Radiographical Spectrum of High-altitude Pulmonary Edema: A Pictorial Essay
1Department of Hematology & Stem Cell Transplant, Army Hospital (R&R), New Delhi, India
2Department of Pulmonology, Base Hospital, New Delhi, India
3,4Department of Pulmonology, Army Hospital (R&R), New Delhi, India
5Department of Radiology, Base Hospital, New Delhi, India
6Department of Oncology, Army Hospital (R&R), New Delhi, India
7Ex Director General, Medical Services (Army), Currently, Vice Chancellor, Sikkim Manipal University, Sikkim, Gangtok, India
8Department of Haemato-Oncology and Bone Marrow Transplant, Apollo CBCC Cancer Care, Ahmedabad, Gujarat, India
Corresponding Author: Puneet Saxena, Department of Pulmonology, Army Hospital (R&R), New Delhi, India, Phone: +91 7798982797, e-mail: email@example.com
How to cite this article: Yanamandra U, Vardhan V, Saxena P, Singh P, Gupta A, Mulajkar D, et al. Radiographical Spectrum of High-altitude Pulmonary Edema: A Pictorial Essay. Indian J Crit Care Med 2021;25(6):668–674.
Source of support: Nil
Conflict of interest: None
Background: High-altitude pulmonary edema (HAPE) is a common cause of hospitalization in high altitude areas with significant morbidity. The clinical presentation of HAPE can overlap with a broad spectrum of cardiopulmonary diseases. Also, it is associated with varied radiological manifestations mimicking other conditions and often leading to unnecessary and inappropriate treatment.
Patients and methods: The primary aim of the study was to study the various radiological manifestations of HAPE through real-world chest radiographs. We present six different chest X-ray patterns of HAPE as a pictorial assay, at initial presentation, and after the resolution of symptoms with supplemental oxygen therapy and bed rest alone.
Results: HAPE can present as bilateral symmetrical perihilar opacities, bilateral symmetrical diffuse opacities, unilateral diffuse opacities, bilateral asymmetrical focal opacities, and even lobar consolidation with lower zone or less commonly upper zonal predilection. These presentations can mimic many common conditions like heart failure, acute respiratory distress syndrome, pulmonary embolism, aspiration pneumonitis, pneumonia, malignancy, and tuberculosis.
Conclusion: A holistic clinical–radiological correlation coupled with analysis of the temporal course can help high-altitude physicians in differentiating true HAPE from its mimics.
Keywords: Chest X-ray, High-altitude pulmonary edema, Imaging, Radiograph.
The allure of the mountains and recreational activities attract hundreds of tourists every year to high altitude (HA). Sojourn in these altitudes for occupational reasons is also on the rise (i.e., military deployment, mining, railways, roadways, and bridge construction). The increased accessibility of air travel has also reduced travel times. These factors have contributed to the increased incidence of high-altitude illnesses (HAIs). Though acute mountain sickness resolves with conservative measures and rests over the next few days, high altitude pulmonary edema (HAPE) and high-altitude cerebral edema require urgent specialist treatment.
HAPE is a form of noncardiogenic pulmonary edema.1 It is the most frequent cause of hospital admissions in HA and is potentially fatal.2,3 The clinical presentation of HAPE can masquerade several other conditions like lower respiratory tract infections (pneumonia), pulmonary thromboembolism (PTE), and coronary artery disease (CAD). Extensive radiological studies such as computed tomography or chest ultrasonography are not always possible due to environmental, geographical, and resource constraints. Thus, in real-world HA settings, physicians often have to rely on conventional (nondigital) chest radiographs with limited resolution.
Healthcare facilities in HA are usually handled by young doctors who need to be sensitized to the different presentations of HAPE. This pictorial review covers the protean imaging manifestations of HAPE from real-world settings with limited resources.
