|Year : 2017 | Volume
| Issue : 3 | Page : 307-310
Etiology and outcome of moderate-to-massive hemoptysis: Experience from a tertiary care center of North India
Ashish Bhalla, Ashok Kumar Pannu, Vikas Suri
Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India
|Date of Web Publication||31-Jul-2017|
Department of Internal Medicine, 4th Floor, F Block, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012
Source of Support: None, Conflict of Interest: None
Background: The aim of this study was to evaluate the etiology of hemoptysis in patients presenting to emergency department of Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India. Method: Prospectively 110 patients presenting to the emergency department with history of hemoptysis were screened for a period of one and half years. Out of these, 64 patients having true hemoptysis were enrolled in the study. The patients were clinically evaluated with detailed history. Radiological evaluation included chest x rays and computerized tomogram. Sputum examination and bronchoscopy was done to establish the etiology. All the patients were conservatively managed using intravenous fluids, antibiotics, anti-tussive and anti-fibrinolytic drugs. Bronchial/pulmonary artery embolization was performed for controlling ongoing bleeding/re-bleeding. All the patients were followed up till discharge or death. Results: The mean age was 41.8 ± 15.16 years with male preponderance. Pulmonary tuberculosis (active/ sequel) was the most common etiology (65%), followed by community acquired pneumonia (10.93%), bronchiectasis (9.3%), carcinoma lung (7.18%) and miscellaneous causes (8.6%). Almost all patients (98%) had severe hemoptysis (>100 ml in 24 hours). Abnormalities in bronchial circulation were present in 59.4% and 14% of patients had pulmonary circulation abnormalities. 65% patients responded to conservative treatment. 23.4% patients under went intervention out of which 73.3% underwent bronchial artery embolization (BAE) and remaining 26.6% underwent pulmonary artery embolization (PAE). One patient died during hospital stay due to necrotizing pneumonia and another left hospital against medical advice (outcome unknown). Conclusions: TB (active/sequel) remains the most common cause of hemoptysis in patients admitted in emergency department. Non-TB causes like primary bronchiectasis, carcinoma lung and pneumonia are other important causes. Conservative management suffices in majority patients for controlling active bleed.
Keywords: Emergency, hemoptysis, tuberculosis
|How to cite this article:|
Bhalla A, Pannu AK, Suri V. Etiology and outcome of moderate-to-massive hemoptysis: Experience from a tertiary care center of North India. Int J Mycobacteriol 2017;6:307-10
|How to cite this URL:|
Bhalla A, Pannu AK, Suri V. Etiology and outcome of moderate-to-massive hemoptysis: Experience from a tertiary care center of North India. Int J Mycobacteriol [serial online] 2017 [cited 2020 Feb 27];6:307-10. Available from: http://www.ijmyco.org/text.asp?2017/6/3/307/211924
| Introduction|| |
Hemoptysis is defined as expectoration of blood from respiratory tract. It can arise in the airways from glottis to alveoli. Often it ranges from streaking of sputum with blood to frank blood without accompanying sputum. Hemoptysis usually results due to bleeding from pulmonary arteries and/or bronchial arteries. Involvement of bronchial vessels is responsible for majority of cases with pulmonary artery being the culprit in <10% of the cases. Severity of hemoptysis is usually classified based on the amount of blood expectorated in 24 h. Hemoptysis is classified as mild (<30 ml), moderate (31–100 ml), severe (100–600 ml), and massive. Massive hemoptysis defined by a number of criteria, often ranging from 100 ml to more than 600 ml over 24 h with respiratory or hemodynamic compromise. The reported mortality ranges from 7% to 30% for nonmassive hemoptysis, to up to 80% for massive hemoptysis., The mortality generally depends on the rate of bleeding. Etiologic classification of hemoptysis is based on the site of origin within the lungs. Common causes of hemoptysis include tracheobronchial source, pulmonary parenchymal source, and primary vascular source. In developing countries like India, pulmonary tuberculosis accounts for the majority of cases of severe and nonsevere hemoptysis, whereas in developed countries where the prevalence of tuberculosis has been significantly decreased, bronchiectasis, bronchitis, and lung cancer are common etiologies.
Our aim of the study was to study the etiology and outcome of patients with hemoptysis presenting to the Emergency Department of Postgraduate Institute of Medical Education and Research, Chandigarh, India, and to compare the results with findings reported in literature.
| Methods|| |
All prospective patients with a history of active hemoptysis, presenting to the emergency department at our institute were screened, and only patients with true hemoptysis were included in the study. Institute Ethics Committee approval was obtained before the recruitment was started.
Patients were enrolled in the study with their knowledge, and a written informed consent was obtained after informing them about the aims and method of the study and the institutional affiliation of the researcher. The study was done by utilizing known investigation modalities, and all the possible treatment options will be given and none was withheld. Confidentiality of data collected from contribution source or individual was maintained.
