ISLAMIC UNIVERSITY IN UGANDA
HABIB MEDICAL SCHOOL
FACULTY OF HEALTH SCIENCES
DEPARTMENT OF INTERNAL MEDICINE
MASAKA REGIONAL REFERRAL HOSPITAL
AHIMBISIBWE ALAPHAEL
215-083011-07652
YEAR 5
SEMESTER 1
Name:Nabakoza Elizabeth
Age: 60 years
Tribe: Muganda
Religion: catholic
Occupation; peasant famer
Marital status; married
Address: mwelu masaka
N.O.K:naluwa reste (Daughter)
Informant; patient
Referral status: self-referral
Nearest health center: Butenga health centre
Doa.24/02/2020
Doc: 26/02/2020
PRESENTING COMPLAINTS
Cough x 3/52
Fever x 2/52
HISTORY OF PRESENTING COMPLAINTS
Patient was relatively well till 3 weeks prior to hospital admission when she
gradually developed a non-productive cough that progressively became severe
that was aggravated by lying flat in bed and required use of approximately 2
pillows to sleep, This was associated with palpitation even at rest, easy
fatigability when walking or waking up from the bed, mild chest pain and
paroxysmal nocturnal dyspnea, she however reported no history of lower limb
swelling, she also reported a history of mild weight loss and no history of
excessive night sweats or contact with a person with chronic cough.
she reported to have developed flue like symptoms that progressed to nasal
congestion with large volumes of clear mucoid nasal discharge, she however
reported no history of nose bleeding, no discharge from the ears ,no hoarseness
of the voice or impaired sense of smell.
2 weeks prior to this hospital admission she suddenly developed a high-grade
fever, slightly relieved by paracetamol with no aggravating factors, this was
associated with chills and rigors. She also reported a history of reduced ability
to hear, however she reported no speech or visual problems, she reported no
history of loss of consciousness, no headache, no history of convulsions, no
numbness or tingling sensations of the limbs.
REVIEW OF OTHER SYSTEMS
Genital urinary system
She reported mild pain on urination to small volume of straw colored urine,
dribbling and intermittent however reported no urine incontinence with no
history of discharge.
Gastrointestinal system.
She reported poor appetite however reported no history of abdominal pain,
abdominal distension, no yellow discoloration, normal bowel habits.
Musculoskeletal system
No history of muscle pain or swelling and no joint pain, swelling or stiffness, or
any form of deformity.
PAST MEDICAL HISTORY
Reported several hospital admissions presenting with similar symptoms of
which the previous hospital admission presented with high grade fevers and
cough, was managed from a clinic with unknown medication.
Reported no history of known chronic diseases such as hypertension, TB and
no history any other chronic use of medications.
No history of known allergies to medications or foods.
She’s HIV negative last tested several years ago.
PAST SURGICAL HISTORY
She reported history of blood transfusion 1 year ago with no transfusion
reaction, no history of surgeries, no history of major trauma like burns,
fracture and no history of accidents.
FAMILY HISTORY
She is 2nd in the family of 6 siblings, she doesn’t know much about her
siblings, both parents died due to unknown cause, she’s a mother to 10
children,4 alive and well,6 died due to unknown cause, the husband is a
known hypertensive patient for unknown duration on treatment
She however reported no anyother known history of chronic illness such as
hypertension or familial illnesses such as asthma.
SOCIAL HISTORY
She is married a peasant farmer, she occasionally takes alcohol for 7 years,
taking approximately 2 bottles in a month with no history of cigarette smoking,
the husband is also a peasant famer occasionally takes alcohol for 20 years,
taking approximately 4litres of wine in a month with, no history smoking
cigarette and is their social and economic supporter. They stay in their 5
roomed, well ventilated permanent house, obtain their water for domestic use
from a tap and drink boiled water, they sleep under treated mosquito net.
SUMMARY.
