CASE REPORT


https://doi.org/10.5005/jp-journals-11006-0055
Indian Journal of Critical Care Case Report
Volume 2 | Issue 3 | Year 2023

Gastroenteritis-triggered BRASH Syndrome in a Patient with Chronic Kidney Disease: A Case Report


Amit Goel1https://orcid.org/0000-0002-9509-5705, Upendra Singh2https://orcid.org/0009-0006-9583-2732, Eshaan Patel3https://orcid.org/0009-0009-9686-130X, Mohd Javed4https://orcid.org/0009-0000-5795-1171

1,3,4Department of Critical Care Medicine, Yatharth Super Speciality Hospital, Greater Noida West, Uttar Pradesh, India

2Department of Nephrology, Yatharth Super Speciality Hospital, Greater Noida West, Uttar Pradesh, India

Corresponding Author: Amit Goel, Department of Critical Care Medicine, Yatharth Super Speciality Hospital, Greater Noida West, Uttar Pradesh, India, Phone: +91 9999849981, e-mail: amgoel3@gmail.com

Received on: 23 March 2023; Accepted on: 09 May 2023; Published on: 23 June 2023

ABSTRACT

Introduction: Patients with chronic kidney disease (CKD) are on regular renal support. However, coexisting comorbidities, ongoing treatment and drug interactions requires exploration of other associated conditions which could prove life-threatening.

Case description: We present here the management of a CKD patient on atrioventricular (AV) node-blocking medications with acute gastroenteritis presenting in shock, refractory bradycardia, and severe hyperkalemia.

Conclusion: Bradycardia, renal failure, AV nodal blocking drugs, shock, and hyperkalemia (BRASH) syndrome is broadly reported in a group of CKD patients receiving long-term AV node blockers. Hypovolemia, renal hypoperfusion, and deranged renal parameters are major risk factors. Largely high morbidity and mortality are associated with BRASH syndrome. However, prompt diagnosis and management can lead to an overall better patient outcome.

How to cite this article: Goel A, Singh U, Patel E, et al. Gastroenteritis-triggered BRASH Syndrome in a Patient with Chronic Kidney Disease: A Case Report. Indian J Crit Care Case Rep 2023;2(3):72-74.

Source of support: Nil

Conflict of interest: None

Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.

Keywords: Acute gastroenteritis, Bradycardia, Bradycardia, renal failure, AV nodal blocking drugs, shock, and hyperkalemia syndrome, Chronic kidney disease, Hyperkalemia.

INTRODUCTION

Here, we present an elderly man with CKD on antihypertensive medications presenting with BRASH syndrome. He made an uneventful recovery with prompt medical management.

CASE DESCRIPTION

A 59-year-old, previously known hypertensive, and stage 4 CKD (not on dialysis) male presented to the hospital with restlessness, uneasiness, mild to moderate grade fever, and multiple episodes of loose motions for 1–2 days. A history of toothache, hiccups, and decreased appetite were also noted. He was on β-blocker (bisoprolol—2.5 mg once a day), calcium channel blockers (CCBs) (amlodipine 5 mg once a day), oral nonsteroidal anti-inflammatory drugs (NSAID), and oral antibiotics for his medical condition. On arrival, he was drowsy yet arousable (Glasgow Coma Scale—12–13), restless, and required 2 L supplemental oxygen to maintain normal oxygen saturations. He had severe bradycardia heart rate—32–36/minute with hypotension blood pressure—80/50 mm Hg. Immediately intravenous (IV) line was secured, and 1 mg adrenaline and 0.6 mg atropine IV bolus were given. Followed by stat 1 L IV normal saline fluid. Vasopressor noradrenaline was started in view of hypotension. Arterial blood gas (ABG) was suggestive of severe metabolic acidosis (pH—7.16, bicarb—12) with hyperkalemia (5.8 mEq/L). The serum potassium level was 6.1 mEq/L. Electrocardiogram (ECG) was suggestive of sinus bradycardia with tented T-waves (Fig. 1). Immediately, antihyperkalemic measures were initiated with a 20 mL injection of calcium gluconate and 100 mL sodium bicarbonate. Salbutamol nebulization for 20–30 minutes and 50% dextrose 100 mL with 20 units of insulin was also initiated. Over the next 1 hour, his heart rate started to improve to 55–60/minute and repeat ABG was suggestive of improvement in acidosis and hyperkalemia. His basic lab investigations were sent, and with ongoing noradrenaline, and antihyperkalemic measures, he was shifted to the intensive care unit for further stabilization.

Fig. 1: Electrocardiogram (ECG)

One session of hemodialysis was done in view of azotemia (blood urea—193 mg/dL, serum creatinine—9.7 mg/dL) and persistent hyperkalemia. He improved hemodynamically and started accepting orally well with no loose motions over the next 2 days. He was shifted to step down care unit after a thorough cardiac evaluation. Later, on day 5, he was discharged in stable condition with necessary instructions for care and follow-up.

DISCUSSION

Bradycardia, renal failure, AV nodal blocking drugs, shock, and hyperkalemia (BRASH) syndrome represents a vicious cycle involving bradycardia, renal failure, AV nodal block, shock, and hyperkalemia. It is frequently observed in the elderly with underlying comorbidities, such as CKD, coronary artery disease, and hypertension. This term was first used and reported by Farkas et al. in 2016.1 However it was underreported earlier, but it has been widely recognized and published in the last couple of years.2-8 Most observed contributing factors leading to the development of BRASH syndrome are old age, kidney dysfunction, the requirement of AV node blocking agents, hypovolemia, and renal hypoperfusion.2 The proposed mechanism in BRASH syndrome is the synergistic effect of AV-nodal blocking agents and hyperkalemia causing refractory bradycardia and hypotension.1 This leads to renal hypoperfusion and further deranged renal function leading to hyperkalemia and reduced drug elimination, initiating a vicious cycle.

