Handbook of Obstetric Anaesthesia

Handbook of Obstetric Anaesthesia

The Simpson Handbook of Obstetric AnaesthesiaDr A S Buchan and Dr G H Sharwood-Smith

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Viewed apart, and in an isolated light, the degree of actual pain (of labour) is as great if not greater than that attendant upon most surgical operations ... Sir James Young Simpson, March 1847Copyright A.S.Buchan and G.H.Sharwood-Smith 1999 all rights reserved. Published by the Royal College of Surgeons of Edinburgh Updated on August1 2002

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INDEX

INDEXAcute renal failure Alveolar ventilation Amniotic fluid embolus Anaesthesia for:cervical suture cord prolapse emergency caesarean section instrumental delivery major obstetric haemorrhage manual removal of placenta placenta praevia post partum evacuation of uterus the pregnant patient Anaphylactic shock Antepartum haemorrhage (APH) Anticoagulant therapy Aortocaval compression Apgar score Assessment of the neonate Audit of epidural analgesia Awareness under general anaesthesia Blood and circulatory changes in pregnancy Blood products Bloody tap Breast feeding and anaesthetic related drugs Caesarean section under regional anaesthesia Cardiac disorders Cardiac Output Cardiopulmonary resuscitation (CPR) Cauda equina syndrome Caudal analgesia Central venous pressure, (multiple refs) Ref1 Ref2 Cervical suture Checklist prior to delivery of infant Clonidine Coagulation, (multiple refs) Ref1 Ref2 Ref3 Ref4 Ref5 Coagulation problems during pregnancy Colloid solutions Combined spinal and epidural (CSE) Complications of pregnancy Continuous spinal analgesia Contraindications for epidural analgesia Convulsions Cord prolapse CPR algorithm Cricoid pressure , (multiple refs) Ref1 Ref2 Ref3 Dermatome chart Diabetes mellitus Difficult intubation Disseminated intravascular coagulation (DIC) Dopamine,(multiple refs) Ref1 Ref2 Ref3 Ref4 Drugs for epidural analgesia Dural blood patch Dural puncture, (multiple refs) Ref1 Ref2 Ref3 Ref4 Eclampsia Entonox, (multiple refs) Ref1 Ref2 Ephedrine, (multiple refs) Ref1 Ref2 Ref3 Ref4 Ref5 Epidural abscess Epidural anaesthesia for Caesarean section Epidural analgesia Epidural catheter difficulties Epidural infusion Epidural infusion regimens Epidural vein catheterisation Ergometrine, (multiple refs) Ref1 Ref2 Failed intubation drill Failure to thread epidural catheter Fetal haemoglobin Fetal heart rate (FHR) monitoring Fibrinogen, (multiple refs) Ref1 Ref2 Gastrointestinal changes in pregnancy General Anaesthesia Glyceryl Trinitrate (GTN) HELLP syndrome Heparin,(multiple refs) Ref1 Ref2 Hepatic changes in pregnancy Hypertension, (multiple refs) Ref1 Ref2 Induction of general anaesthesia Inferior vena cava (IVC) Infiltration and field block anaesthesia for caesarean section Inhalational analgesia Intrathecal opioids, (multiple refs) Ref1 Ref2 Intravenous PCA in labour Links to other obstetric anaesthetic sites Loss of bladder sensation Lower oesophageal sphincter (LOS) Magnesium sulphate, (multiple refs) Ref1 Ref2 Ref3 Ref4 Maintenance of general anaesthesia Major obstetric haemorrhage management Malignant hyperpyrexia Manual removal of placenta Meconium aspiration syndrome Mendelson's Syndrome Mobile epidural, (multiple refs)Ref1 Ref2 Multiple pregnancy Neonatal resuscitation Neonatal resuscitation chart 1 Neonatal resuscitation chart 2 Neurological damage after epidural or spinals Normal delivery of infant Obesity Obstetric haemorrhage Oliguria, (multiple refs) Ref1 Ref2 Oxy-haemoglobin dissociation curve Pain in labour Pain pathways Paracervical block Patient controlled epidural analgesia (PCEA) Phenylephrine Physiological changes at birth Psychological factors Placenta accreta Placenta praevia Placental abruption Plasma volume Positive intravenous test dose Post partum haemorrhage (PPH) Postoperative pain management Pre-eclampsia, (multiple refs) Ref1 Ref2 Ref3 Ref4 Preface Preparation for general anaesthesia Preterm delivery Problems with epidural analgesia Pudendal block Pulmonary aspiration syndrome Pulmonary embolism Pulmonary oedema, (multiple refs) Ref1 Ref2 Ref3 Ref4 Regurgitation,(multiple refs) Ref1 Ref2 Renal changes in pregnancy Respiratory changes in pregnancy Respiratory disorders Resuscitation drug doses Segmental nerve supply to the perineum Serum cholinesterase Spinal anaesthesia for Caesarean section Spinal analgesia Spinal curves Spinal headache, (multiple refs) Ref1 Ref2 Spinal solutions Spinal or epidural haematoma Spiral arteries, (multiple refs) Ref1 Ref2 Steroid treatment regimens Subdural block Suggested technique for epidural analgesia Supine hypotensive syndrome Systemic analgesia Total spinal block Toxic reaction to local anaesthetic Transcutaneous electrical nerve stimulation (TENS) Uterine atony Uterine hypertonus Uterine relaxation with glyceryl trinitrate

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INDEXHypotension, (multiple refs) Ref1 Ref2 Ref3 Ref4 Ref5 Inadequate epidural block Inadvertent dural puncture Indications for epidural analgesia Indications and management of the apnoeic baby Venous air embolus Venous thromboembolus Ventilatory parameters

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Preface

ABOUT THE SIMPSON HANDBOOK OF OBSTETRIC ANAESTHESIA A sound practical and theoretical knowledge of the basic procedures is required to deal with the challenge posed by labour ward emergencies. This handbook which is based on a manual for a large maternity hospital is designed to meet this need. Recent advances in electronic publication have opened up new and exciting opportunities for distributing and updating the handbook. While the approach remains essentially didactic it is now possible to provide an up to date reference base with online links to Medline and revised clinical guidelines in accordance with current practice. Feedback from our readers will play a welcome and essential part in developing the content and technical aspects of the book. We hope that all labour ward staff (medical and midwifery) will find it a useful resource. It should also be a useful revision guide for postgraduate examinations. Hypertext links to obstetric and anaesthetic WWW resources will be developed further as they become available. ACKNOWLEDGEMENTS Several of our anaesthetic and medical colleagues have given their valuable advice in the preparation of the book. We would particularly like to thank the following obstetric anaesthetists: Professor Felicity Reynolds, Dr Vicki Clark, Dr John McClure and Dr Anne McCrae. Mrs Glynis Omond has given us invaluable secretarial assistance. We would also like to acknowledge receipt of a grant from Astra Pharmaceuticals Ltd. towards the costs of multimedia authoring. LEGAL MATTERS AND DISCLAIMER Every effort has been made to ensure that the material in this book conforms to current guidelines and practice in obstetric anaesthesia. Before instituting treatment all dosage schedules should be checked with manufacturers recommendations. Treatment protocols are not intended to be recommendations for a particular patient. Practitioners should always refer to local practice and guidelines before instituting treatment. The publisher, editors and authors can not therefore accept any liability arising from the treatment of any particular patient. A.S. BUCHAN, G.H. SHARWOOD-SMITH December 1999 While publication has been made possible by the support of advertisers the authors wish to emphasise their complete independence in deciding the content of the book ABOUT THE TECHNOLOGY OF THIS PUBLICATION This Book has been specially prepared in HTML format for conventional online viewing, or alternatively for email transmission or Web download as a self installing Windows 95/98/NT program. This program permanently stores the publication on your hard disk as a mini Web site; a single click of the mouse will then run your existing Web browser and allow you read the publication. If you have an intranet then the book can be copied direct to the server (assuming you have the appropriate license). For those who do not use the Windows operating system a zipfile version of the book is available although you will have to manually install it on your machine. This architecture results in maximum compatibility with existing trends in intranet/internet information delivery whilst allowing transfer of publications to machines without a network connection using floppy disks. Optimised compression techniques ensure very small file sizes for publications. There are substantial savings in publication costs and many extra facilities, particularly the ability to send further partial or complete updates by email or download. If the book is installed on an individual PC or Intranet then readers will not suffer from the slowness or expense of online connections although online references are automatically retrieved when necessary. The subscriber also has tangible "ownership" of their publication in that it resides on their own computer. The familiar interface of the subscribers Web browser helps to reduce the learning curve. In addition to the normal hypertext features seen in this publication items such as colour pictures, sound, video and live references to items on the World Wide Web / discussion groups we hope that virtual 3D simulations will soon be included and will be developed in future versions. CHAPTER 1Copyright A. S. Buchan and G.H. Sharwood- Smith 1999 all rights reserved. Published by the Royal College of Surgeons of Edinburgh

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Chapter 1

1 PHYSIOLOGICAL CHANGES IN PREGNANCY

Chapter contents Blood and circulatory changes Respiratory changes Gastrointestinal changes Renal changes Hepatic changes

The following alterations occur in order to meet the increasing metabolic demands of the fetus and prepare the mother for delivery. BLOOD AND CIRCULATORY CHANGES Coagulation During pregnancy - there is increased activation of the coagulation system affecting the normal balance of intravascular coagulation and fibrinolysis. Platelet activity and consumption are increased but there is also a compensatory rise in production. The concentration of most coagulation factors including fibrinogen VII,VIII, IX, X and XII are significantly increased. By contrast factor XIII (fibrin stabilising factor) decreases. Increased levels of antithrombin III, an increase in fibrin degradation products and increased plasminogen concentrations reflect enhanced fibrinolysis. These changes are not detected in a routine coagulation screen which is usually reported as 'normal' At delivery - placental separation prompts a further shift to increased coagulation but a fall in fibrinolysis. The risk of postpartum haemorrhage is reduced but this change is also linked to an increased risk of postpartum thromboembolism. Uterine contraction leading to closure of open placental vessels is also essential in reducing blood loss. Blood volume - plasma volume increases by 45% while the red cell mass increases by only 20%. This results in the physiological anaemia of pregnancy (the haemoglobin falling from 15 g/dl to 12 g/dl at 34 weeks). The blood volume returns to normal 10 - 14 days post partum (Fig 1.1). Haemodynamic changes - progesterone induced vasodilatation causes a 20% decrease in peripheral vascular resistance by term; consequently there is a fall in systolic and diastolic blood pressures. In the last trimester changes in posture may exert significant effects on cardiac output and blood pressure. Cardiac output rises to 50% above the non pregnant level during the third trimester; heart rate and stroke volume both rise by 25%. The central venous pressure, reflecting right ventricular filling pressure, shows no change during normal pregnancy - left ventricular hypertrophy and dilatation accounting for the increased cardiac output. During labour cardiac output rises by a further 15% in the latent phase, 30% in the active phase and up to 45% in the expulsive phase.

