February 5, 2024

There are three types of Brugada Syndrome, but truly, the sodium channel demonstrates the following on the EKG.  

1. Type 1 has an ST-segment elevation in V1-V2 of at least 2mm. This is followed by a negative T wave in V1 and V2, as above.  

2. In Type 2 there is also ST segment elevation in V1 and V2, but this is followed by a biphasic or saddleback T wave.  

3. Type 3 is either a type 1 or type 2 pattern, but the ST segment elevation is less than 2mm.

Let's take a closer look at V1 and V2:

The patient has an EKG described as Brugada Sign. The actual Brugada Syndrome requires that you have clinical signs associated with the EKG, which alone may not be significant without clinical signs. A study from Japan showed almost 800 patients whose routine EKG had Brugada Sign. After eight years of following the patients, none had a fatal cardiac event. The Brugada brothers first described the actual Brugada Syndrome in 1992.  This study found the mean age of death was 41. The diagnosis was made from 2 days old to 84 years old. There are higher incidents in Southeast Asia. Here, it was called SUND, sudden unexplained nocturnal death. In the Philippines, it was referred to as bangungut, or “rise and moan in sleep.”  In Japan, it was called pokkuri, or sudden unexplained phenomena.  In Thailand, it was called Lai Tai, or “death during sleep.”  

The illness is explained by over 60 cardiac sodium channel errors in which 50% can be explained through mutations and the rest are hereditary. The sodium channelopathies can be seen on EKG, and with associated clinical events, the diagnosis can be made. The EKG changes can be transient, but fevers, ischemia, anti-arrhythmic medications like calcium channel blockers, beta-blockers, and Flecainide, as well as cocaine, alcohol, and hypothermia, can bring on these classic EKG changes.

The diagnosis of the EKG changes and clinical events require definitive treatment with an Implanted Cardiac Defibrillator (ICD).  

Clinical signs of Brugada Syndrome require one of the following with the Brugada Sign on the EKG: 

• Dizziness

• Fainting (syncope)

• Gasping labored breathing, particularly at night

• Irregular heartbeats or palpitations

• Extremely fast and chaotic heartbeats

• Documented ventricular fibrillation or polymorphic ventricular tachycardia

• Seizures

The bottom line is syncope can be extremely dangerous when combined with these EKG clinical findings. Thanks for taking the time to consider Brugada Syndrome during syncope evaluations.  

Sincerely,



Don Spaner, MD

UH EMS Institute CMO

February 12, 2024

A wise old professor once said, “If you knew everything you needed to know about how alcohol affects your body, you could skip medical school.” In fact, there is literally no organ not affected by alcohol abuse. My disclaimer, of course, is that we are not talking about responsible alcohol use; we are talking about abuse. It varies from person to person and includes how well the individual metabolizes alcohol. The national definition is more than 15 drinks per week for men and more than 8 drinks per week for women. Again, this varies with the size of the individual and health status. When I interview a patient in the ED who is concerned about possible alcohol abuse, it helps to ask nonjudgmental questions that can help identify someone who may need help. 

Questions include:

• Do you ever need an eye opener (a drink to get going)?” 

• Has anyone asked you, “Do you have a drinking problem?” 

• Do you ever feel guilty about your drinking? 

• Do you feel ill when you go without alcohol? 

• Have you lost a job or been disciplined because of your drinking? 

• Has your family suffered because of your drinking?  

Once a patient is identified, provide a positive sense that the future can be better.  

Let’s do a quick review of how alcohol affects the body:

1. Gastroenterology certainly seems to be the most obvious, with hepatitis, cirrhosis, stomach cancer, throat cancer, pancreatitis, colon cancer, oral cancers, gastric ulcers, and esophageal varices.

2. GU, bladder, and renal cancer also have been associated with alcohol abuse.

3. Cardiac alcoholic cardiomyopathy is a well-known, profoundly damaging event from alcohol.

4. Dermatology: Well-known thinning of the skin and places the patient at high risk for trauma.

5. Neurologic: Cerebral atrophy, including dementia and cerebellar damage including instability.

6. Visual: it impairs contrast sensitivity and increases cataracts, macular degeneration, and glaucoma.

7. Sexuality and alcohol impair erection ability and alter mental status in both sexes.

8. Cardiovascular disease: alcohol is well known to cause hypertension.

9. Pulmonary: it increases lung dysfunction and pulmonary diseases.

10. Musculoskeletal: it is well known to cause muscle atrophy.

Emergency departments help with alcohol emergencies every single day. I remember, as a first-year resident at Mt Sinai in Cleveland, Ohio, we had a hard-core alcoholic who seemed to come in almost every week in very rough conditions. We would sober him up and start the detox process, only to see him again and again. Then he stopped coming. Months went by, and he just vanished. Rumors of an ill-fated demise ensued, and we sadly considered the worst. Just before graduating residency, about a year after I last saw him, he came in with his wife in a suit and tie. He had been sobered for a year and wanted to let us know there is always hope. It was the best graduation present the senior residents could have ever asked for. I felt blessed that he took the time to share this with us, and I think of him often whenever I care for any addiction event. We know how profoundly alcohol can damage the body, but we also have been given a gift to make a difference. Let’s always take the time to use this gift.

