PE in pulmonology KTH BY DR NAWZ SWAT

CASE HISTORY PRESENTATION : 

CASE HISTORY PRESENTATION 1 DR. Muhammad Nawaz TMO Medical E KTH

Pulmonary venousThromboembolism (PE) : 

Pulmonary venousThromboembolism (PE) 2

EPIDEMIOLOGY : 

EPIDEMIOLOGY 3RD LEADING CAUSE OF DEATH 370,000 DEATHS / YEAR EUROPE 300,000 DEATHS / YEAR ---- USA 7% WERE DIAGNOSED CASES OF PE 34% SUDDEN FATAL DEATHS (AUTOPSY) 59% PE CASES UNDETECTED IN HOSPITAL IN DEFFERENT WARDS (AUTOPSY) 3

Risk Factors : 

Risk Factors Hypercoagulability Malignancy Pregnancy Postpartum status (<4wk) ANTI PHOSPOLIPID AS/Estrogen/ OCP’s Genetic mutations (Factor V Leiden, Protein C & S deficiency, Prothrombin mutations, anti-thrombin III deficiency) Venous Stasis Bedrest > 24 hr - -- - STROKES,POST OPERATED Recent cast or external fixator Long-distance AIR travel or prolong automobile travel Vessel wall Injury Recent surgery requiring endotracheal intubation Recent trauma (especially the lower extremities and pelvis) 4

Emboli : 

Emboli Most common embolus is thrombus in veins or heart 50 - 60%(venous) proximal deep veins of lower limbs Pelvic and upper extremeties veins Rarely fat,air,amniotic fluid,forign bodies,septic emboli, and tumors cells 5

Slide 6: 

6 HOW TO DIAGNOSE

HOW TO DIAGNOSE : 

HOW TO DIAGNOSE Clinically very difficult 1st ; clinical findings of PE depend both on size of embolus and patient pre-existing cardiopulmonary status 2nd ; the common signs/sympyoms are not specific for PE like--- 7

DIFFERENTIALS : 

DIFFERENTIALS ACS PNEUMOTHORAX PNEUMONIA COPD CCF,PERICARDITIS TRAUMA RIB FRACTURE 8

Slide 9: 

UPET PIOPED I S/S PE + PE+ PE- Dyspnea 84% 73% 72% Chest pain 74 66 59 COUGH 53 37 36 Leg pain NR 26 24 Hemoptysis 30 13 8 Palpitation NR 10 18 Wheezing NR 9 11 R/R >20/m 92 70 68 CRACKLES 58 51 40 PULSE > =IOO/M 44 30 24 Temp >38c 43 7 12 Loud P2 53 23 3 S3 NR 3 4 Cynosis 19 1 2 Pleural rub etc NR 3 2 9

Slide 10: 

Confusing for Emergency Physician chances of under diagnosis/over diagnosis? 10

Slide 11: 

CLINICAL PRIDICTION RULE FOR PE POINTS S/S DVT + 3 ALTERNATIVE DX LESS LIKELY THAN P.E 3 HEART RATE >100 1.5 IMMOBALIZATION >3 DAYS OR SURGERY IN PAST 4 WEEKS 1.5 PREVIOUS PE OR DVT 1.5 HEMOPTYSIS 1.0 CANCER (ON TREAMENT WITHIN 6MONTH /PALLIATIVE CARE) 1.0 ------------------------------------------------------------- PE LIKELY SCORE >4 PE UNLIKELY =4 OR < 4 11

Slide 12: 

PIOPED II 2006 12 Concern PE PE unlikely Dichotomous clinical probability ASSESSMENT PE likely D-dimer negative Positive >500ng/ml VTE excluded.look D.Ds/follow off anticoagulation Helical CT-PA PE Dx Treat PE Normal study or INTERMEDIATE STUDY doppler scan lowerlimbs or Pulm angiography PE excluded , Look for D.Ds and follow off anticogulation

PIOPED II (NHLBI) 2006 : 

