pulmonary manifestations of inhaled street drugs

HEART & LUNG VOL. 27, NO. 5 297

From the Departments of Medicine and Nursing, Sound ShoreMedical Center of Westchester, and Newark–Beth Israel MedicalCenter(s), New Rochelle and Newark.

Reprint requests: Robert D. Brandstetter, MD, FCCM, AssociateDirector of Medicine, Chief, Critical Care Division Director of Med-ical Education, Sound Shore Medical Center of Westchester, 16Guion Pl, New Rochelle, NY 10802.

Heart Lung®1998;27:297-305.

Copyright © 1998 by Mosby, Inc.0147-9563/98/$5.00 + 0 2/2/92690

HISTORICAL BACKGROUND

Since 1611, when the Jamestown colonists firstharvested tobacco, America has witnessedalmost 4 centuries of inhalation drug abuse.

The first general misuse of tobacco and drugs (opi-ates) occurred during the 16th century, when thesesubstances were used as a substitute for legal cur-rency.1 Drug scares have come and gone in cycles.Today, America is in the midst of its third waragainst illicit drugs, and it may not be the last.

During the 19th century, certain mood-alteringsubstances, such as opiates and cocaine, wereoften regarded as compounds helpful in everyday

life. The first decline in the use of drugs startedafter the initial wave of Asian immigrants in themid-1890s, continuing through the great wars untilthe 1940s. The increasing fear of addiction led tothis decline. This started America’s first war againstdrugs; by the 1930s, possession of opiates wasdeclared illegal in 35 states.

Another cycle of illicit drug abuse surged in the1960s as America entered an age of social experi-mentation. Widespread use of powerful hallucino-gens and so-called uppers and downers fueled athriving black market. In the 1970s, PresidentRichard Nixon declared the second war on drugs.

Since the 1980s, cocaine and marijuana use,along with a variety of other inhaled substances,has soared. This occurred as both drug users andthe pharmaceutical industry came to realize thepotential of obtaining, from inhaled substances,effects similar to those achieved by intravenousinjection. In 1989, President George Bush declaredthe third war on drugs, which remains an ongoingbattle, without an apparent armistice in sight. Druguse has created many of the same problems andconcerns throughout the world as it has in the Unit-

Pulmonary manifestations of inhaled streetdrugs

Roxana Cruz, MD, Mechery Davis, MD, Hilda O’Neil, RN, Frank Tamarin, MD, Robert D. Brandstetter, MD, FCCM, and Monroe Karetzky, MD, New Rochelle, N.Y.,and Newark, N.J.

INSTRUCTIONS TO CE ENROLLEES

The closed-book, multiple-choice examination that follows this article isdesigned to test your understanding of the educational objectives listedbelow.To enroll in Single Topics, see the instructions at the end of this article.

EDUCATIONAL OBJECTIVES

Based on the content of the article, the enrollee should be able to:1. Discuss the background and description of current street drugs.2. Identify presenting symptoms of patients who have used the more common street

drugs.3. Describe some methods of treatment of patients who have used street drugs.

Adverse effects of inhaled street drugs Cruz et al

298 SEPTEMBER/OCTOBER 1998 HEART & LUNG

ed States. The drug culture permeates the soci-ety—from street people up through the middle-and upper-socioeconomic classes. The solution tothe medical and social problems associated withsubstance abuse remains an enigma to the physi-cian as well as to the user and continues to be asource of immense financial profits. This articlereviews the historical aspects and pulmonary man-ifestations of the most frequently encounteredinhaled street drugs: “crack” cocaine, opiates, mar-ijuana, PCP (phencyclidine), and ice (methamphet-amine).

COCAINE

Cocaine is one of the most powerful euphoriantsthat can be ingested. The known use of cocainepredates the Christian era; coca leaves were usedby South American Indians, Incas, and Aztecs, as a“gift of the Sun.”2

Until the 19th century, cocaine was availablefrom coca leaves that were chewed or dissolved inalcohol. The advent of organic chemistry in the1800s changed the drug’s available form. Cocainewas a favorite health tonic; and a key ingredient ofthe first Coca Cola, the “picker-upper” beverage,introduced in 1886. During the 19th century,cocaine was thought to be no more addictive thancoffee or tea. In 1910, after its removal from CocaCola in 1906, cocaine was reported to pose themost serious drug problem America had everfaced.3 Four years later, President Woodrow Wilsonsigned into law the Harrison Narcotic Act, which, inaddition to its opiate provision, permitted only theprescription sale of cocaine in proprietary medi-cines.3 It was outlawed as a health cure completelyin 1915.4 Thus its use gradually declined during the1920s,3 only to emerge once again as a recreationaldrug in the 1960s; it soared out of control through-out American society in the 1980s, with the conver-sion from the use of cocaine hydrochloride (HCL) tocrack cocaine.

