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Year : 2018  |  Volume : 2  |  Issue : 3  |  Page : 48-50

Essence of time in high altitude pulmonary edema – A case report

Department of Anaesthesia, Government Medical College and Hospital, Chandigarh, India

Date of Web Publication25-Feb-2019

Correspondence Address:
Ravneet Kaur Gill
Department of Anaesthesia, Government Medical College and Hospital, Sector 32, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sccj.sccj_31_18

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High-altitude sickness can present with numerous symptoms ranging from headache, blurring of vision, dyspnea on exertion to more critical events such as pulmonary edema and cerebral edema. Rapid ascent, high altitudes of >2500 m, and previous lung disorders are the predisposing factors. Rapid and aggressive management forms the core treatment. Mechanical ventilation should be instituted at the earliest to prevent fatal consequences. Most of the cases are managed at medical centers at high altitudes only. Utmost coordination is required between centers for rapid management. Here, we report a case which was referred to our institute located at foothills with high-altitude pulmonary edema for intensive management.

Keywords: Acute mountain sickness, altitude sickness, high-altitude pulmonary edema

How to cite this article:
Rathi U, Gill RK, Saroa R, Saxena P. Essence of time in high altitude pulmonary edema – A case report. Saudi Crit Care J 2018;2:48-50

How to cite this URL:
Rathi U, Gill RK, Saroa R, Saxena P. Essence of time in high altitude pulmonary edema – A case report. Saudi Crit Care J [serial online] 2018 [cited 2023 Jun 7];2:48-50. Available from: https://www.sccj-sa.org/text.asp?2018/2/3/48/252893

  Introduction Top

Pulmonary edema is a life-threatening disease. High-altitude sickness is a preventable entity. It has a wide spectrum of symptoms ranging from headache, retinal hemorrhages, and peripheral edema to more severe events such as pulmonary edema or cerebral edema, which may end in fatality. Early and aggressive management is the mainstay of treatment to prevent further morbidity and mortality. Most of the patients are treated at nearby medical facilities owing to the necessity for urgent intervention. We had an experience of a patient with high-altitude pulmonary edema (HAPE) who was referred from a hospital to our medical institute, which is located in the foothills of Himalayas, in view of nonavailability of adequate medical resources there.

  Case Report Top

A 25-year-old male (165 cm, 55 kg) student by profession was referred to our institute with a history of breathlessness for 1 day after a trip from a hill station (4000 m from the sea level). He complained of difficulty in breathing and slurring of speech with generalized weakness (which was acute in onset), after which he was admitted to a local hospital where decision for tracheal intubation was taken in view of nonmaintenance of oxygen saturation (SpO2) and referred to higher center for further management as they lacked the necessary expertise and equipment for intensive management. He was received in the emergency department of our institute with 8.0-mm endotracheal tube in situ and SpO2 of 91%. The condition of the patient was assessed and the decision to shift the patient to our intensive care unit was taken. Hemodynamically, the patient was stable. History of frothy secretions was documented. General physical examination was normal. On auscultation of the chest, the patient had bilateral crepitations and decreased air entry in both the lung bases. Rest of the systemic examination was normal. A chest x-ray reported bilateral homogeneous opacities, mostly in the middle zone and lower zone. As the trachea was already intubated, he was then treated with ventilatory support on synchronized intermittent mechanical ventilation with pressure control mode with tidal volume of 450 ml, respiratory rate of 12 min, positive end-expiratory pressure of 12 cm H2O, pressure support of 15 cm H2O, and fraction of inspired oxygen (FiO2) of 100%. Gradually the SpO2 improved to 94%, after which FiO2 was gradually decreased and titrated to maintain the SpO2 of ≥94%. He was sedated with infusion of injection midazolam at 2 ml/h and injection morphine 2 mg/h. Intravenous (IV) injection methylprednisolone 15 mg was given stat, followed by 15 mg infusion over 24 h. IV injection dexamethasone 4 mg tds was also advised.

All blood investigations were within the normal limits. Initially, the arterial blood gases revealed hypoxemia (PaO2 of 57 mmHg) and compensated respiratory alkalosis. After mechanical ventilation, hypoxemia and respiratory alkalosis were resolved, serial chest X-rays showed improvement corresponding with clinical condition [Figure 1] and [Figure 2].
Figure 1: Radiological image showing multiple opacities on admission

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Figure 2: Radiological image showing improvement in the lung parenchyma

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The patient was gradually weaned off from ventilatory support and after adequate criteria of weaning were met, spontaneous breath trial was given which was successful after which the trachea was extubated and treated with noninvasive ventilation for 1 day. Next day, the patient was maintained on venturi mask on oxygen at 6 liters per minute. After 2 days of monitoring, he was shifted to ward on nasal prongs in stable condition.

  Discussion Top

High-altitude illness may manifest with milder symptoms such as headache, dyspnea on exertion to fatal pulmonary, and cerebral edema. The incidence for acute mountain sickness is 15%–40%, whereas the fatal complication comprises only 1% of the spectrum. There is no gender difference in acute mountain sickness, but men tend to develop HAPE more than the female.[1]

Pulmonary edema resulting from high altitude is commonly seen in individuals ascending to altitude of ≥2500 m from the sea level. High-altitude sickness may involve lungs (HAPE) or the central nervous system (high-altitude cerebral edema). The most common cause of mortality from high-altitude sickness is due to HAPE. Individuals with the previous history of similar events are predisposed to the condition as it has a recurrence rate of 60%.[2] Other risk factors which increase the incidence of HAPE is fast ascent, altitudes of >2500 m from sea level, preexisting lung infections, sickle cell disease, pulmonary hypertension, atrial septal defect, and patent foramen ovale.[3]

