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BDS4 > Oral Surgery > Flashcards

Oral Surgery Flashcards

1
Q

Indications for 8 XLA

A

Un-restorable caries
Non-Txable pulpal/periapical pathology
Cellulitis, abscess, osteomyelitis
Resorption of adjacent/tooth
Tooth follicle disease: cyst (dentinogerous), tumour
Tooth in line of jaw surgery: #, orthognathic
Pericoronitis

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2
Q

What is pericoronitis?

A

Soft tissue inflammation related to crown of PE tooth
Most common reason for 8 XLA
Incidence: 70% PE 8s

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3
Q

Discuss acute pericoronitis

A

Symptoms

  • pain + swelling localised to operculum
  • radiation of pain
  • severe: trismus, facial swelling
  • spread of infection to tissue spaces (rare)

Exam

  • EO swelling, lymphadenopathy
  • trismus
  • tender operculum

Management

  • analgesic
  • chlorhexidine
  • operculum debridment (LA)
  • opposing tooth: XLA, smooth cusps
  • affected tooth: XLA
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4
Q

Discuss chronic pericoronitis

A

As acute +

  • pus exuding from beneath operculum
  • x-ray: widening of pericoronal space, sclerosing osteitis
  • traumatised operculum from OE U8

Management: AB

  • temp: 38.5C
  • feel unwell
  • dysphagia
  • recent 8 pain
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5
Q

What are not indications for 8 XLA?

A

Asymptomatic

L. ant. crowding

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6
Q

Local factors affecting 8 XLA

A 
Opening: trismus reason
Bone quality/density
- bisphosphonates
- radiotherapy
- hypercementosis
Tooth
- angulation
- crown size
- crown:root
- root morphology
- caries
Anatomy
- ID canal
- maxillary sinus
- cystic change 
Adjacent teeth
- restorations
- PD
- caries
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7
Q

Additional risks associated w/ U8 and L8 XLA

A

L8

  • temporary/permanent altered sensation lip/chin/tongue
  • 0.2% permanent tongue
  • 0.5% permanent lip/chin

U8

  • OAC
  • # maxillary tuberosity
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8
Q

Dx criteria for MRONJ

A

Previous/current Tx w/ anti-resorptive/angiogenic drug
Exposed bone or bone probed through IO/EO fistula in maxillofacial region persisted >8/52
No Hx radiotherapy jaws
No obvious metastatic disease jaws

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9
Q

Reasons for pt to be taking anti-resorptive/angiogenic

A 
Osteoporosis 
Hypercalcaemia
Bone
- Paget’s
- osteogenesis imperfecta 
- fibrous dysplasia 
Cancer
- w/ bone metastases: breast, prostate, lung, kidney, thyroid, bowel
- w/o bone metastases
- Multiple myeloma 
- other: giant cell lesions, fibrous dysplasia
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10
Q

What are bisphosohonates?

A

Anti-resorptives
Pyrophosphate analogues share C-P-C chemical core
Inhibit bone resorption: osteoclastic apoptosis
High affinity for bone; esp. high turnover areas
Less effect when new bone laid over
Long t1/2: 10y

Oral tablets: 1-10% intestinal absorption
IV: >70% reach bone

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11
Q

Examples of bisphosphonates

A

Alendeonate
Clodronate
Risedronate

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12
Q

What is denosumab?

A 
Anti-resorptive 
RANKL inhibitor: interfere osteoclast function 
Doesn’t bind to bone
Effect diminished 6/12 post-Tx
SC injection
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13
Q

Examples of denosumab

A

Prolia: red. skeletal event osteoporotic pt; take 6/12
XGEVA: red. skeletal event pt w/ bone metastases from solid tumours; 4/52
- higher conc., more freq.

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14
Q

What are anti-angiogenesis drugs?

