IV heparin.
 Urgent referral to the facility where reperfusion is available in consultation with
specialist.

4.5. Rheumatic Heart Disease

Acute rheumatic Fever
Brief description
Acute Rheumatic fever is a systemic illness in which there is inflammation of several
organs. It occurs as non-suppurative complication of group A streptococcus pharyngitis and
may consist of arthritis, carditis, chorea, erythema marginatum, and subcutaneous nodules.
The onset of symptoms occurs 1-3 weeks after the throat infection. Damage to cardiac valves
is the most serious complication and is usually progressive. In developing countries, it is a
major cause of permanent damage to the heart. The disease occurs mainly in children of
school age. The prevalence of rheumatic heart disease in the Ethiopian population among the
asymptomatic school children is 19 per 1000 population. The diagnosis is based on the
modified John‘s criteria approved by WHO in 2003. The diagnostic criteria do have
major and minor manifestations.
Modified Jones Criteria (2003)
Major Criteria
• Carditis
• Polyarthritis
• Chorea
• Subcutaneous nodules
• Erthema marginatum
Minor Criteria
Clinical
• Fever
• Polyarthralgia

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Lab Tests
Acute phase reactants
• Raised ESR
• Positive C-reactive protein
• Leukocytosis.
ECG
Prolonged PR interval
Essential Criteria
Documentation of recent streptococcal infection (within 45 days) is necessary for diagnosis of
ARF, that is one of the following tests should be positive.
1. Positive throat culture
2. Raised or rising streptococcal antibody tire (Anti streptolysin O or Anti DNAse B)
3. Rapid antigen detection tests for Group A Streptococci.

Diagnosis: requires the presence of supporting evidence for preceding streptococcal infection
and the following:
1. Primary episode of Rheumatic Fever or recurrence without established rheumatic heart
disease: Two major, or one major and two minor manifestations.
2. Recurrent attack of Rheumatic fever with established rheumatic heart disease-two minor
manifestations.
3. Rheumatic chorea or insidious onset carditis-neither evidence of preceding streptococcal
infection nor other major manifestation needed.
Treatment Objectives
 Eradicate streptococcal throat infection
 Prevent recurrent episodes of rheumatic fever and further valvular damage
 Treat Heart Failure, if co-existent
 Control inflammation and relive symptoms of arthritis

Non-pharmacologic
 Bed rest if the patient has severe rheumatic carditis or arthritis/arthralgia only.
 Salt restriction if there is associated Heart Failure.
Pharmacologic
 Antibiotic (primary prevention)
 Conventional therapy for Heart Failure
 Anti-inflammatory
o First line
 Aspirin, 4-8 grams per day P.O. in 4 divided doses
 Add a GI prophylaxis – PPI (e.g. Omeprazole 20mg, P.O., BID)

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o Alternative
 Prednisolone (consider its use in severe carditis only), 1–2mg/kg per day
(maximum, 80mg); only required for a few days or up to a maximum of 3
weeks.
 Prevention of recurrent rheumatic fever (secondary prevention)
o First line
 Benzathine penicillin, 1.2 million units or 600,000 units if <30 kg, every
4 weeks. It can be given every 3 weeks, to persons considered to be at
particularly high risk.
o Alternative (if penicillin allergic)
 Erythromycin, 250mg, P.O. BID

Duration of secondary prophylaxis

Category of Patient Duration of Prophylaxis

For 5 years after the last attack or 18 years

of age (whichever is longer)
Rheumatic fever without carditis
For 10 years after the last attack, or 25
Rheumatic fever with carditis with no residual years of age (whichever is longer)
valvular disease or mild mitral regurgitation

Rheumatic fever with persistent valvular disease or

after valve surgery Life long

Further reading
1. M Satpathy, BR Mishra. Rheumatic Fever and Rheumatic Heart Disease.
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD. © 2013,
Jaypee Brothers Medical Publishers
2. STG 3rd edition, 2014

4.6. Valvular Heart Disease

 As a general recommendation, patients with high index of suspicion for valvular heart
disease should get access for evaluation by a specialist. The four common valvular heart

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diseases are discussed below as a general guidance for management at a General

Hospital level. Patients with acute heart failure should be managed as per the guideline.

Mitral Stenosis

Almost all cases of mitral stenosis are due to rheumatic heart disease. Patients are usually
asymptomatic until the mitral valve area is reduced to approximately 1.5 cm2 (normal valve
area is 4 to 6 cm2). The disease is more common in women.

Clinical Features

Symptoms
 Exertional dyspnea, orthopnea, PND
 Palpitations
 Hemoptysis
 Thromboembolism: often associated with AFib
 If RV failure occurs, ascites and edema may develop

Signs
 Mitral stenosis murmur.
 With long-standing disease, will find signs of RVF (e.g., right ventricular heave, JVD,
hepatomegaly, ascites) and/or pulmonary HTN (loud P2).
 All signs and symptoms will increase with exercise and during pregnancy.

Diagnosis
 CXR: Left atrial enlargement (early)
 Echocardiogram—most important test in confirming diagnosis

Treatment
 Consult specialist OR referral to a cardiologist

Aortic Stenosis
 It causes obstruction to left ventricular outflow, which results in LVH. When the aortic
valve area falls below 1 cm2, cardiac output fails to increase with exertion, causing
angina (but may be normal at rest).

Causes
 Calcification of a congenitally abnormal bicuspid aortic valve.
 Calcification of tricuspid aortic valve in elderly.
 Rheumatic fever.

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Clinical Features

Symptoms
 Angina
 Syncope—usually exertional
 Heart failure symptoms, such as dyspnea on exertion, orthopnea, or PND

Signs
 Murmur of aortic stenosis

Diagnosis
 CXR findings: Calcific aortic valve, enlarged LV/LA (late)
 ECG findings: LVH, LA abnormality
 Echocardiography: Valve lesion, degree of stenosis, LVH

Treatment
 Consult specialist OR referral to a cardiologist

Aortic Regurgitation

Also called aortic insufficiency; this condition is due to inadequate closure of the aortic
valve leaflets. For acute aortic regurgitation, mortality is particularly high without surgical
repair.

Causes
 Acute
o Infective endocarditis
o Trauma
o Aortic dissection
o Iatrogenic as during a failed replacement surgery
 Chronic
o Primary valvular: Rheumatic fever, bicuspid aortic valve, Marfan syndrome,
SLE
o Aortic root disease: Syphilitic aortitis, aortic dissection, systemic HTN

Clinical Features

Symptoms
 Dyspnea on exertion, PND, orthopnea
 Palpitations—worse when lying down

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 Angina
 Cyanosis and shock in acute aortic regurgitation (medical emergency)

Physical examination
 Widened pulse pressure—markedly increased systolic BP, with decreased diastolic BP.
 Diastolic decrescendo murmur best heard at left sternal border.
 Peripheral signs of Aortic Regurgitation

Diagnosis
 CXR findings: Enlarged cardiac silhouette, dilated aorta
 ECG findings: LVH
 Echocardiogram
o Assess LV size and function
o Look for dilated aortic root and reversal of blood flow in aorta
o In acute aortic regurgitation, look for early closure of mitral valve

Treatment
 Consult specialist OR referral to a cardiologist

Mitral Regurgitation
 This condition is due to inadequate closure of the mitral valve. It could be acute or
chronic. Acute form is associated with much higher mortality

Causes
 Acute
o Endocarditis (most often Staphylococcus aureus)
o Papillary muscle rupture (from infarction) or dysfunction (from ischemia)
o Chordae tendineae rupture
 Chronic
o Mitral valve prolapse (MVP)
o Rheumatic fever
o Marfan syndrome
o Cardiomyopathy causing dilation of mitral annulus

Clinical Features

Symptoms
 Dyspnea on exertion, PND, orthopnea

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 Palpitations
 Pulmonary edema

Signs
 Murmur of mitral regurgitation

Diagnosis
 CXR findings: Cardiomegaly, dilated LV, pulmonary edema.
 ECG: AFib
 Echocardiogram: MR; dilated LA and LV; decreased LV function.

Treatment
 Consult specialist OR referral to a cardiologist

4.7. Infective Endocarditis

Infective endocarditis is defined as an infection of the endocardial surface of the heart (usually
involves the cusps of the valves) Always suspect endocarditis in a patient with a new heart
murmur and unexplained fever or bacteremia.

Classifications (acute or subacute)

 Acute endocarditis
o Most commonly caused by Staphylococcus aureus (highly virulent).
o Occurs on a normal heart valve.
o If untreated, fatal in less than 6 weeks.
 Subacute endocarditis
o Caused by less virulent organisms, such as Streptococcus viridans and
Enterococcus
o Occurs on damaged heart valves
o If untreated, takes much longer than 6 weeks to cause death

Organisms
 Native valve endocarditis
o Streptococcus viridans is the most common organism in native valve endocarditis.
o Other common organisms include:
 Staphylococcus species (Staphylococcus aureus more commonly than
Staphylococcus epidermidis) and Enterococci.

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 Streptococcus bovis is associated with increased risk of active colonic

malignancy
 HACEK group of organisms: Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella, and Kingella.
 Prosthetic valve endocarditis
o Staphylococci are the most common causes of early-onset endocarditis;
symptoms appear within 60 days of surgery (Staphylococcus epidermidis more
commonly than Staphylococcus aureus).
o Streptococci are the most common cause of late-onset endocarditis; symptoms
appear 60 days after surgery.
 Endocarditis in IV drug users
o Frequently presents with right-sided endocarditis.
o Staphylococcus aureus is the most common cause.
o Other organisms include Enterococci and Streptococci.
o Fungi (mostly Candida) and gram-negative rods (mostly Pseudomonas) are less
common causes.

Diagnosis
 Duke clinical criteria ( see table below): Two major criteria, one major and three minor
criteria, or five minor criteria are required to diagnose infective endocarditis.
 Of note, echocardiographic evidence of vegetations is not necessary to make the
diagnosis as long as sufficient Duke criteria have been met. Treatment should be
initiated if clinical suspicion is high. TEE is better than transthoracic
echocardiography (TTE) in the diagnosis of endocarditis for especially mitral valve
pathology and small aortic vegetations. Most patients should get TTE as an initial
screening test.

Duke Criteria
Major Criteria
1. Sustained bacteremia by an organism known to cause endocarditis
2. Endocardial involvement documented by either echocardiogram
(vegetation, abscess, valve perforation, prosthetic dehiscence) or clearly
established new valvular regurgitation

Minor Criteria
1. Predisposing condition (abnormal valve or abnormal risk of
bacteremia)
2. Fever

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3. Vascular phenomena: Septic arterial or pulmonary emboli, mycotic aneurysms,

intracranial hemorrhage, Janeway lesionsa
4. Immune phenomena: Glomerulonephritis, Osler nodes,b Roth spots,c
rheumatoid factor
5. Positive blood cultures not meeting major criteria
6. Positive echocardiogram not meeting major criteria
Note: Definitive (i.e., highly probable) diagnosis if two major, or one major plus
three minor, or five minor criteria are present.
aJaneway lesions are painless erythematous lesions on palms and soles.
bOsler nodes are painful, raised lesions of fingers, toes, or feet.
cRoth spots are oval, retinal hemorrhages with a clear, pale center.

