Shamimul Hasan et al.

UJP 2013, 02 (05): Page 1-4

Universal Journal of Pharmacy

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Review Article
ISSN 2320-303X

Take Research to New Heights

LUDWIGS ANGINA- AN ALARMING MULTIDISCIPLINARY

CHALLENGE - OVERVIEW OF LITERATURE
Shamimul Hasan1*, Sarah Asif2, Shakeba Quadri3
*1

MDS; Assistant Professor Deptt of Oral Medicine and Radiology Faculty of Dentistry Jamia Millia Islamia New Delhi, India
2
BDS Z.A Dental College & Hospitals Aligarh Muslim University Aligarh, India
3
BDS Z.A Dental College & Hospitals Aligarh Muslim University Aligarh, India

Received 12-07-2013; Revised 10-08-2013; Accepted 12-09-2013

ABSTRACT
Ludwigs angina is a rare, potentially life threatening diffuse cellulitis, usually originating from odontogenic infection.
It usually involves bilateral deep tissue spaces and causes elevation of the tongue, woody brawny induration of the
floor of the mouth, trismus and laryngeal edema. Airway obstruction and cavernous sinus thrombosis are serious
complications and the condition may be fatal. Early diagnosis, prompt airway control, aggressive antibiotic
administration and surgical intervention is essential to combat an unfavourable outcome.
Keywords: Ludwigs angina, airway obstruction, antibiotics.

INTRODUCTION
The clinical entity now known as Ludwig angina (LA)
was described in the times of Hippocrates and Galen.
This serious and potentially fatal disease continues to
be discussed in the otolaryngology and oral surgery
literature. Karl Friedrich Wilhelm von Ludwig provided
a clear description of this disease process in 1836 after
careful observation over time of its clinical course and
postmortem findings. He described the pathophysiology
as rapidly progressive gangrenous cellulitis that began
in the vicinity of the submandibular gland and spread
via continuity rather than through the lymphatic system
1,2,3
.Ludwigs angina is a potentially life threatening
diffuse cellulitis involving the floor of the mouth,
submandibular regions bilaterally and causing
progressive airway obstruction3, typically; ludwigs
angina is characterized by fever, malaise, dyspnea,
dysphagia as well as brawny hard tender swelling of the
floor of the mouth and neck 4,5,6.
Etiology of Ludwigs angina includes odontogenic
infection, penetrating injury of the floor of the mouth,
osteomyelitis, compound fracture of the jaw, otitis
media, submandibular gland sialidenitis, sialolithiasis
*Corresponding author:
Dr Shamimul Hasan
C/O Mohd Javed Khan
C-4, Duplex Quarters, New Sir Syed Nager, Aligarh
09953290676; 09411467630
Email:shamim0571@gmail.com

and tongue piercing2,7,8,9. Of all these, the major cause

is of odontogenic infection, mainly around the second
and third lower molar teeth7,10.
Most odontogenic infections are uncomplicated
resolving following the removal of the cause and
sometimes with antibiotic therapy. However, a few
cases of odontogenic infections do get complicated by
Ludwigs angina amongst others. Several factors which
may either act locally or systemically are responsible
for these complications11,12,13.
Treatment invariably consist of securing the airway
where necessary , aggressive broad spectrum
antimicrobial therapy, and surgical decompression of
the facial planes with removal of source of
infection5,6,14.

DISCUSSION
The danger of airway obstruction from soft tissue
swelling in the head and neck has been appreciated
since antiquity, with specific references being made by
Hippocrates, Galen, Aretius, and Paulus of Aegin.
Wilhelm Frederich von Ludwig in 1836 described
repeated recent occurrence of a certain type of
inflammation of the throat, which, despite the most
skillful treatment, is almost always fatal. 15 It was
known as Morbus Strangulatorius and Garotillo (Spanish
for hangmans loop); all names alluding to the
respiratory obstruction so prominent in disease
morbidity16.
Ludwigs angina is a serious and rapidly progressive
infectious process that spreads by the floor of the

