Oral Surgery Flashcards
Indications for 8 XLA
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
What is pericoronitis?
Soft tissue inflammation related to crown of PE tooth
Most common reason for 8 XLA
Incidence: 70% PE 8s
Discuss acute pericoronitis
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
Discuss chronic pericoronitis
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
What are not indications for 8 XLA?
Asymptomatic
L. ant. crowding
Local factors affecting 8 XLA
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
Additional risks associated w/ U8 and L8 XLA
L8
- temporary/permanent altered sensation lip/chin/tongue
- 0.2% permanent tongue
- 0.5% permanent lip/chin
U8
- OAC
- # maxillary tuberosity
Dx criteria for MRONJ
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
Reasons for pt to be taking anti-resorptive/angiogenic
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
What are bisphosohonates?
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
Examples of bisphosphonates
Alendeonate
Clodronate
Risedronate
What is denosumab?
Anti-resorptive RANKL inhibitor: interfere osteoclast function Doesn’t bind to bone Effect diminished 6/12 post-Tx SC injection
Examples of denosumab
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.
What are anti-angiogenesis drugs?
Medications inhibit formation new blood vessels
Target multiple kinases involved in angiogenesis
Discuss examples of anti-angiogenetic
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
MRONJ pathophysiology
Unknown
Inhibition osteoclast differentiation + function -> apoptosis
- red. bone turnover + remodelling
Inflammation + infection: local, systemic
Angiogenesis inhibition
Others
- soft tissue healing
- innate/acquired immune dysfunction
MRONJ risk factors for bisphosphonates
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
MRONJ risk in cancer pt
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
MRONJ risk for osteoporosis pt
Low risk <1/1000 develop ONJ Oral/IV: similar risk - less potent cf cancer Tx 100x smaller cf cancer Tx Duration: >4y inc. risk
Management strategies for pt before starting anti-resorptive/angiogenic
Pre-dental assessment
- XLA all poor prognosis/unrestorable
- allow mucosal healing before starting drugs
— esp for IV BP + denosumab
Encourage good OH
Smoking cessation
Management strategies for pt on anti-resorptive/angiogenic
Regular dental appt Maintain OH Non-OS Tx done in practice - restorations - endo - prosthesis - NSPT
Prevention of MRONJ
XLA 1 sextant/T
CHX m/w
Flapless surgery
1ry closure w/ split thickness flap (no exposed bone)
Evidence for AB when Tx anti-resorptive/angiogenic pt
Low risk: no evidence
High risk
- pre: amoxicillin 500mg stat
- post: amoxicillin 500mg TDS, CHX, review
Evidence for drug holidays
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
Management goals for MRONJ
Prioritise + support continued oncological Tx
Persevere QoL
Control pain + 2ry infection
Prevent extension + development new necrosis
Local and systemic factors affecting socket healing
Local
- inflammation
- foreign bodies
- bony fragments
- tooth tissue
- radiation exposure -> endarteritis
Systemic
- medications
- smoking
- DM
- malignancy
- diet/nutrition
- vascular disease
Aetiology of alveolar osteitis
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
Risk factors for dry socket
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)
Clinical presentation of dry socket and Ix
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
Management of alveolar osteitis
Reassurance Irrigation - saline - CHX; no evidence Dressing; Alvogyl Smoking cessation Analgesia: ibuprofen, paracetamol Review Repeat (if req.) If no resolution = wrong Dx
Osteomyelitis aetiology
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
Clinical presentation of osteomyelitis
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
Ix and Mx of osteomyelitis
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
What is osteoradionecrosis?
