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FASCIAL SPACES AND ITSIMPLICATIONS IN THE

SPREAD OF INFECTIONS

K.Saravanan

PG Trainee

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• FASCIA• Used to describe broad sheets of dense connective

tissue whose function is to separate structures that must

pass over each other during movement, such as

muscles and glands, and serve as pathways for the

course of vascular and neural structures.

• The function of the fascia may be compared with the

tissue paper in a shirt box.

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• CLASSIFICATION:

• Superficial Fascia

• The superficial fascia is a layer of dense conn. tissue

that courses deep to sub-cutaneous tissue thro out

the entire body.

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Superficial Layer

• Superior attachment – zygomatic process

• Inferior attachment – thorax, axilla.

• Similar to subcutaneoustissue

• Ensheathes platysmaand muscles of facialexpression

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• Deep Cervical Fascia

• Investing fascia

• Parotidomessteric

• Temporal

• Middle Layer

• Sterno hyoid Omohyoid division

• Sterno thyroid – Thyrohyoid division• Visceral division

• Bucco pharyngeal

• Pre tracheal

• Retropharyngeal

• Posterior layer

• Alar division

• Prevertebral division

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Superficial Layer of the Deep CervicalFascia

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Middle Layer of the Deep CervicalFascia

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Deep Layer of Deep Cervical Fascia

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Prevertebral Space

• Entire length of neck

• Anterior border -prevertebral fascia

• Posterior border -vertebral bodies anddeep neck muscles

• Lateral border – transverse processes

• Extends along entirelength of vertebral column

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Visceral Vascular Space

• Entire length of neck

• Carotid Sheath

• ―Lincoln Highway‖

• Lymphatic vessels

can receive drainage

from most of

lymphatic vessels inhead and neck.

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Grodinsky and Holyoke’s (1938)classification of spaces

•Space 1 : Superficial to superficial fascia

• Space 2 : Superficial to the middle layer of deep

cervical fascia

• Space 3 : superficial to the visceral division of middle

layer of deep cervical fascia (Contains pretracheal,

retropharyngeal, lateral pharyngeal)

• Space 3A : Encloses carotid sheath visero vascular

space (Lincoln’s highway by Mosher) Infections of this

space are usually associated with IJV

thrombophebitis or CA erosion.

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• Space 4 :Danger space between alar and

prevertebral fascia, extends from base of skull to post

mediastinum.

• Space 4A : In the post triangle post to

carotid sheath

• Space 5 : Pre vertebral space

• Space 5 A : Enclosed by pre-vertebral

fascia, post to transverse process of vertebrae, as itsurrounds the scalene and spinal postural muscles.

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FASCIAS SPACES OF CLINICALSIGNIFICANCE

• Face : Buccal, Canine, Masticator

• Suprahyoid : Sub lingual, Sub

mandibular , Sub mental, Lateral pharyngeal, Peritonsillar

• Infrahyoid : Pre tracheal

• Space of total neck : Retro pharyngeal, Danger

space, Space of carotid

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• IV. BASED ON THE MODE OF INVOLVEMENT• Direct (Primary)

•

Primary maxillary spaces• Canine

• Buccal

• Infra temporal

• Primary mandibular spaces

• Sub-mental• Sub-mandibular

• Sub-lingual

• Buccal

• Indirect (Secondary)

• Messetric• pterygo mandibular

• Temporal

• Parotid

• Retropharyngeal

• Pre-vertebral

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I. PRIMARY MAXILLARY SPACES

1. CANINE SPACE (INTRA ORBITAL SPACE)

• Thin potential space bet levator angluli oris and levator

labii superioris muscles.

¥ Bounded by

• Superiorly : levator labii superioris, levatorlabii superioris aleque nasi.

• Interiorly : caninus muscle

• Anteriorly : Orbicularis oris

• Posteriorly : Buccinator muscle

• Medially : Antero lateral surface of maxilla.

¥ Etiology• Mostly due to odontogenic infections

• Less frequently by nasal infection.

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¥ Spread• Restricted within levator anguli oris.

• Canine with short root• Restricted above levator anguli oris below levator labii

superioris

• Canine with long root

¥ Clinical Features• Obliteration of naso-labial fold

• Swelling of cheek and upper lip.

• Drooping of angle of mouth

• Edema /swelling of lower eye lid.

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Canine Space Infection

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¥ Treatment

• Incision and Drainage

• Thro intra-oral approach, high in the maxillary labialvestibule by sharp and blunt dissection in region of

lateral incisor and canine.

• With curved – mosquito forceps inserted superior to theattachment of canine muscle, infra orbital space is

entered, pus drained, and rubber drain inserted kept for

1-2 days stayed with sutures.

2. Buccal Space• Potential space between buccinator and messeter

muscle

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¥ Bounded by• Anteriomedially: Buccinator muscle

• Posteriomedially: Messeter overlying the anteriorborder of ramus of mandible.

• Laterally : Forward extension of deepfascia from parotid gland and by plastysma muscle.

• Superiorly : zygo. Process of maxilla andzygo. major and muscles.

• Inferiorly : Limited by attachment of deepfascia to mandible.

¥ Contents• Buccal pad of fat, stenson’s duct facial art

¥ Etiology

• Mostly infections from maxillary and mandibularpremolar and molar teeth.

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¥ Spread• The relation of the root apices to the origin of the

buccinator muscle determines whether infection existsintraorally in the buccal vestibule or extends deeply intothe buccal space.

• Molar infections existing superiorly to the maxillary originof the muscle or inferiorly to the mandibular origin of themuscle enter the buccal space.

