Critical Care

Massive Hemoptysis

Massive hemoptysis has been variably defined with a range of expectorated blood volume from 100 to >1000 mL in 24 hours along with a persistent airway hemorrhage.1 Consensus is lacking on specific thresholds to characterize massive hemoptysis because these numbers can be challenging to reliably obtain and fail to predict the severity of disease.

Increasingly, focus has shifted away from attempts to quantify the volume or rate of bleeding and toward the estimated risk of major sequelae. In the clinical environment, these risks include hemodynamic instability, shock, and hypoxic respiratory failure.

Most cases of hemoptysis seen in the ED are small in volume and associated with bronchitis, with only 1-5% of hemoptysis cases involving massive or life-threatening bleeding.2 Though relatively rare, emergency physicians need to have working knowledge of massive hemoptysis pathophysiology given the high risk of mortality and the need for timely management.

Anatomy
The lungs have a dual blood supply from the pulmonary and bronchial arterial trees. Alveolar perfusion is supplied mostly from the low-pressure pulmonary arteries, while the connective tissues and pleura are fed by the comparatively smaller, but high-pressure circuit of bronchial arteries. The bronchial circulation, which arises from the thoracic aorta, is a small-caliber, high-pressure system that is the source of 90% of cases of massive hemoptysis. Of the remaining, half are actually fed by the pulmonary arterial system, and the rest by the aorta directly, non-bronchial systemic branches such the intercostals, subclavian, or phrenic arteries.3 

Etiology
The most frequent worldwide cause of hemoptysis is tuberculosis. In the West, the cause of as much as half of the cases of hemoptysis remains unestablished, and of the rest, common causes include inflammatory disease of the airway, bronchiectasis, and bronchial carcinoma and metastases.4 Epistaxis and dental bleeding leading to aspiration and expectoration is a common cause of reported non-massive pseudohemoptysis.5

Pathophysiology
The mechanism of respiratory failure in massive hemoptysis is primarily obstruction of the proximal airways with clotted blood, rather than by flooding of the distal airspaces or by cardiovascular collapse due to frank exsanguination. Because the average total volume of the adult tracheobronchial space is approximately 150 to 200 mL, a fairly small collection of blood can swiftly impede gas exchange. Understanding this pathophysiology focuses the resuscitation to the patient’s tracheobronchial blood clearance and avoids false reassurance in the hemoglobin concentration or distribution of disease seen on chest imaging.

Pre-existing impairment of lung function is an important factor in determining the critical rate of hemorrhage for each patient, rather than an independently derived cutoff, and correlates inversely with tolerance of airway bleeding.6

Management
The paramount priority in emergent management of massive hemoptysis is to maintain or establish and then preserve airway patency, in parallel with testing to identify the source of bleeding to then ultimately coordinate further treatment options. Management of massive hemoptysis often requires interdisciplinary input and co-management by pulmonologists, interventional radiologists (IR), thoracic surgeons and intensivists, a collective grouping that should ideally be coordinated early after presentation by the emergency physician.

The conventions of “securing” an airway with an endotracheal tube and universally positioning the patient on to the bleeding side may be inappropriate in some instances. We recommend against routinely committing a patient to intubation and supine or lateral decubitus positioning who is otherwise clearing airway matter without impairment in gas exchange, and instead favor the natural airway and the most comfortable position the patient finds (which is usually upright and coughing).

If intubation is required, a large diameter (8.0 or wider) endotracheal tube should be used to facilitate emergent flexible bronchoscopy. Turning to the affected side can be attempted, theoretically allowing for continued patency and ventilation of the unaffected lung, but only maintained if gas exchange is thereby improved and adequate suctioning is not limited as a result.

In confirmed left-sided bleeding, a right-mainstem intubation can be attempted if the practitioner is confident about managing single-lung ventilation.7 Left-mainstem intubations are more difficult to achieve without fiberoptic bronchoscopy. Double lumen endotracheal intubation is not routinely recommended due to high risk of malposition and numerous complications including bilateral pneumothoraces, pneumomediastinum and carinal rupture.8

The next most important step after securing the airway is to localize the bleeding. An initial chest radiograph (CXR) is quick and inexpensive, but because of its low sensitivity, a negative CXR in a patient with hemoptysis with signs of impaired gas exchange or any perceived limitation in maintaining a clear airway, should always warrant further diagnostic studies. CT angiography (CTA) of the chest has become instrumental in management of severe hemoptysis, primarily by guiding subsequent bronchial artery embolization (BAE). The goal of this procedure is to reduce the systemic arterial perfusion pressure in the bronchial arteries of the affected area sufficiently to stop the bleeding, with a technical success rate ranging from 65 to 92% depending on the focus of bleeding and case series studied.9 This success rate has largely obviated the role of direct surgical control of hemorrhage, at least as a primary approach. Although CTA rarely identifies the exact source of bleeding, it provides rapid identification of abnormalities of the pulmonary and bronchial arterial systems, such as aneurysms or suspect tortuosity, and non-bronchial feeder arteries contributing to or primarily responsible for the hemorrhage, which are crucial information for interventionalist attempting BAE. CT can also identify other causes of hemorrhage, including those known to be recalcitrant to embolization and for which surgery or other treatments such as bronchoscopy may be the preferred management to offer.10 Critical complications of BAE include recurrent bleeding, particularly in patients with chronic lung disease, and rarely, spinal cord ischemia.11

For the rapidly hemorrhaging patient, bronchoscopy can be severely limited in yield while carrying all of the usual risks, and in those instances should be reserved for airway clearance in patients who are already intubated or who cannot tolerate a CT scan.12,13

In the stable patient with no compromise in oxygenation, if the CTA is unrevealing or an endobronchial lesion has been identified, follow up with pulmonology for outpatient bronchoscopy is reasonable.

