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Case 2: Pulmonary Thromboembolism
 

Case 2: Pulmonary Thromboembolism

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    Case 2: Pulmonary Thromboembolism Case 2: Pulmonary Thromboembolism Presentation Transcript

    • TWO CASES WITH HEMOPTYSIS CASE 2
      • PROF.S.SUNDAR’S UNIT
      • Dr.V.Jayaprakash
    • Mr.Marimuthu, 35 years,lorry driver,admitted on 12.2.2009
      • C/O Breathlessness – 1 day
      • H/O Presenting illness:
      • 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
      • H/O orthopnea
      • No H/O chest pain
      • No H/O palpitation/syncope/pedal edema
      • No H/O cough/hemoptysis/wheeze
      • No H/O fever
      • No H/O abdominal pain/abdominal distension/oliguria
      • No H/O swelling of legs
      • PAST H/O :
      • No H/O of similar illness in the past
      • No H/O recent surgery/travel/immobility
      • No H/O DM/SHT/bronchial asthma/TB/CAHD/CVA/ seizure disorder
      • H/O vascular disease of right lower limb 5 years back for which he had undergone bypass surgery
      • PERSONAL HISTORY:
      • Mixed diet
      • Smoker for 10 years; smokes one pack per day
      • Occasionally consumes alcohol
      • FAMILY HISTORY:
      • Nil significant
      • TREATMENT HISTORY:
      • Nil significant
    • GENERAL EXAMINATION
      • Conscious
      • Oriented
      • Afebrile
      • No pallor
      • Central cyanosis
      • No clubbing
      • Dyspneic and tachypneic
      • No pedal edema/calf muscle tenderness
      • No generalised lymphadenopathy
      • BP – 110/80 mmHg
      • PR – 120/min
      • Dorsalis pedis and posterior tibial pulsation absent in both lower limbs
      • RR – 35/min
      • JVP – Not elevated
      • CARDIOVASCULAR SYSTEM:
      • S1S2 heard
      • No murmurs
      • RESPIRATORY SYSTEM:
      • NVBS heard
      • No added sounds
      • ABDOMINAL EXAMINATION:
      • Soft
      • Midline scar+
      • No organomegaly/ Free fluid
      • CENTRAL NERVOUS SYSTEM:
      • No focal neurological deficit
    • PROVISONAL DIAGNOSIS
      • ACUTE BREATHLESSNESS FOR EVALUATION
      • ? Pulmonary Thromboembolism
      • No evidence of DVT clinically
    •  
    • INVESTIGATIONS
      • Urine routine – Normal
      • CBC:
      • Hb – 13 g%
      • TC – 12000
      • DC – P85 L16 E4
      • ESR – 5/12
      • PCV – 42%
      • Platelet – 1.2 lakh
      • Blood sugar ®- 107mg%
      • Urea – 27 mg%
      • Sr creatinine – 0.8 mg%
      • Sr Na+ - 140 mmol/l
      • K+ - 4.1 mmol/l
      • Sr Lipid profile – 186 mg%
    • ECG on admission
    • Chest X ray PA view
      • CHEST X RAY PA VIEW
      • Prominent pulmonary artery
      • ECG
      • Sinus tachycardia
      • RBBB
      • S1 Q3 T3 pattern
      • ST segment depression in lead I and ll
      • ST segment depression in left precordial leads
      • Tall R waves in right precordial leads
    • ECG FINDINGS IN PULMONARY EMBOLISM
      • Low amplitude deflection
      • Right atrial enlargement
      • Right ventricular hypertrophy
      • Right ventricular myocardial ischemia
      • Right ventricular myocardial injury
      • RBBB
      • Atrial tachyarrythmias
    • ECG FINDINGS IN PULMONARY EMBOLISM
      • FRONTAL PLANE LEADS:
      • S1Q3T3 pattern
      • ST segment depresson in standard lead l and ll
      • Right axis deviation
      • Tall peaked T wave in lead ll
      • HORIZONTAL LEADS:
      • T wave inversion in right precordial leads
      • ST segment elevation in right precordial leads
      • ST segment depression in left precordial leads
      • Increase in R amplitude in right precordial leads
      • RBBB
      • ECHOCARDIOGRAM:
      • No RWMA
      • Normal LV systolic function
      • TR mild
      • TRPG 48 mmHg
      • Mild RA/RV dilated
      • D-DIMER LEVEL:
      • 3.27 microgram/ml – POSITIVE
      • (Normal : < 0.5 mcg/ml)
    • FURTHER INVESTIGATIONS
      • CT Chest – Normal study
      • Doppler study of both lower limbs – No evidence of DVT
      • Lupus anticoagulant – Negative
      • Anti CardioLipin Antibody (ACLA) – Normal
      • IgG – 5.11 GPLU/ml (Normal - < 10)
      • IgG – 3.65 mPLU/ml (Normal - <7)
      • Protein C levels – 44.6% (Normal :70 – 140%)
      • Protein S levels – 39.7% (Normal : 60 – 150%)
      • Sr homocysteine level – 20.31 mcmol/l (Normal:5.9 – 16)
      • Antithrombin levels – Not done
      • Factor V Leiden – Not done
      • 15/2/09 18/2/09 23/2/09
      • PT 17.6 26.3 24.2
      • aPTT 36.4 40 40.5
