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Subarachnoid haemorrhage following spinal anaesthesia in an obstetric patient
British Journal of Anaesthesia 86 (3): 442±4 (2001)
Subarachnoid haemorrhage following spinal anaesthesia in an obstetric patient S. M. Eggert* and K. A. Eggers Department of Anaesthesia, Princess of Wales Hospital, Coity Road, Bridgend CF31 1RQ, UK *Corresponding author We describe an obstetric patient who presented for removal of a retained placenta. After insertion of the spinal anaesthetic, she developed a severe headache, and a subarachnoid haemorrhage was diagnosed. We discuss the differential diagnosis of the headache, the occurrence of intracranial haemorrhages after dural puncture and the future management of this patient. Br J Anaesth 2001; 86: 442±4 Keywords: anaesthetic techniques, subarachnoid; anaesthesia, obstetric; complications, haemorrhage Accepted for publication: September 25, 2000
Severe headache in combination with pregnancy and dural puncture has a broad spectrum of differential diagnoses, including postdural puncture headache, pre-eclampsia, migraine, drug-induced headache and intracranial pathologies. The latter include haemorrhages, venous sinus thrombosis and postpartum cerebral angiopathy. Although rare, subarachnoid haemorrhage (SAH) was the second commonest cause of indirect maternal death in the most recent triennial report (1994±1996) on maternal deaths from the UK's Department of Health.1 This diagnosis should be considered when assessing obstetric patients with atypical headaches after dural puncture.
Case report A 29-yr-old, multiparous woman (gravida 4 para 3) presented for removal of a retained placenta. Her previous obstetric history consisted of three spontaneous vaginal deliveries, including one with a retained placenta that was removed uneventfully under spinal anaesthesia 4 years ago. Except for a history of smoking (25 cigarettes per day) and mild asthma, there was no notable medical history, and the patient was normotensive throughout this pregnancy. As there were signs of fetal distress, she required an assisted instrumental delivery. A healthy, normal-sized baby (Apgar score 7 at 1 min and 9 at 5 min) was delivered after 5 h 20 min of labour (second stage 15 min). Medication given during labour included ranitidine 150 mg orally, patientcontrolled Entonox, and Syntometrine 1 mg i.m. on delivery of the baby. One hour after delivery she was moved to theatre for removal of a retained placenta. The anaesthetic registrar performed a spinal anaesthetic with the patient in the right
lateral position, at the level of the L3/4 interspace using a 24G Sprotte needle under standard aseptic conditions. At the ®rst attempt, clear cerebrospinal ¯uid (CSF) was obtained, and this was followed by slow injection of 2.5 ml heavy bupivacaine. At 5 min a sensory block to T6 was achieved and the operation proceeded. Systolic blood pressure ranged between 130 and 90 mm Hg and the intraoperative heart rate was stable at 65±85 beats min±1. Boluses of ephedrine were given as required in 3 mg increments to a total of 15 mg. Five minutes into the operation, the patient complained of a sudden onset of severe, pounding, occipital headache radiating to the frontal region. Neurological examination revealed photophobia, no meningism, no additional motor or sensory de®cits and a Glasgow coma score of 15. Systolic blood pressure recorded at the onset of the headache was 150 mm Hg, with a heart rate of 80 beats min±1. No ECG changes were noted. Further medication given intraoperatively included Augmentin 1.2 g i.v. and an infusion of Syntocinon (30 IU in 500 ml of normal saline over 2 h). The placenta was removed manually and the patient was transferred back to the labour room for observation. She still complained of severe headache and felt nauseated with one episode of vomiting. There was no postural element to the headache. Cyclizine 50 mg i.v. and codeine phosphate 60 mg orally were given. One hour later the headache was still incapacitating. Investigations at this time included a normal coagulation screen (prothrombin time 11.1 s, control 13.2 and activated partial thromboplastin time 31.6 s, control 32.7) and full blood count (haemoglobin 12.3 g dl±1, platelets 292 3~109 litre±1). The on-call medical team was consulted and a cranial computer tomogram performed, which showed a small amount of blood in the left sylvian
Ó The Board of Management and Trustees of the British Journal of Anaesthesia 2001
Subarachnoid haemorrhage after spinal anaesthesia
®ssure and the convexity sulci. The diagnosis of an SAH (grade 1 on the Hunt and Hess scale) was made and the patient was transferred to a neurosurgical unit on the same day. A four-vessel angiogram demonstrated tortuous vasculature on the left, but no apparent lesion. A repeat angiogram 6 weeks later was normal. The patient has made an uneventful recovery.
