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Acute Gastroenteritis

The document details the case of a 7-year-old boy named Sebastian who was admitted to the hospital with acute gastroenteritis, presenting symptoms such as cough, fever, vomiting, and diarrhea. It includes comprehensive medical history, physical examination findings, and management plans, highlighting the importance of hydration and monitoring for dehydration. The document also discusses the epidemiology, etiology, pathogenesis, risk factors, complications, and clinical manifestations of gastroenteritis in children.

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0% found this document useful (0 votes)
107 views44 pages

Acute Gastroenteritis

The document details the case of a 7-year-old boy named Sebastian who was admitted to the hospital with acute gastroenteritis, presenting symptoms such as cough, fever, vomiting, and diarrhea. It includes comprehensive medical history, physical examination findings, and management plans, highlighting the importance of hydration and monitoring for dehydration. The document also discusses the epidemiology, etiology, pathogenesis, risk factors, complications, and clinical manifestations of gastroenteritis in children.

Uploaded by

Afraz farooqui
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

ACUTE

GASTROENTERITIS
BY – SANGRAM LONDHE, KAMLESH CHOUDHARY
SOURCE OF INFO – FATHER

RELIABILITY – 60 %
GENERAL DATA

 Sebastian, Arnejo , 7-year-old, Male, born in


GCGMMC, Filipino, Roman Catholic resides in
Tagbilaran City , Bohol. Was admitted for the 2nd
time in Ramiro Community Hospital on Oct 8th,
2024.
CHIEF COMPLAINT

 COUGH,
FEVER, VOMITTING, LOOSE BOWEL
MOVEMENTS
HISTORY OF PRESENT ILLNESS
 4days PTA - Patient had an onset of cough, productive with
undocumented phlegm as he swallowed it every time. Meptin 5mcg/ml,
5ml was given once a day. (RD – 25mcg/day) Patient felt relief. Patient
was healthy in the interim
 18hrs PTA - Patient had onset of fever (Tmax - 38.4C) he was given
Paracetamol biogenic 250mg/5ml 6ml every 4hrs (RD – 5ml of
250mg/5ml 4 times a day). Patient felt relief.
 12hrs PTA - Patient had 1 episode of vomiting. Watery and milky
content with unrecalled quantity, 1 episode of loose bowel movements,
yellowish brown in color , non foul smelling, non mucoid. Unrecalled
quantity.
 On the time of cousult - Patient already had more than 10 episodes of
vomiting in the morning, consisting of watery and milky content and
unrecalled quantity. Associated with epigastric pain Ps 5/10. Thus,
prompt consult.
PRE-NATAL HISTORY

 Mother's age was 29 years old when she gave birth to the
patient, G2P2, had her first prenatal checking at 3 months
at a private clinic in Tagbilaran City, Bohol and continued to
have the follow-up check ups in the private clinic. She took
TT vaccine, Folic acid, MV, Ferrous Sulphate. Mother did
not have UTI, gestational hypertension, diabetes or any
illnesses during pregnancy. Patient's mother denies
smoking, drinking or use of illicit drug use. Patient had CS
in her first pregnancy.
NATAL HISTORY

 Patient was delivered full term at 39 2/7 weeks of


gestation by caesarean delivery attended by a
resident in GCGMMC due to repetitive
decelerations. The APGAR score of the patient are
unrecalled but patient had a pale body
appearance, good cry, good activity and
immediately after birth.
POST NATAL HISTORY

 The patient's birth weight was 2.9kg. Patients APGAR,


Ballard score, head circumference, chest circumference
and abdominal circumference were unrecalled. Essential
intrapartum and newborn care was done. Patient was again
kept with the mother for breastfeeding initiation and skin to
skin contact. Patient was administered BCG, Vit-k, Hep-B,
and eye prophylaxis
FEEDING HISTORY

 Patient was exclusively breast-feeding for 4 years and then


was shifted to solid.
 Patient only consumes chicken, rice, fish and sometimes
vegetables.
 Patient rarely eats junk food and soda.
IMMUNIZATION HISTORY

 Patient’s parent does not recall number of vaccinations and


the number of doses given to the patient but said he is up
to date as he has always visited the local health centre for
all the vaccinations
DEVELOPMENTAL HISTORY

 Patient’s parents don’t recall the exact months for


developmental milestones but remember a few
mentioned below.
 Making cooing sounds – 2months
 Walking with support – 10 months
 Walking without support – 11 months
 Ride a tricycle – 4 years
 Could do basic math – 6 years
PAST MEDICAL HISTORY

 Patient was admitted once in RCH for AGE (unrecalled


year). Patient did not have any surgeries, no allergies, no
maintenance medication and no recent travel history.
FAMILY HISTORY

