PULMONARY EMBOLISM MANAGEMENT

1. Dr ASHISH NAIR
MBBS, MD ANAESTHESIA,IDCCM
DrNB CRITICAL CARE(SR)

2. THE GREAT MASQUERADER
• Pulmonary thrombo embolism(PTE) is important in (ICU) patients where
diagnosis can be difficult and may be life threatening, with mortality rates in
haemodynamically unstable patients being about 30%.
• A relatively common cardiovascular emergency with high morbidity and
mortality.
• Leading cause of unexpected deaths in hospitalized patients. (5-10%)
• Mortality in patients with PE is around 100% in patients with MPE and
hypotension.
• About 90% of patients with fatal PE die within 1-2 hrs of onset.
• Difficult diagnosis that may be missed
• Early diagnosis and aggressive management is the key to successful
outcome.

3. • Average annual incidence of PE is 1:1000 population
in the western countries.
• The exact incidence of PE in India remains
unknown
Wells PS et al. Clin Chest Med 2003.
INCIDENCE

4. • The overall incidence of PE in adult medical autopsies
was 15.9%.
• PE very significantly contributed to death in (80%).
• PE affected a younger population as 80% of the
overall patients (73% were < 50 yrs)
• Sepsis was the primary diagnosis in 32% of total and
in 42% of fatal cases.
N.Kakkar et al. Clinical and Applied Thrombosis/Hemostasis, 2008
An Autopsy-Based Study
(n=1000 adult medical autopsies)

5. • There is 50% resolution of PE after a month of
treatment.
• About 5% of treated pts with PE develop PAH.
• Recurrence rate of PE - 7% at 6 months.
• Mortality rates after an episode of PE are high
with 25 % of patients dying within one year.
Carson JL et al. NEJM 1992
Natural History

6. Risk stratification in Acute PE
Hypotension
Positive
Troponins
RV
Dysfunction

7. Risk stratification according to expected
PE-related early mortality risk

8. Risk factors for venous thromboembolism
Primary hypercoagulable states (thrombophilia)
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Resistance to activated protein C (inherited factor
V Leiden mutation)
• Hyperhomocysteinaemia
• Lupus anticoagulant (antiphospholipid antibody)
Secondary hypercoagulable states
• Immobility/Surgery/Trauma/Malignancy
• Pregnancy and the puerperium
• Obesity
• Smoking
• Oestrogen-containing oral contraception or
hormone
• replacement therapy
• Indwelling catheters in great veins and the right
heart
• Burns
• Patients with limb paralysis (e.g. spinal injuries)
• Heart failure
• Increasing age

9. Approximately 20-50% episodes of first-time PE are unprovoked
or idiopathic, that occur without a readily identifiable risk factor.
• Patient-related risk factors (Permanent).
• Setting-related risk factors (Temporary - reversible).
PREDISPOSING RISK FACTORS

10. Strong
predisposing factors
Moderate
predisposing
factors
Weak
predisposing
factors
NIL CHF or RF Increasing age
HRT Obesity
Malignancy Varicose veins
OCP Pregnancy /
Postpartum
Paralytic stroke
Previous VTE
Thrombophilia
Patient Related Risk Factors

11. Strong
predisposing
factors
Moderate
Predisposing
factors
Weak
predisposing
factors
Fracture (hip or leg) Arthroscopic knee
surgery
Bed rest >3 days
Hip or knee
replacement
Central venous lines Immobility due to
sitting
Major general surgery Chemotherapy Laparoscopic Surgery
Major trauma Pregnancy/postpartum
Spinal cord injury
Setting Related Risk Factors

13. • Most PE results from DVT of the lower limbs, pelvic veins or inferior vena cava (IVC),
although DVT of the upper limbs, right atrium or ventricle
• Virchow’s triad:
• (1) venous stasis,
• (2) vein wall injury, and
• (3) hypercoagulability of blood does occur.
PATHOPHYSIOLOGY
• Acute pulmonary hypertension increases RV afterload and RV wall tension, which leads to RV dilatation and
dysfunction, with coronary ischaemia being a major contribution
• In massive PE, the combination of coronary ischaemia, RV systolic failure, paradoxical interventricular septal shift
and pericardial constraint leads to left ventricular (LV) dysfunction and obstructive shockting mechanism
• Increased right atrial pressure can open a patent foramen ovale, which may result in right-to-left shunting,
manifested as either refractory hypoxaemia or paradoxical (arterial) embolisation, commonly to the brain,
leading to cerebral infarction

