Space Infections PDF

Space Infections
CONTENTS:
1 Introduction 2
2 History 4
3 Definition of fascial spaces 5
5 Pathophysiology of odontogenic infection 5
6 Pathways of dental infection 7
7 Stages of infection 8
8 Spread of orofacial infection 10
9 Classification of fascial spaces 13
10 Anatomy of fascia 15
11 Primary maxillary spaces 25
12 Primary mandibular spaces 36
13 Secondary fascial spaces 46
14 Complications of space infections 64
15 Localisation of dental infections 78
16 Diagnostic imaging of space infections 79
17 Management of space infections 79
18 Public health significance 92
19 Conclusion 93
20 Reference 93
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Introduction
INTRODUCTION:
Odontogenic infections have two major origins - pulpal and
periodontal. Infection erodes through the thinnest bone and causes infection in
adjacent tissue. When the infection erodes through the cortical plate of the
alveolar process, it appears in predictable anatomic locations, determined by -
• The thickness of the bone overlying the apex of tooth,
• The relationship of site of perforation of bone to muscle attachments of

maxilla and mandible.
Most odontogenic infections penetrate the bone to form vestibular
abscesses. On occasion they erode into fascial spaces directly, which causes
fascial space infection.
The soft tissues of head and neck can be divided into a series of
spaces. Some spaces are normal anatomical spaces containing various
structures (e.g. masticatory space), whereas the others are potential spaces,
identifiable only when involved by a pathological process (e.g. retro-pharyngeal
space). Important anatomical connections exist between these various actual
and potential spaces that can allow for the rapid dissemination of infections
throughout the head and neck and even into the mediastinum.
Conceptually, the fascial planes of the head and neck may be visualised
as a series of “conduits”. The outer envelope which surrounds the head and
neck is composed of skin and superficial fascia (subcutaneous tissues). Two
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Introduction
features of the superficial fascia are that (1) it contains the muscles of facial
expression, including the platysma, and (2) by virtue of its superficial location, it
is readily evaluated on clinical examination and usually doesn’t necessitate
diagnostic imaging of pathological processes.
Anatomically, the deep neck can be divided into a superficial
investing layer, middle or pre-tracheal layer, and deep or pre-vertebral layer.
These spaces are major pathways for the spread of inflammatory processes
and must be thoroughly evaluated in any imaging study.
The spaces that are directly involved are known as fascial spaces of
primary involvement.
• Maxillary primary spaces - canine, buccal and infratemporal spaces.
• Mandibular primary spaces - submental, buccal, submandibular, sublingual

spaces.
Infections can extend beyond these primary spaces into additional
fascial spaces or secondary spaces.
• Masseteric, pterygomandibular, superficial and deep temporal, lateral

pharyngeal, retropharyngeal, and pre vertebral space are secondary spaces.
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History
HISTORY:
In the 1930s the classical anatomical studies of Grodinsky and Holyoke
established the modern understanding of the fascial layers and the potential
anatomical spaces through which infections can spread in the head and neck.
They injected dyed gelatine into the cadaver specimens at selected portals of
entry. Their hypothesis was that these infections spread primarily by hydrostatic
pressure, with the flow of injected fluids guided by the resistance of certain
tissues such as fasciae, muscles and bone.
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Definition
DEFINITION:
Shapiro defined fascial spaces as potential spaces between the
layers of fascia. These spaces are normally filled with loose connective tissues
and various anatomical structures like veins, arteries, glands, lymph nodes etc.
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 bones, muscles or fascial layers. -
Moore, 1975.
The concept of fascial spaces is based on the anatomist’s knowledge that all
spaces exist only ‘potentially’, until fasciae are separated by pus, blood, drains
or surgeon's finger.
PATHOPHYSIOLOGY OF ODONTOGENIC INFECTION:
Once an infection has passed beyond the dental apex and apical
periodontal ligament, a very localised apical osteomyelitis occurs. Bone
destruction in osteomyelitis is very similar to the process of necrosis of the
inflamed dental pulp. Essentially, as the interstitial hydrostatic pressure
increases as result of transudation of extracellular fluid, followed by exudation of
inflammatory cells, the flow of new blood into the regions is compromised. In
soft tissues, the increased interstitial pressure is relieved by swelling. When the
soft tissues are contained within an unyielding mineralised structure, such as
medullary spaces of bone or the pulp canal, the increased pressure cannot be  
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Pathophysiology of Odontogenic Infection
relieved. Therefore, the pulpal or medullary soft tissues die as a result of
ischemia. Tissue breakdown products recruit circulating macrophages and
histiocytes by the process of chemotaxis. As mineralised tissue is encountered
these circulating macrophages coalesce and differentiate into osteoclasts and
resorb mineralised bone.
The process of bone necrosis and resorption expands in a roughly
spherical pattern until a bony cortex is reached. At this point, the process of
bone resorption is slowed by the densely mineralised tissue, thus changing the
shape of the bony cavity that is produced. When the bony cortical layer finally is
breached the infectious process then may enter the soft tissues.
The invading bacterial pathogens that trigger this autolytic
inflammatory process persist throughout its extent. Not only can they spread the
inflammatory process by continued antigen production, but they also can cause
direct destruction. Streptococci, commonly found in the early stages of infection,
can invade tissues by the elaboration of their hyalurodinases, which breakdown
the extracellular glycoproteins of connective tissue.
As the streptococci flourish in their exponential growth phase,
they create an environment conducive to the subsequent growth of the
anaerobic flora of odontogenic infections. They consume the local oxygen
supplies and metabolise nutrients to create a more acidic environment. They
also may produce essential nutrients for the anaerobes present after
about 3 days of clinical symptoms. The anaerobes, including Prevotella and
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Pathophysiology of Odontogenic Infection
Porphyromonas spp., produce collagenase, which destroy collagen, the most
plentiful extracellular matrix protein of connective tissue. As the infection
perforates the bony cortical plate, the process of bacterial inoculation, followed
by the inflammation and necrosis, begins anew in the soft tissues. The most
vulnerable tissue is the areolar tissue that is not well vascularised. It is loose
and easily dissected by relatively low hydrostatic pressures. Thus the spreading
of infection follows the path of least resistance, deflected by denser and better
vascularised structures such as muscle, fascia, organs and bone.
PATHWAYS OF DENTAL INFECTION:
The narrow pulpal foramen at the root apex, although of insufficient
diameter to permit adequate drainage of infected pulp, does serve as a
reservoir of bacteria and permits egress of bacteria into periodontal tissue and
bone. This access explains the occasional problems when antibiotics are alone
used to treat draining fistulas from abscessed teeth. Once the drainage ceases
the bacteria harboured in the pulp chamber subsequently repopulate the
periapical tissues from the untreated pulp, thus reinitiating the infection. Serious
dental infection, spreading beyond the socket, is more commonly the result of
pulpal infection than of periodontal infection. Once infection extends past the
apex of the tooth, the pathophysiological course of a given infectious process
can vary, depending on the number and virulence of the organism, host
resistance, and anatomy of the involved area.
If the infection remains localised at the root apex, a chronic periapical
infection may develop. Frequently, sufficient destruction of bone develops to  

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Pathways of Odontogenic Infection
create a well corticated radiolucency observable on dental radiographs. This
process represents a focal bone infection, “garden variety” radiolucencies
associated with carious teeth should not be confused with true osteomyelitis.
Once infection extends beyond the root apex, it may proceed into
deeper medullary spaces and evolve into widespread osteomyelitis. More
commonly, these processes form fistulous tracts through alveolar bone and exit
into the surrounding soft tissue. This phenomenon is often associated with
sudden soft tissue swelling and a reduction in intrabony pressure, resulting in
lessening of pain. The fistula may penetrate the mucosa or skin, and thus serve
as a natural drain for the abscess.
Once beyond the confines of the dentoalveolar bone, infection may
localise as an abscess or spread through soft tissue as cellulitis or both.
Staphylococci frequently are associated with abscess formation. These
microorganisms produce coagulase, an enzyme that can cause fibrin
deposition in citrated or oxalated blood. Streptococci are associated more
often with cellulitis because they produce enzymes such as streptokinase
(fibrinolysin), hyaluronidase, and streptodornase. These enzymes breakdown
fibrin and connective tissue ground substance, and lyse cellular debris, thus
facilitating rapid spread of the bacterial invaders. Oral infections frequently are
composed of mixed flora, or the bacteria behave in untraditional fashion. Thick
walled abscesses, with little or no blood supply to their lumen, respond slowly or
poorly to antibiotic therapy, whereas cellulitis usually responds well without
surgical drainage.  
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Stages of Infection
STAGES OF INFECTION:
The stages of infection can be divided into inoculation, cellulitis and
abscess based on the inflammatory tissue destructive events.
Initially the inoculation stage is caused by the early spread, probably of
streptococci, into the soft tissues. This stage can be recognised as soft, doughy,
mildly tender soft tissue swelling with little redness.
During the cellulitis stage, the process of inflammation is paramount, resulting
in a deeply reddened, hard, exquisitely painful swelling with loss of function,
such as truisms or the inability to protrude the tongue.
During the third stage, abscess formation, necrosis predominates. A central
softening of the cellulitic region, which may become fluctuant, is present. The
fluid wave is caused by the flow of pus within the abscess cavity.
The final stage in odontogenic infections is resolution, which occurs after
spontaneous or therapeutic drainage. The stages of infection can be used as a
conceptual framework to understand the progression of untreated severe
odontogenic infections through anatomical deep fascial spaces of head and
neck. For example, if a virulent odontogenic infection originating in a lower
molar has flourished in the submandibular space, producing an abscess, it may
have progressed through the inoculation stage to the cellulitis stage in the
neighbouring lateral pharyngeal space. The retropharyngeal area might have
already been inoculated by bacteria carried along the advancing front of
inflammatory oedema.
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Stages of Infection
Characteristic Inoculation Cellulitis Abscess