N.E,60-year-old female from mwelu masaka who presented with a 3week
history of sever non productive cough aggravated by lying flat in bed associated
with easy fatigability, palpitations, paroxysmal nocturnal dyspnea with flue like
symptoms. Also reported a 3-day history of high-grade fevers relieved by
paracetamol associated with chills and rigors with no history of convulsions
and several hospital admissions due recurring chest infections.
DIFFERENTIAL DIAGNOSIS
Left sided heart failure in view of dry cough, history of recurring chest
infections, palpitations, paroxysmal nocturnal dyspnea.
Pneumonia in view of cough, history of fever, mild chest pain flue like
symptoms.
Urinary tract infection; pain of micturition.
PHYSICAL EXAMINATION
GENERAL EXAMINATION
I examined a middle-aged female with bobbing motion of the head, sited in
bed, well-nourished, mild wasted, alert and well kempt in fair general
condition, with no signs of respiratory distress such as nasal flaring or use of
respiratory accessory muscles, with a pink cannula in situ on her right arm.
Her hair was well distributed and was black in color of normal texture not
easily pluck able.
She had no Jaundice with mild pallor of conjunctiva, tongue, palms and sole of
the feet, she had no angular stomatitis, she had no oral sores or ulcerations
and her tongue was of normal size and normal tongue papillae distribution
with dental carries, no central cyanosis with poor oral hygiene, she had 2
missing molar teeth, no lymphadenopathy and she was afebrile with axillary
temperature of 37.4oC.
There was a Quincke’s sign, no finger clubbing, leukonychia, kolionychia, no
splinter hemorrhages. She had no lower limb swelling.
CARDIOVASCULAR SYSTEM
Blood pressures of 108/76 mmhg, Pulse was 90bpm, regular full volume, it
was synchronous with radial pulse of the contralateral arm and no radio
femoral delay, with warm extremities.
She had visible pulsation a neck veins, her jugular venous pressure was not
raised, normal active precordium, the apex beat was in the 5 th intercostal
space, midclavicular axillary line on the left with the trachea centrally located,
no thrills, and no heave.
Auscultation
SI and SII heart sounds were heard with, no added sounds or murmurs, no
basal crepitations.
RESPIRATORY SYSTEM
Inspection
Respiratory rate was 23 breath per minute, not in respiratory distress, her
chest was symmetrical of normal shape, size, no obvious chest wall deformities
seen or any scars or lesions.
Palpation
There was equal chest wall movement and expansion with normal vocal
fremitus. No areas of tenderness, trachea was centrally located with apex beat
in the left 5th intercostal space midclavicular line
Percussion
There was normal resonant percussion note in all lung field
Auscultation
There was bilateral equal air entry, vesicular breath sound present with
bilateral coarse crackles.
ABDOMINAL EXAMINATION
Inspection
Abdomen was Scaphoid, symmetrical, moving with respiration, umbilicus was
inverted. No areas of hyperpigmentation or hypopigmentation of skin, with no
visible collaterals or scars or lesions, no scratch marks.
Palpation
Abdomen was soft, non-tender, spleen was palpably enlarged non tender,
smooth surface with 4cm below the subcoastal margins, liver and kidneys
were not palpably enlarged. No fluid thrill or shifting dullness.
Auscultation
There were low pitch bowel sounds with a frequency of 4 in one minute, no
renal, aortic bruits.
CENTRAL NERVOUS SYSTEM
Patient was alert with a GCS of 15/15, oriented in place, person and time with
no signs of meningeal irritation such as neck stiffness or photophobia with a
negative kerning’s sign.
Cranial nerves;
CNI; I could not asses since I had no familiar scents
CNII; pupils were equal and reactive to light
CNIII, IV, VI; she could follow a pen in a H and x patterns
CNVII-her face was symmetrical on smiling and frowning.
CNIX, X: Her uvula was centrally located
CNXI: She would shrug her shoulders and move her neck against resistance.
CNXII; her tongue was of equal size with no fasciculations.
