- Email: [email protected]
Anaesthetic issues related to postpartum haemorrhage (excluding antishock garments)
Best Practice & Research Clinical Obstetrics and Gynaecology Vol. 22, No. 6, pp. 1043–1056, 2008 doi:10.1016/j.bpobgyn.2008.08.006 available online at http://www.sciencedirect.com
4 Anaesthetic issues related to postpartum haemorrhage (excluding antishock garments) Felicity Plaat *
BA, MBBS, FRCA
Consultant Anaesthetist Queen Charlotte’s & Chelsea Hospital, Department of Anaesthesia, 5th Floor, Hammersmith House, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK
The obstetric anaesthetist is a key member of the multidisciplinary team required to manage postpartum haemorrhage, having been trained in resuscitation and being experienced in managing haemorrhage and in monitoring and caring for the critically ill patient. The diagnosis of shock, initial resuscitation controversies surrounding fluid replacement, cell salvage in obstetrics and monitoring are discussed. Key words: fluid resuscitation; obstetric anaesthesia; postpartum haemorrhage; shock.
INTRODUCTION If the primary role of the obstetrician is definitive treatment of postpartum haemorrhage, then that of the anaesthetist is concerned with supportive measures. Because anaesthetists have expertise in resuscitation, management of hypovolaemic shock, monitoring and care of the critically ill, they are part of the multidisciplinary team, regardless of whether anaesthesia is required. DIAGNOSIS OF HYPOVOLAEMIC SHOCK IN THE OBSTETRIC PATIENT This is complicated by several factors in the obstetric patient. Estimating blood loss in obstetrics is notoriously difficult. Bleeding might be completely hidden and, even when visible, blood loss is often underestimated, particularly if it is large.1,2 This situation can be improved with training3, the use of blood-collecting drapes4, and weighing swabs. * Tel.: þ208 383 3991; Fax: þ208 383 5373. E-mail address: [email protected] 1521-6934/$ - see front matter ª 2008 Elsevier Ltd. All rights reserved.
1044 F. Plaat
However, the clinical diagnosis of hypovolaemia can be difficult. Not only are obstetric patients generally young and fit, but the physiological changes of pregnancy make them particularly well equipped to withstand haemorrhage. In the term parturient, the circulating blood volume is approximately 100 mg/kg body weight, as opposed to 7 mg/kg in the healthy non-pregnant adult, and there is a 30% increase in red-cell volume; cardiac output is increased by 50%. As a result, the signs and symptoms of hypovolaemia might not develop until 1200–1500 mL blood has been lost (30–35% of the circulating volume). An decreased sensitivity to angiotensin II and decreased pulmonary and vascular resistance contribute to the altered response to hypovolaemia.5 An increase in resting heart rate by 15–20 beats/minute, peripheral vasodilation, and the widened pulse pressure in pregnancy can mask the classical signs of shock. The 16% increase in oxygen consumption increases vulnerability to falling haemoglobin concentrations.6 In healthy non-pregnant adults, hypovolaemia can be divided into four stages (Table 1). Such a classification can be useful in the obstetric patient, although the volume of blood loss associated with each stage will be greater.7 It is important, when considering the obstetric patient, to emphasise that the systolic blood pressure is unlikely to fall until 2–3 L have been lost. By this stage, the patient is in extremis and requires immediate transfusion and surgery to survive. A ‘normal BP’ should not be reassuring. Tachypnoea is an early sign. The respiratory rate increases when 15% of the circulating volume is lost. Monitoring of the respiratory rate is mandatory in patients at risk or who have haemorrhaged. Minimal increases in heart rate are easily missed but a sinus tachycardia of greater than 100 beats/minute must be investigated. Some patients, such as those with a low resting rate (athletes, congenital heart block), patients with pacemakers and those on b-blockers, will not become tachycardic in response to hypovolaemia. Paradoxical bradycardia can also occur. Table 1. Classification of shock. Class
Loss of Amount in a 70-kg circulating non-pregnant volume (%) adult (mL)
I II
0e15 15e30
<750 750e1500
III
30e40
1500e2000
IV
>40
>2000
Signs and symptoms
Alert, mild thirst; minimal tachycardia Anxious; pale; tachypnoea; tachycardia; cool peripheries; prolonged capillary refill (>2 s); narrowed pulse pressure (increased diastolic þ normal systolic pressure); decreased urine output Agitated/confused; pale; marked tachypnoea þ tachycardia; cool, pale peripheries; prolonged capillary refill (>2 s); decreased systolic BP; decreased urine output Drowsy/unconscious; grey; severe tachypnoea þ tachycardia; cold peripheries; absent capillary refill; hypotensive; oliguria/anuria
BP, blood pressure; s, seconds. Adapted from Baskett PJF (1990) ABC of major trauma. Management of hypovolaemic shock. British Medical Journal 1453–1457 and Johanson R, Cox C, Grady K, Howell C (2003) Managing obstetric emergencies and trauma: The MOET course manual. London, Royal College of Obstetricians and Gynaecologists’ Press, pp. 97–104.
Anaesthetic issues related to PPH 1045
Other early signs of hypovolaemia that are often overlooked are a narrowed pulse pressure and prolonged capillary refill that occur as the result of vasoconstriction. A falling urine output can be a particularly useful sign when haemorrhage is concealed. Patients should be monitored in well-lit surroundings so that changes in complexion can be noted. Once intravenous access is secured, the response to intravenous fluid boluses can be used as an indicator for the need for further treatment (Table 2). RESUSCITATION: THE IMMEDIATE MANAGEMENT OF POSTPARTUM HAEMORRHAGE Shock is defined as inadequate tissue perfusion. The purpose of resuscitation is to restore/maintain the oxygen delivery to the tissues. The aim is to prevent the onset of the irreversible stage of shock when there is multiple organ failure, increased capillary permeability, acidosis and failure of haemostasis. Resuscitation is based on the ABC approach.7 A patent airway is necessary to allow adequate oxygenation and ventilation for CO2 excretion. The conscious patient should have high-flow oxygen (10–15 L/min), via a facemask with a non-re-breathing bag to deliver w60% oxygen. Arterial oxygen saturations should be kept > 95% if possible. To maintain and protect the airway in the unconscious patient (or the patient with reduced or falling conscious level), the trachea should be intubated with a cuffed tube and 100% oxygen given. Good venous access should be secured as early as possible. Flow rates through different-sized cannulae are listed in Table 3. Most resuscitation manuals recommend two 14G cannulae in the presence of haemorrhage.7 Peripheral venous access might be impossible if there is intense vasoconstriction. Other options include cutdown to a peripheral vein (possible sites include the antecubital fossa, the proximal saphenous vein and the peripheral saphenous vein at the ankle), percutaeous femoral cannulation and central venous cannulation. Although peripheral cutdown can be performed quickly and have few complications, a randomised study in 78 trauma patients of intravenous access by saphenous vein cutdown and femoral cannulation found the time required for the cutdown to be significantly longer (5.6 2.6 min versus 3.2 1.2 min).8 Table 2. Response to resuscitation by intravenous fluids (2L crystalloid). Response type I II
III
Signs improve Initial, temporary improvement with rapid regression to original levels, due to redistribution of fluid to the extravascular compartment or ongoing haemorrhage No improvement with second fluid challenge
IV
No response to rapid infusion of fluid of any type
Intervention needed No further fluid challenge required Second fluid challenge (colloid) required. If vital signs return to normal, redistribution was responsible Continue intravenous infusion of blood or colloid to sustain resuscitation. Surgery required within 1 hour Immediate surgery required
Modified with permission from Johanson R, Cox C, Grady K, Howell C (2003) Managing obstetric emergencies and trauma: The MOET course manual. London, Royal College of Obstetricians and Gynaecologists’ Press, pp. 97–104.
1046 F. Plaat
Table 3. Flow rates through intravenous cannulae. Gauge number* 20G 18G 16G 14G
Colour code Pink Green Grey Orange
Flow rate mL/min** 40e80 75e120 130e220 250e360
*
G refers to a wire gauge classification of the size of the internal diameter of the cannula. It is slightly different to the American and Standard Wire Gauges. ** The British standard for determining flow rate: involves in-vitro testing using distilled water at 22 C, kept at constant pressure. The flow rates are therefore not the same as those achievable clinically.
The disadvantages of femoral cannulation include the prerequisite of a palpable femoral arterial pulse and, in the obstetric setting, lack of access. Central venous access allows monitoring of central pressures but is more difficult and potentially hazardous in the hypovolaemic patient, especially in the presence of impaired coagulation. Complications include air embolism, subcutaneous emphysema, pneumothorax, haemothorax, damage to the common carotid artery, brachial plexus, phrenic nerve, thoracic duct and sympathetic chain. Cardiac perforation has been reported. An aseptic technique must be employed to reduce the risk of catheter-related sepsis and ECG monitoring is required as the catheter tip can induce arrhythmias if inserted too far. The National Institute for Health and Clinical Excellence (NICE) recommends that ‘2-D imaging ultrasound guidance should be considered in most clinical situations where CVC [central vein catheterisation] is necessary whether the situation is elective or emergency’. Those using ultrasound guidance should have prior training.9 When samples have been taken for full blood count, group and cross-match, coagulation profile and biochemistry (urea þ electrolytes, glucose), fluid replacement should be promptly started.
