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 difficult to
regulate as manufacturers
alter formulations in
an attempt to stay one
step ahead of law enforcement [1]. Due
to variable chemical 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]. We report the case of a 59-year-old
man with diffuse,
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 C, and schizophrenia was
admitted to the Medical Intensive Care Unit (MICU) after
a witnessed, generalized tonic-clonicseizure in the waiting room of a psychiatry clinic. The patient admitted to using K2 at least 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 the SpO2 increased to 94%. Initial venous blood
gas revealed lactate of 21mmol/L, pH 6.9, pCO2
57mmHg, and HCO3 of
10mmol/L, which
later normalized and was attributed to the seizure. The
initial arterial pO2 was 50mmHg. Basic
metabolic panel was unremarkable. 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 level. Coagulation
panel was within normal limits. Serum ethanol level was undetectable and 5-panel urine drug screen was negative. Achest X-ray showed diffuse, bilateral pulmonary parenchymalopacities (Figure1). Shortly after
admission
to the MICU 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; the patient had a seizure in the setting of
K2 intoxication and then
hemoptysis with diffuse
air space opacities on chest imaging (Figure
2). At the time of the priorseizure
the patient had a cardiac arrest requiring advanced cardiac
life support and endotracheal intubation.On the current
presentation, the patient’s hypoxia stabilized with the use
of HFNC and he had no further episodes of hemoptysis so bronchoscopy was deferred.
Given the clinical and radiographic
findings, the patient was started
empirically on methylprednisolone for
presumed drug-induced
Diffuse Alveolar Hemorrhage
(DAH). By hospital day two, the patient was weaned from HFNC to low-flow nasal
cannula and was able to maintain appropriate oxygen saturation. Further work-up revealed negative antinuclear antibodies, normal erythrocyte
sedimentation rate and complement levels,
negative anti-glomerular basement membrane and anti-neutrophilcytoplasmic antibodies. He was transferred
out of the MICU
to the general medicine floor and sub sequently to the
psychiatric service for
inpatient treatment
of schizophrenia and substance abuse. Ona presentation to
the ER some months later for an unrelated
chief
complaint, the patient reported
continued abstention from K2 and
a chest X-ray showed resolution of the diffuse airspace disease (Figure 3).
3. Discussion
Our patient presented
on two separate occasions with
DAH and seizures after inhalation
of a SCRA. Two prior
cases of DAH associated with SCRA inhalation have
been reported. The reported toxic
effects of SCRAs include
many central nervous
system, cardiovascular, and
pulmonary effects [1,2]. Some
complications of SCRA abuse
are thought to be due to vasospasm in the affected organs;
cases of acute myocardial
infarction as well 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 with variable 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 DAH and
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 the alveolar 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 confirm the presence
of DAH bronchoscopicallyas our patient’s hypoxic respiratory failure improved without the need for endotracheal intubation and bronchoscopy was deemed
too high-risk. However, given 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
Figure 1: ChestX-ray
on Admission with Diffuse Pulmonary Infiltrates.
Figure 2: Chest CT from Outside Hospital Two Months 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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