Hello to all my colleagues!

For each week of January, I will present brief topics relating to winter emergencies. This week I will discuss Hypothermia. Topics for the rest of January will include snow shoveling-induced coronary ischemia, carbon monoxide poisoning, and frostbite.

Due to the nature of our jobs, emergency health care providers possess a somewhat skewed and unique perspective on life. How many of us gauge our seasons not based solely upon anticipated fun activities and events, but also upon the type and numbers of various seasonal emergencies we are likely to encounter, both in prehospital and emergency department settings? 

Winter of course is no exception: sledding and snowmobile accidents, Influenza and Covid surges, carbon monoxide poisonings, hypothermia and Acute Coronary Syndrome induced by snow shoveling are the “events” that partially define winter for many of us.  

Hypothermia (defined as a core body temperature of less than 35°C ) risk factors include extremes on either end of the age spectrum. The elderly lose their ability to sense cold and generate heat. The very young conserve heat poorly because of high surface area to mass ratio and lack of subcutaneous fat. Radiation and conduction (loss of heat through skin that is in contact with cold or WET CLOTHES) become major mechanisms of heat loss in cold weather.  Diabetics and those with altered sensorium due to alcohol and /or drugs are also susceptible to hypothermia. Trauma victims are at risk for acidosis and hypoperfusion when hypothermia co-exists. 

At 30 - 32 °C, the body loses shivering ability and can no longer generate heat. As the body temperature declines further, metabolism slows significantly, and EKG changes can be observed. The Osborn or “J” wave (elevated and notched J point at the initiation of the ST segment) might be apparent. Dysrhythmias are more likely when the core temperature is ≤ 30 °C, progressing from sinus bradycardia to slow atrial fibrillation, and finally ventricular fibrillation or asystole.

The freezing myocardium is highly irritable and rough handling can precipitate ventricular fibrillation. Hypothermia has four clinical stages. 

· Stage I defines a conscious shivering patient with a core temperature range from 32 – 35 °C. These patients can be warmed by removing them from the cold, changing clothes, and providing warm drinks.

· Stage II defines the non-shivering lethargic victim (28 to < 32 °C). Active external warming (apply heat to body surfaces via warming blankets and radiant heat), warmed humidified oxygen and warmed IV fluids (38 to 42 °C) are effective measures. As the body temperature drops to less than 28 °C, patients are likely to be unconscious with vital signs.

· (Stage III) or without vital signs (Stage IV). Management includes CPR if no vital signs, airway management, rewarming techniques already mentioned, and consideration of ECMO (Extracorporeal Membrane Oxygenation) or cardiopulmonary bypass if available. Hypothermic patients should not be pronounced dead until after they have been rewarmed to 35 °C ideally (although in certain situations termination of resuscitation can be considered earlier). 

I thank you for your perseverance, grit, resilience, and commitment to the patients we serve. I am honored to be your team member.  

Andrew P. Garlisi, MD, MPH, MBA, VAQSF 

Snow  - January 11, 2021

Greetings from Chardon, a paradise for snow lovers! 

And speaking of snow...

Snow shoveling is far from a benign activity and can be a risky endeavor, especially for those over age 55 with risk factors for coronary disease. Over 11,500 visits to the emergency department are due to injury or illness secondary to show shoveling. Seven percent of these visits are heart related. Statistics reveal that there are 34% more heart- related deaths per year in the United States during heavy snowfalls versus on snow-free days.  

The cold weather may induce coronary spasm which, when compounded upon fixed atherosclerotic lesions, precipitate coronary ischemia. Snow shoveling is considered a “rapid exertion” type of activity with intense effort expended immediately upon undertaking the snow shoveling activity, with little to no warmup phase. Additionally, victims are often otherwise sedentary individuals, far from peak conditioning. Such immediate intense exertion causes a rapid spike in heart rate and blood pressure which raises the likelihood of acute coronary ischemia and injury.  

