Manejo de Cefalea Postpuncion Ginecologia y Obst

8/3/2019 Manejo de Cefalea Postpuncion Ginecologia y Obst

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O R IGINA L A R T IC L E

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) alsoknown as spinal (or post-spinal) headache still remains adisabling 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 applicationof regional anesthesia. Accidental dural puncture com-plicating epidural anesthesia varies in incidence from0.19 to 4.4%. The incidence of epidural needle-inducedPDPH headache in pregnant women has been reportedto range 7685%. 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, andtreatment of PDPH in pregnant women.

Keywords Pregnancy

Obstetric anesthesia

Laboranalgesia Epidural Complications Dural puncture Post-dural puncture headache Prevention

Introduction

Epidural analgesia is widely considered as the mosteffective method of providing pain relief during labor,and the number of women receiving epidural analgesiafor labor and delivery is increasing worldwide [13].Post-dural puncture headache (PDPH) also known asspinal (or post-spinal) headache still remains a disabling

complication of needle insertion into the subarachnoidspace. Pregnant women are at particular risk of duralpuncture and the subsequent headache, because of sex,

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 alarge gauge epidural needle has become the most com-mon cause of PDPH in pregnant women. Accidentaldural puncture complicating epidural anesthesia variesin incidence from 0.19 to 4.4% [4, 5]. The incidence ofepidural needle-induced PDPH headache in pregnantwomen has been reported to range 7685%.

Post-dural puncture headache typically occurs on thefirst or second day after dural puncture. In the hospitalsettings the diagnosis, prevention, and treatment of aPDPH is usually be the responsibility of the obstetricanesthesiologist, however it is important for the obste-trician to be familiar with the incidence, pathophysiol-

ogy, symptoms, prevention, and treatment of thiscomplication. As in many countries post-partum womenare being discharged into the community sooner afterdelivery complications arising from labor analgesia(including PDPH) may first present to the obstetriciansduring follow up appointments, and therefore theobstetrician should be familiar with their clinical courseand 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, Bierdemonstrated spinal anesthesia (with subarachnoidinjection of local anestheticcocaine) 1 day, and spinalheadache widely known today as PDPH the followingmorning [6]. Bier surmised that the headache wasattributed to continuous loss (leakage) of cerebrospinalfluid (CSF) from the subarachnoid space (through duraltears). In 1899, Bier published six case reports ofpatients undergoing lower extremities surgery under

K. M. KuczkowskiDepartments of Anesthesiology and Reproductive Medicine,UCSD Medical Center, University of California,200 West Arbor Drive, San Diego, CA 92103-8770, USAE-mail: [email protected].: +1-619-5433247Fax: +1-619-5435424

Arch Gynecol Obstet (2007) 275: 125131DOI 10.1007/s00404-006-0146-y


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spinal anesthesia with cocaine [6]. The needles used weredescribed as large gauge Quincke type spinal needles.

By the early 1900s, there were numerous reports inthe medical literature of the applications (and compli-cations) of spinal anesthesia with large gauge spinalneedles, with the average incidence of PDPH exceeding50% of subjects [7, 8]. In 1951, Whitacre developed thepencil-point needle, which led to a significant reductionin 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-pointdesign, is associated with a lower risk of PDPH thantraditional cutting point needle tips (Quincke-pointneedles) [911]. It has also been established that patientsage, and sex are important determinants of the incidenceof 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 (adense, connective tissue layer surrounding the spinalcord) is of elastic and collagen fibers running it thelongitudinal direction. Clinical studies based on thistheory confirmed that PDPH was more likely when thecutting spinal needle was oriented perpendicular to thedirection of the spinal dura fibers [7]. However, recentelectron microscopic studies (which describe the duramater as consisting of collages fibers arranged in severallayers 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 donot demonstrate any specific orientation.

In 1764, Cotugno first described the presence of acollection of fluid around the brain and spinal cord. In1825, Magendie discovered that this fluid circulatedaround the brain and spinal cord [14]. The total volumeof CSF in the adult subject is approximately 150 ml,50% of which is within the cranium. About 500 ml ofCSF is produced per day [7]. Production of CSF occursprimarily in the choroid plexus, but there is growingevidence of extrachoroidal CSF production [13, 15]. TheCSF pressure in the lumbar region in the supine positionranges between 5 and 15 cm H2O, however, on assuming

the vertical position, this pressure increases to over40 cm H2O.

Although the loss of CSF and subsequent decrease ofthe CSF pressure is not disputed, the actual mechanismproducing the PDPH remains unclear [7, 8, 1626]. Thewidely accepted theory explaining the pathophysiologyof PDPH is based on the assumption of persistentleakage of CSF through the hole made by the spinal orepidural 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 ofCSF leads to intracranial hypotension and a demon-strable reduction in CSF volume and pressure.