A total of 110 patients were screened for a study period of 18 months. Patients having hematemesis, oral bleed, epistaxis, and upper respiratory tract bleeding were excluded from the study. Sixty-four patients with “true hemoptysis” were finally included in the study. After obtaining informed consent from the patients, baseline demographic data such as age, sex, address, and amount of hemoptysis were noted. Severity of hemoptysis is classified as mild (<30 ml), moderate (31–100 ml), severe (101–600 ml), and massive hemoptysis (>600 ml or any amount of bleeding with hemodynamic and respiratory compromise) over 24 h. Duration of hospital stay, interventions done, complications encountered, and final outcome were noted.
Etiological diagnosis was based on clinical history and examination supported by appropriate investigation. Radiography of chest, computed tomography (CT), and digital subtraction angiography were carried out in all to evaluate structural changes in the lung. Sputum examination was carried out for etiological diagnosis including Gram stain and cultures. Sputum was also examined for acid-fast bacilli and fungi. Bronchoscopy and histopathological examination (fine-needle aspiration/biopsy) was carried out wherever indicated. Active tuberculosis was diagnosed on the basis of sputum positivity and radiological features (nodules, alveolar, or interstitial infiltrates) predominantly in upper lobe of the lung (s) along with constitutional symptoms such as weight loss, loss of appetite, and low-grade fever/night sweats. Inactive tuberculosis/sequelae was diagnosed on the basis of the previous history of tuberculosis and radiological features such as fibrocavitary disease predominantly affecting upper lobes, in patients without having systemic symptoms. Bronchiectasis was diagnosed on the basis of clinical history and radiological findings. Lung cancers were diagnosed on the basis of clinical, radiological, bronchoscopic, and histopathological examination.
All patients received conservative management which consisted of maintaining a patent airway, breathing, and circulation. Cough suppressants, bed rest, and antibiotics/antitubercular drugs were initiated wherever indicated. Bronchial/pulmonary artery embolization (BAE/PAE) was considered if hemoptysis was not controlled with conservative management. Descriptive statistics were applied, and results presented as mean with standard deviation and percentage.
| Results|| |
During the study period, a total of 110 patients were screened and 64 patients who had true hemoptysis were included in the study. The study population included 50 males and 14 females. Mean age of patients was 41.7 years. Mean duration of ongoing hemoptysis was 2.1 ± 1.22 days. Majority of patients had severe hemoptysis (98%) and rest had moderate hemoptysis. Baseline laboratory parameters of these patients are provided in [Table 1]. Out of fifty males, thirty were active smoker and ten had quit smoking in the past 6 months. The mean smoking index of the patients was 120.1 ± 44.2 out of forty female patients only two were smokers but had quit in the past 6 months. All the five patients with a diagnosis of bronchogenic carcinoma had quit smoking in the past 1 month. None of the patients was on antiplatelets and anticoagulants at presentation. History and clinical features suggestive of chronic obstructive pulmonary disease (COPD) were found in 33 males and 5 female patients. None of them at presentation had an acute exacerbation of COPD. Two patients had chronic kidney disease and were on conservative management. Mean duration of hospital stay of the patients was 4.81 (±3.22) days.
Majority of the patients had tuberculosis (65%) as the etiology. Active tuberculosis (sputum positivity for acid-fast bacillus) was noted in 40% of patients and sequel of pulmonary parenchymal tuberculosis was present in 60% of patients. Pneumonia (community acquired) was the etiological diagnosis in 10.75% cases. The other important etiologies were bronchogenic carcinoma, vasculitis, and congenital heart disease [Table 2]. Secondary bacterial infections as a cause of active hemoptysis could be diagnosed in 25 patients with inactive tuberculosis (20) and bronchiectasis (5). The most common organism causing infection was Pseudomonas (16) and Klebsiella spp. (9) isolated from sputum. Only one patient had a fungal ball in the preexisting tubercular cavity (inactive tuberculosis) causing active hemoptysis.
Nearly 76.6% patients responded to conservative management and the hemoptysis was controlled. Fifteen (23.4%) patients underwent intervention for controlling ongoing bleeding. Majority, i.e., 46.7% (7/15) of patients underwent intervention for controlling ongoing hemoptysis, whereas 26.7% (4/15) underwent prophylactic embolization due to hypertrophic bronchial arteries with increased risk of re-bleeding. About 26.7% of the patients, who had responded initially to conservative management, had re-bleed within first 48 h. They underwent interventions for recurrence of hemoptysis. Bronchial artery embolization was done in 11 (73.3%) patients, whereas PAE was done in 4 (26.7%) patients. Out of 15 patients who underwent intervention, majority (60%) of the patients had pulmonary parenchymal abnormalities secondary to tuberculosis, and hemoptysis was attributed to increased vascularity in the cavity wall or pseudoaneurysms. One patient died due to basic disease (septic shock with necrotizing pneumonia) and one patient left the hospital against medical advice after the hemoptysis was not controlled with conventional treatment.
