Deep space infections of Head and Neck

DEEP SPACE INFECTIONS
OF HEAD AND NECK
Presented By:
Dr. Sapna K Vadera
(P.G. Student)
Dept. Of OMFS
VSPM’S Dental College and Research Centre, Nagpur
Guided By:
Dr. S.R.Shenoi
(Prof, Guide and H.O.D)
Dept. of OMFS

CONTENTS
• Introduction
• Anatomy & Spaces description
• Aetiology ( General & Specific)
• Microbiology
• Clinical features ( General & Specific)
• Investigations & Radiology
• Management
• Complications of DNS
• Conclusion

INTRODUCTION
Deep neck infections occur within the potential
compartments of the neck between the facial layers.
They are unique among infectious diseases for their
versatility and potential for severe and life threatening
complications such as airway obstruction, mediastinitis,
septic embolization, dural sinus thrombosis, and
intracranial abscess.
Osborn TM, Assael LA, Bell RB. Deep space neck infection: principles of surgical management. Oral and
maxillofacial surgery clinics of North America. 2008 Aug 31;20(3):353-65.

The clinical presentation is widely variable, and often early
symptoms do not reflect the disease severity. The complication
risk depends on the extent and anatomical site.
Diseases that transgress fascial boundaries and spread along
vertically oriented spaces (parapharyngeal, retropharyngeal,
and paravertebral space) have a higher risk of complications
and require a more aggressive treatment compared with those
confined within a nonvertically oriented space (peritonsillar,
sublingual, submandibular, parotid, and masticator space).
INTRODUCTION

The occurrence of deep neck infections has been declining since
the advent of antibiotic therapy. However, they do still occur &
represent challenging diagnostic & treatment problems.
Aggressive monitoring and management of the airway is the
most urgent and critical aspect of care, followed by appropriate
antibiotic coverage and surgical drainage, when needed.
INTRODUCTION

The term Fascia is used to
describe broad sheets of
dense connective tissues
whose function is to
separate structures that
may pass over each Other
during movement such as
muscles & glands & serves
as pathways for the course
of Vascular & neural
structures.
FASCIA
Grodinsky M, Holyoke EA; The fasciae and fascial spaces of head, neck and adjacent regions. American
journal of Anatomy 63:363, 1938

I. Superficial Fascia
II. Deep Fascia
Superficial layer (Investing fascia)
Parotidomasseteric
Temporal
Middle layer
Muscular division
Visceral division
Buccopharyngeal
Pretracheal
Retropharyngeal
Deep layer
Alar division
Prevertebral division

SUPERFICIAL FASCIA

• Layer of dense connective tissue that courses deep to subcutaneous tissue
throughout the body.
• Muscles of facial expression below the mouth lie deep to the fascia and
above the mouth lie superficial to fascia
• Necrotizing Fascitis – infection of superficial fascia causing necrosis of tissue
in subcutaneous space.
• Skin
+ Superficial musculocutaneous aponeurotic system
Superficial fascia (SMAS)
+
Platysma
SUPERFICIAL FASCIA

• Controversy exists that whether it is formed by all three layers of
deep fascia or from alar division or posterior layer
• Anatomically separate from all layers.
• Contains carotid artery, internal jugular vein, and vagus nerve
• Extends from superior mediastinum (beginning of carotid artery)
till jugular foramen and carotid canal at skull base.
CAROTID SHEATH

NUMBERED SPACES OF GRODINSKY &
HOLYOKE- DEEP SPACES OF NECK(1938)

1)Space 1:superficial to superficial
fascia(subcutaneous space)
2)Space 2:space lying superficial to
sternothyroid-thyrohyoid division of middle
layer of deep cervical fascia or between first
and second divisions of middle layer.
3)Space 3:superficial to visceral division of
middle layer of deep cervical fascia contains
pretracheal,retropharyngeal & lateral
pharyngeal spaces.
Space 3a: viscerovascular space (Lincoln's
highway as coined by Mosher)- Is the
carotid sheath.

4) Space 4: Danger space is a potential
space between the alar and prevertebral
fascia it extends from the base of the skull
to the posterior mediastinum ,as far as the
diaphragm.
Space 4a:present in the posterior triangle
of the neck, posterior to the carotid sheath.
5) Space 5: prevertebral space
Space 5a: enclosed by prevertebral fascia,
posterior to the transverse process of the
vertebrae as it surrounds the scalene and
the spinal postural muscles.

