Treatment Modalities in Calcium Channel Blocker Overdose: A Systematic Review.

Calcium channel blocker poisoning is one of the most common poisonings encountered which presents with life-threatening complications. However, there is no unified approach for treating these patients in the existing literature. This study aimed to assess the effects of different treatment modalities used in calcium channel blocker poisoning, as reported by previous studies. The primary outcomes studied were mortality and hemodynamic parameters after treatment. The secondary outcomes were the length of hospital stay, length of intensive care unit stay, duration of vasopressor use, functional outcomes, and serum calcium channel blocker concentrations. A thorough literature search was performed through Ovid, PubMed, Cochrane Library, and Google Scholar from January 2014 to December 31, 2022, to identify all studies analyzing the effects of the treatment of calcium channel blocker poisoning on the desired outcomes. Two reviewers reviewed 607 published articles from January 2014 to December 2022 to identify studies analyzing the effects of the treatment of calcium channel blocker poisoning on desired outcomes. In this review, 18 case reports, one case series, and one cohort study were included. Most patients were treated with an injection of calcium gluconate or calcium chloride. The use of calcium along with dopamine and norepinephrine was found to have lower mortality rates. A few patients were also treated with injection atropine for bradycardia. High-dose insulin therapy was used in 14 patients, of whom two did not survive. In the cohort study, 66 calcium channel blocker toxicity patients were included. These patients were treated with high-dose insulin therapy. A total of 11 patients with calcium channel blocker toxicity succumbed. Although it was found to be associated with improved hemodynamic parameters and lower mortality, side effects such as hypokalemia and hypoglycemia were noted. Intravenous lipid emulsion therapy (administered to eight patients), extracorporeal life support (used in three patients with refractory shock or cardiac arrest), injection glucagon, methylene blue, albumin infusion, and terlipressin were associated with a lower mortality rate as well as improvement in hemodynamic parameters. None of the case reports provided any information on end-organ damage on long-term follow-up.

Quadriparesis and Broad Complex Tachycardia Secondary to Severe Hypokalaemia Induced by Distal Renal Tubular Acidosis as the Initial Manifestation of Sjogren's Syndrome.

Sjogren's syndrome is an autoimmune disorder characterized by lymphocytic infiltration of exocrine glands that typically manifests as dysfunction of the lacrimal or salivary glands. About one-third of Sjogren's syndrome patients exhibit systemic symptoms. In one-third of Sjogren's syndrome cases, renal tubular acidosis (RTA) is present. Hypokalemia is the most prevalent electrolyte disorder in patients with distal RTA. A middle-aged female presented to the emergency department with a complaint of sudden-onset quadriparesis followed by shortness of breath. Her arterial blood gas analysis revealed severe hypokalaemia and metabolic acidosis. ECG revealed broad complex tachycardia, which resolved after starting potassium infusion. On evaluating the cause of normal anion gap metabolic acidosis and hypokalaemia, she was found to have distal renal tubular acidosis (RTA). Furthermore, on evaluating the cause of distal RTA, her SSA/Anti Ro and SSB/Anti La levels came out to be elevated, and a probable diagnosis of Sjogren's syndrome was made. Severe hypokalaemia leading to hypokalaemia quadriparesis and broad complex tachycardia as the initial manifestation of distal RTA due to Sjogren's syndrome is uncommon. Timely recognition and prompt replacement of potassium are key to improved outcomes. It is also important to note that Sjogren's syndrome should be taken into account even in the absence of sicca symptoms, like in our case.

Hiccups and Slurring of Speech: Atypical Presentation of High-Altitude Cerebral Edema.

High-altitude cerebral edema (HACE) is one of the rare and severe form of high-altitude mountain sickness. Usually it presents as headache, altered mental status, ataxia in un-acclimatized person with rapid ascent to high altitude. Here we report a case of a 62-year-old male patient who had history of rapid ascent to high altitude and presented to the department of emergency after descent from high altitude with an atypical presentation as hiccups and slurring of speech. Magnetic resonance imaging (MRI) of brain showed white matter edema suggestive of HACE. The patient improved after treatment with supplemental oxygen, dexamethasone, and acetazolamide. He was discharged after three days of hospital stay with complete resolution of symptoms.