PDPH occurs following procedures that disrupt the integrity of the meninges (ie dura and arachnoid mater).

  Onset of symptoms is generally delayed; 65% of patients experience symptoms within 24 h and 92% within 48 h.

  Onset of symptoms within 1 h is suggestive of pneumocephalus and not PDPH.

  The hallmark of PDPH is its postural nature, with symptoms worsening in the upright position and improving with recumbency.

  Pain and stiffness in the neck and shoulders are common and seen in nearly half of all patients experiencing PDPH.

  Nausea may be reported by a majority of patients.

The severity of PDPH symptoms is directly related to needle size. Larger needles are associated with more severe headaches⁵ and a greater need for definitive treatment measures.⁶ The severity of PDPH after spinal anesthesia varies from mild (11%) to moderate (23%), to severe (67%).²

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.⁷ With careful questioning, nausea may be reported by a majority of patients and can lead to vomiting.²

        Uncommonly, patients may experience auditory or visual symptoms,⁸ and the risk for either appears to be directly related to needle size.^9,10 In a large study of PDPH, these symptoms were present to a clinically significant degree in 0.4% of patients.¹¹ Auditory symptoms are frequently unilateral, and include hearing loss, tinnitus, and even hyperacousis. Subclinical hearing loss, especially in the lower frequencies, appears to be common following spinal anesthesia, even in the absence of PDPH.¹⁰ Closely associated with auditory function, vestibular disturbances (dizziness or vertigo) may also occur. Visual problems include blurred vision, difficulties with accommodation, diplopia, and mild photophobia.⁹ In contrast to headache complaints, nearly 80% of episodes of diplopia involve unilateral cranial nerve palsies.

Clinical Pearls

Incidence

The reported incidence of PDPH varies considerably depending on the technique employed, patient population, definition of PDPH, and duration of follow-up. PDPH is primarily discussed in association with spinal anesthesia; however, it is also frequently observed following diagnostic lumbar puncture, myelography, and accidental durai puncture (ADP) during epidural techniques.

        Rates of PDPH are particularly high (up to 10%) after myelography and diagnostic lumbar puncture, in which large-gauge needles are considered necessary due to the viscosity of contrast material and to facilitate the timely collection of cerebrospinal fluid (CSF).

Clinical Pearls

Rates of PDPH following spinal anesthesia have steadily declined; from an incidence exceeding 50% in Bier’s time, to around 10% in the 1950s,¹¹ until currently a rate of 1% or less can be reasonably expected. This reduction is clearly due to modifications in practice that have followed the identification of risk factors (discussed in the section on Risk Factors). In obstetric patients, a population known to be at high risk for PDPH, meta-analysis demonstrated an incidence of 1.7% using 27-gauge Whitacre needles.¹² Combined spinalepidural techniques have also been associated with a low incidence of PDPH (1.6% in one study of over 2000 obstetric patients).¹³ This observation may be due to several factors, including the ability to successfully use needles of very small diameters (ie, 27 gauge) with a noncutting tip design as well as possible tamponade provided by epidural infusions. Continuous spinal anesthesia using standard 20-gauge catheters (macrocatheters) has been reported by some to be associated with surprisingly low incidences of PDPH (3.4%) compared with single-dose spinal techniques using similar gauge needles.¹⁴ This observation has been attributed to reaction to the catheter, which may promote better sealing of a breach in the meninges. However, deliberate continuous spinal anesthesia has usually been investigated in low-risk populations.

        Epidural techniques are an attractive alternative to spinal anesthesia due to the perceived ability to avoid puncture of the dura. The problem is, however, that ADP cannot be reliably prevented and may be unrecognized at the time in over 25% of patients who eventually develop PDPH.¹⁵ ADP is of greatest concern in the obstetric anesthesia setting, where the incidence may be up to 1.5%.¹² Of these patients, 52–80% will develop PDPH.

Medicolegal Considerations

PDPH is a significant source of concern and dissatisfaction for patients. In parturients who had experienced an ADP, 70% would not choose to have epidural analgesia again, and only 28% would recommend it to a friend or relative.¹⁶ Iatrogenic headaches continue to represent a significant medicolegal liability, as noted by the high frequency of malpractice claims for headache in the American Society of Anesthesiologists Closed Claims Project database. For instance, for obstetric anesthesia claims, headache was the second most common maternal injury (after death) and resulted in payment in 56% of cases.^17,18 Similarly, headache following epidural steroid injections was the most common malpractice claim in pain management practices.¹⁹ For these reasons, the potential for this complication necessitates a proper discussion and informed consent for any procedure that may result in PDPH.

