Secondary spaces

OBJECTIVE
For accomplishment of proper management, maxillofacial surgeon must understand physiologic
and anatomic factors that influence the spread and localization of dental infections.
Understand the microbiology of odontogenic infections.
Understand the signs, symptoms and findings in patients with odontogenic infections.
Review the various pathways of spread of odontogenic infections.
Understand the medical and surgical management of odontogenic infections.
2

INTRODUCTION
Infections are amongst the most challenging and serious conditions that we face.
Data from early 1900’s show that infections caused 1/3 of deaths in the U.S.
1974, U.S Dept. of Health, Education and Welfare (DHEW) ranked head and neck infections as
the number one reason for referring to a clinician.
The incidence of mortality from head and neck infections is low, despite serious morbidity.
3

Space infections of head and neck are very common in Oral and maxillofacial practice.
Depending on the virulence of microorganisms and host resistance, bacterial infections have the
potential to spread beyond the bony confines of jaw bones into surrounding soft tissues.
They flow following the path of least resistance , into loose areolar connective tissue of fascia
surrounding the muscles.
4

Early extraction of offending tooth and incision and drainage tend to shorten the usual course of
infection and minimize the chances of further complications.
In new era of antibiotics, incidence of death due to infection is reduced but due to developing
drug resistance, there is outbreak of new range of infections requiring invention of newer
antibiotics.
5

History
Burns (1811) first described fascial space as an anatomical entity and gave their clinical significance.
In 1836 Wilhelm Frederick von Ludwig described his observations concerning repeated occurrences
of inflammation of throat. Hence most severe orofacial Infection at that time was named as Ludwigs
angina.
Greek author Parker(1879) gave vivid descriptions of infections which produced inflammation of
oral cavity, tonsil and larynx.
6

The term “ Quinsy “ was given by Muckleston in 1928.
In 1929 Mosher called Viscerovascular space as “Lincoln highway”
Space of the body of mandible is described by Coller & Iglesias. (1935)
7

Anatomy of the Cervical Fascia
 The term fascia is used to describe broad sheets of dense connective tissue whose function is to separate
structures that must pass over each other during movement, such as muscles and glands, and serve as pathways for
the course of vascular and neural structures.
 Because bacterial infections appear to spread by hydrostatic pressure, they follow the path of least resistance,
which is the loose, areolar connective tissue that surrounds the muscles enclosed by the fascial layers.
 This type of tissue is destroyed easily by the hyaluronidases and collagenases elaborated by bacteria, thus
opening the potential spaces surrounding the muscles.
9

For example, an odontogenic infection beginning in a lower molar may erode through the thin lingual cortical
plate of the mandible inferior to the attachment of the mylohyoid muscle.
Once the invading organisms have eroded through the cortical bone and periosteum, they enter the submandibular
space directly.
The potential space of the submandibular triangle is filled primarily by areolar connective tissues surrounding
the submandibular gland.
As the infection enters the submandibular space the areolar connective tissue gradually undergoes necrosis; it is
replaced first by cellulitic fluid and then by pus.
Vascular dilation, transudation, and exudation draw fluid into the region, thus increasing the hydrostatic
pressure.
10

Fascia of head and neck
1. Superficial fascia.
2. Deep cervical fascia.
A. Anterior Layer.
◦ Investing Fascia.
◦ Parotidomassetric fascia.
◦ Temporal.
B. Middle Layer.
◦ Sternohyoid- Omohyoid division.
◦ Sternothyroid- thyrohyoid Division.
◦ Visceral Division
1. Buccopharyngeal.
2. Pretracheal
3. Retropharyngeal
C. Posterior Layer.
◦ Alar division.
◦ Prevertebral Division
11
Topazian R, Goldberg M, Hupp Oral and Maxillofacial Infections. 4th Edition. Saunders, Pennsylvania
2009

Layers of deep cervical fascia
12

Superficial Fascia
 The superficial fascia is a layer of dense connective tissue that
courses deep to the subcutaneous tissue throughout the entire body.
 The subcutaneous space is defined as the tissues lying superficial
to the superficial fascia.
 Subcutaneous space infections involve mainly the areolar and
fatty connective tissues known as subcutaneous tissue.
 Below the mouth the muscles of facial expression lie deep to the
superficial fascia, whereas in the upper face the muscles of facial
expression are positioned superficial to this layer.
13

Deep Cervical Fascia
A. Anterior Layer –
 Also known as the investing layer or the enveloping layer or the external layer or the
superficial layer of the deep fascia.
 It has been described using the ‘rule of twos’—it envelops two muscles, two glands and
forms two spaces.
 This layer originates from the spinous processes of the vertebral column and spreads
circumferentially around the neck and splits to cover the sternocleiodomastoid and trapezius
muscles.
 In the midline, inferiorly it splits 2 cms above the manubrium forming the suprasternal
space of Burns.
 The space of burns contains anterior jugular vein, lymph nodes, sternal head of
sternocleidomastoid muscle & interclavicular ligament.
14

Superiorly, it attaches to the hyoid bone and continues
superiorly to enclose the submandibular and parotid glands.
The portion of the fascia covering the masseter muscle and
enclosing the parotid gland is known as the
‘Parotideomassetric fascia’.
It also covers the anterior bellies of the digastrics and the
mylohyoid, thereby forming the floor of the submandibular
space.
At the mandible, the fascia splits into an internal layer,
which covers the medial surface of the medial pterygoid and
attaches to the skull base and an outer layer that covers the
masseter and inserts on the zygomatic arch.
15

B. Middle layer -
Also known as the visceral fascia, the prethyroid fascia and the
pretracheal fascia.
It has two subdivisions,
- The muscular division, which surrounds the infrahyoid strap muscles
- The visceral division, which envelops the pharynx, larynx,
esophagus, trachea and thyroid gland.
The superior extent of the muscular division is the hyoid and thyroid
cartilage, inferiorly it inserts on the sternum and clavicle.
 Surgical significance - This layer of deep cervical fascia should be
divided in the midline to approach the thyroid gland and trachea.
16

The visceral division attaches to the hyoid bone above and surrounds
the trachea, esophagus and thyroid gland.
Above the hyoid, the fascia surrounds the pharynx on the lateral and
posterior sides lying on the superficial side of the constrictor muscles of
the pharynx where it is known as the buccopharyngeal fascia.
It extends inferiorly into the upper mediastinum where it is continuous
with the fibrous pericardium and covers the thoracic trachea and
esophagus.
The retropharyngeal, pretracheal and lateral pharyngeal spaces lie
superficial to this layer.
17

C. Posterior layer
The deep layer of the deep cervical
fascia originates from the spinous
processes of the cervical vertebra and the
ligamentum nuchae.
At the transverse processes of the
cervical vertebra, it divides into an
anterior alar layer and a posterior
prevertebral layer.
18

1. Alar fascia
The alar fascia extends from the base of the skull to the second
thoracic vertebra (T2).
It lies between the visceral layer of the middle fascia and the
prevertebral layer.
It fuses with the retropharyngeal fascia between C6 and T4.
This fusion forms the bottom of the retropharyngeal space and
infections of the retropharyngeal space may rupture the alar fascia
and enter the danger space which is continuous with the posterior
mediastinum (Posterior Lincoln’s highway).
19