Duration 0-3 days 3-7 days >5 days
Pain Mild-moderate Severe and Moderate-severe
generalised & generalised
Size Small Large Small
Localisation Diﬀuse Diﬀuse Circumscribed
Palpation Soft, doughy, Hard, tender Fluctuant, tender
tender
Appearance Normal colour Reddened Peripherally
reddened
Skin quality Normal Thickened Undermined &
shiny
Surface Slightly heated Hot Moderately
temperature heated
Loss of function Minimal or none Severe Moderately
severe
Tissue fluid Edema Serosanguineous Pus
Levels of malaise Mild Severe Moderate-severe
Severity Mild Severe Moderate-severe
Percutaneous Aerobic Mixed Anaerobic
bacteria
Stages of infection 
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Spread of orofacial infection
SPREAD OF OROFACIAL INFECTION:
The routes by which the infections can spread are:
• By direct continuity through the tissues,
• By lymphatics to the regional lymph nodes and eventually into the blood
stream. When the infection gets established in the lymph nodes, secondary
abscesses may develop. The spread of infection from the lymph nodes
into the tissues in secondary areas of cellulitis or tissue space abscess.
• By the bloodstream: Rarely, local thrombophlebitis may propagate along
the veins, entering the cranial cavity via emissary veins to produce
cavernous sinus thrombophlebitis. The micro-organisms or infected emboli
may get swept away into the bloodstream, leading to bacteremia,
septicaemia, or pyemia with the development of embolic abscess.
FACTORS INFLUENCING SPREAD:
Some infections progress more rapidly into deep fascial spaces than others.
This may be because of: (A) General factors, and (B) Local factors.
A. General factors:
It includes - (a) host’s resistance or immunocompetence of the host, and (b)
virulence of microorganisms; and (c) combination of both.
(a) Host resistance: It depends upon: (i) Humoral factors and (ii) cellular
factors.
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• Humoral factors involve immunoglobulins derived from B lymphocytes or

plasma cells and complement.
• Cellular factors include polymorphonuclear leukocytes, monocytes,

lymphocytes, and tissue macrophages.
(b) Virulence of micro organisms: It is determined by invasiveness of the
causative microorganisms. These include production of lytic enzymes, potent
endotoxins and exotoxins and interference with or resistance to host and
humeral and cellular defences.
Rapid progression of infection occurs in necrotising fascitis, especially in
immuno-compromised host, particularly when virulent strains of beta-haemolytic
streptococci are involved.
(c) Compromised host defences:
• Uncontrolled metabolic diseases, such as, uraemia, alcoholism,

malnutrition, severe diabetes.
• Suppressing diseases: Leukemia, lymphoma, malignant tumors.
• Suppressing drugs: Cancer chemotherapeutic drugs, immunosuppressive

drugs. 
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B. Local factors:
Once the balance between host resistance and bacterial pathogenicity is lost in
favour of invading organisms, then the spread of infection progresses. The
following are the barriers:
Intact anatomical barriers:
• Alveolar bone: It is the first locally limiting barrier to further spread of a

periapical infection. As the infection progresses within the bone, it spreads in
the radial manner and extends to the cortical plates. The site of perforation of
the cortex is dependent upon proximity of the root apices to alveolar process.
• Periosteum: It is the next local barrier. This structure is better developed in

mandible; and hence can delay further spread leading to development of a
subperiosteal abscess. It does not provide much resistance and infection
spreads into adjacent surrounding soft tissues.
• Adjacent muscles and fascia: It is the next site of localisation.
The final outcome of spread depends on the host’s defense mechanisms.
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Classification of Fascial Spaces
CLASSIFICATION OF FASCIAL SPACES:
A. Based on the mode of involvement:
• Direct involvement:
Primary spaces - maxillary spaces and mandibular spaces
• Indirect involvement:
Secondary spaces
 
B. Spaces involved in odontogenic infections:
• Primary maxillary spaces:
- Canine
- Buccal
- Infra temporal spaces
• Primary mandibular spaces:
- submental
- buccal
- submandibular
- sublingual
• Secondary fascial spaces:
- masseteric
- pterygo-mandibular
- superficial and deep temporal

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Classification of Fascial Spaces
- lateral pharyngeal
- retro-pharyngeal
- pre vertebral space
- parotid space
C. Based on clinical significance:
• Face:
- buccal
- canine
- masticatory
- parotid
• Supra hyoid:
- sub lingual
- sub mandibular (submaxillary, submental)
- pharyngo-maxillary (lateral pharyngeal)
- peri-tonsillar
• Infra hyoid:
- antero-visceral (pre-tracheal)
• Spaces of total neck:
- retro-pharyngeal
- space of carotid sheath
- danger space. 
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Anatomy of Fascial Spaces
ANATOMY:
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 movements, such as muscles and glands, and serve as pathways for the
course of vascular and neural structures.
The fascia of head
and neck comprise
of outer superficial
fascia and inner
deep cervical fascia.
Superficial and deep cervical fascia
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 which comprise the 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.
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DEEP CERVICAL FASCIA:
Deep cervical fascia is divided into anterior, middle and posterior layers.
A. Anterior layer
1. Investing fascia (over the neck)
2. Parotidomasseteric
3. Temporal
B. Middle layer
1. Sternohyoid-omohyoid division
2. Sternothyroid-thyrohyoid division
3. Visceral division
a) Buccopharyngeal
b) Pre tracheal
c) Retropharyngeal
C. Posterior layer
1. Alar division
2. Prevertebral division
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A. ANTERIOR LAYER:
The anterior layer of the deep cervical fascia is also called the
superficial or investing layer. The anterior layer encircles the neck, splits to
surround the sternocleidomastoid and trapezius muscles, and attaches
posteriorly to the spinous process of the cervical vertebrae. It forms the
superficial border of the submandibular space and splits to form the capsule of
the submandibular gland. As the anterior layer approaches the inferior border of
the mandible, it fuses with the periosteum of the horizontal ramus of the
mandible.
Over the ascending ramus of the mandible it splits to surround the
muscles of mastication, thus forming the masticator space. Superficially the
anterior layer is called the parotidomassetric fascia in this region because it
covers the superficial surface of masseter muscle anteriorly and splits to
surround the parotid gland posteriorly.
Deep cervical fascia
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On the medial side of the ascending ramus of the mandible, it
covers the medial side of the medial pterygoid muscle and attaches to the base
of the skull at the sphenoid bone and pterygoid plates. At the zygomatic arch,
the anterior layer of the deep cervical fascia fuses with the periosteum of the
arch and then rises superiorly to cover the superficial surface of the temporalis
muscle. It attaches to the cranium, terminating at the superficial temporal crest.
Above the zygomatic arch, the temporal fascia divides into 2 layers, between
which is the temporal fat pad, an extension of the buccal fat pad. Similarly the
anterior layer splits at about 2 cm above the manubrium of the sternum to form
the supra-sternal space of Burns, which contains only areolar connective tissue.
It follows the rule of 2, i.e., it splits to surround 2 muscles, SCM and Trapezius;
surrounds 2 glands, submandibular and parotid glands; and forms 2 spaces,
supra-sternal and supra-clavicular spaces.
B. MIDDLE LAYER:
The middle layer of the deep cervical fascia can be divided into three
divisions. The first two are the sternohyoid-omohyoid and the sternothyroid-
thyrohyoid divisions, which comprise the muscular layer. These two divisions
surround the corresponding strap muscles of the neck between the hyoid bone
and the clavicle.
The primary significance of these layers is that they must be divided
in the midline in a surgical approach to the trachea or thyroid gland. They
usually are not involved in the head and neck infections because they do not lie
on the major routes that an orofacial infection may follow to the mediastinum or
chest wall.
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Visceral division of deep cervical fascia
The third division of the middle layer of the deep cervical fascia is
clinically significant. Below the hyoid bone, the visceral division surrounds the
trachea, oesophagus, and thyroid gland. Above the hyoid bone, the visceral
fascia wraps around the lateral and posterior sides of the pharynx, lying on the
superficial (toward the skin) side of the pharyngeal constrictor muscles. In this
region, it is also called the buccopharyngeal fascia. The important deep neck
spaces (i.e., the retropharyngeal, lateral pharyngeal and pretracheal spaces) all
lie on the superficial side of the visceral division of the middle layer of the deep
cervical fascia.
C. POSTERIOR LAYER:
The posterior layer of the deep cervical fascia has two divisions, the
alar and the pre vertebral. The alar fascia passes through the transverse
processes of the vertebrae on either side, posterior to the retropharyngeal
fascia.
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Posterior layer of deep cervical fascia
In the vertical dimension, the posterior layer extends from the base of
the skull to the diaphragm. The alar fascia fuses with the retropharyngeal fascia
at a variable level between the sixth cervical (C6) and the fourth thoracic (T4)
vertebrae. This fusion forms the bottom of the retropharyngeal space. Infections
of the retropharyngeal space may rupture the alar fascia, thus entering the
danger space, which is continuous with the posterior mediastinum.

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The pre vertebral fascia surrounds the vertebrae and the attached
postural muscles of the neck and back. The pre vertebral fascia lies just anterior
to the periosteum of the vertebrae, and infections of the vertebrae, such as
tuberculous osteomyelitis, may enter the pre vertebral space. The pre vertebral
space usually is not invaded by infections arising in the maxillofacial regions.
CAROTID SHEATH:
Carotid sheath and its contents
Controversy exists as to which of the deep cervical fascia contribute to
the carotid sheath. Some believe that the carotid sheath is formed from the alar
division of the posterior layer of the deep cervical fascia whereas others
attribute formation of this important structure to all the three layers of the deep
cervical fascia.
The carotid sheath begins at the origin of the carotid artery in the superior
mediastinum and passes through the pre tracheal space in an upward and
posterior direction. Above the hyoid bone, it lies at the junction of the lateral
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pharyngeal and retropharyngeal spaces. The carotid sheath terminates at the
jugular foramen and the 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.
NUMBERED SPACES OF GRODINSKY AND HOLYOKE:
In their landmark article of 1938 in which they described the deep
fascial spaces of head and neck, Grodinsky and Holyoke used numbers to
indicate various deep neck spaces.
Grodinsky and Holyoke Spaces (1938)
Space 1 lies superficial to the superficial fascia and is therefore synonymous
with the subcutaneous space.
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Space 2 is a group of spaces surrounding the cervical strap muscles, lying
superficial to the sternothyroid-throhyoid division of the middle layer of the deep
cervical fascia, or between the sternothyroid-thyrohyoid division and
sternohyoid-omohoid division.
Space 3 is the potential anatomical space lying superficial to the visceral
division of the middle layer of the deep cervical fascia. Space 3 contains the
pretracheal, retropharyngeal and lateral pharyngeal spaces.
Space 3A is the space of the carotid sheath.(Lincoln’s highway by Mosher)
Space 4 is the potential space that lies between the alar and pre vertebral
divisions of the posterior layer of the deep cervical fascia; this is also called as
danger space.
Space 4A is in the posterior triangle of the neck, posterior to the carotid sheath.
Space 5A is enclosed by the pre vertebral fascia, posterior to the transverse
processes of the vertebrae, as it surrounds the scalene and spinal postural
muscles. 
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Primary Maxillary Space Infections
MAXILLARY SPACE INFECTIONS:
CANINE SPACE:
Canine space is also known as infraorbital space. Contents of the canine
space include angular artery and vein, infraorbital nerve. The neighbouring
space is the buccal space.
BOUNDARIES:
• Quadratus labii superioris muscle defines the infraorbital space.
• Anterior: Nasal cartilages
• Posterior: Buccal space
• Superior: Quadratus labii superioris muscle
• Inferior: oral mucosa

