1139 - Acute Labile Blood Pressures in Chronic Spinal Cord Injury : A Case Report

Case Diagnosis: A 67-year-old male with cervical spinal cord injury (SCI) in 1975, who initially presented with refractory UTI and duodenal ulcers, presented again with labile blood pressures thought to be autonomic dysreflexia (AD). He reported a history of asymptomatic fluctuations in blood pressure (BP) managed with home fludrocortisone.

Case Description:

Initial workup was unremarkable except for C6-C7 enhancement suggestive of mild cord expansion on MRI. Systolic BP readings ranged 70s -200s without headaches, flushing, bradycardia, or piloerection. Urologic, gastrointestinal, wound, and endocrinologic causes were ruled out. He developed SVT with hypotension requiring IV pressors and metoprolol. Cardiology was consulted, who observed he developed hypertension while supine and hypotension while upright. Thus, daily midodrine and nightly metoprolol were added. He received antibiotics for sepsis and underwent a thoracentesis for fluid overload. He declined admission to inpatient rehabilitation and was discharged home in stable condition.

Discussions: This patient showed acute, very labile BP despite being more than 40 years post-injury. While disruption of neuronal communication between brainstem vasomotor centers and spinal sympathetic neurons is considered the mainstay of SCI-related BP issues1, potential reasons for the development of labile BP in chronic SCI patients may be specifically related to reduced baroreceptor sensitivity, which may be a chronic effect of baroreceptor arterial stiffening and long-term physical and cardiac deconditioning2. It is thought that structural changes in the elastic properties of central arteries occur due to repetitive, severe orthostatic stress and substantial increases in sympathetic outflow above the site of injury3. This, coupled with years of immobility and lack of access to proper SCI specialized care, may be one of the factors contributing to this patient’s new cardiovascular impairments.

Conclusions: Very few studies exist that discuss the evolution of blood pressure in chronic SCI patients. This case highlights a potential etiology of such acute cardiovascular developments in this population.