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Dr. Mohit Bindal Senior Lecturer Department Of OMFS

DR.MOHIT BINDAL, Subharti Dental College, SVSU CONTENTS INTRODUCTION HOST DEFENSE AND INFECTION MICROBIOLOGY AND ANTIBIOTIC THERAPY FASCIAE OF HEAD AND NECK CLASSIFICATION OF SPACES MAXILLARY SPACES MANDIBULAR SPACES SECONDARY SPACES COMPLICATIONS OVERALL MANAGEMENT STAGES OF INFECTION CONCLUSION INTRODUCTION  Fascial spaces are potential spaces between the layers of fascia- Shapiro

 Represent major pathways for spread of infections

 When infections spread deeply into soft tissue- involvement following path of least resistance

INFECTIONS AND HOST DEFENSE

 In establishing presence of an infection, interaction occurs among three factors:

1. Host 2. Environment 3. Microorganism

Infection occurs when either host is immunocompromised or when pathogenecity and number of microbes invading host is more

SPREAD OF OROFACIAL INFECTION

FACTORS INFLUENCING SPREAD

 GENERAL FACTORS:

 Host resistance

 Virulence of microorganism

 Medically compromised

 LOCAL FACTORS:

- Intact anatomical barriers

 Alveolar bone

 Periosteum

 Adjacent muscles and fascia. ANATOMICAL CONSIDERATIONS MUSCLE ATTACHMENTS-  Posteriors- Buccinator- midroot level  Anteriors –Intrinsic muscles & risorius- at apex  In - infection above attachment of muscle enters extra oral space  In - infection below attachment of muscle enters extra oral space PREDISPOSING FACTORS

1. Dental caries or periodontal infections 2. Lowered body resistance 3. Trauma

Primary signs & symptoms of these infections: - Redness - Raised temperature - Edema overlying tissue - Tenderness - Loss of function - Lymphadenopathy

MICROBIOLOGY –SPACE INFECTION  Aerobic bacteria (5%) . Gram positive cocci (85%)– MICRO ORGANISMS  Streptococcus species( 90% ) • S.Milleri • S.Sanguis • S.Salivarius 25 MIXED • S.Mutans AEROBIC  Staphylococcus species (6 %) 5 ANAEROBIC 70  Anaerobic bacteria (25%) . Gram positive cocci (30%)- Peptococcus species 33% Pepto Streptococcus species 33% . Gram negative bacilli (50%) – Prevotella species, Porphyromonas species (75%), Fusobacterium -20%  Mixed bacteria (70%)

Indications for antibiotics:  Toxic signs and symptoms, febrile condition or .  Poorly localized extensive abscesses, diffuse cellulitis  Abscesses in systemically compromised patients  Deep fascial space infections  , Osteomyelitis, Fractures  Soft tissue wounds Selection of antibiotics:  Identification of causative organism  Antibiotic sensitivity  Bactericidal drugs preferred  Antibiotics of the narrowest spectrum preferred  The least toxic antibiotic should be selected  Cost of antibiotics

COMMON ANTIBIOTICS

 β-lactams- Penicillins, Cephalosporins, Monobactams, Carbapenems

 Macrolides- Erythromycin, Clindamycin, Azithromycin, Clarithromycin, Aminoglycosides

 Nitromidazoles- Metronidazole

 Quinolones- Ciprofloxacin, Moxifloxacin STAGES OF INFECTIONS

 Stage I – Inoculation- caused by early spread

 Stage II – Cellulitis- inflammatory process

 Stage III – Abscess- necrosis predominates

 Stage IV – Resolution- occurs after spontaneous or therapeutic drainage LAYERS OF NECK SUPERFICIAL FASCIA

 Ensheathes-

1. Platysma

2. Muscles of facial expression

 Dense connective tissue

SUPERFICIAL LAYER OF  Superficial Layer of the Deep Cervical Fascia  Muscles  Sternocleidomastoid  Trapezius  Glands  Submandibular  Parotid  Spaces  Posterior Triangle  Suprasternal space Of Burns

MIDDLE LAYER OF DEEP CERVICAL FASCIA

 Muscular Division  Infrahyoid Strap Muscles

 Visceral Division  , Larynx, Thyroid  , Trachea 

 The deep neck spaces viz. retropharyngeal, lateral pharyngeal & pretracheal lie superficial side of visceral division DEEP LAYER OF DEEP CERVICAL FASCIA

 Arises from spinous processes and ligamentum nuchae.

