BRASH syndrome with a complete heart block- a case report.

INTRODUCTION: BRASH syndrome (Bradycardia, Renal failure, Atrioventricular (AV) nodal blocking agent, Shock and Hyperkalemia) is a recently emerging diagnosis that describes the profound bradycardia seen in patients on AV nodal blockers who present with acute kidney injury (AKI) and hyperkalemia. CASE PRESENTATION: We present a case of a 68 years old female patient with past history of hypertension taking atenolol and Enalapril presented to emergency department with the complaint of loss of consciousness of 02 hours duration. She had 03 days history of fatigue, poor oral intake, decreased urine output, appetite loss, vertigo and global headache. Her vital signs were blood pressure of 60/40 mmHg, absent radial pulse and temperature of 36.4 °C. Her systemic examination was remarkable for dry buccal mucosa; apical heart rate was 22 beats per minute. Glasgow Coma Scale was 13/15. Her laboratory tests showed creatinine of 1.83 mg/dL, blood urea nitrogen of 89 mg/dL and potassium elevated to the level of 6.39 mEq/dL. ECG revealed complete heart block with a normal QT interval and T waves and no U waves with ventricular rate of 22 beats per minute. Her previous medications were discontinued and the patient was resuscitated with intravenous (IV) fluids. She was given 03 doses of 1 mg atropine every 5 minutes but there was no increment in heart rate. She was given 50% dextrose with 10 international units of regular insulin, 1 g of calcium gluconate and Intravenous perfusion of norepinephrine and dopamine. Subsequently, after 14 hours of ICU admission the patient had a cardiac arrest with asystole and resuscitation was attempted but she couldn't survive. CONCLUSION: BRASH syndrome is largely an under-recognized life threatening clinical diagnosis. Physicians should have high index of suspicion for BRASH when they encounter patients with bradycardia, hyperkalemia, and renal failure, as timely diagnosis is crucial in the management.

Pacemaker ECG with the Littmann sign.

Severe hyperkalemia may be concealed in the electrocardiogram (ECG). We present the case of a critically ill patient with severe bradycardia and the BRASH syndrome. In critically ill patients, double counting of the heart rate is frequently a marker of severe hyperkalemia (Littmann sign). In our case, hyperkalemic double counting only appeared in the ECG performed during percutaneous pacing. The Littmann sign helped with the early recognition of hyperkalemia and the BRASH syndrome.

Water quality effects of peat rewetting and leftover conifer brash, following peatland restoration and tree harvesting.

Harvesting of plantation conifers on peatlands is carried out as part of restoration and forestry operations. In particular, in the UK and Ireland, conifer plantations on drained ombrotrophic blanket and raised bogs are increasingly being removed (by harvesting), along with blocking of drainage ditches to help raise water tables to reinitiate and restore bog vegetation and function. However, both tree harvesting and peatland restoration operations can have significant impacts on water quality at local and catchment scales. Previous research has suggested that leaching from leftover decomposing brash (tree tops and branches, including wood and needles) is the primary cause, while other work has suggested that release from rewetted peat also contributes to water quality changes. This research investigates the relative importance of peat rewetting, needles and branches on water quality using mesocosm experiments, to help elucidate the mechanisms behind water quality changes following restoration and harvesting operations. Peat and brash were collected from a drained afforested blanket bog in the Flow Country, Scotland. Short-term mesocosm experiments were conducted by incubating peat, peat + needles and peat + needles + branches with rainwater in quadruplicate. Brash from Sitka spruce (Picea sitchensis) and lodgepole pine (Pinus contorta) was investigated separately, while we also conducted experiments with fresh and aged (∼18 months) brash. Peat, needles and branches all significantly impacted water quality in the order of branches > needles > peat, while concentrations of DOC, PO43-, NH4+, K and Mn were most impacted. Water quality impacts of spruce brash appeared generally greater than pine, while fresh brash had larger effects than aged brash. In our mesocosms, relative contributions to water quality changes were estimated by elemental yields. On average, peat contributed 25.4% (range 0.6-72.3%), while needles and brash contributed 19.7% (range 3.0-37.0%) and 54.9% (range 22.1-70.2%) to yields, respectively. We further estimate that 267 kg C ha-1 (255.8 kg as DOC, 10.7 kg as DIC), 27.4 kg K ha-1, 5.8 kg P ha-1 (as PO43-) and 0.5 kg N ha-1 (as NH4+) could be released from brash, over nine days.

