(BQ) Part 2 book “Contemporary oral and maxillofacial surgery” has contents: Infections, management of oral pathologic lesions, temporomandibular and other facial pain disorders, oral and maxillofacial trauma, management of hospital patients, dentofacial deformities.
Trang 1Odontogenic infections are generally caused by bacteria that
have a propensity to cause abscess formation In addition, the
roots of the teeth provide a pathway for infecting bacteria to
enter the deep tissues of the periodontium and periapical
regions Therefore, odontogenic infections cause deep-seated
abscesses, and they almost always require some form of
surgi-cal therapy Treatments range from endodontic therapy and
gingival curettage to extraction, incision, and drainage of the
deep fascial spaces of the head and neck Antibiotic therapy
is an adjunctive treatment to the required surgery
Prophylac-tic antibioProphylac-tic therapy may prevent distant infections caused by
bacteremias arising from oral-maxillofacial surgical
proce-dures, and such therapy may also prevent some postoperative
wound infections.
This section presents the principles of management and
prevention of infections in dental patients.
Chapter 16 describes the basic management techniques,
including surgery and antibiotic administration, in the
treat-ment of odontogenic infections This chapter also discusses
the principles of antibiotic prophylaxis for the prevention of
wound infection and distant metastatic infection such as
infectious endocarditis.
Chapter 17 presents an overview of complex odontogenic
infections that involve the deep fascial spaces, which may
necessitate hospitalization of the patient Osteomyelitis and
other unusual infections are also discussed.
Chapter 18 presents the indications, rationale, and cal aspects of surgical endodontics Although periapical surgery is occasionally necessary for successful endodontic management, it is necessary for the clinician to choose this treatment modality wisely Therefore, the discussion of the indications and contraindications for endodontic surgery is extensive, and the technical aspects of surgical endodontics are well illustrated.
techni-Chapter 19 presents information about patients at risk for infection and other problems that are caused by compromise
of the patient’s host defense as a result of radiotherapy or cancer chemotherapy These patients are susceptible to a variety of problems, and the prevention and management of these problems are discussed.
Chapter 20 describes maxillary sinus problems that arise from odontogenic infections and other problems Although general practitioners rarely see patients with these problems, they may have to provide diagnoses before referring these patients to the appropriate health care professional for definitive care.
Finally, Chapter 21 discusses salivary gland diseases, marily the obstructive and infectious types The major diag- nostic and therapeutic modalities used in managing these problems are discussed.
pri-IV
Part
Trang 2Principles of Management and Prevention of
Odontogenic Infections
Thomas R Flynn
Principle 2: Choose Correct Antibiotic 313Principle 3: Antibiotic Plasma Level Must Be High 313Principle 4: Time Antibiotic Administration Correctly 313Principle 5: Use Shortest Antibiotic Exposure That Is Effective 313
Prophylaxis Against Total Joint Replacement Infection 316
In dentistry, one of the most difficult problems to manage is an odontogenic infection Odontogenic infections arise from teeth and have a characteristic flora Caries, periodontal disease, and pulpitis are the initiating infections, that can spread beyond teeth to the alveolar process and to the deeper tissues of the face, oral cavity, head, and neck These infections may range from low-grade, well-localized infections that require only minimal treatment to severe, life-threatening deep fascial space infections Although the overwhelming majority of odontogenic infections are readily managed by minor surgical procedures and supportive medical therapy that includes antibiotic administration, the practitioner must constantly bear in mind that these infections occasionally become severe and life threatening within a short time
This chapter is divided into several sections The first section cusses the typical microbiologic organisms involved in odontogenic infections Appropriate therapy of odontogenic infections depends
dis-on a clear understanding of the causative bacteria The secdis-ond sectidis-on discusses the natural history of odontogenic infections When infec-tions occur, they may erode through bone and into the adjacent soft tissue Knowledge of the usual pathway of infection from the teeth and surrounding tissues through bone and into the overlying soft tissue planes is essential when planning appropriate therapy The third section of this chapter deals with the principles of management
of odontogenic infections A series of principles are discussed, with consideration of the microbiology and typical pathways of infection
CHAPTER OUTLINE
NATURAL HISTORY OF PROGRESSION OF ODONTOGENIC
Medical Conditions That Compromise Host Defenses 302
Pharmaceuticals That Compromise Host Defenses 302
Principle 3: Determine Whether Patient Should Be
Treated by General Dentist or Oral-Maxillofacial
Surgeon 303
Principle 4: Treat Infection Surgically 304
Principle 5: Support Patient Medically 306
Principle 6: Choose and Prescribe Appropriate
Antibiotic(s) 306
Determine the Need for Antibiotic Administration 306
Use Empirical Therapy Routinely 307
Use the Narrowest-Spectrum Antibiotic 308
Use the Antibiotic with the Lowest Incidence of Toxicity and Side
Effects 308
Use a Bactericidal Antibiotic, if Possible 309
Be Aware of the Cost of Antibiotics 309
Summary 309
Principle 7: Administer Antibiotic Properly 310
Principle 8: Evaluate Patient Frequently 311
PRINCIPLES OF PROPHYLAXIS OF WOUND
Principle 1: Procedure Should Have Significant Risk of
Infection 312
Trang 3The chapter concludes with a section on the prophylaxis of wound
infection and of metastatic infection
MICROBIOLOGY OF ODONTOGENIC
INFECTIONS
The bacteria that cause infection are most commonly part of the
indigenous bacteria that normally live on or in the host
Odonto-genic infections are no exception because the bacteria that cause
odontogenic infections are part of the normal oral flora: those that
comprise the bacteria of plaque, those found on mucosal surfaces,
and those found in the gingival sulcus These bacteria are primarily
aerobic gram-positive cocci, anaerobic gram-positive cocci, and
anaerobic gram-negative rods These bacteria cause a variety of
common diseases such as dental caries, gingivitis, and periodontitis
When these bacteria gain access to deeper underlying tissues, as
through a necrotic dental pulp or through a deep periodontal pocket,
they cause odontogenic infections As the infection progresses more
deeply, different members of the infecting flora can find better growth
conditions and begin to outnumber the previously dominant species
Many carefully performed microbiologic studies of odontogenic
infections have demonstrated the microbiologic composition of
these infections Several important factors must be noted First,
almost all odontogenic infections are caused by multiple bacteria
The polymicrobial nature of these infections makes it important that
the clinician understand the variety of bacteria that are likely to cause
infection In most odontogenic infections, the laboratory can identify
an average of five species of bacteria It is not unusual to identify as
many as eight different species in a given infection On rare
occa-sions, a single species may be isolated New molecular methods,
which identify the infecting species by their genetic makeup, have
allowed scientists to identify greater numbers and a whole new range
of species, including unculturable pathogens, not previously
associ-ated with these infections In the future, these methods may lead to
a completely new understanding of the pathogenesis of odontogenic
infections
A second important factor is the oxygen tolerance of the bacteria
that cause odontogenic infections Because the mouth flora is a
com-bination of aerobic and anaerobic bacteria, it is not surprising to find
that most odontogenic infections are caused by anaerobic and aerobic
bacteria Infections caused by aerobic bacteria alone account for 6%
of all odontogenic infections Anaerobic bacteria alone are found in
44% of odontogenic infections Infections caused by mixed
anaero-bic and aeroanaero-bic bacteria comprise 50% of all odontogenic infections
(Table 16-1)
The predominant aerobic bacteria in odontogenic infections
(found in about 65% of cases) are the Streptococcus milleri group,
which consists of three members of the S viridans group of bacteria:
Table 16-1 Role of Anaerobic Bacteria in
Data from Brook I, Frazier EH, Gher ME: Aerobic and anaerobic microbiology
of periapical abscess Oral Microbiol Immunol 6:123–125, 1991.
Table 16-2 Major Pathogens in Odontogenic Infections
S anginosus, S intermedius, and S constellatus These facultative
organ-isms, which can grow in the presence or the absence of oxygen, may initiate the process of spreading into deeper tissue (Table 16-2) Miscellaneous bacteria contribute 5% or less of the aerobic species found in these infections Rarely found bacteria include staphylo-
cocci, group D Streptococcus organisms, other streptococci, Neisseria spp., Corynebacterium spp., and Haemophilus spp.
The anaerobic bacteria found in odontogenic infections include
an even greater variety of species (see Table 16-2) Two main groups, however, predominate The anaerobic gram-positive cocci are found
in about 65% of cases These cocci are anaerobic Streptococcus and
Peptostreptococcus Oral gram-negative anaerobic rods are cultured in
about three quarters of the infections The Prevotella and Porphyro
monas spp are found in about 75% of these, and Fusobacterium
organisms are present in more than 50%
Of the anaerobic bacteria, several gram-positive cocci (i.e.,
anaero-bic Streptococcus and Peptostreptococcus spp.) and gram-negative rods (i.e., Prevotella and Fusobacterium spp.) play a more important patho-
genic role The anaerobic gram-negative cocci and the anaerobic gram-positive rods appear to have little or no role in the cause of odontogenic infections; instead, they appear to be opportunistic organisms
The method by which mixed aerobic and anaerobic bacteria cause infections is known with some certainty After initial inoculation into
deeper tissues, the facultative S milleri group organisms can
synthe-size hyaluronidase, which allows the infecting organisms to spread through connective tissues, initiating the cellulitis stage of infection Metabolic byproducts from the streptococci create a favorable envi-ronment for the growth of anaerobes: the release of essential nutri-ents, lowered pH in the tissues, and consumption of local oxygen supplies The anaerobic bacteria are then able to grow, and as the local oxidation–reduction potential is lowered further, the anaerobic bacteria predominate and cause liquefaction necrosis of tissues by
Trang 4Figure 16-1 When infection erodes through bone, it will enter soft tissue through thinnest bone A, Tooth apex is near thin labial bone, so infection
erodes labially B, Right apex is near palatal aspect, so palatal bone will be perforated
Table 16-3 Comparison of Edema, Cellulitis, and Abscess
Characteristic
Edema (Inoculation) Cellulitis Abscess
Duration 0–3 days 1–5 days 4–10 days
Pain, borders Mild, diffuse Diffuse Localized
Size Variable Large Smaller
Color Normal Red Shiny center
Consistency Jelly-like Boardlike Soft center
Progression Increasing Increasing Decreasing
Pus Absent Absent Present
Bacteria Aerobic Mixed Anaerobic
Seriousness Low Greater Less
their synthesis of collagenases As collagen is broken down and
invading white blood cells necrose and lyse, microabscesses form and
may coalesce into a clinically recognizable abscess In the abscess
stage, anaerobic bacteria predominate and may eventually become
the only organisms found in culture Early infections appearing
ini-tially as a cellulitis may be characterized as predominantly aerobic
streptococcal infections, and late, chronic abscesses may be
character-ized as anaerobic infections
Clinically, this progression of the infecting flora from aerobic to
anaerobic seems to correlate with the type of swelling that can be
found in the infected region Thus, odontogenic infections seem to
pass through four stages In the first 3 days of symptoms, a soft,
mildly tender, doughy swelling represents the inoculation stage, in
which the invading streptococci are just beginning to colonize the
host After 3 to 5 days, the swelling becomes hard, red, and acutely
tender as the infecting mixed flora stimulates the intense
inflamma-tory response of the cellulitis stage At 5 to 7 days after the onset of
swelling, the anaerobes begin to predominate, causing a liquefied
abscess in the center of the swollen area This is the abscess stage
Finally, when the abscess drains spontaneously through skin or
mucosa, or it is surgically drained, the resolution stage begins as the
immune system destroys the infecting bacteria, and the processes of
healing and repair ensue The clinical and microbiologic
characteris-tics of edema, cellulitis, and abscess are summarized and compared
in Table 16-3
NATURAL HISTORY OF PROGRESSION OF ODONTOGENIC INFECTIONS
Odontogenic infections have two major origins: (1) periapical, as a
result of pulpal necrosis and subsequent bacterial invasion into the
periapical tissue, and (2) periodontal, as a result of a deep periodontal
pocket that allows inoculation of bacteria into the underlying soft tissues Of these two, the periapical origin is the most common in odontogenic infections
Necrosis of the dental pulp as a result of deep caries allows a pathway for bacteria to enter the periapical tissues Once this tissue has become inoculated with bacteria and an active infection is estab-lished, the infection spreads equally in all directions, but preferen-tially along the lines of least resistance The infection spreads through the cancellous bone until it encounters a cortical plate If this cortical plate is thin, the infection erodes through the bone and enters the surrounding soft tissues Treatment of the necrotic pulp by standard endodontic therapy or extraction of the tooth should resolve the infection Antibiotics alone may arrest, but do not cure, the infection because the infection is likely to recur when antibiotic therapy has ended without treatment of the underlying dental cause Thus, the primary treatment of pulpal infections is endodontic therapy or tooth extraction, as opposed to antibiotics
When the infection erodes through the cortical plate of the lar process, it spreads into predictable anatomic locations The loca-tion of the infection arising from a specific tooth is determined by the following two major factors: (1) the thickness of the bone overly-ing the apex of the tooth and (2) the relationship of the site of perforation of bone to muscle attachments of the maxilla and mandible
alveo-Figure 16-1 demonstrates how infections perforate through bone into the overlying soft tissue In Figure 16-1, A, the labial bone overly-ing the apex of the tooth is thin compared with the bone on the palatal aspect of the tooth Therefore, as the infectious process spreads, it goes into the labial soft tissues In Figure 16-1, B, the tooth
is severely proclined, which results in thicker labial bone and a tively thinner palatal bone In this situation, as the infection spreads through bone into the soft tissue, the infection is seen as a palatal abscess
rela-Once the infection has eroded through bone, the precise location
of the soft tissue infection is determined by the position of the foration relative to the muscle attachments In Figure 16-2, A, the infection has eroded through to the facial aspect of the alveolar process and inferior to the attachment of the buccinator muscle, which results in an infection that appears as a vestibular abscess In
Trang 5per-Figure 16-3 Palatal abscess arising from the palatal root of a maxillary
first premolar
Figure 16-4 Vestibular abscess arising from maxillary incisor Overlying
mucosa is thin because pus is near the surface. (From Flynn TR:
Anatomy of oral and maxillofacial infections In Topazian RG, Goldberg
MH, Hupp JR, editors: Oral and maxillofacial infections, ed 4,
Philadelphia, PA, 2002, WB Saunders.)
Figure 16-2 Relationship of point of bone perforation to muscle attachment determines fascial space involved A, When tooth apex is lower than
muscle attachment, vestibular abscess results B, If apex is higher than muscle attachment, the adjacent fascial space is involved
Figure 16-2, B, the infection has eroded through the bone superior
to the attachment of the buccinator muscle and is expressed as an infection of the buccal space because the buccinator muscle separates the buccal and vestibular spaces
Infections from most of the maxillary teeth erode through the facial cortical plate These infections also erode through the bone below the attachment of the muscles that attach to the maxilla, which means that most maxillary dental abscesses appear initially as ves-tibular abscesses Occasionally, a palatal abscess arises from the apex
of a severely inclined lateral incisor or the palatal root of a maxillary first molar or premolar (Fig 16-3) More commonly, the maxillary molars cause infections that erode through the bone superior to the insertion of the buccinator muscle, which results in a buccal space infection Likewise, on occasion a long maxillary canine root allows infection to erode through the bone superior to the insertion of the levator anguli oris muscle and causes an infraorbital (canine) space infection
In the mandible, infections of incisors, canines, and premolars usually erode through the facial cortical plate superior to the attach-ment of the muscles of the lower lip, resulting in vestibular abscesses
Mandibular molar infections erode through the lingual cortical bone more frequently than in the case of the anterior teeth First molar infections may drain buccally or lingually Infections of the second molar can perforate buccally or lingually (but usually lingually), and third molar infections almost always erode through the lingual corti-cal plate The mylohyoid muscle determines whether infections that
drain lingually go superior to that muscle into the sublingual space
or below it into the submandibular space
The most common odontogenic deep fascial space infection is a vestibular space abscess (Fig 16-4) Occasionally, patients do not seek treatment for these infections, and the process ruptures sponta-neously and drains, resulting in resolution or chronicity of the infec-tion The infection recurs if the site of spontaneous drainage closes Sometimes, the abscess establishes a chronic sinus tract that drains
to the oral cavity or to skin (Fig 16-5) As long as the sinus tract continues to drain, the patient experiences no pain Antibiotic administration usually stops the drainage of infected material tem-porarily, but when the antibiotic course is over, the drainage recurs Definitive treatment of a chronic sinus tract requires treatment of the original causative problem, which is usually a necrotic pulp In such
a case, the necessary treatment is endodontic surgery or extraction of the infected tooth
PRINCIPLES OF THERAPY OF ODONTOGENIC INFECTIONS
This section discusses the management of odontogenic infections A series of principles are useful in treating patients who come to the dentist with infections related to teeth and the gingiva The clinician must keep in mind the information in the preceding two sections of
Trang 6Figure 16-5 Chronic drainage sinus tracts that result from low-grade
infections may drain intraorally (A) or extraorally (B). (A, Courtesy of
Sasha B Ross, DMD B, From Flynn TR, Topazian RG: Infections of the
oral cavity In Waite D, editor: Textbook of practical oral and
maxillofacial surgery, Philadelphia, PA, 1987, Lea & Febiger.)
A
B
Figure 16-6 Patient with severe infection and elevated temperature,
pulse rate, and respiratory rate The patient feels sick and tired; he has a
“toxic appearance.” (From Flynn TR: Surgical management of orofacial
infections Atlas Oral Maxillofac Surg Clin North Am 8:79, 2000.)
this chapter to understand these principles By following these
prin-ciples in a stepwise fashion, the clinician will certainly have met the
standard of care, even though the expected result may not always be
achieved The first three principles are perhaps the most important
in determining the outcome, yet they can be accomplished by the
experienced practitioner within the first few minutes of the initial
patient encounter
Principle 1: Determine Severity of Infection
Most odontogenic infections are mild and require only minor
surgi-cal therapy When the patient comes for treatment, the initial goal is
to assess the severity of the infection This determination is based on
a complete history of the current infectious illness and a physical
examination
Complete history The history of the patient’s infection follows
the same general guidelines as those for any history The initial
purpose is to find out the patient’s chief complaint Typical chief
complaints of patients with infections are “I have a toothache,” “My
jaw is swollen,” or “I have a gum boil in my mouth.” The complaint
should be recorded in the patient’s own words
The next step in history taking is determining how long the
infec-tion has been present First, the dentist should inquire as to time of
onset of the infection How long ago did the patient first have
symp-toms of pain, swelling, or drainage, which indicated the beginning
of the infection? The course of the infection is then discussed Have
the symptoms of the infection been constant, have they waxed and
waned, or has the patient’s condition steadily grown worse since the
symptoms were first noted? Finally, the practitioner should determine the rapidity of progress of the infection Has the infection process progressed rapidly over a few hours, or has it gradually increased in severity over several days to a week?
