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Obstetric emergencies
6 Obstetric emergencies FRANCIS
X. L A H
Emergency obstetric anaesthesia is not for the inexperienced anaesthetist; however, because obstetric procedures are often performed at unsociable hours in isolated units the provision of anaesthesia is frequently delegated to junior hospital medical staff training in anaesthesia. It therefore should come as no surprise, when maternal mortality reports are examined for anaesthetic-related deaths, to read comments such as 'The giving of responsibility to inexperienced anaesthetists was the principal cause of 12 deaths' (1973-1975) or 'There should be a review of anaesthetic services to maternity units with the aim of providing better trained anaesthetists' (19761978) (Department of Health, 1978, 1982). Changes are being implemented. Obstetric anaesthetic sessions are taken up by experienced anaesthetists. These anaesthetists are forming themselves into groups to actively promote interest and research into obstetric anaesthesia. Smaller maternity units are being consolidated into larger units within major general hospitals to make it financially feasible to provide dedicated obstetric anaesthetic sessions. Progress has, however, been slow because of resistance from a variety of groups with vested interests. They must not be allowed to succeed in delaying progress: anaesthetic-related maternal morbidity and mortality can only decrease when experienced anaesthetists provide an emergency obstetric anaesthetic service. Table 1. Rates of direct maternal death per million total pregnancies.
Cause of death
1973-1975
1976-1978
1979-1981 1982-1984
1985-1987
Hypertension Diseases of pregnancy Pulmonary embolism Abortion Haemorrhage Anaesthesia Ectopic pregnancy Amniotic fluid embolism Sepsis Ruptured uterus Other direct
13.2
12.5
14.2
10.0
9.4
12.8 10.5 8.1 10.5 7.4 5.4 7.4 4.3 8.5
18.5 6.0 10.3 11.6 9.0 4.7 6.5 6.0 8.2
9.0 5.5 5.5 8.7 7.9 7.1 3.1 1.6 7.5
10.0 4.4 3.6 7.2 4.0 5.6 1.0 1.2 8.4
9.1 2.3 3.8 1.9 4.1 3.4 2.3 1.9 7.5
Total
88.0
93.4
70.0
55.0
45.6
From Department of Health (1991). Baillikre' s Clinical Anaesthesiology-Vol. 7, No. 2, June 1993 ISBN 0--7020-1734-5
299 Copyright 9 1993, by Bailli6re Tindall All rights of reproduction in any form reserved
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E v e n at this e a r l y s t a g e t h e change~ t h a t h a v e b e e n i m p l e m e n t e d s e e m to b e affecting t h e a n a e s t h e t i c - r e l a t e d m a t e r n a l m o r t a l i t y statistics ( T a b l e 1). In the t r i e n n i u m 1985-1987, e i g h t m o t h e r s d i e d as a d i r e c t result of r e c e i v i n g a n a n a e s t h e t i c . This r e p r e s e n t s a significant r e d u c t i o n f r o m t h e p r e v i o u s r e p o r t , w h e n a n a e s t h e s i a was t h e t h i r d m o s t c o m m o n c a u s e of d e a t h ; it is n o w e q u a l last w i t h r u p t u r e d uterus. M o r g a n (1991) p o i n t s o u t , h o w e v e r , t h a t t h e r e has b e e n an i n c r e a s e in t h e n u m b e r of m a t e r n a l d e a t h s in w h i c h a n a e s t h e s i a m a y h a v e b e e n a contrib u t o r y f a c t o r ( T a b l e 2). W h y this is so is n o t clear. P e r h a p s it reflects t h e Table 2. Main cause of death in which anaesthesia was a contributory factor. Cause of death
Number
Hypertensive disorders Haemorrhage Early pregnancy deaths Genital tract trauma Other direct deaths Cardiac deaths Indirect: phaeochromocytoma Total
3 2 1 2 2 5 1 16
From Department of Health (1991).
Table 3. Maternal deaths associated with anaesthesia.
Operation
Indication
Cause of death
Elective caesarean
Cephalopelvic disproportion Aortic incompetence Fetal distress
Misplaced tracheal tube
1
Epidural/cardiovascular collapse Misplaced tracheal tube
1
Failure to progress, breech Previous caesarean section, ?ruptured uterus Retained placenta
Misplaced tracheal tube
1
Aspiration of gastric contents
1
Kinked tracheal tube
t
Elective caesarean
Cephalopelvic disproportion,
1
Emergency caesarean
Fetal distress
Misplaced tracheal tube after respiratory arrest secondary to complications of epidural anaesthesia Misplaced tracheal tube
Emergency planned caesarean Emergency unplanned caesarean Manual removal of placenta
No. of deaths
1
Late deaths
From Department of Health (1991).
1
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301
changing role of anaesthetists, who are now more closely involved in the management of seriously ill obstetric patients. With the increased interest in obstetric anaesthesia came the increased use of epidural and spinal anaesthesia. The major problems of general anaesthesia, namely difficulty in tracheal intubation and inhalation of gastric contents, are exchanged for cardiovascular depression and local anaesthetic toxicity (Morgan, 1991). However, the incidence of fatalities associated with regional anaesthetic techniques is far less than those associated with general anaesthesia. This is evidenced when the eight deaths in the last triennal report are more closely examined (Table 3). Although many procedures may be associated with maternal death, the emergency caesarean presents the greatest problems for the anaesthetist. The reasons are numerous but many are quite obvious: 9 The operation is often undertaken in haste with an ill-prepared mother. 9 There is often a heightened anxiety associated with anaesthetizing a mother and fetus. 9 Surgery is often performed late at night in isolated units. 9 Maternal physiology during pregnancy predisposes to problems, especially those involving the cardiovascular, respiratory and gastrointestinal systems. PREVENTION OF ANAESTHETIC-RELATED MATERNAL DEATHS Difficult and failed tracheal intubation
Difficult intubation, failed intubation and misplacement of the tracheal tube in the oesophagus appear to account for the majority of maternal deaths associated with anaesthesia. Death is attributable to hypoxia, which usually presents in the form of a cardiac arrest. Resuscitation is sometimes successful in restoring cardiac rhythm and output but death finally ensues because of irreversible brain damage. Scott (1986a) argues that anaesthetists should realize that intubation is not essential and that time should not be wasted on repeated attempts at intubation. It is difficult to give a precise definition of or frequency for failed tracheal intubation but several studies have suggested a failed intubation rate of approximately 1 in every 300 obstetric general anaesthetics (ScotL 1986a). Every anaesthetist must have a simple safe plan of management of failed intubation. Anaesthetic departments where trainees in anaesthesia are involved must prepare guidelines and ensure that each trainee is aware of those guidelines (see Appendix 1).
Preoperative examination Difficult intubation can be predicted in some patients (see Chapter 4); in particular, laryngeal oedema may be present in pre-eclamptic patients.
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Failed intubation drill
The main reason that difficult intubation in obstetrics causes mortality is the erroneous belief of anaesthetists that intubation is essential at all costs. Indeed, in many procedures in which intubation was regarded as essential, laryngeal masks are now routine, and these may be particularly suitable in difficult intubations (McClune et al, 1990). Failed intubation is discussed in detail in Chapter 4. In obstetric anaesthesia attention should be paid to be following. 1.
2. 3. 4.
5. 6.
The lungs must be oxygenated to provide an adequate 'reservoir of oxygen'. Preoxygenation with 100% oxygen for 3 minutes is desirable, and if this is not possible at least five total capacity breaths should be encouraged. Treatment to increase gastric pH should be constituted (see below). Capnography should be used to check adequacy of ventilation, and if there is any doubt about the position of the tube it should be removed. Help should be obtained, preferably from another anaesthetist, if the patient cannot be intubated. Mask and bag ventilation should be instituted with cricoid pressure maintained. Oral airways are preferable to nasal as the latter may produce brisk haemorrhage. If ventilation is difficult cricoid pressure may be eased and alterations to the position of the jaw may help. Transtracheal ventilation, cricothyrotomy and tracheostomy should be reserved for extreme situations. When adequate ventilation is achieved assessment of obstetric urgency may permit allowing the mother to waken and the use of regional block, with the understanding that if respiratory difficulties occur intubation may not be an option.
