Delayed Emergence from Anesthesia Resulting from
Cerebellar Hemorrhage During Cervical Spine Surgery
Koichi Nakazawa, MD, Mamoru Yamamoto, MD, Kunihiko Murai, MD, Seiji Ishikawa, MD,
Tokujiro Uchida, MD, and Koshi Makita, MD
Department of Anesthesiology & Critical Care Medicine, School of Medicine, Tokyo Medical & Dental University,
Tokyo, Japan

Cerebellar hemorrhage is an unpredictable complication of spinal surgery. We encountered a case of cerebellar hemorrhage presenting with delayed emergence from anesthesia and hemiplegia after resection
of an intradural extramedullar tumor from the cervical spine. Postoperative brain computed tomography
revealed hematoma in the cerebellar vermis and right
cerebellar hemisphere. The patient made a gradual

C

erebellar hemorrhage is an unpredictable complication of spine surgery. Only a few case reports of this rare complication have been published (1– 4). The onset of neurological disturbance has
been reported more than 10 h after surgery. According
to previous reports (1– 4), patients were neurologically
intact on awakening from anesthesia and anesthesiologists therefore may not have considered the possible
the development of cerebellar hemorrhage during
spine surgery. The mechanism of such hemorrhage in
spine surgery remains unclear but loss of cerebrospinal fluid (CSF) seems important in the pathogenesis of
this complication (3,4). The literature contains no cases
in which cerebellar hemorrhage became apparent
while diagnosing delayed emergence from anesthesia.
We encountered a case of cerebellar hemorrhage during cervical spine surgery presenting with delayed
emergence from anesthesia. The complication was
suspected to be the result of transient loss of CSF.

Case Report
A 74-yr-old female was scheduled to undergo resection of
an intradural extramedullar tumor of the cervical spine.
Accepted for publication October 1, 2004.
Address correspondence and reprint requests to K. Nakazawa,
MD, Department of Anesthesiology & Critical Care Medicine,
School of Medicine, Tokyo Medical & Dental University, 1–5– 45
Yushima, Bunkyo-ku, Tokyo 1138519, Japan. Address e-mail to
nakazawa.mane@tmd.ac.jp.
DOI: 10.1213/01.ANE.0000148120.33694.12

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Anesth Analg 2005;100:1470–1

recovery with conservative treatment. Although the
mechanism of cerebellar hemorrhage remains speculative, loss of cerebrospinal fluid may play an important role. Cerebellar hemorrhage must therefore be
considered in patients with unexplained neurological deterioration or disturbance on emergence from
anesthesia after spinal surgery.
(Anesth Analg 2005;100:1470 –1)

The tumor was located at the level of C2 and compressed
the spinal cord from the right side. Other than atrial
fibrillation, no remarkable medical history was noted preoperatively. Anticoagulants had not been administered
and no bleeding tendency was clinically observed before
surgery. Anesthesia was induced with propofol 100 mg
and fentanyl 0.1 mg IV. Nasotracheal intubation was facilitated with vecuronium bromide 10 mg under direct
laryngoscopy. Anesthesia was maintained with propofol
6 – 8 mg · kg⫺1 · h⫺1 and fentanyl 1–2 ␮g · kg⫺1 · h⫺1,
and bispectral index (BIS) was monitored to allow the
dose of propofol to be adjusted. After induction of anesthesia, the left radial artery was cannulated to enable
continuous monitoring of arterial blood pressure. Systolic
blood pressure was controlled during anesthesia and
never exceeded 150 mm Hg. After laminectomy and durotomy at the level of C2, the tumor was resected and
the operation completed uneventfully. However, emergence from anesthesia was delayed. On regaining consciousness, the patient was only able to nod her head
in response to verbal commands and right-sided hemiplegia was noted. We considered that manipulation
of the tumor might be responsible for right-sided hemiplegia. When the tidal volume exceeded 8 mL/kg and
BIS exceeded 85, the patient was tracheally extubated
and transferred to the recovery room. Because her level
of consciousness did not improve, brain computed
tomography (CT) was performed 12 h postoperatively,
revealing hemorrhage in the vermis and right cerebellar hemisphere (Figure 1). The patient was treated conservatively and the neurological deficits including drowsiness and paralysis gradually recovered. One month
postoperatively, the hematoma had been completely absorbed and hemiplegia had resolved leaving a mild residual gait ataxia.
©2005 by the International Anesthesia Research Society
0003-2999/05

ANESTH ANALG
2005;100:1470 –1

Figure 1. Plain computed tomographic image of the head 12 h after
surgery revealing hematoma in the cerebellar vermis and right
cerebellar hemisphere.

Discussion
The most common causes of perioperative intracranial
hemorrhage are diverse: use of anticoagulants, high
arterial blood pressure, and underlying intracranial
vascular abnormalities. However, several case reports
have demonstrated that loss of CSF might be another
important factor in the pathogenesis of intracranial
hemorrhage during spine surgery (1– 4). Friedman et
al. (4) reported two cases of cerebellar hemorrhage
after spinal surgery. They speculated that caudal cerebellar displacement or sag resulting from intraoperative loss of CSF causes transient stretching and occlusion of superior cerebellar veins draining in the
cephalad direction into the deep venous system (4).
In the present case, cerebellar hemorrhage was considered to result from loss of CSF after durotomy for
the following reasons. First, although anticoagulant
therapy is a cornerstone of the treatment of chronic
atrial fibrillation, it was not used perioperatively in the
present patient. Second, arterial blood pressure was
continuously monitored throughout the anesthetic
and no episodes of high arterial blood pressure occurred. Relatively mild characteristics of hematoma
formation also suggested that less severe stress was
responsible for the pathomechanism. Third, magnetic
resonance angiography performed postoperatively
also failed to demonstrate a vascular lesion.
Because asymptomatic cerebellar hemorrhages are
unlikely to be detected and because postoperative cranial CT is not routinely performed after spinal surgery, the incidence of cerebellar hemorrhage may exceed that reported (4). In this case, although tidal

CASE REPORTS

1471

volume exceeding 8 mL/kg and BIS more than 85 are
controversial criteria for tracheal extubation, we considered the delayed emergence from anesthesia to be a
transitory residual effect of fentanyl and propofol. In
retrospect, brain CT should have been examined before tracheal extubation.
Cerebellar hemorrhage remote from the site of surgery is seen much more often after supratentorial intracranial surgery, with a reported incidence of 0.08%–
0.29% (5–7). The mechanisms of hemorrhage in spinal
surgery resemble those in supratentorial surgery, with
either transtentorial pressure gradient as a result of
excessive CSF loss or removal of a mass lesion without
substantial CSF loss postulated to be responsible for
disruption of cerebellar venous blood flow and consequent venous hemorrhage (5,8). Although perioperative factors, such as intraoperative positioning, inherent or induced coagulopathies, and arterial blood
pressure, fail to predict the development of remote
cerebellar hemorrhage (5), “head-down” positioning
during opening of the dura might reduce the risk of
this complication, at least in case of spinal surgery (4).
In conclusion, it is important to be aware of this complication as a potential causative factor of unexplained
neurological deterioration or disturbance on emergence from anesthesia after spinal surgery. Early diagnosis and treatment of this complication are of great
importance to patient outcome.

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