Three patients are presented with traumatic spinal cord injury (SCI) complicated by acute heterotopic ossification (HO), and concurrent deep vein thrombosis 15 months, 18 months and 22 years after SCI, accompanied by persistent hyper coagulation. The diagnosis of HO preceded deep vein thrombosis in all three patients. All were treated with etidronate disodium and therapeutic heparin followed by oral anticoagulation. As these patients were not acutely injured, the questions arose as to what predisposed them to deep vein thrombosis and when was the appropriate time to discontinue anticoagulation.Over a course of 3 years following deep vein thrombosis, these patients were monitored for evidence of hypercoagulation by D-dimer assay, plasma fibrino gen estimation, and rate of whole blood clotting by Sonoclot® coagulation analyzer. The activity of acute HO was assessed by three-phase bone scan. A steady state of hypercoagulation, reflected by an increase in all three para meters, ran parallel to the extent of acute HO for the entire observation period. Moreover, hypercoagulation was persistently greater during increased acute HO activity even when the warfarin-induced prothrombin time ratio was 1.2-1.5. In addition, as acute heterotopic ossification activity decreased, the test values returned to near normal during warfarin therapy. However, when warfarin was discontinued, the clotting rate and D-dimer levels were found to again increase. Oral anticoagulation was therefore resumed for these patients and will be continued as long as laboratory evidence of hypercoagulation is presentThe usual practice following an episode of thromboembolism is to di'icontinue anticoagulation after a fixed period of 3 months to 1 year. However in patients with SCI who have acute HO, the hypercoagulation may be 101g term. Laboratory monitoring can assist in identifying those patients who may require a prolonged regimen of anticoagulation. The possible role of acute heterotopic ossification in the development of clotting abnormalities is discussed.

Isotope renography was compared to excretory urography, voiding cystourethrography and endogenous creatinine clearances in 52 spinal cord injury patients. Renogram abnormalities were detected in 86 per cent of the cases. The most common abnormality was the delay of isotope excretion from the renal cortex and pelvis. Anticholinergic medication significantly reduced these excretion delays. A subgroup containing 22 newly injured patients was evaluated separately. Renogram abnormalities in this subgroup were associated with normal excretory urography and normal creatinine clearances. We postulate that the defect producing upper tract deterioration in spinal cord injury begins early, is obstructive to renal drainage, does not increase with time and probably requires early intervention with anticholinergic medication or transurethral sphincterotomy to prevent upper tract damage.

OBJECTIVE.Urinary

SummaryA case of percutaneous endoscopic gastrostomy in a quadriplegic patient with aerophagia and symptomatic chronic gastric distention is presented. Gastrostomy is an accepted proce dure for acute and chronic gastric distention in veterinary medicine. In the aerophagic quadriplegic population, this is a viable therapeutic option after failure of medical therapy.Aerophagia in the adult quadriplegic is a significant clinical problem for which no defmite treatment exists. Gastrostomy for feeding and decompression is an estab lished surgical procedure for various indications, and veterinary surgeons employ it to relieve acute and chronic gaseous distention in cattle and dogs. We present a case in which percutaneous endoscopic gastrostomy (PEG) was performed for relief of symptomatic gastric distention in a high-risk quadriplegic patient whose abdomi nal pain and bloating due to aerophagia were refractory to medical management.In our experience in a Department of Veterans Affairs Spinal Cord Injury Cen ter, we have noted chronic gastric dilatation in many quadriplegic patients, appar ently due to aerophagia, and we have treated several patients medically for upper abdominal pain and bloating. It is interesting to speculate whether this condition is caused by a gastro-pyloric dyssynergia analogous to the bladder and anorectal dys synergias found in spinal cord injury patients, and whether inability to belch through unchecked diaphragmatic pressure on the oesophagus is a contributing factor. The preponderance of older individuals with this condition may point to an aetiologic role for chronic anticholinergic administration in gastric hypotony and hypomotility.Acute gastric dilatation due to aerophagia has been recognised in the young quadriplegic (Sutton et al., 1981) and is a life-threatening late complication of spinal cord injury that may cause aspiration, respiratory compromise, and va gaIly mediated bradycardia. Whether acute and chronic gastric dilatation due to aerophagia share a common mechanism is unknown.

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