Chapter 31
Postpartum Headache
Alison Macarthur BMSc, MD, FRCPC, MSc
Chapter Outline
Postpartum headache is the complaint of cephalic, neck, or shoulder pain occurring during the first 6 weeks after delivery. The incidence of postpartum headache throughout the 6-week postpartum period has not been followed in a prospective manner. However, information is available from an evaluation of women during the first week postpartum,1 from a database that recorded symptoms during pregnancy and in the first week after delivery,2 and from a survey of women at 5 months and 1 year postpartum.3 Goldszmidt et al.1 evaluated 985 women during the first week postpartum and found a 38.7% incidence of headache. The median time to onset of symptoms was 2 days, and the median duration of headache was 4 hours. Benhamou et al.2 examined information collected on pregnant women who delivered at their institution during a 2-year period; exclusion criteria included recognized dural punctures, preterm deliveries, multiple gestation, and/or elective cesarean delivery. Headache was reported by 12% of 1058 patients who had epidural anesthesia without dural puncture and by 15% of 140 patients who delivered without epidural anesthesia. Saurel-Cubizolles et al.3 surveyed 1,286 postpartum women and found the incidence of headache was 22% and 42% at 5 and 12 months, respectively.
Post–dural puncture headache (PDPH) is one of the most common postpartum complications of neuraxial anesthesia. However, physicians and nurses should be aware that a dural puncture is only one of many causes of postpartum headache (Table 31-1). Most headaches are benign or do not require immediate attention; however, the timely diagnosis of some headaches (e.g., cortical vein thrombosis, subdural hematoma) is critical to good outcomes. Knowledge of both benign and nonbenign headaches is important for the anesthesiologist who is frequently the first physician to evaluate the patient with postpartum headache. Difficult diagnostic problems may require the opinion of a neurologist. The purpose of this chapter is to discuss the differential diagnosis of postpartum headache and PDPH in particular.
TABLE 31-1
Differential Diagnosis of Postpartum Headache
* The International Classification of Headache Disorders-II criteria state that caffeine-withdrawal headache occurs on cessation of ≥ 200 mg daily caffeine consumption for more than 2 weeks.4 However, others have suggested that caffeine-withdrawal headache may occur after as little as 3 days’ exposure to 300 mg/day or 7 days’ exposure to 100 mg/day.35
CSF, cerebrospinal fluid; CT, computed tomography; FLAIR, fluid-attenuated inversion recovery; MRA, magnetic resonance angiogram; MRI, magnetic resonance imaging.
Differential Diagnosis of Postpartum Headache
The classification of headaches follows the International Classification of Headache Disorders (ICHD), created in 1988 by the Headache Classification Subcommittee of the International Headache Society. This classification system, which has been updated (ICHD-II), identifies two broad categories of headaches: primary and secondary (Box 31-1).4 Primary headaches are classified as migraine, tension-type headache, cluster headache and trigeminal autonomic cephalalgia, or other. Secondary headaches are attributable to a specific underlying pathologic process. Primary headaches are 20 times more common than secondary headaches among women in the first week postpartum.1
After delivery, women frequently suffer from headache. Stella et al.5 retrospectively reviewed 5 years of hospital records to identify women who had postpartum headaches between 24 hours and 6 weeks after delivery. Ninety-five women met these criteria, and although the incidence of postpartum headache could not be calculated, the study did identify some important features of postpartum headache. Most women (82%) were still in the hospital at time of onset of the headache. Additionally, the demographics of the study population largely reflected the general obstetric population; the mean age was 25 years, 87% of the women had received some type of neuraxial analgesia/anesthesia, and 29% had a cesarean delivery.
Primary Headaches
The postpartum patient can present with a recurrence of her known primary disorder or with the first manifestation of a primary condition. Patients with a history of headache disorders typically are diagnosed with one of the four major types of primary headaches. The most common postpartum headaches are tension-type and migrainous headaches, which account for almost two thirds of headaches during this period.1,2 Tension-type headaches are often circumferential and constricting, can be associated with scalp tenderness, and are usually of mild to moderate severity.
Migraine
Migrainous headaches (or migraines) are defined as recurring cranial pain lasting 4 to 72 hours, often with typical features such as pulsating pain in a unilateral location, nausea, and photophobia.4 Headache with aura is a subtype of migraine that is characterized by focal neurologic symptoms preceding the headache. The prevalence of migraine is approximately 17% in the female population (three times more common than in men) and is more common in patients between 30 and 50 years or age.6 Pregnancy has an ameliorating effect on migraine frequency in the majority of sufferers. However, symptoms may recur soon after delivery, with reports of 34% within the first week postpartum and 55% within the first month.7 Generally, the symptoms are similar to their typical pattern, although often milder and less often unilateral. It is rare for a migraine to manifest for the first time during the postpartum period. There appears to be an association between migraines and preeclampsia, which may reflect an underlying predisposition to cerebral ischemic injury.8
Secondary Headaches
A common secondary headache in the postpartum period is the musculoskeletal headache, exacerbated by the maternal physical exertion of labor and associated sleep deprivation. This headache has accompanying neck and shoulder pain without a history of dural puncture. Approximately 11% to 14% of postpartum headaches are diagnosed as musculoskeletal.1 Other causes of secondary headache are discussed in the following paragraphs.
