venous thrombosis and pulmonary embolism

1. Venous Thrombosis
&
Pulmonary Embolism
• Presenter: Dr Y V Rao
• Moderator: Dr Mamatha H K
• HOD: Dr Arun Kumar Ajjappa
•

2. • Introduction
• Risk factors
• Pathophysiology
• Thromboprophylaxis
• Diagnostic evaluation
• Investigations
• Treatment

3. • The threat of venous thrombosis and acute pulmonary embolism is a daily
concern in the post operative period and ICU.
• Thrombi usually form in proximal leg veins and are often clinically silent,
becoming evident only when a portion of the thrombus breaks loose and
travels to the lungs to become a pulmonary embolus.
• Because it is possible to prevent thrombus formation in the legs , deaths from
pulmonary emboli are considered preventable.

4. Risk Factors
• Surgery
• Trauma
• Malignancy
• Acute medical illness
• ICU-related factors

5. Pathophysiology of thrombosis
Virchow’s triad

6. Pulmonary embolism
• When a thrombus completely or partially obstructs a pulmonary artery or its
branches,
• the alveolar dead space is increased.
• The area, although continuing to be ventilated,
• receives little or no blood flow.
• Thus, gas exchange is impaired or absent in this area.
• In addition, various substances are released from the clot and surrounding area,
causing regional blood vessels and bronchioles to constrict.
• This causes an increase in pulmonary vascular resistance. This reaction compounds
(the ventilation–perfusion imbalance.)

7. • The hemodynamic consequences are increased from the regional
vasoconstriction and reduced size of the pulmonary vascular bed.
• increase in right ventricular work to maintain pulmonary blood flow.
• When the work requirements of the right ventricle exceed its capacity, right
ventricular failure occurs,
• leading to a decrease in cardiac output followed by a decrease in systemic
blood pressure
• the development of shock.

8. Conditions High-risk regimens
Acute medical illness LDUH/LMWH
Major abdominal surgeries LDUH/LMWH+GCS/IPC
Thoracic surgery LDUH/LMWH+GCS/IPC
Cardiac surgeries with complications LDUH/LMWH+IPC
craniotomy IPC
Hip/knee surgery LMWH
Major trauma LDUH/LMWH/IPC
Head/spinal cord trauma LDUH/LMWH+IPC
Above conditions+active bleeding/risk
of bleeding
IPC
Thromboprophylaxis

9. Unfractionated heparin
• Mucopolysaccharide
• Heparin+anti thrombin forms heparin AT complex which inhibits factor
2(10times) and factor 10
• It also binds to plasma protiens,endothelial cells and macrophages
• Platelet binding-heparin induced thrombocytopenia(HIT)

10. HIT
• 2 types
1)non immune type
2)immune type
Pathogenesis:
• Heparin+platelets forms antigenic complex which produces anti bodies
induces thrombosis.
• Anti bodies also binds to endothelial cells forms fibrin -thrombosis

11. Risk factors:
• Flushes for intravascular catheters, heparin coated pulmonary catheters
• HIT is 10times greater with unfractionated heparin than LMWH
• Post orthopaedic and cardiac surgeries
Clinical features:
• Appears after 5 days and in 24hrs in patient with HIT anti bodies

12. Thrombosis:
• Venous>arterial
Diagnosis:
• ELISA for anti bodies for platelet factor 4 heparin complex
Acute management:
• Withhold heparin
• Stop heparin flushes
• Direct thrombin inhibitors: Argatroban, Lepirudin

13. • Argatroban : 2mcg/kg/min and titrate dose to aPTT= 1.5-3*control
• : 0.5mcg/kg/min in liver failure
• : maximum dose 10mcg/kg/min
• Lepirudin : 0.4mg/kg or 0.2mg/kg(renal failure) bolus/ followed by
• 0.15mg/kg/hr titrate dose to aPTT= 1.5-3*control

14. Duration of treatment:
• Recommended until platelet count rises above1.5 lakhs

15. LOW MOLECULAR WEIGHT HEPARIN
• Anti 10 a activity 2- 4times more than anti thrombin activity.
• Reduced binding to plasma proteins.-more potent anticoagulant.
• Reduced binding to endothelial cells and macrophages – longer duration of
action
• Reduced binding to platelets – low risk of HIT –major advantage.
• Major draw back is clearance by kidney.

