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- 1. Directorate of Health Services, Kashmir. HIGH ALTITUDE ILLNESS- Prevention & Management. DR. MOHD YOUSUF NATH MBBS; M.D(INTERNAL MEDICINE) Physician specialist Govt Gousia Hospital
- 2. OUTLINE INTRODUCTION PHYSIOLOGY AT HIGH ALTITUDE HIGH ALTITUDE ILLNESSES Acute Mountain Sickness(AMS) High Altitude Cerebral Edema(HACE) High Altitude Pulmonary Edema(HAPE) RISK FACTORS PREVENTION TREATMENT
- 3. INTRODUCTION Thousands of locals, tourists, religious travellers, trekkers, mountaineers and skiers are attracted to mountainous areas of Kashmir throughout the year. Anyone who travels to high altitude is at risk of developing high-altitude illness. Many people planning high-altitude travel are likely to have a pre-existing medical condition. Appropriate acclimatization is able to prevent altitude (hypoxia) related illnesses.
- 4. Purpose of going to high altitude Amaranth cave 5486 m
- 5. Men at work
- 8. Phase 2 Gandola Height 4200 m
- 11. How high is High altitude? High altitude is usually defined as a height above 2500 meters. However, physiologically, High Altitude> 1500 meters ALTITUDE METERS FEET HIGH 1,500–3,500 (Gulmarg= 2650m) 5,000–11,500 VERY HIGH 3,500–5,500 (Amarnath Cave= 3888m, Kolohai Peak =5425m) 11,500–18,000 EXTREME >5,500m (Mt. Everest= 8849m, K2= 8611 m) >18,000
- 14. Although the risk of acute altitude illness begins with an ascent above 2000 m, and particularly above 2500 m, some persons with chronic medical conditions are at risk at lower elevations. It is long known that the increasing level of hypoxemia due to the reduced inspired oxygen partial pressure with gain in altitude is the primary reason for developing acute mountain sicknesses.
- 15. Hypoxia at high altitude
- 16. High altitude Hackett, PH, Roach, RC. High-Altitude Medicine. In: Wilderness Medicine, 5th ed
- 18. PATHOPHYSIOLOGY AT HIGH ALTITUDE As a person ascends , PI02 decreases which leads hypobaric hypoxemia which in turn stimulates peripheral chemoreceptors and causes increase in ventilation and minute ventilation also increases . This is known as hypoxic ventilatory response. Increase in ventilation causes decrease in pco2 causing respiratory alkalosis. In absence of acclimatization and renal compensatory mechanism , respiratory alkalosis depresses central chemoreceptors thereby decreases ventilation and causes hypoxia . At high altitude , there is increase in sympathetic activity thereby increasing HR,BP,CO,venous tone . Despite increase in HR ,SV is diminished because of low plasma volume due bicarbonate diuresis ,shift of fluid from intravascular spaces and suppression of aldosterone ,
- 19. In reponse to hypoxia , there is cerebral vasodilation which leads to intracellular edema, leading to extravascular ionic edema. Then vasogenic edema with protein extravasation and ultimately loss of integrity of the BBB with extravasation of red cells and micro-hamorrhages. According to tight – fit hypothesis ,persons with a large brain to cranial vault ratio become more symptomatic than individuals with a smaller ratio. The pulmonary vasculature constricts in response to hypoxia resulting in increase in PVR and PA pressure. An exaggerated increase in PA pressure and PVR is associated with susceptibility to HAPE In acclimtation ,a key mediator is hypoxia-inducible factor(HIF), a gene transcription factor that serves as the master regulator of cellular responses to hypoxia, including cellular metabolism, angiogenesis,and erythropoiesis.
- 21. HIF Wilson DF, Roy A, Lahiri S: High Altitude Med Biol 6:97–111, 2005 Cellular adaptation to hypoxia
- 22. Peter Bärtsch et al; Circulation. 2007;116:2191-2202
- 23. AT RISK GROUPS Persons with lung diseases of sufficient severity, such as COPD, Interstitial lung disease or cystic fibrosis. Cyanotic congenital heart disease Obesity Pul. Art. HTN Hemoglobinopathies Pregnancy( in case of high risk pregnancy) Past h/o High Altitude Illness. Poorly controlled Diabetics H/O Seizure disorder.
