J Emerg Med
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Case Reports
Diabetic Ketoacidosis as a Delayed Immune-Related Event after Discontinuation of Nivolumab.
Nivolumab, an anti-programmed cell death-1 (PD-1) monoclonal antibody with immune checkpoint inhibitory activity, represents a novel treatment for several cancers. Immune checkpoint inhibitors cause side effects, known as immune-related adverse events (irAEs) or delayed immune-related events (DIRE), after immunotherapy discontinuation. Type 1 diabetes mellitus (T1DM) and diabetic ketoacidosis have been reported to develop as an irAE during the treatment with nivolumab. Here, we report on a patient who developed T1DM and diabetic ketoacidosis after discontinuation of treatment with nivolumab as a DIRE. ⋯ A 59-year-old man, who received nivolumab for an alpha fetoprotein-producing gastric cancer, presented with acute fatigue 4 months after discontinuation of nivolumab. Throughout therapy with nivolumab, the patient's hemoglobin A1c (HbA1c) level was ≤ 6%. However, 1 month prior to the patient's emergency department visit, he noticed weight loss, and 3 weeks prior to that, his HbA1c was 7.1%. Urinalysis showed ketone bodies, and arterial blood gas analysis suggested metabolic acidosis with hyperglycemia (690 mg/dL), which established the diagnosis of diabetic ketoacidosis. An endogenous insulin deficiency without verifiable anti-islet autoantibodies was confirmed; the patient had a human leukocyte antigen haplotype that does not increase the risk of acute-onset T1DM. We considered that T1DM in this patient developed possibly due to nivolumab. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This case highlights the need for clinicians to be vigilant of the fact that a history of anti-PD-1 monoclonal antibody therapy may increase the risk of diabetic ketoacidosis, whether treatment is ongoing or discontinued.
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Case Reports
Utility of Hypertonic Saline and Diazepam in COVID-19-Related Hydroxychloroquine Toxicity.
Hydroxychloroquine (HCQ) poisoning is a life-threatening but treatable toxic ingestion. The scale of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (COVID-19) and the controversial suggestion that HCQ is a treatment option have led to a significant increase in HCQ use. HCQ poisoning should be at the top-of-mind for emergency providers in cases of toxic ingestion. Treatment for HCQ poisoning includes sodium bicarbonate, epinephrine, and aggressive electrolyte repletion. We highlight the use of hypertonic saline and diazepam. ⋯ We describe the case of a 37-year-old man who presented to the emergency department after the ingestion of approximately 16 g of HCQ tablets (initial serum concentration 4270 ng/mL). He was treated with an epinephrine infusion, hypertonic sodium chloride, high-dose diazepam, sodium bicarbonate, and aggressive potassium repletion. Persistent altered mental status necessitated intubation, and he was managed in the medical intensive care unit until his QRS widening and QTc prolongation resolved. After his mental status improved and it was confirmed that his ingestion was not with the intent to self-harm, he was discharged home with outpatient follow-up. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: For patients presenting with HCQ overdose and an unknown initial serum potassium level, high-dose diazepam and hypertonic sodium chloride should be started immediately for the patient with widened QRS. The choice of hypertonic sodium chloride instead of sodium bicarbonate is to avoid exacerbating underlying hypokalemia which may in turn potentiate unstable dysrhythmia. In addition, early intubation should be a priority in vomiting patients because both HCQ toxicity and high-dose diazepam cause profound sedation.
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Emergency departments (EDs) are faced with a growing number of patients with traumatic brain injury (TBI) using direct oral anticoagulants (DOACs). However, there remains uncertainty about the bleeding risk, rate of hematoma expansion, and the efficacy of reversal strategies in these patients. ⋯ Based on the present findings it can be postulated that TBI patients using DOACs have a low risk for ICH. Hematoma progression occurred, however, in a substantial number of patients. Considering the retrospective nature of the present study, future prospective trials are needed to confirm this finding.