Abstract
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. 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 a consultation with a neurologist or imaging studies. The purpose of this chapter is to discuss the differential diagnosis of postpartum headache and PDPH in particular.
Keywords
Post–dural puncture headache, Chronic headache, Subdural hematoma, Macrocatheters, Microcatheters, Cosyntropin, Epidural blood patch
Chapter Outline
Differential Diagnosis of Postpartum Headache, 724
Post–Dural Puncture Headache, 730
Incidence, 730
Symptoms, 730
Onset and Duration, 731
Imaging, 731
Pathophysiology, 732
Risk Factors, 732
Complications, 735
Prevention, 735
Treatment, 738
Unanswered Questions, 745
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 several sources, including an evaluation of women during the first week postpartum, from a database that recorded symptoms during pregnancy and in the first week after delivery, from a secondary analysis of parturients followed for postpartum pain, and from a survey of women at 5 months and 1 year postpartum. Goldszmidt et al. 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. 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 analgesia without recognized dural puncture and by 15% of 140 patients who delivered without epidural analgesia. Turner et al. evaluated patients at four university hospitals in the United States and Europe and found that 10% reported headache during pregnancy, 3.7% within 72 hours after delivery, and 3.6% at 8 weeks postpartum. A history of headache before pregnancy was predictive of headache during pregnancy and at 8 weeks postpartum but not at 72 hours. A history of intrapartum headaches was independently associated with headaches at 72 hours. Saurel-Cubizolles et al. surveyed 1286 women on their general health following their first or second delivery 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 30.1 ). 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 a consultation with a neurologist or imaging studies. The purpose of this chapter is to discuss the differential diagnosis of postpartum headache and PDPH in particular.
Headache Etiology | Primary Symptoms/Signs | Diagnostic Modality |
---|---|---|
Tension headache | Mild to moderate headache, lasting 30 minutes to 7 days Often bilateral, nonpulsating, and not aggravated by physical activity | History and physical examination |
Migraine | Recurrent moderate to severe headache, lasting 4 to 72 hours Often unilateral, pulsating, and aggravated by physical activity Associated with nausea, photophobia, and phonophobia | History and physical examination |
Musculoskeletal | Mild to moderate headache accompanied by neck and/or shoulder pain | History and physical examination |
Preeclampsia/eclampsia | Hypertension and/or HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome Headache often bilateral, pulsating, and aggravated by physical activity | History and physical examination Laboratory evaluation (alanine aminotransferase [ALT], aspartate transaminase [AST], uric acid, platelet count, urine protein) |
Posterior reversible (leuko)encephalopathy syndrome (PRES) | Severe and diffuse headache with an acute or gradual onset Possible focal neurologic deficits and seizures | History and physical examination MRI |
Stroke | Ischemic or hemorrhagic. Cerebral infarction/ischemia: new headache that is overshadowed by focal signs and/or disorders of consciousness. Subarachnoid hemorrhage : abrupt onset of an intense and incapacitating headache. Often unilateral accompanied by nausea, nuchal rigidity, and altered consciousness. | History and physical examination CT without contrast or MRI (FLAIR sequence) |
Subdural hematoma | Headache usually without typical features Often overshadowed by focal neurologic signs and/or altered consciousness | History and physical examination CT or MRI |
Carotid artery dissection | Late developing headache that is constant in nature Bilateral or unilateral location | History and physical examination. Carotid ultrasonography or MRA |
Cerebral venous and sinus thrombosis | Nonspecific headache that may have a postural component. Often accompanied by focal neurologic signs and seizures | History and physical examination MRV Possible angiography |
Brain tumor | Progressive and often localized headache Often worse in the morning Aggravated by coughing/straining | History and physical examination CT or MRI |
Idiopathic intracranial hypertension (pseudotumor cerebri/benign intracranial hypertension) | Progressive nonpulsating headache Aggravated by coughing/straining Associated with increased CSF pressure and normal CSF chemistry | History and physical examination Lumbar puncture |