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• Superficial: Quadratus labii superioris muscle
• Deep: Levator anguli oris
Canine fossa involvement with infection from dental origin leads to
canine space infection. Maxillary anterior teeth - canines and premolar infection
usually involve the infraorbital space. Sometimes mesiobuccal root of first
molars also cause canine space infection.
Infections of maxillary canine usually appear as labial swelling and
less as palatal swelling. The levator muscle lies over the apex of the canine
root, originating high in the canine fossa of the maxillary wall and inserting in the
angle of mouth.If the canine infection perforates the lateral cortex of maxillary
bone, superior to the origin of the elevator angle oris muscle, the canine space
is involved, filling the space between levator anguli oris and levator labii
superioris. Spontaneous intraoral drainage of the infraorbital space may be
delayed because an abscess in this region must pass around levator anguli oris
to reach vestibular space and the oral mucosa. Alternatively, infraorbital space
infections burrow toward skin on either side of quadratus labii superioris,
pointing through medial or lateral aspect of the lower eyelid.
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CLINICAL FEATURES:
Marked cellulitis of the cheek and upper lip, lateral to the nose is
seen causing obliteration of the nasolabial fold. Drooping of the angle of mouth
is seen. Marked cellulitis of the eyelids and periorbital area is present, forcing
the eyelid to close. Redness and marked tenderness of facial tissues. Offending
tooth is mobile and tender to percussion. In chronic stages, chronic fistula forms
in the cleft area between levator labii superioris alaque nasi and zygomaticus
minor muscles near the medial canthus of the eye.
MANAGEMENT: INCISION AND DRAINAGE.
Drainage best accomplished by an intraoral approach. The
approach is through the mucosa of buccal vestibule in the region of lateral
incisor and canine. A curved mosquito forceps is inserted superior to the
attachment of caninus muscle, and infraorbital space is entered. Pus is
evacuated and a drain is inserted and is secured with a suture.

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COMPLICATIONS OF CANINE SPACE INFECTION:
Cavernous Sinus Thrombosis:
Cavernous sinus thrombosis is a rare but dreaded
complication, caused by ascending thrombophlebitis of the angular vein, which
passes through the infraorbital space. Facial veins are generally valveless, thus
allow bidirectional flow. Septic thrombophlebitis of angular vein may ascend to
the cavernous sinus through the inferior ophthalmic vein, which passes through
the orbit. Cavernous sinus infection, ascending from maxillary teeth, upper lip,
nose or orbit through the valveless anterior and posterior fascial veins, carries
an extremely high mortality rate.
BUCCAL SPACE:
Buccal space is the potential space between buccinator and masseter
muscle. Contents of the buccal space are parotid duct, anterior facial artery and
vein, transverse facial artery and vein, buccal fat pad. Neighbouring spaces of
the buccal space are infraorbital, pterygomandibular and infratemporal spaces.
It communicates with submasseteric space superficially and
posteriorly; medial side of mandible-with pterygomandibular space inferiorly and
infratemporal space superior to the lateral pterygoid; posteriorly with lateral
pharyngeal space.
BOUNDARIES :
Anterior: Angle of mouth
Posterior: Masseter muscle, pterygomandibular space

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Superior: Maxilla, infraorbital space
Inferior: Mandible
Superficial: Subcutaneous tissue and skin
Deep: Buccinator muscle.
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BUCCAL SPACE INFECTION:
Maxillary and mandibular premolars and molars drain in lateral and
buccal direction. Relation of the root apices to origin of the buccinator muscle
determines whether the infection exits intraorally in the buccal vestibule or
extend deep into the buccal space. Molar infections exiting superiorly to the
maxillary origin of the muscle or inferiorly to the mandibular origin of the muscle
enter the buccal space. Involvement of buccal space usually results in swelling
below the zygomatic arch and above the inferior border of mandible. Thus both
the zygomatic arch and the inferior border of mandible are palpable in buccal
space infections.
CLINICAL FEATURES:
Marked cheek swelling associated with a diseased molar or premolar is
seen. When pus accumulates on oral side of the muscle, ’Gum boil’ is seen in
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the vestibule. If pus accumulates lateral to the muscle, prominent extraoral
swelling is seen extending from lower border of mandible to the infraorbital
margin and from the anterior margin of masseter muscle to the corner of mouth.
Sometimes edema of lower eyelid is seen.
SPREAD:
Infection from the buccal space spreads via pterygomandibular space
to the infra temporal space along the fascia, accompanying the Stenson’s duct.
It also spreads to submasseteric space if infection tracks backwards and
penetrates the parotidomasseteric fascia.
INCISION AND DRAINAGE:
Extraoral:
When fluctuance occurs, cutaneous drainage should be performed
inferior to the point of fluctuance with blunt dissection into the depth and
extreme boundaries of the space. Branches of facial nerve should be avoided.
Aspiration of this space is done usually.
Intraoral :
Horizontal incision through 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 curved
mosquito forceps to enter the buccal space.
Drain is placed and secured with suture.

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DIFFERENTIAL DIAGNOSIS:
• Buccal cellulitis: It is caused by Haemophilus influenza. It is seen in infants

and children younger than 3 years which is characterised by high fever at
least 24 hrs before appearance of clinical signs.
• Erysipelas: Rapid onset of dark red swelling associated with otitis media
frequently.
• Crohn’s disease: Recurrent buccal abscesses can occur as a complication

of Crohn’s disease. It is a segmental transmural disease with intermittent
abdominal pain, fever, weight loss and diarrhoea and is characterised by
inflammatory granulomas present over the length of GIT from mouth to anus.
Granulomatous lesions and ulcerations of buccal mucosa can progress to
true buccal space abscesses.
INFRATEMPORAL SPACE:
Infection involves the infratemporal fossa space. Infra temporal space is
also known as retrozygomatic space (by Sicher), as it is partly situated behind
the zygomatic space. The space lies posterior to the maxilla. Laterally, it is
continuous with the deep temporal space. It continuous with the upper part of
pterygomandibular space anteriorly, separated posteriorly by lateral pterygoid
muscle, thereby forming the upper extremity of pterygomandibular space.
BOUNDARIES:
Anterior: Infratemporal surface of maxilla.
!32
Posterior: parotid gland.
Superior: Infratemporal surface of greater wing of sphenoid & by zygomatic
arch.
Inferior: Lateral pterygoid muscle forming the floor of fossa, demarcating
pterygomandibular and infra temporal spaces.
Lateral: Ramus of mandible, temporalis muscle and its tendon.
Medial: Medial pterygoid plate, lateral pterygoid muscle, medial pterygoid
muscle, lower part of temporal fossa of the skull and lateral wall of pharynx.
!33
CONTENTS OF INFRA TEMPORAL FOSSA:
Infra temporal fossa contains the origins of medial pterygoid and
lateral pterygoid muscles. It also contains the pterygoid venous plexus, internal
maxillary artery and vein, mandibular nerve and middle meningeal artery.
INVOLVEMENT:
Buccal roots of maxillary 2nd and 3rd molars, particularly unerupted 3rd
molars are the direct causes for infra temporal space involvement. Local
anaesthesia injections with contaminated needles in the area of tuberosity.
Spread of infection from other spaces.
CLINICAL FEATURES:
• Extraoral:
Trismus is the classic feature of the infra temporal swelling. Bulging of
temporalis muscle is seen with marked swelling of the face on the affected side
in front of ear, overlying the area of TMJ, behind the zygomatic process. Eye is
often closed and is proptosed on the affected side because of the edema
accumulation on that side.
• Intraoral:
Intraorally, swelling is seen in the tuberosity area. Elevation of body
temperature upto 104 ℉ is observed.
!34
• Intraorally:
If trismus is not marked, and fluctuation is detected early, an intraoral
incision is given buccal vestibule opposite the second and third molars. The
exploration is carried out medial to coronoid process and temporalis muscle
upwards and backwards with a sinus forceps, or a curved haemostat. The
space is entered and drained; and a small piece of corrugated rubber drain is
placed and secured to the mucosa with a suture.
!35
• Extraorally:
In severe intractable infection, extraoral incision is only method of
drainage. Incision is made at the upper and posterior edge of temporals muscle,
within the hairline. A sinus forceps is then directed upwards and medially. Pus is
excavated; rubber drain inserted and secured with a suture.
COMPLICATIONS:
Infection of infra temporal space should be considered a serious event
because of proximity of pterygoid plexus of veins, from which infection can track
upwards to the cavernous sinus via: deep facial veins; emissary veins; and via
other foramina directly from infra temporal fossa to the middle cranial fossa. 
!36
Primary Mandibular Space Infections
PRIMARY MANDIBULAR SPACES:
SUBMENTAL SPACE:
The submental space lies below the chin, in the anterior aspect of mandible.
BOUNDARIES:
Anterior: Inferior border of
mandible
Posterior: Hyoid bone
Superior: Mylohyoid muscle
Inferior: Investing fascia
Superficial: Investing fascia
Lateral: Anterior bellies of digastric muscles.
CONTENTS:
The contents of the submental space are anterior jugular vein and
submental lymph nodes.
NEIGHBOURING SPACES:
The neighbouring spaces of the submental space is the
submandibular space on either side of it.
!37
INVOLVEMENT:
Lower anteriors are the most common cause of submental space
infection. Infection resulting from the fracture of symphysis also involves
submental space. Spread of infection from submandibular space is also a
common cause of submental space involvement.
CLINICAL FEATURES:
Extraoral:
Distinct, firm, erythematous swelling is seen in midline below the
anterior border of the mandible. Skin overlying the swelling is board-like and
taut. Fluctuation may be present.
INTRAORAL:
Anterior teeth are either nonvital, fractured or carious.
Offending tooth may exhibit tenderness to percussion and may show mobility.
Considerable discomfort on swallowing is observed.