16. Anticoagulant regimen for Thromboprophylaxis
Unfractionated heparin :
• Usual dose:5000U SC every 12th /8th hrly
• Obesity:5000U SC 8th hrly(BMI<50),7000U SC 8th hrly(BMI>50)
LMWH:
Enoxaparin: usual dose : 40mg SC once daily/30mg SC twice daily.
• obesity : 0.5mg/kg SC once daily(BMI >40)
• renal failure : 30mg SC once daily
• Dalteparin: usual dose:2500 SC OD

17. Mechanical Thromboprophylaxis
• Graded compression stockings
• Intermittent pneumatic compression

18. Diagnostic evaluation:
• DVT is silent only but symptomatic pulmonary embolus appears.
• The clinical presentation of acute pulmonary embolism is non-specific, and
there are no clinical or laboratory findings that will confirm or exclude
the diagnosis of pulmonary embolism.

21. PERC FOR LOW RISK OUTPATIENT POPULATIONS
• This approach has been best studied in the emergency department
1. Age < 50 years
2. HR < 100 bpm
3. SPO2 ≥ 95 %
4. No haemoptysis
5. No oestrogen use
6. No prior DVT or PE
7. No unilateral leg swelling
8. No surgery or trauma requiring hospitalization within the past 4 weeks

22. LABORATORY
1. Leucocytosis
2. Increased ESR
3. Elevated serum LDH
4. ABGs: hypoxemia, hypercapnia, and respiratory alkalosis. Massive PE with
hypotension can cause hypercapnia and a combined respiratory and metabolic
acidosis (due to lactic acidosis)

23. • Elevated Troponin
1. 30-50 % of pts who have a moderate to large PE
2. Due to acute right heart overload
3. Resolve within 40 hrs (more prolonged elevation after acute MI).

24. • ELECTROCARDIOGRAPHY
1. 70 % of pts with acute PE had ECG abnormalities
2. Most commonly
Sinus tachycardia
nonspecific ST-segment and T-wave changes
• S1 Q3 T3 pattern of acute cor pulmonale (acute right heart strain) is classic
infrequent during acute PE
Common among patients with massive acute PE and cor pulmonale

26. ELECTROCARDIOGRAPHY
• The following ECG abnormalities are associated with a poor prognosis
1. Atrial arrhythmias
2. Right bundle branch block
3. Inferior Q-waves
4. Precordial T-wave inversion and ST-segment changes

28. • CXR shows RLL collapse.
Ventilation perfusion scan
showing perfusion defect in right
side + corresponding ventilation
defect

29. • classical’ appearance of a
pulmonary infarction – a
wedge-shaped lesion
peripherally set against the
pleura

30. VENTILATION-PERFUSION (V/Q) SCAN
• The PIOPED study
1. Accuracy is greatest when the V/Q scan is combined with clinical
probability

31. ULTRASOUND
• Only 29 % of pts with PE had venous thrombosis detected by compression
ultrasound

32. D-DIMER
• ELISA (results in >8 hrs)
• Quantitative rapid ELISA (results in 30 min)
• Semi-quantitative rapid ELISA (results in 10 min)
• Qualitative rapid ELISA (results in 10 min)
• Quantitative latex agglutination assay (results in 10 to 15 min)
• Semi-quantitative latex agglutination assay (results in 5 min)
• Erythrocyte agglutination assay (SimpliRED) (results in 2 min)

33. • ANGIOGRAPHY - gold standard in the diagnosis of acute PE
• A negative pulmonary angiogram excludes clinically relevant PE

37. ALVEOLAR DEAD SPACE
• Alveolar dead space fraction (ADF) increases
• 98% pts with PE have an abnormal ADF (defined as >20 %) or a positive D-
dimer
• Common false positive results
• Difficulty obtaining accurate ADF measurements

38. ECHOCARDIOGRAPHY
• Useful if a rapid diagnosis is required to justify the use of thrombolytic
therapy
• PE related mortality increases with RV dysfunction,RV thrombus
• 35% of pts with RV thrombus have PE
• only 4 % of pts with PE have an RV thrombus

39. Echocardiographic findings in PE
• RV dilation and dysfunction
• RV thrombus
• RA dilation
• TR
• Pulm HTN
• Paradoxical septal movement
• Increases in RV pressure will displace the septum towards the LV during systole and/or
diastole
• Dilated and invariable IVC
• McConnell Sign
• Regional wall motion abnormalities that spare the right ventricular apex
• 77% sensitivity, 94% specificity

40. Antithrombotic Therapy
Anticoagulation
• The initial treatment of thromboembolism that is not life-
threatening is anticoagulation with heparin.

