Chemical Poisoning and Exposures
Kodi K. Azari
Roee E. Rubenstein
Chemical burns comprise a group of devastating injuries. Their management requires expertise, especially in the acute injury period when interventions to minimize the extent of tissue damage must be implemented. The knowledge of the specific properties of the offending agent is important to obtain the most optimal result.
There are over 25,000 known products, which can cause a chemical burn as a result of topical exposure, and these agents are extremely diverse. Although more than 60% of hospital admissions for chemical injuries are work related, exposures to harmful chemicals may also occur in household settings. These injuries have significant occupational morbidity, and some patients are not able to return to their jobs. Individuals working in the landfill industry are most susceptible to chemical exposures with industrial cleaners and paper manufacturers following closely behind. Extravasation injuries may occur in with chemotherapeutic and radiological contrast dyes and although often self-limiting, can create significant tissue loss.
Despite a relative paucity of literature on the subject, hand surgeons commonly see chemical burns as the digits are one of the most common locations of chemical burns.
Chemical burns of the hand, like thermal burns, usually cause damage that is limited to the skin. However, some chemical agents may continue to be active at the site of injury, causing assiduous destruction to the tissues even after the spill has been cleaned, and without immediate pain.
Determinants of the extent of tissue damage include the part of the body exposed, the nature and concentration of the chemical agent, the volume of substance in contact with the skin, the comorbid condition of the skin and patient, with the most important being the duration of contact between the skin and the noxious chemical.
Most chemical burns are the result of exposure to either acidic or alkaline agents.
Acid chemicals erode through the skin’s protective stratum corneum, causing fluid shifts and cellular dehydration, damaging cell membranes, and coagulation necrosis. The damage can progress and spread until the agent is lavaged away, sufficiently diluted, or neutralized. Significantly, damaged tissue retains sufficient buffering capacity for acids to limit the depth of tissue damage sustained.
Alkali burns are more dangerous than acid burns. They are clinically more latent, and often victims do not sense the burn until the exposure is prolonged. Furthermore, these burns are considered “hygroscopic” because protein-bound alkali molecules are highly reactive and lipophilic, achieving easy tissue penetration by combining with membrane elements to form fatty
soaps. The damaged tissues have a limited capacity to buffer alkalis, the wound milieu remains basic, and the reactions can continue for days with extensive and deep tissue destruction known as liquefaction necrosis.