Case Presentation: A 51-year-old male with a past medical history of hypertension and schizophrenia maintained on amlodipine, risperidone and benztropine was transported to the ER psychiatric unit by law enforcement. He was detained after he was found wandering the streets demonstrating increased verbal and physical aggressiveness. He was known to the psychiatric unit, with previous admissions for psychosis secondary to schizophrenia. On presentation vitals were solely significant for tachycardia. Physical and mental status examination revealed a disheveled, agitated and combative male who was disoriented to time, person and location. He was actively experiencing visual and auditory hallucinations with psychomotor agitation, intermittent loosening of association, circumstantial and tangential speech and persecutory delusions. Although, initially given one dose of intramuscular haloperidol and benztropine, his psychosis persisted. Biochemical investigations were significant for a serum glucose of 37 mg/dL; All other investigations including alcohol level, toxicology and TSH were normal. Head CT was unremarkable. His HG was treated with intravenous dextrose with complete resolution of psychotic symptoms within one hour of normoglycemia. He needed no further antipsychotic doses save his maintenance risperidone. Post return of normal mentation, further historical enquiry revealed a recent diagnosis of type 2 diabetes mellitus by his PCP, managed on metformin and glimepiride, and poor oral intake. He was discharged on metformin and sitagliptin after extensive DM self-management education; glimepiride was discontinued.
Discussion: In the hypoglycemic state, catecholamine mediated neurogenic symptoms such as diaphoresis, tremors, tachycardia, and anxiety frequently occur. By contrast, neuroglycopenic manifestations of hypoglycemia, that is, lethargy, confusion, focal seizures, hemiplegia and coma, are the direct result of central nervous system glucose deprivation. Uncommonly, they can be the sole presenting complaint in the hypoglycemic patient. In one study, 27% of patients with insulinomas had only neuroglycopenic symptoms [1]. Interestingly, some case reports suggest acute psychosis may be an important neuroglycopenic feature [2]. Psychiatric patients, particularly those with primary psychotic disorders often face a labyrinthine process when seeking emergent medical care including but not limited to anchoring and ascertainment physician bias. If unrecognized, hypoglycemia can lead to neuronal death and functional brain failure [3]. Conversely, in cases of simple hypoglycemia, prompt management often quickly results in normoglycemia and near immediate resolution of symptoms.
Conclusions: The neurogenic response to hypoglycemia is well established. By contrast, neuroglycopenic manifestations are widely variable, often vague and have been erroneously attributed to other diagnoses. The incidence of these symptoms in a patient with a psychiatric illness may also compound diagnostic uncertainty. Clinicians must maintain a high index of suspicion of hypoglycemia in patients presenting with acute psychosis even in the presence of functional illness so as to reduce morbidity, mortality and medicolegal risk.