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Pulmonary Fredric Edward and Complications L. Hildebrand, C. Rosenow Henry D. lii, Tazelaar, of Leukemia Jr., M.D.;* M.D., F.C.C.P;* Thomas M. Habermann, (Chest 98:1233-39) 1990; the parenchyma. Other causes bacterial and other opportunistic rhage, leukemic and lymphomatous ALL = acute lymphocytic leukemia; A.ML acute myelocytic leukemia; AMML acute myelomonocytic leukemia; Ara-C cytosine arabinoside; ARDS acute respiratory distress syndrome; CLLchronic lymphocytic leukemia; CMVcytomegalovirus; HSVherpes simplex virus; JPAinvasive palmonary aspergillosis; PAPpulmonary alveolar phospholipoproteinosis T he leukemias natural are history chronic a diverse and leukemias different with ent upon leukemia, are and the presence or thrombocytopenia. that 98 autopsy dence ofdisorders. of the distinctly are leukemias. These or absence of Hooper’ in found leukemia reported is are selected for patients with specific pulmonary problems or particular leukemias. Moreover, the incidence varies over a wide range, depending upon whether symptoms, chest radiographs, tests, or autopsy findings alone of disease. Pulmonary the conditions differential host, such as the not due patient’s to the must of the patient leukemia itself, are are status, medical in listed abnormalities but immunocompromised a complicating considered leukemia, pulmonary illness. All caused by in 139 with patients Genter leukemia infiltrates, infiltrates for which attributed Hooper’s’ conclusively review at the to determine pulmonary here. causes of pulmo- for in leukemic patients. the infiltrates, infiltrates majority organisms ofpulmonary Sixty infiltrates to 75 percent 82 percent offocal and had infectious causes. pathogens were infiltrates, whereas Table of reported underlying infiltrates, human immunodeficiency and neoplasm the Drug-induced pulmonary disease of the focal accounted in Disease Host process involving complications lymphoid virus of interstitial the leukemia, lungs lym- pneumonia in infection) reaction process community-acquired Unusual most of diffuse bacterial organisms disease unusual carcinoma, Nonspecific for opportunistic phoma, “Unrelated” 35 percent Common 1 -Categories ofPilmonary the immunocompromised of the (1eukemic responsible infection conditions opportunistic deaths in leukemia are due to infection.t57 In Tenholder and Hooper’s’ series of 68 patients with pulmonary Opportunistic or and (cardiogenic pulmonary edema and pneumonia) fibrosis complications proteinosis; ofthe pulmonary Combinations of two disease or therapy veno-occlusive or more of the (pulmonary alveolar disease) above procedures. invasive Medical is responsible Opportunistic medications, of the will not be discussed bacteria are listed in Table 1 should be considered during evalualion ofthese patients in order to narrow the differential diagnosis as much as possible and to avoid unnecessary diagnostic In Tenholder and with function as the index immunocompromised with of the be patients The bone INFECTION Recurrence that diagnosis 1.2,3 Many Table pulmonary are used transplant review summarizes the major complications in leukemia. Infection who came to The true mci- series marrow This nary of neutropenia and pulmonary complications to assess because most in failure (Table 2). These will be discussed. spectrum of pulmonary problems in depend- the type of treatment, percent of leukemic patients had pulmonary complications. difficult common ofsignificant Tenholder and Several are factors, including and time course kocytic reactions, heart unique included infection by organisms, hemorinvolvement, leu- leukemic cell lysis pneumonopathy, hyperleureaction, alveolar proteinosis, adverse drug and other processes including congestive kostasis, The acute different. complications any ofthe multiple the nature group management pulmonary patients M.D.;t M.D4 in 84 a cause the of the Walter etiology instances was to leukemic records Reed of cell ofPulmonary With Leuke,nia ftitients in Hemorrhage Leukemia 10 were infiltration Disease Infection of parenchymal only 2-Causes Army of associated found, Table of From the of Thoracic Diseases and Internal Medicine, the tDivision of Hematology and Internal Medicine, and the tDivision of Pathology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota. I3nt requests: Dt Rosenow, Ma Clinic, Rochester, MN 55905 and lymphomatous involvement Leukostasis Leukemic cell lysis Hyperleukocytic reaction Alveolar proteinosis Adverse drug Opportunistic reactions neoplasms CHEST Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21620/ on 05/10/2017 I 98 I 5 I NOVEMBER, 1990 1233 for most ofthe diffuse diffuse infections the