PATIENTS AND METHODS
We present a series of chest radiographs of HAPE patients managed at a secondary hospital located at an elevation of 3500 m. The radiographs have been chosen to represent the different patterns of HAPE presentation. Each pattern is represented by two radiographs, one at diagnosis and another at discharge. These patients were part of the studies published previously.4,5 These radiographs belong to individuals who ascended to HA as part of the occupational sojourn. All these individuals were young healthy males (age range of 24–32 years) who underwent rigorous clinical and laboratory evaluation before ascending to HA for any comorbidities (hematological, biochemical abnormalities, hypertension, diabetes, any past venous thrombosis, cardiovascular diseases, and life-threatening HAI in the past). All these individuals were subjected to the acclimatization for 7 days on the ascent to the HA. All these individuals developed HAPE within 5 days of arrival to HA during the acclimatization schedule in the absence of any known provocative factors (such as unaccustomed exertion, preceding respiratory tract infection, etc.). Clinical manifestations of all these patients included breathlessness and low oxygen saturation levels on pulse oximetry (SpO2). All patients fit into the diagnosis of HAPE as per the Lake Louis diagnostic criteria for HAPE.6 All patients were managed with only supplemental oxygen therapy and bed rest.4 Standard chest radiography was performed using floor-mounted projection radiography (nondigital equipment of 60 kV, 75 mAs exposure time, and film source distance of 6 ft). Standing posterior–anterior (PA) radiographs at end inspiration were done routinely. The study was conducted in accordance with the declaration of Helsinki, and informed consent was taken from all patients.
Bilateral symmetrical diffuse opacities (Fig. 3)
Lobar consolidation with lower zone predilection (Fig. 9)
Lobar consolidation with upper zone predilection (Fig. 10)
The diagnosis of HAPE as per Lake Louise criteria is based on pulmonary symptoms and signs.6 HAPE may present as cough, initially dry progressing to a productive cough, which may have whitish or blood-tinged sputum. Breathlessness (out of proportion to the amount of exertion), orthopnea, and chest pain are also seen. On examinatin, tachypnea, tachycardia, wheeze, and crackles on auscultation are noted. Often, these cases occur at remote locations with no access to necessary medical facilities. Delay in evacuation to the nearest healthcare facility can be detrimental to the patient. Making a timely correct diagnosis, therefore, assumes utmost importance.
Radiology remains a crucial cornerstone in the diagnosis and management of HAPE. These patients can have clinical–radiological discordance. Lung ultrasonography is a crucial evolving tool in diagnosing HAPE earlier, and its portability can help in field settings in the future.7 We have demonstrated different radiographical manifestations of HAPE. Several differentials for these radiographical patterns are tabulated in Table 1. Reports suggest radiographic evidence of early pulmonary edema even after prolonged high-intensity exertion at HA underlining the importance of chest radiography in this setting.8 Vock et al. also noted many different radio-morphological pictures in HAPE. Radiographic pictures may include unilateral or bilateral, central or peripheral, homogenous, or patchy fluffy opacities, predominantly in the dependent zones of lungs.9
|Bilateral symmetrical perihilar opacities||Bilateral symmetrical diffuse opacities||Unilateral diffuse opacities||Bilateral asymmetrical focal opacities||Lobar consolidation|
|Cardiogenic pulmonary edema
Diffuse alveolar hemorrhage
Acute interstitial pneumonia
Acute eosinophilic pneumonia
Diffuse alveolar hemorrhage
Acute hypersensitivity pneumonitis
Acute interstitial pneumonia
Acute eosinophilic pneumonia
|Unilateral pulmonary edema (as in some cases of mitral regurgitation)
Re-expansion pulmonary edema
Pulmonary embolism (oligemia on the affected side may be misinterpreted as diffuse opacity on the unaffected side)
Bronchogenic carcinoma with metastasis
Allergic bronchopulmonary aspergillosis
Upper-tuberculosis, pneumoconiosis, right upper lobe edema in acute mitral regurgitation
Lower-aspiration pneumonia, asbestosis
Bilateral diffuse opacities is a common manifestation of HAPE seen in up to 40% patients by Vock et al., 81% patients by Li et al., and 85% patients by Kobayashi et al.9–11 Airspace opacification is sharply confined to central, perihilar regions of the lung with sparing of peripheral or subpleural regions in early cases and extending to the periphery in severe cases.12,13 It is essential to rule out differentials as all the patients with bilateral diffuse radiological opacities at HA need not be HAPE, as was reported in a patient of systemic lupus erythematosus with diffuse alveolar hemorrhage.14 Drowning or immersion pulmonary edema can mimic HAPE with bilateral diffuse opacities.13,15
Cardiogenic pulmonary edema is by far the commonest differential of HAPE (Figs. 1 and 2). The presence of an underlying heart disease, bilateral pleural effusion, and cardiomegaly should arouse the suspicion of this differential. Pleural effusion is rarely seen in HAPE but may be seen when patients have delayed presentations. It is vital to interpret cardiomegaly correctly in an anteroposterior film as may be required on certain occasions when a patient is too critical for a routine standing PA film. Increased cardiothoracic ratios have been reported in HAPE even in the absence of overt cardiogenic edema, especially right ventricle and prominence of the pulmonary vasculature (acute cor pulmonale), which rapidly reverses on recovery.10,16,17 Pulmonary hypertension may be appreciated as prominence of the pulmonary trunk (increased bulge below the aortic knuckle at the left mediastinal border) and central pulmonary arteries with peripheral pruning and enlargement of right descending pulmonary artery (interlobar artery) (Figs. 2, 3 and 5). Most importantly, for the same degree of radiological involvement or hypoxia, a patient with cardiogenic pulmonary edema is much more symptomatic than a patient with HAPE.
