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BDS3: Clinical dental sciences > Oral Surgery > Flashcards

Flashcards in Oral Surgery Deck (212)
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1
Q

what does trauma and infection lead to a breakdown of and what does it produce?

A

Trauma and infection lead to the breakdown of membrane phospholipids producing arachidonic acid

2
Q

arachidonic acide can be broken down to form what?

A

Arachidonic acid can be broken down to form prostaglandins

3
Q

what does prostaglandins do to the tissues?

A
  • Prostaglandins sensitise the tissues to other inflammatory products which results in pain
  • They sensitise the tissues to other inflammatory products such as leukotrienes
  • So if prostaglandin production decreases, this will moderate the pain
4
Q

what acid is aspirin?

A

Acetylsalicylic acid

5
Q

what are properties for aspirin?

A

 1) Analgesic
 2) Antipyretic
 3) Anti-inflammatory
 4) metabolic

6
Q

What is mechanism of action for aspirin?

A

 Aspirin inhibits cyclo-oxygenases (COX-1 & 2)
 ∴ reduces production of Prostaglandins
 NB:
* It is more effective at inhibiting COX-1)
* -COX-1 inhibition reduces platelet aggregation (predisposes to damage of the gastric mucosa)

7
Q

what does aspirin inhibit?

A

cyclo-oxygenases (COX-1 & 2)

8
Q

what does aspirin reduce production of?

A

prostaglandins

9
Q

what does cox-1 inhibition reduce?

A

COX-1 inhibition reduces platelet aggregation predisposes to damage of the gastric mucosa)

10
Q

what actions predominate in relation to analgesic properties of aspirin?

A

Peripheral actions predominate.

11
Q

where does the analgesic action result from in aspirin?

A

 The analgesic action results from inhibition of prostaglandin synthesis in inflamed tissues (Cyclo-oxygenase inhibition).

12
Q

what are prostaglandins and what do they affect in terms of anti-inflammatory?

A

Prostaglandins are vasodilators and as such also affect capillary permeability.

13
Q

what does aspirin reduce

A

Aspirin is a good anti-inflammatory and will reduce redness and swelling as well as pain at the site of the injury

14
Q

what are potential adverse /side effects of aspirin?

A
  • 1) GIT problems
  • 2) Hypersensitivity
  • 3) Overdose – tinnitus, metabolic acidosis
  • 4) Aspirin Burns – Mucosal
15
Q

where does GIT problems associated from aspirin tend to happen?

A

mucosal lining of stomach

16
Q

explain the effect prostaglandins have on GIT in relation to aspirin?

A

 inhibit gastric acid secretion
 Increase blood flow through the gastric mucosa
 Help production of mucin by cells in stomach lining (cytoprotective action)

17
Q

what does prostaglandins inhibit?

A

inhibit gastric acid secretion

18
Q

what does prostaglandins increase in relation to GIT and aspirin?

A

Increase blood flow through the gastric mucosa

19
Q

what does prostaglandins help production of in relation to GIT and aspirin?

A

Help production of mucin by cells in stomach lining (cytoprotective action)

20
Q

what is cytoprotective action?

A

Help production of mucin by cells in stomach lining (cytoprotective action)

21
Q

when should their be especially care of in patients with GIT problems and using aspirin?

A

 Ulcers
 Gastro-oesophageal reflux

22
Q

what will patients taking aspirin definitely suffer from in the GIT?

A

o Most patients taking Aspirin will suffer some blood loss from the GIT (not detectable macroscopically and asymptomatic)

23
Q

what kind of side effects do you suffer from when taking aspirin?

A
  1. GIT problems
  2. Hypersensitivity
  3. overdose - tinnitus, metabolic acidosis
  4. aspirin burns - mucosal
24
Q

why kind of hypersensitive side effects could people taking aspirin face?

A

 Acute bronchospasm / asthma type attacks
 Skin rashes / urticaria / angioedema
 Other allergies

25
Q

what is a life threatening overdose of aspirin be?

A

metabolic acidosis

26
Q

what types of overdose reactions can someone with aspirin suffer from?

A

o Hyperventilation
o Tinnitus, deafness
o Vasodilatation & sweating
o Metabolic acidosis (can be life threatening)
o Coma (Uncommon)

27
Q

what causes aspiring burns?

A

salicylic acid

28
Q

how does an aspirin burn occur?

A

Aspirin applied locally to oral mucosa results in a chemical burns

29
Q

what must asprin be taken with?

A

water

30
Q

what are the groups to avoid when taking aspirin?

A
  • Peptic ulceration
  • Epigastric pain
  • Bleeding abnormalities
  • Anticoagulants
  • Pregnancy/lactation
  • Pts on steroids
  • Renal/hepatic impairment
  • Children and adolescents under 16 years
  • Asthma
  • Hypersensitivity to other NSAIDs
  • Taking other NSAIDs
  • Elderly
  • G6PD-deficiceny
31
Q

why don’t you give someone who has a peptic ulcer aspririn?