Treatment
 Consult specialist
 Three sets of blood cultures should be drawn prior to initiating antibiotic therapy
 Parenteral antibiotics based on culture results for extended periods (4 to 6 weeks)
 If cultures are negative but there is high clinical suspicion, treat empirically (See table
below) until the organism can be isolated.
 If patient has intracardiac devices such as pacemaker or ICD, these must be removed.
 Early surgical intervention is warranted for patient with:
o acute heart failure due to valvular damage.
o left-sided infective endocarditis with highly resistant organisms (including
MRSA)
o infective endocarditis complicated by heart block or intracardiac abscess.
o persistent bacteremia or fevers lasting 5 to 7 days after antibiotic initiation.
o recurrent infection in those with prosthetic valves.

Note: Infective endocarditis is almost always fatal if left untreated.

Empiric antibiotic therapy

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Table: Empiric treatment of ―community acquired‖ Native Valve SBE

Duration in
Antibiotic regimen options Dosage and route weeks Comments
Ceftriaxone 2g, IV, once per day 4-6

3mg/kg, IV once per 2 Dose should be adjusted

PLUS day to

Gentamicin OR Creatinine clearance.

Creatinine should be
1mg/kg/dose, IV, TID monitored.

Vancomycin 15mg/kg/dose, IV, BID 4 For patients with severe

or immediate beta-
lactam allergy.
Do not exceed 2g per day
Adjust dose to creatinine
PLUS clearance.

Gentamicin 3mg/kg, IV once per day 2 See above

OR1mg/kg/dose, IV, TID

*Treatment should be modified based on culture and sensitivity results as well as clinical
judgement of response, risk factors and expected organisms.

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Table: Empiric treatment of health care–associated and IV medicine users

endocarditis
Antibiotic-regimen Dosage and route Duration in Comments
weeks
15mg/kg/dose, IV, BID -Do not exceed 2g per day
4
Vancomycin -Adjust dose to creatinine
PLUS clearance.
Gentamicin
3mg/kg, IV once a day

OR 2 See the table above

1mg/kg/dose, IV, TID

Prophylaxis
Scope of patients who qualify for prophylaxis is much narrower than in the past.
Must have both a qualifying cardiac indication AND procedure to warrant
antibiotic prophylaxis.
 Qualifying cardiac indications
o Prosthetic heart valves (including mechanical, bioprosthetic, and transcatheter
valves).
o History of infective endocarditis
o Congenital heart disease
 Unrepaired cyanotic congenital heart disease.
 Repaired congenital heart disease, with prosthetic material, during first 6
months after procedure
o Cardiac transplant with valvulopathy.
 Qualifying procedures
o Dental procedures involving manipulation of gingival mucosa or periapical
region of teeth (extractions, implants, periodontal surgery, cleaning when
bleeding expected).
o Procedures involving biopsy or incision of respiratory mucosa
o Procedures involving infected skin or musculoskeletal tissue

Further reading

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Steven Agabegi, Elizabeth Agabegi. Step-Up to Medicine. 5th edition, 2020

CHAPTER 5: ENDOCRINE DISORDERS

1. Diabetes mellitus
Brief description
 Diabetes mellitus describes a group of disorders which are characterized by persistently high
blood glucose levels.
 Diabetes is the leading cause of cardiovascular disease, chronic kidney disease, visual loss
and non-traumatic amputations worldwide.
 The classification of diabetes includes four clinical classes
1. Type 1 diabetes- results from cell destruction (immune mediated or idiopathic),
leading to absolute insulin deficiency.
2. Type 2 diabetes-results from a progressive insulin secretory defect on the
background of insulin resistance.
3. Gestational diabetes mellitus (GDM)-diabetes diagnosed during pregnancy in
previously non-diabetic woman

Table. Current diagnostic criteria for diabetes mellitus

4. Other specific types of diabetes e.g. genetic defects in cell function genetic
defects in insulin action, diseases of the exocrine pancreas, and medicine induced

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Pre-diabetes Diabetes Remarks

Diagnostic test
100-125mg/dl >126 mg/dl At least 2 tests needed*
Fasting blood glucose
5.7-6.4% > 6.5% At least 2 tests needed*
Hemoglobin A1C#
140-199mg/dl >200mg/dl At least 2 tests needed
02 hour plasma glucose
>200mg/dl Only classic symptoms of
Random blood glucose hyperglycemia or
hyperglycemic crisis

*If both fasting blood sugar and hemoglobin A1C are done initially and both are in the
diabetic range, repeat test is not necessary for the diagnosis.
# If there is significant discrepancy between HbA1C and blood glucose measurements,
use the blood glucose level.
 The clinical course and treatment of the different types of diabetes are different; hence,
classification of the type of diabetes is very important to determine therapy.
 The traditional thinking that type 2 diabetes as the disease of adults and type 1 diabetes as the
disease of children is not accurate as both diseases can occur in both age groups.

Clinical features
Symptoms
 Asymptomatic: there are no recognizable symptoms in the majority of patients individuals
with type 2 diabetes.
 Type 1 diabetic patients tend to be much more symptomatic than type 2 diabetic patients
(weight loss, polyuria, polydipsia).
 Fatigue, unexplained weight loss
 Large amounts of urine (polyuria) and excessive thirst (polydipsia)
 Unexplained weight loss
 Blurred vision
 Recurrent skin infections
 Recurrent itching of the vulva (candida infections)
 Symptoms related to chronic complications can be present at initial diagnosis in type 2
diabetic patients
o Numbness or pain over the lower limbs
o Visual impairment
o Foot abnormalities (ulcer, ischemia, deformity)

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o Body swelling

Investigations and diagnosis

Diagnosis
 The diagnosis diabetes is made based on the diagnostic criteria depicted above.
 Individuals with any one of the following need screening for type 2 diabetes. If the result is
normal, repeat screening every three years; but if the result is in the prediabetes range repeat
the test every year.
o Age 45 or above
o Overweight or obese individuals ( BMI >25kg/m2)
o Physical inactivity
o Hypertension
o HDL < 35mg/dl and/or triglyceride level > 250mg/dl
o Women with history of gestational diabetes mellitus
o Individuals with prediabetes should be tested yearly
o First-degree relative with diabetes
o History of atherosclerotic cardiovascular disease
o Women with polycystic ovary syndrome.
Investigations
 In newly diagnosed patients
o Diagnostic tests: Fasting or random blood glucose, glycated hemoglobin (HbA1c)
o Urine ketones
o Urine albumin
o Blood urea and creatinine
o Fasting lipid profile
o ECG (adults)
 In diagnosed patients, follow up investigations
o Glycemic control: HbA1c, fasting plasma glucose, post prandial plasma glucose
o Screening for complications: Urine albumin/protein, retinal screening by
ophthalmologist, serum creatinine and urea.
o Other cardiovascular risk screening: Lipid profile (if not already on statin).

Treatment

Objectives of treatment
 Relieve symptoms
 Prevent acute hyperglycemic complications
 Prevent/delay chronic complications of diabetes
 Prevent treatment-related hypoglycemia

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 Achieve and maintain appropriate glycemic targets

 Ensure weight reduction in overweight and obese individuals

1.1 Treatment of Type-2 Diabetes Mellitus

Non pharmacologic treatment

A. Medical Nutrition Therapy (MNT): general guidance
1. Principles of nutritional therapy
o Focus on supporting the patient on choosing healthy eating behaviors.
o Consider the literacy of the individual, access to food, and willingness.
o Try to maintain the pleasure of eating as much as possible
o Respect and address the individual preferences, cultural, and religious choices.
o Be nonjudgmental
o Be practical
o Limit food choices when only supported by scientific evidences
o Help overweight and obese individuals to decrease body weight
o Help attain individualized glycemic, blood pressure, and lipid goals.

2. General advice
o Avoid refined sugars: soft drinks with sugar, or adding sugar/honey to teas/other drinks.
o Carbohydrate
- Reduce overall carbohydrate intake
- Carbohydrate sources high in fiber and minimally processed are preferred : whole
grains, non-starchy vegetables, fruits, and dairy products Be encouraged to have
complex carbohydrates
o Fat
- Reduce saturated fat (animal fat) intake: butter, ghee, fatty cuts of meat, cheese.
- Reduce Trans-fat (hydrogenated oil): solidified vegetable oils
- Mono-saturated and polyunsaturated vegetable oils are preferred
o Protein
- Should be left to the individual choice.
- When there is chronic kidney disease, reduction (not stopping) protein intake.
o Sweetened beverages
- Individuals who have had the habit sugar added beverages, taking low-calorie or
nonnutritive- beverages can serve as short-term transition. However, they should be
encouraged to replace with water intake.
B. Exercise

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o Regular moderate-intensity aerobic physical activity : for at least 30 minutes at least 5

days a week (at least 150 min/week)
o Encourage resistance training three times per week.
C. Weight management
o For obese and overweight individuals
- Eating plans (focusing on reduction of overall carbohydrate intake) and exercise
D. Stop smoking
E. Moderation of alcohol intake
o A maximum one drink for women and two drinks for men.
- One drink is roughly equivalent to a bottle of beer, a glass of wine, or a unit of spirit.
F. Self-blood glucose monitoring (SBGM)
G. Screening for micro and macro vascular complications

Pharmacologic treatment
I. Management of blood sugar
A. Target blood glucose
o Target should be individualized.
o In young patients with recent diagnosis, without significant chronic complications,
tight glycemic control should be encouraged.
o Individuals for whom less stringent ( HbA1C < 8 to 8.5%) should be considered
- History of severe hypoglycemia
- The elderly and those limited life expectancy
- Established cardiovascular disease
- Advanced microvascular disease e.g. advanced chronic kidney disease
- Significant comorbid conditions e.g. liver disease, malignancy
- Long duration of diabetes
B. Target in most non-pregnant adults without significant comorbidities: depicted in the
table below.
Table. Glycemic targets for non-pregnant adults without significant comorbidities
TARGET Remark
Fasting capillary glucose 100 -130mg/dl In young, highly motivated, well
HbA1C <7.5% supported patients a hemoglobin
A1C target <6.5% and fasting
blood glucose of 80-130mg/dl can
be aimed, if it can be achieved
without causing recurrent
hypoglycemia.
Post meal capillary glucose <180mg/dl
(1-2hr from the beginning of

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meal)

C. Blood glucose lowering medicines

1. First line: Metformin
o Initial dose 500mg to 1000mg/day daily or in two divided doses with meals.
o Titrate dose every two weeks depending on the fasting blood sugar
o Maximum dose = 2000mg/day (1000mg BID)
- The major side effects of metformin are gastrointestinal intolerance: bloating,
abdominal discomfort, and diarrhea. This can be reduced by gradually
increasing the dose.
- Metformin is contraindicated in patients with advanced chronic kidney disease
(eGFR <30ml/min), advanced liver disease, and hypoxia.

