Diarrhea

Diarrhea is best defined as excessive loss of fluid and electrolyte in the stool. Acute diarrhea is defined as sudden onset of excessively loose stools of >10 mL/kg/day in infants and >200 g/24 hr in older children, which lasts <14 days. When the episode lasts >14 days, it is called chronic or persistent diarrhea.

Normally, a young infant has approximately 5 mL/kg/day of stool output; the volume increases to 200 g/24 hr in an adult. The greatest volume of intestinal water is absorbed in the small bowel; the colon concentrates intestinal contents against a high osmotic gradient. The small intestine of an adult can absorb 10-11 L/day of a combination of ingested and secreted fluid, whereas the colon absorbs approximately 0.5 L. Disorders that interfere with absorption in the small bowel tend to produce voluminous diarrhea, whereas disorders compromising colonic absorption produce lower-volume diarrhea. Dysentery (small-volume, frequent bloody stools with mucus, tenesmus, and urgency) is the predominant symptom of colitis.

The basis of all diarrheas is disturbed intestinal solute transport and water absorption. Water movement across intestinal membranes is passive and is determined by both active and passive fluxes of solutes, particularly sodium, chloride, and glucose. The pathogenesis of most episodes of diarrhea can be explained by secretory, osmotic, or motility abnormalities or a combination of these (Table 298-10).

Secretory diarrhea occurs when the intestinal epithelial cell solute transport system is in an active state of secretion. It is often caused by a secretagogue, such as cholera toxin, binding to a receptor on the surface epithelium of the bowel and thereby stimulating intracellular accumulation of cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP). Some intraluminal fatty acids and bile salts cause the colonic mucosa to secrete through this mechanism. Diarrhea not associated with an exogenous secretagogue can also have a secretory component (congenital microvillus inclusion disease). Secretory diarrhea is usually of large volume and persists even with fasting. The stool osmolality is indicated by the electrolytes and the ion gap is 100 mOsm/kg or less. The ion gap is calculated by subtracting the concentration of electrolytes from total osmolality:

Osmotic diarrhea occurs after ingestion of a poorly absorbed solute. The solute may be one that is normally not well absorbed (magnesium, phosphate, lactulose, or sorbitol) or one that is not well absorbed because of a disorder of the small bowel (lactose with lactase deficiency or glucose with rotavirus diarrhea). Malabsorbed carbohydrate is fermented in the colon, and short-chain fatty acids (SCFAs) are produced. Although SCFAs can be absorbed in the colon and used as an energy source, the net effect is increase in the osmotic solute load. This form of diarrhea is usually of lesser volume than a secretory diarrhea and stops with fasting. The osmolality of the stool will not be explained by the electrolyte content, because another osmotic component is present and the anion gap is >100 mOsm.

Motility disorders can be associated with rapid or delayed transit and are not generally associated with large-volume diarrhea. Slow motility can be associated with bacterial overgrowth leading to diarrhea. The differential diagnosis of common causes of acute and chronic diarrhea is noted in Table 298-11.

Table 298-11 DIFFERENTIAL DIAGNOSIS OF DIARRHEA

From Kliegman RM, Greenbaum LA, Lye PS, editors: Practical strategies in pediatric diagnosis and therapy, ed 2, Philadelphia, 2004, Elsevier, p 272.

Constipation

Any definition of constipation is relative and depends on stool consistency, stool frequency, and difficulty in passing the stool. A normal child might have a soft stool only every 2nd or 3rd day without difficulty; this is not constipation. A hard stool passed with difficulty every 3rd day should be treated as constipation. Constipation can arise from defects either in filling or emptying the rectum (Table 298-12).

A nursing infant might have very infrequent stools of normal consistency; this is usually a normal pattern. True constipation in the neonatal period is most likely secondary to Hirschsprung disease, intestinal pseudo-obstruction, or hypothyroidism.

Defective rectal filling occurs when colonic peristalsis is ineffective (in cases of hypothyroidism or opiate use and when bowel obstruction is caused either by a structural anomaly or by Hirschsprung disease). The resultant colonic stasis leads to excessive drying of stool and a failure to initiate reflexes from the rectum that normally trigger evacuation. Emptying the rectum by spontaneous evacuation depends on a defecation reflex initiated by pressure receptors in the rectal muscle. Stool retention, therefore, can also result from lesions involving these rectal muscles, the sacral spinal cord afferent and efferent fibers, or the muscles of the abdomen and pelvic floor. Disorders of anal sphincter relaxation can also contribute to fecal retention.

