Version May 2024
INTRODUCTION — Spinal cord infarction is a rare but often devastating vascular disorder caused by one of several etiologies. Patients typically present with acute paraparesis or quadriparesis, depending on the level of the spinal cord involved. The severity can vary, and while many patients make some functional recovery, permanent and disabling neurologic deficits remain in many. Specific treatment options are limited.
This topic will review the acute treatment and prognosis of spinal cord infarction. The etiologies, clinical features, diagnosis, and chronic complications of spinal cord infarction are discussed separately.
●(See "Spinal cord infarction: Epidemiology and etiologies".)
●(See "Spinal cord infarction: Clinical presentation and diagnosis".)
●(See "Chronic complications of spinal cord injury and disease".)
The management of acute traumatic spinal cord injury is discussed elsewhere. (See "Acute traumatic spinal cord injury".)
TREATMENT
Acute management — The management of patients with acute spinal cord infarction begins with identifying or excluding high-risk causes such as aortic dissection that require specific treatment to prevent further morbidity. Overall treatment of spinal cord ischemia is directed toward minimizing or reversing neurologic dysfunction and is guided by principles of cerebral infarction and traumatic spinal cord injury. This generally involves optimizing spinal cord perfusion and initiating cause-specific secondary preventive therapies. However, evidence of efficacy for these treatment options used for spinal cord infarction is limited.
Identify high-risk underlying causes that require urgent treatment — The etiology of spinal cord infarction may be apparent in some cases, such as when symptoms occur in the setting of aortic or spinal surgery or during severe systemic hypoperfusion (eg, cardiac arrest). In other cases, the etiology of spinal cord infarction may be uncertain despite initial clinical examination and diagnostic spinal imaging. For patients with an uncertain cause of spinal cord infarction, further diagnostic testing is warranted to identify underlying causes.
Patients with clinical features of or risk factors for high-risk underlying causes of spinal cord infarction require urgent evaluation to guide specific acute treatment and reduce the immediate risk of further morbidity. As examples, this includes patients with spinal cord infarction and additional clinical features or risk factors suggestive of:
●Aortic dissection, aneurysm, or thrombosis (eg, hemodynamic instability, severe chest/back pain, reduced/asymmetric peripheral pulses)
●Vertebral artery dissection (eg, rostral spinal cord infarction, associated brainstem symptoms)
●Infective endocarditis (eg, fever, new heart murmur)
●Bacterial meningitis (eg, fever, meningismus)
Etiologic testing to identify the underlying cause of spinal cord infarction is discussed separately. (See "Spinal cord infarction: Clinical presentation and diagnosis", section on 'Testing for underlying cause'.)
Addressing spinal cord hypoperfusion — Spinal cord infarction may be caused by systemic hypotension or other conditions that cause hypoperfusion of the spinal cord, such as aortic surgery. Strategies to improve inadequate spinal cord perfusion may halt or reverse progression of neurologic symptoms due to acute spinal cord infarction in some patients. Treatment options vary by individual clinical circumstances and available resources. These include:
●Correct systemic hypotension – Correction of hypotension, if present, is typically the first step to improve neurologic deficits due to presumed spinal cord hypoperfusion. This may involve administration of intravenous fluids and/or treatment of specific conditions such as heart failure or anemia.
●Trial of blood pressure augmentation with vasopressors – We attempt a trial of blood pressure augmentation for patients with possible reversible spinal hypoperfusion, such as patients who present acutely (eg, <24 hours), patients with systemic hypotension unresponsive to fluid resuscitation, and those whose symptoms fluctuate with blood pressure changes or improve with recumbent/Trendelenburg positioning. Reversal of neurologic deficits has been reported with blood pressure augmentation in some cases of acute spinal cord infarction due to aortic surgery [1,2] and other cases when symptoms fluctuated with blood pressure changes [3].
The specific blood pressure goal is uncertain. Some experts use a trial of increasing mean arterial perfusion (MAP) to 70 to 85 mmHg or a target MAP of 10 to 20 mmHg above baseline while monitoring for neurologic improvement [4]. An alternative approach for patients with a lumbar drain is to titrate MAP to achieve a spinal perfusion pressure >60 mmHg [5]. Treatment is typically weaned after 24 to 48 hours as tolerated or if contraindications develop. Prerequisites of these treatments include excluding aortic dissection and hemorrhagic causes of symptoms which may worsen with blood pressure augmentation.
