NYSORA - The New York School of Regional Anesthesia: Diagnosis and Managment of Intraspinal, Epidural, and Peripheral Nerve Hematoma

Diagnosis and Managment of Intraspinal, Epidural, and Peripheral Nerve Hematoma
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Richard Claudio  on 2009-03-15 19:43:00
 
Authors: Rasha S. Jabri, MD; Steven Deschner, MD; Honorio T. Benzon, MD
TABLE OF CONTENTS
Introduction
Incidence
History & Physical Examination
Etiology & Location of Hematoma
Diagnosis of SEH
Prevention, Treatment & Prognosis
Spinal Epidural Hematoma: Summary
Peripheral Hematoma after Nerve Blocks
INTRODUCTION
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.
Clinical Pearls
*Hemorrhage into the spinal canal most commonly occursin 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. 	*SEH
occurs primarily in anticoagulated or thrombocytopenic patients. 	*The risk of
spinal hematoma in patients without overt risk factors is less than 1 in
150,000 epidural and less than 1 in 220,000 spinal anesthesias.
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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
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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 symptomsmay includeweakness,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 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.
Clinical Pearls
*The patient 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.
	*Return of sensory or motor deficit several hours after spinal or epidural
block has worn off (with or without back pain) is highly pathognomonic and
should be considered and treated as spinal or epidural hematoma until proven
otherwise.
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
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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 1).23
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DIAGNOSIS OF SEH
Figure 1. Sagittal magnetic resonance images of the thoracolumbar spine. A
large complex epidural hematoma extending from T3 to T10 through T11 is seen
with hypo- and isodense signal characteristics on a T1-weighted image (left;
arrows) and hyperintense signal characteristics on a T2-weighted image (right;
arrows). At the center of the hematoma, the spinal cord abuts the posterior
aspect of the thoracic vertebral bodies (left). No signal abnormalities of the
cord itself are seen.
Reprinted, with permission, from Schwarz SKW, Wong CL, McDonald WN: Spontaneous
recovery from a spinal epidural hematoma with atypical presentation in a
nonagenarian. Can J Anesth 2004;51:557–561.
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 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 onT2-weightedimages.
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 sack 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 mayworsen 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
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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.36
Figure 2. Practical approach to decision-making in work-up and treatment of a
patient with suspected epidural hematoma. CSF = cerebrospinal fluid, MRI =
magnetic resonance imaging, CBC = complete blood count.
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 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 neurologicdysfunction.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.
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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 associatedwith 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 symptomsand surgery, togetherwith 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.
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PERIPHERAL HEMATOMA AFTER NERVE BLOCKS
Figure 3. Neck Hematoma. Sizeable neck hematoma in a patient in whom external
the jugular vein was punctured with an 18-gauge Tuohy-style needle during
insertion of a catheter in the interscalene groove. The hematoma shown was
self-contained and was treated conservatively with local compression.
There have been a few case reports of hematoma after peripheral nerve blocks
(Figure 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 Anesthesia36 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 3days before the block.47 The blocks were
performed near blood vessels in an expandable and noncompressible areas. These
case reports must also be viewed in the context of spontaneous hematomas in
patients who were on anticoagulants.48–51
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.
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