Predictive Value of ONSD and NIRS for PDPH

Postdural puncture headache (PDPH) is defined as a headache that develops within five days following a dural puncture, is fundamentally caused by cerebrospinal fluid (CSF) leakage, and is characterized by neck stiffness, photophobia, and/or auditory symptoms. All cases involving a dural puncture during neuraxial block procedures are at risk for developing PDPH. The reported incidence following spinal anesthesia varies widely, ranging from 1% to 36% .The widespread use of neuraxial techniques in obstetric surgery has led to this complication being observed more frequently, particularly in the young female population.

Any delay in diagnosis or treatment can lead to serious, potentially life-threatening complications such as postpartum major depression, visual impairments, cranial nerve palsies, and subdural hematoma. PDPH and its associated complications not only reduce the mother's quality of life but also negatively impact the newborn care process.

The underlying factor in the accepted hypotheses regarding the pathophysiology of PDPH is excessive CSF loss. Changes in CSF volume can lead to changes in optic nerve sheath diameter (ONSD), which is surrounded by the meninges (arachnoid and dura). Due to the free exchange of CSF between the subarachnoid space and this region, changes in fluid volume result in the expansion or narrowing of the ONSD.

The validity of ultrasound-guided ONSD measurement in assessing intracranial pressure has been demonstrated; as a noninvasive and safe option, this method is utilized as a supportive tool for clinical diagnosis. The strong correlation between CSF pressure and ONSD dynamics highlights the potential of perioperative ONSD measurements in predicting the development of PDPH. This approach may carry clinical significance for patients presenting with high-risk factors, such as the use of a large-gauge needle, a low body mass index, and a prior history of headache or PDPH.

Following a decrease in intracranial CSF pressure, changes are also observed in cerebral vascular circulation. Under the Monro-Kellie doctrine, adenosine-mediated vasodilation occurs in vascular structures to compensate for the decreased CSF volume and lower intracranial pressure (ICP), leading to an increase in cerebral blood volume. Under physiological conditions, this compensatory vasodilation is expected to support cerebral blood flow (CBF), thereby maintaining or increasing cerebral oxygen saturation.

However, spinal anesthesia, which is frequently preferred in cesarean delivery, leads to post-spinal hypotension in 70-80% of cases due to the accompanying sympathetic blockade and systemic vasodilation in the lower extremities. Consequently, venous return and cardiac output decrease, leading to a reduction in systemic perfusion pressure. Therefore, although the Monro-Kellie doctrine triggers intracranial vasodilation (and theoretically increases cerebral blood volume), the concurrently developing severe post-spinal systemic hypotension may exceed the limits of cerebral autoregulation, setting the stage for a drop in net cerebral perfusion pressure and CBF velocity. This conflicting physiological process may lead to cerebral desaturation when compensatory mechanisms prove insufficient.

Currently, there is no reliable and effective method available in clinical practice to predict the development of PDPH. Early prediction and prevention of PDPH would reduce the incidence of postoperative complications, thereby enhancing the quality of recovery and care for both the mother and the newborn.

In this study, by testing the hypothesis that ONSD changes occurring after spinal anesthesia in pregnant women scheduled for elective cesarean delivery are associated with the development of PDPH, a predictive cutoff value for ONSD will be determined to foresee this complication. As a secondary endpoint, we aimed to evaluate the monitoring of cerebral desaturation secondary to post-spinal hypotension via NIRS and to assess the clinical significance of these data in predicting the development of PDPH.