Vascular Injury Secondary to Drug Abuse



Vascular Injury Secondary to Drug Abuse



Gerald S. Treiman, Misty Humphries and Richard L. Treiman



Arterial Injury


Inadvertent intraarterial drug injection (IADI) can result from administration of medication by health care providers or injection of illicit substances. Iatrogenic intraarterial injection was first reported 60 years ago and is estimated to occur in between 1 in 3440 and 1 in 56,000 cases of parenteral medication administration. The incidence following illicit drug administration is unknown but is thought to be more common, although most reports reflect anecdotal experiences involving small numbers of patients.



Pathophysiology


IADI results in injury to the arteries, arterioles, capillaries, and venules. Arterial spasm, embolization of particulate matter, alternations in pH with drug crystallization, platelet aggregation, thromboxane release, and sympathetic-mediated vasospasm have all been proposed to account for ischemic changes. The initial injury appears to affect the venules as the drug and particulate matter pass through the arteriolar and capillary system, then injure venous endothelium, leading to venospasm and venous thrombosis (Figure 1). The venous injury results in outflow obstruction and slowed perfusion, causing stagnation in the arterioles. The result is secondary arteriolar endothelial injury, intimal disruption, and local thrombosis. In addition, outflow obstruction from venous thrombosis increases capillary pressure, leading to increased interstitial pressure and impaired tissue perfusion. The arterial insufficiency, venous injury, and loss of perfusion combine to result in tissue ischemia.


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FIGURE 1 Venous phase of an arteriogram taken 36 hours after intraarterial drug injection demonstrates venous thrombosis with multiple venous microaneurysms.

Secondary arterial injury results from chemical arteritis (inflammation in response to compounds present in the injected substance) and direct endothelial cytotoxic effects. Direct endothelial injury has been confirmed histologically, with vessel wall necrosis occurring within 24 hours after injection. These examinations have found the arterial wall to be amorphous and weakly acidophilic, with destruction of cellular architecture and nuclei. The intima has no viable endothelium, although arteriolar thrombosis might not be apparent for 48 to 72 hours. As the inflammatory response progresses and thrombosis develops, tissue perfusion is further reduced.



Presentation


Almost without exception, patients present with unrelenting severe pain. Following upper extremity injection, the forearm is often edematous and the hand is usually cool. The fingers are commonly mottled, cyanotic, or gangrenous, with impaired sensation and minimal motor function (Figure 2). Radial and ulnar pulses are usually present, and the presence of intact pulses helps distinguish IADI from other causes of acute ischemia (Figure 3). Although distal pulses are often palpable, plethysmography often fails to identify digital pulses owing to distal arterial occlusion.


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FIGURE 2 Hand showing characteristic changes of cyanosis, mottling, and edema after intraarterial drug injection.

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FIGURE 3 Arteriogram of the same patient in Figure 1 demonstrates patency of radial, ulnar, and brachial arteries (A) and digital artery occlusion (B).

Initial examination should assess the extent of ischemia and the status of motor and sensory function because the clinical signs and severity of injury correlate with the ultimate outcome and extent of tissue loss. The likelihood of permanent neurologic dysfunction of tissue loss can be more accurately determined through evaluation of the color, capillary refill, temperature, and sensory function of the affected extremity at the time of initial presentation (Table 1). Patients with three or more abnormal findings are significantly more likely to develop neurologic dysfunction or tissue loss than those with one or two abnormal signs if treatment is not initiated within 48 hours of injury.





Treatment


The fundamental goal of treatment is to prevent arterial, capillary, and venous stasis, maintain tissue perfusion, prevent thrombosis, control local inflammation, and minimize edema. This goal, in turn, is intended to prevent compartmental hypertension, systemic infection, and gangrene.


The largest experience with a defined treatment protocol comes from Los Angeles County–University of Southern California Medical Center, with its effectiveness on 69 patients reported in 1990. In that study, patients were treated with IV heparin sodium 10,000 units, followed by a continuous heparin infusion adjusted to keep the partial thromboplastin time (PTT) at 2 to 2.5 times control, dexamethasone 4 mg IV every 6 hours, and low-molecular-weight dextran (dextran-40) by IV infusion at 20 mL/hour (Box 1). Narcotics were given as required for pain control, the extremity was elevated in an Osborne sling, and early active and passive range of motion were instituted. The protocol was continued for a minimum of 48 hours and continued thereafter until symptoms completely resolved or extremity function no longer improved. Débridement of nonviable or gangrenous tissue was delayed until there was demarcation to allow preservation of as much potentially viable tissue as possible.



BOX 1   Protocol for Treatment of Intraarterial Drug Injection




IV, Intravenous; LMW, low-molecular-weight; PTT, partial thromboplastin time.


From Treiman GS, Yellin AE, Weaver FA, et al: An effective treatment protocol for intraarterial drug injection, J Vasc Surg 12:456–465, 1990.


Patients managed with this protocol with one or two abnormal findings had an excellent prognosis, regardless of the time from injury to the initiation of treatment (Table 2). For patients with more than two abnormal findings, time to initiation of treatment was important. This protocol was not based on randomized clinical data and has not been compared with other management schemas. Nevertheless, early initiation was found to be effective in preventing tissue loss and permanent neurologic dysfunction in patients with more than two abnormal signs.


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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Vascular Injury Secondary to Drug Abuse

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