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3: MED1 Y3 - Cardiovascular [2] > [12] Deep Vein Thrombosis > Flashcards

[12] Deep Vein Thrombosis Flashcards

1
Q

What is a DVT?

A

A venous thrombosus that develops in the deep veins of the body, most commonly the legs or pelvis

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2
Q

How can a DVT lead to a pulmonary embolism?

A

The clot may dislodge and travel to the lungs, causing a pulmonary embolism

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3
Q

What is very clinically important in DVT?

A

Early recognitin and appropriate treatment

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4
Q

What is meant by thrombosis?

A

The formation of a solid mass of blood from the constituents of blood within the circulatory system during life.

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5
Q

Is thrombosis the same thing as clotting?

A

No

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6
Q

What are the three fundamental predisposing factors to thrombosis known as?

A

Virchow’s triad

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7
Q

What is Virchow’s triad?

A
  • Abnormalities to the flow of blood
  • Abnormalities to the blood vessel wall
  • Abnormalities of the constituents of blood
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8
Q

Give two examples of when there are abnormalities to the flow of blood?

A
  • Stagnation
  • Turbulence
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9
Q

Give 3 examples of where there are abnormalities to the blood vessel wall

A
  • Atheroma
  • Direct injury
  • Inflammation
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10
Q

Give three examples of where there may be abnormalities of the constituents of blood

A
  • Smokers
  • Post-partum
  • Post-op
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11
Q

How does the development of venous thrombosis differ from arterial thrombosis, regarding Virchow’s triad?

A

It seems that in venous thrombosis, blood vessel damage is less of a factor than in arterial thromosis

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12
Q

How does a venous thrombosis form?

A

The beginning of a venous thrombosis is thought to be caused by tissue factor, which leads to the conversion of prothrombin to thrombin, and then thrombin causing the conversion of fibrinogen to fibrin

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13
Q

How do venous thrombi appear?

A

As soft, gelatinous, and deep red

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14
Q

How does the cell content of venous thrombi compare to that of arterial?

A

It is higher

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15
Q

What are the risk factors for DVT?

A
  • Previous history of VTE
  • Family history of VTE
  • Cancer
  • Age >60
  • Immobilisation
  • Smoking
  • BMI over 30
  • Male gender
  • Acquired or familial thrombophilia
  • Heart failure
  • Varicose veins
  • Trauma to the vein, or chronic low grade injury e.g. vasculitis, stasis, chemotherapy
  • COCP or HRT
  • Pregnancy
  • Dehydration
  • Antiphospholipid syndrome
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16
Q

Why is the clinical diagnosis of DVT very difficult?

A

It is often missed, and many DVTs progress to PE without the DVT being clinically apparent, and in those with classic clinical signs, only about 1/3 have DVT

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17
Q

What are the classical clinical features of DVT?

A
  • Limb pain and tenderness along the line of the deep veins
  • Swelling of the calf or thigh
  • Pitting oedema
  • Distention of superficial veins
  • Increase in skin temperature
  • Skin discolouration
  • Palpable cord
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18
Q

Is swelling of the calf or thigh usually unilateral or bilateral in DVT?

A

Unilateral

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19
Q

What colour might the skin be in DVT?

A

Erythematous, or occassionally purple/cyanosed

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20
Q

What is a palpable cord?

A

A hard, thickened, palpable vein

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21
Q

What condition can sometimes complicate a diagnosis of DVT?

A

Cellulitis

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22
Q

Why can cellulitis sometimes complicate a diagnosis of DVT?

A
  • Severe signs of DVT can resemble cellulitis
  • Secondary cellulitis may develop with a primary DVT
  • Primary cellulitis may be followed by a secondary DVT
  • Superficial thrombophlebitis may hide an underlying DVT
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23
Q

What are the differential diagnoses of DVT?

A
  • Trauma
  • Superficial thrombophlebitis
  • Post-thrombotic syndrome
  • Peripheral oedema
  • Heart failure caused by heart failure, cirrhosis, or nephrotic syndrome
  • Arteriovenous fistula and congenital vascular abnormalities
  • Vasculitis
  • Ruptured Baker’s cyst
  • Cellulitis
  • Septic arthritis
  • Compartment syndrome
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24
Q

What has been developed as a result of the unreliability of the clinical features of DVT?