A

could result in perforation

32
Q

why don’t you give someone who has a epigastric pain aspririn?

A

may have undiagnosed ulcer

33
Q

why don’t you give somone taking anticoagulants asprin?

A
  • aspirin enhances warfarin and other coumarin anticoagulants
  • displaces warfarin from binding sites on plasma proteins
  • so more free warfarin
  • marjority of warfarin is bound (inactive) if more is released this will become active increasing bleeding tendency
34
Q

why don’t you give someone who is pregnant aspirin?

A
  • especially in 3rd trimester
  • near delivery may cause impairment of platelet function
    *increased risk of haemorrhage
  • increased risk of jaundice in baby
  • can prolong delay labour
35
Q

why don’t you give someone who is lactating aspirin?

A

could cause reye’s syndrome

36
Q

why don’t you give someone who is on steroids aspirin?

A

a quarter of steroid users will develop an ulcer

36
Q

when is it worst to give aspirin to someone pregnant?

A

3rd trimester

37
Q

why don’t you give someone who has a renal/hepatic impairment aspirin?

A
  • aspirin metabolised in liver and excreted in kidney
  • if renal impairment - excretion may be reduced/delayed
  • not complete contraindication but administer with care and avoid if impairment severe
38
Q

where are prostaglandins PGE2 and PGI2 synthesised and what are they?

A

Prostaglandins PGE2 and PGI2 are powerful vasodilators synthesized in the renal medulla and glomeruli respectively, and are involved in the control of renal blood flow and excretion of salt and water

39
Q

Inhibition of renal prostaglandin synthesis may result in?

A
  • sodium retention
  • reduced renal blood flow
  • renal failure,
40
Q

NSAID’s may cause what in kidney?

A

NSAIDs may cause interstitial nephritis and hyperkalaemia.

41
Q

why don’t you give children under 16 aspirin?

A
  • could cause reye’s syndrome
42
Q

what is reye’s syndorme?

A
  • fatty degenerative process in liver profound swelling in brain
43
Q

why don’t you give people with asthma aspirin?

A
  • not completely contraindicated but ask them if they had problems before?
44
Q

why don’t you give people taking other NSAIDs aspirin?

A

increased risk of side effects

45
Q

why don’t you give elderly aspirin?

A
  • more likely to get side effects
  • smaller circulating blood volume
  • on other meds
  • have other med problems
46
Q

aspirin is completely contraindicated in who?

A
  • 1) Children & Adolescents under 16 years; breast-feeding (Reye’s Syndrome)
  • 2) Previous or active peptic ulceration
  • 3) Haemophilia
  • 4) Hypersensitivity to Aspirin or any other NSAID
47
Q

for mild to moderate odontogenic or inflammatory pain what is given?

A

5 day regime of 300mg aspirin tablets
- 40 tablets
- 2 tablets 4 times daily after food

48
Q

if pt has or had peptic ulcer what do they get instead of aspirin?

A
  • paracetamol and proton pump inhibitor
  • either omeprazole or lansoprazole
  • 5 day regime
49
Q

what does ibuprofen have less effect on compared to aspirin?

A

Less effect on platelets

50
Q

what may ibuprofen cause?

A

bronchospasm

51
Q

what ibuprofen regime do you take?

A
  • mild to moderate post op pain
  • 5 day regime
  • 400mg
  • 20 tablets
  • 1 tablet 4 times daily preferably after food
52
Q

what is max adult dose of ibuprofen?

A

2.4g

53
Q

when is there caution when prescribing ibuprofen?

A

 1) Previous or active peptic ulceration
 2) The Elderly
 3) Pregnancy & lactation
 4) Renal, cardiac or hepatic impairment
 5) History of hypersensitivity to Aspirin & other NSAIDs
 6) Asthma
 7) Patient taking other NSAIDs
 8) Patients on long term systemic steroids

54
Q

what are side effects of ibuprofen?

A

 1) GIT discomfort, occasionally bleeding & ulceration
 2) Hypersensitivity reactions e.g. rashes, angioedema & bronchospasm
 3) Others: headache, dizziness

55
Q

what are symptoms of ibuprofen overdose?

A
  • Nausea
  • Vomiting
  • Tinnitus (more serious toxicity very uncommon)
56
Q

how is ibuprofen overdose treated?

A

Activated charcoal followed by symptomatic measures are indicated if more than 400mg/kg has been ingested within the preceding hour.

57
Q

what is mode of action of paracetamol?

A

 Hydroperoxides are generated from the metabolism of arachidonic acid by COX and exert a positive feedback to stimulate COX activity
 - This feedback is blocked by paracetamol, thus indirectly inhibiting COX – especially in the brain

58
Q

what is main site of action of paracetemol?

