Case Of Diffuse Alveolar Hemorrhage Research Articles

A Case of Dupilumab-Induced Diffuse Alveolar Hemorrhage.

Eosinophilic pneumonia is a known side effect of dupilumab; however, diffuse alveolar hemorrhage has not yet been reported in association with dupilumab. We herein report a case of diffuse alveolar hemorrhage caused by dupilumab. A 57-year-old man with severe asthma was unable to discontinue oral steroids and thus was prescribed dupilumab. The patient was admitted to the hospital four weeks after treatment because of suspected eosinophilic pneumonia. Bronchoscopy revealed diffuse alveolar hemorrhage characterized by hemosiderin-phagocytic macrophages in the bronchoalveolar lavage fluid without eosinophils. The steroid dosage improved the respiratory status and resolved the infiltrate shadow. Dupilumab may thus cause diffuse alveolar hemorrhage, which can be differentiated using bronchoscopy.

Systemic lupus erythematosus with diffuse alveolar hemorrhage.

Systemic lupus erythematosus with diffuse alveolar hemorrhage.

Abstract 13671: A Case of Diffuse Alveolar Hemorrhage While on Systemic Anticoagulation for Impella

A 57 year old male with PMH of non-ischemic cardiomyopathy (EF 30%), atrial fibrillation, and VT s/p ICD was admitted to the cardiac intensive care unit for cardiogenic shock. His condition deteriorated necessitating Impella 5.5 implantation as bridge to cardiac transplant. Systemic heparin was started per Impella protocol with a lower anti-Xa goal of 0.2 - 0.3 given post-op bleeding at the R axillary Impella site. Five days post Impella placement he developed bloody secretions from the endotracheal tube requiring multiple blood transfusions and discontinuation of systemic heparin, while maintaining heparin purge. Labs were notable for anti-Xa 0.22, hemoglobin 9.7, and platelets 221. CT Chest demonstrated parenchymal opacities concerning for diffuse alveolar hemorrhage (DAH) which was confirmed via bronchoalveolar lavage; he had no known history of lung disease. High-dose corticosteroids were administered as a high ANA titer (1:128) and low C3 suggested capillaritis. However, decreasing ANA (1: 320) and a negative autoimmune workup decreased the likelihood of a rheumatologic cause for DAH and steroids were discontinued. DAH secondary to acquired von Willebrand syndrome (aVWS) was considered, but factor VIII and vWF activity levels were normal. The bloody secretions improved with inhaled thromboxane and systemic heparin was restarted. Orthotopic heart and kidney transplant was performed with subsequent Impella removal 104 days after Impella placement. Discussion: We present the first documented case of DAH with isolated Impella 5.5 support. Previously reported cases of DAH post-Impella were observed in patients with concurrent ECMO or RVAD. As autoimmune and coagulopathic causes of DAH were excluded, bland DAH secondary to systemic anticoagulation is most likely in this case. This raises a question about how to balance the risk of bleeding with the risk of device thrombosis, stroke and embolic events and when to switch from heparin to sodium bicarbonate purge.

Clinical characteristics of patients with diffuse alveolar hemorrhage diagnosed by cytological examination of 1000 bronchoalveolar lavage samples.

Diffuse alveolar hemorrhage (DAH) is a life-threatening condition due to the extravasation of blood in the alveoli, resulting in hypoxemia and even acute respiratory distress syndrome. This study aimed to describe the clinico-radio-pathological profile of patients diagnosed with DAH and classify it into immune and nonimmune DAH. This was a retrospective analytical study. Of a total of 1000 cases of bronchoalveolar lavage fluids (BALF) received for cytological examination, patients fulfilling the clinical, radiological, and laboratory details of cases satisfying the clinical and cytological criteria of DAH (n=47) were studied. The most common cause of immune DAH was ANCA-associated vasculitis (n=13, 27.6%), and that of nonimmune DAH was infections (n=10, 21.3%). Twenty-nine patients (61.7%) had hemoptysis. The most common radiological finding was ground-glass opacities (n=33, 70.2%). In univariate analysis, female sex, mean hemoglobin at admission, total leucocyte count (TLC), platelet count, and erythrocyte sedimentation rate (ESR) were significantly associated with immune-DAH. However, in multivariate analysis, female sex, higher TLC, high platelets, and high ESR were significantly associated with immune DAH. Patients were treated with corticosteroids (n=25, 46.3%), intravenous cyclophosphamide (n=12, 22.2%), plasma exchange (n=7, 13.0%), intravenous immunoglobulin (n=5, 9.3%) and rituximab (n=5, 9.3%). The overall mortality was 8.5% (n=4). DAH is a life-threatening syndrome that may be classified into immune and nonimmune DAH. Immune-DAH requires aggressive management, whereas nonimmune DAH cases respond best to conservative management.

