Anesth Analg 2005;100:545-546
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000143340.51813.6A
NEUROSURGICAL ANESTHESIA
Cerebellar Hemorrhage Caused by Cerebrospinal Fluid Leak After Spine Surgery
Ehab Farag, MD, FRCA*,
Amgad Abdou, MD
,
Ihab Riad, MD,
Sam R. Borsellino, MD
, and
Armin Schubert, MD, MBA*
Departments of *General Anesthesiology and Neurosurgery, and Division of Anesthesiology and Critical Care Medicine, Cleveland Clinic Foundation; and Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio
Address correspondence and reprint requests to Armin Schubert, MD, MBA, Department of General Anesthesiology/E-31, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195. Address e-mail to schubea{at}ccf.org.
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Abstract
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Spine surgery is associated with a wide range of surgical and anesthetic complications. Excessive cerebrospinal fluid leak can be a cause of cerebellar hemorrhage postoperatively. We report a 43-yr-old patient who had lumbar spine reexploration surgery complicated by a cerebrospinal fluid leak which led to cerebellar hemorrhage manifested by postoperative mental status changes. Early detection and proper management resulted in full recovery.
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Introduction
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Spine surgery is associated with a wide range of perioperative complications. The adverse circulatory and compressive sequelae related to the prone position have been well described (1). However, intracranial bleeding after spine surgery is rare with few published case reports (2–5). None mention that postoperative opioids may mask diagnostically important changes in mental status. In the current report, we describe the occurrence of cerebellar hemorrhage after complex lumbar spine surgery, summarize purported mechanisms, and call attention to the early identification and treatment of this complication to avoid or minimize permanent neurological injury.
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Case Report
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A 43-yr-old woman, height 1.67 m, weight 68 kg, had an L5-S1 fusion using pedicle screw fixation for low back pain. Her symptoms resolved until 2 months later when she was involved in a motor vehicle accident at which time her back pain recurred. She was readmitted for surgical reexploration based on magnetic resonance imaging (MRI) and computerized tomographic (CT) scan investigations. Her medical history revealed a 30-pack-year exposure to cigarettes and migraine headaches. Her medications were oxycodone, bupropion, tizanidine, and esomeprazole. She was scheduled for spinal reexploration of L4-S1 and lateral fusion with iliac crest autograft. Anesthesia was induced with 200 mg of propofol IV; tracheal intubation was facilitated with 50 mg of rocuronium IV. Anesthesia was maintained with a remifentanil infusion and sevoflurane in an air oxygen mixture and muscle relaxation with boluses of rocuronium. Arterial blood pressure ranged from 130/70 to 140/90 mm Hg. Her preoperative arterial blood pressure was 115/64 mm Hg. During her 7-h surgery, the patient received 400 mL of cell salvage blood, 1500 mL of colloid, and 7000 mL of crystalloid. The estimated blood loss was 1300 mL at the end of the surgery. Her hemoglobin was 9.2 g/dL, prothrombin time 13 s, international normalization ratio 1.14, and partial thromboplastin time 27.6 s. She was transferred to the postanesthesia care unit awake, hemodynamically stable, and neurologically intact. The patient used IV patient-controlled analgesia (PCA) with a 0.2-mg hydromorphone demand dose limited to 10 doses/h with a basal rate of 0.2 mg/h, but required additional boluses of hydromorphone. Over the first 36 h after surgery, the patient became increasingly drowsy, but was obeying commands and moving all limbs. This was attributed to opioid overmedication; the PCA basal rate was discontinued and PCA use eventually stopped, all without improvement in mental status. She had received a total of 12 mg of hydromorphone over 36 h. A CT scan was obtained showing cerebral edema and evidence of a posterior fossa lesion. The patient was tracheally intubated and transferred to intensive care. Brain MRI and magnetic resonance angiography showed bilateral symmetric cerebellar hemorrhages (Fig. 1). A right internal carotid artery aneurysm measuring 9 mm in diameter was noted incidentally. A ventricular catheter was placed via the frontal approach with an opening pressure of 5–6 mm Hg, and brain-dehydrating measures were begun. On postoperative day 18 she was discharged to an acute rehabilitation facility. The patient recovered completely except for persistent bouts of lower back pain and right lower extremity pain. Diplopia was present on far lateral gaze bilaterally. Two months after this procedure, the patient had her aneurysm treated endovascularly and was readmitted to the hospital for drainage of a lumbar pseudomeningocele, closure of a dural tear, and partial refusion.
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Figure 1. Magnetic resonance imaging scan obtained after endotracheal intubation and admission to neuro intensive care.
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Discussion
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The proposed mechanism for development of cerebellar hemorrhage caused by intracranial hypotension is an increase in the transluminal venous pressure resulting in blood vessel rupture (6,7). Another theory is the downward displacement of the cerebellum, which in turn causes stretching, and possibly tearing, of the superior vermian veins (8,9). Cerebellar hemorrhage has been observed after cervical, thoracic, and lumbar spine surgery (2–5). Postoperative cerebellar hemorrhage is more prevalent in females than males (10). A major factor associated with the development of remote intracerebral bleeding after spine surgery, as well as after supratentorial surgery, seems to be intracranial hypotension caused by excessive cerebrospinal fluid (CSF) drainage (2–5,11). Low intracranial pressure from excessive CSF drainage indeed seems to have been the cause of our patient’s cerebellar bleed. Our patient’s MRI was consistent with the diagnosis of intracranial hypotension showing dural enhancement during MRI angiography (12–14). Confirming the diagnosis further, a low ventricular opening pressure was present. Moreover, she had neither systemic hypertension nor coagulopathy. Other complications from a CSF leak occur because downward displacement of the brain exerts traction on cranial nerves, leading to diplopia (as observed in our case), visual field defects, vocal cord paralysis, and facial numbness (15,16). Declining mental status after spine surgery should not be dismissed as an opioid effect but should prompt immediate investigation with CT or MRI scans to exclude central causes. To aid with this diagnostic dilemma, opioid reversal should be considered. One must be especially alert for intracranial bleeding when CSF leak or excessive CSF drainage are observed or suspected.
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Footnotes
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Accepted for publication August 10, 2004.
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References
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Abstract
Introduction
