RadioGraphics
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


DOI: 10.1148/rg.274065103
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow CME Test (opens in a new window)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hagan, I. G.
Right arrow Articles by Burney, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hagan, I. G.
Right arrow Articles by Burney, K.
Related Collections
Right arrow General
Right arrowRelated Article
RadioGraphics 2007;27:919-940
© RSNA, 2007


EDUCATION EXHIBIT

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
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
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
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
After reading this article and taking the test, the reader will be able to:


    Introduction
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
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
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
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.


View this table:
[in this window]
[in a new window]

 
Table 1. Cardiovascular Complications of Recreational Drug Abuse

 
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).


Figure 1
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.

 

Figure 2A
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.

 

Figure 2B
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).


Figure 3A
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.

 

Figure 3B
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).


Figure 4
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).


Figure 5A
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.

 

Figure 5B
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.

 

Figure 5C
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).


Figure 6
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.

 

Figure 7
View larger version (108K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 7.  Venous thrombosis in a 27-year-old female IV drug user. Longitudinal image from abdominal US shows thrombosis (arrows) extending up the inferior vena cava.

 

    Respiratory Complications
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
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.


View this table:
[in this window]
[in a new window]

 
Table 2. Respiratory Complications of Recreational Drug Abuse

 
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).


Figure 8A
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.

 

Figure 8B
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.


Figure 9
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.


Figure 10A
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.

 

Figure 10B
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.

 

Figure 11A
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.

 

Figure 11B
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.

 

Figure 12A
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.

 

Figure 12B
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.


Figure 13A
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.

 

Figure 13B
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.

 

Figure 13C
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 {alpha}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
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
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.


View this table:
[in this window]
[in a new window]

 
Table 3. Neurologic Complications of Recreational Drug Abuse

 
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.


Figure 14
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 (3133), 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 (3739) 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 (3133,3941) and embolic events due to endocarditis or injection of particulate material in IV drug users.


Figure 15A
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.

 

Figure 15B
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).


View this table:
[in this window]
[in a new window]

 
Table 4. Distribution of Cerebral Ischemic Complications by Drug

 
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).


Figure 16A
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.

 

Figure 16B
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.

 

Figure 16C
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.

 

Figure 16D
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.

 

Figure 16E
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.

 

Figure 16F
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) (5153) 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.


Figure 17
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
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
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).


Figure 18A
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.

 

Figure 18B
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 to contiguous spread from soft-tissue infection, more frequently these reflect hematogenous seeding of microorganisms (59). A variety of gram-positive and gram-negative bacteria may be responsible and occasionally fungi such as Candida species. In the case of septic arthritis complicating IV drug use, there is frequent involvement of joints not usually associated with septic arthritis such as the sacroiliac (Fig 19a), acromioclavicular, sternoclavicular (Fig 20) (60), and manubriosternal (Fig 21) joints and symphysis pubis, as well as more conventional sites of septic arthritis such as the hip (Fig 19b) (61). The role of hematogenous bacterial seeding is supported by the coexistence of septic arthritis with other hematogenous infectious complications such as septic emboli (Figs 20, 21) and in some cases multifocality of joint infection (Fig 21).


Figure 19A
View larger version (121K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 19a.  Septic arthritis as a complication of IV drug abuse in two patients. (a) Axial unenhanced CT image (window level = 400 HU, window width = 1500 HU) of a 34-year-old man shows sclerosis and erosions at the right sacroiliac joint due to septic arthritis. (b) Coronal short inversion time inversion-recovery MR image of a 36-year-old man shows destruction of the right femoral head and acetabulum, a joint effusion, and extensive abnormal high signal intensity in adjacent soft tissues due to septic arthritis of the hip joint.

 

Figure 19B
View larger version (144K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 19b.  Septic arthritis as a complication of IV drug abuse in two patients. (a) Axial unenhanced CT image (window level = 400 HU, window width = 1500 HU) of a 34-year-old man shows sclerosis and erosions at the right sacroiliac joint due to septic arthritis. (b) Coronal short inversion time inversion-recovery MR image of a 36-year-old man shows destruction of the right femoral head and acetabulum, a joint effusion, and extensive abnormal high signal intensity in adjacent soft tissues due to septic arthritis of the hip joint.

