Pearls & Oy-sters: Delayed traumatic intracerebral hemorrhage caused by cerebral venous sinus thrombosis

DISCUSSION

Delayed traumatic ICH was first described by Bollinger¹ in 1891, who proposed diagnostic criteria including a definite traumatic history, an asymptomatic period after trauma, a delayed event of apoplexy, and absence of previous vascular disease. A variety of possible pathogeneses of delayed traumatic ICH have been proposed and include local or systemic coagulation abnormalities, necrosis of blood vessels in areas of brain injury, transient cerebral dysautoregulation, and reduction of the intracranial pressure either medically or surgically.^2,3 Our patient presented with a clear symptom-free interval and the initial head CT did not show any type of hemorrhage. He did not have coagulation disorders, use of an antithrombotic agent, or previous vascular abnormalities. Therefore, his condition should be compatible with delayed traumatic ICH.¹ Importantly, the finding of focal hyperdensity with air bubbles inside on the initial CT hints at the existence of cerebral venous sinus thrombosis (CVST) and adjacent temporal bone fracture.

Although a causal relationship between the occurrence of delayed ICH and traumatic CVST is not certain, the impairment of venous return originally through the superior sagittal sinus and vein of Labbé may theoretically increase regional intracranial pressure and contribute to delayed ICH. One study showed that the superior sagittal sinus is the most commonly involved head injury–related CVST.⁴ Other cerebral venous sinus, such as sigmoid sinus in our proposed case, is less common, although the association between basilar skull fracture caused by head trauma and transverse/sigmoid venous thrombosis has been mentioned.^4,5

The finding of CVST in our case could have been overlooked if no further neurovascular imaging had been performed.⁶ The concurrent existence of delayed ICH and traumatic CVST is uncommon in head injury patients; another possible explanation for the coexistence of these 2 conditions being rarely reported is the difficulty in identifying CVST on routine noncontrast head CT.⁶ Vascular imaging such as CT angiography/venography or magnetic resonance angiography/venography should be considered for a head injury patient with unusual presentations such as delayed ICH.^7,8

So far, there is no consensus on the treatment of delayed traumatic ICH and CVST. Because the use of anticoagulant in a traumatic patient may increase risk for bleeding, some suggest that the management of patients with traumatic CVST can start with hyperosmolar therapies for intracranial pressure control. There is a paucity of literature regarding choice, dose, concentration, duration, and monitoring parameters of hyperosmolar therapy. Selection of hyperosmolar therapy should be individualized to the patient's condition. Generally, mannitol is dosed 0.25–1.0 g/kg, with low dose in renal impairment. Commercially available hypertonic saline ranges from 3% to 23.4%. Bolus dosing with 250 mL of 3%, 2 mL/kg of 7.5%, or 30 mL of 23.4% hypertonic saline has been advocated.⁹ If further deterioration of neurologic signs happens despite adequate control of increased intracranial pressure, systemic anticoagulation, surgical decompression, and endovascular thrombolysis may be considered.^4,7,10