202411241324

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Tags: Neuraxial block, Obstetrics

Post-dural puncture headache

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
• depression

studies demonstrate an association between PDPH and rare but serious complications such as

• intracranial subdural hematoma
• cerebral venous thrombosis

Definition

The International Classification of Headache Disorders, ICHD-3, classifies PDPH (7.2.1) as a headache

• developing w/i 5 days of lumbar puncture,
• caused by cerebrospinal fluid (CSF) leakage through the dural puncture,
• which remits spontaneously w/i 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
• 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.

Epidemiology

Patient risk factors

• female
• young age
• low BMI
• chronic headache
• pregnancy
• vaginal delivery
• Hx of PDPH
  Needle type
• large bore <24G
• cutting needle
  Accidental dural puncture with a large (16-18G) epidural needle results in PDPH in 50-80% of cases

Presentation

The presentation of a PDPH is typically

• dull,
• throbbing,
• bilateral,
• worsening in the upright position.
  up to 5% of PDPH may present without orthostatic changes.
  Common symptoms include
• neck stiffness,
• nausea,
• vomiting,
• tinnitus,
• hearing changes,
• photophobia,
• visual disturbances,
• vertigo
  These symptoms are thought to be the result of
• descent of brain tissue,
• engorgement or activation of meningeal or cerebral vessels,
• meningeal inflammation
• 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.

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)

In obstetric PDPH, additional diagnostic tools (e.g., radiologic evidence of CSF leak or lumbar puncture demonstrating CSF pressure <60 mm H2O) 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 gadolinium contrast may show

• pachymeningeal (dural) enhancement,
• venous engorgement,
• brain sagging,
• pituitary enlargement.
  In one study, 100% of patients undergoing MRI within 3 days of PDPH onset showed dural enhancement

Postpartum headache

Postpartum headaches are common, affecting approximately 40% of women, with the majority being classified as tension headaches or migraines

Pathophysiology

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

spinal CSF loss > body’s replacement rate (about 300-1000 mL/day)
→ ↓ intracranial CSF volume
→ surpassing compensatory cerebral vasodilation capacity
→ ↓ ICP
→ downward shift of brain structures, known as brain sagging
worsen with 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,
• 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

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

Prevention + treatment

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

Intrathecal insertion of the epidural catheter (intrathecal catheter, ITC), once an accidental dural puncture (ADP) occurs, may provide a functional mode of labour analgesia or caesarean delivery anaesthesia, but does not decrease the risk of PDPH and/or the need for an EBP

neuraxial injection of other substances (e.g., preservative free morphine, saline) into the epidural space or the use of prophylactic EBPs have not consistently shown benefit

Oral caffeine may temporarily reduce symptom severity, but the ingested amount should be limited in obstetric patients and breastfeeding women

Epidural blood patch

Other treatment

There appears to be no consistent association between the volume of CSF loss and the degree of PDPH symptoms
Transient headache symptoms do often occur during drainage of CSF in lumbar punctures and are associated with the volume collected
headache immediately after lumbar puncture procedures is unrelated to persistent PDPH at 24 hours or the need for an EBP

intrathecal catheter controversial

the best practices outlined in the 2024 Guidelines on ITC placement after ADP from the Obstetric Anaesthetists’ Association conclude that there is no evidence-based indication for leaving the ITC in situ after delivery is complete

Various strategies aim to increase the production of CSF. Increased fluid intake, administration of caffeine or other methylxanthines, hydrocortisone and ACTH-analogues, have all been considered but have not proven to contribute to increased CSF production

Epidural single shot saline boluses and continuous epidural or caudal saline infusions have been used as an option for the treatment of PDPH. Sterile saline, injected epidurally, produces a short-lived mass effect which is thought to temporarily reduce CSF flow through dural hole, thus facilitating repair

Various regimens in different patient populations have been studied, and while severity of symptoms reduces, the effect is transient, compared to EBP

IT saline injection may relieve stretching of pain-sensitive structures and secondary vasodilation. Intrathecal injection of saline, either during a spinal procedure, during ADP or through an ITC before removal appears to contribute to reduced incidence and severity of PDPH, though current evidence is not sufficient to recommend this as standard practice

Various treatments for migraine and cluster headache, such as triptans, gabapentinoids, sphenopalatine ganglion block (SPGB) and greater occipital nerve block (GONB), have shown some effectiveness in relieving the symptoms of PDPH, suggesting potential similarities in underlying pathophysiologic mechanisms. Interruption of central sensitization, reduction of inflammation and modulation of pain pathways may contribute to relief of symptoms

The SPGB, typically used in patients with cluster headache and trigeminal neuralgia, is considered to be a minimally invasive alternative treatment option for PDPH

The sphenopalatine ganglion (SPG) is the main extracerebral parasympathetic ganglion, located bilaterally in the pterygopalatine fossa, containing sensory, sympathetic, and parasympathetic fibers that innervate the lacrimal glands, nasal glands, and cerebral blood vessels.
The SPG is connected to the trigeminovascular system, which is implicated in various headache disorders

SPGB appears to temporarily reduce or reverse cerebral reflex vasodilation due to low CSF volume and potentially interrupt trigeminal activation, or modulate inflammatory neurotransmitters involved in pain signalling

An effective SPGB typically provides only temporary symptomatic relief, and repeated treatments may be necessary before PDPH symptoms resolve

Techniques include percutaneous and trans-nasal approaches, the latter being the less invasive, but likely less effective as well

A typical GONB includes bilateral injection of local anaesthetic and corticosteroid near the greater occipital nerves and may modulate trigeminocervical signalling to effect central pain processing pathways. The anti-inflammatory effect of the corticosteroid dose may augment the efficacy of the GONB

Oxygen therapy can be effective in treatment of cluster headache where it may have similar actions as in high altitude headache: inhibiting trigeminal-vascular and autonomic pathway innervation by acting specifically on the PS/facial nerve projections to the cranial vasculature

In treatment resistant PDPH, other means of repairing the meningeal breach have historically been considered, such as the use of fibrin glue
The most common complication, lumbar radiculopathy, occurred 6 times more frequently in the EBP group which also had a significantly longer hospital stay.
the limited evidence present does not support routine use, and complications include anaphylaxis and aseptic meningitis

References

Postdural Puncture Headache Beyond the Evidence - BPRCA