Pediatric emergency medicine trisk 0364 0364
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Food protein–induced enterocolitis syndrome (FPIES)
Bulky, foul-smelling, or diarrheal stools suggest malabsorption secondary to
many causes, which may include formula enteropathies, bacterial overgrowth,
parasites, and cystic fibrosis (see Chapters 91 Gastrointestinal Emergencies and
94 Infectious Disease Emergencies ). In lactose intolerance, bacterial metabolism
of unabsorbed lactose produces intestinal gas causing abdominal distension,
cramping, flatulence, and diarrhea. The severity of the symptoms is related
primarily to the quantity of lactose ingested. Celiac disease may present with
prominent abdominal distension, especially in children younger than 2 years,
along with nonspecific GI symptoms and poor weight gain. Obstipation is a
common cause of abdominal distension. The patient usually has a history of
irregular stooling or chronic constipation. This is often due to a severe functional
disturbance, but pathologic processes, including Hirschsprung disease and other
defects in bowel enervation, and hypothyroidism should be excluded (see Chapter
18 Constipation ).
Extraluminal gas usually causes abdominal distension only when present as
free intraperitoneal air. This may result from intestinal perforation (due to trauma,
inflammation, ulcer, foreign-body ingestion, or other causes) or secondary to a
pneumomediastinum. It is demonstrated with an upright or cross-table lateral
radiograph of the abdomen or on an upright chest radiograph to detect free air
under the diaphragm. Alternatively, point-of-care ultrasound (POCUS) has been
shown to accurately detect free intraperitoneal air. An ileus generally contributes
to the abdominal distension.
Extraluminal fluid in the abdomen may be an effusion, blood, chyle, bile,
urine, or pus. The most common reason in pediatrics for the accumulation of fluid
in the abdominal cavity is secondary to a low serum albumin. This may be the
result of protein loss due to nephrotic syndrome or protein-losing enteropathy, or
due to decreased protein synthesis such as that which occurs in cirrhosis and
malnutrition. There is usually associated peripheral edema and pleural effusion.
Increased venous and lymphatic resistance through the portal and hepatic veins
may also cause accumulation of abdominal fluid. Obstruction of blood flow
through the liver is suggested by distended abdominal wall veins, a history of
hemoptysis, and an enlarged spleen. Although cirrhosis evolves gradually, its
clinical presentation may be abrupt. It results from Wilson disease, α1 -antitrypsin
disease, biliary atresia, and other congenital problems, or occasionally, from
chronic active hepatitis. Decreased clotting factors would be among the many
laboratory findings of cirrhosis. Obstruction of flow at the hepatic veins or above
