Pulmonary Medicine

Alveolar Hemorrhage Syndromes (Diffuse Alveolar Hemorrhage)

What every physician needs to know:

The origins of bleeding from the lungs can be anatomically compartmentalized. Bleeding can arise from the bronchial circulation, small-medium-large pulmonary arteries, and the microcirculation. Diffuse Alveolar Hemorrhage (DAH) is a clinicopathoglogic syndrome characterized by intra-alveolar accumulation of red blood cells that originates from the interstitial capillaries and is associated with hypoxemic respiratory failure. If unrecognized and not treated, it may result in death. All causes of DAH have the common denominator of injury to the alveolar microcirculation, which is made up of the precapillary arterioles, alveolar capillaries, and post capillary venules. The clinical syndrome is characterized by hemoptysis, acute and unexplained anemia, and diffuse pulmonary radiographic infiltrates.

The presence of a hemorrhagic bronchoalveolar lavage (BAL) in serial lavages is diagnostic. DAH has three histopathologic patterns: pulmonary capillaritis, bland hemorrhage and diffuse alveolar damage. These histopathologic patterns are associated with various clinical etiologies. The most common histopathologic pattern found to cause DAH is pulmonary capillarities, typically the setting of a rheumatologic disease. Although a BAL is diagnostic, surgical lung biopsy should be considered if DAH is associated with a negative serologic workup, not part of a systemic disease or if it is refractory to treatment. It is important to establish the cause of DAH since virtually all cases, except those associated with overwhelming diffuse alveolar damage, are potentially reversible. Repeated episodes are common, particularly if DAH is caused by pulmonary capillaritis. Treatment is directed at the underlying etiology and typically includes corticosteroids, total plasma exchange, and immunosuppressant therapy.


DAH is associated with a number of clinical entities and several histopathologic subtypes. Table 1 lists the etiologies of DAH with their associated histopathologic subtypes.

Table 1

Etiology and Histology of Diffuse Alveolar Hemorrhage
Pulmonary Capillaritis Bland Hemorrhage Diffuse Alveolar Damage
Connective Tissue Diseases:Mixed connective tissue diseaseAntiglomerular basement membrane antibody disease(Goodpasture's)PolymyositisPrimary antiphospholipid antibody syndromeRheumatoid arthritisSystemic lupus erythematosis (SLE)Systemic scleroderma Connective Tissue Diseases:Antiglomerular basement membrane antibody disease(Goodpasture's)Systemic lupus erythematosis Infection:Any associated with ARDS Viral
Systemic Vasculitides:ANCA-associated granulomatous vasculitis (Wegener's)Microscopic polyangitisCryoglobulinemiaPauci-immune glomerulonephritisHenoch-Schoenlein purpuraIsolated pulmonary capillaritis (ANCA-positive or -negative)Idiopathic glomerulonephritis Drugs*:Anticoagulant therapyPlatelet glycoprotein IIA/IIIB Drugs*:AmiodaroneCytotoxic agentsNitrofurantoinPenicillaminePropylthiouracilSirolimus
Drugs*:DiphenylhydantoinPropylthiouracilRetinoic acid syndromeOther:Hematopoietic Stem Cell TransplantAcute lung transplant rejectionUlcerative ColitisMyasthenia gravisLeptosporosis Other:Idiopathic pulmonary hemosiderosisMitral stenosisPulmonary veno-occlusive diseaseSubacute bacterial endocarditisLeptosporosisObstructive sleep apnea Connective Tissue Disease:PolymyositisSystemic lupus erthematosis
Other:Crack cocaine inhalationHematopoietic stem cell transplantRadiation therapy ARDS (any cause)
Miscellaneous histologies
Pulmonary veno-occlusive disease
Pulmonary capillary hemangiomatosis
Fibrillary glomerulonephritis
Metastatic renal cell carcinoma
Epithelioid hemangioepithelioma
Choriocarcinoma syndrome

Are you sure your patient has Diffuse Alveolar Hemorrhage? What should you expect to find?

DAH can appear at any age and often appears with a pre-existing systemic disease. DAH may also be the presenting manifestation of an underlying systemic disease. The clinical syndrome includes hemoptysis, acute and unexplained anemia, diffuse radiographic pulmonary infiltrates, and hypoxic respiratory failure of varying degrees of severity. Although hemoptysis is considered the cardinal sign of DAH, it may be absent in up to 33 percent of all patients; therefore, the absence of hemoptysis does not rule out DAH. Hemoptysis may be a dramatic event or it may evolve over days to weeks. The clinical course of DAH is unpredictable; it can vary in severity, but it should be considered a life-threatening event. The symptoms of DAH, other than hemoptysis, tend to be non-specific; they can include but are not limited to fever, chest pain, cough, and dyspnea.

