ORAL INFECTIONS and facial space infections
- 1. Fascial Spaces Def: The Facial spaces are the potential spaces between various layers of fascia normally filled with loose connective tissue and bounded by anatomical barriers, usually of bone, muscle or fascial layers. • Potential spaces into which Odontogenic infections can spread
- 2. continued •Fascial: Thin casing of connective tissue beneath the skin that surrounds and holds every organ, blood vessels, bone, nerve fibers and muscles in place. types •Superficial : loose connective tissue under the dermis. •Deep: Dense connective tissue that surrounds bone, nerves and blood vessels. •Visceral: Suspends organs within their cavity.
- 3. Classification • Based on mode of involvement- - Primary spaces: Those that can be infected via direct spread from periapical or periodontal infections.
- 4. continued -Secondary spaces: Those that are infected via spread from other facial spaces. • Primary maxillary- canine, buccal, infratemporal. • Primary mandibular- submental, sublingual, buccal, submandibular.
- 5. cont’d • Secondary spaces- masseteric, pterygomandibular, superficial & deep temporal, lateral pharyngeal, retropharyngeal, parotid, prevertebral • Based on clinical significance- - Face- Buccal, canine, parotid, masticatory. - Suprahyoid- Sublingual, submental, submandibular, lateral pharyngeal, peritonsillar. Infrahyoid- Pretracheal.
- 6. Cont’ • Spaces of total neck- Retropharyngeal, space of carotid sheath
- 8. Canine Space • It is the region between anterior surface of maxilla and overlying levator muscles of upper lip. • Contains angular artery & vein, infraorbital nerve. Etiology • Maxillary canine & 1stst premolar infection & sometimes • mesiobuccal root of first molars.
- 9. continued Boundaries- • Superiorly: levator superioris alaque nasi and levator labii superioris • Inferiorly: caninus muscle • Medially: anterolateral surface of maxilla • Posteriorly: buccinator mucsle. • Anteriorly: orbicularis oris
- 10. continued Clinical Features- • Swelling of cheek, lower eyelid & upper lip. • Drooping of angle of mouth. • Nasolabial fold obliterated. • Odema of lower eyelid
- 12. Drainage
- 13. Buccal Space Boundaries- • Superiorly: zygomatic arch. • Inferior: inferior border of mandible. • Laterally: skin & subcutaneous tissue. • Medially: buccinator muscle ,buccopharyngeal fascia. • Posteriorly: anterior edge of masseter muscle. • Anteriorly: posterior border of zygomaticus major & depressor anguli oris.
- 14. continued Contents- • Buccal fat pad. • Stenson’s duct. • Facial artery.
- 15. continued Etiology- • Infected mandibular & maxillary premolars & molars. Clinical Features- • Obliteration of nasolabial fold. • Angle of mouth shifted to opposite side. • Swelling in cheek extending to corner of mouth. • Buccal space associated with temporal space – Dumb bell shaped appearance due to lack of swelling over zygomatic arch.
- 17. Infratemporal Space • Boundaries- • Superiorly: infratemporal surface of greater wing of sphenoid. • Inferiorly: lateral pterygoid muscle. • Laterally: temporalis tendon & coronoid process. • Medially: lateral pterygoid plate & lateral pharyngeal wall. • Posteriorly: condyle & lateral pterygoid muscles. • Anteriorly: infratemporal surface of maxilla & posterior surface of zygomatic bone
- 18. continued
- 19. continued • Contents- • Pterygoid plexus of veins. • Internal maxillary artery. • Mandibular nerve & its branches. • Etiology- • Infected maxillary 3rd molars. • Infected needles or contaminated LA solution.
- 20. continued • Clinical Features- • Extra-oral swelling over sigmoid notch area. • Intra-oral swelling in tuberosity area. • Trismus. • Spread of Infection- • To temporal space. • Cavernous sinus thrombosis- infection spreads via pterygoid • plexus of veins.
