Spinal cord infarction (SCI) is a rare but devastating disorder. A majority of infarctions involve anterior spinal cord and present with acute quadriparesis or paraparesis depending on the level of the spinal cord involved; rarely, weakness of a single limb may be seen, and even more rarely hemiparesis mimicking cerebral infarction. The diagnosis is made clinically and by excluding other potential explanations for the patient’s symptoms. Spine magnetic resonance imaging (MRI) may confirm the diagnosis of infarction, although it can be normal in the acute period. Depending on the clinical scenario, urgent MRI may be needed to exclude compressive lesions of the cord which may cause similar symptoms but require a completely different therapeutic approach (e.g., decompressive surgery and/or steroids).
The etiology of SCI is critical to management. The most important distinction is whether SCI occurs in the perioperative or procedural setting or in a spontaneous outpatient setting. The vast majority of SCI occurs periprocedurally, typically complicating aortic surgery.
SCI is a major complication of spinal and descending aortic surgery that puts the spinal cord at risk due to loss or injury of critical intercostal arteries that collateralize the anterior spinal artery. In an effort to reduce this complication, surgical techniques have been developed to identify and reduce this complication, including intraoperative neurophysiologic monitoring (IOM) and the use of lumbar cerebrospinal fluid drains to increase spinal cord perfusion.
If spinal cord ischemia is detected by IOM, spinal cord perfusion is enhanced by increasing systemic blood pressure. Blood pressure goals must be individualized due to the competing risk of hemorrhage or exacerbation of underlying aortic disease. It is reasonable to increase mean arterial pressure in increments of 10 mmHg until there is clinical improvement or it is felt unsafe to increase pressure further. Perfusion can also be augmented by placing a lumbar cerebrospinal fluid drain to reduce intracranial pressure to 8–12 cm H 2 O. In some cases, a lumbar drain will already be present because it was prophylactically placed in the operating room. Additional considerations to augment cord perfusion include surgical vascular manipulations and optimizing oxygen delivery with transfusion.
Reversal of the ischemia in many cases occurs intraoperatively, but if a patient arouses from anesthesia with any degree of weakness, a similar protocol is followed.
SCI is associated with high morbidity and mortality, and patients require substantial supportive care. When there is neurologic improvement, aggressive support should be continued until stability has been present for at least 24 hours. These patients are at high risk for reoccurrence of ischemia, typically manifested as fluctuating or worsening weakness, particularly with even mild instances of hypotension and thus require vigilant observation as they are weaned from SCI treatment. After patients have stabilized, they may begin their typical postoperative care. If patients with complete paralysis do not improve despite aggressive management, the infarction can be considered complete after a 24-hour period and aggressive support can be discontinued.
The mechanisms of spontaneous spinal cord ischemia are diverse and include embolism and severe aortic atherosclerosis, but also unusual causes such as surfer’s myelopathy and fibrocartilaginous emboli. Perhaps the most important and treatable cause is aortic dissection, resulting in loss of perfusion to critical spinal cord collateral blood flow. Computed tomography angiography of the chest should be performed to identify aortic dissection in patients with spontaneous SCI because management typically requires emergent surgical intervention.
While surgical repair of aortic dissection is critical, blood pressure should be supported to augment spinal cord perfusion. Extremity malperfusion syndromes should be excluded, as they often mimic or mask SCI in this setting.
Cervical cord infarction is more often embolic than perfusional. While reperfusion therapies such as thrombolysis are theoretically appealing, there is little data on such treatment and conservative management is generally pursued. Spontaneous thoracic SCI in the absence of aortic dissection is very uncommon, but can be due to atherosclerosis of perforating arteries, surfer’s myelopathy, or fibrocartilaginous emboli. Thoracic ischemia is more likely to be perfusional, as compared to cervical ischemia, so blood pressure and volume support is more critical.
If a patient’s SCI is persistent and greater than 24 hours in length, it is unlikely that aggressive management will change the outcome. If the onset of spontaneous SCI is less than 24 hours, in particular if symptoms are fluctuating or progressing, aggressive management should be pursued, very similar to that undertaken in the perioperative setting.