 

Figure 20A
View larger version (106K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 20a.  Septic arthritis in a 29-year-old IV drug user. Pulmonary CT angiography showed multiple septic emboli. (a) Axial CT image (window level = 150 HU, window width = 600 HU) shows soft-tissue swelling over the right sternoclavicular joint (arrows) with poor definition of the medial clavicle. (b) Oblique axial reformatted image (window level = 500 HU, window width = 2400 HU) of the right sternoclavicular joint shows erosive changes on either side of the joint, a finding consistent with septic arthritis.

 

Figure 20B
View larger version (96K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 20b.  Septic arthritis in a 29-year-old IV drug user. Pulmonary CT angiography showed multiple septic emboli. (a) Axial CT image (window level = 150 HU, window width = 600 HU) shows soft-tissue swelling over the right sternoclavicular joint (arrows) with poor definition of the medial clavicle. (b) Oblique axial reformatted image (window level = 500 HU, window width = 2400 HU) of the right sternoclavicular joint shows erosive changes on either side of the joint, a finding consistent with septic arthritis.

 

Figure 21A
View larger version (95K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 21a.  Clinically unsuspected multifocal septic arthritis in a 28-year-old male IV drug user. The patient presented with chest pain, and pulmonary CT angiography showed septic pulmonary emboli. (a) CT image obtained with a bone window (level = 400 HU, width = 2000 HU) shows destructive changes at the manubriosternal joint (arrows) with soft-tissue swelling, findings strongly suggestive of septic arthritis. (b) Anterior (ANT) and posterior (POST) images from subsequent whole-body bone scintigraphy show increased uptake at the manubriosternal joint, as well as increased activity at the right wrist and left third metacarpophalangeal joint, both of which proved to be additional foci of septic arthritis.

 

Figure 21B
View larger version (136K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 21b.  Clinically unsuspected multifocal septic arthritis in a 28-year-old male IV drug user. The patient presented with chest pain, and pulmonary CT angiography showed septic pulmonary emboli. (a) CT image obtained with a bone window (level = 400 HU, width = 2000 HU) shows destructive changes at the manubriosternal joint (arrows) with soft-tissue swelling, findings strongly suggestive of septic arthritis. (b) Anterior (ANT) and posterior (POST) images from subsequent whole-body bone scintigraphy show increased uptake at the manubriosternal joint, as well as increased activity at the right wrist and left third metacarpophalangeal joint, both of which proved to be additional foci of septic arthritis.

 
Conventional radiography is insensitive in early bone and joint infections. CT and particularly MR imaging demonstrate the bone and soft-tissue changes of infection to much better advantage. Bone scintigraphy may be particularly useful in suspected multifocal septic arthritis (Fig 21).

Diskitis
Hematogenous microbial seeding also renders IV drug users susceptible to infective diskitis and its attendant complications such as epidural abscess formation and cord compression (Fig 22). As with other bone and joint infections in these patients, a variety of bacterial and sometimes fungal agents may be responsible, and negative blood cultures may well necessitate image-guided biopsy to guide appropriate antimicrobial therapy. Conventional radiography has poor sensitivity in the early stages of disease, and MR imaging is the imaging modality of choice, demonstrating intervertebral disk and endplate changes with high sensitivity, allowing distinction of enhancing inflammatory tissue from epidural abscess formation, which may require surgical intervention, and accurately delineating the effects on adjacent neural structures.


Figure 22A
View larger version (84K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 22a.  Infective diskitis in a 43-year-old male IV drug user. Sagittal T2-weighted (a) and gadolinium-enhanced T1-weighted (b) MR images of the thoracolumbar spine show typical changes of diskitis at T11-12 with abnormal signal intensity and destruction of the intervertebral disk and adjacent vertebral end-plates. Enhancing inflammatory tissue bulges the anterior and posterior longitudinal ligaments, and there is associated compression of the spinal cord.

 

Figure 22B
View larger version (86K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 22b.  Infective diskitis in a 43-year-old male IV drug user. Sagittal T2-weighted (a) and gadolinium-enhanced T1-weighted (b) MR images of the thoracolumbar spine show typical changes of diskitis at T11-12 with abnormal signal intensity and destruction of the intervertebral disk and adjacent vertebral end-plates. Enhancing inflammatory tissue bulges the anterior and posterior longitudinal ligaments, and there is associated compression of the spinal cord.