41. Unfractionated Heparin

42. Low-Molecular-Weight Heparin
• Enoxaparin, 1 mg/kg by SC every 12h
• LMWH is cleared by the kidneys, and dose adjustments are necessary in renal
impairment
• In patients with renal failure and thromboembolism who require heparin,
UFH is recommended over LMWH .

43. • LMWH no need to monitor anticoagulant activity, and the ability
to treat outpatients (which could help to reduce hospital
admissions for deep vein thrombosis).
• For these reasons, LMWH is slowly replacing UFH for the initial
management of thromboembolism

44. Monitoring Anticoagulation
• The aPTT can be used , because it is a reflection of coagulation factor IIa activity, and
one of the prominent effects of UFH is inhibition of factor IIa (antithrombin effect).
• The aPTT cannot be used to monitor anticoagulation with LMWH.
• Monitoring of anticoagulation is usually not necessary with LMWH.
• If needed, the anticoagulant response to LMWH can be assessed by measuring factor
Xa activity .

45. Warfarin Anticoagulation
• patients with a reversible cause of venous thromboembolism (e.g., major
surgery),oral anticoagulation with warfarin can be started on the first
day of heparin therapy.
• When the PT reaches an (INR) of 2 to 3, the heparin can be discontinued.
• Oral anticoagulation with Coumadin is continued for at least 3 months
Patients with cancer-related or recurrent VTE require longer periods of
anticoagulation

46. Thrombolytic Therapy
• Pulmonary embolism accompanied by hemodynamic instable
• Hemodynamically stable patients with right ventricular dysfunction
• Cardiac arrest
• The major problem with this is bleeding

47. The two drug regimens shown below are designed to achieve rapid clot
lysis.
• Alteplase: 0.6 mg/kg over 15 minutes.
• Reteplase: 10 Units by bolus injection, and repeat in 30 minutes.

48. • The usual Alteplase dose is 100 mg infused over 2 hours
• Reteplase is not currently approved for treatment of
thromboembolism , but the bolus administration of this drug is
well-suited for rapid clot dissolution .

49. Inferior Vena Cava Filters
• Mesh like filter devices can be placed in the inferior vena cava to
trap thrombi that break
• loose from leg veins and prevent them from traveling to the lungs

50. Indications
A. Patient has proximal deep vein thrombosis in the legs and has one of the
following conditions:
• 1. A contraindication to anticoagulation
• 2. Pulmonary embolization during full anticoagulation
• 3. A free-floating thrombus (i.e., the leading edge of the thrombus is not
adherent to the vessel wall).
• 4. Poor cardiopulmonary reserve and unlikely to tolerate a pulmonary
embolus.

51. B. Patient does NOT have proximal deep vein thrombosis in the legs but has one of
the following conditions:
• 1. Requires long-term prophylaxis of pulmonary embolism (e.g., patients with a
history of recurrent pulmonary embolism)
• 2. Has a high risk of thromboembolism and a high risk of hemorrhage from
anticoagulant drugs (e.g., trauma victims)

52. The Greenfield Filter
• The major advantage of this filter is its elongated, conical
shape, which allows the basket to fill with thrombi to 75% of
its capacity without compromising the cross-sectional area of
the vena cava.
• This limits the risk for vena cava obstruction and
troublesome leg oedema, which plagued earlier models of
IVC filters.

54. References:
• Paul Marino's, The ICU Book, 4th Edition.
• Venous thromboembolism: risks and prevention:Contin Educ Anaesth Crit
Care Pain (2011) 11 (1): 18-23.

55. Thank you