It is vital in obstetric failed intubation to avoid repeated attempts, and to decide early and act quickly when intubation is impossible. Aspiration of stomach contents The physiological changes that occur in pregnancy lead to an increased liability to regurgitation of gastric contents and possible aspiration into the lungs. The risk is further increased by difficult intubation where intrumentation may encourage regurgitation. The methods of reducing that risk are pharmacological and physical. The aim of the pharmacological methods is to reduce the volume of gastric juice as well as increasing its pH. Both the volume and the pH of the gastric juice are critical to the amount of lung damage that will occur upon aspiration. Critical volumes of gastric juice have recently been questioned. Raidoo et al (1990) have suggested that this volume needs to exceed 0.8 ml/ kg before significant lung damage occurs. This is approximately twice the previously commonly quoted figure and translates to approximately 50 ml in the average mother. Much has been written about maintaning the pH of the gastric contents above 2.5 in all labouring women. Thorburn and Moir (1987) pointed out
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that treating all women in labour with some form of antacid therapy is not sensible: each year a very large number of mothers would be receiving treatment in the hope of preventing a condition from which they are not at risk of suffering because they are not going to receive a general anaesthetic. In an Australian survey, Burgess and Crowhurst (1989) showed that antacid prophylaxis was used in less than a quarter of the hospitals surveyed without any increased incidence of problems with aspiration. This does not mean that antacid therapy should cease. Animal work by James et al (1984) has shown that the lower the pH of materials aspirated, the smaller the volume required to produce death. Schwarz et al (1980), in other animal work, have shown that non-acid aspiration is far from being a benign process, especially when the inhaled material is particulate.
Summary of pharmacological agents H2-histamine receptor antagonists. These reduce the amount of gastric acid produced. They have no effect on gastric acid present in the stomach but will slow further production. 9 For emergency anaesthesia: cimetidine 200mg i.m. or ranitidine 50mg i.m., given when the decision is made to operate.
Metoclopramide. This has been shown to accelerate gastric emptying and hence reduce the amount of residual gastric acid in the stomach. This effect may be blocked if there has been prior treatment with opioids. 9 For emergency anaesthesia: metoclopramide 10 mg i.v., given 10 minutes before induction.
Antacid. Any remaining gastric acid should be neutralized with an antacid. The non-particulate antacids are now favoured. 9 For emergency anaesthesia: 30ml 0.3M sodium citrate orally at least 3 minutes before the induction of anaesthesia. The patient should be rotated from side to side after ingestion to ensure adequate mixing with gastric contents. While the pharmacological agents can be used to reduce the amount of gastric juice and its acidity in the stomach, the prevention of regurgitation is dependent upon: 1. 2.
No increase in intragastric pressure. This may be increased by poor airway management with accidental ventilation of the stomach. The production of an effective physical barrier to prevent regurgitant fluid reaching the upper airway. This can be achieved by cricoid pressure (Sellick's manoeuvre) (Sellick, 1961).
Ideally both pharmacological and physical methods should be employed, but the physical remain the most important.
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Regional anaesthesia and analgesia Regional anaesthesia in obstetrics is thought to be safer than general anaesthesia because of the problems associated with intubation. However, there have been a number of deaths associated with regional anaesthetic and analgesic techniques. The causes of these deaths are: 9 Total spinal blockade with cardiovascular and respiratory depression. 9 Profound hypotension _ hypovolaemia. 9 Local anaesthetic toxicity.
Total spinal blockade This can occur when large doses of local anaesthetics are inadvertently injected directly into the subarachnoid space. The onset of the block occurs within 1-2 minutes after completion of the injection. The mother usually complains of numbness in both the lower and upper limbs before becoming apnoeic. Extreme hypotension does not necessarily occur. If resuscitation begins rapidly, the mother may still remain conscious. This is a life-threatening complication and resuscitative efforts must therefore be skilled as well as rapid. Respiratory support is the mainstay of management, with appropriate cardiovascular support if necessary. In most hospitals this would require the presence of a cardiac arrest team if an anaesthetist was not immediately present. The simplest way of avoiding this complication is to treat each injection into the epidural space as a test dose, i.e. never injecting down an epidural catheter a dose that might cause a total spinal block before testing for its effect. In practical terms this means that no more than 3 ml of a concentrated local anaesthetic solution may be injected before assessment. Higher volumes of more dilute local anaesthetic may be injected before total spinal block is achieved. Paech (1990) describes a case in which 10 ml of a 0.125% bupivicaine solution with 5 p~g/mlof fentanyl was injected into the subarachnoid space without producing a total spinal blockade.
Profound hypotension Profound hypotension is more common and of more rapid onset with spinal than with epidural anaesthesia. The hypotension will be even more dramatic in the presence of hypovolaemia. The blockade of the sympathetic nervous system causes dilatation of the peripheral vasculature, leading to a decrease in venous return and cardiac output and a fall in blood pressure. Bromage (1978) showed that decreases of blood volume by as little as 13% were poorly compensated for with lumbar epidural anaesthesia. Preloading of the circulation with adequate fluid (either crystalloid or colloid) before and during the onset of regional blockade is essential. In situations where overloading the circulation may be a problem, such as in pre-eclamptic patients, central venous pressure monitoring is useful. On occasions, the fall in blood pressure can be so dramatic that fluid loading may not be rapid enough and pharmacological intervention will be necessary. Ephedrine is preferred in the obstetric patient because of its
OBSTETRIC EMERGENCIES
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minimal effect on the uteroplacental circulation. If profound hypotension ensues, ephedrine may be ineffective and metaraminol, adrenaline or phenylephrine should be used until appropriate volume loading can be achieved.
Local anaesthetic toxicity Local anaesthetics, when injected systemically, produce toxic effects primarily on the central nervous system but they may also produce direct effects on the cardiovascular system if they are present in high enough concentration. A rising blood level will produce the following sequence of events (Scott, 1986b): 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Numbness of mouth, lips and tongue. Lightheadedness. Tinnitus. Visual disturbance. Slurring of speech. Muscular twitching. Irrational conversation. Unconsciousness. Grand real convulsion. Apnoea.
This sequence of events is the same with all local anaesthetics as the blood concentration increases. Animal studies have shown that bupivacaine differs from the other local anaesthetics in that: (1) the blood level of bupivacaine that produces central nervous system toxicity is only slightly below that which produces cardiovascular collapse; and (2) bupivacaine is associated with the production of ventricular arrhythmias and ventricular fibrillation. Pregnancy renders the patient more sensitive to the cardiovascular toxic effects of bupivacaine (Morishima et al, 1985; Covino, 1986). It is not recommended for use in obstetrics in high concentration (0.75%) because of the profound myocardial depression and prolonged, difficult resuscitations associated with accidental intravascular injections. Reiz and Nath (1986) have summarized the studies on cardiotoxicity of local anaesthetics. If ventricular fibrillation or spontaneously occurring ventricular tachycardia following a toxic dose of bupivacaine occurs, their suggested resuscitation regimen is to begin with effective external cardiac massage. Hypoxia, acidosis and any hyperkalaemia must be rapidly corrected for they potentiate the cardiotoxicity of bupivacaine. Inotropic support should be provided and the use of bretylium may be warranted because the cardiac arrhythmias seem to be of the re-entrant type. Often the ventricular fibrillation is resistant to direct countershock, but after treatment with bretylium it seems to respond to countershock. More recently, De La Coussaye et al (1992) have suggested that clonidine 0.01 mg/kg, given intravenously over a 1 minute period with a 5 Ixg kg -1 min -1 dobutamine
306
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infusion, corrected not only the electrophysiological impairment induced by bupivacaine but also the haemodynamic depression. DEATHS TO WHICH ANAESTHESIA MAY CONTRIBUTE Haemorrhage (Table 4) The management of extensive haemorrhage in the obstetric patient often involves the anaesthetist. The bleeding is usually brisk and may be massive. The majority of deaths associated with haemorrhage stem from initial inadequate resuscitation and prolonged haemorrhage, leading to coagulation problems. Table 4. Obstetric causes of major bleeding in the peripartum period.
