Chapter 71. Diagnosis & Management of Intraspinal, Epidural, & Peripheral Nerve Hematoma

Spinal epidural hematoma (SEH) is an accumulation of blood in the potential space between the dura and the bone. Hemorrhage into the spinal canal most commonly occurs in the epidural space because of the prominent epidural venous plexus. SEH may be spontaneous or may follow minor trauma, such as lumbar puncture or neuraxial anesthesia. It is more likely to occur in anticoagulated or thrombocytopenic patients, or in those with liver disease or alcoholism. Approximately one quarter to one third of all cases are associated with anticoagulation therapy.1,2 Spontaneous bleeding is rare but may be seen with anticoagulation, thrombolysis, blood dyscrasias, coagulopathies, thrombocytopenia, neoplasms, vascular malformations, or vertebral hemagioma.3,4 The peridural venous plexus is usually involved, though arterial sources of hemorrhage also occur.5 SEHs are mostly venous in nature because the venous plexus lacks valves, and the plexus has been shown to permit a reversal in blood flow during pressure increase from physical activity.6 Hematoma sites are usually found in the cervical and thoracic spine.7 Most SEHs are located dorsal to the dural sac because of the firm adherence of the dural sac to the posterior longitudinal ligament in the ventral aspect of the spinal canal. The dorsal aspect of the thoracic or lumbar region is involved commonly, and expansion is limited to a few vertebral levels.

Incidence

SEH represents a rare spinal emergency, with a frequency of less than 1% of spinal space-occupying lesions.8 SEH affects 1 per 1,000,000 people annually.9,10 The actual incidence of neurologic dysfunction resulting from hemorrhagic complications associated with central neural blockade is unknown. In an extensive review of the literature, the calculated incidence was approximated to be less than 1 in 150,000 epidural and less than 1 in 220,000 spinal anesthesias.11 No racial predilection has been reported, but SEH is more frequent in females. Increased age has been associated with more frequent SEH.

Anticoagulant therapy in association with neuraxial analgesia, as well as the length and intensity of anticoagulation, has been identified as one of the most important risk factors for epidural hematoma.12 Decreased weight and concomitant hepatic or renal disease, which may exaggerate the anticoagulant response, represent theoretical concerns for bleeding tendency. Thrombolytic therapy represents the greatest risk factor for bleeding complications.13

History & Physical Examination

The patient is usually in significant distress and usually presents with a severe, localized constant back pain with or without a radicular component that may mimic disc herniation. Associated symptoms may include weakness, numbness, and urinary or fecal incontinence.14,15 The onset of pain is occasionally related to minor straining such as with defecation, lifting, coughing, or sneezing, but in the majority of cases the onset of pain is spontaneous.16,17 Signs of spinal cord and nerve root dysfunction appear rapidly and may progress to paraparesis or paraplegia depending on the level of the lesion. In the lumbar spine, the epidural hematoma may mimic an acute disc herniation. In the cases of epidural hematomas that are related to neuraxial anesthesia or lumbar puncture, the presence of new or progressive postoperative neurologic symptoms should alert the physician to a possible epidural hematoma.

Back pain is enhanced by percussion over the spine, as well as maneuvers that increase intraspinal pressure such as coughing, sneezing, or straining. Depending on the level and the size of the hematoma, physical findings may include unilateral or bilateral weakness, sensory deficits with unilateral or bilateral radicular paresthesias, various alterations in deep tendon reflexes, and alterations of bladder or anal sphincter tone.18

Etiology & Location of Hematoma

The proposed factors that can cause spinal epidural hematoma include trauma, anticoagulation, thrombolysis, lumbar puncture, epidural or spinal anesthesia, interventional spine procedures or surgeries, coagulopathy or bleeding diathesis, hepatic disease with portal hypertension, vascular malformation, disk herniation, Paget disease of the vertebral bones, Valsalva maneuver, and hypertension.19 The most important causes of spontaneous spinal epidural hematoma are clotting disorders, which may be acquired (anticoagulant therapy, malignancies) or congenital (hemophilia).20,21 Vascular malformations are rarely responsible for spontaneous epidural hematomas; only 4% in a series of 158 cases and 6.5% in a series of 199 cases were reported to be due to vascular malformation.22,23 Other less common predisposing factors include systemic lupus erythematosus, ankylosing spondylitis, rheumatoid arthritis, Paget disease, disc herniation, and hypertension.17,24,25 No underlying cause can be identified in about 40% to 50% of cases. The most widely accepted hypothesis is that of venous bleeding. Epidural veins are valveless and are located in the low-pressure epidural space. These veins are unprotected from sudden increases in intraabdominal or intrathoracic pressure (as in the Valsalva maneuver), leading to rupture and hemorrhage.26,27 It has been proposed that an increase in venous pressure in the epidural space, in association with the hemodynamic changes of pregnancy, may predispose to rupture of a preexisting pathologic venous wall.28,29 The epidural venous plexus is most prominent in the thoracic spine.23 Spontaneous SEH most often is located in the thoracic and cervicothoracic region followed by the thoracolumbar location and extends over a few vertebral body levels.8,15,16,23 Spinal epidural hematoma is usually posterior or posterolateral to the thecal sac (Figure 71–1).23

