00004311-200210000-00008

7/29/2019 00004311-200210000-00008

1/14

Update on Postdural

Puncture Headache

Kristopher R. Davignon, MD

Kevin C. Dennehy, MB, BCh, FFARCSI

August Bier described the first postdural puncture headache (PDPH)in 1899. This initial description of PDPH accompanied his publisheddescription of the first successful spinal anesthetic performed in 1898:

After spinal cocainization . . . I carried out the resection of the ankle joint. This wasfollowed by 2 hours after the operation his back and left leg became painful and thepatient vomited and complained of severe headache. The pain and vomiting soonceased, but headache was still present the next day. (Translated by Hinnerk F. W.

Wulf, MD)1

Although this first PDPH was related to an anesthetic, PDPH is not aproblem limited to the specialty of anesthesiology. Dural puncture is aprocedure performed by a host of medical specialists, including neurolo-

gists, neurosurgeons, and interventional radiologists. In the intervening100 years, PDPH remains a significant complication following the perfor-mance of dural puncture.

Incidence

The overall incidence of PDPH has been reported to range from 1%to more than 75%.24 Studies have shown PDPH to occur more frequentlyin women than in men5 and more commonly in younger people6 andin people prone to headaches.7 Traditionally, it has been thought that

young women are at highest risk for PDPH. Pregnancy has been consid-ered a predisposing factor for PDPH. However, other studies have dem-onstrated that the high incidence of PDPH in obstetrics can be attributedto the age and gender alone of this patient population.8 A large prospec-tive study on the incidence and ability to predict the development ofPDPH looked at several variables commonly thought to predispose toPDPH and found only age, a history of previous PDPH, and direction of

89DOI: 10.1097/01.aia.0000033048.48337.24

7/29/2019 00004311-200210000-00008

2/14

the bevel of the needle during dural puncture to be significant. In 1,021

spinal anesthetics, there were no significant differences in the incidenceof PDPH based on gender, duration of postoperative recumbence, ornumber of attempted dural punctures.7

Spinal needle tip and design play a significant role in the developmentof PDPH. Hart and Whitacre described a reduction in PDPH following theintroduction of a pencil-point spinal needle.9 Other studies have rec-ommended the use of the smallest-gauge needle possible with a noncut-ting or pencil-point bevel design.7,10 Needles commonly used for perfor-mance of spinal and epidural anesthesia are demonstrated in Figure 1.

The experience of the physician performing the procedure has alsobeen cited as a risk factor.11 Flaatten and associates, however, could notdemonstrate any effect of experience and training on the incidence ofPDPH after subarachnoid blockade.12 Multiple dural punctures may in-

crease the incidence of PDPH, although this has not been a consistentfinding.7,13

Indirectly, the specialty of the operator may also play a role in theincidence of PDPH. A survey published in the British Medical Journalshowed that about 74% of neurologists and neurosurgeons in the UnitedKingdom used cutting-tip needles and that more than 85% used needleslarger than 22 gauge for dural puncture.14

Figure 1. Needle tips commonlyused for performance of spinal andepidural anesthesia/analgesia.From the top down are a 24GSprotte, 25G Quincke, 25GWhitacre, and 17G Touhy needle.

90 Davignon and Dennehy

7/29/2019 00004311-200210000-00008

3/14

Patient history of PDPH with a previous spinal anesthetic may predis-

pose to development of PDPH with subsequent spinals. Lybecker andcoworkers found that following repeat spinal anesthesia, PDPH developedin 2 of 3 patients with a history of previous PDPH but in only 3 of 114patients without a history of previous PDPH.7

The incidence of PDPH in nonpregnant, mainly elderly patients un-dergoing continuous spinal anesthesia (CSA) has been shown to below.15,16 The situation is less clear with obstetric patients undergoing CSA.Studies have demonstrated the incidence of PDPH to be both unchangedand reduced in these patients.1719 Norris and colleagues showed theincidence of PDPH to be 11% (4 of 35) in the intrathecal catheter groupand 19% (4 of 21) in the control group, which was not statistically differ-ent.17 Cohen and associates18 compared three groups retrospectively afterinadvertent dural puncture during attempted epidural anesthesia for ce-

sarean section. Group 1 subsequently had an epidural catheter placed.Group 2 had an intrathecal catheter placed and removed immediatelypostoperatively. Group 3 had an intrathecal catheter placed with postop-erative analgesia provided with bupivacaine 0.025%, fentanyl 5 g/mL,and epinephrine 2 g/mL infused via the intrathecal catheter for >24hours. The incidence of PDPH was 33% (5 of 15), 47% (8 of 17), and 0(0 of 13) for groups 1 to 3, respectively.