PIOPED II (NHLBI) 2006 PURPOSE: To formulate comprehensive recommendations for the diagnostic approach to patients with suspected pulmonary embolism, based on randomized trials. RECOMMENDATIONS :all patients with suspected pulmonary embolism should undergo an objective clinical pretest probability assessment and D-dimer should be measured by the quantitative rapid enzyme-linked immunosorbent assay (ELISA) wasinigton,michigan state universities etc 2006

Slide 14: 

If pulmonary embolism is not excluded, contrast-enhanced computed tomographic pulmonary angiography (CT angiography) in combination with venous phase imaging (CT venography), is recommended. In pregnant women, ventilation/perfusion scans are recommended by many as the first imaging test following D-dimer and perhaps venous ultrasound. washington ,michigon state universities etc2006 14

PIOPED II 2006 : 

PIOPED II 2006 Md-H-CT-PA SENSITIVITY----83% VS single detector 53% SPECIPECITY---96% VS single detector 81% 15

cont : 

cont But high false negative rate---- 15 ---20% Is it safe to withhold anticoagulation In pt with negative CT-PA ? 16

CHRISTOPER STUDY LARGE …PROSP ….. TRIAL : 

CHRISTOPER STUDY LARGE …PROSP ….. TRIAL Pt with high PTPA SCORE and negative CTPA were followed up off-anticoagulation for 3 months ---- They found a low <2% incedence of subsequent PE. PE were insignificant… So a negative CT-PA almost exclude significant PE 17

CT PA : 

CT PA Few issues…….. Rate of false positive CTPA And over treatment Has not been studied yet 18

Slide 19: 

19

GOLD STANDARD : 

GOLD STANDARD Refference standard for pulmonary angiography 755 pt PA in PIOPED I 97% established diagnosis About 3% PA were non diagnostic 0.8% with negative PA DIED due to PE( autopsy report) 20

MRI ROLE : 

MRI ROLE MORE SENSITIVE THAN DOPPLER U/S……...for dvt . 21

Other investigations : 

Other investigations ECG, CHEST XRAY ABGS D-DIMER TROP I,TROP T, BNP DOPPLER SCAN FOR DVT 22

ECG : 

ECG ECG abnormal in 70% of PE Pts Most Common Findings: Sinus Tachycardia or T-wave changes V1 –V4 Right ventricular strain pattern P pulmonale Right axis deviation RBBB S1-Q3-T3 (occurs in only 30% of PE patients) 23

CXR : 

CXR To exclude other D.Ds To permit V/Q SCAN interpretation 12 % cxr were normal in PIOPED I Atelactasis Infiltrates Minimal effusions and other uncommon signs 24

Chest X-ray of PE : 

Chest X-ray of PE Westermark's sign A dilation of the pulmonary vessels proximal to the embolism along with collapse of distal vessels, sometimes with a sharp cutoff. Hampton’s Hump A triangular or rounded pleural-based infiltrate (heamorrage)with the apex toward the hilum, usually located adjacent to the hilum. 25

Radiographic findings - Hampton’s Hump, Westermark’s Sign : 

Radiographic findings - Hampton’s Hump, Westermark’s Sign 26 Westermark’s Sign Hampton’s Hump

D-dimer Test : 

D-dimer Test BY ELIZA > 500ng/ml Quantitative test have -------- 95-97% sensitivity but only 45% specific for venous thromboembolism In PESHAWAR-----cost 710 PKR False Positives: e.g Sepsis,pragnancy,malignancies, trauma ,surgery,stokes 27

Diagnostic Testing - ABG’s : 

Diagnostic Testing - ABG’s ABGS-----usually show acute respiratory alkalosis The A-a gradient is a better measure of gas exchange than the pO2, but it is nonspecific and insensitive in ruling out PE. but profound hypoxia with a normal CXR in absence of pre existing lung disease------is suspicous for PE. 28 “ Normal A-a gradient significantly decreases PE chances ”.

