2. Presentation Outline
• Objectives
• Introduction
• Applied anatomy-fascial spaces
• Specific entities- aetiology, microbiology, pathogenesis
• Principles of management
• Complications
• Sample Clinical Cases
• References
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3. Objectives
• To understand the relevant anatomy
• To diagnose and distinguish between the common maxillofacial
infections
• To identify and manage key risk factors
• To manage common maxillofacial infections
• To make appropriate decisions including appropriate referrals
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4. Introduction
• Infection is the invasion of an organisms body tissues by disease
causing agents, their multiplication, and the reaction of host
• Chain of infection: 6 components- pathogen, reservoir, portal of exit,
mode of transmission, portal of entry, susceptible host.
• Infections Global burden
• Local picture
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5. Fascial Spaces
• Potential tissue spaces made of delicate meshwork or loose CT
• Primary and secondary fascial spaces
• Primary-become directly involved /infected directly from odontogenic
sources
• Maxillary- infratemporal, canine, buccal
• Mandibular- buccal, perimandibular (sub-mental,sublingual, submandibular)
• Secondary-communicate with primary spaces
eg masticator spaces- 4 compartments-superficial and deep
temporal,infratemporal,masseteric, pterygomandibular(pterygoid) and
Deep cervical fascial spaces eg lateral pharyngeal,retropharngeal,
prevertebral.
• Fascial spaces -are they good or bad?
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10. Ludwig’s Angina
It is an acute,overwhelming and rapidly spreading septic cellulitis, involving peri-
mandibular spaces bilaterally.
ETIOLOGY:
• Odontogenic infection-Extension of infection from mand. 2nd & 3rd molar
teeth into the floor of mouth
• Trauma-soft tx laceration & punctured wounds of oral floor
• Submand. gland sialadenitis & infected malignancy
• Salivary calculi
• Osteomyelitis-e.g compound mand. fracture
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11. Ludwig’s Angina
BACTERIOLOGY: Polymicrobial
• Most common-streptococci viridans and staph.aureus.
• Others-Alpha hemolytic streptococci, peptostreptococci, bacteriodes,
klebsiella, fusiform bacilli & E-coli.
C/F:
• The terrible Ds- dyspnea, dysphagia, odynophagia, drooling, dysarthria,
• Diffuse painful swelling with no signs of localization, Neck pain
• Floor of mouth appears erythematous & edematous, redness of neck
• Fever with chills
• Weakness, fatigue, confusion
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12. Necrotizing Fasciitis Syndrome
• Distinct entity from Ludwig’s angina.
• Rapidly progressive inflammatory infection of the fascia with secondary
necrosis of the subcut. tissues.
• Polymicrobial- anaerobic and gram negative bacteria -symbiosis and
synergy maybe responsible for rapid progress
• Monomicrobial- Group A beta hemolytic streptococcus.
• Spreads along fascial spaces
• Lack of classical tissue inflammatory signs
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13. Necrotizing Fasciitis Syndrome..cont.
• M>F 2-3:1, 4-5th decades, Rare in children(malnutrition, vascular lymphatic
malformations
• Risk factors- DM (20-40%), Ca, ISS, Alcoholism, liver dx (cirrhosis), neutropenia,
organ transplants, vascular disease.
• Note- Approx. 50% of strep. fasciitis occur in young healthy people
• Is preceded by excruciating pain disproportionate with the actual tissue destruction
• Fascial tissue necrosis is often more advanced than it appears
• Putrid discharge, bullae, anaesthesia of overlying skin
• Emphysema- air in tissues- H, N, HS
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14. Necrotizing Fasciitis Syndrome..cont.
• High morbidity and mortality(20-80%)- aggressive treatment indicated
• Late intervention- involvement of deeper muscle layers- myositis,
myonecrosis.
• Prognostic factors- pt characteristics, pathogens , infection site, speed of
treatment
• Poor prognosis- liver and renal dysfunction, gram negative, age
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15. Necrotizing Fasciitis Syndrome..cont.
• Surgery is the primary Rx- wide extensive debridement
• Clindamycin work better than penicillin
• Hemodynamic instability may worsen the skin necrosis
• Resurfacing of the wound done once healthy granulation tissues occurs
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16. Necrotizing Fasciitis Syndrome.. pathogenesis
• Entry of microbes-enzymes and toxins production, bacterial surface protein
expression M1, M3 allows for adherence of strep. to tissues and evasion of
phagocytosis by PMNs, thrombosis, vascular occlusion, ishaemia- necrosis
– damage of superficial nerves- septicemia+ systemic toxicity
• Streptococcus pyrogenic exotoxins (SPEs) A,B,C are directly toxic and
together with streptococcus superantigen lead to production of cytokine
and hypotension.
• Staph. aureus maybe caused by Panton- Valentine leukocidin toxin
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17. Principles of Management
• Prompt diagnosis
• Air management and protection
• Fluid resuscitation and optimal nutrition
• Source control
• Aggressive iv antibiotic therapy-empiric, then definitive after C/S
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18. Principles of Management
• Decompression/Incision and drainage - copious amounts of normal
saline
• Debridement
• Analgesia and management of inflammation
• Identification and management of the risk factor
• Appropriate and early referral
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19. Complications
• Airway obstruction
• Dehydration
• Empyema thoracis, Mediastinitis, aspiration pneumonia, and pleural
effusion
• Cavernous sinus thrombosis, orbital and cerebral abscesses ± meningitis
• Septic shock- MOD if not managed
• Death
• Others- carotid arterial rupture, thrombophlebitis of the IJV, pericardial effusion, osteomyelitis
of the mandible, subphrenic abscess, Lemierre syndrome
Preventive dental care is the best way- regular dental reviews and treatment and good oral hygiene practices.
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Fascial and not facial
Infratemporal space is part of masticator region but is considered a primary fascial space
Are they good or bad?
Infections of the masticator space leads to Trismus
Infections can spread directly from the maxillary 3rd molar to the infratemporal space thus a primary space but often spread secondarily
Note the posturing- open mouth of the patient- dyspnoea
2021 Had gone for witchcraft intervention that did not work. Trismus and severe pain
It is a cellulitis buts its sequelae may lead to abscess
Odontogenic- neglected caries, periodontitis,pericoronitis postprocedural infections,
Breach of defensive- skin barrier- Malignancies, trauma, large cysts
Bruising of the neck creases (poor neck hygiene)- common in paeds
Cardinal signs of Celsus
3 syndromes- type 1 polymicrobial, type 2 streptococcal, type 3 gas gangrene- clostridium polymyonecrosis
Nitrogen, HS and hydrogen, accumulate due to their low solubility in water
Perfusion is a factors of capillary pressure
Hypotension worse in hemodynamic unstable patients
Avoid iodine, hydrogen peroxide snd naocl 80% sensitive to penicillins mean hospitalization about one week
Put a corrugated drain- incise on health skin
Generous debridement
Steroids for suspected laryngeal oedema
Mostly due to late presentations, late diagnosis, inadequate management can lead to increased hospitalization, increased morbidity and mortality and high costs of treatment.
Knowledge is paramount!
Diabetic- poorly controlled
When you have done what is possible you can sit and enjoy your sunset