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Anaesthesia for caesarean delivery in a parturient following a recent cerebrovascular event
International Journal of Obstetric Anesthesia (2009) 18, 55–59 0959-289X/$ - see front matter c 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2007.12.002
CASE REPORT
www.obstetanesthesia.com
Anaesthesia for caesarean delivery in a parturient following a recent cerebrovascular event R. K. Iqbal, R. Russell Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, UK ABSTRACT Ischaemic cerebrovascular events in pregnancy are uncommon. The anaesthetic management of a pregnant patient within six weeks of an ischaemic cerebrovascular event has not previously been reported. Issues raised include consent and minimising further neurological insult. Changes in regional blood flow, cerebral metabolic rate and integrity of the blood brain barrier must be considered although evidence to support regional in preference to general anaesthesia is lacking. We report the case of a woman with known systemic lupus erythematosis and antiphospholipid syndrome who developed idiopathic thrombocytopenic purpura in pregnancy and suffered a thrombotic cerebral vascular accident at 32 weeks of gestation. Ten days later she required urgent caesarean delivery, which was performed under general anaesthesia. There was no deterioration in neurological function following surgery and eight days postoperatively she was transferred to a neuro-rehabilitation centre for further care. The idiopathic thrombocytopenic purpura did not respond to medical therapy following delivery and a second anaesthetic was required for splenectomy four weeks later. c 2008 Elsevier Ltd. All rights reserved.
Keywords: Cerebrovascular event; Ischaemic stroke; Antiphospholipid syndrome; Idiopathic thrombocytopenic purpura; Caesarean delivery; General anaesthesia
Introduction Ischaemic stroke in pregnancy is a rare event. The risk of anaesthesia for non-neurosurgical or non-carotid surgery in patients who have suffered a recent cerebrovascular event is unknown. Indeed, there is little in the literature although in practice non-urgent surgery is usually postponed for six weeks.1 When surgery cannot be postponed, practice is based around the principles employed for anaesthetising patients with haemorrhagic stroke. We present the case of a woman who required urgent caesarean delivery following a recent ischaemic stroke and describe the issues that were raised.
Case report A 33-year-old woman (G3, P1) with known antiphospholipid syndrome (APS), hypothyroidism and systemic lupus erythematosis required urgent caesarean delivery for fetal malpresentation and ruptured memAccepted May 2008 Correspondence to: Robin Russell, Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, OX2 8HT, UK. E-mail address: [email protected]
branes at 33 weeks of gestation. At her first antenatal appointment at 8 weeks, her weight was 81 kg and height 166 cm (BMI 29 kg/m2). Her obstetric history included a first trimester miscarriage and a spontaneous vaginal delivery at 38 weeks of gestation. Due to her history of miscarriage and APS, she had been prescribed aspirin and dalteparin in the first trimester of this pregnancy as in her previous pregnancy. However, unlike her previous pregnancy, on this occasion she developed thrombocytopenia with a platelet count of 30 · 109/L at 9 weeks. Aspirin and dalteparin were stopped and following the exclusion of other causes of thrombocytopenia, including heparin-induced thrombocytopenia, a diagnosis of antenatal idiopathic thrombocytopenic purpura was made at 12 weeks and steroids were prescribed. Platelet counts failed to improve and treatment was supplemented with intravenous immunoglobulin and azathioprine from 15 weeks when her platelet count had fallen to 5 · 109/L. The platelet count increased to 97 · 109/L after 48 h and a platelet transfusion was not given. At 32 weeks, whilst mobilising on the ward following an immunoglobulin infusion, she fell to the floor. Examination revealed a global aphasia with a dense right hemiplegia and hypotonia but no impairment of consciousness. She had a regular heart rate of 108 beats/min
