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DIAGNOSIS OF DEEP VEIN THROMBOSIS AND PULMONARY EMBOLISM

K Suega Hematology Medical Oncology Division Udayana Medical School, Bali

DVT and PE : a CONTINOUS SPECTRUM OF THE SAME DISEASE call VENOUSTHROMBOEMBOLISM (VTE). REPRESENT A SIGNIFICANT HEALTH PROBLEM because of ITS HIGH MORBIDITY and MORTALITY and MOREOVER CHARACTERIZED BY HIGH RATE OF RECURRENCE VTE : age adjusted INCIDENCE 1-2 EVENT/ 1000 POPULATION
STARTING FROM CALF DVT EXTENDED TO PROXIMAL DVT and DEVASTATING PE, based on its SEVERITY and the INTENSITY OF PROTHROMBOTIC STIMULUS ACUTE VTE PRESENT EITHER BY LUNG or LEG SYMPTOMS, but MOST PATIENTS HAVE THROMBUS AT BOTH SITE AT THE TIME OF DIAGNOSTIC

Fabringer etal., ATVB 2009 Kearon et al., Circulation, 2003 Zhu et al., ATVB 2009

EPIDEMIOLOGY
VTE DIFFERS SUBSTANTIALLY WORLWIDE,NECROPSY STUDY : 60% HOSPITAL DEATH HAVING PE. USA : 1 CASE /1000 PERSON/YEAR VTE : LOWER IN ASIAN RACES , INCREASE MARKEDLY WITH AGES AND PREGNANCY ( RR 4,29) PE FOUND IN 29-30% OF ALL PX IN MEDICAL INTENSIVE, 27-33% OF CRITICAL CARE PX, 20-26% OF PX WITH BEDREST PULMONARY DISEASE, 48% OF PX AFTER ARTERY BYPASS GRAFT PE WERE FOUND WITH DVT IN 60-80%, 50% WERE ASYMPTOMATIC DVT : 1 PERSON IN 20 DEVELOP DVT IN THE COURSE OF THEIR LIFE, INCREASED TO 20-70% IN HOSPITALISED PX. UP TO 50% OF DVT BECOME PTS, OBESITY INCREASE THE RISK DVT WERE FOUND WITH ASYMPTOMATIC PE IN 40%
Ramzi et al. Am Fam Phydician,2004 Quellette et al., Medscape , 2011

Quellette et al., Medscape 2011

Thrombosis

LIFEBLOOD THE

CHARITY

Venous thromboembolism
Treatment and secondary prevention

DVT

PE

Deep vein insufficiency

Pulmonary hypertension

Death

Post-thrombotic syndrome

Chronic PE

Ulcus cruris

Deep vein thrombosis

Common femoral vein

Thrombus

Knee

Proximal Distal

PATHOGENESIS

Robert et al., Anesthesiology, 2004

ETIOLOGY
PE
VENOUS STASIS HYPERCUAGULABLE STATE IMMOBILITY SURGERY AND TRAUMA PREGNANCY ORAL CONTRACEPTIVE ESTROGEN REPLACEMENT MALIGNANCY HAREDITARY FACTORS ACUTE MEDICAL ILLNESS

DVT
INCREASED BLOOD VISCOUSITY INCREASED CENTRAL VENOUS PRESSURE ANATOMIC VARIANT MECHANICAL INJURY GENETIC FACTORS COMMON RISK FACTORS MEDENOX STUDY
PRESENCE OF ACUTE ILLNESS AGE OLDER THAN 75 YEARS CANCER HISTORY OF PRIOR VTE

Alikhan et al., Arch Intern Med, 2004 Ramzi et al., AM Fam Physician ,2004 Rugeri et al., Lancet 2001

Risk Factors for Venous Thromboembolism Age >40 yr History of venous thromboebolism Surgery requiring >30 min of anesthesia Prolonged immobilization Cerebrovascular accident