A

Several diagnostic scoring systems

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25
Q

What do diagnostic scoring systems for DVT do?

A

Classify patients as having high, intermediate, or low possibility of developing DVT, based on history and clinical examination

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26
Q

What scores 1 point on the Well’s score?

A

Each of;

  • Entire leg swollen
  • Calf swelling by more than 3cm compared with asymptomatic leg (measured 10cm below tibial tuberosity)
  • Pitting oedema confined to symptomatic leg
  • Localised tenderness along the distribution of the deep venous system (such as the back of the calf)
  • Recently bedridden for three days or more, or major surgery within the previous 12 weeks requiring general or regional anaesthesia
  • Previously documental DVT
  • Collateral superficial veins
  • Active cancer
  • Paralysis, paresis, or recent plaster immobilization of the legs
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27
Q

What do you do if an alternative cause is at least as likely as DVT in the Well’s score?

A

Subtract 2 points

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28
Q

What Well’s score indicates that DVT is likely?

A

2 or more

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29
Q

What should all patients in whom DVT is suspcted, and with a Well’s score of 2 or more be offered?

A

A proximal leg vein ultrasound scan within 4 hours, and then a D-dimer test if the result is negative

or

A D-dimer with interim 24-hour dose of parenteral anticoagulation if an ultrasound scan cannot be carried out within 4 hours. This should be followed by an ultrasound scan within 24 hours

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30
Q

What should all patients in whom DVT is suspected with a Well’s score of 0 or 1 be offered?

A

A D-dimer test

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31
Q

What should patients with suspected DVT, Well’s score of 0 or 1, and a positive D-dimer test be offered?

A

A proximal leg ultrasound scan.

If the ultrasound scan is not available within 4 hours, an interim 24-hour dose of parenteral anticoagulant should be offered

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32
Q

What should DVTs be diagnosed and treated on the basis of?

A

A positive proximal leg vein ultrasound scan

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33
Q

What are D-dimers?

A

Specific cross-linked products of fibrin degradation

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34
Q

How are D-dimers used diagnostically in DVT?

A

They are raised in VTE, with a high sensitivity but poor specificity

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35
Q

Why does D-dimer testing have a poor specificity?

A

Because high concentrations occur in other disorders, such as malignancy, pregnancy, and other conditions where clots form, such as after surgery

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36
Q

What should all patients diagnosed with an unprovoked DVT or PE be offered?

A

Investigations for cancer,

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37
Q

What investigations for cancer should be offered in patients who have had an unprovoked DVT or PE?

A
  • Physical examination
  • CXR
  • Blood tests - FBC, calcium, LFTs
  • Urinalysis

Consider further investigations, e.g. abdomino-pelvic CT scan, mammogram, in all patients over 40

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38
Q

Give two examples of specific conditions that cause DVT that you might choose to test for while investigating a cause

A
  • Antiphospholipid syndrome
  • Hereditary thrombophilia
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39
Q

How quickly should people who are likely to have a DVT be assessed and managed?

A

Same day

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40
Q

What should be offered to patients with confirmed proximal DVT or PE?

A

LMWH or fondaparinux

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41
Q

What should be taken into account when offering patients with confirmed proximal DVT or PE LMWH?

A

Co-morbidities and contraindications

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42
Q

How quickly should LMWH be started in patients with confirmed proximal DVT or PE?

A

As soon as possible

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43
Q

How long should LMWH be continued for in patients with confirmed DVT or PE?

A

At least 5 days, or for those starting warfarin until INR is 2 or above for at least 24 hours - whichever is longer

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44
Q

How soon after confirmed DVT or PE should oral anticoagulants be offered?

A

Within 24 hours after diagnosis

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45
Q

How long after DVT or PE should oral anticoagulation be continued?

A

3 months

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46
Q

What are the options for oral anticoagulation in DVT/PE?

