Abstract
Despite advances in procedural techniques and equipment, postdural puncture headache (PDPH) remains a serious complication of labour epidural analgesia after accidental dural puncture (ADP). Often considered a temporary inconvenience, PDPH can be debilitating in the short term. It can also be associated with chronic manifestations and serious complications.
The precise underlying mechanisms of PDPH are still incompletely understood, and longstanding beliefs of dysregulation of cerebrospinal fluid (CSF) homeostasis due to CSF fluid loss are currently being challenged. The existence of orthostatic headaches unrelated to CSF loss demands consideration of other mechanisms involved, for instance, related to the autonomic nervous system or the release of calcitonin gene-related peptide (CGRP) associated with activation of the meningeal and cerebral arteries.
A multi-society international working group recently provided evidence-based recommendations on the prevention, diagnosis, and management of PDPH resulting from neuraxial procedures. According to the recommendations, there was insufficient evidence to support the routine use of intrathecal catheters or sphenopalatine ganglion blocks to prevent or treat PDPH. Both evidence-based and experimental strategies include stabilizing CSF dynamics through preventing CSF loss, supplementing CSF, or increasing production, and reducing cerebral vasodilation.
Future research in PDPH preventive and therapeutic strategies can be facilitated with standardised definitions, interventions, and outcome measures. Analyses should consider various confounding factors and recognise the complex multifactorial nature of pain experience across diverse populations. Clinical care and research on PDPH will demand a multidisciplinary collaborative effort to elucidate the complexities of its pathophysiology and further improve patient outcome and quality of care.
Abbreviations
ADP –
Accidental dural puncture
ANS –
Autonomic nervous system
CGRP –
Calcitonin gene-related peptide
CNS –
Central nervous system
CSF –
Cerebrospinal fluid
CVT –
Cerebral venous thrombosis
EBP –
Epidural blood patch
GONB –
Greater occipital nerve block
ICHD –
International Classification of Headache Disorders
ITC –
Intrathecal catheter
MRI –
Magnetic resonance imaging
NSAIDs –
Non-steroidal anti-inflammatory drugs
ONSD –
Optic nerve sheath diameter
PDPH –
Postdural puncture headache
POTS –
Postural orthostatic tachycardia syndrome
PRES –
Posterior reversible encephalopathy syndrome
PTSD –
Post-traumatic stress disorder
RCT –
Randomized controlled trial
SAH –
Subarachnoid haemorrhage
SDH –
Subdural hematoma
SIH –
Spontaneous intracranial hypotension
SPGB –
Sphenopalatine ganglion block
TVS –
Trigemino-vascular system
1
Introduction
Postdural puncture headache (PDPH), occurring after intentional or accidental dural puncture (ADP), remains a significant challenge in obstetric anaesthesia due to the high proportion of neuraxial techniques, and prevalence of risk factors such as younger age and female sex. While PDPH has traditionally been considered a relatively benign, self-limited condition, cohort and case-control studies suggest an association between PDPH and long-term morbidities, such as chronic headache, backache, neck pain and depression [ ]. Additionally, studies demonstrate an association between PDPH and rare but serious complications such as intracranial subdural hematoma and cerebral venous thrombosis [ , ].
Unfortunately, our understanding of PDPH is incomplete. There is a paucity of high-quality evidence to support many existing management strategies [ ]. It is not feasible to conduct sufficiently powered prospective studies for which large numbers of patients would be needed, and ethical considerations prevent randomisation [ ]. Here we review the current understanding of PDPH including strategies for prevention, pathophysiology, treatment, and long-term concerns with inclusion of lesser-known strategies for which further research is warranted.
1.1
PDPH definition, epidemiology, and diagnosis
- a.
Definition
The International Classification of Headache Disorders, ICHD-3, classifies PDPH (7.2.1) as a headache developing within 5 days of lumbar puncture, caused by cerebrospinal fluid (CSF) leakage through the dural puncture, which remits spontaneously within 2 weeks, or after sealing of the leak with autologous epidural lumbar patch [ ]. As with other headaches caused by low CSF pressure, headache symptoms may be more severe in the upright position (orthostatic or postural), but this feature is not required for a PDPH diagnosis. A PDPH is frequently accompanied by neck stiffness, tinnitus, photophobia and/or nausea. In anaesthesia practice or after diagnostic lumbar puncture, the diagnosis of PDPH is based on clinical symptoms, without the need to confirm reduced CSF pressure or CSF leakage through imaging.
- b.
Epidemiology
The incidence of PDPH varies based on procedure, needle type, and patient population [ ]. Patient-related risk factors for PDPH include female gender, younger age, low body mass index, chronic headache, pregnancy, vaginal delivery, and history of PDPH [ , ]. A PDPH occurs after 50–60% of spinal techniques when large (<24G) cutting spinal needles are used, but this risk falls dramatically to 0.16–2% with the use of pencil-point needles or smaller (>24G) cutting needles [ ]. Accidental dural puncture with a large (16-18G) epidural needle results in PDPH in 50–80% of cases [ , ]. With increasing utilization of labour epidural analgesia, it has been estimated that up to 15,000 women in Europe and 50,000 in the United States develop PDPH after childbirth every year [ , ].
