Received Date : 24-Oct-2016

Accepted Article Revised Date : 16-Jan-2017

Accepted Date : 22-Feb-2017

Article type : Scientific Article

Necrotising fasciitis as a complication of odontogenic infection: a review of management and case

series

K Bayetto1, A Cheng2, P Sambrook3

1
Oral and Maxillofacial Surgery Unit, Royal Adelaide Hospital, Adelaide, Australia
2
Oral and Maxillofacial Surgery Unit, Royal Adelaide Hospital, Adelaide, Australia
3
Director, Oral and Maxillofacial Surgery Unit, Royal Adelaide Hospital, Adelaide, Australia

Objective: To establish the incidence of head and neck necrotising fasciitis (NF) in the Adelaide Oral
and Maxillofacial Surgery Unit. To review the current literature regarding the management of head
and neck NF. To determine the evidence for the role of hyperbaric oxygen therapy in the
management of NF.

Method: A retrospective audit of all patients admitted to the Royal Adelaide Hospital Oral and
Maxillofacial Surgery Unit 2006-2015 with severe odontogenic infections was carried out. Patient
demographics were recorded and treatment details were collected and analysed.

Results: A total of 672 patients were admitted for management of severe odontogenic infections. Of
these, three were identified as NF. One case was treated using hyperbaric oxygen as an adjunct to
conventional surgical and medical management. Two cases were managed using aggressive surgical
management alone. Two patients survived. The incidence of head and neck NF in South Australia is
48 per 100,000 infections per year.

Conclusion: The first line treatment of severe odontogenic infections remains conventional surgical
and medical management, however hyperbaric oxygen therapy may have an additional role in the
management of NF and other rare severe infections in medically complex patients.

Keywords: cervicofacial, necrotising, fasciitis, odontogenic, infection

Corresponding author:
Andrew Cheng
Oral and Maxillofacial Surgery Unit, Adelaide Dental Hospital,
Frome Road, Adelaide
South Australia, 5000
8222 8223
andrew.cheng@sa.gov.au

This article has been accepted for publication and undergone full peer review but has not
been through the copyediting, typesetting, pagination and proofreading process, which may
lead to differences between this version and the Version of Record. Please cite this article as
doi: 10.1111/adj.12508
This article is protected by copyright. All rights reserved.
 Necrotising fasciitis as a complication of odontogenic infection: a review of management and case
series
Accepted Article
Objective: To establish the incidence of head and neck necrotising fasciitis (NF) in the Adelaide Oral
and Maxillofacial Surgery Unit. To review the current literature regarding the management of head
and neck NF. To determine the evidence for the role of hyperbaric oxygen therapy in the
management of NF.

Method: A retrospective audit of all patients admitted to the Royal Adelaide Hospital Oral and
Maxillofacial Surgery Unit 2006-2015 with severe odontogenic infections was carried out. Patient
demographics were recorded and treatment details were collected and analysed.

Results: A total of 672 patients were admitted for management of severe odontogenic infections. Of
these, three were identified as NF. One case was treated using hyperbaric oxygen as an adjunct to
conventional surgical and medical management. Two cases were managed using aggressive surgical
management alone. Two patients survived. The incidence of head and neck NF in South Australia is
48 per 100,000 infections per year.

Conclusion: The first line treatment of severe odontogenic infections remains conventional surgical
and medical management, however hyperbaric oxygen therapy may have an additional role in the
management of NF and other rare severe infections in medically complex patients.

Keywords: cervicofacial, necrotising, fasciitis, odontogenic, infection

Introduction
Necrotising fasciitis (NF) is an acute, rapidly progressive infection of the fascia and subcutaneous
tissues that is well recognised in various parts of the body, but is less common in the head and neck
region.(1, 2) Necrotising fasciitis of the head and neck is most commonly referred to as cervicofacial
necrotising fasciitis (CNF), and can be subdivided into craniofacial NF, occurring above the lower
border of the mandible, and cervical NF occurring below.(2, 3)

The most common cause of CNF is odontogenic infection, particularly in those patients with chronic
disease or those who are immunosuppressed.(1) (1, 2, 4-10) Other causes include oropharyngeal
infection such as tonsillitis and peritonsillar abscess, insect bites, trauma and post-operative
infection.(2, 4)

