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Cotorogea-Simion, M.;  Pavel, B.;  Isac, S.;  Telecan, T.;  Matache, I.;  Bobirca, A.;  Bobirca, F.;  Rababoc, R.;  Droc, G. Acute Hematologic Malignancy-Associated ARDS. Encyclopedia. Available online: (accessed on 25 June 2024).
Cotorogea-Simion M,  Pavel B,  Isac S,  Telecan T,  Matache I,  Bobirca A, et al. Acute Hematologic Malignancy-Associated ARDS. Encyclopedia. Available at: Accessed June 25, 2024.
Cotorogea-Simion, Mihail, Bogdan Pavel, Sebastian Isac, Teodora Telecan, Irina-Mihaela Matache, Anca Bobirca, Florin-Teodor Bobirca, Razvan Rababoc, Gabriela Droc. "Acute Hematologic Malignancy-Associated ARDS" Encyclopedia, (accessed June 25, 2024).
Cotorogea-Simion, M.,  Pavel, B.,  Isac, S.,  Telecan, T.,  Matache, I.,  Bobirca, A.,  Bobirca, F.,  Rababoc, R., & Droc, G. (2022, September 19). Acute Hematologic Malignancy-Associated ARDS. In Encyclopedia.
Cotorogea-Simion, Mihail, et al. "Acute Hematologic Malignancy-Associated ARDS." Encyclopedia. Web. 19 September, 2022.
Acute Hematologic Malignancy-Associated ARDS

Acute hematologic malignancies are a group of heterogeneous blood diseases with a high mortality rate, mostly due to acute respiratory failure (ARF). Acute respiratory distress syndrome (ARDS) is one form of ARF which represents a challenging clinical condition. 

acute hematologic malignancy acute respiratory distress syndrome pneumonia

1. Pneumonia-Associated ARDS

Pneumonia-induced ARDS management includes, beyond standard ARDS supportive measures, antimicrobial therapy with the goal of eradicating the causative agent. The most recent ECIL guidelines recommend an escalation/de-escalation empirical approach. The choice of antimicrobials should be based on the risk of the patient having contracted a resistant germ, as well as the resistance profile of the commonly encountered microbes in the local healthcare setting [1]. For patients without prior resistant pathogen infection or risk of complicated disease evolution, empiric therapy consists of initial monotherapy (piperacillin/tazobactam 4/0.5 g IV q6h or ceftazidime 2 g IV q8h or cefepime 2 g IV q8h or q12h), for a duration of 7–8 days [1][2]. Should this prove ineffective, with deteriorating patient status or proven microbial resistance, the regimen should be changed. The recommended antibiotic regimen must provide broader coverage: carbapenems (meropenem 1 g IV q8h or imipenem 500 mg IV q6h) or antipseudomonal beta-lactams combined with aminoglycosides (e.g., ceftazidime 2 g IV q8h + amikacin 20 mg/kg IV q24h) or with colistin (e.g., ceftazidime 2 g IV q8h + colistin 9 million UI IV loading dose, then 3 million UI IV q8h) [1][2]. Vancomycin should be added if the hospital reports high rates of methicillin-resistant S. aureus [1][2]. De-escalation strategies follow the inverse steps and are recommended when bacteriological results are available, in case the patient had been infected or colonized with resistant germs, exhibits signs of unfavorable evolution (hypotension, shock), or if the healthcare center often deals with multidrug-resistant germs [1]. For de-escalation, the course of antibiotic treatment lasts for 14 days [1]. Should the patient suffer from Legionella pneumonia, treatment choice is 500 mg levofloxacin IV q12h for 21 days [2][3].

