hiren j. mehta and michael a. jantz1515 chapter 116 interventional bronchoscopy and massive...

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Chapter

116Interventional Bronchoscopy and Massive HemoptysisHiren J. MeHta and MicHael a. Jantz

IntroductIon

Hemoptysis is defined as the expectoration of blood that origi-nates from the lower respiratory tract. Pseudohemoptysis is the expectoration of blood from a source other than the lower respiratory tract such as the nares, oropharynx, larynx, or the gastrointestinal tract. Massive hemoptysis is defined as expec-toration of blood exceeding 200 to 1,000 mL over a 24-hour period, with expectoration of more than 600 mL in 24 hours being the most commonly used definition (1).

In practice, the rapidity of bleeding and ability to maintain a patent airway are critical factors; life-threatening hemop-tysis can alternatively be defined as the amount of bleeding that compromises ventilation (2). Only 3% to 5% of patients with hemoptysis have a massive bleed, with the mortality rate ranging from 20% to as high as 80% in some case series (3–5). Most patients who die from massive hemoptysis do so from asphyxiation secondary to airway occlusion by clot and blood—not from exsanguination. Prognostic factors associ-ated with an increased risk of death from massive hemoptysis include bleeding in excess of 1,000 mL/24 hr, hemoptysis due to neoplasms, radiographic evidence of aspiration, and hemo-dynamic instability (3,6).

EtIology of MassIvE HEMoptysIs

Hemoptysis has multiple causes usually categorized under parenchymal diseases, airway diseases, and vascular diseases. Bleeding may originate from small or large lung vessels. The causes of massive hemoptysis are listed in Table 116.1. Virtu-ally all causes of hemoptysis may result in massive hemoptysis. Infections associated with bronchiectasis, tuberculosis, lung abscess, and necrotizing pneumonia are commonly responsible for the massive bleeding. Other common causes include bron-chogenic carcinoma, mycetoma, invasive fungal diseases, chest trauma, cystic fibrosis, pulmonary infarction, and coagulopa-thy. Although massive hemoptysis is usually due to bleeding from the bronchial circulation, alveolar hemorrhage due to conditions such as granulomatosis with polyangiitis (Wegen-er’s) granulomatosis and Goodpasture syndrome may occa-sionally cause massive hemoptysis (Table 116.2).

anatoMIc sourcEs of HEMoptysIs

The sources of lower respiratory tract bleeding include the pulmonary and bronchial circulations. Two arterial vascular

systems supply blood to the lungs: the pulmonary and the bronchial arteries. The pulmonary arteries provide 99% of the arterial blood to the lungs and are involved in gas exchange. The pulmonary circulation is a low pressure circuit under nor-mal circumstances. The bronchial arteries serving the intrapul-monary airways and lung parenchyma arise from the thoracic aorta at the level of the third through the eighth thoracic vertebrae, originating most commonly at the level of the fifth and sixth vertebrae and drain through the bronchopulmonary anastomosis into the pulmonary veins, which empty into the left side of the heart. Bronchial circulation supplies nourish-ment to the extra- and intrapulmonary airways and to the pulmonary arteries (vasa vasorum), without being involved in the gas exchange (7). Complex capillary anastomoses exist between the pulmonary arteries and the systemic bronchial arteries. When the 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. Like-wise, in chronic inflammatory disorders, such as bronchiec-tasis, chronic bronchitis, tuberculosis, mycotic lung diseases, and lung abscess, as well as in neoplastic diseases, the release of angiogenic growth factors promote neovascularization and pulmonary vessel remodeling, with engagement of collateral systemic vessels (8). These new and collateral vessels are fragile and prone to rupture into the airways.

Angiographic studies of patients with active hemoptysis have demonstrated that bleeding originates from bronchial and pulmonary arteries in 90% and 5% of cases, respectively (1,9). In the remaining 5% of cases, hemoptysis may derive from nonbronchial systemic arteries (9). Very rarely, hemop-tysis has been reported originating from pulmonary and bronchial veins (10) and capillaries (11). A recent study by Noe et al. (12) shows that bleeding from bronchial arteries can coexist with bleeding from nonbronchial and pulmonary arteries in the same patient.

InItIal EvaluatIon

A detailed history and physical examination should be per-formed. Patients with a history of tuberculosis may have bleeding from rupture of a pulmonary artery aneurysm in the cavity lumen, known as a Rasmussen aneurysm, or by break-down of bronchopulmonary anastomoses within the wall of old cavities. Bronchogenic carcinoma should be suspected in smokers older than 40 years of age. Repeated episodes of hemoptysis over months to years suggest bronchiectasis or a carcinoid tumor. Chronic sputum production predating the

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1516 SeCtion 11 respiratory DisorDers

diffuse pulmonary infiltrates. The triad of upper airway dis-ease, lower airway disease, and renal disease suggests granu-lomatosis with polyangiitis (Wegener granulomatosis) (17). Goodpasture syndrome should be suspected in young men with alveolar hemorrhage and microscopic or macroscopic hematuria (18). Patients with a history of systemic lupus ery-thematosus (SLE) may develop alveolar hemorrhage at any time during the course of their disease, and alveolar hemor-rhage may be the initial manifestation (19). Alveolar hemor-rhage should be considered in patients with diffuse pulmonary infiltrates who have recently undergone hematopoietic stem cell or bone marrow transplantation (20). Although uncom-mon, tracheoinnominate artery fistula is an important consid-eration in patients with tracheostomy presenting with massive hemoptysis (21,22). The peak incidence is between the first and second week, although hemorrhage can occur as early as 48 hours and as late as 18 months after the procedure. A sen-tinel self-limited bleed is observed in 35% to 50% of patients. Trauma from suctioning, particularly in the setting of abnor-mal coagulation, may also cause hemoptysis in patients with a tracheostomy tube or in those who have an endotracheal tube (ET) in place. The possibility of traumatic rupture of a pulmo-nary artery should be considered in patients with a pulmonary artery catheter in place (23,24).

