Altitude sickness

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Chronic mountain sickness (CMS) is also known as Monge’s disease, after its first description in 1925 by Carlos Monge. High Altitude Flatus Expulsion was first described by Joseph Hamel in c. 1820. It was rediscovered in 1981 by Paul Auerbach and York Miller. Altitude sickness may be classified according to clinical symptoms and the pathological changes of principally encroached organs into 2 groups acute and chronic. Altitude sickness caused by an increase in pulmonary artery pressure due to the normal pulmonary vasoconstriction induced by hypoxia. Hypoxia leads to increase oxygen delivery to the tissues and increases ventilation, cardiac output and haemoglobin concentrations. These changes improve ventilation-perfusion matching and gas exchange and lead to high altitude pulmonary hypertension. Altitude sickness is brought on by the combination of reduced air pressure and lower oxygen concentration that occur at high altitudes. Common risk factors in the development of altitude sickness include underlying lung disease, substances or conditions that interfere with acclimatization, previous history of high altitude sickness, lack of acclimatization. There is insufficient evidence to recommend routine screening for altitude sickness which include cold pressor test, heart rate variability, pulmonary function test. The important complications of altitude sickness are high altitude pulmonary edema and cerebral edema. Prognosis is generally good, and the 5 year mortality rate of patients with altitude sickness is approximately 12%. Patients with altitude sickness may have a positive history of underlying lung disease and substances or conditions that interfere with acclimatization. Common symptoms of altitude sickness include headache, dizziness, fatigue, cyanosis. Laboratory findings consistent with the diagnosis of altitude sickness include increased the level of hemoglobin, hematocrit and blood urea nitrogen and decreased level of bicarbonate, creatinine and PCO2. An ECG may be helpful in the diagnosis of altitude sickness. Findings on an ECG suggestive of altitude sickness include shortening of R-R interval, shortening of the lengthening of Q-T and in particular for the ST-T flattening and Increase of P wave. X-ray may be helpful in the diagnosis of complications of altitude sickness which include patchy alveolar infiltrates, predominantly in the right central hemithorax, asymmetric pattern of airspace consolidation. CT scan may be helpful in the diagnosis of complications of altitude sickness pulmonary edema and it shows patchy alveolar infiltrates, predominantly in the right central hemithorax. Pharmacologic medical therapies for altitude sickness include acetazolamide, dexamethasone. Pharmacologic therapy for nausea and vomiting of altitude sickness include promethazine, ondansetron. Effective measures for the primary prevention of altitude sickness include avoiding alcohol ingestion, high carbohydrate in diet, adequate hydration, vigorous exertion during the first few days at high altitude, oxygen Enrichment.

Chronic mountain sickness (CMS) is also known as Monge’s disease, after its first description in 1925 by Carlos Monge. High Altitude Flatus Expulsion was first described by Joseph Hamel in c. 1820. It was rediscovered in 1981 by Paul Auerbach and York Miller.

Altitude sickness may be classified according to clinical symptoms and the pathological changes of principally encroached organs into 2 groups acute and chronic.

Altitude sickness caused by an increase in pulmonary artery pressure due to the normal pulmonary vasoconstriction induced by hypoxia. Hypoxia leads to increase oxygen delivery to the tissues and increases ventilation, cardiac output and haemoglobin concentrations. These changes improve ventilation-perfusion matching and gas exchange and lead to high altitude pulmonary hypertension.

Altitude sickness is brought on by the combination of reduced air pressure and lower oxygen concentration that occur at high altitudes.

The incidence of altitude sickness is approximately 53,000 per 100,000 individuals worldwide. The prevalence and mortality rate of altitude sickness depends on altitude. Patients of all age groups may develop altitude sickness. The incidence of altitude sickness increases with age; the median age at diagnosis is 26-45 years. There is no racial predilection to altitude sickness. The majority of altitude sickness cases are reported in Kilimanjaro, Everest region of Nepal.

Common risk factors in the development of altitude sickness include underlying lung disease, substances or conditions that interfere with acclimatization, previous history of high altitude sickness, lack of acclimatization.

There is insufficient evidence to recommend routine screening for altitude sickness which include cold pressor test, heart rate variability, pulmonary function test.

The important complications of altitude sickness are high altitude pulmonary edema and cerebral edema. Prognosis is generally good, and the 5 year mortality rate of patients with altitude sickness is approximately 12%.

