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Case Report

Ludwigs angina: A case report and review of management

Sasikala Balasubramanian, P. Elavenil, S. Shanmugasundaram, J. Himarani, V. B. Krishnakumar Raja

Department of Oral and Maxillofacial Surgery, SRM Dental College and Hospital, Ramapuram, Chennai, Tamil Nadu, India

ABSTRACT
Space infection in the Oral and Maxillofacial region is common from odontogenic origin
especially in the immunocompromised patients. Ludwigs angina which is relatively
uncommon remains a potentially life-threatening condition due to the risk of impending
airway obstruction. Thus, because of its invasive nature, early identification and
management of Ludwigs angina is extremely important.

Key words: Airway obstruction, Ludwigs angina, life-threatening, space infection

INTRODUCTION substance of the tongue in the cleft between the hypoglossus

Ludwigs angina was first described by the German surgeon
Wilhelm Friedrich von Ludwig in 1836as a rapidly and
frequently fatal progressive gangrenous cellulitis and edema
of the soft tissues of the neck and floor of the mouth.[1]
Ludwigs angina is a severe diffuse cellulitis that presents an
acute onset and spreads rapidly, affecting the submandibular,
sublingual, and submental spaces bilaterally resulting in a
state of emergency because of impending airway obstruction.
Ludwigs angina usually starts with submandibular space
infection from second or third lower molar then it spreads
to the sublingual space of the same side. From there it
crosses to the opposite side sublingual space and thence to
the contralateral submandibular space. The involvement of
submental space is by lymphatic spread. It can also start from
sublingual space and progress to the submandibular space.
Infection from the sublingual space spreads posteriorly in the
Address for correspondence:
B Sasikala,
Senior Lecturer, Department of OMFS, SRM Dental College and
Hospital, Ramapuram, Chennai-89, Tamil Nadu, India.
E-mail: sasikalabalasubramanian@yahoo.in
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DOI:
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SRM Journal of Research in Dental Sciences | Vol. 5 | Issue 3 | July-September 2014
and genioglossus muscles and reaches epiglottis which causes
edema of the glottis and respiratory obstruction.[2]
Causes 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, and tongue piercing. Of all
these, the major cause is of odontogenic infection, mainly
from the second and third lower molar teeth.[3]
Predisposing factors are dentalcaries, recent dental treatment
like dental extraction, systemic illness such as diabetes mellitus
(DM), malnutrition, alcoholism, compromised immune
system like AIDS, organ transplantation, and trauma. In
children, it can occur de novo, without any apparent cause.[4]
In Ludwigs angina, patients demonstrate swelling in the floor
of the mouth and neck, pain, malaise, fever, and dysphagia. In
these patients, inability to swallow saliva and stridor indicate
imminent airway compromise. The most feared complication is
airway obstruction due to elevation and posterior displacement
of the tongue and edema of the glottis.[5]
The presence of swelling in the neck and floor of the mouth,
edema of the glottis, makes it difficult to anaesthetize the
patient. Aggressive use of intravenous antibiotics and surgical
decompression with removal of source of infection and airway
management is mandatory to prevent mortality.[6]
CASE REPORT
A 65-year-old patient reported to the Department of Oral
and Maxillofacial Surgery with chief complaints of inability
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Balasubramanian, et al.: Ludwigs angina

