Advances in Anesthesia, Vol. 28, No. 1, 2010
ISSN: 0737-6146
doi: 10.1016/j.aan.2010.07.006
Postdural Puncture Headache
History and current relevance
As one of the earliest recognized complications of regional anesthesia, PDPH has a long and colorful history [1]. Dr August Bier noted this adverse effect in the first patient to undergo successful spinal anesthesia on August 16, 1898. Bier observed: “Two hours after the operation his back and left leg became painful and the patient vomited and complained of severe headache. The pain and vomiting soon ceased, but headache was still present the next day” (italics added) [2]. The following week, Bier and his assistant, Dr August Hildebrandt, performed experiments with cocainization of the spinal cord on themselves. In a description scarcely improved upon in an intervening century, Bier later reported first-hand his experience in the days to follow: “I had a feeling of very strong pressure on my skull and became rather dizzy when I stood up rapidly from my chair. All these symptoms vanished at once when I lay down flat, but returned when I stood up… I was forced to take to bed and remained there for nine days, because all the manifestations recurred as soon as I got up… The symptoms finally resolved nine days after the lumbar puncture” [2]. In medical history, few complications have come to be considered as closely linked to a specific technique as PDPH with spinal anesthesia.
Employing the methods of the early twentieth century, spinal anesthesia was frequently followed by severe and prolonged headache, casting a long shadow over the development and acceptance of this modality. Investigations into the cause of these troubling symptoms eventually led to the conclusion that they were due to persistent cerebrospinal fluid (CSF) loss through the rent created in the meninges. The most notable successful efforts to minimize the loss of CSF were through the use of smaller gauge and “noncutting” needles (as convincingly demonstrated by Vandam and Dripps [3] and Hart and Whitacre [4], respectively, in the 1950s). Despite these significant advances in prevention, PDPH remained a frustratingly common occurrence.
The extensive search for effective treatments for PDPH dates to Bier’s time. Yet efforts through the first half of the 20th century, while often intensive and creative, were questionably worthwhile. In a monograph intended to be a comprehensive review of PDPH from the 1800s through 1960, Dr Wallace Tourette and colleagues [5] cite dozens of separate and far-ranging treatment recommendations, including such interventions as intravenous ethanol, x-rays to the skull, sympathetic blocks, and manipulation of the spine. Unfortunately, before the introduction of the EBP there were no treatment measures that could be described as significant improvements over the simple passage of time. In his 1955 textbook, Complications of Regional Anesthesia, Dr Daniel Moore describes in detail a full 3-day treatment protocol for PDPH. He concludes by noting that 3 days is the usual duration of untreated mild to moderate headaches, but that “nevertheless, the patient feels an attempt to help his problem is being made” [6].
The EBP, a startlingly unique medical procedure, proved to be the breakthrough in the treatment of PDPH. The concept of using autologous blood to “patch” a hole in the meninges was introduced in late 1960 by Dr James Gormley, a general surgeon [7]. Yet Gormley’s brief report went largely unnoticed for nearly a decade because, to the practitioners of the day, an iatrogenic epidural hematoma raised serious concerns of scarring, infection, and nerve damage. The procedure was only later popularized in anesthesia circles, and performed as a true epidural injection, largely through the work of Drs Anthony DiGiovanni and Burdett Dunbar [8]. The EBP procedure was further refined through the 1970s as the volume of blood commonly used increased to 20 mL [9]. Today, the EBP is nearly universally employed as the cornerstone of treatment for severe PDPH [10].
PDPH remains a prominent clinical concern to the present day. Largely due to modifications in practice that followed the identification of risk factors, rates of PDPH following spinal anesthesia have steadily declined; from an incidence exceeding 50% in Bier’s time, to around 10% in the 1950s [3], until currently a rate of 1% or less can be reasonably expected. However, as perhaps the highest risk group, an unfortunate 1.7% of obstetric patients continue to experience PDPH after spinal anesthesia using 27-gauge Whitacre needles [11]. Since epidural techniques intend to avoid meningeal puncture, they are attractive alternatives to spinal anesthesia. Yet occasional ADP, with either the needle or catheter, is unavoidable (or may be unrecognized at the time in more than 25% of patients who eventually develop PDPH) [12]. In nonobstetric situations (eg, interlaminar epidural steroid injections), the rate of ADP should be considerably less than 0.5%. However, ADP is of greatest concern in the obstetric anesthesia setting, where the incidence of this adverse event is around 1.5% [11]. Over half of all patients who experience an ADP will eventually develop headache symptoms, and many studies in obstetric populations report PDPH rates exceeding 75%. In addition to anesthesia interventions, PDPH remains a too-common iatrogenic complication following myelography and diagnostic/therapeutic lumbar puncture (LP). In these situations, rates of PDPH around 10% are commonly cited, as practitioners often continue to use Quincke needles, and large-gauge needles are considered necessary because of the viscosity of contrast material as well as to facilitate the timely collection of CSF. Consequently, there is evidence to suggest that the majority of instances of PDPH now have a nonanesthesia origin [13].
