ANESTHESIA FOR HIGH RISK PATIENT (PRE-ECLAMPSIA AND ECLAMPSIA) Dr.

Susilo Chandra, SpAn Pre-eclampsia is usually defined as hypertension and proteinuria developing during pregnancy after 20 weeks' gestation in a previously normotensive and non-protein uric woman. It is possible to develop non-proteinuric pre-eclampsia and also to have eclamptic seizures with minimal or even no hypertension. Hypertensive disorders of pregnancy are the second major cause of maternal death after thromboembolism in the UK. Pre-eclampsia is a multisystem disease with a variable clinical presentation. All maternal organ systems may potentially be affected. The pathophysiology of pre-eclampsia is still only parrially understood, but it is known that failure of placentation occurs early in pregnancy and this leads to vascular endothelial cell damage and dysfunction. The endothelial cell damage is thought to lead to release of vasoactive sub,ranees, which promote generalised vasoconstriction and reduced organ perfulion. This is exacerbated by the increased sensitivity to circulating catecholamines found in the pre-eclamptic patient. Pre-eclamptic women demonstrate an imbalance of the normal thromboxane/prostacyclin ratio and increased free radical activity. Pre-eclampsia encompasses HELLP syndrome, eclampsia and possibly acute fatty liver of pregnancy. Although the disease is progressive, a mother may be asymptomatic until she presents with an eclamptic fit, and although preeclampsia is a disease of pregnancy, terminated only by delivery, both HELLP syndrome and eclampsia may occur after delivery. The large international CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) trial failed to show universal benefit from low-dose aspirin, suggesting instead that aspirin may be beneficial in selected high-risk women. Problems/special considerations ClinicaL features: Pre-eclampsia is frequently asymptomatic despite significant disease. Symptoms are often non-specific and include headache, visual disturbance and epigastric pain. The most commonly occurring signs are hypertension, oedema and hyperreflexia, although this is subjective and unreliable as a prognostic indicator. Sustained clonus is pathological. Women may also present with the clinical features of pulmonary oedema, cerebral haemorrhage, impaired liver function, placental abruption or coagulopathy. Oedema may also affect the airway. Investigations may reveal abnormal renal and hepatic function, coagulation disorders and pleural and pericardial effusions. Occasionally the clinical presentation may be dramatic - ruptured liver associated with pre-eclampsia has been reported. FetaL effects: Chronic impairment of uteroplacental blood flow causes intrauterine growth retardation and this may be one of the first signs of pre-eclampsia. Hypertension: Hypertension in pregnancy is defined as a single diastolic blood pressure exceeding 110 mmHg or two consecutive readings of at least 90 mmHg at an interval of 4 hours. A systolic arterial pressure of greater than 160 mmHg or a diastolic reading greater than 110 mmHg on two occasions at least 6 hours apart is diagnostic of severe preeclampsia. Treatment of hypertension does not modify the course of the underlying disease process but may reduce the morbidity and mortality attributable to uncontrolled hypertension.

Haemodynamic changes: The normal expansion of blood volume which takes place in early pregnancy fails to occur in pre-eclamptic women and there is therefore a relatively hypovolaemic state. This is exacerbated by leaky capillaries, which allow inappropriate fluid shifts between compartments. Colloid osmotic pressure is low in pre-eclamptic women, and any increased hydrostatic pressure due to iatrogenic fluid overload, impaired left ventricular function or postpartum fluid shifts may therefore readily precipitate pulmonary oedema. Results of the numerous studies (both invasive and non-invasive) of the haemodynamic changes occurring in pre-eclampsia are confusing. There is generalised vasoconstriction and therefore systemic vascular resistance is usually increased. Cardiac index and cardiac output may be high, low or normal but this is frequently a reflection of drug therapy. In severe pre-eclampsia, especially if there is pulmonary oedema, right atrial pressure may not accurately reflect pulmonary artery pressure, and central venous pressure monitoring may therefore be an unreliable guide to treatment. Convulsion: In the UK, 40% of eclamptic fits occur after delivery, most commonly within the first 3 days and rarely more than one week postpartum. Recurrent seizures are associated with increased maternal morbidity and mortality. Magnesium sulphate has been proven to be effective in preventing recurrence of fits in eclampsia; prophylactic use of magnesium sulphate in severe pre-eclamptics is becoming more common, and there is some evidence to support its use. Unfortunately a significant percentage of eclamptic women in the UK have minimal prodromal signs or symptoms and would therefore not be helped by prophylactic magnesium unless it was given to every pregnant woman.

