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8/6/2019 Space Inf Yuva Ppt

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Balance is lost infection occurs

Microbial factors Vs Host factors.

virulence local

quantity humoral

cellular


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Pathophysiology of odentogenic

infections Dental apex apical osteomyelitis incresed interstitial

hydrostatic pressure (increase transudate &exudate)-ischemia- tissue breakdown (recruit macrophages)-macrophages (osteoclast) bone resorption cortexbreached soft tissue areolar ( path of least resistance)deflected by

Muscle

Fascia Organs

Bone.


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Anatomical structures influencing

spread Mandible :

Mentalis.

Buccinator. Temporalis.

Mylohyoid.

Masseter.

Temporalis.

External oblique ridge

Mylohyoid ridge.


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Cervical fascia:

I.Superficail fascia

II. Deep cervical fascia

Anterior layer: Investing fascia

Parotideomasseteric

Temporal

Middle layer:

a. Sternohyoid-omohyoid division.

b. sternothyroid-throhyoid division.

c. Visceral division 1.buccopharyngeal.

2. pretracheal. 3. retropharynmgeal.

Posterior layer: Alar division.

Prevertabreal division.


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Stages of infection Inoculation

Cellulitis

Abscess

Resolution


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BUCCAL SPACE INFECTION (BUCCINATOR

SPACE INFECTION)

BOUNDARIES :Ant. modiolus

Post. buccinator joins sup. Const. muscle.Med. buccinatorLat. skin.Sup. infra orbital space.Inf. lower border of mand.

CONTENTS : buccal fat pad.

stensons duct.facial artery br. (transverse facial artery)


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CLINICAL FEATURES :

this space can be expand to a surprising volume.

SWELLING.

COMMUNICATIONS :

On posteromedial side of mandible buccal space communicates withPTERYGOMANDIBULAR SPACE.

To infra temporal space above left pharyngeal muscle inferiorly.

breaches buccinator posteriorly sub masseteric space.

through temporal extension of BFP sup. Temp. space.

Erodes transverse facial artery reaches pterygoid venous plexus cavernous sinus spreads along subcutaneous space into periorbital spaceabove and even neck below.

Dd :

haemophilus influenza inf infants or children younger than 3 years - cancause non odontogenic buccal space infection.

recurrent buccal space inf as a complication of Cohns disease ( segmentaltransmural intestinal disease).


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CANINESPACE (INFRA ORBITALSPACE)INFECTION

BOUNDARIES Ant. nasal cartilage.

Post. buccal space.

Sup. levator labii superioris

Inf. oral mucosa.

Med. levator labi superioris.

Lat. levator anguli oris.

.CONTENTS

infra orbital nerve and vessels.

CLINICAL FEATURES obliteration of nasolabial fold.

infra (circum) orbital oedema.

sinus near medial canthus of eye. ( inf open between levator labi

superoris and levator labii sup. Alaeque nasi.


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COMMUNICATIONS :

Can spread to cavernous sinus by an ascending thrombophebitis of

angular vein inferior ophthalamic vein cavernous sinus.*

facial veins are valve less*.

Dd Dacryocystitis

nasolacrimal duct.

maxillary sinusitis.

carbuncle.


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VESTIBULARSPACE (DENTO ALVEOLARABSCESS)

Space between oral mucosa and muscles of facial expression.


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DEEPSPACESASSOCIATED WITH MAND.ODONTOGENIC INFECTION

SPACE OF BODY OF MANDIBLE : ( MANDIBULAR SPACE):

BOUNDARIES : periosteal envelope and cortical surface of mandible.

CONTENTS : no contents, but sometimes mental nerve may cross

this space if distended near foramen. CLINICAL FEATURES : Infections which cross bony cortex, but not

periosteum cause this infecton.

mand itself appears enlarged.

quite painful since periosteum ( richly innervated) is dissected from

bone by abscess.


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SUBLINGUALSPACE

BOUNDARIES Sup. : mucosa of oral cavity.

Inf. : mylohyoid.

Ant and lat.: lingual surface of mandible.

