Details of DVT amd Pulmonary embolosm. Basics of Anticoagulations.

1. DEEP VEIN
THROMBOSIS
AND
PULMONARY
EMBOLISM
DR ANKIT GAJJAR

2. Haemostasis
Successful haemostasis depends on
• vessel wall
• platelets
• coagulation system
• fibrinolytic system

3. Blood Vessels
• Normal vascular endothelium possess
antiplatelet, anticoagulant and
profibrinolytic effects to inhibit clot
formation.
• Any damage to this endothelium shift the
balance and expose tissue factors which,
promotes clot formation.

4. Platelets
• adhere to damaged vessel wall
• adhere to each other
• form a platelet plug
• platelet release reaction

5. Platelet Release Reaction
• ADP, thromboxane A2 cause platelet
aggregation
• platelet factor 3 also released which is
important in coagulation
• Coagulation factor V and V|||

6. COAGULATION SYSTEM
• Main molecular components –
Coagulation factors and inhibitors,
Fibrinolysis factors and inhibitors,
Adhesive proteins (e.g. von Willebrand factor,
vWF), Intercellular proteins, Acute-
phase proteins,
Immunoglobulins, Calcium ions,
Phospholipids, Prostaglandins
Certain cytokine.

7. COAGULATION PROCESS- in
vivo
• Initiated mainly by FVIIa bound to tissue factor
(TF; large black arrow), which then activates
both FX (1) and FIX (2) (=initiation phase).
• To increase thrombin generation further,
thrombin activates FV, FVIII and FXI in a
feedback-loop (3) (=amplification).
• Continuation of thrombin generation results
mainly from the ongoing generation of FXa by
FIXa and FVIIIa (=propagation).
• Maximum thrombin generation occurs only after
the formation of fibrin, leading to the formation of
FXIIIa, which then crosslinks the fibrin
monomers (4) (=stabilization)

8. Current model of coagulation and fibrinolysis.

11. Thrombosis
• Definition
Thrombosis is the formation of a solid
mass of blood within the circulatory
system

12. Why does thrombosis occur?
VIRCHOW’S TRIAD
• Abnormalities of the vessel wall
– atheroma
– direct injury
– inflammation

13. Why does thrombosis occur?
• Abnormalities of blood flow(stasis)
- bed rest
- paralysis
• Abnormalities of blood component
– post-partum
– Protein c and s deficiency

14. Risk factors associated withRisk factors associated with
thrombosisthrombosis.• Acquired
1. Age > 70
2. Lupus AC/ SLE
3. Prior thrombus
4. Venous Stasis
5. Malignancy
6. Obesity
7. Hypertension
8. Stroke and Immobility
9. Oral contraceptives
10. Nephrotic Syndrom
11. Inflammatory Bowel
Disease
12. Pregnancy
13. Cigarette smoking
• Inherited.
1 Antiphospholipid
antibody syndrom
2 Factor V leiden
deficiancy
3 AT III deficiency
4 Protein C and S
deficiency
5 Homocysteinemia

15. DVT – Wells Score
• Cancer
• Paralysis or
plaster
immobilization
• Complete Bedrest
> 3 d or surgery in
past 4 wks
• Localized
tenderness
• Entire leg swollen
• Calf > 3cm larger
than unaffected
leg
• Pitting edema
greater than
unaffected leg
• Collateral
superficial veins
The following were assigned a point value of 1 if
present:
• Alternative diagnosis more likely than DVT = - 2 points
• Probability High (≥ 3), Moderate (1-2) or Low (0 or less)
• DVT risk: High – 75%, Moderate – 17%, Low – 3%

16. PULMONARY EMBOLISM
• When venous emboli become dislodged
from their site of origin, they embolize to
the pulmonary arterial circulation or,
paradoxically to the arterial circulation
through a patent foramen ovale
– About 40 - 50% of pts with pelvic or proximal
leg deep venous thrombosis have PE
– Isolated calf or upper extremity venous
thrombosis pose a lower risk for PE

17. Pathophysiology
• Increased pulmonary vascular resistance
• Impaired gas exchange
• Alveolar hyperventilation
• Increased airway resistance
• Decreased pulmonary compliance

