CLINICAL PRACTICE

CASE REPORT

Cervical necrotizing fasciitis originating

with a periapical infection
Trevor Treasure, DDS, MD; William Hughes, DDS; Jeffrey Bennett, DMD

ecrotizing fasciitis is a rapidly

spreading, soft-tissue infection
that involves the subcutaneous
tissues. It has a classic manifestation of necrosis of the subcutaneous fascia. In rare cases, it also may
cause necrosis of the underlying muscle
and overlying skin. The resulting pain is
severe and out of proportion to the clinical
findings.1 This infection produces morbidity and in some instances mortality.
Most cases of necrotizing fasciitis occur in
the extremities, abdomen and perineum.
Cervical necrotizing fasciitis (CNF) is a
rare complication from dental infection
that can lead to involvement of the neck,
mediastinum and chest wall.2 The
reported cases usually are in people who
are immunocompromised, but CNF also
can occur in healthy people. A delay in
seeking treatment for odontogenic infections is a common finding in people who
have CNF. Frequently, the practitioner
misdiagnoses the condition, which leads
to a delay in definitive treatment.2,3 CNF
is polymicrobial. The bacteria involved
are the same species as those that cause
chronic dental infections in the gingival
crevice or periapical infections of the jaw.
Sometimes CNF occurs as a result of minimal skin trauma or a simple tooth
extraction.4 The early stages of CNF may
resemble odontogenic cellulitis or an
abscess.2,3 Imaging studies, in particular
computed tomography (CT), may reveal
gas bubbles in the tissues of the neck,
which are an early sign of CNF.5
Once the practitioner suspects that
CNF is the diagnosis, surgical and medical therapy is warranted. Airway protec-

ABSTRACT
Background. Necrotizing fasciitis is a rapidly spreading, softtissue infection involving the subcutaneous tissues. Necrotizing
fasciitis originating from a dental-related source is rare. Practitioners should be aware that this infection could occur in patients
who are immunocompromised and in patients who are healthy.
Practitioners must treat this disease aggressively with surgical
debridement and intensive medical support.
Case Description. The authors present a case report of a man
with poorly controlled diabetes mellitus in whom a periapical infection progressed into a maxillofacial space abscess and finally cervical necrotizing fasciitis (CNF). A delay in his initial visit to a dentist was evident. The authors observed a successful outcome in the
patient after he underwent several wide surgical debridement procedures, hyperbaric oxygen therapy and a protracted, intensive hospital stay lasting 34 days.
Conclusions. Dentists should suspect that a patient has CNF
when maxillofacial cellulitis or an abscess does not respond to conventional therapy. Findings of spreading skin erythema, induration,
purple discoloration and anesthesia suggest necrotizing fasciitis.
Early computed tomography scans may reveal gas within the deep
tissues of the neck, fascial plane involvement or both.
Clinical Implications. CNF has high morbidity and mortality
rates if rapid aggressive therapy is not pursued. Spread of this
polymicrobial infection can lead to mediastinitis or cranial base
involvement. Mortality is directly proportional to the time to
intervention.
Key Words. Cervical necrotizing fasciitis; flesh-eating bacteria;
immunocompromised patient; diabetes; hyperbaric oxygen therapy.
JADA 2010;141(7):861-866.

Dr. Treasure is a clinical assistant professor, Department of Oral Surgery and Hospital Dentistry, School of Dentistry, Indiana University, 1050 Wishard Blvd., Room R4201, Indianapolis,
Ind. 46202, e-mail ttreasur@iupui.edu. Address reprint requests to Dr. Treasure.
Dr. Hughes is the chief resident, Department of Oral Surgery and Hospital Dentistry, School
of Dentistry, Indiana University, Indianapolis.
Dr. Bennett is a professor and the chairman, Department of Oral Surgery and Hospital
Dentistry, School of Dentistry, Indiana University, Indianapolis.

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CASE REPORT

Figure 1. Tooth no. 18 with a periapical radiolucency and

numerous other carious teeth.

