Case Presentation:
A 21 year old male with no significant past medical or surgical history presented to the hospital with sudden onset of bilateral lower extremity paralysis and paresthesia. He was lifting heavy boxes at work when he felt severe lower back pain that eventually radiated to his legs. The pain was followed by bilateral lower extremity paralysis and paresthesia. His vitals were stable on admission, and physical exam was significant for 0/5 strength of the lower extremities and absence of patellar and achilles reflexes bilaterally. He also had loss of sensation from the umbilicus downward. Labs and lumbar puncture were unremarkable. An initial MRI of the spine showed a probable spinal cord infarction from the inferior aspect of T10 through the conus medullaris terminating at L1. Systemic lupus erythematosus (SLE), lyme disease and syphilis were ruled out. Patient’s presentation was labeled as a work related injury and he was transferred to the rehab service. He was then found to have bilateral iliopsoas hematoma’s prompting further investigation. A rheumatologic work-up was performed yielding a positive Dilute Russell’s viper venom time (dRVVT) and hexagonal phase phospholipid neutralization assay, and elevated cardiolipin IgM. Patient’s spinal cord infarction was attributed to the diagnosis of primary antiphospholipid syndrome (APS) and he was discharged on lifelong anticoagulation with warfarin.
Discussion:
APS is often seen in patients with SLE and is known for causing both venous and arterial thrombosis. It is generally suspected in women who present with spontaneous abortions. We present a unique presentation of APS in a 21 year old healthy male who presented with spontaneous paraplegia. Though primary APS is rare, it is even less common for it to present as sudden paraplegia due to a spinal cord infarct. Since the event occurred during a physical strain, it was easy to miss the diagnosis on initial evaluation. It was further undermined due to the absence of SLE as APS is commonly associated with lupus. Our case illustrates that primary APS can present as spinal cord infarction due to high incidence of thrombosis associated with this disease entity.
Conclusions:
After a thorough literature review, we found only 1 case of primary APS causing spinal cord infarction in a 6 year old boy. When dealing with rare presentations of infarctions, a comprehensive hypercoagulable workup must be pursued, which should include testing for APS. A clinician should always have a broad differential when approaching any patient as rare presentations of rare diseases can otherwise be missed causing significant morbidity and even mortality.