18. Risk Factors
• Virchow’s Triad
• Age >70
• History of varicose veins
• History of MI
• History of malignancy
• History of atrial fibrillation
• History of ischemic stroke
• History of diabetes mellitus
• Previous VTE, obesity, pregnancy
• Use of estrogen

19. Incidence of Fatal PE inIncidence of Fatal PE in
Perioperative settingPerioperative setting
• 0.1-0.8 % during elective general surgery.
• 2-3 % during elective hip replacement.
• 4-7 % of patients undergoing surgery for a
fractured hip.
• Asymptomatic VTE 20-25% of patients after
general surgery and 45-60% of patients post for
hip or knee surgery.

20. Risk CategoriesRisk Categories
• Low ( Fatal PE < 0.001%)
• <40
• No risk factors
• General Anesthesia lasting < 30 mins.
• Minor operative procedures.
• Moderate ( Fatal PE 0.1-0.7%)
• >40
• General Anesthesia for > 30 mins
• <2 of the previous risk factors.

21. Risk CategoriesRisk Categories
• High Risk (Fatal PE-1-5%)
• > 40
• Surgery for Malignancy or Orthopedic procedure
• Surgery lasting > 30 mins.
• Inhibitor deficiency state or any other risk factor.

22. Evaluation and Diagnosis
• Evaluation and
imaging is dependent
upon estimated
pretest probability
(Modified Wells’
Criteria)
• Pretest probability:
– Low (<2 points)
– Intermediate (2-6
points)
– High (>6 points)
VARIABLE POINTS
S/S of DVT 3.0
HR >100 1.5
Immobilization
(bed rest >/= 3d)
OR surgery within
4 weeks
1.5
Prior DVT or PE 1.5
Hemoptysis 1.0
Malignancy
(treated within the
past 6 months or
palliative
1.0
Other diagnoses
less likely than PE
3.0

23. Clinical Features of PTE
Silent Asymptomatic Probably more
frequent than we
realize
Without Infarction Sudden onset of
unexplained
dyspnea
Tachycardia,
Anxiety,
Restlessness
Usually Transient

24. Clinical Features of PTE
With Infarction Dyspnea,
Hemoptysis,
Pleutitic Pain,
Friction Rub,
Brochospasm.
If you wait for
these features,
you will miss
perhaps 60% of
patients with
embolism

25. Clinical Features of PTE
With
Hemodynamic
Impairment
Tachycardia,
loud P2,
Gallop, JVP+
+, rt
ventricular
heave,
Hypotension,
Cyanosis,
Syncope
This means
obstruction of
30-50% of
pulmonary
vascular bed

26. Right Ventricular Dysfunction
• Progressive right heart failure is the usual
immediate cause of death from PE
• As pulmonary vascular resistance
increases, right ventricular wall tension
rises and perpetuates further right
ventricle dilation and dysfunction
• Interventricular septum bulges into and
compresses the normal left ventricle and
lead to decrease in lt ventricular stroke
volume and heart failure.

27. Broad Differential
• Pneumothorax
• Myocardial ischemia
• Pericarditis
• Asthma
• Pneumonia
• MI with cardiogenic shock
• Cardiac tamponade
• Aortic dissection
• Anxiety……..

28. Value of Diagnostic Tests in
PTE
Chest X-Ray Atelectasis(MC),
Elevated diaphragm,
Westermark sign,
Wedge-shaped
opacity(Hampton
Hump), Palla’s sign,
Pleural Effusion
It may be Normal
after acute PE
ECG Sinus
Tachycardia(MC),
S1Q3T3 pattern,
Signs of Rt. Strain.
P-Pulmonale,
Chest X-Ray and
ECG should be
Routine

29. Value of Diagnostic Tests in PTE
Isoenzyme
Pattern
Normal Only helpful
in
distinguishing
PE from MI
Leucocytic
Count
Under 15 000 If over 15 000,
consider
Bacterial
Sepsis

30. Value of Diagnostic Tests in PTE
Arterial Blood
Gases ( ABG )
Hypoxemia,
Hypocapnia,
Resp.
alkalosis
Non-specific
Alveolar-
Arterial
Oxygen
Tension
Difference
Increased
Difference
More
Sensitive but
Non-specific .

