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ANZCA Part 2 > Perioperative Medicine > Flashcards

Perioperative Medicine Flashcards

1
Q

What are the advantages and disadvantages of Warfarin?

A

Advantages

Wide range of indications
Preferred in high-risk patients (especially mechanical valves)
Long safety history
Cheap, widely available antidote
Easy monitoring of degree of anticoagulation
No gastrointestinal upset (2% dabigatran/rivaroxaban)
Inexpensive
Single daily doseN

DISADVANTAGES

Need for monitoring
Highly variable dosing
Increased requirement for bridging
Food interactions
Drug interactions
Initially procoagulant
Slow onset
Long half-life
Increased risk of intracranial bleed (50%)

Possibly increased life-threatening bleed (25%)

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2
Q

What are the indications for NOACS / DOACS?

A

Only licensed for:

Non valvular AF (non inferior / decreased ICH)

Primary prevention VTE prophylaxis post Hip / Knee Surgery

Secondary prevention in other VTE

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3
Q

How does Warfarin , Dabigatran and Rivaroxaban Act?

A

Warfarin INHIBITS the epoxide reductase enzyme which is required to recycle vitamin K and is ESSENTIAL for production of gamma carboxylated coagulation factors. INDIRECT MECHANISM so takes time.

DABIGATRAN - directly inhibits THROMBIN (Factor 2) - it is a PRODRUG

RIVAROXABAN are DIRECT INhibitors of Factor Xa

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4
Q

How do you brige warfarin perioperatively?

A

Mounting evidence suggests bridging Warfarin increases major bleeding and cardiovascular events without a decrease in thromboembolic events.

1) Warfarin should not be interrupted for procedures of low risk
2) Patients at low VTE risk should not be Bridged
3) In patients at highest risk of VTW , but not excessive bleeding risk - consider Bridging
4) intermediate risk - individual risk assessment!

Warfarin needs to be ceased 5 days prior to OT.

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5
Q

How do you bridge DOACs?

A

Not recommended as the duration for the drug to be withheld before surgery is short and restoration of clinical effect is rapid and without PROCOAGULANT effect . Can be contemmplated in patient who has HIGH risk and requires prolonged preoprtative cessation .

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6
Q

How do you quantify Thromboembolic risk ?

A
  • Divided in 3 groups
    • Mechanical Heart Valve
      • every Mitral + Some Aortic
    • AF
      • CHA2DS2VASc
    • Previous VTE
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7
Q

What is your approach to reversal of anticoagulants?

A

Depends on degree of bleeding and if it is life threatening

MINIMAL BLEEDING

  1. discontinue anticoagulant
  2. spontaneous resolution over time
  3. Vitamin K for warfarin

SEVERE BLEEDING

  1. Discontinue anticoagulant
  2. Supportive care (iv fluids, blood products - platelts )
  3. Activated charcoal
  4. Consider dialysis (dabigatran)
  5. DOAC reversal (dabigatran - IDARUCIAZUMAB)
  6. Consider Tranexamic acid 15-30mg/kg
  7. Prothrombin X 50iu/kg
  8. (haem advice - rfVII 90mck/kg or FEIBA
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8
Q

What is in Prothrombin X

What is in FFP

A

Freeze dried powder of FII IX X from plasma of donors

Vials contain 500IU

Contraindications are DIC or Thrombosis

FFP

Seperated and frozen plasma <18hrs

150-300 ml

Has Factors 2 9 10 7

Should be ABO compatible with patients Red Cells

Transfusion reaction, volume (15ml/kg)

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9
Q

What are the most common inherited bleeding disorders?

A

Haemophilia A, B or C (F8, F9 F11 def)

and

VWD 1 , 2a-d , 3 (quan, qual, none)

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10
Q

Discuss Haemophilia and its management

A

Classified as A, B or C depending on deficieny 8,9,11

A and B are X linked recessive - males affected, female carry

~1/3 have no family hx

Factors 8 and 9 important in intrinsic pathway ->thrombin

Routine clotting screen may be normal - maybe prolonged APTT

Definitive diagnosis with factor assay.

