|Year : 2017 | Volume
| Issue : 1 | Page : 31-34
Management of HAPE with bed rest and supplemental oxygen in hospital setting at high altitude (11,500 ft): A review of 43 cases
Sanjay Singhal1, Srinivasa A Bhattachar2, Sumit Rungta3
1 153-General Hospital, Leh, Jammu and Kashmir, India
2 High Altitude Medical Research Centre, Leh, Jammu and Kashmir, India
3 Department of Gastroenterology, King George Medical University, Lucknow, Uttar Pradesh, India
|Date of Web Publication||29-Dec-2016|
Dr. Sanjay Singhal
Chest Specialist and Intensivist, 153-General Hospital, Leh, Jammu and Kashmir
Source of Support: None, Conflict of Interest: None
Objectives: To evaluate the safety and efficacy of treating high-altitude pulmonary edema (HAPE) by bed rest and supplemental oxygen in hospital setting at high altitude. Materials and Methods: In a prospective case series, all patients who were diagnosed clinically with HAPE on admission to our hospital located at a height of 11,500 ft were evaluated and managed with bed rest and oxygen supplementation. Results: A total of 43 patients of HAPE with mean age of 31 years (range 20–48 years) were admitted to our hospital. Infections followed by unaccustomed physical exertion were the predominant risk factors. 95.35% of the patients improved successfully with oxygen and bed rest alone with mean hospital stay of 2.67 ± 1.06 (1–6 days). Two patients (4.65%) required nifedipine and evacuation to lower altitude. Of this, one patient suffering from concomitant viral infection expired 4 days after evacuation to near sea level. Conclusion: Majority of the patients with HAPE where medical facilities are available can be safely treated with bed rest and oxygen supplementation at moderate high altitude without descent.
Keywords: Bed rest, HAPE, outcome, oxygen
|How to cite this article:|
Singhal S, Bhattachar SA, Rungta S. Management of HAPE with bed rest and supplemental oxygen in hospital setting at high altitude (11,500 ft): A review of 43 cases. J Assoc Chest Physicians 2017;5:31-4
|How to cite this URL:|
Singhal S, Bhattachar SA, Rungta S. Management of HAPE with bed rest and supplemental oxygen in hospital setting at high altitude (11,500 ft): A review of 43 cases. J Assoc Chest Physicians [serial online] 2017 [cited 2018 May 25];5:31-4. Available from: http://www.jacpjournal.org/text.asp?2017/5/1/31/196652
| Introduction|| |
High-altitude pulmonary edema (HAPE) is a potentially fatal medical condition that occurs in otherwise healthy individuals within 2–4 days of ascent to altitude above 8000 ft. Delayed onset HAPE, which occurs after more than 6 days of stay at the same altitude, had also been reported. As a person ascends to higher altitudes, the air pressure falls, resulting in the fall of partial pressure of oxygen (PO2) in inhaled air, the arterial PaO2, and oxygen saturation of blood. Hypoxia-induced exaggerated and non-uniform pulmonary vasoconstriction is thought to lead to overperfusion and stress failure in portions of the pulmonary vascular bed.[2‐4] The endothelium may also be affected by inflammation from viral infection or upper respiratory tract infection that may prime the cellular layer for insult. The development of HAPE has been associated with rapid ascent, strenuous exercise, and exposure to cold and previous episode of HAPE. The recent consensus guidelines from the Wilderness Medical Society (WMS) for the management of HAPE emphasize descent as the first treatment priority in the patients with HAPE. The World Health Organization report states 35 million people travel to regions above 3000 m every year. In populations where movement to high altitude in large numbers is predominantly for commercial or industrial reasons, prompt descent as the first treatment of choice results in loss of essential manpower and requires additional transport resources at altitude. However, in patients who have access to oxygen and intense monitoring in hospital setting at moderate altitude, oxygen therapy can be considered as an alternative to descent. We reviewed the characteristics of 43 cases of HAPE admitted to our hospital located at a height of 11,500 ft who were managed with oxygen therapy alone.
| Materials and Methods|| |
During the 1-year study period, 148 patients were admitted with possible diagnosis of HAPE to our hospital located at an altitude of 11,500 ft; out of them, one patient was subsequently diagnosed to have pulmonary embolism. Diagnosis of HAPE was suspected on the following criteria: cough, dyspnea on history, tachypnea, crepts on chest auscultation, resting room air hypoxemia (saturation <90%) determined on pulse oximetry, and presence of pulmonary infiltrates on chest radiograph. Grade of HAPE severity was assessed as per classification given in [Table 1]. Detailed history and medical examination were done to find out the risk factors contributing to development of HAPE. Treatment consisted of bed rest and oxygen inhalation in all patients, nifedipine, and evacuation to lower altitude in few patients who failed to maintain the oxygen saturation on high-flow oxygen inhalation (10–12 L/min). Findings of all patients were recorded including response to treatment, details of entry to high altitude, and height of stay prior to onset of symptoms. Patients already on medications like nifedipine, dexamethasone, or sildenafil before admission to our hospital were excluded from the study. Patients were discharged from the hospital after they were able to maintain oxygen saturation on room air and resolution of radiological opacity.
