Scalp necrosis and giant cell arteritis: case report and issues in wound management

Abstract

Scalp necrosis is rare in patients with giant cell arteritis. Here, we report the case of an 81‐year‐old woman who presented with a management problem that required a truly multidisciplinary approach to treatment. A combined approach of effective wound bed preparation with selective debridement, prolonged antimicrobial therapy, corticosteroid use and careful dressing choices resulted in a successful outcome in a potentially disastrous situation.

Introduction

Scalp necrosis is uncommon in patients with giant cell arteritis, accounting for <1% of cases (1). Approximately, 55 cases (2) have been reported in the rheumatological, dermatological and ophthalmological literature, but to our knowledge, no such cases have appeared in the ‘wound care’ literature. While previous reports have focused primarily upon scalp necrosis as a rare complication of giant cell arteritis, we explore specific issues involved in the wound management of this condition.

Case

An 81‐year‐old female, with a medical history of hypertension, ischaemic heart disease and hypercholesterolaemia, presented to a hospital emergency room with a fronto‐temporal headache. She was evaluated and thought to have had a small ‘cerebrovascular accident’. There was no history of smoking, diabetes mellitus, peripheral neuropathy, joint symptoms, renal disease or intermittent claudication. She was discharged from the hospital, but the following day, in addition to ongoing headache, she had intermittent visual ‘blackouts’. By the second day, she became completely blind.

She returned to the hospital, where a clinical diagnosis of ‘temporal (giant cell) arteritis’ was made after noting some tenderness along the temporal arteries. A temporal artery biopsy confirmed the diagnosis. At the same time, there was concern on the part of her treating physicians that she might also have had ‘shingles’. Because she was already blind, and because of the concern over ‘shingles’, it was decided not to start corticosteroids at that time. She was discharged home.

Four months later, her family noted the development of bilateral scalp ulcers with secondary infection. She was assessed by several dermatologists and had limited scalp debridements. She was started on prednisone 60 mg per day, topical fusidic acid and silver sulfadiazine.

After 2 months of unsuccessful treatments, she was then referred to the regional consultation wound clinic because of deep scalp ulcers. She had a relatively painless, large irregular scalp wound from the anterior hairline to the occipital region, including much of the temporal areas bilaterally. The area of involvement was estimated to be at least 120 cm² in size, with about 20 cm² of exposed skull. There were areas of purulent exudate, granulating tissue and islands of oedematous hair‐bearing scalp as well as dry, exposed parietal and occipital bone. The wound edges were swollen, but there was little tenderness (Figure 1).

Figure 1.

Initial appearance of scalp wound (anterior view).

A heavy growth of methicillin‐sensitive Staphylococcus aureus was isolated from the scalp wound.

Wound management

The exposed parieto‐occipital bones of the skull were dry, and the lambdoid bony sutures were friable at exploration. We elected not to debride the skull bones but to apply a hydrogel (IntraSite Smith & Nephew Ltd) with a non adherent silicone mesh (Mepitel Mölnlycke Ltd) to keep the wound moist and to lessen the risks of dressing adherence to underlying islands of struggling granulation tissue.

Antimicrobial therapy was given via topical and systemic routes. Topical 1% silver sulfadiazine (Flamazine Pfizer Ltd) and intravenous Cefazolin 2 g every 6 hours were chosen for their efficacies against S. aureus. The area was then covered with moist gauze, which was then supported by gauze netting over the head.

Oral prednisone 60 mg per day was used to treat the active underlying giant cell arteritis. Dressings were inspected and changed daily by the community home care service, although the silicone mesh was not removed. Clinic follow‐up was performed every 1–2 weeks, initially, and then once monthly as positive results were realised, in consultation with the community home care service (Figure 2). Intravenous antibiotics were continued for approximately 6 weeks. Prednisone doses were gradually tapered over a period of 4 months to <20 mg per day, as advised by the rheumatology service.

Figure 2.

Initial appearance of scalp wound (posterior view).

Five months after its initial appearance, the wound had granulated well, covering all areas of exposed, formerly dry skull. A bridge of new epithelium had grown across the parietal bones, creating anterior and posterior wound areas. The wound was now about 30–40% smaller than on initial visit. We elected to cover the larger posterior granulating wound with a split thickness skin graft to enhance resolution of the defect. Nine months after its first appearance, the wound had completely closed (Figure 3).

Figure 3.