The next step is eliciting information about the patient’s toms Infections are actually a severe inflammatory response, and the cardinal signs of inflammation are clinically easy to discern These
symp-signs and symptoms are, in Latin terms, dolor (pain), tumor (swelling),
calor (warmth), rubor (erythema, redness), and functio laesa (loss of
function)
The most common complaint is pain The patient should be asked where the pain actually started and how the pain has spread since it was first noted The second sign is tumor (swelling), which is a physi-cal finding that is sometimes subtle and not obvious to the practitio-ner, although it is obvious to the patient It is important that the dentist ask the patient to describe any area of swelling With regard
to the third characteristic of infection, calor (warmth), the patient should be asked whether the area has felt warm to the touch Redness
of the overlying area is the next characteristic to be evaluated The patient should be asked if there has been or is any change in color, especially redness, over the area of the infection Functio laesa (loss
of function) should then be checked When inquiring about this characteristic, the dentist should ask about trismus (difficulty opening the mouth widely) and any difficulty chewing, swallowing (dyspha-gia), or breathing (dyspnea)
Finally, the dentist should ask how the patient feels in general Patients who feel fatigued, feverish, weak, and sick are said to have
malaise Malaise usually indicates a generalized reaction to a
moderate-to-severe infection (Fig 16-6)
In the next step, the dentist discusses treatment The dentist should find out about previous professional treatment and self-treatment Many patients treat themselves with leftover antibiotics, hot soaks, and a variety of other home or herbal remedies Occasion-ally, a dentist may see a patient who had received treatment in an emergency room 2 or 3 days earlier and was referred to a dentist by the emergency room physician The patient might have neglected to follow the emergency room physician’s advice until the infection became severe Sometimes, the patient may not have taken the pre-scribed antibiotic because he or she could not afford to purchase it.The patient’s complete medical history should be obtained in the usual manner through an interview or a self-administered question-naire with verbal follow-up of any relevant findings
Physical examination The first step in the physical examination
is to obtain the patient’s vital signs, including temperature, blood pressure, pulse rate, and respiratory rate The need for evaluation of
Trang 7temperature is obvious Patients who have systemic involvement of infection usually have elevated temperatures Patients with severe infections have temperatures elevated to 101°F or higher (greater than 38.3°C).
The patient’s pulse rate increases as the patient’s temperature increases Pulse rates of up to 100 beats per minute (beats/min) are not uncommon in patients with infections If pulse rates increase to greater than 100 beats/min, the patient may have a severe infection and should be treated more aggressively
The vital sign that varies the least with infection is the patient’s blood pressure Only if the patient has significant pain and anxiety will an elevation occur in systolic blood pressure However, septic shock results in hypotension
Finally, the patient’s respiratory rate should be closely observed
One of the major considerations in odontogenic infections is the potential for partial or complete upper airway obstruction as a result
of extension of the infection into the deep fascial spaces of the neck As respirations are monitored, the dentist should carefully check to ensure that the upper airway is clear and that the patient
is able to breathe without difficulty The normal respiratory rate is
14 to 16 breaths per minute (breaths/min) Patients with mild to moderate infections may have elevated respiratory rates greater than
18 breaths/min
Patients who have normal vital signs with only a mild ture elevation usually have a mild infection that can be readily treated Patients who have abnormal vital signs with elevation of temperature, pulse rate, and respiratory rate are more likely to have serious infection and require more intensive therapy and evaluation
tempera-by an oral-maxillofacial surgeon
Once vital signs have been taken, attention should be turned to the physical examination of the patient The initial portion of the physical examination should be inspection of the patient’s general appearance Patients who have more than a minor, localized infec-tion have an appearance of fatigue, feverishness, and malaise This is referred to as a “toxic appearance” (see Fig 16-6)
The patient’s head and neck should be carefully examined for the cardinal signs of infection (as discussed earlier), and the patient should be inspected for any evidence of swelling and overlying ery-thema The patient should be asked to open the mouth widely, swallow, and take deep breaths so that the dentist can check for trismus, dysphagia, or dyspnea These are ominous signs of a severe infection, and the patient should be referred immediately to an oral-maxillofacial surgeon or to the emergency room A recent study of severe odontogenic infections requiring hospitalization found trismus (maximum interincisal opening less than 20 mm) in 73% of cases, dysphagia in 78%, and dyspnea in 14%
Areas of swelling must be examined by palpation The dentist should gently touch the area of swelling to check for tenderness, amount of local warmth or heat, and the consistency of the swelling
The consistency of the swelling may vary from very soft and almost normal to a firmer, fleshy swelling (described as “doughy”) to an even firmer or hard swelling (described as “indurated”) An indurated swelling has similar firmness to a tightened muscle Another charac-teristic consistency is fluctuance Fluctuance feels like a fluid-filled balloon Fluctuant swelling almost always indicates an accumulation
of liquid pus in the center of an indurated area
The dentist then performs an intraoral examination to try to find the specific cause of the infection Severely carious teeth, an obvious periodontal abscess, severe periodontal disease, combinations of caries and periodontal disease, or an infected fracture of a tooth or the entire jaw may be present The dentist should look and feel for areas of gingival swelling and fluctuance and for localized vestibular swellings or draining sinus tracts
The next step is to perform a radiographic examination This usually consists of the indicated periapical radiographs Occasionally,
Figure 16-7 Cellulitis involving the submental and submandibular
region The cellulitis is indurated on palpation, and the patient is sick.(From Flynn TR: Surgical management of orofacial infections Atlas Oral Maxillofac Surg Clin North Am 8:79, 2000.)
Figure 16-8 Well-localized abscess with fluctuance in the center and
induration at its periphery. (Courtesy of Richard G Topazian, DDS.)
however, extraoral radiographs such as a panoramic radiograph may
be necessary because of limited mouth opening, tenderness, or other extenuating circumstances
After the physical examination, the practitioner should begin to have a sense of the stage of the presenting infection Very soft, mildly tender, edematous swellings indicate the inoculation stage, whereas
an indurated swelling indicates the cellulitis stage (Fig 16-7), and central fluctuance indicates an abscess (Fig 16-8) Soft tissue infec-tions in the inoculation stage may be cured by removal of the odon-togenic cause, with or without supportive antibiotics; infections in the cellulitis or abscess stages require removal of the dental cause of infection plus incision and drainage and antibiotics
Distinctions between the inoculation, cellulitis, and abscess stages are typically related to duration, pain, size, peripheral definition and consistency on palpation, presence of purulence, infecting bacteria, and potential danger (see Table 16-3) The duration of cellulitis is usually thought to be acute and is the most severe presentation of infection An abscess, however, is a sign of increasing host resistance
to infection Cellulitis is usually described as being more painful than
Trang 8an abscess, which may be the result of its acute onset and tissue
distention
Edema, the hallmark of the inoculation stage, is typically diffuse
and jelly-like, with minimal tenderness to palpation The size of a
cellulitis is typically larger and more widespread than that of an
abscess or edema The periphery of a cellulitis is usually indistinct,
with a diffuse border that makes it difficult to determine where the
swelling begins or where it ends The abscess usually has distinct and
well-defined borders Consistency to palpation is one of the primary
distinctions among the stages of infection When palpated, edema
can be very soft or doughy; a severe cellulitis is almost always
described as indurated or even as being “boardlike.” The severity of
the cellulitis increases as its firmness to palpation increases On
pal-pation, an abscess feels fluctuant because it is a pus-filled tissue cavity
Thus, an infection may appear innocuous in its early stages and
extremely dangerous in its more advanced, indurated, rapidly
spread-ing stages A localized abscess is typically less dangerous because it
is more chronic and less aggressive
The presence of pus usually indicates that the body has locally
walled off the infection and that the local host resistance mechanisms
are bringing the infection under control In many clinical situations,
the distinction between severe cellulitis and abscess may be difficult
to make, especially if an abscess lies deeply within the soft tissue In
some patients, an indurated cellulitis may have areas of abscess
for-mation within it (see Chapter 17)
Severe infections occupying multiple deep fascial spaces may be
in an early stage in one anatomic space, and in a more severe, rapidly
progressive stage in another fascial space A severe, deeply invading
infection may pass through ever deeper anatomic spaces in a
predict-able fashion, similar to a house fire, where smoke may be present in
one room, intense heat in another, and open flames near the source
of the fire The goal of therapy in such infections is to abort the spread
of the infection in all involved anatomic spaces These infections are
discussed in detail in Chapter 17
In summary, edema represents the earliest inoculation stage of
infection which is most easily treated Cellulitis is an acute, painful
infection with more swelling and diffuse borders Cellulitis has a hard
consistency on palpation and contains no visible pus Cellulitis may
be a rapidly spreading process in serious infections An acute abscess
is a more mature infection with more localized pain, less swelling,
and well-circumscribed borders The abscess is fluctuant on palpation
because it is a pus-filled tissue cavity A chronic abscess is usually slow
growing and less serious than cellulitis, especially if the abscess has
drained spontaneously to the external environment
Principle 2: Evaluate State of Patient’s Host
Defense Mechanisms
Part of the evaluation of the patient’s medical history is designed to
estimate the patient’s ability to defend against infection Several
disease states and several types of drug use may compromise this
ability Immunocompromised patients are more likely to have
infec-tions, and these infections often become serious more rapidly
There-fore, to manage their infections more effectively, it is important to be
able to identify those patients who may have compromised host
defenses
Medical conditions that compromise host defenses
Delinea-tion of those medical condiDelinea-tions that may result in decreased host
defenses is important These compromises allow more bacteria to
enter the tissues or to be more active, or they prevent the humoral
or cellular defenses from exerting their full effect Several specific
conditions may compromise patients’ defenses (Box 16-1)
Uncontrolled metabolic diseases—such as uncontrolled diabetes,
end-stage renal disease with uremia, and severe alcoholism with
Box 16-1 Compromised Host Defenses
Uncontrolled Metabolic Diseases
• Poorly controlled diabetes
• Alcoholism
• Malnutrition
• End-stage renal disease
Immune System–Suppressing Diseases
• Human immunodeficiency virus/acquired immunodeficiency syndrome
• Lymphomas and leukemias
The second major group of immunocompromising diseases includes those that interfere with host defense mechanisms, for example, leukemias, lymphomas, and many types of cancer These diseases result in decreased white cell function and decreased anti-body synthesis and production
Human immunodeficiency virus (HIV) infection attacks T lymphocytes, affecting a person’s resistance to viruses and other intracellular pathogens Fortunately, odontogenic infections are caused largely by extracellular pathogens (bacteria) Therefore, HIV-seropositive individuals are able to combat odontogenic infections fairly well until acquired immunodeficiency syndrome (AIDS) has progressed to advanced stages, when B lymphocytes are also severely impaired Nonetheless, care for the HIV-seropositive patient with an odontogenic infection is usually more intensive than for the other-wise healthy patient
Pharmaceuticals that compromise host defenses Patients
taking certain drugs are also immunologically compromised Cancer chemotherapeutic agents can decrease circulating white cell counts
to low levels, commonly less than 1000 cells per milliliter (cells/mL) When this occurs, patients are unable to defend themselves effectively against bacterial invasion Patients receiving immunosuppressive therapy, usually for organ transplantation or autoimmune diseases, are compromised The common drugs in these categories are cyclo-sporine, corticosteroids, tacrolimus (Prograf), and azathioprine (Imuran) These drugs decrease the function of T and B lymphocytes and immunoglobulin production Thus, patients taking these medi-cations are more likely to have severe infections The immunosup-pressive effects of some cancer chemotherapeutic agents can last for
up to a year after therapy ends
In summary, when evaluating a patient whose chief complaint may be an infection, the patient’s medical history should be carefully reviewed for the presence of diabetes, severe renal disease, alcoholism with malnutrition, leukemias and lymphomas, cancer chemotherapy, and immunosuppressive therapy of any kind When the patient’s history includes any of these, the patient with an infection must be treated much more vigorously because the infection may spread more
Trang 9urgent criterion is difficulty swallowing (dysphagia) Patients with acutely progressive deep fascial space infections may also have diffi-culty swallowing their saliva Drooling is an ominous sign because the inability to control one’s secretions frequently indicates a narrow-ing of the oropharynx and the potential for acute airway obstruction This patient should also be transported to the hospital emergency room immediately because surgical intervention or intubation may
be required for airway maintenance Definitive treatment of the tion can follow once the airway is secure
infec-Several other criteria should indicate referral to an maxillofacial surgeon Patients who have extraoral swellings such as buccal space infections or submandibular space infections may require extraoral surgical incision and drainage (I&D) as well as hospitalization Next, although infection frequently causes an ele-vated temperature, a temperature higher than 101°F indicates a greater likelihood of severe infection, and this patient should be referred to the hospital Another important sign is trismus, the inabil-ity to open the mouth widely In odontogenic infections, trismus results from the involvement of the muscles of mastication by the inflammatory process Mild trismus can be defined as a maximum interincisal opening between 20 and 30 mm; moderate trismus is an interincisal opening between 10 and 20 mm; and severe trismus is
oral-an interincisal opening of less thoral-an 10 mm
Moderate or severe trismus may be an indication of the spread of the infection into the masticator space (surrounding the muscles of mastication) or, worse, either or both the lateral pharyngeal space and the retropharyngeal space surrounding the pharynx and the trachea In this situation, referral to a specialist is necessary for evalu-ation of upper airway patency In addition, systemic involvement of
an odontogenic infection is an indication for referral Patients with systemic involvement have a typical toxic facial appearance: glazed eyes, open mouth, and a dehydrated, sick appearance When this is seen, the patient is usually fatigued, has a substantial amount of pain, has an elevated temperature, and is dehydrated Finally, if the patient has compromised host defenses, he or she may have to be hospital-ized An oral-maxillofacial surgeon is qualified to admit the patient expeditiously to the hospital for definitive care
In summary, within the first few minutes of the initial patient encounter, the three principles mentioned above allow the dentist to assess the severity of the infection, evaluate host defenses, and expe-ditiously decide on the best setting for the patient’s care In doubtful situations, it is always best to err on the side of caution and refer the patient for a higher level of care Appropriate decision making at this stage can prevent serious morbidity and the occasional mortality that still occur because of odontogenic infections
Principle 4: Treat Infection Surgically
The primary principle of management of odontogenic infections is
to perform surgical drainage and to remove the cause of the infection Surgical treatment may range from something as straightforward as
an endodontic access opening and extirpation of the necrotic tooth pulp to treatment as complex as the wide incision of the soft tissue
in the submandibular and neck regions for a severe infection or even open drainage of the mediastinum
The primary goal in surgical management of infection is to remove the cause of the infection, which is most commonly a necrotic pulp
or deep periodontal pocket A secondary goal is to provide drainage
of accumulated pus and necrotic debris
When a patient has a typical odontogenic infection, the most likely appearance is a carious tooth with a periapical radiolucency and a small vestibular abscess With this presentation, the dentist has the following surgical options: endodontic treatment or extraction, with or without I&D If the tooth is not to be extracted, it should be opened and its pulp removed, which results in elimination of the
rapidly Referral to an oral-maxillofacial surgeon for early and sive surgery to remove the cause and initiate parenteral antibiotic therapy must be considered
aggres-Additionally, when a patient with a history of one of these lems is seen for routine oral surgical procedures, it may be necessary
prob-to provide the patient with prophylactic antibiotic therapy prob-to decrease the risk of postoperative wound infection Use of the guidelines and regimens for prevention of endocarditis published by the American Heart Association (AHA) and American Dental Association (ADA) is
a practical way to manage this problem
Principle 3: Determine Whether Patient Should Be Treated by General Dentist or Oral-Maxillofacial Surgeon
Most odontogenic infections seen by the dentist can be managed with the expectation of rapid resolution Odontogenic infections, when treated with minor surgical procedures and antibiotics, if indi-cated, almost always respond rapidly However, some odontogenic infections are potentially life threatening and require aggressive medical and surgical management In these special situations, early recognition of the potential severity is essential, and these patients should be referred to an oral-maxillofacial surgeon for definitive management As the specialist with the best training and experience
in the management of severe odontogenic infections, the maxillofacial surgeon can optimize the outcomes and minimize the complications of these infections For some patients, hospitalization
oral-is required, whereas others can be managed as outpatients
When a patient with an odontogenic infection comes for ment, the dentist must have a set of criteria by which to judge the seriousness of the infection (Box 16-2) If some or all of these criteria are met, immediate referral must be considered
treat-Three main criteria indicate immediate referral to a hospital gency room because of an impending threat to the airway The first criterion is a history of a rapidly progressing infection This means that the infection began 1 or 2 days before the interview and is growing rapidly worse, with increasing swelling, pain, and other associated signs and symptoms This type of odontogenic infection may cause swelling in deep fascial spaces of the neck, which can compress and deviate the airway The second criterion is difficulty breathing (dyspnea) Patients who have severe swelling of the soft tissue of the upper airway as the result of infection may have difficulty maintaining a patent airway In these situations, the patient often will refuse to lie down, have muffled or distorted speech, and be obvi-ously distressed by breathing difficulties This patient should be referred directly to an emergency room because immediate surgical attention may be necessary to maintain an intact airway The third
emer-Box 16-2 Criteria for Referral to an Oral-Maxillofacial
• Swelling extending beyond the alveolar process
• Elevated temperature (greater than 101°F)
• Severe malaise and toxic appearance
• Compromised host defenses
• Need for general anesthesia
• Failed prior treatment
Trang 10cause and limited drainage through the apical foramen of the tooth
If the tooth cannot be salvaged or is not restorable, it should be
extracted as soon as possible
Extraction provides removal of the cause of the infection and
drain-age of the accumulated periapical pus and debris In addition to the
endodontic procedure or extraction of the tooth, an I&D procedure
may be required for an infection that has spread beyond the periapical
region Incision of the abscess or cellulitis allows removal of the
accu-mulated pus and bacteria from the underlying tissue Evacuation of the
abscess cavity dramatically decreases the load of bacteria and necrotic
debris Evacuation also reduces the hydrostatic pressure in the region
by decompressing tissues, which improves the local blood supply and
increases the delivery of host defenses and antibiotics to the infected
area I&D of a cellulitis serves to abort the spread of the infection into
deeper anatomic spaces The I&D procedure includes the insertion of
a drain to prevent premature closure of the mucosal incision, which
could allow the abscess cavity to re-form It is important to remember
that the surgical goal is to achieve adequate drainage If endodontic
opening of the tooth does not provide adequate drainage of the
abscess, it is essential to perform an I&D
The technique for I&D of a vestibular abscess or cellulitis is
straight-forward (Fig 16-9) The preferred site for intraoral incision is directly
over the site of maximum swelling and inflammation However, it is
important to avoid incising across a frenum or the path of the mental
nerve in the lower premolar region When I&D procedures are
per-formed extraorally, a more complex set of criteria must be met when
selecting a site for the incision Once the area of incision has been
selected, a method of pain control must be used Regional nerve block
anesthesia is preferred when it can be achieved by injecting in an
area away from the site of infection Alternatively, infiltration of local
Figure 16-9 A, Periapical infection of lower premolar extends through buccal plate and creates sizable vestibular abscess B, Abscess is incised with
No 11 blade C, Beaks of hemostat are inserted through incision and opened so that beaks spread to break up any loculations of pus that may exist
in abscessed tissue D, A small drain is inserted to depths of abscess cavity with a hemostat E, The drain is sutured into place with a single black silk
suture Note that pus usually flows out along, rather than through, a tubular drain
Box 16-3 Indications for Culture and Antibiotic
Sensitivity Testing
• Infection spreading beyond the alveolar process
• Rapidly progressive infection
• Previous, multiple antibiotic therapy
• Nonresponsive infection (after more than 48 hours)
• Recurrent infection
• Compromised host defenses
anesthetic solution into and around the area to be drained can be performed Once the local anesthetic needle has been used in an infected site, it should not be reused in an uninfected area
Before the actual incision of the abscess is performed, obtaining a specimen for culture and sensitivity (C&S) testing must be considered
If the decision is made to perform a culture, it is carried out as the initial portion of the surgery (Box 16-3) After the site of surgery has been anesthetized, the surface mucosa is disinfected with a solution such as povidone-iodine (Betadine) and dried with sterile gauze A large-gauge needle, usually 18 gauge, is used for specimen collection
A small syringe, usually 3 mL, is adequate The needle is then inserted into the abscess or cellulitis, and 1 or 2 mL of pus or tissue fluid is aspirated The specimen may contain only tissue fluid and blood instead of pus, yet it commonly provides sufficient bacteria for an accurate culture The specimen is then inoculated directly into aerobic and anaerobic culturettes, which are sterile tubes containing a swab and bacterial transport medium Culturettes and specimen bottles that are appropriate for both aerobes and anaerobes are also available All
Trang 11drain is then sutured to one edge of the incision with a nonresorbable suture The suture should be placed in viable tissue to prevent loss
of the drain because it might tear through friable, nonvital tissue.The drain should remain in place until all the drainage has stopped, usually for 2 to 5 days Removal is done by simply cutting the suture and slipping the drain from the wound
Inoculation-stage infections, that initially appear as edema with a soft, doughy, diffuse, mildly tender swelling, do not typically require I&D Surgical management of infections of this type is limited to removal of the necrotic pulp or removal of the involved tooth Adjunctive antibiotic therapy may be used, according to the indica-tions discussed below
It is critical to keep in mind that the primary method for treating odontogenic infections is to perform surgery to remove the source of the infection and drain the anatomic spaces affected by indurated cellulitis or an abscess Whenever an abscess or cellulitis is diagnosed, the surgeon must drain it Failure to do so may result in worsening
of the infection and failure of the infection to resolve, even if ics are given Even if the tooth cannot be immediately opened or extracted, an I&D should be done
antibiot-Some clinicians believe that I&D of a cellulitis may allow the infection to spread into deeper tissues by opening them up to infect-ing bacteria The experience of others has shown that establishing drainage for a cellulitis serves to abort the spread of infection In a prospective study of 37 patients hospitalized for severe odontogenic infection, approximately 25% of the cases had drainage in the cel-lulitis stage On multivariate analysis, the stage of infection had no significant effect on complications or the length of hospital stay.The algorithm presented in Figure 16-10 is a decision pathway for the management of uncomplicated odontogenic infections, which follows the principles described in this chapter After deciding to treat the patient in the outpatient setting, the dentist should determine
culturettes and specimen bottles have a limited shelf-life, so the tion date should be checked before use Care must be taken to keep the anaerobic culture tube fully upright while open to prevent the escape
expira-of the carbon dioxide that is needed to maintain the tube’s anaerobic environment As discussed before, anaerobic bacteria are almost always present in odontogenic infections, so care must be taken to provide the laboratory with the best specimen to find them The surgeon should request, in writing, a gram stain, aerobic and anaero-bic cultures, and antibiotic sensitivity testing
Once the culture specimen is obtained, an incision is made with
a scalpel blade just through the mucosa and submucosa into the abscess cavity (see Fig 16-9) The incision should be short, usually
no more than 1 cm in length Once the incision is completed, a closed curved hemostat is inserted through the incision into the abscess cavity The hemostat is then opened in several directions to break up any small loculations (cavities of pus) that have not been opened by the initial incision Any pus or tissue fluid that drains out during this time should be aspirated into the suction and should not
be allowed to drain into the patient’s mouth If, however, an adequate specimen has not been obtained with aspiration, aerobic and anaero-bic culturette swabs may be carefully introduced into the wound without contaminating the swabs on the surface mucosa Adequate specimens can be obtained in this manner, even if obvious pus is not present in the wound
Once all areas of the abscess cavity have been opened and all pus has been removed, a small drain is inserted to maintain the opening
The most commonly used drain for intraoral abscesses is a inch sterile Penrose drain A frequently used substitute is a small strip
quarter-of sterilized rubber dam or surgical glove material Take care to note any patient sensitivity to latex when selecting the drain material A piece of drain of adequate length to reach the depth of the abscess cavity is prepared and inserted into the cavity using a hemostat The
Figure 16-10 Management algorithm for odontogenic infections (Data from Flynn TR: Deep fascial space infections In Laskin DM, Abubaker AO,
editors: Decision making in oral and maxillofacial surgery, Chicago, IL, 2007, Quintessence.)
