Anesthesia for High Risk Patient

7/28/2019 Anesthesia for High Risk Patient

1/5

ANESTHESIA FOR HIGH RISK PATIENT

(PRE-ECLAMPSIA AND ECLAMPSIA)

Dr. Susilo Chandra, SpAn

Pre-eclampsia is usually defined as hypertension and proteinuria developing duringpregnancy after 20 weeks' gestation in a previously normotensive and non-proteinuric woman. It is possible to develop non-proteinuric pre-eclampsia and also to haveeclamptic seizures with minimal or even no hypertension.

Hypertensive disorders of pregnancy are the second major cause of maternal deathafter thromboembolism in the UK. Pre-eclampsia is a multisystem disease with avariable clinical presentation. All maternal organ systems may potentially be affected.The pathophysiology of pre-eclampsia is still only parrially understood, but it isknown that failure of placentation occurs early in pregnancy and this leads to vascularendothelial cell damage and dysfunction. The endothelial cell damage is thought tolead to release of vasoactive sub,ranees, which promote generalised vasoconstrictionand reduced organ perfulion. This is exacerbated by the increased sensitivity tocirculating catecholamines found in the pre-eclamptic patient. Pre-eclamptic womendemonstrate an imbalance of the normal thromboxane/prostacyclin ratio andincreased free radical activity.

Pre-eclampsia encompasses HELLP syndrome, eclampsia and possibly acute fattyliver of pregnancy. Although the disease is progressive, a mother may beasymptomatic until she presents with an eclamptic fit, and although preeclampsia is adisease of pregnancy, terminated only by delivery, both HELLP syndrome andeclampsia 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 thataspirin 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, visualdisturbance and epigastric pain. The most commonly occurring signs arehypertension, oedema and hyperreflexia, although this is subjective andunreliable as a prognostic indicator. Sustained clonus is pathological. Womenmay 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 renaland hepatic function, coagulation disorders and pleural and pericardial effusions.Occasionally the clinical presentation may be dramatic - ruptured liverassociated with pre-eclampsia has been reported.

FetaL effects: Chronic impairment of uteroplacental blood flow causes intrauterinegrowth retardation and this may be one of the first signs of pre-eclampsia.

Hypertension: Hypertension in pregnancy is defined as a single diastolic bloodpressure exceeding 110 mmHg or two consecutive readings of at least 90 mmHgat an interval of 4 hours. A systolic arterial pressure of greater than 160 mmHg ora diastolic reading greater than 110 mmHg on two occasions at least 6 hours apart

is diagnostic of severe preeclampsia. Treatment of hypertension does not modifythe course of the underlying disease process but may reduce the morbidity andmortality attributable to uncontrolled hypertension.


2/5

Haemodynamic changes: The normal expansion of blood volume which takesplace in early pregnancy fails to occur in pre-eclamptic women and there istherefore a relatively hypovolaemic state. This is exacerbated by leakycapillaries, which allow inappropriate fluid shifts between compartments. Colloidosmotic pressure is low in pre-eclamptic women, and any increased hydrostatic

pressure due to iatrogenic fluid overload, impaired left ventricular function orpostpartum fluid shifts may therefore readily precipitate pulmonary oedema.

Results of the numerous studies (both invasive and non-invasive) of thehaemodynamic changes occurring in pre-eclampsia are confusing. There isgeneralised vasoconstriction and therefore systemic vascular resistance is usuallyincreased. Cardiac index and cardiac output may be high, low or normal but thisis frequently a reflection of drug therapy. In severe pre-eclampsia, especially ifthere is pulmonary oedema, right atrial pressure may not accurately reflect

pulmonary artery pressure, and central venous pressure monitoring may thereforebe an unreliable guide to treatment.

Convulsion: In the UK, 40% of eclamptic fits occur after delivery, mostcommonly within the first 3 days and rarely more than one week postpartum.

Recurrent seizures are associated with increased maternal morbidity andmortality. Magnesium sulphate has been proven to be effective in preventingrecurrence of fits in eclampsia; prophylactic use of magnesium sulphate insevere pre-eclamptics is becoming more common, and there is some evidence tosupport its use. Unfortunately a significant percentage of eclamptic women in theUK have minimal prodromal signs or symptoms and would therefore not behelped 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 themanagement of pre-eclampsia and eclampsia. There have also been recommendationsthat every obstetric unit should have an 'eclampsia pack' containing everythingnecessary to treat eclamptic women with magnesium.

Women with mild to moderate disease and without major fetal compromise areusually 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 Caesareansection. The anaesthetist should assess the mother, paying particular attention to anysymptoms of pre-eclampsia, drug treatment, the airway, level of hypertension, resultsof haematological and biochemical investigations and proposed mode of delivery.

HypertensionThe first line treatment of hypertension is methyldopa, which has a long safety recordfor the fetus. Labetalol and nifedipine have both been used increasingly in recentyears, 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 tocontinuous 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 asignificantly greater percentage reduction in uteroplacental perfusion)


3/5

Labetalol (10 mg boluses) may be used parenterally in the acute situation, and oralnifedipine capsules (5-10 mg) act within 15-20 minutes. Sublingual nifedipine actsvery rapidly but is no longer recommended because of the risk of uncontrolledhypotension, especially in combination with magnesium sulphate.

Nitroprusside and nitroglycerin have been used in North America for acute control ofhypertension but are not commonly used in the UK.

Angiotensin converting enzyme inhibitors are contraindicated in pre-eclampsia; theiruse is associated with unacceptably high fetal morbidity and mortality.

