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J Oral Maxillofac Surg70:340-344, 2012

Cervicofacial Necrotizing Fasciitis andSteroids: Case Report and

Literature ReviewMatthew Murray, DDS, MD,* Jeffrey Dean, DDS, MD,† and

Richard Finn, DDS‡

Necrotizing fasciitis (NF) is a devastating disease thattypically affects immunocompromised patients butcan also affect healthy patients. The disease can becaused by a monomicrobial or polymicrobial infec-tion and spreads rapidly. Monomicrobial infectionsare usually due to group A streptococcus and areuncommon.

NF can rapidly produce septic shock and requiresimmediate surgical management of the necrotic tis-sue.1 Patients taking corticosteroids can have im-paired immune function, which can increase the riskof infection. We report the case of a 33-year-oldwoman who was taking intravenous corticosteroidsfor traumatic neuritis caused by a motor vehicle col-lision.

She developed NF and required intensive medicaland surgical treatment.

Case Report

A 33-year-old woman was admitted to our hospital aftersustaining multisystem trauma with multiple facial frac-tures, including left optic neuropathy, in a motor vehiclecollision. She did not have any medical comorbidities. Theophthalmology team was consulted for the optic neuropa-thy, and intravenous injections of methylprednisolone 1

*Chief Resident, Department of Oral and Maxillofacial Surgery,

Loma Linda University Medical Center, Loma Linda, CA.

†Assistant Professor, Associate Program Director, Associate Di-

rector for the Advanced Education in OMFS, Department of Oral

and Maxillofacial Surgery, Loma Linda University Medical Center,

Loma Linda, CA.

‡Chief, Department of Oral and Maxillofacial Surgery, Veterans

Administration North Texas Health Care System, Dallas, TX; Profes-

sor, Department of Surgery, Division of Oral and Maxillofacial

Surgery and Department of Cell Biology, The University of Texas

Southwestern Medical Center, Dallas, TX.

Address correspondence and reprint requests to Dr Dean: De-

partment of Oral and Maxillofacial Surgery, Loma Linda University,

11092 Anderson St, Room 3306, Loma Linda, CA 92354; e-mail:

jsdeanddsmd@gmail.com

© 2012 American Association of Oral and Maxillofacial Surgeons

278-2391/12/7002-0$36.00/0

oi:10.1016/j.joms.2011.02.021

340

g/day were begun. Her midface fractures were repaired inthe operating room. The patient had an uneventful postop-erative course until postoperative day 6 when she startedspiking high temperatures and developed electrolyte abnor-malities, including low serum sodium and increasing leuko-cytosis with a left shift. The patient had already been givenantibiotics postoperatively.

On morning rounds, the patient was found to have asmall area of discoloration on her left malar eminence. Thepurplish tissue did not blanch to palpation. She reportedthat the area felt cool and numb to the touch. Within 6hours, the discoloration had progressed over her left face,including the periorbit, and the tissue had become necrotic(Figs 1-3). Initially, she had refused treatment when we firstnoted the discoloration and was insistent on leaving italone. Broad-spectrum antibiotics were started, and consul-tation with her family convinced her of the seriousness ofher situation. She was taken emergently to the operatingroom for debridement 6 hours after we first noted thediscoloration. Tracheostomy secured her airway, and ag-gressive surgical debridement was begun on the patient’sleft face. Very aggressive debridement continued until via-ble bleeding tissue was encountered (Figs 4-6).

FIGURE 1. Frontal view 6 hours after onset of symptoms showingextensive necrosis on left face and periorbital region.

Murray, Dean, and Finn. Cervicofacial Necrotizing Fasciitis.

J Oral Maxillofac Surg 2012.

MJ

MURRAY, DEAN, AND FINN 341

The surgery was terminated when all nonviable tissuehad been removed (Fig 7). The debridement was extensive.The patient was brought back to the intensive care unit,where her condition quickly deteriorated. Within 24 hours,she had died of progression of the NF and refractory septicshock.

