Metabolic encephalopathy secondary to diabetic ketoacidosis: a case report

Abstract

Introduction: Metabolic encephalopathy is a rare but potentially devastating complication of diabetic ketoacidosis (DKA). This case highlights the dramatic cognitive decline of a young man due to metabolic encephalopathy complicating DKA. The aims of this case report are to highlight metabolic encephalopathy as a complication of DKA and to explore the current research in diabetic related brain injury. The importance of investigation and treatment of reversible causes of encephalopathy is also demonstrated.

Case presentation: A 35-year-old man with a background of type 1 diabetes mellitus (T1DM) and relapsing remitting multiple sclerosis (RRMS) presented to the emergency department (ED) in a confused and agitated state. Prior to admission he worked as a caretaker in a school, smoked ten cigarettes per day, took excess alcohol and smoked cannabis twice per week. Following initial investigations, he was found to be in DKA. Despite timely and appropriate management his neurological symptoms and behavioural disturbance persisted. Neuroimaging revealed temporal lobe abnormalities consistent with an encephalopathic process. The patient underwent extensive investigation looking for evidence of autoimmune, infective, metabolic, toxic and paraneoplastic encephalopathy, with no obvious cause demonstrated. Due to persistent radiological abnormalities a temporal lobe biopsy was performed which showed marked astrocytic gliosis without evidence of vasculitis, inflammation, infarction or neoplasia. A diagnosis of metabolic encephalopathy secondary to DKA was reached. The patient's cognitive function remained impaired up to 18 months post presentation and he ultimately required residential care.

Conclusions: Metabolic encephalopathy has been associated with acute insults such as DKA, but importantly, the risk of cerebral injury is also related to chronic hyperglycaemia. Mechanisms of cerebral injury in diabetes mellitus continue to be investigated. DKA poses a serious and significant neurological risk to patients with diabetes mellitus. To our knowledge this is the second case report describing this acute complication.

Keywords: Diabetes mellitus; Diabetic brain injury; Ketoacidosis; Metabolic encephalopathy; Type 1 diabetes.

Fig. 1

Axial FLAIR (a) and saggital FLAIR (b) sequences from last surveillance MRI for his MS taken 2 months prior to presentation shows stable periventricular white matter lesions with evidence of an isolated demyelinating plaque in his right temporal horn. Axial FLAIR (c and d) sequence at presentation shows high signal abnormality in both temporal lobes extending to the insular cortex. Axial diffusion weighted imaging (e) shows no restricted diffusion and susceptibility weighted imaging (f) shows no area of focal haemorrhage

Fig. 2

Astrocytic gliosis. (a) H&E and (b) glial fibrillary acid protein (GFAP) stained sections demonstrate marked astrocytic gliosis characterised by an evenly dispersed proliferation of large reactive astrocytes with abundant eosinophilic cytoplasm and branching processes (arrows)