Discussion Spontaneous SAH is a rare event, ruptured intracranial aneurysms being the main cause (51±80%), followed by hypertensive disease (10±15%) and arteriovenous malformations (AVM) (5±10%). Rarer causes include meningeal infection, tumours and blood dyscrasias.2 3 In 5±10% of spontaneous SAHs, no causative lesion can be identi®ed.3 4 The incidence of spontaneous SAH is estimated to be increased ®ve-fold to 2 in 100 000 deliveries compared with the non-pregnant population, but no reliable data exist.5 Several studies con®rm a higher risk of aneurysmal rupture during pregnancy, whereas the behaviour of an AVM in the pregnant patient is more controversial,5±9 except for an increased risk of rebleeding of an AVM during pregnancy.6 7 The risk of an SAH increases with gestational age, probably because of hormonal and haemodynamic changes of pregnancy. Although one would assume that labour itself poses a particular risk, only 2% of SAHs occur during labour.5 Uterine contractions and the Valsalva manoeuvre performed during vaginal delivery cause a marked transient increase in blood pressure as well as in CSF pressure. This may balance the transluminal pressure across a fragile vessel wall.7 10 According to a recent review,5 there is consensus that an SAH in a pregnant patient should be treated according to the same neurosurgical principles valid for the non-pregnant patient. In our patient, severe headache occurred suddenly a few minutes after insertion of a spinal anaesthetic and about 2 h after vaginal delivery. The differential diagnosis included early onset of a postdural puncture headache, caused by CSF loss and subsequent low CSF pressure. In our case, there was neither suf®cient time for signi®cant CSF loss through a 24G hole in the dura, nor any signi®cant CSF loss during spinal needle insertion. The presentation of headache was atypical, with a sudden, severe onset and no postural element. Pre-eclampsia was considered, but there was no hypertension or proteinuria. Tension headache or migraine was unlikely because the onset of headache was too sudden and severe, with no history of similar headaches. The ephedrine given just before the onset of the headache may have caused a sudden change in blood pressure, resulting in headache. In our patient the headache lasted several hours, extending far beyond the normal period of drug action. After exclusion of the common causes of headache, intracranial pathology was considered and a computer tomogram performed, which revealed the SAH.
