Cutaneous Complications of Intravenous Drug Abuse

P. Del Giudice

Disclosures

The British Journal of Dermatology. 2004;150(1) 

In This Article

Local Cutaneous Complications

Local complications occur at the site or in the area of injection. Two types are described: acute complications occurring within a few hours to 48-72 h after injection, and delayed complications.

Acute Complications

Injection marks. Recent injection marks at the site of injection are present in all IDUs.[20,21]

Cutaneous infections. Cutaneous infections are common in IDUs.[16] Abscesses and cellulitis occur in 22-65% of addicts (Figs 1 and 2).[22,23,24] Vishov et al.[17] reported that 11% of IDUs interviewed had had at least one abscess in the past 6 months and Spijkerman et al.[25] found an incidence of skin abscesses of 33 per 100 person-years. A combination of factors favours cutaneous infection. Tuazon et al.[26] found that 68% of street heroin samples and 89% of the material for injection confiscated in Washington DC were contaminated with various single or multiple pathogens including Clostridium sp., Gram-negative bacteria and fungi. Moustoukas et al.[27] in Chicago, found similar results with 61% of heroin samples contaminated with 1.6 x 102 to 3.7 x 104 organisms per gram. Other risk factors include intradermal injection,[28,29] absence of skin asepsis,[6,28,29] unsterile equipment, poor hygiene,[19] adulterants acting as irritant substances and foreign bodies, and the combination of heroin and cocaine.[28] Spijkerman et al.[25] found that HIV infection, female gender, prostitution, foreign nationality, combined injection of heroin and cocaine, a high frequency of injecting, and obtaining syringes through the needle exchange programme were independently and positively associated with skin abscesses. In addition, the pharmacological properties of the drugs such as the vasoconstrictive effect of cocaine may contribute to infections.[30] The use of alcohol to clean the skin before injection may protect against cutaneous infections.[17,28,29]

Figure 1.

Multiple sites of group A ß-haemolytic Streptococcus A localized necrotizing cellulitis (after surgical excision of necrotizing tissues). Multiple scars of past injection and abscesses. Injection scars over the penis.

Figure 2.

Cutaneous abscess of the thigh after 'skin popping'.

A wide range of pathogens including almost all bacteria and fungi have been isolated in these infections. Single or multiple pathogens may be isolated. Gram-positive cocci are the bacteria most frequently seen. The three most common are Staphylococcus aureus, group A ß-haemolytic Streptococcus and other Streptococci.[2,30,31,32,33,34,35] Anaerobes are the second most common group of bacteria to be isolated, and include Clostridium sp., usually associated with aerobic bacteria. Gram-negative bacteria are less commonly isolated. The source of the pathogens is variable but most originate from the flora of the skin and oropharynx. Indeed some IDUs lick needles, use saliva to clean the skin, to moisten the cotton wool or to dilute the drug.[28,29,30] Irritant substances cause sterile chemical cellulitis and abscesses. Management of abscesses includes incision, drainage and antibiotics active against Staph. aureus, Streptococci and anaerobes.[35]

Necrotizing fasciitis. This is a rare but severe and life-threatening manifestation with a high rate of mortality and amputation.[36,37,38] Necrotizing fasciitis occurs mainly after subcutaneous injection. The use of black tar heroin has been associated with epidemics of abscesses, cellulitis and necrotizing fasciitis.[38] Recent severe cutaneous infections, myonecrosis and sepsis with a high mortality rate have been reported in the U.K. and San Francisco caused by Clostridium novyi, C. perfingens and other Clostridium sp.[39,40] Other local infections include lymphangitis, thrombophlebitis, pyoderma, ecthyma gangrenosum[41] and gas gangrene.[42,43]

The impact of opiate maintenance programmes on the rate of cutaneous infections is an important issue. Bassetti et al.[44] reported no beneficial effect of an injected opiate maintenance programme on the incidence of hospitalization because of current infections, including cutaneous infections. However, Conrad et al.[45] observed a significant decline of cutaneous infections over 18 months of heroin-supported treatment, and Batki et al.[46] a reduction of hospital admissions for abscesses and cellulitis. A reduction of abscesses resulted from a needle and educational programme in IDUs in Bangladesh.[47]

