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302 PART V ORAL AND MAXILLOFACIAL SURGERY
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B
A
A
Temporalis
Temporal
fascia
Zygomatic
arch
Masseter
Masseteric space
B
Figure 28-3. Typical sites of incision and drainage for various fascial space infections. A, Intraoral drainage of pterygoid compartment of masticator space (A) and lateral pharyngeal space (B). B, Masseteric, pterygoid, and temporal compart­ments of the masticator space. Incisions at B and C can be used to drain the submandibular space. C, Suggested locations for incision for extraoral drainage of temporal and lateral pharyngeal space infections. (From Goldberg MH, Topazian RG: Odontogenic infections and deep fascial space infections of dental origin. In Topazian RG, Goldberg MH, editors: Oral and maxillofacial infections, ed 3, Philadelphia, 1994, Saunders.)
C
Superficial
Deep
Temporal
pouch
Internal
pterygoid
CHAPTER 28 OROFACIAL INFECTIONS AND ANTIBIOTIC USE 303
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21. What imaging and laboratory studies are used for diagnosis of odontogenic
infections?
• Radiographsareusedtoidentifythecauseofinfection:periapical,occlusal,andpanoramic
views.
• Imagingstudiesareusedtoidentifytheextentofinfectionandpresenceofpurulentcollection.The
gold standard is computed tomography (CT) with contrast. In some instances, magnetic resonance imaging (MRI), soft tissue films, and ultrasound can be useful.
• Labstudiesareusedtoevaluatetheimmunesystem,whitecellanddifferentialcounts,andculture
and sensitivity from the infection site.
22. What are the principles of therapy for odontogenic infection?
The important components in treatment of odontogenic infection are:
• Determiningtheseverityofinfection  • Determiningwhethertheinfectionisatthecellulitisorabscessstage  • Evaluatingthestateofthepatient’shostdefensemechanisms
Odontogenic infection is treated surgically, pharmacologically, or by medical support of the patient,
including removing the source of infection; incision and drainage; and use of antibiotics, fluids, anal­gesics, and nutritional support.
23. How is the severity of odontogenic infection determined?
By analyzing the history, physical findings, and results of lab and imaging studies.
24. What are the different methods of drainage of odontogenic infections?
• Endodontictreatment  • Extractionoftheoffendingtooth  • Incisionanddrainageofsofttissuecollection
25. What are the surgical principles of incision and drainage?
• Beforeincision,obtainuidforculturethroughaspirationofpususingasyringeandneedle.  • Incisetheabscessinhealthyskinormucosaandinacosmeticallyorfunctionallyacceptableplace,
using blunt dissection and thorough exploration of the involved space.
• Useone-waydrainsinintraoralabscesses;usethrough-and-throughdrainageinextraoralcases.  • Removethedraingraduallyfromdeepsites.
26. What is the percentage of oral bacteria resistant to commonly used antibiotics for
treatment of odontogenic infection?
See Table 28-5.
27. What should be reevaluated during the follow-up appointment after treating a
patient for odontogenic infection?
• Responsetotreatment(subjectiveimprovementofpainandothersubjectivesymptoms)  • Toxicityreactionstoantibiotics  • Recurrenceofinfection  • Secondaryinfection(e.g.,Candida) • Presenceofallergicreactions
Table 28-5. Percentage of Oral Bacteria Resistant to Commonly Used Antibiotics
ORAL BACTEROIDES FUSOBACTERIA
Penicillin 15-30 6 4 0 Erythromycin 0 85 18 0 Clindamycin 4 0 2 0 Metronidazole 0 0 24 100 Cephalexin 10 0 6 18
Adapted from Peterson LJ: Microbiology of head and neck infections, Oral Maxillofac Surg Clin 3:255, 1991.
ANAEROBIC COCCI
ALPHA­STREPTOCOCCI
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28. What are the principles of antibiotic use?