A
  • Warfarin
  • Rivaroxiban
  • Dabigatran
  • Apixiban
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47
Q

What should be done 3 months after starting oral anticoagulation for DVT/PE?

A

Should assess the risks and benefits of continuing anticoagulant treatment

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48
Q

When should you consider continuing oral anticoagulation beyond 3 months after DVT/PE?

A

In patients with unprovoked proximal DVT if their risk of VTE is high, and there is no additional risk of major bleeding

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49
Q

What is heparin?

A

Heparin is a injectable, rapidly acting anticoagulant that is often used acutely to interfere with the formation of thrombi

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50
Q

How does heparin occur naturally?

A

As a macromolecule complexed with histamine in mast cells

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51
Q

What is the physiologic role of heparin?

A

Unknown

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52
Q

What is heparin used for?

A
  • Prevention of venous thromboembolism
  • Treatment of a variety of thromboembolic diseases, such as pulmonary embolism and acute MI
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53
Q

What is unfractionated heparin?

A

A mixture of straight chain, anion glycosaminoglycans with a wide range of molecular weights

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54
Q

Why is unfractionated heparin strongly acidic?

A

Because of the presence of sulfate and carboxylic acid groups

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55
Q

What is LMWH also known as?

A

Enoxaparin

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56
Q

What is LMWH?

A

A heterogenous group of compounds that are 1/3 of the size of unfractionated heparin

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57
Q

How is LMWH produced?

A

By chemical or enzymatic depolymerisation of unfractionated heparin

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58
Q

What is the advantage of heparin over LMWH?

A

Speedy onset of action

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59
Q

Why are LMWH becoming the preferred agent over heparin?

A
  • They can be conveniently injected subcutaneously on a patient weight-adjusted basis
  • They have predictable therapeutic effects
  • They have a more predictable pharmacokinetic profile
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60
Q

What is the result of LMWH being more predictable?

A

They do not need the same intense monitoring that heparin needs, subsequently saving laboratory costs as well as nursing time and costs

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61
Q

What is the mechansim of action of heparin?

A

Heparin acts at a number of molecular targets, but it’s anticoagulant effect is a consequence of binding to antithrombin III, with the subsequent rapid inactivation of coagulation factors

It also acts as a catalyst for the interaction antithrombin III and activated coagulation factors

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62
Q

What happens when heparin binds to antithrombin III?

A

Heparin induces a conformational change in antithrombin III which accelerates it’s rate of action by about 1000x

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63
Q
A
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64
Q

What is the result of the heparin acting as a catalyst for the interaction of antithrombin III and activated coagulation factors?

A

It allows antithrombin III to rapidly combine with, and inhibit, circulating thrombin and factor Xa

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65
Q

What is the mechanism of action of LMWH?

A

They complex with antithrombin III to inactive factor Xa, but this complex does not bind as avidly to thrombin

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66
Q

What is the result of LMWH not causing as much inhibition to thrombin as heparin?

A

LMWHs are less likely to activate resting platelets

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67
Q

What is antithrombin III?

A

An alpha-globulin

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68
Q

What does antithrombin III do>?

A

Inhibits serine proteases, including several clotting factors, including thrombin (IIa) and factor Xa

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69
Q

How does antithrombin III act in the absence of heparin?

A

It interacts very slowly with thrombin and factor Xa

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70
Q

What are the therapeutic applications of heparin?

A
  • Anti-thrombotic drug for the treatment of acute DVT and PE. Also decreases the incidence of recurrent thromboembolic episodes.
  • Prophylaxis to prevent post-operative venous thrombosis in patients undergoing elective surgery, and those in acute phase of MI
  • Preventing thrombosis in extra-corpreal devices, e.g. dialysis machine
  • Anticoagulation in pregnant women with prosthetic heart valves or VTE
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71
Q

Why is heparin used in the anticoagulation of pregnant women?

A

Because it does not cross the placenta, due to it’s large size and negative charge

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72
Q

What is the chief complication of heparin use?

A

Haemorrhage

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73
Q

What is required to minimise the problem of haemorrhage with heparin?