●Placement of lumbar drain with goal intracranial pressure – The placement of a lumbar drain may improve spinal cord perfusion by reducing intracranial and intraspinal pressure. A lumbar drain is typically used prophylactically to prevent spinal cord infarction from aortic surgery [6]. It may be also be attempted for other patients who present acutely (eg, <24 hours) with nonoperative causes of spinal cord infarction, although efficacy data of lumbar drainage in this setting are unavailable. (See 'Following aortic surgery or endovascular repair' below.)
The optimal intracranial pressure target to treat spinal cord ischemia for patients with a lumbar drain is uncertain. We suggest draining cerebrospinal fluid either to a target pressure of 10 to 15 mmHg or at a rate of 10 to 20 mL each hour [7]. We monitor clinically for 24 to 48 hours to assess for improvement of neurologic symptoms then wean step-wise while monitoring for neurologic stability. Lumbar drains are associated with a risk of spinal epidural bleeding or abscess and intracranial hypotension syndrome [6,8,9] and should be used by experienced clinicians in centers experienced with this technique, such as a neurocritical care unit.
Therapies of uncertain or limited benefit
Thrombolytic treatment — Thrombolytic therapy for spinal cord ischemia remains investigational. Protocols for spinal cord infarcts typically follow dosing and inclusion/exclusion criteria used for ischemic cerebral infarction. However, the efficacy and safety of this treatment for spinal cord infarction is uncertain. Thrombolytic therapy has been utilized for spinal cord infarction with apparent success in only a few published case reports [10-13]. (See "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use".)
A significant barrier to thrombolytic treatment in this situation is the initial diagnostic uncertainty that can delay diagnosis beyond the acute thrombolytic treatment window; this includes the need to exclude aortic dissection and spinal vascular malformations, which are contraindications to thrombolytic therapy.
Glucocorticoids — For most patients with spinal cord infarction, we avoid glucocorticoids. Glucocorticoids are not recommended in acute ischemic stroke of the brain, and their benefit in ischemic injury to the spinal cord is unproven [14,15]. In addition, glucocorticoids may worsen neurologic deficits in patients with initially suspected spinal cord infarction who are subsequently found to have myelopathy from a spinal arteriovenous fistula [16].
Glucocorticoids may be administered to select patients with spinal cord infarction determined to be due to an inflammatory condition such as vasculitis. In addition, it may be reasonable to use glucocorticoids to treat progressive myelopathic symptoms when transverse myelitis is suspected but discriminating between ischemic and demyelinating causes is difficult or delayed. The use of glucocorticoids for these conditions is discussed in detail separately.
●(See "Overview of the management of vasculitis in adults", section on 'Approach to treatment'.)
●(See "Transverse myelitis: Treatment and prognosis".)
Treatment for specific underlying causes — Diagnostic evaluation of spinal cord infarction includes assessment of underlying causes. While the etiology of a spinal cord infarct may not be immediately apparent in some cases, clinical circumstances and initial diagnostic testing may identify the cause in other cases (eg, aortic dissection, systemic hypoperfusion, vascular malformation, vertebral artery dissection). Treatment of underlying etiologies may help to hasten recovery, prevent further neurologic deterioration, and reduce the risk of other cause-specific complications. (See "Spinal cord infarction: Epidemiology and etiologies", section on 'Etiologies'.)
Aortic dissection and other acute aortic conditions — Patients with spinal cord infarction due to hypoperfusion from aortic dissection, aneurysm, or thrombosis may require urgent evaluation and treatment of the aortic condition. Acute treatment of these conditions may take priority over treatment of spinal cord infarction to reduce the risk of mortality or progressive morbidity. This includes patients with hemodynamic instability and those with high-risk findings on diagnostic testing. The management of these acute aortic conditions is discussed in detail separately. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Management'.)
Following aortic surgery or endovascular repair — A specific protocol has been developed that appears to be effective in reversing or limiting the neurologic deficits from spinal cord ischemia after aortic surgery and thoracic endovascular aortic repair (TEVAR) [7,17-19]. This employs a combination of blood pressure support and reduction of spinal cord canal pressure with lumbar drains (algorithm 1):
●MAP is increased in increments of 10 mmHg every five minutes (with volume and vasopressor agents) until symptoms resolve, bleeding complications ensue, or additional blood pressure augmentation would cause an unacceptably high risk of bleeding at the surgical bed.
●If a lumbar drain is in place, it should be opened and set to drain at 8 to 12 mmHg. If not in place, a lumbar drain should be placed if there is no response to blood pressure augmentation within 10 to 20 minutes.