Estimates, before the renewed epidemiccaused by the appearance of crack cocaine in 1985,suggested that approximately 25 million Ameri-cans used cocaine primarily by snorting thehydrochloride salt in powder or flake form at leastonce in their lifetime, and that an estimated 3.5million habitual users were between 12 and 35years of age. The smoking of alkaloidal cocaine(freebase or crack cocaine), alone or in combina-tion with other substances, has caused a renewedepidemic, because it is readily smokable and inex-pensive.5

Crack cocaine is a street name given to cocainethat has been processed from cocaine HCL to itsfreebase to facilitate its use by smoking. The termcrack refers to the crackling sound heard when themixture is smoked (heated). Crack cocaine, unlikecocaine (HCL), is resistant to thermal degradationand is lipid soluble. Consequently, rather thaninhalation by the intranasal route (snorting) of thepowder cocaine HCL, crack can be smoked andrapidly absorbed across the epithelial barriers ofthe airways and pulmonary vascular bed—with atransit time of lung to brain of 5 to 10 seconds.Crack cocaine has become the most frequentlyabused controlled substance in the United States.With unit doses, known as “rocks,” the smallestquantity purchaseable, selling for $3 to $5 each,cocaine is no longer a status drug for the affluent;its use has expanded among the lower socioeco-nomic groups. The epidemic use of crack has led toa variety of pulmonary disorders, distinguishing itfrom other inhaled street drugs.

Pulmonary Symptoms, Complica-tions, and Management

Crack cocaine–related pulmonary complicationsoccur in up to 25% of users and range from coughand shortness of breath to fatal pulmonary hemor-rhage (Table I).6-11 The respiratory symptoms usu-ally develop acutely within hours of use, but mayoccur within minutes, or not be manifested foryears.11, 12 The cough may be productive of a char-acteristic black sputum accompanied by wheezingand dyspnea. The black sputum is attributed toinhalation of the carbonaceous residue frombutane- or alcohol-soaked cotton sponges used toignite the cocaine.13 This appears to be the mecha-nism of thermal airway injury, which results insevere reactive airway disease, hemoptysis, andeven tracheal stenosis.14 Another dramatic cause ofthermal injury is the occasional, yet well-publi-cized, intratracheal ignition of the highly volatileether residue used in the processing of the free-base form of cocaine.11

The chest pain reported by crack users may rep-resent a local sensory response caused by acutepulmonary hypertension or bronchoconstrictionfrom the high concentration of inhaled cocaineitself.11 Alternatively, chest pain may be secondaryto thermal injury or, rarely, may be associated withpulmonary infarction or acute myocardial ischemiaand infarction, as well as aortic dissection, pneu-mothorax, or pneumomediastinum from theintrathoracic shearing forces created by forcefulinhalation maneuvers.15,16


Though hemoptysis, attributable to “rupture” oftracheobronchial mucosal vascular elements,11,12 isreported to occur in up to 25% of crack users, overtalveolar hemorrhage is observed in 30% of users atautopsy in those experiencing sudden death fromcocaine overdose.17

There are no significant long-term adverseeffects of habitual crack cocaine smoking on lungmechanics or gas exchange, as reflected by the usu-ally normal values obtained on spirometric testingat rest or with exercise.6,18,19 A significant decreasein specific airway conductance, with resulting bron-choconstriction and clinical findings of wheezing,may occur over time.9 Differences in the results ofvarious studies appear to be related to samplesize, the confounding influences of other smokedsubstances, inadequate control groups, and theamount and purity of freebase cocaine smoked.The pattern of smoking, depth of inhalation, num-ber of puffs taken, and the device used to inhalethe cocaine are all difficult to control.11 However, asrecently suggested, the reduced maximum exer-cise performance in long-term cocaine users was

probably the result of poor motivation throughaltered effort perception.19

The effect of crack cocaine on pulmonary alveo-lar permeability and the findings of noncardiac pul-monary edema and diffuse alveolar hemorrhagemay follow the inhalation of crack cocaine smoke.This may be related to the reported injurious effectof cocaine on the pulmonary vasculature,20 whichalso accounts for the variable findings of a decreaseor no change in the carbon monoxide diffusingcapacity.18,21,22 In spite of these conflicting studies,including an initial report that the habitual smokingof cocaine has no measurable effect on the airway’sepithelial barrier, as reflected by alveolar perme-ability,7 it is generally believed that the clinicalmanifestations of alveolar capillary dysfunction(noncardiac pulmonary edema, alveolar hemor-rhage, and pulmonary vascular involvement) sup-port the argument that pulmonary alveolar perme-ability is compromised with the habitual smokingof crack cocaine.11