- 22. Submental Space • Boundaries- • Roof: mylohyoid muscle. • Inferior: deep cervical fascia, platysma, superficial fascia & skin. • Laterally: anterior belly of digastric. • Posteriorly: submandibular space. • Contents- • Lymph nodes, anterior jugular vein.
- 23. Submental space
- 24. continued Etiology- • Infected mandibular incisors. • Anterior extension of submandibular space. Clinical Features- • Chin appears glossy & swollen. • Pain & discomfort on swallowing
- 26. Sublingual Space Boundaries- • Superiorly: mucosa of floor of mouth. • Inferior: mylohyoid muscle. • Posteriorly: body of hyoid bone. • Anteriorly & laterally: inner aspect of mandibular body. • Medially: geniohyoid,styloglossus,genioglossus muscle.
- 27. Sublingual Space cont’d Contents- • Deep part of Submandibular gland. • Wharton’s duct. • Sublingual gland. • Lingual & hypoglossal nerves. • Terminal branches of lingual artery
- 28. continued Etiology- • Infected mandibular premolar & 1stst molar. Clinical Features- • Swelling of floor of mouth. • Elevated tongue. • Pain & discomfort on swallowing
- 29. Sublingual space
- 31. Submandibular Space • Boundaries- • Superiorly: mylohyoid muscle, inferior border of mandible. • Inferior: anterior & posterior belly of digastric. • Laterally: deep cervical fascia, platysma, superficial fascia & skin. • Medially: hyoglossus,styloglossus,mylohyoid muscle. • Posteriorly: to hyoid bone. • Anteriorly: submental space.
- 32. Submandibular Space con’d • Contents- • Submandibular salivary gland. • Proximal portion of Wharton’s duct. • Lingual & hypoglossal nerves. • Branches of facial artery- palatine,tonsillar,glandular,
- 34. Submandibular Space con’d Etiology- • Infected mandibular 2nd & 3rd molars. • From submental,sublingual spaces. Clinical Features- • Indurated swelling in submandibular region. • Usually bulges over lower border of mandible. Spread of Infection- • Across midline to contralateral space. • To contiguous pharyngeal spaces.
- 37. Pterygomandibular Space Boundaries- Superiorly: lower head of lateral pterygoid muscle. Laterally: medial surface of ramus. Medially: medial pterygoid muscle. Posteriorly: deep part of parotid. Anteriorly: pterygomandibular raphe. Contents- Inferior alveolar neurovascular bundle. Lingual & auriculotemporal nerves. Mylohyoid nerve & vessels.
- 38. Pterygomandibular Space cont’d • Etiology- • Infected mandibular 3rd molars(mesioangular/horizontal) • Pericoronitis. • Infected needles or contaminated LA solution. • Clinical Features- • Absence of extra-oral swelling. • Severe trismus. • Difficulty in swallowing. • Anterior bulging of half of soft palate & tonsillar pillars with deviation of uvula to unaffected side.
- 39. Pterygomandibular Space cont’d • Spread of Infection- • Superiorly to infratemporal space. • Medially to lateral pharyngeal space. • To submandibular space
- 40. Masseteric Space Boundaries- • Superiorly: zygomatic arch. • Inferiorly: inferior border of mandible. • Laterally: masseter muscle. • Medially: ramus of mandible. • Posteriorly: parotid gland & its fascia. • Anteriorly: buccal space & buccopharyngeal fascia. Contents- • Masseteric artery & vein. Etiology- • Mandibular 3rd molars(pericoronitis).
- 41. Cont’ Clinical Features- • Swelling limited to masseter muscle. • Severe trismus & throbbing pain.
- 44. Temporal Spaces Superficial temporal- • Laterally: temporalis fascia. • Medially: temporalis muscle. Deep temporal- • Laterally: temporalis muscle. • Medially: temporal bone & greater wing of sphenoid. Etiology- • From infratemporal or pterygomandibular space.
