Nasal carriage of Staphylococcus aureus in patients undergoing Mohs micrographic surgery is an important risk factor for postoperative surgical site infection: a prospective randomised study.

BACKGROUND: Surgical site infection (SSI) can be a problematic complication of Mohs micrographic surgery (MMS). Previous reports have cited nasal Staphylococcus aureus (S. aureus) carriage as a risk factor for SSI, but none thus far in dermatologic surgery. OBJECTIVE: The aim was to determine the difference in infection rates between nasal carriers of S. aureus and non-carriers, and whether decolonisation with intranasal mupirocin ointment and chlorhexidine wash would reduce the infection rate in nasal carriers. METHODS: In all, 738 patients presenting for MMS at the Oxford Day Surgery and Dermatology underwent a nasal swab to determine their S. aureus carriage status. S. aureus carriers were randomised for decolonisation with intranasal mupirocin ointment and chlorhexidine body wash. Non-carriers were untreated. All patients were followed up for SSI. RESULTS: The rate of SSI was 11 per cent in untreated S. aureus carriers, 4 per cent in treated carriers, and 3 per cent in non-carriers. The difference in infection rate between carriers and non-carriers was significant (P < 0.001). The difference between treated and untreated carriers was also significant (P = 0.05). CONCLUSION: Nasal S. aureus carriage is an important risk factor for SSI in MMS, conferring an over threefold increase in SSI risk. A pre-operative nasal swab provides a simple and effective risk stratification tool. The use of a topical decolonisation regimen reduces the infection rate in carriers to a level approaching non-carriers without exposure to systemic antibiotics.

Assessment and management of chemical exposure in the Mohs laboratory.

BACKGROUND: The correct handling, storage, and disposal of chemicals used in the processing of tissue for Mohs micrographic surgery are essential. OBJECTIVES: To identify the chemicals involved in the preparation of Mohs frozen sections and assess the associated occupational health risks. To quantify exposure levels of hazardous chemicals and ensure that they are minimized. METHODS: A risk assessment form was completed for each chemical. Atmospheric sampling was performed at our previous laboratory for formaldehyde and volatile organic compounds. These data were used in the design of our new facility, where testing was repeated. RESULTS: Twenty-five chemicals were identified. Ten were classified as hazardous substances, 10 were flammable, six had specific disposal requirements, four were potential carcinogens, and three were potential teratogens. Formaldehyde readings at our previous laboratory were up to eight times the national exposure standard. Testing at the new laboratory produced levels well below the exposure standards. CONCLUSION: Chemical exposure within the Mohs laboratory can present a significant occupational hazard. Acutely toxic and potentially carcinogenic formaldehyde was found at high levels in a relatively standard laboratory configuration. A laboratory can be designed with a combination of physical environment and operational protocols that minimizes hazards and creates a safe working environment.

Irritant dermatitis, irritancy and its role in allergic contact dermatitis.

Irritant contact dermatitis is the clinical result of sufficient inflammation arising from release of pro-inflammatory cytokines from skin cells (principally keratinocytes) in response to (usually) chemical stimuli. Different clinical forms may arise. The three main pathophysiological changes seen are skin barrier disruption, epidermal cellular changes and cytokine release. An important role of irritancy in allergic contact dermatitis (ACD) comes from earlier animal and human studies. Evidence is outlined which is consistent with a "danger model" of ACD rather than one based on a traditional "self-nonself" immune model. In such a model an antigenic signal will produce sensitization only in the presence of a danger signal; in the absence of a danger signal tolerance will occur. We propose that the danger signal in ACD is cytokine release from nonimmune skin cells (principally keratinocytes) and that both the antigenic and "danger" signals arises from the hapten.