post-dural puncture headache: pathophysiology, prevention ... · post-dural puncture headache:...

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Post-dural puncture headache:

pathophysiology, prevention and treatmentq

Kenneth D. Candido* MD

Associate Professor of Anesthesiology

Department of Anesthesiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA

Rom A. StevensCaptain, Medical Corps, United States Naval Reserve and Adjunct Professor

Department of Anesthesiology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA

Post-dural puncture headache (PDPHA) has been a vexing problem for patients undergoingdural puncture for spinal anaesthesia, as a complication of epidural anaesthesia, and afterdiagnostic lumbar puncture since Bier reported the first case in 1898. This Chapter discussesthe pathophysiology of low-pressure headache resulting from leakage of cerebrospinal fluid(CSF) from the subarachnoid to the epidural spaces. Clinical and laboratory research overthe last 30 years has shown that use of small-gauge needles, particularly of the pencil-pointdesign, is associated with a lower risk of PDPHA than traditional cutting point needle tips(Quincke-point needles).

A careful history can rule out other causes of headache. A positional component ofheadache is the sine qua non of PDPHA. In high-risk patients (e.g. age ,50 years, post-partum, large-gauge-needle puncture), patients should be offered early (within 24–48 h ofdural puncture) epidural blood patch. The optimum volume of blood has been shown to be12–20 ml for adult patients. Complications of autologous epidural blood patch are rare.

Key words: headache; post-dural puncture; anaesthesia; spinal; complications; treatment.

Post-dural puncture headache (PDPHA) is a possible complication of both spinal andepidural anaesthesia. The first report of PDPHA was described after Professor AugustBier and his Surgical Resident, Dr Hildebrandt, performed spinal anaesthesia on eachother in 1898, using cocaine.1 When Dr Hildebrandt could not attach the syringe withthe local anaesthetic to the needle placed in the subarachnoid space of Professor Bier, aconsiderable amount of cerebrospinal fluid (CSF) was lost. Not wanting to disappointProfessor Bier, Dr Hildebrandt volunteered subsequently to receive a spinal anaesthetichimself. Both men developed significant postural cephalalgia following the experiment,Professor Bier’s lasting for 9 days and Dr Hildebrandt’s commencing the evening of

1521-6896/$ - see front matter Q 2003 Elsevier Ltd. All rights reserved.

Best Practice & Research Clinical AnaesthesiologyVol. 17, No. 3, pp. 451–469, 2003doi:10.1016/S1521-6896(03)00033-8, www.elsevier.com/locate/jnlabr/ybean

q The opinions expressed in this article are those of the authors and do not reflect official policies of the

United States Navy, the Department of Defense, or of the Uniformed Services University of the Health

Sciences.* Corresponding author.

E-mail address: [email protected] (K.D. Candido).

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the procedure and associated with at least two episodes of vomiting. Bier suggestedthat it was the loss of CSF that resulted in his condition, and further postulated that theloss of CSF might be minimized by the use of fine needles and the placement of a fingerinto the hub of the needle, as expeditiously as possible, to prevent further loss.Although Bier may have been the first to speculate on the relationship between lowCSF pressure and PDPHA, the first publication of this theory was made by MacRobertin 1918.2 Thus, PDPHA and its cause have been known since the advent of spinalanaesthesia, and it remains one of the most perplexing limitations of this anaesthetictechnique.

It was not until the reports of Gormley in 19603 and DiGiovanni and Dunbar in19704 that a definitive treatment was known for the syndrome. DiGiovanni and Dunbardescribed the epidural injection of autologous blood in 50 patients suffering fromPDPHA. This proved to be an effective measure to stop the process of CSF leakage andpostural cephalalgia. PDPHA remains the most common postoperative complication ofspinal anaesthesia. Its diagnosis and treatment should be considered part of thestandard armamentarium of the regional anaesthesiologist.

INCIDENCE

The incidence of PDPHA following spinal anaesthesia has been reported to vary from0.2 to 24%.5–9 The generally quoted incidence is ,3%.10 PDPHA is more frequentlynoted in pregnant women receiving spinal anaesthesia, and in patients less than 50 yearsof age. In obstetric patients, a lowering of intra-abdominal pressure after delivery of thefetus may lower epidural pressure11,12, and thus theoretically increase CSF leakagefrom a dural hole. Additionally, hormonal changes at the time of delivery may make thecerebral vasculature especially reactive and predispose parturients to PDPHA.13 Thereis a definite decrease in the incidence of PDPHA in older adults. After the age of 50years, the risk of PDPHA declines appreciably.14,15 There are various theories toexplain the low incidence of PDPHA in older patients; however, there is little evidenceto support these theories.