 
Foreign Bodies
Needles or needle fragments are not infrequently seen at injection sites in the groin (Fig 23) or neck on plain radiographs (62). They are also readily visible at US and CT (Fig 18), which can in addition delineate their relationship to adjacent vessels and collections. Identification of a needle within an abscess (Fig 18) is important, as this may form a nidus for infection that allows recurrence of the abscess after percutaneous drainage.


Figure 23
View larger version (154K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 23.  Oblique radiograph of the left hip in a 27-year-old male IV drug user shows two needles in the groin (arrows).

 

    Other Visceral Complications
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
Miscellaneous visceral complications of drug abuse that may manifest radiologically include acquisition of chronic viral infections, renal disorders, and gastrointestinal disorders. Body packers may also come to the attention of the radiologist.

Acquired Viral Infections
IV drug abuse is a major risk factor for acquisition of blood-borne viral infections through sharing of contaminated needles, including HIV infection and hepatitis B and C. HIV infection is relatively unusual in the United Kingdom IV drug user population with an overall prevalence of 1.5% (63), although on a global basis IV drug use is estimated to account for 5%–10% of all new infections (2). The radiology of HIV infection is a vast subject in its own right and is beyond the scope of this article.

By contrast with the low prevalence of HIV infection, hepatitis C infection is endemic in the United Kingdom IV drug user population with a seropositivity rate varying from 20% to 59% between regions (63,64). The majority of infected patients fail to clear the virus, leading to chronic infection. Hepatosplenomegaly is often observed at US or CT in these patients, often as an incidental finding. Many patients progress to cirrhosis with development of irregular livers and imaging features of portal hypertension (Fig 24).


Figure 24
View larger version (159K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 24.  Cirrhosis due to chronic hepatitis C infection acquired as a result of IV drug use in a 44-year-old man. Contrast-enhanced CT image (window level = 40 HU, window width = 340 HU) shows that the right lobe of the liver has a slightly irregular margin. Recanalization of the umbilical vein (arrowhead), collateral veins in the abdominal wall (arrows), and splenomegaly reflect portal hypertension.

 
Renal Disorders
The renal complications of drug abuse comprise a diverse array of glomerular, tubulointerstitial, and renovascular diseases (65). Such effects are usually chronic and irreversible (66) but may be acute and potentially reversible. Mechanisms include direct renal toxic effects, rhabdomyolysis, acute and chronic glomerulonephritis, accelerated and chronic hypertension, amyloidosis, and renal infarction. Toluene abuse predisposes users to distal renal tubular acidosis and stone formation (67). In general, radiologic features of renal failure are nonspecific, with renal parenchymal disorders manifesting as increased echogenicity with loss of corticomedullary differentiation at US. Radiologic investigation may also detect the complications of chronic renal failure (Fig 25).


Figure 25
View larger version (136K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 25.  Hypercalcemia in a 30-year-old man with a long history of IV drug use. The hypercalcemia was subsequently found to be due to tertiary hyperparathyroidism complicating end-stage renal failure secondary to drug abuse. Bone scintigrams show striking gastric and pulmonary uptake; both findings are recognized features of hyperparathyroidism.

 
Gastrointestinal Disorders and Body Packing
Drug abuse may have a number of adverse effects on the gastrointestinal tract. Opiates are well recognized to cause reduced intestinal motility, leading to chronic constipation and fecal impaction if used regularly. In rare cases, this fecal impaction may cause local pressure necrosis of the bowel wall, resulting in stercoral colitis and perforation (68), which may carry a mortality rate as high as 35% (69). The majority of such perforations occur in the rectum and sigmoid colon (69). Abdominal radiographs are relatively insensitive in the early stages of stercoral perforation, and CT is the investigation of choice. In the presence of fecal impaction, the CT findings of focal wall thickening in distended large bowel and stranding in adjacent fat should raise concern about stercoral colitis, while the presence of extraluminal gas or an abscess suggests that perforation has already occurred (69).

