Intestinal Pseudo-Obstruction - a Review

Postgraduate Medical Journal (1985) 61, 1033-1038 Postgrad Med J: first published as 10.1136/pgmj.61.722.1033 on 1 December 1985. Downloaded from

Review Article

Intestinal pseudo-obstruction - a review

Peter Isaacs' and Ali Keshavarzian2* 'Guy's Hospital, London SE] and2Hammersmith Hospital, London W12, UK.

Introduction Pseudo-obstruction is an abnormality of intestinal After meals, mixing and an aborad movement of the motility severe enough to produce the clinical features contents is produced by segmenting contractions of of intestinal obstruction. the small bowel. Gastric emptying andjejunal motility Normal intestinal motility depends upon the are inhibited by the presence of nutrients in the distal modulation by nerves and hormones of the intrinsic small bowel (Spiller et al., 1984). rhythmical contractility of the smooth muscle syn- Abnormalities of gut motility may be produced by cytium. Contraction occurs when hyperpolarising disorders which affect the gut nerves, muscle layers,

action potentials (spikes or electrical response activity, both of these or abnormal gut collagen and inter- Protected by copyright. ERA) coincide with the peaks of a continuously stitium (See Table I). fluctuating potential difference across the cell mem- brane (slow wave or electrical control activity, ECA) (Brading, 1979). Spike potentials are triggered by Table I Aetiological classification of intestinal pseudo- neurotransmitters but because of the fixed rate of the obstruction slow wave, the rhythmic contractile response also has a fixed maximum rate (3 c.p.m. in stomach, 12 c.p.m. Gut nerve dysfunction in duodenum and 8 c.p.m. in ileum of man; Duthie, Toxic - drugs, heavy metals, insecticides. 1979). The contraction ofthe intestinal muscle coats is Metabolic - amyloidosis, diabetes mellitus, porphyria, integrated by the myenteric plexus whose neurones paraneoplastic Inflammatory - Chagas' disease, varicella, Kawasaki lack specialized neuro-effector junctions but have disease, vancosities containing vesicles which release a wide Genetic - congenital and familial visceral neuropathy. variety of neurotransmitters including acetylcholine, noradrenaline, 5HT, peptides and purines (Burnstock, Gut muscle dysfunction 1982). Nicotinic cholinergic fibres mediate the rapid Familial visceral myopathy. http://pmj.bmj.com/ inhibitory descending reflex and purinergic fibres Dystrophia myotonica. mediate the slower excitatory descending pathway Polymyositis. (Hirst, 1979). The myenteric plexus also propagates the inter-digestive myoelectric complex (IMC) (Sarna Disorders affecting gut muscle andnervefunction Myxoedema. et al., 1981) which, in fasting man, sweeps aborally the Phaeochromocytoma. length of the small intestine at intervals of 15 to Hypoparathyroidism. 195 min, clearing the intestinal lumen. An abnormal Pregnancy. on September 30, 2021 by guest. bacterial population supervenes when IMC are aboli- Enteroglucagonoma. shed or absent. IMCs are stimulated by vagal activity Trauma. (Wingate, 1982), motilin (Itoh et al., 1981) and Jejuno-ileal bypass. suppressed by the ingestion of meals (Heppell et al., 1983). Disorders ofgut collagen andinterstitium Scleroderma. Radiation. Correspondence: P. Isaacs, M.D., M.R.C.P. Gastroen- Strongyloidosis. terology Unit, Victoria Hospital, Blackpool, FY3 8NR. Ehlers-Danlos syndrome. *Present address: Gastrointestinal Division, V.A. Medical Mesenteric panniculitis. Center, Baltimore, MD 21218, USA. Ceroidosis. Accepted: 14 May 1985 i) The Fellowship of Postgraduate Medicine, 1985 1034 P. ISAACS & A. KESHAVARZIAN Postgrad Med J: first published as 10.1136/pgmj.61.722.1033 on 1 December 1985. Downloaded from

