The unusual fi nding of black pigmentation involving the airways from occupational exposure has been
reported in the literature since the early 1940s. The term black bronchoscopy, describing the endobronchial appearance of malignant melanoma, was introduced in 2003. 1 However, a search of the literature reveals multiple etiologies that can cause a black discoloration of the airways ( Table 1 ). Bronchoscopic examination is being performed with increasing frequency in the modern era. Pulmonologists should be fully cognizant of the differential diagnosis of black bronchoscopy. The following is a review of the literature related to the con-ditions causing a black discoloration of the airways.
Congenital Cause
Melanosis
Tracheobronchial melanosis (TBM) is an uncommon fi nding reported in the literature. Previous series have quoted a prevalence of one in every 52 bronchoscopies performed. 2 The common sites affected are the sec-
ondary and the tertiary carina. Men and women are equally affected. 2 Single or multiple areas of dark pig-mentation are encountered incidentally on bronchos-copy performed for unrelated indications. No other mucosal abnormalities or distortions of the airways are noted ( Fig 1D ). Melanosis of the larynx and the oropharynx has been associated with occult malignancy, yet no such relationship has been reported with TBM. 3 In addition, an association between TBM and the mel-anosis involving other body organs or smoking has not been reported. With primary melanoma of the tracheo-bronchial tree being a rare entity, the clinical signif-icance of TBM is not yet defi ned; however, it does need to be differentiated from other causes of black bronchoscopy.
Inborn Error of Metabolism
Alkaptonuria (Ochronosis)
Alkaptonuria is a rare inborn error of metabolism involving the degradation of the amino acids phe-nylalanine and tyrosine. It is a genetic disorder with an autosomal-recessive mode of inheritance. 4 It is caused by a defi ciency of the genes encoding for the homogentisate-1, 2-dioxygenase, which is an important
A presence of black pigmentation involving the endobronchial tree is not uncommon. It was fi rst described in the literature in association with occupational exposure in the early 1940s. However, in 2003, Packham and Yeow formally used the term black bronchoscopy to describe endobron-chial metastasis from a malignant melanoma. Hyperpigmentation of the airway, however, is asso-ciated with multiple etiologies such as congenital disease, inborn errors of metabolism, infections, environmental exposures, neoplasm, and iatrogenic causes. Although the majority of these condi-tions are benign, a proper diagnosis is important for optimal management. In this article, we review the etiology of black bronchoscopy and discuss its presentations and current management guidelines. CHEST 2013; 144(5):1696–1706
Black Bronchoscopy Pichapong Tunsupon , MD ; Tanmay S. Panchabhai , MD ; Danai Khemasuwan , MD , MBA ; and Atul C. Mehta , MD , FCCP
Manuscript received April 23, 2013; revision accepted June 21, 2013. Affiliations: From Internal Medicine, Medicine Institute (Dr Tunsupon) and Pulmonary, Allergy and Critical Care Medicine, Respiratory Institute (Drs Panchabhai, Khemasuwan, and Mehta), Cleveland Clinic, Cleveland, OH Correspondence to: Atul C. Mehta, MD , FCCP, Pulmonary, Allergy and Critical Care Medicine, Respiratory Institute, Cleveland Clinic, Cleveland, OH 44195; e-mail: [email protected]
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however, long-term effi cacy and safety necessitate further evaluation. 4
Infection
Aspergillus niger
Tracheobronchial aspergillosis can present in var-ious clinical forms, such as invasive, ulcerative, or pseudomembranous tracheobronchitis. 7 It predomi-nantly affects the immunocompromised population. Endoscopic fi ndings vary depending on the Aspergillus species involved. One percent of all Aspergillus airway infections following lung transplantation are from the niger species. It is usually encountered in the nosocomial environment and in patients who are suffering from hypogammaglobulinemia and are on long-term itra-conazole therapy. 8 In patients infected with Aspergillus niger , black pigmentation has been reported on FB. In addition to the black pigmentation, white masses of oxalate crystals are also seen; the fungus produces oxalic acid which binds to airway calcium ( Figs 1E-F ). 8 The treatment of endobronchial aspergillosis follows the treatment guidelines for invasive aspergillosis.
