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Arch Gynecol Obstet (2007) 275: 125–131 DOI 10.1007/s00404-006-0146-y

ORIGINAL ARTICLE

ORIGINAL ARTICLE

Krzysztof M. Kuczkowski

The management of accidental dural puncture in pregnant women:

what does an obstetrician need to know?

Received: 8 February 2006 / Accepted: 10 February 2006 / Published online: 11 March 2006 Springer-Verlag 2006

Abstract Post-dural puncture headache (PDPH) also known as spinal (or post-spinal) headache still remains a disabling complication of needle insertion into the sub- arachnoid space. Pregnant women are at particular risk of dural puncture, and the subsequent headache, be- cause of sex, young age, and the widespread application of regional anesthesia. Accidental dural puncture com- plicating epidural anesthesia varies in incidence from 0.19 to 4.4%. The incidence of epidural needle-induced PDPH headache in pregnant women has been reported to range 76–85%. The classic symptoms of PDPH con- sist of photophobia, nausea, vomiting, neck stiffness, tinnitus, diplopia, and dizziness in addition to the often, severe cephalgia. This article reviews the current litera- ture on the pathophysiology, incidence, prevention, and treatment of PDPH in pregnant women.

Keywords Pregnancy Æ Obstetric anesthesia Æ Labor analgesia Æ Epidural Æ Complications Æ Dural puncture Æ Post-dural puncture headache Æ Prevention

Introduction

Epidural analgesia is widely considered as the most effective method of providing pain relief during labor, and the number of women receiving epidural analgesia for labor and delivery is increasing worldwide [13]. Post-dural puncture headache (PDPH) also known as spinal (or post-spinal) headache still remains a disabling complication of needle insertion into the subarachnoid space. Pregnant women are at particular risk of dural puncture and the subsequent headache, because of sex,

K. M. Kuczkowski Departments of Anesthesiology and Reproductive Medicine, UCSD Medical Center, University of California, 200 West Arbor Drive, San Diego, CA 92103-8770, USA E-mail: kkuczkowski@ucsd.edu Tel.: +1-619-5433247 Fax: +1-619-5435424

young age, and the widespread (and increasing) appli- cation of regional anesthesia [4, 5]. Recent advances in spinal needles design have sub- stantially decreased the incidence of PDPH after spinal anesthesia and now accidental dural puncture with a large gauge epidural needle has become the most com- mon cause of PDPH in pregnant women. Accidental dural puncture complicating epidural anesthesia varies in incidence from 0.19 to 4.4% [4, 5]. The incidence of epidural needle-induced PDPH headache in pregnant women has been reported to range 76–85%. Post-dural puncture headache typically occurs on the first or second day after dural puncture. In the hospital settings the diagnosis, prevention, and treatment of a PDPH is usually be the responsibility of the obstetric anesthesiologist, however it is important for the obste- trician to be familiar with the incidence, pathophysiol- ogy, symptoms, prevention, and treatment of this complication. As in many countries post-partum women are being discharged into the community sooner after delivery complications arising from labor analgesia (including PDPH) may first present to the obstetricians during follow up appointments, and therefore the obstetrician should be familiar with their clinical course and therapeutic options available.

History

One of the milestones in the development of spinal anesthesia (and first descriptions of its complications) was the work of the German surgeon Augustus Bier. Using himself as subject, more than 100-year ago, Bier demonstrated spinal anesthesia (with subarachnoid injection of local anesthetic—cocaine) 1 day, and spinal headache widely known today as PDPH the following morning [6]. Bier surmised that the headache was attributed to continuous loss (leakage) of cerebrospinal fluid (CSF) from the subarachnoid space (through dural tears). In 1899, Bier published six case reports of patients undergoing lower extremities surgery under

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spinal anesthesia with cocaine [6]. The needles used were described as large gauge Quincke type spinal needles. By the early 1900s, there were numerous reports in the medical literature of the applications (and compli- cations) of spinal anesthesia with large gauge spinal needles, with the average incidence of PDPH exceeding 50% of subjects [7, 8]. In 1951, Whitacre developed the pencil-point needle, which led to a significant reduction in the incidence of PDPH. Clinical experience and re- search over the last 30 years has shown that use of small- gauge spinal needles, particularly of the pencil-point design, is associated with a lower risk of PDPH than traditional cutting point needle tips (Quincke-point needles) [911]. It has also been established that patient’s age, and sex are important determinants of the incidence of PDPH [8, 12, 13].

