Spontaneous Resolution of Epidural Hematoma after Continuous Epidural Analgesia in a Patient without Bleeding Tendency

A 72-yr-old woman (weight, 42 kg) with stenosis of the bile duct associated with cholelithiasis was admitted for choledochoduodenostomy and cholecystectomy. The patient had no relevant medical history and was on no medication. Except for elevations in aspartate aminotransferase (109 U/l [normal range, 11–32 U/l]), alanine aminotransferase (112 [11– 32] U/l), alkaline phosphatase (230 [6–39] U/l), and total bilirubin (8.9 mg/dl; normal range, 0.3–1.2 U/l), she showed no abnormal findings in preoperative laboratory examinations, including coagulation tests.

The patient received an epidural block combined with general anesthesia. Epidural puncture was performed with an 18-gauge Tuohy needle at the T7–T8 interspace, and the epidural space was easily confirmed on the first attempt without bleeding. An epidural catheter was advanced smoothly 5 cm in the cephalad direction without accompanying paresthesia or pain. During surgery, epidural analgesia was achieved with a mixture of 0.125% bupivacaine and 5 μg/ml fentanyl. The patient received 8 ml of the mixture as an initial dose, and this was followed by continuous administration at a rate of 6 ml/h. The operation was performed without difficulty, and total blood loss during the 3-h surgery was 420 ml.

In the recovery room, the patient had no pain and was able to dorsiflex both feet on request. We reduced the epidural infusion of the 0.125% bupivacaine and 5 μg/ml fentanyl to 4 ml/h for postoperative pain control. On the first postoperative day, the patient had no pain or motor weakness when postoperative evaluation was made by the anesthesiologist. On the second postoperative day, both lower extremities gradually became weak, but the patient did not report her condition to anyone because she considered that this weakness was due to epidural analgesia. On the third postoperative day, the patient informed the nursing staff of her condition, and the anesthesiologist was consulted.

When the patient first complained of lower extremity weakness, she was alert and had no pain. Her vital signs were normal, but she was unable to hold her knees flexed. We immediately discontinued the epidural infusion and consulted a neurosurgeon. The neurologic examination showed hypoesthesia and hypalgesia below the T6 dermatome distribution in the right side and below the T8 in the left side. Both the patellar and the Achilles tendon reflexes were absent. Manual muscle testing revealed that the muscle strength of the iliopsoas and the quadriceps femoris were zero (0/5), and the muscle strength of the tibialis anterior and extensor halluces longus were trace (1/5) in both lower extremities. Cranial nerve and upper extremity examination results were normal. No bleeding or sign of infection was present at the epidural catheter insertion site. Although the postoperative coagulation profile was normal, we suspected an SEH. Emergency magnetic resonance (MR) imaging was ordered, and the epidural catheter was removed before the study. The MR images revealed a hematoma extending from Th6 to Th9 (fig. 1). When the MR imaging was finished, however, the patient began to show signs of recovery from the paraplegia. She could dorsiflex both lower extremities on request. One hour after the MR imaging, she could hold the right knee flexed. Judging from the signs of spontaneous resolution, the neurosurgeon recommended conservative therapy with 8 mg intravenous dexamethasone every 8 h. Several hours after the conservative therapy, the muscle strength and sensory function improved gradually in both lower extremities.

By the fourth postoperative day, the patient had regained the ability to dorsiflex both feet and to hold both knees flexed. On the eighth postoperative day, she was able to stand by herself without assistance, and she was able to walk with a cane by the 14th postoperative day. An MR image obtained on the 14th postoperative day showed that the hematoma remained at the same level but was reduced in size (fig. 2). The patient was discharged from the hospital on the 40th postoperative day without neurologic deficits.

Placement of an epidural catheter may cause SEH more often than expected, but most SEHs remain asymptomatic. 7,8In some patients, however, SEH becomes symptomatic, especially if the patient has a bleeding tendency or is receiving anticoagulation therapy. 1–3Our patient did not have a bleeding tendency and was not receiving anticoagulants. She was also not taking nonsteroidal antiinflammatory drugs, which are known to impair platelet function. Traumatic or difficult epidural puncture can also cause symptomatic SEH even in patients without coagulation-related disorders or treatment. However, in our patient, the epidural block was performed easily and atraumatically by a well-trained anesthesiologist. The epidural congestion related to the compromised hepatic function in our patient may have been a contributing factor in the development of SEH. Hepatic dysfunction accompanied by increased portal pressure can divert blood into the epidural circulation and cause the veins to dilate and bleed easily. 8,9This could have led to the symptomatic change in this case. Spontaneous SEH has been reported in a few cases. 4,10MR study in our case, however, revealed that the SEH was located where the epidural block had been performed; therefore, spontaneous SEH was unlikely, although the cause of this SEH was not clear.

Irrespective of the cause, emergency decompressive laminectomy should be performed for SEH in patients presenting with progressive signs of spinal cord compression. 1,2Lawton et al.  11reviewed that rapid diagnosis of SEH and emergency surgical treatment maximize neurologic recovery, but patients with complete neurologic lesions or long-standing compression can improve substantially with surgery. However, surgical treatment may be unnecessary when the clinical symptoms are not progressive or when early recovery is observed. 5Wagner et al.  6reported that for patients with a stable or improving neurologic status, conservative management monitored by MR imaging might be the treatment of choice. Because our patient began to show signs of recovery from the paraplegia early after we were informed of symptoms, we chose conservative therapy. Our patient's neurologic function improved shortly after removal of the catheter, suggesting that a pressure effect from the epidural infusion may have worsened her functional deficit. This implies that epidural infusion may aggravate the symptoms of SEH, and that removal of the epidural catheter may improve the paraplegia, as occurred in our patient.

The delay in recognizing the SEH in this case should be addressed. As mentioned above, early diagnosis of SEH is key to preventing permanent neurologic deficit. In our hospital, nursing staff and surgeons check the patient's condition often during the postoperative period, and the anesthesiologist makes postoperative rounds on the first postoperative day as a rule. After the postoperative round by the anesthesiologist on the first postoperative day, however, our patient was not given a thorough examination for signs of neurologic dysfunction. Furthermore, our patient did not report her condition because she thought her symptoms were due to the epidural analgesia. Postoperative pain control by epidural analgesia has become popular. Thus, it is important to carefully explain the side effects of epidural block not only to patients but also to nursing staff and surgeons. In addition, patients who have undergone epidural block should be monitored carefully for potential neurologic deficit after surgery, and the postoperative round by the anesthesiologist should be made while patients receive continuous epidural infusion.

The authors thank Wasa Ueda, M.D. (Department of Perioperative Science, Kochi Medical School, Kohasu, Okoh-cho, Nankoku City, Kochi, Japan), for reviewing the manuscript.