MALDIGESTION AND MALABSORPTION
Classically, maldigestion is defined as defective hydrolysis of nutrients, and malabsorption is defined as defective mucosal absorption. Although this distinction may be useful on pathophysiologic grounds, the clinical presentation and complications of maldigestion and malabsorption are similar. When the distinction between these terms is not of clinical relevance, only the terms absorption and malabsorption are used. ETIOLOGY AND PATHOPHYSIOLOGY From a pathophysiologic point of view, mechanisms causing malabsorption can be divided into premucosal (luminal) factors, mucosal factors, and postmucosal factors (vascular and lymphatic). For clinical purposes, this approach is of limited value, because the various clinical pictures caused by malabsorption syndromes are determined mainly by the nature of the malabsorbed substrates. We therefore discuss the mechanisms causing malabsorption on the basis of the malabsorbed substrate.CLINICAL FEATURES AND EVALUATION Diagnosis of malabsorption requires suspecting its presence, confirming its existence, and demonstrating its cause. History and Physical Examination Gastrointestinal : Diarrhea (watery or steatorrhea), Abdominal distention, flatulence , Foul-smelling flatulence or stool , Pain , Ascites . Musculoskeletal : Tetany, muscle weakness, paresthesias , Bone pain, osteomalacia, fractures Cutoneous and Mucosal : Easy bruisability, ecchymoses, petechiae , Glossitis, cheilosis, stomatitis, Edema , Acrodermatitis, scaly dermatitis , Follicular hyperkeratosis , Hyperpigmented dermatitis , Thin nails with spoon-shaped deformity , Perifollicular hemorrhage , Spiral or curly hair . Other : Weight loss, hyperphagia , Growth and weight retardation, infantilism , Anemia , Kidney stones , Amenorrhea, impotence, infertility , Night blindness, xerophthalmia , Peripheral neuropathy , Fatigue, weakness , Neurologic symptoms, ataxia .
Laboratory Findings Blood Cell Count: Hematocrit, hemoglobin(Decreased in iron, vitamin B12, and folate malabsorption or with blood loss) Mean corpuscular hemoglobin or mean corpuscular volume(Decreased in iron malabsorption; increased in folate and vitamin B12 malabsorption ) White blood cells, differential(Decreased in vitamin B12 and folate malabsorption; low lymphocyte count in lymphangiectasia). Biochemical Tests (Serum ): Triglycerides(Decreased in severe fat malabsorption) Cholesterol(Decreased in bile acid malabsorption or severe fat malabsorption) Albumin(Decreased in severe malnutrition, lymphangiectasia, protein-losing enteropathy) Alkaline phosphatase(Increased in calcium and vitamin D malabsorption (severe steatorrhea); decreased in zinc deficiency) Calcium, phosphorus, magnesium(Decreased in extensive small intestinal mucosal disease, after extensive intestinal resection, or in vitamin D deficiency) Zinc(Decreased in extensive small intestinal mucosal disease or intestinal resection) Iron, ferritin(Decreased in celiac disease, in other extensive small intestinal mucosal diseases, and with chronic blood loss)
Other Serum Tests : Prothrombin time(Prolonged in vitamin K malabsorption) β-Carotene(Decreased in fat malabsorption from hepatobiliary or intestinal diseases) Immunoglobulins(Decreased in lymphangiectasia, diffuse lymphoma) Folic acid(Decreased in extensive small intestinal mucosal diseases, with anticonvulsant use, in pregnancy; may be increased in small intestinal bacterial overgrowth ) Vitamin B12(Decreased after gastrectomy, in pernicious anemia, terminal ileal disease, and small intestinal bacterial overgrowth) Methylmalonic acid(Markedly elevated in vitamin B12 deficiency) Homocysteine(Markedly elevated in vitamin B12 or folate deficiency)Stool Tests : Fat(Qualitative or quantitative increase in fat malabsorption) Elastase, chymotrypsin(Decreased concentration and output in exocrine pancreatic insufficiency) pH(Less than 5.5 in carbohydrate malabsorption)
Biopsy : Examination of endoscopic biopsy specimens from the duodenum may be diagnostic or highly suggestive of a variety of small bowel disorders resulting in malabsorption ; follow-up small intestinal biopsy can be used to assess treatment effects. two or three jumbo duodenal or jejunal biopsy specimens usually are sufficient to allow histologic sectioning parallel to the villi and crypts. Specimens also may be obtained with smaller forceps, although the number of specimens obtained must then be increased to four to six. Charaterstic histological feature of malabsorption is villous atrophy. Aspiration : Fluid aspirated from the descending part of the duodenum may be examined microscopically for Giardia lamblia or cultured to detect bacterial overgrowth in patients with diffuse small intestinal motility disorders . ABDOMINAL IMAGING Small Bowel Follow-through and Small Bowel Enteroclysis Abdominal Computed Tomography Magnetic Resonance Imaging of the Small Intestine
DDX of villous atrophy: 1- celiac disease 2- tropical sprue 3- Infection (due to Giardia lamblia, Cryptosporidium) 4-AIDS enteropathy 5- Whipple's disease 6-Drug-induced enteropathy (NSAIDs, colchicine, neomycin) 7-Food protein hypersensitivity (rye, barley, egg, fish, rice, poultry) 8-Immunodeficiency (hypogammaglobulinemia) 9-Lymphoma 10-Prolonged folate or cobalamin deficiency 11- Crohn's disease 12-Protein-calorie malnutrition 13- zollinger Ellison syndrome 14- Chronic radiation damage 15-Traumatic injury
GENERAL APPROACH TO MANAGEMENT Treatment of malabsorptive diseases must be directed against the underlying condition, if possible. In addition, nutritional deficits must be corrected. In pancreatic insufficiency, in disorders of intestinal fat absorption, and in short bowel syndrome, medium-chain triglycerides can be used as a source of dietary calories, these patients, therefore, should consume a diet rich in carbohydrates and medium-chain triglycerides. In bile acid malabsorption after extensive ileal resections, intestinal fat absorption can be improved markedly by oral administration of natural conjugated bile acids or of synthetic cholylsarcosine. Replacement of conjugated bile acids also reduces urinary oxalate excretion and therefore should protect against development of kidney stones. Patients with cystic fibrosis or short bowel syndrome who are unable to absorb vitamin D from their diet may benefit from treatment with an ultraviolet lamp, which emits ultraviolet radiation similar to sunlight.
In patients with malabsorption and an intact colon, fluid depletion must be avoided to prevent kidney stones associated with hyperoxaluria.[326] In patients with malabsorption syndrome, special care should be given to the replacement of vitamins, iron, calcium, and trace elements to avoid deficiency syndromes. In patients with diarrhea, symptomatic treatment with opiates or loperamide can increase the time available for absorption of nutrients.