on 02-Jan-2021 (Sat)

Une expectoration mousseuse, de sang rouge vif, et (si massive) une sensation de suffocation sont caractéristiques de l'hémoptysie vraie.

La revue des systèmes doit rechercher des symptômes suggérant des causes possibles, dont une fièvre et une expectoration (pneumonie); des sueurs nocturnes, une perte de poids et une fatigue (cancer, tuberculose); des douleurs thoraciques et une dyspnée (pneumonie, embolie pulmonaire); des douleurs et un gonflement des jambes (embolie pulmonaire); une hématurie (syndrome de Goodpasture); et un écoulement nasal sanglant (granulomatose avec polyangéïte).

Il faut interroger les patients sur les facteurs de risque étiologiques. Ces facteurs de risque comprennent l'infection par le VIH, la prise d'immunodépresseurs (tuberculose, infection fongique); une exposition à la tuberculose; un tabagisme ancien (cancer); et une immobilisation ou opération récente, un cancer connu, des antécédents personnels ou familiaux de thrombose, une grossesse, une prise d'œstrogènes et des voyages lointains récents (embolie pulmonaire)

Une anamnèse d'épistaxis fréquentes, de formation facile d'ecchymoses, ou de maladie du foie évoque une possible coagulopathie. On doit rechercher la prise d'anticoagulants et d'antiplaquettaires.

Plusieurs signes spécifiques sont importants.

• Une insuffisance rénale ou une hématurie connues évoquent un syndrome réno-pulmonaire (p. ex., syndrome de Goodpasture, granulomatose avec polyangéïte [anciennement appelée maladie de Wegener]).

• La granulomatose avec polyangéïte (anciennement appelée granulomatose de Wegener) peut provoquer des lésions des muqueuses nasales.

• Des télangiectasies visibles évoquent une malformation artérioveineuse.

• Les patients qui présentent une hémoptysie due à un trouble de la coagulation sanguine ont habituellement des symptômes cutanés (pétéchies et/ou purpura) ou des antécédents de prise d'anticoagulant ou d'un traitement médicamenteux antiplaquettaire.

• Une hémoptysie récurrente coïncidant avec les règles évoque fortement une endométriose pulmonaire.

Hémoptysies cryptogénétiques

L'étiologie des hémoptysies reste méconnue dans 30 à 40% des cas, mais le pronostic des hémoptysies cryptogénétiques est généralement favorable, avec habituellement guérison du saignement dans les 6 mois du bilan

L'hémoptysie massive est l'une des rares indications de la bronchoscopie rigide (par opposition à la bronchoscopie flexible), qui permet le contrôle des voies respiratoires, permet un champ visuel plus large qu'une bronchoscopie souple, de meilleures possibilités d'aspiration et est plus adaptée aux interventions thérapeutiques, telles que le traitement par laser.

La bronchite, la bronchectasie, la tuberculose et la pneumonie nécrosante ou l'abcès du poumon sont les causes les plus fréquentes chez l'adulte.

Les infections des voies respiratoires inférieures et l'inhalation de corps étrangers sont les causes les plus fréquentes chez l'enfant.

Criteria for the definition of massive/life-threatening haemoptysis should be better defined.

The epidemiology of haemoptysis has changed over time, particularly in industrialized countries, where bronchiectasis and lung cancer have surpassed tuberculosis as the most frequent causes.

Haemoptysis is defined as the expectoration of blood or blood-streaked sputum from the lower respiratory tract. The term derives from the ancient Greek words haima, meaning blood, and ptysis, meaning spitting

There is a lack of universal consensus on the quantification and severity of haemoptysis events. Haemoptysis is considered scant when involving <5 mL, mild when <20 mL, and moderate when >20 mL

Most authors apply the term massive haemoptysis to bleeding >600 mL/24 hours or >25 mL/hour.

Given the unreliability in both the patient’s and physician’s estimates of expectorated volume, and lack of consensus cut-off volume definition, other authors define haemoptysis as massive in the presence of clinical consequences, such as respiratory failure due to airway obstruction or haemodynamic instability [2].

t has been estimated that volumes of blood in the alveoli above 400 mL are sufficient to significantly alter gas exchange. However, it must be considered than, in many situations, haemoptysis arises in patients with underlying cardiorespiratory disease. These subjects may suffer considerable worsening of gaseous exchange even for smaller quantities of blood.

