Overview of Pulmonary Disease in People Who Inject Drugs

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Overview of pulmonary disease in people who inject

drugs
AUTHOR: Joyce S Lee, MD
SECTION EDITOR: Talmadge E King, Jr, MD
DEPUTY EDITOR: Paul Dieffenbach, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Apr 14, 2023.
INTRODUCTION
People who inject drugs (PWID) are at increased risk for acute and chronic pulmonary
complications. These sequelae may be due to pharmacodynamic properties of the drugs,
effects of intravenous contaminants, or complications of the intravenous route of
administration.
The general pulmonary complications and drug-specific pulmonary diseases that may result
from injection drug use will be reviewed here. Other complications of injection drug use,
such as foreign body granulomatosis, infective endocarditis, opioid use disorder, cocaine
intoxication, and methamphetamine intoxication, are reviewed separately. (See "Substance
use disorders: Clinical assessment" and "Foreign body granulomatosis" and "Right-sided
native valve infective endocarditis" and "Opioid use disorder: Pharmacologic management"
and "Acute opioid intoxication in adults" and "Cocaine: Acute intoxication" and
"Methamphetamine: Acute intoxication".)
PULMONARY COMPLICATIONS
The pulmonary complications associated with intravenous injection of illicit drugs include
pneumonia, septic embolization, noncardiogenic pulmonary edema, foreign body
granulomatosis, emphysema, interstitial lung disease, pulmonary vascular disease,
pneumothorax, and an increased incidence of fatal asthma [1-4].
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Pneumonia — PWID have a 10-fold increased risk of community-acquired pneumonia

compared with the general population [2]. This may be due to a number of factors:
● Concurrent smoking of cigarettes or illicit drugs may impair local lung defenses,
macrophage activity, and mucociliary clearance
● The stupor induced by some injected drugs favors development of aspiration
pneumonia or lung abscess (see "Aspiration pneumonia in adults" and "Lung abscess in
adults")
● Bacteremia may follow injection and may hematogenously infect the lung
● HIV-positive PWID are at substantially higher risk for bacterial pneumonia than HIV-
negative PWID
The organisms that most commonly cause community-acquired pneumonia in this

population include Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae,
Klebsiella pneumoniae, and Escherichia coli, although it is difficult to separate out the
pathogens associated with HIV-positive and HIV-negative injection drug use [5,6].
Antimicrobial therapy is initially empiric and based on the clinical situation, particularly
whether the chest radiograph shows focal or diffuse opacities and whether the patient
meets criteria for hospital admission. In patients presenting with typical symptoms of
bacterial pneumonia with focal consolidation on chest radiograph, the initial antibiotic
regimen will be directed at the most common community-acquired pathogens. (See "Clinical
evaluation and diagnostic testing for community-acquired pneumonia in adults" and
"Bacterial pulmonary infections in patients with HIV" and "Treatment of community-acquired
pneumonia in adults in the outpatient setting" and "Treatment of community-acquired
pneumonia in adults who require hospitalization".)
If the etiology of community-acquired pneumonia is identified using reliable microbiologic

methods, antimicrobial therapy can be focused on that pathogen ( table 1). (See
"Treatment of community-acquired pneumonia in adults who require hospitalization",
section on 'Initial empiric therapy'.)
For patients who have progressive disease despite antibiotic therapy for bacterial
pneumonia, other considerations include fungal and mycobacterial agents. Candida
pneumonia has been reported in PWID when the injection drug is contaminated [2].
Tuberculosis (particularly multidrug-resistant tuberculosis) is more prevalent among PWID

than it is in the general population [7-9]. The excess risk largely relates to covariates which
are more frequent among PWID, such as poverty, homelessness, malnutrition, HIV infection,
and poor medical care. Tuberculosis should be suspected in patients with a longer
prodrome, particularly in the presence of fever or night sweats for more than a week prior to
presentation, or weight loss. In addition, mycobacterial disease should be suspected in
patients with nonresolving pneumonia. (See "Epidemiology of tuberculosis" and "Pulmonary
tuberculosis: Clinical manifestations and complications" and "Nonresolving pneumonia",

