Wilderness and Environmental Medicine, 11, 99-101 (2000)

CASE REPORT

A tragic report of probable high-altitude pulmonaryedema in the Himalayas: preventive implicationsTORREY GOODMAN, MD, FACEP; BUDDHA BASNYAT, MD, MSc, FACP

From Kaiser Permanente, Department of Emergency Medicine, Honolulu, Hawaii (Dr Goodman) and the Himalayan Rescue Association,Nepal International Clinic, Patan Hospital, Kathmandu, Nepal (Dr Basnyat).

High-altitude pulmonary edema (HAPE) is a well-recognized disease entity in trekkers to the NepalHimalayas. We present the case of a patient who had clinical features consistent with HAPE but didnot descend the mountain on time, which contributed to his death. The important factors of thediagnosis, the descent, and the follow-up in Kathmandu are examined.

Key words: high-altitude pulmonary edema, Nepal Himalayas, trekkers

Introduction

High-altitude pulmonary edema (HAPE) is a life-threat­ening form of altitude sickness that has been describedextensively in the literature. I- 4 However, except for astudy4 in 1983, little information from the Himalayashas been published regarding the host of situational fac­tors that may contribute to serious outcomes, includingdeath. This case report illustrates several of those factors,and we examine how they may be avoided.

Case

A 37-year-old, overweight European man on an orga­nized trek presented to the Himalayan Rescue Associa­tion (HRA) clinic at 3500 m in the Annapurna regionof Nepal. His rate of ascent had been conservative. Hecomplained of extreme fatigue of 2 days' duration andshortness of breath accompanying exertion. There wasno cough, dyspnea at rest, orthopnea, or paroxysmalnocturnal dyspnea. He had no significant past medicalhistory and did not smoke tobacco or drink alcohol. Fur­ther discussion revealed that he had no prior strenuoushiking experience and had never been at high altitude(above 2500 m). He denied any headache, nausea, vom­iting, diarrhea, anorexia, or incoordination, and he hadbeen eating and drinking fluids without difficulty. Hisphysical examination was completely unremarkable; he

Corresponding author: Buddha Basnyat, MD, MSc, FACp' NepalInternational Clinic, Lal Durbar GPO Box 3596, Kathmandu. Nepal(e-mail: nic@naxal.wlink.com.np).

had clear lung fields, no respiratory distress, no periph­eral edema, and no ataxia. His blood pressure was 130180 and his pulse was 110 beats per minute. Since a pulseoximeter was not available, we had the patient run ap­proximately 50 m and then observed his respiratory pat­tern. His respiratory rate was initially increased, as ex­pected, but returned to the resting rate of 18 breaths perminute after 1 minute. It was felt that his fatigue anddyspnea on exertion could possibly be due to HAPE.Therefore, the patient and his trek leader were advisedthat he should not continue his ascent toward a 5500-mpass. Because English was not their primary language,an interpreter gave them clear instructions about the se­riousness of the problem and the need for a prompt de­scent.

Unbeknownst to the physicians, the patient remainedat 3500 m while awaiting a flight out from a nearbyvillage airstrip. During that time, he remained alone ina lodge and became progressively sicker. His shortnessof breath worsened substantially; eventually, he was un­able to get out of bed without difficulty. Neither he norhis porter, whom the group had entrusted for his carewhile they continued their trek, recognized the severityof his symptoms, so they did not try to contact the phy­sicians at the HRA aid post. After 4 days, when thepatient tried to mount a horse to ride to the airfield, hecollapsed and was brought to the aid post by bystanders.

On his arrival at the HRA aid post, 4 days after hisinitial presentation, he was severely short of breath atrest and had a respiratory rate of 40 breaths per minute.He had a frequent, dry, wheezy cough, and was only

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able to speak 3 to 4 words between breaths. He stilldenied any nausea, vomiting, or headache but had noteaten anything in 2 days and had only drunk a smallamount of tea. He had a blood pressure of 140/90 anda pulse of 130 beats per minute, and he was afebrile.His pharynx was dry, there was no jugular venous dis­tension, and lung sounds revealed only very slight crack­les in the right middle and lower lobes. The cardiac andgastrointestinal exams were unremarkable, and there wasno peripheral edema.

