Venous Thromboembolism Flashcards
1
Q
What is VTE
A
Venous thromboembolism (VTE) is a disease that includes deep vein thrombosis (DVT) and pulmonary embolism (PE).
2
Q
How do we make blood clot?
A
- Blood vessels are made up of an inner lining of endothelial cells
- When blood vessels are damaged, platelets are used for coagulation
- How does the platelet know when to clot?
o The environment inside the BV is different to the environment outside BV
o Outside BV = collagen (structural protein)
o Step 1: platelet plug: Collagen chemically interacts with platelets to form platelet plugs.
o Step 1 platelet plug is not as strong
o Step 2- fibrin (protein)= strengthens the platelet plug to create a mesh of protein. The fibrin strand is made up of fibrin sub-units which naturally polymerase.
o Fibrinogen (circulates in the blood doesn’t allow fibrin to stick together in the blood where is circulates) fibrin
o How does the fibrinogen know when to stick to stick together?
- Tissue factors- which are outside the endothelial cells that surround wounds that change fibrinogen to fibrin.
- Tissue factors turns thrombin (protein) to its active form to create fibrinogen to fibrin.
3
Q
What is DVT?
A
involves the formation of a blood clot in the deep veins of the calves, legs or pelvis. If part of the blood clot passes in the blood stream it may cause damage elsewhere.
4
Q
Signs and symptoms of DVT
A
- Localised pain
- Asymmetric oedema
- Calf swelling
- Acute chest pain
5
Q
Consequences of VTE?
A
Many diagnosed and treated VTE recover are not fatal. However, there are long-term complications:
- Post-thrombotic syndrome (PTS)- PTS occurs in up to 60% of patients with DVT and results in significant disability and discomfort. 5% - 10% will develop severe PTS with chronic venous ulceration.
- Chronic pulmonary hypertension
- Recurrent VTE
6
Q
The Virchow’s Triad
A
- The increased VTE risk in pregnancy is bought about a combination of these three.
- Hypercoagulability- likely to evolve to protect women against bleeding.
o Activation of coagulation mechanisms
o Increased levels of clotting factors as pregnancy progresses: - Increased fibrinogen up to 3x
- Thrombin, Factor VIII, IX and X levels increase
- Anticougulants decrease (protein S)
- Fibrinolysis increase to dissolve clots.
- Venous stasis
o When the blood is sluggish
o Hormonally-induced (proegesterone) decrease in venous tone- 50% decrease in venous flow in lower extremity by third trimester
o Obstruction to venous flow as uterus enlarges - Vascular endothelial damage
o Trauma to pelvic veins as fetus passes through pelvis
o Other causes, e.g. smoking, pre-eclampsia, diabetes
7
Q
Risk factors for VTE
A
- Family history
- Heart failure
- Varicose Veins with phlebitis
- Known thrombophilias
- Receiving cancer therapy
- Total anaesthetic and surgical time of over 90 minutes.
- Smoking- increase the risk of chronic inflammation
- Hyperemesis- Dehydration
- Cancer- cancer tissue breaks down and create a clot
- The risk of developing VTE depends on the condition and/or procedure for which the patient is admitted and on any predisposing risk factors
8
Q
Pre-existing risk factors for VTE during pregnancy
A
- Previous VTE and family history
- Thrombophilia – Heritable (Antithrombin deficiency, Protein C Deficiency, Protein S Deficiency, Factor V Leiden, Prothrombin gene G20210A) –> with this inherited disease the risk of miscarriage, intrauterine fetal death, placental abruption and severe IUGR increases.
- Thrombophilia – Acquired (antiphospholipid syndrome – persistent lupus anticoagulant- anti-immune response, persistant moderate/high-titre anticardiolipin antibiodies)
- Medical co-morbidities (e.g. heart or lung disease, SLE, Cancer, inflammatory bowel disease or inflammatory polyarthropathy) Nephrotic syndrome, sickle cell disease, intravenous drug users
- Age > 35yrs
- Obesity >30kg/m2
- Smoking
- Gross varicose veins
- Sickle cell anaemia
- Paraplegia: impairment in motor or sensory function of the lower extremities.