2. Prevertebral fascia
The prevertebral fascia lies just anterior to the vertebral
bodies and extends the entire length of the vertebral column.
It travels circumferentially around the neck and covers the
paravertebral muscles, the deep muscles of the posterior
triangle of the neck and the scalene muscles.
This layer of fascia surrounds the brachial plexus and
subclavian vessels and continues laterally as the axillary
sheath.
It may be involved by infections of the vertebral bodies and is
not involved in maxillofacial infections.
20

Carotid Sheath
• It is formed by all three layers of deep fascia or from alar division or posterior layer.
• The carotid sheath begins at the origin of the carotid artery in the superior mediastinum and
passes through the pretracheal space in an upward and posterior direction.
• Above the hyoid bone it lies at the junction of the lateral pharyngeal and retropharyngeal
spaces.
• The carotid sheath terminates at the jugular foramen and carotid canal, where the internal
jugular vein and carotid artery enter the base of the skull, respectively.
• The carotid sheath also contains the vagus nerve.
• The cervical sympathetic chain is attached to the posterior surface of the carotid sheath.
• The carotid, jugular, and vagus nerves each have compartments within the carotid sheath.
21
Topazian R, Goldberg M, Hupp Oral and Maxillofacial Infections. 4th Edition. Saunders, Pennsylvania
2009

PATHOPHYSIOLOGY OF ODONTOGENIC
INFECTIONS
22

Infections and Host defense
In establishing presence of an infection, interaction occurs among three factors.
1. Host
2. Environment
3. Microorganism
In state of Homeostasis , balance exists among these three and disease occurs when
imbalance exists.
25

Infection occurs when host is
immunocompromised or when
pathogenicity and number of microbes
invading host is more.
26

Microbiology –Space infection
Aerobic bacteria (25%)
Gram positive cocci (85%)–
Streptococcus species( 90% ) -
◦ S.Milleri
◦ S.sanguis
◦ S.Salivarius
◦ S.Mutans
Staphylococcus species (6 %)
27

Anaerobic bacteria (75%)
1. Gram positive cocci (30%)
2. Peptococcus species 33%
3. Pepto Streptococcus species 33%
4. Gram positive bacilli (50%)
5. Prevotella species, Porphyromonas species (75%)
6. Fusobacterium -20%
28

Stages of infection
Infections generally pass through these 4 stages before they
undergo complete resolution.
Stage I – Inoculation
Stage II – cellulitis
Stage III –After day 5 underlying abscess undermines skin or mucosa making it compressible.
Stage IV - Finally there is resolution of abscess
29

Factors affecting Spread of Infection
1. Microbial factors-
Level of virulence.
No. of organisms introduced.
2. Host factors-
General state of health.
Integrity of surface defence.
Level of immunity.
Capacity for inflammatory & immune response.
Impact of medical intervention.
3. Combination of both factors.
31

Routes of Spread
Direct spread-
a) Spread into superficial soft tissues as-
Abscess- pathological thick walled cavity filled with pus.
Cellulitis- diffuse subcutaneous/submucous inflammation of soft tissues. Tends to spread along fascial planes.
b) Spread into adjacent fascial spaces.
c) Into deep medullary spaces of bone- osteomyelitis
Indirect spread-
a) Lymphatic routes to regional nodes.
b) Hematogenous route to other organs such as brain.
32

Routes of spread of infection
Superficial
Spread of infection
Direct
Tissue
Indirect
LymphadenopathyBlood
Septicemia
DeathSpread to other
organs
OsteomyelitisMedullary space
Deep
CellutitisAbscess
Facial planes
Airway obstruction –
Ludwigs angina ,
mediastinal obstruction 33

Investigations
 Routine laboratory investigations.
 Radiological examination- helpful in locating offending teeth or other underlying
cause.
 IOPA
 OPG
 Lateral oblique view mandible.
 A-P & Lateral view of neck for soft tissues can be useful in detecting retropharyngeal
space infection.
 Ultrasound of swelling.
 CT scan, MRI help in diagnosing extension of infection beyond maxillofacial region.
35

Fascial Spaces
• Sharpio defined fascial spaces as potential spaces between the layers of fascia.
• These areas are either clefts ( potential spaces between facial layers ) or compartment containing
connective tissue.
• Fascial planes offer anatomic highways for infection to spread from superficial to deep planes.
36

Fascial spaces
The fascial spaces in head and neck 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)
37

Hollinshead’s classification(1958)
Infrahyoid spaces -
1.Visceral compartment
A) Pretracheal / previsceral
B) Retrovisceral
2. Visceral space
3. Other space
I. Cavity within carotid sheath
II. Space between 2 layers of prevertebral fascia
38

CLASSIFICATION OF FASCIAL SPACES
GRODINSKYAND HOLYOKE (1938)
Space 1 – Superficial to superficial fascia
Space 2 – Group of spaces surrounding cervical strap
muscles 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 (Lincoln’s High way)
39

Space 4 – Space lies between alar & prevertebral
division of posterior layer of deep cervical fascia
(Danger space)
Space 4A – Posterior triangle space posterior to
carotid sheath
Space 5 - Prevertebral space
Space 5A- Space enclosed by Prevertebral fascia.
40

BASED ON MODE OF INVOLVEMENT
1. Direct Involvement. (Primary Spaces)
◦ Maxillary Spaces – Canine, buccal, infratemporal
◦ Mandibular Spaces – Submental, Submandibular, Sublingual, Buccal
2. Indirect involvement (Secondary Spaces)
◦ Masseteric
◦ Pterygomandibular
◦ Superficial and deep temporal
◦ Lateral and retro pharyngeal
◦ Prevertebral, parotid, carotid sheath, peritonsillar and danger spaces.
41

Based on clinical significance-
Face- Buccal, canine, parotid, masticatory.
Suprahyoid- Sublingual, submental, submandibular, lateral
pharyngeal, peritonsillar.
Infrahyoid- Pretracheal.
Spaces of total neck- Retropharyngeal, space of carotid
sheath.
42

MASTICATORY SPACES
1. MASSETERIC SPACES
2. PTERYGOMANDIBULAR SPACES
3. SUPERFICIAL TEMPORAL SPACES
4. DEEP TEMPORAL SPACES
44

SUBMASSETERIC SPACE
ANATOMY:
 The same layers of fascia that separate at the inferior border of the mandible to form the space of the
body of the mandible also form the second potential muscular fascial space known as the masticator
space.
 The superficial layer passes upward externally to the masseter muscle but deep to the parotid gland,
Stenson’s duct, seventh nerve, and the superficial temporal artery and vein.
 This layer passes upward over the Zygomatic bone, to which it becomes attached, and from there
upward over the temporal muscle to become attached to the periosteum of the temporal bone
45

BOUNDRIES –
• Anterior: Anterior border of masseter muscle and buccinator.
• Posterior: Parotid gland, and posterior part of masseter.
• Inferior: Attachment of the masseter to the lower border of mandible.
• Medial: Lateral surface of the ramus of mandible.
• Lateral: Medial surface of the masseter muscle.
47

