Perioperative Medicine Flashcards
What are the advantages and disadvantages of Warfarin?
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%)
What are the indications for NOACS / DOACS?
Only licensed for:
Non valvular AF (non inferior / decreased ICH)
Primary prevention VTE prophylaxis post Hip / Knee Surgery
Secondary prevention in other VTE
How does Warfarin , Dabigatran and Rivaroxaban Act?
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
How do you brige warfarin perioperatively?
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.
How do you bridge DOACs?
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 .
How do you quantify Thromboembolic risk ?
- Divided in 3 groups
- Mechanical Heart Valve
- every Mitral + Some Aortic
- AF
- CHA2DS2VASc
- Previous VTE
- Mechanical Heart Valve
What is your approach to reversal of anticoagulants?
Depends on degree of bleeding and if it is life threatening
MINIMAL BLEEDING
- discontinue anticoagulant
- spontaneous resolution over time
- Vitamin K for warfarin
SEVERE BLEEDING
- Discontinue anticoagulant
- Supportive care (iv fluids, blood products - platelts )
- Activated charcoal
- Consider dialysis (dabigatran)
- DOAC reversal (dabigatran - IDARUCIAZUMAB)
- Consider Tranexamic acid 15-30mg/kg
- Prothrombin X 50iu/kg
- (haem advice - rfVII 90mck/kg or FEIBA
What is in Prothrombin X
What is in FFP
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)
What are the most common inherited bleeding disorders?
Haemophilia A, B or C (F8, F9 F11 def)
and
VWD 1 , 2a-d , 3 (quan, qual, none)
Discuss Haemophilia and its management
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.
Discuss the managment of VWD
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
What is in CRYOPRECIPITATE
VIII
VWF
XIII
FIBRINOGEN
Define Prehabilitation
What are the components
What is the current evidence base
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
How would you classify severity of asthma?
Define the following terms
FEV1
FVC
FEV1/ FVC Ratio
DLCO
FEF 25-75%
Maximum voluntary oxygenation
Describe the following flow loops:
1) Fixed obstruction
2) Extra-thoracic variable
3) Intra-thoracic variable
Discuss the pharmalogical management of asthma
How do TCAs work?
What are the implications for anaesthesia?
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.
How do SSRI work?
What are the implications for anaesthesia?
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.
what is serotonin syndrome?
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
How to MAOI work?
What are the anaesthetic implications??
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.
What are the anaesthetic issues with lithium?
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.
Discuss Parkinson’s Disease and its Perioperative Management
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
How does a SGLT2 inhibitor work?
What is the proposed mechanism of EDKA
What is the suggested perioperative management?
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.
