Odontogenic Infection

OdontogenicOdontogenic
Infection 1Infection 1
Dr. Adel I. AbdelhadyDr. Adel I. Abdelhady
BDS, MSc ( Tanta, Eg.), PhD (Egypt,USABDS, MSc ( Tanta, Eg.), PhD (Egypt,USA((
Ass. Prof. Oral and Maxillofacial surgeryAss. Prof. Oral and Maxillofacial surgery,,
Collage of DentistryCollage of Dentistry
King Faisal UniversityKing Faisal University
"Do not let sun sets on prisoned pus"

Odontogenic InfectionOdontogenic Infection
Infection due to
dental cause.
Oral flora is the
main source of OI:
Aerobic and
Anaerobic Gr-ve
and Gr. +ve cocci
and rods.

Oral flora is the main source ofOral flora is the main source of
odontogenic infectionodontogenic infection
bacteriabacteria PercentagePercentage % of Aerobic & Anaerobic% of Aerobic & Anaerobic
AerobicAerobic 7 %7 % Aerobic 25 %Aerobic 25 %
Anaerobic 75 %Anaerobic 75 %
Of the causative organismsOf the causative organisms
(number of patients was 404(.(number of patients was 404(.
AnaerobicAnaerobic 33 %33 %
MixedMixed 60 %60 %

Routes ofRoutes of
odontogenicodontogenic
infectionsinfections
▼▼
PulpalPulpal
oror
PeridontiumPeridontium
oror
SystemicSystemic

Infection Arising and SpreadingInfection Arising and Spreading
 Effectiveness of patientEffectiveness of patient
immune mechanismimmune mechanism
 Microbe---virulenceMicrobe---virulence
 QuantityQuantity
 Failure to drainFailure to drain
accumulation pusaccumulation pus
Balance ImbalanceBalance Imbalance
ScaleScale

The Anatomical Factors InfluencingThe Anatomical Factors Influencing
the direction of spread within thethe direction of spread within the
tissuestissues
 The site of the source of infection , upperThe site of the source of infection , upper
or lower jawor lower jaw
 The point at which the pus escapes fromThe point at which the pus escapes from
the bone to the soft tissues labiobucally orthe bone to the soft tissues labiobucally or
linguopalatallylinguopalatally
 The natural barriers to the spread of pus inThe natural barriers to the spread of pus in
the tissues as layer of fascia , muscle orthe tissues as layer of fascia , muscle or
jaw bonejaw bone

Sequence of odontogenicSequence of odontogenic
infectionsinfections
fascial spaces
Soft tissue &
cortical bone
Erosion of cancellous bone
Periapical through pulp necrosis
Periodontal through deep periodontal pocket

Alveolar
bone
Soft tissue
Fascial space
Alveolar
bone
Soft tissue
Fascial space
Trait of anatomyTrait of anatomy
Tooth andTooth and
PeriodontiumPeriodontium
Caries
Pulpitis
Apical
infection
Caries
Pulpitis
Apical
infection

Odontogenic infectionOdontogenic infection
• Periapical infection
•Periodontal
• Pericoronitis
• Periapical infection
•Periodontal
• Pericoronitis

PericoronitisPericoronitis
Lower third molarLower third molar

Periapical infectionPeriapical infection
Acute-chronic
Periapical
infection
Acute-chronic
Periapical
infection
Fistular
Cellulitis
Intraoral
soft tissue
abscess
Osteomyelitis
Septicemia
Deep fascial
space
infection
Ascending facial-
cerebral infection

Pathways of Periapical infectionPathways of Periapical infection

Changing directionsChanging directions
 Localization andLocalization and
recoveryrecovery
 Acute chronicAcute chronic
 Diffusion or spreadDiffusion or spread
Blood system---Septicemia
lymphoid system---
Lymphadenopathy
From submandibular
space infection
spread to chest region

Inflammation as a Sign of Odontogenic InfectionInflammation as a Sign of Odontogenic Infection
 Inflammation is an important pathologic process oftenInflammation is an important pathologic process often
encountered by dentists . As an indicator of disease, it hasencountered by dentists . As an indicator of disease, it has
been recognized for centuries. Almost 2,000 years ago,been recognized for centuries. Almost 2,000 years ago,
the Roman physicianthe Roman physician CelsusCelsus recognized the warmth,recognized the warmth,
redness, swelling, and pain associated with now is knownredness, swelling, and pain associated with now is known
asas "inflammation“."inflammation“.
 These events caused by a series of cellular and tissueThese events caused by a series of cellular and tissue
responses to some injurious agent. These responses areresponses to some injurious agent. These responses are
directed atdirected at

destroying the incitingdestroying the inciting ‫المحرض‬‫المحرض‬ agent or, rendering itagent or, rendering it
harmless, isolates the agent and prevents its spread toharmless, isolates the agent and prevents its spread to
other locations.other locations.
 All this activity may cause damage or destruction toAll this activity may cause damage or destruction to
normal tissue in the immediate area; the inflammatorynormal tissue in the immediate area; the inflammatory
process cleans up resulting debris and starts restoringprocess cleans up resulting debris and starts restoring
damaged tissuesdamaged tissues

Types of InflammationTypes of Inflammation
 There are two fundamentalThere are two fundamental
types of inflammation:types of inflammation:
acute and chronic.acute and chronic.
 A rapid onset, shortA rapid onset, short
duration, and profoundduration, and profound
signs and symptomssigns and symptoms
characterizecharacterize acuteacute
inflammation.inflammation.
 On the other hand, a slowOn the other hand, a slow
onset, long duration, andonset, long duration, and
less obvious signs andless obvious signs and
symptoms characterizesymptoms characterize
chronic inflammation.chronic inflammation.
 In addition to the two basicIn addition to the two basic
forms (acute and chronic),forms (acute and chronic),
there are two others thatthere are two others that
appear less commonly:appear less commonly:
subacute and granulomatoussubacute and granulomatous
chronic inflammation.chronic inflammation.
Subacute inflammationSubacute inflammation is anis an
ill-defined form that hasill-defined form that has
some clinical features ofsome clinical features of
acute and some of chronicacute and some of chronic
inflammation or predisposeinflammation or predispose
to chronic infection.to chronic infection.
 Granulomatous,Granulomatous, is ais a
special form of chronicspecial form of chronic
inflammation e.g.inflammation e.g.
tuberculosis.tuberculosis.


Life Threatening Infection

Intraoral infection with a skin fistula

Acute InflammationAcute Inflammation
 A series of responses of small bloodA series of responses of small blood
vessels and some blood and tissue cellsvessels and some blood and tissue cells
to "injurious" agents resulting into "injurious" agents resulting in
weakening, destruction, or isolation ofweakening, destruction, or isolation of
the agent.the agent.
 In the first minutes, small blood vesselsIn the first minutes, small blood vessels
(capillaries and venules) increase their(capillaries and venules) increase their
diameter (dilate) allowing more blood todiameter (dilate) allowing more blood to
flow into the area.flow into the area.
 This increased blood flow is fed byThis increased blood flow is fed by
dilation of supplying arterioles, a processdilation of supplying arterioles, a process
known as "active hyperemia" (hyper- =known as "active hyperemia" (hyper- =
increased; -emia = blood). Withincreased; -emia = blood). With
increased blood flow, increased numbersincreased blood flow, increased numbers
of blood cells enter the area too Fever,of blood cells enter the area too Fever,
leukocytosisleukocytosis, abscesses, and cellulitis, abscesses, and cellulitis
may be presentmay be present ..

MicrobiologyMicrobiology
 Odontogenic infections are multi-Odontogenic infections are multi-
microbial:microbial:
 Gram (+) cocci, aerobic and anaerobic:Gram (+) cocci, aerobic and anaerobic:
 Streptococci and their anaerobicStreptococci and their anaerobic
counterpart, peptostreptococcicounterpart, peptostreptococci
 Staphylococci, and their anaerobicStaphylococci, and their anaerobic
counterpart, peptococcicounterpart, peptococci
 Gram (+) rods:Gram (+) rods:
 Lactobacillus, diphtheroids, actinomycesLactobacillus, diphtheroids, actinomyces
 Gram (-) rods:Gram (-) rods:
 Fusobacterium, Bacteroids,Fusobacterium, Bacteroids,

Host FactorsHost Factors
Immunity against intraoral infection isImmunity against intraoral infection is
composed of three sets of mechanisms:composed of three sets of mechanisms:
 Humeral factorsHumeral factors
 Cellular factorsCellular factors
 Local factorsLocal factors
Decrease one of these mechanisms followedDecrease one of these mechanisms followed
by increases the potential for infection andby increases the potential for infection and
spread of infection may be supervene.spread of infection may be supervene.

Humoral FactorsHumoral Factors
 Circulating immunoglobulins, along withCirculating immunoglobulins, along with
complement, combine with microbes tocomplement, combine with microbes to
form opsonins that promote phagocytosisform opsonins that promote phagocytosis
by macrophages.by macrophages.
 IgA prevents colonization of microbes onIgA prevents colonization of microbes on
oral mucosal surfaces.oral mucosal surfaces.
 In the presence of infection, histamine,In the presence of infection, histamine,
serotonin, prostaglandins supportserotonin, prostaglandins support
inflammationinflammation →→ vasodilation and increasedvasodilation and increased
vascular permeability.vascular permeability.

Cellular factorsCellular factors
 Phagocytes engulf and kill microbes,Phagocytes engulf and kill microbes,
removing them, preventing replication.removing them, preventing replication.
 Lymphocytes produce lymphokines andLymphocytes produce lymphokines and
immunoglobulines (aids humoral).immunoglobulines (aids humoral).
 Lymphokines stimulate reproduction ofLymphokines stimulate reproduction of
other lymphocytes, and kills antigens.other lymphocytes, and kills antigens.

Local FactorsLocal Factors
 Specific factors leading to resistance:Specific factors leading to resistance:
 Abundant vascular supply allowingAbundant vascular supply allowing
humoral and cellular response.humoral and cellular response.
 Mechanical cleansing by salivary flow.Mechanical cleansing by salivary flow.
 Secretory IgA contained within saliva.Secretory IgA contained within saliva.

Host defence mechanismsHost defence mechanisms
LocalLocal
defencesdefences
HumoralHumoral
defencesdefences
CellularCellular
defencesdefences
• Intact anatomicIntact anatomic
barrierbarrier
• IndigenousIndigenous
bacteriabacteria
• ImmunoglobulinsImmunoglobulins
• ComplementComplement
• phagocytesphagocytes
• GranulocytesGranulocytes
• MonocytesMonocytes
• LymphocytesLymphocytes

Compromised host defencesCompromised host defences
UncontrolledUncontrolled
metabolic diseasesmetabolic diseases
SuppressingSuppressing
diseasesdiseases
Suppressing drugsSuppressing drugs
 UremiaUremia
 AlcoholismAlcoholism
 MalnutritionMalnutrition
 Severe diabetesSevere diabetes
 LeukaemiaLeukaemia
 LymphomaLymphoma
 MalignantMalignant
tumourstumours
 chemotherapeuticschemotherapeutics
 ImmunosuppressivesImmunosuppressives

Clinical FeaturesClinical Features
 Inflammation is tissue responseInflammation is tissue response
to injury or invasion byto injury or invasion by
microorganisms that involvesmicroorganisms that involves
vasodilation, capillaryvasodilation, capillary
permeability, mobilization ofpermeability, mobilization of
leukocytes, and phagocytosis.leukocytes, and phagocytosis.
 Cardinal signs of inflammationCardinal signs of inflammation::
 Red, hot, swelling, pain, with loss ofRed, hot, swelling, pain, with loss of
functionfunction
 Other findings:Other findings: regionalregional
lymphadenopathylymphadenopathy,, fever, elevated whitefever, elevated white
blood cell count, tachycardia,blood cell count, tachycardia,
tachypnea, dehydration, malaise.tachypnea, dehydration, malaise.