Complications such as bronchiolitis obliteransorganizing pneumonia (BOOP), eosinophilic lung

Cruz et al Adverse effects of inhaled street drugs

Table IIllicit drugs, routes of administration, and adverse pulmonary effects

Substance Route of administration Adverse pulmonary effects

Cocaine HCL Snorting Chronic: Ischemia, necrosis of nasal mucosa; sinuses

Cocaine alkaloid Smoking Acute: Pulmonary edema; cough; bron-(crack) chospasm; aspergillosis

Chronic: Hypersensitivity of eosinophilic pneumonia; bronchitis obliterans; pulmonary angiopathy

Marijuana Smoking Acute: BronchoconstrictionChronic: Bronchitis; squamous metapla-

sia; invasive aspergillosis

Heroin Snorting; smoking Acute: Noncardiogenic pulmonary edema; bronchospasm; eosinophilic pneumonia

Amphetamine HCL Inhalation by pipe; Acute: Noncardiogenic (Ice, speed, crank) snorting; smoking pulmonary edema; retropharyngeal

emphysema

Phencyclidine Snorting; smoking Acute: Dyspnea(PCP, angel dust)



disease, and interstitial pneumonia and pneumo-mediastinum/pneumothorax/pneumopericardiumalso occur.6,9,11 Crack smoking has been associatedwith acute exacerbations of preexisting asthma andhas been reported with near fatal and fatal acutebronchospasm in patients with a previous historyof asthma.14,23,24

Treatment in most cases is supportive (Table II).Symptomatic relief of wheezing and dyspneashould include oxygen therapy and, when appro-priate, beta2 agonists. Sputum should be obtainedwhen available and examined for both routine,community-acquired and opportunistic organisms,because many patients are or have been intra-venous drug abusers, and crack smoking is consid-ered a risk factor for acquired human immunodefi-ciency virus (HIV infection). When indicated,empiric or specific antimicrobial therapy should beinitiated promptly. Hemoptysis should be evaluat-ed for its origin and, when necessary, flexiblefiberoptic bronchoscopy should be used to localizebleeding and to distinguish proximal inflammatoryor thermal burn injury of the airways from distalalveolar hemorrhage. The management of noncar-diac pulmonary edema, which can be severeenough to qualify as a criterion for the definition ofadult respiratory distress syndrome (ARDS), is alsosupportive.25 Patients with biopsy-proven bronchi-

olitis obliterans organizing pneumonia mayimprove rapidly after treatment with cortico-steroids,11 although some patients may progress to death. Patients who present with barotrauma(pneumothorax, pneumomediastinum, pneu-mopericardium) from vigorous inhalation are man-aged with observation and oxygen therapy. Highalveolar oxygen concentrations may enhanceresorption of the free air. Rarely, chest tube inser-tion is indicated for an expanding pneumothorax. Itshould be remembered that the differential diag-nosis for pneumomediastinum with pneumothoraxincludes Pneumocystis carnii pneumonia as well asesophageal perforation, which can be ruled out bya barium swallow.11 The acute syndrome of fever,cough, dyspnea, and eosinophilic pulmonary infil-tration has been termed crack lung and may alsorespond to steroids.26-28

OPIATESThe first reference to the use of opium, which is

found in poppy juice, can be traced back to the thirdcentury BC,29 although it has been around for some6000 years.30 Opium, the Greek term for poppyjuice, became very popular in the Middle East afterbeing introduced by Arab traders in the 18th centu-ry.29 By that time, in the Far East, England had begunsolving its balance-of-trade problems with China by

Table IISymptoms and treatment of illicit drug inhalation

Drug Symptoms Treatment

Cocaine HCL Nasal stuffiness; erosion Nasal packing; corticosteroid of nasal cartilage; internasal cream; intranasal corticosteroidseptum; epistaxis spray