Hypertension
Hypertensive disorders of pregnancy, including preeclampsia, are commonly associated with headaches. Eclampsia is a form of hypertensive encephalopathy that includes headache, visual disturbances, nausea, vomiting, seizures, stupor, and sometimes coma. Seizures may occur in the absence of severe hypertension. Headache is a serious premonitory sign, being present in over 50% of women in whom eclampsia develops.9 Other hypertensive disorders, with or without superimposed preeclampsia, are also associated with headaches both antepartum and postpartum and may lead to encephalopathy. The diagnosis can be complex if the parturient’s labor and delivery course is complicated by a dural puncture.10
Posterior Reversible Leukoencephalopathy Syndrome
Posterior reversible (leuko)encephalopathy syndrome (PRES) was described in 1996 after recognition of consistent symptom presentation and brain magnetic resonance imaging (MRI) findings in a diverse group of patients. Conditions associated with PRES include preeclampsia, uremia, hemolytic-uremic syndrome, and exposure to immunosuppressant drugs.11 Approximately 25% of cases of PRES occur during pregnancy or in the immediate postpartum period. PRES symptoms include headache, seizures, altered mental status, visual changes, and, occasionally, focal neurologic deficits.12
The neuroradiologic features of PRES include symmetric areas of cerebral edema, predominantly involving the white matter regions of the posterior circulation (occipital lobes, posterior parietal and temporal lobes) (Figure 31-1). The pathophysiology of PRES is similar to that of hypertensive encephalopathy in that altered cerebrovascular regulation causes loss of blood-brain barrier integrity. The accompanying vasogenic edema can be reversed by prompt recognition and supportive therapy (e.g., cessation of provocative medications, aggressive treatment of hypertension, seizure prophylaxis). However, irreversible cytotoxic edema with permanent neurologic damage can occur if the initial disorder is not diagnosed early. This syndrome often manifests in the postpartum period, frequently in conjunction with preeclampsia. Distinguishing PRES from preeclampsia or eclampsia is complex because headache, seizures, and focal neurologic deficits, such as temporary loss of vision, are common symptoms of both disorders.13,14 Typical features that distinguish PRES from other postpartum headaches include seizures and focal neurologic deficits, such as temporary loss of vision. Definitive diagnosis is made with MRI.
FIGURE 31-1 Posterior reversible (leuko)encephalopathy syndrome (PRES). Axial fluid-attenuated inversion-recovery (FLAIR) images demonstrate foci of abnormally increased T2 signal (arrows) in the subcortical white matter and cortex of the frontal and parietal lobes involving both anterior and posterior circulations. (From Long TR, Hein BD, Brown MJ, et al. Posterior reversible encephalopathy syndrome during pregnancy: seizures in a previously healthy parturient. J Clin Anesth 2007; 19:145-8.)
Cortical Vein Thrombosis
The incidence of cerebral cortical vein thrombosis is increased during pregnancy and in the puerperium, and is estimated to be 10 to 20 per 100,000 deliveries in developed countries. The incidence appears higher in developing countries (e.g., 450 per 100,000 deliveries in India).15 Often it is difficult to distinguish cortical vein thrombosis from PDPH, because the headache of cortical vein thrombosis may have a postural component. Preceding dural punctures have been reported, and it has been hypothesized that the reductions in cerebrospinal fluid (CSF) pressure and cerebral vasodilation that accompany dural puncture predispose to thrombosis development.16 Associated features may include focal neurologic signs, seizures, and coma. Cerebral infarction may ensue if diagnosis is delayed. Diagnosis is best confirmed by MRI, because computed tomography (CT) appears to identify only one third of cases.17 Treatment of cortical vein thrombosis largely is symptomatic, with the aim of preventing seizures. Anticoagulation therapy is commonly used to treat these patients, with observational and randomized trial studies indicating better outcomes.18
Cerebral Infarction/Ischemia
Cerebral arterial insufficiency is one cause of stroke in pregnancy with an estimated incidence of 4 to 11 per 100,000 deliveries.19 Approximately half of the events occur in the peripartum period, and the clinical presentation often comprises a sudden onset of a nonpostural thunderclap headache, vomiting, seizures, and focal neurologic deficits. Postpartum cerebral angiopathy has been detected with the aid of cerebral angiography, in which a characteristic “arterial beading” pattern indicative of arterial spasm is evident.20 Initial CT and MRI findings are often normal, and intracranial Doppler or angiographic investigations may be necessary to diagnose the arterial ischemia or infarct. Treatment is supportive and may include vasodilator therapy.