The use of cocaine and to a lesser extent amphetamines can cause mesenteric ischemia and infarction, due largely to vasoconstriction in the splanchnic vasculature with or without mesenteric thrombosis (7072), although there may be an additional direct toxic effect of cocaine on the gastrointestinal mucosa (70). Abdominal radiographs may be normal or show nonspecific dilatation of bowel loops and evidence of bowel wall thickening, as well as bowel wall gas (pneumatosis), portal venous gas, and free abdominal gas in established infarction. CT is more sensitive than conventional radiography in detecting these abnormalities (Fig 26) but appearances are variable (70,72,73). Bowel wall thickening is the most common finding, particularly in ischemic colitis (70,73), but cases of small bowel infarction may demonstrate dilated bowel with a thinned wall (73). The bowel wall itself may be hypoattenuating or hyperattenuating depending on the relative amounts of edema and submucosal hemorrhage. Bowel wall enhancement is also variable, depending on the degree of residual blood flow, and a target sign may be produced by the combination of low-attenuation mural edema with mucosal-submucosal and serosal-subserosal enhancement. Mesenteric fat stranding and free fluid are frequent but nonspecific signs. Pneumatosis intestinalis and portomesenteric venous gas are more specific but less common findings, and free abdominal gas may be seen when perforation supervenes.


Figure 26
View larger version (144K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 26.  Cecal infarction in a 32-year-old man with acute abdominal pain and a history of cocaine abuse. Contrast-enhanced CT image of the abdomen shows mixed-attenuation mural thickening of the cecum with stranding in pericecal fat and extraluminal gas. Cecal infarction was confirmed at laparotomy. (Courtesy of Bettina Siewert, MD, Beth Israel Deaconess Medical Center, Boston, Mass.)

 
Body packing refers to the practice of smuggling drugs (usually hashish, cocaine, or heroin) within the human body, either for personal use or financial gain. Handmade or mechanically produced packets of drugs 2–6 cm in diameter are swallowed or inserted into the rectum or vagina. These individuals may present as known or suspected drug couriers, or with complications of body packing such as bowel obstruction, perforation, or intoxication due to packet rupture. On occasion, packets may be identified as an incidental finding when imaging is performed for another reason (Fig 27).


Figure 27A
View larger version (114K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 27a.  Incidentally found drug packet in a 37-year-old man who had recently arrived from Jamaica and was stabbed in the left loin during an argument. (a) Contrast-enhanced CT image of the abdomen (window level = 40 HU, window width = 400 HU) shows the knife track with air in the left paraspinal muscles and retroperitoneum (arrowheads) but no serious visceral injury. (b) CT image shows a high-attenuation tubular structure (arrow) at the rectosigmoid junction. The tubular structure proved to be a drug packet.

 

Figure 27B
View larger version (140K):
[in this window]
[in a new window]
[Download PPT slide]
 
Figure 27b.  Incidentally found drug packet in a 37-year-old man who had recently arrived from Jamaica and was stabbed in the left loin during an argument. (a) Contrast-enhanced CT image of the abdomen (window level = 40 HU, window width = 400 HU) shows the knife track with air in the left paraspinal muscles and retroperitoneum (arrowheads) but no serious visceral injury. (b) CT image shows a high-attenuation tubular structure (arrow) at the rectosigmoid junction. The tubular structure proved to be a drug packet.

 
Conventional abdominal radiography is the initial investigation of choice, although CT has higher sensitivity and specificity (68). Swallowed packets tend to be smaller and rounder, while packets inserted into the rectum or vagina tend to be oval or tubular. As a general guide, hashish is said to be more opaque than stool at conventional radiography, cocaine is of similar opacity to stool, and heroin packets are mostly of gas opacity (74). However, the major determinant of radiographic opacity is the purity of the drug, and different drugs may be of similar opacity (75).


    Conclusions
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 
Recreational drug abuse is best regarded as a multisystem disease with potential complications involving many different organs, sometimes synchronously. The nature of the complications depends on the particular drug, its method of administration, and any impurities contained within it. Although radiology often has a key role to play in identifying these complications, many of the imaging features are nonspecific, and a history of drug abuse may not be forthcoming at presentation. This necessitates a high degree of suspicion on the part of the reporting radiologist and referring clinician, and drug abuse should be considered in any unexplained illness, especially in young people. Owing to the multisystem effects of drug abuse, the discovery of one complication should prompt the radiologist to search for signs of coexistent pathologic conditions, which may alter management.


    Acknowledgments
 
We would like to thank the following people for their help in obtaining some of the images included: Charles J. Wakeley, MB, BS, FRCS(Ed), FRCR; R. Peter Wilde, BM, BCh, MRCP, FRCR; Sally E. King; Mike Darby, MB, ChB, MRCP, FRCR; J. Maurice Gibson, MA, MB, BS, MRCP, FRCR; Martin Johnson, MB, ChB, MD, FRCP; and Bettina Siewert, MD. We would also like to thank Iain D. Lyburn, MB, ChB, MRCP, FRCR; Bettina Siewert; and Mike Darby for their helpful comments regarding the manuscript.