FIGURE 2. Right profile view of patient.

urray, Dean, and Finn. Cervicofacial Necrotizing Fasciitis.Oral Maxillofac Surg 2012.

FIGURE 3. Left profile view of patient with extensive necrosisextending posterior to include ear.

Murray, Dean, and Finn. Cervicofacial Necrotizing Fasciitis.

J Oral Maxillofac Surg 2012.

Discussion

NF is a rapidly spreading, progressive, inflammatoryinfection located in the deep fascia, with secondarynecrosis of the subcutaneous tissues. Characteristi-

FIGURE 4. Necrosis extending deep into temporal/parietal lay-ers, including temporalis muscle.

Murray, Dean, and Finn. Cervicofacial Necrotizing Fasciitis.J Oral Maxillofac Surg 2012.

FIGURE 5. Frontal view of patient after extensive initial debride-ment to bleeding tissue. Deeper tissue still involved.

Murray, Dean, and Finn. Cervicofacial Necrotizing Fasciitis.

J Oral Maxillofac Surg 2012.

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342 CERVICOFACIAL NECROTIZING FASCIITIS

cally, fulminant destruction of tissue is present, withsystemic signs of toxicity and a high mortality rate.The blood vessels become thrombosed, and, ulti-mately, tissue death occurs.

Subcutaneous air is classically described in NF. Ne-crotizing soft tissue infections are typically not asso-ciated with abscesses, although they can originatefrom an untreated or inadequately drained abscess.This can be seen in radiographs or not at all.

NF moves along the deep fascial planes.2 The clin-ical conditions associated with necrotizing infectioninclude drug use, diabetes mellitus, obesity, alcohol-ism, and immunosuppression. Type I NF is a mixedinfection caused by anaerobic and aerobic bacteriaand occurs most commonly after surgical proceduresin patients with comorbidities such as diabetes, com-promised immune function, and peripheral vasculardisease. Common isolates in this group include Staph-ylococcus aureus, streptococci, enterococci, Esche-ichia coli, Peptostreptococcus species, Prevotelland Porphyromonas species, the Bacteroides fragilisroup, and Clostridium species. Type II NF is usuallymonomicrobial infection caused by group A strep-

ococcus that can affect healthy patients. Methicillin-esistant S. aureus has been described with this typef infection. Overall, there are an estimated 3.5 caseser 100,000 persons, with a case-fatality rate of 24%

FIGURE 6. Lateral view of patient after extensive initial debride-ment to bleeding tissue. Deeper tissues still involved.

Murray, Dean, and Finn. Cervicofacial Necrotizing Fasciitis.J Oral Maxillofac Surg 2012.

or NF of all regions.3

Cervical NF can occur from a breach of the integ-rity of the mucous membranes after surgery, trauma,instrumentation, or odontogenic infection.

Odontogenic infection is the greatest cause of NF.A study from France reviewed 45 patients with cervi-cal NF.4 Most (78%) were of dental origin; the remain-ing cases were of pharyngeal origin or had occurredafter surgery or trauma.4 This was confirmed by areport of 11 cases by Wong et al5 and a report of 12ases by Whitesides et al,6 in which all cases were

odontogenic in origin; 2 had concomitant use of cor-ticosteriods. The NF spread to the face in 22%, lowerneck in 56%, and mediastinum in 40%. Spread to themediastinum can be particularly devastating becausethe debridement results in high morbidity and mor-tality. These infections are generally from mixed aer-obic and anaerobic bacteria A type I infection. How-ever, gas can also cause NF or a peritonsillar abscess,which can extend into the deep structures of theneck.

Corticosteriods or glucocorticoids are powerfulagents given to blunt the body’s response to stress orreduce the inflammatory response. They have othereffects on the body’s metabolism and development.Corticosteroids downregulate the body’s anti-inflam-matory proteins and impair margination of whiteblood cells. Blood glucose levels also increase be-cause of gluconeogenesis and by inhibiting glucoseuptake by muscle and adipose tissue. The increasedblood glucose levels serve as fuel for the metabolism

FIGURE 7. Final view after complete debridement to viable tissuewith orbital exoneration.