Non-pulmonary signs and symptoms are those that accompany the underlying etiology. In addition to data from a through history and physical, an unexplained drop in hemotocrit should alert the physician to the possibility of DAH. Chest radiographics are nonspecific and consist with an alveolar filling process that can be patchy, focal, or diffuse in nature. A CT scan of the chest will further define the extent of the disease, and it can help to localize the areas of involvement in which BAL should be performed. Ashemoptysis may be absent in up to a third of patients. The diagnosis is established after sequential BAL reveals worsening RBC counts. BAL will establish the clinical diagnosis of DAH and will exclude infection, but it does not establish the underlying cause. Surgical lung biopsy should be considered if the clinical history or serologic testing is unrevealing. Transbronchial biopsies are insufficient for histopathologicdiagnosis. Surgical lung biopsy should also be considered for patients who are refractory to appropriate treatment.

Beware: there are other diseases that can mimic Diffuse Alveolar Hemorrhage:

Any disease that presents in an acute fashion with hypoxemia respiratory failure and diffuse alveolar infiltrates should be included in the differential diagnosis with DAH. Many patients can present with an acute drop in their hemotocrits for reasons other than DAH. Table 2 lists acute noninfectious diffuse parenchymal lung diseases with their associated histology and clinical etiologies.

Table 2

Imitators of DAH
Acute Exacerbation of Interstitial Lung Disease
Diffuse alveolar damage on backdrop of the underlying ILD
Idiopathic pulmonary fibrosis, Connective-tissue-associated ILD
Acute Interstitial Pneumonitis
Organizing diffuse alveolar damage
Idiopathic (Hamman-Rich syndrome), collagen vascular disease, cytotoxic drugs, infections
Acute Eosinophilic Pneumonia
Eosinophilic infiltration and diffuse alveolar damage
Idiopathic, drugs
Acute Cryptogenic Organizing Pneumonia
Organizing pneumonia
Idiopathic, collagen vascular disease, drugs, radiation, infections
Acute Hypersensitivity Pneumonitis
Granulomatous and cellular pneumonitis with diffuse alveolar damage
Inhaled antigens

How and/or why did the patient develop Diffuse Alveolar Hemorrhage?

Common to all causes of DAH is injury to the basement membrane of the alveolar capillary bed, which injury allows for accumulation of red blood cells into the alveolar space. However, the injury to the basement membrane is unique to the specific systemic disease that underlies the DAH, and in some cases the mechanism of injury remains unknown. The pathogenesis of DAH in the more common causes of DAH will be discussed here. DAH in ANCA-associated granulomatous vasculitis is due to the development of an antibody directed against cytoplasmic proteinase 3 (PR3), which involves cellular immune pathways that result in granulomatous inflammation of the lung.

DAH from microscopic polyangitis, which can be due to pulmonary capillaritis or to diffuse alveolar damage, is associated with a perinuclear ANCA directed against neutrophil myeloperoxidase (MPO). Immune complex deposition and activation of complement with the lung is thought to be the cause of DAH in SLE. Autoantibodies directed against the NC1 domain of the alpha-3 chain of the basement membrane collagen type 4 is central to the pathogenesis of DAH in antiblomerular basement membrane antibody disease. Drug-induced DAH may have a variety of mechanisms as a cause of basement membrane injury. Given the vast numbers drugs that have been reported in the literature to be associated with DAH, Phillip Camus, Pascal Foucher, and the GEPPI have developed and maintained an up-to-date website, www.penumotox.com, with which to search for drugs that have been reported to cause injury to the lungs.

Which individuals are of greatest risk of developing Diffuse Alveolar Hemorrhage?

While several diseases can cause DAH, there are no prospective studies that estimate the relative frequency of DAH. By far the greatest risk factor for the development of DAH is an established diagnosis of a systemic vasculitis. The most common clinical cause of DAH is ANCA-associated granulomatous vasculitis, followed by anti-glomerular basement membrane disease. Epidemiologic studies show that the prevalence and incidence of the autoimmune disorders is increasing, with the overall prevalence of the primary systemic vasculitides of 90 to 257 per million and the incidence is estimated at 10 to 20 per million. In ANCA-associated granulomatous vasculitis, rising ANCA titers correlate with higher rates of relapse; however, the correlation with the development of DAH is has not been studied. In patients with SLE, a single retrospective study found that neuropsychiatric lupus and high SLE disease activity index scores (>10) were independent risk factors for DAH.