Referral tooral andmaxillofacialsurgeon
Inoculationstage
Outpatient therapy
Incision and drainageRemove dental cause extraction
endodontics débridement
Oral antibioticssupportive carecontrol systemic diseasehydration, nutrition
Failure toimprove by72hCellulitis or
abscess stage
Follow-uppreventive andrestorative care
Improvement
by 72h Œtemperature Œfever ŒswellingAssess Severity
airway compromise anatomic location rate of progressionEvaluate Host Defenses medical comorbidities immune compromise systemic reserve
History andphysical examination pain
swelling caries periodontitis pericoronitis
X-ray examination periapical pathosis periodontal bone loss impacted tooth
Odontogenicinfection
Remove dental cause extraction
endodontics débridement
Trang 12should be able to manage their self-care The clinician is responsible
to ensure that patients are provided careful instructions about these important issues
Principle 6: Choose and Prescribe Appropriate Antibiotic
The appropriate antibiotic for treating an odontogenic infection must
be chosen carefully After weighing all factors, the clinician may decide that no antibiotic is necessary at all; in other situations, broad-spectrum or even combination antibiotic therapy may be indicated
A variety of factors must be considered when choosing an antibiotic from the nearly 70 antibiotics currently available Antibiotics must
be viewed as a double-edged sword Although appropriate use may result in dramatic resolution of infections and cure, misuse of anti-biotics provides little benefit to offset the associated risks and expense
of antibiotic administration Studies have shown that even the administration of oral penicillin promotes the growth of penicillin-resistant organisms in the oropharyngeal flora of the patient, the patient’s family, and even the patient’s coworkers or classmates Therefore, the following guidelines are recommended for consider-ation when choosing a specific antibiotic
Determine the need for antibiotic administration A common
misconception is that all infections, by definition, require antibiotic administration This is not necessarily the case In some situations, antibiotics are not useful and may even be contraindicated In making this determination, three factors must be considered: (1) The first factor is the seriousness of the infection when the patient comes to the dentist If the infection has caused swelling, has progressed rapidly, or is diffuse cellulitis, evidence supports the use of antibiotics
in addition to surgical therapy (2) The second consideration is whether adequate surgical treatment can be achieved In many situ-ations, extraction of the offending tooth may result in rapid resolu-tion of the infection Contrary to widely held opinion, extraction of
a tooth in the presence of infection does not promote the spread of infection Several studies have shown that removal of a tooth in the presence of infection hastens the resolution and minimizes the com-plications of the infection, such as time out of work, hospitalization, and the need for extraoral I&D Therefore, prompt removal of the offending tooth (or teeth) in the presence of infection is to be encour-aged; a prior period of antibiotic therapy is not necessary Moreover, when surgery cannot be done immediately, a course of antibiotics does not reliably prevent worsening of the infection In a blinded study of 130 patients presenting to a hospital emergency room with toothache, no significant difference was seen in the progression of infection between the placebo and the antibiotic groups Only the presence of a restoration and a periapical lesion larger than 2 mm predicted subsequent development of spreading infection (3) The third consideration is the state of the patient’s host defenses A young, healthy patient may be able to mobilize host defenses and may not need antibiotic therapy for resolution of a minor infection However, patients who have any type of decreased host resistance, such as those with severe metabolic disease or those receiving cancer chemo-therapy, may require vigorous antibiotic therapy even for minor infections
When these three factors are balanced, several definite indications for antibiotic use in dentistry become clear (Box 16-4) The first
and most common indication is the presence of an acuteonset infection
with diffuse swelling and moderate-to-severe pain This infection is usually in the cellulitis stage; and with appropriate antibiotic therapy, I&D, and treatment of the offending tooth, rapid resolution is expected The second indication is almost any type of infection in a
patient who is immunologically compromised Such patients who have
infections of any severity should be considered candidates for
whether the infection is in the inoculation (edema) stage or if it has
progressed to cellulitis or an abscess In the inoculation stage, the
dental cause of the infection should be treated surgically An
antibi-otic may also hasten resolution of the infection at this stage If the
infection has progressed to cellulitis or an abscess, then an I&D and
the appropriate dental therapy should be performed Sometimes, a
separate I&D is not necessary if the abscess cavity drains completely
through an extraction socket Antibiotic therapy should be used when
complete abscess drainage cannot be achieved by extraction alone
The criteria for referral to an oral-maxillofacial surgeon are
listed in Box 16-2 In summary, in the presence of potential or actual
airway compromise, spread of infection beyond the alveolar process,
medical or immune system compromise, or signs of systemic
in-volvement, immediate referral to an oral-maxillofacial surgeon or, in
life-threatening cases, referral to a hospital emergency room, is
indicated
Principle 5: Support Patient Medically
A patient’s systemic resistance to infection is perhaps the most
impor-tant determinant of a good outcome Host systemic resistance must
be considered in three areas: (1) immune system compromise, (2)
control of systemic diseases, and (3) physiologic reserves
Diseases that compromise the immune system are listed in Box
16-1 Odontogenic infections that occur in patients with immune
system compromise should be treated by a specialist Often,
hospi-talization and medical consultation are required The treatment team
selects therapies designed to enhance the immune response, combat
the infection medically with bactericidal antibiotics, and optimize
surgical management of the infection
Many systemic diseases also reduce the ability of the patient to
resist infection and to undergo treatment In diabetes, for example,
the control of blood sugar is directly correlated with resistance to
infection Host response to a significant infection increases the blood
sugar levels and, therefore, the insulin requirements of a person with
diabetes Moreover, cardiovascular diseases decrease the ability of the
host to respond to the stress of infection and surgery Therefore,
optimizing control of hypertension, cardiac dysrhythmias, and
ath-erosclerotic heart disease is an essential part of the comprehensive
management of odontogenic infections Medications may also affect
the treatment of odontogenic infections For example, the patient
receiving anticoagulant therapy with warfarin (Coumadin) may need
reversal of anticoagulation before surgery can be safely performed
Patients with systemic conditions, especially of the immune,
cardio-vascular, respiratory, hematologic, and metabolic systems, often need
sophisticated medical support from a team of specialists
Even patients without medically compromising diseases may
have reduced or altered physiologic reserves to draw on as they
combat an odontogenic infection Children, for example, are
particu-larly susceptible to dehydration and high fevers Elderly patients,
however, are less able to mount a fever but are susceptible to
dehy-dration Fever increases daily fluid requirements in the adult by about
800 mL/°F/day, and daily caloric requirements by 3% to 5% per
degree Fahrenheit per day However, temperatures up to 103°F may
be beneficial in combating infections Therefore, judicious control of
highly elevated fever, along with active hydration and nutritional
support, are important components of the management of
odonto-genic infections
Because of pain, difficulty swallowing, or both, patients frequently
have not had adequate fluid intake, nutritional intake, or rest During
the immediate post-treatment period, patients should be encouraged
to drink sufficient water or juice so that they urinate regularly and to
take high-calorie nutritional supplements Patients should also be
prescribed adequate analgesics for relief of pain to help them rest
Patients should be given careful postoperative instructions, and they
Trang 13Box 16-6 Effective Orally Administered Antibiotics
Useful for Odontogenic Infections
• Mild pericoronitis (inflammation of the operculum only)
• Drained alveolar abscess
Box 16-4 Indications for Therapeutic Use of Antibiotics
• Swelling extending beyond the alveolar process
antibiotic administration The third indication for antibiotic therapy
is the presence of an infection that has progressed to involvement
of the deep fascial spaces In these situations, the infection is aggressive
enough to have spread beyond the alveolar process of the jaws, indicating that the host defenses are inadequate to contain the infec-
tion The fourth indication is severe pericoronitis, with temperatures
higher than 100°F, trismus, and swelling of the lateral aspect of the face, which occurs most commonly around impacted mandibular third molars Finally, the patient who has osteomyelitis requires antibiotic therapy in addition to surgery to achieve resolution of the infection
On the basis of the same criteria, antibiotic therapy is not cated and is even contraindicated in other situations (Box 16-5) The
indi-first is a minor, chronic, welllocalized abscess, in which case, extraction
of the offending tooth results in complete evacuation of a periapical abscess, provided that the patient’s host defenses are intact and that the patient has no other immunocompromising conditions An example of this is the patient without symptoms and who may require the extraction of teeth with chronic periapical abscesses, a draining parulis, or severe periodontitis A second, similar contrain-
dication is a welllocalized dentoalveolar abscess, with little or no facial
swelling In these situations, endodontic therapy can be performed,
or the tooth can be extracted along with I&D of the swelling on the alveolar process, which will result in rapid resolution in most patients
Third is a localized alveolar osteitis (dry socket) Treatment of the dry
socket is primarily palliative, and dry socket is not treated as an tion Although bacterial pathogens may play a role in the etiology of
infec-a dry socket, the clinicinfec-al problem of infec-alveolinfec-ar osteitis is self-limiting and appears to be caused by premature fibrinolysis (dissolution of a
blood clot) Fourth, patients who have mild pericoronitis with minor
gingival edema and mild pain do not require antibiotics for resolution
of their infection Irrigation with hydrogen peroxide or dine, plus extraction of the partially erupted tooth will result in reso-lution Antibiotics should not be prescribed simply because a patient demands them for a routine toothache or for dental extractions in a patient without any immune system compromise
chlorhexi-In summary, antibiotics should be used when clear evidence exists
of bacterial invasion into deeper tissues that is greater than the host defenses can overcome Patients who have an impaired ability to defend themselves against infection and patients who have infections that are not immediately amenable to surgical treatment should be considered for antibiotic therapy Antibiotics should not be used when no evidence of bacterial invasion of deeper tissues is found Antibiotics do not hasten wound healing and do not provide any benefit for nonbacterial (e.g., viral) conditions Patients who have inflammatory pulpitis have severe pain, but the pain results from the local inflammatory reaction within the pulp, not from bacterial infec-tion spreading into deeper tissues These patients should not rou-tinely be given antibiotic therapy
Use empirical therapy routinely Odontogenic infections are
caused by a highly predictable group of bacteria, and the antibiotic sensitivity of these organisms is well known and consistent As a result, the use of culture and sensitivity (C&S) testing is not necessary for routine odontogenic infections The bacteria that cause odonto-genic infections are overwhelmingly facultative oral streptococci;
anaerobic streptococci, including Parvimonas micra (formerly Pepto
streptococcus micros); and Prevotella and Fusobacterium species Other
species of bacteria may also be cultured from these infections, but they appear to be opportunistic rather than causative Fortunately, the antibiotic susceptibility of causative bacteria is fairly predictable Orally administered antibiotics that are effective against odontogenic infections include penicillin, amoxicillin, clindamycin, azithromycin, metronidazole, and moxifloxacin (Box 16-6) A recent systematic review of randomized clinical trials comparing penicillin or amoxicil-lin with newer antibiotics found that when appropriate dental surgery was done, none of newer antibiotics had a significantly greater clini-cal cure rate than amoxicillin or penicillin
The antibiotics mentioned above (except metronidazole) are effective against aerobic and facultative streptococci, and oral anaer-obes Metronidazole is effective only against obligate anaerobic bac-teria, but the effectiveness of this antibiotic class in odontogenic infections has been shown in a prospective study Several important variations can be found among these antibiotics (See Appendix VI for a detailed description of the various antibiotics.)
Because the microbiology and antibiotic sensitivity of oral gens are well known, it is a reasonable therapeutic maneuver to use one of these antibiotics empirically, that is, administer the antibiotic
patho-on the assumptipatho-on that it is the appropriate drug The drug of choice
is usually penicillin Alternative drugs for use in penicillin-allergic patients are clindamycin and azithromycin Metronidazole is useful only against anaerobic bacteria and should be reserved for a situation
in which only anaerobic bacteria are identified, in combination with
an antibiotic that has antiaerobic activity, such as penicillin, or when other antibiotics are contraindicated
Clearly, patients frequently fail to take the medication correctly
as prescribed In fact, Socrates, in 400 bc, cautioned physicians to
be aware that patients will lie about taking their prescribed medications
Trang 14Reliable data from many studies demonstrate that patient
compli-ance decreases with increasing numbers of pills per day When it is
necessary to take the prescription once daily, patient compliance is
approximately 80% However, when it is necessary to take the pill
two times daily, compliance decreases to 69%, and drops even further
to 35% for four times daily Therefore, if the clinician has a
reason-able choice, he or she should prescribe antibiotics that need to be
taken the fewest times daily to improve patient compliance
For example, amoxicillin and clindamycin are usually taken three
times daily instead of four times daily (as is penicillin) Azithromycin
is taken twice a day, instead of four times daily (as is erythromycin)
Moxifloxacin is taken once daily Thus, when other important factors
such as antibacterial effectiveness, side effects, drug interactions, and
cost are reasonably equal, a drug that needs to be taken less
fre-quently is preferable As discussed subsefre-quently, however, significant
differences exist among these antibiotics in their side effects, drug
interactions, and cost
Routine C&S testing is not cost-effective in the treatment of
routine odontogenic infections However, in some cases, the dentist
should seriously consider sending a specimen for C&S testing (see
Box 16-3) The first case is the rapid onset of severe infection and its
rapid spread Delay in bacterial identification may have disastrous
consequences in this situation; therefore, culturing early in the
clini-cal course is indicated The second case is postoperative infection If
a patient had no signs of infection when the original surgery was
done but returns 3 or 4 days later with an infection, the chances of
nonindigenous bacteria causing the infection are higher Precise
iden-tification of the causative bacteria early on may facilitate the timely
administration of the appropriate antibiotic and, thus, the resolution
of the infection The third case is an infection that does not resolve
as expected In these situations, the clinician should make every effort
to obtain a specimen of pus or tissue fluid for C&S testing The fourth
case is a recurrent infection When the initial infectious problem has
resolved and an infection-free period of 2 days to 2 weeks followed
by a second infection occurs, the probability is high that the infection
is caused by bacteria that are resistant to the previously used
antibi-otic The fifth case is the patient who has compromised host defenses
Patients with immune system compromise have a propensity to
harbor unusual pathogens that can be identified by C&S testing
In the foreseeable future, conventional C&S testing may be
replaced by molecular methods that are currently used only in
research Bacteria can be identified even after they die from their
genetic material, using the polymerase chain reaction to amplify tiny
amounts of bacterial deoxyribonucleic acid (DNA) and ribonucleic
acid (RNA) Single-stranded nucleic acids from an unknown sample
can be hybridized to single-stranded genes from known species,
which would lead to a positive identification of infecting bacteria
These methods have identified the involvement of a large number of
unculturable pathogens in odontogenic infections, the presence of
which was only suspected in the past In the future, these methods
may be able to detect antibiotic-resistance genes directly as well,
which would make it possible to provide a prompt diagnosis of the
infecting species and their antibiotic sensitivity patterns
Use the narrowest-spectrum antibiotic When an antibiotic is
administered to a patient, most of the susceptible bacteria are killed
If the antibiotic is a narrow-spectrum antibiotic, it kills bacteria of a
narrow range For example, penicillin will kill streptococci and oral
anaerobic bacteria but will have little effect on the staphylococci of
the skin and almost no effect on gastrointestinal (GI) tract bacteria
As a result, penicillin has little or no effect on the GI tract and does
not facilitate a multitude of other bacteria developing resistance By
contrast, drugs such as amoxicillin-clavulanate (Augmentin) are
broad-spectrum antibiotics, inhibiting not only streptococci and oral
anaerobes but also a variety of staphylococci and enteric
gram-negative rods Thus, when this antibiotic is given, it has an effect on
Box 16-8 Simple and Complex Odontogenic Infections
Simple Odontogenic Infections
• Swelling limited to the alveolar process and vestibular space
• First attempt at treatment
• Patient who is not immunocompromised
Complex Odontogenic Infections
• Swelling extending beyond the vestibular space
• Failed prior treatment
altera-The ADA’s Council on Scientific Affairs has issued guidelines, which are based on a review of the available scientific literature, recommending that dentists use only narrow-spectrum antibiotics to treat simple infections A list of narrow-spectrum and broad-spectrum antibiotics is provided in Box 16-7 Broad-spectrum antibiotics may
be used for complex infections, which are not defined in the ADA advisory statement Nonetheless, a simple odontogenic infection can
be defined as one involving only the alveolar process or the oral vestibule, in its first course of treatment, and in an immunocompe-tent individual A complex infection may be defined as one that has spread beyond the alveolar process and oral vestibule, with prior treatment failures, or in an immunocompromised patient The char-acteristics of simple and complex odontogenic infections are differ-entiated in Box 16-8
In summary, antibiotics that have narrow-spectrum activity against causative organisms are just as effective as antibiotics that have broad-spectrum activity, but without upsetting normal host microflora populations and increasing the chances of bacterial resistance With appropriate surgery, an appropriate choice can be made from among the commonly used antibiotics on the basis of safety, cost, and the medical history of the patient
Use the antibiotic with the lowest incidence of toxicity and side effects Most antibiotics have a variety of toxicities and side
effects that limit their usefulness These range from mild ones to side effects that are so severe that the antibiotic causing them cannot be used in clinical practice The older-generation antibiotics usually used for odontogenic infections have a surprisingly low incidence of
Trang 15toxicity-related problems The newer-generation antibiotics, however, may have significant toxicities and drug interactions Therefore, it is becoming increasingly important for the clinician to understand the toxicities, side effects, and drug interactions of the drugs he or she may prescribe.