Clinical Pearls

Pathophysiologic Mechanisms Behind PDPH

Despite a great deal of research and observational data, the pathophysiology of PDPH remains incompletely understood.²⁰ It is generally accepted that PDPH results from a disruption of normal CSF homeostasis. 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 H₂0 in the horizontal position (40–50 cm H₂0 in the upright position). A sudden loss of CSF results in the development of typical PDPH symptoms, which resolve promptly with reconstitution of lost CSF volume.²¹ It is thought that PDPH is due to the loss of CSF through a persistent leak in the meninges. In this regard, it has been postulated that the arachnoid mater may be at least as and perhaps more important than the dura mater in the genesis of PDPH.²² However, the actual mechanism by which CSF hypotension generates headache is controversial and currently ascribed to a bimodal mechanism involving both loss of intracranial support and cerebral vasodilation (predominantly venous). Diminished hydrostatic support is thought to cause the brain to sag in the upright position, resulting in traction and pressure on pain-sensitive structures within the cranium (dura, cranial nerves, bridging veins, and venous sinuses). In addition, vasodilation may occur secondary to diminished intracranial CSF volume and reflexively secondary to traction on intracranial vessels.

Clinical Pearls

The neural pathways primarily involved in PDPH include the ophthalmic branch of the facial nerve (CN VI) in frontal pain, cranial nerves IX and X in occipital pain, and cervical nerves Cl through 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.⁸ Visual disturbances usually represent a transient palsy of the nerves that supply the extraocular muscles of the eye (CN III, IV, and, VI). The lateral rectus muscle is most often involved, attributed to the long, vulnerable intracranial course of the abducens nerve (CN VI).⁹

       RISK FACTORS FOR DEVELOPING PDPH

Risk factors for PDPH can be broadly categorized into patient characteristics and procedural details.

Patient Characteristics

Although uncommon in children younger than 10 years of age, PDPH has a peak incidence in the teens and early 20s.²⁴ The incidence then declines over time, becoming infrequent in patients older than 50 years of age. Female gender has long been thought to impart an increased risk for PDPH.¹¹ However, gender has not always constituted an independent risk factor when age-matched nonpregnant populations are studied.²⁴ Pregnancy is generally regarded as a risk factor for PDPH,¹¹ but this consideration partially reflects the young age as well as the high incidence of ADP in the gravid population. Pushing during the second stage of labor, thought to promote the loss of CSF through a hole in the meninges, has been shown to be a significant risk factor for PDPH following ADP. Angle and colleagues noted that the cumulative duration of bearing down correlated with the risk of developing PDPH in patients who had experienced an ADP and that patients who avoided pushing altogether (ie, proceeded to cesarean delivery prior to reaching second stage labor) had a much lower incidence of PDPH (10%) than those who pushed (74%).²⁵ Observed variations in the thickness of the dura (from 0.5 to nearly 2.0 mm) have also been proposed to influence the risk of PDPH, as punctures made where the dura is thicker appear to be less prone to allowing the loss of CSF.²⁶

Clinical Pearls

PDPH appears to have an interesting association with other headaches. Patients who report having had a headache within the week prior to lumbar puncture have been observed to have a higher incidence of PDPH.²⁷ On further analysis, only those with chronic bilateral tension-type headaches were found to be at increased risk.²⁸ A history of unilateral headache²⁸ or migraine²⁹ has not been linked with an increased risk of PDPH. Menstrual cycle, a factor in migraine headaches, did not influence the rate of PDPH in one underpowered pilot study.³⁰ A small but statistically significant increased incidence of PDPH following spinal anesthesia has been reported if patients have a history of previous PDPH.²⁴ Patients with a history of ADP have been shown to have a slightly increased risk of another ADP (and subsequent PDPH).³¹

        A number of other patient characteristics have been demonstrated to be minor risk factors for PDPH, including lower opening pressures,³² lower patient body mass index,^27,33 low CSF substance P concentration,³⁴ and low baseline pain sensitivity.³⁵ Although such findings would appear to be of academic interest only, they may hold important keys to the future prevention and treatment of PDPH.