Fig 1.1 Changes in cardiac output, plasma volume and red blood cell (RBC) volume during pregnancy and the puerperium (modified from Obstetric Analgesia and Anesthesia: 1980 Bonica JJ. World Federation of Anaesthesiologists, Amsterdam.)

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Chapter 1

Aortocaval compression After 24 weeks the gravid uterus may compress the inferior vena cava when the patient lies supine thus reducing venous return and maternal cardiac output. Two compensatory mechanisms exist: An increase in sympathetic tone leading to venous and arterial constriction (this includes the utero-placental circulation) and an increase in heart rate. A collateral circulation allows blood from the lower limbs to flow through the vertebral venous plexus and reach the right side of the heart via the azygos veins. In 10% of mothers these mechanisms are inadequate to maintain a normal blood pressure when supine (supine hypotensive syndrome). If the blood pressure fall is severe, consciousness may be lost. Turning the patient onto her side allows the cardiac output and blood pressure to return to normal as the IVC is decompressed. Falls in maternal cardiac output and blood pressure lead to a reduced placental flow with the risk of fetal hypoxia. By contrast the thicker walled aorta is less prone to compression; however, should it occur blood flow to the kidneys, uterus, placenta and the lower limbs may decrease - inadequate placental perfusion and fetal hypoxia may also follow. During labour uterine contractions displace most of the blood from the uterus and placenta into the azygos system; important consequences of this include intermittent increases in epidural venous pressure and cardiac output. Significance to the anaesthetist Aortocaval compression Anaesthesia - The induction of general anaesthesia or the institution of epidural or spinal blockade reduce sympathetic tone and may unmask aortocaval compression; as a result there is likely to be a fall in maternal cardiac output, blood pressure and placental perfusion. A left lateral tilt should be maintained by appropriately wedging the mother's pelvis. Labour and delivery - The mother should be prevented from lying completely supine. This is especially important during fetal blood sampling or instrumental delivery. Venous distension - Distension of epidural veins increases the chance of vascular damage during performance of regional blocks. It also reduces the volume of the epidural and intrathecal spaces therefore a reduced dose of local anaesthetic is required at term. Resuscitation - During external cardiac massage tilting the patient is essential to allow refilling of the right side of the heart. Immediate delivery also improves venous return and offers the best chance of survival for both mother and baby. Blood loss During vaginal delivery this averages 300 ml, in Caesarean section 750 ml; normally this is well tolerated because of the increased blood volume Cardiac output Venous return increases immediately after delivery due to an autotransfusion secondary to uterine emptying and the removal of IVC occlusion. Normally this additional volume is accommodated by vasodilatation and an increase in cardiac output; however cardiac failure with pulmonary oedema may be precipitated in the following conditions: systemic or pulmonary hypertension, severe cardiac disease and the use of vasopressors including ergometrine. Regional analgesia reduces the large increase in cardiac output which occur during labour and following delivery. It may be of value in patients such as those above with a limited cardiac output Utero-placental circulation


Chapter 1

Fig 1.2 Diagram of the maternal blood supply to the human placenta As pregnancy advances a fibrin matrix replaces the elastic lamina and smooth muscle of the spiral arteries ( Fig. 1.2). Consequently vascular resistance falls and placental blood flow increases. At term the uterine blood flow is around 700 ml/minute (10% of cardiac output); some 80% of this flows via the maternal spiral arteries into the intervillous space where exchange of gases and nutrients occurs between the villi containing the fetal capillaries and the maternal blood. Any reduction in uterine blood flow is therefore detrimental to the fetus. Uterine blood flow = (uterine arterial pressure - uterine venous pressure) uterine vascular resistance An increase in uterine vascular resistance causes a reduction in uterine blood flow. The uterine vascular resistance and venous pressure rise with each contraction. The bigger the contraction the more profound the drop in uterine perfusion. When the intraamniotic pressure rises above 50 - 60 mmHg intervillous perfusion ceases. Hence uterine hypertonus is clearly undesirable. Likely causes of reduced uterine blood flow are Hypotension:- aortocaval compression, blood loss, sympathetic block Hypertension:- essential or pregnancy-induced elevation of blood pressure Uterine Hypertonus:- excess oxytocin, placental abruption, high concentrations of local anaesthetic, ketamine in doses > 1.5 mg/kg, cocaine abuse Vasoconstriction:-sympathetic overactivity due to fear/anxiety or extreme hypoxia, sympathomimetic drugs (a1 adrenergic) with the exception of ephedrine (mainly 1 adrenergic), Fall in cardiac output: - this is not necessarily accompanied by a fall in blood pressure - for example in pre-eclampsia RESPIRATORY CHANGES Anatomy - Capillary engorgement affects all the airways. In particular the false cords and arytenoids may be oedematous. There is a progesterone induced increase in ventilation with tracheal and bronchial dilatation. Although the uterus displaces the diaphragm upwards inspiration is still predominantly due to diaphragmatic contraction. There is a compensatory increase in both the anteroposterior and transverse diameters of the rib cage.


Chapter 1

Fig 1.3 Changes in ventilatory parameters during pregnancy (modified from Obstetric Analgesia and Anesthesia: 1980 Bonica JJ. World Federation of Anaesthesiologists, Amsterdam.)

Lung volumes: A 20% reduction in functional residual capacity is present in the third trimester; this is due to a reduction in both expiratory reserve volume and residual volume. Inspiratory capacity increases and vital capacity is unchanged. Ventilation and blood gases during pregnancy Alveolar ventilation - increases by 70% during the second to third month of gestation. This is mainly due to an increase in tidal volume. Oxygen consumption and carbon dioxide production - both increase progressively to reach 60% above non pregnant levels at term. Pa CO 2 - falls and stabilizes at 4.1 kPa (31 mmHg) by the end of the first trimester; this is due to rising progesterone levels which reset the sensitivity of the respiratory centre to Pa CO 2 Pa O 2 - rises to 14 kPa (105 mmHg) during the third trimester in the erect position; this is due to the fall in Pa CO 2 plus a reduced arteriovenous oxygen difference. The Pa O 2 declines slightly by term - the rise in cardiac output does not keep pace with to the increased oxygen consumption and arteriovenous oxygen difference increases. In the supine position a fall in cardiac output and, in some patients, closure of dependant airways may lead to a fall in Pa O 2 to 1020, urine osmolality is high at >700 mmol/kg. low in sodium - the urine sodium concentration is 250 mmol/l. Intrinsic renal causes - Acute renal failure may result from failure to correct pre-renal factors and may be complicated by exposure to nephrotoxins, e.g., bacteraemia, incompatible blood transfusion, disseminated intravascular coagulation, amniotic fluid embolus, cephalosporin and amino-glycoside antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs) and hepatic failure. The kidney fails to concentrate urine effectively. The urine is: dilute - the specific gravity is 100 > 100 > 200 >8 prolonged

USE OF ANTICOAGULANT THERAPY DURING PREGNANCY AND THE PUERPERIUM In general the risk of venous thrombosis is greater in the days and weeks after delivery than it is during pregnancy. Indications for full anticoagulant therapy


Chapter 7

Deep venous thrombosis (DVT) prophylaxis - (heparin). DVT treatment - (heparin and warfarin) Prosthetic heart valve - (warfarin) Thrombophilia e.g. antithrombin III, proteins C and S deficiency, Factor V Leiden polymorphism - (heparin). Indications for low dose heparin therapy and alternative methods (Adapted from) PROPHYLAXIS AGAINST THROMBOEMBOLISM IN CAESAREAN SECTION (1998 RCOG Working Party Report on Prophylaxis against thromboembolism) Risk assessment profile for thromboembolism in Caesarean section LOW RISK - early mobilisation and hydration Elective Caesarean section - uncomplicated pregnancy and no other risk factors MODERATE RISK - Consider heparin prophylaxis +/- leg stockings Age >35 years Obesity (>80Kg) Para 4 or more Labour 12hours or more Gross varicose veins Current infection Pre-eclampsia Immobility before surgery ( >4days) Major current illness e.g. heart disease, cancer, inflammatory bowel disease, nephrotic syndrome Emergency Caesarean section in labour HIGH RISK - Heparin prophylaxis + leg stockings A patient with three or more risk factors from above Extended major pelvic or abdominal surgery, e.g. Caesarean hysterectomy Patients with a personal or family history of DVT, pulmonary embolism or thrombophilia Paralysis of lower limbs Patients with antiphospholipid antibody (cardiolipin antibody or lupus anticoagulant). The heparin regimen should consist of 7,500 units of subcutaneous standard heparin 12 hourly or enoxaparin (LMWH) 40 mg daily. Anticoagulant drugs Vitamin K antagonists - phenindione, warfarin. Warfarin has a low molecular weight, is lipid soluble and crosses the placenta; it is teratogenic and may cause placental or fetal bleeding. This group of drugs should be avoided in pregnancy if possible; treatment during the first and third trimesters presents the greatest risk. If the balance of risk results in administration during the middle trimester (e.g. for a prosthetic heart valve) a change to heparin is normally made at least 4 weeks before delivery. The prothrombin time, reported as the international normalised ratio (INR), is monitored; the therapeutic range is 2 - 5:1. Excessive anticoagulation or haemorrhage may require intravenous phytomenadione ( Vitamin K), plus FFP if life threatening; close liaison with the haematologist is essential. Unfractionated heparin (UHF) - this is a mucopolysaccharide with a high molecular weight and protein binding capacity, which does not cross the placenta. Coagulation is inhibited by a number of steps including the potentiation of antithrombin III and alterations in platelet function. The activated partial thromboplastin time (APTT) is monitored and the therapeutic range is 1.5 - 2.5:1. If haemorrhage occurs withdrawal of heparin may be sufficient, otherwise protamine is given. When heparin is given in low dose by subcutaneous injection laboratory monitoring is not required.


