Etiopathogenesis, clinical manifestations, diagnostic algorithm and management of malabsorption

Etiopathogenesis, clinical manifestations, diagnostic algorithm and management of malabsorption

Malabsorption means defective passage of digested nutrients into the blood and lymph. It may be global (all nutrients) or selective (one nutrient, e.g. B12).

Distinguish maldigestion (failure of luminal breakdown — pancreatic or bile salt problem) from malabsorption (failure of mucosal uptake or lymphatic transport).

Healthy ageing alone does not cause malabsorption. Pathy's states that although brush-border enzymes fall, digestion and absorption of carbohydrate, fat and protein remain normal in healthy old age.

Age-related changes are selective: vitamin A absorption increases, vitamin D absorption decreases, folate absorption falls slightly, and B12 absorption falls when hypochlorhydria is present.

Small-intestinal motility and transit are essentially preserved with healthy ageing; therefore bacterial overgrowth is rare in the healthy elderly. When it occurs, look for disease, not for age.

Luminal (maldigestion): pancreatic exocrine insufficiency (chronic pancreatitis, pancreatic cancer), bile salt deficiency (cholestasis, ileal resection), and hypochlorhydria from atrophic gastritis or long-term PPI use.

Mucosal: coeliac disease, tropical sprue, Crohn's disease, giardiasis, drug-induced enteropathy (olmesartan, NSAIDs, colchicine), amyloidosis, radiation enteritis.

Post-mucosal (lymphatic/vascular): intestinal lymphangiectasia, lymphoma, chronic mesenteric ischaemia, constrictive pericarditis, right heart failure.

Stasis with bacterial overgrowth (SIBO): Pathy's identifies the classic geriatric mechanism — diabetes with autonomic neuropathy, small-intestinal diverticula, and reduced gastric acid cause stasis and predispose to overgrowth, causing malnutrition and diarrhoea.

Post-surgical causes matter in the elderly: previous gastrectomy, blind loop, ileal resection, and short bowel after mesenteric ischaemia.

In India, always add tropical sprue, intestinal tuberculosis, giardiasis, strongyloidiasis, and HIV enteropathy to the differential — these are far commoner than in Western series.

Classical picture — chronic diarrhoea, steatorrhoea (bulky, pale, offensive, floating stool), weight loss, abdominal bloating and flatulence.

Geriatric picture is atypical and oligosymptomatic: presentation is often only unexplained weight loss, anaemia, fatigue or a metabolic bone disease, with little or no diarrhoea. Diarrhoea may even be absent.

Deficiency-based clues: iron/folate/B12 deficiency anaemia; osteomalacia and proximal myopathy (vitamin D, calcium); bruising (vitamin K); glossitis and cheilitis (B-complex); night blindness (vitamin A); oedema (hypoalbuminaemia); peripheral neuropathy (B12).

Fat-soluble vitamin loss (A, D, E, K) occurs in maldigestion and steatorrhoea, whereas isolated B12 loss suggests ileal or gastric pathology.

Step 1 — Confirm malabsorption and screen: CBC with MCV, iron studies, B12, folate, calcium, phosphate, albumin, prothrombin time, 25(OH)D, TSH. A raised INR that corrects with vitamin K is a useful bedside pointer.

Step 2 — Confirm fat malabsorption: qualitative Sudan III stain of stool (simple, available in India) or 72-hour faecal fat (>7 g/day). Faecal calprotectin distinguishes inflammatory from non-inflammatory causes.

Step 3 — Localise the defect: Mucosal → IgA anti-tTG plus total IgA, then upper GI endoscopy with 4–6 duodenal biopsies (including bulb). Pancreatic → faecal elastase-1; <200 µg/g suggests, <100 µg/g indicates severe exocrine insufficiency; CT/MRCP for structural disease. SIBO → Pathy's: culture of duodenal aspirate or glucose/xylose hydrogen breath test; sensitivity and specificity vary widely, so a negative test after antibiotics increases diagnostic certainty.

Step 4 — Imaging and exclusion of malignancy: CT enterography, capsule endoscopy or enteroscopy for obscure cases; CT angiography if chronic mesenteric ischaemia is suspected (post-prandial pain, food fear, weight loss).

Always exclude malignancy first in the elderly. Weight loss plus altered bowel habit in an older patient requires a low threshold for colonoscopy and cross-sectional imaging before labelling anything "functional".

Treat the cause: lifelong gluten-free diet for coeliac disease; pancreatic enzyme replacement for exocrine insufficiency; tetracycline plus folic acid for tropical sprue; ATT for intestinal tuberculosis.

SIBO (Pathy's): metronidazole, tetracycline or quinolones, or non-absorbed rifaximin, given for one to four weeks, repeated cyclically if recurrent — noting that Pathy's stresses there is a paucity of controlled data to guide practice.

Correct deficiencies aggressively: parenteral iron if oral is not absorbed, B12 (oral high-dose or IM), folate, calcium with vitamin D, and vitamin K where INR is prolonged.

Nutritional rehabilitation: high-energy, high-protein diet; oral nutritional supplements; MCT oil for severe steatorrhoea; lactose restriction if secondary lactase deficiency; involve a dietitian, and monitor for refeeding syndrome in the very depleted.

Symptomatic and stewardship measures: Pathy's notes loperamide and clonidine may help when no cause is found, but warns older patients are especially prone to adverse effects — constipation, urinary retention and glaucoma with loperamide; hypotension, bradycardia, sedation and dry mouth with clonidine. Deprescribe the PPI if the indication has lapsed, since acid suppression drives both B12 deficiency and overgrowth.