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Space infections.pptx

This document discusses space infections that can arise from dental infections. It defines fascial spaces and outlines the pathways of odontogenic (dental) infections. It describes different classifications of infections including by location (e.g. maxillary vs mandibular spaces), etiology, and causative organisms. Specific spaces that can become infected are discussed such as the canine, buccal, and infratemporal fossa. Clinical features, treatment including incision and drainage, and potential spread are covered for each space.

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SPACE INFECTIONS DR SUMAYYA UMARAH ORAL AND MAXILLOFACIAL SURGEON
Content • Introduction • Definition • Pathway of odontogenic infection • Classification • Maxillary space infection • Mandibular space infection • Ludwigs angina • Cavernous sinus thrombophlebitis
Introduction • Occurrence of infectious disease is determined by interaction of host , the microorganism and the environment • In healthy state there is balance among these factors and when the balance is lost disease occurs • Most odontogenic infections arise as a sequel of pulp necrosis caused by caries, trauma, periodontitis
Fascial spaces • Definition : the fascial spaces are the potential spaces between the various layers of fascia normally filled with loose connective tissue and bounded by anatomical barriers , usually of bone , muscle or fascial layers. (Moore – 1975)
Pathways of odontogenic infection • Invasion of dental pulp by bacteria after decay of a tooth • inflammation edema and lack of blood supply • Venous congestion ,pulpal tissue death • Reservoir for bacterial growth • Periodic egress of bacteria into surrounding alveolar bone
Odontogenic infections • Types of infection: acute chronic • Acute stage in acute stage ,infection spreading in the soft tissues can take the following forms of in the clinical situation Abscess Cellulitis Fulminating infections
Difference between cellulitis and abscess cellulitis • Acute phase • Severe and generalized • Large • Diffuse borders • Doughy to indurated • No presence of pus • Greater degree of seriousness • Aerobic bacteria abscess • Chronic phase • Localized • Small in size • Well circumscribed • Fluctuant on palpation • Presence of pus • Less degree of seriousness • Anaerobic bacteria/mixed
Acute infection • The odontogenic infection present in the following forms: 1. Acute periapical abscess: abscess arises and remains in the confine of the alveolar bone 2. Acute dentoalveolar abscess: once the infection has crossed the confines of alveolar bone and comes to lie in the neigbouring soft tissues and gets localized 3. Acute periodontal abscess 4. Acute pericoronal abscess
Differential clinical features between acute periodontal & acute periapical abscess Acute periapical abscess • Pain is severe and throbbing • Common in adults • Pulp gets necrotic and infected • Swelling seen over the apex • Sinus discharge will be present • TOP is present • Mobility in later stages • Arises from the pulp Acute periodontal abscess • Pain is severe and throbbing • Uncommon in children • Pulp is vital • Swelling over the gingival third of the alveolar process • Sinus discharge may be present • TOP is present • Mobility Is seen in early stages • Arises in relation to periodontal pocket
Periodontal abscess Periapical abscess
Chronic stage • In chronic stage the odontogenic infection present itself in the following forms: 1. Chronic fistulous tract or sinus formation: abscess neglected for a long period discharge intraorally or extraorally 2. Chronic osteomyelitis 3. Cervicofacial actinomycosis
General course of odontogenic abscess 1. Early stage: there is intrabony pus collection. The adjoining soft tissues doesnot undergo any necrosis 2. Intermediate stage: perforation of cortex infection progresses soft tissues becomes indurated and brawny small area of central softening can be palpated this represents central necrosis due to loss of blood supply
Microbiology • The aerobic bacteria found in odontogenic infection are gram positive cocci , most are viridans streptococci species , include strep.milleri ,strep.sanguis, strep.salivarius, strep.mutans. • These oral streptococci account for more than 80% of aerobic bacteria in odontogenic infection.
There are two main groups of bacteriodes a.oropharyngeal b. they other group found in the gut • Oropharyngeal bacteriodes :divided into: • Porphyromonas : includes P. assachrolyticus ,P.gingivalis, P.endodontalis • Prevotella:it includes p.buccal p.oralis, p.loeschii, p.denticola prevotella intermedius , porphyromonas gingivalis ,and porphyromonas endodontalis appears to be most pathogenic among them
• Medical therapy • Consists of supportive care –hydration soft or liquid diet rich with protein ,analgesics and use of antiseptic mouthwashes to maintain oral hygiene
Antibiotic therapy i. In non compromised pt with well localized abscess surgical drainage and dental therapy without antibiotic cover. In cases of poorly localized , extensive abscess and diffuse cellulitis , antibiotic therapy is must . ii. In compromised pt as well as in pt with systemic signs and symptoms like trismus, airway compromise, fever antibiotic coverage is mandatory
• Penicillin is the empirical drug of choice. Later on after knowing the lab results of culture and sensitivity testing , specific antibiotic is instituted. • oral clindamycin , Augmentin, 1st and 2nd generation cephalosporin are useful in orofacial infections • in compromised pt , clindamycin alone or in combination with gentamicin, 1st and 2nd generation cephalosporin can be used parenterally.
Surgical therapy • Incision and drainage helps i. To get rid of toxic purulent ii. To decompress the edematous tissues iii. To allow better perfusion of blood , antibiotic and defensive elements iv. To increase oxygenation of infected area
Hiltons method of incision and drainage • The method of opening an abscess ensures that no blood vessel or nerve in the vicinity is damaged and is called Hiltons method • Steps 1. Topical anaesthesia 2. Stab incision: made over max fluctuation in most dependent area along the crease 3. If pus is not encountered, further deepening of surgical site is achieved with sinus forcep 4. Closed forcep is pushed through tough deep fascia and advanced towards the pus 5. Pus flows along the sides of the beak 6. Placement of drain : a corrugated rubber drain is inserted into to the depth of the abscess cavity and external part is secured to the wound margin with the help o suture 7. Drain left for atleast 24 hours
Purpose of keeping the drain • Is to allow the discharge of the tissue fluids and pus from the wound by keeping it patent . • The drain allows for debridement of the abcess cavity by irrigation
Spread of orofacial infection Routes of spread By direct continuity through the tissues By lymphatics to the regional lymph node and eventually into the blood stream. The spread of infection from the lymph nodes to the tissues results in secondary area of cellulitis or tissue space abscess By blood stream: local thrombophlebitis may propagate along the veins entering the cranial cavity via emissary veins to produce cavernous sinus thrombophlebitis. The microorganism or the infected emboli may get swept away in to the blood stream leading to bacteraemia, septicaemia or pyaemia with the development of embolic abscess.