Patients with altitude sickness may have a positive history of underlying lung disease and substances or conditions that interfere with acclimatization. Common symptoms of altitude sickness include headache, dizziness, fatigue, cyanosis.

Physical examination of patients with altitude sickness is usually remarkable for headache, nausea, vomiting and lightheadedness.

Laboratory findings consistent with the diagnosis of altitude sickness include increased the level of hemoglobin, hematocrit and blood urea nitrogen and decreased level of bicarbonate, creatinine and PCO2.

An ECG may be helpful in the diagnosis of altitude sickness. Findings on an ECG suggestive of altitude sickness include shortening of R-R interval, shortening of the lengthening of Q-T and in particular for the ST-T flattening and Increase of P wave.

X-ray may be helpful in the diagnosis of complications of altitude sickness which include patchy alveolar infiltrates, predominantly in the right central hemithorax, asymmetric pattern of airspace consolidation.

CT scan may be helpful in the diagnosis of complications of altitude sickness pulmonary edema and it shows patchy alveolar infiltrates, predominantly in the right central hemithorax.

[MRI]] may be helpful in the diagnosis of complications of high altitude pulmonary edema and it shows increased T2 signal in the white matter of the splenium of the corpus callosum.

There are no other imaging findings associated with altitude sickness.

There are no other diagnostic studies associated with altitude sickness.

Pharmacologic medical therapies for altitude sickness include acetazolamide, dexamethasone. Pharmacologic therapy for nausea and vomiting of altitude sickness include promethazine, ondansetron.

Surgical intervention is not recommended for the management of altitude sickness.

Effective measures for the primary prevention of altitude sickness include avoiding alcohol ingestion, high carbohydrate in diet, adequate hydration, vigorous exertion during the first few days at high altitude, oxygen Enrichment.

There are no established measures for the secondary prevention of altitude sickness.

In order to help understand the factors that make some individuals susceptible to high altitude pulmonary edema (HAPE), the International HAPE Database was set up in 2004.^[1] Individuals who have previously suffered from HAPE can register with this confidential database in order to help researchers study the condition.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Chronic mountain sickness (CMS) is also known as Monge’s disease, after its first description in 1925 by Carlos Monge. High Altitude Flatus Expulsion was first described by Joseph Hamel in c. 1820. It was rediscovered in 1981 by Paul Auerbach and York Miller.

• Altitude sickness was first discovered by Paul Auerbach and York Miller in 1981.^[1]
• High Altitude Flatus Expulsion was first described by Joseph Hamel in 1820.^[2]
• The association between smoking and the development of altitude sickness was first discovered in 1986.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Altitude sickness may be classified according to clinical symptoms and the pathological changes of principally encroached organs into 2 groups acute and chronic.

• Altitude sickness may be classified according to clinical symptoms and the pathological changes of principally encroached organs into 2 groups: ^[1][2]
  • Acute
    • High altitude acute response (HAAR)
    • High altitude pulmonary edema (HAPE)
    • High altitude cerebral edema (HACE)
    • High altitude children cardiopathy (HACC).
  • Chronic
    • High altitude chronic response (HACR)
    • High altitude erythoblastosis (HAEb)
    • High altitude adult cardiopathy (HAAC)
    • High altitude hypertension (HAHyper)
    • High altitude hypotension (HAHypo)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Altitude sickness caused by an increase in pulmonary artery pressure due to the normal pulmonary vasoconstriction induced by hypoxia. Hypoxia leads to increase oxygen delivery to the tissues and increases ventilation, cardiac output and haemoglobin concentrations. These changes improve ventilation-perfusion matching and gas exchange and lead to high altitude pulmonary hypertension.

• It is believed that altitude sickness is secondary to body’s response to hypoxia due to low pressure at high altitude; not just normobaric hypoxia.
• This belief is due the the facts including:^[1]
  • Onset of symptoms occurs after a delay from onset of hypoxia; ranging from hours to days
  • It takes time for symptoms to reverse after oxygen therapy
• Physiological responses in mild to moderate altitude sickness includes:
  • Relative hypoventilation^[2][3]
  • Impaired gas exchange^[4]
  • Fluid retention and redistribution
  • Increased sympathetic drive^[5]
• Physiological responses in moderate to severe altitude sickness includes:
  • Raised intracranial pressure
  • Cerebral edema^[6]

Abbreviations: CBV= Cerebral blood volume, CBF= Cerebral or coronary blood flow, Pcap= Pulmonary capillary pressure, HACE= High-altitude cerebral edema, HAPE= High-altitude pulmonary edema ^{[8][9][10][11]}