- 45. Temporal Space ( Superficial & Deep)
- 46. continued Clinical Features- • Superficial temporal- swelling limited by outline of temporalis fascia. Trismus. Severe pain. • Deep temporal- less swelling, difficult to diagnose. Trismus.
- 48. Deep Neck spaces Extension of Odontogenic infections beyond the primary and secondary spaces is uncommon. When it occurs airway compromise and descending Mediastinitis are posibble complications Posterior spread of Pterygomandibular space infection is to the Lateral Pharyngeal space.
- 49. Lateral Pharyngeal Space Boundaries- • Shape of an inverted cone or pyramid, the base is at sphenoid bone and the apex at hyoid bone. • Anteriorly: pterygomandibular raphe. • Posteriorly: extends to prevertebral fascia. • Laterally: fascia covering medial pterygoid muscle, parotid & • mandible. • Medially: buccopharyngeal fascia on lateral surface of superior constrictor muscle. • Styloid process divides the space into anterior muscular and posterior vascular compartment
- 50. continued Contents- • Anterior compartment: fat, muscle, lymph nodes and • connective tissue. • Posterior compartment: carotid sheath(carotid artery, internal • jugular vein, vagu nerve), cranial nerves IX through XII.
- 51. continued Etiology- • Infected mandibular 3rd molars. • Tonsillar infections. • Pharyngitis. • Parotitis. Spread of Infection- • To retropharyngeal space. • To peritonsillar space.
- 52. continued Clinical Features- Anterior compartment: • Trismus. • Induration & swelling at angle of jaw. • Fever. • Pharyngeal bulging.
- 53. continued Posterior compartment: • Posterior tonsillar pillar deviation. • Neurological involvement. • Thrombosis of internal jugular vein. • Erosion of carotid vessels may occur.
- 54. Retropharyngeal Space • Posteromedial to lateral pharyngeal space and anterior to the prevertebral space . Boundaries- • Anterior: posterior pharyngeal wall. • Posterior: prevertebral fascia. • Superior: skull base. • Inferior: mediastinum. • Laterally: lateral pharyngeal space.
- 55. continued Etiology- • Nasal & pharygeal infections. • Spread from odontogenic infections.
- 56. continued Clinical Features- • Stiffness of neck. • Dysponea. • Dysphagia. • Bulging of posterior pharyngeal wall. Complications- • Airway obstruction. • Aspiration pneumonia. • Acute mediastinitis. • Can spread to Danger space.
- 58. Prevertebral Space • Potential space between two layers of prevertebral fascia (alar and prevertebral layers). • Extends from skull base superiorly to the diaphragm inferiorly. • Mediastinitis is concerned with prevertebral space infections similarly to retropharyngeal space infections
- 59. Danger space • Lies between the Alar fascia and Prevertebral fascia. • Span from base of skull to posterior mediastinum and diaphragm. • Extremely high risk due to high way of infection spread.
- 60. Fascia layers
- 62. Pontential pathways of fascial infections
- 63. Conclusion • Fascial planes offer anatomic highways for infection to spread from superficial to deep planes. • Fascial spaces are contiguous and infection readily spreads from one space to another ( primary to secondary spaces and vice verse). • Infections will always follow the path of least resistance “This is the general Rule of Thumb”
- 64. • The easiest path for bacteria and their by- products to travel depends on bone density, muscle thickness and muscle attachment. • Antibiotic availability in fascial is limited due to poor vascularity. • Treatment of infections depend on I & D
- 65. OBJECTIVES Applied anatomy of fascial space Aetiology, pathogenesis and Diagnosis Principal of management of odontogenic infections Ludwigs angina Necrotising fascitis
- 66. Introduction • Oral cavity consists of more than 500 bacterial taxa several fungal species, few protozoal genera and many viruses as normal residents. • Occurrence of infectious disease is determined by the interaction of host, the organism and the environment. • In healthy state there is a balance among these factors and when the balance is lost disease occurs.
