Mountain Sickness

Mountain sickness

Background: At higher altitudes, there is less oxygen. For example, at 10,000 feet, the air is 14% oxygen while at sea level in NYC, we are breathing in 21% oxygen. Mountain sickness is the manifestation of the body’s response to hypoxia. 

Clinical features: 

Usually only occurs in altitudes greater than 8000 ft unless patients are particularly susceptible to hypoxia (COPD, anemia). This is also why when flying, airplane cabins are usually pressurized to 7-8000 ft. Patients who have experienced altitude sickness are more likely to have repeat episodes when returned to the same altitude. A quicker rate of ascent is also more likely to lead to mountain sickness. Most often presents the 1st night or 2nd night at higher elevations. The average duration of symptoms in cases that self resolve is one day (the body successfully acclimates). 

Clinical criteria (most are CNS symptoms since the brain is most sensitive to hypoxia): An individual above 8000 feet presents with headache and one of the following

- GI symptoms

- Sleep disturbance

- Dizziness/lightheadedness 

The feared complications of mountain sickness are High Altitude Cerebral Edema (HACE) & High Altitude Pulmonary Edema (HAPE). 

Treatment & Prevention:

In mild mountain sickness, the patient can descend to a lower altitude (1000-3000 ft lower) or stop the ascent and acclimate for 12-36 hours. Acetazolamide (125-250 mg BID) can be used to speed up acclimation by increasing respiratory rate from the resultant metabolic acidosis. For patients who have moderate to severe mountain sickness, immediate descent 1000-3000 feet is indicated. Low flow oxygen, especially at night, can be helpful. Hyperbaric oxygen therapy can be considered. Lastly, besides acetazolamide, dexamethasone 4 mg q6 can be considered.

The best preventative measure is gradual ascent. Acetazolamide prophylaxis indicated in those who have previously experienced acute mountain sickness or anticipate a rapid ascent to altitude. Start 24 hours before ascent and continue until 48 hours after reaching final altitude. Dexamethasone can be started the day of ascent and likewise continued until the first two days at altitude. Ibuprofen also helps. 

HACE

Severe and uncommon form of acute mountain sickness. Basically, it is a progression of acute mountain sickness resulting in AMS & ataxia from cerebral edema due to hypoxia. Treatment is immediate descent, supplemental O2, dexamethasone, & acetazolamide. Other treatments for increased ICP (mannitol etc…) are of undetermined benefit.

HAPE

Hypoxic pulmonary vasoconstriction led to pulmonary hypertension and eventual pulmonary edema due to elevated pulmonary artery pressures. Patients can have bilateral opacities on CxR and a better clinical appearance than their O2 saturations suggest. Immediate descent, minimizing exertion, supplemental O2, expiratory positive airway pressure mask (forces some PEEP in a non-intubated patient), nifedipine, & sildenafil (promotes pulmonary artery vasodilation) are possible treatment options.  

https://www.ncbi.nlm.nih.gov/books/NBK430716/

https://wikem.org/wiki/High_altitude_pulmonary_edema

https://wikem.org/wiki/Acute_mountain_sickness

Imray C, Wright A, Subudhi A, Roach R. Acute mountain sickness: pathophysiology, prevention, and treatment. Prog Cardiovasc Dis. 2010 May-Jun;52(6):467-84. doi: 10.1016/j.pcad.2010.02.003. PMID: 20417340

POTD: Winter is Coming.

Let’s talk about FROSTBITE, BRRRRRRR.

Background

• Results from the freezing of tissue that are exposed to temperatures below their freezing point, resulting in direct ice crystal formation and cellular lysis with microvascular occlusion

• Most of the damage occurs as a result of a freeze thaw cycle with endothelial damage and cellular death resulting in osmotic gradient changes, initiation of the arachidonic acid cascade, vasoconstriction, and hematologic abnormalities including thrombosis

• Risk correlated with temperature and wind speed

• Risk is <5% when ambient temperature (includes wind chill) is > –15°C (5°F)

• Most often occurs at ambient temperature < –20°C (–4°F)

• Wetness and humidity increase the risk (water has 25x thermal conductivity of air)

• Can develop within 2-3sec when metal surfaces that are at or below –15°C (5°F) are touched

• Most commonly affects distal part of extremities, face, nose, and ears

• The severity of irreversible damage is most closely related to ambient temperature and length of time the tissue remains frozen

• High-risk groups: outdoor workers, elderly, homeless, drug or alcohol abusers, psychiatric disease, high-altitude or cold-weather athletes, military personnel

• "Hunter's response" - prolonged repeated exposure to cold is protective

Classification

Frostbite is classically categorized into four levels of injury.

Management

The initial treatment in the Emergency Department for all degrees of frostbite is the same. Addressing ABC’s, trauma evaluation, removing wet and constrictive clothing, treatment of concomitant hypothermia (must rewarm to a core temperature of at least 35°C), and identification of other injuries should be confirmed in all cold injury cases if warranted.

• THAWING: Do NOT attempt until the risk of refreezing is eliminated. Refreezing will cause even more severe damage. Rapid active rewarming is the core of therapy and should be initiated as soon as possible. Best performed in a circulating water bath around 37°C to 39°C. Frostbitten faces can be thawed using warm water compresses, and ears may be thawed with small bowls of warm water. Immersion rewarming can be discontinued when the affected area developed a red or purple appearance and becomes pliable to the touch.

• Analgesia: rewarming is very painful, treat your patient's pain!

• Local wound care: Gently dry, elevate, and apply bulky dressing to the affected area. Compartment syndrome is a known complication, so maintain a high suspicion.

• Update tetanus as needed

• Empiric prophylactic antibiotics are not needed and are controversial.

• Surgical management may be required if wet gangrene or infection occurs, but this is typically reserved for late frostbite management after the rewarming phase in days to weeks following initial presentation

Dispo Dispo Dispo

• Patients with superficial local frostbite may be discharged home if social circumstances allow. Patients unable to care for themselves adequately should never be discharged into subfreezing temperatures.

• Significant injuries will require admission.

References:

http://www.emdocs.net/brrr-ed-presentation-evaluation-and-management-of-cold-related-injuries/

http://emedicine.medscape.com/article/926249-treatment#showall

https://wikem.org/wiki/Frostbite

https://www.emrap.org/episode/environmentalem/hypothermia

https://www.emrap.org/episode/environmentalem/frostbite