Chapter 13

Haemoptysis

George Z. Cheng and Momen M. Wahidi

Dept of Medicine, Duke University Medical Center, Durham, NC, USA.

Correspondence: George Z. Cheng, Duke University Medical Center, DUMC Box 102356, Durham, NC 27710, USA. E-mail: george.cheng@duke.edu

Haemoptysis is a commonly encountered clinical entity in pulmonary medicine. Ranging from self-limited blood-streaked sputum (85–95%) to massive bleeding (5–15%), haemoptysis has variable presentations and, ultimately, different management approaches based on the severity of bleeding [1]. Massive haemoptysis can rapidly compromise airways, resulting in asphyxiation rather than exsanguination. Therefore, it should be viewed as a medical emergency requiring prompt intervention. Untreated massive haemoptysis has a mortality rate approaching 50% [2]. A patient with massive haemoptysis should be managed with appropriate positioning, securing the airway to maintain respiratory and cardiovascular function, and correcting any coagulopathy that may contribute to the bleeding [3]. This is quickly followed by evaluation for the source of the bleed via bronchoscopy and HRCT. Bronchoscopy is essential for localisation, isolation and control of the haemorrhage source in the case of endoluminal lesions. HRCT provides a global assessment of the lung tissue, vital mediastinal structures and parenchymal bleeding source [4]. Here, we review the definitions, anatomy, aetiology, and diagnostic and management approaches to haemoptysis with a special focus on massive haemoptysis.

Definitions

Haemoptysis, derived from the Greek root of haima for blood and ptysis for the act of spitting, can be mild to massive. Mild or nonmassive haemoptysis is not life-threatening and often self-limited. The patient maintains adequate ventilation and oxygenation, usually does not require hospitalisation, observation is often the mainstay of management, and additional outpatient workup should be individualised with regard to the patient’s comorbid conditions. Massive haemoptysis is often life-threatening and requires prompt intervention; however, there is no consensus on its definition [5].

Using the amount of expectorated blood as a measurement of haemoptysis is challenging in clinical practice. Patients do not quantify the amount of perceived haemoptysis in millilitres. The description is often more colloquial, in terms of cups or the amount and frequency of haemoptysis, thus leading to grossly inaccurate measurements. The published literature does not have a consensus on what is considered to be massive haemoptysis. Threshold ranges from 100 to 1000 mL over 24 h have been proposed, but none has been universally accepted [1, 6–9].

Pathophysiologically, the conducting airway (i.e. anatomical dead space) volume is ∼150 mL. Therefore, if blood was to fill the conducting airways, there would be significant airway obstruction and interference with ventilation and oxygenation. Furthermore, the clinical response of a patient with haemoptysis often depends on their underlying cardiopulmonary reserve and comorbidities. Any disease states (i.e. neuromuscular weakness, tracheal stenosis and COPD) that interfere with the ability to effectively clear the airway will change the threshold for considering intervention [10, 11]. Therefore, if there is evidence of abnormal gas exchange or haemodynamic instability secondary to haemoptysis, we propose to consider intervention regardless of the amount of bleeding. However, in a patient without gas exchange abnormalities, we proposed to use 100 mL in 1 h (two-thirds of the anatomical dead space) or 300 mL in 24 h (two times the anatomical dead space) as the threshold for intervention.

Anatomy

The lung and its conducting airways receive dual circulation from the bronchial arteries and the pulmonary arteries. There are wide anatomical variations in the origins of bronchial arteries. Generally, bronchial arteries originate from the descending thoracic aorta, most often at the T5–T6 level and less frequently from vertebral or intercostal arteries. Typically, one bronchial artery supplies the right lung and two bronchial arteries supply the left lung. These vessels supply the airways from the trachea to the terminal bronchioles, hilar lymph nodes, visceral pleura and other mediastinum structures (the middle third of the oesophagus, vagus nerve, vasa vasorum of the aorta and pulmonary trunks). Of note, in ∼5% of individuals, the spinal artery originates from the bronchial artery, which has implications for procedures involving embolisation of bronchial arteries [2, 12–15]. The pulmonary arteries carry deoxygenated blood to the alveolar capillary bed and supply the lung parenchyma and the respiratory bronchioles, where anatomical anastomosis with bronchial arteries exists. While bronchial arteries carry only 1% of the total lung blood flow, this is a high-pressure system compared with pulmonary arteries, which form a low-pressure system. As such, 90% of massive haemoptysis has a bronchial artery origin compared with 5% attributable to pulmonary circulation [3, 16]. Of note, chronic inflammatory, infectious or vascular lung diseases can cause significant alterations in vascular anatomy, resulting in enlargement, marked tortuosity and altered anastomosis of bronchial arteries, which lead to increased arterial blood flow and risk of bleeding [13].