56 and a blood pressure of 110/55 mmHg. Examination of other systems was normal. No calf swelling, carotid bruits or abnormalities on her CT brain scan were detected. Her blood tests revealed haemoglobin 9.7 g/dL, white cell count 4.6 · 109/L, platelets 84 · 109/L, prothrombin time 13.2 s (normal range 10-14 s), activated partial thromboplastin time (APPT) 39.8 s (normal range 22-34 s) and fibrinogen 3.8 g/L. Bedside glucose test was 6 mmol/L, which was confirmed in the laboratory. Urea and electrolytes were normal. An electrocardiogram and echocardiogram were normal. A thrombotic cerebrovascular event was diagnosed and, following review by general physicians and neurologists, she was prescribed aspirin 75 mg. Twenty-four h later she was restarted on dalteparin 7500 units in the morning and 10000 units in the evening. At this time she was referred to the obstetric anaesthetists for review. As there was no evidence of fetal compromise, the obstetric plan was to monitor mother and baby but not to proceed with delivery. Ten days after the cerebrovascular event, the membranes ruptured with subsequent onset of labour. Ultrasound examination demonstrated that the baby was in a transverse lie and the decision was made to perform urgent caesarean delivery. Anaesthetic history revealed a previous spinal anaesthetic for manual removal of placenta but no previous general anaesthesia. She had been tolerating oral fluids but had taken nothing by mouth for more than six hours. The last doses of aspirin and dalteparin had been given 14 h earlier. On examination the cardiovascular and respiratory systems were normal. The blood pressure on the ward was 115/70 mmHg with a regular heart rate of 80 beats/min. Neurologically she had an expressive dysphasia but was able to understand and respond to direct questioning by squeezing with her left hand. On the right side she had a dense hemiplegia with motor strength assessed as 0/5. This was accompanied by hypotonia and upward plantar reflexes. She had a Mallampatti class 1 airway, good mouth opening and a thy-
Caesarean delivery following a cerebrovascular event romental distance greater than 6.5 cm. Blood tests taken 4 h previously revealed a platelet count of 147 · 109/L, a prolonged APPT of 62 s (normal range 22-34) and a normal prothrombin time 13 s (normal range 10-13.5). Thromboelastography demonstrated a hypocoagulable state (Fig. 1). In view of the abnormal coagulation profile and the patient’s relative immobility it was decided that the caesarean delivery should be performed under general anaesthesia. Using the system of communication described earlier the patient demonstrated that she preferred not to stay awake during her delivery. The general anaesthetic technique was discussed and, following i.v. ranitidine 50 mg and metoclopramide 10 mg, the patient was transferred to the obstetric operating theatres. On the advice of a senior haematologist protamine 50 mg was given before induction. Due to time constraints it was not possible to obtain a thromboelastograph following protamine administration. A right radial artery line was placed before induction, revealing a blood pressure of 150/70 mmHg. Sodium citrate 0.3M 30 mL was given orally. After pre-oxygenation, a rapid sequence technique with thiopental 500 mg, suxamethonium 150 mg and alfentanil 1 mg was employed and anaesthesia was maintained with isoflurane in oxygen and nitrous oxide. Post-induction blood pressure was 120/60 mmHg and intra-operatively ranged from 110120 mmHg systolic and 50-65 mmHg diastolic. Following delivery oxytocin 5 units diluted in saline 10 mL was administered by slow intravenous injection. Cefuroxime 1.5 g was also given and an oxytocin infusion of 40 units in 500 mL 0.9% saline was started. The slow bolus of oxytocin resulted in a transient decrease in blood pressure to 105/50 mmHg for 5 min. Vasopressors were not needed at induction or during surgery. Surgery lasted 30 min and was uncomplicated with an estimated blood loss of 500 mL. A healthy boy was delivered with Apgar scores of 9 and 10 at 1 and 5 min respectively. Umbilical cord blood gases were normal (arterial pH
Fig. 1 Thromboelastograph with therapeutic dalteparin. The prolonged R time implies a hypocoagulable state, probably due to anticoagulation.
R. K. Iqbal, R. Russell 7.32, base excess -1.9 mEq/L; venous pH 7.34, base excess -2.7 mEq/L). At the end of surgery the patient was extubated when awake. There was no further neurological deterioration and 6 h postoperatively she was breastfeeding on the ward. Postoperative pain was managed with i.v. morphine patient-controlled analgesia. Anti-embolic stockings were used, adequate hydration was ensured and dalteparin was restarted 24 h postoperatively. Within 24 h she started to mobilise with assistance and tolerated a soft diet. Eight days post partum she walked with assistance and was transferred to a neuro-rehabilitation centre. At this time she was able to understand but continued to have expressive dysphasia with inability to name familiar objects. Post partum her platelet count fell again and did not respond to medical therapy of steroids and immunoglobulin. A splenectomy was performed under general anaesthesia four weeks post partum. Since then platelet counts have returned to normal and a year later she is walking unaided. Motor power in the lower limb is 34/5 but remains 3/5 in the upper limb.
