Epidural hematoma related to neuraxial anesthesia is a rare but potentially devastating complication; published reports in patients undergoing epidural catheter placement estimate an incidence of about 1 case in 150,000 anesthetics.1–3 Most often, symptoms arise within a few hours after placement or removal of the catheter.3 Cases of spontaneous epidural hematoma occurring in pregnancy are exceedingly rare; only 6 have been reported in the English-language literature, only 1 of which occurred after delivery.3–7 We found no previous case reports of epidural hematoma presenting more than 1 week after catheter removal. We report a case of an epidural hematoma in a previously healthy woman who presented 9 days after labor and vaginal delivery with epidural analgesia. Written informed consent was obtained from the patient before preparation and submission of the manuscript.
A 32-year-old, G1P0 woman with body mass index of 27 kg/m2 underwent epidural catheter placement during labor. Localization of the epidural space required 2 passes in the midline of the L2-3 interspace with an 18-gauge Tuohy needle. After the epidural space was identified by loss of resistance to saline at 7 cm from the skin, a flexible, wire-embedded catheter (FlexTip Plus®; Arrow International, Reading, PA) was passed without resistance, paresthesia, or discomfort to a distance 6 cm beyond the tip of the needle. The catheter was secured at 13 cm at the skin. Aspiration through the catheter with a 3-mL syringe failed to yield blood or fluid. Lidocaine 45 mg and epinephrine 15 μg were administered without change in heart rate or initiation of motor or sensory loss. Subsequent analgesia was effective, and the remainder of labor and delivery (5 hours) progressed without complication. Shortly after delivery, the patient developed profuse vaginal bleeding and was taken to the operating room for cervical dilation and curettage; surgical anesthesia was successfully administered via the in situ epidural catheter. The cause of the bleeding was not clearly attributed to retained placental fragments or cervical tear. Total estimated blood loss was 750 mL, and 2.5 L lactated Ringer solution was administered. After the procedure, the epidural catheter was removed, and the patient was discharged home 2 days later in excellent condition without complaints.
Nine days later, she presented to the emergency department with severe low back pain and acute, ascending lower extremity paralysis that began 2 hours before arrival. Immediate evaluation by obstetric and anesthesia physicians revealed arterial blood pressure of 190/100 mm Hg and lower extremity paralysis and sensory deficit ascending to the umbilicus. Laboratory values included hematocrit 30%, platelet count 358 × 109/μL, prothrombin time (PT) 14.0 seconds (normal, 12.5–16.0 seconds; international normalized ratio, 1.0), and fibrinogen 236 mg/dL (normal, 202–430 mg/dL). Dexamethasone 12 mg was administered IV and urgent neurosurgical consultation was requested. Magnetic resonance imaging revealed a large, cylindrical heterogeneous fluid collection around the spine extending from C6-7 through the lumbar region, with significant mass effect, cord deformity, and T2 signal prolongation at T9-11; the majority of the blood had collected between T6 and T12 (Fig. 1). Within 2 hours of her arrival at the hospital, she was taken to the operating room to undergo decompression surgery. Baseline laboratory values revealed a hematocrit of 28%, and platelet count, PT, and partial thromboplastin time within normal limits. Neither thromboelastography nor platelet function assay was available in our institution. Because of ongoing blood loss and oozing in the field, 1 pheresis pack of platelets and 4 U fresh frozen plasma were administered, resulting in satisfactory hemostasis. Three units of packed red blood cells were administered during surgery, and at the conclusion of the 4-hour case, blood loss was estimated to be 1.5 L. The paralysis resolved completely over the next 12 hours, and the sensory examination returned to normal over the next week with the exception of an area of paresthesia along the medial aspect of her lower right medial leg.
Neuroangiographic evaluation for spinal arteriovascular malformation was negative. A subsequent detailed history, performed in conjunction with the hematology service, did not reveal personal or family history of abnormal bleeding. The patient was noted to have used ibuprofen 800 mg every 8 hours for 9 days after delivery for low back and generalized musculoskeletal pain. Further laboratory workup conducted 2 weeks after hematoma evacuation included a ristocetin cofactor assay of 88% (reference range, 42%–200%), fibrinogen of 301 mg/dL (normal range, 202–430 mg/dL), and factor VIII activity of 162% (normal, 43%–168%). These values were all within 2 standard deviations of mean values at our institution for a patient who is not pregnant. At 2-month follow-up, the patient had made a complete neurologic recovery.