The incidence of CNF has not been readily reported in the literature and the diagnosis of CNF is often
delayed due to signs and symptoms readily attributable to other soft tissue infections. It is primarily
a clinical diagnosis and is often first suspected in patients who do not respond to conventional
therapy for odontogenic infection. The diagnosis of CNF requires both clinical signs and symptoms
and histopathological findings. Common early signs of CNF include marked cutaneous erythema,
warmth, oedema, pain disproportionate to clinical signs and hyperaesthesia. (1, 2, 4, 5, 9) As CNF
progresses patients may develop tissue crepitus, bullae and skin necrosis with purple-black
discolouration secondary to vessel thrombosis. (1, 2, 4, 5, 9)

CNF is most commonly a polymicrobial infection(1) and its management requires aggressive surgical
debridement as well as adjunctive medical and supportive therapy. The initiation of early empiric
antibiotic therapy is essential and this can then be modified according to culture and sensitivity
results.(7, 11) Hyperbaric oxygen therapy (HBO) has been widely recommended in the literature as an
adjunct in the management of CNF, although there have been no randomised controlled trials to
assess the efficacy of HBO in the management of CNF.

This article is protected by copyright. All rights reserved.

 The aim of this to establish the incidence of head and neck NF in the Adelaide Oral and Maxillofacial
Accepted Article Surgery Unit and to review the current literature regarding the management of head and neck NF
including the role of hyperbaric oxygen therapy.

Methods

A retrospective audit of all patients admitted to the Royal Adelaide Hospital Oral and Maxillofacial
Surgery Unit 2006-2015 with severe odontogenic infections was carried out via retrieval of electronic
records and analysis of a separate odontogenic infection database within the Oral and Maxillofacial
Surgery Unit. Patients diagnosed as having CNF were included in this study. A diagnosis of CNF was
made with a combination of (1) clinical signs and symptoms (2) white cell count (3) serum C-reactive
protein levels (4) intra-operative assessment (5) histopathological specimen results. Information
recorded for these patients included age, gender, presenting symptoms, aetiology, associated
comorbidities, medical and surgical management and complications.

Results

A total of 672 patients were admitted to the Royal Adelaide Hospital for odontogenic infection over
the nine year period from January 2006 to January 2015. Of these patients, three were identified as
being complicated by CNF. This gives the South Australian OMS unit an incidence of odontogenic-
related CNF of 48 per 100,000 odontogenic infections per year.

Case 1

A 78 year old Laotian man with a history of type two diabetes mellitus, hypertension, osteoarthritis,
hypercholesterolaemia, pulmonary fibrosis and a previous right cerebellar stroke was transferred to
our institution from a peripheral hospital after a one week admission with a left side facial swelling
and systemic symptoms after extraction of his tooth 38. On presentation he was febrile and
hypertensive with a white cell count of 17.4 and C-reactive protein of 270. He had a left fluctuant
temporal, parapharyngeal, palatal and buccal space swelling, see Figure 1. A CT showed a left
parapharyngeal and tonsillar abscess measuring 53 x 38 x 65mm with extensive gas noted within the
tissues, see Figures 2 and 3. These radiological findings demonstrate multiple gas collections within
anatomical structures which is different from a usual pattern of invasive streptococcus anginosus
infection. The patient underwent surgical drainage and debridement in theatre with 150ml of pus
drained from the superficial temporal space. He was post-operatively managed in ICU for septic
shock and showed no systemic or local clinical improvement over a number of days. A repeat CT
revealed a recollection of infection and extensive gas within the soft tissues. He was taken to theatre
for two further extensive soft tissue debridements including debridement of the necrotic left
temporalis muscle. Blood cultures showed Streptococcus bacteraemia. Wound swab cultures
showed multiple multi-resistant bacteria including Serratia sp, Citerobacter koseri, Klebsiella oxytoca
and Enterococcus faecalis. On day 23 of admission he was deemed suitable for hyperbaric oxygen
therapy and underwent seven days of treatment. He subsequently clinically improved and was
discharged 39 days after admission.

This article is protected by copyright. All rights reserved.