Very few reports describe intracranial haemorrhages after dural puncture and most of these are subdural haematomas.11±16 A potentially continuing CSF leak leads to low CSF pressure with pulling on the dura and bridging veins, causing postdural puncture headache. If this headache is left untreated, the shearing forces can lead to venous tears and acute or chronic subdural haematoma. Typically, the patient presents with prolonged postdural puncture headache, which becomes treatment-resistant, with loss of the postural element, and neurological symptoms and signs develop. At this point the intracranial haemorrhage is usually diagnosed. Postdural puncture headache should be taken seriously and treated early to minimize the rare but potentially fatal complication of an intracranial haemorrhage. On review of the literature, only three cases of intracerebral haemorrhage17±19 and only one case of an SAH alone20 have been reported after a dural puncture. In the latter, Boettiger and colleagues20 describe a 60-yr-old man who developed an SAH after two consecutive subarachnoid blocks within 2 weeks. They postulate that low CSF pressure exacerbated by the second dural puncture can develop even without postdural puncture headache. The decrease in intracranial pressure could cause an increase in transmural pressure across the arterial wall, thus facilitating the rupture of a potential vascular malformation. In our patient, there was insuf®cient time for a signi®cant CSF leak to develop and, therefore, the pathophysiology of an intracranial haemorrhage, postulated by other authors, may not apply here. Just before the onset of the headache, i.v. ephedrine was given because the systolic blood pressure had dropped to 90 mm Hg. Although the maximum recorded value afterwards was only 150 mm Hg, the pressure was measured non-invasively every 3 min and might have brie¯y been higher. Relatively sudden swings in blood pressure could have facilitated the rupture of a potentially weakened vessel wall before autoregulation became effective. Aneurysms are known to rupture under conditions associated with sudden rises in blood pressure.21 Considering the sequence of the events, there is the possibility that the SAH occurred during or just after labour, although the patient did not complain about headache at that time, and became symptomatic as a result of increased bleeding around the time the spinal block was performed. Potential cardiovascular changes, as discussed earlier, may have contributed to this. On the other hand, the combination of labour, spinal anaesthetic and SAH might have been purely incidental, considering that many spontaneous SAHs occur without obvious trigger event. In one series of 500 patients, 34% of SAHs developed during non-strenuous activities and 12% during sleep.22 Such a coincidence is, however extremely unlikely as the overall incidence of SAHs is so low. The computer tomogram in our patient showed a small SAH. The four-vessel angiogram was negative on the same day and 6 weeks later. According to Latchaw and
443
Eggert and Eggers
colleagues,3 in 10% of SAHs found on CT scan no lesion can be identi®ed on the angiogram. This usually implies a better prognosis, with a rebleeding rate of 4%.4 How should this patient be managed if she presents with another pregnancy? According to Dias and Sekhar,9 maternal and fetal outcomes are similar in parturients with either untreated aneurysms or AVMs, regardless of whether a Caesarian section or a vaginal delivery is performed. Manoeuvres such as shortening the second stage, epidural analgesia and, if necessary, low forceps delivery might decrease the risk of recurrent bleeding during vaginal delivery.9 If this patient requires anaesthetic intervention in the future, we will probably avoid spinal anaesthesia, although case numbers are too small to provide suf®cient evidence favouring a general anaesthetic. If an epidural catheter is considered, it should be inserted by an experienced operator to minimize the risk of a dural tap, which could be disastrous. She should be assessed antenatally by a consultant obstetric anaesthetist to formulate a management plan for labour.
