Surgical management of axillary necrotizing fasciitis: A case report

Authors


  • Conflict interest: none.

Osamu Yamasaki, M.D., Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan. Email: yamasa-o@cc.okayama-u.ac.jp

Abstract

Axillary necrotizing fasciitis (NF) is quite rare and requires special management with respect to debridement and delayed surgical reconstruction. A 76-year-old man presented to our emergency department with a 2-day history of high fever, severe left axillary pain and redness. A few hours later, he developed discoloration and hemorrhagic bulla in the axilla, and the redness enlarged on the trunk. Emergency surgical debridement was performed. The blackish necrosis in the axilla was completely excised and the erythematous areas in the chest wall were cut down to the level of the fascia. Split-thickness skin grafts were applied during the second debridement on the 30th day of hospitalization and negative pressure wound therapy was used. Although the grafts took partially, full thickness axillary defects remained. We performed reconstruction with a pedicled latissimus dorsi flap on day 78. This case highlights some of the important surgical considerations in the management of axillary NF.

Introduction

Necrotizing fasciitis (NF) may occur in almost any anatomic site, but most cases involve the extremities, abdomen and perineum.1 Primary involvement of the axilla is quite rare. Furthermore, NF in the axillary region requires special management with respect to debridement and delayed surgical reconstruction.

Case Report

A 76-year-old man presented to our emergency department with a 2-day history of high fever, severe left axillary pain and redness. He had injured his left palm 4 days earlier. His consciousness was confused. Physical examination revealed redness, swelling, warmth and severe tenderness without obvious signs of necrosis in the left axilla. A rice-sized crust was seen on the left palm. His vital signs were: blood pressure, 90/40 mmHg; pulse, 110 b.p.m.; and body temperature, 39.2°C. The initial blood chemistry results were: white blood cells, 800/mm3; platelet count, 147 000/mm3; C-reactive protein, 29.5 mg/dL; aspartate aminotransferase, 220 IU/L; alanine aminotransferase, 59 IU/L; creatinine phosphokinase, 9520 IU/L; activated partial thromboplastin time, 56.7 s; fibrinogen level, 652 mg/dL, fibrinogen degradation products, 31 ug/mL; D-dimer level, 8.6 ug/mL; and streptolysin O, 106 U/mL (rose to 1602 U/mL at 4 weeks later). He was admitted into our intensive care unit; pressor support with dopamine and i.v. treatment with meropenem, clindamycin and immunoglobulin G were initiated. A few hours later, he developed discoloration and hemorrhagic bulla in the axilla, and the redness enlarged on the trunk (Fig. 1). NF was suspected, and emergency surgical debridement was performed. The blackish necrosis in the axilla was completely excised and the erythematous areas in the chest wall and upper arm were cut down to the level of the fascia, revealing watery fluid and viable fascia (Fig. 2a). Histopathological findings of a blackish necrotic lesion in the axilla revealed mild neutrophil infiltration and intravascular coagulation in the dermis and subcutis (Fig. 2b). No thrombus was observed in the erythematous lesion of the abdominal wall (Fig. 2c). Blood cultures were negative, but the culture of excised fascia was positive for group A streptococci (GAS). The onset of NF, shock, organ failure and the isolation of GAS from a normally sterile site were compatible with the defining characteristics of toxic shock-like syndrome. Meropenem was changed to sulbactam/ampicillin, and gabexate mesilate and platelets were used to treat disseminated intravascular coagulation. Although the redness extended to the forearm and clavicular region on day 1 postoperatively, there was no necrosis in the affected skin. He also developed severe atrial fibrillation. However, his condition gradually improved with mechanical ventilation, antibiotics and hemodialysis. The wounds granulated well after resolution of the infection (Fig. 3a). Split-thickness skin grafts were applied during the second debridement on the 30th day of hospitalization (Fig. 3b) and negative pressure wound therapy was used (Fig. 3c). Although the grafts took partially, full thickness axillary defects remained (Fig. 4a). We performed release of upper arm contractures and reconstruction with a pedicled latissimus dorsi flap on day 78 of hospitalization (Fig. 4b, c). Approximately 4 months after the initial operation, the patient was discharged. His shoulder mobility was preserved, and there was no axillary scar contracture.

