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British Journal of Anaesthesia 96 (2): 262–5 (2006)
doi:10.1093/bja/aei297
Advance Access publication December 16, 2005
Case Report
Epidural haematoma after a combined spinal–epidural
anaesthetic in a patient treated with clopidogrel and dalteparin
N. L. K. Tam1*, C. Pac-Soo1 and P. M. Pretorius2
1
Department of Anaesthesia, Wycombe General Hospital, Queen Alexandra Road, High Wycombe,
Buckinghamshire HP11 2TT, UK. 2Department of Neuroradiology, The Radcliffe Infirmary,
Woodstock Road, Oxford OX2 6HE, UK
*Corresponding author. E-mail: nicolettetam@hotmail.com
Br J Anaesth 2006; 96: 262–5
Keywords: anaesthetic techniques, epidural; blood, anticoagulation; complications,
haematoma; complications, spinal injury
Accepted for publication: November 10, 2005
Antiplatelet agents are being increasingly used as they are
beneficial in reducing the incidence of cerebro-vascular and
ischaemic cardiac events in at-risk populations. Newer more
potent agents such as the thienopyridine derivatives are
being introduced into clinical practice but their effect, especially in combination with other anticoagulants, on the risk
of developing an epidural haematoma after neuraxial blockade is not well documented. We report a case of an epidural
haematoma in a patient who was administered low molecular weight heparin (LMWH) prophylactically against the
development of deep vein thrombosis perioperatively and
received a combined spinal–epidural analgesia for a knee
arthroplasty. She had also been taking regular clopidogrel
which had been stopped 7 days before surgery.
Case report
An 80-yr-old woman weighing 56 kg was admitted for an
elective left total knee arthroplasty. Her significant past
medical history included atrial fibrillation, moderate tricuspid regurgitation, congestive cardiac failure and haemorrhagic gastritis following ingestion of low dose aspirin.
Her current medications included clopidogrel 75 mg once
daily, furosemide 20 mg once daily, verapamil 120 mg once
daily, lansoprazole 30 mg once daily and risedronate 35 mg
once weekly. The clopidogrel was stopped 7 days before
elective surgery. The results of her routine preoperative
blood investigations revealed a normal clotting screen with
an activated partial thromboplastin time of 32 s, prothrombin
time of 10 s and a normal platelet count of 356·109 litre 1.
Plasma urea and creatinine were raised at 10.2 mmol litre 1
(normal range 2.5–7.5) and 116 mmol litre 1 (normal range
50–110), respectively. On a previous hospital admission,
plasma urea was noted to be 15.6 mmol litre 1 and plasma
creatinine 186 mmol litre 1, indicating that the patient has
impaired renal function.
The patient received dalteparin (LMWH) 5000 units s.c.
the night before, 10 h before elective surgery for prophylaxis
against the development of deep vein thrombosis. The
following day, in theatre the patient underwent a combined
spinal–epidural anaesthetic. A 16 gauge Tuohy needle was
inserted at the L4/5 inter-vertebral space in the midline and
the epidural space was identified using the loss of resistance
to saline technique. A 12 cm, 24 gauge Sprotte spinal needle
was advanced into the sub-arachnoid space through the
Tuohy needle and heavy bupivacaine 0.5% (2 ml) and diamorphine 300 mg injected. An epidural catheter was then
threaded into the epidural space and secured over the
patient’s back. The procedures were reported as atraumatic
with no bloody tap or blood in the catheter. The sensory level
was assessed using ethyl chloride spray and the upper limit
of the sensory blockade was T4 on the right and T6 on the
left. Surgery proceeded with the patient receiving propofol
sedation via a target controlled infusion pump.
After surgery, in the post anaesthetic care unit, a test
dose of lidocaine 1% (3 ml) was injected into the epidural
catheter. After 10 min there was no change in the cardiovascular or neurological status of the patient, excluding
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We report a case of a spinal–epidural haematoma occurring in a patient after a combined spinal–
epidural anaesthetic. She had been taking clopidogrel and had received perioperative dalteparin
for thromboprophylaxis. Despite adhering to standard guidelines concerning administration of
low molecular weight heparin perioperatively and stopping the clopidogrel 7 days before the
anaesthetic, the patient developed an epidural haematoma.
Epidural haematoma after spinal–epidural anaesthetic
Discussion
The development of a spinal haematoma is a rare but potentially devastating complication of central neuraxial blockade. Its true incidence is unknown and due to its rarity it is
very difficult to evaluate risk factors prospectively and any
properly powered study would require many thousands of
patients to investigate this. Therefore, data on the incidence
A
B
Fig 1 Axial T2 weighted images at the T12 (A) and L1 (B) levels demonstrate a large epidural haematoma returning low signal (black arrows in A
and B). There is compression of the conus medullaris with increased signal
in the conus indicating a compressive myelopathy (white arrow in A). At the
L1 level, there is compression of the cauda equina (white arrow in B).
of spinal haematoma following neuraxial blockade are
mainly based on audit studies and case reports.