Constipation tends to be self-perpetuating, whatever its cause. Hard, large stools in the rectum become difficult and even painful to evacuate; thus, more retention occurs and a vicious circle ensues. Distention of the rectum and colon lessens the sensitivity of the defecation reflex and the effectiveness of peristalsis. Eventually, watery content from the proximal colon might percolate around hard retained stool and pass per rectum unperceived by the child. This involuntary encopresis may be mistaken for diarrhea. Constipation itself does not have deleterious systemic organic effects, but urinary tract stasis can accompany severe long-standing cases and constipation can generate anxiety, having a marked emotional impact on the patient and family.

Abdominal Pain

There is considerable variation among children in their perception and tolerance for abdominal pain. This is one reason the evaluation of chronic abdominal pain is difficult. A child with functional abdominal pain (no identifiable organic cause) may be as uncomfortable as one with an organic cause. It is very important to distinguish between organic and nonorganic (functional) abdominal pain because the approach for the management is based on this. Normal growth and physical examination (including a rectal examination) are reassuring in a child who is suspected of having functional pain.

A specific cause may be difficult to find, but the nature and location of a pain-provoking lesion can usually be determined from the clinical description. Two types of nerve fibers transmit painful stimuli in the abdomen. In skin and muscle, A fibers mediate sharp localized pain; C fibers from viscera, peritoneum, and muscle transmit poorly localized, dull pain. These afferent fibers have cell bodies in the dorsal root ganglia, and some axons cross the midline and ascend to the medulla, midbrain, and thalamus. Pain is perceived in the cortex of the postcentral gyrus, which can receive impulses arising from both sides of the body. In the gut, the usual stimulus provoking pain is tension or stretching. Inflammatory lesions can lower the pain threshold, but the mechanisms producing pain of inflammation are not clear. Tissue metabolites released near nerve endings probably account for the pain caused by ischemia. Perception of these painful stimuli can be modulated by input from both cerebral and peripheral sources. Psychologic factors are particularly important. Features of abdominal pain are noted in Tables 298-13 and 298-14. Pain that suggests a potentially serious organic etiology is associated with age <5 yr; fever; weight loss; bile or blood-stained emesis; jaundice; hepatosplenomegaly; back or flank pain or pain in a location other than the umbilicus; awakening from sleep in pain; referred pain to shoulder, groin or back; elevated ESR, WBC, or CRP; anemia; edema; or a strong family history of inflammatory bowel disease (IBD) or celiac disease.

Table 298-13 CHRONIC ABDOMINAL PAIN IN CHILDREN

abd, abdominal; EEG, electroencephalogram; GI, gastrointestinal; Hx, history; IVP, intravenous pyelogrophy; O&P, ova and parasites; PE, physical exam; RLQ, right lower quadrant; RUQ, right upper quadrant.

Visceral pain tends to be dull and aching and is experienced in the dermatome from which the affected organ receives innervations. So, most often, the pain and tenderness is not felt over the site of the disease process. Painful stimuli originating in the liver, pancreas, biliary tree, stomach, or upper bowel are felt in the epigastrium; pain from the distal small bowel, cecum, appendix, or proximal colon is felt at the umbilicus; and pain from the distal large bowel, urinary tract, or pelvic organs is usually suprapubic. The pain from the cecum, ascending colon, and descending colon sometimes is felt at the site of the lesion due to the short mesocecum and corresponding mesocolon. The pain due to appendicitis is initially felt in the periumbilical region, and pain from the transverse colon is usually felt in the supra pubic region. The shifting (localization) of pain is a pointer toward diagnosis; for example, periumbilical pain of a few hours localizing to the right lower quadrant suggests appendicitis. Radiation of pain can be helpful in diagnosis; for example, in biliary colic the radiation of pain is toward the inferior angle of the right scapula, pancreatic pain radiated to the back, and the renal colic pain is radiated to the inguinal region on the same side.

Somatic pain is intense and is usually well localized. When the inflamed viscus comes in contact with the somatic organ like the parietal peritoneum or the abdominal wall, pain is localized to that site. Peritonitis gives rise to generalized abdominal pain with rigidity, involuntary guarding, rebound tenderness, and cutaneous hyperesthesia on physical examination.

