Unintentional dural puncture followed by postdural puncture headache is a well-known complication following neuraxial labor analgesia. Risk factors for the development of postdural puncture headache may be related to the patient’s history and characteristics, the neuraxial technique, and obstetrical events. The diagnosis of postdural puncture headache is usually made depending on the clinical presentation (orthostatic headache after a neuraxial procedure). Occasionally, neuroimaging and neurological consultation are warranted. Complications following postdural puncture headache may include transient or permanent hypoacusis, cranial nerve palsies, subdural hematoma, and chronic headache. Evidence is limited regarding the safety and effectiveness of different interventions aimed to prevent or treat postdural puncture headache.
Definition
Unintentional dural puncture (UDP) followed by postdural puncture headache (PDPH) is a well-known complication of neuraxial labor analgesia. The International Classification of Headache Disorders defines PDPH as a headache that occurs within 5 days of a lumbar puncture and is associated with cerebrospinal fluid (CSF) leakage through the dural puncture .
The headache is usually, but not necessarily, orthostatic in nature. It tends to worsen when going from a supine to standing or sitting position and improves when the patient lies down. Associated signs and symptoms are present in more than 50% of patients and may include neck pain or stiffness, photophobia, tinnitus, hypoacusis, and nausea . In most cases, spontaneous resolution of symptoms occurs within 2 weeks of onset, or sooner if autologous epidural blood patch (EBP) is performed . Although most cases resolve without major sequelae, PDPH may limit the interaction between the mother and newborn, is associated with prolonged length of hospitalization and emergency department visits, and, in rare cases, may lead to significant morbidity (e.g., chronic headache, subdural hematoma) .
Pathophysiology
There are two presumed mechanisms behind the development of PDPH:
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CSF loss through the dural rent that leads to the stretching and stimulation of sensory cranial nerve fibers caused by downward shift of the brain.
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Intracranial hypotension that leads to cerebral vasodilation (a compensatory mechanism to maintain intracranial volume) causing a vascular-type headache .
Risk factors
Reported risk factors for the development of PDPH after UDP are those related to the patient’s history and demographic and physical characteristics (previous history of PDPH, young age, female gender, history of chronic headache, lower body mass index (BMI)), the neuraxial technique (large-bore needles, cutting-tip needles, provider’s experience, time of the day the neuraxial procedure was performed), and obstetrical events (second stage pushing) .
In a prospective study, patients with a previous history of PDPH were more likely to develop a new PDPH after a second spinal anesthetic . Age is a well-established risk factor for PDPH . The incidence is higher in young adults (20–30 years old) and lower in those older than 60 years . A possible cause is the lower CSF pressure in the elderly. A systematic review of 18 trials concluded that nonpregnant females are two times more likely to develop PDPH than male subjects . A retrospective study suggested that patients with higher BMI have a lower incidence of PDPH after UDP (39% [BMI ≥ 31.5 kg/m 2 ] vs. 56% [BMI < 31.5 kg/m 2 ]; difference of −17%; 95% CI, −7% to −26%, P = 0.0004) . However, once patients developed PDPH, higher BMI did not confer further protection; the pain intensity at headache presentation and the highest reported pain score were similar between high and low BMI groups ( P = 0.61). In a retrospective study, advanced cervical dilation at the time of labor epidural catheter placement was identified as an obstetrical risk factor for the development of UDP ( P < 0.001) . Multiparity was associated with PDPH after UDP ( P = 0.004). A plausible explanation for the higher risk of UDP associated with greater cervical dilation at the time of epidural catheter placement is that painful contractions, and perhaps the urge to bear down, limit the patient’s ability to remain still during the procedure and increase the risk of UDP.
Diagnosis
Headache is common after delivery . The diagnosis of PDPH is usually made depending on the clinical presentation (orthostatic headache after a neuraxial procedure). If the patient develops focal neurologic signs or complains of a persistent severe headache despite conservative management or the headache becomes nonpositional, neuroimaging and neurological consultation should be considered ( Fig. 1 ) . Contrast-enhanced magnetic resonance imaging (MRI) is more sensitive than computed tomography for the diagnosis of PDPH. MRI signs consistent with intracranial hypotension include compression of the ventricles, reduction of the basal cisterns, caudal displacement of the brain, brainstem and optic chiasm, subdural effusions, cerebellar ectopia, and diffuse pachymeningeal thickening and enhancement .