to open the mouth, pain and difficulty in swallowing with a
swelling in relation to the lower jaw and neck for the past 4
days [Figures 1-3]. On physical examination, he was toxic in
appearance and his vital signs were monitored immediately.
Thetemperature was 100F with a pulse rate of 80 beats per
minute (BPM), blood pressure (BP) of 100/70 mmHg, and a
respiratory rate of 22 breaths per minute. Mouth opening was
limited to 1.5 cm (interincisal distance). Extra-oral swelling
was indurated and non-fluctuant with bilateral involvement
of the submandibular and sublingual region. An infected
third molar had been extracted 3 days earlier. An immediate
diagnosis of Ludwigs angina was made, and the patient was
posted for surgical decompression under local anesthesia
with monitoring of oxygen saturation and vital signs by
anesthesiologist. The blood report was normal except for rise
in erythrocyte sedimentation rate (ESR), total white blood
cell (WBC) count, and neutrophils. In the operating theater,
electrocardiography, noninvasive BP, and pulse oximetry
were used for monitoring vitals. Intravenous access was
obtained and an infusion of normal saline started. Separate
stab incisions was made in relation to the submandibular
space bilaterally and submental space. A sinus forceps was
introduced to open up the tissue spaces and pus was drained
[Figure 4]. The wound was irrigated with normal saline, and
corrugated rubber drain was placed and secured to the skin
with silk sutures [Figure 5]. Intra-operatively, the vitals were
stable. Intravenous administration of Cefotaxime1gbd
(two times), Gentamycin 80 mg bd, Metronidazole 500 mg,
tid (three times a day) were given for 5 days. Postoperative
irrigation was done through the drain which was removed
after 36 hr. Patient recovery was satisfactory. The following
morning the patient was comfortable, with a pulse rate of 68
BPM, BP of 110/70 mmHg and oxyhemoglobin saturation of
97%. The neck swelling had regressed [Figures 6-9].
DISCUSSION
Ludwigs angina in the preantibiotic era which carried a
very high mortality rate of around 50%has dropped down
to around 8-10% today. The bacterial organisms generally
isolated include Streptococci viridans, Staphylococcus aureus,
and Staphylococcus epidermidis. Only 7% of Ludwigs
angina cases are due to group A -hemolytic streptococcus.
Initial antibiotic treatment should be broad spectrum to

Figure 1: Pre operative- frontal view Figure 2: Pre operative- neck view

Figure 3: Pre operative- mouth opening Figure 4: Draining pus

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Balasubramanian, et al.: Ludwigs angina

Figure 6: Immediate post operative - neck view

Figure 5: Drain fixed

Figure 8: Late post operative- neck view

Figure 7: Late post operative- frontal view
of presentation. The surgeons experience, existing resources,
and personnelare all essential factors forassessment.

Tracheal intubation with a flexible bronchoscope by using

topical anesthesia is highly successful in adult patients with
deep neck infections. Tracheostomy using local anesthesia
is recommended if fiberoptic intubation is not feasible,
the clinician is not skillful in the use of awake -fiberoptic
intubation, or when intubation attempts have failed.[8]

Larry W. Moreland et al., from their clinical experience and

Figure 9: Late post operative- mouth opening
cover gram-positive and gram-negative bacteria as well as
anaerobes. Penicillin, metronidazole, clindamycin, and
ciprofloxacin are commonly the antibiotics of choice.[7]
The treatment plan for each patient should bebased on the
phase ofthe infection and associated conditions at the time
SRM Journal of Research in Dental Sciences | Vol. 5 | Issue 3 | July-September 2014
literature review concluded that conservative management of
Ludwigs angina is acceptable in selective cases, provided that
early antibiotic therapy is commenced and any collectable
abscess is drained. They proposed an airway management
protocol for these cases. Patients are then categorized as
having either a severe airway compromise or a stable airway
based on respiratory rate, oxygen saturation, and findings on
fiberoptic laryngoscopy. In the severely compromised group
(patients unable to maintain saturation on room air above
95%, respiratory rate >25, or a significant airway compromise
on fiberoptic laryngoscopy) a definitive airway is required.
They suggested awake, fiberoptic-assisted intubation should
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Balasubramanian, et al.: Ludwigs angina
be attempted first; if this fails then a surgical tracheostomy
is performed under local anesthesia.[9]
In some patients intravenous dexamethasone and nebulized
adrenaline have been used to reduce upper airway edema
to defer or avoid airway instrumentation altogether. Oro-
tracheal intubation by direct laryngoscopy may be difficult
due to distorted airway anatomy, trismus and tissue
immobility. Blind nasal intubation is to be avoided as it could
cause catastrophic bleeding, laryngospasm, airway edema,
rupture of pus into the oral cavity, and aspiration. In skilled
and experienced hands, flexible fiberoptic nasal intubation
is the preferred method of airway management and has a
high rate of success. When fiberoptic bronchoscopy is not
feasible, not available, or has failed, cricothyrotomy and
tracheostomy are the options.[10]
CONCLUSION
Management of Ludwigs angina should be based on
patients clinical condition. It is essential to identify Ludwigs
angina in the earlier stages of the disease, when it is easier
to manage. In advanced cases, airway management and
surgical drainage with organism specific antibiotic therapy
are important in avoiding complications.
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How to cite this article: Balasubramanian S, Elavenil P,
Shanmugasundaram S, Himarani J, Krishnakumar Raja VB. Ludwigs
angina: A case report and review of management. SRM J Res Dent Sci
2014;5:211-4.
Source of Support: Nil, Conflict of Interest: None declared