Non-healing region of bone in irradiated area
- persisted >3/12
- in absence of recurrent malignancy
Staging of ORN
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 #
Prevention of ORN
Full dental assessment + prophylactic XLA
Diet change, F advice
Relieve dentures to avoid mucosal trauma
Regular recall
Good communication w/ hospital
Local + systemic risk factors for osteomyelitis
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
Discuss acute osteomyelitis
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
Discuss chronic osteomyelitis
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
Complications of osteomyelitis
Septicaemia: enter bloodstream
Acute bacterial arthritis: inflammation of joint space
Pathological #: extensive bone weakened
Clinical + radiographic findings of ORN
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
Aetiology of ORN
Irradiation affects bone vascularity
- vessel intima proliferation -> thickening -> occlusion (endertaritis obliterans)
- thrombosis
= loss of vitality (aseptic necrosis)
Mx of ORN
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
Aetiology of facial #s
Road traffic accidents Assault: drugs, alcohol Falls: epilepsy, MS Sports Firearms Dentistry Pathology
Types of #
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
Early Mx of all #s
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
Sites of Md #
Dentoalveolar 3% Condyle: intra/extracapsular 36% Coronoid 2% Ramus 3% Angle 20% Body 21% Para/symphysis 14%
Clinical signs of Md #
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
Tx of Md #s
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
Complications of Md #
Malunion
Delayed union
Non-union
Infection: osteomyelitis, screw/plate
Malocclusion
Nerve injury
TMJ ankylosis
Types of mid. 1/3 #
Alveolar Central Zygomatic complex Orbital Nasal
General features of mid. 1/3 #s
Airway obstruction Ecchymoses: circumorbital, subconjunctival Gross facial oedema Bleeding, CSF leak Mx mobility Occlusal disturbance
Tx for mid. 1/3 #s
Reduction
- correct craniofacial relationship
- correct occlusal relationship
Fixation: in/direct
- external: craniomaxillary, craniomandibular (old)
- internal: plates, wires, wires to Mx splint/antral pack
Types of central mid. 1/3 #s
Le Fort 1/2/3
Discuss Le Fort 1 #
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
Discuss Le Fort 2 #
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
Discuss Le Fort 3 #
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)
Clinical features of zygomatic complex #s
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
Tx indications + modalities for zygomatic complex #s
Indications
- aesthetics
- limited Md/ocular movement
Modality
- reduction
- IO elevation: upper B sulcus incision
- Gillies Lift: EO elevation, temporal incisor
- Poswillo Hook
Clinical features of orbital blow out
No step defect: orbital rim intact - Thin orbital floor + med. wall # Contents herniate into antrum Enophthalmos Diplopia Limited movement
Tx for orbital blowout #
Restore orbital vol. Remove herniated tissue from antrum Graft defect in floor/med. wall - Ti - bone
Effect of benign lesions
Excessive accumulation of cells leads to
- pressure atrophy: adjacent parenchyma
- fibrous capsule: more resistant connective tissue
- obstruction
General features of benign lesions
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)
Indications for removal of benign lesions
Pain Red. function Aesthetics Continual growth Pressure on adjacent structures Weakening of structures Infection
Surgical management methods
Excision Curettage Enucleation Marsupialisation Lithotripsy Laser Diathermy Cryotherapy
Discuss excision + curettage
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
Discuss enucleation
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
Dis/advantages of enucleation
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)
Discuss marsupialisation
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
Dis/advantages of marsupialisation
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
Discuss LASER for soft tissue uses
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
Dis/advantages of laser surgery
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
Uses of diathermy
Coagulation (bipolar)
Fulguration: destruction of small growth/area
Cutting (monopolar)
Disadvantages of diathermy
Burns
Explosions
Electrocution
Pacemakers
Discuss cryotherapy
Tissue denaturation by cold medium
Direct application of NO2 or through cryoprobes (-196C)
Use: fluid filled lesions
Discuss freeze-thaw cycles of cryotherapy
Causes formation of ice-ball
Intracellular ice formation inc. cell volume + disruption occurs on thawing
Repeated cycles -> red. lesion mass
What is effectiveness of cryotherapy dependant on?