¥ Communications• Superiorly : Sub messetric space

• Medially : Pterygomandibular space (inf)

Infratemporal space (sup)

• Posteriorly : lateral pharyngeal space

• Extension of buccal pad: Infratemporal surface

• Thro subcutaneous space: peri-orbital space.

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Spread of Buccal Space Infections

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Clinical FeaturesSwelling from lower border of mandible to infraorbital margin.

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¥ DDCellulitis

• Non-odontogenic buccal space infection or buccalcellulitis caused by H.Influenzae usually seen in

infants/children of 3 years of dark red swellings.

Erysipelas

Recurrent buccal space abscesses

Complication of crohn’s disease -

a

transmural intestinal disease, characterized by

inflammatory granulomas from mouth to anus.

• Antibiotic, corticosteroid or surgical therapy

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¥ Rx

I & D

• I.O Approach – Horizontal incision thro mucosa ofcheek in premolar, molar region and drained.

• E.O Approach – Cutaneous drainage performed inferior

to point of fluctuance with blunt dissection into the depth.

Branch of facial nerve should be preserved. The I & D

should be inferior to stenson’s duct.

3 Infratemporal Space

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3. Infratemporal Space• Also called retro zygomatic space by Sicher .

¥ Bounded by• Laterally : By ramus of mandible

• Medially : Medial pterygoid plate, medialpterygoid muscle. Lateral wall of pharynx.

• Superiorly : By infratemporal surface ofgreater wing of sphenoid, and by zygo. arch.

• Inferiorly : Lateral pterygoid muscle, whichforms floor of the fossa, its lower head marks the borderbet pterygomandibular and infratemporal spaces.

• Anteriorly : Infra temporal surface of maxilla

• Posteriorly : Parotid gland

¥ Contents• both medial and lateral pterygoid muscles

• contains pterygoid plexus maxillary art, mandibular nerveand middle meningeal art.

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¥ Etiology• Inf from buccal roots of maxillary 2nd and 3rd molars

particularly from impacted 3rd molars.

• Max. 3rd molar (mostly)

¥ Clinical features• Trismus, marked swelling of face on affected side in front

of ear, eye often closed and proptosed swelling in thetuberosity area.

¥ Spread• Upward to temporal space.

• Downwards to pterygomandibular space.

• Because of close proximity to pterygoid plexus of veins,

infections travel upwards via deep facial veins or

emissary veins.

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Infra temporal space infection

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¥ I & D

• I.O Approach – an intraoral incision given at the

buccal vestibule opposite to 2nd and 3rd molars,

exploration carried out medial to coronoid process, and

then upwards and backwards with sinus forceps or

curved hemostat, the space is entered and drained by

rubber drain placed and secured with a suture.

• E.O. Approach – In severe infection, this is the only

choice. Incision made at the upper and posterior edge of

temporalis muscle within the hair line, exploration by

sinus forceps directed upwards and medially and

drained.

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II. PRIMARY MANDIBULAR SPACES

1. Sub-mental Space

• It is a midline structure exists below the chin.

¥ Bounded by

• Laterally : Anterior belly of digastric and

lower border of mandible deeply by mylohyoid muscle.

• Superficially : deep cervical fascia, platysma,superficial fascia, skin.

¥ Contents

• Aerolar connective tissue, sub-mental lymph nodes and

anterior jugular veins. ¥ Etiology

• Direct - Infection from mandibular incisors

• Indirect – from sub-mandibular space.

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¥ Clinical Features

• Firm swelling below chin

• Tenderness over the anterior mandibular teeth involved.

¥ I & D

• E.O. Approach– Horizontal incision in the most

inferior portion of the chin, in a natural skin crease,

provides most dependent drainage.• I.O Approach – Labial vestibule thro mentalis muscle

but dependent drainage cannot be established.

¥ Spread• May spread to submandibular spaces.

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Submental Space Infection

2 S b dib l S

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2. Sub-mandibular Space

• Separated from sub-lingual space by the fibers by themylohyoid muscle.

¥ Bounded by

• Anteriomedially: Mylohyoid forming the floor.

• Posteriomedially: Hyoglossus forming floor

• Anterosup. : Ant belly of digastric

• Post. sup. : Post. belly of digastric andstylohyoid.

• Laterally : Skin. Superficial fascia,platysma, superficial layer of deep cervical fascia

¥ Contents

• Sub mandibular salivary gland, sub mandibular lymphnodes, proximal portion of Wharton’s duct, lingual andhypoglossal nerve deep to gland and 5 branches offacial. artery (Asc palatine, tonsillar, sub lingual,glandular and sub mental)

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Submandibular Space

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Submandibular Space Infection

¥ E i l

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¥ Etiology

• Mandibular molars (mostly from 3rd molars)-perforate

Lingual cortical plate.

¥ Clinical Featu res

• Swelling below inferior border of the mandible.

¥ Spread

• Extend into sub-mental space.• Extend into contra-lateral side

• Extend backwards to involve pharyngeal spaces

¥ I & D

• Submandibular approach – incision || to inferior border

of mandible. Careful to avoid damage to submand

gland, facial nerve, lingual nerve

3 S b li l

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3. Sub-lingual space

• Between floor of mouth and the mylohyoid muscle.

¥ Bounded by

•

Superiorly : Mucosa of floor of the mouth• Inferiorly : Mylohyoid muscle

• Medially : Hyoglossus, genioglossus,genio hyoid muscles

• Laterally : Medial side of the mandible.

¥ Contents

• Sublingual glands, sub mandibular duct, hilum of submandibular gland, lingual nerve, sub lingual art and vein.

¥ Etio

• Mostly infections from root apices of the premolar and Istmolar teeth -superior to mylohyoid muscle.