Life-threatening haemoptysis may be defined as any haemoptysis that:

• ◆ Is >100 mL in 24 hours.

• ◆ Causes abnormal gas exchange/airway obstruction.

• ◆ Causes haemodynamic instability.

Independent of its definition, massive/life-threatening haemoptysis involves only a minority of clinical events (generally 5–10%), but related mortality may exceed 50% [1,2]. Mortality is generally more the result of airway compromise with asphyxiation, rather than exsanguination.

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The relative importance of different causes of haemoptysis has changed over time. For centuries, haemoptysis was considered virtually pathognomonic for pulmonary tuberculosis. The following Hippocratic aphorism: ‘The spitting of pus follows that spitting of blood, consumption follows the spitting of this and death follows consumption’ shows how far rooted in history is the association between haemoptysis and tuberculosis

Box 126.1 Causes of haemoptysis

Infection

• ◆ Mycobacterial (tuberculosis and atypical mycobacteria).

• ◆ Fungal infections (including mycetoma).

• ◆ Necrotizing pneumonia.

• ◆ Lung abscess.

• ◆ Parasitic.

• ◆ Septic emboli.

Pulmonary

• ◆ Acute bronchitis.

• ◆ Chronic obstructive pulmonary disease.

• ◆ Bronchiectasis (including cystic fibrosis).

• ◆ Alveolar haemorrhage.

• ◆ Lymphangioleiomiomatosis.

• ◆ Sarcoidosis.

• ◆ Lung transplantation.

Neoplastic

• ◆ Bronchogenic carcinoma.

• ◆ Metastatic lung cancer.

• ◆ Endobronchial tumours (bronchial adenoma, carcinoid).

Cardiovascular

• ◆ Pulmonary embolism (lung infarct).

• ◆ Pulmonary hypertension.

• ◆ Pulmonary artery aneurysm.

• ◆ Bronchial artery aneurysm.

• ◆ Left ventricular heart failure.

• ◆ Mitral stenosis.

• ◆ Arteriovenous malformations.

Vasculitic

• ◆ Wegener’s granulomatosis.

• ◆ Behçet’s disease.

• ◆ Goodpasture syndrome.

• ◆ Systemic lupus erythematosus.

• ◆ Antiphospholipid syndrome.

Traumatic

• ◆ Foreign body aspiration.

• ◆ Blunt or penetrating chest injury.

• ◆ Aortic aneurysm.

Iatrogenic

• ◆ Bronchoscopy.

• ◆ Endobronchial procedures (brachytherapy, dilation, stent placement, laser).

• ◆ Lung biopsy.

• ◆ Pulmonary artery catheterization.

Drugs and toxins

• ◆ Bevacizumab.

• ◆ Solvents.

• ◆ Crack cocaine.

• ◆ Penicillamine.

Haematological

• ◆ Coagulopathy (congenital, acquired, or iatrogenic).

• ◆ Thrombocytopenia.

• ◆ Platelet dysfunction.

Miscellaneous

• ◆ Cryptogenetic.

• ◆ Endometriosis.

• ◆ Broncholitiasis

It has been estimated that in bronchogenic carcinoma, haemoptysis presents at some point in the natural history of the disease in up to 20% of patients. Conversely, haemoptysis may be the presenting symptom in only 7% of patients with lung malignancy [4]‌. Haemoptysis is more likely to occur, and may manifest earlier in (p. 585) the disease course, when carcinoma originates in a major bronchus compared with more peripheral sites

Haemoptysis may be the result of active tuberculosis, generally with small and chronic bouts of blood, although massive haemoptysis has also been described in this context. Inactive mycobacterial disease may be associated with bleeding arising from post-tuberculous thick-walled cavities or bronchiectasis. Rarely, peri-bronchial calcified lymph node may erode into or distort an adjacent bronchus. This condition is known as broncholithiasis and may be associated with symptoms such as cough, recurrent episodes of fever and purulent sputum, and sometimes massive haemoptysis [5]

The reported incidence of haemoptysis in patients with aspergilloma ranges from 54 to 87.5%. Most patients will experience mild and recurrent episodes of haemoptysis, although roughly 10% may develop massive events [6]‌. Invasive pulmonary aspergillosis in immunocompromised subjects is also associated with haemoptysis events, although rarely fatal

Cystic fibrosis, usually in the context of extensive bronchiectasis, has become an increasingly common aetiology of haemoptysis, probably due to the longer survival of affected patients into adulthood. Approximately 40% of patients with cystic fibrosis will develop an episode of haemoptysis during the course of their life, with an average annual incidence of 0.87% [7]‌.

