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Lu et al.: SUBDURAL HEMATOMA AFTER SPINE SURGERY
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instrumentation over L5–S1 and surgical revision was
planned. Hypertension and diabetes mellitus had been
noted for years and were under regular medical treat-
ment. All laboratory data including coagulation status
were within normal limits on admission. Preoperative
blood pressure was 150/80 mmHg with heart rate
around 90 beats·min–1. Anesthesia was induced with
thiopentone 300 mg and fentanyl 100 µg and tracheal
intubation facilitated by succinylcholine 80 mg.
Anesthesia was maintained with isoflurane 4–5% in O
(300 mL·min–1). The arterial hemoglobin O2 satura2-
tion (SpO2) remained between 98–99% during
surgery. The patient was ventilated mechanically and
end-tidal CO maintained between 35–40 mmHg.
The patien2t underwent posterior laminectomy for L5
to S1 fusion with autologous iliac bone graft and stabi-
lization with a variable screw placement system. A dural
tear was identified during the procedure. Primary clo-
sure was performed with 4-O and 5-O silk, and gelfoam
was used to cover the repair site. A subfascial suction
drain was placed and the wound closed layer by layer.
Total perioperative blood loss was 2840 mL. Total fluid
replacement included four units of packed red blood
cell (125 mL per unit; total 500 mL), six units of whole
blood (250 mL per unit; total 1500 mL) and 3000 mL
of crystalloids during the operation.
The patient denied the presence of headache during
the first three days after surgery. On the fourth day, the
patient developed a persistent, throbbing right retro-
orbital and right hemicranial headache with a mild
neck stiffness. However, her vital signs, including tem-
perature, were within normal limits and no abnormali-
ties were found on physical or neurologic examination.
These symptoms were first thought to be due to CSF
leakage, thus she was hydrated with 1000 mL iv fluids
and treated with non-steroidal anti-inflammatory
drugs (NSAIDs). The symptoms improved but did not
disappear. On the seventh postoperative day, the
patient complained of severe headache with nausea and
vomiting that was not related to position changes.
Moreover, general weakness and loss of appetite were
also noted. Again, her medical history revealed no pre-
vious head trauma, coagulation abnormalities, or neu-
rologic disorders. Once more, iv fluids and NSAIDs
were given, and resulted in some improvement. Two
days later, the patient’s condition deteriorated further
and she became drowsy. Neurological examination
revealed a left hemiparesis with left Babinski’s sign and
the Glascow coma scale was 9. Emergent computed
tomography (CT) scan showed a large subdural
hematoma over the right convexity with midline shift
and marked subfascial herniation. Emergent right-pari-
etal burr-hole with drainage was performed under gen-
eral anesthesia without any complication. This second
operation relieved the patient’s symptoms, and she was
discharged 14 days later without any neurological
sequelae.
Discussion
Dural tear is one of the most common complications
of spine surgery, with a prevalence of 1 to 17% in series
reporting from 5 to 450 patients.5–8 The causes of
dural tear during primary operation include eroded or
thin dura, dura adhesion, and redundant dura in
patients diagnosed with a tight spinal stenosis. It is
particularly prevalent in patients who have epidural
fibrosis and scar tissue adherent to the dura during
revision of spine surgery.4 The operative technique
plays a key role in avoiding injury to the dural tissue.
Intracranial subdural hematoma formation has
been reported after dural tear with persistent leakage
of CSF.9 However, the exact pathophysiological
mechanism is not known. One possible explanation is
that CSF leakage reduces intraspinal as well as
intracranial pressure. The altered CSF dynamics may
result in a caudally-directed movement of the spinal
cord and brain, which in turn stretches the pain-sensi-
tive structures, dura, cranial nerves and bridging
veins.1 0 Cerebral veins drain into dural sinuses that are
adherent to the inner table of the skull. Many struc-
tural features, based mainly on electron microscopic
data, imply that bridging veins are more fragile in the
subdural portion than in the subarachnoid space.1 1
Therefore, any traction exerted on the bridging veins
will rupture at their weakest point in the subdural
space. It is presumed that CSF leaked via a dural fistu-
la created by accidental durotomy may cause a caudal
displacement of the brain, which in turn pulls and
tears the bridging vessels, and results in a subdural
hemorrhage and hematoma formation. The symptoms
of such intracranial hematoma are persistent headache,
sometimes accompanied with other symptoms and
signs such as vomiting and a feeling of unreality. In
many cases, somnolence, confusion, even coma are the
symptoms that first lead to the diagnosis. A CT-scan
will confirm the diagnosis and must be performed as
early as it is suspected.
Dehydration may further increase the risk of imbal-
ance between CSF loss and production.12 Dehydration
induced reduction of brain volume could lead to sub-
dural hemorrhage. Low intracranial pressure, as a result
of perioperative dehydration, promotes excessive blood
congestion in the bridging veins with consequent
dilatation and increasing tension of the vessels, which
are further stretched by a downward displacement of
the brain, and consequently more vulnerable to the