A

Medications inhibit formation new blood vessels

Target multiple kinases involved in angiogenesis

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15
Q

Discuss examples of anti-angiogenetic

A

Bevacizumab: Ca Tx

  • monoclonal Ab: sits of cell surface
  • blocks VEGF ligand

Sunitinib: GI stromal, renal cell carcinoma, pancreatic neuroendocrine

  • tyrosine kinase inhibitor
  • blocks angiogenesis
  • blocks cell proliferation
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16
Q

MRONJ pathophysiology

A

Unknown

Inhibition osteoclast differentiation + function -> apoptosis
- red. bone turnover + remodelling
Inflammation + infection: local, systemic
Angiogenesis inhibition

Others

  • soft tissue healing
  • innate/acquired immune dysfunction
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17
Q

MRONJ risk factors for bisphosphonates

A 
Route: oral (0.02%), IV (2-16%)
Duration: oral (4y+), 3 IV infusions 
Dose
Potency 
Tx: OS > trauma > spontaneous 
L > U; post. > ant.
Immunosuppressed: azathioprine, methotrexate, steroids
Immunocompromised: DM, HIV
Chemotherapy, anti-angiogenesis
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18
Q

MRONJ risk in cancer pt

A

Higher risk

Not exposed anti-resorptive/angiogenic: 0-1.9/10000
Exposed bisphosphonates/denosumab: 50-100x inc. risk
Exposed bevacizumab: 20/10000
- inc. w/ concurrent bisphosphonates

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19
Q

MRONJ risk for osteoporosis pt

A 
Low risk
<1/1000 develop ONJ
Oral/IV: similar risk
- less potent cf cancer Tx
100x smaller cf cancer Tx
Duration: >4y inc. risk
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20
Q

Management strategies for pt before starting anti-resorptive/angiogenic

A

Pre-dental assessment
- XLA all poor prognosis/unrestorable
- allow mucosal healing before starting drugs
— esp for IV BP + denosumab

Encourage good OH
Smoking cessation

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21
Q

Management strategies for pt on anti-resorptive/angiogenic

A 
Regular dental appt 
Maintain OH
Non-OS Tx done in practice 
- restorations
- endo
- prosthesis 
- NSPT
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22
Q

Prevention of MRONJ

A

XLA 1 sextant/T
CHX m/w
Flapless surgery
1ry closure w/ split thickness flap (no exposed bone)

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23
Q

Evidence for AB when Tx anti-resorptive/angiogenic pt

A

Low risk: no evidence
High risk
- pre: amoxicillin 500mg stat
- post: amoxicillin 500mg TDS, CHX, review

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24
Q

Evidence for drug holidays

A 
Low evidence 
Probably no harm due to long t1/2
Oncologists can discontinue drug for Ca pt if ONJ develops;
- cancer status
- ONJ extent + severity
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25
Q

Management goals for MRONJ

A

Prioritise + support continued oncological Tx
Persevere QoL
Control pain + 2ry infection
Prevent extension + development new necrosis

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26
Q

Local and systemic factors affecting socket healing

A

Local

  • inflammation
  • foreign bodies
  • bony fragments
  • tooth tissue
  • radiation exposure -> endarteritis

Systemic

  • medications
  • smoking
  • DM
  • malignancy
  • diet/nutrition
  • vascular disease
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27
Q

Aetiology of alveolar osteitis

A

Dry socket

Organised blood clot in XLA socket lost
- never forms: bone disease affecting blood supply
- prematurely lost: smoking, rinsing
- disintegrated: proteolytic bacteria
Bacteria colonise + proliferate
- escape host defence in socket
Further colonisation -> encourage clot lysis
Localised inflammation of alveolar bone
- prevents spread of infection beyond socket

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28
Q

Risk factors for dry socket

A 
Traumatic XLA
Md > Mx; post. > ant.
F, OCP
Smoker: -ve pressure remove clot 
PD, poor OH
Bony disease affecting blood supply
- Paget’s, osteopetrosis, CRT of H+N, cemento-osseous dysplasia 
Previous dry socket
Excessive vasoconstrictor (LA)
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29
Q

Clinical presentation of dry socket and Ix

A

Clinical

  • pain; few days post-XLA
  • no blood clot; grey slough, bone/debris
  • gingival inflammation
  • halitosis, bad taste

Ix

  • completely clinical Dx
  • X-ray for bony fragment if >2/52
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30
Q

Management of alveolar osteitis

A 
Reassurance
Irrigation
- saline
- CHX; no evidence
Dressing; Alvogyl
Smoking cessation
Analgesia: ibuprofen, paracetamol 
Review
Repeat (if req.)
If no resolution = wrong Dx
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31
Q

Osteomyelitis aetiology

A

Inflammation of bone usually due to infection
Source
- haematogenous: rare, poss. children
- direct: XLA, surgery, #, PA lesion (usually)