- 67. • Infections of orofacial and neck region, particularly those of odontogenic origin, have been one of the most common diseases in human beings. • Despite great advances in healthcare, these infections remain a major problem. • Infections range from periapical abscess to superficial and deep neck infections. • Generally spread by following the path of least resistance through connective tissue and along fascial planes. • Infections spread to such an extent, distant from the site of origin, causing considerable morbidity and occasional death.
- 68. • Early recognition of orofacial infection and prompt, appropriate therapy is absolutely essential. • Remember the old adage—“Do not let the sunset on the prisoned pus.”
- 69. ETIOLOGY General classification: It is based on the origin of the infection. • ■ Odontogenic: The majority of infections in orofacial and neck regions belong to this group. -Odontogenic infections arise within the jaw bones, and can be classified as those arising from: ■ Noniatrogenic odontogenic infections: (i) Pulp disease, • (ii) Periodontal disease, (iii) Secondarily infected cysts
- 70. • These manifest in the following forms: (i) Periapical abscess, (ii) Periodontal abscess, (iii) Infected cyst, (iv)Residual abscess (v) Pericoronal infection.
- 71. Iatrogenic odontogenic infections ■ Traumatic: Occasionally, trauma from penetrating wounds of soft and hard tissues of the face can lead to orofacial infections. ■ Postimplant surgery ■ Postreconstructive surgery ■ Infections arising from contaminated needle punctures.
- 72. Others: ■ This group includes instances of orofacial infections arising from other factors, such as infected antrum, salivary gland afflictions, etc. ■ Secondary to oral malignancies
- 73. On the basis of causative organisms: Orofacial infections can be classified as: Bacterial infections: - Odontogenic infections encountered in orofacial region are mostly bacterial infections. - Nonodontogenic infections: (i) Tonsillar, and (ii) Nasal infections which are more common in children, and (iii) Furuncle of overlying skin. - Fungal infections: These infections have slow rate of spread. These are difficult to diagnose in early stages.
- 74. STAGES OF INFECTION Periapical infection/abscess • Dental infection that spreads across the pulp to the area extending beyond the apex of the tooth • localised at that site. • When the localised periapical infection undergoes an acute exacerbation with pus formation within the bony confines, it becomes periapical abscess.
- 75. Dental abscess • When a periapical abscess extends beyond the confines of the dentoalveolar bone into the vestibular space it becomes a classic dentoalveolar abscess. • It remains as a thick-walled cavity containing pus.
- 76. Cellulitis • When a periapical infection fails to localise as abscess, it results in cellulitis where infection rapidly spreads through fascial tissue planes diffusely. • Depends on the virulence of the organism and host resistance, • Bacterial infections have a potential to spread into the surrounding soft tissues, by hydrostatic pressure, following the path of least resistance, into loose areolar connective tissue of the fascia that surrounds the muscles.
- 77. Factors affecting spread of orofacial infection • I. Systemic factors a. Microbial factors • Level of virulence of the causative organism • Number of organisms introduced into the host b. Host factors • General state of health • Integrity of surface Capacity of inflammatory and immune response • Level of immunity • Impact of medical intervention c. Combination of both factors II. Local factors a. Alveolar bone and periosteum b. Neighbouring soft tissues, muscles
- 78. Mechanism of spread of infection Oral infection Originates in dental pulp Originates in periodontal tissue Through root canals Disperse through spongy bone Extended into periapical tissues May perforate cortical plate Spread into various tissues or discharge on free mucous membrane
- 79. Routes of spread The routes by which the infections can spread are as follows: 1. direct continuity through the tissues. 2. lymphatics to the regional lymph nodes and eventually into the bloodstream. When the lymph nodes gets established in lymph nodes, secondary abscesses may develop. • The spread of infection from the lymph nodes into the tissues results in secondary areas of cellulitis or tissue space abscess. 3. Bloodstream: Rarely, local thrombophlebitis may propagate along the veins, entering the cranial cavity via emissary veins to produce cavernous sinus thrombophlebitis. Microorganisms or infected emboli may get swept away into the bloodstream, leading to bacteremia, septicemia, or pyemia with the development of embolic abscesses
- 83. DIAGNOSIS • Evaluation of a patient with odontogenic infection follows the same basic principles of diagnosis as with any oral disease. The steps include 1.Thorough history taking 2. Clinical examination (general and regional) 3. Investigations—laboratory and radiological 4. Diagnosis and treatment planning
- 84. Algorithm for management of odontogenic infections • Assess disease severity and systemic state. • Emergency surgical or medical intervention as needed. • Evaluate patient. • Decide on setting of care (outpatient or admission). • Pus/discharge—swab for culture and sensitivity test. • Start antibiotics empirically and then change as per sensitivity test. • Treat surgically with adjunctive medical support. • Rehabilitate. • Evaluate the patient frequently
- 85. Principles of management of odontogenic infections 1. Treatment of the causes -Most infections have a distinct cause and only surgical treatment will prevent worsening and recurrence, -In advanced infection resulting in space infection and septicaemia, management strategies shift to medical management. - Management of acute odontogenic infections involves both surgical and supportive therapies.