Maternal Antepartum and intrapartum Placenta praevia Placental abruption Ruptured uterus Postpartum Atonic uterus Placental accreta and percreta Trauma to cervix, vagina and perineum Fetal Vasa praevia
Table 5. Estimated total blood volume
in normal pregnancy. Volume (ml) Non-pregnant
4000
Pregnancy 20 weeks 30weeks 40 weeks
4650 5550 5650
From Hytten and Lind (1973).
Table 5 gives the estimated total blood volumes in normal pregnancy. Maternal hypovolaemia and associated hypotension must be corrected immediately by inserting at least two large-gauge lines and administering appropriate replacement fluids (Table 6), as guided by central venous pressure (CVP) measurement, urine output and vital signs. The average CVP in the third trimester is 1.0 kPa (10 cmH20) (Muldoon, 1969). In acute hypovolaemia there is an initial peripheral vasoconstriction which will maintain systemic arterial pressure close to normal. The uterine blood vessels, which at term are maximally dilated, participate in this peripheral vaso-
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Table 6. Maternal hypovolaemia: appropriate fluids for resuscitation. Blood volume lost (%) 10-15 15-30 30-35
35-40 >40
Action
Set up drip; organize crossmatching Replace with Haemaccel or lactated Ringer's (Hartmann's) solution Replace initiallywith Haemaccel or Hartmanns. Give blood when fully crossmatched; ratio of blood to other fluid 1 : 2; blood should be warmed and filtered Restore blood volume as quickly as possible. Blood can generally be crossmatched; ratio of blood to other fluid 1 : 1 Uncrossmatched blood may be used. ABO and Rhesus compatible. Fresh blood, i.e. less than 24-hours-oldis preferable; 5% albumin should be the non-haemoglobinfluid of choice. Ratio of blood to other fluid 1 : 1. Maintain haematocrit at around 30%
constriction so that a reduction in uterine blood flow occurs early. The type of fluid required for replacement depends on the diagnosis. In general, it is wise to use isotonic solutions which remain in the intravascular space and generate an osmotic pressure. While the resuscitation process is in progress the mother is in the left lateral position, if still pregnant, to avoid compression of the inferior vena cava. An obstetric opinion should be sought in order to exclude a bleeding source that can readily be stopped. Often the only course open to the obstetrician to stem the flow of blood is to perform a surgical procedure. Anaesthesia for the hypovolaemic patient is difficult. Intravenous ketamine with reduced doses of thiopentone or propofol may be necessary. Ketamine has the advantage of increasing uterine tone, thereby reducing endometrial bleeding from the site of placental separation. Haemostatic anomalies more readily occur if the placenta is involved in the cause of bleeding, e.g. abruption. It seems that thromboplastins from the placenta and the decidua activate circulating plasminogen and the extrinsic procoagulant system. The end-result of widespread intravascular coagulation and fibrinolysis is thrombocytopenia, hypofibrinogenaemia, consumption of factors V, VII and VIII and the appearance of fibrin degradation products and soluble fibrin monomer complexes (Gilabert and Estelles, 1985). This bleeding disorder may be worsened by the coagulopathy of massive transfusion and the haemodilution of rapid volume replacement. Here, flesh blood is the treatment of choice. One unit of flesh blood (less than 24 hours old) raises the platelet count by 10-15 x 109/1, haemoglobin by 10-15 g/l, haematocrit by 3% and circulating fibrinogen by 0.08--0.125 g/1 (Beller and Uszinski, 1974). If more fibrinogen replacement is required, fresh frozen plasma is another valuable source. Further platelets may be required if the platelet count is less than 50 x 109/1. Once hypovolaemia is corrected, persistently low urine output may herald the onset of renal failure. Administration of low dose dopamine
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(2 Ixg kg -1 min -1) may be useful in establishing the diagnosis and alleviating the problem. Uterine atony sometimes persists into the postpartum period: intramyometrial injection of prostaglandin F2~ may be indicated. On delivery, the neonate often needs aggressive and immediate resuscitation. Neonatal hypovolaemia can be corrected using blood obtained from the fetal surface of the placenta with a heparinized syringe. Anaesthetic agents given to the mother may affect the way the neonate can handle acute haemorrhage.
Hypertensive disorders Approximately 10% of all pregnancies in developed countries are complicated by a hypertensive disorder. Pre-eclampsia is the most common of these. This syndrome can take on many forms, the most frequent being the triad of increased blood pressure, proteinuria and central nervous system irritability. Another, more virulentform of the syndrome presents as epigastric and right hypochondrial pain and is associated with haemolysis, elevated liver enzymes and low platelets. Placental growth is usually compromised with pre-eclampsia, with the fetus at risk in utero. Improvements in placental growth can be achieved with low-dose aspirin regimens (Trudinger et al, 1988) but the definitive treatment for the mother is delivery. Decreasing central nervous system irritability, stabilizing hypertension and correcting any volume deficit should be achieved before the patient is submitted to anaesthesia. The critical time during general anaesthesia is at laryngoscopy and intubation, when there is a sudden sympathetic response (Hodgkinson et al, 1980) which might cause a sharp rise in blood pressure. Intracranial bleeding is a real risk. Many methods have been used to obtund this intubation response, including deep anaesthesia, potent intravenous hypotensive agents, intravenous lignocaine and short-acting opioids, all with limited success. A regional anaesthetic technique would therefore seem preferable but haemostasis may be a problem in some pre-eclamptic patients. This usually takes the form of a reduced platelet count (less than 100 x 109/1) and coagulation defects. If these are present they provide a relative contraindication to regional anaesthesia. This should be balanced against the fact that laryngeal oedema is often present or results from the resuscitative regimens in pre-eclamptics, making tracheal intubation difficult. This gives added impetus to avoiding intubation and choosing a regional anaesthetic regimen. Most obstetric units develop protocols in which inital management is set forth, detailing medications for decreasing cerebral irritability, hypertension control and volume loading. For example: 9 Decreasing cerebral irritability: dilantin; ? magnesium sulphate. 9 Stabilizing hypertension: clonidine; hydralazine; diazoxide. 9 Volume loading: crystalloid (Hartmann's); colloid (5% albumin) in 1:1 ratio monitored by CVP. Carefully titrated to 5-8 cmH20 range.
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Cardiac disease
Since there has been significant improvement in the management of patients with either acquired or congenital heart disease, there have been an increasing number of women with these conditions becoming pregnant and requiring intervention in the management of their labour and delivery. Deaths are most commonly associated with valvular disease or cardiomyopathies. These patients tend to have a relatively fixed cardiac output and therefore poorly tolerate even small changes in heart filling pressures. In administering anaesthesia, the primary considerations are the avoidance of myocardial depression, increases in the workload of the heart and significant alterations in blood pressure. These requisities are best met with a cautiously titrated lumbar epidural block administered early in labour and maintained continuously until after delivery. Prevention of bearing down in the second stage of labour is essential so the technique must abolish the urge to bear down in the second stage and provide excellent conditions for forceps or vacuum extraction. Lumbar epidural anaesthesia can be adjusted so that the appropriate density of block is achieved to TIO. If labour should progress too rapidly for this to be cautiously achieved, a pudendal block supplemented with inhalational analgesia proves satisfactory. Often caesarean section is the mode of delivery chosen for the pregnant patient with severe cardiac disease. Here, lumbar epidural anaesthesia is good choice in that it: 1. 2. 3. 4. 5. 6.
Effectively blocks the stress response from the outpouring of endogenous catecholamines. Does not produce the sympathetic vasopressor or cardiac response seen with rapid sequence induction of general anaesthesia. Decreases myocardial oxygen consumption as an end-result of decreasing preload and afterload of the heart. Has minimal myocardial depressant qualities. Can be initiated slowly, allowing control of associated cardiovascular changes. Can be continued into the postoperative period to provide excellent analgesia.
