DOI: 10.1148/rg.274065103
RadioGraphics 2007;27:919-940
© RSNA, 2007
Radiology of Recreational Drug Abuse1
Ian G. Hagan, BM, BCh, BCh, MRCP, FRCR and
Kashif Burney, MB, BS, MRCS, FRCR
1 From the Departments of Radiology, Bristol Royal Infirmary (I.G.H.) and Southmead Hospital (K.B.), Bristol, England. Presented as an education exhibit at the 2005 RSNA Annual Meeting. Received May 18, 2006; revision requested August 22 and received October 30; accepted October 30. All authors have no financial relationships to disclose.
Address correspondence to I.G.H., Department of Radiology, Cheltenham General Hospital, Sandford Road, Cheltenham GL53 7AN, United Kingdom (e-mail: ian_hagan{at}yahoo.com).
 |
Abstract
|
|---|
Recreational drug abuse is increasing throughout the world. Use of these drugs may result in a diverse array of acute and chronic complications involving almost any body organ, and imaging frequently plays a vital role in detection and characterization of such complications. The nature of the complications depends to a large extent on the drug used, the method of administration, and the impurities associated with the drug. Radiologically demonstrable sequelae may be seen after use of opiates, cocaine, amphetamines and their derivatives such as 3,4-methylenedioxymethamphetamine ("ecstasy"), marijuana, and inhaled volatile agents including amyl nitrite ("poppers") and industrial solvents such as toluene. Cardiovascular complications include myocardial infarction, cardiomyopathy, arterial dissection, false and mycotic aneurysms, venous thromboembolic disease, and septic thrombophlebitis. Respiratory complications may involve the upper airways, lung parenchyma, pulmonary vasculature, and pleural space. Neurologic complications are most commonly due to the cerebrovascular effects of illicit drugs. Musculoskeletal complications are dominated by soft-tissue, bone, and joint infections caused by intravenous drug use. Awareness of the imaging features of recreational drug abuse is important for the radiologist because the underlying cause may not be known at presentation and because complications affecting different body systems may coexist. Intravenous drug abuse in particular should be regarded as a multisystem disease with vascular and infective complications affecting many parts of the body, often synchronously. Discovery of one complication should prompt the radiologist to search for coexisting pathologic conditions, which may alter management.
© RSNA, 2007
|
LEARNING OBJECTIVES FOR TEST 1
|
|---|
After reading this article and taking the test, the reader will be able to:- List the multisystem complications of recreational drug abuse that may be detected with radiology.
- Describe the pathophysiology underlying the multisystem complications of recreational drug abuse.
- Identify the multimodality imaging features of recreational drug abuse.
|
Introduction
|
|---|
The use of recreational drugs is by no means a new phenomenon, having existed as long as civilization itself. In recent times, however, the number of people using recreational drugs seems to be increasing (1,2). In the United Kingdom, for example, government statistics indicate that nearly half of all young people aged 15–24 years have used illegal drugs at some point (3,4), and when questioned nearly one in five 16–24-year-olds reported the use of such drugs in the preceding month (4). On a wider scale, 5% of the global population aged 15–64 years has used illicit drugs at least once in the past year (2). When statistics such as these are viewed in conjunction with the potential adverse effects of recreational drug use, it can be seen that this constitutes a substantial public health problem. The size of this health burden is difficult to measure accurately, but one independent United Kingdom study found that 6.9% of all patient attendances in an inner-city emergency department were directly or indirectly related to illegal drug use (5).
The medical complications of recreational drug use are diverse, involving almost any body organ, and vary greatly according to the substance used and the route by which it is taken. They can be due to the physical or mechanical effects of the method of administration, the direct chemical or pharmacologic effects of the drug, the effects of adulterants or filler agents mixed with the primary active drug, the microbiologic sequelae of drug administration, and finally the social and behavioral consequences of drug use, including an increase in risk-taking behavior and an association with violent crime and prostitution.
For a large number of these complications, imaging plays a key role in their detection and characterization. Furthermore, the illicit nature of recreational drug use means that at the time a patient presents with a complication in either the acute or chronic setting, the underlying cause may not be known, and it is the reporting radiologist who may be the first to suggest the diagnosis. For these reasons, it is vital that radiologists have an awareness of the imaging spectrum of drug abuse, and it is this spectrum that we attempt to describe and illustrate in this article. The drugs covered include cocaine, amphetamines and their derivatives such as 3,4-methylenedioxymetham-phetamine (MDMA) (commonly known as "ecstasy"), opiates, cannabis, and inhaled volatile agents, including amyl and butyl nitrites (commonly known as "poppers") and industrial solvents such as toluene. The radiologically demonstrable effects of the use of these drugs on various body systems are reviewed, including cardiovascular, thoracic, neurologic, musculoskeletal, and other soft-tissue and visceral complications. Maternal drug use also has a number of deleterious effects on the developing fetus, but these aspects are not covered herein.
|
Cardiovascular Complications
|
|---|
The adverse effects of recreational drugs on the cardiovascular system can be divided into cardiac, arterial, and venous complications. Table 1 summarizes cardiovascular complications by particular drug.
Cardiac Complications
Cocaine, amphetamine, and amphetamine derivatives such as MDMA may cause intense coronary vasoconstriction (6,7). Cocaine may in addition stimulate platelet activation (8). These factors may lead to acute myocardial ischemia and infarction (6,7) and their associated complications, even in the presence of otherwise normal coronary arteries (Fig 1). Chronic use of these drugs may result in dilated cardiomyopathy (Fig 2), but this is often reversible with cessation of the drug (9).
