infection Flashcards
acute dentoalveolar abscess
localised suppurative inflammation involving teeth and supporting structures
what the the pathogens mostly in an acute dentoalveolar abscess?
anaerobes
acute dentoalveolar abscess - how do pathogens gain entry to PA tissue?
through necrotic pulp or PDL
acute dentoalveolar abscess S+S
pain on biting (pressure on apical pathology)
pyrexia
lymphadenopathy
what can lack of appropriate tx of an acute dentoalveolar abscess lead to/
chronic dentoalveolar abscess
- persistent low-grade chronic infection
granuloma can be asymptomatic until acute stage of infection
cardinal signs of inflammation
tenderness
pain
redness
swelling
feature of chronic infection
sinus formation (IO or EO) may stimulate epithelial cells and initiate development of cyst
common odontogenic sources of infection
PA infection
- PA abscess
- apical periodontitis
- cellulitis - spreading of infection into surrounding
tissues
pericoronitis
- impaction of food and bacteria
- swelling and inflammationpath of spread - PA infection
caries pulpitis PA infection alveolar bone localised STs fascial space
PA infection U tooth directions of spread
nasal passage MS oral cavity buccal sulcus buccal space lateral to buccinator
PA infection L tooth directions of spread
FOM: above/below mylohyoid
oral cavity
buccal space
path of spread - pericoronitis
operculum food trapping/bacterial ingress pericoronitis localised STs fascial space
pericoronitis L8 directions of spread
buccal space masticatory space lat pharyngeal space sublingual space submandibular space
fascial space involvement
if infection continues to spread, it can travel into the fascial spaces, some of which can lead to EO swelling
primary fascial spaces
palatal vestibular canines buccal submental submandibular sublingual
where does a palatal fascial space infection often originate from?
U laterals
canine fascial space
eats through maxillary bone nasolabial fold obliteration orbital region involvement can cause CST cranial spread through external angular vein levator anguli oris and oculi
buccal fascial space
U and L premolars/molars can spread into: - temporal space superiorly - submandibular space inferiorly - masseteric space posteriorly
submental fascial space
L incisors and canines
has perforated through lingual cortex
also if have infected mandibular fracture to symphysis
taut skin, can be a bit red
submandibular fascial space
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
sublingual fascial space
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”
Ludwig’s angina
bilateral submental, submandibular and sublingual swelling
medical emergency - refer to hospital
hard swelling, often diffuse cellulitis
FOM raised, trismus, difficulty breathing, tongue swollen
secondary fascial spaces
if infection continues to spread
temporal, masseteric, pterygomandibular, lateral pharyngeal, retropharyngeal, prevertebral spaces
parotid, superficial, deep temporal
consequence of infection spreading to secondary fascial spaces
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
SIRS
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
sepsis
life-threatening condition caused by an overreaction of the body’s immune response to infection
diagnosis: SIRS + infection present
septic shock
sepsis with persistent hypotension despite adequate fluid replacement
worst outcome of sepsis
organ failure and death
management of infection
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)
can’t remove source of infection immediately
e.g. unable to numb pt
still important to I+D as much pus as possible to reduce swelling
special investigations
xray
sensitivity testing
referral CT/MRI/US
HPC
when had previously spread systemic symptoms pain mouth opening changed colour/consistency getting bigger/smaller
MH
drug allergies
diabetes
immunocompromised
DH
recent tx
had before
SH
any responsibilities e.g. kids
when last ate and drank - don’t let them if even small chance of GA
sepsis 6
give O2 (high-flow) give IV antibiotics give IV fluids take blood cultures measure urine output measure lactate
EO examination
facial profile - asymmetry, LNs, colour change
TMJ
MofM
SOB
IO exam
perio, carious teeth
sinus tract
deviation of uvula (parapharyngeal spread) - risk of aspiration
determining severity
onset, progression, history, trismus, systemic symptoms
pt factors e.g. diabetic/on steroids
warning signs
warning signs to refer
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
pt observations
hr 60-100bpm
bp 90/60 - 120/80 mmHg
temp 36-38 degrees
O2 sats 95-100%
aspiration of pus
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
indications for prescribing ABs
local measures have failed (e.g. tooth ext but swelling and infection remains)
pt systemically unwell
cellulitis
infection spreading
SDCEP refer to A and E or urgent OMFS
significant trismus
FOM swelling
eye involvement
difficulty breathing
complications
SIRS and sepsis multiorgan failure death scars orbital infections CST - bulging eye, loss of vision - headache - CNs paralysed mediastinitis pericarditis
in practice guidelines
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)
swab
rub it over area
problems
- easily contaminated by oral bacteria
- anaerobes exposed to air
amoxicillin
500mg
send 15
x3 daily
5 dys
metronidazole
200/400mg
send 15
x3 daily
5 days
not if heavy drinker/warfarin
if penicillin allergy
adjunct if spreading infection/pyrexia
phenoxymethylpenicillin
250mg
send 40
2 x4 daily
5 days
when should you use second line antibiotics?