2. Leukostasis, Leukemic Infiltration of the Lung, Pulmonary Lysis Syndrome

Leukostasis is mostly a complication of myeloid leukemias (acute myelomonocytic or monocytic, and chronic during the blast crisis), especially those with leukocyte counts over 50,000/mm3, although the degree of hyperleukocytosis does not necessarily correlate with the severity of the symptoms [4][5]. Leukostasis consists of white blood cell build-up inside small vessels, not only in the lungs, but also brain and heart, among other places, which explains the symptoms associated with this condition (acute respiratory failure, acute myocardial infarction, right ventricular overload, headaches, dizziness, tinnitus, coma, intracranial bleeding, peripheral ischemia, mesenteric infarction, priapism etc.) [4][6][7]. Leukostasis occurs not just due to increased viscosity and low flow in the pulmonary circulation, but also because of cytokines (mostly IL-1 and TNF-α) released by the pathologic cells [4][7]. The cytokine buildup leads to increased expression of adhesion molecules on endothelial cells (such as selectins and ICAM-1), leukocyte aggregation and activation, and secretion of matrix metalloproteinases, causing endothelial damage, increased vascular permeability, and subsequent extravasation of fluid, blood, and leukemic cells [4][7][8]. This migration from the intravascular to the interstitial and alveolar spaces is the basis for the radiologic opacities and the hypoxic respiratory failure that constitute hallmarks of ARDS [7]. However, the aforementioned hypoxemia has yet another causative mechanism—the occlusion of pulmonary capillary vessels, mimicking a pulmonary embolism, which explains how patients with histologically diagnosed leukostasis can be hypoxemic, yet show no abnormalities on chest X-rays [7].
Leukemic infiltration of the lung entails blasts building up in the pulmonary extravascular space, without any other discernible causes (infectious, hydrostatic, or otherwise) [9]. Leukostasis causes migration of leukemic cells into the interstitium. Thus, leukostasis and leukemic pulmonary infiltration are not two separate entities, but rather two sides of the same coin [7]. The two seem to occur more often in myeloid leukemia patients, but infiltration, unlike leukostasis, is even less correlated with hyperleukocytosis. However, it should be suspected in patients with a blast ratio exceeding 40% of total peripheral blood leukocytes [4][10]. The symptomatology is rather sparse, with the patient usually complaining about cough, fever, and dyspnea [4]. Imagistic findings include thickening of the interlobular septa or the bronchovascular bundles, as well as non-systematized “ground-glass” opacities [4][7][9].
Management of ARDS in the case of leukostasis and leukemic infiltration includes, beyond general supportive measures, therapies meant to reduce blood viscosity and deplete the number of leukocytes in the pulmonary vasculature and parenchyma [4]. Thus, patients should receive generous infusions of isotonic intravenous solutions, while avoiding blood transfusions for as long as the patient’s clinical status does not call for urgent action [4]. For leukodepletion, clinicians can resort to either chemotherapy, in the shape of hydroxyurea, or leukapheresis, a process in which the patient’s blood is run through a device containing a centrifuge, which mechanically separates cellular elements from plasma, before being fed back into the blood vessels [4][11]. In case of rapid degradation of clinical status, leukapheresis should be the preferred option, as it leads to a quicker drop in leukocyte levels [11]. However, in promyelocytic leukemia, this procedure should not be used, for two reasons: due to the disseminated intravascular coagulation which contraindicates apheresis, and because of the usually lower than normal white blood cell count [11][12]. Leukapheresis does not influence the long-term survival [11][13][14][15][16][17].
Hydroxyurea has been used as the mainstay of leukodepletion therapy for many decades, as it effectively lowers the number of leukocytes, with a low occurrence of acute tumor lysis syndrome, albeit over a longer period of time (24–48 h after initiation of therapy) [4][18]. Some studies have proven its usefulness in preventing short-term mortality [4][11][19]. Hydroxyurea acts by inhibiting ribonucleotide reductase, preventing the synthesis of deoxyribonucleotides, and halting the cell cycle in the S phase [20].
Due to the involvement of cytokines in leukostasis, corticosteroids have proven themselves useful in reducing leukemic pulmonary infiltration, mortality, and relapse incidence, as well as improving overall and disease-free survival [5][21]. Corticoids act by binding to cytoplasmic glucocorticoid receptors, which then relocate to the nucleus, exerting effects predominantly by induction of gene transcription (selective acetylation of histones) and increasing the expression of anti-inflammatory products such as IL-10 and IκB-α (inhibitor of NFκB) [22][23]. Conversely, they also bind and inhibit other proteins that act as histone acetyltransferases and activators, but for proinflammatory genes, thus switching them off [22]. Another mechanism relies on destabilization of mRNA molecules that encode for inflammatory proteins [20].
Pulmonary lysis syndrome, also known as acute lysis pneumopathy, occurs after initiation of cytostatic treatment [4][10]. However, it does not owe its effects to its direct mechanism of action, but rather to the massive destruction of tumor cells, which release their cytotoxic contents, producing diffuse alveolar damage or lung hemorrhage [4][10]. The incriminated components include reactive oxygen species, enzymes, and damage-associated molecular patterns (cellular components such as DNA, histones, heat shock proteins, uric acid) [4][24]. White blood cell count appears inconsequential, as cases have been reported in patients with fewer than 50,000 leukocytes per mm3 [4]. The clinical presentation is typical for acute respiratory failure, while imaging typically shows bilateral “ground-glass” opacities [17]. Manifestations usually appear within 48 h of induction of therapy, but exceptions were noted by studies by both Azoulay et al. and Kunitomo et al., at 15 and 14 days, respectively [25][26].