 Splits into two layers at the transverse processes:

 Alar layer

 Superior border – skull base

 Inferior border – upper mediastinum at T1-T2

 Prevertebral layer

 Superior border – skull base

 Inferior border – coccyx

 Envelopes vertebral bodies and deep muscles of the neck.

 Extends laterally as the axillary sheath.

CLASSIFICATION OF FASCIAL SPACES BASED ON CLINICAL SIGNIFICANCE - TOPAZIAN FASCIAL SPACES

FACE SUPRAHYOID INFRAHYOID TOTAL NECK

Buccal Sublingual Anterovisceral Retro (Pretracheal) pharyngeal Canine Submandibular Masticatory Pharyngomaxillary space

Parotid CLASSIFICATION OF FASCIAL SPACES BASED ON MODE OF INVOLVEMENT

FASCIAL SPACES

DIRECT (Primary spaces) INDIRECT (Secondary spaces)

Masseteric

Pterygomandibular MAXILLARY MANDIBULAR Superficial & Deep Canine Submental Temporal

Buccal Buccal Lateral Pharyngeal

Infratemporal Submandibular Retropharyngeal

Sublingual Prevertebral & Parotid Spaces CLASSIFICATION OF FASCIAL SPACES ACCORDING TO GRODINSKY AND HOLYOKE (1938) Space 1 – Superficial to superficial fascia Space 2 – Group of spaces surrounding cervical strap muscle lying superficial to sternothyroid-thyrohyoid division of middle layer of deep cervical fascia. Space 3 – Space lying superficial to visceral division of middle layer of deep cervical fascia Space 3A – Carotid sheath space or viscerovascular space Space 4 – Space lies between alar & prevertebral division of posterior layer of deep cervical fascia () Space 4A – Posterior triangle space posterior to carotid sheath Space 5 - Space 5A- Space enclosed by Prevertebral fascia BUCCAL SPACES ANTERIOR POSTERIOR SUPERIOR INFERIOR MEDIAL LATERAL Modiolus of Pterygomandib Maxilla, Lower Border Buccinator Of ular Raphe, infraorbital Of Mandible Muscle, Masseter space Buccopharyng eal Fascia

CONTENTS: Buccal pad of fat, Stenson’s duct , Anterior and transverse facial artery LIKELY SOURCE OF INFECTION: Maxillary & mandibular premolars and molars BUCCAL SPACES- COMMUNICATIONS

 Superficial Temporal Space

 Lateral Pharyngeal Space

BUCCAL SPACES CLINICAL FEATURES:  Vestibular abscess  Extra oral swelling

TREATMENT:  Antibiotic prophylaxis  Intra oral horizontal vestibular incision through of cheek in the premolar, molar region. ANTERIOR POSTERIOR SUPERIOR INFERIOR MEDIAL LATERAL

Nasal Quadratis Oral mucosa Quadratis Levator anguli cartilages labii labii oris superioris superioris

CONTENTS : Angular artery and vein, Infraorbital nerve. LIKELY SOURCE OF INFECTION : Maxillary canine or first premolar CANINE SPACE CLINICAL FEATURES :  Swelling lateral to the nose  Obliteration of the ,  Swelling of the upper lip,  Edema occurs in the upper and lower lid that may close the eye

TREATMENT:  Antibiotic prophylaxis  Mucosa of buccal vestibule in incisor and canine region

