Abstract A 24-year-old male with a history of type 1 diabetes mellitus presented to the emergency department with altered mental status, tachypnea, and bradycardia. Shortly following his arrival, the patient suffered a cardiac arrest with 15 minutes of downtime. He received one shock for ventricular fibrillation with subsequent ROSC. Laboratory evaluation confirmed severe DKA and he was admitted to the MICU for management of DKA and post-arrest care. His MICU course was complicated by brief upper GI bleeding that resolved spontaneously, anuric AKI requiring renal replacement therapy and NSTEMI. Following clinical resolution of his DKA over the next several days, he was extubated to HFNC. Shortly after extubation, he endorsed bilateral lower extremity paralysis with loss of sensation at the T4 dermatome. Stat MRI imaging revealed cylindrical cord T2 hyperintensity extending from C5 to T10, with cord expansion from T1 to T6 (Fig 1). Brain imaging showed no acute infarction or cerebral edema.Spinal cord ischemia following cardiac arrest is a rare but increasingly recognized complication, particularly in the setting of prolonged hypoxia. The thoracic cord (T3-T8) is especially vulnerable as it is the longitudinal watershed zone between the anterior spinal artery territory and the artery of Adamkiewicz. In this case, the combination of DKA-induced metabolic derangements and global hypoperfusion during cardiac arrest likely contributed to the development of spinal cord infarction. DKA itself is associated with increased risk of both cerebral and spinal cord infarctions, as well as other neurological sequelae such as cerebral edema and myelinolysis. Neurological complications of DKA are unpredictable and may occur despite appropriate management. The overlap of metabolic acidosis, hyperglycemia, and hypoxic injury increases the risk of poor neurological outcomes, particularly in young adults. Early recognition of focal deficits and prompt neuroimaging are essential for diagnosis. Management is primarily supportive, focusing on optimizing hemodynamics, correcting metabolic abnormalities, and initiating rehabilitation. Aspirin was initiated with intensive risk factor modification. Steroids are not recommended due to their lack of proven benefit. Ultimately, he was discharged from inpatient rehabilitation with continued outpatient therapy. He remains a T4 incomplete paraplegic. He demonstrated renal recovery without further need for hemodialysis. This case highlights the importance of vigilance for spinal cord injury in post-arrest DKA patients, especially when new focal neurological deficits arise. Further research is needed to clarify the incidence, risk factors, and optimal management strategies for hypoxic-ischemic spinal cord injury in this population. This abstract is funded by: None
Adivi et al. (Fri,) studied this question.