Diagnosis of SEH

Clinical findings of SEH usually include neurologic deficit during the acute stage; the motor and sensory deficits may rapidly develop into paraplegia, quadriplegia, or autonomic dysfunction. Patients usually present with acute axial spine pain that radiates to corresponding dermatomes and evolving focal neurologic deficit with signs of nerve root or spinal cord compression.30 The epidural hematoma usually presents itself within the first 24–48 h after surgery. Early clinical signs are increased pain or focal neurologic deficit, often in areas not present preoperatively or in areas affected by the surgery. Any new or progressive neurologic symptoms warrant immediate clinical evaluation and diagnostic work-up to rule out any space-occupying lesion including epidural hematoma. A new or progressive neurologic deficit occurring in the presence of epidural analgesia mandates immediate discontinuation of the infusion, with the catheter left in place, to rule out any contribution from the local anesthetic. If the epidural infusion is the cause of the neurologic manifestation, a return of sensory and motor function should be noted. Otherwise, an immediate work-up and radiographic imaging studies should be obtained and a consultation with a neurosurgeon sought.

In view of acute axial back pain with deterioration of neurologic deficits, pathologic entities associated with nerve root and spinal cord compression need to be evaluated immediately, to differentiate miscellaneous lesions simulating SEH. The clinical presentation of a patient with suspected epidural hematoma may resemble epidural abscess, spinal cord disease, neoplasms, and acute disc herniation. The differential diagnoses of new or progressive postoperative neurologic symptoms include surgical neuropraxia, prolonged or exaggerated neuraxial block, anterior spinal artery syndrome, exacerbation of a preexisting neurologic disorder, and presentation of a previously undiagnosed neurologic condition.

Complete blood count with platelets should be ordered to assess the extent of bleeding and to determine the presence of infection. Prothrombin time and activated partial thromboplastin time determine the presence of bleeding diathesis.

Rapid diagnostic radiographic evaluation is essential to minimize delay in treatment of spinal epidural hematoma. Currently, magnetic resonance imaging (MRI) is the diagnostic imaging of choice for spinal emergencies because it allows rapid, noninvasive evaluation of the vertebral column and the spinal cord in all planes. Spinal MRI may delineate the location of an epidural hematoma and identify an associated vascular malformation; it will provide information about the extent of the hematoma as well as the degree of cord compression. MRI is also helpful in determining the age of the hematoma (see Figure 71–1).17,31,32 The chronologic characteristics of an MRI of a spinal epidural hematoma are similar to those seen with intracranial hemorrhage. In the hyperacute stage (first 6 h), the spinal epidural hematoma appears as isointense as the spinal cord on T1-weighted images and mildly hyperintense and heterogeneous on T2-weighted images, as a result of the presence of intracellular oxyhemoglobin. In an acute stage (7–72 h) the hematoma is still isointense on T1-weighted images and becomes hypointense on T2-weighted images. This is due to the presence of intracellular deoxyhemoglobin, which causes T2 shortening. As the concentration of methemoglobin increases, the hematoma becomes hyperintense and homogeneous on T1- and T2-weighted images. Gadolinium-enhanced magnetic resonance arteriography (MRA) may further define the extent of an arteriovenous malformation.

Conventional CT may diagnose an epidural hematoma, but may give false-negative results if the hematoma is isodense to the thecal sac or the spinal cord and if the image quality is affected by artifacts often seen in upper thoracic region.32 Spinal computed tomography (CT) scanning may be nondiagnostic in the thoracic spine, where resolution is poorer than in the lumbar and cervical spine because of the high contrast between the lung parenchyma and vertebral bone.

Conventional angiography may be required to definitely demonstrate the presence of a vascular malformation.17,27 Myelography, and later CT, used to be the main diagnostic modalities for diagnosing epidural hematomas.33 Myelography and CT-myelography may show an epidural lesion with partial or complete spinal block, but is not specific; it is invasive and may worsen the clinical status. Although myelography can demonstrate signs of compression with visualization of nonspecific contrast blockade or extradural convex compression, it cannot be used to determine the nature and the real extent of the lesion.34 Combined with spinal CT scanning, SEH can be viewed as an intraspinal biconvex and hyperdense lesion with the density equivalent to blood.35

Prevention, Treatment, & Prognosis

Lumbar puncture or epidural anesthesia should be avoided in individuals who are on anticoagulant therapy, following thrombolysis, or when a bleeding diathesis is suspected. Anesthesiologists are urged to be up to date on their knowledge of anticoagulation protocols, new anticoagulant medications, and new guideline recommendations. The decision to perform neuraxial blockade and the timing of catheter removal in a patient receiving antithrombotic therapy should be made on an individual basis, weighing the risks of spinal hematoma with the benefits of regional anesthesia for a specific patient. The American Society of Regional Anesthesia has published consensus statements on neuraxial anesthesia and anticoagulation with current updates, which provides an up-to-date source for guidelines in the decision-making process in performing neuraxial anesthesia in a patient with risk factors (see Chapter 70, Neuraxial Anesthesia and Peripheral Nerve Blocks in Patients on Anticoagulants).36