2. Alternative to Metformin
o If Metformin is contraindicated a sulfonylurea can be started ( see below for the
sulfonylurea)
o Basal insulin can also be started as an alternative( see for indications for starting
insulin in type 2 diabetes)

3. Add on to Metformin: If glycemic target is not achieved by metformin alone after

three months, add either of the following.
o Sulfonylureas : Glibenclamide, Glimepiride, Gliclazide
OR
o Basal insulin

4. Initiating two oral agents at diagnosis

o Patients with severe hyperglycemia at presentation (Fasting blood sugar > 250mg/dl
or HbA1C>10%) and prefer oral agents than insulin, need to be started on a
combination of metformin and sulfonylurea.

5. Sulfonylureas
o Glibenclamide (Glyburide)
- Starting dose is 2.5-5mg/day, 30 minutes before breakfast.
- Titrate dose slowly to maximum of 20mg/day
- When 10mg/day is needed, divide the total dose into two, with the larger dose
in the morning.
- Avoid in the elderly and patients with renal impairment.
o Glimepiride

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- Starting dose is 1-2 mg/day, 30 minutes before breakfast.

- Titrate dose slowly to maximum of 8mg/day
o Gliclazide, modified release
- Starting dose 30mg/day
- Titrate the dose slowly to a maximum dose 120mg/day
o The major side of sulfonylureas is hypoglycemia.
- Individuals should be educated about the risk, manifestations, prevention and
treatment of hypoglycemia.
- Sulfonylureas should be avoided or given at lower doses in individuals at high
risk of hypoglycemia (e.g. the elderly, with significant comorbidities, history
of hypoglycemia)
6. Insulin therapy in type 2 diabetes
Indications for insulin therapy
 Failure to control blood glucose with oral medicines
 Temporary use for major stress, e.g. surgery, medical illness
 Severe kidney or liver failure
 Pregnancy
 In patients difficult to distinguish type 1 from type 2 diabetes
 Ketonuria
 Unexplained weight loss accompanied by poorly controlled blood sugar
 Initial therapy for a patients presenting with very high blood sugar
o HbA1C >10% or fasting blood glucose >250 mg/dl or random glucose
consistently >300 mg/d

o Dosing basal insulin in type 2 diabetes

- If started on as an add on therapy to Metformin
 Starting dose = NPH 10 units at bed time
 A higher dose might be started for higher blood glucose
 Dose increment 2-4 units in 3-7 days with self-monitoring of blood
sugar
- If started as a replacement for oral agents
 Starting dose = NPH 15 -20 units at bed time
 A higher dose might be started for higher blood glucose
 For doses above 20units divided in two ( about 2/3 in the morning and
1/3 in the evening)
 Dose increment 2- 4 units in 3-7 days with self-monitoring

o Addition of prandial regular insulin

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- Indications to start regular insulin before meal

 If FBS is well controlled but HbA1c is above target
 If HbA1c is above target despite increasing basal insulin to >0.5
unit/Kg/day
- Dosing prandial regular insulin
 Starting dose of prandial insulin : Regular insulin 4units
 Preferred time : before the largest meal of the day
 Dose increment 1-2 units in 2-3 days with self-monitoring of the
next pre-meal blood glucose

D. Other oral diabetic medications for the care of patients with type 2 diabetes
mellitus.
o The above recommendations on the choice of pharmacotherapy for type 2 diabetes
indicate sulfonylureas or basal insulin to be the preferred add-on therapies next to
metformin. This is mainly based on cost related factors.
o There are other medications which have been extensively studied and demonstrated to
have benefits for different groups of patients with type 2 diabetes.
o For patients who can afford to buy or get access to these medications, decision on
which agent to add to Metformin, combine with Metformin from the beginning or
sometimes start an initial treatment should be individualized based on the following
factors.
- The need for weight loss
- Risk of hypoglycemia in the patient
- the presence of cardiovascular disease
- The presence of chronic kidney disease.
o The following table shows the list of the available medications at the time of
publication, their mechanism of action and the preference(see the table below)

Class of Available drugs Mechanism of Clinical sates in which Common side

medication and formulations glucose the drug is most effects
in Ethiopia lowering beneficial
SGLT2 Dapagliflozin 10mg Increased  Heart failure  Increased
inhibitors or 5mg tablet urinary  Early stages of CKD urination
(Sodium glucose  Compelling need to  Vulvovagina
glucose Dosage: 5 or 10mg, excretion by decrease the risk l fungal
transporter -2 po, once daily the kidneys hypoglycemia infections
inhibitors)  Compelling need to and UTI
decrease weight loss or  Might
reduce weight increase the

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 Need to improve risk of DKA

glycemic control  Avoid in
 Additional benefit of BP advanced
lowering CKD
DPP4- Saxagliptin 2.5 or  Inhibition of  Compelling need to  Upper
inhibitors 5mg DPP-4 decrease the risk respiratory
(Dipeptidyl ( also as fixed drug enzyme, hypoglycemia tract
peptidase -4 combination with increase the  Need for intensification infections
inhibitors) Metformin 500mg level of of glycemic control  Headache
or 1000mg) incretins.  Weight neutral (no  Dose
 Increases increment or significant reduction
Dosage: 2.5 -5mg, glucose- decrement) need in
po, once daily dependent
patients
insulin
Vildagliptin 50mg secretion. with CKD.
(also as fixed drug  Reduce
combination with glucose
Metformin 500mg release from
or 1000mg) liver after
meals
Dosage: 50mg, po,
once daily or BID

E. Management of other cardiovascular(CV)risks

1. Cardiovascular risk calculation
- All patients 10 year cardiovascular risk factor needs to be calculated (see
section on ischemic heart disease)
2. Blood pressure management (See section on hypertension)
- Target blood pressure: <130/80mmHg
- First line if there is proteinuria: ACE inhibitors or ARBs
- First line if no proteinuria: Calcium channel blocker, thiazide diuretics
or ACE inhibitors or ARBs.
- Preferred two drug combinations for patients with proteinuria
 ACE inhibitors/ARB + Calcium channel blockers
 ACE inhibitors/ARB + Thiazide diuretics
- Preferred combination for patients with no proteinuria
 Calcium channel blockers + ACE inhibitors/ARB
 Calcium channel blockers + Thiazide diuretics
- Preferred three drug combinations

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 ACE inhibitors/ARB + calcium channel blockers + Thiazide

diuretic
3. Lipid lowering therapy
- Indications
1. Age above 40 without additional CV risk
 Start moderate intensity statin
 Make it high intensity if there is additional CV risk
2. All ages with a history of cardiovascular risk
 Start high intensity statin
3. Age 20-39 years with one or more CV risk factor

4. Antiplatelet therapy
- Aspirin ( 81-162mg/day)
 It is only indicated for patients who have CV disease (coronary
artery disease, ischemic stroke or peripheral arterial disease)

1.2 Treatment of Type 1 Diabetes Mellitus

Non pharmacologic treatment
 See in the management type 2 Diabetes

Pharmacologic
 Insulin is the main stay of treatment in type 1 diabetes
 Insulin regimen in type 1 Diabetes Mellitus :
1. Conventional insulin therapy
- It encompasses simpler non-physiologic insulin regimens.
- These include single daily injections, or two injections per day (including a
combination short-acting and -NPH insulin)
2. Intensive insulin therapy
- It describes treatment with >3 injections/day or continuous insulin infusion
- It requires frequent monitoring of blood sugar: fasting, before lunch, before dinner &
before bed.
- It also requires the following
 Counting and recording carbohydrates.
 Adjusting insulin doses in response to given glucose patterns.
 Coordinating diet, exercise, and insulin therapy.
 Responding appropriately to hypoglycemia
3. Designing insulin therapy

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- Total insulin dose per day Initiation, 0.2 to 0.4 units/kg/day

- Maintenance – highly variable roughly 0.6 to 0.7 units/kg/day
- Regimen options-with NPH and regular insulin

A. Preferred regimen: NPH with premeal regular insulin

o NPH before breakfast and at bed time
PLUS
o Regular Insulin three times daily injection: before breakfast, lunch, and dinner

B. Other options: If the patient work, routines, social circumstances, and support do
not allow the patient to do the preferred regimen
o NPH with pre-breakfast and pre-dinner regular insulin
o Mixed NPH and regular insulin -70/30 (70% NPH & 30% regular)
o Twice daily NPH injections only: Before breakfast and before bedtime

1.3 Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar

state (HHS)
Brief description
 Diabetic ketoacidosis (DKA) is a condition in which there is a severe deficiency of insulin
resulting in very high blood glucose.
 Fat is broken down as an alternative source of energy with ketones/ketoacids as a by-product.
 This state of severe hyperglycemia and ketone body production results in severe metabolic,
fluid and electrolyte abnormalities.
 DKA often occurs in type 1 diabetes patients but may also occur in type 2 diabetes.
 The most common settings in which DKA occurs include:
o Previously undiagnosed and untreated diabetes
o Interruption therapy
o Stress of inter-current illness (e.g. infection, myocardial infarction, stroke,
surgery, complicated pregnancy etc.)
 Hyperglycemic hyperosmolar state (HHS) is a hyperglycemic emergency that occurs in type
2 DM due to relative insulin deficiency and inadequate fluid intake.
 Apart from acidosis the manifestations, risk factors and management of HHS is similar to
DKA

Clinical features
Symptoms
 Excessive urination

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 Excessive thirst and drinking of water

 Nausea, vomiting
 Abdominal pain
 Symptoms of infection or other precipitants
Signs
 Deep and fast breathing
 Low blood pressure
 Fast and weak pulse
 Alteration in sensorium or collapse
 Dehydration with dry skin, reduced skin turgor or sunken eyes
 -Fruity' breath (smell of acetone) in DKA
 Evidence of infection, recent surgery, stroke etc.

Investigations and diagnosis

Diagnosis
 Diagnosis of DKA or HHS is made with the presence of severe hyperglycemia, clinical
features and ketone in the urine (in case of DKA)
 Sometimes DKA can occur in relatively lower blood sugar (euglycemic DKA)

Investigations
 Random blood glucose : usually >300mg/dl)
 Urine glucose (usually >3+)
 Urine ketones (usually >2+)
 BUN and Creatinine
 Serum electrolytes, particularly serum potassium
 Investigations for precipitants: CBC, blood film for malaria parasites and others based on the
suspected precipitating factors

Treatment
Objectives of treatment
 Replace fluid losses
 Replace electrolyte losses and restore acid-base balance
 Replace deficient insulin
 Seek the precipitating cause and treat appropriately

Non Pharmacologic
 Admit to intensive care unit (or a ward patient can be very closely observed)
 Closely monitor fluid input and urine output

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Pharmacologic
1. Replace fluids: Individualize fluid needs based on the patient hydration status; the
following is a guide to severely dehydrated patients.
o Initial fluid
- 1000ml NS the first hour.
- Reassess for hydration status: if still severely dehydrated, give another 1000ml
NS over the next 01 hour.
o Subsequent fluid
- Depends on the hydration status and urine output of the patient.
- On average give about 250 mL/hour (1000ml over 04 hour) in the first 24 hours
or until patient is able to take enough oral fluids.
- Reassess the patient hydration status to decide subsequent Iv fluid needs.
o Changing fluid
- Change the NS to 5% DW9D when plasma glucose reaches 250 mg/dl in DKA
and 300mg/dl in HHS.
o HHS requires more fluid.
o Assess hydration status, BP and urine output frequently.
o In patients with impaired kidney function and cardiac disease more frequent monitoring
must be performed to avoid iatrogenic fluid overload.