Management options The Report on Confidential Enquiries into Maternal Deaths in the United Kingdom strongly recommends that every obstetric unit should have written guidelines for the management of pre-eclampsia and eclampsia. There have also been recommendations that every obstetric unit should have an 'eclampsia pack' containing everything necessary to treat eclamptic women with magnesium. Women with mild to moderate disease and without major fetal compromise are usually offered a trial of vaginal delivery, whilst those with severe pre-eclampsia (especially at less than 37 weeks' gestation) are likely to be delivered by Caesarean section. The anaesthetist should assess the mother, paying particular attention to any symptoms of pre-eclampsia, drug treatment, the airway, level of hypertension, results of haematological and biochemical investigations and proposed mode of delivery. Hypertension The first line treatment of hypertension is methyldopa, which has a long safety record for the fetus. Labetalol and nifedipine have both been used increasingly in recent years, either instead of, or in addition to, methyldopa. Hydralazine is the most commonly used agent for management of acute hypertension. Administration of small repeated intravenous boluses (e.g. 5 mg) is preferable to continuous infusion. Hydralazine acts primarily as a vasodilator and should therefore be used with caution and preferably in conjunction with gentle volume replacement. Acute vasodilatation may cause an uncontrolled fall in blood pressure and thus provoke fetal distress. (Reduction in maternal blood pressure is associated with a significantly greater percentage reduction in uteroplacental perfusion)

Labetalol (10 mg boluses) may be used parenterally in the acute situation, and oral nifedipine capsules (5-10 mg) act within 15-20 minutes. Sublingual nifedipine acts very rapidly but is no longer recommended because of the risk of uncontrolled hypotension, especially in combination with magnesium sulphate. Nitroprusside and nitroglycerin have been used in North America for acute control of hypertension but are not commonly used in the UK. Angiotensin converting enzyme inhibitors are contraindicated in pre-eclampsia; their use is associated with unacceptably high fetal morbidity and mortality. Convulsions Magnesium sulphate is now the drug of choice in pre-eclampsia, and there should be a magnesium pack on every labor ward (see, Chapter 82, Magnesium sulphate, p. 198). There is no place for chlormethiazole or phenytoin in the prophylaxis or treatment of eclampsia. Diazepam is still used to terminate eclamptic fits, although magnesium sulphate is also effective, and it would seem logical to treat with a single agent rather than two. Some authorities claim that eclamptic fits are self-limiting and that no treatment other than initiation of the magnesium sulphate regimen is needed. Analgesia for labor Regional analgesia is the method of choice. Good analgesia prevents hypertensive episodes associated with contraction pain. Well conducted epidural analgesia may be beneficial to the compromised fetus by improving uteroplacental perfusion. A combination of low-dose local anaesthetic and opioid may be given by continuous infusion or intermittent bolus dose, and this can obviously then be supplemented as necessary should instrumental or operative delivery be required. A pre-epidural platelet count should be performed (if trends suggest that platelet numbers are decreasing significantly a platelet count should be repeated immediately before epidural injection is commenced). Current guidelines from the Obstetric Anaesthetists' Association suggest that a platelet count of at least 80 X 109/l is advisable before instituting central neural blockade. It is important to remember that any stated lower safe limit is entirely arbitrary, and the relative risks and benefits of regional analgesia and anaesthesia must be considered for each patient. Several studies have confirmed that if the platelet count is at least 100 X 109/l there is no need to perform further coagulation studies. In some centres thromboelastography has been used as an indicator of coagulation and fibrinolytic status, but this is not widely available. Bleeding time has been suggested as a clinical tool for assessment of coagulation, but a normal range for bleeding time has not been established in pregnancy and there is considerable inter- and intraobserver variability in its measurement. If epidural analgesia is contraindicated, it is important to control the blood pressure by using appropriate agents (hydralazine, nifedipine, labetalol) and to provide alternative analgesia. Patient-controlled intravenous opioids offer the mother the psychological benefit of being in control of her analgesia and are more predictable than intramuscular opioids. Combined spinal-epidural analgesia may be used, but arguably offers few advantages compared with epidural alone.