 Case 2
Accepted Article A 64 year old Caucasian male with a history of type two diabetes mellitus, ischaemic heart disease
and diverticulitis was transferred to our institution via the Royal Flying Doctors Service from rural
New South Wales with a 1 day history of Ludwig’s angina. On presentation he was febrile with
trismus and stridor and marked erythema extending from the mandibular border to the sternum. He
was systemically unwell with marked tachycardia and confusion. He was initially admitted under the
Ear Nose and Throat team who proceeded to a fibre optic intubation and an emergency
tracheostomy. Twenty four hours later Oral and Maxillofacial surgery were asked to review the
patient and he was found to have an ongoing Ludwig’s angina, pus discharge from the tracheostomy
site, a grossly carious dentition and extensive gas within the tissues on CT, see figure 4. He was taken
to theatre for an incision and drainage and multiple tooth extractions. Wound swab cultures showed
multi-resistant Klebsiella pneumoniae, Proteus mirabilis, Serratia species, Klebsiella oxytoca,
Stenotrophomonas maltophilia which were treated with intravenous antibiotics. A repeat CT post-
operatively showed a recollection within the right retropharyngeal and parapharyngeal spaces with
extensive gas formation. Post-operatively the upper thorax cellulitis rapidly spread and the patient
was taken back to theatre multiple times for extensive transcervical debridement of necrotic fascia
as well as partial resection of the sternocleidomastoid muscle. He continued to deteriorate on the
ward and died of spontaneous cardiac arrest.

Case 3

A medically well 32 year old female intravenous drug user presented to the emergency department
with a two week history of increasing facial swelling and a lower right side vestibular abscess. On
examination she was systemically unwell with peri-oral necrotising fasciitis and multi-organ
dysfunction. She was taken to theatre for a full dental clearance, drainage of the abscess and
debridement of necrotic tissue. Wound swabs and blood cultures both grew Staphylococcus aureus
and Candida tropicalis. She underwent testing for a variety of infectious diseases which were all
negative. Post-operative ICU support was given with little clinical improvement. She had progressive
loss of her upper lip and cheek due to spreading peri-oral necrotising fasciitis, as well as developing
intracranial complications. The patient survived and underwent extensive rehabilitation with
significant long-term impairments including partial blindness, hemiparesis and cognitive impairment.

Discussion

The Royal Adelaide Hospital contains the only Oral and Maxillofacial Surgery unit in South Australia.
It covers a population area of two million people and manages all odontogenic infections as a
centralised service. The hospital employs a standardised management protocol for all odontogenic
infections which includes a multi-disciplinary approach. All cases have input from Oral and
Maxillofacial Surgery, Ear Nose and Throat Surgery, Anaesthetics, Intensive Care and Infectious
Diseases physicians. The management protocol ensures that the majority of odontogenic infections
are definitively managed within four hours of arrival at hospital and all the post-operative care is
carried out in a single centre.

The incidence of CNF is not commonly described in the literature. Wong et al in 2000 reported an
incidence of 2.6% among hospitalised infections within the Oral and Maxillofacial Surgery unit in
Tainan, Taiwan.(8) The incidence of CNF in our population was 48 per 100,000 odontogenic infections
per year, which is significantly lower.

This article is protected by copyright. All rights reserved.

 CNF is more common in patients with chronic disease and immune suppression. Patients with
obesity, malnutrition, diabetes, immune suppression, renal failure, alcoholism, malignancy and
Accepted Article intravenous drug use are all at increased risk. (1, 2, 4, 5, 12, 13) All three of our patients with CNF had
underlying chronic disease which included diabetes mellitus, drug abuse and hepatitis B infection.

Early diagnosis of necrotising fasciitis is essential to allow early aggressive treatment to improve
patient outcomes.(2) Misdiagnosis is common as early signs and symptoms are equivocal and appear
similar to cellulitis and other soft tissue infections.(5, 13-16) As CNF progresses patients become
systemically unwell and display signs of shock.(5) Myonecrosis is a late sign thought to be due to
vessel thrombosis.(1, 11, 17, 18) Two of our three patients had myonecrosis present on surgical
exploration and required extensive debridement of necrotic muscle tissue. As yet there are no
accepted diagnostic criteria for cervicofacial necrotising fasciitis and the diagnosis is mainly clinical.
In the three cases identified in our own institution, the early signs and symptoms were typical of
odontogenic infection and they were initially treated as such. After further investigation and
management CNF was diagnosed. The diagnosis of CNF was ultimately made with a combination of
(1) clinical signs and symptoms (2) white cell count >11.0x109/L (3) C-reactive protein levels >8.0
mg/L (4) intra-operative identification of necrotic tissue and (5) histopathological specimen results,
see Table 2. Typically in our hospital the management of odontogenic infection does not include the
histopathological analysis of tissue specimens, but in the three cases of CNF soft tissue specimens
were sent for histopathological analysis based on the intra-operative findings of extensive spreading
necrotic infection.