Lateral pharyngeal space
Retropharyngeal space
Peritonsillar space
Space 3a- carotid sheath
Space 4- dangerous space
Complications

LATERAL PHARYNGEAL
SPACE
It has been described as conical in shape, with its base the
pterous portion of temporal bone & its apex at the hyoid
bone.
It is divided into an anterior & posterior compartment by the
styloid process & its musculature.
(Fascial condensation called the aponeurosis of zuckerkandl
and testut which divides this space into anterior and
posterior division(prestyloid and poststyloid)

BOUNDARIES:

Contents:
Pre styloid
• Medial—tonsillar fossa
• Lateral—medial
pterygoid
• Contains fat, connective
tissue, nodes
Post styloid
• Carotid sheath
• Cranial nerves IX, X, XII
LATERAL PHARYNGEAL
SPACE

CLINICAL
FEATURES
Anterior compartment :
Pain, Dysphagia & trismus.
Fever & chills.
Swelling at the angle of mandible, medial bulging of the pharyngeal
wall & signs of systemic toxicity.
LATERAL PHARYNGEAL
SPACE

Posterior compartment:
Systemic signs of fever & toxicity.
Trismus is uncommon.
Medial bulging of the pharyngeal wall
seen with anterior compartment is not
present.
Swelling if present is usually behind the
palatopharyngeal arch & thus is often
missed on examination.
LATERAL PHARYNGEAL
SPACE

LATERAL PHARYNGEAL
SPACE
Osborn TM, Assael LA, Bell RB. Deep space neck infection: principles of surgical management.
Oral and maxillofacial surgery clinics of North America. 2008 Aug 31;20(3):353-65.

SOURCE & SPREAD OF INFECTION
Lateral pharyngeal space
Pterygo mandibular
space
Submandibular
space
Peritonsillar
space
Sublingual
space
Cavernoous sinus
thrombosis
Retropharyngeal
space
Carotid Space Danger Space
Prevertbral space
Meningitis
Brain abscess Mediastinitis

TREATMENT : INCISION & DRAINAGE
EXTRAORAL APPROACH
Extraoral Inciaion & Drainage Of
Lateral Pharyngeal Space Abscess.
A-incision Line
B-direction For Insertion Of Hemostat
Incision Is Made Along Anterior
Border Of Sternomastoid
Extending From Below The Angle
Of Mandible To The Middle Third
Of Submandibular Gland
Curved Hemostat Is Inserted
Medially Behind The Mandible As
Well As Superiorly Until Abscess
Cavity Is Reached
A Rubber Drain Is Introduced &
Secured In Position With Suture

INTRAORAL APPROACH
A Vertical Incision Is Placed Over The
Pterygomandibular Raphe.
Sinus Forcep Or Curved Hemostat Is
Passed Through Pterygomandibular
Raphe Along The Medial Surface Of
The Mandible, Medial To Medial
Pterygoid & Lateral To Superior
Constrictor Is Then Divided
Posteriorly

RETROPHARYNGEAL
SPACE INFECTION
● Midline space b/w pharygobasilar fascia, which attaches
the pharyngeal constrictor to the base of skull and pre
vertebral fascia
Extension - Base of the skull
Mediastinum

Boundaries :
Anterior- superior and middle
pharyngeal constrictor muscle
Posterior- Alar fascia
Superior- skull base
Inferior- Fusion of alar and
prevertebral fasciae at c6-T4
Lateral – carotid sheath and lateral
pharyngeal space
RETROPHARYNGEAL
SPACE INFECTION

CLINICAL EVALUATION
• Children less than 4 yrs commonly affected.
• In adults it manifests as cold abscess.
• Sore throat, dysphagia, odynophagia, difficulty handling secretions.
• Hot potato voice.
Early signs:
•Refusal to take food.
•Cervical lymphadenopathy.
•Slight neck rigidity.
•Noisy breathing due to laryngeal
edema.
Late signs
•Neck tilts towards involved side.
•Hyperextended complete inability
to flex the neck.
•Respiratory embarssment may
occur if abscess not ruptured or
drained.

Contents
Areolar connective tissues,
lymph nodes that drains
Waldeyer’s ring.
Waldeyer’s ring
RETROPHARYNGEAL
SPACE INFECTION

PARAPHARYNGEAL
SPACE
PERITONSILLAR
SPACE
PREVERTEBRAL
SPACE
MEDIASTINITIS
DANGER SPACESource & Spread Of Infection
RETROPHARYNGEAL
SPACE
RETROPHARYNGEAL
SPACE INFECTION

• EXTRAORAL APPROACH
• Suprahyoid portion
• Infrahyoid portion
RETROPHARYNGEAL
SPACE INFECTION

• INTRAORAL APPROACH
RETROPHARYNGEAL
SPACE INFECTION

PERITONSILLAR SPACE
Consists of an area of loose connective tissue between the fibrous
capsule of palatine tonsil medially and superior constrictor laterally.
Clinical evaluation
• 3-7 days history of pharyngitis
without resolution
• Severe sore throat, dysphagia,
odyonophagia and referred
otalgia.
• Speech is muffled and
classically discribed as ‘hot
potato’
Marra S, Hotaling AJ. Deep neck infections. American journal of otolaryngology. 1996 Sep
1;17(5):287-98.