Subarachnoid Hemorrhage
Subarachnoid hemorrhage (SAH) occurs secondary to aneurysmal or nonaneurysmal causes. The risk for SAH due to nonaneurysmal causes appears to be increased during pregnancy. A 2012 U.S. population–based study estimated an overall incidence of peripartum SAH at 5.8 per 100,000 deliveries.21 The classic presentation consists of the sudden onset of a severe headache that is unlike any previous headache. Associated symptoms may be present, such as decreased level of consciousness and focal deficits. Pregnancy may increase the risk for bleeding because of increased blood volume and hormonal changes that affect arterial integrity. Two thirds of all cases in pregnancy occur in the postpartum period, but maternal mortality appears to be less than in nonpregnant patients.21 Other factors associated with SAH during pregnancy include advanced maternal age, African American race, hypertensive disorders, smoking history, alcohol abuse, and intracranial venous thrombosis. Suspicion of SAH necessitates urgent investigation by CT scan, because nonsurgical therapies (e.g., endovascular ablation) are available and long-term sequelae can be minimized.
Subdural Hematoma
In rare instances, dural puncture is associated with the subsequent development of a subdural hematoma (see later discussion). In several case reports, the identification of the subdural hematoma was preceded by symptoms of a PDPH.22 Dural puncture results in leakage of CSF and decreased intracranial pressure (ICP). Presumably, the reduction in ICP causes stress on bridging cerebral vessels, which may precipitate bleeding. Neurologic signs of subdural hematoma are variable but include evidence of increased ICP (e.g., headache, somnolence, vomiting, confusion) and focal abnormalities.
Carotid Artery Dissection
A rare, vascular cause of postpartum headache is spontaneous carotid artery dissection. Borelli et al.23 reviewed the 19 known published cases of postpartum carotid artery dissection. The mean interval from delivery to headache onset was 9.3 days. The headaches were constant in character and both unilateral and bilateral. Stricken woman appeared older (mean age, 35 years) than the average parturient. Diagnosis was made after carotid vessel ultrasonography or magnetic resonance angiography.
Brain Tumor
Intracranial tumors may manifest as postpartum headache. Headache that is dull rather than throbbing may be an early feature of a brain tumor. Nausea, vomiting, seizures, and/or focal neurologic signs may be present. Neurologic examination may reveal evidence of increased ICP. Case reports suggest that atypical presentation of the headache, either with persisting headache symptoms in the supine position or exacerbation after epidural blood patch, should prompt further neuroradiologic investigations.24,25
Idiopathic Intracranial Hypertension
Parturients with idiopathic intracranial hypertension (i.e., increased ICP in the absence of a mass lesion, also known as pseudotumor cerebri or benign intracranial hypertension) have headache and visual disturbances, usually in the antepartum period. The features of the postpartum headache of pseudotumor cerebri mimic the usual chronic headache symptoms experienced by the patient. The diagnosis largely is one of exclusion (see Chapter 49). Treatment involves reduction of CSF pressure, either with glucocorticoids, carbonic anhydrase inhibitors, diuretics, or serial lumbar punctures. Case reports describe the use of an intrathecal catheter for labor analgesia26 and administration of epidural blood patch for PDPH in patients with idiopathic intracranial hypertension.27
Spontaneous Intracranial Hypotension
Spontaneous intracranial hypotension develops because of CSF leakage secondary to dural tears. The tears usually occur at the thoracic spinal level and are not associated with prior spinal intervention.28 Diagnosis requires radioisotope cisternography and CT myelography, which may also identify the level of the leak. Presentation of this disorder is identical to that of PDPH, because the pathophysiology is the same. The only difference is the lack of a prior neuraxial procedure in spontaneous intracranial hypotension. One case report has described the development of a postural headache 4 days after a spontaneous vaginal delivery without neuraxial anesthesia.29 The patient was found to have a cervicothoracic dural leak.