AVOIDANCE OF HYPOTHERMIA Whichever fluid used and regime followed, it is imperative that the fluids are warmed as part of the strategy to prevent hypothermia, (defined as core temperature <35 C). Due to tissue hypoperfusion and inadequately warmed fluids. The detrimental effects of hypothermia include: Shift of the oxyhaemoglobin dissociation curve to the left, impairing oxygen delivery to the tissues. Shivering, increasing oxygen consumption and lactic acidosis. Impaired hemostasis. Impaired response to recombinant activated factor VII (rFVIIa). Hypothermia impairs platelet aggregation10,11, enhances fibrinolysis12 and impairs clotting factor function. Johnston et al found that at 35 C, without dilution, the function of all factors in the coagulation cascade was reduced by as much as 35%. At 33 C, factors XI and XII functioned at only 17% and 32% of normal capacity.13
Anaesthetic issues related to PPH 1047
Hypothermia potentiates dilutional coagulopathy Prothrombin time (PT) and activated partial thromboplastin time (APTT) values do not reflect the effects of hypothermia as blood samples are prewarmed in the laboratory prior to testing. In trauma patients, hypothermia is associated with worsened survival rates and increased blood loss.14 Various fluid-warming devices are available, several of which combine warming, using countercurrent water technology with pressure infusion, for example the Level 1 (Level 1 Technologies, Inc., Rockland, MA; Figure 1). Problems with such devices include insufficient warming at high flow rates, the risk of fluid overload and fatal venous air embolism.15 FLUID THERAPY The ideal fluid for resuscitation would have the oxygen-carrying capacity and volumeexpanding properties of blood. It would, however, be entirely synthetic, eradicating the need to cross-match and the risk of infection, and making it acceptable those whose beliefs prohibit the use of blood. Blood substitutes Several modified haemoglobin products are under development, including artificial red cells made from biodegradable polymers and polymerised haemoglobin developed from out-of-date bank blood. Non-human sources of haemoglobin and recombinant-based products are also being developed. Problems with these haemoglobin solutions include a short half-life; their lack of protective antioxidant enzymes, which could theoretically worsen reperfusion injury; and their tendency to cause vasoconstriction. One multi-centre, randomised, controlled trial of a cross-linked haemoglobin in trauma patients was terminated early due to concerns about pulmonary hypertension and increased mortality in the study group.16
Figure 1. Forced air warming system.
1048 F. Plaat
Perfluorocarbons are compounds that, when infused intravenously, can transport oxygen and carbon dioxide. Problems currently being investigated include the need for 100% inspired oxygen to make oxygenation effective, uptake by the reticuloendothelial system and interference with laboratory tests.17 Despite intense interest in the development of a blood substitute, there is nothing likely to be available in the immediate future. CLEAR FLUIDS: THE CRYSTALLOID–COLLOID DEBATE Intravenous infusion of any clear fluid will initially expand the intravascular space. How long the expansion lasts depends on how freely the fluid crosses the vascular endothelium: crystalloid solutions cross freely, whereas colloid do so more slowly. Because colloids have a higher osmolality than plasma, they expand the intravascular volume by more than the volume infused by drawing water intravascularly. Isotonic solutions such as Hartmann’s solution (Ringer’s lactate) or 0.9% saline are distributed between the intravascular and extravascular (interstitial) spaces in a ratio of 1:3. (5% dextrose is metabolised rapidly leaving pure water, which is distributed between the extracellular and intracellular compartments in a ration of 1:2. Thus, only a tiny proportion remains intravascular, making it unsuitable for intravascular volume replacement.) From the above, it is clear that colloids achieve intravascular volume expansion more efficiently: a smaller volume is required (2–4 less than the volume of crystalloid), and the effect is longer lasting. Colloid oncotic pressure is better maintained.18 Because smaller volumes are required, colloid resuscitation is associated with less interstitial oedema. Interstitial oedema has deleterious effects on gas exchange, wound healing and myocardial compliance. In critically ill patients, a positive fluid balance is associated with higher mortality.19 Hydroxyethyl starch solutions cause plasma expansion that lasts of up to 24 hours compared with only a few hours in the case of gelatine derivatives (Haemaccel, gelofusin). Despite these theoretical advantages, a recent trial comparing saline and albumin for resuscitation of patients in intensive care found no difference in outcome.20 Crystalloids are much cheaper than colloids. They are not associated with a risk of anaphylaxis and do not interfere with hemostasis (both gelatins and hydroxyethyl starch solutions have been implicated).21,22 Newer colloids, such as hydroxyethyl starch HES130/0.4 (Voluven), appear to have less effect on coagulation.23 Normal saline is not recommended as large volumes are associated with the development of a hyperchloraemic acidosis. This can complicate the interpretation of blood-gas data and can result in inappropriate clinical intervention.24 The clinical significance of the hyperchloraemic acidosis is still unclear. However, there is an argument for the use balanced fluid resuscitation using fluid (both crystalloids and colloids) containing physiological balance of electrolytes to avoid such disturbances.25 NORMOTENSIVE OR HYPOTENSIVE RESUSCITATION? There is a growing body of evidence to suggest that overvigorous fluid resuscitation increases the rate of uncontrolled haemorrhage and might be associated with increased risk of a poor outcome. Intravenous fluid loading increases ventricular preload
Anaesthetic issues related to PPH 1049
and increases blood pressure, which might reverse vasoconstriction increasing haemodynamic instability, as well as directly displacing fibrin clots. Clear fluids dilute the oxygen-carrying capacity of blood, dilute the concentrations of clotting factors and platelets, and reduce viscosity. In animal models of uncontrolled haemorrhage, aggressive fluid administration is associated with decreased survival.26 To test this in humans, Bickell et al assigned 598 adults who had suffered penetrating torso injuries with initial systolic blood pressure <90 mm Hg to either conventional or delayed fluid administration.27 In the former – conventional – group, Ringer’s lactate infusion was started at the scene; in the study group, fluid was withheld until the patient arrived in theatre. The latter group had better survival (70% versus 62%), fewer complications and shorter hospital stays. The transport times in this study were relatively short; fluid resuscitation was not unduly delayed. Dutton and colleagues randomised patients suffering both blunt and penetrating injuries to resuscitation protocols aimed at maintaining the systolic BP to either 100 mm Hg (normal) or 70 mm Hg, (low).28 Despite the latter group having a higher average injury score, mortality was the same in both groups. Although hypotensive resuscitation might be inappropriate in the pregnant patient because of the reliance of the placental circulation on maternal venous return, following delivery there might be benefits in the more cautious use of clear fluids, especially crystalloids, before surgical control of haemorrhage has been achieved. TRANSFUSION STRATEGIES There is agreement that when 30% or more of the circulating blood volume is lost, blood transfusion is required to maintain sufficient oxygen delivery to the tissues. Oxygen delivery is the function of cardiac output oxygen content: O2 content ¼ %O2 saturation [Hb] 1.34 When haemorrhage is very brisk, immediate access to blood can be life saving: all obstetric units should keep a couple of units of O-negative blood immediately available as group-specific blood requires 30 minutes and fully cross-matched blood an hour or more to prepare. In patients with known red-cell antibodies, the risk of a haemolytic transfusion reaction must be balanced against the risks of withholding transfusion. Recently, there has been a change in what is perceived to be an optimum haemocrit or haemoglobin concentration. Traditionally, the target was a packed cell volume (PCV) of 30% and haemoglobin concentration of 10 g/dL. However, there is growing evidence that concentrations as low as 7 g/dL are well tolerated in healthy, normovolaemic patients. A lower hematocrit decreases blood viscosity, increasing cardiac output and improving tissue oxygenation.29 Current guidelines state that red cells are rarely required when the haemoglobin concentration is >10 g/dL, and almost always needed when it is <6 g/dL. At intermediate concentrations, the need for transfusion depends on the individual clinical situation.30 During postpartum haemorrhage, the haemoglobin concentration to likely to be changing rapidly and oxygen demand in the peripartum period is greater than in the non-pregnant patient. Thus, it seems prudent to aim for the upper end of the recommended range of haemoglobin concentrations.
1050 F. Plaat
Coagulopathy is a common complication of major haemorrhage and particularly of obstetric haemorrhage. The causes include dilution, disseminated intravascular coagulation (DIC), hypothermia and acidosis. The careful use of warmed fluids to prevent hypothermia and acidosis has been discussed. Traditional policy for transfusion of products dictated that replacement should be guided by laboratory coagulation test results: blood products are indicated if the PT and APTT >1.5 normal control. During a major haemorrhage, laboratory test results are rarely available in time and empiric regimes such as at least one unit of fresh frozen plasma (FFP) for every four units packed red blood cells (PRBC) are widely advocated.31 Recently, however, such regimes have been challenged. Ho and colleagues argue that such regimes are based on old studies, which used whole blood and not packed cells for transfusion.32 A unit of whole blood contains the equivalent of one unit of PRBC þ one unit FFP: thus, such regimes are bound to result in dilutional coagulopathy and the equivalent of whole blood should be given from the start. Using a computer model of exsanguination, Hirshberg et al showed that prolongation of PT is the sentinel event of dilutional coagulopathy and occurs early.33 The key to preventing coagulopathy is to start FFP infusion before the PT becomes abnormal. This could be achieved by using a replacement ratio of PRBC:plasma of 3:2 or to transfuse FFP concurrently with the first units of PRBC. In practice, the latter would be complicated by the delay required as the FFP is thawed. Platelets do not need to be replaced so rapidly but should be kept >50 109/L. Because platelets are not kept by all transfusion laboratories, a level of 75–100 109/L should trigger a request for platelets. Platelets should be transfused through a fresh giving set, not one previously used for blood.29 The most common serious complication of massive transfusion is that the patient is given the wrong blood. This is more likely in the emergency situation. Other complications include transfusion reactions and hypocaelcaemia (PRBC contain citrate). Transfusion-related acute lung injury (TRALI), although uncommon, can also occur and is five or six times more likely after blood products compared to PRBC. More efficient use of blood and blood products is facilitated by the use of near patient testing. The Haemacue device allows haemoglobin estimation at the bedside using a drop of peripheral blood. It has been validated for use in obstetric patients.34 The thromboelastogram (TEG) allows bedside estimation of global haemostasis. It has been described as the ideal method for monitoring hemostasis during massive obstetric haemorrhage due to the fast feedback time, although this has been disputed. During a debate in 2005, a majority of UK obstetric anaesthetists rejected the motion that every labour ward should have a TEG.35 Although there has been less work on the use of the platelet function analyser (PFA) as a bedside test of coagulation in obstetrics, currently it appears to be less reliable than TEG in obstetric patients.36 Cell salvage in obstetrics Cell salvage (Figure 2) has been used in over 400 documented cases in obstetrics.37 It can reduce or obviate the need for allogenic blood and has been used for emergency as well as elective procedures.38 Due to the high and rising cost of blood and blood products, cell salvage can be justified on financial grounds. One unit reported that 60% of the total cost of disposables for a whole year was covered by the reduction
Anaesthetic issues related to PPH 1051
Figure 2. Cell salvage machine Didecot Electa (Sorin) (reproduced with permission).
