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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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https://youtu.be/ReGHxASrwo8

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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ACLS for Cardiac Arrest in Pregnancy

9/7/2023

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https://youtu.be/WRiChBdfGc8

ACLS for In-Hospital Cardiac Arrest in Pregnancy

IHCA in pregnancy

In-Hospital Cardiac Arrest (IHCA) in pregnancy is a medical emergency that affects both the mother and the fetus.
The management of these patients requires a rapid and coordinated response from a multidisciplinary team of healthcare professionals, including obstetricians, anesthesiologists, cardiologists, neonatologists, and cardiothoracic surgeons.
The basic and advanced cardiac life support (BLS and ACLS) algorithms should be implemented as usual.
However, the physiologic and anatomic changes of pregnancy require some modifications to these protocols.
Randomized trials of approaches to the management of pregnant patients with IHCA are lacking.
Therefore, recommendations for modifications to BLS and ACLS protocols are based on expert opinion and data from small case series and small cohort studies.

ACLS algorithm for IHCA in pregnancy

The ACLS algorithm for IHCA in pregnancy includes the following steps:
Perform BLS and ACLS as would occur in any adult patient.
Chest compression and ventilation recommendations for the pregnant patient are the same as nonpregnant patients.
The mother should be placed supine for chest compressions.
Manual left uterine displacement (LUD) should be used to relieve aortocaval compression during resuscitation.
The energy required for defibrillation during cardiac arrest in pregnancy would be the same as for the nonpregnant patient.
If magnesium is being administered, stop it, and provide calcium gluconate or calcium chloride.
Fetal assessment should not be performed during resuscitation.
Fetal monitors should be removed or detached as soon as possible to facilitate perimortem Cesarean delivery (PMCD) without delay or hindrance.
If ROSC (return of spontaneous circulation) occurs, move to post-cardiac arrest care.
Pregnant women who remain comatose after resuscitation from cardiac arrest should receive targeted temperature management and fetal heart rate monitoring with OB/GYN support.
If ROSC does not occur within 5 minutes, consider perimortem Cesarean delivery.
The neonate should be evaluated for neonatal resuscitation.

Advanced Airway for IHCA in pregnancy

In pregnancy, a difficult airway is common.
Use the most experienced provider.
Provide endotracheal intubation or supraglottic advanced airway.
Perform waveform capnography or capnometry to confirm and monitor endotracheal tube placement.
Once an advanced airway is in place, give 1 breath every 6 seconds (10 breaths per minute) with continuous chest compressions.

Potential Etiology of Maternal Cardiac Arrest

A: Anesthetic complications
B: Bleeding
C: Cardiovascular
D: Drugs
E: Embolic
F: Fever (infections)
G: General nonobstetric causes of cardiac arrest (H's and T's)
H: Hypertension

Perimortem Cesarean Delivery (PMCD)

PMCD is a surgical delivery of a fetus from a mother in cardiac arrest.
It is performed when the mother has not responded to CPR after 4 minutes.
The goal of PMCD is to increase the chances of survival for both the mother and the fetus.
PMCD is recommended for fetuses at least 20 weeks gestation.
The decision to perform PMCD is made on a case-by-case basis, considering the fetus’ gestational age, the mother's medical condition, and the availability of resources, and skill of the medical team.
PMCD should be performed as quickly as possible.
Maternal and fetal survival rates following PMCD vary greatly based on multiple factors.

Take Home Message

In conclusion, in-hospital cardiac arrest in pregnancy requires a specialized approach to resuscitation.
The primary focus is on resuscitating the mother, and fetal monitoring should not be used during the resuscitation.
Oxygenation and airway management is crucial in the resuscitation of a pregnant woman.
Amiodarone should be avoided due to the risk of fetal thyroid and neurodevelopmental complications.

Perimortem Cesarean delivery should be considered if ROSC does not occur within 5 minutes.

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Hypermagnesemia

9/6/2023

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https://youtu.be/_OXM26wVgFU

Hypermagnesemia

Hypermagnesemia is a serum magnesium concentration greater than 2.6 mg/dL.
Causes of hypermagnesemia include: renal failure, increased magnesium intake such as laxatives and antacids, treatment of eclampsia with intravenous MgSO4, and lithium-based psychotropic drugs which can reduce magnesium excretion.

Clinical presentations

Clinical presentations of hypermagnesemia include: lethargy, drowsiness, hypotension, nausea, vomiting, facial flushing, urinary retention, ileus, loss of DTRs, respiratory depression, respiratory arrest, oliguria, shortness of breath, and cardiac arrest (> 15 mg/dL).
At serum magnesium concentrations greater than 6 mg/dL, the ECG shows prolongation of the PR interval, widening of the QRS complex, increased T-wave amplitude, and irregular conduction.

Treatment

The withdrawal of the magnesium infusion is usually sufficient to treat most cases of hypermagnesemia when the patient has normal renal function.
Hydration should be initiated with saline diuresis and furosemide.
Administration of intravenous furosemide can increase magnesium excretion when volume status and renal function are adequate.
In patients who have severe complications, calcium gluconate or calcium chloride can be used to treat hypermagnesemia.
These medications work by increasing the levels of calcium in the blood, which can help counteract the muscle and heart effects of excess magnesium.
Patients who have ARF or ESRD may require hemodialysis. Peritoneal dialysis can also be used to effectively remove magnesium in patients who cannot tolerate hemodialysis.

