Gastroenterol Clin N Am 1988;17:357; Dis Colon Rectum 2000:289

Cause: Diverticulosis with secondary infection.

Epidem: Diverticulosis present in almost all patients age > 40 yr in U.S. if on a low-bulk diet. Increased risk in alcoholics (Brit J Surg 1999;86:1067).

Pathophys: Low-residue diet leads to increased intracolonic pressures causing outpocketings.

Sx: Left lower quadrant pain, usually, although may be anywhere.

Si: Localized abdominal tenderness (LLQ in 67% < 40 yr of age); fever; tachycardia (Am J Emerg Med 2000;18:140).

Crs: Variable, with obesity as risk for accurate diagnosis and surgical treatment, if needed.

Cmplc: Perforation; peritonitis; partial obstruction; abscess; fistulas; and/or bleeding from diverticulosis alone.

Diff Dx: Intestinal gas; gastroenteritis; abdominal wall muscle strain; colitis; hernia; right-sided angiodysplasia of the colon, often seen in elderly and associated with aortic stenosis.

Lab: CBC with diff showing leukocytosis in 91%, consider UA in atypical cases.

Gastroenterol Clin N Am 1991;1:691

Cause: Inadvertent ingestion of foreign body or large food bolus.

Epidem: 80% peds.

Pathophys: Pediatric esophagus with 5 natural narrowings, adults may have rings, webs, dysmotility, or mass lesions.

Sx: Foreign body sensation anywhere from oropharynx to epigastrium, inability to swallow saliva.

Si: Drooling is almost pathognomonic.

Crs: If no foreign body on exam or plain film, no hypersalivation, and no obstruction or foreign body on barium swallow, then expectant management OK (Jacep 1979;8:101), except as noted under “Cmplc.”

Lab: CXR to r/o aspiration, and to identify location if radio-opaque. Consider lateral neck film or abdominal film if unable to locate object in chest. Barium swallow if still uncertain.

Emergency Management: For esophageal foreign bodies without an acute abdomen:

Chest Surg Clin N Am 1994;4:819

Cause: Full thickness esophageal tear, known as Boerhaave’s syndrome (named after the Danish physician who first diagnosed this after the Danish grand admiral had vomited portions of a duck). May occur secondary to a weakened esophagus or after violent emesis, but the hx is nonspecific most of the time. Ingested sharp or corrosive foreign bodies, or direct penetrating trauma are also risk factors.

Epidem: Uncommon, many diagnoses made postmortem. If diagnosis made promptly, outcome as good as with esophageal perforation secondary to endoscopy (Chest 1987;92:995).

Pathophys: Cause as above, leakage of enteric contents causes the secondary mediastinitis. One hypothesis is lack of muscularis mucosa at site of rupture (Am J Surg 1989;158:420).

Sx: Hx of vomiting; chest pain, abdominal pain, fever, otherwise nonspecific.

Si: Rales; subcutaneous emphysema.

Crs: Worse with delayed diagnosis; classic triad of vomiting, chest pain, and subcutaneous emphysema is not common (Am Surg 1999;65:449).

Cmplc: Mediastinitis—mortality > 70% with delayed diagnosis.

Diff Dx: Stomach rupture (Jama 1982;247:811); tension pneumothorax; bronchial tear; pulmonary embolus.

Lab: Low SaO₂; pleural fluid for food particles if radiographic studies equivocal (Chest 1992;102:976).

Gastrointest Endosc Clin N Am 1999;9:175; Drug Ther Bull 2000;38:37; Nejm 2001;345:669)

Cause: End-stage hepatic failure has many etiologies, one of the four major complications is hemorrhage, and esophageal bleeding is the most life threatening. Other complications are ascites, renal failure, and encephalopathy.

Pathophys: Portal hypertension leading to varices; bleeding from depressed prothrombin and fibrinogen; depressed platelets from bleeding and hypersplenism; perhaps diminished platelet function from increased BUN; increased plasminogen activators due to diminished hepatic filtration.