SUB MANDIBULAR SPACE ANTERIOR POSTERIOR SUPERIOR INFERIOR LATERAL MEDIAL Anterior belly Posterior belly Inferior & Digastric Platysma, Mylohyoid, of digastric Of digastric, medial tendon Investing Hypoglossus, Stylohyoid, surface of fascia Superior Stylopharyngus mandible Constrictor

CONTENTS: , Facial artery & vein LIKELY SOURCE OF INFECTION : Mandibular molars SUB MANDIBULAR SPACE

CLINICAL FEATURES : Induration and erythema Obliteration of the mandibular line & extending to the level of No trismus

SUMBANDIBULAR SPACE  I & D through Extra-oral incision.

 Incision – 2 stab incisions given over dependent part below lower border of mandible

 Curved hemostat inserted & blunt dissection through subcutaneous fat

 Drain is placed & dressing is given

SUBMANDIBULAR SPACE- COMMUNICATION .

. Lateral pharyngeal space

.

. Contralateral spaces

SUB LINGUAL SPACE ANTERIOR POSTERIOR SUPERIOR INFERIOR MEDIAL LATERAL

Lingual Submandibular Oral mucosa Mylohyoid Muscles of Lingual surface of space muscle Surface mandible of mandible

CONTENTS : Sublingual glands, Wharton’s duct, Lingual nerve, Sublingual artery & vein LIKELY SOURCE OF INFECTION : Mandibular premolars & molars SUB LINGUAL SPACE CLINICAL FEATURES :  Elevation of tongue  Edema and induration of floor of mouth  Tongue cannot be extended beyond of upper lip

COMMUNICATIONS:  Infection through buccopharyngeal gap into lateral pharyngeal space  Infection along posterior border of mylohyoid into

SUB LINGUAL SPACE TREATMENT:-

 Antibiotic prophylaxis

 Incision made Intraorally over lingual sulcus at the base of the alveolar process

 Haemostat passed beneath in an antero posterior direction and drain is placed.

SUB ANTERIOR POSTERIOR SUPERIOR INFERIOR SUPERFICIAL DEEP

Inferior Fascia between Mylohyoid Investing Investing Fascia Anterior border of Hyoid and fascia bellies of mandible inferior border digastric of mandible

CONTENTS : Anterior Jugular veins, Lymph Nodes LIKELY SOURCE OF INFECTION : Lower anteriors SUB MENTAL SPACE CLINICAL FEATURES :  Limited to point of chin & to region immediately below it  Fullness of submental space  Limitation of swelling to hyoid bone

TREATMENT:  Transverse incision in skin below symphysis of the mandible and blunt in upward and backward, Drain & dressings are placed.

MASTICATORY SPACE  These are secondary spaces, well differentiated and communicate with each other

PTERYGOMANDIBULAR SPACE ANTERIOR POSTERIOR SUPERIOR INFERIOR MEDIAL LATERAL

Buccal space Deep lobe Lateral Inferior Medial Ascending Of Parotid Pterygoid border of pterygoid Ramus of gland mandible muscle mandible

CONTENTS : Mandibular division of trigeminal nerve, inferior alveolar artery & vein LIKELY SOURCE OF INFECTION : Lower third molars PTERYGOMANDIBULAR SPACE CLINICAL FEATURES :  No external swelling, trismus  Dysphagia  Medial displacement of lateral wall of pharynx  Uvula displaced to opposite side

INCISION AND DRAINAGE: Intraorally : Sicher’s incision along the pterygomandibualr raphe Extraorally : In cases of severe trismus, incision is placed behind the angle of the mandible SUBMASSETRIC SPACE ANTERIOR POSTERIOR SUPERIOR INFERIOR MEDIAL LATERAL

Buccal space Zygomatic Inferior Ascending Masseter arch border of ramus of muscle mandible mandible

