Intracranial hypotension associated with CSF hypovolemia can occur spontaneously from cryptic CSF leaks, after trauma, or from iatrogenic causes, especially lumbar puncture. It is not widely known that it increases the risk of complications from craniotomy. We present two cases in which patients with CSF hypovolemia experienced posture-dependent deteriorations in level of consciousness after craniotomy.
Case report.
Patient 1.
A 59-year-old woman sought treatment for progressive headache. CT and MRI demonstrated bilateral subdural fluid collections with diffuse pachymeningeal enhancement and a left subdural hematoma with mild left to right shift. She had a craniotomy with evacuation of the hematoma and dural biopsy. This showed only thrombus and normal dura. Headache persisted postoperatively, and she became progressively more obtunded despite head elevation. CT showed bifrontal pneumocephalus and effacement of the suprasellar cistern. By postoperative day 5, she was responsive only to pain and had no voluntary eye movements. Pupils were reactive at 4 mm, but plantar responses were extensor. Neurology was consulted. Further history disclosed the preoperative headaches were orthostatic. Reanalysis of the radiologic studies suggested preoperative spontaneous intracranial hypotension. An MRI confirmed further herniation and buckling of the brainstem. She awoke within hours of being placed in the Trendelenburg position. Further imaging studies revealed a CSF leak in the lower thoracic spine. She recovered after a 20-mL lumbar epidural blood patch.
Patient 2.
A 46-year-old man had squamous cell cancer of the frontal sinus with erosion into the anterior cranial fossa. A bifrontal craniotomy with osteotomies of the anterior fossa floor and tumor resection was performed. A lumbar drain was placed to “relax” the brain during the operation. A pericranial flap was placed to help prevent a cranial CSF leak.
The lumbar drain was removed on postoperative day 2. The patient was allowed to sit up. He became progressively obtunded. CT was thought to show increasing brain edema. During repeat craniotomy, the pericranial flap was edematous and was removed. The frontal dura appeared relaxed. Postoperatively, the patient was kept in the supine position, and he improved for 2 days. He was extubated and allowed to sit up. He again became progressively lethargic and was unable to follow commands. CT on postoperative day 5 revealed pneumocephalus and effacement of the suprasellar cistern. He recovered after a 15-mL lumbar epidural blood patch.
Discussion.
Spontaneous intracranial hypotension (SIH) may be associated with descent of the brainstem and subdural hygromas and hematomas.1 Chronic alterations in level of consciousness have been described.2,3⇓ Acute deterioration after craniotomy in the setting of underlying SIH (our first case) has not been previously recognized. Deterioration in other cases after craniotomy with coincident use of a lumbar drain (similar to our second case) has been reported.4,5⇓ We believe the positional deterioration in these cases was the result of acute brainstem displacement provoked by opening the hypovolemic intrathecal space to atmospheric pressure.
In the normal state, the dural sac and CSF constitute part of a closed system along with the brain and blood. The inter-relationships of these three volumes are defined by the Monro–Kellie hypothesis.6 A loss of CSF allows the intracranial pressure to decrease, but an increase in intracranial venous volume acts to compensate for the loss. The combined CSF and blood volumes also contribute a property of buoyancy that helps to physically support the brain when the head is upright. The normal upright intracranial pressure is −5 to +5 cm H2O, referenced to the foramen of Monro. Orthostatic headache does not occur until the upright pressure decreases to near −30 to −35 cm H2O.7
After craniotomy, the Monro–Kellie hypothesis no longer applies because the system has been “opened.” When open to atmosphere, the previously negative intracranial pressure increases, and air may enter the subarachnoid space. An air–fluid level appears. Because of the underlying CSF hypovolemia, the buoyancy effect of the remaining CSF in keeping the brain afloat becomes more critical, and a position-dependent caudal herniation of the brain may occur. Focal deficits may occur after a unilateral craniotomy.6 Craniotomies performed in patients with normal amounts of CSF are not subject to this herniation because their preserved volume of CSF continues to provide adequate buoyant support to the brain (figure).
Figure. Craniotomy in the setting of normal CSF volume exposes the intracranial contents to atmospheric pressure, but this approximates the underlying preoperative intracranial pressure, and the buoyancy provided by the CSF results in no significant shift in the brain’s position (A, B). In patients with CSF hypovolemia, craniotomy opens the previously negative intracranial pressure to atmospheric pressure (C, D). The loss of CSF buoyancy allows a posture-dependent descent of the brain. Air enters the thecal sac. The presence of pneumoencephaly on postoperative imaging is an important clue that this syndrome may be present.
Subdural fluid collections are relatively common in patients with SIH. Surgery to drain these fluid collections is usually unnecessary. If surgery is attempted, these patients are at an increased risk of brain herniation. The relatively paradoxical maneuver of placing a patient with rostrocaudal herniation in the Trendelenburg position can be potentially life saving in this situation.
- Received June 8, 2003.
- Accepted September 11, 2003.
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