9
Q
Obstetrics risk factors
A
- Multiple pregnancy
- CTG: position and immobile for prolonged periods
- Lithotomy position:
o Increase in intra-abdominal pressure - Assisted reproductive therapy: IVF -increase hormones
- Ovarian hyperstimulation syndrome
- Pre-eclampsia
- Caesarean section (Prolonged labour, mid cavity rotational instrumental delivery)
- PPH (>1litre) Requiring transfusion (Prolonged labour, mid cavity rotational instrumental delivery
10
Q
Thromboembolism in Pregnancy: Diagnosis
A
DVT:
- Leg pain or discomfort
- Usually of sudden onset
- Especially in left legs
- Swelling, tenderness
- High Temperature
- Lower abdominal pain
- Increase of WBC
- Investigate leg symptoms
- Consider different differential diagnoses
- Doppler USS
- MRI Scan
- Bloods: D-Dimers (particles from the clotting cascade and if the levels are normal -> we can exclude DVT)- NOT RECOMMENDED IN PREGNANCY.
11
Q
Investigations & Management
A
- If a DVT or PE is diagnosed (or strongly suspected) in pregnancy, anticoagulation with LMW heparin should be commenced
- LMWH should be given in doses titrated against the woman’s booking or early pregnancy weight.
- Once daily or in two divided doses
- Prior to this bloods for FBC, COAG, U+Es and LFTs.
- When VTE occurs at term, consideration should be given to the use of intravenous unfractionated heparin which is more easily manipulated.
- LMWH and unfractioned heparin
o Fragmin (delteparin)
o Clexane (enoxoparin sodium)
o Smaller molecule enables increased uptake and therefore lower, less frequent doses of heparin are required (once daily).
o Once she is in established labour or thinks that she is in labour, she should not inject any further heparin.
o Where delivery is planned, either by elective caesarean section or induction of labour, LMWH maintenance therapy should be discontinued 24 hours prior to planned delivery.
o Regional anaesthetics should not be undertaken until at least 24 hours after the last dose
o LMWH should not be given for 4 hours after the use of spinal anaesthesia or after the epidural catheter has been removed, and the epidural catheter should not be removed within 12 hours of the most recent injection
o Postnatally: stockings, hydration and early mobilisation - Heparin
o Does not cross the placenta
o Not excreted in the breast milk
o But may have hazards on prolonged use: - Osteoporosis - Heparin-induced thrombocytopaenia - Allergy o Inconvenient to use
- Warfarin
o Oral anticoagulant that interferes with the action of vitamin K (used in the liver as a co-enzyme in the production of a number of clotting factors)
o Readily crosses the placenta and is a known teratogen, therefore not used in pregnancy (but is considered safe postpartum & with breastfeeding)
o Crosses placenta
o Teratogenic effects
o Warfarin embryopathy
o Intracerebral Hge in-utero
o Haemorrhagic complications to mother and baby during labour
o Not excreted in breast milk
12
Q
Side effects of LMWH and warfarin
A
- Most serious adverse effect is haemorrhage – mild or severe
- May need antagonist drugs to reverse the effects
- Vitamin K for warfarin
- Protamine sulphate for heparin
- IV clotting factors may be required
- Risks when considering regional blockade
- e.g. epidural haematoma
- Long-term heparin use may lead to:
- Heparin-induced thrombocytopenia
- Osteoporosis
- Fetal haemorrhage
- Risks are lower with LMWH – recommended for use in pregnancy (RCOG, 2004).
13
Q
Other drugs used in managing VTE
A
- Aspirin; acts by preventing platelet aggregation but no controlled trials and one study found no better than a placebo = RCOG does not recommend
- Streptokinase is a fibrinolytic drug used to dissolve clots that have already occurred, e.g. dissolving large PE or coronary thromboses (only usually used PN)
- Both drugs carry a risk of haemorrhage and are C/I where there is active bleeding or patient has a history of cerebral bleeding
- ACUTE VTE IN PREGNANCY SHOULD BE TREATED WITH AN IV HEPARIN BOLUS OF 5000 IU FOLLOWED BY CONTINUOS INFUSION OF 2000 IU
14
Q
Midwifery/medical care
A
- Family history of VTE should be established at booking and referral to the obstetric team should be made.
- Guidelines for VTE should be adhered to.
- Women on heparin for more than 6 weeks should be fully informed of the signs of complication to report.
- Skills in active resuscitation
- Health promotion strategies such as measures to avoid DVT
- Contraception
- Prophylaxis: Compression socks
15
Q
Signs and symptoms of PE and what is it?
A
- Blockage in one artery (blood vessels) in the lungs.
- Clinical signs are related to the size of the clot that is obstructing the pulmonary circulation
- Large or multiple emboli will prevent adequate oxygenation of blood
- Result is poor venous return to the heart and decreased cardiac output
- Dyspnoea
- Major PE:
o Collapse; hypotension; chest pain; breathlessness; cyanosis; abdominal pain; right sided heart failure; enlarged liver, blood stained sputum - Smaller emboli:
o Unexplained pyrexia; cough; haemoptysis; chest pain; breathlessness