Chapter 7

Low molecular weight heparin (LMWH) - heparin is fractionated to produce LMWH which inhibits activated factors II and X with little effect on platelet function; a longer action means that only a single daily subcutaneous dose is required e.g. enoxaparin. Factor Xa activity is not normally monitored. Aspirin - this inhibits cyclo-oxygenase which is required for prostacyclin production (vasodilator, decreased platelet aggregation) and thromboxane A2 production (vasoconstriction, increased platelet aggregation) in platelets and the vascular endothelium. Suppression of thromboxane A2 is greater and of longer duration than that of prostacyclin - so the net effect is vasodilatation and decreased platelet aggregation. Aspirin shows very limited efficacy in preventing DVT. It has been used in an attempt to improve fetal outcome in pre-eclampsia but published evidence has not been favourable. Anticoagulants with epidurals and spinals Full anticoagulation with warfarin or heparin is a contraindication to spinal and epidural techniques. Haematoma in the vertebral canal is rare and can arise spontaneously. The risk of this complication is slightly increased when spinal or epidural analgesia is performed in a patient to whom low dose subcutaneous heparin, including LMWH, is being administered. The risk appears to be greatest for epidural catheterisation. The increase in cases associated with LMWH recently reported from America may be related to the larger doses given there. The risk may be minimised by applying a few basic precautions: Weigh the small increased risk against the benefits of an epidural in the situation presenting and discuss the matter fully with the patient Use a skilful atraumatic technique Before performing a central nerve block: 4 hours should be allowed after the last dose and 1 hour before the next dose of UHF 10-12 hours should be allowed after the last dose and 4 hours before the next dose of LMWH Continue to monitor the patient for signs of cord compression for the entire duration of anticoagulant therapy. Aspirin therapy interferes with platelet function, an effect which may persist for 7 days after stopping treatment. The risk of haematoma formation appears to be very slight if the coagulation screen is normal. Extra care when inserting and removing the catheter is a sensible precaution. FURTHER READING Lechner RB. Hematologic and coagulation disorders. In: Chestnut DH ed. Obstetric Anesthesia. St Louis: Mosby, 1994; 815-845. Howell CJ, Clowes NWB. The management of major obstetric haemorrhage. Current Anaesthesia and Critical Care 1995; 6: 218223. Scottish Obstetric Guidelines and Audit Project . The Management of Postpartum Haemorrhage. 1998; click here for WWW link Harmer M. Maternal mortality is it still relevant? Anaesthesia 1997; 52: 99-100.Click here for Medline link Donaldson MDJ, Seaman MJ, Park GR. Massive Blood Transfusion. British Journal of Anaesthesia 1992; 69: 621-630.Click here for Medline link Bell K. Blood transfusion in the critically ill: coagulopathy and hypoalbuminaemia. British Journal of Intensive Care 1996; 6:10-15. Bell K. Blood transfusion in the critically ill: volume replacement and transfusion of red cells. British Journal of Intensive Care 1995; 6: 218-273. Checketts MR and Wildsmith JAW. Central nerve block and thromboprophylaxis - is there a problem? British Journal of Anaesthesia 1999; 82:164-167.Click here for Medline link NEXT CHAPTER


Chapter 7


Chapter 8

8. MATERNAL RESUSCITATION Chapter contents Cardio-pulmonary resuscitation CPR Algorithm Resuscitation drug dosages Convulsions Anaphylactic shock Pulmonary embolismVenous thromboembolus: Amniotic fluid embolus: Venous Air Embolus

Pulmonary oedema Malignant hyperpyrexia CARDIO-PULMONARY RESUSCITATION (CPR) Cardiac arrest is rare with an incidence of 1:30,000 pregnancies. The survival of mother and fetus depends on prompt recognition and treatment. Main causes of cardiac arrest

Anaesthetic ProblemsFailed intubation Aspiration of gastric contents Total spinal anaesthesia Drug induced reactions Local anaesthetic toxicity

Obstetric ProblemsMassive haemorrhage Amniotic fluid embolism Venous and/or air embolism Intracranial haemorrhage Magnesium toxicity After 26 weeks of pregnancy aortocaval compression is likely. If cardiac arrest occurs the complete absence of any vascular tone leads to a reduction in venous return to the right side of the heart. External cardiac compression may therefore be ineffective, as the heart is empty. The patient must be tilted to at least a 30 angle. This is best achieved using a specially wedged board, although it is possible to use a "human wedge".

Fig 8.1

Wedged board

Human wedge

If CPR is not effective (15:2 ratio) in generating a powerful pulse (100/min) or adequate perfusion within 3 - 4 minutes and there is


Chapter 8

no other obvious remediable cause, e.g. massive haemorrhage, bilateral tension pneumothorax or pulmonary embolus, the fetus must be delivered while CPR is continuing; effective cardiac filling and output should then occur. Early delivery may also save the baby (the fetus is more resistant to hypoxia than the mother).

THE CHAIN OF SURVIVAL Early Access Early Basic Life Support

Early Defibrillation

Early Advanced Life Support

For every minute that elapses following the onset of a shockable arrhythmia, there is 5-10% less chance of survival. Early defibrillation is critical; therefore it should not be delayed if available and appropriate. Administration of 200, 200 and 360 joule shocks, given in sequence if required with a monophasic defibrillator, should not take any longer than 30 seconds. As soon as the shocks have been delivered, B.L.S must be restarted immediately. Available data suggests that defibrillation is safe in all phases of pregnancy and labour as only a small amount of current penetrates the uterus. Biphasic defibrillators are effective at lower energy levels e.g. 200 J. They reverse current flow during defibrillation and are as effective or better than monophasic defibrillators. ADVANCED LIFE SUPPORT ALGORITHM FOR THE MANAGEMENT OF CARDIAC ARREST IN ADULTS

Note: each successive step is based on the assumption that the one before has been unsuccessful

Resuscitation Council UK. Table 8.1 Resuscitation drug doses


Chapter 8

TRACHEAL DRUGS made up in a all doses based on INTRAVENOUS volume of 10 a 70 kg woman ml saline Epinephrine 1:10,000 0.1-1 mg 2 mg 10 ml = 1 mg Atropine 1 mg 2 mg 0.6 mg/ml 3 mg Amiodarone in 20 ml 5% dextrose 300 mg second dose 150 mg

COMMENT a and receptor stimulant Infusion 5 mg:500 ml saline (10 g/ml) Increases heart rate Completely blocks the vagus nerve, used in asystole Used in refractory fibrillation. Consider as early as fourth shock Used in refractory fibrillation Membrane stabilisation, reduces tendency to tachyarrythmias Inotropic action

Bretylium tosylate 500 mg 50 mg/ml Mexiletine 150 mg bolus 25 mg/ml Calcium gluconate 10% 10 ml (0.225 mmol Ca/ml) Lidocaine 2% Adenosine 100 mg 6 mg 200 mg

Infusion 1.5 g:500 ml 3 mg/ml then 12 mg x 3 every 2 min Not as routine, only refractory cases, pH to be measured as soon as possible -blocker used for supraventricular arrythmias (SVT)

Sodium bicarbonate 50 ml 8.4% Metoprolol 5 mg (1 mg/ml)

Any effects of these drugs on the fetus can be addressed after delivery, resuscitation of the mother is the prime consideration. Algorithms for treatment of Periarrest Arrhythmias can be accessed here

BRADYCARDIA BROAD COMPLEX TACHYCARDIA NARROW COMPLEX TACHYCARDIA CONVULSIONS Main causes Eclampsia, epilepsy and local anaesthetic toxicity. Consider all obstetric convulsions eclamptic in origin despite a normal blood pressure until proved otherwise. Premonitory signs Eclampsia - May be NONE: severe frontal headache with visual disturbance, photophobia, nausea and vomiting, right upper quadrant pain. Epilepsy - Aura, history of epilepsy, anticonvulsant therapy. Local anaesthesia - Numbness of the tongue and circumoral tissues, light-headedness, dizziness, difficulty focusing, tinnitus, slurred speech, shivering and muscle twitching.


Chapter 8

Management Turn the patient on her side to avoid aortocaval compression. Maintain and protect the airway, administer 100% oxygen. Ensure fetal monitoring. Follow one of the two regimes:Diazepam 5 - 20 mg i.v. (more than 30 mg may cause neonatal hypotonia) Intravenous thiopentone 50 mg increments - suxamethonium, cricoid pressure and intubation may be required. If eclampsia is suspected once convulsions have ceased then the magnesium sulphate protocol is followed. ANAPHYLACTIC SHOCK Common labour ward causes:- antibiotics, suxamethonium, latex, oxytocin, NSAIDs and colloids. An anaphylactic reaction is where previous sensitisation has occurred and vasoactive substances e.g. histamine, serotonin are released from mast cells in response to an IgE antibody mediated reaction. An anaphylactoid reaction is where there is no antibody mediation in mast cell release. Management Stop the administration of all suspected drugs and curtail surgery if appropriate. Maintain the airway, give 100% oxygen, and avoid aortocaval compression. Give epinephrine 1:10,000 (1 mg:10 ml saline) i.v. as 0.5 - 1 ml boluses, titrate as necessary for hypotension and bronchospasm. Start rapid intravascular volume expansion with crystalloid or colloid. Specific measures Hypotension - Elevate the legs, establish monitoring with ECG and possibly CVP and arterial line. Circulatory support with catecholamines. Bronchospasm aminophylline salbutamol 250 - 500 mg i.v. slowly 250 g i.v. slowly 2.5 - 5 mg nebulised in 3 ml saline Antihistamines chlorpheniramine Steroids hydrocortisone 100 - 200 mg i.v. 10 - 20 mg i.v.

