Mismanagement of Severe Altitude Illness in a Tertiary Hospital in Nepal: A Cautionary Tale

To the Editor:

High altitude pulmonary edema (HAPE) is a potentially lethal noncardiogenic pulmonary edema ¹ that accounts for the majority of deaths from high-altitude illness. ² The availability of health care facilities at high altitude in the Himalayas saves the lives of many trekkers, mountaineers, porters, and pilgrims. However, patients with HAPE that are airlifted to hospitals in Kathmandu (1300 m) are sometimes mismanaged because HAPE and high-altitude cerebral edema (HACE) are unfamiliar to these urban practitioners. We present the case of a porter who experienced HAPE and HACE and was mismanaged when he was airlifted to a hospital in Kathmandu.

A 28-year-old male porter, a resident of Nepal who was previously healthy, was part of a Korean team climbing Island peak (6189 m). He presented to the emergency department of a teaching hospital in Kathmandu with a 4-day history of fatigue and dizziness and a 3-day history of shortness of breath and cough.

The team started from Lukla (2680 m) and took 7 days to reach Island peak base camp (5100 m), where the patient reported headache, fatigue, and dizziness. The patient was started on acetazolamide 250 mg twice daily, which was provided by a nonmedical team member. The next morning, he felt better and continued to high camp (5600 m), but again in the evening, he reported headache, dizziness, fatigue, and nausea and vomited once. While helping team members fetch water and snow, he became ataxic and fell down. The same evening, he was assisted by another porter and descended to base camp, where he stayed overnight with an additional symptom of dry cough. The following day, the patient developed shortness of breath and coughs with pink frothy sputum and descended further to Dingboche (4410 m). He stayed overnight and was administered oxygen along with acetazolamide 250 mg. The next day, he was severely ataxic and fatigued and was evacuated on a stretcher from Tyangboche (3800 m) to Namche Bazar. At Namche Bazar, his oxygen saturation by pulse oximeter was reported as 37%. He was then airlifted to Kathmandu (1300 m).

At the teaching hospital, he appeared well and was oriented to time, place, and person, with blood pressure of 110/60 mm Hg, pulse of 82 beats·min^-1, respiratory rate of 26 breaths·min^-1, and improved saturation of 92% on room air. He was afebrile and acyanotic. On auscultation, coarse crackles were heard on bilateral basal lung fields. He was ataxic on tandem walking test, with otherwise normal neurological findings.

Red and white blood cell counts, electrolytes, urea, and creatinine were normal. Electrocardiogram showed normal sinus rhythm. Chest radiograph showed heterogeneous opacities in the left middle and lower zones and right lower zone (Figure 1). The patient was given intravenous (IV) furosemide 80 mg, oral acetazolamide 250 mg, and oral dexamethasone 8 mg, but oxygen was not administered. He was kept on observation overnight. He reported dizziness the next morning with a fall in blood pressure to as low at 70/40 mm Hg. He was then resuscitated with IV fluids. In the evening, the patient improved and decided to leave the hospital against the doctor’s advice with a blood pressure of 90/60 mm Hg, a saturation of 96% on room air, and no crackles on auscultation. Later, he reported feeling well at 1-week phone follow-up.

Figure 1

Chest radiograph of the patient showing heterogeneous opacities in the left middle and lower zones and right lower zone.

Our patient clearly experienced HAPE and HACE, as manifested by severe ataxia and radiograph showing patchy infiltrates in the lower and middle zones. The Wilderness Medical Society (WMS) ³ has devised evidence-based guidelines for the treatment of HAPE and HACE. The approach suggested for HAPE is descent, oxygen supplementation when available, and nifedipine as an adjunctive therapy. The WMS states that there is no role for diuretics in the treatment of HAPE, ³ and the International Climbing and Mountaineering Federation (UIAA) guideline clearly discourages the use of furosemide. ⁴ A hyperbaric bag (Gamow bag) can be used for both HAPE and HACE when descent is not possible, and its temporary use in extremis can improve a patient’s condition enough to necessitate less emergent evacuation.

Prompt descent to Namche Bazar and then to Kathmandu from 5600 m along with oxygen supplementation likely saved the life of our patient, as descent is the mainstay of treatment. Administration of dexamethasone 8 mg was indicated for the treatment of HACE. Because the patient was maintaining saturation (92%) in the hospital, the idea of observing the patient without administration of oxygen also was reasonable. However, the use of furosemide 80 mg IV is against the current WMS guidelines. The reason for the patient’s dizziness and hypotension was likely the administration of 80 mg IV furosemide in addition to acetazolamide. If not for his youth and lack of comorbidities, this patient could have had more complications (stroke, myocardial infarction) due to administration of furosemide.

The approach to management of patients with HAPE and HACE should be based on guidelines such as those put forth by WMS ³ and UIAA. ⁴ Especially in the tertiary centers of Nepal, which are more likely to treat these kinds of patients, following the established guidelines not only save lives, but it helps porters like our patient avoid spending money on unnecessary investigations because this population usually has no health insurance and has to pay out of pocket. It is imperative for physicians in tertiary hospitals of Kathmandu and other city centers who are increasingly seeing patients with HAPE and HACE being helicoptered down to be familiar with the pathophysiology and treatment of altitude illness; otherwise, more harm than good may occur.

This case was presented in abstract form at the 7th World Congress of Mountain & Wilderness Medicine, Telluride, CO. ⁵