15. Circulatory collapse &
eventually death.
Fall in LV CO and BP
Reduced LV filling during
diastole
RVD & Resultant bulge
of the IVS into the LV
PE - Consequences
RV
RA
LV
LA

16. Precipitates myocardial
ischemia and infarction
Compression & decrease
in perfusion of RCA
Increased RV wall tension
& decrease in Aortic
pressure
PE - Consequences

17. V/Q mismatch
Release of mediators
Hypoxemia
Bronchoconstriction
Lung edema
Lung hemmorhages
Respiratory Failure
PE - Consequences

18. • Massive PE is acute PE characterized by
the presence of hemodynamic instability
(defined by the presence of SBP < 90 mm
Hg).
• Submassive PE is acute PE defined by the
presence of right ventricular dysfunction
but without hemodynamic instability.
(saddle PE)
• Non-massive PE is acute PE without any of
the features of massive or submassive PE.
Definition

19. Classification
• Massive Pulmonary Embolism
• Acute PE with sustained hypotension (SBP 90 mm Hg for at least 15 minutes
or requiring inotropic support,
• Not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or
left ventricular [LV] dysfunction), pulselessness, or
• Persistent profound bradycardia (HR 40 bpm with signs or symptoms of
shock).
• Submassive PE
• Low risk PE

20. Classification
• Massive Pulmonary Embolism
• Submassive PE
• Acute PE without systemic hypotension (SBP> 90 mm Hg) but with either RV dysfunction or
myocardial necrosis
• RV dysfunction means the presence of at least 1 of the following:
• RV dilation
• RV systolic dysfunction
• Elevation of BNP (90 pg/mL) or
• Elevation of N-terminal pro-BNP (500 pg/mL); or
• ECG changes
• new complete or incomplete right bundle-branch block,
• anteroseptal ST elevation or depression, or
• anteroseptal T-wave inversion
• S1Q3T3 pattern
• Myocardial necrosis is defined as either of the following:
• Elevation of troponin I (0.4 ng/mL) or
• Elevation of troponin T (0.1 ng/mL)
• Low risk PE

21. Classification
• Massive Pulmonary Embolism
• Submassive PE
• Low risk PE
• Acute PE and the absence of the clinical markers of adverse prognosis that
define massive or submassive PE.
• 70 to 75% of patients
• Excellent prognosis

22. Symptom or Sign Percent
Dyspnea 82
Respiratory Rate >20/min 60
Heart Rate >100 beats/min 40
Chest pain 49
Cough 20
Syncope 14
Hemoptysis 7
Goldhaber SZ, et al. Lancet 1999.
CLINICAL PRESENTATION

23. Symptoms PE confirmed (n - 219) PE excluded (n - 546)
Dyspnoea 80% 59%
Chest pain (pleuritic) 52% 43%
Chest pain (substernal) 12% 8%
Cough 20% 25%
Haemoptysis 11% 7%
Syncope 19% 11%
Signs
Tachypnoea (>20/min) 70% 68%
Tachycardia (>100/min) 26% 23%
Signs of DVT 15% 10%
Fever 7% 17%
Cyanosis 11% 9%
Miniati et al. Resp Crit Care Med 1999, Stein PD et al. Chest 1997
Prevalence of Symptoms & Signs in
Suspected PE

24. Diagnosis-Probability Assessment
• Implicit clinical judgment is fairly accurate: “Do you think this patient
has a PE?”
• Validated prediction rules standardize clinical judgment
• Wells
• Geneva

25. Variables Points
Predisposing factors
Previous PE or DVT 1.5
Immobilization (>3 d) or Surgery in previous 4 wks 1.5
Malignancy 1
Symptoms
Hemoptysis 1
Clinical signs
Heart rate > 100/min 1.5
Clinical signs and symptoms of DVT 3
Clinical judgement
Alternative diagnosis less likely than PE 3
Clinical Probability – Low (0-1), Intermediate (2-6), High (≥ 7)
Well’s Score

27. PERC RULE ( for low risk patients)
• Hormones
• Age > 50yrs
• DVT or PE history
• Coughing up blood(Hemoptysis)
• Lower extremity swelling
• O2 saturation < 95%
• Tachycardia
• Surgery or trauma in past 4 weeks
If none of the 8 PERC features are present in a patient that has deemed low risk by
well’s criteria or by clinical gestalt, then no further tests are indicated.