tion and radical surgical debridement of necrotic

tissue are mandatory. A benefit of performing
surgery is that it gives the clinician the opportunity to diagnose CNF definitively by inspecting
the tissue and performing a biopsy. The surgeon
should make a transcervical neck incision to
create a wide exposure to the contents of the
patients neck and submandibular region.
Necrotic subcutaneous fascia will be evident
when the incision is made and the affected site is
opened up. The surgeon must make the incision
in advance of the line of necrosis to prevent subcutaneous spreading along facial planes. The surgeon may need to perform a tracheostomy to protect the patients airway owing to severe neck
swelling. Ventilator support is required in
patients with severe cases of CNF, owing to acute
respiratory failure. Practitioners frequently use
cardiovascular intensive measures such as intravenous (IV) fluids and medications to support the
patients blood pressure and heart rate.
Hyperbaric oxygen therapy (HBO) is an adjunctive treatment for CNF. Although it has not been
shown to be effective in randomized clinical trials,
it has shown a beneficial effect in some case series.6
Overwhelming sepsis, mediastinitis and multiple organ failures are common in patients with
CNF. Mortality rates range from 0 to 33 percent.2
If mediastinum involvement occurs, the mortality
rate is approximately 50 percent.2,3
In this article, we report a case of a man with
poorly controlled diabetes mellitus whose periapical abscess of tooth no. 18 became a maxillofacial space abscess and then, across several days,
CNF involving the submandibular, submental
and parapharyngeal spaces. The entire anterior
aspect of the neck and upper left chest wall eventually became involved in the necrotic process.
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Because of his worsening condition, a 54-year-old

obese man with a chief complaint of pain and
swelling on the left side of his mandible and neck
was transferred by a physician at another hospital
to the Indiana University Medical Center in June
2008. Seven days earlier, the patient had seen a
general dentist, who referred him to an oral surgeon for definitive treatment that was to include
making incisions and placing drains, as well as
extracting teeth. The patient delayed seeking treatment for one week until the swelling had increased
substantially and he went to the emergency department of the other hospital. The patients medical
history was significant for hypertension, but he did
not take medication for this condition. He had substantial trismus and could open his mouth to only
20 millimeters. The oral surgeon observed that the
patient was mentally obtunded and had difficulty
swallowing. The submandibular, submental and
lateral pharyngeal spaces were involved with the
initial odontogenic infection.
After the patient was admitted to the Indiana
University Medical Center, we obtained a
panoramic radiograph that revealed carious teeth
nos. 3, 4 and 16 through 20 and a periapical
abscess around the apexes of tooth no. 18 (Figure
1). We conducted laboratory tests, the results of
which showed that the patient had numerous
abnormal values (Table). We determined that the
patient had undiagnosed, uncontrolled diabetes
mellitus (blood glucose level = 340 milligrams per
deciliter, glycated hemoglobin = 11.5 percent) and
acute renal failure (serum creatinine level =
2.7 mg/dL). The acute renal failure was secondary
to dehydration. The patient was febrile (99.5F)
and malnourished (albumin level = 1.7 grams per
deciliter) and had an elevated white blood cell
(WBC) count (17.9 109 cells per liter). There also
was evidence of mild metabolic acidosis (serum
bicarbonate level = 18 milliequivalents per liter).
We consulted hospitalists to manage his blood glucose level and insulin dosing. After the patient
was rehydrated with IV fluids, his serum creatinine level was within normal limits and, thus, his
renal failure was treated.
ABBREVIATION KEY. CNF: Cervical necrotizing
fasciitis. CT: Computed tomography. H: Head. HBO:
Hyperbaric oxygen therapy. ICU: Intensive care unit.
IV: Intravenous. PEG: Percutaneous endoscopic
gastrostomy. WBC: White blood cell.

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C L I N I C A L P R A C T I C E CASE REPORT

TABLE

Patients abnormal laboratory test results and vital signs at admission.

TEST

VALUE

REFERENCE RANGE

White Blood Cell Count (  10 9 Cells per Liter)

17.9

4.5-11

Blood Glucose (Milligrams per Deciliter)

340

70-105

Blood Urea Nitrogen (mg/dL)

56

7-18

Serum Creatinine (mg/dL)

2.7

0.5-1.2

Serum Bicarbonate (Milliequivalents per Liter)

18

19-23

Serum Albumin (Grams per Deciliter)

1.7

3.5-5.0

Serum Chloride (mEq/L)

Glycated Hemoglobin (%)

94

98-106

11.5

4.0-5.9

99.5

98.6 0.8

Vital Signs
Temperature (F)
Respiratory rate (breaths per minute)

20

12-20

Pulse (beats per minute)

97

60-100 in adults

123/85

< 120/< 80 (normal), 139-120/80-89 (prehypertension),

> 140/> 90 (stage 1 hypertension)

Blood pressure (millimeters of mercury,

systolic/diastolic)

