Deep vein thrombosis Pulmonary embolism

EPIDEMIOLOGY

2 MILLION VENOUS THROMBOTIC EVENTS OR VTE 500,000 ARE DEEP VEIN THROMBOSIS 200,000 PULMONARY EMBOLISM

 OVER

150 YEARS, VIRCHOW POSTULATED THAT THROMBUS FORMATION AND PROPAGATION RESULTED FROM ABNORMALITIES

BLOOD FLOW VESSEL WALL BLOOD COMPONENTS

1. BLOOD FLOW- VENOUS STASIS ABNORMALITIES OF HAEMOORHEOLOGY AND TURBULENCE AT VESSEL BIFURCATIONS AND STENOTIC REGIONS

2. Vessel walls- impaired function of vessel wall Abnormalities in the endothelium, such as atherosclerosis, and associated vascular inflammation

3.Blood components- changes in blood constituents Abnormalities in coagulation and fibrinolytic pathways

 Initiated

by action of tissue factor (TF) in Factor VII after injury to vessels exposes the subendothelium and promotes platelet adhesion and aggregation to forma primary platelet plug

 The

process is completed by actions of multiple components and factors in the blood that generate thrombin, potent rateregulating enzyme, which interacts with fibrinogen and Factor XIII to form an insoluble clot

 Malignancies,

sustain venous damage (surgical procedure) there is up regulation of thrombin. TF, fibrin and thrombin have angiogenic properties that can interfere with tissue properties by degrading matrix metalloproteinases, promoting cell migration and enhancing metastasis.

 Tumors

up regulate the production of TF and plasminogen activator inhibitor-1 (PAI-1) again promoting generation of procoagulant activity

 In

addition to postsurgical reactions, there is increase in fibrinogen, Factor V, Factor VIII, and Von Willebrand factor which promote platelet adhesion and function

 Increases

platelet number, normal fibrinolytic response is blunted by the increase PAI-1 and thrombin, activable fibrinolysis inhibitor (TAFI)

 Fibrinolytic

system is non-functional following surgery Preventings degradation of fibrin

 Venous

stasis is the cornerstone of post operative thrombosis Results to platelet activation, promoting adhesions of platelets to endothelial cells lining the vessel, stressed to procoagulant mode These encourage the development of a thrombus

 The

most common type of VTE is DVT DVT is the formation of a blood clot in a deep vein, usually in a calf or thigh muscle

 Venous

return from the lower extremity is decreased by half during surgical procedures because of the impact of muscle relaxation from anesthetic agents Lower extremity blood flow has been shown to decrease to about 75% of the normal drainage flow immediately after surgery

 This

is an important reflection of virchows triad on the role of adequate vessel flow. This reduction in flow persists for about 14 days after surgery because of the loss of muscl pumping function in the legs

 The

major site of thrombus formation is the soleal venous sinuses of the calf

 Another

contributing factor to venous stasis during prolonged surgery is the use of tight packing of the intestines in the upper abdomen with obstruction of the underlying vena cava

 Thrombus/

clot embolizes to the lungs Mild PE, could be asymptomatic, or severe enough to cause an immediate cardiac attack

 AGE

>40 YEARS OLD OBESITY >20% ABOVE IDEAL WEIGHT PROLONGED SURGERY IMMOBILITY (PRE-, PERI-, POST OPERAITVE) PELVIC MALIGNANCY PRIOR VTE TRAUMA

 THOMBOPHILIA
DIABETES HEART

FAILURE PRIOR RADIATION CHRONIC OBSTRUCTIVE PULMONARY DISEASE VARICOSE VEINS SEPSIS ACUTE INFLAMMATORY DISEASE WITH IMMOBILIZATIOI\N

 Molecular

Hypercoagulable state

Deficiency anti thrombin Protein C Protein S Heparin cofactor II Factor V Leiden Prothrombin variant 20210A

 Antiphopholipid

antibodies

Lupus anticoagulant Anticardiolipin

Hyperhomocystinuria Dysfibrinogenemia Dec

plasminogen Dec Plasminogen activators Heparin-induced thrombocytopenia

 Pregnancy
Estrogen

therapy (OCP) Inflammatory bowel disease Nephrotic syndrome Hyperviscosity

Classically = calf pain, tenderness, swelling, redness and Homans sign

Overall sens/spec = 3-91% Unreliable for diagnostic decisions Up to 50% have none of these

Wells developed and tested a clinical prediction model for DVT

 Swelling

in one or both legs Pain or tenderness Warmth in the skin of the affected leg Red or discolored skin Visible surface veins Leg fatigue

Dyspnea, pleuritic pain and cough most common symptoms Tachypnea, rales and tachycardia most common signs