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Sublingual Space Infection

¥ Cli i l f t

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¥ Clinical features

• Brawny tender swelling of the floor of the mouth which is

raised pushing tongue superiorly.

¥ Spread

• To the contra lateral side

• To the sub mandibular space

• To the lat pharyngeal space then the buccopharyngeal

gap

• To the sub lingual space

¥ I & D

• I.0 – an incision placed on the mucosa close tothe lingual cortical plate close to sub lingual plica (to

preserve lingual nerve) || to Wharton’s duct, and

explored thro sinus forceps and drained.

• SECONDARY POTENTIAL SPACES

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• SECONDARY POTENTIAL SPACES1.PAROTID SPACE

¥ Bounded by• The space is formed by splitting of the ant layer of

the deep cervical fascia and lies post. to the masticatorspace

• Inferiorly

• Stylomandibular ligament which separates the parotidspace from the submand space.

¥ Contents

• Parotid gland, parotid lymph nodes, facial nerve, ECAand retromand vein.


• Severe pain referred to ear• Presence of swelling over the messeter muscle

¥ Spread• To submesstric, pterygomondibular, and lat pharyngeal

spaces.

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Parotid Space

• Suprahyoid

• Superficial layer of deepfascia

• Dense septa fromcapsule into gland

• Direct communication toparapharyngeal space

• Contains

• External carotid artery• Posterior facial vein

• Facial nerve

• Lymph nodes

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¥ I & D

• Retromand incision placed, sinus forceps inserted, bluntdissection of parotid fascia is done and drained.

2. Masticator space• Anatomical compartment enclosed by the splitting of the

ant layer of deep cervical fascia around the muscle ofmastication.

• Contains

• Sub-messeteric

• Pterygomandibular

• Temporal spaces

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Masticator and TemporalSpaces

• Suprahyoid

• Formed by superficial layerof deep cervical fascia

• Masticator space• Antero-lateral to

pharyngomaxillary space.• Contains

• Masseter

• Pterygoids• Body and ramus of the

mandible• Inferior alveolar nerves and

vessels• Tendon of the temporalis

muscle

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Masticator space infections

• Symptoms; trismus, painful swelling, dysphagia etc

• Anatomy ;

1 Sub – messetric space

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1.Sub – messetric space

• Lies between ant layer of deep cervical fasciareferred as parotido messetric fascia and the lat

surface of ascending ramus of mandible

¥ Bounded by• Ant : Ant border of messeter muscle and buccinator

• Post : Parotid gland and post part of messeter• Inf : Attachment of messeter to lower border of

mandible

• Med: Lateral surface. of ramus of mandible

• Lat: Medial surface. of messeter muscle

¥ Contents• Messeter muscle, messeteric nerve, superficial

temporal art and vein

¥ Etiology

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¥ Etiology• Infections from

• Pericoronitis of 3rd molars (impacted)

¥ C/F• Extended facial swelling continued to outline of

messeter muscle,

• trismus is hallmark of this condition.

¥ Spread• Communicate, with pterygomandibular space thro

sigmoid notch.• No separation exits bet. this space and Sup temporal

space.

¥ I & D

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¥ I & D

• I.O. App- Incision placed vertically over the lower

part of ant border of ramus of mandible, sinus forceps

passed along the lat surface of ramus downwardsand backwards, and drained.

• E.o. app -when trismus in severe, an incision is

placed in the skin behind the angle of mandible, and

drained.

2.Pterygomandibular space

• This is the most frequently affected compartment insevere odontogenic infections.

¥ Bounded by

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¥ Bounded by• Lat : medial surface of ramus of mandible

• Med: lat surface of medial Pterygoid.

• Post : parotid gland• Ant : pterygomandibular raphae

• Sup : lat pterygoid muscle forms the roof

¥ Contents

Mandibular nerve -Ant. trunk ,Post trunk- lingual,inf. alv nerve

mylohyoid nerve,inf alveolar art.

¥ Etio• Most commonly by pericoronitis of mand 3rd molar

• Needle track infections occur, when used for inf. alv.Nerve block..

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¥ C/F

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¥ C/F

• Trismus caused by edema and inflammation of

medial pterygoid, swollen ant tonsillar pillar and

deviation of uvula to opp side,dysphagia. ¥ Spread

• Post to lat pharyngeal space

• Into infra temporal fossa and beneath temporal fascia

¥ I & D

• I.O app- a vertical incision of about 1.5 cm, made on

the ant and medial aspect of ramus of mandible,

sinus forceps is inserted and drained.• E.o. app - an incision placed in the skin below the

angle of mandible, sinus forceps inserted towards the

medial side of ramus in an upward, backward

direction and drained.

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3 Temporal space

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3.Temporal space• Fascial space in relation to temporalis muscle

• Superficial temporal -between temporal fascia, a

continuation of parotido messetric fascia and thetemporalis muscle

• Deep temporal space- bet temporalis muscle and thetemporal bone

¥ C/F• Pain, trismus, swelling over temporal region

¥ Spread• Secondary to pterygopalatine and infratermporal

space

¥ I & D- e,o. app• Incision in temporal region above hairline, 45 to zygo

arch, hemostat inserted and drained above and belowtemporalis muscle.