Physical Examination

The physical examination may provide clues to the diagno-sis of massive hemoptysis. A saddle nose deformity and/or septal perforation suggest Wegener granulomatosis. Stridor or unilateral wheezing indicates a possible laryngeal tumor, tracheobronchial tumor, or airway foreign body. Pulmonary embolism should be considered in patients with tachypnea,

TABLE 116.1 Potential Causes of Massive Hemoptysis

NeoplasmBronchogenic cancer

Metastasis (parenchymal or endobronchial)

carcinoid

leukemia

Infectiouslung abscess

Bronchiectasis

tuberculosis

necrotizing pneumonia

Fungal pneumonia

septic pulmonary emboli

Mycetoma (aspergilloma)

Pulmonary ParenchymaBronchiectasis

cystic fibrosis

sarcoidosis (fibrocavitary)

Diffuse alveolar hemorrhage

airway foreign body

Cardiac/VascularMitral stenosis

pulmonary embolism/infarction

arteriovenous malformation

Bronchoarterial fistula

ruptured aortic aneurysm

Bronchial artery aneurysm

Congestive Heart Failurepulmonary arteriovenous fistula

Iatrogenic/TraumaticBlunt or penetrating chest trauma

tracheal/bronchial tear or rupture

tracheoinnominate artery fistula

Bronchoscopy

pulmonary artery rupture from pulmonary artery catheter

endotracheal tube suctioning trauma

Hematologiccoagulopathy

Disseminated intravascular coagulation

thrombocytopenia

Drugs/Toxinsanticoagulants

antiplatelet agents

thrombolytic agents

crack cocaine

hemoptysis implies a diagnosis of chronic bronchitis, bron-chiectasis, or cystic fibrosis. Pulmonary embolism should be suspected in patients with a history of deep venous thrombosis or risk factors for pulmonary thromboembolism. A febrile ill-ness with sputum production, night sweats, and weight loss suggests a lung abscess or tuberculosis. Excessive anticoagula-tion, thrombolytic therapy, and coagulopathy may also cause hemoptysis (13,14). In children with hemoptysis, the most likely diagnoses are carcinoid tumors, vascular anomalies, and aspiration of foreign bodies (15,16). Alveolar hemorrhage should be suspected in patients with dyspnea, hypoxemia, and

TABLE 116.2 Causes of Alveolar Hemorrhage

Goodpasture syndrome

Vasculitis/collagen vascular disease

Wegener granulomatosis

Microscopic polyangiitis

system lupus erythematosus

Mixed connective tissue disorder

systemic sclerosis (scleroderma)

rheumatoid arthritis

Henoch–schonlein purpura

Mixed cryoglobulinemia

Behçet syndrome

Diffuse alveolar damage

antiphospholipid syndrome

idiopathic pulmonary hemosiderosis

Hematopoietic stem cell/bone marrow transplantation

coagulopathy

Mitral stenosis

lymphangioleiomyomatosis

Drugs/toxins

isocyanates

trimellitic anhydride

D penicillamine

nitrofurantoin

all trans retinoic acid

crack cocaine

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Chapter 116 interventional Bronchoscopy and Massive Hemoptysis 1517

a pleural friction rub, and lower extremity phlebitis. Diffuse rales on examination raises the possibility of diffuse alveolar hemorrhage, diffuse parenchymal lung disease, or cardiac dis-ease as the cause of the hemoptysis. The presence of telangi-ectasias of the skin or mucous membranes suggests hereditary hemorrhagic telangiectasia or a connective tissue disease as the cause. Ecchymoses or petechiae suggest a hematologic abnor-mality or coagulopathy. Clubbing of the fingers may be a sign of a lung carcinoma, bronchiectasis, and cystic fibrosis. The finding of pulsation of the tracheostomy tube is of concern for the development of a tracheoinnominate fistula.

Laboratory Studies

Laboratory studies, including a complete blood count (CBC), coagulation studies, urinalysis, and chest radiograph, should be obtained in all patients. The CBC may suggest an infectious process or hematologic disorder as the cause of hemoptysis and indicate the need for blood transfusion. Coagulation stud-ies may provide evidence for a hematologic disorder as the cause for the hemoptysis, or may identify a coagulopathy that is causing or contributing to the bleeding from another dis-ease. Hematuria may be noted on urinalysis, which suggests the diagnosis of Goodpasture syndrome, Wegener granuloma-tosis, or another systemic vasculitis.