As a result of continuous CSF loss/leakage the adultsubarachnoid pressure of 515 cm H2O may be reducedto 4 cm H2O or less. The rate of CSF loss through thedural hole is generally greater than the rate of CSFproduction, particularly with needle sizes greater than25 GA. The sudden decrease in the CSF volume mayalso activate adenosine receptors, thus producing arte-rial and venous vasodilatation and subsequently clinicalsymptoms of PDPH. Richardson et al. [26] reported thatCSF density in pregnant women, who are particularlysusceptible to PDPH, is significantly lower than the CSFdensity in non-pregnant subjects.

Incidence

Post-dural puncture headache is an iatrogenic compli-cation of neuraxial blocks for labor analgesia. There isconsiderable 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 attributableto the use of large gauge, cutting edge spinal needles wasnearly 70%. Over time the use of fine gauge spinal hasproduced a great reduction in the incidence of thiscomplication [8]. The clinical signs of PDPH may beobserved following intentional dural puncture associ-ated with the administration of spinal anesthesia orcombined spinal-epidural anesthesia or unintentionaldural puncture during epidural anesthesia [27].

Spinal anesthesia is a popular anesthetic techniquefor Cesarean delivery. The incidence of PDPH after

spinal anesthesia varies greatly between studies. Theincidence is 40% with a 20 GA needle; 25% with a25 GA needle; 210% with a 26 GA needle, and lessthan 2% with a 29 GA needle [8]. However, technicaldifficulties are common when spinal block is attemptedwith needles of 29 GA or smaller. The principal factorresponsible for the development of PDPH is the size ofthe dural perforation. Other factors such as the shape ofthe dural perforation and the orientation of the spinalneedle have a less significant role. Therefore, a balancehas to be struck between the risk of dural puncture andPDPH and technical failure [7]. Most experts agree that2527 GA needles probably represent the optimum

needle size for spinal anesthesia. Clinical and laboratorystudies confirmed that pencil-point needles producefewer PDPHs than cutting edge spinal needles.

As previously stated, the pregnant woman is at par-ticular risk of dural puncture (and the subsequentPDPH) because of sex, young age, and the widespreadapplication of neuraxial anesthesia [13, 18, 2022, 2832]. Loss of resistance to air confers a higher risk ofdural puncture than loss of resistance to fluid (normalsaline) [18]. Unintentional dural puncture complicating

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epidural anesthesia vary in incidence from 0.19 to 4.4%.The incidence of epidural needle-induced PDPH inparturients has been reported to range 7685% [13]. Ithas been suggested that the incidence of unintentionaldural puncture during epidural anesthesia is inverselyrelated to operator experience.

Symptoms

Post-partum headache in a parturient almost alwaysraises concerns about accidental dural puncture duringadministration of labor analgesia. PDPH is a well-

known complication of procedures in which the duramater of the spinal cord is punctured. The classicsymptoms of PDPH consist of photophobia, nausea,vomiting, neck stiffness, tinnitus, diplopia, and dizzinessin addition to the often, severe cephalgia (Table 2). Itmay seem more accurate to call the clinical spectrum ofsymptoms that follow dural puncture, the post-duralpuncture syndrome, rather than PDPH, which falselyimplies the headache as the only manifestation [13]. Theheadache is usually severe and throbbing, frontal inorigin, with radiation to the occiput, and is exacerbatedby sitting or standing. The positional nature of theheadache and dramatic improvement on assuming the

supine position remains the standard diagnostic crite-rion for this condition. The differential diagnosis ofPDPH is often clear from the history of dural punctureand the presence of a severe postural headache. How-ever, it is important to consider alternative causes ofheadache (Table 3).

Prevention

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

PDPH to appear. The incidence of epidural needle-in-duced PDPH in pregnant women following duralpuncture with a large bore (e.g., 18 GA) needle has beenreported to range 7685% [13]. Although a few mea-sures have been proposed to prevent PDPH (subarach-noid injection of normal saline, insertion of the epiduralcatheter into the subarachnoid space through the dural

hole), none have been shown to work with certainty todate [7, 8, 12, 19, 24, 2835].

In 2003, Kuczkowski and Benumof [15] reported thatfollowing accidental dural puncture with an 18 GAepidural needle in pregnant women, sequential (Table 4)(1) injection of the CSF in the glass syringe back into thesubarachnoid space through the epidural needle, (2)insertion of a epidural catheter into the subarachnoidspace, (3) injection of small amount of preservative freesaline (35 ml) into the subarachnoid space through thesubarachnoid catheter, (4) administration of bolus andthen continuous intrathecal labor analgesia, and (5)leaving the catheter in situ in the subarachnoid space for

a total of 1220 h decreased the incidence of PDPHfrom 7685 to 14% [15].