Spontaneous intracranial hypotension | No history of dural trauma Diffuse, dull headache worsening within 15 minutes of sitting or standing Associated with neck stiffness, nausea, tinnitus, and photophobia CSF opening pressure < 60 mm H 2 O in the sitting position | History and physical examination Lumbar puncture Radioisotope cisternography CT myelography |
Pneumocephalus | Frontal headache Often an abrupt onset immediately after dural puncture Symptoms can worsen with upright posture | History and physical examination CT or MRI |
Meningitis | Headache is most frequent symptom Often diffuse Intensity increases with time Associated with nausea, photophobia, phonophobia, general malaise, and fever | History and physical examination Lumbar puncture |
Sinusitis | Frontal headache with accompanying facial pain Development of headache coincides with nasal obstruction Purulent nasal discharge, anosmia, and fever | History and physical examination Nasal endoscopy CT or MRI |
Caffeine withdrawal | Onset of headache within 24 hours of cessation of regular caffeine consumption a Often bilateral and pulsating Relieved within 1 hour of ingestion of caffeine 100 mg | History and physical examination |
Lactation headache | Mild to moderate headache associated temporally with onset of breast-feeding or with breast engorgement | History and physical examination |
Ondansetron headache | Mild to moderate headache associated with ondansetron intake | History and physical examination |
Post–dural puncture headache | Headache within 5 days of dural puncture Worsens within 15 minutes of sitting or standing Associated with neck stiffness, tinnitus, photophobia, and nausea | History and physical examination Possible MRI |
a The International Classification of Headache Disorders criterion states that caffeine-withdrawal headache occurs on cessation of ≥ 200 mg daily caffeine consumption for more than 2 weeks. 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.
Differential Diagnosis of Postpartum Headache
The classification of headaches follows the International Classification of Headache Disorders (ICHD), created in 1988 by the Headache Classification Committee of the International Headache Society. This classification system, which was updated in 2018 (3rd edition), identifies two broad categories of headaches: primary and secondary ( Box 30.1 ). Primary headaches are classified as migraine, tension-type headache, trigeminal autonomic cephalalgia, or other primary headache disorders associated with recurring activities (e.g., coughing, strenuous exertion, sexual activity). 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. In a study of 95 women identified with postpartum headache at a single center, Stella et al. noted that tension-type/migraine headache was the most common cause (47%) of postpartum headache. Preeclampsia/eclampsia and PDPH comprised 24% and 16% of cases, respectively.
Primary
- •
Migraine
- •
Tension-type headache
- •
Trigeminal autonomic cephalagias
- •
Cluster headache
- •
- •
Other primary headaches
Secondary
- •
Headache attributed to:
- •
Head and/or neck trauma
- •
Cranial or cervical vascular disorder
- •
Nonvascular intracranial disorder
- •
A substance or its withdrawal
- •
Infection
- •
Disorder of homeostasis
- •
Disorder of the cranial structures (e.g., eyes, ears, nose, sinuses, teeth, mouth)
- •
Psychiatric disorder
- •
- •
Lesions of cranial neuralgias and other facial pain
- •
Other headache disorders
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 migraine headaches, which account for almost two-thirds of headaches during this period. Tension-type headaches are often circumferential and constricting, can be associated with scalp tenderness, and are usually of mild to moderate severity.
Migraine
Migraine headaches 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. In the United States, the estimated overall age-adjusted 3-month prevalence of migraine is 19% in females and 9% in males, and is more common between 18 and 44 years of age. 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. 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. Pregnant women with severe migraine experience higher rates of adverse labor and delivery outcomes (e.g., preterm delivery, preeclampsia, low birth weight) but a lower rate of cesarean delivery than the general population. The higher rates of preeclampsia may reflect an underlying predisposition to cerebral ischemic injury.
