|

Case Report Acute Gastroenteritis

01 March 2010 – 09 May 2010

Faculty of Medicine Pelita Harapan University

Siloam Hospital Kebon Jeruk

Tutor : Dr. H. Tajoedin Sp.PD

By : Eva Yuliana

171.2004.0032

Acute Gastroenteritis

INTRODUCTION

Gastroenteritis is a nonspecific term for various pathologic states of the gastrointestinal tract. The primary manifestation is diarrhea, but it may be accompanied by nausea, vomiting, and abdominal pain.

The inflammation is caused most often by an infection from certain viruses or less often by bacteria, their toxins, parasites, or an adverse reaction to something in the diet or medication. Worldwide, inadequate treatment of gastroenteritis kills 5 to 8 million people per year, and is a leading cause of death among infants and children under 5.

The severity of illness may vary from mild and inconvenient to severe and life threatening. Appropriate management requires extensive history and assessment and appropriate, general supportive treatment that is often etiology specific.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 2

Acute Gastroenteritis

CASE

I. Patient IdentityName : Mr. RAge : 15 y.oSex : MaleDate of Admission: 3 March 2010

II. Anamnesis ( autoanamnesis, 5 March 2010 )

Chief ComplaintVomiting

Present IllnessThe patient came to Siloam Kebon Jeruk hospital with a chief complaint of vomiting since one day before admission. Vomiting occurred each time after each meal and drink. There was presence of Diarrheas for more than 10 times. Stool appeared yellow in color, watery and slimy in consistency, with no signs of fibrous or blood component. Urination frequency and urine quantity were both decreased. Urine was dark-yellow in color, with no pain upon urination. Other physical symptoms that followed were colic stomach ache, nauseous, headache, weakness, continuous thirst, and coldness on both hands and feet. No features of fever, heartthrobs, or increase respiration were found. This patient could not remember what he had eaten or drunk before experiencing this sickness.

Past Medical HistoryThe patient was previously hospitalized in the same hospital two weeks ago, for Dengue Hemorrhagic Fever. He was discharged four days before he got readmitted. He’s got a history of childhood asthma. Apart from his asthma medication, he does not have any history of long term medication and is allergic to sulfonamide.

Family HistoryNone of this patient’s family member is experiencing this sort of sickness. This patient’s Dad shared the same medical history of asthma. No family member has a history of hypertension, nor diabetes mellitus.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 3

Acute Gastroenteritis

Social history This Patient is a high school student who comes from a middle economical family.

III. Physical Examination ( 5 March 2010 )

General State : Moderately ill

Consciousness : Compos Mentis

GCS : E4M6V5

Height : 175 cm

Weight : 96 kg

Nutritional state : IMT = 31.34 kg/m2

Blood pressure : 110/70

Pulse : 78 x/minute

Temperature : 36 oC

Respiration : 16 x/minute

Skin : Warm and dry, turgor is adequate, color is normal.

There is no icterus, purpura, rash, or unusual pigmentation

noted.

Head : Normocephaly and atraumatic; no lesions noted.

Hair : Short and black.

Face : oval in shape, symmetrical, involuntary movement (-), edema (-)

Eyes : Eyelids ptosis (-), exopthalmos (-), laceration (-).

Swollen lacrimal gland (-), cornea is without lesion,

anemic conjunctiva (-), Scleral icterus (-),

pupils are equal, measuring approximately 3 mm -3 mm in

diameter, round, reactive to light

direct light reflex (+,+), indirect light reflex (+,+).

Extraocular movements are conjugated, without signs of

Nystagmus or strabismus.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 4

Acute Gastroenteritis

Ears : Normal in appearance, auditory canal appear clean and without

Lesion, hearing is adequate, pain upon tragus’s pressure (-)

Nose : Septum appears to be within normal limits and without

deviation. Nasal mucosa appear pink without any abnormal

discharge. No nasal polyp or other lesion are noted, frontal and

maxillary sinuses are nontender, pernapasan cuping hidung (-),

Mouth : Lips are without cyanosis or pallor. Surface is rather dry. Buccal

mucosa is normal in appearance. Teeth appear to be in good

condition.