2. Administer short-acting insulin

o Regular Insulin
- 10units IV and 10 units IM, stat,
Then
- If there is perfuser: 0.1units/kg per hour by continuous IV infusion.
- If there is no perfuser: 5 units, I.M, every hour.
o Goal
- Reduce serum glucose by 50 to 70 mg/dl in the 2-3 hours
- If the drop is <50mg/dl in 2-3 hours, double the regular insulin.
- If the drop is faster, reduce the dose by half for continuous infusion and give the
IM insulin every 2 hour.

3. Potassium
o All patients with DKA have potassium depletion irrespective of the serum K+ level.
- If the initial serum K+ is <3.3 mmol/l, do not administer insulin until the K is
corrected.
- If the initial serum K + is >5.3 mmol/l, do not supplement K until the level
reaches < 5.3.

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- If K+ determination is not possible delay initiation of K replacement until there is

a reasonable urine put(>50 ml/hr)
o Add intravenous KCl in the IV fluids
- Add 40–60 mmol/l of IV fluid when serum K+ < 3.7 mmol/l
- Add 20-40 mmol/l of IV fluid when serum K+ < 3.8-5.2 mmol/l
o The serum potassium should be maintained between 4.0 and 5.0 mmol/l

4. Precipitant identification and treatment

o Noncompliance, infection, trauma, infarction. Initiate appropriate workup for
precipitating event (cultures, CXR, ECG)

5. Follow up of response
o Blood glucose every 1–2hrs
o Urine ketones every 4hr
o Electrolytes (especially K+) every 6 h for first 24 h.

6. Continuation of treatment
o The above treatment should continue until the patient is stable, clinically acidosis
improves, and patient is able to take oral feeding.
o The urine ketone might still be positive, as it usually lags behind the improvement of
acidosis.

7. Transition
o Once the patient is able to take oral feeding and clinically the acidosis improved.
- Reduce regular insulin : 2-3 units hourly (5 units every 2 hour) or for continuous
infusion by 0.05/kg per hour
- Overlap regular insulin with subcutaneous NPH insulin for 2-3 hours
- NPH insulin dosing
 If previously on insulin: start the pre DKA or pre HHS dose
 If Insulin naïve: 80% of the 24 hour requirement or 0.5 to 0.8kg/day
(divided in to basal and bolus)
1.4 Hypoglycemia in Diabetes
Brief description
 Hypoglycemia is a blood sugar level low enough to cause symptoms and signs.
 It is a common complication of glucose lowering therapy in diabetes.
 Sulfonylureas and insulin are the most common causes of hypoglycemia.

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 The elderly, patients with impaired kidney function and multiple comorbidities are at higher
risk of hypoglycemia.
 A value <70mg/dl is agreed as alert level to define hypoglycemia in diabetes.
 It should be remembered some patients might be symptomatic at levels>70mg/dl and some
might not develop symptoms at level <70mg/dl.
 Pseudohypoglycemia is an event during which the person with diabetes reports typical
symptoms of hypoglycemia but with a measured blood glucose concentration >70 mg/dl.
These patients commonly have chronically high blood sugar and they experience symptoms
of hypoglycemia at plasma glucose levels >70 mg/dl as glucose levels starts to improve.
 Whipple‘s triad is a combination of three essential elements useful for the diagnosis of
hypoglycemia in general.
1. Symptoms and signs of hypoglycemia
2. Documented low blood glucose level
3. Relief of symptoms up on correction of the low blood glucose.
 Hypoglycemia unawareness is a situation where symptoms of hypoglycemia are not felt by
the patient in spite of having low blood glucose levels. It is a common and challenging
problem is patients with long standing diabetes.

Clinical features
 The symptoms of hypoglycemia are classified in to adrenergic and neuroglycopenic
Adrenergic(autonomic) Neuroglycopenic ( brain glucose
deprivation)

Difficulty concentrating
Palpitation Difficulty in speaking
Tremor Blurred vision
Anxiety Incoordination
Hunger Confusion
Sweating Loss of consciousness
Tingling Seizure

 Asymptomatic: diabetic patients with hypoglycemia can be asymptomatic; this

hypoglycemia unawareness results from autonomic dysfunction.

Investigations and diagnosis

Diagnosis
 The diagnosis of hypoglycemia is diabetes is made with either of the following
o A documented blood glucose level <70mg/dl

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OR
o Presence of symptoms which improve with treatment
 Classification of diabetes associated hypoglycemia based on severity
Level 1 Blood glucose 54-70 mg/dl
Level 2 Blood glucose <54 mg/dl
Level 3 A severe event characterized by altered mental and/or
physical status requiring assistance for treatment of
hypoglycemia

Investigations
 Glycemia related: FBS, postprandial blood sugar and HbA1c
 Creatinine and urea

Treatment
Objectives of treatment
 Reverse hypoglycemic symptoms
 Prevent brain damage
 Prevent recurrence

Non-pharmacologic
 The main stay of management of level 1-2 (mild to moderate) and level-3 (severe)
hypoglycemia with preserved consciousness taking or providing glucose rich
food/drinks(sweets).
o Pure glucose is preferred but any carbohydrate rich food can be used
- Give 04 teas spoon of sugar diluted in water
- Monitor blood sugar every 20-30 minutes
- If no improvement repeat the above
- Once blood sugar improves, the patient must take a meal or snack
o Alternatives: regular soft drinks
- 200ml of Mirinda® or Cola® contains about 20gram sugar can replace
the above.
o Avoid protein rich foods as they increase insulin response
 For hypoglycemia unawareness: a 2-3 weeks period of avoiding hypoglycemia through
frequent self-monitoring of blood glucose and keeping the blood glucose at higher levels may
restore awareness.

Pharmacologic
 In patients who present to health facilities with decreased level of consciousness from severe
hypoglycemia

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o 40% Dextrose (20ml vial)

- Give 03 vials IV, fast
- Monitor blood sugar every 20-30 minutes
- If blood sugar is <70mg/dl, give another 03 vials of 40% dextrose and start
5-10% dextrose infusion. Continue to monitor blood sugar every 20-30
minutes.
- When the patient can take orally give regular meal or snack. .

Prevention of hypoglycemia in diabetics

 Self-monitoring of blood sugar
 Patient, family/care giver education
o A standardized education on rigorous avoidance of hypoglycemia
o On conditions which increase the risk of hypoglycemia
- Fasting or delayed meals
- Consumption of alcohol
- Intense exercise
o Symptoms of hypoglycemia and possibility of hypoglycemia unawareness
o Treatment of hypoglycemia at earliest warning symptoms or at <70mg/dl
o Adjusting glycemic targets to higher levels, if hypoglycemia is recurrent
o Reporting episodes of hypoglycemia to physician

1.5 Chronic complications of diabetes

Brief description
 The complications of diabetes are classified in two major groups
1. Microvascular: Diabetic kidney disease, retinopathy and nephropathy
2. Macrovascular: coronary artery disease, stroke and peripheral vascular disease
 Diabetic foot disease is also a major complication which results from multifactorial causes
 Prevention, detection, delaying progression and supportive management of these
complications is an important part of care of patients with diabetes
 Prevention of these complications can be achieved through optimal glycemic control, optimal
blood pressure management, lipid control, quitting smoking and maintaining a healthy life
style.
 Screening, follow up, prevention and treatment of the microvascular complications is
summarized in the table below

Table: screening and management of chronic complication of diabetes

Initial screening Follow up Prevention& Treatment
screening
Nephropathy  T1DM-after 5 years  No  Optimize glycemic control

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 T2DM - at nephropathy -  Optimize BP control

diagnosis annually  ACEi/ARB for proteinuria
 Screening tool:  Nephropathy-
- Albuminuria 2x/yr
- Creatinine, eGFR  Refer if eGFR
<30ml/min
Retinopathy  T1DM-after 5 years  No  Optimize glycemic control
 T2DM – at retinopathy-  Optimize BP control
diagnosis in 1-2yr  Optimize lipid control
 Before and at time  Retinopathy-
of pregnancy 1yr  Pan retinal laser
 Sight photocoagulation
 Screening tool: threatening  Intravitreous injections of
- Dilated eye retinopathy - anti– vascular endothelial
examination by more frequent growth
ophthalmologist evaluation
 ASA is not in patients with
retinopathy
Neuropathy  T1DM-after 5 years Annually  Optimize glycemic control
 T2DM – at  Symptomatic management
diagnosis
 Painful neuropathy
Screening tool o Amitriptyline: 12.5-50mg
 Careful history PO/bedtime
 Temperature/
pinprick &  Gastroparesis
vibration o Metoclopromide 10mg
sensation PO, TID( syrup preferred)
 10-g monofilament Alternatives( 2nd line)
testing o Domperidone 10mg PO
TID
o Erythromycin syrup, 50-
250mg, TID

 Diabetic diarrhea
o Symptomatic treatment
Loperamide 2-4mg,PO,
6-8hrly
or
Codeine 30mg, PO,6-
8hrly
o Treatment of bacterial
overgrowth: Antibiotics 7-
10days

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Norfloxacin 400mg, BID

Or
Metronidazole500mg TID
+ Cephalexin 500mg
TID/or Cotrioxazole
960mg BID

 Postural hypotension
o Change posture slowly
o Elevate head by 10-200
o Dorsiflexion of feet and
handgrip( before standing
o Tensing legs by
crossing(when standing)

 Bladder dysfunction
o Remove drugs which
worsen it (Amitriptyline,
calcium channel blockers)
o Strict voluntary voiding
schedule
o Crede maneuver(lower
abdominal pressure by
hands)
o If severe: Self intermittent
catheterization

 Erectile dysfunction
Use PDE5 inhibitors
- Take 01hr before sexual
encounter
- On empty stomach
- Avoid use with nitrates
o Sidenafil 25-100mg (start
with 50mg
o Vardanfil 10-20mg
o Tadalafil 10-20mg

If refractory
o Tadalafil2.5-5mg/daily

Diabetic foot Initial visit Every visit

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 Optimize glycemic control

Screening tools  Stop smoking
- Assessment of skin  Pain management in
& foot deformities painful peripheral
- Neurologic exam neuropathy
- Peripheral arterial  Education on foot care
disease evaluation  Specialized therapeutic
foot ware for patients with
callous deformities, ulcers,
or amputation

Further reading
1. American Diabetes Association Standards of Medical care in diabetes—2020.
2. International Diabetes Federation. Recommendations For Managing Type 2 Diabetes In
Primary Care, 2017. www.idf.org/managing-type2-diabetes
3. Mohan, V., Khunti, K., Chan, S.P. et al. Management of Type 2 Diabetes in Developing
Countries: Balancing Optimal Glycaemic Control and Outcomes with Affordability and
Accessibility to Treatment. Diabetes Ther 11, 15–35 (2020). https://doi.org/10.1007/s13300-
019-00733-9

2. Dyslipidemia and metabolic syndrome

Brief descriptions
I. Metabolic syndrome
 The metabolic syndrome is defined as the co-occurrence of risk factors for atherosclerotic
cardiovascular disease (ASCVD) and future development of type 2 diabetes.
 Abdominal obesity and the associated insulin resistance are considered to be main pathogenic
mechanism behind the metabolic syndrome.
 The most important clinical implication of diagnosing metabolic syndrome is intensification
of life style and pharmacologic based ASCVD risk reduction.