!38
SPREAD:
The infection from the submental space moves posteriorly to involve
submandibular space. It may discharge on the face in the submental region.
Horizontal incision in the most inferior portion of chin provides
dependent drainage. Kelly’s forceps or sinus forceps is inserted through the
incision, upward and backward. Small piece of drain is inserted in the abscess
cavity, and is secured to one of the margins with a suture.
SUBMANDIBULAR SPACE:
Grodinsky and Holyoke used the term submandibular space to
describe all the peri-mandibular spaces, which are now described separately as
submandibular, submental and sublingual spaces.
!39
The submandibular space lies between the anterior and
posterior bellies of digastric muscles, in the inferior border of the mandible.
Mylohyoid muscle separates the sublingual space above, from the
submandibular space below, attaching to the lingual surface of the mandible
BOUNDARIES:
Anterior: Anterior belly of digastric muscle.
Posterior: Posterior belly of digastric muscle, stylohyoid muscle,
stylopharyngeus muscle.
Superior: Inferior and medial surfaces of mandible.
Inferior: Digastric tendon.
Superficial: Platysma muscle, investing fascia.
Deep: Mylohyoid, hypoglossus, superior constrictor muscles.
!40
CONTENTS:
The contents of the submandibular space are submandibular gland,
submandibular lymph nodes, facial artery and vein.
The neighbouring spaces of the submandibular gland are sublingual,
submental, lateral pharyngeal, buccal spaces.
INVOLVEMENT:
Lower molars are the most common causes of the submandibular
space infection. Spread of infection from submandibular gland also involves the
submandibular space. Spread of infection from submental space, sublingual
space also involves the submandibular space.
CLINICAL FEATURES:
• Extraoral:
Firm swelling in the submandibular region below the inferior border of
mandible is observed along with tenderness of swelling and redness of
overlying skin.
• Intraoral:
Diseased molars tender to percussion can be observed. Dysphagia
and moderate trismus are associated with submandibular space infection.
!41
MANAGEMENT:
Surgical drainage, antibiotics, and definitive care of the primary
dental infection. Incision is performed through the skin below and parallel to the
inferior border of mandible.
Blunt dissection is carried to depths of space extending to
anterior and posterior margins. Deep abscess loculations should be entered
with a small closed clamp, probing in all directions while attempting to avoid
damage to the submandibular gland, the facial artery, and the lingual nerve. The
contralateral space should not be entered unless it is involved in infection; if
necessary, however a through-and-through drain can be placed into both the
sides, as in Ludwig’s angina.
!42
SPREAD:
Infection from submandibular space infection speeds into submental
space due to lack of major anatomical barriers. Spread to submandibular space
on contralateral side occurs due to the same. It also spreads to sublingual
space via the posterior border of mylohyoid muscle and spreads backwards to
involve para-pharyngeal spaces.
Differential diagnosis should include acute sialadenitis, sublingual
trauma or foreign body, and submandibular lymphadenitis. These may produce
a secondary overlying cellulitis that further confuses the diagnosis.
SUBLINGUAL SPACE:
Sublingual space is the V-shaped trough lying lateral to muscles of
tongue. It is a paired space which communicates anteriorly with the submental
space.
BOUNDARIES:
Anterior: Lingual surface of mandible.
Posterior: Submandibular space.
Superior: Oral mucosa.
Inferior: Mylohyoid muscle.
Medial: Muscles of tongue.
Lateral: Lingual surface of mandible.
!43
CONTENTS:
The contents of the sublingual space are the sublingual glands,
Wharton’s ducts, lingual nerve, sublingual artery and vein.
The neighbouring spaces of sublingual spaces are submandibular,
submental, lateral pharyngeal, visceral (trachea and oesophagus) spaces.
!44
INVOLVEMENT:
Infection of the sublingual space is most frequently from the lower
premolars, molars (especially the first molar). Direct trauma to the sublingual
region of mandible can also involve the sublingual space. Spread of infection
from surrounding submental and submandibular spaces are also frequent.
CLINICAL FEATURES:
• Extraoral:
Extraorally, little or no swelling is seen. Lymph nodes may be
enlarged and tender. Pain and discomfort on deglutition is observed. Speech
may be affected.
• Intraoral:
Brawny, erythematous, tender swelling of the floor of the mouth,
beginning close to the mandible and spreading toward the midline or beyond is
observed. Elevation of the tongue and floor of the mouth is raised, leading to
airway obstruction.Tongue protrusion beyond
the vermilion border of the lip will be affected.
• Intraorally:
An incision is given through the mucosa parallel to Wharton’s duct
bilaterally. Sinus forceps is then inserted and opened to evacuate the pus.
!45
• Extraorally:
When both the submental and sublingual spaces contain pus, they
can be drained via a skin incision placed in the submental region, pushing a
closed sinus forceps through the mylohyoid muscle.
Similarly, when the submandibular space is involved, sublingual
space can be accessed by an incision in the skin overlying the submandibular
space, via the submandibular space.
SPREAD:
The infection from sublingual space crosses midline and affects the
space on opposite side. It may also involve the submandibular space via the
posterior border. Submental space can be involved inferiorly. Lateral pharyngeal
space can be involved via the bucco-pharyngeal gap.
Cellulitis accompanying impacted sialolith in Wharton’s duct.
Radiographs of teeth and occlusal films of the floor of the mouth should be used
in diagnosis.
!46
Secondary Fascial Spaces
SECONDARY FASCIAL SPACES:

MASTICATORY SPACES:
Masticatory space is an anatomical compartment enclosed by splitting
of the anterior layer of the deep cervical fascia around the muscles of
mastication, following those muscles to their attachments to the cranium and
skull base. Infections generally affect discrete portions of the masticatory space
like the submasseteric space, pterygomandibular, superficial temporal and deep
temporal spaces.
The masticatory space as a whole is bound by fascia, contains the
muscles of mastication and the internal maxillary artery and the mandibular
nerve. It communicates freely with buccal, submandibular and parapharyngeal
spaces. Swelling may not be the prominent sign in masticatory space infections,
because infectious process exists deep to large muscle masses that obscure
much observable swelling.
Surgical access to the various compartments of masticator space is
complicated by the containment of the infectious process by the muscle
masses. Although drainage of entire masticator space from the intraoral space
is possible and occasionally practical, access from an extraoral incision is
easier technically and more prudent. Sichers’ suggested an intraoral approach
to all compartments via incision along pterygomandibular raphe (less feasible in
infectious patient with trismus). Oral approach could compromise the airway
postoperatively because of persistent bloody or purulent oozing and intraoral
drains may be difficult to maintain and can be aspirated if loosened
inadvertently.
!47
!48
SUBMASSETERIC SPACE:
The submasseteric space lies between anterior layer of deep cervical
fascia, locally referred to as parotidomasseteric fascia, and the lateral surface of
ascending ramus of mandible.
BOUNDARIES:
Anterior: Buccal space.
Posterior: Parotid gland.
Superior: Zygomatic arch.
Inferior: Inferior border of mandible.
Medial: Ascending ramus of mandible.
Lateral: Masseter muscle.
CONTENTS:
The contents of the submasseteric space are masseteric artery and
vein.
Sub-masseteric spaces communicates freely with buccal,
pterygomandibular, superficial temporal, parotid spaces.
INVOLVEMENT:
Infections from the lower third molars, fracture of angle of mandible
frequently involve the sub-masseteric space. Contaminated mandibular block
!49
anaesthetic injections also cause infection. Spread from nearby contiguous
spaces; trauma/surgery through or near muscles is seen. As a complication of
circumzygomatic wiring for mid face trauma, this space may be involved.
CLINICAL FEATURES:
Inflammation and edema of overlying masseter muscle is observed with
tenderness over the angle of the mandible. Inflammatory process results in
significant trismus, hallmark of this condition, exception in immunosuppressed
patients, who may not exhibit the classic signs of inflammation or the unique
signs of deep space infection. Submasseteric swellings can be differentiated
from parotid swellings, as they obscure the ear lobe whereas the parotid
swellings elevate it.
• Intraoral:
Incision is made vertically over the lower part of anterior border of the ramus of
the mandible, deep to the bone. A sinus forceps are passed along the lateral
surface of the ramus downwards and backwards and the pus is drained; drain
inserted and secured with suture.