CONTENTS : Massetric artery & vein LIKELY SOURCE OF INFECTION: Lower 3rd molar SUBMASSETRIC SPACE CLINICAL FEATURES:  Mild swelling over angle of mandible

 Deep seated severe throbbing pain

 Trismus

 Tenderness over the mandibular ramus

lobes are obscured SUBMASSETRIC SPACE TREATMENT: Intra oral Vertical incision along external oblique line

Haemostat is passed

 Drain is placed

Extra oral Incision beneath angle of mandible

Blunt dissection through fibres

Drainage with plastic or rubber catheter to withstand muscle contraction. SUPERFICIAL TEMPORAL SPACES ANTERIOR POSTERIOR INFERIOR MEDIAL LATERAL Posterior Fusion of Zygomatic arch Lateral surface Temporal surface of temporalis of temporalis Fascia lateral orbital fascia with muscle rim pericranium

CONTENTS: Temporal fat pad, temporal branch of LIKELY SOURCE OF INFECTION: Upper & Lower molars DEEP TEMPORAL SPACES ANTERIOR SUPERIOR INFERIOR MEDIAL LATERAL Posterior wall of Attachment of Lateral Temporal bone Temporalis maxillary sinus, temporalis to pterygoid muscle Pterygomaxillary cranium muscle fissure, posterior surface of

CONTENTS: , inferior & vein, mandibular division of trigeminal nerve LIKELY SOURCE OF INFECTION: Upper molars SUPERFICIAL & DEEP TEMPORAL SPACES CLINICAL FEATURES :  Characteristic dumbell shaped swelling (Superficial)  Mild swelling over temporal region (Deep)

TREATMENT:  Intraoral- vertical incision made medial to upper extent of anterior border of the ramus  Haemostat  Passed superiorly along lateral aspect of the coronoid (Superficial) Passed supero-medially (Deep)  Extra oral incision- slightly superior to zygomatic arch

INFRATEMPORAL SPACE ANTERIOR POSTERIOR SUPERIOR INFERIOR MEDIAL LATERAL Maxillary Mandibular Infratemporal Lateral Lateral Temporalis tuberosity condyle crest of pterygoid pterygoid Tendon, sphenoid muscle plate Coronoid process

CONTENTS: Pterygoid plexus, internal maxillary artery and vein , mandibular division of trigeminal nerve INFRATEMPORAL SPACE CLINICAL FEATURES:  Marked Trismus  Swelling of face in front of ear, over TMJ, behind zygomatic process  Eye is closed and proptosed

INFRATEMPORAL SPACE TREATMENT: INTRAORAL Incision is made into buccolabial fold lateral to maxillary third molar- Kruger

Curved hemostat is inserted behind maxillary tuberosity

 Vertical incision made medial to upper extent of the anterior border of the ramus- Laskin

Curved hemostat is passed superiorly into infratemporal region, drain is inserted

EXTRAORAL Horizontal incision above the zygomatic arch

Curved hemostat is directed in inferior and medial direction to enter infratemporal space

Insertion of drain.

PREVERTEBRAL SPACE  Formed by deep cervical fascia  Extends from skull base to coccyx  Fascia attaches to transverse process of cervical vertebra dividing it into anterior and posterior compartments

Anterior compartment : -Vertebral bodies. -Spinal cord. -Vertebral arteries. -Phrenic nerve. -Prevertebral and

Posterior compartment : -Posterior vertebral elements. -Paraspinous muscles. PERITONSILLAR SPACE INFECTION (QUINCY)

Clinical evaluation:

 3-7 days H/o pharyngitis

 Severe sore , dysphagia,

Odyonophagia and referred otalgia.

 The speech is muffled and classically

described as hot potato voice.