A

Careful monitoring of bleeding time

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74
Q

How is excessive bleeding caused by heparin administration managed?

A

Cessation of the drug, or with administration of protamine sulfate

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75
Q

How does protamine sulfate work?

A

When infused slowly, it combines ionically with heparin to form a stable 1:1 inactive complex.

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76
Q

How is protamine sulfate administered?

A

IV

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77
Q

How long does the onset of action of protamine sulfate normally take?

A

5 minutes

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78
Q

What does of protamine sulfate is administered?

A

1mg of protamine sulfate per 100 units of heparin

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79
Q

Why is it very important to titrate the dose of protamine sulfate?

A

Because protamine sulfate is a weak anticoagulant, so excess amounts may trigger bleeding episodes, or worsen bleeding potential

80
Q

Other than bleeding potential, what are the adverse effects of protamine sulfate?

A
  • Hypersensitiivty
  • Thrombocytopenia
  • Abnormal liver function tests
  • Osteoporosis in long-term therapy
81
Q

How long does the anticoagulation effect of heparin take?

A

It occurs within minutes of IV administration, or 1-2 hours after SC injection

82
Q

When does the maximum anti-factor Xa activity of LMWH occur?

A

About 4 hours after SC injection

83
Q

How is heparin administered?

A

It must be given parenterally, either by SC injection or IV

84
Q

Why must heparin be administered parenterally?

A

Because it does not readily cross membranes

85
Q

How is immediate anticoagulation achieved with heparin?

A

Administration in an IV bolus

86
Q

What is given after immediate anticoagulation is achieved using an IV bolus?

A

Lower doses, or a continuous infusoin of heparin, for 7-10 days

87
Q

How is the dose of heparin titrated after a DVT/PE?

A

It is titreated so the aPTT is 1.2-2.5% normal

88
Q

How are LMWH administered?

A

SC

89
Q

Is it necessary to monitor aPTT with LMWH?

A

Not usually

90
Q

Why is it not usually necessary to monitor aPTT with LMWHs?

A

As the plasma levels and pharmacokinetics are predictable

91
Q

What happens to heparin in the blood?

A

It binds to many proteins that neutralise it’s activity

92
Q

What results from heparin binding to proteins that neutralise it’s activity in the blood?

A
  • Resistance to the drug
  • Unpredictable pharmacokinetics
93
Q

In which patients is heparin binding to plasma proteins variable?

A

Patients with thromboembolic diseases

94
Q

Where does heparin distribute in the body?

A

It is generally restricted to the circulation

95
Q

How is heparin inactivated in the body?

A

It can be taken up by the monocyte/macrophage system, where it undergoes depolymerisation and desulfation to inactive products

96
Q

What is the result of heparin being inactived by the monocyte/macrophage system?

A

Heparin has a longer half-life in patients with hepatic impairment

97
Q

How is heparin, LMWH, and inactive metabolites excreted from the body?

A

Urine

98
Q

What is the result of heparin and LMWH being excreted to urine?

A

Renal insufficient prolongs the half life

99
Q

What is the half life of heparin?

A

1.5 hours

100
Q

What is the half life of LMWH?

A

3-7 hours

101
Q

Does heparin dose need to be adjusted in renal impairment?

A

Yes

102
Q

What is warfarin?

A

A coumarin anticoagulant that antagonises the cofactor function of vitamin K

103
Q

Why is the clinical use of warfarin decreasing?

A

Because of the increasing availability of LMWHs and platelet aggregate inhibitors, which are preferred due to the potential morbidity assocatied with the use of warfarin

104
Q

What monitoring is required in warfarin?

A

Careful monitoring of INR

105
Q

Does careful monitoring of INR in warfarin prevent bleeding complications?

A

No, not in many patients

106
Q

How is vitamin K involved in coagulation?

A

Several of the protein coagulation factors require vitamin K cofactor dependent post-translational modification

107
Q

Which protein coagulation factors require vitamin K as a cofactor?

A
  • II
  • VII
  • IX
  • X
108
Q

What happens in vitamin K cofactor dependent post-translational modification?

