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BRASH Syndrome

9/23/2023

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https://youtu.be/IBrU4LfuaYE

BRASH Syndrome

BRASH syndrome is a constellation of symptoms that includes bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock, and hyperkalemia.
The syndrome is caused by medication-induced AV nodal blockade, such as beta-blockers or calcium channel blockers, leading to bradycardia, poor tissue perfusion with decreased cardiac output, shock, renal failure, and subsequent hyperkalemia, which further exacerbates bradycardia.
In this lecture, we will discuss the pathophysiology, clinical features, and management of BRASH syndrome.

Pathophysiology:

Population at risk of developing BRASH syndrome are elderly patients with vulnerable renal function who are prone to volume depletion and, at the same time, taking AV nodal blocking agents such as beta-blockers.
BRASH syndrome is a vicious cycle in the setting of medications, hyperkalemia, and renal failure.
- Renal failure causes hyperkalemia.
- Hyperkalemia synergizes with AV node blockers to cause bradycardia and hypoperfusion.
- Hypoperfusion, in turn, causes worsening of the renal failure.
The inciting factor of BRASH syndrome is generally considered to be something that prompts acute kidney injury, often hypovolemia of some sort. Rather than AV nodal blocker overdose or severe hyperkalemia causing conduction problems, the combination of AV nodal blocker use and moderate hyperkalemia has a synergistic effect on cardiac conduction, causing further bradycardia that results in renal failure and shock.

Clinical Features:

Patients with BRASH syndrome may present with heterogeneous, nonspecific symptoms, including generalized weakness, dizziness, and syncope.
While it is commonly precipitated by beta-blockers or calcium channel blockers, other agents such as amiodarone, digoxin, and octreotide are also associated with the onset of the disease.

Management:

Treatment of BRASH syndrome is supportive, but most effective when the syndrome is promptly recognized and all symptoms and signs are simultaneously managed.
Physicians should be familiar with its existence in order to avoid diagnostic and treatment delay.
Clinicians should aim to treat hyperkalemia, bradycardia, hypovolemia, and renal hypoperfusion, simultaneously.
Shock is managed with intravenous fluid resuscitation.
Epinephrine infusion may be needed to treat severe bradycardia.
Hyperkalemia is managed with intravenous calcium, intracellular potassium-shifting medications, and loop diuretics.
Bradycardia is managed with intravenous calcium and epinephrine (or isoproterenol).
Cardiac pacing is rarely needed.
Renal failure is managed with intravenous rehydration. Severe cases of renal failure may require hemodialysis.

Pitfalls:

The most common error in managing BRASH syndrome is fixating on a single component of the syndrome, for example, hyperkalemia, and focusing solely on management of that problem, for example, emergent dialysis; meanwhile, other aspects of the syndrome are overlooked, for example, the patient might remain under-resuscitated, bradycardic, and malperfused.

Take Home Message:

In conclusion, BRASH syndrome is a relatively new clinical entity that includes bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia.
It is caused by medication-induced AV nodal blockade leading to bradycardia, shock, renal failure, and subsequent hyperkalemia, which further exacerbates bradycardia.
BRASH syndrome may present with heterogeneous, nonspecific symptoms, including generalized weakness, dizziness, and syncope, which could be easily misdiagnosed if clinicians are unaware of the association between AV nodal blocking agents and the possible consequences of bradycardia, renal injury, and shock.

Treatment is supportive, but most effective when the syndrome is recognized and all symptoms and signs are managed simultaneously.

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Euglycemic DKA Secondary to SGLT2 Inhibitors

9/20/2023

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https://youtu.be/6PJUfHHwPlw

Euglycemic DKA Secondary to SGLT2 Inhibitors

Euglycemic Diabetic Ketoacidosis (EDKA) is a serious, rare complication of diabetes occurring in both type 1 and type 2 diabetes.
It is characterized by euglycemia (blood glucose less than 250 mg/dL) despite severe metabolic acidosis (arterial pH less than 7.3, serum bicarbonate less than 18 mEq/L) and presence of ketones.
SGLT2 inhibitors, a class of newer oral antidiabetic medications (canagliflozin, dapagliflozin, empagliflozin, ertugliflozin), can directly lead to EDKA.
SGLT2 inhibitors can directly and indirectly stimulate glucagon secretion

Pathophysiology:

SGLT2 inhibitors are drugs used to treat type 2 diabetes by inhibiting glucose reabsorption in the proximal renal tubules, leading to urinary glucose excretion and a decrease in blood glucose levels.
The mechanism of EDKA with SGLT2 inhibitors involves the lowering of insulin production and an increase in glucagon secretion, which promotes a shift of glucose to fat metabolism and stimulates lipolysis and ketogenesis.
With SGLT2 inhibitor use, EDKA can easily be triggered by surgery, infection, trauma, major illness, reduced food intake, persistent vomiting, gastroparesis, dehydration, and reduced insulin dosages.
The U.S. Food and Drug Administration (FDA) issued a drug communication warning about the increased risk of euglycemic diabetic ketoacidosis with the use of sodium-glucose-cotransporter 2 inhibitors in May 2015.