Potential routes of spread of periapical infection Muscles and fascial attachments determine the direction of spread. Extensions beyond this attachments lead to deep space involvement
Factors influencing spread • General factors a) Host resistance :depends upon : humoral factor cellular factor i. Humoral factors involve immunoglobulins derived from B lymphocytes or plasma cells ii. Cellular factors include pmn leucocytes , monocytes ,lymphocytes and tissue macrophages
b. Virulence of micro organisms : determined by invasiveness of the causative micro organisms. These include production of lytic enzymes , potent endotoxins & exotoxins c. Compromised host defences : uncontrolled metabolic diseases, such as alcoholism , malnutrition , severe diabetes 2. Suppressing diseases: leukaemia , lymphoma , malignant tumours 3. Suppressing drugs: cancer chemotherapeutic drugs , immunosuppressive drugs
Local factors • Intact anatomical barriers: i. alveolar bone : first local limiting barrier to further spread of periapical infection ii. Periosteum : this structure is better developed in mandible and hence can delay further spread leading to the development of a sub periosteal abscess iii. Adjacent muscles and fascia : next site for localization
Evaluation of patient with orofacial infection • If the patient i. Is toxic ii. Exhibits CNS changes iii. Airway compromise • Then, i. Immediate hospitalization ii. Aggressive medical treatment iii. Aggressive surgical intervention
History taking • Physical examination General examination Regional examination Extra oral examination • Inspection • Palpation Intra oral examination Radiological examination
classification Mode of involvement etiology Causative organism Based on
Mode of involvement Primary max spaces Primary mandibular spaces Secondary fascial spaces
Primary max space • Canine • Buccal • infratemporal Primary mandibular space • Submental • Sublingual • Submandibular • buccal Secondary fascial spaces • Pterygomandibular • Superficial and deep temporal • Masseteric • Pharyngeal • Retropharyngeal • Prevertebral • parotid
Based on etiology General classification • Odontogenic • Traumatic • Implant surgery • Reconstructive surgery • Infection arising from contaminated needle puncture • Others( including from factors such as infected antrum , salivary gland afflictions)
On the basis of causative organism • Bacterial infection • Fungal • Viral • Odontogenic infection • Non odontogenic infection  Tonsillar infection  Nasal infection  Furuncle overlying skin
Canine fossa involvement [infraorbital space] • Odontogenic infection • Nasal infection • Periapical abscess of cuspids. periapical abscess which discharges bucally from an upper canine or first premolar may lead to accumulation of pus in canine fossa
• Involvement :teeth which frequently give rise to abscess are maxillary canine and premolars and sometimes mesiobuccal root of maxillary first molar • The periapical abscess discharges bucally superior to origin of canninus muscle and pus accumulates in canine fossa
Surgical anatomy-boundaries • Superiorly levator labii superiors alaque nasi,levator labii superioris,zygomaticus minor muscle • Inferiorly ,caninus muscle • Anteriorly, orbicularis oris • Posteriorly, buccinators • Medially, anterolateral surface of maxilla
Clinical features • Swelling of the cheek and upper lip • Obliteration of nasolabial fold • Drooping of the angle of mouth • Edema of the lower eye lid • extra oral –early phase: on first or second day,inflamma- tory enlargement of upper lip, and angle of mouth is seen to drop. • late phase-usually occur on the second or third day • Marked periorbital edema forcing eyelid to close • Redness and marked tenderness of the facial tissues
• When the infection progress to chronic stage, it may result in production of chronic fistula in the cleft area between levator labii superiors alaque nasi and zygomaticus minor muscle near the medial canthus of eye • intraoral: the offending teeth is mobile and is tender on percussion
Treatment • Incision and drainage : • The approach to this area is through the mucosa of buccal vestibule in the region of lateral incisor and canine. A curved mosquito forcep is inserted superior to the attachment of caninus muscle ,and the infraorbital space is entered.
Buccal space involvement • Buccal space is the potential space between buccinator and masseter BOUNDARIES • Anteromedially :buccinator • Posteromedially:masseter overlying the anterior border of ramus of mandible • Laterally :platysma muscle • Inferiorly:limited by the attachment of deep fascia to the mandible and by depressor anguli oris • Superiorly: the zygomaticus process of the maxilla and zygomaticus major and minor muscle
• Contents :buccal pad of fat, stensons duct, facial artery • TEETH COMMONLY INVOLVED maxillary and mandibular molars and premolars
CLINICAL FEATURES • Gum boil is seen in the vestibule • Prominent dome shaped extraoral swelling extending from lower border of mandible to the infraorbital margin and from the anterior margin of masseter muscle to the corner of the mouth. SPREAD: continuation with the pterygomandibular space to infratemporal space along the fascia
Treatment • Incision and drainage :horizontal incision thro the oral mucosa of the cheek in the premolar ,molar region. • If the pus is lateral to the muscle then the muscle is penetrated with the mosquito forcep to enter the buccal space
Infratemporal fossa space • Also called retrozygomatic space as it is situated behind the zygomatic bone • Involvement :infections arise from infection of buccal roots of the max 2nd and 3rd molar • Local anaesthesia injection with contaminated needle in the area of tuberosity
BOUNDARIES • Bounded laterally by ramus of mandible temporalis muscle and its tendon • Medially by medial pterygoid plate ,lateral pterygoid muscle lower part of temporal fossa of the skull and lateral wall of pharynx • Superiorly by infratemporal surface of greater wing of sphenoid and by zygomatic arch • Inferiorly by the lateral pterygoid muscle which forms the floor of the fossa • Anteriorly infratemporal surface of maxilla • Posteriorly parotid gland
Clinical features Extraoral: • Trismus • Bulging of temporalis muscle • Marked swelling of the face on the affected side infront of the ear • The eye is often closed Intraoral: swelling of the tuberosity. • Elevation of temperature up o 104 F
Incision and drainage • Intraoral approach: if trismus is not marked and fluctuation is detected early , intraoral incision is given in the buccal vestibule . • extraoral approach: incision is made at upper and posterior end of the temporalis muscle within the hairline .the sinus is then directed upwards and medially and pus is evacuated.
Potential primary spaces related to lower jaw SUBMENTAL SPACE • Involvement: originating from the six anterior mandibular teeth; then perforate the cortical plate below the origin of mentalis muscle labially and mylohyoid lingually. BOUNDARIES: Lateral: lower border of the mandible and anterior bellies of digastric muscle Superior: mylohyoid muscle Inferior: suprahyoid portion of the investing layer of deep cervical fascia which is in turn covered by platysma
Contents: submental lymph node and jugular veins .the lymph nodes lies embedded in adipose tissues and hence submental abscess tend to remain well circumscribed. CLINICAL FEATURES: Extraoral finding :distinct firm swelling in the midline, beneath the chin. Intraoral findings : ant teeth are either non vital fractured or carious . • The offending tooth may exhibit tenderness to percussion and may show mobility • Pt may experience discomfort on swallowing
Incision and drainage • Performed by making transverse incision in the skin below the symphysis of mandible. Dissection is carried by inserting sinus forcep through the incision, upward and backward. • SPREAD posteriorly to involve the submandibular space • It may discharge on the face in the submental region.