Necrotizing pneumonia, lung abscess, and lung gangrene caused by bacteria, such as Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus pneumoniae, other Streptococcus spp. and Actinomyces spp. may be associated with haemoptysis in up to 15% of cases [8]‌

Pulmonary hypertension is reported as the underlying cause of haemoptysis in 0.2–4% of cases [11]. Conversely, in patients with Eisenmenger syndrome, haemoptysis is a more common finding

In female patients with thoracic endometriosis haemoptysis represents an early clinical manifestation, occurring at an earlier age, whereas pneumothorax tends to manifest in more advanced disease. In over 80% of cases the right hemithorax is involved [12]

Diffuse alveolar haemorrhage is a rare cause of haemoptysis associated with disruption of the alveolar–capillary barrier. It should be suspected in case of haemoptysis, anaemia and bilateral infiltrates on the chest radiograph. The infiltrates are the result of distal inhalation of blood.

Diffuse alveolar haemorrhage may be associated with Goodpasture’s syndrome, where antibodies to type IV collagen are deposited along the alveolar and glomerular basement membranes, giving rise to haemoptysis. Diffuse alveolar haemorrhage is also associated with systemic vasculitis, such as Wegener’s granulomatosis or microscopic polyangiitis. Less commonly, diffuse alveolar haemorrhage may be associated with other immunological conditions, such as systemic lupus erythematosus, Henoch–Schönlein purpura, IgA nephropathy, rheumatoid arthritis, Behçet’s syndrome, and cryoglobulinaemia. Infectious processes, such as leptospirosis, malaria, and cytomegalovirus infection may present alveolar haemorrhage. A number of drugs are also associated with diffuse alveolar haemorrhage, such as propylthiouracil, carbimazole, and crack cocaine [ 13]

In a sizable number of cases, even after extensive diagnostic work-up, a definitive cause for haemoptosyis is not found. These cases are termed as cryptogentic haemoptysis. The incidence of cryptogenetic haemoptysis varies between different reports, with most being between 15 and 30% [14]. Most of these studies have, however, not systematically used CT evaluation on all patients

The lungs are furnished with a dual blood supply, the bronchial arteries and the pulmonary arteries. The former account for only about 1% of arterial supply to the lung and bring nutrients to the lung parenchyma, the bronchi, and vasa vasorum of the pulmonary arteries and veins

The bronchial arteries are a high-pressure circulation system. They have a variable anatomy in terms of origin and branching distribution. They generally originate from the descending thoracic aorta, at the level of the 3rd–8th thoracic vertebral body, more commonly between T5 and T6 (70–83.3% of cases) [ 15]. The right bronchial artery often arises together with the first aortic intercostal artery to form the intercostobronchial (ICBT) trunk, which usually branches off from the right lateral surface of the descending thoracic aorta. The left bronchial arteries conversely tend to arise from the more anterior surface of the descending thoracic aorta.

In approximately 20–30% of cases aberrant bronchial arteries branch off from other systemic arteries, such as the aortic arch, brachiocephalic artery, subclavian artery, internal mammary artery, inferior phrenic artery, or abdominal aorta. In addition, during chronic inflammatory processes collateral blood supply may be recruited from non-bronchial systemic arteries through transpleural vessels. These collateral non-bronchial vessels may derive from ramifications of subclavian, axillary, internal mammary arteries, as well as from subdiaphragmatic arteries. True bronchial arteries (both normal variants and aberrant) can be distinguished from these non-bronchial systemic arteries in that their trajectory into the pulmonary parenchyma parallels the bronchovascular axes. In contrast, non-bronchial systemic collateral vessels do not run parallel to the airways and have a more unpredictable origin from infradiaphragmatic arteries or from the supra-aortic great vessels or their branches, and enter the parenchyma through the inferior pulmonary ligament or through the adherent pleura; their course is not parallel to that of the bronchi

