Case Presentation: A 47-year-old female with a history significant for poorly controlled T1DM and hypothyroidism presented after being found unresponsive following episodes of vomiting for the past 24 hours. The patient was found to have DKA, high anion gap metabolic acidosis, and shock with blood pressure of 65/31. Labs showed blood glucose levels of 983, sodium bicarbonate of 3, potassium of 7.0, pH < 6.8, anion gap 37, and lactic acid of 2.0 with ketones on urinalysis. IV fluids, insulin, steroids, norepinephrine-epinephrine infusion, and bicarbonate were initiated. The patient was admitted to the ICU due to continuing hypotension requiring fluid boluses and vasopressors. Blood glucose levels began to normalize 23 hours after admission. On day 3 of admission, the patient became fully oriented and reported new numbness in the left upper extremity and lower extremities. On exam, there was no spontaneous movement or withdrawal to stimuli of the lower extremities. There was absent sensation to light touch and temperature in bilateral lower extremities. The patient initially did not have bowel incontinence but later developed incontinence requiring a catheter. CT and MRI of the head were negative for acute abnormalities, with MRI of total spine showing suspected intramedullary hemorrhage centered at C5. The patient was transferred to a tertiary care center for continued work-up. Lumbar puncture and serum studies were performed due to concern for inflammatory and autoimmune processes; however, work-up came back negative. Diffusion MRI of cervical and thoracic spine was performed which confirmed suspicion of an acute/subacute infarct as the cause of the patient’s symptoms. Despite treatment with high-dose steroids and plasmapheresis, the patient was discharged to rehabilitation with continued paraplegia and remains wheelchair-bound.
Discussion: Spinal cord infarction leading to tetraplegia is a rare complication of DKA, with less than ten reported cases in adults. In one case, a 17-year-old patient developed pulmonary and cerebral edema along with multiple infarctions of the brain and cervical spinal cord; whereas in a second case, a 23-year-old patient developed pulmonary edema, cardiac failure, and spinal cord infarction. The etiology of spinal cord infarction remains unclear given its rare presentation. Numerous studies exist regarding the causes of cerebral edema which may be applied to this case including the rapid infusion of fluids due to a hyperosmolar state, hypoxia, hypotension, and increased risk of thrombosis in DKA. Considering that the patient had a history of multiple hospitalizations for DKA and was hypotensive for an unknown amount of time, injury could likely be multifactorial. While spinal cord infarctions continue to be a rare complication of DKA, this case emphasizes the importance of further research into the association of this complication in order to prevent life-altering complications of diabetes. In addition, these patients also require multidisciplinary and extensive evaluation to rule out other mimics of the illness.
Conclusions: Ischemic spinal cord injury is a rare complication of diabetic ketoacidosis. A further understanding of its etiology is required to prevent life-altering complications of diabetes.