Submandibular space • The space lies between ant and post bellies of digastric muscle. The upper part lies beneath the inferior border of mandible and the lower part lies deep to the investing layer of deep cervical fascia . • Involvement: infections originating from mandibular molars. • The pus perforates the lingual cortical plate of mandible inferior to the attachment of mylohyoid muscle and passes directly to the submandibular space • It is involved as an extension of infection from submental space • Also involved by an infection originating from post part of sublingual space • Also involved from infection originating from middle third of the tongue ,posterior • part of the floor of the mouth, maxillary teeth cheek , maxillary sinus and palate.
BOUNDARIES • Anteromedially ,the floor is formed by the mylohyoid muscle which is covered by loose areolar tissue and fat • Posteromedially ,the floor is formed by the hyoglossus muscle • Superolaterally,medial surface of mandible below the mylohyoid ridge • Anterosuperiorly,anterior belly of digastric • Posterosupriorly, post belly of digastric stylohyoid and stylopharyngeus muscle • Laterally , platysma and the skin
Clinical features Extraoral :firm swelling in submandibular region ,below the inferior border of the mandible • Some degree of tenderness • Redness of the overlying skin Intraoral: teeth are sensitive to percussion • Teeth are mobile • Dysphagia • Moderate trismus
Incision and drainage • Incision of about 1.5 to2cm length is made 2 cm below the lower mandible in the skin creases . • Skin and subcutaneous tissues are incised . • The sinus forcep is inserted thro the incision superiorly and posteriorly on the lingual side of the mandible below the mylohyoid to release the pus from the submandibular space
spread • There are no major anatomic barrier between the two submandibular and submental spaces • There are no major anatomic barrier hence infection can spread easily across the midline and involve submandibular space on the contralateral side • Infection can spread backwards to involve para pharyngeal space • The submandibular space communicates with the sub lingual space around the posterior border of mylohyoid muscle.
Differential diagnosis • Lymphoma arising in the lymph node of upper neck • TB lymphadenitis
Sublingual space • This space is v shaped trough lying lateral to the muscle of the tongue including hyoglossus genioglosssus and geniohyoid • Involvement : teeth involved are mandibular incisors canines premolars • The infection perforates lingual plate below the level of the mucosa of the floor of the mouth and passes into the sublingual space.
Boundaries • Superiorly by the mucosa of the floor of the mouth • Inferiorly :mylohyoid muscle • Laterally: medial side of the mandible • Medially :hyoglossus genioglossus and geniohyoid muscles • Posteriorly :hyoid bone • Laterally and inferiorly by the mylohyoid muscle and the lingual side of the mandible
Contents • Includes genioglossus geniohyoid hyoglossus muscle • It also contains • deep part of submandibular salivary gland • sublingual salivary gland • Lingual nerve • Hypoglossal nerve
Clinical features • Extraoral : there is little or no swelling .the lymph node may be enlarged and tender • Pain and discomfort on deglutition • Speech may be affected • Intraoral: firm painful swelling seen in the floor of the mouth • The tongue may be pushed superiorly. this will bring about airway obstruction • The ability to protrude the tongue beyond the vermillion border of upper lip is affected
Incision and drainage • Intraorally:incision is made close to the lingual cortical plate as the imp structure at this site is sublingual nerve which is deeply placed and less likely to be damaged by this approach. The sinus forcep is inserted and opened to evacuate pus. • Extraoral: drained via skin incision placed in the sub mental region.
spread • Infection always crosses the midline, and can affect the spaces on the opposite side • Infection can also spread via the lymphatics to the submental or submandibular lymph nodes.
Masticatory spaces • It comprises of the following spaces 1. pterygomandibular 2. submasseteric 3. temporal –superficial temporal 4. deep temporal
Submassetric space • When the pus accumulates between the ramus of the mandible and the masseter muscle , it produces a submassetric space abscess. • Involvement :infection originates from the lower 3rd molar resulting from(i) pericoronitis • (ii) periapical abscess
Boundaries • Anterior : ant border of masseter muscle and buccinators • Posterior : parotid gland and posterior part of masseter • Inferior : attachment of masseter to lower border of mandible • Medial : lateral surface of ramus of mandible • Lateral : medial surface of masseter
Contents • masseteric nerve , superficial temporal artery , transverse facial artery • It contains muscle of mastication, ramus ,posterior • part of mandible and branches of mandibular division of • trigeminal nerve
Clinical features • External facial swelling is moderate in size :swelling extending from lower border of mandible to the zygomatic arch and anteriorly to the ant border of masseter and posteriorly to the post border of the mandible • Tenderness over the angle of the mandible • Almost complete limitation of mouth opening • pyrexia
Incision and drainage • Intraoral approach: incision made vertically over the lower part of anterior border of the ramus of the mandible ,deep to the bone. • A sinus forcep is passed along the lateral surface of the ramus downwards and backwards. • Extraoral approach : when the mouth cannot be opened ,an incision is placed in the skin behind the angle of mouth to open the abscess by Hiltons method
• Involvement : pericoronitis related to mandibular 3rd molar • Infection can also be because of contaminated needle used for an IANB • At times can also originate from max 3rd molar following PSA injection Pterygomandibular space infection
Boundaries • Lateral: medial surface of ramus of mandible • Medial : lateral surface of medial pterygoid muscle • Posterior: parotid gland • Anterior :pterygomandibular raphe • Superior :lat pterygoid muscle forms the roof to pterygomandibular space • Contents: lingual nerve , mandibular nerve , inferior alveolar artery , mylohyoid nerve and vessel
Clinical features • Even the established cases of pterygomandibular space infection doesnot cause much swelling of face over the submandibular region . • Severe degree of limitation of mouth opening • Tenderness over the area of swollen tissues medial to ant border of ramus of mandible • Dysphagia is present • Redness and the edema of the area around the 3rd molar • Uvula is swollen • Difficulty in breathing
Incision and drainage • Intraoral :Vertical incision approx. 1.5 cm in length is made on anterior and medial aspect of ramus of mandible . Sinus forcep is inserted in the abscess cavity , opened and closed and withdrawn . The pus is evacuated • Extraoral :incision is taken in the skin below the angle of the mandible. A sinus forcep is inserted towards the medial side of the ramus in an upward and backward direction • . Pus is evacuated
Spread • Infection may spread superiorly along the medial surface of the ramus to involve the infratemporal fossa • Infection may spread posteriorly to lateral pharyngeal space and then to retropharyngeal space • Can also spread around the front of ramus of mandible to involve the buccal space
