Teaching Case

A 24-year-old female presented acutely with severe neck pain after being displaced from an inflatable dinghy towed by a Jet Ski. There was no loss of consciousness or neurological symptoms. On presentation, the patient was neurologically intact with only severe upper neck pain.

An initial CT cervical spine was provisionally reported with no fracture or malalignment. She was discharged home with oral analgesia.

Subsequent radiology consultant review the following morning identified a cervical subdural haematoma and the patient was recalled urgently for a complementary MRI study.

MRI cervical and thoracic spine revealed extensive subdural haematoma extending from the clivus to T8 without evidence of cord compression, fracture or a ligamentous injury. The rest of the spine or brain was not imaged at this point as the patient was transferred to a tertiary neurosurgical centre.

Subsequent MRI of her entire neuroaxis confirmed extensive subdural blood extending from the craniocervical junction to the lumbar canal. Small volume subdural haemorrhage was also noted along the tentorium cerebellum, thought to be contiguous with the spinal subdural.

The pathophysiology of spinal subdural haematoma (SSDH) is not fully understood and there have been several proposed mechanisms. In contrast to the pathophysiology of intracranial SDHs, there are no bridging veins in the spinal subdural space [1]. Rader proposed that, in trauma, a sudden increase in thoracoabdominal pressure increases the pressure in spinal vessels as they cross the subdural and subarachnoid spaces causing rupture [2].
An alternative proposed mechanism suggests that raised intracranial pressure increases shearing forces between the spinal subdural and subarachnoid spaces resulting in tearing and bleeding of the inner dural layer [3]. In contrast to epidural haemorrhage, blood within the subdural space at the clivus is not constrained by ligamentous attachments and is free to diffuse caudally as well as cranially into the ventral and retrocerebellar parts of the posterior fossa [4].

Though it has been postulated that SSDH may result from caudal redistribution of intracranial SDH to the most dependent areas, based on the site of maximal pain, we consider it unlikely in this case [1, 5].

MRI is most the appropriate imaging modality to visualise spinal haematoma, though non-contrast CT is useful in compartmentalising the haematoma [6]. The typical CT appearance of SSDH is a hyperdense lesion within the dural sac, distinct from adjacent low-density epidural fat [6]. MRI typically demonstrates a subdural-extramedullary heterogeneous mass of variable signal intensity which may show clumping, loculation, and streaking of blood within the dural space [6]. Extension into the posterior fossa is an indicator of its subdural location [7].

Definitive surgical decompression of SSDH is not well established and depends on the clinical scenario. Prompt neurosurgical management is required in patients with severe neurological deficits (Grade D or worse on the Frankel grading scale) to prevent irreversible neurological damage [3, 8]. Patients without neurological symptoms or with mild symptoms may be managed conservatively [9]. Our patient did not show neurological deficits and made a full recovery following conservative management. Importantly, the finding of a traumatic SSDH requires imaging of the whole neuroaxis, ideally with MRI [6].