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• W2016806618 abstract "Epidural hematoma after spinal or epidural anesthesia has been acknowledged as a rare but a serious complication, which may cause permanent neurologic deficits even though emergency laminectomy is performed [1,2]. Previous reports have highlighted the substantial risk of this complication in patients receiving the subsequent anticoagulant or antiplatelet therapy [3,4]. We report a case of epidural hematoma accompanied by paraparesis after epidural anesthesia in the patient with hepatic cirrhosis, which was complicated by mild prolongation of prothrombin time and depression of platelet count. Case Report A 69-yr-old woman with a 2-yr history of hepatic cirrhosis was admitted and scheduled for partial resection of right lower lobe of the lung under a diagnosis of lung cancer. All biochemical laboratory data were within normal range except the slight increase of serum transaminase enzymes. Although platelet count was slightly decreased, the bleeding time by the Duke method was at the lower limit of the normal range Table 1. Prothrombin time was barely prolonged and fibrinogen was at the lower limit of normal range, whereas activated partial thromboplastin time and fibrin degradation product were within normal range Table 1. The patient had not taken any antiinflammatory drugs such as aspirin for more than a year.Table 1: Data of Bleeding and Coagulation Tests During the Perioperative PeriodA combination of epidural block with general anesthesia was planned for the surgery. On arrival at the operation room, the patient was placed in the left decubitus position. A 17-gauge Tuohy needle was advanced through the lateral approach in the T7-8 interspace into the epidural space, which was confirmed by loss of resistance technique. Since dark blood was noted to drip from the needle, it was immediately removed and was reinserted into the T9-10 interspace without any difficulties. No blood was withdrawn at this time, and a catheter was easily advanced 5 cm cephalad into the epidural space. There was no paresthesia nor any unusual pain during the procedure. General anesthesia was induced with thiopental and succinylcholine intravenously; the trachea was intubated, and anesthesia was maintained with isoflurane in nitrous oxide and oxygen. Twenty minutes after the surgical incision, 5 mL of 1% mepivacaine was administered through the epidural catheter after it was reconfirmed that no blood had been withdrawn from the catheter. Ninety minutes after the incision, blood was withdrawn via the epidural catheter when the second administration of mepivacaine was planned. After 3 mL of normal saline was administered, local anesthetics were discontinued for the remainder of the surgery. The total amount of blood loss during the 2-h surgery was 180 g. After surgery, bleeding was noted at the insertion point of the catheter which was then removed. During emergence from general anesthesia in the operation room, the patient was able to dorsiflex both feet on request. The patient was transferred to the general ward. Five hours after the surgery, a complaint by the patient of the weakness of both lower extremities was followed up by the surgeons. Because the neurologic abnormalities gradually worsened during the first postoperative day (POD 1), the surgeons consulted the neurologist the next day. The neurologic examination indicated moderately depressed muscle motor tone of both lower extremities with hypesthesia and hypalgesia; the patient could not hold her knees flexed. An emergency magnetic resonance imaging (MRI) was performed and revealed a posteriorly placed hematoma extending from T4-8 on both T1-proton density and T2-weighted images Figure 1. Because the neurologic findings had stabilized for several hours and seemed unlikely to get worse, the spine surgeon suggested conservative therapy with systemic administration of hypertonic glycerol and steroid. Both platelet count and prothrombin time were further depressed on the POD 1 compared to preoperative data Table 1. The latter was reversed on POD 3 by the infusion of 5 units of fresh frozen plasma for 2 days. By POD 4, the paraplegia had gradually improved; the patient was able to dorsiflex the right foot, but was unable to dorsiflex or move the left foot. Ten days after the surgery, the neurologic findings were further improved and the patient was able to stand and walk without assistance. The MRI on POD 14 showed that the area of hematoma was reduced but was still present at the same level Figure 2. The patient was discharged 1 mo after the surgery with mild hypesthesia on lower left leg.Figure 1: Sagittal magnetic resonance imaging view of the spine 2 days after surgery. A low intense lesion (black arrow), present behind the