Cocaine alkaloid Dyspnea; cough with carbonaceous Oxygen; inhaled bronchodilators;(crack) sputum; thermal burns of face or corticosteroids

upper airway; chest pain; hemoptysis;exacerbation of asthma; fever, with pulmonary infiltrates shown on chest radiograph

Heroin Asthma Oxygen; bronchodilators; cortico-steroids; naloxone; oxygen; bronchodilators

Marijuana Asthma Oxygen; bronchodilators

Methamphetamine HCL Barotrauma; dyspnea with pulmonary Oxygeninfiltrates; does not produce bronchoconstriction


selling opium in exchange for tea. This laid the foun-dation for conflict with China’s rulers, who rejectedthis practice because of the great addiction inChina’s population; but England persisted, whichresulted in the Opium War of 1839.30 Until the 19thcentury, opium was ingested by chewing or dissolv-ing poppy plants in an alcoholic beverage to dilutethe impact of the active agent.

The crude product of opium was brought toAmerica by European colonists, who regarded it as a familiar recourse for pain relief. During the last years of his life, Benjamin Franklin regularlytook opium in alcohol to alleviate the pain of kid-ney stones. In 1806, morphine was isolated fromopium.29 In 1874, diacetylmorphine, better knowntoday as heroin, was synthesized from morphine.3

By the late 1890s, heroin cough syrup was widelyavailable. In the mid-nineteenth century, the hypo-dermic syringe was perfected, and manufacturersexploited the market. As a result of easier intra-venous access, higher doses of opium were morereadily available in America. More than 400,000Civil War soldiers, most of whom were presumablywounded, returned home as drug addicts.

Doctors continued to prescribe opium and mor-phine through the early 1800s, despite evidence ofits addictive powers.30 Interestingly, a number ofsurveys showed that, by 1900, two thirds to threequarters of American opiate addicts were womenbeing treated for painful uterine and ovarian dys-function. One of the most famous examples of thiswas playwright Eugene O’Neill’s mother, EllaO’Neill, who was treated with morphine during andafter a difficult obstetrical delivery in 1908. Shebecame addicted, and it took a quarter of a centu-ry for her to free herself from morphine. This storyis described by her son in his play “A Long Day’sJourney into Night.”31

In 1912, 12 nations signed a pact that requiredeach country to enact domestic legislation control-ling and eliminating the legal dispensing of mor-phine from clinics, thereby criminalizing its use aswell as the narcotic trade. The goal was to restrictnarcotics to medicinal use. During the 1920s and1930s, the opiate problem declined3; however,another cycle started again in the 1950s, whenheroin use increased.30 During the 1930s, only 17%of opioid abusers were black; but, by the end of thel950s, more than 50% of heroin-related deaths wererepresented by blacks as minority use of opioidsbecame widespread.30 Fatal drug overdose was themost feared consequence of heroin abuse in thelate 1960s and 1970s. Although heroin abuseslacked off in the 1980s, its introduction back onto

the street in the mid-1990s may reflect the fear ofthe medical consequences associated with crackcocaine among its users and dealers. Curiouslyenough, smoking of heroin originated in Shanghaiin the 1920s, and it involved the use of porcelainbowls and bamboo tubes. “Chasing the dragon,” arefinement of this form of heroin smoking, surfacedin Hong Kong in the 1950s.32 This techniqueinvolves the inhalation of the heroin vapors whenthe drug is heated on tinfoil over a flame. The tech-nique later spread to other parts of Southeast Asiaand the United States.

The recognized pulmonary complications fromopiate abuse (heroin, morphine, and codeine),such as the pulmonary hypertension labeled “blue-velvet” disease, a term derived from the glow ofthe heated preparation when liquefied, have prin-cipally been from intravenous injection of “filler”impurities. Currently, in response to AIDS aware-ness programs and market conditions of fallingprices as well as increased production and purity ofproduct, the nonparenteral use of heroin—sniffing,snorting, and smoking—has become the preferredmode of usage. The most formidable inhalationmorbidities include noncardiac pulmonary edemaand airway inflammation, progressing to bronchiec-tasis and, rarely, secondary lung abscess from aspi-ration. Recent reports have extended our under-standing of the harmful pulmonary effects of heroinwhen it is inhaled.


