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We present a case of a previously healthy 64-year-old man who presented initially with chest pain and inferior ST elevation acute coronary syndrome. Primary angiography revealed minor left coronary disease and an occluded proximal right coronary artery. Oral loading doses of aspirin 300 mg and prasugrel 60 mg were prescribed. Given significant thrombus burden, intravenous weight-adjusted glycoprotein IIb/IIIa inhibitor abciximab (0.25 mg/kg) and unfractionated heparin (70 units/kg) boluses were given and a 6 Fr Export (Medtronic, Minnesota, USA) aspiration catheter restored thrombolysis in myocardial infarction III flow. Two resolute integrity (Medtronic, Minnesota, USA) drug-eluting stents were successfully deployed. Chest pain and ECG changes resolved, and abciximab infusion (0.125 µg/kg/min) was continued for 12 h. The next morning, the patient developed severe lower back pain with urinary retention, loss of anal sphincter tone, bilateral lower limb areflexia, grade 0 power deficits and T12 sensory level. Urgent MRI of the spine demonstrated an extensive T7–T12 intradural haematoma with spinal cord compression on T2-weighted sagittal (figure 1) and axial sequences (figure 2). Digital subtraction angiography did not reveal any underlying vascular malformation. The patient underwent urgent neurosurgical exploration and evacuation of the intradural haematoma, thoracic laminectomy and posterior durotomy. Repeat MRI 2 weeks later showed no residual haematoma (figure 3), and although paraplegia persisted, aspirin was cautiously restarted. The patient was transferred for rehabilitation and remarkably, after 5 months of intensive therapy, ambulated independently with a frame, regained bladder and bowel function, and was discharged home.

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Figure 1

Thoracolumbar spine MRI T2-weighted sequence. Sagittal view showing extensive hyperintense acute intradural haematoma from T7 to T12 (white arrow).

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Figure 2

Thoracolumbar spine MRI T2-weighted sequence. Axial view showing large hyperintense acute intradural haematoma (white arrow) with significant spinal cord compression.

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Figure 3

Thoracolumbar spine MRI T2-weighted sequence. Sagittal view demonstrating postoperative resolution of haematoma and cord compression.

Non-traumatic spinal intradural extramedullary haematomas (SIEH) are extremely rare. The majority require emergency attention as they can rapidly progress to spinal cord compression. In the largest series of 101 cases of spinal subdural haematomas, the thoracolumbar region was most frequently affected, without a gender predominance.1 Causes of non-traumatic SIEH include iatrogenic (lumbar puncture, spinal anaesthesia/surgery), anticoagulation, haematological disorders, vascular malformations, tumours and an idiopathic aetiology.2 Only 41 cases due to anticoagulation have been reported in the literature in patients on warfarin or low molecular weight heparin. Typical clinical features are sudden onset back or radicular pain with paraplegia and bowel or bladder paralysis. Meningism and headache may be the initial symptoms with predominantly subarachnoid bleeding. MRI is the gold standard for diagnosis of spinal haematomas. The classical finding in intradural haematomas is a concave loculated delineation of isointensity compared with the spinal cord on T1-weighted images, and variable signal hyperintensity on T2-weighted images.3 This is in contrast to epidural spinal haematomas, which appear broad-based and convex. Prompt neurosurgical evacuation and decompression is essential as prognosis is inversely related to duration of cord compression.1

This is the first report of a rare but serious complication in the era of potent antithrombotic therapies in ACS. While these agents have led to significant recent improvements in cardiovascular outcomes, the competing bleeding risk may drive adverse events. Clinicians should be vigilant in monitoring these patients, particularly those at higher risk.