Ann Thorac Surg 2008;86:634-637. doi:10.1016/j.athoracsur.2008.02.021
© 2008 The Society of Thoracic Surgeons
Case Reports
Reversible Unilateral Brain Edema Presenting With Major Neurologic Deficit After Valve Repair
Eelco F.M. Wijdicks, MD*,
Norbert Campeau, MD,
Thoralf Sundt, MD
Department of Neurology, and Division of Critical Care Neurology, Diagnostic Radiology, Cardiovascular Surgery, Mayo Clinic College of Medicine, Rochester, Minnesota
Accepted for publication February 1, 2008.
* Address correspondence to Dr Wijdicks, Mayo Clinic College of Medicine, Department of Neurology and Division of Critical Care Neurology, 200 First St SW, Rochester, MN 55905 (Email: wijde{at}mayo.edu).
| Dr Sundt discloses that he has a financial relationship with Atricute Inc, Bolton Medical, Jarvik Heart Inc, Medtronic Inc, Sorin Group/Carbomedics, St. Jude Medical, Thoratec Corporation, W. L. Gore & Associates Inc, and Boston Scientific Corp.
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Abstract
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Brain edema after cardiac surgery is unusual and often asymptomatic. We encountered a 34-year-old man who had postoperative left flaccid hemiplegia and anosognosia after undergoing composite root replacement and closure of a patent foramen ovale. Computed tomographic and magnetic resonance imaging (MRI) scans showed profound white matter changes indicative of brain edema predominantly in the right hemisphere. His symptoms resolved spontaneously within 3 days with resolution of MRI abnormality. No evidence of cerebral infarction was documented on diffusion-weighted imaging and apparent diffusion coefficient mapping, or on the follow-up MRI obtained 25 days after presentation. The cause for the unilateral brain edema is unknown, but the patient's clinical course and imaging are supportive for a variant of a hyperperfusion syndrome or reversible encephalopathy. The outcome was excellent.
Neurologic complications after valve surgery typically involve ischemic strokes [1–5]. Patients may have localized findings, such as a new speech abnormality or hemiparesis and rarely postoperative stupor from multiple hemispheric infarctions [1]. Brain edema after normothermic cardiopulmonary bypass has been described, but these patients have remained asymptomatic and changes were only detected with serial MRI scans [3]. We describe a patient with strikingly unilateral brain edema with complete resolution but presenting with a major neurologic deficit suggesting an ischemic stroke. We believe that this presentation has not been previously reported.
A 34-year-old man underwent uneventful composite root replacement and closure of patent foramen ovale under moderate hypothermia (34°C) with central aortic cannulation using a Terumo Capiox SX25 membrane oxygenator (Terumo Cardiovascular Systems, Ann Arbor, MI) and cardioplegic arrest. The patient had a history of prior graft replacement of the ascending aorta for acute DeBakey type I dissection, reoperation for aneurysmal dilatation of the aortic arch, and subsequent repair of Crawford extent II thoracoabdominal aortic aneurysm. The latter two procedures were performed at our institution under profound hypothermia with circulatory arrest, with the last having been performed 3 months previously.
Postoperatively, the patient was noted to have a left hemiparesis immediately on withdrawal of sedation. This was preceded by vigorous shaking of his leg. On examination, he did not open his eyes to pain but followed commands, had intact brainstem reflexes, a spontaneous clonus on the left side, and flaccid left arm and left leg weakness. There was no forced eye deviation or any facial asymmetry. A marked left-sided anosognosia was noted. Initial computed tomographic scan of the brain obtained on the day of surgery showed no clear abnormalities. An MRI scan of the brain (Fig 1) obtained the following day showed a striking pattern of signal change with diffuse areas of increased T2-signal throughout the subcortical and deep white matter of the right cerebral hemisphere, and only minimal signal change within the left temporal and occipital lobes. There was no evidence of restricted diffusion to suggest acute infarction. The apparent diffusion coefficient map showed increased diffusion corresponding to the right hemispheric signal changes. The T2 signal change did not follow a specific vascular territory. The follow-up computed tomographic scan on postoperative day 3 showed areas of hypointensity in a similar distribution to that seen on the prior MRI scan. There was no evidence for intracranial hemorrhage. Twenty-four hours later, he was markedly improved, and no neglect was detected. His left arm was still weak, but he was able to lift it against gravity and above his head. When he was examined 48-hours later, all neurologic deficits did resolve. An MRI of the brain obtained on postoperative day 5 demonstrated development of some restricted diffusion within the splenium of the corpus callosum, and white matter within the mid and posterior right centrum semiovale. No gadolinium enhancement was noted. An MRI performed 25 days after the presentation showed complete resolution of the abnormalities without evidence for encephalomalacia or gliosis.