A

A number of the protein coagulation factors’ glutamic acid resiudes are carboxylated to form gamma-carboxyglutamic acid residues

109
Q

What is the importantance of gamma-carboxyglutamic acid residues on coagulation factors?

A

They bind calcium ions, which are essential for the interaction between the coagulation factors and platelet membranes

110
Q

What happens in the carboxylation reaction of protein coagulation factors?

A

Vitamin-K dependant carboxylase adds CO2 to form a COOH group on glutamic acid. The reduced vitamin K cofactor is converted to vitamin K epoxide in the reaction

111
Q

How is vitamin K regenerated from vitamin K epoxide?

A

By the enzyme vitamin K epioxide reductase

112
Q

What is the clinical importance of vitamin K epoxide reductase?

A

This is the enzyme that warfarin inhibits

113
Q

What does warfarin treated result in, in terms of clotting factors?

A

The production of clotting factors with reduced activity (10-40% normal) due to the lack of sufficient gamma-carboxyglutamic acid side chains

114
Q

How long does it take for warfarin to take effect?

A

The effects of warfarin are not seen for 8-12 hours after drug administration, and peak effects may be delayed by 72-96 hours

115
Q

Why is the onset of action of warfarin delayed?

A

As this is the time it takes to deplete the pool of circulating clotting factors

116
Q

How can the anticoagulation effects of warfarin be overcome?

A

Administration of vitamin K

117
Q

How long does vitamin K reversal of warfarin action take?

A

24 hours

118
Q

Why does vitamin K reversal of warfarin take 24 hours?

A

Because this is the time necessary for the degradation of already synthesised clotting factors

119
Q

What are the indications for warfarin therapy?

A
  • DVT and PE
  • Atrial fibrillation
  • Mechanical prosthetic valves
  • Thrombosis associated with inherited thrombophilia conditions
  • Cardiac thrombus
  • CVA, especially with AF
  • Cardiomyopathy
120
Q

What is the principle adverse effect of warfarin?

A

Haemorrhage

121
Q

What is important as a result of the risk of haemorrhage on warfarin?

A

To frequently monitor and adjust the anticoagulnt effect

122
Q

How can minor bleeding on warfarin be manged?

A

Withdrawl of the drug and administration of oral vitamin K

123
Q

How is severe bleeding on warfarin managed?

A

Greater doses of vitamin K given IV

Whole blood, frozen plasma, and plasma concentrates of blood factors may also be used for rapid reversal

124
Q

Give 2 rare complications of warfarin

A
  • Skin lesions
  • Necrosis
125
Q

What is purple toe syndroem?

A

A painful, blue-tinged discolouration of the toe caused by cholesterol emboli from plaques, which has been observed with warfarin therapy

126
Q

What factors can alter warfarins therapeutic response?

A
  • Drugs
  • Changes in environment
  • Diet
  • Physical state
127
Q

By what mechanisms can drugs increase the action of warfarin

A
  • Inhibition of hepatic metabolism
  • Inhibition of platelet function
  • Reduction of vitamin K from gut bacteria
  • Albumin displacement
  • Decrease GI absorption of vitamin K
128
Q

Give 5 drugs that inhibit hepatic metabolism to interact with warfarin

A
  • Amiodarone
  • Quinolone
  • Metronidazole
  • Cimetidine
  • Alcohol (acute intoxication)
129
Q

Give an example of a drug that inhibits platelet function to interact with warfarin

A

Aspirin

130
Q

Give an example of a drug that reduces vitamin K from gut bacteria to interact with warfarin

A

Cephalosporin antibiotics

131
Q

Give an example of a drug that causes albumin displacement to interact with warfarin

A

NSAIDs

132
Q

How do drugs that cause albumin displacement or decrease the GI absorption of vitamin K vary in their interaction compared to other mechanisms?

A

They have less of an effect

133
Q

Give 3 examples of drugs that inhibit the action of warfarin?

A
  • Anti-epileptics, except sodium valproate
  • Rifampicin
  • St Johns Wort
134
Q

How do drugs that inhibit the action of warfarin do so?

