Causes and Management of Massive He Mop Ty Sis

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Causes and management of massive hemoptysis in adults

David H Ingbar, MD

UpToDate performs a continuous review of over 350 journals and other resources.

Updates are added as important new information is published. The literature review

for version 14.1 is current through December 2005; this topic was last changed onNovember 29, 2004. The next version of UpToDate (14.2) will be released in June

2006.

INTRODUCTION Massive hemoptysis is variably defined as expectoration of blood

exceeding 100 to 600 mL over a 24-hour period. Its significance is derived from twofeatures: it is often a sign of an important underlying disease, and the hemoptysis

itself may be life-threatening due to asphyxiation. While only five percent of

hemoptysis is massive, some studies report a mortality rate of up to 80 percent. Thecauses and the general management of massive hemoptysis will be discussed here,

while the diagnostic approach to this problem is covered elsewhere. (See "Diagnostic

approach to massive hemoptysis in adults"). Causes and evaluation of hemoptysis

that is not massive are also considered separately. (See "Etiology and evaluation ofhemoptysis in adults").

Several comprehensive reviews are available for those seeking additional information

[1-3], but there are virtually no large series of patients with massive hemoptysis.The only exceptions are two retrospective modern series of 120 patients with

massive hemoptysis reported from South Africa [4] and 29 patients from Israel [5].

CAUSES OF MASSIVE HEMOPTYSIS Before assuming a lower respiratory source ofthe bleeding, it is important to consider whether the blood may be coming from a

non-pulmonary source, such as the upper airway or the gastrointestinal tract. Thismay be a difficult distinction that requires careful examination by an otolaryngology

and/or gastrointestinal subspecialist, respectively. As an example, blood from theupper gastrointestinal tract can be aspirated and coughed up, or blood from the

lungs can be swallowed and be present in the stomach. Alkaline pH, foaminess, orthe presence of pus may sometimes suggest the lungs as the primary source of

bleeding rather than the stomach.

There are numerous causes of massive hemoptysis originating from the lowerrespiratory tract, the most common and important of which will be discussed here

(show table 1).
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The literature from the 1940s through the 1960s supports three major etiologiesaccounting for 90 percent of cases: tuberculosis (TB); bronchiectasis; and lung

abscess. Most of these reports were from municipal hospitals that cared for patientsat higher risk of infectious lung diseases due to their living conditions and underlying

illnesses. Most experts believe that the frequency of each of these etiologies has

decreased significantly over the past thirty years.

Two modern studies of predominantly nonmassive hemoptysis demonstrated that TB

and bronchiectasis presently account for fewer cases of hemoptysis than in the past[6,7].

TB accounted for six and seven percent of cases and bronchiectasis for onlyone percent in these outpatient retrospective studies.

Bronchitis was the attributed cause of hemoptysis in 23 and 37 percent ofpatients, including 27 percent of cases of massive hemoptysis in one series[7]. However, since computed tomography (CT) of the chest was rarely done
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in these patients, it is likely that many of the patients with bronchitis also had

bronchiectasis.

One series reported information about 22 patients with massive hemoptysis(defined as more than 200 mL over 24 hours): six patients had bronchitis and

four had TB, while no other etiology accounted for more than one case [7].

In the United States, invasive medical procedures and the increased number of

patients with immuno-compromising neutropenia or thrombocytopenia probably

contribute significantly to present cases of massive hemoptysis. In addition, thesurvival of more patients with cystic fibrosis into adulthood has made this a more

common etiology of massive hemoptysis [8]. Similarly, early recognition andtreatment of arteriovenous malformations (AVM) have increased the survival of

patients with hereditary hemorrhagic telangiectasia (HHT), and now more than eightpercent of these patients have episodes of massive pulmonary bleeding [9]. (See

"Pulmonary AVMs, including hereditary hemorrhagic telangiectasia: Etiology andclinical features").