PE Assign Pretest Probability

 The

following were assigned a point value of 1 if present

Paralysis or plaster immobilization Bedrest > 3 d or surgery in past 4 wks Localized tenderness

Entire leg swollen Calf > 3cm larger than unaffected leg Pitting edema greater than unaffected leg Collateral superficial veins

Alternative diagnosis more likely than DVT = - 2 points Probability High ( 3), Moderate (1-2) or Low (0 or less) DVT risk: High 75%, Moderate 17%, Low 3%

 Single

most important step in the diagnosis of pulmonary embolism May be done based on clinical judgment or aided by a clinical scoring system Modified Wells Criteria is the most widely used and studied Reliably stratifies patients by likelihood of PE to allow selection of safe (<2% VTE risk if no anticoagulation) management strategy

 33

year old, female 4 major surgeries due to intestinal obstruction Prolonged surgery Immobilization post-operative Post blood transfusion

 Signs

and symptoms

On and off low grade fever of unknown origin Upper extremity pain and edema on the left, 7th post operative day Sudden onset of cough, chest pain, dyspnea tachycardia

 EKG CXR

arrythmia

 Drug

fever Thrombophlebitis

Venography
Invasive,

use of contrast dye Increased risk in patients with renal compromise

 I125 labeled

Fibrinogen scanning

It involves the intravenous injections of isotopelabeled fibrinogen, which is expected to be incorporated into the evolving thrombus and can be imaged by a scintillation scanner. Because of the use of isotopes, it is technically cumbersome and rarely used, despite many large studies

Plethysmography based on the principal of electrical resistance in specific areas of the body. When there is resistance to blood flow that is due to a thrombus, there is marked reduction in the electrical resistance over that vessel.

Impedance

Doppler Ultrasound Doppler ultrasound, often with computer color enhancement measurement of flow velocity in larger blood vessels. In this technique, a reflected sound signal is converted to both an audible form and visual image on a computer screen. In the presence of a thrombosis, there is a decrease in the reflected signal that can be heard or, more likely, can be visualized.

 Real-Time

Ultrasound Compression Ultrasound Duplex Doppler Ultrasound

real-time and Doppler methods in a procedure known as B mode visualize the vessel and identify any thrombus in it

 Light

Reflection Rheography Radioisotope Imaging Indirect Computed Tomography Venography

 Magnetic

Resonance Imaging/Magnetic Resonance Imaging Venography

differences in signal intensities to distinguish flowing blood from stagnant blood

 Nonimaging

Methods automated quantitative D-dimer assay

Blood test to measure fibrin degradation fragments generated by fibrinolysis Indicates thrombotic process Used as an adjunct to non-invasive testing

 Sensitive

d-dimer testing can rule out DVT in low-moderate risk patients

 With

symptoms of DVT Positive D Dimer

Goals To prevent PE Halt further thrombus formation Dissolve existing thrombus

Cornerstone

of DVT Dose adjusted IV unfractionated heparin which preventsbformation of new thrombi

 Bolus

dose of heparin: 5000-10000 U EV Initial maintenance dose of heparin: 32000 U EV per 24h by continuous infusion or 17000 U subcutaneously to be repeated after adjustment at 12h

 Adjust

dose of heparin at 6h according to normogram. Maintain aPTT 2 times the control Repeat aPTT 6 times every hour until in therapeutic range and then daily (see nomogram) Start warfarin 10mg at 24h and 10mg next day.

 Overlap

heparin and warfarin for at least 4

days Perform PT daily and adjust warfarin dose to maintain INR at 2.0-3.0 Continue heparin for a minimum of 5 days, then stop if INR has been in therapeutic range for at least 2 consecutive days.

 Continue

warfarin for 3 months and monitor PT daily until in therapeutic range, then 3 times during first week, twice weekly for 2 weeks , or until dose response is stable, and then every 2 weeks Obtain pretreatment hemoglobin level, platelet count, PT, and aPTT. Repeat platelet count daily until heparin stopped.

 Low

Risk > Hospitalized medical patients without risk factors > Surgical patients under age 40, surgery lasting < 30 minutes, no additional risk factors

Ambulatory leg exercises

Moderate risk >Hospitalized medical patients with one or more risk factors>>Low dose heparin >Surgical patients over age 40 having abdominal or thoracic surgery lasting > 30 minutes>>Lowdose heparin > Neurosurgery or others patients with high bledding risk-Intermittent pneumatic compression odf legs

High risk Hip fracture>> Warfarin(low dose regimen) Hip replacement >Warfarin(low dose regimen) or LMWH Knee replacement >>Warfarin(low dose regimen) and intermittent pneumatic compression of the legs Gynecology Malignancy Intermittent pneumatic compression of legs

 Bleeding