Risk Factors Related to the Procedure and Equipment

Needle size and tip design are the most important procedural factors.⁵ Needle size is directly related to the risk of PDPH, with larger needles resulting in a higher incidence of symptoms.¹¹ “Noncutting” needles are associated with a reduced incidence of PDPH than occurs with “cutting” (eg, Quincke) needles of the same size. Noncutting needles, also referred to as pencil-point, blunt tip, atraumatic, or conical tip, include the Whitacre, Sprotte, European, Pencan, and Gertie Marx needles. Although originally thought to be less traumatic than cutting needles, electron microscopy has shown noncutting needles to produce a more traumatic hole in the dura, perhaps resulting in a better inflammatory healing response.³⁶ The influence of needle size on risk of PDPH appears to be less for noncutting needles than cutting needles (eg, the reduction in the incidence of PDPH between 22- and 26-gauge sizes is greater for cutting than noncutting needles). Some needles, such as the Greene and Atraucan, appear to be acceptable combinations of cutting and noncutting features.³⁷

Clinical Pearls

Inserting cutting needles with the bevel parallel to the long axis of the spine reduces the risk of PDPH.^24,38,39 This observation was for many years attributed to a “spreading” rather than cutting of longitudinally oriented durai fibers. However, scanning electron microscopy reveals the dura to be made of many layers of concentrically directed fibers,⁴⁰ and the importance of needle bevel insertion is most likely due to the longitudinal tension on the dura and its influence on CSF leakage through holes with differing orientations.

Clinical Pearls

A greater number of dural punctures increases the rate of PDPH.41 The angle of approach to the dura may be another important consideration, due to the dura-arachnoid relationship. Experimental and clinical evidence suggest that paramedian⁴² (vs midline) and oblique⁴³ (vs 90-degree) approaches may allow for better sealing of a dural puncture, reducing CSF loss and resulting in a lower incidence of PDPH. The operator’s experience, comfort, and skill are clearly associated with the incidence of ADP during epidural procedures, but have not consistently been a significant risk factor for other central neuraxial techniques. The possible contribution of operator fatigue, especially for ADP, remains to be determined.

        A number of procedural details do not appear to influence the rate of development of PDPH, including patient position at the time of dural puncture,27 bloody tap during spinal anesthesia,⁴⁴ addition of narcotics to spinal block,⁴³ and volume of spinal fluid removed (for diagnostic purposes).²’ The specific local anesthetic used may affect the rate of nonspecific headache but does not appear to influence the need for epidural blood patch (EBP).⁴⁶

Practical Approach to Evaluating Patients Presenting with Headache After a Neuraxial Anesthetic

A careful history with a brief consideration of other possible diagnoses is usually sufficient to differentiate PDPH from other causes of headache (Table 73–1). Most nonpostward puncture headaches will not have a strong positional nature, as seen in PDPH. Vital signs (normal blood pressure and absence of fever) and a basic neurologic exam should be documented. Bilateral jugular venous pressure, briefly applied, tends to worsen headaches secondary to intracranial hypotension. Laboratory studies are usually not necessary for the diagnosis of PDPH and, if obtained, are generally unremarkable (most commonly, magnetic resonance imaging may show meningeal enhancement, and lumbar puncture reveal increased CSF protein and low opening pressures).

        It should be noted that benign headaches are common in the perioperative setting, even in the absence of durai puncture, and have generally been noted to be less severe than PDPH⁷ (causes may include anxiety, dehydration, hypoglycemia, anxiety, and caffeine withdrawal). It has even been proposed that some nonpostdural puncture headaches may be due to contamination of the central neuraxis with skin preparation solutions.⁴⁷ The majority of headaches following durai puncture will be benign nonspecific headaches. In a careful analysis of headache following spinal anesthesia using strict criteria for PDPH, Santanen and colleagues found an incidence of nonspecific headache of 18.5%, with an incidence of true PDPH of only 1.5%.⁴⁸ In an obstetric population, Grove noted postpartum headache in 23% of patients who had not had any regional anesthesia.⁴⁹

Clinical Pearls

        Exacerbation of chronic headache (eg, tension, cluster, or migraine) is usually notable for a history of similar headaches. Hypertensive headache has a clear association with significant hypertension. Pneumocephalus can produce a positional headache that does not respond to EBP and can be difficult to distinguish from PDPH, but is readily diagnosed with computed tomography.⁵⁰ Sinusitis may be associated with purulent nasal discharge and tenderness over the affected sinus and is often improved with assuming an upright position. A number of other benign causes are possible.