Oral tissue examinationOral tissue examination
 Examine quality and consistency:Examine quality and consistency:
 Soft to fluctuant (fluid filled) to hardSoft to fluctuant (fluid filled) to hard
(indurated)(indurated)
 Color and temperature determineColor and temperature determine
the presence and extent ofthe presence and extent of
infectioninfection
 Normal v abnormal tissueNormal v abnormal tissue
architecture:architecture:
 Distortion of mucobuccal foldDistortion of mucobuccal fold
 Soft palate symmetric with uvula inSoft palate symmetric with uvula in
midlinemidline (deviation → involvement of(deviation → involvement of
lateral pharyngeal space(lateral pharyngeal space(
 Nasolabial fold, circumorbital areasNasolabial fold, circumorbital areas

Examination, con’tExamination, con’t..
 Identify causative factors:Identify causative factors:
 Tooth, root tip, foreign body, etc.Tooth, root tip, foreign body, etc.
 Vital signs should be taken:Vital signs should be taken:
 TemperaturesTemperatures >> 101 to 102°F accompanied101 to 102°F accompanied
by an elevated heart rate indicate systemicby an elevated heart rate indicate systemic
involvement of the infection and increasedinvolvement of the infection and increased
urgency of treatment.urgency of treatment.

How to diagnoseHow to diagnose??
 Local Signs and SymptomsLocal Signs and Symptoms
 Systemical Signs and SymptomsSystemical Signs and Symptoms
Signs and Symptoms

Local Signs and SymptomsLocal Signs and Symptoms
 PainPain
 SwellingSwelling
 Surface erythemaSurface erythema
 Pus formationPus formation
 Limitation of motionLimitation of motion
LocallyLocally

Systemical Signs and SymptomsSystemical Signs and Symptoms
 FeverFever
 LymphadenopathyLymphadenopathy
 MalaiseMalaise
 Toxic appearanceToxic appearance
 LeukocytosisLeukocytosis

Management of odontogenicManagement of odontogenic
infectioninfection
 Prevention of the odontogenic infection is thePrevention of the odontogenic infection is the
golden standardgolden standard
 Mild odontogenic infection can be easilyMild odontogenic infection can be easily
treated with simple antibiotictreated with simple antibiotic
 Complex odontogenic infection may requireComplex odontogenic infection may require
an incision and drainagean incision and drainage
 Complicated odontogenic infection mayComplicated odontogenic infection may
require patient admission and hospitalizationrequire patient admission and hospitalization
 Any odontogenic infection should be treatedAny odontogenic infection should be treated
promptly and not be underestimated!promptly and not be underestimated!
Why?Why?

To avoid the following complicationsTo avoid the following complications::
 Scaring and sinus & fistulaScaring and sinus & fistula
formation.formation.
 Loss of bone and teethLoss of bone and teeth
 Spread to potential fascialSpread to potential fascial
spaces and airwayspaces and airway
 Orbital and intracranialOrbital and intracranial
spread via facial andspread via facial and
angular veinsangular veins
 Spread into the neck, withSpread into the neck, with
large vessel complicationslarge vessel complications
 Septic shock from gram –veSeptic shock from gram –ve

The routes by which theThe routes by which the
infection can spreadinfection can spread
 1-By direct continuity through the tissues1-By direct continuity through the tissues
 2-By the lymphatics to the regional nodes and2-By the lymphatics to the regional nodes and
eventually into the bloodstream, secondaryeventually into the bloodstream, secondary
abscess may develop.abscess may develop.
 3-By bloodstream ,local thrombophlebitis may3-By bloodstream ,local thrombophlebitis may
propagate along the veins, entering cranialpropagate along the veins, entering cranial
cavity via emissary vein to produce cavernouscavity via emissary vein to produce cavernous
sinus thrombophlebitis , organism or infectedsinus thrombophlebitis , organism or infected
emboli may be swept into blood stream leadingemboli may be swept into blood stream leading
to bacteraemia , septicemia or pyaemiato bacteraemia , septicemia or pyaemia

Site at Which Pus AccumulatesSite at Which Pus Accumulates
 Pus tends to accumulate in specific regions whichPus tends to accumulate in specific regions which
are referred to as tissue spaces, none of which areare referred to as tissue spaces, none of which are
actually spaces until pus has been formed.actually spaces until pus has been formed.
 Some of these potential spaces are compartmentsSome of these potential spaces are compartments
which contain structure such as SG,LN, BPF thesewhich contain structure such as SG,LN, BPF these
structures surrounded by loose connective tissue .structures surrounded by loose connective tissue .
 Pus destroys the loose connective tissue andPus destroys the loose connective tissue and
separate the anatomical boundaries of theseparate the anatomical boundaries of the
compartmentcompartment as it increase in volume, soas it increase in volume, so
creating an abscess cavity bounded bycreating an abscess cavity bounded by
fascia , muscle and bonefascia , muscle and bone

AnatomyAnatomy
Fascial space loose connective tissue
Among skin, maxillary and muscle
•Purulent--- spreading way
•Do not exist in healthy state
•Become filling during infection

Thank you & have a nice
day
Thank you & have a nice
day

Odontogenic Infection 2Odontogenic Infection 2
BDS, MSc ( Tanta, Eg.(, PhD (Egypt,USABDS, MSc ( Tanta, Eg.(, PhD (Egypt,USA((
Tanta UniversityTanta University

CellulitisCellulitis
initial stage of infectioninitial stage of infection
 Diffuse, warm, erythematousDiffuse, warm, erythematous
indurated, hard painfulindurated, hard painful
swelling that is tender toswelling that is tender to
palpation.palpation.
 Inflammatory response notInflammatory response not
yet forming a true abscess.yet forming a true abscess.
 Microorganisms have justMicroorganisms have just
begun to overcome hostbegun to overcome host
defenses and spread beyonddefenses and spread beyond
tissue planes.tissue planes.

True abscess formationTrue abscess formation
 As inflammatory responseAs inflammatory response
matures, may develop a focalmatures, may develop a focal
accumulation of pus.accumulation of pus.
 May have spontaneousMay have spontaneous
drainage intraorally ordrainage intraorally or
extraorally.extraorally.
 Abscess is a pocket of tissueAbscess is a pocket of tissue
containing necrotic tissue,containing necrotic tissue,
bacterial colonies,and deadbacterial colonies,and dead
white cells, the area may orwhite cells, the area may or
may not be fluctuant, the pat.may not be fluctuant, the pat.
Is often is a febrile, oftenIs often is a febrile, often
cused by anaerobic bacteria.cused by anaerobic bacteria.

Cellulitis Vs AbscessCellulitis Vs Abscess
Diffuse swelling
Localized swelling

Differences between cellulitis and abscessDifferences between cellulitis and abscess
CharacteristicsCharacteristics CellulitisCellulitis AbscessAbscess
DurationDuration AcuteAcute 3-5 days3-5 days Chronic 5 daysChronic 5 days
PainPain Sever andSever and
generalizedgeneralized
LocalizedLocalized
SizeSize LargeLarge SmallSmall
LocalizationLocalization Diffuse bordersDiffuse borders WellWell
circumscribedcircumscribed
PalpationPalpation Doughy to induratedDoughy to indurated Fluctuant, tenderFluctuant, tender
Presence of pusPresence of pus NoNo YesYes
Degree ofDegree of
seriousnessseriousness
GreaterGreater lessless
BacteriaBacteria AerobicAerobic AnaerobicAnaerobic

Types of odontogenic infectionTypes of odontogenic infection
 Simple, localised and controllableSimple, localised and controllable
 PeriapicalPeriapical
 PeriodontalPeriodontal
 VestibularVestibular
 PalatalPalatal
 Complex, invasive and may be dangerousComplex, invasive and may be dangerous
 Fascial spacesFascial spaces
 LungLung
 BrainBrain
 MediastinumMediastinum
 Metastatic infection to the heart subacuteMetastatic infection to the heart subacute
bacterial endocarditisbacterial endocarditis

Simple odontogenic infectionSimple odontogenic infection

Infection of fascial spacesInfection of fascial spaces

Potential fascial spacesPotential fascial spaces
Primary MandibularPrimary Mandibular
spacesspaces
Primary MaxillaryPrimary Maxillary
spacesspaces
Secondary fascialSecondary fascial
spacesspaces
SublingualSublingual
 BuccalBuccal
SubmandibularSubmandibular
SubmentalSubmental
CanineCanine
BuccalBuccal
InfratemporalInfratemporal
MassetericMasseteric
PterygomandibularPterygomandibular
Superficial and deepSuperficial and deep
temporaltemporal
Lateral pharyngealLateral pharyngeal
RetropharyngealRetropharyngeal
PrevertebralPrevertebral

Potentially Infected Fascial Spaces

Fascial SpacesFascial Spaces
 Bound by the fascial layers investingBound by the fascial layers investing
muscles of the body, they contain variousmuscles of the body, they contain various
structures.structures.
 Delineate different regions in the body.Delineate different regions in the body.
 These areThese are potential spaces.potential spaces.
 They are not true spaces, or voids, butThey are not true spaces, or voids, but
infections and body’s biochemicalinfections and body’s biochemical
response can "dissect" along these fascialresponse can "dissect" along these fascial
layers as a means of spreadinglayers as a means of spreading

Fascial LayersFascial Layers
 Two main fascial layers in head andTwo main fascial layers in head and
neck are superficial (lying closest toneck are superficial (lying closest to
the surface) and deep cervical fasciathe surface) and deep cervical fascia
(cloaking anterior and posterior(cloaking anterior and posterior
regions of the neck).regions of the neck).

Superficial Cervical FasciaSuperficial Cervical Fascia
 Continuation of deltopectoral fascia of ant.Continuation of deltopectoral fascia of ant.
chest wall, Camper’s fascia of abdomen.chest wall, Camper’s fascia of abdomen.
 Contains the intrinsic muscles of the faceContains the intrinsic muscles of the face
and neck innervated by CN VII.and neck innervated by CN VII.
 Most associated infections result fromMost associated infections result from
cellulitis, folliculitis, carbuncle, furuncle, orcellulitis, folliculitis, carbuncle, furuncle, or
trauma to overlying skin.trauma to overlying skin.
 Although there is potential for spread toAlthough there is potential for spread to
deeper layers, treatment is usually directdeeper layers, treatment is usually direct
incision over the fluctuance.incision over the fluctuance.

Deep Cervical FasciaDeep Cervical Fascia
 Contains muscles, viscera, andContains muscles, viscera, and
neurovascular bundles in fascial sheets.neurovascular bundles in fascial sheets.
 Acts as the lubricating system ofActs as the lubricating system of
musculoskeletal system.musculoskeletal system.
 The continuation and bony attachmentsThe continuation and bony attachments
form the planes and compartmentsform the planes and compartments
containing deeper structures.containing deeper structures.