A

central nervous system, such as in the thalamus

59
Q

cautions when prescribing paracetamol to who>

A

 1) Hepatic impairment
 2) Renal impairment
 3) Alcohol dependence

60
Q

what are side effects of paracetemol?

A

 Side effects are rare but:
 1) Rashes
 2) Blood disorders
 3) Hypotension reported on infusion
 4) Liver damage (and less frequently kidney damage) following overdose

61
Q

what is paracetamol regime?

A

for mild to moderate odontogenic or post op pain
- 5 days
- tablets 500mg
- 40 tablets
- 2 tablets 4 times daily

62
Q

what is max dose of paracetemol?

A

 Adults: 1-2 tablets (0.5-1g) 4-6 hourly
* Max. Dose: 4g daily (8 tablets)

63
Q

what dose children paracetamol dose depend on?

A

: Depends on weight/age – see BNF

64
Q

what must you always warn patients on for paracetemol?

A

Always warn patients of maximum dose and emphasise that they should not exceed this!

65
Q

what may paracetamol over does cause?

A

severe hepatocellular necrosis, and less frequently, renal tubular necrosis

66
Q

how much paracetamol overdose is deadly?

A

As little as 10-15g (20-30 tablets) or 150mg/kg of paracetamol taken within 24 hours may cause severe hepatocellular necrosis, and less frequently, renal tubular necrosis

67
Q

when is liver damage of paracetamol overdose maximal?

A

Liver damage is maximal at 3-4 days after ingestion-> LIVER FAILURE -> Death

68
Q

what is there a lack of and what happens if someone overdoses on paracetamol?

A

Therefore, despite a lack of significant early symptoms, patients who have taken an overdose of paracetamol should be transferred immediately to hospital

69
Q

where do opioids act?

A

spinal cord in dorsal horn pathways
- central regulation of pain

70
Q

what are problems of opioids?

A
  • dependence
  • tolerance
  • effects on smooth muscle
  • constipation
  • urinary and bile retention
71
Q

what is CNS effect of opioids?

A
  • 1) Pain centre (alters awareness/perception of pain)
  • 2) Higher centres
  • 3) Respiratory centre
  • 4) Cough centre
72
Q

what are side effects of opioids?

A
  • Nausea
  • Vomiting
  • drowsiness
     Larger doses produce respiratory depression & hypotension
73
Q

what are effects of opioids enhanced by?

A

alcohol

74
Q

who re contraindications of giving opioids to?

A

 Acute respiratory depression
 Acute alcoholism
 Raised intracranial pressure/head injury
* Interferes with respiration
* Affects pupillary responses vital for neurological assessment

75
Q

what is codeine taken with?

A

Usually in combination with NSAIDs or Paracetamol e.g. Co-codamol (8mg Codeine : 500mg Paracetamol)

76
Q

what is used to treat trigeminal neuralgia?

A

o 100 or 200 mg tablets
o Starting dose 100mg once or twice daily (but some patients may require higher initial dose)
o Increase gradually according to response
o Usual dose 200mg 3-4 times daily, up to 1.6g daily in some patients

77
Q

what are other drugs for trigeminal neuralgia?

A

o Gabapentin
o Phenytoin

78
Q

what are clinical features of trigeminal neuralgia?

A

o 1) Severe spasms of pain: ‘Electric shock’, lasts seconds
o 2) Usually unilateral
o 3) Older age-group
o 4) Trigger spot identified
o 5) Females more than males
o 6) Periods of remission
o 7) Recurrences often greater severity

79
Q

what are 3 basic modes of action for tooth elevation?

A
  • wheel and axle
  • lever
  • wedge
80
Q

why do teeth fracture?

A

o Thick cortical bone
o Root shape
o Root number
o Hypercementosis
o Ankylosis
o Caries
o Alignment

81
Q

how is debridement done?

A
  • physical
  • bone file or handpiece to remove sharp edges
    *mitchell trimmer or veronica currette to remove soft tissue debris
  • irrigation
    *sterile saline to into socket and under flap
  • suction
    *aspirate into socket and under flap
    *check socket for retained apices
82
Q

what are aims of suturing?

A
  • reposition tissues
  • cover bone
  • prevent wound breakdown
  • achieve haemostasis
  • encourage healing by primary intention
83
Q

what is haemostasis peri-operative?

A

 LA with vasoconstrictor
 Artery forceps
 Diathermy
 Bone wax

84
Q

what is haemostasis post-operative?

A

 Pressure
 LA with vasoconstrictor
 Diathermy
 Whitehead’s Varnish Pack
* Iodoform, Gum Benzoin, Storax, Balsam Tolu, Ethyl Ether
 Surgicel
 Sutures

85
Q

what are stages of surgery?

A

o Anaesthesia
o Access
o Bone removal as necessary
o Tooth division as necessary
o Debridement
o Suture
o Achieve haemostasis
o Post-operative instructions
o Post-operative medication

86
Q

if sutures non-absorbable?

