Spread of Oral Infections in Fascial Spaces

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SPREAD OF ORAL INFECTIONS IN FASCIAL SPACES BHARATHREDDY

Transcript of Spread of Oral Infections in Fascial Spaces

SPREAD OF ORAL INFECTIONS IN FASCIAL

SPACES

BHARATHREDDY

THE CONCEPT OF FASCIAL “SPACES” IS BASED ON

ANATOMIST’S KNOWLEDGE THAT ALL “SPACES” EXIST

POTENTIALLY, UNTIL FASCIAE ARE SEPARATED BY PUS,

BLOOD, DRAINS OR SURGEONS FINGER.

WHEN DENTAL INFECTIONS SPREAD DEEPLY INTO SOFT

TISSUE RATHER THAN EXITING THROUGH ORAL OR

CUTANEOUS ROUTES,FASCIAL SPACES MAY BECOME

INVOLVED FOLLOWING PATH OF LEAST RESISTANCE.

Classification of facial spaces According to topazian

ON FACE: BUCCAL CANINE MASTICATOR MASSETER PTERYGOID ZYGOMATICO TEMPORAL PAROTID

SUPRAHYOID:

SUBLINGUAL SUBMANDIBULAR SUBMAXILLARY SUBMENTAL PHARYNGOMAXILLARY PERITONSILLAR

INFRAHYOID:

ANTEROVISCERAL (PRETACHEAL)

SPACES OF TOTAL NECK:

RETROPHARYNGEAL DANGER SPACE SPACE OF CAROTID SHEATH

FASCIAL LAYER

SUPERFICIAL LAYER DEEP LAYER

SUPERFICIAL OR ANTERIOR LAYERMIDDLE LAYERPOSTERIOR LAYER

THESE DEVIDE, UNITE, BLEND AND FUSE TO FORM VARIOUS COMPARTMENTS OR SPACES

Previsceral fascia( sagittal section)

BUCCAL SPACE

BOUNDRIES

SUPERIORLY : ZYGOMATIC ARCHINFERIORLY : LOWER BORDER OF MANDIBLE ANTERIORLY : MODIOLUS OF MOUTHPOSTERIORLY : PTERYGOMANDIBULAR RAPHEMEDIALLY : BUCCINATOR MUSCLE AND BUCCOPHARYNGEAL FASCIA LATERALLY : SKIN OF CHEEK

BUCCAL SPACE ABSCESS

CONTENTS

STENSEN’S DUCT MAXILLARY ARTERY BUCCAL FAT PAD

SOURCE OF INFECTION

MAXILLARY AND MANDIBULAR MOLAR REGION

OR

EVEN BICUSPID

IF CONFINED TO BUCCINATOR:

INFECTION DRAINS INTRA ORALLY IN BUCCAL VESTIBULE

CROSSES BUCCINATOR:

INFECTION DRAIN DEEP INTO BUCCAL SPACE AND EXTRA ORAL DRAINAGE

CANINE SPACE

INFREQUENTLY INVOLVED IN ODONTOGENIC INFECTIONS

LEVATOR ANGULI ORIS OVERLIES THE APEX OF CUSPID ROOT . ORIGIN OF THE MUSCLE IS HIGH IN CANINE FOSSA WHEREAS ITS INSERTION IS THE ANGLE OF MOUTH AND ZYGOMATIC MUSCLE.

IF CUSPID INFECTION PERFORATES THE LATERAL CORTEX OF MAXILLARY BONE SUPERIOR TO INSERTION OF MUSCLE POTENTIAL CANINE SPACE BECOME INVOLVED

MASTICATOR SPACES

CONSIST OF MESSETERIC PTERYGOID TEMPORAL

THESE ARE WELL DIFFERENTIATED BUT COMMUNICATE WITH EACH OTHER AND WITH BUCCAL, SUBMANDIBULAR AND PARAPHARYNGEAL SPACES

SORCE OF INFECTION

THIRD MOLAR (PERICORONITIS, DENTAL CARIES INDUCED ABSCESS ETC) INFECTION OF MAXILLARY CANINE USUALLY PRESENT AS LABIAL SULCUS SWELLING AND LESS COMMONLY AS PALATAL SWELLING