Morbid obesity may diminish the incidence of PDPH for unclear rea-sons.20

Symptoms

The classic description of PDPH is that of a frontal or occipital head-ache that is present or aggravated by assuming the upright position andessentially disappears when returning to the supine position. In fact, thisis just what Bier described in 1899.1 The pain may be throbbing in nature,often radiates to the neck, and is extremely variable in severity.21 Othersymptoms include nausea, vomiting, neck stiffness, and ocular and audi-tory disturbances (photophobia, diplopia, hypoacusia, tinnitus), as well ascranial nerve palsy.19 The onset and duration of PDPH can be extremely

variable. Most occur within 48 hours of dural puncture and are self-limited, lasting only days. However, there are case reports of chronicPDPH lasting as long as a year.22

Differential Diagnosis

Diagnosis of PDPH may be a challenge when there is no history ofobvious dural puncture or the symptoms are different from those de-scribed above. PDPH should not be ruled out solely on the basis of lack of

Postdural Puncture Headache 91

7/29/2019 00004311-200210000-00008

4/14

documentation of dural puncture. Symptoms are not always specific for

PDPH, and other illnesses may mimic PDPH. The differential diagnosis isbroad and is listed in Table 1.

Morbidity

PDPH may occur in conjunction with or be the cause of other patho-logical processes. There are several case reports involving patients withdural puncture and PDPH who have subsequently developed subduralhematoma, cerebral venous thrombosis, and even pituitary apoplexy.2325

Stocks and coworkers described a postpartum patient who was treatedwith an epidural blood patch (EBP) for PDPH and then developed gen-eralized seizures secondary to cortical vein thrombosis.26 Mantia de-

scribed a patient whose postpartum course was complicated by PDPH andthe subsequent development of an intracranial hemorrhage.27 Shearerand colleagues described the development of cortical blindness and gen-eralized seizures in eight patients with PDPH. They documented cerebralartery vasospasm in three of these patients.28

These complications may represent a spectrum of disorders related tothe pathophysiological processes that occur with PDPH and unfortunatelyare not well described.

Pathophysiology

Bier, who first described PDPH, also first suggested that the headachewas caused by loss of cerebrospinal fluid (CSF).1 It was postulated that thisloss of CSF results in dilatation of, and traction on, pain-sensitive intra-cranial vascular structures.29 This is illustrated in Figure 2. Evidence thatfavors this explanation includes that lumbar puncture can significantlyreduce CSF volume. Kunkle and associates demonstrated that drainage of

Table 1. Differential Diagnosis of PDPH

Subdural hematoma

Subarachnoid hemorrhage

Benign intracranial hypertension

Malignant hypertension

MeningitisCaffeine withdrawal

Pneumocephalus

Intracranial vein thrombosis

Migraine


7/29/2019 00004311-200210000-00008

5/14

20 mL of CSF consistently produces headache.29 If the CSF drainage isthen followed with intrathecal or epidural injections of saline, headachehas been shown to be relieved31,32 and epidural and subarachnoid pres-sures have been elevated.32

The role of pressure in the intrathecal space in the development ofPDPH is not clear. It has not been shown to correlate with the develop-ment of PDPH. If the loss of CSF is responsible for the PDPH, then lowpressures should be recorded in the intrathecal space. Marshall demon-strated pressures of 0 and 5 mmHg in two patients without headache andpressures of 105 and 150 mmHg in two patients with headache.33

The amount of CSF leak, as demonstrated on MRI, has not beenshown to correlate with the incidence of headache.34 However, needlegauge and design have been shown to play a significant role in the devel-opment of PDPH. Larger needles with a cutting rather than pencil pointdesign have been shown to increase the incidence of PDPH.

