July 29, 2024

This week we will be discussing anaphylaxis. Anaphylaxis is an acute life-threatening systemic reaction that results from the sudden release of inflammatory mediators. It can cause hypotension, bronchoconstriction, mucosal edema, and decreased cardiac contractility. It is mediated by mast cell degranulation, resulting in the release of histamine, tryptase, and tumor necrosis factor (TNF)-alpha.

Establishing the incidence of anaphylaxis in a large population is difficult because studies are based on self-reports or ED visits, and they may focus on severe reactions and underestimate mild or moderate reactions. Unrecognized first-time reactions and hospitalized patients may be missed if they do not have a discharge diagnosis of anaphylaxis. There was no standard definition for anaphylaxis until the publication of consensus guidelines in 2006.

The causes of anaphylaxis are numerous and include food, medications, stinging insects, latex, and exercise. Food is the most common cause of anaphylaxis in the outpatient setting, such as peanuts, tree nuts, fish, shellfish, cow milk, soy, and eggs. Current estimates suggest a prevalence of food allergy in North America of 6% in young children. Prior tolerance to a food does NOT exclude the development of an allergy. Food allergens account for 30% of fatal cases of anaphylaxis, which leads to approximately 200 deaths in the US per year. The highest risks for severe food-induced anaphylaxis are allergy to peanuts/tree nuts, other food allergies, and a history of asthma.

Medications are the second most common cause of anaphylaxis in children. The most frequent culprits are antibiotics, particularly beta-lactam antibiotics (e.g., Augmentin = Amoxicillin plus beta-lactam) and non-steroidal anti-inflammatory drugs (NSAIDs).

Stings by bees, vespids (i.e., yellow jackets, hornets, wasps), and stinging fire ants can cause anaphylaxis. Approximately 0.4-0.8% of children report systemic allergic reactions to insect stings. At least 50 cases of fatal anaphylaxis to insect stings occur annually in the U.S. For venom allergy children, the risk of a systemic reaction to an insect sting (even into adulthood) is 30%. Skin symptoms alone occur in 60% of children, and these can be treated symptomatically with cold compresses, oral antihistamines, and oral analgesics.  

Latex is an “emerging” cause of anaphylaxis. The most common mode is direct contact with latex products, such as medical gloves, catheters, and dental instruments. It can also be inhaled. Certain patient subsets have prevalence of a latex allergy as high as 75%. Children born with spina bifida, those with bladder extrophy, and those requiring frequent bladder catheterizations are particularly at risk.  

Exercise-induced anaphylaxis is caused by mast cell mediator release from exercise and physical exertion. Symptoms typically start within a few minutes of exercise. Normally, high levels of exertion, like jogging and aerobics, are most at risk, although some patients experience symptoms with low levels of exertion, like walking. A co-trigger or co-factor is usually present, such as eating certain foods, medications, alcoholic beverages, menstruation, or high-pollen exposure.  

Idiopathic anaphylaxis is when a causative allergy or inciting physical factor is not found. This is a diagnosis of exclusion after a thorough detailed history has been completed, appropriate allergy testing has been performed, and other mimickers of anaphylaxis have been excluded. This is considerably rare in adults and even less frequent in children.  

Diagnosis of anaphylaxis is clinically based on prompt recognition of signs and symptoms, which include: 

• Abdominal cramping  

• Angioedema

• Cough

• Diarrhea  

• Dizziness

• Dyspnea

• Flushing 

• Hives

• Pruritus 

• Stridor 

• Syncope

• Vomiting

• Wheezing 

It typically involves two or more organ systems: Mucocutaneous (i.e., skin), respiratory, cardiac, and gastrointestinal (GI). Skin findings are the most common but are not required to diagnose anaphylaxis.  

Treatment of anaphylaxis includes multiple medications. Epinephrine is widely recommended as first-line therapy for anaphylaxis despite no high-quality trials. It serves the dual purpose of stabilizing mast cells and treating angioedema, bronchospasms, and vasodilation. The dose is 0.01 mg/kg (max 0.5 mg) of 1mg/ml Epinephrine administered intramuscularly (IM). It should not be given subcutaneously. In addition, the preferred site is the lateral thigh over the deltoid/shoulder due to better absorption. Furthermore, about 1 in 10 reactions will require an additional dose of epinephrine.  