A

Most of these drugs work by inducing hepatic enzymes, thereby increasing the metabolism of warfarin

135
Q

What disease states can affect the therapeutic action of warfarin?

A
  • Vitamin K deficiency
  • Hepatic diseases that impair synthesis of clotting factors or affects warfarin metabolism
  • Hypermetabolic setates
  • Neoplastic disease
  • Hyperlipidaemia
  • Hypothyroidism
136
Q

What are the contraindications to warfarin use?

A

Pregnancy

137
Q

Why should warfarin never be used in pregnancy?

A

Because it is teratogenic, and can cause abortion of birth defects

138
Q

What should be used instead of warfarin if anticoagulant therapy is needed during pregnancy?

A

Heparin or LMWH

139
Q

Is warfarin rapidly absorbed after oral administration?

A

Yes

140
Q

What is the oral bioavailability of warfarin?

A

100%

141
Q

What effect does food have on the absorption of warfarin?

A

It may delay absorption, but it does not affect the extent of absorption

142
Q

What % of warfarin is bound to plasma albumin?

A

99%

143
Q

What is the result of the high protein binding of warfarin on its distribution?

A

It prevents diffusion into CSF, urine, and breast milk

144
Q

Can warfarin be displaced from it’s albumin binding site?

A

Yes, drugs that have a higher affinity for the binding site can displace it

145
Q

What happens when warfarin is displaced from it’s albumin binding sites by drugs with a higher affinity?

A

It leads to a trasient elevated activity

146
Q

What problems can drugs that affect warfarin binding to plasma proteins cause?

A

Drug interactions and viability in the therapeutic response to warfarin

147
Q

What is the half-life of warfarin?

A

The average half life is about 40 hours, but this is highly variable among individuals

148
Q

How is warfarin metabolised?

A

By the CYP450 system

149
Q

What is warfarin metabolised to?

A

Inactive metabolites

150
Q

What happens to the inactive metabolites of warfarin?

A

After conjugation to glucuronic acid, they are excreted in uine and faeces

151
Q

What is INR?

A

A measure adopted to measure warfarin concentration

152
Q

What is the purpose of measuring warfarin using INR?

A

It corrects for variations that would occur with various thromboplastin reagents, among difficult hospitals or the same hospital when they recieve new batches of reagent

153
Q

Why is it important INR is maintained within the optimal range?

A

Because warfarin has a narrow therapeutic index

154
Q

Other than INR, what can be used to measure warfarin therapy?

A

The prothrombin time

155
Q

What is prothrombin time a measure of?

A

The extrinsic pathway

156
Q

What INR range should be aimed for in DVT?

A

2.0-3.0

157
Q

What INR range should be aimed for in atrial fibrillation?

A

2.0-3.0

158
Q

What INR range should be aimed for in atrial fibrillation?

A

2.0-3.0

159
Q

What INR range should be aimed for in mechanical prosthetic valves?

A

2.5-4.5

160
Q

What INR range should be aimed for in patients with recurrent thrombosis on warfarin?

A

2.5-4.5

161
Q

What INR range should be aimed for in thrombosis associated with inherited thrombophilia conditions?

A

2.5-4.5

162
Q

How should should warfarin therapy be continued for after DVT?

A

3-6 months

163
Q

How should should warfarin therapy be continued for after PE?

A

6 months

164
Q

How should should warfarin therapy be continued for in atrial fibrillation?

A

Until risk > benefit

165
Q

What is rivaroxiban?

A

An oral anticoagulant medication

166
Q

What is the mechanism of action of rivaroxiban?

A

It is a highly selective inhibitior of both free factor Xa and factor Xa bound to the prothrombinase complex. Through this, it interrupts the intrinsic and extrinsic pathway of the blood coagulation cascade, inhibiting thrombin formation and the development of thrombi

167
Q

What is the advantage of rivaroxiban over warfarin?

A

It provides predictable anticoagulation, so dose adjustment, routine coagulation monitoring, and dietary restrictions are not needed

168
Q

What is the most serious adverse effect of rivaroxiban?