Life threatening complication of orofacial infection • Which may be classified as • Those relate to lower jaw (a)ludwigs angina (b) descending deep cellulitis of the neck (c) carotid sheath invasion • Those related to upper jaw (a)cavernous sinus thrombosis ,Dural meningitis ,osteomyelitis of skull (b) retro bulbar cellulitis with possibility of blindness
Ludwig's angina • Definition;it is the massive firm brawny cellulitis/induration and acute toxic stage involving simultaneously ,the submandibular, sublingual and submental spaces bilaterally . • the term Ludwig angina was coined by Camerer in 1837 • this condition had established its unique identity with three ” f ”s • It was to be FEARED • rarely becomes FLUCTUANT • it was often FATAL
Etiology 1.Odontogenic : a) Acute dentoalvelolar abscess b) Acute periodontal abscess c) Acute pericoronal abscess: in relation to erupting 2nd and 3rd molar which can extend to following spaces i. Submandibular spaces ii. Buccal space iii. Sublingual space iv. Pterygomandibular space
2. Iatrogenic : use of contaminated needle for giving LA 3. Traumatic injuries to orofacial region :mandibular fractures ,deep lacerations and penetrating injuries 4. Osteomyelitis 5. Sublingual and submandibular sialadenitis 6. Cervical lymphoid tissues
Pathology • The condition is a cellulitis – a diffuse inflammation of soft tissues which is not circumscribed or confined to one area but in contrast to the abscess ,tends to the spread thro tissues spaces and along fascial planes. • Involvement : mandibular 2nd and 3rd molars
Clinical features • Pt looks very toxic , very ill and dehydrated • There is pyrexia anorexia chills and malaise • Dysphagia • Impaired speech • Hoarseness of voice
Extraoral examination • Firm and brawny hard swelling in the bilateral submandibular and submental regions which soon extends down to the anterior part of the neck to the clavicle. • Swelling is non pitting minimally or non fluctuant associated with severe tenderness • Classically shows ill defined borders with induration. • Severe muscle spasm may lead to trismus. • Typically mouth may remain open due to edema of the sublingual tissues leading to raised tongue almost touching the palatal vault • Airway obstruction • There may be dilatation of alae nasi , raising of thoracic inlet by the scalene and sternocleidomastoid muscle and indrawing of the tissues above the clavicle
• Cyanosis may occur due to hypoxia • Fatal death may occur in untreated cases of Ludwig's angina within 10 to 24 hours due to asphyxia • Intraorally: swelling develops rapidly which involves sublingual tissues and distends or raises the floor of the mouth, woody edema of the floor of the mouth and the tongue • Increased salivation , stiffness of tongue movement and difficulty in swallowing • Backward spread of infection leads to edema of glottis, resulting in respiratory obstruction • Stridor being alarming sign of this fatal extension needing emergency intervention to keep airway patent
Spread • Due to anatomical continuity of various spaces with submandibular space infection may track to • submasseteric petrygomandibular space parapharyngeal space para tonsillar spaces Worsening the airway
• Infection from the submandibular region may spread downwards along and the deep investing layer of deep cervical fascia , towards the clavicle and subsequently to mediastinum.
Principles of treatment • The treatment is based on combination of following factors • Early diagnosis • Maintenance of patent airway • Intense and prolonged antibiotic therapy • Extraction of offending tooth • Surgical drainage or decompression of fascial spaces
Airway maintenance • Intubation of patient: blind intubation should be avoided . Nasoendotacheal intubation is far more reliable. • surgical airway: required in case of severe upper resp obstruction . • Laryngotomy cricothyroidotomy (tracheotomy) is preferred over tracheostomy because of : • Identification of landmarks is difficult due to associated massive edema and tissue distortion • The surgery itself may lead to spread of infection to deeper tissues due to additional incision required .
Surgical intervention • It has two aims: (i) remove the cause (ii) Surgical decompression Removal of the cause : removing of offending tooth may facilitate the evacuation of the pus Surgical decompression : it reduces pressure of edematous tissues on the airway reducing respiratory embarassement • It allows prompt drainage
Antibiotic therapy • Plays a vital role in managing Ludwig's angina. • Penicillin are first line antibiotics in treating such infections as it covers majority of aerobic gram +ve microbial flora . • Administerd in the form of aqueous Pn g 2 to 4 million units IV 4 to 6 hourly or;500 mg six hourly orally . • Ampicillin or amoxicillin ; 500mg 6 and 8 hourly IV and orally respectively • Cloxacillin; 500mg orally 8 hourly • In case of allergic to Pn; erythromycin 600mg 6 to 8 hourly
• Gentamicin 80mg IM B.D • Clindamycin IV 300 to 600 mg 8 hourly • Metronidazole 400mg 8 hourly
Hydration • Pt should be encouraged to have liquids and if required iv ,fluids can maintain hydration and calories.
A simple prototype protocol A. Preoperative 1.Airway assessment 2.Etiological findings :further radiographs OPG, and other radiograph 3.Risk factor consideration: diabetes immunodeficiency status 4.Hydration :pulse and urine output 5.Chest radiograph to rule out pneumonia 6.Evaluate lab data: blood counts
B.Perioperative i. Intubation ii. Removal of cause iii. Antibiotics C .postoperative i. Extubate after confirming adequate airway ii. Irrigations of drains periodically iii. Culture reports to adjust antibiotics accordingly iv. Regular follow up
Cavernous sinus thrombophlebitis • Occur as a result of superior spread of odontogenic infection via haematogenous route • Formation of thrombus in cavernous sinus / communicating branches • Unusual occurrence ,rarely result of infected tooth • Serious, life threatening infection
• 2 routes • External route(anteriorly)-infection enters -face & lip –sup or inf ophthalmic vein-sup orbital fissure-cavernous sinus • Internal route(posteriorly)-pterygoid plexus –emissary vein – cavernous sinus
Microbiology streptococci and staphylococci and gram – ve bacteria Clinical features • Swelling of the face and eye • Pain in the eye • Edema of conjunctiva • Pulsating exopthalmus
Treatment • Antibiotic therapy • Neurosurgical consultation • Anticoagulants • Surgical drainage
Conclusion we being dental surgeons must understand anatomy of fascial spaces ,spread of infection and proper management for the prevention of further complications and betterment of health of the patient.
Space infections.pptx

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Space infections.pptx

  • 1.
    SPACE INFECTIONS DR SUMAYYAUMARAH ORAL AND MAXILLOFACIAL SURGEON
  • 2.
    Content • Introduction • Definition •Pathway of odontogenic infection • Classification • Maxillary space infection • Mandibular space infection • Ludwigs angina • Cavernous sinus thrombophlebitis
  • 3.
    Introduction • Occurrence ofinfectious disease is determined by interaction of host , the microorganism and the environment • In healthy state there is balance among these factors and when the balance is lost disease occurs • Most odontogenic infections arise as a sequel of pulp necrosis caused by caries, trauma, periodontitis
  • 4.
