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High Altitude Illness
1) High altitude illness includes acute mountain sickness (AMS), high altitude cerebral edema (HACE), and high altitude pulmonary edema (HAPE). AMS causes headache, nausea, fatigue, and dizziness. HACE is a neurological deterioration in someone with AMS. HAPE causes cough, dyspnea, and chest tightness. (2) Risk factors for these illnesses include rapid ascent, exertion, prior history, age under 50, and underlying lung/heart conditions. (3) Treatment depends on the illness but may include descent, oxygen, medications like dexamethasone or nifedipine, and hyperbaric bags that simulate lower altitudes.
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High Altitude Illness
- 1. HIGH ALTITUDE ILLNESS Dr. ParthaDas ER, Fortis Hospital, Kolkata
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- 4. Lake Louise self-assessment AMSscoring system Each symptom is graded on a scale of 0–3; the presence of headache plus a score greater than or equal to 3 is usually considered positive for AMS. Mild AMS 2-4, Moderate AMS 5-9, Severe AMS >10 Ref: Rambam Maimonides Medical Journal January 2011w Volume 2w Issue 1w e0022 Headache None (0) to anticipating (3) GI symptoms None (0), mild nausea (1), moderate nausea/vomiting (2), severe nausea/vomiting (3) Fatigue/ Weakness None (0) to severe or incapacitating (3) Dizziness/ light headedness None (0) to incapacitating (3) ↓ sleep last night Slept well (0) to no sleep at all (3)
- 5. BLOOD GASES &ALTITUDE Ref: Tintinalli’s Emergency Medicine, 6th ed. Altitude (meters) PaO2 (mmHg) SaO2 % PaCO2 (mmHg) Sea level 90-95 96 40 1524 (5000 ft.) 75-81 95 35.6 2286 (7500 ft.) 69-74 92-93 31-33 4572 (15000 ft.) 48-53 86 25 6096 (20000 ft.) 37-45 76 20 7620 (25000 ft.) 32-39 68 13 8848 (29029 ft.) 26-33 58 9.5-13.8
- 6. RISK FACTORS Rapid ascent Physicalexertion at high altitudes (including climbing) P/H/O high altitude sickness Younger individuals (<50 years) Obesity Pre existing lung/cardiac disease Sleeping @ 7000-9000 ft.
- 7. AMS Typically occurs @altitudes > 2500m/8200ft C/F headache/dizziness Nausea/vomiting Fatigue/irritability (Often misdiagnosed as hangovers from alcohol) Generally benign & self limiting Onset : 4-12 hours after ascent
- 8. HACE • Cytotoxic ratherthan vasogenic • Progressive neurological deterioration in someone with AMS or HAPE. (seen rarely as an isolated entity) • May occur 12 hours after onset of AMS & requires 2-4 days for development • C/F: Headache Altered mental status Ataxia Nausea/vomiting Papilledema/ Retinal Hemorrhages CN palsies
- 9. FREQUENCY OF NEUROLOGICFEATURES IN 44 PATIENTS WITH HACE Table 1 lists the neurological findings in the largest series published to date (Dickinson, 1983) HIGH ALTITUDE MEDICINE & BIOLOGY Volume 5, Number 2, 2004 © Mary Ann Liebert, Inc. Disturbance of consciousness 31 (70%) Ataxia 27 (61%) Papilledema 23 (52%) Urinary retention/ incontinence 21 (48%) Abnormal plantar reflexes 15 (34%) Abnormal limb tone/ power 6 (14%) Abducens Nerve palsy 2 Anisocoria 2 Visual field loss 2 Speech difficulty 1 Hearing loss 1 Flapping tremor 1
- 10. HAPE • Usually occurs2-4 days after ascent • Life threatening • Usually at altitudes >2300m • C/F cough (usually dry→frothy +/- blood stained) Dyspnea (even at rest) Chest tightness Orthopnea/ Tachypnea Fever +/- Coarse crepitations on auscultation Cyanosis
- 11. PEOPLE AT RISKFOR HAPE • Pulmonary hypertension – Intra cardiac shunts – Patent ductus arteriosus – Drug-induced (Fenfluramine/ SSRIs) – Chronic venous thrombotic disease