The practical significance of PDPH is illustrated in being noted in the American Society of Anesthesiologists Closed Claims Project database as one of the most frequent claims for malpractice involving obstetric anesthesia [14], regional anesthesia [15], and chronic pain management [16]. Justifiably, headache is the most commonly disclosed risk when obtaining consent for spinal and epidural anesthesia [17]. The potentially serious nature of this complication necessitates inclusion in informed consent involving any procedure that may result in PDPH. As part of this discussion, patients should also be apprised of the normal delayed onset of symptoms and given clear instructions for the timely provision of advice or management should they experience adverse effects.
Pathophysiology
It has long been accepted that PDPH results from a disruption of normal CSF homeostasis. However, despite a great deal of research and observational data, the pathophysiology of PDPH remains incompletely understood [18].
CSF is produced primarily in the choroid plexus at a rate of approximately 0.35 mL/min and reabsorbed through the arachnoid villa. The total CSF volume in adults is maintained around 150 mL, of which approximately half is extracranial, and gives rise to normal lumbar opening pressures of 5 to 15 cm H2O in the horizontal position (40–50 cm H2O in the upright position). It has been shown experimentally that the loss of approximately 10% of total CSF volume predictably results in the development of typical PDPH symptoms, which resolve promptly with reconstitution of this deficit [19]. It is agreed that PDPH is caused by the loss of CSF through a persistent leak in the meninges. In this regard, it has been postulated that the cellular arachnoid mater (containing frequent tight junctions and occluding junctions) is perhaps more important than the more permeable and acellular dura mater in the genesis of PDPH [20]. This tenet has led some, including this author, to advocate the term “meningeal puncture headache” (MPH) as more accurate and descriptive than PDPH [21,22]. However, “postdural puncture headache” is used in this review as it is the more common terminology at the present time. Regardless of nomenclature, it is also important to acknowledge that references to “dural puncture” throughout the medical literature (including this article) actually describe puncture of the dura-arachnoid and are more correctly termed “meningeal puncture.” Furthermore, the apparent role of the arachnoid mater calls into question the significance of the many published studies concerning PDPH of isolated in vitro dura mater.
Multiple neural pathways are involved in generating the symptoms of PDPH. These pathways include the ophthalmic branch of the trigeminal nerve (CN V1) in frontal head pain, cranial nerves IX and X in occipital pain, and cervical nerves C1 to C3 in neck and shoulder pain [23]. Nausea is attributed to vagal stimulation (CN X). Auditory and vestibular symptoms are secondary to the direct communication between the CSF and the perilymph via the cochlear aqueduct, which results in decreased perilymphatic pressures in the inner ear and an imbalance between the endolymph and perilymph [24]. Significant visual disturbances may represent a transient palsy of the nerves supplying the extraocular muscles of the eye (CN III, IV, and, VI). Here, the lateral rectus muscle is most often involved, which is attributed to the long, vulnerable intracranial course of the abducens nerve (CN VI) [25]. Other, much less frequent cranial nerve palsies of the trigeminal (CN V), facial (CN VII), and auditory (CN VIII) nerves have also been reported [26].
Clinical presentation and characteristics
Onset
Onset of symptoms is generally delayed, with headache usually beginning 12 to 48 hours and rarely more than 5 days following meningeal puncture. In their landmark observational study, Vandam and Dripps reported onset of headache symptoms within 3 days of spinal anesthesia in 84.8% of patients for whom such data were available [3]. More recently, Lybecker and colleagues [27] performed a detailed analysis of 75 consecutive patients with PDPH following spinal anesthesia (primarily using 25-gauge cutting-point needles). Although none of their patients noted the onset of symptoms during the first hour following meningeal puncture, 65% experienced symptoms within 24 hours and 92% within 48 hours. An onset of symptoms within 1 hour of neuraxial procedures is suspicious for pneumocephalus, especially in the setting of an epidural loss-of-resistance technique using air [28]. Occasional reports of unusually delayed onset of PDPH highlight the importance of seeking a history of central neuraxial instrumentation whenever positional headaches are evaluated [29].