28. MODIFIED PIOPED CRITERIA FOR DIAGNOSIS
OF PULMONARY EMBOLUS
• Determines the probability of pulmonary embolus following a
V/Q scan.
• Classification
High probability
• 2 or more large mismatched segmental defects or equivalent
moderate /large defects with a normal x ray.
• Any perfusion defect substantially larger than radiographic
abnormality.

29. Intermediate probability
• Multiple perfusion defects with associated radiographic opacities
• > 25 % of a segment and less than 2 mismatched segmental perfusion
defects with
normal radiograph
one moderate segmental
one large or two moderate segmental
one large and one moderate segmental
• Three moderate segmental
• Triple match-solitary moderate – large matching segmental defect with
matching radiograph
• Difficult to characterise high or low probability

30. Low probability
• Non segmental defects ,small effusion, blunting costophrenic angle,
cardiomegaly ,elevated diaphragm, ectatic aorta
• Any perfusion defect with substantialy larger radiographic abnormality
• Matched ventilation and perfusion defects with normal chest
radiograph
• Small subsegmental perfusion defects
• Normal scan
• No perfusion defects

31. DVT
• Non-compressible venous segment
• Increased venous diameter : acute thrombus
• Decreased venous diameter : chronic thrombus
• Loss of phasic flow on Valsalva maneuver
• Absent colour flow : if completely occlusive
• Increased flow in superficial veins
• Lack of flow augmentation of calf squeeze

32. ULTRASOUND & DOPPLER– LOWER
EXTREMITIES

33. ECG
• sinus tachycardia (which is non-specific), the most frequent ECG
abnormalities
• non-specific S–T depression and T-wave inversion in the anterior leads,
reflecting right heart strain.
• The pattern of a deep S-wave in lead I and a Q-wave and inverted T-wave in
lead III (S1Q3T3) is
• classical, but infrequently present.
• left- or right-axis deviation, P pulmonale, right bundle-branch block and
atrial arrhythmias.
• The ECG is also useful in excluding acute myocardial infarction and
pericarditis.

35. ECG
RV strain - T inversions in V1–V4,
Classic S1Q3T3 type,
Incomplete or complete RBBB

36. CXR
• Focal oligemia (Westermark's sign)
• Peripheral wedged-shaped density above the
diaphragm (Hampton's hump)
• Enlarged right descending PA (Palla's sign).
• Cardiomegaly with pleural effusion
• Atelectasis (loss of lung volume)
• Enlargement of a MPA (Fleischner’s sign)
• Pulmonary parenchymal infiltrate
• Pulmonary congestion

37. Westermark’s sign

38. Westermark sign, with hilar enlargement

39. Hampton’s hump
Dome shaped pleural based opacity due to lung infarction.
Pulmonary infarct is dome shaped instead of being wedge
shaped because of double blood supply with preserved
bronchial arteries resulting in sparing of the expected apex of
the wedge.

40. 2D ECHO
• the most common being RV dilatation, RV hypokinesis, paradoxical
interventricular septal motion toward the LV, tricuspid regurgitation and
pulmonary hypertension.
• The pattern of RV hypokinesis with apical sparing is considered
pathognomonic for PE.
• The presence of RV dysfunction correlates with mortality.
• a negative echocardiography does not exclude PE.
• TTE: Transthoracic echocardiography will also allow estimation of pulmonary
arterial pressure, identification of intracardiac thrombi (which usually requires
surgical embolectomy) and aids in differential diagnosis by excluding aortic
dissection and pericardial tamponade.
• Transoesophageal echocardiography has the additional benefit of directly
identifying embolus in the proximal pulmonary arteries, which is common in
patients with haemodynamically significant PE.

