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Manu Chopra
MD, DNB, MNAMS
Pulmonologist
 High altitude: 1500-3500m above sea level
 Very high altitude: 3500-5500m
 Extreme altitude: above 5500m
6April 2016 6
• Hackett PH, Roach RC. High
altitude medicine. Widerness
medicine 2007
Tibetan plateau &
Himalayan valleys
(8848m)
Andes
(6962m)
Ethiopian highlands (4620m)
ALTITUDETYPE FROM SEA-
LEVEL (In feet)
HIGH 8,000 – 12,000
VERY HIGH 12,000 – 18,000
EXTREMELY Above 18,000
Manali 2050m
Nainital 2084m Shimla 2205m
Srinagar 1585m
Mussoorie 2006m
Mt K2 8611m
Kanqchenjunga- 8,586 M
Mt Everest
8848m
Nanga Parbat 8126m Dhaulagiri 1 8167m
Thiksey monastery Leh
3650m
Ladakhi
Kedarnath
3553m
KorzokVillage Ladakh
4600m
KibberVillage
4270m
Tabo Monastery Spiti 3280m
 BAROMETRIC PRESSURE
 HEAVY SNOW
 WINDY CLIMATE
 FREEZINGTEMPERATURES
 DANGERS
 RADIATION
6April 2016 22
Barometric pressure versus altitude
Altitude (m) Altitude (feet)
Barometric
Pressure (mm
Hg)
Inspired PO2 (mm
Hg)
0 0 760.0 159.1
1,000 3,280 674.4 141.2
2,000 6,560 596.3 124.9
3,000 9,840 525.8 110.1
4,000 13,120 462.8 96.9
5,000 16,400 405.0 84.8
6,000 19,680 354.0 79.1
8,000 26,240 267.8 56.1
8,848 29,028 253.0 43.1
6April 2016 25
6April 2016 27
 A combination of air
temperature and
wind speed that
affects the freezing
rate of exposed
skin.
Wind Chill/Frostbite Chart
As this chart indicates, if the actual temperature is -200 F and the wind is blowing 15
mph, the cold effect on your bared skin is -450 F. At this temperature, frostbite can
begin in as little as 10 minutes.
6April 2016 30
−16 °C to -60 °C
6April 2016 31
6April 2016 32
5% increase in UV
rays/ 300m gain +
snow reflection
Air Lungs Blood Tissue
•Delivery of atmospheric O2 to the tissues normally involve 3
stages---with a drop in PO2 at each stage.
•When the starting PO2 is lower than normal, body
undergoes acclimatization so as to—
(i)↓ pressure drop during transfer
(ii)↑ oxygen carrying capacity of blood
(iii) ↑ ability of tissues to utilize O2
• Starts within 10- 15 min of exposure  1500m
• Mechanism
VENTILATORY ACCLIMATIZATION
Ascent to altitude
Hypoxia
Carotid body stimulation
Respiratory centres stimulation
Increased ventilation
Improved hypoxia
Decreased PCO2
CO2 + H2O H2CO3 HCO3
- + H+
 1.Ventilation & perfusion matching
 IncreasedVentilation = Increased cardiac output
Increased Pulmonary Perfusion
 Alveolar hypoxia triggers Hypoxic Pulmonary
vasoconstriction
-redistribution of blood flow to areas less
perfused at sea level
- improved gas exchange
LUNG DIFFUSION
Major rate limiting step
• High altitude   O2 diffusion, because of
– a lower driving pressure for O2 from the air to the
blood ( low Po2)
–  and inadequate time for equilibration ( decreased
transit Time)
– Long term adaptation – diffusing capacity increases
Cardiac output increases
Tachycardia:
Increased catecholamine release & sensitivity
Also d/t peripheral chemo. Response  CO 
oxygen delivery to the tissues
Stroke Vol decreases
 Increase in Hb conc in 1-2 days
 initially – hemoconcentration ( diuresis)
 later – increased RBC production due to
increased erythropoietin
 Hypoxia is the primary stimulus for
erythropoietin secretion
 Se erythropoietin levels increase in 24-48 hrs
decline within 3 weeks
 Plasma to cytoplasm – 10mmHg
 Cytoplasm to mitochondria – 1-2mmHg
 Diminished ms fibre
 Increased myoglobin conc
 Increased levels of enzymes involved in
oxidative phosphorylation
 Cerebral Blood flow
Cerebral bld flow increases initially due to hypoxia
Hypocapnia cerebral vasoconstriction bld flow
decreases
 13% greater than sea level
 Improved O2 delivery
 Motor, sensory & cognitive abilities impair
 New tasks are learned with difficulty at
3048m
 Short term memory impaired
 Arterial So2 85% - impair concentration and
fine motor coordination
 Arterial So2 75% - poor judgement and
irritability
 Diuresis & natriuresis
 Peripheral venous constriction →
increased central volume →
decreased ADH and aldosterone →
diuresis →
decreased plasma volume and hyperosmolality.