The respiratory symptoms noted with inhaledheroin are a combination of indirect systemiceffects and direct pulmonary toxicity. Shortness ofbreath, wheezing, and upper-airway obstructionfrom edema have been reported with heroin smok-ing.33,34 An acute eosinophilic pneumonia has alsobeen reported,35 as well as noncardiogenic pul-monary edema after intranasal use.30

The most serious pulmonary complication frominhaling heroin fumes is the provocation of severeand even fatal exacerbations of asthma.34,36 This issimilar to the acute episodes of bronchospasmreported with cocaine smoking in asthmatics; all ofthe patients described with asthmatic symptomsafter heroin inhalation had a previous history ofasthma.

The mechanisms provoking bronchoconstrictionare multifactorial. Opiates are powerful releasers ofhistamines, which can produce inflammation andedema. This can be particularly problematic inasthmatics who are atopic. Another potential dan-




ger of heroin use in acute asthma is the central res-piratory-depression effect of opiates. This conse-quence of heroin may compromise the normalcompensatory respiratory responses to an asthmat-ic attack. Accordingly, in the susceptible individual,respiratory acidosis and hypoxemia may be has-tened. Management should include administeringnaloxone, an opiate antagonist, whenever the sys-temic manifestation of ventilatory depression fromopioid use is suspected.

MARIJUANAMarijuana, otherwise known as cannabis (from

its source the hemp plant Cannabis sativa), dope, orpot, has been used by ingestion or smoking through-out the world since the pre-Christian era, just asalcohol is today. It is a good source of fiber (hemp)and is useful for pharmacologic purposes in thetreatment of asthma, as well as an antiseptic, ananalgesic, an antidepressant, and in the treatmentof such neurologic disorders as tetanus.37

Marijuana was originally introduced in Americaduring a period of drug intolerance in the early1900s and was used as a cure for morphine addic-tion. Initially, unrecognized as a euphoriant, it wasnot included in the Harrison Narcotics Act of 1914;but, by the 1930s, it lost its image as a medicine,and became a disreputable intoxicant. However, inthe 1960s, the demand for marijuana once againincreased when its use spread from urban areas tocollege campuses. It then declined in the 1970s and1980s, but there is now evidence of a comeback.3

When marijuana is smoked, because it affectsthe brain and the circulatory system, it gives theuser a “high.” The eyes become bloodshot; theuser loses an awareness of time, has cognitive diffi-culties with memory, and does not think clearly.38

Although numerous pharmacologic constituentshave been identified in marijuana, the main psy-chotropic ingredient is delta-9-tetrahydrocannabi-nol (9-THC), a highly soluble lipid that is rapidlyabsorbed through the mucosal membranes.

Recently, controversy has centered on the med-ical conditions for which marijuana may be benefi-cial, and further studies appear to be warranted asto marijuana’s role in the treatment of AIDS wastingsyndrome, glaucoma, neuropathic pain, and nau-sea from cancer chemotherapy. Questions concern-ing how to design clinical trials of marijuana smok-ing that will produce valid results have doggedresearchers for years and continue to do so. In viewof its unique smell when smoked, maintainingblinded studies is difficult. Puff volume can differfrom 1 smoking episode to another; some people

simply cannot tolerate smoking, and it presents arisk for reactive airway disease.39

Pulmonary Symptoms, Function,and Complications

The pulmonary manifestations of inhaling mari-juana may be mild or fulminant, depending on theabsence or presence of underlying lung disease.Studies performed with college students, compar-ing heavy versus light users of marijuana, havebeen difficult in view of the ever-present variableof multiple substance abuse.38 Studies have shownthat smoke from marijuana does contain irritantsthat elicit cough and produce abnormalities in air-way dynamics and bronchial mucosal histopatholo-gy. This is particularly so in habitual smokers.Accordingly, the regular smoking of marijuanacould cause a nonspecific airway hyperresponsive-ness (AHR) or augment the AHR associated withtobacco use.39,40 Previous studies have shown thatthough the first puff may cause acute airway relax-ation,41 subsequent inhalations cause progressiveairway hyperactivity, perhaps reflecting the bron-chitic symptoms reported to be associated withchronic use.38,39