Allergy is the major side effect of penicillin Approximately 2% or 3% of the total population is allergic to penicillin Patients who have allergic reactions to penicillin, as exhibited by hives, itching, or wheezing, should not be given penicillin again Penicillin does not have other major side effects or toxicities in the normal dose range used by dentists
Likewise, azithromycin and clindamycin have a low incidence of toxicity and side effects Clindamycin may cause severe diarrhea,
called pseudomembranous colitis or antibioticassociated colitis Several
other drugs such as ampicillin and oral cephalosporins also cause this problem However, with clindamycin and other antibiotics, this problem is usually confined to severely ill and debilitated patients and is rare in other patients The elimination of much of the anaero-bic gut flora allows the overgrowth of another antibiotic-resistant
bacterium, Clostridium difficile This bacterium produces toxins that
injure the gut wall, which results in colitis Patients who take mycin, amoxicillin, or cephalosporins should be warned of the pos-sibility of profuse watery diarrhea and should be told to contact their prescribing dentist if it occurs
clinda-Among the new members of the macrolide (erythromycin) family, azithromycin has the best combination of effectiveness, low toxicity, and infrequent drug interactions Erythromycin is no longer consid-ered effective against the oral pathogens, and it shares with clarithro-mycin the propensity to cause drug interactions involving the liver microsomal enzyme system
Moxifloxacin is a new member of the fluoroquinolone class of antibiotics that has much better effectiveness against the oral patho-gens compared with older members of this class However, it has significant toxicities, including muscle weakness and mental cloud-ing, and serious, potentially fatal drug interactions with many com-monly used drugs Moxifloxacin is also contraindicated in children under 18 years and pregnant females because of interference with the growth of cartilage As a new antibiotic, moxifloxacin is expensive
Moxifloxacin should be reserved for use by specialists treating severe, recalcitrant infections for which no other effective drug is available
Oral cephalosporins such as cephalexin and cefadroxil have lost much of their effectiveness in treating odontogenic infections These antibiotics are no longer commonly used for treating odontogenic infections, even though they are associated with only mild toxicity problems As with penicillin, the cephalosporins may cause allergic reactions Cephalosporins should be given cautiously to patients with penicillin allergies because these patients may also be allergic to cephalosporins Patients who have experienced an anaphylactic type
of reaction to penicillin should not be given a cephalosporin because
of increased chance for that life-threatening event to recur
Tetracyclines, like cephalosporins, are no longer considered useful for treating odontogenic infections, except when they are used topi-cally in very high local concentrations, such as when they are inserted into periodontal pockets They have minor toxicities for most patients (i.e., the commonly encountered GI problems of nausea, abdominal cramping, and diarrhea) Some patients may experience photosensi-tivity while they are taking this drug systemically and should be warned to stay out of the sun Finally, tetracyclines when taken by pregnant women may produce tooth discoloration in their infants when taken by those who are in the tooth development stages of their lives (under 12 years of age) In the latter case, the discoloration is the result of chelation of the tetracycline to calcium, which results in incorporation of the tetracycline into developing teeth
Metronidazole has mild toxicities, the most prominent being the typical GI disturbances discussed previously The drug may also
produce a disulfiram effect; that is, the patient taking metronidazole who also consumes ethanol may experience sudden, violent abdomi-nal cramping and vomiting
Use a bactericidal antibiotic, if possible Antibiotics may kill
bacteria (i.e., bactericidal antibiotics) or interfere with their growth (i.e., bacteriostatic antibiotics) Bactericidal antibiotics usually inter-fere with cell wall production in newly forming, growing bacteria The resultant defective cell wall is not able to withstand the osmotic pressure differential between the cytoplasm and the environment, and the bacterial cells lyse (i.e., die) The antibiotic actually kills the bacteria, so the white blood cells, complement, and antibodies of the host play a less important role in fighting the bacteria
Bacteriostatic antibiotics interfere with bacterial reproduction and growth This slowing of bacterial reproduction allows host defenses
to move into the area of infection, phagocytize the existing bacteria, and kill them Bacteriostatic antibiotics require reasonably intact host defenses This type of antibiotic should be avoided in patients who have compromised host defense systems
For patients with compromised host defenses, bactericidal otics should be the drugs of choice For example, the bactericidal antibiotic penicillin would be preferred over the bacteriostatic antibiotic azithromycin in a patient who is receiving cancer chemotherapy
antibi-Be aware of the cost of antibiotics Antibiotics vary widely in
cost to patients Newer-generation drugs tend to be more expensive, whereas older-generation drugs, which are made by a variety of com-panies, tend to be less expensive Generic drugs also tend to be less expensive than their brand-name counterparts Generic equivalents for the newer-generation drugs are not available When other factors are equal, the clinician should prescribe the less expensive antibiotic
Table 16-4 provides a cost comparison among commonly used antibiotics
Summary Antibiotics should be used to assist the dentist in
treating patients with infections that are spreading beyond the lar processes of the jaws and to prevent endocarditis or infection of prosthetic-implanted devices arising from bacteremia induced by dental manipulations Surgical treatment of the infection remains the primary method of treatment in most patients; antibiotic therapy plays an adjunctive role Antibiotics are especially important in patients who have infections that are spreading beyond the alveolar process and in patients with compromised host defense mechanisms When antibiotic therapy is to be used for treating a routine odonto-genic infection, empiric antibiotic therapy with a narrow-spectrum antibiotic is recommended because the microbiology of odontogenic infections is well known and usually consistent from patient to patient The antibiotic of choice for odontogenic infections is still
alveo-a penicillin The penicillins halveo-ave been shown to be alveo-as effective alveo-as other antibiotics in several prospective studies and systematic reviews Penicillins are bactericidal; have a narrow spectrum of action against pathogens, including streptococci and oral anaerobes, which are responsible for odontogenic infections; have low toxicity; and are inexpensive Among penicillins, amoxicillin may be preferable to penicillin V because the dosage is less frequent, which increases compliance with the prescribed regimen, and its cost is often slightly lower than that of penicillin V
Although about 25% of Prevotella strains are resistant to
penicil-lins, when used in conjunction with adequate surgery, they almost always result in cure Amoxicillin-clavulanate (Augmentin) is a broad-spectrum penicillin that should be reserved for complex infections
Amoxicillin may be used for prophylaxis of endocarditis and late prosthetic joint infections, according to the formal guidelines of the ADA in conjunction with the AHA and the American Academy of Orthopaedic Surgeons (AAOS) An alternative drug is azithromycin, which is a useful medication for patients who are allergic to
Trang 16Table 16-4 Cost Comparison of Orally Administered Antibiotics
Antibiotic Usual Dose Usual Interval Weekly Retail Cost, 2011** Amoxicillin Cost Ratio
Usual doses and intervals are for moderate infections and are not to be considered prescriptive.
Amoxicillin Cost Ratio = Retail Cost of Antibiotic for 1 week/Retail Cost of Amoxicillin for 1 week.
**Retail Cost/1 week = Retail price charged for a 1-week prescription at a large national pharmacy chain (Courtesy of Tricia McKinley, CHPT and Rachel Ouellette, CHPT.)
penicillin Clindamycin is also a useful alternative for patients with
penicillin allergy or in special situations in which resistant anaerobic
bacteria are suspected Metronidazole may be useful, especially when
anaerobic bacteria are suspected It may be used in combination with
another antibiotic that kills facultative and aerobic oral pathogens
Because of the need to limit the development of resistance and
because of its toxicities and drug interactions, moxifloxacin should
be restricted to prescription by only specialists in the treatment of
severe infections
Principle 7: Administer Antibiotic Properly
Once the decision is made to prescribe an antibiotic to the patient, the drug should be administered in the proper dose and at the proper dose interval The manufacturer usually recommends the proper dosage and administration Provision of plasma levels that are suf-ficiently high to kill the bacteria that are sensitive to the antibiotic but are not so high as to cause toxicity is adequate The peak plasma level of the drug should usually be at least four or five times the
Trang 17present Dental implants are increasingly common foreign bodies, and the ability of bacteria to find shelter from the immune system
in the surface gaps and irregularities of an implant can perpetuate the infection until the implant is successfully débrided or removed.Finally, the antibiotic that was given to the patient may be prob-lematic The dentist first ascertains whether the patient has been compliant with the dose regimen The patient must have the prescrip-tion filled and must take the antibiotic according to directions Many patients fail to follow the instructions of their dentists as carefully as they should Sometimes, a patient may not have the prescription filled because he or she cannot afford it The dentist should use the most cost-effective antibiotic available and should directly ask the patient whether or not a particular prescription is affordable Another problem to consider is whether the antibiotic reached the infected area The penetration of antibiotics into abscess cavities is poor Failure of the antibiotic to reach the area may be related to inade-quate surgery or drainage, inadequate blood supply to the local area,
or a dose that is too low to be effective against the bacteria Another antibiotic-related problem is incorrect identification of causative bac-teria If a culture was not performed at the initial surgical treatment
or if no surgical treatment was done at the initial therapy, the dentist should obtain a specimen for C&S testing Finally, it is possible that the wrong antibiotic was prescribed for the infection, which may be because of inaccurate identification of bacteria or the increasing anti-
biotic resistance of oral bacteria For example, 25% to 35% of Pre
votella organisms are resistant to penicillin but rarely cause persistent
infection if penicillin is given and adequate surgery is done However,
if the patient has a persistent, low-grade infection that does not resolve despite adequate surgery, prescribing an antianaerobic anti-biotic such as clindamycin is appropriate
The clinician must also examine the patient to look specifically for toxicity reactions and untoward side effects Patients may report complaints such as nausea and abdominal cramping but may fail to associate watery diarrhea with the drug Specific questions with regard to expected toxicities is important to their early recognition.The dentist should also be aware of the possibility of secondary infections or superinfections The most common secondary infection encountered by dentists is oral or vaginal candidiasis This is the
result of an overgrowth of Candida organisms because the normal
flora has been altered by the antibiotic therapy Other secondary infections may arise as normal host flora is altered, but they are not seen with significant frequency in the management of odontogenic infections
Finally, the dentist should monitor the patient carefully once the infection has resolved to check for recurrent infection Recurrence would be seen in a patient who had incomplete therapy for the infec-tion A variety of factors may account for this For example, the patient may have stopped taking the antibiotic too early The drain may have been removed too early, allowing the drainage site to seal too early and re-establishing the infectious process If infection does recur, surgical intervention and reinstitution of antibiotic therapy should be considered
PRINCIPLES OF PREVENTION OF INFECTION
The use of antibiotics to treat an established infection is a accepted and well-defined technique These drugs provide major assistance for the patient in overcoming an established infection The use of antibiotics for prevention (i.e., prophylaxis) of infection is less widely accepted The final section of this chapter discusses the use of antibiotics for prophylaxis of two distinct types of infection The use
well-of antibiotics to prevent wound infection after surgery is presented first, followed by a discussion of antibiotic use to prevent metastatic infection
minimal inhibitory concentration for the bacteria involved in the infection
Clearly, some patients stop taking their antibiotics after acute symptoms have subsided and rarely take their drugs as prescribed after 4 or 5 days Therefore, the antibiotic that would have the highest compliance would be the drug that could be given once a day for not more than 4 or 5 days Studies have shown that for odontogenic infections a 3- or 4-day course of a penicillin, combined with appropriate surgery, has been as effective as a 7-day course of the antibiotic
At the clinical follow-up examination, additional prescription of antibiotics may be necessary in the case of infections that do not resolve rapidly The clinician must make it clear to the patient that the entire prescription must be taken If for some reason the patient
is advised to stop taking the antibiotic early, all remaining pills or capsules should be discarded Patients should be strongly discour-aged from keeping small amounts of unused antibiotics to self-treat
a sore throat next winter Casual self-administration of antibiotics is not only useless, but also may be hazardous to the health of the individual as well as that of the community
Principle 8: Evaluate Patient Frequently
After surgery and antibiotic therapy, the patient should be carefully monitored for response to treatment and complications In most situ-ations, the patient should be asked to return to the dentist 2 to 3 days after completion of the original therapy Typically, the patient is seen
to be much improved If therapy had been successful, swelling and pain would have decreased dramatically The dentist should check the I&D site to determine whether the drain should be removed at this time Other parameters such as body temperature, trismus, swell-ing, and the patient’s subjective feelings of improvement, should also
be evaluated
If response to treatment is not satisfactory, the patient should be examined carefully for clues to the reason for failure (Box 16-9) The most common cause of treatment failure is inadequate surgery A tooth may have to be re-evaluated for extraction, or an extension of the infection into an area not detected during the first treatment may have to be incised and drained It may be necessary to admit such a patient to the hospital for purposes of airway security, further surgery, and intravenous antibiotic therapy
A second reason for failure is depressed host defense mechanisms
A review of the patient’s medical history should be performed, and more careful, probing questions should be asked In addition to immunocompromising diseases, conditions that diminish physio-logic reserves, for example, dehydration, malnutrition, and pain, should also be considered and corrected, if necessary
A third reason for treatment failure is the presence of a foreign body Although this is unlikely in an odontogenic infection, the dentist may consider taking a careful history and a periapical radio-graph of the area to ensure that a radiopaque foreign body is not
Box 16-9 Reasons for Treatment Failure
• Drug not reaching site
• Drug dose too low
• Wrong identification of bacteria
• Wrong antibiotic
Trang 18PRINCIPLES OF PROPHYLAXIS OF
WOUND INFECTION
On the one hand, the use of antibiotics for prophylaxis of
postopera-tive wound infections may be effecpostopera-tive and desirable in certain
situations On the other hand, little scientific evidence supports
the effectiveness of prophylactic antibiotics in dentistry and
oral-maxillofacial surgery If, however, prophylactic antibiotics are
effec-tive in preventing postoperaeffec-tive wound infections and bloodborne
infections of distant sites, they would have three distinct advantages:
(1) Prophylactic antibiotics may reduce the incidence of
postopera-tive infection and, thereby, reduce postoperapostopera-tive morbidity When a
patient becomes infected after surgery, wound healing and recovery
are substantially delayed (2) Appropriate and effective antibiotic
prophylaxis may reduce the cost of health care By decreasing the
incidence of postoperative infection, the patient can be saved the
expense of returning to the dentist, buying more antibiotics, and
missing additional days of work Third, appropriate use of
prophy-lactic antibiotics requires a shorter-term administration, rather than
therapeutic use, thus possibly decreasing the total amount of
antibi-otics used by the population
On the other hand, when they are used inappropriately,
prophy-lactic antibiotics are, actually in fact, associated with an increased risk
of postoperative infection, typically by a bacterium resistant to these
prophylactic antibiotics The use of prophylactic antibiotics has
several other disadvantages, as discussed earlier First, they may alter
host flora The body is populated with a variety of bacteria that have
a symbiotic relationship with the host When antibiotics are
admin-istered, some of these bacteria are eliminated, allowing the
over-growth of antibiotic-resistant and perhaps more pathogenic bacteria
that may then cause infection Second, as several studies have shown,
antibiotic administration in one patient allows antibiotic-resistant
organisms to spread to the patient’s family and to the community
Third, in certain situations, the risk of infection is so low that the
antibiotic does not significantly decrease the incidence of infection
Fourth, the use of prophylactic antibiotics may encourage lax surgical
and aseptic techniques on the part of the dentist The attitude of, “Oh
well, the patient is on antibiotics,” is an unacceptable excuse when
the principles of atraumatic tissue handling and surgical asepsis are
violated Fifth, the cost of the antibiotic must be considered Although
the cost for a single event for a single patient may be small, the cost
for many surgeries for many patients can be enormous Finally, the
toxicity of the drug to the patient must be also kept in mind All drugs
have the potential to cause injury to the patient Although most
antibiotics used by dentists have low toxicity, the possibility of
toxic-ity is always present The principles of prophylactic antibiotic use are
summarized in Box 16-10
Principle 1: Procedure Should Have
Significant Risk of Infection
To justify the prophylactic administration of antibiotics to reduce the
incidence of infection, the surgical procedure must have a high
Box 16-11 Factors Related to Postoperative Infection
• Size of bacterial inoculum
• Duration of surgery
• Presence of foreign body, implant, or dead space
• State of host resistance
Box 16-10 Principles of Prophylactic Antibiotic Use
• Find out if the risk of infection is significant
• Choose the correct narrow-spectrum antibiotic
• Confirm that the antibiotic level is high
• Ensure that the antibiotic is in the target tissue before surgery
• Use the shortest effective antibiotic exposure
enough incidence of infection Clean surgery done with strict ence to basic surgical principles usually has an incidence of infection
adher-of about 3% Infection rates adher-of 10% or more are usually considered unacceptable, and the prophylactic use of antibiotics must be strongly considered for such infection-prone procedures For the dentist doing routine office surgery, this means that most office procedures per-formed on healthy patients do not require prophylactically adminis-tered antibiotics The incidence of infection after tooth extraction, frenectomy, biopsy, minor alveoloplasty, and torus reduction is extremely low; therefore, antibiotics would provide no benefit This
is true even in the presence of periapical infection, severe titis, and multiple extractions
periodon-However, several surgical factors may influence the dentist to strongly consider the use of antibiotic prophylaxis (Box 16-11): The first and most obvious factor that may lead to infection is a bacterial inoculum of sufficient size The usual surgical procedure performed
in the mouth rarely involves sufficient bacterial inoculation to cause infection unless an acute infection with cellulitis or an abscess is already present The second factor is surgery that involves a pro-longed procedure In hospital surgeries, the incidence of postopera-tive infection increases significantly with operations lasting longer than 4 hours A third factor that may prompt the use of antibiotics
is the insertion or presence of a foreign body, most commonly a dental implant Most data seem to suggest that the use of antibiotics may decrease the incidence of infection when foreign bodies such as dental implants are inserted into the jaws
The final and most important factor for most dentists in ing which patients should receive prophylactic antibiotics is whether the patient’s host defenses are depressed Patients who have a com-promised ability to defend themselves against infection should receive antibiotics prophylactically because they are likely to have a higher incidence of more severe infection All patients receiving cancer chemotherapy or immunosuppressives should receive anti-biotics prophylactically, even when minor surgical procedures are performed Patients receiving immunosuppressives for organ trans-plantation will be taking these drugs for the remainder of their lives and should be given preventive antibiotics accordingly Patients receiving cancer chemotherapy will receive cytotoxic drugs for 1 year
determin-or less, but should be given antibiotics prophylactically fdetermin-or at least a 1-year period after the cessation of their chemotherapy This is also advisable for those receiving radiation therapy to the jaw Patients with end-stage renal disease, including those receiving kidney dialy-sis, are immunocompromised and require antibiotic prophylaxis for oral surgical procedures
The most common immunocompromising disease, however, is diabetes mellitus The incidence of postoperative infection in persons with diabetes is directly correlated with elevations of blood sugar The oral surgical management of persons with diabetes based on their blood glucose is summarized in Table 16-5 The glycosylated hemoglobin test, or hemoglobin A1c, is a good measure of the level
of diabetes control over the previous 3 to 4 months Before complex reconstructive oral-maxillofacial surgery such as the placement of dental implants, the dentist is wise to ensure that acceptable intermediate-term control of blood glucose has been achieved, as measured by a hemoglobin A1c of 7% or less The American Diabetes Association recommends a therapeutic target hemoglobin A1c level
Trang 19is that the drug be given in a dose at least two times the usual peutic dose Use of the same prophylactic doses recommended by the AHA for prophylaxis of infective endocarditis is reasonable For penicillin or amoxicillin, this is 2 g; for clindamycin, 600 mg; and for azithromycin, 500 mg.