 Cheyne-Stokes Respirations
 Above 10,000 ft (3,000 m) most people experience a periodic
breathing during sleep.The pattern begins with a few shallow
breaths increases to deep sighing respirations  falls off
rapidly.
 During period of breathing-arrest, person often becomes
restless & may wake with a sudden feeling of suffocation.
 Can disturb sleeping patterns exhausting the climber.
 O2 & acetazolamide help
 At high altitude air is thin. To make up for it, the
blood gets thick, respiration ↑ & circulation
improves, provided adequate time is given &
body functions properly  still some limitations
remain as implied!!!
• Process by which people gradually adjust to high altitude
• Determines survival and performance at high altitude
• Series of physiological changes
 O2 delivery
hypoxic tolerance +++
• Acclimatization depends on
• severity of the high-altitude hypoxic stress
• rate of onset of the hypoxia
• individual’s physiological response to hypoxia
Acclimatisation
6April 2016 50
 FIRST STAGE ACCLIMAZATION(Above 2700 m and up to
3600 m):The acclimatization period will be for 6 days as
under:
 (i) First and second day: Rest except for short walks in the
unit lines only, not involving any climbs.
 (ii) Third and fourth day: walk at slow pace for 1.5 -3Km
avoid steep climbs.
 (iii) Fifth and sixth day: walk upto 5 Km and climb upto 300
m at a slow pace.
6April 2016 51
 SECOND STAGE ACCLIMATIZATION(Above 3600 m and
up to 4500 m):This is carried out for 4 days as under:
 (i ) First & Second day: Slow walk for a distance for 1.5 -3 Km avoid
steep climbs.
 (ii) Third day: slow walk and climb upto 300 m.
 (iii) Fourth day: Climb 300 m without equipment.
 THIRD STAGE ACCLIMATIZATION:(Above 4500 m):This
also lasts for 4 days and is on the same lines as second stage
acclimatization.
6April 2016 52
maladaptation
ACUTE
 Acute Mountain Sickness
 High Altitude Pulmonary
Oedema
 High Altitude Cerebral
Oedema
CHRONIC
 Chronic Mountain Sickness
 Pulmonary Arterial
Hypertension of HA
 High altitude retinopathy
 UV keratitis
 Thrombotic episodes
 Hypothermia
 Local cold injury
(A) Chilblains
(B) Trench foot
(C) Frost bite
6April 2016 55
Relationships of the Different
Forms of Altitude Illness
Altitude illness may be an interrelated spectrum :
AMS HAPE
HACE
Acute Mountain Sickness :
Etiology
22-50% travellers
Typically occurs at altitude > 8000 feet
Rarely occurs at altitude 6000 to 8000 feet
No predeliction based on gender
More likely if :
• Rapid ascent
• Lack of acclimatization
• Exertion soon after arrival
• Alcohol intake
• Sedatives (sleeping pills)
• Narcotics
Acute Mountain Sickness :
Pathophysiology
Much individual variation in susceptibility
Likely mild cerebral oedema develops
 “Tight fit hypothesis”
 Symptoms:
▪ Headache
+
▪ Fatigue
▪ Nausea &Vomiting
▪ Impaired night vision
▪ Anorexia
▪ Dizziness
▪ Sleep Disturbance
 Signs: no characteristic finding
▪ Mild tachycardia
▪ Peripheral oedema
▪ Crackles
Acute Mountain Sickness :
Differential Diagnosis
Dehydration
Hypothermia
Exhaustion
Alcohol hangover
Respiratory/ CNS infection
Psychiatric disorders
Carbon monoxide poisoning
 Mild
 Rest and stop ascent
 Descend if not
improved after 24
hours
 Drink fluids
 Simple analgesics
Resolves 1-3 days
 Moderate/Severe
 Descend ≥ 100m
 Acetazolamide
 Dexamethasone
 Hyperbaric O2
 Prevention
 Following acclimatization
protocols
 Medications
6April 2016 62
Progression of Acute Mountain
Sickness
If ascent is continued or accelerated
by a patient with untreated AMS, HAPE
or HACE may occur and death may
result
 Usually get AMS before HACE
 Mental status changes +/ ataxia
 Confusion, ataxia, stupor
 focal neurologic signs
 May lead to coma, irreversible neurological
damage or death
 Incidence 0.53% - 1.25%
 Other causes of encephalopathy
 CO poisoning
Hypertensive crisis
Hypoxia
Meningitis
Hypoglycemia
Hypothermia
 Ataxia (e.g. poor heel – toe walking)
 Focal neurological signs
Papilloedema & retinal
haemorrhages
 IMMEDIATE DESCENT
 Do NOT wait until morning if HACE occurs at
night
 Oxygen
 Hyperbaric bag (to facilitate descent if
necessary NOT replace it)
 Dexamethasone
 Commonest cause (54%)of Hospital admission due
to HAA related illnesses
 Most common cause of death from high altitude
illness.