CONTENTS:
 Ramus of the mandible,
 All of the muscles of mastication,
 Fat pad surrounding the attachment of the temporal muscle to the coronoid process
The upper part of the masticator space is divided into two parts by the temporal muscle.
48

POSSIBLE SOURCES OF INFECTIONS:
 The masticator space may be infected by extension of infection from the space of the body of
the mandible, from the parotid space, from the lateral pharyngeal space, or from suppurative
middle ear diseases.
 It is occasionally infected by septic material carried on the point of the needle during the course
of injection to anesthetize the inferior alveolar nerve.
49

CLINICAL FEATURES -
 External facial swelling is moderate in size & is confined to the outline of the masseter muscle, i.E.
The swelling is seen extending from the lower border of the mandible to the zygomatic arch; and
anteriorly to the anterior border of masseter; and posteriorly to the posterior border of the mandible.
 There is tenderness over the angle of the mandible.
 Limitation of mouth opening.
 Fluctuation may be absent; and if present, cannot be elicited, because the muscle lies between the
pus and the surface.
 Pyrexia and malaise.
50

 The ramus of the mandible is more dependent upon blood supply from the overlying muscle than
the body of the mandible, which is supplied by inferior alveolar artery.
 As a result, ischemic changes may take place in that part of bone denuded by periosteum by a
submasseteric abscess so that a low-grade osteomyelitis of lateral cortical plate may occur with
sequestrum formation.
 Often submasseteric infection leads to subperiosteal new bone deposition beneath the periosteum.
 Necrosis of the muscle can also occur.
52

SPREAD:
 Infections in the lower portion of the space cannot easily extend downward because of the firm
attachment of the periosteum to the bone about the angle of the mandible.
 The fused layers forming the anterior and posterior boundaries of the space also discourage
extension either anteriorly or posteriorly.
 The infection may spread upward to involve either the superficial or deep temporal spaces.
 These spaces are also sometimes infected due to osteomyelitis arising in the zygomatic bone or in
the temporal bone.
53

INCISION AND DRAINAGE:
Intraoral:
Occasionally an abscess in the masticator space may point intraorally, in which event the space
may be drained by a vertical incision inside the mouth along the anterior border of the masseter
muscle. Through this incision, by blunt dissection, either the portion of the space lateral to the
ramus or that portion of the space medial to the ramus may be explored.
54

Extraoral angle approach:
 The space also may be drained through an incision about 4 cm. long passing through the skin and
subcutaneous fascia in a curved fashion below and behind the angle of the mandible.
 Through this incision it is possible by blunt dissection to explore that portion of the masticator space
either medial to or lateral to the ramus of the mandible.
 In cases of extensive infection where either the superficial or deep temporal spaces are also involved,
through-and-through drainage should be established between the incision made to drain the lower part
of the space and the incision made for drainage of the superficial and deep temporal spaces.
55

PTERYGOMANDIBULAR SPACE
INFECTION
 The pterygomandibular space is a compartment situated between the medial
Surface of the ramus of the mandible and the medial pterygoid muscle.
Involvement:
(i) Pericoronitis related to the mandibular third molar.
(ii) Septic fractures of mandibular ramus.
58

BOUNDARIES
• Lateral: Medial surface of ramus of mandible.
• Medial: Lateral surface of medial pterygoid muscle.
• Posterior: Parotid gland (deep portion).
• Anterior: Pterygomandibular raphae.
• Superior: Lateral pterygoid muscle forms roof to the pterygomandibular space.
59

Contents:
 Lingual nerve
 Mandibular nerve,
 Inferior alveolar or mandibular artery
 Mylohyoid nerve and vessels
 Loose areolar connective tissue
60

CLINICAL FEATURES:
1. Even the established cases of pterygomandibular space infections, do not cause much
swelling of face over the submandibular region.
2. Severe degree of limitation of mouth opening.
3. Tenderness can be elicited over the area of swollen soft tissues medial to anterior border of
ramus of the mandible.
4. Dysphagia
5. Medial displacement of the lateral wall of the pharynx
6. Redness and edema of the area around the third molar
7. Midline of the palate is displaced to the unaffected side
8. Uvula is swollen.
9. Difficulty in breathing.
61

INCISION AND DRAINAGE
The abscess usually tends to point at the anterior border of the ramus of the
mandible and drainage can be easily done by intraoral route.
Intraoral: a vertical incision, approximately 1.5 cm in length, is made on
the anterior and medial aspect of the ramus of mandible. A sinus forceps in
inserted in the abscess cavity, opened and closed and withdrawn. The pus is
evacuated, a rubber drain is introduced and is secured in position with a
suture.
62

Extraoral:
An incision is taken in the skin by extraoral
submandibular ‘Risdon’s incision’. A sinus
forceps is inserted towards the medial side of
the ramus in an upward and backward
direction. Pus is evacuated and the drain is
placed insitu and sutured in position.
63

Spread
 Occasionally, infection may spread superiorly along the medial surface of ramus to involve the
Infratemporal fossa and beneath the temporal fascia.
 The infection can spread posteriorly to lateral pharyngeal space and then to retropharyngeal space.
 It can also spread around the front of the ramus of the mandible to involve the buccal space.
 It can also spread around the front of the ramus of the mandible extending anteroinferiorly below the
lower border and under the superior constrictor to involve the submandibular space.
64

TEMPORAL SPACE INFECTION
ANATOMIC LOCATION
The temporal space is the superior continuation of the infratemporal space.
This space is divided into superficial and deep temporal spaces.
The superficial temporal space is bounded laterally by the temporal fascia
and medially by the temporalis muscle, while the deep temporal space is
found between the medial surface of the temporalis muscle and the temporal
bone.
65

SUPERFICIAL TEMPORAL SPACE INFECTION
BOUNDRIES OF SUPERFICIAL TEMPORAL SPACE –
Laterally - Skin, temporal fascia
Medially - Lateral aspect of temporalis muscle
Inferiorly - Superior surface of lateral pterygoid muscle
Superiorly and posteriorly - Attachment of temporalis to cranium, anterior
border
Anteriorly - Posterior wall of maxillary sinus, pterygomandibular fissure
66

ETIOLOGY -
 Maxillary & mandibular molars
CONTENTS –
Temporal fat pad
Temporal branch of facial nerve
NEIGHBOURING SPACES –
Buccal space
Deep temporal space
67

DEEP TEMPORAL SPACE INFECTION
BOUNDRIES OF DEEP TEMPORAL SPACE –
Laterally – medial surface of Temporalis muscle
Medially - Lateral surface of the temporal bone
Inferiorly – Superior surface of lateral pterygoid muscle
Superiorly and posteriorly - Attachment of temporalis to cranium,
anterior border
Anteriorly - Attachment of the fascia to the orbital process of the
zygoma
68

ETIOLOGY -
 Maxillary molars
CONTENTS –
Pterygoid plexus
Internal maxillary artery & vein
Mandibular division of trigeminal nerve
Skull base foramina
NEIGHBOURING SPACES –
Buccal space
Superficial Temporal space
69