    Fascial spaces • Definition: the fascial spaces are the potential spaces between the various layers of fascia normally filled with loose connective tissue and bounded by anatomical barriers , usually of bone , muscle or fascial layers. (Moore – 1975)
  • 5.
    Pathways of odontogenicinfection • Invasion of dental pulp by bacteria after decay of a tooth • inflammation edema and lack of blood supply • Venous congestion ,pulpal tissue death • Reservoir for bacterial growth • Periodic egress of bacteria into surrounding alveolar bone
  • 6.
    Odontogenic infections • Typesof infection: acute chronic • Acute stage in acute stage ,infection spreading in the soft tissues can take the following forms of in the clinical situation Abscess Cellulitis Fulminating infections
  • 7.
    Difference between cellulitisand abscess cellulitis • Acute phase • Severe and generalized • Large • Diffuse borders • Doughy to indurated • No presence of pus • Greater degree of seriousness • Aerobic bacteria abscess • Chronic phase • Localized • Small in size • Well circumscribed • Fluctuant on palpation • Presence of pus • Less degree of seriousness • Anaerobic bacteria/mixed
  • 8.
    Acute infection • Theodontogenic infection present in the following forms: 1. Acute periapical abscess: abscess arises and remains in the confine of the alveolar bone 2. Acute dentoalveolar abscess: once the infection has crossed the confines of alveolar bone and comes to lie in the neigbouring soft tissues and gets localized 3. Acute periodontal abscess 4. Acute pericoronal abscess
  • 9.
    Differential clinical featuresbetween acute periodontal & acute periapical abscess Acute periapical abscess • Pain is severe and throbbing • Common in adults • Pulp gets necrotic and infected • Swelling seen over the apex • Sinus discharge will be present • TOP is present • Mobility in later stages • Arises from the pulp Acute periodontal abscess • Pain is severe and throbbing • Uncommon in children • Pulp is vital • Swelling over the gingival third of the alveolar process • Sinus discharge may be present • TOP is present • Mobility Is seen in early stages • Arises in relation to periodontal pocket
  • 10.
  • 11.
    Chronic stage • Inchronic stage the odontogenic infection present itself in the following forms: 1. Chronic fistulous tract or sinus formation: abscess neglected for a long period discharge intraorally or extraorally 2. Chronic osteomyelitis 3. Cervicofacial actinomycosis
  • 12.
    General course ofodontogenic abscess 1. Early stage: there is intrabony pus collection. The adjoining soft tissues doesnot undergo any necrosis 2. Intermediate stage: perforation of cortex infection progresses soft tissues becomes indurated and brawny small area of central softening can be palpated this represents central necrosis due to loss of blood supply
  • 13.
    Microbiology • The aerobicbacteria found in odontogenic infection are gram positive cocci , most are viridans streptococci species , include strep.milleri ,strep.sanguis, strep.salivarius, strep.mutans. • These oral streptococci account for more than 80% of aerobic bacteria in odontogenic infection.
  • 14.
    There are twomain groups of bacteriodes a.oropharyngeal b. they other group found in the gut • Oropharyngeal bacteriodes :divided into: • Porphyromonas : includes P. assachrolyticus ,P.gingivalis, P.endodontalis • Prevotella:it includes p.buccal p.oralis, p.loeschii, p.denticola prevotella intermedius , porphyromonas gingivalis ,and porphyromonas endodontalis appears to be most pathogenic among them
  • 15.
    • Medical therapy •Consists of supportive care –hydration soft or liquid diet rich with protein ,analgesics and use of antiseptic mouthwashes to maintain oral hygiene
  • 16.
    Antibiotic therapy i. Innon compromised pt with well localized abscess surgical drainage and dental therapy without antibiotic cover. In cases of poorly localized , extensive abscess and diffuse cellulitis , antibiotic therapy is must . ii. In compromised pt as well as in pt with systemic signs and symptoms like trismus, airway compromise, fever antibiotic coverage is mandatory
  • 17.
    • Penicillin isthe empirical drug of choice. Later on after knowing the lab results of culture and sensitivity testing , specific antibiotic is instituted. • oral clindamycin , Augmentin, 1st and 2nd generation cephalosporin are useful in orofacial infections • in compromised pt , clindamycin alone or in combination with gentamicin, 1st and 2nd generation cephalosporin can be used parenterally.
  • 18.
    Surgical therapy • Incisionand drainage helps i. To get rid of toxic purulent ii. To decompress the edematous tissues iii. To allow better perfusion of blood , antibiotic and defensive elements iv. To increase oxygenation of infected area
  • 19.
    Hiltons method ofincision and drainage • The method of opening an abscess ensures that no blood vessel or nerve in the vicinity is damaged and is called Hiltons method • Steps 1. Topical anaesthesia 2. Stab incision: made over max fluctuation in most dependent area along the crease 3. If pus is not encountered, further deepening of surgical site is achieved with sinus forcep 4. Closed forcep is pushed through tough deep fascia and advanced towards the pus 5. Pus flows along the sides of the beak 6. Placement of drain : a corrugated rubber drain is inserted into to the depth of the abscess cavity and external part is secured to the wound margin with the help o suture 7. Drain left for atleast 24 hours
  • 22.
    Purpose of keepingthe drain • Is to allow the discharge of the tissue fluids and pus from the wound by keeping it patent . • The drain allows for debridement of the abcess cavity by irrigation
  • 24.
    Spread of orofacialinfection Routes of spread By direct continuity through the tissues By lymphatics to the regional lymph node and eventually into the blood stream. The spread of infection from the lymph nodes to the tissues results in secondary area of cellulitis or tissue space abscess By blood stream: local thrombophlebitis may propagate along the veins entering the cranial cavity via emissary veins to produce cavernous sinus thrombophlebitis. The microorganism or the infected emboli may get swept away in to the blood stream leading to bacteraemia, septicaemia or pyaemia with the development of embolic abscess.
  • 25.
    Potential routes ofspread of periapical infection Muscles and fascial attachments determine the direction of spread. Extensions beyond this attachments lead to deep space involvement
  • 26.
    Factors influencing spread •General factors a) Host resistance :depends upon : humoral factor cellular factor i. Humoral factors involve immunoglobulins derived from B lymphocytes or plasma cells ii. Cellular factors include pmn leucocytes , monocytes ,lymphocytes and tissue macrophages
  • 27.
    b. Virulence ofmicro organisms : determined by invasiveness of the causative micro organisms. These include production of lytic enzymes , potent endotoxins & exotoxins c. Compromised host defences : uncontrolled metabolic diseases, such as alcoholism , malnutrition , severe diabetes 2. Suppressing diseases: leukaemia , lymphoma , malignant tumours 3. Suppressing drugs: cancer chemotherapeutic drugs , immunosuppressive drugs
  • 28.