There is considerable controversy regarding whether non-pregnant women are atany increased risk of developing PDPHA following dural puncture. A study by Lybeckeret al included no parturients, and found no gender differences in the incidence ofPDPHA following spinal anaesthesia.16 The literature on obstetrics suggests anincidence of PDPHA of up to 75% following dural puncture using 17- or 18-gaugeneedles. Norris demonstrated that orientating the epidural needle bevel parallel to thefibres of the dura decreases the incidence of PDPHA in labouring women followinginadvertent dural puncture from 75 to 31%.17,18 For reasons yet unexplained, morbidobesity may decrease the incidence of PDPHA following epidural needle puncture ofthe dura.19 Thus, there are several potential patient-related factors which can affect theincidence of PDPHA.

In addition to patient-related factors, there are several technical factors which canaffect the incidence of PDPHA. The incidence of PDPHA after dural puncture withepidural anaesthesia is markedly less when saline is used for the loss of resistancetechnique versus air (10 versus 65%).20 While the incidence of unrecognized duralpuncture may occur in up to 1.5% of attempted epidural punctures21, the incidence ofPDPHA following attempted epidural block may be as high as 81–91%.22–25 Rotating anepidural needle once inside the epidural space may increase the risk of dural puncture(and hence PDPHA) and is therefore not recommended.26,27

452 K. D. Candido and R. A. Stevens

The most important technical factor in determining the incidence of PDPHA isundoubtedly the size of the dural hole produced during puncture. There are two majorrelevant sub-topics to this issue: needle size, and design of the needle point. There is adirect relationship of PDPHA to spinal needle tip diameter.28 The larger the diameter ofthe needle, the more frequent and more severe the headache. There is an incidence of.80% with 16-gauge needles versus 5% with 26-gauge needles; the overall incidencewas 11% of 10 098 spinals in one large study.11 Use of small-gauge pencil-point spinalneedles has reduced the incidence to about 0.02–1.5%.29–31 This latter factor isthought to be due to the smaller dural hole produced by a pencil-point needlecompared with that produced by a cutting (Quincke) point needle, resulting in lessleakage of CSF leakage.

For example, Flaatten et al compared the incidence of PDPHA after spinalanaesthesia using either 27-gauge pencil-point (non-cutting) versus 27-gauge Quincke(cutting) needles. There were 301 patients in the study; 153 in the pencil-point group,and 148 in the Quincke group. There were three PDPHAs in the pencil-point group,versus 12 in the Quicke group. A meta-analysis of other studies totalling 1131 patientsshowed a relative risk of developing PDPHA of 0.38 (95% confidence interval, 0.19–0.75) in the pencil-point (non-cutting) group compared with the Quincke group.32

However, there is an increased failure rate of spinal anaesthesia associated with 27-gauge spinal needles.33–35 PDPHA risk is increased if repeat dural puncture occurs afterfailed attempts at spinal block, even when needles of fine gauge are used.36 Multiplesmall dural holes can result in the same loss of CSF as from one large hole. As verysmall-gauge needles have an increased failure rate, a reasonable compromise is a 24-gauge pencil-point needle, which is currently the favourite spinal needle used by thepresent authors.

Although the highest incidence of PDPHA may occur in obstetric patients, as manyas 40% of parturients who do not receive any neuraxial anaesthesia whatsoevercomplain of headache in the peripartum period.37 This emphasizes the need to rule outother causes of headache in any patient, including tension headache, migraine headache,caffeine withdrawal headache, sinusitis and pre-eclampsia. One must also consider thepossibility of headache due to a pneumocephalus (from using the loss of resistancetechnique with air to identify the epidural space). In the case of pneumocephalus,usually the headache is worse in the recumbent position, and it typically resolves overseveral hours. Consideration must also be given to the possibility of subarachnoidhaemorrhage, intracranial haemorrhage, subdural haematoma, or cortical veinthrombosis.38,39 Typically, these other causes of headache can be differentiated fromPDPHA by lack of a postural component to the headache.