Altitude hypoxemia

Brain

Lung

Vasodilation

Uneven vasoconstriction

↑CBV

↑CBF

↑PAP

Overperfusion

Focal/regional overperfusion

↑Pcap

↑Pcap

Vasogenic edema

Capillary leak

HACE

HAPE

• Monge disease is also known as chronic mountain disease, commonly present in individuals acclimatized to high altitudes.^[12]
• Monge disease is a maladaptive state due to hypoxia on high altitudes.
• SENP1 (an erythrocyte regulator) and ANP32D (an oncogene) present on chromosome 12q13 are commonly involved in Monge disease.
• Symptoms include severe polycythemia, headache, fatigue, somnolence, and depression.
• Blood viscosity is increased due to polycythemia leading to complications such as strokes and myocardial infarctions in early adulthood.

There is no gross pathologic findings associated with altitude sickness.

There is no microscopic findings associated with altitude sickness.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Altitude sickness is brought on by the combination of reduced air pressure and lower oxygen concentration that occur at high altitudes.

Altitude sickness may be caused by:^[1][2]

• Ascending to a great height too rapidly
• Live at or near sea level and travel to a high altitude
• Alcohol or other substances have interfered with acclimatization
• Medical problems involving the heart, nervous system, or lung

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell);

Organ system			Diseases	Clinical manifestations											Diagnosis					Other features
				Symptoms						Physical exam
				Loss of consciousness	Agitation	Weight loss	Fever	Chest pain	Cough	Cyanosis	Clubbing	JVD	Peripheral edema	Auscultation	CBC	ABG	Imaging	Spirometry	Gold standard
Acute Dyspnea	Respiratory system	Chest and Pleura, Lower airway	Bronchiolitis[1]	–	–	–	+	+/-	+	–	–	–	–	Wheeze and Crackles	↑WBC	Normal	Bronchovascular markings	↓Vt	Clinical assessment	Respiratory syncytial virus (RSV)
			COPD exacerbation[2]	–	+	–	+	+	+	+	+/-	+/-	+/-	Wheeze, Rhonchi, and Crackles	↑WBC, ↑RBC	Respiratory alkalosis	Hyperexpansion	↓ FEV1/FVC	Clinical assessment	Acute exacerbations of chronic bronchitis (AECB)
			Lung carcinoma[3]	–	–	+	–	–	+	+	+	–	–	Wheeze and Crackles	Normal	Normal	Mass lesion, hilar lymphadenopathy	↓Vt, ↑RV	Bronchoscopy	Paraneoplastic syndromes, such as SIADH and lambert-Eaton
			Pneumonia[4]	–	–	–	+	+	+	–	–	–	–	Wheeze, Rhonchi, and Crackles	↑WBC, neutrophilia	Normal	Lobar consolidation	Normal	Chest X-ray and CT Scan	productive cough
	Cardiovascular system		Pulmonary edema[5]	+/-	+	–	+	+	+	+	+	+	+	Basal crackle	Normal	Respiratory alkalosis	Bat wing pattern, air bronchograms	↓Vt, ↑RV	Cardiac Catheterization	Tachypnea
Chronic Dyspnea	Respiratory system	Chest and Pleura, Lower airway	Bronchiectasis[6]	–	–	–	+	+	+	+	+	–	–	Rhonchi, Wheezing, Crackles	↑WBC, neutrophilia	↓O2, ↑CO2	Tram-track opacities	↑ FEV1/FVC	High resolution computed tomography (HRCT)	Chronic productive cough
			Interstitial lung disease[7]	–	–	–	–	+	+	+	+	–	–	Rhonchi, Wheezing, Crackles	Normal	↓O2, ↑CO2	Peripheral pulmonary infiltrative opacification	↑ FEV1/FVC	High resolution computed tomography (HRCT)	Pneumoconiosis
			Sarcoidosis[8]	–	–	+/-	–	+/-	+	+	–	–	–	Crackles	Normal	↓O2, ↑CO2	Hilar adenopathy	↑ FEV1/FVC	High resolution computed tomography (HRCT)	Hypercalcemia, high ACE
			Alveolitis[9]	–	–	–	+	+	+	–	–	–	–	Basal crackle	↑WBC, neutrophilia	Normal	Basal reticulonodular opacification	↑ FEV1/FVC	High resolution computed tomography (HRCT)	Dry cough
			Cystic fibrosis[10]	–	–	+	+	–	+/-	+	+	–	–	Rhonchi, Wheezing, Crackles	Normal	Metabolic alkalosis	Thick-walled bronchiectasis	↓ FEF75%/FVC	Sweat test	Absent vas deferens
			Tuberculosis[11]	–	–	+	+	+	+	+/-	–	–	–	Rhonchi, Wheezing, Crackles	↑WBC	↓O2, ↑CO2	Patchy consolidation or poorly defined linear and nodular opacities	Restrictive, obstructive, or mixed	IFN-γ release assay (IGRA) Acid-fast staining	Night sweat
	Autoimmune		Wegener’s granulomatosis[12]	–	–	+/-	–	–	+	–	–	–	–	Wheezing, Crackles	↓ RBC	↓O2, ↑CO2	Cavitate nodules, ground-glass opacity	↓ FEV1/FVC	Biopsy demonstrating a granulomatous vasculitis	Chronic rhinosinusitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