CLINICAL FEATURES OF TEMPORAL
SPACE INFECTIONS
Mild swelling in the temporal area
The swelling is not very conspicuous due to the presence of the
tenacious temporal fascia in case of superficial pouch involvement and
in case of the deep pouch, due to the presence of the temporalis muscle
and overlying fascia.
Trismus due to the spasm of the temporalis muscle
The superficial pouch infection extents below the zygomatic arch in
the massetric area producing a classical ‘dumbbell’- shaped swelling
70

 Extraoral incision in temporal region, well above the hairline, 45º to
zygomatic arch.
 The hemostat is inserted above and below the temporalis muscle.
 The care should be taken not to damage the branches of facial nerve.
 The incision can be placed above and parallel to the zygomatic arch.
The temporal fascia is divided to evacuate the contents of the
superficial pouch and the temporalis muscle is pierced open to drain the
contents of the deep pouch.
71

LATERAL PHARYNGEAL SPACE
 The lateral pharyngeal space, which is also known as the
pharyngomaxillary space, is a potential cone-shaped space or cleft
with its base uppermost at the base of the skull and its apex at the
greater horn of the hyoid bone.
 The space is divided into two by a short layer of condensed fascia
called aponeurosis of Zuckercandl and Testut joining the styloid
process to tensor veli palatini as anterior and posterior compartments.
72

 If the anterior compartment becomes infected, the patient exhibits pain, fever, chills, medial
bulging of lateral pharyngeal wall, deviated uvula, dysphagia and trismus.
 If the posterior compartment becomes infected, there is absence of trismus along with visible
swelling, but respiratory obstruction, septic thrombophlebitis of IJV may ensue in late stages.
73

ETIOLOGY –
Odontogenic, secondary to a grossly carious molar, pericoronitis or tooth extraction.
Thrombosis of the internal jugular vein or of peritonsillar veins
Metastatic tumors with secondary infection of the internal jugular lymph node chain
Iatrogenic introduction of organisms during infiltration for a mandibular nerve block
administration of an anesthetic during tonsillectomy
By backward spread from sublingual, submandibular and pterygomandibular space infections.
Lateral spread from tonsillar abscess.
75

SOURCE & SPREAD OF INFECTION
76
Peritonsillar infections that penetrate the pharyngeal constrictor muscles enter the lateral
pharyngeal space.
Sublingual space infections can enter the lateral pharyngeal space in the posterior part of the
floor of the mouth through the buccopharyngeal gap.
Submandibular space infections can pass around the posterior belly of the digastric muscle or
the stylohyoid muscle to enter the lateral pharyngeal space.

Retropharyngeal space infections, possibly caused by necrotic breakdown of retropharyngeal
lymph nodes, can spread easily into the lateral pharyngeal space because no membranous or
muscular barrier exists between these two spaces.
Infections may encircle the airway by spreading from one lateral pharyngeal space to the other
through the retropharyngeal space.
77

BOUNDARIES
Anteriorly: Superior and middle pharyngeal constrictor muscle
Posteriorly: Carotid sheath, stylohyoid, styloglossus and
stylopharyngeous
Superiorly: Base of skull
Inferiorly: Hyoid bone
Medially: Superior pharyngeal constrictors
Laterally: Medial pterygoid muscle and capsule of parotid gland
78

CONTENTS
Anterior compartment (Prestyloid) :
Lymph nodes, ascending pharyngeal, facial artery, loose
areolar connective tissue.
Posterior compartment (Poststyloid):
Carotid sheath, glossopharyngeal nerve, spinal accessory
nerve, hypoglossal nerve and cervical sympathetic trunk.
79
Osborn TM, Assael LA, Bell RB. Deep space neck infection: principles of surgical management. Oral and
maxillofacial surgery clinics of North America. 2008 Aug 31;20(3):353-65.

CLINICAL FEATURES
Clinical picture is grave, because of generalized septicemia and respiratory embarrassment due to
edema of the larynx. General constitutional symptoms in the form of malaise and pyrexia are
present.
80

Anterior compartment:
1. Extraoral:
Brawny induration of the face, above the angle of the mandible. This induration may extend
downward to the submandibular region, as well as, upwards to the parotid region on the ipsilateral
side
Fever
Pharyngeal bulging
81

2. Intraoral:
The anterior part of the lateral pharyngeal wall may be swollen;
that pushes the soft palate and the palatine tonsil towards the
midline.
Marked trismus may be present.
Severe pain arising from the collection of pus between the
medial pterygoid and superior constrictor.
Dysphagia
82

Posterior compartment:
 The clinical picture is dominated by septicemia.
 Usually little or no trismus is present.
 Slight pain is present.
 External swelling is less extensive.
 There is subtle swelling in lateral neck, just above the hyoid bone, between posterior belly of digastric and
sternocleidomastoid muscle externally.
Internal swelling involves the lateral wall of pharynx behind the palatopharyngeal arch.
83
Osborn TM, Assael LA, Bell RB. Deep space neck infection: principles of surgical management. Oral and
maxillofacial surgery clinics of North America. 2008 Aug 31;20(3):353-65.

MANAGEMENT -
Immediate hospitalization
Maintenance of airway
Incision and drainage
Removal of the causative agent & antibiotic therapy initiated empirically and adjusted when
results of culture and antibiotic sensitivity tests have been obtained.
85

1. Intraoral
- Transpharyngeal approach
- Lateral approach
2. Extraoral
86

TRANSPHARYNGEALAPPROACH
Made through the tonsillar fossa.
This approach is not recommended because adequate drainage is very difficult to obtain.
87

LATERALAPPROACH
Performed by making an incision medial to the pterygomandibular
raphe
A sinus forceps or curved hemostat is passed through the
pterygomandibular raphae along the medial surface of the mandible,
medial to the medial pterygoid and just lateral to the superior
constrictor is then divided posteriorly to the pus pocket.
88

EXTRAORALAPPROACH -
An incision is made along the anterior border of
sternocleidomastoid muscle, extending from below the angle of the
mandible, to the middle third of submandibular gland.
 A 3 to 5 cm incision is placed low over the submandibular space
just superior and parallel to the hyoid bone.
 The posterior end should lie just over the anterior border of
sternocleidomastoid muscle.
 The dissection is carried through skin, subcutaneous tissue,
superficial fascia, and platysma muscle to expose the superficial or
anterior layer of deep cervical fascia
89

 The fascia is exposed sufficiently to identify
submandibular gland and the posterior belly of digastric
muscle.
The dissection is then carried further just posterior to the
posterior belly of digastric muscle in a superior, medial,
and posterior direction.
 The dissection of lateral pharyngeal space is completed
when the surgeon is able to palpate the endotracheal tube
medially, the ipsilateral transverse processes of the
vertebrae posteromedially, and the carotid sheath
posterolaterally.
90

COMBINED APPROACH -
 A mucosal incision is made lateral to the pterygomandibular
raphe, and a large curved clamp is passed medial to the medial
pterygoid muscle in a posteriorinferior direction.
 The tip of the clamp is delivered through the skin by a
cutaneous incision between the angle of the mandible and the
sternocleidomastoid muscle.
91

COMPLICATIONS -
According to sharpio –
1. Mediastinitis
2. Jugular thrombosis
3. Edema of the larynx
4. Ludwig’s angina
5. Hemorrhage from erosion and blowout of the large vessels
6. Osteomyelitis of the mandible
7. Pneumonia
8. Vagus involvement (sudden death)
9. Meningitis
10. Parotid abscess
93