When choosing a specific antibiotic as part of treatment of odontogenic infection, adhere to the follow-
ing principles:
• Usethecorrectandnarrow-spectrumantibiotic.  • Usetheleasttoxicdrugwiththefewestsideeffects.  • Usebactericidaldrugswheneverpossible.  • Beawareofdrugcost.  • Ensureeffectiveoraladministrationthroughtheuseofproperdoseandproperdosage
interval.
• Continuetheantibioticforanadequatelengthoftime.  • Administertheantibioticsthroughtheproperroute.
29. What are the most commonly used antibiotic formulations for oral and maxillofa-
cial infections?
See Table 28-6.
Table 28-6. Formulations for Antibiotics Commonly Used in
DRUG TYPES FORMULATIONS UNIT DOSE
Penicillin G
Potassium Generic, Pfizerpen VialforIM,IV 1-, 5-, and 20-million U Sodium generic VialforIM,IV 5-million U Repository Bicillin CR VialforIM 300-600,000 U/mL PenicillinV Generic, Betapen Tablets 250, 500 mg
Ampicillin Generic, Omnipen, Capsules 250, 500 mg
Amoxicillin Generic, Amoxil, Capsule 250, 500 mg
Amoxicillin- clavu-
lanate
Oxacillin Generic, Prostaphlin Capsules 250, 500 mg
Dicloxacillin Generic, Dynapen, Capsules 250, 500 mg
Cephalexin Generic,Keex Capsules/Pulvules 250, 500 mg
Cephradine Generic, Anspor, Capsules 250, 500 mg
Oral and Maxillofacial Infections
VK,PenVeeK,Veetids Oral solution 125, 250 mg/5 mL
Polycillin, Oral suspension 250 mg/5 mL Principen Pediatric drops 100 mg/mL
Vial 125, 250, 500, 1000,
2000 mg
Polymox, Trimox, Oral suspension 125, 250 mg/5 mL Wymox Pediatric drops 50 mg/mL Augmentin Tablets 250, 500 mg
Tablets (chewable) 125, 250 mg Oral suspension 125, 250 mg/5 mL
Oral solution 250 mg/5 mL VialsforIM,IV 250, 500, 1000 mg
Pathocil Oral suspension 62.5 mg/5 mL
Tablets 250, 500, 1000 mg Oral suspension 125, 250 mg/5 mL Pediatric drops 100 mg/mL
Velosef Oral suspension 125, 250 mg/5 mL
VialforIM,IV 250, 500, 1000 mg
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Table 28-6. Formulations for Antibiotics Commonly Used in
DRUG TYPES FORMULATIONS UNIT DOSE
Cefazolin Generic, Ancef, VialforIM,IV 250, 500, 1000 mg
Cefaclor Ceclor Pulvules 250, 500 mg
Cefoxitin Mefoxin VialforIM,IV 1000 mg
Erythromycin
Base Generic, ERYC,
Estolate Generic, Ilosone Tablets 250, 500 mg
Ethylsuccinate Generic, EES, Ery Tablets 400 mg
Clindamycin Generic, Cleocin Capsules 75, 150, 300 mg
Chloramphenicol Chloromycetin Capsule 250 mg
Vancomycin Generic,Vancocin Capsules 125, 250 mg
Metronidazole Generic, Flagyl, Tablets 250 mg
Nystatin Generic, Mycostatin, Tablets 500,000 U
Clotrimazole Mycelex Troche 10 mg Ketoconazole Nizoral Tablets 200 mg Acyclovir Zovirax Capsules 200 mg
IM, Intramuscular; IV, intravenous. Adapted from Hupp JR: Antibacterial, antiviral, and antifungal agents, Oral Maxillofac Surg Clin 3:273–286, 1991.