Usually bacterial: Strep., Staph., Prevotella, Porphyromonas
Forms in confined spaces of Md: medullary cavity (bone marrow space)

Eventual necrosis -> liquefaction + pus formation
- sub-periosteal reactive bone formation try to prevent spread

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32
Q

Clinical presentation of osteomyelitis

A

Pain: pus formation in confined space

  • throbbing, entire Md
  • poorly localised cf dry socket
Swelling: oedematous, collection (localised pus), bone
Exposed necrotic bone +/- suppuration
- 1/+ IO/EO sinuses 
Paraesthesia: CNV3; lip + chin numbness 
- if ID canal affected

Lymphadenopathy
Pyrexia, malaise
Trismus

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33
Q

Ix and Mx of osteomyelitis

A

Ix

  • pus sample; AB sensitivity
  • X-ray: plain, CBCT, CT
  • bloods: leukocytosis

Mx
- empirical AB therapy
— clindamycin (good bony penetration)
- removal + debridement (if severely contaminated)
- long term AB; Outpatient Parenteral AB Therapy

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34
Q

What is osteoradionecrosis?

A

Non-healing region of bone in irradiated area

  • persisted >3/12
  • in absence of recurrent malignancy
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35
Q

Staging of ORN

A

Notani

1: confined to alveolar bone
2: limited to alveolar bone +/- mandible above level of mandibular canal
3: extended to mandible below level of mandibular canal w/ skin fistula or pathological #

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36
Q

Prevention of ORN

A

Full dental assessment + prophylactic XLA
Diet change, F advice
Relieve dentures to avoid mucosal trauma
Regular recall
Good communication w/ hospital

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37
Q

Local + systemic risk factors for osteomyelitis

A

Local

  • Md > Mx
  • red. vascularity/vitality
  • medications: bisphosphonates
  • irradiation: CRT
  • bony disease: Paget’s, osteopetrosis

Systemic: immunodeficient;

  • DM
  • leukaemia
  • agranulocytosis
  • medications: corticosteroids, CRT
  • malnutrition: osteomalacia, Ricket’s
  • age
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38
Q

Discuss acute osteomyelitis

A

Acute exudative inflammation reaction within bone
- dense neutrophilic infiltrate within bone marrow
Compression + thrombosis of periosteal vessels -> ischaemic necrosis
Reactive bone formation; min. cf chronic

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39
Q

Discuss chronic osteomyelitis

A

More common

Clinical: dif. pain nature + duration

  • low level dull ache
  • always present

cf acute

  • localised sclerotic bone
  • CRT more likely implicated

Mx

  • corticotomy: holes made in bone, allow periosteum vascularity to permeate
  • AB beads
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40
Q

Complications of osteomyelitis

A

Septicaemia: enter bloodstream
Acute bacterial arthritis: inflammation of joint space
Pathological #: extensive bone weakened

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41
Q

Clinical + radiographic findings of ORN

A 
Clinical: similar to COM
- sterile: asymptomatic 
- infection -> intractable OM
— spreads rapidly 
— painful necrosis 
— sloughing of orofacial soft tissues 
- healing slower/none
- no periosteal reaction; bone acellular

Radiographic: similar to OM

  • ill defined
  • mottled
  • mixed radiodensity
  • bony sequestra
  • haphazard trabecula
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42
Q

Aetiology of ORN

A

Irradiation affects bone vascularity
- vessel intima proliferation -> thickening -> occlusion (endertaritis obliterans)
- thrombosis
= loss of vitality (aseptic necrosis)

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43
Q

Mx of ORN

A

Conservative: AB, analgesic, OH
Hyperbaric O2 therapy: inc. O2 supply
Surgery: resection + reconstruction

Medications: pentoxifylline, tocopherol

  • anti-radiation fibrosis, antioxidant
  • scavenge free radicals -> prevent oxidation

Severe cases surgical reconstruction only option

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44
Q

Aetiology of facial #s

A 
Road traffic accidents
Assault: drugs, alcohol 
Falls: epilepsy, MS
Sports 
Firearms
Dentistry 
Pathology
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45
Q

Types of #

A

Simple (closed): no communication w/ external structure
Compound (open): communication w/ skin/mucosa/PDL
Comminuted: multiple fragments
Complicated: involves important structure (artery)
Green stick: partial, children
Pathological: due to disease