Based on the Lake Louis criteria, the diagnosis ofHAPE was made, and the patient was given oxygen 2Llmin for half an hour, 10 mg of nifedipine, and 250 mgof acetazolamide orally, and placed in a hyperbaric bagfor 4 hours. He had a transient episode of hypotensionshortly after the nifedipine was given. After coming outof the hyperbaric bag, he was much improved and hada respiratory rate of 20 breaths per minute, and the rightlung crackles were resolved. The patient was kept at theclinic through the night and was encouraged to drinksubstantial amounts of fluids. His status worsened againafter 4 hours when he was noted to have a respiratoryrate of 32 breaths per minute while sleeping and, whenawakened, was barely able to stand because of weaknessand dyspnea. His lungs once again had only very slightcrackles, and the frequent dry cough continued. He wasplaced back in the hyperbaric bag for another 4 hoursand arrangements were initiated for helicopter evacua­tion. The helicopter was not able to arrive for another 8hours, during which time the patient was given inter­mittent oxygen, beta-agonist inhaler treatments, acet­azolamide, and 2 L of warm oral fluids. No further ni­fedipine was given because of the transient decrease inhis blood pressure after his first dose. His respiratorystatus slowly improved, his lungs became clear, and hisresting respiratory rate decreased to 18 breaths per mi­nute. However, when the helicopter arrived, there wasstill substantial dyspnea with any exertion, and the pa­tient had not urinated in over 12 hours; however, therewas no palpable bladder distension or urge to urinate.

When the helicopter arrived, verbal and written re­ports were given to the doctor on board. This physicianapparently had no experience regarding acute mountainsickness (AMS) or HAPE. On arrival in Katmandu, thepatient went directly to his hotel rather than being seenat a travel medicine clinic or a hospital. The patient wasassigned a room on the third floor of a hotel without anelevator. After going to his room for a while, he returneddownstairs and was found to be very short of breath. Adoctor was called, but unfortunately, the patient died be­fore the arrival of the doctor.

Goodman and Basnyat

Discussion

In summary, at 3500 m in the Nepal Himalayas, a 37­year-old German trekker presented with a disease entityconsistent with RAPE. However, because of a delay indescent, the patient's condition worsened. When the pa­tient was finally evacuated, he was taken to his hotel andnot evaluated in a medical setting. He died in the hotel.

This case illustrates several factors that are commonlypresent in deaths from altitude-related illnesses in theHimalayas. The first significant error was that, once itwas determined that the patient needed to descend, hisgroup left him alone with a porter that had no knowledgeof AMS or HAPE and did not speak his language. Thishappens regularly every season in the Himalayas. If agroup member has to descend, it is mandatory thatsomeone from the party who speaks the patient's lan­guage and understands AMS needs to accompany himor her.

This case report also illustrates the importance of rec­ognizing patients with the probable diagnosis of HAPE,and that HAPE may be characterized by extreme fatigueand dyspnea caused by ordinary exertion without othersymptoms or signs. A careful history and physical ex­amination of the patient and the careful observation ofthe evolution of the disease process is essential in allcases of altitude-related illnesses. This is especially truein the case of HAPE, because it may not be precededby signs and symptoms of AMS such as headache andnausea,5 and it may not initially qualify for the LakeLouise criteria.

Although the patient's presentation was in keepingwith HAPE, he had no obvious high-altitude cerebraledema and was given acetazolamide-a substance thathas no known useful effect on HAPE. In fact, somewould argue that if he had respiratory acidosis due tosevere RAPE, acetazolamide would be contraindicated.Hence, the administration of this drug could be ques­tionable, although studies have shown that people withsevere HAPE may have high-altitude cerebral edema(for which acetazolamide would be useful) and vice ver­sa.6

Another important factor here was the language bar­rier between the patient and the physician. Perhaps thephysician speaking in English was perceived to not haveappropriately articulated the gravity of the situation, and,equally likely, the patient and the trip leader who didnot speak English fluently may have failed to grasp theimportance of descent. Even with other disease entitiessuch as gastroenteritis, language barriers are known byone of us (B.B.) to play havoc with diagnosis and treat­ment in travel clinics in Kathmandu, especially whenEnglish is not the main medium of communication.