| Results|| |
During the 1-year study period, 148 patients were admitted with possible diagnosis of HAPE to our hospital located at an altitude of 11,500 ft; out of them, one patient was subsequently diagnosed to have pulmonary embolism. A total of 104 patients were excluded from the study, as 96 patients were receiving medications like nifedipine, sildenafil, or dexamethasone before admission to the hospital and eight patients developed HAPE after more than 6 days of entry in high altitude. This atypical presentation has been found to be more severe with higher mortality in the experience at our center; therefore, oxygen alone therapy was not considered for these patients. Thus, only 43 patients were included in the study. All 43 patients were young males with mean age of 31 years (range 20–48 years), physically active (moderate to high intensity physical activity for 1 h at least 4–5 times a week), and having no previous medical comorbidites. Seven patients were newly inducted to high altitude and the remaining 36 patients had previously entered high altitude (mean number of inductions − 2.4) with history of previous HAPE in four patients. Clinical characteristics of all 43 patients are presented in [Table 2]. First symptoms started around the second day after entry in high altitude at mean height of 12,319 ft (range 10,500–17,720 ft). Virtually all patients experienced cough and dyspnea, and all showed crepitations on pulmonary examination. All patients were having hypoxemia and radiographic pulmonary infiltrates on hospital admission. Majority of the cases of HAPE (36 patients; 83.7%) were admitted in winter as compared to only seven patients (16.3%) who were admitted in summer. A total of 20 patients with HAPE were evacuated to our hospital from height greater than 11,500 ft, which led to resolution of symptoms to some extent, thus leading to the difference in grading of severity in clinical and radiological criteria as given in [Table 3]. Infection was found to be the predominant risk factor in the development of HAPE [Table 3]. Majority of the patients (41, 95.35%) improved successfully with oxygen and bed rest alone with mean hospital stay of 2.67 ± 1.06 (1–6 days). Two patients were not able to sustain on oxygen alone and required nifedipine along with evacuation to lower altitude; out of them, one recovered [Table 4] and the second patient who was evacuated was suffering from concomitant viral infection. After evacuation to near sea level, the patient was placed on ventilator, and he expired after 4 days of evacuation. Autopsy of the patient who expired also confirmed the diagnosis of HAPE.
| Discussion|| |
HAPE is thought to be a result of altitude-related hypoxia-induced pulmonary vasoconstriction which may be regionally heterogeneous, leading to areas of underperfusion and overperfusion.[2‐4] The combination of higher flow in areas of better alveolar ventilation and weaker vasoconstriction in presence of high pulmonary artery pressure could result in stress failure of pulmonary capillaries leading to HAPE. Although pulmonary vasoconstriction and stress failure of pulmonary capillaries have been proposed as mechanism of HAPE, inflammation may trigger, potentiate, or exacerbate the formation of edema., Physical exertion itself is shown to be associated with pulmonary edema in subclinical form., Hence, the release of vasoactive, inflammatory mediators during infection could have resulted in priming of pulmonary endothelium manifesting as HAPE in response to exertion (as in some of our cases). Animal experiments have demonstrated rise in oxygen consumption and ventilation in hypoxic conditions on cold exposure, (number of cases with HAPE were more in winter as compared to summer). Evidence is also suggestive of altered nitric oxide dynamics in pulmonary endothelium on cold exposure increasing the likelihood of HAPE. Decreased NO levels have been attributed by authors toward increased leukocyte adherence due to hypoxia in animals experiments conducted on endothelium in other tissues. These combined effects of cold on oxygen consumption, ventilation, and mediator synthesis by pulmonary endothelium could probably increase risk of HAPE in susceptible individuals in winters. Infection, exertion, poor acclimatization, and cold were found to be the main risk factors for the development of HAPE in our study as is documented in various other studies.,
WMS guidelines for the management of HAPE emphasize descent and supplemental oxygen aimed at maintaining oxygen saturation above 90% as the cornerstone of management. Previous studies have demonstrated that patients with mild HAPE can improve with bed rest alone, although oxygen supplementation will result in rapid recovery., Successful management of HAPE with bed rest and supplemental oxygen at moderate altitude without descent has been documented in a smaller number in another study. Hence, in hospital setting with access to oxygen and intense monitoring, patients may not need to descend to lower elevation and can be treated with oxygen supplementation at the current elevation, which is in concurrence with our experience in management of HAPE with oxygen alone at the same altitude. Oxygen administration like descent results in increased oxygen availability in alveoli. This causes resolution and reversal of pathophysiological changes occurring in HAPE in response to hypoxia. Among other management modalities, continuous positive airway pressure may also improve oxygenation, although the effect on outcomes has only been evaluated in smaller numbers in studies., Nifedipine (potent pulmonary vasodilator) at a dose of 60 mg daily in divided doses can be added in patients who worsen or fail to improve with oxygen and bed rest. Beta-agonists and phosphodiesterases have not been assessed for effectiveness in systemic studies, though reports are available of their use in HAPE. Diuretics have no role in the management of HAPE, as patients are already likely to have volume depletion.
| Conclusion|| |
Majority of the patients with HAPE where medical facilities are available can be safely managed with bed rest and oxygen supplementation without descent; however, it requires intense monitoring and preparation of contingencies for prompt evacuation in severe or non-responsive cases.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Singhal S, Bhattachar SA, Paliwal V, Pathak K. Delayed-onset high-altitude pulmonary edema. Int J Adv Med Health Res 2014;1:96-8.