section on 'Tuberculosis'.)
The use of injection drugs is a strong risk factor for the acquisition of HIV infection. PWID
who present with pneumonia should be assessed for possible HIV infection. In the presence
of known HIV infection, a variety of opportunistic pulmonary infections in addition to
tuberculosis may occur. (See "Evaluation of pulmonary symptoms in persons with HIV".)
Septic emboli — Septic pulmonary emboli can originate in the peripheral veins at sites of
thrombophlebitis or they can arise from heart valves that have been damaged and infected
due to injection drug use. Right-sided valve (tricuspid) endocarditis is generally found to be
more common among PWID than left-sided. (See "Pathogenesis of vegetation formation in
infective endocarditis" and "Right-sided native valve infective endocarditis", section on
'Clinical manifestations'.)
Patients typically present with fever, but generally do not have an audible murmur or
peripheral stigmata of infective endocarditis. Blood cultures are usually positive. The
radiographic manifestations of septic pulmonary emboli include ill-defined, nodular
pulmonary opacities, cavities, abscesses, infarction, and pulmonary gangrene ( image 1).
The evaluation and treatment of infective endocarditis in PWID is discussed separately. (See
"Right-sided native valve infective endocarditis".)
Noncardiogenic pulmonary edema — Noncardiogenic pulmonary edema (NPE) refers to

the radiographic evidence of alveolar fluid accumulation without hemodynamic evidence to
suggest a cardiogenic etiology and is caused by increased pulmonary capillary permeability.
NPE can occur following intravenous injection of cocaine and, more commonly, opioids [3,10-
12]. Acute respiratory distress syndrome (ARDS) is a more severe form of NPE, associated
with severe hypoxemia and the need for mechanical ventilatory support. (See
"Noncardiogenic pulmonary edema" and "Acute respiratory distress syndrome:
Epidemiology, pathophysiology, pathology, and etiology in adults", section on 'Etiologies and
predisposing factors'.)
The exact pathophysiology of NPE due to opioid overdose (eg, heroin or methadone) is
unknown, but may include a direct effect of the drug, cerebral edema (neurogenic), or
possibly negative pressure. Patients with central nervous system depression due to a drug
overdose can develop upper airway obstruction. Breathing against the obstruction can
create a strong negative pressure across the alveoli, which causes pulmonary capillary
leakage. (See "Noncardiogenic pulmonary edema", section on 'Opioid overdose' and
"Noncardiogenic pulmonary edema", section on 'Neurogenic pulmonary edema'.)
Patients typically present with decreased mental status and evidence of respiratory
insufficiency (eg, tachypnea, tachycardia, hypoxemia). Patients with NPE due to opiate
intoxication typically have severe respiratory depression requiring naloxone reversal. Co-
intoxication with alcohol or cocaine is present in approximately 50 percent [11]. The majority
of these patients are hypoxemic on arrival in the emergency department [10,11].
Imaging findings in PWID with NPE were described in a series of 27 patients with opiate-
related NPE: 74 percent had bilateral, ground-glass opacities suggestive of pulmonary
edema, while unilateral pulmonary edema or focal opacities were noted in the remainder
[10].
The diagnosis of NPE in PWID is based on the clinical presentation and exclusion of
processes in the differential diagnosis, which includes the other causes of ARDS that may
complicate injection drug use, such as sepsis, pneumonia (bacterial, viral, fungal), aspiration,
cardiogenic pulmonary edema, and pulmonary embolism. (See "Noncardiogenic pulmonary
edema".)
For most PWID with NPE, treatment is supportive. Symptoms and signs typically resolve in 24
hours with supportive care (eg, supplemental oxygen), although approximately one-third of
patients require mechanical ventilation for 24 to 48 hours. (See "Acute opioid intoxication in
adults" and "Noncardiogenic pulmonary edema", section on 'Treatment'.)
Foreign body granulomatosis — Drug users sometimes pulverize tablets intended for oral
use, dissolve them in water, and inject them intravenously. Talc, starch, cotton, and cellulose
are used as filler agents in these tablets and may be carried by the bloodstream until they
lodge in the pulmonary capillary bed; chronic inflammation and multiple foreign body
granulomas in the lungs may ensue.
Patients may be asymptomatic or may present with nonspecific complaints such as dyspnea,
cough, or an increase in sputum production. Computed tomography (CT) typically shows
diffuse, small nodules (2 to 3 mm) or ground-glass opacities ( image 2). Pulmonary
hypertension, emphysema, and interstitial fibrosis can occur if the process is severe. The
diagnosis and management of foreign body granulomatosis are discussed separately. (See
"Foreign body granulomatosis".)
Bullous lung disease and emphysema — Emphysema and bullous lung disease have been
described in association with HIV infection, but HIV-negative PWID can also develop these
complications, particularly when methadone, methylphenidate, or talc-containing drugs are
injected [13-15]. (See "Foreign body granulomatosis".)
In one series, the prevalence of bullous lung damage and emphysema among intravenous
drug users (as assessed by chest radiographs) was 2 percent [16]. The bullous cysts were
noted predominantly in the upper lobes and in the lung periphery, with sparing of the
central portions of the lungs [16,17]. Other reports of patients who injected talc-containing
drugs have reported a predominance of bullous changes in the lower lobes [18,19]. Patients
present with cough and dyspnea, and usually have combined obstructive and restrictive
defects on pulmonary function testing.
A separate cross-sectional study of 516 participants who injected drugs demonstrated an