Assessment of patients with CT scanning may assist in the diagnosis of CNF. Abnormal gas collections
within the cervical tissues on CT scan is consistent with CNF infection and is seen in 54.5-64% of
cases.(8, 16) Other CT findings consistent with CNF include thickening of the subcutaneous fat, diffuse
enhancement of the cervical fascia, enhancement and thickening of musculature and fluid collection
within neck compartments.(16) All three patients with CNF seen at our institution demonstrated
extensive gas collections on CT as well as muscle thickening and enhancement.

The microbiology of CNF infections is variable, with the majority being polymicrobial.(1, 2, 7, 8, 11, 12, 18, 19)
Both aerobic and anaerobic bacteria are commonly found. In the three patients we managed with
CNF, all had polymicrobial infection with multi-resistant organisms, as shown in table 1. An
interesting feature of the isolated organisms is that they are mostly non-standard oral bacteria. We
found that there was broad resistance to amoxycillin within the isolated organisms. This is a
significant issue in the management of CNF, especially as the emergence of multi-resistant
organisms is increasing worldwide and particularly in the Asia-Pacific region. This emphasises the
importance of wound swabs being used for microbiological culture and sensitivity to determine the
specific bacterial resistance patterns.

The management of cervical necrotising fasciitis involves early aggressive surgical debridement and
patients commonly require repeated surgical debridement of necrotic tissue.(1, 2, 4, 7, 8, 11, 15, 17, 19) In a
case series of 10 patients by Mohammedi in 1999, patients required a mean of five surgical
explorations.(1) A retrospective study of 38 patients found that the early intervention in CNF
improved prognosis, which is supported by other studies.(5, 13) Early broad-spectrum empiric
antibiotic therapy is essential, with modification of antibiotic treatment once microbial culture and
sensitivity results become available.(2, 7, 13) Antibiotic therapy may not be effective due to vascular
thrombosis which is common in NF and may inhibit the delivery of antibiotics to the site of
infection.(1) Airway management is essential and tracheostomy should be considered for definitive
airway management.(9)

This article is protected by copyright. All rights reserved.

 The use of hyperbaric oxygen therapy (HBO) in managing CNF has been suggested by multiple
authors as being a useful adjunct.(2, 5-7, 12, 14, 17, 18) Multiple retrospective studies in the literature have
Accepted Article small cohorts and small or no control groups. These studies have varying results including both
increased and decreased numbers of surgical debridements compared to patients not receiving HBO
therapy.(12, 20) Some studies have suggested an overall mortality benefit in patients receiving
adjunctive HBO therapy in the management of CNF, whilst others have found no mortality benefit.(12,
21)
There are no prospective randomized controlled trials on the efficacy of hyperbaric oxygen in the
management of CNF due in part to the rarity of the condition. HBO is said to augment the immune
response to infection, accelerate wound healing as well as being directly bactericidal to anaerobic
bacteria.(12) In our own institution HBO is available and can be used for both ward patients and
intensive care patients who are intubated and ventilated. In the initial period of treatment of CNF
our patients are generally managed in the intensive care unit and remain intubated and ventilated
for airway protection. The movement of these patients for HBO therapy requires careful planning
and transfer to a separate part of a large hospital. The transfer of an intubated patient is costly in
both time and medical personnel and carries multiple risks including dislodgement of the
endotracheal tube and destabilisation of an acutely unwell patient. Given that there is no scientific
evidence to suggest that HBO is a highly effective adjunct in the management of CNF we did not
employ HBO in the early stages of management of this condition, preferring to focus on multiple
surgical debridements and supportive medical therapy including intravenous antibiotics. In one case
we did use HBO in the management of CNF once the patient was medically stabilised, extubated and
being cared for on a general surgical ward.