Pathophysiology

Bier is credited with the first description of the patho- physiology (leakage of CSF) of PDPH [6], and today there is no doubt that loss of CSF initiates the syndrome [7]. The classical description of the spinal dura mater (a dense, connective tissue layer surrounding the spinal cord) is of elastic and collagen fibers running it the longitudinal direction. Clinical studies based on this theory confirmed that PDPH was more likely when the cutting spinal needle was oriented perpendicular to the direction of the spinal dura fibers [7]. However, recent electron microscopic studies (which describe the dura mater as consisting of collages fibers arranged in several layers parallel to the surface) have challenged this clas- sical description of the anatomy of the spinal dura mater [8]. These new studies revealed that each layer of the dura consists of both collagen and elastic fibers that do not demonstrate any specific orientation. In 1764, Cotugno first described the presence of a collection of fluid around the brain and spinal cord. In 1825, Magendie discovered that this fluid circulated around the brain and spinal cord [14]. The total volume of CSF in the adult subject is approximately 150 ml, 50% of which is within the cranium. About 500 ml of CSF is produced per day [7]. Production of CSF occurs primarily in the choroid plexus, but there is growing evidence of extrachoroidal CSF production [13, 15]. The CSF pressure in the lumbar region in the supine position ranges between 5 and 15 cm H 2 O, however, on assuming the vertical position, this pressure increases to over 40 cm H 2 O. Although the loss of CSF and subsequent decrease of the CSF pressure is not disputed, the actual mechanism producing the PDPH remains unclear [7, 8, 1626]. The widely accepted theory explaining the pathophysiology of PDPH is based on the assumption of persistent leakage of CSF through the hole made by the spinal or epidural needle and decrease in CSF volume or pressure, or both, which leads to shifts of intracranial contents

and traction on pain sensitive structures [7, 8]. Loss of CSF leads to intracranial hypotension and a demon- strable reduction in CSF volume and pressure. As a result of continuous CSF loss/leakage the adult subarachnoid pressure of 5–15 cm H 2 O may be reduced to 4 cm H 2 O or less. The rate of CSF loss through the dural hole is generally greater than the rate of CSF production, particularly with needle sizes greater than 25 GA. The sudden decrease in the CSF volume may also activate adenosine receptors, thus producing arte- rial and venous vasodilatation and subsequently clinical symptoms of PDPH. Richardson et al. [26] reported that CSF density in pregnant women, who are particularly susceptible to PDPH, is significantly lower than the CSF density in non-pregnant subjects.

Incidence

Post-dural puncture headache is an iatrogenic compli- cation of neuraxial blocks for labor analgesia. There is considerable variability in the incidence of PDPH, which is affected by several factors including age, gender, pregnancy, and needle type (design) and size (Table 1) [8, 12, 13]. In 1989, the incidence of PDPH attributable to the use of large gauge, cutting edge spinal needles was nearly 70%. Over time the use of fine gauge spinal has produced a great reduction in the incidence of this complication [8]. The clinical signs of PDPH may be observed following intentional dural puncture associ- ated with the administration of spinal anesthesia or combined spinal-epidural anesthesia or unintentional dural puncture during epidural anesthesia [27]. Spinal anesthesia is a popular anesthetic technique for Cesarean delivery. The incidence of PDPH after spinal anesthesia varies greatly between studies. The incidence is 40% with a 20 GA needle; 25% with a 25 GA needle; 2–10% with a 26 GA needle, and less than 2% with a 29 GA needle [8]. However, technical difficulties are common when spinal block is attempted with needles of 29 GA or smaller. The principal factor responsible for the development of PDPH is the size of the dural perforation. Other factors such as the shape of the dural perforation and the orientation of the spinal needle have a less significant role. Therefore, a balance has to be struck between the risk of dural puncture and PDPH and technical failure [7]. Most experts agree that 25–27 GA needles probably represent the optimum needle size for spinal anesthesia. Clinical and laboratory studies confirmed that pencil-point needles produce fewer PDPHs than cutting edge spinal needles. As previously stated, the pregnant woman is at par- ticular risk of dural puncture (and the subsequent PDPH) because of sex, young age, and the widespread application of neuraxial anesthesia [13, 18, 2022, 2832]. Loss of resistance to air confers a higher risk of dural puncture than loss of resistance to fluid (normal saline) [18]. Unintentional dural puncture complicating

