Case 2: Pulmonary Thromboembolism

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Case 2: Pulmonary Thromboembolism

  1. 1. TWO CASES WITH HEMOPTYSIS CASE 2 <ul><li>PROF.S.SUNDAR’S UNIT </li></ul><ul><li>Dr.V.Jayaprakash </li></ul>
  2. 2. Mr.Marimuthu, 35 years,lorry driver,admitted on 12.2.2009 <ul><li>C/O Breathlessness – 1 day </li></ul><ul><li>H/O Presenting illness: </li></ul><ul><li>The patient was apparently alright 1 day back when he developed acute onset of breathlessness,stationary in course,class 4,aggravated by exertion and relieved by rest and sitting posture </li></ul><ul><li>H/O orthopnea </li></ul><ul><li>No H/O chest pain </li></ul><ul><li>No H/O palpitation/syncope/pedal edema </li></ul>
  3. 3. <ul><li>No H/O cough/hemoptysis/wheeze </li></ul><ul><li>No H/O fever </li></ul><ul><li>No H/O abdominal pain/abdominal distension/oliguria </li></ul><ul><li>No H/O swelling of legs </li></ul><ul><li>PAST H/O : </li></ul><ul><li>No H/O of similar illness in the past </li></ul><ul><li>No H/O recent surgery/travel/immobility </li></ul><ul><li>No H/O DM/SHT/bronchial asthma/TB/CAHD/CVA/ seizure disorder </li></ul><ul><li>H/O vascular disease of right lower limb 5 years back for which he had undergone bypass surgery </li></ul>
  4. 4. <ul><li>PERSONAL HISTORY: </li></ul><ul><li>Mixed diet </li></ul><ul><li>Smoker for 10 years; smokes one pack per day </li></ul><ul><li>Occasionally consumes alcohol </li></ul><ul><li>FAMILY HISTORY: </li></ul><ul><li>Nil significant </li></ul><ul><li>TREATMENT HISTORY: </li></ul><ul><li>Nil significant </li></ul>
  5. 5. GENERAL EXAMINATION <ul><li>Conscious </li></ul><ul><li>Oriented </li></ul><ul><li>Afebrile </li></ul><ul><li>No pallor </li></ul><ul><li>Central cyanosis </li></ul><ul><li>No clubbing </li></ul><ul><li>Dyspneic and tachypneic </li></ul><ul><li>No pedal edema/calf muscle tenderness </li></ul><ul><li>No generalised lymphadenopathy </li></ul><ul><li>BP – 110/80 mmHg </li></ul><ul><li>PR – 120/min </li></ul><ul><li>Dorsalis pedis and posterior tibial pulsation absent in both lower limbs </li></ul><ul><li>RR – 35/min </li></ul><ul><li>JVP – Not elevated </li></ul>
  6. 6. <ul><li>CARDIOVASCULAR SYSTEM: </li></ul><ul><li>S1S2 heard </li></ul><ul><li>No murmurs </li></ul><ul><li>RESPIRATORY SYSTEM: </li></ul><ul><li>NVBS heard </li></ul><ul><li>No added sounds </li></ul><ul><li>ABDOMINAL EXAMINATION: </li></ul><ul><li>Soft </li></ul><ul><li>Midline scar+ </li></ul><ul><li>No organomegaly/ Free fluid </li></ul><ul><li>CENTRAL NERVOUS SYSTEM: </li></ul><ul><li>No focal neurological deficit </li></ul>
  7. 7. PROVISONAL DIAGNOSIS <ul><li>ACUTE BREATHLESSNESS FOR EVALUATION </li></ul><ul><li>? Pulmonary Thromboembolism </li></ul><ul><li>No evidence of DVT clinically </li></ul>
  8. 9. INVESTIGATIONS <ul><li>Urine routine – Normal </li></ul><ul><li>CBC: </li></ul><ul><li>Hb – 13 g% </li></ul><ul><li>TC – 12000 </li></ul><ul><li>DC – P85 L16 E4 </li></ul><ul><li>ESR – 5/12 </li></ul><ul><li>PCV – 42% </li></ul><ul><li>Platelet – 1.2 lakh </li></ul><ul><li>Blood sugar ®- 107mg% </li></ul><ul><li>Urea – 27 mg% </li></ul><ul><li>Sr creatinine – 0.8 mg% </li></ul><ul><li>Sr Na+ - 140 mmol/l </li></ul><ul><li>K+ - 4.1 mmol/l </li></ul><ul><li>Sr Lipid profile – 186 mg% </li></ul>