Although some case reports have described successful conservative management of epidural hematoma, urgent surgical decompression is the treatment of choice for SEH causing acute compromise of cord function.37 A practical approach to management of suspected epidural hematoma is displayed in Figure 71–2. Nonoperative treatment with good outcome was mainly reported in hematomas localized at the cauda equina level and those with mild neurologic deficit.20 Although not all spinal hematomas are treated with emergency laminectomy and spontaneous resolution of deficits has been reported in the literature,38 the decision to observe or surgically intervene is a neurosurgical one. The critical factors for recovery after SEH are the level of preoperative neurologic deficit and the operative interval.20,39 In complete preoperative sensorimotor loss, surgery within 36 h of onset of symptoms correlates with favorable outcome.31 Laminectomy is followed by evacuation of the hematoma, coagulation of bleeding sites, and inspection of the dura. The dura is then tented to the bone and, occasionally, epidural drains are employed for as long as 24 h. The prognosis is worse when there is a delay between the injury and surgical intervention.31 It was noted that complete neurologic recovery was unlikely if more than 8 h has elapsed between the development of paralysis and surgical intervention.40 Recovery without surgery is rare, and surgical consultation for consideration of emergent decompressive laminectomy must be obtained as soon as possible. The overall mortality rate is 8%.41 Functional recovery is related primarily to the length of time the symptoms are present, and recovery after 72 h of symptoms, although rare,42 has been reported.43 Prognosis for neurologic recovery primarily depends on the patient's preoperative neurologic status and duration of neurologic dysfunction.26,44 Since neurologic outcome is linked to early diagnosis and intervention, consultation with a neurosurgeon about the potential emergent evacuation of the hematoma should be obtained as soon as possible.26 Complications of SEH include neurologic deficits, paraplegia, spasticity, neuropathic pain, and urinary or fecal sphincter dysfunction.

Spinal Epidural Hematoma: Summary

Spinal epidural hematoma comprises a heterogeneous group of disorders with the final common result of hemorrhage in the spinal epidural space. SEH may be acute or chronic, spontaneous, posttraumatic, or iatrogenic. Its occurrence appears to be particularly associated with acquired coagulopathy from medications and disease states. MRI plays an especially important diagnostic role. Surgery needs to be performed as rapidly as possible because the interval between the onset of symptoms and surgery, together with the preoperative clinical status, determine the clinical outcome.

Since spinal epidural hematoma is a rare and potentially reversible cause of spinal cord compression, it is essential that the diagnosis be made as early as possible to enable full recovery. Since spinal hematoma may occur even in the absence of identifiable risk factors, vigilance in monitoring any new neurologic symptoms is critical in allowing early evaluation of neurologic dysfunction and prompt intervention. It is a potentially reversible cause of spinal cord and root compression, and the prompt diagnosis and treatment of this relatively rare condition are important. When accomplished rapidly, surgical decompression can result in full functional recovery.

There have been a few case reports of hematoma after peripheral nerve blocks (Figure 71–3). There were two case reports of psoas hematoma after lumbar plexus block.45,46 In one patient, enoxaparin was give 19.5 h before the block and 4.5 h after the block.45 Note that the intervals between the block and the administration of enoxaparin were within the guidelines recommended by the American Society of Regional Anesthesia,36 although the patient also took aspirin. The enoxaparin was discontinued, and resorption of the hematoma was observed. In the other reported cases, warfarin and heparin infusion were administered 8 h after the block and, in another patient, enoxaparin was given 40 h after the block.46 Another case of psoas hematoma was reported after lumbar sympathetic block. One patient was on ticlopidine during the block, and the other patient took clopidogrel 3 days before the block.47 In these case reports, the blocks were performed near blood vessels in an expandable and noncompressible area. These case reports must also be viewed in the context of spontaneous hematomas in patients who were on anticoagulants.48–51

As stated in Chapter 70, the symptoms of hematoma after peripheral nerve block include pain (flank or paravertebral pain or groin pain in psoas bleeding), tenderness in the area, fall in hemoglobin/hematocrit, fall in blood pressure, and sensory and motor deficit. CT scan is used in the diagnosis. In one case report,52 ultrasound demonstrated the presence of renal subcapsular hematoma. The increased use of ultrasound in peripheral nerve blocks will make it easier for clinicians to follow suspected cases of bleeding after peripheral nerve blocks.

Treatments of hematoma after peripheral nerve blocks usually include surgical consult, blood transfusion as necessary, and watchful waiting versus surgical drainage. In the case reports of psoas hematoma,45,52 no surgical evacuation of the hematoma was performed. The patients regained their sensory and motor status in a few days to 4 months after the diagnosis. The expandable nature of the site probably helped decreased the possibility of irreversible nerve ischemia. Since there are no published guidelines on anticoagulants and peripheral nerve blocks, anesthesiologists should individualize their decision on the advisability of performing peripheral nerve blocks in patients on anticoagulants. Anesthesiologists should discuss the risks and benefits of the block with the patient and the surgeon. If a block is performed, the patient should be followed very closely after the block and observed for signs and symptoms of peripheral hematoma.