II. Dyslipidemia
 Dyslipidemias are disorders of lipoprotein metabolism that may result in the following
abnormalities: High total cholesterol (TC), high low-density lipoprotein cholesterol (LDL-
C), high non-high-density lipoprotein cholesterol (HDL-C), high triglycerides (TG), or low
HDL-C.
 Serum cholesterol and its lipoprotein carriers (LDL, and VLDL) are known to be related to
atherosclerotic cardiovascular disease (ASCVD).

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 LDL-cholesterol is the dominant form of atherogenic cholesterol.

 HDL-cholesterol is not atherogenic.
 Although LDL-Cholesterol is a primary cause of atherosclerosis, other major cardiovascular
risk factors contribute a lot.
 The major cardiovascular risk factors include cigarette smoking, hypertension, diabetes,
other non-LDL abnormalities and old age
 LDL-C is calculated with the formula: LDL= Total-cholesterol–(triglycerides/5) – HDL.
When triglyceride level is above 400mg/dl, this equation is sufficiently accurate.

III. Atherosclerotic cardiovascular disease (ASCVD) risk calculation and prevention

 Coronary artery disease, ischemic stroke, and peripheral arterial disease the major
atherosclerotic cardiovascular diseases (ASCVD)
 Primary prevention of ASCVD is a preventive strategy implemented in individuals at
increased risk before the development of the ASCVD.
 Secondary prevention is a preventive strategy implemented in individuals who have past or
current ASCVD.
 ASCVD risk calculation tools are validated tools of predicating the probability of
developing these diseases in the future, generally expressed as the percentage probability in
the coming 10 years.
 Decision on treatment and intensity of treatment of dyslipidemia for primary prevention
should be based on the calculated ASCVD risk.

Clinical features
 Central obesity
 High blood pressure
 Xanthelasmas and xanthomas
 If ASCVD has already developed: angina pain, intermittent claudication, transient ischemic
attacks

Diagnosis and Investigations

 The diagnosis of metabolic syndrome is based on the presence of three of the following five
risk factors
No Risk factor Defining level

1. Waist circumference Men >102 cm Women > 88 cm

Triglycerides
2. >150 mg/dl

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HDL cholesterol Men <40 mg/dl Women <50mg/dl

3.

Blood pressure 130/85 mm Hg

4.
Fasting glucose >100 mg/dl
5.

 For calculation of ASCVD risk use the AHA/ACC 2013 ASCVD Risk Calculator which
available as freely downloadable tools for smartphones or online use.
 After calculating the 10yr ASCVD, categorize individuals in the age 40-75year in to the
following risk categories.

<5% = LOW RISK 5 to < 7.5% = BORDERLINE

7.5 to< 20% = INTERMEDIATE >20% = HIGH

 The presence of CKD, metabolic syndrome, inflammatory diseases like rheumatoid arthritis
and HIV, premature menopause, family history of premature ASCVD increase the risk and
are considered das risk modifiers.
 Additional investigations
o FBS and HbA1C
o Urinary protein/albumin
o Creatinine and urea/eGFR

Treatment
Objectives of treatment
 Reduction of future development of ASCVD
 Prevention of early mortality

Non- pharmacologic management

 Life-style modification
o Diet
- Diet that emphasizes intake of vegetables, fruits, whole grains, legumes
- Healthy protein sources (low-fat milk products), low-fat chicken (without the
skin),and fish
- Limits intake of sweets, sugar-sweetened beverages, and red meats
o Weight Control
o Physical Activity

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- At least 150 minutes per week (e.g. At least ½ hour 5-7x/wk) of moderate-
intensity physical activity or 75 minutes of vigorous intensity.
- Moderate intensity physical activity: typical example brisk walking
- Vigorous intensity physical activity: typical example Jogging, running or biking

Pharmacologic treatment
 Statin therapy
 The intensity of statin therapy is divided into 3 categories
o High-intensity statin = lowers LDL-C levels by ≥50%
o Moderate-intensity statin = lowers LDL-C levels by 30% to 49%,
o Low-intensity statin therapy = lowers LDL-C levels by <30%

Table. Intensity of statin therapy

High intensity Moderate intensity Low intensity
Atorvastatin 40-80mg 10-20mg -
(commonly used 40mg) ( commonly used 20mg)
Rosuvastatin 20-40mg 5-10mg -
(commonly used 20mg) (commonly used 10mg)
Simvastatin - 20-40mg 10mg
Lovastatin - 40mg 20mg

Table. Indications of statin therapy

High intensity statin Moderate intensity Low intensity

1. Anyone with LDL-C 1. Anyone with DM + age 40- 1. Age 40-75yr,

>190mg/dl 75yr Borderline risk (5-
2. Secondary prevention 2. No DM + Age 40-75 + 7.5%) + multiple
3. Age 40-75yr and ASCVD ASCVD RISK 7.5-20% + risk risk enhancers
risk >20% enhancers 2. If moderate
4. DM, age 40-75yr +risk 3. Age 20-39yr, LDL>160mg/dl intensity therapy is
enhancers and family history of not tolerated
premature ASCVD
4. If high intensity therapy is not
tolerated

 Statin safety
o Statin therapy is usually well tolerated and safe.
o Some side effects are seen occasionally.
o The most common side effect a statin-associated muscle symptom. Myalgia is more
common than genuine myositis, or the very rare rhabdomyolysis.
o If muscle symptoms are mild, another statin can be rechallenged with a lower
intensity.

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o Statins increase the risk of new onset diabetes modestly but it should not be reason
not to start or withdraw statins.
 Other pharmacologic treatments in metabolic syndrome
o Hypertension and diabetes should be treated as per the standard treatment guideline.

Further reading
1. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to
reduce cardiovascular risk. European Heart Journal (2020) 41, 111188.
doi:10.1093/eurheartj/ehz455.
2. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA
Guideline on the Management of Blood Cholesterol. Circulation. 2019;139:e1082–e1143.
DOI: 10.1161/CIR.0000000000000625. https://www.ahajournals.org/journal/circ

3. Thyroid disorders
3.1 Goiter
Brief description
 Goiter (Goitre) refers to an enlarged thyroid gland.
 The most common cause of Goiter in Ethiopia is endemic goiter, which results from iodine
deficiency and/or regular the regular consumption of goitrogenic.
 Goitrogenic foods are foods that inhibit thyroid hormone synthesis e.g. Millet, cabbage, kale
etc.
 Goiter can be present with normal or abnormal thyroid function.

Causes of goiter
1. Endemic goiter( iodine deficiency and/or regular consumption
goitrogenic foods)
 Simple
 Toxic
2. Grave‘s disease
3. Thyroiditis
4. Physiologic goiter( pregnancy and puberty)
5. Benign thyroid tumor( adenoma)
6. Thyroid cancer

Clinical features

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Symptoms
 Majority of individuals with goiter do not have symptoms
 Swelling in anterior neck
 Disfigurement
 Compression of symptoms from large goiter or growth behind the sternum( retrosternal
goiter) : hoarseness of voice, stridor, difficulty of swallowing
 Occasional postural dizziness
 Symptoms of hyperthyroidism or hypothyroidism ( see next ) may be present

Signs
 Visible or Palpable thyroid gland
 Enlarged( engorged) neck veins
 Signs of hyperthyroidism or hypothyroidism ( see next) may be present

WHO Grading of goiter size ( mainly for epidemiologic purposes)

Grade 0: Group 0: normal thyroid, no palpable or visible goiter
Grade 1: A goiter that is palpable but not visible when the neck is in the
normal position
Grade 2: A goiter that is clearly visible and palpation is when the neck is in
normal position

Investigations and diagnosis

Diagnosis
 The diagnosis of goiter is based on physical examination.
 The next step two steps in the evaluation are the following
1. Determining thyroid function test : serum TSH(Thyroid stimulating hormone)
2. Thyroid ultrasound
o Ultrasound features that make thyroid nodules suspicious for malignancy:
- Hypoechogenicity
- Microcalcification
- Hypervascularity
- Irregular borders
- Taller than wide
o Thyroid imaging reporting and data system (TI-RADS) is a helpful ultrasound
based risk stratification system to identify thyroid nodules with high risk for
malignancy.
- TI-RADS 4b and 5 nodules need FNAC.

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- TI-RADS 4a and 3 lesions may need FNAC is they are large or rapidly
growing.
3. Evaluation for possible malignancy: FNAC( Fine needle aspiration biopsy)

Goiter:
Determine TSH

TSH: normal
TSH: Low TSH: High

- Thyroid ultrasound No need for thyroid - Thyroid ultrasound -

- FNAC: dpending on ultrasound - FNAC: dpending on
TI-RADs score of the Evlauate as TI-RADs score of the
ultraound hyperthyroidism ultraound

Treatment
Objectives of treatment
 The goal of treatment for goiter depends on clinical presentation
1. Improving physical compression symptoms: surgical treatment
2. Addressing aesthetic concerns(disfigurement): surgical treatment
3. Correcting hyperthyroidism or hypothyroidism : pharmacologic treatment

Non-pharmacologic treatment
 The main non-pharmacologic treatment of goiter is surgical management.
 The main indications for surgery( thyroidectomy ) are the following
1. Thyroid cancer
2. Compression symptoms
3. Toxic multi-nodular goiter: after correcting the thyrotoxicosis
4. Aesthetic concerns

Pharmacologic treatment

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 There is no specific pharmacologic treatment for decreeing the size of uninvestigated goiter.
Routine of iodine or Lugol’s solution to decrease the size of a grossly enlarged
nodular goiter should be avoided.

