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ORIGINAL ARTICLE
Year : 2022  |  Volume : 24  |  Issue : 1  |  Page : 11-16

Role of point-of-care ultrasound in grading the severity and early diagnosis of high-altitude pulmonary edema at a peripheral hospital


1 Department of Anaesthesia, 403 Field Hospital, Ladakh, India
2 Department of Anaesthesia and Critical Care, Command Hospital (Southern Command), Pune, Maharashtra, India

Date of Submission21-Sep-2020
Date of Decision10-Jan-2021
Date of Acceptance23-Jan-2021
Date of Web Publication21-Jan-2022

Correspondence Address:
Dr. Deepak Dwivedi
Department of Anaesthesia and Critical Care, Command Hospital (Southern Command), Pune - 411 040, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmms.jmms_138_20

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  Abstract 


Background and Aims: Troops deployed at high-altitude area (HAA) suffer from various high-altitude illnesses (HAIs) including high-altitude pulmonary edema (HAPE). There are various criteria to diagnose and assess the severity of HAPE, but point-of-care ultrasound (POCUS) of the lung has also been used in isolation by physicians. The aim is to assess whether POCUS of the lung improves the ability to diagnose the severity of HAPE. Methodology: A retrospective, cross-sectional descriptive study was planned for the patients treated for HAPE (n = 46) at our hospital from January 2019 to March 2020. Prehospital admission data, hospital admission data, and discharge data for the first-time inductees and reinductees were collected from the central hospital admission registry and central database of the medical department and intensive care unit. Results: The incidence of HAPE was 2.2 per 1000. First-time inductees (n = 30) were affected more when compared to reinductees (n = 16) and the maximum were at the third stage of HAA. POCUS of the lung facilitated the diagnosis of the six patients with mild HAPE with no positive radiological features. Conclusions: POCUS of the lung should be routinely used by the medical officers deployed at high altitudes. It will increase the diagnostic rate of HAPE with meticulous grading of the severity, thereby aiding in formulating the case-specific treatment protocol.

Keywords: Acclimatization, chest X-ray, high-altitude pulmonary edema, lung ultrasound, point-of-care ultrasound


How to cite this article:
Sud S, Kumar Y, Bharadwaj S, Dwivedi D, Kumar A, Garg A. Role of point-of-care ultrasound in grading the severity and early diagnosis of high-altitude pulmonary edema at a peripheral hospital. J Mar Med Soc 2022;24:11-6

How to cite this URL:
Sud S, Kumar Y, Bharadwaj S, Dwivedi D, Kumar A, Garg A. Role of point-of-care ultrasound in grading the severity and early diagnosis of high-altitude pulmonary edema at a peripheral hospital. J Mar Med Soc [serial online] 2022 [cited 2022 Aug 13];24:11-6. Available from: https://www.marinemedicalsociety.in/text.asp?2022/24/1/11/336183




  Introduction Top


Siachen glacier in the western Himalayas is the most glaciated area outside the polar regions, consisting of around 22 glaciers.[1] The treacherous terrain of Siachen is uninhabitable owing to extreme climatic conditions, altitude ranging from 3050 m (10,000 feet) to 7010 m (23,000 feet) above sea level and temperature varying between _30°C and _60°C. In addition, strong wind blizzards (185–300 km/h) and massive crevasses worsen the situation.[1] Soldiers deployed at these altitudes are prone to various high-altitude illnesses (HAIs), such as acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), high-altitude cerebral edema (HACE), cerebral venous thrombosis, pulmonary thromboembolism, mesenteric vein thrombosis, deep-vein thrombosis, and cerebrovascular accidents.[2] Among all the HAIs, AMS is most common (40%–90%), followed by HAPE (0.2%–7%) and HACE (0.5%–1%).[3] HAI is mainly because of a decrease in temperature, ambient humidity, and barometric pressure, leading to the decreased partial pressure of oxygen in atmosphere which, in turn, decreases oxygen availability at cellular mitochondria. This hypobaric hypoxia at the cellular level triggers a series of physiological responses, which help most individuals to adapt and tolerate the low oxygen conditions. However, in some cases, maladaptive responses occur leading to HAI.[3] Diagnosis of HAPE requires clinical evaluation and various radiological examinations (chest X-ray, lung ultrasound [LUS], and computed tomography [CT] of the chest). LUS has been shown to be a reliable bedside tool for surveillance and diagnosis of HAPE.[4] Indian armed forces prior to induction to high-altitude areas (HAAs) follow a well-documented acclimatization schedule.[5] Still, the annual incidence of HAPE in Indian armed forces is 0.15 per thousand soldiers per year.[1] Therefore, we planned this research with a primary objective to study the incidence and factors responsible for HAPE at our peripheral hospital located at high altitude and as a secondary objective to see whether the incorporation of point-of-care ultrasound (POCUS) of the lung improves the ability to assess the severity of HAPE.