44. RV dilatation
RV hypokinesia
Dilatation of pulmonary arteries
Moderate to severe TR
Increase in PAP
Paradoxical RV septal motion
Reduced LV cavity dimension &
CO
Right heart thrombi
Thromboemboli in PA (TEE)
Echocardiographic Findings in PE

45. D-dimer
• Sensitivity of >95% and a specificity around 40% (Elisa)
• Normal D-dimer levels excludes acute PE in patients with
either a low or a moderate probability of PE. (High NPV) –
“RULE OUT TEST”
• D-dimer is NOT useful for confirming PE (Low PPV)
• The sensitivity of the D-dimer is > 80% for DVT and >95% for
PE.
Stein PD et al. Ann Intern Med 2004
Based on the new ESC guidelines, instead of a fixed-
cut off level of D-dimers (500 ng/mL), an age-adjusted
cut-off level of D-dimers should be considered to
exclude PE in patients
with low or intermediate clinical possibility for PE and
in those where PE is unlikely

46. Brain Natriuretic Peptides (BNPs)
• Increases in PE
• Reflect the severity of RVD and haemodynamic
compromise
• Elevated levels of BNP or NT-pro-BNP in PE were at
higher risk of
• In-hospital adverse events (OR 6.8, 95% CI 4.4–10)
• 30-day all-cause mortality (OR 7.6, 95% CI 3.4–17)
Klok FA et al. Am J Respir Crit Care Med 2008

47. Cardiac Troponins
• Increases in PE due to RV microinfarction.
• Predict an increase in major complications and
mortality from PE.
• Positive troponin T - 44% in-hospital mortality
Negative troponin T - 3% in-hospital mortality
Gianitsis E et al. Circulation 2000

48. Compression ultrasonography (CUS)
CT Venography
• CUS shows a DVT in 30–50% of pts with PE.
(Sensitivity - 90%, Specificity - 95%)
• The only validated diagnostic criterion for DVT is
incomplete compressibility of the vein.
• CT venography with CT angiography – adds significant
amount of radiation.

49. • Ventilation scans- a gaseous radionuclide xenon or
technetium DTPA in an aerosol form is inhaled
• Perfusion scans - IV injection of radioactive technetium
macro-aggregated albumin (Tc99m-MAA).
• A Gamma Camera acquires the images for both phases
of the study.
• Valid option in dye allergy or renal failure
V/Q Scan

50. Scintigraphy
(ventilation perfusion lung scan)
Advantages:
Very high sensitivity 98% (it was the imaging modality of choice in
diagnosis of pulmonary embolism).
Disadvantages:
The main one was high percentage of non diagnostic intermediate
probability scans.
Very low specificity 10%.

51. Scintigraphic findings for acute pulmonary
embolism
• Ventillation perfusion mismatch.
Ventillation scan Perfusion scan

52. V/Q Scan Interpretation
RESULT INTERPRETATION SIGNIFICANCE
Normal No Perfusion Deficit Excludes PE
Low
Probability
Perfusion Deficit with
matched Ventilation Deficit
Non Diagnostic
Intermediate
Probability
Perfusion Deficit that
corresponds to
Parenchymal Abnormality
on CXR
Non Diagnostic
High
Probability
Multiple Segmental
Perfusion Deficits with
Normal Ventilation
Diagnostic for PE

53. • Sensitivity and specificity: 41% and 97%
• Normal perfusion scan excludes PE.
• High-probability V/Q scan Confirms PE.
• May need further tests to exclude PE, if negative in pts
with high clinical probability. (low PPV)
• May NOT be reliable for the diagnosis of PE in the
presence of pre-existing pulmonary disease (pleural
effusion, COPD)
• Lower radiation exposure than Spiral CT
PIOPED II study, 2008
V/Q Scan Interpretation

54. • Imaging test of choice for the diagnosis of PE
• Sensitivity of 83% and Specificity of 96%
• Positive MDCT confirms PE
• A negative MDCT excludes PE in patients with a
non-high clinical probability of PE (NPV 90%)
• A negative MDCT despite a high clinical
probability – Further tests required. (NPV 60%)
PIOPED II study, 2008
MDCT Pulmonary Angiography
The PIOPED II trial observed a sensitivity of 83% and a
specificity of 96% for MDCT

55. CT Pulmonary Angiography

56. CT pulmonary angiography showing filling defects at the
bifurcation of right and left pulmonary arteries
CT Pulmonary Angiography