3. Drug-Induced ARDS

Drugs administered in the treatment of hematological malignancy could lead to ARDS not only through their intrinsic action towards the lung, but also by way of their interaction with the neoplastic cells. The incidence varies from 0.1 to 15% [27].
The pathophysiology of drug-induced ARDS is complex, with incriminated mechanisms ranging from idiosyncratic reactions to anaphylaxis, capillary leak syndrome, or reactive oxygen species and inflammatory cytokine production [28]. The relevant drugs incriminated in lung damage leading to ARDS are: bleomycin, mitomycin-C, cyclophosphamide, gemcitabine, cytarabine, GM-CSF, and vinca alkaloids [29][30][31][32]. Bleomycin and mitomycin-C increase reactive oxygen species production [29][30]. Gemcitabine increases cytokine release [29][30]. Cytarabine has a direct toxic effect [31]. GM-CSF increases neutrophil adhesion to lung endothelium, due to higher expression of glycoproteins, and superoxide production [31]. Vinca alkaloids cause endothelial dysfunction by disrupting the organization of tubulin [32].
Of particular interest is all-trans retinoic acid (ATRA), which is used in acute promyelocytic leukemia, where a chromosomal translocation leads to a change in the function of the retinoic acid receptor [33]. Consequently, the gene responsible for cell maturation and differentiation no longer responds to physiological ATRA doses [33]. Thus, the myeloid cells remain trapped in their promyelocyte stage [33]. Another drug used in acute promyelocytic leukemia is arsenic trioxide, which increases degradation of the mutant receptor in the lysosome [34]. The administration of either of these drugs could lead to retinoic acid syndrome, a particular type of drug-induced ARDS. This is an entity which appears in 2 to 31% of patients treated with such drugs, mostly when treatment consists of these alone, during the induction phase, usually 10 days after the initiation of the treatment [35]. When ATRA binds to the retinoic acid receptor, immature cells are forced to differentiate. This changes the profile of secreted cytokines (IL-1β, IL-6, IL-8), increasing expression of lymphocyte function-associated antigen 1 (a molecule involved in the migration of leukocytes), intercellular adhesion molecule 1, matrix metalloproteinase 9, and cathepsin G [36][37]. These changes increase the vascular permeability and facilitate lung infiltration [36][37]. Some of the cytokines are also involved in altering hemostasis [35][36]. Thus, retinoic acid syndrome-associated ARDS manifests itself as leukemic infiltration of the lung and alveolar hemorrhage. Management of this pathology consists of intravenous dexamethasone (10 mg i.v. q12h), stopping the administration of the incriminated drug, and the addition of a different cytostatic agent in cases of leukocytosis [36].