spinal cord, is displacing the cord anteriorly at T4-8.Figure 2: Sagittal magnetic resonance imaging view of the spine 2 wk after surgery. A hyperintense lesion (black arrow), indicating subacute hematoma, is still slightly displacing the cord anteriorly at T4-8.Discussion Epidural hematoma usually occurs due to the insertion of a needle into the epidural space, vascular abnormalities in the epidural venous plexus, and/or anticoagulant or antiplatelet therapy [3-5]. Most reports, however, indicate that intra- or postoperative anticoagulation therapy combined with the epidural or subarachnoidal approach is the main reason for excessive bleeding in the epidural space [1,6]. The only report of a patient who developed epidural hematoma and paraplegia without any coagulation disorder involved many lumbar punctures, which were considered traumatic enough to cause bleeding [5]. Since the epidural anesthesia in this case was performed by a well-trained anesthesiologist with more than 10 yr experience, we believe that the procedure by the epidural approach was not done in a rough manner compared to other cases. Considering the benefits of placing an epidural catheter for perioperative pain management, we decided to apply epidural anesthesia to this patient, even though mild coagulation disorder was found. As seen in this case, hepatic cirrhosis is usually accompanied by coagulopathy, associated with depressed platelet count and with the reduction in coagulation factors, mainly due to hypersplenism and/or depressed protein synthesis [7]. Although the platelet count was slightly depressed preoperatively, the normal bleeding time indicated that the platelet function was intact, and that the patient probably had no problem with the primary coagulation process. However, the prolonged prothrombin time suggested the moderate deterioration of the secondary coagulation process, while activated partial thromboplastin time was within normal range. Furthermore, the preoperative data on fibrinogen and fibrin degradation product suggested that fibrynolysis, which possibly might be accelerated in hepatic cirrhosis, was not observed in this case [8]. In addition to the coagulation abnormalities, hepatic cirrhosis causes portal vein hypertension, resulting in the development of collateral venous flow from splanchnic circulation [7]. The epidural veins, like the azygous or hemiazygous thoracic veins would be swollen and their walls would become thin. Thus, in patients with hepatic cirrhosis, the epidural venous plexus can be damaged easily by attempting an epidural puncture and then neurologic deficits become more readily apparent, with less blood pooling in the limited epidural space. Even when the epidural veins are ripped by epidural puncture, the bleeding is usually minimal and the blood leaks through the intervertebral foramina. Distended epidural venous plexus might be able to interrupt these routes. Therefore, we believe that various factors associated with hepatic cirrhosis were probably responsible for the development of epidural hematoma in this case. After signs of prolonged weakness, it is desirable to take active diagnostic measures much sooner than occurred in our case report. Although it has been emphasized that only emergency decompressive laminectomy is able to provide good outcome [1], this case indicated the possibility of spontaneous remission of hematoma and compressive force on the spinal cord by conservative therapy, as previously reported [9,10]. Given the fact that neurologic deficits were improved by treatment with glycerol and steroid administration, edema of the spinal cord, rather than the compressive force of hematoma, was the primary cause of the neurologic sequale. Rao and El-Etr [11] reported 3993 cases with continuous epidural or subarachnoid anesthesia and intraoperative heparin therapy without clinical evidence of an epidural hematoma. Another report showed that none of 950 patients receiving oral anticoagulants at the time of epidural catheter placement developed neurologic dysfunction [12]. However, the second MRI examination of the spinal cord Figure 2 might suggest that the presence of a hematoma in itself does not always cause neurologic deficits. Epidural hematoma may occur more often than expected and with no clinical symptoms after the insertion of an epidural catheter. We conclude that the indication for epidural anesthesia should be considered carefully in patients with hepatic cirrhosis. If epidural anesthesia is undertaken in such patients, a suspicion of epidural hematoma is warranted." @default.
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• W2016806618 title "Epidural Hematoma After Epidural Anesthesia in a Patient with Hepatic Cirrhosis" @default.
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