57. Partial eccentric filling defect with acute angle
with the vessel wall

58. Intraluminal filling defect
(polo mint sign)

59. Intraluminal filling defect
(railway track sign)

60. Enlargment of the occluded vessel

63. Ancillary findings of acute pulmonary embolism
(atelectatic band)

65. • MR utilizes gadolinium contrast agent, which is not
nephrotoxic.
• MR imaging should be considered for suspected PE
with renal insufficiency or contrast dye allergy.
• MR pulmonary angiography detects large proximal PE
but is not reliable for smaller segmental and
subsegmental PE.
MR (Contrast Enhanced)
Pulmonary Angiography

66. Pulmonary MRA
• Pulmonary hypertension with dilated central pulmonary arteries and
pruning of peripheral pulmonary arteries

68. Pulmonary Angiography
• Now rarely employed
• Performed when the results of non-invasive imaging
are equivocal.
• Mortality due to pulmonary angiography -0.2%
• Risk of local bleeding is markedly increased due to
thrombolysis after pulmonary angiography.
Agnell D et al. Arch Intern Med 2002

69. Pulmonary angiographic findings
Primary signs:
The only primary sign of acute pulmonary embolism is filling defect.
Secondary signs:
Abrupt occlusion of pulmonary artery.
Areas of oligemia with pruning of the branching vessels.

71. Pulmonary Angiography
Pulmonary angiogram showing intraluminal filling

73. HISTORICAL ASPECTS
Peitho trial
Fibrinolysis for patients with intermediate risk
Conclusion – In patients with intermediate risk pulmonary embolism,
fibrinolytic therapy prevented hemodynamic decompensation but
increased the risk of major hemorrhage and stroke
Moppet trial
Moderate pulmonary embolism treated with thrombolysis
Conclusion-low dose thrombolysis is safe and effective in moderate
PE

74. Mappet trial 1
Management strategies and determinants of outcome in acute major
pulmonary embolism -multicentre registry 1997
Conclusion- Thrombolysis may favorably affect the clinical outcome of
hemodynamically stable patients with major pulmonary embolism.
Mappet trial 2
Importance of cardiac troponins I and T in risk stratification of
patients with acute pulmonary embolism
Conclusion-CTni and CTnT may be a novel , particularly useful tool for
optimizing the management strategy in patients with acute PE.
Mappet trial 3
Management strategies and prognosis of pulmonary embolism
Heparin plus alteplase compared with heparin alone in patients with
Sub massive PE.
Conclusion – alteplase may improve clinical course and prevent further
clinical or hemodynamic deterioration.

75. Pioped 1 study
Provide a comprehensive criteria for v/q lung scan interpretation
Conclusion -study support the use of v/q lung scanning in the diagnostic
evaluation of patients with suspected reammendments to the original pioped
criteria should reinforce the role of v/q lung scanning in patients with suspected
PE
Pioped 2 study
The accuracy of multidetector CTA for the diagnosis of acute PE.
Conclusion-In pts with suspected PE multidetector cta-ctv has a higher
diagnostic sensitivity than does cta alone. with similar specificity. The predictive
value of either cta-ctv is high with concordant clinical assessment but additional
testing is necessary when the clinical probability is inconsistent with imaging
results.
Pioped 3 study
Gadolinium enhanced mra for PE
Conclusion mrpa should only be considered at centres that routinely perform it
well and only for patients for whom standard tests are contraindicated.

78. DIAGNOSTIC
ALGORITHMS

81. Suspected PE with shock or hypotension

82. Suspected PE without shock or hypotension

83. Prognostic assessment

85. TREATMENT

87. • Respiratory support
• Inotropic support
• IV Fluids
• Anticoagulation
• Thrombolysis
• Embolectomy (Surgical /
Percutaneous catheter)
Primary
Therapy
TREATMENT

88. IV UFH
(bolus 80 U/kg followed by infusion at 18 U/kg/h)
S/C LMWH
Enoxaparin (1mg/kg BD), Tinzaparin, Dalteparin
S/C Fondaparinux
5 mg (<50 kg) 7.5 mg (50-100 kg), 10 mg (>100 kg) OD
Anticoagulation

89. Anticoagulation
IV UFH is the preferred
anticoagulant of choice:
1. Hypotension
2. Severe renal failure
3. High risk bleeding

90. Streptokinase
Urokinase
rtPA
THROMBOLYSIS
(Approved Thrombolytic Agents)

92. Loading
dose
2.5 million IU
over 30 mins
Maintenance
dose
1 million IU/hr
over 12-24 hrs.
Accelerated
regimen
1.5 million IU
over 2 hrs
THROMBOLYSIS
Streptokinase