View larger version (171K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1. Acute anterior myocardial infarction after cocaine use in a 41-year-old man. Cranial right anterior oblique view from left coronary angiography shows an ill-defined filling defect (arrows) in the mid left anterior descending artery. The filling defect is due to a soft thrombus. The coronary vessels are otherwise normal.
|
|
View larger version (107K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2a. Cocaine-induced dilated cardiomyopathy in a 48-year-old man. (a) Contrast-enhanced computed tomographic (CT) image (window level = 40 HU, window width = 400 HU) shows dilatation of the left ventricle and a filling defect in the ventricle (arrow), which represents a mural thrombus. (b) CT image obtained 6 months later, after abstinence from cocaine and treatment with warfarin, shows that the heart is normal in size and no thrombus is seen.
|
|
View larger version (92K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2b. Cocaine-induced dilated cardiomyopathy in a 48-year-old man. (a) Contrast-enhanced computed tomographic (CT) image (window level = 40 HU, window width = 400 HU) shows dilatation of the left ventricle and a filling defect in the ventricle (arrow), which represents a mural thrombus. (b) CT image obtained 6 months later, after abstinence from cocaine and treatment with warfarin, shows that the heart is normal in size and no thrombus is seen.
|
|
Intravenous (IV) drug users are at risk of developing endocarditis (10), particularly tricuspid endocarditis, as a consequence of bacteremia produced by nonsterile injection techniques. Vegetations are well demonstrated with transthoracic (Fig 3) or transesophageal echocardiography and may occasionally be visualized at multidetector CT of the thorax. In addition to local valvular complications, vegetations may lead to septic embolization, and in the case of right-sided endocarditis such embolization occurs to the lungs (discussed later).
View larger version (92K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3a. Endocarditis of the tricuspid valve in a 24-year-old male IV drug user. Parasternal short-axis views from echocardiography, obtained during systole (a) and diastole (b), show a mobile echogenic mass (arrow) related to the tricuspid valve, a finding consistent with a vegetation. Chest radiography showed multiple septic pulmonary emboli. LV = left ventricle, RA = right atrium, RV = right ventricle.
|
|
View larger version (103K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3b. Endocarditis of the tricuspid valve in a 24-year-old male IV drug user. Parasternal short-axis views from echocardiography, obtained during systole (a) and diastole (b), show a mobile echogenic mass (arrow) related to the tricuspid valve, a finding consistent with a vegetation. Chest radiography showed multiple septic pulmonary emboli. LV = left ventricle, RA = right atrium, RV = right ventricle.
|
|
Arterial Complications
Aortic dissection after cocaine use is well recognized (7,11,12), the combination of systemic hypertension and the positive inotropic and chronotropic cardiac effects produced by this drug engendering the conditions favoring the development of aortic dissection. The radiologic appearances of cocaine-induced aortic dissection are the same as those of dissection due to other causes, including the presence of an intimal flap and intramural and mediastinal hematoma. These features are well demonstrated with both multidetector CT and magnetic resonance (MR) imaging, though for reasons of accessibility and speed in the emergency setting the former of these modalities is generally preferred.
IV drug use may result in a variety of local arterial complications at the injection site. Inadvertent arterial puncture may result in traumatic arterial dissection and even arterial occlusion with consequent acute limb ischemia. Arterial puncture may also result in formation of a false aneurysm. These lesions have a typical appearance at duplex ultrasonography (US) (Fig 4), consisting of a cavity communicating with an adjacent artery via a neck and containing turbulent pulsatile flow. At injection sites with restricted acoustic windows such as the medial subclavian vessels, CT (particularly CT angiography), MR imaging, and catheter angiography can provide a definitive diagnosis of arterial false aneurysm if US proves problematic. Chest radiography may suggest the diagnosis by demonstrating an extrapleural mass over the medial lung apex with a discrete inferior margin and an ill-defined superior margin (13).
View larger version (109K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4. False aneurysm in a 36-year-old female IV drug user. Transverse image from duplex US of the left groin shows a jet that communicates between the common femoral artery and an anterior cavity via a narrow neck.
|
|
Not infrequently, the nonsterile nature of injections leads to infection of false aneurysms, resulting in mycotic aneurysm formation (14). The presence of gas within the aneurysm is a rare but pathognomonic feature of infection and is best seen at CT (13,14). Complications include rupture with possible limb loss (15). Mycotic aneurysms may form elsewhere in the circulation due to hematogenous bacterial seeding and subsequent arterial wall damage (Fig 5).