Diffuse Alveolar Hemorrhage: A Rare Underlying Disease in a Child with Chronic Respiratory Symptoms

Background: Diffuse lung disease (DLD), conventionally known as interstitial lung disease (ILD), encompasses a spectrum of diseases involving the pulmonary parenchyma with impairment of gaseous exchange. Most of the diseases under DLD have similar presentations, but appropriate investigations can delineate the exact disease. Diffuse alveolar hemorrhage (DAH) is one of the diseases under this umbrella group of DLD. Clinical Description: A 3-year-old girl suffering from persistent breathlessness and intermittent hypoxic exacerbations over 1 year, presented to us with acute respiratory worsening. She was underweight with stunting and had severe pallor. She had received blood transfusions in previous hospitalizations. Chest-X-ray shows reticular opacities, with High Resolution Computed Tomography (HRCT) chest showing bilateral diffuse ground glass opacities involving all lobes with the prominent pulmonary artery. The broncho-alveolar lavage showed hemosiderin-laden macrophages, thereby confirming alveolar hemorrhage. Antinuclear antibody was positive, though double-stranded DNA and Anti-neutrophil cytoplasmic antibody were negative. The child was thus diagnosed with a case of DAH, probably, immune mediated. Management: The child was treated with supportive care, including oxygen, intravenous fluids, antibiotics, and packed red cell transfusion. Even after improvement in hemoglobin, oxygen dependency persisted. The child was then administered Intravenous Immunoglobulin and prednisolone, to which the child showed a response with gradual weaning off oxygen. Conclusions: In any child presenting with persistent respiratory symptoms, especially exercise intolerance, over a prolonged period with intermittent hypoxic exacerbations, a pediatrician should consider diagnoses beyond infections and multitrigger wheezing. Such manifestations, particularly if associated with failure to thrive, may be due to DLD. DAH, a rare form of DLD, may be a possibility in such children.

Venovenous Extracorporeal Membrane Oxygenation in Diffuse Alveolar Hemorrhage Secondary to Anti-neutrophil Cytoplasmic Autoantibody-associated Vasculitis: Starting without Systemic Anticoagulation.

Regarding extracorporeal membrane oxygenation (ECMO) support against hemorrhagic conditions, there seems to be a dilemma when deciding between maintaining the circuit patency by systemic anticoagulation and increasing the risk of bleeding. We herein report two cases of diffuse alveolar hemorrhage (DAH) caused by myeloperoxidase (MPO) anti-neutrophil cytoplasmic autoantibody-associated vasculitis (AAV) successfully treated with venovenous (VV)-ECMO support, both initially started without systemic anticoagulation. Under anticoagulation-free ECMO management, we should consider the shortcomings of frequent circuit exchange and hemorrhagic diathesis related to circuit-induced disseminated intravascular coagulation (DIC).

A CASE OF TYPE 1 CRYOGLOBULINEMIA PRESENTING WITH DIFFUSE ALVEOLAR HEMORRHAGE

A CASE OF TYPE 1 CRYOGLOBULINEMIA PRESENTING WITH DIFFUSE ALVEOLAR HEMORRHAGE

A RARE MANIFESTATION OF SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): DIFFUSE ALVEOLAR HEMORRHAGE

A RARE MANIFESTATION OF SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): DIFFUSE ALVEOLAR HEMORRHAGE

P30 A case of small bowel and leukocytoclastic vasculitis associated with acitretin therapy