Other important clinical causes of DAH that are not vasculitic in nature are infection, ARDS, the use of anticoagulants with supertherapeutic bleeding times, and the use of IIB/IIIA medications following percutaneous interventions.

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

Diagnostic evaluation is outlined in Table 3. Serologic studies should be directed to confirm the diagnosis of an underlying autoimmune or connective tissue disease. Coagulation studies and peripheral blood smear should be performed as well. Urinalysis should be performed with microscopic evaluation, as the presence of red blood casts will alert the physician to the possibility of a pulmonary-renal syndrome.

Table 3

Diagnostic Evaluation for patients with DAH
Serologic Non-serologic
Complete blood cell counts, Comprehensive metabolic panel, Coagulation studies, Blood smear Urinalysis with microscopic evaluation
ANA, RF, anti-CCP, P-ANCA, C-ANCA (MPO, PR3), Anti-GBM antibodies, Anti-ds DNA, Antiphospholipid antibodies, Anti-Smith Transthoracic echocardiogram
Complements, Cryoglobulins CT chest
Serial chest X-rays

What imaging studies will be helpful in making or excluding the diagnosis of Diffuse Alveolar Hemorrhage?

The radiographic findings of DAH are nonspecific. They consist of an alveolar filling process that can be focal, patchy, or diffuse in nature. Chest CT scans will confirm the chest radiographic findings and will more accurately define the extent of the disease as compared to chest X-rays. Chest X-rays should be performed to follow changes in the extent of the disease, as well as the patient's response to therapy. Chest CT scan should be done at the time of clinical suspicion--and prior to bronchoscopy if possible--in order to localize involved regions. Serial chest CT is not indicated. Figure 1 shows a typical X-ray and the associated CT scan of a patient with SLE-associated DAH.

Figure 1.

Chest X-ray and CT scan illustrating the alveolar filling process of DAH

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of Diffuse Alveolar Hemorrhage?

Pulmonary function tests are rarely indicated in the acute settings. An increased diffuse capacity of carbon dioxide (DLCO) should alert the physician to the possibility of alveolar hemorrhage. Pulmonary function testing should be performed following resolution of DAH, particularly in those patients who are at risk of recurrence of DAH (i.e., systemic vasculitis), as repeated episodes are associated with interstitial fibrosis and emphysematous changes.

Transthoracic echocardiography should be performed to rule out the presence of valvular disease as a cause of DAH.

What diagnostic procedures will be helpful in making or excluding the diagnosis of Diffuse Alveolar Hemorrhage?

Diffuse alveolar hemorrhage is a syndrome rather than a final diagnosis, and its presence should prompt further evaluation for the underlying etiology. The classic triad of DAH is that of hemoptysis, falling hematocrit, and diffuse radiographic infiltrates. However, hemoptysis may be absent in up to a third of the patients at time of presentation; therefore, its absence should not preclude the diagnosis. If a diagnosis of DAH is suspected, bronchoscopy with sequential lavage should be performed in an area that is most involved; this can be determined by CT chest.

The bronchoscope is wedged in a subsegmental bronchus proximal to the region of involvement, and three aliquots of 30 to 60 mL of saline are instilled and withdrawn. If the returned BAL aspirate clears with each aliquot, the bleeding is bronchial in origin. If the BAL becomes progressively more hemorrhagic, the diagnosis of DAH is confirmed. A false negative lavage occurs if the BAL is performed in an uninvolved region of the lung. The presence of hemosideren-laden macrophages on the BAL (>20%) is helpful in detecting DAH as well. Bronchoalveolar lavage fluid should be sent for bacterial cultures and viral PCR.

Serologic studies that investigate an autoimmune disease should be performed, as the turn-around time for specific tests may delay diagnosis. Tissue biopsy is the most efficient manner in which to confirm the diagnosis. If there is a suspicion for a pulmonary-renal syndrome, arenal biopsy with direct immunofluorescence should be pursued, as this procedure has a low morbidity rate. Immunofluorescence will show "clusters" immune complex deposition in SLE, linear deposition in the basement membranes in anti-glomerular basement membrane disease, and the absence of immune complex deposition in ANCA-associated granulomatous vasculitis and microscopic polyangitis.