!50
• Extraoral:
When the mouth cannot be opened, an
incision is placed in the skin behind the angle
of the mandible to open the abscess by
Hilton’s method. A rubber drain is inserted
and secured in position with a suture.
Dressing applied.
PTERYGOMANDIBULAR SPACE:
Pterygomandibular space is the most frequently affected anatomical
compartment.
BOUNDARIES:
Anterior: Buccal space.
Posterior: Parotid gland.
Superior: Lateral pterygoid
muscle.
Inferior: Inferior border of
mandible.
Medial: Medial pterygoid
muscle.
Lateral: Ascending ramus of mandible.
!51
CONTENTS:
The contents of the pterygomandibular space include mandibular division of
trigeminal nerve, inferior alveolar artery and vein.
Pterygomandibular space communicates with buccal, lateral pharyngeal,
submasseteric, deep temporal, parotid spaces.
INVOLVEMENT:
Infection of the pterygomandibular space can be from lower third
molars, fracture of angle of mandible, infection from contaminated needles used
for inferior alveolar nerve block.
CLINICAL FEATURES:
Little extraoral swelling is seen in pterygomandibular space infections.
Trismus, caused by edema and inflammation of the medial pterygoid muscle,
hinders the view of the swollen anterior tonsillar pillar and the deviation of the
uvula to the opposite side. Dysphagia is present. Edema of soft palate present.
Tenderness can be elicited over the area of swollen soft tissues medial to
anterior boxer of ramus of mandible.
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.
!52
• Intraoral:
A vertical incision approximately, 1.5 cm in length,
is made on the anterior and medial aspect of the
mandible. A sinus forceps is placed in the abscess
cavity, opened and closed and withdrawn. Pus is
evacuated; drain placed and secured.
• Extraoral:
An incision is made on the skin below the angle of mandible. A sinus forceps is
inserted towards the medial side of the ramus in an upward and backward
direction. Pus is evacuated and drain inserted and secured.
SPREAD:
Infection from pterygomandibular space spreads along the medial surface of
ramus to involve infra temporal fossa and beneath the temporal fascia;
posteriorly to the lateral pharyngeal space and then to the retropharyngeal
space; spreads around the front of the ramus to involve the buccal space;
spreads around the front of the ramus extending anteroinferiorly below the
lower border and under the superior constrictor to involve the submandibular
space.
!53
TEMPORAL SPACES:
SUPERFICIAL TEMPORAL SPACE:
Superficial temporal space lies between the temporal fascia, which is the
continuation of parotidomasseteric fascia, and the temporalis muscle.
BOUNDARIES:
Anterior: Posterior surface of lateral orbital rim.
Posterior: fusion of temporal fascia with the pericraniums at the posterior edge
of temporalis muscle.
Inferior: Zygomatic arch and areolar connective tissue medial to it.
!54
CONTENTS:
Superficial temporal space contains temporal fat pad, temporal branch of
facial nerve.
Superficial temporal space communicates with buccal, deep temporal
spaces.
INVOLVEMENT:
Infection from upper and lower molars may involve the superficial
temporal space. Buccal space infections may spread to the superficial temporal
space following the temporal fat pad.
DEEP TEMPORAL SPACE:
Deep temporal space is present deep to superficial temporal space.
BOUNDARIES:
Lateral: Temporalis muscle.
Medial: Squamous temporal bone and sphenoid bone.
Inferior: Superior surface of the lateral pterygoid muscle.
Superior and posterior: Attachment of the temporalis muscle to the cranium at
the temporal crest.
!55
Anterior: Posterior wall of the maxillary sinus, the pterygomaxillary fissure, and
the posterior surface of the orbit, including inferior orbital fissure.
CONTENTS:
Contents of the deep temporal space are the internal maxillary artery
and vein, mandibular division of trigeminal nerve.
CLINICAL FEATURES:
Pain and trismus is usually present. Swelling over temporal region may
or may not be present.
Extraoral incision in temporal region, well above the hairline, 45º to
zygomatic arch. The haemostat is inserted above and below the temporalis
muscle.
PARAPHARYNGEAL SPACES:
Paraphayngeal spaces include lateral and retro pharyngeal spaces.
These spaces form a ‘ring’ around the pharynx and together form a pathway for
spread of orofacial infections in neck and mediastinum. The parapharyngeal
spaces communicate directly with the submandibular space anteroinferiorly and
retromandibular space posteriorly. These spaces separate the muscles of
mastication from the muscles of deglutition.
!56
LATERAL PHARYNGEAL SPACE:
Lateral pharyngeal space is shaped like an inverted pyramid with its
base at the base of the skull and its apex at the hyoid bone.
!57
A short layer of fascia runs from the anterior layer of the deep cervical fascia
overlying the medial pterygoid muscle, across the styloid process and the
styloid muscles to the buccopharyngeal fascia. This fascial condensation is
called as aponeurosis of Zuckerkandl and Testut, which divides the lateral
pharyngeal space into anterior(prestyloid) and posterior (poststyloid)
compartments.
Anterior compartment has little content except areolar connective tissue.
The posterior compartment contains the cranial nerves IX, X, XI, XII, carotid
sheath and its contents, and the cervical sympathetic chain, attached to
posterior surface of the carotid sheath. These structures give rise to the
ominous clinical signs of cranial nerve and carotid sheath involvement that
occur in severe infections of the lateral pharyngeal space.
BOUNDARIES:
Anterior: superior and middle pharyngeal constrictor muscles, stylohyoid and
posterior belly of digastric muscle.
Posterior: Carotid sheath and scalene fascia.
Superior: Skull base.
Inferior: Hyoid bone.
Medial: Pharyngeal constrictors, buccopharyngeal fascia, retropharyngeal
space.
Lateral: Medial pterygoid muscle sup & anterior layer of deep cervical fascia
inferiorly
!58
CONTENTS:
Lateral pharyngeal space contains carotid artery, internal jugular vein,
vagus nerve, cervical sympathetic vein.
Lateral pharyngeal space communicates with the pterygomandibular,
submandibular, sublingual, peritonsillar, retropharyngeal spaces.
INVOLVEMENT:
Infection from the lower third molars may reach the lateral pharyngeal
space. Lateral pharyngeal space may be involved due to tonsillitis, pharyngitis,
parotitis, otitis, mastoiditis, infection from neighbouring spaces, herpetic
gingivostomatitis involving pericoronal tissue.
CLINICAL FEATURES:
Only visible swelling may be between the posterior belly of digastric and
the anterior border of SCM, just superior to the hyoid bone. On palpation, a
tender fullness of this region also suggests the correct diagnosis. Intraorally,
only mild to moderate trismus may be noted, unless the masticatory space is
involved. Palatoglossus arch is blunted on the affected side with deviation of
uvula to the unaffected side. Anterior tonsillar pillar is edematous and tender.
The patient’s head may tilt toward shoulder of unaffected side to position the
upper airway over the deviated trachea and larynx. Grave because of
generalised septicemia and respiratory compromise due to edema of the larynx.
!59
ANTERIOR COMPARTMENT:
Patient exhibits pain, fever, chills, medial bulging of the lateral
pharyngeal with deviation of the palatal uvula from the midline, dysphagia,
swelling below the mandible and usually trismus.
POSTERIOR COMPARTMENT:
Noted for absence of trismus and visible swelling, but respiratory
obstruction, septic thrombosis of the internal jugular vein, and carotid artery
haemorrhage may occur in patients at a late stage of infection.
MANAGEMENT:
Therapy consists of antibiotics, surgical drainage, and tracheostomy
if indicated. The surgical approach may be oral, by incision of the lateral
pharyngeal wall, or external, by exposure of carotid sheath near the lateral tip of
hyoid bone after retraction of the SCM. Blunt dissection along the posterior
order of the digastric muscle leads to lateral pharyngeal space.
In the combined intraoral and extra oral 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 posterior-inferior
direction; tip delivered through skin by cutaneous incision between angle of
mandible and sternocleido-mastoid muscle.
!60
SPREAD:
Infection can spread:
• Upwards through various foramina such as, foramen ovale,
foramen lacerum, and jugular foramen present at the base of the
skull, producing brain abscess, menginitis or sinus thrombosis.
• Downwards into the carotid sheath towards the mediastinum; a
pathway which Mosher called the ‘Lincoln’s highway’ of the neck.
RETROPHARYNGEAL SPACE:
Oesophagus and trachea are enclosed by middle layer of deep cervical
fascia, which extends laterally to the carotid sheath creating an anterior neck
compartment- pretracheal (previsceral) space and a posterior retropharyngeal
space(retrovisceral).
The posterior space lies behind the oesophagus and pharynx and
extends inferiorly to the upper mediastinum and superiorly to the base of the
skull. The retropharyngeal space extends vertically from the base of the skull to
the fusion of retropharyngeal fascia with the alar fascia at level between C6 and
T4 vertebrae.
BOUNDARIES:
Anterior: Superior and middle pharyngeal constrictor muscles.
Posterior: Alar fascia.
Superior: Skull base.
!61
Inferior: Fusion of alar and pre vertebral fascia at C6-T4.
Lateral: Carotid sheath and lateral pharyngeal space.
CONTENTS:
Retropharyngeal space contains areolar connective tissue and lymph
nodes that drain the adenoidal tissues of the posterior pharyngeal wall.
!62
INVOLVEMENT:
The lateral and retropharyngeal spaces contain a rich supply of lymph
nodes that drain Waldeyer’s ring. When these nodes are overwhelmed or
necrotic, a fascial space infection may develop. Retropharyngeal space
infection may also occur due to nasal and pharyngeal infections in children,
dental infections through contiguous spaces, oesophageal trauma or foreign
bodies and tuberculosis.
CLINICAL FEATURES:
Dysphagia, dyspnea, nuchal rigidity, oesophageal regurgitation, and fever
characterise infections of retropharyngeal space.
If the pharynx can be visualised, a bulging of the posterior wall may
be observed and is usually more prominent unilaterally because of the
adherence of the median raphe of the pre vertebral fascia.
If it is not treated in time, there is a risk of:
• Obstruction of the upper respiratory tract, due to displacement of the
posterior wall of the pharynx anteriorly.
• Rupture of the abscess and aspiration of pus into the lungs, with
asphyxiation resulting.
• Spread of infection into the mediastinum.
!63
MANAGEMENT:
Management of retropharyngeal space requires prompt surgical
drainage and allows little time for delay, debate, or decision by committee. For
the fear of aspiration or airway obstruction by pus pouring from the ruptured
space during passage of an endotracheal tube, tracheostomy is usually
indicated.
Drainage can be performed transorally with the patient under local
anaesthesia in the extreme Trandelenburg position and with constant
suctioning. In the transoral technique, an incision is made through the midline in
the posterior pharyngeal mucosa, and the abscess is opened by blunt
dissection.
Extraoral approach provides more dependable drainage. An incision
along the anterior border of SCM and parallel to it, inferior to hyoid bone. This
muscle and the carotid sheath are retracted laterally, and blunt finger dissection
is carried deeply. Blunt finger dissection deep to the inferior constrictor muscles
opens the retropharyngeal space abscess. Deep drains are placed and
maintained until all clinical and laboratory signs of infection are no longer
apparent.
COMPLICATIONS:
Infections of the retropharyngeal space are ominous because of their ability to
impinge on the airway directly and potential involvement of the danger space.
The alar fascia divides the retropharyngeal fascia from the danger space, once
an aggressive necrotising infection has fully distended the retropharngeal

!64
space, pressure necrosis and enzymatic destruction of the alar fascia may allow
the infection to perforate the danger space. The overall mortality rate for
retropharyngeal infections of all causes is approximately 10%.
PRETRACHEAL SPACE:
The pre-tracheal space lies in front of trachea.
BOUNDARIES:
Superior: Fusion of the visceral division and sternothyoid-thyrohyoid division.
Inferior: superior and anterior mediastinum.
Anterior: Deep surface of sternothyroid-thyrohyoid fascia
Posterior: Superficial surface of visceral fascia.
Lateral: Retropharyngeal space.
!65
As a result of dense fusion of fascial layers above the extent of this space,
infections from jaws and oral cavity usually do not descend into the pretracheal
space.
VISCERAL SPACE:
Visceral space is the space enclosed by the visceral division of
the middle layer of deep cervical fascia. It extends upto the mediastinum and
contains viscera like pharynx, larynx, trachea, oesophagus and thyroid glands.
Infections of these organs drain into the lumen of pharynx,
oesophagus, or trachea or pierce the visceral fascia anteriorly to enter the pre
tracheal space.
!66
DANGER SPACE:
The danger space is so called because of its communication with the
mediastinum. It extends from the base of the skull superiorly to the diaphragm
inferiorly. The contents of the danger space are areolar connective tissue.
In the chest, danger space is continuous with posterior mediastinum
which contains the vena-cava, aorta, thoracic duct, trachea, and oesophagus.
Therefore, infections that pass through the danger space into the mediastinum
can erode into or compress blood vessels, lower airway, and upper digestive
tracts.
CAROTID SHEATH:
The carotid sheath encloses common carotid artery, internal
jugular vein and vagus nerve. The carotid sheath space is involved by infection
from the submandibular, infra temporal and parapharyngeal spaces.
Infections that erode the carotid sheath use disruption of any of the
structures associated with it, including expanding hematoma in the neck,
bleeding episodes, variations in heart rate or speech function, or septic emboli.
!67
Complications of Space Infections
COMPLICATIONS OF SPACE INFECTIONS:

CAVERNOUS SINUS THROMBOPHLEBITIS:
INVOLVEMENT:
Cavernous sinus thrombophlebitis is a serious condition consisting
of formation of thrombus in the cavernous sinus or its communicating branches.
Infection of head, face and intraoral structures above the maxilla, particularly,
lead to this disease. There are two routes by which infection may reach
cavernous sinus.
EXTRAORAL ROUTE:
Infections from the face and lip are carried by facial and angular veins
and nasofrontal veins (danger area of the face) to the superior ophthalmic vein,
which enters the cavernous sinus through the superior orbital fissure, while in
internal system, dental infection is by the way of pterygoid plexus from the
posterior maxillary region, from here through the inferior orbital fissure into the
terminal part of the ophthalmic vein and then through the superior orbital fissure
into cavernous sinus. The infection spreading by the facial or external route is
very rapid with a short fulminating course because of the large, open system of
the veins leading directly to cavernous sinus. In contrast, infection spreading
through the pterygoid or internal route reaches the cavernous sinus only
through the small, twisting passages and has a much slower course. The other
pathway from the pterygoid plexus, is an emissary vein, which connects the
cavernous sinus with the pterygoid plexus of veins. It passes through an
opening of the base of the greater sphenoid wing, the foramen of Vesalius or
!68
through the fibrocartilage filling the foramen lacer or foramen ovale. Infection
usually involves one side initially, but can spread to the opposite side through
the circular veins.
Rapid complications and occasionally death can result, from
infections by virulent organisms from the upper part of the face, because:
• The short distance from the facial regions to the sinuses of the brain through
the superiorly draining venous system,
• Frequent and complicated anastomoses of these veins leading to direct

communications with the sinuses.
• The lack of protective valves that other venous systems of the body possess
and which factor is significantly absent in the facial vessels involved in this
complication.
!69
MICROBIOLOGY:
The various bacteria implicated are streptococci and staphylococci and some
gram negative bacteria.
CLINICAL FEATURES:
Generalised constitutional
symptoms, high fluctuating
fever, chills, rapid pulse and
sweating.
• Initial symptoms: it
presents with:
(ii) swelling of the face, with
edematous involvement of the eyelids. Pain in the eye and tenderness to
pressure;
(iii) Venous obstruction leading to marked edema and congestion of eyelids;
(iv) Pulsating exophthalmos, where carolid pulse is transmitted through
retrobulbar edema;
(v) Cranial nerve involvement: oculomotor, trochlear, abducens, ophthlamic
division of trigeminal nerve, and carotid sympathetic plexus. It results in
ophthalmoplegia, paresis or paralysis of the abducens nerve is diagnosed
by the weakness or paralysis of the lateral rectus muscle of the eye. The
weakness of the other muscles of the eye, culminates in paralysis,

!70
diminished or absent corneal reflex, ptosis and dilation of pupil, exophthalmos,
photophobia with profuse lacrimation and pain in the disturbution of the
ophthalmic division of the 5th cranial nerve.
(vi) Papilledema with multiple retinal hemorrhages, (if retina can be visualised)
and chemises, epistaxis, due to increased intracranial pressure and
decreased venous return.
• Late symptoms: if left untreated, thrombophlebitis spreads to other side,
and bilateral signs can be seen.
• Advanced stage: There may be signs of advanced toxaemia and
meningitis, producing stiffness of the neck, with positive Kernig’s sign and
Brudzinski’s signs and Biot’s respiration. Unless it is treated early, the
prognosis is poor. Septecemia with leukocytosis and severe acidosis with a
positive blood culture.
TREATMENT:
• Antibiotic therapy: IV chloramphenicol 1 g 6 holy.
• Heparinization, to prevent extension of thrombosis, heparin 20,000 units in
1,500 ml of 5% dextrose or dicoumarol 200 mg may be given orally, for the
first day, and 100 mg daily, thereafter.
• Neurosurgical consultation.
• Mannitol: it reduces edema.
• Anticoagulants: it prevents venous thrombosis.
• Surgical drainage. 
!71
LUDWIG’S ANGINA:
Ludwig’s angina is a firm, acute, toxic cellulitis of the submandibular
and sublingual spaces bilaterally and of the submental space. Ludwig’s angina
was first described by Wilhelm Friedreich von Ludwig in 1836. The term
‘Ludwig’s angina’ coined by Camerer in 1837. The three ‘fs’ associated with
Ludwig’s angina became evident even before the first written description of the
disease: it was to be feared, it rarely became fluctuant, and it often was fatal.
Ludwig’s angina is also called as Marbus strangulatorius, angina maligna,
angina ludovici, Garrotillo.
ETIOLOGY:
1. Odontogenic: cause in majority of cases.
• Acute dentoalveolar abscess - mandibular 2nd and 3rd molars.
• Acute periodontal abscess - deep abscess involve sublingual

spaces.
• Acute periocoronal abcess - in relation to erupting mandibular
!72
3rd molars, which can extend to: submandibular space, buccal

space, sublingual space, pterygomanibular space, infected
mandibular cyst also can spread to form Ludwig’s angina.
2. Iatrogenic: use of contaminated needle for giving LA.
3. Traumatic injuries to orofacial region:
• Mandibular fractures, the chances of developing Ludwig’s

angina are
more, if the fracture is compounded and comminuted.
• Deep lacerations or penetrating injuries such as punctured

wounds.
4. Osteomyelitis: secondary to compound mandibular fractures; acute

exacerbation of chronic osteomyelitis of mandible.
5. Submandibular and sublingual sialadenitis: Acute/chronic infection

of glands.
6. Secondary infections of oral malignancies: secondary infections of

the oral
malignancies leaving to condition.
7. Miscellaneous causes: Rare causes such as-
• Infection in the tonsils or pharynx such as purulent tonsillitis,

etc.
• Foreign bodies such as fish bone, etc.
• Oral soft tissue lacerations.
8. Cervical lymphoid tissues.
!73
The term pseudo-Ludwig’s angina has been applied to the cases
of non dental origin, they are also referred to as pseudo-Ludwig phenomena.
PATHOLOGY:
It is a cellulitis which tends to spread through tissue spaces &
along fascial planes. It occurs in the presence of organisms that produce
significant amounts of hyaluronidase and fibrinolysins that act on hyaluronic
acid and fibrin. Streptococci, the potent producer of hyaluronidase are always
associated with Ludwig’s angina.
MICROBIOLOGY:
Staphylococci, Streptococci, E. coli, Pseudomonas, and anaerobes like
Bacteroides spp, anaerobic Streptococci, Peptostreptococcus, Fusospirochetes
are the contemporary organisms associated with Ludwig’s angina. In early
stages with almost no putrefaction, mixed aerobic and anaerobic infection is
seen. Later stages with frank putrefaction, more anaerobic infection is seen.
INVOLVEMENT:
Mandibular second and third molars are the frequently associated
cause of the Ludwig’s angina. The bone around these teeth is usually thicker on
the buccal aspect than lingual side. The teeth with root apices below the
mylohyoid muscle, infection spreads primarily to the submandibular space.
Hence, submandibular space plays vital role in development and progress of
the disease while the spread is dependent on the muscles in the area.
!74
PATHWAY OF INVOLVEMENT:
The condition usually follows a submandibular space infection caused
by a periapical infection, or pericoronitis around mandibular third molar. The
infection then spreads to the sublingual space on the same side, around the
deep part of the submandibular gland. The submental space is involved by
lymphatic spread. The condition may also occur in converse manner, i.e.,
spread from sublingual to submandibular spaces.
SPREAD:
From the sublingual spaces, the infection may spread backwards in the
substance of the tongue along the course of sublingual artery. Infection reaches
region of epiglottis and produces swelling around the laryngeal inlet. Infection
may track to submasseteric, pterygomandibular spaces and more posteriorly,
parapharyngeal, paratonsillar spaces- worsening airway compromise.
Infection from submandibular space can spread downwards along
and beneath the investing layer of deep cervical fascia, towards clavicle and
subsequently to mediastinum. Uncommonly, infection can spread below and
reach close to carotid sheath, pterygopalatine fossa, leading to cavernous sinus
thrombosis with subsequent meningitis.
CLINICAL FEATURES:
1. General examination:
General constitutional symptoms, patient looks toxic, very ill &
dehydrated with pyrexia, anorexia, chills and malaise can be observed. Marked
!75
pyrexia, with difficulty in swallowing, impaired speech and hoarseness of voice
can be observed.
2. Regional examination:
• Extraoral examination:
• Firm/hard brawny swelling in the bilateral submandibular and submental
regions, which soon extends down to the anterior part of clavicles can be
observed.
• Swelling is non pitting, minimally or non fluctuant associated with severe
tenderness. Classically, the swelling shows ill-defined borders with
induration.
• Severe muscle spasm may lead to trismus with restricted mouth opening
and also jaw movements. Typically mouth remains open due to edema of
sublingual spaces leading to raised tongue almost touching the palatal
vault. In extreme cases, tongue may actually protrude from the mouth;
tongue movements are reduced.

!76
• Airway obstruction is seen. Respiratory rate may be seen to be raised;
breathing being shallow with accessory muscles of reparation being used.
There may be dilation of alas nasi, raising of thoracic inlet by scalenes and
sternocleido-mastoid muscles and in-drawing of tissues above the clavicle.
Cyanosis may occur due to progressive hypoxia.
• Fatal death may occur in untreated case of Ludwig’s angina within 10-24
hrs due to asphyxia.
• Intraoral examination:
• The swelling involves the sublingual tissues, and distends or raises the
floor of the mouth, woody edema of the floor of the mouth and tongue.
Tongue may be raised against palate. Increased salivation, stiffness of
tongue movements, difficulty in swallowing.
• Backward spread of infection leads to edema of glottis, resulting in
respiratory obstruction.
• Stridor is the alarming sign of this fatal extension needing emergency
intervention to keep airway patent.
• Reduced control of muscles and jaw posture - excessive saliva, even
drooling.
• Progressive dyspnea - caused by backward spread of infection, until in
untreated case, edema of the glottis causes a complete respiratory
obstruction.
!77
FATE OF LUDWIG’S ANGINA:
Ludwig’s angina, if untreated, can be fatal within 12-24 hrs; death
arising from asphyxia. Established cases become more complicated with
involvement of other spaces. Other causes of death include septicemia/septic
shock, mediastinitis and aspiration pneumonia. With newer antibiotics, mortality
rate 75% to 4%. However, the possible fatal outcome of new cases cannot be
ignored.
PRINCIPLES OF TREATMENT:
Ludwig’s angina should be taken as life threatening emergency. It is
best treated by aggressive intervention- based on combination of following
factors:
i) Early diagnosis,
ii) maintenance of airway,
iii) intense and prolonged antibiotic therapy,
iv) extraction of the offending teeth,
v) surgical drainage of spaces.
A nasopharyngeal tube and a tracheostomy kit should be kept ready
near the patient. Evaluation of blood gases gives an indication of the degree of
respiratory obstruction and may indicate the need for tracheostomy even if the
patient is not in distress.
!78
SURGICAL MANAGEMENT:
Bilateral incision into the submandibular spaces with blunt dissection
to the midline suffices, if a through and through drain or bilateral drains meeting
in the midline are placed. This along with drainage of sublingual spaces,
relieves the intense pressure of the oedematous tissue on the airway and
provides specimens for culture. The platysma and supra hyoid fascias are
incised by this approach and the fascia of the submandibular gland is entered.
The mylohyoid muscle should be divided and the sublingual spaces is entered.
A closed clamp should be inserted through the median raphe of the mylohyoid
muscle and advanced to the hyoid bone at the base of the tongue.
Generally, little pus is obtained because the infection
often represents cellulitis of the fascia spaces rather than true abscess
formation. In some cases, especially late or fully developed ones, purulent flow
is produced. Sequelae after adequate drainage are uncommon. However,
inadequate drainage or premature closure of the surgical wounds may lead to
reinfection. Late spread to other spaces or generalised sepsis may occur.
Failure to extract the offending tooth could cause reinfection. Secondary
revision of scarring may be necessary for cosmetic reasons or to repair stenosis
of Wharton’s duct.
!79
ANTIBIOTIC THERAPY:
IV antibiotics with proper dosage and frequency are necessary. The
following drugs can be given:
• Penicillin G - 2-4 million units, IV 4-6 hourly; or 500 mg 6 hourly orally.
• Ampicillin/ amoxycillin - 500 mg 6 and 8 hourly, IV and orally respectively.
• Cloxacillin - 500 mg orally, 8 hourly.
• For people allergic to penicillin: Erythromycin 600 mg 6-8 hourly.
• Gentamicin - 80 mg, BID.
• Clindamycin- IV 300-600 mg 8 hourly, orally or IV.
• Metronidazole - 400 mg 8 hourly orally or IV.
• Cephalosporins are given in cases of resistant infections.
SIMPLE PROTOTYPE PROTOCOL:
1. Preoperative:
• Airway assessment.
• Etiological findings. Radiographs- OPG, others.
• Risk factor consideration. Diabetes, immunodeficiency.
• Hydration. Bp, pulse and urine output.
• Temperature.
• Chest radiographs- to rule out pneumonia.
• Evaluate laboratory data - blood counts and proteins.
• Consider emergency airway preparations.
!80
2. Perioperative:
• Intubation.
• Removal of cause.
3. Postoperative:
• Extubate after confirming adequate airway.
• Irrigation of drains periodically.
• Culture reports- adjust antibiotics accordingly.
• Re-evaluating laboratory counts.
• Monitoring course of infection - if necessary, re-exploration or