Table 1 Factors affecting the incidence of PDPH

1

Age

2

Gender

3

Pregnancy

4

Needle size

5

Needle design

6

Number of attempts

7

History of previous PDPH

epidural anesthesia vary in incidence from 0.19 to 4.4%. The incidence of epidural needle-induced PDPH in parturients has been reported to range 76–85% [13]. It has been suggested that the incidence of unintentional dural puncture during epidural anesthesia is inversely related to operator experience.

Symptoms

Post-partum headache in a parturient almost always raises concerns about accidental dural puncture during administration of labor analgesia. PDPH is a well- known complication of procedures in which the dura mater of the spinal cord is punctured. The classic symptoms of PDPH consist of photophobia, nausea, vomiting, neck stiffness, tinnitus, diplopia, and dizziness in addition to the often, severe cephalgia (Table 2). It may seem more accurate to call the clinical spectrum of symptoms that follow dural puncture, the post-dural puncture syndrome, rather than PDPH, which falsely implies the headache as the only manifestation [13]. The headache is usually severe and throbbing, frontal in origin, with radiation to the occiput, and is exacerbated by sitting or standing. The positional nature of the headache and dramatic improvement on assuming the supine position remains the standard diagnostic crite- rion for this condition. The differential diagnosis of PDPH is often clear from the history of dural puncture and the presence of a severe postural headache. How- ever, it is important to consider alternative causes of headache (Table 3).

Prevention

In general, the larger the gauge of the needle breaching the dura mater, the more likely it is for the symptoms of

Table 2 Symptoms of PDPH in pregnant women

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Table 3 Differential diagnosis of PDPH in pregnant women

1

Post-dural puncture headache

2

Non-specific headache

3

Migraine

4

Caffeine-withdrawal headache

5

Meningitis

6

Sinus headache

7

Pregnancy induced hypertension

8

Drugs (amphetamine, cocaine)

9

Pneumocephalus-related headache

10

Cerebral vein thrombosis

11

Subdural hematoma

12

Subarachnoid hematoma

13

Brain tumor

14

Lactation headache

PDPH to appear. The incidence of epidural needle-in- duced PDPH in pregnant women following dural puncture with a large bore (e.g., 18 GA) needle has been reported to range 76–85% [13]. Although a few mea- sures have been proposed to prevent PDPH (subarach- noid injection of normal saline, insertion of the epidural catheter into the subarachnoid space through the dural hole), none have been shown to work with certainty to date [7, 8, 12, 19, 24, 2835]. In 2003, Kuczkowski and Benumof [15] reported that following accidental dural puncture with an 18 GA epidural needle in pregnant women, sequential (Table 4) (1) injection of the CSF in the glass syringe back into the subarachnoid space through the epidural needle, (2) insertion of a epidural catheter into the subarachnoid space, (3) injection of small amount of preservative free saline (3–5 ml) into the subarachnoid space through the subarachnoid catheter, (4) administration of bolus and then continuous intrathecal labor analgesia, and (5) leaving the catheter in situ in the subarachnoid space for a total of 12–20 h decreased the incidence of PDPH from 76–85 to 14% [15]. Since their original report [15] the authors encoun- tered (2004–2005) eight more pregnant women [16] in whom the performance of epidural analgesia was com- plicated by an accidental dural puncture with an 18 GA epidural needle. In all eight additional cases, the acci- dental dural puncture was followed by the same five maneuvers and no PDPH was reported in any of these patients. These additional eight cases combined with the original seven patients (N=15) suggest that following an accidental dural puncture with an 18 GA epidural nee-

1

Nausea

Table 4 Prevention of PDPH in pregnant women

2

Vomiting

 