        Serious causes of headache are rare but must be excluded. It is important to remember that lateralizing neurologic signs, fever/chills, seizures, or changes in mental status are not consistent with a diagnosis of PDPH. Meningitis tends to be associated with fever, leukocytosis, changes in mental status, and meningeal signs (eg, nuchal rigidity).⁵¹ Subdural hematoma (SDH), long recognized as a potential complication of durai puncture, is believed due to intracranial hypotension resulting in excessive traction on cerebral vessels, leading to their disruption. Practioners should maintain a high index of suspicion for SDH, which is often preceded by classic PDPH symptoms but progresses to lose its postural component and may include disturbances in mentation and focal neurologic signs.⁵² It has been proposed that early definitive treatment of severe PDPH may serve to prevent SDH.⁵³ Subarachnoid hemorrhage, most commonly due to rupture of a cerebral aneurysm or arteriovenous malformation, is usually associated with the sudden onset of excruciating headache followed by a decreased level of consciousness or coma.⁵⁴ Preeclampsia/eclampsia often presents with headache and may only become evident in the postpartum period.^55,56 Durai venous sinus thrombosis (DVST) is usually seen in the postpartum obstetric population, in whom headache symptoms may progress to seizures, focal neurologic signs, and coma.⁵⁷ Predisposing factors for DSVT include hypercoagulability, toxemia, and dehydration. Reports of other intracranial pathology (intracranial tumor, intracerebral hemorrhage, etc) misdiagnosed as PDPH are extremely uncommon and will be detected with a thorough neurologic evaluation.⁵⁴

        Diagnosis of PDPH can be particularly challenging in patients who have undergone lumbar puncture as part of a diagnostic work-up for headache. In these situations, headache should have changed in quality, the most common difference being a new postural nature. Occasionally, if the benign diagnostic possibilities cannot be narrowed down with certainty, a favorable response to EBP can provide definitive evidence for a diagnosis of PDPH.

       PREVENTION STRATEGIES

A number of recommendations can be made to decrease the risk of PDPH, but several long-standing practices, namely prolonged recumbency and aggressive hydration, do not appear to be useful.^58,59

Subarachnoidal Needle Placement

Prevention of PDPH in the setting of spinal anesthesia involves appropriate patient selection and careful attention to technique. Patients younger than 40 years of age are at particularly high risk for PDPH, and alternatives to spinal anesthesia should perhaps be sought in these individuals unless the benefits are sufficiently compelling (as they appear to be in the obstetric population). Using needles with a lower risk of PDPH is the most important technical means of reducing the risk of PDPH with spinal anesthesia. As a rule, the smallest noncutting needles feasible should be employed. However, extremely small needles are more difficult to place, have a slow return of CSF, may be associated with multiple punctures of the dura, and may result in a higher rate of unsuccessful block. Therefore, it appears that the best compromise between the risk of PDPH and ease of placement is a 24- to 27-gauge noncutting needle. If cutting tip needles are used, the bevel should be directed parallel to the long axis of the spine.

        It has been suggested that intravenous caffeine (500 mg caffeine sodium benzoate within 90 min after spinal anesthesia) reduces the incidence of moderate to severe headache.⁶⁰ However, the applicability of these data is questionable as this study involved the use of 22-gauge Quincke needles in a relatively young patient population.

Epidural Needle Placement

Unlike spinal anesthesia, patient selection appears to play a minimal role in the prevention of ADP during attempted epidural techniques. The use of a noncompressible medium (saline or local anesthetic) for loss-of-resistance generally results in a lower incidence of ADP than using air.⁶¹ The risk of PDPH following ADP can probably also be reduced by always using the smallest gauge epidural needle possible (yet equipment options in this regard are limited with catheter techniques.

        Optimal bevel orientation for epidural needle insertion remains a matter of debate. Although incidence of PDPH following ADP may be reduced by directing the needle bevel parallel to the long axis of the spine,³⁸ this technique necessitates a 90-degree rotation of the needle for catheter placement. Consequently, the possibility of durai trauma with needle rotation has prompted some to suggest always inserting epidural needles with the bevel facing the direction of desired catheter placement.⁶³

Strategies to Reduce the Risk of PDPH After ADP

Since not all patients who experience an ADP will develop PDPH, and only a portion of those who do will require definitive treatment, a cautious approach in this regard is suggested. Several immediate measures following ADP have been proposed to prevent the development of PDPH. Replacing the stylet prior to needle withdrawal is a simple and possibly effective means of lowering the incidence of PDPH. This recommendation is based on observations of lumbar punctures performed using 21 -gauge Sprotte needles and is theorized to decrease the possibility of an arachnoid mater “wick” through the dura.⁶⁴ Charsley and Abrams performed a subarachnoid injection of 10 mL of saline following ADP and noted a significantly reduced need for EBP in the treated group.⁶⁵ Their analysis is limited by the small number of patients studied, and further investigation is clearly indicated. Ayad and colleagues recommend placement of a subarachnoid catheter for 24 h following ADP.⁶⁶ In their obstetric population, catheter placement resulted in a rate of PDPH of only 6.2%, with an expected incidence under these conditions of over 50%. This impressive reduction in the incidence of PDPH, however, has not been noted in studies in which catheters have been left in place for less than 24 h.