RETROPHARYNGEAL SPACE
INFECTION
Retropharyngeal Space: Prevertebral Space
It is a potential midline space between the
pharyngobasilar fascia, which attaches the pharyngeal
constrictors to the base of skull, and alar fascia.
95

ETIOLOGY -
Otologic
Pharyngeal or nasopharyngeal infections can directly spread to the retropharyngeal space
Upper respiratory infections
Odontogenic infections
Cervical osteomyelitis
Foreign body introduction
Regional trauma
Spread by the lymphatics
Progression from lateral pharyngeal space
96

BOUNDARIES
Laterally - Carotid sheath, lateral pharyngeal space
Superiorly - Base of the skull
Inferiorly - Fusion of retropharyngeal fascia
Anteriorly & posteriorly - Deep cervical fascia and
alar fascia
Medially - Midline septum
97

CLINICAL FEATURES:
Fever
Sialorrhea
Stiff neck
Sore throat
Dysphagia
Possible stridor
Leukocytosis
Occasional lateral neck erythema and swelling.
98

Lateral soft tissue radiographs of the neck are extremely useful and
may reveal considerable widening of the retropharyngeal space, well
beyond the 3- to 6-mm width in normal adults at the second vertebra
(or >14 mm in children).
99

MANAGEMENT -
Maintainence of airway
Aggressive antibiotic therapy
INCISION AND DRAINAGE:
INTRAORALLY –
Patient should be under local anesthesia in the extreme Trendelenburg position and with constant
suctioning.
In the transoral technique, an incision is made through the midline of the posterior pharyngeal
mucosa, and the abscess is opened by blunt dissection.
100

EXTRAORALLY –
The space can be safely divided into two – (a) Suprahyoid portion, and (b) Infrahyoid
portion.
Suprahyoid portion:
 The suprahyoid portion of retropharyngeal space can be approached by using the same
incision described for lateral pharyngeal space.
 The space is approached through the lateral pharyngeal space, hence the dissection is
the same, until the lateral pharyngeal space is further explored by blunt finger dissection.
 The dissection is continued until the surgeon is able to palpate the contralateral
transverse processes of the vertebrae, the endotracheal tube from its posterior aspect,
and if necessary the opposite carotid artery.
101

Infrahyoid portion:
 If the space is involved below the hyoid bone, then the posterior end of the
low submandibular incision described above is extended inferiorly along the
anterior border of sternocleidomastoid muscle.
 As the dissection passes deep to anterior layer of deep cervical fascia, the
sternocleidomastoid muscle is retracted posterolaterally to expose the carotid
sheath.
 The loose connective tissue lying between the carotid sheath and the
esophagus is bluntly dissected medially and posteriorly to expose the visceral
fascia, which surrounds the trachea, oesophagus and thyroid gland.
 Blunt dissection with finger is used to follow the visceral fascia into the
retropharyngeal space.
 Multiple soft drains are then placed in the superior and inferior portions of
the retropharyngeal space as well as in the lateral pharyngeal space.
102

CAROTID SHEATH SPACE
Infections that have eroded into the carotid sheath may cause disruption of any of the structures
associated with it, including expanding hematoma in the neck, bleeding episodes ("herald
bleeds"), variations in heart rate or speech function, or septic emboli.
Involvement of the cervical sympathetic chain may cause Horner's syndrome on the affected
side, which is characterized by miosis (pupillary constriction), ptosis (drooping of the lid caused
by inactivation of Muller's muscle), and anhidrosis (decreased sweating of the affected side of the
head, neck, and upper extremity).
105

DANGER SPACE
Potential space between the alar and prevertebral divisions of
the deep layer of the deep cervical fascia
Boundaries -
• Superiorly:-base of the skull.
• Inferiorly:- upper border of diaphgram.
• Laterally:- fusion of alar and prevertebral fascia at transverse
process of cervical and thoracic vertebrae.
• Anteriorly:- alar fascia.
• Posteriorly:- prevertebral fascia.
106

WHY DANGER SPACE???
At the inferior border it continous with the posterior mediastinum containing vena cava ,arch
of aorta, thoracic duct, trachea and oesophagus.
Erosion of major blood vessels, lower airway and upper digestive tract
Death of patient.
107

COMPLICATIONS
Osborn TM, AssaelLA,Bell RB.Deepspaceneckinfection: principles of surgical management. Oral and
maxillofacial surgery clinics of North America. 2008Aug31;20(3):353-65.
 Ludwig’s Angina
 Cavernous Sinus Thrombosis
 Carotid artery erosion
 Necrotizing Fascitis
 Internal jugular vein thrombosis
 Mediastinitis
 Pyopneumothorax
 Bronchial erosion
 Purulent Pericarditis
 Pleural effusion

Historical Background
• A rare disorder, Ludwig’s angina is a serious, potentially life- threatening infection
of the neck and the floor of the mouth.
• Originally, described by Wilhelm Frederick von Ludwig in 1836.*
Nguyen VD, Potter JL, Hersh-Schick MR. Ludwig angina: an uncommon and potentially lethal neck infection.
AJNR Am J Neuroradiol 1992;13:215–9
LUDWIG’S ANGINA

It isdefined asacute, ‘non- suppurating
necrotising cellulitis’ involving the
submandibular, sublingual and submentalspaces,
bilaterally.
 This condition is notorious for its aggressiveness,
rapid progression to airway compromise and high
mortality when not treated promptly.
Nguyen VD,Potter JL,Hersh-SchickMR. Ludwig angina: an uncommon and potentially lethal neckinfection.
AJNRAmJNeuroradiol 1992;13:215–9

BACTERIOLOGY -
 Poly-microbial and predominantly involves the oral
flora.
 Organisms most often isolated are
Streptococcus Viridans and Staphylococcus Aureus.
Anaerobes
Bacteroides
Peptostreptococci
Peptococci
122
NguyenVD,Potter JL,Hersh-SchickMR.Ludwig angina: an uncommon and potentially lethal neck
infection. AJNRAmJNeuroradiol1992;13:215–9
Gram-positive bacteria
• Fusobacterium nucleatum
• Spirochetes
• Candida
• Eubacteria
• Clostridium
Gram-negative bacteria
• Neisseria species
• E coli
• Pseudomonas species
• Haemophilus influenzae

 Predisposing conditions
 Diabetes mellitus
 Neutropenia
 Alcoholism
 Aplastic anemia,
 Glomerulonephritis
 Age range - 12 years to 84 years
 Male > female (3:1 to 4:1)

ETIOLOGY
Originates from,
• Second or third mandibular molars.
Other less commonly causes,
• Sialadenitis
• Peritonsillar abscess
• Open mandibular fracture
• Infected thyroglossal duct cyst
• Epiglottitis
• Intravenous injections of drugs into the neck
• Traumatic bronchoscopy
• Endotracheal intubation
• Oral lacerations
• Tongue piercing
• Upper respiratory infections
• Trauma to the floor of the
mouth.

