A thorough history and physical evaluation are crucial in providing rapid detection of SCI. This, together with neuroimaging, can aid in expedited detection of SCI. Suspected patients are managed with hemodynamic support to maximize blood pressure, lumbar drainage to lower the cerebrospinal fluid (CSF) pressure is often indicated to increase spinal perfusion and halt the progression of the injury.[27][3] Maintenance of optimal hemodynamic stability should be at a mean arterial pressure above 90mm Hg, accomplished with volume replacement and vasopressor support, along with proper monitoring for improvement or complications via serial neurological examinations over 12 to 48 hours.[1][27][3]

A review of 49 patients undergoing endovascular repair of descending thoracic aneurysm and thoracoabdominal aortic aneurysms facilitated by continuous intraoperative motor/somatosensory-evoked potential (MEP/SEP), cerebrospinal fluid drainage, and use of iliofemoral conduits allowed for early prediction and management of SCI.[35] Serial neurological evaluations are crucial particularly in the postoperative setting and must be performed immediately after dissipation of anesthesia and the patient awakens with the involvement of complete neurological examination in addition to Glasgow Coma Scale and National Institutes of Health Stroke Scale assessments performed according to previously published guidelines by the American Spinal Injury Association.[36] Transient loss in vibration and proprioception in the lower extremities can commonly occur during the first few hours; postoperative patients possess an elevated susceptibility to epidural hematoma due to anticoagulants during surgery.[1]

 Laboratory Evaluation

Laboratory examinations are can differ depending on the clinical presentation they can include copper, zinc, vitamin B12, Lyme disease serology, varicella-zoster viral serology, HIV serology, syphilis serology, human T-lymphotropic virus 1 serology, antinuclear antibody, anti-neutrophil cytoplasmic antibody, anti-cyclic citrullinated peptide, angiotensin-converting enzyme, aquaporin-4-IgG, myelin oligodendrocyte glycoprotein, hypercoagulable profile, and paraneoplastic autoantibody assessment.[17]

CSF Analysis

Lumbar punctures are performed in certain SCI cases. CSF analysis includes red blood cell count, white blood cell count and differential, protein, and glucose. Further analysis may be comprised of IgG index, cytology, flow cytometry, gram stain, oligoclonal bands, bacterial culture, Lyme disease serology and polymerase chain reaction (PCR), cryptococcal antigen, paraneoplastic autoantibodies, venereal diseases, varicella-zoster virus PCR, Epstein-Barr virus PCR, enterovirus PCR, cytomegalovirus PCR, mycobacterium tuberculosis PCR, and cultures.[17] Elevated protein levels and white blood cells may occasionally occur, although not specific, arising from embolism, celiac plexus block, and vasculitis.[3][37][9]

Neuroimaging

While radiography can be equivocal in certain cases, it remains to be a fundamental aspect of SCI diagnosis. Magnetic resonance imaging (MRI) at 1.5 Tesla (T) including sagittal and axial T1 and T2-weighted sequences and diffusion-weighted imaging (DWI) with contrast are often employed to identify and localize SCI.[13][7] DWI has become increasingly sensitive in SCI diagnosis, particularly during the acute phase (less than 24 hours).[38][31] Initial MRI findings can be unremarkable during the early stages; a second MRI days later is necessary.[31][17] Particular signs on imaging have correlations to SCI; they are not highly specific - however, their presence has been correlated to the vasculature that is involved. Spinal cord swelling and “pencil-like” hyperintensities on T2-weighted images (T2WI), enhancement on post-contrast T1-weighted images and hyperintense signal on DWI are among the frequently encountered imaging features of SCI.[7][31] Spinal cord edema will eventually get replaced with atrophy in the chronic phase.[9][13][3] The presence “owl’s eyes pattern” hyperintensities on axial T2WI is associated with ASA infarcts.[17] Vertebral body infarcts also develop and can be visualized on MRI; they are associated with radicular artery occlusion.[22] Computed tomography (CT) can deliver a diagnosis in cases where there are contraindications to MRI as in epidural hematoma or if the patient is clinically unstable. MRI is performed postoperatively in order to rule out spinal cord compression.[3][1] If neuroimaging illustrates structural lesions or abnormalities, an emergent neurosurgical consultation is warranted. Otherwise supportive measures continue to be carried out while exploring other etiologies.

