The authors present cases of two Emergency Department patients who presented with cocaine-related
pneumomediastinum. These cases illustrate the diagnostic examinations necessary to confirm the diagnosis,
so appropriate monitoring and management can be initiated.
Dr. Mangi is a Resident in the Department of Surgery and
Dr. Mullins is a Resident in the Department of Radiology at the
Massachusetts General Hospital. Both are also Officers at
Harvard Medical School. Dr. McLoud is staff radiologist at the
Massachusetts General Hospital and Professor of Radiology at
Harvard Medical School, Boston, MA.
The inhalation of alkaloid cocaine (free-basing, mixing the
solid cocaine salt with a solvent to render it "smokeable") is a
recent phenomenon that surged in popularity among recreational drug
users in the early 1980s because of its relatively low cost and
easy availability. The earliest report of pulmonary complications
related to free-basing cocaine was in 1981.
Several additional reports of pneumothorax, pneumomediastinum, and
pneumoperitoneum were documented in the 1980s.
Retropharyngeal emphysema has also been described in association
with cocaine free-basing.
There have been only two case reports in the past 9 years, however,
which may be due to decreased use of the substance.
In 1999, the authors evaluated two patients in the Emergency
Department (ED) of Massachusetts General Hospital with
cocaine-related pneumomediastinum. Both were young males, who had
recently used free-based cocaine. They presented several hours
thereafter with subcutaneous emphysema, pneumomediastinum, and
leukocytosis. The purpose of this report is to re-emphasize the
clinical presentation, evaluation, and management of this
Patients and methods
Two patients presented to the ED and were subsequently admitted
to the General Surgical and Medical Services for observation. The
patients were interviewed directly by one of the authors (surgery
housestaff), and the radiological and medical records were reviewed
by two of the authors (radiology and surgery housestaff). All
authors reviewed radiographic images.
Patient number one
A previously healthy 24-year-old man developed sudden pain in
the back of his neck followed by violent coughing after inhaling
free-based cocaine. He subsequently noted right facial and neck
swelling accompanied by mild substernal chest discomfort,
aggravated by coughing and deep breathing. Following 8 hours of
sleep, he awoke with extensive swelling over his entire face and
anterior chest wall. He initially presented to a community hospital
and then transferred to the ED of our institution.
History revealed that he was otherwise healthy, did not take any
medications and had no known allergies to drugs. On physical
examination, he did not appear to be in any distress, his heart
rate was 85 beats per minute (bpm) with a blood pressure of 160/100
mm Hg, and an blood oxygen saturation of 100% on room air. There
was extensive subcutaneous air in his cheeks, neck, and upper
chest. There was no cardiac rub on auscultation. The patient was
able to swallow and no cough was observed. A white blood cell (WBC)
count of 16,700 had been recorded at the outside facility and had
increased to 18,200 upon presentation to our ED several hours
A chest radiograph revealed an extensive pneumomediastinum. A
contrast-enhanced chest CT was performed, which excluded
mediastinal fluid collection, pneumothorax, pleural effusion, and
pneumoperitoneum (figure 1). Mediastinal air was noted to involve
the deep fascial layers of the neck and chest, and surrounded the
great vessels in
the mediastinum. Gastrografin swallow, followed by a barium
not demonstrate any evidence of esophageal tear. The patient was
admitted to the hospital and observed overnight. The subcutaneous
air resolved, and his WBC count fell to 11,700 the following
morning. He was then discharged.
Patient number two
A previously healthy 19-year-old man inhaled free-based cocaine,
and while bearing down after inhaling the drug, felt a "pop" in his
chest. He subsequently developed constant pleuritic and substernal
chest pain. He proceeded to inhale cocaine once more, and then
attempted to sleep. Upon awakening, his chest pain had worsened,
and he sought medical attention at the ED. The patient's past
medical history was remarkable for a congenital atrial septal
defect. He did not take any prescription medications and had no
known drug allergies.
On examination, the patient was in no apparent distress and was
afebrile. The heart rate was 70 bpm, his blood pressure was 110/80
mm Hg, and the room air arterial blood oxygen saturation was 94%. A
pericardial rub was noted on auscultation. There was no evidence of
subcutaneous emphysema. His WBC count was 15,100.