Since their original report [15] the authors encoun-tered (20042005) eight more pregnant women [16] inwhom the performance of epidural analgesia was com-plicated by an accidental dural puncture with an 18 GAepidural needle. In all eight additional cases, the acci-dental dural puncture was followed by the same fivemaneuvers and no PDPH was reported in any of thesepatients. These additional eight cases combined with theoriginal seven patients (N=15) suggest that following anaccidental dural puncture with an 18 GA epidural nee-

Table 1 Factors affecting the incidence of PDPH

1 Age2 Gender3 Pregnancy4 Needle size5 Needle design6 Number of attempts7 History of previous PDPH

Table 2 Symptoms of PDPH in pregnant women

1 Nausea2 Vomiting3 Neck stiffness4 Photophobia5 Difficulty in accommodation6 Diplopia7 Dizziness8 Tinnitus9 Hyperacusis10 Hearing loss11 Cephalgia

Table 3 Differential diagnosis of PDPH in pregnant women

1 Post-dural puncture headache2 Non-specific headache3 Migraine4 Caffeine-withdrawal headache5 Meningitis6 Sinus headache7 Pregnancy induced hypertension8 Drugs (amphetamine, cocaine)9 Pneumocephalus-related headache

10 Cerebral vein thrombosis11 Subdural hematoma12 Subarachnoid hematoma13 Brain tumor14 Lactation headache

Table 4 Prevention of PDPH in pregnant women

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

2 Passing the epidural catheter through the duralhole into the subarachnoid space

3 Injecting of 35 ml of preservative free saline intothe subarachnoid space through the subarachnoid catheter

4 Administering bolus and then continuous intrathecallabor analgesia through the subarachnoid catheter

5 Leaving the subarachnoid catheter in situ for a total of 1220 h

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dle in parturients, sequential performance of these fivemaneuvers decreased the incidence of PDPH from7685% [13] to 6.6% (PDPH occurred only in one out ofour total number of 15 pregnant patients) [16]. All ofthese five components were aimed at maintaining CSFvolume.

The replacement of the escaped CSF volume byinjecting the small amount of CSF filling the syringeback into the subarachnoid space and 35 ml of pre-servative-free normal saline seems a low risk maneuver;however, the replacement of this small amount of CSFvolume seems of questionable significance when onetakes 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, otherstudies did find that the immediate injection of 10 mlintrathecal normal saline through the epidural needleafter a dural puncture reduced the incidence of PDPHfrom 62 to 32% [19].

Four other reports have suggested that leaving thecatheter in the dural hole for several hours may decreasethe incidence of PDPH [19, 2830]. First, Cohen et al.

reported a 20% incidence of PDPH in a group of tenpregnant women receiving continuous spinal analgesiavia a 20 GA catheter inserted after accidental duralpuncture [28]. Second, Dennehy et al. found in threepatients that immediate insertion of a subarachnoidcatheter after accidental dural puncture followed byintermittent injections of local anesthetics with opioidsduring labor and delivery prevented PDPH in all threepatients [29]. Third, Cohen et al. in a retrospective studyfound in 13 Cesarean section patients a zero incidence ofPDPH when accidental dural puncture was followedpost-operatively by continuous spinal analgesia througha subarachnoid catheter [30]. Fourth, Charsley et al.

found in six patients that subarachnoid catheter place-ment following accidental dural puncture, and injectionof 10 ml of normal saline prior to removal of the sub-arachnoid catheter effectively prevented PDPH in all sixpatients [19]. These four reports are supported by theobservation that the incidence of PDPH is near zeroafter continuous spinal anesthesia in non-pregnant pa-tients [32].

Two different mechanisms to explain the decreasedincidence of PDPH after subarachnoid catheter insertionhave been postulated; first, the intrathecal catheterplugs the dural tear, decreasing or stopping the effluxof CSF from the subarachnoid space [29], and second,

inserting a catheter in the dural hole leads to aninflammatory reaction, with edema or fibrin exudatessubsequently sealing the dural tear after catheter re-moval [34]. Others described formation of fibrin aroundthe chronic (at least 57 days) intrathecal catheter atthe dural tear in an experimental animal study [35].Thus, in addition to directly plugging the dural hole, thelong-term presence of the intrathecal catheter may alsopromote an inflammatory response around the duralhole, which facilitates dural closure after catheter re-moval.

At this time it is difficult to speculate on the relativeimportance of the five maneuvers originally describedby Kuczkowski and Benumof [15] in decreasing theincidence of PDPH. The authors speculated that theimmediate insertion of the epidural catheter into thesubarachnoid space (short-term plugging) withcareful attention to minimize additional CSF loss andthe prolonged presence of the catheter in the sub-arachnoid space (long-term plugging), seemed themost likely mechanisms of prevention of continuousleakage of CSF and subsequent development of PDPH[15, 16].