The pulmonary arteries are a low-pressure circulation system that account for 99% of the arterial supply to the lungs and are responsible for gas exchange. The bronchial and pulmonary systems are in close proximity at the level of the vasa vasorum where they are interconnected by numerous anastomoses. These communications cause a physiological right-to-left shunt that involves approximately 5% of the total cardiac output

Bleeding in the lungs may originate from bronchial arteries, pulmonary arteries, bronchial capillaries, and alveolar capillaries. Bronchial arteries are the most common site of bleeding causing haemoptysis, being involved in approximately 90% of cases [16]. In only 5% of cases does haemoptysis origin from the pulmonary vessels. In the remaining 5% of cases bleeding arises from ectopic bronchial arteries or other non-bronchial systemic arteries (including the aorta)

The most common cause of bleeding from the pulmonary circulation is Rasmussens’s aneurysm. In the walls of cavitary lesions, bronchial or pulmonary arteries may be subject to deformation causing pear-shaped dilatations, which are, in truth, pseudo-aneurysmatic lesions, which may be eroded due to chronic inflammatory derangement. These aneurysms are traditionally considered responsible for haemoptysis in TB patients. However, the development of hypervascularized, dilated, tortuous bronchial vessels, often anastomotic with the pulmonary circulation, in the absence of true aneurysms, may be equally involved in these patients.

In certain situations, the thin-walled capillary communications between the high-pressure systemic bronchial arterial system, and the lower pressure pulmonary arterial system can vasodilate and enlarge. Conditions causing reduced pulmonary arterial perfusion, such as chronic thromboembolic disease and vasculitic disorders, in which there is a reduction in pulmonary arterial supply distal to the emboli, can lead to a gradual increase in the bronchial arterial contribution [3]‌, thereby increasing the importance of bronchial-to-pulmonary artery anastomoses in regions of the lung that are deprived of their pulmonary arterial blood flow. Experimental studies have suggested that the increased bronchial arterial blood flow is due to neovascularization [3]. The anastomotic vessels, which are subjected to increased systemic arterial pressure, are often thin-walled, and prone to rupture into the alveoli or bronchial airways, giving rise to haemoptysis

During acute or chronic tracheobronchitic events, inflammation of the mucosa with vascular engorgement, desquamation, atrophy, and erosion, may lead to bleeding. Infective agents, such as Aspergillus spp. may release fungal endotoxins that exert haemolytic activity. Inflammatory processes release angiogenic growth factors, thus promoting neo-angiogenesis and recruitment of collateral supplies from adjacent vessels and increased anastomoses between bronchial and pulmonary arterial systems [17]

The hypoxic micro-environment associated with tumour growth causes cellular activation of hypoxia-inducible factor (HIF). HIF up-regulation promotes transcription of pro-angiogenic cytokines [20]. Hypoxaemia-induced angiopoietin 2 release plays an important role in initiating vessel sprouting in concert with VEGF. In contrast with angiopoietin-1, which stabilizes blood vessels, angiopoietin 2 destabilizes blood vessels, thus favouring bleeding. The new vessels associated with chronic inflammatory or tumoural pro-angiogenesis are usually thin-walled and fragile, and thus prone to rupture into the airways, therefore causing haemoptysis

Furthermore, a large volume of expectorated blood alone should not define massive hemoptysis, but rather an amount of blood sufficient to cause a condition that threatens the patient’s life can be a more correct and functional definition of severe hemoptysis (4, 5).

Asphyxia due to the flooding of the airways rather than exsanguination is usually the cause of death, and it is commonly accompanied by cardiovascular collapse. The mortality rate from untreated massive hemoptysis is more than 50% (6).

Hemoptysis has multiple causes usually categorized under parenchymal diseases, airway diseases, and vascular diseases.