Chest Radiograph

The chest radiograph is an important study to identify the cause and side of bleeding. The chest radiograph may dem-onstrate abnormalities such as lung masses, cavitary lesions, atelectasis, focal infiltrates, and diffuse infiltrate. Single or multiple pulmonary cavities suggest neoplasm, tuberculosis, fungal disease, lung abscess, septic pulmonary emboli, para-sitic infection, or Wegener granulomatosis as the cause for hemoptysis. The presence of a mass within a cavitary lesion indicates a possible mycetoma (aspergilloma). The appearance of a new air–fluid level in a cavity or infiltrate around a cav-ity is suggestive of the site of bleeding. A solitary pulmonary nodule that has vessels going toward the nodule may be an arteriovenous malformation. Diffuse pulmonary infiltrates suggest diffuse alveolar hemorrhage (Table 116.2), bleeding from coagulopathy, lung contusions from blunt chest trauma, hemorrhage with multiple areas of aspiration, or pulmonary edema with a cardiac cause for hemoptysis. Chest radiographs may be normal or nonlocalizing in 20% to 45% of patients (25,26). Therefore, in patients presenting with hemoptysis, a negative CXR warrants other diagnostic studies.

Computed Tomography

Computed tomography (CT) represents a noninvasive and highly useful imaging tool in the clinical context of hemoptysis, allowing a comprehensive evaluation of the lung parenchyma, airways, and thoracic vessels by using contrast material. Mul-tidetector CT (MDCT) may identify the bleeding site in 63% to 100% of patients with hemoptysis (27); the role of CT in the management of massive hemoptysis is however somewhat controversial. CT may demonstrate abnormalities that are not visible on the chest radiograph. It is helpful in the diagnosis of bronchiectasis (28), although abnormalities from bronchiec-tasis can usually be appreciated on the chest radiograph. CT

with contrast may detect pulmonary emboli, thoracic aneu-rysms, or arteriovenous malformations. CT scans may also demonstrate cavitation with a surrounding infiltrate, the halo sign, which suggests a necrotizing infection such as aspergil-losis or mucormycosis (29,30). Some studies have noted that CT scanning before bronchoscopy may increase the yield of bronchoscopy (31). In one retrospective study of 80 patients with large or massive hemoptysis, chest CT was superior to chest radiograph or bronchoscopy in determining the cause of bleeding, and was similar to bronchoscopy in successfully localizing the site of bleeding (32). CT is useful to create a detailed and accurate map of the thoracic vasculature that may guide further treatment, depicting the number and origin of bronchial arteries and the coexistence of an additional non-bronchial arterial supply. CT can thus assist in choosing ecto-pic vessels amenable to embolization, preventing recurrence after initial successful embolization, reducing angiography procedure time, fluoroscopy radiation dose, contrast load, and decreasing iatrogenic complications (12). Some authors have argued that transport of the potentially unstable patient with massive hemoptysis may not be judicious, however; thus, the patient should be adequately stabilized prior to obtaining a chest CT.

Angiography

Angiography can determine the site of bleeding in 90% to 95% of cases. However, in one case series, routine use of diagnostic angiography provided a diagnosis not identified on bronchos-copy in only 4% of patients (33). Angiography can be helpful in detecting a pseudoaneurysm that has formed after healing of a pulmonary artery tear from pulmonary artery catheter-ization (34). As previously noted, the bronchial arteries and other collateral systemic arteries account for the source of bleeding in most cases with massive hemoptysis. Pulmonary angiography is usually performed only when there is suspi-cion for pulmonary aneurysms, arteriovenous malformations, and pulmonary embolism. Technetium labeled red blood cell or colloid studies rarely provided any information that is not obtained by bronchoscopy and chest CT. The use and timing of bronchoscopy will be discussed in a subsequent section.

Bronchoscopy

Bronchoscopy, performed with either a rigid or flexible endo-scope, is helpful for identifying active bleeding and for checking the airways in patients with massive hemoptysis. The capabil-ity and success of bronchoscopy in localizing the bleeding site may vary according to the rate and severity of the hemorrhage. Hirshberg et al. (4) found that bronchoscopy was more effec-tive in finding the bleeding site in patients with moderate to severe hemoptysis (64% and 67%) than in those with mild hemoptysis (49%). Bronchoscopy has an overall lower sensi-tivity than MDCT in detecting the underlying causes of bleed-ing (25,27,31). Nevertheless, bronchoscopy yields additional information on endobronchial lesions and allows samples for tissue diagnosis and microbial cultures.

Other Studies

Depending on the suspected causes of massive hemopty-sis, additional studies may be indicated. Echocardiography

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may be performed if a cardiac cause is considered. If diffuse alveolar hemorrhage syndromes are suspected, laboratory testing, including antiglomerular basement membrane anti-body, antineutrophilic cytoplasmic antibody, antinuclear antibody, rheumatoid factor, complement levels, cryoglobu-lins, and antiphospholipid antibodies, should be performed, depending on the causes that are being considered. Trans-bronchial lung biopsy, open lung biopsy, or kidney biopsy may be indicated in some cases of alveolar hemorrhage to establish a diagnosis.