ALSO BY CONTAMINATED MANDIBULAR BLOCK INJECTIONS OR DIRECT TRAUMA

HERE, CLINICALLY THE HALLMARK OF INFECTION IS TRISMUS

SUBLINGUAL SPACE BILATERAL V SHAPED SPACE

BOUNDRIES:SUPERIORLY : SUBLINGUAL MUCOUS MEMBRANEINFERIORLY : MYLOHYOID MUSCLEPOSTERIORLY : HYOID BONEANTERIORLY : LINGUAL SURFACE OF MANDIBLELATERALLY : LINGUAL SURFACE OF MANDIBLEMEDIALLY : GENIOGLOSSUS, GENIOHYOID, STYLOGLOSSUS

om

COMMUNICATIONS

ANTERIORLY : SUBMENTAL SPACE

POSTERIORLY : SUBMANDIBULAR SPACE

SOURCE OF INFECTION

PREMOLARS

PERIODONTAL INFECTION OF INCISORS

LINGUAL INJECTIONS

INFECTION OF WHARTSON’S DUCT

SIALIDINITIS

IMPORTANT CLINICAL FEATURES

RAISED TONGUE WHITE DISCOLORATION OF FLOOR OF MOUTH BRAWNY ERYTHEMATOUS TENDER SWELLING OF FLOOR OF MAOUTHOPEN MOUTHDRIBBLING OF SALIVAWHITE COLLAR APPEARANCEDYSPHAGIADYSPNOEAOTHER FEATURES OF TOXEMIA

NO EXTRA ORAL DRAINAGE,ONLY INTRA ORAL DRAINAGE

D/D: CELLULITIS WITH INFECTED SIALOLITH

SUBMANDIBULAR SPACE

SEPARATED FROM OVERLYING SUBLINGUAL SPACE BY

MYLOHYOID MUSCLE

BOUNDRIES LATERALLY : SUBMANDIBULAR SKIN,SUPERFICIAL FASCIA,PLATYSMA, LOWER BORDER OF MANDIBLE

MEDIALLY : MYLOHYOID, HYPOGLOSSUS. STYLOGLOSSUS

INFERIORLY : ANTERIOR AND POSTERIOR BELLY OF DIGASTRIC

POSTERIORLY : HYOID BONE

SUBMANDIBULAR SPACE INFECTION

CONTENTS

SUBMANDIBULAR SALIVARY GLAND AND LYMPH NODES

FACIAL ARTERY

WHARTSON’S DUCT

LINGUAL NERVE

HYPOGLOSSAL NERVE

SOURCE OF INFECTION

MANDIBULAR SECOND AND THIRD MOLAR

SOMETIMES EVEN FIRST MOLAR

SECONDARY TO ADJOINING SPACES-SUBLINGUAL OR SUBMENTAL

D/D: ACUTE SIALADENITIS SUBMANDIBULAR LYMPHADENITIS

SUBMENTAL SPACE

BOUNDRIES

SUPERIORLY : INFERIOR BORDER OF MANDIBLE

INFERIORLY : MYLOHYOID MUSCLE

POSTERIORLY : MYLOHYOID MUSCLE

LATERALLY : ANTERIOR BELLY OF DIGASTRIC

SOURCE OF INFECTION

MANDIBULAR INCISORS OR FROM SUBMANDIBULAR SPACE

Presentation The patient presents with a swollen face and occasionally swollen neck. Toothache or facial pain may or may not be a feature.

There is often general malaise and possibly rigors with fever.

Patients may complain of trismus (inability to open the mouth fully), pain or difficulty in swallowing, drooling, sore throat and a hoarse voice.

Examination

Specific attention should be paid to the location of swelling, size, flactuance, any possible pointing and coexistent lymph node enlargement.

Good oral examination should include

presence of halitosis, evidence of intraoral pus drainingany tongue elevation, any sublingual or

submandibular swelling, swelling in the mandibular or maxillary sulci, palatal swelling especially of the soft palate

or uvula, general dental state patency of salivary outlets (parotid,

submandibular and sublingual), nature of saliva produced (clear, thick, pus?).

Suspect teeth should be tapped with a metallic object to elicit any tenderness to percussion.

Swelling should be palpated bimanually if possible with a finger of one hand intraorally and and the second hand extraorally (pushing towards the oral site).

The neck should be evaluated for swelling, lymphadenopathy and possible tracheal deviation.

Aetiology of major facial infections

Teeth can contribute by:

Potential route of spread of pulpal infection

(1) Decay (caries) reaching the dental pulp=pulpitis, this in turn spreads to supporting bone resulting in

(2) periapical abscess which in turn may spread subperiosteally.

