PATHOPHYSIOLOGY OF ACUTE GASTROENTERITIS

Ingestion of fecally contaminated food & water Direct invasion of the bowel wall
Stimulation and destruction of mucosal lining of the bowel wall Pain ulceration
bleeding
Endotoxins are released
Attempted defecation (tenesmus) Digestive & absorptive malfunction
hematochezia hematemesis Nausea & vomiting
melena
Excessive gas formation GI distention Flatus Secretion of F&E in the intestinal
lumen Increase peristaltic movement Increase secretion of Cl & HCO3 ions in the
bowel
Hyperactive bowel sound (borborygmi)
Mild diarrhea (2-3 stools) F&E imbalance Increase protein in the lumen
Inhibition of Na reabsorption hypernatremia Metabolic acidosis
LI is overwhelmed & unable to reabsorb the lost fluid Intense diarrhea (>10x) (w
atery stool) Serious fluid volume deficit Hypotension Hypovolemic shock
Kussmauls breathing
Death
Acute gastroenteritis is usually caused by bacteria and protozoan. In the Philip
pines, one of the most common causes of acute gastroenteritis is E. histolytica.
The pathologic process starts with ingestion of fecally contaminated food and w
ater. The organism affects the body through direct invasion and by endotoxin bei
ng released by the organism. Through these two processes the bowel mucosal linin
g is stimulated and destroyed the eventually lead to attempted defecation or ten
esmus as the body tries to get rid of the foreign organism in the stomach. The c
lient with acute gastroenteritis may also report excessive gas formation that ma
y leads to abdominal distention and passing of flatus due to digestive and absor
ptive malfunction in the system. Feeling of fullness and the increase motility o
f the gastrointestinal tract may progress to nausea and vomiting and increasing
frequency of defecation. Abdominal pain and feeling of fullness maybe relieved o
nly when the patient is able to pass a flatus. As the destruction of the bowel c
ontinues the mucosal lining erodes due to toxin, direct invasion of the organism
and the action of the hydrochloric acid of the stomach. As the protective coati
ng of the stomach erodes the digestive capabilities of the acid helps in destroy
ing the stomach lining. Pain or tenderness of the abdomen is then felt by the pa
tient. When the burrows or ulceration reaches the blood vessels in the stomach b
leeding will be induced. Dysentery may be characterized by melena or hematochezi
a depending on the site and quantity of bleeding that may ensue. Signs of bleedi
ng may be observed also through hematemesis. As the bowel is stimulated by the o
rganism and its toxin, the intestinal tract secretes water and electrolytes in t
he intestinal lumen. The body secretes and therefore lost Chloride and bicarbona
te ions in the bowel as the body try to get rid of the organism by increasing pe
ristalsis and number of defecation. Sodium and water reabsorption in the bowel i
s inhibited with the lost of the two electrolytes. Mild diarrhea is characterize
d by 2-3 stool, borborygmi (hyperactive bowel sound),fluid and electrolyte imbal
ance and hypernatremia. When the condition continue to progress, protein in the
body is excreted to the lumen that further decreases the reabsorption and the bo
dy become overwhelmed that leads to intense diarrhea with more than 10 watery st
ool. Serious fluid volume deficit may lead to hypovolemic shock and eventually d
eath.