Discussion This case raises several issues. The first and perhaps most under-reported would be anaesthesia in the presence of a recent cerebrovascular event. The estimated incidence of ischaemic cerebrovascular complications during pregnancy has been quoted as 8.1 per 100 000 pregnancies.2 Prognosis is poor compared to the nonpregnant state. The presence of a recent cerebrovascular event poses specific challenges including consent, maintenance of cerebral blood flow and planning of postoperative care. Ischaemic stroke is usually due to the presence of a clot in a cerebral blood vessel. This results in an area of ischaemia in which irreversible neuronal death occurs. The area is surrounded by the ischaemic penumbra, which is potentially viable neuronal tissue where blood flow is maintained by collateral circulation, although due to a loss of autoregulation perfusion is pressure-dependant. Neuronal death may occur if there is further compromise to oxygen supply. A rise in systemic arterial pressure may be the response necessary to maintain blood flow in this area and therefore treatment of hypertension in the acute stage is controversial. The argument for treating hypertension is to decrease the risk of haemorrhage and minimise oedema.3 However, oedema may be exacerbated by ischaemia induced by lowering blood pressure. Optimal blood pressure following ischaemic stroke is uncertain. The blood pressure may fluctuate in the first 24 h and patients may demonstrate hypersensitivity to blood pressure treatment.4 Eighty percent of stroke patients have elevated blood pressure although two thirds
57 are normotensive at ten days. Current advice by the British Hypertension Society is for raised blood pressure to remain untreated for one to two weeks after an ischaemic stroke.5 Blood pressure may then be treated under close supervision, with restoration of pre-treatment values if there is neurological deterioration. There is no evidence to suggest what level of blood pressure will ensure adequate cerebral blood flow and avoid further neurological injury. In this case the woman at no point demonstrated an elevated blood pressure following her neurological event. Although there are reports in the literature of general anaesthesia for caesarean delivery in irreversible maternal brain injury,6 there are no reports of anaesthesia in the situation we have described in which surgery and anaesthesia could make the neurological injury worse. Anaesthesia within six weeks of a cerebrovascular event is associated with a 20-fold increase in mortality in the non-pregnant state. Animal and human studies have shown that cerebral autoregulation is impaired up to a month after cerebral ischaemia.3 Following upper motor neuron lesions there is a potential for exaggerated hyperkalaemia when using suxamethonium.7 Cardiovascular instability can ensue in susceptible patients. The underlying pathophysiology is an increase in the number and surface area of acetylcholine receptors, increased sensitivity of the receptor to agonists and changes in the receptor leading to a prolonged ‘open’ state with resultant prolonged potassium leak from muscle into plasma. Arguments for the use of suxamethonium in this case include its rapid offset, the absence of cardiovascular problems in our patient and awareness of the limitations of airway assessment tools. Alternatively the non-depolarising agent rocuronium could have been used to facilitate tracheal intubation. This would have minimised the risk of cardiovascular instability although had there been difficulty with intubation its prolonged duration of action might have caused problems. Antiphospholipid syndrome refers to the presence of autoantibodies to phospholipids. Clinically these patients are susceptible to venous and arterial thromboses with 50% of reported cases occurring during pregnancy. Transient ischaemic episodes secondary to thrombosis have been reported during pregnancy in these patients.8 Their coagulation status is complex. The tendency is towards hypercoagulability, although traditional laboratory assays for coagulation may be abnormal. Interpretation of APTT in individuals who suffer with APS is difficult as APTT is a phospholipid-dependant laboratory test and is usually prolonged. Interestingly APTT on the day of the cerebrovascular event was 39.8 s but 10 days later it had climbed to 62 s. Dalteparin had been started 48 h after the cerebrovascular event but one would not expect this to result in such a rise in APTT. However it is possible that the high doses used in
58 the presence of lupus anticoagulant produced further interference with the laboratory assay for APTT. Thromboelastography has been advocated to aid assessment of coagulation status in this group of patients.8 Central neuraxial blockade has been reported in the presence of significantly prolonged laboratory values for APTT without adverse consequences.8 Low-dose aspirin may contribute to complications with regional techniques but clinically in isolation has not led to greater complications.9 Thromboelastography is a non-specific global test of coagulation that can detect both hypo- and hypercoagulability. In the case described, the highly abnormal thromboelastograph in the presence of high-dose dalteparin and regular aspirin was considered to increase the risk associated with a regional technique. The thromboelastogram did not, however, give values for MA and G that reflect maximum strength of clot dependant on fibrinogen