View larger version (154K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5a. Renal mycotic aneurysm in a 33-year-old male IV drug user with endocarditis who presented with hematuria and clot retention. US showed an aneurysm in the upper pole of the right kidney. (a) Coronal reformatted image from contrast-enhanced CT (window level = 40 HU, window width = 500 HU) shows an intrarenal aneurysm (black arrows) arising from an upper pole renal artery (white arrows). No enhancement of the renal parenchyma is seen surrounding the aneurysm; there is low-attenuation material extending into the renal pelvis and upper ureter (arrowheads), a finding that represents blood. (b) Selective conventional arteriogram shows a jet of contrast material (arrow) entering the aneurysm. (c) Image obtained later in the angiographic series shows incomplete opacification of the aneurysm (arrowheads) due to the presence of thrombosis. The aneurysm was successfully treated with coil embolization followed by nephrectomy.
|
|
View larger version (133K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5b. Renal mycotic aneurysm in a 33-year-old male IV drug user with endocarditis who presented with hematuria and clot retention. US showed an aneurysm in the upper pole of the right kidney. (a) Coronal reformatted image from contrast-enhanced CT (window level = 40 HU, window width = 500 HU) shows an intrarenal aneurysm (black arrows) arising from an upper pole renal artery (white arrows). No enhancement of the renal parenchyma is seen surrounding the aneurysm; there is low-attenuation material extending into the renal pelvis and upper ureter (arrowheads), a finding that represents blood. (b) Selective conventional arteriogram shows a jet of contrast material (arrow) entering the aneurysm. (c) Image obtained later in the angiographic series shows incomplete opacification of the aneurysm (arrowheads) due to the presence of thrombosis. The aneurysm was successfully treated with coil embolization followed by nephrectomy.
|
|
View larger version (178K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5c. Renal mycotic aneurysm in a 33-year-old male IV drug user with endocarditis who presented with hematuria and clot retention. US showed an aneurysm in the upper pole of the right kidney. (a) Coronal reformatted image from contrast-enhanced CT (window level = 40 HU, window width = 500 HU) shows an intrarenal aneurysm (black arrows) arising from an upper pole renal artery (white arrows). No enhancement of the renal parenchyma is seen surrounding the aneurysm; there is low-attenuation material extending into the renal pelvis and upper ureter (arrowheads), a finding that represents blood. (b) Selective conventional arteriogram shows a jet of contrast material (arrow) entering the aneurysm. (c) Image obtained later in the angiographic series shows incomplete opacification of the aneurysm (arrowheads) due to the presence of thrombosis. The aneurysm was successfully treated with coil embolization followed by nephrectomy.
|
|
Arteriovenous fistula formation is usually a sequela of a mycotic aneurysm (14) and may lead to septicemia or endocarditis. US, CT angiography, MR angiography, and conventional angiography are all useful in diagnosis.
Venous Complications
Deep venous thrombosis is common in IV drug users. Once sites for IV injection in the arms have been exhausted, drug users will move on to use the femoral vein at the groin or less commonly the subclavian or jugular veins. 
Almost all regular IV drug users have some chronic nonocclusive thrombus at the regular injection site (Fig 6). Intermittently, additional acute thrombus will develop, propagating to a varying extent (Fig 7), and US is well suited for assessment of these complications. Nonsterile injection makes superimposed infection in the form of septic thrombophlebitis a frequent occurrence. Irregular thickening of the vein wall at US is suggestive of this complication. Occasionally, gas may be seen within the vein at CT, although the presence of gas without vessel wall thickening may simply reflect air introduced at injection. Infected and noninfected thrombus may break off, resulting in septic and conventional pulmonary emboli, respectively (discussed later).
View larger version (162K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 6. Chronic nonocclusive thrombus in a 28-year-old male IV drug user. Longitudinal US image of the common femoral vein shows the regular injection site, which is indicated by a hypoechoic scar extending from the skin to the vessel. A chronic nonocclusive thrombus (T) is seen in the vein with acquired venous stenosis.
|
|
|
Respiratory Complications
|
|---|
The respiratory complications of drug abuse may involve the upper airways, lungs, and pleura and include pneumonia, pulmonary edema, pulmonary hemorrhage, drug-induced granulomatosis, emphysema, and pneumothorax. Table 2 summarizes respiratory complications by particular drug.
Upper Respiratory Tract Complications
Bronchitis, epiglottitis, and sinusitis have all been reported after both nasal insufflation of cocaine hydrochloride and smoking of alkaloidal (freebase or crack) cocaine. In particular, the nasal septum seems to be highly sensitive to the local vasoconstriction caused by nasal cocaine use, and septal perforation due to ischemic necrosis is a common complication of chronic cocaine use. A more aggressive intranasal and pharyngeal destructive process simulating midline granuloma disease and Wegener granulomatosis clinically and radiologically has been described in heavy cocaine use (16). A history of cocaine use should be sought when these two diagnoses are being considered, as the treatment of cocaine nose is clearly different.
Pneumonia
For reasons that are not entirely clear, there seems to be an increased prevalence of bacterial pneumonia among IV drug users (17). In addition, any consciousness-altering drug places the drug user at risk of aspiration pneumonia (18), and this is particularly true of opiates. The local anesthetic effect of cocaine in the pharynx may also lead to aspiration events (19). As with other causes of aspiration pneumonia, it is the dependent portions of the lung in the supine position that are most often involved, specifically the apical and posterior segments of the upper lobes and apical segments of the lower lobes. Consolidation with or without volume loss is seen at these sites at chest radiography or CT. Aspiration of volatile organic compounds such as amyl and butyl nitrites (commonly known as "poppers") during attempted inhalation of vapors may lead to the development of lipoid pneumonia (Fig 8).
