SUN-189 Tramadol Induced Hypoglycemia Masquerading as a Seizure Disorder

Abstract

Main cause of hypoglycemia is exogenous insulin and its secretagogues. Herein we report a patient presenting with seizures treated with topiramate for last 10 years. During ER visits for seizures, plasma glucose(PG) was 1.5-1.8 mM/l with undetectable insulin, C peptide, proinsulin and normal responses of HGH, ACTH and cortisol, excluding insulinoma, exogenous insulin, insulin secretagogues and HGH, cortisol or ACTH deficiency. CT scans excluded Tumor secreting IGF2. Further inquiry revealed high daily dose tramadol use confirmed by elevated urine levels. Withdrawal of tramadol resulted in remission of hypoglycemia and seizures confirming unique presentation of tramadol-induced hypoglycemia. Clinical case: 57 y/o Caucasian woman presented to ER with post seizure confusion. Next of kin reported recurrent seizures over past 10 years being treated with topiramate. She was also receiving amitriptyline HS and tramadol 50 mg TID ‘for neuropathic pain’, KCL and spironolactone for hypokalemia attributed to topiramate. Physical examination revealed confusion, with no focal neurological deficit, pulse 68/min, BP 114/72 mm. Rest of the examination was unremarkable. Laboratory tests showed PG, 2.5 mM/l and K, 3.1 mM/L, normal ECG and EEG. Patient was resuscitated with glucose and K infusion and discharged. During several visits to ER at different hospitals for seizure, PG was <3mM/l, with undetectable levels of insulin <0.2 uU/ml, C peptide < 0.78 ng/ml, pro insulin <4.1 with normal responses of cortisol 25-45 /dl, HGH 2.5-8.8 ng/ml, ACTH 50-85 pg/ml and prolactin 15-19 pg/ml. Concurrent IGF2 levels were 650-950 ng/ml (N-331-936). During 1 visit, PG rose to 8 mM/l on resuscitation with 50 ml D/50. However, PG declined to <3 mM/l within half hour and pattern persisted for 4 hrs. Hence, she was admitted into ICU for observation, while administering infusion of 10% dextrose and 2000 kcal diet. During 48 hrs, PG remained between 5-8 mM/l while receiving infusion. However, following discontinuation, symptomatic hypoglycemia (<3mM/l) returned within an hour. She was retained for observation. Hypoglycemia was thought to be induced by tramadol because of previous reports of hypoglycemia on propoxifen administration and tramadol belonging to same group. Literature search revealed rare reports implicating tramadol in onset of hypoglycemia. Urine toxicology showed elevated levels of tramadol 0.834 mg/l (N-0.1-0.3) and metabolite desmethyltramadol 9913 ng/ml. Neither a seizure nor hypoglycemia and hypokalemia ensued following discontinuation of tramadol, glucose infusion, KCL and spironolactone during next 48 hours. Finally patient is free of seizures and hypoglycemia for past 9 months. Conclusion- a unique presentation of tramadol induced hypoglycemia mascerading as a seizure disorder. Tramadol induced hypoglycemia may be attributed to non-suppressible IGF2 documented by elevated IGF2/PG.