significant nonopportunistic infiltrate reasonable Several and associates5 permits 193 patients of which Sixty percent Kiebsiella cases clinician pneunioniae, Staphylococcus ( Pneumocystis) are Granulocytopenia the common absolute of infection. With there is a steady increase cells/pA there 100 fatal decreasing respiratory consequences likelihood In addition, cells/pi in below and the leukemic biopsy-proven locytopenia patients.9”#{176} In a study causes trum can is of subse(IPA) with and others” found grantsmost important factor in been shown development episodes granu- to of of hemop- in these ated They u’9 and hairy-cell leukemia had found combmant but and the and most common, pulmonary infil- cell-medi- These infections in one series.#{176}Prior approaches, patients no infectious complicathan re- longer interferon-a (2 ‘ -deoxycoformycmn) the natural toxicities.21 my- kansasii to impaired to live significantly However, Pentostatin my- atypical , distinctly changing and its infectious atypical granulomatous and coccidioido- monocytopenia. 9 of 186 patients chemotherapeutic tions patients due of Gram- Mycobacterium in been with and being with causes bacteria, chills, probably immunity were reported to effective sec- Infectious Disseminated with by fever, are spec- complications infections, M aviurn-intracellulare trates. infections, defects in cell-mediated are the primary causes Opportunistic blastomycosis also major A wide Gram-negative infections, to be are infections.’”5 infectious fungal are characterized tract leukemia. mortality.m6m7 including may thought and respiratory leukemia, and are pathogens is involved bacteria, cobacterial and persisted has the viruses lymphatic include positive and to the harmful increase incidence from frequent from in acute of morbidity bacteremias of patients and as respiratory ofviruses mycosis, A rapidly an recovery chemotherapy of IPA, with of morbidity especially 500 it Also, leukemia, important and below of granulocytopenia IPA, Gerson to be the single In childhood in incidence, further.8 more. cavitation pneumonitis mci- with 12,13 cobacterial infections, determine the probability of infection, and particular importance in the development and quent course ofinvasive pulmonary aspergillosis in for ce11s/i.l granulocyte count and damage mucosa and cilia are particularly of chemotherapy which also of infection. the duration after course disease, if granulocytopenia ondary to granulocytopenia, immunity, and monocytopenia factor 1,000 or In hairy-cell protozoans incidence, increase increase and demonstrated count counts Gram-negative infections and has been is a marked tract. coli, pathogens.56 neutrophil dence tysis. Mucorales, predisposing correlation locytopenia worsen the more almost aeruginosa, HSV), is a Inajor A direct between less acute setting, (Candida, (CMV, viruses infections. hospital in in the respiratory due to Escherichia Fungi a weeks pulmonary infection of the 50 percent three for type to offer development approaching microbial causes Balducci and Pseudomonas aureus. Aspergillus), of in a general were located of these were half the the the Clearly, but and associated differential diagnosis. have described the in patients with leukemia. reported leukemic other their studies of infection below abnormalities. begin as focal infiltrates, between opportunistic organisms of pulmonary more infectious may disparity history of the are disease ‘p ....,, Fmcuiu: 1A. Chest roentgenogram of a patient with acute myelomonocytic pulmonary hemorrhage. B. Massive pulmonary hemorrhage in a 67-year-old leukemia associated with a low I)latelet count secondary to chemotherapy magnification, x 64). 1234 leukemia (AMML) and man with acute lymphocytic (hematoxylin-eosin, original Pulmonary Complications Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21620/ on 05/10/2017 of Leukemia (Hildebrand et a!) HEMORRhAGE Alveolar hemorrhage patients with is often leukemia. found at autopsy It is frequently 1.23-28 other pulmonary pathologic conditions, pneumonia from invasive aspergillosis, ally involves blood vessels.’ Alveolar usually not suspected or because patients hemoptysis occurs in this setting. The the before hemorrhage seen of acute leukemia. In bleeding function, was severe enough but hemoptysis patients and in none a pneumonic pat1 A). Unless it is may sometimes cells4i.l is presenP’27 20,000 cells/pA. Associated findings may occult pulmonary mimic if the platelet rhage was pulmonary percent and ofdiffuse the usually but, as stated than noted common cause (11 percent alveolar cause percent of of infiltrates, in possibly monary hemorrhage determined hemorrhage LEUKEMIC the may rapid and chemotherapy is be diffuse), pleural, pen(Fig 3 A and B).31#{176} CLL histologic picture to an non-Hodgkin’s This is charac- deterioration, fever, progres- and involve- sites, including the lung. This in patients who have had no The disease mediastinal, prognosis remissions treated of disease may hepatosplenomegaly, previous chemotherapy.’ bronchial,37 pleural,7’ based at die themselves transfonmation. extranodal may occur long-term who were found involvement or high-grade clinical adenopathy, chial.39’#{176}The as the especially . who infiltrates Leukemic Richter’s of lavage pulmonary a low-grade from are of patients cell 2). intermediate by infiltrates symptomatic (both focal or endobronchial convert terized cell leukemic (Fig parenchymal bronchial, hemosiderin INVOLVEMENT percent but to A of pul- macrophage LYNIPII0NIATous to 66 leukemia,’3’ of 3 to patients.7 measurement is the leukemic in 31 uncommon an incidence through bronchoalveolar is a disorder of exclusion. ANI) Pulmonary due with quantitative content Alveolar autopsy patients. Other series hemorrhage is a less immunocompromised effective ment process above, is poor may be penand endobron- in these have been aggressively patients, but reported in patients with anthracyclmne- programs.37 hemor- of noninfectious of focal and Contributing 8 sive 20,000/pi. that common lymphoma, of it is below and roentgenographic and mask a diagnosis were excluded in these that de novo pulmonary aggressive to death . In almost count of less than and fever is greater infiltrates). the diagnosis for invasive aspergillosis must be undertaken, Hooper’ the most infiltrates of these, was hemorrhage, count Tenholder 12 percent infection an aggressive search cause of hemorrhage is an or open lung some degree of of 50 autopsied to compromise pulmonary was absent in all of these made prior a platelet 50,000 of may microscopically of them pulmonary hemorrhage all documented cases, death in less than one-fourth chest roentgenogram artifact induced by transbronchoscopic biopsy. Bodey and co-workers found pulmonary hemorrhage in 54 percent cases to particularly which generhemorrhage is diagnosed show a well-localized infiltrate(s), tern, or a diffuse infiltrate (Fig massive (Fig 1 B), the pathologist assume in related problems suggest pulmonary LEUKOSTASIS, LEUKEMIC HYPERLEUKOCYI’IC 78 There are three unusual CELL LYSIS, ANI) REAc-nioN pulmonary complications 31” 74. S #{149} .‘::#{149} ., ‘. .‘ S 0m - , S. -‘ __ - . p Fu tIRE 2A. Chest roentgenograin of a patient with chronic lyinplocytic involvement. B. Open-lung biopsy specimen shows mature lymplax.ytes right), characteristic of’ pulmonary involvement h chronic IVmplak’tic original magnification, X 4(X)). leukemia dena)nstrates interstitial tracking along t vessel (upper k’uke,nia (hemnatoxvlin-eosin, CHEST Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21620/ on 05/10/2017 I 98 I 5 1 NOVEMBER. 1990 1235 ‘I . - Ut : ‘.‘ . ‘. 1:. 0 4 *_ ‘. t:r J? p._.. . #{149} I, C ,‘ , #{149}‘.,. . 3bb.S _ .1_ . :i . . .;e #{149} ?#{149} ‘ - ‘ “ . ,- ‘ , ‘I t t :: :?:,. c,.. ‘M’’..i # unique leukemia: to . acute respiratory leukocyte an or l)last autopsy review nonlymphocytic leukemia leukemia, McKee vascular “leukostasis” l)y ()CCILI5iOI1 with cell count in a group leukemia failure. developing Each diffuse hours after dying from respiratory phenomenon This support. lysis patients kocyte and infarctions, edema. and blast oxygen being stances therapy. leukemic postulated associated by and local of vascular these small tissue damage and by blast cells, with the toxic and thromboplastic injury sub- released by these cells as a result of chemoThe lack of deformability of myeloblastic cells has been substantiated; it is further that biopsy A third but chemotherapy may alter the aggregation.45 symptoms leukemic In and with myeloblastic count nadir. In infiltrates Each diffuse leukemia had an alveolar specific condition, cell cell co-workers.4 fever, without similar five specimens characteristic and dam- therapy. by a different mech- of these nisms respiratory counts adaptation. the same in the cerebral lung, accounting sumal)ly above, distress; and a slow did not presumably associated It must of extreme to the and leukostatic it was to a “hyperleukocytic” leukemia leukocyte falsely pathologic microhemorrhages, proposed rise acute culatory scribed died, who associated In addition ofmnjury chronic patients revealed pulmonary leukostasis with the accumulation of blast cells in arterioles edema. a rapid with count greater than 245,000/pA and blasts, with a rapid increase in the and number of blasts over several capillaries, alveolar analysis. worsen and demonstrating all recovered and symptoms, interstitial