Emergency Medicine Investigations

Diffuse Alveolar Hemorrhage Due to Synthetic Cannabinoid Inhalation

Mark H Adelman1*, Michael Thorp2, Young Im Lee3, Robert L Smith4

1NYU Langone Medical Center, New York

2Langone Medical Center, New York

3Mount Sinai Beth Israel Hospital, New York

4New York Harbor Healthcare System, New York

*Corresponding author: Mark H Adelman, NYU Langone Medical Center, 462 First Avenue, NBV 7N24, New York, USA.Tel: +12122636479; Email: mark.adelman2@nyumc.org

Received Date: 25 July, 2017; Accepted Date: 14 August, 2017; Published Date: 21 August, 2017

Citation: Adelman MH, Thorp M, Im Lee Y, Smith RL (2017) Diffuse Alveolar Hemorrhage Due to Synthetic Cannabinoid Inhalation. Emerg Med Inves: 153. DOI: 10.29011/2475-5605.000053


1. Introduction

Synthetic Cannabinoid Receptor Agonists (SCRAs, aka “K2” , “Spice,” and other street names) are an increasingly popular drug of abuse and are difficulto regulate as manufacturers alter formulations in an attempt to stay one step ahead of law enforcement [1]. Due to variablchemical compositions and more potent agonism of endogenous cannabinoid receptors than naturally occurring Δ(9)-tetrahydrocannabinol, clinical presentation is unpredictable and often far more severe than that of cannabis intoxication [2]Wreport the case of a 59-year-old man witdiffuse, bilateral pulmonary in filtrates after SCRA inhalation.

2. Case Presentation

A 59-year-old man with a history of cocaine, alcohol, and K2 abuse, Hepatitis Cand schizophrenia was admitted tthe Medical Intensive Care Unit (MICU) after a witnessed, generalized tonic-clonicseizure in the waitinroom of a psychiatry clinic. The patient admitted tusinK2 aleast three times in the days prior.

Initial vital signs in the emergency department were notable for a pulse oximetry (SpO2) reading of 86% on a non-rebreather mask. High-Flow Nasal Cannula(HFNC) was applied at 40Lpm, FiO2 of 80% and thSpO2 increased t94%. Initial venous blood gas revealed lactate of 21mmol/L, pH 6.9, pCO2 57mmHgand HCO3 of 10mmol/L, which later normalized and was attributed tthe seizure. The initial arterial pO2 was 50mmHgBasic metabolic panel waunremarkable. Ahepatic panel was notable for elevated alkaline phosphatase and elevated trasaminases. Complete blood count demonstrated white blood cell count of 17.4/µL with 63% lymphocytes, hemoglobin 15.3 g/dL and a normal platelet levelCoagulation panel wawithin normal limits. Serum ethanol level was undetectable and 5-panel urine drug screen wanegative. Achest X-ray showed diffuse, bilateral pulmonary parenchymalopacities (Figure1). Shortly after admission to thMICU the patient had a witnessed episode of small-volume hemoptysis.

Collateral information was obtained from an outside hospital where the patient had been admitted previously; thpatient had a seizure in the settinof K2 intoxication and then hemoptysis witdiffuse air space opacities on chest imaging (Figure 2). At the time of the priorseizure thpatient had a cardiac arrest requiring advanced cardiac life support and endotracheal intubation.Othe current presentation, the patient’s hypoxia stabilized with the use of HFNC and he had no further episodes of hemoptysis so bronchoscopy wadeferred.

Given the clinical and radiographic findings, thpatient was started empirically on methylprednisolone for presumed drug-induced Diffuse Alveolar Hemorrhage (DAH). By hospital datwo, thpatient waweaned from HFNC tlow-flow nasal cannula and was able to maintain appropriate oxygen saturation. Further work-up revealed negative antinucleaantibodies, normal erythrocyte sedimentation rate and complement levels, negative anti-glomerular basement membrane and anti-neutrophilcytoplasmic antibodies. He watransferred out of thMICU to thgeneral medicine floor and sub sequently tthe psychiatric service for inpatient treatment of schizophrenia and substance abuseOna presentation to thER some months later for aunrelated chief complaint, thpatient reported continued abstention from K2 and a chest X-ray showed resolution of thdiffuse airspace disease (Figure 3).

3. Discussion                                                                 

Our patient presented on two separate occasions with DAand seizures after inhalation of a SCRA. Two prior cases of DAassociated with SCRA inhalation have been reported. The reported toxic effects of SCRAs include many central nervous system, cardiovascularand pulmonary effects [1,2]. Some complications of SCRA abuse are thought to be dutvasospasm in the affected organs; cases of acute myocardial infarction awell as is chemic and hemorrhagic stroke have been reported in SCRA users, including younger patients without traditional cardiovascular risk factors [3,4]. Similarly, “Crack Lung” is a well-described complication of free-base cocaine inhalation witvariable manifestations that include DAH; while the underlying cause is not fully understood, proposed mechanisms of alveolar damage include the high temperature of volatilized cocaine and cocaine-induced vasoconstriction in pulmonary capillary beds [5]. Notably, our patient’s urine toxicology screen was negative for cocaine metabolites, thus “Crack Lung” is an unlikely cause of DAH in this case.

DAH secondary to SCRA use was first described in 2011 by Loschner, et al. in a 19-year-old man who presented with hemoptysis [6]. Their patient had bronchoscopic confirmation of DAand reported daily K2 use. The patient improved with mechanical ventilation and empiric methylprednisolone. Similarly, Alhadi and colleagues presented a case of a previously healthy chronic K2 user with diffuse, bilateral pulmonary infiltrates [7]. Bronchoscopy with serial bronchoalveolar lavage revealed bloody, non-clearing secretions. Achronic, lymphocytic in filtrate was seen on transbronchialbiopsy. The patient improved with mechanical ventilation and methylprednisolone; work-up of thalveolar hemorrhage was negative for infectious, malignant, rheumatologic or vasculitis-related etiologies. Furthermore, four SCRA compounds were detectable in the patient’s blood, urine orsaliva.

We were not able to confirthe presence of DAH bronchoscopicallyas our patient’s hypoxic respiratory failure improvewithout the need for endotracheal intubation and bronchoscopy wadeemed too high-risk. Howevergiven the patient’s clinical presentation and imaging findings, otherwise negative laboratory results, and dual temporal association with K2 use, it is most likely that this presentation represents another case of DAH secondary to inhaled SCRAs.

4. Conclusion

Our case highlights diffuse alveolarhemorrhage as are but important adverse effect of synthetic cannabinoid receptor agonistuse. As in other forms of drug-induced DAH, with drawal of the offending drug is likely the most important intervention. Howeveras the underlying mechanism remains unknown but may be inflammatory in nature, glucocorticoid therapyis a reasonabladjunct to supportive care for patients that present with hemoptysis and acute respiratory failure. The increasing prevalence of SCRA abuse underscores thurgent need to further characterize the cause of this potentially life-threatenincomplication.


Figure 1: ChestX-ray oAdmission with Diffuse Pulmonary Infiltrates.





Figure 2: Chest Cfrom Outside Hospital TwMonths Prior to Admission with Bilateral Airspace Consolidations and Ground Glass Opacities.




Figure 3: Chest X-ray Three Months after Admission with Resolution of Infiltrates.


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