ManagEMEnt of MassIvE HEMoptysIs

Airway Protection and Stabilization

Once the diagnosis of massive hemoptysis is established, the initial priorities are to protect the airway and stabilize the patient. In general, the patient with massive hemoptysis should be monitored in the ICU setting, even if intubation and mechanical ventilation are not required. Large bore IV access should be established and supplemental oxygen provided. Blood should be drawn for a CBC, arterial blood gas analysis, coagulation studies, electrolytes, renal function tests, and liver function tests. The patient should be type and cross-matched for blood, with 4 to 6 units of packed red blood cells always available. Correction of thrombocytopenia and coagulopathy, if present, with appropriate blood products should be con-sidered. Attempts to lateralize the site of bleeding should be made in anticipation of steps to prevent aspiration into the nonbleeding lung; the patient may be positioned in a lateral decubitus position with the bleeding lung down.

Airway patency must be ensured in patients with massive hemoptysis, as deaths from this process are predominantly due to asphyxiation. Most patients with ongoing massive hemoptysis will require intubation and mechanical ventila-tion, although select patients who are not hypoxemic and are able to keep the airway clear on their own may not require intubation. Although intubation generally preserves oxygen-ation and facilitates blood removal from the lower respiratory tract, the ET can become obstructed by blood clots, leading to the inability to oxygenate and ventilate the patient. The larg-est possible ET should be inserted to allow the use of bron-choscopes with a 2.8- to 3.0-mm working channel for more effective suctioning and to allow for better ventilation with the bronchoscope in the airway for prolonged periods of time. In severe cases, the mainstem bronchus of the nonbleeding lung can be selectively intubated under bronchoscopic guidance to preserve oxygenation and ventilation from the normal lung.

Some authors have recommended the use of a double-lumen ET to isolate the normal lung and permit selective intubation. Although double-lumen ETs have been used successfully in the airway management of massive hemoptysis, there are several potential pitfalls. First, placement of a double-lumen ET is dif-ficult for less experienced operators, particularly with a large amount of blood in the larynx and oropharynx. Second, the individual lumens of the ET are significantly smaller than a standard ET and are at significant risk of being occluded by blood and blood clots. Last, positioning of the double-lumen ET and subsequent bronchoscopic suctioning of the distal airways require a small pediatric bronchoscope with work-

ing channels of 1.2 to 1.4 mm. Adequate suctioning of large amounts of blood and blood clots through such bronchoscopes is extremely problematic. In one series of 62 patients with massive hemoptysis, death occurred in four of seven patients managed with a double-lumen ET due to loss of tube position-ing and aspiration (35). In general, we do not recommend the use of double-lumen ETs for airway management in massive hemoptysis. As an alternative to selective mainstem bronchial intubation or intubation with a double-lumen ET, an ET that incorporates a bronchial blocker, such as the Univent tube, may be used.

Localization of Source and Cause of Hemoptysis

Once the patient is stabilized and airway patency is achieved, the source of bleeding should be localized as precisely as pos-sible, and the cause of bleeding determined. Identification of the cause and location of the bleeding potentially allows for more specific therapy. Methods of localization include patient history, physical examination, chest radiograph, chest CT, bronchoscopy, and angiography. In one study of 105 patients with hemoptysis, patients themselves were able to localize the side of bleeding in 10% of cases, but with an accuracy of 70% when able to do so (36); localization by a physical examination performed by a physician was possible in 43% of patients. Chest radiographs were able to localize bleeding in 60% of cases. Bronchoscopy was accurate in localizing the source of bleeding in 86% of patients. In another study, 9 of 24 patients were able to accurately localize the side of their bleeding (37). Chest radiographs should be routinely obtained to help localize the source of bleeding and determine the cause. As discussed earlier, chest CT may provide additional informa-tion beyond the chest radiograph, and may be more accurate in localizing the bleeding and determining the cause, although concerns about transporting a potentially unstable patient out of the ICU exist (7,38). Bronchoscopy and angiography remain the modalities for localizing the source of hemoptysis and offer potential therapeutic intervention.

Early—rather than delayed—bronchoscopy should be per-formed to increase the likelihood of localizing the source of bleeding. Bronchoscopy performed within 48 hours of bleed-ing onset successfully localized bleeding in 34% to 91% of patients, depending on the case series, as compared to success-ful localization in 11% to 52% of patients if delayed bronchos-copy was performed (39). Bronchoscopy performed within 12 to 24 hours may provide an even higher yield. Bedside flexible bronchoscopy should not be performed to establish a diag-nosis of a tracheoarterial fistula such as a tracheoinnominate fistula (21,40).

Bronchoscopic Therapies to Control Hemoptysis

Rigid bronchoscopy is the most efficient means of clearing the airways from blood clots and secretions, ensuring effective tamponade of the bleeding airway and safe isolation of the nonaffected lung, thereby preventing asphyxia and preserv-ing ventilation. However, it requires a trained bronchoscopist, who is not always readily available. A variety of maneuvers can be performed with the flexible bronchoscope to control bleeding.