Aetiology

There are many causes for haemoptysis originating from the lower respiratory tract, including but not limited to infectious, inflammatory, malignant, haematological, vascular, iatrogenic and toxin-related categories. Historically, three aetiologies account for 90% of massive haemoptysis, i.e. bronchiectasis, tuberculosis and lung abscess [1]. However, more recent epidemiological data suggest that the causes of haemoptysis are evolving, with bronchogenic carcinoma, mycetomas and cryptogenic haemoptysis becoming more prominent [17–19].

Bronchiectasis

Bronchiectasis is the result of recurrent infectious and inflammatory processes, characterised by abnormal bronchial wall thickening with a dilated lumen, chronic sputum production associated with cough and airflow obstruction. Chronic airway inflammation in bronchiectasis leads to increased tortuosity and enlargement of the bronchial arteries to the affected bronchial tree. In addition, there is a corresponding increase in the submucosal and peribronchial capillary plexus. Rupture of either the bronchial artery or the capillary plexus will lead to significant haemoptysis. This pattern often occurs in patients with disease entities that predispose them to recurrent infections, such as cystic fibrosis, rheumatological disease, allergic bronchopulmonary aspergillosis, immunodeficiency, ciliary dysfunction, haematological malignancies, recurrent aspiration and nontuberculous mycobacteria infection [20, 21].

Tuberculosis

While the incidence and distribution of tuberculosis have changed in recent decades secondary to advances in antimycobacterial therapy, it remains a prominent cause of massive haemoptysis in areas of the world where tuberculosis is prevalent, such as South-East Asia and Africa [6, 22, 23]. Tuberculosis can lead to haemoptysis both in prior and active infection. With prior tuberculosis infection, massive haemoptysis can occur when calcified lymph nodes or broncholiths erode into an airway interrupting a bronchial artery, due to bronchiectasis as a result of prior tuberculosis infection or as a result of a superimposed fungal infection within the lung cavity due to prior pulmonary tuberculosis. With active tuberculosis infection, significant bleeding often occurs due to the necrosis of bronchial vessels adjacent to the airway involved in active infection, which can occur in both cavitary and noncavitary disease. Active tuberculosis can also lead to Rasmussen’s aneurysm, where infectious processes lead to slow expansion of the pulmonary artery, resulting in eventual rupture of the vessel wall due to chronic inflammation [24, 25].

Fungal infections

Fungal infections leading to massive haemoptysis in patients with cavitary lung disease are most often attributed to Aspergillus. Aspergilloma or mycetoma is formed from Aspergillus hyphae, cellular debris, fibrin and mucin within a lung cavity. The chronic inflammatory process leads to bronchial artery dilation and hypertrophy surrounding these cavities, and predisposes these areas to bleed. Patients with aspergilloma report haemoptysis very frequently, ranging from 50% to 90% during their disease course [1]. Angio-invasive fungal infections from Aspergillus or Mucor in immunocompromised hosts (such as those undergoing stem cell transplantation) can result in haemoptysis during the engraftment phase when the neutrophil count begins to rise. Neutrophil infiltration of the infected lung parenchyma initiates the inflammatory response that leads to disruption of bronchial vessels and results in massive haemoptysis [26–29].

Lung abscess

Lung abscesses arise from polymicrobial/anaerobic infections secondary to aspiration or necrotising pneumonias and can result in massive haemoptysis due to either tissue necrosis or bronchial artery rupture. The risk factors for developing haemorrhage from a lung abscess include thrombocytopenia or coagulopathy from systemic disease such as liver failure or bone marrow suppression [30]. In a recent review of patients who underwent anatomical lung resection for haemoptysis, lung abscess was an independent predictor of death along with advanced age, renal failure, sarcoidosis and extent of resection [31].