Initial CT scans revealed a contrast material

enhanced abscess in the left parapharyngeal
space and in the left submandibular space. There
was no evidence on the CT scan of gas or fascial
plane involvement of the neck.
The patient was taken emergently to the operating room, where we performed a fiber-optic
nasotracheal intubation owing to the patients
trismus and neck and oropharyngeal edema. We
made several submandibular incisions and placed
and secured drains into the maxillofacial spaces
to drain the deep neck infection. We also
extracted teeth nos. 3, 4 and 16 through 20. The
patient was admitted to the intensive care unit
(ICU) while still intubated and received ventilation. During the next several days, the patient did
not recover from his critical condition. Under
most circumstances, patients begin to recover
after these initial interventions. On hospital day
six, the patient again became febrile (100F) and
had an elevated WBC count (15.9 109 cells/L).
We performed an incision and drainage procedure
again, as well as a formal tracheostomy. Antibiotic therapy, which began with 900 mg of clindamycin 900 every eight hours, was changed to
4 g of piperacillin and 0.5 g of tazobactam every
six hours. Piperacillin was recommended by members of the infectious disease service to provide
coverage for both gram-positive aerobic and gramnegative aerobic and anaerobic bacteria. Contained within this combination antibiotic is
tazobactam, a potent inhibitor of groups 2 and 4
penicillinase. Members of the general surgery

service placed a percutaneous endoscopic gastrostomy (PEG) tube into the patient several days
later to feed him.
The results of cultures we obtained two days
postoperatively showed a polymicrobial infection.
The hospitals laboratory technicians isolated
-hemolytic streptococci, Eikenella species, Enterobacter species, Haemophilus species and Neisseria species.
By hospital day nine, we noted that the patient
was developing CNF. We noticed a fetid odor with
copious dishwaterlike purulent drainage coming
from the drains. The patients skin over the left
side of his neck had developed anesthesia, was
indurated and had a purple-brown discoloration
(Figure 2). New CT scans revealed gas below the
mandible, below the thyroid cartilage and within
the deep tissues of the neck, with fascial plane
involvement (Figure 3). During surgery, we made
a transcervical incision into this tissue that
revealed minimal bleeding. We observed a black,
necrotic fascia in the subcutaneous tissues
(Figure 4). We removed all of the platysma and
digastric muscles. We performed three more
serial debridement procedures of necrotic tissue
during the next several hospital days. We
debrided the entire anterior aspect of the neck
and upper left chest wall (Figure 5). We instituted
HBO therapy for 90 minutes at 2.4 atmospheres
with the patients breathing 100 percent oxygen.
He had 20 HBO treatments. We packed the
wounds with wet-to-dry gauze twice daily. The
patient was hospitalized for 34 days, after which
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Figure 2. The zone of the spreading erythema traveling down the

left neck onto the chest wall on hospital day six.

Figure 3. Sagittal computed tomography scanning revealing gas

within tissues below the angle of the mandible and deep within the
neck. H: Head.

Figure 4. Incision into the subcutaneous tissues revealing necrosis

of fascia and little bleeding on hospital day nine.

we discharged him to a physical rehabilitation

center.
During the patients hospital stay, we consulted 10 services, including ICU and critical care
for ventilator management, infectious disease for
intravenous antibiotic agent recommendations
and general surgery for placement of the PEG
tube. Otolaryngologists helped us debride the
patients chest wall, and the hospitalists managed
the patients diabetes mellitus and hypertension.
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Figure 5. The entire anterior aspect of the neck exposed to the

clavicle to debride fascia and necrotic muscle.

Members of the HBO therapy team, nutrition

service, wound team, social work service and diabetes education service helped us manage the
treatment of this patient.
The patient eventually recovered and was
treated successfully for his diabetes mellitus and
hypertension. At the four-month follow-up
appointment, the wounds were well healed and

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C L I N I C A L P R A C T I C E CASE REPORT

there was no evidence of residual infection or

tissue loss (Figure 6).
DISCUSSION

Confederate States of America Army surgeon

Joseph Jones, MD, wrote the first modern account
of necrotizing fasciitis in 1871.7 He described the
condition of hospital gangrene that occurred in
wounded Civil War soldiers. Wilson1 coined the
term necrotizing fasciitis in 1952 to describe the
condition of spreading necrosis in the fascia
layers below the skin. In severe cases, however,
the skin and muscles also can be necrotichence
the term flesh-eating bacteria. Malnutrition,
difficulty swallowing, trismus, obtundation and
dehydration frequently are observed in patients
with CNF. We observed all of these conditions in
the patient in our case at his first visit.
In patients with CNF, the overlying skin usually appears erythematous or dusky, indurated
and thickened and can be hypoesthetic or anesthetic.2,3,8 Making an incision into the affected
tissue produces virtually no bleeding. Drainage
appears dishwaterlike, and the blood vessels are
thrombosed. The fetid odor indicating necrotic
tissue is characteristic of established CNF. A case
series from Taiwan, across 10 years, suggests
that the incidence of CNF accounts for 2.6 percent
of all odontogenic infections.9
Early in its development, practitioners might
misdiagnose CNF as odontogenic cellulitis or an
abscess. Common to virtually all reported dental
cases of CNF is a patient who is immunocompromised and who delays seeking treatment for an
odontogenic infection, which occurred in the case
we report. Diabetes, renal disease, alcoholism,
smoking, underlying malignancy, human immunodeficiency virus and advancing age are risk factors for CNF.2,3,8 However, it also can occur in
someone who is immunocompetent. A pediatric
patient was reported to have developed CNF after
routine third molar extraction.4
CT scans that are obtained early give the clinician the best chance for recognizing CNF. Gas
bubbles will be seen in the neck around the fascial planes and possibly the carotid artery and
jugular vein. Air-fluid levels and fascial plane
blurring also can be seen on CT scans.5,10 The
patient in our case report had gas in the tissues
below the mandible, below the thyroid cartilage
and within the deep tissues of the neck, with fascial plane involvement.
A patient with CNF typically is febrile and has

