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Posterior Reversible Encephalopathy Syndrome with Vasospasm in a Postpartum Woman After Postdural Puncture Headache Following Spinal Anesthesia

Ho, Chiu-Ming MD, PhD; Chan, Kwok-Hon MD

doi: 10.1213/01.ane.0000278128.26896.b2
Obstetric Anesthesiology: Case Report

We describe a postpartum woman who, after an uneventful pregnancy, developed posterior reversible encephalopathy syndrome after spinal anesthesia, complicated by postdural puncture headache.

IMPLICATIONS: This report describes the successful management of a postpartum woman with cerebral vasospasm-induced posterior reversible encephalopathy syndrome. This syndrome is associated with irreversible brain damage if not recognized or treated incorrectly.

From the Department of Anesthesiology, Taipei Veterans General Hospital and National Yang-Ming University, Taipei, Taiwan.

Accepted for publication June 1, 2007.

Supported, in part, by grants (V95C1-034) from Taipei Veterans General Hospital, Taiwan.

Address correspondence and reprint requests to Chiu-Ming Ho, MD, PhD, Department of Anesthesiology, Taipei Veterans General Hospital, 201, Sec. 2, Shih-Pai Rd., Taipei 11217, Taiwan. Address e-mail to

Posterior reversible encephalopathy syndrome (PRES) is a rare acute neurologic condition characterized by headache followed by deterioration, including confusion, seizure, or cortical visual disturbances (1,2). Transient changes on neuroimaging with findings of edema in the symmetric bilateral posterior regions of cerebral hemispheres, usually with a reversible course, are often seen (1,2). The syndrome has occurred in patients with hypertensive encephalopathy, renal failure, immunosuppression, and postpartum eclampsia (1–7). Although postdural puncture headache is a well-described complication of spinal anesthesia in cesarean delivery (8), PRES has not been associated with postdural puncture headache after spinal anesthesia in postpartum women (1–7). This report describes a postpartum woman after an uneventful pregnancy who developed PRES after spinal anesthesia which was complicated by a postdural puncture headache.

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A 33-year-old primipara (62 kg, 158 cm) underwent cesarean delivery under spinal anesthesia in the 40th week of gestation because of failure to progress. Her medical history and laboratory examinations were unremarkable. No signs of preeclampsia, such as edema, proteinuria, arterial hypertension, or neurologic complaints had been observed during pregnancy.

After an initial IV preload of lactated Ringer’s solution (800 mL), a spinal block was performed with 27-gauge Quincke needle at L3–4, using a midline approach. On the first attempt, clear cerebrospinal fluid (CSF) was obtained, followed by slow injection of 12 mg 0.5% hyperbaric bupivacaine to achieve a T-4 sensory level for surgery, which proceeded uneventfully, with the patient exhibiting stable vital signs. The patient delivered a healthy girl (2876 g; Apgar score, 8–9). The mother’s vital signs were normal in the postoperative care unit; motor and sensory block had totally worn off 3 h after spinal anesthesia.

The patient did well until 2 days postsurgery when she developed a severe postural headache (visual analog scale, VAS, 8/10) over the bifrontal area, particularly when in an erect position; it was relieved by being recumbent. The diagnosis of postdural puncture headache was made. The headache improved (VAS, 2/10) after 4 days of supportive therapy, including oral analgesics (acetaminophen, 2 g/d), aggressive intravascular hydration (lactated Ringer’s solution, 3000 mL/d), and bed rest (8). Surprisingly, the patient complained of a severe throbbing headache (VAS, 10/10) over the occipital area, which was no longer postural. During this throbbing headache, her arterial blood pressure was 130 mm Hg (systolic) over 75 mm Hg (diastolic). The patient gradually presented with somnolence, confusion, visual hallucinations, right-sided facial and limb numbness, and slurred speech within a day. Routine hematologic biochemical tests as well as chest roentgenogram and echocardiogram, were normal. Noncontrasted computed tomographic scanning of the patient’s brain was unremarkable. Diagnostic lumbar puncture revealed an open pressure of 21 cm H2O; CSF was clear and showed no inflammatory signs. The next day, magnetic resonance (MR) imaging of the brain revealed edema of the bilateral posterior parietooccipital lobes with hyperintense signal on T2-weighted signal (Fig. 1A) and fluid-attenuated inversion recovery signal (Fig. 1B), with the same regions showing hypointense signal on T1-weighted signal. Diffusion-weighted images showed small patchy hyperintense areas within the bilateral posterior parietooccipital regions (Fig. 1C) and the hypointensity on apparent diffusion coefficient map of these areas showed restricted diffusion, which were consistent with cytotoxic edema in the early phase of cerebral ischemia. The MR angiography showed diffuse vasospasm of the main arteries of bilateral cerebral hemispheres, especially posterior circulations (Fig. 2A). MR venography revealed no evidence of thrombosis in the cerebral venous sinus. Transcranial Doppler showed high flow with turbulence at the right proximal middle cerebral artery and bilateral posterior cerebral arteries. During this period of hospitalization, no episode of marked hypertension was noted; the patient’s arterial blood pressure was within the range of 110–140 mm Hg (systolic) over 60–80 mm Hg (diastolic) before and throughout the development of clinical symptoms. Because intravascular magnesium sulfate may relieve maternal cerebral vasospasm (9–11), intravascular magnesium sulfate (16 g/d) treatment was immediately started. One day later, the headaches and numbness had subsided. Five days after initiation of the magnesium treatment, the patient reported no headache, and the neurologic examination was normal and the magnesium treatment was discontinued. Her arterial blood pressure was within the range of 100–125 mm Hg (systolic) over 60–80 mm Hg (diastolic) during the time of magnesium treatment. Repeat MR imaging 1 wk later demonstrated dramatic improvement, with a slight residual signal of the previous abnormalities; moreover, MR angiography showed complete resolution of the previously diffuse cerebral vasospasm (Fig. 2B). At that time, her transcranial Doppler was also normal. The patient was then discharged with no neurologic deficit and remained asymptomatic on the outpatient service 1 mo later.