| Discussion|| |
Etiology of hemoptysis can vary from infections to malignancy, and it may differ in developed countries when compared to developing countries, where infections still are a major etiological factor. Within a geographic region, the etiology may change over a period of time due to changing epidemiology of diseases. In developed countries, studies done during the 1940s and 1950s noted tuberculosis to be an important cause of hemoptysis. A study by Abbott in 1940 in the USA (Atlanta) reported tuberculosis to be responsible for hemoptysis in 22% patients, with bronchiectasis and malignancy being other important etiologies. Subsequent studies done during 1977–1985, 1974–1981, and 1980–1995 in developed countries demonstrated a decreasing trend of tuberculosis from 22% to 1% with proportional rise in the other etiologies.,,
Earliest study from India in 1960 by Rao reported tuberculosis to be the most common cause of hemoptysis. The scenario has remained unchanged in our country. Tuberculosis still remains the most common cause of hemoptysis as evident from our study (65%) and other recently reported studies from India.,,, As evident from our study, both active and inactive tuberculosis are an important cause of hemoptysis. Structural damage caused by tubercular bacillus can subsequently result in pooling of secretions and infections, resulting in hemoptysis in patients with inactive tuberculosis. Secondary bacterial infections are common. Secondary fungal infections can also occur and often difficult to diagnose in resource-constraint countries because of similar presentation to tuberculosis and may require CT thorax, serum precipitating antibodies to Aspergillus species, respiratory cultures, and even lung biopsy or videothoracoscopy in some cases. In our study, secondary bacterial infections were present in patients with inactive tuberculosis and bronchiectasis, but fungal ball was demonstrable in only one patient with inactive tubercular cavity.
In developed countries, nontubercular causes such as malignancy, bronchiectasis, and pneumonia have evolved as important causes of hemoptysis in posttuberculosis era. Incidence of malignancy, in various reported studies looking at epidemiology of hemoptysis from developed countries, ranges from 5% to 44%.,,,, Indian studies have not reported very high incidence of lung malignancy as etiology of hemoptysis. In the present study too, malignancy was responsible for active hemoptysis in 6.25% patients only. Other Indian studies too have also reported similar findings (0%–6.6%).,,,,, It implies that in India, malignancy is an important cause but is not as common as it is in developed countries, where it has taken over infections to emerge as a major cause of hemoptysis [Table 3].
In our study, community-acquired pneumonia (bacterial) was present in 10.72% whereas other studies from India have reported it to be ranging from 1.7% to 25.5%.,, Bronchiectasis was present in 9.3% in our study which is slightly lower than 13.6% reported by Rao in 1960. More recent studies from India have reported the incidence of bronchiectasis to range between 3.8% and 21% whereas studies from developed world have reported bronchiectasis to range from 21% (1940–1947) to 19% (1980–1995).,,,,,,
This highlights the fact that structural lung damage is an important etiological factor responsible for hemoptysis, which could result from tuberculosis in developing countries and bronchiectasis due to various etiologies in developed countries. Secondary bacterial and fungal infection in bronchiectasis and inactive pulmonary tubercular lesions was responsible for causing hemoptysis in our patients, as has been the experience from developed countries, justifying the use of antibiotics in management.,
Most of the patients respond to management with conservative treatment and BAE/PAE for controlling hemoptysis is required only in few patients. In our study, <25% patients required intervention for controlling bleeding/preventing re-bleed. Since bronchial artery is the most common source of bleeding, bronchial artery embolization can save many lives by controlling ongoing bleed. In our study, only one patient died and the death was not directly related to hemoptysis. One patient left against medical advice when hemoptysis was not controlled (outcome not known). Observed mortality was low compared other studies reported from India which ranges from 8.2% to 18.8% in various studies., Studies from Thailand and Singapore have reported similar mortality ranging from 17.8% to 13%, respectively. Other studies have documented mortality ranging from 9% to 10%.,, The reason for low mortality in our study could be the proactive embolization undertaken by us. This further strengthens our belief that aggressive management of moderate-to-severe hemoptysis can help in saving many lives.
| Conclusion|| |
Tuberculosis still remains an important cause of hemoptysis in India. Both active tuberculosis and posttubercular sequelae can result in hemoptysis, whereas in the Western world, nontubercular causes such as malignancy, bronchiectasis, and bronchitis are leading causes of hemoptysis. Posttuberculosis sequelae constituted a most common cause of hemoptysis in our study, thus emphasizing the importance of controlling tuberculosis. Early and aggressive intervention with the use of vessel embolization can reduce mortality.
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| References|| |
Cahill BC, Ingbar DH. Massive hemoptysis. Assessment and management. Clin Chest Med 1994;15:147-67.