Disorders of gut nerves al., 1979). In endemic areas Chagas' disease produces widespread abnormality of gut function (Oliveira et Drugs which inhibit intestinal motility are the most al., 1983) due to the inflammatory reaction in the common cause of acute pseudo-obstruction, par- myenteric plexus (Smith, 1980). ticularly atropine-like drugs (Faulk et al., 1978), phenothiazines (Sriram et al., 1979), clonidine (Bear & Steer, 1976), tricyclic antidepressants and vincristine Disorders of gut muscle (Rosenberg & Caridi, 1983). A wide variety ofdiseases may damage the myenteric plexus but the mor- Failure of development of duodenal musculature has phological changes have to be extensive before symp- been reported (Handelsman et al., 1965) but inherited toms are produced (Smith, 1982). Congenital abnor- metabolic abnormalities of gut and muscle usually malities of the myenteric plexus are usually evident present later. Hereditary visceral myopathy is a degen- soon after birth because of vomiting or obstruction eration ofthe longitudinal muscle coat inherited as an and are sometimes associated with pyloric hypertro- autosomal dominant (Schuffier & Pope, 1977) Sub- phy and malrotation of the gut (Tanner et al., 1976), clinical achalasia-like abnormality of the oesophagus patent ductus arteriosus (Harris et al., 1976) or or intestinal pseudo-obstruction may occur in associa- urogenital tract plexus degeneration (megacystis- tion with urogenital tract smooth muscle degeneration microcolon-intestinal hypoperistalsis) (Jountz, 1981), (Faulk, 1978). An autosomal recessive-type associated which is probably due to cholinergic neurone loss. with ophthalmoplegia has been described (Anuras et Inherited generalized disease of the autonomic al., 1983). Investigations of relatives may help in nervous system (familial dysautonomia, Riley-Day making the diagnosis and in genetic counselling. syndrome) and congenital ganglioneuromatosis (Car- Skeletal muscle disorders such as dystrophia ney et al., 1976) lead to small bowel pseudo-obstruc- myotonica (Lewis & Daniel, 1981) and polymyositis tion, pyloric hypertrophy and megacolon probably (Patterson & Rios, 1959) may produce abnormal because both adrenergic and cholinergic nerves are gastric and duodenal motility. Protected by copyright. involved. Familial myenteric plexus degeneration (Schuffler et al., 1978) is associated with generalized evidence of Disorders affecting gut muscle and nerve autonomic dysfunction, ataxic gait and hypotonia. The pupils are hyper-reactive to pilocarpine suggest- A wide variety of metabolic abnormalities may affect ing a denervation hypersensitivity due to cholinergic both gut nerve and muscle function. Myxoedema neurone degeneration. Other families exhibit an slows small bowel transit (Shafer et al., 1984) achalasia-like abnormality of the oesophagus and sometimes producing acute pseudo-obstruction abnormal duodenal motility which responded normally, (Salerno & Grey, 1978). Congenital hypopara- to cholinergic agents suggesting deficiency of non- thyroidism may also produce intestinal pseudo-obs- adrenergic inhibitory mechanisms (Lewis et al., 1978). truction (Cockel et al., 1973). In diabetes mellitus, autonomic neuropathy is com- Pregnancy slows intestinal transit and renders IMCs mon, gastric emptying is frequently impaired (Loo et less frequent (Scott et al., 1983) and pseudo-obstruc- al., 1984) but small bowel pseudo-obstruction is rare. tion is particularly frequent following Caesarian sec- http://pmj.bmj.com/ Acute colonic dilatation may occur as a terminal event tion (Ravo et al., 1983). in severe diabetes (Paley et al., 1961). Abdominal pain, vomiting, constipation or pseudo- Intestinal pseudo-obstruction is also usually a ter- obstruction may be presenting symptoms of phaeo- minal event in secondary amyloidosis (Legge et al., chromocytoma (Turner, 1983) and the risks of 1970) but in familial amyloidosis with polyneuropathy, laparotomy in both this condition and in myxoedema episodic diarrhoea and constipation are typical. The are particularly high. amyloid deposition in gut nerve is responsible for the A unique patient with an enteroglucagonoma had abnormal gut response to cholinergic agents (Battle et chronic constipation and villous hyperplasia (Gleeson on September 30, 2021 by guest. al., 1979). Rarer degenerative disease of the myenteric et al., 1971) but no other peptide hormone secreting plexus such as glycolipid deposition in Fabry's disease tumours have been reported as causing pseudo-obs- (Friedman et al., 1984) and porphyria (Gorchein et al., truction. 1982) may present as pseudo-obstruction syndromes. The mechanism of acute pseudo-obstruction of the In Europe and North America infective neuropath- colon after blunt abdominal trauma with sepsis (Ad- ies are rare but have been reported following varicella dison, 1983) may be akin to pseudo-obstruction ofthe (Walsh, 1982) and in some sporadic cases ofmyenteric colon after jejunal-ileal bypass which is improved by plexus damage, immune reactions to an infective agent antibiotic therapy, suggesting that the bacterial similar to that seen in mucocutaneous lymph node production ofsubstances toxic to gut nerve and muscle syndrome (Kawasaki disease) is possible (Franken et is responsible. INTESTINAL PSEUDO-OBSTRUCTION 1035 Postgrad Med J: first published as 10.1136/pgmj.61.722.1033 on 1 December 1985. Downloaded from