Necrotizing ulcers. Cutaneous necrosis and necrotizing ulcers may develop as a result of several combined factors mainly 'skin popping', toxicity and the irritant properties of the drug and adulterants, vascular thrombosis and infection (Fig. 3).[31,48,49,50,51,52,53,54] For example, quinine used as an adulterant has caustic effects. In addition some drugs such as cocaine have potent vasoconstrictive and thrombotic effects.[11,12] Although bacteria may be cultivated from necrotic ulcers, most authors consider the mechanism to be related not to an infection but to a direct effect of the drug or adulterants. However, in some cases infection may contribute to the formation of ulcerated lesions even though it is difficult to demonstrate the respective contribution of each factor.[53] Indeed Hoeger et al.[55] reported a synergistic cocaine and streptococcal cutaneous necrosis. Some bullous lesions, nodules and chemical cellulitis and abscesses share identical physiopathology and may precede necrosis and ulceration.[3,4,53,56]

Figure 3.

Necrotizing ulcer after morphine sulphate tablet injection.

Cutaneous necrosis also results from arterial thrombosis after direct intra-arterial injection such as scrotal skin necrosis after pudendal artery injection.[41]

False aneurysm and mycotic aneurysms. False aneurysm and mycotic aneurysm are rare but serious complications. The lesion manifests as a pulsatile mass located in the area of major arteries. In some case it may present as a non-pulsatile inflammatory mass and may be mistaken for a cutaneous abscess.[16,57,58,59] Inappropriate incision is disastrous. False aneurysm is caused by vascular injuries after drug injection. Staph. aureus is the main pathogen in mycotic aneurysms. Most cases involve the femoral artery following groin injection but other locations such as the upper limbs have been described.[57,60] The treatment is difficult, and is based on ligation and surgical excision of the aneurysm.[61,62,63,64,65]

Thrombophlebitis. Injecting drug use is considered a risk factor for deep vein thrombosis.[66] The repeated trauma of venepuncture, local infections and the irritating qualities of the drugs and adulterants are the main cause of superficial and deep venous thrombosis.[14,67,68] Septic thrombosis is responsible for bacteraemia, with Staph. aureus as the most frequent pathogen.[69] High-risk locations include iliofemoral and upper limb deep thrombosis.[59,69,70,71,72]

Intra-arterial injections. Inadvertent or deliberate direct intra-arterial injection of drugs may cause severe tissue ischaemia and necrosis.[58,73,74,75,76,77,78,79,80] Immediately after injection, the patient feels intense pain and burning; within a few hours a marked oedema appears, followed by cyanosis in the territory of the artery (Fig. 4).[73,74,75,76,77,78,79,80] In the most severe cases necrosis occurs, leading to amputation. Several mechanisms have been suggested to explain the vascular injury. A direct vasoconstriction may be caused by cocaine or amphetamines. The local chemical toxicity of drugs or adulterants cause chemical endarteritis resulting in vasospasm and thrombosis. Finally the mixture may contain microparticles that act as emboli. This is particularly the case when oral drug formulations such as crushed tablets are injected. The result is a peripheral ischaemia, oedema and compartment syndrome, which worsen the ischaemia.[73,74,75,76,77,78,79,80]

Figure 4.

Livedoid purpuric feature after direct intra-arterial buprenorphine tablets injection of the brachial artery.

The management of intra-arterial drug injection is difficult. Most authors suggest an elevation of the limb, analgesia and heparinization. In the case of compartment syndrome, urgent surgical decompression is indicated. Many treatments have been used including vasodilators, anticoagulants, corticosteroids, prostaglandin inhibitors, and others.[73,74,75,76,77,78,79,80]

Delayed Complications

Hyperpigmentation. Weidman and Fellner[3] found that hyperpigmentation at the site of injection was the most common cutaneous finding, present in 54% of subjects it is related to scars and tracks along the injected veins (Fig. 5). Hyperpigmentation results from a postinflammatory process following the various skin injuries.

Figure 5.

Pigmented 'pop scars' of the leg following cocaine injection.