(2) Periapical abscess may occur in seemingly intact but devitalised teeth (trauma, cracks or decay under fillings).

(3) Periapical and periodontal abscess may form as a result of chronic gingivitis and supporting bone and soft tissue loss (periodontal disease) - note again the tooth may be entirely intact clinically and radiographically.

(4) Erupting teeth (especially partially impacted lower third molars) can result in inflammation and infection of the gum flap preventing eruption (operculum) with swelling pus etc. around the crown (pericoronitis). (5) Retained roots supragingival or subgingival.

JAWS(1)Can develop cysts or tumours that

can range from odontogenic (=dental origin) to either primary or secondary malignancy. Most are derived from the dental apparatus and although benign can nevertheless continuously grow and become secondarily infected on breaching the surrounding bone.

(2)Osteomyelitis although rare can be the result of chronic infection as mentioned before.

(3) Osteoradionecrosis occurs readily in irradiated jaws subjected to further trauma (such as extractions).

(4) Rarer are tuberculosis, Actinomycosis and syphilitic osteomyelitis. (5) Most jaw fractures in the tooth bearing segments are by definition compound to the oral cavity and can easily be infected by the oral microbes. (6) Extraction sites again are comparable to compound fractures and it is surprising that infection is so relatively rare.

Major salivary glands

(1) May be the subject of either viral or bacterial

infections often superimposed on obstruction of ducts (stone,

stricture, etc).

(2) Tumours rarely also become secondarily

infected.

Paranasal sinuses

(1)May be primarily infected, obstruct and result in facial swelling.

(2)May become infected secondary to infected teeth protruding into the maxillary sinus (upper premolar and molar teeth often do).

(3)Tumours or cysts may become infected.

(4)Fractures such as the orbital floor are by definition compound to the “outside” and may result in orbital cellulitis.

Investigations In many cases careful history and examination will make diagnosis clear, however certain investigation will still be necessary.

Plain X rays

(1)The OPG (orthopantomogram) is invaluable in displaying the teeth, whole of mandible, tooth bearing segment of the maxilla as well as parts of the maxillary sinuses. Use for any suspected fractures of the mandible, periapical abscesses and bony cysts and tumours. Will show impacted third molars ('wisdom teeth').

(2)Occipito-mental 15 and 30 degrees (“Water’s view”) will show both maxillary sinuses (effusion?), orbital floor and most fractures of the maxilla.

(3) Mandibular occlusal views and lateral oblique views may demonstrate stones in the submandibular gland.

(4) 'Puffed cheek' view may demonstrate stones in the parotid duct.

Sialography: Can be used for suspected gland obstruction however CT sialogram is the gold standard.

Ultrasound

Useful in confirming collections as well as a guide to aspiration. Will also show stones in salivary ducts and glands.

CT scan

With axial and coronal views will demonstrate exact extent of the swelling, potential airway compromise and is invaluable to both the surgeon and anaesthetist. However patients unwell enough to potentially obstruct their airway should be taken straight to theatre rather than risk an emergency in the radiology dept.

Microbiology of any pus or discharge.

The usual blood tests.

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 4 IS THE SPACE BETWEEN PREVERTIBRAL AND ALAR FASCIA

PTERYGOMANDIBULAR SPACE

PTERYGOID SPLEXUSEMISSERY VEINS

CAVERNOUS SINUS THROMBOSIS

LATERAL PHARYNGEAL SPACE

RETROPHARYNGEAL SPACE

MEDIASTINUMCAROTID SHEATHDANGER SPACE 4

EVOLUTIVE STAGES OF ODONTOGENIC INFECTION

AN INITIAL PERIOD OF PERIAPICAL CONTAMINATION BY BACTERIA GENERALLY ORIGINATING FROM ROOT CANAL

CLINICAL PERIOD WITH SIGNS AND SYMPTOMS –ACUTE APICAL PERIODONTITIS, DEVELOMENT OF A PERIAPICAL ABSCESS

PERIOSTEUM RUPTURES AND INFECTION GAINS ECCESSTO SURROUNDING SOFT TISSUES PRODUCING CELLULITIS ( PHLEGMON )

FINAL RESOLUTION PERIOD AND GENERATION OF REPAIR TISSUE.