    Footnotes
 

Abbreviations: CNS = central nervous system, HIV = human immunodeficiency virus, IV = intravenous, MDMA = 3, 4-methylenedioxymetham-phetamine, PRES = posterior reversible encephalopathy syndrome

See also the article by Restrepo et al (pp 941–956) in this issue.


    References
 Top
 Abstract
 LEARNING OBJECTIVES FOR TEST...
 Introduction
 Cardiovascular Complications
 Respiratory Complications
 Neurologic Complications
 Musculoskeletal Complications
 Other Visceral Complications
 Conclusions
 References
 

  1. Strang J. Substance abuse: the size of the problem. Medicine 1995;23:41–45.
  2. United Nations Office on Drugs and Crime. 2005 world drug report. New York, NY: United Nations Publications, 2005.
  3. National Centre for Social Research/National Foundation for Educational Research. Drug use, smoking and drinking among young people in England in 2004. London, England: Department of Health, 2005.
  4. Ramsay M, Baker P, Goulden C, et al. Drug misuse declared in 2000: results from the British Crime Survey. Home Office Research Study 224. London, England: Home Office Research, 2001.
  5. Binks S, Hoskins R, Salmon D, Benger J. Prevalence and healthcare burden of illegal drug use among emergency department patients. Emerg Med J 2005;22:872–873.[Abstract/Free Full Text]
  6. Hollander JE, Hoffman RS, Burstein JL, Shih RD, Thode HC Jr, Cocaine-associated Myocardial Infarction Study Group. Cocaine-associated myocardial infarction: mortality and complications. Arch Intern Med 1995;155:1081–1086.[Abstract/Free Full Text]
  7. Kumar K, Holden WE. Drug-induced pulmonary vascular disease: mechanisms and clinical patterns. West J Med 1986;145:343–349.[Medline]
  8. Togna G, Tempesta E, Togna AR, Dolci N, Cebo B, Caprino L. Platelet responsiveness and biosynthesis of thromboxane and prostacyclin in response to in vitro cocaine treatment. Haemostasis 1985;15:100–107.[Medline]
  9. Chokshi SK, Moore R, Pandian NG. Reversible cardiomyopathy associated with cocaine intoxication. Ann Intern Med 1989;111:1039–1040.[Abstract/Free Full Text]
  10. Miro JM, del Rio A, Mestres CA. Infective endocarditis in intravenous drug users and HIV-1 infected patients. Infect Dis Clin North Am 2002; 16:273–295.[CrossRef][Medline]
  11. McDermott JC, Schuster MR, Grummy AB, Archer CW. Crack and aortic dissection. Wis Med J 1993;92:453–455.[Medline]
  12. Chang RA, Rossi NF. Intermittent cocaine use associated with recurrent dissection of the thoracic and abdominal aorta. Chest 1995;108:1758–1762.[Medline]
  13. Gotway MB, Marder SR, Hanks DK, et al. Thoracic complications of illicit drug use: an organ system approach. RadioGraphics 2002;22(spec no):S119–S135.[Abstract/Free Full Text]
  14. Roszler MH, McCarroll KA, Donovan KR, Rashid T, Kling GA. The groin hit: complications of parenteral drug abuse. RadioGraphics 1989;9:487–508.[Abstract]
  15. Yellin AE. Ruptured mycotic aneurysm: a complication of parenteral drug abuse. Arch Surg 1977; 112:981–986.[Abstract/Free Full Text]
  16. Daggett RB, Haghighi P, Terkeltaub RA. Nasal cocaine abuse causing an aggressive midline intranasal and pharyngeal destructive process mimicking midline reticulosis and limited Wegener’s granulomatosis. J Rheumatol 1990;17:838–840.[Medline]
  17. Louria DB, Hensle T, Rose J. The major medical complications of heroin addiction. Ann Intern Med 1967;67:1–22.[Abstract/Free Full Text]
  18. McCarroll KA, Roszler MH. Lung disorders due to drug abuse. J Thorac Imaging 1991;6:30–35.[Medline]
