From Volume 49, Issue 6, June 2022 | Pages 500-504
Necrotizing fasciitis is a rare complication of dental infection and is associated with a significant mortality rate. Prompt recognition and urgent referral are therefore essential. Surgical debridement and broad-spectrum intravenous antibiotic therapy are the mainstay of management. This report outlines a case of necrotizing fasciitis of odontogenic origin in an otherwise healthy 32-year-old patient.
Necrotizing fasciitis (NF) is a rare but severe complication of odontogenic infection.1,2 The infection spreads rapidly from the peri-apical tissues via the fascial spaces, causing necrosis of the soft tissue layers while not respecting anatomic boundaries. As a result, the patient is often systemically unwell and a mortality rate of 9.8% is associated with NF of odontogenic origin.2
Prompt diagnosis is crucial, with early surgical intervention and appropriate antimicrobial therapy being key in obtaining a good outcome.3,4,5 Patients often require aggressive surgical resection of necrotic tissues, which can lead to significant morbidity in both form and function in the head and neck.6
This case report documents NF originating from a dental source. It highlights NF as a severe complication of a common dental presentation and outlines the basic principles of management of NF to the dental team. In doing so, the authors hope to inform the readership of the crucial role they may play in expediting care and improving outcomes for these patients.
A 32-year-old male presented to accident and emergency with a 1-day history of left-sided submandibular swelling. On questioning, the patient reported approximately 1 week of toothache in the left lower jaw, fever and night sweats of 3 days, and recent onset odynophagia. He had been unable to seek dental care due to service limitations during the COVID-19 pandemic.
The patient was medically fit and well otherwise, taking no regular medicines. He smoked three cigarettes per day and drank approximately 16 units of alcohol per week. The patient's vital signs are summarized in Table 1, with tachycardia and tachypnoea evident.
| Heart rate | 102 bpm |
| Respiratory rate | 22 bpm |
| Blood pressure | 116/83 |
| Oxygen saturation | 98% |
| Temperature | 36.7°C |
On examination, there was a slight left submandibular swelling with associated tenderness. The skin over the neck was erythematous and it had no features of necrosis. Intra-orally, there was tenderness associated with the LL7 and LL8. The floor of the mouth was slightly raised with no obvious signs of a collection.
An OPT radiograph (Figure 1) showed grossly carious teeth LL7, LL8 and distal caries in tooth UL8. There is PDL widening evident around the apices of LL7. Initial blood investigations (Table 2) identified a leukocytosis, hyponatraemia, markedly raised C-reactive protein and acute kidney injury. A CT scan showed a 22 x 9-mm gas-containing collection in the left level 1B area of the neck, in keeping with the appearance of necrotizing fasciitis (Figure 2).
| Parameter and reference range | Result |
|---|---|
| White cell count (4.5–13.0 x 109/L) | 19.5 x 109/L |
| C-reactive protein (0–10 mg/L) | 384 mg/L |
| Sodium (135–145 mmol/L) | 133 mmol/L |
| Creatinine (50–120 µmol/L) | 197 µmol/L |
| eGFR (>60 ml/min) | 38 ml/min |
Intravenous antibiotics were commenced as per the local microbiology guidelines for NF: flucloxacillin (2 g 4-hourly), clindamycin (600 mg 6-hourly), metronidazole (500 mg 8-hourly), benzylpenicillin (2.4 g 6-hourly) and gentamicin (320 mg 24-hourly).
The patient was taken to theatre for removal of teeth LL7, LL8 and UL8 and exploration of the left neck. Exploration of left neck levels 1B, 2A and 3 revealed dishwater-like fluid associated with necrotic fascial tissue. Necrotic tissue was excised until healthy bleeding margins were encountered and irrigated copiously with normal saline.
There was a planned return to theatre around 12 hours after the first procedure to assess the adequacy of the first debridement and to assess whether there had been any progression of disease. Further exploration of the left neck revealed a small amount of purulent fluid in level 5, which was washed out copiously. Exploration of the right neck revealed healthy tissues.
Microbiology samples cultured Streptococcus anginosus with a resistance to clindamycin and clarithromycin. Tissue samples from the left neck showed histopathological findings consistent with necrotizing fasciitis.
The patient remained in ITU for a total of 4 days. Piperacillin and tazobactam were added to the antibiotic regimen, with clindamycin being discontinued on the advice of the local microbiology service. The patient was discharged home on oral co-amoxiclav 7 days after admission to hospital.