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Balloon Tamponade

Endobronchial tamponade via flexible bronchoscopy can prevent aspiration of blood into the contralateral lung and preserve gas exchange in patients with massive hemoptysis. Endobronchial tamponade can be achieved with a 4-Fr Fog-arty balloon-tipped catheter. The catheter may be passed directly through the working channel of the bronchoscope, or the catheter can be grasped with biopsy forceps placed though the working channel of the bronchoscope prior to introduction into the airway of the bronchoscope and catheter. The catheter is held in place adjacent to the bronchoscope by the biopsy forceps, and both are then inserted as a unit into the airway. The catheter tip is inserted into the bleeding segmen-tal orifice, and the balloon is inflated. If passed through the suction channel, the proximal end of the catheter is clamped with a hemostat, the hub cut off, and a straight pin inserted into the catheter channel proximal to the hemostat to main-tain inflation of the balloon catheter. The clamp is removed, and the bronchoscope is carefully withdrawn (41–43). The catheter can safely remain in position between 15 minutes and 1 week, until hemostasis is ensured by surgical resection of the bleeding segment or bronchial artery embolization. It should be deflated for a few minutes three times a day, in order to pre-serve mucosal viability and to check for bleeding recurrence. Right heart balloon catheters have been used in a similar fash-ion (44). A modified technique for placement of a balloon catheter has been described using a guidewire for insertion. A 0.035-in soft-tipped guidewire is inserted through the working channel of the bronchoscope into the bleeding segment. The bronchoscope is withdrawn, leaving the guidewire in place. A balloon catheter is then inserted over the guidewire and placed under direct visualization after reintroduction of the broncho-scope (45). The use of endobronchial blockers developed for unilateral lung ventilation during surgery may hold promise for management of massive hemoptysis in tamponading bleed-ing and preventing contralateral aspiration of blood (46). The Arndt endobronchial blocker is placed through a standard ET and directly positioned with a pediatric bronchoscope. Suctioning and injection of medications can be performed through the lumen of the catheter after placement. The Cohen tip deflecting endobronchial blocker is also placed through a standard ET and directed into place with a self-contained steering mechanism under bronchoscopic visualization. At this time, there is limited published experience with these blockers in the setting of massive hemoptysis, although the author has successfully used them for this application.

Other Bronchoscopic Techniques

Additional bronchoscopic techniques may be useful as tempo-rizing measures in patients with massive hemoptysis. Broncho-scopically administered topical therapies, such as iced sterile saline lavage or topical 1:10,000 or 1:20,000 epinephrine solution, may be helpful (47). Direct application of a solution of thrombin or a fibrinogen–thrombin combination solution has been used (48). The use of bronchoscopy-guided topical hemostatic tamponade therapy using oxidized regenerated cel-lulose mesh has recently been described (49). Endobronchial placement of a silicone spigot can prove adequate for tempo-rary control of bleeding, allowing patients to stabilize before endovascular embolization (50). Successful tamponade and

isolation of the bleeding site in patients with massive hemopty-sis can be achieved by the placement of covered self-expanding airway stents blocking the orifice of the bleeding airway (51). Although anecdotal, the author has had success with topical application of a sodium bicarbonate solution.

For patients who have hemoptysis due to endobronchial lesions, particularly endobronchial tumors, hemostasis may be achieved with the use of neodymium:yttrium aluminum garnet (Nd:YAG) laser phototherapy, electrocautery, argon plasma coagulation (APC), or cryotherapy via the bronchoscope.

Angiography and Embolization

Angiography can identify the bleeding site in more than 90% of cases. As noted, the bronchial arteries are the most frequent source of bleeding in massive hemoptysis. In some cases, systemic vessels other than the bronchial arteries can be the source of bleeding (52). The pulmonary arteries may be the source for massive hemoptysis in 8% to 10% of cases (53). Visualization of extravasated dye from a vessel is relatively uncommon. Signs suggesting a particular vessel is the source of bleeding include vessel tortuosity, increased vessel diameter, and aneurysmal dilatation.

Bronchial artery embolization has been widely used to control massive hemoptysis, as a temporary measure to sta-bilize patients before surgical resection or medical treatment (antibiotics/antituberculous drugs) or as a definitive thera-peutic approach in patients who refuse surgery, who are not considered as candidates for surgery (poor lung function, bilateral pulmonary disease, comorbidities), or patients in whom surgery is contraindicated. Bronchial artery emboli-zation is considered the most effective nonsurgical modality for treatment of massive hemoptysis. The immediate success rates from bronchial artery embolization range from 51% to 100% (3,9,37,54–66). This wide range of success rates across multiple studies can be partially attributed to heterogeneity with regard to analysis of results with some series, including patients in whom bronchial artery cannot be canalized or that spinal artery was seen coming off the bronchial vessel prevent-ing embolization in the final analysis (61). Embolization has been performed with Gelfoam, polyurethane particles, poly-vinyl alcohol particles, and vascular coils. Sclerosing agents may cause subsequent lung necrosis and should be avoided. Recurrence of bleeding, although usually nonmassive, has been noted in 16% to 46% of patients (9,54). Recurrence of hemoptysis may be due to incomplete embolization of the bronchial vessels, recanalization of the embolized arteries, presence of nonbronchial systemic arteries, or development of collateral circulation in response to continuing pulmonary inflammation (60,67). Repeat embolization may be required in some patients (37,59,63,68). Complications include chest pain, fever, vessel perforation and intimal tears, and emboli-zation of material to mesenteric and extremity arteries. The most serious complication is embolization of the anterior spi-nal artery, which may arise from the bronchial artery, with subsequent spinal artery infarction and paraparesis; the risk of this occurrence is less than 1%.