Surgical lung biopsy should be considered if tissue diagnosis cannot be made with other tissue, if serologic studies are unrevealing, or if DAH is refractory to treatment. Transbronchial biopsy is insufficient in terms of providing the histopathologic diagnosis and should not be performed.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of Diffuse Alveolar Hemorrhage?

There are no genetic tests available to confirm the diagnosis of DAH. Blood tests are directed at confirming the presence of an autoimmune or connective tissue disease.

If you decide the patient has Diffuse Alveolar Hemorrhage, how should the patient be managed?

Establishment of the underlying cause of DAH requires a heightened clinical suspicion and a directed diagnostic evaluation. The goal of management is to stabilize the patient, halt the progression of the disease process, and limit end organ damage. Early institution of therapy can prevent the mortality that is associated with DAH and can help prevent the associated morbidity. Treatment should be directed at the underlying cause of DAH. However, in clinical practice, patients can present with a rapidly progressive, fulminant course that does not allow adequate time for diagnostic studies to confirm the underlying diagnosis. In such cases, institution of empiric treatment is appropriate.

The cornerstone of treatment for the most common cause of DAH, systemic vasculitis, is pulse dose steroids. Unfortunately, no randomized control trials exist to guide therapy, and dosing is based on expert opinion. Methylprednisolone should be administered in 500 mg to 1 gm in divided doses over three days, followed by 0.5 mg/kg/day. If stabilization does not occur following pulsed dose steroids, then the following therapies should be considered.

Total Plasma Exchange (TPE)

TPE is an extracorporeal blood purification used to remove large molecular-weight substances from the plasma. If clinical suspicion remains high for the presence of a system vasculitis or an autoimmune disease, consideration should be given to the institution of TPE. The use of TPE is well established in anti-GBM disease, as well as in renal disease associated with ANCA-associated granulomatous vasculitis. A retrospective study in which twenty patients with DAH that was due to systemic vasculitis were treated with TPE following steroids and cyclophosphamide. All twenty patients showed resolution of hemorrhage following an average of 6.4 treatments.


Cyclophosphamide can be given more easily in patients with a pre-existing diagnosis of systemic vasculitis and should be considered in appropriate patients with severe vasculitis. Careful consideration should be given to its empiric use because of the potential for prolonged toxicity and its delay in therapeutic effects, which may be up to three weeks following administration. Cyclophosphamide has a substantial side effect profile, including bone marrow suppression--which may prohibit its use in the intensive care unit--and hemorrhagic cystitis. Despite these reservations, the combination of pulse corticosteroids and cyclophosphamide has dramatically decreased mortality in patients with systemic vasculitis.

If the decision is made to begin cyclophosphamide, intravenous therapy has advantages over oral administration, particularly in the critically ill patient. Intravenous versus oral administration is equally effective for induction of remission in the ANCA-associated vasculitides and less risk of neutropenia. A typical dosage protocol for intravenous administration is 15 mg/kg given two weeks apart for three weeks. Adequate hydration and pretreatment with MESNA should be utilized to help decrease the risk of hemorrhage cystitis. Careful monitoring of complete blood counts and renal function should be performed. Appropriate dose adjustments should be made if there is evidence of neutropenia or renal injury.


Rituximab is an anti-CD20 monoclonal antibody that targets B-cells. Pulse dose corticosteroids and IV cyclophosphamide are considered the current standard of treatment for DAH that is due to systemic vasculitis; however, the side effect profile and the potential for severe immunosuppressive may limit the use of cyclophosphamide. Recently, the RAVE-ITN, a randomized, double-blind, double-dummy, noninferiority trial, was published. It showed that the use of rituximab in patients with ANCA-associated vasculitis was as effective in inducing remission as cyclophosphamide. There are increasing numbers of case reports that suggest that the use of rituximab in DAH in other connective tissue diseases is effective. As with any immunosupressant therapy, careful consideration to the risks and benefits of treatment should be given on an individual basis and should be administered in consultation with an experience specialist.

Supportive Measures

Supportive measures should be undertaken to prevent morbidity. In the critically ill patient, the use of lung-protective strategy to ventilate and correct an underlying coagulopathy should be performed. Infection is an important cause of mortality in patients who are immunosupressed , so care should be given to prevent iatrogenic infections.

Salvage Therapies

Salvage therapies are used in to prevent death in critically ill patients for whom rapid stabilization is required in order to prevent death and to allow established therapies time to have effect . They include Extracorporal Membrane Oxygenation (ECMO) and the use of human recombinant factor VIIa (rf VIIa).


