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Oral Disease for FINALS > Bacterial orofacial infections - their causes, spread and control > Flashcards

Bacterial orofacial infections - their causes, spread and control Flashcards

1
Q

Range of bacterial infections (11)

A 
Dental caries
Chronic & aggressive periodontitis 
Dentoalveolar abscess
Periodontal abscess
Acute streptococcal gingivostomatitis
ANUG & Noma
Tuberculosis
STDs – syphilis, gonorrhoea
Actinomycosis
Acute bacterial sialadenitis
Osteomyelitis
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2
Q

Classical signs of acute inflammation are diagnostic (5)

A 
Swelling
 Redness
 Pain or tenderness
 Heat
 Loss of function
-may also be systemic signs such as pyrexia or malaise as well as regional lymphadenopathy
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3
Q

Abscess formation (4)

A

Pus-filled pathoogical cavity
Can form as part of inflammatory response to acute infection
Acute exacerbations of chronic inflammation can also occur, followed by periods of quiescence
Every abscess should be drained

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4
Q

How can abscess formation be determined clinically (3)

A

‘Fluctuance’ to gentle palpation
Pressure exerted by 1 finger should be detected by another finger as ‘bounce’
If no fluctuance then cellulitis is present, which does not need drainage

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5
Q

Radiographs in diagnosis of an acute dentoalveolar abscess (3)

A

Radiographs do not typically show any change in periapical tissues
Because it take ~10 days for sufficient bone loss to occur to be detectable on an intra-oral film
Earliest sign is widening of perio ligament space

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6
Q

Clinical presentation of apical abscess - where will the abscess be (2)

A

Pus from an acute dentoalveolar abscess takes the track of least resistance through cancellous bone and points on nearest epithelial surface
Usually on buccal aspect of maxillary or mandibular alveolus, where overlying bone is thinnest, but can be palatally/ lingually

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7
Q

General measures: principles of acute infection (3)

A 
Admission if unwell
-IV abx + surgical drainage
Analgesia
-NSAIDS (pain relief and anti-pyrexial)
Control of infection
-abx given blindly as it not practical to await results of culture and sensitivity testing
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8
Q

Local measures: principles of acute infection (4)

A

Removal of the cause
Drainage Prevention of spread
Restoration of function

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9
Q

Abx used for dental abscesses (3)

A

Typically amoxicillin and metronidazole are used in combination, and changes made only in the face of microbiological results.

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10
Q

Local measures: removing the cause (2)

A

Most important principal
E.g. extraction of non-vital or hopelessly mobile teeth, removal of sequestrae (dead bone), foreign bodies or salivary calculi

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11
Q

Local measures: drainage (3)

A

Pus should always be drained and a surgical incision leaves less scarring than spontaneous drainage, particularly through skin
Abx not substitute

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12
Q

Drainage of IO abscesses (8)

A

Adequate anaesthesia – need to have sufficient anaesthesia to allow a painless incision. Use 2% lignocaine with adrenaline injected into the overlying mucosa, not into the abscess cavity.
Horizontal incision parallel to the occlusal surface of the teeth 1 – 2cm in length.
Take into account local anatomy eg mental nerve
Use a no. 11 blade held backwards with an upward sweep
Open the abscess cavity with artery forceps (Hilton’s method).
Hot salt water mouthwashes afterwards will encourage any remaining pus to drain.
Incising an abscess cavity to drain it is almost always sufficient for intra-oral abscesses. However, when pus has to pass through several tissue planes in order to escape, for example in deep neck abscesses, a drain can be inserted into the abscess cavity which is exteriorized into the mouth or onto the skin surface (sometimes both: through-and-through).

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13
Q

Local measures: prevention of spread (2)

A

This is achieved by drainage, use of antimicrobials and rest. Rest is difficult in the orofacial region, but trismus when present achieves this naturally.

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14
Q

Local measures: restoration of function (2)

A

Review the patient after the acute phase to ensure that things have settled and function has been restored. Sometimes trismus can persist and need treatment eg. Therabite.

