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It Is Not Always the Epidural: A Case Report of Anterior Spinal Artery Ischemia in a Trauma Patient

Matos, Jennifer R. MD; George, Renuka M. MD; Wilson, Sylvia H. MD

doi: 10.1213/XAA.0000000000000764
Case Reports

Motor vehicle collisions impact millions of people annually resulting in multiinjury trauma. Anesthesiologists are consulted for rib fracture analgesia to improve respiratory mechanics and prevent intubation. This report describes a trauma patient who developed hypotension and lower extremity weakness after epidural placement for multiple rib fractures. Initially, hypotension was attributed to neuraxial sympathectomy. However, physical examination also indicated anterior spinal artery ischemia. Regional anesthesia and acute pain teams must be able to both identify contraindications and complications of regional techniques and discern when complications are not a result of regional interventions to initiate prompt management and definitive care.

From the Department of Anesthesia and Perioperative Medicine, Medical University of South Carolina, Charleston, South Carolina.

Accepted for publication February 14, 2018.

Funding: None.

The authors declare no conflicts of interest.

This case was presented at the 2017 Regional Anesthesia and Acute Pain Medicine Meeting of the American Society of Regional Anesthesia and Pain Medicine in San Francisco, CA, April 6–8, 2017.

Address correspondence to Jennifer R. Matos, MD, Department of Anesthesia and Perioperative Medicine, Medical University of South Carolina, 167 Ashley Ave, Suite 301, MSC 912, Charleston, SC 29425. Address e-mail to

Rib fractures are associated with increased morbidity and mortality. Management strategies to improve patient outcomes focus on both respiratory care and analgesia with multimodal medications and interventional pain therapies.1 Epidural analgesia provides excellent pain relief and augments respiratory mechanics following rib fractures in trauma patients. By decreasing sensation to the affected ribs, epidural analgesia improves vital capacity breaths, limits the likelihood of atelectasis, and may lead to shorter duration of mechanical ventilation.2 Despite its benefits neuraxial analgesia can also be associated with untoward side effects and complications.3 Regional anesthesia and acute pain teams must be prepared to recognize and treat these complications as they arise. However, they must also know when the epidural is not the culprit. We present a case of sudden hypotension coupled with loss of bilateral lower extremity motor function, pain, and temperature sensation with sparing of proprioception and fine touch attributed initially to thoracic epidural analgesia, but subsequently diagnosed as anterior spinal artery (ASA) ischemia by the regional anesthesia team.

The patient provided written consent for publication of this case.

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A 48-year-old male cyclist with history of ulcerative colitis sustained multiple injuries when struck by a motor vehicle traveling at 50 mph. At the scene, he was hypotensive with percent oxygen saturation in 70 seconds and underwent emergency needle decompression of a left pneumothorax. He was urgently taken to the operating room for an exploratory laparotomy and left-sided chest tube placement. Intraoperatively, a small bowel laceration, a mesenteric artery tear, and a liver injury with a subcapsular hematoma were repaired. During surgery, a phenylephrine infusion (20–30 µg/min) was administered for blood pressure (BP) support. At the conclusion of surgery, his vital signs were stable without vasopressors: heart rates 70–80 beats per minute, BP 118/56 mm Hg, and percent oxygen saturation 100% (Fio2 0.5). Arterial blood gas: pH 7.31, Paco2 44, Pao2 100, bicarbonate 22 mEq/L. He was extubated and transferred to the intensive care unit. Other injuries included bilateral rib fractures, sternal fracture with pulmonary contusions, descending perioaortic hematoma without direct aortic trauma, and bilateral small internal carotid artery dissections with no signs of extravasation on angiogram. Trauma injury scores4,5 are summarized in the Table.



Six hours postoperatively, when he was unable to generate volumes over 500 mL with spirometry, the regional anesthesia service was contacted for interventional analgesia for his rib fractures. After confirmation of normal coagulation parameters, hemodynamic, and an intact neurologic physical examination, the patient was consented for thoracic epidural analgesia. After 1 unsuccessful left paramedian approach, a thoracic epidural (T8–9) was inserted on the first midline pass and secured after a negative test dose (3 mL, lidocaine 1.5% with epinephrine 5 µg/mL). Because baseline BPs were in the 90s/50s mm Hg, an epidural infusion (0.1% bupivacaine, epinephrine 2 µg/mL) was initiated (5 mL/h) without a bolus dose. The regional anesthesia service remained at the bedside for 20 minutes. Epidural placement was well tolerated and initial hemodynamics remained unchanged.

Approximately 30 minutes after epidural infusion initiation and 50 minutes after the test dose, the regional service was called for systolic BPs in the 70s and neurologic changes. The epidural was stopped with <3 mL administered. Physical examination revealed bilateral lower extremity paralysis, loss of sensation to pain and temperature, and bilateral vision loss. Notably lower extremity proprioception and fine touch remained intact. American Spinal Injury Association Impairment scores based on the regional anesthesia team assessments are detailed in the Table.6 Neither blood nor cerebrospinal fluid (CSF) could be aspirated from his epidural catheter.