Not all headaches following spinal anaesthesia are due to leakage of CSF. Gurmanikproposed that the mild headache occasionally following spinal anaesthesia might resultfrom a chemical irritation or chemical meningitis due to povidone-iodine antisepticused to prepare the skin prior to performing the block.40,41

PDPHA may result not from epidural or spinal needle puncture, but rather fromepidural catheter puncture of the dura mater. From the anaesthesia records of about9000 epidural techniques for obstetrical analgesia, Kalas and Hehre identified 19epidural catheter punctures resulting in PDPHA in six of these patients (31.6%); in thisseries, there were 99 epidural needle punctures of the dura, resulting in 48 PDPHA(48.5%).42 In a larger series (26 490 labouring patients receiving epidural analgesia), twoout of six (33%) patients with documented catheter-induced dural puncture developedPDPHA.43 Following continuous spinal anaesthesia using 20-gauge catheters, theincidence of PDPHA seems to be low (about 1%).44,45 Intrathecal catheters (20-gauge)

Post-dural puncture headache 453

placed through 18-gauge needles did not have a higher incidence of PDPHA thansmaller continuous catheters placed through 20-gauge needles or compared with‘single-shot’ spinal anaesthesia using 22-gauge pencil-point needles.46 The reason forthis low incidence of PDPHA after continuous spinal anaesthesia is not known. Somehave speculated that an inflammatory reaction around the catheter reduces the loss ofCSF via the dural hole. There is little direct evidence to support this hypothesis.

PDPHA infrequently occurs following combined spinal/epidural anaesthesia (CSE).Inadvertent dural puncture does occur with similar frequency following CSE comparedwith lumbar epidural anaesthesia.47 There are several possible explanations for thisobservation. First, the reduced incidence of PDPHA following CSE may be due to theepidural needle acting as an introducer for the spinal needle, reducing the number ofattempts to puncture the dura using the spinal needle. Second, 25- to 27-gauge spinalneedles are used for CSE, and the incidence of PDPHA following their use is low (,2%). Third, the injection of local anaesthetic (LA) into the epidural space during CSEreduces leakage of CSF through the dura secondary to increased epidural pressure.Fourth, epidural opioids may provide a prophylactic effect against PDPHA.48–52 Again,direct evidence for these possible explanations is lacking at present.

CLINICAL FEATURES OF PDPHA

A history of dural puncture and a postural component of the headache are essentialfactors in making a diagnosis of PDPHA. PDPHA usually occurs within a minimum of afew hours following dural puncture. The onset of headache usually occurs within thefirst or second day after dural puncture but may occur 5 days or more later. For the first24–48 h following dural puncture, loss of CSF exceeds production. Eventually, the duralrent is repaired by fibroblasts forming a fibrin seal. However, there are reports ofchronic PDPHA occurring up to 5 months following dural puncture.11 Bed restfollowing dural puncture has not been shown to prevent, but merely to postpone, thedevelopment of PDPHA.53 In almost all cases, including chronic PDPHA, a history ofworsening the headache when assuming the sitting or standing position, due to alowering of CSF pressure, can be elicited.

The typical location of the headache is bifrontal and/or occipital. Occasionally,symptoms involve the neck and upper shoulders. Intensity ranges from mild toexcruciating. Classically it is worse in the upright position or during coughing orstraining. Symptoms usually subside with recumbency. There may be associated nausea,loss of appetite, photophobia, and changes in hearing acuity and tinnitus, as well asdepression. In severe cases, there may be diplopia and cranial nerve dysfunction andnerve palsies secondary to traction on those nerves. All of these symptoms can beexplained by low CSF pressure (see below).

PATHOPHYSIOLOGY

Any theory explaining PDPHA must account for the relationship of the headache to theloss of CSF. One theory states that the loss of CSF through a dural hole results inintracranial tension or traction on nerves and meningeal vessels. There is support forthis theory from audiometric studies performed on patients who developed temporaryhearing loss and PDPHA after dural puncture.54–59 These studies also documented


improvement in hearing acuity and resolution of the headache following epidural bloodpatch. The bimodal theory of the pathophysiology of this syndrome was first publishedby Kunkle et al in 1943.60 The bimodal theory suggests that there is a combination ofboth low CSF pressure and resultant cerebral vasodilatation in reaction to thestretching of vessels.

