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Similar to Pulmonary embolism
Pulmonary embolism
- 2.
- 3. Perspective A commondisorder and potentially deadly Occurs in approximately 1% of all hospitalized patients and accounts for around 5% of in-hospital deaths. It is a common mode of death in patients with stroke, malignancy and pregnancy. Diagnosis is highly elusive. Autopsy reports suggest it is commonly “missed” diagnosed
- 4. Presentation isoften “atypical”. Signs and symptoms are frequently vague and nonspecific. Untreated mortality rate of 20% - 30%, plummets to 5% with timely intervention.
- 5. Case A 48-year-oldwoman is brought to the emergency room complaining of a sudden onset of dyspnea. She reports she was standing in the kitchen making dinner, when she suddenly felt as if she could not get enough air, her heart started racing, and she became lightheaded and felt as if she would faint. On examination, she is tachypneic with a respiratory rate of 28 breaths per minute, oxygen saturations 84% on room air, heart rate 124 bpm, and blood pressure 118/89 mm Hg. She appears uncomfortable, diaphoretic, and frightened. Her right leg is moderately swollen from mid-thigh to her feet, and her thigh and calf are mildly tender to palpation. Her chest x-ray is interpreted as normal.
- 6. Epidemiology & Pathophysiology Thrombi commonly form in deep veins of calf and propagate into the proximal veins of the leg from where they embolize. 80% of pulmonary emboli arise from the propagation of proximal lower limb DVT Remaining 20% arise from Pregnancy related DVT Upper extremity DVT Air, fat and amniotic fluid embolism.
- 7. • THROMBOSIS:TRIGGERED BY (VIRCHOW’STRIAD) • 1.VENOSTASIS • 2.VESSEL WALL INFLAMMATION • 3.HYPERCOAGULABILITY • ALL CLINICAL RISK FACTORS FOR DVT/PE HAVE THEIR BASIS IN ONE OR MORE ELEMENTS OF THE TRIAD. Risk Factors
- 8. Vessel Injury Recentsurgery Recent major trauma Venous Stasis Prolonged bed rest Recent cast or external fixator Long-distance travel or long flight
- 9. Acquired Inherited Malignancy Pregnancy OCPs Lupus anticoagulant Nephrotic syndrome Factor V Leiden mutation Protein C deficiency Protein S deficiency Antithrombin III deficiency Hypercoagulable State
- 10. Symptoms Signs Dyspnea>80% Pleuritic chest pain Sub-sternal chest pain Cough Hemoptysis Leg pain Tachypnea >90% Tachycardia Loud P2 3rd or 4th heart sound Crackles Cyanosis Clinical Presentation
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- 12. Wells’ Score Clinical symptomsof DVT (leg swelling, pain with palpation) 3.0 Other diagnosis less likely than PE 3.0 Heart rate >100 1.5 Immobilization (≥3 days) or surgery in the previous four weeks 1.5 Previous DVT/PE 1.5 Hemoptysis 1.0 Malignancy 1.0 Wells criteria High >6.0 Moderate 2.0 to 6.0 Low <2.0 Modified Wells criteria PE likely >4.0 PE unlikely ≤4.0
- 13. P A TI E N T S W I T H H I G H O R I N T E R M E D I A T E C L I N I C A L S U S P I C I O N O F P U L M O N A R Y E M B O L I S M S H O U L D B E P U T O N A N T I C O A G U L A T I O N B E F O R E S T A R T I N G I N V E S T I G A T I O N S Investigations & Diagnosis
- 14. ECG Sinus tachycardia S1Q3T3 RBBB RAD P Pulmonale Simultaneous T wave inversion in inferior+anteroseptal leads
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- 20. ECHO RV enlargement RV free wall hypokinesia with sparing of apex (McConnell sign 94% specificity) Septal flattening/ leftward septal shift/Paradoxical septal motion Assessment of pulmonary artery pressure TR Right chamber emboli Alternative diagnoses like pericardial effusion, pericardial temponade, aortic dissection, LVF TEE can identify central pulmonary embolism
- 23. D-Dimer Elevated inthrombosis, malignancy, pregnancy, MI, sepsis, elderly and hospitalized patients Useful when low clinical probability for PE Levels <500ng/ml rule out PE where clinical probability is low. In high probability patients proceed to CTPA, negative d-dimer can miss up to 15% of patients in this group
- 24. ABGs Hypoxemia Hypocapnia Respiratory alkalosis Increased A-a gradient Pulse oximetry Decreased oxygen saturation
- 25.
- 26. CT Pulmonary Angiography First-line diagnostic test Quick and non-invasive Allows direct visualization of emboli Provides alternative diagnoses like aortic dissection, ACS, consolidation, pneumothorax May miss small peripheral emboli
- 28. V/Q scan Seldomused nowadays Used when CTPA is contra-indicated Gives high, intermediate or low probability for PE depending upon perfusion defects. Normal scan rules out PE. May not be useful if pre-existing lung disease.