Ochroconis gallopava
Dematiaceous fungi (dark-pigmented fungi) are char-acterized by the presence of melanin or melanin-like pigments. 9 Infections caused by this group of fungi include mycetoma, chromoblastomycoses, and phae-ohyphomycosis. There has been an increase in the incidence of infections caused by these fungi, partic-ularly in solid-organ transplant recipients. 9 Of particular
liver enzyme that degrades homogentisic acid (HGA), a metabolite in the phenylalanine and tyrosine degra-dation pathway. The term ochronosis describes the accumulation of homogentisic acid in collagenous tis-sues of the body, resulting in dark gray pigmentation of the connective tissue and the cartilages, involving multiple organ systems. A history of early-onset degen-erative arthritis, multiple joint replacements, and val-vular heart disease suggest alkaptonuria along with the dark-colored airways. 4 The severity of symptoms pro-gressively increases beyond 30 years of age. The phys-ical examination may reveal the darkening of sclera and ear cartilage. The involvement of the respiratory system with ochronosis is most frequently diagnosed during autopsy. However, a premortem case of alkap-tonuria has been reported as diagnosed with fl exible bronchoscopy (FB). 5 The bronchoscopic examination reveals hyperpigmentation of the airways, including the epiglottis, larynx, bronchial cartilages, and mucosa. Hyperpigmentation of the bronchial mucosa extends distally from the trachea to the small bronchioles, and the involved bronchial mucosa is typically covered with dry black secretions ( Figs 1A-C ).
The diagnosis of alkaptonuria is based on gas chromatographic-mass spectrophotometric assays that measure urine and plasma HGA levels. 6 Effective man-agement of alkaptonuria is not clearly described. Nei-ther high-dose vitamin C nor protein restriction has effectively reduced urinary HGA excretion. Nitisi-none, a triketone herbicide that reversibly inhibits 4-hydroxyphenylpyruvate-dioxygenase, has been shown to reduce urinary HGA excretion by . 80% in a murine model. It can also decrease HGA production in humans;
Table 1— Black Bronchoscopy: Etiology, Differential Diagnosis, and Diagnostic Methods
Etiology Differential Diagnoses Diagnostic Method
Congenital Melanosis By excluding other conditionsInborn error
metabolismAlkaptonuria (ochronosis) Measurement of urine and plasma HGA levels
Infection Aspergillus niger Endobronchial biopsy and culture Ochroconis gallopava Transbronchial biopsy and culture
Healed TB Prior history of TB infection and pigment location at lymph node stationsEnvironmental
exposuresAnthracosis and anthracofi brosis By history, endobronchial biopsy and microscopic examination under polarized light
Soot inhalation History of exposure to fi reArgyria By history and endobronchial biopsy
Iatrogenic Charcoal aspiration History of charcoal useAmiodarone History of amiodarone use and resolution after discontinuation of the drugTricoptysis History of prior airway reconstruction surgery
Endobronchial ignition History of thermal ablation
HGA 5 homogentisic acid.
