When a Cure Becomes a Curse: The Complex Clinical Scenario Involving Amiodarone Therapy and BRASH (Bradycardia, Renal failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia) Syndrome.

BRASH [bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock, and hyperkalemia] syndrome is a recently recognized clinical condition that is rare but can be potentially life-threatening. Its pathogenesis is characterized by a self-perpetuating cycle of bradycardia that is potentiated by the concomitant occurrence of medication use, hyperkalemia, and renal failure. AV nodal blocking agents are commonly implicated in BRASH syndrome. We report a case of a 97-year-old female patient with a medical history of heart failure with preserved ejection fraction, atrial fibrillation, hypertension, hyperlipidemia, and hypothyroidism who presented to the emergency department with a one-day history of diarrhea and vomiting. Upon presentation, the patient was hypotensive, bradycardic, and had severe hyperkalemia, acute renal failure, and anion gap metabolic acidosis, raising concern for BRASH syndrome. The treatment of each component of BRASH syndrome resulted in the resolution of the symptoms. The association of BRASH syndrome with amiodarone, the only AV nodal blocking agent in this particular case, is not commonly reported.

Chronicle of Hypoxemia: Transfusion-Associated Circulatory Overload Versus Transfusion-Related Acute Lung Injury.

The preeminent causes of blood transfusion-related morbidity and mortality are transfusion-associated circulatory overload (TACO) and transfusion-related acute lung injury (TRALI). These occur within hours of blood transfusion and lead to acute respiratory distress. The differentiation between TACO and TRALI has always been a great challenge in the context of underlying etiology, whether it is volume overload or lung injury, or both. This is a case report of a 64-year-old female with multiple comorbidities, who was brought to the emergency department with generalized weakness. She was hemodynamically unstable and encephalopathic. Her hemoglobin was 6.5 gm/dl with no active evidence of bleeding. She was started on a norepinephrine drip and one unit of packed red blood cells was transfused. A few hours post-transfusion, she became extremely tachypneic and hypoxic. A chest x-ray post-transfusion showed diffuse bilateral fluffy alveolar infiltrates and the N-terminal (NT)-pro hormone Brain Natriuretic Peptide (NT-proBNP) was significantly elevated. The transfusion reaction workup was negative. Due to worsening hypoxia, she required a rapid transition from non-invasive to invasive mechanical ventilation. The chronology of this case report depicts a unique presentation of acute respiratory distress and the course of hypoxemia.

Independent Predictors of Mortality in COVID-19 Myocardial Injury: The Role of Troponin Levels, GRACE Score, SOFA Score, and TIMI Score.

Background Coronavirus disease 2019 (COVID-19) infection is associated with troponin elevation, which is associated with increased mortality. However, it is not clear if troponin elevation is independently linked to increased mortality in COVID-19 patients. Although there is considerable literature on risk factors for mortality in COVID-19-associated myocardial injury, the Global Registry of Acute Coronary Events (GRACE), Thrombolysis in Myocardial Infarction (TIMI), and Sequential Organ Failure Assessment (SOFA) scores have not been studied in COVID-19-related myocardial injury. This data is important in risk-stratifying COVID-19 myocardial injury patients. Methodology Of the 1,500 COVID-19 patients admitted to our hospitals, 217 patients who had troponin levels measured were included. Key variables were collected manually, and univariate and multivariate cox regression analysis was done to determine the predictors of mortality in COVID-19-associated myocardial injury. The differences in clinical profiles and outcomes of COVID-19 patients with and without troponin elevation were compared. Results Mortality was 26.5% in the normal troponin group and 54.6% in the elevated troponin group. Patients with elevated troponins had increased frequency of hypotension (p = 0.01), oxygen support (p < 0.01), low absolute lymphocyte (p < 0.01), elevated blood urea nitrogen (p < 0.01), higher C-reactive protein (p < 0.01), higher D-dimer (p < 0.01), higher lactic acid (p < 0.01), and higher Quick SOFA (qSOFA), SOFA, TIMI, and GRACE (all scores p < 0.01). On univariate cox regression, troponin elevation (hazard ratio (HR) = 1.85, 95% confidence interval (CI) = 1.18-2.88, p < 0.01), TIMI score >3 (HRv = 1.79, 95% CI = 1.11-2.75, p = 0.01), and GRACE score >140 (HR = 2.27, 95% CI = 1.45-3.55, p < 0.01) were highly associated with mortality, whereas cardiovascular disease (HR = 1.40, 95% CI = 0.89-2.21, p = 0.129) and cardiovascular risk factors (HR = 1.15, 95% CI = 0.73-1.81, p = 0.52) were not. After adjusting for age, use of a non-rebreather or high-flow nasal cannula, hemoglobin <8.5 g/dL, suspected or confirmed source of infection, and qSOFA and SOFA scores (HR = 1.18, 95% CI = 1.07-1.29, p < 0.01) were independently associated with mortality, whereas troponin (HR = 1.08, 95% CI = 0.63-1.85, p = 0.76), TIMI score (HR = 1.02, 95% CI = 0.99-1.06, p = 0.12) and GRACE scores (HR = 1.01, 95% CI = 0.99-1.02, p = 0.10) were not associated with mortality. Conclusions Our study shows that troponin, GRACE score, and TIMI score are not independent predictors of mortality in COVID-19 myocardial injury. This may be because troponin elevation in COVID-19 patients may be related to demand ischemia rather than acute coronary syndrome-related. This was shown by the association of troponin with a higher degree of systemic inflammation and end-organ dysfunction. Therefore, we recommend SOFA scores in risk-stratifying COVID-19 patients with myocardial injury.