Boundaries:
Medially- capsule of palatine tonsil
Laterally- superior pharengeal constrictor
Superiorly- anterior tonsillar pillar
Inferiorly- posterior tonsillar pillar
PERITONSILLAR SPACE
https://classconnection.s3.amazonaws.com/694/flashcards/4655694/jpeg/3 143B44F4EC00781C322.jpeg

Peritonsillar infection may drain through the mucosa into the oropharynx or
may perforate the superior constrictor and the visceral fascia to enter the
lateral pharyngeal space rather than spreading laterally the infection spreads
vertically
PERITONSILLAR SPACE
1;17(5):287-98.

PRETRACHEAL SPACE
BOUNDARIES:
Anterior: Sternothyroid- thyroid fascia
Posterior: Retropharyngeal space
Superior: Thyroid cartilage
Inferior: Superior mediastinum
Medial: Sternothyroid- Thyrohyoid fascia
Lateral: Visceral fascia over trachea &
thyroid gland.
1;17(5):287-98.

CAROTID SPACE
LINCOLN’S HIGHWAY - (MOSHER)
• Potential space within the
carotid sheath.
• Extends from the jugular
foramen and carotid canal
to the mediastinum.
• Contents:
Carotid A, IJV, Vagus Nerve
Cervical sympathetic plexus
1;17(5):287-98.

CAROTID SPACE
INFECTION
Clinical features
• Expanding hematoma of neck, bleeding episodes
• Spread to chest
• Septic venous thrombosis
• Horner's syndrome
Ptosis-----inacitvation of Muller’s Muscle
Miosis
Anhydrosis
1;17(5):287-98.

DANGER SPACE
Potential space between the
alar and prevertebral divisions
of the deep layer of the deep
cervical fascia
Boundaries
• Superiorly:-base of the skull.
• Inferiorly:- upper border of
diaphgram.
• Laterally:- fusion of alar and
prevertebral fascia at transverse
process of cervical and thoracic
vertebrae.
• Anteriorly:- alar fascia.
• Posteriorly:- prevertebral fascia.
https://classconnection.s3.amazonaws.com/50/flashcards/3569050/jpg/danger_space1338471011692-142CE73A2582D1C0A4F.jpg

WHY DANGER SPACE???
At the inferior border it
continous with the
posterior mediastinum
containing vena cava ,arch
of aorta, thoracic duct,
trachea and oesophagus.
Erosion of major blood
vessels, lower airway and
upper digestive tract
Death of patient.
http://images.slideplayer.com/21/6274898/slides/slide_57.jpg
1;17(5):287-98.

Contents
• In cervical region is loose areolar
connective tissue.
• In the chest, danger space is
continue with the posterior
mediastinum which contains vena
cava, aorta, thoracic duct, trachea
& oesophagus.
• Infection can erode to compress
the major vessels, lower airway &
upper digestive tract.
DANGER SPACE
1;17(5):287-98.

Clinical features
• Severe dysnea.
• Pain .
• Widened mediastinum.
Treatment
• Thoracotomy for
drainage.
DANGER SPACE
http://images.slideplayer.com/21/6274898/slides/slide_573233.jpg
Marra S, Hotaling AJ. Deep neck infections. American journal of otolaryngology. 1996 Sep 1;17(5):287-98.

MICROBIOLOGY
• Staphylococcus aureus - Most common in the preantibiotic
era.
• Since the advent of antibiotics, aerobic streptococcal
species & non- streptococcal anaerobes have become the
bacteria predominantly responsible for DNS.

• At present, the most commonly isolated anaerobes include
Peptostreptococcus, Fusobacterium nucleatum & Bacteroides
melaninogenicus.
• In odontogenic infections, the most common of the
streptococcal species is the alpha- nonhemolytic streptococci,
whereas infections of pharyngeal origin have the hemolytic
group A strains more commonly isolated.
• The anaerobe Eikenella Corrodes is becoming increasingly
isolated in head & neck infections.
MICROBIOLOGY

CLINICAL FEATURES
(GENERAL)
Symptoms:
Generalized- Fever
Chills
Malaise
Loss of appetite
Localized- Odynophagia
Dysphagia
Sore throat
Neck stiffness
Neck pain
Trismus
voice changes