• Until 1960 – Pneumonia
• 1960 - Pulmonary edema (Houston)
6April 2016 69
Non cardiogenic pulmonary edema
 Manifests within 2-4 days of ascent >2400m
(8000 feet)
 2nd night
 Pulmonary hypertension
 Exaggerated Hypoxic Pulmonary vasoconstriction
 High levels of ET1
 Increased sympathetic tone
 Lower levels of NO
 Uneven hypoxic vasoconstriction
 Pulmonary Endothelium Fragility
 Abnormal alveolar fluid resorption
 Symptoms: AMS
 Reduced exercise
tolerance
 Dry cough
 Dyspnea at rest
 Blood stained sputum
 Mental changes
 Signs: better than expected
 Tachycardia
 Tachypnoea
 Low grade fever
 Pallor
 Cyanosis
 Crackles
 Signs of RV strain
▪ RV heave, Loud P2
 Pneumonia
 Pulm embolism
 MI
 Asthma
 Pulm Infarction
6April 2016 73
6April 2016 74
General Specific
Descent
Rest – carry the patient
Hydration
Hyperbaric chamber
Oxygen - CPAP
Drug therapy
Nifedipine
Tadalafil/ sildenafil
 Acclamatisation
 Drugs
Nifedipine
Salmetrol
Tadalafil
Dexamethasone
6April 2016 76
6April 2016 77
6April 2016 78
Avalanche
 50 to 100 miles per hour
Can be as fast as 200 miles per
hour
Can generate impact pressures
> 150 lbs/square inch
 (can destroy even concrete
structures)
Occur with greatest frequency
on slopes of 30 to 45 degrees
Causes of death in avalanche
Direct impact trauma of snow blocks or ice
Indirect trauma of hitting against objects
such as trees or rocks
Hypoxia from encasement in snow
Hypothermia
Restrictive chest compression
Radiation Exposure
 High altitude retinopathy
 UV keratitis
 pain, photophobia, tearing,
erythema, chemosis, eyelid
swelling
 24 h to heal, analgesics and cold
comp.
 Wear sunglasses
 UV dermatitis
Miscellaneous Altitude Related
Medical Problems
Immune suppression
–probably related to tissue hypoxia
–wounds slower to heal & more likely to get infected
–wound infections can show antibiotic resistance
Prothrombotic state leading to various Thrombosis
High altitude peripheral edema
 Khumbu cough
 Purulent bronchitis and painful throat near
universal at very high altitude
 respiratory heat loss, bronchospasm and mucosal
cracking (dry and cold effects)
 coughing can lead to rib #s
 Antibiotics no use
 wear your balaclava – there are face masks that
act as HME
 1. Chronic mountain sickness- due to
excessive erythrocytosis
 Described in 1928 Monge’s disease
 Young and middle aged men
 Low Landers who ascend to HA
 High Landers with / without respiratory disease
 Increased blood volume, PAH, haematocrit >60%
 CNS symptoms dominate
 Plethoric florid faces, dark red conjunctiva, haemorrage below nail
 2. High altitude pulmonary hypertension
 Without polycythemia
 Non Freezing
Chilblain
Trench foot
 Freezing
Frost bite
Chilblains
Medical problems in high altitude- Height does matter
Medical problems in high altitude- Height does matter
Medical problems in high altitude- Height does matter
Medical problems in high altitude- Height does matter
Medical problems in high altitude- Height does matter
Medical problems in high altitude- Height does matter
Medical problems in high altitude- Height does matter

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Medical problems in high altitude- Height does matter

  • 1. Manu Chopra MD, DNB, MNAMS Pulmonologist
  • 2.