- 86. Incision and drainage • Incision and drainage (I&D) is the foremost surgical method in treating space infection. • Create an escape route for the necrotic tissues, pus and microbes from • the tissue space. Objectives - Removal of dead tissue, pus, toxins and infective material that facilitate better immune defence mechanism. - Effectively reduce the surface area of infected tissue and thus minimising the dosage of antibiotic required. -Blunt dissection into the tissue spaces breaks the pus locules and fibrous barrier, thus facilitating reach of the antibiotics into the infective site. - Drainage is used for culture and sensitivity (C&S) based on which empirical antibiotic therapy may be continued or changed
- 87. Antibiotic therapy • Odontogenic infections are caused by a highly predictable group of bacteria, -Choice of the initial antibiotic is empirical. More than 90% of odontogenic infections are caused by aerobic and anaerobic streptococci, peptostreptococci, prevotella, fusobacterium and bacteroides.
- 88. SUPPORTIVE THERAPY - Analgesics, -nonsteroidal antiinflammatory drugs (NSAIDs) and nutritional support are mandatory. -Patients with infection and fever present a considerable loss of body fluids—250 mL for every degree (centigrade) temperature rise. -Ambulatory patients must drink 8–10 glasses of water or any other liquid. -Intravenous fluids can be given to those patients who are hospitalised to improve hydration. -The daily calorie requirement also increases by up to 13% for each degree (centigrade) above normal body temperature. -Thermal agents should be used to aid the body defences and not in a futile attempt to regulate localisation. - Potential risk of onset of respiratory impairment, requiring airway monitoring, perhaps even on an emergency basis, by means of endotracheal intubation, or tracheotomy.
- 89. LUDWIG’S ANGINA
- 91. Definition • Ludwig’s angina is a form of a firm, acute, toxic and severe diffuse cellulitis/induration that spreads rapidly, bilaterally affecting the submandibular, sublingual and submental spaces. • It was first described by Wilhelm Friedreich Von Ludwig in 1836. • The word ‘angina’ derived from Latin word ‘angere’ meaning suffocation or choking sensation; and the word ‘Ludwig’ from the person who first described it.
- 94. Aetiology • Ludwig’s angina is a disease primarily of dental origin although various causes can also be related. 1. Odontogenic infection • Dental aetiology has been reported as the causative factor in 90% of cases,either as primary dental infection or as post extraction phenomena, following infection of the second and third mandibular molars.
