|Year : 2016 | Volume
| Issue : 1 | Page : 23-25
High altitude pulmonary edema (HAPE) with pulmonary embolism
Srinivasa Alasinga Bhattachar1, Sanjay Singhal2, Vivek Paliwal2, Vineet Kumar Malhotra1, Atul Kotwal3
1 Department of Physiology, High Altitude Medical Research Centre, Jammu and Kashmir, India
2 Department of Medicine, 153-General Hospital, Leh, Jammu and Kashmir, India
3 Department of Community Medicine, 153-General Hospital, Leh, Jammu and Kashmir, India
|Date of Web Publication||4-Mar-2016|
153-General Hospital, Leh, Jammu and Kashmir
Source of Support: None, Conflict of Interest: None
High altitude pulmonary edema (HAPE) is a life-threatening condition occurring at heights above 2500 meter mostly within 2-4 days of entry in high altitude. Postmortem studies showed evidence of thrombi in cases of HAPE suggesting possible role of thrombosis in the pathogenesis of HAPE. Here, we are presenting the two cases of HAPE with pulmonary embolism, and the possibility of pulmonary embolism should be considered in cases of HAPE with persistent radiographic opacities despite oxygen or descent.
Keywords: High altitude, pulmonary edema, pulmonary embolism
|How to cite this article:|
Bhattachar SA, Singhal S, Paliwal V, Malhotra VK, Kotwal A. High altitude pulmonary edema (HAPE) with pulmonary embolism. Heart India 2016;4:23-5
|How to cite this URL:|
Bhattachar SA, Singhal S, Paliwal V, Malhotra VK, Kotwal A. High altitude pulmonary edema (HAPE) with pulmonary embolism. Heart India [serial online] 2016 [cited 2020 Jul 10];4:23-5. Available from: http://www.heartindia.net/text.asp?2016/4/1/23/178117
| Introduction|| |
High altitude pulmonary edema (HAPE) is a life-threatening condition occurring at heights above 2500 meter mostly within 2-4 days of entry in high altitude. The exact pathophysiology of HAPE is not completely understood. But nonuniform vasoconstriction of pulmonary vasculature leading excess blood flow to better ventilated areas thus leading to stress failure of pulmonary capillaries is believed to be one of the possible mechanisms of pulmonary edema.,, Postmortem studies showed evidence of thrombi in cases of HAPE suggesting the possible role of thrombosis in the pathogenesis of HAPE. The present case report describes cases of HAPE with pulmonary embolism.
| Case Report|| |
Case 1 summary
A 32-year-old male was evacuated to our hospital located at 3500 m from a location at similar height with history of fatigue, breathlessness, and dry cough since 24 h. He was reinducted to high altitude after absence of 30 days from high altitude. He also complained of headache, nausea, vomiting, and loss of appetite. The severity score of these symptoms as per the Lake Louise criteria was 11 that is suggestive of severe acute mountain sickness (AMS). The patient had one previous episode of HAPE, approximately 1 year back, for which he was evacuated to near sea level after the initial management. He was reinducted to high altitude after 2 months of staying at near-sea level and subsequent stay was uneventful after acclimatization. The examination revealed height: 172 cm, weight: 81.75 kg, pulse 100/min, blood pressure 140/90 mmHg, respiratory rate-24/min, SpO2 60% on room air. Chest auscultation revealed bilateral creps in infrascapular and infraaxillary regions. Chest radiograph revealed alveolar opacities in bilateral middle and lower zones. Routine hematological investigations revealed hemoglobin level of 14.2 g%, total leukocyte count and 10,500 cells/mm 3 with neutrophil predominant. The metabolic and biochemical profile was normal. The patient was initially managed with oxygen inhalation to maintain oxygen saturation above 90% and was advised to take bed rest. Serial x-ray examination showed significant resolution of opacities but a single localized opacity in right lower zone persisted till fifth day of hospitalization. Contrast enhanced computerized tomography of chest revealed filling defect in segmental arterial branches supplying posterior and lateral basal segments of right lower lobe with no evidence of pulmonary infarction [Figure 1]. The color Doppler of lower limb was normal. The patient was managed with low-molecular-weight heparin and later shifted on long-term oral anticoagulants. After stabilization, he was shifted to a tertiary care center at near-sea level. Subsequent recovery of the patient was uneventful. The follow-up of the patient did not reveal any procoagulant condition.