        Provided an epidural catheter can be successfully placed following ADP, prophylactic epidural saline has been used in hopes of reducing the incidence and severity of PDPH. Efforts have included both bolus (eg, 50 mL as a single injection or every 6 h for four doses) and continuous infusion techniques (commonly 600–1,000 mL over 24 h). In the largest analysis of this approach (n = 241), Stride and Cooper reported a reduction in the incidence of PDPH from 86% in a conservatively treated control group to 70% with epidural saline infusion.⁶⁷ Trivedi and colleagues noted a similar reduction in PDPH (from 87% to 67%) in 30 patients who received a single prophylactic “saline patch” (40–60 mL) following completion of the obstetric procedure.⁶⁸ Other studies of epidural saline have noted this modest decrease in the incidence of PDPH. Stride and Cooper also reported a lower incidence of severe headache (from 64% to 47%), but this effect has been inconsistently seen by other investigators, and there is no definitive evidence that epidural saline reduces the eventual need for EBP. Despite the paucity of data, a survey in North America published in 1998 reported 25% of tertiary care obstetrical centers using prophylactic epidural saline infusions.⁶⁹ Such observations appear to be due more to a desire to “do something” and the perceived safety of the practice rather than any proven efficacy. The 1999 National Obstetric Anesthetic Database in the United Kingdom reported epidural saline infusion/bolus used as immediate management in only 7% of cases of ADP.⁷ Importantly, epidural saline does not appear to reduce the success rate of EBP. Although the epidural administration of saline is generally benign, transmitted pressure not uncommonly results in back and eye pain and has caused retinal hemorrhage.

Prophylactic Epidural Blood Patch: When, How, in Whom

The risk-benefit of prophylactic measures should be most favorable in those having the greatest likelihood of developing PDPH, such as obstetric patients experiencing an ADP with an epidural needle. However, investigations into the efficacy of the prophylactic EBP in this setting have yielded mixed results.⁷⁰ Scavone and colleagues, for example, in a prospective, randomized, double-blind study in an obstetric population found that the prophylactic EBP shortened the total duration of symptoms but failed to reduce the incidence of PDPH or subsequent need for EBP.⁷¹ Currently, due to concerns of exposing patients to a potentially unnecessary and marginally beneficial procedure, most centers do not utilize the prophylactic EBP as a routine measure.⁶⁹

        If employed prophylactically, the EBP should be performed only after any spinal or epidural local anesthetic has worn off, as premature administration has been associated with excessive cephalad displacement of local anesthetic.⁷² Residual epidural local anesthetic may also inhibit coagulation of blood, further decreasing the efficacy of EBP.⁷³

       TREATMENT STRATEGIES FOR PDPH

Once the diagnosis has been made, patients should be provided a straightforward explanation of the cause, natural history, and treatment options for PDPH. A treatment algorithm, based primarily on the severity of symptoms, can serve as a useful guide for management (Figure 73–1).

Time

PDPH is a complication that tends to resolve spontaneously. Prior to the introduction of definitive therapy for PDPH (ie, the EBP), the natural history of the disorder was documented by Vandam and Dripps as they followed 1011 episodes of PDPH after spinal anesthesia using cutting needles of various sizes.¹¹ Although their analysis is flawed by a lack information on duration in 9% of patients, if one considers their observed data, spontaneous resolution of PDPH was seen in 59% of cases within 4 days and 80% within 1 week. More recently, Lybecker and coworkers followed 75 episodes of PDPH and, although providing an EBP to 40% of their patients, noted in the untreated patients a median duration of symptoms of 5 days with a range of 1 to 12 days.² These data, although generally reassuring, also illustrate the sometimes prolonged duration of untreated PDPH.’Indeed, Vandam and Dripps noted 4% of patients still experiencing symptoms 712 months after spinal anesthesia.¹¹ Similar observations of prolonged symptoms have been reported following diagnostic lumbar puncture⁷⁴ and ADP.⁷⁵ A number of case reports exist of successful treatment of PDPH months or years after known⁷⁶ or even occult durai puncture.⁷⁷

Figure 73–1. Treatment decision-making algorithm for postdural puncture headache.

Related posts:

Regional Anesthesia in the Patient with Preexisting Neurologic Disease. The History of Local Anesthesia. Stimulating Catheters. Ultrasound-Assisted Nerve Blocks in Adults. Cutaneous Blocks for the Upper Extremity. Cervical Plexus Block.

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