ADVANCES IN THE MANAGEMENT OF
DENTAL INFECTIONS
The lion's share of dental practices involves dealing with the effects of microorganisms on the structures of the teeth and jaws. Caries and periodontal disease
affect almost every individual. Despite the universality of this assault on the mouth,
relatively few people develop overt, acute, serious infection of the jaws. We owe this
to the many defense mechanisms in place that localize and minimize the potential for
tissue invasion. These include individual and professional interventions like oral
hygiene and dental restorations. These, of course, augment the natural defense of
the saliva and its components (IgA), mucosal barriers and the cell mediated and
humoral immune system. By necessity; therefore, an infective process must hurdle
one or more of these barriers in order to establish itself. From that point of view, the
question of why a particular person should present with a particular infection may
assume paramount importance in the management of the illness.
The factors which bring about an infection may be thought of as the interplay of three
sets of determinants: Bug factors, local factors and host factors.
1. Bug factors involve adaptations of the organism in question to defeat the natural
defense barriers. For example the stickiness of Streptococcus mutans or the ability of
other species to live in anaerobic environments.
2. Local factors include holes in teeth or recent wounds, traumatic or surgical. It
also involves the sheer numbers of bacteria available in a given mouth. Furry teeth
not only have more bugs available to start an infection, they have broader section of
species that can take advantage of the openings that occur.
3. Host factors involve the relative presence or absence of the systemic defense
mechanisms. A good example being the leukemic patient with decreased numbers of
functional white blood cells.
Not only is this a complex process in terms of the number of interconnecting
variables; it is a dynamic, changing process with time. As a wound heals, it presents
a smaller and smaller "window of opportunity" for organisms to exploit. Conversely,
an established early infection with Streptococcal species may open ever larger
volumes of tissue by the elaboration of destructive enzymes (such as collagenase
and hyaluronidase) and toxins. Further, the character of the infection evolves with
time. Whereas an initial facial cellulitis consists of primarily aerobic Streptocci, as the
oxygen tension is lowered by the bacteria and the body responds by walling off the
part, anaerobic species take over. In other words, the patient presenting on Monday
with a facial swelling due to cellulitis will be entirely different in terms of extent and
composition compared to Friday's frank abcess in the same patient.
Consideration of the process of infection allows the clinician to appreciate that the
moment that a patient presents with a problem is but a phase in an ongoing series of
events. This is by no means a new concept, but it does put management into
context. In the absence of, in spite of or because of clinical intervention, the patient's
illness is going to evolve. It is going to get better or get worse. Management must
therefore have two capabilities: anticipation and reaction. Anticipation of possible
scenarios and preparation for them. Reaction to actual events as they transpire.
Management, being dynamic, must be thought of as a process rather than an
event.
A. Diagnosis:
The first step in this process is the establishment of a diagnosis. The diagnosis
consists of four basic pieces of information:
1. Cause: where did the infection originate
2. Extent: what spaces does the infection now occupy
3. Causative organism: which species are present at this time
4. Systemic considerations: fever, dehydration, sepsis, airway, shock, etc.
Sources of infections of the jaws may be broadly classified into four major
categories:
1. Pulpal: carious spread to the pulp
2. Periodontal: deep infected pockets
3. Pericoronal: associated with a partially erupted tooth
4. Post-traumatic: post injury or surgery
These represent the main portals of entry into tissue. Early intervention is often
aimed at eliminating the cause, eg. tooth removal, and therefore turning off the
ongoing supply of organisms to deeper tissues. Which deeper tissue that may be
involved next can often be predicted by establishing the source and through applied
anatomy anticipate natural planes of spread. Occasionally; however, the cause is
obscure or possibly irrelevant. This again refers to the dynamic nature of many
infections.
Having gained access to tissue the infection, through time, can spread through a
number of stages:
1. Primary: the immediate point of access, eg. the pulp
2. Secondary: spread to adjacent tissue, eg. the PDL and bony cavity
3. Tertiary: break out to adjacent soft tissue spaces, eg. buccal space
4. Quaternary: fascial spread to deep spaces, eg. parapharyngeal
Exact establishment of just where the infection has spread to is probably the most
important point to assess. This is particulary true of those that have reached the
quaternary stage. Deep space infections involving the para-and retropharyngeal
spaces directly threaten the airway, the great vessels of the neck and the structures
of the mediastinum. Assessment of signs and symptoms will allow the clinician to
"map out the spread of the infection and thereby assess progress through time or
anticipate problems. This will be highlighted during discussion of the "danger"
signals.