Introduction/BackgroundAcitretin is an oral retinoid that is used to treat a number of skin conditions including acne. It is generally well tolerated and common side-effects such as gastrointestinal upset, mucosal and skin reactions are usually mild. However, we present what we believe to be the first reported case of small bowel and leukocytoclastic vasculitis (LCV) caused by acitretin and this required prompt treatment with intravenous glucocorticoids and cyclophosphamide to induce remission.Description/MethodA 53-year-old caucasian male presented to the Emergency Department with severe bilateral foot pain for four days and a purpuric rash which initially affected the soles of his feet and spread to affect all four limbs, both hands and abdomen. He was three weeks into his second course of acitretin 20mg daily for a flare of psoriasis, having ceased treatment three months before due to a suspected iatrogenic rosacea type reaction. He had generalised abdominal pain and recent constipation. Observations demonstrated a sinus tachycardia at 130 beats per minute only and examination revealed widespread patchy non-blanching palpable purpura and deep ulcers over the soles of both feet. There was mild abdominal distension and global tenderness but no peritonism. The remainder of the physical examination was unremarkable. Initial blood tests showed: haemoglobin 156 g/L, white cell count 13 x 109/L (neutrophilia: 10.6 x 109/L), platelets 514 x 109/L, CRP 123 mg/L, ESR 12 mm/hr, normal renal and liver function. Detailed immunology, microbiology and viral screens were negative including anti-neutrophil cytoplasmic antibodies (ANCA) and cryoglobulins. Urine dipstick was unremarkable. Abdominal x-ray showed distended small bowel loops and CT demonstrated significant intestinal wall oedema suggestive of small bowel vasculitis. Skin biopsy demonstrated typical changes of leukocytoclastic vasculitis. After surgical review he was managed conservatively on the high dependency unit with intravenous methylprednisolone 1g daily for three days followed by intravenous hydrocortisone and one dose of cyclophosphamide (15mg/kg). Total parenteral nutrition was initiated, and his bowel symptoms settled after two weeks. His skin significantly improved and he was discharged after four weeks’ inpatient stay. Actretin was stopped indefinitely, and he has remained in remission over three years later. Prednisolone was successfully tapered at a slow rate, and no further cyclophosphamide was required. His psoriasis is currently managed well with oral methotrexate.Discussion/ResultsLCV is a small vessel vasculitis which mostly occurs in the cutaneous form but can be life-threatening with systemic involvement. Around 50% of cases are idiopathic, with infections (15-20%), autoimmune diseases (15-20%) and malignancy (<5%) being well-recognised causes.Drug-induced LCV accounts for nearly 15% of cases and antibiotics, non-steroidal anti-inflammatories, anti-epileptics and TNF-alpha blockers are well-known precipitants. It usually occurs within three weeks after commencement of the medication, and the timing of re-introduction of acitretin in our patient makes it likely to be the cause. Up to 90% of LCV cases resolve within weeks to months after addressing the precipitating cause, with or without oral steroids. However, a 2% mortality is reported, likely due to systemic involvement and given the severity of our patient’s presentation, it was decided to commence immunosuppression in view of the skin biopsy and CT findings. (A biopsy of the small bowel was considered but would have delayed treatment).To our knowledge there are no published case reports linking LCV and small bowel vasculitis to acitretin therapy. However, there have been several case reports of LCV and other vasculitides caused by all-trans-retinoic acid (ATRA) and isotretinoin (first generation retinoids). Yamada et al. (1999) reported a severe case of haemonecrosis of the ileum, as a complication of ATRA treatment for acute promyelocytic leukaemia. Surgical intervention was required and histology demonstrated LCV.Isotretinoin was attributed to cause 5 out of 11 LCV cases reviewed by Dwyer et al. (1989). Turan et al. (2012) reported a case of a Henoch-Schonlein Purpura secondary to isotretinoin that improved with discontinuing treatment and three weeks of fluocortolone 20mg daily. More recently, a case of diffuse alveolar haemorrhage due to isotretinoin-induced granulomatosis with polyangiitis was described by Assuncao et al. (2018), which remitted with intravenous methylprednisolone and cyclophosphamide.Key learning points/ConclusionAlthough very rare, consider retinoids including acitretin in cases of drug-induced LCV and small bowel vasculitis.Symptoms usually improve on cessation of the treatment alone, but immunosuppression might be required for more severe cases.Future case series could help guide treatment choices.