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Temporal Space Infection

Para pharyngeal spaces

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Para pharyngeal spaces• They include

I. Lat pharyngeal space

II. Retro pharyngeal space

I. Lat pharyngeal space• Shaped like an inverted pyramid with its base at

the base of the skull and apex at the hyoid bone. ¥ Bounded by

• Sup : base of the skull

• Inf : hyoid bone

• Ant : pterygomandibular raphe

• Post : bounded by stylohyoid muscle, upp part of

carotid sheath, prevertebral fascia

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Lateral Pharyngeal space

• Suprahyoid

• aka – Parapharyngeal space

• Superior—skull base• Inferior—hyoid• Anterior—

ptyergomandibular raphe• Posterior—prevertebral

fascia•

Medial—

buccopharyngealfascia• Lateral—superficial layer of

deep fascia

• Lat: ascending ramus of mandible insertion of medial

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• Lat: ascending ramus of mandible, insertion of medial

pterygoid, med surface of deep lobe of parotid gland.

• Med: bounded by pharyngeal wall, sup and mid

constrictors, stylopharyngeus & buccopharyngealfascia.

¥ Contents

• This space is divided into 2 compartments by the

fascial condensation across the styloid process called―aponeurosis of zukerkandl and testut‖ into

• Ant compartment (per styloid)

• Post compartment (post styloid)

• Ant compt : lymph nodes, ascending pharyngeal artery,

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Ant compt : lymph nodes, ascending pharyngeal artery,

loose aerolar connective tissue.

• Post compt : IX, X, XI, XII nerves, carotid sheath and

contents, cervical sym chain lies post to sheath. ¥ Etiology

• Infection from mand 3rd molars.

• Pharyngitis,tonsilitis parotitis, otitis, mastoiditis, and

herpetic gingivo stomatitis• From sub-lingual, Sub-mandibular, retro pharyngeal

pterygomandibular space infections.

¥ C/F

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¥ C/F • Ant compt : medial bulging of lateral pharyngeal wall

with deviation of palatal uvula from midline,dysphagia, swelling below angle of mandible, usually

trismus.

• Post comp : resp obstruction septic thrombosis of IJV,C.A hemorrhage.

¥ Spread

• Upwards thro O ovale, O lacerum, J.O present at thebase of the skull, and produce brain abscess,meningitis or sinus thrombosis.

• Downwards into carotid sheath towards mediastinum-

Lincoln’s highway’ of neck ¥ Inv

• CT is more useful in diagnosing lateral pharyngealinfections, contrast enhanced CT is more valuable aidin diagnosing lat pharyngeal infections .

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Presentation

• Lateral pharyngeal Space

• Fever, chills, malaise

• Pain, dysphagia, trismus

• Medial bulge of lateral

pharyngeal wall

• Cause—infection of

pharynx, tonsil, adenoids,dentition, parotid, mastoid,

suppurative lymphadenitis,

extension from other deep

neck spaces

¥ I & D

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¥ I & D • I.o. app: by incision placed along the lat pharyngeal

wall.

•

e.o.app : A 3.5 cm incision placed over the submandspace sup and || to hyoid bone, along the post belly ofdigrastric, after retraction of st.mastoid ,leads toexposure of carotid sheath, Blunt dissection alongthe post border of digastric muscle leads to lat

pharyngeal space.• In the combined intra oral and extra oral approach, a

mucosal incision is made lateral to thepterygomandibular raphe, and a large curved clamp ispassed medial to the medial pterygoid muscle in a

posterior-inferior direction. The tip of the clamp isdelivered thro the skin by a cutaneous incisionbetween the angle of mandible and of sternomastoidmuscle.

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II Retropharyngeal space

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II. Retropharyngeal space • Potential midline space between pharyngo-basillar

fascia, from the base of the skull to the fusion of

retropharyngeal fascia ¥ Bounded by

• laterally - carotid sheath

• Continuous with retro-pharyngeal space into post

mediastinum of T6 vertebrae.

¥ Contents

• Loose aerolar con. tissue, lymph nodes that drain

adenoid tissues of post pharyngeal wall.

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Retropharyngeal Space

• Entire length of neck.

• Anterior border - pharynx andesophagus (buccopharyngealfascia)

•

Posterior border - alar layer ofdeep fascia• Superior border - skull base• Inferior border – superior

mediastinum• Combines with buccopharyngeal

fascia at level of T1-T2

• Midline raphe connects superiorconstrictor to the deep layer ofdeep cervical fascia.

• Contains retropharyngeal nodes.

¥ Etiology

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¥ Etiology• Mostly from nasal and pharyngeal infection in

children

• Dental infection from lat pharyngeal space• TB

• Foreign bodies, trauma

¥ C/F

• Dysphagia, dyspnoea, nuchal rigidity, esophagealregurgitation, fever, bulging of post wall of pharynxunilaterally.

¥ Inv

• Radiography: lat soft tissue radiographies of neck isuseful by revealing increase in widening ofretropharyngeal space, [normal 6 mm at C2 and 20mm at C6]

• CT scans.

¥ I & D i.o app

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pp• Pt kept under LA in extreme trendelenburg position

and with constant suctioning , incision placed thro themidline of the post pharyngeal mucosa ,opened by

blunt dissection.

Caution • Pus pouring from ruptured space may be riskful by

aspiration or airway obstruction and in that

tracheotomy is indicated. E.o.app

• An incision placed along its ant border of st.mastoidmuscle, || to it, inf to hyoid bone, carotid sheath

retracted laterally, blunt finger dissection is carrieddeeply, avoiding hypoglossal nerve to the level ofhypo pharynx. Blunt dissection deep to inf constrictormuscles opens retropharyngeal space. Then drainsare placed.

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Block diagram showing the relationships of the prevertebral space (1), the danger space (2),

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g g p f p p ( ), g p ( ),the visceral compartment (3), the parapharyngeal spaces and the carotid sheaths (4), thesubmandibular space (5), the masticator spaces (6), and the parotid gland (7).

