High-Altitude Illness — SAQ

Stem

A 26-year-old fit male Indian Army soldier is deployed to a forward post in eastern Ladakh at 4300 m. He flew in from sea level the previous day, was driven directly to altitude and slept at the post overnight. On the morning of the second day he reports a bilateral throbbing headache, nausea and poor sleep, which he attributes to tiredness. By evening he is staggering when he walks, confused and drowsy. An hour later his tent-mate is found to be breathing fast at 32/min with a dry cough that is now producing pink frothy sputum, cyanosed, with bibasal crackles and an SpO2 of 72% on room air. Both have been cooking inside the closed tent. The medical post has oxygen, a portable hyperbaric bag and a limited pharmacy (acetazolamide, dexamethasone, nifedipine).^[3][19][20]

Questions

a) What two life-threatening diagnoses have developed, and which single clinical sign clinches each? (2 marks)

The soldier has developed high-altitude cerebral oedema (HACE) — the cardinal sign is ataxia (staggering, cannot walk a straight line heel-to-toe), accompanied by confusion and drowsiness. Ataxia at altitude is HACE until proven otherwise. His tent-mate has developed high-altitude pulmonary oedema (HAPE) — the cardinal features are exertional dyspnoea progressing to dyspnoea at rest with a dry then pink-frothy cough, cyanosis, bibasal crackles and a marked fall in SpO2 (72% is a marked fall; treat as HAPE rather than quoting an unsourced expected SpO2 band for 4300 m). Both syndromes are caused by ascent to altitude under hypobaric hypoxia and are fatal if untreated.^[19]

b) Outline the immediate field management of BOTH patients. State the definitive treatment. (2 marks)

For both, the definitive treatment is immediate descent — AMS/HACE typically 300 to 1000 m; HAPE at least 1000 m or until symptoms resolve. The immediate field bundle is: stop all ascent; high-flow oxygen by mask targeting SpO2 over 90%; sit the HAPE patient upright, keep both warm and at rest; begin descent (carry the ataxic/confused HACE patient — never let an ataxic patient descend unaided as he will fall); use the portable hyperbaric chamber as a temporising measure if descent is impossible (weather, terrain, darkness) — it must not delay descent; and administer the specific adjuncts (see c, d).^[3][9]

c) For the HACE patient, give the drug, dose, route, timing and mechanism. State one precaution. (2 marks)

Drug: dexamethasone. Dose: 8 mg loading then 4 mg every 6 hours, orally (or IM/IV if unable to swallow). Mechanism: reduces vasogenic cerebral oedema by stabilising the blood-brain barrier; consciousness typically improves within hours. Precaution: dexamethasone and oxygen buy time, they do not cure — never let them delay descent; rebound cerebral oedema occurs on abrupt withdrawal, so taper after recovery. WMS: acetazolamide may be added as an adjunct to dexamethasone in HACE, with dexamethasone remaining primary; a published field case used 250 mg twice daily. Do not invent an 8-hourly HACE acetazolamide dose. Do not give sedatives, opioids or benzodiazepines — they blunt the hypoxic ventilatory drive.^[3][12]

d) For the HAPE patient, give the WMS nifedipine regimen and the WMS rules on diuretics and PDE-5 inhibitors. (2 marks)

Drug: nifedipine 30 mg extended-release orally every 12 hours or 20 mg extended-release every 8 hours (WMS 2019). A short-acting 10 mg loading dose is no longer used (hypotension). Mechanism: calcium-channel blockade lowers pulmonary artery pressure. Do not combine nifedipine with sildenafil or tadalafil. PDE-5 inhibitors are for HAPE treatment only if descent, oxygen/hyperbaric AND nifedipine are unavailable. Salmeterol is not recommended for HAPE prevention (WMS 2B) and has no treatment recommendation. WMS: diuretics should not be used for HAPE (Grade 1C). Do not invent morphine/nitrate “contraindications” as WMS HAPE rules.^[3][9][17]

e) The group cooked inside the closed tent. State one mimic of AMS that you must exclude before attributing the soldier's morning headache to AMS, and the bedside finding that points to it. (1 mark)

Carbon monoxide poisoning — from cooking inside a closed tent. Suspicion is heightened when multiple group members are affected and symptoms resolve when the stove is extinguished. The bedside clue is that pulse oximetry reads falsely normal (the device cannot distinguish carboxyhaemoglobin from oxyhaemoglobin); confirmation requires a co-oximeter (arterial blood gas) measuring carboxyhaemoglobin. Treatment: move to fresh air and 100% oxygen; fatal CO exposure has occurred from a cook stove in a closed tent at altitude, and mild-to-moderate CO poisoning mimics AMS. Do not quote unsourced CO half-life numbers here.^[20]

f) Name three preventive measures that, if applied to future troop deployments, would reduce the incidence of high-altitude illness. (1 mark)

1. Graded, staged ascent — "climb high, sleep low"; above 3000 m, sleeping elevation not more than 500 m per day and a rest day every 3 to 4 days (WMS 2019). Do not teach a 2700–3000 m Indian AF band as a Roach 2018 result.
2. Pharmacological prophylaxis — acetazolamide 125 mg every 12 h (WMS prophylaxis); nifedipine 30 mg ER q12h or 20 mg ER q8h for HAPE-susceptible individuals.
3. Education and field discipline — recognise early symptoms and stop ascending with any AMS; never cook inside closed tents; avoid alcohol, sedatives and opioids; ensure hydration and a high-carbohydrate diet; carry oxygen, a portable hyperbaric chamber and the standard pharmacy; never let an ataxic patient descend unaided.^[3]

References28ShowHide

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