Acute respiratory distress and hemoptysis: a case report of drug-induced lung injury aka “crack lung”
Case Report

Acute respiratory distress and hemoptysis: a case report of drug-induced lung injury aka “crack lung”

Manuel Reichert1 ORCID logo, Tobias Holtz2

1Department of Internal Medicine III, St. Bernward’s Hospital, Hildesheim, Lower Saxony, Germany; 2Department of Radiology, St. Bernward’s Hospital, Hildesheim, Lower Saxony, Germany

Contributions: (I) Conception and design: M Reichert; (II) Administrative support: M Reichert; (III) Provision of study materials or patients: Both authors; (IV) Collection and assembly of data: Both authors; (V) Data analysis and interpretation: Both authors; (VI) Manuscript writing: Both authors; (VII) Final approval of manuscript: Both authors.

Correspondence to: Manuel Reichert, BSc, MD. Department of Internal Medicine III, St. Bernward’s Hospital, Hildesheim, Lower Saxony, Germany; Medical Department II-Cardiology and Intensive Care Medicine, City Hospital (Städtisches Krankenhaus), Salzdahlumer Straße 92, 38118 Braunschweig, Lower Saxony, Germany. Email: sci.reichert@mailbox.org.

Background: With the increasing use of inhaled drugs such as cocaine and amphetamines, drug-induced lung injury has become a relevant condition in emergency settings. “Crack lung” is a well-documented, acute pulmonary syndrome associated with inhalation of cocaine, characterized by respiratory distress, hemoptysis, and various radiographic findings. While the syndrome is more common among younger individuals, it can present in older patients, often triggered by the acute use of inhalative drugs.

Case Description: A 60-year-old obese male with no significant history of lung or cardiac disease presented to the emergency department with sudden-onset dyspnea, severe hemoptysis, palpitations, and tachycardia. Vital signs indicated hypertension (180/110 mmHg) and hypoxia [peripheral capillary oxygen saturation (SpO2) of 80% on room air]. The electrocardiogram (ECG) revealed sinus tachycardia but no right bundle branch block (RBBB). Laboratory tests were mostly unremarkable, and a computed tomography (CT) scan ruled out pulmonary embolism but showed diffuse bronchial wall thickening consistent with bronchitis or atypical pneumonia. During the clinical interview, the patient admitted to recent use of inhaled cocaine and amphetamines, leading to the diagnosis of early-stage “crack lung”. After stabilization by administration of oxygen, bronchodilatators and prednisolone, the patient was discharged with follow-up care focusing on cessation of drug use and monitoring for potential lung damage. Bronchoscopically, there was no evidence of another cause of hemorrhage such as tumor growth.

Conclusions: This case highlights the importance of recognizing drug-induced lung injury in patients presenting with acute respiratory distress and hemoptysis. As the use of inhaled drugs such as cocaine continues to rise in Germany, awareness of conditions like “crack lung” is essential for timely diagnosis and management. Steroids may play a role in reducing inflammation, but further research is needed to establish standardized treatment protocols for this condition.

Keywords: Case report; crack lung; drug-induced lung injury; hemoptysis; respiratory distress


Received: 19 December 2024; Accepted: 05 March 2025; Published online: 02 July 2025.

doi: 10.21037/acr-24-283


Highlight box

Key findings

• We here present a case of a 60-year-old obese male with no significant lung or cardiac history presented with acute dyspnea, hemoptysis, and tachycardia. Computed tomography (CT) ruled out the initial suspicion of pulmonary embolism (PE). Instead, diffuse bronchial wall thickening, consistent with bronchitis or atypical pneumonia, was found. Later the patient admitted to having smoked a mixture of crack cocaine and amphetamine.

What is known and what is new?

• “Crack lung” is a recognized syndrome caused by inhalative cocaine inhalation, typically characterized by respiratory distress, hemoptysis, and bronchial inflammation. There is no evidence regarding standardized therapy strategies. Treatment focuses mostly on supportive care. However, systemic corticosteroid is often discussed to reduce inflammatory damage of the lungs.

• This manuscript adds another case of drug-induced lung damage, emphasizing the importance of differential diagnostic thinking. Furthermore, it becomes clear once again that, particularly with increasing case numbers of this disease, randomized studies on therapy recommendations, especially regarding the potential benefits of corticosteroids, are urgently needed.