and platelet function and number. There are several possible explanations for this. The first, and most likely, is that the R time was so prolonged that it was not possible to give an accurate value for MA. Alternatively, and less likely, is that the MA could not be reached due to a hypercoagulable state in which maximum amplitude of clot was not achieved in the time that the sample was evaluated or to a technical error with conducting the assay. We used thromboelastography as an aid for clinical decision making with the awareness that this has not been validated in obstetric practice and has the obvious limitation in that it is an in vitro test for coagulation. Protamine was administered on haematological advice in order to minimise intraoperative bleeding and not in order to perform a neuraxial block. Protamine neutralisation of dalteparin is incomplete and the dose of protamine required is controversial; it has been argued that doses of less than 1 mg per 100 units of dalteparin are not effective.10 Therefore the dose used in our case may not have been adequate. The anaesthetic technique in these patients should be chosen on an individual basis and should maximise haemodynamic stability. Advantages of a regional technique would have included reduced blood loss, reduction in the risk of deep vein thrombosis and the ability to monitor neurological signs. In this particular case a regional technique was considered contraindicated because high-dose dalteparin had been administered 14 h earlier. The American Society of Regional Anesthesia recommends that neuraxial block should be avoided for 24 h in patients on therapeutic doses of low-molecular-weight heparin. Even had a regional technique been an option on haemostatic grounds, general anaesthesia might have been preferred to reduce the chance of hypotension, which could have resulted in greater ischaemic injury.3 Moreover, had neurological function deteriorated during surgery, it would be difficult, although not impossible, to differentiate between complications of a central neuraxial block
Caesarean delivery following a cerebrovascular event and hypotension as the cause. Other challenges would include difficulty in assessing sensory block given the dense right-sided hemiparesis with partial loss of sensation. This combination of treatment with aspirin and highdose dalteparin and a hypocoagulable thromboelastograph led to the decision to use general anaesthesia with anti embolic precautions and to strive to maintain haemodynamic stability. There is no consensus as to the optimal agents for haemodynamic stability when general anaesthesia is employed. Opioids are widely used to obtund the laryngeal response to intubation, with alfentanil being the agent of choice in our unit. There has been recent interest in the use of remifentanil due to its short duration of effect. A 1-lg/kg remifentanil bolus at induction attenuates haemodynamic changes at intubation, albeit with a risk of transient, but significant, neonatal depression.11 Finally, valid informed consent has three requirements. An individual must make an autonomous decision, demonstrate capacity and competency to make the decision and be given the right information.12 Capacity is the ability to understand the information being given, process the information into a decision, and communicate the decision. In this case, the anaesthetic options were discussed with the patient and she was able to communicate a preference. However, the degree to which the information was understood, retained and used to come to a decision was less clear. Anaesthetic management of obstetric patients following a recent ischaemic stroke poses unique challenges. Cases may be further complicated by the presence of conditions that make interpretation of coagulation status difficult. Although we report the successful management of a patient following a recent stroke with general anaesthesia, the choice of anaesthetic technique should be made on an individual case basis, with techniques directed at minimising further neurological injury. The principles are largely extrapolated from knowledge of neurophysiology and evidence from neurosurgical practice.
Acknowledgement We would like to thank Professor Christopher Redman of the Nuffield Department of Obstetrics and Gynaecology for his help in the preparation of the manuscript.
References 1. Blaisdell W F, Clauss R H, Galbraith J G, Imparato A M, Wylie E J. Joint study of extracranial arterial occlusion. IV. A review of surgical considerations. JAMA 1969; 209: 1889–95. 2. Grosset D G, Ebrahim S, Bone I, Warlow C. Stroke in pregnancy and puerperium: what magnitude of risk. J Neurol Neurosurg Psychiatry 1995; 58: 129–31.
R. K. Iqbal, R. Russell 3. Powers W J. Acute hypertension after stroke: The scientific basis for treatment decisions. Neurology 1993; 43: 461–7. 4. Connell J E, Gray C S. Treating hypertension after stroke. Br Med J 1994; 308: 1523–4. 5. British Hypertension Society. Fact file stroke 04/2006 www.bhsoc.org. 6. Feldman D M, Borgida A F, Rodis J F, Campbell W A. Irreversible maternal brain injury during pregnancy: a case report and review of the literature. Obstet Gynecol Surv 2000; 55: 708–14. 7. Martyn J A J, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states. Etiologic factors and molecular mechanisms. Anesthesiology 2006; 104: 158–69. 8. Ringrose D K. Anaesthesia and the antiphospholipid syndrome: a review of 20 obstetric patients. Int J Obstet Anesth 1997; 6: 107–11.