3

Neck stiffness

1 Injecting the CSF in the glass syringe back into the subarachnoid space through the epidural needle

4

Photophobia

5

Difficulty in accommodation

2 Passing the epidural catheter through the dural hole into the subarachnoid space

6

Diplopia

7

Dizziness

3 Injecting of 3–5 ml of preservative free saline into the subarachnoid space through the subarachnoid catheter

8

Tinnitus

9

Hyperacusis

4 Administering bolus and then continuous intrathecal labor analgesia through the subarachnoid catheter

10

Hearing loss

11

Cephalgia

5 Leaving the subarachnoid catheter in situ for a total of 12–20 h

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dle in parturients, sequential performance of these five maneuvers decreased the incidence of PDPH from 76–85% [13] to 6.6% (PDPH occurred only in one out of our total number of 15 pregnant patients) [16]. All of these five components were aimed at maintaining CSF volume. The replacement of the escaped CSF volume by injecting the small amount of CSF filling the syringe back into the subarachnoid space and 3–5 ml of pre- servative-free normal saline seems a low risk maneuver; however, the replacement of this small amount of CSF volume seems of questionable significance when one takes into consideration the total volume of CSF (150 ml) and the rate of production of CSF (0.35 ml/ min) in the subarachnoid space. Nevertheless, other studies did find that the immediate injection of 10 ml intrathecal normal saline through the epidural needle after a dural puncture reduced the incidence of PDPH from 62 to 32% [19]. Four other reports have suggested that leaving the catheter in the dural hole for several hours may decrease the incidence of PDPH [19, 2830]. First, Cohen et al. reported a 20% incidence of PDPH in a group of ten pregnant women receiving continuous spinal analgesia via a 20 GA catheter inserted after accidental dural puncture [28]. Second, Dennehy et al. found in three patients that immediate insertion of a subarachnoid catheter after accidental dural puncture followed by intermittent injections of local anesthetics with opioids during labor and delivery prevented PDPH in all three patients [29]. Third, Cohen et al. in a retrospective study found in 13 Cesarean section patients a zero incidence of PDPH when accidental dural puncture was followed post-operatively by continuous spinal analgesia through a subarachnoid catheter [30]. Fourth, Charsley et al. found in six patients that subarachnoid catheter place- ment following accidental dural puncture, and injection of 10 ml of normal saline prior to removal of the sub- arachnoid catheter effectively prevented PDPH in all six patients [19]. These four reports are supported by the observation that the incidence of PDPH is near zero after continuous spinal anesthesia in non-pregnant pa- tients [32]. Two different mechanisms to explain the decreased incidence of PDPH after subarachnoid catheter insertion have been postulated; first, the intrathecal catheter ‘‘plugs’’ the dural tear, decreasing or stopping the efflux of CSF from the subarachnoid space [29], and second, inserting a catheter in the dural hole leads to an inflammatory reaction, with edema or fibrin exudates subsequently sealing the dural tear after catheter re- moval [34]. Others described formation of fibrin around the ‘‘chronic’’ (at least 5–7 days) intrathecal catheter at the dural tear in an experimental animal study [35]. Thus, in addition to directly plugging the dural hole, the long-term presence of the intrathecal catheter may also promote an inflammatory response around the dural hole, which facilitates dural closure after catheter re- moval.

At this time it is difficult to speculate on the relative importance of the five maneuvers originally described by Kuczkowski and Benumof [15] in decreasing the incidence of PDPH. The authors speculated that the immediate insertion of the epidural catheter into the subarachnoid space (‘‘short-term plugging’’) with careful attention to minimize additional CSF loss and the prolonged presence of the catheter in the sub- arachnoid space (‘‘long-term plugging’’), seemed the most likely mechanisms of prevention of continuous leakage of CSF and subsequent development of PDPH [15, 16]. Canovas et al. [4] attempted to assess the effectiveness of continuous subarachnoid analgesia for labor and as prophylaxis for (PDPH) in 12 pregnant women who suffered accidental dural puncture. The authors con- cluded that continuous subarachnoid analgesia after accidental dural puncture was first, a safe way to provide analgesia during labor, and second, it reduced the inci- dence of PDPH [4]. Further studies are needed.

Treatment

Theophylline, caffeine, sumatriptan, epidural saline, epidural dextran, and epidural blood patch (EBP) in- clude some of the current treatment modalities for PDPH (Table 5). However, only the EBP seems to have apparent benefits [8, 13, 15, 18].