Ozgül MA, Turna A, Yildiz P, Ertan E, Kahraman S, Yilmaz V. Risk factors and recurrence patterns in 203 patients with hemoptysis. Tuberk Toraks 2006;54:243-8.
Thompson AB, Teschler H, Rennard SI. Pathogenesis, evaluation, and therapy for massive hemoptysis. Clin Chest Med 1992;13:69-82.
Conlan AA, Hurwitz SS, Krige L, Nicolaou N, Pool R. Massive hemoptysis. Review of 123 cases. J Thorac Cardiovasc Surg 1983;85:120-4.
Yeoh CB, Hubaytar RT, Ford JM, Wylie RH. Treatment of massive hemorrhage in pulmonary tuberculosis. J Thorac Cardiovasc Surg 1967;54:503-10.
Abbott OA. The clinical significance of pulmonary hemorrhage; a study of 1316 patients with chest disease. Dis Chest 1948;14:824-42.
Johnston H, Reisz G. Changing spectrum of hemoptysis. Underlying causes in 148 patients undergoing diagnostic flexible fiberoptic bronchoscopy. Arch Intern Med 1989;149:1666-8.
Santiago S, Tobias J, Williams AJ. A reappraisal of the causes of hemoptysis. Arch Intern Med 1991;151:2449-51.
Hirshberg B, Biran I, Glazer M, Kramer MR. Hemoptysis: Etiology, evaluation, and outcome in a tertiary referral hospital. Chest 1997;112:440-4.
Rao P. Hemoptysis as a symptom in a chest clinic. Indian J Chest Dis 1960;2:219.
Prasad R, Garg R, Singhal S, Srivastava P. Lessons from patients with hemoptysis attending a chest clinic in India. Ann Thorac Med 2009;4:10-2.
] [Full text]
Talwar D, Chudiwal J, Jain R, Kumar S. Massive hemoptysis in a respiratory ICU: Causes, interventions and outcomes-Indian study. Crit Care 2012;16 Suppl 1:1-520.
Nawal SK, Heda MR. Hemoptysis: A prospective analysis of 110 cases. Asian J Biomed Pharm Sci 2013;3:1-3.
Singh SK, Tiwari KK. Etiology of hemoptysis: A retrospective study from a tertiary care hospital from Northern Madhya Pradesh, India. Indian J Tuberc 2016;63:44-7.
Ofori A, Steinmetz AR, Akaasi J, Asafu Adjaye Frimpong GA, Norman BR, Obeng-Baah J, et al.
Pulmonary aspergilloma: An evasive disease. Int J Mycobacteriol 2016;5:235-9. [Full text]
Pursel SE, Lindskog GE. Hemoptysis. A clinical evaluation of 105 patients examined consecutively on a thoracic surgical service. Am Rev Respir Dis 1961;84:329-36.
van Kralingen KW, van Kralingen-Heijboer AC, Zimmerman M, Postmus PE. Management of hemoptysis in a Third World city hospital: A retrospective study. Tuber Lung Dis 1995;76:344-8.
Souders CR, Smith AT. The clinical significance of hemoptysis. N
Engl J Med 1952;247:790-3.
Moersch HJ. Clinical significance of hemoptysis. J Am Med Assoc 1952;148:1461-5.
Suri JC, Goel A, Singla R. Cryptogenic hemoptysis: Role of fiberoptic bronchoscopy. Indian J Chest Dis Allied Sci 1990;32:149-52.
Jindal SK, Gilhotra R, Behera D. Fiberoptic bronchoendoscopic examination in patients with haemoptysis and normal chest roentgenogram. J Assoc Physicians India 1990;38:548-9.
Sharma SK, Dey AB, Pande JN, Verma K. Fiberoptic bronchoscopy in patients with haemoptysis and normal chest roentgenograms. Indian J Chest Dis Allied Sci 1991;33:15-8.
McGuinness G, Beacher JR, Harkin TJ, Garay SM, Rom WN, Naidich DP. Hemoptysis: Prospective high-resolution CT/bronchoscopic correlation. Chest 1994;105:1155-62.
Angrill J, Agustí C, de Celis R, Rañó A, Gonzalez J, Solé T, et al.
Bacterial colonisation in patients with bronchiectasis: Microbiological pattern and risk factors. Thorax 2002;57:15-9.
Reechaipichitkul W, Latong S. Etiology and treatment outcomes of massive hemoptysis. Southeast Asian J Trop Med Public Health 2005;36:474-80.
Ong TH, Eng P. Massive hemoptysis requiring intensive care. Intensive Care Med 2003;29:317-20.
Corey R, Hla KM. Major and massive hemoptysis: Reassessment of conservative management. Am J Med Sci 1987;294:301-9.
[Table 1], [Table 2], [Table 3]
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