 Trismus is not present

 Needle aspiration instead of open incision and drainage - JOMS,Vol 51,2009

LATERAL PHARYNGEAL SPACE  Inverted pyramid shape with base at base of skull and apex at hyoid bone

 Medial- pharyngeal constrictor

 Lateral- & deep cervical fascia

 Anterior- palatal musculature, buccinator, superior constrictor, stylohyoid and posterior belly of digastric  Posterior- carotid sheath,

LATERAL PHARYNGEAL SPACE  Infection spreads from peritonsillar infection, sublingual, submandibular & retropharyngeal space infections

 May encircle airway by spreading from one side to another

 Patients head may tilt to unaffected side to position upper airway over deviated trachea and LATERAL PHARYNGEAL SPACE CLINICAL FEATURES:  Firm swelling with surrounding erythema lateral and anterior to sternocleidomastoid muscle  Difficulty in flexing and turning of neck  Trismus, Dysphagia, Dyspnoea

TREATMENT:  Hospitalization with IV antibiotics  Airway protection  Surgical approach always through neck not through oral cavity  Incision is made at the level of hyoid bone across the SCM muscle RETROPHARYNGEAL SPACE

 Extends from base of skull to retropharyngeal fascia (between 4th and 6th thoracic vertebra)

 Lateral border- lateral pharyngeal space and carotid sheath

 Separated in midline by septum

 Contains areolar tissue, lymph nodes draining Waldeyer’s ring  Infections impinge directly on airway, involve danger space

RETROPHARYNGEAL SPACE

CLINICAL FEATURES: • Dysphagia • Cervical lymphadenopathy. • Slight neck rigidity • Noisy breathing due to laryngeal edema. • Neck tilts towards involved side. • Hyperextended complete inability to flex the neck. RETROPHARYNGEAL SPACE- COMMUNICATION  Posterior- pre-vertebral space

 Lateral- carotid artery (haemorrhage, pseudoaneurysm, thrombosis) and jugular vein (thrombosis)

 Anterior-compression and compromise of the airway

 Inferior- mediastinum resulting in mediastinitis

DANGER SPACE

• Entire length of neck

• Anterior border - alar layer of deep fascia

• Posterior border - prevertebral layer

• Extends from skull base to diaphragm

• Contains loose areolar tissue

• Infection may enter mediastinum & compress major vessels, lower airway and upper digestive tract

• 71% mediastinitis cases- infection from retropharyngel space through danger space: Mediastinitis following cervical suppuration, Pearse, 1938 CAROTID SPACE

 Encloses common & internal carotid arteries, internal jugular vein and vagus nerve

 Named “Lincoln’s Highway” by Mosher in 1929

 Extends from jugular foramen & carotid canal to mediastinum

 Infection eroding this space may cause-

 Expanding hematoma in neck  Bleeding episodes( herald bleeds)  Horner’s syndrome- miosis, ptosis and anhidrosis MEDIASTINUM

• Extension of infection from deep neck spaces into the mediastinum is clinically seen as – chest pain – severe dyspnea ,Unremitting fever, – Radiographic demonstration of mediastinal widening. LUDWIG’S ANGINA Ludwig’s angina is a firm, acute, rapidly progressing polymicrobial toxic cellulitis of the submandibular and sublingual spaces bilaterally and of the submental space resulting in life threatening airway compromise.

• Wilhelm Friedrich von Ludwig

1. Rapidly spreading gangrenous cellulitis. 2. Originates in the region of submandibular gland but never involves one single space 3. Arises from extension by continuity and not by lymphatics 4. Produces gangrene with serosanguinous, putrid infiltration but very little or no frank pus. LUDWIG’S ANGINA- BACTERIOLOGY  Polymicrobial - predominantly oral flora

 Organisms isolated - Streptococcus viridans and Staphylococcus aureus

 Anaerobes - bacteroides, peptostreptococci, and peptococci.

 Other gram-positive bacteria- Fusobacterium nucleatum, Aerobacter aeruginosa,spirochetes, and Veillonella, Candida, Eubacteria, and Clostridium species.