The association of the possible role of daily mar-ijuana smoking in the development of chronicobstructive pulmonary disease (COPD) has beenstudied recently.42 Approximately 400 healthyyoung adults were stratified into 4 groups (onlymarijuana smokers, marijuana and tobacco smok-ers, only tobacco smokers, and nonsmokers). Thegroups were evaluated by means of forced expira-tory volume in 1 second (FEV1) measurements overa period of 8 years. In neither men nor women wasmarijuana smoking associated with greaterdeclines in the FEV1 than was nonsmoking; nor wasan additive effect of marijuana plus tobacco noted;or a significant relationship between the number ofmarijuana cigarettes per day and the rate ofdecline in the FEV1 over time. Accordingly, in thispreliminary study, declining lung function, as mea-sured by FEV1, is not seen in young marijuanasmokers over a short period of time.42 However,after chronic use, it has been shown to be associat-ed with a decrease in the diffusing capacity and,when used in combination, it may cause moreimpairment in gas exchange than cigarette smokingalone.43,44 This has been attributed to a greaterretention of particulate matter and an altered pat-tern of inhalation, greater puff volume, and reten-tion time, which cause higher carboxyhemoglobinlevels.42,43 There appears to be significantbronchial mucosal histopathology as a result of


marijuana smoking.44,45 Habitual marijuana smok-ers have histopathologic abnormalities in the tra-cheobronchial mucosa similar to those found intobacco smokers.46

It is not clear whether marijuana smoking canincrease the risk of lung cancer.37 One report from theUniversity of California at Los Angeles suggests that 1to 3 marijuana joints per day produce the sameamount of morphologic changes in the lung as 5tobacco cigarettes per day and, thus, a higher poten-tial for dysplastic mucosal abnormalities.8 Moreimportant, the polynuclear aromatic hydrocarbons,many of which are known carcinogens that arefound in the particulate phase of both tobacco and marijuana, are found in marijuana smoke in amounts 50% to 70% higher than in tobaccosmoke.47 These data from an animal model suggest apotent etiologic factor in the development of respi-ratory tract cancer. Users have been reported to havecancer of the mouth, larynx, and lung develop.37

Meaningful studies are difficult to perform, con-sidering the legal issues surrounding marijuanasmoking and the social stigma of such a habit. Stud-ies are controversial, in light of the recent inquiriesinto the use of marijuana for its positive medicinalproperties,48 patients with comorbid conditions,and the danger of bronchopulmonary aspergillosisin asthmatics, as well as49 invasive aspergillosis inimmunocompromised patients.50,51,52

ICE (METHAMPHETAMINE)Ice, a new name for an old drug, in its pure form

is methamphetamine hydrochloride. Methamphet-amine and related phenylisopropylamines havebeen considered stimulants for centuries.53 Someform of these drugs was used in China more than5000 years ago and in East Africa in the early 1300sfor strength and suppression of fatigue andappetite.53 Amphetamine is a synthetic form ofephedrine and was introduced in 1932 as a bron-chodilator for the treatment of nasal and bronchialcongestion associated with colds.

During World War II, soldiers of both sides usedit to fight fatigue and enhance performance. In the1950s, legally manufactured tablets of the longer-acting methamphetamine were used nonmedicallyby college students and truck drivers as well as ath-letes. However, when the actions of amphetamineon the central nervous system were discovered(euphoria), it was quickly adopted by drug abusers,and its distribution and manufacture were progres-sively restricted, although epidemics of ampheta-mine abuse continued to occur in the 1960s and1970s.

Now a new type of methamphetamine has beenintroduced in the form of a relatively pure crys-talline hydrochloride salt called ice, because of itstransparent, sheet-like crystals. The drug is alsoreferred to as crystal and glass. When ice containsimpurities and is inhaled, it is called speed. The drugis inhaled, as with cocaine, either by snorting it orby smoking it in its freebase form. This creates aresponse, according to abusers, similar to that of anintravenous dose; it gives the abuser a “rush” or“flash,” a sense of energy and self-confidence, anda feeling of well-being. It has a similar effect ascocaine; however, the effects of amphetamines lastfor hours. The effects on the central nervous systemof even small amounts of ice include irritability,insomnia, tremors, and seizures that can result indeath. Ice has fueled the clandestine drug marketsince the late 1980s and is now known as the drugof the 1990s.

Pulmonary Symptoms and Complications

Although most of the side effects associated withsmoking or snorting ice are systemic, some pul-monary symptoms are experienced, and rare com-plications can occur.53 Dyspnea, with shallow respi-rations, can result within seconds of smoking ice.This has been reported to be associated with pul-monary edema.54 Absence of bronchoconstrictionand wheezing may be explained by the pharmacol-ogy of methamphetamine, because it has potentbronchodilator effects. Chest pain, when experi-enced, appears to be cardiac in origin, because theactive substance of methamphetamine has potentvasoconstrictive effects.