Motor exam
Right upper Left upper Right lower Left lower
limb limb limb limb
Muscle bulk Normal Normal Normal Normal
Muscle tone Normal Normal Normal Normal
Reflexes Normal Normal Normal Normal
Power 4 4 4 4
Sensory exam
Her senses of pain, touch and proprioception were intact in both the upper
limbs and the lower limbs.
Impression
Urinary tract infection in view of pain on micturition.
Aortic regurgitation in view of Corrigan sign, Quincke’s sign.
Heart failure secondary to aortic regurgitation
Pneumonia in view of cough, bilateral course crackles.
FOLLOW UP AND MANAGEMENT.
Plan
Admit to ward (female ward)
IV fluids N/S; 1.5 liters start
Soluble insulin 20IU
10IU-IM
10IU-IV
Monitor RBS according to the sliding scale.
Tabs. Lasix 80 mg b.d x 2/52
Tabs. Nifedipine 20mg b.d x 2/52
15/02/2020
Reviewed a 4o year old female known diabetic patient being managed for Heart
failure secondary to anemia today still complains of non-productive cough,
generalized body swelling and mild epigastric pain.
On examination
On examination
Middle aged female, in a fair general condition, sleeping in bed, no jaundice,
and moderate pallor, afebrile with axillary temperature of 36.2 Co
Cardiovascular system
Bp; 114/70mmhg, Pulse; 86bpm regular, JVP; not raised, Precordium; normal
active, Heart sounds SI, SII are heard and normal with no added sounds, with
the Spo2 of 93%.
Respiratory system
The respiratory rate was 22 bpm which was high, signs of respiratory distress
with nasal flaring, intercostal. Bilateral equal air entry, bronchial vesicular
sound were present, bilateral wheeze, bilateral coarse crackles.
Per abdomen
Grossly distended, soft, moving with respiration, mild tenderness in the LUQ,
the liver and the spleen are palpably enlarged organs. Bowel sounds were
present 6/minute, low pitched, no renal bruits or aortic bruits.
Central nervous system
GCS: alert, conscious, oriented (PPT).
Impression
- Heart failure secondary to anemia.
Plan
Continue with IV medications of Lasix, ceftriaxone, ampiclox
Continue with syrup lactulose
Tabs. Captopril 12.5mg t.d.s x 1/12
Tabs. Spironolactone 25mg o.d x 1/12
Tabs. FEFO I o.d x 2/52
Mixtard PB; 15IU, PS; 8IU
18/02/2020
Reviewed a 4o year old female known diabetic patient being managed for Heart
failure secondary to anemia today still complains of non-productive cough,
generalized body swelling and mild epigastric pain.
On examination
On examination
Middle aged female, in a fair general condition, sleeping in bed afebrile, no
jaundice, and moderate pallor, afebrile with axillary temperature of 35.7 Co
Cardiovascular system
Bp; 110/70mmhg, Pulse; 76bpm regular, JVP; not raised, Precordium; normal
active, Heart sounds SI, SII are heard and normal with no added sounds, with
the Spo2 of 94%.
Respiratory system
The respiratory rate was 22 bpm which was high, signs of respiratory distress
with nasal flaring, intercostal. Bilateral equal air entry, bronchial vesicular
sound were present, bilateral wheeze, bilateral coarse crackles.
Per abdomen
Grossly distended, soft, moving with respiration, mild tenderness in the LUQ,
the liver and the spleen are palpably enlarged organs. Bowel sounds were
present 6/minute, low pitched, no renal bruits or aortic bruits.
Central nervous system
GCS: alert, conscious, oriented (PPT).
Impression
Heart failure secondary to anemia.
Chronic kidney disease
Plan
Continue with IV medications of Lasix, ceftriaxone, ampiclox
Continue with syrup lactulose, Captopril, Spironolactone.
Mixtard PB; 15IU, PS; 8IU(6.2mmol/l)
20/02/2020
Reviewed a 4o year old female known diabetic patient being managed for Heart
failure secondary to anemia today still complains of non-productive cough,
generalized body swelling and mild epigastric pain.