46
Q

Early Mx of all #s

A

ABC

Control bleeding
Other serious injuries: head, cervical spine, abdomen, thorax 
Other #s
CSF leak 
Ocular damage 
Red. + immobilise if compromising airway 
Lacerations 
Antimicrobial + tetanus prophylaxis
47
Q

Sites of Md #

A 
Dentoalveolar 3%
Condyle: intra/extracapsular 36%
Coronoid 2%
Ramus 3%
Angle 20%
Body 21%
Para/symphysis 14%
48
Q

Clinical signs of Md #

A 
Occlusal derangement: open bite 
Step deformity 
Para/anaesthesia 
Mobility across #
Pain, tenderness 
Swelling: haematoma (sublingual), oedema
IO bleeding 
Loose teeth 
Dysphagia 
Limited movement/trismus 
Otorrhoea: blood, CSF
49
Q

Tx of Md #s

A

Reduction: bring #s closer together

  • compound/open: surgical exposure
  • simple/closed: fast (manipulation), slow (elastic traction)

Fixation: relocate

  • indirect: inter-Mx #; Leonard buttons/eyelets/archbar/IMF screws
  • direct: screw/plate/wire/pin

Immobilisation: prevent movement

Rehabilitation

  • soft diet
  • jaw exercises
  • elastics
  • occlusal adjustment
50
Q

Complications of Md #

A

Malunion
Delayed union
Non-union

Infection: osteomyelitis, screw/plate
Malocclusion
Nerve injury
TMJ ankylosis

51
Q

Types of mid. 1/3 #

A 
Alveolar 
Central 
Zygomatic complex 
Orbital 
Nasal
52
Q

General features of mid. 1/3 #s

A 
Airway obstruction 
Ecchymoses: circumorbital, subconjunctival 
Gross facial oedema
Bleeding, CSF leak 
Mx mobility 
Occlusal disturbance
53
Q

Tx for mid. 1/3 #s

A

Reduction

  • correct craniofacial relationship
  • correct occlusal relationship

Fixation: in/direct

  • external: craniomaxillary, craniomandibular (old)
  • internal: plates, wires, wires to Mx splint/antral pack
54
Q

Types of central mid. 1/3 #s

A

Le Fort 1/2/3

55
Q

Discuss Le Fort 1 #

A

Anatomy

  • low level, sub-zygomatic
  • detachment of alveolar process w/ palate from Mx complex
  • sup. floor of nose + antrum

Clinical: Mx move independently

  • local injury evidence: bruising, oedema (B sulcus)
  • gagging on post. teeth, ant. OB
  • altered sound on percussion
56
Q

Discuss Le Fort 2 #

A

Anatomy

  • pyramidal
  • sub-zygomatic
  • through lat. + ant. walls Mx sinus and through infraorbital margin
  • join across bridge nose

Clinical: nose move independently

  • rapid facial swelling: bruising, oedema
  • bilateral, circumorbital + subconjunctival ecchymoses
  • epistaxis
  • infraorbital anaesthesia
  • interference w/ ocular movement
57
Q

Discuss Le Fort 3 #

A

Anatomy

  • high level
  • supra-zygomatic
  • through lat. walls orbits + orbital floor
  • detachment of zygomatic bones @ frontozygomatic suture across zygomatic arch

Clinical: orbits move

  • as Le Fort 2
  • subconjunctival ecchymoses (outer quadrant cf inner LF2)
58
Q

Clinical features of zygomatic complex #s

A 
Ecchymoses: circumorbital, subconjunctival 
Cheek oedema
Zygoma tenderness + flattening 
Limited ocular movement 
Diplopia 
Strabismus 
Limited lat. excursion to injury 
Limited opening/closing 
Epistaxis 
Para/anaesthesia (gum, cheek)
Infraorbital rim notch 
Dimple over zygomatic arch
59
Q

Tx indications + modalities for zygomatic complex #s

A

Indications

  • aesthetics
  • limited Md/ocular movement

Modality

  • reduction
  • IO elevation: upper B sulcus incision
  • Gillies Lift: EO elevation, temporal incisor
  • Poswillo Hook
60
Q

Clinical features of orbital blow out

A 
No step defect: orbital rim intact 
- Thin orbital floor + med. wall #
Contents herniate into antrum 
Enophthalmos 
Diplopia
Limited movement
61
Q