31. Value of Diagnostic Tests in PTE
Radioactive
Scanning
Abnormal Lung
Perfusion with
Normal
Ventilation .
High,
Intermediate
and Low
Probability .
A Normal
Perfusion Scan
with a Normal
CXR rules out
PE .

32. Value of Diagnostic Tests in PTE
Pulmonary
Angiogram
Intravacular
Filling Defect or
Vessel Cut-off
Gold standard.
The Most
Reliable but
Invasive
D-Dimers A Good (>90%)
Negative
Predictive Test
Elevated in DIC,
Pregnancy,
Severe Infection,
Trauma,
Malignancy,
Surgery, Liver
Disease

33. Value of Diagnostic Tests in
PTE
Spiral Computed
Tomography
Cases with
Ventilation-
Perfusion scan of
Intermediate
Probability
More sensitive to
proximal emboli
not for peripheral
Clinical
Assessment
Clinical Scoring
Plus ECG,
Radiographic
Findings,
Perfusion Scan.
This may restrict
the need for
Angiography to a
minority.

34. Interpretation of V/Q scan
Interpretation Clinical
suspicion
Probability of
PE Interpretation
High probability High or
intermediate
96% Treat for PE
Intermediate
Intermediate
Intermediate
Low
33%
12%
Need further
evaluation
Need further
evaluation
Low
Low
High
Low
16%
4%
Need further
evaluation
No PE
Normal Low 2% No PE
34

35. Echocardiogram
- Assess right and left ventricular function
– Diagnostic of PE if hemodynamics by echo
are consitent with clinical hx
– Help to differrntiate conditions which mimics
PE like cardiac tamponade, acute mocardial
infarction and aortic dissection.

36. Duplex US with compression of the
lower extremities
• Non-invasive test that accurately detects
proximal DVT in LE (70-80% of pts with
PE have concomitant proximal DVT)
• Often used in workup of PE before going
to more invasive procedure.

37. Treatment of acute pulmonary
embolism
• Treat as for any respiratory distress inclding O2,
monitoring, inotropes…..
• HEPARIN THERAPY
-- Unfractionated heparin
-- Low molecular weight heparin
• ORAL ANTICOAGULANT THERAPY
-- Warfarin
• THROMBOLYTIC THERAPY
-- Urokinase
-- Streptokinase
-- r t-PA (Alteplase)
• INFERIOR VENA CAVAL INTERRUPTION

38. HEPARIN
• A loading dose of 5,000 U followed by 1,000 U/h.
OR a bolus dose of 10,000 to 15,000 U.
• Weight based dosing
A bolus dose of 80 U/kg followed by start a drip of
18 U/kg/hr.
Check aPTT at 6 hrly and keep it 50 – 80 sec or 1.5 to
2 times than control.
Heparin should be continue for at least 4 days
total and for at least 2 days of therapeutic APTT
is achived.

39. Sites of Action of Heparin
CONTACT PHASECONTACT PHASE
XII activationXII activation
XI IXXI IX
TISSUE FACTORTISSUE FACTOR
TF:VIIaTF:VIIa
THROMBINTHROMBIN
fibrinogenfibrinogen
prothrombinprothrombin
XaXa
VaVa
VIIIaVIIIa
CaCa++++
plateletsplatelets
CLOTCLOT
monocytmonocyt
eses plateletsplatelets
macrophagemacrophage
ss
FIBRINOLYSIS ACTIVATIONFIBRINOLYSIS ACTIVATION
FIBRINOLYSIS INHIBITIONFIBRINOLYSIS INHIBITION
NATURALNATURAL
ANTICOAGULANTANTICOAGULANT
SS
(APC, ATIII)(APC, ATIII)
XX
PhospholipiPhospholipi
d surfaced surface
CaCa++
++
CaCa++
++
CaCa++
++
CaCa++
++
CaCa++
++
CaCa++
++
UF HEPARINUF HEPARIN
LMWHLMWH
ATIIIATIII