References 1 Department of Health. Why Mothers Die: Report on Con®dential Enquiries into Maternal Deaths in the United Kingdom 1994±1996. London: The Stationary Of®ce, 1998 2 Young BJ, Seigerman MH, Hurst RW. Subarachnoid hemorrhage and aneurysms. Semin Ultrasound CT MR 1996; 17: 265±77 3 Latchaw RE, Silva P, Falcone SF. The role of CT following aneurysmal rupture. Neuroimaging Clin N Am 1997; 7: 693±708 4 Duong H, Melancon D, Tampieri D, Ethier R. The negative angiogram in subarachnoid haemorrhage. Neuroradiology 1996; 38: 15±9 5 Mas JL, Lamy C. Stroke in pregnancy and the puerperium [review]. J Neurol 1998; 245: 305±13 6 Wiebers DO. Subarachnoid hemorrhage in pregnancy. Semin Neurol 1988; 8: 226±9 7 Horton JC, Chambers WA, Lyons SL, Adams RD, Kjellberg RN. Pregnancy and the risk of hemorrhage from cerebral arteriovenous malformations. Neurosurgery 1990; 27: 867±71
444
8 Robinson JL, Hall CS, Sedzimir CB. Arteriovenous malformations, aneurysms, and pregnancy. Neurosurgery 1974; 41: 63±70 9 Dias MS, Sekhar LN. Intracranial hemorrhage from aneurysms and arteriovenous malformations during pregnancy and the puerperium [review]. Neurosurgery 1990; 27: 855±65 10 Hunt HB, Schifrin BS, Suzuki K. Ruptured berry aneurysms and pregnancy. Obstet Gynecol 1974; 43: 827±37 11 Jack TM. Post-partum intracranial subdural haematoma. A possible complication of epidural analgesia. Anaesthesia 1979; 34: 176±80 12 Pavlin DJ, McDonald JS, Child B, Rusch V. Acute subdural hematomaÐan unusual sequelae to lumbar puncture. Anesthesiology 1979; 51: 338±40 13 Newrick P, Read D. Subdural haematoma as a complication of spinal anaesthetic. Br Med J 1982; 285: 341±2 14 Edelman JD, Wingard DW. Subdural hematomas after lumbar dural puncture. Anesthesiology 1980; 52: 166±67 15 Skoldefors EK, Olofsson CI. Intracranial subdural haematoma complicates accidental dural trap during labour. Eur J Obstet Gynecol Reprod Biol 1998; 81: 119±21 16 Vaughan DJA, Stirrup CA, Robinson PN. Cranial subdural haematoma associated with dural puncture in labour. Br J Anaesth 2000; 84: 518±20 17 Benzon HT. Intracerebral hemorrhage after dural puncture and epidural blood patch: nonpostural and noncontinuous headache. Anesthesiology 1984; 60: 258±9 18 Mantia AM. Clinical report of the occurrence of an intracerebral hemorrhage following post-lumbar puncture headache. Anesthesiology 1981; 55: 684±5 19 Wedel DJ, Mulroy MF. Hemiparesis following dural puncture. Anesthesiology 1983; 59: 475±7 20 BoÈttiger BW, Diezel G. Akute intrakranielle Subarachnoidalblutung nach wiederholter SpinalanaÈsthesie. Anaesthesist 1992; 41: 152±7 21 Pulsinelli WA. Cerebrovascular diseases, aneurysmal subarachnoid hemorrhage. In: Bennett JC, Plum F, editors. Cecil's Textbook of Medicine. Philadelphia: W. B. Saunders, 1996; 2073±6 22 Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000; 342: 29±36
Subarachnoid haemorrhage following spinal anaesthesia in an obstetric patient S. M. Eggert* and K. A. Eggers Department of Anaesthesia, Princess of Wales Hospital, Coity Road, Bridgend CF31 1RQ, UK *Corresponding author We describe an obstetric patient who presented for removal of a retained placenta. After insertion of the spinal anaesthetic, she developed a severe headache, and a subarachnoid haemorrhage was diagnosed. We discuss the differential diagnosis of the headache, the occurrence of intracranial haemorrhages after dural puncture and the future management of this patient. Br J Anaesth 2001; 86: 442±4 Keywords: anaesthetic techniques, subarachnoid; anaesthesia, obstetric; complications, haemorrhage Accepted for publication: September 25, 2000
Severe headache in combination with pregnancy and dural puncture has a broad spectrum of differential diagnoses, including postdural puncture headache, pre-eclampsia, migraine, drug-induced headache and intracranial pathologies. The latter include haemorrhages, venous sinus thrombosis and postpartum cerebral angiopathy. Although rare, subarachnoid haemorrhage (SAH) was the second commonest cause of indirect maternal death in the most recent triennial report (1994±1996) on maternal deaths from the UK's Department of Health.1 This diagnosis should be considered when assessing obstetric patients with atypical headaches after dural puncture.
