Post-dural puncture headache: pathogenesis, prevention and treatment

J. A. Aldrete1, J. Barrios-Alarcon2, S. Sagadai3, A. Hunningher4, R. Bell4 and D. K. Turnbull5

1 Chipley, FL, USA 2 São Paulo, Brazil 3 Stockport, UK 4 London, UK 5 Sheffield, UK

Editor—The review article on PDPH by Turnbull and Shepherd1 emphasized that, for the needle hole to heal, it is imperative to have an inflammatory reaction on the dural wall, discarding any therapeutic modalities that do not initiate inflammation.

The authors claim that epidural blood patches (EBPs) seal the puncture by initiating an inflammatory response, whereas in fact it has been shown that they do so by blood moving from the epidural toward the subarachnoid space through the orifice until a clot is formed that would act as a ‘plug’.2 A gradient has to be established, increasing the epidural pressure to higher levels so the fluid passes into the intrathecal space and tampons the orifice. However, in most of these punctures, the superficial layer of the arachnoid is also perforated; this is precisely the meningeal layer that may initiate an inflammatory process that may progress to radiculitis3 (transient nerve root irritation) demonstrated by ‘enhancement’, and oedema and swelling of the nerve roots,4 5 leading in some cases to arachnoiditis.5 Their endorsement of prophylactic EBP may result in unnecessary, expensive and hazardous treatment, as not all the patients that have an incidental dural puncture develop PDPH. There is not only the feasibility of another dural puncture, but also the possibility of injecting the blood subdurally or intrathecally.6

Surprisingly, the authors also dismissed the advantages of using lumbar epidural injections of colloids, citing only one brief series7 but ignoring the first report by Barrios-Alarcon and colleagues8 applied in post-partum patients with PDPH, and later confirmed by Salvador and colleagues9 in a similar population. There was no mention of the effectiveness of epidural caudal dextrose infusion (3 ml h–1) after an initial bolus of Dx in relieving PDPH in 13 patients in whom one EBP had failed,10 and in the one patient with persisting post-dural headache after three EBPs did not relieve it.11 Lander and Korkon12 noted insignificant inflammatory changes in the intradural structures of goats destroyed 7 days post epidural dextran, whereas in the animals that received EBP, a marked inflammatory response was noted. Blood is a highly irritant substance to neural tissue; attempting to explain the complex pathophysiology of PDPH on the need to create inflammation appears simplistic. By promoting inflammatory changes around the dural hole to stop the PDPH, we would favour the concept that the formation of tissue substances (cytokines and leukotrienes), which have been suggested as precipitators of the ‘inflammatory cascade’, results in the neurological deficit noted after EBP in some cases.5 6 13 Research needs to be directed to genomically identify those patients that may be more susceptible to developing PDPH and to determine the circumstances that may produce arachnoiditis when invasive procedures are done within the vertebral canal.

J. A. Aldrete1

J. Barrios-Alarcon2

1Chipley, FL, USA

2São Paulo, Brazil

Editor—I read with interest the review article ‘Post-dural puncture headache: pathogenesis, prevention and management’,1 and congratulate the authors for the excellent review of the topic. However, I would like to draw your attention to a few issues relating to it.

The incidence of post-dural puncture headache (PDPH) quoted for 25 G Whitacre spinal needles is rather high (0–14.5%). Quaynor and colleagues14 had quoted an incidence of 4.7% only. It is not clear whether Drs Turnbull and Shepherd have included patients with post-dural puncture related headache,15 in their calculation to arrive at this higher figure. I could not find any other study where the PDPH rates were this high for 25 G Whitacre spinal needles.

Drs Turnbull and Shepherd claim that there is enough evidence,1619 to show that perpendicular orientation of the needle bevel is preferable. In contrast to the authors’ statement, three of the four references1618 cited in this review are clearly in favour of parallel orientation of the bevel along the long axis of the dura to reduce the incidence of PDPH, and the fourth one is inconclusive. The fourth reference cited is an experimental study on cadaver dura in which Dittmann and colleagues19 found that bevel orientation had a minor role in determining the size and shape of the dural defect; alteration in the direction of the bevel changed only the shape of the defect. They did not study leak rates or measure the size of the dural defect.

Cruickshank and Hopkinson20 measured the fluid loss in a dural puncture model and found no significant difference in the volume of fluid lost when comparing bevel alignments. However, median flow rates were lower for the parallel approach.

Further review of the literature showed that a meta-analyses,21 which reviewed 450 publications on PDPH, did not comment about the effects of bevel orientation. In another study22 on human cadaveric dura, Angle and colleagues demonstrated reductions in leak rates with perpendicular orientation of the bevel, but this did not reach statistical significance. The authors concluded that further studies are warranted on this issue. Thus, the issue of bevel orientation still remains unresolved.

Replacing the stylet before withdrawing the needle after a diagnostic lumbar puncture has been mentioned in the literature2325 as a technique to reduce PDPH. Though it is more relevant to diagnostic lumbar punctures, I think it deserves to be mentioned in a review article on PDPH.

S. Sagadai

Stockport, UK

Editor—We thank Turnbull and Shepherd for their valuable summary on the pathogenesis, prevention and treatment of PDPH.1 A further point for discussion is the treatment of Jehovah’s witnesses with PDPH.

Many Jehovah’s witnesses will not accept even autologous blood unless it is in a continuous circuit with the systemic circulation. The usual technique for carrying out an EBP may not therefore be acceptable. Although some of the alternatives to the EBP such as caffeine, epidural dextran 40, or fibrin glues may be acceptable to Jehovah’s witnesses, the EBP remains the gold standard for the treatment of PDPH.