Peritonsillar abscess (quinsy):

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(q y)

• Localized inf in the conn.tissue bed between the tonsil

and sup. Constrictor muscle between the ant and post

and pillars of fauces. ¥ Etiology:

Pharyngitis

Complication of pericoronal abscess.

¥ C/F : pain on throat, dysphagia, hot potato in mouth

voice-characteristic, drooping of saliva

¥ Spread : to lat pharyngeal space

¥ I & D: i.o incision at the most prominent part of softpalate where fluctuation is the maximal.

Pericoronitis

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• Inflammation surrounding the crown of a partiallyerupted or unerupted tooth.

¥ Etiology: impacted teeth mostly mand 3rd molars. ¥ C/F :

• Acute: Well localized severe pain, pus discharge fromunderneath gingival pad, restricted mouth opening,enlarged lymph nodes on that side.

• chronic : asymptomatic or mild discomfort .

¥ Spread• To buccal space

• vestibular spaces• To submandibular pterygomandibular and

submessetric spaces

• Extraction of impacted tooth and drainage established.

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• Anatomicalconsiderationin dento

alveolarinfections

•MICROBIOLOGY

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MICROBIOLOGY

• The aerobic bacteria found

• in odontogenic infection are primarily G+ive cocci,mostly, s.viridans, s.milleri, s.sanguis, s.salivarius,s.mutans. They account for 80% of aerobic bacteriafound in odontogenic infection.

• The anaerobes are peptostreptococcus andbacteriodes. oropharyngeal bacteriodes are

• Porphyromonas – p.gingivalis,p.endodonticalis,p.asacrolyticus,

• Prevotella - p.melaninogenicus, p.buccalis,p.intermedia, p.oralis, p.looschi, p.dentocola.

• Other gp of anaerobes of g-ive rods are• Fusobacterium.

• among these, bacteriodes, fusobacterium,eikenella, are the org. most commonly identified inodontogenic infections.

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•PATHOPHYSIOLOGY

•

Spread of orofacial infection Routes of spread • By direct continuity thro the tissues.

• By lymphatics to regional lymph nodes.• By blood stream, e.g. Thrombo phlebitis, C.V.

thrombosis.

• Factors influencing spread

Depends upon

a. General factors

b. Local factors

a. General factors

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fHost resistance : depends upon

• Humoral factors that involve IgGs from Blym or plasma cells and complement.

• Cellular factors include PMN leucocytes,monocytes, lymphocytes and tissuemacrophages.

• virulence of micro organisms:

• Determined by invasiveness of causativemicro-org. these include production of lyticenzymes, potent exotoxins, endotoxins.

• Combination of both

• Compromised host defenses:

-Uncontrolled metabolic diseases like,diabetes, malnutrition, alcoholism

--Suppressing diseases like leukemia,lymphoma

--Suppressing drugs, cancer

chemotherapeutic drugs immunosuppressivedru s.

b Local factors

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b. Local factors

• Alveolar bone: 1st locally limiting barrier to farther

spread of a periapical infection. The site of

perforation of cortex is dependent upon proximity ofthe root apices to alveolar process.

• Periosteum : next local barrier. This is better

developed in mandible, produces some delay to

dev. of sub-periosteal abscess.• Adj muscles and fascia .

• so in broad context, pathways of dental infections

depends upon

Virulence of micro org

Resistance of host

Anatomy of involved area

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• As the interstitial hydrostatic pressure increases as aresult of the transudation of extra cellular fluid,

followed by the exudation of inflammatory cells, theflow of new blood into the region is compromised.

• In soft tissues the increased interstitial fluid pressureis relieved by swelling.

• when the soft tissues are contained within an

unyielding mineralized structure, such as themedullary space of bone or the pulp canal , theincreased pressure cannot be relieved.

• So, the pulpal or medullary soft tissues die as a

result of ischemia.• Tissue breakdown products recruit circulating

macrophages and histiocytes by the process ofchemotaxis.

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• As mineralized tissue is encountered thesecirculating macrophages coalesce and differentiate

into osteoclasts, which resorb mineralized bone.• The invading bacterial pathogens that trigger this

autolytic inflammatory process persist thro out itsextent.

• Streptococci, commonly found in early stages of

infection, can invade tissues by their elaboration ofhyaluronidase, which break down the extra cellularglyco proteins of con. tissue.

• As the streptococci flourish in their exponential

growth phase, they create an environment conductiveto subsequent growth of anaerobic flora ofodontogenic infections.

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• They consume O2 supplies and metabolize nutrientsto create a more acidic environment.

• They also may produce essential nutrients for theanaerobes present after about 3 days of clinicalsymptoms.

• The anaerobes including prevotella andporphyromonas sp, produce collagenases, whichdestroy most plentiful extra cellular matrix protein ofcon. tissue.

• As the infection perforates the bony cortical plate, theprocess of bacterial inoculation, followed byinflammation and necrosis, begins anew in the softtissues.

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• The most vulnerable tissue is aerolar con. tissue that

is not well vascularised.

• It is loose and easily directed by relatively lowhydrostatic pressures.

• Thus spreading infection follows the path of least

resistance deflected by denser and better

vascularized structures such as muscle, fascia,organs and bone.

• The deep facial infections are deflected or contained

by the structures that define the anatomical deep

facial spaces.

• EXAMINATION AND DIAGNOSIS

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EXAMINATION AND DIAGNOSIS

EXAMINATION

• Patient with orofacial infection may presentthemselves with various signs and symptoms ranging

from unimportant to extremely serious. So, a wide

assessment is a must.

• If the pt is toxic, exhibiting CNS changes, airway

compromised, then immediate hospitalization,

aggressive medical therapy and surgical intervention

should be done under intubation and tracheotomy.