A

 If extended retention periods are required
 Must be removed postoperatively
 Closure of OAF or exposure of canine tooth

87
Q

if sutures absorbable?

A

 Holds tissue edges together temporarily
 If removal of suture not possible/desirable
 Vicryl-breakdown via absorption of water into filaments causes polymer to degrade
 ?may mean review not required

88
Q

when is lingual nerve at risk?

A

 Incision of flap
 Raising of buccal and lingual flaps
 Retraction of flap
 Bone removal
 Extraction with forceps

89
Q

when 3rd molar is removed what nerves can be damaged?

A

 Lingual*
 Inferior alveolar*
 Mylohyoid
 Buccal

90
Q

what meds are usually given when 3rd molar removed?

A

o Analgesia
 Ibuprofen
 Cocodamol
 Paracetemol
o Other
 Chlorhexidine
o Antibiotics not routinely required

91
Q

what are Complications of Lower Third Molar Removal?

A

o Pain
o Swelling
o Bruising
o Trismus
o Paraesthesia/anaesthesia-lip/tongue

92
Q

what are aims of peri-radicular surgery?

A

 Establish a root seal at the apex of a tooth or at the point of perforation of a lateral perforation
 To remove existing infection
* Curettage, enucleation of cyst
* Removal of apical part of root which may have infected lateral canals

93
Q

how is removal of apex done?

A

o Remove 3mm
o Minimal angle to allow visualisation
o Try to keep cut at right angles to root to minimise surface area
o Allows curettage

94
Q

what retrogade seal is used for bone removal?

A

zin oxide (eugenol)

95
Q

what retrogade seal is used for apex removal?

A

MTA

96
Q

what are peri-op complications?

A

o Difficult access
o Abnormal resistance
o tooth/root fracture
o Jaw fracture
o Involvement of maxillary antrum
o Tuberosity fracture

97
Q

what are example of difficult access peri-op complication?

A

 Trismus
 Reduced aperture of mouth (congenital/syndromes – microstomia; scarring)
 Crowded/malpositioned teeth

98
Q

what are example of abnormal resistance peri-op complication?

A

 Thick cortical bone
 Shape/form of roots e.g. divergent roots/hooked roots
 Number of roots e.g. 3 rooted lower molars
 Hypercementosis
 Ankylosis

99
Q

what are example of tooth/root fracture peri-op complication?

A

consider
- caries
- alignment
- size
- root morphology
*fused
*convergent or divergent
*extra root
*hypercementosis
*ankylosis

100
Q

what are example of jaw fracture peri-op complication?

A
  • usually mandible
  • radiograph essential
  • application of force
101
Q

if jaw fracture occurs what do you do?

A
  • inform patient?
  • post op radiograph
  • refer (phone call)
  • ensure analgesia
  • stabilise
  • if delay, antibiotic
102
Q

what is inolvement of maxillary antrum peri-op complication?

A
  • OAF/OAC
  • loss of root into antrum
  • fractured tuberosity
103
Q

how to diagnose involvement of maxillary antrum?

A
  • size of tooth
  • radiographic position of roots in relation to antrum
  • bone at trifurcation of roots
  • bubbling of blood
  • nose holding test ( careful as can create OAC)
  • direct vision
  • good light and cution
  • blunt probe (careful as to not create an OAC)
104
Q

what are risk factors of peri-op complications involvement of maxillary antrum?

A
  • extraction of upper molars and premolars
  • close relationship of roots to sinus on radiograph
  • last standing molars
  • large bulbous roots
  • older patient
  • previous OAC
  • recurrent sinusitis
105
Q

what is management of involvement of maxillary antrum? if small or sinus intact?

A
  • inform patient
  • encourage clot
  • suture margins
  • antibiotic
  • post op instructions
106
Q

what is management of involvement of maxillary antrum? if large or lining torn?

A
  • close with buccal advancement flap
  • antibiotics and nose blowing instructions
107
Q

how do you confirm root in antrum?

A
  • confirm radiographically by OPT, occlusal or periapical
108
Q

how to diagnose tuberosity fracture?

A
  • Noise
  • Movement noted both visually or with supporting fingers
  • More than one tooth movement
  • Tear on palate
109
Q

what does neurapraxia mean?

A

contusion of nerve/continuity of epineural sheath and axons maintained

110
Q

what does axonotmesis mean?

A

continuity of axons but not epineural sheath disrupted

111
Q

what does neurotmesis mean?

A

complete loss of nerve continuity/nerve transected

112
Q

what does anaesthesia mean?

A

numbness

113
Q

what does paraestheisia mean?

A

tingling

114
Q

what does dyaesthesia mean?

A

unpleasant sensation/pain

115
Q

what does hypoaesthesia mean?

A

reduced sensation

116
Q

what does hyperaesthesia mean?