Transcutaneous electrical nerve stimulation, Entonox and non-pharmacological methods of analgesia are not suitable for the pre-eclamptic mother in established labor. They do not provide reliable analgesia and increase the likelihood of general anaesthesia being used if delivery by emergency Caesarean section is required. Anaesthesia for Caesarean section Regional anaesthesia is preferable to general both for the mother and for the fetus. There is vasoconstriction of the uteroplacental vasculature in pre-eclampsia and this may be relieved by epidural anaesthesia. There is some evidence that addition of adrenaline to epidural bupivacaine negates this benefit. Although the use of spinal anaesthesia in pre-eclampsia is controversial, there is evidence that uterine artery velocity and neonatal condition are unaffected by spinal anaesthesia if systolic arterial pressure remains at least 80% of baseline measurement. Combined spinal-epidural anaesthesia confers the benefits of dense anaesthesia (especially of the sacral nerve roots) with the flexibility of epidural anaesthesia and postoperative analgesia. Use of a smaller dose of intrathecal local anaesthetic and subsequent use of the epidural to extend the level of anaesthesia facilitates haemodynamic stability. There is controversy about the need for volume preloading before instituting regional anaesthesia in obstetric practice. The pre-eclamptic mother may exhibit greater sensitivity to ephedrine than the usually normotensive mother. General anaesthesia may be necessary if there is great urgency to deliver the mother or if regional anaesthesia is contraindicated by coagulopathy or major haemorrhage. Extreme prematurity does not contraindicate regional anaesthesia and nor, necessarily, does eclampsia. The additional risks of general anaesthesia for Caesarean section are compounded in the pre-eclamptic woman by the potential for a significantly compromised airway and the hypertensive response to intubation and extubation. There may also be potential drug interactions, especially between magnesium sulphate and neuromuscular blocking agents. Laryngeal oedema is uncommon but may be sufficient to obscure all normal anatomy at laryngoscopy. Each obstetric theatre should include microlaryngeal endotracheal tubes on the intubation trolley for this eventuality. Uncontrolled hypertension in response to tracheal intubation may provoke cardiac arrhythmias, myocardial ischaemia or cerebrovascular catastrophe. Numerous agents have been used to attenuate this response but the commonly used agents in the UK are fentanyl 1-4 g/kg or alfentanil 7-10 g/kg and labetalol 10-20 mg. Other opioids and -blockers, lignocaine and droperidol may be used; magnesium sulphate 30 mg/kg also appears to be effective. Monitoring All women with moderate or severe pre-eclampsia should have continuous electronic fetal monitoring, including monitoring during development of regional anaesthesia. There is a trend towards more invasive maternal monitoring, and othe use of central venous pressure catheters provides useful guidance for fluid admistration during regional anaesthesia. Access via the antecubital fossa rather than via neck veins is

recommended, especially in the undelivered mothcr. Direct arterial pressure monitoring is more accurate than non-invasive methods in poorly controlled hypertension, since the measurement error with non-invasive equipment is known to be greater at very high or very low pressure. The relative benefits of intra-arterial monitoring must be balanced the familiarity of midwifery staff with their use. The need for pulmonary artery cathererisation is an indication for transfer to an intensive care unit, and it is important to remember that pulmonary artery catheters are associated with morbidity and mortality. All pre-eclamptic women should have a urinary catheter inserted and an accurate hourly fluid balance recorded. Fluid management is controversial. The risk of volume overload and iatrogenic pulmonary oedema must be balanced against the risk of hypotension if vasodilators are given without concomitant replacement. Postoperative management The risks of deterioration in blood pressure control, of HELLP syndrome and of eclampsia do not end immediately with delivery of the placenta. Women with moderate and severe pre-eclampsia should be monitored in a high-dependency environment for at least 48 hours after delivery. Invasive monitoring and antihypertensive treatment should be continued during this time.

Key points Pre-eclampsia and eclampsia are the second cause of maternal death in the World. Pre-eclampsia can only be effectively treated by delivery of the placenta, although symptomatic treatment attenuates maternal morbidity. Effective control of hypertension reduces cardiovascular and cerebrovascular morbidity and mortality. HELLP syndrome is part of the spectrum of pre-eclampsia and may not be preceded by significant pre-eclampsia. Eclampsia may occur without premonitory symptoms or signs, and 40% of eclamptic fits occur after delivery. Although the classic presentation of the disease is hypertension, proteinuria and oedema occurring after 20 weeks of pregnancy, pre-eclampsia is a multisystem disease and may present atypically.