Med.: genioglossus and intrinsiic muscles of tongue. Post.: sup, post, and medial portion of sub mand space.

CONTENTS : sublingual gland, sub mandibular duct, hilum of sub

mandibular gland, lingual nerve, sub lingual artery and vein.

CLINICAL FEATURES :

elevation of tongue and restriction in movement.

can cause epiglotitis in severe case ( infection dissects intrinsic (m)

tongue and reach epiglotis).


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Communications:

Pass around mylohyoid sub mandibular. Buccopharyngeal gap (sup and middle const) to lateral pharyngeal

space along styloglossus.

Anteriorly breach mylohyoid enter sub mental.

Dd sialolith in whartons duct.

sub lingual gland infection.


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SUB MANDIBULARSPACE (SUBMAXILLARY,SUB MYLOHYOID)

INFECTIONBOUNDARIES:

Ant.: anterior belly of digastric.

Post.: post belly of digastric, stylohyoid.

Sup.: inf and lingual border of mand. Below the mylohyoid lines.

Med.: mylohyoid (m).

Inf.: digastric tendon.

Sup.: platysma (m) and inv lar of deep fascia.

CONTENTS:

sub mandibular salivary gland, lymph nodes, facial artery and vein, poximal portion of whartons duct, lingualand hypoglossal nerve.

CLINICAL FEATURES : swelling in the typical region.

COMMUNICATIONS :

posteriorly -infection crosses post belly of digastric (or) along lateral surface of pharyngeal const (m) to lt

pharyngeal space. Anteriorly crosses ant belly to sub mental cross mylohyoid sub lingual space.

Dd acute sialadenitis, sub lingual trauma , sub lingual lymph adenitis.


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SUB MENTALSPACE

BOUNDARIES: Lat. : ant belly of digastric.

Sup. : deep cervical fascia, platysma and skin.

Deep: mylohyoid (m).

Ant.: inferior br of mandible. Post.: hyoid bone.

CONTENTS: areolar CT, sub mental lymph nodes, ant jugular vein.

CLINICAL FEATURES: swelling in chin and sub mental region.

COMMUNICATIONS :

post submandibular.sup.- sub lingual ( unlikely).

Dd

plunging ranula, sub mental lymph adenitis.


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MASTICATORSPACE

Anatomical compartment enclosed by splitting of anterior layer of deep

cervical fascia around , muscles of mastication.

Sub masseteric

Pterygomandibular

Sup and deep temporal space infection.


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SUB MASSETERICSPACE

BOUNDARIES: Med: lat surface of ramus.

Lat: parotidomassetric fascia.

Inf: pterygomassetric sling.

Sup: par.mas.fascia fusing with lateral surface of zygo arch. Ant. Buccal space.

Post: parotid gland.

CONTENTS:

Masseter, submasseteric artery and vein.

CLINICAL FEATURES: TRISMUS

no obvious extra oral swelling.

osteomyelitic changes ( sometimes young patients sub periosteal osteosclerosis PA

view).


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COMMUNICATIONS:

Through sigmoid notch to pterygomandibular space.

Sup. Continuous with sup and deep temporal space.

To buccal space anteriorly.

Lt. pharyngeal and parotid space post.

Dd parotid infection ( elevate ear lobe, submandibular abscure it).


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PTERYGOMANDIBULARSPACE

Lat: lingual surface of ascending branch of ramus.

Med: medial pterygoid.

Inf.: pterygo mass sling.

Sup: lt. pterygoid.

Ant: buccinator fusing with superior const (m).

Post: parotid gland.

CONTENTS: IAN vessels, motor supply to med pteryg and masseter and

sensory nerve like lingual, auriculotemporal, mylohyoid, IAN.

CLINICAL FEATURE:

trismus ( edema and inflammation of med pteryg (m).

No obvious extra oral swelling.

Deviation of uvula to opposite side.

Swollen ant tonsillar pillar.


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COMMUNICATION :

Spreads to Lt pharyngeal space by passing around ant border of med

pteryg muscle.