Sincerely,



Don Spaner, MD

February 19, 2024

Cyanide is a rapidly acting substance that is traditionally known as a poison. Hydrogen cyanide was first isolated from Prussian blue dye in 1786, and cyanide was first extracted from almonds around 1800. Cyanide can exist as a gas, hydrogen cyanide salt, and potassium cyanide. Natural substances in some foods, such as lima beans and almonds, can release cyanide. Cyanide is also found in manufacturing and industrial sources such as insecticides, photographic solutions, plastics manufacturing, and jewelry cleaner. It has been used as a poison in mass homicides and suicides. The firefighter and patient’s greatest exposure is house fires with burning plastics and an industry that uses hydrogen cyanide in metal works. Online data shows that about 35% of fire victims show signs of cyanide toxicity. In hospitals, sodium nitroprusside, AKA nipride, is an intravenous medication for hypertensive emergencies that has five cyanide molecules on the chemical. It can cause cyanide poisoning if used over an extensive period. Although nipride is still widely used, it is always limited to less than three days.

Intravenous and inhalation of cyanide produce a more rapid onset of signs and symptoms than exposure via the oral or transdermal route. The toxicity of cyanide is linked mainly to the cessation of aerobic cell metabolism. Cyanide reversibly binds to the ferric ions’ cytochrome oxidase three within the mitochondria. It effectively halts cellular respiration by blocking the reduction of oxygen to water.

Cyanide's main effect is that it inhibits oxidative phosphorylation, a process where oxygen is utilized to produce essential cellular energy sources in the form of ATP. It binds to the enzyme cytochrome C oxidase and blocks the mitochondrial transport chain. After that, cellular hypoxia and the depletion of ATP occur, leading to metabolic acidosis. The utilization of oxygen by the tissue occurs, followed by the impairment of vital functions.

We must put cyanide poisoning on our differential diagnosis that involves smoke inhalation, fire victims, and industrial hydrogen cyanide use victims. Testing for cyanide in the hospital is complicated and requires a send-out, so even our decisions in the emergency department are clinically driven. The lack of ATP production leads to shock and poor brain and cardiac perfusion. So, the following three events should tell the provider that it is time to emergently treat cyanide poisoning. 

1. Exposure to cyanide (plastics burning, industrial use of hydrogen cyanide, or chemical exposure to cyanide-producing drugs)

2. Altered mental status (lack of brain perfusion)

3. Shock and hypotension in the above setting

Combining these three clinical findings is enough to use the Cyanokit immediately. Remembering our basics is critical, and this includes NO MOUTH TO MOUTH! Decontamination is also critical to reduce continued exposure. Clothes need to be removed and skin washed if dermal exposure is suspected. The antidote needs to be started stat as death from cyanide poisoning occurs in minutes to hours, rapid diagnosis and care are critical for survival. Hydroxycobalamin is the antidote of choice for acute cyanide poisoning, especially if the patient has coexisting carbon monoxide poisoning. The older Cyanokit had three drugs and impaired oxygen caring capacity and should only be used if Cyanokit II is not available. The standard dose is 5 grams given intravenously (IV over 15 minutes; be aware that this antidote turns urine dark red; this is not due to myoglobinuria). Remember to use the glass vial and vented tubing supplied with these kits.

Cyanide poisoning is extremely dangerous and rapidly fatal if not considered. Be prepared to look for early signs of cyanide toxicity, dilated pupils, headache, confusion with exposure, and act fast. If you recognize exposure, hypotension, and significantly altered mental state, treat immediately.

Sincerely,



Don Spaner, MD

February 26, 2024

The BEES Card is a great way to remind you of the right patient, proper medication, correct dose, right route, and right documentation. Take home is a simple weight-based rule of thumb. If your patient is less than 30Kg (66#), they get 0.15mg epinephrine IM. If they are over 30Kg (66#), they get 0.3mg epinephrine IM.

I’m looking forward to having this practical completed ASAP at all our departments utilizing EMTs. Together, we can save more lives. Thanks for taking the time to review IM epinephrine for EMTs.

Sincerely,



Don Spaner, MD CMO