  • 3.
  • 4.
  • 5.
  • 6.  High altitude: 1500-3500m above sea level  Very high altitude: 3500-5500m  Extreme altitude: above 5500m 6April 2016 6 • Hackett PH, Roach RC. High altitude medicine. Widerness medicine 2007 Tibetan plateau & Himalayan valleys (8848m) Andes (6962m) Ethiopian highlands (4620m)
  • 7. ALTITUDETYPE FROM SEA- LEVEL (In feet) HIGH 8,000 – 12,000 VERY HIGH 12,000 – 18,000 EXTREMELY Above 18,000
  • 8.
  • 9. Manali 2050m Nainital 2084m Shimla 2205m Srinagar 1585m Mussoorie 2006m
  • 10. Mt K2 8611m Kanqchenjunga- 8,586 M Mt Everest 8848m Nanga Parbat 8126m Dhaulagiri 1 8167m
  • 11. Thiksey monastery Leh 3650m Ladakhi Kedarnath 3553m KorzokVillage Ladakh 4600m KibberVillage 4270m Tabo Monastery Spiti 3280m
  • 12.
  • 13.
  • 14.
  • 15.
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22.  BAROMETRIC PRESSURE  HEAVY SNOW  WINDY CLIMATE  FREEZINGTEMPERATURES  DANGERS  RADIATION 6April 2016 22
  • 24. Altitude (m) Altitude (feet) Barometric Pressure (mm Hg) Inspired PO2 (mm Hg) 0 0 760.0 159.1 1,000 3,280 674.4 141.2 2,000 6,560 596.3 124.9 3,000 9,840 525.8 110.1 4,000 13,120 462.8 96.9 5,000 16,400 405.0 84.8 6,000 19,680 354.0 79.1 8,000 26,240 267.8 56.1 8,848 29,028 253.0 43.1
  • 26.
  • 28.  A combination of air temperature and wind speed that affects the freezing rate of exposed skin.
  • 29. Wind Chill/Frostbite Chart As this chart indicates, if the actual temperature is -200 F and the wind is blowing 15 mph, the cold effect on your bared skin is -450 F. At this temperature, frostbite can begin in as little as 10 minutes.
  • 30. 6April 2016 30 −16 °C to -60 °C
  • 32. 6April 2016 32 5% increase in UV rays/ 300m gain + snow reflection
  • 33.
  • 34. Air Lungs Blood Tissue •Delivery of atmospheric O2 to the tissues normally involve 3 stages---with a drop in PO2 at each stage. •When the starting PO2 is lower than normal, body undergoes acclimatization so as to— (i)↓ pressure drop during transfer (ii)↑ oxygen carrying capacity of blood (iii) ↑ ability of tissues to utilize O2
  • 35. • Starts within 10- 15 min of exposure  1500m • Mechanism VENTILATORY ACCLIMATIZATION Ascent to altitude Hypoxia Carotid body stimulation Respiratory centres stimulation Increased ventilation Improved hypoxia Decreased PCO2 CO2 + H2O H2CO3 HCO3 - + H+
  • 36.  1.Ventilation & perfusion matching  IncreasedVentilation = Increased cardiac output Increased Pulmonary Perfusion  Alveolar hypoxia triggers Hypoxic Pulmonary vasoconstriction -redistribution of blood flow to areas less perfused at sea level - improved gas exchange
  • 37. LUNG DIFFUSION Major rate limiting step • High altitude   O2 diffusion, because of – a lower driving pressure for O2 from the air to the blood ( low Po2) –  and inadequate time for equilibration ( decreased transit Time) – Long term adaptation – diffusing capacity increases
  • 38. Cardiac output increases Tachycardia: Increased catecholamine release & sensitivity Also d/t peripheral chemo. Response  CO  oxygen delivery to the tissues Stroke Vol decreases
  • 39.
  • 40.  Increase in Hb conc in 1-2 days  initially – hemoconcentration ( diuresis)  later – increased RBC production due to increased erythropoietin  Hypoxia is the primary stimulus for erythropoietin secretion  Se erythropoietin levels increase in 24-48 hrs decline within 3 weeks
  • 41.