Synthesis of 13R,20-dihydroxy-docosahexaenoic acid by site-directed mutagenesis of lipoxygenase derived from Oscillatoria nigro-viridis PCC 7112.

Lipoxygenases (LOXs) are implicated in the biosynthesis of pro- and anti-inflammatory lipid mediators involved in immune cell signaling, most of which catalyze peroxidation of polyunsaturated fatty acids by distinct regio- and stereoselectivity. Current reports suggested that conserved amino acid, Gly in R-LOXs and Ala in S-LOXs, in the catalytic domain play an important role in determining the position as well as the stereochemistry of the functional group. Recently, we have confirmed that the catalytic specificity of cyanobacterial lipoxygenase, named Osc-LOX, with alanine at 296 was 13S-type toward linoleic acid, and producing a 17S- hydroxy-docosahexaenoic acid from docosahexaenoic acid (DHA). Here, we aimed to change the catalytic property of LOX from13S-LOX to 9R-LOX by replacing Ala with Gly and to produce a lipid mediators different from the wild-type using DHA. Finally, we succeeded in generating human endogenous a 13R-hydroxy-docosahexaenoic acid and a 13R,20-dihydroxy-docosahexaenoic acid from DHA through an enzymatic reaction using the Osc-LOX-A296G. Our study could enable physiological studies and pharmaceutical research for the 13R,20-dihydroxy-docosahexaenoic acid.

Anaphylaxis induced bradycardia, renal failure, AV-nodal blockade, shock, and hyperkalemia: A-BRASH in the emergency department.

The emergency department (ED) is responsible for managing a variety of acute illnesses including undifferentiated shock. A newer less recognized syndrome termed BRASH - bradycardia, renal failure, AV-node blockers, shock and hyperkalemia - is a cycle of synergy between hyperkalemia and AV-blockade that can result in shock. This entity is more common amongst the elderly, considering polypharmacy and co-morbid diseases. Some cases have an inciting trigger of hypovolemia. Anaphylaxis is a potentially lethal form of shock that most emergency physicians (EP) treat in the ED. The two entities have never occurred simultaneously. Herein, we report a case of anaphylaxis induced BRASH syndrome occurring in an elderly diabetic man. The EP should be aware of this unique presentation of BRASH. It was concluded that the patient's anaphylaxis, caused hypovolemia, coupled with polypharmacy, and physiological stress, precipitated this severe form of shock and multi-organ system failure.

BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia.

BACKGROUND: BRASH syndrome, or Bradycardia, Renal Failure, AV blockade, Shock, and Hyperkalemia, has recently become recognized as a collection of objective findings in a specific clinical context pertaining to emergency medicine and critical care. However, there is little emergency medicine and critical care literature specifically evaluating this condition. OBJECTIVE: We sought to define and review BRASH syndrome and identify specific management techniques that differ from the syndromes as they present individually. DISCUSSION: BRASH syndrome is initiated by synergistic bradycardia due to the combination of hyperkalemia and medications that block the atrioventricular (AV) node. The most common precipitant is hypovolemia or medications promoting hyperkalemia or renal injury. Left untreated, this may result in deteriorating renal function, worsening hyperkalemia, and hemodynamic instability. Patients can present with a variety of symptoms ranging from asymptomatic bradycardia to multiorgan failure. BRASH syndrome should be differentiated from isolated hyperkalemia and overdose of AV-nodal blocking medications. Treatment includes fluid resuscitation, hyperkalemia therapies (intravenous calcium, insulin/glucose, beta agonists, diuresis), management of bradycardia (which may necessitate epinephrine infusion), and more advanced therapies if needed (lipid emulsion, glucagon, or high-dose insulin infusion). Understanding and recognizing the pathophysiology of BRASH syndrome as a distinct entity may improve patient outcomes. CONCLUSIONS: BRASH syndrome can be a difficult diagnosis and is due to a combination of hyperkalemia and medications that block the AV node. Knowledge of this condition may assist emergency and critical care providers.

John Goodsir: discovering Sarcina ventriculi and diagnosing Darwin's dyspepsia.