4. Radiotherapy-Induced ARDS

Management options for hematologic malignancies go beyond pharmacological means. Radiation therapy is also useful, especially in lymphomas, where irradiating affected lymph nodes in selected patients leads to excellent 5-year survival and relapse rates [38]. Its use also extends to leukemia, but more as prophylactic, post-chemotherapy, or palliative therapy [38]. However, body tissues are also susceptible to radiation damage, with the lungs being the most sensitive of the thoracic organs and radiation pneumonitis occurring at doses as low as 15–16 Gy [38]. The radiation-induced death of endo- and epithelial cells leads to a vicious circle of inflammation, increased vascular permeability, and cytokine release, while infiltrating macrophages amplify tissue damage by producing reactive oxygen and nitrogen species and cytokines [39]. The cytokine milieu varies with the time elapsed since the pulmonary injury [39]. The first 2 weeks are characterized by high levels of TNF-α, IL-1 and -6, fibroblastic and platelet-derived growth factors. On a tissular level, this stage is characterized by vascular congestion and intra-alveolar edema, leukocyte infiltration, and pneumocyte apoptosis [39]. In later stages (about 6–8 weeks after the original insult), TGF-β1 expression increases, while vascular and alveolar linings begin to detach, leading to capillary lumen reduction and thrombi formation, and to alveolar collapse with associated fibrin exudation and hyaline membranes, respectively [39].
Radiation pneumonitis could occur months, even years, after radiotherapy [40][41]. In such patients, the triggering factor was proven to be a round of chemotherapy, although cases have been reported where immunotherapy was incriminated instead [39][42]. The mechanisms involved in radiation recall pneumonitis are still being investigated. However, postulated theories include: (1) constant subliminal inflammatory cytokine secretion; (2) changes in local stem cell function, either increased turnover (which increases their susceptibility to antineoplastic agents) or reduced proliferation; (3) accumulation of the anticancer drug due to local changes in angiogenesis and vascular permeability [41][42]. The severity of symptoms does not appear to be correlated with the time elapsed between radio- and chemotherapy [39]. One could mistake radiation recall for chemotherapy-induced lung damage; however, in the case of radiation recall pneumonitis, the ground-glass opacities and infiltrates conform to the shape of the previously irradiated areas [41].
Treatment of ARDS induced by radiation therapy consists mainly of intravenous corticosteroids [39]. Furthermore, some prophylactic options exist, which dampen the effects radiation has on the lung tissue: pentoxifylline, with its TNF-α and IL-1 suppressing action leading to an improvement in symptoms, and amifostine, which acts by scavenging free radicals and by inducing tissular hypoxia, with protective effects [39][43].

5. Hematopoietic Stem Cell Transplantation-Related ARDS

While chemo- and radiotherapy have remission and symptom control as their goals, stem cell transplantation has been used with curative effects [44]. There are multiple types of transplantation, but the two most widely used are autologous and allogeneic.
Autologous transplant involves harvesting stem cells from the patient, either directly from the bone marrow or from the blood after marrow stimulation [45]. Then the patient undergoes myeloablative therapy, which destroys the malignant cells, along with their own hematopoietic cells, and has the harvested stem cells reimplanted, in hope that they would resume their function [45]. While considered a curative therapy option, relapse rates remain high, mostly due to the stem cell harvest contamination by neoplastic cells [46].
Allogenic HSCT requires a donor, related to the patient or not, with HLA antigen matching [47]. While the complications and non-relapse mortality rate of allogenic HSCT is worse than that of the autologous one, lower relapse rates offset the difference, leading to similar long-term survival [47]. The benefit of allogenic grafts is an immune reaction mediated by minor histocompatibility antigens, which prevents the subsequent growth of leukemic cells [48]. The minor histocompatibility antigen is usually expressed on cells belonging to the immune system, including the malignant ones [48]. However, the donor cells sometimes react with epithelial cells, which also express such antigens, leading to graft vs. host disease [48]. GVHD occurs due to pre-existent damage to the host tissues, through the underlying disease or the preconditioning chemotherapy, which leads to an elevated state of inflammation in the body, culminating in ARDS [49]. Of note is the occurrence of GVHD in autologous stem cell transplant recipients, in spite of the complete cellular antigen matching [50][51]. The putative mechanism is the loss of self-reactive cell suppression, either through direct regulatory T cell expression inhibition (caused by specific agents, such as thalidomide derivatives), or through poor thymus function owing to cytotoxic therapy [50].
Other mechanisms related to hematopoietic SCT, which led to ARDS, are diffuse alveolar hemorrhage, peri-engraftment respiratory distress syndrome (PERDS), and cryptogenic organizing pneumonia [52].
Diffuse alveolar hemorrhage is an exclusion diagnosis, being defined as lung hemorrhage-induced ARDS in the absence of any infection within 1 week after hematopoietic stem cell transplantation [50]. The diffuse alveolar hemorrhage can last between 1 week and 1 month, during the engraftment period, when neutrophil production increases, causing them to flow towards the pulmonary vasculature [52]. To establish the diagnosis, bronchoalveolar lavages must be performed [53]. The bronchoalveolar lavage must appear increasingly bloody as time passes or contain macrophages which are loaded with hemosiderin in proportion higher than 20% [53]. The initial pulmonary lesion is caused by high-dose radiotherapy, releasing host antigens into the circulation, which are then recognized by donor T cells, in the case of allogeneic stem cell transplants, leading to their activation and inflammatory cytokine production [53].
Diffuse alveolar hemorrhage can also occur in autologous transplant recipients [50][53]. The T cells might be activated by compounds such as lipopolysaccharides, which end up in the bloodstream following gastrointestinal epithelium damage, as is the case in mucositis (caused by melphalan, a drug used in the treatment of multiple myeloma) or GVHD [50][53]. GVHD leads to alveolitis, manifesting as alveolar hemorrhage and increased counts of alveolar leukocytes, regardless of post-transplantation leukopenia [54]. Consequently, the endothelial swelling and medial hyperplasia leads to narrower vessel lumina, increasing the extravasation of erythrocytes into the lung parenchyma [54]. Outcomes for diffuse alveolar hemorrhage appear remarkably poor, with reported mortality rates between 64 and 100% [53][54]. Supportive therapy includes platelet transfusions, clotting factor (recombinant factor VIIa) or antifibrinolytic drug intake, and ventilatory support, while corticosteroids are largely unhelpful [53][54]. The recombinant factor VIIa, particularly when administered locally, through bronchoscopy, overcomes any preexisting tissue factor pathway inhibitors and leads to bleeding control [54].
ES occurs within 4 days of engraftment, which is defined as the first of 3 consecutive days when neutrophil levels maintain themselves at over 500/mm3, and it is caused by the engrafted neutrophils’ production of inflammatory cytokines and degranulation, leading to systemic endothelial damage [55][56]. A particular manifestation of ES is periengraftment respiratory distress syndrome, whose reported incidence rates vary from 2.5 to 25% [53]. The risk factors for PERDS are female gender, a quick immune function recovery, autologous HSCT, less intensive pre-conditioning therapy or GM-CSF instead of G-CSF, and the need of preengraftment platelet transfusions [53][57]. PERDS has a very similar clinical presentation to that of acute GVHD and, while self-limited, can be severe enough to warrant corticosteroid therapy (3 days of 1–2 mg/kg iv methylprednisolone q12h), along with supportive therapy [52][53].