Tounge : symmetrical in shape, shows no lesions or tremor, movement

is free in every direction.

Throat : Pharyngeal mucosa is pink and does not reveal any lesion,

Exudates, erythema, or evidence of tonsils inflammation. Gag

reflex is intact. Uvula is centered.

Neck :Neck is supple. Full range of motion is present. There is no

evidence of tracheal deviation or neck lymphadenopathy, as well

as supraclavicular lymphadenopathy. Jugular vein pressure is 5 –

3 H2O. Thyroid gland is in normal size, it’s palpation does not

reveal any nodule or masses. Hepatojugular reflex is not

examined.

Back :Spinal curvature is normal, there is no scoliosis, kyphosis, or

tenderness present. Full range of motion is present.

Toraks -inspection :Symmetrical, no susbternal-intercostal retraction, normal

intercostals space, no enlargement nor shrinkage, no venectation, no tumor. Movement is accordingly to respiration.

-Palpation : No signs of mass, no sign of axilar lymphadenopathy.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 5

Acute Gastroenteritis

Lung

-Palpation : Tactile fremitus is not increased nor decresed. Equal bilaterally.

-Percussion: Lung fields are resonant throughout.

Lung – Liver border : right midclavicular line ICS V

Lung – gaster border : left anterior axilar line ICS

-auscultation: vesicular breath sound, ronchi (-/-), wheezing (+/+)

Heart

-Inspection : Apical impulse is not visible

-Palpation : Apical impulse is strong, felt on ICS V

-Percussion : Right Heart border is on ICS IV, 1 cm lateral to left parasternal

line

Left heart border is on ICS V, 1 cm medial to left midclavicular

line.

-Auscultation: S1S2 are regular, murmur (-), gallop (-).

Abdomen

-Inspection :Abdominal wall is normal size and contour. There are no

capillary dilatations, striae albae is seen on the surface,

Abdominal wall moves accordingly to respiration

-Palpation :Abdominal wall is supple, no abdominal distention or masses.

Pain on epigastric pressure is present, no pain on other

abdominal field.

-Percussion : Tympanic on all four abdominal quadrants.

-Auscultation : Normoactive bowel sounds and no abdominal bruits.

Liver : Not palpable

Spleen : Not palpable

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 6

Acute Gastroenteritis

Kidney : Flank pain (CVA tenderness ) is (-), Ballottement (-).

Extremity : Both hands and feet are normal in size and shape

Acrals are chilly, no sign of cyanotic

Capillary refill time is 1 second

No edema on all four extremities

No tremor on all four extremities

Anogenitalia : Not examined.

IV. Supportive

Laboratorium test ( 5 February 2010 )

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 7

Acute Gastroenteritis

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 8

TEST Result UNIT Reference

Ranges

HEMATOLOGY

Hemoglobin 17.3 g/dL 13.0 – 18.0

Leukocyte count 10.1 103/µL 4.0 – 10.0

Diff. Leukocyte count

Basophil 0 % 0-1

Eosinophil 0 % 0-4

Band neutrophil 0 % 2-6

Segmented neutrophi 70 % 50-70

Lymphocyte 27 % 20-40

Monocyte 3 % 2-8

ESR 43 mm 0-15

Erythrocyte count 6.11 106/µL 4.50 – 6.20

Acute Gastroenteritis

ElectrocardiogramKesan : sinus Rhythm

HR 84 bpm ECG normal

V. ResumeA patient, male, 15 y.o., came to Siloam Kebon Jeruk hospital with a chief complaint of vomiting since one day before admission. Vomiting occurred each time after each meal and drink. There was presence of Diarrheas for more than 10 times. Stool appeared yellow in color, watery and slimy in consistency, with no signs of fibrous or blood component. Urination frequency and urine quantity were both decreased. Urine was dark-yellow in color, with no pain upon urination. Other physical symptoms that followed were colic stomach ache, nauseous, headache, weakness, continuous thirst, and coldness on both hands and feet. No features of fever, heartthrobs, or increase respiration were found. This patient could not remember what he had eaten or drunk before experiencing this sickness.

