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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