In the normal human, 450–500 ml of CSF is produced per day (0.3 ml/min). Thenormal CSF volume is 150 ml, which is divided about equally between intracranial andspinal CSF.61 The major portion of CSF (90%) is produced from filtration of blood inchoroid plexuses in the lateral, third and fourth ventricles of the brain and issubsequently absorbed back into blood by the arachnoid granulations found in thesuperior sagittal and transverse venous sinuses. The other 10% of CSF is derived frombrain substance itself. There is a slow movement or circulation of CSF from theventricles to the intracranial subarachnoid space and then to the venous sinuses. Thespinal subarachnoid space is in effect a ‘backwater’ in which there is very littlemovement of CSF except by simple diffusion and postural changes. As the bodygenerates its entire CSF volume three times per day, all that is necessary to treat aPDPHA is to stop the leakage of CSF.

Decreased brain ‘buoyancy’ owing to low intracranial pressure causes traction onstructures supporting the brain and cranial nerves. A caudal shift of the brain occurswith a decreased volume of CSF, causing dural stretching and traction on pain-sensitiveintracranial structures (cerebral vessels, falx cerebri and tentorium). The trigeminal,glossopharyngeal and vagus nerves are thought to be involved. Vagal traction maystimulate chemoreceptors in the medulla to produce nausea. Traction on the abducensand trochlear nerves can lead to ocular muscle paralysis, with strabismsus and doublevision resulting. Hearing loss has also been reported, due to low CSF pressuretransmitted to the inner ear via the cochlear aqueduct.62 This decrement in hearing isfully reversible once normal subarachnoid pressure is restored.

Although there is no evidence that the body compensates for a loss of CSF byincreasing its production, venous dilatation does occur, which partially compensates forloss of intracranial volume. This phenomenon may be responsible for the sensation ofpressure that is experienced with PDPHA. When standing, the intracranial pressuredecreases and intracranial venous distention increases, worsening the headache. Whensupine, equalization of intracranial cisternal and lumbar CSF pressures takes place, sono expansion of the venous system occurs, and the headache improves. Neck pain mayresult from tension on cervical nerves 1–3.63 Neck pain may develop into a myofascial-like pain. Trigger point injections are sometimes helpful in treatment.

Intracranial subdural haematoma is a very rare complication of prolonged reductionof CSF pressure. This has been associated with a 14% mortality rate, and a high rate ofpersistent neurological complications in those who survive64,65, emphasizing the needto diagnose and treat persistent PDPHA expeditiously.

The amount of CSF loss depends upon the size and shape of the dural hole and thepressure difference between the subarachnoid and epidural spaces. The design of thespinal needle tip and orientation of a cutting needle bevel are both factors indetermining the rate of CSF loss (see below). In one in vitro study performed usinghuman postmortem thoracolumbar dura mater (Figure 1), the median loss of CSFvolume in 5 min was significantly less with a 22-g Whitacre needle than with a 22-gQuincke. There was a 21% reduction in leakage of CSF if the Quincke needle bevel wasparallel to the large axis of the vertebral column. Orienting the Quincke needle bevel inthe longitudinal axis promotes separation instead of cutting of dural fibres.66 However,this cadaver study has been disputed by anatomical and in vitro analyses.67 A classic


clinical study by Mihic demonstrated that the incidence of PDPHA is lower when aQuincke needle bevel is oriented parallel to the longitudinal fibres.68

The size of a dural hole relates to outside diameter of a given spinal needle, as well asto bevel configuration. Cutting fewer fibres of the dura reduces the size of the duralhole. Needle tips that stretch dural fibres should reduce the size of a resulting hole, incomparison to tips that cut fibres; hence the rationale for using pencil-point needlesrather than cutting needles.12,69–72 The dura mater consists of tough fibrous tissue thatvaries in thickness, even in the same individual. Fibres run longitudinally, but alsotransversely. In 1988, Dittmann et al reported that dural fibres are not uniformlyparallel, and that the thickness of the dural sac varies. They described the so-called ‘tincan lid’ phenomenon: needle perforation of the dura with a Quincke needle resemblesthe top of an almost completely opened tin can with the lid hinged at its base. The holetends to be ellipsoidal when the needle is inserted through a thick section of dura. Bycontrast, when a needle of the same gauge and design perforates a thinner section ofdura, the resultant orifice is larger, and it closes much more slowly.73 A hole left in thedura resembles an opened tin can rather than a neat punched out hole. The resultingflap may fall back into place, virtually sealing the hole (Figures 2–4). Quincke needlesproduce an oval or ellipsoidal hole, as opposed to Whitacre or Sprotte needles, whichproduce a more rounded hole.74

Figure 1. MRI confirmation of cerebrospinal fluid collection following dural puncture at L2–L3. Thearrows demonstrate the fluid mass (sagittal spin echo proton density). (Reproduced with permissionfrom Reference 61.)