Rupture of the Pulmonary Artery

The pulmonary artery may potentially be ruptured from right heart catheterization. This complication should be suspected

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in patients who develop hemoptysis with a pulmonary artery catheter in place. Balloon tamponade and contralateral selec-tive intubation should be performed (69). The catheter should be withdrawn 5 cm with the balloon deflated, and the balloon then reinflated with 2 mL of air and allowed to float back into the ruptured vessel to occlude it. Patients who stop bleeding should undergo angiographic evaluation to localize the tear and identify the formation of a pseudoaneurysm (34,70). If a pseudoaneurysm is identified, embolization of the affected ves-sel should be considered to prevent subsequent hemorrhage.

Surgery

Emergency surgery for control of massive hemoptysis is per-formed less often due to the advent of bronchial artery embo-lization. Mortality rates for surgical management of massive hemoptysis range from 1% to 50% (3,71–76). Surgical resec-tion of the source of bleeding offers definitive treatment as long as the lesion can be completely resected and the patient is able to tolerate resectional surgery. It is often difficult to accu-rately determine if these patients will be able to tolerate sur-gery, as they are often too ill to undergo pulmonary function tests, or are intubated and thus unable to perform pulmonary function tests. Surgical resection may be considered in patients when bronchial artery embolization is unavailable, if bleeding continues despite embolization, or if the cause of the hemoptysis is unlikely to be controlled with embolization.

Surgery also remains the strategy of choice for the manage-ment of massive hemoptysis caused by diffuse and complex arteriovenous malformations, iatrogenic PA rupture, chest trauma, and mycetoma not responding to other therapeutic strategies, or associated with recurrent life-threatening hemop-tysis as outlined above. Bronchovascular fistulae—with ensuing massive bleeding, is most often encountered following surgery, local infection, associated with vascular aneurysms and, less frequently, following lung transplantation surgery—are also managed by surgical repair once the patient is stabilized (1).

Diffuse Alveolar Hemorrhage

Patients with diffuse alveolar hemorrhage syndromes are not candidates for bronchial artery embolization or surgery; treat-ment for these groups of patients is pharmacologic. Cortico-steroids are typically used and are effective for a wide range of the alveolar hemorrhage syndromes (77). Doses of 1 to 2 mg/kg/day of methylprednisolone have been most commonly used. For life-threatening alveolar hemorrhage, initial doses of 500 to 1,000 mg/day of methylprednisolone have been rec-ommended. For Goodpasture disease, granulomatosis polyan-giitis, and other vasculitides, adjunctive cytotoxic therapy or plasmapheresis may be considered.

prognosIs

Factors associated with high mortality in patients with massive hemoptysis include a bleeding rate of at least 1,000 mL within a 24-hour period, aspiration of blood in the contralateral lung, massive bleeding requiring single lung ventilation, and broncho-genic carcinoma as an underlying etiology (3,6). Patients seem to fare better when tuberculosis, bronchitis, or bronchiectasis are responsible for the massive hemoptysis. Patients who experience

recurrent bleeding following embolization for massive hemop-tysis have significantly higher mortality (78). Overall mortality rates for massive hemoptysis range from 9% to 38% (58,61,79), with significant reduction in mortality in recent years since bron-chial artery embolization is considered as first-line therapy.

IntErvEntIonal BroncHoscopy

Interventional bronchoscopy is a field that utilizes minimally invasive techniques for the management of a variety of tra-cheobronchial disorders. There are a number of circumstances for which interventional bronchoscopy has application in the ICU. The most common need for such procedures arises from central airway obstruction (CAO), both malignant and benign in etiology. Other potential situations that interven-tional bronchoscopy may be of benefit include management of hemoptysis and management of persistent airleaks.

Malignant Airway Obstruction

CAO from malignancy may arise from endoluminal tumor, submucosal tumor infiltration, extrinsic compression by a tumor mass, extrinsic compression by malignant mediastinal adenopathy, or a combination of these pathologies. Bron-chogenic carcinoma is the most common cause of malignant airway obstruction. The exact prevalence of airway obstruc-tion in patients with lung cancer is not clear although it has been estimated that 20% to 30% of patients will develop large airway obstruction (80). Patients with other malignan-cies may also develop endobronchial metastases. Cancers of the thyroid, colon, breast, kidney, and esophagus as well as melanoma have been most commonly noted to cause endo-bronchial metastases. As a result of the airway obstruction, patients may experience respiratory distress, hypoxemia, or frank respiratory failure requiring mechanical ventilation. Postobstructive pneumonia may also occur.

Benign Airway Obstruction

Patients may develop tracheal stenosis or tracheal webs fol-lowing endotracheal intubation. The reported incidence ranges from 10% to 22%, although only 1% to 2% of patients are symptomatic or have severe stenosis (81). Most stenoses occur at the site of the ET cuff, thought to be due to decreased regional blood flow as a result of pressure of the cuff on the tracheal wall. A similar incidence has been reported following tracheostomy tube placement (82). While patients may develop stenoses or webs at the site of the tra-cheostomy tube cuff, tracheal stenosis following tracheostomy tube placement typically occurs around the tracheal stomal site. This is thought secondary to abnormal wound healing with excess granulation tissue formation around the tracheal stoma (81). In addition, patients may develop focal tracheo-malacia at the level of the stoma secondary to cartilaginous damage (dynamic A-shaped tracheal stenosis) (83). Patients may also develop airway obstruction secondary to granulation tissue above the tracheostomy tube and at the tip of the tra-cheostomy tube. Finally, patients may also develop tracheal or bronchial stenosis as a consequence of systemic disease, such as granulomatous polyangiitis (Wegener granulomatosis), relapsing polychondritis, sarcoidosis, and tracheobronchial

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amyloidosis. In about 3% to 5% of cases of tracheal stenosis, there is no known inciting process for the development of the stenosis and such cases are labeled idiopathic (84).