The differential diagnosis of PDPH in the obstetric population is broad, ranging from benign or nonurgent conditions (tension-type headache, migraine, caffeine withdrawal, and lactation headaches) to more serious disorders (preeclampsia, meningitis, subarachnoid hemorrhage, and sagittal sinus thrombosis) ( Table 1 ) . In a prospective study over a 3-month period, 39% of women had a headache in the first week after delivery. PDPH was the sixth most common cause of headache (the most common was tension-type headache, 38% of all headaches) . PDPH was diagnosed in 4.7% women with headache.
| Diagnosis | Clinical presentation | Key features |
|---|---|---|
| Primary | ||
| Tension-type headache | Bilateral location Pressing or tightening nature Not worsened by physical activity No nausea or vomiting Photophobia or phonophobia may be present Usual duration: 30 min to 7 days | Most common type of recurring headache |
| Migraine | Unilateral location Usually frontotemporal Pulsating quality ± Aura Nausea and/or vomiting Photophobia and/or phonophobia Usual duration: 4–72 h. | Remission occurs during pregnancy and recurrence is common after delivery |
| Secondary | ||
| Preeclampsia | Headache associated with hypertension and proteinuria (in the absence of proteinuria, other evidence of organ dysfunction include thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, and cerebral or visual symptoms) | Magnesium sulfate should be administered for seizure prophylaxis |
| Meningitis | Typically acute presentation Headache associated with neck stiffness, nausea, fever, and changes in mental state and/or other neurological signs and symptoms | |
| Subarachnoid hemorrhage | Sudden or thunderclap onset May be isolated or associated with focal neurological deficits | |
| Dural sinus thrombosis | Non-specific headache: most often diffuse, progressive, and severe but can be unilateral and sudden (even thunderclap) or mild and migraine-like. | Very misleading. A recent persisting headache should raise suspicion, particularly in the presence of an underlying prothrombotic condition |
| Posterior reversible leukoencephalopathy syndrome | Headache accompanied by mental status changes, visual disturbances or blindness, seizure, and neuroimaging findings of cortical and subcortical edema. | Rarely occurs without seizures Often associated with hypertensive encephalopathy, preeclampsia, eclampsia, renal failure, immunosuppressive therapy, or chemotherapy |
Complications
Complications following PDPH include hypoacusis, diplopia, subdural hematoma, and chronic headache . Dural sinus thrombosis has been reported in women with PDPH .
Chronic headache
In a retrospective case–controlled study, women with UDP reported an increase in the likelihood of backache and a 28% incidence of chronic headache 12–24 months after delivery . Further prospective studies are required to confirm this finding.
Hypoacusia
Muffled hearing or tinnitus has been reported after UDP, and low-frequency hearing loss has been documented after spinal anesthesia . The presumed mechanism is endolymphatic hydrops caused by the loss of CSF and equalization of CSF and perilymphatic pressures . In a cohort-controlled study, women who were treated with an EBP after UPD during labor underwent an audiometric test several years after delivery (mean 5.2 years); the results were compared with those of a control group of healthy women . Minor hearing loss was detected in the UDP group compared to the control group.
Oculocranial nerve palsies
Diplopia secondary to oculocranial nerve palsy (oculomotor, trochlear, and abducens nerves) may occur after dural puncture . A 2004 systematic review identified 94 reported cases. The abducens nerve was the most commonly affected. The presumed mechanism is traction on nerves secondary to loss of the normal CSF “cushion” .
Dural sinus thrombosis
Dural sinus thrombosis has been reported after UDP and successful treatment with an EBP . Cerebral venous dilation from loss of CSF and postpartum hypercoagulability may explain these cases. The occurrence of new neurological symptoms, including the development of a nonpostural headache, should heighten the suspicion of dural sinus thrombosis.