6. TRALI in Patients with Acute Hematologic Malignancy

Since bone marrow suppression in hematological malignancies is either a consequence of the disease itself, or a desired effect of medication (as is the case in myeloablative therapy), cytopenia in at least one blood cell line occurs in almost all patients [58]. Once the levels of a particular component reach a critically low value, blood product transfusions should be performed [59][60]. The transfusion threshold for hemoglobin and platelets is 7 g hemoglobin/100 mL whole blood and 10 × 103 platelets/mm3 whole blood, respectively (numbers apply in the absence of active bleeding) [59][60]
TRALI is defined as pulmonary edema occurring within 6 h post-transfusion, in the absence of other ARDS-precipitating factors or evidence of circulatory overload [61]. It occurs in roughly 1 in every 1000 blood product recipients, with the incidence being 50 to 80 times higher in intensive care settings [61]. However, patients with hematologic malignancy develop this complication less frequently than other patient categories, most likely due to the associated neutropenia [61]. Mortality stands at approximately 10%, while mechanical ventilation requirement occurs in 70 to 90% of cases [62]. Risk factors associated with TRALI are the total number of administered blood products, previously pregnant donors, chronic alcohol and tobacco use, pretransfusion shock, and positive fluid balance [61][62]. The occurrence of TRALI can most often be attributed to the presence of leukocyte antibodies in the plasma contained in blood products [61]. The antibodies bind their corresponding recipient antigens and trigger an immune reaction culminating in resident neutrophil activation, capillary leak, and lung injury [61].
TRALI in neutropenic patients might occur due to antibodies binding directly to endothelial cells, which are then damaged by reactive oxygen species produced through the activation of the complement cascade or monocytes [61]. It has been proven that even platelets are capable of secreting proinflammatory mediators, while also migrating into alveolae, augmenting leukocytic infiltration [61]. Finally, erythrocyte transfusion bags might carry significant amounts of proinflammatory factors (reactive oxygen species, cytokines, etc.), which can trigger acute lung injury in the recipient [61][62].
TRALI is self-limited, with patients recovering within 3 to 4 days. In some cases, corticosteroids or diuretic therapy might prove useful [3]. In order to reduce the occurrence rate, mitigation strategies have been implemented: collecting plasma-rich products only from male donors or nulliparous females, antibody screening in female thrombocyte apheresis donors (since this product contains a significant amount of plasma), or pooling together plasma and platelets from multiple donors, to dilute or neutralize any residual antibodies [62].


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