High-altitude pulmonary edema

Last, this case highlights the fact that physicians whoassume care for patients with altitude-related illnessesmust have experience in this field. When this patient wasfinally evacuated, he had improved substantially but wasstill quite ill. Hospitalization, or at least reevaluation, ata clinic with physicians experienced in altitude medi­cine, was warranted upon arrival in Katmandu. The phy­sician on the helicopter who accepted care of this patientmay have made an error in judgment if he allowed thepatient to simply go to his hotel alone, unless, of course,the patient refused further medical attention once inKathmandu. Even though rapid recovery after descent isthe rule for altitude sickness, hospitalization with bedrest, oxygen, and, rarely, mechanical ventilation may berequired for patients severely affected with HAPE.7

The major limitation of this case report is that thediagnosis of HAPE in this patient was based solely onthe clinical criteria. In this overweight patient at highaltitude, pulmonary embolism alone or in coexistencewith HAPE could easily account for his sudden death.However, cycles of improvement and deterioration afterhyperbaric bag treatment on 2 occasions would seem tosuggest HAPE as the primary process. Hyperbaric treat­ment bags only help to buy time, and the positive effectsalmost always wear off over time if descent is not in­stituted promptly. Myocardial infarction, because the pa­tient had no chest pain, is a less likely diagnosis. Hyp­oxemia due to HAPE or pulmonary embolism could cer­tainly have triggered a fatal arrhythmia. Pneumonia mayhave been concurrently present with HAPE but wasprobably not the primary cause because this young pa­tient remained afebrile. Valvular heart disease is also un­likely because the cardiac examination was normal. Inshort, we clearly do not know the exact cause of thepatient's death, but his presentation was certainly inkeeping with HAPE, and at high altitude, it is safest toassume that the symptom complex as presented here is

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related to altitude illness so that descent should beprompt.

In conclusion, this case illustrates several situationalfactors that are commonly present in altitude-relateddeaths in the Himalayas. The most significant one is thata patient should never be left alone, or with someoneunable to care for them, while the rest of the party con­tinues on its trek. Second, timely descent should alwaysbe the rule, and this must be clearly communicated toall parties involved. Third, there should be a high indexof suspicion for HAPE in patients who complain of ex­treme fatigue and dyspnea on exertion at altitude re­gardless of whether they have other signs of AMS orHAPE. And last, medical care of individuals with alti­tude-related illnesses should only be undertaken by med­ical professionals with specific training in this specialty.

References

1. Hultgren HN. High altitude pulmonary edema: current con­cepts. Ann Rev Med. 1996;47:267-284.

2. Grissom CK, Elstad MR. The pathophysiology of high al­titude pulmonary edema. Wilderness Environ Med. 1999;10:88-92.

3. Bezruchka S. High altitude medicine. Med Clin North Am.1992;76:1481-1497.

4. Dickinson J, Heath D, Gosney J, Williams D. Altitude re­lated deaths in seven trekkers in the Himalayas. Thorax.1983;38:646-656.

5. Lake Louise consensus on definition and quantification ofaltitude illness. In: Sutton JR, Coates' G, Houston CS, eds.Hypoxia: Mountain Medicine. Burlington, VT: Queen CityPress; 1992:327-330.

6. Hackett PH, Roach RC. High altitude medicine. In: Auer­bach PS, ed. Wilderness Medicine Management of Wilder­ness and Environmental Emergencies. 3rd ed. St Louis,MO: Mosby; 1995:1-37.

7. Litch lA. Endotracheal intubation and mechanical ventila­tion following respiratory arrest from high altitude pulmo­nary edema. Wilderness Med J. 1999;170:174-176.