JRSM >
Volume 96, Number 12 >
Pp. 591-592
Departments of Neurosurgery and Neuroanaesthesia, National Hospital for Neurology and Neurosurgery, London, UK
Correspondence to: Dr Ahmed Ibrahim, 38 C Camden Road, London NW1 9DR, UK E-mail: aibrahim{at}doctors.net.uk
The use of low-molecular-weight heparin in neurosurgical patients is controversial.
CASE HISTORY
A man of 53 sustained a small frontal contusion in a fall (Figure 1). Initially, he was fully alert and oriented and he was admitted for observation to the local hospital. There was no relevant medical history, and blood results including a clotting screen were normal. A week later he became acutely breathless and was found to have a PaO2 of 9 kPa and raised D-dimers. A pulmonary embolus was suspected and he was started on enoxaparin 120 mg once a day. Within a few hours of receiving the first dose of this low-molecular-weight heparin the patient's level of consciousness began to deteriorate. He was opening his eyes, making incomprehensible sounds and flexing his limbs to painful stimuli (Glasgow coma score 9). A repeat head scan revealed considerable progression of the frontal contusion (Figure 2). After intubation he was transferred to our unit, and on arrival his activated partial thromboplastin time (APTT) was 67 seconds (normal range 22-41). He was managed conservatively in the intensive care unit; an intracranial pressure monitor was not inserted for fear of inducing further haemorrhage. The next day spiral CT of the chest showed no evidence of pulmonary embolus. The APTT gradually improved and was normal within four days. Thereafter he made a good recovery.
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COMMENT
In patients already receiving anticoagulants, the special hazards of head injury are well known. In a retrospective study the case fatality was 50% compared with 20% in a group not receiving anticoagulants.1 The question of thromboembolism prophylaxis in neurosurgical patients is difficult: these patients are commonly immobile for long periods and are prone to deep vein thrombosis, yet haemorrhage into the operation site is more dangerous than in other forms of surgery where heparin prophylaxis is advocated. Nurmohamed and co-workers2 used fractionated or low-molecular-weight heparin in addition to compression stockings postoperatively in neurosurgical patients and reported a clinically significant decrease in venous thromboembolism without increased risk of major bleeding, and Constantini et al.3 found no excess risk from perioperative low-molecular-weight heparin, in a randomized comparison with 0.9% saline, in patients having brain surgery. These studies were in elective neurosurgery. In emergency work, Norwood and colleagues4 gave enoxaparin, 30 mg 12-hourly, to 177 patients admitted with blunt injury and with documented intracranial haemorrhage. Progression of intracranial haemorrhage, on CT, was seen in 4% and the authors concluded that enoxaparin could be used for prophylaxis if started 24 hours or more after the acute admission.
In the case described here, cerebral haemorrhage worsened when a low-molecular-weight heparin was given a week after the original injury—and there were no apparent aggravating factors such as clotting derangements or sepsis. Although the aim was therapeutic rather than prophylactic (pulmonary embolism was suspected), the case does illustrate the hazards of these agents. Most of the published evidence on anticoagulation in head-injured patients is retrospective and thus insecure. For prophylaxis at least, until better evidence emerges, we would favour mechanical measures (antiembolism stockings, intermittent calf compression, physiotherapy) rather than heparins.
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