    Local factors • Intactanatomical barriers: i. alveolar bone : first local limiting barrier to further spread of periapical infection ii. Periosteum : this structure is better developed in mandible and hence can delay further spread leading to the development of a sub periosteal abscess iii. Adjacent muscles and fascia : next site for localization
  • 29.
    Evaluation of patientwith orofacial infection • If the patient i. Is toxic ii. Exhibits CNS changes iii. Airway compromise • Then, i. Immediate hospitalization ii. Aggressive medical treatment iii. Aggressive surgical intervention
  • 30.
    History taking • Physicalexamination General examination Regional examination Extra oral examination • Inspection • Palpation Intra oral examination Radiological examination
  • 31.
  • 32.
  • 33.
    Primary max space •Canine • Buccal • infratemporal Primary mandibular space • Submental • Sublingual • Submandibular • buccal Secondary fascial spaces • Pterygomandibular • Superficial and deep temporal • Masseteric • Pharyngeal • Retropharyngeal • Prevertebral • parotid
  • 34.
    Based on etiology Generalclassification • Odontogenic • Traumatic • Implant surgery • Reconstructive surgery • Infection arising from contaminated needle puncture • Others( including from factors such as infected antrum , salivary gland afflictions)
  • 35.
    On the basisof causative organism • Bacterial infection • Fungal • Viral • Odontogenic infection • Non odontogenic infection  Tonsillar infection  Nasal infection  Furuncle overlying skin
  • 36.
    Canine fossa involvement[infraorbital space] • Odontogenic infection • Nasal infection • Periapical abscess of cuspids. periapical abscess which discharges bucally from an upper canine or first premolar may lead to accumulation of pus in canine fossa
  • 37.
    • Involvement :teethwhich frequently give rise to abscess are maxillary canine and premolars and sometimes mesiobuccal root of maxillary first molar • The periapical abscess discharges bucally superior to origin of canninus muscle and pus accumulates in canine fossa
  • 38.
    Surgical anatomy-boundaries • Superiorlylevator labii superiors alaque nasi,levator labii superioris,zygomaticus minor muscle • Inferiorly ,caninus muscle • Anteriorly, orbicularis oris • Posteriorly, buccinators • Medially, anterolateral surface of maxilla
  • 39.
    Clinical features • Swellingof the cheek and upper lip • Obliteration of nasolabial fold • Drooping of the angle of mouth • Edema of the lower eye lid • extra oral –early phase: on first or second day,inflamma- tory enlargement of upper lip, and angle of mouth is seen to drop. • late phase-usually occur on the second or third day • Marked periorbital edema forcing eyelid to close • Redness and marked tenderness of the facial tissues
  • 40.
    • When theinfection progress to chronic stage, it may result in production of chronic fistula in the cleft area between levator labii superiors alaque nasi and zygomaticus minor muscle near the medial canthus of eye • intraoral: the offending teeth is mobile and is tender on percussion
  • 41.
    Treatment • Incision anddrainage : • The approach to this area is through the mucosa of buccal vestibule in the region of lateral incisor and canine. A curved mosquito forcep is inserted superior to the attachment of caninus muscle ,and the infraorbital space is entered.
  • 42.
    Buccal space involvement •Buccal space is the potential space between buccinator and masseter BOUNDARIES • Anteromedially :buccinator • Posteromedially:masseter overlying the anterior border of ramus of mandible • Laterally :platysma muscle • Inferiorly:limited by the attachment of deep fascia to the mandible and by depressor anguli oris • Superiorly: the zygomaticus process of the maxilla and zygomaticus major and minor muscle
  • 43.
    • Contents :buccalpad of fat, stensons duct, facial artery • TEETH COMMONLY INVOLVED maxillary and mandibular molars and premolars
  • 44.
    CLINICAL FEATURES • Gumboil is seen in the vestibule • Prominent dome shaped extraoral swelling extending from lower border of mandible to the infraorbital margin and from the anterior margin of masseter muscle to the corner of the mouth. SPREAD: continuation with the pterygomandibular space to infratemporal space along the fascia
  • 45.
    Treatment • Incision anddrainage :horizontal incision thro the oral mucosa of the cheek in the premolar ,molar region. • If the pus is lateral to the muscle then the muscle is penetrated with the mosquito forcep to enter the buccal space
  • 47.
    Infratemporal fossa space •Also called retrozygomatic space as it is situated behind the zygomatic bone • Involvement :infections arise from infection of buccal roots of the max 2nd and 3rd molar • Local anaesthesia injection with contaminated needle in the area of tuberosity
  • 48.
    BOUNDARIES • Bounded laterallyby ramus of mandible temporalis muscle and its tendon • Medially by medial pterygoid plate ,lateral pterygoid muscle lower part of temporal fossa of the skull and lateral wall of pharynx • Superiorly by infratemporal surface of greater wing of sphenoid and by zygomatic arch • Inferiorly by the lateral pterygoid muscle which forms the floor of the fossa • Anteriorly infratemporal surface of maxilla • Posteriorly parotid gland
  • 49.
    Clinical features Extraoral: • Trismus •Bulging of temporalis muscle • Marked swelling of the face on the affected side infront of the ear • The eye is often closed Intraoral: swelling of the tuberosity. • Elevation of temperature up o 104 F
  • 50.
    Incision and drainage •Intraoral approach: if trismus is not marked and fluctuation is detected early , intraoral incision is given in the buccal vestibule . • extraoral approach: incision is made at upper and posterior end of the temporalis muscle within the hairline .the sinus is then directed upwards and medially and pus is evacuated.
  • 51.
    Potential primary spacesrelated to lower jaw SUBMENTAL SPACE • Involvement: originating from the six anterior mandibular teeth; then perforate the cortical plate below the origin of mentalis muscle labially and mylohyoid lingually. BOUNDARIES: Lateral: lower border of the mandible and anterior bellies of digastric muscle Superior: mylohyoid muscle Inferior: suprahyoid portion of the investing layer of deep cervical fascia which is in turn covered by platysma
  • 52.
    Contents: submental lymphnode and jugular veins .the lymph nodes lies embedded in adipose tissues and hence submental abscess tend to remain well circumscribed. CLINICAL FEATURES: Extraoral finding :distinct firm swelling in the midline, beneath the chin. Intraoral findings : ant teeth are either non vital fractured or carious . • The offending tooth may exhibit tenderness to percussion and may show mobility • Pt may experience discomfort on swallowing
  • 53.
    Incision and drainage •Performed by making transverse incision in the skin below the symphysis of mandible. Dissection is carried by inserting sinus forcep through the incision, upward and backward. • SPREAD posteriorly to involve the submandibular space • It may discharge on the face in the submental region.
  • 54.