A summary of the frequency of etiologies of massive hemoptysis as reported inseveral series is presented in Table 2 (show table 2) [4,5,10].
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Tuberculosis TB can cause massive hemoptysis through multiple mechanisms:

Active cavitary or noncavitary lung disease can cause small or large amountsof bleeding. Most of these patients have sputum smears that stain positivelyfor acid-fast bacilli.

Active disease can cause sudden rupture of a Rasmussen's aneurysm [11].This is an aneurysm of the pulmonary artery that slowly expands into an

adjacent cavity because of inflammatory erosion of the external vessel wall

until it bursts. There is some uncertainty about whether these aneurysms alsocan arise from bronchial arteries.

Inactive TB can cause bleeding due to residual bronchiectasis, erosion of abroncholith through a vessel and into an airway, or by leaving a cavity thatsubsequently acquires a mycetoma.

Rarely, scar carcinomas form in areas of old tuberculous pneumonitis andmay cause hemoptysis.

In the South African series, patients usually had bronchiectasis or cavitation,but approximately one third had noncavitary active disease [4].

Apart from the Rasmussen's aneurysm, the source of bleeding in each of thesecauses is usually the bronchial arterial circulation.

Bronchiectasis Chronic airway inflammation in bronchiectasis causes hypertrophyand tortuosity of the bronchial arteries that accompany the regional bronchial trees,

with expansion of the submucosal and peribronchial plexus of vessels. This

circulation is under systemic blood pressure, so that rupture of either the tortuousvessels or the capillary plexus causes rapid bleeding.

Bronchiectasis may result from prior bacterial or viral infection, cystic fibrosis, TB,host immune defects, or impairment of the mucociliary clearance apparatus (ciliary

dyskinesia, which in the primary form may be associated with Kartagener'ssyndrome, and Young's syndrome). (See "Clinical manifestations and diagnosis of

bronchiectasis" and see "Primary ciliary dyskinesia (Immotile-cilia syndrome)").

Fungal infections Fungal infections are increasing in frequency, especially inimmunocompromised patients or those with preexisting cavitary disease. Hemoptysis

occurs in 50 to 90 percent of patients with aspergilloma and may be massive, butthe exact cause of bleeding is uncertain. Invasive parenchymal fungal infections also

frequently cause hemoptysis, particularly the angioinvasive fungi Aspergillus and

Mucor. The accompanying lung infarction probably augments the likelihood ofbleeding from necrotizing infection. Bleeding may be somewhat more likely when

bone marrow production of neutrophils is returning, since local inflammation mayincrease [12]. (See "Aspergilloma", see "Clinical features and diagnosis of invasive

aspergillosis", and see "Mucormycosis (Zygomycosis)").

Other lung infections Other lung infections, particularly lung abscess, can cause

massive hemoptysis. Bleeding may occur acutely from necrosis of lung tissue or from

rupture of hypertrophied bronchial arteries in the setting of chronic inflammation. In
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other countries, parasitic infections are very common etiologies of hemoptysis,

particularly paragonimiasis in Southeast Asia. Severe leptospirosis may be

complicated by massive alveolar bleeding and hemoptysis [13].

Bronchogenic carcinoma Bronchogenic carcinoma is an infrequent cause of

massive bleeding, although it commonly causes nonmassive hemoptysis. Hemoptysis

occurs at presentation in seven to 10 percent and sometime during the course inapproximately 20 percent of patients with lung cancer. In one large series, three

percent of lung cancer patients had massive, terminal hemoptysis [14]. Most

patients with hemoptysis had small, sentinel bleeding episodes in the prior weeks,

but in 20 percent the initial episode of hemoptysis was massive. The patients withmassive hemoptysis typically had large, centrally located tumors, especially

squamous cell carcinoma.

Hemoptysis is also common in patients with bronchial carcinoid tumors, and the

amount of bleeding is quite variable.