Subdural hematoma
Subdural hematoma is a rare but serious complication following neuraxial procedures. Its presumed cause is traction and rupture of the bridging veins after CSF loss and caudal displacement of the brain. In a literature review of 56 cases, PDPH was identified as the first symptom in most patients who developed an intracranial subdural hematoma after neuraxial analgesia/anesthesia; subsequently, the headache became nonpostural in 83% of patients .
Prevention
The best method to avoid PDPH is to minimize the risk of UDP, and if dural puncture is planned, it is best to use techniques and equipment associated with a lower risk of development of PDPH. In a systematic review and meta-analysis, no intervention was identified as effective in reducing the incidence of UDP if an experienced operator performed the procedure. The use of a combination of spinal-epidural technique, fluid versus air as the loss-of-resistance medium, and ultrasound-guided insertion failed to decrease the risk of UDP . A single retrospective study found that pushing during the second stage of labor (versus first stage intrapartum cesarean delivery) was associated with a higher risk of PDPH . Given that the incidence of UDP cannot be decreased, research has focused on the prevention of PDPH after UDP .
Technique and equipment
Anesthesiologists can alter the incidence of PDPH by optimizing equipment and techniques. Use of smaller versus larger epidural needles (18- vs. 16-gauge) is associated with a lower incidence and severity of PDPH after UDP . A single low-quality study found that orientation of the bevel of the epidural needle in the sagittal (versus transverse) plane was associated with a decreased incidence of PDPH . In one study, the use of pencil-point epidural needles (e.g., Sprotte) compared with Tuohy needles was associated with a lower risk of PDPH after UDP .
Conservative measures
Neither bed rest nor hyperhydration were found to be protective against PDPH in a systematic review and meta-analysis . Abdominal binders, which were previously used to increase epidural pressure and prevent CSF leakage, are impractical and have shown no benefit in the prevention of PDPH.
Prophylactic epidural saline or colloid solution
Bolus or continuous infusion of saline through the epidural catheter was believed to prevent PDPH by briefly increasing the epidural pressure or by causing an inflammatory reaction of the dura, resulting in the sealing of the dural puncture. A systematic review and meta-analysis found no reduction in the incidence of PDPH with these practices . Case reports and small studies evaluated the prophylactic injection of dextran or hydroxyethyl starch solutions through the epidural catheter after UDP . The safety and efficacy of injecting these solutions into the neuraxial canal remain unclear.
Caffeine
Small studies using different doses of oral caffeine showed no significant risk reduction for developing PDPH with caffeine intake . Moreover, caffeine induces restlessness and insomnia; one case of postpartum seizures after oral caffeine therapy was reported .
Epidural morphine
A prospective, randomized, double-blind trial compared prophylactic epidural morphine administration and normal saline placebo for the prevention of PDPH after UDP . Parturients were randomly allocated to receive either morphine (3 mg) or normal saline placebo shortly after delivery and again 24 h later. Morphine was associated with a lower incidence of PDPH and need for EBP but with a higher incidence of nausea and vomiting (44%). Although no safety concerns were identified, the authors of this review recommend caution when using this technique. Epidural morphine crosses the dura at a higher rate in the presence of a large dural rent compared to intact dura. The resulting higher concentration of intrathecal morphine may be associated with an increased risk for respiratory depression. Larger trials are needed to confirm the benefit and safety of prophylactic epidural morphine administration.
Intravenous cosyntropin
Cosyntropin is an analog of ACTH and has been reported to successfully treat PDPH . The mechanism of action whereby ACTH and its analogs treat PDPH is not known. Expansion of blood volume (by the stimulation of aldosterone-driven water retention), increased production of CSF, anti-inflammatory action, and direct interaction with opioid receptors have been proposed as possible mechanisms . A single randomized, controlled, double-blind trial compared the prophylactic administration of intravenous cosyntropin 1 mg to normal saline placebo in women with UDP . The incidence of PDPH was reduced from 69% in the control group to 33% in the cosyntropin group ( P = 0.001) and the need for EBP was lower in the treatment group (11%) than in the control group (30%). These encouraging findings require confirmation in larger trials; moreover, safety, particularly with regards to breastfeeding, should be assessed.
