EM@3AM: Crack Lung

Author: Holly Conger, MD (EM Resident Physician, UT Southwestern Medical Center, Dallas, TX) // Reviewed by: James Dazhe Cao, MD (@JamesCaoMD, Associate Professor of EM, Medical Toxicology, UT Southwestern Medical Center, Dallas, TX); Alex Koyfman, MD (@EMHighAK); and Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 45-year-old male with a history of cocaine use presents to the emergency department (ED) complaining of one day of worsening shortness of breath, cough, and fever. He is coughing up sputum streaked with blood. He endorses smoking crack cocaine the night before his symptoms started but denies injecting, using other drug use, or vaping.

Vital signs include blood pressure 152/86 mmHg, heart rate 110 beats per minute, temperature 38°C, respiratory rate 23, oxygen saturation 86% on room air. Exam reveals a man in moderate respiratory distress. He has no signs or symptoms of hypervolemia. Chest x-ray (CXR) demonstrates diffuse alveolar infiltrates bilaterally. Computed tomography (CT) chest demonstrates diffuse ground glass opacities bilaterally that spare the periphery and is negative for pulmonary embolism (PE) or aortic dissection.

Question: What is the most likely diagnosis?

Answer: Crack lung


  • 20 million people worldwide are estimated to have used cocaine at least once between the ages of 15-641
  • Cocaine can be used in the salt or base form
    • Cocaine salt can be injected, snorted, or absorbed across any mucus membrane
    • Cocaine base, or “crack” cocaine, can be smoked1-3
  • “Crack Lung” refers to the acute pulmonary injury associated with smoking crack cocaine



  • Acute pulmonary syndrome that occurs after inhaling freebase cocaine
  • Exact etiology of crack lung remains unclear1
  • Hemorrhagic alveolitis and diffuse alveolar injury may result from direct cellular toxicity from cocaine and/or contaminants, inflammatory reaction, thermal injury, barotrauma, and vasospasm leading to ischemia4,5
  • Vasospasm can lead to ventilation/perfusion mismatch similar in presentation to a PE6
  • Crack lung is occasionally associated with peripheral and pulmonary eosinophilia1,3,5
  • Indistinguishable from alveolar hemorrhage, hypersensitivity pneumonitis, and eosinophilic disease radiologically but rapidly resolves after cocaine cessation

Clinical Presentation:

  • Lung injury occurs within 48 hours of smoking crack cocaine
  • Symptoms are due to an inflammatory reaction and diffuse alveolar injury
  • Imaging demonstrates diffuse alveolar infiltrates, ground glass opacities that spare the periphery, and alveolar/interstitial edema3-8, 10
  • Most commonly presents with dyspnea
  • Other common symptoms include:
    • Back pain
    • Chest pain
    • Cough
    • Fever
    • Hemoptysis
    • Hypoxia
    • Tachypnea
  • May present with signs of acute cocaine intoxication
    • Agitation
    • Anxiety
    • Cardiac dysrhythmias
    • Dilated pupils
    • Hypertension
    • Psychosis
    • Tachycardia


  • Hypoxia with progression to respiratory failure and acute respiratory distress syndrome (ARDS)
  • Pneumothorax or pneumomediastinum from barotrauma during smoking or after due to lung damage, increased risk with Valsalva after smoking9
Figure 1: Chest x-ray from patient with crack lung (source: https://radiopaedia.org/articles/crack-lung?lang=us)


Figure 2: CT chest from patient with crack lung
(Source: https://www.rcpjournals.org/content/clinmedicine/17/2/186)


  • Most evaluation focused on ruling out other causes of similar symptoms
  • Social history: crack cocaine use, specifically looking for smoking as the route of administration, use of other intoxicants or illegal substances common with cocaine use
  • History and physical to determine if heart failure or hypervolemia possible etiology for respiratory distress (may be used in conjunction with brain natriuretic peptide)
  • CBC – evaluate for signs of infection or hemorrhage
  • EKG – look for signs of cardiac toxicity or ischemia from the cocaine use
  • CXR – evaluate the pattern of lung injury and look for possible focal consolidations
  • Chest CT or CT Angiogram – consider in patients with undifferentiated cause of respiratory distress or concern for possible PE based on history, exam, and risk factors
  • Infectious disease evaluation – only in patients with concern for possible infectious etiology to guide antimicrobial treatment
  • Urine drug screen for cocaine
    • Do note that urine cocaine immunoassay detects a cocaine metabolite, benzoylecgonine
    • Reflects recent use and may not indicate active intoxication


  • Acute coronary syndrome
  • Acute eosinophilic pneumonia
  • ARDS
  • Diffuse alveolar hemorrhage
  • E-cigarette and vaping product associated lung injury (EVALI)
  • Pneumonia, especially atypical infections such as legionella or tuberculosis
  • Pulmonary embolism
  • Heart failure
  • Septic embolism