drainage.
• Regular follow-up.
4. Irrigation:
• Copious irrigation of wound drain with antibacterial solution.
• Typically, bacitracin - mixture of H2O2 and normal saline
recommended.
COMPLICATIONS:
Complications of Ludwig’s angina include osteomyelitis, maxillary
sinusitis, localised respiratory tract disturbances, digestive tract disturbances.
More serious complications of Ludwig’s angina include: Life threatening airway
obstruction, septicaemia, distant metastatic foci, mediastinitis, pericarditis,
internal jugular vein thrombosis, neurological complications/intracranial
involvement leading to meningitis, epidural abscess/ brain abscess, cavernous
sinus thrombosis. Involvement of carotid sheath leads to carotid artery erosions.
And finally death. 

!81
Localisation of Dental Infections
LOCALISATION OF DENTAL INFECTIONS:
Teeth in upper jaw:
Teeth in lower jaw: 
!82
Diagnostic Imaging of Space Infections
DIAGNOSTIC IMAGING OF SPACE INFECTIONS:
Conventional Radiography:
• IOPA
• OPG
• Lat view of the mandible
• A-P and lat view of the neck for soft tissues(retro)
Other Diagnostic Aids:
• CT Scan - gold standard for H & N imaging.
• MRI
• Nuclear medicine
• Xeroradiography
MANAGEMENT OF SPACE INFECTIONS:
The management of fascial infections, either mild or severe, always has 5
goals:
1. Medical support of the patient, with special attention to correcting host

defence compromises where they exist;
2. Administration of proper antibiotics in appropriate doses;
3. Surgical removal of the source of infection as early as possible;
4. Surgical drainage of infection, with placement of proper drains; and
5. Constant re-evaluation of the resolution of the infection. 
!83
Management of Space Infections
PRINCIPLES OF MANAGEMENT OF SPACE INFECTION:
The eight steps in the management of odontogenic infections are as follows:
1. Determine the severity of infection.
2. Evaluate host defenses.
3. Decide on the setting of care.
4. Treat surgically.
5. Support medically.
6. Choose and prescribe antibiotic therapy.
7. Administer the antibiotic properly.
8. Evaluate the patient frequently.  
1. DETERMINE THE SEVERITY OF THE INFECTION:
A careful history and a brief but thorough physical examination should
allow the treating surgeon to determine the anatomic location, rate of
progression, and the potential for airway compromise of a given infection. The
host defenses, including immune system competence and the level of systemic
reserves that can be called upon by the patient to maintain homeostasis, are
largely determined by history.
Three major factors must be considered in determining the severity of an
infection of the head and neck: anatomic location, rate of progression, and
airway compromise.
!84
ANATOMIC LOCATION:
The anatomic spaces of the head and neck can be graded in severity by
the level to which they threaten the airway or vital structures, such as the heart
and mediastinum or the cranial contents. The buccal, infraorbital vestibular, and
subperiosteal spaces can be categorized as having low severity because
infections in these spaces do not threaten the airway or vital structures.
Infections of anatomic spaces that can hinder access to the airway due to
swelling or trismus can be classified as having moderate severity. Such
anatomic spaces include the masticatory space, whose components may be
considered separately as the submasseteric, pterygomandibular, and superficial
and deep temporal spaces, and the perimandibular spaces (submandibular,
!85
submental, and sublingual). Infections that have high severity are those in which
swelling can directly obstruct or deviate the airway or threaten vital structures.
These anatomic spaces are the lateral pharyngeal and retropharyngeal, the
danger space, and the mediastinum. Cavernous sinus thrombosis and other
intracranial infection also have high severity.
In 1999 Flynn and colleagues devised a severity score (SS) that
assigned a numerical value of 1 to 4 for involvement of each of the low,
moderate, severe, or extreme severity anatomic spaces, respectively. Thus, a
patient with cellulitis or abscess of the right buccal (SS = 1), right
pterygomandibular (SS = 2), and right lateral pharyngeal (SS = 3) spaces would
have a total severity score of 6, which is the sum of the values assigned to each
of the three anatomic spaces.
RATE OF PROGRESSION:
Upon interviewing the patient with an infection, the surgeon can
appraise the rate of progression by inquiring about the onset of swelling and
pain and comparing those times to the current signs and symptoms of swelling,
pain, trismus, and airway compromise.
Odontogenic infections generally pass through three stages before they
resolve. During the first 1 to 3 days the swelling is soft, mildly tender, and
doughy in consistency. Between days 2 and 5 the swelling becomes hard, red,
and exquisitely tender. Its borders are diffuse and spreading. Between the fifth
and seventh days the center of the cellulitis begins to soften and the underlying
abscess undermines the skin or mucosa, making it compressible and shiny. The
!86
yellow colour of the underlying pus may be seen through the thin epithelial
layers. At this stage the term fluctuance is appropriately applied. Fluctuance
implies the palpation of a fluid wave by one hand as the abscess is compressed
by the other hand.
The final stage of odontogenic infection is resolution, which generally
occurs after spontaneous or surgical drainage of an abscess cavity. The
swelling then begins to decrease in size, redness, and tenderness. The
resolving swelling may stay firm for some time, however, as the inflammatory
process is involved in removing necrotic tissue and bacterial debris.
AIRWAY COMPROMISE:
The most frequent cause of death in reported cases of odontogenic
infection is airway obstruction. Therefore, the surgeon must assess current or
impending airway obstruction within the first few moments of evaluating the
patient with a head and neck infection.
In partial airway obstruction, abnormal breath sounds will be
evident, consisting of stridor or coarse airway sounds suggestive of fluid in the
upper airways. The patient may assume a special posture that straightens the
airway, such as the “sniffing position,” in which the head is inclined forward and
the chin is elevated, as if one were sniffing a rose.
Other such postures include a sitting patient with the hands or elbows
on the knees and the chest inclined forward with the head thrust anterior to the
shoulders, which also straightens the airway and may allow secretions to drool
outward onto the floor or into a pan. Occasionally a patient with a lateral
!87
pharyngeal space infection will incline the neck toward the opposite shoulder in
order to position the upper airway over the laterally deviated trachea.
2. EVALUATE HOST DEFENSES:
IMMUNE SYSTEM COMPROMISE:
The medical conditions that can
interfere with proper function of the
immune system, which is, of course,
essential to the maintenance of host
defense against infection. Diabetes is
listed first because it is the most
common immune-compromising disease.
SYSTEMIC RESERVE:
The host response to severe infection can place a severe
physiologic load on the body. Fever can increase sensible and insensible fluid
losses and caloric requirements. A prolonged fever may cause dehydration,
which can therefore decrease cardiovascular reserves and deplete glycogen
stores, shifting the body metabolism to a catabolic state. The surgeon should
also be aware that elderly individuals are not able to mount high fevers, as often
seen in children. Therefore, an elevated temperature at an advanced age is not
only a sign of a particularly severe infection, but also an omen of decreased
cardiovascular and metabolic reserve, due to the demands placed on the
elderly patient’s physiology.
!88
The physiologic stress of a serious infection can disrupt previously
well- established control of systemic diseases such as diabetes, hypertension,
and renal disease. The increased cardiac and respiratory demands of a severe
infection may deplete scarce physiologic reserves in the patient with chronic
obstructive pulmonary disease or atherosclerotic heart disease, for example.
Thus, an otherwise mild or moderate infection may be a significant threat to the
patient with systemic disease, and the surgeon should be careful to evaluate
and manage concurrent systemic diseases in conjunction with direct
management of the infection.
3. DECIDING ON THE SETTING OF CARE:
In deciding whether to admit the patient with a serious odontogenic infection, it
is generally safer to err on the side
of hospital admission. The
inpatient setting affords the patient
with continual professional
monitoring, supportive medical
care, the availability of radiologic
and medical consultative services,
and, most importantly, a team that can rapidly secure the airway should it
become compromised.
4. TREAT SURGICALLY:
AIRWAY SECURITY:
Immediate establishment of airway security and early aggressive surgical
!89
therapy are the most important intervention steps in the management of severe
odontogenic infections.
The involvement of moderate or high severity anatomic spaces
generally necessitates a more complicated airway management procedure, as
well as surgical intervention in anatomic locations that are not amenable to
profound local anesthesia. An infection that is rapidly progressing through the
anatomic fascial planes, as in necrotizing fasciitis, indicates the prompt
establishment of a secure airway, even if for anticipatory reasons, as well as the
possible need to extend the anatomic dissection into regions that had not been
contemplated preoperatively. Sometimes general anesthesia is required for
patient management reasons alone, especially in the patient who is not able to
cooperate, such as a young child or mentally handicapped individual.
An infrequently used surgical technique that may aid in
protecting the air-way during intubation or tracheotomy is needle
decompression. In this technique, under local anesthesia an abscess of the
pterygomandibular, lateral pharyngeal, submandibular, or sublingual space is
aspirated with a large-bore needle in order to decompress the surrounding
tissues. This manoeuvre may decrease the risk of abscess rupture through taut,
distended oropharyngeal tissues during instrumentation of the airway. Additional
benefits of this procedure are the redirection of pus drainage into the oral cavity
or onto the skin, where it can easily be removed, and obtaining an excellent
specimen for culture and sensitivity testing.
!90
SURGICAL DRAINAGE:
In general, surgery for management of severe odontogenic infections is
not difficult. Given a thorough knowledge of the anatomy of the deep fascial
spaces of the head and neck, the surgeon should be able, by using appropriate
anatomic landmarks, to use small incisions and blunt dissection without direct
exposure and visualization of the entire infected anatomic space.
Lest the surgeon crush a vital structure within the beaks of a
hemostat during blunt dissection, it is crucial to insert the instrument closed,
then open it at the depth of penetration, and then withdraw the instrument in the
open position. A hemostat should never be blindly closed while it is inside a
surgical wound. Another important principle of surgical incision and drainage is
the need to dissect a pathway for the drain that includes the locations where
pus is most likely to be found.
!91
The advantages of through-and- through drainage are the provision
of two pathways for the egression of pus, placement of the incisions in healthy
tissue in cosmetically acceptable areas, and the ability to irrigate the infected
wound with uni-directional flow from one incision to the other. Wound irrigation
is facilitated especially by the use of a Jackson Pratt–type drain, which is
noncollapsible and perforated.
TIMING OF INCISION AND DRAINAGE:
Much of the surgical literature on the management of deep fascial
space infections of the head and neck advocates an expectant approach to
surgical drainage of deep neck infections. The overall strategy of this approach
is to use parenteral antibiotic therapy as a means of controlling, localizing, or
even eradicating the soft tissue infection. Failure of the medical approach is
determined by patient deterioration, impending airway compromise, and the
identification of an abscess by CT or clinical examination or both.
CULTURE AND SENSITIVITY TESTING:
Infections that present in the low severity anatomic spaces are not in
an anatomic position that is likely to threaten the airway or vital structures. In
the absence of immunologic or systemic compromise, such infections are very
unlikely to become serious or life threatening. Straightforward treatments, such
as removal of the involved teeth, intraoral incision and drainage, and empiric
antibiotic therapy, are almost always successful.
!92
When an infection involves anatomic spaces of moderate or
greater severity, or when there is significant medical or immune system
compromise, culture and sensitivity testing as early as possible in the course of
infection is important because the final result of antibiotic sensitivity testing can
be delayed for as much as 2 weeks when fastidious or antibiotic-resistant
organisms are involved.
5. SUPPORT MEDICALLY:
Medical supportive care for the patient with a severe
odontogenic infection is composed of hydration, nutrition, and control of fever in
all patients. Maintenance or reestablishment of electrolyte balance and the
control of systemic diseases may also be a crucial part of the necessary
supportive medical care for some cases, and the reader is referred to
appropriate texts for a more comprehensive discussion of these matters.
6. CHOOSE AND PRESCRIBE ANTIBIOTIC THERAPY:
Mild or outpatient infections have been shown in a number of
studies to respond well to the oral penicillins. There was no significant
difference in pain or swelling at 7 days of therapy between penicillin and various
other antibiotics, including clindamycin, amoxicillin, amoxicillin-clavulanate, and
cephradine, although these parameters improved more rapidly during the first
48 hours of therapy with the alternative antibiotics.
In most of the cases, the involved tooth or teeth were treated with
extraction or root canal therapy is done. Incision and drainage is performed as
necessary. Therefore, penicillin continues to be a highly effective antibiotic for

