Presentation is loading. Please wait.

Presentation is loading. Please wait.

Department of Medicine Manipal College of Medical Sciences

Similar presentations

Presentation on theme: "Department of Medicine Manipal College of Medical Sciences"— Presentation transcript:

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

. 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

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

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



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PULMONARY ANGIOGRAPHY (has been largely superseded by CTPA)

58 .


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


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!!

Download ppt "Department of Medicine Manipal College of Medical Sciences"

Similar presentations

Ads by Google