- 30. Compression or duplexUSG For DVTs before proceeding to invasive tests like pulmonary angiography
- 31. Pulmonary Angiography GoldStandard Performed in an Interventional Cath Lab Positive result is a “cutoff” of flow or intraluminal filling defect “Court of Last Resort”
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- 35. Pulmonary Embolism Symptoms Right Heart Strain VitalsManagement Minor Asymptomatic No Stable Discharged with LMWH to Coumadin bridge Small to medium Symptomatic No Stable Admitted in Ward LMWH to Coumadin bridge Sub-massive Symptomatic Yes Stable In ICU Heparin infusion to coumadin bridge Massive Symptomatic Yes Unstable ICU O2 Fluids Thrombolysis Or embolectomy
- 36. Heparin Available asLMWH or Unfractionated Heparin FDA approved dosing: LMWH: 1 mg/kg B.D Unfractionated: 80 units/kg (or 5000 U) bolus then 18 units/kg/hr or 1300U/h LMWH is preferred in pregnant patients
- 37. Fondaparinux A syntheticpentasaccharide Alternative to LMWH DOSING: 5 mg OD (for body weight below 50 kg) 7.5 mg OD (for body weight b/w 50–100 kg) 10 mg OD (for body weight above 100 kg)
- 38. Warfarin (Coumadin) Vit.K antagonist Inhibits hepatic synthesis of factor II, VII, IX, X, protein C & S. Patient is anticoagulated with heparin before initiating warfarin therapy because it causes temporary hypercoagulable state in first 5 days of treatment. Target INR is 2. 0– 3.0 Warfarin alternatives are rivaroxaban, apixaban, dabigatran & endoxaban.
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- 40. Thrombolytic Therapy Documentedmassive PE with Persistent hypotension Syncope with persistent hemodynamic compromise Significant hypoxemia Cardiogenic shock
- 41. Alteplase 100 mgIV over 2 hour IV anticoagulation is started immediately after alteplase. Streptokinase Loading dose 250,000 IU then 100,000 IU per hour for 24 hour. Maximum three million units per 24 hour.
- 42. Complications of ThrombolyticTherapy 1. ICH 2. Retroperitoneal & GI bleeding 3. Bleeding from surgical wounds
- 43. Contraindications Absolute 1. Activeinternal bleeding 2. Stroke in last 2 months Relative 1. Surgery or trauma in last 6 weeks 2. Uncontrolled hypertension
- 44. Other Treatment Options Embolectomy Before thrombolytic therapy this was only therapy for massive PE Now it is performed when thrombolysis is contraindicated Carries a 40% operative mortality IVC Filter Anticoagulation is contraindicated Recurrent VTE despite anticoagulation
- 45.
- 46. • LMWH SC+ oral anticoagulation (6 months ) • LMWH (pregnancy) • Recurrance / unknown origin / permanantly increased risk like anti phospholipid syndrome (throughout life)
- 47. Rivaroxaban Factor Xa inhibitor 15mg BD for Ist 3 weeks then 20mg OD for next 6 months No need of monitoring
- 48.
- 49. • INDICATIONS • Contraindicationsto anticoagulation • Failed anticoagulation • Developed a complication due to anticoagulation • Severe cardiopulmonary compromise where the next PE will be lethal IVC Filter
- 50. C O NS I D E R E D W H E N P A T I E N T ' S P R E S E N T A T I O N I S S E V E R E E N O U G H T O W A R R A N T T H R O M B O L Y S I S ( E . G . , P E R S I S T E N T H Y P O T E N S I O N ) , B U T T H R O M B O L Y S I S E I T H E R F A I L S O R I S C O N T R A I N D I C A T E D . Embolectomy
- 51. Catheter embolectomy Rheolytic:injecting pressurized saline through the catheter's distal tip, which macerates the emboli Rotational: rotational catheter fragmentation
- 52. Surgerical Embolectomy Performedon cardiopulmonary bypass with clots extracted from the opened PAs under direct visualization Indicated only when 1.Systemic hypotension due to PE in a patient in whom thrombolysis is contraindicated Possible: echocardiographic evidence of an embolus trapped within a patent foramen ovale, the right atrium, or the right ventricle 2.Limited to large medical centers because an experienced surgeon and cardiopulmonary bypass are required
- 53. • S UD D E N C A R D I A C D E A T H • O B S T R U C T I V E S H O C K • A R R Y T H M I A S • H Y P O X I A • L U N G I N F A R C T I O N Complications
- 54. Massive PE occlusionof the pulmonary artery that exceeds 50% of its cross-sectional area, resulting in progressive hemodynamic compromise Usually presenting with systolic blood pressure < 90 mmHg. obstruction of the PA to this degree initiates a cascade of physiologic events, which if not interrupted early, ultimately results in cardiac arrest and death in up to 70% of patients in the first hour
- 55. Medical treatment ofMassive PE Supplemental oxygen High dose IV heparin Hemodynamic support IV fluids (empiric 500 mL) increased right ventricular (RV) wall stress can decrease the ratio of RV oxygen supply to demand. (ischemia, deterioration of RV function, and worse RV failure) Vasopressors (no evidence for which one) Norepinephrine, epinephrine, or dopamine usually first line Thrombolytics (if no contraindications)
- 56. • IMMEDIATE MORTALITYIS HIGH IN THOSE WITH RIGHT VENTRICULAR DYSFUNCTION OR CARDIOGENIC SHOCK. • ONCE ANTICOAGULATION IS STARTED, THE RISK OF MORTALITY FALLS RAPIDLY. • THE RISK OF RECURRENCE IS HIGHEST IN THE FIRST 6–12 MONTHS AFTER THE INITIAL EVENT. Prognosis
- 57. • INITIAL RESUSCITATIONIS KEY . • EMPIRIC ANTICOAGULATION SHOULD BE CONSIDERED WHEN THE DIAGNOSIS CANNOT BE A MADE IN A TIMELY MANNER. • ANTICOAGULATION SHOULD BE PROMPTED WITH APPROPRIATE AGENT(S). • IVF FILTER SHOULD BE CONSIDERED WHEN ANTICOAGULATION IS NOT AN OPTION. Summary