Psychological

Post-dural puncture headache during the post-partum period is almost always a complication of neuraxial anesthesia. The parturient is usually aware that her headache is an iatrogenic problem, and she may be an- gry, resentful and/or depressed [7]. Headache may make it difficult to care for the newborn and to interact with other family members. It is therefore important to give the parturient a thorough explanation of the reason for the headache, the anticipated time course, and the therapeutic options available [8]. Additionally a severe PDPH may delay discharge from the hospital and may have economic consequences (increased cost). It is essential to discuss the EBP as a therapeutic option early. In the US PDPH associated with regional anes- thesia is the third most common reason for litigation in the obstetric anesthesia database.

Posture

The final diagnosis of PDPH requires demonstration of the postural component of the headache; partial relief in horizontal position and worsening on assumption of the vertical position. Therefore supine position may be preferred by patients and should be recommended.

Hydration

Increased oral hydration (preferably with caffeinated beverages) remains a popular first step therapy for PDPH. However, there is little (if any) evidence that this increased fluid intake has any therapeutic effect [8]. Nevertheless, no parturient with the diagnosis of PDPH should restrict her oral fluid intake and become dehy- drated.

Caffeine

Caffeine is a central nervous system stimulant, which produces cerebral vasoconstriction. It is available in an oral and intravenous form. The oral preparation is well absorbed from oral mucosa with peak blood levels reached in approximately 30 min [8]. Caffeine easily crosses the blood-brain barrier and has a long half-life of 3–8 h. Several studies however, showed that the benefi- cial effect of caffeine might be transient. Caffeine ap- pears in breast milk in very small amounts.

Theophylline

Theophylline is another member of the methylxantine family available in long-acting oral preparations, which might be a suitable alternative to caffeine for the treat- ment of PDPH in pregnant women (Table 5). Theoph- ylline is a potent cerebral vessel vasoconstrictor.

Sumatriptan

Sumatriptan is a serotonin agonist that affects predom- inantly type 1D receptors. It promotes cerebral vaso- constriction in a similar way to caffeine. Sumatriptan has been advocated to the treatment of migraine and recently, for PDPH [8, 13, 18]. This drug is expensive and must be given by subcutaneous injections.

Adrenocorticotropic hormone

The proposed mechanisms of action of the adrenocor- ticotropic hormone (ACTH) include increased beta-

Table 5 Treatment of PDPH in pregnant women

1

Psychological support

2

Posture

3

Hydration

4

Caffeine

5

Theophylline

6

Sumatriptan

7

Adrenocorticotropic hormone

8

Abdominal binder

9

Epidural saline

10

Epidural dextran

11

Subarachnoid catheter

12

Epidural blood patch

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endorphin levels and increased intravascular volume. However, this therapy is not widely used in clinical practice and deserves further investigation.

Abdominal binder

Abdominal binder causes increases in intra-abdominal pressures, and subsequently increases in CSF pressures. This may reduce the symptoms of PDPH.

Epidural saline

It has been speculated that an epidural injection of saline would, in theory, produce the same ‘‘mass effect’’ as autologous EBP, and restore normal CSF dynamics. Advocates of an epidural saline infusion (or boluses) maintain that the lumbar injection of saline raises epi- dural and subarachnoid pressures [19]. However, to date no studies have demonstrated either a sustained rise in CSF pressure or accelerated closure of the dural hole (tear) following administration of epidural saline [8]. It is therefore difficult to conclude from the evidence that epidural saline administration will restore normal CSF dynamics.

Epidural dextran

It has been suggested that the high viscosity and high molecular weight of dextran may slow its removal from the epidural space. However, it is unlikely that dextran would act any differently to normal saline in the epidural space [8, 13]. Any pressure increase with the epidural and subarachnoid space would, like saline, be short- lived. Additionally, it has been reported that dextran does not demonstrate any inflammatory response that would promote the dura healing process.

Subarachnoid catheters

It has been suggested that placement of a subarachnoid catheter through the dural hole following an accidental dural puncture with a large gauge epidural needle, may provoke an inflammatory reaction that will seal the puncture site [15, 19, 2830, 3235]. Histological animal and human studies with long-term subarachnoid cathe- ters confirm the presence of an inflammatory reaction at the catheter insertion site. Further studies are needed [36, 37].