In 1842, when John Goodsir was Conservator to the Museum of the RCSEd, he saw a 19-year-old male patient who vomited a large volume of acidic, fermented-smelling, watery fluid every morning. Under his microscope, Goodsir found the vomitus to be populated with a micro-organism he named Sarcina ventriculi, which he considered to be causative. In so-doing, Goodsir became one of the first people to link a specific micro-organism with a disease. Goodsir recommended small doses of creosote as an antiseptic and claimed that the boy was eventually cured of the vomiting condition. In August of 1863 Charles Darwin was hugely celebrated by the scientific community and the public, but he had suffered from severe stomach problems all his adult life and at this point, he was vomiting daily. He read Goodsir's paper and contacted him and asked if he could send some vomitus samples to Edinburgh in the hope that Goodsir might find Sarcina in it and solve the mystery of his debilitating stomach symptoms and perhaps cure them with creosote. Goodsir examined samples in his microscope, but failed to find Sarcina. Sadly, Darwin went on to suffer constantly from severe stomach problems, recently attributed to lactose intolerance, until he died in 1882, some 20 years later.

Not only Van Gogh: a case of BRASH syndrome with concomitant digoxin toxicity.

BACKGROUND: Bradycardia, renal failure, atrioventricular (AV) node blocking, shock, and hyperkalemia syndrome is a potentially life-threatening clinical condition characterized by bradycardia, renal failure, atrioventricular (AV) node blocking, shock, and hyperkalemia. It constitutes a vicious circle in which the accumulation of pharmacologically active compounds and hyperkalemia lead to hemodynamic instability and heart failure. CASE PRESENTATION: A 66-year-old Caucasian female patient was admitted to the emergency department presenting with fatigue and bradycardia. Upon examination, the patient was found to be anuric and hypotensive. Laboratory investigations revealed metabolic acidosis and hyperkalemia. Clinical evaluation suggested signs of digoxin toxicity, with serum digoxin concentrations persistently elevated over several days. Despite the implementation of antikalemic measures, the patient's condition remained refractory, necessitating renal dialysis and administration of digoxin immune fab. CONCLUSION: Bradycardia, renal failure, atrioventricular (AV) node blocking, shock, and hyperkalemia syndrome is a life-threatening condition that requires prompt management. It is important to also consider potential coexisting clinical manifestations indicative of intoxication from other pharmacological agents. Specifically, symptoms associated with the accumulation of drugs eliminated via the kidneys, such as digoxin. These manifestations may warrant targeted therapeutic measures.

Unexpected Presentations of Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia (BRASH) Syndrome: A Report of Two Cases.

Bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia syndrome is an underrecognized phenomenon in which renal injury leads to hyperkalemia and inadequate clearance of atrioventricular nodal-blocking agents. The compounding effect of both insults can lead to a bradyarrhythmia that, in severe cases, can rapidly progress to cardiogenic shock. The degree of resulting pathology is usually out of proportion to either insulting agent given that there is a synergistic effect. Treatment strategies for this condition are not entirely clear, but it appears as if these patients often do not warrant aggressive interventions and can be managed medically. We report two cases with early recognition and simple medical management with resulting favorable outcomes.

A Case of BRASH (Bradycardia, Renal Dysfunction, Atrioventricular Node Blockade, Shock, and Hyperkalemia) Syndrome Following Initiation of a Sodium-Glucose Cotransporter-2 (SGLT-2) Inhibitor and a Loop Diuretic.

BRASH (bradycardia, renal dysfunction, atrioventricular node blockade, shock, and hyperkalemia) syndrome is a recently recognized clinical process that can be fatal if not adequately and promptly treated. As such, it is important for clinicians to recognize the syndrome. This case demonstrates an example of BRASH syndrome in a 73-year-old patient with heart failure occurring after initiation of dapagliflozin, a drug not previously associated with this phenomenon in the literature. Given the increasingly appreciated clinical utility of sodium-glucose cotransporter-2 (SGLT-2) inhibitors, prescribers must respect their potential side effects in patients with underlying comorbidities and remember the importance of re-evaluating renal function after initiation of these medications. Here, we review the pathophysiology of BRASH, the renal effects of SGLT-2 inhibitors, and the importance of educating patients on volume management and diuretic dose titration at home.

BRASH (Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia) Syndrome: A Frequently Underrecognized Condition Often Confused With Simple Hyperkalemia.