      • INR 1.6 2.8 2.68
    •  
    • FINAL DIAGNOSIS
      • PULMONARY THROMOEMBOLISM
      • PROTEIN C DEFICIENCY
      • PROTEIN S DEFICIENCY
      • NO DEEP VENOUS THROMBOSIS
    • TREATMENT GIVEN
      • Supportive measures
      • Unfractionated Heparin
      • Acenocoumarol
      • Folic acid tablets
      • B – complex supplements
    • VENOUS THROMBOEMBOLIC DISORDERS (DVT & PE)
      • ETIOLOGY: Stasis, Hypercoagulability, Venous endothelial injury
      • STASIS : Immobilisation (Trauma,Surgery,Immobilisation)
      • HYPERCOAGULABLE STATES :
      • Inherited : Prothrombin gene mutation, partial protein C deficiency, partial protein S deficiency, partial antithrombin deficiency,factor V Leiden, hyperhomocystinemia
      • Acquired : Malignancy, nephrotic syndrome, estrogen use, pregnancy, HIT,APA syndrome, sickle cell disease, marrow fat embolism, amniotic fluid embolism
    • CLINICAL PRESENTATION (Signs and symptoms of DVT & PE are neither sensitive nor specific)
      • CLINICAL DECISION RULES:
      • Clinical variable Score
      • Signs and symptoms of DVT 3.0
      • Alternative diagnosis less likely than PE 3.0
      • Heart rate >100/min 1.5
      • Immobilisation>3 days,Surgery within 4 wks 1.5
      • Prior PE or DVT 1.5
      • Hemoptysis 1.0
      • Cancer 1.0
      • High clinical likelihood of PE if the point score exceeds 4.0
    • ASSESSMENT OF SEVERITY OF PE
      • MASSIVE PE:
      • Systemic Arterial Hypotension
      • MODERATE TO LARGE PE:
      • RV Hypokinesias in Echocardiography
      • Normal Systemic Arterial Pressure
      • SMALL TO MODERATE PE:
      • Normal Right Heart Function
      • Normal Systemic Arterial Pressure
    • LABORATORY STUDIES
      • D-DIMER:
      • Cross linked fibrin degradation product that may be increased during acute illness or VTE.
      • It has a low positive predictive value and specificity – If positive, requires further evaluation.
      • It has high negative predictive value-If negative,it excludes DVT.
    • 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
    • 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
    • IMAGING - DVT SPECIFIC TESTING
      • Duplex Examination -
      • Compressive ultrasound performed with doppler testing
      • Venography
      • MRI
      • CT Venography
    • PE SPECIFIC TESTING
      • NONSPECIFIC TESTS:
      • ~ ECG,Troponin levels, Chest Radiography
      • ~ Determine pretest probability of PE along with D-Dimer assay
      • CONTRAST ENHANCED SPIRAL(HELICAL) CHEST CT:
      • ~ Relatively accurate for large(proximal) PE, but sensitivity is low for small(distal) emboli
      • ~ Clinical suspicion that is discordant with the objective finding should lead to further testing
      • V/Q SCANNING:
      • Requires administration of radioactive material(via both inhaled and i.v. routes)
      • V/Q scan can be classified as normal, non diagnostic or high probability for PE
      • Use of clinical suspicion improves the accuracy of V/Q scan
      • When both the findings are discordant, further testing should be performed
      • MR ANGIOGRAPHY
      • PULMONARY ANGIOGRAPHY
    • TREATMENT
      • UNFRACTIONATED HEPARIN (UFH):
      • 80 U/kg bolus followed by infusion of 18 U/kg/hr.
      • Continued for atleast 4-5 days and until INRs of atleast 2 are achieved on 2 consecutive days with warfarin therapy.
      • LMWH:
      • VKAs(Vitamin K Antagonists), Warfarin or Acenocoumarol:
      • Started as 5 mg PO and dose adjusted according to INR
      • INR should be done frequently during the first month,because multiple dose adjustments are usually necessary to achieve therapeutic INR
      • Once a stable dose is achieved, INR monitoring should be done atleast 4 weeks.
      • THROMBOLYTIC THERAPY- INDICATIONS:
      • Refractory Systemic Hypotension
      • ? Right Ventricular Dysfunction
      • ANTITHROMBIN III INFUSION:
      • In patients with congenital antithrombin lll deficiency - during an acute thromotic episode
    • INVASIVE SPECIAL THERAPIES
      • IVC FILTERS:
      • 1] Acute DVT states in which there is absolute contraindication to anticoagulation
      • 2] Recurrent thromboembolic episodes
      • CATHETER EMBOLECTOMY
      • SURGICAL EMBOLECTOMY
    • 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
    • COURSE OF THE ILLNESS
      • 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.
    •  
    • ACKNOWLEDGEMENTS
      • THE PATIENT AND HIS FAMILY
      • IMCU TEAM
      • thank you