in banked blood used on one patient.39 In 2005, nearly 40% of units in the UK used cell salvage in obstetrics, although problems with gaining sufficient experience to use it successfully in the emergency situation have been reported.40 The two possible complications of cell salvage in obstetrics – amniotic fluid embolism and undetected rhesus immunisation – have not been reported. It is recommended
1052 F. Plaat
that a leucocyte depletion filter is used, which has shown to reduce fetal squames and phosholipid lamellar bodies to close to zero in salvaged blood.41 As an added precaution, most units use conventional suction until the placenta and as much amniotic fluid as possible has been removed. Fetal red cell contamination does occur: 2 to 19 mL fetal blood can be re-transfused. Kleihauer testing should be undertaken as soon as possible and increased doses of anti-D immunoglobulin might be required.42 The use of cell salvage in obstetrics is now endorsed by several national organisations in the UK, including CEMACH, NICE, the RCOG and the Obstetric Anaesthetists’ Association. Where it is not available, consideration should be given to the transfer out of patients who refuse autologous blood and blood products. MONITORING REQUIRED IN POSTPARTUM HAEMORRHAGE To determine the severity of shock, the response to treatment and to detect concealed haemorrhage, continuous monitoring of multiple parameters is essential. This requires Level 2 critical care (or Level 1 if the patient is ventilated or there is multiorgan failure).43 As discussed above, in addition to ECG, oxygen saturation and blood pressure, respiratory rate in the conscious patient and core temperature in all patients should be monitored closely. Signs of impaired peripheral infusion should be sought regularly and frequently. Early warning scoring systems have been shown to improve detection of worsening physiological parameters in no-obstetric patients44 and are being adapted for use in obstetrics. Many such charts are now being evaluated (R. Jones, personal communication) and it is recommended that they be used to monitor all seriously and critically ill patients, including those at risk of or who have suffered postpartum haemorrhage. Central venous pressure monitoring will be necessary to direct volume replacement in most cases of postpartum haemorrhage. However, as previously described, it is a potentially hazardous procedure and unpleasant for the conscious patient. In the presence of impaired haemostasis, prior administration of blood products might be necessary. Because patient are often unstable and repeated arterial blood samples are required to monitor response to resuscitation, an arterial line if often required. The radial artery is most commonly cannulated but the brachial, femoral and dorsalis pedis arteries offer alternative sites. The use of a pulmonary artery flotation catheter (PAFC) to measure cardiac output is becoming less common as concerns grow about well-documented hazards and unproven clinical benefits. The risks of insertion and use include pneumothorax, arrhythmias, valve damage, pulmonary artery rupture and pulmonary infarction.45 A Cochrane database systematic review on the use of PAFCs for adult patients in intensive care could not demonstrate any difference in mortality or hospital length of stay with their use.46 Less invasive, safer monitoring techniques are gaining popularity. Doppler provides a means of real-time continuous cardiac output monitoring by measuring the velocity of blood flow in the aorta. The oesophageal Doppler incorporates a transducer at the tip of a flexible probe, which is inserted into the oesophagus via the oral route. Newer models have been designed for use in the awake patient. The suprasternal Doppler measures cardiac output via a handheld stationary probe, which directs a continuous
Anaesthetic issues related to PPH 1053
ultrasound beam at the ascending or aortic arch.47 The measurement of cardiac output by Doppler has been validated against thermodilution methods and has been used to successfully monitor cardiac function in a range of physiological states including pregnancy.48 Pulse contour cardiac output monitoring is also less invasive than the PAFC as it utilises information from central venous (usually femoral) and arterial lines. This method involves both pulse contour analysis of the arterial trace and intermittent transpulmonary thermodilution (PiCCO) or lithium chloride dilution (LiDCO). In the latter, lithium chloride is injected via central venous catheter and a lithium-sensitive electrode is sited in a peripheral arteryvia a standard arterial catheter. A lithium dilution curve is constructed, from which cardiac output is calculated and a continuous display of cardiac output is produced.49 More recently, a method by which lithium is injected via a peripheral vein has been evaluated.50 Adequacy of resuscitation can be assessed by improving cardiovascular variables, urine output and correction metabolic acidosis, anaemia and coagulopathy. Conventionally, tissue hypoperfusion was monitored by observing the magnitude of the base deficit as a measure of metabolic acidosis. However, as mentioned previously, this might not arise purely as a result of tissue hypoxia.51 Lactate is a by-product of anaerobic metabolism. Levels rise when peripheral perfusion leads to tissue hypoxia (type A lactic acidosis). It is easily measured by many blood gas machines and is recommended as a method for monitoring adequacy of tissue oxygenation. A study of ITU patients showed that it correlated better with mortality and morbidity than base deficit.52 A separate study of medical and surgical patients found that the combination of the two variables appeared superior to either lactate or base deficit alone in predicting survival.53 An initial increase in lactate levels that can occur when perfusion improves might represent washout from previously underperfused tissues. Lactic acidosis (type B) might also arise from non-hypoxic causes (e.g. in diabetes, hepatic and renal failure). The anion gap will be increased by hypoxia but not by other causes of metabolic acidosis, such as hyperchloraemic acidosis. The anion gap has to be corrected for the level of albumin, as hypoalbuminaemia will tend to reduce it. ANAESTHESIA FOR POSTPARTUM HAEMORRHAGE The appropriate anaesthetic technique will depend on the clinical situation but a senior experienced obstetric anaesthetist should always be directly involved. In the elective situation, when heavy bleeding is anticipated (e.g. caesarean section for placenta praevia) a regional technique can be used. Evidence suggests that blood loss is reduced when regional rather than general anaesthesia is used at caesarean section.54 A survey of obstetric anaesthetists in the UK revealed that the majority would be willing to use regional anaesthesia for patients undergoing elective surgery with minor placenta praevia. One-third would do so if the patient was bleeding but not haemodynamically compromised. The more experienced the anaesthetists, the more willing they were to offer regional anaesthesia. The two obstetricians who answered this survey, however, preferred general anaesthesia.55 A retrospective study by Parekh and colleagues found a significantly reduced blood loss and need for transfusion in women with placenta praevia under going caesarean section under regional anaesthesia.56
1054 F. Plaat
If regional anaesthesia is offered, it is essential that the patient is made aware that conversion to general anaesthesia might be required. Adequate preparations should be made to deal with sudden blood loss, including appropriate intravenous access, monitoring and instantly available blood and or blood products, and a method for warming intravenous fluids. In the haemodynamically unstable patient, when there is uncorrected hypovolaemia, where hemostasis is impaired or where the airway is at risk (semi- or unconscious patient) general anaesthesia is indicated. Should the patient need transfer – to the intensive care or the radiology department – the anaesthetist must provide appropriate monitoring and, if necessary, anaesthesia or sedation. In the UK, the majority of labour-ward theatres do not have the facilities for interventional radiological procedures and transfer to the radiology suite can be a considerable logistical challenge. If interventional radiology is considered, it is important to take into account that this might necessitate both the anaesthetist and anaesthetic support staff leaving the labour ward to accompany the patient.
Practice points Management of postpartum haemorrhage requires a multidisciplinary approach, with communication and co-operation between all specialties involved. The anaesthetist must be involved as early as possible and involved in the antenatal care of at-risk patients. There must be direct involvement of an experienced obstetric anaesthetist. Anaesthetists can contribute by organizing practice drills for managing postpartum haemorrhage and teaching resuscitation skills.