  Methodology Top


A retrospective, cross-sectional descriptive record-based study was planned at our hospital after obtaining approval from the institutional review board. Data were obtained from the central hospital admission registry and central database of the medical department and intensive care unit (ICU) for the duration of January 2019 to March 2020 and a total of 46 patients qualified for the study.

The study included all serving personnel of all age groups admitted to our ICU as a suspected case of HAPE and managed as per our institutional protocol. The data were segregated as prehospital admission data, hospital admission data, and discharge data. It was also segregated on the basis of first-time inductees and reinductees. Reinductees are the ones re-entering the HAA after the absence of more than 10 days.

Prehospital admission data included age (years), sex, body mass index (kg/m2), duration of induction (days), presentation of symptoms, high-altitude stage where symptoms occurred, duration of symptoms before reporting to our hospital, first-time inductee into HAA or re-inductee, previous history of HAPE, and comorbidities. These data are represented in [Table 1]. The first stage of HA lies between 2700 and 3600 m, the second stage between 3600 and 4500 m, and >4500 m is the third stage.[6]
Table 1: Prehospital admission data

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Hospital admission data included symptoms and signs, clinical examination findings such as heart rate (HR), respiratory rate (RR), oxygen saturation (SpO2), body temperature, noninvasive blood pressure (BP), electrocardiography (ECG), lung auscultation findings, radiological findings (X-ray chest, LUS, and CT chest), echocardiography, routine blood test reports, treatment given, and complications if any. Discharge data included the duration of stay in the hospital, whether the patient transferred to any other hospital, and the final outcome.

In our hospital, we use Li et al. criteria for diagnosis and confirmation of HAPE.[7] For the diagnosis of HAPE, criteria 1, 2, and 3 must be met. These findings along with those in criteria 4, 5, 6, 7, and/or 8 are then used to confirm HAPE [Table 2]. Severity Grading criteria as described by Zhou Q et al. in their study was routinely used in our hospital for determining the severity of HAPE.[8] We modified the criteria by adding LUS to it and coined it as “ Modified Severity Grading Criteria” for HAPE to observe how much change happened in assessing the severity of HAPE [Table 3].
Table 2: Diagnostic criteria of high-altitude pulmonary edema

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Table 3: Modified Severity Grading Criteria of high-altitude pulmonary edema

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Point-of-care lung ultrasound

LUS was done as a point of care depending on the expertise available. LUS was performed using the MINDRAY digital ultrasonic diagnostic imaging system, Model DP-8500 (SHENZHEN Mindray Bio-Medical Electronics Co., Ltd, China) with a convex 3.5 curvilinear broadband 2.0–5.0MHz probe. Scanning was done in sitting, supine, or near supine position depending on the comfort of a patient with the probe placed perpendicular over the intercostal spaces. Scanning of both lungs was done along the parasternal, midclavicular, anterior axillary, and midaxillary lines [Figure 1]. For the right lung, the scanning was done from the second to the fifth intercostal spaces and for the left lung from the second to the fourth intercostal spaces. B-lines at each scanning site were counted from zero to ten. Zero implied complete absence of B- lines, whereas a complete homogenous white screen in a single scanned zone represented 10 B-lines. In situations where B-lines were confluent and difficult to assess, percentage of the screen occupied with B-lines was divided by ten A B line score <5 was regarded negative for HAPE, whereas a B line score >5 was observed positive for HAPE.[9] A B line score <5 indicated no HAPE, 6–15 score indicated mild HAPE, 16–30 score was moderate HAPE, and >30 score meant severe HAPE.
Figure 1: Lung ultrasound scanning for B-lines in various areas (a) Parasternal area (b) Midclavicular area (c) Anterior axillary area (d) Mid axillary area

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  Results Top


The most common presentations in the descending order were breathlessness (100%), cough (93.4%), and headache (30.4%), with pink frothy sputum being the least (4.3%). Fever was seen in five patients and HACE was seen in one patient. Tachycardia was present in 25 patients with 15 patients having HR more than 110/min indicating severe HAPE. Tachypnea was present in all 46 patients with RR ranging between 20 and 40/min. SpO2 on room air was in the range of 50%–85% on presentation with an average of 68%, which gradually improved on treatment. Raised BP was present in 24 patients. Two patients of severe HAPE had low BP and needed inotropic support. Raised total leukocyte count was seen in 23 patients, while raised hemoglobin was observed in 19 patients.

