SAT060 Hyperosmolar Hyperglycemic State Presenting As Seizures
Recommended Citation
Faber A, Levy S. SAT060 Hyperosmolar Hyperglycemic State Presenting As Seizures. J Endocr Soc 2023; 7:A497.
Document Type
Conference Proceeding
Publication Date
10-5-2023
Publication Title
J Endocr Soc
Abstract
Introduction: Hyperosmolar hyperglycemic state (HHS), also known as hyperosmotic hyperglycemic nonketotic state (HHNK), is one of the most severe complications of diabetes mellitus. HHS is a medical emergency defined by high serum osmolality and hyperglycemia as well as the absence of ketoacidosis in most cases. Wepresent an unusual case of a young man presenting with seizures who on further investigation was found to have HHS. Case Description: A 44-year-old man presented to the hospital for a possible seizure at home. His medical history is significant for EBV+ B-cell lymphoma receiving chemotherapy, HIV on HAART therapy, and prior history of cryptococcus meningitis in 2019. He did not have history of seizures or diabetes mellitus. He reported that five days prior to admission, he began experiencing polydipsia and polyuria, which later progressed to lethargy. The day of admission his mother found him on the floor with generalized body shaking with significant shaking of the right arm, urinary incontinence, and blood in his mouth from tongue biting. He was taken to the hospital due to concern for seizure. Workup revealed elevated blood glucose of 972 and elevated serum osmolality of 322. He did not present with overwhelming ketosis; his beta-hydroxybutyrate was 0.57, he did not have an anion gap, and ketones were not present in his urine. His A1c was elevated at 9.9%. The differential diagnosis for this patient's seizure included chemotherapy side effect, intracranial pathology, infectious etiology in the setting of known HIV, or HHS. Hematology evaluated the chemotherapy regimen and stated it was not likely the cause of his seizures. Neurology assessed the patient with a CT head, MRI brain, EEG, and lumbar puncture, all of which were negative. The CSF from the lumbar puncture underwent intensive testing, which was negative for HSV, VDRL, CMV, EBV, VZV, Lyme disease, and JC virus. Neurology initially started the patient on anti-seizure medication, however later stated his seizure was likely provoked from hyperglycemia and discontinued the medication. Infectious workup included chest X-ray, blood cultures, and urinalysis, all of which were negative. Endocrinology was consulted and recommended initiating basal and bolus insulin as well as testing for GAD antibodies. Unfortunately, the patient left the hospital against medical advice and GAD antibody testing was not completed. Discussion: The most common symptoms of HSS include hyperglycemia, polyuria, and polydipsia. Though neurological symptoms can occur, they are not common. The neurologic symptoms are typically not seen until the serum osmolality reaches 320 - 330 mOs/kg, and this patient's serum osmolality was elevated at 322 mOs/kg. Though seizure is not well understood in hyperglycemia, treatment for HHS-induced seizures focuses on aggressive management of the underlying hyperglycemic state.
Volume
7
First Page
A497