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ents, lung transplant recipients have the highest inci-dence of O gallopava infections. 10 Common pulmonary presentations include nodules and nonresolving infi l-trates with upper and middle lung predominance. Cough may or may not be present. 11 Involvements of
Figure 1. A-C, Ochronosis. Note the dark black pigments involv ing the (A) upper, (B) middle, and, (C) lower trachea. (Courtesy of Mohamad Bakry, MD, Pulmonary and Critical Care Medicine, New York Methodist Hospital.) D, Incidental fi nding of endobronchial melanosis in a patient undergoing bron-choscopy for an unrelated indication. Note the black pigmentation involving the bronchial mucosa. E, Black pigmentation of Aspergillus niger colonization involving right upper lobe bronchus in a lung transplant recipient. Note the white calcium oxalate particles at the base. (Reprinted with permission from Singhal et al. 8 ) F, Calcium oxalate crystals under the microscope. (Reprinted with permission from Singhal et al. 8 )
interest to the topic of discussion is the genus Ochro-conis which include species gallopava , constricta , and humicola . O gallopava infections generally involve the lung with extrapulmonary involvement especially of CNS and skin. 10 Among solid-organ transplant recipi-
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Figure 2. A, Ochroconis gallopava . Note the black pigmentation involving the left upper lobe bronchus in an immunocompetent patient with positive fungal cultures on BAL. (Courtesy of Wes Shepherd, MD, Interventional Pulmonology, Virginia Commonwealth University Medical Center.) B, Healed endo-bronchial Mycobacterium tuberculosis (MTB). Note the dark pigmentation involving the right upper lobe bronchus (with fibrosis). C, Left lower lobe bronchus. Note the dark pigmentation involv ing the left lower lobe bronchus. D, Anthracostenosis. Note the severe narrowing and black pigmenta-tion involving the right lower lobe bronchus in an elderly coal miner. (Reprinted with permission from Mireles-Cabodevila et al. 18 ) E, Anthracostenosis. Note that the endobronchial biopsy specimen revealed anthracotic pigments (arrow). (Reprinted with permission from Mireles-Cabodevila et al. 18 ) F, Anthracostenosis. Note that polarized microscopy revealed silica particles (arrow). (Reprinted with permission from Mireles-Cabodevila et al. 18 )
airways could present with black pigmentation and growth similar to A niger ( Fig 2A ). Diagnosis is made by transbronchial biopsies and fungal culture. Antifungal
therapy anecdotally has been decided based on sensi-tivities. Rarely, cases of O gallopava have been reported in the non-solid-organ transplant population as well. 12
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Healed endobronchial Mycobacterium tuberculosis (MTB) often leaves black pigmentation within the airways. Multiple areas of dense peribronchial fi bro-sis and the deposition of black pigment are observed during bronchoscopy. In addition, multiple calcifi ed intrathoracic lymph nodes on CT scan of the chest raise suspicion for a past history of MTB 13 ( Figs 2B-C ). The proposed pathophysiology of black pigmentation associated with MTB could be explained by possible intrabronchial perforation involving infected lymph nodes burdened with pigment-laden macrophages into the adjacent bronchial mucosa. After years of heal-ing and fi broblastic proliferation, airway stenosis may develop. 14 We presume that the black pigments are the residue of the MTB organisms. Based on current data, an anti-TB regimen may resolve atelectasis and bron-chial narrowing. However, hyperpigmentation is con-sidered irreversible. 13
Environmental Causes
Anthracosis and Anthracofi brosis
Anthracosis refers to the deposition of carbon par-ticles in the airways and the lung parenchyma. It is found among those who smoke cigarettes or reside or work in areas heavily polluted with atmospheric soot. The deposition of carbon within the bronchial mucosa or lung parenchyma does not induce infl ammation or fi brosis. Most anthracotic particles are usually removed by mucociliary clearance; however, a small amount of carbon particles, phagocytosed by macrophages, remain within the bronchioles. 15 Anthracofi brosis and anthra-costenosis are the terms which describe the fi ndings of bronchial obliteration, along with an anthracotic (black) pigmentation covering the bronchial mucosa, without an associated history of cigarette smoking 16,17 ( Figs 2D-F 18 ). The fi brotic aspect of anthracofi brosis is associated with occupational exposure to silica. High-risk occupations include coal mining, masonry, and those with exposure to woodsmoke. 19-21 Anthracofi bro-sis related to chronic biomass or woodsmoke exposure is usually found in nonsmoking elderly women using natural fuels for indoor cooking. 19,22
Common manifestations of anthracofi brosis are chronic cough, dyspnea, wheezing, and rhonchi. 16,19,22 COPD of the chronic bronchitis type with a minimal response to bronchodilators is the usual manifestation in the majority of patients. 22 Characteristic CT scan fi ndings include peribronchial thickening and oblit-eration, leading to lobar atelectasis, predominantly involving the right upper and middle lobes, surrounded by enlarged and/or calcifi ed peribronchial, hilar, or mediastinal lymph nodes. 14 A high proportion of crys-talline silica in hilar lymph nodes and lung parenchyma
raises the possibility of lymph node perforation into the bronchial walls, preceding the chronic healing pro-cess. The mechanism is similar to that described in MTB-associated fi brosis. The gold standard for the diagnosis is based on mineralogic analyses by trans-mission electron microscopy showing high percent-ages of crystalline silica and nonfi brous silicates, such as mica and kaolin particles, in lung tissue and BAL fl uid. 20 Cases of bronchogenic carcinoma have been reported in association with anthracofi brosis 23 ; in addi-tion, poorly differentiated adenocarcinomas have been found to develop in severely anthracotic lungs. 24 How-ever, this occurrence seems to be coincidental rather than a cause- effect relationship.