Pneumocephalus
The subdural or subarachnoid injection of air used for identification of the epidural space may be associated with the sudden onset of severe headache, sometimes accompanied by neck pain, back pain, or changes in mental status.30 Headache symptoms can mimic PDPH in that they are worse in the sitting position and may be relieved by lying down. Radiologic studies confirm the presence of intracranial air; the headache typically resolves over the first week. Administration of oxygen by nasal cannula or face mask may hasten resorption of the air and speed recovery, although this has yet to be proven with pneumocephalus after neuraxial anesthesia.31
Meningitis
The severe headache of meningitis typically manifests within the first several postpartum days (see Chapter 32). It is accompanied by fever, nuchal rigidity, and the presence of Kernig and Brudzinski signs. Lethargy, confusion, vomiting, seizures, and a rash also may occur. The most common pathogen is Streptococcus viridans.32,33 These organisms are found in the upper airway and vagina; the causative organism has been linked to the oropharyngeal flora of the proceduralist in a number of reports of iatrogenic meningitis after dural puncture procedures. Aseptic technique during the neuraxial procedure, including donning of a mask by the proceduralist, is of paramount importance. The diagnosis is confirmed by examination and CSF culture.
Sinusitis
Headache caused by inflamed paranasal sinuses is associated with purulent nasal discharge and, occasionally, fever. Pain may be unilateral or bilateral, depending on the extent of the disease, and the skin over the affected sinus may be tender. Frontal sinus infection causes headache in the frontal region. Ethmoidal and sphenoidal sinus infections cause periorbital pain, and maxillary sinus infection may cause diffuse facial discomfort. The sinuses fill overnight, and pain typically is worse on awakening. Pain improves in the upright position, which assists drainage.34
Caffeine Withdrawal
The withdrawal of caffeine may lead to headache, increased fatigue, and anxiety. Caffeine withdrawal headaches may occur after just 3 days’ exposure to 300 mg/day or 7 days’ exposure to 100 mg/day of caffeine.35 Normal-sized caffeinated drinks usually contain 50 to 100 mg of caffeine per serving. Although caffeine withdrawal headache has not been documented as a cause of postpartum headache, if the parturient has been drinking beverages with caffeine during the pregnancy the diagnosis should be considered.
Lactation Headache
Askmark and Lundberg36 reported episodes of intense headache during periods of breast-feeding in a woman known to suffer from migraine. Onset of headaches occurred within the first few minutes of breast-feeding, and the headaches resolved after cessation of nursing. The headaches were associated with an increase in plasma vasopressin concentration. Headaches have also been described in women with breast engorgement who either have elected not to breast-feed or have reduced the frequency of breast-feeding.37
Ondansetron
Sharma and Panda38 reported a case in which a woman received ondansetron for nausea and vomiting after uneventful spinal anesthesia for cesarean delivery. Several hours later she developed a severe frontal headache that was worse in the upright position and in the morning and evening hours. The symptoms abruptly stopped after the discontinuation of ondansetron.38 Headache is a common side effect of ondansetron (incidence, 3% to 17%), owing to its antagonism of serotonin 5-HT3 receptors, and should be considered in the differential diagnosis of postpartum headache.
Post–Dural Puncture Headache
Incidence
PDPH may occur after intentional dural puncture with a spinal needle or unintentional dural puncture with an epidural or other needle. A meta-analysis of studies of PDPH in obstetric patients (n = 328,769) calculated a pooled risk for unintentional dural puncture with any epidural needle of 1.5% (95% confidence interval [CI], 1.5% to 1.5%).39 After a dural puncture with an epidural needle, the risk for PDPH was 52.1% (95% CI, 51.4% to 52.8%) (Figure 31-2). The rate of PDPH after dural puncture with spinal needles ranged between 1.5% and 11.2%, depending on the needle size and type of needle (see later discussion) (Table 31-2).39–43 Although PDPH is often considered a “minor” complication of dural puncture, it was the cause of 14% of obstetric claims in the American Society of Anesthesiologists (ASA) Closed-Claims Project database (see Chapter 33).
FIGURE 31-2 Meta-analysis of post–dural puncture headache (PDPH) frequency for epidural needles in the obstetric population. The dots represent the percentages of patients experiencing the event. The horizontal lines represent the 95% confidence interval (CI). (From Choi PT, Galinski SE, Takeuchi L, et al. PDPH is a common complication of neuraxial blockade in parturients: a meta-analysis of obstetric studies. Can J Anaesth 2003; 50:460-9.)
Symptoms
Patients typically experience headache pain in the frontal and occipital regions, but location is not diagnostic. Pain often radiates to the neck, which may be stiff. Some women have a mild headache that permits full ambulation. In others, pain is severe and incapacitating. Symptoms are worse in the upright position and are usually relieved in the horizontal position. Abdominal compression may relieve pain in some patients. The ICHD-II defines PDPH as occurring within 15 minutes of moving to an upright position (sitting or standing) and resolving within 15 minutes of moving to the supine position, and requires one of the following symptoms to be present: headache, neck stiffness, tinnitus, hypacusis, photophobia, or nausea.4
Lybecker et al.44 reported the incidence of these symptoms in a prospective study of 75 nonobstetric patients with PDPH (Table 31-3). Cranial nerve palsy, thought to be secondary to nerve traction due to low CSF volume, is occasionally associated with PDPH. The sixth cranial nerve is most susceptible to traction during its long intracranial course. The traction results in failure of the involved eye to abduct, and patients may have diplopia. Hearing loss is usually in the low-frequency range and may be secondary to endolymph and perilymph imbalance and alteration of hair cell position in the inner ear.45 The risk for hearing loss appears to be increased with advanced age (> 40 years) and dural puncture with larger-gauge needles. Other rare symptoms associated with PDPH include seizures,46,47 vertigo,48 bilateral forearm pain,49 abdominal pain, and diarrhea.50 In all these case reports the headache and associated symptoms cleared after therapy with an epidural blood patch.
