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David A. Connett, DO, FACOFP, dist

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David A. Connett, DO, FACOFP, dist

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Nothing to disclose – including pharmaceuticals

Disclosures

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Acute Mountain Sickness (AMS)

High Altitude Cerebral Edema (HACE)

High Altitude Pulmonary Edema (HAPE)

Decompression Sickness (DCS)

High Altitude Syndromes

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High Altitude-5,000 feet to 11,500 feet (1500-3500 m) • Highest U.S. ski resorts

• Minor impairment of arterial oxygen transport arterialSaO2> 90%

• AMS common with rapid ascent above 8000 feet

Very High Altitude-11,500 feet to 18,000 feet (3500-5500 m) • High peaks in the lower 48, Europe

• Maximum arterial SaO2 < 90%, PAO2<60 torr

• Most common range for serious altitude sickness

Extreme Altitude-over 18,000 feet (above 5500 m) • Denali, Himalaya, Karakoram, Andes

• Marked hypoxemia and hypercapnia

High Altitude

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Oxygen Levels at Altitude

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Barometric pressure falls with increasing altitude in logarithmic fashion

Partial pressure of oxygen decreases resulting in hypoxia

Altitude changes with distance from equator, hypoxia worse at the poles.

Pressure is lower in winter than in summer.

Temperature decreases with altitude 1000 feet for every 3.56°F

Ultraviolet light increases by 4% every thousand feet

Environment at High Altitude

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Pathophysiology Acute Mountain Sickness

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Hypoxic Ventilatory Response (HVR)

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Pathophysiology Acute Mountain Sickness

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Pathophysiology of HAPE

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Components of endothelial activation/dysfunction in acute lung injury (ALI). This schematic cartoon illustrates the components of endothelial activation including

1) Endothelial cell-leukocyte interactions,

2) Endothelial cell-platelet-neutrophil interactions, and

3) Structural changes between endothelial cells. RBC, red blood cell; MLCK, myosin light chain kinases; PASMC, pulmonary artery smooth muscle cell.

Pathophysiology of HAPE

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Pathophysiology of HAPE

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Acute • Ventilation

• Heart rate

• Cerebral blood flow

• Diuresis increased hematocrit

Chronic • Increase in pulmonary ventilation

• Increase and diffusing capacity in the lung

• Red blood cell count due to erythropoietin

• Metabolism (tissue changes over years)

• Increase in the number of mitochondria

• Augmentation of the cytochrome oxidase system

Factors Increased by Acclimatization

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Rapid ascent and exposure to the altitude at the summit of Mount Everest 29,028 feet results in loss of consciousness in a few minutes and death shortly thereafter.

Acclimatization occurs over time

Ability to acclimatize varies from individuals

Just a few days at sea level may make one susceptible to AMS or HAPE

Acclimatization to High Altitude

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“Climb high. Sleep low.”

High carbohydrate diet

Mild exercise-avoid exertion

Avoid alcohol and sleeping medications

Other Aids to Acclimatization

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In the setting of a recent gain in altitude, there is precedence of headache and at least one of the following: • Gastrointestinal (anorexia, nausea or vomiting)

• Fatigue or weakness

• Dizziness or lightheadedness

• Difficulty sleeping

Lake Louis Consensus definitions of High Altitude Acute Mountain Sickness

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Rapid ascent to 8200 feet from altitudes below 5000 feet for unacclimatized

Headache • Throbbing, by temporal or occipital worse at night

Fatigue

Dizziness/lightheadedness

Anorexia and nausea

Difficulty sleeping

Acute Mountain Sickness

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Mild Headache

Insomnia

Shortness of Breath while Exercising

May continue climbing

More time for acclimatization

Mild Acute Mountain Sickness

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Headache may be severe

Some lassitude

Weakness

Loss of appetite

Nausea

Beginning to lose coordination - ataxia

Begin to descend

Moderate Acute Mountain Sickness

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Viral illness

Hangover

Exhaustion

Dehydration

Hypothermia

Sedatives/hypnotic medications

Carbon monoxide

Acute Mountain Sickness Differential Diagnosis

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Usually self-limited

If untreated may persist for weeks

May precede HACE or HAPE

Responds well to treatment

Acute Mountain Sickness

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In the presence of a recent gain in altitude, the presence of the following: • Two of the following symptoms:

• Dyspnea at rest

• Cough

• Chest tightness or congestion

• At least two of the following signs: • Crackles or wheezing and at least one lung field

• Central cyanosis

• Tachypnea

• Tachycardia

Lake Louis Consensus definitions of High Altitude High Altitude Pulmonary Edema (HAPE)

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The most common cause of death from high-altitude illness.

Most often after second night at new altitude

Apparent abrupt onset

May occur in the absence of Acute Mountain Sickness

High Altitude Pulmonary Edema

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Early symptoms: fatigue, weakness, dyspnea on exertion, dry cough

Progression to tachycardia, tachypnea, and orthopnea and dyspnea at rest – marked shortness of breath even at rest

Pink or blood-tinged sputum is a very late finding

Crackles usually start in right axilla

May also have headache, lassitude, reduced urine output, peripheral edema and ataxia.

HAPE Symptoms and Signs

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Severity Percent Symptoms

Mild 65 Headache, anorexia, nausea and malaise

Moderate 30 Unrelieved headache, vomiting, reduced urine output

Severe 5 Altered consciousness, ataxia, rales, cyanosis, dyspepsia at rest, possible papilledema

Distribution of Symptoms and signs in 154 Trekkers Nepal with AMS

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Study Group Number at Risk per Year

Sleeping Altitude (feet)

Maximum Altitude Reached (feet)

Average Rate of Assent (days low altitude)

Percent with AMS

Percent with HAPE and/or HACE

Western State Visitors

30 million 6500 ft. 8000 ft. >9800 ft.

11,500 ft. 1-2 18-20 22 27-42

0.01

Mount Everest

6000 18,000 ft. 1-2 (fly in) 10-13(walk)

47 23

1.6 0.05

Mount Denali 800 20,321 feet 3-7 30 2-3

Mount Rainier 6000 14,409 ft. 1-2 67 -

Indian soldiers Unknown 18,000 ft. 1-2 2.3-15.5

Incidents of Altitude Illness in Various Groups

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Can be considered “end-stage” or severe acute Mountain sickness. In the setting of a recent gaining altitude there is either: • The presence of a change in mental status and/or ataxia in a person

with Acute Mountain Sickness

• Or the presence of both mental status changes and ataxia any person without Acute Mountain Sickness

Lake Louis Consensus definitions of High Altitude High Altitude Cerebral Edema (HACE)

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Progression of cerebral signs and symptoms of Acute Mountain Sickness • Headache, vomiting

Truncal ataxia (other focal neurologic deficits may also occur)

Severe lassitude

Altered consciousness or coma

Weakness or paralysis on one side of the body

Amnesia or hallucinations

Especially common with High Altitude Pulmonary Edema - Shortness of breath, dry cough

High Altitude Cerebral Edema

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Late Symptoms • Ataxia (appendicular to

truncal) • Irrationality • Hallucinations • Visual disturbances • Focal neurological deficits • Abnormal reflexes

Early Symptoms • Headache • Anorexia • Nausea • Emesis • Photophobia • Fatigue • Irritability • Decrease socialization

High Altitude Cerebral Edema

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High-altitude retinopathy – maintain good fluid intake to reduce hemoconcentration, spontaneously resolves

Peripheral edema – treat with a diuretic in the absence of AMS, HACE or HAPE; condition spontaneously resolves on descent

Venous stasis and thrombotic complications – stay active keep well hydrated and descend if needed

Altitude pharyngitis and bronchitis – suck on hard candy, brie through a facemask and drink plenty of fluids

Ultraviolet keratitis ( snow blindness) – remove contact lenses, patch affected eye, use oral analgesics to decrease pain; prevented by wearing sunglasses

