3.11 Small Intestinal Disease, Ischemia & Gastrointestinal Complications of HIV

1. Small Intestinal Bacterial Overgrowth

Excess colonic-type bacteria in the small bowel produce bloating, flatulence, diarrhea and malabsorption. It arises whenever the mechanisms that normally keep the small bowel sparsely colonized fail:

• Anatomic stasis: surgical blind loops, strictures, diverticula, adhesions
• Motility failure: diabetic autonomic neuropathy, scleroderma, chronic intestinal pseudo-obstruction
• Loss of the ileocecal valve after resection
• Achlorhydria from long-term acid suppression

The distinctive laboratory pattern is a low vitamin B12 with a normal or high folate: bacteria consume B12 while synthesizing folate. Fat malabsorption follows bacterial deconjugation of bile salts, producing steatorrhea and fat-soluble vitamin deficiency.

Diagnosis uses carbohydrate breath testing (an early hydrogen rise) or, less commonly, jejunal aspirate culture. Treatment is a course of antibiotics — rifaximin is commonly used — plus correction of the underlying anatomic or motility problem, without which recurrence is the rule.

2. Short Bowel Syndrome

Malabsorption after extensive resection. The functional consequences depend on which segment was lost, and this is the reasoning the exam tests.

Terminal ileal disease or resection is the highest-yield item. Bile salts that escape ileal reabsorption enter the colon:

• Limited resection (< ~100 cm): unabsorbed bile salts irritate the colon, producing bile-acid (choleretic) diarrhea that responds to a bile-acid sequestrant such as cholestyramine.
• Extensive resection (> ~100 cm): the bile-salt pool is depleted, producing steatorrhea that worsens with a sequestrant and requires fat restriction and medium-chain triglycerides instead.

Giving cholestyramine to the wrong patient makes them worse — a classic distractor.

Other consequences of ileal resection: lifelong vitamin B12 supplementation, calcium oxalate kidney stones (unabsorbed fatty acids bind calcium, leaving oxalate free for absorption — enteric hyperoxaluria), and gallstone formation.

3. Post-Bariatric Complications

The blueprint lists gastric bypass complications explicitly.

• Nutritional deficiencies: iron, vitamin B12, folate, thiamine, calcium, vitamin D, copper and zinc. Thiamine deficiency can present acutely as Wernicke encephalopathy after protracted post-operative vomiting and is a medical emergency.
• Dumping syndrome: early (30 minutes; osmotic, with cramping, diarrhea and vasomotor symptoms) versus late (1–3 hours; reactive hyperinsulinemic hypoglycemia). Both are managed by dietary modification.
• Internal hernia: intermittent postprandial pain after Roux-en-Y that can progress to closed-loop obstruction; imaging may be normal between episodes and a high index of suspicion is required.
• Marginal ulceration at the gastrojejunal anastomosis, strongly associated with smoking and NSAID use.

4. Ischemic Bowel Disease

Three distinct syndromes that are frequently confused.

Acute mesenteric ischemia is the emergency. Early in its course the abdomen is soft and unimpressive while the patient reports severe pain — the discordance is the diagnosis. Lactate rises late, so a normal lactate must not be used to exclude it. Peritoneal signs indicate infarction and are a late finding. Embolic occlusion in a patient with atrial fibrillation is the classic vignette.

Ischemic colitis is far more common, involves the watershed areas (splenic flexure, rectosigmoid), and typically resolves with supportive care; the rectum is usually spared because of dual blood supply.

5. Infectious Gastroenteritis

Most acute diarrheal illness is self-limited and requires only oral rehydration. The exam focuses on when not to follow that rule.

Indications for stool testing: severe illness, fever, bloody stool, immunocompromise, recent antibiotics, hospitalization, or persistent symptoms.

Inflammatory (invasive) pathogens — Shigella, Campylobacter, Salmonella, Shiga toxin-producing Escherichia coli, Entamoeba histolytica — cause fever, bloody stool and fecal leukocytes. Non-inflammatory pathogens — norovirus, enterotoxigenic E. coli, Vibrio, preformed toxins from Staphylococcus aureus or Bacillus cereus — cause watery diarrhea without fever.

The single most important antibiotic rule: in suspected Shiga toxin-producing E. coli (including O157:H7), antibiotics and antimotility agents are contraindicated, because they increase the risk of hemolytic uremic syndrome. Suspect it when bloody diarrhea occurs with little or no fever.

Other associations worth knowing: Campylobacter preceding Guillain-Barré syndrome; Yersinia mimicking appendicitis with right lower quadrant pain; Vibrio vulnificus after raw shellfish, especially dangerous in iron overload and cirrhosis; and post-infectious irritable bowel syndrome after any of these.

6. Gastrointestinal Complications of HIV Infection

The likely pathogen tracks the CD4 count, and this stratification is the testable structure.

Esophageal disease is a common presentation:

• Candida — the most common cause; oral thrush plus dysphagia justifies empiric fluconazole, with endoscopy reserved for non-responders.
• Cytomegalovirus — large, solitary, linear or deep ulcers; treated with ganciclovir.
• Herpes simplex virus — multiple small, shallow, well-circumscribed ulcers; treated with acyclovir.
• Idiopathic aphthous ulceration — a diagnosis of exclusion treated with corticosteroids or thalidomide.

Cytomegalovirus colitis at CD4 counts below 50 causes abdominal pain, bloody diarrhea, fever and weight loss, and may perforate. Serology is inadequate for diagnosis; colonoscopic biopsy demonstrating intranuclear inclusions is required.

Chronic watery diarrhea with a normal CD4 count on suppressive antiretroviral therapy is more likely to be a medication adverse effect — protease inhibitors are the usual culprits — than an opportunistic infection. Ultimately, the definitive treatment for most HIV-associated gastrointestinal opportunistic disease is immune reconstitution with effective antiretroviral therapy; pathogen-directed treatment alone rarely produces durable control when the CD4 count remains low.