On successfully completing this topic, you will be able to:
recognise the risk factors for thromboembolism and understand the need for appropriate risk assessment and thromboprophylaxis
recognise the features of pulmonary embolism and have an early suspicion of the diagnosis
describe the treatment of suspected pulmonary embolism, including massive, life-threatening pulmonary embolism.
Introduction and incidence
The risk of venous thromboembolism (VTE) is significantly increased in pregnancy overall, due to a variety of important changes in the coagulation and vascular systems. There may also be a variety of other factors that can contribute to an individual’s risk.
Thrombosis and thromboembolism have been the leading cause of direct maternal deaths in the UK since 1985 except for the period 2006–08 when it was overtaken by genital tract sepsis. The 2009–2012 report has shown a rise in deaths from thromboembolism and the rate is once again above 1 per 100,000 maternities. These deaths are being reported in detail in 2015.
The incidence of antenatal pulmonary embolism in the UK has recently been estimated in a prospective case–control study by UKOSS (the UK Obstetric Surveillance System) at 1.3/10 000 maternities, with a case fatality rate of 3.5% and significant severe morbidity.2 There were 143 women with antenatal pulmonary embolisms in the study.
The period covered by the 2006–08 report where deaths fell, was the first triennium since the publication of the RCOG guideline, ‘Thromboprophylaxis during pregnancy, labour and after normal vaginal delivery,’ in 2004.3 It is possible that the very significant fall in the rate of deaths from thromboembolism is a result of better identification of risk factors and more aggressive prophylaxis as a result of this guideline.
Of the 16 deaths from pulmonary embolism, three women died in the first trimester of pregnancy, two died after miscarriage and three after perimortem CS in the third trimester. The remaining eight died in the postpartum period, two after vaginal delivery and six after CS.
Of the 18 deaths overall, six were associated with ‘major’ substandard care and four with ‘minor’ substandard care (56% of cases). In seven women, there was inadequate thromboprophylaxis, in six there was failure to investigate chest symptoms and five cases involved a failure of appropriate referral to a consultant obstetrician.
Risk factors for VTE
Well-known additional risk factors for thromboembolism include:
obesity
increasing maternal age
increasing parity
previous VTE
thrombophilia congenital (e.g. antithrombin 3 deficiency, protein C and S deficiency, activated protein C resistance) and acquired (lupus anticoagulant and antiphospholipid antibody)
operative delivery
surgical procedures in pregnancy or the puerperium.
Other recognised risk factors are: immobility; hypertensive disorders; hyperemesis; dehydration and excessive blood loss. Medical disorders such as: homocysteinuria; sickle cell disease; inflammatory bowel disease; nephritic syndrome; certain cardiac conditions and myeloproliferative disorders also increase the risk of VTE.
Risk factors were identified in only 99 of the 143 cases (70%) in the UKOSS report2 (and 14 of the 16 deaths in Saving Mothers’ Lives1), but also in 49% of controls. In the UKOSS survey, however, after adjustment, only multiparity and obesity were associated with a significantly raised odds ratio for antenatal pulmonary embolism. Saving Mothers’ Lives also suggests that obesity is the most important risk factor, with many classic risk factors notably absent, perhaps as a result of better identification of risk factors with appropriate prophylactic treatment.
Pathophysiology
Hypercoagulability, as a result of one or more factors, results in formation of thrombus in the leg veins, on the left in up to 90% of cases and affecting the proximal ileofemoral veins in most cases. Emboli can reach the pulmonary arteries, with potentially fatal consequences. Deep vein thrombosis confined to the calf is rare in pregnancy.
Obstruction of the pulmonary arteries and release of vasoactive substances from platelets elevates pulmonary vascular resistance. The resulting increase in alveolar dead space and redistribution of blood flow impairs gas exchange. Right ventricular afterload increases, resulting in right ventricular dilatation, dysfunction and ischaemia.
Stimulation of irritant receptors causes alveolar hyperventilation. Reflex bronchoconstriction increases airway resistance and pulmonary oedema decreases pulmonary compliance.
Clinical presentation of pulmonary embolism
Pulmonary embolism can present as a massive, life-threatening event, or as a less-severe combination of symptoms with pleuritic chest pain, with or without dyspnoea, and possibly low-grade fever and haemoptysis. Clinical diagnosis of pulmonary embolism is difficult and commonly delayed because the significance of symptoms may not be appreciated by the woman or her attendants, and because there may be few signs on examination (Table 11.1).
| Findings | Occurrence in patients with proven pulmonary embolism (%) |
|---|---|
| Tachypnoea | 89 |
| Dyspnoea | 81 |
| Pleuritic pain | 72 |
| Apprehension | 59 |
| Cough | 54 |
| Tachycardia | 43 |
| Haemoptysis | 34 |
| Temperature > 37°C | 34 |
Although, with less severe symptoms, the differential diagnoses include chest infection, cardiac causes and pneumothorax, pulmonary embolism carries the highest risk. It should be the presumed diagnosis: treatment should be started and continued until embolism has been excluded, or a different diagnosis confirmed.
Massive pulmonary embolism may present with hypotension, severe dyspnoea, cyanosis and circulatory collapse; with central chest pain as a result of right ventricular myocardial ischaemia; or as sudden collapse, cardiac arrest or death. In this emergency situation, there may be right-sided heart failure, with increased jugular pressure, liver distension and subtle cardiac signs. As with less-severe pulmonary embolism, the presentation can be confused with that of other severe cardiopulmonary conditions, but a high index of suspicion must be maintained to avoid delay in beginning the appropriate management of a potentially life-threatening situation.
Management
The immediate management of a woman presenting with significant symptoms suggestive of pulmonary embolism, or of collapse possibly due to this condition, follows the structured approach to the severely ill patient:
1 Remember the risk factors for thromboembolism and maintain a high index of suspicion in women presenting with chest pain, dyspnoea, tachycardia or collapse.
2 Ensure a safe environment, approach the patient, ’shake and shout’ if necessary.
3 Call for help: senior obstetrician, anaesthetist, on-call medical team and, in an unexplained maternal collapse or cardiac arrest, the cardiac arrest team.
A – Assess and ensure an adequate airway, administer high flow oxygen.
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