Figure 2. Scanning electron micrograph of a dural puncture hole made by a 25-gauge Quincke (cutting)needle. View is from the inner (intrathecal) side of the dura mater. Note the ‘open-tin-can’ configuration.(Photograph courtesy of Drs Mark Johnson and Vladimer Bittner)(Reproduced with permission fromReference 61).

Figure 3. Scanning electron micrograph of a dural puncture hole made by a 25-gauge Quincke (cutting)needle. View is from the outer (epidural) side of the dura. (Photograph courtesy of Drs Mark Johnson andVladimer Bittner)(Reproduced with permission from Reference 61).


The arachnoid mater is closely applied to the dura mater, but is not attached to it.For CSF to leak, the hole in the dura must be closely aligned to a hole in the arachnoidmater. An angled approach to the subarachnoid space, such as a paramedian approach,is associated with a lower incidence of PDPHA75,76, although at least one study doesnot support this contention.77 In summary, pencil-point needles produce smaller duralholes, a reduced loss of CSF, and lower rates of PDPHA than do Quincke point needlesof the same size. When using a Quincke point needle, a paramedical approach producesa decreased loss of CSF and a lower incidence of PDPHA. A lower incidence of PDPHAis seen when the bevel of the Quincke needle is oriented parallel to the longitudinal axisof the body.

TREATMENT

Based on the theories of PDPHA discussed above, it should seem readily apparent thatthe goal is to restore CSF pressure. It should be kept in mind that the natural history ofPDPHA is one of resolution with time, with up to 90% resolving within 10 days ofonset.78 It is essential to consider other possible diagnoses of headache prior toembarking upon treatment. Failing to recognize other potential causes might result intreatment failures, or worse, in misdiagnosis of other life-threatening causes ofcephalalgia.

In cases where the headache appears to be related to the dural puncture, i.e. ispostural in nature, conservative measures may be attempted for headache. These

Figure 4. Scanning electron micrograph of a dural puncture hole made by a 25-gauge Whitacre (non-cutting)needle. View is from the inner (intrathecal) side of the dura mater. Note that the fibres are ‘torn’ rather than‘cut’, resulting in an ellipsoidal configuration. (Photograph courtesy of Drs Mark Johnson and VladimerBittner)(Reproduced with permission from Reference 61).


include the use of non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen,bed rest (to avoid symptoms, not to prevent onset), and possibly weak opioidanalgesics. In cases where the patient is unlikely to lie flat, such as a mother who has justdelivered a baby, and who will have an over-riding need to get out of bed to care for hernewborn, conservative measures are not likely to be effective. Abdominal binders forcemore venous blood through the epidural venous plexus, and although not advocated bythe present authors, might have a place in very mild cases or in cases where the patientwishes to exhaust all non-invasive modalities prior to considering epidural blood patch.Aggressive hydration of patients (to try to stimulate CSF production) is of no provenbenefit. Additionally, this manoeuvre will result in a brisk diuresis and will subsequentlyinterfere with instructions to lie flat.

Caffeine, a methylxanthine, has a cerebral vasoconstrictor effect, and may have someefficacy in the management of PDPHA; however, caffeine is also a diuretic. Caffeine isinexpensive, widely available, and most importantly is associated with minimal risk.Camann et al evaluated 40 postpartum patients with headache in a randomized, double-blind, placebo-controlled study. Caffeine 300 mg orally versus placebo resulted in a300% reduction in the visual analogue pain score at 4 h after administration, but therewas no difference at 24 h.79 Caffeine may also be administered parenterally. Forintravenous use, caffeine is combined with sodium benzoate to enhance solubility.Sechzer and Abel performed a randomized, double-blind, placebo-controlled studyconsisting of 41 patients with PDPHA who received either placebo or intravenouscaffeine 500 mg. All 41 patients subsequently received intravenous caffeine 500 mg,regardless of initial treatment or outcome, and 71% ultimately achieved relief ofheadache. Their conclusion was that intravenous caffeine is a safe and effective methodfor treating PDPHA.80,81 However, placebo-controlled studies of either oral orintravenous caffeine have not shown a reduction in the number of patients subsequentlyrequiring epidural blood patch.