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Shamimul Hasan et al. UJP 2013, 02 (05): Page 1-4

mouth affecting simultaneously to submandibular,
sublingual and submental spaces. The infection
generally begins as cellulites, then it turns into
fasciitis, and finally, into real abscess that results in a
woody and hard swelling of the floor of the mouth and
suprahioid region in a bilateral form, with displacement
of the tongue and airway affectation17.
ETIOLOGY
Ludwigs angina usually originates from an odontogenic
infection, especially from the second or third lower
molars. These teeth have roots that lie at the level of
the mylohyoid muscle, and abscesses here can spread
to the submandibular space. Other less commonly
reported causes of Ludwigs angina include 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, and trauma to the floor of the mouth.
Predisposing conditions include diabetes mellitus,
neutropenia,
alcoholism,
aplastic
anemia,
glomerulonephritis, dermatomyositis, and systemic
lupus erythematosus18.
PATHOPHYSIOLOGY
The development of Ludwigs angina is facilitated by
the anatomy of the floor of the mouth. Periapical
dental abscesses of the second and third molars
penetrate the inner cortex of the mandible. Because
these roots extend inferiorly to the mandibular
insertion of the mylohyoid muscle, submandibular
infection ensues. Communication around the posterior
margin of the mylohyoid muscle produces rapid
involvement of the sublingual and contralateral spaces.
The mandible, hyoid, and superficial layer of the deep
cervical fascia limit tissue expansion as edema
develops. This leads to superior and posterior
displacement of the floor of the mouth and tongue
base. The resulting airway compromise can be insidious
until it is nearly complete, when abrupt asphyxiation
occurs1.
The organisms most commonly cultured from oral
infections
include
Streptococcus
viridans
and
Staphylococcus aureus, as well as anaerobic B.
melaninogenicus and peptostreptococcus19. Isolation of
gram-negative organisms like H. influenza, E. coli,
Pseudomonas, and Neisseria are not frequent.
CLINICAL FEATURES
Most cases of Ludwigs angina occur in previously
healthy persons. Most affected patients are between
age 20 and 60 years, although an age range from 12
days to 84 years has been reported 18. There is a male
predominance (3:1 to 4:1) of the disorder. Patients
with Ludwigs angina typically have a history of recent
dental extraction or of poor oral hygiene and dental
pain. Clinical findings are consistent with sepsis and
include fever, tachypnea, and tachycardia. Patients

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may be anxious, agitated, and confused. The disease is

recognized by 5 identifiable characterstics:
(1) Submandibular cellulitis; (2) Involvement of more
than 1 space; (3) Progression of cellulitis to gangrene
with serosanguineous infiltration and minimal
purulence; (4) Extension of cellulitis to connective
tissue fascia; and (5) Spread of cellulitis by continuity,
not via the lymphatics2.
Many patients with Ludwigs angina demonstrate a
Bull neck appearance as the inflammation spreads to
the submandibular region, giving the appearance of a
large Double chin. Hoarseness, stridor, respiratory
distress, decreased air movements, cyanosis, and a
sniffing position (characterstic position assumed by
patients with impending upper airway compromise
consisting of an upright posture with the neck thrust
forward and the chin elevated) are all signs of
impending airway catastrophe. More specifically, they
may have a muffled tone at higher registers (Hot
potato voice) caused by edema of the vocal
apparatus; this finding should be a warning to clinicians
of potentially severe airway compromise. Adenopathy
and fluctuance are not usually seen in patients with
ludwigs angina.
DIAGNOSIS AND INVESTIGATIONS
Awareness and recognition of the possibility of
Ludwigs angina is the first and most essential step in
the diagnosis and management of this serious
condition. The presence of brawny induration of the
floor of the mouth in a suggestive clinical presentation
should prompt the clinician to move rapidly toward
airway stabilization first, followed by further diagnostic
confirmation.
Plain radiographs of the neck and chest often show
soft-tissue swelling, the presence of gas, and the
extent of airway narrowing. Sonography has been used
to identify fluid collections in the soft tissues, as has
gallium citrate Ga-67 scanning. Panoramic radiographic
views of the jaw may show a dental focus of infection.
After the airway patency is assured, CT scanning is a
valuable modality to show the extent of soft-tissue
swelling, the presence of gas, fluid collection, and
airway compromise. Magnetic resonance imaging is
another elegant modality that can be considered in
some patients18.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of Ludwigs angina includes
angioneurotic edema, lingual carcinoma, sublingual
hematoma (following anticoagulation), salivary gland
abscess, lymphadenitis, cellulitis, and peritonsillar
abscess.
TREATMENT OPTIONS
Ludwig's angina was formerly invariably fatal but now,
with adequate surgical and antibiotic treatment, has a
much reduced rate of mortality6. It remains, however,
a potentially life-threatening condition because of the
risk of impending airway obstruction. Thus, because of

