British Journal of Neurosurgery, December 2014; 28(6): 785–786 © 2014 The Neurosurgical Foundation ISSN: 0268-8697 print / ISSN 1360-046X online DOI: 10.3109/02688697.2014.913778
SHORT REPORT
Early onset of PRES in a patient with a subarachnoid haemorrhage due to a ruptured intracranial aneurysm Hiroki Kuroda1, Hiroshi Kashimura2, Toshiyuki Murakami2, Hidehiko Endo2, Tomohiko Mase2 & Kuniaki Ogasawara2 1Department of Neurosurgery, Iwate Prefectural Miyako Hospital, Miyako, Japan, and 2Department of Neurosurgery, Iwate
Medical University, Morioka, Japan
headache. On arrival, her blood pressure was 191/76 mmHg. She was subsequently started on a nicardipine drip; her systolic blood pressure (SBP) was between 102 and 144 mmHg, and diastolic blood pressure (DBP) was between 43 and 52 mmHg. The patient was alert and fully oriented without focal neurological deficits (Hunt and Hess grade II). A CT scan revealed a diffuse SAH. CT angiography demonstrated a saccular aneurysm located at the bifurcation of the left internal carotid and posterior communicating arteries. Arterial vasospasm was not observed in the anterior or posterior circulation. Forty hours later, she successfully underwent neck clipping of the aneurysm via a craniotomy under general anaesthesia. Anaesthesia was induced with an intravenous continuous infusion pump of 1% propofol and remifentanil and an intravenous bolus injection of fentanyl and rocuronium. SBP and DBP during the operation were 70–125 mmHg and 35–50 mmHg, respectively. When the patient recovered from general anaesthesia, she was fully oriented without focal neurological deficits. However, subsequent CT revealed a new hypodensity in the bilateral occipito-parietal lobes (Fig. 1). On the following day, she became somewhat lethargic. We identified no causes for this lethargy, including infection, electrolyte imbalance, hydrocephalus, or metabolic disorders. Thus, she underwent triple-H (hypertension, hypervolemia, and haemodilution) therapy. We intended to maintain her SBP between 140 and 190 mmHg. CT on the fifth postoperative day revealed enlargement of the hypodensity in the bilateral occipito-parietal lobes, and fluid-attenuated inversion recovery and T2-weighted MR imaging on the eighth postoperative day showed high intensity in those regions, which exhibited no abnormal findings on diffusion-weighted MR imaging. MR angiography on the same day revealed no evidence of vasospasm. She remained lethargic until the 12th postoperative day, when she complained of worsening headache. CT revealed hyperdensity in the bilateral occipito-parietal lobes (Fig. 2). She subsequently underwent a nicardipine drip, resulting in a decrease in SBP
Abstract Posterior reversible encephalopathy syndrome (PRES) is rarely associated with subarachnoid haemorrhage (SAH). We present a case involving a patient who developed PRES, prior to induction of hypertensive therapy, 2 days after the onset of a SAH due to a ruptured intracranial aneurysm. Keywords: hyperperfusion; hyperdynamic therapy; posterior reversible encephalopathy syndrome; subarachnoid haemorrhage
Introduction Posterior reversible encephalopathy syndrome (PRES) is manifested as a subacute change in neurological status and reversible white matter oedema in the bilateral occipitoparietal lobes on computed tomography (CT) or magnetic resonance (MR) imaging. PRES is triggered by an abrupt elevation of systemic arterial blood pressure. Its heralding features are failure of autoregulation, breakdown of the blood-brain barrier, and extravasation of fluid and protein into the brain parenchyma. PRES is rarely associated with a subarachnoid haemorrhage (SAH); this syndrome reportedly occurs between 6 and 17 days after a SAH and is related to hyperdynamic therapy for cerebral vasospasm.1,2 We describe a case involving a patient who developed PRES, prior to induction of hyperdynamic therapy, 2 days after the onset of a SAH due to a ruptured intracranial aneurysm. PRES is a rare part of the differential diagnosis when a patient deteriorates late following SAH. As in the present case, PRES can be easily and mistakenly ascribed to vasospasm, resulting in more harm when the patient is given further hypertensive therapy.
Case report A 52-year-old woman with a history of hypertension was transferred to our hospital after the sudden onset of a
Correspondence: Hiroki Kuroda, MD, Department of Neurosurgery, Iwate Prefectural Miyako Hospital, 1-11-26 Sakikuwagasaki, Miyako 027-0096, Japan. Tel: ⫹ 81-19-362-4011. Fax: ⫹ 81-19-363-6941. E-mail: [email protected] Received for publication 2 December 2013; accepted 6 April 2014
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786 H. Kuroda et al.
Fig. 1. A CT scan immediately after neck clipping, 2 days after the onset of the SAH, showing new hypodense lesions in the bilateral occipital lobes.
to 110–130 mmHg (DBP to 60–85 mmHg). Her consciousness and headache improved gradually.