Other intravenous agents that have been used in an attempt to relieve PDPHAinclude sumatriptin and adrenocorticotropic hormone; both have demonstrated someefficacy, but have limited evidence to support their use. Sumatriptin, a 5-HT agonist, isfurther limited by its 2-h plasma half-life.82

EPIDURAL INJECTIONS

Autologous epidural blood patch (AEBP) has become the ‘gold standard’ in thetreatment of PDPHA. As there is some risk of infection when injecting blood into theepidural space, we will discuss the efficacy of some other aqueous agents which havebeen injected into the epidural space to treat PDPHA. Prior to considering the use ofepidural injections of blood or other substances to relieve the symptoms of PDPHA,there needs to be a clearly negative history of sepsis and coagulopathy. HIV infection isnot considered to be a contraindication to AEBP (see below).

Dextran and 0.9% NaCl (saline) injections into the epidural space function by thesame basic mechanism, i.e. to transiently increase pressure in the epidural space, whichsubsequently decreases the leakage of CSF and restores subarachnoid pressure.Unfortunately, this effect is only transient. Dextran, being of large molecular weight,stays in the epidural space longer than saline and provides increased pressure for longerperiods of time. Bolus injection of epidural dextran 20 ml has relieved headacherefractory to bed rest, hydration or caffeine, with long-lasting relief occurring within


10 min of injection. Unfortunately, the success rate is moderate. Anaphylaxis has beenreported following the use of dextran for this purpose.83,84

Injection of 0.9% NaCl (saline) into the epidural space after unintended duralpuncture dates back to 1950, when Rice and Dobbs reported immediate relief ofheadache in 99.5% of cases with a 54% recurrence rate.85 Usubiaga et al and Baysingeret al showed that intermittent injections of saline 10–30 ml relieved headache, withoutreported re-occurrence.86,87 It is believed that the mechanism of action of both salineand dextran involves an increase in epidural pressure which reduces outflow of CSF,while a fibrin clot forms over the dural puncture site.63,88 Other studies show verylimited effects of prophylactic epidural saline infusions on the prevention of PDPHA,particularly in postpartum patients.22,24,89

AUTOLOGOUS EPIDURAL BLOOD PATCH

The autologous epidural blood patch was first described by Gormley in 1960, and laterpopularized by DiGiovanni et al.3,4,90 The suspected mechanism of action of AEBP is bytamponade of the dural leakage while raising the subarachnoid pressure. Elevation ofsubarachnoid and epidural pressures remains so only for about 20 min.86,91 MRIevidence confirms a mass effect after injection of epidural blood, with gradualresolution over about 7 h (Figure 5 A–C).92 Unlike saline, dextran or other fluids,blood is not removed quickly from the epidural space93, and it potentially exerts atamponade effect for much longer periods of time. The autologous blood is thought toform a fibrin clot over a dural rent, allowing CSF volume (and hence, pressure) tonormalize as new CSF is generated.94

Abouleish et al summarized 524 cases of AEBP reported by 11 centres.95 Persistentsymptomatic relief of PDPHA following epidural blood patch was .95%, particularlywhen using volumes of blood .15 ml. In this review, using volumes of blood greaterthan 20 ml offered no advantage as it is known that 20 ml spreads about 9–10 spinalsegments when administered to patients in the sitting position.12

Some studies have demonstrated lower success rates, with only 61–75% of patientsdemonstrating sustained benefit. These lower success rates may reflect dural punctureoccurring with large-bore epidural needles versus smaller-gauge spinal needles.22,63,96,97

In obstetrical studies, the success rate of epidural blood patch for PDPHA is lower,because the dural hole made by 17-gauge Tuohy needles results in a large leakage of CSF,necessitating a second blood patch in as many as 29% of patients.22,23,25

