Pulmonary embolism can be a presentation of underlying occult malignancy.Also , sometimes it can be the most challenging one to manage and needs thorough knowledge of available modalities and research.

2. • A 47 year old lady presented with complaints of
dyspnea on minimal exertion since two weeks
right sided chest pain since 1 week
On examination,
PR-121/min regular
BP-128/70mm hg
RR-26/min
Spo2-92% (Room Air)

3. • R.S. – Air entry reduced in right infra scapular area
• C.V.S. - S1,S2 Normal, tachycardia,JVP (N)
Differentials :
1.Pneumonia/pleural effusion (h/o fever 2 weeks before onset)
2.Acute Myocardial infarction
3.congestive heart failure
4.Pneumothorax
5.Pulmonary Embolism

4. • Past History-Saphenous vein thrombosis on treatment since June
2014
treatment with Dabigatran 150mg twice a day
• H/O air travel 3 days back with exacerbation of underlying symptoms

5. June
DVT
Oct 9
Air travel
Oct 11
Pulmonary
embolism

7. Laboratory investigations
• Hb-12.7
• Tlc- 13410
• Dlc- P75 L17 M3 E5 B0
• Platelet count-112000
• INR-1.31
• APTT-37.2
• Sr.creatinine-0.6
• D-dimer levels-18.69

8. Ecg-sinus tachycardia

9. Chest Xray
Right sided pleural effusion
Right lower lobe collapse

10. Right descending pulmonary artery -thromboembolism

11. CECT CHEST
• Pulmonary embolism,right pleural effusion and pericardial effusion
Venous Doppler of lower limbs-12/10/2018
• Complete recanalization of left GSV
• Deep veins normal

12. • 2decho
• Severe TR with Pulmonary Hypertension
• PASP-105mm hg
• Dilated Right atrium and Right ventricle
• Rv Systolic dyscfunction
• LV –no RWMA, normal LV function,EF-55%
• ‘d shaped’ LV
• Paradoxical septal motion
• No clot /vegetation

13. Treatment
• Lmwh at 1mg/kg twice a day started
• Dabigatran was stopped
• Plan was bridging therapy of heparin and warfarin
• But clinically dyspnea,tachypnea,tachycardia persistent

14. Risk factors in this patient
• Symptomatic
• Echocardiography-RV dysfunction and RV enlargement
• In view of this ,Anticoagulation alone was not enough

15. • Rapid reversal of right heart failure was needed.

16. Fibrinolysis was planned
rTPA ALTEPASE 100mg was used.
Screening echocardiography done
No reversal of RV dysfunction

17. Fibrinolysis with rTPA failed /Re-embolization
Patient symptomatic and HD unstable
UROKINASE used -2.5 lakh units/hour
Inotropic support with MILRINONE
Haemodynamic stability
Symptoms resolved

18. SECONDARY PREVENTION
Inferior Vena Cava Filter
Indications in this patient-Recurrent PE
Right Heart Failure on presentation
Two fibrinolytic agents used already
Placed on
Started on FONDAPARINUX 7.5mg od
Improved and shifted to wards

19. Role of antifibrinolytic agents in Pulmonary embolism

20. • According to ACCP,EVIDENCE BASED CLINICAL GUIDELINES
• Potential indications for thrombolytic therapy in VTE
• 1.Presence of hypotension related to PE
• 2.Presence of severe hypoxemia
• 3.Right Ventricular dysfunction
• 4.Extensive DVT

21. Mechanism of fibrinolytic therapy in PE
• 1.dissolves anatomically obstructing thrombus
• 2.Prevent release of serotonin which exacerbates pulmonary
hypertension
• 3.lyses source of thrombus in pelvic or deep leg veins,decreasing
likelihood of recurrent PE

22. Place of fibrinolysis as per FDA
• Approved indication –only massive pulmonary embolism
• Controversial role in Submassive PE with RV dysfunction
• EUROPEAN MULTICENTERED RT of Submassive PE using tenecteplase
showed that death or haemodynamic collapse was reduced by 56%
• However, 2%- hemorrhagic stroke

23. Contraindications to fibrinolysis
• 1.Intracranial disease
• 2.Recent surgery
• 3.Trauma

24. Guidelines for thrombolytic therapy
• Clear documentation of PE (or DVT)
• Contraindications carefully reviewed
• Initiate or continue other supportive therapy
• Discontinue heparin during thrombolytic infusion

25. Choice of thrombolytic agent
• Depends upon institutional policy
• Streptokinase(stk) or Urokinse(UK) and Recombinant tissue
plasminogen activator(rTPA) are available choices
• STK-preferred as cheap
Rtpa-fast relief of RV function desired
Urokinase usually given through catheter into pulmonary artery
Thrombolysis is effective up to 10-14 days after the onset of symptoms

26. Dosing schedules
• 1.Streptokinase
• IV bolus 2,50,000 units over 30 mins followed by infusion of
1,00,000units/hr for 12-24hrs
• 2.rTPA-iv bolus of 50 mg/hr-total 100mg
• 3.Urokinase
• 4400units /kg directly into pulmonary artery for 10 minutes
followed by 4400units/kg/hr for 12-24 hrs

27. drawbacks
• High cost
• Danger of severe and fatal bleeding
• Intracranial-1-3%
• Life expectancy not necessarily increased
• Failed thrombolysis -8 to 10%
• Allergic reactions to STK

33. Definition of failure of thrombolysis
• A.persistent hypotensive state
• B.ECHO evidence of Persistent RV dysfunction
• C.Residual pulmonary vascular obstruction >30% at the 10th day after
thrombolysis on Right herat catheterization or CT Pulmonary
Angiography