overall prevalence of obstructive lung disease (OLD) of 18.2 percent, as determined by
spirometry [20]. Very few reported a prior diagnosis of emphysema (10.6 percent) despite a
high prevalence of respiratory symptoms (44.7 percent). After adjustment for age, pack-years
smoked, and Black race, injection drug use was associated with a 13 percent (95% CI 1-27)
increased odds of OLD for every five years of injection drug use.
Interstitial lung disease — Interstitial lung disease in PWID is generally associated with
foreign body granulomatosis, but may also be a nonspecific finding due to previous episodes
of infection, aspiration, or infarction. Lymphocytic interstitial pneumonia, a rare interstitial
lung disease in the general population, is seen with increased frequency in HIV-infected
individuals. In addition, organizing pneumonia, sarcoidosis, drug hypersensitivity, and
immune reconstitution syndrome can develop in HIV-infected patients. (See "Foreign body
granulomatosis" and "Approach to the adult with interstitial lung disease: Clinical evaluation"
and "Approach to the adult with interstitial lung disease: Diagnostic testing" and "Evaluation
of pulmonary symptoms in persons with HIV", section on 'Causes of pulmonary disease in
persons with HIV'.)
Pulmonary hypertension — Pulmonary hypertension may be induced by obstruction or

obliteration of the pulmonary vascular bed from multiple causes, including foreign body
granulomatosis, emphysema, or interstitial disease. Patients who are HIV-positive may
develop pulmonary arterial hypertension (PAH) with plexiform lesions and medial
hypertrophy. The evaluation and management of pulmonary hypertension associated with
HIV infection is discussed separately. (See "Pulmonary arterial hypertension associated with
human immunodeficiency virus" and "Treatment and prognosis of pulmonary arterial
hypertension in adults (group 1)".)
Drugs with sympathomimetic properties (eg, cocaine, methamphetamine) can produce

transient pulmonary vasoconstriction. It also appears that chronic use of these drugs can
lead to irreversible injury and production of a syndrome indistinguishable from primary
pulmonary hypertension. In one retrospective study, patients with idiopathic PAH were ten
times more likely to use stimulants (ie, amphetamines, methamphetamines, or cocaine) than
patients with PAH due to known risk factors, such as collagen vascular disease, congenital
heart disease, or anorexigen use [21]. (See "The epidemiology and pathogenesis of
pulmonary arterial hypertension (Group 1)", section on 'Drugs and toxins'.)
Pneumothorax and pneumomediastinum — Pneumothorax may result from unsuccessful

attempts to inject drugs into the central circulation via the subclavian and jugular veins
("pocket shots"). It has also been reported as a complication of crack cocaine use, septic
pulmonary emboli, and drug-related bullous disease [22,23]. (See 'Cocaine' below.)
Pneumomediastinum is associated with inhalation of crack cocaine and, less commonly,

intranasal cocaine [24]. It is most likely due to performance of a Valsalva maneuver after
inhalation, rather than an effect of the drug. Approximately 20 percent also had a
pneumothorax. (See "Pulmonary complications of cocaine use", section on 'Pneumothorax
and pneumomediastinum'.)
Asthma — PWID with asthma appear to have an increased risk of fatal asthma [25-28] (see
"Identifying patients at risk for fatal asthma", section on 'Minor risk factors'):
● One toxicologic study of 92 cases of fatal asthma in Chicago found evidence of

substance abuse, most commonly cocaine or opiates, in 32 percent of individuals [25].
It is unclear whether the drugs themselves or other unidentified factors are responsible
for the increased asthma fatalities. Optimal use of asthma medicines is less frequent
among drug users [26], and antiinflammatory medications were being utilized by just
two patients in the Chicago series.
● A retrospective review of 152 urban asthma patients found that intubation and
mechanical ventilation were required more often among patients presenting with an
acute exacerbation if they use cocaine (31 versus 11.5 percent) or heroin (17 versus 2.3
percent), compared with nonusers [27].
Amyloidosis — Bilateral pulmonary nodules containing amyloid (AA) protein have been
reported in PWID with HIV disease [29]. (See "HIV infection and malignancy: Management
considerations", section on 'Plasma cell disorders'.)
DRUG-SPECIFIC COMPLICATIONS
Cocaine — Cocaine is an alkaloid with anesthetic and central nervous system stimulant
properties. It can be inhaled nasally or injected; a heat-stable form produced by boiling with
bicarbonate can be smoked (“free-basing”). There is a higher incidence of clinically apparent
pulmonary complications when cocaine is smoked versus used intravenously or intranasally.
The pulmonary complications associated with the use of cocaine are multiple and can be
divided into acute and chronic pulmonary disorders.
● Acute pulmonary complications – The acute complications of injection cocaine use