Infra temporal of deep temporal space by passing around Lt pteryg

muscle superiorly.


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SUPERFICAIL TEMPORALSPACE

BOUNDARIES: Med: temporalis.

Lat : temporalis fascia.

Ant: post surface of Lt orbital rim.

Post : fusion of temp. fascia with pericranium. Inf : zyg arch and areolar CT medial arch where it communicates with sub masset space.

CONTENTS :

Above 2 cm from zyg arch fascia splits to enclose buccal fat pad,

small veins.

CLINICAL FEATURES: trismus, swelling above zyg arch.

COMMUNICATION :

buccal space temporal extension of BFP

pteryg and submassetric as they are continuous.


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DEEP TEMPORALSPACE (TEMPORALPOUCHES)

Lat : temporalis.

Med : squamous temporal bone.

Inf : superior surface of lateral pteryg muscle.

Sup. And post : temporalis muscle to cranium.

Ant : post wall of maxillary sinus, pterygomaxillary fissure, post surface of orbit.

Infra temporal space is portion of temporal space that lies inferior to

infra temporal crest of sphenoid bone.

CLINICAL FEATURES: TRISMUS, swelling ( may not be obvious)


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CONTENTS:

Pterygo venous plexus, maxillary artery and branches andsphenopalatine ganglion.

COMMUNICATION :- 1). Cavernous sinus through pterygoid venous plexus which connects

cavernous sinus by emisary through 3 foramens - ovale, Lacerum ,versalis. 2) Infection from buccal space erode transverse FACIAL Ptg. venous plexus 3). Directly from Ptg & sub massetric.


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Pharyngeal space infection

Lateral pharyngeal space:- [ Pharyngomaxillary space , Para pharyngeal space ]

Pyramidal space withBase (sup):- Base of skull.

Apex (Inf) :- Hyoid bone

Med:- Pharyngeal constr. (m) [ overling visceral div. of middle layer of deepcervical fascia called buccopharyngeal fascia].

Lat :- laterosup med ptg. (m)

L. infer ant. Layex of deep ceroical fascia.

Ant:- Ant. sup:- Palatine (m)

middle :- buccinator + sup. Const.

Inferior :- stytoid (m)

post belly of digastric.

Post :- Post medially retropharyngeal.


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Post lateral carotid sheath.

facial condensation from

to

ant layer of styloid process Buccopharyngeal fascia

Deep cervical styloid (m)

Fascia

divides Lateral . ph. Space into

Anterior &

posterior compartment

Aponeurosis of this facial cond ZUCKERKANDL & TESTUT


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CONTENTS :-

Anterior compt :- Loose areolar C.T. (pre-styloid)

Posterior compt (Post- Styloid) :- cranial nerves IX,X,XI,XII ,carotid sheath and its contents.

Cervical symp. Chain attached to posterior sutface of carotid sheath.

CLINICAL FEATURE :-

Ant. Compt:- pain, fever, chills, palatoglossal arch may be blunted on affected side with uvula tounaffected side.

In the frontal view only visible swelling will be between post belly of digastric and ant br of SCM justsup to hyoid bone below angle of mandible.

Trismus.

Post compt: - absence of trismus.

visible swelling.

but may have respiratory obstruction, septic thrombosis ofIJV, carotid artery

haemorrhage.CT is much helpful in diagnosis of post compt infection.


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COMMUNICATIONS:

To sub lingual space buccopharyngeal gap.

Peri tonsillar inf that penetrates pharyngeal constrictor (m) enters Lt

Ph space.

From sub mandibular crossing post belly of digastric reach Lt

pharyngeal space.

From retropharyngeal directly to Lt pharyn space.


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Space Ptg Lt Ph peritonsillar

Anatomy bet mand & med pteryg bet med pty & sup cons bet sup cons & mucous

memb

Limitation of extreme mod. Some

opening.

External little none(except none

swelling in angle of mand.

Swelling in some over good deal of pillar of little in faucial pillar most

in

oral cavity med aspect of ant fauces but little soft soft tissue.

br of ramus tissue.