Crystalloids can also be given once IV access has been obtained. This helps the patient since anaphylaxis causes vasodilation and increased vascular permeability, leading to rapid third spacing of fluid. There is minimal evidence, but guidelines recommend 1-2 L as an IV bolus.  

Antihistamines have a role in the treatment of anaphylaxis, but they should NOT be used as the initial management. H1 blockers reduce cutaneous manifestations and H2 blockers reduce GI symptoms, but they are also associated with increased rates of biphasic reactions.  

There is no quality evidence that steroids improve outcomes in anaphylaxis and that their use decreases incidence of biphasic reactions. Albuterol can be used as an adjunctive treatment, but there is minimal evidence for its use in anaphylaxis. There is a 4.7% incidence of a biphasic reaction with a median onset of 11 hours.  

If a patient with anaphylaxis were to arrest, attempt intubation with a single attempt and a paralytic if allowed/available. Consider early cricothyroidotomy. Give lots of epinephrine, both IM and IV per protocol. Be prepared for obstructive lung physiology and pneumothoraces.  

Be safe and have a great summer,

Jeffrey Luk, MD

July 22, 2024

Heat stroke is a true environmental emergency! The patient’s temperature regulatory mechanism in the brain is lost, which leads to uncontrolled hyperthermia. Cell death and damage to the brain, liver, and kidneys occur. There is no absolute core temperature at which heat stroke begins, but the body temperature is usually at least 105°F. Mortality for heat stroke is up to 70%. The classic clinical triad for heat stroke is high body temperature, the absence of sweating, and mental status changes. The patient will often have preceding malaise or flu-like symptoms with hot skin that can be moist or dry. The patient will experience deep, fast breathing progressing to shallow and slow breathing as well as a rapid full pulse to a slow heart rate. The patient will feel confused, disoriented, and could be unconscious. There also may be possible seizure activity.  

There are two forms of heat stroke, classical and exertional: 

• Classical heat stroke generally affects the very young, debilitated elderly, and/or chronically ill. It is caused by increased external heat gain with decreased internal heat loss. The general scenario is a heat wave with no air conditioning plus medications that affect temperature regulation. This type of heat stroke tends to be a gradual onset over several days leading to severe dehydration and hot, dry skin.  

• Exertional heat stroke tends to occur in young, healthy patients who are physically active in the heat. It is usually due to excessive exertion with prolonged heat exposure and poor acclimatization. Sweating ceases with the onset of heat stroke, BUT the patient may still be very diaphoretic because of sweating prior to onset.  

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Heat stroke causes widespread damage to every organ system. The central nervous system is the first to be involved and the last to recover. The cerebellum is especially sensitive so the patient may display poor coordination. Mental confusion begins with a core temperature of 38° C (101° F) and the CNS ceases functioning at temperatures above 42°C (107.6°F). The liver is particularly susceptible to heat injury, which causes liver failure, bleeding disorders, and hypoglycemia. Kidney failure occurs due to damage from products of muscle breakdown. Severe build-up of acids in the body occurs from lactic acid production.  

The first step in managing heat stroke is to transfer the patient to a cooler environment and remove constrictive clothing. ABCs need to be addressed and the airway may need to be supported, possibly with intubation. Apply cardiac monitoring and obtain an EKG since cardiac arrhythmias are common. Attempt to obtain info on the duration, magnitude, and conditions of the heat exposure, as well as underlying medical conditions and medications.  

The cornerstone of therapy for heat stroke is rapid cooling. One can use cool IV fluids and ice packs to the groin and axilla, but the BEST treatment is immersing the patient in an ice bath or covering the patient with ice to cool the patient to around 101° F to limit neurological sequelae. 

Remember that prevention is better than treating. Keep an eye out for your colleagues when it is hot. Make sure to maintain adequate fluid intake since thirst is a poor indicator of hydration.  

Be safe and have a great summer,

Jeffrey Luk, MD

July 15, 2024

Heat edema is a type of minor heat illness. It consists of peripheral edema of an unknown cause, generally located in the ankle and wrist, and occurs in the first few days of heat exposure. It is usually self-limited and does not require any intervention other than elevation of the extremities.

Another type of minor heat illness is heat tetany. It presents as spasms in the hands and feet and is secondary to breathing fast, resulting in a decrease in carbon dioxide and ionized serum calcium. It is often seen in conjunction with other heat syndromes or causes of hyperventilation since it may be an attempt to compensate for exercise-induced lactic acidosis. It should resolve with reversal of the hyperventilation.