In patients with a history of or suspected bronchiectasis presenting with hemoptysis, broad spectrum antibiotics covering gram positive and gram negative pathogens are recommended even in the absence of other symptoms of active infection.14 Novel treatment options including inhaled lysine analogues (antifibrinolytics), ice-cold saline lavages, endobronchial application of vasopressors, direct tamponade with topical hemostatic agents, argon beam therapy, endobronchial stenting, and extracorporeal membrane oxygenation as a bridge to definitive treatment have all been described, but are not well-studied or universally recommended.15-22

Disposition
All patients with diagnosed or presumed massive hemoptysis should be admitted to the hospital for close monitoring of airway clearance and gas exchange given the high rates of complications and limited predictive value of blood volume produced and extent of disease depicted by radiography. A multidisciplinary approach should always be considered, even for palliation of incurable or unresolvable disease burden, with an aim to diagnose if not directly treat the specific cause of bleeding.


References
1. Ibrahim WH. Massive haemoptysis: the definition should be revised. Eur Respir J. 2008;32(4): 1131-1132.
2. Walls RM, Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, PA: Elsevier; 2018.
3. Radchenko C, Alraiyes AH, Shojaee S. A systematic approach to the management of massive hemoptysis. J Thorac Dis. 2017;9(Suppl 10):S1069-S1086.
4. Santiago S, Tobias J, Williams AJ. A reappraisal of the causes of hemoptysis. Arch Intern Med. 1991;151(12):2449-2451.
5. Cordovilla R, et al. Diagnosis and Treatment of Hemoptysis. Arch Bronconeumol. 2016;52(7):368-377.
6. Ittrich H, Bockhorn M, Klose H, Simon M. The Diagnosis and Treatment of Hemoptysis. Dtsch Arztebl Int. 2017;114(21):371-381.
7. Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med. 2000;28(5):1642-1647.
8. Klein U, Krazai W, Bloos F, et al. Role of Fiberoptic Bronchoscopy in Conjunction with the Use of Double-lumen Tubes for Thoracic Anesthesia A Prospective Study. Anesthesiology. 1998;88(2):346-350.
9. Larici AR, Franchi P, Occhipinti M, et al. Diagnosis and management of hemoptysis. Diagn Interv Radiol. 2014;20(4):299-309.
10. Khalil A, Fedida B, Parrot A, Haddad S, Fartoukh M, Carette MF. Severe hemoptysis: From diagnosis to embolization. Diagn Interv Imaging. 2015;96(7-8):775-788.
11. Kalva SP. Bronchial artery embolization. Tech Vasc Interv Radiol. 2009;12(2):130-138.
12. Nielsen K, Gottlieb M, Colella S, Saghir Z, Larsen KR, Clementsen PF. Bronchoscopy as a supplement to computed tomography in patients with haemoptysis may be unnecessary. Eur Clin Respir J. 2016;3:31802.
13. Torbiarczyk JM, Sobczak PA, Torbiarczyk KK, et al. Is bronchoscopy always justified in diagnosis of haemoptysis? Adv Respir Med. 2018;86(1):13-16.
14. Landsberg JW. Clinical practice manual for pulmonary and critical care medicine. Philadelphia, PA: Elsevier; 2017.
15. Prutsky G, Domecq JP, Salazar CA, Accinelli R. Antifibrinolytic therapy to reduce haemoptysis from any cause. Cochrane Database Syst Rev. 2012;18(4):CD008711.
16. Breuer H, Charchut S, Worth H, Trampisch HJ, Glanzer K. Endobronchial versus intravenous application of the vasopressin derivative glypressin during diagnostic bronchoscopy. Eur Respir J. 1989;2(3):225-228.
17. Morice RC, Ece T, Ece F, Keus L. Endobronchial Argon Plasma Coagulation for Treatment of Hemoptysis and Neoplastic Airway Obstruction. Chest. 2001;119(3):781-787.
18. Valipour A, Kreuzer A, Koller H, Koessler W, Burghuber OC. Bronchoscopy-guided topical hemostatic tamponade therapy for the management of life-threatening hemoptysis. Chest. 2005;127(6):2113-2118.
19. Brandes JC, Schmidt E, Yung R. Occlusive Endobronchial Stent Placement as a Novel Management Approach to Massive Hemoptysis from Lung Cancer. J Thorac Oncol. 2008;3(9):1071-1072.
20. Bellam BL, Dhibar DP, Suri V, Sharma N, Varma SC, Malhotra S, Bhalla A. Efficacy of tranexamic acid in haemoptysis: A randomized, controlled pilot study. Pulm Pharmacol Ther. 2016;40:80-83.
21. Gagnon S, Approach to Hemoptysis in the Modern Era. Can Respir J. 2017;1565030.
22. Fagundes Júnior AAP, Chaves RB, Santos ARD, Oliveira HA, Paschoal MH. Massive hemoptysis successfully treated with extracorporeal membrane oxygenation and endobronchial thrombolysis. Rev Bras Ter Intensiva. 2018;30(1):116-120.

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