Signs:
Neck swelling
Elevation of the floor of the mouth
Bulging of Pharyngeal wall
Pyrexia
CLINICAL FEATURES
(GENERAL)

In addition to a “ hot potato” voice, airway signs include,
• Dyspnea
• Stridor
• Shortness of breath
These signs are seen in advanced disease, & immediate steps to secure
the airway are required to prevent airway obstruction or airway arrest.
CLINICAL FEATURES
(GENERAL)

Any bleeding ranging from ecchymosis of the neck skin to frank
blood from the ear, nose, or mouth , may present a sentinel or
herald bleed, resulting from infectious involvement of the carotid
artery with a potentially lethal outcome.
CLINICAL FEATURES

CLINICAL FEATURES
(SPECIFIC)
LATERAL PHARYNGEAL SPACE:
Anterior compartment :
• Pain, Dysphagia & trismus.
• Fever & chills.
• Swelling at the angle of mandible, medial bulging of the pharyngeal
wall & signs of systemic toxicity.

Posterior compartment:
• Systemic signs of fever & toxicity.
• Trismus is uncommon.
• Medial bulging of the pharyngeal wall seen with anterior compartment is
not present.
• Swelling if present is usually behind the palatopharyngeal arch & thus is
often missed on examination.
CLINICAL FEATURES
(SPECIFIC)

RETROPHARYNGEAL SPACE
• Early in the presentation, diagnosis
may be difficult, especially in
children.
• Sore throat is not a typical complaint,
trismus is minimal.
• Slight elevation of temperature.
• A “hot potato” voice , when present,
is secondary to supraglottic swelling.
CLINICAL FEATURES
(SPECIFIC)
http://sajs.redbricklibrary.com/index.php/sajs/
article/viewFile/1767/486/849

• When the swelling is below the nasopharynx , a mass along the posterior
pharyngeal will be seen off the midline.
• Cervical lymphdenopathy
• Irritability
• If there is severe respiratory distress , mediastinal extension should be
considered.
CLINICAL FEATURES
(SPECIFIC)

INVESTIGATIONS
• Routine haematology shows a raised WBC & ESR. The biochemical
profile is usually normal.
• Blood cultures should be sent to identify organisms & their
antibiotic sensitivity.

RADIOLOGY
Numerous radiographic techniques are available to evaluate deep infections.
These include,
• Chest X-ray
• Lateral neck X-ray
• Ultrasonography
• CT/CECT
• MRI

CHEST X-RAY
It may provide information as to the possibility of complications resulting
from DNS , such as Mediastinal extension, Lung abscess, & Pyopneumothorax.
The presence of an infiltrate on chest X-ray can suggest aspiration , & it may
document mediastinal involvement necessitating aggressive management of
a patient.
http://images.radiopaedia.org/images/321795
/45bab6d8322888287fa7ae74a726ee.jpg

LATERAL CERVICAL X-RAY
• Simplest & most readily
available
• It is applicable in those cases
in which there is suspicion of
Retropharyngeal or
Prevertebral space
involvement.
• These lateral cervical films are
interpreted by measuring the
distance from the anterior
aspect of the vertebral body
to the air column of the
posterior pharyngeal wall.
https://www.google.co.in/search?q=lateral+x+ray+neck+for+space+inf
ection&espv=2&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiT2pKSoI
bSAhUHTo8KHV5MDXgQ_AUICCgB&biw=1366&bih=589#imgrc=_JLGn
hWxRDJqjM

• Increased thickness of the distance
from the anterior aspect of the
vertebral body to the air column in
the posterior pharyngeal wall (O7
mm at C-2), loss of cervical lordosis,
and presence of air in the soft
tissues suggest space involvement.
• At the level of C-2, the normal
distance may be as wide as 7mm in
both adults & children.
• At the level of C-6, the normal
distance may be as much as 22mm
in adults & 14mm in children.
https://images.radiopaedia.org/images/7562625/
6a3a639c4ce32043453951916fd862_jumbo.JPG
LATERAL CERVICAL X-RAY

CT/CECT

MRI

PRINCIPLES OF MANAGEMENT
OF SPACE INFECTIONS
1. Airway- Assessment & Secure
2. Incision & Drainage & Extraction (If possible)
3. Swab for Culture & antibiotic Sensitivity tests
4. Empirical Antibiotic therapy
5.Hydration- Fluid & Electrolyte balance & supportive care
6.Culture Specific Antibiotics

Criteria for admission of odontogenic infections at high risk of deep
neck space infection. European Annals of Otorhinolaryngology,
Head and Neck diseases(2015),
http://dx.doi.org/10.1016/j.anorl.2015.08.007
Criteria for admission of
odontogenic infections at high
risk of deep neck space
infection