A

increased/heightened sensation

117
Q

what are most bleeds due to?

A

 Most bleeds due to local factors – mucoperiosteal tears or fractures of alveolar plate/socket wall

118
Q

what t do if soft tissue bleed?

A
  • pressure
  • sutures
  • LA with adrenaline (vasoconstrictor)
  • diathermy (cauterise/burn vessels precipitate proteins which from proteinaecous plug in vessel)
  • ligatures/haemostatic forceps (artery clips) for larger vessles
119
Q

what if bleed in bone?

A
  • pressure
  • LA on a swab or injected into socket
  • haemostatic agents
  • blunt isntrument
  • bone wax
  • pack
120
Q

if TMJ dislocation what do you do?

A

 Relocate immediately (analgesia and advice on supported yawning)
 If unable to relocate try local anaesthetic into masseter intra-orally
 If still unable to relocate – immediate referral

121
Q

what does eccymosis mean?

A

bruising

122
Q

what are causes of trismus?

A
  • related to surgery (oedema / muscle spasm)
  • related to giving LA – IDB
    (medial pterygoid muscle spasm)
  • Haematoma – medial pterygoid or less likely masseter (haematoma/clot organises and fibrose)
  • damage to TMJ – oedema/joint effusion
123
Q

how does IDB cause trismus?

A

medial pterygoid spasm

124
Q

when managing a patient with anticoag or antiplatelet drug? what do you do?
is dental tx likely to cause bleed?

-yes

A

is medication time limited?

125
Q

when managing a patient with anticoag or antiplatelet drug? what do you do?
is dental tx likely to cause bleed?

-no

A

treat with caution using standard procedures and taking care to avoid causing bleeding

126
Q

when managing a patient with anticoag or antiplatelet drug? what do you do?
is medication time limited?

-yes

A

delay non-urgent invasive dental procedures where possible

127
Q

when managing a patient with anticoag or antiplatelet drug? what do you do?
is medication time limited?

-no

A

does patient have other relevant medical complications?

128
Q

when managing a patient with anticoag or antiplatelet drug? what do you do?
does patient have other relevant medical complications?

-no

A

which drug type is the patient taking?

129
Q

when managing a patient with anticoag or antiplatelet drug? what do you do?
does patient have other relevant medical complications?

-yes

A

consult with prescribing clinician, specialist, or general medical practitioner

130
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • DIrect oral anticoagulant? (DOAC) - like apixiban or diagbtran
  • low bleeding risk procedure
A

-treat without interrupting medication
- treat early in day, limit initial treatment and assess bleeding before continuing staging extensive or complex procedures, strongly consider packing and suturing

131
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • DIrect oral anticoagulant? (DOAC) - like apixiban, diabigatran
  • high bleeding risk procedure
A

-advise patient to miss or delay morning dose before treatment
- treat early in day, limit initial treatment and assess bleeding before continuing staging extensive or complex procedures, strongly consider packing and suturing
- advise patient when to restart medication

132
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • vitamin K antagonist like warfarin?
A
  • check INR, ideally no more than 24 hours before procedure up to 72 hours if patient is stably anticoagulated
  • if INR below 4 :
  • treat without interupting medication

consider limiting initial treatment and staging extensive or complex procedures strongly consider suturing and paxking

  • if INR >4 or above, Delay invasive treatment or refer if urgent
133
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • injectable anticoagulant like dalterprin
  • prophylactic (low dose)
A
  • treat without interrupting meds
  • consider limiting initial treatment and staging extensive or complex procedures strongly consider suturing and packing
134
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • injectable anticoagulant like dalterprin
  • prophylactic (high dose)
A
  • consult with prescribing clinician
  • consider limiting initial treatment and staging extensive or complex procedures strongly consider suturing and packing
135
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • antiplatelet
  • aspirin alone
A
  • treat without interrupting medication
    consider limiting initial treatment and staging extensive or complex procedures and use local haemostatic measures
136
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • antiplatelet
  • clopidogrel or other antiplatelet + aspirin
A
  • treat without interupting meds
  • expect prolonged bleeding limit initial treatment area and consider staging extensive or complex procedures, strongly consider suturing and packing
137
Q

when managing a patient with anticoag or antiplatelet drug? and dental tx likely to bleed, meds is not time limited and has no medical complications what do you do for the different types of drugs?

  • antiplatelet + anticoagulant
A
  • consult with patients prescribing clinican
138
Q

dental procedures low risk of post op bleeding?

A
  • simple extractions 1-3 teeth
  • drainage intra oral swellings
  • detailed 6ppc
  • RSD
  • direct or indirect supragingival margin restorations
139
Q

dental procedures higher risk of post op bleeding?

A
  • complex extractions that will cause large wound or more than 3 teeth out
  • flap rasining procedures
  • gingival recontouring
  • biopsies
140
Q

what if on apixiban or diabgatran what is dose schedule after high risk treatment?

