What Illegal Substance Causes Face and Mouth Sores?

When individuals use illegal substances, they sometimes develop severe, non-healing sores or deep ulcerations on the face, mouth, and other parts of the body. These devastating skin and soft tissue injuries are generally not a direct result of the primary illegal substance itself, such as an opioid or stimulant. Instead, the wounds are telltale signs of exposure to potent, non-pharmaceutical compounds mixed into the drug supply to increase volume or enhance psychoactive effects. These contaminants introduce severe toxicity to the body’s vascular and immune systems, leading to necrosis, which is the death of body tissue. Understanding the specific nature of these adulterants is necessary to grasp the heightened dangers associated with the current illicit drug market.

Xylazine The Current Public Health Concern

The substance currently causing the most alarm and the majority of these necrotic skin lesions is Xylazine, commonly known on the street as “tranq” or “tranq dope.” Xylazine is a powerful sedative and analgesic developed for use in large animals, such as horses and cattle, but it is not approved for human consumption. It is now frequently used as an adulterant, particularly in the illicit fentanyl supply, where it is often combined with other substances to prolong the euphoric effects of the opioid.

The presence of Xylazine presents a complex danger because it is a non-opioid, meaning that the opioid-reversal medication naloxone has no effect on its sedative properties. Users exposed to Xylazine frequently present with deep, slow-healing wounds that have a characteristic appearance of purple or gray patches of dead tissue. These ulcers can appear at injection sites but are also frequently found in distant areas like the face, mouth, limbs, and back. The severity of the tissue damage significantly increases the risk of systemic infection, which can lead to life-threatening conditions like sepsis.

The Mechanism Behind Severe Tissue Damage

The profound tissue destruction associated with Xylazine exposure stems from two intertwined physiological and behavioral mechanisms. The primary biological cause is Xylazine’s powerful action as an alpha-2 adrenergic agonist, which results in intense vasoconstriction. This physiological process causes the narrowing of blood vessels, drastically reducing blood flow to peripheral tissues throughout the body, even those far from the injection site.

This lack of blood flow, known as ischemia, deprives the skin and underlying soft tissue of necessary oxygen and nutrients, leading to cellular death and subsequent necrosis. The resulting wounds are distinct because they are caused by a systemic lack of circulation rather than a localized infection or trauma. Compounding this effect, Xylazine causes severe bradycardia and hypotension, further compromising the body’s overall ability to circulate blood effectively and heal minor injuries.

The second mechanism relates to the profound and prolonged sedation Xylazine induces, which can last for many hours. This extended period of immobility leads to a high risk of developing pressure sores, also called decubitus ulcers, as users remain unconscious and still for long durations. Users may also neglect existing wounds or suffer injuries while sedated, and the compromised circulation prevents these minor wounds from healing naturally. The combination of systemic ischemia and behavioral factors results in the rapid development of deep, necrotic lesions that can expose underlying bone and tendon.

Levamisole A Historical Contaminant

Before the emergence of Xylazine, another adulterant, Levamisole, was historically recognized for causing similarly severe, but clinically distinct, skin damage. Levamisole is an anti-parasitic medication used in veterinary medicine, and it was widely used to bulk illegal cocaine supplies in the 2000s and early 2010s.

Unlike Xylazine’s direct vasoconstriction, Levamisole-induced sores are primarily caused by an autoimmune reaction known as vasculitis. This reaction involves the body’s immune system mistakenly attacking and damaging the walls of small and medium-sized blood vessels. This damage leads to inflammation, microvascular thrombosis, and tissue death.

The lesions resulting from Levamisole exposure often present as purpuric, net-like patches with central necrosis, a pattern known as retiform purpura. These unique sores frequently affect the ears, nose, and cheeks, in addition to the extremities, making them visually distinct from the ulcers caused by Xylazine. The systemic nature of the immune response often leads to other complications, including a severely decreased white blood cell count, which leaves the user highly vulnerable to infection.

Specialized Medical Treatment for Drug-Induced Sores

Treating these drug-induced ulcers presents a significant challenge because the wounds are often extensive and resistant to standard care. A multidisciplinary team including wound care specialists, infectious disease physicians, and surgeons is often required for successful management.

The first step involves debridement, which is the surgical or enzymatic removal of the dead, necrotic tissue and eschar to allow healthy tissue to regenerate. Because the compromised tissue is highly susceptible to bacterial invasion, broad-spectrum antibiotics are necessary to treat or prevent secondary infections, which often include aggressive strains like methicillin-resistant Staphylococcus aureus. Pain management is another complex factor, as patients with these wounds frequently require substantial doses of pain medication.

In cases where the tissue damage is severe and exposes bone or tendon, advanced reconstructive techniques, such as the application of dermal substitutes or skin grafting, may be necessary to achieve wound closure. However, these procedures carry a high risk of failure if the patient continues to use the contaminated substance, as the ongoing vascular damage will prevent the graft from healing. The immediate medical goal is to prevent systemic infection and limb loss, which can ultimately necessitate amputation if the necrosis is too widespread.