Odontogenic infection is very common in the general population, with 6.3% of adult teeth exhibiting apical periodontitis.7 In most cases, the infection is confined to the peri-apical tissues with local abscess formation. If left unmanaged, infection can spread to other regions of the maxillofacial region via fascial spaces.8,9 There is also the potential for haematogenous spread and resultant septicaemia.6 NF differs from cellulitis and abscess formation in that there is a rapidly advancing front of necrosis and typical systemic illness.4 Dentists can aid in the management of these rare cases by prompt identification and appropriate referral. Furthermore, prevention of dental caries and management of necrotic teeth will reduce the prospective risk of occurrence of NF.
Most cases occur in the upper and lower limbs, abdomen and groin region.10 The head and neck region is rarely involved, comprising around 1–10% of all cases of NF – due in part to the rich blood supply.11One Danish study reported an annual incidence of head and neck NF of 2 cases in 1,000,000.12 Of head and neck NF, odontogenic infections comprise around 50% of infective sources, with pharyngeal, laryngeal, tonsillar and skin infections comprising the remainder of cases.13,14 Mandibular second and third molar teeth are the most common origins of infection, with their peri-apical regions being inferior to the mylohyoid line.14 There is an approximate 3: 1 male to female preponderance and a mean age of 49 years for NF in the maxillofacial region.13
Risk factors for NF include those that impair immune function. Common examples include diabetes mellitus, malnutrition, alcoholism, elderly, cirrhosis, corticosteroid therapy, HIV, illicit intravenous drug use and obesity.2,8,10,14
The aetiology of NF is variable. Bacterial inoculation can result from trauma to the skin, insect bites, surgical procedures, intravenous drug use, burns and localized infections.3,4 Bacterial proliferation and release of exotoxins results in local tissue damage. There is resultant capillary occlusion and damage to vascular epithelium, causing fluid leakage, which correlates to the erythema and oedema seen clinically. The advancing infective front rapidly spreads to damage larger venules and arterioles, thereby causing ischaemic necrosis of adjacent tissue and deeper structures.3 Gas production by the rapidly proliferating bacteria often results in a characteristic crepitus of the skin.3
The term ‘necrotizing fasciitis’ may therefore be misleading as it suggests purely fascial layer involvement; ‘necrotizing soft tissue infection’ has been proposed as an alternative as it reflects the fact that any soft tissue layer can be involved, including skin and muscle.1 Other necrotizing infections also exist in the head and neck, including noma – a fulminant and progressive soft tissue infection, originating from necrotizing periodontal disease.15 Gas gangrene is another necrotizing infection, characterized by gas production by anaerobic clostridium bacteria.16 Similar to necrotizing fasciitis, rapid surgical debridement is essential in managing these related conditions.
Bacterial toxins and mass-production of inflammatory cytokines result in haemodynamic compromise – with shock, organ dysfunction and death being potential consequences.1,2,5,6,10,12,13,14 Careful assessment, monitoring and management of the patient are essential, with ICU-level care in addition to early surgical intervention.1,10
NF can be classified based on the microbiology of the infection: type-I NF involves a mix of both aerobes and anaerobes with a typical preponderance for immunocompromised patients; type-II NF is monomicrobial, with Group A Streptococcus being the most common species, and is the most prevalent type in otherwise healthy individuals.4 This case is a type-II NF.
Early diagnosis is key; however, in the initial stages of the disease, a benign clinical presentation can make differentiation from non-necrotizing infections (eg cellulitis, abscess) difficult.5,17 Clinical features have been classified as early, intermediate or late by Wang et al and are summarized in Table 3.18
| Stage | Clinical features |
|---|---|
| Early | Tenderness to palpation (beyond apparent area of skin involvement) |
| Intermediate | Blister or bullae formation |
| Late | Crepitus of skin |
Poorly defined erythema, oedema and calor (warmth) may be seen early on in the infection as the necrotic process is taking place at deeper soft tissue levels. As the condition progresses, the changes on the skin's surface become more apparent.18
Intense pain on palpation that is disproportionate from the clinical appearance is considered a red flag sign.3,13 Blistering and bullae formation on the skin surface represent underlying ischaemia and help to discern from non-necrotizing soft tissue infections.18 Signs in the later stages of infection include skin crepitus – as the rapidly advancing bacterial front produces gas in the soft tissues.5,11,18