When rapidly inhaled as a vapor with a pipe, icecondenses in the lung. This technique has beenassociated with barotrauma, such as the report ofisolated retropharyngeal emphysema.55 The mech-anism for this injury seems to be related to theincrease in the retropharyngeal pressure caused bya Valsalva maneuver (often performed to enhancethe effect of the smoked ice), also by “bystander”assistance: CPR-like mouth-to-mouth exhalation(boost). Such barotrauma injury is similar to thatdescribed with marijuana, crack cocaine, and hero-in abuse, in which an increase in intra-alveolarpressure can result in pneumothorax pneumome-diastinum or pneumopericardium.11 Althoughretropharyngeal emphysema is self-limiting, hospi-tal admission and close observation are stillmandatory.55 Rarely, ice may be associated with thelate development of noncardiac pulmonary edema.Pulmonary hypertension may occur after long-




standing abuse of the less pure form of ice: “crank”methamphetamine.56

PHENCYCLIDINE (PCP)Phencyclidine was developed in 1959. It was first

used as an anesthetic in animals and then as a gen-eral anesthetic in humans. It fell into disuse quick-ly, and was discontinued in humans in 1965,because patients experienced agitation or deliri-um, or a combination of both, when they emergedfrom anesthesia. By the 1970s, it was 1 of the mostwidely abused drugs in the United States, used inany one of 3 ways: snorted, smoked, or eaten.29,57,58

Its prevalence declined in the 1980s. The com-pound is relatively easy to synthesize, and it isreadily soluble in water and alcohol. It is knownamong drug users by a number of street names,including PCP, angel dust, crystal, supergrass,ozone, whack, rocket fuel, and peace pill. Thesecontradictory connotations reflect PCP’s bizarre andvolatile effects. The drug is now illicitly produced,and its purity varies widely. Phencyclidine is a cen-tral nervous system stimulant and, although it isresponsible for feelings of strength and power,recent studies support chronic abusers’ experi-ences of rage, anger, and violent behavior, includ-ing criminal and self-destructive activity.30


The pulmonary manifestations associated withthe snorting or smoking of PCP appear to be relat-ed to the drug’s systemic effects. Symptoms arenoted within 30 to 60 seconds of snorting it and 1 to5 minutes after smoking it. When the drug issmoked, it is applied to a leafy material such asmint, parsley, or even marijuana. Hyperventilation,with shallow respirations, may be additionallyaccompanied by dyspnea when PCP is smoked.Isolated pulmonary complications have been rare,although aspiration in the setting of overdose andcoma may be encountered. Respiratory and cardiacarrest may develop at high PCP doses.

Management includes reassurance and continu-ous sedation with a benzodiazepine for anxiety orhaloperidol for psychosis. Acidification of the urinemay facilitate drug excretion.

CONCLUSIONInhaled street drugs constitute a group of

abused pharmacologic agents that are toxic to therespiratory system. These illicitly obtained drugsare frequently combined or laced with additionalsubstances that promote airway injury because of

their noxious and often volatile properties. Recog-nizing the signs and symptoms of airway involve-ment from inhaled street drugs is difficult, becausethe clinical presentation is similar to other acuterespiratory disorders. This is particularly true whenreasons for wheezing, shortness of breath, chestpain, and hemoptysis are being considered. Labo-ratory tests are nonspecific and generally limited tocomplete blood count, urine drug screen, arterialblood gas, sputum Gram stain, peak expiratory flowrate, and chest radiograph. The incrimination of aninhaled street drug as the definitive cause for clin-ical and laboratory findings rests on suspicion forits presence and the history taken from the patient,friends, or possibly law enforcement officers. Themanagement of the pulmonary complications relat-ed to inhaled street drugs is principally supportive.All patients should be carefully monitored andsupplemental oxygen administered. Specific thera-peutic measures are offered on an individual basis,such as ventilator support for respiratory failureand chest tube placement for clinically significantpneumothorax.

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15. Warner E. Cocaine abuse. Arch Intern Med 1993;119:226-35.16. Weiner D, Putnum CE. Pain in the chest in a user of cocaine.

JAMA 1987;258:2087-8.17. Rao AN, Polos PG, Walther FA. Crack abuse and asthma: a

fatal combination. NY State J Med 1990;90:511-2.18. Tashkin DP, Khalsa ME, Gorelick D, et al. Pulmonary status of

habitual cocaine smokers. Am Rev Respir Dis 1992;145:92-100.