Discussion In the present case, a CT scan showed hypodensity in the bilateral occipito-parietal lobes. In addition, although these lesions exhibited high intensity on fluid-attenuated inversion recovery and T2-weighted MR imaging, diffusion-weighted MR imaging revealed no abnormal findings in those lesions. These radiological findings may be attributed to typical PRES. The symptoms in our patient deteriorated with the development of the haemorrhage after hyperdynamic therapy and resolved after cessation of hyperdynamic therapy. These findings were also consistent with PRES. PRES reportedly occurs between 6 and 17 days after a SAH, and hyperdynamic therapy for vasospasm after a SAH may induce development of PRES.1,2 Sustained high blood pressure during hyperdynamic therapy may overcome the upper limits of autoregulation, resulting in forced vasodilation. This leads to the mechanical rupture of vascular endothelial cell junctions. The breakdown of the blood-brain barrier allows extravasation of plasma proteins and water and the subsequent formation of oedema. The present case exhibited PRES on CT, prior to induction of hyperdynamic therapy, 2 days after the onset of the SAH.
Fig. 2. A CT scan on the 12th postoperative day revealing hyperdense lesions in the bilateral occipital lobes.
A catecholamine surge at the time of the aneurysm rupture stimulates a sympathetic storm, leading to an abrupt increase in blood pressure. This acute hypertension at the onset may have resulted in early PRES in the present case. Symptoms of PRES often mimic those of an acute SAH. Several investigators have also reported that abnormal high-intense lesions often develop in the early stage of SAH; these lesions are not related to surgery and appear on diffusion-weighted MR imaging, as in the present case. The pathogenesis of these abnormal high-intense lesions remains unknown.3 PRES may be one of the events during this pathogenesis, although this hypothesis has not been stated. Declaration of interest: The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Amin-Hanjani S, Schwartz RB, Sathi S, Stieg PE. Hypertensive encephalopathy as a complication of hyperdynamic therapy for vasospasm: report of two cases. Neurosurgery 1999;44:1113–6. 2. Jang HW, Lee HJ. Posterior reversible leukoencephalopathy due to “triple H” therapy. J Clin Neurosci 2010;17:1059–61. 3. Sato K , Shimizu H, Fujimura M, et al. Acute-stage diffusionweighted magnetic resonance imaging for predicting outcome of poor-grade aneurysmal subarachnoid hemorrhage. J Cereb Blood Flow Metab 2010;30:1110–20.
Copyright of British Journal of Neurosurgery is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
SHORT REPORT
Early onset of PRES in a patient with a subarachnoid haemorrhage due to a ruptured intracranial aneurysm Hiroki Kuroda1, Hiroshi Kashimura2, Toshiyuki Murakami2, Hidehiko Endo2, Tomohiko Mase2 & Kuniaki Ogasawara2 1Department of Neurosurgery, Iwate Prefectural Miyako Hospital, Miyako, Japan, and 2Department of Neurosurgery, Iwate
Medical University, Morioka, Japan
headache. On arrival, her blood pressure was 191/76 mmHg. She was subsequently started on a nicardipine drip; her systolic blood pressure (SBP) was between 102 and 144 mmHg, and diastolic blood pressure (DBP) was between 43 and 52 mmHg. The patient was alert and fully oriented without focal neurological deficits (Hunt and Hess grade II). A CT scan revealed a diffuse SAH. CT angiography demonstrated a saccular aneurysm located at the bifurcation of the left internal carotid and posterior communicating arteries. Arterial vasospasm was not observed in the anterior or posterior circulation. Forty hours later, she successfully underwent neck clipping of the aneurysm via a craniotomy under general anaesthesia. Anaesthesia was induced with an intravenous continuous infusion pump of 1% propofol and remifentanil and an intravenous bolus injection of fentanyl and rocuronium. SBP and DBP during the operation were 70–125 mmHg and 35–50 mmHg, respectively. When the patient recovered from general anaesthesia, she was fully oriented without focal neurological deficits. However, subsequent CT revealed a new hypodensity in the bilateral occipito-parietal lobes (Fig. 1). On the following day, she became somewhat lethargic. We identified no causes for this lethargy, including infection, electrolyte imbalance, hydrocephalus, or metabolic disorders. Thus, she underwent triple-H (hypertension, hypervolemia, and haemodilution) therapy. We intended to maintain her SBP between 140 and 190 mmHg. CT on the fifth postoperative day revealed enlargement of the hypodensity in the bilateral occipito-parietal lobes, and fluid-attenuated inversion recovery and T2-weighted MR imaging on the eighth postoperative day showed high intensity in those regions, which exhibited no abnormal findings on diffusion-weighted MR imaging. MR angiography on the same day revealed no evidence of vasospasm. She remained lethargic until the 12th postoperative day, when she complained of worsening headache. CT revealed hyperdensity in the bilateral occipito-parietal lobes (Fig. 2). She subsequently underwent a nicardipine drip, resulting in a decrease in SBP
