Kidney Week

Abstract: SA-PO064

BRASH Syndrome: Familiar Yet Difficult to Manage, a Case Series

Session Information

• AKI: Clinical, Outcomes, and Trials - Management
  October 26, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Truong, Hong Hieu, Ascension Saint Francis, Evanston, Illinois, United States

Hong Hieu Truong, MD

• Adhikari, Pabitra, Ascension Saint Francis, Evanston, Illinois, United States

Pabitra Adhikari, MD

• Sorour, Laith S., Ascension Saint Francis, Evanston, Illinois, United States

Laith S. Sorour, MD

• Albanna, Muhammad, Ascension Saint Francis, Evanston, Illinois, United States

Muhammad Albanna, MD

• Gogia, Sopiko, Ascension Saint Francis, Evanston, Illinois, United States

Sopiko Gogia

• Vo, Le Y Nhi, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Ho Chi Minh, Viet Nam

Le Y Nhi Vo, MD

• Begiashvili, Valiko, Ascension Saint Francis, Evanston, Illinois, United States

Valiko Begiashvili, MD

Introduction

BRASH syndrome is characterized by the combined effects of AV nodal blockers and Renal dysfunction, leading to Hyperkalemia, severe Bradycardia, and Shock . Although the connection between these medications and renal failure has been known for years, managing the syndrome remains challenging.

Case Description

Case 1: A 78-year-old woman with atrial fibrillation and severe mitral valve stenosis (MVS) presented with fatigue. She was taking metoprolol, diltiazem. Upon arrival at the emergency department (ED), her heart rate (HR) of 50 beats per minute (bpm), blood pressure (BP) of 65/30 mmHg, and a potassium (K+) level of 8.3 mEq/L, and creatinine level of 5.17 mg/dl from a baseline of 1.23 mg/dl. She was given norepinephrine, home medications were stopped, and hyperkalemia treatment was initiated, resulting in lowering her K+ level to 4.8 mEq/L and an increase in HR to 77 bpm. Echocardiography later revealed pulmonary hypertension from MVS, which was identified as the underlying cause of her AKI. Kidney function gradually improved with furosemide within the context of cardiorenal syndrome stemming from MVS. Upon discharge, her creatinine level was 1.9 mg/dl

Case 2: An 84-year-old male with hypertension (HTN), chronic kidney disease (CKD), and benign prostatic hypertrophy (BPH) was on carvedilol. In the ED, his HR was 18 bpm, BP was 92/43 mmHg, K+ level was 8.1 mEq/L, and creatinine was 2.7 mg/dL (baseline 1.96 mg/dL). A bladder scan showed significant urinary retention. Foley catheter placement helped resolve the obstruction. He was also hypothermic, with rectal temperature of 90.9°F, and passive warming methods were employed. He received hyperkalemia treatment without response. Both pacing attempts and atropine administration were unsuccessful. IV dobutamine was also started for hypotension. His HR increased to 40 bpm. Immediate dialysis was performed for life-threatening hyperkalemia, reducing K+ level to 5.2 mEq/L. His HR improved slowly to 50 bpm. Cardiology was consulted and diagnosed BRASH syndrome on top of sick sinus syndrome

Discussion

BRASH syndrome affects patients with various levels of kidney function, from normal eGFR to ESRD on dialysis. It can involve multiple etiologies or just a single cause. Most patients improve with supportive care, but standard hyperkalemia and bradycardia treatment protocols should be followed.