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15
Q

Microbial aetiology of dentoalveolar abscesses (7)

A 
Black-pigmented anaerobes
 Fusobacterium
 Anaerobic cocci (Peptostreptococcus, Parvimonas)
Streptococcus
non-pigmented anaerobes
Eubacterium
spirochaetes
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16
Q

Symptoms of periodontal abscess (4)

A

Pain
Swelling - small localised to diffuse
Lymphadenopathy and fever may be present
Facial or neck cellulitis rare

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17
Q

Periodontal abcess - Tooth usually vital (3)

A

pre-existing periodontal pockets that become occluded (foreign body)
Trauma to the periodontium
Secondary infection of lateral periodontal cyst

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18
Q

Periodontal abscess - radiography (1)

A

Radiolucency on lateral aspect of root

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19
Q

Diabetic patients - periodontal abscesses (2)

A

Multiple seen in poorly controlled diabetes

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20
Q

Microbial aetiology of periodontal abscesses (2)

A

Same as chronic perio + candida

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21
Q

Treatment of periodontal abscesses (2)

A

Drain and debride

22
Q

Sptreptococcal gingivostomatitis (2)

A

Rare in non-compromised hosts
-most frequently follows tonsillitis
Severe inflammation of the gingivae with marked pain
Caused by S.pyogenes
-complications - fasciitis, tissue destruction, rheumatic heart disease, nephritis etc.
Differentiate from drug and viral causes

23
Q

Treatment of streptococcal gingivostomatitis (1)

A

Requires prompt treatment with penicillin

24
Q

Acute ulcerative gingivitis (3)

A

Poor oral hygiene, smoking, stress
Ulceration + destruction of interdental papilla - invasion of tissue
Halitosis, bad taste, malaise, lymphadenopathy

25
Q

Cancrum oris or Noma (5)

A

Usually preceded by ANUG and recent debilitating illness
Infection
-viral (e.g. measles)
-bacterial infection (e.g. Tuberculosis, scarlet fever)
-parasitic infection (e.g.malaria)
Immune-suppressive drugs/disease
Malnutrition
F. necrophorum, P. intermedia, T. vincentii, T.denticola, T.forsythia, a-streptococci

26
Q

Tuberculosis (3)

A

Increasing incidence in UK particularly among immigrants
Rare in oral cavity
-usually 2º to pulmonary TB
-cough or cervical lymphadenopathy
Can result in delayed healing after tooth extraction
- 2˚ osteomyelitis

27
Q

Tuberculosis investigation (3)

A

Biopsy- ZN
Culture – LJ 4-6 wks
(Serology), PCR, reactive T cells

28
Q

Tuberculosis - histology (2)

A

Epithelioid granulomas

Giant cells and caseation

29
Q

Syphilis - primary lesion (4)

A

Chancre on lip or tongue.
Ulcer, local oedema, painless
Smear shows spirochaetes
Lymphadenopathy

30
Q

Secondary syphilis (4)

A

~6 weeks after healing
Snail track ulcers
Lymphadenopathy
Skin rash

31
Q

Tertiary syphilis (3)

A

Now rarely seen in western world
Gumma on palate, tongue or tonsil
-firm, necrotic centre surrounded by inflamed tissue,
Leukoplakia on dorsum of tongue and increased incidence of oral cancer

32
Q

Congenital syphilis (2)

A

Hutchinson’s incisors

Mulberry molars

33
Q

Gonorrhoea (4)

A

Pharynx and any part of oral mucosa can be affected
Pain and lymphadenopathy
Variable appearance
-Ulceration
-Oedema
-Pseudomembranes
Direct examination of a smear and/or culture necessary to diagnose Neisseria gonorrhoeae

34
Q

Actinomycosis caused by (3)

A

Actinomyces israelii, A.oris, A.naeslundii

35
Q

Treatment for actinomycosis (2)

A

Surgical drainage & debridement

Antibiotics 6-8 weeks

36
Q

Acute bacterial sialadenitis features (3)

A

Ascending infection – mainly parotid,
Usually failure of secretion
-Sjögren’s syndrome, gland pathology, sialolithiasis, drugs
Unilateral, firm, red swelling, extreme pain, trismus, possibly febrile, milking duct releases pus

37
Q

Sampling for acute bacterial sialadenitis (4)

A 
Difficult
Microbial causes
-oral streptococci
-oral anaerobes
-staphylococcus aureus
38
Q

Tx for acute bacterial sialadenitis (2)

A

Amoxicillin, flucloxacillin

39
Q

Exploration of acute bacterial sialadenitis (2)

A

sialography AFTER resolution, possibly surgical exploration

40
Q

Angular cheilitis causes (3)

A

Haematological deficiency – Fe, vitamin B2,3,6,12
Candida sp., Staph. aureus, (Strep. pyogenes) – alone or mixed
Treat with miconazole, nystatin or fusidic acid, depending on cause

41
Q

Spread of infection - anatomy (3)

A

The spread of dentoalveolar infections is governed by the site of origin and the surrounding tissue planes that are limited by fascial layers and muscle insertions. The position of the apices of the originating tooth relative to muscles and fascia will influence the clinical presentation

42
Q

Fascial planes and tissue spaces

A

The neck is surrounded by multiple layers of fascia, of which the deep cervical fascia is the most important. These fascial layers continue superiorly and split around various structures to form tissue spaces. Fascial planes and tissue spaces are an anatomical framework for understanding how infection can spread.