Additional Diagnostic Evaluations

Additional examinations that can confirm SCI and rule out other etiologies include magnetic resonance angiography, computed tomography angiography, full spinal magnetic resonance angiography, thoracoabdominal computed tomography angiography, digital subtraction angiography and electromyography (EMG).[17] The presence of denervation is discernable with the use of EMG to localize the origin of the ischemic deficit.[9]

Prompt surgical management is necessary in cases of vascular compression and acute aortic event in addition to maintaining hemostatic equilibrium.[31] In the setting of aortic surgery, lumbar drainage and blood pressure augmentation are often options for management.[17] A review of spinal manifestations of patients with vertebral artery dissection revealed the use of anticoagulation was the sole form of therapy in spinal ischemia; antiplatelet therapy was also administered in conjunction with anticoagulants.[4] Another investigation used antiplatelet therapy in all 36 participants, including aspirin and clopidogrel.[22] Rehabilitation efforts have proven to be successful in achieving good outcomes.[17] Cases of vasculitis implore the use of corticosteroid therapy.[3] Decompression sickness treatment is with hyperbaric oxygen.[39]

Neoplastic transformation, disk herniation, epidural abscesses, and epidural hematoma share a similar phenotype with SCI.[3] Multiple sclerosis has similar MRI findings; therefore distinguishing the two is crucial. This differentiation necessitates a thorough CSF analysis and paraneoplastic panel evaluation. Spinal cord compression can originate from spinal cord neoplasms and impede circulation, thus mimicking clinical manifestations of SCI. Infectious or autoimmune transverse myelitis and intramedullary hemorrhage or neoplasm can also present similarly to SCI.[40]

Timely diagnosis and management are essential for improving the outcome and prognosis of SCI. SCI is reversible, and a good functional outcome is attainable with prompt recognition and adequate management; the severity of neurological deficits generally determines the prognosis.[41][37] A study investigating the clinical manifestations, evaluations, and treatment of 36 patients with acute spinal stroke demonstrated favorable outcome including complete and incomplete recovery in 23 (64%) patients, no recovery in 12 (33%) patients, gait assistance required in 18 (50%), 11 (31%) were wheelchair-bound upon discharge and the favorable prognosis was associated with unilateral infarcts.[22] A prospective study including patients with SCI enrolled within 10 days of symptom onset, analysis of clinical and MRI findings demonstrated worst outcome in patients with proprioceptive deficits at the onset, this study also reported the development of pain in half of the patients.[37] Long-term outcome was assessed in 30 patients with SCI and compared to those with cerebral infarction; showed lower mortality rate, higher re-employment rate, and worse functional outcome.[42]

Loss of motor and sensory modalities, including paresthesias and paralysis, may persist in some instances, increasing the risk for cardiovascular and pulmonary diseases. Some SCI patients continue to suffer from chronic pain,[37][42] along with urinary and bowel dysfunction.SCI patients have reported other secondary complications to include: respiratory infections, spasticity, blood pressure fluctuation, and pressure sores.[43]

The National Institute of Neurological Disorders and Stroke (NINDS) provides a wide variety of educational material and information for patients with spinal cord injuries. Patients are encouraged to explore all the resources available, including clinical trials, patient organizations, and publications in this regard. Facilitation of community support and outreach for patients and caregivers come from organizations such as Christopher and Dana Reeve Foundation, Paralyzed Veterans of America, and the United Spinal Association.

Improving overall outcomes and achieving high-quality results requires joint efforts and full participation from patients and healthcare teams. Health care professionals must exercise concerted efforts in early detection of symptoms, triaging, and providing an expedited workup for patients with suspected spinal cord injuries. Proper and effective communication must take place between the interprofessional team, including emergency physicians, neurologists, neuroradiologists, neurosurgeons, other specialists, physiatrists, and specialized nursing staff to achieve higher quality care. Nurses who manage patients with spinal cord infarction should be aware of the potential complications like urinary retention, pressure sores, DVT, and contractures. The dietitian should be involved in the management of nutrition.

Pharmacist involvement comes with the initiation of antiplatelet or anticoagulation therapy. The pharmacist can verify dosing, check for drug interactions, and help change agents where any contraindications exist. They can also assist nursing in the monitoring of pharmaceutical therapy. These activities will be reported to the managing physician, especially in the event of any issues encountered.

The rehabilitation phase involves direct medical care from physiatrists and nursing staff. The nursing staff has a crucial role in monitoring ventilation and lung function, monitor cardiovascular function, stable blood pressure, and prevent infections and other complications from occurring. The patients’ effort during the rehabilitation period has a considerable impact on the recovery process. Only through such an interprofessional team approach can the morbidity of spinal cord infarction be lowered and patient outcomes optimized. [Level 5]