A CT scan revealed a pneumomediastinum (figure 2A), which was
confirmed on contrast-enhanced chest CT (figure 2B). Mediastinal
air was noted to extend into the soft tissues of the neck. There
was no pleural effusion, pneumothorax, or pneumoperitoneum. A
gastrografin swallow was normal. An echocardiogram showed no
evidence of cardiac tamponade physiology. The patient was admitted
to the medical service. Prior to discharge, his WBC count fell to
6,700. The patient was followed with serial chest radiography that
documented decrease in the pneumomediastinum. He was discharged
with uneventful follow-up.
Mediastinal emphysema may be an ominous finding, suggestive of
either traumatic or spontaneous exertional
tracheobronchial or esophageal disruption. Extrapleural tears of
the central major bronchi or distal trachea may occur after severe
blunt trauma leading to a pneumomediastinum. Disruption of the
esophagus either from instrumentation and balloon dilatation or
following violent vomiting (Boerhaave's syndrome) also produces
mediastinal emphysema. "Spontaneous" pneumomediastinum usually
occurs following a sudden or prolonged increase in intrathoracic
pressure (for example, Valsalva maneuver, status asthmaticus, and
barotrauma from mechanical ventilation). The mechanism involves the
rupture of alveoli within the lung parenchyma with subsequent
dissection of air centrally along the bronchovascular bundles to
the hila (interstitial emphysema) and rupture into the mediastinum.
Mediastinal emphysema following crack cocaine inhalation is due to
the latter mechanism.
Pneumomediastinum reported in the setting of free-based cocaine
use is thought to develop as the patient performs a Valsalva
maneuver in order to intensify the euphoria. The resultant increase
in intrathoracic pressure is transmitted to the alveoli, which
subsequently rupture, thereby resulting in pneumomediastinum.
Mediastinal air then dissects into the planes of least resistance,
resulting in cervical subcutaneous emphysema and, occasionally,
pneumoperitoneum. Pneumothorax is unlikely as the air tracks
centrally along the bronchovascular bundles. True pneumopericardium
is uncommon and usually occurs as a result of iatrogenic
instrumentation. Pseudopneumopericardium may be effected by
adjacent air in the fascial planes of the mediastinum.
Patients who develop subcutaneous emphysema and
pneumomediastinum in the setting of cocaine inhalation appear
relatively well, despite the impressive amounts of air that are
seen in the mediastinum and cervical soft tissues. Dyspnea is rare
but intermittent pleuritic substernal chest discomfort and sudden
onset of facial and neck swelling are very frequent. Moderate
leukocytosis is common, likely secondary to the sympathomimetic
effects of the cocaine.
There is usually no history of chest trauma or a history of
antecedent vomiting, but a history of illicit drug use is often
difficult to obtain. Physical examination reveals neck and upper
torso subcutaneous emphysema without other findings. Patients are
most often hemodynamically stable.
The presence of mediastinal air on standard chest radiographs in
the absence of a history of other etiologic factors should raise
suspicion of free-based cocaine use. Extensive subcutaneous air may
obscure a pneumomediastinum and a CT may be confirmatory.
Typically, thoracic CT is performed to evaluate mediastinal fluid
collections or hematoma, possible tamponade of the heart or
vessels, or small pneumothoraces not appreciated on the chest
radiograph. In most cases, neck CT would not change management.
Echocardiography is recommended if suspicion for tamponade
physiology is raised by the clinical evaluation. In the right
clinical setting, a gastrografin swallow may be necessary to
exclude an esophageal tear in patients who may be intoxicated and
whose history is therefore unreliable.
In the acute setting, the patient should be monitored with
standard pulse oximetry, cardiac monitoring, and electrocardiogram.
Management consists of close observation. The leukocytosis
typically resolves quickly, and the pneumomediastinum and
subcutaneous emphysema will also quickly resolve without residual
effects. The rapid and early institution of drug counseling cannot
be overemphasized. AR
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