On examination
Middle aged female, in a fair general condition, sleeping in bed afebrile, no
jaundice, and moderate pallor, afebrile with axillary temperature of 36.4 Co
Cardiovascular system
Bp; 120/70mmhg, Pulse; 91bpm regular, JVP; not raised, Precordium; normal
active, Heart sounds SI, SII are heard and normal with no added sounds, with
the Spo2 of 93%.
Respiratory system
The respiratory rate was 16 bpm which was high, signs of respiratory distress
with nasal flaring, intercostal. Bilateral equal air entry, bronchial vesicular
sound were present, bilateral wheeze, bilateral coarse crackles.
Per abdomen
Grossly distended, soft, moving with respiration, mild tenderness in the LUQ,
the liver and the spleen are palpably enlarged organs. Bowel sounds were
present 6/minute, low pitched, no renal bruits or aortic bruits.
Central nervous system
GCS: alert, conscious, oriented (PPT).
Impression
Heart failure secondary to anemia.
Chronic kidney disease
Diabetic nephropathy
Plan
Do Urinalysis
Do renal scan
Do reticulocyte count
Caps .Flucamox 500mg t.d.s x 5/7
Mixtard PB; 10 IU, PS; 5 IU (RBS: 4.6mmol/l)
22/02/2020
Reviewed a 4o year old female known diabetic patient being managed for Heart
failure secondary to anemia today still complains of non-productive cough,
generalized body swelling and mild epigastric pain.
On examination
On examination
Middle aged female, in a fair general condition, sleeping in bed afebrile, no
jaundice, and moderate pallor, afebrile with axillary temperature of 35.7 Co
Cardiovascular system
Bp; 120/70mmhg, Pulse; 91bpm regular, JVP; not raised, Precordium; normal
active, Heart sounds SI, SII are heard and normal with no added sounds, with
the Spo2 of 96%.
Respiratory system
The respiratory rate was 16 bpm which was high, signs of respiratory distress
with nasal flaring, intercostal. Bilateral equal air entry, bronchial vesicular
sound were present, bilateral wheeze, bilateral coarse crackles.
Per abdomen
Grossly distended, soft, moving with respiration, mild tenderness in the LUQ,
the liver and the spleen are palpably enlarged organs. Bowel sounds were
present 6/minute, low pitched, no renal bruits or aortic bruits.
Central nervous system
GCS: alert, conscious, oriented (PPT).
Impression
Heart failure secondary to anemia.
Chronic kidney disease
Diabetic nephropathy
Plan
Discharge the patient home on;
Caps .Flucamox 500mg t.d.s x 5/7
Tabs. Captopril 12.5mg t.d.s x 1/12
Tabs. Spironolactone 25mg o.d x 1/12
Tabs. FEFO I o.d x 2/52
Mixtard PB; 15IU, PS;8IU
PATIENT WITH AORTIC REGURGITATION
Definition;
Aortic regurgitations the diastolic flow of blood from the aorta into the left
ventricles and this is due to incompetence of the aortic valve or any
disturbance of the valvular apparatus such as the leaflets, annulus of the aorta
resulting into diastolic flow of blood into the left ventricle.
Cause
Aortic regurgitation is caused by disease of the valve leaflets or enlargement of
the aortic root. In the developing world, most common cause of AR is
rheumatic heart disease, in developed countries, AR is most often due to aortic
root dilation or a congenital bicuspid aortic valve.
Valvular disease;
congenital malformation (mostly bicuspid aortic valve)
infective endocarditis
nonvalvular disease;
idiopathic (systemic hypertension, suggesting that altered
elasticity and/or geometry of the aortic root may have been the cause of
valve incompetence)
Marfan syndrome or forme fruste.
In this patient the cause was not established however she resided in Uganda
which is among the developing countries with the possible cause of rheumatic
heart disease.
Epidemiology
Men>women, Rare in less than 50 years of age but the risk increases
progressively. This patient was a female and she was 60 years which was 10
years above the estimated age.
