EPIDURAL catheters are commonly used in today's anesthetic practice, and complications are rare. However, hematomas within the spinal canal leading to compression of the spinal cord remain a major concern. In particular, anticoagulation and bleeding disorders are considered to be risk factors for hematoma formation after neuroaxial blockade. We report a case of paraplegia that developed after removal of a thoracic epidural catheter during low-molecular-weight heparin (LMWH) treatment. The patient's symptoms improved spontaneously, and restitution was complete after conservative treatment.

Case Report

A 73-yr-old woman (height, 149 cm; weight, 61 kg) was scheduled to undergo left nephrectomy because of a kidney tumor. Her past medical history was unremarkable except for a previous hysterectomy and possible asbestosis. Preoperative coagulation studies and platelet count were within the normal range. Following admission, the patient had been treated with a LMWH (enoxaparin, 40 mg subcutaneously every morning). Since a combined general and epidural anesthesia was planned, no enoxaparin was administered on the day of surgery, i.e. , the last dose was given approximately 24 h before anesthesia.

An epidural catheter (20 gauge) was inserted uneventfully at the T12–L1 interspace via  an 18-gauge Tuohy needle in the awake patient using the loss-of-resistance technique with normal saline. Neither blood nor cerebrospinal fluid could be aspirated via  the catheter, and a test dose of 3 ml bupivacaine, 0.5%, did not evoke sensory deficits. General anesthesia was induced with fentanyl (5 μg/kg), etomidate (20 mg), and rocuronium (0.5 mg/kg); the trachea was intubated; and anesthesia was maintained with nitrous oxide (60% end tidal) and sevoflurane (0.7% expired). Another 8 ml bupivacaine, 0.5%, was administered epidurally, and anesthesia and nephrectomy proceeded uneventfully except for a splenectomy due to surgical injury to the spleen. The patient was extubated after surgery and transferred to a general ward. For analgesia, a continuous epidural infusion of 0.25% bupivacaine (4–8 ml/h) was administered. This yielded sufficient analgesia without gross sensory or motor deficits. When the patient was visited by an anesthesiologist on the first postoperative day, analgesia was satisfactory and gross neurologic examination was normal. Treatment with LMWH was continued, and no other drugs impairing coagulation or platelet function were given postoperatively.

On the morning of the third postoperative day, a surgeon removed the epidural catheter without consulting an anesthesiologist. Unfortunately, enoxaparin (40 mg subcutaneously) had been administered approximately 2 h earlier. Immediately after catheter removal, the patient complained of severe back pain, and over the next 2 h, paraplegia of both legs developed. The attending anesthesiologist on call was informed. Examination revealed a complete palsy of the left leg and impossible flexion of the right hip. The left patellar reflex and the anal sphincter reflex were absent. Other muscular reflexes were normal, and a Babinski sign was not observed. Sensory deficits did not occur at any time.

An urgent magnetic resonance image (MRI) was obtained and revealed an inhomogeneous epidural mass compressing the dural sac from T11–T12 to T12–L1, consistent with an epidural hematoma (fig. 1). A neurosurgical consultation was requested immediately. At the time of the neurosurgical examination, a slight improvement of the motor impairment was observed. Thus, immediate surgical intervention was not considered by the neurosurgeon to be indicated, and a decision toward a conservative trial was made. Treatment with corticosteroids (dexamethasone, 40 mg intravenously initially and 4 mg orally four times daily for 1 week) and physical therapy were initiated. The motor deficits gradually disappeared completely over the next 4 days. The epidural mass was still present in a MRI obtained after 3 days but was smaller in size and did not compress the dural sac (fig. 2).

Fig. 1. Sagittal magnetic resonance imaging section at the T12–L1 level after removal of an epidural catheter revealing an epidural mass (*) extending from T12 to L1 compressing the dural sac.

Fig. 1. Sagittal magnetic resonance imaging section at the T12–L1 level after removal of an epidural catheter revealing an epidural mass (*) extending from T12 to L1 compressing the dural sac.

Fig. 2. Magnetic resonance imaging study of the lumbar spine 3 days after removal of an epidural catheter. The epidural mass (*) is smaller but still present.

Fig. 2. Magnetic resonance imaging study of the lumbar spine 3 days after removal of an epidural catheter. The epidural mass (*) is smaller but still present.


Epidural hematoma is a very rare but typical complication of epidural anesthesia. In a large retrospective and prospective study, no signs suggesting epidural hematoma were recognized in 4,185 patients receiving a thoracic epidural catheter. 1However, several cases of spinal or epidural hematoma after neuraxial blockade in patients receiving LMWH have been published, 2,3and investigators expressed their concern about patients receiving LMWH being at an increased risk for those particular complications. 4In 1997, the Food and Drug Administration issued a public health advisory regarding reports of epidural or spinal hematomas with the concurrent use of LMWH and spinal–epidural anesthesia or spinal puncture. Similar recommendations were issued by the German Society of Anesthesiology and Intensive Care Medicine in the same year. 5There is consensus that when LMWH is used perioperatively, neuroaxial block should be delayed for 10 to 12 h after the last dose. 6,7The same time interval has been recommended between LMWH administration and removal of a spinal or epidural catheter. 6 

Enoxaparin has an elimination half-life of 2.3–3.0 h, and its antithrombotic effect lasts for about 24 h. 8LMWHs also undergo renal elimination and do accumulate in patients with renal failure. 8Whether nephrectomy in our patient altered LMWH elimination can only be speculated.

Reversing the effects of LMWH is difficult. Protamine neutralizes the antithrombin activity of LMWH, normalizing the activated partial thromboplastin time; however, its antagonizing effect on antifactor Xa activity is incomplete. 9If LMWH effects are to be reversed, protamine seems to have a lesser effect compared to its antagonizing abilities after unfractionated heparin treatment.

Cases of epidural hematoma developing after catheter removal have been reported. 10,11The treatment of choice is laminectomy and surgical evacuation of the hematoma. The rapidity of surgical intervention correlates with the outcome. 12There are, however, also reports of patients that have been managed successfully without surgical intervention following epidural hematomas of either posttraumatic or spontaneous origin. 13,14In most of those cases, improving clinical condition led to the decision for conservative management. Novel in our case is the conservative management of an epidural hematoma developing as a complication after epidural anesthesia with complete resolution of the neurologic symptoms. Initial regression of symptoms during diagnostic workup led to the conservative approach.

An epidural hematoma occurred after removal of an epidural catheter. The physician removing the catheter was not trained in anesthesiology and was unaware of the risk when an epidural catheter is removed shortly after LMWH administration. This supports the view that postoperative neuroaxial blockade should be supervised by anesthesia personnel and that manipulations of epidural catheters should only be made by educated physicians. Particular caution is warranted when anticoagulants or platelet aggregation inhibitors are administered. Following administration of LMWHs, removal of epidural catheters should be delayed for 10–12 h.

The management of suspected epidural hematoma should include a thorough neurologic examination, an urgent MRI or computed tomography scan, and immediate consultation with a neurosurgeon. Surgical intervention remains the treatment of choice in patients with neurologic deficits; however, a conservative approach may be indicated in patients showing early clinical improvement.


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