Anaphylaxis algorithm can be accessed here:-

Investigation Immediate - mast cell tryptase, the principle protein content of mast cell granules is released with histamine and other amines in anaphylactic and anaphylactoid reactions. Plasma concentration is raised 1 - 6 h after a reaction. Normal level 0.8 - 1.5 ng/ml Anaphylactic reactions occur at concentrations >20ng/ml


Chapter 8

Long term - referral to allergist for skin testing and specific IgE antibody detection by radio-allergosorbent test (RAST)

PULMONARY EMBOLISM This is the commonest cause of maternal death in the United Kingdom. Emboli may be thrombus, amniotic fluid or air. The physiological changes that occur depend on the degree of obstruction to blood flow through the pulmonary artery and the increase in dead space ventilation. These may lead to pulmonary hypertension, right ventricular strain and cardiac failure. During anaesthesia an early sign is an abrupt fall in end tidal PCO 2 Venous thromboembolus The risk of venous thrombosis is increased in pregnancy due to the relatively hypercoagulable state, particularly in the postpartum period. The presentation includes retrosternal discomfort, dyspnoea, pleuritic pain, haemoptysis, profound collapse, raised central venous pressure and cardiac arrest. The ECG shows:S1 Q 3 T3 pattern with prominent S wave in lead I, Q wave and inverted T in lead III Sinus tachycardia T wave inversion in leads V1 -V3 Right bundle branch block Low amplitude deflection A ventilation perfusion scan will show normal ventilation with a segmental perfusion defect. Pulmonary angiography may demonstrate an intraluminal filling defect and/or the abrupt termination of a branch vessel. Management of minor thromboembolism Heparinisation - 5,000 -10,000 i/u i.v. followed by a continuous infusion of 1,000-2,000 i/u per hour. Monitored with the APPT - therapeutic range 1.5-2.5. Antenatally heparin is given sc - 12,000 i/u 12 hourly. Postnatally oral warfarin is started at the same time as i.v. heparin - 10 mg/day for 2days. Subsequent dosage depends on the INR - therapeutic range 2-3. Management of massive thromboembolism Oxygen therapy, cardiac massage and intermittent positive pressure ventilation (IPPV) An intravenous bolus of heparin - 15,000 i/u should be given. Cardiovascular support with a norepinephrine infusion 4 mg in 500 ml of saline A pulmonary angiogram should be obtained immediately: if this is not available thrombolytic therapy must be started with streptokinase in a loading dose of 600,000 units with a maintenance dose of 100,000 u/h for 24 hours. The thrombin time should be maintained at a level of 1 times the control value. Amniotic fluid embolus (Anaphylactoid Syndrome of Pregnancy) The incidence is 1 in 30,000 pregnancies with a maternal mortality rate approaching 85%, It can occur during labour (70%), after Caesarean delivery (19%), or after vaginal delivery (11%). The presenting features are Sudden collapse Excessive bleeding in labour or post partum Seizures Dyspnoea Fetal bradycardia There is a history in 41% of mothers of atopy (asthma, eczema, hay fever) or allergy, often to drugs.


Chapter 8

There is a biphasic response to the presence of amniotic fluid (or meconium) in the maternal circulation causing release of substances that produce pulmonary vascular spasm, pulmonary hypertension, hypoxic injury to the pulmonary capillaries and heart. This leads to left ventricular failure and subsequent adult respiratory distress syndrome. Coagulopathy may be related to the presence of a factor X activator in amniotic fluid. Diagnosis is made on clinical grounds. The presence of fetal cells in the maternal blood is NOT pathognomonic and they are commonly detected in normal patients. In primates it has been shown that infusions of large amounts of amniotic fluid do NOT cause the syndrome. Minor degrees of the syndrome are probably quite common. Management Cardiopulmonary resuscitation with the patient wedged if the fetus is still in utero Deliver the fetus and placenta as soon as possible Insert 2 large peripheral cannulae, CVP line, urinary catheter, arterial line and if possible a pulmonary artery catheter Aspirate blood from the right side of the heart Monitor ECG, pulse, blood pressure, CVP and pulmonary artery wedge pressure Cardiovascular support with dopamine and epinephrine DIC management in consultation with the Haematology Department Venous air embolus This can occur during Caesarean section particularly at the time of uterine incision and placental separation. It has been shown that subclinical venous air embolism occurs in up to 50% of patients at this time; the risk is increased when the uterus is exteriorised and the patient is head down. A head up tilt has been advocated during surgery for Caesarean section. A patent foramen ovale is present in 20 - 25 % of patients and paradoxical air embolism is possible although very rare in clinical practice. Large air embolism will result in frothing of blood in the right ventricle causing an air lock and cardiac arrest. The diagnosis is made with a precordial or oesophageal Doppler probe. A mill wheel murmur is accompanied by hypotension, a fall in SpO 2 , end tidal PE CO 2 and an increase in central venous pressure. Management 100% oxygen must be given Stop the nitrous oxide to reduce the air bubble size Replace the uterus if exteriorised Flood the wound with fluid to prevent further aspiration of air. Place the patient in a head down position on the left side to allow any air to collect in the apex of the right ventricle Aspirate air from the right atrium via a central venous line. Provide cardio-respiratory support as necessary. Internal cardiac massage may be required - access to the great vessels will permit direct aspiration of air (or amniotic fluid) . PULMONARY OEDEMA Maternal pulmonary oedema is associated with: Pre-eclampsia - capillary permeability is increased and colloid osmotic pressure falls due to proteinuria. There may also be an element of left ventricular failure secondary to severe hypertension. Antihypertensive therapy with -blockers may contribute to this. Fluid overload - due to over-treatment of severe haemorrhage, or fluid challenges in pre-eclamptic patients. Myocardial disease - e.g. cardiomyopathy of pregnancy or myocardial ischaemia. The use of tocolytic therapy for premature labour with -adrenergic agonists, e.g., ritodrine, isoxuprine, salbutamol. Tachycardia is a prominent feature. Steroid therapy for fetal lung maturation may be a contributory factor It presents with tachycardia, tachypnoea, hypoxia and cyanosis. An early sign is a fall in oxygen saturation. On auscultation of the chest, basal crepitations and rhonchi are heard. Chest x-ray shows fluffy shadowing or the more extensive butterfly wing appearance. Management


Chapter 8

Oxygen Sedation with i.v. morphine to relieve agitation / anxiety and reduce the pre-load by venodilatation. Diuretic therapy with frusemide 40 - 80 mg i.v., repeated as necessary. Dopamine 2 - 5 g/kg / min may be required i.v.. Intubation and IPPV may be necessary with positive end expiratory pressure (PEEP) Treatment of the underlying cause

MALIGNANT HYPERPYREXIA (MH) The incidence is 1:30,000 of all general anaesthetic administered. Not every patient with a genetic predisposition developes a MH crisis during exposure to triggering agents which include all volatile anaesthetics and depolarising muscle relaxants. MH presents with the following

signs:

Unexplained tachycardia Tachypnoea A rise in body temperature which increases by more than 2 C/h An abnormal reaction to suxamethonium - trismus is an early sign of this Cyanosis Muscular rigidity developing later during the anaesthetic Increased oozing is usually a sign of DIC A fall in SpO 2 , a rise in PE CO 2 , metabolic acidosis and hyperkalaemia A diagnosis of MH should be assumed if suspicions are aroused. Management Discontinue inhalational agents, terminate surgery CALL FOR HELP. Hyperventilate with 100% oxygen 2 - 3 times the predicted minute volume Give dantrolene 2 mg/kg i.v.. Repeat as necessary up to a total of 10 mg/kg Cool with 1 - 2 litres iced saline i.v., apply surface cooling over the major vessels, and lavage to the pleural or peritoneal cavities. Consider cardiopulmonary bypass via femoro-femoral circulation Correct metabolic acidosis with sodium bicarbonate, monitor blood gases and pH and correct hyperkalaemia. Treat arrhythmias if severe. Establish the following monitoring: SpO 2 , ECG, arterial cannulation, a muscle temperature probe, central venous cannulation, urinary catheter, blood pressure and a fluid balance chart. Investigations should include the following: blood gases, haemoglobin, urea, electrolytes, clotting screens and CPK level Admit to the intensive care unit Late management must include screening of the patient and her family for MH susceptibility In the management of known MH or MH susceptible patients, the technique of choice is regional anaesthesia. The administration of general anaesthesia requires the following conditions:A clean anaesthetic machine with disposable tubing and no vaporisers The circuit which has been flushed with 10 litres of oxygen for at least 20 minutes before use A cooling blanket on the operating table, Dantrolene and ice must be available. Only 'safe' drugs must be used SAFE Diazepam, thiopentone, propofol, methohexitone. Nitrous oxide Atracurium, pancuronium, vecuronium, mivacurium,, rocuronium Succinylcholine Halothane, enflurane, isoflurane, desflurane, sevoflurane UNSAFE