ConvulsionsMagnesium sulphate is now the drug of choice in pre-eclampsia, and there should bea 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 ofeclampsia. Diazepam is still used to terminate eclamptic fits, although magnesiumsulphate is also effective, and it would seem logical to treat with a single agent ratherthan two. Some authorities claim that eclamptic fits are self-limiting and that notreatment other than initiation of the magnesium sulphate regimen is needed.

Analgesia for laborRegional analgesia is the method of choice. Good analgesia prevents hypertensiveepisodes associated with contraction pain. Well conducted epidural analgesia may be

beneficial to the compromised fetus by improving uteroplacental perfusion. Acombination of low-dose local anaesthetic and opioid may be given by continuous

infusion or intermittent bolus dose, and this can obviously then be supplemented asnecessary should instrumental or operative delivery be required. A pre-epidural

platelet count should be performed (if trends suggest that platelet numbers aredecreasing significantly a platelet count should be repeated immediately beforeepidural injection is commenced). Current guidelines from the ObstetricAnaesthetists' Association suggest that a platelet count of at least 80 X 109/l isadvisable before instituting central neural blockade. It is important to remember thatany stated lower safe limit is entirely arbitrary, and the relative risks and benefits ofregional analgesia and anaesthesia must be considered for each patient. Severalstudies have confirmed that if the platelet count is at least 100 X 109/l there is no needto perform further coagulation studies. In some centres thromboelastography has beenused as an indicator of coagulation and fibrinolytic status, but this is not widelyavailable. Bleeding time has been suggested as a clinical tool for assessment ofcoagulation, but a normal range for bleeding time has not been established in

pregnancy and there is considerable inter- and intraobserver variability in itsmeasurement.

If epidural analgesia is contraindicated, it is important to control the blood pressureby using appropriate agents (hydralazine, nifedipine, labetalol) and to providealternative analgesia. Patient-controlled intravenous opioids offer the mother the

psychological benefit of being in control of her analgesia and are more predictablethan intramuscular opioids.

Combined spinal-epidural analgesia may be used, but arguably offers few advantagescompared with epidural alone.


4/5

Transcutaneous electrical nerve stimulation, Entonox and non-pharmacologicalmethods of analgesia are not suitable for the pre-eclamptic mother in establishedlabor. 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 sectionRegional anaesthesia is preferable to general both for the mother and for the fetus.There is vasoconstriction of the uteroplacental vasculature in pre-eclampsia and thismay be relieved by epidural anaesthesia. There is some evidence that addition ofadrenaline to epidural bupivacaine negates this benefit. Although the use of spinalanaesthesia in pre-eclampsia is controversial, there is evidence that uterine arteryvelocity and neonatal condition are unaffected by spinal anaesthesia if systolicarterial 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 andsubsequent use of the epidural to extend the level of anaesthesia facilitateshaemodynamic stability.

There is controversy about the need for volume preloading before instituting regionalanaesthesia in obstetric practice. The pre-eclamptic mother may exhibit greatersensitivity 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 inthe pre-eclamptic woman by the potential for a significantly compromised airway andthe hypertensive response to intubation and extubation. There may also be potentialdrug interactions, especially between magnesium sulphate and neuromuscular

blocking agents.Laryngeal oedema is uncommon but may be sufficient to obscure all normal anatomyat laryngoscopy. Each obstetric theatre should include microlaryngeal endotrachealtubes on the intubation trolley for this eventuality.Uncontrolled hypertension in response to tracheal intubation may provoke cardiacarrhythmias, myocardial ischaemia or cerebrovascular catastrophe. Numerous agentshave been used to attenuate this response but the commonly used agents in the UKare fentanyl 1-4 g/kg or alfentanil 7-10 g/kg and labetalol 10-20 mg. Other opioidsand -blockers, lignocaine and droperidol may be used; magnesium sulphate 30mg/kg also appears to be effective.

MonitoringAll women with moderate or severe pre-eclampsia should have continuous electronicfetal 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 duringregional anaesthesia. Access via the antecubital fossa rather than via neck veins is


5/5

recommended, especially in the undelivered mothcr. Direct arterial pressuremonitoring is more accurate than non-invasive methods in poorly controlledhypertension, 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-arterialmonitoring must be balanced the familiarity of midwifery staff with their use. The

need for pulmonary artery cathererisation is an indication for transfer to an intensivecare unit, and it is important to remember that pulmonary artery catheters areassociated with morbidity and mortality.

All pre-eclamptic women should have a urinary catheter inserted and an accuratehourly fluid balance recorded. Fluid management is controversial. The risk of volumeoverload and iatrogenic pulmonary oedema must be balanced against the risk ofhypotension if vasodilators are given without concomitant replacement.

Postoperative managementThe risks of deterioration in blood pressure control, of HELLP syndrome and of

eclampsia do not end immediately with delivery of the placenta. Women withmoderate and severe pre-eclampsia should be monitored in a high-dependencyenvironment for at least 48 hours after delivery. Invasive monitoring andantihypertensive 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 cerebrovascularmorbidity and mortality.

HELLP syndrome is part of the spectrum of pre-eclampsia and may not bepreceded by significant pre-eclampsia.

Eclampsia may occur without premonitory symptoms or signs, and 40% ofeclamptic fits occur after delivery.

Although the classic presentation of the disease is hypertension, proteinuria andoedema occurring after 20 weeks of pregnancy, pre-eclampsia is a multisystemdisease and may present atypically.

Documents

Anesthesia for High Risk Patient