Congestive heart failure


Cancer Fracture of pelvis, femur, or tibia Obesity Pregnancy or recent delivery Estrogen therapy Inflammatory bowel disease Genetic or acquired thrombophilia Antithrombin III deficiency Protein C deficiency Protein S deficiency Prothrombin G20220A mutation Factor V Leiden Anticardiopilin antibody syndrome Lupus anticoagulant

PATHOPHYSIOLOGY
PE
RESPIRATORY COSENQUENSES
INCREASED ALV. DEAD SPACE HYPOXEMIA HYPERVENTILATION

DVT
VENOUS STASIS RESULTS IN AN INCREASED BLOOD VISCOSITY DECREASED WALL CONTRACTILITY AND VEIN VALVE DYSFUNCTION CHRONIC VENOUS INSUFFICIENCY

HEMODYNAMIC CONSEQUENSES
PULMONARY VASC. RESISTENCE RIGHT VENTRICULAR FAILURE

Glhaber et al.,Circulatin ,2003 Riedei et al.,Postgrad Med,2004 Patel et al., Medscape, 2011

PHYSICAL EXAMINATION
PE
MAY VARY, ATYPICAL MOST PX HAVE NO OBVIOUS SYMPTOMS, SHOCK ( MASSIVE PE) SIGNS OF RHF PIOPED III PLEURITIC CHEST PAIN (66%) DYSPNEU (73%) COUGH (37%) HEMOPTYSIS (13%) (SIGNS&SYMPTOMS CANTCONFIRM, WITHOUT IT COULDNT EXCLUDE PE)

DVT
HOMAN SIGN ODEMA PAINFULL TENDERNESS DISCOLORATION OF SKIN PHLEGMASIA CERULEA DOLENS PHLEGMASIA ALBA DOLENS

( NO SINGLE OR COMBINED SIGNS &SYMPTOMS IS SIGNIFICANTLY ACCURATE )

Patel et al., Medscape,2011 Quellette et al., Medscape 2011

Rules for Predicting the Probability of Embolism* Variable Risk factors Clinical signs and symptoms of deep venous thrombosis An alternative diagnosis deemed less likely than pulmonary embolism Heart rate > 100 beats/min Immobilization or surgery in the previous 4 wk Previous deep venous thrombosis or pulmonary embolism Hemoptysis Cancer (receiving treatment, treated in the past 6 mo or palliative care) Clinical probability Low Intermediate High *Adapted from Wells et al 3.0 3.0 No. of points

1.5 1.5 1.5 1.0 1.0

<2.0 2.0-6.0 >6.0

SUPPORTIVE DIAGNOSTIC MODALITIES


PE
CHEST RADIOGRAPHY ECG ECHOCARDIGRAPHY V/Q SCANING CT SCANING MRI ANGIOGRAPHY

DVT
COMPRESSIVE SONOGRAPHY IMPEDANCE PLETHYSMOGRAPHY SCINTIGRAPHY CT VENOGRAPHY MRI, NUCLEAR IMAGING VENOGRAPHY

Quellette et al., PE Work up, Medscape,2011

LABORATORIUM EVALUATION
D DIMER TROPONIN BRAIN NATRIURETIC PEPTIDE (BNP) GAS ANALYSE BIOMARKERS FOR VTE OTHER RISK FACTORS

D-dimer testing has been proposed as a non-invasive, inexpensive, rapid, and simple test in the evaluation of suspected VTE. D-dimer assays detect the presence of plasmin-mediated degradation products of fibrin. Levels increase following a thrombotic event with normalization within 15 to 20 days. Recent trauma or surgery, cancer, intravascular coagulation, serious infection, and other conditions can elevate D-dimer levels so D-dimer assays are typically sensitive but not specific.

Different D-dimer assays have been developed. There is no standard D-dimer level, the units of measure vary, the data from one test cannot be transferred to another, and each laboratory needs to establish and validate cut-off points for the test(s) they are using.
Measurement of systemic D dimer, an index of ongoing thrombus formation and lysis, can aid clinical diagnosis in venous thromboembolic conditions.