Physical examination showed relatively stable hemodynamic with blood pressure : 110/70, pulse : 78 x/min, temperature : 360C, respiratory : 16x/min. Lips looked dried, present of pain on epigastric pressure, and all four extremities are chilly.

Significant features found on laboratory test are; leukocyte count : 10.100/μl, ESR : 43mm, platelet count : 630.000/μl, blood ureum : 62 mg/dL, blood creatinin : 2.40 mg/dL, and occult blood on stool sample had a positive result.

VI. Differential Diagnosis Gastroenteritis ( viral, bacterial, parasite ) Botulism Dyspepsia syndrome Drugs ( sorbitol, cholinergics, caffeine) Inflammatory bowel disease Dehydration Acute Renal Failure

VII. Working Diagnosis- Acute viral gastroenteritis

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 9

Acute Gastroenteritis

- Acute Renal Failure- Post primary DHF

VIII. TherapyThe mainstay of therapy in gastroenteritis is rehydration- Bed rest- Soft-food, no fiber diet- Ringer lactate 500ml, 20 dpm- Oral rehydration solution → oralit- Attapulgit ( Toxin absorbent ) → Diagit 600 mg 3 x 1- Sucralfate (GIT mucosa protector ) → Smecta - Probiotic ( lactobacillus ) → Rillus 1 x 1- Proton Pump Inhibitor → Pantozol IV 2 x 1- Ondansetron ( antiemetic ) → Ondeval 5cc 3 x 1

IX. PrognosisAd vitam : dubia ad bonam

Ad functionam : dubia ad bonam

Ad sanationam : dubia ad bonam

Gastroenteritis Discussion

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 10

Acute Gastroenteritis

Definition

Gastroenteritis is defined by the incidence of inflammation of the stomach and the intestines. Can cause

nausea and vomiting and/or diarrhea. Gastroenteritis has numerous causes: including infectious

organisms (viruses, bacteria, etc.), food poisoning, and stress.

Etiology

Viral (50-70%)

Norovirus

Caliciviruses

Rotavirus

Adenovirus

Parvovirus

Astrovirus

Coronavirus

Pestivirus

Torovirus

Bacterial (15-20%)

Shigella

Salmonella

C jejuni

Yersinia enterocolitica

E coli - Enterohemorrhagic O157:H7, enterotoxigenic, enteroadherent, enteroinvasive

V cholera

Aeromonas

B cereus

C difficile

Clostridium perfringens

Parasitic (10-15%) Drug-associated diarrhea

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 11

Acute Gastroenteritis

Antibiotics, due to alteration of normal flora Laxatives, including magnesium-containing antacids Colchicine Quinidine Cholinergics Sorbitol

Other unknown causes

Patophysiology

Infectious agents usually cause acute gastroenteritis. These agents cause diarrhea by adherence, mucosal invasion, enter toxin production, and/or cytotoxin production.

These mechanisms result in increased fluid secretion and/or decreased absorption. This produces an increased luminal fluid content that cannot be adequately reabsorbed, leading to dehydration and the loss of electrolytes and nutrients.

Diarrheal illnesses may be classified as follows:

Osmotic, due to an increase in the osmotic load presented to the intestinal lumen, either through excessive intake or diminished absorption

Inflammatory (or mucosal), when the mucosal lining of the intestine is inflamed Secretory, when increased secretory activity occurs Motile, caused by intestinal motility disorders

The small intestine is the prime absorptive surface. The colon then absorbs additional fluid, transforming a relatively liquid fecal stream in the cecum to well-formed solid stool in the rectosigmoid.

Disorders of the small intestine result in increased amounts of diarrheal fluid with a concomitantly greater loss of electrolytes and nutrients.

Microorganisms may produce toxins that facilitate infection. Enterotoxins are generated by bacteria (ie, enterotoxigenic Escherichia coli, Vibrio cholera) that act directly on secretory mechanisms and produce typical, copious watery (rice water) diarrhea. No mucosal invasion occurs. The small intestines are primarily affected, and elevation of the adenosine monophosphate (AMP) levels is the common mechanism.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 12

Acute Gastroenteritis

Cytotoxin production by bacteria (ie, Shigella dysenteriae, Vibrio parahaemolyticus, Clostridium difficile, enterohemorrhagic E coli) results in mucosal cell destruction that leads to bloody stools with inflammatory cells. A resulting decreased absorptive ability occurs.