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Shamimul Hasan et al. UJP 2013, 02 (05): Page 1-4

its invasive nature, early recognition and treatment of
Ludwig's angina is extremely important.
The first therapeutic consideration in patients with
Ludwigs angina is the airway management, because it
is mandatory to preserve it early by means of a
fiberoptic nasotracheal intubation or tracheostomy.
Medical management with antibiotics, improved dental
care and dexamethasone in the early stages of the
disease has minimized the need for surgical
intervention to control the airway10. Different
antimicrobial regimen have been recommended to
cover in broad-spectrum the polymicrobial aetiology
(gram - positives, gram-negatives, aerobes and
anaerobes). Antibiotics used before obtaining the
culture and the antibiogram results, have been
penicillin
G
intravenous,
clindamycin
or
metronidazole20. Aminoglucosides have been also
associated in some studies 21. Other alternatives
described are ticarcilin, sulbactam-ampicilin or
piperacilin-tazobactam. Cervical incision and surgical
dbridement are indicated when there is suppurative
infection, radiologic evidence of fluid collection or
soft-tissue air, clinical fluctuance, crepitus, or a
purulent needle aspirate. Drainage is also indicated
when there is no clinical improvement after 24 at 48
hours of intravenous antibiotics. The delay in the
realization of the surgical intervention has been related
to mortality increase. It has been demonstrated that
early elimination of the dental focus of the infection
reduces the time of recovery17. Intravenous
dexamethasone and nebulized adrenaline have been
used to reduce upper airway edema in such cases to
defer or avoid airway instrumentation altogether22 .
In an exhaustive review of the literature, from 1945 to
1979, 75 cases of Ludwig angina were found, and the
authors strongly advocate elective tracheostomy under
local anaesthesia. However, there may be good reason
to avoid tracheostomy7. Cellulitis of the neck with in
volvement of the tracheostomy site makes it a more
difficult procedure. Moreover, surgical dissection of the
fascial planes in the neck may actually open and
contaminate the pathways, leading to life-threatening
mediastinal invasion19. More recent reviews of
anesthesia management report good results without the
use of tracheostomy15. Other options for airway
management
may
include
orotracheal,
blind
nasotracheal,
and
fiber
optic
intubation
or
cricothyroidotomy with jet insufflation.
The prognosis in Ludwigs angina depends primarily on
immediate protection of the airway and then on
prompt antibiotics, and possibly surgical treatment of
the infection. Mortality in the preantibiotic era was
50% but, with the advent of current therapies, has
declined to less than 5%.
COMPLICATIONS
The most serious complication of Ludwig's angina is
asphyxia caused by expanding edema of soft tissues of

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the neck23. Another common cause of death is the

acute loss of airway during interventions to control the
condition24. The possible serious complications include
sepsis,
pneumonia,
empyema,
pericarditis,
mediastinitis, and pneumothorax .

CONCLUSION
Ludwigs angina, a potentially alarming condition, is a
deep tissue infection that causes respiratory distress.
Clinical manifestations are bizarre, hence, accurate
diagnosis and treatment planning is required for the
survival of the patient. Mutidisciplinary approach
involving the dental surgeons, anaesthetists and ENT
(Ear Nose and Throat) specialists play an important role
in managing this fatal disease. Aggressive antibiotic
intervention, adequate hygiene maintainence may be
sufficient in the early stages, if correct diagnosis is
established.

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Source of support: Nil, Conflict of interest: None Declared

Universal Journal of Pharmacy, 02(05), Sep-Oct 2013