Abstract
Pulmonary complications are common following hematopoietic cell transplantation (HCT) and contribute significantly to its morbidity and mortality. Diffuse alveolar hemorrhage is a devastating non-infectious complication that occurs in up to 5% of patients post-HCT. Historically, it carries a high mortality burden of 60–100%. The etiology remains ill-defined but is thought to be due to lung injury from conditioning regimens, total body irradiation, occult infections, and other comorbidities such as graft vs. host disease, thrombotic microangiopathy, and subsequent cytokine release and inflammation. Clinically, patients present with hypoxemia, dyspnea, and diffuse opacities consistent with an alveolar disease process on chest radiography. Diagnosis is most commonly confirmed with bronchoscopy findings of progressively bloodier bronchoalveolar lavage or the presence of hemosiderin-laden macrophages on microscopy. Treatment with glucocorticoids is common though dosing and duration of therapy remains variable. Other agents, such as aminocaproic acid, tranexamic acid, and activated recombinant factor VIIa have also been tried with mixed results. We present a review of diffuse alveolar hemorrhage with a focus on its pathogenesis and treatment options.
Highlights
Hematopoietic cell transplant (HCT) is increasingly used as a treatment for various malignant and non-malignant disease processes
While the evidence is limited, this study suggests that intrapulmonary cytokine levels may be a helpful biomarker in diagnosis and development of precise immunomodulatory therapies for Diffuse alveolar hemorrhage (DAH)
The rationale for pulse dosing is to maximize the immediate non-genomic effects leading to faster recovery of clinical symptoms, minimize the inflammatory damage from disease, and limit the adverse effects associated with long term glucocorticoid use (73)
Summary
Hematopoietic cell transplant (HCT) is increasingly used as a treatment for various malignant and non-malignant disease processes. The rationale for pulse dosing is to maximize the immediate non-genomic effects leading to faster recovery of clinical symptoms, minimize the inflammatory damage from disease, and limit the adverse effects associated with long term glucocorticoid use (73) Treatment at these doses are limited in duration of therapy and require either discontinuation or rapid decreases after a maximum of 5 days (64, 73, 76). Prospective studies are greatly needed to develop treatment regimens as mortality for DAH remains high At this time, in cases of DAH thought to be caused by inflammationinduced alveolar damage, we advocate for the use of high dose glucocorticoid therapy to achieve maximal genomic and nongenomic effects and minimize side effects. DAH, diffuse alveolar hemorrhage; HCT, hematopoietic cell transplant; Allo, allogeneic; Auto, autologous; BM, bone marrow; UNS, unspecified; IV, intravenous; MP, methylprednisolone; Hosp, hospital; BAL, bronchoalveolar lavage; RF, respiratory failure; MOF, multiple organ failure
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