Figure 2. Pathophysiology of PDPH. The pressure differentialbetween the epidural andintrathecal space as measured inthe lumbar region favors CSFleakage. CSF leakage leads todescent of the brain, with resultanttraction on pain-sensitiveintracranial vessels and thetentorium. Pain is referred via thetrigeminal nerve (V) to the frontalregion, via the glossopharyngealand vagus nerves (IX, X) to theocciput, and via the upper cervicalnerves (C1,2,3) to the neck andshoulders. (Reprinted with

permission from Brownridge30

)


7/29/2019 00004311-200210000-00008

6/14

The other major mechanism thought to be responsible for PDPH is

cerebral vasodilatation. Following the removal of CSF in swine, cerebralblood flow increased and then promptly returned to baseline followingEBP.35 The effectiveness of cerebral vasoconstrictors such as caffeine andtheophylline supports the theory of a cerebrovascular etiology to PDPH.

Prevention

Prevention of PDPH would be preferred to treatment, assuming thatit remains both cost-effective and without serious risk to the patient. Pre-

vention may be especially appropriate for patients at the highest risk forPDPH, namely young patients with a history of PDPH who suffer duralpuncture with a large-gauge needle. It would be least appropriate for

those who are less susceptible (e.g., older male for single-shot spinal an-esthetic). At this point there is no definite preventative therapy, thoughseveral possibilities have been postulated to be effective.

One of the earliest prophylactic measures was epidural administrationof saline. Craft and associates reported the potential benefits of epidurallyadministered saline after accidental dural puncture in 1973. They injected60 mL normal saline postdelivery and again the following day. This re-sulted in a headache rate of 12.5, compared to 76.5% in controls.36

Charsley and colleagues reported their experience in 28 patients withaccidental dural puncture subsequently given 10 mL normal saline intothe subarachnoid space, either through the epidural needle or through asubarachnoid catheter. They demonstrated a significant reduction in theincidence of headache as well as a significant reduction in the number of

epidural blood patches between those who received intrathecal saline andthose who did not.31

Keeping patients in the supine position after dural puncture alleviatesthe symptoms of PDPH. This, however, has been shown in more than onestudy not to prevent PDPH and merely delays the presentation.37,38

Prophylactic EBP was performed following the reported success byGormley of therapeutic EBP in 1960.39 In 1978 Loeser and associateslooked at the timing of EBP, finding a 71% failure rate if EBP was done24 hours after puncture.40 This was supported by Palahniuk andcolleagues, who found prophylactic EBP to be ineffective.41 However,more recent investigations have placed this in question. Evidence fromnewer studies demonstrating the effectiveness of prophylactic EBP may berelated to larger volumes of blood being used. Palahniuk and colleagueshad used only 5 to 10 mL blood. Cheek and coworkers reported 10 casesof successful prophylactic EBP using 17 to 20 mL autologous blood.42 Ina randomized study done by Colonna-Romano and Shapiro, the incidenceof PDPH after unintentional dural puncture with a 17-gauge Tuohy


7/29/2019 00004311-200210000-00008

7/14

needle in obstetric patients was reduced from 80% to 21% by prophylactic

EBP.3

Although prophylactic EBP has been shown to be effective, it is hardlythe treatment of choice. In Colonna-Romano and Shapiros study, even inthe control group, where 80% of parturients with wet tap had PDPH,only 35% required EBP. In the study group 21% of parturients had aPDPH after prophylactic EBP, and 75% of these (14% of the total studypopulation) underwent a second EBP.3 It is not necessary to identify theepidural space a second time when performing a prophylactic EBP, butthe risks associated with injecting blood into the epidural space are in-curred by a larger group of patients. Dural puncture with a 17-gaugeneedle resulted in 35% of patients receiving EBP versus 114% if prophy-lactic EBP was performed, as some patients had both prophylactic andrescue EBP.3

The placement of a subarachnoid catheter after unintentional duralpuncture may reduce the incidence of PDPH. The incidence of PDPHafter continuous spinal anesthesia is low.43 Denny and colleagues used an18-gauge needle to insert a 20-gauge catheter into the subarachnoid spaceof 117 mainly elderly patients undergoing surgery of the lower limb orlower abdomen and, described an incidence of PDPH of less than 1%.15