Carotid SheathCarotid Sheath
 Contains, carotid artery, internal jugularContains, carotid artery, internal jugular
vein, and vagus nerve.vein, and vagus nerve.
 Ansa cervicalis, sympathetic trunk, andAnsa cervicalis, sympathetic trunk, and
lymphatics are adjacent, but not within.lymphatics are adjacent, but not within.
 Intrathoracic propagation may lead toIntrathoracic propagation may lead to
mediastinitis, empyema, and pericarditis.mediastinitis, empyema, and pericarditis.

Cervical Fascia CFCervical Fascia CF
 Superficial LayerSuperficial Layer
 Deep LayerDeep Layer
 Subdivisions notSubdivisions not
histologically separatehistologically separate
 SuperficialSuperficial
 Enveloping layerEnveloping layer
 Investing layerInvesting layer
 MiddleMiddle
 Visceral fasciaVisceral fascia
 Prethyroid fasciaPrethyroid fascia
 Pretracheal fasciaPretracheal fascia
 Deep layer of DCFDeep layer of DCF

Superficial fasciaSuperficial fascia
 Superior attachment –Superior attachment –
zygomatic processzygomatic process
 Inferior attachment –Inferior attachment –
thorax, axilla.thorax, axilla.
 Similar toSimilar to
subcutaneous tissuesubcutaneous tissue
 Ensheathes platysmaEnsheathes platysma
and muscles of facialand muscles of facial
expressionexpression

Superficial Layer of the DeepSuperficial Layer of the Deep
Cervical FasciaCervical Fascia
 Completely surrounds theCompletely surrounds the
neck.neck.
 Arises from spinousArises from spinous
processes.processes.
 Superior border – nuchalSuperior border – nuchal
line, skull base, zygoma,line, skull base, zygoma,
mandible.mandible.
 Inferior border – chest andInferior border – chest and
axillaaxilla
 Splits at mandible andSplits at mandible and
covers the massetercovers the masseter
laterally and the mediallaterally and the medial
surface of the medialsurface of the medial
pterygoid.pterygoid.
 EnvelopesEnvelopes
 SCMSCM
 TrapeziusTrapezius
 SubmandibularSubmandibular
 ParotidParotid
 Forms floor ofForms floor of
submandibular spacesubmandibular space

Deep Neck SpacesDeep Neck Spaces
 Described in relation to the hyoid.Described in relation to the hyoid.
 Entire length of neckEntire length of neck
 Superficial spaceSuperficial space
 RetropharyngealRetropharyngeal
 DangerDanger
 PrevertebralPrevertebral
 Vascular visceralVascular visceral
 SuprahyoidSuprahyoid
 SubmandibularSubmandibular
 PharyngomaxillaryPharyngomaxillary
(Parapharyngeal)(Parapharyngeal)
 ParotidParotid
 PeritonsillarPeritonsillar
 TemporalTemporal
 MasticatorMasticator
 InfrahyoidInfrahyoid
 Anterior visceralAnterior visceral

Superficial SpaceSuperficial Space
 Entire length of neckEntire length of neck
 Surrounds platysmaSurrounds platysma
 Contains areolar tissue,Contains areolar tissue,
nodes, nerves and vesselsnodes, nerves and vessels
 Subplatysmal FlapsSubplatysmal Flaps
 Involved with cellulitis andInvolved with cellulitis and
superficial abscessessuperficial abscesses
 Treat with incision alongTreat with incision along
Langer’s lines, drainageLanger’s lines, drainage
and antibioticsand antibiotics

Retropharyngeal SpaceRetropharyngeal Space
 Entire length of neck.Entire length of neck.
 Anterior border - pharynx andAnterior border - pharynx and
esophagus (buccopharyngealesophagus (buccopharyngeal
fascia)fascia)
 Posterior border - alar layer ofPosterior border - alar layer of
deep fasciadeep fascia
 Superior border - skull baseSuperior border - skull base
 Inferior border – superiorInferior border – superior
mediastinummediastinum
 Combines withCombines with
buccopharyngeal fascia atbuccopharyngeal fascia at
level of T1-T2level of T1-T2
 Midline raphe connectsMidline raphe connects
superior constrictor to the deepsuperior constrictor to the deep
layer of deep cervical fascia.layer of deep cervical fascia.
 Contains retropharyngealContains retropharyngeal
nodes.nodes.

Parotid SpaceParotid Space
 Superficial layer of deepSuperficial layer of deep
fasciafascia
 Dense septa fromDense septa from
capsule into glandcapsule into gland
 Direct communication toDirect communication to
parapharyngeal spaceparapharyngeal space
 ContainsContains
 External carotid arteryExternal carotid artery
 Posterior facial veinPosterior facial vein
 Facial nerveFacial nerve
 Lymph nodesLymph nodes

Odontogenic Infection 3Odontogenic Infection 3
BDS, MSc ( Tanta, Eg.), PhD (Egypt,USABDS, MSc ( Tanta, Eg.), PhD (Egypt,USA))
Tanta UniversityTanta University

Fascial Layers of the Neck
 Two main fascial divisions exist, the superficial cervical
fascia and the deep cervical fascia.
 Superficial cervical fascia
 just deep to the dermis
 surrounds the muscles of fscial expression
 includes the superficial musculoaponeurotic system (SMAS)
 extends from the epicranium to the axillae and chest
 space deep to this layer contains fat, neurovascular bundles,
and lymphatics

Deep cervical fascia
 encloses the deep neck spaces
 3 layers, the superficial, middle, and deep
layers of the deep cervical fascia.

The superficial layer of the deep cervical fascia
 investing fascia that surrounds the neckencompasses the
sternocleidomastoid muscle, trapezius, muscles of
mastication, and submandibular and parotid glands,
limited superiorly by the nuchal ridge, mandible, zygoma,
mastoid, and hyoid bones
 Inferiorly, it is bounded by the clavicles, sternum,
scapula, hyoid, and acromion, contributes to the fascia
covering the digastric muscle and to the lateral aspect of
the carotid sheathIn its course from the hyoid bone to the
medial table of the ramus of the mandible, it envelops the
anterior belly of the digastric muscle and forms the floor
of the submandibular space
 Laterally, this fascia helps to define the parotid and
masticator spaces

The middle layer of the deep cervical
fascia
 2 divisions, muscular and visceral
 muscular division surrounds the strap muscles (ie,
sternohyoid, sternothyroid, thyrohyoid, omohyoid) and
the adventitia of the great vessels
 visceral division surrounds the constrictor muscles of the
pharynx and esophagus to create the buccopharyngeal
fascia and the anterior wall of the retropharyngeal space
 Both the muscular and visceral divisions contribute to the
formation of the carotid sheath
 also envelops the larynx, trachea, and thyroid gland
 attaches to the base of the skull superiorly and extends
inferiorly as low as the pericardium via the carotid sheath

The deep layer of the deep cervical
fascia
 2 divisions, prevertebral and alar
 prevertebral division adheres to the anterior aspect of the vertebral
body and extends laterally to the transverse processes of the
vertebrae.
 alar division lies between the prevertebral division and the visceral
division of the middle layer and defines the posterior border of the
retropharyngeal space
 surrounds the deep neck muscles and contributes to the carotid
sheath
 Posteriorly, the muscular division of the middle layer of the deep
cervical fascia fuses with the alar division of the deep layer of the
deep cervical fascia at the level of thoracic vertebrae 1-2 (T1-T2).

Sublingual spaceSublingual space 11
 Borders:Borders:
 Anterior – mandibleAnterior – mandible
 Posterior – submandibular spacePosterior – submandibular space
 Superior – oral mucosaSuperior – oral mucosa
 Inferior – mylohyoidInferior – mylohyoid
 Medial – tongue musclesMedial – tongue muscles
 Lateral – mandibleLateral – mandible
 Contains sublingual gland, lingual nerve, sublingual a &Contains sublingual gland, lingual nerve, sublingual a &
v Wharton's duct, hypoglossal nerve.v Wharton's duct, hypoglossal nerve.
 Infection would lead to dysphagia, pain, elevation ofInfection would lead to dysphagia, pain, elevation of
the floor of mouth and sup. displacement of tonguethe floor of mouth and sup. displacement of tongue..

Sublingual spaceSublingual space 22

Submandibular spaceSubmandibular space 11
 Anterior – anterior belly of digastricAnterior – anterior belly of digastric
 Posterior – posterior belly ofPosterior – posterior belly of
digastric/stylohyoid/digastric/stylohyoid/
stylopharyngeusstylopharyngeus
 Superior – mylohyoid/mandibleSuperior – mylohyoid/mandible
 Inferior – digastric tendon andInferior – digastric tendon and
hyoidhyoid
 Deep –Deep –
mylohyoid/mylohyoid/hyoglossus/styloglhyoglossus/stylogl
 Superficial –Superficial – platysma / faciaplatysma / facia

Pathways of spread of submandibularPathways of spread of submandibular
space infection from mandibular molarspace infection from mandibular molar

Submandibular SpaceSubmandibular Space
 Likely cause
 Lower molars
 Neighboring space
 Sublingual
 Lateral pharyngeal
 Submental
 Buccal
 Contents
 Submandibular gland
 Lymph nodes
 Hypoglossal nerve
 Nerve to mylohyoid
 Facial artery and vein
 S/S
 Extraoral below
inferior border
 May obliterate
inferior border
 Site for I&D
 Extraoral -
Submandibular
incision

Submandibular SpaceSubmandibular Space

Submental spaceSubmental space
 Sup.Sup. MylohyoidMylohyoid
 Inf.Inf. Platysma, Skin,Platysma, Skin,
 Ant.Ant. Lingual mandibleLingual mandible
 Post.Post. HyoidHyoid
 Med.Med. Common space, no medial wallCommon space, no medial wall
 Lat.Lat. Medial MandibleMedial Mandible
 Causes: from mand. incisor teeth or continuationCauses: from mand. incisor teeth or continuation
form submandibular space infection andform submandibular space infection and
SymphysisSymphysis fracturefracture

Ludwig’s anginaLudwig’s angina
 Hippocrates in 1836, a postmortem findings,Hippocrates in 1836, a postmortem findings,
Karl Friedrich WilhelmKarl Friedrich Wilhelm von Ludwigvon Ludwig
 A rapidly progressive gangrenous cellulitisA rapidly progressive gangrenous cellulitis
originating in submandibular gland.originating in submandibular gland.
 Inflammatory distention of the fascial planesInflammatory distention of the fascial planes
of the neck can lead to respiratory tractof the neck can lead to respiratory tract
obstruction and death.obstruction and death.
 It extends by continuity rather than lymphaticIt extends by continuity rather than lymphatic
spread.spread.
 Mortality rate exceeds 50% during the pre-Mortality rate exceeds 50% during the pre-
antibiotic era, attributed to overwhelmingantibiotic era, attributed to overwhelming
sepsis.sepsis.

 Infection of 5 spaces;Infection of 5 spaces;
submental, and bilateralsubmental, and bilateral
submandibular andsubmandibular and
sublingual spaces.sublingual spaces.
 Foul serosanguinous fluid,Foul serosanguinous fluid,
no frank purulence. Fascia,no frank purulence. Fascia,
muscle, connective tissuemuscle, connective tissue
involvement, sparinginvolvement, sparing
glandsglands

Signs and symptomsSigns and symptoms::
 Brauny oedema of theBrauny oedema of the
spaces.spaces.
 Paucity of pusPaucity of pus
(therefore not an(therefore not an
abscess).abscess).
 No lymphadenopathy.No lymphadenopathy.
 Minimal inflammation ofMinimal inflammation of
pharynx.pharynx.