Referred pain from extraintestinal locations, due to shared central projections with the sensory pathway from the abdominal wall, can give rise to abdominal pain, as in pneumonia when the parietal pleural pain is referred to the abdomen.

Gastrointestinal Hemorrhage

Bleeding can occur anywhere along the GI tract, and identification of the site may be challenging (Table 298-15). Bleeding that originates in the esophagus, stomach, or duodenum can cause hematemesis. When exposed to gastric or intestinal juices, blood quickly darkens to resemble coffee grounds; massive bleeding is likely to be red. Red or maroon blood in stools, hematochezia, signifies either a distal bleeding site or massive hemorrhage above the distal ileum. Moderate to mild bleeding from sites above the distal ileum tends to cause blackened stools of tarry consistency (melena); major hemorrhages in the duodenum or above can also cause melena.

Table 298-15 DIFFERENTIAL DIAGNOSIS OF GASTROINTESTINAL BLEEDING IN CHILDHOOD

Erosive damage to the mucosa of the GI tract is the most common cause of bleeding, although variceal bleeding secondary to portal hypertension occurs often enough to require consideration. Prolapse gastropathy producing subepithelial hemorrhage and Mallory-Weiss lesions secondary to mucosal tears associated with emesis are causes of upper intestinal bleeds. Vascular malformations are a rare cause in children; they are difficult to identify. Upper intestinal bleeding is evaluated with an EGD (esophagogastroduodenoscopy). Evaluation of the small intestine is facilitated by capsule endoscopy. The capsule-sized imaging device is swallowed in older children or placed endoscopically in younger children. Lower GI bleeding is investigated with a colonoscopy. In brisk intestinal bleeding of unknown location, a tagged red blood cell (RBC) scan is helpful in locating the site of the bleeding. Occult blood in stool is usually detected by using commercially available fecal occult blood testing cards, which are based on a chemical reaction between the chemical guaiac and oxidizing action of a substrate (hemoglobin), giving a blue color. The guaiac test is very sensitive, but random testing can miss chronic blood loss, which can lead to iron-deficiency anemia. GI hemorrhage can produce hypotension and tachycardia but rarely causes GI symptoms; brisk duodenal or gastric bleeding can lead to nausea, vomiting, or diarrhea. The breakdown products of intraluminal blood might tip patients into hepatic coma if liver function is already compromised and can lead to elevation of serum bilirubin.

Abdominal Distention and Abdominal Masses

Enlargement of the abdomen can result from diminished tone of the wall musculature or from increased content: fluid, gas, or solid. Ascites, the accumulation of fluid in the peritoneal cavity, distends the abdomen both in the flanks and anteriorly when it is large in volume. This fluid shifts with movement of the patient and conducts a percussion wave. Ascitic fluid is usually a transudate with a low protein concentration resulting from reduced plasma colloid osmotic pressure of hypoalbuminemia and/or from raised portal venous pressure. In cases of portal hypertension, the fluid leak probably occurs from lymphatics on the liver surface and from visceral peritoneal capillaries, but ascites does not usually develop until the serum albumin level falls. Sodium excretion in the urine decreases greatly as the ascitic fluid accumulates and, thus, additional dietary sodium goes directly to the peritoneal space, taking with it more water. When ascitic fluid contains a high protein concentration, it is usually an exudate caused by an inflammatory or neoplastic lesion.

When fluid distends the gut, either obstruction or imbalance between absorption and secretion should be suspected. The factors causing fluid accumulation in the bowel lumen often cause gas to accumulate, too. The result may be audible gurgling noises. The source of gas is usually swallowed air, but endogenous flora can increase considerably in malabsorptive states and produce excessive gas when substrate reaches the lower intestine. Gas in the peritoneal cavity (pneumoperitoneum) is usually due to perforated viscus and can cause abdominal distention depending on the amount of gas leak. A tympanitic percussion note, even over solid organs such as the liver, indicates a large collection of gas in the peritoneum.

An abdominal organ can enlarge diffusely or be affected by a discrete mass. In the digestive tract, such discrete masses can occur in the lumen, wall, omentum, or mesentery. In a constipated child, mobile, nontender fecal masses are often found. Congenital anomalies, cysts, or inflammatory processes can affect the wall of the gut. Gut wall neoplasms are extremely rare in children. The pathologic enlargement of liver, spleen, bladder, and kidneys can give rise to abdominal distention.

Jaundice

See Chapters 96.3 and 348.