Approach to Malabsorption Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: This is a core cause for chronic diarrhoea, unexplained weight loss, and nutritional deficiencies that you will be asked to clerk and work up from the clinic or wards.
High-Yield Definition: Malabsorption is a state of impaired nutrient absorption by the small intestine, which can be global, affecting most nutrients, or partial, affecting specific ones. (Source: UpToDate, 2024).
Clinical One-Liner: Basically, the gut isn't absorbing food properly, so the patient is losing weight and getting specific deficiencies despite eating.
II. Etiology & Risk Factors
The causes can be broken down by the stage of digestion that's affected. It's a useful way to frame your thinking.
1. Pre-mucosal (Intraluminal Phase Defect): Problems with breaking down food.
Chronic Pancreatitis: A big one here, often due to alcohol or idiopathic. Lack of lipase leads to fat malabsorption.
Bile Acid Deficiency: Can occur in cholestatic liver disease or after ileal resection (e.g., in Crohn's disease).
2. Mucosal (Intestinal Phase Defect): The gut lining itself is the problem.
Celiac Disease: Immune-mediated damage to villi from gluten. Less common than in the West, but we see it.
Tropical Sprue: A classic diagnosis in our region. A post-infectious syndrome causing chronic diarrhoea and malabsorption in those living in or returning from tropical areas.
Inflammatory Bowel Disease (IBD): Specifically Crohn's disease affecting the small bowel.
Infections: Giardiasis, Whipple's disease (rare but classic), and importantly in Malaysia, Tuberculous enteritis.
Lactose Intolerance: Very common in the Asian population. Enzyme deficiency, not structural damage.
3. Post-mucosal (Absorptive Phase Defect): Nutrients are absorbed but can't be transported.
Lymphatic Obstruction: Can be congenital (lymphangiectasia) or acquired (e.g., lymphoma, radiation damage).
Key Risk Factors:
Modifiable: High alcohol intake (chronic pancreatitis), recent travel to endemic areas (infectious causes).
Non-modifiable: Family history (Celiac, IBD), prior abdominal surgery (short bowel syndrome, bacterial overgrowth), history of radiation.
III. Quick Pathophysiology
Think simply. The link between the cause and the symptoms is direct.
Fat Malabsorption (Steatorrhoea): No lipase (pancreatitis) or bile salts means fat stays in the gut lumen. This fat pulls water in osmotically, causing bulky, oily, foul-smelling stools that are hard to flush. This is the hallmark.
Mucosal Damage (e.g., Celiac, Tropical Sprue): The villi are flattened, drastically reducing the surface area for absorption. The proximal bowel is rich in villi for absorbing iron and folate, which is why you see microcytic or macrocytic anaemia first.
Vitamin Deficiencies: Fat-soluble vitamins (A, D, E, K) are absorbed along with fat. No fat absorption means no vitamin absorption. This leads to bruising/bleeding (Vit K), bone pain (Vit D), and neurological symptoms (Vit E).
IV. Clinical Assessment
Red Flags & Immediate Actions:
Haemodynamic instability (Hypotension, Tachycardia): → Alert senior, secure two large-bore IV cannulas, start fluid resuscitation.
Signs of severe dehydration (e.g., confusion, reduced urine output): → Catheterise for urine monitoring, start IV fluids, check renal profile and electrolytes urgently.
Severe electrolyte disturbance on ECG (e.g., peaked T-waves, prolonged QT): → Get senior help immediately, start specific electrolyte correction.
Signs of bleeding (melaena, haematemesis, extensive purpura): → Check FBC/coagulation profile, order GXM, alert senior/gastroenterology team.
History:
Common (>50%): Chronic diarrhoea, significant unintentional weight loss, abdominal bloating/flatulence.
Less Common (10-50%): Steatorrhoea (ask specifically: "Are your stools oily, pale, floating, or difficult to flush?"), abdominal pain, peripheral oedema (from hypoalbuminaemia).
