Department of Anaesthesia, Princess of Wales Hospital, Coity Road, Bridgend CF31 1RQ, UK*Corresponding author
Accepted for publication: September 25, 2000
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Abstract |
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Br J Anaesth 2001; 86: 4424
Keywords: anaesthetic techniques, subarachnoid; anaesthesia, obstetric; complications, haemorrhage
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Introduction |
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Case report |
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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 first attempt, clear cerebrospinal fluid (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 6585 beats min1. 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 deficits 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 min1. 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 dl1, platelets 292 x109 litre1). The on-call medical team was consulted and a cranial computer tomogram performed, which showed a small amount of blood in the left sylvian fissure 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.
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Discussion |
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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 sufficient time for significant CSF loss through a 24G hole in the dura, nor any significant 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.1116 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 haemorrhage1719 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 insufficient time for a significant 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 briefly 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 colleagues,3 in 10% of SAHs found on CT scan no lesion can be identified 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 sufficient 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.
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References |
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