THROMBOEM-BOLISM

PRESENTED BY:-SHIPRA OMAR

M.PHARM(CLINICAL PHARMACY) 1st sem

SGRRITS, DEHRADUN

INTRODUCTION:- Thromboembolism/ deep vein thrombosis/ thromboembolic

disorder.

 deep vein thrombosis, is the formation of a blood clot (thrombus) within a deep vein.

In 1856, German pathologist Rudolf Virchow postulated the interplay of three processes resulting in venous thrombosis, now known as Virchow's triad a decreased blood flow rate (venous stasis) increased tendency to clot (hypercoagulability) and changes to the blood vessel wall.

CHAPTER 1:- (A) DEFINITION:-

Deep vein thrombosis is the formation of a blood clot in one of the deep veins of the body, usually in the leg, calf thigh etc.

(B):- EPIDEMOLOGY :-o About 1 in 1000 adults per year has DVT  inNorth American and European populations.o VTE is rare in children.

o Occurs generally due to deficiencies in protein S, protein C, and antithrombin.

o VTE is common, with an incidence of 25%. PE is now the commonest cause of maternal death, and deep vein thrombosis may result in not only PE but also subsequent morbidity.

o diagnosis is missed generally

Classification of level of VTE risk

Low risk Moderate risk High risk Highest risk

· Minor surgery in patients <40years with no additional riskfactors

· Surgery inpatients 40-60years with noadditional risk factors

· Minor surgeryin patients with additional risk factors

· Surgery inpatients >60years, or age 40-60 with additional risk factors (prior VTE, cancer, molecular hyper-coagulability)

· Surgery inpatients with multiple risk factors (age >40, cancer, prior VTE)

· Hip or knee arthroplasty, hip fracture surgery

· Major trauma, spinal cord injury

(C):- SIGHNS & SYMPTOMS:- Pain

Swelling

Redness or discolouration

Signs and symptoms alone are not sufficiently sensitive  to make a diagnosis, but when considered in conjunction with known risk factors  can help determine the DVT

Phlegmesia cerulea dolens is a very large and dangerous type of DVT.

It is characterized by an acute and almost total venous occlusion of the entire extremity outflow, including the iliac and femoral veins.

(D) CAUSES :-

Rudolf virchow has identified and given the causes and risk factors that play a kingpin role in the formation of emboli which furthur leads to thrombo embolism/ deep vein thrombosis.

(E) RISK FACTORS :- Cancer Broken leg/ hip Trauma Major surgery Prolonged immobility Inherited Congestive heart failure Unhealthy food habits, smoke, diabetes, hypertension

ACQUIRED:-

Old age Major surgery Inactivity and immobilization Pregnancy Combined oral contraceptives Obesity Polycythemia

polycythemia and polycythemia rubra vera)is a neoplasm in which the bone marrowmakes too many red blood cells. It may also result in the overproduction of white blood cells and platelets.

Most of the health concerns associated with polycythemia vera are caused by the blood being thicker as a result of the increased red blood cells

INHERITED :-

Antithrombin deficiency Protein C deficiency Protein S deficiency Factor V leiden Dysfibrinogenemia Non- O blood type

(F):- PATHOPHYSIOLOGY :- (ACC TO VIRCHOW TRIAD) :-

Stasis

Hypercoagulability

Injury to the vessel wallDamage to the vessel wall can be produced by direct trauma such as major hip or knee surgery, stab wounds or insertion of venous catheters, by direct invasion from cancer cells, or as a consequence of age. Support structures in vessel walls deteriorate with age, leading to weakness and a predisposition to damage from distension.

Injury to the vessel wall

Hypercoagulability

StasisStasis describes the slowing or even cessation of blood flow. This commonly occurs in veins as a result of immobility or paralysis and can lead to concentration and subsequent activation of coagulation factors. Stasis can also cause the vessel walls to become distended, resulting in endothelial damage.

Injury to the vessel wall

Stasis

HypercoagulabilityThe term hypercoagulability means an increased propensity to clot. Hypercoagulability can occur as a result of a genetic defect, stasis, malignancy or hormone changes such as during pregnancy, during administration of oral contraceptives or hormone replacement therapy.

(II):-

Coagulation system is called cascade consisting of proteins and different factors

DVT occurs due to the abnormalities in antithrombin factor and protein C

Arterial thrombosis is caused by RBCs and platelets that form plaque i.e.: heart attack

Venous thrombosis took place due to fibrin and WBCs

Followed by deposition of fibrin on the endothelial surface which generally prevents clotting

Followed by inflammation

It generally took place in the valves of veins

Due to hypoxemia

Abrupt blood flow and formation of ROS

DVT

OTHER RISK OF DVT: CTEPH It is the important cause of hypertension which leads to pulmonary

embolism

Unresolved thrombus becomes organized and fibrosed leading to obstruction to blood flow

If untreated leads to pulmonary hypertension, left ventricular dysfunction and is fatal to led to death of patient

HISTROY OF CTEPH:-Honey moon period:- exists during which the pulmonary hypertension exists. During this time hypertrophy of right ventricle took place in effort to maintain cardiac output in presence of increased pulmonary resistance.