Heat syncope is a brief loss of muscle tone in the body with or without loss of consciousness. Vital signs are typically normal by the time of examination. It occurs early in exposure to a new heat stress and is often preceded by dehydration or the presence of drugs that affect the normal mechanisms to compensate for heat. The etiology is usually mild dehydration in combination with the rerouting of blood into the extremities for cooling. Treatment includes rest, rehydration with electrolyte-containing fluids, and gradual return to activity.

Heat rash is common in acclimatization, in tropical areas, and in those with tight clothes. It is an intensely itchy, red, slight raised, or fluid-filled rash. It is caused by the plugging, dilation, and rupture of sweat glands followed by skin maceration from sweating. Therapy is to keep the skin cool and dry, avoid powders to prevent further plugging, avoid tight clothing, and antihistamines for itching as needed.

Heat cramps are painful intermittent spasms in the hands, arms, legs, and abdominal muscles. The patient may feel dizzy or faint. Vitals are stable. The skin is moist and warm. The patient’s body temperature is normal or slightly increased. Treatment includes removing the patient from the heat by placing in a cool, shaded area or air conditioning. You can treat the patient with oral fluid and electrolyte replacement; if the patient cannot take oral fluid, then IV fluid with normal saline is appropriate.

Heat exhaustion is the most common heat illness in the prehospital setting. Common presenting symptoms are normal or slightly elevated temperature, cool and clammy skin, heavy sweating, tachycardia, tachypnea, and hypotension. The patient may report a headache, anxiety, and numbness/tingling in extremities, but the patient should NOT have any evidence of mental status changes. Most patients present with a combined picture of salt and water depletion. Treat the patient by removing them from the heat and place in a cool shaded environment or air conditioning. Place the patient in a shock position as necessary. Rehydration with IV fluids may require up to 4L of more. Without termination of the heat stressor and immediate treatment, symptoms may progress to frank heat stroke.

Be safe and have a great summer,

Jeffrey Luk, MD

July 8, 2024

Heat illness is defined as the inability of your body to cope with heat stress. It is very prevalent, so we must understand how our bodies regulate temperature and what happens when it is overwhelmed. If heat illness is unrecognized and untreated, it can seriously harm the body. For example, heat stroke in athletes is second only to head and C-spine injuries as a cause of death. However, not all forms of heat-related illness require emergency treatment. Risk factors for heat illness include the following: 

• The young and old are at the most risk since they cannot remove themselves from hot environments.  

• Heat waves, especially when individuals do not have air conditioning or it is not properly functioning.  

• Patients with multiple medical conditions, such as cardiovascular disease, diabetes, and psychiatric problems.  

• Patients on various medications, such as antihistamines, beta-blockers, antipsychotics, and diuretics.  

• An individual’s level of acclimatization (i.e., the process of becoming physically adjusted to the environment). 

• Length and intensity of exposure.  

• Other environmental factors, such as humidity, sunshine, and wind.  

Heat illness is usually a combination of multiple processes: 

• Increased heat gain. 

• Increased heat production due to an increase in exertion.  

• Decreased heat loss.

The body adapts to heat through multiple mechanisms: 

• Radiation, which is the transfer of heat via electromagnetic waves. It accounts for almost 65% of heat loss in a cool environment, but it can also be a major source of heat gain.  

• Evaporation, which is the conversion of a liquid (e.g., sweat) to a gas on the skin, which requires energy. It is a major source of heat loss via sweating but becomes ineffective in humidity over 75%.  

• Convection, which is heat loss to surrounding air via the wind. It accounts for 20% of heat loss.  

• Conduction, which is the transfer of heat between two objects via direct contact. It accounts for 2% of heat loss.  

Heat dissipates through multiple mechanisms. In the first phase, heat radiates from small blood vessels in the skin. Increased heat loss occurs as the circulatory system adjusts blood flow from the core to the outside parts of the body (i.e., extremities). Blood flow is decreased to the intestines and the heart rate increases. In the second phase, active heat loss occurs by sweating and the evaporation of sweat. Sweat glands are stimulated by the sympathetic nervous system, which increases losses via evaporation.  

In acclimatization, the body adapts to repeated heat stress over 10 to 60 days. Although this process will protect against heat illness, as the temperature one feels when the skin is wet and is exposed to moving air approaches 86°F, even young, well-acclimated individuals are susceptible to vigorous or prolonged physical activity.

Be safe and have a great summer,

Jeffrey Luk, MD