Epidural anaesthesia is best avoided in patients who are likely to develop right-to-left shunts or have pulmonary hypertension because of the risks associated with uncontrolled hypotension. When general anaesthesia is necessary, deep planes of anaesthesia are indicated. Pretreatment with fentanyl, up to 5 ixg/kg, are well tolerated by the pregnant patient with cardiac disease and will significantly attenuate the sympathetic discharge and hypertensive response associated with intubation. If further blood pressure control is required then B-blocker therapy with peripheral vasodilatation is indicated. Amniotic fluid embolism
This is an uncommon complication of pregnancy but, if it does occur, has a very high rate of mortality.
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Clinically, the presentation is one of an acute anxious patient who suddently develops respiratory distress, usually without any chest pain. It is often associated with an obstetric event such as rupturing of the membranes. Amniotic fluid and its contents leak into the maternal circulation, leading to the mechanical blockage of the pulmonary vessels. An anaphylactoid reaction often accompanies this, with resultant bronchospasm and pulmonary vasoconstriction. Severe hypoxia and acute pulmonary hypertension leading to acute pulmonary oedema often leads to the death of the mother. Mothers who survive nearly all develop a diffuse intravascular coagulopathy. The prime objects of treatment are: 1. 2. 3.
Improvement of oxygenation. Support of the cardiovascular system. Treatment of the coagulopathy.
Severe ventilation-perfusion defects that develop with the entry of amniotic fluid into the pulmonary circulation are the cause of the hypoxia. Intubation and positive pressure ventilation with positive end expiratory pressure and 100% oxygen is required. Bronchodilators help overcome the bronchospasm. Inotropic support of the heart is required because rightsided and left-sided heart failure ensue. The coagulopathy is difficult to control and is often complicated by massive bleeding associated with uterine atony. This bleeding must be controlled and intravascular volume must be maintained. Fresh blood has the advantage in this situation, with further correction of clotting deficiencies with fresh frozen plasma and platelets (Clark, 1991). C A R D I O P U L M O N A R Y RESUSCITATION IN THE P R E G N A N T PATIENT
Cardiac arrest in late pregnancy (Table 7) occurs in 1 in 30 000 pregnancies and survival after such an event is exceptional (unless it occurs under anaesthesia) (Rees and Willis, 1988). Resuscitation of the pregnant patient is made more difficult because of aortocaval compression by the gravid uterus. Even minor degrees will have a profound effect on the success or failure of the resuscitative efforts (Marx, 1982). It is therefore imperative that uterine displacement be maintained during cardiopulmonary resusciTable 7. Causesof cardiac arrest in late pregnancy. Acute hypoxia Anaestheticmishap Major pulmonaryembolism Major haemorrhage Amnioticfluidembolism Myocardialinfarction Local anaesthetictoxicity Electrocution Trauma
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tation. Effective wedging should not greatly effect the position of the torso, and chest compressions should still be possible without difficulty. If circumstances make this approach impractical then the uterus should be manually deviated to the left and slightly cephalad. If it is possible to raise the patient's legs, this simple manoeuvre will also help to improve venous return. If haemodynamic stability cannot be achieved even though uterine displacement is thought effective, abdominal delivery of the fetus should be performed immediately. Prompt delivery will assist maternal resuscitation and recovery. Marx (1982) reviewed five cases where resuscitation was required for more than 10 minutes. The three patients who underwent immediate caesarean section survived with no neurological deficit, whereas those in whom delivery was delayed suffered irreversible brain damage. POSTOPERATIVE CARE OF THE OBSTETRIC PATIENT Good anaesthetic management dictates that no mother should leave the operating room until she is fully conscious, orientated and able to protect her own airway. If there is any doubt, the anaesthetist should remain with the patient until those criteria are satisfied. A number of deaths have been associated with inadequate postoperative care. Inadequate reversal of neuromuscular blockade has led to hypoxia and eventual cardiac arrest. The reversal of neuromuscular blockade should be checked either by the use of a nerve stimulator or by the patient's ability to keep her head raised from a pillow. Inadequate staffing of the postpartum wards has led to a number of deaths from respiratory obstruction, haemorrhage and aspiration of stomach contents. It is vitally important that postnatal wards are staffed with trained nurses and that all mothers are observed carefully for at least 24 hours after an anaesthetic. This observation should consist, as a minimum, of regular assessments of pulse rate, blood pressure, respiratory rate, level of consciousness and blood loss. With the best possible anaesthetic care by experienced anaesthetists maternal anaesthetic mortality and morbidity can be kept to a minimum. This is what is strived for by modern obstetric units. This is what is expected by obstetric patients. SUMMARY
This chapter reviews the situations where obstetric emergencies have led to maternal mortality or morbidity. Failed intubation, aspiration of stomach contents, regional anaesthesia and analgesia mortality are reviewed and an appropriate course of action when confronted with these situations outlined. In addition, situations where anaesthesia or analgesia may be difficult are reviewed. Massive haemorrhage, hypertensive disorders of pregnancy, cardiac disease in pregnancy, amniotic fluid embolism, cardiopulmonary resuscitation and postoperative care of the obstetric patient are outlined and problems in their management highlighted.
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APPENDIX
1
Guidelines for management of failed intubation at caesarean section
9 All patients undergoing general anaesthesia: 1. Careful antacid prophylaxis (before induction) 2. Preoxygenated 9 If cords not visualized at laryngoscopy then only one attempt at intubation. 9 If not rapidly successful then organize the most skilled help available
~
~Obstetric reasons DECIDE for ~ . . . . . nt morbidity potential9
DISCONTINUE ~ ANAESTHESIA
1.
2.
Ventilate via face mask with 100% oxygen and allow patient to awaken
When awake proceed with a form of regional anaesthesia
PROCEED with ANAESTHESIA Patient supine + Trendelenberg Cricoid pressure maintained until spontaneously breathing and then released
Ventilate via face mask with 100% oxygen and 1.5 MAC of volatile agent
9 IF DIFFICULT TO VENTILATE 1. Use an oral airway 2. Laryngeal mask 3. Triple airway manoeuvre 9 As a last resort Cricothyroid puncture: large-bore (12 G) i.v. cannula. Connect via 3.5 mm endotracheal tube connector and ventilate via anaesthetic circuit Tracheostomy
REFERENCES
Belier G & Uszinski M (1974) Disseminated intravascular coagulation in pregnancy. Clinical Obstetrics and Gynaecology 17: 250-278. Bromage P (ed) (1978) Textbook Epidural Analgesia chap. 10, pp 366-369. London: WB Saunders. Burgess R & Crowhurst J (1989) Acid aspiration prophylaxis in Australian obstetric hospitals. Anaesthesia and Intensive Care 17: 492-495. Clark S (1991) Amniotic fluid embolism. Critical Care Clinics 7: 877-882. Covino B (1986) Toxicity of local anaesthetics in Obstetrics. III. Overview. Clinical Anaesthesia 4: 109--111. De La Coussaye J, Bassoul B, Brugada J e t al (1992) Reversal of electrophysiologic and hemodynamic effects induced by high dose bupivacaine by the combination of clonidine and dobutamine. Anesthesia and Analgesia 74" 703-711. Department of Health (1978) Report on Confidential Enquiries into Maternal Deaths in England and Wales 1973-1975. London: HMSO.