Transthoracic M-mode Echocardiography Demonstrating Cardiac Tamponade.

A 67-year-old man presented to the emergency department for two weeks of progressive shortness of breath with orthopnea and new-onset back pain. On admission, vital signs were normal, and physical exam was remarkable for jugular vein distention with the rest of the cardiovascular exam in normal limits. A bedside transthoracic echocardiogram showed a large circumferential pericardial effusion with M-mode analysis revealed diastolic collapse of the right ventricle (RV) and > 40% tricuspid inflow respiratory variation in Doppler. Emergency pericardiocentesis yielded 800 cm3 of yellow-colored fluid. Subsequently, the patient underwent lymph node biopsy showing tumor cells consistent with squamous cell carcinoma of unknown origin. This case highlights the use of bedside echocardiogram and M-mode imaging for the diagnosis of cardiac tamponade.

Platypnea-Orthodeoxia Syndrome: A Rare and Treatable Cause of Positional Dyspnea.

Platypnea-orthodeoxia means low oxygen saturation and dyspnea in the upright posture which improves on lying down. The causes can be classified into the intrapulmonary shunt, intracardiac shunt, and ventilation-perfusion mismatch. A 62-year-old male presented with shortness of breath, which had worsened over a period of one year. Various investigations were done to rule bacterial, viral infection, pulmonary embolism, and other respiratory and cardiac causes. The initial echocardiogram showed an ejection fraction of 55%. The patient was observed to be having dyspnea only in the upright position. In the recumbent position, the dyspnea disappeared with a marked improvement in oxygen saturation. A repeat echocardiogram with a bubble study was done which showed an atrial septal defect. Surgical closure of the defect was performed which improved the patient's oxygen saturation to baseline normal. This case demonstrates that a vigilant approach is required in cases of dyspnea, keeping in mind the not-so-common phenomenon like platypnea-orthodeoxia syndrome.

Disseminated adenovirus infection in heart and kidney transplant.

Presently described is a case of disseminated adenovirus infection in a heart-kidney transplant recipient that was successfully treated with cidofovir. There are several reports of adenovirus infections in adult solid organ transplant recipients and the prognosis is usually poor, with mortality rates of 40% to 60%. Severe disseminated adenovirus infections have been associated with increased risk of adverse transplant events, such as rejection, ventricular dysfunction, allograft vasculopathy, graft loss, and the need for re-transplantation. The patient's lack of clinical improvement, the onset of hemorrhagic cystitis and acute kidney injury were factors in our decision to temporarily discontinue administration of immunosuppressive agents and start an antiviral agent. It is important to suspect adenovirus in transplant patients when they do not respond to antibiotics and cultures are negative. Early diagnosis and treatment are critical to improving outcomes in immunocompromised patients.