CONFLICTS OF INTEREST The author has recently written a review of B-Lynch C, Keith LG, Lalonde AB & Karoshi M. (eds) (2006) A textbook of postpartum haemorrhage. London: Sapiens Publishing. REFERENCES 1. Newton M, Mosey IM, Eglie GE et al. Blood loss during and immediately after delivery. Obstet Gynecol 1961; 17: 9–18. 2. Toledo P, McCarthy RJ, Hewlett BJ et al. The accuracy of blood loss estimation after simulated vaginal delivery. Anesth Analg 2007; 105: 1736–1740. *3. Bose P, Regan F & Paterson Brown S. Improving the accuracy of estimated blood loss at obstetric haemorrhage using clinical reconstructions. Br J Obstet Gynaecol 2006; 113: 919–924. 4. Patel A, Goudar SS, Geller SE et al. Drape estimation versus visual assessment for estimating postpartum haemorrhage. Int J Gynaecol Obstet 2006; 93: 220–224. 5. Allsop J, Navaneetham N & Cooper J. Maternal physiology. In Collis R, Plaat F & Urquhart J (eds.). Textbook of obstetric anaesthesia. London: Greenwich medical Media, 2002, pp. 21–38. 6. Pernoll ML, Metcalfe J, Schlenker TL et al. Oxygen consumption at rest and during exercise in pregnancy. Respir Physiol 1975; 25: 285–294. 7. Johanson R, Cox C, Grady K et al. Managing obstetric emergencies and trauma: the MOET course manual. London: RCOG Press, 2003. 97–104.
Anaesthetic issues related to PPH 1055 8. Westfall MD, Price RK, Lambert M et al. Intravenous access in the critically ill trauma patient: a multicentred, prospective, randomised trial ofsaphenous cutdown and percutaneous, femoral access. Ann Emerg Med 1994; 23: 541–545. 9. National Institute for Health and Clinical Excellence (NICE). TA49 Central venous catheters – ultrasound locating devices: guidance. Available from: www.nice.org.uk/guidance; 2002. 10. Gubler KD, Gentileloo LM, Hassantash SA et al. The impact of hypothermia on dilutional coagulopathy. J Trauma 1994; 36: 847–851. *11. Wolberg AS, Meng ZH, Monroe III DM et al. A systematic evaluation of the effect of temperature on coagulation enzyme activity and platelet function. J Trauma 2004; 56: 1221–1228. 12. Paul J, Cornillon B, Baguet J et al. In-vivo release of a heparin-like factor in dogs during profound hypothermia. J Thorac Cardiovasc Surg 1981; 82: 45–48. 13. Johnston TD, Chen Y & Reed II RL. Functional equivalence of hypothermia to specific clotting factor deficiencies. J Trauma 1994; 37: 413–417. 14. Jurkovitch GJ, Greiser WB, Luterman A et al. Hypothermia in trauma victim: an ominous predictor of survival. J Trauma 1987; 27: 1019–1024. 15. Adhikary GS & Massey SR. Massive air embolism: a case report. J Clin Anesth 1998; 10: 70–72. 16. Sloan EP, Koenigsberg M, Gens D et al. Diaspirin cross-linked haemoglobin (DCLHb) in the treatment of severe traumatic hemorrhagic shock: a randomised control efficacy trial. JAMA 1999; 282: 1857– 1864. 17. Ma Z, Monk TG, Goodnough LT et al. Effect of haemoglobin and perflubron-based oxygen carriers on common clinical laboratory tests. Clin Chem 1997; 43: 1732–1737. 18. Norberg A, Brauer KI, Prough DS et al. Volume turnover kinetics of fluid shifts after hemorrhage, fluid infusion, and the combination of hemorrhage and fluid infusion in sheep. Anesthesiol 2005; 102: 985– 994. 19. Mitchell JP, Schukker D, Calandrino FS et al. Improved outcome based on fluid management in critically ill patients requiring pulmonary artery catheterization. Am Rev Respir Dis 1992; 145: 990–998. *20. Finfer S, Bellomo R, Boyce N et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350: 2247–2256. 21. Evans PA, Garnett M, Boffard K et al. Evaluation of the effect of colloid (Haemaccel) on the bleeding time in the trauma patient. J R Soc Med 1996; 89: 101–104. 22. Kapiotis S, Quehenberger P, Eichler HG et al. Effect of hydroxyethyl starch on the activity of blood coagulation and fibrinolysis in healthy volunteers: a comparison with albumin. Crit Care Med 1994; 22: 606–612. 23. Langeron O, Doelberg M, Ang ET et al. Voluven, a lower substituted novel hydroxyethyl starch (HES 130/0.4), causes fewer effects on coagulation in major orthopedic surgery than HES 200/0.5. Anesth Analg 2001; 92: 855–862. 24. Brill SA, Stewart TR, Brundage SI et al. Base defficit does not predict mortality when secondary to hyperchloraemic acidosis. Shock 2002; 17: 459–462. *25. Boldt J. The balanced concept of fluid resuscitation. Br J Anaesth 2007; 99: 312–315. 26. Capone A, Safar P, Stezoski SW et al. Uncontrolled hemorrhagic shock outcome model in rats. Resuscitation 1995; 24: 143–152. *27. Bickell WH, Wall MJ, Pepe PE et al. Immediate versus delayed resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994; 331: 1105–1109. 28. Dutton RP, Mackenzie CF & Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma 2002; 52: 1141–1146. 29. Van der Linden P, Gilbart E, Paques P et al. Influenceof hematocrit on tissue O2 extraction capabilities during acute hemorrhage. Am J Physiol 1993; 264: 1942–1947. *30. Stainsby D, MacLennan S, Thomas D, et al. Guidelines in the management of major blood loss. British Committee for Standards in Haematology 2006. 31. Turner DAB. Emergency anaesthesia. In Aitkinhead AR, Rowbotham DJ & Smith G (eds.). Textbook of anaesthesia. 4th edn. Edinburgh: Churchill Livingstone, 2001, pp. 619–628. *32. Ho AMH, Karmakar MJ & Dion PW. Are we giving enough coagulation factors during major trauma resuscitation? Am J Surg 2005; 190: 279–284. 33. Hirshberg A, Dugas M & Banez EI. Minimizing dilutional coagulopathy in exsanguinating hemorrhage: a computer simulation. J Trauma 2003; 54: 454–463.
1056 F. Plaat 34. Yau R, Kathigamanathan T, Plaat F et al. Evaluation of the haemocue for measuring haemoglobin concentrations in the obstetric population. Int J Obstet Anesth 2002; 11(S): 8. 35. Hunt BI, Lyons G & Watson HG. Thromboelastography should be available on every labour ward. Int J Obstet Anesth 2005; 14: 324–327. 36. Vincelot A, Nathan N, Collet D et al. Platelet function during pregnancy: an evaluation using the PFA100 analyzer. Br J Anaesth 2001; 87: 890–893. *37. Catling S. Blood conservation techniques in obstetrics; a UK perspective. Int J Obstet Anesth 2007; 16: 241–249. 38. Catling SJ, Freites O, Krishnan S et al. Clinical experience with cell salvage in obstetrics: 4 cases from one UK centre. Int J Obstet Anesth 2002; 11: 128–134. 39. Dowse C, Gardner I, Laxton C et al. Investing in intra-operative cell salvage: experience of a Bristol teaching hospital. Int J Obstet Anesth 2008; 17(S): 49. 40. Dharmarajah A, Bedson R, Plaat F et al. Introducing cell salvage in obstetric practice: the first year’s experience. Int J Obstet Anesth 2008; 17(S): 50. 41. Waters JH, Biscotti C, Potter PS et al. Amniotic fluid removal during cell salvage in the caesarean section patient. Anesthesiology 2000; 92: 1531–1536. 42. Catling SJ, Williams S & Fielding AM. Cell salvage in obstetrics: an evaluation of the ability of cell salvage combined with the leucocyte depletion filtration to remove amniotic fluid from operative blood loss at caesarean section. Int J Obstet Anesth 1999; 8: 79–84. 43. RCoA, RCM, RCOG, RCPCH. Safer childbirth: minimum standards for the organisation and delivery of care in labour. London: RCOG Press, 2007. 44. Chatterjee MT, Moon JC, Murphy R et al. The ‘‘OBS’’ chart: an evidence based approach to re-design of the patient observation chart in a district general hospital setting. Postgrad Med J 2005; 81: 663–666. *45. Fujitani S & Baldisseri MR. Hemodynamic assessment in a pregnant and peripartum patient. Crit Care Med 2005; 33(Suppl): S354–S361. 46. Harvey S, Young D, Brampton W et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Syst Rev 2006; (3): CD003408. 47. Gan T. The esophageal Doppler as an alternative to the pulmonary artery catheter. Curr Opin Crit Care 2000; 6: 214–221. 48. Bray JK, Fernando R, Patel NP et al. Suprasternal Doppler estimation of cardiac output: standard versus sequential combined spinal epidural anesthesia for Cesarean delivery. Anesth Analg 2006; 103: 959–964. 49. Linton RAF, Band DM & Haire KM. A new method of measuring cardiac output in man using lithium dilution. Br J Anaesth 1993; 71: 262–266. 50. Jonas MM, Kelly FE, Linton RAF et al. A comparison of lithium dilution cardiac output measurement made using central and antecubital fossa venous injection of lithium chloride. J Clin Monit Comput 1999; 15(S): 25–28. *51. Morris CG & Low J. Metabolic acidosis in the critically ill: part I. Anaesthesia 2008; 63: 294–301. 52. Husain FA, Martin MJ, Mullenix PS et al. Serum lactate and base deficit as predictor of mortality and morbidity. Am J Surg 2003; 185: 485–491. 53. Smith I, Kumar P, Molloy S et al. Base excess and lactate as prognostic indicators for patients admitted to intensive care. Intensive Care Med 2001; 27: 74–83. 54. Afolabi BB, Lesi FE & Merah NA. Regional versus general anaesthesia for caesarean section. Cochrane Database Syst Rev 2006; (18). CD004350. 55. Bonner SM, Haynes SR & Ryall D. The anaesthetic management of Caesarean section for placenta praevia: a questionnaire survey. Anaesthesia 1995; 50: 992–994. 56. Parekh N, Husaini SW & Russell IF. Caesarean section for placenta praevia: a retrospective study of anaesthetic management. Br J Anaesth 2000; 84: 725–730.