Case report A 29-yr-old, multiparous woman (gravida 4 para 3) presented for removal of a retained placenta. Her previous obstetric history consisted of three spontaneous vaginal deliveries, including one with a retained placenta that was removed uneventfully under spinal anaesthesia 4 years ago. Except for a history of smoking (25 cigarettes per day) and mild asthma, there was no notable medical history, and the patient was normotensive throughout this pregnancy. As there were signs of fetal distress, she required an assisted instrumental delivery. A healthy, normal-sized baby (Apgar score 7 at 1 min and 9 at 5 min) was delivered after 5 h 20 min of labour (second stage 15 min). Medication given during labour included ranitidine 150 mg orally, patientcontrolled Entonox, and Syntometrine 1 mg i.m. on delivery of the baby. One hour after delivery she was moved to theatre for removal of a retained placenta. The anaesthetic registrar performed a spinal anaesthetic with the patient in the right
lateral position, at the level of the L3/4 interspace using a 24G Sprotte needle under standard aseptic conditions. At the ®rst attempt, clear cerebrospinal ¯uid (CSF) was obtained, and this was followed by slow injection of 2.5 ml heavy bupivacaine. At 5 min a sensory block to T6 was achieved and the operation proceeded. Systolic blood pressure ranged between 130 and 90 mm Hg and the intraoperative heart rate was stable at 65±85 beats min±1. Boluses of ephedrine were given as required in 3 mg increments to a total of 15 mg. Five minutes into the operation, the patient complained of a sudden onset of severe, pounding, occipital headache radiating to the frontal region. Neurological examination revealed photophobia, no meningism, no additional motor or sensory de®cits and a Glasgow coma score of 15. Systolic blood pressure recorded at the onset of the headache was 150 mm Hg, with a heart rate of 80 beats min±1. No ECG changes were noted. Further medication given intraoperatively included Augmentin 1.2 g i.v. and an infusion of Syntocinon (30 IU in 500 ml of normal saline over 2 h). The placenta was removed manually and the patient was transferred back to the labour room for observation. She still complained of severe headache and felt nauseated with one episode of vomiting. There was no postural element to the headache. Cyclizine 50 mg i.v. and codeine phosphate 60 mg orally were given. One hour later the headache was still incapacitating. Investigations at this time included a normal coagulation screen (prothrombin time 11.1 s, control 13.2 and activated partial thromboplastin time 31.6 s, control 32.7) and full blood count (haemoglobin 12.3 g dl±1, platelets 292 3~109 litre±1). The on-call medical team was consulted and a cranial computer tomogram performed, which showed a small amount of blood in the left sylvian
Ó The Board of Management and Trustees of the British Journal of Anaesthesia 2001
Subarachnoid haemorrhage after spinal anaesthesia
®ssure and the convexity sulci. The diagnosis of an SAH (grade 1 on the Hunt and Hess scale) was made and the patient was transferred to a neurosurgical unit on the same day. A four-vessel angiogram demonstrated tortuous vasculature on the left, but no apparent lesion. A repeat angiogram 6 weeks later was normal. The patient has made an uneventful recovery.
Discussion Spontaneous SAH is a rare event, ruptured intracranial aneurysms being the main cause (51±80%), followed by hypertensive disease (10±15%) and arteriovenous malformations (AVM) (5±10%). Rarer causes include meningeal infection, tumours and blood dyscrasias.2 3 In 5±10% of spontaneous SAHs, no causative lesion can be identi®ed.3 4 The incidence of spontaneous SAH is estimated to be increased ®ve-fold to 2 in 100 000 deliveries compared with the non-pregnant population, but no reliable data exist.5 Several studies con®rm a higher risk of aneurysmal rupture during pregnancy, whereas the behaviour of an AVM in the pregnant patient is more controversial,5±9 except for an increased risk of rebleeding of an AVM during pregnancy.6 7 The risk of an SAH increases with gestational age, probably because of hormonal and haemodynamic changes of pregnancy. Although one would assume that labour itself poses a particular risk, only 2% of SAHs occur during labour.5 Uterine contractions and the Valsalva manoeuvre performed during vaginal delivery cause a marked transient increase in blood pressure as well as in CSF pressure. This may balance the transluminal pressure across a fragile vessel wall.7 10 According to a recent review,5 there is consensus that an SAH in a pregnant patient should be treated according to the same neurosurgical principles valid for the non-pregnant patient. In our patient, severe headache occurred suddenly a few minutes after insertion of a spinal anaesthetic and about 2 h after vaginal delivery. The differential diagnosis included early onset of a postdural puncture headache, caused by CSF loss and subsequent low CSF pressure. In our case, there was neither suf®cient time for signi®cant CSF loss through a 24G hole in the dura, nor any signi®cant CSF loss during spinal needle insertion. The presentation of headache was atypical, with a sudden, severe onset and no postural element. Pre-eclampsia was considered, but there was no hypertension or proteinuria. Tension headache or migraine was unlikely because the onset of headache was too sudden and severe, with no history of similar headaches. The ephedrine given just before the onset of the headache may have caused a sudden change in blood pressure, resulting in headache. In our patient the headache lasted several hours, extending far beyond the normal period of drug action. After exclusion of the common causes of headache, intracranial pathology was considered and a computer tomogram performed, which revealed the SAH.