Abstract Posterior reversible encephalopathy syndrome (PRES) is rarely associated with subarachnoid haemorrhage (SAH). We present a case involving a patient who developed PRES, prior to induction of hypertensive therapy, 2 days after the onset of a SAH due to a ruptured intracranial aneurysm. Keywords: hyperperfusion; hyperdynamic therapy; posterior reversible encephalopathy syndrome; subarachnoid haemorrhage
Introduction Posterior reversible encephalopathy syndrome (PRES) is manifested as a subacute change in neurological status and reversible white matter oedema in the bilateral occipitoparietal lobes on computed tomography (CT) or magnetic resonance (MR) imaging. PRES is triggered by an abrupt elevation of systemic arterial blood pressure. Its heralding features are failure of autoregulation, breakdown of the blood-brain barrier, and extravasation of fluid and protein into the brain parenchyma. PRES is rarely associated with a subarachnoid haemorrhage (SAH); this syndrome reportedly occurs between 6 and 17 days after a SAH and is related to hyperdynamic therapy for cerebral vasospasm.1,2 We describe a case involving a patient who developed PRES, prior to induction of hyperdynamic therapy, 2 days after the onset of a SAH due to a ruptured intracranial aneurysm. PRES is a rare part of the differential diagnosis when a patient deteriorates late following SAH. As in the present case, PRES can be easily and mistakenly ascribed to vasospasm, resulting in more harm when the patient is given further hypertensive therapy.
Case report A 52-year-old woman with a history of hypertension was transferred to our hospital after the sudden onset of a
Correspondence: Hiroki Kuroda, MD, Department of Neurosurgery, Iwate Prefectural Miyako Hospital, 1-11-26 Sakikuwagasaki, Miyako 027-0096, Japan. Tel: ⫹ 81-19-362-4011. Fax: ⫹ 81-19-363-6941. E-mail: [email protected] Received for publication 2 December 2013; accepted 6 April 2014
785
786 H. Kuroda et al.
Fig. 1. A CT scan immediately after neck clipping, 2 days after the onset of the SAH, showing new hypodense lesions in the bilateral occipital lobes.
to 110–130 mmHg (DBP to 60–85 mmHg). Her consciousness and headache improved gradually.
Discussion In the present case, a CT scan showed hypodensity in the bilateral occipito-parietal lobes. In addition, although these lesions exhibited high intensity on fluid-attenuated inversion recovery and T2-weighted MR imaging, diffusion-weighted MR imaging revealed no abnormal findings in those lesions. These radiological findings may be attributed to typical PRES. The symptoms in our patient deteriorated with the development of the haemorrhage after hyperdynamic therapy and resolved after cessation of hyperdynamic therapy. These findings were also consistent with PRES. PRES reportedly occurs between 6 and 17 days after a SAH, and hyperdynamic therapy for vasospasm after a SAH may induce development of PRES.1,2 Sustained high blood pressure during hyperdynamic therapy may overcome the upper limits of autoregulation, resulting in forced vasodilation. This leads to the mechanical rupture of vascular endothelial cell junctions. The breakdown of the blood-brain barrier allows extravasation of plasma proteins and water and the subsequent formation of oedema. The present case exhibited PRES on CT, prior to induction of hyperdynamic therapy, 2 days after the onset of the SAH.
Fig. 2. A CT scan on the 12th postoperative day revealing hyperdense lesions in the bilateral occipital lobes.
A catecholamine surge at the time of the aneurysm rupture stimulates a sympathetic storm, leading to an abrupt increase in blood pressure. This acute hypertension at the onset may have resulted in early PRES in the present case. Symptoms of PRES often mimic those of an acute SAH. Several investigators have also reported that abnormal high-intense lesions often develop in the early stage of SAH; these lesions are not related to surgery and appear on diffusion-weighted MR imaging, as in the present case. The pathogenesis of these abnormal high-intense lesions remains unknown.3 PRES may be one of the events during this pathogenesis, although this hypothesis has not been stated. Declaration of interest: The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Amin-Hanjani S, Schwartz RB, Sathi S, Stieg PE. Hypertensive encephalopathy as a complication of hyperdynamic therapy for vasospasm: report of two cases. Neurosurgery 1999;44:1113–6. 2. Jang HW, Lee HJ. Posterior reversible leukoencephalopathy due to “triple H” therapy. J Clin Neurosci 2010;17:1059–61. 3. Sato K , Shimizu H, Fujimura M, et al. Acute-stage diffusionweighted magnetic resonance imaging for predicting outcome of poor-grade aneurysmal subarachnoid hemorrhage. J Cereb Blood Flow Metab 2010;30:1110–20.
Copyright of British Journal of Neurosurgery is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
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