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. 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 coma. Seizures may occur in the absence of severe hypertension. Headache is a serious premonitory sign, present in more than 50% of women in whom eclampsia develops. About one-half of the cases of postpartum eclampsia occur within 48 hours after delivery, and the remainder occur between 2 days and 4 weeks after delivery. Occipital or frontal thunderclap headache, blurred vision, scotomas, photophobia, and altered mental status are some of the potential presenting symptoms. Other hypertensive disorders, with or without superimposed preeclampsia, are also associated with headaches both antepartum and postpartum and may lead to encephalopathy.
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, infection, malignancy, and exposure to immunosuppressant drugs. Approximately 25% of cases of PRES occur during pregnancy or in the immediate postpartum period. Mayama et al. conducted a retrospective cohort study to assess the incidence of PRES in women with eclampsia and preeclampsia with neurologic symptoms. PRES occurred in 92.3% of women with eclampsia and in 19.2% of women with preeclampsia with neurologic symptoms. PRES symptoms include headache, seizures, altered mental status, visual changes, and, occasionally, focal neurologic deficits.
The pathophysiology of PRES is believed to be 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) in 70% to 90% of cases. However, irreversible cytotoxic edema with permanent neurologic damage can occur if the initial disorder is not diagnosed early.
The neuroradiologic features of PRES typically include symmetric areas of cerebral edema, predominantly involving the white matter regions of the posterior circulation (occipital lobes, posterior parietal and temporal lobes) ( Fig. 30.1 ). MRI is the “gold standard” for diagnosing PRES because it can provide information about cerebral involvement earlier than computed tomography (CT).
Stroke
The physiologic changes that occur during pregnancy (e.g., venous stasis, edema, hypercoagulability) render these patients susceptible to stroke, and headache is a common presenting symptom. Approximately 50% of strokes occur within the first 6 weeks postpartum. Strokes can be ischemic or hemorrhagic.
The evaluation and treatment of stroke during pregnancy should mimic that performed for nonpregnant patients. Treatment will depend on the etiology. In addition to supportive care, acute reperfusion therapy with fibrinolytic agents (recombinant tissue plasminogen activator) and intra-arterial mechanical thrombectomy should be considered in pregnant women with qualifying strokes.
Ischemic strokes account for approximately 87% of all strokes. Causes of ischemic stroke include cerebral venous sinus thrombosis, preeclampsia/eclampsia, thromboembolism related to valvular heart disease, and profound and persistent hypotension (e.g. cervical arterial dissection, amniotic fluid embolism). The clinical presentation often comprises new onset headache that is overshadowed by focal neurologic signs and/or disorders of consciousness.
Hemorrhagic strokes can be subclassified into intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH), with a 10% and 3% incidence, respectively. Hemorrhagic stroke in pregnancy and the postpartum period is relatively more common than in the nonpregnant state. Conditions associated with hemorrhagic stroke include preeclampsia/eclampsia, aneurysms, and arterio-venous malformations.
Subarachnoid Hemorrhage
Subarachnoid hemorrhage usually occurs secondary to ruptured aneurysms or arterio-venous malformations. The classic presentation is sudden onset of a severe headache that is unlike any previous headache (“worst headache of my life”). Associated symptoms may include neck stiffness, nausea, vomiting, decreased level of consciousness, and focal neurologic deficits. Suspicion of SAH necessitates urgent investigation by CT imaging; nonsurgical therapies (e.g., endovascular ablation) are available, and long-term sequelae can be minimized with early therapy.
Subdural Hematoma
Although usually associated with head trauma, subdural hematomas can occur spontaneously during pregnancy or can be associated with dural puncture (see later discussion). In several case reports, identification of the subdural hematoma was preceded by symptoms of PDPH. Dural puncture results in leakage of cerebrospinal fluid (CSF) and decreased intracranial pressure (ICP). Presumably, the reduction in ICP causes stress on bridging cerebral vessels, which precipitates tearing and bleeding. Spontaneous subdural hematomas have been reported in parturients with diseases associated with angiopathy, such as preeclampsia and fatty liver disease of pregnancy. 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. reviewed the 19 known published cases of postpartum carotid artery dissection in 2011. The mean interval from delivery to headache onset was 9.3 days. The headaches were constant in character and both unilateral and bilateral. Stricken women appeared older (mean age, 35 years) than the average parturient. Diagnosis was made after carotid vessel ultrasonography or magnetic resonance angiography.