overlap with those of inhaled crack cocaine; the most common are acute pulmonary
edema and pulmonary hemorrhage.
• Acute noncardiogenic pulmonary edema (NPE) presents with the rapid onset of
dyspnea, hypoxemia, and diffuse opacities on chest radiograph; altered mental
status is frequently also present in PWID. Treatment is supportive and includes
supplemental oxygen and ventilator support, if necessary. Clinical improvement
generally occurs within 24 to 48 hours. (See 'Noncardiogenic pulmonary edema'
above and "Noncardiogenic pulmonary edema".)
• Pulmonary hemorrhage can occur with or without frank hemoptysis and is

commonly found on autopsy in asymptomatic cocaine users [30]. The causes of
hemorrhage are probably multifactorial and may include NPE, pulmonary infarction,
infection, and pulmonary hypertension. Treatment is supportive. (See "Pulmonary
complications of cocaine use".)
• Cardiogenic edema may result from cocaine-induced coronary artery spasm,

myocardial ischemia, and left ventricular dysfunction ( image 3). The diagnosis is
suspected in patients with dyspnea, diffuse pulmonary opacities on chest imaging,
an elevated brain natriuretic peptide, and/or reduced left ventricular function by
echocardiogram. The diagnosis and treatment are discussed separately. Of note,
beta-adrenergic antagonists (ie, beta-blockers) are avoided in cocaine-related
cardiovascular disease because they may create unopposed alpha-adrenergic
stimulation. (See "Clinical manifestations, diagnosis, and management of the
cardiovascular complications of cocaine abuse", section on 'Clinical manifestations'
and "Cocaine: Acute intoxication", section on 'Cardiovascular complications' and
"Treatment of acute decompensated heart failure: General considerations".)
• Pneumothorax and pneumomediastinum are also reported in association with

cocaine inhalation. (See 'Pneumothorax and pneumomediastinum' above.)
● Chronic pulmonary complications – The chronic pulmonary complications of injection

cocaine use include foreign body granulomatosis, lung scarring due to repeated
pulmonary infections and pulmonary infarction, and pulmonary arterial hypertension
(PAH) [31]. (See 'Foreign body granulomatosis' above and 'Interstitial lung disease'
above and 'Pulmonary hypertension' above.)
Opioids — Opiates are naturally occurring alkaloids from the poppy plant; the term “opioids”
includes natural opiates (eg, morphine, codeine) and synthetic derivatives that also bind to
opioid receptors in the brain (eg, heroin, hydrocodone). Use of heroin (diacetyl morphine) is
rising in the United States, and increasingly pure formulations of the drug are available. Most
of the direct morbidity and mortality related to opiate use occur after acute intoxication and
are due to anaphylaxis, noncardiogenic pulmonary edema, acute respiratory acidosis, and
aspiration pneumonitis. (See "Acute opioid intoxication in adults".)
● Massive release of histamine from mast cells and basophils may follow narcotic
injection due to an anaphylactoid reaction to the narcotics themselves or to adulterants
or contaminants. Shock, bronchospasm, and upper airway edema may ensue [32]. (See
"Anaphylaxis: Emergency treatment".)
● Heroin-induced noncardiogenic pulmonary edema usually develops rapidly within the

first few hours following injection, but rarely occurs as late as 24 hours. This
complication can also occur with other opiates such as codeine and methadone, as well
as fentanyl-heroin mixtures [33]. Oxygen therapy and noninvasive positive pressure
ventilation or intubation with mechanical ventilation may be required. Improvement
can occur rapidly, but full resolution generally requires two to three days. (See
'Noncardiogenic pulmonary edema' above and "Noncardiogenic pulmonary edema".)
● Diffuse alveolar hemorrhage has been described as a complication of heroin overdose,

although it is not known whether the hemorrhage was due to a contaminant in the
heroin or a consequence of noncardiogenic pulmonary edema with capillary leak [34].
Contamination of heroin by cocaine or levamisole was thought to be unlikely in the
reported patients as the urine cocaine and antineutrophil cytoplasmic antibody (ANCA)
tests were negative. (See 'Cocaine' above and "Cocaine: Acute intoxication", section on
'Levamisole'.)
● Narcotics powerfully suppress central respiratory drive. Acute administration may