Clinical Presentation of Legionella pneumophila Serogroup 1-Associated Pneumonia and Diffuse Alveolar Hemorrhage: A Case Report and Literature Review

Patient: Female, 44-year-old Final Diagnosis: Legionella pneumophila serogroup 1-associated pneumonia and diffuse alveolar hemorrhage Symptoms: Dyspnea Medication:— Clinical Procedure: Bronchoalveolar lavage Specialty: Infectious Diseases Objective: Rare disease Background:We report a case of diffuse alveolar hemorrhage (DAH) caused by Legionella pneumophila serogroup (SG) 1 and review the existing literature to identify risk factors and determine the prognosis of patients with Legionella pneumonia-associated DAH.Case Report:A 44-year-old woman was admitted to our hospital following the presentation of dyspnea for a few days. Chest computed tomography (CT) findings revealed “crazy-paving” pattern in the right upper lobe implicating DAH and consolidation in the lower lobe. Analysis of the bronchoalveolar lavage (BAL) fluid revealed DAH, with further analyses identifying L. pneumophila SG 1 as the causative agent. The patient was successfully treated with levofloxacin and a red blood cell transfusion and discharged on the 32nd day of hospitalization. A literature review of 6 reported cases (including our case) of Legionella pneumonia-associated DAH revealed that the median age of patients with DAH was 59 years (range, 44–75 years), involving female patients in 4 cases (67%) and the use of immunosuppressive drugs in 2 cases (33%). Three cases were BAL Legionella polymerase chain reaction (PCR)-positive and 4 cases were diagnosed using a urinary Legionella antigen test (one case was simultaneously PCR-positive). These infections were caused by L. pneumophila SG 1 in three cases and SG 3 in one case. Mechanical ventilation was used in 5 cases (83%) and one patient had an unfavorable prognosis. Steroids for DAH were used in 5 cases (83%), and 2 cases responded to this treatment.Conclusions:Our case highlights that clinicians should be aware of Legionella spp. as a cause of DAH in an immunocompe-tent host with “crazy-paving” pattern on chest CT, and perform a urinary antigen test and BAL PCR for diagnosis.

DIFFUSE ALVEOLAR HEMORRHAGE DUE TO HYDRALAZINE-INDUCED LUPUS

TYPE: Case Report TOPIC: Pulmonary Manifestations of Systemic Disease INTRODUCTION: Hydralazine is a known cause of drug-induced lupus and has been associated with ANCA-associated vasculitis (AAV) primarily involving the kidney, with rare pulmonary complications. We report a case of Hydralazine-induced lupus presenting as diffuse alveolar hemorrhage (DAH) in the absence of renal disease or AAV. CASE PRESENTATION: An 86 year-old female presented to the hospital due to one week of dyspnea and hemoptysis. She was started on Hydralazine 100mg BID five months prior. CTA of the chest revealed extensive bilateral central ground-glass opacities with relative sparing of the peripheral lungs. She had an unrevealing infectious and cardiac workup. Urinalysis showed bland sediment. Bronchoscopy revealed blood throughout the tracheobronchial tree and serial lavage aliquots were consistent with DAH. Autoimmune studies noted a positive ANA titer of ≥1:1280, and positive anti-histone IgG of 163AU/mL. The remaining studies were normal, including complement, anti-dsDNA, anti-Smith, anti-GBM, ANCA titers, PR3 and MPO antibodies, rheumatoid factor, anti-CCP, anti-RNP, and anti-SSA/SSB. Hydralazine was discontinued and the patient was started on systemic corticosteroids with complete resolution. DISCUSSION: Few cases of DAH attributed to Hydralazine have been reported in the literature. This case is unique in that there was no nephritis or AAV based on the antibody biomarker distribution. CONCLUSIONS: We report a case of DAH as a result of Hydralazine-induced lupus in the absence of renal involvement or AAV. Discontinuation of the offending agent, early bronchoscopy, autoimmune workup, and systemic corticosteroids are paramount to successful patient outcomes. Further investigation is necessary, as there currently exist no randomized trials to guide therapy. DISCLOSURE: Nothing to declare. KEYWORD: diffuse alveolar hemorrhage

Diffuse alveolar hemorrhage: An underreported complication of transplant associated thrombotic microangiopathy.

Hematopoietic stem cell transplantation-associated thrombotic microangiopathy (TA-TMA) and diffuse alveolar hemorrhage (DAH) are well recognized post-transplant complications that carry a high risk of mortality; however, the risk of DAH complicating the course of transplant patients with TA-TMA is not well understood. We conducted a ten-year retrospective study at our institution to determine the incidence of DAH in a cohort of pediatric patients with TA-TMA and described their presentation and outcomes. Additionally, autopsy slides, when available, were reviewed to assess for histological evidence of microvascular injury and alveolar hemorrhages. A total of 58 pediatric patients with TA-TMA were identified. Of these, 14 (24%) had DAH. Majority of DAH cases occurred within a week of TA-TMA diagnosis (n = 8, 57%, range 0-698 days). Mortality was 100% for patients with DAH and TA-TMA. Infections were found to be a significant risk factor for DAH in TA-TMA. Autopsy was performed in 11 of the 14 patients, and pulmonary slides were available for review in ten cases. 70% cases had pathological evidence of microvascular injury, concerning for pulmonary TA-TMA. We conclude that DAH is a potentially fatal complication in patients with TA-TMA and may be a result of pulmonary microangiopathy.