Tx for orbital blowout #

A 
Restore orbital vol.
Remove herniated tissue from antrum 
Graft defect in floor/med. wall
- Ti
- bone
62
Q

Effect of benign lesions

A

Excessive accumulation of cells leads to

  • pressure atrophy: adjacent parenchyma
  • fibrous capsule: more resistant connective tissue
  • obstruction
63
Q

General features of benign lesions

A 
Encapsulated; esp. if in solid organ 
Shape: round (moulded by surrounding tissues)
Size: small cf malignant 
Slow growing 
Bleeding + ulceration rare 
Can prod. hormones (endocrine tissue)
64
Q

Indications for removal of benign lesions

A 
Pain
Red. function 
Aesthetics 
Continual growth 
Pressure on adjacent structures 
Weakening of structures 
Infection
65
Q

Surgical management methods

A 
Excision 
Curettage 
Enucleation 
Marsupialisation 
Lithotripsy 
Laser
Diathermy
Cryotherapy
66
Q

Discuss excision + curettage

A

Excision
- cut lesion out
- suitable for small lesions; won’t leave large defect
- direct important
— long axis parallel skin creases/wrinkles
— along muscle will cause scaring

Curettage: scrape out

67
Q

Discuss enucleation

A

Removal of whole lesion/cyst w/ lining/capsule

Suitable for large lesions
Incise mucosa over lesion + dissect lesion out

Success is dependent on

  • complete removal of lining
  • uneventful healing
  • no 2ry infection blood clot
68
Q

Dis/advantages of enucleation

A

Adv

  • cavity closed to mouth
  • little aftercare req.
  • complete lining available for histology

Disadv

  • recurrence; if incomplete lining removal
  • blood clot may be infected
  • haemorrhage
  • vital teeth apices/structures may be damaged
  • large cyst may weaken jaw
  • can’t visualise cavity (1ry closure)
69
Q

Discuss marsupialisation

A

Decompress cyst be creating largest poss. surgical window consistent w/ anatomy
- relieve intro-cystic pressure -> regresses in size until eliminated

Incomplete lining removal + make continuous w/ mouth/antrum

Hole must be large enough to prevent closure + cyst recreation

  • pack
  • wait for granulation tissue
  • 6/12
70
Q

Dis/advantages of marsupialisation

A

Adv

  • less bone removal (avoid pathological # Md)
  • cavity visible
  • save associated tooth (dentigerous cyst)
  • avoid damage adjacent structures

Disadv

  • pt needs to keep clean
  • whole lining not available for histology
  • epithelial lining may be friable + difficult to suture
  • several appts; repack cavity as shrinks + repairs
  • orifice may closure -> cyst reform
  • bony infill may not occur
71
Q

Discuss LASER for soft tissue uses

A

CO2 laser

Method

  • beam hits
  • temp rise -> proteins denature + thrombosis
  • cellular H2O boils -> ruptures cells -> tissue vaporised
  • once desiccated, temp rise more + adjacent tissues heat (carbonisation)

Uses

  • cutting: vaporisation
  • coagulation: protein denaturation -> cell death + haemostasis
  • har tissue surgery
72
Q

Dis/advantages of laser surgery

A

Adv

  • dry working field
  • red. blood loss
  • red. post-op oedema, pain, fibrosis
  • fibre-optic delivery; reach places not poss. w/ surgery

Disadv

  • cost
  • complexity
  • no specimen for pathology
73
Q

Uses of diathermy

A

Coagulation (bipolar)
Fulguration: destruction of small growth/area
Cutting (monopolar)

74
Q

Disadvantages of diathermy

A

Burns
Explosions
Electrocution
Pacemakers

75
Q

Discuss cryotherapy

A

Tissue denaturation by cold medium
Direct application of NO2 or through cryoprobes (-196C)

Use: fluid filled lesions

76
Q

Discuss freeze-thaw cycles of cryotherapy

A

Causes formation of ice-ball

Intracellular ice formation inc. cell volume + disruption occurs on thawing
Repeated cycles -> red. lesion mass

77
Q

What is effectiveness of cryotherapy dependant on?