Chemotherapy and bone marrow transplantation Patients undergoing

chemotherapy for leukemia or those who have received a bone marrow transplantmay have sudden and massive pulmonary hemorrhage that is frequently fatal. (See"Pulmonary complications after autologous hematopoietic cell transplantation"). The

etiology is uncertain, but postmortem pathology suggests that it is due to diffuse

lung injury, presumably from a combination of drugs, radiation, and/orthrombocytopenia. There may also be contributions from underlying fungal or viral

infection. These patients are at risk for developing diffuse alveolar hemorrhage andrespiratory failure even in the absence of hemoptysis. Usual treatment includes high-

dose glucocorticoids, and platelet transfusion if thrombocytopenia is present. The

optimal dose and duration of steroid therapy is not clearly defined in this setting.

Immunologic lung diseases A number of diffuse parenchymal lung diseases with

an immunologic basis may cause massive bleeding. Specific etiologies includeGoodpasture's syndrome, Wegener's granulomatosis, systemic lupus erythematosus

(SLE), and idiopathic pulmonary hemosiderosis. Pathologically, many of thesediseases have components of pulmonary capillaritis, particularly SLE, Wegener's

granulomatosis, and microscopic polyangiitis.

The causes and features of diffuse alveolar hemorrhage are summarized in Table 3(show table 3A-3B) [15,16].
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Surprisingly, the degree of hemoptysis may be much less than the amount ofbleeding, since the alveolar location of the bleeding may not stimulate the cough

reflex to the same degree that occurs with other, predominantly larger airway

locations of bleeding. However, recognizing diffuse alveolar hemorrhage anddiagnosing its underlying etiology is important because of the necessity of early

treatment with steroids, possibly cytotoxic drugs, and/or plasmapheresis. (See"Treatment of anti-GBM antibody disease (Goodpasture's syndrome)", see "Initial

and maintenance therapy of Wegener's granulomatosis and microscopic polyangiitis",and see "Pulmonary manifestations of systemic lupus erythematosus in adults").

Cardiac and vascular disease Cardiovascular etiologies infrequently cause massive

hemoptysis.

Pulmonary arteriovenous malformations may bleed, whether they are singleor multiple and whether or not they are part of hereditary hemorrhagic

telangiectasia (HHT or Osler-Weber-Rendu syndrome) [9,17].
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Mitral stenosis used to be common, but now is rare. There is calcification andincreased resistance in the pulmonary veins, accompanied by reversal of

blood flow from the pulmonary capillaries into the bronchial veins. Theresulting submucosal bronchial varices may rupture, causing "cardiac

apoplexy." Cardiopulmonary bypass can markedly reduce such bleeding when

it is life-threatening.

Hemoptysis from pulmonary emboli is usually scant in volume, but maybecome massive after anticoagulation or the use of thrombolytic agents.

Pulmonary artery catheterization can result in iatrogenic pulmonary arteryperforation.

Septic pulmonary emboli from right-sided infective endocarditis occasionallymay result in massive bleeding.

Congenital heart disease or severe pulmonary hypertension can also causesignificant hemoptysis.

Aortic aneurysm can present with either submassive or massive hemoptysis.ACUTE MANAGEMENT The acute and general management of patients with

massive hemoptysis is difficult for several reasons:

There are a multitude of potential etiologies. The course of bleeding is unpredictable. As an example, sometimes a small,

sentinel bleed heralds a massive, asphyxiating bleed.

It is frightening to see patients dying from asphyxiation, even in spite ofintubation.

There is no consensus regarding the optimal management of these patients,and there are no large series of patients studied.

Initial priorities are insuring adequate airway protection, ventilation, and

cardiovascular function [18]. Patients with poor gas exchange, rapid ongoinghemoptysis, hemodynamic instability, or severe shortness of breath should be orally

intubated with a large bore endotracheal tube (size 8.0 or greater). Coagulationdisorders should be rapidly reversed. Early consultation with pulmonary medicine

and thoracic surgery should be obtained, possibly supplemented by invasiveradiology. Once the patient is stabilized, early bronchoscopy should be performed.

