ESPE Abstracts

Introduction: Reduced consciousness during diabetic ketoacidosis (DKA) is an acute medical emergency which necessitates rapid escalation of care. Rarely it can point towards unusual co-morbidities too. We report a case of new- onset type 1 diabetes (T1D) presenting with severe DKA in a teenager, complicated by an evolving neuropathy.

Case report: A previously healthy 17-year-old girl presented in severe DKA following a 4-day history of vomiting, lethargy and recent history of polydipsia. She recently returned from a holiday when all family members had COVID (initial history was taken from family via telemedicine). She also intentionally lost weight by physical exercise during covid lockdown. On presentation she needed intubation and ventilation in intensive care unit. Due to profound encephalopathy she underwent CT and MRI head which were normal. Despite resolution of DKA with standard treatment protocol, she had fluctuating level of consciousness and increasing oxygen requirements. She was started on antibiotics and antiviral for chest consolidation and presumed viral meningitis respectively. She was also treated with antifungal medication for positive candida on blood culture. Due to confusion, evolving bulbar palsy with aspiration pneumoniae and seizure activity further head CT and MRIs were done which were normal. Subsequently an EEG showed features of encephalopathy but no epileptiform waves. She eventually underwent nerve conduction studies and electromyography which was suggestive of widespread demyelinating radiculoneuropathy and the cerebrospinal fluid protein was high on lumbar puncture, both consistent with the clinical diagnosis of Guillain- Barre syndrome (GBS). She was commenced on a course of plasma exchanges which improved her neurological status. Due to persistent neuropathic pain, she received extensive input from neuropsychology, speech and language, physiotherapy and occupational therapy teams. Before discharge she was started on continuous glucose monitoring in view of impaired hypoglycaemia awareness. Her GAD antibodies were positive, but her extensive autoimmune polyneuropathy screen was negative.

Conclusion: The case shows a rare combination of GBS, T1D with DKA and COVID-19 infection in our patient. It also highlights the challenges associated with neurological manifestations during DKA. A short prodrome and severe DKA may have been precipitated by the concomitant COVID-19 infection. Persistent neurological symptoms presented a conundrum and eventually led to the diagnosis of GBS in a newly diagnosed T1D patient. It’s very plausible that COVID-19 infection played part in GBS too. This underpins the importance of thinking broadly on differential diagnoses when a patient presents in severe DKA and evolving abnormal neurology.