Pathophysiology
The inability of the aortic valve leaflets to remain closed or coapted during
diastole results in a portion of the left ventricular stroke volume leaking back
from the aorta into the left ventricle. The added volume of regurgitant blood
produces an increase in left ventricular end-diastolic volume and an elevation
in wall stress. The heart responds with compensatory myocardial hypertrophy.
The combination of hypertrophy and chamber enlargement raises the total
stroke volume. The net effect is that forward stroke volume and hence cardiac
output are initially maintained despite the regurgitant lesion. Although left
ventricular volume is increased, end-diastolic pressure remains normal due to
an increase in ventricular compliance. Thus, the heart initially adapts well to
chronic AR, functioning as a very efficient and compliant high output pump.
An additional factor that plays a role in left ventricular performance is vascular
adaptation. One study found that in some patients, total arterial elastance,
determined by measuring left ventricular pressure and left ventricular volumes
during different loading conditions, decreases to maximize left ventricular work
and maintain performance while in other patients elastance increases,
enhancing afterload excess and leading to a reduction in left ventricular work
and pump performance; this is most apparent in those with impaired left
ventricular contractility
Clinical features.
AR may remain asymptomatic for decades, even if there is progressive
ventricular dilatation, however, there is a large regurgitant volume, the patient
may complain of symptoms related to the increased mass of the enlarged left
ventricle. These include:
A sense of pounding and an uncomfortable awareness of the heartbeat,
pronounced when lying down or lying on the left side.
Atypical chest pain
Palpitations due to tachycardia or premature beats.
Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea,
paroxysmal nocturnal dyspnea, and eventual pulmonary edema) occur in
the presence of left ventricular dysfunction.
Angina pectoris. The presence of angina suggests either underlying coronary
artery disease or, if there is marked left ventricular hypertrophy,
subendocardial ischemia. Some patients also develop abdominal discomfort at
this time due to splanchnic ischemia.
In this patient she presented with a sense of pounding, palpitation ,mild chest
pain, dyspnea on exertion or rest, orthopnea, paroxysmal nocturnal dyspnea,
and eventual pulmonary edema.
Investigations.
Recommendations for the use of echocardiography in patients with
symptomatic and asymptomatic murmurs and for testing for the diagnosis and
initial evaluation of patients with AR.
Electrocardiogram (ECG); reflects the adaptive changes that occur in the left
ventricle as a result of the volume overload. Left ventricular hypertrophy
typically leads to an increase in the amplitude of the QRS complexes with
concurrent ST and T wave changes, indicative of underlying chronic ischemia.
There is often evidence of left atrial hypertrophy and the axis may be leftward.
Among asymptomatic or only mildly symptomatic patients with pure AR, the
presence or absence of repolarization abnormalities on the resting or exercise
ECG (ST segment depression) correlates with left ventricular size and function.
Chest radiograph; The routine chest radiograph shows cardiomegaly due to
the dilatation of the left ventricle, which enlarges in an inferior and leftward
direction. There is usually no calcification of the aortic valve and aortic root
unless there is associated aortic stenosis. The ascending aorta (and often the
aortic arch or knob) are typically markedly dilated.
Left atrial enlargement does not occur unless there is significant left
ventricular dysfunction. Thus, its presence in patients with mild to moderate
AR suggests associated mitral valve disease.
Echocardiogram; Echocardiography is part of the standard evaluation of
patients with AR and Characteristic echocardiographic findings include the
following:
The valve leaflets may be normal or abnormal, depending upon the
etiology of the AR. Abnormalities that may be seen include thickening,
vegetations, calcification, and prolapsed or flail leaflets
The aortic root is often dilated and there may be evidence of an
aneurysm (dissecting or saccular).
There is often high frequency, diastolic fluttering of the anterior leaflet of
the mitral valve which is due to the diastolic regurgitant jet of blood from
the aorta.