19. Marques-Magallanes JA, Royal SN, Cooper CB, Kleerup EC,Tashkin DP. Impact of habitual cocaine smoking on the phys-iologic response to maximum exercise. Chest 1997;112:1008-16.

20. Murray RJ, Smialek JE, Golle M, Albin RJ. Pulmonary arterymedical hypertrophy in cocaine users without foreign particlemicroembolization. Chest 1989;96:1050-3.

21. Weiss RD, Goldenheim PD, Mirin SM, Hales CA, MendelsonJH. Pulmonary dysfunction in cocaine smokers. Am J Psychia-try 1981;138:1110-2.

22. Tashkin DP, Simmons MS, Coulson AH, Clark VA, Gong HJ.Respiratory effects of cocaine “freebasing” among habitualusers of marijuana with or without tobacco. Chest 1987;92:638-44.

23. Rubin RB, Neugarten J. Cocaine associated asthma. Am J Med1990;88:339-42.

24. Levenson T, Greenberger PA, Donoghue ER, Schultz L. Asthmadeaths compounded by substance abuse: an assessment offatal asthma. Chest 1996;110:604-10.

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26. Oh PJ, Balter MS. Cocaine-induced eosinophilic lung disease.Thorax 1992;47:478-9.

27. Kissner DG, Lawrence WD, Seles JE, Flint AI. Crack lung: pul-monary disease caused by cocaine abuse. Am Rev Respir Dis1987;136:1250-2.

28. Forrester JM, Steele AW, Waldron JA, Parsons PE. Crack lung:an acute pulmonary syndrome with a spectrum of clinical andhistopathological findings. Am Rev Respir Dis 1990;147:462-7.

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CE TEST INSTRUCTIONS

Test identification No. H0981 Minimum passing score: 70%Contact hours: 1.0 Florida Content Code: 2502

This continuing education activity is administered and sponsored by Buchanan & Associates, which isaccredited as a provider of Continuing Education in Nursing by the American Nurses CredentialingCenter’s Commission on Accreditation; California Board of Nursing Provider No. CEP9473; Florida Board ofNursing Provider No. 271 1004; and the Iowa Board of Nursing Provider No. 244.

This test was written by Jean Marshall, MS, RN. Single Topics. To receive CE credit for this test, mark your answers on the answer form that follows the

test, complete the enrollment information, and submit it with the $9.00 processing fee (in U.S. dollars) toBuchanan & Associates. Answer forms must be postmarked by September 17, 2001. Within 3 weeks ofreceiving your test form, Buchanan & Associates will send a CE certificate.

1. When were opiates first declared illegal in the United

States?

a. 1920s

b. 1930s

c. 1940s

d. 1970s

2. Thermal airway injury causes the following EXCEPT:

a. Hemoptysis

b. Tracheal stenosis

c. Severe reactive airway disease

d. Bronchoconstriction

3. Chest pain reported by crack users is LEAST likely

caused by:

a. Pulmonary hypertension

b. Acute myocardial ischemia

c. Bronchoconstriction

d. Thermal injury

4. What is the treatment for bronchiolitis obliterans orga-

nizing pneumonia (BOOP)?

a. Beta agonists

b. Corticosteroids

c. Antibiotics

d. Naloxone

5. Symptoms of acute “crack lung” include the following

EXCEPT:

a. Cough

b. Dyspnea

c. Fever

d. Tracheal stenosis

6. “Blue velvet” disease is

a. Pulmonary hypertension

b. Tracheal stenosis

c. Hemoptysis

d. Bronchospasm

7. Diacetylmorphine is more commonly known as:

a. Morphine

b. Heroin

c. Cocaine

d. Crystal

8. Pulmonary effects of heroin causing the most morbidity

include the following EXCEPT:

a. Noncardiac-related pulmonary edema

b. Airway inflammation

c. Lung abscess

d. Pulmonary hypertension

9. Amphetamine was introduced in 1932 as a:

a. Depressant

b. Bronchodilators for nasal congestion

c. Systemic stimulant

d. Hypertensive agent

10. “Whack” is also called:

a. THC

b. PCP

c. Grass

d. Ice



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Article Title: Pulmonary manifestations of inhaled street drugs

Test ID No. H0981 Fee: $9.001.0 Contact hours Expires: September 17, 2001

Florida Content Code: 2502

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pulmonary manifestations of inhaled street drugs

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