Various theories have been postulated which show a genetic predisposition to HAPE. At the molecular level, various pathways are involved in the pathogenesis which include renin–angiotensin–aldosterone system, nitric oxide pathway, and hypoxia-inducible factor pathway.[4],[5] Localized areas of pulmonary capillaries stress failure are characteristic of HAPE. High altitudes lead to physiological response in the body, which is characterized by increase in respiratory rate, increase in heart rate, but with a lower stroke volume. Longer exposure leads to polycythemia, increase in myoglobin, and hypoxic pulmonary vasoconstriction.[6]

Kurtzman and Caruso advocate pretreatment with a carbonic anhydrase inhibitor, oxygen inhalation, and proper hydration to reduce the risk.[7] Initial presentation of HAPE includes breathlessness, dyspnea on exertion, headache, and chest congestion. As the disease advances, bilateral coarse crepts and pink frothy sputum are seen. Arterial blood gas analysis mostly show hypoxemia and respiratory alkalosis. Similar findings of arterial blood gas analysis were seen in our patient.[6]

To prevent HAPE, the major predictor is the rate of ascent which should be gradually over few days. It should not exceed 350 m/day, as it will provide ample time for the body to acclimatize to the new altitude.[3] However, once an individual starts to show the spectrum of HAPE, the patient should be brought to 1000 m as soon as possible and oxygen therapy started with an aim to maintain the SpO2 of >90%.

Few drugs have been found to play a role in reversing the effect. These include phosphodiesterase inhibitors, such as tadalafil or sildenafil, which cause pulmonary vasodilation and decrease pulmonary artery pressure, thus providing relief.[8] Another physiological challenge is to maintain normothermia as it will reduce the sympathomimetic effects of hypothermia.

Steroid cover will lead to decrease in pulmonary artery pressure. The recommended dose of dexamethasone is 8 mg initially followed by 4 mg every 6 h.[9] Nitric oxide inhalation[10] and portable hyperbaric bags such as Gamow bag[11] both have shown improvement in the clinical picture.

Our patient also received intensive treatment at the earliest which fastened the process of recovery. The decision of tracheal intubation and mechanical ventilation at the primary medical facility with the aim to maintain the SpO2 of >90% was lifesaving. The adjuvant drug therapy also plays a role in the recovery. This entity demands aggressive management at the earliest to prevent the fatal consequences. Our institute rarely sees such cases as most of these are handled at the nearby centers only. Even so, such cases should be managed with paramount enthusiasm. Such cases are given the first line of management at medical center located at high altitudes only. Apt care received at this point can change the course of the disease. The medical centers should be suitably equipped as well as the staff properly trained. The higher centers most deal with cases toward end of the spectrum of the disease. A well-coordinated team coordination is required between both the centers, so as the treatment is not hampered. The emphasis is on making a team and a registry for HAPE patients both at the level of high altitudes and at the lower plains, so as to fast track such patients.

  Conclusion Top

HAPE is a life-threatening disease which is preventable by gradual ascent, but once it manifests, the aim should be to maintain arterial saturation of >90%. Drug therapy may be helpful to alleviate the symptoms and may fasten the recovery process. Time is of essence and treatment should not be delayed. A team-oriented effort is required at all levels.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.


We are thankful to the department of anesthesia at government medical college Chandigarh for support.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Goyal R, Mosenifar Z. High Altitude Pulmonary Oedema. Available from: https://www.emedicine.medscape.com/article/300716-overview#a2?src=soc_gp_. [Last accessed on 2018 Nov 24].  Back to cited text no. 1
Jensen JD, Vincent AL. Altitude illness, pulmonary syndromes, high altitude pulmonary edema (HAPE). In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2018. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430819/. [Last updated on 2017 Oct 10].  Back to cited text no. 2
Pennardt A. High-altitude pulmonary edema: Diagnosis, prevention, and treatment. Curr Sports Med Rep 2013;12:115-9.  Back to cited text no. 3
Luo Y, Gao W, Chen Y, Liu F, Gao Y. Rare mitochondrial DNA polymorphisms are associated with high altitude pulmonary edema (HAPE) susceptibility in Han Chinese. Wilderness Environ Med 2012;23:128-32.  Back to cited text no. 4
Whitlow KS, Davis BW. High altitude pulmonary edema in an experienced mountaineer. Possible genetic predisposition. West J Emerg Med 2014;15:849-51.  Back to cited text no. 5
Bhagi S, Srivastava S, Singh SB. High-altitude pulmonary edema: Review. J Occup Health 2014;56:235-43.  Back to cited text no. 6
Kurtzman RA, Caruso JL. High-altitude illness death investigation. Acad Forensic Pathol 8(1):83-97.  Back to cited text no. 7
Fagenholz PJ, Gutman JA, Murray AF, Harris NS. Treatment of high altitude pulmonary edema at 4240 m in Nepal. High Alt Med Biol 2007;8:139-46.  Back to cited text no. 8
Maggiorini M. High altitude-induced pulmonary oedema. Cardiovasc Res 2006;72:41-50.  Back to cited text no. 9
Archer S, Michelakis E. The mechanism(s) of hypoxic pulmonary vasoconstriction: Potassium channels, redox O(2) sensors, and controversies. News Physiol Sci 2002;17:131-7.  Back to cited text no. 10
West JB; American College of Physicians, American Physiological Society. The physiologic basis of high-altitude diseases. Ann Intern Med 2004;141:789-800.  Back to cited text no. 11


  [Figure 1], [Figure 2]


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