Bronchogenic carcinoma

Roughly 20–60% of lung cancer patients will experience varying degrees of haemoptysis, with ∼7–10% at the time of presentation [1]. Recent evidence suggests that lung cancer patients represent over half of the patients who present with massive haemoptysis [32, 33]. Among patients with massive haemoptysis, eight out of 10 had sentinel-bleeding events in the weeks prior to presentation. Large, endobronchial, centrally located tumours (such as squamous cell carcinoma) are more likely to be associated with haemoptysis. This is especially true with the use of bevacizumab (an antiangiogenesis agent that leads to tumour cavitation) in squamous cell lung cancer, where six out of 66 patients had haemoptysis and there were four fatal outcomes during the phase II trial [34]. Furthermore, metastatic lesions to the lung are also associated with haemoptysis. Melanoma, colon, breast and prostate cancer have a propensity for endobronchial metastasis, whereas renal cell carcinoma, thyroid cancer and sarcomas tend to form parenchymal lesions in the lung. These lesions have a tendency to cause bleeding due to necrosis, mucosal invasion or local angiogenesis [10].

Cryptogenic haemoptysis

Cryptogenic or idiopathic haemoptysis refers to haemoptysis without a clear aetiology after clinical assessment, radiographic studies and fibreoptic bronchoscopy evaluation. In the reported literature, cryptogenic haemoptysis encompasses 7–42% of haemoptysis cases. When these patients with cryptogenic haemoptysis are followed, 6–10% will eventually be diagnosed with lung cancer, especially in smokers and those over 40 years old [17, 35, 36]. Cryptogenic/idiopathic haemoptysis is a diagnosis of exclusion. Immunological lung diseases (e.g. Goodpasture’s syndrome, granulomatosis with polyangiitis, microscopic polyangiitis and systemic lupus erythematosus) or cardiovascular defects (e.g. pulmonary arteriovenous malformations, bronchial Dieulafoy’s lesion, mitral stenosis, pulmonary hypertension, pulmonary emboli and aortic aneurysms) should be excluded prior to reaching a diagnosis. In young female patients, thoracic endometriosis (catamenial haemoptysis) or lymphangioleiomyomatosis (spontaneous pneumothorax and haemoptysis in the setting of cystic lung disease) should be considered [11].

The aetiology of haemoptysis is variable. A useful approach is to consider anatomical location and the disease process that is involved (table 1). Clinical suspicion will ultimately direct diagnostic and management approaches.

Diagnostic approaches

When evaluating a patient with haemoptysis, it is essential to determine that the haemorrhage is coming from the lung and not from the supraglottic airway (i.e. epistaxis) or gastrointestinal tract (i.e. haematemesis). If pseudohaemoptysis is suspected, then evaluation by otolaryngology or gastroenterology will be essential for diagnosis and management. Typically, haemoptysis is alkaline, bright red colour with oxygen saturation close to that of arterial blood, whereas haematemesis tends to be acidic, dark coffee ground colour with oxygen saturation close to that of venous blood. Careful examination of the oral and nasal passage can provide clues to bleeding in the naso- or oropharynx [9].

History and physical examination are important to haemoptysis evaluation, in that pertinent findings will guide clinical evaluation and therapeutic intervention. For example, a history of infectious exposure, fever and cough will lead one to consider pulmonary cavitary lesions, whereas a history of haemoptysis corresponding with menstruation will lead one to consider catamenial haemoptysis. Clinical presentation of the patient will ultimately triage the urgency of diagnostic workup and management.

Laboratory evaluation of a patient presenting with haemoptysis should be targeted. A complete blood count, coagulation studies, a basic metabolic panel, a hepatic function panel, arterial blood gases, urinalysis, and blood typing and cross-matching should be obtained as the initial assessment. Correction of underlying coagulopathy will aid in controlling haemoptysis. Urinalysis will provide clues to possible pulmonary renal syndromes (i.e. presence of blood in the urine may trigger a workup for vasculitis).

Radiological workup

Chest imaging is one of the cornerstones of diagnostic evaluation in haemoptysis. The goal is to localise the bleeding site so as to direct management. Chest radiography is inexpensive, ubiquitous and can rapidly provide lateralising information. While chest radiography is commonly the initial imaging study, it has significant limitations. In one series, chest radiography only provided the location in 46% and the cause in 35% of haemoptysis cases [37]. Furthermore, patients with haemoptysis secondary to malignancy had normal chest radiography ∼25% of the time [36]. Therefore, when evaluating haemoptysis, a normal chest radiograph is not sufficient and should warrant additional workup either with bronchoscopy or a multidetector CT (MDCT) scan.