It is not necessary to perform FB if patients are asymptomatic. However, if the history suggests a high probability for malignancy, the procedure should be considered. 20
No defi nitive treatment exists for anthracofi brosis. In a single case report, a partial resolution of bron-chial narrowing following treatment with corticoste-roids and tamoxifen was documented. 19,25,26 Despite treatment, however, the multiple patchy areas of black pigmentation remained unchanged. 19 Other measures, including antibiotics, bronchodilators, physiotherapy, and postural drainage, remain of limited value. 22
Soot Inhalation
Residential fi res are a major cause of inhalation injury affecting airways and lung parenchyma. In the past, in association with skin burns and the exposure to carbon monoxide and nitric oxide, systemic shock and wound sepsis were the major causes of death in these patients. Currently, inhalation injury is the most frequent cause of death in burn patients. 27 The mor-tality rate from soot inhalation alone is approximately 10%. A combination of smoke inhalation and skin burns increases this rate to 30% to 90%. 28
The diagnosis of inhalation injuries is based on appropriate history and medical fi ndings (eg, facial burns, nostril edema). 29 Laryngeal edema following the soot inhalation could rapidly progress to acute upper airway obstruction and may necessitate intuba-tion and mechanical ventilation. 30
Presently, FB is the standard procedure for the diag-nosis of smoke inhalation. 31 Bronchoscopic fi ndings are characterized by multiple, focal, large black-and-gray edematous plaques involving the tracheobronchial mucosa, extending distally to the small bronchioles 32 ( Fig 3A 33 ). The fi ndings are usually associated with atelectasis and pneumonia, as seen on chest radiographs, as a consequence of a marked decrease in surfactant production. 34 Histologic examination reveals disruption of the tracheobronchial mucosa with focal necrosis and the formation of a pseudomembrane composed
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way suction, and pharmacologic agents, such as bron-chodilators, racemic epinephrine, and mucolytic agents. In addition, FB is very effective for secretion and cell debris removal. If left untreated, airways could become completely obstructed, subsequently causing lobar
of mucus, cell debris, fi brinous exudate, neutrophils, and bacteria. 28
The fundamental concept in managing smoke inha-lation is secretion clearance by means of therapeutic coughing, chest physiotherapy, early ambulation, air-
Figure 3. A, A case of soot inhalation. Note the thick layer of soot involving the lower trachea. (Reprinted with permission from Ribeiro et al. 33 ) B, Endobronchial argyria. Note the well-demarcated area of grayish-black pigmentation involving upper trachea in a patient using a silver tracheostomy tube over 30 y. C, Endobronchial biopsy revealing silver particles in the submucosa without vascular involvement (arrows). (Reprinted with permission from Schreiber et al. 43 ) D, Endobronchial metastatic melanoma produc ing total obstruction of the left main stem bronchus in a patient with prior history of melanoma. (Reprinted with permission from Das et al. 50 ) E-F, A case of activated charcoal aspiration and black bronchoscopy . (Reprinted with permission from Rajamani and Allen. 55 )
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atelectasis and postobstructive pneumonia. 34 The com-bination of inhalation injury and pneumonia results in a 60% increase in mortality from burns. 28