TABLE 31-3
Symptoms Associated with Post–Dural Puncture Headache
| Symptom | Incidence (%) |
| Nausea | 60 |
| Vomiting | 24 |
| Neck stiffness | 43 |
| Ocular* | 13 |
| Auditory† | 12 |
* Ocular symptoms include photophobia, diplopia, and difficulty in accommodation.
† Auditory symptoms include hearing loss, hypacusis, and tinnitus.
Data 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; 39:605-12.
Onset and Duration
Headache typically occurs on the first or second day after dural puncture; by ICHD-II criteria, it must appear within 5 days of dural puncture.4 However, Choi et al.39 found that PDPH can occur up to 7 days after dural puncture, and one case report identified a woman who developed a PDPH 12 days after labor neuraxial analgesia.51 Ninety-five percent of PDPH headaches last less than a week. The National Obstetric Anaesthesia Database project of the Obstetric Anaesthetists’ Association demonstrated that 75% of 975 women with PDPH had difficulty with performing activities of daily living.52 Rarely, symptoms may persist for months or even years.53 Webb et al.54 found that 18% of women who sustained a dural puncture with a 17-gauge Tuohy needle suffered from chronic headaches compared with 5% of women in a matched cohort who did not sustain dural puncture with an epidural needle. These findings require confirmation, but they suggest that there may be long-term sequelae from dural puncture with a large-gauge needle.
Imaging
Imaging investigations are not routinely recommended for the postpartum patient with a PDPH unless the symptoms suggest other diagnoses or the diagnosis of PDPH is in doubt. Contrast-enhanced MRI is the method of choice to study the meninges and has revealed characteristic findings of PDPH.55,56 These findings include (1) marked, diffuse pachymeningeal thickening and enhancement; (2) compression of the ventricles; (3) caudal displacement of the brain, brainstem, and optic chiasm; (4) cerebellar ectopia; (5) pituitary enlargement and enhancement; (6) and expansion of the superior sagittal sinus. The enlarged venous sinus may represent compensatory venous expansion in response to low CSF pressure. The presence of intracranial air on CT imaging (after using a loss-of-resistance to air technique to identify the epidural space) may help differentiate headache due to pneumocephalus from a low-CSF pressure headache.57
Pathophysiology
Debate continues regarding the precise etiology of PDPH symptoms. The original theory was that pain-sensitive nerve fibers were stimulated by a downward shift of the brain secondary to a loss of CSF volume. German surgeon August Bier58 is credited with the first description of successful spinal anesthesia and PDPH after his pioneering work on spinal anesthesia with cocaine. Bier and his assistant, Hildebrandt, performed spinal anesthesia on each other; using blows to the shin with an iron hammer and application of a burning cigar to the skin they demonstrated adequate sensory blockade.58 Both experienced severe PDPH. The assistant forced himself to work the next day, but Bier stayed home for 9 days. Bier suggested the PDPH might be caused by CSF loss. Today there is no doubt that leakage of CSF initiates the syndrome. Kunkle et al.59 consistently produced PDPH by draining 20 mL of CSF from volunteers. Symptoms were immediately relieved by subarachnoid injection of saline to restore initial CSF pressure.
Total CSF volume is estimated to be 150 mL, and the production rate is approximately 0.35 mL/min or a daily rate of 500 mL. The rate of CSF leakage through a dural hole may exceed the rate of CSF production. If this occurs, low CSF pressure results in a loss of the cushioning effect provided by intracranial fluid.
CSF pressure during labor is normal between contractions but increases significantly during painful contractions and expulsive efforts. Effective epidural analgesia attenuates this increase in CSF pressure.60 In a study of five women with unintentional dural puncture, epidural pressures were normal preceding the development of headache.61 However, with development of headache symptoms, the mean epidural pressure measurements were found to decrease significantly.
