What Is the Optimal Management of Postdural Puncture Headache?

INTRODUCTION

Despite advances in equipment and regional anesthetic techniques, postdural puncture headache (PDPH) remains a persistent problem. In some cases, the headache is mild in intensity and brief in duration, without significant sequelae; however, this is not always the case. PDPH is occasionally severe enough to leave patients bedridden and can delay hospital discharge. PDPH can be prolonged, with reports of symptoms lasting months or even years. There is evidence that unintentional dural puncture with a Tuohy needle can lead to the development of chronic headache. Untreated PDPH can lead to the development of persistent cranial nerve palsies and even subdural hematoma. ^, Finally, despite the perception among physicians that PDPH is merely a nuisance, it is a surprisingly frequent, and sometimes a distressingly costly, source of litigation.

A wide range of both conservative and invasive treatments for PDPH has been described in the literature, sometimes with scant scientific support. The rationale for the more common treatments of PDPH in this review are based on our current understanding of the pathophysiology of PDPH. Because there are so few well-controlled studies of the treatment of PDPH, however, many of the treatment recommendations will be based on case reports, observational studies, and personal experience. A century after August Bier first described PDPH, the optimal management of PDPH is a question that remains unanswered.

PATHOPHYSIOLOGY

This chapter deals primarily with the treatment of PDPH; however, it should be remembered that our primary goal should be the prevention of PDPH. As in many other areas of medicine, prevention is far preferable to treatment. There are numerous risk factors for PDPH that cannot be modified, but the two most important are needle shape and size. The use of small pencil-point needles for spinal anesthesia (25- or 27-gauge Whitacre, Sprotte, Gertie Marx, or Atraucan needles) will reduce the incidence of headache after dural puncture to 1% or less, even in high-risk populations. Although in practice many attempt to use the smallest possible gauge noncutting needle, a recent Cochrane review suggests that needle gauge plays only a small role in further decreasing headache when these needles are used. Given the technical difficulties of successfully placing a very small-gauge noncutting needle, initial use of a 25-gauge needle should produce an acceptable rate of spinal headache. If a cutting needle (e.g., Quincke) is used, insertion of the needle with the bevel parallel to the longitudinal axis of the body will significantly decrease the risk of headache. When epidural anesthesia is performed, the option of using such small needles is not possible; we must instead rely on meticulous technique. The use of the combined spinal–epidural technique may reduce the risk for accidental dural puncture; the incidence of headache requiring autologous epidural blood patch (EBP) has been reported to be no higher with this technique than with traditional epidural anesthesia. ^,

An understanding of the pathophysiology of PDPH is essential when considering its treatment. There are two competing yet somewhat complementary theories. The first is predicated on the belief that the continued leak of cerebrospinal fluid (CSF) from a dural puncture leads to a loss of fluid from the intracranial compartment. The loss of the cushioning effect of CSF allows the brain to sag within the skull, which places traction on the pain-sensitive meninges, an effect that becomes most apparent in the upright position. This suggests that the treatment of PDPH should be based on minimizing the leak of CSF, increasing CSF production, or translocating CSF from the spinal to the intracranial compartment. Correlation of the degree of CSF spread within the epidural space with the severity of headache supports the role of this mechanism in the pathophysiology of PDPH.

The second theory postulates that the loss of CSF causes intracranial hypotension, which leads to compensatory cerebral vasodilation. This suggests that PDPH is similar to migraine headache, a theory supported both by the similarly increased incidence of migraine and PDPH in women and by MRI studies that demonstrate enhanced cerebral blood flow in PDPH. This theory suggests not only that PDPH will be relieved by restoration of intracranial CSF volume but also that cerebral vasoconstrictors might provide symptomatic relief.

OPTIONS

The treatment of PDPH is traditionally divided into conservative and, for want of a better term, aggressive treatment ( Box 50.1 ).

EVIDENCE