Treatment

  • Factors and blood products*
  • recombinant factors VII and IX (A and B) - free from disease
  • expensive!
  • must be screened for factor inhibitors! if high risk then need Factor Eight Inhibitor Bypass Assay (FEIBA)

CRYOPRECIPITATE (VIII, VWF, X111, fibrinogen)

PROTHROMBIN X (II, VII, IX, X, protein c and s) (replaced by specific factors)

Recombinant factor VIIa (binds platelets and activated X - generates thrombin)

FFP not really used anymore

Pharmacological

1) DDAVP - released vWF increasing VIII levels (mainly A and VWD)
2) Tranexamic acid - inhibits conversion of plasminogen to plasmin.

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11
Q

Discuss the managment of VWD

A

most common inherited bleeding disorder incidence 1/100 but only clinically relevant 1/10000

VWF normally released from endothelium - binds factor 8, decreasing its clearance also helps with platelet adhesion and aggregation.

3 types 1,2,3

1 = quantative problem

2 = qualitative problem (A-D)

3 = no VWF factor

Diagnosis

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12
Q

What is in CRYOPRECIPITATE

A

VIII

VWF

XIII

FIBRINOGEN

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13
Q

Define Prehabilitation

What are the components

What is the current evidence base

A

Prehabilitation is a preoperative conditioning intervention that aims to prevent or attenuate surgery-related functional decline and its consequences.

“multi modal” prehabilitation comprises of physical, nutritional, and psychological

Goals of nutritional = promote anabolism avoid malnutrition

Evidence shows a positive effect of prehabilitation on perioperative fitness BUT had not yet shown improvement in post op complications, length of stay, tumour progression, response to medical treatment and survival.

Should be personalized approach targeting high risk patients

Do you postpone surgery (cancer) to prehabilitate?

Screen (DASI, 6mWD) + HADS -> Assess -> Intervene –> Re-assess

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14
Q

How would you classify severity of asthma?

A
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15
Q

Define the following terms

FEV1

FVC

FEV1/ FVC Ratio

DLCO

FEF 25-75%

Maximum voluntary oxygenation

A
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16
Q

Describe the following flow loops:

1) Fixed obstruction
2) Extra-thoracic variable
3) Intra-thoracic variable

A
17
Q

Discuss the pharmalogical management of asthma

A
18
Q

How do TCAs work?

What are the implications for anaesthesia?

A

TCAs - depression and chronic pain eg amitriptyline

Prevent presynaptic reuptake of NA and 5HT

Also have anti-muscarinic, anti-histaminergic and anti a1 adrenergic effect

IMPLICATIONS

abrupt withdrawl no recommended mainly due to cholenergic side effects and worsening depression/pain

MAY cause potentiation of indirect sympathomimetics - suggest cautiously use DIRECT acting to avoid hypertensive crises

Drugs that increase endogenous catecholamines eg Ketamine and Pancuronium should be used with caution .

Can caues sedation and loser seizure threshold

Potentiated by administration of other anticholenergic agents

CVS: widening QRS complex and QT prolongation with increasing dose.

Avoid Tramaol due to risk of serotonin syndrome.

19
Q

How do SSRI work?

What are the implications for anaesthesia?

A

SSRI =inhibition of pre-synaptic serotonin reuptake.

IMPLICATIONS

LOW risk - continue

abrupt withdrawl may provoke discontinuation syndrome

-dizziness, GI upset, variety psychiatric symptoms.

SSRI (mainly fluoxeyinr) interfer with CYP2D6 of codiene to morphine.

SSRIs interfer with platelet function so slight increase bleeding risk with NSAID

Consider serotonin syndrome.

20
Q

what is serotonin syndrome?

A

Iatrogenic condition

Behaioural symptoms ( agitation and confusion)

Motor activity ( muscle rigidity, hyper-reflexia)

autonomic instABILITY (hyperthermia, tachycardia, diarrhoea, labile BP)

Seizure, rhabdomyolysis, renal failure, arrhythmias may also occure

Dx is NMS

21
Q

How to MAOI work?

