|Year : 2014 | Volume
| Issue : 3 | Page : 179-182
Necrotizing fasciitis of odontogenic origin in a nonimmunocompromised patient: A rare case report
NC Sangamesh1, KC Vidya2, GS Roopa3, Santosh B Sakri4
1 Department of Oral Medicine and Radiology, Institute of Dental Science, Bariely, Uttar Pradesh, India
2 Department of Oral and Maxillofacial Surgery, Institute of Dental Science, Bariely, Uttar Pradesh, India
3 Departments of Dental Public Health, JKK Nataraja Dental College, Komarapalyam, Tamil Nadu, India
4 Departments of Dental Public Health, Surender Dental College and Hospital, Sri Ganganagar, Rajasthan, India
|Date of Web Publication||19-Sep-2014|
Santosh B Sakri
Department of Dental Public Health, Surender Dental College and Hospital, Sri Ganganagar, Rajasthan
Source of Support: None, Conflict of Interest: None
Necrotizing fasciitis is a rapidly spreading infection involving the superficial fat, fascial layers with necrosis of skin and is a disfiguring condition that is fatal. Head and neck are an unusual site, which is rarely affected. It is characterized by its fulminating, devastating and rapid progressive course. It usually occurs in patients with systemic conditions such as diabetes mellitus, renal disease, cardiovascular disease, HIV infections, etc. A case of cervical necrotizing fasciitis of odontogenic origin occurring in a nonimmunocompromised patient is reported here who was treated successfully by surgical debridement and antibiotic therapy.
Keywords: Cervical necrotizing fasciitis, odontogenic, surgical debridement
|How to cite this article:|
Sangamesh N C, Vidya K C, Roopa G S, Sakri SB. Necrotizing fasciitis of odontogenic origin in a nonimmunocompromised patient: A rare case report. J Sci Soc 2014;41:179-82
|How to cite this URL:|
Sangamesh N C, Vidya K C, Roopa G S, Sakri SB. Necrotizing fasciitis of odontogenic origin in a nonimmunocompromised patient: A rare case report. J Sci Soc [serial online] 2014 [cited 2020 Oct 31];41:179-82. Available from: https://www.jscisociety.com/text.asp?2014/41/3/179/141216
| Introduction|| |
Necrotizing fasciitis is a rare and rapidly spreading superficial infection along facial planes causing necrosis of fascia, superficial fat, overlying skin, and blood vessels with characteristic sparing of muscles and bone. 
Necrotizing fasciitis was actually first described by Hippocrates in 5 th century BC, who described this as a complication of erysipelas. In late 18 th century, Sir Gilbert Blane, Thomas Trotter, and Leonard Gillespie British naval surgeons described necrotizing fasciitis in detail. In 1871, Jones called it "hospital gangrene," which was the first description of necrotizing fasciitis in US, in 1918 Pfanner described "necrotizing erysipelas," but the name "necrotizing fasciitis" was given by Wilson in 1952 to describe tissue death and associated fascial plane involvement characteristic of the disease. 
Necrotizing fasciitis is caused by polymicrobial or mixed aerobic and anaerobic microorganisms resulting in massive tissue destruction and toxic shock syndrome. Cases affecting the head and neck regions are unusual and rare. ,
However, in contrast to an abscess or cellulites, which resolve after antibiotic therapy or incision and drainage, treatment of necrotizing fasciitis requires thorough surgical debridement of necrotic tissue.  Without aggressive medical and surgical intervention, the patient usually becomes toxic, frequently requiring critical care support, with the potential for severe cosmetic deformity, and death if not treated appropriately in a timely manner. 
| Case report|| |
A 53-year-old male patient reported to the Dental Hospital with the complaint of swelling and discharge in the left lower one-third of the face and the upper part of neck for the past 2 days.
He had been seen previously by a dentist who drained abscess giving extraoral incision that yielded pus and the patient was put on a course of routine antibiotics and analgesics. However, the patient was not relieved of symptoms. A day later patient developed swelling in the upper part of the neck associated with severe pain, fever, and dysphagia. It was at this stage that patient reported to the outpatient dental department.
There was no relevant medical history. Patient's physical examination was unremarkable and his vital signs were as follows: Blood pressure −110/70 mm Hg, pulse −94 b/min, respiratory rate −16 cycles/min and the patient was febrile with temperature −102°F.
Examination of the site revealed a diffuse swelling on the left lower third of the face extending from ala-tragal line to 4 cm below the lower border of the mandible toward the upper part of the neck. Skin over the swelling was slightly stretched, shiny generalized erythematous appearance [Figure 1] with foul smelling purulent discharge from the incised area. Few blackish dusky spots were present. On palpation, the swelling was tender with the rise of local temperature. Submandibular and upper group of cervical lymph nodes were palpable and tender. There was no involvement of the parotid gland as there was no rise of ear lobule.
|Figure 1: Swelling showing shiny unusually erythematous with orange peel appearance|
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Intraoral examination showed 12 mm mouth opening, vestibular obliteration with 27, 28 and relevant teeth were tender on percussion. Provisionally diagnosis of buccal and submandibular space infection secondary to carious 27 and 28 were made. Orthopantomograph was taken, which showed carious 27 and 28 [Figure 2].
