Negative pressure wound therapy, staged excision and definitive closure with split-thickness skin graft for axillary hidradenitis suppurativa: a retrospective study
Bilateral axillary hidradenitis is a chronic, suppurative and scarring disease that is most effectively treated by complete excision of all hair-bearing tissues. We assessed our staged procedure for excision and placement of a split-thickness skin graft for bilateral axillary hidradenitis in terms of costs, outcomes and timing of excision.
An IRB approved retrospective case analysis was performed on patients that underwent bilateral axillary hidradenitis skin excision with eventual placement of split-thickness skin grafting using the current LSUHSC/University Health hidradenitis surgical treatment protocol. Using ICD-9 codes (705.83) and CPT codes (11041, 11042, 11451, 11600, 11601, 11602, 11603, 11604) we reviewed cases performed at our institution from 1 January 2008 to 24 February 2014 and we selected patients based on bilateral axillary involvement (alone) and >1 year history of active disease. Patients were excluded if resection of tissue encompassed regions outside of the immediately adjacent axillary.
A total of seven patients matching criteria for bilateral axillary hidradenitis were selected for analysis. Clinical course, cost and surgical techniques were assessed. Of the seven patients, six required admission throughout their treatment due to lack of funding making use of negative pressure wound therapy at home not possible. These patients stayed an average of 10 days with a mean hospital charge of $35,178 and a mean hospital provider charge of $10,019. No recurrence was demonstrated. All patients attained full range of motion, post-grafting. No patient required a further operation due to graft failure.
Split-thickness skin grafting without use of bilayer dermal regenerative templates yielded definitive results with acceptable cosmesis and functionality, without the added cost of treatments such as a bilayer dermal regenerative template.
Hidradenitis suppurativa (HS) is a chronic suppurative and scarring disease of the skin and underlying subcutaneous tissues that typically manifests in axillae, inguinal, anogenital/perineum, and inframammary regions resulting in painful and unsightly lesions.1,2 The prevalence of HS is 0.3 to 4% in industrialised countries and primarily affects younger (mean age of onset 23 years) individuals of African American descent with a female to male ratio of 4:1.2,3 Axillae are the most frequently affected sites, therefore, interest has developed in treating HS affecting axillae in a manner that is cost-effective, well tolerated by the patient, expedient and definitive.3
Pathogenesis and aetiology of HS has often been disputed and previously thought of as a disorder of apocrine origin; however, it is now widely accepted that the key component of HS pathogenesis involves follicular infundibular occlusion as opposed to inflammatory or infectious processes of the apocrine glands.4,5 The apocrine glands still play a critical role as evidenced by the age of onset of the disease. Patients with HS present in post-pubertal ages (following maturation of apocrine sweat glands including those of the axillae, groin, inflammatory folds).4 There have been rare cases of individuals presenting before the age of 10; these individuals underwent precocious puberty resulting in an increase in apocrine gland development/maturation.4 Patients with HS typically present with complaints of burning, itching, tenderness and hyperhidrosis of the affected areas, which tend to be violet in appearance.4,6 The disease process originates from a double comedone secondary to follicular occlusion caused by keratinous debris. The occlusion results in neighbouring apocrine inflammation.1,2,4 Follicular occlusion with subsequent rupture causes extensive and deep dermal inflammation leading to the development of epithelialised, fistulous tracts.1 Occlusion and rupture of follicular units occurs simultaneously with healing and cicatrisation leading to a permanently altered dermis, which results in a chronic recurring process of draining fistulous tracts and abscess formation.1,2,4 The process of chronic scar formation, leading to sinus tract formation, creates a hospitable environment for various species of Staphylococcus and Streptococcus bacteria to grow.5,6
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