Carbon monoxide poisoning and its effect on QTc prolongation.

Carbon monoxide (CO) poisoning has been associated with direct toxicity to the cardiovascular system by causing arrhythmias through prolongation of QTc. It has been reported to have arrhythmogenic potential likely due to its action on the cardiac membranes. We present a case of a 69-year-old man who presented to the emergency department for evaluation of a syncopal episode after exposure to CO. His carboxyhemoglobin level was elevated at 10.5% on admission, electrocardiogram revealed QTc interval of 622 msec. He was treated with hyperbaric oxygen and a repeat electrocardiogram 15 h after hyperbaric oxygen initiation showed improvement in QTc to 490 msec and his carboxyhemoglobin level decreased to 1.8%. There is a direct association between acute CO poisoning and QTc prolongation as reported in patient cases and evidence of it was seen by investigators who worked on rats and found that this phenomenon occurs due to the action of nitric oxide on the late Na + channels affecting repolarization. The resolution after hyperbaric oxygen could be due to decrease in the CO concentration and the absence of nitric oxide synthase activation further propagating the QT prolongation, however, further research would have to be performed to consolidate this.

Miller Fisher syndrome with bilateral vocal cord paralysis: a case report.

BACKGROUND: Miller Fisher syndrome is a variant of acute inflammatory demyelinating polyneuropathy classically characterized by ataxia, ophthalmoplegia, and areflexia. Miller Fisher syndrome can present with uncommon symptoms such as bulbar, facial, and somatic muscle palsies and micturition disturbance. CASE PRESENTATION: We describe the case of a 76-year-old white man with new-onset ataxia, stridor, areflexia, and upper and lower extremity weakness who required intubation at presentation. An initial work-up including imaging studies and serum tests was inconclusive. Eventually, neurophysiological testing and cerebrospinal fluid analysis suggested a diagnosis of Miller Fisher syndrome. Our patient responded to treatment with intravenous immunoglobulin and supportive therapy. CONCLUSION: The occurrence of acute or subacute descending paralysis with involvement of bulbar muscles and respiratory failure can often divert clinicians to a diagnosis of neuromuscular junction disorders (such as botulism or myasthenia gravis), vascular causes like stroke, or electrolyte and metabolic abnormalities. Early identification of Miller Fisher syndrome with appropriate testing is essential to prompt treatment and prevention of further, potentially fatal, deterioration.

When it is not just DKA; diabetic ketoacidosis as a first presentation of pancreatic adenocarcinoma.

Pancreatic cancer is the fourth leading cause of cancer related-deaths in the United States. Early symptoms of pancreatic cancer are nonspecific, and most cases are diagnosed at an advanced stage. DKA as a first presentation of pancreatic adenocarcinoma is a seldom reported condition. We present a case of a 59 year old female with type 2 diabetes, who presented to the emergency department with confusion, abdominal pain, polyuria and polydipsia. Laboratory workup showed a high anion gap metabolic acidosis and a blood glucose level of 419 mg/dl with positive serum ketones. She was diagnosed with DKA and admitted to the ICU. A CT abdomen/pelvis was performed to assess for pancreatic pathology as her DKA took longer time to resolve, it showed a pancreatic mass with multiple lesions in the liver. She had biopsies done which were positive for poorly differentiated pancreatic ductal adenocarcinoma. DKA occurs less commonly in patients with type 2 diabetes. Common precipitating factors for DKA in type 2 diabetes include medication noncompliance, infection, or possibly treatment with SGLT2 inhibitors. DKA as a first presentation of pancreatic cancer has been reported more with endocrine islet cell tumors but rarely with adenocarcinoma of the exocrine pancreas. Studies have shown that diabetes is an independent risk factor for development of pancreatic cancer. Other studies suggested that diabetes might be a result of pancreatic cancer or a paraneoplastic effect. One study suggested that diabetes associated with pancreatic cancer occurs at a resectable stage of the disease.