Ludwig’s angina with bilateralLudwig’s angina with bilateral
involvement of sublingual andinvolvement of sublingual and
submandibular spacessubmandibular spaces

Infection in multi-spaceInfection in multi-space

Surgical interventionSurgical intervention
 DecompressionDecompression
sublingual andsublingual and
submandibular spaces.submandibular spaces.
Incision andIncision and
drainagedrainage
 DebridementDebridement

Masticator and Temporal SpacesMasticator and Temporal Spaces
 SuprahyoidSuprahyoid
 Formed by superficial layer ofFormed by superficial layer of
deep cervical fasciadeep cervical fascia
 Masticator spaceMasticator space
 Antero-lateral toAntero-lateral to
pharyngomaxillary space.pharyngomaxillary space.
 ContainsContains
 MasseterMasseter
 PterygoidsPterygoids
 Body and ramus of theBody and ramus of the
mandiblemandible
 Inferior alveolar nervesInferior alveolar nerves
and vesselsand vessels
 Tendon of the temporalisTendon of the temporalis
musclemuscle

Submasseteric spaceSubmasseteric space
 BordersBorders
 Anterior – buccal spaceAnterior – buccal space
 Posterior – parotid glandPosterior – parotid gland
 Superior – zygomatic archSuperior – zygomatic arch
 Inferior – inferior border of mandibleInferior – inferior border of mandible
 Superficial – masseterSuperficial – masseter
 Deep – ramusDeep – ramus
 Infection causes trismus.Infection causes trismus.
 Communicates with temporalCommunicates with temporal
fossafossa

Submasseteric spaceSubmasseteric space
 Likely causes
 Lower third molar
 Angle fracture
 Contents
 Masseteric artery
and vein
 Buccal
 Pterygomandibular
 Superficial temporal
 Parotid
 Swelling
 Extraoral over the
masseter/ascending
ramus
 Site of I&D
 Intraoral
 Extraoral –
submandibular
approach

Pathway of spread fromPathway of spread from
masseteric space infectionmasseteric space infection

Infection in masseteric spaceInfection in masseteric space

Superficial and Deep temporalSuperficial and Deep temporal
 Superficial Temporal spacSuperficial Temporal spac
 Anterior – superificalAnterior – superifical
temporalis fasciatemporalis fascia
 Posterior – superficialPosterior – superficial
 Superior – pericraniumSuperior – pericranium
 Inferior – masseteric spaceInferior – masseteric space
 Medial – temporalis muscleMedial – temporalis muscle
 Lateral – superficialLateral – superficial

Deep temporal
 Anterior – temporalis
muscle/infratemporal
space
 Posterior – temporalis
 Superior – temporalis
muscle attachment
 Lateral - temporalis
 Inferior –
infratemporal space
 Medial - squamous
temporal bone

 Likely cause
 Upper molars
 Extension from
submasseteric/pterygomandibular
/infratemporal spaces
 Neighboring spaces
 Submasseteric
 Infratemporal
 Contents
 Temporal arteries and veins
 Swelling
 Above zygomatic arch and
behind lateral orbital rim
 Almost always associated
with trismus
 Site of I&D
 Intraoral – incision at
superior aspect of ascending
ramus and dissect
posteriorly and superiorly on
temporalis into superficial
temporal space then
medially through temporalis
into deep temporal space
 Extraoral – incision parallel
to zygomatic branch of VII,
slightly superior to zygomatic
arch

Infratemporal spaceInfratemporal space
 The infratemporal fossa spaceThe infratemporal fossa space
forms the upper extremity offorms the upper extremity of
pterygomandibular spacepterygomandibular space
 Anterior – maxillary tuberosityAnterior – maxillary tuberosity
 Posterior – mandibular condylePosterior – mandibular condyle
 Superior – infratemporal crest ofSuperior – infratemporal crest of
sphenoid/deep temporal spacesphenoid/deep temporal space
 Inferior – lateral pterygoidInferior – lateral pterygoid
/pterygomandibular spac/pterygomandibular spac
 Medial – lateral pterygoidMedial – lateral pterygoid
plate/pterygopalatine foramenplate/pterygopalatine foramen
 Lateral – coronoidLateral – coronoid
process/temporalis tendonprocess/temporalis tendon

Infratemporal spaceInfratemporal space
 Contains maxillary artery, and pterygoidContains maxillary artery, and pterygoid
plexus of veins.plexus of veins.
 Communicates with submassetric andCommunicates with submassetric and
pterygo-mandibular spaces.pterygo-mandibular spaces.
 One of the potential spaces forOne of the potential spaces for
displacement of maxillary third molars.displacement of maxillary third molars.

Infratemporal space
 Likely cause
 Upper molars
 Extension from
neighboring sites
 Deep temporal
 Contents
 Internal maxillary artery
 Pterygoid plexus of
veins
 V3
 Swelling
 Not clinically seen –
behind tuberosity
 Trismus due to
involvement of
muscles of
mastication
 Site of I&D
 Intraoral – from
pterygomandibular
space
 Extraoral –
submandibular
approach

Buccal spaceBuccal space
 Sup.Sup. ZygomaZygoma
 Inf. deep fascia Inferior border of mandibleInf. deep fascia Inferior border of mandible
 AntromediallyAntromedially Buccinator ms.Buccinator ms.
 Posteromedially Masseter ms.Posteromedially Masseter ms.
 Lat.forward extension of deep fascia fromLat.forward extension of deep fascia from the capsule ofthe capsule of
parotid gland and platysma ms.parotid gland and platysma ms.
 Contains facial artery, vein, and nerve; Stenson’s duct,Contains facial artery, vein, and nerve; Stenson’s duct,
buccal fat pad.buccal fat pad.
 The buccal fat pad acts as an impediment for spread ofThe buccal fat pad acts as an impediment for spread of
infection from buccal to lateral pharyngeal space.infection from buccal to lateral pharyngeal space.

Pathway of spread for buccalPathway of spread for buccal
space infectionspace infection

Buccal space infectionBuccal space infection

Canine spaceCanine space
 If the canine root is short pus from periapical abscessIf the canine root is short pus from periapical abscess
will emerge below the origin of levator anguli oris inwill emerge below the origin of levator anguli oris in
buccal vestibule but if long pus will emerges betweenbuccal vestibule but if long pus will emerges between
levator labii superiors and levator labii superiors alaquelevator labii superiors and levator labii superiors alaque
nasinasi
 Sup.Sup. Origin of levator musclesOrigin of levator muscles
 Inf .Inf . Orbicularis orisOrbicularis oris
 Ant.Ant. Skin, subQSkin, subQ
 Post.Post. MaxillaMaxilla
 Med.Med. Levator labii alaquae nasiiLevator labii alaquae nasii
 Lat.Lat. Zygomaticus majorZygomaticus major
 Contains angular artery and vein, infraorbital foramen.Contains angular artery and vein, infraorbital foramen.
 These provide a path of communication to cavernousThese provide a path of communication to cavernous
sinus via ophthalmic vein, leading to cavernous sinusitissinus via ophthalmic vein, leading to cavernous sinusitis
and brain abscess.and brain abscess.

Areas of spread in infraorbitalAreas of spread in infraorbital
space infectionsspace infections

Pterygomandibular SpacePterygomandibular Space
Borders:Borders:
Anterior – pterygomandibularAnterior – pterygomandibular
raphe/buccal spaceraphe/buccal space
Posterior – parotidPosterior – parotid
Superior – lateral pteygoidSuperior – lateral pteygoid
Inferior – inferior border ofInferior – inferior border of
mandiblemandible
Lateral – ramusLateral – ramus
Medial – medial pterygoidMedial – medial pterygoid
Infection would causes trismus.Infection would causes trismus.
 Commonly would lead to para-Commonly would lead to para-
pharyngeal space involvement.pharyngeal space involvement.

Pterygomandibular SpacePterygomandibular Space
 Likely causes
 Lower third molar
 Angle fracture
 Contents
 V3
 Inferior alveolar vein and artery
 Buccal
 Deep temporal
 submasseteric
 Parotid
 Peritonsillar
 Swelling
 Intraoral over medial
aspect of ramus
 Not usually any
extraoral
 Trismus due to
involvement of medial
pterygoid
 Site of I&D
 Intraoral
 Extraoral -
submandibular

Lateral (Para) pharyngeal spaceLateral (Para) pharyngeal space
 Anterior – pterygomandibular
raphe, sublingual and
submandibular spaces
 Posterior –
retropharyngeal/carotid sheath
 Superior – skull base
 Inferior – hyoid bone
 Medial – superior and middle
constrictors and its coveringand its covering
buccopharyngeal fasciabuccopharyngeal fascia
 Lateral – medial
pterygoid/parotid capsule
 Note: Divided into anterior
(muscular) and posterior
(vascular) compartments, by the
stylohyoid process/ligaments
and muscles
Cone shapeCone shape

Lateral (para) pharyngeal spaceLateral (para) pharyngeal space
 Likely causes
 Lower third molars
 Tonsillar abscess
 Neighboring
spaces
 Submandibular
 Sublingual
 Retropharyngeal
 Peritonsillar
 Contents
 Anterior compartment
 Loose CT
 Lymph nodes
 Ascending pharyngeal
artery
 Posterior compartment
 carotid sheath (ie, carotid
artery, internal jugular vein,
vagus nerve)
 glossopharyngeal
 hypoglossal nerves
 superior sympathetic chain
lymphatics
 accessory nerve

S/S Of Parpharyngeal space
anterior compartment
 bulging of lateral pharyngeal wall
 deviation of uvula
 trismus
 swelling at angle indicates extension to inferior extent of
anterior compartmen
 Posterior compartment
 Posterolateral wall and posterior tonsillar pillar edema
 Minimal trismus
 Cranial nerve involvement (IX-XII)
 Horner’ syndrome (ptosis, miosis, anhidrosis) from
involvement of superior sympathetic chain

I&D Parpharyngeal space
Site of I&D
 Intraoral – anterior compartment
 Extraoral – posterior compartment
(submandibular approach – with finger
dissection to identify hyoid, digastric and
styloid process)
 Carotid space – same as posterior compartment
lateral pharyngeal

Pharyngomaxillary Space orPharyngomaxillary Space or
ParapharyngealParapharyngeal
 Communicates
with several deep
neck spaces.
 Parotid
 Masticator
 Peritonsillar
 Submandibular
 Retropharyngeal

Lateral (para) pharyngeal spaceLateral (para) pharyngeal space
 Infection manifests as:Infection manifests as:
 Trismus, DysphagiaTrismus, Dysphagia
 FeverFever
 Pharyngeal bulgePharyngeal bulge
 Induration at mandibular angleInduration at mandibular angle
 If the posterior compartment is involved:If the posterior compartment is involved:
 sepsissepsis
 dyspneadyspnea
 minimal trismusminimal trismus
 ? hearing loss due to blockade of Eustachian tube? hearing loss due to blockade of Eustachian tube

Retropharyngeal space
 Borders
 Anterior – superior and middle constrictor
muscles
 Posterior – alar fascia
 Superior – cranial base
 Inferior – fusion of alar and prevertebral
fascia (upper mediastinum - C6-T4)
 Medial – midline
 Lateral – lateral pharyngeal space/carotid
sheath

 Likely causes
 Extension from
lateral pharyngeal
 Prevertebral
 Mediastinum
 Contents
 Branches of cranial
nerves IX,X
 Pharyngeal vessels
 S/S
 Bulge in posterior wall of
pharynx
 Odynophagia/dysphagia
 Fever/leukocytosis/chills
 Sialorrhea/respiratory
distress
 Site of I&D
 Extraoral
 incision along anterior
border of SCM below hyoid
 muscle and carotid sheath
are retracted laterally
 finger inserted posterior to
inferior constrictor for blunt
dissection
 transoral
 for localized infections

 Patient who have infection of the lateralPatient who have infection of the lateral
pharyngeal space have serious potentialpharyngeal space have serious potential
problems. When the it is involved, theproblems. When the it is involved, the
Odontogenic infection is severe and may beOdontogenic infection is severe and may be
progressing at a rapid rate.progressing at a rapid rate.
 Another possible problem is the contents of theAnother possible problem is the contents of the
space, especially those of the posteriorspace, especially those of the posterior
compartment, as thrombosis of the internalcompartment, as thrombosis of the internal
jugular vein, erosion of the carotid artery or itsjugular vein, erosion of the carotid artery or its
branches and interference of cranial nerve IXbranches and interference of cranial nerve IX
through XII. The other serious complication arisethrough XII. The other serious complication arise
if the infection progress from the lateralif the infection progress from the lateral
pharyngeal to retropharyngeal space.pharyngeal to retropharyngeal space.