A retrospective study has revealed that patients with a 30% to 59% surface-area burn and pneumonia who underwent at least one bronchoscopy required shorter duration mechanical ventilation (21 days vs 28 days, P 5 .0001), ICU stay (35 vs 39 days, P 5 .04), as well as overall hospital stay (45 days vs 49 days, P 5 .009) than otherwise. In addition, the mortality rate was reduced by 18% in the bronchoscopy group. 27 A prospective study proposes a graded severity of soot inhalation according to the depth of mucosal injury. This classifi cation is based on FB being performed within the fi rst 24 h after the injury ( Tables 2 , 3 ). 35 FB helps predict outcomes and leads to the development of effective treatment guidelines. Histologic exam-ination reveals that the deeper the mucosal damage, the higher the rate of acute lung injury and the mor-tality rate. 35 Thus, early bronchoscopy is highly desir-able for patients with an inhalation injury. 35,36
Argyria and Argyrosis
Argyria is a term which describes chronic silver exposure which causes an irreversible, blue-gray dis-coloration of the skin (argyria) and sclera (argyrosis). 37,38 Cases of argyria associated with occupational expo-sure and drug consumption have been reported since the early 1940s. 39,40 The duration of exposure varies from months to years prior to the diagnosis. 39,40 Silver particles can enter the body via inhalation, ingestion, or a parenteral route. 38,41,42 The deposition of silver particles could be confi ned to one area through pro-longed direct contact or be widespread in distribution, involving organs such as the trachea, skin, liver, kidneys, corneas, gingival, mucous membranes, nails, and spleen ( Fig 3B). 43 Argyria is proposed as a mechanism of detoxifying silver from the bloodstream by its excretion into the tissues in form of a harmless silver-protein com-plex. 44 Sparse data are available on the possible toxic effects of silver deposition in organ tissues. 38 Patients who report high levels of silver exposure and present
Table 2— Classifi cation of Endobronchial Burns According to the Depth of Mucosal Damage
Group Finding
G 0 NegativeG b Confi rmed positive by biopsyG 1 Mild mucosal edema and hyperemia, with or without
carbon sootG 2 Severe mucosal edema and reddening, with or without
carbon sootG 3 Ulcerations, necrosis, and absence of both cough refl ex
and bronchial secretions
G 5 group. Adapted with permission from Chou et al. 35
Table 3— Correlation of ALI and Mortality by Group
Adapted with permission from Chou et al. 35 ALI 5 acute lung injury. See Table 2 legend for expansion of other abbreviation.
with plasma silver levels above the normal range could develop neuropathy. 45
Histologic examination reveals tiny dark-brown par-ticles of silver deposited in the affected areas, espe-cially the internal elastic lamina of small vessels. 39 This fi nding is visually distinguishable from the typical coarse deposition of black pigment seen in anthracosis. 37,43 Chronic inhalation of silver vapors could result in the discoloration of bronchial mucosa and alveoli. 39 How-ever, no reports of signifi cant clinical consequences, except for chronic cough, mild bronchitis, emphyse-matous change, and reduction in lung volumes, were found. 46 A single case report described an unusual bronchoscopic fi nding of a dark hyperpigmented area with a distinctive demarcation in a patient in prolonged contact with a silver tracheostomy tube. Histologic examination revealed dark fi ne pigments underneath the epithelium, without the involvement of blood vessels ( Fig 3C ). 43
Neoplasms
Endobronchial Melanoma
Several endobronchial neoplasms exhibit dark pig-ments. Primary melanoma of the lung is a rare tumor involving 0.01% of all lung tumors. 47 Metastatic mel-anoma is the more common endobronchial lesion than its primary counterpart. Endobronchial melanomas, when metastatic, usually present after the onset of the primary tumors. It is vital to rule out an occult primary tumor if melanoma of the lung is suspected on bron-choscopy. The pathogenesis of endobronchial mela-nomas has been revised by Kiryu et al 48 who have classifi ed endobronchial melanomas into four devel-opmental modes: type 1, direct metastasis to the bron-chus; type 2, bronchial invasion by a parenchymal metastatic lesion; type 3, bronchial invasion by medi-astinal or hilar lymph node metastasis; and type 4, a peripheral lesion extending along the proximal bronchus.