59 9. Collaborative Group. CLASP: a randomised trial of low dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy). Lancet 1994; 343: 619–29. 10. Woltz M, Weltermann A, Nieszpaur-Los M et al. Studies on the neutralizing effects of protamine on unfractionated and low molecular weight heparin (dalteparin) at the site of activation of the coagulation system in man. Thromb Haemost 1995; 73: 439–43. 11. Ngan Kee W D, Khaw K S, Ma K C, Wong A S Y, Lee B B, Ng F F. Maternal and neonatal effects of remifentanil at induction of general anesthesia for caesarean delivery. A randomised double blind controlled trial. Anesthesiology 2006; 104: 14–20. 12. Hope T, Savulesco J, Hendrick J. Medical Ethics and Law: The Core Curriculum. Edinburgh: Churchill Livingstone, 2003.
CASE REPORT
www.obstetanesthesia.com
Anaesthesia for caesarean delivery in a parturient following a recent cerebrovascular event R. K. Iqbal, R. Russell Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, UK ABSTRACT Ischaemic cerebrovascular events in pregnancy are uncommon. The anaesthetic management of a pregnant patient within six weeks of an ischaemic cerebrovascular event has not previously been reported. Issues raised include consent and minimising further neurological insult. Changes in regional blood flow, cerebral metabolic rate and integrity of the blood brain barrier must be considered although evidence to support regional in preference to general anaesthesia is lacking. We report the case of a woman with known systemic lupus erythematosis and antiphospholipid syndrome who developed idiopathic thrombocytopenic purpura in pregnancy and suffered a thrombotic cerebral vascular accident at 32 weeks of gestation. Ten days later she required urgent caesarean delivery, which was performed under general anaesthesia. There was no deterioration in neurological function following surgery and eight days postoperatively she was transferred to a neuro-rehabilitation centre for further care. The idiopathic thrombocytopenic purpura did not respond to medical therapy following delivery and a second anaesthetic was required for splenectomy four weeks later. c 2008 Elsevier Ltd. All rights reserved.
Keywords: Cerebrovascular event; Ischaemic stroke; Antiphospholipid syndrome; Idiopathic thrombocytopenic purpura; Caesarean delivery; General anaesthesia
Introduction Ischaemic stroke in pregnancy is a rare event. The risk of anaesthesia for non-neurosurgical or non-carotid surgery in patients who have suffered a recent cerebrovascular event is unknown. Indeed, there is little in the literature although in practice non-urgent surgery is usually postponed for six weeks.1 When surgery cannot be postponed, practice is based around the principles employed for anaesthetising patients with haemorrhagic stroke. We present the case of a woman who required urgent caesarean delivery following a recent ischaemic stroke and describe the issues that were raised.
Case report A 33-year-old woman (G3, P1) with known antiphospholipid syndrome (APS), hypothyroidism and systemic lupus erythematosis required urgent caesarean delivery for fetal malpresentation and ruptured memAccepted May 2008 Correspondence to: Robin Russell, Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, OX2 8HT, UK. E-mail address: [email protected]
branes at 33 weeks of gestation. At her first antenatal appointment at 8 weeks, her weight was 81 kg and height 166 cm (BMI 29 kg/m2). Her obstetric history included a first trimester miscarriage and a spontaneous vaginal delivery at 38 weeks of gestation. Due to her history of miscarriage and APS, she had been prescribed aspirin and dalteparin in the first trimester of this pregnancy as in her previous pregnancy. However, unlike her previous pregnancy, on this occasion she developed thrombocytopenia with a platelet count of 30 · 109/L at 9 weeks. Aspirin and dalteparin were stopped and following the exclusion of other causes of thrombocytopenia, including heparin-induced thrombocytopenia, a diagnosis of antenatal idiopathic thrombocytopenic purpura was made at 12 weeks and steroids were prescribed. Platelet counts failed to improve and treatment was supplemented with intravenous immunoglobulin and azathioprine from 15 weeks when her platelet count had fallen to 5 · 109/L. The platelet count increased to 97 · 109/L after 48 h and a platelet transfusion was not given. At 32 weeks, whilst mobilising on the ward following an immunoglobulin infusion, she fell to the floor. Examination revealed a global aphasia with a dense right hemiplegia and hypotonia but no impairment of consciousness. She had a regular heart rate of 108 beats/min