Other Altitude Related Disorders

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# 1 AMS symptoms at altitude are AMS until proven otherwise

# 2 Don’t ascend further if you have symptoms

# 3 Descend if very ill or not improving. Descend immediately for ataxia or decreased consciousness

#4 Don’t let anyone with AMS descend alone

Acute Mountain Sickness Management The Golden Rules

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Prevention • Acetazolamide (Diamox) 125 mg twice a day (or 500 mg slow release

daily)

• Start 12 hours before assent

• Continue first day at altitude

Sleep • Acetazolamide (Diamox) 62.5-280 mg at dinner time

Prevention Acute Mountain Sickness

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The mainstay of treatment of AMS is rest, fluids, and mild analgesics: acetaminophen (Tylenol), aspirin, or ibuprofen. These medications will not cover up worsening symptoms.

The natural progression for AMS is to get better, and often simply resting at the altitude at which you became ill is adequate treatment. Improvement usually occurs in one or two days, but may take as long as three or four days. • Dehydration is a common cause of headache at altitude. Drink one

liter of fluid, and take acetaminophen or aspirin. • If the headache resolves quickly and totally (and you have no other

symptoms of AMS) it is very unlikely to have been due to AMS.

Descent is also an option, and recovery will be quite rapid.

Treating Acute Mountain Sickness

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Stop ascent, rest, acclimatize at same altitude

Acetazolamide, 125 to 150 mg twice a day, to speed acclimatization

Symptomatic treatment as necessary with analgesics and anti-medics or

Descend 1500 feet or more

Treatment Mild Acute Mountain Sickness

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Low-flow oxygen, if available

Acetazolamide, 125 two 250 mg twice a day with or without Dexamethasone, 4 mg PO,IM, IV q 6hr

Hyperbaric therapy or Immediate descent

Treatment Moderate Acute Mountain Sickness

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0.14 atmosphere (102 torr) above ambient pressure

14,000 feet simulates 8000 feet

CO2 buildup minimal if used properly (and maybe helpful)

Instant Descent Inside a Bag

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Minimize exertion and keep warm

Oxygen, 4 to 6 L/min until improving it, then 2 to 4 L/min

Dexamethasone, 4 mg PO,IM, IV q 6hr

Treatment HAPE

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Graded ascent

Nifedipine for HAPE susceptibles • 20 mg orally every eight hours or 30 mg every 12 hours-starting 24

hours before arrival and continuing for three days

HAPE Prevention

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Tadalafil and Sildenafil

Phosphodiesterase-5 (PDE-5) inhibitors that augment the pulmonary vasodilatory effects of nitric oxide by blocking the degradation of cyclic guanosine monophosphate (cGMP), the intracellular mediator of nitric oxide. Nitric oxide is a potent pulmonary vasodilator and reduces hypoxic pulmonary vasoconstriction (HPV) and pulmonary hypertension in HAPE.

Both Tadalafil and sildenafil have been shown to be effective as prophylaxis for HAPE, but neither has been studied as treatment.

Nevertheless, based upon their mechanism of action, both Tadalafil and sildenafil may be effective adjunct treatments for established HAPE when neither oxygen nor descent is available options. These drugs may have advantages over nifedipine because they lower PA pressure with less risk of lowering systemic blood pressure. The appropriate dose for treatment is unknown but might be similar to that used for prophylaxis (Tadalafil 10 mg by mouth every 12 hours; sildenafil 50 mg by mouth every eight hours).