View larger version (128K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 8a. Lipoid pneumonia in a 52-year-old man with a persistent area of consolidation in the right lower lobe that was unresponsive to antibiotics. After biopsy with inconclusive results, surgical resection revealed lipoid pneumonia, and the patient gave a history of accidental aspiration of "poppers" (amyl or butyl nitrite). (a) High-resolution CT image (window level = –500 HU, window width = 1500 HU) shows a rounded area of consolidation in the right lower lobe. (b) CT image shows thickened interlobular septa and subtle tree-in-bud abnormalities just below the area of consolidation; these are features of lipoid pneumonia.
|
|
View larger version (121K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 8b. Lipoid pneumonia in a 52-year-old man with a persistent area of consolidation in the right lower lobe that was unresponsive to antibiotics. After biopsy with inconclusive results, surgical resection revealed lipoid pneumonia, and the patient gave a history of accidental aspiration of "poppers" (amyl or butyl nitrite). (a) High-resolution CT image (window level = –500 HU, window width = 1500 HU) shows a rounded area of consolidation in the right lower lobe. (b) CT image shows thickened interlobular septa and subtle tree-in-bud abnormalities just below the area of consolidation; these are features of lipoid pneumonia.
|
|
Pulmonary Edema
Cardiogenic pulmonary edema may be seen in drug users as a result of the adverse myocardial effects described earlier. Many drugs can also produce noncardiogenic pulmonary edema, especially in overdose. Although this complication is classically associated with opiate overdose (20), it is well described in cocaine use (21), particularly with IV use of cocaine hydrochloride and smoking of crack cocaine, as well as with amphetamine and its derivatives such as MDMA (Fig 9). The exact mechanism of lung injury in these cases is not clear, but possible explanations include a direct toxic effect on the alveolar-capillary membrane, immune response activation, and neurogenic pulmonary edema secondary to the central nervous system (CNS) effects of the drug.
View larger version (156K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 9. Acute noncardiogenic pulmonary edema in a 19-year-old man after an overdose of MDMA. Chest radiograph shows bilateral perihilar airspace shadowing with normal heart size and no pleural effusion.
|
|
Radiographic findings are similar to those of other causes of pulmonary edema, most commonly taking the form of bilateral perihilar airspace opacification (Fig 9). In contrast to cardiogenic pulmonary edema, pleural effusion and cardiomegaly are usually absent. Heart size is not a reliable discriminator, however, because in cardiogenic pulmonary edema due to drug-induced acute myocardial ischemia or drug-induced cardiac arrhythmia the heart size may well be normal. Typically, radiographic abnormalities resolve rapidly—often within hours—although edema may be more protracted with longer-acting agents such as methadone (22).
Pulmonary Hemorrhage
There are many reports of pulmonary alveolar hemorrhage after cocaine use (23), particularly with crack cocaine. Chest radiography demonstrates multifocal airspace shadowing that may be indistinguishable from pulmonary edema, and high-resolution CT usually shows bilateral scattered or diffuse ground-glass opacities. As with pulmonary edema, radiographic abnormalities in drug-induced pulmonary hemorrhage typically clear rapidly, although chronic pulmonary hemorrhage has been identified in cocaine users in autopsy studies (24).
Pulmonary Embolism and Septic Embolization
Deep venous thrombosis in IV drug users may be complicated by pulmonary embolism, which may be detected with ventilation-perfusion scintigraphy or CT pulmonary angiography (Fig 10). Septic emboli may result as a consequence of septic thrombophlebitis, tricuspid valve endocarditis (see the section on cardiac complications), or simply injection of microorganisms with the drug. Radiographic findings consist of multiple pulmonary nodules with or without cavitation (Fig 11). CT demonstrates multiple ill-defined peripheral pulmonary nodules, some of which may show cavitation (Fig 12). These peripherally located pulmonary abscesses may rupture into the pleural space, leading to empyema, pyopneumothorax (Fig 12), or occasionally bronchopleural fistula formation.
View larger version (93K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10a. Acute pulmonary embolism in a 38-year-old male IV drug user. (a) Pulmonary CT angiogram (window level = 40 HU, window width = 400 HU) shows a filling defect in a right lower lobe pulmonary artery (arrow). (b) CT image shows a small area of pulmonary infarction just beyond the embolus.
|
|
View larger version (136K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10b. Acute pulmonary embolism in a 38-year-old male IV drug user. (a) Pulmonary CT angiogram (window level = 40 HU, window width = 400 HU) shows a filling defect in a right lower lobe pulmonary artery (arrow). (b) CT image shows a small area of pulmonary infarction just beyond the embolus.
|
|
View larger version (155K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 11a. Septic pulmonary emboli in a 26-year-old male IV drug user. (a) Chest radiograph shows at least two pulmonary nodules (short arrows). A strong diagnostic clue is provided by the syringe (long arrows) in the patient’s shirt pocket. (b) Magnified view of the left lung base shows the syringe.
|
|
View larger version (138K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 11b. Septic pulmonary emboli in a 26-year-old male IV drug user. (a) Chest radiograph shows at least two pulmonary nodules (short arrows). A strong diagnostic clue is provided by the syringe (long arrows) in the patient’s shirt pocket. (b) Magnified view of the left lung base shows the syringe.
|
|
View larger version (104K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 12a. Pyopneumothorax complicating septic emboli in a 28-year-old male IV drug user. (a) Contrast-enhanced thoracic CT image (window level = –500 HU, window width = 1500 HU) shows cavitating lesions in the left upper lobe. (b) CT image obtained inferiorly to a shows right-sided pyopneumothorax due to rupture of a peripheral pulmonary abscess into the pleural space.