- 95. Aetiology cont’d 2. Traumatic injuries of orofacial region • Compound/comminuted mandibular fractures • Oral soft tissue lacerations • Puncture wounds of floor of the mouth • Osteomyelitis secondary to compound mandibular fracture • Trauma: mandibular fracture, facial fracture, tongue piercing
- 96. Aetiology cont’d 3. Submandibular and sublingual sialadenitis 4. Secondary infections of oral malignancies 5. Pharyngeal infection or tonsillitis. 6. Iatrogenic: Use of contaminated needle for giving local anaesthesia 7. Cervical lymphoid tissues 8. Miscellaneous: Foreign bodies such as fish bone
- 97. Predisposing factors ● Diabetes ● HIV/AIDS ● Neutropenia ● Alcoholism ● Aplastic anemia ● Glomerulonephritis ● Dermatomyositis ● Systemic lupus erythematous
- 98. Bacteriology • Commonly mixed infections involving both aerobes and anaerobes • Commonly alpha-hemolytic Streptoccoci, staphylococci and bacteriodes group • Rarely does it involve H.Influenza, E. Coli and Pseudomonas.
- 99. Pathophysiology
- 101. Pathophysiology cont’d • Infection extends contiguously to involve the sublingual and thus the entire submandibular space in a symmetrical manner. • This leads to a presentation of the cardinal signs of inflammation i.e. redness, pain, swelling, loss and function and pus • Cellulitis of the submandibular space may spread directly along the styloglossus muscle into the parapharyngeal space and from there to the retropharyngeal space and the superior mediastinum
- 102. clinical features General examination • General constitutional symptoms: Patient looks toxic, very ill, dehydrated, • chills and malaise. • Marked pyrexia • Difficulty in swallowing (dysphagia) • Impaired speech and hoarseness of voice
- 103. Clinical features cont’d Regional examination Extraoral examination: • Bilateral suprahyoid swelling is observed, with a hard, cardboard-like consistency. • Swelling is firm/hard brawny involving bilateral submandibular and submental regions. • It is nonpitting, not-fluctuating and tender on palpation. • Airway obstruction and cyanosis may occur due to progressive hypoxia
- 105. Clinical features cont’d • Early presentation has no suppuration but occurs late in the course of disease. Further, this phenomenon appears very rapidly and does not respect any anatomic barrier. • Mouth remains open due to the oedema of sublingual tissues and there is a resultant raised tongue with restricted movements. • Shallow breathing with accessory muscles of respiration being used and respiratory rate may be raised • Severe muscle spasm leading to trismus with restricted mouth opening and also jaw movement. • Fatal death may occur in untreated case of ludwig’s angina within 10–24 h due to asphyxia.
- 106. Clinical features cont’d Intraoral examination: • Swelling develops rapidly and involves sublingual spaces causing elevation of tongue against the palate. • Increased salivation, stiffness of tongue, dysphagia, odynophagia with hot potato speech is noted. • Drooling of saliva due to reduced control of muscles and jaw posture. • Backward spread of infection leading to oedema of the glottis, which leads to obstruction of airway. • Development of Stridor being the alarming sign for fatal extension necessitating emergency intervention to keep airway patent.
- 107. Clinical features cont’d Hallmark clinical features ● Bilateral Involvement of submandibular,sublingual and submental spaces with brawny edema. ● The swelling is firm, non fluctuant, non pitting and tender. ● Elevated tongue ● Airway obstruction ● Paucity of pus ● Trismus General features ● Fever ● Dehydration ● Anorexia ● Malaise ● Dysphagia ● Shallow breathing ● Hoarseness of the voice ● Drooling • Odynophagia
- 109. Investigations • Lab tests- Hemoglobin, CBC, blood glucose. • Panoramic xray • Cervical profile and posterior-anterior radiographs. • Ultrasound • CT Scan
