BLIND LOOP SYNDROM
The normal duodenum and
jejunum contain less than 104/mL
organisms which are usually derived from saliva.
In bacterial overgrowth there may be 108-1010/mL organisms, most of which are normally found only in the colon.
Disorders which impair the normal physiological mechanisms controlling bacterial proliferation in the intestine predispose to bacterial overgrowth
The most important are:
() loss of gastric acidity,
() impaired intestinal motility
() structural abnormalities which allow colonic bacteria to gain access to the small intestine.
Causes of small bowel bacterial overgrowth
1- Hypo- or achlorhydria: * Pernicious anaemia *Partial gastrectomy *Long-term PPI therapy
2- Impaired intestinal motility: * Scleroderma *Diabetic autonomic neuropathy *Chronic intestinal pseudo-obstruction
3- Structural abnormalities: *Gastric surgery *Jejunal diverticulosis *Enterocolic fistulas (e.g. Crohn s disease) *Extensive small bowel resection *Strictures (e.g. Crohn s disease) 4- Impaired immune function: *Hypogammaglobulinaemia
Pathophysiology
() diabetic autonomic neuropathy :
reduces small bowel motility and affects enterocyte secretion.
() In scleroderma, bacterial overgrowth occurs because the circular and longitudinal layers of the intestinal muscle are fibrosed, and motility is abnormal.
() In idiopathic hypogammaglobulinaemia : the IgA and IgM levels in serum and jejunal secretions are reduced. these will lead to Chronic diarrhoea and malabsorption occur because of bacterial overgrowth and recurrent gastrointestinal infections particularly giardiasis
Clinical features
The patient presents with watery diarrhoea and/or steatorrhoea with anaemia due to B12 deficiency. These arise because of deconjugation of bile acids, which impairs micelle formation, and because of bacterial utilisation of vitamin B12.
There may also be symptoms from the underlying intestinal cause
Investigations
() Serum vitamin B12 concentration is low, whilst folate levels are normal or elevated because the bacteria produce folic acid. ()Barium follow-through or small bowel enema may reveal blind loops or fistulas.
() Endoscopic duodenal biopsies exclude mucosal disease such as coeliac disease. Jejunal contents for bacteriological examination can be aspirated at endoscopy; the laboratory analysis requires anaerobic and aerobic culture techniques.
()The diagnosis can often be made non-invasively using the glucose hydrogen or 14C-glycocholic acid breath tests.
Bacteria within the small bowel cause an early rise in breath hydrogen from glucose or 14C from 14C-glycocholate.
()Hypogammaglobulinaemia can be diagnosed by measurement of serum immunoglobulins and by intestinal biopsy which shows reduced or absent plasma cells and nodules of lymphoid tissue (nodular lymphoid hyperplasia).
Management
() treat The underlying cause of small bowel bacterial overgrowth. () Tetracycline 250 mg 6-hourly for 7 days is then the treatment of choice, although up to 50% of patients do not respond adequately. () Metronidazole 400 mg 8-hourly or ciprofloxacin 250 mg 12-hourly is an alternative.
()Some patients require up to 4 weeks of treatment and, in a few, continuous rotating courses of antibiotics are necessary. ()Intramuscular vitamin B12 supplementation is needed in chronic cases.
()Patients with motility disorders such as diabetes and scleroderma may benefit from antidiarrhoeal drugs (diphenoxylate 5 mg 8-hourly orally or loperamide 2 mg 4-6-hourly orally).
() In hypogammaglobulinaemia treatment should focus on control of giardiasis and, if necessary, immunoglobulin infusions
Whipple s disease
This rare condition is characterised by infiltration of small intestinal mucosa by foamy macrophages which stain positive with periodic acid-Schiff (PAS) reagent.
The disease is a multisystem one and almost any organ can be affected, sometimes long before gastrointestinal involvement becomes apparent
Pathophysiology
The disease is caused by infection with the Gram-positive bacillus Tropheryma whipplei which is resident within macrophages in the bowel mucosa.
Villi are widened and flattened; densely packed macrophages occur in the lamina propria.
These may obstruct lymphatic drainage, causing fat malabsorption
Clinical features
() Gastrointestinal (> 70%) :Diarrhoea, steatorrhoea, weight loss, bloating, protein-losing enteropathy, ascites, hepatosplenomegaly
() Musculoskeletal (65%) : Seronegative large joint arthropathy, sacroiliitis
() Cardiac (10%) : Pericarditis, myocarditis, endocarditis, coronary arteritis
() Neurological (10-40%) : Apathy, fits, dementia, myoclonus, meningitis, cranial nerve lesions
() Pulmonary (10-20%) Chronic cough, pleurisy, pulmonary infiltrates
() Haematological (60%) Anaemia, lymphadenopathy
() Other : Fever, pigmentation
Management
() Whipple s disease is often fatal if untreated but responds well, at least initially, to intravenous ceftriaxone 2 g daily for 2 weeks, followed by oral co-trimoxazole for at least 1 year.