Bleeding from the small vessels usually causes a focal or diffuse alveolar hemorrhage and is mainly due to immunologic, vasculitic, cardiovascular, and coagulatory causes ( Table 1 ). Causes of bleeding from the large vessels include infectious, cardiovascular, congenital, neoplastic, and vasculitic diseases ( Table 2 )

tabl 1 : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4463269/table/t1-dir-20-4-299/
tabl 2 : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4463269/table/t2-dir-20-4-299/

Complex capillary anastomoses exist between the pulmonary arteries and the systemic bronchial arteries (9). When pulmonary circulation is compromised (e.g., in thromboembolic disease, vasculitic disorders, or in hypoxic vasoconstriction), the bronchial supply gradually increases causing a hyperflow in the anastomotic vessels, which become hypertrophic with thin walls and tend to break into the alveoli and bronchi, giving rise to hemoptysis

Bronchial arteries are the principal sources of hemoptysis amenable to treatment (5). Searching the bronchial arteries origin before treatment is helpful, because over 30% have an abnormal origin that may lead to endovascular treatment failure. The bronchial arteries commonly originate from the upper portion of the descending thoracic aorta. The origin is defined orthotopic if the arteries arise from the descending aorta at the level of the vertebral bodies of T5–T6 (or at the carina). When the bronchial arteries originate at other levels, including aortic branches, they are referred to as ectopic (18)

Cauldwell et al. (19) reported the most frequent types of origin of orthotopic bronchial arteries in a population of 150 adult cadavers ( Fig. 1 ). Usually, two or three branches of the bronchial arteries run parallel with the major bronchi and generate a peribronchial plexus by anastomosing with each other (20). Arterioles from this plexus perforate the muscular layer and create a parallel plexus in the bronchial submucosa. In normal conditions the diameter of bronchial arteries is less than 1.5 mm at the origin and less than 0.5 mm more distally (21). They are usually considered hypertrophic and a potential source of hemoptysis when larger than 2 mm at the origin (22).

Fig : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4463269/figure/f1-dir-20-4-299/

Hemoptysis may also arise from nonbronchial systemic arteries, which enter the pulmonary parenchyma through transpleural adhesions due to chronic inflammatory processes (tuberculosis, mycosis) or through pulmonary ligaments (20) and anastomose with the pulmonary arterial circulation (8)

Pulmonary arterial origin of hemoptysis is possible (23). Persistent hemoptysis despite appropriate embolization of the systemic arteries suggests a pulmonary arterial source of bleeding. Khalil et al. (24) investigated the potential causes of pulmonary arterial hemoptysis, including diseases causing necrosis (active tuberculosis, pulmonary abscess, aspergillosis, and necrotic lung carcinoma), vasculitis (Behçet disease or Hughes-Stovin syndrome), trauma by Swan-Ganz catheter, and pulmonary arteriovenous malformation (PAVM)

Nevertheless, the sensitivity of CXR in this context is not high. Hirshberg et al. (28) reported only 50% positive diagnostic yield for CXR. Revel et al. (29) demonstrated that CXR may identify the bleeding site in 46% of cases and the bleeding cause in 35% only. In a study by Herth et al. (30), nearly a quarter of patients presenting with hemoptysis due to malignancy showed normal CXR. Therefore, in patients presenting with hemoptysis, a negative CXR warrants other diagnostic studies, including bronchoscopy and/or MDCTA

Although rigid bronchoscopy may have a role in massive hemoptysis due to its ability to maintain airway patency (6), flexible fiberoptic bronchoscopy has the advantage of being carried out at the patient’s bedside without anesthesia and in the intensive care unit, and is therefore more frequently used (10).

Bronchoscopy has an overall lower sensitivity than MDCT in detecting the underlying causes of bleeding (8, 25–27, 29). In a study by Revel et al. (29), the cause of bleeding was identified in 8% of the patients, with bronchoscopy and in 77%, with MDCT. Nevertheless, bronchoscopy yields additional information on endobronchial lesions and allows samples for tissue diagnosis and microbial cultures (10). Moreover, with bronchoscopy cold saline solution can be instilled directly into the airways at the level of the bleeding source, if identified, and balloon inflation or laser coagulation may be used to control hemorrhage, even though the efficacy of these procedures is not proved and depends mostly on the practitioner’s skill (32)