Epidural blood patch

The EBP for the treatment of PDPH was introduced by Gormley in 1960 [38]. Two theories have been proposed

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to explain EBP efficiency in the treatment of PDPH [13, 15, 23, 25]. The first theory suggests that the autologous blood injected in the epidural space forms a clot, which adheres to the dura mater and directly patches the hole. The second theory suggests that the volume of blood injected in the epidural space increases CSF pressure, thus reducing traction of pain sensitive brain structures, leading to relief of symptoms. The optimal volume of blood to be injected in the epidural space remains con- troversial. At the University of California, San Diego the optimum volume of autologous blood has been shown to be 14–20 ml for most adult patients (K.M. Kuczkowski, Unpublished data). Complications of autologous EBP are rare, and a success rate is up to

94%.

Conclusion

Epidural analgesia is widely considered as the most effective method of providing pain relief during labor, and the number of women receiving epidural analgesia for labor and delivery is increasing worldwide [13]. Pregnant women are at particular risk of dural puncture, and the subsequent headache, because of sex, young age, and the widespread application of regional anesthesia [7, 8]. The diagnosis, prevention and treatment of a PDPH in the labor and delivery suite is usually the responsi- bility of the obstetric anesthesiologist, however it is paramount for the obstetrician to be familiar with the clinical course of this syndrome, and the usual treatment strategies. The novel technique of preventing the PDPH (by maintaining the CSF volume) introduced by Kucz- kowski and Benumof [15, 16] is an intriguing one, however, further prospective, randomized and blinded studies to examine its clinical significance are indicated. Several treatment modalities for PDPH are available, however, only the EBP seems to have apparent benefits [13]. Before any treatment is initiated it is important to consider alternative causes of peripatum headache.

References

1. Kuczkowski KM (2004) Ambulatory labor analgesia: what does an obstetrician need to know? Acta Obstet Gynecol Scand

83:415–424

2. Practice Guidelines for Obstetrical Anesthesia (1998) The task force on obstetrical anesthesia. House of Delegates, American society of anesthesiologists, 520 Northwest Highway, Park Ridge, IL

3. Kuczkowski KM (2003) New and challenging problems (and solutions) in obstetric anesthesia: introduction. J Clin Anesth

15:165

4. Canovas L, Morillas P, Castro M et al (2005) Treatment of accidental dural puncture during obstetric epidural analgesia. Rev Esp Anestesiol Reanim 52:263–266

5. Kuczkowski KM, Fernandez CL (2005) Accidental dural puncture in an obstetric patient, continuous spinal labor analgesia and post-dural puncture headache. Rev Esp Aneste- siol Reanim 52:581–582

6.

Bier A (1989) Versuche uber Cocainisirung des Ruken Markes. Dtsch Z Chir 51:361–369

7.

Kuczkowski KM (2004) Post-dural puncture headache in the obstetric patient: an old problem—new solutions. Minerva Anestesiol 70:823–830

8.

Turnbull DK, Shepherd DB (2003) Post-dural puncture head- ache: pathogenesis, prevention and treatment. Br J Anaesth

91:718–729

9.

Hafer J, Rupp D, Wollbruck M et al (1997) The effect of needle type and immobilization on postspinal headache. Anaesthesist

46:860–866

10.

Seupaul RA, Somerville GG, Viscusi C et al (2005) Prevalence

of

postdural puncture headache after ED performed lumbar

puncture. Am J Emerg Med 23:913–915

11.

Birnbach DJ, Kuroda MM, Sternman D, Thys DM (2001) Use

of

atraumatic spinal needles among neurologists in the United

States. Headache 41:385–390

12.

Brownridge P (1983) The management of headache following accidental dural puncture in obstetric patients. Anaesth Inten- sive Care 11:4–15

13.

Collier CB (2000) Complications of regional anesthesia. In:

Birnbach DJ, Gatt SP, Datta S (eds) Textbook of obstetric anesthesia. Churchill Livingstone, NY, pp 504–523

14.