Hultgren HN, Grover RF, Hartley LH. Abnormal circulatory responses to high altitude in subjects with a previous history of high altitude pulmonary edema. Circulation 1971;44:759-70.
Maggiorini M, Mélot C, Pierre S, Pfeiffer E, Greve I, Sartori C et al.
High-altitude pulmonary edema is initially caused by an increase in capillary pressure. Circulation 2001;103:2078-83.
Hopkins SR, Garg J, Bolar DS, Balouch J, Levin DL. Pulmonary blood flow heterogeneity during hypoxia and high-altitude pulmonary edema. Am J Respir Crit Care Med 2005;171:83-7.
Kaminsky DA, Jones K, Schoene RB, Voelkel NF. Urinary leukotriene E4 levels in high-altitude pulmonary edema. A possible role for inflammation. Chest 1996;110:939-45.
Jones BE, Stokes S, Mckenzie S, Nilles EJ. Management of high altitude pulmonary edema in the Himalaya: A review of 56 cases presenting at Pheriche Medical Aid Post (4240 m). Wilderness Environ Med 2013;24:32-6.
Luks AM, McIntosh SE, Grissom CK, Auerbach PS, Rodway GP, Schoene RB et al.
Wilderness Medical Society Consensus Guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med 2010;21:146-55.
Dumont L, Lysakowski C, Tramèr MR, Kayser B. Controversies in altitude medicine. Travel Med Infect Dis 2005;3:183-8.
Scoene RB, Hultgren HN. High-altitude pulmonary edema. In: Hornbein TF, Schoene RB, editors. High Altitude: An Exploration of Human Adaptation. New York: Marcel Dekker; 2001. p. 782.
Bärtsch P, Mairbäurl H, Maggiorini M, Swenson ER. Physiological aspects of high-altitude pulmonary edema. J Appl Physiol 2005;98:1101-10.
Durmowicz AG, Noordeweir E, Nicholas R, Reeves JT. Inflammatory processes may predispose children to high-altitude pulmonary edema. J Pediatr 1997;130:838-40.
Eldridge MW, Braun RK, Yoneda KY, Walby WF. Effects of altitude and exercise on pulmonary capillary integrity: Evidence for subclinical high-altitude pulmonary edema. J Appl Physiol 2006;100:972-80.
Pratali L, Cavana M, Sicari R, Picano E. Frequent subclinical high-altitude pulmonary edema detected by chest sonography as ultrasound lung comets in recreational climbers. Crit Care Med 2010;38:1818-23.
Blake CI, Banchero N. Effects of cold and hypoxia on ventilation and oxygen consumption in awake guinea pigs. Respir Physiol 1985;61:357-68.
Johnson TS, Young JB, Landsberg L. Norepinephrine turnover in lung: Effect of cold exposure and chronic hypoxia. J Appl Physiol Respir Environ Exerc Physiol 1981;51:614-20.
Isa KB, Kawasaki N, Ueyama K, Sumii T, Kudo S. Effects of cold exposure and shear stress on endothelial nitric oxide synthase activation. Biochem Biophys Res Commun 2011;412:318-22.
Wood J, Mattioli L, Gonzalez N. Hypoxia causes leukocyte adherence to mesenteric venules in non-acclimatized, but not in acclimatized rats. J Appl Physiol 1999;87:873-81.
Schoene RB. Illnesses at high altitude. Chest 2008;134:402-16.
Koul PA, Khan UH, Hussain T, Koul AN, Malik S, Shah S et al.
High altitude pulmonary edema among “Amarnath Yatris”. Lung India 2013;30:193-8.
Marticorena E, Hultgren HN. Evaluation of therapeutic methods in high altitude pulmonary edema at 4240 m in Nepal. High Alt Med Biol 2007;8:139-46.
Zafren K, Reeves JT, Schoene R. Treatment of high-altitude pulmonary edema by bed rest and supplemental oxygen. Wilderness Environ Med 1996;7:127-32.
Schoene R, Roach R, Hackett P, Harrison G, Mills WJ Jr. High altitude pulmonary edema and exercise at 4,400 m on Mount Mckinley. Effect of expiratory positive airway pressure. Chest 1985;87:330-3.
Larson EB. Positive airway pressure for high-altitude pulmonary oedema. Lancet 1985;1:371-3.
[Table 1], [Table 2], [Table 3], [Table 4]