Oral and Maxillofacial Infections
Kefzol
Oral suspension 125, 250 mg/5 mL
Tablets 250, 500 mg Ilotycin, E-mycin, Ery-Tab
Tablets (chewable) 125 mg
Oral suspension 125, 250 mg/5 mL
Pediatric drops 100 mg/mL
Ped, Eryzole, Tablets (chewable) 200 mg Pediamycin Oral suspension 200, 400 mg/5 mL Pediatric drops 100 mg/2.5 mL
Oral solution 75 mg/5 mL VialforIM,IV 250, 500, 750 mg
Oral suspension 150 mg/5 mL
VialforIV 1000 mg
Oral solution 250 mg/5 mL
VialforIV 500, 1000 mg
Protostat VialforIV 500 mg
Nilstat Oral suspension 100,000 U/mL
Pastilles 200,000 U
Ointment 5% concentration
VialforIV 500 mg
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30. What is the minimal inhibitory concentration (MIC) of antibiotics?
MIC is a measure of sensitivity of bacteria. For an antibiotic to have maximum antibiotic efficacy in
treatment of specific infections, the concentration of the antibiotic at the site of infection should be 3 to 4 times the MIC. Concentrations >4 times the MIC are not more effective.
31. What is the beta-lactam group of antibiotics?
These antibiotics, which have in common a beta-lactam ring in their structures, comprise three classes:
penicillins, cephalosporins, and carbapenems. Penicillins and cephalosporins encompass many different antibiotics that are commonly used for odontogenic infection. Imipenem is an example of the carbapenems.
32. What was the first carbapenem to be used clinically?
Imipenem was the first clinically available carbapenem. It has the broadest antibacterial activity of any
currently used systemic antibiotic and, therefore, is reserved for use in treatment of severe head and neck infections.
33. What is the mode of action of penicillin?
Penicillin affects bacteria by two mechanisms:
1. It inhibits bacterial cell wall synthesis.
2. It activates endogenous bacterial autolytic processes that cause cell lysis. The bacteria must be actively dividing, and the cell wall must contain peptidoglycans for this action. Penicillin inhibits enzymes necessary for cell wall synthesis.
34. How do bacteria build up resistance to antibiotics?
Anantibiotic’sabilitytopenetratecellwallsandbindtoenzymesplaysanessentialroleinresistance
of antibiotics. Specifically, bacteria build resistance by two mechanisms:
1. Alteration in cell wall permeability to prevent antibiotics from inhibiting peptidoglycan synthesis
2. Bacterial production of beta-lactamase that causes beta-lactams to become ineffective
35. What are the pediatric and adult dosages for the most commonly used
antibiotics?
See Table 28-7.
36. What is the antimicrobial spectrum of the most common antibiotics used in treat-
ments for oral and maxillofacial infections?
See Table 28-8.
37. When should antibiotics be used?
• Acute-onsetinfection  • Involvementoffascialspaces  • Diagnosedosteomyelitisofthejaw  • Patientswithcompromisedhostdefences  • Infectionwithdiffuseswelling  • Severepericoronitis
38. When are prophylactic antibiotics for prevention of odontogenic infections not
necessary?
Antibiotics have minimal or no benefits in the treatment of chronic well-localized abscess, minor
vestibular abscess, dry socket, and root canal sterilization.
39. What are the indications for prophylactic antibiotics?
• Topreventlocalwoundinfection  • Topreventinfectionatthesurgicalsitecausinglocalwoundinfection  • Topreventmetastaticinfectionatadistantsusceptiblesiteduetohematogenousbacterialseeding
from the oral flora (e.g., subacute bacterial endocarditis, prosthetic joint replacement) following oral surgical procedures