  • Mainstay of treatment is maintaining adequate oxygenation throughout duration of symptoms
    • Similar to treatment of other causes of ARDS
    • May require supplemental oxygen, ventilatory support, intubation for respiratory failure
  • Judicious use of fluids to reduce edema formation
  • Broad-spectrum antibiotics are usually initiated until infectious etiologies are ruled out
  • Limited evidence supporting use of steroids in crack lung but may be of benefit when used in acute eosinophilic pneumonia11
    • Bronchoalveolar lavage fluid will demonstrate >25% eosinophils1,3,4,11
    • Steroids may worsen some infectious etiologies, so withhold steroids if infection remains high on the differential


  • Determined by degree of respiratory compromise versus failure
    • Patients requiring low rates of supplemental oxygen may be stable for admission to the floor
    • Patients requiring intubation or non-invasive ventilatory support at risk of decompensating may require intensive care unit or step-down unit level care
  • Patients may be discharged with follow up and resources for substance use disorder treatment after symptoms resolve
    • Patients should be counselled on the risk of developing chronic pulmonary toxicity with continued use of crack cocaine5,7,8


Clinical Pearls:

  • Crack cocaine is the free base form of cocaine that can be smoked and can result in diffuse alveolar injury, inflammation, and hemorrhage termed “crack lung”
  • Patients with present within 48 hours of crack cocaine use and have signs and symptoms most commonly including some of the following: chest pain, cough, dyspnea, fever, hemoptysis, hypoxia, and tachypnea
  • Evaluation should include investigation for alternative causes of ARDS and other symptoms in addition to gathering drug use history if possible
  • Management focuses on supportive care, particularly maintaining adequate oxygenation throughout the duration of the symptoms, ranging from supplemental oxygen to intubation


  1. Smollin CG, Hoffman RS. Cocaine. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw Hill; 2019. Accessed August 13, 2022. https://accesspharmacy-mhmedical-com.foyer.swmed.edu/content.aspx?bookid=2569&sectionid=210259752
  2. Greenberg, A., Stammers, K., Moonsie, I., & José, R. J. (2017). Image of the month: All puffed out – a case of crack lung. Clinical Medicine17(2), 186–187. https://doi.org/10.7861/clinmedicine.17-2-186
  3. Almeida, R. R., Zanetti, G., Souza, A. S., Jr, Souza, L. S., Silva, J. L., Escuissato, D. L., Irion, K. L., Mançano, A. D., Nobre, L. F., Hochhegger, B., & Marchiori, E. (2015). Cocaine-induced pulmonary changes: HRCT findings. Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia41(4), 323–330. https://doi.org/10.1590/S1806-37132015000000025
  4. Haim, D. Y., Lippmann, M. L., Goldberg, S. K., & Walkenstein, M. D. (1995). The Pulmonary Complications of Crack Cocaine. Chest107(1), 233–240. https://doi.org/10.1378/chest.107.1.233
  5. Hagan, I. G., & Burney, K. (2007). Radiology of recreational drug abuse. Radiographics : a review publication of the Radiological Society of North America, Inc, 27(4), 919–940. https://doi.org/10.1148/rg.274065103
  6. Ramachandaran, S., Khan, A. U., Dadaparvar, S., & Sherman, M. S. (2004). Inhalation of Crack Cocaine Can Mimic Pulmonary Embolism. Clinical Nuclear Medicine29(11), 756–757. https://doi.org/10.1097/00003072-200411000-00028
  7. Richards, J. R., & Le, J. K. (2020). Cocaine Toxicity. Retrieved from PubMed website: https://www.ncbi.nlm.nih.gov/books/NBK430976/
  8. Zimmerman, J. L. (2012). Cocaine intoxication. Critical Care Clinics28(4), 517–526. https://doi.org/10.1016/j.ccc.2012.07.003
  9. Maeder, M., & Ullmer, E. (2003). Pneumomediastinum and Bilateral Pneumothorax as a Complication of Cocaine Smoking. Respiration70(4), 407–407. https://doi.org/10.1159/000072905
  10. Restrepo, C. S., Carrillo, J. A., Martínez, S., Ojeda, P., Rivera, A. L., & Hatta, A. (2007). Pulmonary Complications from Cocaine and Cocaine-based Substances: Imaging Manifestations. RadioGraphics27(4), 941–956. https://doi.org/10.1148/rg.274065144
  11. Forrester, J. M., Steele, A. W., Waldron, J. A., & Parsons, P. E. (1990). Crack lung: an acute pulmonary syndrome with a spectrum of clinical and histopathologic findings. The American review of respiratory disease142(2), 462–467. https://doi.org/10.1164/ajrccm/142.2.462

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