obstruction membrane and thus promote The observation that pulmonary 1236 with causes as a result consumption perpetuated from hemorrhage, leukostasis This 48 three and distention of and venules by leu- aggregates, penivascular hypoxemia with specimens congestion cell respi- within initiated, capillaries, arterioles, of hypoxemic, infiltrates Tissue demonstrated pulmonary type acute cell of the high blast of leukemic has been observed by Vernant and co-workers7 in 25 leukemic patients with acute respiratory distress; failure despite ventilatory was termed “leukemic cell pneumonopathy.” days days. and severely Tryka symptoms, in five patients four open-lung age, by pulmonary blasts, was nuclei pneumonopathy study, all had a leukocyte 35 to 80 percent leukocyte count pulmonary let,kenia (hematoxvlin- iii’elo,nonoc’tic angulated with acute nonlymphocounts of greater than l)ecafl’le chemotherapy acute anism, 200,000/pJ. a second this within in all patients than patients leukocyte .4 ‘ after chemotherapy in patients with counts has led to a similar description developed acute myelogenous pulmonary infiltration and vessel described 70 to 90 percent in- common.4149 aggregates greater to with chronic of and 200,000/p.l, ratory lysis (Table due are discovered or small associates’ cytic or leukemic and reaction cell patients Gollins4’ a leukocyte Myers cell and counts 206 .itt . leukeiuic infiltrate in patient with shows leukernic cells with irregular, reaction failure cell of 7’ .R.#{149}-’L5, -., lysis with Patients In leukemic hyperleukocytic ,t X 1(X)). leukostasis, and iiietimiiiathy, 2). creased niagnification. . _% ‘-‘.“. original ,,a##{149}’ 4.:lt#{149} .,, f!lb, eoSin, .‘ - . - Ft( t’ RF: 3A . Chest roentgeiiograin shows (ANI NI L). B. I ugh-power inagiiification :v ,_#{149}‘Jl -4:’ .#{234}Q.. .,. ? , h ‘ . #{149}s iv_ . ,, :‘ “. ‘ :;Fs.-11. Q’ #{149}I. #{149}V’ also state however, rate show patients of increase the same vasculature for the and with in their respiratory as a consequence Guttner hyperleukocytic mechanoted that correlated of microcir- associates48 dereaction occurring as commonly somnolence and as in the confusion with this acute respiratory distress. be remembered, however, that conditions leukocytosis or thrombocytosis may cause low Pa02 values This phenomenon a result of increased Pulmonary Ofl Complications Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21620/ on 05/10/2017 peripheral blood gas of pseudohypoxia is preoxygen consumption by of Leukemia (Hildebrand et a!) these numerous ce1ls.’ diagnosis of hypoxemia, between sampling This may lead particularly and analysis nonproductive to an incorrect if there ofthe gram is a delay peripheral though blood the specimen. ALVEOLAR must PAP diagnosis An also association included been an coexistent made found various leukemia. 22 hematologic All had infections by group opportunistic of5 that on the defective (8.5 of34 the evidence pool ofintracellular additional Noa substances macrophages of PAP, et al52 suggested that characteristic of leuke- monocytes are and from results and in phospho- macrophages are load of debris, not recruited ADVERSE Adverse drug opportunistic patient not only to recurrent infections, but also to PAP DRUG reactions infection, REACTIONS affecting the pulmonary lung can edema, and The onset be insidious, with busulfan. is associated of drug-induced pulmonary disease subacute, or chronic-the last Most drug-induced pulmonary with fever, but not necessarily fever. It is rarely sweats. Fever associated may precede with the shaking onset chills leuin in can especially disease a daily or night of symptoms with be the chest roentgeno- of exclusion. may show some as well as other a drug features exclusion Even atypia of cells finding is not diagpulmonary disease taking histologic corticosteroids. disease known to consistent of other of Several states with causes. acute It is (Ara-G) oftreatment dyspnea produces and with a unique completion.7’ fever ofthe mimics patients minimal changes fluid. there onset occurs the drug.57 roentgenograms specimens show with proteinaceous edema with corticosteroids; and receiving occur. Chest and histologic parenchymal The ARDS Hemoptysis may also show a diffuse infiltrate percent confused picture of noncardiogenic pulmousually beginning during treatment or 30 days veolar portive drug-induced are frequently arabinoside clinicopathologic nary edema, diffuse intra-al- Treatment is supis approximately 50 mortality. was Ofl of the first drugs recognized an adverse effect on the lungs. A review with an estimated incidence of 6 percent to of 56 was Busulfan produce cases recently published. mal infiltrates seen asymmetric