AIRWAY
PROTECTION
Intubation:
Direct laryngoscopy: possible risk of
rupture and aspiration
Flexible fiberoptic intubation
Tracheostomy:
Ideally : Planned, awake, local
anesthesia
Abscess may overlie trachea
Distorted anatomy and tissue planes
http://pocketdentistry.com/wpcontent/uploads/285/F000177f
017-004a-9780323091770.jpg
https://image.slidesharecdn.com/presentation2016-
160318141136/95/deep-neck-space-infections-24-
638.jpg?cb=1458310356

SEVERITY SCORE OF FACIAL SPACE INFECTION

ALGORITHM FOR AIRWAY MANAGEMENT OF
PATIENTS WITH HEAD & NECK INFECTIONS
Zide MF, Limchayseng LRG . Complications of head & neck infections. Oral Maxillofac Clin North Am
1991;3;355

EMPIRICAL ANTIBIOTIC THERAPY
Odontogenic infections-
mixed bacterial flora
Penicilins/ 3rd gen
Cephalosporin
+
Metronidazole
Peterson’s Principles of Oral & maxillofacial Surgery. Vol.I, 3rd Eition

ANTIBIOTIC THERAPY
Empirical antibiotic treatment:
Initial empiric antimicrobial therapy should include broad coverage for beta-
lactamase–producing bacteria, including Staphylococcus
aureus, Streptococcus pyogenes, Streptococcus viridans, anaerobic gram-
negative bacilli, and Peptostreptococcus species, until culture results are
obtained to help direct treatment.
For cases with an oral or odontogenic source of infection:
Oxacillin - 50-100 mg/kg/d oral or 2 g IV 8 hourly
Ceftriaxone- 200mg 12 hourly or 1g IV 12 hourly
Clindamycin-150mg 6 hourly or 600 mg IV 8 hourly or
Metronidazole – 400mg oral 8 hourly or 500 mg IV 8hourly
Gidley PW, Ghorayeb BY, Stiernberg CM. Contemporary management of deep neck space infections.
Otolaryngology—Head and Neck Surgery. 1997 Jan;116(1):16-22.

• If methicillin-resistant S aureus (MRSA) is suspected,
add vancomycin 1000 mg (15 mg/kg) IV 12h or
• If MRSA, Nosocomial Inf., Pseudomonas-linezolid 600 mg IV 12h
Duration of therapy
Parenteral therapy is indicated until the patient is afebrile, with a clear
clinical improvement in symptoms for 48h. Afterwards, the patient may
transition to oral antibiotics and complete a 2- to 3-wk course of
treatment. Longer courses may be required when complications are
present.
CULTURE SPECIFIC
ANTIBIOTIC
Gidley PW, Ghorayeb BY, Stiernberg CM. Contemporary management of deep neck space infections.
Otolaryngology—Head and Neck Surgery. 1997 Jan;116(1):16-22.

Treatment algorithm for Deep Neck Infections

Treatment algorithm for Deep Neck Infections
Marra S, Hotaling AJ. Deep neck infections. American journal of otolaryngology. 1996 Sep 1;17(5):287-98.

INCISION AND DRAINAGE

COMPLICATIONS
Ludwig’s Angina
Cavernous Sinus Thrombosis
Carotid artery erosion
Necrotizing Fascitis
Internal jugular vein thrombosis
Mediastinitis
Pyopneumothorax
Bronchial erosion
Purulent Pericarditis
Pleural effusion

Historical Background
• A rare disorder, Ludwig’s angina is a serious, potentially life-
threatening infection of the neck and the floor of the mouth.
• Originally, described by Wilhelm Frederick von Ludwig in 1836.*
• The term “Ludwig’s Angina” was coined by Camerer in 1837,
who presented cases which included classic description of the
entity as done in the previous year by W. F. Ludwig.
LUDWIG’S ANGINA
Nguyen VD, Potter JL, Hersh-Schick MR. Ludwig angina: an uncommon and potentially lethal neck infection.
AJNR Am J Neuroradiol 1992;13:215–9

It is defined as acute, ‘non-
suppurating necrotising cellulitis’
involving the submandibular,
sublingual and submental spaces,
bilaterally.
This condition is notorious for its
aggressiveness, rapid progression to
airway compromise and high mortality
when not treated promptly.
LUDWIG’S ANGINA

• Mortality rate exceeds 50% during the pre antibiotic era, in
antibiotic era the mortality reduced below 5%.
• Untreated, the mortality is close to 100 %, both from the
acute sepsis and from airway obstruction.
• In the early 1900s the deadly role of mechanical
respiratory obstruction was realized.
LUDWIG’S ANGINA