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Department of Health (1982) Report on Confidential Enquiries into Maternal Deaths in England and Wales 1976-1978. London: HMSO. Department of Health (1991) Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1985-1987. London: HMSO. Gilabert J & Estelles A (1985) Abruptio placentae and disseminated intravascular coagulation. Acta Obstetrica et Gynaecologica Scandinavica 64: 35-39. Hodgkinson R, Husain F & Hayashi R (1980) Systemic and pulmonary blood pressure during caesarean section in parturients with gestational hypertension. Canadian Anaesthetic Society Journal 27: 389-394. Hytten J & Lind D (1973) Diagnostic Indices in Pregnancy, p 37. London: Ciba and Geigy. James C, Modell J, Gibb C et al (1984) Pulmonary aspiration---effect of volume and pH in the rat. Anesthesia and Analgesia 63: 665-668. McClune S, Reagan M & Moore J (1990) Laryngeal mask airway for caesarean section. Anaesthesia 45: 227-228. Marx G (1982) Cardiopulmonary resuscitation of late pregnant women. Anesthesiology 56: 156. Morgan M (1991) Getting there (editorial). Anaesthesia 45: 709-711. Morishima H, Pederson H & Finster M (1985) Bupivacaine toxicity in pregnant and nonpregnant ewes. Anesthesiology 63: 134-135. Muldoon M (1969) The use of central venous pressure monitoring in abruptio placentae. British Journal of Obstetrics and Gynaecology 76: 225-228. P aech M (1990) Inadvertent spinal anaesthesia with 0.125 % bupivacaine and fentanyl during labour. Anaesthesia and Intensive Care 18: 400-402. Raidoo D, Rocke D, Brock-Utne J e t al (1990) Critical volume for pulmonary acid aspiration: reappraisal in a primate model. British Journal of Anaesthesia 65: 248-250. Rees G & Willis B (1988) Resuscitation in late pregnancy. Anaesthesia 43: 347-349. Reiz S & Nath S (1986) Cardiotoxicity of local anaesthetic agents. British Journal of Anaesthesia 58: 736-746. Schwarz D, Wynne J, Gibbs C et al (1980) The pulmonary consequences of aspiration of gastric contents at pH values greater than 2.5. American Review of Respiratory Disease 121: 119-126. Scott DB (1986a) Endotracheal intubation a friend or foe? British Medical Journal 292: 157-158. Scott D (1986b) Toxic effects of local anaesthetic agent on the central nervous system. British Journal of Anaesthesia 58: 732-735. Sellick B (1961) Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet ii: 404-406. Thorburn J & Moir D (1987) Antacid therapy for emergency caesarean section. Anaesthesia 42: 352-355. Trudinger B, Cook C, Thompson R et al (1988) Low dose aspirin therapy improves fetal weight in umbilical placental insufficiency. American Journal of Obstetrics and Gynecology 159: 681-685.
X. L A H
Emergency obstetric anaesthesia is not for the inexperienced anaesthetist; however, because obstetric procedures are often performed at unsociable hours in isolated units the provision of anaesthesia is frequently delegated to junior hospital medical staff training in anaesthesia. It therefore should come as no surprise, when maternal mortality reports are examined for anaesthetic-related deaths, to read comments such as 'The giving of responsibility to inexperienced anaesthetists was the principal cause of 12 deaths' (1973-1975) or 'There should be a review of anaesthetic services to maternity units with the aim of providing better trained anaesthetists' (19761978) (Department of Health, 1978, 1982). Changes are being implemented. Obstetric anaesthetic sessions are taken up by experienced anaesthetists. These anaesthetists are forming themselves into groups to actively promote interest and research into obstetric anaesthesia. Smaller maternity units are being consolidated into larger units within major general hospitals to make it financially feasible to provide dedicated obstetric anaesthetic sessions. Progress has, however, been slow because of resistance from a variety of groups with vested interests. They must not be allowed to succeed in delaying progress: anaesthetic-related maternal morbidity and mortality can only decrease when experienced anaesthetists provide an emergency obstetric anaesthetic service. Table 1. Rates of direct maternal death per million total pregnancies.
Cause of death
1973-1975
1976-1978
1979-1981 1982-1984
1985-1987
Hypertension Diseases of pregnancy Pulmonary embolism Abortion Haemorrhage Anaesthesia Ectopic pregnancy Amniotic fluid embolism Sepsis Ruptured uterus Other direct
13.2
12.5
14.2
10.0
9.4
12.8 10.5 8.1 10.5 7.4 5.4 7.4 4.3 8.5
18.5 6.0 10.3 11.6 9.0 4.7 6.5 6.0 8.2
9.0 5.5 5.5 8.7 7.9 7.1 3.1 1.6 7.5
10.0 4.4 3.6 7.2 4.0 5.6 1.0 1.2 8.4
9.1 2.3 3.8 1.9 4.1 3.4 2.3 1.9 7.5
Total
88.0
93.4
70.0
55.0
45.6
From Department of Health (1991). Baillikre' s Clinical Anaesthesiology-Vol. 7, No. 2, June 1993 ISBN 0--7020-1734-5
299 Copyright 9 1993, by Bailli6re Tindall All rights of reproduction in any form reserved
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E v e n at this e a r l y s t a g e t h e change~ t h a t h a v e b e e n i m p l e m e n t e d s e e m to b e affecting t h e a n a e s t h e t i c - r e l a t e d m a t e r n a l m o r t a l i t y statistics ( T a b l e 1). In the t r i e n n i u m 1985-1987, e i g h t m o t h e r s d i e d as a d i r e c t result of r e c e i v i n g a n a n a e s t h e t i c . This r e p r e s e n t s a significant r e d u c t i o n f r o m t h e p r e v i o u s r e p o r t , w h e n a n a e s t h e s i a was t h e t h i r d m o s t c o m m o n c a u s e of d e a t h ; it is n o w e q u a l last w i t h r u p t u r e d uterus. M o r g a n (1991) p o i n t s o u t , h o w e v e r , t h a t t h e r e has b e e n an i n c r e a s e in t h e n u m b e r of m a t e r n a l d e a t h s in w h i c h a n a e s t h e s i a m a y h a v e b e e n a contrib u t o r y f a c t o r ( T a b l e 2). W h y this is so is n o t clear. P e r h a p s it reflects t h e Table 2. Main cause of death in which anaesthesia was a contributory factor. Cause of death
Number
Hypertensive disorders Haemorrhage Early pregnancy deaths Genital tract trauma Other direct deaths Cardiac deaths Indirect: phaeochromocytoma Total
3 2 1 2 2 5 1 16
From Department of Health (1991).
Table 3. Maternal deaths associated with anaesthesia.
Operation
Indication
Cause of death
Elective caesarean
Cephalopelvic disproportion Aortic incompetence Fetal distress
Misplaced tracheal tube
1
Epidural/cardiovascular collapse Misplaced tracheal tube
1
Failure to progress, breech Previous caesarean section, ?ruptured uterus Retained placenta
Misplaced tracheal tube
1
Aspiration of gastric contents
1
Kinked tracheal tube
t
Elective caesarean
Cephalopelvic disproportion,
1
Emergency caesarean
Fetal distress
Misplaced tracheal tube after respiratory arrest secondary to complications of epidural anaesthesia Misplaced tracheal tube
Emergency planned caesarean Emergency unplanned caesarean Manual removal of placenta
No. of deaths
1
Late deaths
From Department of Health (1991).
1
OBSTETRIC EMERGENCIES
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changing role of anaesthetists, who are now more closely involved in the management of seriously ill obstetric patients. With the increased interest in obstetric anaesthesia came the increased use of epidural and spinal anaesthesia. The major problems of general anaesthesia, namely difficulty in tracheal intubation and inhalation of gastric contents, are exchanged for cardiovascular depression and local anaesthetic toxicity (Morgan, 1991). However, the incidence of fatalities associated with regional anaesthetic techniques is far less than those associated with general anaesthesia. This is evidenced when the eight deaths in the last triennal report are more closely examined (Table 3). Although many procedures may be associated with maternal death, the emergency caesarean presents the greatest problems for the anaesthetist. The reasons are numerous but many are quite obvious: 9 The operation is often undertaken in haste with an ill-prepared mother. 9 There is often a heightened anxiety associated with anaesthetizing a mother and fetus. 9 Surgery is often performed late at night in isolated units. 9 Maternal physiology during pregnancy predisposes to problems, especially those involving the cardiovascular, respiratory and gastrointestinal systems. PREVENTION OF ANAESTHETIC-RELATED MATERNAL DEATHS Difficult and failed tracheal intubation
Difficult intubation, failed intubation and misplacement of the tracheal tube in the oesophagus appear to account for the majority of maternal deaths associated with anaesthesia. Death is attributable to hypoxia, which usually presents in the form of a cardiac arrest. Resuscitation is sometimes successful in restoring cardiac rhythm and output but death finally ensues because of irreversible brain damage. Scott (1986a) argues that anaesthetists should realize that intubation is not essential and that time should not be wasted on repeated attempts at intubation. It is difficult to give a precise definition of or frequency for failed tracheal intubation but several studies have suggested a failed intubation rate of approximately 1 in every 300 obstetric general anaesthetics (ScotL 1986a). Every anaesthetist must have a simple safe plan of management of failed intubation. Anaesthetic departments where trainees in anaesthesia are involved must prepare guidelines and ensure that each trainee is aware of those guidelines (see Appendix 1).