Very few reports describe intracranial haemorrhages after dural puncture and most of these are subdural haematomas.11±16 A potentially continuing CSF leak leads to low CSF pressure with pulling on the dura and bridging veins, causing postdural puncture headache. If this headache is left untreated, the shearing forces can lead to venous tears and acute or chronic subdural haematoma. Typically, the patient presents with prolonged postdural puncture headache, which becomes treatment-resistant, with loss of the postural element, and neurological symptoms and signs develop. At this point the intracranial haemorrhage is usually diagnosed. Postdural puncture headache should be taken seriously and treated early to minimize the rare but potentially fatal complication of an intracranial haemorrhage. On review of the literature, only three cases of intracerebral haemorrhage17±19 and only one case of an SAH alone20 have been reported after a dural puncture. In the latter, Boettiger and colleagues20 describe a 60-yr-old man who developed an SAH after two consecutive subarachnoid blocks within 2 weeks. They postulate that low CSF pressure exacerbated by the second dural puncture can develop even without postdural puncture headache. The decrease in intracranial pressure could cause an increase in transmural pressure across the arterial wall, thus facilitating the rupture of a potential vascular malformation. In our patient, there was insuf®cient time for a signi®cant CSF leak to develop and, therefore, the pathophysiology of an intracranial haemorrhage, postulated by other authors, may not apply here. Just before the onset of the headache, i.v. ephedrine was given because the systolic blood pressure had dropped to 90 mm Hg. Although the maximum recorded value afterwards was only 150 mm Hg, the pressure was measured non-invasively every 3 min and might have brie¯y been higher. Relatively sudden swings in blood pressure could have facilitated the rupture of a potentially weakened vessel wall before autoregulation became effective. Aneurysms are known to rupture under conditions associated with sudden rises in blood pressure.21 Considering the sequence of the events, there is the possibility that the SAH occurred during or just after labour, although the patient did not complain about headache at that time, and became symptomatic as a result of increased bleeding around the time the spinal block was performed. Potential cardiovascular changes, as discussed earlier, may have contributed to this. On the other hand, the combination of labour, spinal anaesthetic and SAH might have been purely incidental, considering that many spontaneous SAHs occur without obvious trigger event. In one series of 500 patients, 34% of SAHs developed during non-strenuous activities and 12% during sleep.22 Such a coincidence is, however extremely unlikely as the overall incidence of SAHs is so low. The computer tomogram in our patient showed a small SAH. The four-vessel angiogram was negative on the same day and 6 weeks later. According to Latchaw and
443
Eggert and Eggers
colleagues,3 in 10% of SAHs found on CT scan no lesion can be identi®ed on the angiogram. This usually implies a better prognosis, with a rebleeding rate of 4%.4 How should this patient be managed if she presents with another pregnancy? According to Dias and Sekhar,9 maternal and fetal outcomes are similar in parturients with either untreated aneurysms or AVMs, regardless of whether a Caesarian section or a vaginal delivery is performed. Manoeuvres such as shortening the second stage, epidural analgesia and, if necessary, low forceps delivery might decrease the risk of recurrent bleeding during vaginal delivery.9 If this patient requires anaesthetic intervention in the future, we will probably avoid spinal anaesthesia, although case numbers are too small to provide suf®cient evidence favouring a general anaesthetic. If an epidural catheter is considered, it should be inserted by an experienced operator to minimize the risk of a dural tap, which could be disastrous. She should be assessed antenatally by a consultant obstetric anaesthetist to formulate a management plan for labour.