Gram-positive bacteria
• Fusobacterium nucleatum
• Spirochetes
• Candida
• Eubacteria
• Clostridium
Gram-negative bacteria
• Neisseria species
• E coli
• Pseudomonas species
• Haemophilus influenzae
• The bacteriology of Ludwig’s
angina is poly-microbial and
predominantly involves the oral
flora.
• Organisms most often isolated
are Streptococcus Viridans and
Staphylococcus Aureus.
• Anaerobes
Bacteroides
Peptostreptococci
Peptococci
LUDWIG’S ANGINA

Predisposing conditions
• Diabetes mellitus
• Neutropenia
• Alcoholism
• Aplastic anemia,
• Glomerulonephritis
Age range - 12 days to 84 years.
Male > female (3:1 to 4:1).
LUDWIG’S ANGINA

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

SIGN & SYMPTOMS
• It is a massive firm, bilateral submandibular
swelling which soon extends down the
anterior part of the neck to the clavicle.
• Bulls neck appearance
• It elevates the floor of the mouth and forces
the tongue up against the palate.
• Marked pyrexia.
• Deglutition and speech are difficult.
• Airway obstruction
• Cynosis may occur due to progressive
hypoxia
• Fatal death may occur in untreated cases of
Ludwigs angina within 10 -12 hrs due to
asphyxia
LUDWIG’S ANGINA

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

INVESTIGATIONS
Plain radiographs of neck and chest
Panoramic radiographic
CT scan
LUDWIG’S ANGINA

Plain Radiographs Of The Neck May Show Soft-tissue Swelling, The
Presence Of Gas, And The Extent Of Airway Narrowing
LUDWIG’S ANGINA

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

TREATMENT
Primary goal:
• Preserve the
oropharyngeal airway.
Secondary goal:
• Antibiotic agent or
incision and drainage.
LUDWIG’S ANGINA

LUDWIG’S ANGINA
Nguyen VD, Potter JL, Hersh-Schick MR. Ludwig angina: an uncommon and potentially lethal neck infection. AJNR Am J
Neuroradiol 1992;13:215–9

Airway management-
-Blind intubation avoided
-Nasoendotrcheal
intubation is far more
reliable
- Cricothyoidotomy are
always preferred over
tracheostomy
LUDWIG’S ANGINA

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

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

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

LUDWIG’S ANGINA

The incisions must be bilateral, extraoral, parallel,
and medial to the inferior border of the mandible, at
the premolar and molar region
LUDWIG’S ANGINA

• Large venous space situated in the middle
cranial fossa, on either side of body of the
sphenoid bone.
• Each sinus is about 2 cm long and 1 cm
wide.
• Interior is divided into a number of spaces
or caverns by trabeculae.
CAVERNOUS SINUS THROMBOSIS

BOUNDRIES
Anterior - extends into medial
end of superior orbital fissure.
Posterior - upto apex of petrous
temporal bone.
Medial – Pitutary above and
sphenoid below
Lateral – temporal lobe and uncus
Superior – optic chiasma
Inferior - endosteal dura mater,
greater wing of sphenoid

CONTENTS
Superior to inferior (within the lateral
wall of the sinus)
• Oculomotor nerve (CN III)
• Trochlear nerve (CN IV)
• Ophthalmic nerve, the V1 branch
of the trigeminal nerve (CN V)
• maxillary nerve, the V2 branch of
CN V

Abducens nerve (CN VI) runs through
the middle of the sinus alongside
the Internal carotid artery (with
sympathetic plexus)
These nerves, except the CN V2, pass
through the cavernous sinus to enter
the orbital apex through the superior
orbital fissure.
CONTENTS

VENOUS CONNECTIONS
OF CAVERNOUS SINUS

DANGEROUS AREA OF FACE
• Flow of blood in all tributaries & communication
are reversible as they possess no valve
• Spread of infection can lead to thrombosis of
cavernous sinus
• The cavernous communicate with dangerous
area of face through 2 routes
 Superior opthalmic vein
 Deep facial veins , pterygoid plexus of vein ,
emissary vein.

SPREAD OF INFECTION TO
CAVERNOUS SINUS
1. Infection of the upper lip, vestibule of the nose and eyelids 
spread by way of the angular, supraorbital and supratrochlear
veins to the ophthalmic veins. Commonest route of infection.
2. Intranasal operations on the septum, turbinates or ethmoid /
sphenoid sinus infection  through the ethmoidal veins.