- c.
Clinical presentation and diagnosis
The presentation of a PDPH is typically dull, throbbing, and bilateral, often with worsening in the upright position. However, up to 5% of PDPH may present without orthostatic changes [ ]. Common symptoms include neck stiffness, nausea, vomiting, tinnitus, hearing changes, photophobia, visual disturbances, and vertigo [ ]. These symptoms are thought to be the result of descent of brain tissue, engorgement or activation of meningeal or cerebral vessels, meningeal inflammation and temporary dysfunction of the first three cervical and cranial nerves [ , ]. Auditory symptoms, reported in 20% of cases, result from either involvement of the vestibulocochlear nerve or cochlear dysfunction [ ].
Postpartum headaches are common, affecting approximately 40% of women, with the majority being classified as tension headaches or migraines ( Table 1 ) [ ]. It is crucial to consider other potential causes when assessing postpartum headaches. In cases where hypertension is present, new-onset or worsening preeclampsia should be evaluated as a possible diagnosis. Such headaches may involve posterior reversible encephalopathy syndrome (PRES), though this is rare. Severe and rapidly worsening headache symptoms, especially when accompanied by focal neurological signs or altered consciousness, require immediate neurological assessment and neuroimaging to rule out rare but potentially life-threatening conditions, such as subarachnoid haemorrhage, subdural hematoma, cerebral venous thrombosis, ischemic stroke, or an undiagnosed intracranial tumor [ ]. To aid in the accurate diagnosis of postpartum headaches, Lim et al. recommend using the PARTUM mnemonic ( Table 2 ) [ ].
| Condition | Common Presentation |
|---|---|
| Tension headache | Bilateral, tightening headache |
| Migraine headache | Unilateral, pulsating headache |
| Preeclampsia with severe features/eclampsia | Headache associated with hypertension or seizure attributed to preeclampsia |
| Posterior Reversible Encephalopathy Syndrome (PRES) | Headache, visual disturbances, altered mentation, hypertension, ± seizure |
| Cerebral venous thrombosis (CVT) | Severe headache of gradual onset, typically non-positional |
| Meningitis/sepsis | Severe headache, fever, nuchal rigidity, vomiting, + Kernig or Brudzinski’s signs |
| Subdural hematoma (SDH) | Progressively worsening headache, with possible decreased consciousness |
| Postdural puncture headache (PDPH) | Fronto-occipital headache, often worse when upright |
| Cerebral venous infarction | +/− Headache, focal neurologic deficits |
| Intracerebral or subarachnoid haemorrhage (SAH) | Headache with focal neurologic deficits, “worst headache ever” (SAH) |
| Idiopathic intracranial hypertension | Headache, visual symptoms, ± nausea |
| Reversible cerebral vasoconstriction syndrome | “Thunderclap” headache |
| P | Pressure | Blood pressure for pre-eclampsia/eclampsia |
|---|---|---|
| A | Anaesthetic | Postdural puncture headache (PDPH) |
| R | Reversible | Reversible vasoconstriction syndrome or posterior reversible encephalopathy syndrome (PRES) |
| T | Thrombosis | Cerebral venous sinus thrombosis (CVT), ischemic stroke |
| U | Use your brain | There are so many other causes of headache: musculoskeletal, tension-type, meningitis, caffeine withdrawal, etc. |
| M | Migraine | If they improved during pregnancy, likely to recur in the first week postpartum |
Although PDPH has often been described as self-limiting, early studies reported chronic headache after spinal anaesthesia and recent cohort and case-control studies in obstetrics describe an increased risk of chronic headache, backache, postpartum depression and post-traumatic stress disorder (PTSD) [ ]. A recent anonymous online survey of individuals on a PDPH-patient advocacy website reported severe long-term consequences such as persistent headache and disability in patients previously diagnosed and treated for PDPH after lumbar puncture, epidural anaesthesia, or spinal surgery [ ]. Given the retrospective nature of data on chronic headache after PDPH, the possibility of bias is significant [ ]. Nonetheless, mounting evidence for an association of PDPH with chronic headache and other sequelae warrant further attention and consideration for longer-term follow-up.
In obstetric PDPH, additional diagnostic tools [e.g., radiologic evidence of CSF leak or lumbar puncture demonstrating CSF pressure <60 mm H 2 O)] are not typically used, and PDPH remains a clinical diagnosis [ ]. If the headache presentation is atypical, changes over time, or symptoms appear which cannot be explained by CSF loss or raise suspicion of serious complications, then imaging is warranted [ ]. Neuroimaging can rule out other pathology and either directly or indirectly demonstrate signs of CSF leakage. Spinal MRI, CT, or digital subtraction myelography can display the amount and site of CSF leakage. However, this finding can be nonspecific, often unaccompanied by clinical PDPH symptoms, or clinical symptoms can be present without signs of spinal CSF leakage [ , ]. Cranial MRI using a gadolinium-based contrast agent may show pachymeningeal (dural) enhancement, venous engorgement, brain sagging, or pituitary enlargement. In one study, 100% of patients undergoing MRI within 3 days of PDPH onset showed dural enhancement ( Fig. 1 ) [ ].