Chapter 8

Local anaesthetic drugs Oxytocin, PGF2 a, ergometrine Nitroglycerine, magnesium sulphate Ephedrine, epinephrine, norepinephrine FURTHER READING The American Heart Association in Collaboration with the International Liaison Committee on Resuscitation (ILCOR) Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - An International Consensus on Science. Resuscitation 2000; 46: 1-448 The 1998 European Resuscitation Council Guidelines for Adult Advanced Life Support. In: Bossaert L (ed.). European Resuscitation Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 36-37. The 1998 European Resuscitation Council Guidelines for the management of the airway and ventilation during resuscitation. In: Bossaert L (ed.). European Resuscitation Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 129-158. Kudenchuk PJ, Cobb LA, Copass MK et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. New England Journal of Medicine 1999; 341: 871-878.Click here for Medline link The Association of Anaesthetists of Great Britain and Ireland and The British Association of Allergy and Immunology. Suspected anaphylactic reactions associated with anaesthesia. Published by: The Association of Anaesthetists of Great Britain and Ireland 1995. MedicAlert Foundation (Registered Charity) Fletcher SJ, Parr MJA. Amniotic fluid embolism: a case report and review. Resuscitation 2000: 43;141-146 Click here for Medline link Halsall P, Ellis FR. Malignant hyperthermia. Current Anaesthesia and Critical Care 1996; 7; 3: 158-166. NEXT CHAPTER


Chapter 9

9. NEONATAL RESUSCITATION

Chapter contents Physiological changes Checklist before delivery Normal delivery Assessment of the neonate Indications for positive pressure ventilation Resuscitation chart 1 Resuscitation chart 2

PHYSIOLOGICAL CHANGES AT BIRTH The infants first breath expands the lungs and reduces pulmonary vascular resistance, thus allowing increased pulmonary blood flow. Clamping the umbilical cord increases systemic vascular resistance and these changes together with a rising arterial PO2 result in closure of the foramen ovale and ductus arteriosis to establish a pulmonary and systemic circulation. The arterial PO2 slowly increases and may take up to six weeks to reach adult values, due to intrapulmonary shunting of venous blood which may be as high as 20% in the first few days of life. As the lungs expand surfactant function becomes well established and less negative pressure is required to allow air entry. Each subsequent breath therefore requires less effort. Blood from the umbilical vessels has the following values Table 9.1 Umbilical vein (UV) pH PaCO 2 kPa PaO 2 kPa Base excess mmol /l 7.24 - 7.49 3.0 - 6.5 2.0 - 6.4 - 9.0 to - 3 .5 (23 -49 mmHg) (15 - 48 mmHg) Umbilical artery (UA) 7.15 - 7.43 4.0 - 10 0.5 - 4.5 (31 - 74 mmHg) (4 - 34 mmHg)

-11.2 to - 6.2

Some degree of acidosis is common at birth. Cerebral palsy is unlikely to be related to intrapartum hypoxia unless cord pH at birth is < 7.00. Most infants with a pH as low as this develop normally. Umbilical arterial samples are a better reflection of fetal status than venous. Normal acid base status is achieved after 1 - 2 hours. CHECKLIST BEFORE DELIVERY Switch on radiant warmer. Check oxygen supply, connections and self inflating bag. Maximum pressure control blow-off is set at 25 cm water. Suction apparatus, oral mucus extractor and fine suction catheters, laryngoscopes, endotracheal tubes Dry and warm towels Drugs naloxone 400 g/ml epinephrine 100 g/ml or 1/10,000 concentration dextrose 5-10% solutions sodium bicarbonate 0.5 mmol/ml or 4.2% concentration NORMAL DELIVERY


Chapter 9

The mouth and oropharynx are always aspirated first as stimulation of the nose may cause the neonate to gasp and inhale any pharyngeal contents. The suction catheter must not be passed too far into the mouth as stimulation of the hypopharynx can cause laryngospasm and bradycardia. As neonates have poor thermoregulation they should be dried and wrapped in warm towels. Most newborn babies do not need any resuscitation and after they have been dried they can be returned to their mothers. ASSESSMENT OF THE NEONATE Apgar score The Apgar scoring system at 1 minute and 5 minutes is in common use and gives information about the severity and prognosis of asphyxia. In pre-term infants the score is more likely to be affected by gestational age than by asphyxia. Table 9.2 Apgar scoring system Clinical Sign 0 A: Appearance (colour) P: Pulse G: Grimace (reflex irritability) A: Activity (muscle tone) R: Respiratory effort Score 10 = optimal condition Score 6 or less = depression, resuscitative measures required Heart rate This is a reliable indicator of the newborns degree of distress. It can be evaluated by palpation of the pulse at the base of the umbilical cord or auscultation of apical heart sounds. If the heart rate is greater than 100 beats/min and spontaneous respirations are present assessment continues. If the heart beat is less than 100 beats/min positive pressure ventilation with 100% oxygen should be started immediately. If the heart rate is less than 60 beats/ min and not increasing despite effective ventilation with 100% oxygen, chest compression should be initiated. Colour The infant may be cyanotic despite adequate ventilation and a heart rate greater than 100 beats/min. It has been suggested that an Apgar minus colour score (A-C) is of better prognostic value as colour does not correlate well with the acid base state of the infant at birth. INDICATIONS FOR POSITIVE PRESSURE VENTILATION Apnoea Heart rate less than 100 beats/min Persistent central cyanosis despite the administration of 100% oxygen Effective ventilation can usually be provided with a bag and mask; the infant should be positioned with neck slightly extended (rolled towel 2.5 cm thick placed under the shoulders). Initial inflation pressures may need to be as high as 50 cmH2 0, the first five or six breaths require that inspiration is held for 1-2 seconds to establish an adequate functional residual capacity for continued spontaneous ventilation. If adequate ventilation as indicated by effective chest movement is not achieved then immediate intubation of the trachea and ventilation are performed. The time taken from birth to the babys first gasp and to the onset of regular respiration should be recorded. Assisted ventilation should be at a rate of 40 - 60 breaths/min, and chest compression at a rate of 120/min (i.e. a ratio of 3:1). There is evidence that air is as effective as 100% oxygen in term babies. !00% oxygen has little advantage and may increase oxygen free radical damage. If gas mixing facilities are available 40% oxygen is recommended. Blue, pale Absent No response Limp Absent Apgar Score 1 Body pink, extremities blue Less than 100 Grimaces Some flexion of extremities Weak cry or shallow 2 Completely pink More than 100 Cries Active, well flexed Good strong cry


Chapter 9

Factors affecting resuscitation Maternal sedation Meconium stained amniotic fluid Fetal heart rate abnormalities during labour Operative delivery Prolapsed cord Abnormal presentation Prolonged labour Infection Maternal health problems e.g. pre-eclampsia, diabetes mellitus, antepartum haemorrhage Naloxone is used if apnoea is due to maternal opioid sedation. The recommended dose is 100 g kg-1 i.m. The indications and management of the apnoeic baby are illustrated in figs 9.1& 9.2.

Fig 9.1 Resuscitation chart 1 Note: if there is particulate meconium and the baby is unresponsive, proceed at once to fig 9.2 MECONIUM ASPIRATION SYNDROME If the liquor is meconium stained during delivery then the pharynx must be aspirated before the first breath, the trachea intubated and any remaining meconium aspirated by direct suction. The indications and management of meconium aspiration can be seen in fig 9.2 CIRCULATION Lack of improvement in the heart rate is usually due to inadequate ventilation. Check face mask seal or tracheal tube position. If the newborn fails to respond to ventilation then chest compression must commence at a rate of 120/min, ventilation occurring every third compression. Epinephrine 10-30 g kg-1 i.v. (0.1-0.3 ml kg-1 of 1:10,000 solution) via the umbilical venous catheter flushed with saline 2ml and repeated as necessary with a third dose of 100 g kg-1 . If there is no response or evidence of severe acidosis sodium bicarbonate 1-2 mmol kg-1 i.v. is given slowly over 2-3 minutes


Chapter 9

Hypovolaemia requires active volume replacement which is indicated when:-

1. Evidence of acute fetal loss 2. Pallor persisting after oxygenation 3. Faint pulses with a good heart rate but poor response to resuscitation including adequate ventilationFluid replacement 10-20 ml kg-1 is given with 4.5% albumin, whole blood or plasma.

(a) Consider while preparing for (b) (c) depending on local policy. * may vary with individual circumstances and local guidelines Fig 9.2 Resuscitation chart 2

Figs 9.1 and 9.2 from Guidelines for resuscitation of babies at birth; Royal College of Paediatrics and Child Health and Royal College of Obstetricians and Gynaecologists 1997. BMJ Publishing Group, London.

FURTHER READING Zideman DA. Resuscitation. British Journal of Anaesthesia; 83: 157-168.1999 Click here for Medline link


Chapter 9

Resuscitation Council (UK). Newborn Life Support; Resuscitation Guidelines 2000. Paediatric Life Support: (including the recommendations for resuscitation of babies at birth). European Resuscitation Council. Resuscitation; 37(2): 95 - 96. 1998 Click here for Medline linkThe 1998 European Resuscitation Council Guidelines. Resuscitation of babies at birth. APPENDICES


APPENDICES

APPENDICES Normal female clinical chemistry and haematology values Composition of colloid solutions and blood products Epidural infusion regimens for labour Catecholamine infusions Fetal heart rate (FHR) monitoring Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1991-1993 & 1994-1996 Guidelines for the management of severe pre-eclampsia from the Report on Confidential Enquiries into Maternal Deaths in UK 1997-1999 Breast feeding and anaesthetic related drugs Side effects of drugs associated with obstetric anaesthesia Dermatome chart and segmental nerve supply to the perineum Magnesium sulphate in the management of eclampsia Neurological damage following epidural/spinal blockade after delivery Steroid treatment regimens Links to other obstetric anaesthetic sites

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Chapter 8

8. MATERNAL RESUSCITATION Chapter contents Cardio-pulmonary resuscitation CPR Algorithm Resuscitation drug dosages Convulsions Anaphylactic shock Pulmonary embolismVenous thromboembolus: Amniotic fluid embolus: Venous Air Embolus

Pulmonary oedema Malignant hyperpyrexia CARDIO-PULMONARY RESUSCITATION (CPR) Cardiac arrest is rare with an incidence of 1:30,000 pregnancies. The survival of mother and fetus depends on prompt recognition and treatment. Main causes of cardiac arrest

Anaesthetic ProblemsFailed intubation Aspiration of gastric contents Total spinal anaesthesia Drug induced reactions Local anaesthetic toxicity

Obstetric ProblemsMassive haemorrhage Amniotic fluid embolism Venous and/or air embolism Intracranial haemorrhage Magnesium toxicity After 26 weeks of pregnancy aortocaval compression is likely. If cardiac arrest occurs the complete absence of any vascular tone leads to a reduction in venous return to the right side of the heart. External cardiac compression may therefore be ineffective, as the heart is empty. The patient must be tilted to at least a 30 angle. This is best achieved using a specially wedged board, although it is possible to use a "human wedge".