Retropharyngeal space infectionsRetropharyngeal space infections
 The retropharyngeal space lies behind the softThe retropharyngeal space lies behind the soft
tissue of the posterior aspect of the pharynx it istissue of the posterior aspect of the pharynx it is
bounded anteriorly by superior pharyngealbounded anteriorly by superior pharyngeal
constrictor muscle and posteriorly by the alarconstrictor muscle and posteriorly by the alar
layer of the prevertebral fascialayer of the prevertebral fascia
 The space begun at the base of skull andThe space begun at the base of skull and
extends inferiorly to the level of vertebra C7 orextends inferiorly to the level of vertebra C7 or
T1, where the alar fascia fuses anteriorly withT1, where the alar fascia fuses anteriorly with
the buccopharyngeal fascia.the buccopharyngeal fascia.
 Its danger when it is become infected theIts danger when it is become infected the
infection can extend inferiorly to posteriosuperiorinfection can extend inferiorly to posteriosuperior
mediastinummediastinum

 The final danger of retropharyngealThe final danger of retropharyngeal
space infection is progressivespace infection is progressive
involvement of the prevertebral space.involvement of the prevertebral space.
which is separated from retropharyngealwhich is separated from retropharyngeal
space by alar layer of prevertebral fasciaspace by alar layer of prevertebral fascia
if this fascia is perforated and the spaceif this fascia is perforated and the space
is involved .is involved .
 The prevertebral space extends from theThe prevertebral space extends from the
base of the skull to the diaphragmbase of the skull to the diaphragm
infection of this space can extends to theinfection of this space can extends to the
thorax and mediastinumthorax and mediastinum

 When the retropharyngeal or prevertebralWhen the retropharyngeal or prevertebral
spaces or both are involved as a result ofspaces or both are involved as a result of
odontogenic infection the patient is alwaysodontogenic infection the patient is always
seriously ill .The following potentialseriously ill .The following potential
complications:complications:
 1-Upper airway obstruction1-Upper airway obstruction
 2-Rupture of the retropharyngeal space2-Rupture of the retropharyngeal space
abscess and aspiration of pus to the lungabscess and aspiration of pus to the lung
and asphyxiationand asphyxiation
 3-Spread of infection into the mediastinum3-Spread of infection into the mediastinum
which results of severe infection in thewhich results of severe infection in the
thoraxthorax

Potential Pathways of Spread ofPotential Pathways of Spread of
Odontogenic InfectionsOdontogenic Infections

Cavernous sinus thrombosisCavernous sinus thrombosis
 Cavernous sinus contains; CN III, IV, VCavernous sinus contains; CN III, IV, V
(ophthalmic division) and VI, and internal carotid(ophthalmic division) and VI, and internal carotid
artery.artery.
 Valveless veins of head and neck result in aValveless veins of head and neck result in a
"venous lake" throughout the midface and skull"venous lake" throughout the midface and skull
base.base.
 This will result in retrograde flow dependent onThis will result in retrograde flow dependent on
pressure gradient;pressure gradient;
 Thus infection may spread from midface toThus infection may spread from midface to
cavernous sinus and other parts of brain viacavernous sinus and other parts of brain via
sup. and inf. ophthalmic veinssup. and inf. ophthalmic veins,, or emissaryor emissary
veins connecting pterygoidveins connecting pterygoid plexusplexus throughthrough
ovale and lacerum foramina to the cranial vault.ovale and lacerum foramina to the cranial vault.

 Earliest sign is vascularEarliest sign is vascular
congestion in periorbital,congestion in periorbital,
scleral and retinal veinsscleral and retinal veins
 Other signs include;Other signs include;
periorbital edemaperiorbital edema
proptosis ,dilated pupilsproptosis ,dilated pupils
abscent of corneal reflexabscent of corneal reflex
nausea, vomiting,nausea, vomiting,
diplopia, visualdiplopia, visual
impairment,impairment,
ophthalmoplegia,ophthalmoplegia,
photophobia,photophobia,
papilledema.papilledema.

 What are the pathways of odontogenicWhat are the pathways of odontogenic
infection to the cavernous sinus…..twoinfection to the cavernous sinus…..two
routes:routes:
 Anterior routeAnterior route: via angular and inferior: via angular and inferior
ophthalmic veinophthalmic vein
 Posterior route:Posterior route: via the transverse facialvia the transverse facial
vein and the pterygoid venous plexusvein and the pterygoid venous plexus

Principles of Management of
Odontogenic Infections
 Determine Severity of Infection
 Three major factors
 Anatomic location
 Rate of progression
 Airway compromise

2-Rate of Progression
 Onset of swelling
 Pain
 Trismus
 Airway compromise

Stages of odontogenic infections
 Days 1-3 - onset
 Soft
 Doughy
 Mildly tender
 Small, minimal
edema
 Aerobic bacteria
 Least severe
 Days 2-5 - cellulitis
 Hard
 Red
 hot
 ++ tender
 Diffuse and
spreading borders
 Mixed aerobic and
anaerobic
 Serosanguinous
fluid

 Day >5
 Cellulitis softens and abscess becomes apparent
 Compressible and shiny
 Fluctuant
 Tender
 Pus filled
 Moderate to severe
 Anaerobic
 Resolution
 After spontaneous or surgical drainage
 Swelling decreases
 May remain firm for weeks due to
inflammation and wound healing

Airway Compromise
 Most frequent cause of death is airway
compromise
 Complete obstruction requires
 Intubation
 Tracheostomy
 Cricothirotomy – emergency situations
 Partial airway obstruction
 Stridor
 Coarse breath sounds
 Drooling
 Accessory muscle use

 Trismus
 Ominous sign
 MIO of less than 20mm should be considered a
masticator space abscess until proven otherwise
 Need to observe the oropharynx and position of the
uvula to assess for swelling
 Pulse oximeter
 Below 94% is ominous sign
 Indicated insufficient oxygenation
 Radiographs
 Soft tissue radiographs of cervical airway
 CT scan (with contrast) – also identifies pus

Evaluate Host Defenses
 Immune system compromise
 Diabetes (WBC defect in phagocytosis and
chemotaxis and impaired vascular flow through small
vessels)
 Steroid therapy
 Organ transplant
 Malignancy
 Chemotherapy
 Chronic renal disease
 Malnutrition
 Alcoholism
 End stage AIDS (controversial – more defect of T
cells)

 Systemic Reserve
 Fever
 increases insensible fluid
loss and caloric
requirement
 ominous sign in elderly
patients (normally not
able to mount fever as
younger people)
 physiologic stress may
disrupt control of
systemic disease
 difficult glucose control
in diabetics
 Indications for hospital
admission
 Temperature > 38.3
 Increases fluid loss
 Dehydration
 Physical signs
 Dry skin
 Loss of turgor
 Chapped lips
 Dry mucous
membranes
 Elevated BUN
 Elevated urine
specific gravity

Possible need for hospitalizationPossible need for hospitalization
 Immunocompromised patient:Immunocompromised patient: diabetic,diabetic,
alcoholic, malnourishmentalcoholic, malnourishment
 Systemic involvement:Systemic involvement: fever >39 C, malaise,fever >39 C, malaise,
dehydrationdehydration
 Patient compliance:Patient compliance: patient is incapable of selfpatient is incapable of self
carecare
 Rapid spread:Rapid spread: Trismus, paresthesiaTrismus, paresthesia
 Need for parenteral antibioticsNeed for parenteral antibiotics
 Special features:Special features: resistant organisms,resistant organisms,
osteomyelitis, actinomycosisosteomyelitis, actinomycosis

Possible need for hospitalizationPossible need for hospitalization
 Airway compromise or threat to airway
 Trismus
 Airway swelling
 Masticator space infection
 Perimandibular space infections
 Rapidly spreading cellulites
 IV antibiotics
 Need for GA for I&D
 Need for control of systemic disease
 Decreased systemic reserve (elderly)
 Elevated WBC – more a predictor of length of stay

Diagnostic workshop for infectionDiagnostic workshop for infection
1. Patient assessment1. Patient assessment
 Physical examination:Physical examination:
 Head and neckHead and neck
 OphthalmologicOphthalmologic
 NeurologicalNeurological
2. Imaging2. Imaging
3. Lab studies:3. Lab studies:
Serum chemistrySerum chemistry
 HaematologyHaematology
UrinalysisUrinalysis
Culture and antibioticCulture and antibiotic
sensitivity testingsensitivity testing
Sampling techniquesSampling techniques

11..Patient assessmentPatient assessment
History:History:
duration of infection, sequence of events, antibioticduration of infection, sequence of events, antibiotic
prescribed, habits,prescribed, habits,
 Physical examination:Physical examination:
 Head and neck:Head and neck: Swelling, asymmetry, abscessSwelling, asymmetry, abscess
versus cellulitis, lymphadenopathy, trismus, sinusversus cellulitis, lymphadenopathy, trismus, sinus
discharge, draining fistulae, pharyngeal fullness, rashesdischarge, draining fistulae, pharyngeal fullness, rashes
 Neurological:Neurological: altered mental status, neck rididity,altered mental status, neck rididity,
fetor and sensory deficits, nausea, seizuresfetor and sensory deficits, nausea, seizures
 OphthalmologicOphthalmologic:: Proptosis, ophthalmoplegia andProptosis, ophthalmoplegia and
photophobiaphotophobia
 Mediastinal:Mediastinal: dyspnea, chest pain, distended neckdyspnea, chest pain, distended neck
veins, widened mediastinum.veins, widened mediastinum.

22..ImagingImaging
• Plane filmsPlane films
 Dental structures.Dental structures.
 Bone changesBone changes are evident after 5 - 14 days ofare evident after 5 - 14 days of
infection (33% - 50% demineralization).infection (33% - 50% demineralization).
 CT, MRI & UltrasonographyCT, MRI & Ultrasonography
Determine extent of space and cavities infectionDetermine extent of space and cavities infection
 Nuclear bone scansNuclear bone scans (Tc 99m & Ga 67)(Tc 99m & Ga 67)
Localizes active foci, diagnosis of biologic activityLocalizes active foci, diagnosis of biologic activity
e.g. osteolytic and osteoblastic and healinge.g. osteolytic and osteoblastic and healing
responses in osteomyelitisresponses in osteomyelitis..