  9. 10. ECG on admission
  10. 11. Chest X ray PA view
  11. 12. <ul><li>CHEST X RAY PA VIEW </li></ul><ul><li>Prominent pulmonary artery </li></ul><ul><li>ECG </li></ul><ul><li>Sinus tachycardia </li></ul><ul><li>RBBB </li></ul><ul><li>S1 Q3 T3 pattern </li></ul><ul><li>ST segment depression in lead I and ll </li></ul><ul><li>ST segment depression in left precordial leads </li></ul><ul><li>Tall R waves in right precordial leads </li></ul>
  12. 13. ECG FINDINGS IN PULMONARY EMBOLISM <ul><li>Low amplitude deflection </li></ul><ul><li>Right atrial enlargement </li></ul><ul><li>Right ventricular hypertrophy </li></ul><ul><li>Right ventricular myocardial ischemia </li></ul><ul><li>Right ventricular myocardial injury </li></ul><ul><li>RBBB </li></ul><ul><li>Atrial tachyarrythmias </li></ul>
  13. 14. ECG FINDINGS IN PULMONARY EMBOLISM <ul><li>FRONTAL PLANE LEADS: </li></ul><ul><li>S1Q3T3 pattern </li></ul><ul><li>ST segment depresson in standard lead l and ll </li></ul><ul><li>Right axis deviation </li></ul><ul><li>Tall peaked T wave in lead ll </li></ul><ul><li>HORIZONTAL LEADS: </li></ul><ul><li>T wave inversion in right precordial leads </li></ul><ul><li>ST segment elevation in right precordial leads </li></ul><ul><li>ST segment depression in left precordial leads </li></ul><ul><li>Increase in R amplitude in right precordial leads </li></ul><ul><li>RBBB </li></ul>
  14. 15. <ul><li>ECHOCARDIOGRAM: </li></ul><ul><li>No RWMA </li></ul><ul><li>Normal LV systolic function </li></ul><ul><li>TR mild </li></ul><ul><li>TRPG 48 mmHg </li></ul><ul><li>Mild RA/RV dilated </li></ul><ul><li>D-DIMER LEVEL: </li></ul><ul><li>3.27 microgram/ml – POSITIVE </li></ul><ul><li>(Normal : < 0.5 mcg/ml) </li></ul>
  15. 16. FURTHER INVESTIGATIONS <ul><li>CT Chest – Normal study </li></ul><ul><li>Doppler study of both lower limbs – No evidence of DVT </li></ul><ul><li>Lupus anticoagulant – Negative </li></ul><ul><li>Anti CardioLipin Antibody (ACLA) – Normal </li></ul><ul><li>IgG – 5.11 GPLU/ml (Normal - < 10) </li></ul><ul><li>IgG – 3.65 mPLU/ml (Normal - <7) </li></ul><ul><li>Protein C levels – 44.6% (Normal :70 – 140%) </li></ul><ul><li>Protein S levels – 39.7% (Normal : 60 – 150%) </li></ul><ul><li>Sr homocysteine level – 20.31 mcmol/l (Normal:5.9 – 16) </li></ul><ul><li>Antithrombin levels – Not done </li></ul><ul><li>Factor V Leiden – Not done </li></ul><ul><li>15/2/09 18/2/09 23/2/09 </li></ul><ul><li>PT 17.6 26.3 24.2 </li></ul><ul><li>aPTT 36.4 40 40.5 </li></ul><ul><li>INR 1.6 2.8 2.68 </li></ul>
  16. 18. FINAL DIAGNOSIS <ul><li>PULMONARY THROMOEMBOLISM </li></ul><ul><li>PROTEIN C DEFICIENCY </li></ul><ul><li>PROTEIN S DEFICIENCY </li></ul><ul><li>NO DEEP VENOUS THROMBOSIS </li></ul>
  17. 19. TREATMENT GIVEN <ul><li>Supportive measures </li></ul><ul><li>Unfractionated Heparin </li></ul><ul><li>Acenocoumarol </li></ul><ul><li>Folic acid tablets </li></ul><ul><li>B – complex supplements </li></ul>