MDCT may identify the bleeding site in 63% to 100% of patients with hemoptysis (25, 34) and has the ability to uncover the potential underlying causes of bleeding, such as bronchiectasis, pulmonary infections, lung cancer, etc., being superior to bronchoscopy in this respect. MDCT also has the advantage of showing distal airways beyond the level of the bronchoscope (25, 26, 28, 33), and it has a sensitivity of more than 90% in identifying endobronchial lesions (10)

Nevertheless, there are some limitations in characterizing lesions such as endobronchial blood clots that may mimic a tumor and visualizing an endobronchial process in the presence of acute bleeding filling the bronchial lumen (35). In these cases bronchoscopy remains an important complementary diagnostic tool (10). It has been affirmed that the combined use of MDCT and bronchoscopy provides the best accuracy in assessing patients with hemoptysis (34). Numerous authors have suggested that MDCT should be carried out before eventual bronchoscopy in all patients with hemoptysis (5, 27).

In cases of hemoptysis, vessel analysis should include the bronchial and nonbronchial arteries and the pulmonary arterial circulation. A MDCTA of the chest performed before treatment is of value because the number and the origin of bronchial arteries may be carefully evaluated and the coexistence of an additional nonbronchial arterial supply may be easily depicted to determine the optimal angiographic approach (4, 36). Recognition of more than one arterial supply before endovascular treatment in patients presenting with massive hemoptysis, will assist in choosing ectopic vessels amenable to embolization and in preventing recurrences of hemoptysis after initial successful embolization (15)

The term hemoptysis refers to expectoration of blood originating from the lower respiratory tract (ie, from below the vocal cords). Pseudohemoptysis, expectoration of blood that comes from the upper respiratory tract and/or the upper gastrointestinal tract, can mimic hemoptysis

The most common causes of non-life-threatening hemoptysis in developed countries are acute bronchitis, bronchiectasis, and bronchial neoplasms (primary or secondary) [1-6]. In contrast, in developing countries, infections due to Mycobacterium tuberculosis and Paragonimus westermani and non-cystic fibrosis (CF)-related bronchiectasis are more common causes [1,7-9]

In bronchitis, minor amounts of hemoptysis may be seen during an acute flare but hemoptysis is unusual during the chronic phase. Life-threatening hemoptysis from acute bronchitis is unusual

In bronchiectasis, minor amounts of blood that are mixed with expectorated phlegm (“streaky” in appearance) are commonplace during the chronic phase. Less commonly, larger amounts that appear as bright red blood and clots may occur during an acute flare. In contrast to acute bronchitis, bronchiectasis is a common cause of life-threatening hemoptysis. Non-life-threatening hemoptysis is likely due to the chronic airway inflammation that is characteristic of bronchiectasis, while life-threatening hemoptysis is likely due to rapid bleeding from a ruptured tortuous bronchial artery or from hypertrophied submucosal and peribronchial blood vessels

The most common clinical pattern of hemoptysis due to lung cancer is intermittent small amounts of hemoptysis lasting more than two weeks. Less commonly, bronchogenic carcinoma causes life-threatening hemoptysis.

Non-life-threatening hemoptysis occurs in 7 to 10 percent of patients with lung cancer at the time of presentation and in approximately 20 percent of patients at some time during the course of their illness [10].

Fistulas – Fistula formation between a blood vessel and the tracheobronchial tree can occur when there is chronic vascular inflammation (eg, aortic aneurysm, aortic surgery such as stent placement, aortic infection, or an indwelling vascular device) or airway inflammation (eg, tracheobronchial medical device such as an airway stent). Vascular fistulas are at high risk of causing life-threatening hemoptysis, which is often heralded by smaller non-life threatening episodes of bleeding

Infection — A number of lung parenchymal infections, especially tuberculosis, mycetoma, lung abscess, and necrotizing pneumonia can cause hemoptysis, most often due to erosion into blood vessels. Hemoptysis from infection can be life-threatening, particularly among patients with an aspergilloma and tuberculosis [25,26]. Among those with aspergilloma, hemoptysis is relatively common, occurring in up to 40 percent of patients in some series. In the developing world, P. westermani is a common cause of hemoptysis, and hemorrhagic dengue fever is associated with hemoptysis in about one-fourth of patients [27]. Hemoptysis is a late manifestation of Ebola virus. Other infections are listed in the table (table 1).