HAPE Prevention

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Dexamethasone 8 mg every 12 hours (also helps to prevent Acute Mountain Sickness)

Tadalafil 10 mg every 12 hours (no benefit for Acute Mountain Sickness)

Salmeterol 125 µg every 12 hours (some benefit for Acute Mountain Sickness)

All regimes start 24 hours prior to assent and continue at altitude

HAPE Prevention

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Dexamethasone • Indicated with contraindication to Acetazolamide

• Also used in conjunction with acetazolamide for rapid ascent above 10,000 feet (rescue)

• Dosage 4 mg every six hours

Other Drugs to Prevent Acute Mountain Sickness

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Immediate descent or evacuation

Oxygen, 2 to 4 L/min

Dexamethasone, 4 mg PO,IM, IV q 6hr

Hyperbaric therapy

Treatment HACE

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Rapid ascent to altitudes over 10,000 feet

Past history of recurrent Acute Mountain Sickness

Treatment of Acute Mountain Sickness

Periodic breathing or poor sleep

Indications for Acetazolamide

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Contraindications • Uncompensated left heart failure • Pulmonary hypertension • Sickle cell anemia • Moderate-severe COPD • Seizure disorders

Cautions • History of left heart failure • Cardiac arrhythmias • Cerebral vascular disease • Sleep apnea • Sickle Trait

High Altitude Medical Contraindications/Cautions

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Distribution of DCS

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Decompression sickness (DCS) results from the formation of nitrogen bubbles in the tissues or circulation as a result of inadequate elimination of nitrogen after a dive.

The formation of nitrogen bubbles may occur following a dive and ascending to high altitudes in a short period of time to include a pressurized commercial aircraft.

Bubbles that form are trapped in the joints called the “bends.”

Bubbles that are formed in circulation may become trapped in the brain or spinal cord resulting in serious neurological compromise or death.

DCS may also occur in very high altitudes with aircraft or spacecraft without a dive to precipitate the response.

Decompression Sickness

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Pulmonary DCS

Skin Bends

Inner Ear Decompression Sickness

Limb Bends

Central Nervous System (CNS) DCS

Cerebral Decompression Sickness

Decompression Sickness

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Dalton’s Law - in a mixture of non-reacting gases, the total pressure exerted is equal to the sum of the partial pressures of the individual gases.

Henry’s Law - the amount of dissolved gas is proportional to its partial pressure in the gas phase. In diving more gas is dissolved in solution when at pressure.

Gas Laws - Dalton and Henry

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Decompression Sickness

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Boyles Law - Air Embolism vs Bends

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Gas (air) entry into the circulation from ruptured pulmonary veins or patent foramen ovale

Air bubbles travel in the arterial blood supply and the tissues

Air bubbles become lodged in tissues blocking blood flow

Air Embolism

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Occurs within 2-3 minutes

Cardiac arrest or arrhythmias

Neurological focal paralysis, sensory disturbance, seizures, altered mental status

Air Embolism

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Physiological Atmospheric Divisions

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Pathophysiology of Bubbles in DCS

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Dive Table “Pushing Your Tables”

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Altitude Decompression Risk Assessment

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Altitude Decompression Risk Assessment

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Classification DCS

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Risks at Altitude

1. Can happen over 18k ft, especially repeated ascents

2. Is a substantial risk over 30k ft.

3. Is a much greater risk after diving.

4. Risk is related to altitude and rate of ascent.

5. In gliders, is a risk in wave flights.

6. In pressurized aircraft, is likely in depressurization accidents.

7. Can results in permanent injury.

1. Must seek a bariatric physician ASAP

2. 100% oxygen rebreathing

Two principal factors control the risk of a diver suffering DCS:

1.The rate and duration of gas absorption under pressure – the deeper or longer the dive the more gas is absorbed into body tissue in higher concentrations than normal (Henry's Law);

2.The rate and duration of outgassing on depressurization – the faster the ascent and the shorter the interval between dives the less time there is for absorbed gas to be offloaded safely through the lungs, causing these gases to come out of solution and form "micro bubbles" in the blood.

Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON). DON can develop from a single exposure to rapid decompression.

Principle Factors for DCS

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Symptoms Frequency and Onset

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“Skin Bends”

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Spinal Cord Bends – Infarction of Cord

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Bends Prevention

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DCS Management

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DCS Management US Navy Table 6

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DCS Management

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Important Safety Tip

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Questions