  18. 20. VENOUS THROMBOEMBOLIC DISORDERS (DVT & PE) <ul><li>ETIOLOGY: Stasis, Hypercoagulability, Venous endothelial injury </li></ul><ul><li>STASIS : Immobilisation (Trauma,Surgery,Immobilisation) </li></ul><ul><li>HYPERCOAGULABLE STATES : </li></ul><ul><li>Inherited : Prothrombin gene mutation, partial protein C deficiency, partial protein S deficiency, partial antithrombin deficiency,factor V Leiden, hyperhomocystinemia </li></ul><ul><li>Acquired : Malignancy, nephrotic syndrome, estrogen use, pregnancy, HIT,APA syndrome, sickle cell disease, marrow fat embolism, amniotic fluid embolism </li></ul>
  19. 21. CLINICAL PRESENTATION (Signs and symptoms of DVT & PE are neither sensitive nor specific) <ul><li>CLINICAL DECISION RULES: </li></ul><ul><li>Clinical variable Score </li></ul><ul><li>Signs and symptoms of DVT 3.0 </li></ul><ul><li>Alternative diagnosis less likely than PE 3.0 </li></ul><ul><li>Heart rate >100/min 1.5 </li></ul><ul><li>Immobilisation>3 days,Surgery within 4 wks 1.5 </li></ul><ul><li>Prior PE or DVT 1.5 </li></ul><ul><li>Hemoptysis 1.0 </li></ul><ul><li>Cancer 1.0 </li></ul><ul><li>High clinical likelihood of PE if the point score exceeds 4.0 </li></ul>
  20. 22. ASSESSMENT OF SEVERITY OF PE <ul><li>MASSIVE PE: </li></ul><ul><li>Systemic Arterial Hypotension </li></ul><ul><li>MODERATE TO LARGE PE: </li></ul><ul><li>RV Hypokinesias in Echocardiography </li></ul><ul><li>Normal Systemic Arterial Pressure </li></ul><ul><li>SMALL TO MODERATE PE: </li></ul><ul><li>Normal Right Heart Function </li></ul><ul><li>Normal Systemic Arterial Pressure </li></ul>
  21. 23. LABORATORY STUDIES <ul><li>D-DIMER: </li></ul><ul><li>Cross linked fibrin degradation product that may be increased during acute illness or VTE. </li></ul><ul><li>It has a low positive predictive value and specificity – If positive, requires further evaluation. </li></ul><ul><li>It has high negative predictive value-If negative,it excludes DVT. </li></ul>
  22. 24. LABORATORY ASSESSMENT OF INHERITED THROMBOPHILIC STATES Prothrombin gene mutation G20210A G20210A mutation Partial protein C deficiency Partial protein S deficiency Protein C activity Protein S activity, Free protein S antigen Factor V Leiden Activated protein C resistance, if positive confirm with Factor V Leiden PCR Hyperhomocystinemia Fasting plasma homocysteine levels
  23. 25. LABORATORY ASSESSMENT OF ACQUIRED THROMBOPHILIC STATES ANTIPHOSPHOLIPID ANTIBODY SYNDROME LUPUS ANTICOAGULANT, ANTICARDIOLIPIN ANTIBODY, BETA 2 GLYCOPROTEIN 1 PNH RBC OR WBC FLOW CYTOMETRY FOR LOSS OF CD55,CD59 MYELOPROLIFERATIVE DISORDER JAK – 2 MUTATION
  24. 26. IMAGING - DVT SPECIFIC TESTING <ul><li>Duplex Examination - </li></ul><ul><li>Compressive ultrasound performed with doppler testing </li></ul><ul><li>Venography </li></ul><ul><li>MRI </li></ul><ul><li>CT Venography </li></ul>
  25. 27. PE SPECIFIC TESTING <ul><li>NONSPECIFIC TESTS: </li></ul><ul><li>~ ECG,Troponin levels, Chest Radiography </li></ul><ul><li>~ Determine pretest probability of PE along with D-Dimer assay </li></ul><ul><li>CONTRAST ENHANCED SPIRAL(HELICAL) CHEST CT: </li></ul><ul><li>~ Relatively accurate for large(proximal) PE, but sensitivity is low for small(distal) emboli </li></ul><ul><li>~ Clinical suspicion that is discordant with the objective finding should lead to further testing </li></ul>