Pulmonary artery pseudoaneurysms – Pulmonary artery pseudoaneurysms (Rasmussen aneurysm), which are usually caused by infection, neoplasms, or trauma, have a predilection for peripheral pulmonary arteries and may be single or multiple [32]. Active tuberculosis and paragonimiasis may cause sudden rupture of a Rasmussen aneurysm [33,34]. Bleeding is more likely to be life-threatening

Pulmonary or bronchial artery aneurysms – Hughes-Stovin syndrome, which may be a variant of Behçet syndrome, is characterized by the presence of multiple pulmonary and/or bronchial aneurysms that can cause life-threatening hemoptysis [31].

Pulmonary embolism (thrombotic, fat, septic) – Hemoptysis is a rare presenting manifestation of pulmonary embolism and is usually non-life-threatening unless the patient is receiving anticoagulant therapy. The presumed mechanism is pulmonary infarction, which usually occurs with smaller, more distal thromboembolism

Any etiology associated with non-life-threatening hemoptysis (table 1) can also cause life-threatening hemoptysis, but a few etiologies account for most episodes of the latter. While comprehensive epidemiologic data are lacking, common causes of life-threatening hemoptysis in developed countries include bronchiectasis (most often cystic fibrosis [CF]-related), tuberculosis (TB), airway neoplasms (primary and metastatic), and fungal infections (particularly aspergilloma) [54-56]

Active TB – Life-threatening hemoptysis due to active TB can occur in the setting of cavitary or noncavitary disease. The cause of the bleeding is usually due to bronchial arterial vessel ulceration [10]. Less often, active TB may cause sudden rupture of a Rasmussen aneurysm (ie, pseudoaneurysm) of the pulmonary artery [33]. There is some uncertainty about whether similar pseudoaneurysms can also arise from TB-infected bronchial arteries

Prior TB – There are multiple causes of hemoptysis due to inactive prior TB. These include the erosion of a healed calcified lymph node (ie, broncholith) through a bronchial artery and into an airway, bronchiectasis due to structural lung damage from prior TB, a mycetoma in an old TB lung cavity, and scar carcinoma in areas of healed TB. Late rupture of a Rasmussen aneurysm also may occur in patients with prior TB [61]

In many patients, aspergillomas (and mycetomas) are asymptomatic and non-progressive for prolonged periods of time. However, hemoptysis occurs in 50 to 90 percent of patients, at some point in their life [10,25,26]. Hemoptysis is generally non-life-threatening but in rare cases, can be life-threatening. The exact cause of bleeding due to an aspergilloma is uncertain.

Invasive parenchymal fungal infections – Invasive parenchymal fungal infections may also cause hemoptysis, particularly infections caused by the angioinvasive fungi including Aspergillus (acute or chronic necrotizing aspergillosis) and Mucor [10,64]. The fungi destroy parenchymal and vascular structures, thereby inducing hemorrhage

There is increasing recognition of subacute progressive aspergillus infection in patients with chronic underlying lung disease, including severe chronic obstructive pulmonary disease (COPD). When invasive parenchymal fungal infection occurs after hemopoietic stem cell transplantation, bleeding may be more likely when bone marrow production of neutrophils returns (about day 100), since local inflammation may increase [65].

Acute dimorphic fungal infections (eg, histoplasmosis, blastomycosis) rarely cause hemoptysis and, when they do, it is likely a consequence of mucosal erosion. Prior histoplasmosis has been reported as a potential cause of hemoptysis, either due to the erosion of a calcified lymph node through an airway and vessel, or the effects of fibrosing mediastinitis.

Bronchogenic cancer accounts for approximately 5 to 30 percent of cases of life-threatening hemoptysis, depending on the report [66-68]. In many cases, life-threatening bleeding may be heralded by smaller, sentinel bleeding events during the prior weeks [69]. Patients typically have large, centrally located tumors, especially squamous cell carcinoma. In a case series of 125 patients with life-threatening hemoptysis related to non-small cell lung cancer, bleeding was due to bronchial artery involvement in 82 percent, while bleeding due to involvement of the main pulmonary artery was rare (6 percent) [70]. Approximately half these patients had squamous cell carcinoma

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