MDCT or HRCT scan

A CT scan should be performed in the setting of gross or recurrent haemoptysis, especially in patients with increased cancer risk (i.e. more than 30 pack-years smoking history, over 40 years of age), suspected bronchiectasis or with unrevealing chest radiography. A HRCT scan without contrast is ideally used in patients with self-limiting haemoptysis without risk factors for cancer and those with renal dysfunction. An MDCT scan with contrast or angiography should be done for patients with active bleeding or those with a high risk of cancer who are being considered for embolisation procedures [38–40]. MDCT angiography is noninvasive and highly accurate in characterising thoracic, bronchial, ectopic nonbronchial and pulmonary arteries that may be involved in bleeding, correctly identifying the bleeding vessel up to 85% of the time [40]. Pathological characteristics of bronchial arteries include increased tortuosity and diameter ≥2 mm. High-resolution volumetric reconstructions of bronchial arteries can effectively aid in procedural planning [2]. The major limitations of CT scans are the time that is required to obtain the image and the supine position of the patient that may impair airway clearance.

Bronchoscopy

Flexible and rigid bronchoscopies are essential techniques for identifying and treating haemoptysis causes in the airway. Flexible bronchoscopy is able to localise the bleeding source in 73–93% of patients [37, 41]. Studies have demonstrated that early bronchoscopy (i.e. during active bleeding episodes or within 48 h of cessation) can better localise the active bleeding source; however, clinical diagnosis and outcome did not vary [42, 43]. Importantly, rigid bronchoscopy should be considered as the first line for evaluation and treatment of massive haemoptysis, as it affords adequate suction for evacuating blood and clots, and concurrent ventilation and airway maintenance. However, use of rigid bronchoscopy is limited by the need for general anaesthesia, experience in its use, and the restricted airway accessibility to the trachea and main bronchi. Therefore, flexible bronchoscopy is often performed through the rigid bronchoscope to achieve adequate airway evaluation and bleeding control involving distal airways (figure 1a) [44–47].

Figure 1. a) Massive haemoptysis with refresh blood coming from both the left and right mainstem. b) SURGICEL application (Ethicon, Somerville, NJ, USA) to the anterior segment of the right upper lobe. Reproduced with kind permission of J. Cárdenas-García (Penn State Milton S. Hershey Medical Center, Hershey, PA, USA). c) Fogarty balloon occlusion to the right upper lobe. d) Arndt endobronchial blocker (Cook Medical, Bloomington, IN, USA) to the left mainstem.

Diagnostic complements

Bronchoscopy is complementary to the use of a CT scan. Bronchoscopy is better for detection of airway bleeding sources, whereas a CT scan provides information on lung parenchymal and vascular abnormalities. One study showed that a CT scan more effectively identified the cause of the bleed (77% versus 8%), but was not superior to bronchoscopy in detecting the bleeding site (70% versus 73%) [37]. However, in patients with no appreciable bleeding source on a CT scan, bronchoscopy can aid in detecting the source of the bleed [48]. Most importantly, bronchoscopy can obtain samples from lavage and tissue for microbiology, cytology and histopathology examination.

Management

Patients with haemoptysis are triaged based on severity of bleeding. Not all patients who present with haemoptysis require hospitalisation; in particular, those with self-limiting and intermittent blood-streaked sputum can often be managed as outpatients. However, patients with massive haemoptysis should be considered as a medical emergency and require multidisciplinary management teams, including emergency physicians, intensivists, pulmonologists, interventional radiologists and cardiothoracic surgeons, and the possible involvement of otolaryngologists and gastroenterologists. The therapeutic goal is to maintain airway patency, localise and stop the bleeding source, and monitor for any haemodynamic instability and recurrent bleed [4, 9, 38].

General considerations

The patient presenting with active massive haemoptysis should be admitted to the intensive care unit for close monitoring; it is necessary to provide supplemental oxygen and empiric antibiotics, obtain laboratory studies for workup of haemoptysis, maintain total fasting, and insert adequate large bore intravenous access for resuscitation. It is important to stress that once the side of active bleeding is known, the patient should be placed in the lateral decubitus position with the bleeding side down. With this positioning, one can delay the spillage of blood into the nonbleeding side. In general, intubation should be considered only if the patient cannot maintain his/her airway. As the patient’s native cough reflex is often more efficient than the suction catheters available for blood clearance, endotracheal intubation should not be done routinely without consideration. However, if there is any sign of fatigue or ventilation defects, intubation with a large (8.5–9.0 mm diameter) bore endotracheal tube will allow adequate suctioning and therapeutic flexible bronchoscopy. Ideally, in the setting of experienced bronchoscopists, rigid bronchoscopy should be performed to ensure the most efficient means of clearing the airway and treatment of airway bleeding source or blocking off active bleeding lung segments in order to prevent asphyxia.