thera-Principle 4: Time Antibiotic Administration Correctly
For the antibiotic to be maximally effective in preventing tive infection, the antibiotic must be given 2 hours or less before the surgery begins The time of dosing before surgery varies, depending
postopera-on the route used, allowing for absorptipostopera-on of the antibiotic into tissues at the time of wounding For the oral route, this is usually 1 hour; with the intravenous route, a much shorter preoperative dosing interval is possible This principle has been clearly established in many animal and human clinical trials Antibiotic administration that occurs after surgery is greatly decreased in its efficacy or has no effect at all on preventing infection; evidence indicates that prophy-lactically administered antibiotics given 2 hours or more after surgery may increase the risk of wound infection
If the surgery is prolonged and an additional antibiotic dose is required, intraoperative dose intervals should be shorter (i.e., one half the usual therapeutic dose interval) Therefore, penicillin and clindamycin should be given every 3 hours during prolonged surgery This ensures that the peak plasma levels will stay adequately high and avoids periods of inadequate antibiotic levels in the tissue fluids
Principle 5: Use Shortest Antibiotic Exposure That Is Effective
For the antibiotic prophylaxis to be effective, the antibiotic must be given before the surgery begins, and adequate plasma levels must be maintained during the surgical procedure Once the surgical proce-dure is completed, continued antibiotic administration produces little, if any, benefit If the procedure is a short operation, a single preoperative dose of antibiotics is adequate Considerable amounts
of animal and human clinical data demonstrate that the prophylactic use of antibiotics is necessary only for the time of surgery; after closure of the wounds and formation of the blood clots, migration
of bacteria into the wound and underlying tissues occurs at such a low level that additional antibiotics are not necessary
Summary
The use of antibiotics for prophylaxis of postoperative wound tion may be effective It may reduce patient pain, morbidity, cost, and total antibiotic use Appropriate antibiotic prophylaxis does little to alter host flora Most dental procedures on healthy patients do not require antibiotic prophylaxis A few select patients who are to undergo long surgical procedures or the insertion of foreign bodies such as dental implants should be considered for prophylaxis Patients who have compromised host defenses because of poorly controlled metabolic diseases or certain diseases that interfere with host defenses or who are taking drugs that suppress the immune system should also be given prophylactic antibiotics The drug of choice is a narrow-spectrum antibiotic that is effective against caus-ative organisms, is nontoxic, and is bactericidal Penicillin fits these criteria the best
infec-When the antibiotic is given, it should be taken before the surgery begins, at a normal dose twice that of therapeutically administered antibiotics If the surgery is prolonged, interim doses at half the normal dose interval should be used High plasma levels should be
Table 16-5 Dental Treatment for Patients with Diabetes, Based on Fingerstick Blood Glucose Testing
Finger Stick Blood Glucose (mg/dL%) Dental Treatment
Less than 85 Administer glucose; postpone elective
treatment85–200 Stress reduction; consider antibiotic
prophylaxis for extraction200–300 Stress reduction; antibiotic prophylaxis;
referral to primary care physician300–400 Avoid elective treatment; referral to
primary care physician or emergency room at nearby hospital
Greater than 400 Avoid elective treatment; send to
emergency room at nearby hospital
of 7% or less Withholding dental implant therapy and working with the patient’s physician can help motivate the patient to achieve effec-tive long-term control of diabetes Although prophylactically admin-istered antibiotics are helpful in patients with diabetes, perioperative control of blood sugar levels is paramount
Principle 2: Choose Correct Antibiotic
The choice of antibiotic for prophylaxis against infections after surgery of the oral cavity should be based on the following criteria:
First, the antibiotic should be effective against the organisms most likely to cause infection in the oral cavity As previously discussed, facultative streptococci are usually the originally invading organism
in oral infection Second, the antibiotic chosen should be a spectrum antibiotic
narrow-By using a narrow-spectrum antibiotic, the risk of altering host flora is minimized Third, the antibiotic should be the least toxic antibiotic available for the patient Finally, the drug selected should
be a bactericidal antibiotic Because many of the routine prophylactic uses of antibiotics in the dental office are for patients with compro-mised host defenses, it is important to ensure that the antibiotic effectively kills the bacteria
Taking into account these four criteria, the antibiotic of choice for prophylaxis before oral surgery is penicillin or amoxicillin These two
antibiotics are effective against the causative organism (i.e., Streptococ
cus), have a narrow spectrum of activity, have low toxicity, and are
bactericidal For patients allergic to penicillin, the best choice is clindamycin Clindamycin is a narrow-spectrum antibiotic, fairly effective against oral streptococci, and is bacteriostatic The third choice for oral administration for prophylaxis is azithromycin
Azithromycin, another narrow-spectrum antibiotic, is reasonably effective against the usual organisms, and it is also bacteriostatic
Principle 3: Antibiotic Plasma Level Must
Be High
When antibiotics are used prophylactically, the antibiotic level in the plasma must be higher than when antibiotics are used therapeuti-cally The peak plasma levels should be high to ensure diffusion of the antibiotic into all of the fluid and tissue spaces where the surgery
is going to be performed The usual recommendation for prophylaxis
Trang 20maintained during the surgical procedure, but no additional
antibiot-ics are necessary after surgery
PRINCIPLES OF PROPHYLAXIS AGAINST
METASTATIC INFECTION
Metastatic infection is defined as infection that occurs at a location
physically separate from the portal of entry of the bacteria The classic
and most widely understood example of this phenomenon is
bacte-rial endocarditis, which may arise from bacteria that are introduced
into the circulation as a result of tooth extraction, for example The
incidence of metastatic infection can be reduced if antibiotic
admin-istration is used to eliminate the bacteria before they can establish
an infection at the remote site
For metastatic infection to occur, several conditions must be met
(Box 16-12) The first and most important is a susceptible location
in which an infection can be established An example of this is the
deformed heart valve with its altered endothelial surface onto which
an irregularly surfaced vegetation has formed
Bacterial seeding of the susceptible area must also take place This
seeding occurs as the result of a bacteremia in which bacteria from
the mouth are carried to the susceptible site Most likely, a
quantita-tive factor is involved in this seeding process because the body
experi-ences multiple episodes of small bacteremias as a result of normal
daily activities such as chewing and toothbrushing Turbulent blood
flow across a deformed heart valve can traumatize the endothelial
lining of the valve, which can then precipitate the deposition of
platelets and fibrin, resulting in nonbacterial thrombotic
endocardi-tis (NBTE) Subsequently, bacterial proteins, called adhesins,
recog-nize the fibrin and platelet matrix of NBTE Some staphylococci and
oral streptococci, especially Streptococcus sanguis, Streptococcus mitis,
and Streptococcus oralis, have these adhesins, which explains their
association with infective endocarditis
Also necessary for the establishment of metastatic infection is
some impairment of the local host defenses Once bacteria have
attached to NBTE, they are protected from white blood cell
phagocy-tosis by a thin coating of fibrin and an extracellular matrix
synthe-sized by bacteria, resulting in a biofilm More than 90% of the
bacteria existing within a mature cardiac vegetation are in a
metaboli-cally inactive state, which also renders them less susceptible to
bac-tericidal antibiotics Bacteria inhabiting such a biofilm coating on
foreign bodies such as a prosthetic joint or dental implants are not
easily phagocytized by white blood cells or killed by antibiotics, as
in endocarditis
Prophylaxis Against Infectious Endocarditis
Historically, the rationale for antibiotic prophylaxis of infectious
endocarditis (IE) after dental procedures has been based on the
fol-lowing facts: Bacteremias have been shown to cause IE;
viridans-group streptococci are part of the normal oral flora and have been
commonly found in IE; dental procedures can cause bacteremias
because of Streptococcus viridans; a large number of case reports
associ-ate dental procedures with subsequent IE; S viridans is generally
Box 16-12 Factors Necessary for Metastatic Infection
• Distant susceptible site
• Hematogenous bacterial seeding
• Impaired local defenses
Box 16-13 Cardiac Conditions Associated with the
Highest Risk of Adverse Outcome from Endocarditis for Which Prophylaxis with Dental Procedures Is Recommended
• Prosthetic cardiac valve
• Previous infective endocarditis
• Congenital heart disease (CHD)*
• Unrepaired cyanotic CHD, including palliative shunts and conduits
• Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure†
• Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
• Cardiac transplant recipients who have cardiac valvulopathy
† Prophylaxis is recommended because endothelialization of prosthetic material occurs within 6 months after the procedure.
*Except for the conditions listed above, antibiotic prophylaxis is no longer recommended for any other form of CHD.
susceptible to the antibiotics recommended for prophylaxis of IE; antibiotic prophylaxis has been shown to prevent experimental endo-
carditis caused by S viridans in animals; the risk of significant adverse
reaction to the antibiotic is low in an individual patient, and the morbidity and mortality of IE are high When this occurs, the patient must be treated in the hospital with high doses of intravenous anti-biotics for prolonged periods Often, the damaged native heart valve must be surgically replaced with a prosthetic valve Although initial recovery from bacterial endocarditis approaches 100%, recurrent epi-sodes reduce the 5-year survival rate of patients with this disease to approximately 60%
Recent evidence puts into question the likelihood, however, that prophylactic antibiotics prevent IE in human beings Antibiotics do not consistently prevent bacteremias after dental procedures Bacte-remias after chewing, toothbrushing, and other daily activities occur far more frequently than after dental procedures Endocarditis has been shown to occur despite appropriate antibiotic prophylaxis for dental procedures Only a small proportion of IE cases are from dental procedures, and very few cases of IE would be prevented by antibiotic prophylaxis for dental procedures, even it if were 100% effective
The AHA has had formal recommendations for the prevention of
IE after dental treatments since 1960 The latest formal tions appeared in May 2007 Dentists must stay abreast of revised recommendations as they are published by the AHA and the ADA These new guidelines take into account that a very small number of cases of IE might be caused by dental procedures and might be pre-vented by antibiotic prophylaxis New emphasis has been correctly placed on the establishment and maintenance of optimal oral health
recommenda-in patients with recommenda-increased risk for IE
The new guidelines indicate prophylaxis only for the patients at highest risk of endocarditis, including those with previous endocar-ditis, prosthetic heart valves, cyanotic congenital heart defects that have not been repaired or have remaining partial defects after repair, and heart transplant patients with valvulopathy This will signifi-cantly decrease the number of dental patients for whom prophylaxis
is indicated A list of the conditions that pose the highest risk of endocarditis can be found in Box 16-13
Recent evidence also indicates that the magnitude of bacteremia caused by a given dental procedure is not necessarily correlated with
Trang 21the incidence of IE Therefore, the new guidelines have simplified the description of dental procedures for which antibiotic prophylaxis should be used to the following description: “All dental procedures that involve manipulation of gingival tissue or the periapical region
of teeth or perforation of the oral mucosa” (Box 16-14) Prophylaxis
is not required for routine local anesthetic injections through noninfected tissue, dental radiographs, placement of removable prosthodontic or orthodontic appliances, adjustment of orthodontic appliances, placement of orthodontic brackets, shedding of decid-uous teeth, and bleeding from trauma to the lips or oral mucosa (Box 16-15)
Bacterial endocarditis prophylaxis is achieved for most routine conditions with the administration of 2 g of amoxicillin orally a half hour to 1 hour before the procedure (Table 16-6) Amoxicillin is the drug of choice because it is better absorbed from the GI tract and provides higher and more sustained plasma levels Amoxicillin is an effective killer of viridans-group streptococci, which include the organisms that most commonly cause IE after bacteremias from the oral cavity
For patients who are allergic to penicillin, two alternative drugs have been recommended The first recommended drug is clindamy-cin, with a dose of 600 mg orally 1 hour before surgery If the patient’s allergy to penicillin is mild and not of an anaphylactic type, a first-generation cephalosporin such as cephalexin may be prescribed
Although erythromycin is no longer recommended, the newer rolide antibiotics, azithromycin or clarithromycin, are acceptable alternative drugs If the patient is unable to take oral medication, parenteral administration can be used
mac-For the pediatric patient, the dose of the drugs that are given must
be reduced The recommendations include clear guidelines for proper pediatric dosing (see Table 16-6)
Box 16-15 Dental Procedures in Which Prophylaxis Is
Not Recommended
• Restorative dentistry
• Routine local anesthetic injection
• Intracanal endodontic therapy and placement of rubber dams
• Orthodontic appliance adjustment
• Shedding of primary teeth
Box 16-14 Dental Procedures for Which Endocarditis
Prophylaxis Is Recommended for Patients
of orthodontic appliances, placement of orthodontic brackets, shedding of deciduous teeth, and bleeding from trauma to the lips or oral mucosa.
Table 16-6 Antibiotic Regimens for Prophylaxis of Bacterial Endocarditis
REGIMEN30–60 MIN BEFORE PROCEDURE
Situation Agent Adults Children*
Oral Amoxicillin 2 g 50 mg/kgParenteral Ampicillin 2 g IM or IV 50 mg/kg
IM or IVCefazolin/
ceftriaxone† 1 g IM or IV 50 mg/kg
IM or IVPenicillin
allergy, oral
Cephalexin† 2 g 50 mg/kg
Clindamycin 600 mg 20 mg/kgAzithromycin/
clarithromycin
500 mg 15 mg/kg
Penicillin allergy, parenteral
Cefazolin/
ceftriaxone†
1 g IM or IV 50 mg/kg
IM or IVClindamycin 600 mg IM
or IV
20 mg/kg
IM or IV
*Total children’s dose should not exceed adult dose.
† Cephalosporins should not be used in patients with immediate-type hypersensitivity reaction to penicillins Other first-generation or second- generation oral cephalosporins may be substituted in equivalent adult or pediatric doses.
IM, Intramuscularly; IV, intravenously.