Smith et al., Technology Assessment Committee, 2003

RECOMMENDED DIAGNOSTIC STRATEGIC : DIAGNOSTIC ALGORITHM


HEMODYNAMIC STATUS CO-MORBIDITIES ONSET OF THE SYMPTOMS AVAILABILITIES

Riedel, Postgrad Med.,2004

Suspected Pulmonary Embolism New or worsening dyspnea, chest pain or sustained hypertension without another obvious cause Clinical probability assesment

Hemodynamically stable

Hemodynamically unstable

Low or intermediate clinical probability D-dimer testing

High clinical Probablility

Not critically

Critically ill and high clinical probability

Multidetector CT available Normal Elavated Multidetector CT

Multidetector CT available Transthoraric or transesophageal echocardiography

Pulmonary embolism ruled out

Negative

Pulmonary embolism confirmed

Pulmonary embolism confirmed

No right ventric -cular dysfunction Search for Alternative diagnosis

Treatment and secondary prevention of VTE


VTE event

Acute

Continue

Heparin or LMWH together with a VKA (e.g. warfarin) until an INR of 2.0-3.0 is achieved

VKA (e.g. warfarin) INR 2.0-3.0

VTE - treatment options

Acute

Long-term

Anticoagulation - UFH/LMWH Thrombolysis Thrombectomy Inferior vena cava filters (IVCF)

Anticoagulation - VKAs (e.g. warfarin) - LMWH Stockings

7th ACCP recommendations - Initial treatment for acute DVT or PE


Confirmed DVT or non-massive PE Initial treatment with sc LMWH or iv UFH (or sc if DVT)
[Grade 1A] for at least 5 days [Grade 1C]

Start VKA with LMWH or UFH on day 1 [Grade 1A] Stop LMWH or UFH when INR stable >2.0 [Grade 1A] High clinical suspicion of VTE
Anticoagulation until outcome of diagnostic
tests [Grade 1C+]

Bller H et al. Chest 2004;126:401S428S

Treatment and secondary prevention of VTE


VTE event Decision point

Acute

Continue

How long? 3-6-12 months or lifelong Risk of VTE (5-7%/year) vs. Risk of bleeding (3-4%/year)

Heparin or LMWH VKA (e.g. warfarin) together with a INR 2.0-3.0 VKA (e.g. warfarin) untill an INR of 2.0-3.0 is achieved

7th ACCP recommendations - Long-term treatment for DVT or PE


First episode with a transient risk factor 3 months after distal or proximal DVT [Grade 1A] At least 3 months after PE [Grade 1A]

First episode of idiopathic DVT/PE VKA for at least 612 months [Grade 1A] but consider indefinite duration [Grade 2A] Two or more episodes of DVT/PE Suggest indefinite treatment [Grade 2A]
Target INR 2.5 (range 2.03.0) [Grade 1A]

Bller H et al. Chest 2004;126:401S428S

Long-term treatment of DVT


Recurrence rate of VTE in patients with DVT dependent on Underlying risk factors for DVT Duration of treatment
Decision regarding duration of treatment dependent on Underlying risk factors for DVT Risk of haemorrhage from oral anticoagulation Patient preference Numerous regimens studied to improve benefit of long-term treatment while reducing the dose

SUMMARY
DVT AND PE WERE A CONTINOUUM SPECTRUM OF SAME DISEASE WHICH SHARED COMMON RISK FACTORS AS WELL AS PATHOGENIC PROTHROMBOTIC STIMULUS CLINICAL PRESENTATION ALONE INSUFFICIENTLY ACCURATE, THEREFORE INCORPORATING INTO VALIDATED CLINICAL PROBABILITY SCORE LEAD TO MORE APPROPRIATE DIAGNOSTIC STRATEGIES TO ESTABLISH THE DIAGNOSIS OF DVT AND PE BEST CHOSEN AVAILABLE SUPPORTIVE DIAGNOSTIC MODALITIES AID CONFIRMATION THE EXISTENCE OF THE DISEASE (DVT,PE)