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RETROPHARYNGEALSPACE(RETROESOPHAGEAL,

RETROVISCERALSPACE)BOUNDARIES:

Lat : carotid sheath and lt pharyngeal space.

Sup : skull base.

Inf : alar fascia with visceral division of middle layer of deep cervicalfascia ( retropharyngeal fascia) C6 T4.

Post : alar fascia.

Ant : sup and middle pharyngeal const(m)

midline septum divides right from left.

CONTENTS:

areolar CT, rich supply of lymph nodes that drains waldeyers ring.


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CLINICAL FEATURES:

can be caused from oesophageal trauma, nasal pharyngeal infection,

through dental infection of contiguous space or necrosis lymph nodes

involved.

Dysphagia, dyspnea, nuchal rigidity, oesophagus regurgitation, with

fever.

Bulging in posterior wall either to one side can be visualized.

Lateral soft tissue radiograph of neck.

Widening of retropharyngeal space

C2 - < 6mm

C6 - < 20mm.

COMMUNICATIONS : it has to breach only alar fascia to reach danger

space.

continuous to Lt pharyngeal space.


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MANAGEMENT OFFACIALSPACEINFECTION

HOST, NOT ANTIBIOTICS CURES INFECTION

Presence of infection :- local and systemic sign.

State of host defense :- depressed defense may be a)

physiological, b) disease, c) congenital, d) drug induced.

Principles for choosing antibiotics:1. Identify causative organism aerobes and anaerobes, GPC-Str GPC-Strp, GNB-E.coli GNB-fuso

bactereobes

2. Determine sensitivity: Majority is sensitive to penicillin

3. Use a specific , narrow spectrim antibiotics:- Broad spectrum resitance , super injections.

4. Least toxic.

1. Bactericidal rather than bacterostatic

1. Less resistance to hostt.

2. Faster results.

3. Flexibility with dose.

Cost and patient complaince- od 80%, bid 69%, qid 35%


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2.Principles of antibiotic administration

1. Dose- 3-4 times MIC

2. Time interval- 4 times t1/2.

3. Proper route4. consistency in route

5. combinations

3 . Patient monitoring

4. Causes of failure:

Inadequate surgical drainage Depressed host defence

Presence of foreign body

Antibiotic problems- not reaching, adequate wrong choice, diagnosis.


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5. Complications:- adverse reaction, toxicity, ACC, superinfection.


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Incision and drainage

Hiltons method:

Objectives:

To drain pus and maintain drainage.

Relive pressure - vascularity( o2

supply)

By increasing vascularity- access to bodies defence mech. And

antibiotics to reach the site.

Converts spectrum of organism present- Anaerobic Aerobic

environment.

Reduces the load and narrows spectrum of antibiotics required.


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Principles in placing incision:-

Healthy skin

Esthetics

Dependent drainage

Explore and break compartments

Place drain and suture

Dont leave the drain for long period

Regular re-exploration and irrigation


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Cavernous sinus thrombosis

Anatomy- wide venous space on the lateral slope of sphenoid body in

middle cranial fossa.

Receive superior and inferior opthalmic vien, central retinal vein,

middle meningeal vein

Drains superior and inferior petrosal sinus IJV into right and left

connected by inter cavernous sinus

Relations internal carotid, abducens within sinus

III, IV, V lateral to sinus.

sphenoid sinus medially

pituitary sinus supero medially.

Pathways of spread- 1) emissary veins- pterygoid plexuses

parietal group connects sup.

Temporal

to sup. Saggital sinus


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2) Anastomosis of veins:-

anterior route- upper lip, ala of nose, anterior part of nose

infraorbital vein communicates through angular vein to

superopthalmic vein,.

From sup. Opthalmic vein cavernous sinus.

posterior route- transverse facial vein

pterygoid venous plexus

inferior alveolar vein retromandibular vein

From pterygoid venoud plexus ---- cavernous sinus (through

emissery vein)


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Clinical features

Headache, fever, malaise prior to occular symptoms

Orbital fullness, pain and visual disturbance

The earliest clinical sign of cavernous thrombosis is congestion of

retina of unaffected eye- inter cavernous sinus thrombosis.