produce hypercapnia, acute respiratory acidosis, and if severe, cardiopulmonary arrest
and death. (See "Acute opioid intoxication in adults".)
● Narcotics also diminish the level of consciousness and depress the cough reflex. These
actions render narcotic users less able to protect the airway and more likely to develop
aspiration pneumonitis (due to infection or aspirated gastric contents) and lung
abscess. Lower lobe bronchiectasis has been reported among heroin users and may
result from prior episodes of aspiration or pulmonary infection [35]. (See "Aspiration
pneumonia in adults" and "Lung abscess in adults".)
● In a case report, an intravenous heroin user developed respiratory failure due to

organizing pneumonia; scattered, nonnecrotizing granulomata and multinucleated
giant cells with foreign body particles were also noted [36].
Methylphenidate and methamphetamine — Methylphenidate and methamphetamine are

sympathomimetic stimulants that are sometimes injected intravenously by PWID. General
signs and symptoms of toxicity include restlessness, tachycardia, hypertension, diaphoresis,
and confusion. Long-term use of methylphenidate can lead to bullous emphysema.
● Methylphenidate – Intravenous methylphenidate has been associated with the

development of hemoptysis, chest pain, and wheezing. One series of 22 patients
hospitalized following methylphenidate use reported that 80 percent had one or more
of these findings [37]. Excess adrenergic activity and vasospasm may underlie these
complications.
Habitual intravenous use of methylphenidate has been associated with the

development of panlobar emphysema after one to six years [18,38]. Emphysema
primarily involves the lower lobes of the lungs and has a similar radiographic
appearance to alpha-1 antitrypsin deficiency. The relative contribution of
methylphenidate, foreign body granulomatosis, and concomitant smoking in the
genesis of emphysema among these patients is unclear, but one study compared the
findings on chest computed tomography (CT) of patients with foreign body
granulomatosis who abused intravenous methylphenidate with others who did not
[39]. A significantly increased prevalence of lower lobe panacinar emphysema was
demonstrated in patients abusing methylphenidate, and was frequently associated
with a fine micronodular pattern and ground-glass attenuation. (See 'Bullous lung
disease and emphysema' above.)
● Methamphetamine – Methamphetamine ("speed" or "crank") is a stimulant drug that

has similar effects to cocaine. It can be smoked or administered intravenously or
intranasally. There are rare case reports of acute noncardiogenic pulmonary edema and
pulmonary hypertension following the inhalation of methamphetamine, but
complications of intravenous use are not well documented. Cardiogenic pulmonary
edema can complicate methamphetamine intoxication, possibly related to fluid
resuscitation in the setting of acute hypertension. (See "Methamphetamine: Acute
intoxication", section on 'Clinical features' and "Methamphetamine: Acute intoxication",
section on 'Fluid resuscitation'.)
The evaluation and management of acute methamphetamine intoxication are discussed

separately. (See "Methamphetamine: Acute intoxication".)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Stimulant use
disorder and withdrawal".)
SUMMARY AND RECOMMENDATIONS
● Pulmonary disease associated with IV drug use – Pulmonary complications

associated with intravenous (IV) injection of illicit drugs include pneumonia, septic
embolization, foreign body granulomatosis, emphysema, interstitial lung disease,

organizing pneumonia, pulmonary vascular disease, pneumothorax,
pneumomediastinum, and an increased incidence of fatal asthma. (See 'Pulmonary
complications' above.)
• Community-acquired pneumonia – People who inject drugs (PWID) have a 10-fold

increased risk of community-acquired pneumonia compared with the general
population; common causative organisms include Streptococcus pneumoniae,
Staphylococcus aureus, Haemophilus influenzae, Klebsiella pneumoniae, and Escherichia
coli. In addition, those who develop HIV/AIDS are at risk for opportunistic pulmonary
infections (eg, tuberculosis, atypical mycobacteria, Pneumocystis jirovecii,
cytomegalovirus). (See 'Pneumonia' above.)
• Foreign body granulomatosis – When tablets intended for oral use are pulverized
and injected intravenously, the insoluble agents in the tablets (eg, talc, cotton, and
cellulose) can be trapped in the pulmonary vasculature, migrate through the vessel
walls, and initiate a granulomatous inflammatory response in the perivascular
interstitium. This disease process, known as foreign body granulomatosis, can lead
to development of progressive interstitial lung disease, emphysema, and pulmonary
hypertension. (See 'Foreign body granulomatosis' above and "Foreign body
granulomatosis".)
• Emphysema and bullous lung disease – Emphysema and bullous lung disease may
result from concomitant cigarette smoking but are also associated with HIV infection
and intravenous injection of methadone, methylphenidate, and talc-containing
drugs. (See 'Pulmonary complications' above.)
• Pneumothorax – Pneumothorax may result from unsuccessful attempts to inject