    Submandibular space • Thespace lies between ant and post bellies of digastric muscle. The upper part lies beneath the inferior border of mandible and the lower part lies deep to the investing layer of deep cervical fascia . • Involvement: infections originating from mandibular molars. • The pus perforates the lingual cortical plate of mandible inferior to the attachment of mylohyoid muscle and passes directly to the submandibular space • It is involved as an extension of infection from submental space • Also involved by an infection originating from post part of sublingual space • Also involved from infection originating from middle third of the tongue ,posterior • part of the floor of the mouth, maxillary teeth cheek , maxillary sinus and palate.
  • 56.
    BOUNDARIES • Anteromedially ,thefloor is formed by the mylohyoid muscle which is covered by loose areolar tissue and fat • Posteromedially ,the floor is formed by the hyoglossus muscle • Superolaterally,medial surface of mandible below the mylohyoid ridge • Anterosuperiorly,anterior belly of digastric • Posterosupriorly, post belly of digastric stylohyoid and stylopharyngeus muscle • Laterally , platysma and the skin
  • 57.
    Clinical features Extraoral :firmswelling in submandibular region ,below the inferior border of the mandible • Some degree of tenderness • Redness of the overlying skin Intraoral: teeth are sensitive to percussion • Teeth are mobile • Dysphagia • Moderate trismus
  • 58.
    Incision and drainage •Incision of about 1.5 to2cm length is made 2 cm below the lower mandible in the skin creases . • Skin and subcutaneous tissues are incised . • The sinus forcep is inserted thro the incision superiorly and posteriorly on the lingual side of the mandible below the mylohyoid to release the pus from the submandibular space
  • 59.
    spread • There areno major anatomic barrier between the two submandibular and submental spaces • There are no major anatomic barrier hence infection can spread easily across the midline and involve submandibular space on the contralateral side • Infection can spread backwards to involve para pharyngeal space • The submandibular space communicates with the sub lingual space around the posterior border of mylohyoid muscle.
  • 60.
    Differential diagnosis • Lymphomaarising in the lymph node of upper neck • TB lymphadenitis
  • 61.
    Sublingual space • Thisspace is v shaped trough lying lateral to the muscle of the tongue including hyoglossus genioglosssus and geniohyoid • Involvement : teeth involved are mandibular incisors canines premolars • The infection perforates lingual plate below the level of the mucosa of the floor of the mouth and passes into the sublingual space.
  • 62.
    Boundaries • Superiorly bythe mucosa of the floor of the mouth • Inferiorly :mylohyoid muscle • Laterally: medial side of the mandible • Medially :hyoglossus genioglossus and geniohyoid muscles • Posteriorly :hyoid bone • Laterally and inferiorly by the mylohyoid muscle and the lingual side of the mandible
  • 63.
    Contents • Includes genioglossusgeniohyoid hyoglossus muscle • It also contains • deep part of submandibular salivary gland • sublingual salivary gland • Lingual nerve • Hypoglossal nerve
  • 64.
    Clinical features • Extraoral: there is little or no swelling .the lymph node may be enlarged and tender • Pain and discomfort on deglutition • Speech may be affected • Intraoral: firm painful swelling seen in the floor of the mouth • The tongue may be pushed superiorly. this will bring about airway obstruction • The ability to protrude the tongue beyond the vermillion border of upper lip is affected
  • 65.
    Incision and drainage •Intraorally:incision is made close to the lingual cortical plate as the imp structure at this site is sublingual nerve which is deeply placed and less likely to be damaged by this approach. The sinus forcep is inserted and opened to evacuate pus. • Extraoral: drained via skin incision placed in the sub mental region.
  • 66.
    spread • Infection alwayscrosses the midline, and can affect the spaces on the opposite side • Infection can also spread via the lymphatics to the submental or submandibular lymph nodes.
  • 67.
    Masticatory spaces • Itcomprises of the following spaces 1. pterygomandibular 2. submasseteric 3. temporal –superficial temporal 4. deep temporal
  • 68.
    Submassetric space • Whenthe pus accumulates between the ramus of the mandible and the masseter muscle , it produces a submassetric space abscess. • Involvement :infection originates from the lower 3rd molar resulting from(i) pericoronitis • (ii) periapical abscess
  • 69.
    Boundaries • Anterior :ant border of masseter muscle and buccinators • Posterior : parotid gland and posterior part of masseter • Inferior : attachment of masseter to lower border of mandible • Medial : lateral surface of ramus of mandible • Lateral : medial surface of masseter
  • 70.
    Contents • masseteric nerve, superficial temporal artery , transverse facial artery • It contains muscle of mastication, ramus ,posterior • part of mandible and branches of mandibular division of • trigeminal nerve
  • 71.
    Clinical features • Externalfacial swelling is moderate in size :swelling extending from lower border of mandible to the zygomatic arch and anteriorly to the ant border of masseter and posteriorly to the post border of the mandible • Tenderness over the angle of the mandible • Almost complete limitation of mouth opening • pyrexia
  • 72.
    Incision and drainage •Intraoral approach: incision made vertically over the lower part of anterior border of the ramus of the mandible ,deep to the bone. • A sinus forcep is passed along the lateral surface of the ramus downwards and backwards. • Extraoral approach : when the mouth cannot be opened ,an incision is placed in the skin behind the angle of mouth to open the abscess by Hiltons method
  • 73.
    • Involvement :pericoronitis related to mandibular 3rd molar • Infection can also be because of contaminated needle used for an IANB • At times can also originate from max 3rd molar following PSA injection Pterygomandibular space infection
  • 74.
    Boundaries • Lateral: medialsurface of ramus of mandible • Medial : lateral surface of medial pterygoid muscle • Posterior: parotid gland • Anterior :pterygomandibular raphe • Superior :lat pterygoid muscle forms the roof to pterygomandibular space • Contents: lingual nerve , mandibular nerve , inferior alveolar artery , mylohyoid nerve and vessel
  • 75.
    Clinical features • Eventhe established cases of pterygomandibular space infection doesnot cause much swelling of face over the submandibular region . • Severe degree of limitation of mouth opening • Tenderness over the area of swollen tissues medial to ant border of ramus of mandible • Dysphagia is present • Redness and the edema of the area around the 3rd molar • Uvula is swollen • Difficulty in breathing
  • 76.
    Incision and drainage •Intraoral :Vertical incision approx. 1.5 cm in length is made on anterior and medial aspect of ramus of mandible . Sinus forcep is inserted in the abscess cavity , opened and closed and withdrawn . The pus is evacuated • Extraoral :incision is taken in the skin below the angle of the mandible. A sinus forcep is inserted towards the medial side of the ramus in an upward and backward direction • . Pus is evacuated
  • 77.
    Spread • Infection mayspread superiorly along the medial surface of the ramus to involve the infratemporal fossa • Infection may spread posteriorly to lateral pharyngeal space and then to retropharyngeal space • Can also spread around the front of ramus of mandible to involve the buccal space
  • 78.