What are the anaesthetic implications??

A

enzymes involved in the breakdown of amine neurotransmitters (5HT and NA). MAO A and MAO B (tyramine)

either reversible or irreversble - selective or non selective.

moclobemide = reversible MAO A

IMPLICATIONS

irreversable - long duration of action. stop 2 weeks~!

PROFOUND PRESSOR EFFECT - indirect and direct , metabolism of indirect is inhibited, resulting in potentiation.

DIRECT is preffered if required.

Pethidine + MAO = serotonin crisis.

22
Q

What are the anaesthetic issues with lithium?

A

used in mania, bipolar, refractory depression.

MOA poorly understood, mimics Na and decreases neuronal activity in CNS and PNS

Narrow TI and high side effect profile

minor - continue , major suggest 24-49 stop

Can affect ADH, cardiac dysrhythmias, GI disturbance and tremor. ataxia renal failure coma in high doses.

Prolongs NDMB, ( decrease NT release in CNS) and reduction in anaesthetic agent requirements.

Solely excreted by the kidneys! Careful fluid balance , avoid nephrotoxics. NSAIDs reduce Li excretion by kidneys so Avouid.

23
Q

Discuss Parkinson’s Disease and its Perioperative Management

A

PD is an idiopathic neurodegenerative disease characterized by tremor, muscle rigidity and bradykinesia.

aetiology unknown but interplay between genetics, environmental and infectious factors

Results from cellular degeneration of dopaminergic cells in the substantia nigra and subsequent lack of dopamine. ALSO tyrosine B hydroxylase - rate limiting step - also diminishes,

PREOP

Assessing severity of PD

Currenty drug treatment - consider interactions

Will PO be availiable post op

Consider optimisation by neurologist.

INTRAOP

Airway - assess bulbar function - sialorrhoea - may need glycopyrolate.

Dysphagia - risk of aspiration

GA vs Regional - risk/benefit - may not tolerate Regional due to tremor and rigidity. Monitoring may be difficult.

Avoid - Droperidol/Metoclopramide (D2 antagonism)

Diathermy and DBS - may need to switch off and use non polar

POSTOP

CNS - risk of post op delirium - quietiapine no haloperidol

antiemetics

make sure can use PCA

24
Q

How does a SGLT2 inhibitor work?

What is the proposed mechanism of EDKA

What is the suggested perioperative management?

A

1) oral non-inuslin glucose lowering agents. Target SGLT2 receptor in PCT to prevent reuptake of glucose by the kidney. Reduce HbA1C ~2%, low hypo risk.

Trials have shown they also cardioprotective and reno-protective.

T1/2 ~12-16 hrs

2) EDKA - BSL <14, Ketone >0.7 and acidosis.

Fasting promotes formation of ketone bodies. In times of high glucagon there is an amplification of breakdown of fat to Acetyl CoA and production of ketone bodies.

SGLT2i also stimulate alpha cells, and increase plasma glucagon stimulating lipolysis, and ketogenesis in the liver. This glucagon/insulin ratio shift stimulates glucogenolysis and gluconeogenesis, thus increasing hepatic glucose output.

This is futher exacerbated by sugical stress leading to insulin resistance through increased release of catecholamines and cortisol.

The increase in glucose is excreted through the action on SGLT2 which affects the homeostatic picture and failure to supress glucagon.

3)

Risk Assessment

Type of Surgery

Low Risk - 48 hrs ( can be less) , certainly on the day of surgery

Check BSL and Blood Ketones on arrival

Post Op - Rpt ketones, restart SGLT2 asap

Major surgery

Atleast 2 days, consider more regular monitoring eg 4hrly, consider involving endocrinology.

Colonoscopy - “match the fast” ie when lost fibre starts

if combined preperation consider splitting and continuing other OHG.

ANZCA Part 2 (23 decks)

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