Extracorporal membrane oxygenation (ECMO) is a life-saving therapy in neonates and children with severe respiratory failure. It requires access to a skilled perfusionist and a tertiary care center with experienced surgeons. ECMO has a relative contraindication in patients with systemic disease; however, several case reports describe the use of ECMO in cases of severe respiratory failure that was due to DAH in systemic vasculitis. Although these reports suggest ECMO can be used, care should be given to choosing the appropriate patient for this therapy, which should be considered a last-line therapy.

Human recombinant factor VIIa

The process of hemostasis requires an intact coagulation factor and normal vascular endothelium. The process of clot formation begins following injury to the vascular endothelium which releases factor VII. The circulating factor VII binds to tissue factor found on stromal cells and fibroblasts creating the VIIa/TF complex, thus initiating the extrinsic coagulation cascade. Several case reports have shown the effective return of hemostasis in patients with DAH when Human rf Vlla is given via bronchoscopic administration or nebulized treatment. Use of rf VIIa can be considered as salvage therapy in the patient with fulminant alveolar hemorrhage that is refractory to supportive medical therapy.

What is the prognosis for patients managed in the recommended ways?

The natural history and prognosis is dependent upon the underlying cause of DAH. If DAH goes untreated, it has a high rate of morality, with patients dying of progressive respiratory failure. In those patients who are aggressively treated with appropriate diagnosis directed treatment, the mortality rate remains high, ranging from 13 percent to 50 percent, depending on the underlying diagnosis and side effects of treatment.

What other considerations exist for patients with Diffuse Alveolar Hemorrhage?

Best hospital and critical care practices should be applied to all patients with DAH. Treatment is directed at the underlying diagnosis with the goal of halting the progression of the hemorrhage and preventing death from respiratory failure. Despite best practices, patients may develop repeated episodes of DAH, with which long-term pulmonary sequela may occur, such as evidence of pulmonary fibrosis and emphysema. Consultation with specialists experienced in treating the disease and its complications is recommended.

What’s the evidence?

Diaz, J, Calamia, KT, Lee, AS. "Pulmonary vasculitis in the intensive care unit.". J of Intens Care Med . vol. 26. 2011. pp. 88.

This review discusses the epidemiology, disease presentation, clinical and diagnostic considerations and treatment of patients with pulmonary vasculitis in intensive care units.

Lara, AR, Schwarz, MI. "Diffuse alveolar hemorrhage.". Chest . vol. 137. 2010. pp. 1164.

This review defines the clinicalpathologic syndrome of diffuse alveolar hemorrhage (DAH) and describes the various conditions that can result in DAH with discussion regarding treatment for the specific conditions.

Zamora, MR, Warner, ML, Tuder, RM. "Diffuse alveolar hemorrhage and systemic lupus erythematosus: clinical presentation, histology, survival and outcome.". Medicine. vol. 76. 1997. pp. 192-202.

This retrospective study describes the clinicopathologic presentation of DAH in patients with systemic lupus erythematosus (SLE). Fifteen patients were reviewed, the majority of whom were female (66%) and who had a median age of 27 years. Hemoptysis, which was present at the time of admission in only 42 percent of the patients, was associated with lupus nephritis in fourteen of the fifteen patients. Pulmonary capillaritis was the most common histopathologic pattern associated with DAH.

Schwarz, MI, Mortenson, RL, Colby, TV. "Pulmonary capillaritis: the association with progressive irreversible airflow limitation and hyperinflation.". Am rev Respir Dis. vol. 148. 1993. pp. 507-511.

This prospective study describes the development of irreversible obstructive lung disease as a consequence of repeated episodes of DAH and pulmonary capillaritis.

Hunt, DP, Weil, R, Nicholson, AG, Burke, MM, Du Bois, RM, Wells, AU. "Pulmonary capillaritis and its relationship to the development of emphysema in hypocomplementaemic urticarial vasculitis syndrome". Sarcoidosis Vasc Diffuse Lung Dis. vol. 23. 2006. pp. 70-72.

This case report describes the development of progressive obstructive lung disease and the development of emphysema with coexisting capillaritis in a non-smoking patient with hypocomplementemic urticarial vasculitis syndrome.

Lane, SE, Watts, R, Scott, DG. "Epidemiology of systemic vasculitis.". Curr Rheumatol Rep. vol. 7. 2005. pp. 270-275.