Not all patients with PDPH symptoms have decreased CSF pressure, and not all patients with a significant CSF leak experience symptoms. The pain of PDPH may be caused, in part, by an increase in cerebral blood flow (and cerebral vasodilation) as a consequence of low CSF pressure or volume. This phenomenon has been observed in animals.62,63 The inverse relationship between intracranial blood volume and CSF volume reflects the body’s effort to maintain a constant intracranial volume.64 The lumbar CSF compartment is a dynamic structure and acts as a reservoir for intracranial CSF volume adjustment.65 The occurrence of cerebral vasodilation may explain the relief of headache symptoms with vasoconstrictors such as caffeine, theophylline, and sumatriptan.
Risk Factors
In a classic study of 10,098 spinal anesthetics published in 1956, Vandam and Dripps66 noted that three patient factors influenced the incidence of PDPH: age, gender, and pregnancy. The analysis did not allow determination as to whether these factors were independent risk factors. Subsequently, other risk factors for development of PDPH have been identified.
Age
Extensive evidence supports the observation that PDPH is uncommon in patients older than 60 years of age and is most common in patients who are younger than 40 years of age.67 In the elderly, the dura may be inelastic and less likely to gape after puncture. CSF leakage may be impeded by adhesions and calcification. The cerebrovascular system also may be less reactive in older patients. Further, this group is less active physically and older patients may be less likely to complain.
Gender
Vandam and Dripps66 observed a twofold higher incidence of PDPH after spinal anesthesia in women than in men (14% versus 7%, respectively). This difference may be related to differences in cerebrovascular reactivity, because it is well known that migraine headaches occur predominantly in females and are influenced by hormonal changes. Women may have enhanced vascular reactivity, or perhaps changes in cerebral blood flow are more likely to produce pain in women than in men. A meta-analysis of randomized clinical trials identified a twofold higher risk for PDPH in nonpregnant females than in males.68
Vaginal Delivery
Vandam and Dripps66 also observed a high incidence of PDPH (22%) in women who received spinal anesthesia for vaginal delivery. This high incidence may be a result of the mechanical consequences of expulsive efforts during the second stage of labor and/or postpartum hormonal changes in cerebrovascular reactivity. Expulsive efforts in the second stage may increase CSF leakage. This possibility has prompted some physicians to restrict maternal pushing after dural puncture and to use forceps to shorten the second stage of labor. In a 20-year retrospective review of 460 parturients who experienced unintentional dural puncture during labor at the Birmingham Maternity Hospital in the United Kingdom, Stride and Cooper69 did not identify a lower incidence of PDPH in women who underwent prophylactic forceps delivery than in those who had spontaneous vaginal delivery. In contrast, in a retrospective review of the records of 33 laboring women who had experienced unintentional dural puncture, Angle et al.70 found that women who were allowed to push were much more likely to develop PDPH (relative risk [RR], 7.4; 95% CI, 1.1 to 48.2) and also were more likely to require an epidural blood patch.
Morbid Obesity
In a retrospective study, Faure et al.71 found that morbidly obese patients are less susceptible to PDPH and are also less likely to receive an epidural blood patch for treatment of PDPH, suggesting either a reduced severity of PDPH or anesthesia provider reticence to perform an epidural blood patch in this patient population. Possible but unproven explanations of a lower incidence and severity of PDPH in obese patients include increased abdominal pressure (which may reduce the extent of CSF leakage) and/or reduced physical activity in these patients. Other confounding factors, such as differences in the mode of delivery (higher rate of cesarean delivery) and neuraxial opioid administration, may also play a role. In contrast to these findings, Webb et al.54 found that the median body mass index was greater in women who developed PDPH after unintentional dural puncture with a Tuohy needle than in women who did not develop PDPH.
History of Previous Post–Dural Puncture Headache
A history of PDPH after previous spinal anesthesia is associated with the development of PDPH with subsequent spinal anesthesia.72 A cohort of nonobstetric women with a history of previous spinal anesthesia was monitored prospectively after a second spinal anesthesia procedure. Those with a previous history of PDPH were 2.3 times more likely (95% CI, 1.0 to 5.1) to have a second PDPH than women without a history of headache (24.2% versus 10.6%, respectively). This finding suggests that certain individuals are predisposed to the development of PDPH.
Multiple Dural Punctures
Seeberger et al.73 found that multiple dural punctures significantly increased the risk for PDPH. Surgical patients who received a second spinal injection owing to failure of the initial spinal puncture had a 4.2% incidence of PDPH compared with a 1.6% incidence among patients who had a single dural puncture.
Neuraxial Anesthetic Technique
Technical factors related to the neuraxial technique influence the incidence of PDPH.
Epidural Needle Size/Design.