Scarring. Scars and, in particular, needle tracks are the main stigmata of narcotic abuse (Figs 1, 5 and 6).[19,21,56] Horowitz[81] found that 76% of 74 IDUs examined had scars along a vascular distribution, mainly the ante-cubital area and the dorsum of the hand. The presence of scarring was related to the duration of drug abuse.[81] Fifty-three per cent of the subjects who had stopped injection for more than 5 years still had scarring.[81] Repeated injections along a superficial vein result in venous thrombosis and subsequent fibrosis to form linear cord-like hypopigmented or hyperpigmented scars ('railroad tracks') pathognomonic of intravenous drug addiction.[6]'Pop scars' form irreversible irregular round or oval hypopigmented or hyperpigmented, atrophic or hypertrophic scars, or keloids, 0.5-3 cm in diameter (Fig. 5).4,[8] Other scars result from various skin injuries from trauma, infections, necrosis, burns, suicide scars, etc.

Figure 6.

Digits show cocaine injection scars and beginning of digit retraction.

'Shooting tattoos.' These result from the 'cooking' of the drug, flaming of needles and soot deposition or the introduction of foreign materials in the dermis.[19,81,82] Common tattoos are a means of disguising scars.

Chronic venous insufficiency and ulcers. Pieper et al.[67,68,83] found that 88% of people with a history of injection drug abuse had clinical evidence of chronic venous insufficiency. Risk factors for the development of venous insufficiency include vein trauma, necrotic ulcers, superficial and deep vein thrombosis and blockage of the lymphatic system by repeated infections and the sclerosing effects of adulterants.[67,68,83] Both lymphatic blockage and venous impairment contribute to chronic oedema of the lower extremities. Delayed leg ulcers occur at sites of past subcutaneous injection as a result of lymphatic and venous vessel damage.[67,68,83]

Cutaneous nodules, panniculitis, sclerosis and ulcers. The drug and adulterants can cause a dermal inflammatory reaction which may be a foreign body granuloma or a nonspecific nongranulomatous inflammation with or without detectable foreign bodies. Cutaneous nodules, panniculitis and dermal sclerosis result from the chronic dermal inflammatory process.[7,82] Hahn et al.[76] demonstrated starch or talc granuloma in five of nine skin nodules. The lesions may break down and ulcerate, producing chronic ulcers.[84,85] Chronic infections, such as underlying osteitis, may be associated.[86] The vascularized granulation tissue in and around the ulcer may used as a site for drug injection.[85,86,87]

In some instances chronic dermal inflammation evolves into a severe dermal fibrosis. Pentazocine abuse was responsible for extensive 'woody' cutaneous fibrosis.[48,49,50,51]

Histopathological analysis and examination of tissues under polarized light can show the presence of birefringent material, such as starch, talc and other foreign particles.[7,82,86]

Raynaud's phenomenon and peripheral ischaemia. Heng and Haberfeld[84] reported multiple large skin ulcers with kidney and liver injury after intravenous cocaine injection and suggested that the multiple infarcted lesions were caused by the vasoconstrictive and thrombotic effects of the cocaine. Cocaine has been associated with vascular disorders such as Raynaud's phenomenon and digital necrosis.[88,89]

Complications Related to the Site of Injection

No area of the skin is spared by addicts. Specific locations of injection become the sites of particular complications.

Hands. These are a common site of injection, mainly the dorsum of the hand and the digits (Figs 3 and 6).15,31,[34,90-92] Infection may affect all the anatomical structures of the hand causing abscesses, cellulitis, necrotizing fasciitis, tenosynovitis, arthritis, osteitis and osteomyelitis. Destruction of the articular cartilage causes finger deformities.[92] Volkman's ischaemia and bullae may occur following coma. Radial or brachial intra-arterial injections may cause hand ischaemia and digital necrosis.

With repeated injections, the hands become chronically swollen. This phenomenon, called 'puffy hand' syndrome by Abeles,[93] seems to be specific to addiction.[13,94] The 'puffy hand' syndrome is a form of lymphoedema caused by the sclerosing action of the drugs.[92,93,94] Neviaser et al.[94] demonstrated that the cause of 'puffy hand' was a lymphatic obstruction. The swelling persists even after the addict stops injections.

Penis. Penile veins are used for injection, particularly the dorsal vein of the penis, resulting in penile necrotizing ulcers (Fig. 1).[95,96]

Neck. Jugular vein injection may be complicated by descending cervical cellulitis and mediastinitis with a high rate of mortality.[97,98]

Groin. Direct pudendal artery injections cause penile and scrotal necrotizing ulcers.[41,77,78] Abscesses, false and mycotic femoral aneurysms and iliofemoral venous thrombosis complicate groin injections.[21,60,69]

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