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oral surgery 4th year > infection > Flashcards

infection Flashcards

1
Q

acute dentoalveolar abscess

A

localised suppurative inflammation involving teeth and supporting structures

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2
Q

what the the pathogens mostly in an acute dentoalveolar abscess?

A

anaerobes

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3
Q

acute dentoalveolar abscess - how do pathogens gain entry to PA tissue?

A

through necrotic pulp or PDL

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4
Q

acute dentoalveolar abscess S+S

A

pain on biting (pressure on apical pathology)
pyrexia
lymphadenopathy

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5
Q

what can lack of appropriate tx of an acute dentoalveolar abscess lead to/

A

chronic dentoalveolar abscess
- persistent low-grade chronic infection
granuloma can be asymptomatic until acute stage of infection

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6
Q

cardinal signs of inflammation

A

tenderness
pain
redness
swelling

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7
Q

feature of chronic infection

A 
sinus formation (IO or EO)
may stimulate epithelial cells and initiate development of cyst
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8
Q

common odontogenic sources of infection

A 
PA infection
 - PA abscess
 - apical periodontitis
 - cellulitis - spreading of infection into surrounding 
    tissues
pericoronitis
 - impaction of food and bacteria
 - swelling and inflammation
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9
Q

path of spread - PA infection

A 
caries
pulpitis
PA infection
alveolar bone
localised STs
fascial space
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10
Q

PA infection U tooth directions of spread

A 
nasal passage
MS
oral cavity
buccal sulcus
buccal space lateral to buccinator
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11
Q

PA infection L tooth directions of spread

A

FOM: above/below mylohyoid
oral cavity
buccal space

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12
Q

path of spread - pericoronitis

A 
operculum
food trapping/bacterial ingress
pericoronitis
localised STs
fascial space
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13
Q

pericoronitis L8 directions of spread

A 
buccal space
masticatory space
lat pharyngeal space
sublingual space
submandibular space
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14
Q

fascial space involvement

A

if infection continues to spread, it can travel into the fascial spaces, some of which can lead to EO swelling

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15
Q

primary fascial spaces

A 
palatal
vestibular
canines
buccal
submental
submandibular
sublingual
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16
Q

where does a palatal fascial space infection often originate from?

A

U laterals

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17
Q

canine fascial space

A 
eats through maxillary bone
nasolabial fold obliteration
orbital region involvement
can cause CST
cranial spread through external angular vein
levator anguli oris and oculi
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18
Q

buccal fascial space

A 
U and L premolars/molars
can spread into:
 - temporal space superiorly
 - submandibular space inferiorly
 - masseteric space posteriorly
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19
Q

submental fascial space

A

L incisors and canines
has perforated through lingual cortex
also if have infected mandibular fracture to symphysis
taut skin, can be a bit red

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20
Q

submandibular fascial space

A

commonly teeth where roots below mylohyoid, usually 7+8 (rarely 6/premolars)
can’t palpate border of mandible
often present w trismus
pain and redness over swelling

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21
Q

sublingual fascial space

A

L incisors, canines, premolars, mesial root 6
roots lie above mylohyoid attachment
diff swallowing/breathing
tongue displaced posteriorly and medially
raised FOM
voice can sound different “hot potato”

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22
Q

Ludwig’s angina

A

bilateral submental, submandibular and sublingual swelling
medical emergency - refer to hospital
hard swelling, often diffuse cellulitis
FOM raised, trismus, difficulty breathing, tongue swollen

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23
Q

secondary fascial spaces

A

if infection continues to spread
temporal, masseteric, pterygomandibular, lateral pharyngeal, retropharyngeal, prevertebral spaces
parotid, superficial, deep temporal

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24
Q

consequence of infection spreading to secondary fascial spaces

A

can lead to infection becoming life-threatening - trismus, difficulty breathing, speaking and swallowing
need hospital for IV ABs, +/- EO I+D - after EO drainage drains are inserted into the fascial spaces up to 48hrs post-op
if infection not txed - can lead to sepsis

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25
Q

SIRS

A

body’s response to a stimulus, such as infection or trauma

diagnosis: 2 or more of
- temp <36 or >38 degrees
- hr >90bpm
- resp rate >20bpm
- WBC count <4000/mm3 or >12000/mm3 or >10% immature (band) forms

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26
Q

sepsis

A

life-threatening condition caused by an overreaction of the body’s immune response to infection
diagnosis: SIRS + infection present

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27
Q

septic shock

A

sepsis with persistent hypotension despite adequate fluid replacement

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28
Q

worst outcome of sepsis

A

organ failure and death

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29
Q

management of infection

A 
history
exam
resuscitative (ABC) and supportive tx
special investigations
take pt observations (baseline in case infection progresses)
remove source of infection - RCT/ext
remove any pus accumulated - I+D of swelling (if no drainage through RCs/socket - establish drainage
(ABs)
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30
Q

can’t remove source of infection immediately

A

e.g. unable to numb pt

still important to I+D as much pus as possible to reduce swelling

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31
Q

special investigations

A

xray
sensitivity testing
referral CT/MRI/US

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32
Q

HPC

A 
when
had previously
spread
systemic symptoms
pain
mouth opening
changed colour/consistency
getting bigger/smaller
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33
Q

