1. Table 27.1 Risk factors for arterial thrombosis
(atherosclerosis).
Positive family history
Male sex
Hyperlipidaemia
Hypertension
Diabetes mellitus
Gout
Polycythaemia
Hyperhomocysteinaemia
Cigarette smoking
ECG abnormalities
Elevated CRP, IL6, fibrinogen, lipoprotein-associated
phospholipase A2
Lupus anticoagulant
Collagen vascular diseases
Behçet’s disease
CRP, C-reactive protein; ECG, electrocardiogram.
Table 27.2 Hereditary and acquired risk
factors for venous thrombosis.
Hereditary haemostatic disorders
Factor V Leiden
Prothrombin G20210A variant
Protein C deficiency
Antithrombin deficiency
Protein S deficiency
Dysfibrinogenaemia
ABO blood group
Hereditary or acquired haemostatic disorders
Raised plasma levels of factor VIII
Raised plasma levels of fibrinogen
Raised plasma levels of homocysteine
Acquired disorders
Lupus anticoagulant
Oestrogen therapy (oral contraceptive and HRT)
Heparin-induced thrombocytopenia
Pregnancy and puerperium
Surgery, especially abdominal, hip and knee
surgery
Major trauma
Malignancy
Acutely ill hospitalized medical patients
including cardiac or respiratory failure,
infection, inflammatory bowel disorders
Myeloproliferative disease
Hyperviscosity, polycythaemia
Stroke
Pelvic obstruction
Nephrotic syndrome
Dehydration
Varicose veins
Age
Obesity
Paroxysmal nocturnal haemoglobinuria
Behçet’s disease
HRT, hormone replacement therapy.

2. Table 27.3 Clinical associations of lupus
anticoagulant and anticardiolipin antibodies.
Venous thrombosis: deep venous thrombosis/
pulmonary embolism, renal, hepatic, retinal veins
Arterial thrombosis
Recurrent fetal loss
Thrombocytopenia
Livedo reticularis
NB. Recurrent fetal loss may also occur in other types of
thrombophilia.
Table 27.4 Deep vein thrombosis: clinical
assessment: the Wells score.
Points
Active cancer (treatment ongoing or
within previous 6 months or palliative)
1
Paralysis, plaster 1
Bed more than 3 days, surgery within
1
4 weeks
Tenderness along veins 1
Entire leg swollen 1
Pitting oedema 1
Collateral veins 1
Alternative diganosis likely –2
Low probability 0–1
High probability 2 or more
Table 27.5 Comparison of unfractionated heparin with low molecular weight heparin.
Unfractionated heparin Low molecular weight heparin
Mean molecular weight 15 4.5
in kilodaltons (range) (4–30) (2–10)
Anti-Xa : anti-IIa 1 : 1 2 : 1 to 4 : 1
Inhibits platelet function Yes No
Bioavailability 50% 100%
Half-life
intravenous 1 hour 2 hours
subcutaneous 2 hours 4 hours
Elimination Renal and hepatic Renal
Monitoring APTT Xa assay (usually not needed)
Frequency of heparin-induced
High Low
thrombocytopenia
Osteoporosis Yes Less frequent
APTT, activated partial thromboplastin time.

3. Table 27.6 Oral anticoagulant control tests.
Target levels recommended by the British
Society for Haematology.
Target INR Clinical state
2.5
(2.0–3.0)
Treatment of DVT, pulmonary
embolism, atrial fibrillation,
recurrent DVT off warfarin;
symptomatic inherited
thrombophilia, cardiomyopathy,
mural thrombus, cardioversion
3.0
(2.5–3.5)
Recurrent DVT while on
warfarin, mechanical prosthetic
heart valves, antiphospholipid
syndrome (some cases)
DVT, deep venous thrombosis; INR, international
normalized ratio.
Table 27.7 Drugs and other factors that interfere with the control of coumarin (e.g. warfarin)
therapy.
Potentiation of coumarin anticoagulants Inhibition of coumarin anticoagulants
Drugs that increase the effect of coumarins
Reduced coumarin binding to serum albumin
Sulphonamides
Inhibition of hepatic microsomal degradation of
coumarin
Cimetidine
Allopurinol
Tricyclic antidepressants
Metronidazole
Sulphonamides
Alteration of hepatic receptor site for drug
Thyroxine
Quinidine
Decreased synthesis of vitamin K factors
High doses of salicylates
Some cephalosporins, other antibiotics
Liver disease
Decreased synthesis of vitamin K factors
Decreased absorption of vitamin K
e.g. Malabsorption, antibiotic therapy, laxatives
Drugs that depress the action of coumarins
Acceleration of hepatic microsomal degradation
of coumarin
Barbiturates
Rifampicin
Enhanced synthesis of clotting factors
Oral contraceptives
Hereditary resistance to oral anticoagulants
Pregnancy
NB. Patients are also more likely to bleed if taking antiplatelet agents (e.g. NSAIDs, dipyridamole or aspirin); alcohol in large
amounts enhances warfarin action.

4. Table 27.8 Recommendations on the
management of bleeding and excessive
anticoagulation by the British Committee for
Standards in Haematology (third edition 1998;
2005 update).
INR 3.0–6.0 (target
INR 2.5)
Reduce warfarin dose
or stop
INR 4.0–6.0 (target
INR 3.5)
Restart warfarin when
INR <5.0
INR 6.0–8.0 Stop warfarin*
No bleeding or minor
bleeding
Restart when INR <5.0
INR >8.0 Stop warfarin*
No bleeding or minor
bleeding
Restart warfarin when
INR <5.0
If other risk factors for
bleeding give
0.5–2.5 mg vitamin K
orally
Major bleeding Stop warfarin
Give prothrombin
complex concentrate
50 units/kg, in
preference
FFP 15 mL/kg (when
available)
Give 5 mg vitamin K
(i.v. or oral)
FFP, fresh frozen plasma; INR, international normalized
ratio; i.v., intravenous.
* 1 mg vitamin K may be given orally to rapidly reduce the
INR to the therapeutic range within 24 hours in all patients
with an INR above the therapeutic range and no bleeding.
Table 27.9 Contraindications to thrombolytic
therapy.
Absolute
contraindications
Relative
contraindications
Active gastrointestinal
bleeding
Aortic dissection
Head injury or
cerebrovascular
accident in the past
2 months
Neurosurgery in the
past 2 months
Intracranial aneurysm
or neoplasm
Proliferative diabetic
retinopathy
Traumatic
cardiopulmonary
resuscitation
Major surgery in the
past 10 days
Past history of
gastrointestinal
bleeding
Recent obstetric
delivery
Prior arterial puncture
Prior organ biopsy
Serious trauma
Severe arterial
hypertension
(systolic pressure
>200 mmHg,
diastolic pressure
>110 mmHg)
Bleeding diathesis

5. Table 27.10 Antiplatelet therapy in patients
with an acute coronary syndrome and in
those undergoing percutaneous coronary
intervention (PCI). (After Lange R.A. and Hillis
L.D. (2004) N Engl J Med 350, 277–80.)
Drug
Target/patient
group Duration
Acute coronary syndrome
Aspirin All Life-long
Clopidogrel All 9–12 months
Glycoprotein IIb/IIIa inhibitors
Abciximab None –
Eptifibatide High risk 48–72 hours
Tirofiban High risk 48–72 hours
Patients undergoing PCI
Aspirin All Life-long
Clopidogrel All 9–12 months
Abciximab High risk 12 hours after
PCI
Eptifibatide High risk 18–24 hours
after PCI
Tirofiban None –