Preoperative examination Difficult intubation can be predicted in some patients (see Chapter 4); in particular, laryngeal oedema may be present in pre-eclamptic patients.
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Failed intubation drill
The main reason that difficult intubation in obstetrics causes mortality is the erroneous belief of anaesthetists that intubation is essential at all costs. Indeed, in many procedures in which intubation was regarded as essential, laryngeal masks are now routine, and these may be particularly suitable in difficult intubations (McClune et al, 1990). Failed intubation is discussed in detail in Chapter 4. In obstetric anaesthesia attention should be paid to be following. 1.
2. 3. 4.
5. 6.
The lungs must be oxygenated to provide an adequate 'reservoir of oxygen'. Preoxygenation with 100% oxygen for 3 minutes is desirable, and if this is not possible at least five total capacity breaths should be encouraged. Treatment to increase gastric pH should be constituted (see below). Capnography should be used to check adequacy of ventilation, and if there is any doubt about the position of the tube it should be removed. Help should be obtained, preferably from another anaesthetist, if the patient cannot be intubated. Mask and bag ventilation should be instituted with cricoid pressure maintained. Oral airways are preferable to nasal as the latter may produce brisk haemorrhage. If ventilation is difficult cricoid pressure may be eased and alterations to the position of the jaw may help. Transtracheal ventilation, cricothyrotomy and tracheostomy should be reserved for extreme situations. When adequate ventilation is achieved assessment of obstetric urgency may permit allowing the mother to waken and the use of regional block, with the understanding that if respiratory difficulties occur intubation may not be an option.
It is vital in obstetric failed intubation to avoid repeated attempts, and to decide early and act quickly when intubation is impossible. Aspiration of stomach contents The physiological changes that occur in pregnancy lead to an increased liability to regurgitation of gastric contents and possible aspiration into the lungs. The risk is further increased by difficult intubation where intrumentation may encourage regurgitation. The methods of reducing that risk are pharmacological and physical. The aim of the pharmacological methods is to reduce the volume of gastric juice as well as increasing its pH. Both the volume and the pH of the gastric juice are critical to the amount of lung damage that will occur upon aspiration. Critical volumes of gastric juice have recently been questioned. Raidoo et al (1990) have suggested that this volume needs to exceed 0.8 ml/ kg before significant lung damage occurs. This is approximately twice the previously commonly quoted figure and translates to approximately 50 ml in the average mother. Much has been written about maintaning the pH of the gastric contents above 2.5 in all labouring women. Thorburn and Moir (1987) pointed out
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that treating all women in labour with some form of antacid therapy is not sensible: each year a very large number of mothers would be receiving treatment in the hope of preventing a condition from which they are not at risk of suffering because they are not going to receive a general anaesthetic. In an Australian survey, Burgess and Crowhurst (1989) showed that antacid prophylaxis was used in less than a quarter of the hospitals surveyed without any increased incidence of problems with aspiration. This does not mean that antacid therapy should cease. Animal work by James et al (1984) has shown that the lower the pH of materials aspirated, the smaller the volume required to produce death. Schwarz et al (1980), in other animal work, have shown that non-acid aspiration is far from being a benign process, especially when the inhaled material is particulate.
Summary of pharmacological agents H2-histamine receptor antagonists. These reduce the amount of gastric acid produced. They have no effect on gastric acid present in the stomach but will slow further production. 9 For emergency anaesthesia: cimetidine 200mg i.m. or ranitidine 50mg i.m., given when the decision is made to operate.
Metoclopramide. This has been shown to accelerate gastric emptying and hence reduce the amount of residual gastric acid in the stomach. This effect may be blocked if there has been prior treatment with opioids. 9 For emergency anaesthesia: metoclopramide 10 mg i.v., given 10 minutes before induction.
Antacid. Any remaining gastric acid should be neutralized with an antacid. The non-particulate antacids are now favoured. 9 For emergency anaesthesia: 30ml 0.3M sodium citrate orally at least 3 minutes before the induction of anaesthesia. The patient should be rotated from side to side after ingestion to ensure adequate mixing with gastric contents. While the pharmacological agents can be used to reduce the amount of gastric juice and its acidity in the stomach, the prevention of regurgitation is dependent upon: 1. 2.
No increase in intragastric pressure. This may be increased by poor airway management with accidental ventilation of the stomach. The production of an effective physical barrier to prevent regurgitant fluid reaching the upper airway. This can be achieved by cricoid pressure (Sellick's manoeuvre) (Sellick, 1961).
Ideally both pharmacological and physical methods should be employed, but the physical remain the most important.
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Regional anaesthesia and analgesia Regional anaesthesia in obstetrics is thought to be safer than general anaesthesia because of the problems associated with intubation. However, there have been a number of deaths associated with regional anaesthetic and analgesic techniques. The causes of these deaths are: 9 Total spinal blockade with cardiovascular and respiratory depression. 9 Profound hypotension _ hypovolaemia. 9 Local anaesthetic toxicity.
Total spinal blockade This can occur when large doses of local anaesthetics are inadvertently injected directly into the subarachnoid space. The onset of the block occurs within 1-2 minutes after completion of the injection. The mother usually complains of numbness in both the lower and upper limbs before becoming apnoeic. Extreme hypotension does not necessarily occur. If resuscitation begins rapidly, the mother may still remain conscious. This is a life-threatening complication and resuscitative efforts must therefore be skilled as well as rapid. Respiratory support is the mainstay of management, with appropriate cardiovascular support if necessary. In most hospitals this would require the presence of a cardiac arrest team if an anaesthetist was not immediately present. The simplest way of avoiding this complication is to treat each injection into the epidural space as a test dose, i.e. never injecting down an epidural catheter a dose that might cause a total spinal block before testing for its effect. In practical terms this means that no more than 3 ml of a concentrated local anaesthetic solution may be injected before assessment. Higher volumes of more dilute local anaesthetic may be injected before total spinal block is achieved. Paech (1990) describes a case in which 10 ml of a 0.125% bupivicaine solution with 5 p~g/mlof fentanyl was injected into the subarachnoid space without producing a total spinal blockade.
Profound hypotension Profound hypotension is more common and of more rapid onset with spinal than with epidural anaesthesia. The hypotension will be even more dramatic in the presence of hypovolaemia. The blockade of the sympathetic nervous system causes dilatation of the peripheral vasculature, leading to a decrease in venous return and cardiac output and a fall in blood pressure. Bromage (1978) showed that decreases of blood volume by as little as 13% were poorly compensated for with lumbar epidural anaesthesia. Preloading of the circulation with adequate fluid (either crystalloid or colloid) before and during the onset of regional blockade is essential. In situations where overloading the circulation may be a problem, such as in pre-eclamptic patients, central venous pressure monitoring is useful. On occasions, the fall in blood pressure can be so dramatic that fluid loading may not be rapid enough and pharmacological intervention will be necessary. Ephedrine is preferred in the obstetric patient because of its
OBSTETRIC EMERGENCIES
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minimal effect on the uteroplacental circulation. If profound hypotension ensues, ephedrine may be ineffective and metaraminol, adrenaline or phenylephrine should be used until appropriate volume loading can be achieved.
Local anaesthetic toxicity Local anaesthetics, when injected systemically, produce toxic effects primarily on the central nervous system but they may also produce direct effects on the cardiovascular system if they are present in high enough concentration. A rising blood level will produce the following sequence of events (Scott, 1986b): 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Numbness of mouth, lips and tongue. Lightheadedness. Tinnitus. Visual disturbance. Slurring of speech. Muscular twitching. Irrational conversation. Unconsciousness. Grand real convulsion. Apnoea.