drugs into the central circulation via the subclavian and jugular veins ("pocket
shots"). It has also been reported as a complication of septic pulmonary emboli and
drug-related bullous disease. (See 'Pneumothorax and pneumomediastinum'
above.)
● Pulmonary complications of IV cocaine – Complications of intravenous injection of

crack cocaine include noncardiogenic and cardiogenic pulmonary edema, acute and
recurrent alveolar hemorrhage, and interstitial lung disease due to foreign body
granulomatosis. (See 'Cocaine' above.)
● Pulmonary complications of IV opioids – Pulmonary complications related to opioid

injection typically occur in the setting of acute intoxication and are due to anaphylaxis,
noncardiogenic pulmonary edema, hypoventilation with acute respiratory acidosis, and
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aspiration pneumonitis. (See 'Opioids' above and "Acute opioid intoxication in adults"
and "Opioid intoxication in children and adolescents".)
● Pulmonary complications of IV amphetamines – Intravenous injection of

methylphenidate has been associated with hemoptysis, chest pain, and wheezing;
excess adrenergic activity and vasospasm may underlie these complications. Foreign
body granulomatosis and emphysema are complications associated with long-term
use. Methamphetamine ("speed" or "crank") is a stimulant drug that has similar effects
to cocaine and is rarely associated with noncardiogenic pulmonary edema and
pulmonary hypertension. (See 'Methylphenidate and methamphetamine' above.)
ACKNOWLEDGMENT
The UpToDate editorial staff acknowledges Jill P Karpel, MD (deceased), who contributed to
an earlier version of this topic review.
Use of UpToDate is subject to the Terms of Use.
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33. Algren DA, Monteilh CP, Punja M, et al. Fentanyl-associated fatalities among illicit drug
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34. Riccardello GJ Jr, Maldjian PD. Pulmonary hemorrhage in acute heroin overdose: a report
of two cases. Emerg Radiol 2017; 24:709.
35. Banner AS, Rodriguez J, Sunderrajan EV, et al. Bronchiectasis: a cause of pulmonary
symptoms in heroin addicts. Respiration 1979; 37:232.
36. Bishay A, Amchentsev A, Saleh A, et al. A hitherto unreported pulmonary complication in
an IV heroin user. Chest 2008; 133:549.
37. Parran TV Jr, Jasinski DR. Intravenous methylphenidate abuse. Prototype for prescription
drug abuse. Arch Intern Med 1991; 151:781.
38. Sherman CB, Hudson LD, Pierson DJ. Severe precocious emphysema in intravenous
methylphenidate (Ritalin) abusers. Chest 1987; 92:1085.
39. Ward S, Heyneman LE, Reittner P, et al. Talcosis associated with IV abuse of oral
medications: CT findings. AJR Am J Roentgenol 2000; 174:789.
Topic 4337 Version 19.0
GRAPHICS
Recommended antimicrobial therapy for specific pathogens causing

community-acquired pneumonia in adults
Alternative
Organism Preferred antimicrobial(s)
antimicrobial(s)
Streptococcus pneumoniae
Penicillin nonresistant; Penicillin G, amoxicillin Macrolide, cephalosporins (oral

MIC <2 mcg/mL* [cefpodoxime, cefprozil,
cefuroxime, cefdinir] or
parenteral [cefuroxime,
ceftriaxone, cefotaxime]),
clindamycin, doxycycline,
respiratory fluoroquinolone ¶
Penicillin resistant; MIC Agents chosen on the basis of Vancomycin, linezolid, high-dose
≥2 mcg/mL* susceptibility, including amoxicillin (3 g/day with
cefotaxime, ceftriaxone, penicillin MIC ≤4 mcg/mL)
fluoroquinolone
Haemophilus influenzae
Non-beta-lactamase Amoxicillin Fluoroquinolone, doxycycline,

producing azithromycin, clarithromycin Δ
Beta-lactamase producing Second- or third-generation Fluoroquinolone, doxycycline,

cephalosporin, amoxicillin- azithromycin, clarithromycin Δ
clavulanate
Mycoplasma Macrolide, a tetracycline Fluoroquinolone

