Case Reports in Critical Care

Introduction. Aluminum phosphide (rice tablet) was first introduced as a pesticide in India. Rice tablets are commonly used in Iran due to their high efficacy against rodents and insects, low cost, and availability. Aluminum phosphide is a lethal poison without antidote and causes cardiocirculatory collapse and has negative inotropic cardiac effect. Human and animal studies showed that high dose insulin had positive cardiac inotropic effects. GIK (glucose, insulin, and potassium) assists heart uptake of carbohydrates that are the major fuel substrate of the myocard muscle under stressed conditions and leading to correction of acidosis, increased myocardial contractility, and peripheral vascular resistance. Case Presentation. In this manuscript, a young woman with aluminum phosphide poisoning was described to have presented with hypotension, hypoxemia, and severe metabolic acidosis. In contrast to our previous experiences that approximately all rice tablet poisoning patients with shock were dead despite full conservative treatment, this patient miraculously was saved with high dose intravenous regular insulin infusion and was discharged from the hospital with good condition and without any complications. Conclusion. Rice tablet poisoning has high fatality rate, and to date, no antidote is available. GIK is suggested as a potential life saving treatment for critical rice tablet poisoning patients with symptoms and signs of shock.

Point-of-care ultrasound (POCUS) is becoming a frequently utilized imaging tool in the emergency department (ED) as it can aid in early diagnosis of many pathologies. This is a case report of a 55-year-old male who presented to the emergency department by ambulance for sudden onset chest pain followed by a syncopal episode. Point-of-care echocardiogram revealed a large pericardial effusion with a significantly dilated aortic root, concerning for aortic dissection. Patient was emergently taken for a computed tomography (CT) scan, which was only remarkable for an ascending thoracic aortic aneurysm but failed to show an aortic dissection flap. On repeat POCUS, a dissection intimal flap, large pericardial effusion with tamponade physiology, and aortic regurgitation were identified and later confirmed on transesophageal echocardiogram. This case report details a rare pathology that was correctly identified on initial POCUS before it was seen on CT scan.

Symmetrical peripheral gangrene (SPG) is a rare clinical syndrome characterized by an acute onset of ischemic damage in two or more extremities without obstruction or vasculitis of supplying vessels. Body parts commonly affected include toes, hands, scrotum, and earlobes, increasing the risk of limb amputation and impairing the quality of life. The vascular injury mechanism is disseminated intravascular coagulation. SPG may manifest unpredictably in conditions associated with septic shock, low output states, vasospastic conditions, myeloproliferative disorders, or hyperviscosity syndrome. A review on the topic is presented based on a 3-case series of SPG that required amputation of fingers and toes after the administration of vasopressors in a septic shock context.

Remdesivir (RDV) is an approved treatment for hospitalized patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. There is limited literature on the cardiac adverse effects of RDV. We report a case of a patient who developed hemodynamically unstable bradycardia after the initiation of RDV that resolved after discontinuing RDV.

Plasmapheresis for the treatment of hypertriglyceridemia is relatively uncommon and mostly reported either in patients experiencing hypertriglyceridemia-induced acute pancreatitis or patients with therapy-resistant familial hypercholesterolemia. Standard therapies for hypertriglyceridemia include dietary modification and lipid-lowering medication. For severe hypertriglyceridemia, the risk of pancreatitis increases significantly as triglyceride levels increase above 1000 mg/dL, and current therapies are unable to reduce triglyceride levels rapidly enough. Here, we report a case of a 48-year-old male patient who presented to the emergency department due to an amitriptyline overdose. In addition to being started on IV sodium bicarbonate therapy, an intravenous 20% fat emulsion bolus at 1.5 mL/kg was administered followed by 0.25 mL/kg/min infusion for 4 hours as a strategy to absorb lipophilic amitriptyline. Two days posttreatment, he was noted to have substantial hypertriglyceridemia (serum triglycerides: 6,475 mg/dL). His amylase was within the normal range at 37 U/L (reference range: 20-100 U/L), his lipase was low at 40 U/L (reference range: 75-390 U/L), and he was without evidence of any clinical sequelae secondary to hypertriglyceridemia (e.g., pancreatitis). Due to the severity of his hypertriglyceridemia, plasmapheresis was initiated urgently for rapid reduction in serum triglyceride levels to prevent pancreatitis and end-organ damage. He underwent a 1-plasma volume exchange with 5% albumin as the replacement fluid. This reduced his triglyceride levels to 185 mg/dL (reference range: 3-149 mg/dL). His symptoms secondary to his amitriptyline overdose were also resolved. Here, we report a 2-step process of intravenous lipid emulsion followed by plasmapheresis for amitriptyline overdose.

Background. Lactic acidosis is a well-known complication of metformin accumulation in diabetic patients with kidney failure. However, it is not usual to raise the diagnosis of metformin-associated lactic acidosis when patients have normal kidney function. The causes of metformin-induced high lactate include the accumulation of normal doses of metformin in chronic kidney disease, an overdose of this drug without kidney failure, or an increase in lactate production due to the inhibition of liver gluconeogenesis. Case Presentation. We report the case of a 61-year-old diabetic man who was brought to the emergency room in a comatose state. His family reported abdominal pain with diarrhea in the last two days. He was found to have severe lactic acidosis with normal serum creatinine. He was on a regular dose of metformin, and his family denied any other medical history or any alcohol abuse. He showed no signs of infection, his liver enzymes were slightly elevated, and he had severe anemia. His hemodynamics deteriorated quickly within hours, and an abdominal computed tomography scan revealed no abnormalities. He underwent a laparotomy that ruled out mesenteric ischemia and revealed an abnormal liver. The liver biopsy later confirmed the diagnosis of cirrhosis. Conclusions. We discuss here the probable causes of severe lactic acidosis and the role of metformin in exacerbating this acid-base disturbance in cirrhotic patients. Future research is needed to determine whether these patients might benefit from dialysis.