ECG abnormality was seen in 25 patients, which included sinus tachycardia, T-wave inversion, ST-segment abnormality, R-wave in V1–V2, S wave in V5–V6, and right-axis deviation. Sinus tachycardia was present in 25 patients, significant ST-segment depression in 3 cases over lateral and inferior wall leads, and significant ST elevation was seen in 2 cases over anterior leads. T-inversion was seen in 16 patients, with five patient's having T-wave inversion in limb leads only, while nine patients had T-inversion in both chest and limb leads. These changes probably reflect some degree of pulmonary arterial hypertension concomitantly present with pulmonary edema. R-waves in V1–V2 were seen in 7 patients, while S-waves in V5–V6 were seen in 8 patients, suggestive of right ventricular overload which is commonly seen in HAPE. These ECG changes reverted to normal within 2–7 days (average 4 days).

Application of modified severity grading criteria for HAPE was successful in detecting additional six patients and graded them into mild category, which were initially missed by the chest X-ray on admission. Data of radiological findings based on the severity of HAPE employing X-ray of the chest, LUS, and CT of the chest are presented in [Table 4].
Table 4: Radiological assessment of severity of high-altitude pulmonary edema, employing X-ray of the chest, lung ultrasound, and computed tomography chest

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The incidence of HAPE was 2.2 per 1000 which was calculated based on the total number of troops inducted into the Siachen sector from January 2019 to March 2020. The total number of HAPE cases were observed more in first-time inductees, in comparison to reinductees [Table 4]. The duration that the reinductees stayed at lower altitudes varied from 15 to 121 days. Maximum cases of HAPE occurred at the third stage [Table 4]. Twenty-four patients were evacuated by air to our hospital. The average duration of hospitalization was 8.14 days. Thirty-two (69.5%) patients were evacuated by the air route to a tertiary care hospital in plains.


  Discussion Top


HAPE is a potential life-threatening emergency, manifesting as noncardiogenic pulmonary edema, commonly seen due to the rapid ascend of lowlanders to HA.[10] The most common risk factors for developing HAPE are high altitude, low atmospheric temperature, male, rapid ascent (>600 m/day), nil/incomplete acclimatization, vigorous exercise, comorbidities, and possible genetic predisposition.[10] The most likely mechanism for developing HAPE is exaggerated hypoxic pulmonary vasoconstriction of smaller arteries and veins, causing overdistension of the vessel wall with opening of the cellular junctions and stress failure of the alveolar–capillary membrane leading to raised pulmonary artery pressure (PAP) and high permeability, noncardiogenic pulmonary edema with normal pulmonary capillary wedge pressure.[11] Common causes of high PAP in HAPE are increased sympathetic activity, elevated endothelin-1 levels, and decreased nitric oxide.[12]

Diagnosis of HAPE at such peripherally located hospitals has taken a leap with the availability of diagnostic tools such as POCUS and CT of the chest which have impacted the outcome by early diagnosis and management. Literature also reiterates the role of POCUS which has brought a transformative change in clinical practice by improving the speed and accuracy of diagnostic testing, minimizing the delay in initiation of definitive therapy by medical care providers without the radiation risk, and thus leading to the reduction in the morbidity and mortality.[13]

Incidence of 5.5% HAPE in the Indian army has been documented by Virmani in the eastern Himalaya sector and 1.42 per 1000 in the western Himalaya sector by Bhalwar et al., whereas it was 2.2 per 1000 in our study.[14],[15] The increased incidence in our study as compared to Bhalwar et al. could be due to sudden exposure to high altitude and cold temperature, as majority of soldiers in our area were inducted by air. Majority of the cases of HAPE occurred in the third decade of life (63.1%) and at the third stage of HAA (48%) as was observed by Virmani.[14]

The global percentage of first-time inductees developing HAPE varies between 41.6% and 75% and was comparable with our study (65.3%, n = 30). However, the proportion was much lower (35%, n = 16) when was compared globally (64.3% to 85%), this could be explained by the strict adherence of the acclimatisation schedule in our area [Table 5]. Two reinductees suffered severe HAPE after completely recovering from an earlier episode of mild HAPE. Their reinduction was in accordance with the guidelines issued by draft DGAFMS Memorandum 2001, “problems of high-altitude.”[16] As per these guidelines, only patients with severe HAPE, recurrent HAPE (>1 episode), or with associated pulmonary arterial hypertension are unfit for HAA. The occurrence of HAPE during the first 24 h of induction was lesser (36.9%) in comparison to global figures (52.4%–61.8%).[14] This was achieved by ensuring complete bed rest. Six cases of HAPE which occurred after 5 days of acclimatization could be due to undue physical exertion or genetic predisposition for HAPE. The common genes predisposing an individual for HAPE are associated with the renin–angiotensin–aldosterone system pathway, hypoxia-inducible factor pathway, the nitric oxide pathway, and vascular endothelial growth factor. Other genes associated with HAPE are pulmonary surfactant proteins, tyrosine hydroxylase, adrenergic receptor, and pulmonary surfactant proteins.[17] The proportion of the population developing HAPE at the third stage was much higher (50%, n = 23) in our study when compared with the global proportions which vary between 2% and 21% [Table 5]. This increase could be explained by the increased number and duration of the deployed troops at these extreme HAA.
Table 5: Distribution of data based on type of inductees and at various stages of high altitude