Cold dry air is also a major trigger for airways, making breathing difficult. A phenomenon known as Exercise-Induced Bronchospasm (EIB) occurs in approximately 80% of Americans diagnosed with asthma, and at least in 10% of the general population. A major contributor to EIB is mouth breathing, especially in colder temperatures.   

Mouth breathing offers less resistance to inhaled air, but the downside is when the nose is bypassed, cold dry air cannot be properly warmed and humidified. The nasal turbinates are a series of passageways that warm and humidify the air we breathe. Mouth breathing bypasses the nose introducing cold air directly into the bronchial tubes.  Cells lining the bronchial passages are forced to work overtime in an attempt to warm and humidify the air which causes the release of mediators of inflammation, such as histamine and leukotrienes.  These chemical mediators cause bronchospasm.   

Symptoms include coughing, shortness of breath, tightness in the chest, and of course wheezing. Although cold weather bronchospasm is more likely to affect athletes participating in winter sports (football, skiing, ice skating), anyone participating in physical activity could be susceptible to bronchospasm including joggers and yes...snow shovelers.   

Asthmatics can alleviate symptoms by taking a few puffs of a bronchodilator such as Albuterol prior to or after exercise, or a pill such as Singulair (a leukotriene antagonist) an hour or two prior to exertion.  For non-asthmatics, wearing a mask or cloth scarf over the mouth helps warm the inhaled air and may mitigate symptoms. 

Stay warm my friends... 

Andrew P. Garlisi, MD

January 18, 2021

I will never forget my shift in Geneva nearly two decades ago when 19 victims of carbon monoxide poisoning flooded our emergency department. Victims included one infant and three toddlers. Several families had gathered in one dwelling utilizing a faulty space heater. 

Carbon Monoxide (CO) Poisoning is responsible for approximately 50,000 visits to the emergency department in the U.S.  Seasonal first-time activation of furnaces and confinement to the indoors (more stringent now than ever due to Covid lockdowns) are reasons that carbon monoxide poisonings spike during the winter months.  Structure fires are common sources of CO poisoning in addition to burns, smoke inhalation, and cyanide poisoning. CO is a silent killer, invisible, and odorless. It poisons cellular metabolism.    

Cells need energy (ATP) to function. Cells produce this energy by taking oxygen plus glucose from the blood to produce carbon dioxide, water, and ATP (energy required to sustain life). Three major biochemical stages are needed to convert oxygen plus glucose to ATP energy: glycolysis, Kreb's Cycle, and Electron Transport Chain. These stages are sequential and involve multiple enzymatic chemical reactions. Carbon monoxide poisons the cells via two main mechanisms:    

1. CO kicks oxygen off the hemoglobin molecule and occupies the oxygen binding sites. With less oxygen going to cells, metabolism and energy production are impaired.    

2. Carbon monoxide interferes with the enzymes, which are required for the third and final stage of cellular metabolism -- the Electron Transport Chain.    

Carbon monoxide signs and symptoms are categorized broadly as mild, moderate and severe.   

• Mild symptoms are "flu-like" and include headache, nausea, vomiting, and fatigue. These symptoms correlate roughly with CO levels from 10 to 20%.     

• Moderate symptoms and signs include worsening headache, confusion, drowsiness, and tachycardia, seen with CO levels between 20 to 40%.    

• Severe poisoning may cause loss of consciousness, seizures, stroke, STEMI, and cardiorespiratory failure (levels greater than 40%).    

• Remember that the CO levels for signs and symptoms are NOT SPECIFIC and will VARY. A diabetic with heart disease can manifest life-threatening symptoms at CO levels less than 25% due to underlying diseases. The same would be true of patients with COPD and other chronic illnesses.    

Because early symptoms are vague, CO poisoning is often misdiagnosed. Clues include flu without fever, dead pets, multiple victims in the same dwelling, and power outages in winter. Treatment includes immediate removal of victims from the scene. Providing 100% oxygen by tight-fitting mask is the conventional therapy. With non-rebreather 100% oxygen, CO levels will generally return to levels less than 10% within 2 to 4 hours.  