Conclusion

CNF is a rapidly spreading, aggressive infection that requires early diagnosis and management to
improve patient outcomes. The first line treatment of CNF is aggressive surgical debridement,
empirical intravenous antibiotics and supportive therapies. Hyperbaric oxygen therapy whilst
theoretically may be of benefit as an adjunctive treatment has not been demonstrated in trials to be
efficacious in the management of head and neck CNF. We recommend conventional surgical and
medical supportive therapies with use of hyperbaric oxygen therapy in stable ward patients where
practicable.

References

1. Mohammedi I, Ceruse P, Duperret S, Vedrinne J, Bouletreau P. Cervical necrotizing fasciitis:

10 years' experience at a single institution. Intensive Care Med. 1999 Aug;25(8):829-34.

2. Oguz H, Yilmaz MS. Diagnosis and management of necrotizing fasciitis of the head and neck.
Curr Infect Dis Rep. 2012 Apr;14(2):161-5. DOI: 10.1007/s11908-012-0240-1.

3. Lanisnik B, Cizmarevic B. Necrotizing fasciitis of the head and neck: 34 cases of a single
institution experience. Eur Arch Otorhinolaryngol. 2010 Mar;267(3):415-21. DOI:
10.1007/s00405-009-1007-7.

4. Panda NK, Simhadri S, Sridhara SR. Cervicofacial necrotizing fasciitis: can we expect a
favourable outcome? J Laryngol Otol. 2004 Oct;118(10):771-7. DOI:
10.1258/0022215042450698.

This article is protected by copyright. All rights reserved.

 5. Thakur JS, Verma N, Thakur A, Sharma DR, Mohindroo NK. Necrotizing cervical fasciitis:
Prognosis based on a new grading system. Ear Nose Throat J. 2013 Mar;92(3):149-52.
Accepted Article
6. Mathieu D, Neviere R, Teillon C, Chagnon JL, Lebleu N, Wattel F. Cervical necrotizing fasciitis:
clinical manifestations and management. Clin Infect Dis. 1995 Jul;21(1):51-6.

7. Flanagan CE, Daramola OO, Maisel RH, Adkinson C, Odland RM. Surgical debridement and
adjunctive hyperbaric oxygen in cervical necrotizing fasciitis. Otolaryngol Head Neck Surg.
2009 May;140(5):730-4. DOI: 10.1016/j.otohns.2009.01.014.

8. Tung-Yiu W, Jehn-Shyun H, Ching-Hung C, Hung-An C. Cervical necrotizing fasciitis of

odontogenic origin: a report of 11 cases. J Oral Maxillofac Surg. 2000 Dec;58(12):1347-52;
discussion 53. DOI: 10.1053/joms.2000.18259.

9. Bakshi J, Virk RS, Jain A, Verma M. Cervical necrotizing fasciitis: Our experience with 11 cases
and our technique for surgical debridement. Ear Nose Throat J. 2010 Feb;89(2):84-6.

10. Shaikh N, Ummunissa F, Hanssen Y, Al Makki H, Shokr HM. Hospital epidemiology of

emergent cervical necrotizing fasciitis. J Emerg Trauma Shock. 2010 Apr;3(2):123-5. DOI:
10.4103/0974-2700.62108.

11. Umeda M, Minamikawa T, Komatsubara H, Shibuya Y, Yokoo S, Komori T. Necrotizing fasciitis

caused by dental infection: a retrospective analysis of 9 cases and a review of the literature.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003 Mar;95(3):283-90. DOI:
10.1067/moe.2003.85.

12. Krenk L, Nielsen HU, Christensen ME. Necrotizing fasciitis in the head and neck region: an
analysis of standard treatment effectiveness. Eur Arch Otorhinolaryngol. 2007
Aug;264(8):917-22. DOI: 10.1007/s00405-007-0275-3.

13. Malik V, Gadepalli C, Agrawal S, Inkster C, Lobo C. An algorithm for early diagnosis of
cervicofacial necrotising fasciitis. Eur Arch Otorhinolaryngol. 2010 Aug;267(8):1169-77. DOI:
10.1007/s00405-010-1248-5.