Liu and associates performed a similar study with 87 patients having or-thopedic surgery where patients were allocated to have the catheter im-mediately withdrawn or left in situ for 12 to 24 hours. The prolongedintrathecal catheter group had an incidence of PDPH of 7.5% vs 10.6% inthe controls. This difference was not statistically significant, and they didnot report how many patients required treatment of their PDPH.44 How-ever, in 1990 Norris and Leighton evaluated the role of an intrathecal

catheter after unintended dural puncture in the parturient and foundthat while the requirement for EBP was reduced from 19% to 11%, this

was not statistically significant.17 More recently Dennehy and Rosaeg de-scribed three cases of intrathecal catheter insertion after unintended du-ral puncture in parturients and where no subsequent PDPH occurred.45

The proposed mechanism for the reduced incidence of PDPH is de-creased loss of CSF while the intrathecal catheter is in situ and increasedfibrin deposition secondary to irritation of the dura by the catheter. In allof the above studies, the time that the catheter was left in place wasextremely variable, and this may be the key to reduction of PDPH.

Combined spinal-epidural anesthesia may prevent the development ofPDPH. Cox and colleagues reviewed over 6,000 obstetric patients whoreceived CSE with less than two dural punctures by a 27-gauge Whitacreneedle and found the incidence of PDPH to be 0.13%.46

There has been speculation that intrathecal opioids are protectiveagainst PDPH. Abboud and coworkers administered intrathecal morphineand bupivacaine or intrathecal bupivacaine for cesarean section andfound that there was no difference in the incidence of PDPH (22% and


7/29/2019 00004311-200210000-00008

8/14

19%, respectively) or requirement for EBP (8% and 0%, respectively)

between the two groups.47

Probably the most important preventative measures that should betaken when planning dural puncture are needle choice and possibly ori-entation. If we believe that PDPH is a result of CSF leak, then it would belogical to think that any strategy to reduce CSF loss would reduce theincidence of PDPH. Traditionally this has been accomplished by usingsmaller-gauge needles, turning cutting bevels longitudinally to preventtransverse cutting of longitudinally oriented dural fibers, and using pen-cil-point needles to part instead of cut dural fibers.48 In vivo, these strat-egies have diminished the incidence of PDPH.10 However, the mechanismby which they provide this effect may not be as originally suspected. First,

when the dura is examined under the electron microscope, the duralfibers appear to be randomly organized as opposed to the traditionally

believed longitudinal orientation.49

Second, when comparing Quinckewith Whitacre needles, it appears that the pencil-point needle actuallycauses more dural trauma, contrary to popular belief.50 This, of course,brings into question the mechanisms by which it is believed that pencil-point needles and longitudinal passage of cutting needles reduce theincidence of PDPH. It may be that the tension on the dural fibers in thelongitudinal axis is more important than which way the fibers run. This

would allow longitudinal cut to pull closed more easily.48 Reina and as-sociates postulate that perhaps traumatic passage of the pencil-pointneedle produces an inflammatory plug that seals the dura.49 To supportthe theory that less CSF leak occurs with pencil-point needles, Holst andcolleagues using an electron microscope measured CSF leakage withSprotte, Whitacre, Quincke, and Atraucan needles in vitro. They found all

pencil-point needles to have less CSF leakage.50Whatever the mechanism, there are good data to suggest that the use

of smaller-gauge pencil-point needles reduces the incidence of PDPH.Halpern and Preston published a meta-analysis looking at cutting versusnoncutting needles and small versus large spinal needles. They found onlyone study reporting a lower incidence of PDPH with a cutting needle. This

was comparing a 29-gauge Quincke needle with a 22-gauge Whitacreneedle. The difference was not statistically significant, but this makes itimpossible to conclude that a noncutting needle is better than a cuttingneedle regardless of size. The conclusions of the meta-analyses were thatnoncutting needles for spinal anesthesia produce a lower incidence ofPDPH than cutting needles. In addition, smaller needles produce lessheadache than larger needles of the same type.10

Some practitioners still prefer to use epidural anesthesia as opposedto spinal anesthesia because it theoretically should not cause PDPH. How-ever, Lambert and associates, have demonstrated that the incidence ofPDPH from epidural anesthesia is about 1.1% to 1.7% due to uninten-tional dural puncture and the associated high incidence of PDPH with


7/29/2019 00004311-200210000-00008

9/14

such a large-bore needle puncture.4 This incidence is similar to that re-

ported by the same group using a 25-gauge Whitacre needle for spinalanesthesia. Therefore, there seems to be no benefit to epidural over spinalanesthesia with regard to the incidence of PDPH.