A

usual dose - twice a day
- morning dose - miss
- post op - usual time in evening

  • as long as no earlier than 4 hours after haemostasis has been achieved
141
Q

what if on rivroxban or edoxaban what is dose schedule after high risk treatment?

A

usual dose - once a day

  • if dose morning - delay - until 4 hours after haemostasis has been achieved
  • if evening dose - usual time in evening if 4 hours after haemostasis
142
Q

what is secondary bleeding?

A
  • often due to infection
  • commonly 3-7 days
  • usually mild ooze but can occasionally be a major bleed
  • medication related
143
Q

what is surgicel?

A

oxidises regenerated cellulose

144
Q

what are haemostatic agents?

A
  • Adrenaline containing LA – vasoconstrictor
  • Oxidised regenerated cellulose – Surgicel / equitamp
  • Haemocollagen Sponge –absorbable/meshwork for clot formation
  • Thrombin liquid and powder
  • Floseal
145
Q

what are systemic haemostatic aids?

A
  • Vitamin K (necessary for formation of clotting factors)
  • Anti-Fibrinolytics e.g. Tranexamic acid (prevents clot breakdown/stabilises clot – systemic tablets or mouthwash)
  • Missing Blood Clotting Factors
  • Plasma or whole blood
  • Desmopressin
146
Q

what is tranexamic acid?

A

anti fibrolytic

147
Q

what does tranexamic acid do?

A

prevents clot breakdown/stabilises clot

148
Q

if bleeding severe what do you do?

A

o If bleeding severe get pressure on immediately / arrest the bleed
o Calm anxious patient / separate from anxious relatives
o Clean patient up / remove bowls of blood / blood-soaked towels
o Take a thorough but rapid history while dealing with haemorrhage

o Get inside mouth/good light & suction
o Mouth often filled with large jelly-like clot
o Remove clot
o Patient may be vomiting if blood swallowed
o Identify where bleeding from

149
Q

what are post extraction instructions?

A

o Do not rinse out for several hours (better not to rinse till next day, then avoid vigorous mouth rinsing – wash clot away)
o Avoid trauma - do not explore socket with tongue or fingers/hard food
o Avoid hot food that day
o Avoid excessive physical exercise and excess alcohol – increase blood pressure

150
Q

what is Advice on control of bleeding?

A

 Biting on damp gauze/tissue
 Pressure for at least 30min (longer if bleeding continues)
 Points of contact if bleeding continues

151
Q

what is dry socket called?

A

alveolar osteitis

152
Q

what happens in dry socket?

A

o Normal clot disappears (appear to be looking at bare bone/empty socket – partially or completely lost blood clot)
o Main feature – intense pain (described as worse than toothache/patient kept awake at night)

153
Q

when does dry socket appear?

A

3-4 days after extraction

154
Q

how long does it take to resolve? dry socket?

A

o Takes 7-14 days to resolve

155
Q

symptoms of dry socket?

A

 Usually throbs/can radiate to patient’s ear/often continuous and can keep patient awake at night
 The exposed bone is sensitive and is the source of the pain
 Characteristic smell/bad odour & patient frequently complains of bad taste

156
Q

what is localised osteitis?

A

inflammation affecting lamina dura

157
Q

what are predisposing factors to dry socket?

A

 Molars more common – risk increases from anterior to posterior
 Mandible more common
 Smoking – reduced blood supply
 Female
 Oral Contraceptive Pill
 Local Anaesthetic – vasoconstrictor
 ?infection from tooth
 ?haematogenous bacteria in socket
 Excessive trauma during extraction
 Excessive mouth rinsing post extraction (clot washed away)
 Family history/ previous dry socket

158
Q

what is management of dry socket?

A

 Supportive – reassurance / systemic analgesia
 LA
 Irrigate socket with warm saline (wash out food and debris)
 Curettage/debridement
 Antiseptic Pack (Alvogyl)
 Advise patient on Analgesia and hot salty mouthwashes
 Review patient / change packs and dressings (as soon as pain resolves get packs out to allow healing)
 Generally, do not prescribe antibiotics as it is not infection
 Remember to check initially that it is a dry socket and that no tooth fragments or bony sequestra remain

159
Q

what is sequestrum?

A

o Usually bits of dead bone (can see white spicules coming through gingivae – patient often thinks you have left a part of the tooth)
o Can also be pieces of amalgam/tooth
o Delays healing/remove

160
Q

what is infected socket?

A

o But occasionally see an infected socket with pus discharge
 check for remaining tooth/root fragments/bony sequestra/foreign bodies. Treatment
 radiograph/explore/irrigate/remove any of the above/consider antibiotics.

161
Q

when is infected socket more commonly seen?