 Gram-negative organisms Neisseria species, Escherichia coli,Pseudomonas species, Haemophilus influenzae, and Klebsiella species LUDWIG’S ANGINA Clinical features :  Toxic, ill, dehydrated

 Difficulty in deglutition

 Firm, brawny swelling

 Mouth slightly open, Hot potato voice

 Respiratory difficulties, cyanosis, increased respiratory rate, stridor

 Increased salivation, stiffness of tongue, Elevation of floor of mouth

LUDWIG’S ANGINA SPREAD

 ACCORDING TO KRUGER,TOPAZIAN,LUDWIG

THIRD MOLARS - SUBMANDIBULAR SPACE - SUBLINGUAL SPACE - CONTRALATERAL SUBMANDIBULAR AND SUBMENTAL SPACE INVOLVEMENT

 ACCORDING TO LASKIN

SUBLINGUAL SPACE - SPREADS BILATERALLY - SUBMANDIBULAR AND SUBMENTAL SPACE - BACKWARD SPREAD TO SUBSTANCE OF TONGUE - INFECTION REACHES EPIGLOTTIS - SWELLING AROUND LARYNGEAL INLET

PRINCIPLES OF MANAGEMENT OF LUDWIG’S ANGINA

• Hospitalization

• Securing the airway

• Anaesthetic implications

• Early I.V. antibiotics & hydration

• External surgical exploration with division of and drainage

• Medical supportive therapy

• Review and re-evaluation in the post op period

LUDWIG’S ANGINA MANAGEMENT

 Early diagnosis and hospitalization

 Maintenance of airway: i} cricothyrotomy/laryngotomy ii} Nasoendotracheal intubation using fibre optic laryngoscope.

 Anaesthesia: LA into superficial tissue of neck or if intubated then G.A.

 I.V. analgesics

 Removal of cause: Extraction of offending tooth which facilitates evacuation of pus LUDWIG’S ANGINA MANAGEMENT

Bilateral incision, Midline incision Blunt dissection

Initially no pus, but later on profuse pus drains out Drain placement LUDWIG’S ANGINA MANAGEMENT Antibiotic therapy:  Penicillin– 2-4MU i.v. 4hourly, then penicillin V- 500mg orally slowly.  Amoxicillin- 500mg TID orally  Cloxacillin-500mg TID orally  Erythromycin-600mg 6-8hourly  Clindamycin-600mg i.v. 300-400mg orally TID  Cephalosporin

Treatment of dehydration: excess oral fluid intake or i.v. fluid infusion

LUDWIG’S ANGINA RISKS  Posteriorly into larynx causing suffocation, death

 Spread of infection to mediastinum

 Septicaemia and septic shock

 Venous and thrombosis, carotid sheath erosion

 Brain abscess and meningitis.

 Aspiration pneumonia

 Pericarditis.

 Death

COMPLICATIONS OF SPACE INFECTION

 Scar formation

 Sinus tract formation

 Cavernous sinus thrombosis

 Necrotising fascitis CAVERNOUS SINUS  Large venous space situated in the middle cranial fossa

 Interior divided into number of caverns by trabeculae

ANTERIOR POSTERIOR MEDIAL LATERAL SUPERIOR INFERIOR Medial end of Apex of Pitutary Temporal lobe Optic chiasma Endosteal superior petrous above and and uncus dura mater, orbital fissure temporal bone sphenoid greater wing below of sphenoid

CONTENTS DANGEROUS AREA OF FACE

The cavernous communicate with dangerous area of face through 2 routes:

 Superior opthalmic vein

 Deep facial veins , pterygoid plexus of vein , emissary vein. SPREAD OF INFECTION TO CAVERNOUS SINUS 1. Infection of upper lip, vestibule of nose and eyelids  Angular, supraorbital and supratrochlear veins to ophthalmic veins

2. Intranasal surgeries on septum, turbinates or ethmoid / sphenoid sinus infection  Ethmoidal veins

3. Surgeries on tonsil, , osteomyelitis of maxilla, and deep cervical abscess  spread through pterygoid plexus or by direct extension to the internal jugular vein.