The patient was placed supine and 1-L crystalloid bolus administered. BP immediately improved (systolic BPs in the 90s mm Hg) coupled with return of vision and right lower extremity motor function. However, with 30° head elevation, BP decreased and right lower extremity strength and sensation lessened. These recovered with supine positioning and another 1-L intravenous crystalloid bolus. Due to concern for ASA ischemia, neurosurgery was consulted. They removed the epidural and placed a lumbar drain (L3–4 interspace) but did not measure opening pressure. With maintenance of mean arterial pressures (MAPs) >75 mm Hg, all neurologic symptoms were completely resolved by the conclusion of lumbar drain placement. A magnetic resonance imaging (MRI), performed 2.5 hours after lumbar drain placement and 3.5 hours after initial neurologic changes, showed no spinal cord compression or hematoma to account for his symptoms. Because of neurologic recovery with increased MAP goals and initial CSF drainage, neurosurgery elected to drain CSF by volume per hour (goal 5–10 mL/h) rather than based on CSF pressure. The lumbar drain was removed 3 days after placement.

Hemodynamics was stable without vasopressors after the first day. The patient made a complete recovery from his traumatic and neurologic injuries. He was discharged home on posttrauma day 8 and remained neurologically intact in clinic evaluation 1 week later.

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The ASA is primarily supplied by the artery of Adamkiewicz, which arises from intercostal and numerous smaller arteries, and supplies blood to the anterior two-thirds of the spinal cord. ASA interruption can lead to ischemia or infarction of the anterior and lateral columns of the spinal cord. Patients with ASA ischemia present with flaccid paralysis, because of corticospinal tract involvement, and loss of sensation to pain and temperature, because of spinothalamic tract involvement, below the level of the insult. However, proprioception, vibration sense, and fine touch are maintained because these arise from the posterior or dorsal columns supplied by 2 posterior spinal arteries.7 Bilateral symptoms are common, but unilateral presentations are not unusual. Hypotension can be both a cause and a manifestation of spinal cord ischemia. Although not seen in our patient, respiration can be affected adversely with cervical spine injuries leading to dysfunction of descending pathways and to diaphragmatic paresis.8 Our patient’s transient vision loss was likely ischemic optic neuropathy caused by systemic hypotension and resolved with hemodynamic support.9 Vision loss is not a typical finding for ASA ischemia.

ASA ischemia is a rare but potentially devastating disorder, which can lead to lifelong disability requiring extensive therapy and support, both physical and emotional. Because mortality rates approach 20%,10 swift recognition and neurosurgical involvement is vital for possible hematoma evacuation, relief of other cord compression, and evaluation for thrombosis. Diagnosis is clinical, but spinal MRI is used for confirmation and exclusion of other etiologies. In the acute phases, MRI is not very sensitive; swelling of the spinal cord with central focal hyperintensity is consistent with ischemia and usually appears after 24 hours.11 However, normal MRI with classic neurologic examination findings is typical with ASA ischemia.11,12 Vascular imaging can be difficult given that the smaller vessels supplying the ASA are only visible on dedicated spinal catheter angiograms.13

Once ASA ischemia is suspected, restoration of spinal cord perfusion pressure is crucial to minimize chronic neurologic sequelae. Ischemia results in edema and increased pressure around the spinal cord. Because spinal cord perfusion pressure is related to both MAP and CSF pressure,14 ASA ischemia treatment requires decreasing CSF pressure to minimize ischemic changes and elevating MAP to improve spinal cord perfusion. Lumbar drain placement facilitates prevention and treatment of elevated CSF pressures and minimizes the risk of reperfusion injury to the spinal cord.13 Hypotension is treated with judicious crystalloid administration, because aggressive administration may worsen spinal cord edema and ischemia, and combined with vasopressors.15 Vasopressor therapy targets both α and β receptors to balance the risks of vasospasm, systemic ischemia, and masking low fluid volumes.15

Sudden hypotension and neurologic changes in a polytrauma patient may have several etiologies including undiagnosed injury from trauma, epidural hematoma, stroke, hypovolemic or neurogenic shock, continued effects of anesthesia, and ASA ischemia. First, undiagnosed injuries must be excluded and supportive care administered. Epidural hematoma can present with neurologic changes and was high on the differential. However, the atraumatic catheter placement, normal coagulation, and intact lower extremity proprioception and fine touch made this unlikely, as later confirmed with MRI. The transient nature of the symptoms and symptomatic improvement with increased MAP made embolic and hemorrhagic strokes unlikely. Neurogenic and hypovolemic shock were also considered. Neurogenic shock, defined by bradycardia, hypovolemia, and temperature dysregulation, is caused by spinal cord injury. Conversely, hypovolemic shock presents with hypotension and tachycardia caused by reduced intravascular volume. However, neither of these present with reversible motor and sensory deficits. Although continued effects of anesthesia may impact BP changes, they would be unlikely to cause the described neurologic deficits. As trauma can directly disrupt the autoregulatory mechanisms maintaining spinal cord blood flow and indirectly cause vasospasm, systemic hypotension, and inflammatory processes,15 this is likely the cause of ASA ischemia in our patient.

Understanding the etiology behind this patient’s symptoms led to prompt and correct treatment. The regional anesthesia and acute pain team is uniquely qualified to know and interpret epidural side effects and complications. In our situation, the patient’s hypotension and severe neurologic changes were initially attributed as side effects of an epidural infusion. By evaluating the neuraxial catheter, epidural volume infused and performing a detailed neurologic examination, the team expedited both the diagnosis and treatment of ASA ischemia and contributed to the patient’s full neurologic recovery.

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Name: Jennifer R. Matos, MD.

Contribution: This author helped care for the patient and write the manuscript.

Name: Renuka M. George, MD.

Contribution: This author helped write the manuscript.

Name: Sylvia H. Wilson, MD.

Contribution: This author helped care for the patient and write the manuscript.

This manuscript was handled by: Raymond C. Roy, MD.

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