33..Lab studiesLab studies
A. Serum chemistryA. Serum chemistry
 In Fever and dehydrationIn Fever and dehydration
 ↓↓Na++ and Cl- if ↑ sweatingNa++ and Cl- if ↑ sweating
 ↑↑ Na++ and Cl- if volume depletedNa++ and Cl- if volume depleted
 K and HCO3 remain unchangedK and HCO3 remain unchanged
 Bl. U/N may be ↑Bl. U/N may be ↑
 In septic shock → exaggeration of the above findingsIn septic shock → exaggeration of the above findings
 Evidence of acute renal failure:Evidence of acute renal failure:
 K, Cl and volume retentionK, Cl and volume retention
 Renal (metabolic) acidosisRenal (metabolic) acidosis
 ↓↓ HCO3-HCO3-
 Albumen may ↓ in osteomyelitis and necrotizing infection.Albumen may ↓ in osteomyelitis and necrotizing infection.

B. HaematologyB. Haematology
 Leukocytosis >12, 000/ mm3Leukocytosis >12, 000/ mm3
 Normocytic, normochromic anaemiaNormocytic, normochromic anaemia
 Thrombocytosis (> 500,000/mm3Thrombocytosis (> 500,000/mm3
 ↑↑ ESR with most of the bacterial and fungalESR with most of the bacterial and fungal
infection but no ↑ in viral infection.infection but no ↑ in viral infection.
C. UrinalysisC. Urinalysis
 Proteinuria with extensive infectionProteinuria with extensive infection
 Oliguria and anaemia in septic shock.Oliguria and anaemia in septic shock.

D. Sampling techniques:D. Sampling techniques:
 AspirationAspiration
 SwabbingSwabbing
 Tissue sample The specimen has to beTissue sample The specimen has to be
transferred directly to lab.transferred directly to lab.
 AspirateAspirate
 Dark, malodorous pusDark, malodorous pus,, is indicative of anaerobic infections.is indicative of anaerobic infections.
 White-yellow pusWhite-yellow pus,, implicates aerobic gram-positive cocciimplicates aerobic gram-positive cocci
 Dark-stained fluidDark-stained fluid,, is often produced by gram-negative entericis often produced by gram-negative enteric
bacteriabacteria
 Sulphur granules,Sulphur granules, in yellowish exudatesin yellowish exudates implicates actinomycesimplicates actinomyces
 Gas,Gas, with or without puswith or without pus, suggests clostridial or anaerobic, suggests clostridial or anaerobic
infections.infections.

OdontogenicOdontogenic
Infection 4Infection 4
BDS, MSc ( Tanta, Eg.), PhD (Egypt,USABDS, MSc ( Tanta, Eg.), PhD (Egypt,USA))
Collage of DentistryCollage of Dentistry

POTENTIAL SPREAD
OF INFECTION
FROM LOWER
THIRD
MOLAR
SUPERIORLY
INFRATEMPORAL AND MASTICATOR SPACE
POSTERO INFERIORLY
PTERYGOMANDIBULAR
SPACE
INFERIORLY
SUBMANDIBULAR SPACE
LUDWIG’S ANGINA
ANTERIORLY,BUCCALY
BUCCAL SPACE
BUCCALY
MESSETRIC
SPACE

NOTE : DANGER SPACE IS THE SPACE BETWEEN
PREVERTIBRAL AND ALAR FASCIA
PTERYGOMANDIBULAR SPACE
PTERYGOID SPLEXUS
EMISSERY VEINS
CAVERNOUS SINUS
THROMBOSIS
LATERAL PHARYNGEAL SPACE
RETROPHARYNGEAL SPACE
MEDIASTINUM
CAROTID SHEATH
DANGER SPACE

F. Culture and antibiotic sensitivity testingF. Culture and antibiotic sensitivity testing::
Even if there is no pus aspiratedEven if there is no pus aspirated forfor C&SC&S
 IndicationsIndications
 Rapidly spreading or extensive infectionRapidly spreading or extensive infection
 Infection in compromised patientInfection in compromised patient
 Infection not responding to antibioticsInfection not responding to antibiotics
 Recurrent infectionRecurrent infection
 OsteomyelitisOsteomyelitis
 Postoperative infectionPostoperative infection
 Infections with unusual features:Infections with unusual features:
 Tissue necrosisTissue necrosis
 Gas productionGas production
 Chronic or multiple fistulae or sinus tractsChronic or multiple fistulae or sinus tracts
 Hospital-acquired infections (NOSOCOMIAL)Hospital-acquired infections (NOSOCOMIAL)

Principles of infection managementPrinciples of infection management
 Once diagnosis of infection is established, theOnce diagnosis of infection is established, the
principles of treatment are common.principles of treatment are common.
 ABC’s first,ABC’s first,
 Secure and maintain a patent, functional airway, andSecure and maintain a patent, functional airway, and
IV access for fluids and medications.IV access for fluids and medications.
 In case of respiratory distress or embarrassment,In case of respiratory distress or embarrassment,
intubation should be strongly considered.intubation should be strongly considered.
 Fiberoptic intubation or surgical airway, "cric" orFiberoptic intubation or surgical airway, "cric" or
"trach" may be necessary if oedema has distorted"trach" may be necessary if oedema has distorted
the anatomy.the anatomy.
1. Vital signs:

Support medicallySupport medically
 HydrationHydration
 NutritionNutrition
 Control feverControl fever
 Fever below 39.4 isFever below 39.4 is
beneficialbeneficial
 Promotes phagocytosisPromotes phagocytosis
 Increases blood flow toIncreases blood flow to
areaarea
 Increases metabolicIncreases metabolic
raterate
 Enhances antibodyEnhances antibody
functionfunction

 Fever in older patient usually indicatesFever in older patient usually indicates
significant infectionsignificant infection
 Should control fever in elderly at a lowerShould control fever in elderly at a lower
temperature because of increased CV andtemperature because of increased CV and
metabolic demandsmetabolic demands
 Other methods for fever controlOther methods for fever control
 Cool water or alcohol sponge bathCool water or alcohol sponge bath
 Chilled drinksChilled drinks
 Immersion in bath of tepid waterImmersion in bath of tepid water
 Correct electrolyte imbalancesCorrect electrolyte imbalances
 Control systemic diseaseControl systemic disease

22..Medical therapyMedical therapy
Nutritional supportNutritional support
Daily requirements:Daily requirements:
 Adult male, 20-30 k Cal/kg body wt/d. (younger ↑Adult male, 20-30 k Cal/kg body wt/d. (younger ↑
require and elder ↓)require and elder ↓)
 Sepsis → ↑ caloric require. (13%/1 C° )Sepsis → ↑ caloric require. (13%/1 C° )
 Protein requirement for young adult is 0.45g/kg/d.Protein requirement for young adult is 0.45g/kg/d.
 Iron, Magnesium, and other trace elements must beIron, Magnesium, and other trace elements must be
monitored.monitored.
 Blood cultures: Indicated for all serous head and neckBlood cultures: Indicated for all serous head and neck
infections (2 culture bottle 5 cc bl. Each for aerobicinfections (2 culture bottle 5 cc bl. Each for aerobic
and anaerobic).and anaerobic).

Medical therapyMedical therapy
Antibiotic therapyAntibiotic therapy
 Therapeutic Indications:Therapeutic Indications:
 Extensive or unusual infectionsExtensive or unusual infections
 Systemic spread or sepsisSystemic spread or sepsis
 Chronic and /or non responsive infectionsChronic and /or non responsive infections
 Debilitated patientDebilitated patient
 Infections in an operative site or in the hospitalisedInfections in an operative site or in the hospitalised
patientpatient
● Oral rout: on empty stomach, 2gs Penicillin reachesOral rout: on empty stomach, 2gs Penicillin reaches
high peak after 1 hour.high peak after 1 hour.
● Parenteral root is indicated in sever infectionParenteral root is indicated in sever infection

Indications for antibiotic useIndications for antibiotic use

33..Removal of the source ofRemoval of the source of
infectioninfection
 Ultimate goal of treatment is directed at removing theUltimate goal of treatment is directed at removing the
source of infection.source of infection.
 For odontogenic infections, this means endodonticFor odontogenic infections, this means endodontic
treatment, or extraction of the offending dentition.treatment, or extraction of the offending dentition.
 Should be done concurrently with establishment ofShould be done concurrently with establishment of
drainage of the involved space (s).drainage of the involved space (s).
 Antimicrobial aids in eliminating infections from the body.Antimicrobial aids in eliminating infections from the body.
But are not curative so long as the source of infection isBut are not curative so long as the source of infection is
present.present.
 In OMFS, treatment is incision and drainage (I&D) of theIn OMFS, treatment is incision and drainage (I&D) of the
involved space and removal of the causative agent.involved space and removal of the causative agent.

Removal of the causeRemoval of the cause

44..Surgical treatmentSurgical treatment
 Sterile preparation and draping.Sterile preparation and draping.
 Aspiration of the swelling for investigation &Aspiration of the swelling for investigation &
samplingsampling
 Place 1-2 cm incision in a healthy skin orPlace 1-2 cm incision in a healthy skin or
mucosa not over most fluctuant areamucosa not over most fluctuant area
 Place skin incision in aesthetically acceptablePlace skin incision in aesthetically acceptable
area.area.
 blunt dissection with instrument and/or finger.blunt dissection with instrument and/or finger.
 Use shortest and most direct route to theUse shortest and most direct route to the
space.space.
 Secure drains, penrose or red rubberSecure drains, penrose or red rubber
catheters, avoid gauze drainscatheters, avoid gauze drains

Surgical drainage and incisionSurgical drainage and incision
 How to judge the pus formation?How to judge the pus formation?
 Purposes of surgical drainage and incisionPurposes of surgical drainage and incision
 Principles of surgical drainage and incisionPrinciples of surgical drainage and incision

How to judge the pus formationHow to judge the pus formation??
Three stagesThree stages
InoculationInoculation
CellulitisCellulitis
AbscessAbscess
 Duration--- >5 daysDuration--- >5 days
 Palpation---Palpation---
FluctuantFluctuant
 Appearance---Appearance---
ReddenedReddened
 Needle aspirationNeedle aspiration
 B-ultrasoundB-ultrasound
 CTCT
CharacteristicCharacteristic

Fluctuant examinationFluctuant examination

44..Surgical treatmentSurgical treatment
 Sterile preparation and draping.Sterile preparation and draping.
 Aspiration of the swelling for investigation &Aspiration of the swelling for investigation &
samplingsampling
 Place 1-2 cm incision in a healthy skin orPlace 1-2 cm incision in a healthy skin or
mucosa not over most fluctuant areamucosa not over most fluctuant area
 Place skin incision in aestheticallyPlace skin incision in aesthetically
acceptable area.acceptable area.
 blunt dissection with instrument and/orblunt dissection with instrument and/or
finger.finger.
 Use shortest and most direct route to theUse shortest and most direct route to the
space.space.
 Secure drains, penrose or red rubberSecure drains, penrose or red rubber
catheters, avoid gauze drainscatheters, avoid gauze drains

11--Incision & drainageIncision & drainage

Site of incision and drainageSite of incision and drainage
for FSfor FS
 Submandibular:Submandibular: Below inf mandible, inBelow inf mandible, in
submandibular trianglesubmandibular triangle
 Masticator:Masticator: E/O at Inferior border ofE/O at Inferior border of
mandible, I/O at pterygomandibular raphaemandible, I/O at pterygomandibular raphae
 Temporal:Temporal: Above zygomatic arch, I/O atAbove zygomatic arch, I/O at
raphaeraphae
 Infratemporal:Infratemporal: Above and lateral toAbove and lateral to
maxillary tuberositymaxillary tuberosity
 Buccal:Buccal: Inf. mandible, I/O buccal mucosaInf. mandible, I/O buccal mucosa
inf to Stenson’s duct.inf to Stenson’s duct.
 Lat Pharyngeal:Lat Pharyngeal: Angle of mandible, I/O atAngle of mandible, I/O at
raphae.raphae.

