day 4 - presentasi vte, kuliah sm okt 2012

8/12/2019 Day 4 - Presentasi VTE, Kuliah Sm Okt 2012

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DIAGNOSIS OF DEEP VEIN THROMBOSIS

AND PULMONARY EMBOLISM

K Suega

Hematology Medical Oncology Division

Udayana Medical School,

Bali


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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


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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 PULMONARYDISEASE, 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


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LIFEBLOOD

THE

ThrombosisCHARITY

Venous thromboembolismTreatment and secondary prevention

Ulcus crurisChronic PE

PE

DVT

Post-thromboticsyndrome

Death

Deep veininsufficiency

Pulmonaryhypertension


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Deep vein thrombosis

Common femoral vein

Thrombus

KneeProximal

Distal


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PATHOGENESIS

Robert et al., Anesthesiology, 2004


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ETIOLOGY

PEVENOUS STASIS

HYPERCUAGULABLE STATE

IMMOBILITY

SURGERY AND TRAUMA

PREGNANCY

ORAL CONTRACEPTIVE

ESTROGEN REPLACEMENT

MALIGNANCY

HAREDITARY FACTORSACUTE MEDICAL ILLNESS

DVTINCREASED 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 YEARSCANCER

HISTORY OF PRIOR VTE

Alikhan et al., Arch Intern Med, 2004

Ramzi et al., AM Fam Physician ,2004Rugeri et al., Lancet 2001


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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


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PATHOPHYSIOLOGY

PERESPIRATORY COSENQUENSES

INCREASED ALV. DEAD SPACE

HYPOXEMIA

HYPERVENTILATION

HEMODYNAMIC CONSEQUENSES

PULMONARY VASC. RESISTENCE

RIGHT VENTRICULAR FAILURE

DVTVENOUS STASIS RESULTS IN AN

INCREASED BLOOD VISCOSITY

DECREASED WALL CONTRACTILITY

AND VEIN VALVE DYSFUNCTION

CHRONIC VENOUS INSUFFICIENCY

Glhaber et al.,Circulatin ,2003

Riedei et al.,Postgrad Med,2004

Patel et al., Medscape, 2011


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PHYSICAL EXAMINATION

PEMAY VARY, ATYPICALMOST 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)

DVTHOMAN SIGNODEMA

PAINFULL

TENDERNESS

DISCOLORATION OF SKIN

PHLEGMASIA CERULEA DOLENS

PHLEGMASIA ALBA DOLENS

( NO SINGLE OR COMBINED SIGNS

&SYMPTOMS IS SIGNIFICANTLY

ACCURATE )

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


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Rules for Predicting the Probability of Embolism*

Variable No. of points

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)

3.0

3.0

1.5

1.5

1.5

1.0

1.0

Clinical probabilityLow

Intermediate

High

6.0

*Adapted from Wells et al


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SUPPORTIVE DIAGNOSTIC MODALITIES

PE

CHEST RADIOGRAPHY

ECG

ECHOCARDIGRAPHYV/Q SCANING

CT SCANING

MRI

ANGIOGRAPHY

DVT

COMPRESSIVE SONOGRAPHY

IMPEDANCE PLETHYSMOGRAPHY

SCINTIGRAPHYCT VENOGRAPHY

MRI, NUCLEAR IMAGING

VENOGRAPHY

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


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LABORATORIUM EVALUATION

D DIMER

TROPONIN

BRAIN NATRIURETIC PEPTIDE (BNP)

GAS ANALYSEBIOMARKERS FOR VTE

OTHER RISK FACTORS


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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 increasefollowing 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


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RECOMMENDED DIAGNOSTIC

STRATEGIC : DIAGNOSTIC ALGORITHM

HEMODYNAMIC STATUS

CO-MORBIDITIES

ONSET OF THE SYMPTOMS

AVAILABILITIES

Riedel, Postgrad Med.,2004


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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

Pulmonary

embolism

confirmed

D-dimer testing

Critically ill and high

clinical probability

Not criticallyHigh clinical

Probablility

Negative

Multidetector

CT

Pulmonary

embolism

ruled out

Normal Elavated

Pulmonary

embolism

confirmed

Transthoraric or

transesophageal

echocardiography

Multidetector CT

available

Multidetector CT

available

Search forAlternative diagnosis

No right ventric

-cular dysfunction

T d d


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VTE event

Acute Continue

Treatment and secondary

prevention of VTE

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


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VTE - treatment options

Acute Long-term

Anticoagulation

- UFH/LMWH

Thrombolysis

Thrombectomy

Inferior vena cava filters (IVCF)

Anticoagulation

- VKAs (e.g. warfarin)

- LMWH

Stockings


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7thACCP 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

T t t d d


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VTE event

Acute Continue

Heparin or LMWH

together with a

VKA (e.g. warfarin)untill an INR of 2.0-3.0

is achieved

VKA (e.g. warfarin)

INR 2.0-3.0

3-6-12 months or lifelong

Decision point

Risk of VTE (5-7%/year)

vs.Risk of bleeding (3-4%/year)

How long?

Treatment and secondaryprevention of VTE


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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

7thACCP recommendations

- Long-term treatment for DVT or PE

Long term treatment of DVT


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Long-term treatment of DVT

Recurrence rate of VTE in patients with DVT dependent onUnderlying risk factors for DVT

Duration of treatment

Decision regarding duration of treatment

dependent onUnderlying 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


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SUMMARY

DVT AND PE WERE A CONTINOUUM SPECTRUM OF SAMEDISEASE WHICH SHARED COMMON RISK FACTORS AS WELL

AS PATHOGENIC PROTHROMBOTIC STIMULUS

CLINICAL PRESENTATION ALONE INSUFFICIENTLY

ACCURATE, THEREFORE INCORPORATING INTO VALIDATEDCLINICAL 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)


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day 4 - presentasi vte, kuliah sm okt 2012

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