40. Heparin - Problems
bleeding
• unable to inhibit thrombin bound to clot
• unable to inhibit Xa bound to clot
• ongoing thrombin generation
• Direct inhibits platelets aggregation.
• Thrombocytopenia – HIT syndrom
• Allergic reaction
• Osteoporosis on long term use in higher dose

41. Heparin - Problems
• Heparin induce thrombocytopenia (HIT)
• Incidence: 1-5% of pt on UFH
• Due to antibodies formed against heparin-
platelet factor 4 complax on long term use
of heparin and it destroys the platelets.
• Lepirubin and argatobran used in HIT
syndrom which are direct thrombin
inhibitors.
• Immunoassay: anti-heparin-PF4 antibody

42. • In HIT, warfarin can be start when PLT
start to increase but direct thrombin
inhibitors should be cont. until normal PLT.
• After 4-5 days of warfarin and if PLT are
normal check INR, if it is 2-3, stop DTI’s.

43. Monitoring
1) PTT
assay 4-6 hrs after bolus dose and every
24 hrs theraafter
target for prophylaxis: 60-92 secs.
target for therapy: 92-125 secs.
2) PLATELET COUNT
check PLT count to detect HIT, if count
drops 30-50%, stop heparin and start
alternative anticoagulant.

44. Low Molecular Weight HeparinLow Molecular Weight Heparin
• Dalteparin, enoxaparin and tinzaparin
• All act to inhibit Factor Xa.
• Smaller effect on APTT and clotting
time
• Indicated in THA an TKA prophylaxis as
lower incidence of thrombosis.

45. Low molecular weight heparin
• Greater bioavailability (70-90%) when given
as subcutaneous injection.
• The duration of the anticoagulant effect is
greater (once or twice daily)
- The anticoagulant response is highly
correlated with body weight, permitting
administration of a fixed dose
- Laboratory monitoring is not necessary
except in pregnancy, morbid obesity and
renal failure
- Less likely to induce thrombocytopenia

46. Low molecular weight heparin
• no difference in risk of bleeding
• risk of accumulation
– renal clearance
– minimal filter clearance
• increased cost
• None are approved in pregnancy, spinal
cord injury, trauma with high risk of
bleeding or neurosurgery.

47. • Enoxaparin sodium
• for t/t 1mg/kg twice daily
• For prophylaxis 40 mg sc od.
• Oral anticoagulant should be initiated and
enoxaparin sodium should br continue
until therapeutic effect (INR 2-3)
• Dalteparin 200 U/kg is approved as a
monotherapy.
• Dose should be reduced in CRF.
Low molecular weight heparin

48. Heparin antagonist
• Protamine sulfate
• For Every 100 U of heparin 1mg of
protamine is given.
• Risk of hypersensitivity reaction is
common,

49. Fondaparinux
• Low molecular weight pentasaccaride.
• Inhibits Factor Xa.
• Once a daily s.c. injection is required in to treat
DVT and PE as a ‘bridge’ to warfarin.
<50 kg – 5 mg
50 – 100 kg – 10 mg
>100 kg – 15 mg
- Dose reduced in renal dysfunction.
- Monitoring: anti Xa-heparin assay
PTT is insensitive

50. Fondaparinux
• No monitoring is required and does not
cause HIT syndrom.
• Lower incidence of thromboembolism
when compared to enoxaparin after THA,
TKA, and Hip fracture surgery 12.5% vs.
27.8%.

51. Warfarin
• It is taken orally. Begin with 5 mg.
• Warfarin therapy can be started on day
one of heparin therapy.
• INR ratio of 2-3 considered therapeutic.
• Monitor daily using PT, until stable INR for
2 days, then 2-3 times weekly for 2 weeks
and then monthly.
• Continue using at least for 6 months.

52. MECHANISM OF ACTION
• Competitive antagonists of vitamin K,
needed for synthesis of clotting factors
II (prothrombin), VII, IX and X.
• The onset of action is slow at least 5
days.
• They require once-daily dosage at a
fixed time.