BRASH syndrome, defined by bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia, is a relatively new and often underrecognized condition. In this article, we present a case of an elderly female who developed an episode of syncope. She was found to have refractory shock and bradycardia in the emergency department. Laboratory results and other findings led to the diagnosis of a BRASH syndrome, which was refractory to medical therapy alone, requiring transvenous pacing, hemodialysis, and vasopressor support.

Bradycardia, Renal Failure, Atrioventricular Nodal Block, Shock, and Hyperkalemia (BRASH) Syndrome-Induced Atrial Fibrillation: A Case Report.

BRASH syndrome is a syndrome that comprises bradycardia, renal failure, atrioventricular nodal block, shock, and hyperkalemia. This syndrome is usually associated with a junctional rhythm. Early recognition of this clinical entity is crucial for appropriate management. In this case report, we describe a 70-year-old female who presented with BRASH syndrome-induced atrial fibrillation with a slow ventricular response.

Bradycardia, Renal Failure, Atrioventricular Block, Shock, and Hyperkalemia (BRASH) Syndrome Emergence in a Unique Intersection of COVID-19 and End-Stage Renal Disease: A Case Report.

Bradycardia, renal failure, atrioventricular (AV) block, shock, and hyperkalemia (BRASH) syndrome is a rare clinical entity that poses challenges for healthcare practitioners. It is characterized by bradycardia, renal failure, atrioventricular (AV) obstruction, shock, and hyperkalemia. This case is an interesting instance of BRASH syndrome in the setting of COVID-19 infection and end-stage renal disease (ESRD). Initial laboratory results revealed macrocytic anemia, renal dysfunction, acidosis, and mild hyponatremia, along with hyperkalemia. An electrocardiogram (EKG) and telemonitoring showed dopamine-resistant persistent bradycardia until transvenous temporary pacemaker placement was done, which resolved the bradycardia. Anti-hyperkalemic therapy, avoiding AV nodal-blocking medication, and temporary pacemaker placement were all part of the management. After receiving hemodialysis, the patient gradually recovered. Bradycardia improved and potassium normalized. The intricate interaction between hyperkalemia and AV nodal obstruction that causes BRASH syndrome results in severe bradycardia and shock. To the best of our knowledge, this is the first case of BRASH syndrome in a patient with an active COVID-19 infection in a previously vaccinated patient. Even though case reports make up the majority of the material currently in publication, to fully comprehend the mechanisms underlying this illness, more research is required, as early detection of this syndrome is crucial for better patient outcomes.

Rare presentation of BRASH syndrome with hypoglycemia and altered mental status.

BACKGROUND: BRASH syndrome (bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia) is a rare clinical condition with potentially severe outcomes. Patients with BRASH syndrome can present with diverse signs and symptoms and are usually in critical condition, but if recognized early, the syndrome is treatable and may have a favorable prognosis. CASE PRESENTATION: This case study presents a 74-year-old patient with a history of multiple chronic conditions who was brought to the emergency department with a suspected cerebrovascular accident, altered mental status, and bradycardia. A head computed tomography scan was unremarkable but laboratory results showed hyperkalemia, acidosis, and renal failure with concomitant progressive hypoglycemia. The patient was diagnosed with a BRASH syndrome characterized by a vicious cycle of atrioventricular nodal blockade induced by the potentiated effect of beta-blockers or calcium channel blockers, in combination with progressive hypoglycemia due to the suspected accumulation of anti-diabetic medications, which influenced the presentation and initial triage in the emergency department. She was admitted to the intensive care unit for further management, where she continued to improve and was ultimately discharged in a relatively stable condition. CONCLUSION: This case study highlights the importance of considering rare and atypical presentations of medical conditions, particularly in elderly patients who may have multiple comorbidities. Early recognition and prompt management of such cases are crucial for improving patient outcomes.

Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock and Hyperkalemia (BRASH) Syndrome: A Clinical Case Study.

