LUDWIG’S ANGINA
Definition
• Ludwig’s angina is a form of firm, acute, toxic and
severe diffuse cellulitis that spreads rapidly,
bilaterally, affecting the submandibular, sublingual
and submental spaces and resulting in a woody
swelling.
Etiology
Dental infection most commonly the mandibular
3rd molar in 90% of cases.
Oral soft tissue lacerations.
Puncture wounds of the floor of the mouth.
Submandibular gland sialadenitis.
Secondary infections of oral malignancies.
MICROBIOLOGY
Streptococci are most commonly reported
Clinical Features
Bilateral suprahyoid swelling with hard
consistency,non fluctuating & painful on
palpation
Swelling is characterized by rapid onset
Difficulty in breathing (dyspnea),
Difficulty in swallowing (odynophagia)
Restricted tongue movements, elevated tongue,
inability to open the mouth, salivation
Patients may exhibit muffled voice due to edema
of vocal apparatus (hot potato voice)
Firm, brawny swelling in bilateral submandibular
& submental and sublingual spaces, non
fluctuant,tender with ill defined borders
Open mouth due to edema of sublingual tissue
Airway obstruction due to edema of the glottis and
floor of the mouth
Infection can spread to involve the masticator
space and Para pharyngeal space in the latter
stages of the disease
Signs & Symptoms
General examination:
1) Patient looks toxic
2) Marked pyrexia
3) Chills and malaise
4) Dysphagia
5) Impaired speech
6) Hoarseness of voice
7) Patient looks dehydrated
8) Respiratory rate is raised.
The cardinal signs of Ludwig’s angina are:
1. Bilateral involvement of more than a single deep
tissue space
2. Putrid infiltration but little or no frank pus
3. Involvement of connective tissue, fascia, and
muscle but not glandular structures
4. Spread via facial space continuity rather than by
lymphatic system
Diagnosis and Investigations
• Ultra-Sonography : Used to identify fluid
collection in the soft tissues.
• O.P.G
• C.T. Scan
• M.R.I
• Culture & sensitivity
• Blood investigations:
a) WBC count
b) Hb%
c) ESR ….. ALWAYS RAISED IN INFECTIONS
d) HIV & Hbs-Ag
e) RBS
PRINCIPLES OF MANAGEMENT
• Early diagnosis.
• Maintenance of patent airway.
• Intense and prolonged antibiotic therapy.
• Extraction of the offended teeth.
• Surgical drainage / decompression of facial spaces.
• Proper post operative care.
Antibiotic Therapy
•
Antibiotic therapy (intravenous) should be
intense
•
Choice of antibiotics include
Penicillin+metronidazole
or
Clindamycin
METRONIDAZOLE
• Immediate infusion of Metronidazole - 500mg
• Brings about rapid improvement
• Repeated every 8 hours
Steroids
• Reduce edema
• Used routinely when airway compromise
suspected
• Dexamethasone- 10 - 20mg IV
4 - 6mg 6th hourly for 8 doses
Complications
• Septicemia.
• Obstruction of upper respiratory airways.
• Aspiration pneumonia.
• Spread of infection into Para pharyngeal spacesmediastinum-produce thoracic empyema
OSTEOMYELITIS
DEFINITION
In Greek osteon means bone
myelos means marrow
itis
means inflammation
“ Osteomyelitis may be defined as an
inflammatory condition of bone, that begins
as an infection of medullary cavity and
haversian systems and extends to involve the
periosteum of the affected area ”
CLASSIFICATION
• Simplest and the most used is based on
presence or absence of suppuration
• Based on clinical course
Based on suppuration
SUPPURATIVE
ACUTE SUPPURATIVE
CHRONIC SUPPURATIVE
- PRIMARY
- SECONDARY
INFANTILE
NON SUPPURATIVE
CHRONIC SCLEROSING
- FOCAL
- DIFFUSE
GARRE’S SCLEROSING
ACTINOMYCOTIC
SPECIFIC INFECTIVE
- TUBERCULOSIS
- SYPHILIS
RADIATION
CLASSIFICATION
• BASED ON CLINICAL COURSE
ETIOPATHOGENESIS
Infection
3 culprits
Trauma
Ischemia
PROCESS OF OSTEOMYELITIS
Acute inflammation following infection
⇃
Hyperemia,
⇃
Capillary permeability ↑and infiltration of granulocytes
⇃
Tissue necrosis
⇃
Destruction of bacteria, vascular thrombosis & Pus forms
⇃
Intramedullary pressure ↑ as pus accumulates -> anesthesia
compression
⇃
Vascular collapse, venous stasis and ischemia
⇃
Pus accumulates with Stripping of
periosteum
⇃
vascular supply reduced
⇃
periosteum penetration and mucosal
fistulas
⇃
chronic Inflammation->granulation tissue
& lysis of bone
⇃
separation of necrotic bone (sequestra)
⇃
sheath of new bone (involucrum)
CLINICAL FEATURES
INCIDincidENCEe:
10 / 100,000
AGE:
10 – 30 YEARS
SITE:
MANDIBLE > MAXILLA (83% : 1%)
BODY - 20%
ANGLE - 18%
RAMUS - 7%
CONDYLE - 2%
Acute oml
GEN. CONSTITUTIONAL SYMPTOMS
DEEP, BORING, INTENSE CONTINUOUS PAIN
PARAESTHESIA OR ANAESTHESIA OF LIP
FACIAL CELLULITIS OR INDURATED
SWELLING
FOETID ODOUR
TEETH – TENDER
TRISMUS
Chronic oml
PAIN IS MINIMAL
NONHEALING WOUNDS WITH INDURATION
INTRA ORAL OR EXTRA ORAL SINUS
THICKENED OR WOODEN CHARACTER OF BONE
ENLARGEMENT OF MANDIBLE
PATHOLOGICAL #S
LOOSE , TENDER TEETH
Radiographic evaluation
• 30-60% destruction min 4-8 days to 3 wks.
• Mouth eaten appearance, scattered areas of
bone destruction
• Islands of sequestrae in radiolucent areas
surrounded by involucrum
INVESTIGATIONS
Histopathology
• Blood and aspirate culture.
• FNAC (infants.)
• Samples for culture should be taken from infected cavity wall,
sequestrum, granulation tissue, involucrum and sinus tract
(misleading).
• Organism can be identified and tested for antibiotic sensitivity.
MANAGEMENT
A. Conservative
B. Surgical
CONSERVATIVE MANAGEMENT
• Supportive therapy- e.g. nutrition.
• Control of pain- using analgesics and
sedatives.
• Antimicrobial agents.
ANTIMICROBIAL THERAPY
• Penicillin remains the time- honoured
antibiotic of choice for osteomyelitis.
• Then after obtaining culture and sensitivity
report specific therapy is started.
Surgical management –
Incision & drainage
Extraction of teeth
Closed wound irrigation & drainage
Intra-arterial antibiotics
Sequestrectomy
Sequestrectomy with saucerization
Trephination or Fenestration
Decortication
Resection
Hyperbarbic oxygen therapy
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