Diffuse alveolar hemorrhage secondary to immune thrombocytopenic purpura: a case report and literature review

Diffuse alveolar hemorrhage (DAH) is a potentially life-threatening disease that can be caused due to several underlying disorders. The diagnosis and management of DAH remains challenging given its nonspecific presentation and lack of uniform criteria for the diagnosis. The management of DAH involves treating the causative underlying condition. On extensive review of the literature, only fewer than 10 cases of DAH associated with immune thrombocytopenic purpura (ITP) were found. The outcomes in DAH associated with ITP were also found to be variable in the reported cases, ranging from clinical recovery to mortality. We present a 45-year-old man with ITP who developed DAH, and a review of the available literature.

DIFFUSE ALVEOLAR HEMORRHAGE WITH LATE PRESENTING RIGHT VENTRICULAR THROMBI

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Diffuse alveolar hemorrhage is a life threatening emergency that can be caused by multiple etiologies. Pulmonary capillaritis, one common etiology, is particularly associated with autoimmune or inflammatory diseases. We present a challenging case of diffuse alveolar hemorrhage with associated acute hypoxic respiratory failure due to isolated pulmonary capillaritis with multiple late presenting intracardiac thrombi. CASE PRESENTATION: A 20 year-old woman presented with four days of myalgias, fever, and shortness of breath. Testing for pulmonary embolism and SARS-CoV2 was negative. She was diagnosed with pneumonia and treated with ceftriaxone and azithromycin. She then developed blood tinged mucous which was concerning for diffuse alveolar hemorrhage and received three days of pulse dose steroids. Seven days after initial presentation, she required escalation to intensive care. Her oxygen saturation was 96% on 70% FiO2 and 50 liters of pressure and subsequently required intubation for hypoxic respiratory failure. Imaging revealed diffuse bilateral infiltrates and bronchoscopy with lavage yielded mild endobronchial bleeding, but no overt hemorrhage. Pathology demonstrated neutrophilic capillaritis with diffuse alveolar damage. Prior outpatient autoimmune workup was significant only for mildly positive anti-nuclear antibody (speckled pattern 1:80). Transthoracic echocardiogram performed after intubation revealed two right ventricular thrombi that were not present on prior echocardiogram from admission. We initiated a heparin infusion in the setting of her alveolar bleeding and continued treatment with methylprednisolone. She then developed acute hemodynamic changes concerning for pulmonary embolism but stabilized without further intervention. The patient's oxygenation improved and she was successfully extubated. An antiphospholipid syndrome screen returned positive for a Dilute Russell Viper Venom Time (though notably value was 1.25 and upper limit of normal is 1.24) and anticoagulation was transitioned to warfarin prior to discharge home. DISCUSSION: Concurrent hemorrhage and hypercoagulability is a difficult management dilemma that many clinicians will face in the hospital setting. This case highlights the degree of suspicion required to evaluate for thromboembolic phenomena even in a patient with hemorrhage. In this young patient with no significant past medical history, autoimmune etiologies must be considered for her presentation of diffuse alveolar hemorrhage, which can also cause a concurrent hypercoagulable state. Despite mildly positive lupus anticoagulant screen, remainder of autoimmune workup was negative and suspicion low for systemic autoimmune disease. CONCLUSIONS: Bedside clinical judgement must drive decision making in the balance between worsening bleeding with anticoagulation or considering intervention for hemodynamically significant thromboembolic events. REFERENCE #1: Stoots SA, Lief L, Erkan D. Clinical Insights into Diffuse Alveolar Hemorrhage in Antiphospholipid Syndrome. Curr Rheumatol Rep. 2019;21(10):56. Published 2019 Sep 6. doi:10.1007/s11926-019-0852-7 REFERENCE #2: Park MS. Diffuse alveolar hemorrhage. Tuberc Respir Dis (Seoul). 2013;74(4):151-162. doi:10.4046/trd.2013.74.4.151 DISCLOSURES: No relevant relationships by Micah Fisher, source=Web Response No relevant relationships by David Wilhoite, source=Web Response