BRASH syndrome, which stands for Bradycardia, Renal failure, Atrioventricular (AV) Nodal blockade, and shock, is a relatively new clinical condition. Bradycardia develops because of the synergistic effect of AV-nodal blockers and hyperkalemia in a renal failure resulting in a vicious cycle of progressive bradycardia, renal hypoperfusion, and hyperkalemia. We present a case of an 88-year-old man with chronic systolic heart failure, atrial fibrillation, stage 3 chronic kidney disease, and dementia who presented to our emergency department with poor oral intake and weakness. He was found to have symptomatic bradycardia in the 30s secondary to hyperkalemia and beta-blockers in the setting of acute renal failure from dehydration, raising concern for BRASH syndrome. Treatment of each component conservatively resulted in complete resolution without the need for aggressive measures such as dialysis or pacing. This case report also discusses the pathophysiology, management, and the need for recognizing this underdiagnosed and novel clinical condition.

Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia (BRASH) Syndrome: A Rising Entity of Severe Bradycardia.

Bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia (BRASH) syndrome is an entity recently coined to describe this clinical pentad. Although the condition is rare, early recognition is paramount. It ensures prompt appropriate intervention is administered, as conventional management for bradycardia as guided by advanced cardiac life support (ACLS) is ineffective in the BRASH syndrome. Here, we describe a case of an elderly lady with hypertension and chronic kidney disease presenting to the emergency department with dyspnoea and confusion. She was found to have bradycardia, hyperkalemia, and acute kidney injury. Notably, she had recent changes in her medications in view of poorly controlled hypertension two days before the presentation. Her Bisoprolol 5mg every morning was changed to Carvedilol 12.5mg twice daily, and Amlodipine 10mg every morning was changed to Nifedipine long-acting 60mg twice daily. Initial treatment with atropine for bradycardia was ineffective. However, when the BRASH syndrome was identified and treated, the patient's condition improved, and she averted complications such as multiorgan failure without the need for dialysis or cardiac pacing. Early detection of bradycardia via smart devices could be considered in patients at higher risk of BRASH syndrome.

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.

A Case of Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalaemia (BRASH) Syndrome in an Elderly Male and Its Management: A Case Report and Literature Review.

BRASH syndrome, characterized by bradycardia, renal dysfunction, atrioventricular (AV) nodal blockage, shock, and hyperkalemia, is a rare but potentially life-threatening condition resulting from the interplay between AV nodal blockers and hyperkalemia. This complex syndrome poses significant challenges in diagnosis and management, with patients often presenting with bradycardia and high potassium levels. This case report highlights the need for increased awareness of BRASH syndrome, especially in an aging population and evolving cardiovascular treatments. Early recognition and a comprehensive, multidisciplinary approach are crucial for improving outcomes in affected patients.

A Case Report on Uremic Toxins and Their Effects on Cardiac Rhythm: Understanding Junctional Ventricular Escape Rhythm in Renal Failure.

Understanding the reasons behind junctional ventricular escape rhythm is crucial for guiding the clinical management of patients. Various factors such as acidosis, hyperkalemia, metabolic toxins, digoxin toxicity, and BRASH syndrome (comprising bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock, and hyperkalemia) should be considered when dealing with a symptomatic unstable patient in a hospital. In this case, we present an example where metabolic toxins, specifically uremia, in combination with other factors, lead the patient to enter a ventricular escape rhythm, ultimately resulting in cardiogenic shock. The main objective of this case study is to illustrate how uremic metabolic acidosis contributes to AV nodal blockade, leading to a junctional ventricular escape rhythm within the context of BRASH.

Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock and Hyperkalaemia Syndrome Involving Digoxin Toxicity: A Case Report.

Bradycardia, renal failure, atrioventricular nodal blockade, shock and hyperkalemia (BRASH) syndrome is named after the pentad of symptoms experienced by patients with this clinical entity, and is propagated via a synergistic mechanism. Herein, we describe a case of an 81-year-old male who presented with bradycardia, dyspnoea on exertion, and confusion. He was also initially found to be in cardiogenic shock. In a setting of elevated digoxin levels, acute renal failure and hyperkalemia, he was diagnosed with BRASH syndrome. Prompt interventions of continuous renal replacement therapy and digoxin antibody administration were performed to treat this patient. His renal function improved and his hyperkalemia and bradycardia resolved over the course of 4 days, and the patient was discharged to a subacute rehabilitation facility after stabilization. BRASH syndrome is a clinical entity requiring prompt diagnosis for life-saving treatment, including renal replacement therapy, vasoactive medications, transvenous pacing, and reversing agents, when appropriate.