56 and a blood pressure of 110/55 mmHg. Examination of other systems was normal. No calf swelling, carotid bruits or abnormalities on her CT brain scan were detected. Her blood tests revealed haemoglobin 9.7 g/dL, white cell count 4.6 · 109/L, platelets 84 · 109/L, prothrombin time 13.2 s (normal range 10-14 s), activated partial thromboplastin time (APPT) 39.8 s (normal range 22-34 s) and fibrinogen 3.8 g/L. Bedside glucose test was 6 mmol/L, which was confirmed in the laboratory. Urea and electrolytes were normal. An electrocardiogram and echocardiogram were normal. A thrombotic cerebrovascular event was diagnosed and, following review by general physicians and neurologists, she was prescribed aspirin 75 mg. Twenty-four h later she was restarted on dalteparin 7500 units in the morning and 10000 units in the evening. At this time she was referred to the obstetric anaesthetists for review. As there was no evidence of fetal compromise, the obstetric plan was to monitor mother and baby but not to proceed with delivery. Ten days after the cerebrovascular event, the membranes ruptured with subsequent onset of labour. Ultrasound examination demonstrated that the baby was in a transverse lie and the decision was made to perform urgent caesarean delivery. Anaesthetic history revealed a previous spinal anaesthetic for manual removal of placenta but no previous general anaesthesia. She had been tolerating oral fluids but had taken nothing by mouth for more than six hours. The last doses of aspirin and dalteparin had been given 14 h earlier. On examination the cardiovascular and respiratory systems were normal. The blood pressure on the ward was 115/70 mmHg with a regular heart rate of 80 beats/min. Neurologically she had an expressive dysphasia but was able to understand and respond to direct questioning by squeezing with her left hand. On the right side she had a dense hemiplegia with motor strength assessed as 0/5. This was accompanied by hypotonia and upward plantar reflexes. She had a Mallampatti class 1 airway, good mouth opening and a thy-
Caesarean delivery following a cerebrovascular event romental distance greater than 6.5 cm. Blood tests taken 4 h previously revealed a platelet count of 147 · 109/L, a prolonged APPT of 62 s (normal range 22-34) and a normal prothrombin time 13 s (normal range 10-13.5). Thromboelastography demonstrated a hypocoagulable state (Fig. 1). In view of the abnormal coagulation profile and the patient’s relative immobility it was decided that the caesarean delivery should be performed under general anaesthesia. Using the system of communication described earlier the patient demonstrated that she preferred not to stay awake during her delivery. The general anaesthetic technique was discussed and, following i.v. ranitidine 50 mg and metoclopramide 10 mg, the patient was transferred to the obstetric operating theatres. On the advice of a senior haematologist protamine 50 mg was given before induction. Due to time constraints it was not possible to obtain a thromboelastograph following protamine administration. A right radial artery line was placed before induction, revealing a blood pressure of 150/70 mmHg. Sodium citrate 0.3M 30 mL was given orally. After pre-oxygenation, a rapid sequence technique with thiopental 500 mg, suxamethonium 150 mg and alfentanil 1 mg was employed and anaesthesia was maintained with isoflurane in oxygen and nitrous oxide. Post-induction blood pressure was 120/60 mmHg and intra-operatively ranged from 110120 mmHg systolic and 50-65 mmHg diastolic. Following delivery oxytocin 5 units diluted in saline 10 mL was administered by slow intravenous injection. Cefuroxime 1.5 g was also given and an oxytocin infusion of 40 units in 500 mL 0.9% saline was started. The slow bolus of oxytocin resulted in a transient decrease in blood pressure to 105/50 mmHg for 5 min. Vasopressors were not needed at induction or during surgery. Surgery lasted 30 min and was uncomplicated with an estimated blood loss of 500 mL. A healthy boy was delivered with Apgar scores of 9 and 10 at 1 and 5 min respectively. Umbilical cord blood gases were normal (arterial pH
Fig. 1 Thromboelastograph with therapeutic dalteparin. The prolonged R time implies a hypocoagulable state, probably due to anticoagulation.