53. SIDE-EFFECTS
• Haemorrhage
• Skin necrosis. In patients with heterozygous
for protein C or protein S deficiency
• Other (rare):
– Hypersensitivity
– Skin rashes
– Alopecia

54. CONTRAINDICATIONS
• Stroke.
• Recent Peptic Ulcer.
• Uncooperative patients.
• Uncontrolled hypertension.
• Alcoholism.
• Recent trauma or surgery to the CNS or eye.
• Uncompensated cirrhosis.
• Elderly patients greater risk of major bleeding.
• Pre-existing haemostatic defect.

55. PREGNANCY
• Teratogenic during the first trimester (mainly
between 6 and 12 weeks). Should be avoided.
• Risk of fetal bleeding. Abortion rate doubled.
• Heparin generally preferred.
• If used, should be discontinued no later than
36 weeks or 2-3 weeks before expected
delivery and anticoagulation maintained with
heparin.
• Patients should be warned of the risk before
conception.

56. BLEEDING
• Reversal of oral anticoagulation effect
depends upon synthesis of new
coagulation factors, which can take several
days.
• Major bleeding manage with prothrombin
complex concentrate.
• It can be expedited by:
–Vitamin K1 (lower the INR in 12 to 24 hours)
–Infusion of fresh frozen plasma (FFP)

57. Thrombolytic therapy
• Successful thrombolytic therapy rapidly
reverses the rt heart failure and lower the
death rate and recurrent PE by:
(1) dissolving pulmonary arterial thrombus.
(2) preventing release of serotonin and other
factor which causing pulmonary
hypertension.
(3) lysis of thrombus in deep leg veins which
will prevent recurrent PE.

58. INDICATION
• Presence of hypotension related to PE.
• Presence of hypoxemia.
• substantial perfusion defect
• Rt ventricular dysfunction due to PE
• Extensive deep vein thrombosis with h/o
recurrent embolic episodes.

59. CONTRAINDICATION
ABSOLUTE
• Hemorrhagic stroke
• Active intracranial neoplasm
• Recent intracranial surgery or trauma (<2months)
• H/o intracranial bleeding (<6 months)
RELATIVE
• Bleeding diasthesis
• Uncontrolled hypertension (SBP>200 or DBP>110)
• Cardiopulmonary resuscitation
• Surgery within priveous 10 days.
• Thrombocytopenia (PLT<1,00,000)

60. Approved regimen
• Recombinant Tissue plasminogen
activator (alteplase)
100mg iv over 2 hr
Streptokinase
250,000 u iv loading dose iv for 30 mns
f/b 1,00,000 u/hr for 24 hr.
• Urokinase
1000 u/kg iv loading dose for 10 mns
f/b 1000 u/hr for 24 hr.

61. General guidelines for administration

62. About administration
• Intravenous route
-- primary method of delivery
• Rapid infusion
-- Shorter regimens may not only prove efficacious but also
reduce the risk of hemorrhagic complications
• Catheter-directed therapy
-- for massive PE, may induce major bleeding

63. Catheter-directed therapy
• Local delivery of streptokinase
-- Extensive lysis (by perfusion scan and pulmonary
arteriography at 12 to 24 hour follow-up)
• Intrapulmonary versus peripheral
alteplase
-- no advantage over the intravenous route
• Direct delivery into clot
--Enhanced thrombolysis, relatively low doses
-- Could prove advantageous over the intravenous route

64. 68
Surgical
• Embolectomy
– Prefininolytic therapy this was only therapy for
massive PE
– Carries a 40% operative mortality
– Alternative is Transvenous Catheter
Embolectomy

65. Inferior Vena CavaInferior Vena Cava
FiltersFilters
• Indications
1. Absolute contraindication to anticoagualtion.
2. Life threatening hemorrhage on
anticoagulation.
3. Recurrent venous thrombosis despite
adequate anticoagulaion.

66. IVC FiltersIVC Filters
– Non significant reduction in the incidence of
fatal pulmonary embolism.
– Significant increase in the number of
subsequent DVT’s by providing nidus for clot
formation.