The high rate of PDPH after unintentional dural puncture with an epidural needle has led investigators to alter the epidural needle design or size in an attempt to reduce headache incidence or severity. Data on the success of this endeavor are conflicting. In an in vitro study using cadaver dura, no differences were found in fluid leak rate among punctures made with Hustead, Tuohy, Crawford, and Sprotte epidural needles.74 In contrast, in an in vivo study, Morley-Forster et al.75 observed a lower incidence of PDPH with the use of an 18-gauge Sprotte needle than with the use of the standard 17-gauge Tuohy needle, despite no difference in the unintentional dural puncture rate. A pilot study has examined the use of a 19-gauge Tuohy needle with 23-gauge epidural catheter.76
Spinal Needle Design.
Historically, the beveled Quincke needle (Figure 31-3) has been the most widely used needle for dural puncture for both diagnostic and anesthetic purposes (see Chapter 12). A modification of the Quincke needle, the Atraucan needle, has a cutting tip and a double bevel, which is intended to cut a small dural hole and then dilate it.40 Clinical experience with the Atraucan needle has been generally good,40,41 although studies appear to suggest that the use of this needle is associated with a higher risk for PDPH than the use of a non-cutting, pencil-point needle (see Table 31-2).42
FIGURE 31-3 Designs of spinal needle tips (not to scale). (Drawing by Naveen Nathan, MD, Northwestern University Feinberg School of Medicine, Chicago, IL.)
In 1951, Hart and Whitacre77 introduced a solid-tipped, pencil-point spinal needle with a lateral injection port, which is now known as the Whitacre design (see Figure 31-3). They believed that their new needle would stretch and separate rather than cut the dural fibers and result in a lower incidence of PDPH. Currently, both 25- and 27-gauge Whitacre needles are very popular, and studies have confirmed the anticipated low incidence of PDPH.39 A randomized comparison of 27-gauge Quincke and Whitacre needles in outpatients undergoing spinal anesthesia found a lower incidence of PDPH in the Whitacre needle group.78 In vitro evidence suggests that fluid leak through the dural puncture site is lower after use of a pencil-point needle than after use of a beveled needle.79 With the recognition that pencil-point spinal needle tips reduce the incidence of PDPH, other tip designs have appeared. In 1987, Sprotte et al.80 reported experience with the use of a new needle that was designed to reduce the risk for neural and dural trauma (see Figure 31-3). The Sprotte needle has a solid oval tip and a longer orifice than the Whitacre needle. The incidence of PDPH was 0.02% with its use in a heterogeneous patient population of almost 35,000 patients.80 Subsequent studies have shown the incidence of PDPH with the Sprotte needle is lower than that with Quincke needles of smaller gauge (see Table 31-2).39 There are currently many other non-cutting spinal needle products available and all are associated with a low PDPH rate.
Spinal Needle Size.
With the Quincke needle, the incidence and severity of PDPH are directly related to the size of the needle. The incidence of PDPH appears to be lower with a 27-gauge needle than with 25- and 26-gauge needles (see Table 31-2). A similar relationship may exist with pencil-point needles. When needles smaller than 27-gauge are used, the incidence of PDPH is very low, but technical problems with needle insertion and failure to produce adequate anesthesia are more common.81 Locating the epidural space before insertion of the spinal needle (e.g., using the epidural needle as an introducer needle) may improve the success rate with these fine-gauge needles.
The current popularity of spinal anesthesia in obstetric patients is largely a result of new needle technology, which has led to a reduction in the incidence of PDPH. Because of the morbidity associated with PDPH, every effort should be made to use a needle associated with a low incidence of PDPH (e.g., a small-gauge, non-cutting needle).82 There are times when urgency or body habitus will dictate the use of a larger needle, but there is seldom justification for using a Quincke needle larger than 27-gauge.
Direction of Bevel of the Quincke Needle.
Studies have confirmed that puncturing the dura mater with a Quincke needle bevel parallel to the long axis of the spine reduces the incidence of PDPH by 70% compared with a perpendicular orientation.83 An early study by Franksson and Gordh84 demonstrated that orientation of the bevel of a Quincke spinal needle parallel to the long axis of the spine produced less dural trauma than occurred when the bevel was inserted perpendicularly. These investigators thought that the dural fibers were predominantly longitudinal in direction. Electron microscopy has revealed that the dural structure is far more complex than originally proposed. Fink and Walker85 noted that the dura consists of multidirectional interlacing collagen fibers with both transverse and longitudinal elastic fibers. They suggested that the insertion of the needle with the bevel parallel to the long axis of the spine most likely results in less tension on the dural hole and, therefore, a smaller aperture with less CSF leak. In vitro studies of bevel orientation and fluid leak have provided conflicting results.86–88 Despite confusing anatomic evidence, clinical experience strongly supports insertion of the Quincke needle with the bevel parallel to the long axis of the spine.83
Direction of the Bevel of the Tuohy Needle.