Bronchoscopic treatment

Several strategies are available for efficient bronchoscopic treatment of the bleeding airway. The operator should be familiar with techniques of effective suctioning, maintaining a clear bronchoscopic visual field and clot evacuation [49]. Endobronchial pharmacological and mechanical therapies are reviewed in the following subsections. In general, pharmacological therapies that can reach distal airways are more effective on peripheral sites of bleeding, while mechanical therapies are often limited to the more central sites of bleeding where visualisation of the bleeding source is required for effective therapy delivery.

Ice saline lavage

Endobronchial irrigation with normal saline at 4°C (ice saline) for massive haemoptysis has been used since the 1980s. The initial report of ice saline treatment for massive haemoptysis examined 12 consecutive patients with at least 600 mL of haemoptysis in 24 h. All patients were treated with rigid bronchoscopy. The bleeding side was repeatedly irrigated with ice saline at 4°C in 50 mL aliquots, where each aliquot was left in for 30–60 s prior to suction removal. On average, 500 mL (range 300–750 mL) per patient was used to stop bleeding. One out of the 12 patients had transient sinus bradycardia that resolved without intervention. Two out of the 12 patients had recurrent bleeding that required repeat ice saline lavage. The mechanism of action of ice saline was attributed to cold-induced vasoconstriction and clot formation [50]. Ice saline irrigation can be used with a flexible bronchoscope via a large bore endotracheal tube; however, there is less control of selective ventilation and suction. Unfortunately, most of the data with ice saline is from retrospective case series and no current randomised control trial for evaluation of ice saline use in massive haemoptysis has been performed [9].

Pharmacological therapy

Topical epinephrine, tranexamic acid, fibrinogen–thrombin complex, n-butyl-2-cyanoacrylate and oxidised regenerated cellulose have been reported in controlling haemoptysis. However, their efficacy in massive haemoptysis is not known due to a lack of high-quality studies. Additionally, topical agents are often diluted and washed away by the blood in the airway, thus decreasing their true efficacy. We will briefly review their use here.

Topical endobronchial application of epinephrine has been used to achieve local vasoconstriction and bleeding control in the setting of endobronchial biopsy or TBB. The safety profile of diluted epinephrine (1:10 000) applied in 2 mL aliquots up to a maximum dose of 0.6 mg has had very long experiential support [51]. However, the use of epinephrine in massive haemoptysis is limited to a case report [52]. Unintended hypertension and tachyarrythmias can also occur, and therefore endobronchial epinephrine should be avoided in the elderly, in patients with coronary artery disease and in the setting of carcinoid tumours [53].

Use of an antifibrinolytic drug, i.e. tranexamic acid, via oral or i.v. administration, in patients following major surgery has been well established [54]. However, there is only limited evidence for its use in controlling haemoptysis from any cause [55]. In recent reports, both topical application (500 mg tranexamic acid in 15 mL of normal saline) and intralesional injection (250–500 mg tranexamic acid in 2.5–5 mL of normal saline) appear to decrease endobronchial bleeding related to malignancy and bronchoscopic biopsies [56, 57]. In a recent randomised study comparing endobronchial epinephrine (1 mg in 20 mL of saline) with tranexamic acid (500 mg in 20 mL of saline) there appears to be no difference in the efficacy between these agents in controlling haemoptysis [58]. Finally, there is one case series of four patients (three with lung cancer and one with bronchiectasis) with moderate haemoptysis (100 mL per 24 h) successfully treated with nebulised tranexamic acid (250–500 mg in 2.5–5 mL every 8 h) [59]. While these are encouraging reports, there is still insufficient data to recommend the routine use of tranexamic acid, especially in the setting of massive haemoptysis. Furthermore, tranexamic acid at a high dose and in susceptible populations (i.e. the elderly, renal failure, cardiac disease and those with prior neurological defects) can lead to seizures [60]. This adverse effect has also been reported in haemoptysis treatment with tranexamic acid [61].