Diarrheal illness occurs when microbial virulence overwhelms normal host defenses. A large inoculum may overwhelm the host capacity to mount an effective defense. Normally, more than 100,000 E coli are required to cause disease, while only 10 Entamoeba or Giardia cysts may suffice to do the same. Some organisms (eg, V cholera, enterotoxigenic E coli) produce proteins that aid their adherence to the intestinal wall, thereby displacing the normal flora and colonizing the intestinal lumen.

In addition to the ingestion of pathogenic organisms or toxins, other intrinsic factors can lead to infection. An alteration of normal bowel flora can create a biologic void that is filled by pathogens. This occurs most commonly after antibiotic administration, but infants are also at risk prior to colonization with normal bowel flora.

The normally acidic pH of the stomach and colon is an effective antimicrobial defense. In achlorhydric states (ie, caused by antacids, histamine-2 [H2] blockers, gastric surgery, decreased colonic anaerobic flora), this defense is weakened.

Hypomotility states may result in colonization by pathogens, especially in the proximal small bowel, where motility is the major mechanism in the removal of organisms. Hypomotility may be induced by antiperistaltic agents (eg, opiates, diphenoxylate and atropine [Lomotil], loperamide) or anomalous anatomy (eg, fistulae, diverticula, antiperistaltic afferent loops) or is inherent in disorders such as diabetes mellitus or scleroderma.

The immunocompromised host is more susceptible to infection, as evidenced by the wide spectrum of diarrheal pathogens in patients with AIDS.

Diagnosis

Laboratory Studies

Determination of laboratory tests: The patient's evaluation should be based on the clinical assessment and the need to do the following:

o Further evaluate the seriousness of the condition (degree of dehydration and electrolyte derangement).

o Determine a specific etiologic agent.o Evaluate the patient for noninfectious etiologies.o Patients who require further workup include those who appear seriously ill or

dehydrated; those who have high fevers, bloody stools, severe abdominal pain,

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 13

Acute Gastroenteritis

or persistent diarrhea; and those who are immunocompromised or whose condition is suspected of having an epidemic diarrheal etiology.

o History, epidemiologic considerations, and the physical examination should be the primary guides in determining whether any further diagnostic evaluation is necessary, followed by microscopic examination of the stool.

1. Stool studies and culture

2. Routine laboratory tests

o Routine laboratory tests (CBC, electrolytes, renal function) may not be helpful or indicated in making a diagnosis. These tests may be useful as indicators of severity of disease, especially in elderly or very young patients, although that determination is best made clinically.

o Electrolytes and BUN tests are indicated in patients with severe diarrhea or dehydration to rule out hyponatremia or hypernatremia. Decreased serum bicarbonate suggests severe dehydration, especially in children. Acidosis secondary to bicarbonate loss in the stools and/or from hypovolemia-induced lactic acidosis may be present. Hypokalemia may also occur.

o A CBC may be indicated with a prolonged course, severe diarrhea, or toxicity. The WBC count is usually increased in Salmonella infections but normal or low with significant left shift in Shigella infections. The WBC count is otherwise variable. Eosinophilia may be present in parasitic infections.

3. Enzyme-linked immunosorbent assay

o Commercially available immunofluorescent antibody and enzyme immunoassays are also available for Giardia and Cryptosporidium organisms. C difficile toxin assays can be performed when antibiotic-associated diarrhea is suspected.

o Rotavirus: Enzyme-linked immunosorbent assay (ELISA) is available in less than 2 hours but is not sensitive enough in adults.

o Giardia: ELISA is more than 90% sensitive in susceptible populations (eg, people who camp or travel to endemic areas). Consider ELISA prior to ova and parasite examination or string test.