Abnormalities of gut collagen and interstitium horizontal sections through the gut wall fixed as a sheet (Smith, 1982) (Figure 1) will show abnormalities In comparison with skeletal muscle, smooth muscle not seen by routine histological techniques (Krish- contains much more collagen and disordered collagen namurthy & Schuffier, 1983) and special stains to metabolism produces intestinal dysmotility. show fibrous tissue and muscle will help differentiate The excess collagen in scleroderma leads to bowel systemic sclerosis from chronic idiopathic intestinal symptoms ranging from pseudo-obstruction, vol- pseudo-obstruction (Schuffier & Beegle, 1979), alth- vulus, perforation and diverticulosis (Krishnamurthy ough even electron microscopic appearances may be et al., 1983). Steatorrhoea appears to be due to normal in some cases. Suction biopsy of the jejunal bacterial overgrowth occurring in the absence ofIMCs mucosa is useful in excluding coeliac disease but the (Rees et al., 1982). nerve fibres visible in these specimens are not known Irradiation-induced recurrent pseudo-obstruction to reliably reflect changes in the myenteric plexus. is also related to gut fibrosis and is particularly likely If a treatable cause for pseudo-obstruction cannot after pelvic irradiation (Lopez et al., 1981) and similar be found, management is directed to reducing gaseous fibrosis may result in severe strongyloidiasis (Barth- distension, combatting bacterial overgrowth and olomew, 1977). Mesenteric panniculitis (Tytgat et al., stimulating intestinal motility. Schuffier (1981) finds 1980), malignant disease of the mesentery or rare infiltrative disorders, such as ceroidosis (Boller et al., 1976), may produce intestinal pseudo-obstruction mainly by reducing compliance of the bowel wall, but some involvement of the nerve supply may occur.

and Investigation management ofintestinal pseudo- Protected by copyright. obstruction A carefully taken history will frequently detect clues to the presence of intestinal dysmotility. Previous laparotomies with negative findings, oesophageal or intestinal dysfunction in relatives (Schuffier & Pope, 1976) or clinical features suggesting abnormal motility in more than one area of the gut should suggest chronic idiopathic intestinal pseudo-obstruction. A history or clinical features of scleroderma, thyroid disease, diabetes or skeletal myopathy should be sought and a careful drug and radiotherapy history obtained. The investigation of dysmotility could require the elimination of a wide variety of metabolic and en- http://pmj.bmj.com/ docrine causes (Snape, 1981) but clearly the investigation plan should be tailored to the clinical problem. Assessment of oesophageal motility by manometry, cineradiography or scintigraphy is of value in assess- ing patients with presumed visceral myopathy. Radiological examination of the small intestine, preferably by barium infusion, is essential to eliminate sub-acute small bowel obstruction (Schuffler et al., on September 30, 2021 by guest. 1976). Jejunal manometry detects pseudo-obstructive Figure 1 Examples of myenteric plexus pathology. motility but because intubation in itselfwill accelerate (top) Myenteric plexus from the small intestine of a child intestinal motility (Read et al., 1983), non-invasive of 7 months dying from total peristaltic failure. The transit measurements using breath hydrogen monitor- extrinsic trunks are normal and well formed but do not ing after ingestion of non-absorbed carbohydrates appear to communicate at all with the ganglia which may be preferred as a contain neurones without processes. first assessment. Oower) A myenteric ganglion from a patient dying from If a laparotomy is carried out and no obstructing carcinoma of the bronchus. The ganglion is invaded by lesion is found, a full thickness biopsy of the intestine lymphocytes and there is severe neuronal damage. Re- should be considered, particularly when a previous produced from Smith (1982) by kind permission of the laparotomy has also been negative. Silver stains of author. 1036 P. ISAACS & A. KESHAVARZIAN Postgrad Med J: first published as 10.1136/pgmj.61.722.1033 on 1 December 1985. Downloaded from