Murray, Dean, and Finn. Cervicofacial Necrotizing Fasciitis.

J Oral Maxillofac Surg 2012.

MURRAY, DEAN, AND FINN 343

of harmful bacteria, and the impaired immune re-sponse allows for the quick proliferation of infectiousagents.

Many reports have been published of patients withNF who had been taking steroids. NF has been asso-ciated in many patients with systemic lupus erythem-atosus. In a retrospective review, 8 cases of NF wereseen in the lupus population, all of whom were takingsystemic corticosteroids.7 Corticosteroid therapy, es-pecially in doses greater than prednisone 20 mg/dayor its equivalent, has been associated with an in-creased susceptibility to infection.8,9 However, theincreased risk of infection has been documented inpatients with systemic lupus erythematosus beforethe corticosteroid era. It is unclear whether oral,intravenous, or injectable corticosteroids have thegreatest risk of developing an infection. A 55-year-oldwoman with no comorbidities or lifestyle risk factorspresented with swelling of the right hand 5 days aftera triamcinolone and lignocaine injection of the middlefinger.10

Another 41-year-old woman developed NF 2 days af-ter a shoulder injection with 40 mg of depomedrone.11

Other studies have reported oral, intravenous, or inject-able use of steroids, without a predilection for 1 route.Transplant patients are also immunosuppressed and areoften taking steroids. One such patient presented withNF 9 years after kidney transplantation.12 NF can occurat any age, as shown by a 14-month-old infant who hadidiopathic nephritic syndrome and developed NF whilereceiving prednisolone.13 Trauma and steroid use, lead-ing to NF, has been previously reported. A 68-year-oldman who was taking steroids fell on his right elbow anddeveloped a necrotizing infection 3 days later.14

Many clinical features should raise the suspicion ofNF. The infection typically begins with an area oferythema that quickly spreads within the courseof hours to days. The redness spreads rapidly, and themargins of infection can move out into normal skinwithout being raised or sharply demarcated. As thedisease progresses, the skin will turn dusky or pur-plish at the infection site. Multiple identical patchescan develop to produce a large area of gangrenousskin as the infection spreads. The most importantsigns are tissue necrosis, bullae, putrid discharge, se-vere pain, gas production, rapid spread through thefascial planes, and the absence of the classic tissueinflammatory signs. A positive “finger test” result ischaracterized by a lack of resistance to finger dissec-tion in normally adherent tissues. Systemic findingscan include, fever, tachycardia, and hypotension.

Laboratory values can also aid in the diagnosis ofNF. Useful laboratory tests and findings include com-plete blood count, with the differential showing a leftshift; an electrolyte panel with low serum sodium,

elevated glucose, elevated blood urea nitrogen, ele-

vated creatine, elevated lactate; elevated coagulationprofile, blood and tissue cultures (deep tissue sam-ples); elevated creatine phosphokinase; urinalysis;and arterial blood gas. A risk score, the LaboratoryRisk Indicator for Necrotizing Fasciitis, was retrospec-tively designed and validated in a separate cohortstudy in which 6 laboratory parameters were used.15

Points are assigned according to the different labora-tory values: serum C-reactive protein greater than 150mg/L (4 points), white blood count of 15 to 25 (1point), white blood count greater than 25 (2 points),hemoglobin 11 to 13.5 g/dL (1 point), hemoglobinless than 11 g/dL (2 points), serum creatine greaterthan 1.6 mg/dL (2 points), and serum glucose greaterthan 180 g/dL (1 point). A score of 5 or less indicatesa probability of less than 50% for NF. A total score ofgreater than 6 should raise the suspicion of NF; 75% to80% of the cases of NF had a score of 8 or more.