- 110. Diagnosis • Clinically • FBC: leukocytosis • Culture and gram stain • Imaging • CT Scan: Imaging modality of choice for the diagnosis of Ludwig's angina and other deep neck space infections • Panoramic X-ray: To identify possible odontogenic sources • Cervical, profile and posterior-anterior radiographs: For any tracheal deviation and raising volume in the soft tissues • Ultrasound: Has been recommended to differentiate cellulitis, abscess and adenopathy in head and neck infection
- 111. Differential diagnosis • Cellulitis • Peritonsillar abscess • Sublingual hematoma • Lingual CA • Lymphadenitis
- 112. Complications • Spread of infection to the parapharyngeal and retropharyngeal spaces • Airway obstruction due to laryngeal edema • Septicemia • Aspiration pneumonia
- 113. Treatment objectives: 1.Airway management 2.Early antibiotic therapy 3.Incision and drainage(I and D) 4.Nutrition and hydration support 5.Extraction of the offending tooth Treatment
- 114. 1. Airway management • Tracheostomy: Was the gold standard in the past. Has risk of spreading infection to the mediastinum • Cricothyroidotomy: Has a much lower risk of mediastinal infection • Blind nasal intubation (BNI) • Fiber optic nasotracheal intubation: Useful especially in deep neck infections
- 115. 2. Medical management • It is important to gain IV access- for fluid and antibiotic administration. Antibiotics used to treat Ludwigs Angina are: • Penicillins with beta lactemase inhibitors • 2nd, 3rd and 4th generation cephalosporins • Metronidazole • Ampicillin/ Sulbutum and Clindamycin
- 116. 3 Surgical management • Principles (Topazian and Golberg) • Incise in healthy skin and mucosa when possible, not at the site of maximum fluctuance, because wounds tend to heal with an unsighty scar • Place the incision in a natural skin fold • Place the incision in a dependent position • Dissect bluntly • Place a drain; and • Remove drains when wounds become minimal.
- 117. Cont’d • Bilateral submandibular incisions as well as mid line submental incisions • Incision approximately 5 to 4 cm below the angle of the mandible and below the inferior extent of swelling roughly parallel to the inferior border of mandible • Intra oral incision: if localized to sublingual space • Extra oral incision: if involving sub maxillary space
- 119. 4.Nutrition and Hydration support • Put patient on I.V fluids to rehydrate • for energy if by oral patient cant feed, a nasogastric tube may be tried as I.V suplements are administered.
- 120. 5. Removal of causative agent • in this case its the offending tooth • foreign body ; Fish bone broken needle in the bone(medial surface of ramus of mandible)
- 121. NECROTISING FASCITIS
- 122. CONTENTS • Definition • Epidemiology • Aetiology • Classification • Risk factors • Spread • Clinical manifestation • Workup • Diagnosis • Management • DDX • Complications • Prevention
- 123. NECROTISING FASCITIS • Life-threatening, progressive, rapidly spreading, inflammatory infection located in the deep fascia • Infection rapidly destroys the skin and soft tissue beneath it. • Also known as ‘’flesh-eating’’ bacteria
- 124. Why is it dangerous? 1. Its difficult to diagnose. 2. Extremely toxic. 3. Spreads rapidly.
- 125. Epidemiology • Overall morbidity and mortality is 70 -80% • Male 3 : Female 1 • Often affects adults , pediatric cases are rare.
- 126. Aetiology • Its a direct sequela of bacterial infection ; 1. Odontogenic infections 2. Tonsillar or pharyngeal infections 3. Trauma 4. Salivary gland infections
- 127. Causative Organisms • Aerobic microorganisms, particularly Group A-haemolytic Streptococcus and • Staphylococcus, were initially considered to be the causal agents in necrotising fasciitis. • It was later demonstrated that the strict anaerobes played a very important role, representing a mixed or synergistic infection. • Microorganisms of the Bacteroides genus, Proteus, coliforms and Peptostreptococcus have been isolated, as have been Enterobacter and Pseudomonas.
