Nonketotic Hyperglycemia-Induced Occipital Lobe Seizures
Abstract number :
2.417
Submission category :
18. Case Studies
Year :
2019
Submission ID :
2421859
Source :
www.aesnet.org
Presentation date :
12/8/2019 4:04:48 PM
Published date :
Nov 25, 2019, 12:14 PM
Authors :
Aljoharah Alakkas, UCSD; Patrick Chen, UCSD; Michael Chen, UCSD; Katherine Longardner, UCSD; Jonathan Bui, UCSD; David Piccioni, UCSD
Rationale: The nonketotic hyperosmolar hyperglycemic (NKHH) state is defined as hyperglycemia (> 600 mg/dL) and hyperosmolality (> 350 mOsm/L) without ketosis [1]. The term 'nonketotic hyperglycemia' (NKH) is used when these criteria are not met. Seizures are a rare complication of NKHH/NKH and can be the initial manifestation of diabetes mellitus [2]. Seizures in NKH/NKHH are mainly in the form of focal motor seizures with/without loss of awareness; rarely, however, occipital seizures have been reported [4-7]. Methods: A 53-year-old woman presented to the emergency room for evaluation of six days of new-onset headaches. Her medical history was significant for poorly-controlled type 2 diabetes mellitus, hypertension, Grave’s disease, and coronary artery disease post stenting. She had no migraine history. Six days prior to presentation, the headaches started suddenly in the left maxillary region and progressed to the left orbitm and radiated to the back of the left side of the head. The severity was 7–10/10. She simultaneously reported seeing colored lights, described as “discotheque” in the right eye and obscuration of the right side of the visual field. In the emergency room, ESR was 93. An ophthalmologic exam revealed only glaucomatous optic nerves without evidence of temporal arteritis. A neurological exam revealed a dense right homonymous hemianopsia. Lab tests revealed glucose of 492, sodium of 131, measured osmolality of 292, ESR of 93, TSH of 16.44, FT4 of 0.83, and HgbA1c of 13.2%. Results: MRI of brain with and without contrast revealed elevated cortical blood flow to the left parietal-occipital cortex without mass lesion or underlying abnormalities. Prolonged EEG revealed left occipital sharp waves in the occipital leads consistent with epilepsia partialis continua. Initial treatment for status epilepticus was unsuccessful with intravenous levetiracetam and valproic acid loads. An insulin drip was initiated with concordant electrographic and clinical improvement with normoglycemia. On follow up, the patient's symptoms had resolved, she continued home insulin, and levetiracetam was tapered. Conclusions: Seizures are a rare complication of NKH/NKHH and can be the initial manifestation of diabetes mellitus [2]. We report a case of occipital lobe seizures secondary to hyperglycemia that did not meet the criteria for NKHH. Recognition of the role of hyperglycemia in seizures is vital because such seizures tend to be focal, refractory to AEDs, and respond mainly to insulin therapy and hydration [2, 3]. Funding: No funding
Case Studies