R. K. Iqbal, R. Russell 7.32, base excess -1.9 mEq/L; venous pH 7.34, base excess -2.7 mEq/L). At the end of surgery the patient was extubated when awake. There was no further neurological deterioration and 6 h postoperatively she was breastfeeding on the ward. Postoperative pain was managed with i.v. morphine patient-controlled analgesia. Anti-embolic stockings were used, adequate hydration was ensured and dalteparin was restarted 24 h postoperatively. Within 24 h she started to mobilise with assistance and tolerated a soft diet. Eight days post partum she walked with assistance and was transferred to a neuro-rehabilitation centre. At this time she was able to understand but continued to have expressive dysphasia with inability to name familiar objects. Post partum her platelet count fell again and did not respond to medical therapy of steroids and immunoglobulin. A splenectomy was performed under general anaesthesia four weeks post partum. Since then platelet counts have returned to normal and a year later she is walking unaided. Motor power in the lower limb is 34/5 but remains 3/5 in the upper limb.
Discussion This case raises several issues. The first and perhaps most under-reported would be anaesthesia in the presence of a recent cerebrovascular event. The estimated incidence of ischaemic cerebrovascular complications during pregnancy has been quoted as 8.1 per 100 000 pregnancies.2 Prognosis is poor compared to the nonpregnant state. The presence of a recent cerebrovascular event poses specific challenges including consent, maintenance of cerebral blood flow and planning of postoperative care. Ischaemic stroke is usually due to the presence of a clot in a cerebral blood vessel. This results in an area of ischaemia in which irreversible neuronal death occurs. The area is surrounded by the ischaemic penumbra, which is potentially viable neuronal tissue where blood flow is maintained by collateral circulation, although due to a loss of autoregulation perfusion is pressure-dependant. Neuronal death may occur if there is further compromise to oxygen supply. A rise in systemic arterial pressure may be the response necessary to maintain blood flow in this area and therefore treatment of hypertension in the acute stage is controversial. The argument for treating hypertension is to decrease the risk of haemorrhage and minimise oedema.3 However, oedema may be exacerbated by ischaemia induced by lowering blood pressure. Optimal blood pressure following ischaemic stroke is uncertain. The blood pressure may fluctuate in the first 24 h and patients may demonstrate hypersensitivity to blood pressure treatment.4 Eighty percent of stroke patients have elevated blood pressure although two thirds
57 are normotensive at ten days. Current advice by the British Hypertension Society is for raised blood pressure to remain untreated for one to two weeks after an ischaemic stroke.5 Blood pressure may then be treated under close supervision, with restoration of pre-treatment values if there is neurological deterioration. There is no evidence to suggest what level of blood pressure will ensure adequate cerebral blood flow and avoid further neurological injury. In this case the woman at no point demonstrated an elevated blood pressure following her neurological event. Although there are reports in the literature of general anaesthesia for caesarean delivery in irreversible maternal brain injury,6 there are no reports of anaesthesia in the situation we have described in which surgery and anaesthesia could make the neurological injury worse. Anaesthesia within six weeks of a cerebrovascular event is associated with a 20-fold increase in mortality in the non-pregnant state. Animal and human studies have shown that cerebral autoregulation is impaired up to a month after cerebral ischaemia.3 Following upper motor neuron lesions there is a potential for exaggerated hyperkalaemia when using suxamethonium.7 Cardiovascular instability can ensue in susceptible patients. The underlying pathophysiology is an increase in the number and surface area of acetylcholine receptors, increased sensitivity of the receptor to agonists and changes in the receptor leading to a prolonged ‘open’ state with resultant prolonged potassium leak from muscle into plasma. Arguments for the use of suxamethonium in this case include its rapid offset, the absence of cardiovascular problems in our patient and awareness of the limitations of airway assessment tools. Alternatively the non-depolarising agent rocuronium could have been used to facilitate tracheal intubation. This would have minimised the risk of cardiovascular instability although had there been difficulty with intubation its prolonged duration of action might have caused problems. Antiphospholipid syndrome refers to the presence of autoantibodies to phospholipids. Clinically these patients are susceptible to venous and arterial thromboses with 50% of reported cases occurring during pregnancy. Transient ischaemic episodes secondary to thrombosis have been reported during pregnancy in these patients.8 Their coagulation status is complex. The tendency is towards hypercoagulability, although traditional laboratory assays for coagulation may be abnormal. Interpretation of APTT in individuals who suffer with APS is difficult as APTT is a phospholipid-dependant laboratory test and is usually prolonged. Interestingly APTT on the day of the cerebrovascular event was 39.8 s but 10 days later it had climbed to 62 s. Dalteparin had been started 48 h after the cerebrovascular event but one would not expect this to result in such a rise in APTT. However it is possible that the high doses used in