Less commonly, the opacities may be more diffuse without any central predilection (Fig. 3), as seen in most cases of acute respiratory distress syndrome and often in viral pneumonia and several noninfective interstitial pneumonitides (Table 1).
Unilateral pulmonary edema as a radiological presentation has been reported in HAPE previously, as also illustrated in Figures 4 and 5 above.18–20 Predominantly unilateral radiographic involvement was variably reported from 15 to 60%.9–11 Right lung predilection and predominance were shown in patients with unilateral and bilateral edema, respectively.9,11 Since HAPE presenting as unilobar or multilobar consolidation is rare, it is imperative to be aware of such a radiological picture (Figs. 6 to 10). Rounded opacities that may be misinterpreted as metastasis can sometimes be seen (Figs. 8). The mechanism of HAPE is uneven sheer stress of pulmonary capillaries along with capillary stress failure in areas of heterogeneous and over-perfused capillaries. Owing to the apicobasal pressure gradient, commonly involved zones are lower lung zones, i.e., the dependent zones. However, it is not unusual for HAPE to involve upper or mid-zone, as seen in Figure 10, and in endemic areas can mimic tuberculosis. In any given individual developing recurring HAPE, there is no predilection to any specific zone, as was reported by Kobayashi et al. in a patient with recurrent HAPE.10 There is no clear pathophysiological mechanism for atypical findings of HAPE. Some authors, though, have suggested a prior trauma or damaged lung tissue as a cause for zone predilection, but the same has not been proven. Asymmetrical perfusion due to a variety of causes like unilateral pulmonary artery agenesis/hypoplasia or unilateral embolism, prolonged lateral decubitus positioning, and cardiac disorders, mainly mitral regurgitation, have been suggested as plausible mechanisms for unilateral pulmonary edema in HAPE. Though none of the patients described in this manuscript had any forthcoming history, clinical findings, or echocardiography features to suggest any of the above.18,19,21–24
The clinical presentation of HAPE can overlap with a broad spectrum of cardiopulmonary diseases. While HAPE can be managed by supplemental oxygen therapy and bed rest with minimal or no pharmacotherapy, more severe disorders like PTE and CAD need urgent specialist care.4 Special caution is required in differentiating pneumonia from HAPE to avoid unnecessary overuse of antibiotics. Owing to the clinical overlap between HAPE and other cardiopulmonary conditions, relying solely on radiographic findings without emphasis on history and examination can lead to wrong diagnosis and poor outcomes. Despite severe hypoxia, HAPE patients do well with oxygen therapy and other conservative measures. Correct diagnosis can avoid unnecessary intubation and other potentially harmful therapeutic measures. A systematic approach is, therefore, warranted in all patients with suspected HAPE while maintaining a low threshold to seek specialist care. Such an approach has been described in detail in the supplement attached.
This study is limited by the relatively poor quality of radiographs with no incidence calculation of different radiological patterns, and the lack of supporting CT scan images. Most areas at such altitudes lack in healthcare infrastructure, and advanced imaging technology is often not available.
No fixed radiographical appearance is associated with HAPE, and it can masquerade many conditions. A high index of suspicion should be maintained in all patients visiting HA, particularly in the first few days of arrival. Unusual radiological presentation of HAPE should be kept in mind when the differential diagnosis is considered in HA settings.
Uday Yanamandra https://orcid.org/0000-0002-0546-6585
Vasu Vardhan http://https://orcid.org/0000-0002-2180-218X
Puneet Saxena https://orcid.org/0000-0003-1111-1008
Priyanka Singh https://orcid.org/0000-0002-2468-8394
Amul Gupta https://orcid.org/0000-0002-0076-9317
Deepak Mulajkar https://orcid.org/0000-0001-9775-0032
Rajan Grewal https://orcid.org/0000-0001-5305-0990
Velu Nair https://orcid.org/0000-0002-8710-1925
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