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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
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
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
IF CONFINED TO BUCCINATOR:
INFECTION DRAINS INTRA ORALLY IN BUCCAL VESTIBULE
CROSSES BUCCINATOR:
INFECTION DRAIN DEEP INTO BUCCAL SPACE AND EXTRA ORAL DRAINAGE
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
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
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
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
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.
(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.
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
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
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
• 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