FB exhibiting a black, sticky endobronchial lesion raises a possibility of either a primary or a metastatic melanoma 49 ( Fig 3D 50 ). The differential diagnosis, how-ever, also includes melanocytic carcinoid, schwannoma,
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the infl ammatory response in the lungs. In an animal model, the direct instillation of activated charcoal into the lungs resulted in increased microvasculature per-meability and pulmonary edema. The aspiration of charcoal can also present as a spiculated, PET-positive mass years after aspiration and can be confused with lung cancer. 58
If FB demonstrates charcoal in the endobronchial tree ( Figs 3E-F ), 55,59 washings are performed to miti-gate the severity of complications. Overall manage-ment is supportive care with mechanical ventilation, inhaled bronchodilators, and repeated bronchoscopy to facilitate clearance. 60 The best method to prevent charcoal aspiration is to provide adequate airway pro-tection with endotracheal intubation in patients with impaired mental status. 55
Amiodarone
Amiodarone is an effective agent against various cardiac arrhythmias. However, its use is limited by pulmonary toxicity. Amiodarone and its metabolite accumulate in lung tissue at levels 100- to 500-fold higher than serum. 61 Pulmonary complications develop in 5% to 15% of patients on 500 mg or more daily and in 0.1% to 0.5% of patients on doses up to 200 mg daily. 62 There are two possible mechanisms of pulmo-nary toxicity: (1) a direct toxic effect and (2) an immune-mediated hypersensitivity reaction. 63 Patients may present with: interstitial pneumonia, organizing pneu-monia, ARDS, pulmonary nodules, alveolar hemor-rhage, and pulmonary fi brosis. 64 Hyperpigmentation of the airway is reported in one case ( Fig 4A ). 65 The possible mechanism may be the chronic accumulation of amiodarone in the submucosal tissue from its long-term use. Discontinuation of the drug results in the resolution of bronchial pigmentation ( Fig 4B ). 65 How-ever, drug toxicity may initially continue to progress due to the long half-life of amiodarone. Regardless, a rechallenge of amiodarone is not recommended due to the risk of pulmonary fi brosis.
Tricoptysis
The condition of tricoptysis can be iatrogenic in origin. In a single case report, the patient presented with a gradual onset of shortness of breath, hoarse-ness, wheezing, and coughing of hair. This patient had undergone reconstruction surgery for a benign laryn-geal tumor, which used a mucosal fl ap. FB revealed an extensive meshwork of black hair fi laments, below the epiglottis, partially covering the vocal cords. Some hairs were covered by thick mucus ( Fig 4C ). Most patients with a laryngeal tumor who undergo flap reconstruction require postoperative radiation to minimize ectopic hair growth. However, this patient did not receive external beam radiation. Laser hair
or paraganglioma. 47 The diagnosis mainly rests upon histologic identifi cation. Occasionally, the metastatic lesion may lose its pigmentary characteristic and be labeled as amelanotic melanoma. Because primary melanoma of the lung is exceedingly rare, strict diag-nostic criteria have been established: junctional changes (ie, dropping off or nesting of melanoma cells just beneath the bronchial epithelium), the invasion of the bronchial epithelium by melanoma cells in an area where the bronchial epithelium is not ulcerated, and no demonstration of a tumor elsewhere at the time of diagnosis. 51 The prognosis is poor for both primary and metastatic melanomas of the lung. Median survival after the diagnosis of metastatic disease is approxi-mately 15 months, as the endobronchial condition represents advanced stage disease. 52 Surgical resection followed by chemotherapy and immunotherapy has been reported in a few instances, but long-term prog-nosis is not yet defi ned.
Teratomas
The term tricoptysis refers to the expectoration of hairs in the sputum. Tricoptysis is seen in 15% of the cases of intrapulmonary teratoma. A mature teratoma may rupture and release its contents into airways, resulting in a recurrent cough, hemoptysis, and tri-coptysis. 53 Involved airways exhibit dark black areas due to the presence of hair. Excision of the tumor is the treatment of choice for a mature teratoma even though the tumor is benign. A benign teratoma may potentially transform into a malignancy. 54
Iatrogenic Causes
Charcoal Aspiration
Activated charcoal is considered an effective GI decontaminant for acute intoxication with select drugs. Charcoal prevents absorption by binding directly to the toxic drug and creating a passive diffusion gra-dient from the bloodstream, across the GI lumen (GI dialysis). 55 Patients with an altered mental status are at high risk of aspiration of activated charcoal into the lungs, especially if the airway is not adequately protected. Aspiration is reported in 1.7% of patients who receive charcoal alone and 2.3% of those who also undergo gastric emptying. 56 The aspiration of gas-tric contents occurs concomitantly with charcoal aspi-ration, which frequently results in severe pulmonary complications.