  19. Lacagnina S, Vomero E, Jacobson M, Gold AR. Hypodermic needle aspiration in a freebase cocaine user [letter]. Chest 1990;97:1275–1276.
  20. Morrison WJ, Wetherill S, Zyroff J. The acute pulmonary edema of heroin intoxication. Radiology 1970;97:347–351.[Medline]
  21. Hoffman CK, Goodman PC. Pulmonary edema in cocaine smokers. Radiology 1989;172:463–465.[Abstract/Free Full Text]
  22. Schaaf JT, Spivack ML, Rath GS, Snider GL. Pulmonary edema and adult respiratory distress syndrome following methadone abuse. Am Rev Respir Dis 1973;107:1047–1051.[Medline]
  23. Godwin JE, Harley RA, Miller KS, Heffner JE. Cocaine pulmonary hemorrhage and hemoptysis. Ann Intern Med 1989;110:843.[Abstract/Free Full Text]
  24. Bailey ME, Fraire AE, Greenberg SD, Barnard J, Cagle PT. Pulmonary histopathology in cocaine abusers. Hum Pathol 1994;25:203–207.[CrossRef][Medline]
  25. Robertson CH Jr, Reynolds RC, Wilson JE 3rd. Pulmonary hypertension and foreign body granulomas in intravenous drug users: documentation by cardiac catheterization and lung biopsy. Am J Med 1976;61:657–664.[CrossRef][Medline]
  26. Ward S, Heyneman LE, Reittner P, Kazerooni EA, Godwin JD, Muller NL. Talcosis associated with IV abuse of oral medications: CT findings. AJR Am J Roentgenol 2000;174:789–793.[Abstract/Free Full Text]
  27. Pare JP, Cote G, Fraser RS. Long-term follow-up of drug users with intravenous talcosis. Am Rev Respir Dis 1989;139:233–241.[Medline]
  28. Weisbrod GL, Rahman M, Chamberlain D, Homan SJ. Precocious emphysema in intravenous drug abusers. J Thorac Imaging 1993;8:233–240.[Medline]
  29. Johnson MK, Smith RP, Morrison D, Laszlo G, White RJ. Large lung bullae in marijuana smokers. Thorax 2000;55:340–342.[Abstract/Free Full Text]
  30. Stern EJ, Frank MS, Schmutz JF, Glenny RW, Schmidt RA, Godwin JD. Panlobular pulmonary emphysema caused by i.v. injection of methylphenidate (Ritalin): findings on chest radiographs and CT scans. AJR Am J Roentgenol 1994;162:555–560.[Abstract/Free Full Text]
  31. Daras M, Tuchman AJ, Koppel BS, Samkoff LM, Weitzner I, Marc J. Neurovascular complications of cocaine. Acta Neurol Scand 1994;90:124–129.[Medline]
  32. Levine SR, Brust JC, Futrell N, et al. Cerebrovascular complications of the use of the "crack" form of alkaloidal cocaine. N Engl J Med 1990;323:699–704.[Abstract]
  33. Brown E, Prager J, Lee HY, Ramsey RG. CNS complications of cocaine abuse: prevalence, pathophysiology, and neuroradiology. AJR Am J Roentgenol 1992;159:137–147.[Abstract/Free Full Text]
  34. Madden JA, Konkol RJ, Keller PA, Alvarez TA. Cocaine and benzoylecgonine constrict cerebral arteries by different mechanisms. Life Sci 1995; 56:679–686.[CrossRef][Medline]
  35. Reneman L, Habraken JB, Majoie CB, Booij J, den Heeten GJ. MDMA ("Ecstasy") and its association with cerebrovascular accidents: preliminary findings. AJNR Am J Neuroradiol 2000;21:1001–1007.[Abstract/Free Full Text]
  36. Squier MV, Jalloh S, Hilton-Jones D, Series H. Death after ecstasy ingestion: neuropathological findings. J Neurol Neurosurg Psychiatry 1995;58:756.[Free Full Text]
  37. Andersen SN, Skullerud K. Hypoxic/ischaemic brain damage, especially pallidal lesions, in heroin addicts. Forensic Sci Int 1999;102:51–59.[CrossRef][Medline]
  38. Benyo Z, Wahl M. Opiate receptor-mediated mechanisms in the regulation of cerebral blood flow. Cerebrovasc Brain Metab Rev 1996;8:326–357.[Medline]
  39. Niehaus L, Meyer BU. Bilateral borderzone brain infarctions in association with heroin abuse. J Neurol Sci 1998;160:180–182.[CrossRef][Medline]