() Symptoms usually resolve quickly and biopsy changes revert to normal in a few weeks.
()Long-term follow-up is essential, as relapse occurs in up to one-third of patients. in which case the same therapy is repeated or else treatment with doxycycline and hydroxychloroquine is necessary
Ileal resection
Malabsorption may occur as a complication of small bowel resection. Vitamin B12 and bile salt malabsorption develops .
Unabsorbed bile salts pass into the colon, stimulating water and electrolyte secretion and resulting in diarrhoea
()Parenteral vitamin B12 supplementation is necessary.
() Diarrhoea usually responds well to colestyramine, a resin which binds bile salts in the intestinal lumen.
()Aluminium hydroxide is an alternative therapy
Short bowel syndrome
It is defined as malabsorption resulting from extensive small intestinal resection or disease.
Irrespective of the cause, three main types of patient are seen:
1- Jejunal resection with intact ileum and colon. This is uncommon and nutritional support is rarely needed.
2-Jejunum-colon patients (jejuno-ileal resection with jejunocolic anastomosis).
3- Jejunostomy patients (jejuno-ileal resection and colectomy)
Aetiology of short bowel syndrome
Children:
-Congenital anomalies (e.g. mid-gut volvulus, atresia)
-Necrotising enterocolitis
Adults :
-Crohn s disease
-Mesenteric infarction
-Radiation enteritis
-Volvulus
Management
() In the immediate post-operative period, total parenteral nutrition (TPN) should be started.
() PPI therapy is given to reduce gastric secretions.
() Enteral feeding can be cautiously introduced after 1-2 weeks under careful supervision and slowly increased as tolerated.
() For patients with a jejunostomy, parenteral saline is likely to be necessary if less than 100 cm of jejunum remains. If less than 75 cm of small bowel remains, TPN is also needed
() Replacement of vitamin B12, calcium, vitamin D, magnesium, zinc and folic acid.
() Antidiarrhoeal agents, e.g. loperamide (2-4 mg 6-hourly) or codeine phosphate (30 mg 4-6-hourly).
() Octreotide (50-200 ?g 8-12-hourly by subcutaneous injection) reduces gastrointestinal secretions and is useful in such individuals.
() Despite these measures, some patients require long-term home TPN for survival and this is best managed in specialist centres.
() Small bowel transplantation is an option but rejection and graft-versus-host disease remain significant hurdles
Radiation enteritis and proctocolitis
() Intestinal damage occurs in 10-15% of patients undergoing radiotherapy for abdominal or pelvic malignancy.
() The risk varies with total dose, dosing schedule and the use of concomitant chemotherapy
Pathophysiology
() The rectum, sigmoid colon and terminal ileum are most frequently involved.
() Radiation causes acute inflammation, shortening of villi, oedema and crypt abscess formation. These usually resolve completely but in some patients an obliterative endarteritis affecting the endothelium of submucosal arterioles develops over 2-12 months.
() Fibroblastic proliferation produces progressive ischaemic fibrosis over years and may lead to adhesions, ulceration, strictures, obstruction or fistula to adjacent organs.
Clinical features
()In the acute phase there is nausea, vomiting, cramping abdominal pain and diarrhoea. When the rectum and colon are involved, rectal mucus, bleeding and tenesmus occur.
()The chronic phase develops after 5-10 years produces one or more of the following problems
Proctocolitis
- Bleeding from telangiectasia
- Small bowel strictures
- Fistulas: rectovaginal, colovesical, enterocolic
- Adhesions
- Malabsorption: bacterial overgrowth, bile salt malabsorption (ileal damage)
Investigations
() In the acute phase the rectal changes at sigmoidoscopy resemble those of ulcerative proctitis .
() The extent of the lesion is determined by colonoscopy.
()Barium follow-through examination shows small bowel strictures, ulcers and fistulas
Management
() Diarrhoea in the acute phase is treated with codeine phosphate, diphenoxylate or loperamide in standard dosage.
() Local corticosteroid enemas help proctitis,
() antibiotics may be required for bacterial overgrowth.
() Nutritional supplements are necessary when malabsorption is present. Colestyramine (4 g as a single sachet) is useful for bile salt malabsorption.
() Endoscopic laser or argon plasma coagulation therapy may reduce bleeding from proctitis.
() Surgery should be avoided, if possible, because the injured intestine is difficult to resect and anastomose, but it may be necessary for obstruction, perforation or fistula
Abetalipoproteinaemia
This rare autosomal recessive disorder is caused by deficiency of apolipoprotein B which results in failure of chylomicron formation. It leads to fat malabsorption and deficiency of fat-soluble vitamins.
Jejunal biopsy reveals enterocytes distended with resynthesised triglyceride and normal villous morphology
() Serum cholesterol and triglyceride levels are low.
() acanthocytosis, retinitis pigmentosa and a progressive neurological disorder with cerebellar and dorsal column signs.
()Symptoms may be improved by a low-fat diet supplemented with medium-chain triglycerides and vitamins A, D, E and K