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Virmani and Rao et al. had a majority of HAPE cases during June–December, whereas we had cases between October and March.[14],[18] The most probable reason for this variation may be that in the winter months, there is a further drop of barometric pressure leading to increased hypoxia and HAPE.[19] Increased incidence of respiratory tract infections (10.8%) when compared to global rate (2.2%%–7.8%) could be due to the repeated exposure to extremely dry and freezing atmospheric conditions. Lower incidence of pink frothy secretions (4.3%) seen was due to the lesser number of severe HAPE cases.[14] Increased hemoglobin levels seen could be due to polycythemia of high altitude and was not related to the severity of HAPE. One patient had associated HACO which was treated successfully with cerebral decongestants. The higher average duration of hospitalization (8.14 days) seen in our study in comparison to Virmani (7.14 days) was due to bad weather, resulting in nonavailability of aircrafts for transferring the patients to plains.[14] There were eight patients of severe HAPE who were initially treated with HAPE bags at their high-altitude posts, as the evacuation was delayed due to inclement weather.

LUS being portable, user friendly, and with no radiation risk has become an integral part of the standard operating procedure for the management of HAPE patients in our hospital [Figure 2]. Literature, shows that LUS had higher sensitivity than moist rales (0.98 vs. 0.81, P < 0.01 using the McNemar test) and X-ray chest (0.98 vs. <0.93, P < 0.05 using the McNemar test) in diagnosing HAPE before treatment.[9] Therefore, we have included LUS in our treatment protocol for HAPE and were able to diagnose six patients of mild HAPE whose X-rays of the chest were inconclusive, but LUS showed B lines score between 05 and 15, which could be due to the lag in the X-ray findings when compared to the clinical worsening due to timely evacuation. Hence, the use of 'Modified Severity Grading Criteria' may help in clinching diagnosis in mild HAPE category by 30% which could be easily missed on X-ray of the chest.
Figure 2: Treatment algorithm of High-altitude pulmonary edema

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It is recommended to have a multicentric randomized controlled study to validate the modification of Yang et al. criteria with the incorporation of LUS for establishing the sensitivity of the diagnoses and grading of HAPE.


  Conclusions Top


LUS not only helps in the early diagnosis and grading of HAPE patients but also allows in assessing the efficacy of treatment by repeated and frequent scans. Regular use of LUS by medical officers of hospitals deployed in HAA will go a long way not only in diagnosing HAPE cases at an early stage but also in assessing their response to therapeutic interventions.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Mehta SR, Chawla A, Kashyap AS. Acute mountain sickness, high altitude cerebral oedema, high altitude pulmonary oedema: The current concepts. Med J Armed Forces India 2008;64:149-53.  Back to cited text no. 2
    
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Luks AM, Swenson ER, Bartsch P. Acute high-altitude sickness. Eur Respir Rev 2017;26:1-14.  Back to cited text no. 3
    
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Zhou Q. Standardization of Methods for Early Diagnosis and On-Site Treatment of High-Altitude Pulmonary Edema, Pulmonary Medicine; 2011. p. 1-9.  Back to cited text no. 8
    
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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. 10
    
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Pennardt A. High-altitude pulmonary edema: Diagnosis, prevention, and treatment. Curr Sports Med Rep 2013;12:115-9.  Back to cited text no. 12
    
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Virmani SK. High altitude pulmonary oedema-an experience in Eastern Himalaya. Med J Armed Forces India 1997;53:163-8.  Back to cited text no. 14
    
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Bhalwar R, Singh R, Ahuja RC, Misra RP. Nested case-control analysis of the risk factors for high altitude pulmonary oedema. Med J Armed Forces India 1995;51:189-93.  Back to cited text no. 15
    
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Ahmad FM, Sharma N. High altitude and its illness. Med J Armed Forces India 2005;61:307.  Back to cited text no. 16
    
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Luo Y, Zou Y, Gao Y. Gene polymorphisms and high-altitude pulmonary edema susceptibility: A 2011 update. Respiration 2012;84:155-62.  Back to cited text no. 17
    
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    Figures

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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