HISTORY TAKING• History of onset, duration, previous treatment if any,

previous history of infection, if any helps in arriving at

accurate diagnosis.

Physical examination

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Physical examination

• Includes

• Gen-examination:

• Recording vital signs

• Regional examination & inspection:

• Includes

• Skin, fascia, head and neck.• Swellings /fistula, sinus

• Palpation:

• Swelling –size,tenderness,fixation,fluctuation

• Color, consistency,• Regional lymph nodes.

I.O.examination:

• teeth-decayed ,trismus

• Percussion of tooth

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• These basic principles of pt evaluation must be

observed if an accurate diagnosis and appropriate

treatment are to be achieved.

Investigations

Include

Lab investigations

• Complete blood Picture, c-reacting protein, ESR,

blood glucose levels. Blood cultures, gram staining

,culture sensitivity..• The isolation, identification and susceptibility testing

of microrg associated with infection are imp

components in determination of diagnosis and

appropriate therapy for may infectious diseases.

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Specimen acquisition and transport

• When possible collect specimen before administration of

antimicrobial therapy.

• Minimize contamination of the specimen with indigenous

flora.• Collect an appropriate amt of specimen for the tests

reqd.

• Use of sterile collection containers with pt name,

identification no., specific source, date and time ofcollection.

• Optimum time for specimen transport to laboratory is

less than 2 hrs.

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Aspiration

• Collection of aspirate specimen in head and neck

infections should use an extra oral approach to eliminate

contamination with oral flora.

• The site should be cleansed with germicidal soap

/alcohol.

• If i.o. app must be used, use of chlorhexidine minimizes

contamination with oral flora.

• Inj of LA into infected site should be avoided bcoz of

inhibitory eff of anesthetic agents on bacteria.

• Should accomplish a needle and syringe .

• Should be transferred to a sterile tube containing sodiumpolyanotrol sulfonate (SPS), anti coagulants.

Antimicrobial Therapy

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o Empherical therapy

• The choice of appropriate antimicrobial agent for

treatment of an infection depends on• Antimicrobial therapy must be directed as specifically as

possible against the infecting org.

• Antimicrobial agent should be chosen that will exhibit

appropriate pharmacological properties and activityagainst target orgs.

• host factors like age, renal / hepatic fn, site of infection

and previous adverse drug reactions must be evaluated.

• Effectiveness of antimicrobial agent to deliver adequateconc. at the site of infection

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• Surgical intervention often augments empherical therapy

bcoz drainage of necrotic tissue are necessary foreffective action of the antimicrobial at the site of

infection.

•

Rationale for susceptibility testing • Goal of susceptibility testing is to predict the likely

outcome of treating a specific organism with a

particular antimicrobial agent.

• To determine MIC & MBC.

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Imaging

• CT with contrast• Pros

• Widely available• Faster (5-15 minutes)• Abscess vs cellulitis• Less expensive

• Cons• Contrast• Radiation• Uniplanar• Dental artifacts

• MRI• Pros

• MRI superior to CT ininitial assessment

• More preciseidentification of space

involvement (multiplanar)• Better detection of

underlying lesion• Less dental artifact• Better for floor of mouth• No radiation

• Non iodine contrast• Cons

• Cost• Pt cooperation• Slower (19 to 35 minutes)

•TREATMENT

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SURGICAL INCISION & DRAINAGE Incision and drainage rid the body of toxic purulent

material and decompress the tissues, allowing betterperfusion of blood containing antibiotics anddefensive elements and increased oxygenation of the

infected area. Incision and drainage are best performed at the

earliest sign of this ripening.

In many odontogenic infections, surgical drainage

can be accomplished by extraction of offending tooth. Removal of tooth serves to eliminate the bacteria’s

portal entry to deeper tissues.

The following principles should be used whenpossible with incision and drainage

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possible with incision and drainage.

Incise in healthy skin and mucosa whenever

possible. An incision placed at the site of maximumfluctuance where the tissues are necrotic orbeginning to perforate may result in a puckeredunaesthetic scar.

Place the incision in an esthetically acceptable area,such a under the shadow of jaw or in a natural skinfold or crease.

When possible, place the incision in a dependent

position to encourage drainage by gravity.

Dissect bluntly, with a closed surgical clamp or fingerthro deeper tissues and explore all positions of theabscess cavity thoroughly so that compartmentalized

area of pus are disrupted and excavated.

Pl d i d t bili ith t

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Place a drain and stabilize with sutures.

Consider use of thro and thro drains in bilateral,submandibular space infections.

Do not leave drains in place for an overly extendedperiod. Remove them when drainage becomes

minimal.

The presence of drain itself may produce someexudate and can be a portal for sec. bacterial

invaders.

Clean wound margins daily under sterile conditions toremove clots and debris.

ANTIBIOTIC THERAPY

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ANTIBIOTIC THERAPY

Principles for choosing appropriateantibiotic

• Identification Of causative org

• Determination of antibiotic sensitivity

• Use of specific narrow spectrum antibiotic• Use of least toxic antibiotic

• Pt drug history

• Use of bactericidal rather than bacteriostatic drugs

• Use of antibiotic with a proven history of success.• Cost of antibiotic.

• Encourage pt compliance.

Principles of antibiotic administration

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• Proper dose

• Proper time interval

• Proper route of administration• Consistency of route of administration

• Combination antibiotic therapy.

• PT MONITORING Response to treatment• Most commonly, the response begins by 2nd day and

initially is a subjective sense of feeling better.

• Ideally antibiotics should be given until all offendingbacteria have been eradicated. It is reached by 3rdday after pt become asymptomatic when no tempand no or little swelling present.

