Factitious diarrhea: Clinical manifestations, diagnosis, and management

INTRODUCTION — Factitious diarrhea may be due to a self-induced true increase in stool volume or the creation of an apparent increase in stool volume by the addition of various substances to the stool. Early diagnosis of factitious diarrhea can prevent patient self-harm as well as iatrogenic complications arising from unnecessary tests and treatments. This topic will review the clinical manifestations, diagnosis, and management of factitious diarrhea. Other causes of chronic diarrhea and the clinical features, diagnosis, and management of factitious disorder are discussed separately. (See "Approach to the adult with chronic diarrhea in resource-abundant settings" and "Factitious disorder imposed on self (Munchausen syndrome)".)

EPIDEMIOLOGY — More than 90 percent of patients with factitious diarrhea are women and have a history of work in the healthcare field [1]. These patients often seek care from many clinicians and have multiple hospital admissions in an effort to establish the cause of the diarrhea. They also have a higher incidence of anorexia nervosa, suggesting a common underlying psychiatric basis [2,3].

Surreptitious laxative misuse is the most frequent cause of factitious diarrhea and often presents as chronic watery diarrhea of unknown etiology. In one study in which 47 patients at a tertiary referral center for evaluation of diarrhea of unclear etiology were screened for laxative use, seven patients (15 percent) tested positive for laxatives [4].

CLINICAL MANIFESTATIONS

Clinical presentation — Patients with factitious diarrhea often present with a history of frequent, large-volume, watery diarrhea [5,6]. Patients report between 10 and 20 bowel movements a day, with 24-hour stool volumes ranging from 300 to 3000 mL. More than 50 percent of patients complain of nocturnal bowel movements. Patients may also report associated blood in the stool.

In patients with factious diarrhea due to laxatives, diarrhea is often associated with cramping abdominal pain due to an increase in the fluid content of the stool and enhanced gastrointestinal motility. Lethargy, generalized weakness, and dizziness or lightheadedness may result from orthostatic hypotension due to dehydration. Weight loss is common, and in severe cases, patients may have malnutrition and cachexia due to diarrhea, concurrent nausea or vomiting, or diminished nutrient absorption. As an example, rhein (an anthraquinone) and bisacodyl (a diphenolic laxative) impair glucose absorption and may also cause mild steatorrhea and gastrointestinal protein loss. (See "Mechanisms, causes, and evaluation of orthostatic hypotension", section on 'Symptoms' and "Management of chronic constipation in adults", section on 'Stimulant laxatives'.)

Laboratory findings — Hypokalemia is frequently present due to losses in the diarrheal fluid. Hypovolemia-induced secondary hyperaldosteronism may also contribute by increasing colonic potassium secretion. (See "Pathophysiology and clinical features of primary aldosteronism".)

Chronic diarrhea caused by laxative abuse often results in metabolic alkalosis [5-8]. The alkalosis may be due in part to hypokalemia impairing the intestinal reabsorption of chloride, thereby diminishing bicarbonate secretion into the intestinal lumen via chloride-bicarbonate exchange. Loss of a high-chloride, low-bicarbonate solution can raise the plasma bicarbonate concentration, and both volume depletion and hypokalemia prevent excretion of the excess bicarbonate in the urine. (See "Pathogenesis of metabolic alkalosis".)

Moderate to severe hypermagnesemia can occur if a magnesium-containing laxative is used, particularly in patients in whom urinary magnesium excretion is impaired because of volume depletion [9,10]. (See "Hypermagnesemia: Causes, symptoms, and treatment", section on 'Causes of hypermagnesemia'.)

Imaging findings — Cathartic colon is a rarely seen but severe manifestation of prolonged laxative use [11,12]. It is characterized by dilation of the large bowel, with decreased or absent haustrations noted on plain abdominal films or barium enema. The changes are usually most marked in the right colon but can affect the entire colon.

DIAGNOSIS — The diagnosis of factitious diarrhea is based on a self-induced true increase in stool volume or the creation of an apparent increase in stool volume by the addition of substances (eg, urine, water) to the stool. Although laboratory testing and endoscopic findings may be supportive of the diagnosis of factitious diarrhea, they are limited in their sensitivity and specificity. The diagnosis requires a high index of suspicion, and test results need to be interpreted in the context of the patient's history.

