The epidural blood patch (EBP) is regarded by many as the gold-standard treatment of postdural puncture headache (PDPH).1 Since its introduction in 1960 by Gormley,2 the EBP has been commonly used to treat PDPH from spinal anesthesia, dural puncture with epidural anesthesia, and diagnostic and therapeutic lumbar puncture. EBP has a reported success rate of >75%.3 Recent reports have suggested that EBP may have possible utility in the treatment of PDPH after placement of lumboperitoneal (LP) shunt.4,5 We present a case of a patient with pseudotumor cerebri (idiopathic intracranial hypertension) who had a LP shunt placed for persistent headaches and subsequently developed symptoms similar to a PDPH that were successfully treated with an EBP. Written consent was obtained from the patient for the publication of this case report.
A 31-year-old, African American woman presented with intractable headache, nausea, and vomiting after an LP shunt placement 5 days before admission. The patient had a history of pseudotumor cerebri diagnosed 2 years before this presentation, and she had been treated with intermittent lumbar punctures to relieve headaches associated with elevated intracranial pressures. This intermittent therapy eventually failed, resulting in intracranial pressures exceeding 45 mm Hg. She subsequently underwent LP shunt placement by a neurosurgeon.
The patient’s headaches before shunt placement manifested in a parietooccipital distribution with a constant, throbbing quality and without postural variance. She also experienced associated blurred vision, nausea, and vomiting. After LP shunt placement, the patient continued to suffer from headaches that differed in quality from those she experienced before the surgery. She described them as having a frontotemporal distribution, throbbing in nature, with associated nausea and vomiting. They became worse when sitting, standing, or with a Valsalva maneuver and were alleviated with supine position. She denied photophobia, phonophobia, or visual disturbances. The patient had a previous history of PDPH following prior lumbar punctures and noted that her headache after the LP shunt placement felt similar to previous PDPHs. Those headaches had resolved without EBP treatment. Conservative treatments including acetaminophen, caffeine, hydration, and bed rest provided no relief. The patient presented to the hospital emergency department on postoperative days 4 and 5 for her headache symptoms, and was readmitted for pain control and intravenous fluids. An anesthesiology consult for possible placement of an EBP was then ordered.
After complete history and physical were performed and other causes of headache were deemed unlikely, EBP placement was offered to the patient on postoperative day 7. Informed consent was obtained. Typical risks of the procedure (failure to relieve the headaches, inadvertent dural puncture, infection) and additional risks due to the shunt placement (damage to the shunt catheter and perhaps an increased risk of infection) were discussed with the patient. Due to concern for damaging the indwelling LP shunt catheter, fluoroscopic guidance was used for the procedure, which was performed by a general anesthesiologist and an anesthesiology resident.
The patient was brought to the fluoroscopic suite and placed in the prone position. The LP shunt catheter was noted at the L2–L3 interspace, so the L4–L5 interspace was chosen for the EBP. Standard aseptic technique was used. An 18-gauge Hustead needle was advanced to loss of resistance in the midline at L4–L5 under fluoroscopic guidance. Twenty milliliters of the patient’s blood, aseptically obtained from her arm, were injected into the epidural space. The patient noted immediate relief of her headache on completion of the procedure and was discharged home the next day. In subsequent follow-ups in the neurosurgery clinic at 1 week and 5 weeks after EBP placement, the patient did not have a recurrence of her headache.
The exact mechanism by which a PDPH occurs has been debated in the literature.1 However, loss of cerebrospinal fluid (CSF) from the intrathecal space has been shown to correlate with PDPH symptoms because Kunkle et al6 consistently produced PDPH symptoms by withdrawing 20 mL of CSF in test subjects. Furthermore, these subjects had immediate resolution (albeit temporary) by subsequent injection of 20 mL of saline solution (thus restoring CSF pressures). In a study examining postpartum epidural pressures when unintentional dural puncture occurred, normal epidural pressures correlated with no PDPH symptoms and significantly decreased mean epidural pressures were associated with PDPH symptoms.7 While these findings suggest loss of CSF pressure causes PDPH symptoms, not all patients with PDPH have decreased CSF pressures.8 Similarly, not all patients with significant postdural puncture leaks develop PDPH symptoms.8 A proposed mechanism by which PDPH could occur with normal CSF pressures is that PDPH symptoms may arise from cerebral vasodilatation. In this proposed mechanism, while there is still CSF loss, CSF pressures remain normal through increased cerebral blood flow (cerebral vasodilatation), and thus, it is this vasodilatation that causes the actual symptoms rather than the lower CSF pressures alone.9
The mechanism by which our patient experienced symptoms of PDPH is uncertain. We proposed that she had a leak around the LP shunt catheter causing an excess loss of CSF beyond what was being shunted by the LP catheter. Because conservative measures had failed previously, we decided to treat with an EBP.
Although the method by which an EPB relieves PDPH symptoms is not completely understood, possible mechanisms include formation of a clot at the dural tear or site of CSF leak, increasing CSF pressure, and causing cerebral vasoconstriction.10 Therefore, the resolution of our patient’s headaches after the EBP could have resulted from increasing CSF pressures as well as a clot formation around the LP catheter, thereby diminishing further leakage of CSF. Another possible explanation is that a large volume of CSF was lost during catheter placement causing CSF pressures to drop, and the normal production of CSF was insufficient to restore CSF volume due to an ongoing leak.
A previous case of PDPH after LP shunt placement was reported in which the headache recurred after the blood patch and was attributed to the type of valve used for the shunt,4 providing only transient symptomatic relief. Because our patient’s headache had not recurred at 5 weeks post-EPB placement, it was thought that her PDPH symptoms were not related to the LP shunt valve and were rather due to excess CSF loss during the LP shunt placement, or persistent CSF loss through a leak around the LP catheter.
While the optimal volume of injected blood remains disputed, we chose to infuse 20 mL of autologous blood because this volume has been shown to have greater efficacy than smaller volumes.2 Previous studies have shown that when 12–18 mL of blood were injected, a 9 spinal segment spread was observed with cephalad spread predominating.11 Given these reports, we felt confident that there would be sufficient cephalad spread of the EBP from the L4–L5 interspace to cover the LP shunt entry located at the L2–L3 interspace.
In summary, our patient presenting with PDPH symptoms after placement of an LP shunt had a successful resolution of symptoms after EBP administration 7 days postoperatively. While the exact mechanism by which our patient was experiencing PDPH symptoms is unknown, the EBP administration proved to be not only therapeutic, but also diagnostic as well, by ruling out LP shunt catheter malfunction through the successful resolution of symptoms. Given the current trend toward the development of more and more medical devices that are placed into the epidural and intrathecal spaces (intrathecal pumps, spinal cord stimulators, etc), EBP administration in the presence of an indwelling medical device may be required on an increasingly frequent basis.
Name: Jonathan Ferns, MD.
Contributions: This author helped write the manuscript and manage the case.
Name: Michael McCartney, MD.
Contributions: This author helped write the manuscript and manage the case.
This manuscript was handled by: Kent H. Rehfeldt, MD.
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