This sequence of events is the same with all local anaesthetics as the blood concentration increases. Animal studies have shown that bupivacaine differs from the other local anaesthetics in that: (1) the blood level of bupivacaine that produces central nervous system toxicity is only slightly below that which produces cardiovascular collapse; and (2) bupivacaine is associated with the production of ventricular arrhythmias and ventricular fibrillation. Pregnancy renders the patient more sensitive to the cardiovascular toxic effects of bupivacaine (Morishima et al, 1985; Covino, 1986). It is not recommended for use in obstetrics in high concentration (0.75%) because of the profound myocardial depression and prolonged, difficult resuscitations associated with accidental intravascular injections. Reiz and Nath (1986) have summarized the studies on cardiotoxicity of local anaesthetics. If ventricular fibrillation or spontaneously occurring ventricular tachycardia following a toxic dose of bupivacaine occurs, their suggested resuscitation regimen is to begin with effective external cardiac massage. Hypoxia, acidosis and any hyperkalaemia must be rapidly corrected for they potentiate the cardiotoxicity of bupivacaine. Inotropic support should be provided and the use of bretylium may be warranted because the cardiac arrhythmias seem to be of the re-entrant type. Often the ventricular fibrillation is resistant to direct countershock, but after treatment with bretylium it seems to respond to countershock. More recently, De La Coussaye et al (1992) have suggested that clonidine 0.01 mg/kg, given intravenously over a 1 minute period with a 5 Ixg kg -1 min -1 dobutamine
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infusion, corrected not only the electrophysiological impairment induced by bupivacaine but also the haemodynamic depression. DEATHS TO WHICH ANAESTHESIA MAY CONTRIBUTE Haemorrhage (Table 4) The management of extensive haemorrhage in the obstetric patient often involves the anaesthetist. The bleeding is usually brisk and may be massive. The majority of deaths associated with haemorrhage stem from initial inadequate resuscitation and prolonged haemorrhage, leading to coagulation problems. Table 4. Obstetric causes of major bleeding in the peripartum period.
Maternal Antepartum and intrapartum Placenta praevia Placental abruption Ruptured uterus Postpartum Atonic uterus Placental accreta and percreta Trauma to cervix, vagina and perineum Fetal Vasa praevia
Table 5. Estimated total blood volume
in normal pregnancy. Volume (ml) Non-pregnant
4000
Pregnancy 20 weeks 30weeks 40 weeks
4650 5550 5650
From Hytten and Lind (1973).
Table 5 gives the estimated total blood volumes in normal pregnancy. Maternal hypovolaemia and associated hypotension must be corrected immediately by inserting at least two large-gauge lines and administering appropriate replacement fluids (Table 6), as guided by central venous pressure (CVP) measurement, urine output and vital signs. The average CVP in the third trimester is 1.0 kPa (10 cmH20) (Muldoon, 1969). In acute hypovolaemia there is an initial peripheral vasoconstriction which will maintain systemic arterial pressure close to normal. The uterine blood vessels, which at term are maximally dilated, participate in this peripheral vaso-
OBSTETRIC EMERGENCIES
307
Table 6. Maternal hypovolaemia: appropriate fluids for resuscitation. Blood volume lost (%) 10-15 15-30 30-35
35-40 >40
Action
Set up drip; organize crossmatching Replace with Haemaccel or lactated Ringer's (Hartmann's) solution Replace initiallywith Haemaccel or Hartmanns. Give blood when fully crossmatched; ratio of blood to other fluid 1 : 2; blood should be warmed and filtered Restore blood volume as quickly as possible. Blood can generally be crossmatched; ratio of blood to other fluid 1 : 1 Uncrossmatched blood may be used. ABO and Rhesus compatible. Fresh blood, i.e. less than 24-hours-oldis preferable; 5% albumin should be the non-haemoglobinfluid of choice. Ratio of blood to other fluid 1 : 1. Maintain haematocrit at around 30%
constriction so that a reduction in uterine blood flow occurs early. The type of fluid required for replacement depends on the diagnosis. In general, it is wise to use isotonic solutions which remain in the intravascular space and generate an osmotic pressure. While the resuscitation process is in progress the mother is in the left lateral position, if still pregnant, to avoid compression of the inferior vena cava. An obstetric opinion should be sought in order to exclude a bleeding source that can readily be stopped. Often the only course open to the obstetrician to stem the flow of blood is to perform a surgical procedure. Anaesthesia for the hypovolaemic patient is difficult. Intravenous ketamine with reduced doses of thiopentone or propofol may be necessary. Ketamine has the advantage of increasing uterine tone, thereby reducing endometrial bleeding from the site of placental separation. Haemostatic anomalies more readily occur if the placenta is involved in the cause of bleeding, e.g. abruption. It seems that thromboplastins from the placenta and the decidua activate circulating plasminogen and the extrinsic procoagulant system. The end-result of widespread intravascular coagulation and fibrinolysis is thrombocytopenia, hypofibrinogenaemia, consumption of factors V, VII and VIII and the appearance of fibrin degradation products and soluble fibrin monomer complexes (Gilabert and Estelles, 1985). This bleeding disorder may be worsened by the coagulopathy of massive transfusion and the haemodilution of rapid volume replacement. Here, flesh blood is the treatment of choice. One unit of flesh blood (less than 24 hours old) raises the platelet count by 10-15 x 109/1, haemoglobin by 10-15 g/l, haematocrit by 3% and circulating fibrinogen by 0.08--0.125 g/1 (Beller and Uszinski, 1974). If more fibrinogen replacement is required, fresh frozen plasma is another valuable source. Further platelets may be required if the platelet count is less than 50 x 109/1. Once hypovolaemia is corrected, persistently low urine output may herald the onset of renal failure. Administration of low dose dopamine
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(2 Ixg kg -1 min -1) may be useful in establishing the diagnosis and alleviating the problem. Uterine atony sometimes persists into the postpartum period: intramyometrial injection of prostaglandin F2~ may be indicated. On delivery, the neonate often needs aggressive and immediate resuscitation. Neonatal hypovolaemia can be corrected using blood obtained from the fetal surface of the placenta with a heparinized syringe. Anaesthetic agents given to the mother may affect the way the neonate can handle acute haemorrhage.
Hypertensive disorders Approximately 10% of all pregnancies in developed countries are complicated by a hypertensive disorder. Pre-eclampsia is the most common of these. This syndrome can take on many forms, the most frequent being the triad of increased blood pressure, proteinuria and central nervous system irritability. Another, more virulentform of the syndrome presents as epigastric and right hypochondrial pain and is associated with haemolysis, elevated liver enzymes and low platelets. Placental growth is usually compromised with pre-eclampsia, with the fetus at risk in utero. Improvements in placental growth can be achieved with low-dose aspirin regimens (Trudinger et al, 1988) but the definitive treatment for the mother is delivery. Decreasing central nervous system irritability, stabilizing hypertension and correcting any volume deficit should be achieved before the patient is submitted to anaesthesia. The critical time during general anaesthesia is at laryngoscopy and intubation, when there is a sudden sympathetic response (Hodgkinson et al, 1980) which might cause a sharp rise in blood pressure. Intracranial bleeding is a real risk. Many methods have been used to obtund this intubation response, including deep anaesthesia, potent intravenous hypotensive agents, intravenous lignocaine and short-acting opioids, all with limited success. A regional anaesthetic technique would therefore seem preferable but haemostasis may be a problem in some pre-eclamptic patients. This usually takes the form of a reduced platelet count (less than 100 x 109/1) and coagulation defects. If these are present they provide a relative contraindication to regional anaesthesia. This should be balanced against the fact that laryngeal oedema is often present or results from the resuscitative regimens in pre-eclamptics, making tracheal intubation difficult. This gives added impetus to avoiding intubation and choosing a regional anaesthetic regimen. Most obstetric units develop protocols in which inital management is set forth, detailing medications for decreasing cerebral irritability, hypertension control and volume loading. For example: 9 Decreasing cerebral irritability: dilantin; ? magnesium sulphate. 9 Stabilizing hypertension: clonidine; hydralazine; diazoxide. 9 Volume loading: crystalloid (Hartmann's); colloid (5% albumin) in 1:1 ratio monitored by CVP. Carefully titrated to 5-8 cmH20 range.