67. Conclusion
• The primary therapy for acute pulmonary
embolism is anticoagulation with heparin
and warfarin to prevent additional
thromboembolism.
• Thrombolysis, why not?
-- Heparin for well-tolerated PEs : extremely good
prognosis
-- Inherent risk of thrombolysis : bleeding

68. Conclusion
• The role of thrombolytic therapy in the
management of acute massive pulmonary
embolism remains controversial
• Although there is more rapid dissolution of venous
thromboemboli, the risk of serious bleeding with
thrombolysis remains a concern( intracerebral
hemorrhage occurs more frequently with
thrombolytic agents than with heparin).

69. Conclusion
• Catheter-directed therapy with low-dose
thrombolytic therapy can be considered
• Direct intraembolic therapy may be superior to
intravenous therapy
• The shorter interval between the onset of
symptoms and the initiation of therapy, the greater
response

70. Newer drugs
• Rivaroxaban – factor Xa inhibitors
• Dabigatran – direct thrombin inhibitor
• Both drugs has rapid onset of action and
short half life and as efficacious as
warfarin so initial parentral ‘bridging’ is not
required.
• Also effective in preventing TVE after THR
and TKR.

71. ModalitiesModalities
Non-pharmacologic
1. Early Ambulation
2. Elastic Stockings
3. Intermittent
Pneumatic
Compression
devices
4. IVC Filters

72. Early AmbulationEarly Ambulation
• The earlier the better
• Lower incidence of VTE, Shorter length of
stay, earlier return to the community,
fewer complications and lower 6 month
mortality.
• Used with elastic stockings for low risk
patients as only form of prophylaxis.

73. Elastic stockingsElastic stockings
• Improve venous flow and reduce vessel
wall damage secondary to passive venous
dilatation.
• Fit properly, above knee and continue use
throughout hospitalization and rehab
period.
• Not recommended as solo prophylaxis for
moderate and high risk patients

74. Intermittent pneumaticIntermittent pneumatic
compression devicescompression devices
• Exact mechanism whereby they prevent VTE is
unclear.
• Reduce venous stasis.
• Promote the clearance of pro-thrombotic
coagulation factors.
• Possibly increase local plasminogen activator
• Only effective when used continuously
• Not recommended as the primary agent in high
risk patients and Hip and knee surgery.

75. PERIOPERATIVE MANAGEMENT
• PERIOPERATIVE WARFARIN
• SURGERY WITH RISK OF DANGEROUS
BLEEDING (and not at high risk of thrombosis)
– Omit warfarin 3-4 days before surgery
– Check INR day before surgery to check
adequate progress in reversal
– Consider small dose on vit K (0.5-1 mg) if INR>2
– Consider alternative prophylaxis against
thromboembolism (e.g. sc heparin)
– Restart warfarin as soon as practical post-op

76. PERIOPERATIVE WARFARIN
• After warfarin is stopped it takes about 4
days for the INR to reach 1.5.
• MINOR SURGERY
– Omit warfarin 2-3 days prior surgery
– Check INR pre-operatively
– INR<2.5 is safe for most minor surgery
– Restart warfarin on day of surgery

77. PERIOPERATIVE WARFARIN
PATIENT AT RISK OF RECURRENT
THROMBOSIS
– Stop warfarin and check INR daily
– When INR<2 start iv heparin infusion (adjust
APTT ratio to 1.5-2.5)
– Stop heparin 6 h pre-op. Re-start 12 hours
post-op, without bolus dose. Check APTT 12
h later.
– Restart warfarin when possible