Presentation
The cardinal feature of PDPH is a postural nature, with headache symptoms worsening in the upright position and relieved, or at least improved, with recumbency. The International Classification of Headache Disorders further describes this positional quality as worsening within 15 minutes of sitting or standing, and improving within 15 minutes after lying [30]. Headache is always bilateral, with a distribution that is frontal (25%), occipital (27%), or both (45%) [27]. Headaches are typically described as “dull/aching”, “throbbing”, or “pressure-type”.
The severity of headache symptoms, a feature with important ramifications for treatment, varies considerably among patients. Although there is no widely accepted severity scale, one practical approach is to have patients simply rate their headache intensity using a 10-point analog scale, with 1 to 3 classified as “mild,” 4 to 6 “moderate,” and 7 to 10 “severe.” Lybecker and colleagues [27] further categorized patients according to restriction in physical activity, degree of confinement to bed, and presence of associated symptoms (Fig. 1). A prospective analysis of PDPH after spinal anesthesia using the Lybecker classification system demonstrated that 11% were mild, 23% moderate, and 67% severe.
Fig. 1 Classification of severity of postdural puncture headache (PDPH).
(Adapted from Lybecker H, Djernes M, Schmidt JF. Postdural puncture headache (PDPH): onset, duration, severity, and associated symptoms. An analysis of 75 consecutive patients with PDPH. Acta Anaesthesiol Scand 1995;39:606; with permission.)
Associated Symptoms
If headaches are severe, they are more likely to be accompanied by a variety of other symptoms. Pain and stiffness in the neck and shoulders is common, and seen in nearly half of all patients experiencing PDPH [31]. With questioning, nausea may be reported by a majority of patients and can lead to vomiting [27].
Patients uncommonly may experience auditory or visual symptoms [24], and the risk for either appears to be directly related to needle size [25,32]. In the large study of PDPH by Vandam and Dripps [3], each was seen to a clinically apparent degree in 0.4% of patients. Auditory symptoms include hearing loss, tinnitus, and even hyperacousis, and can be unilateral. It is interesting to note that subclinical hearing loss, especially in the lower frequencies, has been found to be common following spinal anesthesia, even in the absence of PDPH [32]. Closely associated with auditory function, vestibular disturbances (dizziness or vertigo) may also occur. Visual problems include blurred vision, difficulties with accommodation, mild photophobia, and diplopia [25]. In contrast to headache complaints, which are consistently bilateral, nearly 80% of episodes of diplopia secondary to meningeal puncture involve unilateral cranial nerve palsies.
Risk factors
Patient Characteristics
The patient characteristic having the greatest impact on risk of PDPH is age. Uncommonly reported in children younger than 10 years, PDPH has a peak incidence in the teens and early 20s [33]. The incidence then declines over time, becoming much less frequent in patients older than 50 years (Fig. 2). Females have long been recognized as being at increased risk for PDPH, and a systematic review of published studies found the odds of developing PDPH were significantly lower for male than age-matched nonpregnant female subjects (odds ratio = 0.55; 95% confidence interval, 0.44–0.67) [34]. The etiology behind this gender difference is not clear. Body mass index (BMI; calculated as the weight in kilograms divided by height in meters, squared) appears to be a mixed risk factor. Morbid obesity presents obvious technical difficulties for central neuraxial procedures, increasing the likelihood of multiple needle passes and ADP [35]. However, low BMI has been reported as an independent risk factor for PDPH [36] and high BMI (ie, obesity) may actually decrease risk, possibly due to a beneficial effect of increased intra-abdominal pressure [37].
Pregnancy has traditionally been regarded as a risk factor for PDPH [3], but this consideration partially reflects the young age as well as the high incidence of ADP in the gravid population. Although controversial, pushing during the second stage of labor, thought to promote the loss of CSF through a hole in the meninges, has been reported to influence the risk of PDPH following ADP. Angle and colleagues [38] noted that the cumulative duration of bearing down correlated with the risk of developing PDPH in patients who had experienced an ADP. These investigators also found that patients who avoided pushing altogether (proceeded to cesarean delivery before reaching second stage of labor) had a much lower incidence of PDPH (10%) than those who pushed (74%).
PDPHs appear to have an interesting association with other headaches. Patients who report having had a headache within the week prior to LP have been observed to have a higher incidence of PDPH [36]. On further analysis, only those with chronic bilateral tension-type headaches were found to be at increased risk [39]. A history of unilateral headache [39] or migraine [40] has not been linked to an increased risk of PDPH. Menstrual cycle, a factor in migraine headaches, did not influence the rate of PDPH in one small pilot study [41]. Patients with a history of previous PDPH, particularly women, appear to have an increased risk for new PDPH after spinal anesthesia [42]. With epidural procedures, patients with a history of ADP have been shown to be at slightly increased risk for another ADP (and subsequent PDPH) [43].