A

o Infection more commonly seen after minor surgical procedures involving soft tissue flaps and bone removal

162
Q

OAF/OAC what is acute and chronic

A

acute - oral antral communication
chronic - oral antral fistula

163
Q

how to diagnose oral antral communication?

A

 Size of tooth
 Radiographic position of roots in relation to antrum
 Bone at trifurcation of roots
 Bubbling of blood
 Nose holding test (careful as can create an OAF)
 Direct vision
 Good light and suction - echo
 Blunt probe (take care not to create an OAF)

164
Q

what is chronic OAF manageemnt?

A

o Excise sinus tract
o Buccal Advancement Flap

165
Q

how to do foreign body retrieval in antrum?

A

 Flap Design
 Open fenestration with care
 Suction – efficient and narrow bore
 Small curettes
 Irrigation or ribbon gauze
 Close as for oro-antral communication

166
Q

is caldwell-luc approach?

A
  • Root in Antrum – Retrieval
    o Caldwell-Luc approach:
     Buccal sulcus
     Buccal window
167
Q

what is osteomyelitis?

A

inflammation of bone marrow

168
Q

what is patient often in regards to osteomyelitis

A

Patient often systemically unwell/raised temperature

169
Q

what happens in deep seated infection in regards to osteomyelitis?

A

In deep seated infection may see altered sensation due to pressure on IAN

170
Q

where does osteomyelitis usually begin and spread to?

A

 Usually begins in medullary cavity involving the cancellous bone
 Then extends and spreads to cortical bone
 Then eventually to periosteum (overlying mucosa red and tender)

171
Q

what happens with invasion of bacteria into cancellous bone?

A

Invasion of bacteria into cancellous bone causes soft tissue inflammation and oedema in the closed bony marrow spaces

172
Q

what happens in enclosed bone marrow space of osteomyelitis?

A

 Oedema in an enclosed space leads to increased tissue hydrostatic pressure – higher than blood pressure of feeding arterial vessels
 Compromised blood supply results in soft tissue necrosis
 Involved area becomes ischaemic & necrotic

173
Q

why does bacteria proliferate in regards to osteomyelitis?

A

 Bacteria proliferate because normal blood borne defences do not reach the tissue
 The osteomyelitis spreads until arrested by antibiotic and surgical therapy

174
Q

why doesn’t osteomyelitis tend to happen in maxilla?

A

Can occur in maxilla but maxilla supplied by several arteries – rich blood supply

175
Q

why does osteomyelitis tend to happen in mandible?

A

Mandible – primary blood supply inferior alveolar artery and dense overlying cortical bone limits penetration of periosteal blood vessels – so poorer blood supply and more likely to become ischaemic and infected

176
Q

what are major predisposing factors to osteomyelitis?

A

odontogenic infections & fractures of mandible

177
Q

ostemyelitis is rare unless what?

A

osteomyelitis still rare unless host defences compromised
 Compromised host defence:
* Diabetes/ Alcoholism/ IV Drug Use/ Malnutrition/ Myeloproliferative Disease (e.g. leukaemias, sickle cell disease, chemotherapy treated cancer)

178
Q

what is early osteomyelitis difficult to distinguish from?

A

dry socket or localised infection in the socket

179
Q

when does lost bone be detectable radiographically?

A

10-12 days

180
Q

what is chronic osteomyelitis?

A

Chronic osteomyelitis – (+/- pus) – bony destruction in the area of infection

181
Q

what does osteomyelitis look radiographically?

A

increased radiolucency (uniform or patchy with a ‘moth-eaten appearance)

182
Q

what is areas of radipacity within radiolucent region of osteomyelitis?

A

unresorbed islands of bone – sequestra

183
Q

what may there be an increase of when viewing chronic osteomyelitis radiographically?

A

 In long-standing chronic osteomyelitis there may be an increase in radiodensity surrounding the radioluscent area – an involucrum
 This is the result of an inflammatory reaction – bone production increased

184
Q

what is treatment of osteomyelitis?

A
  • Medical and Surgical Treatment
  • Investigate host defences – Blood investigations/glucose levels – seek medical consultation
185
Q

what is antibiotic treatment of osteomyelitis?

A
  • Antibiotics – penicillins generally 1st line drug – effective against odontogenic infections & good bone penetration
  • Longer courses than normal
  • Often weeks in acute osteomyelitis (some suggest at least 6 weeks after resolution of symptoms)/months in chronic osteomyelitis (in some cases up to 6 months)
  • Severe acute osteomyelitis may require hospital admission and IV antibiotics (if systemic symptoms)
186
Q

how long are you on antibiotics for acute osteomyelitis?

A

6 weeks after resolution of symptoms

187
Q

how long are you on antibiotics for chronic osteomyelitis?

A

6 months after resolution of symptoms

188
Q

what is surgical treatment of osteomyelitis?