Take Home Message

In conclusion, hypermagnesemia is a serum magnesium > 2.6 mg/dL.
The major cause is renal failure.
Symptoms include hypotension, respiratory depression, and cardiac arrest.
Diagnosis is by measurement of serum magnesium concentration.
Treatment includes intravenous calcium gluconate and possibly furosemide.

Hemodialysis can be helpful in severe cases.

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Inspirational Medical Quotes

9/6/2023

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https://youtu.be/erMuI-UIUdg

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Dengue Fever and Tourniquet Test

9/3/2023

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https://youtu.be/zqQgUNVD-w8

Dengue fever and tourniquet test

Dengue fever is a mosquito-borne viral disease that is widespread in tropical and subtropical regions.
The World Health Organization has outlined diagnostic criteria for making the diagnosis of dengue infection, which includes the use of the tourniquet test.
The tourniquet test is a marker of capillary fragility and it can be used as a triage tool to support diagnostic decision-making during the initial febrile phase which may last 2 to 7 days after the development of fever.

Symptoms and signs of dengue fever

Dengue fever follows a distinct pattern with three phases: febrile phase, critical phase, and convalescent or recovery phase.
During the febrile phase, there is an abrupt onset of fever for 2 to 5 days, along with other symptoms such as headache, muscle, bone, and joint pain, nausea, vomiting, pain behind the eyes, swollen glands, and rash. The fever pattern is classically biphasic or "saddleback", breaking and then returning for 1 or 2 more days.
The critical phase usually occurs around the time the fever subsides and lasts for 1 to 2 days. During this phase, there is a risk of developing severe dengue, which can cause serious bleeding, a sudden drop in blood pressure, shock, and death.
The convalescent or recovery phase begins after the critical phase and can last for several days to weeks. During this phase, the symptoms gradually improve, and the patient recovers.

Tourniquet test

The tourniquet test, also known as the Rumpel-Leede or Hess test, is a simple diagnostic tool that can be used to assess capillary fragility.
The test involves inflating a blood pressure cuff on the upper arm to a pressure midway between the systolic and diastolic blood pressure for five minutes. After five minutes, the cuff is deflated and the number of petechiae in a 2.5 cm x 2.5 cm area on the forearm is counted.
A positive tourniquet test is defined as the presence of 10 or more petechiae per 2.5 cm x 2.5 cm area.

Diagnostic accuracy of the tourniquet test

A systematic review and meta-analysis of diagnostic test accuracy found that the tourniquet test has poor diagnostic performance, with a pooled sensitivity and specificity of 58% and 71%, respectively. However, the tourniquet test is still widely used in resource-poor settings despite currently available evidence demonstrating only a marginal benefit in making a diagnosis of dengue infection alone.

Summary

The tourniquet test is a simple and inexpensive diagnostic tool that can be used to support diagnostic decision-making during the initial, acute, febrile phase of dengue infection.
However, the test has poor diagnostic performance and should not be relied upon as the sole diagnostic tool for dengue fever.
Other diagnostic tests, such as nucleic acid amplification tests and serological tests, should also be used to confirm the diagnosis of dengue fever.

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LEMON Mnemonic (Difficult Airway)

9/3/2023

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https://youtu.be/Dek6gi_uV8M

The LEMON Mnemonic

The “LEMON” mnemonic facilitates airway assessment for predicting difficult intubation.

L: Look externally:

This involves visually inspecting the patient's airway for any signs of difficulty, such as facial trauma, facial trauma, large incisors, beard or mustache, large tongue, or abnormal anatomy

E: Evaluate the 3-3-2 rule:

This rule assesses the patient's mouth opening (3 fingerbreadth), hyoid-mental distance (3 fingerbreadth), and the thyroid-to-hyoid distance (2 fingerbreadth). These measurements can indicate potential difficulties in intubation.

M: Mallampati score:

The Mallampati score evaluates the visibility of the patient's tonsils and uvula. The Modified Mallampati Score:
Class I: Soft palate, uvula, fauces, pillars visible.
Class II: Soft palate, major part of uvula, fauces visible.
Class III: Soft palate, base of uvula visible.
Class IV: Only hard palate visible.
A high Mallampati score (class 3 or 4) is associated with more difficult intubation as well as a higher incidence of sleep apnea.

O: Obstruction:

This assessment looks for any signs of airway obstruction, such as tumors or foreign bodies. Upper airway obstructions usually present with stridor, so listen carefully.

N: Neck mobility:

Neck mobility is evaluated to determine if there are any limitations that could affect intubation.

Summary:

“LEMON” is a quick and easy mnemonic that can help healthcare professionals identify patients who may have difficult airways, allowing them to plan for alternative approaches to airway management. It has been validated and used in emergency departments and other clinical settings to predict difficult intubation.

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<<Previous

BRASH Syndrome

Euglycemic DKA Secondary to SGLT2 Inhibitors

Neurogenic shock and Spinal Shock

ACLS Pretest and Answers (Part 3)

Pitfalls in Traumatic Cardiac Arrest

ACLS for Cardiac Arrest in Pregnancy

Hypermagnesemia

Inspirational Medical Quotes

Dengue Fever and Tourniquet Test

LEMON Mnemonic (Difficult Airway)

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Twitter: @jackcfchong
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AuthorTwitter: @jackcfchongjackcfchong@gmail.com

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Author
Twitter: @jackcfchong
jackcfchong@gmail.com