Eur Spine J (2006) 15: 95–99
DOI 10.1007/s00586-005-0987-2

CASE REPORT

Deniz Konya
Serdar Ozgen
M. Necmettin Pamir

Cerebellar hemorrhage after spinal surgery:
case report and review of the literature

Received: 22 December 2004
Revised: 26 April 2005
Accepted: 12 June 2005
Published online: 9 July 2005
Ó Springer-Verlag 2005

D. Konya (&) Æ S. Ozgen Æ M. N. Pamir
Marmara University Hospital,
Neurosurgery, Istanbul, Turkey
E-mail: drdkonya@hotmail.com
Tel.: +90-216-3264559
Fax: +90-216-3275249

Abstract Recent reports indicate
that cerebellar hemorrhage after
spinal surgery is infrequent, but it is
an important and preventable problem. This type of bleeding is thought
to occur secondary to venous
infarction, but the exact pathogenetic mechanisms are unknown. This
report details the case of a 48-yearold woman who developed remote
cerebellar hemorrhage after spinal
surgery. The patient presented with
a herniated lumbar disc, spinal stenosis, and spondylolisthesis, and
underwent multiple-level laminectomy, discectomy, and transpedicular
fixation. The dura mater was opened
accidentally during the operation.
There were no neurologic deficits in
the early postoperative period;
however, 12 h postsurgery the patient complained of headache. This

Introduction
Cerebellar hemorrhage after spinal surgery is extremely
rare, but is a very serious clinical problem due to the
location of the bleeding. Some authors suggest that
remote cerebellar hemorrhage (RCH) or hemorrhagic
infarction occurs due to venous infarction, but the
pathophysiology and etiology of this condition are
unknown [4, 7, 13, 14, 16]. It has been proposed that
cerebellar sag resulting from intraoperative or postoperative cerebrospinal fluid (CSF) drainage might stretch
and occlude the bridging cerebellar veins that course
cephalad, leading to hemorrhagic venous infarction [4, 9,

became more severe, and developed
progressive dysarthria and vomiting
as well. Computed tomography
demonstrated small sites of remote
cerebellar hemorrhage in both cerebellar hemispheres. The patient was
treated medically, and was discharged in good condition. At
6 months after surgery, she was
neurologically normal. The case is
discussed in relation to the ten previous cases of remote cerebellar
hemorrhage documented in the literature. The only possible etiological
factors identified in the reported case
were opening of the dura and largevolume cerebrospinal fluid loss.
Keywords Cerebellar hemorrhage Æ
Dural injury Æ Hemorrhagic
infarction Æ Spinal surgery

14, 16]. Peroperative patient positioning is another factor
that is widely suspected to contribute to RCH, but the
relevance of this is unclear [4, 12]. We report a case in
which RCH occurred after spinal surgery, and discuss
possible causative factors.

Case
A 48-year-old woman presented with pain in her lower
back and both legs. Investigation revealed a herniated
disc at L4–L5, stenosis of the lumbar spinal canal, and
spondylolisthesis at L4–L5. She was operated in prone

96

position via a posterior approach. The surgery involved
L3–L5 laminectomies, L4–L5 discectomy, and screw
fixation of the L3–L5 pedicles. The dura mater was
damaged intraoperatively, and was sutured in watertight
fashion.
Approximately 100 ml of CSF escaped before the
dura was closed. When this accidental opening of the
dura occurred, the patient’s blood pressure dropped
immediately, and the decrease was attributed to the CSF
leakage. The anesthesiologist administered routine
treatment for hypotension (10 mg intravenous ephedrine
sulfate), and blood pressure returned to normal range
within approximately 10 min. Prior to closure, a hemovac drain was placed in the epidural space.
When the patient awoke from anesthesia, she was
neurologically intact. Her blood pressure was normal in
the immediate postoperative period. At 12 h after surgery she complained of headache, and over the next 12 h
she exhibited progressive dysarthria, developed a severe
headache, and began vomiting. By the end of the first
day, the patient was conscious but only responsive to
commands. In the first 24 h after surgery, 580 ml of
serosanguineous fluid were removed via the hemovac
drain.
Cranial computed tomography (CT) at 24 h showed
small sites of hemorrhage in both cerebellar hemispheres, just below the tentorium (Fig.1). The results of
laboratory investigations, including platelet count, and a
clotting screen, were all in the normal range.
Fig. 1 Cranial computed
tomography scanning done
24 h after spinal surgery
showed cerebellar hemorrhage
or venous infarction in the
cerebellum (arrows)

The patient was managed conservatively with antiedema treatment (4 mg intravenous dexamethasone
every 6 h), analgesics, and bed rest. Her neurological
status did not deteriorate further after hemorrhage was
detected. Repeat CT at 48 h postsurgery showed no
enlargement of the hemorrhage sites and no hydrocephalus. Nine days after the operation, the patient was
discharged in good condition with full mobility and with
no neurologic deficits. At 6 months after surgery, she
was neurologically normal.

