Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Necrotizing Fasciitis of the Head and Neck Necrotizing fasciitis is a soft tissue infection that causes necrosis of fascia and subcutaneous tissue, but spares skin and muscle initially. The groin, abdomen and extremities are the most frequent sites involved by this disease. The eyelids, scalp, face and neck are rarely involved, with only 40 cases reported in the literature. The first description of the disease was by Joseph Jones in 1871 when he referenced more than 2600 cases during the civil war. Various names have been ascribed to this lesion including hospital gangrene, necrotizing erysipelas, streptococcal gangrene, and suppurative fasciitis. In 1952, Wilson first used the term "necrotizing fasciitis," which is the most accurate term to describe this disease. The disease in the head and neck can be divided into two groups because it behaves differently in each area. The first group is the scalp and eyelids, where the disease is most commonly caused by trauma followed by infection. In the eyelids there are anatomic barriers that limit the spread of infection outside the orbit. The opposite orbit is frequently involved because the path of least resistance is across the nasal bridge. The organism most commonly isolated is Group A b-hemolytic strep alone or in combination with S aureus. There have been no fatalities reported in this group. The other group includes the face and neck. Dental infections are the most common etiology, followed by trauma, peritonsillar and pharyngeal abscesses, and osteoradionecrosis. This group has a rapidly progressive course with 65% of cases in one series developing extension into the chest wall and mediastinum, and a mortality rate of 27%. The bacteriology consists of anaerobes, gram negative rods, group A b-hemolytic strep, and staph species. The onset of symptoms is usually 2 to 4 days after the insult. The skin is smooth, tense and shiny with no sharp demarcation, and develops a dusky discoloration with poorly defined borders. There is localized necrosis of skin which is secondary to thrombosis of nutrient vessels as they pass through the zone of involved fascia. If untreated, this will progress to frank cutaneous gangrene. Clinically there is sudden pain and swelling and the skin becomes warm, erythematous, and edematous and can be mistaken for cellulitis or erysipelas. Three zones of skin are recognized and include a wide peripheral zone of erythema surrounding a tender dusky zone, and a central zone of necrosis that eventually ulcerates. There can be anesthesia of the skin from involvement of the cutaneous nerves as they pass through necrotic subcutaneous tissue. Soft tissue crepitance is common from gas formation. These patients often have a low-grade fever and can be anemic and jaundiced from bacterial hemolysis. Massive amounts of fluid can be sequestered with resultant hyponatremia, hypoproteinemia, and dehydration. Hypocalcemia can develop from necrosis of subcutaneous fat and subsequent saponification. Evaluation should consist of routine blood work looking for metabolic abnormalities as mentioned. Cultures of the wound and blood should be obtained and sent for routine and anaerobic cultures. If there is any question about subcutaneous necrosis, the wound can be probed to ascertain the presence and extent of fascial involvement. Imaging studies that are helpful include plain soft tissue films of the neck looking for gas in soft tissues and retropharyngeal widening; chest x-ray to evaluate the mediastinum for widening and to look for pleural effusions; and CT scanning which is probably the single most useful study because it can detect gas in areas inaccessible to palpation, identify areas where infection has spread preoperatively, and can detect vascular thrombosis, erosion of vessels, or mediastinitis. These patients should be treated with broad spectrum antibiotics after cultures have been obtained. Penicillin is the drug of choice for streptococcus-group A, B, C, G, and H, strep viridans and most clostridia. Clindamycin is adequate therapy against anaerobes resistant to penicillin, and an aminoglycoside should be used to cover gram negative bacilli. Debridement of all necrotic tissue is the most important aspect in the treatment of these patients. Immediate surgical exploration is indicated in the presence of subcutaneous emphysema, rapidly advancing infection despite 24 to 48 hours of medical therapy, obvious fluctuance, or skin necrosis in an area of cellulitis. It is important to remember that fascial necrosis usually extends further than cutaneous involvement. Several factors have been found to influence survival in necrotizing fasciitis. A delay of greater than 24 hours is associated with a much higher mortality rate (70%) than in those patients treated in less than 24 hours (36%). Diabetes mellitus and atherosclerosis are also associated with a much higher mortality rate and chronic renal failure, obesity, immunosuppression, and malnutrition have all been found to influence survival rates adversely. The complications that have been associated with necrotizing fasciitis of the head and neck include necrosis of the chest wall fascia, mediastinitis, pleural effusion, pericardial effusion, empyema, airway obstruction, arterial erosion, jugular vein thrombophlebitis, septic shock, lung abscess, and carotid artery thrombosis. The most important aspects in the care of these patients are the early recognition and correction of metabolic abnormalities, broad spectrum antibiotic coverage, and early radical debridement of all necrotic tissue. Case Presentation A 8-year-old Latin male had been in good health until June 1990 when he developed vesicular eruptions over his face, neck and chest and was diagnosed with chicken pox. His neck became swollen and tender and this was followed shortly thereafter by erythema. At this time he was seen by his primary physician who prescribed amoxil. The erythema and edema spread quickly to involve the right side of his face, neck and upper chest. He was admitted to Polly Ryan Hospital and treated with intravenous Claforan and Nafcillin. CT scanning revealed soft tissue swelling of his neck and bilateral submandibular fluid collections. He was transferred to Texas Children's Hospital on and an Otolaryngology consult was obtained. On examination he was febrile to 102°F, tachycardic, hypotensive, and had marked edema and erythema on the right side from the tragus to the upper chest, and on the left from the mandible to the upper chest. There was exquisite tenderness to palpation in the submandibular region and there was an inflamed, crusted pock mark in the mid-aspect of the right side of the neck. Laboratory evaluation was remarkable for a white count of 17.5 with 70% segmented neutrophils and 13% bands and a sodium of 131. On admission, his antibiotics were changed to penicillin, clindamycin and amikacin. He was taken to the operating room emergently and exploration of his neck revealed necrosis of the subcutaneous fat and fascia. All necrotic tissue was debrided and Penrose drains were placed. Postoperatively, he required aggressive fluid supplementation and vasopressors to adequately maintain his blood pressure. He remained intubated in the intensive care unit for five days and during this time his wounds were managed with frequent dressing changes and debridement at the bedside. Seven days later, he was taken back to the operating room for additional debridement and drainage of his neck wounds. The final culture grew only group A ß-hemolytic streptococcus. After seven days of triple antibiotics he was changed over to penicillin for an additional seven days, and then discharged home. Oral clindamycin was prescribed for ten days. His wounds were managed as an outpatient and eventually healed by secondary intention without complication. Bibliography Bahna M, Canalis RF. 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Yamaoka M, Furusawa K, Kiga M, Iguchi K, Hirose I. Necrotizing buccal and cervical fasciitis. J Cranio Maxillo Fac Surg 1990;8:223-224. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2006 Baylor College of Medicine
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