1. Department of Medicine Manipal College of Medical Sciences
PULMONARY
EMBOLISM
ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal

2. Clinically significant obstruction of part or all of the pulmonary vascular tree, usually caused by thrombus from a distant site

4. Massive P E
Medium size P E
Small P E

5. Incidence Account for up to 15% of all post-operative deaths
Commonest cause of death following elective surgery
Commonest cause of maternal death
Improved diagnostic methods mean that it is probably reported more frequently

6. Pathophysiology
75% thrombi generated in deep venous system of the lower limbs and pelvis

7. Prolonged immobilization
Anti coagulant factor deficiencies
Auto immune disorders
Certain cancers
Platelet disorders
Smoking
Contraceptive pills
Heart failure
Increased viscosity
Small blood clots
Prolonged immobilization

8. Score Wells scoring system (to asses the clinical probability of DVT)
Active cancer (patient receiving treatment for cancer within the previous 6 months or currently receiving palliative treatment) 1
Paralysis, paresis or recent plaster immobilisation of the lower extremities
Recently bedridden for 3 days or more, or major surgery within the previous 12 weeks requiring general or regional anaesthesia
Localised tenderness along the distribution of the deep venous system
Entire leg swollen
Calf swelling at least 3 cm larger than that on the asymptomatic side (measured 10 cm below tibial tuberosity)
Pitting oedema confined to the symptomatic leg
Collateral superficial veins (non-varicose)
Previously documented DVT
Alternative diagnosis at least as likely as DVT -2
Clinical probability
Total score
DVT unlikely
< 2
DVT likely
≥ 2

9. RISK FACTORS FOR VENOUS THROMBOEMBOLISM.
RISK FACTORS FOR VENOUS THROMBOEMBOLISM
Surgery
Major abdominal/pelvic surgery
Hip/knee surgery
Post-operative intensive care
Obstetrics
Pregnancy/puerperium
Cardiorespiratory disease
COPD
Congestive cardiac failure
Other disabling disease

10. Lower limb problems Malignant disease Miscellaneous Fracture
Varicose veins
Stroke/ spinal cord injury
Malignant disease
Abdominal pelvic
Advanced/metastatic
Concurrent chemotherapy
Miscellaneous
Increasing age
Previous proven VTE
Immobility
Thrombotic disorders
Trauma .

11. Cancer and venous thromboembolism (VTE)
Previously undiagnosed cancer is frequent in patients with unprovoked VTE
prevalence of previously undiagnosed cancer in patients with unprovoked (idiopathic) VTE (venous thromboembolism) was 6.1% (95% CI, 5.0% to 7.1%) at baseline and 10.0% (CI, 8.6% to 11.3%) from baseline to 12 months
risk of cancer was 4-fold greater in patients with unprovoked VTE (10%) than in those with a clear precipitating factor (2.6%)
an extensive screening strategy using computed tomography of the abdomen and pelvis statistically significantly increased the proportion of previously undiagnosed cancer detected from 49.4% (CI, 40.2% to 58.5%) (with limited screening alone - history and examination, routine blood tests, CXR) to 69.7% (CI, 61.1% to 77.8%) in patients with unprovoked VTE

12. Inherited Thrombophilia
(propensity to develop thrombosis due to an abnormality in the coagulation system )
% of patients with VTE have an identifiable inherited thrombophilia
Antiphospholipid syndrome
Among the identified acquired thrombophilic states, it is the most common
lupus anticoagulant (LA)
anticardiolipin antibodies (ACA)
Deficiency of Protein C & S & antithrombin III
small protein molecule that inactivates several enzymes of coagulation system
Factor V leiden
COAGULATION
COAGULATION - - - -
Protein C & S
Anti thrombin III
Protein C & S
Anti thrombin III +
Factor V

13. These usually need to interact with an additional acquired risk factor to cause VTE
Inherited
thrombophilia
Dehydration
Pulmonary embolism
(DVT) + =

14. Symptoms of DVT Warmth, swelling, redness, and /or pain in a leg
DVT of the calf – symptoms in the calf
In thigh – symptoms in both thigh &/or calf
Vast majority of DVTs occurs in only one leg at a time
Other medical conditions can cause pain and/ or swelling in the legs

15. Thrombi can develop in The heart following AV shunts
Atrial fibrillation
Myocardial infarction
Prosthetic valve
Endocarditis
In association with intraventricular septal defects (paradoxical emboli)
AV shunts
With central venous access

16. Clinical features

17. Clinical features are:
Very varied
Non specific
Strong degree of suspicion required for diagnosis
All information has to be examined carefully before giving a verdict
Wow ! What a
geeeenius yar !!
I am “Saarlak Homes”
Like a detective

18. Cardiovascular collapse
The clinical features of PE depend upon
Size of embolism
Pre existing state of myocardium & lung parenchyma
Co-morbidity
Encompass a spectrum from
Small emboli with few or no
haemodynamic consequences
Cardiovascular collapse

