INTRODUCTION — Spinal cord infarction is a rare disorder caused by a wide variety of pathologies. 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 most. Specific treatment options are unfortunately limited.
This topic discusses the prognosis and acute treatment of spinal cord infarction. The causes, clinical symptoms, and diagnosis of spinal cord infarction are discussed separately. The management of chronic complications of spinal cord infarction is also discussed separately. (See "Spinal cord infarction: Epidemiology and etiologies" and "Spinal cord infarction: Clinical presentation and diagnosis" and "Disorders affecting the spinal cord" and "Chronic complications of spinal cord injury and disease".)
TREATMENT
General medical care — Depending on the level and severity of spinal cord ischemia, patients are at risk for a number of systemic as well as neurologic complications in the first days and weeks. Some of these are potentially life-threatening and can exacerbate the neurologic injury. Early intervention can avoid and ameliorate many of these. 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.
Cardiovascular complications — 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.
Bradycardia can occur in severe, high cervical (C1 through C5) lesions and may require external pacing or administration of atropine.
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 be a potential concern after spinal cord infarction involving the cervical and upper thoracic cord as well. (See "Chronic complications of spinal cord injury and disease", section on 'Autonomic dysreflexia'.)
Respiratory complications — The incidence of pulmonary complications (respiratory failure, pulmonary edema, pneumonia, and pulmonary embolism) is highest with higher cervical lesions and is also common with 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"). Signs of impending respiratory failure, such as increased respiratory rate, declining forced vital capacity, rising pCO2, or falling pO2, indicate urgent intubation and ventilation with positive pressure support.
With a goal of preventing atelectasis and pneumonia, chest physiotherapy should be instituted as soon as possible; patients may also need frequent suctioning. (See "Respiratory complications in the adult patient with chronic spinal cord injury", section on 'Respiratory insufficiency' and "Respiratory complications in the adult patient with chronic spinal cord injury", section on 'Pulmonary infection'.)
Venous thromboembolism and pulmonary embolism — Patients with significant paraparesis after spinal cord infarction should be treated to prevent deep venous thrombosis. We consider patients with acute spinal cord infarction to have a similar risk to those with spinal cord injury and treat accordingly. Specific recommendations are provided separately. (See "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)
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.
Urinary catheterization — Initially, an indwelling urinary catheter should be placed 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 cannot sweat below the lesion. Their temperature may vary with the environment and need to be maintained.
Functional recovery — Occupational and physiotherapy should be started as soon as possible. Psychological counseling should also be offered to patients and relatives as early as possible.
Specific treatments
Thrombolysis — Thrombolytic therapy for spinal cord ischemia remains investigational at this time.
Thrombolytic therapy has been utilized with apparent success in only a few published case reports of spinal cord infarction [1,2]. A significant barrier to thrombolytic treatment in this situation is the initial diagnostic uncertainty that can delay diagnosis beyond the treatment window; this includes the need to exclude aortic dissection and vascular malformations, which are contraindications to thrombolytic agents.
Corticosteroids — Systemic corticosteroids have not been studied in acute ischemic injury to the spinal cord and are not recommended in acute ischemic stroke involving the brain [3]. We do not recommend the use of steroids to treat spinal cord infarction; however, in rare cases when it is not clear whether a patient has an ischemic versus a demyelinating spinal cord lesion, it may be reasonable to use corticosteroids pending a firm diagnosis. (See "Treatment of acute exacerbations of multiple sclerosis in adults", section on 'Initial therapy with glucocorticoids'.)
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) [4-7]. This employs a combination of blood pressure support and reduction of spinal cord canal pressure with lumbar drains (algorithm 1):
●Mean arterial pressure 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 acceptable.
●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, and 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 provides evidence of its efficacy. Nonetheless, the number of patients in whom this treatment has been reported is small [8].
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.
Other underlying cause — If an underlying etiology is found, it should be treated (ie, systemic vasculitis, aortic dissection, cardiogenic embolism), usually with a goal toward preventing further deterioration and secondary events rather than treating the primary injury. Vascular malformations of the spinal cord should be repaired if present. Repair of the malformation may prevent further neurologic decline, and in some instances lead to improved neurologic function [9,10].
The use of antiplatelet treatment in patients with underlying vascular risk factors or comorbid vascular disease is recommended to prevent other secondary atherothrombotic events. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)
PROGNOSIS — Small case series 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 20 percent [8,11-14]. 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 dying. 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 [15].
●Functional outcomes – Among survivors, most make some improvement in functional deficits. Independent gait is achieved by 11 to 46 percent, while 20 to 57 percent do not achieve ambulatory status [8,11-13,16-19]. One case series with prolonged follow-up noted that gradual improvement occurred in many patients long after hospital discharge [14].
Poor prognostic factors for recovery include severe impairment at presentation, female sex, advanced age, and lack of improvement in the first 24 hours [11,13,14,16-18,20,21].
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. The management of these conditions is discussed 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 medical care – Depending on the level and severity of spinal cord ischemia, patients are at risk for potentially life-threatening complications. 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 medical care' above.)
Similar to patients with traumatic spinal cord injury, patients with significant paraparesis after spinal cord infarction are at high risk of venous thromboembolism and should receive interventions to prevent this complication. Specific recommendations are provided separately. (See "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)
●Specific therapies – There are no therapies proven to reverse or limit ischemic spinal cord injury.
A protocol for managing patients in the setting of thoracoabdominal aneurysm surgery is presented (algorithm 1), but this requires independent, prospective demonstration of its safety and efficacy. (See 'Specific treatments' above.)
●Secondary prevention – Underlying causes should be treated in order to prevent secondary events. As an example, patients with atherosclerotic risk factors or underlying comorbid atherosclerotic vascular disease will benefit from antiplatelet therapy and management of atherosclerotic risk factors to prevent future stroke and myocardial infarction. Specific recommendations are provided separately. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)
●Prognosis – Mortality after spinal cord infarction is primarily influenced by the underlying etiology; however, patients with high cervical cord lesions are at risk of potentially life-threatening complications.
Survivors of spinal cord infarction often make some functional improvements, but most have significant, residual neurologic deficits. (See 'Prognosis' above.)