 Patient's parents don't have any illnesses like


Hypertension, Diabetes Mellitus, Asthma, Cardiac problems
or Cancer history.
 History on Maternal side – Hypertension to grandfather,
(Diabetes mellitus, Breast cancer) to grandmother
 History on Paternal side – Hypertension to grandfather
PERSONAL AND SOCIAL HISTORY
 Patient is the 2nd child in the family. Birth Rank 2/2. Patient is in
Grade 2. Patient has an elder sister aged 10 years.
 Patient's father is 37 years old and is a government employee
graduated from USPF, Cebu
 Patient's mother is 36 years old and is also a government
employee graduating from Cebu Normal University , Cebu .
Patient’s family is financially stable.
 Patient's father is an occasional drinker, Patient's parent denied
smoking or any illicit drug use.
 No pets in the house.
ENVIRONMENTAL HISTORY

 Patient lives in a concrete house located in a semi crowded


area.
 They have water from a purified refilling station.
 Garbage is collected twice a week.
 Area around their house is clean and have endemic
disease dengue in their area.
REVIEW OF SYSTEMS
 Review of systems
 General:
 Awake, alert, conscious, not in respiratory distress

 Respiratory:
 Productive cough started 4 days ago.
 Improvement noted with increased fluid intake.
 No shortness of breath, but mild discomfort during deep breaths.
 No wheezing or audible stridor.
 No nasal congestion or runny nose.

 ENT (Ear, Nose, Throat):


 No sore throat
 No ear pain or discharge.
 No significant voice changes or hoarseness.
 Cardiovascular:
 No chest pain or palpitations.
 No swelling in the extremities.

 Gastrointestinal:
 Vomiting x 10 episodes consisting of pre ingested liquid.
 Loose bowel movements x 1
 Normal appetite, though slightly decreased due to fatigue.

 Musculoskeletal:
 No generalized body aches.
 No joint pain or swelling.

 Neurological:
 No headaches.
 No confusion, dizziness, or seizures.

 Skin:
 No rash, hives, or other skin changes noted.
 Urinary:
 No pain or discomfort during urination.
 No changes in urinary frequency or color.
PHYSICAL EXAMINATION

VITAL SIGNS ANTROPOMETRICS


HR- 131 bpm HEIGHT – 131cm
O2 – 97% WEIGHT – 27kg
BP – 110/70
T – 36.2 C BMI – 15.7 - underweight
RR – 24cpm
 Skin: (-) rash, (-) pallor, (-) jaundice, warm to touch, Poor skin turgor and mobility, (-)
lesions/masses
 HEENT: Normal head size and symmetry, (-) swelling, (-) erythema, pupil are of normal
size and reactive to light, (-) eye discharge , acentric sclera, pink palpable conjunctive ,
(-) nasal discharge, (-) alar flaring, , normal ear size, (-) lesions, Symmetric nose, (-)
masses or lesions, (-) nasal discharge, moist lips and oral mucosa, (-) vein distention, (-)
lymphadenopathy.
 C/L: , Symmetric chest, (-) chest retraction, equal chest expansion, (-)tenderness,

(+)resonance in both lung fields, clear breath sound,


 CVS: (-)cyanosis, (-)tenderness regular rhythm, Distinct heart sounds, no murmurs
 Abd: (-) lesions or masses,(-)hernia ,hyperactive bowel sounds,(+) tenderness in
epigastric region on light palpation, , Soft , flabby
 Muscoskeleton: Full range of motion in all joints, normal gait and posture, (-) asymmetry,
normal muscle tone and strength. (-)edema, strong peripheral pulses, CRT<2sec
 Neuro : Alert, oriented, lethargic, normal coordination and balance for age, appropriate
fine and motor skills, good interaction with parents and health care providers.
 Neurologic: alert, oriented to place, person and time
 CN I - Not assessed
 CN II- Pupils are equally reactive to light and accommodation
 CN III, IV, VI- Intact extraocular movements
 CN V- not assessed
 CN VII- No facial asymmetry
 CN VIII- whisper test positive
 CN IX, X- able to swallow, (-) Gag Reflex
 CN XI- Able to shrug shoulder
 CN XII- tongue midline
 Muscle strength- 5/5 on both the upper and lower extremities
ADMITTING DIAGNOSIS

Acute gastroenteritis with mod


dehydration
BASIS

 Fever,
 Loose bowel movements,
 Epigastric pain,
 Vomiting.
1)Peptic ulcer 2) Typhoid fever 3) Appendicitis