OBSTETRIC EMERGENCIES
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Cardiac disease
Since there has been significant improvement in the management of patients with either acquired or congenital heart disease, there have been an increasing number of women with these conditions becoming pregnant and requiring intervention in the management of their labour and delivery. Deaths are most commonly associated with valvular disease or cardiomyopathies. These patients tend to have a relatively fixed cardiac output and therefore poorly tolerate even small changes in heart filling pressures. In administering anaesthesia, the primary considerations are the avoidance of myocardial depression, increases in the workload of the heart and significant alterations in blood pressure. These requisities are best met with a cautiously titrated lumbar epidural block administered early in labour and maintained continuously until after delivery. Prevention of bearing down in the second stage of labour is essential so the technique must abolish the urge to bear down in the second stage and provide excellent conditions for forceps or vacuum extraction. Lumbar epidural anaesthesia can be adjusted so that the appropriate density of block is achieved to TIO. If labour should progress too rapidly for this to be cautiously achieved, a pudendal block supplemented with inhalational analgesia proves satisfactory. Often caesarean section is the mode of delivery chosen for the pregnant patient with severe cardiac disease. Here, lumbar epidural anaesthesia is good choice in that it: 1. 2. 3. 4. 5. 6.
Effectively blocks the stress response from the outpouring of endogenous catecholamines. Does not produce the sympathetic vasopressor or cardiac response seen with rapid sequence induction of general anaesthesia. Decreases myocardial oxygen consumption as an end-result of decreasing preload and afterload of the heart. Has minimal myocardial depressant qualities. Can be initiated slowly, allowing control of associated cardiovascular changes. Can be continued into the postoperative period to provide excellent analgesia.
Epidural anaesthesia is best avoided in patients who are likely to develop right-to-left shunts or have pulmonary hypertension because of the risks associated with uncontrolled hypotension. When general anaesthesia is necessary, deep planes of anaesthesia are indicated. Pretreatment with fentanyl, up to 5 ixg/kg, are well tolerated by the pregnant patient with cardiac disease and will significantly attenuate the sympathetic discharge and hypertensive response associated with intubation. If further blood pressure control is required then B-blocker therapy with peripheral vasodilatation is indicated. Amniotic fluid embolism
This is an uncommon complication of pregnancy but, if it does occur, has a very high rate of mortality.
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Clinically, the presentation is one of an acute anxious patient who suddently develops respiratory distress, usually without any chest pain. It is often associated with an obstetric event such as rupturing of the membranes. Amniotic fluid and its contents leak into the maternal circulation, leading to the mechanical blockage of the pulmonary vessels. An anaphylactoid reaction often accompanies this, with resultant bronchospasm and pulmonary vasoconstriction. Severe hypoxia and acute pulmonary hypertension leading to acute pulmonary oedema often leads to the death of the mother. Mothers who survive nearly all develop a diffuse intravascular coagulopathy. The prime objects of treatment are: 1. 2. 3.
Improvement of oxygenation. Support of the cardiovascular system. Treatment of the coagulopathy.
Severe ventilation-perfusion defects that develop with the entry of amniotic fluid into the pulmonary circulation are the cause of the hypoxia. Intubation and positive pressure ventilation with positive end expiratory pressure and 100% oxygen is required. Bronchodilators help overcome the bronchospasm. Inotropic support of the heart is required because rightsided and left-sided heart failure ensue. The coagulopathy is difficult to control and is often complicated by massive bleeding associated with uterine atony. This bleeding must be controlled and intravascular volume must be maintained. Fresh blood has the advantage in this situation, with further correction of clotting deficiencies with fresh frozen plasma and platelets (Clark, 1991). C A R D I O P U L M O N A R Y RESUSCITATION IN THE P R E G N A N T PATIENT
Cardiac arrest in late pregnancy (Table 7) occurs in 1 in 30 000 pregnancies and survival after such an event is exceptional (unless it occurs under anaesthesia) (Rees and Willis, 1988). Resuscitation of the pregnant patient is made more difficult because of aortocaval compression by the gravid uterus. Even minor degrees will have a profound effect on the success or failure of the resuscitative efforts (Marx, 1982). It is therefore imperative that uterine displacement be maintained during cardiopulmonary resusciTable 7. Causesof cardiac arrest in late pregnancy. Acute hypoxia Anaestheticmishap Major pulmonaryembolism Major haemorrhage Amnioticfluidembolism Myocardialinfarction Local anaesthetictoxicity Electrocution Trauma
OBSTETRIC EMERGENCIES
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tation. Effective wedging should not greatly effect the position of the torso, and chest compressions should still be possible without difficulty. If circumstances make this approach impractical then the uterus should be manually deviated to the left and slightly cephalad. If it is possible to raise the patient's legs, this simple manoeuvre will also help to improve venous return. If haemodynamic stability cannot be achieved even though uterine displacement is thought effective, abdominal delivery of the fetus should be performed immediately. Prompt delivery will assist maternal resuscitation and recovery. Marx (1982) reviewed five cases where resuscitation was required for more than 10 minutes. The three patients who underwent immediate caesarean section survived with no neurological deficit, whereas those in whom delivery was delayed suffered irreversible brain damage. POSTOPERATIVE CARE OF THE OBSTETRIC PATIENT Good anaesthetic management dictates that no mother should leave the operating room until she is fully conscious, orientated and able to protect her own airway. If there is any doubt, the anaesthetist should remain with the patient until those criteria are satisfied. A number of deaths have been associated with inadequate postoperative care. Inadequate reversal of neuromuscular blockade has led to hypoxia and eventual cardiac arrest. The reversal of neuromuscular blockade should be checked either by the use of a nerve stimulator or by the patient's ability to keep her head raised from a pillow. Inadequate staffing of the postpartum wards has led to a number of deaths from respiratory obstruction, haemorrhage and aspiration of stomach contents. It is vitally important that postnatal wards are staffed with trained nurses and that all mothers are observed carefully for at least 24 hours after an anaesthetic. This observation should consist, as a minimum, of regular assessments of pulse rate, blood pressure, respiratory rate, level of consciousness and blood loss. With the best possible anaesthetic care by experienced anaesthetists maternal anaesthetic mortality and morbidity can be kept to a minimum. This is what is strived for by modern obstetric units. This is what is expected by obstetric patients. SUMMARY
This chapter reviews the situations where obstetric emergencies have led to maternal mortality or morbidity. Failed intubation, aspiration of stomach contents, regional anaesthesia and analgesia mortality are reviewed and an appropriate course of action when confronted with these situations outlined. In addition, situations where anaesthesia or analgesia may be difficult are reviewed. Massive haemorrhage, hypertensive disorders of pregnancy, cardiac disease in pregnancy, amniotic fluid embolism, cardiopulmonary resuscitation and postoperative care of the obstetric patient are outlined and problems in their management highlighted.
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APPENDIX
1
Guidelines for management of failed intubation at caesarean section
9 All patients undergoing general anaesthesia: 1. Careful antacid prophylaxis (before induction) 2. Preoxygenated 9 If cords not visualized at laryngoscopy then only one attempt at intubation. 9 If not rapidly successful then organize the most skilled help available
~
~Obstetric reasons DECIDE for ~ . . . . . nt morbidity potential9
DISCONTINUE ~ ANAESTHESIA
1.
2.
Ventilate via face mask with 100% oxygen and allow patient to awaken
When awake proceed with a form of regional anaesthesia
PROCEED with ANAESTHESIA Patient supine + Trendelenberg Cricoid pressure maintained until spontaneously breathing and then released
Ventilate via face mask with 100% oxygen and 1.5 MAC of volatile agent
9 IF DIFFICULT TO VENTILATE 1. Use an oral airway 2. Laryngeal mask 3. Triple airway manoeuvre 9 As a last resort Cricothyroid puncture: large-bore (12 G) i.v. cannula. Connect via 3.5 mm endotracheal tube connector and ventilate via anaesthetic circuit Tracheostomy
REFERENCES
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