  40. Citron BP, Halpern M, McCarron M, et al. Necrotizing angiitis associated with drug abuse. N Engl J Med 1970;283:1003–1111.[Medline]
  41. Fredericks RK, Lefkowitz DS, Challa VE, Troost BT. Cerebral vasculitis associated with cocaine abuse. Stroke 1991;22:1437–1439.[Abstract/Free Full Text]
  42. Di Lazzaro V, Restuccia D, Oliviero A, et al. Ischaemic myelopathy associated with cocaine: clinical, neurophysiological, and neuroradiological features. J Neurol Neurosurg Psychiatry 1997;63:531–533.[Abstract/Free Full Text]
  43. Bartzokis G, Goldstein IB, Hance DB, et al. The incidence of T2-weighted MR imaging signal abnormalities in the brain of cocaine-dependent patients is age-related and region-specific. AJNR Am J Neuroradiol 1999;20:1628–1635.[Abstract/Free Full Text]
  44. Lyoo IK, Streeter CC, Ahn KH, et al. White matter hyperintensities in subjects with cocaine and opiate dependence and healthy comparison subjects. Psychiatry Res 2004;131:135–145.[CrossRef][Medline]
  45. Neuwelt EA. Mechanisms of disease: the blood-brain barrier. Neurosurgery 2004;54:131–142.[CrossRef][Medline]
  46. Kinoshita T, Moritani T, Shrier DA, et al. Diffusion-weighted MR imaging of posterior reversible leukoencephalopathy syndrome: a pictorial essay. Clin Imaging 2003;27:307–315.[CrossRef][Medline]
  47. Port JD, Beauchamp NJ Jr. Reversible intracerebral pathologic entities mediated by vascular auto-regulatory dysfunction. RadioGraphics 1998;18:353–367.[Abstract]
  48. D’Costa DF, Gunasekera NP. Fatal cerebral oedema following trichloroethane abuse. J R Soc Med 1990;83:533–534.[Medline]
  49. Kramer L, Bauer E, Schenk P, Steininger R, Vigel M, Mallek R. Successful treatment of refractory cerebral oedema in ecstasy/cocaine-induced fulminant hepatic failure using a new high-efficacy liver detoxification device (FPSA-Prometheus). Wien Klin Wochenschr 2003;115:599–603.[Medline]
  50. Matthai SM, Davidson DC, Sills JA, Alexandrou D. Cerebral oedema after ingestion of MDMA ("ecstasy") and unrestricted intake of water. BMJ 1996;312:1359.[Medline]
  51. Wolters EC, van Wijngaarden GK, Stam FC, et al. Leukoencephalopathy after inhaling heroin pyrolysate. Lancet 1982;2:1233–1237.[Medline]
  52. Tan TP, Algra PR, Valk J, Wolters EC. Toxic leukoencephalopathy after inhalation of poisoned heroin: MR findings. AJNR Am J Neuroradiol 1994;15:175–178.[Abstract]
  53. Keogh CF, Andrews GT, Spacey SD, Forkheim KE, Graeb DA. Neuroimaging features of heroin inhalation toxicity: "chasing the dragon." AJR Am J Roentgenol 2003;180:847–850.[Abstract/Free Full Text]
  54. Aydin K, Sencer S, Ogel K, Genchellac H, Demir T, Minareci O. Cranial MR findings in chronic toluene abuse by inhalation. AJNR Am J Neuroradiol 2002;23:1173–1179.[Abstract/Free Full Text]
  55. Rosenberg NL, Grigsby J, Dreisbach J, Busenbark D, Grigsby P. Neuropsychologic impairment and MRI abnormalities associated with chronic solvent abuse. J Toxicol Clin Toxicol 2002;40:21–34.[CrossRef][Medline]
  56. Pascual-Leone A, Dhuna A, Anderson DC. Cerebral atrophy in habitual cocaine abusers: a planimetric CT study. Neurology 1991;41:34–38.[Abstract/Free Full Text]
  57. Pezawas LM, Fischer G, Diamant K, et al. Cerebral CT findings in male opioid-dependent patients: stereological, planimetric and linear measurements. Psychiatry Res 1998;83:139–147.[CrossRef][Medline]
  58. Tunkel AR, Pradhan SK. Central nervous system infections in injection drug users. Infect Dis Clin North Am 2002;16:589–605.[CrossRef][Medline]
  59. Firooznia H, Golimbu C, Rafii M, Lichtman EA. Radiology of musculoskeletal complications of drug addiction. Semin Roentgenol 1983;18:198–206.[CrossRef][Medline]