Rule in - Rule in - Rule in -


Abdominal pain Dairrhea Abdominal pain
Vomiting Vomiting Vomiting
Abdominal pain
Rule out
Hematemesis Rule out Rule out
Weight loss Rash ( rose spots) (-) Psoas sign
Headache
Constipation
MANAGEMENT

 Management -
 Maintenance fluid - Isotonic - 2025ml over 4hrs (75ml/kg)
 PCM 250mg/5 ml - 10ml every feveric episode.
 (RD - 15mg/kg)
 Zinc 20mg/day for 14 days
 Oral ORS intake ( mild dehydration - 50ml/kg = 1350 in 4hrs )
 50ml ORS per vomiting episode.
 Monitor for lethargy and signs of severe dehydration
CASE DISCUSSION

ACUTE GASTROENTERITIS
ACUTE GASTROENTERITIS

 The term gastroenteritis denotes infections of the gastrointestinal


tract caused by bacterial, viral, or parasitic pathogens.

 The most common manifestations are diarrhea and vomiting, which


can also be associated with systemic features such as abdominal pain
and fever.

 The term gastroenteritis captures the bulk of infectious cases of


diarrhea.
EPIDEMIOLOGY

 Diarrheal disorders in childhood account for a large proportion (9%) of


childhood deaths, with an estimated 0.71 million deaths per year
globally, making it the second most common cause of child deaths
worldwide.
 Global mortality may be declining rapidly, but the overall incidence of
diarrhea has only declined from 3.4 to approximately 2.9 episodes per
child-year in the past 2 decades
 The decline in diarrheal mortality, despite the lack of significant
changes in incidence, is the result of preventive rotavirus vaccination
and improved case management of diarrhea, as well as improved
nutrition of infants and children.
ETIOLOGY

 Gastroenteritis is the result of infection acquired through the fecal–


oral route or by ingestion of contaminated food or water.
 Enteropathogens that are infectious in a small inoculum (Shigella,
enterohemorrhagic Escherichia coli, Campylobacter jejuni,
noroviruses, rotavirus, Giardia lamblia, Cryptosporidium parvum, Ent
amoeba histolytica)
 Rotavirus and the noroviruses (small round viruses such as Norwalk-
like virus and caliciviruses) are the most common viral agents,
 Food sources include poultry, leafy vegetables, beef, fruits and nuts,
vine-stalk vegetables, and many other foods.
 Rotavirus infections (the most common identifiable viral cause of
gastroenteritis in all children)
PATHOGENESIS

 Pathogenesis and severity of bacterial disease depend on whether


organisms have preformed toxins, produce secretory or toxins, or are
invasive, and on whether they replicate in food.
 Enteropathogens elicit noninflammatory diarrhea through entero
toxin production by some bacteria, destruction of villus (surface) cells
by viruses, adherence by parasites, and adherence and/or
translocation by bacteria. Inflammatory diarrhea is usually caused by
bacteria that directly invade the intestine or produce cytotoxins with
consequent fluid, protein, and cells (erythrocytes, leukocytes) that
enter the intestinal lumen.
 Some viruses, such as rotavirus, target the microvillus tips of the
enterocytes and can enter the cells by direct invasion or calcium
dependent endocytosis. This can result in villus shortening and loss of
enterocyte absorptive surface through cell shortening and loss of
microvilli
 Most bacterial pathogens elaborate enterotoxins; the rotavirus
protein NSP4 acts as a viral enterotoxin. Bacterial enterotoxins can
selectively activate enterocyte intracellular signal transduction and
can also affect cytoskeletal rearrangements with subsequent
alterations in the water and electrolyte fluxes across enterocytes.
 ETEC colonizes and adheres to enterocytes of the small bowel via its
surface fimbriae (pili) and induces hypersecretion of fluids and
electrolytes into the small intestine through 1 of 2 toxins: the heat
labile enterotoxin or the heat-stable enterotoxin.
RISK FACTORS
 Seasonal exposure to organisms such as rotavirus
 Major risks include environmental contamination and increased
exposure to enteropathogens. Additional risks include young age,
immunodeficiency, measles, malnutrition, and lack of exclusive or
predominant breastfeeding.
 The majority of cases of diarrhea resolve within the 1st week of the
illness. A smaller proportion of diarrheal illnesses fail to resolve and
persist for longer than 2 wk.
 Persistent diarrhea is defined as episodes that began acutely but last
for 14 or more days.
COMPLICATIONS

