ABSTRACT
Diabetic ketoacidosis (DKA) can cause significant morbidity and mortality in patients with type 1 or type 2 diabetes mellitus. DKA causes an approximate annual hospitalization rate of 6.3% and in-hospital case-fatality rate of 0.4%. A subset of DKA cases termed euglycemic diabetic ketoacidosis (eu-DKA) is characterized by euglycemia (<200 mg/dL), high anion gap metabolic acidosis, and an increased plasma ketone concentration. This clinical syndrome comprises approximately 2.6% to 3.2% of total DKA admissions, making it a rare condition. In this case report, a male patient was diagnosed with coronavirus disease 2019 (COVID-19) three days prior to arriving at the emergency department. Upon evaluation, he displayed severe acidemia and was diagnosed with eu-DKA. He was started on intravenous regular insulin and D5 one-half normal saline, which markedly improved his metabolic status. Notably, his admission was uncomplicated by respiratory symptoms of COVID-19. It is proposed that his eu-DKA was catalyzed by his recent COVID-19 infection. Recent studies that have shown COVID-19 may increase lipolysis and induce ketogenesis in susceptible patients.
ABSTRACT
Coronavirus disease 2019 (COVID-19) was designated as a global pandemic by the World Health Organization (WHO) on March 11, 2020. The Cochrane Database of Systematic Reviews documents that COVID-19 has a wide range of common symptoms, which have made it difficult to characterize the disease. To date, the neurological symptoms of stuttering and word-finding difficulties have not been reported in confirmed COVID-19 cases. This case report describes the clinical course of a 53-year-old female that presented to the emergency department (ED) twice with varying symptoms consistent with COVID-19. At the second ED visit, she complained of new-onset stuttering and word-finding difficulties and tested positive for COVID-19 using the polymerase chain reaction (PCR) nasopharynx test. When contacted, the patient stated that her speech issues persisted at least seven days after discharge from her second ED visit. As a result, the virus may cause symptoms of an acute neurological event and should be taken into diagnostic consideration. These neurological findings may be explained by the recent discovery of the COVID-19 spike protein's ability to destabilize the blood-brain barrier (BBB) and enter the central nervous system (CNS). Increased classification of unrecognized COVID-19 symptoms and complications may aid in the characterization, surveillance, and prevention of the disease.
ABSTRACT
OBJECTIVES: To present three patients with severe coronavirus disease 2019 infection who developed life-threatening hyperpyrexia while being treated with dexmedetomidine for sedation. DATA SOURCES: Clinical records. STUDY SELECTION: Case report. DATA EXTRACTION: Relevant clinical information. DATA SYNTHESIS: We describe three patients, a 60-year-old female, 43-year-old female, and 46-year-old male, who were hospitalized in surge ICUs during the coronavirus disease 2019 pandemic in the early spring of 2020. All developed hyperpyrexia, defined as a temperature above 41.1°C, following an increase in dexmedetomidine dosing to above 1.5 µg/kg/hr. Fevers resolved following discontinuation of dexmedetomidine. CONCLUSIONS: While the exact mechanism of hyperpyrexia remains unclear, findings in this study suggest that high doses of dexmedetomidine infusion are associated with hyperpyrexia in a seemingly dose-dependent fashion in critically ill patients with coronavirus disease 2019. Coronavirus disease 2019 infection causes a hyperinflammatory state characterized by pro-inflammatory cytokine dysregulation. Dexmedetomidine, a centrally acting alpha-2 agonist, may alter hypothalamic temperature regulation through disturbances in neurotransmitter expression and metabolism. We postulate that the use of high-dose dexmedetomidine in a hyperinflammatory state may increase the risk of developing hyperpyrexia in this severe disease state.