Cerebral Rebleeding by Spinal Anesthesia in a Patient with Undiagnosed Chronic Subdural Hematoma

The patient was a 69-yr-old man who sustained a mild head trauma after falling down, for which he was admitted to the emergency department. Neurologic examination and cranial computed tomography scan were normal. He was discharged on the same day. However, mild nonspecific headache that did not require any treatment appeared on the 4th day and disappeared on the 7th day. On the 10th day, the patient was scheduled to undergo right inguinal hernia repair. Physical examination was unremarkable, and the patient agreed to undergo spinal anesthesia. With the patient in the sitting position, spinal anesthesia was performed at the L3–L4 interspace with a 25-gauge pencil-point needle, using 12 mg isobaric bupivacaine, which resulted in adequate bilateral T8 sensory block. The patient remained hemodynamically stable throughout the procedure. Postoperatively, the patient experienced after few hours later a mild fronto-occipital headache that was more intense in the sitting position, suggesting a post–dural puncture headache. The headache was treated by analgesics (paracetamol), bed rest, and hydration. However, on the next day, the characteristics of the headache changed to a severe nonpostural headache associated with right hemiplegia. Urgent cranial computed tomography revealed a 2.5-cm-thick acute-on-chronic left subdural hematoma shifting the brain laterally and compressing the ventricles (fig. 1). Immediate surgical evacuation was achieved and showed an acute-on-chronic hematoma. The patient’s condition improved rapidly, and he was discharged home 7 days later after uneventful recovery and with full resolution of his symptoms.

Spinal anesthesia can be followed by post–dural puncture headache and even cerebral hemorrhage.1,2It is postulated that the hemorrhage is caused by sudden decrease in intracranial pressure consequent to the loss of cerebrospinal fluid at the lumbar puncture site. Sudden caudal shift of the brain may cause traction on the arachnoid mater, venous structures (bridging veins), or both and may lead to bleeding from ruptured vessels. Intracranial subdural hematoma is rare but could be a lethal complication as evident from the deaths recorded as a complication of lumbar puncture.3–7Electron microscopic data on human bridging veins show that the thinnest parts of the bridging veins’ walls are in the subdural space and the thickest are in the subarachnoid portion.8This implies that bridging veins are more fragile in the subdural portion than in the subarachnoid space. Traction on the bridging veins may cause a rupture at their weakest point in the subdural space, which results in subdural hematoma. The current report shows that spinal anesthesia which is known to cause subdural hematoma can also produce rebleeding in a patient with undiagnosed subdural hematoma, resulting in acute-on-chronic subdural hematoma. The acute-on-chronic subdural hematoma was diagnosed by the computed tomography scan and confirmed during surgical evacuation of the hematoma. Because our patient had no coagulation disorders and was not receiving any anticoagulants, it is possible that the spinal anesthesia, which resulted in cerebral spinal fluid leakage, cerebrospinal fluid hypovolemia, and subsequent intracranial hypotension, was the most likely cause of the subdural rebleeding and might have produced a dramatic brain herniation syndrome. The brain herniation, rebleeding, or both may precipitate severe neurologic deterioration, which may be transient or persistent.9 

In summary, the current report shows that spinal anesthesia in a patient with subdural hematoma may produce subdural rebleeding, resulting in brain herniation syndrome and subsequent neurologic deterioration.