Some studies are suggesting CPAP with 100% oxygen for patients who are conscious and cooperative with serious symptoms. Dramatic reductions of CO levels within one hour are documented with CPAP. High Flow Nasal Oxygen (HFNC Airvo, Vapotherm) has also been studied as a treatment option for CO poisoning but results are inconclusive. Hyperbaric oxygen should be considered for pregnant patients with CO levels greater than 10%, patients with significant signs and symptoms with CO levels greater than 25%, and those with neurological deficits and cardiac ischemia. Hyperbaric oxygen reduces the half-life of carbon monoxide to 20 minutes.    

It is better to err on the side of treating with HBO2 because the benefits of treating outweigh the risks. The only major contraindication for HBO2 is a patient with untreated pneumothorax. The benefit of the HBO2 is faster restoring of normal oxygenation of hemoglobin, and improved oxygen delivery and reducing reperfusion injury to ischemic tissue. Also, there is a benefit to the reduction and prevention of delayed neuropsychiatric syndromes, which are difficult to predict based on the poisoning.   

There is also the special case of treating pregnant patients in which the fetal hemoglobin has a greater affinity for CO than hemoglobin in the mother's red blood cells. The fetus acts as a sink for the CO, so pregnant patients may have fewer symptoms and lower COHb when compared to patients with similar exposures. Because of the increased toxicity of CO for the fetus, and difficulty with evaluating, it is recommended to have a low threshold for HBO2 treatment for the pregnant patient.  

I have tried to find an updated list of available hyperbaric chambers used for acute carbon monoxide treatment. I asked our Transfer Center if they could have such a list available for when we have a patient that requires urgent hyperbaric treatment. I also notified poison control for an updated list, and--they are working on it. I believe St. Vincent Charity Medical Center still offers acute hyperbaric treatment for adults, but I am not sure about pediatric victims.  The Ohio State University Medical Center offered acute hyperbaric treatment for pediatric patients in the past. The University of Pittsburgh also offers acute hyperbaric treatment. I am working on updating this list and will let you know if I find further information.   

Thank you for your dedication and commitment to our patients! 

Andrew Garlisi MD, MPH, MBA, VAQSF 

Frostbite - January 25, 2021

As we approach the end of our first month of the 2021 winter season, I will wrap up the discussion of winter emergencies with frostbite.

Frostbite has played significant roles in military history and was recorded during Hannibal’s trek across the Italian Alps prior to invading Rome. The first formal description of the condition was in 1813 by Dominique Larrey, a physician in Napoleon’s army, who was devastated by frostbite and hypothermia during the invasion of Russia. The soldiers were forced to slit open the bellies of horses to warm their badly frostbitten hands during the brutal winter. Nearly one million combatants fell victim to frostbite during the first and second world wars. 

Pathophysiology

Frostbite is caused by cold-induced damage to the skin and underlying structures, and can occur at temperatures above and below freezing. Tissue damage is caused by capillary vessel stasis and thrombosis. Cutaneous vasoconstriction occurs at 15 °C (59° F) which reduces blood flow. As the temperature drops to 10 °C (50° F), cold-induced vasodilation (the so-called “hunting response”) occurs whereby vasoconstriction is interrupted by a period of vasodilation in an effort to protect the extremity from cold damage. BUT, as returning blood from the periphery begins to decrease core body temperature, blood flow to the extremity shuts down, and the tissue temperature drops. This further results in capillary endothelial damage, increased platelet affinity and plasma leakage from the intravascular space, increased RBC stasis, vessel thrombosis and eventual frostbite. Once the tissue temperature drops below 0 °C (32° F), frostbite occurs; ice crystals literally from within the tissues, the tissue injures, and necrosis occurs, which can result in amputation. 