Signs of venous congestion: Chemosis

Edema of eyelid

Periorbital edema

Signs of increased retrobulbur pressure:

-Exophthalamus (pulsatile) Ophthalamoplagia.

meningeal signs nauchal rigidity.

Systemic signs chills, fever, delirium, shock..


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Investigation :

CT, MRI.

Treatment :

aggressive antibiotics.

anticoagulants.

treat the primary cause source of infection.


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Ludwigs angina


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Ludwigs anginaA sensation of chocking and suffocation

angina

Wilhelm Friedrich Von Ludwig (1836)-Ludwigs.

Rapidly spreading cellulitis involving

BILATERAL submandibular ,sublingual and

submental space infection.


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Causes: 90% dental cause (spread from unilateral

submandibular / sublingual )

Compound fracture of mandible, puncturewounds in floor of mouth, secondary inf.

From malignancies- pseudo ludwigs

angina.


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Mortality rate: Pre-antibiotic era - 50%

Post -antibiotic era - 5%

But if untrated even now 100% mortality.


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Microbiology: Mostly Streptococci or mixed oral flora.

Contemporary reports Staph,GNB,E. coli

and Pseudomonas.Anerobes like

Bacteroides,Peptostreptococcus,Prevotella

melanogenicus ,P.oralis ,P. corrodens.


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Clinical features: Bilateral infection of sub-lingual and sub-

mandibular spaces with brawny edema

Elevated floor of the mouth, tongue almosttouching the palate.

Airway obstruction

Paucity of pus are hallmark signs


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Ludwigs angina


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Systemic features:

Pyrexia

Dehydration

Dysphagia Dyspnoea

Hoarseness of voice.


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Extra oral features:

Warm and tender swelling

Hard to firm brawny swelling extendingfrom bilateral submandibular andsubmental region sometimes anterior partof neck up to calvicle.

Unable to close mouth,saliva drooling

Respiratory distress noticed by the use ofaccessory muscles of respiration (SCM)


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Intra-oral features:

Trismus

Elevated floor of the mouth.

Tongue -displaced upwards andbackwards.

Increased salivation.


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Danger signs ofLudwigs:

Dysphagia

Dyspnoea

Hoarseness of voice. Stridor


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Management:

Early diagnosis

Airway management

Intense and prolonged antibiotic therapy Extraction of affected teeth.

Hydration

Early surgical drainage.


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Management:

DEATH IS DUE TO AIRWAY

OBSTRUCTION NOT BY SEPSIS

Anatomic reasons- tongue pushedbackwars obscures visualising airway by

broncoscope.

Swelling in neck make the task of

performing tracheostomy difficult.


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Management:

Use of muscle relaxant ,sedative and

norcotics are avoided as it can cause more

respiratory depression. Incision and drainage is preferred to reduce

pressure around airways.


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Bilateral submandibular and submental

incisions are placed. If required intra oral

sublingual incisions can also be made. Trough and through drains also can be

placed.


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Management:

Remove the cause at the earliest.

Supportive therapy

Hydrate the patient


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Complications of ludwigs:

Death due to airway compromise.

Aspiration of pus

Septicemia Mendiastinitis.


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Necrotising fascitis.


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Rapidly spreading infection causes

necrosis of tissues in sub-cutaneous space

by thrombosis of vessels that supplysuperficial muscle and skin.

Commonly seen in abdomen.


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Causes:

Dental

Salivary

Tonsillar Ear

Spreads along fascial planes.


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Microbiology:

Polymicrobial

Bacteroides melani

Fusobacterium Bacteroids oralis

Siprochates

Spread to proximity of major vessel in neck -fatal.


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Management:

Aggressive antibiotics, exentsive surgical

debridement like fasciotomy irrigation with

hydrogen peroxide Hyperbaric oxygen therapy


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o Coexist with some immunocompromised

states like diabetes ,uremeia

o Apart from local mangement such

immunocompromised states too.


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Thank you


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