- 128. Classification 1. Types 1- Polymicrobial NF (Aerobic & Anaerobic) - common after surgical procedures. 2. Type 2 –Monomicrobial NF ( Group A hemolytic streptococcus)
- 129. Risk factors Local • Primary odontogenic infection • Post extraction/post surgical infections • Salivary gland infections • Dermatological infections • Complication of Ludwig’s angina • Trauma
- 130. Risk factors cont’d Systemic • Immuno-suppression illnesses e.g proorly controlled DM ,cancer , HIV • Chronic renal failure • Liver disease • malnutrition • advanced age • Idiopathic • Malignancy
- 131. Spread • The ability of necrotizing fasciitis to move rapidly along fascial planes and cause tissue necrosis is secondary to its polymicrobial composition and the synergistic effect of the enzymes produced by the bacteria. • It primarily involves fascia then involves subcutaneous tissues and skin. • The bacteria from odontogenic origin(bacterial enzymes and toxins) via hematogenous spread invades soft tissues causing vascular thrombosis & occlusion results in ischemia and necrosis of fat and fascia.
- 132. Clinical manifestations Early signs and symptoms • Non-specific flu- like symptoms e.g fever, chills, nausea, weakness , dizziness. • Skin becomes tender, warm to touch, erythematous and begins to swell. • Experience pain greater than expected from the appearance of the wound. • Clinically indistinguishable from other possible soft tissue infections due to the non- specific symptoms.
- 134. Advanced symptoms • Excessive swelling over the affected area. • Multiple discolored patches develop to produce a large area of gangrenous skin. • Initial necrosis appears as a massive destruction of skin and subcutaneous tissue. • Skin and subcutaneous tissue are loosened. • Large, dark marks become blisters filled with yellow-green necrotic fluid.
- 136. Critical symptoms • 30% of people develop hemorrhagic bullae – makes them anemic. • Vasculature of the skin become inflamed and thrombosed. Results in necrotic eschars(similar to deep thermal burns). • Deeper muscle layers are involved. • Patients become numb because of nerve damage and progressing gangrene in the area. • Unconsciousness occurs as the body becomes too weak to fight off infections along with severe decrease in blood pressure. • Toxins released leads to septic shock with high fever, respiratory failure, heart failure and renal failure.
- 137. Work-up Inspection • Patient looks seriously ill • Erythematous neck region • Dusky/purplish discoloration • Blood blisters • Edematous Palpation • Local crepitations • Local tenderness
- 138. Work-up cont’d Internal examination(open wound) • Yellowish green necrotic fascia • Purulent discharge • Dark foul smelling necrotic fascia
- 139. Diagnosis (laboratory & imaging studies) • Complete blood cell count – high WBC count(>14,000/uL) , - reduced sodium(<135mmol/L) - elevated BUN level(>15mg/ml) • Elevated creatinine phosphokinase – indicates tissue breakdown. • Abnormal C-reactive protein(>10mg/L) – clinically active inflammation. • Antibiotic culture and sensitivity tests • X-ray – gas in subcutaneous fascial planes • C.T. scan – necrosis with asymmetric fascial thickening and gas in tissues. • MRI scanning NOTE: Imaging studies are useful for early diagnosis of Necrotizing fasciitis ,detecting gas in soft tissues and deep spaces of the neck.
- 140. (Surgical diagnosis) • Finger test – 2cm long incision is made under LA. Lack of fascial resistance , active bleeding and foul smelling fluid constitute a positive finger test. • Biopsy – Gold standard for detecting and diagnosing Necroitizing fasciitis either by taking tissues during or after debridement.
- 141. Management • Early diagnosis and treatment is vital. • Treatment goals; 1. Immediate resuscitation of patient 2. Administration of empirical antibiotics and analgesia 3. Identify causative agent and treatment of underlying systemic conditions. 4. Early , serial and aggressive debridement followed by skin grafts 5. Adequate nutritional support NOTE: Wash and dress wounds(adsorptive dressing and
- 142. DDX 1. Cellulitis 2. Ludwig’s angina 3. Retropharyngeal abscess
- 143. Complications • Mediastinitis • Septic shock • Sepsis • Death
- 144. Prevention • Most people are in good health before they become infected. • Basic hygienic practices reduce chances of infection • Keep all wounds clean. • Watch out for signs of infection(increase pain , swelling ,pus , fever) • Seek medical attention as soon as you notice symptoms of flesh – eating disease.
- 145. THE END