Norris et al.89 examined two groups of women who received epidural anesthesia with a Tuohy needle. In one group the bevel was kept perpendicular to the long axis of the spine. In the other group the needle entered the epidural space with the bevel parallel to the long axis and the needle was then rotated 90 degrees before insertion of the catheter. The authors observed a decreased incidence of PDPH in the latter group. However, some anesthesiologists argue that rotation of the needle within the epidural space may increase the risk for unintentional dural puncture. Richardson and Wissler90 randomized laboring women to a cephalad or lateral orientation of the Tuohy bevel during epidural needle insertion. The needle was not rotated before insertion of the epidural catheter. There was no difference in dural puncture or PDPH rates, but catheter insertion was easier with a cephalad orientation of the bevel.
Midline or Paramedian Approach.
There is conflicting evidence as to whether the spinal needle approach affects the incidence of PDPH. Haftalvi91 reported no cases of PDPH in a retrospective survey of 4465 spinal anesthesia procedures. This investigator used a paramedian approach with a 20-gauge Quincke needle, and the skin was punctured 3 cm from the midline. He suggested that tangential dural puncture creates a dural flap and prevents PDPH. In contrast, Viitanen et al.,92 prospectively monitoring obstetric patients after administration of single-shot spinal analgesia for labor (27-gauge Quincke needle), observed PDPH in 3 of 85 (3.5%) patients in whom the midline approach was used, compared with 15 of 127 (11.8%) patients in whom the paramedian approach was used. Using a rigid paper cylinder model of the dura, Kempen and Mocek93 studied median and paramedian punctures with a 22-gauge Quincke needle in different orientations. With midline punctures, all entry and exit holes were of uniform size regardless of bevel orientation and no dural flaps were seen. After paramedian punctures, flaps formed when the needle bevel faced the cylinder surface with a near-tangential angle of perforation, suggesting it may be beneficial to insert the needle via the paramedian approach to reduce the incidence of PDPH. Currently, data are insufficient to recommend either the median or paramedian approach in regard to subsequent PDPH.
Skin Preparation.
In a nonrandomized, nonblinded study reported in a letter, Gurmarnik94 found that the removal of dried povidone-iodine solution from the skin before placement of the spinal needle was associated with a lower incidence of PDPH (6% versus 0%). This investigator recommended removal of the povidone-iodine solution before insertion of the spinal needle and suggested that chemical meningismus resulting from povidone-iodine introduced into the intrathecal space by the spinal needle contributed to PDPH. This finding has not been confirmed by other investigators. Simsa95 suggested that using an introducer needle so the spinal needle does not touch the povidone-iodine solution may be preferable and accomplish the same goal. (Editors’ note: We do not recommend removal of povidone-iodine [or other solutions used for skin antisepsis] before initiating neuraxial analgesia, because povidone-iodine works by desiccating bacteria, and removing the povidone-iodine reduces its antibacterial effect. Rather, the solution should be allowed to dry on the skin.)
Air versus Saline Method of Locating the Epidural Space.
The medium (air or saline) used for the loss-of-resistance technique to identify the epidural space has not clearly been shown to influence the incidence of PDPH. Many anesthesia providers have adopted the loss-of-resistance-to-saline technique in the belief that it is associated with a lower incidence of unintentional dural puncture and PDPH than the use of air.96 However, the data are inconsistent, and not all studies have found a difference.97,98 In a meta-analysis of prospective randomized studies comparing air to saline and the incidence of both unintentional dural puncture and PDPH, no difference in either outcome was found.99 Segal and Arendt100 suggested that a randomized study of air versus saline may not be the best approach to study headache rate; the study design may lead to overestimation of the difference between air and saline, should one exist, because it is impossible to blind the anesthesia provider to technique and it forces the provider to use a less preferred technique. They performed a retrospective study comparing air with saline; the rate of unintentional dural puncture was not different between groups. However, among anesthesia care providers who had a preference for one technique, use of their preferred technique was associated with fewer unintentional dural punctures. Thus, current data do not support a difference in the incidence of PDPH between air and saline used for the loss-of-resistance technique to identify the epidural space, and one should certainly not change techniques hoping it may decrease headache rates.
Choice of Local Anesthetic Drug for Spinal Anesthesia.
Naulty et al.101 reported that the use of bupivacaine-glucose or lidocaine-glucose for spinal anesthesia was associated with a higher incidence of PDPH than the use of tetracaine-procaine. They postulated that osmotic, cerebral irritant, and/or cerebrovascular effects of the glucose could be responsible for these findings. Whether this finding is applicable to other non–glucose-containing local anesthetic preparations, such as plain bupivacaine, is unknown.
Continuous Spinal Anesthesia.
A multicenter trial published in 2008 reexamined the safety and use of 28-gauge microcatheters for spinal labor analgesia.102
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