Some patients at risk for bacterial endocarditis may be taking daily doses of penicillin to prevent recurrence of rheumatic fever or may already be taking an antibiotic for other reasons In these patients, the streptococci may be relatively resistant to penicillin The recom-mendation for this situation is that the dentist should use clindamy-cin, azithromycin, or clarithromycin for prophylaxis of endocarditis The cephalosporins should be avoided because of possible cross-resistance with the penicillins If possible, the procedure should be postponed until 10 or more days after the antibiotic is completed, thus allowing a more normal oral flora to be re-established
If a particular patient requires a series of dental treatments that requires antibiotic prophylaxis, a period of 10 or more days between appointments is appropriate The reason for the interval is that the continuous administration of antibiotics for several days or more may promote colonization of the patient by bacteria that are resistant
to the antibiotic being given, thus making prophylaxis more likely to fail The 10-or-more day antibiotic-free period may allow antibiotic-sensitive organisms to repopulate the oral flora However, it has been shown that baseline antibiotic resistance levels are not re-established for several months after a course of antibiotics For this reason, the number of dental visits should also be minimized, consistent with the patient’s tolerance level
Occasionally, unexpected bleeding may occur during dental ment in a patient who is at risk for endocarditis, or a patient may not inform the dentist of the indication for antibiotic prophylaxis before the beginning of the procedure In this situation, appropriate antibi-otic prophylaxis should be administered as soon as possible Prophy-laxis given longer than 4 hours after the bacteremia may have limited prophylactic benefit
treat-Patients at risk for IE should have a comprehensive prophylaxis program that includes excellent oral hygiene with excellent periodic
Trang 22professional care Special care should be taken for the establishment
of an effective preventive program, and all incipient dental and
peri-odontal disease should be treated If surgery is required, the mouth
can be rinsed preoperatively with an antibacterial agent such as
chlorhexidine Preoperative oral antiseptic rinses have been shown to
reduce the magnitude of bacteremias (the number of bacteria
enter-ing the bloodstream), although they are not a substitute for antibiotic
prophylaxis
Finally, it is important for the dentist to understand that even
when appropriate measures are taken to prevent bacterial
endocardi-tis, it may still occur Patients should be informed of this and advised
to return to the dentist or to their primary care physician if any of
the signs and symptoms of bacterial endocarditis, especially fever and
malaise, occur
Prosthetic valve endocarditis occurs when the tissue around the
cardiac valve implant becomes infected Such infections are caused
by the same bacteria that cause typical native valve endocarditis
Prosthetic valve endocarditis is a much more serious illness than
native valve endocarditis because loosening of the heart valve may
result in death The 1-year survival rate for patients who have
pros-thetic valve endocarditis is about 50% The AHA currently states that
the standard oral regimens are adequate for most patients with
pros-thetic heart valves
Prophylaxis in Patients with Other
Cardiovascular Conditions
Several other cardiovascular conditions require the clinician to
con-sider the administration of prophylactic antibiotics for the
preven-tion of metastatic infecpreven-tion In coronary artery bypass grafting
(CABG), the coronary arteries are reconstructed with vascular grafts
Because CABG does not predispose patients to metastatic infection,
these patients should not be given prophylactic antibiotics before a
dental procedure is performed
Patients with a transvenous pacemaker have a battery pack
implanted in their chests, with a thin wire that runs through the
superior vena cava into the right side of the heart These patients do
not require prophylactic antibiotics when dental procedures are
per-formed Similarly, coronary artery angioplasty, with or without stent
placement, is not an indication for endocarditis prophylaxis
Patients receiving renal dialysis frequently have an arteriovenous
shunt surgically constructed in their forearms to provide the dialysis
team ready access to the bloodstream Metastatic infection may occur
in these shunts after bacteremia Therefore, the dentist should contact
the patient’s nephrologist or renal dialysis team to discuss the best
management
Patients who have hydrocephaly may have decompression with
ventriculoatrial shunts Because these shunts may induce valvular
dysfunction, antibiotic prophylaxis may be required Consultation
with the patient’s neurosurgeon should be considered
Patients who have had severe atherosclerotic vascular disease and
have had alloplastic vascular grafts placed to replace portions of their
arteries do not appear to be at risk for metastatic infection from
dental procedures Therefore, the AHA does not recommend
antibi-otic prophylaxis for nonvalvular cardiovascular devices, including
coronary artery stents and vena caval filters The exception to this rule
is for I&D of abscesses at other sites, including the oral cavity
Prophylaxis Against Total Joint
Replacement Infection
Patients who have undergone total replacement of a joint with a
prosthetic joint may be at risk for hematogenous spread of bacteria
and subsequent infection These late prosthetic joint infections result
in severe morbidity because the implant is usually lost when tions occur There has been great concern that the bacteremia caused
infec-by tooth extraction may result in such infections However, the recent literature suggests that bacteremias from oral procedures are not likely to cause prosthetic joint infections It appears that the bactere-mia after oral surgery is of a transient nature and does not expose the implant and periimplant tissues to bacteria long enough to cause infection
Instead it appears that the hematogenous spread of prosthetic joint infections is caused by chronic infections elsewhere in the body that result in chronic septicemias These infections are typically urogenital, gastrointestinal, pulmonary, or skin infections, but established odontogenic infections may also cause a septicemia
of sufficient magnitude to cause a total joint infection
In 2003 the American Dental Association (ADA) and the ican Academy of Orthopaedic Surgeons (AAOS) issued a revised joint recommendation concerning the management of patients with prosthetic total joints In 2009, the American Academy of Ortho-paedic Surgeons issued an advisory statement recommending that all patients with prosthetic joints receive antibiotic prophylaxis before dental procedures, regardless of the length of time following implantation
Amer-This apparent controversy has been resolved by the joint tion of an evidence-based guideline and report that evaluates the currently available scientific evidence on the causation of late pros-thetic joint infections following dental procedures The 3 recom-mendations of the American Dental Association and the American Academy of Orthopaedic Surgeons are:
publica-1. The practitioner might consider discontinuing the practice
of routinely prescribing prophylactic antibiotics for patients with hip and knee prosthetic joint implants undergoing dental procedures (Strength of
Recommendation: Limited)
2. We are unable to recommend for or against the use of topical oral antimicrobials in patients with prosthetic joint implants or other orthopaedic implants undergoing dental procedures (Strength of Recommendation: Inconclusive)
3. In the absence of reliable evidence linking poor oral health to prosthetic joint infection, it is the opinion of the work group that patients with prosthetic joint implants or other orthopaedic implants maintain appropriate oral hygiene (Strength of Recommendation: Consensus)
The report also states: “Practitioners should be cautious in ing whether to follow a recommendation classified as Limited, and should exercise judgment and be alert to emerging publications that report evidence Patient preference should have a substantial influ-encing role.”
decid-The first recommendation is classified as limited because the limited amount of currently available reliable scientific evidence does not substantiate that dental procedures cause late prosthetic joint infections It further does not indicate that antibiotic prophylaxis reliably prevents such infections The limited available data is incon-clusive, but points toward a lack of causation of late prosthetic joint infection by dental procedures Therefore the use of prophylactic antibiotics before dental procedures is not justified by the scientific evidence available to date
The second recommendation is classified as inconclusive because the studies performed to date have come to inconsistent conclusions, from which no clear recommendation can be generated
The third recommendation is based upon the consensus of the expert panel, rather than on any scientific studies
Recently published case series have not found any association between late prosthetic joint infection and dental procedures, whether antibiotic prophylaxis was used or not These studies must
Trang 23be interpreted with caution, however, because they did not guish between prosthetic joint infections caused by oral pathogens and those caused by other pathogens, such as Staphylococcus aureus, the source of which primarily is the skin.
distin-When considering the use of a prophylactic antibiotic in the patient with a prosthetic joint, the clinician must weigh the risk of allergic reaction to the antibiotic, the development of antibiotic resis-tance in the host and in the community, and the cost against the low incidence of prosthetic joint infections, the questionable causation of these infections by dental procedures, and the lack of proven effective-ness of antibiotic prophylaxis in preventing these infections
Until determinative scientific evidence is available, the clinician must use sound judgment in deciding whether to use antibiotic prophylaxis in the patient with a prosthetic joint
When there is disagreement between the dentist, the patient, or the patient’s physician over the need for antibiotic prophylaxis, clear
BIBLIOGRAPHY
ADA Council on Scientific Affairs: Combating
antibiotic resistance JADA 135:484–487,
2004
American Academy of Orthopaedic Surgeons, American Association of Orthopaedic Surgeons: Information statement: Antibiotic prophylaxis for bacteremia in patients with joint replacements Accessed February 28,
2012, from http://www.aaos.org/about/
papers/advistmt/1033.asp.American Academy of Orthopaedic Surgeons, American Dental Association Prevention of orthopaedic implant infection in patients undergoing dental procedures: Evidence-based guideline and evidence report
http://www.ada.org/sections/
professionalResources/pdfs/PUDP_
guideline.pdf; accessed online 12/30/2012
American Dental Association, American Academy of Orthopaedic Surgeons:
Antibiotic prophylaxis dental patients with
total joint replacements J Am Dent Assoc
Conover MA, Kaban LB, Mulliken JB:
Antibiotic prophylaxis for major maxillofacial surgery: One-day vs
five-day therapy Otolaryngology
95:554, 1986
Doern GV, Ferraro MJ, Brueggemann AB, Ruoff KL: Emergence of high rates of antimicrobial resistance among viridans group streptococci in the United States
Antimicrob Agents Chemother 40:891–894,
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Field EA, Martin MV: Prophylactic antibiotics for patients with artificial joints undergoing oral and dental surgery: Necessary or
not? Br J Oral Maxillofac Surg 29: 341–346,
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Flynn TR: What are the antibiotics of choice for odontogenic infections, and how long should the treatment course last?
Oral Maxillofac Surg Clin N Am
23(November):519–536, 2011
Flynn TR, Halpern LR: Antibiotic selection in
head and neck infections Oral Maxillofac
Heimdahl A, Von Konow L, Satoh T, et al:
Clinical appearance of orofacial infections
of odontogenic origin in relation to
microbiological findings J Clin Microbiol
22:299, 1985
Jacobson JJ, Schweitzer SO, Kowalski CJ:
Chemoprophylaxis of prosthetic joint patients during dental treatment: A
decision-utility analysis Oral Surg Oral Med
Oral Pathol 72:167, 1991.
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the polymerase chain reaction and its
clinical application J Oral Maxillofac Surg
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Kuriyama T, Absi EG, Williams DW, Lewis MA:
An outcome audit of the treatment of acute dentoalveolar infection: Impact of
penicillin resistance Br Dent J 198:
759–763, 2005
Kuriyama T, Karasawa T, Nakagawa K, et al:
Antimicrobial susceptibility of major pathogens of orofacial odontogenic infections to 11 beta-lactam
antibiotics Oral Microbiol Immunol
17(5):285–289, 2002
Kuriyama T, Nakagawa K, Karasawa T, et al:
Past administration of beta-lactam antibiotics and increase in the emergence of beta-lactamase-producing bacteria in patients with orofacial
odontogenic infections Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 89:186–192,
2000
Lewis MA, Carmichael F, MacFarlane TW, Milligan SG: A randomised trial of co-amoxiclav (Augmentin) versus penicillin V in the treatment of acute
dentoalveolar abscess Br Dent J 175:
Little JW, Jacobson JJ, Lockhart PB;
American Academy of Oral Medicine: The dental treatment of patients with joint replacements: A position paper from the American Academy of Oral
Medicine J Am Dent Assoc 141(6):
667–671, 2010
Pallasch TJ: Antibiotic prophylaxis: Problems
in paradise Dent Clin N Am 47:665–679,
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Paterson SA, Curzon MEJ: The effect of amoxicillin versus penicillin V in the treatment of acutely abscessed primary
Peterson LJ: Contemporary management of
deep infections of the neck J Oral
Sakamoto H, Kato H, Sato T, Sasaki J:
Semiquantitative bacteriology of closed
odontogenic abscesses Bull Tokyo Dent Coll
39:103–107, 1998
Sclar DA, Tartaglione TA, Fine MJ: Overview
of issues related to medical compliance with implications for outpatient management of
infectious disease Infect Agents Dis
3:266, 1994
communication between all parties is required to clarify all relevant facts, the recommendations of professional associations, and scien-tific data and to arrive at a consensus Ultimately, the dentist is responsible for his or her own treatment decisions and should not render care that he or she thinks is not in the best interest of the patient
If a patient who has a total joint replacement needs treatment of
an established odontogenic infection, aggressive therapy for the infection is necessary to prevent seeding of the bacteria into the prosthesis, causing odontogenic infection of the prosthetic joint This aggressive treatment should include extraction, I&D, and the use of high-dose bactericidal antibiotics, possibly given IV The clinician should strongly consider performing C&S testing because if a pros-thetic joint infection does occur, it would be useful to know which bacteria are likely the causative organisms along with their antibiotic sensitivity
Trang 24Takai S, Kuriyama T, Yanagisawa, et al:
Incidence and bacteriology of
bacteremia associated with
various oral and maxillofacial
surgical procedures Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 99:292–298,
2005
Wilson W, Taubert KA, Gewitz M, et al:
American Heart Association:
Prevention of infective endocarditis:
Guidelines from the American Heart Association: A guideline from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease
Committee, Council on Cardiovascular Disease in the Young, and the Council
on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group
J Am Dent Assoc 139(Suppl):3S–24S, 2008.
Trang 25this becomes a vestibular or a deeper fascial space abscess is mined primarily by the relationship of the attachment of the nearby muscles to the point at which the infection perforates the bony corti-cal plate Most odontogenic infections penetrate the facial cortical plate of bone to become vestibular abscesses On occasion, infections erode into other deep fascial spaces directly (Fig 17-1) Fascial spaces are fascia-lined tissue compartments filled with loose, areolar con-nective tissue that can become inflamed when invaded by microor-ganisms The resulting process of inflammation passes through stages that are seen clinically as edema (inoculation), cellulitis, and abscess
deter-In healthy persons, the deep fascial spaces are only potential spaces that do not exist The loose areolar tissue within these spaces serves
to cushion the muscles, vessels, nerves, glands, and other structures that it surrounds and to allow relative movement between these structures During an infection, this cushioning and lubricating tissue has the potential to become greatly edematous in response to the exudation of tissue fluid and then to become indurated when poly-morphonuclear leukocytes, lymphocytes, and macrophages migrate from the vascular space into the infected interstitial spaces Ulti-mately, liquefactive necrosis of white blood cells and this connective tissue leads to abscess formation, and spontaneous or surgical drain-age typically leads to resolution This is the pathophysiology of the stages of infection that clinicians see as edema, when bacteria inocu-late the tissues of a particular anatomic space; cellulitis, when an intense inflammatory response causes all of the classic signs of inflammation and abscess, when small areas of liquefactive necrosis coalesce centrally to form pus within tissues
On the basis of the relationship between the point at which the infection erodes through alveolar bone and surrounding muscle attachments, infections arising from any maxillary or mandibular tooth can cause vestibular, buccal, or subcutaneous space infections Infections passing beyond the alveolar process on the deep (toward the oral cavity) side of the nearby muscle of facial expression invade the vestibular space, and those that enter soft tissue on the superficial (toward skin) side of those muscles enter the buccal or the subcutane-ous space Infections arising from maxillary teeth also tend to spread into the infraorbital, palatal, orbital, and infratemporal spaces, and the maxillary sinus (Box 17-1) Mandibular dental infections also tend to spread into the submandibular, sublingual, submental, and
Odontogenic infections are usually mild and readily treated with the
appropriate surgical procedure with or without supplemental
antibi-otic therapy Infections that spread beyond teeth into the oral
vesti-bule are usually managed by intraoral incision and drainage (I&D)
procedures, as well as dental extraction, root canal therapy, or
gin-gival curettage, as appropriate The principles of management of
routine odontogenic infections are discussed in Chapter 16 Some
odontogenic infections are serious and require management by
oral-maxillofacial surgeons, who have extensive training and experience
in this area Even after the advent of antibiotics and improved dental
health, serious odontogenic infections still sometimes result in death
These deaths occur when the infection reaches areas distant from the
alveolar process The purpose of this chapter is to present an overview
of deep fascial space infections of the head and neck originating in
teeth, as well as several less common but important infections of the
oral cavity
DEEP FASCIAL SPACE INFECTIONS
The pathways of odontogenic infection extending from the teeth
through bone and into surrounding soft tissues are discussed in
Chapter 16 As a general rule, infection erodes through the thinnest
adjacent bone and causes infection in the adjacent tissue Whether
Complex Odontogenic Infections
Thomas R. Flynn
Trang 26Table 17-2 lists the likely causative teeth, contents, neighboring spaces into which infection may spread, and surgical approaches for drainage of the more commonly infected deep fascial spaces of the head and neck.
Infections Arising from Maxillary Teeth
Because the apices of upper lateral incisors and the palatal roots of upper premolars and molars are closest to the palatal cortical plate, infection arising from these teeth can erode through bone without perforating the periosteum The potential subperiosteal space in the palate is the palatal space
The infraorbital space is a thin potential space between the levator anguli oris and the levator labii superioris muscles The infraorbital space becomes involved primarily as the result of infections from the maxillary canine tooth or by extension of infections from the buccal space The canine root is often sufficiently long to allow erosion to occur through the alveolar bone that is superior to the origin of the levator anguli oris and below the origin of the levator labii superioris muscle When this space is infected, swelling of the anterior face obliterates the nasolabial fold (Fig 17-5) Spontaneous drainage of infections of this space commonly occurs near the medial or the lateral canthus of the eye because the path of least resistance is to either side of the levator labii superioris muscle, which attaches along the center of the inferior orbital rim
The buccal space is bounded by the overlying skin of the face on the lateral aspect and the buccinator muscle on the medial aspect
Figure 17-1 As infection erodes through bone, it can express itself in
a variety of places, depending on thickness of overlying bone and
relationship of muscle attachments to site of perforation This illustration
notes six possible locations: vestibular abscess (1), buccal space (2),
palatal abscess (3), sublingual space (4), submandibular space (5), and
maxillary sinus (6). (Adapted from Flint PW Haughey BH, Lund VJ et al,
editors: Cummings otolaryngology: Head and neck surgery, ed 5,
Philadelphia, PA, 2010, Mosby.)
MylohyoidmusclePlatysmamuscle
Buccinator
muscle
2
211
5436
Box 17-1 Anatomic Spaces Involved in
• Maxillary and other paranasal sinuses
• Cavernous sinus thrombosis
Deep Fascial Space Infections Associated with Mandibular Teeth
• Space of the body of the mandible
into the deeper fascial spaces of the neck, such as the lateral
pharyngeal, retropharyngeal, carotid, and pretracheal spaces From
there, such infections can spread into the danger space and the
medi-astinum In addition, infections can rise superiorly through the
sinuses or vascular structures to invade the brain or the intracranial
dural sinuses such as the cavernous sinus
Infections of the deep fascial spaces can be classified as having
low, moderate, or high severity, according to their likelihood of
threatening the airway or other vital structures Low-severity
infec-tions are not likely to threaten the airway or vital structures
Moderate-severity infections hinder access to the airway by causing trismus or
elevation of the tongue, which can make endotracheal intubation
difficult High-severity infections can directly compress or deviate the
airway or damage vital organs such as the brain, heart, lungs, or skin
(as in necrotizing fasciitis, popularly known as flesh-eating bacterial
infection.) Determining the exact anatomic location of infection is a
key step in determining its severity A classification of the deep fascial
spaces according to their severity is listed in Box 17-2 Examples of
low-, moderate-, and high-severity infections are shown in Figures
17-2 to 17-4 Table 17-1 lists the anatomic borders of the more
com-monly infected deep fascial spaces of the head and neck
Infections Arising from Any Tooth
As discussed in Chapter 16 and previously in this chapter, maxillary
or mandibular teeth can cause infections of the buccal, vestibular, or
subcutaneous spaces The buccal space is actually a portion of the
subcutaneous space, which extends from head to toe Thus, a
long-standing buccal space abscess tends to drain spontaneously through
skin at its inferior extent near the inferior border of the mandible
Trang 27Figure 17-2 Low-severity infections that are not likely to threaten the airway or vital structures A, Vestibular space abscess under the upper lip
B, Cellulitis of the space of the body of the mandible (A, from Topazian RG, Goldberg MH, Hupp JR, editors: Oral and maxillofacial infections, ed 4,
Philadelphia, PA, 2002, Saunders.)
• Deep temporal (includes infratemporal)
High Severity—Direct Threat to the Airway or Vital Structures
• Deep neck spaces
infec-Involvement of the buccal space usually results in swelling below the zygomatic arch and above the inferior border of the mandible Infections may follow the extensions of the buccal fat pad into the superficial temporal space, the infratemporal space, the infraorbital space, and the periorbital space, as illustrated in Figure 17-7 Because the fascial layers that pass over the zygomatic arch are tightly bound down to bone, swelling above and below the zygomatic arch can cause the relatively dimpled appearance over the left zygomatic arch,
as seen in Figure 17-7 The zygomatic arch and the inferior border of the mandible remain palpable in buccal space infections
The infratemporal space lies posterior to the maxilla The space is bounded medially by the lateral pterygoid plate of the sphenoid bone and superiorly by the base of the skull Laterally and superiorly, the infratemporal space is continuous with the deep temporal space (Fig 17-8) Essentially, the infratemporal space is the bottom portion of the deep temporal space The space contains branches of the internal maxillary artery and the pterygoid venous plexus Importantly, emis-sary veins from the pterygoid plexus pass through foramina in the base of the skull to connect with the intracranial dural sinuses Because the veins of the face and the orbit do not have valves, blood-borne infections may pass superiorly or inferiorly along their course The infratemporal space is the origin of the posterior route by which infections may spread into the cavernous sinus (Fig 17-9) The infra-temporal space is rarely infected, but when it is, the cause is usually
an infection of the maxillary third molar
Periapical or periodontal infections of posterior maxillary teeth may erode superiorly through the floor of the maxillary sinus Approximately 20% of cases of maxillary sinusitis are odontogenic Odontogenic maxillary sinus infections may also spread superiorly
Trang 28Figure 17-3 Moderate-severity infections that hinder access to the airway A, Submasseteric space abscess that is causing severe trismus B, Infection
of the space of the body of the mandible and submandibular space. (A, From Topazian RG, Goldberg MH, Hupp JR, editors: Oral and maxillofacial
infections, ed 4, Philadelphia, PA, 2002, Saunders.)