if don’t respond to 1st line or severe infection with spreading cellulitis
consequence of 2nd line ABs
c dificile infection
co-amoxiclav
250/125
send 15
x3 daily
5 days
clindamycin
150mg
send 20
x4 daily
5 days
which AB has the side effect of AB associated colitis?
clindamycin
clarithromycin
250mg
send 14
x2 daily
7 days
primary fascial spaces
palatal vestibular canines buccal submental submandibular sublingual
secondary posterior potential spaces
masticatory
lateral pharyngeal
retropharyngeal
prevertebral
masticatory spaces
superficial temporal deep temporal infratemporal pterygomandibular masseteric
describe the stages between caries/(trauma) and an infected apical radicular cyst
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
can you diagnose an abscess radiographically?
no can only see a radiolucency
so unlikely to see if an acute abscess
what does pain result from in an abscess?
usually from build up of pressure as pus builds up
c-fibres
innervate pulp
really hard to localise pulpal pain
a-fibres
innervate PDL
good pain localisation
when infection spreads to periodontium pt will be able to localise pain well
pulp hyperaemia
pain - lasts for seconds - stimulated by hot/cold or sweet foods - resolves after stimulus caries approaching pulp - can still treat tooth without treating pulp
acute pulpitis clinical features
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
acute periodontitis
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
traumatic periodontitis
cause - parafct diagnosis - TTP - normal vitality - radiographs - widening of PDL space examine occlusion tx - therapy for parafct
dental abscesses
acute apical abscess - commonest pus producing infection
other possible causes
- PD abscess
- pericoronitis
- sialadenitis (infection of salivary glands)
abscesses MOs
polymicrobial
anaerobes
acute apical abscess
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
5 cardinal signs of inflammation
heat redness swelling pain loss of fct
once abscess perforates through bone
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
reversible pulpitis
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
irreversible pulpitis
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
site of swelling depends on
position of tooth in arch
root length
muscle attachments
potential spaces in proximity to lesion
periapical granuloma (chronic apical periodontitis)
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
aetiology of radicular cyst
caries/trauma/PDD death of pulp apical bone inflammation dental granuloma stimulation of epithelial rests of malassez epithelial proliferation periapical cyst formation
where does infection spread?
along path of least resistance
path of spread maxillary teeth
buccal space
buccal sulcus
maxillary sinus
maxillary palatal spread
less likely to spread palatally - dense bone
likely in U2s as root lies palatally
v painful - taut tissues
path of spread mandibular teeth
buccal space
buccal sulcus
sublingual (anteriors)
submandibular (posteriors)
posterior potential spaces
masticatory space
lateral pharyngeal space
retropharyngeal space
prevertebral space
masticatory spaces
superficial temporal deep temporal infratemporal pterygomandibular masseteric
what symptoms will pt have if infection spreads into masticatory space?
severe trismus
may/may not have swelling depending on where it spreads
- unlikely if lingual spread
- swelling if buccal spread
CST
brain spread possible
infratemporal space - pterygoid venous plexus
route of spread into chest
retropharyngeal space
prevertebral space
upper anteriors spread of infection
lips
nasolabial region
lower eyelid
2s - palate (less common)
upper posteriors spread of infection
cheek
infratemporal region
maxillary antrum (v rare)
palate (less common)
lower anteriors spread of infection
mental and submental space
lower posteriors spread of infection
buccal space submasseteric space sublingual space submandibular space lateral pharyngeal space
which part of a swelling should you incise?
the most fluctuant part
but take into account proximity of nerves etc
Ludwig’s angina
bilateral cellulitis of the sublingual and submandibular spaces
IO features of Ludwig’s angina
raised tongue
diff breathing
diff swallowing
drooling
EO features of Ludwig’s angina
diffuse redness and swelling bilaterally in SM region
systemic features of Ludwig’s angina
raised hr, resp rate, temp, WCC
EO drain
to allow rest of pus to drain
remove when it has stopped draining pus
OM predisposing factors
bisphosphonates impaired vascularity of bone foreign bodies compound fractures impaired host defences
mechanisms of AB resistance
altered target site
enzyme inactivation
reduced uptake
breakpoint
a chosen conc of an AB which defines whether a species of bacteria is susceptible or resistant to the AB
clinical resistance
when infection is highly unlikely to respond to even max doses of AB