  • 42.  Plasma to cytoplasm – 10mmHg  Cytoplasm to mitochondria – 1-2mmHg  Diminished ms fibre  Increased myoglobin conc  Increased levels of enzymes involved in oxidative phosphorylation
  • 43.  Cerebral Blood flow Cerebral bld flow increases initially due to hypoxia Hypocapnia cerebral vasoconstriction bld flow decreases  13% greater than sea level  Improved O2 delivery
  • 44.  Motor, sensory & cognitive abilities impair  New tasks are learned with difficulty at 3048m  Short term memory impaired  Arterial So2 85% - impair concentration and fine motor coordination  Arterial So2 75% - poor judgement and irritability
  • 45.
  • 46.  Diuresis & natriuresis  Peripheral venous constriction → increased central volume → decreased ADH and aldosterone → diuresis → decreased plasma volume and hyperosmolality.
  • 47.  Cheyne-Stokes Respirations  Above 10,000 ft (3,000 m) most people experience a periodic breathing during sleep.The pattern begins with a few shallow breaths increases to deep sighing respirations  falls off rapidly.  During period of breathing-arrest, person often becomes restless & may wake with a sudden feeling of suffocation.  Can disturb sleeping patterns exhausting the climber.  O2 & acetazolamide help
  • 48.  At high altitude air is thin. To make up for it, the blood gets thick, respiration ↑ & circulation improves, provided adequate time is given & body functions properly  still some limitations remain as implied!!!
  • 49. • Process by which people gradually adjust to high altitude • Determines survival and performance at high altitude • Series of physiological changes  O2 delivery hypoxic tolerance +++ • Acclimatization depends on • severity of the high-altitude hypoxic stress • rate of onset of the hypoxia • individual’s physiological response to hypoxia Acclimatisation
  • 51.  FIRST STAGE ACCLIMAZATION(Above 2700 m and up to 3600 m):The acclimatization period will be for 6 days as under:  (i) First and second day: Rest except for short walks in the unit lines only, not involving any climbs.  (ii) Third and fourth day: walk at slow pace for 1.5 -3Km avoid steep climbs.  (iii) Fifth and sixth day: walk upto 5 Km and climb upto 300 m at a slow pace. 6April 2016 51
  • 52.  SECOND STAGE ACCLIMATIZATION(Above 3600 m and up to 4500 m):This is carried out for 4 days as under:  (i ) First & Second day: Slow walk for a distance for 1.5 -3 Km avoid steep climbs.  (ii) Third day: slow walk and climb upto 300 m.  (iii) Fourth day: Climb 300 m without equipment.  THIRD STAGE ACCLIMATIZATION:(Above 4500 m):This also lasts for 4 days and is on the same lines as second stage acclimatization. 6April 2016 52
  • 54. ACUTE  Acute Mountain Sickness  High Altitude Pulmonary Oedema  High Altitude Cerebral Oedema CHRONIC  Chronic Mountain Sickness  Pulmonary Arterial Hypertension of HA
  • 55.  High altitude retinopathy  UV keratitis  Thrombotic episodes  Hypothermia  Local cold injury (A) Chilblains (B) Trench foot (C) Frost bite 6April 2016 55
  • 56. Relationships of the Different Forms of Altitude Illness Altitude illness may be an interrelated spectrum : AMS HAPE HACE
  • 57. Acute Mountain Sickness : Etiology 22-50% travellers Typically occurs at altitude > 8000 feet Rarely occurs at altitude 6000 to 8000 feet No predeliction based on gender More likely if : • Rapid ascent • Lack of acclimatization • Exertion soon after arrival • Alcohol intake • Sedatives (sleeping pills) • Narcotics
  • 58. Acute Mountain Sickness : Pathophysiology Much individual variation in susceptibility Likely mild cerebral oedema develops  “Tight fit hypothesis”
  • 59.  Symptoms: ▪ Headache + ▪ Fatigue ▪ Nausea &Vomiting ▪ Impaired night vision ▪ Anorexia ▪ Dizziness ▪ Sleep Disturbance  Signs: no characteristic finding ▪ Mild tachycardia ▪ Peripheral oedema ▪ Crackles
  • 60. Acute Mountain Sickness : Differential Diagnosis Dehydration Hypothermia Exhaustion Alcohol hangover Respiratory/ CNS infection Psychiatric disorders Carbon monoxide poisoning
  • 61.  Mild  Rest and stop ascent  Descend if not improved after 24 hours  Drink fluids  Simple analgesics Resolves 1-3 days  Moderate/Severe  Descend ≥ 100m  Acetazolamide  Dexamethasone  Hyperbaric O2  Prevention  Following acclimatization protocols  Medications
  • 63. Progression of Acute Mountain Sickness If ascent is continued or accelerated by a patient with untreated AMS, HAPE or HACE may occur and death may result
  • 64.  Usually get AMS before HACE  Mental status changes +/ ataxia  Confusion, ataxia, stupor  focal neurologic signs  May lead to coma, irreversible neurological damage or death  Incidence 0.53% - 1.25%
  • 65.  Other causes of encephalopathy  CO poisoning Hypertensive crisis Hypoxia Meningitis Hypoglycemia Hypothermia
  • 66.  Ataxia (e.g. poor heel – toe walking)  Focal neurological signs Papilloedema & retinal haemorrhages
  • 67.  IMMEDIATE DESCENT  Do NOT wait until morning if HACE occurs at night  Oxygen  Hyperbaric bag (to facilitate descent if necessary NOT replace it)  Dexamethasone
  • 68.