●If there is no response to treatment, spinal imaging is performed to exclude epidural hematoma. Magnetic resonance imaging (MRI) is preferred, but in cases where MRI is contraindicated or the patient is not stable enough to undergo MRI, computed tomography (CT) is performed as an alternative study.
●Vasopressors are slowly weaned over the ensuing 24 to 48 hours with close monitoring of neurologic function. After vasopressor support is weaned, the lumbar drain should be capped then removed 24 hours later if neurologic function remains stable.
While this protocol has not been evaluated in a controlled study, the temporal association of the intervention with the observation of improvement in some cases provides evidence of its efficacy. Nonetheless, the number of patients in whom this treatment has been reported is small [20].
The use of this treatment protocol in spinal cord infarction due to other causes has not been studied. While these interventions could be considered, the benefit is questionable, particularly given the usually long delay from onset of symptoms to initiation of therapy in these settings.
Thrombotic complication of venoarterial extracorporeal membrane oxygenation — Spinal cord infarction may occur as a complication of peripheral venoarterial extracorporeal membrane oxygenation (V-A ECMO).
Management of these critically ill patients can be challenging due to ongoing need for V-A ECMO and anticoagulation and because required monitoring and treatment regimens can limit access to spinal cord imaging. Intensity of anticoagulation is typically increased in patients with aortic thrombosis, if possible. (See "Extracorporeal life support in adults: Management of venoarterial extracorporeal membrane oxygenation (V-A ECMO)", section on 'Cardiac or aortic thrombosis'.)
Other measures for patients with spinal cord infarction in the setting of V-A ECMO may include a trial of blood pressure augmentation and/or placement of a lumbar drain to reduce intraspinal pressure, if possible. However, use of lumbar drains is often limited by ongoing anticoagulation and severity of illness. If possible, removal of the V-A ECMO device or modification of cannula sites can be considered.
Spinal vascular malformation — Spinal vascular malformations may be identified by spinal MRI or spinal angiography. Repair of the malformation may prevent further neurologic decline and, in some instances, lead to improved neurologic function [21,22]. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.)
Vertebral artery dissection — Patients with cervical spinal cord infarction due to vertebral artery dissection are managed in the same manner as patients with cerebral infarction from dissection. Treatment consists of reperfusion therapy for eligible patients, antithrombotic therapy, blood pressure management, and control of metabolic derangements. The management of patients with vertebral artery dissection is discussed in greater detail separately. (See "Cerebral and cervical artery dissection: Treatment and prognosis".)
Cryptogenic — The underlying cause of spinal cord infarction may remain uncertain even after a thorough diagnostic evaluation (see "Spinal cord infarction: Clinical presentation and diagnosis", section on 'Testing for underlying cause'). For patients with a cryptogenic spinal cord infarction, we typically start antithrombotic therapy with aspirin at 81 mg daily.
We also use high-dose statins (hydroxymethylglutaryl CoA reductase inhibitors) when atherosclerotic risk factors are present and treat for other cerebrovascular risk factors such as hypertension and diabetes mellitus, similar to patients with ischemic cerebral stroke. (See "Overview of secondary prevention for specific causes of ischemic stroke and transient ischemic attack".)
Prevention and management of complications — Patients with spinal cord infarction are at risk for systemic as well as neurologic complications, typically in the first days and weeks after symptom onset. Some of these can exacerbate the neurologic injury and may be life-threatening. Early intervention can avoid and ameliorate the risk of complication-related morbidity and mortality.
General measures — Patients with moderate to severe acute deficits resulting from a high thoracic or cervical cord infarct should be admitted to an intensive care unit with close monitoring of vital signs and neurologic status. Spinal cord infarction involving these rostral levels is associated with an elevate risk of hemodynamic instability, respiratory failure, and other cardiorespiratory complications.
Cardiovascular complications
●Hemodynamic instability and neurogenic shock – Hypo- and hypertension may accompany neurologic symptoms in cervical and rostral thoracic infarcts. Blood pressure abnormalities may also lead to myocardial infarction or impairment of kidney function and may also worsen neurologic symptoms.
Neurogenic shock refers to hypotension, usually with bradycardia, attributed to interruption of autonomic pathways in the spinal cord causing decreased vascular resistance. Patients with spinal cord infarction may also have hemodynamic instability related to the underlying etiology.
