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.

1. SPACE INFECTIONS
DR SUMAYYA UMARAH
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 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

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 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

6. 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

7. 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

8. 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

9. 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

10. Periodontal abscess Periapical abscess

11. 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

12. 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

13. 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.

14. 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

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. 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

17. • 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.

18. 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

19. 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

22. 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

24. 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.

25. 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

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 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

28. 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

29. 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

30. History taking
• Physical examination
General examination
Regional examination
Extra oral examination
• Inspection
• Palpation
Intra oral examination
Radiological examination

31. classification
Mode of
involvement
etiology
Causative
organism
Based on

32. Mode of
involvement
Primary max
spaces
Primary
mandibular
spaces
Secondary fascial
spaces

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
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)

35. On the basis of 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 :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

38. 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

39. 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

40. • 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

41. 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.

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 :buccal pad of fat, stensons duct, facial artery
• TEETH COMMONLY INVOLVED
maxillary and mandibular molars and premolars

44. 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

45. 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

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 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

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 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

52. 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

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
• 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.

56. 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

57. 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

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 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.

60. Differential diagnosis
• Lymphoma arising in the lymph node of upper neck
• TB lymphadenitis

61. 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.

62. 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

63. Contents
• Includes genioglossus geniohyoid 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 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.

67. Masticatory spaces
• It comprises of the following spaces
1. pterygomandibular
2. submasseteric
3. temporal –superficial temporal
4. deep temporal

68. 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

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
• 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

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: 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

75. 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

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 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

78. 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

79. 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

80. 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

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 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

83. Clinical features
• Pt looks very toxic , very ill and dehydrated
• There is pyrexia anorexia chills and malaise
• Dysphagia
• Impaired speech
• Hoarseness of voice

84. 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

85. • 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

86. 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

87. • 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.

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
• 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 .

92. 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

93. 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

94. • Gentamicin 80mg IM B.D
• Clindamycin IV 300 to 600 mg 8 hourly
• Metronidazole 400mg 8 hourly

95. Hydration
• Pt should be encouraged to have liquids and if required iv ,fluids can
maintain hydration and calories.

96. 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

97. 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

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 staphylococci and 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 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.