|
|
View larger version (106K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 12b. Pyopneumothorax complicating septic emboli in a 28-year-old male IV drug user. (a) Contrast-enhanced thoracic CT image (window level = –500 HU, window width = 1500 HU) shows cavitating lesions in the left upper lobe. (b) CT image obtained inferiorly to a shows right-sided pyopneumothorax due to rupture of a peripheral pulmonary abscess into the pleural space.
|
|
Pulmonary Granulomatosis
Insoluble filler agents in oral medications such as talc (magnesium silicate), starch, and cellulose may cause a spectrum of pulmonary abnormalities when oral medications are abused intravenously, by eliciting a foreign-body granulomatous reaction. The particles may occlude small pulmonary vessels leading ultimately to pulmonary hypertension (25). If the particles migrate into perivascular connective tissues, a granulomatous response manifesting as diffuse small nodular opacities at chest radiography and high-resolution CT (18,26) may be seen.
Over time, perihilar and upper lobe conglomerate masses may develop (18,26,27), redolent of the progressive massive fibrosis seen in pneumoconiosis, and these masses may be of high attenuation at CT. Other radiologic findings may be seen in combination, including ground-glass opacification, pulmonary hyperinflation with lower lobe–predominant panlobular emphysema, cardiac and vascular features of pulmonary hypertension, and reactive mediastinal lymphadenopathy. Although patients with drug-induced pulmonary granulomatosis may be essentially asymptomatic at diagnosis, progression to severe respiratory insufficiency can occur in due course.
Emphysema
A striking pattern of large upper lobe bullae formation has been reported in regular marijuana users (Fig 13) (28). Although it is difficult to discount entirely the role of concomitant tobacco consumption in these cases, the relatively young age of the patients and low cumulative tobacco exposure suggest at least an additive role for marijuana in the pathogenesis. It is likely that the pathophysiologic mechanism for large bulla formation involves a combination of direct pulmonary toxic effects with pleural pressure swings and airway barotrauma brought about by the high inspiratory pressures produced in marijuana smoking.
View larger version (140K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 13a. Bullous emphysema in a 27-year-old man with a long history of heavy marijuana use and only modest tobacco consumption. (a) Chest radiograph obtained at presentation shows a large left-sided pneumothorax. There are also bullae at the right apex. (b) High-resolution CT image (window level = –500 HU, window width = 1500 HU) obtained after reinflation of the left lung shows large bilateral apical bullae. The remainder of the lungs was normal. (c) Follow-up chest CT image obtained 4 years later after continued heavy marijuana use shows progression of the bullous lung disease.
|
|
View larger version (119K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 13b. Bullous emphysema in a 27-year-old man with a long history of heavy marijuana use and only modest tobacco consumption. (a) Chest radiograph obtained at presentation shows a large left-sided pneumothorax. There are also bullae at the right apex. (b) High-resolution CT image (window level = –500 HU, window width = 1500 HU) obtained after reinflation of the left lung shows large bilateral apical bullae. The remainder of the lungs was normal. (c) Follow-up chest CT image obtained 4 years later after continued heavy marijuana use shows progression of the bullous lung disease.
|
|
View larger version (99K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 13c. Bullous emphysema in a 27-year-old man with a long history of heavy marijuana use and only modest tobacco consumption. (a) Chest radiograph obtained at presentation shows a large left-sided pneumothorax. There are also bullae at the right apex. (b) High-resolution CT image (window level = –500 HU, window width = 1500 HU) obtained after reinflation of the left lung shows large bilateral apical bullae. The remainder of the lungs was normal. (c) Follow-up chest CT image obtained 4 years later after continued heavy marijuana use shows progression of the bullous lung disease.
|
|
The development of upper lobe bullous emphysema has also been observed in IV drug users (29), and the IV abuse of methylphenidate has been linked specifically to the development of lower lobe panlobular emphysema (30). The radiologic features closely resemble those of 
1-antitrypsin deficiency, consisting of pulmonary hyperinflation with lower zone hyperlucency at chest radiography and simplification of lower lobe pulmonary architecture at high-resolution CT.
Pneumothorax
Pneumothorax may complicate drug abuse for various reasons (18). It may be due to attempted subclavian or jugular vein puncture in IV drug users, rupture of drug-related bullae (Fig 13), or rarely rupture of peripheral pulmonary abscesses due to septic embolization (Fig 12). The large airway pressure changes involved in inhalational maneuvers employed in crack or cannabis use may also lead to rupture of distal airways. Air may then track into the pleural space or mediastinum, manifesting as pneumothorax or pneumomediastinum respectively (18).
|
Neurologic Complications
|
|---|
Aside from the increased risk of accidental and nonaccidental cranial trauma associated with the behavioral effects of drug use, it is cerebrovascular effects that dominate the spectrum of drug-related neurologic complications, leading to hemorrhagic and ischemic events. Other complications include posterior reversible encephalopathy syndrome (PRES), diffuse cerebral edema, toxic leukoencephalopathies, cerebral atrophy, and CNS infection. Table 3 summarizes neurologic complications by particular drug.
Intracranial Hemorrhage
The sympathomimetic effects of cocaine and amphetamines result in systemic vasoconstriction and increased cardiac output, which in turn can lead to severe acute hypertension and subsequent intracranial hemorrhage. Hemorrhage is most commonly intracerebral, particularly in the basal ganglia territory (Fig 14), although primary intraventricular hemorrhage and subarachnoid hemorrhage have been described (31,32). Case series indicate that approximately one-half of all patients with cocaine-related intracranial hemorrhage have an underlying vascular lesion such as a cerebral aneurysm or arteriovenous malformation (33) that has been unmasked by the hypertensive effects of the cocaine, and this should be borne in mind when investigating these patients.