  60. Wohlgethan JR, Newberg AH, Reed JI. The risk of abscess from sternoclavicular septic arthritis. J Rheumatol 1988;15:1302–1306.[Medline]
  61. Roca RP, Yoshikawa TT. Primary skeletal infections in heroin users: a clinical characterization, diagnosis and therapy. Clin Orthop Relat Res 1979;144:238–248.[Medline]
  62. Kurtzman RS. Complications of narcotic addiction. Radiology 1970;96:23–30.[Medline]
  63. Health Protection Agency, Health Protection Scotland, National Public Health Service for Wales, CDSC Northern Ireland, CRDHB, and the UASSG. Shooting up: infections among injecting drug users in the United Kingdom 2004. London, England: Health Protection Agency, October 2005.
  64. Serfaty MA, Lawrie A, Smith B, et al. Risk factors and medical follow up of drug users tested for hepatitis C: can the risk of transmission be reduced? Drug Alcohol Rev 1997;16:339–347.[CrossRef][Medline]
  65. Crowe AV, Howse M, Bell GM, Henry JA. Substance abuse and the kidney. QJM 2000;93:147–152.[Abstract/Free Full Text]
  66. Perneger TV, Klag MJ, Whelton PK. Recreational drug use: a neglected risk factor for end stage renal disease. Am J Kidney Dis 2001;38:49–56.[Medline]
  67. Kaneko T, Koizumi T, Takezaki T, Sato A. Urinary calculi associated with solvent abuse. J Urol 1992;147:1365–1366.[Medline]
  68. Tessier DJ, Harris E, Collins J, Johnson DJ. Stercoral perforation of the colon in a heroin addict. Int J Colorectal Dis 2002;17:435–437.[CrossRef][Medline]
  69. Heffernan C, Pachter HL, Megibow AJ, Macari M. Stercoral colitis leading to fatal peritonitis: CT findings. AJR Am J Roentgenol 2005;184:1189–1193.[Abstract/Free Full Text]
  70. Linder JD, Monkemuller KE, Raijman I, Johnson L, Lazenby AJ, Wilcox CM. Cocaine-associated ischemic colitis. South Med J 2000;93:909–913.[Medline]
  71. Johnson TD, Berenson MM. Methamphetamine-induced ischemic colitis. J Clin Gastroenterol 1991;13:687–689.[Medline]
  72. Osorio J, Farreras N, Ortiz De Zarate L, Bachs E. Cocaine-induced mesenteric ischemia. Dig Surg 2000;17:648–651.[CrossRef][Medline]
  73. Wiesner W, Khurana B, Ji H, Ros PR. CT of acute bowel ischemia. Radiology 2003;226:635–650.[Abstract/Free Full Text]
  74. Ichikawa K, Tajima H, Murakami R, et al. Diagnostic imaging of "body packers" [in Japanese]. Nippon Igaku Hoshasen Gakkai Zasshi 1997;57:89–93.[Medline]
  75. Hergan K, Kofler K, Oser W. Drug smuggling by body packing: what radiologists should know about it. Eur Radiol 2004;14:736–742.[CrossRef][Medline]

Related Article

Pulmonary Complications from Cocaine and Cocaine-based Substances: Imaging Manifestations
Carlos S. Restrepo, Jorge A. Carrillo, Santiago Martínez, Paulina Ojeda, Aura L. Rivera, and Ami Hatta
RadioGraphics 2007 27: 941-956. [Abstract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
Am. J. Neuroradiol.Home page
T.-Y. Chen, H.-J. Lee, T.-C. Wu, and Y.-K. Tsui
MR Imaging Findings of Medulla Oblongata Involvement in Posterior Reversible Encephalopathy Syndrome Secondary to Hypertension
AJNR Am. J. Neuroradiol., April 1, 2009; 30(4): 755 - 757.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow CME Test (opens in a new window)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hagan, I. G.
Right arrow Articles by Burney, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hagan, I. G.
Right arrow Articles by Burney, K.
Related Collections
Right arrow General
Right arrowRelated Article


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
RADIOGRAPHICS RADIOLOGY RSNA JOURNALS ONLINE