Once frostbite has occurred, a phenomenon known as reperfusion injury happens when blood is returned to the injured extremity. Arachidonic acid and prostaglandins are released from the damaged cells, causing vasoconstriction sludging of cells, leading to potential further tissue loss. 

NOTE: If a partially thawed extremity is REFROZEN, tissue injury damage and loss is greatly increased.

Risk Factors

Frostbite is seen at all ages but is most commonly encountered in those between 30 to 50 years old.  The elderly diabetics are at higher risk. Hands, feet, ears, face and nose tissues are most susceptible to frostbite. Cold temperature, duration of cold exposure, wind chill, and wetness all increase severity of injury. People involved in winter sports, the military, and homeless individuals are often at risk to frostbite. 

Clinical Presentation / Definition of Terms

Trench Foot: Is also known as immersion foot; This is usually associated with non-freezing temperatures, and wet environment, and requires exposure for hours or days to wetness. Early symptoms include numbness, painful paresthesia and cramps. The extremity appears cold, pale, and exhibits decreased sensation. Tissue loss is uncommon.

Chilblains (Pernio) is precipitated by exposure to nonfreezing temperatures and dry environment. This results from exposure to cold, damp air. Skin lesions develop after 12 hours and are characterized by erythema, itching, and burning paresthesia. Women with Raynaud’s phenomenon are at greatest risk. 

Frostnip and Frostbite occurs with freezing temperatures in either wet or dry environments. Frostnip is an early response to cold exposure and is reversible. The first sign is pale, painful itchy skin. If not warmed, the skin will progress to frostbite. 

Frostbite has degrees depending on the depth of tissue involvement and damage. Superficial frostbite includes first and second degree injury. Deep frostbite includes third and fourth degree categories. A bone scan or MRI might be needed in determining the true extent of injury.

First Degree Frostbite is superficial and results in no permanent damage. The skin is numb, swollen and erythematous—but soft. Eventually, after a few weeks, the skin surface may slough off. 

Second Degree Frostbite reveals clear blisters early on and the skin hardens. It will take a few weeks for the total extent of injury to be declared. Generally the hardened blistered skin dries, blackens and peels. The patient may experience permanent insensitivity to cold and numbness. 

Third Degree involves layers of tissue below the skin. Signs include blood-filled blisters and blue-grey skin discoloration. Weeks after the injury pain persists and a black crust (eschar) develops. Long term skin ulceration can occur. Structures below the skin surface can be damaged including growth plates of bone.

Fourth Degree frostbite involves muscle, nerves, tendon and bone. Early on, the skin appears colorless, rock hard and painless upon rewarming. The skin eventually mummifies and necrosis necessitates amputation. Often, autoamputation will occur, and may take up to two months to determine the true extent of damage. 

Treatment

Proper clothing like gloves, good nutrition, and avoidance of fatigue and alcohol is the best prevention.

Frostnip treatment can be initiated in the field via breath, body heat or other heat sources. Frostbite treatment should be initiated as soon as possible but ONLY if refreezing can be prevented. Cold, wet clothing should be removed and replaced. 

The affected area should be rewarmed in circulating water ideally heated to 104° - 107° F (40 to 42° C). Warming takes up to one hour and can be very painful, so pain management is essential. Rewarming with dry heat can be dangerous because the frozen insensitive skin cannot detect heat and burns may result. 

Rubbing injured tissues can result in more tissue damage! Ibuprofen can be given in the field to prevent clotting and inflammation. Ibuprofen blocks the arachidonic acid cascade. 

Tetanus prophylaxis should be provided. White, clear blisters can be aspirated or debrided, but hemorrhagic blisters should not be debrided. Avoid early surgical intervention--the true extent of tissue injury will not be apparent for several weeks. Some experts recommend tPA with heparin for those individuals with potential for large area amputations who present within 24 hours of injury, unless contraindications exist.

Thank you and Happy New Year to you and your families!

Andrew Garlisi, MD, MPH, MBA, VAQSF