  26. 28. <ul><li>V/Q SCANNING: </li></ul><ul><li>Requires administration of radioactive material(via both inhaled and i.v. routes) </li></ul><ul><li>V/Q scan can be classified as normal, non diagnostic or high probability for PE </li></ul><ul><li>Use of clinical suspicion improves the accuracy of V/Q scan </li></ul><ul><li>When both the findings are discordant, further testing should be performed </li></ul><ul><li>MR ANGIOGRAPHY </li></ul><ul><li>PULMONARY ANGIOGRAPHY </li></ul>
  27. 29. TREATMENT <ul><li>UNFRACTIONATED HEPARIN (UFH): </li></ul><ul><li>80 U/kg bolus followed by infusion of 18 U/kg/hr. </li></ul><ul><li>Continued for atleast 4-5 days and until INRs of atleast 2 are achieved on 2 consecutive days with warfarin therapy. </li></ul><ul><li>LMWH: </li></ul><ul><li>VKAs(Vitamin K Antagonists), Warfarin or Acenocoumarol: </li></ul><ul><li>Started as 5 mg PO and dose adjusted according to INR </li></ul><ul><li>INR should be done frequently during the first month,because multiple dose adjustments are usually necessary to achieve therapeutic INR </li></ul><ul><li>Once a stable dose is achieved, INR monitoring should be done atleast 4 weeks. </li></ul>
  28. 30. <ul><li>THROMBOLYTIC THERAPY- INDICATIONS: </li></ul><ul><li>Refractory Systemic Hypotension </li></ul><ul><li>? Right Ventricular Dysfunction </li></ul><ul><li>ANTITHROMBIN III INFUSION: </li></ul><ul><li>In patients with congenital antithrombin lll deficiency - during an acute thromotic episode </li></ul>
  29. 31. INVASIVE SPECIAL THERAPIES <ul><li>IVC FILTERS: </li></ul><ul><li>1] Acute DVT states in which there is absolute contraindication to anticoagulation </li></ul><ul><li>2] Recurrent thromboembolic episodes </li></ul><ul><li>CATHETER EMBOLECTOMY </li></ul><ul><li>SURGICAL EMBOLECTOMY </li></ul>
  30. 32. LONG TERM TREATMENT WITH VITAMIN K ANTAGONISTS FOR DVT AND PE First episode of DVT or PE secondary to a transient risk factors 3 mon Recommendation applies to both proximal and calf vein thrombosis First episode of idiopathic DVT or PE 6 – 12 mon Continuation of therapy after 6 -12 mon to be considered First episode of DVT or PE with a documented thrombophilic abnormality 6 – 12 mon Continuation of therapy after 6 -12 mon to be considered First episode of DVT or PE with documented antiphospholipid or >= 2 thrombophilic abnormality 12 mon Continuation of therapy after 12 mon to be considered
  31. 33. COURSE OF THE ILLNESS <ul><li>His breathlessness improved, was able to walk about 100 m without breathlessness. Except for sinus tachycardia, ECG features of PE disappeared. He was discharged at request on 27.2.2009 with advice to continue acitrom and to get readmitted after 3 days for planning CT Angiogram. But he came for admission the next day itself with massive hemoptysis; cause - ?acitrom related ?massive pulmonary embolism and infarct. He was treated with vitamin K, FFP and blood transfusion; shifted to IMCU for intensive care. Evaluation revealed prolonged coagulation parameters. PT- 48 seconds, INR- 4.3. Massive hemoptysis recurred and the patient had hypoxia and altered sensorium. Despite the best possible efforts, the patient succumbed to his illness. </li></ul>
  32. 35. ACKNOWLEDGEMENTS <ul><li>THE PATIENT AND HIS FAMILY </li></ul><ul><li>IMCU TEAM </li></ul>
  33. 36. <ul><li>thank you </li></ul>

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