40. When are prophylactic antibiotics indicated for prevention of local wound infection?
• Whentheproceduretobeperformedhasahighincidenceofinfection  • Wheninfectionsmayhavegraveconsequences  • Whenthepatient’simmunesystemiscompromised  • Whenthesurgicalprocedurelastslongerthan3hours  • Whenthesurgicalprocedurehasahighdegreeofcontamination
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Table 28-7. Pediatric and Adult Antibiotic Dosages
ANTIBIOTIC
ROUTE(S) OF ADMINISTRATION ADULT DOSE
PEDIATRIC DOSE/ DAY
Penicillin G IM,IV 6-12 × 10 U/4 hr 100,000 U/kg ÷ 3 PenicillinV PO 500 mg qid 50 mg/kg ÷ 3 or 4
Ampicillin PO,IM,IV 500 mg qid PO 25 mg/kg ÷ 4 Amoxicillin PO 250 mg qid PO 25 mg/kg ÷ 3 Amoxicillin-
PO 250-500 mg tid 20 mg/kg ÷ 3
clavulanate
Oxacillin IM,IV 500-1000 mg q6h 50-200 mg/kg ÷ 4 Dicloxacillin PO 250-500 mg q6h 12.5-50 mg/kg ÷ 4 or 5 Cephalexin PO 500 mg qid 25-50 mg/kg ÷ 4 Cephradine PO,IV 500 mg qid 25-50 mg/kg ÷ 3 Cefazolin IM,IV 1 g q8h 25-50 mg/kg ÷ 3 or 4 Cefaclor PO 500 mg q6h 20 mg/kg ÷ 3 Cefoxitin IM,IV 500 mg q6h 80-160 mg/kg ÷ 4 or 5 Erythromycin PO,IV 500 mg qid 40 mg/kg ÷ 4 Clindamycin PO,IM,IV 300-450 mg q6h 10-20 mg/kg ÷ 4 Chloramphenicol PO,IV 500-750 mg q6h PO 75-100 mg/kg ÷ 4 Vancomycin IV 500 mg q6h 50 mg/kg ÷ 4 Metronidazole PO 500 mg tid 30-40 mg/kg Nystatin Topical, PO 0.5-2 million U/day ÷ 2-4 Infants: 800,000 U ÷ 4
Older children:
1.6 million U ÷ 4
Clotrimazole Topical 10 mg × 5 times/day <3 yr: Safety not
established
3 yr: 10 mg × 5 times/
day
Ketoconazole PO 200-400 mg qd 3.3-6.6 mg/kg Acyclovir Topical,PO,IV 600 mg ÷ 3 PO Safety in children not
established
15mg/kg÷3IV
IM, Intramuscular; IV, intravenous; PO, orally; qid, four times a day; tid, three times a day; q6h, every 6 hours;
q8h, every 8 hours; qd, daily.
Adapted from Hupp JR: Antibacterial, antiviral, and antifungal agents, Oral Maxillofac Surg Clin 3:273–286, 1991.
41. What is the antibiotic of choice for treatment of odontogenic infection?
The empiric therapy is penicillin or penicillin plus metronidazole, if the patient is not allergic to
antibiotics and is not immunocompromised. In patients who are allergic to penicillin, clindamy- cin is an excellent alternative. Definitive antibiotic therapy should be based on culture and sensitivity.
42. What is the mechanism of action, route of excretion, and spectrum of the most
commonly used antibiotics for oral and maxillofacial infection?
See Table 28-9.
43. What are the possible causes of failure of antibiotic therapy?
• Inadequatesurgicaltreatment  • Depressedhostdefences
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Table 28-8. Antimicrobial Spectrum of Common Antibiotics Used in the
ANTIBIOTIC SPECTRUM ANTIBIOTIC SPECTRUM
Penicillin Streptococcus (except
Ampicillin and
amoxicillin
Amoxicillin plus
clavulanate
Oxacillin and
dicloxacillin
Cephalexin,
cephradine, and cefazolin
Cefaclor Same as cephalexin plus:
Cefoxitin Same as cephalexin plus:
Adapted from Peterson LJ: Principles of antibiotic therapy. In Tobazian RG, Goldberg MH, editors: Oral and
maxillofacial infections, ed 3, Philadelphia, 1994, Saunders.
