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Paralytic Ileus and Urinary Retention Due to Hypothyroidism Motor Spastic BRITISH MEDICAL JOURNAL VOLUME 285 14 AUGUST 1982 477 Br Med J (Clin Res Ed): first published as 10.1136/bmj.285.6340.477-a on 14 August 1982. Downloaded from Glaxo Group Research Limited for providing ranitidine and placebo and performing the ranitidine assay. Allan R, Dykes P. A study of the factors influencing mortality rates from gastrointestinal haemorrhage. Qy Med 1976;180:533-50. 2 Jones FA. Haematemesis and melaena with special reference to causation and to the factors influencing the mortality from bleeding peptic ulcers. Gastroenterology 1956;30:166-90. 3MacDougall BRD, Bailey RJ, Williams R. H2 receptor antagonists and antacids in the prevention of acute gastrointestinal haemorrhage in fulminant hepatic failure. Lancet 1977 ;i :617-9. 4 LaBrooy SJ, Misiewicz JJ, Edwards T, et al. Controlled trial of cimetidine in upper gastrointestinal haemorrhage. Gut 1979;20:892-5. 5 Domschke W, Lux G, Domschke S. Furan H2-antagonist ranitidine inhibits pentagastrin stimulated gastric secretion stronger than cimeti- dine. Gastroenterology 1980;79:1267-71. (Accepted 18 May 1982) Division of Medicine, Selly Oak Hospital, Birmingham B29 6JD JOHN DAWSON, BM, MRCP, senior registrar (present address: department of medicine, Queen Elizabeth Hospital, Birmingham B15) ROY COCKEL, MB, FRCP, consultant physician Paralytic ileus and urinary Supine plain abdominal x-ray film showing bladder retention due to hypothyroidism distension and dilated loops oflarge and small intestine. Peripheral neuropathy is a recognised complication of hypothyroidism. innervation to skeletal muscles and the urinary tract musculature may Skeletal muscles, the intestines, and the urinary tract may all be be similarly affected. affected. We report an unusual case in which the patient presented The peripheral and autonomic neuropathy of hypothyroidism may with paralytic ileus and bladder retention, and despite biochemical take many weeks to recover, but even severe atony of the bladder evidence of severe hypothyroidism physical signs of myxoedema were and paralytic ileus are eventually reversible. It is important to con- absent. The patient eventually responded to replacement treatment. sider hypothyroidism as a cause of autonomic or peripheral neuro- pathy even in the absence of overt signs of myxoedema. Correspondence and requests for reprints should be addressed to: Dr A W Case report Nathan, Department of Cardiology, St Bartholomew's Hospital, London A 67-year-old woman was admitted with a history of increasing malaise, EClA 7BE. constipation, difficulty with walking, and urinary incontinence. On examina- tion she was dehydrated and had a distended, tympanic abdomen with scanty Ord WM. Report of the Clinical Society of London. Lancet 1879;ii:577-9. bowel sounds. The bladder was palpable above the umbilicus and this was 2 Wells I, Smith B, Hinton M. Acute ileus in myxoedema. Br MedJ 1977; confirmed radiologically (see figure). She had global muscle wasting with i:211-2. profound weakness of limb and facial muscles. External signs of myxoedema were absent. She had a normochromic, normocytic anaemia (haemoglobin concentration 8 g/dl) due to combined folate (1.1 /Lg/l) and iron (690 /g/l) (Accepted 11 May 1982) http://www.bmj.com/ deficiencies. Plasma urea (22 mmol/l) and creatinine (194 ,tmol/l) concentra- tions were both raised. Urine microscopy showed red and white blood cells, and urine culture grew Escherichia coli. Intravenous urography indicated Royal Free Hospital, London NW3 2QG bilateral hydronephrosis with a distended bladder. A barium enema showed A W NATHAN, MB, MRCP, medical registrar severe dilatation of the large intestine with no obvious physical obstruction, C W H HAVARD, MD, FRCP, consultant physician an appearance typical of intestinal pseudoobstruction. Electromyographic findings were typical of a severe, predominantly motor polyneuropathy. Thyroid function tests indicated severe primary hypothyroidism with a serum thyroxine concentration of < 10 nmolIl, and a raised thyroid-stimulating hormone concentration of 45 mU/l. on 30 September 2021 by guest. Protected copyright. We considered her diagnosis to be hypothyroid polyneuropathy affecting her intestines, urinary tract, and skeletal muscles. Despite intravenous rehydration, blood transfusion, urinary catheterisation, and the administra- Motor spastic paraplegia and tion of thyroxine her condition continued to deteriorate. Nasogastric and unilateral infranuclear facial palsy rectal suction were begun, together with intravenous hyperalimentation and intravenous triiodothyronine (up to 60 pg/day). This regimen had to be con- complicating tetanus tinued for eight weeks before the patient could receive a conventional diet, but her recovery thereafter