MH

A

drug allergies
diabetes
immunocompromised

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34
Q

DH

A

recent tx

had before

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35
Q

SH

A

any responsibilities e.g. kids

when last ate and drank - don’t let them if even small chance of GA

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36
Q

sepsis 6

A 
give O2 (high-flow)
give IV antibiotics
give IV fluids
take blood cultures
measure urine output
measure lactate
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37
Q

EO examination

A

facial profile - asymmetry, LNs, colour change
TMJ
MofM
SOB

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38
Q

IO exam

A

perio, carious teeth
sinus tract
deviation of uvula (parapharyngeal spread) - risk of aspiration

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39
Q

determining severity

A

onset, progression, history, trismus, systemic symptoms
pt factors e.g. diabetic/on steroids
warning signs

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40
Q

warning signs to refer

A 
fever
dehydration
crossing midline
rapid progression of swelling
increasing trismus
quality/location of swelling
elevation of tongue/firmness of FOM
difficulty speaking and swallowing
eye involvement
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41
Q

pt observations

A

hr 60-100bpm
bp 90/60 - 120/80 mmHg
temp 36-38 degrees
O2 sats 95-100%

42
Q

aspiration of pus

A

may take from a swelling to do culture and sensitivity of bacteria
allows for more targeted AB tx
in taking an aspiration you also decrease the size of the swelling
in case it doesn’t respond to AB therapy so you can see what it will be sensitive to

43
Q

indications for prescribing ABs

A

local measures have failed (e.g. tooth ext but swelling and infection remains)
pt systemically unwell
cellulitis
infection spreading

44
Q

SDCEP refer to A and E or urgent OMFS

A

significant trismus
FOM swelling
eye involvement
difficulty breathing

45
Q

complications

A 
SIRS and sepsis
multiorgan failure
death
scars
orbital infections
CST
 - bulging eye, loss of vision
 - headache
 - CNs paralysed
mediastinitis
pericarditis
46
Q

in practice guidelines

A 
establish diagnosis
document - pulse, temp, resp rate
remove cause
I+D
emergency referral: phone ahead (OMFS)
 - send referral letter w pt to A and E
(ABs)
47
Q

swab

A

rub it over area
problems
- easily contaminated by oral bacteria
- anaerobes exposed to air

48
Q

amoxicillin

A

500mg
send 15
x3 daily
5 dys

49
Q

metronidazole

A

200/400mg
send 15
x3 daily
5 days

not if heavy drinker/warfarin
if penicillin allergy
adjunct if spreading infection/pyrexia

50
Q

phenoxymethylpenicillin

A

250mg
send 40
2 x4 daily
5 days

51
Q

when should you use second line antibiotics?

A

if don’t respond to 1st line or severe infection with spreading cellulitis

52
Q

consequence of 2nd line ABs

A

c dificile infection

53
Q

co-amoxiclav

A

250/125
send 15
x3 daily
5 days

54
Q

clindamycin

A

150mg
send 20
x4 daily
5 days

55
Q

which AB has the side effect of AB associated colitis?

A

clindamycin

56
Q

clarithromycin

A

250mg
send 14
x2 daily
7 days

57
Q

primary fascial spaces

A 
palatal
vestibular
canines
buccal
submental
submandibular
sublingual
58
Q

secondary posterior potential spaces

A

masticatory
lateral pharyngeal
retropharyngeal
prevertebral

59
Q

masticatory spaces

A 
superficial temporal
deep temporal
infratemporal
pterygomandibular
masseteric
60
Q

describe the stages between caries/(trauma) and an infected apical radicular cyst

A 
pulp hyperaemia (increased blood flow)
acute pulpitis - chronic pulpitis
acute apical periodontitis
 - out into PDL - no longer just pulpal
acute apical abscess
(chronic sinus)
chronic apical infection (granuloma)
 - collection of granulation tissue
radicular cyst
 - not everyone gets this, genetic? doesn't tend to cause 
   pain
infected apical radicular cyst
 - causes pain
61
Q

can you diagnose an abscess radiographically?

A

no can only see a radiolucency

so unlikely to see if an acute abscess

62
Q

what does pain result from in an abscess?