Sx/Si: Hematemesis, melena.

Crs: Cause of death in 20% of patients with cirrhosis.

Complc: Coagulopathy; encephalopathy.

Diff Dx: See Upper GI Bleed p 127.

Lab: Hemoccult emesis and stool, CBC with diff, PT/PTT, type and cross for PRBCs.

(Gastrointest Endosc Clin N Am 1999;9:287)

Cause: Cholelithiasis may cause lodging of stones in the cystic duct, the common duct, or they may pass to the duodenum. Colic (misnomer) is an obstructed gallbladder, usually due to stones but may be due to a mass lesion. Cholecystitis is inflammation/infection
of the gallbladder; acalculous cholecystitis is inflammation without stones. Cholangitis is infection of the biliary system, and may be due to a gallstone lodged in the common duct.

Epidem: Cholecystitis is F/M 2:1, with stones present in 10% of adult women in U.S., 70% of Southwestern Native American women. Higher incidence of stone with the following:

Pathophys: Stones are usually mucin protein + cholesterol, less often with bilirubin and calcium.

Sx: Steady epigastric or right upper quadrant pain (colic is a misnomer in this case), radiates to right scapula, nausea, vomiting—temporary relief after vomiting.

Si: Fever, pressure at the right subcostal area inhibits patient from taking deep breath when prompted secondary to pain [Murphy’s sign—97% sensitivity (Ann EM 1996;28:267)].

Crs: Those with stones will have a 10-20% chance of having symptoms over 20-30 yr; after first symptoms, 50% will recur over 20 yr, with 25-50% getting complications—these are the low numbers, it may be higher.

Cmplc: Pancreatitis; cholangitis; hydrops, emphysema, or empyema of gallbladder; perforation and peritonitis; gallstone ileus is rare—a small bowel obstruction from a gallstone that has lodged at the ileocecal valve after eroding through the gallbladder into the duodenum; perhaps gallbladder cancer—cause and effect in these cases is uncertain.

Diff Dx: Chronic acalculous cholecystitis [seen mainly in white females (Jsls 1999;3:221)]; hepatitis; PUD; pyelonephritis; Saint’s triad—hiatal hernia, colonic diverticulosis, and cholelithiasis.

Lab: CBC with diff, LFTs, amylase, lipase—the elderly may have moderate to severe disease with little supportive serum laboratory data, age ≥ 65 yr (Acad Emerg Med 1997;4:51); Perhaps CRP (Eur J Surg 1992;158:365); gallbladder US (Gastrointest Radiol 1986;11:334); consider HIDA scan (Radiology 1982;144:369), if US equivocal—No dye in gallbladder is consistent with cholecystitis, no dye into duodenum is consistent with common duct stone. Abdominal x-ray usually not helpful, even for emphysematous cholecystitis (Brit J Radiol 1997;70:986)—US better. If UA obtained, may show WBCs, but should lack bacteria.

Am J Clin Pathol 2000;113:12; hep A (Vaccine 1992;10:S15); hep B (Nejm 2004;350:1118; Vaccine 1998;16:S11; Microbiol Mol Biol Rev 2000;64:51); hep C (Cmaj 2000;102:827; J Clin Gastroenterol 2000;30:125)

Cause: Hepatitis in general is inflammation of the liver from infectious, autoimmune, toxin, or metabolic disorder. Common causes are mononucleosis, hepatitis A, hepatitis B, hepatitis C, ethanol, and autoimmune hepatitis (Biomed Pharmacother 1999;53:255).

Lab: CBC with diff, LFTs, amylase, lipase, monospot; PT/PTT, if suspect fulminant hepatitis (Vaccine 1992;10:S21); Get CPK, especially if LDH > AST (SGOT) > ALT (SGPT) to r/o myopathy—may also check aldolase.