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• In a uncomplicated odontogenic infection,

improvement would be expected to begin by the

2nd day of therapy and marked resolution by 3rdday.

• Allowing antibiotics additional 2 days results in a 5

day course of antibiotics.

• Occasionally resolution may take longer than 4 days.

So a 7 days course of antibiotics is necessary.

• By observing pt’s progress closely, the clinician can

individualize the treatment for the proper duration of

therapy

Causes of failure in treatment of

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Causes of failure in treatment ofinfection

• Inadequate surgical treatment• Depressed host defenses

• presence of foreign body

• Antibiotic problems

• Drug not reaching infection• Dose not adequate

• Wrong bacterial diagnosis

• Wrong antibiotic

• Rx for immuno compromised pts

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• Diabetes mellitus

• Blood glucose level [198-270mgidl]

• Impaired activation of complement

• Impaired granulocyte adherence

• Impaired Chemo taxis

• Impaired Phagocytosis

• T and dysfn. -CMI impaired

• Reversed by insulin administration

• On surgical exp, optimization of glucose homeostasis

should substantially reduce the risk of infectiouscomplications.

• Prophylactic antibiotic can be provided.

• Cortico steroid therapy

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• Suppress inflammation by impaired recruitment of

leucocytes, decreased production of T lymphocytes. So

increased susceptibility to infections.• Prophylactic antibiotic can be provided

• In established oral or facial infection in the immuno

compromised host, treatment should be directed toward

minimization of magnitude and duration of pathogenexposure.

• Rx directed at removal o source of infection and

nonviable is imperative.

• COMPLICATIONS

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• Ludwig’s angina

• Firm, acute, toxic, cellulitis of the sub-mand and sub

lingual spaces bilaterally and of the sub-mental spaces.

¥ Etiology

• Odontogenic cause: 90% of cases- most common.

• Non-odontogenic causes:

• Sub-mand gland sialadenitis

• Comp. mand #

• Oral soft tissue lacerations.

• Punctured wounds of oral floor.• Sec infections of oral malignancies

• Called as pseudo- Ludwig’s angina.


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¥ Clinical features ¥ On gen examinat ion

• Patient may be toxic, ill, dehydrated, with pyrexia,anorexia, chills and malaise, impaired speech and

hoarseness of voice.

¥ On e.o exam

• Firm brawny swelling in bilateral sub mand and submental regions.

• Tongue movements reduced.

• Airway obstruction.

¥ On i.o exam • Raises floor of mouth, increased salivation, stiffness

of tongue movements, and difficulty

L d i ’ A i

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Ludwig’s Angina

¥ MicrobiologyG i St h

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• G+ive Staph,

• G-ive - E.coli, pseudomonas,

• Anerobes-bacteroides pepto streptococcus spp., p-melanogenicus p.oralis, p.corrodens.

¥ Pathology

• The condition is a diffuse inflammation of soft tissueswhich spread thro tissue spaces and along fascialplanes.

• Spreading infection occurs in the presence of org thatproduce hyaluronidase and fibronolysis which act tobreak down or dissolve respectively hyaluronic acid andfibrin.

• Streptococci – hyaluronidase associated within Ludwig’sangina.

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¥ Spread • Ant- submandibular space – sub messetric,

ptreygomand spaces

• Post – Para pharyngeal, Para tonsillar spaces.

¥ Fate

• If untreated, can be fatal within 12-24 hrs.

• Death due to asphyxia.• Other causes may be septicemia, septic shock,

mediastinitis, and asp. Pneumonia

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Antimicrobial therapy

• Given in IV

• Penicillin and derivatives

• Cloxacillin

• Gentamicin

• Clindamycin

• Metronidazole• Cephalosporins

COMPLICATIONS

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COMPLICATIONS

• Life threatening airway obstructions

• Septicemia

• Mediastinitis

• Pericarditis

• IJV thrombosis

• Meningitis

• C.S. Thrombosis

• brain abscess• Death

MEDIASTINITIS • It is an infection involving the connective mediastinal

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• It is an infection involving the connective mediastinaltissue that fills the interpleural space and surrounds themedian thoracic organs.

¥ Etiology• Odontogenic infection from submand, Para pharyngeal

space, buccal space, spread to midiastinum.

• Descending necrotizing mediastinitis (DNM)

• Most lethal form of descending infection spreads alongfascial planes from an orophayngeal source thro theneck to gain access to mediastinum

• Necrosis occurs because the infection is often

polymicrobial and gas producing.• Predisposing factors: Diabetes, alcoholism, malnutrition

and immuno suppression.


U itti hi h f t h di t h

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• Unremitting high fever, tachycardia, tachyopnea,

hypotension, pleuritic chest pain, dyspnoea, retrosternal

discomfort, Brawny edema. ¥ R/F

• CT scan of neck and chest reveal size and location of

mediastinal fluid collection with or without gas bubbles,

pericardial effusion, empyema and airway patency. ¥ Treatment

• Consists of extensive, long-term antibiotic therapy andsurgical drainage of mediastinum.

INVOLVEMENT OF CAROTID SHEATH

• Fascial condensation surrounding IJV CCA and Vagus

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• Fascial condensation surrounding IJV, CCA and Vagus

nerve.

• Lies below st. mastoid muscle and most commonly affectabove post belly of omohyoid muscle.

¥ Etiology

• Inf from submand space, infra temp space and Para

pharyngeal space. ¥ Clinical Features

• Chills, septicemia, fever

• Herald bleeds – intermittent bleeding episodes from

nose or pharynx caused by incipient erosions of CA orIJV.