Prophylactic epidural blood patch
A prophylactic EBP (PEBP) involves the injection of autologous blood (usually 15–20 mL) into the epidural space through an epidural catheter sited for labor analgesia after UPD, after the resolution of neuraxial blockade and before the removal of the catheter after delivery . The proposed mechanism is to prevent CSF leak through the dural defect by the clotted blood, facilitating sealing of the dural perforation.
Several randomized controlled trials of varying qualities have compared PEBP to conservative treatment. A 2010 systematic review and meta-analysis included nine studies and concluded that PEBP resulted in a reduction in the incidence of PDPH compared to control treatment . However, in a sensitivity analysis that included four randomized controlled trials, no benefit of a prophylactic blood patch was found. The quality of the nonrandomized trials was poor, and the highest quality trial (randomized, double-blind, controlled (sham procedure)) found no correlation between the incidence of PDPH and the need for a therapeutic blood patch but found a shorter duration of symptoms in the PEBP group . In contrast, a study published in 2014 found a significantly lower incidence of PDPH in women randomized to receive a prophylactic blood patch (18%) than those who received conservative treatment (80%) . However, the study was not double blinded (patients were aware of their treatment group) and intent-to-treat analysis was not performed. Thus, further study of PEBP for the prevention of PDPH is warranted.
Intrathecal insertion of an epidural catheter
Intentional placement of an epidural catheter through the dural rent into the intrathecal space is an attractive alternative to reattempting epidural analgesia after UDP; the spinal administration of local anesthetics and opioids will provide excellent labor analgesia. Moreover, labor analgesia can easily be converted to surgical anesthesia if an emergency cesarean delivery becomes necessary. Several retrospective series have suggested that the presence of an intrathecal catheter, particularly one that remains in place for 12–24 h, reduces the risk of PDPH after catheter removal. While in situ, the catheter mechanically obstructs the dural hole and prevents CSF from leaking. It may also induce an inflammatory reaction that promotes dural healing when the catheter is removed. In a 2010 meta-analysis, no reduction in the incidence of PDPH was identified when a catheter was left in the subarachnoid space at the time of UDP .
However, in a 2013 meta-analysis, the authors found a significant reduction in the requirement for EBP in women who had an intrathecal catheter compared to those who did not (relative risk (RR) 0.64; 95% confidence interval (CI) 0.49 to 084), although there was no difference in the incidence of PDPH (RR 0.82; 95% CI 0.67 to 1.01). Of note, most of the studies included in the analysis were retrospective or observational trials. Well-designed prospective studies are difficult to conduct because of logistical and ethical concerns. Two trials in which women were quasi-randomized to groups according to the time of delivery found no difference between groups in the incidence of PDPH and the need for EBP . The quasi-randomized study by Russell was prematurely stopped and was consequently underpowered to detect small differences . Surprisingly, although there was no difference in the incidence of PDPH, the author supported the placement of an intrathecal catheter after UDP to minimize patient suffering (no additional punctures and subsequent complication risk, e.g., repeat UDP) . In the past 3 years, several retrospective studies have been published addressing this practice. These studies found a lower incidence of PDPH in women who received intrathecal catheters than those who received epidural catheters.
As with all neuraxial techniques, intrathecal catheters carry both risks and possible benefits. In a retrospective review of complications associated with the use of large-bore intrathecal catheters in obstetric anesthesia (epidural catheters sited in the intrathecal space), no serious complications (meningitis, abscess, hematoma, arachnoiditis, and cauda equina syndrome) were reported . Drug error is probably the most important risk. Because intrathecal catheters are not routinely used, adequate communication (labeling of the catheter, verbal warning to all obstetric staff involved, and written details in the patient’s record) is required to avoid unintentional intrathecal injection of drugs intended for the epidural space; the significantly higher epidural local anesthetic dose will cause total spinal anesthesia if injected intrathecally .
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