Fig 8.1

Wedged board

Human wedge

If CPR is not effective (15:2 ratio) in generating a powerful pulse (100/min) or adequate perfusion within 3 - 4 minutes and there is

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Chapter 8

no other obvious remediable cause, e.g. massive haemorrhage, bilateral tension pneumothorax or pulmonary embolus, the fetus must be delivered while CPR is continuing; effective cardiac filling and output should then occur. Early delivery may also save the baby (the fetus is more resistant to hypoxia than the mother).

THE CHAIN OF SURVIVAL Early Access Early Basic Life Support

Early Defibrillation

Early Advanced Life Support

For every minute that elapses following the onset of a shockable arrhythmia, there is 5-10% less chance of survival. Early defibrillation is critical; therefore it should not be delayed if available and appropriate. Administration of 200, 200 and 360 joule shocks, given in sequence if required with a monophasic defibrillator, should not take any longer than 30 seconds. As soon as the shocks have been delivered, B.L.S must be restarted immediately. Available data suggests that defibrillation is safe in all phases of pregnancy and labour as only a small amount of current penetrates the uterus. Biphasic defibrillators are effective at lower energy levels e.g. 200 J. They reverse current flow during defibrillation and are as effective or better than monophasic defibrillators. ADVANCED LIFE SUPPORT ALGORITHM FOR THE MANAGEMENT OF CARDIAC ARREST IN ADULTS

Note: each successive step is based on the assumption that the one before has been unsuccessful

Resuscitation Council UK. Table 8.1 Resuscitation drug doses


Chapter 8

TRACHEAL DRUGS made up in a all doses based on INTRAVENOUS volume of 10 a 70 kg woman ml saline Epinephrine 1:10,000 0.1-1 mg 2 mg 10 ml = 1 mg Atropine 1 mg 2 mg 0.6 mg/ml 3 mg Amiodarone in 20 ml 5% dextrose 300 mg second dose 150 mg

COMMENT a and receptor stimulant Infusion 5 mg:500 ml saline (10 g/ml) Increases heart rate Completely blocks the vagus nerve, used in asystole Used in refractory fibrillation. Consider as early as fourth shock Used in refractory fibrillation Membrane stabilisation, reduces tendency to tachyarrythmias Inotropic action

Bretylium tosylate 500 mg 50 mg/ml Mexiletine 150 mg bolus 25 mg/ml Calcium gluconate 10% 10 ml (0.225 mmol Ca/ml) Lidocaine 2% Adenosine 100 mg 6 mg 200 mg

Infusion 1.5 g:500 ml 3 mg/ml then 12 mg x 3 every 2 min Not as routine, only refractory cases, pH to be measured as soon as possible -blocker used for supraventricular arrythmias (SVT)

Sodium bicarbonate 50 ml 8.4% Metoprolol 5 mg (1 mg/ml)

Any effects of these drugs on the fetus can be addressed after delivery, resuscitation of the mother is the prime consideration. Algorithms for treatment of Periarrest Arrhythmias can be accessed here

BRADYCARDIA BROAD COMPLEX TACHYCARDIA NARROW COMPLEX TACHYCARDIA CONVULSIONS Main causes Eclampsia, epilepsy and local anaesthetic toxicity. Consider all obstetric convulsions eclamptic in origin despite a normal blood pressure until proved otherwise. Premonitory signs Eclampsia - May be NONE: severe frontal headache with visual disturbance, photophobia, nausea and vomiting, right upper quadrant pain. Epilepsy - Aura, history of epilepsy, anticonvulsant therapy. Local anaesthesia - Numbness of the tongue and circumoral tissues, light-headedness, dizziness, difficulty focusing, tinnitus, slurred speech, shivering and muscle twitching.


Chapter 8

Management Turn the patient on her side to avoid aortocaval compression. Maintain and protect the airway, administer 100% oxygen. Ensure fetal monitoring. Follow one of the two regimes:Diazepam 5 - 20 mg i.v. (more than 30 mg may cause neonatal hypotonia) Intravenous thiopentone 50 mg increments - suxamethonium, cricoid pressure and intubation may be required. If eclampsia is suspected once convulsions have ceased then the magnesium sulphate protocol is followed. ANAPHYLACTIC SHOCK Common labour ward causes:- antibiotics, suxamethonium, latex, oxytocin, NSAIDs and colloids. An anaphylactic reaction is where previous sensitisation has occurred and vasoactive substances e.g. histamine, serotonin are released from mast cells in response to an IgE antibody mediated reaction. An anaphylactoid reaction is where there is no antibody mediation in mast cell release. Management Stop the administration of all suspected drugs and curtail surgery if appropriate. Maintain the airway, give 100% oxygen, and avoid aortocaval compression. Give epinephrine 1:10,000 (1 mg:10 ml saline) i.v. as 0.5 - 1 ml boluses, titrate as necessary for hypotension and bronchospasm. Start rapid intravascular volume expansion with crystalloid or colloid. Specific measures Hypotension - Elevate the legs, establish monitoring with ECG and possibly CVP and arterial line. Circulatory support with catecholamines. Bronchospasm aminophylline salbutamol 250 - 500 mg i.v. slowly 250 g i.v. slowly 2.5 - 5 mg nebulised in 3 ml saline Antihistamines chlorpheniramine Steroids hydrocortisone 100 - 200 mg i.v. 10 - 20 mg i.v.

Anaphylaxis algorithm can be accessed here:-

Investigation Immediate - mast cell tryptase, the principle protein content of mast cell granules is released with histamine and other amines in anaphylactic and anaphylactoid reactions. Plasma concentration is raised 1 - 6 h after a reaction. Normal level 0.8 - 1.5 ng/ml Anaphylactic reactions occur at concentrations >20ng/ml


Chapter 8

Long term - referral to allergist for skin testing and specific IgE antibody detection by radio-allergosorbent test (RAST)

PULMONARY EMBOLISM This is the commonest cause of maternal death in the United Kingdom. Emboli may be thrombus, amniotic fluid or air. The physiological changes that occur depend on the degree of obstruction to blood flow through the pulmonary artery and the increase in dead space ventilation. These may lead to pulmonary hypertension, right ventricular strain and cardiac failure. During anaesthesia an early sign is an abrupt fall in end tidal PCO 2 Venous thromboembolus The risk of venous thrombosis is increased in pregnancy due to the relatively hypercoagulable state, particularly in the postpartum period. The presentation includes retrosternal discomfort, dyspnoea, pleuritic pain, haemoptysis, profound collapse, raised central venous pressure and cardiac arrest. The ECG shows:S1 Q 3 T3 pattern with prominent S wave in lead I, Q wave and inverted T in lead III Sinus tachycardia T wave inversion in leads V1 -V3 Right bundle branch block Low amplitude deflection A ventilation perfusion scan will show normal ventilation with a segmental perfusion defect. Pulmonary angiography may demonstrate an intraluminal filling defect and/or the abrupt termination of a branch vessel. Management of minor thromboembolism Heparinisation - 5,000 -10,000 i/u i.v. followed by a continuous infusion of 1,000-2,000 i/u per hour. Monitored with the APPT - therapeutic range 1.5-2.5. Antenatally heparin is given sc - 12,000 i/u 12 hourly. Postnatally oral warfarin is started at the same time as i.v. heparin - 10 mg/day for 2days. Subsequent dosage depends on the INR - therapeutic range 2-3. Management of massive thromboembolism Oxygen therapy, cardiac massage and intermittent positive pressure ventilation (IPPV) An intravenous bolus of heparin - 15,000 i/u should be given. Cardiovascular support with a norepinephrine infusion 4 mg in 500 ml of saline A pulmonary angiogram should be obtained immediately: if this is not available thrombolytic therapy must be started with streptokinase in a loading dose of 600,000 units with a maintenance dose of 100,000 u/h for 24 hours. The thrombin time should be maintained at a level of 1 times the control value. Amniotic fluid embolus (Anaphylactoid Syndrome of Pregnancy) The incidence is 1 in 30,000 pregnancies with a maternal mortality rate approaching 85%, It can occur during labour (70%), after Caesarean delivery (19%), or after vaginal delivery (11%). The presenting features are Sudden collapse Excessive bleeding in labour or post partum Seizures Dyspnoea Fetal bradycardia There is a history in 41% of mothers of atopy (asthma, eczema, hay fever) or allergy, often to drugs.