34. • No firm guidelines but various options are
• 1.wait and watch using anticoagulants only
• 2.Repeat thrombolytic therapy with alternative thrombolytic agent
• 3.Rescue surgical embolectomy
• 4.Catheter fragmentation/embolectomy

36. Surgical embolectomy
• Digonnet et al concluded that Rescue surgical embolectomy improved
outcome in massive PE
• Also noticed 100% success in all cases of submassive PE
• Post operative complication –ARDS,Mediastinitis,AKI and neurological
adverse events

37. Catheter Embolectomy
• Indicated when full dose of thrombolytic agents are contraindicated
• Patient unwilling for surgical embolectomy
• Pharmacomechanical-physical fragmentation of thrombus + low dose
thrombolysis through catheter
• Complications-perforation,dissection of pulmonary artery,pericardial
tamponade ,cardiac arrhythmias and bleeding

38. Anticoagulant therapy in PE
• Given irrespective of thrombolysis or embolectomy
• Prevents
• 1. formation of new thrombus
• 2.Fibrin deposition
• 3 Recurrent embolism

39. methods
• 1.Unfractinated heparin
• Initial bolus-80u/kg followed by 18u/kg/hr
• Target aPTT of 2-3 times upper limit of laboratory normal
• 2.Low molecular weight heparin
• 1mg/kg twice daily with normal renal function
• 3.Fondaparinux
• Weight based once daily ,adjust for impaired renal function

40. • Vitamin K antagonist
• Long term anticoagulation for 3-6 months
• Initited at a dose of 5mg
• Dose titration to achieve an INR of 2 to 3
• NOACS
• DIRECT THROMBIN INHIBITORS: argatroban or bivalirudin
• Rivoroxaban
• 15mg twice daily for 3 weeks ,then 20mg once daily

41. Miscellaneous option in PE
• INFERIOR VENA CAVAL FILTERS
• Indications:
• a.active bleeding that precludes anticoagulation
• b.recurrent venous thrombosis despite anticoagulation
• c.Prevention of recurrent PE in patients with RV failure who are not
candidates of thrombolysis
• D.Prophylaxis of extremely high risk individuals
• Complications-nidus for clot formation

42. • Sildenafil
• Ganiere et al have reported improvement 120 minutes after
administration of sildenafil (50mg TDS) in a patient with Massive PE
with persistent respiratory failure even after thrombolytic therapy
• Sildenafil was then gradually withdrawn without any adverse effect

43. • Pulmonary embolism
• The great masquerader

44. Acute pulmonary embolism
• Obstruction of the pulmonary artery or one of its branches by
thrombus/tumour/air/fat
• Classified into
• Massive PE(5-10%)
• Thrombosis affecting half of pulmonary vasculature
• Dyspnea,syncope,hypotension and cyanosis-hallmarks
• Present with cardiogenic shock die from multiorgan failure

45. • Submassive PE(20-25%)
• RV dysfunction despite normal systemic arterial pressure
• Low risk PE(70-75%)
• Excellent prognosis
• Saddle PE
• Lodges at the bifurcation of the main pulmonary artery
• Most saddle pe are submassive

46. • Prognosis
• Mortality rate of acute PE
• -30% without treatment due to recurrent PE
• 2-8% with anticoagulant therapy

47. Poor prognostic factors
• RV dysfunction
• Rv thrombus
• Elevated BNP
• Elevated troponin

48. • Meta –analysis of seven studies
• RV dysfunction was associated with a 2 fold increase in PE related
mortality
• Bnp and mortality
• Troponin and mortality

49. • Stratmann et al told , about pulmonary hypertension in PE
• If its non haematogenous obstruction-60 to 70% of the pulmonary
artery be obstructed to increase PAP
• But if its due to combination of mechanical obstruction and
vasoconstriction-25 to 30% of the pulmonary artery must be
obstructed to increase PAP

50. Risk factors
• Immobilization
• Surgery within the last 3 months
• Stroke,pareisis,paralysis
• History of venous thromboembolism
• Malignancy
• Prior PE
• Obesity
• Hypertension
• High cigarette smoking

51. symptoms Frequency(%)
dyspnea 73
Pleuritic chest pain 66
cough 37
haemoptysis 13
sign
tachypnea 70
rales 51
tachycardia 30
4th heart sound 24
Loud P2 23
Circulatory collapse 8

52. • D-dimer levels are raised
• Sensitivity of D-dimer is >95% for PE
• Useful ‘rule out’ test
• Elevated cardiac biomarkers-troponin,plasma heart type fatty acid
binding protein,NT-proBNP
• ABG-hypoxemia.hypocapnia and respiratory alkalosis

53. • Ecg-sinus tachycardia,S1Q3T3 sign
• Rv strain and t wave inversion in v1 to v4
• Venous utrasonography-to look for DVT

54. Chest xray findings of pulmonary embolism

55. • Contrast enhanced CT scan of chest-
• Principal imaging test
• Sixth order branches of pul artery visualized
• Four chamber view of heart
• Rules out pneumonia,emphysema,pulmonary fibrosis,pulmonary
mass and aortic pathology,early stage cancer

56. • Lung scanning
• Second line diagnostic
• Not eligible for iv contrast
• Unfortunately many have non diagnostic scans
• Contrast enhanced MR imaging
• Detects large proximal PE but not reliable for smaller segmental and
subsegmental

57. • Echocardiography-MC Connel sign of PE
• Can identify saddle.right main or left main PE
• Rules out condition that mimic PE
• Ct angiography
• 1.intraluminal filling defect
• 2.cut off of vessels

58. Flow chart