4 Anaesthetic issues related to postpartum haemorrhage (excluding antishock garments) Felicity Plaat *
BA, MBBS, FRCA
Consultant Anaesthetist Queen Charlotte’s & Chelsea Hospital, Department of Anaesthesia, 5th Floor, Hammersmith House, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK
The obstetric anaesthetist is a key member of the multidisciplinary team required to manage postpartum haemorrhage, having been trained in resuscitation and being experienced in managing haemorrhage and in monitoring and caring for the critically ill patient. The diagnosis of shock, initial resuscitation controversies surrounding fluid replacement, cell salvage in obstetrics and monitoring are discussed. Key words: fluid resuscitation; obstetric anaesthesia; postpartum haemorrhage; shock.
INTRODUCTION If the primary role of the obstetrician is definitive treatment of postpartum haemorrhage, then that of the anaesthetist is concerned with supportive measures. Because anaesthetists have expertise in resuscitation, management of hypovolaemic shock, monitoring and care of the critically ill, they are part of the multidisciplinary team, regardless of whether anaesthesia is required. DIAGNOSIS OF HYPOVOLAEMIC SHOCK IN THE OBSTETRIC PATIENT This is complicated by several factors in the obstetric patient. Estimating blood loss in obstetrics is notoriously difficult. Bleeding might be completely hidden and, even when visible, blood loss is often underestimated, particularly if it is large.1,2 This situation can be improved with training3, the use of blood-collecting drapes4, and weighing swabs. * Tel.: þ208 383 3991; Fax: þ208 383 5373. E-mail address: [email protected] 1521-6934/$ - see front matter ª 2008 Elsevier Ltd. All rights reserved.
1044 F. Plaat
However, the clinical diagnosis of hypovolaemia can be difficult. Not only are obstetric patients generally young and fit, but the physiological changes of pregnancy make them particularly well equipped to withstand haemorrhage. In the term parturient, the circulating blood volume is approximately 100 mg/kg body weight, as opposed to 7 mg/kg in the healthy non-pregnant adult, and there is a 30% increase in red-cell volume; cardiac output is increased by 50%. As a result, the signs and symptoms of hypovolaemia might not develop until 1200–1500 mL blood has been lost (30–35% of the circulating volume). An decreased sensitivity to angiotensin II and decreased pulmonary and vascular resistance contribute to the altered response to hypovolaemia.5 An increase in resting heart rate by 15–20 beats/minute, peripheral vasodilation, and the widened pulse pressure in pregnancy can mask the classical signs of shock. The 16% increase in oxygen consumption increases vulnerability to falling haemoglobin concentrations.6 In healthy non-pregnant adults, hypovolaemia can be divided into four stages (Table 1). Such a classification can be useful in the obstetric patient, although the volume of blood loss associated with each stage will be greater.7 It is important, when considering the obstetric patient, to emphasise that the systolic blood pressure is unlikely to fall until 2–3 L have been lost. By this stage, the patient is in extremis and requires immediate transfusion and surgery to survive. A ‘normal BP’ should not be reassuring. Tachypnoea is an early sign. The respiratory rate increases when 15% of the circulating volume is lost. Monitoring of the respiratory rate is mandatory in patients at risk or who have haemorrhaged. Minimal increases in heart rate are easily missed but a sinus tachycardia of greater than 100 beats/minute must be investigated. Some patients, such as those with a low resting rate (athletes, congenital heart block), patients with pacemakers and those on b-blockers, will not become tachycardic in response to hypovolaemia. Paradoxical bradycardia can also occur. Table 1. Classification of shock. Class
Loss of Amount in a 70-kg circulating non-pregnant volume (%) adult (mL)
I II
0e15 15e30
<750 750e1500
III
30e40
1500e2000
IV
>40
>2000
Signs and symptoms
Alert, mild thirst; minimal tachycardia Anxious; pale; tachypnoea; tachycardia; cool peripheries; prolonged capillary refill (>2 s); narrowed pulse pressure (increased diastolic þ normal systolic pressure); decreased urine output Agitated/confused; pale; marked tachypnoea þ tachycardia; cool, pale peripheries; prolonged capillary refill (>2 s); decreased systolic BP; decreased urine output Drowsy/unconscious; grey; severe tachypnoea þ tachycardia; cold peripheries; absent capillary refill; hypotensive; oliguria/anuria
BP, blood pressure; s, seconds. Adapted from Baskett PJF (1990) ABC of major trauma. Management of hypovolaemic shock. British Medical Journal 1453–1457 and Johanson R, Cox C, Grady K, Howell C (2003) Managing obstetric emergencies and trauma: The MOET course manual. London, Royal College of Obstetricians and Gynaecologists’ Press, pp. 97–104.
Anaesthetic issues related to PPH 1045
Other early signs of hypovolaemia that are often overlooked are a narrowed pulse pressure and prolonged capillary refill that occur as the result of vasoconstriction. A falling urine output can be a particularly useful sign when haemorrhage is concealed. Patients should be monitored in well-lit surroundings so that changes in complexion can be noted. Once intravenous access is secured, the response to intravenous fluid boluses can be used as an indicator for the need for further treatment (Table 2). RESUSCITATION: THE IMMEDIATE MANAGEMENT OF POSTPARTUM HAEMORRHAGE Shock is defined as inadequate tissue perfusion. The purpose of resuscitation is to restore/maintain the oxygen delivery to the tissues. The aim is to prevent the onset of the irreversible stage of shock when there is multiple organ failure, increased capillary permeability, acidosis and failure of haemostasis. Resuscitation is based on the ABC approach.7 A patent airway is necessary to allow adequate oxygenation and ventilation for CO2 excretion. The conscious patient should have high-flow oxygen (10–15 L/min), via a facemask with a non-re-breathing bag to deliver w60% oxygen. Arterial oxygen saturations should be kept > 95% if possible. To maintain and protect the airway in the unconscious patient (or the patient with reduced or falling conscious level), the trachea should be intubated with a cuffed tube and 100% oxygen given. Good venous access should be secured as early as possible. Flow rates through different-sized cannulae are listed in Table 3. Most resuscitation manuals recommend two 14G cannulae in the presence of haemorrhage.7 Peripheral venous access might be impossible if there is intense vasoconstriction. Other options include cutdown to a peripheral vein (possible sites include the antecubital fossa, the proximal saphenous vein and the peripheral saphenous vein at the ankle), percutaeous femoral cannulation and central venous cannulation. Although peripheral cutdown can be performed quickly and have few complications, a randomised study in 78 trauma patients of intravenous access by saphenous vein cutdown and femoral cannulation found the time required for the cutdown to be significantly longer (5.6 2.6 min versus 3.2 1.2 min).8 Table 2. Response to resuscitation by intravenous fluids (2L crystalloid). Response type I II
III
Signs improve Initial, temporary improvement with rapid regression to original levels, due to redistribution of fluid to the extravascular compartment or ongoing haemorrhage No improvement with second fluid challenge
IV
No response to rapid infusion of fluid of any type
Intervention needed No further fluid challenge required Second fluid challenge (colloid) required. If vital signs return to normal, redistribution was responsible Continue intravenous infusion of blood or colloid to sustain resuscitation. Surgery required within 1 hour Immediate surgery required
Modified with permission from Johanson R, Cox C, Grady K, Howell C (2003) Managing obstetric emergencies and trauma: The MOET course manual. London, Royal College of Obstetricians and Gynaecologists’ Press, pp. 97–104.
1046 F. Plaat
Table 3. Flow rates through intravenous cannulae. Gauge number* 20G 18G 16G 14G
Colour code Pink Green Grey Orange
Flow rate mL/min** 40e80 75e120 130e220 250e360
*
G refers to a wire gauge classification of the size of the internal diameter of the cannula. It is slightly different to the American and Standard Wire Gauges. ** The British standard for determining flow rate: involves in-vitro testing using distilled water at 22 C, kept at constant pressure. The flow rates are therefore not the same as those achievable clinically.
The disadvantages of femoral cannulation include the prerequisite of a palpable femoral arterial pulse and, in the obstetric setting, lack of access. Central venous access allows monitoring of central pressures but is more difficult and potentially hazardous in the hypovolaemic patient, especially in the presence of impaired coagulation. Complications include air embolism, subcutaneous emphysema, pneumothorax, haemothorax, damage to the common carotid artery, brachial plexus, phrenic nerve, thoracic duct and sympathetic chain. Cardiac perforation has been reported. An aseptic technique must be employed to reduce the risk of catheter-related sepsis and ECG monitoring is required as the catheter tip can induce arrhythmias if inserted too far. The National Institute for Health and Clinical Excellence (NICE) recommends that ‘2-D imaging ultrasound guidance should be considered in most clinical situations where CVC [central vein catheterisation] is necessary whether the situation is elective or emergency’. Those using ultrasound guidance should have prior training.9 When samples have been taken for full blood count, group and cross-match, coagulation profile and biochemistry (urea þ electrolytes, glucose), fluid replacement should be promptly started.