EBV-ASSOCIATED ATYPICAL HEMOLYTIC UREMIC SYNDROME PRESENTING WITH DIFFUSE ALVEOLAR HEMORRHAGE

TOPIC: Pulmonary Manifestations of Systemic Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Atypical Hemolytic Uremic Syndrome (aHUS) is a severe form of thrombotic microangiopathy that presents with nonimmune hemolytic anemia, thrombocytopenia, and renal failure. Diffuse alveolar hemorrhage (DAH) due to disruption of alveolar-capillary basement membrane is an exceedingly rare presentation of aHUS. CASE PRESENTATION: A 19-year-old-male presented with acute respiratory distress, hemoptysis, tachypnea, tachycardia, elevated blood pressure, and oliguria. One month prior the patient was diagnosed with infectious mononucleosis associated with thrombocytopenia and splenomegaly. Initial labs demonstrated hemolytic anemia, thrombocytopenia, and acute renal failure. CT chest showed diffuse bilateral central alveolar opacities concerning for alveolar hemorrhage. Patient was stabilized with supplemental oxygen and urgent hemodialysis was initiated. Further studies revealed schistocytes on peripheral blood smear, hypocomplementemia, borderline low activity of ADAMTS-13, positive IgM/IgG to EBV nuclear antigen and a renal biopsy consistent with acute thrombotic microangiopathy affecting nearly all blood vessels and glomeruli. Serologies were negative for ANA, anti-dsDNA, ANCA, Anti-GBM ab, rheumatoid factor, HIV, HBV, and HCV. Patient was diagnosed with EBV infection associated Atypical Hemolytic Uremic Syndrome (aHUS) and received treatment with plasmapheresis and eculizumab. With this treatment, patients' respiratory distress, hemoptysis, and renal function improved, following which he was discharged with outpatient hemodialysis. He continues follow up with hematology and nephrology. DISCUSSION: aHUS is much less frequent than Shiga-toxin mediated hemolytic uremic syndrome. Endothelial injury and thrombotic microangiopathy are hallmarks of this complement mediated process. It is associated with high risk of ESRD. Recent advances in therapeutics targeted at complement regulatory proteins including Eculizumab, have offered better outcomes. DAH is a life-threatening complication that has rarely been reported with aHUS. Treatment of diffuse alveolar hemorrhage depends on etiology. In our patient, diagnosis and targeted management of aHUS helped improve hemoptysis and respiratory distress from DAH. CONCLUSIONS: Atypical HUS can present with acute onset renal failure and diffuse alveolar hemorrhage in some instances. Association with EBV infection is extremely rare. REFERENCE #1: Joseph C, Gattineni J. Complement disorders and hemolytic uremic syndrome. Curr Opin Pediatr. 2013;25(2):209-15. REFERENCE #2: Hong JY, Jung JY, Kang YA, Bae YS, Kim YS, Kim SK, et al. Delayed Hemolytic Uremic Syndrome Presenting as Diffuse Alveolar Hemorrhage. Korean J Crit Care Med. 2014;29(1):43-7 REFERENCE #3: Al-Shyoukh A, Younis M, Abughanimeh O, Tahboub M, Hamarshi MS. An Unusual Case of Diffuse Alveolar Hemorrhage as a Clinical Manifestation of Atypical Hemolytic Uremic Syndrome: A Case Report. Cureus. 2019;11(7):e5059-e. DISCLOSURES: No relevant relationships by zainub ajmal, source=Web Response No relevant relationships by Sana Ghalib, source=Web Response No relevant relationships by Boris Shkolnik, source=Web Response No relevant relationships by Fatima Tuz Zahra, source=Web Response