SIGN &SYMPTOMS
 It is a massive firm, bilateral submandibular swelling which
soon extends down the anterior part of the neck to the
clavicle.
 The consistency - ‘wood like’ or brawny induration.
 Bulls neck appearance
 The swelling of the submental space - classical double chinned
appearance.

 It elevates the floor of the mouth and forces the tongue up
against the palate.
 Marked pyrexia.
 Deglutition and speech are difficult.
 Airway obstruction
 Cynosis may occur due to progressive hypoxia
126

DIAGNOSIS
FOUR Cardinal signs -
• Bilateral involvement of more than a single deep-tissue space;
• Gangrene with serosanguinous, putrid infiltration but little or no frank pus;
• Involvement of connective tissue, fasciae, and muscles but not glandular structures;
• Spread via fascial space continuity rather than by the lymphatic system.

INVESTIGATIONS
• Plain radiographs of neck and chest
• Panoramic radiograph
• CT scan
128

PlainRadiographsOf TheNeck May Show Soft-tissueSwelling, The
PresenceOf Gas,And The Extent Of Airway Narrowing

CT scan showing , edema, inflammation & air in soft tissue. adjacent to
Right & Left mandible

TREATMENT
Primary goal:
• Preserve the oropharyngeal airway.
Secondary goal:
• Incision and drainage.
• Aggressive antibiotic therapy

Airway management-
-Blind intubation avoided
-Nasoendotreacheal intubation is
far more reliable
- Cricothyoidotomy are always preferred
over tracheostomy

ANTIBIOTIC AGENT
Early aggressive antibiotic therapy:
• Ampicillin 2-4g/day IV or Ceftriaxone 1gm IV 12hourly
• Gentamycin 1-4mg/kg/day IV or Amikacin 500mg 8hourly
IV dexamethasone, given for 48h, has been beneficial in reducing edema.

SURGICAL DECOMPRESSION
Serves 3 purpose:
• It reduces tension within the tissue plane and prevents the further spread of the edema and
infection.
• As the pressure in the tissue drops, the circulation of the tissue improves which
facilitates resorption of the edema.
• It drains the septic material, if any and prevents further bacteremia. The edema reduces
gradually.

Bilateral submandibular incisions and if
required a midline submental incision 1 cm
below the inferior border of the mandible are
sufficient to drain the involved space.
In most of the cases, little or no pus can be
drained out by surgical intervention, as it is
cellulitis. But in later stages or postsurgical
period profuse pus may be seen draining.
136

SURGICAL DECOMPRESSION
The incisions must be bilateral, extraoral, parallel, and medial
to the inferior border of the mandible, at the premolar and
molar region

 Cavernous sinus thrombosis (CST) is a
serious condition consisting of formation of
thrombus in cavernous sinus or its
communicating branches.
139

Causes of Cavernous Sinus Thrombosis -
• Sinusitis: eg sphenoid & ethmoid sinusitis
• Dental infections: especially maxillary dental abscess/cellulitis, retropharyngeal & parapharyngeal
abscess,etc
• Orbital cellulitis
• Otitis media
• Microbial Infections such as boils/furuncle on upper lip ( danger area of face)
• Fungal infections , generalized inflammatory conditions of body like systemic lupus erythematous,
• Sometimes mechanical causes leading to clot formation like- trauma or head injury, Neurosurgical
procedures like Lumbar puncture
142

CLINICAL FEATURES -CST
1.Sepsis ---
2.Venous Obstruction ---
3.Cranial nerve involvement ----

DIAGNOSIS OF CAVERNOUS SINUS THROMBOSIS
CLINICAL IMAGING
 CT –scan – Contrast enhanced
 MRI
Eagleton's Criteria*
1)Known site of infection.
2)Evidence of blood stream infection.
3) Early sign of venous obstruction in retina, conjunctiva
or eyelids.
4)Paresis of III, IV, VI cranial nerves resulting
from inflammatory edema.
5)Abscess forms and neighboring tissues involved
6) Evidence of meningeal irritation.
Kruger GO.Textbook of oral and maxillofacial surgery. CVMosby; 1984.

CAVERNOUS SINUS ON MRI BRAIN
LevineSR,TwymanRE,Gilman S:Therole of anticoagulation in cavernoussinusthrombosis. Neurology, 2008; 38:517–22

TREATMENT OF CAVERNOUS SINUS THROMBOSIS
Antibiotics - {empiric cover - gram+ve,-ve & anaerobic}
-3rd Gen.Cephalosporin+ Vancomycin+ Metronidazole
- If fungal origin - Amphotercin-B 10mg/kg/day
Anti-coagulants - Intravenous Heparin 24000-30000 units/day
Steroids - Controversial
Hydrocortisone- 100 mg IV q6h
152

Surgery -
Exploration of Cavernous sinus – Not performed routinely
 Removal of Septic focus
 Extraction of odontogenic focus
 Surgical drainage of paranasal Sinuses
 Debridement of Fungal paranasal sinusitis
153

MEDIASTINITIS
 Serious potentially fatal condition – descending neck infection to
the mediastinum.
 Complex anatomical space.
Contents:
 Superior: Carotid A. ,Aortic arch, vagus N. ,subclavian V. ,
thoracic duct, Trachea, Oesophagus, thymus..
 Anterior: No major structure
 Middle: Heart, termination of great vessels, phrenic nerves
 Posterior: Thoracic aorta, superior vena cava, azygos vein, thoracic duct,
vagus nerve.
Osborn TM, AssaelLA,Bell RB.Deepspaceneckinfection: principles of surgical management. Oral and maxillofacial surgery clinics of
North America. 2008Aug31;20(3):353-65.

Clinical features
• Severe retrosternal pain.
• severe dyspnoea,dysphagia.
• High fever with chills.
• oedema with creptations in the upper thorax.
Pretracheal
Retropharyngeal space
Lateral pharyngeal
Infratemporal space
Submandibular space
MEDIASTINITIS
Carotid Space

Management:
Team approach - Aggressive antibiotics + Surgical Drainage+ removal of Source of
infection
Transcervical approach - Wide incision in the anterior border of sternocledomastoid muscle
reaching all the way to mediastinum through blunt dissection, through pretracheal space.
Osborn TM, AssaelLA,Bell RB.Deepspaceneckinfection: principles of surgical management. Oral and
maxillofacial surgery clinics of North America. 2008Aug31;20(3):353-65.

BRAIN ABSCESS
Brain abscesses are rare, but they represent a serious
infection of the brain parenchyma in which a localized
area of suppuration develops.
They may be the result of direct head injury, a
complication of neurosurgical procedures, or the result of
secondary infections from distant sites.
158

 Rarely, odontogenic infections are implicated in the etiology of brain abscesses.
 Can occur from bacteremia accompanying odontogenic infection microorganisms reaching
brain produces -
1. Inflammation.
2. Localized edema.
3. Septic thrombosis.
159

CLINICAL FEATURES:
1. Headache.
2. Nausea, vomiting.
3. Papilloedema, hemiplegia.
4. Convulsions.
5. Stupor.
6. Confusion.
7. Changes in personality.
160
TREATMENT:
1. Drug therapy – Antibiotics,
steroids and mannitol.
2. Early diagnosis and treatment.
3. Surgery to be done for
incision and drainage.