Fibrinogen–thrombin complex for endobronchial treatment of haemoptysis has been in clinical use since the 1980s. The initial report of 33 patients (19 treated with thrombin alone and 14 treated with fibrinogen–thrombin complex) showed promising results in managing massive haemoptysis (>200 mL of blood) [62]. In 1998, fibrinogen–thrombin complex became commercially available as TISSEEL in the USA (Baxter International, Deerfield, IL, USA) and TISSUCOL elsewhere in the world. Bronchoscopic application of TISSUCOL achieved immediate bleeding control in 11 patients with massive haemoptysis (>150 mL per 12 h) refractory or unable to undergo bronchial artery embolisation (BAE). However, three patients had a relapse of bleeding within 12 months of treatment [63]. In addition to TISSEEL, glue material such as n-butyl-2-cyanoacrylate has been used endobronchially in haemoptysis management [64, 65]. Despite these encouraging reports, there is a lack of high-quality controlled studies to recommend routine use in patients with massive haemoptysis.

Oxidised regenerated cellulose (SURGICEL; Ethicon, Somerville, NJ, USA) is a topical haemostatic agent that is biocompatible, absorbable, sterile and bactericidal. SURGICEL and its family of products (SURGICEL SNoW, FIBRILLAR and Nu-KNIT) have broad surgical applications. Endobronchial SURGICEL treatment was first described in 57 patients with massive haemoptysis (>150 mL·h⁻¹ or >150 mL on one occasion) who were refractory to topical ice saline and epinephrine treatment. SURGICEL mesh was cut into strips (maximum 30×40 mm), pulled into the flexible bronchoscope’s working channel with a biopsy forceps and introduced into the bleeding lobar or subsegmental airway to achieve haemostasis. Bleeding was arrested in 56 out of the 57 (98%) treated patients. Six patients had bleeding recurrence within 3–6 days post-treatment. These patients subsequently underwent BAE and two out of six had repeat endobronchial treatment. Five patients developed post-obstructive pneumonia [66]. While the initial experience with SURGICEL is encouraging, the treatment is limited to distal airways and recurrence of bleeding is possible with absorption of the haemostatic SURGICEL plug (figure 1b). Finally, post-obstructive pneumonia risk is significant, especially considering four out of five patients with post-obstructive pneumonia had lobar haemostatic treatment [67].

Mechanical therapy

Physical occlusion of the bleeding airway segment aims to prevent spillage of blood into the healthy lung segments, to allow time for clot formation and to prevent further deterioration of the respiratory status. Once the bleeding side is determined, isolation of the healthy lung can be immediately achieved by selective intubation of the healthy lung with a large bore endotracheal tube. For example, if the blood is coming from the right lung, the left mainstem can be selectively intubated to maintain ventilation of the left lung. Caution should be exercised when selectively intubating the right mainstem due to the close proximity to the right upper lobe take-off. A double-lumen endotracheal tube can be used for selective intubation and lung isolation; however, the use of such tubes is not advocated in haemoptysis due to the small lumen that prohibits therapeutic bronchoscopy. Endobronchial blockers, silicone plugs, and endobronchial stents and valves have been used to achieve airway occlusion in haemoptysis patients. They are reviewed in the following paragraphs.

Balloon occlusion can be used in combination with an endotracheal tube to isolate the bleeding lung and allow therapeutic bronchoscopy treatment. The use of a Fogarty balloon for treatment of massive haemoptysis has been reported since the 1970s [68–70]. However, the Fogarty balloon catheter is placed via the bronchoscope’s working channel and cannot be left in place (figure 1c). To overcome these limitations, different approaches have been described to enable placement of the Fogarty balloon parallel to the bronchoscope [71, 72]. Several systems have been developed to allow long-term balloon tamponade of the airway. The commercially available systems for balloon occlusion include the Arndt endobronchial blocker (Cook Medical, Bloomington, IN, USA), Cohen Flextip endobronchial blocker (Cook Medical), Rusch EZ-Blocker (IQ Medical Ventures, Rotterdam, The Netherlands) and Fuji Uniblocker (Fuji Systems, Tokyo, Japan). The characteristics of each system are summarised in table 2. To date, there are no studies comparing the effectiveness and ease of placement of the different endobronchial blockers in the setting of massive haemoptysis (figure 1d).

Table 2. Endobronchial blockers

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