Imaging studies such as soft tissue radiography,computed tomography, and magnetic resonance im-aging are most useful when gas is present. Gas is ahighly specific finding but not very sensitive. Often,imaging studies show only soft tissue swelling, whichcan be seen in patients with trauma or who have justundergone surgery. The imaging findings should notdelay surgery if the suspicion of NF is high. Treatmentof NF includes aggressive debridement, antibiotics,and intensive care treatment. Broad-spectrum antibi-otics should be instituted early and adjusted by sub-sequent Gram stain, speciation, and sensitivities. De-bridement should be performed daily to ensure thatall necrotic tissue is removed and only viable tissueremains. Multiple deep tissue biopsy specimensshould be taken at the initial debridement site andshould be followed up closely. Early debridement isessential. McHenry et al16 found that the averageinterval from admission to surgery was 90 hours fornonsurvivors versus 25 hours for survivors. Once thetissue remains healthy, the patient will no longerrequire operating room debridement. Patients willneed a team approach in the surgical intensive careunit, and guidelines such as the surviving sepsis cam-paign should be followed. Appropriate monitors, in-vasive lines, cultures, and laboratory tests should beinstituted early to stop sepsis.

Patients will require coverage for the large debride-ments and often require multiple skin grafting or flapprocedures for the large defects.17

Adjunctive hyperbaric oxygen (HBO) therapymight decrease the mortality and limit the extent ofdebridement in patients with NF and Fournier’s gan-grene, but the results have been conflicting. HBOtherapy has been used for wound healing because ofits ability to improve oxygen delivery to hypoxictissues. HBO therapy augments netrophil bactericidal

activity, forms oxygen free radicals, and limits clos-

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344 CERVICOFACIAL NECROTIZING FASCIITIS

tridial exotoxin and other bacterial pathogens. Oneobservational study of 26 patients with Fournier’sgangrene found a much lower mortality rate amongHBO-treated patients (7% vs 42%).18 Another observa-tional study of 29 patients with NF noted significantlyfewer debridements and a lower mortality rate (23%vs 66%) when HBO therapy was used.19 However, alarge study of 42 patients with Fournier’s gangrenesuggested increased mortality, morbidity, and cost oftherapy among patients treated with HBO therapy.20

When used to treat acute infections, HBO therapyshould be started early. One protocol used is 2 to 3daily 90-minute dives at 3 atm. These high pressuresmaintain the tissue oxygen tension at greater than 300mm Hg, sufficient to inhibit clostridial spore and exo-toxin production.21,22 The use of HBO therapy shouldbe weighed against the cost, with the national averagebeing $275/hour,4 and the repeated transportationrom the intensive care unit to the dive chamber,hich can be risky in itself. Also, not every facility has

ccess to an HBO therapy chamber and transport toutside facilities is too risky for a patient in need ofritical care.Intravenous immunoglobulin has been used for

reatment, particularly when a group A streptococcalnfection or clostridial toxins are present. The studiesave been controversial and difficult to compare,iven the small number of patients and differentethods used. A double-blind, placebo-controlled

rial compared intravenous immunoglobin and pla-ebo as an adjunctive therapy. The mortality rate was.6-fold greater in the placebo group, but statisticalignificance was not reached, possibly owing to themall sample size.23

In our case, antibiotics were administered early,and aggressive debridement was performed. Multipletissue biopsy specimens were sent, and the patientreceived intensive care treatment. However, becauseof the rapid spread of the disease, the patient quicklywent into septic shock, and her mental status changesprogressed rapidly. NF is an uncommon disease thatcan be extremely devastating. Expedient managementof the disease is necessary, because any delay canresult in significant morbidity and mortality. The inci-dence of NF could likely increase in the future owingto the greater number of patients with compromisedimmune function and the use of medications thatcould reduce the patients’ ability to fight infection.Steroids are commonly used preoperatively, intraop-eratively, and postoperatively and for many medicaldiseases, including certain traumatic events. Cautionin using steroids for post-traumatic events is advised.Awareness of the patients’ medical conditions and

monitoring of the patients’ medications could also

help in reducing the incidence of this most devastat-ing complication.

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