78. Recommended management of patients on regular
oral anticoagulants
Risk factors Regimen
Low
risk
No history of thromboembolism. Last
venous thromboembolic episode >3
months. Last arterial thromboembolic event
>1 month. Mechanical heart valve without
previous thromboembolic event. No
permanent patient-specific risk factors (e.g.
cancer, thrombophilia, immobilization etc.)
Preoperative. Stop warfarin 3–5 days before
surgery. If INR<2 start LMWH or UFH at
prophylactic doses until surgery (time between
last heparin injection and surgery depends on
dose and type of heparin)
Postoperative. Give LMWH or UFH starting 12–
24 h after surgery at prophylactic doses until
INR>2. Start warfarin within 24–48 h after surgery
High
risk
Last venous thromboembolic episode <3
months.Last arterial thromboembolic event
<1 month.Mechanical heart valve with
previous thromboembolic events. Atrial
fibrillation. Permanent patient-specific risk
factors (e.g. cancer, thrombophilia,
immobilization etc.)
Preoperative. Stop warfarin 3–5 days before
surgery. If INR<2 start UFH i.v. at therapeutic
doses until 4–6 h before surgery. Alternatively,
LMWH can be given at therapeutic doses; last
injection must be ≥24 h before surgery
Postoperative. 8–12 h after surgery start UFH
i.v. (or LMWH s.c.) at increasing doses until
therapeutic level is reached, continue until INR>2.
Start warfarin within 24–48 h after surgery
2011 the British Journal of Anaesthesia
Volume93, Issue2 Pp. 275-287.

79. Final ppt
Minor
bleeding
Warfarin dosage
INR 2 -3.5 Decrease dose
INR 3.5 5 Stop drug, reinstitute at lower dose
INR 5-8 Stop drug, give 2.5 mg vit k po
INR >8 1) Stop drug, give 5 mg vit k po
2) Consider 10ml.kg FFP or 25U /kg PCC (prothrombin complex
concentrate’s)
Major bleeding Warfarin dosage
INR 2-3.5 Stop drug and give 5 mg vit k s.c. or iv repeat sos
INR 3.5-5 Stop drug, give vit k 5-10 mg s.c. or iv, repet sos
INR 5-8 Stop drug, give 5-10 mg vit k s.c. 0r iv, repeat sos
Give 15ml/kg FFP or 25-50 U/kg PCC
INR >8 Stop drug, give 5-10 mg vit k s.c. 0r iv, repeat 6 hrly
Give 15ml/kg FFP or 25-50 U/kg PCC

80. PERIOPERATIVE HEPARIN
If pt on UFH - stop it 4-6 hrs brfore surgery.
LMWH
In prophylactic dose or s.c, – stop before 12-18 hrs
In higher dose - stop before 24-30 hrs
If patient has receive 2 hrs before – C/I for neuraxial
technique
The first dose of LMWH should be administered no earlier
than 24 hours postoperatively (surgical) hemostasis
If the risk of bleeding is more after surgery, LMWH start after
48-72 hrs.

81. PERIOPERATIVE HEPARIN
• Indwelling catheters should be removed prior to
initiation of LMWH thromboprophylaxis or if
continuous technique is used, the epidural
catheter may be left indwelling overnight and
removed the following day, with the first dose of
LMWH administered at least 2 hours after
catheter removal.
• Single daily regimen is benificial than twice daily
dosing.
• If the patient on UFH, heparinize the patient 1 hr
after neueaxial technique and catheter should be
remove 2-4 hrs after the last heparin dose and re-
heparinisation done 1 hr after removal of catheter.

82. ANTIPLATELETS
• Aspirin – stop 48 hrs before surgery. (in high risk
only)
• Clopidogrel – stop 7 days before surgery.
in emergency steroids and aprotinin will
reduce BT.
• Ticlodipine – stop 14 days before surgery.
• Abciximab – stop 24-48 hrs before surgery.
C/I 4-6 weeks after surgery.
Combination of these drugs with other
anticoagulant will increase risk of bleeding.

83. GUIDELINES
• TIME INTERVALS BETWEEN NEURAXIAL NEEDLE
PLACEMENT AND LMWH ADMINISTRATION SHOULD
BE MAINTAINED.
• Monitoring the patient after surgery to detect paralysis
suggestive of an early epidural haematoma.
• ANTI Xa MONITORING NOT MANDATORY; IT DOES
NOT PREDICT THE RISK OF BLEEDING.
- PRESENCE OF BLOOD DURING NEEDLE AND
CATHETER PLACEMENT DOES NOT NECISSATE
POSTPONEMENT. BUT INITIATION OF LMWH
SHOULD BE DELAYED FO 24 HRS POSTOPERATIVE.