Prevention
 The most common cause of goiter, endemic goiter is mainly caused by iodine deficiency.
 Correction iodine deficiency at community level is an effective strategy,
 Universal iodization of salt is the preferred method of prevention.
 In iodine deficient community to prevent the consequences of iodine deficiency in children,
iodine supplementation for pregnant women, lactating women and children less than 2 years.
o Medication for prevention :
- Iodized oil capsule, strength 190 mg of iodine per capsule

Category Dosage
Children less than 6 months Exclusive breast feeding, treat the mother
Children 6 months to 1 year 1 capsule (190 mg) once a year
Children from 1 to 2 year 2 capsules (380 mg) once a year
Pregnant or lactating women 2 capsules (380 mg) once a year

Further reading
1. MARK A. KNOX. Thyroid nodules. American Family Physician. 2013;Volume 88, Number
3. www.aafp.org/afp
2. WHO/NHD/01.1 Assessment of Iodine Deficiency Disorders and Monitoring their
Elimination, A guide for programme managers, second edition.
3. M Andersson, B de Benoist, F Delange and J Zupan. Prevention and control of iodine
deficiency in pregnant and lactating women and in children less than 2-years-old:
conclusions and recommendations of the Technical Consultation. Public Health Nutrition:
10(12A), 1606–1611. doi: 10.1017/S1368980007361004

3.2 Thyrotoxicosis
Brief description
 A condition resulting from an excess of thyroid hormones,
 If left untreated, significant weight loss and cardiac complications, including Heart Failure,
may occur. .
 Causes

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o Grave‘s disease (autoimmune, common in females)

o Toxic multinodular goiter
o Toxic adenoma
o Thyroiditis (causes transient thyrotoxicosis which progresses to normal or
hypothyroid state later)
o Iatrogenic causes (side effect of medications containing iodine e.g. amidarone)
Clinical features
Symptoms
 Weight loss despite increased appetite
 Excessive sweating
 Heat intolerance
 Palpitations
 Nervousness and irritability
 Menstrual irregularity , mainly oligomenorrhea
 Increased hair loss
 In thyroiditis there could be neck pain and

Signs
 Tachycardia with or without irregularity : Sinus tachycardia or atrial fibrillation
 High blood pressure
 Goiter often present but not always
o Smooth and diffuse goiter in Grave's disease
o Irregular goiter in toxic multi-nodular goiter
o Single thyroid nodule in toxic adenoma
o Thyroiditis: there could tenederness
 Tremors and brisk deep tendon reflexes
 Moist palms
 Exophthalmos (Staring or protruding eye, lid lad/retraction in Grave‘s disease)

Investigations and diagnosis

Investigations
 TSH
 Free T4, if TSH is abnormal
 ECG
 Thyroid imaging and cytology are not generally necessary in the work up of
hyperthyroidism.

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Diagnosis
 TSH is the best initial diagnostic test.
 If the TSH is low, it suggests hyperthyroidism
 A low TSH result should be followed by Free T4 and total T3 determinations. Rarely Free T3
determination may be needed.
o TSH normal = excludes hyperthyroidism
o TSH is low and high Free T4 or T3 = Primary hyperthyroidism
o If TSH is low, Free T4 and T3 normal= subclinical hyperthyroidism

Treatment
Objectives of treatment
 Improve symptoms
 Prevent or treat complications

Non pharmacologic treatment

 Avoid stimulants e.g. Caffeine
 Partial thyroidectomy; should only be done after a state of euthyroidism is
achieved with medical therapy
 Radioiodine therapy

Pharmacologic treatment
1. Anti-thyroid drugs
 First line
o Carbimazole
- Initial dose 30-40mg/day divided in 2-3 doses
- Maximum dose 60mg/day
- Maintenance dose : variable but commonly 5-15mg/day
- Titrated down the dose based on thyroid function tests:
 In the initial few months based on Free T4 levels and T3
 After the first few months follow up is based on TSH
 Second line /alternative
o Propylthiouracil (PTU)
- PTU is the first line in pregnant women
- Initial dose: 300 - 400mg/day in 3 divided doses
- Maximum dose 900mg/day
- Maintenance dose: Variable but commonly 100-200mg/day

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- Agranulocytosis is a rare but serious adverse effect of PTU. It should be

suspected if patients develop fever, sore throat or other features of infection
- Hepatotoxicity is another serious adverse effect of PTU

 Duration of treatment with anti-thyroid drugs

o Depends on the specific cause of the hyperthyroidism
- In Grave‘s disease: hyperthyroidism generally resolves in 1.5 - 2 years;
hence, if euthyroid state is achieved the anti-thyroid drug needs to be discontinued in 15
to 2 years.
- In toxic multinodular goiter or toxic adenoma: treatment should continue
until thyroidectomy or radioiodine therapy is done

2. Adjunct pharmacologic treatment

o Beta blockers: for symptom control until euthyroid state is achieved.
- Propranolol, 20-40mg, PO every 8-12 hours
OR
- Atenolol 25-100mg, PO, daily
OR
- Metoprolol 25-100mg, PO, daily or in two divided doses

Further reading
1. Douglas S. Ross, Henry B. Burch, David S. Cooper, M. Carol Greenlee et al. 2016 American
Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and
Other Causes of Thyrotoxicosis. THYROID Volume 26, Number 10, 2016. DOI:
10.1089/thy.2016.0229
2. Igor Kravets. Hyperthyroidism: Diagnosis and Treatment. American Family Physician.
2016;93(5):363-370. www.aafp.org/afp.
3. Gabriella Bathgate. New diagnosis of hyperthyroidism in primary care.
BMJ 2018;362:k2880 doi: 10.1136/bmj.k2880.

3.3 Hypothyroidism
Brief description
 The body requires thyroid hormones for normal metabolism and growth.
 Hypothyroidism is a condition in which there is a reduction in thyroid hormone production.
 In adults, it may be the cause of a slow metabolic rate, systemic problems and dementia.
 The most common reason is decreased production by thyroid glands ( called primary
hypothyroidism), rarely it could be caused by pituitary abnormalities ( secondary)

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 Antibody-related thyroid gland destruction, surgical removal of the thyroid, pituitary lesions
or surgery, congenital, severe iodine deficiency are the major causes.
 Myxedema coma describes the most severe state of hypothyroidism and is a medical
emergency.

Clinical features
Symptoms
 Patients could remain asymptomatic for several years or they might not recognize the
symptoms themselves.
 Intolerance to cold environments, constipation, weight gain, hair loss, dry skin
 Hoarse voice, lethargy, memory loss, depressed reflexes, dementia
 Abnormal menstrual periods and sub-fertility (in adult females)

Signs
 Puffy face, pallor, slow pulse (usually <60 per minute)
 Goiter may be present

Investigations and diagnosis

Diagnosis
 The diagnosis of hypothyroidism is usually delayed due to lack of recognition.
 A very high index of suspicion should be maintained in any adult woman who presented with
fatigue or non-specific symptoms.
 TSH is the best screening test
o TSH >20 micro unit/ml : highly suggestive primary hypothyroidism
o Normal TSH: excludes primary hypothyroidism
o Mildly elevated TSH (<20microunits/ml): needs freeT4 determination
o Mildly elevated TSH with normal free T4: subclinical hypothyroidism
Investigations
 TSH
 Free T4

Treatment
Objectives of treatment
 Correct level of thyroid hormones gradually
 Improve symptoms
 Prevent complications

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Non Pharmacologic treatment

 None

Pharmacologic treatment
 Levothyroxine
o Starting dose
- Young patients with no cardiovascular disease 100mcg/day
- Elderly patients with no obvious cardiac disease 50mcg/day
- Patients with established cardiac disease 25-50mcg/day
o Dose adjustment
- Dose adjustment should be made after at least 2-3 months of therapy
- Dose increments by 25-50mcg/day in 2- 3months
- Achieving TSH is the target of treatments
- After normalization of TSH, annual follow up of TSH suffices

Further reading
1. Onyebuchi Okosieme, Jackie Gilbert, Prakash Abraham, Kristien Boelaer et al. Management
of primary hypothyroidism: statement by the British Thyroid Association Executive
Committee. Clinical Endocrinology (2015), 0, 1–10.doi: 10.1111/cen.12824.
2. Birte Nygaard. Primary Hypothyroidism. American Family Physician; March 15, 2015,
Volume 91, Number 6. www.aafp.org/afp
3. Michelle So, Richard J MacIsaac, Mathis Grossmann. Hypothyroidism: Investigation and
management Australian Family Physician; Vol. 41, no. 8, August 2012.

4. Adrenal disorders
4.1 Adrenal Insufficiency
Brief description
 Adrenal insufficiency is a clinical condition where the amount of cortisol is insufficient to
meet the body's needs.
 It results in fluid, electrolyte imbalance and hypoglycemia.
 It may also result in acute circulatory collapse (shock), in a state commonly referred to as
adrenal crisis. Adrenal crisis is a medical emergency.
 Adrenal insufficiency could result from pathologies of the adrenal gland itself (called
primary) or the pituitary gland (secondary).
 Relative adrenal insufficiency is very common in critical ill patients
 Common causes of adrenal insufficiency

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o Infectious : Tuberculosis, HIV, Meningococcemia

o Autoimmune destruction of the adrenal gland (Addison's disease)
o Sudden cessation of corticosteroid therapy after prolonged use
o Pituitary failure from severe postpartum hemorrhage
o Pituitary surgery or tumors
o Stress (e.g. infection, severe trauma, surgery, and dental procedures) are major
precipitants of adrenal crisis.

Clinical features
Symptoms
 Easily fatigued
 Vague abdominal complaints/abdominal pain
 Nausea, vomiting, diarrhea, collapse, dehydration, craving for salt

Signs
 Low blood pressure (postural drop in blood pressure)
 Darkening of oral mucosa, gums, skin, palms and soles in some patients

Investigations and diagnosis

Diagnosis
 The diagnosis of adrenal insufficiency is usually delayed and patients suffer from delayed
diagnosis
 A high index of clinical suspicion is the most important element in the diagnosis.
 Early morning (8-9AM) serum cortisol <3mcg/dl is strongly indicative and >18mcg/dl
excludes the diagnosis.
 Confirmation of adrenal insufficiency needs dynamic testing: refer patients to a hospital
where there is endocrine service.

Investigations

 Basal( morning) serum cortisol

 Serum electrolytes: sodium and potassium
 Blood sugar
 CXR, Abdominal ultrasound: to assess the possible cause
 HIV screening
 In adrenal crisis: CBC, ESR, Cultures

Treatment

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Objectives of treatment
 Correct the fluid and electrolyte imbalance
 Replace corticosteroids
 Identify cause and treat any precipitating factor

Non pharmacologic treatment

 Encourage fluid and salt intake

Pharmacologic treatment
I. Acute therapy: do not wait for confirmation, start treatment based on clinical suspicion
o Intravenous fluid replacement
- DNS( 0.9% Sodium Chloride I with5% dextrose ),1000ml, 4-6 hourly
o Hydrocortisone
- 200 mg stat, followed by 50-100 mg, IV, 6 hourly.
- If there is a plan to take sample for serum cortisol, give dexamethasone 4mg
IV every 12hr.
o Do not rush to change the intravenous hydrocortisone to oral maintenance therapy.
o Start maintenance oral therapy when the patient is stable enough to be discharged.

II. Adjunct treatment

o Treat infection, if present or suspected, with appropriate medication.

III. Maintenance therapy

o Glucocorticosteroids: If available oral hydrocortisone is preferred.
- Hydrocortisone (tablet), PO, 15 -20mg/day in two to three divided doses.
OR
- Prednisolone 5mg , PO, on the morning and 2.5mg in the evening (or 5mg in
the morning alone)
OR
- Dexamethasone 0.5mg, PO, once in the morning
o Additional Mineralocorticoid
- Fludrocortisone 0.1mg/day. If on hydrocortisone reduce the dose to
0.05mg/day.
o Sick day glucocorticosteroids dosing
- Patients SHOULD NOT STOP treatment if they become ill, rather they
should increase the doses.
- For minor illness such upper respiratory tract infections and fever: Triple the
dose for three days (3x 3 rule).
- For emotional stress double the dose for three days.
- If there is vomiting : need intravenous hydrocortisone

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- For surgery and labor: give intravenous hydrocortisone preoperatively and

until the patient takes oral dose
 For minor surgery: 25-50mg IV hydrocortisone
 For major sugary: 100-150mg hydrocortisone/day in two to three
divided doses.