THE TECHNIQUE OF AUTOLOGOUS EPIDURAL BLOOD PATCH

The procedure is performed only after a careful history to exclude other causes ofheadache. Contraindications to blood patch include infection at the skin puncture siteor untreated sepsis. Informed consent is obtained and risks, benefits and alternativesare explained. Strict sterile technique is mandatory. While some authors recommendthe administration of prophylactic antibiotics for the procedure, the present authors donot. The patient is placed in either the sitting position (for obese patients to facilitateidentification of the midline) or the lateral decubitus position (particularly if theheadache is severe). Rarely, if fluoroscopy is being utilized, the prone position may beselected. After carefully identifying a prominent vein in an upper extremity, a sterile skin


prep and drape is performed. Concomitantly, a skilled anaesthesiologist chooses eitherthe previous level of puncture (if this can be discerned following multiple needleattempts), or, alternatively, one level below the previous injection site. These are thepreferred interspaces to inject into, because blood preferentially rises cephaladfollowing its injection into the lumbar epidural space with a patient in the sittingposition.92,93,98 Once the anaesthesiologist has gained entrance into the epidural spaceat the selected level, the phlebotomy should proceed with the withdrawal of at least20 ml of venous blood. It is important to wait until epidural entry has been successful,because the venous blood might otherwise clot if it is withdrawn too early. The blood iscarefully, and aseptically, transferred to the anaesthesiologist, who injects it slowlythrough the epidural needle until one of several endpoints occurs: (a) if the patientcomplains of backache or worsening headache during the performance of the epidural

Figure 5. (A) MRI demonstrating autologous blood in the epidural space. Blood is primarily seated at L2–L3,but extends as high as T12 and as caudad as L4. (Reproduced with permission from Reference 61). (B) MRIdemonstrating T2-weighted image of autologous blood in the epidural space. In this view, there is less contrastbetween the blood and other anatomical structures including bone and soft tissues. The arrows indicate themass of blood primarily seated at L2–L3. (Reproduced with permission from Reference 61). (C) MRIdemonstrating adjacent slice to Figure 5(A) and (B). Here, the regional morphology of the spinal cord, bloodpooling along the thecal sac and its anterior layering (arrow) is shown. (Reproduced with permission fromReference 61).


injection, or (b) once at least 15 ml have been successfully injected without complaintby the patient. Patients are typically placed supine for up to 30–60 min following theprocedure to reduce the leakage of CSF, out from the dural hole. A period of 30–60 min is long enough for the fibrin clot to form. The patient is advised to avoidstraining, bending or heavy lifting for 2–3 days to allow the dural hole to heal.

As regards the optimum volume of autologous blood to be injected epidurally,Taivainen et al found that using 10 ml standard in all patients was equivalent to 10–15 ml variably administered based upon height; there was no significant difference inearly or late success rates between groups in this one study.96 Others have advocatedmore generous volumes. Crawford found that 20 ml was associated with 96% success,versus 70% success using 6–15 ml.99 The ideal time to perform an epidural blood patchis within 24 h of puncture.95 Treatment failure after blood patch may reflect continuedtransdural leak100; in this case, the blood patch should be repeated while keeping thepatient flat for 24 h afterwards to reduce the flow of CSF through the dural hole.

Complications following AEBP include the following: backache (35%), neck ache(0.9%) and transient temperature elevations (5%) lasting 24–48 h. Bleeding, infection,repeat dural puncture, and arachnoiditis from blood injected into the subarachnoidspace have been reported. There have been at least two cases of facial nerve paralysisreported following autologous blood patch, both of which resolved spontaneously.

Figure 5 (continued )


Lowe and McCullough suggested that the aetiology is ischaemia of the 7th nerveresulting from decreased blood supply after an increase in intracranial pressure due tothe injection of blood in the epidural space.101 There has also been at least one case ofintractable dizziness, vertigo, tinnitus and ataxia.102,103 Blood patch has occasionallybeen associated with vasovagal syncope.104

Subsequent epidural anaesthesia is probably not affected by a previously performedepidural blood patch; however, there exists considerable controversy regarding thissubject. Ong et al identified 29 parturients who had epidural anaesthetics after previousblood patch; there was a 59% success rate in this group, compared with an 88–92%success rate in individuals who did not have previous blood patch. These authors alsoreviewed 17 patients who had dural puncture without subsequent blood patch; in only65% was subsequent epidural anaesthesia successful.105 A study by Hebl et al failed todemonstrate any difference in success of subsequent epidural anaesthesia betweenpatients who received epidural anaesthesia following blood patch (29 cases) versusindividuals who had not undergone blood patch procedures. This corresponds tofindings of other investigators.106–108 Thus, we believe that there is little reason not tooffer epidural anaesthesia to a patient who has previously undergone epidural bloodpatch. Despite concerns of meningitis, arachnoiditis or CNS spread of HIV infectionoccurring after a patch, to date these have not been demonstrated to occur followingan AEBP.109