AVOIDANCE OF HYPOTHERMIA Whichever fluid used and regime followed, it is imperative that the fluids are warmed as part of the strategy to prevent hypothermia, (defined as core temperature <35 C). Due to tissue hypoperfusion and inadequately warmed fluids. The detrimental effects of hypothermia include: Shift of the oxyhaemoglobin dissociation curve to the left, impairing oxygen delivery to the tissues. Shivering, increasing oxygen consumption and lactic acidosis. Impaired hemostasis. Impaired response to recombinant activated factor VII (rFVIIa). Hypothermia impairs platelet aggregation10,11, enhances fibrinolysis12 and impairs clotting factor function. Johnston et al found that at 35 C, without dilution, the function of all factors in the coagulation cascade was reduced by as much as 35%. At 33 C, factors XI and XII functioned at only 17% and 32% of normal capacity.13
Anaesthetic issues related to PPH 1047
Hypothermia potentiates dilutional coagulopathy Prothrombin time (PT) and activated partial thromboplastin time (APTT) values do not reflect the effects of hypothermia as blood samples are prewarmed in the laboratory prior to testing. In trauma patients, hypothermia is associated with worsened survival rates and increased blood loss.14 Various fluid-warming devices are available, several of which combine warming, using countercurrent water technology with pressure infusion, for example the Level 1 (Level 1 Technologies, Inc., Rockland, MA; Figure 1). Problems with such devices include insufficient warming at high flow rates, the risk of fluid overload and fatal venous air embolism.15 FLUID THERAPY The ideal fluid for resuscitation would have the oxygen-carrying capacity and volumeexpanding properties of blood. It would, however, be entirely synthetic, eradicating the need to cross-match and the risk of infection, and making it acceptable those whose beliefs prohibit the use of blood. Blood substitutes Several modified haemoglobin products are under development, including artificial red cells made from biodegradable polymers and polymerised haemoglobin developed from out-of-date bank blood. Non-human sources of haemoglobin and recombinant-based products are also being developed. Problems with these haemoglobin solutions include a short half-life; their lack of protective antioxidant enzymes, which could theoretically worsen reperfusion injury; and their tendency to cause vasoconstriction. One multi-centre, randomised, controlled trial of a cross-linked haemoglobin in trauma patients was terminated early due to concerns about pulmonary hypertension and increased mortality in the study group.16
Figure 1. Forced air warming system.
1048 F. Plaat
Perfluorocarbons are compounds that, when infused intravenously, can transport oxygen and carbon dioxide. Problems currently being investigated include the need for 100% inspired oxygen to make oxygenation effective, uptake by the reticuloendothelial system and interference with laboratory tests.17 Despite intense interest in the development of a blood substitute, there is nothing likely to be available in the immediate future. CLEAR FLUIDS: THE CRYSTALLOID–COLLOID DEBATE Intravenous infusion of any clear fluid will initially expand the intravascular space. How long the expansion lasts depends on how freely the fluid crosses the vascular endothelium: crystalloid solutions cross freely, whereas colloid do so more slowly. Because colloids have a higher osmolality than plasma, they expand the intravascular volume by more than the volume infused by drawing water intravascularly. Isotonic solutions such as Hartmann’s solution (Ringer’s lactate) or 0.9% saline are distributed between the intravascular and extravascular (interstitial) spaces in a ratio of 1:3. (5% dextrose is metabolised rapidly leaving pure water, which is distributed between the extracellular and intracellular compartments in a ration of 1:2. Thus, only a tiny proportion remains intravascular, making it unsuitable for intravascular volume replacement.) From the above, it is clear that colloids achieve intravascular volume expansion more efficiently: a smaller volume is required (2–4 less than the volume of crystalloid), and the effect is longer lasting. Colloid oncotic pressure is better maintained.18 Because smaller volumes are required, colloid resuscitation is associated with less interstitial oedema. Interstitial oedema has deleterious effects on gas exchange, wound healing and myocardial compliance. In critically ill patients, a positive fluid balance is associated with higher mortality.19 Hydroxyethyl starch solutions cause plasma expansion that lasts of up to 24 hours compared with only a few hours in the case of gelatine derivatives (Haemaccel, gelofusin). Despite these theoretical advantages, a recent trial comparing saline and albumin for resuscitation of patients in intensive care found no difference in outcome.20 Crystalloids are much cheaper than colloids. They are not associated with a risk of anaphylaxis and do not interfere with hemostasis (both gelatins and hydroxyethyl starch solutions have been implicated).21,22 Newer colloids, such as hydroxyethyl starch HES130/0.4 (Voluven), appear to have less effect on coagulation.23 Normal saline is not recommended as large volumes are associated with the development of a hyperchloraemic acidosis. This can complicate the interpretation of blood-gas data and can result in inappropriate clinical intervention.24 The clinical significance of the hyperchloraemic acidosis is still unclear. However, there is an argument for the use balanced fluid resuscitation using fluid (both crystalloids and colloids) containing physiological balance of electrolytes to avoid such disturbances.25 NORMOTENSIVE OR HYPOTENSIVE RESUSCITATION? There is a growing body of evidence to suggest that overvigorous fluid resuscitation increases the rate of uncontrolled haemorrhage and might be associated with increased risk of a poor outcome. Intravenous fluid loading increases ventricular preload
Anaesthetic issues related to PPH 1049
and increases blood pressure, which might reverse vasoconstriction increasing haemodynamic instability, as well as directly displacing fibrin clots. Clear fluids dilute the oxygen-carrying capacity of blood, dilute the concentrations of clotting factors and platelets, and reduce viscosity. In animal models of uncontrolled haemorrhage, aggressive fluid administration is associated with decreased survival.26 To test this in humans, Bickell et al assigned 598 adults who had suffered penetrating torso injuries with initial systolic blood pressure <90 mm Hg to either conventional or delayed fluid administration.27 In the former – conventional – group, Ringer’s lactate infusion was started at the scene; in the study group, fluid was withheld until the patient arrived in theatre. The latter group had better survival (70% versus 62%), fewer complications and shorter hospital stays. The transport times in this study were relatively short; fluid resuscitation was not unduly delayed. Dutton and colleagues randomised patients suffering both blunt and penetrating injuries to resuscitation protocols aimed at maintaining the systolic BP to either 100 mm Hg (normal) or 70 mm Hg, (low).28 Despite the latter group having a higher average injury score, mortality was the same in both groups. Although hypotensive resuscitation might be inappropriate in the pregnant patient because of the reliance of the placental circulation on maternal venous return, following delivery there might be benefits in the more cautious use of clear fluids, especially crystalloids, before surgical control of haemorrhage has been achieved. TRANSFUSION STRATEGIES There is agreement that when 30% or more of the circulating blood volume is lost, blood transfusion is required to maintain sufficient oxygen delivery to the tissues. Oxygen delivery is the function of cardiac output oxygen content: O2 content ¼ %O2 saturation [Hb] 1.34 When haemorrhage is very brisk, immediate access to blood can be life saving: all obstetric units should keep a couple of units of O-negative blood immediately available as group-specific blood requires 30 minutes and fully cross-matched blood an hour or more to prepare. In patients with known red-cell antibodies, the risk of a haemolytic transfusion reaction must be balanced against the risks of withholding transfusion. Recently, there has been a change in what is perceived to be an optimum haemocrit or haemoglobin concentration. Traditionally, the target was a packed cell volume (PCV) of 30% and haemoglobin concentration of 10 g/dL. However, there is growing evidence that concentrations as low as 7 g/dL are well tolerated in healthy, normovolaemic patients. A lower hematocrit decreases blood viscosity, increasing cardiac output and improving tissue oxygenation.29 Current guidelines state that red cells are rarely required when the haemoglobin concentration is >10 g/dL, and almost always needed when it is <6 g/dL. At intermediate concentrations, the need for transfusion depends on the individual clinical situation.30 During postpartum haemorrhage, the haemoglobin concentration to likely to be changing rapidly and oxygen demand in the peripartum period is greater than in the non-pregnant patient. Thus, it seems prudent to aim for the upper end of the recommended range of haemoglobin concentrations.
1050 F. Plaat
Coagulopathy is a common complication of major haemorrhage and particularly of obstetric haemorrhage. The causes include dilution, disseminated intravascular coagulation (DIC), hypothermia and acidosis. The careful use of warmed fluids to prevent hypothermia and acidosis has been discussed. Traditional policy for transfusion of products dictated that replacement should be guided by laboratory coagulation test results: blood products are indicated if the PT and APTT >1.5 normal control. During a major haemorrhage, laboratory test results are rarely available in time and empiric regimes such as at least one unit of fresh frozen plasma (FFP) for every four units packed red blood cells (PRBC) are widely advocated.31 Recently, however, such regimes have been challenged. Ho and colleagues argue that such regimes are based on old studies, which used whole blood and not packed cells for transfusion.32 A unit of whole blood contains the equivalent of one unit of PRBC þ one unit FFP: thus, such regimes are bound to result in dilutional coagulopathy and the equivalent of whole blood should be given from the start. Using a computer model of exsanguination, Hirshberg et al showed that prolongation of PT is the sentinel event of dilutional coagulopathy and occurs early.33 The key to preventing coagulopathy is to start FFP infusion before the PT becomes abnormal. This could be achieved by using a replacement ratio of PRBC:plasma of 3:2 or to transfuse FFP concurrently with the first units of PRBC. In practice, the latter would be complicated by the delay required as the FFP is thawed. Platelets do not need to be replaced so rapidly but should be kept >50 109/L. Because platelets are not kept by all transfusion laboratories, a level of 75–100 109/L should trigger a request for platelets. Platelets should be transfused through a fresh giving set, not one previously used for blood.29 The most common serious complication of massive transfusion is that the patient is given the wrong blood. This is more likely in the emergency situation. Other complications include transfusion reactions and hypocaelcaemia (PRBC contain citrate). Transfusion-related acute lung injury (TRALI), although uncommon, can also occur and is five or six times more likely after blood products compared to PRBC. More efficient use of blood and blood products is facilitated by the use of near patient testing. The Haemacue device allows haemoglobin estimation at the bedside using a drop of peripheral blood. It has been validated for use in obstetric patients.34 The thromboelastogram (TEG) allows bedside estimation of global haemostasis. It has been described as the ideal method for monitoring hemostasis during massive obstetric haemorrhage due to the fast feedback time, although this has been disputed. During a debate in 2005, a majority of UK obstetric anaesthetists rejected the motion that every labour ward should have a TEG.35 Although there has been less work on the use of the platelet function analyser (PFA) as a bedside test of coagulation in obstetrics, currently it appears to be less reliable than TEG in obstetric patients.36 Cell salvage in obstetrics Cell salvage (Figure 2) has been used in over 400 documented cases in obstetrics.37 It can reduce or obviate the need for allogenic blood and has been used for emergency as well as elective procedures.38 Due to the high and rising cost of blood and blood products, cell salvage can be justified on financial grounds. One unit reported that 60% of the total cost of disposables for a whole year was covered by the reduction
Anaesthetic issues related to PPH 1051
Figure 2. Cell salvage machine Didecot Electa (Sorin) (reproduced with permission).