 Delays in diagnosis and delays in the institution of appropriate


therapy.
 Without early and appropriate rehydration, many children with acute
diarrhea would develop dehydration with associated complications.
These can be life-threatening in infants and young children.
 Inappropriate therapy can lead to prolongation of the diarrheal
episodes, with consequent malnutrition and complications such as
secondary infections and micronutrient deficiencies (iron, zinc,
vitamin A).
CLINICAL MANIFESTATIONS
 Usually the ingestion of preformed toxins (e.g., those of S. aureus) is
associated with the rapid onset of nausea and vomiting within 6 hr, with
possible fever, abdominal cramps, and diarrhea within 8-72 hr.
 Watery diarrhea and abdominal cramps after an 8-16 hr incubation
period are associ ated with enterotoxin-producing C. perfringens and B.
cereus.
 Abdominal cramps and watery diarrhea after a 16-48 hr incubation
period can be associated with noroviruses, several enterotoxin-producing
bacteria, Cryptosporidium, and Cyclospora, and also have been a notable
feature of influenza virus H1N1 infections. Several organisms, including
Salmonella, Shigella, C. jejuni, Yersinia enterocolitica, enteroinvasive or
hemorrhagic (Shigatoxin-producing) E. coli, and V. parahaemolyticus,
produce diarrhea that can contain blood as well as fecal leukocytes in
association with abdominal cramps, tenesmus, and fever; these features
suggest bacterial dysentery and fever.
 Bloody diarrhea and abdominal cramps after a 72-120 hr incubation
period are associated with infections from Shigella and also Shigatoxin-
producing E. coli, such as E. coli O157:H7.
CLINICAL EVALUATION
 Assessing the degree of dehydration and acidosis and provide rapid
resuscitation and rehydration with oral or intravenous fluids as
required
 Obtaining appropriate contact, travel, or exposure history.
 Clinically determining the etiology of diarrhea for institution of prompt
antibiotic therapy
 Prompt antibiotic therapy, if indicated. Although nausea and vomiting
are nonspecific symptoms, they indicate infection in the upper
intestine. Fever suggests an inflammatory process but also occurs as
a result of dehydration or coinfection (e.g., urinary tract infection,
otitis media). Fever is common in patients with inflammatory
diarrhea. Severe abdominal pain and tenesmus indicate involvement
of the large intestine and rectum. Features such as nausea and
vomiting and absent or low-grade fever with mild to moderate
periumbilical pain and watery diarrhea indicate small intestine
involve ment and also reduce the likelihood of a serious bacterial
infection.
Stool Examination

 Microscopic examination of the stool and cultures can yield important


information on the etiology of diarrhea.
 Stool specimens could be examined for mucus, blood, and leukocytes.
Fecal leukocytes indicate bacterial invasion of colonic mucosa,
 Stool cultures should be obtained as early in the course of disease as
possible from children with bloody diarrhea in whom stool microscopy
indicates fecal leukocytes, in outbreaks with suspected hemolytic-
uremic syndrome, and in immunosuppressed children with diarrhea.
TREATMENT

 The broad principles of management of acute gastroenteritis in


children include oral rehydration therapy, enteral feeding and diet
selection, zinc supplementation, and additional therapies such as
probiotics.
ORAL REHYDRATION AND ENTERAL FEEDING
ZINC SUPPLEMENTATION

 All children older than 6 mo of age with acute diarrhea in at-risk areas
should receive oral zinc (20 mg/day) in some form for 10-14 days
during and continued after diarrhea
Additional Therapies
 T he use of probiotic nonpathogenic bacteria for prevention and therapy of
diarrhea has been successful in some settings although the evidence is
inconclusive to recommend their use in all settings.
 In addition to restoring beneficial intestinal flora, probiotics can enhance host
protec tive immunity such as downregulation of proinflammatory cytokines
and upregulation of anti inflammatory cytokines.
 Antimotility agents (loperamide) are contraindicated in children with
dysentery and probably have no role in the management of acute watery
diarrhea in otherwise healthy children. Similarly, antiemetic agents, such as
the phenothiazines, are of little value and are associated with potentially
serious side effects (lethargy, dystonia, malignant hyperpyrexia). Nonetheless,
ondansetron is an effective and less-toxic antiemetic agent and as indicated
previously, is a useful adjunct to the treatment of vomiting in ambulatory
settings with reduced risk of intravenous fluid requirements and
hospitalization. Because persistent vomiting can limit oral rehydration
therapy, a single sublingual dose of an oral dissolvable tablet of ondansetron
(4 mg 4-11 yr and 8 mg for children older than 11 yr [generally 0.2 mg/kg])
may be given.
PREVENTION

 Promotion of Exclusive Breastfeeding


 Rotavirus Immunization
 Improved Water and Sanitary Facilities and Promotion of Personal and
Domestic Hygiene
 Improved Case Management of Diarrhea

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