CAVERNOUS SINUS THROMBOSIS- DIAGNOSIS

 Eagleton’s criteria for Cavernous Sinus Thrombosis:

1. Sepsis 2. Early obstructive signs 3. Ocular nerve paralysis 4. Surrounding soft tissue abscesses 5. Symptoms of a complicated disease

CAVERNOUS SINUS THROMBOSIS

Characterized by multiple cranial neuropathies

Clinical feature -

 General feature of infection

 Exopthalmos & tender eye ball

 Oedema of eyelid & chemosis of conjuctiva

Oculomotor feature –

 External opthalmoplegia ,Ptosis

 Slight exophthalmos,Dilated pupil with loss of accomdation reflex TREATMENT Septic cavernous sinus thrombosis –  Early and aggressive antibiotic administration.

 Broad-spectrum coverage for gram-positive, gram-negative, and anaerobic organisms

 Antibiotic therapy should include a penicillinase-resistant penicillin plus a third generation cephalosporin.

 Vancomycin may be added for MRSA.

 IV antibiotics are recommended for a minimum of 3-4 weeks

 Corticosteroid therapy ( adrenal insufficiency due to cranial nerve dysfunction or pituitary necrosis)

DIAGNOSTIC IMAGING OF FASCIAL & NECK SPACES

•Plain film- AP & Lateral view

•MRI

•CT

•Ultrasound PRINCIPLES OF INCISION AND DRAINAGE  Incise healthy skin and mucosa when possible

 Incision placed at site of maximum fluctuance

 Incision in esthetically acceptable area

 Incision should be in dependent position

 Dissect bluntly with closed surgical clamp or finger, through deeper tissues

 Clean wound margins daily under sterile conditions

 Place a drain and stabilize it with sutures

GENERAL MANAGEMENT 1. Determine severity Assess history of onset and progression perform physical examination of area: - Determine character and size of swelling - Establish presence of trismus

2. Evaluate host defenses : -Diseases that compromise the host - Medications that may compromise the host

3. Relieve pressure - Remove the cause of infection - Drain pus by performing incision and drainage

GENERAL MANAGEMENT

4. Select antibiotic Determine: - Most likely causative organisms based on history - Host defense status - Allergy history - Prescribe drug properly (route, dose and dosage interval, and duration) - Culture & sensitivity 5. Administration of steroids to reduce edema 6. Follow up  Monitor frequently  Out-patient follow up in 2-3 days  Decreased swelling, discharge, airway edema, malaise in 2-3 day STAGES OF INFECTION CHARACTERISTIC INOCULATION CELLULITIS ABSCESS Duration 0-3 days 3-7 days More than 5 days

Pain Mild- moderate Severe & generalized Moderate – severe and localized Size Small Large Small Localization Diffuse Diffuse Circumscribed Palpation Soft, doughy, mildly Hard, exquisitely tender Fluctuant, tender tender Appearance Normal color Reddened Peripherally reddened Skin Quality Normal Thickened Centrally undermined, shiny Surface temperature Slightly heated Hot Moderately heated Loss of function Minimal or none Severe Moderately severe Tissue fluid Edema Serosanguinous, flecks of Pus pus Levels of malaise Mild Severe Moderate- severe Severity Mild Severe Moderate- severe Percutaneous bacteria Aerobic Mixed Anaerobic CONCLUSION  Thorough knowledge of anatomy is necessary to diagnose and manage the space infections.

 To be alert to the potential seriousness of these infections-never to be dismissed as simple dental abscess

 In severe cases the systemic management of the patient is also very important

 Incidence and severity have diminished with advent of antibiotic therapy

 Deep fascial infections must be recognized promptly and treated as an emergency

 Repeat diagnostic and therapeutic measures may be necessary until the very end