Referral
 Ambulatory patients with suspected adrenal insufficiency should be referred for specialist
evaluation, diagnosis and management.
 Acutely sick patients who are suspected to have adrenal insufficiency should be started
treatment without any delay.

Further reading
1. Evangelia Charmandari, Nicolas C Nicolaides, George P Chrousos. Adrenal insufficiency.
Lancet 2014; 383: 2152–67. http://dx.doi.org/10.1016/S0140-6736(13)61684-0.
www.thelancet.com.
2. Stefan R. Bornstein, Bruno Allolio, Wiebke Arlt, Andreas Barthel et al. Diagnosis and
Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice
Guideline. J Clin Endocrinol Metab, February 2016, 101(2):364–389. doi: 10.1210/jc.2015-
1710. press.endocrine.org/journal/jcem.
4.2 Cushing's syndrome
Brief description
 Cushing‘s syndrome is a clinical syndrome which results from high levels. of cortisol in the
blood and is associated with various changes in the body.
 It results in unexplained and rapid weight gain resulting in the development of obesity,
hypertension, diabetes and osteoporosis.
 The major causes are pituitary tumor/adenoma, adrenal tumor or prolonged and excessive
intake corticosteroids.

Clinical features
Symptoms
 Symptoms could be subtle as they develop very slowly or asymptomatic
 Weight gain
 Change in body habitus and shape: obesity, facial fullness
 Excessive facial hair
 Easy fatigability
 Easy bruising of the skin
 Menstrual irregularity

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 Labile mood

Signs
 High blood pressure
 Truncal obesity
 Prominent supraclavicular fat pad, rounded or moon'
 Striae: Wide (>1cm) and purplish or red
 Hirsutism
 Proximal muscle weakness
Proximal myopathy, wide purple/red striae, and easy bruising are highly predictive of
crushing‘s syndrome

Investigations and diagnosis

Diagnosis
 The diagnosis of Cushing‘s syndrome starts with high index of clinical suspicion; however,
confirmation requires biochemical tests.
 The first step in the diagnosis is to exclude exogenous steroid use (oral, IM, IV)
 Whom to screen with biochemical tests?
o Those with clinical features highly predictive of Cushing‘s syndrome
o Osteoporosis or hypertension in young adults
o Incidental adrenal mass
 The biochemical testing requires the following three steps
1. Confirming high cortisol
2. Determine if the high cortisol is ACTH-dependent or ACTH-independent
3. Determine the source of ACTH ( if it is ACTH-dependent)
 Patients with suspected Cushing‘s syndrome should be referred either directly or after doing
screening test

Investigations
 Screening biochemical test options
1. 1mg overnight dexamethasone suppression test
- Give 1 mg of dexamethasone at 11 PM to 12 AM (midnight), and
measurement of serum cortisol at 8 AM the next morning.
- A morning cortisol level above 1.8 mcg/dl (50nmol/l) is suggestive of
Cushing‘s syndrome.
2. 24 hour urine free cortisol: Level 3-4 times the upper limit of normal is highly
suggestive
3. Late evening(11 PM) salivary cortisol

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 Other supportive investigations

o Blood sugar, lipid profile
o Serum electrolytes
 Confirmatory tests should only be ordered and interpret by specialist.
 Imaging should not be ordered without having biochemical confirmation.

Treatment
Objectives of treatment
 Normalize plasma level of cortisol
 Correct metabolic and electrolyte abnormalities
 Correct blood pressure

Non pharmacologic treatment

 Surgery: the main stay of treatment of Cushing‘s syndrome is surgery (pituitary or adrenal
gland surgery depending on the cause)
 The surgery should be done in referral hospitals with experience in doing surgery.

Pharmacologic
 Manage hypertension and diabetes as per the standard treatment guidelines and refer patient
for definitive treatment.

Referral
 All patients suspected to have Cushing syndrome should be referred to a referral hospital
with endocrine, neurosurgical and endocrine surgery services.

Further reading

1. Lynnette K. Nieman . Recent Updates on the Diagnosis and Management of Cushing‘s

syndrome. Endocrinol Metab 2018;33:139-146. https://doi.org/10.3803/EnM.2018.33.2.139.
2. Lynnette K. Nieman, Beverly M. K. Biller, James W. Findling, John Newell-Price et al. The
diagnosis of Cushing‘s syndrome: An Endocrine Society Clinical Practice Guideline. J Clin
Endocrinol Metab, May 2008, 93(5):1526–1540.

5. Mineral and bone disorders

5.1 Vitamin D deficiency in adults
Brief description

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 Vitamin D is vital in skeletal health.

 Vitamin D‘s role in extra skeletal health (cancer, cardiovascular disease, infectious diseases
and immune dysregulation) is not clear.
 Overt vitamin D deficiency, characterized by hypocalcemia, hypophosphatemia or
osteomalacia is not common in adults but low level of vitamin D with no clinical features
associated with it (subclinical deficiency) appears to be very common.
 Adults with prolonged vitamin D deficiency, rarely develop osteomalacia. The optimal serum
vitamin D (25(OH) D) level needed for skeletal health is controversial.
 Experts agree a 25(OH) D less than 20ng/mL is likely to be suboptimal for skeletal health.
 Common causes of vitamin D deficiency include decreased intake or absorption, dark skin,
reduced sun exposure, drugs which increase vitamin d metabolism (e.g. Phenytoin).

Clinical features
 Asymptomatic: the majority of patients with vitamin D deficiency are asymptomatic
 Symptoms and signs related to osteomalacia: bone pain and tenderness, muscle weakness,
and pathological fracture.

Investigation and diagnosis

 Whom to screen for vitamin D deficiency?
o The current evidence is insufficient to assess the balance of benefits and harms of
screening for vitamin D deficiency in asymptomatic adults.
o It is advisable to screen older individuals, home-bound adults, obese patients,
patients with others features of mal
o Symptomatic individuals should definitely be screened: low serum calcium,
hyperphosphatemia, pathological fractures, suspected osteomalacia or
osteoporosis.
 Cut-off point for defining deficiency
o < 20ng/ml………deficiency
o 20-30 ng/ml……..insufficient for skeletal health
o >30ng/ml…..... …sufficient for skeletal health
 Other investigations

o Serum calcium , phosphorus, PTH, alkaline phosphatase level are important in

patients who are symptomatic

Treatment

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Objectives of treatment
 Prevent fractures in vulnerable individuals
 Prevent and correct skeletal symptoms

Non-pharmacologic treatment
 Dietary advice
 Adequate sun exposure for institutionalized or home-bound elderly
 Exercise

Pharmacologic treatment
1. Vitamin D levels <20ng/ml
o Vitamin D3 or D2, 50,000 IU once per week for 8 weeks
o Followed by maintenance therapy 800IU daily
o Additional calcium 1000mg/day
o Follow up 25(OH) D level: after three to four months of maintenance therapy
2. Vitamin D levels 20 - 30ng/ml
o Vitamin D3 or D2 800 IU/daily
o Additional calcium 800-100omg/day
o Follow up 25(OH) D level: after three to four months of maintenance therapy
3. Vitamin D levels >30ng/ml
o No active treatment
o In older individuals with a level between 20-30ng/ml vitamin D3 or D2 600-
800mg/day can be given.

Further reading

1. Stefan Pilz, Armin Zittermann, Christian Trummer, Verena Theiler-Schwetz et al. Vitamin D
testing and treatment: a narrative review of current evidence. Endocrine Connections
(2019) 8, R27–R43. https://ec.bioscientifica.com. https://doi.org/10.1530/EC-18-0432.
2. Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an Endocrine Society
Clinical Practice Guideline. J Clin Endocrinol Metab, July 2011, 96(7):1911–1930
jcem.endojournals.org.

5.2 Osteoporosis
Brief description
 Osteoporosis literally means porous bone.
 It is a skeletal disorder characterized by low bone mass and bone architecture deterioration
leading to bone fragility and increased risk of fracture.

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 The three major types of osteoporosis

1. Postmenopausal (type I)
2. Involutional (type II) : in both old men and women older due to subtle
increase in both resorption
3. Secondary (type III) : due to other diseases or drugs
 The major risk factors for osteoporosis are older age, early menopause, excessive alcohol
use, excessive caffeine intake, tobacco use, low physical activity level, low body weight, low
vitamin D or calcium intake, history of falls or fractures, family history of osteoporotic
fractures.
 Major causes of secondary osteoporosis
o Cancer: Multiple myeloma, bone metastases
o Inactivity or immobilization
o Chronic kidney disease
o Endocrine disorders: Cushing‘s syndrome, hyperthyroidism
o Chronic inflammatory diseases : Rheumatoid arthritis, SLE, IBD
o Medication: long term use of steroids, anticonvulsants, loop diuretics, PPI
o Malnutrition

Clinical features
Symptoms
 Patients with osteoporosis are asymptomatic until they develop fracture
 Symptoms related to fracture
o Pain
o Impaired mobility
o Respiratory difficulty
o Deformity
Signs
 The signs are related to the presence of fractures
o Loss of height
o Kyphosis
o Chest deformity,
o Rib-pelvis overlap
o Protuberant abdomen

Investigation and diagnosis

Diagnosis
 The diagnosis of osteoporosis can be made based on clinical or bone mineral density
measurement
1. Clinical osteoporosis diagnosis

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-
One or more fragility (low trauma fracture) of the spine, hip, femoral neck,
wrist that happens in high risk individuals.
2. Bone mineral density (BMD) based diagnosis: Dual energy x-ray
absorptiometry (DEXA) scan is used to measure bone density.
- T and Z scores are used to report DEXA scan findings.
- The T-score is a comparison of a person's bone density with that of a healthy
30-year-old of the same sex.
- The Z-score is a comparison of a person's bone density with that of an average
person of the same age and sex
 Diagnosis of Osteoporosis (lumbar Spinal or hip, 1/3 radial) : T-
score ≤ –2.5
 Diagnosis of severe/established osteoporosis: ≤ –2.5 + one or more
fragility fractures

Investigations
 BMD measurement: DEXA scan
 X-ray of the spine
o It is not diagnostic but can help in the diagnostic process
o X-ray related changes occur very late
o Increased lucency, cortical thinning, increased density of end plate, anterior
wedging and biconcavity of vertebrae are the major signs
 Vitamin D( 25(OH)D, calcium, phosphorus and PTH level

Treatment
Objectives of treatment
 Prevent fragility fracture
 Decrease/prevent disability

Non-pharmacologic treatment
 Prevention of falls
 Muscle strength and balance exercises
 Diet: adequate calorie, calcium and Vitamin D intake
 Decrease alcohol intake
 Decrease caffeine intake
 Quit smoking
 Sun exposure

Pharmacologic treatment
 First line: Bisphosphonates

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o Indications to start bisphosphonates

- The presence one or more fragility fracture (commonly hip or spine)
- DEXA scan diagnosis T-score ≤ –2.5
- Long term corticosteroid steroid use : prophylactic
o Check serum vitamin D and calcium level. Correct deficiencies before starting
bisphosphonates.
o Specific bisphosphonate doses for treatment of osteoporosis

Therapeutic dose
-
70mg PO per week
Alendronate
150mg PO per month
Ibandronate
5mg IV per year
Zolendronic acid

o Specific bisphosphonate doses for prevention of osteoporosis in long-term

corticosteroid users.