MENINGITIS
Odontogenic infections rarely spread intracranially to cause
complications such as thrombosis of the cavernous sinus,
abscess, or meningitis.
Meningitis is most common neurological complication
resulting from infection to the orofacial region.
161

Clinical features:
1. Headache.
2. Fever.
3. (Kernig’s & Brudzinkis sign).
Lumbar puncture usually shows rise in protein level and
drop in glucose level.
162

Treatment:
1. Chloromphenicol and penicillin G.
2. Antibiotics to continue unless fever subsides.
3. Proper electrolyte balance level should be maintained.
4.Control of cerebral edema into consideration.
163

CERVICAL NECROTIZING
FASCITIS
DEFINITION:
NF is defined as a relatively rare infection, is characterised by rapidly progressing necrosis of the
fascia and subcutaneous fat, with subsequent necrosis of overlying skin. Muscle involvement is
minimal or non-existent.
164

Necrotizing fasciitis is classified microbiologically
into four types based on the microbiologic etiology -
1. Type I – It is a polymicrobial and the most common type of
Necrotizing Fasciitis
2. Type II is usually monomicrobial and due to Gram-positive
organisms.
3. Type III is a gram-negative monomicrobial infection.
4. Type IV is caused by fungal organisms
165

NF can also be classified based on Clinical dermatological features into three stages:
Stage 1: defined with signs such as erythema, tenderness beyond the erythema, swelling, and hot skin.
Stage 2: defined by the formation of skin bullae, blister, and skin fluctuation.
Stage 3: manifests with haemorrhagic bullae, crepitus, skin necrosis, and gangrene.
166

CLINICAL FEATURES -
• Extreme rapidity with which the disease progresses
• A tendency to turn subcutaneous tissues into putrid, pulpy substance.
• Severe pain together with a smell which is peculiar and extremely
offensive.
• Starts at the site of any small wound or scratch, attacking mainly
immunologically compromised patients but also seen in healthy adults.
Unhygienic surroundings also play an important role in establishing NF.
169

Extensive swelling and erythema bilaterally.
Mucosal sloughing of floor of mouth.
Area of fluid enhancement at periphery without involvement of
cranial base.
The lesion is usually dark, extremely foul-smelling with
purulent exudative discharge and poorly defined edges.
Crepitation and bursting of gas bubbles on compression
Soft in consistency and covered by necrotic skin with visibility
of pulsations of underlying arteries.
170

Treatment:
1. Securing airway.
2. Broad spectrum antimicrobial therapy with penicillin and cephalosporin.
3. Intensive care support.
4. Prompt surgical debridement.
172

PRINCIPLES OF
MANAGEMENT OF
ODONTOGENIC
INFECTIONS
174

Principle 1 - Determine Severity of Infection
Principle 2 - Evaluate State of a Patient’s Host Defense Mechanism
Principle 3 - Determine Whether Patient Should Be Treated by General Dentist
or Oral &
Maxillofacial Surgeon
Principle 4 - Treat Infection Surgically
Principle 5 - Support Patient Medically
Principle 6 - Choose & Prescribe Appropriate ANTIBIOTICS
Principle 7 - Administer Antibiotic Properly
Principle 8 - Evaluate the Patient Frequently
175
Peterson. Ellis. Hupp. Tucker – Contemporary oral & maxillofacial surgery -4th edition

Principle 1 - Determine Severity of
Infection
Most odontogenic infections are mild and require only minor surgical therapy
Severity can be determined by; history & physical examination
176

Complete History
 Chief complaint recorded in patient’s own words.
 Determine how long the infection has been present;
o Time of onset/beginning of infection by asking the patient, first appearance of symptoms;
Pain, swelling, or drainage
o Progression of infection; symptoms of infection has been
Constant,
waxed and waned (undergo alternate increased or decreased)
grown worse
o Rapidity of progress of infection; has the infection progress over a few hours or over days to a week?
177

Information about patient’s symptoms; (Signs of inflammation)
o Most common complaint is pain. – ask location & spread of pain (Dolar)
o Ask the patient for swelling – sometimes hidden & sometime visible (tumor)
o Ask whether the area of infection or swelling is warm to touch. (calor)
o Ask patient, if there is any change in color (redness) over the area of infection or redness. (rubor)
o Functio laesa – trismus (maximum inter – incisal opening less than 20 mm), difficulty chewing,
difficulty swallowing (dysphagia), difficulty in breathing.
178

Determine the general health of patient
o Malaise; fatigued, pyrexia , weak & sick patients.
Ask about previous dental treatments (professional or self – treatment)
179

Physical Examination
Examine patient’s vital signs.
o Pulse rate increases with increase in temperature of patient.
 Pulse rate of greater than 100 beats/minute indicate severe infection.
o Blood pressure is not altered by infection. But it is the pain & anxiety in a patient which
increases the blood pressure.
– B.P decreases in septic shock.
180

o Normal respiratory rate is 14 – 16 breaths/minute
 Mild to moderate infection – respiratory rate greater than 18 breaths/minutes.
 In odontogenic infection, there is potential for partial or complete airway upper airway
obstruction as a result of extension of the infection into the deep fascial spaces of head & neck. –
that’s why respiratory rate should be observed.
181

Inspect patient’s general appearance.
 Toxic Appearance; it is a patient with severe infection
and elevated temperature, pulse & respiratory rate, and
feeling sick & tired.
182

Palpation of swelling if present; check for;
o Tenderness
o Amount of heat
o Consistency of swelling
 Fleshy swelling – doughy swelling
 Firm or hard swelling – indurated swelling
 Fluctuant swelling – feeling like fluid filled balloon.
- This type has liquid pus in the center of indurated area.
183

Perform intra oral examination to find the cause of infection.
Perform radiographic examination
Perform the staging of infection.
o Cellulitis is most severe presentation of infection.
o An abscess is sign of increasing host resistance to infection.
 Presence of pus indicates that the body has locally walled off the infection and that the local host
resistance mechanisms are bringing the infection under control.
184

185
James R. Hupp & Elie M. Ferneini – Head, Neck & orofacial infections

Principle 2 - Evaluate State of a
Patient’s Host Defense Mechanism
It is evaluated in the medical history; in which we estimate the patient’s ability to defend
against infection.
o This ability can be REDUCED BY;
 Medical conditions
 Drugs
186

Medical Conditions that Compromise
Host defense
187

Drugs that Compromise Host
Defense
Cancer chemotherapy drugs
Immune suppressive drugs – organ transplantation & auto immune disease
o Cyclosporine
o Corticosteroids
o Tacrolimus (Prograf)
o Azathioprine (Imuran)
188

Principle 3 - Determine Whether
Patient Should Be Treated by General
Dentist or Oral & Maxillofacial
Surgeon
Criteria for referral to an OMFS
189

Criteria for Immediate Hospital
Emergency Room Admission
Threat to Airway or vital structures
Rapidly progressing infection
Difficulty breathing (dyspnea)
o Patient will refuse to lie down, have quiet or distorted speech
Difficulty swallowing (dysphagia)
o Drooling is ominous sign
Temperature > 101 F (38.3 C)
 Toxic Appearance: glazed eyes, open mouth & dehydrated, sick appearance, fatigued, high
temperature.
190