19. Thrombi/embolus can be
Massive
Medium
Small

20. Acute massive PE

21. Large clot lodge at the bifurcation of the main
pulmonary arteries causing haemodynamic
compromise

22. Pathophysiology: Major haemodynamic effects: ↓ Cardiac output
Acute right heart failure
Symptoms:
Severe dyspnoea
Faintness or collapse
Central chest pain
Apprehension
on sitting up ?
Platypnoea

23. (some times)
Isolated dyspnoea: Acute breathlessness in the absence of circulatory collapse
Suspect PE: sudden onset of unexplained breathlessness, in the presence of risk factors for VTE

24. Usually normal. May be subtle oligaemia
Chest X-ray:
Usually normal. May be subtle oligaemia
Wester mark sign

25. Westermark’s Sign

26. ECG:
S1 Q3 T3 anterior T-wave inversion
Right bundle branch block (RBBB)

27. S1-Q3-T3

28. Right heart strain or acute cor pulmonale
Tall peaked p-waves in II,III,AVF
Right axis deviaton (S>R in lead I)
Right bundle branch block

29. Arterial blood gases:
Markedly abnormal with ↓ PaO2 and ↓ PaCO2
Metabolic acidosis

30. Acute small/medium PE .

31. Smaller clot travel more distally
May infarct lung
Pulmonary infarction is an uncommon consequence because of the bronchial arterial collateral circulation
Causes pleural involvement ± effusion
Symptoms:
Pleuritic chest pain
Restricted breathing
Haemoptysis
Found most often in the lower lobes, where blood flow is greater

32. Collapse (clinical deterioration) (10%)
Some times
Collapse (clinical deterioration) (10%)
In an elderly patient with limited cardio respiratory reserve
Can rapidly decompensate with even a relatively small PE
Clinical findings non-specific and reflect the underlying disease process, rather than the PE itself

33. Signs:
Tachycardia
Pleural rub
Crackles or crepitations
Effusion (often blood-stained)
Low-grade fever

34. ECG:
Sinus tachycardia
Arterial blood gases:
May be normal or ↓ PaCO2

35. Chest X-ray: Pleuropulmonary opacities Pleural effusion Linear shadows
Raised hemidiaphragm

36. .
X Ray findings

37. Pulmonary infarction – triangular opacity with base towards periphery – Hamptons sign

38. Fleischner lines

39. Chronic PE Pathophysiology: Symptoms: Signs:
Chronic occlusion of pulmonary microvasculature
right heart failure
Symptoms:
Exertional dyspnoea
Late symptoms of pulmonary hypertension or right heart failure
Signs:
May be minimal early in disease
Later-RV heave
loud, split P2
Terminal-right heart failure

40. Chest X-ray: features of pulmonary hypertension
Enlarged pulmonary artery trunk
enlarged heart
prominent RV
ECG:
RV hypertrophy and strain
Arterial blood gases:
Exertional ↓ PaO2 or desaturation on formal exercise testing

41. DIAGNOSIS DIFFICULT Ask three questions: Varied clinical features
Physical - signs non-specific
Lack of sensitive and specific diagnostic tests
Ask three questions:
Is the clinical presentation consistent with PE?
Does the patient have risk factors for PE?
Is there any alternative diagnosis that can explain the patient's presentation?
DIAGNOSIS

42. BTS PRE-TEST CLINICAL PROBABILITY SCORING
A. Patient has clinical features compatible with PE:
raised respiratory rate
± haemoptysis
± pleuritic chest pain
Plus 2 other factors:
1. Absence of another reasonable clinical explanation
2. Presence of a major risk factor
A. + 1 and HIGH
A. + 1 or 2: INTERMEDIATE
A. alone: LOW pre-test clinical probability

43. Investigations

44. In > 80% cases the X ray & ECG are normal
All patients with suspected PE should have
chest X-ray
ECG
arterial blood gas analysis
Help to exclude important differential diagnoses

45. Variety of radiographic appearances -usually non-specific
Suspect P E in
Normal X ray in an acutely breathless and hypoxaemic patient
bilateral changes in a patient presenting with unilateral pleuritic chest pain
Most important role of the chest X-ray is to exclude important D D
heart failure
pneumonia
pneumothorax
tumour

46. Arterial blood gases
Ventilation-perfusion mismatch and reduced cardiac output with a low mixed venous oxygen saturation and hyperventilation
Arterial blood gases show a
Reduced PaO2 and a normal or low PaCO2
Normal in a significant minority
Metabolic acidosis may be seen in acute massive PE with cardiovascular collapse

47. Bedside echocardiography extremely helpful in:
differential diagnosis
assessment of acute circulatory collapse
Acute dilatation of the right heart usually present in massive PE
Thrombus may be visible
Alternative diagnoses
left ventricular failure
aortic dissection
pericardial tamponade
Can be established with confidence

48. Patient with acute pulmonary hypertension
due to pulmonary embolism
After clot lysis

49. SPECIFIC INVESTIGATIONS
D-dimer & other circulating markers
Ventilation-perfusion scanning
Pulmonary angiography
CTPA & MRPA