View larger version (142K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 14. Intracerebral hemorrhage related to cocaine use in a 40-year-old man. Unenhanced cranial CT image (window level = 40 HU, window width = 100 HU) shows acute hemorrhage in the left basal ganglia with intraventricular extension.
|
|
There is an increased risk of CNS complications with the alkaloidal form of cocaine, which is smoked and achieves higher CNS concentrations more rapidly than nasal insufflation of cocaine hydrochloride (32). While cocaine hydrochloride and amphetamines are more likely to result in hemorrhagic CNS complications, ischemic complications are at least as likely as hemorrhagic complications with crack cocaine (31,32).
Ischemic Stroke
The mechanism of ischemic stroke related to cocaine and amphetamine use is multifactorial, involving their hemodynamic and vasoconstrictive effects (31–33), and cocaine has also been shown to have a thrombogenic effect via platelet activation (8,31,32). Interestingly, although the risk of ischemic stroke is highest in the first few hours after taking cocaine, there may be a delay in stroke onset as long as 1 week, possibly due to the formation of longer-acting secondary metabolites (34). Ischemic strokes are also well recognized as a complication of MDMA (35,36) (Fig 15) and heroin (37–39) use, thought to be due to vasoconstriction produced by serotonin release and activation of muopioid receptors, respectively. Less common causes of drug-related ischemic events include cerebral vasculitis in amphetamine, cocaine, and possibly heroin users (31–33,39–41) and embolic events due to endocarditis or injection of particulate material in IV drug users.
View larger version (153K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 15a. Acute cerebral infarction after MDMA use in a 21-year-old woman. (a) Axial fluid-attenuated inversion-recovery MR image shows cortical and subcortical high signal intensity in the right frontal lobe. (b) Axial T2-weighted MR image shows fixed gaze deviation to the left. Gaze disorders are among the toxic effects of MDMA.
|
|
View larger version (144K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 15b. Acute cerebral infarction after MDMA use in a 21-year-old woman. (a) Axial fluid-attenuated inversion-recovery MR image shows cortical and subcortical high signal intensity in the right frontal lobe. (b) Axial T2-weighted MR image shows fixed gaze deviation to the left. Gaze disorders are among the toxic effects of MDMA.
|
|
The radiologic features of drug-induced ischemic strokes are the same as those of other causes of ischemic stroke, with low attenuation at CT and high signal intensity at T2-weighted MR imaging; in the acute phase, restricted diffusion is demonstrated at diffusion-weighted MR imaging, the latter being the most sensitive technique for diagnosis. MR angiography and cerebral angiography may show vasospasm or occlusion of the major cerebral arteries, and vasospasm and vasculitis can be difficult to distinguish with these techniques.
Although the radiologic features of individual ischemic lesions are the same, the location of these lesions varies somewhat with different agents, as summarized in Table 4. Infarcts related to cocaine and amphetamine often involve the cerebral white matter, particularly in the middle cerebral artery territory (31,32). The distribution of serotonin receptors in the brain renders the occipital cortex and globus pallidus most susceptible to MDMA-induced ischemia, and globus pallidus necrosis is a common postmortem finding in MDMA users (35,36). Infarcts caused by heroin are frequently seen in so-called watershed territories such as the cerebellum or hippocampus (37,39) and most commonly of all involve the globus pallidus (37). Ultimately, however, any part of the CNS may be involved by drug-induced ischemia, including the spinal cord (42).
In the chronic setting, ischemic lesions in cerebral white matter in excess of that expected for age have been reported in chronic cocaine and opiate users, even in those who are asymptomatic (43,44). Such lesions are more common in cocaine users (44) and in this group are strongly age related (43).
Posterior Reversible Encephalopathy Syndrome
Hypertensive crisis brought on by cocaine or amphetamine use may result in PRES. This is due to failure of cerebrovascular autoregulation at very high blood pressures, resulting in cerebral hyper-perfusion, blood-brain barrier disruption, and vasogenic edema (45). Patients present with headache, altered mental status, and occasionally seizures. The subcortical white matter and cortex of the posterior circulation are most commonly involved, with the basal ganglia and brainstem much less frequently so.
CT findings may be fairly subtle, with patchy symmetric low attenuation in the posterior parietal and occipital lobes (Fig 16). MR imaging more readily demonstrates abnormalities as bilateral areas of cortical or subcortical high signal intensity in the same locations (Fig 16). Unlike the cytotoxic edema of acute cerebral infarction, the vasogenic edema of PRES is not usually associated with restricted diffusion at diffusion-weighted MR imaging (46). Progression to cerebral infarction or hemorrhage is rare, and complete resolution of clinical and radiologic abnormalities can be expected with successful medical management of hypertension (47) (Fig 16).