Figure 6. The patient four months after surgery.

elevated WBC counts. The patient also might be

hypotensive and tachycardic. Rapid surgical
debridement is warranted to stop the necrosis
from spreading. The practitioner should make a
transcervical neck incision in the submandibular
region to open the fascial planes from the
mandible to the clavicle. Intensive medical
therapy includes administering IV fluids to the
patient and prescribing medications that increase
blood pressure to support the patients blood pressure and heart rate. A tracheostomy or endotracheal intubation with a ventilator may be necessary to manage a patients respiratory failure.
Although antibiotic agents are not a substitute
for radical surgical debridement, high-dose IV
broad-spectrum antibiotic agents initially should
be prescribed to help eradicate these mixed softtissue infections. The practitioner must prescribe
antibiotic agents before culture results are available or the results of antibiotic sensitivity assays
are returned. Once the latter are returned, the
patient should begin a directed antibiotic agent
regimen for the bacterial species involved. We recommend consulting with other specialists to help
manage the patients complex medical condition.
The prognosis may be grim in patients who do
not seek treatment in a timely manner. The
average mortality rate reported in several retrospective studies is between 20 and 30 percent.2,3,8,9,11 Most deaths occurred in patients who
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were immunocompromised. The spread of CNF

can occur down the neck away from the oral
cavity into the mediastinum, superiorly into the
cranial base or both. Both situations may be fatal.
The cause of death can be erosion of the carotid
artery and jugular vein, overwhelming sepsis and
multisystem organ failure.3,8,9,11
CONCLUSIONS

Rapid recognition and rapid intervention are the

keys to successful treatment of patients with
CNF. Mortality is directly proportional to the
time to intervention.12 Reconstruction with
muscle flaps or skin grafts may be necessary to
replace missing tissues after the initial infective
process is contained. After having CNF, patients
typically have to undergo a long rehabilitation
period before they can return to an active, functional lifestyle.
Disclosure. None of the authors reported any disclosures.
1. Wilson B. Necrotizing fasciitis. Am Surg 1952;18(4):416-431.
2. Quereshy FA, Baskin J, Barbu AM, Zechel MA. Report of a case of

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cervicothoracic necrotizing fasciitis along with a current review of

reported cases. J Oral Maxillofac Surg 2009;67(2):419-423.
3. Lin C, Yeh FL, Lin JT, et al. Necrotizing fasciitis of the head and
neck: an analysis of 47 cases. Plast Reconstr Surg 2001;107(7):
1684-1693.
4. Ricalde P, Engroff SL, Jansisyanont P, Ord RA. Paediatric necrotizing fasciitis complicating third molar extraction: report of a case. Int
J Oral Maxillofac Surg 2004;33(4):411-414.
5. Yamaoka M, Furusawa K, Uematsu T, Yasuda K. Early evaluation
of necrotizing fasciitis with use of CT. J Craniomaxillofac Surg 1994;
22(5):268-271.
6. Jallali N, Withey S, Butler PE. Hyperbaric oxygen as adjuvant
therapy in the management of necrotizing fasciitis. Am J Surg 2005;
189(4):462-466.
7. Jones J. Investigations upon the nature, causes and treatment of
hospital gangrene as it prevailed in the Confederate armies 1861-1865,
part II. In: Hamilton FH, ed. Surgical Memoirs of the War of the Rebellion. Vol. II. New York: Hurd and Houghton; 1871:143-570.
8. 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;58(2):144-151.
9. 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;58(12):1347-1352.
10. Becker M, Zbren P, Hermans R, et al. Necrotizing fasciitis of the
head and neck: role of CT in diagnosis and management. Radiology
1997;202(2):471-476.
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;95(3):283-290.
12. Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis:
current concepts and review of the literature. J Am Coll Surg 2009;
208(2):279-288.

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