Case 2: Pulmonary Thromboembolism

TWO CASES WITH HEMOPTYSISTWO CASES WITH HEMOPTYSISCASE 2CASE 2

PROF.S.SUNDAR’S UNIT

Dr.V.Jayaprakash

Mr.Marimuthu, Mr.Marimuthu, 35 years,lorry driver,admitted on 12.2.200935 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 EXAMINATIONGENERAL 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/minDorsalis 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 DIAGNOSISPROVISONAL DIAGNOSIS

ACUTE BREATHLESSNESS FOR EVALUATION

? Pulmonary Thromboembolism

No evidence of DVT clinically

INVESTIGATIONSINVESTIGATIONS

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 admissionECG on admission

Chest X ray PA viewChest 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 EMBOLISMECG 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 EMBOLISMECG 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 INVESTIGATIONSFURTHER 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 DIAGNOSISFINAL DIAGNOSIS

PULMONARY THROMOEMBOLISM

PROTEIN C DEFICIENCY

PROTEIN S DEFICIENCY

NO DEEP VENOUS THROMBOSIS

TREATMENT GIVENTREATMENT GIVEN

• Supportive measures

• Unfractionated Heparin

• Acenocoumarol

• Folic acid tablets

• B – complex supplements

VENOUS THROMBOEMBOLIC DISORDERS (DVT & PE)VENOUS THROMBOEMBOLIC DISORDERS (DVT & PE)

• ETIOLOGY: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 PRESENTATIONCLINICAL PRESENTATION (Signs and symptoms of DVT & PE are neither sensitive nor specific)(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 PEASSESSMENT 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 STUDIESLABORATORY 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 LABORATORY ASSESSMENT OF INHERITED THROMBOPHILIC STATESTHROMBOPHILIC 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 LABORATORY ASSESSMENT OF ACQUIRED THROMBOPHILIC STATESACQUIRED 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 TESTINGIMAGING - DVT SPECIFIC TESTING

• Duplex Examination -

Compressive ultrasound performed with doppler testing

• Venography

• MRI

• CT Venography

PEPE SPECIFIC TESTING 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

TREATMENTTREATMENT

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 THERAPIESINVASIVE 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 LONG TERM TREATMENT WITH VITAMIN K ANTAGONISTS FOR DVT AND PEANTAGONISTS 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 ILLNESSCOURSE 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.

ACKNOWLEDGEMENTSACKNOWLEDGEMENTS

• THE PATIENT AND HIS FAMILY

• IMCU TEAM

thank you