in banked blood used on one patient.39 In 2005, nearly 40% of units in the UK used cell salvage in obstetrics, although problems with gaining sufficient experience to use it successfully in the emergency situation have been reported.40 The two possible complications of cell salvage in obstetrics – amniotic fluid embolism and undetected rhesus immunisation – have not been reported. It is recommended
1052 F. Plaat
that a leucocyte depletion filter is used, which has shown to reduce fetal squames and phosholipid lamellar bodies to close to zero in salvaged blood.41 As an added precaution, most units use conventional suction until the placenta and as much amniotic fluid as possible has been removed. Fetal red cell contamination does occur: 2 to 19 mL fetal blood can be re-transfused. Kleihauer testing should be undertaken as soon as possible and increased doses of anti-D immunoglobulin might be required.42 The use of cell salvage in obstetrics is now endorsed by several national organisations in the UK, including CEMACH, NICE, the RCOG and the Obstetric Anaesthetists’ Association. Where it is not available, consideration should be given to the transfer out of patients who refuse autologous blood and blood products. MONITORING REQUIRED IN POSTPARTUM HAEMORRHAGE To determine the severity of shock, the response to treatment and to detect concealed haemorrhage, continuous monitoring of multiple parameters is essential. This requires Level 2 critical care (or Level 1 if the patient is ventilated or there is multiorgan failure).43 As discussed above, in addition to ECG, oxygen saturation and blood pressure, respiratory rate in the conscious patient and core temperature in all patients should be monitored closely. Signs of impaired peripheral infusion should be sought regularly and frequently. Early warning scoring systems have been shown to improve detection of worsening physiological parameters in no-obstetric patients44 and are being adapted for use in obstetrics. Many such charts are now being evaluated (R. Jones, personal communication) and it is recommended that they be used to monitor all seriously and critically ill patients, including those at risk of or who have suffered postpartum haemorrhage. Central venous pressure monitoring will be necessary to direct volume replacement in most cases of postpartum haemorrhage. However, as previously described, it is a potentially hazardous procedure and unpleasant for the conscious patient. In the presence of impaired haemostasis, prior administration of blood products might be necessary. Because patient are often unstable and repeated arterial blood samples are required to monitor response to resuscitation, an arterial line if often required. The radial artery is most commonly cannulated but the brachial, femoral and dorsalis pedis arteries offer alternative sites. The use of a pulmonary artery flotation catheter (PAFC) to measure cardiac output is becoming less common as concerns grow about well-documented hazards and unproven clinical benefits. The risks of insertion and use include pneumothorax, arrhythmias, valve damage, pulmonary artery rupture and pulmonary infarction.45 A Cochrane database systematic review on the use of PAFCs for adult patients in intensive care could not demonstrate any difference in mortality or hospital length of stay with their use.46 Less invasive, safer monitoring techniques are gaining popularity. Doppler provides a means of real-time continuous cardiac output monitoring by measuring the velocity of blood flow in the aorta. The oesophageal Doppler incorporates a transducer at the tip of a flexible probe, which is inserted into the oesophagus via the oral route. Newer models have been designed for use in the awake patient. The suprasternal Doppler measures cardiac output via a handheld stationary probe, which directs a continuous
Anaesthetic issues related to PPH 1053
ultrasound beam at the ascending or aortic arch.47 The measurement of cardiac output by Doppler has been validated against thermodilution methods and has been used to successfully monitor cardiac function in a range of physiological states including pregnancy.48 Pulse contour cardiac output monitoring is also less invasive than the PAFC as it utilises information from central venous (usually femoral) and arterial lines. This method involves both pulse contour analysis of the arterial trace and intermittent transpulmonary thermodilution (PiCCO) or lithium chloride dilution (LiDCO). In the latter, lithium chloride is injected via central venous catheter and a lithium-sensitive electrode is sited in a peripheral arteryvia a standard arterial catheter. A lithium dilution curve is constructed, from which cardiac output is calculated and a continuous display of cardiac output is produced.49 More recently, a method by which lithium is injected via a peripheral vein has been evaluated.50 Adequacy of resuscitation can be assessed by improving cardiovascular variables, urine output and correction metabolic acidosis, anaemia and coagulopathy. Conventionally, tissue hypoperfusion was monitored by observing the magnitude of the base deficit as a measure of metabolic acidosis. However, as mentioned previously, this might not arise purely as a result of tissue hypoxia.51 Lactate is a by-product of anaerobic metabolism. Levels rise when peripheral perfusion leads to tissue hypoxia (type A lactic acidosis). It is easily measured by many blood gas machines and is recommended as a method for monitoring adequacy of tissue oxygenation. A study of ITU patients showed that it correlated better with mortality and morbidity than base deficit.52 A separate study of medical and surgical patients found that the combination of the two variables appeared superior to either lactate or base deficit alone in predicting survival.53 An initial increase in lactate levels that can occur when perfusion improves might represent washout from previously underperfused tissues. Lactic acidosis (type B) might also arise from non-hypoxic causes (e.g. in diabetes, hepatic and renal failure). The anion gap will be increased by hypoxia but not by other causes of metabolic acidosis, such as hyperchloraemic acidosis. The anion gap has to be corrected for the level of albumin, as hypoalbuminaemia will tend to reduce it. ANAESTHESIA FOR POSTPARTUM HAEMORRHAGE The appropriate anaesthetic technique will depend on the clinical situation but a senior experienced obstetric anaesthetist should always be directly involved. In the elective situation, when heavy bleeding is anticipated (e.g. caesarean section for placenta praevia) a regional technique can be used. Evidence suggests that blood loss is reduced when regional rather than general anaesthesia is used at caesarean section.54 A survey of obstetric anaesthetists in the UK revealed that the majority would be willing to use regional anaesthesia for patients undergoing elective surgery with minor placenta praevia. One-third would do so if the patient was bleeding but not haemodynamically compromised. The more experienced the anaesthetists, the more willing they were to offer regional anaesthesia. The two obstetricians who answered this survey, however, preferred general anaesthesia.55 A retrospective study by Parekh and colleagues found a significantly reduced blood loss and need for transfusion in women with placenta praevia under going caesarean section under regional anaesthesia.56
1054 F. Plaat
If regional anaesthesia is offered, it is essential that the patient is made aware that conversion to general anaesthesia might be required. Adequate preparations should be made to deal with sudden blood loss, including appropriate intravenous access, monitoring and instantly available blood and or blood products, and a method for warming intravenous fluids. In the haemodynamically unstable patient, when there is uncorrected hypovolaemia, where hemostasis is impaired or where the airway is at risk (semi- or unconscious patient) general anaesthesia is indicated. Should the patient need transfer – to the intensive care or the radiology department – the anaesthetist must provide appropriate monitoring and, if necessary, anaesthesia or sedation. In the UK, the majority of labour-ward theatres do not have the facilities for interventional radiological procedures and transfer to the radiology suite can be a considerable logistical challenge. If interventional radiology is considered, it is important to take into account that this might necessitate both the anaesthetist and anaesthetic support staff leaving the labour ward to accompany the patient.
Practice points Management of postpartum haemorrhage requires a multidisciplinary approach, with communication and co-operation between all specialties involved. The anaesthetist must be involved as early as possible and involved in the antenatal care of at-risk patients. There must be direct involvement of an experienced obstetric anaesthetist. Anaesthetists can contribute by organizing practice drills for managing postpartum haemorrhage and teaching resuscitation skills.
CONFLICTS OF INTEREST The author has recently written a review of B-Lynch C, Keith LG, Lalonde AB & Karoshi M. (eds) (2006) A textbook of postpartum haemorrhage. London: Sapiens Publishing. REFERENCES 1. Newton M, Mosey IM, Eglie GE et al. Blood loss during and immediately after delivery. Obstet Gynecol 1961; 17: 9–18. 2. Toledo P, McCarthy RJ, Hewlett BJ et al. The accuracy of blood loss estimation after simulated vaginal delivery. Anesth Analg 2007; 105: 1736–1740. *3. Bose P, Regan F & Paterson Brown S. Improving the accuracy of estimated blood loss at obstetric haemorrhage using clinical reconstructions. Br J Obstet Gynaecol 2006; 113: 919–924. 4. Patel A, Goudar SS, Geller SE et al. Drape estimation versus visual assessment for estimating postpartum haemorrhage. Int J Gynaecol Obstet 2006; 93: 220–224. 5. Allsop J, Navaneetham N & Cooper J. Maternal physiology. In Collis R, Plaat F & Urquhart J (eds.). Textbook of obstetric anaesthesia. London: Greenwich medical Media, 2002, pp. 21–38. 6. Pernoll ML, Metcalfe J, Schlenker TL et al. Oxygen consumption at rest and during exercise in pregnancy. Respir Physiol 1975; 25: 285–294. 7. Johanson R, Cox C, Grady K et al. Managing obstetric emergencies and trauma: the MOET course manual. London: RCOG Press, 2003. 97–104.