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- 13. PEDIATRIC CONSIDERATIONS • AMS insmall children & infants can be manifested by :- • ↑ Fussiness • ↑ Irritability • ↓ Appetite & vomiting • Sleep disturbances
- 14. INVESTIGATIONS • HAPE • Bloodgas – E/o hypoxemia & respiratory alkalosis • CXR – Patchy alveolar infiltrates with batwing distribution Kerly B lines +/- • ECG – Sinus tachy E/o Right heart strain
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- 16. Contd… • HACE • CT/MR-Vasogenic edema of white matter
- 17. DIFFRENTIALS • AMS: Alcoholhangover CO poisoning (from wood combustions inside camps) Viral syndrome Encephalitis/ Meningitis • HAPE: High altitude bronchitis Pneumonia PE (more rapid onset + pleuritic chest pain) • HACE: CVA/TIA FND suggests vascular lesions
- 18. Grade based onACCP classification of clinical evidence for guidelines
- 19. MANAGEMENT HAPE: • Immediate evacuationto ↓ altitudes • O2 delivery or simulated descent in hyperbaric chamber/ Gamow bag • ET intubation for airway protection • Beta agonist inhalers & nebulization • Tab. Nifedipine 10mg stat, then 20-30 mg TID • Consider Furesemide Ref – Tintinalli’s emergency medicine, 6th ed.
- 20. Contd… Grade based onACCP classification of clinical evidence for guidelines
- 22. GAMOW BAG • Gamowbag uses ↑PaO2 for therapy of hypobaric injury • Inflated to simulate a ↓ altitude. • Advantage: portable for field use. • HAPE: 2-4 hours, HACE: 4-6 hours of treatment • Named after its inventor, Dr. Igor Gamow
- 23. Contd… HACE: • Immediate evacuationto ↓ altitude • Dexamethasone 8mg i/v stat, then 4mg i/v QID • Hyperbaric O2
- 24. Contd… AMS: • Acetazolamide 250-500mgBD (5mg/kg/day in 2- 3 divided doses) • Prophylaxis 250mg BD (start 24 hours before ascent) • Peds 5mg/kg BD • Paracetamol for headache • Promethazine/ Ondansetron for vomiting • Halt ascent until symptoms subside • Supplemental O2
- 25. PREVENTION • Gradual ascent(1000-1200 ft. per day) & also allowing time for pre-acclimatization • Low sleeping altitudes & avoid sleeping tablets • Keep warm & well hydrated • ↑ carb diet & avoid alcohol • Gingko Bilboa extract (80-120mg BD) • Acetazolamide 125-250mg BD or Dexa 4mg QID – 24 hours before or after ascent • Tadalafil (10mg BD to start 1 day prior ascent)
- 26. OTHER HIGH ALTITUDE CONDITIONS •High altitude bronchitis/ pharyngitis • Chronic mountain polycythemia • UV keratitis (snow blindness) • Peripheral edema • High altitude retinopathy • Acute exacerbation of COPD/CAD • Hypothermia
- 27. REFERENCES • Hackett PH,Roach RC: High-altitude medicine, in PA Auerbach (ed): Wilderness Medicine. St Louis, Mosby, 2001, p 2. • Emedicine.medscape.com • Tintinalli’s Emergency Medicine, 6th ed. • HIGH ALTITUDE MEDICINE & BIOLOGY Volume 5, Number 2, 2004, © Mary Ann Liebert, Inc. • www.radiopedia.com • HAPE Diagnosis, Prevention & Treatment (Vol.12 Number 2 March/April 2013 - Andre Pennardt, MD, FACEP, FAWM)
Editor's Notes
- #13 The pathogenesis is considered to be from the altered permeability of the alveolar-capillary barrier secondary to intense pulmonary vasoconstriction and high capillary pressure 1,4. This, in turn, induces endothelial leakage, which results in interstitial and alveolar oedema without diffuse alveolar damage.
- #16 B/L interstitial oedema with peribronchial cuffing. Batwing distribution. Kerley B lines +/-
- #17 MR is also helpful in confirming HACE & in evaluating causes of FNDs.