Thromboprophylaxi

s & RA
Dr Siva
Dr senthilnathan M
Moderated by: Prof A S BADHE

Introduction
The incidence of neurologic dysfunction is < 1 in

1,50,000 for epidural and < 1 in 2,20,000 for

spinal anaesthesia.
The decision to perform spinal or epidural

technique in patients who are on antithrombotic

medications is based upon individual patient
selection, benefits of RA.
There is small but definite risk of bleeding in

these patients.

Risk factors for VTE

Surgery
Trauma
Immobility
Carcinoma
Cancer therapy
Venous compression
Previous VTE
Pregnancy
HRT

Estrogen containing

OCPs
SERMs
Erythropoiesis
stimulating agents
IBD
Nephrotic syndrome
Obesity
Central venous catheter
Inherited or acquired
thrombophilia

VTE risk in hospitalised

patients
Low
risk

DVT
risk

Minor surgery in mobile patients

Medical patients who are fully
mobile
< 10%

No specific thromboprophylaxis
Options Early & aggressive ambulation

VTE risk in hospitalised

patients
Moderate
risk

DVT risk

Options

Most general, open gynecologic, urologic

surgeries
Medical patients in bed rest or sick

10 to 40%

LMWH, LDUH ( 2 or 3 times/day), fondaparinux

Mechanical thromboprophylaxis for high
bleeding risk

VTE risk in hospitalised

patients
Hip or knee arthroplasty, hip # surgery
High Major trauma, spinal cord injury
risk

DVT
risk

40 to 80%

LMWH, Fondaparinux, VKA

Medical thromboprophylsxis for high risk
Options
bleeding

Risk of bleeding
Bleeding is a major complication of

anticoagulation & thrombolytic therapy.

It is classified as major, if
Intracranial
Intraspinal
Intraocular
Mediastinal
Retroperitoneal
Requiring hospitalisation
Transfusion

Risk of bleeding
Overall risk factors for spinal hematoma
includes,
Spinal cord or vertebral abnormalities
Underlying coagulopathy
Catheter placement in patients on anticoagulation
therapy
Difficulty in needle placement

Risk of bleeding
Large fluctuation in anticoagulation effect

leads to increased risk of bleeding.

INR between 2 to 3 associated with low risk of

bleeding.
Hemorrhagic complications during therapeutic

anticoagulation with I.V or s.c heparin is < 3%

Risk is slightly lower with LMWH.

Spinal hematoma
It can be spontaneous or events disturbing

spinal vessels.

Clinical presentation:
Paraparesis

to paraplegia- MC
Sensory deficit
Loss of sphincter tone
Severe back pain, radicular pain

Spinal hematoma
Anatomical considerations:

Batsons plexus, longitudinal venous plexus, sparse

in midline- major source of epidural hematoma.

Disruption of radicular vessels- subdural &

subarachnoid hematomas.

Artery of Adamkiewicz sometimes enter the spinal

cord as radicular artery of cauda equina. 78% from
left side.

Spinal hematoma
The postoperative numbness & weakness

-attributed to LAs- delay in diagnosis.

Unexpected motor deficit, stop the LA infusion

and assess the patient.

Symptoms usually noted on POD 1.
Neurological outcome : Laminectomy within 8

hours of onset of neurological dysfunction.

Warfarin
Warfarin acts indirectly by inhibiting Vit K

dependent clotting factors factors II, VII, IX, X.

The effects of warfarin are not apparent until

significant amount of biologically inactive

factors are synthesized.
It depends upon half-life of these factors.

Warfarin
Factor

Half-life hrs

Factor VII

6-8

Factor IX

24

Factor X

25-60

Factor II

50-80

Warfarin
INR is based on values from patients who

were on stable anticoagulant doses for at

least 6 weeks.
So INR is less reliable in early course of

warfarin therapy.
Clotting factor activity of 40% for each

factor is adequate for normal or near normal

hemostasis.