93. Loading
dose
4400 IU/kg
over 10 mins,
Maintenance
dose
4400 IU/kg/hr
over 12-24 hrs.
Accelerated
regimen
3 million IU over 2
hrs
THROMBOLYSIS
Urokinase

94. 100mg
over 2 hrs
Accelerated Regimen Over 1.5 hrs
15mg bolus
0.75mg/kg (50mg) over 30mins
0.5 mg/kg (35mg) over 60 mins
THROMBOLYSIS
rtPA

95. Reteplase
(Two IV boluses of 10 U each 30 mins
apart)
Tenecteplase
0.5mg/kg (30-50mg) bolus over 5 secs
THROMBOLYSIS

96. • Prior intracranial hemorrhage (ICH)
• Cerebral vascular lesion / neoplasms
• Ischemic stroke in preceding 6 months
• Active bleeding or bleeding diathesis (excluding
menses)
• Recent major trauma / surgery / head injury within 3
wks
Contraindications of Thrombolysis in PE
(Absolute)

97. • Uncontrolled HTN (SBP >180 mm Hg or DBP >110
mm Hg)
• Traumatic resuscitation
• Recent (within 2-4 wk) internal bleeding
• Noncompressible vascular punctures
• Pregnancy or within 1 week of postpartum
• Active peptic ulcer
• Oral anticoagulant therapy with (INR) >1.7 or PT
>15 seconds
Contraindications of Thrombolysis in PE
(Relative)

99. NEW ORAL ANTICOAGULANTS: (nVk antagonists)
• Various studies on non – vitamin K – dependent new oral anticoagulants show
following results:
• 1. In RECOVER trial – the direct thrombin inhibitor Dabigatran (150 mg BD)
was compared with warfarin for the treatment of VTE – with regard to efficacy
Dabigatran was non – inferior to warfarin.
• 2. In EINSTEIN-PE trial – single oral drug treatment with direct factor Xa
inhibitor Rivaroxaban (15 mg twice daily for 3 weeks, followed by 20 mg once
daily) was tested against Enoxaparin / warfarin & was found to be non –
inferior.

100. 3. The AMPLIFY study – compared single oral drug treatment using direct factor Xa
inhibitor Apixaban (10 mg twice daily for 10 days, followed by 5 mg once daily) with
conventional therapy (Enoxaparin / Warfarin)
• The primary efficacy outcome was recurrent symptomatic VTE or death related to
VTE.
• Apixaban was non – inferior to conventional therapy for the primary efficacy
outcome.
4. The Hokusal-VTE study – compared the direct factor Xa inhibitor Edoxaban (60
mg OD, reduced to 30 mg OD if CrCL is 30 – 50 ml/min or body weight is < 60 kg)
with conventional therapy (UFH or Enoxaparin/Warfarin)
• Edoxaban was non – inferior to warfarin with respect to primary efficacy outcome
of recurrent symptomatic VTE or fatal PE.

102. Valuable Therapeutic Option in pts with:
1. Failed thrombolysis
2. Contraindication to thrombolysis
EMBOLECTOMY
(Surgical / Percutaneous catheter)

103. SURGICAL EMBOLECTOMY:
• The merit of surgical pulmonary embolectomy for pts with
massive PE, is questionable since the advent of
thrombolytic therapy.
• It is associated with peri-operative mortality of 25 – 50%.
• It is indicated in pts with PE & hypotension who have
absolute contraindications to thrombolytic therapy or if
thrombolytic therapy has failed.
• It may also be useful when pts have free – floating intra-
cardiac thrombus.

104. PERCUTANEOUS EMBOLECTOMY: include either
• embolus extraction techniques (pure percutaneous
embolectomy) or
• embolus destruction technique ( including catheter-
directed thrombolytic therapy & percutaneous thrombus
fragmentation technique)
• Success rates are over 80% with reasonable
complications.
• Should be considered in pts with contra-indications to
systemic thrombolytic therapy who are in specialised
centers.

105. • Oral
Anticoagulation
• IVC filters
Secondary
prevention
TREATMENT

106. • INFERIOR VENACAVA FILTERS: (IVC – Filters)
• This is another method to prevent further embolisation.
• Placed in the infra – renal portion of IVC.
• If thrombus is identified in renal veins, supra – renal
placement may be indicated.
• Absolute indications are:
• - absolute contra-indications to anti-coagulants
• - new or recurrent PE despite anti-coagulation
• - complications resulting from anti-coagulation.
• Other recommended indications include:
• - pts with extensive DVT
• - following surgical embolectomy
• - following thrombolytic therapy.