Spinal epidural hematoma is a rare but potentially devastating event, classified as spontaneous (occurring without apparent cause or with delayed onset after minor injury), or secondary to identifiable cause, including spinal or epidural anesthesia. Patients at higher risk for hematoma after epidural anesthesia include those with advanced age, spinal stenosis, coagulopathy (longstanding or acute), platelet inhibition, arteriovenous malformation, or multiple punctures.8 Overall, hematomas related to neuraxial anesthesia seem to be less frequent in the obstetrical compared with the elderly surgical population.2 There are also rare reports of spontaneous epidural hematoma in parturients that occur in the absence of neuraxial block, and delay in recognition and management has resulted in devastating consequences.2,9 This particular case was unusual because it occurred more than 1 week after epidural catheter removal, beyond the timeframe previously described after an inciting event.10
A systematic review of 613 reported cases of spinal and epidural hematoma demonstrates that trauma, neuraxial anesthesia, coagulopathy, arteriovenous malformation, or a combination of these factors, are frequently associated with hematoma; 30% were found to have no identifiable cause.3 In all, 63 cases were associated with neuraxial anesthesia. Of these 63 cases, coagulation status was known in 49; 34 of 49 had confirmed coagulopathy or were receiving concurrent anticoagulation therapy; and 41 of these 49 patients developed symptoms within 72 hours of the neuraxial procedure (Fig. 2).3 Five pregnant patients were among this group of 63; 1 had an elevated PT from hepatic disease related to the pregnancy, another was classified as hypertensive, and the remaining 3 had no identifiable risk factors.
What may have put our patient at risk? The presence of postpartum hemorrhage may have been related to numerous factors other than coagulation disorder, but could also have been related to a subtle disorder of coagulation that was not detected during her workup after surgery.11,12 Although the values of her PT, fibrinogen, and subsequent ristocetin cofactor assay and factor VIII activity were within the normal range for a nonpregnant patient, these may have been falsely normal given the typical changes in coagulation state that accompany pregnancy and the early postpartum period, when circulating levels of clotting factors may be 20% to 200% above nonpregnant levels and do not fully return to nonpregnancy baseline values until 8 weeks postpartum.13
Additionally, we questioned whether the hematoma could have been related to the patient's nonsteroidal antiinflammatory drug (NSAID) use, or to NSAIDs in combination with a subtle impairment in coagulation function. Antiplatelet drugs, including nonselective NSAIDs and aspirin, taken within 1 week of surgery, have been associated with increased risk of hematoma after craniotomy and hip arthroplasty.14,15 However, there is consensus among experts that NSAID use does not increase risk of epidural hematoma. This consensus is based on prospective studies of hundreds of NSAID users undergoing neuraxial anesthesia8 and epidural steroid injection.11 Use of thromboelastography or other platelet function assays at the time of presentation might have established whether NSAID use contributed to the development of this epidural hematoma. A more thorough hematologic evaluation, performed further out from the peripartum period, would be needed to exclude an underlying bleeding disorder; to date, the patient has declined further workup.
In either case, it is possible that inadequate hemostasis caused gradual expansion of a small collection of blood that was initiated by epidural placement or removal. Over days, this small asymptomatic hematoma may have slowly continued to bleed and expand, eventually reaching a critical size sufficient to cause dramatic symptoms. The predominantly thoracic location of the hemorrhage, higher than the site of epidural puncture, does not argue against the epidural catheter as the primary cause. First, the catheter tip may have extended a considerable distance in a cephalad direction, and catheter removal may have initiated trauma at that location. Second, blood from a hematoma secondary to needle trauma in the lumbar region may have collected preferentially in the thoracic epidural space because of anatomic factors such as the relatively narrower dimension of the spinal cord, convexity of the thoracic spine, the relatively lower intrathoracic pressure, and greater capacity of the thoracic epidural space.16,17
Given the prolonged period of time between catheter manipulation and presentation of symptoms, it is possible that this patient's condition resulted from factors other than epidural catheter placement. However, we think it more likely that the event was related to epidural catheter placement/removal, with possible contributing factors including elevated venous pressure related to the pregnancy, platelet inhibition from persistent NSAID use, and hypertension. The relative contribution of these various factors, if any, however, remains undetermined.
Pregnancy is characterized by a relatively hypercoagulable state, effectively reducing the risk of epidural hematoma. However, the epidural space houses an extensive venous system containing tributaries from the spinal cord and vertebral bodies that drain into the external vertebral venous plexus and become more engorged during pregnancy. Because this venous system does not contain valves, and exists within a low-pressure environment, any pressure exerted proximally because of a Valsalva maneuver, vomiting, or mechanical compression of the vena cava can dramatically increase the transmural venous pressure, leaving the veins vulnerable to injury. It has been postulated that spontaneous epidural hematoma may occur from preexisting faults in the venous wall exacerbated by well-described mechanical and hyperdynamic conditions existing in the peripartum period.4–7,18
Numerous studies have demonstrated the most favorable outcomes when a symptomatic hematoma is decompressed within 36 hours, and some authors suggest even faster intervention, within 6 hours.19,20 In this case, intervention occurred within 4 hours of the onset of symptoms. Through emergent, definitive treatment, the patient made a full recovery, illustrating the importance of prompt recognition and treatment of epidural hematoma to maximize the patient's chance of a favorable outcome.
PJG helped with patient consent, data collection, and manuscript preparation; WRM helped with manuscript preparation; and REM helped with data collection, manuscript preparation, and construction of figures.
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