3. Operations on the tonsil, peritonsillar abscess, surgery or
osteomyelitis of the maxilla, dental extraction and deep cervical abscess
 spread by pterygoid plexus or by direct extension to the internal
jugular vein.
4. Involvement of the middle ear and mastoid with lateral sinus
phlebitis or thrombosis  retrograde spread through the petrosal
sinuses to the cavernous sinus.
SPREAD OF INFECTION TO
CAVERNOUS SINUS

ETIOLOGY OF CST
SEPTIC CST
Infectious
ASEPTIC CST
Trauma
Postsurgery
Rhinoplasty
Cataract extraction
Basal skull (including maxillary)
Tooth extraction
Hematologic
Acute lymphocytic leukemia
Malignancy
Nasopharyngeal tumor

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

COMPLICATION OF CAVERNOUS SINUS
THROMBOSIS
• Intracranial extension of infection may result in meningitis,
encephalitis, brain abscess, pituitary infection, and epidural and
subdural empyema.
• Cortical vein thrombosis can result in hemorrhagic infarction.
• Extension of the thrombus to other sinuses can occur.
Levine SR, Twyman RE, Gilman S: The role of anticoagulation in cavernous sinus thrombosis. Neurology, 2008; 38: 517–22

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

CAVERNOUS SINUS ON CT HEAD
Cavernous sinus

CAVERNOUS SINUS ON MRI BRAIN
AXIAL SECTION CORONAL SECTION

CAVERNOUS SINUS ON MRI BRAIN

Antibiotics ---{empiric cover - gram+ve,-ve & anaerobic} -
--3rd Gen.Cephalosporin+ Vancomycin+ Metronidazole
- If fungal origin - Amphotercin-B (liposomal) 10mg/kg/day
Anti-coagulation--- Intravenous Heparin 24000-30000 units/day
Steroids--- Controversial
Hydrocortisone- 100 mg IV q6h
Surgery---- Exploration of Cavernous sinus – Not performed routinely
--- Removal of Septic focus
--- Extraction of odontogenic focus
---Surgical drainage of paranasal Sinuses
---Debridement of Fungal paranasal sinusitis
TREATMENT OF CAVERNOUS SINUS
THROMBOSIS

The indication of anticoagulation is still debated because of possible bleeding
complications and an eventual suppressive role of the thrombus on the
extension of the infectious thrombophlebitis.
Although, no randomized controlled studies have been conducted, early anticoagulant
therapy may have a beneficial effect on mortality and morbidity, reducing oculomotor
sequelae, blindness, and motor sequelae as well as the risk of hypopituitarism.
(studied in only 7 cases)
TREATMENT OF CAVERNOUS SINUS
THROMBOSIS

PROGNOSIS
100% mortality prior to effective antimicrobials
Typically, death is due to sepsis or central nervous system (CNS)
infection.
With aggressive management, the mortality rate is now less than 30%.
Morbidity, however, remains high, and complete recovery is rare.
Roughly one sixth of patients are left with some degree of visual
impairment, and one half (50 %) have cranial nerve deficits.

NECROTIZING FASCIITIS
• Necrotizing fasciitis of the head and neck is an
uncommon, potentially fatal , soft tissue infection
characterized by extensive necrosis and gas formation in
the subcutaneous tissue and fascia.
• Necrotizing fasciitis (NF) is a rapidly spreading, soft tissue
infection characterized by diffuse necrosis of fasciae and
subcutaneous tissues. Necrotizing fasciitis has a
potentially fatal outcome.
Cervical necrotizing fasciitis caused by dental infection: A review and case report
Anisha Maria and K. Rajnikanth Natl J Maxillofac Surg. 2010 Jul-Dec; 1(2): 135–138.

• Occurs in all age but <40 yr common
• Joseph Jones, an American army surgeon, described this
entity in 1871 during the civil war. He named it “hospital
gangrene”
• In 1924, Melany reviewed 20 cases of “streptococcal
gangrene.” He was the one to note that subcutaneous
necrosis is the hallmark of necrotizing fasciitis. It
predominantly affects the tissues of the abdominal wall, the
perineum and the extremities, but can be seen maxillofacial
region also.

• Necrotizing fasciitis of the neck is rare and usually occurs
secondary to dental infection, gingivitis, or pulpitis.
• It is most often a mixed synergistic infection involving both
aerobes and obligate anaerobes.
• Necrotizing fasciitis is a polymicrobial infection of aerobic,
anaerobic, gram positive and gram negative bacteria.
Streptococcal species is the most common organism, but
enterobacter, fusobacterium, bacteroides, staphylococci
and diptheroids have all been isolated from these wounds.