Chapter 8

There is a biphasic response to the presence of amniotic fluid (or meconium) in the maternal circulation causing release of substances that produce pulmonary vascular spasm, pulmonary hypertension, hypoxic injury to the pulmonary capillaries and heart. This leads to left ventricular failure and subsequent adult respiratory distress syndrome. Coagulopathy may be related to the presence of a factor X activator in amniotic fluid. Diagnosis is made on clinical grounds. The presence of fetal cells in the maternal blood is NOT pathognomonic and they are commonly detected in normal patients. In primates it has been shown that infusions of large amounts of amniotic fluid do NOT cause the syndrome. Minor degrees of the syndrome are probably quite common. Management Cardiopulmonary resuscitation with the patient wedged if the fetus is still in utero Deliver the fetus and placenta as soon as possible Insert 2 large peripheral cannulae, CVP line, urinary catheter, arterial line and if possible a pulmonary artery catheter Aspirate blood from the right side of the heart Monitor ECG, pulse, blood pressure, CVP and pulmonary artery wedge pressure Cardiovascular support with dopamine and epinephrine DIC management in consultation with the Haematology Department Venous air embolus This can occur during Caesarean section particularly at the time of uterine incision and placental separation. It has been shown that subclinical venous air embolism occurs in up to 50% of patients at this time; the risk is increased when the uterus is exteriorised and the patient is head down. A head up tilt has been advocated during surgery for Caesarean section. A patent foramen ovale is present in 20 - 25 % of patients and paradoxical air embolism is possible although very rare in clinical practice. Large air embolism will result in frothing of blood in the right ventricle causing an air lock and cardiac arrest. The diagnosis is made with a precordial or oesophageal Doppler probe. A mill wheel murmur is accompanied by hypotension, a fall in SpO 2 , end tidal PE CO 2 and an increase in central venous pressure. Management 100% oxygen must be given Stop the nitrous oxide to reduce the air bubble size Replace the uterus if exteriorised Flood the wound with fluid to prevent further aspiration of air. Place the patient in a head down position on the left side to allow any air to collect in the apex of the right ventricle Aspirate air from the right atrium via a central venous line. Provide cardio-respiratory support as necessary. Internal cardiac massage may be required - access to the great vessels will permit direct aspiration of air (or amniotic fluid) . PULMONARY OEDEMA Maternal pulmonary oedema is associated with: Pre-eclampsia - capillary permeability is increased and colloid osmotic pressure falls due to proteinuria. There may also be an element of left ventricular failure secondary to severe hypertension. Antihypertensive therapy with -blockers may contribute to this. Fluid overload - due to over-treatment of severe haemorrhage, or fluid challenges in pre-eclamptic patients. Myocardial disease - e.g. cardiomyopathy of pregnancy or myocardial ischaemia. The use of tocolytic therapy for premature labour with -adrenergic agonists, e.g., ritodrine, isoxuprine, salbutamol. Tachycardia is a prominent feature. Steroid therapy for fetal lung maturation may be a contributory factor It presents with tachycardia, tachypnoea, hypoxia and cyanosis. An early sign is a fall in oxygen saturation. On auscultation of the chest, basal crepitations and rhonchi are heard. Chest x-ray shows fluffy shadowing or the more extensive butterfly wing appearance. Management


Chapter 8

Oxygen Sedation with i.v. morphine to relieve agitation / anxiety and reduce the pre-load by venodilatation. Diuretic therapy with frusemide 40 - 80 mg i.v., repeated as necessary. Dopamine 2 - 5 g/kg / min may be required i.v.. Intubation and IPPV may be necessary with positive end expiratory pressure (PEEP) Treatment of the underlying cause

MALIGNANT HYPERPYREXIA (MH) The incidence is 1:30,000 of all general anaesthetic administered. Not every patient with a genetic predisposition developes a MH crisis during exposure to triggering agents which include all volatile anaesthetics and depolarising muscle relaxants. MH presents with the following

signs:

Unexplained tachycardia Tachypnoea A rise in body temperature which increases by more than 2 C/h An abnormal reaction to suxamethonium - trismus is an early sign of this Cyanosis Muscular rigidity developing later during the anaesthetic Increased oozing is usually a sign of DIC A fall in SpO 2 , a rise in PE CO 2 , metabolic acidosis and hyperkalaemia A diagnosis of MH should be assumed if suspicions are aroused. Management Discontinue inhalational agents, terminate surgery CALL FOR HELP. Hyperventilate with 100% oxygen 2 - 3 times the predicted minute volume Give dantrolene 2 mg/kg i.v.. Repeat as necessary up to a total of 10 mg/kg Cool with 1 - 2 litres iced saline i.v., apply surface cooling over the major vessels, and lavage to the pleural or peritoneal cavities. Consider cardiopulmonary bypass via femoro-femoral circulation Correct metabolic acidosis with sodium bicarbonate, monitor blood gases and pH and correct hyperkalaemia. Treat arrhythmias if severe. Establish the following monitoring: SpO 2 , ECG, arterial cannulation, a muscle temperature probe, central venous cannulation, urinary catheter, blood pressure and a fluid balance chart. Investigations should include the following: blood gases, haemoglobin, urea, electrolytes, clotting screens and CPK level Admit to the intensive care unit Late management must include screening of the patient and her family for MH susceptibility In the management of known MH or MH susceptible patients, the technique of choice is regional anaesthesia. The administration of general anaesthesia requires the following conditions:A clean anaesthetic machine with disposable tubing and no vaporisers The circuit which has been flushed with 10 litres of oxygen for at least 20 minutes before use A cooling blanket on the operating table, Dantrolene and ice must be available. Only 'safe' drugs must be used SAFE Diazepam, thiopentone, propofol, methohexitone. Nitrous oxide Atracurium, pancuronium, vecuronium, mivacurium,, rocuronium Succinylcholine Halothane, enflurane, isoflurane, desflurane, sevoflurane UNSAFE


Chapter 8

Local anaesthetic drugs Oxytocin, PGF2 a, ergometrine Nitroglycerine, magnesium sulphate Ephedrine, epinephrine, norepinephrine FURTHER READING The American Heart Association in Collaboration with the International Liaison Committee on Resuscitation (ILCOR) Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - An International Consensus on Science. Resuscitation 2000; 46: 1-448 The 1998 European Resuscitation Council Guidelines for Adult Advanced Life Support. In: Bossaert L (ed.). European Resuscitation Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 36-37. The 1998 European Resuscitation Council Guidelines for the management of the airway and ventilation during resuscitation. In: Bossaert L (ed.). European Resuscitation Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 129-158. Kudenchuk PJ, Cobb LA, Copass MK et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. New England Journal of Medicine 1999; 341: 871-878.Click here for Medline link The Association of Anaesthetists of Great Britain and Ireland and The British Association of Allergy and Immunology. Suspected anaphylactic reactions associated with anaesthesia. Published by: The Association of Anaesthetists of Great Britain and Ireland 1995. MedicAlert Foundation (Registered Charity) Fletcher SJ, Parr MJA. Amniotic fluid embolism: a case report and review. Resuscitation 2000: 43;141-146 Click here for Medline link Halsall P, Ellis FR. Malignant hyperthermia. Current Anaesthesia and Critical Care 1996; 7; 3: 158-166. NEXT CHAPTER


COMPOSITION OF COLLOID SOLUTIONS AND BLOOD PRODUCTS

COMPOSITION OF COLLOID SOLUTIONS AND BLOOD PRODUCTS COLLOID SOLUTIONS Colloid Fluid Gelofusin Haemaccel Composition succinylated gelatine polygelin (urea-linked) Molecular Weight 35,000 30,000 Plasma Half Life Allergic Reaction 4 hours 0.38% 2-4 hours 0.38% Remarks

Pentastarch

hydroxyethyl starch 250,000

12-16 hours

0.0014%

Dextran 70

glucose polymer

70,000

12 hours

0.008%

Plasma Protein Solution (PPS)

4.5% protein (85% 70,000 albumin in saline)

> 24 hours

0.003%

Contains 10 times more Ca and K than gelofusin. This may lead to clotting in heating coils when mixed with citrated blood or FFP Taken up by the reticuleondothial system, final elimination from body very slow. Long term effect of this is unknown Inhibits platelet aggregation and renders fibrin more susceptible to fibrinolytic enzymes. Take blood sample before use. Maximum volume I litre 1998 controversial meta-analysis suggested relatively increased mortality

COMPOSITION OF BLOOD PRODUCTS Blood Products Red cells in additive solution Pack Volume 300 ml Contents Red cells after removal of almost all plasma made up with saline, adenine, dextrose +/- mannitol All clotting factors except platelets Fibrinogen, fibrinectin, Von Willebrand factor, factors VIII & Xlll Platelets Remarks Must be ABO +Rh (D) compatible Haematocrit is 0.55-0.65 Flows like blood. ABO compatibility preferred Transfuse when fibrinogen < 1gm Must be ABO + Rh(D) compatible Transfuse when < 50,000

Fresh frozen plasma Cryoprecipitate Platelet concentrate

300 ml 10 - 20 ml 50 - 60 ml

FURTHER READING Cochrane Injuries Group Albumin Reviewers. Human albumin administration in critically ill patients: systematic review of randomised controlled trials. British Medical Journal 1998; 317: 235-40. Click here for Medline link

file:///C|/Users/Administrator/Downloads/shoa%20current%20MASTER/composition_of_colloid_solutions.htm[20/1/2011 6:58:29 p]

Chapter 3

3. EPIDURAL ANALGESIA IN LABOUR Chapter contents Indications Contraindications Drugs Suggested basic technique ProblemsBloody tap; Positive intravenous test dose; Toxic reaction to local anaesthetic; Failure to thread epidural catheter; Inadequate block; Obesity ;Hypotension; Loss of bladder sensation; Inadvertent dural puncture; Management of spinal headache; Subdural block; Total spinal block; Epidural catheter difficulties; Spinal/epidural haematoma; Epidural abscess

Maintenance of epidural analgesiaIntermittent bolus doses; Epidural infusion; Patient Controlled Epidural Analgesia (PCEA); Mobile epidura l

Audit of epidural analgesia INDICATIONS Maternal request Prolonged and painful labour (often in primiparous patients) Malpresentation Anticipated or actual instrument delivery Trial of labour Pre-eclampsia Diabetes Uncoordinated uterus managed by oxytocin infusion Multiple pregnancy Cardiac and respiratory disease Epidural analgesia should be administered with caution if any of the following apply: Previous Caesarean section - Sudden analgesic failure may be due to uterine rupture. A dense sensory blockade must be avoided in order to demonstrate this important sign. Central nervous system disorders - In multiple sclerosis there is no evidence that demyelination can be provoked by epidural analgesia. In cerebrovascular accident, porphyria and other rare conditions the pathophysiology should be discussed with a senior colleague and if necessary the relevant specialist before a decision is made. Spinal deformity - Technical difficulty may increase the risk of dural puncture and failure, the caudal route may be the preferred option. CONTRAINDICATIONS Full anticoagulant therapy Coagulopathy. Platelet count must be greater than 80 x 10 9 /l Hypovolaemic shock Local or systemic sepsis Refusal by patient Raised intracranial pressure Fixed cardiac output Lack of appropriately trained staff DRUGS The three most commonly used drugs are all amide local anaesthetics. They differ in important respects: rate of onset, duration, potency, degree of motor blockade, cardiac and neurotoxicity. In labour it is generally desirable to minimise motor blockade in order to increase maternal mobility and hopefully reduce the rate of instrumental delivery. This can be achieved by the correct choice of drug, concentration, volume and sometimes by the addition of an opioid e.g. fentanyl.