84. GUIDELINES
• Regarding the risk of epidural haematoma during
placement and removal of an epidural catheter to be
similar and therefore applying the same rules.
• Suggesting the use of low concentrations of local
anaesthetics in combination with opioids (and
epinephrine), limited to minimizing sensory and motor
block.
• Not discussing whether stopping antiplatelet or antico
agulation therapy is advisable just to allow neuraxial
anaesthesia or analgesia to be instituted, given the fact
that stopping such therapy per se may result in major
complications, possibly linked to postoperative
hypercoagulability.

85. • If neuraxial blocks at or near the time of fibrinolytic
and thrombolytic therapy, neurological monitoring
should be continued for an appropriate interval
• Interval of monitoring should not be more than two
hours between neurologic checks
• Epidural catheter infusion should be limited to drugs
minimizing sensory and motor block
• No definitive recommendation for removal of
neuraxial catheters in patients who unexpectedly
receive fibrinolytic and thrombolytic therapy
• The measurement of fibrinogen level (one of the
last clotting factors to recover) may be helpful
Thrombolytic therapy

86. • No need to discontinuation of
anticoagulant therapy in patient posted for
dental, dermatological and cataract
surgery.

87. CONTRAINDICATIONS RA
• Prothrombin time (PT) INR>1.5*
• APTT >40 s
• Platelet count <50 000 µl−1
• As most PT reagents are very sensitive to FVII
deficiency, the INR is often determined by the FVII level.
Therefore, the cut-off level of the INR that constitutes a
contraindication for neuraxial anaesthesia can vary
according to whether the course of the INR is increasing
or decreasing. If the INR is increasing, the cut-off level
would be INR>1.5 (FVII levels are mostly about 40%). If
the INR is decreasing (e.g. after ceasing coumarin
therapy), the cut-off level would be INR>1.2

88. DVT Prophylaxis guidelinesDVT Prophylaxis guidelines
Drug Abdominal
Surgery
Total Hip
Replacement
Total Knee
Replacement
Medicaly ill
pts
Unfract-
ionated
Heparin
5000 U
SC q8-12
Warfarin Start post
operation
Target INR
2-3
Start post
operation
Target INR
2-3
1 mg PO qd
for
indwelling
catheter.
Enoxaparin
40 mg SC
qd, 1st
dose
1-2 hrs
preop
30 mg SC
q12h, 1st
dose 12-24 h
post op or 40
mg SC qd
starting 12h
preop
30 mg SC
q12h, 1st
dose
12-24 h post
op
40 mg SC
qd, 1st
dose
1-2 hrs
preop

89. DVT Prophylaxis guide (Continued)DVT Prophylaxis guide (Continued)
Drug Abdominal
Surgery
Total Hip
Replacement
Total Knee
Replaceme
nt
Daltepari
n
2500 IU SC
q24h, preop
(Moderate
risk) or 5000
IU SC q24, 1st
dose q8-12h
preop (High
risk Patients)
2500 IU SC q24h,
2h preop and 6h
postop then 5000
IU SC
q24(Moderate
risk) or 5000 IU
SC q8-12h, then
q24h postop
(High risk
Patients)

90. DVT Prophylaxis guide (Continued)DVT Prophylaxis guide (Continued)
Drug Abdominal
Surgery
Total Hip
Replacemen
t
Total Knee
Replacement
Fonda-
parinux
2.5 mg SC 6
h postop,
then 2.5 mg
SC qd
2.5 mg SC 6
h postop,
then 2.5 mg
SC qd

91. DVT Prophylaxis guide (Continued)DVT Prophylaxis guide (Continued)
• Thoracic surgery – low dose UFH or IPC
• Neurosurgery – IPC
• Neurosurgery for brain tumour - low dose UFH /
LMWH + IPC + predischarge venous USG
• Cancer surgery – LMWH prophylaxis for 1
month
• benign gyenecologic surgery - low dose UFH
• Long haul air travel – LMWH (for high risk pt)
• Anticoagulant C/I - IPC

92. NEVER EVER STOP THINKING
FOR BENEFITS
VS HARMFUL EFECTS