Figure 17-4 High-severity infections that are likely to obstruct the airway or threaten vital structures A, Lateral pharyngeal space abscess
B, A 14-year-old patient had impacted third molars removed Two days later, he became feverish and developed right facial and periorbital erythema
Over the next 24 hours, the skin over the #32 site changed to dark purple and black, as shown The diagnosis of necrotizing fasciitis was made, and
he was immediately taken to the operating room, where drains were placed and plans made for débridement of affected tissues See also Figure 17-26. (B, Courtesy of Dr Robert Ord, Department of Oral and Maxillofacial Surgery, Baltimore College of Dental Surgery, University of Maryland,
Baltimore.)
B A
through the ethmoid sinus or the orbital floor to cause secondary
periorbital or orbital infections Periorbital or orbital infection rarely
occurs as the result of odontogenic infection, but when either does
occur, the presentation is typical: redness and swelling of the eyelids
and involvement of the vascular and neural components of the
orbit This is a serious infection and requires aggressive medical and
surgical intervention from an oral-maxillofacial surgeon and times other specialists Figure 17-10 shows the clinical and radio-graphic appearance of a case of odontogenic infection extending from the maxillary sinus through the ethmoid sinus into the orbit.When maxillary odontogenic infections erode into the infraor-bital vein in the infraorbital space or the inferior ophthalmic vein via
Trang 29some-Table 17-1 Borders of the Deep Fascial Spaces of the Head and Neck
Space Anterior Posterior Superior Inferior
Superficial or Medial*
Deep or Lateral†
Buccal Corner of mouth Masseter muscle
Pterygomandibular space
MaxillaInfraorbital space
Oral mucosa Quadratus labii
superioris muscle
Levator anguli oris muscleMaxillaSubmandibular Anterior belly
digastric muscle
Posterior belly digastric muscleStylohyoid muscle Stylopharyngeus muscle
Inferior and medial surfaces
of mandible
Digastric tendon
Platysma muscleInvesting fascia
Mylohyoid muscleHyoglossus muscleSuperior constrictor musclesSubmental Inferior border of
mandible
Hyoid bone Mylohyoid muscle Investing fascia Investing fascia Anterior bellies of
digastric muscles†
Sublingual Lingual surface of
mandible
Submandibular space
Oral mucosa Mylohyoid
muscle
Muscles of tongue*
Lingual surface of mandible†
Pterygomandibular Buccal space Parotid gland Lateral pterygoid
muscle
Inferior border
of mandible
Medial pterygoid muscle*
Carotid sheath and scalene fascia
Skull base Hyoid bone Pharyngeal
constrictors and retropharyngeal space*
Medial pterygoid muscle†
Retropharyngeal Superior and middle
pharyngeal constrictor muscles
Alar fascia Skull base Fusion of alar
and prevertebral fasciae at C6-T4
Carotid sheath and lateral pharyngeal space†
Pretracheal
Sternothyroid-thyrohyoid fascia
Retropharyngeal space
Thyroid cartilage Superior
mediastinum
thyrohyoid fascia
Sternothyroid-Visceral fascia over trachea and thyroid gland
Figure 17-5 A, Infraorbital space abscess that is about
to drain medial to the attachment of the levator labii superioris muscle B, Infraorbital space abscess with
chronic cutaneous drainage medial to the levator labii superioris muscle. (A, From Topazian RG, Goldberg
MH, Hupp JR, editors: Oral and maxillofacial infections,
ed 4, Philadelphia, PA, 2002, Saunders B, From
Topazian RG, Goldberg MH, Hupp JR, editors:
Oral and maxillofacial infections, ed 4, Philadelphia,
PA, 2002, Saunders.)
Trang 30Cavernous sinus thrombosis is an unusual occurrence that is rarely the result of an infected tooth Like orbital cellulitis, cavernous sinus thrombosis is a serious, life-threatening infection that requires aggres-sive medical and surgical care Cavernous sinus thrombosis has a high mortality even today Figure 17-11 illustrates the rapid extension of
the sinuses, they can follow the common ophthalmic vein through
the superior orbital fissure and extend directly into the cavernous
sinus This is the anterior route to the cavernous sinus Intravascular
inflammation caused by the invading bacteria stimulates the clott-
ing pathways, resulting in a septic cavernous sinus thrombosis
Table 17-2 Relations of the Deep Fascial Spaces of the Head and Neck
Space Likely Causes Contents
Neighboring Spaces
Approach for Incision and Drainage
Buccal Upper premolars
Upper molars
Parotid ductAnterior facial artery and vein
InfraorbitalPterygomandibular
Intraoral (small)Extraoral (large)Lower premolars Transverse facial artery and vein
Buccal fat pad
Infratemporal
Infraorbital Upper canine Angular artery and vein
Infraorbital nerve
Buccal Intraoral
Submandibular Lower molars Submandibular gland
Facial artery and veinLymph nodes
SublingualSubmentalLateral pharyngealBuccal
Extraoral
Sublingual Lower premolars
Lower molarsDirect trauma
Sublingual glandsWharton’s ducts
SubmandibularLateralPharyngeal
IntraoralIntraoral-extraoral
Lingual nerveSublingual artery and vein
Visceral (trachea and esophagus)Pterygomandibular Lower third molars
Fracture of angle of mandible
Mandibular division of trigeminal nerve
Buccal Intraoral
Inferior alveolar artery and vein Lateral pharyngeal
SubmassetericDeep temporalParotidPeritonsillar
Intraoral-extraoral
Submasseteric Lower third molars
Fracture of angle of mandible
Masseteric artery and vein Buccal Intraoral
PterygomandibularSuperficial temporalParotid
Intraoral-extraoral
Infratemporal and
deep temporal
Upper molars Pterygoid plexus
Interior maxillary artery and vein
Mandibular division of trigeminal nerveSkull base foramina
BuccalSuperficial temporalInferior petrosal sinus
IntraoralExtraoralIntraoral-extraoral
Superficial
temporal
Upper molarsLower molars
Temporal fat padTemporal branch of facial nerve
BuccalDeep temporal
IntraoralExtraoralIntraoral-extraoralLateral pharyngeal Lower third molars
TonsilsInfection in neighboring spaces
Carotid arteryInternal jugular veinVagus nerveCervical sympathetic chain
PterygomandibularSubmandibularSublingualPeritonsillarRetropharyngeal
IntraoralIntraoral-extraoral
From Flynn TR: Anatomy of oral and maxillofacial infections In Topazian RG, Goldberg MH, Hupp JR, editors: Oral and maxillofacial infections, ed 4, Philadelphia, PA,
2002, WB Saunders With permission.
Trang 31Figure 17-6 A, Buccal space lies between buccinator muscle and overlying skin and superficial fascia This potential space may become involved via
maxillary or mandibular molars (arrows) B, Typical buccal space infection, extending from the level of the zygomatic arch to the inferior border of the
mandible and from the oral commissure to the anterior border of the masseter muscle. (A, Adapted from Flint PW Haughey BH, Lund VJ et al, editors:
Cummings otolaryngology: Head and neck surgery, ed 5, Philadelphia, PA, 2010, Mosby B, From Flynn TR: The swollen face Emerg Med Clin North
Am 15:481–519, 2000.)
Buccalspace
Figure 17-7 Buccal space infection that has followed the extensions of
the buccal fat pad into the infraorbital, periorbital, and superficial temporal spaces. (From Flynn TR: The swollen face Emerg Med Clin
North Am 15:481–519, 2000.)
a case of orbital cellulitis into cavernous sinus thrombosis; nately, the most vulnerable structure in the cavernous sinus, the abducens (sixth cranial) nerve, was spared
fortu-Infections Arising from Mandibular Teeth
Although many infections arising from mandibular teeth erode into the vestibular space, they may also spread into other deep fascial spaces Initially, such mandibular infections tend to enter the space
of the body of the mandible, the submandibular, sublingual, mental, or masticator spaces From there, severe infections can spread into the deep fascial spaces of the neck, and even extend into the mediastinum to threaten the heart, lungs, and great vessels
sub-The space of the body of the mandible, like the palatal space, is
a subperiosteal space Thus, if an infection erodes through the buccal cortical bone but does not perforate the periosteum, it can essentially peel the periosteal layer of soft tissue off the bony surface Clinically, this results in a swelling that assumes the shape of the underlying
mandible It can appear as if the bone itself has been enlarged, as in
Figure 17-12
If an infection arising from a mandibular posterior tooth rates the buccal cortical bone and the periosteum inferior to the attachment of the buccinator muscle, then the buccal space is involved (see Fig 17-6, A)
perfo-In their landmark work on the anatomy of the deep fascial spaces
of the head and neck, Grodinsky and Holyoke identified the illary space as one large space that encompasses the three anatomic
submax-spaces referred to separately today as submandibular, sublingual, and
submental spaces.1-3 One may collectively refer to them as
perimandibu-lar spaces The sublingual and submandibuperimandibu-lar spaces have the medial
border of the mandible as their lateral boundary These two spaces are involved primarily by lingual perforation of infection from mandibu-lar molars, although they may be involved by premolars as well The factor that determines whether the infection is submandibular or sub-lingual is the attachment of the mylohyoid muscle on the mylohyoid ridge of the medial aspect of the mandible (Fig 17-13) If the infec-tion erodes through the medial aspect of the mandible above this line, the infection will be in the sublingual space This is most com-monly seen with premolars and the first molar If the infection erodes through the medial aspect of the mandible inferior to the mylohyoid line, the submandibular space will be involved The mandibular third molar is the tooth that most commonly involves the submandibular space directly The second molar may involve the sublingual or sub-mandibular space, depending on the length of individual roots.The sublingual space lies between the oral mucosa of the floor of the mouth and the mylohyoid muscle (Fig 17-14, A) The posterior border of the sublingual space is open, and therefore, it freely com-municates with the submandibular space Clinically, little or no extra-oral swelling is produced by an infection of the sublingual space, but much intraoral swelling is seen in the floor of the mouth on the infected side The infection often becomes bilateral, and the tongue becomes elevated (see Fig 17-14, B)
The submandibular space lies between the mylohyoid muscle and the overlying superficial layer of the deep cervical fascia (Fig 17-15) The posterior extent of the submandibular space communi-cates with the deep fascial spaces of the neck Infection of the
Trang 32progress with alarming speed and, thus, may produce upper airway obstruction that often leads to death The most common cause of Ludwig’s angina is an odontogenic infection In the 1940s, before penicillin was available, Williams found a way to reduce the mortality
of Ludwig’s angina from 54% to 10% by instituting a protocol of initially securing the airway and then performing early and aggressive I&D procedures.4,5 These landmark studies established the principles
of airway security and prompt, aggressive surgery and demonstrated that antibiotic therapy plays only a supportive role in the manage-ment of severe odontogenic infections
The submandibular and sublingual spaces join together at the posterior edge of the mylohyoid muscle At the posterior edge of this junction is the buccopharyngeal gap, where the styloglossus and stylohyoid muscles pass between the superior and middle pharyngeal constrictor muscles on their way to the tongue and the hyoid bone, respectively Submandibular or sublingual space infections can pass through the buccopharyngeal gap to enter the lateral pharyngeal space, which is one of the deep fascial spaces of the neck In addition, submandibular space infections can pass around the posterior belly
of the digastric muscle to enter the lateral pharyngeal space directly These are the pathways by which submandibular and sublingual space infections can spread into the deep fascial spaces of the neck and beyond
In most of the reported case series of severe odontogenic tions, the submandibular space is the most frequently involved In a recent series of severe odontogenic infections requiring hospitaliza-tion, however, the submandibular space was involved in 54% of cases, and the masticator space was involved in 78% of cases The pterygomandibular portion of the masticator space was involved in 60% of cases The mandibular third molar is the most commonly associated tooth, and it frequently causes infections of the pterygo-mandibular portion of the masticator space.6,7
infec-submandibular space causes swelling that can look like an inverted
triangle, with the base at the inferior border of the mandible, the
sides determined by the anterior and posterior bellies of the digastric
muscle, and the apex at the hyoid bone (Fig 17-16)
The submental space lies between the anterior bellies of the right
and left digastric muscles and between the mylohyoid muscle and the
overlying fascia (Fig 17-17) Isolated submental space infections are
rare, caused by infections of the mandibular incisors More commonly,
submental space involvement is the result of the spread of a
subman-dibular space infection, which can easily pass around the anterior
belly of the digastric muscle to enter the submental space Such an
aggressive infection can then easily pass from the submental space to
the contralateral submandibular space to involve all three spaces
When the perimandibular spaces (submandibular, sublingual,
and submental) are bilaterally involved in an infection, it is known
as Ludwig’s angina This infection is a rapidly spreading cellulitis that
can obstruct the airway and commonly spreads posteriorly to the
deep fascial spaces of the neck
Severe swelling is almost always seen, with elevation and
displace-ment of the tongue, and a tense, hard, bilateral induration of the
submandibular region superior to the hyoid bone The patient usually
has trismus, drooling, and difficulty swallowing and sometimes
breathing The patient often experiences severe anxiety over the
inability to swallow and maintain an airway This infection may
Figure 17-8 The masticator space is bounded by the fascia overlying
the masseter muscle, medial pterygoid muscle, temporalis muscle, and
the skull The superficial and deep temporal spaces are separated from
each other by the temporalis muscle The lateral pterygoid muscle
divides the pterygomandibular space from the infratemporal portion
of the deep temporal space, and the zygomatic arch divides the
submasseteric space from the superficial temporal space. (Adapted from
Flint PW Haughey BH, Lund VJ et al, editors: Cummings otolaryngology:
Head and neck surgery, ed 5, Philadelphia, PA, 2010, Mosby.)
Deep temporal spaceSphenoid boneInfratemporalspace
LateralpterygoidmuscleHamular processMedialpterygoidmusclePterygomandibularspace
Mandible
Figure 17-9 Hematogenous spread of infection from the jaw to the
cavernous sinus may occur anteriorly via the inferior or superior ophthalmic vein or posteriorly via emissary veins from the pterygoid plexus. (Adapted from Flint PW Haughey BH, Lund VJ et al, editors:
Cummings otolaryngology: Head and neck surgery, ed 5, Philadelphia,
PA, 2010, Mosby.)
CavernoussinusEmissary vein
Superiorophthalmicvein
Retromandibular
veinInternaljugularvein
Facialvein
Pterygoidplexus
InferiorophthalmicveinAngularvein
Trang 33the pupil B, Computed tomography scan demonstrating opacification of the right maxillary and ethmoid sinuses and subperiosteal thickening along
the medial and inferior orbital walls. (From Feigin RD, Cherry J, Demmler-Harrison GJ, et al, editors: Feigin and Cherry’s textbook of pediatric infectious
diseases, ed 6, Philadelphia, PA, 2009, Saunders.)
Figure 17-11 Cavernous sinus thrombosis A, Infraorbital and buccal space abscess with extension into the periorbital and orbital spaces
B, The same patient, 4 hours later, with continued spread of the infection to the superficial and deep temporal spaces, cavernous sinus, and the
opposite orbit C, The same patient, 2 weeks later On voluntary gaze toward the affected right side, both eyes turn toward the right, demonstrating
that the right abducens nerve was not injured. (A and B, From Waite D, editor: Textbook of practical oral and maxillofacial surgery Philadelphia, PA,
A
C
B
Trang 3415:481–519, 2000.) muscle Linguocortical plate perforation by infection from premolars and
first molar causes sublingual space infection, whereas infection from third molar involves submandibular space. (Adapted from Flint PW,
Haughey BH, Lund VJ, et al, editors: Cummings otolaryngology: Head and neck surgery, ed 5, Philadelphia, PA, 2010, Mosby.)
Figure 17-14 A, The sublingual space lies between the oral mucosa and the mylohyoid muscle The space is primarily involved by infection from
mandibular premolars and first molar B, Severe sublingual space abscess that has elevated the tongue into the palate such that only the ventral
surface of the tongue and floor of the mouth are visible. (A, Adapted from Flint PW, Haughey BH, Lund VJ et al, editors: Cummings otolaryngology:
Head and neck surgery, ed 5, Philadelphia, PA, 2010, Mosby B, From Waite D, editor: Textbook of practical oral and maxillofacial surgery,
Philadelphia, PA, 1987, Lea & Febiger.)
Mylohyoidmuscle
Sublingualabscess
Figure 17-15 The submandibular space lies between the mylohyoid
muscle and anterior layer of the deep cervical fascia, just deep to the
platysma muscle, and includes the lingual and inferior surfaces of the
mandible below the mylohyoid muscle attachment. (Adapted from Flint
PW, Haughey BH, Lund VJ et al, editors: Cummings otolaryngology:
Head and neck surgery, ed 5, Philadelphia, PA, 2010, Mosby.)
Submandibular glandMylohyoid muscleSubmandibular abscessPlatysma muscle
Figure 17-16 Typical submandibular space infection demarcated by
both bellies of the digastric muscle, the inferior border of the mandible, and the hyoid bone. (From Flynn TR: The swollen face Emerg Med Clin
North Am 15:481–519, 2000.)
Trang 35Figure 17-17 Submental space infection appears as discrete swelling in
central area of submandibular region
Figure 17-18 Masticator space infection, with all compartments involved A, Frontal view demonstrating the swelling anterior to and obscuring
the ear and in the temporal region B, Oblique view demonstrating the dimpling of the swelling over the zygomatic arch, with temporal and
submasseteric swelling above and below. (A, from Flynn TR: The swollen face Emerg Med Clin North Am 15:481–519, 2000.)