A

Absolute temp change
Rate of change
No. cycles
T of temp decrease

78
Q

Dis/advantages of cryotherapy

A

Adv

  • no cutting
  • tissue intact + no bleeding
  • done w/o LA

Disadv

  • cost
  • no pathology specimen
  • large amount post-op swelling + ulceration
  • depigmentation (lip)
79
Q

Function of maxillary sinus

A

Moisten + warm inhaled air
Lighten skull
Resonance
Immunological (URT)

80
Q

What is oro-antral communication?

A

Communication b/w mouth + maxillary sinus

81
Q

Predisposing factors for OAC

A 
XLA UMs
Tooth-antrum relationship/proximity 
Submerged teeth
Large antrum 
Hypercementosis 
Bone loss (perio)
Excessive force 
Surgery near sinus (cyst removal)
82
Q

Dx of OAC

A 
Hollow sound when aspirator in socket (gentle)
Bubbling bleeding
Air entry into mouth when holding nose 
Antral lining/bone on roots
X-ray: defect in floor
83
Q

OAC Tx

A

Prevention better
Tx before sinus becomes infected

Small: horizontal mattress suture
Large: buccal advancement flap
Acrylic plate/obturator
Antral regime

84
Q

Post-op instructions following OAC Tx

A

No smoking or nose blowing
Don’t drink through straw
Sneeze with mouth open

Antral regime

  • AB prescription
  • inhalations: Karvol
  • nose drops: ephedrine
85
Q

Discuss oro-antral fistula

A

OAC that has epithelialised
- at least 48-72h later

Clinical

  • regurgitation of food/fluids into nose
  • epistaxis
  • chronic sinusitis
  • antral mucosa prolapse into mouth
  • X-ray: fluid in sinus

Tx

  • AB pre-surgery; clean antrum
  • excise fistula tract; 2 epithelialised edges won’t heal
  • buccal advancement flap +/- buccal fat pad
86
Q

Predisposing factors for # tuberosity

A 
Lone standing UMs
Hypercementosis
Bulbous/splayed roots 
Large antrum
Excessive force
87
Q

Dx + Tx # tuberosity

A

Dx: feel tooth + bone moving together

Tx
- small
— raise buccal flap
— dissect # bone + tooth out under direct vision 
— close: prevent OAC
— post-op instructions 
- large
— leave, allow to heal 8/52
— surgical XLA
— AB
88
Q

Aetiology of acute sinusitis

A 
Influenza 
Cold leading to 2ry bacterial infection 
Measles
Whooping cough 
Penetrating injury 
Dental related
89
Q

Predisposing factors for acute sinusitis

A

Poor/dec. drainage
Virulent infection
Deviated septum
Debilitated pt

90
Q

Clinical findings of acute sinusitis

A 
Constant nagging pain mid-face
Pyrexia
Tenderness (esp. when moving head)
Mucopurulent discharge 
Facial swelling, cheek oedema
Teeth TTP but vital 
Lack of transillumination
X-ray: opacity
91
Q

Tx of acute sinusitis

A

Medical

  • bed rest
  • AB
  • decongestants
  • inhalations
  • analgesic

Surgical

  • antral washouts; remove fluid if unresponsive to medical
  • intranasal antrostomy (enlarge ostium)
92
Q

Complications of acute sinusitis

A

Spread to other sinuses
Laryngitis
Otitis media
Chronicity

93
Q

Discuss chronic sinusitis

A

Aetiology: same + inadequate Tx acute

Clinical

  • mucopurulent discharge
  • thickened antral mucosa
  • nasal obstruction
  • X-ray: opacity
  • no transillumination

Tx
- medical: same
- surgical
— antral washout
— intranasal antrostomy (create drainage point)
— Caldwell-Luc (remove irreversibly damaged mucosa)
— Functional Endoscopic Sinus Surgery (enlarge nasal passage)

Complications: same

94
Q

Steps involved in normal haemostasis

A

Vessel vasoconstriction
1ry haemostasis: platelet aggregation -> platelet plug
2ry haemostasis: blood coagulation -> fibrin clot
Fibrin degradation by plasmin to dissolve clot

95
Q

Discuss normal mechanism of vessel vasoconstriction

A

Local factor-mediated neurogenic vasoconstriction
Small vessels + capillaries closed by pure platelet plug w/o blood clots
Larger wounds req. clot

96
Q

What pathological conditions predispose to clot formation?