References 1 Department of Health. Why Mothers Die: Report on Con®dential Enquiries into Maternal Deaths in the United Kingdom 1994±1996. London: The Stationary Of®ce, 1998 2 Young BJ, Seigerman MH, Hurst RW. Subarachnoid hemorrhage and aneurysms. Semin Ultrasound CT MR 1996; 17: 265±77 3 Latchaw RE, Silva P, Falcone SF. The role of CT following aneurysmal rupture. Neuroimaging Clin N Am 1997; 7: 693±708 4 Duong H, Melancon D, Tampieri D, Ethier R. The negative angiogram in subarachnoid haemorrhage. Neuroradiology 1996; 38: 15±9 5 Mas JL, Lamy C. Stroke in pregnancy and the puerperium [review]. J Neurol 1998; 245: 305±13 6 Wiebers DO. Subarachnoid hemorrhage in pregnancy. Semin Neurol 1988; 8: 226±9 7 Horton JC, Chambers WA, Lyons SL, Adams RD, Kjellberg RN. Pregnancy and the risk of hemorrhage from cerebral arteriovenous malformations. Neurosurgery 1990; 27: 867±71
444
8 Robinson JL, Hall CS, Sedzimir CB. Arteriovenous malformations, aneurysms, and pregnancy. Neurosurgery 1974; 41: 63±70 9 Dias MS, Sekhar LN. Intracranial hemorrhage from aneurysms and arteriovenous malformations during pregnancy and the puerperium [review]. Neurosurgery 1990; 27: 855±65 10 Hunt HB, Schifrin BS, Suzuki K. Ruptured berry aneurysms and pregnancy. Obstet Gynecol 1974; 43: 827±37 11 Jack TM. Post-partum intracranial subdural haematoma. A possible complication of epidural analgesia. Anaesthesia 1979; 34: 176±80 12 Pavlin DJ, McDonald JS, Child B, Rusch V. Acute subdural hematomaÐan unusual sequelae to lumbar puncture. Anesthesiology 1979; 51: 338±40 13 Newrick P, Read D. Subdural haematoma as a complication of spinal anaesthetic. Br Med J 1982; 285: 341±2 14 Edelman JD, Wingard DW. Subdural hematomas after lumbar dural puncture. Anesthesiology 1980; 52: 166±67 15 Skoldefors EK, Olofsson CI. Intracranial subdural haematoma complicates accidental dural trap during labour. Eur J Obstet Gynecol Reprod Biol 1998; 81: 119±21 16 Vaughan DJA, Stirrup CA, Robinson PN. Cranial subdural haematoma associated with dural puncture in labour. Br J Anaesth 2000; 84: 518±20 17 Benzon HT. Intracerebral hemorrhage after dural puncture and epidural blood patch: nonpostural and noncontinuous headache. Anesthesiology 1984; 60: 258±9 18 Mantia AM. Clinical report of the occurrence of an intracerebral hemorrhage following post-lumbar puncture headache. Anesthesiology 1981; 55: 684±5 19 Wedel DJ, Mulroy MF. Hemiparesis following dural puncture. Anesthesiology 1983; 59: 475±7 20 BoÈttiger BW, Diezel G. Akute intrakranielle Subarachnoidalblutung nach wiederholter SpinalanaÈsthesie. Anaesthesist 1992; 41: 152±7 21 Pulsinelli WA. Cerebrovascular diseases, aneurysmal subarachnoid hemorrhage. In: Bennett JC, Plum F, editors. Cecil's Textbook of Medicine. Philadelphia: W. B. Saunders, 1996; 2073±6 22 Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000; 342: 29±36