Warfarin
During first few days of warfarin therapy, the

PT primarily reflects the reduction in factor VII.

INR of 1.5 is associated with factor VII activity

of 40%
Thus INR of < 1.5 during warfarin therapy

should have normal hemostasis.

Warfarin Interactions
Medications can affect the other components

of clotting mechanisms without affecting the

INR.
These include
Aspirin
NSAIDs
UFH
LMWH
Antiplatelet drugs

Perioperative management of
patients on warfarin
Preoperative management:

Discontinue warfarin at least 5 days prior.

Assess INR 1 to 2 days before surgery, if > 1.5, consider 1-2

mg of oral vitamin K.

For urgent reversal, consider 2.5 to 5 mg of oral or iv Vit K.

For immediate reversal, consider FFP.

No bridging for low risk of thromboembolism.

Perioperative management of
patients on warfarin
Preoperative management : at high risk of

thromboembolism

Bridge with therapeutic LMWH or iv heparin.

Last dose of LMWH administered 24 hours before

surgery.

IV heparin should be discontinued 4 hours before

surgery.

Risk stratification
Risk

Prosthetic
valve

AF

VTE

High

Any mitral
valve, older
aortic valve,
stroke or TIA
within 6
months

CHADS2 score
of 5 or 6,
recent stroke
or TIA, RHD

Recent-3 mon,
severe
thrombophilia

Moderate

Bileaflet aortic
valve
prosthesis and
one of the
following- prior
stroke, TIA,
DM, HTN, age
> 75years

CHADS2 score
3 or 4

VTE in 3 to 12
mon, recurrent
VTE, less
severe
thrombophilia,
active cancer

Low

Bileaflet aortic

CHADS2 score

VTE > 12 mon

Postoperative MX of patients on
warfarin

Regional anesthetic management

of patients on oral anticoagulants

Regional anesthetic management

of patients on oral anticoagulants

Regional anesthetic management

of patients on oral anticoagulants

Regional anesthetic management

of patients on oral anticoagulants
Low dose warfarin during epidural analgesia -

monitor the INR daily.

Assess sensory & motor function.
Remove catheter when INR is < 1.5.
Neurologic assessment.

Regional anesthetic management of

patients on oral anticoagulants
INR between 1.5 to 3 & without concurrent

medications- remove catheter

Neurological assessment until INR normalises.
INR > 3, withhold or reduce the dose of

warfarin.

Antiplatelet medications
These agents include,

NSAIDs including aspirin

Thienopyridine derivatives ( Ticlopidine, Clopidogrel)

Gp IIb / IIIa receptor antagonist ( abciximab,

tirofiban, eptifibatide)

NSAIDs
NSAIDs inhibit COX enzyme and prevent

synthesis of thromboxane A2.

Platelets in these patients have normal

adherence to subendothelium.
Aspirin- irreversible inhibition of COX 1.
Platelets do not exhibit COX 2 enzyme, so COX

2 inhibitors do not affect platelet function.

Ticlopidine, Clopidogrel
MOA: inhibiting ADP induced platelet aggregation.
Interfere with platelet-fibrinogen binding and

subsequent platelet- platelet interactions.

Concomitant use with aspirin increase -

hemorrhagic events.
Ticlopidine aplastic anemia, TTP, agranulocytosis

Gp IIb/IIIa inhibitors
MOA: inhibiting platelet-fibrinogen, platelet-

von Willebrand factor binding.

They block final common pathway for platelet

aggregation.
During therapy, puncture of non-compressible

sites and epidural procedures should be

avoided.

Perioperative management of
patients on antiplatelet therapy

Perioperative management of
patients on antiplatelet therapy

Regional anesthetic management of

patients on antiplatelet therapy

Regional anesthetic management of

patients on antiplatelet therapy

Platelet count

Preeclampsia

Preeclampsia

THANK
YOU