Diagnosis:

DM patients taking SGLT2 inhibitor with malaise, weakness, dyspnea, nausea, vomiting, drowsiness, altered mental status, or general discomfort, should undergo DKA screening.
DKA screening tests include serum pH and blood or urine ketone testing.
Euglycemic DKA usually exhibits normoglycemia with finger stick glucose below 250 mg/dL.

Laboratory Evaluation of euglycemic DKA includes:

CBC, electrolytes, glucose, chloride, and osmolarity. Anion gap calculation is important for precise management.
BUN, creatinine, AST, and Bilirubin.
Arterial or venous blood gases.
Serum or urine ketones, and serum beta-hydroxybutyric acid. Note that, the urine ketone screening cannot detect beta-hydroxybutyrate.
Lactic acid.
Blood and/or urine cultures, if infection is suspected.
Chest radiograph, and ECG to exclude ACS.

Treatment:

Treatment for euglycemic DKA is similar to typical DKA.
SGLT2 inhibitor should be discontinued as soon as euglycemic DKA is diagnosed.
After volume expansion with crystalloid, the foundation of therapy is a combination of dextrose and insulin infusion until acidosis resolves.
Insulin infusion is crucial and should not be avoided because of normal glucose levels.
Ketosis does not resolve with IV hydration alone.
Sodium bicarbonate infusion is not indicated
Potassium should be carefully monitored as total body potassium will likely be depleted, and intravenous supplementation of potassium and other electrolytes may be needed.
Insulin should not be administered unless potassium is above 3 mEq per liter.
20 to 40 mEq per liter of KCl may be added if initial potassium is below 5 mEq per liter.
Check finger stick glucose every 1 hour and electrolytes every 4 hours at a minimum.
Patients may require ICU admission.
Treatment with intravenous fluid resuscitation and insulin should continue until the anion gap closes and acidosis has resolved.

Pitfalls:

Although SGLT2 inhibitors have been shown to have benefits on cardiovascular and kidney health, they are not recommended to be used in type 1 DM because of the high risk of euglycemic DKA.
Euglycemic DKA can occur in pregnant women even without the use of SGLT2 inhibitors.
Euglycemic DKA in pregnant women is associated with an increased maternal and fetal mortality risk if not promptly identified and treated.
Fetal mortality rate is estimated to be 10 to 35%.

Conclusion:

In conclusion, euglycemic DKA can occur in both type 1 and type 2 DM.
SGLT2 inhibitors can directly result in euglycemic DKA.
Early diagnosis and treatment can significantly improve morbidity and mortality.
Vigilant monitoring of capillary or urine ketones by patients can diagnose euglycemic DKA before it becomes severe.

Treatment includes a combination of dextrose and insulin infusion until acidosis resolves.
SGLT2 inhibitor should be discontinued as soon as euglycemic DKA is diagnosed.

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Neurogenic shock and Spinal Shock

9/20/2023

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https://youtu.be/ndvdK7ICgyE

Neurogenic shock and Spinal Shock

Neurogenic shock is a form of distributive shock resulting from the loss of sympathetic tone in the autonomic nervous system, often due to spinal cord injury above T6 or severe brain injury. This leads to hypotension, bradycardia, and vasodilation.
Spinal shock, on the other hand, is a transient state of areflexia and loss of sensorimotor function below the level of spinal cord injury. It is a physiological response immediately following a spinal cord injury, characterized by the absence of reflexes and muscle weakness. It may last from hours to weeks and can improve once the secondary injury, such as swelling, resolves.

The differences between neurogenic shock and spinal shock.

Neurogenic shock primarily involves a drop in blood pressure due to autonomic nervous system disruption, while spinal shock is characterized by a loss of reflexes and motor function.
Neurogenic shock is usually sustained, whereas spinal shock due to incomplete spinal cord injuries may be temporary and reversible.

The similarities between neurogenic shock and spinal shock.

Both neurogenic and spinal shocks are associated with spinal cord injuries.
They can cause a loss of function and sensation below the level of injury.