An adequate blood pressure is believed to be critical in maintaining adequate perfusion to the ischemic, but not yet infarcted, spinal cord. Close monitoring with symptomatic treatment is warranted to minimize these effects. (See "Acute traumatic spinal cord injury".)
Bradycardia can occur in severe, high cervical (C1 through C5) lesions and may require external cardiac pacing or administration of atropine.
●Autonomic dysreflexia – Autonomic dysreflexia, a phenomenon characterized by episodic paroxysmal hypertension with headache, bradycardia, flushing, and sweating, is most often described after a traumatic spinal cord injury, but may also occur in the subacute or chronic phases after a spinal cord infarction involving the cervical or upper thoracic cord.
Management strategies to reduce frequency and severity of episodes include careful monitoring and optimization of blood pressure, treating pain and avoiding other triggers (eg, bladder distention), and the use of agents such as nifedipine to prevent attacks. (See "Chronic complications of spinal cord injury and disease", section on 'Autonomic dysreflexia'.)
Pulmonary complications — Several pulmonary complications may accompany spinal cord infarction, especially with cervical lesions and high thoracic lesions. Weakness of the diaphragm and chest wall muscles leads to impaired clearance of secretions, ineffective cough, atelectasis, and hypoventilation. (See "Respiratory physiologic changes following spinal cord injury".)
Pulmonary complications include:
●Acute respiratory failure
●Pneumonia
●Pulmonary edema
Chest physical therapy should be started for patients with ineffective cough or impaired clearance of secretions to prevent atelectasis and pneumonia. Sputum Gram stain and culture are warranted for patients with pneumonia to help guide antibiotic therapy. These issues are discussed in detail separately. (See "Respiratory complications in the adult patient with chronic spinal cord injury", section on 'Pulmonary infection'.)
Patients with spinal cord infarction should be monitored for respiratory insufficiency. Signs of impending respiratory failure include increased respiratory rate, declining forced vital capacity, rising partial pressure of carbon dioxide (pCO2), or falling partial pressure of oxygen (pO2) and may indicate a need for intubation and ventilation with positive pressure support. Patients with respiratory failure who require intubation may need respiratory muscle training to wean from ventilatory support, and some may require long-term assisted ventilation. (See "Respiratory complications in the adult patient with chronic spinal cord injury", section on 'Respiratory insufficiency'.)
Venous thromboembolism and pulmonary embolism — All patients with immobility due to acute spinal cord infarction should receive prophylaxis for deep venous thrombosis. We consider patients with acute spinal cord infarction to have a similar risk to those with acute spinal cord traumatic injury and treat accordingly. Specific recommendations are provided separately. (See "Respiratory complications in the adult patient with chronic spinal cord injury", section on 'Prophylaxis'.)
Other medical complications
●Pressure sores – Pressure sores are most common on the buttocks and heels and can develop quickly in immobilized patients. Such patients should be turned side to side (log-rolled) every two to three hours to avoid pressure sores. Special mattresses can also be used to ameliorate this complication. (See "Prevention of pressure-induced skin and soft tissue injury", section on 'Support surfaces'.)
●Urinary catheterization – Patients with moderate to severe deficits including bladder dysfunction initially require an indwelling urinary catheter to avoid bladder distension. Three or four days after injury, intermittent catheterization should be substituted, as this reduces the incidence of bladder infections. (See "Chronic complications of spinal cord injury and disease", section on 'Bladder dysfunction'.)
●Gastrointestinal stress ulceration – Patients with spinal cord infarction, particularly those that affect the cervical cord, are at high risk for stress ulceration and should receive prophylaxis with proton pump inhibitors. (See "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention".)
●Temperature control – Patients with a cervical spinal cord injury may lack vasomotor control and be unable to sweat below the lesion. Their temperature may vary with the environment and need to be maintained.
Functional recovery — Physical and occupational therapy should be started as soon as possible. Patients with neurologic dysfunction due to spinal cord infarction should be screened for depression, and counseling should be included as part of comprehensive rehabilitation, as indicated.
PROGNOSIS — Functional outcome after spinal cord infarct varies according to the spinal level and severity of initial neurologic deficits. Many patients improve with rehabilitation and time, but most have some persistent dysfunction. Case series and cohort studies have attempted to define the range of outcomes following spinal cord infarction.
●Case fatality – The case fatality rate varies depending on the case mix included in the series but is often reported between 10 and 23 percent [20,23-26]. Patients presenting in the setting of cardiac arrest and acute aortic rupture or dissection and those with high cervical lesions are at greatest risk of death. Patients with spinal cord infarction have a higher mortality rate after hospital discharge, in part related to the high prevalence of underlying vascular risk factors [27].
