Cervical necrotizing fasciitis of odontogenic origin

Case report

A 42-year-old woman presented to the oral and maxillofacial team via accident and emergency with an initial complaint of a dental abscess from the lower left quadrant that had been present for the previous 10 days. She had no past relevant medical history. Clinical examination revealed large bilateral submental and submandibular swelling (Figure 1). A developing area of necrosis in the anterior neck, with discharge, was noted (Figure 2). There was also an area of erythema extending from her neck onto her chest wall. On palpation, crepitus was felt in the tissues of her neck and chest wall. A diagnosis of CNF was made. Empirical intravenous antibiotics (tazocin 4.5 g three times a day and clindamycin 1.2 g four times a day) and fluid resuscitation was administered. An OPT revealed the suspected source of infection to be the lower left second premolar (Figure 3). Incidentally, the OPT also demonstrated gas locules. A CT scan of the neck and thorax revealed the presence of a large amount of gas extending from the neck to the sternum (Figures 4 and 5). Following intubation, the initial debridement involved removal of all necrotic tissues, which extended from the anterior neck to sternal notch and chest wall and laterally to the posterior border of sternomastoid muscle. All grossly carious teeth were extracted. Two further episodes of debridement were subsequently required to halt the progress of the disease. Microbiological culture of tissue yielded a mixture of Streptococcus pyogenes, and Staphylococcus and Pseudomonas species. A pectoralis major muscle flap with split thickness skin graft was used to reconstruct the surgical defect in the neck. Unfortunately, a defect developed, with breakdown at the pectoralis major donor site due to the weight of the breast, which subsequently healed by secondary intention (Figure 6). The patient recovered, but unfortunately developed a fixed flexion deformity of her neck due to underlying scarring and fibrosis of her tissue. The scar band was then excised and reconstructed with a left radial forearm free flap, which has improved her function (Figure 7).

Discussion

CNF is a rare, but often fatal infectious disease process with a mortality rate of 9.8%.¹ Predisposing factors for this pathology include alcoholism, diabetes, HIV infection, immunocompromised status, chronic renal failure, malignancy, intravenous drug abuse and obesity.⁵ A systematic review by Gunaratne et al reported that CNF was particularly prevalent in individual with diabetes and alcoholism.² Random venous blood glucose and HbA1C testing is required to test known or newly diagnosed diabetics since adequate glucose control is needed to ensure that the efficacy of treatment is not compromised. In some resource-poor African countries, poor nutritional status and unmanaged oral cavity infections resulting from dental caries, periodontitis, and untreated mandibular fractures with osteomyelitis led to a higher rate of CNF when compared with the rest of the world.⁶

The clinical progression of CNF can often confound clinicians because, initially, the overlying skin may have a benign appearance, which progresses to become erythematous and tense, mirroring cellulitis or erysipelas.² Further disease progression and thrombosis of the underlying nutrient vessels coursing through the affected fascia, results in a skin that becomes dusky, and in later stages, purplish-blue necrotic areas may become more apparent.⁷ Initial localized pain may be replaced by paraesthesia and anaesthesia as cutaneous nerves are destroyed or compressed by the resulting infection.⁶ Clinical examination of the neck may reveal crepitus as a result of gas-producing micro-organisms.⁸

Imaging in CNF plays an important role in diagnosis, planning of surgical debridement, assessing response to treatment and identifying disease progression.² Due to its speed and availability, CT imaging is often the imaging of choice. CT imaging allows the evaluation of any vascular erosion, mediastinitis, progression of infection and the presence of gas bubbles at the infected area.⁶ As disease progression is dynamic, serial CT imaging may provide more information in assessing the deteriorating patient.

The aetiology of CNF is often dental in origin, making up 47% of cases studied.² The second and third mandibular molars are often implicated due to the anatomical position of the root apices below the mylohyoid line. Other rarer sources of CNF include supraglottitis, tonsillar or peritonsillar infection, traumatic/iatrogenic injury, major salivary gland infections, cutaneous infections, otitis media, mastoiditis, malignancy and radiotherapy.²

A range of micro-organisms has been recovered from CNF, including species of Streptococcus, Staphylococcus, Prevotella, Peptostreptococcus and Bacteroides.⁵² Collagenases and hyaluronidases produced by Group A Streptococci cause necrosis and liquefaction of fascia and fat, which occurs early in the disease process.⁸ Separation of skin from underlying tissues produces the classical ‘dishwater pus’, which often has an offensive smell due to the presence of strict anaerobes.⁹

A multidisciplinary approach is required to manage these cases successfully. Effective management includes early diagnosis, airway control, aggressive resuscitation, initial broad spectrum antimicrobial therapy, removal of the source of infection with prompt and radical surgical debridement, repeated evaluation, supportive critical care and reconstructive/rehabilitation.⁷ Aggressive surgical debridement assists in halting the progression of CNF, and prevents the further release of inflammatory mediators that cause systemic complications.⁷ Involved skin, subcutaneous fat and fascia is removed until bleeding edges are encountered. If encountered, necrotic muscle should also be debrided. Patients should be closely evaluated as repeated surgical debridement is often required. Although the risk of blowout is rare with CNF, a local muscle flap can be used to cover the carotid artery system if it is exposed.⁹ Reconstruction of any surgical defect can only be undertaken once there is complete resolution of the disease process.

Empirical antimicrobial therapy may vary between hospitals, but the aim is to cover for Gram-positive, Gram-negative and strictly anaerobic bacteria.² Once culture and antibacterial susceptibility results are available, a more targeted antimicrobial therapy can be provided. The choice of antibiotic therapy may include nitro-imidazoles, cephalosporins, penicillins and aminoglycosides.

Hyperbaric oxygen therapy (HBO) has been used as form of treatment to reduce mortality, duration of hospitalization and the number of surgical debridements.² The high concentration of oxygen induces free radical formation, which is believed to assist neutrophil-mediated phagocytosis.¹⁰ HBO also improves vascularization to the infected area by promoting angiogenesis, collagen formation and capillary budding into the wound.¹¹ However its use is significantly limited by availability, and the logistics of transferring the unwell patient for treatment.

Conclusion

CNF is a relatively uncommon, rapidly progressive and often life-threatening soft tissue infection. Early diagnosis, aggressive antibiotic and surgical treatment play a vital role in the management of the disease. In patients with resultant skin or soft tissue defects, physical rehabilitation and reconstructive procedures may also be required.