Treatment of Oral and Maxillofacial Infections
group D)
Staphylococcus
(non–beta-lactamase–
producing)
Treponema Actinomyces
Oral anaerobes
Same as penicillin plus:
Escherichia coli H. influenzae Proteus mirabilis
Same as ampicillin plus:
Klebsiella Staphylococcus aureus Staphylococcus epidermidis Enterococci Gonococci
Beta-lactamase–producing
staphylococci
Streptococcus (except
group D)
Staphylococcus E. coli Proteus mirabilis Klebsiella
H. influenzae
Enterobacter Bacteroides fragilis
Oral anaerobes
Erythromycin Streptococcus
Clindamycin Oral anaerobes
Chloramphenicol Oral anaerobes
Vancomycin
Metronidazole
Staphylococcus Mycoplasma Haemophilus influenzae Legionella
Streptococcus Staphylococcus
Actinomyces Bacteroides fragilis
Streptococcus Staphylococcus H. influenzae E. coli Salmonella Shigella Rickettsia
Bacteroides fragilis
Oral anaerobes
Streptococcus Staphylococcus
Oral anaerobes
• Presenceofforeignbody  • Problemsassociatedwithuseofantibiotics(e.g.,patientcompliance,inadequatedose,antibiotic-
related infection, use of wrong antibiotic)
44. What is antibiotic-associated colitis (AAC)?
AAC is a toxic reaction associated with the use of an antibiotic that causes alteration of colonic flora
leading to the overgrowth of Clostridium difficile. The toxins from C. difficile cause pseudomembra- nous colitis or AAC, which is manifested clinically as profuse, watery diarrhea that may be bloody; cramping; abdominal pain; fever; and leukocytosis.
45. What are the risk factors for AAC?
Risk factors associated with AAC are related to the type of antibiotic and patient-related factors.
Clindamycin, which originally was thought to be the main antibiotic associated with AAC, has now been recognized to be associated with only one-third of cases. Ampicillin is associated with one-third,
Table 28-9. Profiles of the Most Commonly Used Antibiotics for Oral and Maxillofacial Infection
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PENICILLIN V ERYTHROMYCIN CLINDAMYCIN CEPHALEXIN CEFADROXIL METRONIDAZOLE DOXYCYCLINE AMOXICILLIN NYSTATIN
Bactericidal or
Bactericidal Bacteriostatic Both Bactericidal Bactericidal Bactericidal Bacteriostatic Bactericidal Bactericidal
bacteriostatic
Spectrum Streptococci,
oral anaerobes
Gram-positive
cocci, oral anaerobes
Gram-positive
cocci, anaerobes
Gram-positive
cocci, some gram-negative rods, oral anaerobes
Gram-positive
cocci, some gram­negative rods, oral
Anaerobes Gram-positive
cocci, some gram-negative rods, oral anaerobes
Gram-positive
cocci, E. coli, H. influenzae, oral anaerobes
Candida
organisms
anaerobes
Dose-
interval
250-
500 mg qid
250-500 mg qid 150-300 mg q6h 500 mg qid 500 mg bid 250 mg qid 100 mg bid 250 mg tid 200,000 U
lozenge qid
Metabolized Kidney Liver Liver Kidney Kidney Liver Liver Kidney Toxicity and
side effects
Allergy Nausea, vomiting,
cramping, diarrhea
Nausea,
vomiting, cramping, diarrhea, antibiotic-
Allergy, antibiotic-
associated colitis
Allergy,
antibiotic­associated colitis
Nausea, vomiting,
cramping, diarrhea, disulfi­ram-like effect
Teeth coloration,
photo-sensi­tivity, nausea, vomiting, diarrhea
Allergy, antibiotic-
associated colitis
associated colitis
Primary
indication
Drug of
choice
Useful alternative
for mild infection
Useful alterna-
tive, especially for resistant
Bactericidal drug
required
Bactericidal drug
required
Only anaerobic
bacteria involved
Broad-spectrum
in mild infec­tions
Broader spectrum
needed
Candidosis
anaerobes
qid, Four times a day; bid, twice a day; q6h, every 6 hours; tid, three times a day. Adapted from Peterson LJ: Principles of management and prevention of odontogenic infection. In Peterson LJ, Ellis E, Hupp J, et al., editors: Contemporary oral and maxillofacial surgery, ed 2, St Louis,
1993, Mosby.