43
Q

3 different parts to deep cervical fascia (3)

A

Investing layer
Visceral layer
Prevertebral fascia

44
Q

Spread in the mandible - antomy

A

How infection spreads from a mandibular tooth depends on the relation of the tooth to the insertion of 2 muscles: buccinator and mylohyoid. Buccinator attaches to the lateral (buccal) cortex of the mandible, adjacent to the molar teeth, and mylohyoid attaches to the mylohyoid ridge, which is on the medial (lingual) cortex.
Abscesses that track laterally, above buccinator point in the mouth. Those below buccinator point onto the facial skin.
Abscesses that track medially above mylohyoid point in the sublingual space. Those below mylohyoid point into the submandibular space
Infection from lower 2nd and 3rd molars can also track posteriorly into either the masticator space or the parapharyngeal/retropharyngeal spaces.
A sub-masseteric abscess causes profound trismus, and the patient will not be able to open their mouth
Spread into the parapharyngeal and/or retropharyngeal spaces is dangerous due to possible airway compromise and tracking of pus into the chest via the retropharyngeal space.

45
Q

Spread in the maxilla

A

Most maxillary dental abscesses track buccally, as the bone is thinnest here, to point in the mouth, but abscesses arising from upper lateral incisors and palatal roots of 1st molars can point palatally.
The relationship between the tooth apices and the levator anguli oris and buccinator muscles determines whether the abscess points in the oral cavity or on the skin of the cheek. The apex of the upper canine tooth can occasionally be situated above the origin of levator anguli oris, and infection can therefore present at the medial canthus of the eye, deep to levator labii superioris.

46
Q

Presentation of deep neck space infection (5)

A

These are rare, but most are dental in origin, typically from mandibular 2nd/3rd molars as their apices are often below the mylohyoid muscle.

Presenting features include:
 Fever
 Pain
 Sore throat
 Difficult or painful swallowing (dysphagia, odynophagia)
 Trismus
47
Q

Management of deep neck space infection (3)

A

The same principals of management of intra-oral abscesses apply, namely general and local measures, but broadly speaking the mainstays are:
Airway management
Intravenous antibiotics
Surgical drainage

48
Q

Complications of orofacial infections - cavernous sinus thrombosis

A 
The cavernous sinus is a venous sinus that surrounds the pituitary gland. It receives blood from the orbits, skull vault and cerberal hemispheres. At the medial canthus of the eye there is communication between the facial and opthalmic veins. Infection from an upper anterior tooth can, very rarely, drain into the cavernous sinus, causing venous thrombosis.
The presenting symptoms are:
 Opthalmoplegia (no eye movements)
 Ptosis (drooping upper lid)
 Proptosis (bulging eye)
 Chemosis (red eye)
49
Q

When are antibiotics indicated (5)

A 
When systemic symptoms present
-fever, malaise, nausea etc.
Spreading infections 
Chronic infection despite drainage 
-e.g. actinomycosis
Immuno- or medically compromised
Conditions difficult to resolve without or that speed up recovery
-osteomyelitis, ANUG, sialadenitis
LOCAL MEASURES FIRST - ABX USUALLY NOT FIRST LINE TX
50
Q

How to use anti-microbials (3)

A

Must be aimed at the organism(s) present
Dose must achieve 4-8 times MIC in blood
-keep up-to-date with BNF
Must be present long enough to penetrate adequately to the site - but not too long

51
Q

Selection of agent (3)

A

Broad spectrum agents
-associated with rise in C. difficile disease
-care when prescribing to elderly and GI disease (including proton pump inhibitors and reflux disease)
Empirical use
-main drugs are amoxicillin, pen V, metronidazole and erythromycin
-clindamycin, co-amoxiclav, clarithromycin no advantage
Do not prescribe for
-pulpitis
-prevention of dry socket
-in difficult extractions in immunocompromised

52
Q

Reasons why antibiotics fail (4)

A 
Agent does not reach the site
-inadequate drainage
-poor blood supply
-presence of a foreign body 
-inadequate duration
Impaired defences
-immunocompromised (bacteriostatic agent used)
Inappropriate agent - resistance
-inherent; acquired (mutation, plasmids) 
Poor patient compliance

Oral Disease for FINALS (34 decks)

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