14. Whitesides L, Cotto-Cumba C, Myers RA. Cervical necrotizing fasciitis of odontogenic origin:
a case report and review of 12 cases. J Oral Maxillofac Surg. 2000 Feb;58(2):144-51;
discussion 52.

15. Lin C, Yeh FL, Lin JT, Ma H, Hwang CH, Shen BH, et al. Necrotizing fasciitis of the head and
neck: an analysis of 47 cases. Plast Reconstr Surg. 2001 Jun;107(7):1684-93.

16. Becker M, Zbaren P, Hermans R, Becker CD, Marchal F, Kurt AM, et al. Necrotizing fasciitis of
the head and neck: role of CT in diagnosis and management. Radiology. 1997
Feb;202(2):471-6. DOI: 10.1148/radiology.202.2.9015076.

17. Wolf H, Rusan M, Lambertsen K, Ovesen T. Necrotizing fasciitis of the head and neck. Head
Neck. 2010 Dec;32(12):1592-6. DOI: 10.1002/hed.21367.

This article is protected by copyright. All rights reserved.

 18. Bahu SJ, Shibuya TY, Meleca RJ, Mathog RH, Yoo GH, Stachler RJ, et al. Craniocervical
necrotizing fasciitis: an 11-year experience. Otolaryngol Head Neck Surg. 2001
Accepted Article Sep;125(3):245-52. DOI: 10.1067/mhn.2001.118182.

19. Lee JW, Immerman SB, Morris LG. Techniques for early diagnosis and management of
cervicofacial necrotising fasciitis. J Laryngol Otol. 2010 Jul;124(7):759-64. DOI:
10.1017/S0022215110000514.

20. Riseman JA, Zamboni WA, Curtis A, Graham DR, Konrad HR, Ross DS. Hyperbaric oxygen
therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery.
1990 Nov;108(5):847-50.

21. Shupak A, Shoshani O, Goldenberg I, Barzilai A, Moskuna R, Bursztein S. Necrotizing fasciitis:

an indication for hyperbaric oxygenation therapy? Surgery. 1995 Nov;118(5):873-8.

Table 1. Multi-resistant organisms in three patients with CNF

Organisms isolated from wound: Resistance patterns:

Patient 1 Klebsiella pneumoniae Amoxycillin,

Proteus mirabilis Amoxycillin, Amoxycillin/ Clavulanic acid,
Cephalexin, Cephazolin,
Serratia species Amoxycillin, Amoxycillin/ Clavulanic acid,
Cephalexin, Cephazolin, Ceftriaxone
Klebsiella oxytoca Amoxycillin, Cpehalexin, Cephazolin
Stenotrophomonas maltophilia Amoxycillin, Amoxycillin/ Clavulanic acid,
Cephalexin, Cephazolin, Gentamicin

Patient 2 Staphylococcus aureus Amoxycillin

Patient 3 Klebsiella oxytoca Amoxycillin

Citrobacter koseri Amoxycillin
Serratia species Amoxycillin, Amoxycillin/ Clavulanic acid,
Cephazolin, Ceftriaxone

This article is protected by copyright. All rights reserved.

 Table 2 Histopathology Results
Accepted Article Histopathology of the three cases examined
Necrosis
Gram positive cocci on gram stain
Active inflammatory infiltrate within tissue
Abscess formation
Figure 1. Temporal spread of infection
This article is protected by copyright. All rights reserved.
Accepted histopathological appearance of CNF2
Necrosis of superficial fascia
Presence of microorganisms within destroyed
fascia and dermis with Gram stain
PMN infiltrate of deep dermis and fascia
Fibrinous thrombi of arteries and veins passing
through fascia
Angiitis and fibrinoid necrosis of arterial and
venous walls
Absence of muscle involvement
 Figures 2 and 3. Demonstrates tonsillar and parapharyngeal spread of infection, gas within the
tissues indicative of necrotising fasciitis
Accepted Article

This article is protected by copyright. All rights reserved.

 Figure 4 Demonstrates extensive spread of infection and gas within the tissues indicative of
necrotising fasciitis in Patient 2
Accepted Article

This article is protected by copyright. All rights reserved.