!93
uncomplicated odontogenic infections, owing to its low cost and low incidence
of unwanted side effects.
Clindamycin has become the empiric antibiotic of choice for odontogenic
infections that are serious enough to warrant hospital admission.
Most resistance to penicillin that occurs among the oral pathogens
is due to synthesis of β-lactamase. Therefore, it is reasonable to use penicillin
plus a β-lactamase inhibitor such as ampicillin-sulbactam or a penicillin plus
metronidazole as alternative antibiotics for serious odontogenic infections. The
penicillins and metronidazole have the advantage of crossing the blood-brain
barrier when the meninges are inflamed. Clindamycin, on the other hand, does
not cross the blood-brain barrier. Therefore, it is appropriate to use penicillin
plus metronidazole or ampicillin-sulbactam when there is a risk of an
odontogenic infection entering the cranial cavity.
7. ADMINISTER THE ANTIBIOTIC PROPERLY:
The tissue level of antibiotics determines their effectiveness.
Those tissue levels are of course dependent on the antibiotic’s level in serum,
through which the antibiotic must pass in order to achieve therapeutic levels in
soft tissues, bone, brain, and abscess cavities. Administration of antibiotics by
the oral route requires that the drug successfully navigate the vagaries of the
highly acidic stomach, the chemical qualities of ingested foods, and the basic
intestinal tract. Once an antibiotic is absorbed by the gastric or intestinal
mucosa, it may then be subject to first pass metabolism in the liver and
subsequent excretion though the bile. Part of the excreted antibiotic may then
!94
be reabsorbed by the intestine, resulting in enterohepatic recirculation. For
these reasons orally administered antibiotics achieve much lower serum levels
at a slower rate than when they are injected directly into the vascular system
intravenously.
8. EVALUATE THE PATIENT FREQUENTLY:
In outpatient infections that have been treated by tooth extraction
and intraoral incision and drainage, the most appropriate initial follow-up
appointment is usually at 2 days postoperatively for the following reasons:
• Usually the drainage has ceased and the drain can be discontinued at this
time.
!95
• There is usually a discernible improvement or deterioration in signs and
symptoms allowing the next treatment decisions to be made.
For odontogenic deep fascial space infections that are serious
enough for hospitalization, daily clinical evaluation and wound care are
required. By 2 to 3 postoperative days the clinical signs of improvement should
be apparent, such as decreasing swelling, defervescence, cessation of wound
drainage, declining white blood cell count, decreased malaise, and a decrease
in airway swelling such that extubation can be considered.
!96
Public Health Significance
PUBLIC HEALTH SIGNIFICANCE:
• We need to have knowledge about space infections, because in rural setups
where dental health is often neglected, treatment should be offered before it
becomes fatal. This can be achieved by correct diagnosis and management
of space infections.
• Based on the severity of the infection, immediate treatment or referral can be
done, depending on the risk to airway or vital structures.
• Be able to inform the patient the sequelae of neglecting the dental infection,
which can become fatal to the person.
• To be able to identify the space infection, in order to be able to do treatment/
treatment plan.
CONCLUSION:
• Odontogenic infections are a serious risk to the patient’s health and life, if
these are not managed at proper time.
• Life threatening complications can occur in medically compromised
patients.
• Management of odontogenic infections is primarily surgical supported with
medical care. Antibiotics are required in high intravenous doses as an
adjunct and not as a primary treatment. Control of underlying systemic
disease is also equally important as the control of infection to prevent
mortality and morbidity.  

!97
References
REFERENCES:
1. Richard G. Topazian. Oral and Maxillofacial infections. 4th edition.
Philadelphia: W.B.Saunders. 2002. Pg. 158-213.
2. Larry J. Peterson. Contemporary oral and maxillofacial surgery. 4th edition.
New Delhi: Elsevier. 2004. Pg. 277-93.
3. Neelima AM. Textbook of oral and maxillofacial surgery. 4th edition. New
Delhi:Jaypee brothers. 2016. Pg. 833-885.
4. Laskin D M. Management of odontogenic infections of head and neck. vol 4.
1970.
5. Fragiskos. D. Fragiskos. Oral Surgery. Berlin: Springer. 2007.
6. Henry Gray. Gray’s anatomy. 2nd edition. Philadelphia: Elsevier; 2010.
!98

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Space Infections

Odontogenic infections have two major origins - pulpal and

alveolar process, it appears in predictable anatomic locations, determined by -

• The thickness of the bone overlying the apex of tooth,

• The relationship of site of perforation of bone to muscle attachments of

Most odontogenic infections penetrate the bone to form vestibular

fascial space infection.

spaces. Some spaces are normal anatomical spaces containing various

identifiable only when involved by a pathological process (e.g. retro-pharyngeal

space). Important anatomical connections exist between these various actual

neck is composed of skin and superficial fascia (subcutaneous tissues). Two

is readily evaluated on clinical examination and usually doesn’t necessitate

diagnostic imaging of pathological processes.

Anatomically, the deep neck can be divided into a superficial

investing layer, middle or pre-tracheal layer, and deep or pre-vertebral layer.

and must be thoroughly evaluated in any imaging study.

• Maxillary primary spaces - canine, buccal and infratemporal spaces.

• Mandibular primary spaces - submental, buccal, submandibular, sublingual

Infections can extend beyond these primary spaces into additional

fascial spaces or secondary spaces.

• Masseteric, pterygomandibular, superficial and deep temporal, lateral

In the 1930s the classical anatomical studies of Grodinsky and Holyoke

tissues such as fasciae, muscles and bone.

Shapiro defined fascial spaces as potential spaces between the

bounded by anatomical barriers usually of bones, muscles or fascial layers. -

PATHOPHYSIOLOGY OF ODONTOGENIC INFECTION:

periodontal ligament, a very localised apical osteomyelitis occurs. Bone

destruction in osteomyelitis is very similar to the process of necrosis of the

inflamed dental pulp. Essentially, as the interstitial hydrostatic pressure

increases as result of transudation of extracellular fluid, followed by exudation of

soft tissues are contained within an unyielding mineralised structure, such as

relieved. Therefore, the pulpal or medullary soft tissues die as a result of

ischemia. Tissue breakdown products recruit circulating macrophages and

histiocytes by the process of chemotaxis. As mineralised tissue is encountered

these circulating macrophages coalesce and differentiate into osteoclasts and

resorb mineralised bone.

The process of bone necrosis and resorption expands in a roughly

The invading bacterial pathogens that trigger this autolytic

direct destruction. Streptococci, commonly found in the early stages of infection,

can invade tissues by the elaboration of their hyalurodinases, which breakdown

the extracellular glycoproteins of connective tissue.

As the streptococci flourish in their exponential growth phase,

they create an environment conducive to the subsequent growth of the

anaerobic flora of odontogenic infections. They consume the local oxygen

supplies and metabolise nutrients to create a more acidic environment. They

about 3 days of clinical symptoms. The anaerobes, including Prevotella and

Porphyromonas spp., produce collagenase, which destroy collagen, the most

plentiful extracellular matrix protein of connective tissue. As the infection

vascularised structures such as muscle, fascia, organs and bone.

PATHWAYS OF DENTAL INFECTION:

The narrow pulpal foramen at the root apex, although of insufficient

diameter to permit adequate drainage of infected pulp, does serve as a

the bacteria harboured in the pulp chamber subsequently repopulate the

apex of the tooth, the pathophysiological course of a given infectious process

resistance, and anatomy of the involved area.

If the infection remains localised at the root apex, a chronic periapical

infection may develop. Frequently, sufficient destruction of bone develops to

create a well corticated radiolucency observable on dental radiographs. This

infection may develop. Frequently, sufficient destruction of bone develops to  