Canovas et al. [4] attempted to assess the effectivenessof continuous subarachnoid analgesia for labor and asprophylaxis for (PDPH) in 12 pregnant women whosuffered accidental dural puncture. The authors con-cluded that continuous subarachnoid analgesia afteraccidental dural puncture was first, a safe way to provideanalgesia 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 forPDPH (Table 5). However, only the EBP seems to haveapparent benefits [8, 13, 15, 18].

Psychological

Post-dural puncture headache during the post-partum

period is almost always a complication of neuraxialanesthesia. The parturient is usually aware that herheadache is an iatrogenic problem, and she may be an-gry, resentful and/or depressed [7]. Headache may makeit difficult to care for the newborn and to interact withother family members. It is therefore important to givethe parturient a thorough explanation of the reason forthe headache, the anticipated time course, and thetherapeutic options available [8]. Additionally a severePDPH may delay discharge from the hospital and mayhave economic consequences (increased cost). It isessential to discuss the EBP as a therapeutic optionearly. In the US PDPH associated with regional anes-

thesia is the third most common reason for litigation inthe obstetric anesthesia database.

Posture

The final diagnosis of PDPH requires demonstration ofthe postural component of the headache; partial relief inhorizontal position and worsening on assumption of thevertical position. Therefore supine position may bepreferred by patients and should be recommended.

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Hydration

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

Caffeine

Caffeine is a central nervous system stimulant, whichproduces cerebral vasoconstriction. It is available in anoral and intravenous form. The oral preparation is wellabsorbed from oral mucosa with peak blood levelsreached in approximately 30 min [8]. Caffeine easilycrosses the blood-brain barrier and has a long half-life of38 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 methylxantinefamily available in long-acting oral preparations, whichmight 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. Sumatriptanhas been advocated to the treatment of migraine andrecently, for PDPH [8, 13, 18]. This drug is expensiveand must be given by subcutaneous injections.

Adrenocorticotropic hormone

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

endorphin levels and increased intravascular volume.However, this therapy is not widely used in clinicalpractice 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 salinewould, in theory, produce the same mass effect asautologous 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 dateno 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 istherefore difficult to conclude from the evidence thatepidural saline administration will restore normal CSFdynamics.

Epidural dextran

It has been suggested that the high viscosity and highmolecular weight of dextran may slow its removal fromthe epidural space. However, it is unlikely that dextranwould act any differently to normal saline in the epidural

space [8, 13]. Any pressure increase with the epiduraland subarachnoid space would, like saline, be short-lived. Additionally, it has been reported that dextrandoes not demonstrate any inflammatory response thatwould promote the dura healing process.

Subarachnoid catheters

It has been suggested that placement of a subarachnoidcatheter through the dural hole following an accidentaldural puncture with a large gauge epidural needle, mayprovoke an inflammatory reaction that will seal the

puncture site [15, 19, 2830, 3235]. Histological animaland human studies with long-term subarachnoid cathe-ters confirm the presence of an inflammatory reaction atthe catheter insertion site. Further studies are needed[36, 37].

Epidural blood patch

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

Table 5 Treatment of PDPH in pregnant women

1 Psychological support2 Posture3 Hydration4 Caffeine5 Theophylline6 Sumatriptan7 Adrenocorticotropic hormone8 Abdominal binder9 Epidural saline10 Epidural dextran11 Subarachnoid catheter12 Epidural blood patch

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to explain EBP efficiency in the treatment of PDPH [13,15, 23, 25]. The first theory suggests that the autologousblood injected in the epidural space forms a clot, whichadheres to the dura mater and directly patches the hole.The second theory suggests that the volume of bloodinjected in the epidural space increases CSF pressure,thus reducing traction of pain sensitive brain structures,leading to relief of symptoms. The optimal volume ofblood to be injected in the epidural space remains con-troversial. At the University of California, San Diegothe optimum volume of autologous blood has beenshown to be 1420 ml for most adult patients (K.M.Kuczkowski, Unpublished data). Complications ofautologous EBP are rare, and a success rate is up to94%.

Conclusion

Epidural analgesia is widely considered as the mosteffective method of providing pain relief during labor,

and the number of women receiving epidural analgesiafor 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 PDPHin the labor and delivery suite is usually the responsi-bility of the obstetric anesthesiologist, however it isparamount for the obstetrician to be familiar with theclinical course of this syndrome, and the usual treatmentstrategies. 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 blindedstudies 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 toconsider alternative causes of peripatum headache.

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