One potential solution described by Kanumilli and colleagues26 is to establish a circuit from an 18 G needle in an antecubital vein to the epidural space, using a 30 inch (73.5 cm) extension tube plus a further 36 inch (88 cm) male–male extension tube, with a 3-way tap to enable aspiration and subsequent injection.

Brimacombe and colleagues argue that turning a 3-way tap interrupts the continuous circuit.27 They suggest attaching the 3-way tap directly onto the Tuohy needle, with aspiration of the blood from a venous cannula via a 150 cm low volume narrow bore extension into a syringe. Blood is then injected into the epidural space without turning the 3-way tap. The blood should flow preferentially into the epidural space, aided by the high resistance from the narrow bore extension. They also suggest inflating a blood pressure cuff on the arm (over the cannula). It may, however, be better to manually occlude the cannula or apply a surgical tourniquet to ensure that the pressure remains high and constant.

We telephoned the UK Jehovah’s Witness hospital information service (the central office for the local hospital liaison committees) for their comment.28 They indicated that there is no specific ruling on blood patches, but that they felt that a blood patch is more likely to be acceptable as it is different in principle from sustaining life with a blood transfusion. They advised that patients should be made fully aware of their treatment options and exactly how the procedure is carried out. They added that the hospital liaison committee may be invited to join this discussion in a supportive role but they should not influence the patient’s decision. Appropriate consent should be obtained before carrying out the procedure.

A. Hunningher

R. Bell

London, UK

Editor—I welcome the discussion that this review has generated.1 In reply to Drs Aldrete and Barrios-Alarcon: though the mode by which the EBP promotes closure of the dural perforation may be open to discussion, compression of the subarachnoid space and tamponade of the cerebrospinal fluid (CSF) leak appears likely.29 Furthermore, there is no doubt that blood patching is an effective method of alleviating the symptoms related to dural perforation and persistent CSF leak, and failure to initiate effective treatment in the presence of CSF leak can lead to significant disability,30 and even death. However, correct identification of the position of the needle tip in the absence of MRI scanning is difficult, particularly where CSF may have contaminated the epidural space. Arachnoiditis may therefore follow EBP when the Tuohy needle is misplaced.31 As the authors emphasize, physicians need to be aware of arachnoiditis complicating EBP. The development of safe, effective therapies to manage PDPH should perhaps, be a future goal. With this in mind, Drs Aldrete and Barrios-Alarcon have previously reported significant success with symptom resolution and absence of long term complication by administration of epidural Dextran 40,32 either as a bolus or an infusion. The absence of inflammatory activity, when compared with blood patching, in the intradural structures of sheep12 where epidural Dextran 40 was introduced suggests Dextran 40 controls the CSF leak through compression of the subarachnoid space. Usubiaga,33 however, has demonstrated that subarachnoid compression after an epidural bolus of crystalloid solutions is only temporary. Kroin and colleagues,34 in a rat model of CSF leak, demonstrated that a 3 h infusion of epidural Dextran 40 or saline does not maintain CSF pressure in the presence of a CSF leak. This was in contrast to epidural blood or fibrin glue. Thus, while the administration of solutions such as Dextran 40 is attractive and could avoid some of the described complications of EBP, the evidence for its efficacy is poor.

The impression of Drs Aldrete and Barrios-Alarcon was that the review endorsed the use of prophylactic blood patching. The objective of the review was to be impartial. Nevertheless, after dural perforation with a Tuohy needle in the parturient, the incidence of PDPH is high. In this situation where the symptoms are particularly disabling and frustrating,30 the early application of a patch may be beneficial, if it were to prove as effective as some studies have suggested.35 I accept though, their concerns that prophylactic blood patching attracts an unnecessary risk of arachnoiditis.

The arrangement of collagen fibres within the spinal dura mater interested Dr Sagadai. In recent years, the classical description of parallel arrangement of collagen fibres running from caudad to cephalad has been questioned.36 37 If the arrangement were not uniform, but consisted of groups of fibres passing in all directions, this contradicts the consensus that bevel orientation of Quincke type needles will influence subsequent CSF leak. Laboratory studies favour the obvious conclusion that the larger the dural perforation the greater the leak.20 37 In contrast, clinical studies observing the influence of bevel orientation have generally supported the parallel approach.17 I would therefore concur with Dr Sagadai that the issue of bevel orientation is unresolved. On the other hand, the popularity of Quincke type spinal needles for lumbar puncture and spinal anaesthesia is diminishing with the development of modern spinal needles. The issue of bevel orientation for spinal anaesthesia should become of less clinical significance.

Dr Sagadai correctly stated that replacing the stylet before withdrawing the needle has been considered a method of limiting PDPH after diagnostic lumbar puncture. In the study by Strupp and Brandt,25 this reduced the PDPH rate from 16 to 5%, when a 21 G Sprotte needle was used. However, diagnostic lumbar puncture is still frequently performed with large gauge needles: 22 G, 20 G and even 18 G. Neurologists should be encouraged to use smaller gauge, pencil point needles as a means of limiting PDPH.38

Dr Sagadai correctly identified an error in the table listing the incidence of dural puncture headaches related to 25 G Whitacre needles. The correct figure should have read 0–4.7% not 0–14.5%.

Drs Hunningher and Bell posed the question of the Jehovah’s Witness and EBP. I am grateful that I have not had the opportunity to put their method into practise, but the method they suggested deserves consideration.

D. K. Turnbull

Sheffield, UK

References

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