DIFFUSE ALVEOLAR HEMORRHAGE: A RARE COMPLICATION OF ACUTE MYELOID LEUKEMIA

TOPIC: Pulmonary Manifestations of Systemic Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Diffuse alveolar hemorrhage (DAH) is a life-threatening pulmonary syndrome affecting individuals with hematologic malignancies with increased incidence post bone marrow transplant. We present a rare case of DAH presumably related to pulmonary leukemic infiltration (PLI) in a newly diagnosed Acute Myelogenous Leukemia (AML) patient. CASE PRESENTATION: A 55-year-old female, previously healthy, presented to the emergency room with a 1-week history of dyspnea, cough, and epistaxis. Laboratory data were relevant for leukocytosis (WBC 150,000/mm3) with 84% blasts, thrombocytopenia (platelets 15,000/mm3), and anemia (Hb 8.9 g/dL). CT angiography of the chest was negative for pulmonary embolism but showed scattered bilateral ground-glass opacities (GGO). Peripheral blood flow cytometry revealed AML. She underwent leukapheresis with an appropriate response. On day 5 of admission, she was transferred to the intensive care unit for increased oxygen requirement and required endotracheal intubation the day after. Chest CT showed significant worsening in bilateral GGO and septal thickening. WBC 27,000/mm3, Hb 7.7 g/dL, and platelets 50,000/mm3. Bronchoscopy with serial bronchoalveolar lavages (BAL) showed an increasingly bloody return. BAL cell differential was significant for 75% blasts. She was treated with platelet transfusion, nebulized tranexamic acid, high dose corticosteroids, and empiric antibiotic therapy. Emergent induction chemotherapy (daunorubicin + cytarabine) was started. Repeat bronchoscopy in 48h showed resolution of DAH and undetectable blasts in BAL. She was extubated on day 7 post-intubation, and her respiratory status improved back to baseline. DISCUSSION: Pulmonary opacities in leukemia may be the result of an infectious process, pulmonary edema, drug toxicity, diffuse alveolar hemorrhage, intravascular leukostasis, or pulmonary leukemic infiltrates. Though the timing of pulmonary complications, clinical presentation, and chest CT findings may help identify the etiology, diagnosis is frequently challenging, and early BAL may be of benefit. In this patient, worsening respiratory status and pulmonary infiltrates despite leukapheresis excluded leukostasis and suggested PLI. Hemoptysis is absent in more than one-third of patients with DAH. She had no hemoptysis, and DAH was subsequently diagnosed with bronchoscopy. We believe that early diagnosis of PLI, excellent response to induction chemotherapy, along with other supportive measures led to a favorable outcome. CONCLUSIONS: Early recognition of acute respiratory failure etiology in patients with leukemia and pulmonary infiltrates is essential. Albeit rare, DAH should always be on the differential as early identification and treatment can likely improve outcomes. REFERENCE #1: Nanjappa S, Jeong DK, Muddaraju M, Jeong K, Hill ED, Greene JN. Diffuse Alveolar Hemorrhage in Acute Myeloid Leukemia. Cancer Control. 2016 Jul;23(3):272-7 REFERENCE #2: Nucci M, Nouér SA, Anaissie E. Distinguishing the Causes of Pulmonary Infiltrates in Patients with Acute Leukemia. Clin Lymphoma Myeloma Leuk. 2015 Jun;15 Suppl: S98-103. DISCLOSURES: No relevant relationships by Tony Abdo, source=Web Response No relevant relationships by Samiksha Gupta, source=Web Response No relevant relationships by SYED HUSSAIN, source=Web Response No relevant relationships by Miloni Parmar, source=Web Response

A rare case of diffuse alveolar hemorrhage caused by acute mycoplasma pneumoniae pneumonia

ABSTRACT Mycoplasma pneumoniae is a common bacterial pathogen that causes atypical community-acquired pneumonia. Illness onset can be gradual and progressive over weeks. Patients typically have cough, pharyngitis, malaise, and tracheobronchitis. Although symptoms are frequently mild, the initial presentation can be severe with numerous complications. We present a case of a 28-year-old male who presented with 1 day of significant hemoptysis. He was intubated for airway protection and underwent bronchoscopy, which showed multiple blood clots in several lung lobes, consistent with diffuse alveolar hemorrhage (DAH). His workup was negative for pulmonary embolism, coagulopathy, and vasculitis. He tested positive for rhinovirus and mycoplasma pneumoniae IgM (negative IgG). He was ultimately discharged home with oral doxycycline to complete a 10-day course. DAH is a rare presentation and life-threatening complication of mycoplasma pneumonia. Although there is a reported association between DAH and rhinovirus, our patient improved with antibiotics making mycoplasma pneumoniae the likely culprit. When encountering hemoptysis or alveolar bleeding, clinicians should have low suspicion for atypical infections and start appropriate antibiotics early in the clinical course.