Anaesthetic issues related to PPH 1055 8. Westfall MD, Price RK, Lambert M et al. Intravenous access in the critically ill trauma patient: a multicentred, prospective, randomised trial ofsaphenous cutdown and percutaneous, femoral access. Ann Emerg Med 1994; 23: 541–545. 9. National Institute for Health and Clinical Excellence (NICE). TA49 Central venous catheters – ultrasound locating devices: guidance. Available from: www.nice.org.uk/guidance; 2002. 10. Gubler KD, Gentileloo LM, Hassantash SA et al. The impact of hypothermia on dilutional coagulopathy. J Trauma 1994; 36: 847–851. *11. Wolberg AS, Meng ZH, Monroe III DM et al. A systematic evaluation of the effect of temperature on coagulation enzyme activity and platelet function. J Trauma 2004; 56: 1221–1228. 12. Paul J, Cornillon B, Baguet J et al. In-vivo release of a heparin-like factor in dogs during profound hypothermia. J Thorac Cardiovasc Surg 1981; 82: 45–48. 13. Johnston TD, Chen Y & Reed II RL. Functional equivalence of hypothermia to specific clotting factor deficiencies. J Trauma 1994; 37: 413–417. 14. Jurkovitch GJ, Greiser WB, Luterman A et al. Hypothermia in trauma victim: an ominous predictor of survival. J Trauma 1987; 27: 1019–1024. 15. Adhikary GS & Massey SR. Massive air embolism: a case report. J Clin Anesth 1998; 10: 70–72. 16. Sloan EP, Koenigsberg M, Gens D et al. Diaspirin cross-linked haemoglobin (DCLHb) in the treatment of severe traumatic hemorrhagic shock: a randomised control efficacy trial. JAMA 1999; 282: 1857– 1864. 17. Ma Z, Monk TG, Goodnough LT et al. Effect of haemoglobin and perflubron-based oxygen carriers on common clinical laboratory tests. Clin Chem 1997; 43: 1732–1737. 18. Norberg A, Brauer KI, Prough DS et al. Volume turnover kinetics of fluid shifts after hemorrhage, fluid infusion, and the combination of hemorrhage and fluid infusion in sheep. Anesthesiol 2005; 102: 985– 994. 19. Mitchell JP, Schukker D, Calandrino FS et al. Improved outcome based on fluid management in critically ill patients requiring pulmonary artery catheterization. Am Rev Respir Dis 1992; 145: 990–998. *20. Finfer S, Bellomo R, Boyce N et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350: 2247–2256. 21. Evans PA, Garnett M, Boffard K et al. Evaluation of the effect of colloid (Haemaccel) on the bleeding time in the trauma patient. J R Soc Med 1996; 89: 101–104. 22. Kapiotis S, Quehenberger P, Eichler HG et al. Effect of hydroxyethyl starch on the activity of blood coagulation and fibrinolysis in healthy volunteers: a comparison with albumin. Crit Care Med 1994; 22: 606–612. 23. Langeron O, Doelberg M, Ang ET et al. Voluven, a lower substituted novel hydroxyethyl starch (HES 130/0.4), causes fewer effects on coagulation in major orthopedic surgery than HES 200/0.5. Anesth Analg 2001; 92: 855–862. 24. Brill SA, Stewart TR, Brundage SI et al. Base defficit does not predict mortality when secondary to hyperchloraemic acidosis. Shock 2002; 17: 459–462. *25. Boldt J. The balanced concept of fluid resuscitation. Br J Anaesth 2007; 99: 312–315. 26. Capone A, Safar P, Stezoski SW et al. Uncontrolled hemorrhagic shock outcome model in rats. Resuscitation 1995; 24: 143–152. *27. Bickell WH, Wall MJ, Pepe PE et al. Immediate versus delayed resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994; 331: 1105–1109. 28. Dutton RP, Mackenzie CF & Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma 2002; 52: 1141–1146. 29. Van der Linden P, Gilbart E, Paques P et al. Influenceof hematocrit on tissue O2 extraction capabilities during acute hemorrhage. Am J Physiol 1993; 264: 1942–1947. *30. Stainsby D, MacLennan S, Thomas D, et al. Guidelines in the management of major blood loss. British Committee for Standards in Haematology 2006. 31. Turner DAB. Emergency anaesthesia. In Aitkinhead AR, Rowbotham DJ & Smith G (eds.). Textbook of anaesthesia. 4th edn. Edinburgh: Churchill Livingstone, 2001, pp. 619–628. *32. Ho AMH, Karmakar MJ & Dion PW. Are we giving enough coagulation factors during major trauma resuscitation? Am J Surg 2005; 190: 279–284. 33. Hirshberg A, Dugas M & Banez EI. Minimizing dilutional coagulopathy in exsanguinating hemorrhage: a computer simulation. J Trauma 2003; 54: 454–463.
1056 F. Plaat 34. Yau R, Kathigamanathan T, Plaat F et al. Evaluation of the haemocue for measuring haemoglobin concentrations in the obstetric population. Int J Obstet Anesth 2002; 11(S): 8. 35. Hunt BI, Lyons G & Watson HG. Thromboelastography should be available on every labour ward. Int J Obstet Anesth 2005; 14: 324–327. 36. Vincelot A, Nathan N, Collet D et al. Platelet function during pregnancy: an evaluation using the PFA100 analyzer. Br J Anaesth 2001; 87: 890–893. *37. Catling S. Blood conservation techniques in obstetrics; a UK perspective. Int J Obstet Anesth 2007; 16: 241–249. 38. Catling SJ, Freites O, Krishnan S et al. Clinical experience with cell salvage in obstetrics: 4 cases from one UK centre. Int J Obstet Anesth 2002; 11: 128–134. 39. Dowse C, Gardner I, Laxton C et al. Investing in intra-operative cell salvage: experience of a Bristol teaching hospital. Int J Obstet Anesth 2008; 17(S): 49. 40. Dharmarajah A, Bedson R, Plaat F et al. Introducing cell salvage in obstetric practice: the first year’s experience. Int J Obstet Anesth 2008; 17(S): 50. 41. Waters JH, Biscotti C, Potter PS et al. Amniotic fluid removal during cell salvage in the caesarean section patient. Anesthesiology 2000; 92: 1531–1536. 42. Catling SJ, Williams S & Fielding AM. Cell salvage in obstetrics: an evaluation of the ability of cell salvage combined with the leucocyte depletion filtration to remove amniotic fluid from operative blood loss at caesarean section. Int J Obstet Anesth 1999; 8: 79–84. 43. RCoA, RCM, RCOG, RCPCH. Safer childbirth: minimum standards for the organisation and delivery of care in labour. London: RCOG Press, 2007. 44. Chatterjee MT, Moon JC, Murphy R et al. The ‘‘OBS’’ chart: an evidence based approach to re-design of the patient observation chart in a district general hospital setting. Postgrad Med J 2005; 81: 663–666. *45. Fujitani S & Baldisseri MR. Hemodynamic assessment in a pregnant and peripartum patient. Crit Care Med 2005; 33(Suppl): S354–S361. 46. Harvey S, Young D, Brampton W et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Syst Rev 2006; (3): CD003408. 47. Gan T. The esophageal Doppler as an alternative to the pulmonary artery catheter. Curr Opin Crit Care 2000; 6: 214–221. 48. Bray JK, Fernando R, Patel NP et al. Suprasternal Doppler estimation of cardiac output: standard versus sequential combined spinal epidural anesthesia for Cesarean delivery. Anesth Analg 2006; 103: 959–964. 49. Linton RAF, Band DM & Haire KM. A new method of measuring cardiac output in man using lithium dilution. Br J Anaesth 1993; 71: 262–266. 50. Jonas MM, Kelly FE, Linton RAF et al. A comparison of lithium dilution cardiac output measurement made using central and antecubital fossa venous injection of lithium chloride. J Clin Monit Comput 1999; 15(S): 25–28. *51. Morris CG & Low J. Metabolic acidosis in the critically ill: part I. Anaesthesia 2008; 63: 294–301. 52. Husain FA, Martin MJ, Mullenix PS et al. Serum lactate and base deficit as predictor of mortality and morbidity. Am J Surg 2003; 185: 485–491. 53. Smith I, Kumar P, Molloy S et al. Base excess and lactate as prognostic indicators for patients admitted to intensive care. Intensive Care Med 2001; 27: 74–83. 54. Afolabi BB, Lesi FE & Merah NA. Regional versus general anaesthesia for caesarean section. Cochrane Database Syst Rev 2006; (18). CD004350. 55. Bonner SM, Haynes SR & Ryall D. The anaesthetic management of Caesarean section for placenta praevia: a questionnaire survey. Anaesthesia 1995; 50: 992–994. 56. Parekh N, Husaini SW & Russell IF. Caesarean section for placenta praevia: a retrospective study of anaesthetic management. Br J Anaesth 2000; 84: 725–730.