CRACK LUNG (2013)
White blood cells stuffed with products of combustion fill the lungs of a chronic user of crack cocaine.
“Complications of chronic substance abuse” is a phrase that appears with relative frequency on death certificates. While the short-term risks of alcohol abuse or the use of illicit drugs are well-documented, the effects of chronic substance abuse on an individual’s health receive far less press. A negative post- mortem toxicology report does not negate the pathological effects of years of substance abuse. The ravages of long-term drug abuse are easily seen at high magnification. Some presentations are so striking as to have earned themselves a moniker – in this case, “crack lung”. Crack lung is a syndrome of lung damage marked by the presence of macrophages (white blood cells adapted to engulf and destroy bacteria, dead or dying cells, cellular debris, and foreign material) filled with brownish-black foreign material within the airspaces of the lung. The brownish-black pigment generated from crack use remains within the macrophages of the lung indefinitely and is visible microscopically. The presence of pigment- laden macrophages results from inhalation of products of combustion during crack use. Unlike
cigarettes, crack pipes lack a filter and users often breathe in large fragments of partially burned material. Macrophages patrol the bloodstream and tissues and engulf such material. This photomicrograph is representative of the lungs of a long-term abuser of crack cocaine.
Physiologically, the inhalation of heated crack cocaine (cocaine treated with sodium bicarbonate, which lowers the temperature of vaporization and makes it smokable) leads to marked increases in heart rate, blood pressure, and vascular constriction. Using a hot crack pipe may cause burns of the fingers (sometimes severe enough to obliterate the fingerprints), lips, oral cavity, and airway. Used chronically, the physiological effects of crack – so named for the crackling noises producing during its manufacture – are progressive and potentially deadly. Microscopic findings consistent with crack lung strongly suggest a history of chronic substance abuse to the astute pathologist and should spur histologic examination of the heart for thickening of the intramyocardial vessels, myocyte hypertrophy, and accelerated atherosclerosis that may have caused disability and death long after the cessation of drug use