Therapy

Despite all that is being accomplished in preventative measures,PDPH is still a problem for a small percentage of patients after duralpuncture. PDPH is a self-limiting problem usually lasting between 1 and 6

weeks,21 but it has been reported to last for months.22 PDPH can beextremely debilitating and incapacitating and often requires treatment.Therapy for PDPH runs a large spectrum from simple hydration andnonsteroidal anti-inflammatory drugs to EBP or surgical correction with adural patch or fibrin glue (Table 2).

The simplest therapy for PDPH is positioning the patient supine.However, this is impractical when ambulation is necessary. Hydration isanother simple treatment that is employed frequently for PDPH, but thereis little or no evidence to support it.

Conservative therapy is limited to a few pharmacological agents. Caf-feine has been given orally or intravenously. It also exists in coffee andother beverages and foods. Camann and colleagues51 compared 300 mgoral caffeine and placebo and found caffeine to provide superior relieffrom PDPH as rated by visual analogue scale scores. Fewer EBPs wereperformed in the caffeine group, but the difference was not statistically

significant (35% vs. 55%). They noted that a 150-mL cup of drip-grindcoffee contains approximately 150 mg of caffeine. Theophylline, anothermethylxanthine, has also been used to treat PDPH.

The mechanism of action for either of these drugs is not entirely clear,but many speculate it relates to their cerebral vasoconstrictive properties.Though most would classify caffeine as conservative therapy, it is not

without its risks. Case reports of caffeine causing seizure as well as tran-sient atrial fibrillation exist.5254

Table 2. Treatment of PDPH

Conservative Invasive

Hydration Epidural blood patchNSAIDs Epidural saline

Caffeine PO/IV Epidural fibrin glue

Sumatriptan SC/IN Surgical repair

ACTH IV/IM


7/29/2019 00004311-200210000-00008

10/14

Sumatriptan is a serotonin agonist that is used commonly to treat

migraine headaches. It is expensive and is administered orally, subcuta-neously, or nasally. It may be efficacious in treating PDPH.21 Controlledtrials have not been done and, like caffeine, sumatriptan has potential sideeffects.

Adrenocorticotropic hormone (ACTH) also has been proposed as analternative to EBP for treatment of PDPH. Foster reported a 70% successrate with ACTH administered for PDPH. He uses 1.5 IU/kg infused in-travenously over 1 hour in 1 or 2 liters of Ringers lactate, or 250 mLnormal saline in a subsequent case report.55,56 Collier described initiallyusing 20 units of intramuscularly injected long-acting ACTH and thenlater using tetracosactrin 1 mg IM when long-acting ACTH was no longeravailable.57 The mechanism of action is unknown. Evaluation with con-trolled studies has not been done.

Unfortunately, conservative measures are often inadequate. LumbarEBP remains the most effective treatment modality available to the anes-thesiologist. Since its introduction in 1960 by Gormley, EBP has been used

with only minor modifications to treat severe PDPH.39 The mechanism bywhich EBP is effective is unknown. Some suspect that injection of bloodinto the epidural space increases subarachnoid pressure and thereby re-lieves some of the tension on pain-sensitive structures in the CNS. Othersbelieve the blood forms a platelet and fibrin plug to seal the rent left inthe dura, thereby stopping the leakage of CSF. Likely, it is a combinationof both these modalities that offers relief to those suffering from PDPH.This would explain the very fast onset of symptomatic relief and the pro-longed and often permanent duration of action.58

The timing of EBP is controversial. Some have suggested that delay of

at least 4 days increases the effectiveness of EBP. Safa-Tisseront and co-workers found a significant increase in EBP failure if EBP was performedwithin 3 days of dural puncture.58 Loeser and colleagues also report abenefit in delaying EBP.40 However, in both of these studies the delaybetween dural puncture and EBP was not controlled, and bias may play asignificant role. Patients with worse PDPH (perhaps secondary to moresignificant CSF leak) may have received EBP earlier than others, therebyexplaining the decreased success. In fact, many have advocated EBP earlyand even prophylactically (as has already been discussed).