Discussion
Intracerebral hematoma after craniotomy is one of the
most common and important complications in neurosurgery practice [2, 6, 10, 14]. Some of these hematomas
occur at the surgical site, whereas others develop at remote locations. Hemorrhage after cranial or spinal
surgery can occur in the intracerebral, cerebellar, epidural, or subdural compartments. Numerous authors
have reported cases in which RCH developed as a delayed complication of spinal surgery [1, 3, 4, 5, 8, 9, 11,
13]. Chadduck [3] first described RCH after a spinal
procedure in 1981. Most recently, Thomas et al. [13]
documented a case in which supratentorial and infratentorial intraparenchymal hemorrhage developed after
spinal operations. There has been increased interest in
RCH in the past 10 years, but no specific etiological

97

factors have yet been identified for this type of hemorrhage after spinal surgery.
We conducted a detailed literature review of a total of
ten cases of RCH that have been reported to date, and
found no correlations between RCH and age, sex,
pathology operated, or type of interventions performed
[1, 3, 4, 5, 8, 9, 11, 13] (Table 1). Seven of these patients
were male and three were female, and the age range was
34–75 years (median, 50 years). Four individuals were
operated for intradural pathologies, and the other six for
extradural pathologies. RCH was detected between 16
and 120 h (median, 47 h) after surgery.
All ten individuals exhibited severe headache and
decreased level of consciousness in association with
RCH, and the consciousness levels ranged from a state
of awake, anxious, and agitated to comatose state. The
two important features of our case that shares with these
ten previous cases are opening of the dura and consequent loss of CSF.
Different authors have proposed several pathological
mechanisms for RCH, but none has been proven scientifically. Chadduck [3] postulated that elevated blood
pressure might cause an increased gradient between
intravascular pressure and CSF pressure, and thus induce hemorrhage into the cerebellar parenchyma. Andrews and Koci [1] speculated that their case of
cerebellar infarction resulted from transient traction,
kinking, or spasm of the superior cerebellar arteries, and
that hemorrhage occurred upon reperfusion. Some
researchers have theorized that excessive CSF drainage
per- or postoperatively could cause the cerebellum to
become inferiorly dislocated, with possible tearing of the
superior vermian veins [4, 13, 16]. However, work by
Wang et al. [15] suggest that placement of a closedsuction drain in the epidural space does not aggravate
CSF leakage. They observed no untoward effects on the
cerebellum; thus, we felt that it was safe to use this type
of drainage in our case.
As mentioned, peroperative patient positioning is one
factor that is believed to lead to RCH after cranial surgery [4, 12]. It is known that, in patients who undergo
pterional craniotomy, hyperextension of the neck and
subsequent turning of the head to the side can cause
relative obstruction of the ipsilateral jugular vein [12].
In our case, both the neurosurgery and anesthesiology
teams took care to ensure that there was no excessive neck
hyperextension intraoperatively. The above-mentioned
ten patients with RCH were operated in three different
positions, and the data from these cases indicate no
causative relationship between patient positioning and
this type of hemorrhage after spinal surgery (Table 1).
Several other factors, including arterial hypertension, anticoagulation therapy, coagulopathy, aneurysm, and arteriovenous malformations, have also been
identified as possible predisposing factors for RCH [10,
13, 14]. Our patient had no history of hypertension