was uninterrupted. The paralytic ileus resolved and micturition returned to normal, as did her gait. Repeat barium studies We describe a patient with tetanus who developed a purely motor and intravenous urography showed no abnormality. She was discharged home spastic paraplegia and left facial palsy, both of which resolved feeling well, taking only oral thyroxine (200 jig/day). completely. Comment Case report Though combined intestinal and urinary tract involvement in A 20-year-old man was admitted to hospital in October 1980 with a three- hypothyroidism has previously been reported, the combination of day history of body stiffness and inability to stand and asymmetry of the face "internal myxoedema" together with a skeletal polyneuropathy has for the previous two days. He had injured his right foot 15 days before. There not been described. Ord,' in an early description of myxoedema in was no history of head injury, discharge from the ears, or eating seeds of described connective Lathyrus sativus. Examination showed a blood pressure of 130/80 mm Hg, 1879, necropsy findings including widespread lockjaw, abdominal rigidity, and opisthotonos. He was also having frequent tissue infiltration with mucoid degeneration in nervous and muscular tetanic spasms. Facial asymmetry was due to left-sided facial palsy and tissue. More recently, Wells et a12 suggested that the intestinal com- spasm of facial muscles on the right, giving the appearance of a hemi- ponent was caused by an autonomic polyneuropathy with Schwann risus sardonicus. Hearing and taste were normal. Neurological examination cell degeneration possibly due to mucopolysaccharide deposition; the showed purely motor, upper motor neurone spastic paraplegia with hyper- 478 BRITISH MEDICAL JOURNAL VOLUME 285 14 AUGUST 1982 Br Med J (Clin Res Ed): first published as 10.1136/bmj.285.6340.477-a on 14 August 1982. Downloaded from reflexia and bilateral extensor plantar reflexes. Power in the legs was grade 2 inhalation. These became sustained, and he was in cardiopulmonary arrest and remained so during the clinical phase of tetanus, with gradual recovery on admission. Asystole was converted to ventricular fibrillation by intra- subsequently. No sensory or sphincteric abnormality was observed during the venous injection of 2 ml of 1:1000 adrenaline and 10 ml 10% calcium illness. gluconogalactogluconate. Cardioversion resulted in a supraventricular The patient was given 20 000 IU antitetanus serum intramuscularly after tachycardia, which was converted to sinus rhythm by 10 mg sotalol given a sensitisation test. Injections of diazepam, chlorpromazine, and pheno- intravenously. Spontaneous respiration was not restored, and artificial barbitone were used to control the spasms, with adequate parenteral and ventilation was instituted after muscle relaxation by suxamethonium. Urine oral feeding. He made an uneventful recovery from tetanus, and about one analysis showed large amounts of strychnine.5 He remained deeply comatose month after onset plain radiography of the thoracolumbar spine, cerebro- but was free of convulsions. Nine hours after admission he had a fatal spinal fluid examination (including a Venereal Disease Research Laboratory cardiac arrest. test), and myelography showed nothing abnormal. He still had the facial Three of the four remaining patients complained of pain and stiffness in palsy but could stand with support. Hyperreflexia and extensor plantar the paravertebral muscles within 30 minutes of inhalation. Convulsions, responses were still evident. At follow up two months after discharge the characterised by risus sardonicus, opisthotonus, flexor spasm of upper facial palsy was barely discernible and he could walk unaided. Mild hyper- limbs, and extensor spasm of lower limbs, occurred with minimal sensory reflexia with equivocal plantar responses were elicited. Follow up at one year stimuli. They were treated in a quiet dark room. Diazepam 10 mg intra- showed no neurological deficit. venously controlled convulsions and was repeated one hour later in two patients in whom convulsions recurred. Diazepam was continued in an oral dose of 5 mg six-hourly, and the patients remained free of convulsions. Comment Hyperaesthesia and hyperreflexia with associated paravertebral myalgia persisted for 48 to 72 hours. Diazepam was discontinued 72 hours after This patient showed the characteristic features of tetanus, and 12 admission. Serum creatine phosphokinase activity was raised in all patients days before onset he had injured his foot. In view of the paraplegia (mean 1980 IU/1; normal < 130 IU/l), and estimation of isoenzymes showed was considered; lathyrism is common in this region.l The raised muscle-type (MM) creatine kinase activity, indicating damage to lathyrism skeletal muscle during the convulsions.
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