Anemia is often a complication following spinal cord injury which interferes with the patient's rehabilitation. Hematological profiles of 65 male patients with traumatic spinal cord injury revealed a 52.3% incidence of mild anemia. The age, duration or level of injury had no correlation with the incidence and type of anemia. The anemia was normocytic-normochromic in 32%, normocytic mild hypochromic in 56%, and microcytic hypochromic in 12% of the patients. Factors in pathogenesis included decubitus ulcers, urinary tract infections, acute and chronic blood loss, and folic acid deficiency due to psychosocial maladjustment, alcohol and/or drug abuse. Often, multiple factors were operative in changing proportions. The success of management depends on a careful assessment of causes and removal of inciting factors. The most common type of anemia was that due to chronic disorder, associated with either decubitus ulcers and/or urinary tract infections. Since this type of anemia mimics iron deficiency in presentation it should be differentiated from the latter by evaluation of iron status. Normal hemoglobin levels can be attained only after the chronic disorder is eliminated. Unpredictable fluctuations of hemoglobin level secondary to changes in plasma volume due to autonomic hyperreflexia are common in SCI patients, and should be taken into account for diagnosis and follow-up in therapy.

Protamine is a considerably weaker anticoagulant than heparin. At a concentration in plasma of 0.05 mg (5 units/ml), heparin rendered the plasma incoagulable, while protamine produced only a mild-to-moderate lengthening of activated partial thromboplastin time (APTT) and prothrombin time (PT). Protamine concentrations between 0.3 and 1.0 mg/ml of plasma produced marked prolongation of APTT and PT, but the thrombin time (TT) was shortened. Between protamine concentrations of 1 and 2 mg/ml of plasma, the fibrinogen was precipitated to a variable degree, the APTT and PT were more than 200 sec, and the TT was moderately prolonged. High doses of protamine prolonged APTT, simulating heparin effect. Although APTT is prolonged both by heparin and protamine, TT is either normal or shortened in protamine excess and prolonged in heparin excess. To differentiate between the protamine and heparin excess, a combination of APTT and TT, supplemented by an estimation of fibrinogen and fibrin-fibrinogen split products, is recommended. The significance of these observations in the interpretation of the tests on blood coagulation is discussed.

Abstract. Fifty acute SCI patients are reviewed retrospectively for incidence of deep vein thrombosis and pulmonary embolism and the problems encountered in the diagnosis. The possible role of some risk factors in triggering thromboembolism and the consequent implications in anticoagulant therapy are discussed.

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.

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