No abstract

Appropriate wound dressing selection is guided by an understanding of wound dressing properties and an ability to match the level of drainage and depth of a wound. Wounds should be assessed for necrosis and infection, which need to be addressed prior to selecting an ideal dressing. Moisture-retentive dressings include films, hydrogels, hydrocolloids, foams, alginates, and hydrofibers and are useful in a variety of clinical settings. Antimicrobial-impregnated dressings can be useful in wounds that are superficially infected or are at higher risk for infection. For refractory wounds that need more growth stimulation, tissue-engineered dressings have become a viable option in the past few decades, especially those that have been approved for burns, venous ulcers, and diabetic ulcers. As wounds heal, the ideal dressing type may change, depending on the amount of exudate and depth of the wound; thus success in wound dressing selection hinges on recognition of the changing healing environment.

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Covering wounds, acute and chronic, is one of the most fundamental activities of any medical practitioner. Although wound dressings primarily serve to contain the "good" and keep out the "bad," research has characterized more specifically the sophisticated interaction between the human wound bed and its dressing counterpart. Wound dressings for today's chronic wounds come in many flavors, ranging from the classic types of moisture-retentive dressings to silver-coated varieties to biologic dressings serving as skin substitutes. Moisture-retentive dressing types include foams, films, hydrogels, hydrocolloids, and alginates. Appropriate use of these dressings can help to keep the wound bed moist, which allows for epithelial migration, angiogenesis, retention of growth factors, autolytic debridement, and maintenance of electrical gradients.

Immune checkpoint inhibitors such as ipilimumab and targeted BRAF inhibitors have dramatically altered the landscape of melanoma therapeutics over the past few years. Agents targeting the programmed cell death-1/ligand (PD-1/PD-L1) axis are now being developed and appear to be highly active clinically with favorable toxicity profiles. We report two patients with BRAF V600E mutant melanoma who were treated with anti-PD-1 agents as first-line therapy without significant toxicity, followed by vemurafenib at disease progression. Both patients developed severe hypersensitivity drug eruptions with multi-organ injury early in their BRAF inhibitor treatment course. One patient subsequently developed acute inflammatory demyelinating polyneuropathy (AIDP) and the other developed anaphylaxis upon low-dose vemurafenib rechallenge. Further investigation of the immune response during combination or sequences of melanoma therapeutics is warranted. Furthermore, clinicians should maintain a high index of suspicion for these toxicities when vemurafenib is administered following an anti-PD-1 agent.