- 24. Contraindications to Travel above 2500 m. Advanced COPD (FEV1 <30% of predicted value or requirement for continuous oxygen therapy) Advanced cystic fibrosis (FEV1 <30% of predicted value) Advanced restrictive lung disease (TLC <50% of predicted value or requirement for continuous oxygen therapy) Decompensated heart failure High-risk pregnancy Myocardial infarction or stroke within the past 90 days Poorly controlled seizure disorder Pulmonary hypertension (systolic PAP >60 mm Hg) Sickle cell disease Unstable angina Untreated, high-risk cerebrovascular abnormality(aneurysm or AV malformation)
- 25. ACUTE HIGH ALTITUDE ILLNESS • Acute mountain sickness (AMS) • High altitude cerebral edema (HACE) • High altitude pulmonary edema (HAPE)
- 28. AMS 50% at 3500m Most at 5000m Females > Males ETOH hangover Resolves in average 15 hours, max 4 days Symptoms: Headache Fatigue Nausea & Vomiting Impaired night vision Anorexia Dizziness Sleep Disturbance Signs: Mild tachycardia Peripheral oedema Ataxia may represent severe AMS or HACE Mild:3-5 Moderate: 6-9 Severe: 10-12
- 30. D/D - AMS • Clinical history • No confirmatory laboratory tests • Supplemental oxygen may be used to support the clinical diagnosis • Differentials : – dehydration – hypothermia – exhaustion – alcohol hangover – carbon monoxide poisoning – respiratory or cerebral infections
- 31. Mx Mild Moderate to Severe ◦ Rest and stop ascent ◦ Descend if not improved after 24 hours ◦ Drink fluids ◦ Simple analgesics ◦ Low flow oxygen if available ◦ Descend ◦ Acetazolamide ◦ Dexamethasone ◦ Hyperbaric O2 (Gamow bag) • Continue for 24 -72 hours after symptoms resolve or descent accomplished Symptoms resolve following descent of 300 to 1000 m. Required descent vary between persons
- 32. IMMEDIATE DESCENT DEXAMETHASONE HYPERBARIC BAG HACE Progressive decline of mental function & consciousness Usually get AMS before HACE Behavioural change Hallucinations Disorientation & confusion Decreased consciousness Coma Headache not responding to NSAIDs and associated vomiting indicates probable progression of AMS to HACE BUDDY SYSTEM Ataxia (e.g. poor heel – toe walking) Focal neurological signs Papilloedema & retinal haemorrhages False sense of security when symptoms diminish NIGHT • Does not facilitate acclimatization and further ascent should be delayed until the patient is asymptomatic while off the medication
- 33. Copyrights apply
- 35. Descent • Descent remains the single best treatment for AMS and HACE • Should descend until symptoms resolve • Symptoms resolve following descent of 300 to 1000 m • Required descent vary between persons Tom Smedley & Michael PW Grocott, British J pain 2013
- 36. Acetazolamide • 125 to 250 mg orally every 12 hours • Continue for 24 hours after symptoms resolve or descent accomplished • Relieves symptoms, improves arterial oxygenation, and prevents further impairment of pulmonary gas exchange • Accelerates acclimatisation process Grissom CK et al; Ann Intern Med. 1992;116 (6):461.
- 37. Dexamethasone • Does not facilitate acclimatization and further ascent should be delayed until the patient is asymptomatic while off the medication • 8-mg dose (IM/IV/PO) followed by 4 mg q6h until symptoms resolve • False sense of security when symptoms diminish Tom Smedley & Michael PW Grocott, British J pain 2013
- 38. Noticed only after 24-48hr and occurs after the 2nd night Appears better than expected for the severity of hypoxemia Rapid correction of the SpO2 and clinical status with supplemental O2 in the setting of a severe infiltrative lung process seen on radiograph is virtually pathognomonic for HAPE CXR - patchy alveolar infiltrates, predominantly in the right central hemithorax, which become more confluent and bilateral as the illness progresses USG – Ultrasound lung comets HAPE
- 39. PATHOPHYSIOLOGY Pulmonary edema Raised Capillary pressure Permeability Edema formation Hypoxia Exaggerated pulmonary vasoconstriction (non uniform)
- 40. • Supplemental O2 and Rest - mild to moderate HAPE • Supplemental O2 is first-line therapy • Descent atleast 500 to 1000 m • Gamow Bag • Pharmacology
- 41. Pathophysiology - HAPE Maladaptive responses to the hypoxia
- 42. Oxygen therapy • Supplemental O2 and rest while remaining at high altitude are sufficient treatment for mild to moderate HAPE • Supplemental O2 is first-line therapy – reduces pulmonary artery (PA) pressure – reverses capillary leak – reduces both the heart and respiratory rates
- 43. Descent / Hyperbaric chamber • Atleast 500 to 1000 m • Passive descent recommended • Also treats acute mountain sickness • Portable hyperbaric chamber – good temporizing measure before definitive therapy – if oxygen is not available – descent is unsafe or impossible
- 44. Pharmacologic therapy • Nifedipine • PDE5 inhibitors – Sildenafil – Tadalafil – Strong physiologic rationale present, but no studies have evaluated therapeutic benefit
- 45. Copyrights apply
- 47. Simplified treatment regimen for various high-altitude illnesses.