Absolute temp change
Rate of change
No. cycles
T of temp decrease
Dis/advantages of cryotherapy
Adv
- no cutting
- tissue intact + no bleeding
- done w/o LA
Disadv
- cost
- no pathology specimen
- large amount post-op swelling + ulceration
- depigmentation (lip)
Function of maxillary sinus
Moisten + warm inhaled air
Lighten skull
Resonance
Immunological (URT)
What is oro-antral communication?
Communication b/w mouth + maxillary sinus
Predisposing factors for OAC
XLA UMs Tooth-antrum relationship/proximity Submerged teeth Large antrum Hypercementosis Bone loss (perio) Excessive force Surgery near sinus (cyst removal)
Dx of OAC
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
OAC Tx
Prevention better
Tx before sinus becomes infected
Small: horizontal mattress suture
Large: buccal advancement flap
Acrylic plate/obturator
Antral regime
Post-op instructions following OAC Tx
No smoking or nose blowing
Don’t drink through straw
Sneeze with mouth open
Antral regime
- AB prescription
- inhalations: Karvol
- nose drops: ephedrine
Discuss oro-antral fistula
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
Predisposing factors for # tuberosity
Lone standing UMs Hypercementosis Bulbous/splayed roots Large antrum Excessive force
Dx + Tx # tuberosity
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
Aetiology of acute sinusitis
Influenza Cold leading to 2ry bacterial infection Measles Whooping cough Penetrating injury Dental related
Predisposing factors for acute sinusitis
Poor/dec. drainage
Virulent infection
Deviated septum
Debilitated pt
Clinical findings of acute sinusitis
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
Tx of acute sinusitis
Medical
- bed rest
- AB
- decongestants
- inhalations
- analgesic
Surgical
- antral washouts; remove fluid if unresponsive to medical
- intranasal antrostomy (enlarge ostium)
Complications of acute sinusitis
Spread to other sinuses
Laryngitis
Otitis media
Chronicity
Discuss chronic sinusitis
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
Steps involved in normal haemostasis
Vessel vasoconstriction
1ry haemostasis: platelet aggregation -> platelet plug
2ry haemostasis: blood coagulation -> fibrin clot
Fibrin degradation by plasmin to dissolve clot
Discuss normal mechanism of vessel vasoconstriction
Local factor-mediated neurogenic vasoconstriction
Small vessels + capillaries closed by pure platelet plug w/o blood clots
Larger wounds req. clot
What pathological conditions predispose to clot formation?
Atheroma Vessel fragility (long term steroids) Abnormal vessel Vascular lesions Altered haemodynamics
Discuss 1ry haemostasis mechanism
Exposed collagen (damaged endothelium) binds + activates platelets
Platelet factors released from granules; ADP, Thromboxane A2
More platelets attracted
Platelet plug formed
Causes of thrombocytopenia
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
Causes of disturbed platelet function
Drugs: aspirin, NSAIDs, clopidogrel
Von Willibrand’s disease: defective/red. vWF
Defective granule prod./function; uraemia, haematological malignancy
Briefly outline coagulating cascade
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)
Congenital clotting disorders
Haemophilia A (CF8C deficient) Haemophilia B (CF9 deficient) Von Willibrand’s disorder (vWF deficient/abnormal)
Acquired clotting disorders
Anticoagulant: warfarin, heparin, NOACs VitK deficiency/malabsorption: CF2/7/9/10 Liver disease Disseminated intravascular coagulation Large vol. blood transfusions
Systemic methods of achieving haemostasis
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
Most common local haemostatic agents
Packs Suture Oxidised cellulose (Surgicel, Oxycel) Adrenaline Tranexamic acid m/w
Discuss Mx of thrombocytopenia + haemophilia pt
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
Mx of warfarin pt
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
Drug interactions w/ warfarin
Metronidazole Fluconazole + azole antifungals NSAIDs Alcohol Barbiturates
Mx of NOAC pt
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
Mx of anti-platelet pt
Aspirin: don’t stop
Others: don’t stop
Simple precautions
- pack
- suture
- tranexamic acid
Avoid NSAIDs
Define 1ry, reactionary + 2ry bleeding
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