Acute complications of charcoal aspiration include airway obstruction, bronchospasm, hypoxemia, and pneumonia. Late complications include ARDS, bron-chiolitis obliterans, bronchopleural fi stula, and even death. 57 Although charcoal is an inert and nonabsorbable agent, it exerts a strong immunogenicity and activates
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tion (F io 2 ). 70 Strategies have been proposed to decrease the occurrence of endotracheal fi re during laser pho-toresection, as well as argon plasma coagulation. 68,71-75 Endobronchial ignition, irrespective of the energy source, is an emergency. To avoid delay in the man-agement, the operating room personnel should be trained to manage the circumstances promptly. A step-by-step protocol should be established. When a fl ash fi re is detected, all anesthetic agents should be imme-diately discontinued, followed by endotracheal tube removal and extinguishing the fi re with saline. The patient should receive pure oxygen ventilation by mask prior to reintubation. 69 The tracheobronchial tree should be reevaluated for the removal of any foreign particles. Daily FB should be performed to detect complications and delineate the extent of injury. 69 Ste-roids should be initiated with a gradual tapering as the patient improves. Daily tracheal cultures should be obtained for the early detection of changing micro-biology. Prophylactic antibiotics, such as penicillin
removal or fulguration techniques may be necessary to remove hairs permanently from this location. 66
Endobronchial Ignition
An endobronchial ignition during the thermal abla-tion of an airway lesion resulting in black discoloration has been reported on several occasions. Such compli-cations can occur during the use of a laser, electrocau-tery, or argon plasma coagulation. Burned mucosa as a result of tracheal fi re exhibit black debris, based on the degree of injury ( Fig 4D ). 67,68 The black carbona-ceous debris deposited in the airways, in addition to the toxic vapors from a burn, could produce chemical injury and chronic mucosal infl ammation. 69 Severe endobronchial burns can also lead to the perforation of the airways and fi stula formation with surrounding structures.
Major factors contributing to the endobronchial ignition include the types of endotracheal tube, bron-choscope and laser used, and high oxygen concentra-
Figure 4. A, Black pigmentation involving left lower lobe, in a patient on amiodarone therapy. (Reprinted with permission from Küpeli et al. 59 ) B, Note resolution of the pigments following the discontinuation of the amiodarone. (Reprinted with permission from Küpeli et al. 59 ) C, A case of iatrogenic tricoptysis . Note the hair growth from the anterior wall of the subglottic trachea. (Courtesy of Mohamed B. Bakry, MD, New York Methodist Hospital). D, Endobronchial ignition during laser photoresection. Note the black sloughing in the bronchial mucosa. (Reprinted with permission from Krawtz et al. 68 )
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and cephalosporin, should be initiated and later adjusted, based on bacteriologic fi ndings. 69 In severe laryngopharyngeal injury, tracheostomy is necessary to prevent airway obstruction. A high-humidity nebu-lizer will facilitate the clearing of secretions because burned airways with impaired mucociliary function are prone to form mucus plugs, resulting in postob-structive pneumonia. 69
Conclusion
The presence of black pigmentation involving the bronchial mucosa is a relatively uncommon and, hence, underrecognized condition. In this article, we provide a comprehensive review on the etiology of black bron-choscopy. In most of the cases, diagnosis can be made by reviewing the history of exposure to hazardous substance and by performing endobronchial biopsies and cultures. In case these basic diagnostic tests are unable to reveal the etiology, special diagnostic tests may be needed such as microscopic examination under polarized light and measurement of urine and plasma HGA levels ( Table 1 ). Overall, it is important for a bronchoscopist to recognize the full range of possible etiologies of this rare entity for its optimal management.
Acknowledgments
Financial/nonfi nancial disclosures: The authors have reported to CHEST that no potential confl icts of interest exist with any companies/organizations whose products or services may be dis-cussed in this article.
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