pneumoniae/Chlamydophila
pneumoniae
Legionella species Fluoroquinolone, azithromycin Doxycycline
Chlamydophila psittaci A tetracycline Macrolide
Coxiella burnetii A tetracycline Macrolide
Francisella tularensis Doxycycline Gentamicin, streptomycin
Yersinia pestis Streptomycin, gentamicin Doxycycline, fluoroquinolone
Bacillus anthracis (inhalation) Ciprofloxacin, levofloxacin, Other fluoroquinolones; beta-

doxycycline (usually with second lactam, if susceptible; rifampin;
agent) clindamycin; chloramphenicol
Enterobacteriaceae Third-generation cephalosporin, Beta-lactam-beta-lactamase

carbapenem ◊ (drug of choice if inhibitor § , fluoroquinolone
extended-spectrum beta-
lactamase producer)
Pseudomonas aeruginosa Antipseudomonal beta-lactam ¥ Aminoglycoside plus

plus (ciprofloxacin or (ciprofloxacin or levofloxacin ‡ )
levofloxacin ‡ or aminoglycoside)
Burkholderia pseudomallei Carbapenem, ceftazidime Fluoroquinolone, TMP-SMX
Acinetobacter species Carbapenem Cephalosporin-aminoglycoside,

ampicillin-sulbactam, colistin
Staphylococcus aureus
Methicillin susceptible Antistaphylococcal penicillin † Cefazolin, clindamycin
Methicillin resistant Vancomycin or linezolid TMP-SMX
Bordetella pertussis Macrolide TMP-SMX
Anaerobe (aspiration) Beta-lactam-beta-lactamase Carbapenem

inhibitor § , clindamycin
Influenza virus Refer to associated topic

reviews**
Mycobacterium tuberculosis Isoniazid plus rifampin plus Depends on susceptibility

ethambutol plus pyrazinamide pattern; refer to associated topi
reviews
Coccidioides species For uncomplicated infection in a Amphotericin B

normal host, no therapy
generally recommended; for
therapy, itraconazole,
fluconazole
Histoplasmosis Itraconazole ¶¶ Amphotericin B ¶¶
Blastomycosis Itraconazole ¶¶ Amphotericin B ¶¶
Choices should be modified on the basis of susceptibility test results and advice from local specialists.
Refer to local references for appropriate doses.
Preferred agent may change over time due to changing resistance patterns and depends on many
factors, including severity of illness. Refer to associated UpToDate topic reviews for updated and
detailed treatment recommendations for each pathogen.
MIC: minimum inhibitory concentration; ATS: American Thoracic Society; CDC: United States Centers
for Disease Control and Prevention; IDSA: Infectious Diseases Society of America; TMP-SMX:
trimethoprim-sulfamethoxazole.
* The 2 mcg/mL threshold is for nonmeningitis dosing. The threshold is lower for meningitis dosing.
¶ Levofloxacin, moxifloxacin, gemifloxacin (not a first-line choice for penicillin-susceptible strains);

ciprofloxacin is appropriate for Legionella and most gram-negative bacilli (including H. influenzae).
Δ Azithromycin is more active in vitro than clarithromycin for H. influenzae.
◊ Imipenem-cilastatin, meropenem, ertapenem.
§ Piperacillin-tazobactam, ampicillin-sulbactam, ticarcillin-clavulanate (not available in the United

States), or amoxicillin-clavulanate.
¥ Ceftazidime, cefepime, aztreonam, imipenem, meropenem, or piperacillin (not available in the

United States).
‡ 750 mg daily.
† Nafcillin, oxacillin, flucloxacillin.
** Choice of antiviral regimen depends on type of influenza virus and expected resistance pattern.
(Refer to the UpToDate topic on antiviral drugs for the treatment of influenza in adults.)
¶¶ Preferred agent depends on severity of illness. Refer to associated UpToDate topic reviews for full
discussions.
Adapted with permission from: Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American
Thorac Society Consensus Guidelines on the Management of Community-acquired Pneumonia in Adults. Clin Infect Dis 2007;
44:S27. Copyright © 2007 University of Chicago Press.
Graphic 64816 Version 14.0
Septic embolization in an intravenous drug user with tricuspid valve

endocarditis
Chest radiograph shows multiple ill-defined nodular opacities, some with cavitation. This is an
example of multifocal patchy opacification.
Courtesy of Paul Stark, MD.
Talc granulomatosis
Talc granulomatosis in an intravenous drug user with multiple, partially confluent, bilateral
micronodules.
Hydrostatic pulmonary edema
Pulmonary edema in a "butterfly distribution" due to left ventricular failure. Chest radiograph shows
large perihilar opacities in patient with enlarged cardiac silhouette.

