35 year old female shop assistant presents with “diarrhoea for five months"

Definition

Passing a stool weight or volume greater than 200g or 200mL per 24hours, and it is a symptom instead of a disease

Fundamental process that causes all diarrheal diseases is incomplete absorption of water from intestinal luminal contents

Condition of altered intestinal water and electrolyte transport

Step 1: Make sure to identify what patient means by diarrhoea

Distinguish from decal incontinence where problem is anal sphincter dysfunction instead of dysregulated intestinal fluid or electrolyte absorption

Distinguish from fecal impaction: patients with chronic constipation may develop fecal impaction from inability to expel a large fecal mass through the anus and rectal distention causes relaxation of internal anal sphincter and there is induction of secretions proximal to obstructing stool, liquid stool then passes around the impaction

Step 2: Rule out drug-induced diarrhoea

Diarrhoea is an adverse effect of nearly all medications, make sure to establish temporal relationship between starting use of drug and onset of diarrhoea. E.g. antacids, nutritional supplements that contain Mg2+, antibiotics, PPIs, SSRIs, NSAIDs

Caffeine may cause increased intestinal fluid secretion by elevating intracellular cAMP levels

Antibiotics alter colonic bacterial flora that may then decrease colonic bacterial fermentation of malabsorbed carbohydrates or lead to Clostridium difficile infection

Mesenteric vasoconstriction agents decrease mesenteric blood flow and causes malabsorption

NSAIDs or mycophenolate mofetil are agents that incite intestinal inflammation, thus causing diarrhoea

Chemotherapy causes intestinal or colonic crypt damage, thus impairing water absorption and resulting in apoptotic enterocolopathy

Step 3: Distinguish Acute from Chronic Diarrhoea

Evaluate duration of diarrhoea. Acute: <2wks, Chronic: >4wks

Acute diarrhoea is straightforward as most commonly caused by infection and is self-limited. Note: stool testing and other studies are indicated in the presence of certain clinical or epidemiological features

Chronic diarrhoea warrants diagnostic evaluation, is less likely to resolve on its own and presents a broad differential diagnosis.

Step 4: Categorise diarrhoea as inflammatory, fatty or watery

Inflammatory diarrhoea

Frequent, small-volume, bloody stools and many be accompanied by tenesmus, fever, or severe abdominal pain

Indicates disrupted and inflamed mucosa

Idiopathic Inflammatory Bowel Disease (Crohn disease or ulcerative colitis)

Ischemic colitis

Infectious (C. difficile, CMV, TB, entamoeba histolytica)

Uncommon: Radiation colitis and neoplasia

Fatty stools

Hx of weight loss, greasy or bulky stools that are difficult to flush, and oil in toilet bowl that requires a brush to remove

Misconception that floating stools are indicative steatorrhea! Floating stools indicate gas production by colonic bacteria, not steatorrhea

Fat malabsorption

Inadequate mucosal transport

Fat maldigestion

Celiac disease

Defective hydrolysis of triglycerides

Pancreatic exocrine insufficiency (chronic pancreatitis)

Inadequate duodenal bile acid concentration (small intestinal bacterial overgrowth SIBO) or cirrhosis

Watery diarrhoea

Osmotic

Secretory

Due to ingestion of poorly absorbed ions or sugars (CATIONS: magnesium; ANIONS: phosphate, sulphate which are contained in laxatives and antacids. Stool volume decreases with fasting.

Disruption of epithelial electrolyte transport. Stool volume remains same with fasting. Mechanism involves either net secretion of ions (chloride or bicarbonate) or inhibition of net sodium absorption

Distinguish osmotic and secretory process by noting response to fasting and calculating the fecal osmotic gap

Carbohydrate malabsorption from ingestion of poorly absorbed sugars or sugar alcohols (e.g. sorbitol or xylitol). Results in stool pH < 6 because as carbohydrates reach the colon they are fermented by bacteria, releasing short-chain fatty acids and making the stool water acidic. Lactose intolerance in Africa, Asia, and Latin America.

Infection

Bile acid malabsorption

Non osmotic laxatives

Inflammatory bowel disease (microscopic colitis, Crohn disease, ulcerative colitis)

Disordered regulation (post-vagotomy, diabetic neuropathy)

Peptide-secreting endocrine tumours

Neoplasia (colon carcinoma, lymphoma, villous adenoma)

Idiopathic or epidemic secretory diarrhoea

Step 5: Consider factitious diarrhoea

Intentionally self-inflicted disorder, frequently surreptitious laxative ingestion, most commonly in women of higher socioeconomic status and often employed in medical field

Can use colonoscopy to evaluate factitious diarrhoea as pseudo-melanosis coli is potential clue found on colonoscopy (brownish discolouration of colonic mucosa caused by accumulation of lipofuscin pigment in macrophages of lamina propria, occurs with use of anthraquinone laxatives)

Stool osmolality can never be less than that of plasma, so a low osmolality of <290 mOsm/kg can only result from adding a hypotonic solution such as water or urine to the stool

High stool osmolality of >600 mOsm/kg can be due to addition of hypertonic solutions such as tomato juice or blood

Ulcerative colitis: Haematochezia and tenesmus in Hx, signs usually non-specific, extra intestinal manifestations such as erythema nodosum, uveitis, iritis, episcleritis, arthritis

Hx of DM, past surgery, coeliac or Crohn disease, symptoms include bloating, wind, flatulence, cramping and diarrhoea

Family Hx of coeliac disease or personal Hx of other autoimmune diseases e.g. T1DM, autoimmune thyroid disease with those symptoms, other symptoms are classic abdo symptoms of bloating, N&V, abdo pain, weight loss

Non-specific signs but dermatitis herpetiformis which is a pruritic vesicular rash over the extensor surfaces, if found, is highly suggestive; aphthous mouth ulceration

Hx of pancreatitis, alcohol abuse, CF

Surgical Hx of resection of part of ileum usually >50cm, or due to abnormalities of apical bile salt transporter located in ill enterocytes

Older patients with Hx of vascular disease and on antihypertensive meds; symptoms include cramping abdo pain and mild to severe haematochezia; Signs include abdo tenderness and blood on rectal exam

Significant radiation exposure to abdomen (prostate cancer in men and uterine cancer in women), haematochezia common

ABx use, travel history, contact history, immunosuppression

Crohn's disease: chronic abdo pain, bloating, weight loss, with family Hx of inflammatory bowel disease; signs may include distention consistent with stricture and obstruction, abdo masses secondary to abscess or phlegmon

Gastrinoma

Abdominal pain, erosive esophagitis, enlarged gastric folds, duodenal ulcers

Carcinoid

Flushing, enlarged nodular liver from metastases

VIPoma

Hypokalemia, achlorhydria

Somatostatinoma

DM, cholelithiasis, hypochlorhydria

Glucagonoma

DM, DVT, depression, necrolytic migratory erythema