PATHOLOGY Recurrent PTE in pulmonary artery

Organisation of these thrombi

Organization of thrombus due to slow blood flowIn obstructed pulmonary artery

Increased PVR

Pulmonary hypertension

OTHER RISK OF DVT: B) PULMONARY EMBOLISM When the thrombus or plaque deposits on the endothelial wall, it

restrict the flow of blood into the capillaries

When the plaque becomes hard

A fraction of plaque gets detached and travels with the blood to the heart and then goes to pulmonary veins leads to PE

Furthur leads to hypoxia

Decreased perfusion due to clot in vessel

Increases risk of heart attack and stroke

(G):- DIAGNOSIS:- ABG CXR-

ECG D-Dimer test CT angio Gold standard ECHO Physical examination

Hampton hump

Westermarck sign

i. PHYSICAL EXAMINATION

Decolouration Edema Pitting after pressure applied on calf Pain Ulceration

ii. ABG TEST (ARTERIAL BLOOD GAS)

An arterial blood gas (ABG) is a blood test that is performed using blood from an artery. It involves puncturing an artery with a thin needle and syringe and drawing a small volume of blood. The most common puncture site is the radial artery at the wrist but sometimes the femoral artery & other sites are used. The blood can also be drawn from an arterial catheter. 

iii.CXR TEST

Chest X-rayDone to check pulmonary embolism

A. Hamptons humpB. Westermarck sign

A. HAMPTONS HUMP:- Radiological test Opacification of lungs Dome shaped Lung embolism Named after the name of a scientist Otis Hampton (1940)

B. WESTERMARCK SIGN Radiography

Occurs due to obstruct blood flow in the lung

For detection and conformation of PE

iv. ECG:-

SI QIII TIII

Done to check arterial flutter, hypertension, hypoxia

Seen depression or elevation on T wave

1.

2.

3.

v. D-DIMER TEST & ULTRASONO GRAPHY:- A. ELISA B. LATEX & BLOOD AGGLUTION

vi. CT ANGIO:-

Painted blood vessel is filled in heart (either side) Clot in blood vessel can be determineA type of crystal study

vii. GOLD STANDARD:- Accurate test for PE Directly estimate the presence of emboli in the blood vessels Advantageous for d-dimer negetive result Invasive Rarely used May cause genetic risks May cause anaphylaxis Phelbitis (vein inflammation)

viii. ECHO:- By checking tricuspid valve To estimate right ventricular functioning If found

Increased frequency

High work load

Presence of clot any where in lungs

(G):- MANAGEMENT OF THERAPY

(H):- TREATMENT:- Anticoagulants are primarily used. For example:- heparin, caumarins (warfarin) Blood thinners can also be used. Example:- aspirin Thrombolytics used in case of stroke Act by dissolving the clot n preventing clot formation. IVC filters are used

ANTICOAGULANTS:- Heparin prevents extension of the thrombus

Heparin's anticoagulant effect is related directly to its activation of antithrombin III. Antithrombin III, the body's primary anticoagulant, inactivates thrombin and inhibits the activity of activated factor X in the coagulation process.

ANTICOAGULATION FOR FAST RECOVERY:-

Heparin products Heparin IV(unfractionated)

Heparin fractionated

Heparin IV Infused intravenously By drip For unstable patients Immediate use

CONTD.... Dose:- 80 unit/kg bolus 18 unit/kg after 80 units Quick action Disadvantage;-o Turned off if bleeding took placeo May cause heparin induced thrombocytopenia

Heparin fractionated :- Low molecular weight Given sub cutaneously Syn:- enoxiprin (lovanox)

dose;-o 1mg/kg for 12 houro If GFR is <30 then, 1mg/kg for 24 houro No blood level test needed to performo Stable patiento May cause incidence of hits

Superior bioavailability Superior or equivalent safety and efficacy Subcutaneous once- or twice-daily dosing No laboratory monitoring* Less thrombocytopenia Earlier/facilitated

ADVANTAGES OF LOW-MOLECULAR-WEIGHT HEPARIN OVER

STANDARD UNFRACTIONATED HEPARIN

B. WARFARIN:- For slow therapy Vitamin K antagonist Dose:- 5mg/day- 10mg/day Acton 2,7,9,10 factor In case of deficient protein C and S anticoagulants)- vitamin K

dependent Takes 2-3 days to takes speed Medication duration:- 3-6 months to 6-9 month

Disadvantage:- Cause interaction with antibiotics:- Kill bacteria- that produce vitamin K- decreased

vitamin K level- bleeding increased Interact with aspirin n cause internal bleeding

(I):- THROMBOLYTIC THERAPY:-

Advantages prompt resolution of symptoms, prevention of pulmonary embolism, restoration of normal venous circulation, preservation of venous valvular function, and prevention of postphlebitic syndrome

Disadvantage;- Clot propagation, Rethrombosis Subsequent Embolization Heparin therapy and oral anticoagulant therapy always must follow

a course of thrombolysis. Thrombolytic therapy is also not effective once the thrombus is

adherent and begins to organize The uncertainty regarding thrombolytic therapy likely will continue

(J):- SURGERY

when anticoagulant therapy is ineffective unsafe, contraindicated. The major surgical procedures for DVT are clot removal and partial interruption of the

inferior vena cava to prevent pulmonary embolism.

This patient underwent a thrombectomy. The thrombus has been laid over the approximate location in the leg veins where it developed.

(K):-IVC FILTERS:- Indications for insertion of an inferior vena cava filter Pulmonary embolism with contraindication to

anticoagulation Recurrent pulmonary embolism despite adequate

anticoagulation

Thank you

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