Ongoing AV nodal-blocking medications put these groups of patients at very high risk of persistent life-threatening bradycardia, even with moderate hyperkalemia.1-3 β-blockers and CCBs are the most frequently incriminated medications in this category for BRASH syndrome.4,5 Other triggering agents are angiotensin-converting enzyme inhibitors, potassium-sparing diuretics, and nephrotoxic drugs like aminoglycoside antibiotics and NSAIDs.1,8 Combination of one or more of these precipitating factors may be present, as in our case-AV-nodal blocking agents, NSAIDs, sepsis, and hypovolemia (loose motion).

The clinical presentation is variable, ranging from asymptomatic bradycardia, cardiogenic shock, multisystem organ failure, and even death in some cases.2,8 Eliciting thorough history and a strong clinical suspicion is required to diagnose BRASH syndrome, especially in patients with renal dysfunction presenting with bradycardia, with ongoing AV-nodal blocking agents.2,6 ECG may show a constellation of findings varying from normal pattern to sinus bradycardia to arrhythmias due to AV node block.3,6-8 Junctional rhythm present occasionally can prove life-threatening.

Management of BRASH syndrome includes early recognition and rectification of underlying triggering factors. Standard management as per advanced cardiac life support, including atropine and cardiac pacing, would not be sufficient for bradycardia.2,3 Prompt measures should be taken to break the vicious cycle of bradycardia, decreased cardiac output, renal hypoperfusion, and hyperkalemia. However, IV fluid and vasopressors should be started aggressively; they have been shown to respond better to agents with positive chronotropic effects on β-1 receptors viz isoproterenol, adrenaline, dopamine, and dobutamine. Isoproterenol has rather shown to have a favorable outcome in these scenarios.2 Antihyperkalemic measures must be started immediately for the management of hyperkalemia—(1) IV calcium for cardiac membrane stabilization; (2) IV insulin with glucose and continuous nebulization with β 2 agonist for intracellular potassium shifting; (3) IV sodium bicarbonate, if severe metabolic acidosis is present; (4) kaliuresis with loop diuretics-furosemide should be tried once hypovolemia is corrected; (5) calcium polystyrene sulfonate powder (potassium-binding resin) may be tried enterally once the airway is secured; (6) urgent dialysis in refractory cases.8

Cases with refractory AV nodal blockade due to β-blocker may need to be treated specifically with high-dose insulin euglycemic therapy or IV glucagon. Intralipid emulsion-lipid sink and extracorporeal therapies may also be tried as rescue measures.3,8

CONCLUSION

History, thorough clinical examination, strong clinical suspicion, and prompt treatment is the key to the management of BRASH syndrome. AV nodal-blocking drugs should be avoided in patients having renal dysfunction. This may unfold life-threatening refractory bradycardia and shock with moderate hyperkalemia. A clear understanding and recognition of the pathophysiology of BRASH syndrome can facilitate a more comprehensive and organized management strategy for these patients and a better outcome.

ORCID

Amit Goel https://orcid.org/0000-0002-9509-5705

Upendra Singh https://orcid.org/0009-0006-9583-2732

Eshaan Patel https://orcid.org/0009-0009-9686-130X

Mohd Javed https://orcid.org/0009-0000-5795-1171

REFERENCES

1. Farkas J. Pulm Crit–BRASH Syndrome: Bradycardia, Renal Failure, Av Blocker, Shock, Hyperkalemia. Available from: https://emcrit.org/pulmcrit/brash-syndrome-bradycardia-renal-failure-av-blockershock-hyperkalemia/. Last assessed on 22 Mar 2023.

2. Farkas JD, Long B, Koyfman A, et al. BRASH Syndrome: bradycardia, renal failure, AV blockade, shock, and hyperkalemia. J Emerg Med 2020;59(2):216–223. DOI: 10.1016/j.jemermed.2020.05.001

3. Pata R, Lutaya I, Mefford M, et al. Urinary tract infection causing bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia (BRASH) syndrome: a case report and a brief review of the literature. Cureus 2022;14(8):e27641. DOI: 10.7759/cureus.27641

4. Bailuni Neto JJ, Siqueira BL, Machado FC, et al. BRASH syndrome: a case report. Am J Case Rep 2022;23:e934600. DOI: 10.12659/AJCR.934600

5. Grigorov MV, Belur AD, Otero D, et al. The BRASH syndrome, a synergistic arrhythmia phenomenon. Proc (Bayl Univ Med Cent) 2020;33(4):668–670. DOI: 10.1080/08998280.2020.1784637

6. Shah P, Silangruz K, Lee E, et al. Two cases of BRASH syndrome: a diagnostic challenge. Eur J Case Rep Intern Med 2022;9(4):003314. DOI: 10.12890/2022_003314

7. Khan A, Lahmar A, Ehtesham M, et al. Bradycardia, renal failure, atrioventricular-nodal blockade, shock, and hyperkalemia syndrome: a case report. Cureus 2022;14(3):e23486. DOI: 10.7759/cureus.23486

8. Singh O, Juneja D, Goel A. Life-threatening complication in a patient with chronic kidney disease: BRASH syndrome. Indian J Crit CareCase Rep 2022;1(3):70–72. DOI: 10.5005/jp-journals-11006-0023

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