Transorbital ultrasound for optic nerve sheath diameter (ONSD) measurement could possibly aid in the diagnosis and monitoring of PDPH, as changes in CSF pressure are transmitted along the optic nerve sheath [ ]. Increased ONSD has been demonstrated after successful epidural blood patch (EBP) or closure of CSF leaks and is associated with a decrease in intracranial venous volume and blood flow [ , ].
2
The pathophysiology of PDPH
Postdural puncture headache (PDPH) was first accurately described by Dr. August Bier in 1899, who linked the condition to CSF loss and emphasized minimizing CSF loss during procedures. A similar orthostatic headache can occur with spontaneous intracranial hypotension (SIH), even without prior trauma or medical intervention [ ]. The CSF leak is often perceived to result from a dural tear; however, the primary barrier preventing CSF leakage is not the dura mater, with its 70–80 permeable layers of randomly arranged collagen and fibrinogen fibers, but rather the impermeable arachnoid mater ( Fig. 2 ) [ ].
When spinal CSF loss exceeds the body’s replacement rate (estimated to be about 300–1000 mL/day), the reduction in intracranial CSF volume—and eventually pressure, once the compensatory cerebral vasodilation capacity is surpassed—can cause a downward shift of brain structures, known as brain sagging [ , ]. This phenomenon can be accentuated in the upright position. The headache symptoms are thought to relate in part to traction on pain-sensitive structures such as meninges, arteries near the base of the brain, and anchoring veins draining into the sagittal, transverse, and other venous sinuses [ ].
Another feature of PDPH appears to involve cerebral vasodilation, as a reflex response to traction on intracranial pain-sensitive vessels and/or a compensatory mechanism caused by a reduction in CSF volume. This compensatory mechanism of haemostatic intracranial volume regulation (Monro-Kellie doctrine) is displayed when a loss in intracranial CSF volume is accompanied by an increase in cerebral blood volume (via vasodilation) [ , ].
Dilation of the meningeal arteries and activation of the trigemino-vascular system (TVS) involving release of calcitonin gene-related peptide (CGRP) may also contribute to headache symptoms like those of migraine headaches [ , ]. Another hypothesis suggests that lumbar CSF loss increases spinal compliance caudally, leading to low intracranial CSF pressure in the upright position, and subsequently to intracranial venous dilation [ ]. Lastly, neurotransmitters and modulators involved in pain perception, such as substance P, may play a role. Reduced CSF levels of substance P have been associated with an increased incidence of PDPH following lumbar puncture [ ].
It is notable that orthostatic headaches can occur without CSF disturbances in autonomic dysfunction syndromes like orthostatic hypotension or postural orthostatic tachycardia syndrome (POTS), when compensatory baroreflex mechanisms fail to adapt to postural changes [ , ]. In over 40% of cases, POTS coexists with other headache disorders, such as migraine or SIH, or develops after successful SIH treatment, which suggests a contribution of autonomic dysfunction [ ]. Further research is needed to elucidate the ANS mechanisms involved in the evolution of PDPH, and to identify potential therapeutic targets that modulate this activity.
2.1
Current evidence-based preventive and therapeutic management strategies for PDPH
- a.
Summary
The rare occurrence of PDPH and variability in clinical presentation make gathering of high-quality evidence difficult. Recently, a multidisciplinary group published expert- and evidence-based recommendations using the US Preventative Services Task Force grading guidelines [ ]. Recommendations assigned levels of certainty give clinicians a framework for the prevention, identification and management of PDPH ( Table 3 ) [ , ]. The main procedural recommendation for spinal anaesthesia/analgesia or lumbar puncture to minimize the risk of PDPH is to use a high gauge (small caliber), pencil point needle whenever feasible [ , ]. There is currently insufficient evidence to support other suggested preventative strategies, such as particular patient or needle positioning, postprocedural bed rest, hydration, or medications [ ].
| Procedural factors | ||
|---|---|---|
| Non-cutting spinal needles | A | |
| Narrower gauge cutting spinal needles | A | |
| Conservative treatments | ||
| Paracetamol (acetaminophen) and NSAIDs offered to all patients with PDPH | B | |
| Short-term opioid use if regular analgesics ineffective | C | |
| Caffeine offered in the first 24 h of symptoms | B | Maximum dose of 900 mg/day, 200–300 mg if breastfeeding) |
| Adequate hydration maintained with oral fluids | C | |
| Bedrest to lower severity of symptoms | C | Beware of increased risk of thromboembolism |
| Invasive treatments | ||
| Greater occipital nerve block (after spinal anaesthesia with 22-G or smaller spinal needle) | C | Headache recurrence risk |
| Epidural blood patch | B | Offered if PDPH does not respond to conservative treatment and impairs daily activities. |
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Initiation and maintenance of neuraxial labour analgesia: A narrative review
Preeclampsia and eclampsia: Enhanced detection and treatment for morbidity reduction
Navigating coagulopathy in obstetric hemorrhage: The role of point-of-care testing
Morbid obesity: Optimizing neuraxial analgesia and cesarean delivery outcomes
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