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and the cephalosporins are associated with the last third. Patient-related factors for AAC include previous gastrointestinal procedures, medically compromised patients, advanced age, female gender, inflammatory bowel disease, cancer chemotherapy, and renal disease.
46. What is the diagnosis of and treatment for AAC?
In addition to the clinical signs and symptoms, the diagnosis of AAC is usually made based on positive
C. difficile culture and C. difficiletoxininthepatient’sstool.Sigmoidoscopyisoccasionallyusedto confirm the diagnosis. Treatment includes discontinuation of the causative antibiotics, use of alternate antibiotics if necessary, restoration of fluid and electrolyte balance, and administration of anticlos­tridial antibiotics. The usual choice is oral vancomycin or oral metronidazole.
47. What is Ludwig’s angina?
Ludwig’sanginaisbilateral,brawny,board-likeindurationofthesubmandibular,sublingual,andsubmen-
tal spaces due to infection of these spaces. The term angina is used because of the respiratory distress caused by the airway obstruction. This obstruction can occur suddenly, due to the possible extension of the infection from the sublingual space posteriorly to the epiglottis, causing epiglottis edema.
48. How is Ludwig’s angina treated?
TheprinciplesoftreatmentofLudwig’sanginaareearlydiagnosis,promptsurgicalintervention,and
definitive airway management. After securing an airway, surgical drainage of each individual space should begin even before fluctuance becomes palpable externally. Appropriate antibiotics and man­agement of the host defense mechanism are also important.
49. What is erysipelas?
Erysipelas is a superficial cellulitis of the skin that is caused by beta-hemolytic streptococci and by
group B streptococci. It usually presents with warm, erythematous skin and spreads rapidly from release of hyaluronidase by the bacteria. It is associated with lymphadenopathy and fever and has an abrupt onset with acute swelling. It may affect the skin of the face. Treatment consists of parenteral penicillin.
50. What is cervicofacial necrotizing fasciitis?
Cervicofacial necrotizing fasciitis is a very aggressive infection of the skin and superficial fascia of the
head and neck and is commonly seen in diabetic and immunocompromised patients. It carries a high mortality rate from sepsis of the dead tissue in the affected area. The etiologic factors of cervicofacial necrotizing fasciitis include odontogenic infections; burns; cuts; abrasions; contusions; peritonsillar abscess and boils of the head and neck region; surgery; and trauma.
51. Which organisms are involved in necrotizing fasciitis of the head and neck?
The causative organisms of necrotizing fasciitis include aerobes and obligate anaerobes in synergistic
combinations. In a study of 16 patients with necrotizing fasciitis, two distinctive types of bacterial findings were found. Both types had identical clinical presentations. Type I patients had anaerobic and facultative anaerobic bacteria, such as Enterobacteriaceae and streptococci other than group A. Type II patients had group A streptococci (pyogenous) alone or in combination with anaerobic bacte­ria. Group A streptococci and staphylococci were not isolated from type I patients.
52. What are the clinical features of necrotizing fasciitis of the head and neck?
The initial presentation of necrotizing fasciitis is usually deceivingly benign, although the extent of
tissue and fascial destruction far exceeds the external evidence of infection. The rate of infection is usually rapid, and the patient often has a concomitant systemic disease, such as diabetes mellitus, arteriosclerosis, obesity, malnutrition, or alcoholism.