The clinician's judgment about whether there is blood accumulating in the lungs, the

patient's current physiologic status, and the patient's underlying pulmonary reserveall influence the need for aggressive intervention. Patients who are clinically stable,

have adequate gas exchange and hemodynamics, and have intermittent or slowinghemoptysis can be evaluated with a detailed history and physical examination

followed by a more considered diagnostic evaluation. (See "Diagnostic approach tomassive hemoptysis in adults").
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Protection of the nonbleeding lung Protection of the nonbleeding lung is a major

priority in the acute management of ongoing hemoptysis. Spillage of blood into the

non-bleeding lung can either block the airway with clot or fill the alveoli and preventgas exchange. Unfortunately, protection of the nonbleeding lung requires

identification of the likely site of bleeding, which may not be readily apparent.

If the location or side of bleeding is known, placing the bleeding lung in a dependentposition may prevent blood spillage into the nonbleeding lung. An alternative

strategy involves placement of a typical, single lumen endotracheal tube into eitherthe right or left mainstem bronchus. This is easier to achieve with bleeding from the

left lung, when one wants to selectively intubate the right mainstem bronchus.However, a potential problem is that right mainstem bronchial intubation often

blocks the right upper lobe bronchus. The approach of selective intubation is less

practical when the right lung is bleeding, because selective intubation of the leftmainstem bronchus may be quite difficult.

A third alternative is the placement of a double lumen endotracheal tube specially

designed for selective intubation of the right or left mainstem bronchi [19]. In

general, selective intubation of the left lung is preferable, since there is little risk ofobstructing the right upper lobe bronchus with the bronchial cuff. While double

lumen tubes are conceptually appealing, there are a number of practical problemswith their use:

They may be difficult to place, even by experienced anesthesiologists,especially when patients are bleeding rapidly.

Insuring proper placement is difficult, and a tube that was properly positionedmay move when the patient's position changes. When the tube moves, either

blood spillage or bronchial obstruction may result. Consequently, patientswith double lumen tubes usually should be paralyzed and should not be

moved unless absolutely necessary.

The individual lumen size often is small and may prohibit passage of abronchoscope and necessitate a tube change for diagnostic procedures.

Individuals caring for the patient must be knowledgeable about determiningwhether or not the tube is properly positioned.

The small endotracheal tube lumen may predispose to intra-tube clot andairway obstruction.

Given these difficulties, the use of double lumen endotracheal tubes is not

recommended except in patients who are exsanguinating and/or asphyxiating from

their bleeding, and when no other approaches are possible.

Use of bronchoscopy in acute management A bronchoscopic option for protecting

the non-bleeding lung is balloon tamponade of the bleeding site, involving placementof a four French 100 cm Fogarty balloon catheter in the segmental or subsegmental

bronchus leading to the bleeding site. The balloon is left inflated for 24 to 48 hours,and the patient is then observed for rebleeding with the balloon deflated for several
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hours [3]. There is a potential risk of ischemic mucosal injury and postobstructive

pneumonia, but these complications have not been reported.

Bronchoscopic techniques used to slow or stop bleeding have included lavage withiced saline and application of topical epinephrine (1:20,000), vasopressin, thrombin,

or a fibrinogen-thrombin combination [20]. None of these methods has been tested

in controlled trials. Anecdotally and in our experience, topical epinephrine sometimeshas seemed to slow or stop bleeding. Issues regarding the use of flexible fiberoptic

versus rigid bronchoscopy are discussed elsewhere. (See "Diagnostic approach to

massive hemoptysis in adults").

If bronchoscopy visualizes a localized bleeding mucosal lesion, laser therapy orelectrocautery may be considered, if available. Both techniques can be used through

a flexible or rigid bronchoscope. Since excellent visualization of the bleeding site isrequired, the rigid bronchoscope may be preferred because of its better suction

capability. (See "Bronchoscopic laser resection" and see "Endobronchialelectrocautery").