Tryba1 reported that the incidence of spinal haematoma
after epidural and spinal anaesthesia are 1 in 150 000 and 1 in
220 000, respectively. The incidence of spontaneous spinal
haematoma is rarer still and is estimated at 1 patient per
1 000 000 patients per year.2
Several factors increase the risk of patients developing a
spinal haematoma following neuraxial blockade.3 These
include advanced age, female gender, bony spinal pathology
that may necessitate multiple attempts resulting in traumatic
insertion of either spinal or epidural needle or catheter and
coagulopathy.
Altered patient’s blood coagulation, due either to
an inherent coagulopathy or to the administration of
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sub-arachnoid placement of the catheter. A continuous
infusion of 0.25% bupivacaine was then started, initially
at 7 ml h 1 for postoperative analgesia. Subsequently
that evening the patient reported increasing pain over the
operated site and also over her lumbar back region. A bolus
dose of 10 ml 0.25% bupivacaine was administered via the
epidural catheter and the rate of infusion increased to 9 ml
h 1. The intensity of the pain subsequently decreased and
the infusion rate was reduced to 6 ml h 1. Thromboprophylaxis was resumed using a single daily dosing regimen of
dalteparin 5000 units s.c. and local guidelines were adhered
to, that is, the second dose of the LMWH was administered
24 h after the initial preoperative dose and in the case
described here, it was 14 h after the insertion of the epidural
catheter.
The following day after surgery, the patient was inadvertently administered a dose of clopidogrel 75 mg together with
her usual medications. The physiotherapist, during her daily
visit, noted some numbness and weakness of the right, nonperated leg which she attributed to the epidural analgesia.
Assessment of the left leg was not possible because of the
recent knee surgery. The epidural analgesia was maintained
for a total duration of 72 h until the third postoperative day
when the catheter was removed. This was 12 h after the last
dose of dalteparin and 48 h after the inadvertent single dose
of clopidogrel.
Assessment of the patient 5 h after removal of the epidural
catheter showed that motor weakness was still present in the
right leg. This was again attributed to persistent epidural
block. The patient continued to have weakness of the hip
flexors and quadriceps together with reduced sensation over
the dorsum of the right foot. Neurosurgical opinion was
sought but as the magnetic resonance imaging (MRI) facility
was not available in the hospital at the time of the incident,
there was a further delay of 48 h before the patient was
transferred to a neurosurgical centre.
At the neurosurgical centre, an MRI of the spine was
performed and it revealed an epidural haematoma at the
T12/L1 level (Fig. 1A and B). The patient underwent an
urgent T12 to L2 laminectomy and evacuation of the
haematoma. There was minimal improvement in the neurological symptoms affecting her right leg in the first 24 h
after surgery. Her neurological progress continues to be
assessed by the neurosurgical team and 1 month after
surgery there had not been any significant improvement
in her symptoms.
Tam et al.
adjustment may be necessary for patients with a creatinine
clearance of <30 ml min 1.
The anaesthetist involved reported that the procedure
itself was atraumatic, that is, there was no report of blood
in the epidural needle or catheter and the needle was inserted
at the L4/5 interspace. However, the neurosurgeon who
evacuated the haematoma reported that the catheter
appeared to have been inserted at a higher level of L2/3
and that the epidural haematoma extended from T12 to
L2, compressing mainly the right side of the thecal sac.
Identification of body surface landmarks for neuraxial
blockade is frequently inaccurate11 and probably accounts
for the discrepancy observed between the neurosurgical
findings and the level of insertion reported by the anaesthetist. The discrepancy may well have been compounded by the
finding that the patient had osteoporotic wedge compression
fractures of the bodies of T12, L1 and L2 vertebrae and
partial collapse of L3 as identified by the MRI scan.
Spinal haematomas may also occur at the time of removal
of the epidural catheter. However, we do not believe that this
was the case in our patient. Although the effect of clopidogrel on the inhibition of platelet aggregation has been shown
to occur 2–3 days after administration,12 the abnormal
neurology had been noted in the patient before receiving
the inadvertent dose of clopidogrel and there had not been
any further reported increase in motor or sensory symptoms
after the catheter had been removed.
It is very important to diagnose spinal haematomas early on
so that prompt investigation and treatment are initiated.
However, this is often difficult to achieve because the increasing motor and sensory blockade are often attributed to the
action of the local anaesthetic agent. This has been highlighted in the American Society of Anesthesiologists Closed
Claims database which reported that delays in diagnosis of
spinal haematomas was often due to attributing the postoperative weakness or numbness to persisting local anaesthetic
effect rather than spinal cord ischaemia.13 Successful neurological recovery following evacuation of a spinal haematoma
depends on the interval between onset of symptoms and timing of surgery. Lawton and colleagues14 have observed an
improved outcome in patients that were operated on within
12 h of developing symptoms compared with those operated
on later. Vandermeulen and colleagues4 have suggested an
even shorter interval of <8 h for successful recovery.
This case highlights the need for continued vigilance and
close neurological monitoring regarding the use of epidural
anaesthesia in the presence of combinations of anticoagulant
agents and antiplatelet agents.
References
264
1 Tryba M. Epidural regional anesthesia and low molecular
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We believe that the epidural haematoma occurred at
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