Overview of Pulmonary Disease in People Who Inject Drugs

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21/2/24, 20:12 Overview of pulmonary disease in people who inject drugs - UpToDate

Official reprint from UpToDate®

Overview of pulmonary disease in people who inject

Literature review current through: Jan 2024.

Pneumonia — PWID have a 10-fold increased risk of community-acquired pneumonia

The organisms that most commonly cause community-acquired pneumonia in this

If the etiology of community-acquired pneumonia is identified using reliable microbiologic

Tuberculosis (particularly multidrug-resistant tuberculosis) is more prevalent among PWID

tuberculosis: Clinical manifestations and complications" and "Nonresolving pneumonia",

Noncardiogenic pulmonary edema — Noncardiogenic pulmonary edema (NPE) refers to

A separate cross-sectional study of 516 participants who injected drugs demonstrated an

Pulmonary hypertension — Pulmonary hypertension may be induced by obstruction or

Drugs with sympathomimetic properties (eg, cocaine, methamphetamine) can produce

Pneumothorax and pneumomediastinum — Pneumothorax may result from unsuccessful

Pneumomediastinum is associated with inhalation of crack cocaine and, less commonly,

● One toxicologic study of 92 cases of fatal asthma in Chicago found evidence of

● Acute pulmonary complications – The acute complications of injection cocaine use

• Pulmonary hemorrhage can occur with or without frank hemoptysis and is

• Cardiogenic edema may result from cocaine-induced coronary artery spasm,

• Pneumothorax and pneumomediastinum are also reported in association with

● Chronic pulmonary complications – The chronic pulmonary complications of injection

● Heroin-induced noncardiogenic pulmonary edema usually develops rapidly within the

● Diffuse alveolar hemorrhage has been described as a complication of heroin overdose,

● Narcotics powerfully suppress central respiratory drive. Acute administration may

● In a case report, an intravenous heroin user developed respiratory failure due to

Methylphenidate and methamphetamine — Methylphenidate and methamphetamine are

● Methylphenidate – Intravenous methylphenidate has been associated with the

Habitual intravenous use of methylphenidate has been associated with the

● Methamphetamine – Methamphetamine ("speed" or "crank") is a stimulant drug that

The evaluation and management of acute methamphetamine intoxication are discussed

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● Pulmonary disease associated with IV drug use – Pulmonary complications

embolization, foreign body granulomatosis, emphysema, interstitial lung disease,

• Community-acquired pneumonia – People who inject drugs (PWID) have a 10-fold

• Pneumothorax – Pneumothorax may result from unsuccessful attempts to inject

● Pulmonary complications of IV cocaine – Complications of intravenous injection of

● Pulmonary complications of IV opioids – Pulmonary complications related to opioid

● Pulmonary complications of IV amphetamines – Intravenous injection of

Use of UpToDate is subject to the Terms of Use.

1. Hind CR. Pulmonary complications of intravenous drug misuse. 1. Epidemiology and

6. Madeddu G, Porqueddu EM, Cambosu F, et al. Bacterial community acquired pneumonia

8. Frieden TR, Sterling T, Pablos-Mendez A, et al. The emergence of drug-resistant

Recommended antimicrobial therapy for specific pathogens causing

Penicillin nonresistant; Penicillin G, amoxicillin Macrolide, cephalosporins (oral

Non-beta-lactamase Amoxicillin Fluoroquinolone, doxycycline,

Beta-lactamase producing Second- or third-generation Fluoroquinolone, doxycycline,

Mycoplasma Macrolide, a tetracycline Fluoroquinolone

Legionella species Fluoroquinolone, azithromycin Doxycycline

Chlamydophila psittaci A tetracycline Macrolide

Coxiella burnetii A tetracycline Macrolide

Francisella tularensis Doxycycline Gentamicin, streptomycin

Yersinia pestis Streptomycin, gentamicin Doxycycline, fluoroquinolone

Bacillus anthracis (inhalation) Ciprofloxacin, levofloxacin, Other fluoroquinolones; beta-

Enterobacteriaceae Third-generation cephalosporin, Beta-lactam-beta-lactamase

Pseudomonas aeruginosa Antipseudomonal beta-lactam ¥ Aminoglycoside plus

Burkholderia pseudomallei Carbapenem, ceftazidime Fluoroquinolone, TMP-SMX

Acinetobacter species Carbapenem Cephalosporin-aminoglycoside,

Methicillin susceptible Antistaphylococcal penicillin † Cefazolin, clindamycin

Methicillin resistant Vancomycin or linezolid TMP-SMX

Bordetella pertussis Macrolide TMP-SMX

Anaerobe (aspiration) Beta-lactam-beta-lactamase Carbapenem

Influenza virus Refer to associated topic