Calthorpe N (2004) The history of spinal needles: getting to the point. Anaesthesia 59:1231–1241

15.

Kuczkowski KM, Benumof JL (2003) Decrease in the incidence of post-dural puncture headache: maintaining CSF volume. Acta Anaesthesiol Scand 47:98–100

16.

Kuczkowski KM (2005) Decreasing the incidence of post-dural puncture headache: an update. Acta Anaesthesiol Scand 49:594

17.

Sandesc D, Lupei MI, Sirbu C et al (2005) Conventional treatment or epidural blood patch for the treatment of different etiologies of post dural puncture headache. Acta Anaesthesiol Belg 56:265–269

18.

Kuczkowski KM (2003) Post dural puncture headache, intra- cranial air and obstetric anesthesia. Anaesthesist 52:798–800

19.

Charsley MM, Abram SE (2001) The injection of intrathecal normal saline reduces the severity of postdural puncture headache. Reg Anesth Pain Med 26:301–305

20.

Kuczkowski KM, Benumof JL (2003) Once a post-dural puncture headache patient always post-dural puncture head- ache patient? Acta Anaesthesiol Belg 54:167–168

21.

Kuczkowski KM (2005) Once a post-dural puncture headache patient—always post-dural puncture headache patient: an up- date. Acta Anaesthesiol Belg 56:23

22.

Choi PT, Galinski SE, Lucas S et al (2002) Examining the evidence in anesthesia literature: a survey and evaluation of obstetrical postdural puncture headache reports. Can J Ana- esth 49:49–56

23.

Ferre JP, Gentili ME (1999) Seven months’ delay for epidural blood patch in post-dural puncture headache. Eur J Anaes- thesiol 16:257–258

24.

Flaatten H, Felthaus J, Larsen R et al (1998) Postural post- dural puncture headache after spinal and epidural anaesthesia.

A

double blind study. Acta Anaesthesiol Scand 42:759–764

25.

Taivainen T, Pitkanen M, Tuominen M, Rosenberg PH (1993) Efficacy of epidural blood patch for postdural puncture head- ache. Acta Anaesthesiol Scan 37:702–705

26.

Richardson MG, Wissler R (1996) Density of human cerebro- spinal fluid. Reg Anesth 21:29

27.

Kuczkowski KM (2006) The management of accidental dural puncture. Anaesthesia 61:68

28.

Cohen S, Daitch JS, Goldiner PL (1989) An alternative method for management of accidental dural puncture for labor and delivery. Anesthesiology 70:164–165

29.

Dennehy KC, Rosaeg OP (1998) Intrathecal catheter insertion during labour reduces the risk of post-dural puncture headache. Can J Anaesth 45:42–45

30.

Cohen S, Amar D, Pantuck EJJ et al (1994) Decreased inci- dence of headache after accidental dural puncture in Cesarean delivery patients receiving continuous postoperative intrathecal analgesia. Acta Anaesthesiol Scand 38:716–718

31. Norris MC, Leighton BL (1990) Continuous spinal anesthesia after unintentional dural puncture in parturients. Reg Anesth

15:285–287

32. Peterson DO, Borup JL, Chestnut JS (1983) Continuous spinal anesthesia, case review and discussion. Reg Anesth 8:109–111

33. Kallos T, Smith TC (1972) Continuous spinal anesthesia with hypobaric tetracaine for hip surgery in lateral decubitus. An- esth Analg 51:766–773

34. Denny N, Masters R, Pearson D et al (1987) Postdural punc- ture headache after continuous spinal anesthesia. Anesth Analg

66:791–794

35. Yaksh TL, Noueihed RY, Durant PAC (1986) Studies of the pharmacology and pathology of intrathecally administered

131

4-anilinopeperidine analogues and morphine in the rat and cat. Anesthesiology 64:54–66

36. Chan BO, Paech MJ (2004) Persistent cerebrospinal fluid leak:

a complication of the combined spinal-epidural technique. Anesth Analg 98:828–830

37. Kuczkowski KM (2004) Does an epidural catheter impede or stimulate dural inflammatory response and normal dural clo- sure after dural puncture? Anesth Analg 99:1266

38. Gormley JB (1960) Treatment of postspinal headache. Anes- thesiology 21:565–566