SCI
Marlou Abril, DO
New York Medical College/Metropolitan Hospital Center
Astoria, New York, United States
Daniel Furhang, N/A, BS
Medical Student
New York Medical College
Valhalla, New York, United States
Jeremy Frank, MD
Resident Physician
NYMC/Metropolitan Hospital Center
New York, New York, United States
Ozan Soyer, MD
Resident Physician
New York Medical College / Metropolitan Hospital
Bronx, New York, United States
Marlou Abril, DO
New York Medical College/Metropolitan Hospital Center
Astoria, New York, United States
A 39-year-old male with polysubstance use disorder and chronic paraplegia from a prior spinal cord stroke presented with acute bilateral upper extremity weakness and numbness. On admission, the patient was septic and had a urine toxicology positive for cocaine. MRI findings were concerning for cervical spinal cord infarction. Given these findings, he was empirically started on broad-spectrum antibiotics for suspected septic emboli versus epidural abscess. However, given that echocardiography demonstrated no evidence of endocarditis and blood cultures speciated Providencia Rettgeri, septic emboli and epidural abscess were ultimately ruled out, leading to de-escalation and, ultimately, discontinuation of antibiotics. Although his Gram-negative bacteremia was ultimately attributed to pyelonephritis, as his urinalysis was suggestive of an infection, the clinical presentation and imaging findings were convincingly linked to cocaine use as the precipitant of his cervical spinal cord infarct. Ultimately, the patient was medically stabilized and was discharged to an acute inpatient rehabilitation facility.
Discussions:
This case highlights the atypical mechanism of cocaine induced spinal cord infarction. Although acute spinal cord ischemia accounts for approximately 25% of nontraumatic lesions, substance-induced spinal cord infarctions are extremely rare. The overlap in clinical findings, along with the lack of distinction between cocaine-related versus other most common forms of acute spinal cord ischemia, posed a considerable diagnostic challenge. Nonetheless, substance use as an etiology should always be ruled out in any acute nontraumatic myelopathy. From a rehabilitation framework, the patient’s new functional decline prompted a redefinition of care goals, the implementation of compensatory strategies to maximize functional independence, and focused interventions aimed at enhancing his upper and lower extremity strength and mobility.
Conclusions:
In conclusion, cocaine induced spinal cord infarction is an atypical cause of acute myelopathy that requires diagnostic consideration and coordinated rehabilitation efforts to maximize functional outcomes.
