PATHOPHYSIOLOGY OF ACUTE GASTROENTERITIS

Ingestion of fecally
contaminated food & water

Direct invasion of Endotoxins are

the bowel wall released

Stimulation and destruction of

mucosal lining of the bowel wall
Pain
ulceration Attempted defecation
(tenesmus)
bleeding

Digestive & absorptive

hematochezia melena malfunction

hematemesis
Excessive gas
formation
Nausea &
vomiting
GI distention

Flatus

Secretion of F&E in Increase secretion of Cl & HCO3

the intestinal lumen ions in the bowel

Increase peristaltic
movement

Hyperactive bowel Mild diarrhea Inhibition of Na

sound (borborygmi) (2-3 stools) reabsorption

F&E imbalance hypernatremia

Metabolic
Increase protein in acidosis
the lumen

LI is overwhelmed & unable Kussmauls

to reabsorb the lost fluid breathing

Intense diarrhea (>10x)

(watery stool)

Serious fluid
volume deficit

Hypotension Hypovolemic shock

Death
 Acute gastroenteritis is usually caused by bacteria and protozoan. In the Philippines, one of the most
common causes of acute gastroenteritis is E. histolytica. The pathologic process starts with ingestion of fecally
contaminated food and water. The organism affects the body through direct invasion and by endotoxin being
released by the organism. Through these two processes the bowel mucosal lining is stimulated and destroyed the
eventually lead to attempted defecation or tenesmus as the body tries to get rid of the foreign organism in the
stomach.
The client with acute gastroenteritis may also report excessive gas formation that may leads to
abdominal distention and passing of flatus due to digestive and absorptive malfunction in the system. Feeling of
fullness and the increase motility of the gastrointestinal tract may progress to nausea and vomiting and
increasing frequency of defecation. Abdominal pain and feeling of fullness maybe relieved only when the
patient is able to pass a flatus.
As the destruction of the bowel continues 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 coating of the stomach erodes
the digestive capabilities of the acid helps in destroying the stomach lining. Pain or tenderness of the abdomen
is then felt by the patient. When the burrows or ulceration reaches the blood vessels in the stomach bleeding
will be induced. Dysentery may be characterized by melena or hematochezia depending on the site and quantity
of bleeding that may ensue. Signs of bleeding may be observed also through hematemesis.
As the bowel is stimulated by the organism and its toxin, the intestinal tract secretes water and
electrolytes in the intestinal lumen. The body secretes and therefore lost Chloride and bicarbonate ions in the
bowel as the body try to get rid of the organism by increasing peristalsis and number of defecation. Sodium and
water reabsorption in the bowel is inhibited with the lost of the two electrolytes.
Mild diarrhea is characterized by 2-3 stool, borborygmi (hyperactive bowel sound),fluid and electrolyte
imbalance and hypernatremia. When the condition continue to progress, protein in the body is excreted to the
lumen that further decreases the reabsorption and the body become overwhelmed that leads to intense diarrhea
with more than 10 watery stool. Serious fluid volume deficit may lead to hypovolemic shock and eventually
death.