The amount of autologous blood injected during EBP also is underdebate. Gormley used just 2 or 3 mL of blood in his early blood patch. 39

DiGiovanni and Dunbar reported the use of 10 mL, with success in 41 of45 patients.59 Crawford described the use of 20 mL blood with a resulting96% success rate.60Vakharia and colleagues looked at the spread of bloodafter EBP by MRI and found 20 mL to spread an average of 4.6 interver-tebral spaces.61 Szeinfeld and associates evaluated the spread of bloodusing technetium-labeled red blood cells and found spread of 9 spinalsegments with the injection of on average 14.8 mL.62 The spread of blood


7/29/2019 00004311-200210000-00008

11/14

and volume of blood injected correlated reasonably well (see Fig. 1).

However, this does not help answer the question How much bloodshould we inject? as we really dont know if spread of blood correlateswith any clinically significant endpoint.

Crul and coworkers put forth a new idea in a recent case report. Theyuse fibrin glue (Tissucol, duo 500; Immuno AG, Vienna, Austria) injectedinto the epidural space to treat a persistent PDPH. In their report, a29-year-old woman had undergone spinal anesthesia for knee ligamentrepair. An EBP was performed for PDPH but was unsuccessful, and thepatient remained unable to return to work. They then injected just 3 mLof epidural fibrin glue and the patient had complete relief from hersymptoms and no recurrence 7 months after surgery.63 Such innovativenew techniques are quite interesting, and with further study epiduralfibrin glue may enter the repertoire of the anesthesiologist in the battle

against PDPH.

Conclusions

One hundred years after the first spinal anesthetic and the emergenceof neuraxial blockade, PDPH remains a significant source of morbidity forpatients. This is particularly true in the obstetric population, when duralpuncture is often with a 17- or 18-gauge epidural needle and where eventhe incidence of PDPH after puncture with a smaller-gauge pencil-pointneedle presents a significant amount of morbidity. It is our duty to con-tinue to find ways to prevent and treat PDPH.

References

1. Wulf HFW. The centennial of spinal anesthesia. Anesthesiology 1998;89:500506.

2. Smedstad KG. Dealing with post-dural puncture headacheis it different in obstetrics?Can J Anaesth 1998;45:69

3. Colonna-Romano P, Shapiro BE. Unintentional dural puncture and prophylactic epi-dural blood patch in obstetrics. Anesth Analg 1989;69:522523

4. Lambert DH, Hurley RJ, Hertwig L, et al. Role of needle gauge and tip configurationin the production of lumbar puncture headache. Reg Anesth 1997;22:6672

5. Flaatten H, Rodt S, Rosland J, et al. Postoperative headache in young patients afterspinal anaesthesia. Anaesthesia 1987;42:202204

6. Vandam LD, Dripps RD. Long-term follow-up of patients who received 10,098 spinalanesthetics. JAMA 1956;161:586591

7. Lybecker H, Moller JT, May O, et al. Incidence and prediction of postdural punctureheadache. Anesth Analg 1990;70:389394

8. Morewood GH. A rational approach to the cause, prevention and treatment of post-dural puncture headache. Can Med Assoc J 1993;149:10871093

9. Hart JR, Whitacre RJ. Pencil-point needle in prevention of postspinal headache. JAMA1951;147:657658


7/29/2019 00004311-200210000-00008

12/14

10. Halpern S, Preston R. Postdural puncture headache and spinal needle design. Anes-thesiology 1994;81:13761383

11. Choi A, Laurito CE, Cunningham FE. Pharmacologic management of postdural punc-ture headache. Ann Pharmacother 1996;30:831839

12. Flaatten H, Berg CM, Brekke S, et al. Effect of experience with spinal anaesthesia on thedevelopment of post-dural puncture complications. Acta Anaesthesiol Scand 1999;43:3741

13. Seeberger MD, Kaufmann M, Staender S, et al. Repeated dural punctures increase theincidence of postdural puncture headache. Anesth Analg 1996;82:302305