107. • Early complications:
• - insertion site thrombosis (10% of pts)
• - placement in SVC, carries risk of pericardial tamponade
• Late complications:
• - recurrent DVT (20% of pts)
• - post thrombotic syndrome (in up to 40% pts)
• - occlusion of IVC in 22% pts at 5 years.
• 8 yr follow-up of a randomized study on 400 pts with DVT (with
or without PE) who had received anticoagulant for initial 3
months showed – pts with permanent IVC filters had reduced
risk of recurrent PE – at the cost of increased risk of recurrent
DVT – no overall effect on survival.

108. • Non – permanent IVC filters are classified as temporary or
retrievable devices.
• Temporary filters must be removed within few days.
• Retrievable filters can be left in place for longer periods.
• Non – permanent filters should be removed as soon as it is
safe to use anticoagulants.
• If left in situ for longer periods – late complications like filter
migration, tilting or deformation, penetration of the caval wall
by filter limbs, fracturing of the filter & embolisation of the
device occurs.
• There is no evidence to support the use of IVC filters in pts
with free-floating thrombi in proximal veins & in pts posted for
thrombolysis, surgical embolectomy or pulmonary
thrombendarterectomy.

109. Long Term Anticoagulation
• Initiation of vitamin K antagonists (Warfarin) is
recommended on the first treatment day. (INR
target: 2.0-3.0) (Grade 1A)
• Duration of oral anticoagulation (3 mths for
secondary PE, > 3 mths for idiopathic PE)
• Recurrence of unprovoked PE - indefinite
treatment is recommended.
• Dabigatran, Rivaroxaban, Apixaban - currently
under phase III trials.
Kearon C et al. JAMA 2006

110. Duration of anticoagulation
• Patients with PE should receive at least
3 months of anticoagulant treatment
• The risk of recurrence if anticoagulants
are stopped after 6 or 12 months can
expected to be similar to that after 3
months
• Indefinite treatment reduces the risk for
recurrent VTE by about 90%, but this
benefit is partially offset by a 1% or
higher annual risk of major bleeding.
• Patients with cancer are candidates for
indefinite anticoagulant treatment
after an initial episode of PE
• For cancer patients LMWH for 6 months
after that it could be either LMWH or
VKA till the disease is active

111. Duration of Anticoagulation
• For patients with provoked PE, treatment with a VKA for 3 months is
preferable
• Unprovoked PE should be treated with VKA for at least 3 months.
After this period, indefinite anticoagulation therapy should be
considered for patients with a first unprovoked proximal DVT or PE
and a low risk of bleeding
• Lifelong treatment is recommended for most patients with a second
unprovoked DVT or PE

112. NOACs for extended treatment

113. CONCURRENT HAEMODYNAMIC SUPPORT:
• Shocked pts with PE (massive PE) need urgent
• haemodynamic support in addition to attempts at
• embolus destruction and
• prevention of further embolisation.
• 1) IV FLUIDS:
• Volume loading can improve haemodynamic status in pts with massive PE
• But excessive fluid therapy may worsen RV function (by mechanical
overstretch), which in turn affects LV function.
• There fore modest fluid challenges (500ml) may help to increase cardiac index

114. • 2) VASOPRESSORS:
• Use of vasopressors is often necessary, in parallel with
pharmacological, surgical or interventional reperfusion.
• Nor epinephrine appears to improve RV function via direct
positive inotropic effect, while also improving RV coronary
perfusion by stimulation of peripheral vascular α-receptors
there by increasing MAP.
• RVCPP = MAP – RVPm
• RVCPP – RV coronary perfusion pressure.
• MAP – mean arterial pressure
• RVPm – mean RV pressure
• RVPm = CVP + 1/3 (PAPs – CVP)
• CVP – central venous pressure
• PAPs – systolic pulmonary arterial pressure.