Patients with oral and maxillofacial
infections who had extraordinary clinical
symptoms such as extensive swelling,
redness, fever, crepitations or a marked
increase in serum CRP (C-reactive protein)
should be strongly suspected of having
necrotizing fasciitis.
The necrotizing fasciitis infections are
poorly localized and are characterized by
inflammation and necrosis, extending
deep to what is normal appearing skin.

1. Begin high dose empirical broad spectrum antibiotic therapy.
• IV Benzyl penicillin 2.4 g, 4 hourly + flucloxacillin 1 g, 6 hourly +
metronidazole 500 mg, 8 hourly or
• IV cefotaxim 2 gm, 8 hourly + metronidazole 500 mg, 8 hourly or
clindamycin 900 mg, 8 hourly or
• IV imipenem/cilastatin 500 mg, 6 hourly or add penicillin 20 million units(if
gram negative cocci present).
2. At least two blood culture and sensitivity specimens should be taken 20
min apart as well as specimens from the wound at a point away from any
open wound to rule out contamination.
3. A CT scan will be helpful in detecting gas in the tissues and blood serum
C-reactive protein (CRP) will be raised (11.7–33.7 mg/dl) and leukocytosis
present (11,80038,700/mm3).

4. ICU care and constant monitoring of all vital parameters and nutritional
support and care of the systemic diseases like diabetes mellitus.
5. Tracheostomy if necessary to maintain the airway.
6. Surgical debridement will be required minimum twice or more times. Excision
of all necrotic tissue is done till normal appearing tissue appears which bleeds
freely on incising. Extension of the infection is easily overlooked at the first
procedure, so a second procedure is required after 24 h. Wound should be left
open and insert drains into deeper fascial planes.
7. Irrigation with 0.5% H2O2 is done as often as possible.
8. Hyperbaric oxygen therapy (1.5 h at 2.5 ATA for 15 days) has been used as an
adjunct in the treatment of necrotizing fasciitis and can be used if available.

9. When the wound is seen to be granulating healthy, a skin graft
can be placed over the site or an attempt at primary closure can
be made.
It takes about 20–40 days for a patient to recover completely from
this infection.
Necrotizing fasciitis of the head and neck is a rare disease, but
dentists may encounter it because dental infection is the main
cause of this disease. The reduction in mortality of this disease
depends upon its early detection and adequate surgical treatment.

MEDIASTINITIS
Serious potentially fatal condition – descending
neck infection to the mediastinum.
Complex anatomical space.
Contents:
Superior: Carotids,Aortic arch,
vagus.N,subclavians, thoracic duct, Trachea,
Oesophagus,thymus..
Anterior: No major structure
Middle: Heart, termination of great vessels,
phrenic nerves
Posterior: Thoracic aorta, superior vena cava,
azygos vein, thoracic duct, vagus nerve..

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

Management: Team approach- (CT Surgeons), Aggressive antibiotic Rx+ Surgical
Drainage+ removal of Source of infection
Trans cervical approach - wide incision @ anterior border of sternocledo mastoid
muscle reaching all the way to mediastinum through blunt dissection, through pre
tracheal space.

CAROTID ARTERY RUPTURE
• Mortality of 20-40%
• Majority from internal carotid,
less from external carotid, and
fewer from common carotid
artery.

Clinical features
• Expanding hematoma of neck, bleeding episodes(herald bleeds)
• Spread to chest
• Septic venous thrombosis
• Horner's syndrome
Treatment:
Incision and drainage at anterior border of sternomastoid
Ligation
Patching or grafting
Ptosis-----inacitvation of Muller’s Muscle
Miosis
Anhydrosis
CAROTID ARTERY RUPTURE

INTERNAL JUGULAR
VEIN THROMBOSIS
Swelling and pain along SCM
Bacteremia, septic embolization, dural sinus thrombosis
IV drug abusers
Treatment:
IV antibiotic therapy
Anticoagulation
Ligation and excision

CONCLUSION
Complex head and neck anatomy often makes early recognition of
DNIs challenging, and a high index of suspicion is necessary to avoid
any delay in treatment. Abscesses left untreated can rupture
spontaneously into the pharynx, leading to aspiration. Asphyxia
resulting from direct pressure or from sudden rupture of the
abscess and also from hemorrhage is the major complication of
these infections.
Other complications include extension of infection laterally to
the side of the neck, or dissection into the posterior
mediastinum through facial planes and the prevertebral space,
cerebral abscess, meningitis, and sepsis. Death can occur from
aspiration, airway obstruction, erosion into major blood vessels,
or extension to the mediastinum. Surgical drainage and
antimicrobial therapy are essential for the prompt recovery and
prevention of complications of these abscesses, such as
bacteremia, aspiration pneumonia, and lung abscess after
spontaneous rupture.

Deep space infections of Head and Neck

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