The incidence of altitude sickness is approximately 53,000 per 100,000 individuals worldwide. The prevalence and mortality rate of altitude sickness depends on altitude. Patients of all age groups may develop altitude sickness. The incidence of altitude sickness increases with age; the median age at diagnosis is 26-45 years. There is no racial predilection to altitude sickness. The majority of altitude sickness cases are reported in Kilimanjaro, Everest region of Nepal.

• The incidence of altitude sickness is approximately 53,000 per 100,000 individuals worldwide.^[1][2]

• The prevalence of altitude sickness is approximately as following:^[2][3]
  • 9000 per 100,000 individuals of people at 2850 m
  • 13000 per 100,000 individuals of people at 3050 m
  • 34000 per individuals of people at 3650 m
  • 53,000 per 100,000 individuals of people at 4559 m

• The mortality rate of altitude sickness is approximately as following:^[4][5]
  • 289 per 100,000 individuals in men below 300 m of altitude
  • 242 per 100,000 individuals in men at altitudes above 1500 m
  • 104 per 100,000 individuals in women at below 300 m of altitude
  • 74 per 100,000 individuals in women at altitude 1500 to 1960 m

• Patients of all age groups may develop altitude sickness.^[6]
• The incidence of altitude sickness increases with age; the median age at diagnosis is 26-45 years.^[7]

• There is no racial predilection to altitude sickness.

• Female are more commonly affected by altitude sickness than male.^[5]

• The majority of altitude sickness cases are reported in Kilimanjaro, Everest region of Nepal.^[5][8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Common risk factors in the development of altitude sickness include underlying lung disease, substances or conditions that interfere with acclimatization, previous history of high altitude sickness, lack of acclimatization.

• Common risk factors in the development of altitude sickness include underlying lung disease, substances or conditions that interfere with acclimatization, previous history of high altitude sickness, lack of acclimatization.

• Common risk factors in the development of altitude sickness include:^[1][2][3]
  • Home elevation
  • Maximum altitude
  • Rate of ascent
  • Latitude
  • Age
  • Female sex
  • Intensity of exercise
  • Lack of acclimatization
  • Genetic make-up
  • Pre-existing diseases
  • Substances or conditions that interfere with acclimatization
  • Previous history of high altitude sickness
  • Sleeping altitude
  • Current respiratory infection

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

There is insufficient evidence to recommend routine screening for altitude sickness which include cold pressor test, heart rate variability, pulmonary function test.

• Screening among patients with altitude sickness include:^[1][2][3][4]
  • Cold pressor test
    • Put one hand above the wrist for 1 min in ice water (4-5°C)
    • Measuring blood pressure on the opposite arm at 15 seconds intervals
    • Difference between peak and basal blood pressure determines the level of vascular reactivity
  • Heart rate variability
    • Participants resting in supine position and wear a chest strap from a heart rate monitor watch
    • After 5 minutes rest period, heart rate is collected on a beat-by-beat basis for 10 minutes
  • Pulmonary function test
    • Measure flow-volume loop, maximal voluntary ventilation, forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC) and peak expiratory flow

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

The important complications of altitude sickness are high altitude pulmonary edema and cerebral edema. Prognosis is generally good, and the 5 year mortality rate of patients with altitude sickness is approximately 12%.

• Common complications of altitude sickness include:^[1]
  • Cerebral edema
  • Pulmonary edema
  • Respiratory distress
  • Retinal hemorrhage

• Prognosis is generally good, and the 5 year mortality rate of patients with altitude sickness is approximately 12%.^[2]

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