●Functional outcomes – Among survivors, most make some improvement in functional deficits. Independent gait is achieved by 11 to 46 percent, while 20 to 62 percent remain nonambulatory [20,23-25,28-32]. Outcomes may be better among patients with spontaneous compared with periprocedural spinal cord infarcts [32]. One case series with prolonged follow-up noted that gradual improvement occurred in many patients at long-term follow-up (mean three years) after hospital discharge [26].
Poor prognostic factors for recovery include severe impairment at presentation, female sex, advanced age, and lack of improvement in the first 24 hours [23,25,26,28-30,33,34].
Patients with residual deficits after spinal cord infarction must often contend with a variety of other complications including bladder, bowel, and sexual dysfunction, spasticity, and chronic pain. These conditions are discussed in detail separately. (See "Chronic complications of spinal cord injury and disease".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)
SUMMARY AND RECOMMENDATIONS
●Acute treatment – The acute treatment of spinal cord infarction begins with identifying or excluding high-risk causes such as aortic dissection that require specific treatment to prevent further morbidity. Specific treatment of spinal cord infarction is directed toward minimizing or reversing neurologic dysfunction. Treatment generally involves optimizing spinal cord perfusion and initiating cause-specific secondary preventive therapies. (See 'Acute management' above.)
•Evaluate for high-risk causes – Patients with clinical features or risk factors for high-risk causes require urgent evaluation to guide specific acute treatment and reduce immediate risk of further morbidity. This includes patients with spinal cord infarction and additional clinical features or risk factors suggestive of (see 'Identify high-risk underlying causes that require urgent treatment' above):
-Aortic dissection
-Vertebral artery dissection
-Infective endocarditis
-Bacterial meningitis
•Strategies to optimize spinal cord perfusion – Strategies to improve inadequate spinal cord perfusion may halt or reverse progression of neurologic symptoms due to acute spinal cord infarction in some patients. Treatment options vary by individual clinical circumstances and available resources and include treating systemic hypotension, augmenting blood pressure with vasopressors, and/or using a lumbar drain to reduce intraspinal pressure and improve spinal perfusion. (See 'Addressing spinal cord hypoperfusion' above.)
•Treat underlying causes – Underlying etiologies should be identified and treated to help hasten recovery, prevent further deterioration, and reduce the risk of other cause-specific complications. (See 'Treatment for specific underlying causes' above.)
●Management of complications – Patients with spinal cord infarction are at risk for systemic as well as neurologic complications, typically in the first days and weeks after symptom onset. Early intervention can avoid and ameliorate the risk of complication-related morbidity and mortality. (See 'Prevention and management of complications' above.)
•Triage – Patients with moderate to severe deficits resulting from a high thoracic or cervical cord infarct should be admitted to an intensive care unit with close monitoring of vital signs and neurologic status. (See 'General measures' above.)
•Hemodynamic instability – Hemodynamic monitoring with symptomatic treatment of abnormal blood pressure and/or heart rate is warranted. Management strategies to reduce frequency and severity of autonomic instability include careful monitoring and optimization of blood pressure, treating pain and avoiding other triggers (eg, bladder distention), and the use of agents such as nifedipine to prevent attacks. (See 'Cardiovascular complications' above.)
•Respiratory insufficiency and infection – Chest physical therapy should be started for patients with ineffective cough or impaired clearance of secretions to prevent atelectasis and pneumonia. Patients with signs of impending respiratory failure may need intubation and ventilation with positive pressure support, including those with increased respiratory rate, declining forced vital capacity, rising partial pressure of carbon dioxide (pCO2), or falling partial pressure of oxygen (pO2) levels. (See 'Pulmonary complications' above.)
•Deep venous thrombosis – All patients with immobility due to acute spinal cord infarction should receive prophylaxis for deep venous thrombosis. (See 'Venous thromboembolism and pulmonary embolism' above.)
•Other complications – Patients with spinal cord infarction should also be assessed for other medical complications common in hospitalized or immobilized patients such as pressure sores, urinary dysfunction, gastrointestinal stress ulcers, and temperature dysregulation. (See 'Other medical complications' above.)
●Prognosis – Functional outcome after spinal cord infarct varies according to the level and severity of initial neurologic deficits. Many patients improve with rehabilitation and time, but most have some persistent dysfunction. (See 'Prognosis' above.)
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