Principles of surgical drainage &Principles of surgical drainage &
incisionincision
 Place the incision in an estheticallyPlace the incision in an esthetically
acceptableacceptable
 Place the incision in a dependent positionPlace the incision in a dependent position
to encourage drainage by gravityto encourage drainage by gravity
 Dissect bluntly through deeper tissuesDissect bluntly through deeper tissues
and explore all pockets and portions ofand explore all pockets and portions of
the abscessthe abscess
 Place a drain and stabilize it with suturesPlace a drain and stabilize it with sutures

Principles of surgical drainage &Principles of surgical drainage &
incisionincision

Fascial spaces incision andFascial spaces incision and
drainagedrainage

Although no purulence is expressed, I&DAlthough no purulence is expressed, I&D
will alter the microenvironment whichwill alter the microenvironment which
promoted the infection.promoted the infection.
 This disruption of the balance amongstThis disruption of the balance amongst
different organism, together with adifferent organism, together with a
competent immune system and aid ofcompetent immune system and aid of
antimicrobials will lead to resolution of theantimicrobials will lead to resolution of the
infection.infection.
 If the infective source is removedIf the infective source is removed
simultaneously, the above manoeuvre issimultaneously, the above manoeuvre is
curative.curative.
Incision & drainage

Principles of infectionPrinciples of infection
managementmanagement

Establishment of DrainageEstablishment of Drainage

Drainage, con’tDrainage, con’t

Penrose drain in place to providePenrose drain in place to provide
drainage for vestibular abscessdrainage for vestibular abscess

 How the patientHow the patient
feels- Malaisefeels- Malaise
 PreviousPrevious
treatmenttreatment
 Self treatmentSelf treatment
 Past MedicalPast Medical
HistoryHistory
Severity of the InfectionSeverity of the Infection

 UncontrolledUncontrolled
metabolic diseasesmetabolic diseases
 AlcoholismAlcoholism
 MalnutritionMalnutrition
 DiabetesDiabetes
 Suppressing diseasesSuppressing diseases
 LeukemiaLeukemia
 LymphomaLymphoma
 Malignant TumorsMalignant Tumors

 Incision and drainageIncision and drainage
 Dependent siteDependent site
 Incision in healthyIncision in healthy
tissuetissue
 Adequate drainageAdequate drainage
 Exploration of allExploration of all
involved spacesinvolved spaces
 IrrigationIrrigation
Surgical TreatmentSurgical Treatment
Intraoral Aspiration

Surgical TreatmentSurgical Treatment

Purposes of surgical drainage &Purposes of surgical drainage &
incisionincision
 Get rid the body of toxic purulent materialGet rid the body of toxic purulent material
 Decompress the tissuesDecompress the tissues
 Allowing better perfusion of blood containingAllowing better perfusion of blood containing
antibiotics and defensive elementsantibiotics and defensive elements
 Increased oxygenation of the infected areaIncreased oxygenation of the infected area

AntibioticsAntibiotics
E. Antimicrobial susceptibility testingE. Antimicrobial susceptibility testing
 Based onBased on MICMIC ((Minimum InhibitoryMinimum Inhibitory
ConcentrationConcentration))
Therapeutic antibiotic dose is 3-4 times theTherapeutic antibiotic dose is 3-4 times the
MIC; and 8 times in compromised hosts.MIC; and 8 times in compromised hosts.
 Minimal Bactericidal Concentration (MBC):Minimal Bactericidal Concentration (MBC):
is the antimicrobial concentration that killsis the antimicrobial concentration that kills
99,9 % of bacteria.99,9 % of bacteria.
 Organisms are considered antibioticOrganisms are considered antibiotic
resistant if MBC> MIC by 32-fold.resistant if MBC> MIC by 32-fold.

22..Medical therapyMedical therapy::
Antibiotic therapyAntibiotic therapy a : Prophylactica : Prophylactic
 Principles of prophylactic antibiotic usePrinciples of prophylactic antibiotic use
CriteriaCriteria AdvantagesAdvantages DisadvantagesDisadvantages
 Significant risk ofSignificant risk of
infectioninfection
 Choose correctChoose correct
antibioticantibiotic
 High levelHigh level
 Timing (when)Timing (when)
 Shortest effectiveShortest effective
 ReducesReduces
incidence ofincidence of
infectioninfection
 Reduces healthReduces health
 care costscare costs
 Reduces totalReduces total
antibiotic useantibiotic use
 Allows fewerAllows fewer
resistant bacteriaresistant bacteria
 Alter hostAlter host
 flora?flora?
 Benefit?Benefit?
 Cost?Cost?
 Toxicity?Toxicity?

 Pharmacokinetics:Pharmacokinetics: What the bodyWhat the body
does to a drugdoes to a drug
 Pharmacodynamics:Pharmacodynamics: What the drugWhat the drug
does to a bodydoes to a body
 It can’t hurt and it might help shouldIt can’t hurt and it might help should
not be the reason you are prescribingnot be the reason you are prescribing
antibioticsantibiotics

Principles of antibioticPrinciples of antibiotic
administrationadministration
 Proper doseProper dose
 Proper time intervalProper time interval
 Proper route of administration (oral,Proper route of administration (oral,
parenteral)parenteral)
 Combination antibiotic therapy to obtainCombination antibiotic therapy to obtain
potentiation, to delay development of drugpotentiation, to delay development of drug
resistance, to broaden the spectrum of anti-resistance, to broaden the spectrum of anti-
infective druginfective drug

 Synergism:Synergism: A drug interact with another toA drug interact with another to
produced increased activityproduced increased activity
 Antagonism:Antagonism: Is a drug with opposite actionIs a drug with opposite action
to other drug, it inhibit its actionto other drug, it inhibit its action
 Mode of action of Antibiotics:Mode of action of Antibiotics:
 1-Interference with the cell wall1-Interference with the cell wall
 2-Interference with biochemical activity2-Interference with biochemical activity
 3-Inhibition of protein synthesis3-Inhibition of protein synthesis
 4.Interference with cell metabolism4.Interference with cell metabolism

Referral or notReferral or not??

F. Antimicrobial susceptibility testingF. Antimicrobial susceptibility testing
 Based onBased on MICMIC ((Minimum InhibitoryMinimum Inhibitory
ConcentrationConcentration))
Therapeutic antibiotic dose is 3-4 times theTherapeutic antibiotic dose is 3-4 times the
MIC; and 8 times in compromised hosts.MIC; and 8 times in compromised hosts.
 Minimal Bactericidal Concentration (MBC):Minimal Bactericidal Concentration (MBC):
is the antimicrobial concentration that killsis the antimicrobial concentration that kills
99,9 % of bacteria.99,9 % of bacteria.
 Organisms are considered antibioticOrganisms are considered antibiotic
resistant if MBC> MIC by 32-fold.resistant if MBC> MIC by 32-fold.

Principles of Antibiotic TherapyPrinciples of Antibiotic Therapy
 Use EmpiricUse Empiric
TherapyTherapy
 Use narrowestUse narrowest
spectrum drugspectrum drug
 Use antibiotic withUse antibiotic with
the lowest toxicitythe lowest toxicity
 Use bactericidalUse bactericidal
 Be aware of Cost $$Be aware of Cost $$
$$

Antibiotic TherapyAntibiotic Therapy
 Initial therapyInitial therapy
 Cover Gram positive cocci andCover Gram positive cocci and
anaerobesanaerobes
 If pt is diabetic, should considerIf pt is diabetic, should consider
covering gram negatives empirically.covering gram negatives empirically.
 Unasyn, Clindamycin, 2Unasyn, Clindamycin, 2ndnd
generationgeneration
cephalosporin.cephalosporin.
 PCN, gentamicin and flagyl -PCN, gentamicin and flagyl -
developing nationsdeveloping nations..
 IV abx alone (based on retro andIV abx alone (based on retro and
parapharyngeal infections)parapharyngeal infections)
 Patient stability and nature of lesion.Patient stability and nature of lesion.
 Cellulitis/phlegmon by CT.Cellulitis/phlegmon by CT.
 Abscesses in clinically stable patient.Abscesses in clinically stable patient.
 If no clinical improvement in 24 - 48If no clinical improvement in 24 - 48
hours proceed to surgicalhours proceed to surgical
interventionintervention..

Indications for Culture andIndications for Culture and
Ab. Sensitivity TestingAb. Sensitivity Testing
 Rapidly spreadingRapidly spreading
infectioninfection
 Post-op infectionPost-op infection
 Non-responsiveNon-responsive
infectioninfection
 Recurrent infectionRecurrent infection
 Compromised hostCompromised host
defensesdefenses

Antibiotic Associated ColitisAntibiotic Associated Colitis
 DiagnosisDiagnosis
 Profuse wateryProfuse watery
diarrhea >10 per daydiarrhea >10 per day
 CrampingCramping
 FeverFever
 toxin assaytoxin assay
 Tissue cultureTissue culture
 TreatmentTreatment
 D/C current ABD/C current AB
 Fluid managementFluid management
 AntibioticsAntibiotics
 MetronidazoleMetronidazole
 Vancomycin POVancomycin PO

Reasons for Treatment FailureReasons for Treatment Failure
 Inadequate SurgeryInadequate Surgery
 Depressed hostDepressed host
responsesresponses
 Foreign bodyForeign body
 Antibiotic problemsAntibiotic problems
 Patient noncompliancePatient noncompliance
 Drug not reaching theDrug not reaching the
sitesite
 Drug dose too lowDrug dose too low
 Wrong antibioticWrong antibiotic

Antibiotic TherapyAntibiotic Therapy
 Removal of the cause, drainage,Removal of the cause, drainage,
and supportive care more importantand supportive care more important
than antibiotic therapy.than antibiotic therapy.
 Infections are cured by the patient’sInfections are cured by the patient’s
defenses,defenses, notnot antibiotics.antibiotics.
 Risks of allergy, toxicity, sideRisks of allergy, toxicity, side
effects, resistance andeffects, resistance and
superinfection causing serious orsuperinfection causing serious or
potentially fatal consequences mustpotentially fatal consequences must
be considered.be considered.

Antibiotic therapy, con’tAntibiotic therapy, con’t..
 Oral infections are typically polymicrobial.Oral infections are typically polymicrobial.
 Antibiotic effectiveness dependent uponAntibiotic effectiveness dependent upon
adequate tissue (not serum) concentrationadequate tissue (not serum) concentration
for an appropriate amount of time.for an appropriate amount of time.
 Antibiotics should be prescribed for at leastAntibiotics should be prescribed for at least
one week – adequate tissue concentrationone week – adequate tissue concentration
achieved in 24-48 hours, with bacteriocidalachieved in 24-48 hours, with bacteriocidal
activity occurring over the next 3-5 days.activity occurring over the next 3-5 days.