fibrosis and as well In the 84 series months. There The onset is insidious. on chest roentgenogram may mimic idiopathic as other entities such pneumonia, percent are and by Massin and mortality with hundreds of case Parenchymay be pulmonary as CMV miliary associates,59 an disease, tuberculosis. average reports there was onset at an 41 of methotrexate pneumonitis occurring mainly in children being treated for acute lymphatic leukemia. This reaction is predominantly a hypersensitivity reaction in that over half of the cases are associated with eosinophilia and the onset initiating mimic kemic infiltration and must always be considered the differential diagnosis of pulmonary infiltrates patients with leukemia who are undergoing treatment with chemotherapeutic agents.M patient have and Pneumocystis because of errors in chemotaxis, causing further filling of the alveoli with proteinaceous substances. Chemotherapeutic agents may inflict further damage to these functions. Thus, the altered cell-mediated immunity in leukemia, manifested by impaired macrophage function, predisposes the opportunistic pulmonary the and in up to one-fourth and proliferation derived effect of acute et aP feature drug within Golde lipoproteins in the alveoli. Defective unable to phagocytize the increased and species, antimicrobial is a major this tion (15 percent), from macrophage of leukemic specimens pneumonocyte that cause pulmonary ARDS. Cytosine nine with concurrent (Candida promote PAP Excessive of type II pneumocytes accumulation with biopsy. in vitro function circulating and percent) reviewed Bedrossian et ale’ and Prakash the macrophage dysfunction mias may desquamation a review Bedrossian malignancies, asymmetric bilatinfiltrates, and “secondary Several of these had coexisting alveolar chemotactic In fungi patients and is a disease important to consider a diagnosis of pulmonary drug effect because it is frequently fatal, even after the responsible drug has been stopped and after interven- and or bacteria, particularly and associates52 described at open-lung Based PAP, disorders, including alveolar infiltrates and in whom hematologic eral alveolar-interstitial PAP” were present. infections hematologic of to date, patients Aspergillus, Mucorales) cardia species. Prakash similar patients. between incidence reported I! requires differential pneumonias. of PAP co-workers5’ the in leukemic increased opportunistic cases in infiltrates has malignancies, of 260 be histologic type dyspnea, It characteristic of drug effect, this nostic. A diagnosis ofdrug-mnduced PROTEINOSIS ofpulmonary cough, abnormality. a few adding cases is within a few days to several weeks the medication. The reaction disappears days of either corticosteroids. in which tissue but tissue eosinophilia usually fatal pulmonary intrathecal administration just discontinuing In at least is available, the one-third granulomas is uncommon. edema has been of methotrexate. of in drug or of the are seen, An acute reported and with CONCLUSION Several practical considerations this review Infection is the infiltrates, with local infections CHEST Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21620/ on 05/10/2017 can be derived from most common cause of being more common I 98 I 5 I NOVEMBER, 1990 1237 than using diffuse. blood These cultures can be diagnosed and specimens bronchoalveolar lavage, and open-lung biopsy. Pulmonary infiltrates may be attributable to new pulmonary processes, such as cardiogenic pulmonary edema, pulmonary which are emboli, unrelated patient’s and chemotherapeutic to the underlying immunocompromised above, for potentially effect, or the These standard infiltrates condi- leukocyte count greater dication for count, treatment. discussed than urgent or an absolute 100,000 cells/pi, intervention, alkalinization urine, and in- rapid hy- and hydroxyurea followed these instances it is essential by chemoto prepare for possible cell respiratory distress with lysis pneumonopathy available and ventilatory Craft J, with DJ, Chest 1980; 2 Rosenow in Mayo Proc 4 Krowka cations Rice L, Shenkenberg infections marrow L, GP, in 7 Singer C, study 8 Kurrle H, offiO E, et al. Bhaduri Risk respiratory 1981; HC. factors Pulmonary H-Y, a Med Moore Neiman RS, SL, 87:237-46 RB, 26 Thigpen Narboni C. of Walzer 27 Fever 494 and consecutive PD, D, Yu B. patients: PA. 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Young Res 1985; Leukemic T Hyperleukocytosis Massin F, Fur pneumonopathie 26:263-82 cell 59 lysis A, Reybet-Degat du busulfan. 0, Camus Rev Mal Respir P, Jeannin 1987; L. La 4:3-10 pneumo- CHEST Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21620/ on 05/10/2017 I 98 I 5 I NOVEMBER, 1990 1239