Doppler echocardiography (transthoracic or transesophageal) is the most
sensitive noninvasive technique for detecting the regurgitant jet
The left ventricular end-systolic and end-diastolic volumes are increased
in chronic AR. Wall motion appears to be increased in parallel with the
enhanced stroke volume. When left ventricular decompensation occurs,
systolic shortening is reduced and end-systolic volume increases.
echocardiography can determine the stage of the disease according to left
ventricular function, which in turn may determine the need for corrective
surgery.
Severity of AR; Echocardiography can determine the severity of the aortic
regurgitation. Severe chronic AR is considered to be present if one or more of
the following findings are present on echocardiography (or magnetic resonance
imaging):
A regurgitant fraction ≥50 percent
A vena contracta width >6 mm
A regurgitant volume ≥60 mL (which should be considered relative to
body size)
Other noninvasive tests;
Cardiac catheterization; The role of contrast angiography of the left ventricle
in the assessment of chronic AR is increasingly limited because of the use of
echocardiography. Nevertheless, angiography can permit assessment of the
following parameters, which allows determination of the stage of disease
according to left ventricular function:
Determination of the size and systolic function (ejection fraction) of the
left ventricle
Aortic root dimension and associated disorders (eg, dissection, sinus of
Valsalva aneurysm)
Aortic valve movement and the number of leaflets
A semiquantitative assessment of the severity of AR
The 2006 ACC/AHA guidelines recommended cardiac catheterization in only
indicated when noninvasive tests are inconclusive or provide discrepant results
from clinical findings. Cardiac catheterization should be performed with aortic
root angiography and measurement of left ventricular pressure to assess the
severity of the regurgitation, aortic root size, and left ventricular function.
MANAGEMENT.
ACUTE AORTIC REGURGITATION
Patients with acute severe AR may respond to intravenous diuretics
and vasodilators (such as sodium nitroprusside),
stabilization is usually short-lived and operation is indicated urgently.
Surgery is the treatment of choice and is usually necessary within 24 h of
diagnosis.
CHRONIC AORTIC REGURGITATION
Diuretics, vasodilators (ACE inhibitors, dihydropyridine
calcium channel blockers, or hydralazine) may be useful as well.
vasodilators extend the compensated phase of chronic severe AR before the
onset of symptoms or the development of LV dysfunction is more controversial
Systolic blood pressure should be controlled (goal <140 mmHg) in patients
with chronic AR
Cardiac arrhythmias and systemic infections are poorly tolerated in patients
with severe AR and must be treated promptly and vigorously.
Patients with syphilitic aortitis receive a full course of penicillin therapy
Beta blockers and the angiotensin receptor blocker losartan may be useful to
retard the rate of aortic root enlargement in young patients with Marfan’s
syndrome and aortic root dilation contraindication in severe AR with an
associated aortopathy.
In this patient was initiated of tabs.lasix 20 mg o.d for 1 month
,tabs.captopril 12.5mg o.d for also 1 month and she was initiated in the
hypertensive clinic for adequate follow up.
SURGICAL TREATMENT
patients with chronic severe AR usually do not become symptomatic until
after the development of myocardial dysfunction
when delayed too long (defined as >1 year from onset of symptoms or
LV dysfunction), surgical treatment often does not restore normal LV function.
clinical follow-up and noninvasive testing with echocardiography at
approximately 6- to 12-month intervals are necessary if operation is to be
undertaken at the optimal time
Operation can be deferred as long as the patient both
remains asymptomatic and retains normal LV function without
severe chamber dilation.
AVR is indicated for the treatment of severe AR in symptomatic patients
irrespective of LV function
Operation should be carried out in asymptomatic patients with severe AR and
progressive LV dysfunction defined by an LVEF <50%, an LV end systolic
dimension >50 mm, or an LV diastolic dimension >65 mm. Smaller dimensions
may be appropriate thresholds in individuals of smaller stature.
Patients with severe AR without indications for operation should be followed by
clinical and echocardiographic examination every 6–12 months.
In this patient was counselled about the surgical management however
she could not due to financial constrains and she was not investigated to
asses her status for surgery.