 PenicillinPenicillin (bacteriocidal) drug of choice for(bacteriocidal) drug of choice for
treatment of odontogenic infections (5% incidenttreatment of odontogenic infections (5% incident
of allergy).of allergy).
 ClindamycinClindamycin (batericiodal) 1(batericiodal) 1stst
line afterline after
penicillin; effective against anaerobes; stoppenicillin; effective against anaerobes; stop
taking at first sign of diarrhea.taking at first sign of diarrhea.
 CephalosporinCephalosporin (slightly broader spectrum and(slightly broader spectrum and
bacteriocidal); cautious use in penicillin-allergicbacteriocidal); cautious use in penicillin-allergic
patients → cross-sensitivity; if history ofpatients → cross-sensitivity; if history of
anaphylaxis to penicillin, do not use.anaphylaxis to penicillin, do not use.

 ErythromycinErythromycin (bacteriostatic) good 2(bacteriostatic) good 2ndnd
line drug afterline drug after
penicillin; use enteric-coated to reduce GI upset.penicillin; use enteric-coated to reduce GI upset.
Erythromycin is less effective than penicillinErythromycin is less effective than penicillin
 MetronidazoleMetronidazole (bacteriocidal) excellent against(bacteriocidal) excellent against
anaerobes only.anaerobes only.
 AugmentinAugmentin (amoxicillin + clavulanic acid) kills(amoxicillin + clavulanic acid) kills
penicillinase-producing bacteria that interferes withpenicillinase-producing bacteria that interferes with
amoxicillin; expensive.amoxicillin; expensive.
 VancomycinVancomycin for methicillin-resistant staphylococcifor methicillin-resistant staphylococci
(MRS)(MRS)
 QuinolonesQuinolones for chronic osteomyelitis.for chronic osteomyelitis.

Antibiotic therapyAntibiotic therapy
 Combination therapy may be indicated in:Combination therapy may be indicated in:
 Life-threatening infectionsLife-threatening infections
 Necrotizing fasciitisNecrotizing fasciitis
 Chronic osteomyelitis (Quinolones have goodChronic osteomyelitis (Quinolones have good
bone penetration)bone penetration)
 Prevention of resistant organisms e.g.Prevention of resistant organisms e.g.
bacteroids and staphylococcibacteroids and staphylococci
 Combination therapy involves a BSA (penicillin)Combination therapy involves a BSA (penicillin)
and drug active against gram-negative or one ofand drug active against gram-negative or one of
the beta lactamase inhibitor combinations.the beta lactamase inhibitor combinations.

 Adjusting antibiotic therapyAdjusting antibiotic therapy::
 Nonresponsive or super-infectionsNonresponsive or super-infections
 Culture and antibiotic sensitivity testsCulture and antibiotic sensitivity tests
resultsresults
 ToxicityToxicity::
 Aminoglycosides (nephro-and ototoxicity)Aminoglycosides (nephro-and ototoxicity)
 Clindamycin, cephalosporinsClindamycin, cephalosporins
(pseudomembranous colitis)(pseudomembranous colitis)
 Erythromycin (hepatotoxicity in high doses)Erythromycin (hepatotoxicity in high doses)
 Penicillins and cephalosporins (hypersensitivityPenicillins and cephalosporins (hypersensitivity

Adjunct to antibiotic administrationAdjunct to antibiotic administration
 Nystatin for fungal superinfection (Candida)Nystatin for fungal superinfection (Candida)
 Hyperbaric oxygen therapyHyperbaric oxygen therapy::
 Increase vascularityIncrease vascularity
 Aids in bone healingAids in bone healing
 Increases antibiotic delivery to tissues.Increases antibiotic delivery to tissues.

Antibiotic resistanceAntibiotic resistance mechanismsmechanisms
1. alteration in permeability of bacterial cell wall1. alteration in permeability of bacterial cell wall
for the drugfor the drug
2. changes in the target sites for the drug in the2. changes in the target sites for the drug in the
bacterial cell wallbacterial cell wall
3. bypassing metabolic reactions blocked by the3. bypassing metabolic reactions blocked by the
drugdrug
4. drug inactivation4. drug inactivation
 1-3 = tolerance 4 = antibiotic destructive1-3 = tolerance 4 = antibiotic destructive
cross resistance = bacteria resistant to onecross resistance = bacteria resistant to one
antibiotic: is the resistance to other forms ofantibiotic: is the resistance to other forms of
the antibiotic which are chemically closelythe antibiotic which are chemically closely
relatedrelated

Antibiotic resistanceAntibiotic resistance
1. Natural1. Natural 2. Acquired2. Acquired
11. Natural. Natural
 Due to:Due to:
 the production of enzymes by bacteriathe production of enzymes by bacteria
nullifying the antibiotic effect e.g:nullifying the antibiotic effect e.g:
Penicllinase production by Staph. Aureus orPenicllinase production by Staph. Aureus or
 by the virtue of morphological/biologicalby the virtue of morphological/biological
factors which exclude the natural targetfactors which exclude the natural target
areas of the bacteria to the action of theareas of the bacteria to the action of the

Antibiotic resistanceAntibiotic resistance
2. Acquired2. Acquired
 Bacteria can adapt and become resistant as anBacteria can adapt and become resistant as an
adaptive reaction to prolonged or continuousadaptive reaction to prolonged or continuous
use of an antibiotic mediated by mutationuse of an antibiotic mediated by mutation
 Mutation- natural mutants (chromosomal) theMutation- natural mutants (chromosomal) the
removal of the dominant antibiotic sensitiveremoval of the dominant antibiotic sensitive
strains by the administration of antibiotics allowsstrains by the administration of antibiotics allows
these bacteria to proliferate freely withoutthese bacteria to proliferate freely without
competition e.g strept viridanscompetition e.g strept viridans

Choosing a suitable antibioticChoosing a suitable antibiotic
 Patient FactorsPatient Factors
 allergyallergy
 renal/hepatic functionrenal/hepatic function
 immuno-compromiseimmuno-compromise
 oral toleranceoral tolerance
 severity of illnessseverity of illness
 age/weightage/weight
 pregnancy/breastpregnancy/breast
feedingfeeding
 oral contraceptive/otheroral contraceptive/other
medicationmedication
 Microbial FactorsMicrobial Factors
 culture and sensitivityculture and sensitivity
 likely organisms’likely organisms’
sensitivitysensitivity

Factors that determine degree of placentalFactors that determine degree of placental
transfer:transfer:
 Lipid solubilityLipid solubility
 Ionization of compoundIonization of compound
 Protein bindingProtein binding
 Placental foetal blood flowPlacental foetal blood flow
Considerations in the pregnant or lactating
patient with infection:

Approx. sameApprox. same
as maternalas maternal
20% to 50 of20% to 50 of
maternalmaternal
10% to 15 of10% to 15 of
maternalmaternal
Penicillins,Penicillins,
amoxicillin,amoxicillin,
ampicillin,ampicillin,
methicillin,methicillin,
sulfonamides,sulfonamides,
chloramphenicol,chloramphenicol,
and tetracyclinsand tetracyclins
AminoglycosidesAminoglycosides
(not safe for(not safe for
pregnant, notpregnant, not
absorbed fromabsorbed from
bowel)bowel)
Cephalosporins,Cephalosporins,
clindamycin, andclindamycin, and
erythromycinerythromycin
Foetal serum concentrationsFoetal serum concentrations

Breast milk concentrationsBreast milk concentrations
Approx. sameApprox. same
as maternalas maternal
50% to 70 of50% to 70 of
maternalmaternal
Less than 25% ofLess than 25% of
maternalmaternal
Sulfonamides,Sulfonamides,
Metronidazole andMetronidazole and
isoniazidisoniazid
ChloramphenicolChloramphenicol
and erythromycinand erythromycin
Cephalosporins,Cephalosporins,
clindamycin, andclindamycin, and
erythromycinerythromycin

 Symptom subside?Symptom subside?
vital signs, trismus, swelling, p’t feelingvital signs, trismus, swelling, p’t feeling
 Failure reason?Failure reason?
etiology, surgery, host immune,etiology, surgery, host immune,
foreign body, antibioticsforeign body, antibiotics
 Adverse effectAdverse effect
 Secondary infectionsSecondary infections

Summary of infection managementSummary of infection management
InsureInsure
VitalVital
signssigns
2. Obtain2. Obtain
drainagedrainage
3. Maintain3. Maintain
drainagedrainage
4. Remove4. Remove
the causethe cause
5. Provide5. Provide
supportivesupportive
carecare
• AirAir
wayway
• PulsePulse
• BPBP
• AdequateAdequate
accessaccess
• BluntBlunt
dissectiondissection
• AllAll
loculationsloculations
enteredentered
• All involvedAll involved
spacesspaces
• DependentDependent
drainagedrainage
• MaintenanceMaintenance
of Patencyof Patency
• PulpPulp
extirpationextirpation
• ToothTooth
extractionextraction
• NecroticNecrotic
tissuetissue
/debris./debris.
• FluidsFluids
• RestRest
• NutritionNutrition
• WarmthWarmth
• AntibioticAntibiotic

 Inadequate surgeryInadequate surgery
 Depressed host defencesDepressed host defences
 Foreign bodyForeign body
 Antibiotic problemsAntibiotic problems
 Patient non-compliancePatient non-compliance
 Drug not reaching siteDrug not reaching site
 Drug dosage too lowDrug dosage too low
 Wrong bacterial diagnosisWrong bacterial diagnosis
 Wrong antibioticWrong antibiotic
Reasons for treatment failureReasons for treatment failure

Case report 1Case report 1
Pt ; 38/FPt ; 38/F
 CC ; swellingCC ; swelling
 PI ; mouth opening limitation, dysphagia, Rt buccal &PI ; mouth opening limitation, dysphagia, Rt buccal &
sub mn swelling and rednesssub mn swelling and redness
 Dx ; masticatory spce, lat. Pharyngeal space abscessDx ; masticatory spce, lat. Pharyngeal space abscess
 Tx ; I & D X 2Tx ; I & D X 2
 (submn & submental, deep neck carotid sheath(submn & submental, deep neck carotid sheath
area)area)
 anti theraphy ( aug + micronomycin + flagyl)anti theraphy ( aug + micronomycin + flagyl)
 fluid etc supplementary tx (O2 etc)fluid etc supplementary tx (O2 etc)
 lab ; WBC 30260, segmental neutrophil 85.9%, CRPlab ; WBC 30260, segmental neutrophil 85.9%, CRP
36.536.5

Masseteric space and
parapharyngeal
infection preoperative
Masseteric space and
Parapharyngeal
infection postoperative

Case report 2Case report 2
 Pt ; 30/MPt ; 30/M
 CC ;transfer from ENT d/t deep neck infectionCC ;transfer from ENT d/t deep neck infection
from dental originfrom dental origin
 PI ; both submn swelling & TdPI ; both submn swelling & Td
mouth opening limit, dysphagia, dyspnea,mouth opening limit, dysphagia, dyspnea,
neck Td & redness, #38 area pusneck Td & redness, #38 area pus
 DX ; submn & mental space abscessDX ; submn & mental space abscess
pretracheal space abscesspretracheal space abscess
descending necrotizing mediastinitisdescending necrotizing mediastinitis

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