    Life threatening complicationof orofacial infection • Which may be classified as • Those relate to lower jaw (a)ludwigs angina (b) descending deep cellulitis of the neck (c) carotid sheath invasion • Those related to upper jaw (a)cavernous sinus thrombosis ,Dural meningitis ,osteomyelitis of skull (b) retro bulbar cellulitis with possibility of blindness
  • 79.
    Ludwig's angina • Definition;itis the massive firm brawny cellulitis/induration and acute toxic stage involving simultaneously ,the submandibular, sublingual and submental spaces bilaterally . • the term Ludwig angina was coined by Camerer in 1837 • this condition had established its unique identity with three ” f ”s • It was to be FEARED • rarely becomes FLUCTUANT • it was often FATAL
  • 80.
    Etiology 1.Odontogenic : a) Acutedentoalvelolar abscess b) Acute periodontal abscess c) Acute pericoronal abscess: in relation to erupting 2nd and 3rd molar which can extend to following spaces i. Submandibular spaces ii. Buccal space iii. Sublingual space iv. Pterygomandibular space
  • 81.
    2. Iatrogenic :use of contaminated needle for giving LA 3. Traumatic injuries to orofacial region :mandibular fractures ,deep lacerations and penetrating injuries 4. Osteomyelitis 5. Sublingual and submandibular sialadenitis 6. Cervical lymphoid tissues
  • 82.
    Pathology • The conditionis a cellulitis – a diffuse inflammation of soft tissues which is not circumscribed or confined to one area but in contrast to the abscess ,tends to the spread thro tissues spaces and along fascial planes. • Involvement : mandibular 2nd and 3rd molars
  • 83.
    Clinical features • Ptlooks very toxic , very ill and dehydrated • There is pyrexia anorexia chills and malaise • Dysphagia • Impaired speech • Hoarseness of voice
  • 84.
    Extraoral examination • Firmand brawny hard swelling in the bilateral submandibular and submental regions which soon extends down to the anterior part of the neck to the clavicle. • Swelling is non pitting minimally or non fluctuant associated with severe tenderness • Classically shows ill defined borders with induration. • Severe muscle spasm may lead to trismus. • Typically mouth may remain open due to edema of the sublingual tissues leading to raised tongue almost touching the palatal vault • Airway obstruction • There may be dilatation of alae nasi , raising of thoracic inlet by the scalene and sternocleidomastoid muscle and indrawing of the tissues above the clavicle
  • 85.
    • Cyanosis mayoccur due to hypoxia • Fatal death may occur in untreated cases of Ludwig's angina within 10 to 24 hours due to asphyxia • Intraorally: swelling develops rapidly which involves sublingual tissues and distends or raises the floor of the mouth, woody edema of the floor of the mouth and the tongue • Increased salivation , stiffness of tongue movement and difficulty in swallowing • Backward spread of infection leads to edema of glottis, resulting in respiratory obstruction • Stridor being alarming sign of this fatal extension needing emergency intervention to keep airway patent
  • 86.
    Spread • Due toanatomical continuity of various spaces with submandibular space infection may track to • submasseteric petrygomandibular space parapharyngeal space para tonsillar spaces Worsening the airway
  • 87.
    • Infection fromthe submandibular region may spread downwards along and the deep investing layer of deep cervical fascia , towards the clavicle and subsequently to mediastinum.
  • 90.
    Principles of treatment •The treatment is based on combination of following factors • Early diagnosis • Maintenance of patent airway • Intense and prolonged antibiotic therapy • Extraction of offending tooth • Surgical drainage or decompression of fascial spaces
  • 91.
    Airway maintenance • Intubationof patient: blind intubation should be avoided . Nasoendotacheal intubation is far more reliable. • surgical airway: required in case of severe upper resp obstruction . • Laryngotomy cricothyroidotomy (tracheotomy) is preferred over tracheostomy because of : • Identification of landmarks is difficult due to associated massive edema and tissue distortion • The surgery itself may lead to spread of infection to deeper tissues due to additional incision required .
  • 92.
    Surgical intervention • Ithas two aims: (i) remove the cause (ii) Surgical decompression Removal of the cause : removing of offending tooth may facilitate the evacuation of the pus Surgical decompression : it reduces pressure of edematous tissues on the airway reducing respiratory embarassement • It allows prompt drainage
  • 93.
    Antibiotic therapy • Playsa vital role in managing Ludwig's angina. • Penicillin are first line antibiotics in treating such infections as it covers majority of aerobic gram +ve microbial flora . • Administerd in the form of aqueous Pn g 2 to 4 million units IV 4 to 6 hourly or;500 mg six hourly orally . • Ampicillin or amoxicillin ; 500mg 6 and 8 hourly IV and orally respectively • Cloxacillin; 500mg orally 8 hourly • In case of allergic to Pn; erythromycin 600mg 6 to 8 hourly
  • 94.
    • Gentamicin 80mgIM B.D • Clindamycin IV 300 to 600 mg 8 hourly • Metronidazole 400mg 8 hourly
  • 95.
    Hydration • Pt shouldbe encouraged to have liquids and if required iv ,fluids can maintain hydration and calories.
  • 96.
    A simple prototypeprotocol A. Preoperative 1.Airway assessment 2.Etiological findings :further radiographs OPG, and other radiograph 3.Risk factor consideration: diabetes immunodeficiency status 4.Hydration :pulse and urine output 5.Chest radiograph to rule out pneumonia 6.Evaluate lab data: blood counts
  • 97.
    B.Perioperative i. Intubation ii. Removalof cause iii. Antibiotics C .postoperative i. Extubate after confirming adequate airway ii. Irrigations of drains periodically iii. Culture reports to adjust antibiotics accordingly iv. Regular follow up
  • 99.
    Cavernous sinus thrombophlebitis •Occur as a result of superior spread of odontogenic infection via haematogenous route • Formation of thrombus in cavernous sinus / communicating branches • Unusual occurrence ,rarely result of infected tooth • Serious, life threatening infection
  • 100.
    • 2 routes •External route(anteriorly)-infection enters -face & lip –sup or inf ophthalmic vein-sup orbital fissure-cavernous sinus • Internal route(posteriorly)-pterygoid plexus –emissary vein – cavernous sinus
  • 102.
    Microbiology streptococci and staphylococciand gram – ve bacteria Clinical features • Swelling of the face and eye • Pain in the eye • Edema of conjunctiva • Pulsating exopthalmus
  • 103.
    Treatment • Antibiotic therapy •Neurosurgical consultation • Anticoagulants • Surgical drainage
  • 104.
    Conclusion we being dentalsurgeons must understand anatomy of fascial spaces ,spread of infection and proper management for the prevention of further complications and betterment of health of the patient.