Rare (<10% but classic clues): Easy bruising (Vit K def.), bone pain/fractures (Vit D/Ca def.), night blindness (Vit A def.), tetany (Ca/Mg def.), glossitis/angular cheilitis (B vitamin def.).
Pertinent Negatives: Ask about fever/night sweats (r/o TB, lymphoma), blood in stool (r/o active IBD/malignancy), recent antibiotic use (r/o C. difficile).
Physical Examination:
General: Look for muscle wasting, signs of dehydration, pallor.
Peripheries: Check for peripheral oedema, clubbing (IBD), bruising.
Face: Conjunctival pallor, glossitis, angular cheilitis.
Abdomen: May be distended and tympanitic. Check for tenderness or organomegaly.
Neurology: Check for peripheral neuropathy (B12 deficiency).
Clinical Pearl: Don't just rely on the patient's description of diarrhoea. Ask to see the stool chart or the stool itself. The greasy sheen of steatorrhoea is unmistakable once you've seen it.
V. Diagnostic Workflow
Differential Diagnosis:
1. Chronic Pancreatitis:
Points For: History of heavy alcohol use, epigastric pain radiating to the back.
Points Against: Absence of typical pain, no history of acute pancreatitis.
How to Differentiate: Low Fecal Elastase-1 is the most sensitive non-invasive test. CT abdomen may show pancreatic calcification.
2. Celiac Disease:
Points For: Disproportionately severe iron deficiency anaemia, dermatitis herpetiformis rash.
Points Against: Not as common in our population, diet is rice-based not wheat-based.
How to Differentiate: Serology (Anti-TTG IgA) followed by OGD with duodenal biopsy showing villous atrophy.
3. Tuberculous Enteritis:
Points For: Constitutional symptoms (low-grade fever, night sweats), concomitant lung findings on CXR, history of contact. A great mimic.
Points Against: No constitutional symptoms, rapid onset.
How to Differentiate: Colonoscopy with biopsy of terminal ileum (look for caseating granulomas), imaging (CT shows mural thickening of ileocaecal region).
Investigations Plan:
Bedside / Initial (First Hour):
Stool Examination: Look at the stool. Send for microscopy (ova, cysts, fat globules with Sudan stain).
First-Line Labs & Imaging:
FBC: To check for anaemia. Look at the MCV (can be low, normal, or high).
Renal Profile, LFT: Check electrolytes and albumin level.
Nutritional Screen: Iron studies, Vitamin B12, Folic acid.
Coagulation Profile (PT/INR): Functional test for Vitamin K deficiency.
C-Reactive Protein (CRP): May be elevated in IBD or infective causes.
Confirmatory / Second-Line: This is directed by your clinical suspicion.
For Pancreatic Cause: Fecal Elastase-1. CT Abdomen.
For Mucosal Cause: OGD with duodenal biopsy (for Celiac, Whipple's). Colonoscopy with ileal biopsy (for Crohn's, TB).
Serology: Celiac screen (Anti-TTG IgA).
Breath Tests: Hydrogen breath test for Small Intestinal Bacterial Overgrowth (SIBO) or lactose intolerance.
VI. Staging & Severity Assessment
We don't "stage" malabsorption like cancer. We assess its severity based on the clinical and biochemical impact.
Mild: Minimal weight loss (<5% body weight), subclinical or single nutrient deficiency (e.g., isolated iron deficiency).
Moderate: Significant weight loss (5-10% body weight), multiple nutrient deficiencies, mild hypoalbuminaemia without oedema.
Severe: Weight loss >10%, severe hypoalbuminaemia (<25 g/L) with oedema/anasarca, significant electrolyte abnormalities, complications like osteoporosis or coagulopathy.
The severity dictates the urgency of management and whether the patient needs admission versus outpatient workup.
VII. Management Plan
Management is entirely dependent on the underlying cause. Your initial role is to stabilise and investigate.
Immediate Stabilisation (The ABCDE Plan for a severe case):
A/B: Administer high-flow oxygen if hypoxic or severely unwell.