The masticator space is formed by the splitting of the anterior
layer of the deep cervical fascia, also called the superficial or the
invest-ing layer of the deep cervical fascia, to surround the muscles of
mastica-tion This fascia separates at the inferior border of the mandible to
pass laterally over the masseter muscle and medially over the medial
surface of the medial pterygoid muscle Medially, this fascia
termi-nates at its attachment to the pterygoid plates and sphenoid bone
Laterally, this fascia, at that location called the parotideomasseteric
fascia, rises over the masseter muscle and fuses with the periosteum
over the zygomatic arch Above the zygomatic arch, this fascia, at that
location called the temporalis fascia, rises over the lateral surface of
the temporalis muscle and terminates at the insertion of the
tempo-ralis muscle on the cranium This fascial envelope, as well as the
surfaces of the skull that form its medial border, is the masticator
space Within this space, four compartments that exist are referred
to as separate spaces They are (1) the submasseteric space, between
the masseter muscle and the lateral surface of the ascending ramus
of the mandible; (2) the pterygomandibular space, between the medial
pterygoid muscle and the medial surface of the ascending ramus;
(3) the superficial temporal space, between the temporalis fascia and the temporalis muscle; and (4) the deep temporal space, between the
temporalis muscle and the skull The zygomatic arch separates the submasseteric and superficial temporal spaces, and the lateral ptery-goid muscle separates the pterygomandibular and the deep temporal spaces The infratemporal space is actually the inferior portion of the deep temporal space, between the lateral pterygoid muscle and the infratemporal crest of the sphenoid bone These four compartments
of the masticator space clinically behave like separate spaces because,
in most cases, only one compartment of the masticator space becomes infected However, particularly severe or longstanding masticator space infections can involve all four compartments, as illustrated in
Figure 17-18.The submasseteric space is involved by infection most commonly
as the result of spread from the buccal space or from soft tissue tion around the mandibular third molar (pericoronitis) Occasion-ally, an infected mandibular angle fracture causes a submasseteric space infection When the submasseteric space is involved, the mas-seter muscle also becomes inflamed and swollen, as seen clinically and radiographically in Figure 17-19 Because of the involvement of the masseter muscle, the patient also has moderate to severe trismus caused by inflammation of the masseter muscle
infec-The pterygomandibular space is the site into which local thetic solution is injected when an inferior alveolar nerve block is performed Infections of this space spread primarily from the man-dibular third molar When the pterygomandibular space alone is involved, little or no facial swelling is observed; however, the patient almost always has significant trismus Therefore, trismus without swelling is a valuable diagnostic clue for pterygomandibular space infection On physical examination, with a good light and a tongue depressor, the clinician can see swelling and erythema of the anterior tonsillar pillar on the affected side and deviation of the uvula to the opposite side On computed tomography (CT) examination, fluid collection may be detected between the medial pterygoid muscle and the mandible; the airway is often compressed and deviated by the
Trang 36anes-Deep Cervical Fascial Space Infections
Extension of odontogenic infections beyond the spaces described above is an uncommon occurrence However, when it does happen, involvement of the deep cervical spaces may have serious life-threatening sequelae Infection of the deep fascial spaces of the neck can compress, deviate, or completely obstruct the airway, invade vital structures such as the major vessels, and allow extension of the infec-tion into the mediastinum and the vital structures it contains.Infection extending posteriorly from the pterygomandibular, submandibular, or sublingual spaces first encounters the lateral
swelling, as shown in Figure 17-20 Occasionally, this clinical picture
is caused by needle track infection from a mandibular block
The superficial and deep temporal spaces rarely become infected
and usually only in severe infections When these spaces are involved,
the swelling that occurs is evident in the temporal region, superior
to the zygomatic arch and posterior to the lateral orbital rim The
tight attachment of the anterior layer of the deep cervical fascia to
the zygomatic arch prevents swelling there so that when either of the
temporal spaces and the submasseteric space are both infected, an
hourglass shape can be detected in the frontal view, as shown in
Figures 17-7 and 17-18
Figure 17-20 A, Pterygomandibular space abscess due to a carious lower third molar, with swelling of the anterior tonsillar pillar and deviation of
the uvula to the opposite side B, Computed tomography scan of a pterygomandibular space abscess caused by a lower third molar Note the fluid
collection between the distended medial pterygoid muscle and the ascending ramus of the mandible, as well as the displacement and compression of the airway. (A, From Flynn TR, Topazian RG: Infections of the oral cavity In Waite D, editor: Textbook of practical oral and maxillofacial surgery,
Philadelphia, PA, 1987, Lea & Febiger.)
Figure 17-19 Submasseteric space abscess A, Trismus caused by a right submasseteric space abscess, at maximum oral opening Note that the
lobe of the right ear is obscured by the right submasseteric swelling, whereas the left ear lobe is visible The device taped to the right neck is an intravenous line in the external jugular vein This patient had no accessible veins in the upper extremities because of scarring by previous intravenous drug abuse B, Computed tomography image of a submasseteric space abscess that illustrates the fluid between the edematous masseter muscle and
the ascending ramus of the mandible. (From Topazian RG, Goldberg MH, Hupp JR, editors: Oral and maxillofacial infections, ed 4, Philadelphia, PA,
2002, Saunders.)
Trang 37Figure 17-21 The lateral pharyngeal space is located between the medial pterygoid muscle laterally and the superior pharyngeal constrictor medially
The retropharyngeal and danger spaces lie between the pharyngeal constrictor muscles and the prevertebral fascia The retropharyngeal space lies between the superior constrictor muscle and the alar fascia The danger space lies between the alar layer and the prevertebral fascia. (From Flynn TR:
Anatomy and surgery of deep fascial space infections In Kelly JJ, editor: Oral and maxillofacial surgery knowledge update 1994, Rosemont, IL, 1994,
American Association of Oral and Maxillofacial Surgeons.)
Scalene FasciaSternocleidomastoid m
Jugular V
Sympathetic chainI.C.A
ParotidGlandPost Facial v
Stylohyoid m
LateralPharyngeal SpaceStyloglossus m
SkinMandible
I.C.A - Internal Carotid arteryE.C.A - External Carotid artery
P.F - Internal Carotid arteryA.F - Alar Fascia
V.F - Visceral Fascia
Aponeurosis
of Zuckerkandeland Testut
pharyngeal space This space extends from the base of the skull at the sphenoid bone to the hyoid bone inferiorly The space is medial to the medial pterygoid muscle and lateral to the superior pharyngeal constrictor muscle (Fig 17-21) The space is bounded anteriorly by the pterygomandibular raphe and extends posteromedially to the retropharyngeal space The styloid process and associated muscles and fascia divide the lateral pharyngeal space into an anterior com-partment, which contains primarily loose connective tissue, and a posterior compartment, which contains the carotid sheath and cranial nerves IX (glossopharyngeal), X (vagus), and XII (hypoglossal)
The clinical findings of lateral pharyngeal space infection include trismus as the result of inflammation of the medial pterygoid muscle;
lateral swelling of the neck, especially between the angle of the dible and the sternocleidomastoid muscle; and swelling of the lateral pharyngeal wall, causing it to bulge toward the midline Patients who have lateral pharyngeal space infections have difficulty swallowing and usually have a high temperature and become very sick Figure 17-22 illustrates the clinical appearance of the patient and the CT image of lateral pharyngeal space infection
man-Patients who have infection of the lateral pharyngeal space have several serious potential problems When the lateral pharyngeal space
is involved, the odontogenic infection is severe and may be ing at a rapid rate Another possible problem is the direct effect of the infection on the contents of the space, especially those of the posterior compartment These problems include thrombosis of the internal jugular vein, erosion of the carotid artery or its branches, and interference with cranial nerves IX, X, and XII A third serious com-plication arises if the infection progresses from the lateral pharyngeal space to the retropharyngeal space or beyond
progress-The retropharyngeal space lies behind the soft tissue of the terior aspect of the pharynx The retropharyngeal space is bounded anteriorly by the pharyngeal constrictor muscles and the retropha-ryngeal fascia, and posteriorly by the alar fascia (see Fig 17-21)
pos-The retropharyngeal space begins at the base of the skull and ends inferiorly at a variable point between the sixth cervical (C6) and fourth thoracic (T4) vertebrae, where the alar fascia fuses anteriorly with the retropharyngeal fascia (Fig 17-23) The retropharyngeal space contains only loose connective tissue and lymph nodes, so it provides little barrier to the spread of infection from one lateral pharyngeal space to the other to encircle the airway, as illustrated in
Figure 17-24 Moreover, when the retropharyngeal space becomes
involved, the major concern is that the infection can rupture the alar fascia posteriorly to enter the danger space (Fig 17-25)
The danger space lies between the alar fascia anteriorly and the prevertebral fascia posteriorly The danger space extends from the base of the skull to the diaphragm, and it is continuous with the posterior mediastinum (see Fig 17-23) The prevertebral space
is rarely involved in odontogenic infections because the prevertebral fascia fuses with the periosteum of the vertebral bodies Prevertebral space infections are usually caused by osteomyelitis of the vertebrae.The mediastinum is the space between the lungs, and it contains the heart, the phrenic and vagus nerves, the trachea and the main stem bronchi, the esophagus, and the great vessels, including the aorta and the inferior and superior vena cava A patient with medi-astinitis can have an overwhelming infection that compresses the heart and lungs; interferes with the neurologic control of heart rate and respiration; ruptures into the lung, trachea, or esophagus; and even spreads into the abdominal cavity The mortality of mediastini-tis is high, even with modern methods of care such as open thoracic surgical drainage and close follow-up with serial CT scans
Necrotizing fasciitis is referred to by laypersons as “flesh-eating bacteria” infection It is not a specific “flesh-eating bacterium” that causes this infection Rather, it is the result of the rapid spread of infection on the superficial surface of the anterior, or investing, layer
of the deep cervical fascia, just deep to the platysma muscle Necrosis
of the overlying platysma, subcutaneous tissue, and skin occurs because of thrombosis and occlusion of the arterioles that pass through the platysma to provide blood supply to overlying tissue Early in its course, this infection causes skin vesicles and then a dusky purple discoloration of overlying skin due to ischemia, as shown in
Figure 17-4, B Later, frank necrosis and undermining of skin requires surgical débridement of large areas of skin, as illustrated in Figure 17-26 When necrotizing fasciitis is suspected, emergency surgery, high-dose broad-spectrum antibiotic therapy, treatment of underly-ing medical conditions such as diabetes, and correction of fluid and electrolyte imbalances are necessary
Management of Fascial Space Infections
Management of infections, mild or severe, always has five general goals: (1) medical support of the patient, with special attention to protection of the airway and correcting host defense compromises
Trang 38The patient’s airway must be continually monitored, and cheal intubation or tracheotomy should be performed, if warranted Airway security is the prime concern in the management of severe odontogenic infections Medical management of the patient with a serious infection must include a thorough assessment and support of host defense mechanisms, including analgesics, fluid requirements, and nutrition High-dose bactericidal antibiotics are usually necessary and are almost always administered intravenously.
endotra-Several large studies, performed as early as the 1950s, have shown that extraction of teeth in the presence of infection hastens the resolu-tion of the infection and reduces the morbidity of the infection by such measures as decreased time out of work, shortened or avoided hospitalization, and reduced need for extraoral I&D Occasionally, tooth extraction has been blamed for subsequent severe infections requiring hospitalization However, the infection that necessitated the tooth extraction had most likely become severe enough to warrant hospital care and more aggressive surgery Severe odontogenic infec-tions that ultimately result in hospitalization require shorter hospital stay and fewer complications when some form of dental treatment preceded hospitalization.8
Surgical management of fascial space infections almost always requires a generous incision and aggressive exploration of the involved fascial spaces with a hemostat One or more drains are usually required to provide adequate drainage and decompression of the infected area Because the I&D must be extensive, it is usually done in an operating room, with the patient placed under general anesthesia The locations of various I&D sites are depicted in
Figure 17-22 Lateral pharyngeal space abscess A, Left lateral pharyngeal space abscess with extraoral swelling (arrow) and trismus B, Intraoral view
of the same patient, illustrating swelling of the anterior tonsillar pillar and blunting of the palatouvular fold C, A boy with a left lateral pharyngeal
space abscess who is deviating his head toward the right shoulder to place the upper airway over his deviated trachea D, Computed tomography at
the level of the hyoid bone, showing a lateral pharyngeal space infection that is deviating the airway to the opposite side. (From Topazian RG,
Goldberg MH, Hupp JR, editors: Oral and maxillofacial infections, ed 4, Philadelphia, PA, 2002, Saunders.)
• Evaluate host defenses
• Determine the setting of care
• Treat surgically
• Support medically
• Choose and prescribe appropriate antibiotic(s)
• Administer antibiotic appropriately
• Re-evaluate frequently
where they exist; (2) surgical removal of the source of infection as
early as possible; (3) surgical drainage of the infection, with proper
placement of drains; (4) administration of correct antibiotics in
appropriate doses; and (5) frequent re-evaluation of the patient’s
progress toward resolution Although the intensity of treatment is
greater in complex odontogenic infections, the principles of surgical
and medical management of fascial space infections are the same as
those for less serious infections; these principles are described in
detail in Chapter 16 and are summarized in Box 17-3 Conscientious
application of these principles cannot guarantee an ideal result in
any given case, but it should ensure that the standard of care has
been met
Trang 39tissue necrosis The failure of microcirculation in cancellous bone is
a critical factor in the establishment of osteomyelitis because the involved area becomes ischemic and the cellular component of bone becomes necrotic Bacteria can then proliferate because normal bloodborne defenses do not reach tissue, and the osteomyelitis spreads until it is arrested by medical and surgical therapy
Although the maxilla can also become involved in osteomyelitis,
it does so rarely compared with the mandible The primary reason for this is that the blood supply to the maxilla is much richer and is derived from several arteries, which form a complex network of feeder vessels Because the mandible tends to draw its primary blood supply from the inferior alveolar artery and because the dense overly-ing cortical bone of the mandible limits penetration of periosteal blood vessels, the mandibular cancellous bone is more likely to become ischemic and, therefore, infected
In spite of the many opportunities that bacteria have to enter into cancellous bone via dental infections, osteomyelitis of the mandible rarely occurs if the host defenses are reasonably intact The major predisposing factors for osteomyelitis of the jaws are preceding odon-togenic infections and fractures of the mandible (Fig 17-28) Even these two events rarely cause infections of bone unless host defenses are suppressed by such problems as diabetes, alcoholism, intravenous drug abuse, malnutrition, and myeloproliferative diseases (e.g., leu-kemias, sickle cell disease, or chemotherapy-treated cancer).Recent carefully performed investigations on the microbiology of osteomyelitis of the mandible have adequately demonstrated that the primary bacteria of concern are similar to those causing odontogenic
infections, that is, streptococci, anaerobic cocci such as
Peptostrepto-coccus spp., and anaerobic gram-negative rods such as those of the
Figure 17-27 Ample clinical experience and experimental evidence indicate that even if no abscess formation can be detected by palpa-tion, needle aspiration, radiographic examination, or open surgical drainage, an infection in the cellulitis stage will resolve more rapidly
if incised and drained The surgeon must not wait for unequivocal evidence of pus formation In the preantibiotic era, surgical treatment was the only method of therapy for infections, and early and aggres-sive surgical therapy was frequently curative for these severe infec-tions One must remember that aggressive surgical exploration is still the primary method of therapy for serious odontogenic infections of the head and neck
OSTEOMYELITIS
The term osteomyelitis literally means inflammation of the bone
marrow Clinically, osteomyelitis implies an infection of bone myelitis usually begins in the medullary cavity, involving cancellous bone; then it extends and spreads to cortical bone and eventually to the periosteum Invasion of bacteria into cancellous bone causes soft tissue inflammation and edema within the closed bony marrow spaces As with the dental pulp, soft tissue edema that is enclosed by unyielding calcified tissue results in increased tissue hydrostatic pres-sure that rises above the blood pressure of the feeding arterial vessels
Osteo-The resulting severe compromise of the blood supply then causes soft
Figure 17-23 The retropharyngeal and the alar fascia fuse at a variable
level between the C6 and T4 vertebrae, which forms a pouch at the inferior extent of the retropharyngeal space If infection passes through the alar fascia to the danger space, the posterosuperior mediastinum will most likely soon become involved The inferior boundary of the danger space is the diaphragm, which puts the entire mediastinum
at risk
Alar fascia
Prevertebral fascia
Retropharyngealspace
Dangerspace
Buccopharyngealfascia
Mediastinum
Figure 17-24 Postoperative computed tomography scan of a patient
with a previously placed drain (arrow) in the left pterygomandibular
space The infection has now spread through the left lateral pharyngeal space and the retropharyngeal space to the right lateral pharyngeal space, thus encircling, compressing, and deviating the airway. (From Flynn TR: Surgical management of orofacial infections:
Atlas Oral Maxillofac Surg Clin North Am 8:77–100, 2000.)
Trang 40penetration If the patient has a serious acute osteomyelitis, ization may be required for intravenous administration of antibiotics, which can then be followed by home intravenous therapy via a peripherally inserted central catheter or oral therapy, especially with fluoroquinolones, which are very well absorbed orally.
hospital-Surgical treatment of acute or chronic suppurative osteomyelitis consists primarily of removing obviously nonvital teeth in the area
of the infection, any wires or bone plates that may have been used
to stabilize a fracture in the area, or any necrotic, loose pieces of bone Bone specimens are sent for aerobic and anaerobic cultures, sensitiv-ity testing, and histopathologic examination In addition, corticot-omy (removal or perforation of the bony cortex) and excision of necrotic bone (until actively bleeding bone tissue is encountered) may be necessary For acute osteomyelitis that results from jaw frac-ture, the surgeon must stabilize the mobile segments of the mandible, usually by open reduction and rigid internal fixation Immobility of the fracture segments aids in the resolution of osteomyelitis.Chronic osteomyelitis requires not only aggressive antibiotic therapy but also aggressive surgical therapy Because of the severe compromise in the blood supply to the area of osteomyelitis, the patient is usually admitted to the hospital and given high-dose intra-venous antibiotics to control the infection The surgeon should obtain culture material at the time of surgery so that the selection of an anti-biotic can be based on the specific microbiology of the infection.Therapy for acute and chronic osteomyelitis, most authorities agree, should ensure that antibiotics are continued for a much longer time than is usual for odontogenic infections For mild acute osteo-myelitis that has responded well, antibiotics should be continued for
at least 6 weeks after resolution of symptoms For severe chronic osteomyelitis that has been difficult to control, antibiotic administra-tion may continue for up to 6 months This is especially true in
genera Fusobacterium and Prevotella Traditional investigation of the
microbiology of osteomyelitis of the jaws has used culture specimens
from surface drainage of pus (contaminated with Staphylococcus
organisms) and not anaerobic culture techniques (and thereby have
not grown anaerobes) Thus, osteomyelitis of the mandible differs
substantially from osteomyelitis of other bones in which
staphylo-cocci are the predominant bacteria
Acute suppurative osteomyelitis shows little or no radiographic
change because at least 10 to 12 days are required for lost bone to be
detectable radiographically Chronic osteomyelitis usually
demon-strates bony destruction in the area of infection The appearance is
one of increased radiolucency, which may be uniform in its pattern,
or patchy with a moth-eaten appearance Areas of radiopacity also
may occur within radiolucency These radiopaque areas represent
islands of bone that have not been resorbed and are known as
seques-tra In longstanding chronic osteomyelitis, an area of increased
radiodensity surrounding the area of radiolucency, called an
involu-crum, may be present This is the result of a reaction in which bone
production increases as a result of the inflammatory reaction
Osteomyelitis is treated medically as well as surgically Because
patients with osteomyelitis may have depressed host defense
mecha-nisms, the clinician must take these compromises into account during
the treatment and seek medical consultation, when necessary
Acute osteomyelitis of the jaws is primarily managed by the
administration of surgical débridement, removal of causative factors,
and appropriate antibiotics The precipitating event, condition, or
both must be carefully managed If the event is a fracture of the
mandible, careful attention must be given to accurate reduction and
stable fixation The antibiotics of choice include clindamycin,
penicil-lins, and fluoroquinolones because of their effectiveness against
the flora of odontogenic infections and their good-to-excellent bone
Figure 17-25 A, The normal retropharyngeal soft tissue shadow is narrow (6 mm or less) at C2 and 20 mm or less at C6 on plain radiographic films
B, When the retropharyngeal space is infected, the soft tissue becomes substantially thicker, and the width of the oropharyngeal air shadow
decreases. (From Flint PW, Haughey BH, Lund VJ et al, editors: Cummings otolaryngology: Head and neck surgery, ed 5, Philadelphia, PA, 2010,
Mosby.)