  • 69.  Commonest cause (54%)of Hospital admission due to HAA related illnesses  Most common cause of death from high altitude illness. • Until 1960 – Pneumonia • 1960 - Pulmonary edema (Houston) 6April 2016 69
  • 70. Non cardiogenic pulmonary edema  Manifests within 2-4 days of ascent >2400m (8000 feet)  2nd night
  • 71.  Pulmonary hypertension  Exaggerated Hypoxic Pulmonary vasoconstriction  High levels of ET1  Increased sympathetic tone  Lower levels of NO  Uneven hypoxic vasoconstriction  Pulmonary Endothelium Fragility  Abnormal alveolar fluid resorption
  • 72.  Symptoms: AMS  Reduced exercise tolerance  Dry cough  Dyspnea at rest  Blood stained sputum  Mental changes  Signs: better than expected  Tachycardia  Tachypnoea  Low grade fever  Pallor  Cyanosis  Crackles  Signs of RV strain ▪ RV heave, Loud P2
  • 73.  Pneumonia  Pulm embolism  MI  Asthma  Pulm Infarction 6April 2016 73
  • 74. 6April 2016 74 General Specific Descent Rest – carry the patient Hydration Hyperbaric chamber Oxygen - CPAP Drug therapy Nifedipine Tadalafil/ sildenafil
  • 79.
  • 80.
  • 81. Avalanche  50 to 100 miles per hour Can be as fast as 200 miles per hour Can generate impact pressures > 150 lbs/square inch  (can destroy even concrete structures) Occur with greatest frequency on slopes of 30 to 45 degrees
  • 82. Causes of death in avalanche Direct impact trauma of snow blocks or ice Indirect trauma of hitting against objects such as trees or rocks Hypoxia from encasement in snow Hypothermia Restrictive chest compression
  • 83. Radiation Exposure  High altitude retinopathy  UV keratitis  pain, photophobia, tearing, erythema, chemosis, eyelid swelling  24 h to heal, analgesics and cold comp.  Wear sunglasses  UV dermatitis
  • 84. Miscellaneous Altitude Related Medical Problems Immune suppression –probably related to tissue hypoxia –wounds slower to heal & more likely to get infected –wound infections can show antibiotic resistance Prothrombotic state leading to various Thrombosis High altitude peripheral edema
  • 85.  Khumbu cough  Purulent bronchitis and painful throat near universal at very high altitude  respiratory heat loss, bronchospasm and mucosal cracking (dry and cold effects)  coughing can lead to rib #s  Antibiotics no use  wear your balaclava – there are face masks that act as HME
  • 86.  1. Chronic mountain sickness- due to excessive erythrocytosis  Described in 1928 Monge’s disease  Young and middle aged men  Low Landers who ascend to HA  High Landers with / without respiratory disease  Increased blood volume, PAH, haematocrit >60%  CNS symptoms dominate  Plethoric florid faces, dark red conjunctiva, haemorrage below nail  2. High altitude pulmonary hypertension  Without polycythemia
  • 87.  Non Freezing Chilblain Trench foot  Freezing Frost bite