Diffuse Alveolar Hemorrhage in the ED: Pearls & Pitfalls

Authors: Sumir Shah, DO, MS (EM Resident Physician, University at Buffalo), Eric Cioe, MD, MPH (Director of Global Health, Staten Island Univ Hospital), and Julie Endrizzi, MD (EM Resident Physician, Univ of Rochester) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)


A 45-year-old male with a past medical history of hypertension and a prior gunshot wound presents to your emergency department (ED) with non-radiating, mid-sternal, pleuritic chest pain. The patient also complains of a cough, tactile fever, diaphoresis and chills that started earlier in the morning. He states that he was worried by the specks of red in his otherwise yellow phlegm. The patient admits to marijuana (THC) use, but denies any other illicit drug or alcohol use. He also denies loss of consciousness, seizures, dysuria, or any other symptoms. Emergency Medical Services (EMS) reports that he was given 324mg of aspirin (ASA) en route.

Vital signs upon ED arrival:  Blood pressure (BP) 122/81, Pulse (P) 110, Respiratory Rate (RR) 18, Temperature (T) 35°Celsius (C), and Oxygen saturation (SpO2) 96% on room air.

On exam, the patient is diaphoretic and has diffuse bilateral rales in all lung zones. The remainder of the exam is unremarkable. Laboratory tests demonstrate a white blood cell (WBC) count of 36.4, a hemoglobin (Hgb) of 13.1, and a lactate of 2.9. Urinalysis shows 1+ ketones, 2+ blood, 2+ WBC, 1+ bacteria, 1+ squamous epithelial cells, and a protein of 30. Urine toxicology is positive for THC and cocaine.

The patient is sent for a chest x-ray (CXR), followed by a computed tomography (CT) scan of the chest, showing findings similar to below:

Pic 1 DAHPic 2 DAH

Figure A                                                      Figure B

Figure A: CXR showing new diffuse ground glass opacification of the bilateral lungs, with tiny centrilobular nodules.

Figure B: CT Chest showing diffuse bilateral alveolar ground glass opacities with inter- and intralobular thickening.


Diffuse alveolar hemorrhage (DAH) is a life-threatening medical emergency that is associated with pulmonary disease, bronchial disease and/or trauma. DAH is characterized by bleeding of the pulmonary microvasculature into the alveoli. It is imperative to understand this pathophysiology as many clinical findings are nonspecific and thus, the diagnosis may be difficult to ascertain. (2,7)

DAH is characterized by 3 distinct histological types: Pulmonary Capillaritis, Bland Damage, and Diffuse Alveolar Damage. (9) The most common, Pulmonary Capillaritis, is defined as neutrophilic predominant infiltration of the alveolar septa leading to fibrinoid necrosis of the alveolar and capillary walls. This occurs because the neutrophils undergo cell damage, which causes accumulation of debris, and toxic radicals that undermine the integrity of the cell wall. (6) Drugs such as hydralazine, propylthiouracil (PTU), and carbimazole can trigger this process, but it can also occur due to a number of vasculitides. (8)

The second histologic type of damage is known as Bland Damage. (9) In this subtype, the RBCs leak into the alveoli without histologic findings of inflammation or destruction. This is associated with many of the same diseases that cause capillaritis, such as thrombocytopenia and Anti-GBM (Goodpasture’s) disease, but is also associated with mitral valve pathology. (3,8)

The final subtype of DAH is Diffuse Alveolar Damage. This subtype is defined as edema of the alveolar septa and by formation of hyaline membranes that line the alveolar spaces. (6) This subtype tends to be the most familiar as it encompasses Acute Respiratory Distress Syndrome (ARDS). ARDS has a variety of causes that range from infection to crack cocaine use. (1)

Back to the Case…

Our patient was believed to have presented with his symptoms due to acute crack cocaine ingestion. Cocaine, the most common toxic cause of DAH, is a popular drug in the United States (US). The Drug Abuse Warning Network (WARN) estimates the prevalence is at or above 1.2% in Americans. It is also estimated that 25-60% of users develop respiratory symptoms, known as crack lung, within the first 48 hours. Symptoms of crack lung can range from shortness of breath (SOB) and cough to acute lung injury, ARDS or barotrauma. These symptoms can be further exacerbated in asthma patients because bronchoconstriction commonly occurs. (8,5,10)

Pearl: The most common adulterants of cocaine include the anti-fungal Levamisole and the beta adrenergic agonist Clenbuterol. These have been associated with agranulocytosis, hyperglycemia and hypokalemia. (8)

Pic 3 DAH

Clinical Presentation

The clinical presentation of these patients is often non-specific. It is important to consider the symptoms, imaging, and labs as a group to come to the most accurate diagnosis. Most commonly, patients will present with cough, dyspnea, fever, and hemoptysis. The examination is frequently nonspecific and will most likely consist of diffuse rales or crackles in all lung fields. (2,5)

Pearl: 33% of DAH patients present without hemoptysis due to the large absorptive capacity of the lungs. (9)


In general, cough, dyspnea, hemoptysis, and a positive bronchoalveolar lavage (BAL) for RBCs is enough to establish the diagnosis of DAH. (7) However due to the non-specific nature of the clinical symptoms it is also important to consider the patient’s past medical history for recent infections, drug use, toxic exposures, and known co-morbidities such as systemic vasculitis or mitral valve disease. These can all be used as clues to identify a cause.