While NF is a clinical diagnosis, a diagnostic tool based on blood results has been developed to aid clinicians in the diagnostic process: the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC).19 This cumulative scoring system assigns a value to six different blood parameters (Table 4) and serves to indicate the likelihood of NF as a diagnosis, thereby aiding clinicians in differentiating between necrotic and non-necrotic soft tissue infections.19 The patient in this case was positive for NF according to LRINEC with a cumulative score of 9 (Table 4). A total LRINEC score ≥6 has been shown to be highly sensitive and specific for NF; however, LRINEC appears to have differing validities in different geographical population groups.20
| Parameter | Score | Patient's score | |
|---|---|---|---|
| C-reactive protein (mg/L) | <150 | 0 | |
| ≥150 | 4 | 4 | |
| White cell count (x109/L) | <15 | 0 | |
| 15–25 | 1 | 1 | |
| >25 | 2 | ||
| Haemoglobin (g/L) | >135 | 0 | 0 |
| 110–135 | 1 | ||
| <110 | 2 | ||
| Sodium (mmol/L) | ≥135 | 0 | |
| <135 | 2 | 2 | |
| Creatinine (µmol/L) | ≤141 | 0 | |
| >141 | 2 | 2 | |
| Glucose (mmol/L) | ≤10 | 0 | 0 |
| >10 | 1 | ||
| Total | 9 |
Imaging can serve as a useful adjunct in the diagnosis and surgical planning in cases of NF.14,21 It must be emphasized, however, that the imaging process should not delay the surgical management or in the management of septic patients.22 Computed tomography (CT) scans are often the imaging modality of choice, owing to proven increased sensitivity compared with plain radiographs and more rapid acquisition in the emergency setting when compared with magnetic resonance imaging (MRI) and ultrasonograpy.22 CT findings are in keeping with the pathophysiology of NF: soft-tissue inflammation and necrosis present as dermal thickening, increased soft-tissue attenuation, inflammatory fat stranding, and possible superficial or deep fluid or gas in the subfascial planes.5,22 Indeed, gas in the soft tissue may be considered a hallmark of the necrotizing infective process.14,21
The goals of management in odontogenic NF include haemodynamic stabilization, removal of the source, surgical debridement of necrotic tissue, antimicrobial therapy and delayed reconstruction where appropriate. 1,2,6,13,14,17,21
Early surgical debridement is the fundamental principle in successful management of NF.1,5,6,13,17,21 Timing of surgical intervention is the most significant prognostic determinant of patient outcome.1,6,13 Radical debridement of all necrotic soft tissues is essential to halt the spread of the necrosis. Common surgical findings include grey-white dishwater-like fluid, offensive malodour and non-bleeding soft tissues.8,10,13,17 The margins of the debridement must extend beyond the edge of necrosis perceived clinically (while being mindful of cosmetic and functional implications) because this ensures clearance of micro-organisms from the peripheries of the wound that have not yet became necrosed, but would otherwise, if left.1,14,17 A planned return to theatre for further exploration of the wound is recommended, usually the following day after initial surgical debridement.1,3,10,21Histo pathological and microbiological sampling is also necessary to support the diagnosis and guide antimicrobial therapy.1,5,10,21,23
Antibiotics serve as an adjunct to timely surgical intervention. High-dose, broad-spectrum empirical intravenous antibiotic therapy should be commenced as soon as possible, and ongoing consultation with the local microbiology service is advised.1,5Microbiological sampling will aid in definitive antibiotic selection. The antibiotic regimen used in this case is in keeping with the literature consensus – where it is proposed that gram-positive, gram-negative and anaerobic cover is given.1,8,10,12,13
Hyperbaric oxygen therapy (HBO) is an adjuvant therapy in management of NF. High concentrations of oxygen have been shown to assist immune function and promote angiogenesis and collagen formation in the wound.12,13 The impact of HBO on patient outcome is unclear, and the literature base in equivocal.2,3,5 In one Danish institution, an HBO protocol whereby the patient received HBO three times in the first 24 hours and twice per day thereafter was proven to be significant in reducing the mortality rate associated with head and neck NF.12,24 Accessibility and logistical issues may make HBO unrealistic in many cases. Surgical debridement and appropriate antibiotic therapy remains the mainstay of management.5,23
Complications arising from odontogenic NF can be severe. These include thrombosis of major blood vessels, airway obstruction, organ failure and death.12,13,14,25
Descending necrotizing mediastinitis (DNM) involves the downward spread of infection from the head and neck region via the deep cervical fascial planes to the mediastinum.13 The mediastinum houses many important structures – DNM is associated with a mortality rate of 25–50%.25
In addition, extensive surgical debridement in the head and neck can be drastic and disfiguring. There may be resection of important facial features including eyes and lips. Free-flap reconstruction may be required.6,13
NF is a rare and severe complication of dental infections. Despite its rarity, dentists should be aware of NF to ensure prompt recognition and appropriate management. Rapidly evolving signs and symptoms should prompt emergency referral to hospital. Early surgical debridement with serial planned debridement and appropriate antibiotic therapy are essential in determining patient outcome. This case serves as a reminder of the serious consequences of unmanaged dental infection.