Headed scalp wound.

Discussion

Giant cell arteritis is typically a condition of women over 55 years of age. Its complications are well known. Our patient's most important initial problem was visual loss as a result of ischaemic optic neuropathy, secondary to inflammation involving the medium and large extra‐cranial branches of the external carotid artery, likely involving the posterior ciliary branches, supplying the optic nerve. Visual loss may occur in up to 20% of affected persons with giant cell arteritis. They are at greatest risk within the first 2 months of diagnosis, even if corticosteroid therapy has already been started. Headache has been reported to occur in two‐thirds of such patients (1).

Scalp necrosis associated with giant cell arteritis, on the contrary, is a very uncommon complication (3). Curry et al. describes 24 cases in his 1997 review (4) of the medical literature, indicating that the affected patient population is elderly with a mean age of 77 years, predominantly female, presenting with headache and usually other serious complications (80%), such as visual loss, gangrene of the tongue and involvement of the nasal septum. The mean interval from the onset of giant cell arteritis to scalp necrosis was 3 months in 18/24 cases.

Just over half of the patients in that cohort had bilateral scalp involvement with only one patient having 80% involvement. The current hypothesis is that the presence of these complications may represent a more aggressive variant (5) of vasculitis, which must involve a greater number of medium‐sized arteries, particularly those supplying the scalp.

Mortality risk has been reported to be as high as 40% (6).

In our case, we believe that the following factors contributed to delayed wound healing: wound ischaemia, unresolved secondary infection of the scalp wound, persistent dryness of the wound and advanced patient age. The most pressing initial management priority was effective preparation of the wound bed for healing. The TIME concept (7) was followed systematically with:

• • repeated sharp debridement of loose, necrotic tissue and exudate,
• • local and systemic treatment of the staphylococcal infection to restore bacterial balance,
• • hydrogel cover to achieve moisture balance to promote new cell growth,
• • careful attention to the skin edge to facilitate islands of tissue to coalesce and join,
• • treatment of the underlying vasculitis, along with advice to enhance patient nutrition, relieve stress factors, monitor glucose, minimise potential gastric symptoms and bolster psychological support.

Scalp tissue ischaemia was the main factor that initiated the wound, particularly in the absence of previous anti‐inflammatory therapy. Secondary infection contributed to further destruction of tissue, culminating in a wide wound that defied early resolution.

A major concern was viability of the outer table of the skull, in the light of the loss of blood supply to the outer periosteum. Scalp damage involved the loss of all four layers of the scalp: skin, connective tissue layer, epicranial aponeurosis and underlying loose areolar tissue. The exposed periosteum is normally supplied by branches from the external carotid arteries, such as the superficial temporal, posterior auricular and occipital arteries, which in turn pass through the loose areolar tissue to supply the periosteum. These branches had been destroyed. Fortunately, the outer table had not been breached, but some areas along the posterior bony sutures were friable. The vascular supply to the cortex and inner table is provided by branches of the middle meningeal artery. We were impressed with the scalp's regenerative capacity over desiccated skull bones, which themselves appeared to heal with appropriate bed preparation and treatment of the vasculitis. Possibly, blood supply from the skull cortex as well as regenerating granulation tissue preserved the periosteum.

To restore moisture balance, we used a hydrogel and a non adherent silicone dressing. These were chosen to provide an optimal moist environment for the skull and for support of new tissue without risking that new growth during dressing changes. Because of the high microbial load of S. aureus in the wound, a combined approach of topical and systemic antibiotics was used to treat the infection.

High‐dose corticosteroid (prednisone 60 mg/day) is the accepted initial approach to the treatment of active giant cell arteritis and was chosen to treat the vasculitis that contributed to the tissue ischaemia (1).

Wound healing was slow, but consistent, with progressive bridging of granulation tissue islands across the top of the skull. Towards the end of the course of treatment, grafting of the remaining open surface hastened wound closure.

Summary

• • This case presents the problems encountered in managing a complex wound associated with scalp necrosis caused by giant cell arteritis.
• • Using a structured approach to wound bed preparation and following the TIME method to wound management reverse serious skull desiccation and infection, with resultant scalp wound healing.

Acknowledgements

The authors acknowledge the technical expertise of Dr Carolyn Levis, Division of Plastic Surgery, and Dr Al Cividino, Division of Rheumatology, Hamilton Health Sciences and McMaster University, Hamilton, Ontario.