Figure 1

Figure 1

Figure 2

Figure 2

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Clinical symptoms, as well as neuroimaging findings in this patient, are compatible with PRES (1–7). The patient presented with severe headache over the occiptal area, decreased awareness, confusion, visual disturbances, and altered sensorium. These occurred 5 days after an episode of typical postdural puncture headache, after spinal anesthesia for cesarean delivery. The MR imaging revealed cytotoxic edema of the cerebrum involving bilateral posterior parietooccipital lobes; MR angiography and transcranial Doppler showed diffuse cerebral vasospasm. These findings indicate that the lesion of PRES in this patient was associated with ischemia-induced cytotoxic edema.

Although the exact mechanism for PRES remains unknown (1,2), the temporal association of encephalopathy with diffuse cerebral vasospasm after an episode of postdural puncture headache may have been causative in this patient. Persistent leakage of CSF through the dural opening left by the lumbar puncture needle can result in sagging of the brain and traction on nerves and meningeal vessels (8,12,13). Presumably, the diminished volume of CSF in the cerebral ventricle may collapse the ventricle (14). This traction might cause mechanical stimulation on the arterial wall and, in theory, could induce vasospasm (14,15). Clearly, more clinical data are needed to prove this putative mechanism of collapsed ventricle-induced vasospasm. Previous studies have demonstrated that vasospasm can occur during the acute phase of PRES (16–18). An earlier report described eight postpartum women with postdural puncture headache who developed cortical blindness and seizure (19); angiography and xenon flow studies performed in three of them showed diffuse cerebral artery vasospasm (19). In the current patient, diffuse cerebral artery vasospasm, possibly due to the traction of this vessel by anatomic brain displacement, could provide an explanation for the development of PRES after spinal anesthesia. Furthermore, lack of evidence for systemic vasculopathy argues against an immune-mediated vasculitis in our patient. In addition, fluid accumulation, as part of aggressive intravascular hydration for treatment of postdural puncture headache, may have accentuated the tendency for brain edema, resulting in the development of PRES. All these observations suggest that diffuse cerebral vasospasm after an episode of postdural puncture headache after spinal anesthesia could have caused PRES in this patient.

PRES has been reported to be reversible (1); however, irreversible brain damage can sometimes occur due to late recognition or incorrect treatment (6,20). Importantly, treating the underlying problem usually leads to symptom resolution without neurologic deficit, as was seen in this patient. Therefore, acute treatment for cerebral vasospasm is essential. Nimodipine, a calcium antagonist, has been shown to be associated with a reduced rate of infarction because of cerebral vasospasm (21), but the efficacy of magnesium, a drug with calcium antagonist properties (22), in treating cerebral vasospasm is comparable to that of nimodipine (23). Several clinical studies have also shown that intravascular magnesium sulfate safely relieved maternal cerebral vasospasm (9–11). All syndromes subsided after magnesium treatment for 5 days, and the abnormal findings on neuroimaging had almost subsided 12 days later.

We describe the successful management of a postpartum woman with cerebral vasospasm-induced PRES, associated with postdural puncture headache after spinal anesthesia as another condition underlying PRES.

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