What is the implication, and what should change now?

• The symptom complex of hemoptysis, dyspnea, and tachycardia strongly suggests PE or bronchial carcinoma but inhalation use of illicit substances should always be considered.

• This applies not only to young patients. The importance of a targeted medical history is highlighted here.

• The application of corticosteroids is discussed, but randomized studies are needed to further investigate their potential benefit. Until then, it remains an individual decision.


Introduction

Acute respiratory distress and hemoptysis can be symptomatic of various severe pulmonary conditions, the most dangerous being pulmonary embolism (PE). Dyspnea due to pulmonary injury based on inhalation of toxic agents is an important differential diagnosis in an emergency. Amongst others, the rising number of patients presenting airway affection by consumption of drugs such as cocaine, heroin and nitrous oxide (NO2) in Europe in general and Germany in particular leads to an inevitable consideration of those etiologies of dyspnea in the emergency department (ED) (1,2). Here, we describe a case of a 60-year-old male with acute dyspnea, hemoptysis and tachycardia upon inhalative cocaine and amphetamine consumption. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-24-283/rc).


Case presentation

A 60-year-old, obese male was presented to the ED at 2 a.m. with sudden onset of dyspnea, severe hemoptysis, palpitations, and tachycardia. The patient had no significant past medical history of lung or cardiac disease, recent trauma, surgery, or thromboembolic events. Well’s Score for PE (3) was 5.5 points, the revised Geneva Score (4) was 8 points, and the PE rule-out criteria (PERC) (5) was not fulfilled.

Vital signs on arrival were:

  • Heart rate: 110 bpm;
  • Blood pressure: 180/110 mmHg;
  • Respiratory rate: 22/min;
  • Peripheral capillary oxygen saturation (SpO2): 80% on room air, improving to 88% with 4 L/min of supplemental O2;
  • Temperature: 36.8 ℃.

Arterial blood gas (ABG):

  • pH 7.368, partial pressure of carbon dioxide (pCO2) 39.0 mmHg, partial pressure of oxygen (pO2) 61.2 mmHg, haemoglobin (Hb) 15.6 g/dL, oxygen saturation (sO2) 92.1%;
  • Electrolytes: potassium 3.9 mmol/L, sodium 142 mmol/L, calcium 1.23 mmol/L, chloride 110 mmol/L;
  • Glucose: 87 mg/dL, lactate 0.7 mmol/L;
  • Base excess: −2.9 mmol/L;
  • HCO3: 22.1 mmol/L.

The electrocardiogram showed sinus tachycardia at 110 bpm, a right bundle branch block (RBBB) was not seen and no ST-segment elevation or depression was detected (Figure 1). Transthoracic echocardiography showed no right ventricle dilatation, D-Sign or McConell’s sign and no wall motion abnormalities. Laboratory tests revealed a slightly elevated white blood cell count (11.5×103/µL) and slightly elevated creatinine levels with a reduced GFR (73 mL/min). No other lab abnormalities were found.

Figure 1 12-lead ECG showed sinus tachycardia without signs of right heart strain (no SIQIII pattern, no right bundle branch block), no ERS or acute ischemic signs. ECG, electrocardiogram; ERS, early repolarization syndrome.

Due to the primary high probability of PE, a CT pulmonary angiogram was performed immediately (Figure 2). Surprisingly, there was no evidence of a thromboembolism. However, the scan revealed diffuse infiltrative changes with thickened bronchial walls, consistent with bronchitis or atypical pneumonia. No tumor, pneumothorax or bone fractures were detectable. Being further interviewed in detail, the patient admitted having inhaled “free base”, a mixture of cocaine and amphetamine, right before symptoms started.

Figure 2 Computed tomography scan shows bipulmonary alveolar densities primarily in the central zones with noticeable sparing of the subpleural space. Accentuated thickening of the bronchial walls (red arrow).

The patient received a Bolus of 20 mg prednisolone, and inhalative salbutamol in the ED and was admitted to the medical ward.