58 the presence of lupus anticoagulant produced further interference with the laboratory assay for APTT. Thromboelastography has been advocated to aid assessment of coagulation status in this group of patients.8 Central neuraxial blockade has been reported in the presence of significantly prolonged laboratory values for APTT without adverse consequences.8 Low-dose aspirin may contribute to complications with regional techniques but clinically in isolation has not led to greater complications.9 Thromboelastography is a non-specific global test of coagulation that can detect both hypo- and hypercoagulability. In the case described, the highly abnormal thromboelastograph in the presence of high-dose dalteparin and regular aspirin was considered to increase the risk associated with a regional technique. The thromboelastogram did not, however, give values for MA and G that reflect maximum strength of clot dependant on fibrinogen and platelet function and number. There are several possible explanations for this. The first, and most likely, is that the R time was so prolonged that it was not possible to give an accurate value for MA. Alternatively, and less likely, is that the MA could not be reached due to a hypercoagulable state in which maximum amplitude of clot was not achieved in the time that the sample was evaluated or to a technical error with conducting the assay. We used thromboelastography as an aid for clinical decision making with the awareness that this has not been validated in obstetric practice and has the obvious limitation in that it is an in vitro test for coagulation. Protamine was administered on haematological advice in order to minimise intraoperative bleeding and not in order to perform a neuraxial block. Protamine neutralisation of dalteparin is incomplete and the dose of protamine required is controversial; it has been argued that doses of less than 1 mg per 100 units of dalteparin are not effective.10 Therefore the dose used in our case may not have been adequate. The anaesthetic technique in these patients should be chosen on an individual basis and should maximise haemodynamic stability. Advantages of a regional technique would have included reduced blood loss, reduction in the risk of deep vein thrombosis and the ability to monitor neurological signs. In this particular case a regional technique was considered contraindicated because high-dose dalteparin had been administered 14 h earlier. The American Society of Regional Anesthesia recommends that neuraxial block should be avoided for 24 h in patients on therapeutic doses of low-molecular-weight heparin. Even had a regional technique been an option on haemostatic grounds, general anaesthesia might have been preferred to reduce the chance of hypotension, which could have resulted in greater ischaemic injury.3 Moreover, had neurological function deteriorated during surgery, it would be difficult, although not impossible, to differentiate between complications of a central neuraxial block
Caesarean delivery following a cerebrovascular event and hypotension as the cause. Other challenges would include difficulty in assessing sensory block given the dense right-sided hemiparesis with partial loss of sensation. This combination of treatment with aspirin and highdose dalteparin and a hypocoagulable thromboelastograph led to the decision to use general anaesthesia with anti embolic precautions and to strive to maintain haemodynamic stability. There is no consensus as to the optimal agents for haemodynamic stability when general anaesthesia is employed. Opioids are widely used to obtund the laryngeal response to intubation, with alfentanil being the agent of choice in our unit. There has been recent interest in the use of remifentanil due to its short duration of effect. A 1-lg/kg remifentanil bolus at induction attenuates haemodynamic changes at intubation, albeit with a risk of transient, but significant, neonatal depression.11 Finally, valid informed consent has three requirements. An individual must make an autonomous decision, demonstrate capacity and competency to make the decision and be given the right information.12 Capacity is the ability to understand the information being given, process the information into a decision, and communicate the decision. In this case, the anaesthetic options were discussed with the patient and she was able to communicate a preference. However, the degree to which the information was understood, retained and used to come to a decision was less clear. Anaesthetic management of obstetric patients following a recent ischaemic stroke poses unique challenges. Cases may be further complicated by the presence of conditions that make interpretation of coagulation status difficult. Although we report the successful management of a patient following a recent stroke with general anaesthesia, the choice of anaesthetic technique should be made on an individual case basis, with techniques directed at minimising further neurological injury. The principles are largely extrapolated from knowledge of neurophysiology and evidence from neurosurgical practice.
Acknowledgement We would like to thank Professor Christopher Redman of the Nuffield Department of Obstetrics and Gynaecology for his help in the preparation of the manuscript.
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