PREVENTION

Using small-gauge, pencil-point spinal needles for spinal anaesthesia minimizes thelikelihood of PDPHA.11,12,110 When using a Quincke point needle, aligning the spinalneedle bevel longitudinally so as to separate the longitudinal dural fibres, rather thanshearing the fibres, further minimizes dural leakage of CSF.111 The use of a paramedianapproach to the subarachnoid space has been touted as a means of reducing PDPHA.112

Avoiding multiple puncture holes in the dura mater in also recommended to avoidPDPHA. There is little advantage in using small (25–29 gauge) Quincke point needlescompared with 24-gauge pencil-point needles.111,113 –115 In summary, most authoritiessuggest using smaller-gauge, non-cutting needles, minimizing the number of punctureattempts, and aggressive follow-up of the patients to detect PDPHA when duralpuncture (intentional or unintentional) does occur, so that early treatment can beinstituted.

PROPHYLACTIC BLOOD PATCH

Some have suggested that blood patch be performed as a prophylactic measure (i.e.prior to the development of a headache) in cases of unintended dural punctureoccurring after the insertion of 17–18-gauge epidural needles into the subarachnoidspace, particularly when there has been loss of considerable quantities of CSF. To date,there have been no large, prospective studies to advocate for this practice, although it iswidely practiced. Existing studies regarding prophylactic epidural blood patch are limitedby small patient numbers.116,117 Also, there have been limitations suggested by thesmall volumes of blood injected in some reviews.118 If one chooses to performprophylactic AEBP, some caveats are in order; one should avoid prophylactic AEBP


immediately following LA epidural top-off dose administration, because the resultanthigh epidural pressure has resulted in at least one case of total spinal block.119 Also, thepresence of LA in the epidural space may theoretically interfere with subsequent bloodclot formation.120 There are strong advocates for prophylactic blood patch, particularlyif an epidural catheter is in place, avoiding the need for another epiduralpuncture.121–123 Given the low additional risk, as long as strict sterile technique isemployed, prophylactic epidural blood patch in high-risk patients (e.g. young, post-partum, large-gauge needle puncture) would seem to be worthwhile and is certainlyjustifiable. However, this decision needs to be individualized to the patient.

SUMMARY AND CONCLUSIONS

Post-dural puncture headache (PDPHA) continues to be a vexing problem for patientsand anaesthesiologists. Avoidance of this problem is the best treatment strategem.Using small-gauge (e.g. 24- or 25-gauge) pencil-point needles has been shown tominimize PDPHA. Early diagnosis, by eliciting a history of a postural headache followinga lumbar puncture, and by ruling out other causes of headache, and early treatmentwith AEBP has been shown to be the most effective treatment of PDPHA. This is mostimportant in patients younger than 50 years of age, postpartum patients, and thosewhose dural puncture was performed with large ($22-gauge) needles. Although thenatural history of untreated PDPHA is gradual resolution of the headache over 5–7days, chronic PDPHA has been reported. The authors recommend using 24-gaugepencil-point needles for spinal anaesthesia and minimizing the number of duralpunctures to reduce the risk of PDPHA in patients at high risk for this complication.

Practice points

† using small-gauge pencil-point needles can minimize the risk of PDPHA. Theauthors recommend a 24-gauge Sprotte or Whitacre needle. The paramedianapproach may have a lower risk of PDPHA than a midline approach

† if a headache occurs in a patient following dural puncture, a careful history canrule-in or rule-out PDPHA. The sine qua non of a PDPHA is a positional changein the headache. In high-risk patients (young, postpartum, large-gauge duralpuncture), an AEBP should be performed within 24–48 h of onset of headache.In a patient with an epidural catheter in place, consideration should be given toprophylactic epidural blood patch

† alternatives to AEBP are not nearly as effective, although short-term relief fromheadache is often seen. The optimum volume of epidural blood appears to be15–20 ml. Treatment failures do occur, and chronic PDPHA has been reported.Therefore, follow-up of the patient is important

Research agenda

† the optimum timing of epidural blood patch with respect to dural puncture hasnot been determined

† the optimum treatment of chronic PDPHA has not been determined


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