Procedural Details
Needle size and tip design are the most important procedural factors related to PDPH (Fig. 3) [44]. Needle size is directly related to the risk of PDPH. Meningeal puncture with larger needles is associated with a higher incidence of PDPH [3], more severe headache and associated symptoms [44], a longer duration of symptoms [45], and a greater need for definitive treatment measures [46]. Needle tip design is also a major influence, with “noncutting” needles clearly associated with a reduced incidence of PDPH compared with “cutting” (usually Quincke) needles of the same gauge. In general, noncutting needles have an opening set back from a tapered (“pencil-point”) tip and include the Whitacre, Sprotte, European, Pencan, and Gertie Marx needles. Adding to this somewhat confusing terminology, noncutting needles are sometimes still incorrectly referred to as “atraumatic” needles, despite being shown with electron microscopy to produce a more traumatic rent in the dura than cutting needles (perhaps resulting in a better inflammatory healing response) [47]. The influence of needle size on risk of PDPH appears to be greatest for cutting needles (for example, the reduction seen in the incidence of PDPH between 22- and 26-gauge sizes is greater for cutting than noncutting needles). Insertion of cutting needles with the bevel parallel to the long axis of the spine significantly reduces the incidence of PDPH [48]. This observation was for many years attributed to a spreading rather than cutting of longitudinal-oriented dural fibers. However, scanning electron microscopy reveals the dura to be made of many layers of concentrically directed fibers [49], and the importance of needle bevel insertion is now thought to be related to longitudinal tension on the meninges, particularly in the upright position, and its influence on CSF leakage through holes having differing orientations.
Not surprisingly, a greater number of meningeal punctures have been shown to increase the rate of PDPH [50]. The degree of experience/comfort/skill of the operator is clearly associated with the incidence of ADP during epidural procedures, with higher ADP rates consistently reported when procedures are performed by residents [51,52]. The risk of ADP also appears to be higher for procedures done at night, strongly suggesting a significant contribution of operator fatigue [53].
Several procedural details do not appear to influence the rate of development of PDPH, including patient position at the time of meningeal puncture, “bloody tap” during spinal anesthesia, addition of opiates to spinal block, and volume of CSF removed (for diagnostic purposes) [1].
Prevention
Although prophylaxis is most simply thought of as preventing any symptoms of PDPH, in the clinical context this issue is deceptively complex. It is important to appreciate that significant “prevention” may encompass several other end points, such as a reduced incidence of severe PDPH, a shorter duration of symptoms, or decreased need for EBP. Unfortunately, despite the clear relevance of this issue, the overall quality of evidence for preventive measures is generally weak [54,55].
General Measures
Though only recently used for neuraxial techniques, the use of ultrasonography for regional anesthesia holds some promise in reducing the risk of PDPH. Ultrasonography can decrease the number of needle passes required for regional procedures and has been shown to accurately predict the depth of the epidural space [56]. Further study is ongoing to define this potential for ultrasonography to reduce the incidence of ADP and PDPH.
Pharmacologic measures, notably caffeine, continue to be widely used in hopes of decreasing the incidence of PDPH following meningeal puncture [10]. In support of this practice, one small study (n = 60) found that intravenous caffeine (500 mg caffeine sodium benzoate within 90 minutes after spinal anesthesia) significantly reduced the incidence of moderate to severe headache [57]. However, generalizing these results to other clinical settings is difficult, as this investigation involved the use of 22-gauge Quincke needles in a relatively young patient population. In another study, oral caffeine (75 or 125 mg) administered every 6 hours during the first 3 days following spinal anesthesia failed to influence the rate of PDPH [58]. A critical review of the available evidence fails to support the use of caffeine in prevention of PDPH [59]. More recently, a small pilot study raised the possibility of using the long-acting 5-HT receptor agonist frovatriptan (2.5 mg/d orally for 5 days) in the prevention of PDPH [60]. At present, however, there is no proven pharmacologic prophylaxis for PDPH.
A recent survey of United States anesthesiologists reported that bed rest and aggressive oral and intravenous hydration continue to be employed by a sizable majority as prophylactic measures against PDPH [10]. However, a systematic review of the literature regarding bed rest versus early mobilization after dural puncture failed to show any evidence of benefit from bed rest, and suggested that the risk of PDPH may actually be decreased by early mobilization [61]. It is notable that the practice of United States anesthesiologists regarding bed rest is in direct contrast to that seen in United Kingdom maternity units, where 75% encourage mobilization as early as possible following ADP as prophylaxis against PDPH [62]. Likewise, a randomized prospective trial of increased oral hydration following LP failed to decrease the incidence or duration of PDPH [61]. In summary, at this time there is no evidence to support the common recommendations of bed rest or aggressive hydration in the prevention of PDPH.
