Seizure as the first presentation of diabetes mellitus

Abstract

Seizures comprise 1% of emergency room (ER) admissions. Herein, we present a case of focal seizure due to severe hyperosmolality from a markedly elevated glucose level. The correction of hyperglycemia with fluids and insulin infusion abated the seizures and no anti-epileptic medications were given. Two years later, the patient has remained seizure free. We aim to emphasize that nonketotic hyperosmolar state can be a precursor for seizures and hence the importance of the routine checking of the blood sugar. A 66-year-old African American man with a past medical history of alcoholic liver cirrhosis (Child A) presented to the ER after his family noticed an episode of rigorous shaking of his upper and lower extremities that lasted for 5 minutes during which he was unconscious followed by a period of confusion. Upon arrival, he was noted to have focal right upper extremity seizure activity. The family confirmed that the patient never had seizures nor was there any family history of seizure disorder. There was no history of fever, head trauma, exposure to toxins or drugs. He is a chronic alcoholic who quit drinking 4 years ago without any recent alcohol intake. The family mentioned that 2 months prior to admission, he started complaining of polyuria, nocturia, polydipsia and weight loss but did not seek medical advice. He was never diagnosed with diabetes mellitus before. On examining the patient after the seizure episode, he was afebrile, vitally stable, confused without neck rigidity or notable focal weakness. His random blood sugar was 1026 mg/dl with a normal anion gap and without acetone in the blood or ketones in urine. His calculated serum osmolality was 339. Urine screen was negative for any drugs or toxins and ethanol level was less than 10. His HbA1c was 16.1, calcium level was 9.5 mg/dl, magnesium level was 2 mg/dl and white blood cell (WBC) count was 4300. Liver function tests revealed an ammonia level of 53 µmol/l (normal [N] 11–35), prothrombin time 10.8 (N 9.3–11.8), International Normalized Ratio (INR) level 1.07, albumin 3.3 gm/dl, aspartate transaminase (AST) 26, alanine transaminase (ALT) 24 and total bilirubin of 0.5 mg/dl. Table 1 demonstrates the progression of the blood sugars, electrolytes, kidney functions and calculated serum osmolality during the first 24 hours after admission. CT scan of the brain revealed a chronic lacunar infarct in the putamen of the left basal ganglia but no intracranial bleed or an evident acute ischemic stroke (Figure 1). Electroencephalogram did not reveal any epileptiform discharge activity. Table 1. The progression of the basic metabolic panel and osmolality during the first 24 hours of admission. Figure 1. CT scan of the brain revealing a chronic lacunar infarct in the putamen of the left basal ganglia but negative for intracranial bleed or evident acute ischemic stroke. The patient was started on an insulin drip and normal saline infusion with improvement of his blood sugar. On examining the patient 2 hours later, he was fully conscious, alert and oriented with a normal neurological examination. The patient had laboratory evidence of urinary tract infection and was treated with a course of ciprofloxacin. No anti-epileptic medications were given for the seizures which did not recur during his hospital stay. The patient was discharged on insulin glargine and aspart. On follow up 2 years after the seizure episode, the patient had satisfactory control of his diabetes mellitus without any recurrence of seizures. In the United States, there are 1 million ER visits yearly for seizures which comprise approximately 1 % of all ER admissions [Pallin et al. 2008]. In this report, a patient presented with witnessed focal seizures that was attributed to the markedly elevated serum osmolality. Seizures were abolished and did not recur after control of his blood sugar. Focal seizures as the presenting feature of nonketotic hyperglycemia have been initially described by Maccario and colleagues [Maccario et al. 1965]. Other reports have further illustrated the association [Tiamkao et al. 2003; Hennis et al. 1992; Grant and Warlow, 1985]. The underlying pathophysiology of hyperosmolality-induced seizures is the cellular dehydration and subsequent dysfunction of brain cells. Moreover, the plasma hypertonicity can cause a focal reduction in blood flow and seizures in susceptible individuals. Hyperglycemia also increases gamma-aminobutyric acid metabolism and decreases the seizure threshold. However, the high osmolality alone cannot explain the focal seizures because most patients presenting with high serum osmolality do not have seizures [Daniels et al. 1969]. Interestingly, the described presentation occurred in a patient with nonketotic hyperglycemia and not in cases with diabetic ketoacidosis. A ketogenic diet has been described to have an anticonvulsant effect, especially in patients with partial seizures [Schwartz et al. 1983]. Early recognition of the underlying hyperosmolality is mandatory to establish the diagnosis and to avoid the unnecessary use of prophylactic anti-epileptic medications [Ozer et al. 2003], especially given that phenytoin can worsen the hyperglycemia [Carter et al. 1981]. In conclusion, we present a case where marked increase in the serum osmolality due to nonketotic hyperglycemia was a seizure trigger. We emphasize the importance of the routine checking of the blood sugar in patients presenting with seizures and that lowering the blood sugar with institution of insulin and fluids is the definite cure without the need for anticonvulsants, which are even unfavorable.