50. D-dimer
D-dimer: degradation product of fibrin undergoing endogenous fibrinolysis
Low D-dimer has a high negative predictive value useful screening test
Non-specific elevation of the D-dimer
myocardial infarction
pneumonia
sepsis
Suggestive clinical picture in a high-risk patient must be investigated further even when D-dimer level is normal

51. Ventilation-perfusion scanning
Most popular method to confirm PE
Available only in few centres
A normal V/Q scan virtually excludes PE
Low probability scan in the presence of a low clinical probability makes PE unlikely
High probability scan in a patient with a high clinical probability establishes diagnosis

53. CTPA & MRPA Replaced conventional pulmonary angiography
Can exclude PE
Highlight an alternative diagnosis
Role limited in small peripheral emboli
Utility of contrast-enhanced magnetic resonance scanning is also being explored
Both CT and MRI may allow simultaneous visualisation of the pelvic and leg veins

54. conventional pulmonary angiography

55. CTPA

56. MRPA

57. What is 'gold standard' for diagnosis of PE ?
PULMONARY ANGIOGRAPHY
(has been largely superseded by CTPA)

58. .

59. MANAGEMENT

60. Management of acute massive PE (mortality20%)
Oxygen - 100%
IV access
Send baseline bloods, including clotting profile
Perform ECG

61. Different oxygen delivery systems
Nasal canula
Non re – breather masks

62. Analgesia (if required) Management of cardiogenic shock
Opiates – morphine sulphate
Management of cardiogenic shock
fluids
inotropes
to maintain right ventricular filling

63. ANTI
COAGULATION
ANTI
COAGULATION

64. faster L.M.W.H Unfractionated Heparin molecular weight: 3000 Da
No need for monitoring of
PT -coagulation parameter
need for monitoring of
smaller risk of bleeding
risk of bleeding is more
Smaller risk of thrombocytopenia
risk of thrombocytopenia MORE
Anticoagulant effect: not
Reversible with protamine
sulphate
Acts by inhibiting Xa
Reversible with protamine sulfate.
Inhibits both Xa & thrombin (by augmenting antithrombin III)
Onset Of action:
faster
Slower

65. Anticoagulation Heparin Start IV heparin unless Active GI bleeding or
Intracerebral haemorrhage:
Bolus dose ,000 units or 80 IU/kg
Maintenance infusion of 1300 IU/hr or 18 units/kg/hr
Adjust infusion rate until PT of control
Check hours after initial bolus and hours after any dose change

66. Low molecular weight heparin (LMWH)
as effective as standard unfractionated intravenous heparin
Unfractionated heparin should be considered in massive PE (faster onset of action) as a first dose bolus prior to commencement of LMWH

67. Oral anticoagulation
Should only be commenced once PE is proven -along with Heparin
Target INR heparin stopped

68. Length of warfarin anticoagulation
Temporary risk factor: weeks.
First episode of idiopathic PE: 3 months is currently recommended
Recurrent idiopathic PE:
no guidelines
risk of bleeding balanced with risk of recurrent event.
often long-term anticoagulation
Persisting risk factors: lifelong anticoagulation
recommended

69. Thrombolysis Massive PE presenting with hypotension
No active GI bleeding
No intracerebral haemorrhage
Risk of major haemorrhage is times that of heparin
Embolectomy
if thrombolysis is contraindicated

70. Agents used Alteplase Streptokinase Urokinase
suspected massive PE, 50 mg IV alteplase immediately
Streptokinase
units in 20 minutes with units/h for 24 hours (plus hydrocortisone to prevent further circulatory instability)
Urokinase

71. IVC filter placement Acute VTE with an absolute
contraindication to anticoagulation
Patients with massive PE who survive (in whom a second PE may be fatal)
Recurrent VTE despite adequate anticoagulation

72. summary Analgesia Oxygen IV fluids & inotrops Anticoagulation
Heparin & LMWH initially
Oral anticoagulats when proved
Thrombolysis
Embolectomy
IVC filter placement

73. Rare causes Air embolism Amniotic fluid embolism
Neck vein cannulation,
intrauterine manipulations -criminal abortion
bronchial trauma
barotrauma causing air to enter the pulmonary vein and left heart
Amniotic fluid embolism
1 in 25, ,000 live births
third commonest cause of maternal death,
most common cause of death in the immediate post-partum period.
Amniotic fluid enters circulation because of torn fetal membranes
in Caesarean section,
uterine or cervical trauma, or uterine rupture

74. Fat embolism
during surgery
trauma
fracture of long bone (such as the femur or pelvis)
Fat emboli are small and multiple, and so have widespread effects.
Symptoms 1-3 days after the insult, and are predominantly:
Pulmonary - shortness of breath, hypoxemia
Neurological - agitation, delirium, or coma
Dermatological - petechial rash
Haematological - anaemia, low platelets
Steroid prophylaxis of high risk patients reduces the incidence
Mortality rate approximately 5-15%

75. Happiness keeps you sweet,
Trials keep you strong!
Sorrows keep you Human,
Life keeps you out of wrong!!