Bailey et al.1 examined the lungs of dead cocaine abusers and found the most common pulmonary findings were pulmonary congestion (88%), edema (77%), and acute/chronic alveolar hemorrhage (71%). These findings have been also reported by Murray et al.2-3 found hemosiderin-laden macrophages in 35% (7/20) of the victims of cocaine intoxication and opined that occult alveolar hemorrhage occurs more frequently in cocaine users than is clinically recognized. They also noted pulmonary artery medial hypertrophy in 20% (4/20) of these cocaine abusers who had no histologic evidence of foreign material embolization. The cause of the alveolar hemorrhage was thought to be ischemic damage to the capillary endot-helium from constriction of the pulmonary vascular bed after cocaine inhalation, or as a direct toxic effect of cocaine on the capillary endothelium. Neither hypothesis is proven. Hemosiderin-laden macrophages may be seen in bronchoalveolar lavage fluid or in bronchoscopy biopsy specimens. One cocaine abuser who presented with diffuse alveolar hemorrhage had no vasculitis. Electron microscopy did not demonstrate any disruption in the alveolar or capillary basement membranes.3 Pulmonary hemorrhage has not only been associated with alkaloidal
Figure 2.3.1 Abundant blood-tinged foam escapes from the end of the endotrachial tube in this drug abuser with pulmonary edema.
"crack" cocaine smoking, but also with intravenous and nasal routes4 of administration. Pulmonary congestion in fatal cocaine intoxication is usually caused by the slow cessation of cardiac function associated with brain stem hypoxia during seizures or direct cocaine toxicity.
Fatal and non-fatal pulmonary edema (Figure 2.3.1) has been reported in cocaine smokers without obvious cardiac or central nervous system disease.5-8 Some of these patients had resolution of the pulmonary edema without specific treatment and chest radiographs have shown normal cardiac silhouettes. No reports have shown any hemodynamic data from these patients with pulmonary edema. One patient underwent bronchoalveolar lavage and had an elevated protein level (4x normal) suggesting that the edema was due to altered alveolar capillary permeability.7 Bronchial biopsy usually revealed no histologic abnormalities7 or only "mild interstitial inflammatory changes".8
Pneumonitis, as defined by widening of the alveolar septae with a polymorphous infiltrate (lymphocytes, neutrophils, macrophages, eosinophils) or fibrosis, was seen in one fourth of the victims studied by Bailey et al.1 Patel et al.9 describe a patient with broncholitis obliterans and organizing pneumonia (BOOP) associated with regular free-base use in the weeks prior to the onset of clinical symptoms (non-productive cough, fever, dyspnea). An open lung biopsy demonstrated patchy bronchocentric interstitial and intra-alveolar chronic inflammation (lymphocytes, macrophages, and few polymorphonuclear leukocytes and eosinphils) with granulation tissue and collagen occupying bronchioles and adjacent alveolar ducts. The blood vessels were normal. A hypersensitivity reaction to cocaine or an adulterant was the presumed cause. This mechanism also presumably causes "crack lung", a clinical syndrome with chest pain, hemoptysis, and diffuse alveolar infiltrates associated with smoking "crack" cocaine.10-11 Finally, 11% of the cocaine fatalities had polarizable material, usually talc, within the lungs. Most of these victims were, not unexpectedly, intravenous drug abusers.
Cocaine users who smoked cocaine free base or "crack" may forcefully blow smoke into another user's mouth to augment the drug's effect. Smokers also prolong the Valsalva maneuver to avoid expiring the precious cocaine smoke. The resulting increased intra-alveolar pressure ruptures the alveolar walls, allowing air to dissect along the perivascular tissues into the mediastinum and surrounding cavities. These mechanisms have produced various forms of barotrauma including pneumothorax, pneumo-mediastinum,12-14 pneumopericardium,15 pneu-moperitoneum,16 and subcutaneous emphysema. In the few cases,17 where the duration of cocaine use prior to clinical symptoms was accurately known, patients freebased cocaine for 8 to 12 hours and snorted cocaine for 1 to 2 hours. The clinical course of cocaine-associated barotrauma is generally non- fatal. This barotrauma is not specific for cocaine smokers and has been described in marijuana smokers.18
Smoking cocaine can cause acute severe exacerbation of asthma in chronic asthmatics.19,20 Insufflation of cocaine hydrochloride has also been associated with near-fatal status asthmaticus.21 Blackened sputum and pulmonary cytologic specimens with excessive carbonaceous material
have been associated with crack cocaine use.22 This is most likely from inhalation of nonvolatilized impurities when crack and its tarry residue are smoked: As crack is smoked, a dark, tarry residue forms on the inside of the pipe's bowl and barrel. Many smokers consider this residue to be concentrated cocaine and they scrape it free, reheat it, and vigorously inhale it.
The long-term pulmonary effects and pathology of smoking cocaine are unknown. Pulmonary function studies are confounded by the fact that cocaine smokers also smoke tobacco and marijuana in addition to cocaine. Cocaine smokers have a reduced diffusing capacity of carbon monoxide, but no spirometric abnormalities have been demonstrated.23
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.