• Palsies of X, XI, and XII nerves.

• Hornor’s syndrome &. Hematoma of neck.

¥ Complications

• Thrombophlebitis of IJV

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• Thrombophlebitis of IJV

• If lateral pharyngeal space is undrained the CCA may

become eroded with fatal consequence. ¥ Rx

I & D – Incision made on ant border of st.mastoid

muscle, above the region of omohyoid.

CAVERNOUS SINUS THROMBOSIS

• Condition consisting of formation of thrombus in thecavernous sinus or its communicating branches.

¥ Spread• 2 routes

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2 routes

• Ext. route – infection from face and lip carried by facialand angular veins (danger area of face) to the

sup.opthalmic vein enters cav. Sinus thro sup. Orbitalfissure.

• Int. route – dental infection carried by way of pterygyoidplexus from the post maxillary region to inf ophthalmic

vein.• The internal spreading by facial or external route is veryrapid because open system of the veins leading directlyto cavernous sinus.

• The other pathway from pterygoid of veins thro emissary

veins. ¥ Pathophysio

• Short distance from facial regions to sinuses of brain

• Lack of protective valves.

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¥ Cli i l f

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• Swelling of face with edematous eyelids

• Pain of eye and tenderness to pressure.

• Edema of conjunctiva due to impaired venous return.

• Posteriorly exophthalmus.

• Cranial nerve involvement – opthalmoplegia

• Advanced stage – bilateral signs seen.

• Paralysis of abducent nerve by weakness or paralysis of

lateral rectus muscle of eye.

¥ Treatment

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Antibiotic therapy

• Heparinization to prevent thrombosis 20,000 units in

1500 ml of 5% dextrose or dicumarol 200 mg, on 1st day

and 100mg daily.

• Neurosurgical consultation

• Mannitol reduces edema

• Anticoagulants

Surgical drainage

• BRAIN ABSCESS:

¥ Eti l

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¥ Etiology• Bacteremia accompanying odontogenic infection - inflam

– edema – thrombosis.

¥ Clinical Features• Headache, vomiting, hemiplegia, papilloedema, aphasia,

hemi sensory deficit, hemi anopia and abducens palsy. ¥ Treatment• Drug therapy

• Surgery to provide drainage.

• Meningitis

• Most common neurological complications resulting from

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• Most common neurological complications resulting from

the infection in orofacial region.

¥ Clinical Features• Headache, stiffness of neck, vomiting, convulsions

• Kernig’s sign: strong passive resistance when an attempt

is made to extend the knee from flexed thigh position.

• Brudenski’s sign: abrupt neck flexion in the supineposition resulting in involuntary flexion of the knees.

¥ Treatment

• Penicillin G.

• Proper hydration and electrolytic balance.

• DANGER SPACE

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• DANGER SPACE

• Extends from base of skull superiorly to diaphragm

inferiorly.

• Laterally at the fusion of alar and prevertebral fascia at

the transverse process of c-6 and t-4 vertebrae.

• Infections from retropharyngeal space, pass thro danger

space into mediastinum can erode into or compress

major vessels, lower airway and upper digestive tract.

Danger Space

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Danger Space

• Entire length ofneck

• Anterior border -

alar layer of deepfascia• Posterior border -

prevertebral layer• Extends from

skull base todiaphragm• Contains loose

areolar tissue.

SUBCUTANEOUS SPACE

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• SUBCUTANEOUS SPACE• Occupies the potential space between superficial fascia

along the muscles of facial expression and skin.

• Necrotizing fasilitis, a rapidly spreading infection, causes

necrosis of tissues in the subcutaneous space by

thrombosis of vessels that supply the superficial muscles

and skin.

• In the nerve, they follow platysma muscle inferiorly to its

terminus and ant chest wall, can also affect deeper

structures.

CONTROL AND PREVENTION OFINFECTION IN A SURGICAL

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INFECTION IN A SURGICALPATIENT

Factors in wound infection

Surgical infection control

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• Factors in woundinfection

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• Surgical infection control

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• Surgical infection may be defined as any infectionthat occurs in a patient who has undergone a

surgical procedure.

• The following important factors relating to woundsepsis include the surgeon, assistant, nursing andtechnical personal, the type and length of surgical

procedure, invasive technology and theimplantation of foreign devices, equipment andeven its circulation thro operating room.

• Pathogenic gram-negative bacilli can survive on

the hands for more than 2 hrs.

• Povidone – iodine (10%) solution correctly is thesafest and most efficacious slim preparation formaxillofacial pt and surgical scrub (7.5%).

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•Medial literature on gloves reliability reveals that

pin holes exist in 2% and 9% of used latex gloves,

almost 19,000 bacteria can pass thro a single pin

hole in 20 min.Even blood can also pass thro pin

holes.

•Wearing of double layer of gloves when handling

HIV pts are necessary.

•Masks and protective eye shields are defensive

against blood splashes, which occur most frequently

when power-driven saws and drills are used.

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Thank You

• Diagnostic imaging technique • CT scan- gold standard in head and neck imaging.

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• Shows complete extent of inflammatory process.

• Accuratively demonstrate the status of airway andinvolvement of lymph nodes.

• Contrast enhanced axial CT sections should beperformed in the axial plane in 5mm increments thro allthe involved fascial spaces and the major lymph node

chains receiving drainage from involved regions of headand neck.

• MRI- Though it has been used in evaluation of head andneck, it is not extensively used in deep fascial spaceinfections.

• Has no. of disadvantages in the evaluation of head andneck infections including length of imaging time, andsimilar appearances of abscesses and cellulitis on T2 –weighed images. And also more expensive.

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