Figure 1.

 Blackish necrosis in the axilla and widespread intense erythema from upper arm to trunk were observed.

Figure 2.

 (a) Appearance after extensive debridement in the axillary and chest. (b) No thrombus was observed in the erythematous lesion of the abdominal wall (hematoxylin–eosin [HE], original magnification ×40). (c) Mild neutrophil infiltration and intravascular coagulation in the dermis and subcutis of the chest (HE, ×40).

Figure 3.

 (a) The wounds granulated well 1 month after first debridement. (b) Split-thickness skin grafts for the axillary defects. (c) Negative pressure wound therapy for the axillary defects.

Figure 4.

 (a) Full thickness axillary defects after split thickness skin graft. (b) Pedicled latissimus dorsi flap for filling and covering the axillary defects.

Discussion

In large series of 166 patients with NF, the extremities were the most common site of infection (57.8%), followed by the abdomen (12.1%), perineum (12.1%), buttocks (10.2%), head and neck (8%), and chest (5%).1 To the best of our knowledge, only a few cases of NF involving the axillary region have been reported;2,3 they were not reports specialized in the anatomic site.

Axillary NF may be recorded as chest wall NF. The characteristics of NF in the chest wall adjacent to the axilla are quite different from other sites. Many cases were associated with an underlying condition or surgical procedures such as tube thoracostomy for empyema and esophagectomy for cancer.4 Because of the delay in diagnosis and inadequate debridement, chest wall NF has been highly lethal. Furthermore, wound closure has been difficult in patients who survived the initial septic phase.4 We believe that a minor trauma of the palm in this case was a portal of entry for a bacterial pathogen and the infection developed in the axilla with hematogenous or lymphatic spread from the distant site. Therefore, the pathogenesis might be different from that of chest wall NF.

As a delay in diagnosis and surgical debridement of NF is likely to increase mortality,5 it is important to perform early and adequate debridement. A specific surgical approach is required, depending on the body region involved. Fournier’s gangrene is a surgical emergency, necessitating early aggressive drainage and debridement, but colostomy or orchiectomy may still be necessary despite these measures.6 In patients with cervical NF, careful determination of the depth and extent of the infection is essential because of the proximity to vital structures of the neck. Surgical management may be necessary to prevent airway obstruction.7 NF in the axillary region also requires special consideration. The infection may be widespread in the upper extremity and the trunk. Furthermore, it is necessary to cover the exposed axillary neurovascular structure and to avoid axillary contractures.

Treatment of NF entails a radical excisional debridement. The extent of debridement has been a topic of debate. Sarani et al.8 recommended that the excision boundaries in NF should be at least as wide as the rim of cellulitis. Wong et al.9 proposed a different approach to the debridement in NF, involving the classification of the affected area into the three surgical zones: (i) necrotic tissue, which is completely excised; (ii) infected but potentially salvageable soft tissue, which is carefully assessed and progressively cut back; and (iii) non-infected skin, which is left alone. For the widespread redness on the trunk in this case, we choose the latter; the erythematous skin did not become necrotic.

Delayed surgical reconstruction is necessary for full thickness axillary defects due to NF, as in other reconstructive situations such as burn contractures and hidradenitis suppurativa. A variety of flaps are available to cover defects of the axilla, including thoracodorsal artery perforator flap, scapular/parascapular fasciocutaneous flap, latissimus dorsi, pectoralis major flap and free flaps.10 However, the vascular pedicle of these regional flaps may be absent. Although a wide surgical skin defect of the chest wall remained in this case, the vascularity of the latissimus dorsi was preserved. Therefore, this procedure was performed easily in comparison with other flaps. In axillary NF, an appropriate flap should be chosen after considering the necrotic extent of the attached skin. In conclusion, this case highlights some of the important surgical considerations in the management of axillary NF.

Ancillary