Evaluation — Factitious diarrhea is often suspected in patients in whom organic causes of chronic diarrhea have been ruled out. An approach to the evaluation of a patient with chronic diarrhea is discussed in detail, separately. (See "Approach to the adult with chronic diarrhea in resource-abundant settings", section on 'Initial evaluation'.)

Evaluation of a patient with factitious diarrhea includes the following:

●History in a patient with factitious diarrhea may provide several clues to support the diagnosis. These include high rates of healthcare utilization; evasiveness in providing history; refusal to grant access to prior medical records; inconsistencies in the history, examination, and laboratory tests; and a lengthy and extensive prior clinical evaluation that is negative. Room searches for laxatives, a common practice in the past, are no longer advisable for legal reasons.

●Laboratory studies, including stool osmolality, electrolytes, osmotic gap, and a laxative screen. Laboratory testing should also include a complete blood count and differential, C-reactive protein, sedimentation rate, serum electrolytes, total protein and albumin to assess the volume and nutritional status and to detect electrolyte derangements. (See 'Laboratory findings' above and 'Stool osmolality' below and 'Stool electrolytes and osmotic gap' below.)

●Colonoscopy if not previously performed as part of the evaluation for chronic diarrhea [13]. (See "Approach to the adult with chronic diarrhea in resource-abundant settings", section on 'Initial evaluation' and 'Endoscopy' below.)

Stool osmolality — A 24-hour stool specimen should be evaluated for stool osmolality. Normal fecal fluid has an osmolality close to that of plasma (290 mOsm/kg) [13]. Stool osmolality <250 mOsm/kg suggests that factitious diarrhea may be from the addition of water or hypotonic urine to the stool as the colon cannot dilute stool to an osmolality that is less than that of plasma [13-15].

Stool osmolality >400 mOsm/kg (particularly with a high sodium concentration >90 mmol/L) may be due to the addition or the contamination of stool by concentrated urine. If the stool is not examined quickly, stool osmolality can also increase due to breakdown of carbohydrates by bacteria into smaller, osmotically active molecules [13]. Urine contamination of stool can be confirmed by demonstrating high concentrations of urea in fecal fluid.

Stool electrolytes and osmotic gap — Stool sodium, potassium, magnesium, and phosphate should be measured in patients suspected of having factitious diarrhea [9]. Stool magnesium >90 mEq/L and phosphate >33 mmol/L suggest magnesium- and phosphate-induced diarrhea, respectively [16]. (See "Management of chronic constipation in adults", section on 'Osmotic agents'.)

The osmotic gap is calculated by subtracting twice the measured concentrations of sodium and potassium from 290 mOsmol/kg, which is the expected osmolality of freshly passed diarrheal stool (calculator 1). An osmotic gap exceeding 75 mOsmol/kg can be due to laxatives containing magnesium, sorbitol, lactose, lactulose, or polyethylene glycol as the active ingredients. An osmotic gap less than 75 mOsmol/kg may be due to the use of a secretory laxative (eg, senna, bisacodyl) or osmotic diarrhea caused by a sodium-containing laxative. A negative osmotic gap is suggestive of a phosphate- or sulfate-containing laxative. (See "Management of chronic constipation in adults", section on 'Other laxatives'.)

Laxative screen — We suggest laxative screening on a stool specimen for diphenolic laxatives (eg, bisacodyl) and polyethylene glycol-containing laxatives [17]. As patients consume one or more laxatives at a time, or may rotate laxatives, specimens should be screened for both osmotic and stimulant laxatives. Analysis of stool should repeated if negative if there is a high index of suspicion, as laxatives may be ingested intermittently.

Laxative screens have several limitations. Laxative screens cannot reliably detect anthraquinones (eg, senna, cascara), and assays do not exist for several other laxatives (eg, castor oil and mineral oil). Stool screens for diphenolic laxatives have limited sensitivity and specificity and therefore the possibility of false-positive and false-negative results must be considered while interpreting the results [18]. Although laxatives can also be detected in blood, plasma concentrations are lower than stool or urine concentrations. (See 'Stool electrolytes and osmotic gap' above.)