A 
Atheroma
Vessel fragility (long term steroids)
Abnormal vessel
Vascular lesions 
Altered haemodynamics
97
Q

Discuss 1ry haemostasis mechanism

A

Exposed collagen (damaged endothelium) binds + activates platelets
Platelet factors released from granules; ADP, Thromboxane A2
More platelets attracted
Platelet plug formed

98
Q

Causes of thrombocytopenia

A 
Production failure 
- general marrow failure
— marrow aplasia 
— megaloblastic anaemia
— leukaemia, myeloma 
— myelofibrosis
- megakaryocyte depression
- drugs; alcohol, chemotherapy 
- viruses
- chemicals
- congenital 
Survival Failure
- autoimmune
— idiopathic thrombocytopenia purpura 
— SLE
- HIV
- malaria 
- chronic lymphocytic leukaemia 
- non-autoimmune
— disseminated intra-vascular coagulation 
— drugs; aspirin, cytotoxics, valproate
99
Q

Causes of disturbed platelet function

A

Drugs: aspirin, NSAIDs, clopidogrel
Von Willibrand’s disease: defective/red. vWF
Defective granule prod./function; uraemia, haematological malignancy

100
Q

Briefly outline coagulating cascade

A

Intrinsic pathway: activated by damage within blood vessel

  • contact activation pathway
  • contact w/ exposed collagen

Extrinsic pathway: activated by damage outside blood vessel

Both activate CFX -> common pathway + clot formation
- fibrinogen -> cross-linked fibrin (stable clot)

101
Q

Congenital clotting disorders

A 
Haemophilia A (CF8C deficient)
Haemophilia B (CF9 deficient)
Von Willibrand’s disorder (vWF deficient/abnormal)
102
Q

Acquired clotting disorders

A 
Anticoagulant: warfarin, heparin, NOACs
VitK deficiency/malabsorption: CF2/7/9/10
Liver disease
Disseminated intravascular coagulation 
Large vol. blood transfusions
103
Q

Systemic methods of achieving haemostasis

A

CF8/9

  • fresh frozen plasma
  • purified factors
  • cryoprecipitate

Desmopressin

  • synthetic analogue vasopressin
  • stim. release: CF8, vWF, tPA

Tranexamic acid

  • synthetic derivative lysine
  • anti-fibrinolytic

Platelets
VitK

104
Q

Most common local haemostatic agents

A 
Packs
Suture
Oxidised cellulose (Surgicel, Oxycel)
Adrenaline 
Tranexamic acid m/w
105
Q

Discuss Mx of thrombocytopenia + haemophilia pt

A

Thrombocytopenia

  • bleeding when platelets <50x10^9
  • transfusion pre-XLA (consult haematologist)
  • additional: pack + suture

Haemophilia
- Tx in hospital in conjunction w/ haematologist
- req.
— factor replacement
— desmopressin
— systemic tranexamic acid
- caution w/ ID blocks, infiltration where poss.
- additional: pack + suture
- adverse: immune response to factor, infectious disease spread

106
Q

Mx of warfarin pt

A

Never stop warfarin

Check INR <72h pre-Tx
- >4.0 postpone
Tx at start of day

Atraumatic as poss.
Additional
- pack + suture
- 5% tranexamic m/w QDS
Carefully check haemostasis
Care if prescribing
107
Q

Drug interactions w/ warfarin

A 
Metronidazole 
Fluconazole + azole antifungals 
NSAIDs
Alcohol
Barbiturates
108
Q

Mx of NOAC pt

A

Apixaban + dabigatran: BDS

  • miss morning dose
  • take normal evening dose

Rivaroxaban + edoxaban: ODS

  • morning: delay, 4h post-haemostasis
  • evening: take as normal

Additional: pack + suture

109
Q

Mx of anti-platelet pt

A

Aspirin: don’t stop
Others: don’t stop

Simple precautions

  • pack
  • suture
  • tranexamic acid

Avoid NSAIDs

110
Q

Define 1ry, reactionary + 2ry bleeding

A

1ry

  • immediate, occurs during procedure
  • soft tissue, inflammation, damage to blood vessel, bony bleed, granuloma

Reactionary

  • few hrs later (up to 24h)
  • loss of clot, bleeding disorder/anti-platelet/coagulation medications, adrenaline wearing off

2ry

  • few days later
  • infection, bleeding disorder/anti-coagulation medication

BDS4 (10 decks)

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