Cerebral Venous and Sinus Thrombosis
Cerebral venous and sinus thrombosis (CVST) is an uncommon cause of stroke (less than 1% of all strokes) that results from thrombosis of the cerebral venous system, including dural venous sinuses, and deep and superficial cerebral veins. Approximately 2% of pregnancy-associated strokes are attributable to CVST. The most frequent symptoms in women with CVST are headache (86.1%) and epileptic seizures (26.8%). Diagnosis is best confirmed by MRI in combination with magnetic resonance venography; CT imaging identifies only one-third of cases. Treatment of cortical vein thrombosis includes anticoagulation and treatment of seizures and increased ICP. Anticoagulation therapy is recommended for patients with acute CVST, even in selected patients with intracranial hemorrhage. Thrombolysis may be a therapeutic option in a select group of patients with small hemorrhagic infarct and continued neurologic deterioration. Steroid therapy is not recommended.
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.
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 (see Chapter 48 ). The features of postpartum pseudotumor cerebri mimic the usual chronic headache symptoms experienced by the patient (i.e., nonspecific and varying in type, location, and frequency) and associated symptoms (e.g., visual loss, diplopia, nausea, vomiting, pulsatile tinnitus). The diagnosis largely is one of exclusion. Treatment involves reduction of CSF pressure, either with glucocorticoids, carbonic anhydrase inhibitors, diuretics, or surgical interventions (e.g., optic nerve sheath fenestration, cerebrospinal fluid diversion via lumboperitoneal or ventriculoperitoneal shunt, or intracranial venous sinus stenting). Since CSF volume is rapidly replaced, serial lumbar punctures are of limited value and should be reserved for patients who refuse or cannot undergo conventional medical or surgical therapy. Case reports describe the use of an intrathecal catheter for labor analgesia and administration of epidural blood patch for PDPH in patients with idiopathic intracranial hypertension.
Spontaneous Intracranial Hypotension
Spontaneous intracranial hypotension is an uncommon cause of headache that develops following CSF leakage secondary to dural tears. The tears usually occur at the thoracic spinal level and are not associated with prior spinal intervention. MRI of the brain with contrast will confirm the diagnosis of intracranial hypotension. MRI of the spine, CT cisternography, or CT myelography with contrast or radioisotope can help identify the exact location of CSF 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. Spontaneous intracranial hypotension has been reported during pregnancy and in the postpartum period.
Pneumocephalus
The subdural or subarachnoid injection of air used for identification of the epidural space may be associated with the sudden onset of severe frontotemporal headache, sometimes accompanied by neck pain, back pain, or changes in mental status. Headache is caused by meningeal irritation by air, and symptoms can mimic those of PDPH in that they are worse in the sitting position and may be relieved by lying down. Roderick et al. noted that 2 mL of air injected into the subarachnoid space was sufficient to provoke a symptomatic pneumocephalus. CT is more sensitive than MRI to confirm the presence of air density areas within the cranial cavity. The headache typically occurs soon after air entrance into the intrathecal space and resolves within 3 to 5 days with reabsorption of the air. Treatment is symptomatic. Administration of oxygen by nasal cannula or face mask may hasten resorption of the air and speed recovery, although this therapy has yet to be proven for pneumocephalus after neuraxial anesthesia.