Expiratory central airway collapse—comprises two sepa-rate entities: tracheobronchomalacia (TBM), characterized by weakness of the airway cartilages, and excessive dynamic airway collapse (EDAC)—which is defined as excessive bulg-ing of the posterior membrane into the airway lumen during expiration without cartilage collapse—may produce significant airway obstruction (85). Focal tracheomalacia may result from prolonged intubation, tracheostomy tube placement, vascu-lar abnormalities such as vascular rings, and space occupying lesions of the mediastinum such as a large thyroid goiter. Focal tracheomalacia and bronchomalacia can occur following radia-tion therapy; diffuse TBM can result from relapsing polychon-dritis, and EDAC is associated with COPD, asthma, and obesity.

History and Evaluation

Symptoms depend on the location and degree of airway nar-rowing as well as concurrent thoracic pathology. Dyspnea is the most common symptom. Dyspnea on exertion typically occurs when the tracheal diameter is reduced to 8 mm; stridor may be noted when the tracheal diameter decreases to 5 mm (86). Air-way narrowing of this degree increases susceptibility to acute obstruction from mucus plugs or blood clots. This is thought to be the reason why 50% of these patients present with acute respiratory distress. CT may be used as the initial evaluation modality for tracheobronchial obstruction. MDCT with thin collimation (0.6–1.5 mm) over the entire chest during a single breath hold at full inspiration allows acquisition of volumetric high resolution data sets. Reconstruction of axial overlapped thin slices permits multiplanar reformations of high quality. CT is useful for diagnosing the nature of the obstruction, identifying the precise anatomical location, the characteristics of the lesion,

and the extent of disease, including distal airway patency and local vascular anatomy (87,88). Multiplanar reformations in sagittal, coronal, or oblique planes eliminate the known limi-tation of axial images including detection of subtle airway stenoses, underestimation of the longitudinal extent of narrow-ing, inadequate evaluation of the airways oriented obliquely to the axial plane, and the difficulty in displaying complex three-dimensional anatomy of the airways. In addition, virtual bronchoscopy imaging can be performed using CT images con-structed during postprocessing. Flexible bronchoscopy can be used as a diagnostic modality although ideally bronchoscopy, either flexible or rigid, is performed in conjunction with a bron-choscopic therapeutic intervention. Caution should be taken in performing bronchoscopy in high-grade tracheal or bilat-eral mainstem obstruction if an interventional pulmonologist/ thoracic surgeon is not available as a diagnostic bronchoscopy may precipitate acute, complete airway occlusion.

Interventional Bronchoscopy Techniques

Various interventional bronchoscopy modalities are available to manage malignant or benign CAO. Mechanical debulking and dilatation may be performed with a rigid bronchoscope to relieve obstruction from endoluminal tumor as well as benign stenoses. Rigid bronchoscopy may also be used in conjunction with other ablative modalities, and has some advantages over interventions performed via flexible bronchoscopy including the ability to ventilate the patient through the rigid broncho-scope, use of larger suction catheters to manage blood in the airway, and use of larger forceps to remove tumor and debris.

A variety of ablative techniques are available for relieving obstruction from endoluminal tumor (Table 116.3). Laser, electrocautery, and APC utilize heat thermal energy for tissue destruction. Microdebriders have been used in conjunction with rigid bronchoscopy for mechanical debulking; these

TABLE 116.3 Comparison of Ablative Modalities

Therapy Mechanism of Action Advantages Disadvantages

nd:yaG laser noncontact, thermal energy from laser light

Deep tissue penetration and hemostasis, good for major tissue debulking

potential damage to adjacent tissue

nd:yap laser noncontact, thermal energy from laser light

Better hemostasis than that of nd:yaG laser

less tissue penetration than that of nd:yaG laser

carbon dioxide laser

noncontact, thermal energy from laser light

More precise ablation than that of other lasers, shallow penetration

Minimal hemostasis, bulky equipment limits use in airways

argon plasma coagulation

noncontact, thermal energy from ionized argon gas

Good hemostasis, preferential flow to uncoagulated tissue, bends around corners

shallow penetration, not ideal for major tissue debulking

electrocautery contact, thermal electrical energy inexpensive, multiple accessory types for different situations, good hemostasis

requires frequent cleaning of contact device, less precision than laser

cryotherapy repeated cycles of freezing and thawing

Good for foreign body removal, no risk of airway fire

not for acute airway use due to delayed tissue destruction, requires follow-up bronchoscopic tissue removal

Brachytherapy Direct implantation of radiation source into/next to target lesion

concentrated, long lasting, localized tissue effect

not for acute airway use due to delayed tissue destruction, higher risk of hemor-rhage and other complications

photodynamic therapy

preferential uptake of photosen-sitizer by malignant cells with nonthermal laser–activated phototoxic reaction

potentially curative for early mucosal squamous cell cancers

not for acute airway use due to delayed tissue destruction, requires follow-up bronchoscopic tissue removal, 4–6 wks of skin photosensitivity

Microdebrider Mechanical removal of tissue by rotating blade and suction

no risk of airway fire Device length limits to proximal airway use

nd:yaG, neodymium:yttrium aluminum garnet; nd:yap, neodymium:yttrium aluminum perovskite. adapted from Hsia D, Musani ai. interventional pulmonology. Med Clin North Am. 2011;95(6):1095–1114.