14. Serpell MG, Haldane GJ, Jamieson DRS, et al. Prevention of headache after lumbarpuncture: questionnaire survey of neurologists and neurosurgeons in United Kingdom.Br Med J 1998;316:17091710

15. Denny N, Masters R, Pearson D, et al. Postdural puncture headache after continuousspinal anesthesia. Anesth Analg 1987;66:791794

16. Kallos T, Smith TC. Continuous spinal anesthesia with hypobaric tetracaine for hipsurgery in lateral decubitus. Anesth Analg 1972;51:766773

17. Norris MC, Leighton BL. Continuous spinal anesthesia after unintentional dural punc-ture in parturients. Reg Anesth 1990;15:285287

18. Cohen S, Amar D, Pantuck EJ. et al. Decreased incidence of headache after accidentaldural puncture in cesarean delivery patients receiving continuous postoperative intra-thecal analgesia. Acta Anesthesiol Scand 1994;38:7168

19. Weeks SK. Postpartum headache. In Chestnut DH, ed. Obstetric Anesthesia: Principlesand Practice, ed 2. St. Louis: Mosby, 1999:621638

20. Faure E, Moreno R, Thisted R. Incidence of postdural puncture headache in morbidlyobese parturients [letter]. Reg Anesth 1994;19:361363

21. Lybecker H, Djernes M, Schmidt JF. Postdural puncture headache (PDPH): onset,duration, severity, and associated symptoms. An analysis of 75 consecutive patients withPDPH. Acta Anaesthesiol Scand 1995;39:605612

22. Klepstad P. Relief of postural post dural puncture headache by an epidural blood patch12 months after dural puncture. Acta Anaesthesiol Scand 1999;43:964-966

23. Anand A. Post-dural puncture headache associated with cerebral venous thrombosis. Br

J Anaesth 2000;85:32632724. Acharya R, Chhabra SS, Ratra M, et al. Cranial subdural haematoma after spinal an-aesthesia. Br J Anaesth 2001;86:893895

25. Lennon M, Seigne P, Cunningham AJ. Pituitary apoplexy after spinal anaesthesia. Br JAnaesth 1998;81:616618

26. Stocks GM, Wooler DJA, Young JM, et al. Postpartum headache after epidural bloodpatch: investigation and diagnosis. Br J Anaesth 2000;84:407410

27. Mantia AM. Clinical report of the occurrence of an intracerebral hemorrhage followingpost-lumbar puncture headache. Anesthesiology 1981;55:684685

28. Shearer VE, Jhaveri HS, Cunningham FG. Puerperal seizures after post-dural punctureheadache. Obstet Gynecol 1995;85:255260

29. Kunkle EC, Ray BS, Wolff HG. Experimental studies on headache. Arch Neurol 1943;49:323358

30. Brownridge P. The management of headache following accidental dural puncture inobstetric patients. Anaesth Intens Care 1983;11:415

31. Charsley MM, Abram SE. The injection of normal saline reduces the severity of post-dural puncture headache. Reg Anesth Pain Med 2001;26:301305

32. Usubiaga JE, Usubiaga LE, Brea LM, et al. Effect of saline injections on epidural andsubarachnoid space pressures and relation to postspinal anesthesia headache. Anesth

Analg 1967;46:293296

33. Marshall J. Lumbar puncture headache. Neurol Neurosurg Psychiatr 1950;13:7174


7/29/2019 00004311-200210000-00008

13/14

34. Iqbal J, Davis LE, Orrison WW. An MRI study of lumbar puncture headaches. Headache1995;35:420422

35. Boezaart AP. Effects of cerebrospinal fluid loss and epidural blood patch on cerebralblood flow in swine. Reg Anesth Pain Med 2001;26:401406

36. Craft JB, Epstein BS, Coakley CS. Prophylaxis of dural puncture headache with epiduralsaline. Anesth Analg 1973;52:228231

37. Carbaat PAT, van Crevel H. Lumbar puncture headache: controlled study on thepreventive effect of 24 hours bed rest. Lancet 1981;2:11331135

38. Cook PT, Davies MJ, Beavis RE. Bed rest and postlumbar puncture headache. Theeffectiveness of 24 hours recumbency in reducing the incidence of postlumbar punc-ture headache. Anaesthesia 1989;44:389391

39. Gormley JB. Treatment of postspinal headache. Anesthesiology 1960;21:56556640. Loeser EA, Hill GE, Bennett GM, et al. Time vs. success rate for epidural blood patch.