115. • Dopamine & Dobutamine may be considered for pts of
PE with low cardiac index.
• However raising cardiac index above physiological values
may aggravate ventilation – perfusion mismatch by
redistributing flow from obstructed to non-obstructed
vessels.
• Vasodilators decrease pulmonary arterial pressure &
pulmonary vascular resistance, but may be harmful due
to lack of specificity – cause systemic vasodilatation & fall
in MAP.
• There fore Isoprenaline, Nitroglycerine, Nitroprusside &
Dobutamine or Milrinone should be considered only if
MAP is adequate.

116. • SELECTIVE PULMONARY VASODILATORS:
• Inhaled nitric oxide may improve haemodynamic status &
gas exchange of severely hypoxemic PE pts.
• Inhaled prostacyclin is an alternative.
• OTHER MANAGEMENT ISSUES:
• Hypoxaemia and hypocapnia (due to dead space
ventilation & hyperventilation) require high flow oxygen.
• Intubation & mechanical ventilation often necessary in pts
with massive PE.
• Care should be taken to limit positive intrathoracic
pressure by applying PEEP with caution – as it may
reduce venous return & worsen RV failure in pts with
massive PE.

117. • Low tidal volumes (approximately 6 ml/kg lean body
weight) should be used to keep end-inspiratory plateau
pressure ˂ 30 cm H2O.
• To guide resuscitation central venous catheter (before
administering thrombolytic therapy) should be secured.
• Extracorporeal membrane oxygenation (ECMO) should
be considered for pts with PE who have had
cardiopulmonary arrest or have very severe shock.

119. AHA PE GUIDELINES
• Anticoagulation with LMWH ,UFH or fondaparinux. –I/A
• While working up PE, if pretest is moderate or high and there are no
contraindications, start anticoagulation during work up. –I/C
• Fibrinolysis is reasonable for patients with massive PE and acceptable risk
of bleeding complications.-II a/B
• Fibrinolysis may be considered for patients with submassive PE; judged to
have clinical evidence of adverse prognosis and low risk of bleeding
complications – II b/C
• Fibrinolysis is not recommended for patients with submassive PE with only
mild dysfunction – III/B
• Fibrinolysis is not recommended for undifferentiated cardiac arrest – III/B

120. • Either catheter embolectomy or surgical
embolectomy can be considered depending on
institutional and operator preference- IIa/C
• Either of interventional or surgical options are
reasonable if the patient is still unstable in massive PE
after fibrinolysis- IIa/C
• Also reasonable in massive PE , if the patient has a
contraindication to lysis-IIa/C
• May be considered in lieu of fibrinolysis in patients of
submassive PE and evidence of adverse prognosis-
IIb/C
• Not recommended for patients with PE at low risk-
III/C

121. • Pulmonary embolism in pregnancy:
• Risk of VTE increases during pregnancy and during post partum period, PE is the
leading cause of death.
• DVT and PE are common during all trimester of pregnancy and 6- 12 week after
delivery.
• Diagnosis:
• The diagnostic approach to patient with PE is same as non pregnant women
nuclear perfusion scan is in pregnancy as is a chest CT scan.
• Treatment:
• Heparin(LMWH) and fibrinolysis are safe in pregnancy.
• Warfarin is contraindicated because it crosses placenta and causes fetal
malformation.
• Unfraction heparin is category C drug.
• Women experiencing TE event during pregnancy a full dose of LMWH can be
start and continue till pregnancy and 4-6 weeks postpartum.

123. • Complications of pulmonary embolism are:
• Sudden cardiac death
• Obstructive shock
• Atrial or ventricular arrhythmias
• Secondary pulmonary arterial hypertension
• Severe hypoxemia
• Cor pulmonale
• Lung infarction
• Pleural effusion
• Heparin induced thrombocytopenia
• Thrombo phebitis

125. Supportive Care:
• Compression and stockings:
• For a patients who had a proximal DVT, the use of elastic compression
stocking provides a safe and effective adjunctive treatment that can limit
post phebilitic syndrome
• Socking with a pressure of 30-40mmhg at the ankle reduces the risk of post
phlebitic syndrome.
• True gradient compression stockings are highly elastic and provide a
compression gradient more at ankle and gradually reduces till thigh, this
reduces capacitive venous volume by approx 70% and increase velocity of
blood flow in deep vein which are effective in prophylaxis of thrombo
embolism and prevent prognosis of thrombus in patient with DVT and PE.
• In pregnant women stockings of pressure 30 -40mm hg are use to prevent
DVT and prevent development of varicose vein.