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debriders are composed of a serrated blade rotating at 1,000 to 3,000 rpm attached to a hollow suction tube (89). These modalities, as well as mechanical debulking with the rigid bronchoscope, have the advantage of achieving immediate airway patency. Either silicone or self-expanding metal stents will often be placed to maintain airway patency once the air-way is de-obstructed. Other techniques such as standard cryo-therapy, brachytherapy, and photodynamic therapy have the disadvantages of not achieving immediate airway patency and thus would not be the procedures of choice for patients in the ICU with CAO. A modification of the method of cryotherapy, referred to as cryorecanalization, is able to achieve immediate airway patency, however (90).

For benign tracheal or bronchial stenosis, dilatation with the rigid bronchoscope or balloon bronchoplasty via rigid or flex-ible bronchoscopy may be performed (91). In some cases laser, electrocautery, or APC may be used as an adjunct to mechanical/ balloon dilatation (92,93); some patients may require future repeat procedures. For patients who require repeated dilatation procedures, surgical intervention should be considered (94). If surgery is not feasible or contraindicated due to medical comor-bidities, stent placement may be considered, although some clinicians prefer a trial of temporary stent placement before considering surgery. In general, silicone stents should be used for benign stenoses although the authors have had good success with the use of fully covered, self-expanding, metal stents that can be easily removed, similar to silicone stents.

For patients with TBM and EDAC causing respiratory fail-ure, stent insertion can be considered to allow liberation from mechanical ventilation. Complications related to long-term stent placement in these patient populations are not insignifi-cant however. Self-expanding metal stents can potentially frac-ture and cause granulation tissue. If uncovered metallic stents are used, removal at a later time if complications develop can be challenging. Silicone stents do not have issues with frac-turing, but can cause granulation tissue and can migrate if a standard tracheal stent is used; a silicone Y stent is most com-monly used in these patients. Consideration should be given for surgical management with tracheobronchoplasty once the patient is stabilized (85). Patients with focal tracheal cartilagi-nous malacia due to prolonged intubation or tracheostomy

tube should typically not be managed with stent placement, as the need for the stent will be lifelong, and eventual compli-cations are likely. Patients should be evaluated for resection of the pathologic segment and end-to-end anastomosis (95). If the patient is not a candidate for surgery, placement of a tracheostomy tube to bypass the segment may be required.

Outcomes for Airway Interventions in the ICU

Interventional bronchoscopy procedures can be successful in allowing patients to be liberated from mechanical ventilation (Table 116.4). Likewise, in a study by Noppen et al. 15 patients, who were ventilator/artificial airway dependent patients, were treated for airway obstruction after being referred for failed attempts at weaning from mechanical ventilation or from their tracheostomy cannula (96). All patients had benign disease, with most patients having postintubation tracheal stenosis or tracheomalacia. Median duration of mechanical ventilation prior to referral was 30 days (range, 7–105 days); 14 of the 15 patients were extubated/decannulated immediately fol-lowing the intervention. Similarly, 36 patients with respira-tory failure or impending respiratory failure due to malignant airway obstruction were treated emergently by Jeon et al. (97); of the 36 patients, 34 had a successful outcome. Over-all survival ranged from 3 days to 69 months with a median of 23.6 months. Interventional bronchoscopy can have a sig-nificant impact on critically ill patients with CAO and may allow for successful withdrawal from mechanical ventilation, hospitalization in a lower level of care environment, relief of symptoms, and extended survival.

TABLE 116.4 Results of Interventional Pulmonary Procedures in Patients Requiring Mechanical Ventilation

Author Number of Patients on MV Cause of CAO Interventional Modality Successfully Liberated from MV

stanopoulos et al., 1993 (98) 17 Malignant laser 9/17

saad et al., 2003 (99) 16 Malignant 8Benign 8

stent 14/16

zannini et al., 1994 (100) 6 Malignant 1Benign 5

stent 6/6

colt and Harrell, 1997 (101) 19 Malignant 11Benign 8

laser and/or dilatation and/or stent

10/19

shaffer and allen, 1998 (102) 8 Malignant 6Benign 2

stent 7/8

chan et al., 2002 (103) 4 Malignant stent 4/4

lippman et al., 2002 (104) 3 Malignant 2Benign 1

stent 3/3

lin et al., 2008 (105) 26 Malignant 21Benign 5

stent 14/26

razi et al., 2010 (106) 7 Malignant stent ± electrocautery 3/7

Murgu et al., 2012 (107) 12 Malignant laser and/or stent 9/12

cao, central airway obstruction; MV, mechanical ventilation.

• Massive hemoptysis is defined as expectoration of blood exceeding 200 to 1,000 mL in 24 hours.

• Bleeding in massive hemoptysis originates from bron-chial and pulmonary arteries in 90% and 5% of cases respectively.

Key points

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