Risk factors and outcomes of immune and non-immune causes of diffuse alveolar hemorrhage: a tertiary-care academic single-center experience.

Diffuse alveolar hemorrhage (DAH) is a rare but potentially life-threatening emergency that has both immune and non-immune etiologies. The objective of this investigation was to compare the risk factors and outcomes of immune and non-immune causes of DAH at a tertiary-care academic center. This was a retrospective observational study conducted at a University center. We reviewed all chest radiographs spanning 12years (2007-2019) at our institute with the words "diffuse alveolar hemorrhage" in the body of their report, and ascertained cases of DAH through a detailed chart review. We used Chi-squared test to determine the differences in risk factors and outcomes between immune versus non-immune causes of DAH. We performed logistic regressions to assess whether baseline demographics and clinical features influence four critical outcomes: death, shock, renal failure, and severe anemia requiring transfusions. Over the 12-year period, there were 88 patients with DAH, 55 with non-immune and 33 with immune etiologies. Among immune causes of DAH, granulomatosis with polyangiitis (GPA) (10.2%), microscopic polyangiitis (MPA) (9%) and systemic lupus erythematosus (SLE) (9%) were most common. Among non-immune causes of DAH, coagulopathy (6.8%), decompensated heart failure (4.5%) and infection (3.4%) were most common. Patients with non-immune causes of DAH were 45.8% more likely to die and 20.7% less likely to experience sustained remission (p = 0.001). Patient with immune causes of DAH were 21% more likely to have extra-pulmonary findings and 23.7% more likely to have received hemodialysis (HD). The presence of extra-pulmonary findings was statistically significantly correlated with the number of blood products received, the need for HD and non-statistically significantly correlated with likelihood of death. Patients with immune causes of DAH were 71.5% more likely to receive multimodal therapy including corticosteroids. Immune-mediated DAH is associated with a better prognosis than non-immune DAH, despite its greater association with extra-pulmonary findings and requirement for hemodialysis.

A Case of Diffuse Alveolar Hemorrhage Accompanied by Pneumococcal-positive Bronchial Casts

A Case of Diffuse Alveolar Hemorrhage Accompanied by Pneumococcal-positive Bronchial Casts

DIFFUSE ALVEOLAR HEMORRHAGE AS CLINICAL PRESENTATION OF GPA

TYPE: Abstract Publication TOPIC: Diffuse Lung Disease PURPOSE: We describe a case of diffuse alveolar hemorrhage (DAH) as a presenting clinical manifestation of ANCA-associated vasculitis (AAV) leading to pulmonary-renal syndrome (PRS), a rare complication with a high mortality rate. METHODS: A 52-yo male presented with a one-week history of malaise and dry cough. Lung examination showed decreased breath sounds. Chest x-ray demonstrated diffuse bilateral opacities. CT showed diffuse alveolar filling. Labs were significant for normocytic anemia 8.1(g/dL), renal failure (Cr 3.14 (mg/dL)) and PaO2 74mm HG on 100% oxygen. Vancomycin, piperacillin/tazobactam, and azithromycin were initiated. Urinalysis showed hematuria and proteinuria. Autoimmune workup revealed CRP 213 mg/L, ESR 56 mm/h, ANCA (+), C-ANCA 1:1280, PR3+ >8. Due to rapidly decreasing hemoglobin and respiratory failure patient was intubated and bronchoscopy confirmed DAH. Patient was treated with pulse steroids for five days, cyclophosphamide, and plasmampharesis. Intermittent hemodialysis initiated for renal failure and anuria. Patient was extubated on day 7 and renal biopsy on day 10 confirmed acute necrotizing glomerulonephritis consistent with AAV. RESULTS: We report a case of GPA with sudden onset of hypoxic respiratory failure progressing to PRS. Severities of presenting symptoms and findings in patients with GPA vary considerably from asymptomatic to acute alveolar hemorrhage with respiratory failure. CONCLUSIONS: Although DAH is a rare manifestation of the disease, occurring only in 5% to 10% of patients, it acts as a precursor of severe vasculitis. CLINICAL IMPLICATIONS: Early detection of GPA is essential since it may lead to rapid clinical deterioration; high of index of suspicion and early management significantly improves morbidity and mortality. DISCLOSURE: No significant relationships. KEYWORDS: Diffuse Alveolar Hemorrhage, ANCA Vasculitis