that patients with idiopathic pseudo-obstruction are ileostomy became obstructed with impacted hard most comfortable on a low-lactose and low-fibre diet faeces. Small bowel pseudo-obstruction complicating which minimizes gas production. Treatment of bac- jejuno-ileal bypass is an indication that the bypass terial overgrowth with intermittent antibiotic therapy should be reversed (Wills, 1978) but colonic dilatation can produce periods of prolonged improvement can temporarily be controlled by antibiotics active especially in scleroderma, possibly because the abnor- against obligate anaerobes (Barry et al., 1977). mal bacterial population itself is contributing to the Chronic symptoms and severe malabsorption may abnormal motility (Justus et al., 1983). A wide variety necessitate parenteral nutrition (Greenall, 1983) and of drugs has been used to stimulate gut motility, some patients on total parenteral nutrition long-term including combinations ofcholinergic and adrenolytic may be enabled to take some social meals without pain agents. Neely & Catchpole (1971) improved post- and distension if a subtotal resection of their small operative ileus with a combination of guanethidine intestine is carried out (Anuras, 1978). 20 mg intravenously followed by repeated doses of Colonic pseudo-obstruction may be distinguishable bethanechol 2.5 mg subcutaneously or prostigimine from luminal obstruction by the presence of normal 0.05 mg intravenously and this regime was also used faecal consistency and haustral pattern on plain with benefit in patients with chronic idiopathic intes- abdominal X-ray (Byrne et al., 1981). Persisting tinal pseudo-obstruction by Ballet et al. (1982). There dilatation of the transverse colon or the caecum to have been no double-blind trials of drugs in pseudo- more than 12 cm indicates a risk of perforation obstruction other than one ofmetoclopramide, which (Melzig & Terz, 1978) which is usually caecal (Bern- proved ineffective (Lipton & Knauer, 1980). Non- ton, 1983). A barium enema given without bowel steroidal anti-inflammatory drugs appeared to be preparation can sometimes relieve colonic pseudo- useful in rare patients with excessive circulating pros- obstruction (Dudley, 1958) in addition to giving taglandins (Luderer et al., 1983) although the response diagnostic information, but preferably the colon is may not be sustained. For an acutely dilated gut, decompressed by colonoscopy, either directlyProtected by copyright. intubation and aspiration followed by a gradual (Nivatvongs et al., 1982) or by leaving a tube in the reintroduction of elemental diet has been successful caecum (Groff, 1983). Colonoscopy also detects (Gibbons & Sullivan, 1978). mucosal necrosis which is a strong indication for Unfortunately, idiopathic intestinal pseudo-obs- colectomy. Colostomy in this condition carries a high truction is often diagnosed only after a number of mortality and probably should not be performed negative exploratory laparotomies. Resection is best (Addison, 1983). avoided (Schuffier & Deitch 1980) but may be ben- The syndromes ofintestinal pseudo-obstruction are eficial to patients with severe localized abnormalities. a continuing challenge to the clinician and our increas- Radical resection of a megaduodenum may be neces- ing understanding of abnormalities of gut muscle and sary if there is no improvement after a duodenojejun- nerve renders it likely that more forms of intestinal ostomy (Newton, 1968). Because bacterial overgrowth dysmotility will be detected as investigative techniques in the dilated gut leads to high septic complication improve. rate, antibiotic preparation of the bowel as for colon surgery is recommended (Schuffier & Deitch, 1980). In some patients with severe small bowel distension Acknowledgements http://pmj.bmj.com/ temporary ileostomy is of value (Keshavarzian et al., 1983) although we have observed one patient with My thanks to Catherine Weeks and Joan Hodskinson for idiopathic intestinal pseudo-obstruction in whom the their patient secretarial assistance.

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