Anesthesiology 1978;49:14714841. Palahniuk RJ, Cumming M. Prophylactic blood patch does not prevent post lumbar

puncture headache. Can Anesth Soc J 1979;26:13213342. Cheek TG, Banner R, Sauter J, et al. Prophylactic extradural blood patch is effective. Br

J Anaesth 1988;61:34034243. Benzon HT, Wong CA. Postdural puncture headache: mechanisms, treatment and

prevention. Reg Anesth Pain Med 2001;26:29329544. Liu N, Montefiore A, Kermarec N, et al. Prolonged placement of spinal catheters does

not prevent postdural puncture headache. Reg Anesth 1993;18:11011345. Dennehy KC, Rosaeg OP. Intrathecal catheter insertion during labour reduces the risk

of post-dural puncture headache. Can J Anaesth 1998;45:424546. Cox M, Lawton G, Fowrie-Mohan S, et al. Ambulatory extradural analgesia (letter). Br

J Anaesth 1995;75:11447. Abboud TK, Zhu J, Reyes A, et al. Effect of subarachnoid morphine on the incidence

of spinal headache. Reg Anesth 1992;17:343648. Liu SS, McDonald SB. Current issues in spinal anesthesia. Anesthesiology 2001;94:888

90649. Reina MA, de Leon-Casasola OA, Lopez A, et al. An in vitro study of dural lesions

produced by 25-gauge Quincke and Whitacre needles evaluated by scanning electron

microscopy. Reg Anesth Pain Med 2000;25:39340250. Holst D, Mollmann M, Ebel C, et al. In vitro investigation of cerebrospinal fluid leakage

after dural puncture with various spinal needles. Anesth Analg 1998;87:1331 133551. Camann WR, Murray RS, Mushlin PS, et al. Effects of oral caffeine on postdural punc-

ture headache: a double blind, placebo-controlled trial. Anesth Analg 1990;70:18118452. Cohen SM, Laurito CE, Curran MJ. Grand mal seizure in a postpartum patient follow-

ing intravenous infusion of caffeine sodium benzoate to treat persistent headache. JClin Anesth 1992;4:4851

53. Bolton VE, Leicht CH, Scanlon TS. Postpartum seizure after epidural blood patch andintravenous caffeine sodium benzoate. Anesthesiology 1989;70:146149

54. McSwiney M, Phillips J. Postdural puncture headache. Acta Anaesthesiol Scand 1995;39:990995

55. Foster P. ACTH treatment for post-lumbar puncture headache. Br J Anaesth 1994;73:429

56. Kshatri AM, Foster PA. Adrenocorticotropic hormone infusion as a novel treatment for

postdural puncture headache. Reg Anesth 1997;22:43243457. Collier BB. Treatment for postdural puncture headache. Br J Anaesth 1994;72:36636758. Safa-Tisseront V, Thormann F, Malassine P, et al. Effectiveness of epidural blood patch

in the management of post-dural puncture headache. Anesthesiology 2001;95:33433959. DiGiovanni AJ, Dunbar BS. Epidural injections of autologous blood for postlumbar-

puncture headache. Anesth Analg 1970;49:268271


7/29/2019 00004311-200210000-00008

14/14

60. Crawford JS. Experiences with epidural blood patch. Anaesthesia 1980;35:51351561. Vakharia SB, Thomas PS, Rosenbaum AE, et al. Magnetic resonance imaging of cere-

brospinal fluid leak and tamponade effect of blood patch in postdural puncture head-ache. Anesth Analg 1997;84:585590

62. Szeinfeld M, Ihmeidan IH, Moser MM, et al. Epidural blood patch: evaluation of thevolume and spread of blood injected into the epidural space. Anesthesiology 1986;64:820822

63. Crul BJP, Gerritse BM, van Dongen RTM, et al. Epidural fibrin glue injection stopspersistent postdural puncture headache. Anesthesiology 1999;91:576577.


00004311-200210000-00008

Documents

Transcript of 00004311-200210000-00008