The clinical features of this condition are usually manifested as smooth, tense, and shiny skin, with no sharp demarcation in the area involved. As the disease progresses, the pathognomonic signs of the condition include dusky purplish discoloration of the skin, small purplish patches with ill-defined borders, formation of blisters or bullae, subcutaneous fat, necrosis of the fascia, and gangrene of the overlying skin. Typically, the drainage in these patients yields “dishwater”—a purplish, foul-smelling discharge. Systemic features of necrotizing fasciitis include sepsis, hypotension, hypertension, hyperpyrexia, jaundice, and hemoglobinuria.
53. What is the treatment for necrotizing fasciitis?
Treatment for necrotizing fasciitis includes antibiotics, fluid replacement, nutrition, and daily debride-
ment to remove devitalized tissues. However, the cornerstone of treatment is debridement of the necrotic tissue and daily monitoring to assure adequate removal. Appropriate antibiotics and medical
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support are also important. Medical support includes fluid and electrolyte replacement, monitoring of the intravascular volume, and management of the underlying medical condition. Hyperbaric oxygen treatment has also been suggested for promotion of vascularization of infected tissue.
After resolution of infection, the resulting soft tissue defect is reconstructed with a skin graft and/or regional or local tissue flaps. Penicillin, clindamycin, and aminoglycosides are effective antimi­crobial agents for this condition.
54. What is the associated morbidity of cervicofacial necrotizing fasciitis?
The mortality rate of cervicofacial necrotizing fasciitis approaches 28% and when associated with
extension into the mediastinum and sepsis, rates as high as 41% and 64% have been reported, respectively. Some of the reported predisposing factors associated with the development of cervi­cofacial necrotizing fasciitis include diabetes mellitus, poor dental hygiene, obesity, alcoholism, and immunocompromised states.
55. What are the common granulomatous infections with recognized head and neck manifestations?
See Table 28-10.
56. What are the classifications of salivary gland infections?
Salivary gland infections can be classified based on clinical, microbiologic, or mechanical causes.
Accordingly, they are classified as acute or chronic, bacterial or viral, and obstructive or nonobstruc­tive (involvement by systemic granulomatous diseases). The bacterial and viral infections include mumps and acute, chronic, and recurrent sialadenitis. The obstructive infections include sialolithiasis, mucous plugs, stricture/stenosis, and foreign bodies. Systemic granulomatous infections (nonob- structive) include tuberculosis, actinomycosis, fungal infections, and sarcoid.
57. Which studies should be included in evaluation of chronic salivary gland infection?
Complete blood count with differential, Gram stain, and culture and acid-fast staining of the salivary
secretions are all useful in evaluating patients with salivary gland infection. Plain films (occlusal and
Table 28-10. Common Granulomatous Infections with
Head and Neck Manifestations
DISEASE CAUSATIVE ORGANISM
Actinomycosis Actinomyces israelii (anaerobic
gram-positive bacillus)
Cat scratch disease Unnamed gram-negative bacillus Indolent regional lymphadenitis Glanders Pseudomonas mallei (gram-negative
bacillus)
Leishmaniasis Leishmania (protozoal parasite) Mucocutaneous ulcerations Leprosy Mycobacterium leprae (acid-alcohol-fast
bacillus)
Scleroma Klebsiella rhinoscleromatis (gram-
negative bacillus)
Syphilis (tertiary) Treponema pallidum (spirochete) Gumma of soft tissue or bone Tuberculosis Mycobacterium tuberculosis (acid-fast
aerobic bacillus)
Tularemia Francisella tularensis (gram-negative
coccobacillus)
Adapted from Wood RS: Chronic granulomatous infections, Oral Maxillofac Surg Clin 3:405–422, 1991.
TYPICAL CLINICAL APPEARANCE
Painless, slowly enlarging soft
tissue cervicofacial infection with fistulae
Farcy: draining facial abscesses,
lymphadenopathy
Facial leproma, nasomaxillary
destruction,paresthesiaofV2 andVII
Chronic destructive lesion of naso-
maxillary complex
Scrofula: indolent cervical lymph-
adenitis, ulcerations of palate or tongue
Oropharyngeal ulcerations