This paper describes the epidemiology of the primary systemic vasculitides over a ten-year period and reports an increase the incidence in a well-defined population with the greatest incidence occurring in the elderly population.

Kwok, SK, Moon, SJ, Ju, JH, Park, KS, Kim, WU, Cho, CS, Kim, HY, Park, SH. "Diffuse alveolar hemorrhage in systemic lupus erythematosus: risk factors and clinical outcome: results from affiliated hospitals of Catholic University of Korea". Lupus. vol. 20. 2011. pp. 102-7.

Patients with SLE were studied in a retrospective fashion in order to establish risk factors for the development of DAH. The authors found that those with evidence of neuropsychiatric disease or those who had a high disease activity score were at increased risk of developing DAH.

Klemmer, PJ, Charlermskulrat, MD, Reif, MS, Hogan, SL, Henke, DC, Falk, FJ. "Plasmapheresis therapy for diffuse alveolar hemorrhage in patients with small-vessel vasculitis.". Am J Kidney Dis. vol. 42. 2003. pp. 1149.

This retrospective study evaluated the treatment efficacy of total plasma exchange (TPE) coupled with immunosuppressant therapy versus immunosuppressant therapy alone in patients with systemic vasculitis andDAH. TPE with immunosuppressant therapy was more effective thanimmunosuppressant therapy alone and was well tolerated.

Jayne, DR, Gaskin, G, Rsmussen, N. "Randomized trial of plasma exchange orhigh-dosage methylprednisolone as adjunctive therapy for severe renal vasculitis.". J Am Soc Nephrol. vol. 18. 2007. pp. 2180.

A randomized controlled trial comparing intravenous methylprednisoloneversus TPE in patients with acute renal failure secondary to antineutrophil cytoplasmic associated (ANCA) antibody associated vasculitides. The primary end point was need for dialysis at 3 months.There was a 24% risk reduction for dialysis in patients who received TPE. Patient survival and adverse events were equivalent.

Levy, JB, Turner, AN, Rees, AJ, Pusey, CD. "Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression.". Ann Intern Med. . vol. 134. 2001. pp. 1033.

A retrospective review of treatment efficacy in patients with anti-glomerular basement membrane antibody disease. Treatment included prednisolone, cyclophosphamide and TPE. Of the 71 patients reviewed, 44 had pulmonary hemorrhage and 90 percent were controlled with this regimen.

de Groot, K, Harper, L, Jayne, DR. "Pulse versus daily oral cyclophosphamide for induction of remission in antineutrophil cytoplasmic antibody-associated vasculitis: a randomized trail.". Ann Intern Med . vol. 150. 2009. pp. 670.

This randomized controlled trial compared the effectiveness of pulsed versus oral cyclophosphamide in inducing remission in patients with ANCA-associated vasculitis. No difference was found in the time to remission in either group. The pulsed group had a lower total cumulative dose of the drug compared to the oral group so it had lower rates of toxicity.

Stone, JH, Merkel, PA, Spiera, R. "Rituximab versus cyclophosphamide for ANCA-associated vasculitis.". N Engl J Med . vol. 363. 2010. pp. 221.

In this randomized, non-inferiority trial, patients with ANCA-associated vasculitis were treated with cyclophosphamide and glucocorticoids or rituximab. Rituximab therapy was not inferior to the cyclophosphamide and glucocorticoid treatment and may be more effective at inducing remission during relapse. In the subgroup of patients with alveolar hemorrhage, no difference was found between treatments. However, those patients severe enough to require mechanical ventilation were excluded from the trial.

Ahmed, SH, Aziz, T, Cochran, J, Highland, K. "Use of extracorporeal membrane oxygenation in a patient with diffuse alveolar hemorrhage.". Chest . vol. 126. 2004. pp. 305.

A case report describing the experience of a patient with DAH that was due to ANCA-associated vasculitis with severe hypoxic respiratory failure, necessitating the institution of extracorporeal membrane oxygenation.

Heslet, L, Nielsen, JD, Levi, M. "Successful pulmonary administration of activated recombinant factor VII in diffuse alveolar hemorrhage.". Crit Care. vol. 10. 2006. pp. R177.

This prospective study reviewed the treatment efficacy of intrapulmonary administration of recombinant Factor VIIa in patients with DAH. Of the six patients who received treatment, all achieved hemostatic control following administration. Two patients had repeat treatments, and three patients died because of complications not related to therapy.
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