C: IV access. Correct fluid deficits and electrolyte imbalances (e.g., IV Potassium, IV Magnesium). Be cautious with fluid in severe hypoalbuminaemia.
D: Check capillary blood glucose.
E: Look for sources of sepsis if febrile.
Nutritional Support: Give IV Pabrinex (B vitamins) if malnutrition is severe, especially in alcoholics. Consider parenteral nutrition in discussion with the nutrition support team for severe cases.
Definitive Treatment (The Ward Round Plan - Cause-specific):
Chronic Pancreatitis: Pancreatic Enzyme Replacement Therapy (PERT), e.g., Creon®. Dose is titrated to effect, taken with meals. Plus, absolute alcohol cessation and pain management.
Celiac Disease: Lifelong strict gluten-free diet. Refer to a dietitian.
Tropical Sprue: A course of antibiotics (e.g., Tetracycline) and Folic acid supplementation for several months.
IBD / TB: Refer to Gastroenterology/ID for specific management (immunosuppression or anti-tuberculous therapy).
SIBO: A course of non-absorbable antibiotics like Rifaximin.
Long-Term & Discharge Plan:
Dietitian referral is crucial.
Supplementation of deficient vitamins and minerals (oral or parenteral).
Regular follow-up to monitor nutritional status and weight.
Bone density scan (DEXA) to screen for osteoporosis.
VIII. Complications
Immediate: Dehydration, electrolyte disturbances leading to arrhythmias.
Short-Term: Worsening nutritional status, opportunistic infections due to malnutrition.
Long-Term:
Metabolic Bone Disease (Osteoporosis/Osteomalacia): Due to chronic Vitamin D and Calcium deficiency.
Anaemia: Iron, B12, or folate deficiency.
Nephrolithiasis: Increased oxalate absorption in fat malabsorption can lead to calcium oxalate stones.
Increased malignancy risk: Small bowel adenocarcinoma/lymphoma in long-standing Celiac disease; colorectal cancer in IBD.
IX. Prognosis
Prognosis is entirely dependent on the underlying cause and patient adherence.
Good: Excellent for correctly diagnosed and managed Celiac disease or lactose intolerance.
Variable: Good for PERT-adherent chronic pancreatitis patients who stop alcohol. More challenging in severe Crohn's disease.
Poor: In cases of extensive short bowel syndrome or refractory disease.
Key Prognostic Factors: The underlying diagnosis, the extent of small bowel affected, and adherence to treatment.
X. How to Present to Your Senior
Be concise and structured.
"Dr, for review please. This is Mr. [Name] in Bed [X], a [age]-year-old gentleman referred for investigation of chronic diarrhoea and 10kg weight loss over 6 months.
His main issue is frequent, bulky, and oily stools. Clinically, he has signs of malnutrition with muscle wasting and conjunctival pallor.
My main differential is malabsorption, likely secondary to chronic pancreatitis given his significant alcohol history. Other differentials include IBD or an infective cause like TB.
I have sent off a full nutritional screen, stool studies including fecal elastase, and an FBC.
I would like to ask about arranging for a CT abdomen to look at the pancreas and whether we should start empirical vitamin supplementation."
XI. Summary & Further Reading
Top 3 Takeaways:
Always suspect malabsorption in patients with unexplained weight loss, chronic diarrhoea, or anaemia.
Steatorrhoea is the clinical hallmark of fat malabsorption; ask about it specifically.
Your initial job is to investigate broadly (bloods, stool) and then narrow down with specific tests (endoscopy, imaging) based on your top differentials.
Key Resources:
UpToDate: "Approach to the adult with malabsorption" - This is your best starting point for a comprehensive overview.
Amboss: "Malabsorption Syndromes" - Excellent for quick revision and question-based learning.
Malaysian Society of Gastroenterology & Hepatology (MSGH): Check for local guidelines on specific causes like IBD.
Now, go and apply this. Don't just order tests; think about what you're looking for.