A
  • Drain pus if possible
  • Remove any non-vital teeth in the area of infection
  • Remove any loose pieces of bone
  • In fractured mandible
    o remove any wires/ plates/screws in the area
  • Corticotomy
    o removal of bony cortex
  • Perforation of bony cortex
  • Excision of necrotic bone (until reach actively bleeding bone tissue)
189
Q

what needs to happen in osteomyelitis cases?

A

Osteomyelitis needs referred to local OS or OMFS unit

190
Q

what is endarteritis?

A

reduced blood supply

191
Q

what is osteoradionecrosis?

A

bone within radiation beam becomes virtually non-vital

192
Q

why is mandible more commonly affected in osteoradionecrosis?

A

poorer blood supply

193
Q

how to prevent osteoradionecrosis?

A
  • Scaling/Chlorhexidine mouthwash leading up to extraction
  • Careful extraction technique
  • Antibiotics, chlorhexidine mouthwash and review
  • Hyperbaric oxygen (to increase local tissue oxygenation & vascular ingrowth to hypoxic areas) before and after extraction
  • Take advice/refer patient for extraction
194
Q

what is hyperbaric oxygen?

A

to increase local tissue oxygenation & vascular ingrowth to hypoxic areas

195
Q

what is treatment of osteoradionecrosis?

A
  • Irrigation of necrotic debris
  • Antibiotics not overly helpful unless secondary infection
  • Loose sequestra removed
  • Small wounds (under 1cm) usually heal over a course of weeks/months
  • Severe cases – resection of exposed bone, margin of unexposed bone and soft tissue closure
  • Hyperbaric oxygen
196
Q

what are bisphosphonates used to treat?

A

osteoporosis, Paget’s Disease & malignant bone metastases

197
Q

what do bisphosphonates do?

A

They inhibit osteoclast activity and so inhibit bone resorption and therefore bone renewal

198
Q

apart from bisphosphonates what other drugs do you need to look out for in terms of MRONJ?

A

[RANK-L] inhibitors) - Denosumab - Stops production of osteoclasts.

o Antiangiogenic They are basically divided into two types of drugs: Monoclonal antibodies that stop the receptor or growth factor (bevacizumab) and small molecules, which determine the block by binding the tyrosine kinase receptor (sunitinib and sorafenib).

199
Q

what does MRONJ mean?

A

medical induced osteonecrosis

200
Q

what are higher risk bisphosphonates?

A

IV

201
Q

what are risk factors for MRONJ?

A

o 1: Dental treatment
o 2: Duration of bisphosphonate drug therapy
o 3: Dental Implants - unknown
o 4: Other concurrent medication
o 5: Previous drug history
o 6: Drug holidays

202
Q

how does duration of bisphosphonate relate to risk?

A

Increased dose and increased duration both increase the risk of MRONJ

203
Q

what is duration of denosumab and anti-angiogenic effect on bone?

A

Denosumab’s effect on bone turnover diminishes after 9 months of finishing treatment

Anti-angiogenic drugs are not thought to remain in the body for extended periods of time

204
Q

what do you do for patient with osteoporosis who are being treated with 6 monthly subcutaneous injections of denosumab?

A

Patients with osteoporosis who are being treated with six monthly subcutaneous injections of denosumab may have treatment one month prior to drug administration. Resume drug after soft tissue closure.

205
Q

who are at low risk of MRONJ?

A
  • bisphosphonates orally and IV < 5 years and not taking glucocortico steroids
  • denousumab and not taking glucocorticosteroids
206
Q

who are at high risk of MRONJ?

A
  • oral and IV bisphosphonates >5 years
  • bisphosphonates or denosumab + glucocortico steroids
  • any anti-resorptive drug or antio-genionic drug as part of management of cancer
  • pateints with previous diagnosis of MRONJ
207
Q

how to manage MRONJ?

A
  • Prevent invasive treatment
  • Extractions in primary care setting
  • No benefit of referral to secondary care based purely on their exposure to these drugs
  • Guidance considers patients in two groups
    o Initial management (prior to commencing drug or just commenced)
    o Continuing management (established drug regime)
208
Q

what are the 2 groups of patients guidance has broken them into for MRONJ?

A

o Initial management (prior to commencing drug or just commenced)
o Continuing management (established drug regime)

209
Q

what is actinomycosis?

A

 The bacteria have low virulence and must be inoculated into an area of injury or susceptibility
 It erodes through tissues rather than follow typical fascial planes and spaces

210
Q

what does actinomycosis present as?

A

 Multiple skin sinuses and swelling
 Thick lumpy pus
* colonies of Actinomyces look like sulphur granules on histology

211
Q

what is treatment of actinomycosis?

A
  • I&D of pus accumulation
  • Excision of chronic sinus tracts
  • Excision of necrotic bone & foreign bodies
  • High dose antibiotics for initial control (often IV)
  • Long-term oral antibiotics to prevent recurrence
  • Antibiotics: Penicillins, doxycycline or clindamycin