Principle 4 - Treat Infection
Surgically
The principal of management of odontogenic infections is;
o Remove the cause of infection (Primary Goal)
o Surgical drainage of accumulated pus and necrotic debris (Secondary Goal)
Surgical Options for management of simple uncomplicated odontogenic
infections.
o Endodontic treatment or Extraction with or without Incision & Drainage (I&D)
191

Reasons for performing I&D
Remove the accumulated pus & bacteria from the tissues.
Decreases the load of bacteria & necrotic debris.
Reduce hydrostatic pressure by decompressing tissues.
o Improve the local blood supply
o Increase the delivery of host defences & antibiotics.
Prevent the spread of infection into deeper anatomic spaces.
192

PLACEMENT OF DRAIN
a. A soft rubber drain is inserted into the depth of the abscess cavity; and external part is secured to the wound margin
with the help of sutures.
b. Drain is left for at least 2 – 5 days.
c. Purpose of Drains -
i. Allow the discharge of tissue fluids and pus from the wound by keeping it patent.
ii. Maintain the opening
iii. Allow debridement of abscess cavity by irrigation.
d. The most commonly used drain for intra oral abscess is a quarter inch sterile Penrose drain.
i. Alternatively, thin strip of rubber dam can be used as a substitute (allergy if absent)
196

Principle 5 - Support
Patient Medically
For good outcome, patient’s ability to resist infection should also be good.
There are certain diseases decrease this resistance ability, that’s why they should treated effectively.
o Immune system compromising diseases
o Diabetes - infection itself does not increase the glucose level in body, but it is the host response to that infection
which raise the blood sugar.
- Control of blood sugar is directly proportional to resistance to infection.
o CVS disease should also be controlled.
o Medications - Anticoagulants
199

During infection body’s physiologic reserves are altered.
o Children are particularly susceptible to dehydration & high fever during infection
o Old patients are less susceptible to fever, but in them dehydration occurs during infection.
o Fever increases daily fluid requirements by about 800mL/F/day. & daily caloric intake by 3% - 5% per degree
Fahrenheit per day.
- However, temperature up to 103 F may be beneficial in combating infection.
o So, fever should be carefully controlled, with active hydration and nutritional support.
Prescribe analgesic for relief of pain and to make patient rest.
200

Principle 6 - Choose & Prescribe
Appropriate ANTIBIOTICS
Before choosing specific antibiotic, first of all determine the need for antibiotic administration
– means, whether the patient needs antibiotic or not!!!
 Some misconceptions & Wrong Statements -
o All infections require antibiotics
o Extraction of offending tooth in presence of infection increase the chances of spread of
infection.
o Prior to extraction, antibiotics prevent the worsening of infection.
201

 So, the need for antibiotics can be determined from following 3 factors -
o Seriousness of infection.
o Whether adequate surgical treatment can be achieved
- Sometimes extraction of tooth resolves the infection without antibiotics.
o State of patient’s host defenses
- Young, healthy patient may not need antibiotic while aged patient with systemic disease will need
antibiotics.
202

Antibiotics do not speed up the wound healing and do not provide any benefit for nonbacterial conditions.
So, after determining the need for antibiotics, we should use empirical therapy, means give antibiotics on
the assumption that it is the appropriate drug.
Orally administered antibiotics that are effective against odontogenic infections are;
o Penicillin – Drug of Choice.
o Amoxicillin
o Clindamycin
o Azithromycin
o Metronidazole
o Moxifloxacin
204

Patient’s compliance decreases with increasing numbers of pills per day.
o Once daily – compliance 80%.
o 2x daily – compliance 69%.
o So On…
o So try to prescribe those antibiotics which can be taken few times a day.
205

Routinely culture & sensitivity testing is not recommended.
They are to be done in or indicated in;
o Infection spreading beyond alveolar process
o Rapidly progressing infection
o Post-operative infection
206

- If patient returns after 3 to 4 days with an infection, the chances of nonindigenous bacteria
causing infection are higher
o Previous, multiple antibiotic therapy
o Nonresponsive infection (after more than 48 hours)
o Recurrent infection
o Compromised host defense.
207

Use the NARROW – SPECTURM antibiotic; Advantages of Narrow – Spectrum antibiotics;
o kills/inhibit narrow range bacteria, little or no effect on GI tract & skin bacteria.
While, B R O A D spectrum antibiotics, inhibit not only oral bacteria, but can also cause death of
skin, GIT and other areas’ bacteria, and also result in overgrowth of resistant bacteria.
o This resistance in patient can spread to his/her families, coworkers, community etc.
208

So, in Simple infections as defined below, narrow spectrum antibiotics are prescribed. While,
in complex; broad spectrum.
Antibiotics that have narrow spectrum are as much effective as wide spectrum bacteria but
without upsetting normal host bacteria & development of resistance.
209

210

Use Bactericidal Antibiotic, if possible
o Bactericidal antibiotics interfere with cell wall production in newly forming, growing bacteria.
- The defective cell wall is not able to withstand the osmotic pressure and bacterial cell die without
attack from host defense cells.
o Bacteriostatic antibiotics interfere with bacterial reproduction and growth.
- They slow the bacterial reproduction and allows host defense cells to phagocytize the bacteria
o That’s why bacteriostatic antibiotics should be avoided in immunocompromised patients. & in
these immunocompromised patient bactericidal antibiotics are drug of choice.
Use cost effective antibiotics
218

Principle 7 - Administer Antibiotic
Properly
The drug should be administered in the proper dose and at the proper dose interval.
Plasma level of drug should be high enough to kill the bacteria but not so high to cause toxicity.
o Peak plasma levels should be at least four to five times the minimal inhibitory concentration of
bacterial.
Choose drug which could be given once a day for not more than 4 – 5 days to get more compliance.
At follow – up additional prescription of antibiotic is necessary in case of infection that do not
resolve rapidly.
219

Principle 8 - Evaluate the
Patient Frequently
In this, patient is monitored for response to treatment and complications.
If therapy is successful, the dentist should check the I&D site to determine whether the drain
should be removed at this time and other parameters such as temperature, trismus, swelling &
patient’s subjective feelings should be evaluated.
If therapy is UNSUCCESSFUL, the patient should be examined for clues to reason of failure
of treatment.
The patient should be examined for toxicity reactions.
220

222
James R. Hupp & Elie M. Ferneini – Head, Neck & orofacial infections

REFERENCES
1. James R. Hupp & Elie M. Ferneini – Head, Neck & orofacial infections
2. Peterson. Ellis. Hupp. Tucker – Contemporary oral & maxillofacial surgery -4th edition
3. Osborn TM, Assael LA, Bell RB. Deep space neck infection: principles of surgical management. Oral
and maxillofacial surgery clinics of North America. 2008 Aug 31;20(3):353-65.
4. Nguyen VD, Potter JL, Hersh-Schick MR. Ludwig angina: an uncommon and potentially lethal neck
infection. AJNR Am J Neuroradiol 1992;13:215–9
5. Esquivel Bonilla D, Huerta Ayala S, Molina Moguel JL. Report of 16 cases of Ludwig’s angina: 5-year
review. Pract Odontol. 1991;12(4):23-4, 28.
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