Cerebral vasoconstrictors and postdural puncture headache: the big squeeze

I. Rice1, D. Radhakrishnan2, C. Nelson-Piercy2, C. Oliver2 and S. White2

1 Southampton, UK 2 London, UK

Editor—Puerperal seizures following dural puncture have been reported in the literature.13 However, some of these cases were complicated by the use of an i.v. infusion of caffeine, a cerebral vasoconstrictor that is known to be epileptogenic. Oliver and White4 report three cases of puerperal seizures associated with postdural puncture headache (PDPH) and the use of cerebral vasoconstrictors, namely Synacthen and sumitryptan. Two of us (CNP, DR) were involved in the management of two of these cases. One of these (case three) had developed borderline hypertension at term, was intermittently hypertensive during labour, had proteinuria 1+ before induction of labour, and was noted to be hypertensive before her seizure. She also had 1+ proteinuria after the seizure and a raised urate. Thus pre-eclampsia and therefore eclampsia as a cause of the seizure cannot be excluded.

We have recently reported a further case of post partum tonic clonic seizure related to severe PDPH,5 where we discuss the possible aetiology and the difficulty distinguishing such cases from eclampsia. Transient hypertension and proteinuria after the seizures reported by Shearer and colleagues,2 and ourselves,5 add to this difficulty.

The effect of low cerebrospinal fluid (CSF) volume caused by dural puncture on cerebral haemodynamics is debatable. Animal research shows that decreased CSF pressure leads to cerebral vasodilatation, and that an epidural blood patch can reverse this.6 This would support the use of cerebral vasoconstrictors such as caffeine, Synacthen and sumitryptan in the symptomatic treatment of PDPH.

However, in the cases reported by Shearer and colleagues,2 cerebral angiography and xenon flow studies showed evidence of cerebral vasoconstriction. These authors surmised that seizures following PDPH are a result of cerebral vasoconstriction, caused by the cerebral shift secondary to a decrease in CSF volume. The women reported by Oliver and White4 suffered seizures following the treatment of PDPH with vasoconstrictors, supporting the theory of Shearer and colleagues.2

Oliver and White4 suggest that those with subclinical pre-eclampsia may be at increased risk of cerebral infarcts should their PDPH be treated with cerebral vasoconstrictors. Pre-eclampsia leads to an increase in middle cerebral artery blood flow, as measured by transcranial Doppler, even in those with a minimal increase in blood pressure.7 Zatik and colleagues8 recently reported the effect on cerebral haemodynamics of breath holding tests in pre-eclamptic women. Their results suggest that cerebral arteriolar dilatation in response to an increase in carbon dioxide is preserved in pre-eclampsia. This would indicate that the increase in cerebral blood flow velocity is because of cerebral vasoconstriction, rather than dilatation of the resistance arterioles.

We would agree with Oliver and White that the use of cerebral vasoconstrictors in patients in whom pre-existing vasoconstriction is suspected (i.e. those with pre-eclampsia) is unwise. Indeed, it is often difficult to exclude pre-eclampsia in women with neurological symptoms, including headache, postpartum. Similarly the use of caffeine, Synacthen, or sumitryptan is also inappropriate in those suffering PDPH, since there is evidence that these patients have cerebral vasospasm. For these reasons, it should no longer be considered safe to use vasoconstrictors for the symptomatic relief of PDPH.

I. Rice1

D. Radhakrishnan2

C. Nelson-Piercy2

1Southampton, UK

2London, UK

Editor—We thank Drs Rice, Radhakrishnan and Nelson-Piercy for their correspondence regarding our three case reports discussing the use of cerebral vasoconstrictors and Synacthen in the treatment of PDPH.4 We have read with interest the additional references quoted by Rice and colleagues and are pleased that they add further weight to our original premise that cerebral vasoconstrictors do not have a place in the treatment of PDPH.

We note their comments regarding our third case report, in which CNP and DR were involved in the management. We would like to clarify some of the details. According to the case notes, there was no history of pregnancy-induced hypertension. During labour, this woman had intermittent increases in blood pressure. We believe that in this case, the intermittent pain of labour caused by contractions most adequately and simply explains this particular phenomenon. There was no sustained elevation of her diastolic or systolic pressure; if there was, it certainly was neither documented nor treated. Far more importantly, for the first six days post delivery the woman was normotensive and the first documented elevated blood pressure occurred immediately prior to her seizure. However, we do indeed accept that the serum urate concentration was slightly elevated.

It would seem that our colleagues have not fully grasped the thrust of our article: sub-clinical pre-eclampsia exists, but is hard to identify. Whether the ‘fit’ in this third case represents a reaction to treatment, a failure of treatment, or a simple example of eclampsia is irrelevant. The whole point of the argument is that it indeed could have been eclampsia, but this patient still received a vasoconstrictor. If a patient is thought to be pre-eclamptic, then the correct action is to treat this potentially life-threatening condition. It would, as we recommended, also be wise to avoid unproven therapies for PDPH.

C. Oliver

S. White

London, UK

References

1 Bolton VE, Leicht CH, Scanlon TS. Postpartum seizure after epidural blood patch and intravenous caffeine sodium benzoate. Anesthesiology 1989; 70: 146–9[ISI][Medline]

2 Shearer VE, Jhaveri HS, Cunningham FG. Puerperal seizures after post dural puncture headache. Obstet Gynecol 1995; 85: 225–60[Abstract/Free Full Text]

3 Van de Velde M, Corneillie M, Vanacker B, et al. Treatment for postdural puncture headache associated with late postpartum eclampsia. Acta Anaesth Belg 1999; 50: 99–102[Medline]

4 Oliver CD, White SA. Unexplained fitting in three parturients suffering from postdural puncture headache. Br J Anaesth 2002; 89: 782–5[Abstract/Free Full Text]

5 Rice I, Mountfield J, Radhakrishnan D, Nelson-Piercy C. Puerperal seizures associated with post dural puncture headache. Int J Obstet Anesth 2003, in press

6 Boezaart AP. Effects of cerebrospinal fluid loss and epidural blood patch on cerebral blood flow in swine. Reg Anesth Pain Med 2001; 26: 402–6

7 Williams KP, McLean C. Peripartum changes in maternal cerebral flow velocity in normotensive and preeclamptic women. Anesth Analg 1996; 82: 666–8[ISI][Medline]

8 Zatik J, Aranyosi J, Settakis G, et al. Breath holding test in preeclampsia: lack of evidence for altered cerebral vascular reactivity. Int J Obstet Anaesth 2002; 11: 160–3





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