Following, a flexible bronchoscopy was performed (Figure 3). This revealed a massive diffuse oozing hemorrhage in both bronchial systems from the deep subsegments, primarily the left lower lobe and the right upper lobe. Hemostasis was achieved using 1 x 10 adrenaline in each, resulting in effective bleeding control. Additionally, samples were taken for microbiological examination. An infection could not be detected.

Figure 3 Bronchoscopy revealed a massive diffuse hemorrhage in both bronchial systems from the deep subsegments, primarily the left lower lobe and the right upper lobe.

During the hospital stay, a chest X-ray was also performed, but no relevant pathologies were found.

Taken together, this case shows a monogenic, relevant pulmonary bleeding due to inhalative noxa inhalation, i.e., cocaine and amphetamine.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Oral informed consent was obtained from the patient, witnessed by ED team members (two nurses and one medical intern/final-year medical student) for the publication of this case report and accompanying images. Due to the patient’s early discharge, the ED team failed to obtain written informed consent.


Discussion

By far, the most common cause of the symptom complex consisting of shortness of breath, hemoptysis, and sinus tachycardia is PE (6). Clinical scores estimating the probability have been established for a long time (3-5). Medical professionals working in emergency departments have been aware of this disease for decades. Nevertheless, it remains essential to approach each individual case with differential diagnostic thinking, regardless of the clinical probability of an underlying cause.

The case presented here stresses the importance of thinking outside the box. Although the symptoms and clinical signs presented here highly suggest PE, initiating the corresponding therapy i.e., anticoagulation could have worsened the later found pulmonary hemorrhage. Earlier studies have already described the clinical presentation and radiological findings of patients suffering from “crack lung” (7-10). Considering the rising incidence of inhalation drug use in the USA and Europe stresses the need for awareness of those etiologies of lung injury in the ED (1,2).

Current guidelines for both disciplines, Emergency Medicine and Pulmonology, lack therapeutic recommendations. Steroid therapy may help in reducing inflammation and improving symptoms, though its role should be individualized based on clinical response. To our knowledge, no studies on the effects of steroids in the management of “crack lung” have been executed, although this supportive therapy is discussed regularly on this topic. This should be performed in the future. We performed data research using both, a “classic” PubMed/ Google Scholar and an AI search. However, we could find neither broad nor current evidence of acute therapy strategies. Most literature is based on case reports such as this article. The existing data commenting in particular on corticosteroids is based on older articles (11-13) or in vitro/animal models (14). Some case reports stated clinical and radiological improvement upon administration of methylprednisolone or prednisolone (15,16). An existing UpToDate article confirmed the lack of data regarding “crack lung” (17). Therefore, evidence on the topic is quite sparse. Taking into account the previously mentioned increasing incidence (1,2), systematic randomized controlled trials (RCTs) are necessary but difficult to perform due to the previously rather rare presentation in the emergency departments.

Regarding long-term prognosis, Vidyasankar et al. presented a 10-year follow-up of a 48-year-old female with continued inhalative cocaine consumption (18). Over the observed period, the lung damage progressed severely. In our search, we found no more long-term observations of such patients.

Nonetheless, in any case of hemoptysis, bronchoscopy is inevitable to exclude neoplastic or infectious causes such as tuberculosis.


Conclusions

This case highlights the importance of considering drug-induced lung injury, such as “crack lung” in patients presenting with acute respiratory distress, hemoptysis, and tachycardia, especially in the context of recent inhalation of illicit substances. Even though conditions like pulmonary embolism or bronchial carcinoma are more commonly suspected, inhaled drugs like cocaine and amphetamines can cause significant pulmonary damage in both young and older patients. A thorough medical history and prompt differential diagnosis are crucial for appropriate management. Further research is needed to establish standardized treatment protocols, including the role of corticosteroids in reducing inflammation.


Acknowledgments

None.


Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-24-283/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-24-283/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-24-283/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Oral informed consent was obtained from the patient, witnessed by ED team members (two nurses and one medical intern/final-year medical student) for the publication of this case report and accompanying images. Due to the patient’s early discharge, the ED team failed to obtain written informed consent.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.


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doi: 10.21037/acr-24-283
Cite this article as: Reichert M, Holtz T. Acute respiratory distress and hemoptysis: a case report of drug-induced lung injury aka “crack lung”. AME Case Rep 2025;9:81.

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