of pyrethroid poisoning is rare. When documented, rhythms are consistent with transient complete heart blocks or sinus arrest. The cardiac manifestations in our patient were uncommon and unexpected. We postulate that the EKG findings seen were reflective of
concomitant cocaine intoxication. This case highlights the importance of considering mixed toxicities and the effect of environmental toxicities in patients presenting with cardiac conduction abnormalities.
THE IMPORTANCE OF RECOGNIZING BRASH WITH MILD HYPERKALEMIA Chloe d’Aquin Spears, MD; Department of Medicine; LSU Health New Orleans, New Orleans, LA.
Introduction: BRASH is a clinical syndrome and acronym defined by bradycardia, renal dysfunction, AV nodal blockade, shock and hyperkalemia. It is often mistaken for beta blocker toxicity or undifferentiated shock in cases where hyperkalemia is mild.
evaluate for obstructive shock and found to have no pericardial effusion or signs of right heart strain. The cause of his shock is thought to be secondary to BRASH syndrome in the setting of hypovolemia due to decreased oral intake in response to uremic symptoms. AV nodal blockade from high dose beta blocker combined with poor renal reserve likely put him into a cycle of hyperkalemia and AV nodal block leading to worsening bradycardia, hypoperfusion, and shock. As the labetalol washed out of his system, his hemodynamics improved, and he was weaned off vasopressor support. His course was complicated by progression to end-stage renal disease, cardiac arrest during a tunneled line placement, and new atrial fibrillation diagnosis. He was discharged days later in stable condition. He unfortunately represented a month later with a STEMI leading to cardiac arrest and subsequently expired. Discussion: This case illustrates the importance of recognizing BRASH syndrome with mild hyperkalemia. Common precipitants of BRASH syndrome are hypovolemia, medications that increase serum potassium, and renal injury. It is important to recognize BRASH and correct even mild hyperkalemia to stop the cycle of worsening bradycardia and shock.
Case: A 77-year-old man with renal cell carcinoma status post nephrectomy, chronic kidney disease and hypertension presented with fatigue, shortness of breath, nausea, decreased appetite and decreased urinary output for one week. His medications were labetalol, amlodipine, calcitriol, patiromer, furosemide, and ferrous sulfate. He had no recent medication changes or dose adjustments. He was hypotensive despite fluid resuscitation and required vasopressors. He was bradycardic with initially borderline elevation in his potassium at K 5.1 mEq/L. His BUN and Cr were doubled compared to their baseline two months prior. He was initially managed for undifferentiated shock. He was covered with broad spectrum antibiotics, received glucagon and calcium for concern of beta blocker toxicity, and given albuterol, furosemide and potassium binders for hyperkalemia. An emergent transthoracic echocardiogram was obtained to
INVASIVE MUCORMYCOSIS IN PATIENT WITH ACUTE LIVER FAILURE Kierha Baker MD, Yanming Yang MD, Matthew Brown MD, Department of Medicine, Ochsner Clinic Foundation, New Orleans, LA.
Introduction: Rhinocerebral mucormycosis is a rare opportunistic infection caused by the inhalation of spores of either Rhizopus or Mucor species, affecting the paranasal sinuses and brain. The most important predisposing factors include immunocompromised individuals but even amongst high-risk patients, it accounts for only 8.3%-13% of all fungal infections. Due to the mucor species harboring a ketone reductase system, it grows aggressively in acidic conditions such as diabetic ketoacidosis, resulting in a fulminant and life-threatening disease, with
overall mortality 30-70% despite treatment. Early intervention is critical, however clinical signs of rhinocerebral mucormycosis are nonspecific. Case: A 33-year-old male with type 1 diabetes, hypertension, and alcohol abuse initially presented with jaundice and malaise. He had a distended abdomen, cognitive impairment, and right eyelid apraxia. Labs were consistent with diabetic ketoacidosis and acute liver failure with computed tomography (CT) of the abdomen/pelvis showing 7
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