View larger version (78K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16a. PRES due to cocaine-induced malignant hypertension in a 23-year-old man with headaches, confusion, seizures, and very high blood pressure after cocaine use. (a) Unenhanced cranial CT image shows subtle cortical and subcortical low attenuation in the parieto-occipital region bilaterally. (b, c) Axial T2-weighted MR images show abnormal high signal intensity in the same location (b) and more inferiorly in the occipital lobes (c), findings typical of PRES. Owing to clinical symptoms of a spinal cord syndrome, images of the entire spine were obtained. (d) Sagittal T2-weighted MR image shows abnormal central high signal intensity throughout the spinal cord. This finding is highly unusual for PRES and raised concern about spinal infarction. However, the patient responded well to medical management of the hypertension. (e, f) Repeat axial (e) and sagittal (f) T2-weighted MR images obtained 4 weeks later show complete resolution of the radiologic abnormalities.
|
|
View larger version (154K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16b. PRES due to cocaine-induced malignant hypertension in a 23-year-old man with headaches, confusion, seizures, and very high blood pressure after cocaine use. (a) Unenhanced cranial CT image shows subtle cortical and subcortical low attenuation in the parieto-occipital region bilaterally. (b, c) Axial T2-weighted MR images show abnormal high signal intensity in the same location (b) and more inferiorly in the occipital lobes (c), findings typical of PRES. Owing to clinical symptoms of a spinal cord syndrome, images of the entire spine were obtained. (d) Sagittal T2-weighted MR image shows abnormal central high signal intensity throughout the spinal cord. This finding is highly unusual for PRES and raised concern about spinal infarction. However, the patient responded well to medical management of the hypertension. (e, f) Repeat axial (e) and sagittal (f) T2-weighted MR images obtained 4 weeks later show complete resolution of the radiologic abnormalities.
|
|
View larger version (157K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16c. PRES due to cocaine-induced malignant hypertension in a 23-year-old man with headaches, confusion, seizures, and very high blood pressure after cocaine use. (a) Unenhanced cranial CT image shows subtle cortical and subcortical low attenuation in the parieto-occipital region bilaterally. (b, c) Axial T2-weighted MR images show abnormal high signal intensity in the same location (b) and more inferiorly in the occipital lobes (c), findings typical of PRES. Owing to clinical symptoms of a spinal cord syndrome, images of the entire spine were obtained. (d) Sagittal T2-weighted MR image shows abnormal central high signal intensity throughout the spinal cord. This finding is highly unusual for PRES and raised concern about spinal infarction. However, the patient responded well to medical management of the hypertension. (e, f) Repeat axial (e) and sagittal (f) T2-weighted MR images obtained 4 weeks later show complete resolution of the radiologic abnormalities.
|
|
View larger version (148K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16d. PRES due to cocaine-induced malignant hypertension in a 23-year-old man with headaches, confusion, seizures, and very high blood pressure after cocaine use. (a) Unenhanced cranial CT image shows subtle cortical and subcortical low attenuation in the parieto-occipital region bilaterally. (b, c) Axial T2-weighted MR images show abnormal high signal intensity in the same location (b) and more inferiorly in the occipital lobes (c), findings typical of PRES. Owing to clinical symptoms of a spinal cord syndrome, images of the entire spine were obtained. (d) Sagittal T2-weighted MR image shows abnormal central high signal intensity throughout the spinal cord. This finding is highly unusual for PRES and raised concern about spinal infarction. However, the patient responded well to medical management of the hypertension. (e, f) Repeat axial (e) and sagittal (f) T2-weighted MR images obtained 4 weeks later show complete resolution of the radiologic abnormalities.
|
|
View larger version (126K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16e. PRES due to cocaine-induced malignant hypertension in a 23-year-old man with headaches, confusion, seizures, and very high blood pressure after cocaine use. (a) Unenhanced cranial CT image shows subtle cortical and subcortical low attenuation in the parieto-occipital region bilaterally. (b, c) Axial T2-weighted MR images show abnormal high signal intensity in the same location (b) and more inferiorly in the occipital lobes (c), findings typical of PRES. Owing to clinical symptoms of a spinal cord syndrome, images of the entire spine were obtained. (d) Sagittal T2-weighted MR image shows abnormal central high signal intensity throughout the spinal cord. This finding is highly unusual for PRES and raised concern about spinal infarction. However, the patient responded well to medical management of the hypertension. (e, f) Repeat axial (e) and sagittal (f) T2-weighted MR images obtained 4 weeks later show complete resolution of the radiologic abnormalities.
|
|
View larger version (157K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16f. PRES due to cocaine-induced malignant hypertension in a 23-year-old man with headaches, confusion, seizures, and very high blood pressure after cocaine use. (a) Unenhanced cranial CT image shows subtle cortical and subcortical low attenuation in the parieto-occipital region bilaterally. (b, c) Axial T2-weighted MR images show abnormal high signal intensity in the same location (b) and more inferiorly in the occipital lobes (c), findings typical of PRES. Owing to clinical symptoms of a spinal cord syndrome, images of the entire spine were obtained. (d) Sagittal T2-weighted MR image shows abnormal central high signal intensity throughout the spinal cord. This finding is highly unusual for PRES and raised concern about spinal infarction. However, the patient responded well to medical management of the hypertension. (e, f) Repeat axial (e) and sagittal (f) T2-weighted MR images obtained 4 weeks later show complete resolution of the radiologic abnormalities.
|
|
Diffuse Cerebral Edema
Patients present with diffuse cerebral edema after recreational drug use for a variety of reasons, and generally it indicates a poor prognosis. It may reflect anoxic brain injury after drug-induced cardiac arrest or severe respiratory depression in the case of opiate overdose, or may be a manifestation of fulminant multiorgan failure in drug overdose (48,49). A particular mechanism of cerebral edema has been reported in association with the use of MDMA as a dance drug in clubs. Aware of the risks of hyperthermia and dehydration in this setting, MDMA users often consume large quantities of water. In some cases, this has led to severe cerebral edema due to dilutional hyponatremia (50). Radiologic features include loss of gray-white matter differentiation with diffuse low attenuation at CT and high signal intensity at T2-weighted MR imaging, as well as effacement of sulci and basal cisterns.