Endoscopy — Patients with a history of anthraquinone-containing laxative use may have melanosis coli. However, the presence of melanosis coli is not specific and has been reported in patients with chronic colitis [19]. Melanosis coli is not associated with the use of osmotic or diphenolic laxatives. On endoscopy, melanosis coli appears as a dark brown discoloration of the colon with lymph follicles shining through as pale patches (picture 1). While melanosis coli usually affects the proximal colon, the entire colon may be involved [20]. If melanosis coli is not evident on endoscopy, it can be demonstrated histologically by finding lipofuscin pigment in the macrophages of the lamina propria [21]. Melanosis coli can develop within four months of the onset of anthraquinone-containing laxatives and can disappear in the same amount of time if it is discontinued. (See "Approach to the adult with chronic diarrhea in resource-abundant settings", section on 'Initial evaluation'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of factitious diarrhea includes other causes of chronic diarrhea. The differential diagnosis for chronic diarrhea and the evaluation of chronic diarrhea are discussed in detail, separately. (See "Approach to the adult with chronic diarrhea in resource-abundant settings".)

MANAGEMENT — The initial management of factitious diarrhea consists of correction of electrolyte abnormalities, dehydration, and malnutrition. (See "Treatment and prevention of hyperkalemia in adults" and "Hypomagnesemia: Evaluation and treatment".)

Patients with factitious diarrhea should be referred to a psychiatrist for evaluation and management of an associated psychiatric disorder (eg, factitious disorder). (See "Factitious disorder imposed on self (Munchausen syndrome)", section on 'Diagnostic criteria' and "Factitious disorder imposed on self (Munchausen syndrome)", section on 'Differential diagnosis' and "Factitious disorder imposed on self (Munchausen syndrome)", section on 'Specific treatment'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute diarrhea in adults".)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Factitious diarrhea may be due to a self-induced true increase in stool volume or the creation of an apparent increase in stool volume by the addition of various substances (eg, urine, water) to the stool. More than 90 percent of patients with factitious diarrhea are women and have a history of work in the healthcare field. Patients often have high rates of healthcare utilization. Surreptitious laxative use is the most frequent cause of factitious diarrhea. (See 'Epidemiology' above.)

●Clinical features – Patients often presents as watery diarrhea that is high in frequency and volume. The diarrhea is often associated with cramping abdominal pain. Lethargy, generalized weakness, and dizziness or lightheadedness may result from orthostatic hypotension due to dehydration. Weight loss is common, and in severe cases, patients may have malnutrition and cachexia due to diarrhea. Patients with factitious diarrhea due to laxative abuse may have hypokalemia and metabolic alkalosis due to dehydration and hypermagnesemia due to the use of magnesium-containing cathartics. (See 'Clinical manifestations' above.)

●Evaluation – Factitious diarrhea is suspected in patients in whom organic causes of chronic diarrhea have been ruled out. In addition to the history, evaluation of the patient with suspected factitious diarrhea should include laboratory studies and a colonoscopy if not previously performed for evaluation of chronic diarrhea. (See 'Evaluation' above.)

●Diagnosis – The diagnosis of factitious diarrhea is based on a self-induced true increase in stool volume or the creation of an apparent increase in stool volume by the addition of substances (eg, urine, water) to the stool. Although laboratory testing and endoscopic findings may be supportive of the diagnosis of factitious diarrhea, they are limited in their sensitivity and specificity. The diagnosis requires a high index of suspicion, and test results need to be interpreted in the context of the patient's history. (See 'Diagnosis' above.)

•Stool tests – Stool osmolality <250 mOsm/kg suggests that factitious diarrhea may be from the addition of water, and stool osmolality >400 mOsm/kg may be due to contamination with concentrated urine. An osmotic gap exceeding 75 mOsmol/kg can be due to laxatives containing magnesium, sorbitol, lactose, lactulose, or polyethylene glycol as the active ingredients. An osmotic gap less than 75 mOsmol/kg may be due to the use of a secretory laxative (eg, senna, bisacodyl). Stool magnesium >90 mEq/L and phosphate >33 mmol/L suggest magnesium- and phosphate-induced diarrhea, respectively. (See 'Stool osmolality' above and 'Stool electrolytes and osmotic gap' above.)

•Colonoscopy findings – Patients with a history of anthraquinone-containing laxative use may have melanosis coli. However, the presence of melanosis coli is not specific and has been reported in patients with chronic colitis. (See 'Endoscopy' above.)

●Management – The initial management of factitious diarrhea consists of correction of electrolyte abnormalities, dehydration, and malnutrition. Patients with factitious diarrhea should be referred to a psychiatrist for evaluation and management of an associated psychiatric disorder (eg, factitious disorder). (See 'Management' above and "Factitious disorder imposed on self (Munchausen syndrome)", section on 'Management'.)