Summary

In summary, it is possible for a patient with a spinal cord injury above T6 to experience both neurogenic shock and spinal shock at the same time.

While neurogenic shock is characterized by hypotension, bradycardia, and temperature dysregulation, spinal shock is characterized by flaccid paralysis, loss of reflexes, and loss of bowel and bladder control.

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ACLS Pretest and Answers (Part 3)

9/10/2023

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https://youtu.be/6I_SiRS5cCs

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Pitfalls in Traumatic Cardiac Arrest

9/10/2023

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Pitfalls in the Management of Traumatic Cardiac Arrest

In this lecture, we will discuss 12 pitfalls in the management of traumatic cardiac arrest, a stressful resuscitation scenario that requires the coordinated skills of emergency medical personnel, surgeons, and intensivists.

Pitfall 1

PEA is the most common rhythm.
The most common cardiac rhythm in traumatic cardiac arrest is pulseless electrical activity (PEA). Unlike medical cardiac arrest, ventricular fibrillation is uncommon in traumatic cardiac arrest, and therefore, AED is less helpful in the management of traumatic cardiac arrest.

Pitfall 2

Inadequate treatment specific for trauma.
Despite differences in pathophysiology, traumatic cardiac arrest is frequently treated similarly to medical cardiac arrest, such as chest compressions, epinephrine, and fluids, which may not be effective for traumatic cardiac arrest.

Pitfall 3

Failure to identify reversible causes.
Reversible causes of cardiac arrest in trauma include bleeding, tension pneumothorax, cardiac tamponade, cervical cord injury, and intracranial hemorrhage, which must be promptly managed.

Pitfall 4

Chest compressions alone have no role in traumatic cardiac arrest.
Chest compressions could potentially worsen injuries or delay critical interventions to treat reversible causes.
Nevertheless, chest compressions are still recommended if there's a treatable underlying medical cause of arrest.

Pitfall 5

De-emphasize epinephrine use.
Epinephrine should be considered in traumatic cardiac arrest if there is an underlying medical condition.
Prioritizing epinephrine in traumatic cardiac arrest resuscitations may not be beneficial in cases of hypovolemia or obstructive shock

Pitfall 6

Intubation should not be delayed to address alternative reversible causes of arrest in traumatic cardiac arrest patients, especially those with head, neck, or facial injuries.

Pitfall 7

Resuscitative thoracotomy may be harmful.
While it can be life-saving in specific situations, the procedure is invasive, carries high risks, and may be considered futile in some cases.
Resuscitative thoracotomy should only be considered in specific, life-threatening situations, in order to relieve cardiac tamponade, repair cardiac injuries, control pulmonary bleeding, or repair aortic injuries.

Pitfall 8

Excessive crystalloids may be harmful.
It is important to use crystalloids judiciously and to consider the use of a massive transfusion protocol for patients with massive blood loss.
Massive transfusion protocols are designed to interrupt the lethal triad of acidosis, hypothermia, and coagulopathy that develops with massive transfusion.

Pitfall 9

Needle decompression may not be effective, perform finger thoracostomy instead.
Finger thoracostomy involves making an incision with a scalpel and penetrating directly into the thoracic cavity with forceps and a gloved finger to relieve the tension.
Bilateral finger thoracostomy is recommended in traumatic cardiac arrest.

Pitfall 10

Survivability based on POCUS.
A systematic review suggested that traumatic cardiac arrest patients without cardiac activity on point-of-care ultrasound (POCUS) have a negligible chance of survival.
However, this conclusion is limited by a small sample size.

Pitfall 11

Deciding when to continue resuscitation efforts in traumatic cardiac arrest cases is ethically challenging, considering the balance between potential survival and prolonged suffering.
Decision should be made on a case-by-case basis, considering the patient's clinical status, the reversible causes of arrest, the use of resources, and the patient's quality of life.

Pitfall 12

Resource allocation in mass casualty events.
Allocating resources to traumatic cardiac arrest patients in mass casualty events can be contentious, as it impacts the care of other injured individuals.

Take home message

Traumatic cardiac arrest is a complex and challenging medical scenario that demands careful consideration of its unique characteristics.
Healthcare providers must prioritize the management of reversible causes and be aware of the controversies surrounding traumatic cardiac arrest treatment.

As research continues, the healthcare community should adapt and evolve to improve outcomes for these critically injured patients.

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BRASH Syndrome

Euglycemic DKA Secondary to SGLT2 Inhibitors

Neurogenic shock and Spinal Shock

ACLS Pretest and Answers (Part 3)

Pitfalls in Traumatic Cardiac Arrest

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Twitter: @jackcfchong
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