Chapter 3

Lidocaine is generally administered in a concentration of 2%, has a rapid onset (10-15 minutes) and a relatively short duration (45 min). Inadvertent intravenous injection carries the lowest incidence of toxic effects. Bupivacaine 0.1-0.5% has a slower onset (20 minutes for maximal effect) than lidocaine but a longer duration. It has four times the potency of lidocaine and is relatively more cardiotoxic. Used in the correct dosage it is generally without problem; with accidental i.v. injection there is a risk of delayed cardiac conduction leading to bradycardia, heart block and ultimately a potentially irreversible ventricular fibrillation. Cardiac toxicity is usually preceded by signs of major CNS toxicity i.e. convulsions. Ropivacaine 0.1-0.5% has a similar onset and duration to bupivacaine but it is less cardiotoxic and may produce relatively less motor blockade. SUGGESTED BASIC TECHNIQUE A description of technique cannot replace practical experience with a senior colleague. A safe method should be selected and adhered to until confident and competent. Establish the indications for epidural anaesthesia and review the patients relevant obstetric, medical and anaesthetic history. Explain the procedure and obtain the patients informed verbal consent. Set up a reliable intravenous infusion of saline or Ringer Lactate with, at least, a 17 gauge intravenous cannula. Check that an ampoule of ephedrine 30 mg is immediately available. Record the baseline blood pressure and pulse. Arrange the patient either in the left lateral or sitting position according to preference. Put on a face mask, scrub, glove and gown up. Apply a suitable topical antiseptic solution to the skin and underlying tissues Site the epidural in the L2/3 or nearest convenient interspace using a saline or air loss of resistance technique. Measure the epidural space-skin distance using the cm graduations on the Tuohy epidural needle Insert the catheter 5 - 6 cm into the epidural space, withdraw the needle and then withdraw the catheter to leave 3 - 4 cm in the space or until the meniscus in the catheter falls. Ensure that blood or cerebrospinal fluid (CSF) does not flow back either by capillary action or direct aspiration. Administer an epidural test dose e.g. 4 ml of 2% lidocaine. Inadvertent intravenous injection rapidly produces tinnitus and facial paraesthesia - maintain verbal contact; ask about any symptoms in a non specific way to avoid suggestion. After 5 min record pulse and blood pressure and check for evidence of intrathecal placement (established sensory and motor blockade) - if in doubt wait and reassess after a further 5 min. If the test dose is negative and blood pressure and fetal heart rate are stable administer a bolus dose of 5 - 8 ml of 0.25% bupivacaine. (see alternative maintenance regimes) Progress over the next three contractions should indicate the efficacy of the block. An increase in skin temperature over the feet and legs is a useful sign and demonstrates the onset of an autonomic block. Continue with top-ups or an epidural infusion according to preference. Monitoring the block The following information should be monitored and recorded: Maternal blood pressure and pulse - these should be recorded every five minutes for twenty minutes following a top up and at least half hourly thereafter Fetal heart rate Extent of block Sensory: it is important to record the upper and lower segmental sensory limits of the block bilaterally. These may be identified by testing with a cotton wool ball (light touch), blunt needle (pinprick) or ethyl chloride (cold sensation). Starting from an area of skin with an established block the patient will report light touch, pinprick and cold sensation in sequence as the unblocked area is approached. This progression usually spans three segmental levels. In practice it is sufficient to select and continue with a single method of testing. Motor: this can be assessed on the following practical scale which is based on straight leg raising 0 = full power 1 = able to lift but a little weak 2 = able to lift but very weak


Chapter 3

3 = unable to lift straight leg Site and severity of any persisting pain Mode of administration of local analgesia i.e. top ups, infusion or PCEA Details of maintenance doses prescribed and when actually administered

PROBLEMS Bloody tap - This is caused by puncture of a distended epidural vein by the needle or the catheter and may lead to inadvertent intravenous injection of local anaesthetic or to the formation of an epidural haematoma. In order to minimise this risk the epidural needle or catheter should not be advanced during a uterine contraction. Management is as for positive intravenous test dose Positive intravenous test dose - The test dose should always be given after gentle aspiration and if positive then the catheter should be withdrawn and resited in an adjacent interspace. Toxic reaction to local anaesthetic - rarely this may occur despite a negative test dose. Early central nervous system signs are slurred speech and tinnitus; with increasing toxicity there may be muscle twitching followed by convulsions. Circulatory signs include hypotension, bradycardia and possibly cardiac arrest. Failure to thread epidural catheter Inject additional saline or lidocaine (3 - 6 ml) down the needle in an attempt to open up the epidural space. Carefully rotate the Tuohy needle through 180 (risk of dural tear). Do not withdraw the catheter through the needle (risk of dividing catheter). Ask the patient to straighten her back by slowly extending her hips. If associated with marked paraesthesia or failure of the above methods, resite in an adjacent interspace. Inadequate block - This may be caused by the catheter entering the paravertebral space via an intervertebral foramen which results in a unilateral lumbar plexus block. Occasionally connective tissue appears to sub-divide the epidural space causing a unilateral block. Additionally there may be persistent low backache with rectal or sacral pain. Use posture and the effect of gravity to help the spread of additional local anaesthetic. The addition of fentanyl 50 mg or clonidine 100 - 150 mg may be of value. If all these fail the catheter should be resited at an early stage. Obesity Explain that the procedure may be difficult. Use the sitting position. Ask patient to point to the midline of her back. Identify and mark the midline by initially palpating the upper thoracic spines. Palpate the iliac crest and draw a line bisecting the midline. Infiltrate subcutaneously for 5 cm above and below this point using 1% lidocaine. Use a suitable needle to probe and mark the midline and a spine and interspace. If necessary use a long (15 cm) Tuohy needle to reach the epidural space. Hypotension - Initial symptoms are often due to the rate of fall rather than the absolute level of blood pressure. The complaint is of nausea, dizziness or sleepiness. Turn the patient onto her side (preferably left) to avoid aortocaval compression. Give 250 ml saline or Ringer Lactate rapidly and elevate the foot of the bed. In the absence of a rapid response ephedrine is administered intravenously in 6 mg increments until stability is restored. Loss of bladder sensation - blockade of sacral roots may result in a failure of the patient to sense bladder distension. The patient should be encouraged to empty her bladder two hourly or before top ups. If the bladder becomes distended it is necessary to pass a urinary catheter. Neglect may result in retention of urine and post partum bladder atony . Inadvertent dural puncture


Chapter 3

There are two alternative strategies 1. Resite the epidural in an adjacent space. Be cautious with the first dose of local anaesthetic as the tip of the catheter may be adjacent to the dural puncture site and allow some solution to enter the subarachnoid space. The anaesthetist must always give this dose. Provided a normal initial response is obtained the epidural may be conducted in the usual fashion but with an awareness of the potential for high blockade. If the patient is able to deliver spontaneously, then this should be allowed. A long period of strenuous pushing should be avoided as this may increase the rate of CSF loss. After delivery, an epidural infusion of Ringer lactate should be set up via the epidural catheter and filter, aiming to run in one and a half litres over twenty-four hours. The patient should remain in bed while the infusion is in progress, thereafter she should be allowed to mobilise normally. 2. The needle tip is left in the subarachnoid space and an end-hole catheter inserted two cm only. The catheter must be clearly marked as being in the subarachnoid space. All top ups should be given by the anaesthetist. Care should be taken to avoid excessive loss of CSF. With the patient in the lateral or supine wedged position, give 1 ml of 0.125% plain bupivacaine followed by 0.5ml increments of 0.125% or 0.25% bupivacaine until satisfactory analgesia is achieved. Consider adding an opioid e.g. 12.5 mg fentanyl. It is important to appreciate that plain bupivacaine is slightly hypobaric at body temperature and that sudden movements of the patient may cause displacement of the local anaesthetic in the CSF leading to a high block. For Caesarean section, manual removal and rotational forceps delivery, 0.5% hyperbaric bupivacaine should be used, administered in 0.5 to 1ml increments, until adequate anaesthesia is achieved. Management of spinal headache Development of a spinal headache is characterised by severe, disabling fronto-occipital pain with radiation to the neck and shoulders. There may be neck stiffness. In the upright position the brain becomes unsupported by CSF within the cranium. This results in traction on meninges, venous sinuses and cerebral vessels. A compensatory dilatation of blood vessels takes place with an increase in cerebral blood flow. The pain may be completely relieved by lying supine. It is very important to discuss the nature of the problem and the management options with the patient. Conservative treatment of spinal headache Bedrest Encourage the patient to take oral fluids. Paracetamol, dihydrocodeine or similar analgesia at regular intervals. Consider sumatriptan. It is a serotonin agonist and may relieve pain due to cerebral vas

Handbook of Obstetric Anaesthesia

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