|Figure 1: Contrast enhanced computerized tomography of chest revealed filling defect in segmental arterial branches supplying posterior and lateral basal segments of right lower lobe suggestive of pulmonary embolism|
Click here to view
Case 2 summary
A 49-year-old male was evacuated from a location at 4900 m and shifted to our hospital that was located at 3500 m. The patient presented with history of breathlessness, cough with pinkish sputum, along with headache, anorexia, fatigue, dizziness, and insomnia since one day. Symptoms severity score of 7 as per Lake Louise criteria was suggestive of moderate AMS. He was reinducted to high altitude after an absence of 30 days from high altitude and his symptoms started on the fifth day of acclimatization. Clinical examination at our hospital revealed a pulse rate of 108/min, respiratory rate of 36/min, blood pressure of 150/110 mmHg, temperature of 98.2° F, and oxygen saturation of 64% at room air. Chest auscultation revealed bilateral diffuse crepitus. Other systemic evaluation was unremarkable. Chest radiograph revealed diffuse bilateral alveolar opacities. The patient was managed with oxygen inhalation to maintain oxygen saturation above 90% and bed rest. He improved substantially with a pulse rate of 80/min, body temperature of 98° F, blood pressure of 130/82 mmHg, respiratory rate 20/min, and SpO2 92% with oxygen. Despite improvement, he was not able to maintain oxygen saturation at room air and chest radiograph showed persistent opacity in the right lower zone on the fourth day of hospitalization. Subsequently, he was planned for contrast-enhanced computerized tomography (CECT) of thorax that was suggestive of pulmonary embolism in right lower lobar branch. The color Doppler of lower limb was normal. He was started on low-molecular-weight heparin and was switched over to long-term oral anticoagulants. His recovery was uneventful, and the patient was discharged on oral anticoagulants. Subsequent work-up of this patient did not reveal any procoagulant condition.
| Discussion|| |
HAPE is a life-threatening condition characterized by nonuniform vasoconstriction of pulmonary blood vessels in response to hypoxia. This condition occurs commonly with 2-4 days of entry in high altitude, though delayed form of HAPE developing after 6 days of induction in high altitude has also been described. Studies have described postmortem appearance of lungs in patients with HAPE., Pulmonary vessels are found to be engorged and thrombi are often found in small pulmonary arteries and septal capillaries. Evidence suggests enhanced fibrin formation in HAPE. Further investigation on the role of coagulation abnormities in pathophysiology of HAPE proved that the disruption of endothelial membrane results in activation of coagulation cascade. However, the association of HAPE with coagulation and fibrinolytic abnormalities are corroborated. The findings of pulmonary small artery thrombosis in case of our patients are likely to be a result of a similar phenomenon. Previous history of HAPE (case 1) is suggestive of HAPE susceptibility and re-entry in high altitude could have probably resulted in manifestation of the process of thrombosis in pulmonary blood vessels associated with HAPE that is commonly reported in postmortem studies. Similar findings of HAPE with pulmonary embolism have been reported. The reported case  also mentions of headache present along with other findings of HAPE (though Lake Louise score was not reported) suggestive of AMS with HAPE like in our cases. The reported case mentions  persistently elevated pulmonary artery pressure and persistent infiltrates on chest radiograph despite improvement in oxygenation. This is similar to our cases where localized opacity in right lower zone persisted despite the improvement in other parameters. Our both cases presented as HAPE with AMS with persistent radiographic opacities despite clinical improvement, but none had symptom of chest pain. Pulmonary embolism has been described commonly in lowlanders at high altitude. It has been reported that troops staying at high altitude are 30 times at greater risk to develop thrombosis. Though studies , have reported thrombosis after prolonged stay at high altitude, cases in our study were recent entrants to high altitude that presented with HAPE. The finding of pulmonary embolism in cases of HAPE alters the management strategy and necessitates prompt evacuation of the patients to centers at near-sea level even when facilities for oxygen and intense monitoring are available at the center. Further studies on thrombosis in cases of HAPE are required to prevent morbidity or mortality due to the failure to diagnose and manage pulmonary embolism in cases of HAPE.
| Conclusion|| |
The possibility of pulmonary embolism should be considered in cases of HAPE with persistent radiographic opacities despite oxygen therapy or descent.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
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 F, 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.
Bärtsch P, Lämmle B, Huber I, Haeberli A, Vock P, Oelz O, et al
. Contact phase of blood coagulation is not activated in edema of high altitude. J Appl Physiol (1985) 1989;67:1336-40.
Stream JO, Grissom CK. Update on high-altitude pulmonary edema: Pathogenesis, prevention, and treatment. Wilderness Environ Med 2008;19:293-303.
Singhal S, Bhattachar SA, Paliwal V, Pathak K. Delayed-onset high-altitude pulmonary edema. Int J Adv Med Health Res 2014;1:96-8.
Nayak NC, Roy S, Narayanan TK. Pathologic features of altitude sickness. Am J Pathol 1964;45:381-91.
Arias-Stella J, Kruger H. Pathology of high altitude pulmonary edema. Arch Pathol 1963;76:147-57.
Schoene 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. 787-802.
Bartsch P, Waber U, Haeberli A, Maggiorini M, Kriemler S, Oelz O, et al
. Enhanced fibrin formation in high-altitude pulmonary edema. J Apply Physiol (1985) 1987;63:752-7.
Ren Y, Cui F, Lei Y, Fu Z, Wu Z, Cui B. High-altitude pulmonary edema is associated with coagulation and fibrinolytic abnormalities. Am J Med Sci 2012;344:186-9.
Nakagawa S, Kubo K, Koizumi T, Kobayashi T, Sekiguchi M. High-altitude pulmonary edema with pulmonary thromboembolism. Chest 1993;103:948-50.
Anand AC, Jha SK, Saha A, Sharma V, Adya CM. Thrombosis as a complication of extended stay at high altitude. Natl Med J India 2001;14:197-201.
Kumar S. High altitude induced deep venous thrombosis: A study of 28 cases. Indian J Surg 2006;68:84-8.