A-a oxygen gradient : 

A-a oxygen gradient common measure of oxygenation     A-a oxygen gradient = PAO2 - PaO2. PaO2 is measured by arterial blood gas, while PAO2 is calculated using the alveolar gas equation:   PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 ÷ R) where FiO2 is the fraction of inspired oxygen (0.21 at room air), Patm (760 mmHg at sea level), PH2O (47 mmHg at 37 degrees C), PaCO2 , and R is the respiratory quotient. The respiratory quotient is approximately 0.8 at steady state, but varies according to the relative utilization of carbohydrate, protein, and fat. The A-a gradient calculated using this alveolar gas equation may deviate from the true gradient by up to 10 mmHg. This reflects the equation's simplification from the more rigorous full calculation and the imprecision of several independent variables (eg, FiO2 and R). The normal A-a gradient varies with age and can be estimated from the following equation, assuming the patient is breathing room air (show calculator 1) [3] : A-a gradient = 2.5 + 0.21 x age in years The A-a gradient increases with higher FiO2. When a patient receives a high FiO2, both PAO2 and PaO2 increase. However, the PAO2 increases disproportionately, causing the A-a gradient to increase. 29

Diagnostic Testing : 

Diagnostic Testing Echocardiography Consider in every patient with a documented pulmonary embolism TEE and TTE help in management Early fibrinolysis can reduce mortality 50% 30

others : 

others Trop T,Trop I,plasma BNP raised usually Not useful in diagnosis But correlates with adverse out come 31

Slide 32: 

32 RISK STRATIFICATION NORMAL BP+ RV ANTICOAGULATION ALONE OR IVC FILTERS HYPOTENSION RESUSSITATE AND PRIMARY THERAPY THROMBOLYTIC THERAPY OR EMBOLICTOMY MANAGEMENT

THROMBOLYTIC THERAPY : 

THROMBOLYTIC THERAPY STREPTOKINASE,UROKINASE IN HIGH RISK FOR DEATH BEST 24 HOUR-------1ST WEEK 250,OOO IU -------- Tissue PA 100mg continous IV over 2hr IN FIRST 14 DAYS AFTER PE 33

Treatment : 

Treatment Anticoagulants Heparin (UFH) Provides immediate thrombin inhibition, which prevents thrombus extension Does not dissolve existing clot Dosage---80 IU / kg IV( 5000 iu ) bolus then 18 IU / kg / hr(1200 iu) IV continuous infusion for 5-7 days. Warfarin is safely started concurrently with heparin. FractionatedHeparin convenient alternative Enoxaparin ,Nadroparin s/c 12 hrly 34

Slide 35: 

35 IV HEPARIN NOMOGRAM based on body weight Start after 6 hours of IV bolus dose 35

Optimal duration of anti coagulation : 

Optimal duration of anti coagulation Dvt- 1st----3—6 months(reversible RF) PE ---1st---6 months---12months(revsible RF) In cases of non reversible RF or recurrent TE Life long anticoagulation or filters are recomended 36

Conti ’ : 

Conti ’ 2. IVC filters 37

Primary prevention : 

Primary prevention VTE Often remains clinically silent and presents with mortality and morbidity. The importance of prophylaxis is very significant, yet remained under used Prophylactic low dose sub-cutaneous UFH / LMW- FH 38

prognosis : 

prognosis In US PE estimated ---50000 death anually Mostly PE not recognized antemortem but postmortem on autopsy…. Outlook of early diagnosed and treated PE is good Overall prognosis depends on underlying disease and not PE itself. Chronic P-HTN ---1% Deaths from recurrent thromboemboli -<3% Perfusion defects resolve in most survivors 39

Slide 40: 

Stockings below knee don’t help in bed bound patients 40 Thigh high elastic stockings

Intermittent pneumatic compression : 

Intermittent pneumatic compression USE OF IPC DEVICES IN HIGH RISK INDIVISUALS 41

PREVENTION IS THE BEST : 

PREVENTION IS THE BEST A MESSAGE TO COMMUNTY Encourage self service and Walk in airoplanes. Obesity,diet and exercise awareness Early mobilization in postop and pragnant women. 42

Slide 43: 

43 THANK YOU