Spinal Technique
Replacing the stylet after CSF collection but before needle withdrawal is an effective means of lowering the incidence of PDPH after LP. This recommendation is based on a prospective, randomized study of 600 patients using 21-gauge Sprotte needles. In this setting, replacing the stylet reduced the incidence of PDPH from 16.3% to 5.0% (P <.005). This safe and simple maneuver is theorized to decrease the possibility of a wicking strand of arachnoid mater from extending across the dura (Fig. 4) [63].
Continuous spinal anesthesia (CSA) has been reported by some to be associated with surprisingly low incidences of PDPH compared with single-dose spinal techniques using similar gauge needles [64]. This observation has been attributed to reaction to the catheter, which may promote better sealing of a breach in the meninges. Continuous spinal anesthesia with small-gauge needles and catheters (“microcatheters”) is an appealing option when titration of spinal drug is desirable and duration of surgery is uncertain, but is currently unavailable in the United States, where the risk of PDPH with CSA remains concerning when using “macrocatheters” of approximately 20-gauge. For this reason, deliberate CSA may be underutilized and has been investigated almost exclusively in low-risk populations.
Epidural Technique
The issue of air versus liquid for identification of the epidural space with the loss-of-resistance technique has long been a source of controversy. Each method has acknowledged advantages and disadvantages, but neither has been convincingly shown to result in a lower risk of ADP [65]. In this case, operator preference and experience would be expected to strongly influence performance, and the overriding significance of this factor is illustrated in fewer instances of ADP noted when the medium is chosen at the anesthesiologist’s discretion [66].
Bevel orientation for epidural needle insertion remains a matter of debate. Norris and colleagues [67] found the incidence of moderate to severe PDPH after ADP was only 24% when the needle bevel was oriented parallel to the long axis of the spine (compared with 70% with perpendicular insertion). This orientation resulted in fewer therapeutic EBPs administered to patients in the parallel group (P<.05). However, this technique necessitates a controversial 90° rotation of the needle for catheter placement [68]. It seems that several factors regarding parallel needle insertion (lateral needle deviation, difficulties with catheter insertion, and dural trauma with needle rotation) are of greater concern to practitioners. Most respondents (71.3%) to a survey of United States anesthesiologists preferred to insert epidural needles with the bevel perpendicular to the long axis of the spine (consistent with the intended direction of catheter travel) [10].
Combined spinal-epidural (CSE) techniques have been reported to be associated with a low incidence of PDPH. While providing the advantages of a spinal anesthetic, CSE appears to have no increased incidence of PDPH or need for EBP when compared with plain epidural analgesia [69]. This observation may be due to several factors, including the ability to successfully use extremely small (eg, 27-gauge) noncutting spinal needles and tamponade provided by epidural infusions.
Measures to Reduce the Risk of PDPH after ADP
The risk-to-benefit ratio of prophylaxis should be most favorable in situations having the greatest likelihood of developing severe PDPH. Therefore, most efforts to reduce the risk of PDPH after ADP have been in the obstetric patient population. Several prophylactic measures, discussed below, are worthy of consideration and have been used alone or in combination [70]. However, because not all patients who experience an ADP will develop PDPH, and only a portion of those who do will require definitive treatment (ie, an EBP), a cautious approach in this regard is still generally warranted.
Stylet replacement
Although there have not been any studies to support the use of this technique in the setting of ADP, replacing the stylet is a simple and effective means of lowering the incidence of PDPH after LP [63]. Given the innocuous nature of this maneuver, if no other prophylactic measures are taken, there seems to be little reason not to replace the stylet before epidural needle removal in the event of ADP.
Subarachnoid saline
Limited evidence indicates that the subarachnoid injection of sterile preservative-free saline following ADP may be associated with a significant reduction in the incidence of PDPH and need for EBP. In one small study (n = 43), immediate injection of 10 mL saline through the epidural needle substantially reduced the incidence of PDPH (32%, compared with 62% in a matched control group) and resulted in a significant reduction in the need for EBP (P = .004) [71]. The injection of saline and the reinjection of CSF have been speculated as important in the prevention of PDPH by maintaining CSF volume [70]. However, given the relatively rapid rate of CSF regeneration, it may be that the benefit of fluid injection following ADP is actually in preventing a wicking strand of arachnoid (as proposed for stylet replacement). Further investigation into this issue is clearly needed.
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