Treatment

Rehydration

The primary treatment of gastroenteritis in both children and adults is rehydration, i.e., replenishment of water and electrolytes lost in the stools. This is preferably achieved by giving

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 14

Acute Gastroenteritis

the person oral rehydration therapy (ORT) although intravenous delivery may be required if a decreased level of consciousness or an ileus is present.[16][17] Complex-carbohydrate-based Oral Rehydration Salts (ORS) such as those made from wheat or rice have been found to be superior to simple sugar-based ORS.

Sugary drinks such as soft drinks and fruit juice are not recommended for gastroenteritis in children under 5 years of age as they may make the diarrhea worse. Plain water may be used if specific ORS are unavailable or not palatable.

Diet

It is recommended that breastfed infants continue to be nursed on demand and that formula-fed infants should continue their usual formula immediately after rehydration with oral rehydration solutions. Lactose-free or lactose-reduced formulas usually are not necessary.[20] Children receiving semisolid or solid foods should continue to receive their usual diet during episodes of diarrhea. Foods high in simple sugars should be avoided because the osmotic load might worsen diarrhea; therefore, soft drinks, juice, and other high simple sugar foods should be avoided.[20] The practice of withholding food is not recommended and immediate normal feeding is encouraged.[21] The BRAT diet (bananas, rice, applesauce, toast and tea) is no longer recommended, as it contains insufficient nutrients and has no benefit over normal feeding.

Pharmacologic therapy

Gastroenteritis is usually an acute and self-limited disease that does not require pharmacological therapy. Metoclopramide and ondansetron however may be helpful in children.

Antibiotics

Antibiotics are usually not useful for gastroenteritis, although they are sometimes used if symptoms are severe or a susceptible bacterial cause is isolated or suspected. If antibiotics are decided on, a fluoroquinolone or macrolide is often used.[

Pseudomembranous colitis, usually caused by antibiotics use, is managed by discontinuing the causative agent and treating with either metronidazole or vancomycin.

Antimotility agents

Antimotility drugs have a theoretical risk of causing complications, clinical experience however has shown this to be unlikely. They are thus discouraged in people with bloody diarrhea or diarrhea complicated by a fever.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 15

Acute Gastroenteritis

Loperamide, an opioid analogue, is commonly used for the symptomatic treatment of diarrhea. Loperamide is not recommended in children as it may cross the immature blood brain barrier and cause toxicity.

Bismuth subsalicylate (BSS), an insoluble complex of trivalent bismuth and salicylate, can be used in mild-moderate cases.

Antiemetic drugs

Antiemetic drugs may be helpful for vomiting in children. Ondansetron has some utility with a single dose associated with less need for intravenous fluids, fewer hospitalizations, and decreased vomiting. Metoclopramide also might be helpful.

Probiotics

Some probiotics have been shown to be beneficial in preventing and treating various forms of gastroenteritis. Fermented milk products (such as yogurt) also reduce the duration of symptoms.

Zinc

The World Health Organization recommends that infants and children receive a dietary supplement of zinc for up to two weeks after onset of gastroenteritis. A 2009 trial however did not find any benefit from supplementation.

Complication

Dehydration is the most common outcome that is caused by vomiting and diarrhea. In acute diarrhea, loss of water through vomiting and diarrhea would lead to hypokalemia and metabolic asidosis.

Acute renal failure is the early result of the state of being dehydrated, in which the kidneys are not receiving enough fluid supply. When hypovolemic state is not treated, this condition will lead to acute tubular necrosis, which eventually would cause multiple organ failure.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 16

Acute Gastroenteritis

Bibliography

1. CDC. Outbreaks of gastroenteritis associated with noroviruses on cruise ships--United States,

2002. MMWR Morb Mortal Wkly Rep. Dec 13 2002;51(49):1112-5. [Medline]

2. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL. Harrison's Principles of Internal

Medicine. New York: McGraw-Hill, 2005. ISBN 0-07-139140-1.

3. Seamens CM, Schwartz G. Food-borne illness: differential diagnosis and targeted management. Emerg

Med Rep. 1998;19:120-131.

Clinical Clerkship of Internal Medicine DivisionSiloam Hospital Kebon Jeruk-Pelita Harapan UniversityMarch 1 – May 9, 2010

Page 17