Toxic Leukoencephalopathy
Nonischemic white matter damage has been described with some drugs. A specific leukoencephalopathy has been ascribed to the inhalation of heroin vapor (pyrolysate) (51–53) when the drug is heated on tinfoil, a practice known as "chasing the dragon." It is likely that the disorder is due to an impurity in the heroin rather than the heroin per se, but in any event it is unique to this method of administration. Patients present with cerebellar or extrapyramidal syndromes. Imaging features are characteristic (52,53), with symmetric low attenuation at CT and high signal intensity at T2-weighted MR imaging in the cerebellar white matter, cerebral peduncles, and posterior limb of the internal capsule, with sparing of the anterior limb of the internal capsule and subcortical white matter. Histologic analysis demonstrates spongiform degeneration in the affected areas (51).
A more nonspecific leukoencephalopathy is seen in chronic inhalant abuse of industrial solvents such as toluene, consisting of patchy demyelination and gliosis in cerebral and cerebellar white matter, seen as diffuse high signal intensity in these regions on T2-weighted MR images (54,55). Such lesions can be explained by the high affinity of these lipophilic volatile agents for myelin, and the extent of the lesions seems to correlate with neuropsychologic deficits in these patients (54,55). Symmetric thalamic low signal intensity on T2-weighted MR images reflecting iron deposition may also be seen in this group (55).
Cerebral Atrophy
Cerebral atrophy is a feature of chronic use of many different drugs, including cocaine (56), amphetamines, opiates (57), and inhaled organic solvents (54,55), being a nonspecific sequela of the different cerebral insults described earlier. There seems to be preferential cerebral volume loss in the frontal lobes and to a lesser extent in the temporal lobes in these patients, although solvent abusers with predominant cerebellar and brainstem atrophy have been described.
Infection
CNS infection complicating IV drug abuse occurs most frequently in the context of endocarditis (58), particularly left-sided endocarditis. Septic emboli from valvular vegetations may result in cerebral infarction, brain abscess (Fig 17), or mycotic aneurysm formation. IV drug use is also a risk factor for human immunodeficiency virus (HIV) infection, which is itself associated with a wide variety of CNS infections, but these are beyond the scope of this article.
View larger version (120K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 17. Cerebral abscess in a 25-year-old male IV drug user. Contrast-enhanced cranial CT image (window level = 40 HU, window width = 100 HU) shows a small enhancing lesion in the left caudate nucleus (arrow).
|
|
|
Musculoskeletal Complications
|
|---|
The musculoskeletal complications of drug abuse are dominated by soft-tissue, bone, and joint infections related to IV drug use.
Soft-Tissue Infections
A spectrum of soft-tissue infective complications is seen in IV drug users. Cellulitis is a common complication at injection sites, especially in drug users who have exhausted all peripheral venous access and resort to subcutaneous injection of drugs (known as "skin popping"). US, which is often performed to look for any associated collection, demonstrates diffuse soft-tissue swelling and reduced echogenicity of subcutaneous fat. If performed, CT will show stranding in subcutaneous fat and MR imaging will show high signal intensity on T2-weighted and short inversion time inversion-recovery images in the affected areas.
Infections may spread to involve deeper soft tissues in the form of pyomyositis or even necrotizing fasciitis. MR imaging is the modality of choice for demonstrating the extent of these deeper soft-tissue infections.
Subcutaneous and muscular abscess formation are also common injection site complications. These collections are often of mixed echogenicity at US and can be impossible to distinguish from hematoma. Duplex assessment is important to exclude false aneurysm formation. If there is a suggestion of superior or deep extension from the groin, CT or MR imaging will be useful in further anatomic delineation. The iliopsoas muscle is the most commonly involved muscle due to extension of an abscess from the groin (Fig 18) (13).
View larger version (112K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 18a. Iliopsoas abscess in a 30-year-old male IV drug user. (a) Axial contrast-enhanced abdominal CT image (window level = 40 HU, window width = 400 HU) shows an abscess in the right groin, within which a needle fragment (arrow) is visible. Note the flexed hip position adopted by the patient. (b) Sagittal oblique reformatted image from the same study shows the superior extent of the iliopsoas abscess (arrows). The needle fragment is seen inferiorly.
|
|
View larger version (144K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 18b. Iliopsoas abscess in a 30-year-old male IV drug user. (a) Axial contrast-enhanced abdominal CT image (window level = 40 HU, window width = 400 HU) shows an abscess in the right groin, within which a needle fragment (arrow) is visible. Note the flexed hip position adopted by the patient. (b) Sagittal oblique reformatted image from the same study shows the superior extent of the iliopsoas abscess (arrows). The needle fragment is seen inferiorly.
|
|
Osteomyelitis and Septic Arthritis
Although bone and joint infections in IV drug users can occur due 
Top
Abstract
LEARNING OBJECTIVES FOR TEST...