Knowledge of the organism in question is a tremendous aid in selection of
appropriate antibiotic therapeutics. Unfortunately, this information is usually only
available after necessary treatment has begun. This forces us into empirical
management on the basis of the "most likely" pathogens. The vast majority of dental
infections begin with aerobic gram positive Streptococcus species. This presents
clinically as the firm indurated swelling of a facial cellutitis. With time, this evolves
into the predominantly anaerobic, mixed abcess. This is more localized with the
fluctuance of pus formation deep in the tissue.
While this interesting information on a statistical basis over a large sample of
patients, it may not apply to the individual sitting in your large sample of patients, it
may not apply to the individual sitting in your office. For this reason, the submission
of a sample of infective material to a laboratory for culture and sensitivity at the
earliest possible moment can be critical. While in many cases empirical use of
antibiotics will help to clear an infection, the occasional case that continues to worsen
may benefit tremendously from a timely culture and sensitivity report.
A crucial aspect of diagnosis that must be established at the time of presentation are
systemic considerations. These involve the underlying health of the individual
independent of the infection as well as the systemic toxic effects of the infection.
Systemic illness, for example, diabetes, may point the way to a potential role in
etiology as well as highlight management consideration during the course of the
illness. Systemic toxicity, for example, fever, dehydration or even septic shock
illustrate the seriousness of the infection, dictate management and by their
disappearance denote improvement.
We have now established a diagnosis with respect to the cause, extent and systemic
effects of the infection. Further we have a "best guess" for the guilty organism. From
here we move to the next stage of management which is treatment.
B. Treatment:
The first point to note is that the treatment for each individual is individualized.
Systemic health considerations and severity of infection both dictate the nature and
order of steps. Never the less, some basic generalizations apply. Priorities are as
follows:
1. Airway
a) Anatomical considerations: Generally, the more posterior the infection, the
more seriously endangered is the airway. In addition, assessment is difficult
because of the almost universal trimus that is superimposed. If there is
suspicion of significant danger to the airway, hospital management is
mandatory. Airway involvement tends to progress rapidly and artificial or
surgical procurement of an airway is best managed in the OR.
2. Systemic Health ( fever, dehydration, generalized toxicity)
a) Antipyretics (NB with children because of the danger of convulsions)
b) Fluid management to restore losses due to fever and limitation of oral
intake.
3. Initiation of antibiotics .......IF INDICATED
a) For the minor infection.....are they necessary?
b) For the early infection.....mostly aerobic strep, therefore use Penicillin.
c) For the established infection....superimposed anaerobes....add Flagyl
d) For the penicillin allergic..... clindamycin (depends on the nature of the
allergy....consult with patient's physician)
e) For the non-resolving infection...C and S report is crucial, blood cultures or
non-drained abcess
f) For the resistant organism....C and S
g) Dose - more serious....larger
h)Timing - more serious....often
i) Route - more serious....IV
j) Combination - more serious....second drug, avoid combination of
bacteriostatic and bactericidal antibiotics, eg. tetracyclines and penicillin
4. Surgery.......IF INDICATED
a) Of the cause.....eg. Pulpal infection .vs. pericoronitis
b) Of the secondary spread.....either intra- or extra-oral
c) Of the true abcess.....mandatory incision and drainage with C&S
5. Follow up monitoring
a) Symptoms.....pain, malaise
b) Signs.....temperature and pulse
c) Laboratory.....blood culture
d) Clinical progress.....swelling, trimus, regional lymphadenopathy
6. Modification of therapy
a) In the face of worsening
b) In the face of the C and S report
c) In the face of improvement
d) In the face of complications
C. Danger signs of serious infection
A special note at this stage should be made regarding the signs and symptoms of
serious, potentially dangerous infections. These arise as a function of organism
virulence, anatomical spread or poor underlying health of the patient. Twelve big
danger signs must be watched for:
1. Significant trimus: airway
2. Significant odynophagia: airway
3. Dysphagia: airway
4. Dyspnea: airway
5. Elevation of the tongue: airway
6. Deviation of the uvula: airway
7. Bilateral swelling: airway, virulent
8. Rapid severe swelling: virulent
9. Chest pain: mediastinal spread
10. Obvious overt systemic toxicity: virulence, systemic health
11. Eye signs: cavernous sinus thrombosis
12. Clouding or loss of consciousness: cavernous sinus thrombosis, CNS spread
I would like to close by highlighting the following. Infections are dynamic
changing clinical problems that require sustained vigilance and prompt
responses to events as they transpire. Effective responses are born of
thorough knowledge of anatomy, the infective process and the underlying
patient.