and did not develop this problem peroperatively or
postoperatively, and no arteriovenous malformation
was apparent on CT angiography. None of the factors
listed above is universally accepted, and none is believed to be the sole cause of RCH. The pattern of
RCH observed on the CT scans after spinal surgery in
our case was similar to those patterns that had been
reported by other authors after supratentorial operations [2, 4, 14]. In the two cases of RCH described by
Friedman et al. [4], the hemorrhage had occurred in
the superior portion of the vermis and in the superior
part of the cerebellar hemisphere. In our case, the
hemorrhage was in both cerebellar hemispheres, just
below the tentorium.
Small cerebellar hematomas can be managed medically and followed with serial imaging; however, large
hematomas that cause significant mass effect in the
posterior fossa may require surgical decompression
[1, 3, 4, 5, 8, 11]. Compression of the fourth ventricle
and resultant non-communicating hydrocephalus
should be managed with CSF diversion procedures
[1, 5]. Decompression is necessary if there are signs and
symptoms of brainstem compression due to increased
intracranial pressure, and in such cases, evacuation of
the hematoma should be performed immediately. Expanded suboccipital craniectomy and duraplasty are
the procedures used to decompress the posterior
fossa. Of the ten previously reported cases of RCH,
four were managed medically with anti-edema drugs
(dexamethasone), analgesics and bed rest, and the
other six were managed both surgically and medically
(Table 1). All four of the patients, who were treated
with medical management alone, had small hematomas. After surgery, these individuals were awoke and
responsive to commands only, and their neurological
status did not deteriorate after the hemorrhage was
detected.
The other six patients were treated with posterior
fossa decompression or CSF diversion. In all of these
cases, neurological status deteriorated with time after
hemorrhage, changing from awake state to semicomatose or comatose state. As these reports indicate that
treatment for RCH depends on the patient’s neurological status as well as the on the nature of the lesion.
In summary, based on the experience with RCH to
date, it appears that this type of hemorrhage can
occur after any type of spinal surgery, regardless of
body positioning. The previously reported ten cases as
well as our current case feature CSF loss due to the
opening of the dura intraoperatively. Large-volume
CSF loss intraoperatively or postoperatively may be
an etiologic factor in RCH. We believe that it is
important to consider the possibility of RCH in any
patient who exhibits unexplained neurological deterioration after the dura mater has been opened during
spinal surgery and when a large volume of CSF has

Sitting
Supine
Prone
Prone
Prone

Prone
Prone
Prone
Prone

59/M
75/M
36/M
40/F
57/F

62/M
34/M
43/M
56/M
38/F
48/F

Cervical spinal stenosis
(ED)a Chadduck [3]
Revision of cervical fusion
(ED)a Mikawa et al. [8]
Lumbar scoliosis (ED)a
Andrews and Koci [1]

Postdiscectomy syndrome
(ED)a Gobel et al. [5]
Spondylolisthesis (ED)a
Gobel et al. [5]

Cervical intramed. tumor
(ID) Satake et al. [11]

Cervical schwannoma
(ID) Morandi et al. [9]

T9–T10 herniated disc
(ID) Friedman et al. [4]
Lumbar spinal stenosis
(ED)a Friedman et al. [4]
Thoracolumbar tumor (ID)
Thomas et al. [13]
Lumbar herniated disc+
spinal stenosis (ED)a
Current case (2004)
36 h postoperative

120 h postoperative

48 h postoperative

48 h postoperative

18 h postoperative

18 h postoperative

72 h postoperative

48 h postoperative

36 h postoperative

16 h postoperative

48 h postoperative

Time of
infarction

Both CHs

Supra-infratentorial

Both CHs

Right CH+
left temporal
hemorr.
Right CH

Cerebell. and
supracerebellar layer

Right CH+
Hydrocephalus
Both CHs+
Hydrocephalus

Both CHs+
Hydrocephalus

Left CH+
Hydrocephalus
Both CHs

Hemorrhage
location

a

CH cerebellar hemisphere, EVD external ventricular drain, Mn meningitis, ID intradural, ED extradural
Dura opened accidentally in all ED cases

Prone

Prone

Patient
positioning

Age (years)/
Sex

Primary pathology/Author

Anti-edema drugs and
serial imaging
Anti-edema drugs and
serial imaging
Anti-edema drugs and
serial imaging
Anti-edema drugs and
serial imaging

Anti-edema drugs and
serial imaging

Postoperative
fossa decomp.

Postoperative fossa
decomp.+EVD
EVD

Postoperative fossa
decomp.+EVD
Postoperative fossa
decomp.+EVD
EVD

Treatment

Table 1 Clinical parameters and outcome for the ten previously reported cases of remote cerebellar hemorrhage and the current case

Recovery

Mild dysarthria and ataxia
(residual disability)
Mild dysarthria and ataxia
(residual disability)
Recovery

Mn (6 weeks postoperative)+
sinus thrombosis (4 months
postoperative)
(residual disability)
Diplopia, dizziness, and nausea
(3 months postoperative)
(residual disability)
Recovery

Quadraparetic, min.
hand motor function
(residual disability)
Recovery

Alert, conversive, able to eat
(residual disability)
Exitus

Result

98

99

been lost intraoperatively or postoperatively. Such
patients should undergo immediate neuroradiological
examination. Small hematomas due to RCH can be

managed medically and then monitored with serial
imaging, but larger lesions that cause significant mass
effect in the posterior fossa must be treated surgically.

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complication of an occult postoperative
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