Arteriographic embolization The other option for the patient who continues tobleed is arteriographic embolization, either as "semi-definitive" treatment or as abridge to elective surgery. In the hands of experienced angiographers, embolization

successfully stops bleeding more than 85 percent of the time, especially if the

bronchial circulation and the systemic arterial supply are carefully defined [21,22].

Early technical failures account for 5 to 10 percent of the patients who have

unsuccessful control of bleeding; this usually results from inability to cannulate the

bronchial artery or failure to identify and embolize all collateral systemic feedervessels. Collateral systemic feeder vessels arising from the gastric, intercostal,

internal mammary, renal, and hepatic arteries have been reported [22-26].

Routine post-embolization thoracic aortography may improve detection of bleedingfrom the systemic circulation. In a prospective series of 76 patients managed at a

single center, 14 percent of all bleeding vessels were not seen during initial bronchialartery embolization, but were visible when aortography was performed [27]. These

vessels arose most commonly from the intercostal and inferior phrenic arteries.

Unfortunately, embolization is only "semi-definitive," because rebleeding occurs in a

significant minority (eg, at least 10 to 20 percent) of patients over the next 6 to 12

months [10,28-30]. Late rebleeding may be due to incomplete embolization,revascularization, or recanalization. Acute complications of arteriographic

embolization include bronchial wall necrosis and ischemic myelopathy due toinadvertent embolization of a spinal artery [31], but are uncommon when the

arteriographers are experienced in this procedure [32].

Surgery Patients with lateralized, uncontrollable bleeding should be assessed early

for possible surgery in case the bleeding remains brisk and unresponsive to other

measures. This assessment ideally includes pulmonary function tests, but often thesepatients are too ill for physiologic testing, and historical data are therefore used to

estimate the patient's ability to undergo lung resection. Relative contraindications to

surgery include severe underlying pulmonary disease, active TB, diffuse underlyinglung disease (cystic fibrosis, multiple AVMs, multifocal bronchiectasis), and diffuse

alveolar hemorrhage.
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Morbidity and mortality are significantly greater with emergent surgery for persistent

massive bleeding compared with elective surgery in the nonbleeding patient. In most

series of emergent therapy, surgical mortality for treatment of massive hemoptysis isapproximately 20 percent, with morbidity occurring in an additional 25 to 50 percent

of patients. Common complications include empyema, bronchopleural fistula,

postoperative pulmonary hemorrhage, lung infarction, respiratory insufficiency,

wound infection, and hemothorax. The first two complications are especially frequentafter emergent surgery. (See "Sequelae and complications of pneumonectomy").

RESULTS OF ACUTE TREATMENT Considering arteriographic embolization and all

other techniques short of surgery as "medical therapy," several retrospective studieshave compared medical and surgical treatment for massive hemoptysis [1]. The

older literature clearly favors surgery as having a much lower mortality. However,the highest risk patients in these studies were not considered to be surgical

candidates and were managed with medical therapy. Reports from the 1980s

suggested that the mortality rates from medical and surgical therapy areapproximately comparable in patients who qualified as surgical candidates. However,

medically treated patients probably have a higher risk of rebleeding within the firstsix months.

RECOMMENDATIONS Based on the above data, the following is a reasonableapproach to the patient with massive hemoptysis:

First, stabilize the patient and then perform early bronchoscopy along withother appropriate diagnostic studies. (See "Diagnostic approach to massivehemoptysis in adults").

If the patient continues to bleed aggressively, arteriography is mostreasonable for localization and therapy.

If bleeding persists despite embolization or if the patient is too ill to go toangiography, then blockade therapy or a double lumen tube should be

considered in preparation for rigid bronchoscopy in the operating room withpossible lung resection if warranted.

While surgery remains the only truly definitive therapy, it should not be usedin the acute emergent setting unless it cannot be avoided.
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Documents

Causes and Management of Massive He Mop Ty Sis