A

usually from build up of pressure as pus builds up

63
Q

c-fibres

A

innervate pulp

really hard to localise pulpal pain

64
Q

a-fibres

A

innervate PDL
good pain localisation
when infection spreads to periodontium pt will be able to localise pain well

65
Q

pulp hyperaemia

A 
pain
 - lasts for seconds
 - stimulated by hot/cold or sweet foods
 - resolves after stimulus
caries approaching pulp - can still treat tooth without treating pulp
66
Q

acute pulpitis clinical features

A

constant severe pain
reacts to thermal stimuli
poorly localised pain
referral of pain
no/min response to analgesics - hard for blood to get in
open symptoms less severe - less build up of pressure

67
Q

acute periodontitis

A 
easy to diagnose
TTP
tooth non-vital (unless traumatic)
slight increase in mobility
radiographs 
 - loss of clarity of LD
 - radiolucent shadow - may indicate an 'old' lesion e.g. flare up of an apical granuloma
 - delay in changes at the apex - widening of apical PD space
68
Q

traumatic periodontitis

A 
cause - parafct
diagnosis
 - TTP
 - normal vitality
 - radiographs - widening of PDL space
examine occlusion
tx - therapy for parafct
69
Q

dental abscesses

A

acute apical abscess - commonest pus producing infection
other possible causes
- PD abscess
- pericoronitis
- sialadenitis (infection of salivary glands)

70
Q

abscesses MOs

A

polymicrobial

anaerobes

71
Q

acute apical abscess

A

clinical features - reflect stage of abscess
- initially almost identical to acute apical periodontitis (before eroding through bone and into ST)
symptoms
- severe unremitting pain
- acute tenderness in fct
- acute TTP
BUT no swelling, redness or heat yet - get when spreads into STs

72
Q

5 cardinal signs of inflammation

A 
heat 
redness
swelling
pain
loss of fct
73
Q

once abscess perforates through bone

A

pain often remits (unless in palate)
swelling, redness and heat in STs
as swelling increases pain returns
initial reduction in TTP as pus escapes into STs

74
Q

reversible pulpitis

A 
a level of inflammation in which returning to a normal state is possible if noxious stimuli removed
mild/mod pain when stimulated
no pain without stimulus
subsides <5secs
no mobility
no pain on percussion
75
Q

irreversible pulpitis

A

a higher level of inflammation in which pulp has been damaged beyond recovery
sharp, throbbing, severe pain upon stimulus
- can be spontaneous/no stimulation
pain persists after stimulus removed >5secs
tx - RCT or ext

76
Q

site of swelling depends on

A

position of tooth in arch
root length
muscle attachments
potential spaces in proximity to lesion

77
Q

periapical granuloma (chronic apical periodontitis)

A

mass of chronically inflamed granulation tissue at apex of tooth
- plasma cells, lymphocytes, and few histocytes with fibroblasts and capillaries
not a true granuloma because not granulomatous inflammation
= has epithelial histocytes mixed with lymphocytes and GCs

78
Q

aetiology of radicular cyst

A 
caries/trauma/PDD
death of pulp
apical bone inflammation
dental granuloma
stimulation of epithelial rests of malassez
epithelial proliferation
periapical cyst formation
79
Q

where does infection spread?

A

along path of least resistance

80
Q

path of spread maxillary teeth

A

buccal space
buccal sulcus
maxillary sinus

81
Q

maxillary palatal spread

A

less likely to spread palatally - dense bone
likely in U2s as root lies palatally
v painful - taut tissues

82
Q

path of spread mandibular teeth

A

buccal space
buccal sulcus
sublingual (anteriors)
submandibular (posteriors)

83
Q

posterior potential spaces

A

masticatory space
lateral pharyngeal space
retropharyngeal space
prevertebral space

84
Q

masticatory spaces

A 
superficial temporal
deep temporal
infratemporal
pterygomandibular
masseteric
85
Q

what symptoms will pt have if infection spreads into masticatory space?

A

severe trismus
may/may not have swelling depending on where it spreads
- unlikely if lingual spread
- swelling if buccal spread

86
Q

CST

A

brain spread possible

infratemporal space - pterygoid venous plexus

87
Q

route of spread into chest

A

retropharyngeal space

prevertebral space

88
Q

upper anteriors spread of infection

A

lips
nasolabial region
lower eyelid
2s - palate (less common)

89
Q

upper posteriors spread of infection

A

cheek
infratemporal region
maxillary antrum (v rare)
palate (less common)

90
Q

lower anteriors spread of infection

A

mental and submental space

91
Q

lower posteriors spread of infection

A 
buccal space
submasseteric space
sublingual space
submandibular space
lateral pharyngeal space
92
Q

which part of a swelling should you incise?

A

the most fluctuant part

but take into account proximity of nerves etc

93
Q

Ludwig’s angina

A

bilateral cellulitis of the sublingual and submandibular spaces

94
Q

IO features of Ludwig’s angina

A

raised tongue
diff breathing
diff swallowing
drooling

95
Q

EO features of Ludwig’s angina

A

diffuse redness and swelling bilaterally in SM region

96
Q

systemic features of Ludwig’s angina

A

raised hr, resp rate, temp, WCC

97
Q

EO drain

A

to allow rest of pus to drain

remove when it has stopped draining pus

98
Q

OM predisposing factors

A 
bisphosphonates
impaired vascularity of bone
foreign bodies
compound fractures
impaired host defences
99
Q

mechanisms of AB resistance

A

altered target site
enzyme inactivation
reduced uptake

100
Q

breakpoint

A

a chosen conc of an AB which defines whether a species of bacteria is susceptible or resistant to the AB

101
Q

clinical resistance

A

when infection is highly unlikely to respond to even max doses of AB

oral surgery 4th year (9 decks)

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