Meningitis
Meningitis is a complication of neuraxial procedures, and the associated severe headache typically manifests within 12 hours to several days following the procedure (see Chapter 31 ). Headache is accompanied by fever, nuchal rigidity, and the presence of Kernig and Brudzinski signs. Lethargy, confusion, vomiting, seizures, and a rash also may occur. Various strains of Streptococcus, organisms typically found in the upper airway and vagina, have been linked to bacterial meningitis after neuraxial procedures. In several cluster cases, the involved organisms in the patients’ CSF were matched with the proceduralists’ nasopharyngeal swabs, confirming that these cases of post–dural puncture bacterial meningitis were the result of droplet contamination. Aseptic technique during the neuraxial procedure, including donning of a face mask by the proceduralist, is of paramount importance. The diagnosis of meningitis is confirmed by examination and CSF culture, and warrants immediate treatment.
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. The sinuses fill overnight, and pain typically is worse on awakening. Pain improves in the upright position, which assists drainage.
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. 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, the diagnosis should be considered if the parturient has been drinking caffeinated beverages during the pregnancy.
Lactation Headache
Askmark and Lundberg 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.
Ondansetron
Sharma and Panda 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. Headache is a common side effect of ondansetron (incidence, 3% to 17%), owing to its antagonism of serotonin 5-HT 3 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%). After a dural puncture with an epidural needle, the risk for PDPH was 52.1% (95% CI, 51.4% to 52.8%) ( Fig. 30.2 ). 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 30.2 ). Although PDPH is often considered a “minor” complication of dural puncture, it was the cause of 12% of obstetric claims in the American Society of Anesthesiologists (ASA) Closed-Claims Project database.
Needle Design | Gauge | n/N | Frequency of PDPH (%) a | 95% Confidence Interval b |
---|---|---|---|---|
Quincke | 24 | 15/238 | 11.2 | 10.2–12.2 |
25 | 114/1792 | 6.4 | 5.3–7.6 | |
26 | 139/2467 | 5.6 | 5.6–5.7 | |
27 | 34/1167 | 2.9 | 2.0–4.0 | |
Atraucan | 26 | 16/350 | 4.6 | 2.6–7.3 |
Whitacre | 22 | 1/68 | 1.5 | 1.2–2.8 |
25 | 137/6992 | 2.0 | 1.6–2.3 | |
27 | 13/820 | 1.6 | 0.08–2.7 | |
Sprotte | 24 | 57/1767 | 3.5 | 3.5–3.5 |
Polymedic | 25 | 22/292 | 6.6 | 5.9–7.4 |
BD | 26 | 205/2560 | 5.8 | 5.6–5.9 |
Gertie Marx | 24 | 8/201 | 4.0 | 1.7–7.7 |
a Estimates based on binomial probability estimation.
b Superscript numbers indicate reference citations at the end of the chapter.
Symptoms
The ICHD-3 beta classification defines PDPH as a headache occurring within 5 days of a lumbar puncture, caused by cerebrospinal fluid (CSF) leakage through the dural puncture. It is usually accompanied by neck stiffness and/or subjective hearing symptoms. PDPH usually remits spontaneously within 2 weeks, or after sealing of the leak with an autologous epidural blood patch. The headache is invariably orthostatic, but this is not a diagnostic criterion. Usually headache symptoms occur immediately or within seconds of assuming an upright position and resolve quickly (within 1 minute) after lying horizontally. Alternatively, the symptoms may exhibit delayed response to postural change, worsening after minutes or hours of being upright and improving, but not necessarily resolving, after minutes or hours of being horizontal.
Van de Velde et al. published a 10-year retrospective review of unintentional dural puncture and PDPH in obstetric patients. Of 65 patients diagnosed with PDPH, 55% reported associated symptoms such as nausea, photophobia, tinnitus, and vertigo. Headache was frontal in 34 patients, occipital in 9 patients, and combined frontal and occipital in 15 patients. In 7 patients, headache was not localized to a specific area. In a retrospective review of 75 patients with PDPH after spinal anesthesia, symptoms associated with headache included nausea, vomiting, neck stiffness, and ocular and auditory symptoms ( Table 30.3 ).