Chest x-ray will show patchy alveolar infiltrates similar to pulmonary edema, however there will likely not be any Kerley-B lines, pleural effusions, or peri-bronchial cuffing. Ground-glass opacities and interlobular thickening may be seen on high resolution CT scan of the chest. (4,8)

Pearl: RBC-tagged nuclear imaging is of limited usefulness in diagnosing DAH. (8)

Although laboratory studies on their own are often nonspecific, they can sometimes yield clues to the diagnosis. (6) Commonly ordered lab tests include blood cultures, arterial blood gas (ABG) to evaluate level of hypoxia, complete blood count (CBC) with differential to evaluate anemia, chemistry, liver tests, blood urea nitrogen (BUN) ancreatinine for renal function, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), urinalysis, and urine toxicology. (8) If the patient has a relevant past medical history or a pulmonary-renal syndrome disease, specific antibodies such as cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA), perinuclear anti- neutrophil cytoplasmic antibodies (P-ANCA), anti-nuclear antibody (ANA), anti-glomerular basement membrane (Anti-GBM), and rheumatoid factor should also be considered. (4) Serial pulmonary function testing can also help guide the clinician. Chronic DAH can cause restrictive changes.  Additionally, acute as well as chronic DAH can increase the diffusing capacity for carbon monoxide (DLCO). This is because blood in the alveoli can absorb carbon monoxide at a rapid rate. Both of these factors can be indirectly measured via pulmonary function tests, however both hemodynamic instability and patient cooperation can limit the value and reliability of these tests. (8)

Pearl: Transbronchial biopsy done concurrently with BAL is unlikely to help establish a diagnosis of DAH. (8)


Management of DAH has two goals. The first, which is more relevant for emergency medicine physicians, is to manage the airway, identify and stop any offending agent (s) if applicable, and administer immunosuppressive agents. The mainstay for moderate to severe DAH is methylprednisone (500-2000mg x 5 days IV followed by prednisone 1mg/kg PO) and cyclophosphamide (2mg/kg/day adjusted for renal function). The next goal is treating the specific underlying etiology. (1,8)

Pearl: Recent research shows that recombinant activated human factor VII is showing promise in treating DAH caused by ANCA-vasculitis and SLE, but further investigation must be done. (8)


  • DAH is a medical emergency characterized by bleeding of pulmonary microvasculature into the alveoli.
  • The clinical presentation is nonspecific – most commonly the patient will present with cough, dyspnea, fever, and hemoptysis. Though 33% will present without hemoptysis.
  • Cough, dyspnea, hemoptysis, and bronchoalveolar lavage (BAL) positive for RBCs is enough for a diagnosis
  • Consider the patient’s timeline of symptoms – acute hemorrhagic events are more likely to be caused by toxins than vasculitides.
  • Protecting the airway is the most important part of management. Then identify and stop the offending agent if possible and administer immunosuppressive
  • Mainstay for moderate to severe DAH is methylprednisone (500-2000mg x 5 days IV followed by prednisone 1mg/kg PO) and cyclophosphamide (2mg/kg/day adjusted for renal function)

References & Further Reading:

  1. Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Mosby/Elsevier; 2010
  2. Collard HR, Schwarz MI. Diffuse alveolar hemorrhage. Clin Chest Med 2004;25:583–592, vii.
  3. Nguyen T, Martin MK, Indrikovs AJ. Plasmapheresis for diffuse alveolar hemorrhage in a patient with Wegener’s Granulomatosis: case report and review of the literature. J Clin Apher 2005;20:230–
  4. Ioachimescu, O. C., and J. K. Stoller 2008 Diffuse alveolar hemorrhage: diagnosing it and finding the cause. Cleve Clin J Med 75(4):258, 260, 264-5 passim.
  5. Kissner, Dana G., et al.1987 Crack Lung: Pulmonary Disease Caused by Cocaine Abuse. American Review of Respiratory Disease 136(5):1250-1252.
  6. Park, Moo Suk 2013. Diffuse alveolar hemorrhage. Tuberculosis and respiratory diseases 74(4):151-162.
  7. Sogomonian, R., et al. 2015 Refractile foreign material deposits and alveolar hemorrhage in crack cocaine smoker. Respir Med Case Rep 16:48-50.
  8. uptodate.com
  9. http://lifeinthefastlane.com/ccc/diffuse-alveolar-haemorrhage/
  10. https://www.thieme-connect.com/products/ejournals/html/10.1055/s-2002-35552

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