Then, the patient was subjected to routine investigative procedures such as complete blood count, random blood sugar, HIV, and hepatitis B surface antigen. All the reports were within the normal limits except for the increased neutrophil count. Patient's physical fitness data was obtained from the physician. The patient was admitted for surgical debridement. Empirically, the patient was put on amoxicillin + clavulinic acid 1.2 g intravenously every 8 th hourly, amikacin 500 mg intravenously every 12 th hourly, metranidazole 500 mg infusion every 8 th hourly along with diclofenac sodium 75 mg intramuscularly every 8 th hourly. Then the patient was shifted to the operating room. Under general anesthesia, he underwent aggressive incision (submandibular) and drainage. A copious quantity of pus was released. Massive necrosis of the subcutaneous fat, fascia, and skin was appreciated and surgically the diagnosis of cervical necrotizing fasciitis was made. 27 and 28 were extracted and the specimen was sent for culture and antibiotic sensitivity testing. All necrotic tissue was debrided thoroughly along with fasciectomy and involved areas were irrigated with tetracycline 400 mg capsule mixed with normal saline. Later on corrugated rubber drain was placed for the residual pus. The patient was receiving the same drug regime as above until the culture report came. The culture and sensitivity report came as involvement of both aerobic and anaerobic microorganisms, and then the patient was asked to continue the same medications. After 48 h rubber drain was removed and the patient was returned to the operating room for additional irrigation and debridement of the wound and open dressing was given regularly until the time, he was discharged. No growth was appreciated on the culture.
On the 4 th postoperative day, the patient's condition had improved remarkably. Much of the edema had resolved. On the 8 th postoperative day, shrinkage in the size of the wound along with healing sloppy edges was appreciated. Patient was then discharged from the hospital with 1 week course of oral antibiotics and analgesics (amoxicillin + clavulinic acid 625 mg every 8 th hourly, amikacin 500 mg every 8 th hourly, metronidazole 400 mg every 8 th hourly along with diclofenac sodium 50 mg every 8 th hourly). Follow-up after 12 days, patient improved dramatically [Figure 3].
| Discussion|| |
There are only about 68 reported cases in world literature of cervical necrotizing fasciitis.  Immunocompromised patients are at increased risk of developing necrotizing fasciitis. ,, However, in this case report, the patient was nonimmunocompromised.
The causative organism may be a single agent, commonly Group A β-hemolytic streptococci or Staphylococcus aureus or may be a polymicrobial involving Gram-positive and Gram-negative aerobic, anaerobic bacteria and fungi. However, many authors have found culture reports to be negative in the cases they have reported. 
Initially, there are cellulites, which lead to invasion of the deeper tissues. Clinically, at this stage skin changes of erythema and edema are seen. Progressive tissue necrosis causes an invasion by the normal flora. Continuous bacterial overgrowth and synergy, causes a decrease in oxygen tension and development of local ischemia and proliferation of anaerobic organisms. In 4-5 days, gangrene is evident and after 8-10 days necrotic tissue separates from the underlying ischemic, but viable tissue. 
As the disease progresses, pathognamonic signs of necrotizing fasciitis appear "…a dusky discoloration of skin appearing as small purplish patches with ill-defined borders. Concomitantly blisters or bullae of few millimeters in diameter appear on the skin of the involved area. The skin beneath blisters becomes necrotic and blue in color. Localized necrosis of skin is secondary to thrombosis of nutrient vessels as they pass through the zone of involved fascia." 
The cervical necrotizing fasciitis of odontogenic origin involves mandibular second and third molar frequently as the apices of these teeth extend below mylohyoid insertion. Infective process originating from these teeth easily traverse into the submandibular space. In our case, maxillary second molar was culprit which was consistent with findings of many authors. 
In necrotizing fasciitis of odontogenic origin disease takes the usual path of spread, which invades deep tissue planes in early stage. It is only when the infective process gets to superficial fascia, spread becomes rapid and typical features of necrotizing fasciitis begin to show. This mode of presentation can be misleading to unsuspecting clinician and makes the early diagnosis difficult. 
However, some findings may present clinically when one is suspicious of cervical necrotizing fasciitis:
- Odontogenic infection that spreads to neck and anterior chest.
- Abnormal accumulation of gas in the tissue.
- Very rapid progression of infection.
- Orange peel appearance of the involved skin which change to dusky discoloration as the disease progresses.
Owing to the edema of the overlying tissue or the absence of gas, subcutaneous crepitus may be absent,  which were also seen in our case.
The key to accurate and prompt diagnosis of necrotizing fasciitis versus a typical odontogenic infection lies in the clinician's ability to fully appreciate the patient's history, presenting condition and accurately progressing disease process.  If there is a high index of suspicion clinical diagnosis of necrotizing fasciitis can be made by prompting early surgical exploration to confirm the diagnosis and perform appropriate debridement. 
The cornerstone of treatment is surgical debridement. All necrotic tissue must be removed until healthy bleeding tissue is encountered. Reluctance to debride fascial soft tissues aggressively and avoid unsightly disfigurement often leads to under treatment of the disease early in its course. Multiple surgical debridements in the operating room are usually needed. 
After surgical debridement, wounds are left open and packed with povidine-moistuned gauze, which is changed frequently. It is important to prevent pooling of secretions in the wound that may provide a culture medium for further bacterial growth. Along with debridement, appropriate antibiotic coverage is imperative. 
Hyperbaric oxygen therapy has been gaining support as an adjunctive treatment for Necrotizing fasciitis. Recently, published reports cite a 50% reduction in mortality when hyperbaric oxygen therapy is used along with surgery to treat necrotizing fasciitis,  but its role in necrotizing fasciitis as mentioned by other authors needs further evaluation. 
Once the infection has been resolved, the defect can initially be covered with a split thickness skin graft and reconstructed secondarily by advancement flaps or revascularized free flaps if necessary. 
| Conclusion|| |
Early clinical diagnosis has to be made as there is a direct relationship between morbidity, mortality and time lapse before the start of appropriate treatment. Necrotizing fasciitis of head and neck is rare, but potentially fatal disease that all dentists should be aware of as prompt diagnosis and recognition are the first and most important steps in its management. A delay in diagnosis would result in further disastrous morbidity and mortality.
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[Figure 1], [Figure 2], [Figure 3]