Prophylactic dose
o
o 35mg PO per week
Alendronate
150mg PO per month
Ibandronate
5mg IV every two years
Zoledronic acid
o Duration of therapy for osteoporosis: After 5-10 years of oral
bisphosphonates or 3-6 years of IV bisphosphonates, a 3- 5 year
discontinuation (holidays) should be given if there is no fracture in between.
o Contraindications: esophageal disorder, advanced CKD (eGFR <30ml/min)
o Common adverse effects: Esophageal ulcerations, perforations, bleeding,
sever muscular/bone /joint pains are
o Administration of oral bisphosphonates
- In empty stomach (in the morning after an overnight fasting)
- With a full glass of water
- Wait for at least 30 minutes before taking food, other beverages (other
than water) or other medications.
- Stay upright for at least 30 minutes before reclining (sleeping),
o IV Zoledronic acid: For patients who do not tolerate or can‘t adhere to the
dosing precautions of oral bisphosphonates.

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- Zoledronic acid administration:

 Give paracetamol 1000mg, 30 minutes before administration.
 Reconstitute powder with 5 ml of sterile water for injection
 Once the powder is fully dissolved, dilute further in 100 ml NS or
D5W.
 Give the infusion over at least 15 minutes.
 Additional pharmacologic therapy
o Vitamin D: 800IU/day

Further reading
1. American association of clinical endocrinologists/American college of endocrinology
clinical practice guidelines for the diagnosis and treatment of postmenopausal
osteoporosis— 2020 update. ENDOCRINE PRACTICE Vol 26 (Suppl 1) May 2020.
http://www.endocrinepractice.org. DOI: 10.4158/GL-2020-0524
2. Treatment of Low BMD and Osteoporosis to Prevent Fractures: Updated Guideline from
the ACP. Ann Intern Med. June 6, 2017;166(11):818-839.
http://annals.org/aim/article/2625385/treatmentlow-bone-density-osteoporosis-prevent-
fractures-menwomen-clinical.

CHAPTER 6: GASTROINTESTINAL TRACT AND

HEPATOBILIARY DISEASES
1. Dyspepsia and Peptic Ulcer Disease

Brief description
 Dyspepsia describes a wide and common clinical entity which presents in one of the three
ways:
1. Epigastric pain/burning (epigastric pain syndrome)
2. Postprandial fullness
3. Early satiety
 Dyspepsia is caused by a number of disorders. The most common cause is functional (non-
ulcer) dyspepsia followed by peptic ulcer disease.
 Gastro esophageal reflux disease (GERD), gastric cancer, medication induced dyspepsia,
biliary pain, chronic abdominal wall pain and pancreatitis are other possible causes.

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Clinical features
 Depending on the type of dyspeptic syndrome patients may present with predominant
epigastric burning sensation/pain/discomfort, postprandial discomfort and fullness or be
unable to finish a regular meal.
ALARM SIGNS( need to be further investigation for cancer)
o Advanced age (>55years)
o Previous gastric surgery
o Unintended weight loss
o Persistent vomiting
o Hematemesis
o Progressive dysphagia/Odynophagia
o Otherwise unexplained anemia
o Palpable abdominal mass
o Lymphadenopathy
o Jaundice

Investigations
 H. Pylori test: IgG serology or stool antigen or 13C-urea test
 Hemoglobin/hematocrit, stool for occult blood-when indicated
 Upper GI endoscopy

 H. Pylori test needs to be done for the following patients

o Long standing dyspepsia
o Younger than 55 year
o No alarm symptoms
o No use of Non-steroidal anti-inflammatory drugs
o No features of GERD (Gastro Esophageal Reflux Disease)
 ―Test and treat‖ for H. Pylori can be practiced in these group of individuals

Treatment
Objectives of treatment
 Decrease symptoms/improve quality of life
 Prevent development of complications

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Non pharmacologic
 Avoid offending foods/drinks

Pharmacologic
I. H. Pylori negative
 First line : Proton pump inhibitors
o Omeprazole, 20mg P.O., twice per day for 4-8 weeks
o Esomeprazole, 40mg P.O., daily for 4-8 weeks
o Pantoprazole, 40mg P.O., BID for 4-8 weeks
 Alternatives:H2 receptor blockers
o Cimetidine, 400mg P.O., BID for 4-8 weeks
o Ranitidine, 150mg P.O. BID for 4-8 weeks
o Famotidine, 20-40mg P.O. daily for 4-8 weeks
II. H. Pylori positive: H. pylori eradiaction therapy
 First line therapy
o All drugs for 7-14 days
- Amoxicillin, 1gm, P.O. BID
PLUS
- Clarithromycin, 500mg, P. O., BID
PLUS
- PPI
 Alternative (for penicillin allergic patients).
o This regimen has a higher failure rate.
o All drugs for 7-14 days
- Clarithromycin, 500mg P.O. BID
PLUS
- Metronidazole, 500mg, P.O. BID
PLUS
- PPI

2. Gastroesophageal reflux disease (GERD)

Brief description
 Gastroesophageal reflux refers to the return of stomach contents in to the esophagus.
 Some degree of brief reflux occurs physiologically; usually after a meal or during sleep.
 GERD refers to a pathologic reflux associated with symptoms and complications.
 GERD is a common in primary care practice. Due to its symptoms it can also be
misdiagnosed.

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 Based on the endoscopic appearance GERD is classified in to two types: Erosive and non-
erosive.
 Erosive GERD (Erosive esophagitis) is diagnosed when there are endoscopically visible
breaks in the esophageal mucosa while non-erosive GERD shows no visible mucosal injury
on endoscopy.
 GERD is associated with significant esophageal or extraesophageal complications.
o Esophageal complications
- Barrett's esophagus: a precancerous change in the esophageal mucosa(from
squamous epithelium to columnar epithelium)
- Esophageal stricture: which manifests with solid food dysphagia and intermittent
food impaction?
o Extraesophageal complications
- Triggering Asthma
- Laryngeal and pharyngeal reflux: which manifests with chronic cough, repetitive
throat cleaning, hoarseness of voice

Clinical manifestations

Symptoms
 The two major symptoms of GERD which are considered classic (typical) are heartburn
and regurgitation.
o Heartburn is a commonly described by patients as a burning sensation behind the
sternum (retrosternal area).
o Regurgitation is defined as back flow of gastric contests in to the mouth or
pharynx. Patients feel an acidic (sour) content coming to the mouth mixed with
small amounts of undigested food.

 Other symptoms
o Chest pain: GERD associated chest pain can mimic angina (pain from ischemic heart
disease)
o Triggering asthma attacks (wheezing)
o Hoarsens of voice
o Persistent cough
o Nausea
o Sensation of a lump in the throat (Globus sensation)
o Increased salivation (Water brash)

Diagnosis and investigations

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Diagnosis
 In patients with typical symptoms i.e. heartburn or regurgitation, the diagnosis of GERD can
be considered on clinical grounds without additional investigations, if there are no alarm
signs. In such cases empiric therapy should be started.

Investigations
 Upper GI (gastrointestinal) endoscopy
o Endoscopy is not necessary to make a diagnosis of GERD but it is indicated in
patients with alarm features to see evaluate for possible malignancy.
o The alarm features are weight loss, age above 60 years, iron deficiency anemia,
dysphagia, persistent vomiting or family history of cancer in parents or siblings.
o If GERD symptoms have been there for more than 5-10 years, endoscopy can be
considered to look for evidence of Barrett's esophagus.
Treatment
Objectives of treatment
 Relive symptoms
 Decrease the risk of complications such as Barrett‘s esophagus, esophageal stricture

Non-pharmacologic treatment
1. Life style modifications
 Weight loss in overweight and obsess patients.
 Avoiding meals 2 -3 hours before bed is also advisable.
 Head elevations to 15-20 cm during sleep.
 Dietary selection should not be forced or recommended universally unless patients identify
the specific food item as triggering factor. e.g. caffeine, , spicy foods, food with high fat
content, carbonated beverages, and chocolate)
 Other life style modifications are not supported by evidence.
2. Surgery
 Surgical intervention (usually fundoplication) in GERD patients is rarely indicated. Surgery
ma may be considered in the following circumstances:
o Large hiatal hernia causing the reflux symptoms
o Evidence of aspiration
o Esophagitis refractory to medical therapy
o Persistent symptoms documented as being caused by refractory GERD: after
checking compliance to PPI and optimizing PPI use.
Pharmacologic treatment
 First line: Proton-pump inhibitors (PPIs)
o No major difference in between the available PPIs

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- Omeprazole 40mg PO daily for 8 -12 weeks

OR
- Esomeprazole 40mg PO daily for 8-12 weeks
OR
- Pantoprazole 40mg PO daily for 8-12 weeks
 Stop therapy on symptom resolution to assess response
 After the first 8 -12 weeks, resume therapy as needed,
o Intermittent

OR
o On demand
 Alternatives: If PPIs are not available and the symptoms are mild Histamine-2 receptor
blockers (H2 blockers) can be considered as alternatives.
- Cimetidine 400mg BID for 8 weeks
OR
- Ranitidine 150mg BID for 8 weeks
OR
- Famotidine 20mg BID for 8 weeks

Referral
 Patients with alarm symptoms need to be referred without any delay after the initial
evaluation.
 Patients with persistent symptoms after 8 weeks of therapy should be referred for specialist
evaluation and follow up.

Further reading
1. Philip O. Katz Lauren B. Gerson, and Marcelo F. Vela. Guidelines for the Diagnosis and
Management of Gastroesophageal Reflux Disease. Am J Gastroenterol 2013; 108:308 – 328;
doi: 10.1038/ajg.2012.444
2. World Gastroenterology Organisation Global Guidelines: GERD, Global Perspective on
Gastroesophageal Reflux Disease. Update October 2015.
https://www.worldgastroenterology.org/guidelines/global-guidelines

3. Gastrointestinal Bleeding
3.1 Upper Gastrointestinal (GI) Bleeding
Brief description
 Upper GI bleeding refers to gastrointestinal blood loss originating from the gastrointestinal
tract is proximal to the ligament of Treitz at the duodenojejunal junction.

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 It can be overt or occult bleeding.

 Overt upper GI bleeding can manifest in the following ways:
o Hematemesis: vomiting of frank red blood or a ―coffee-grounds‖ material.
o Melena: Passage of black, tarry stool
o Hematochezia: passage of bright red or maroon (dark red) blood from the rectum.
Upper GI bleeding causes hematochezia rarely, when it is massive and very acute.
 Occult upper GI bleeding present with symptoms anemia such as lightheadedness, or a
positive fecal occult blood test on