CELLULITIS(PHLEGMON)• TYPES1. SEROUS CIRCUMSCRIBED ACUTE

CELLULITIS AFFECTING SINGLE ANATOMIC SPACE

2. SUPPURATIVE CIRCUMSCRIBED ACUTE CELLULITIS WITH PLURULENT SUPPURATION

3. DIFFUSE ACUTE CELLULITIS• LUDWIIG’S ANGINA• PERIPHARYNGEAL CELLULITIS• NECROTIZING FASCIITIS

4. CHRONIC CELLULITIS

CLINICAL MANIFESTATIONS

• SHARP PULSATILE PAIN• REDENING AND WARMTH OF

SKIN AND MUCOSA• POORLY DELIMITED SWELLING

THAT ERASES THE SKIN FOLDS AND SULCI

• LOSS OF FUNCTION • FEVER

LUDWIG’S ANGINAFIRST DESCRIPTION IN 1836 BY DR.VON

LUDWIGANGINA: CHOAKING SENSATION

DEFINITION

ARCHER: IT’S A BILATERAL,ACUTE,RAPIDLY SPREADING, SEPTIC,INFLAMMATORY,INDURATED,WOODEN HARD CELLULITIS OF FLOOR OF MOUTH

• THOMA: IT’S A GANGRENOUS CELLULITIS OF LOOSE ALVEOLAR TISSUE WHICH ORIGINATES IN SUBMANDIBULAR SPACE AND SPREADS RAPIDLY TOWARDS FLOOR OF MOUTH

• KILLEY-KEY-SEWARD: IT’S A CLINICAL DIAGNOSIS AND IS THE NAME GIVEN TO BRAWNY CELLULITIS OCCURING BILATERALLY AT SUBMANDIBULAR REGION WHICH ALSO INVOLVE SUBLINGUAL SPACE

SPREAD OF INFECTION

• ACCORDING TO KRUGER,TOPAZIAN,LUDWIG

THIRD MOLARS

SUBMANDIBULAR SPACE

SUBLINGUAL

CONTRALATERAL SUBMANDIBULAR AND SUBMENTAL SPACE INVOLVEMENT

• LASKINSUBLINGUAL SPACE

SPREADS BILATERALLY

SUBMANDIBULAR AND SUBMENTAL SPACE

BACKWARD SPREAD TO SUBSTANCE OF TONGUE

INFECTION REACHES EPIGLOTTIS

SWELLING AROUND LARYNGEAL INLET

MICROORGANISM INVOLVED ARE MOJORITILY STREPTOCOCCUS HEMOLYTICUS

ETIOLOGYPERODONTAL, PERICORONAL OR

PERIAPICAL ABSCESS OF MANDIBULAR MOLARS

NON ODONTOGENIC CAUSES (PSEUDO LUDWIG)

COMPOUND FRACTURE OF MANDIBLENEEDLE INJURY TO FLOOR OF MOUTHFISH BONE INJURYSIALIDINITIS

LUDWIG’S ANGINA

SIGNS AND SYMPTOMS

• MASSIVE,FIRM,HARD BOARD LIKE,BRAWNY NON PITTING SWELLING OF NECK EXTENDING DOWN TO CLAVICLE

• OPEN MOUTH• DRIBBLING OF SALIVA• RAISED FLOOR OF MAOTH• SHINY MUCOSA• WHITE COLLAR APPEARANCE• STIFF TONGUE TOUCHING PALATE• DYSPHAGIA, DYSPNOEA• EDEMA OF GLOTTIS

• AIRWAY OBSTRUCTION• OTHER FEATURES OF TOXEMIA

SEQUELEIT CAN CAUSE MEDIASTINITIS LEADING TO

ASPIRATION PNEUMONIA AND DEATH DUE TO RESPIRATORY PARALYSIS

IT CAN INVOLVE PTERYGOID COMPARTMENT AND VIA PTERYGOID PLEXUS CAN CAUSE CAVERNUS SINUS THROMBOSIS

IT CAN CAUSE SEPTICEMIA OR BACTEREMIA BECAUSE OF HEMATOLOGICAL SPREAD

GENERAL MANAGEMENT

• PROPER HISTORY TAKING AND EXAMINATION AND INVESTIGATIONS

• ANTIBIOTIC – ANALGESIC THERAPY• ANTIINFLAMMATORY DRUGS• FLUID BALANCE AND AIRWAY

ESTABLISHMENT WHERE REQUIRED• REMOVAL OF FOCUS OF INFECTION• ESTABLISHMENT OF DRAINAGE• ADEQUATE MEDICAL CONSULTATION

AND REFFERAL

THANK YOU