A

Bleeding, including severe internal bleeding

169
Q

How does the bleeding risk of rivaroxiban compare to warfarin?

A

It is associated with higher risks of bleeding in the GI tract

170
Q

Is there an antidote for rivaroxiban?

A

No

171
Q

What is the problem with there not being an antidote for rivaroxiban?

A

Serious bleeding may be more difficult to manage

172
Q

In what patients does rivaroxiban have predictable pharmacokinetics?

A

A wide spectrum of patients, irrespective of age, gender, weight, and race

173
Q

Over what dose range does rivaroxiban have a flat rose response?

A

5-40mg

174
Q

How long does the effects of rivaroxiban last for?

A

Approx 8-12 hours, but factor Xa activity does not return to normal within 24 hours

175
Q

What is the result of factor Xa not returning to normal under 24 hours after rivaroxiban?

A

Dose daily dosing is possible

176
Q

How are DVTs prevented?

A
  • Avoid dehydration
  • Encourage early mobilisation
  • Stop oral contraceptives or HRT containing oestrogen 4 weeks before surgery
  • Mechanical prophylaxis
  • Pharmacological prophylaxis
177
Q

Wbat is the purpose of vena cava filters?

A

They stop a DVT developing into a PE

178
Q

When should a temporary inferior vena cava filter be considered?

A

In patients with very high risk of VTE, if there are contraindications to pharmacological and mechanical prophyalxis

179
Q

What can be used in the mechanical prophylaxis of DVT?

A
  • Graduated compression stockings
  • Intermittent pneumatic compression
  • Foot impulse devices
180
Q

How can graduated copmresion stockings be used to decrease the risk of DVT?

A

Either alone or in combination with pharmacological prophylaxis in high risk patietns

181
Q

Should graduated compression stockings be used routinely for surgical inpatients?

A

Yes

182
Q

What should staff members trained in the use of compression do when a patient is given compression stockings?

A
  • Show the patient how to wear them correctly
  • Monitor their use
  • Provide assistance when needed
183
Q

How long should patients be advised to wear graduated compression stockings for?

A

From admission until they return to their normal level of mobility

184
Q

Give two conditions where the use of graduated compression stockings is contraindicated?

A
  • Established PVD
  • Diabetic neuropathy
185
Q

When can intermittent pneumatic compression or foot impulse devices be used?

A

Instead of, or as well as, graduated compression stockings while patients are in hospital

186
Q

How long should intermittent pneumatic compression or foot impulse devices be used for?

A

As long as possible before surgery

187
Q

What are the options for pharmacological prophylaxis of DVT?

A
  • Fondaparinux sodium
  • Low molecular weight heparin, or synthetic alternatives
  • Unfractionated heparin
188
Q

What should the choice of pharmacological prophylaxis for DVT depend on?

A
  • Co-morbidities, e.g. CKD
  • Patient’s wishes
  • Local policies
189
Q

What should always be considered when giving thromboprophylaxis?

A

The risk of bleeding

190
Q

What is the recurrence rate of first episode DVT or PE without anticoagulation?

A

50%

191
Q

What is the most serious complication of DVT?

A

PE

192
Q

In what kind of DVT is the risk of PE higher?

A

Proximal PE

193
Q

What is post-thrombotic system?

A

Chronic venous hypertension

194
Q

What can post-thrombotic system result in?

A
  • Pain
  • Swelling
  • Hyperpigmentation
  • Dermatitis
  • Ulcers
  • Gangrene
  • Lipodermatosclerosis
195
Q

Why might post-thrombotic syndrome develop after DVT?

A

Due to damage to the deep veins and their valves

196
Q

What % of DVT patients are affected by post-thrombotic syndrome?

A

20-40%

197
Q

What are the risk factors for post-thrombotic syndrome?

A
  • Older age
  • Obesity
  • History of previous ipsilateral DVT
  • Iliofemoral location of DVT
  • Failure to recover promptly from acute symptoms
  • Insufficient quality of oral anticoagulant therapy

3: MED1 Y3 - Cardiovascular [2] (19 decks)

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