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Fig 1. Serial magnetic resonance imaging (MRI) examinations of the brain showing the development of reversible signal change predominantly involving the right cerebral hemisphere. (A) An MRI obtained on the day after surgery demonstrates diffuse areas of increased T2 signal within the right hemispheric white matter. Diffusion-weighted images including ADC map are negative for acute ischemia, and show increased diffusion in the areas of signal change consistent with edema. (B) An MRI obtained on postoperative day 5 demonstrates development of restricted diffusion signal (confirmed on the ADC map) within the splenium of the corpus callosum and the right centrum semiovale. No pathologic enhancement is noted after administration of the gadolinium. The nonenhancing areas of T2 signal change in the right hemisphere have increased slightly and become more confluent since the prior MRI. (C) All changes are resolved on the MRI study obtained on postoperative day 25 without evidence for developing encephalomalacia or gliosis.
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During his postoperative stay, he was on nitroprusside infusion, but at no point was there evidence of postoperative hypertension. He initially complained of postoperative headaches, but they resolved spontaneously. The carotid ultrasound studies were normal. Intraoperative transesophageal echocardiogram was unrevealing.
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Comment
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We present here for the first time unilateral brain edema after aortic valve replacement. Most remarkably, our patient presented with hemibody neglect, and a profound left hemiparesis suggesting an infarction in the middle cerebral artery territory. However, computed tomographic and MRI scans showed a transient emergence of brain edema in the white matter that was essentially unilateral and completely reversible. The MRI (diffusion weighted images with apparent diffusion coefficient mapping) was helpful in excluding ischemic infarction as the cause of these changes.
We can only surmise this abnormality represents a variant of hyperperfusion syndrome or reversible encephalopathy. Sudden forced dilatation of cerebral arteries may disrupt the blood brain barrier and cause extravasation of fluid and resulting edema. It remains puzzling in our case example that the blood brain barrier was breached on one side. Hypertensive surges causing a reversible encephalopathy syndrome known to present unilaterally in some cases can be considered, but the patient blood pressures were well controlled with a vasodilator [6]. Whether relative hypotension caused ischemia in the white matter, a known watershed area, is unlikely because again MRI characteristics of ischemia were absent. Inadvertently directing too much flow from the aortic cannula to the innominate artery can be considered as a possible mechanism, but a straight-tipped cannula was inserted into the Dacron neoaorta (DuPont, Wilmington, DE) in this patient and this makes maldistribution of flow to one brachiocephalic vessel unlikely.
Diffusion-weighted MRI scans after cardiac surgery are rarely performed. The largest study published from John Hopkins University involved 14 patients who underwent diffusion-weighted MRI scans, but concentrated largely on ischemic deficits. Diffusion-weighted MRI scan was more sensitive in documenting ischemic changes than a computed tomographic scan. Two patients had a fluctuating deficit, but the diffusion-weighted MRI scan showed a clear diffusion-weighted abnormality suggesting an infarction [5]. Other studies have noted that aortic valve replacement is associated with high incidences of postoperative diffusion-weighted image lesions, but again, all of these abnormalities are ischemic in origin.
Reversible encephalopathy syndrome can have atypical distributions and manifestations, as noted in two recent large series [7, 8]. The distribution of reversible encephalopathy syndrome is not limited to the posterior cerebral hemispheres and has been shown to involve the remainder of the cerebral hemispheres, brainstem, pons, and cerebellum. These patient series have also shown that reversible encephalopathy syndrome is not limited to white matter, but can involve cortex and deep nuclei. Awareness of variations in the appearance of reversible encephalopathy syndrome is important.
The true mechanism of the reversible white matter changes in this patient after aortic valve surgery remains unclear. The clinical course and imaging are supportive for a variant of a hyperperfusion syndrome-reversible encephalopathy. This case is of clinical interest due to the complete resolution of profound neurologic and MRI abnormalities that initially may have been clinically confounded as cerebral infarction.
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References
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- Floyd TF, Shah PN, Price CC, et al. Clinically silent cerebral ischemic events after cardiac surgery: their incidence, regional vascular occurrence, and procedural dependence Ann Thorac Surg 2006;81:2160-2166.[Abstract/Free Full Text]
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- Knipp SC, Matatko N, Schlamann M, et al. Small ischemic brain lesions after cardiac valve replacement detected by diffusion-weighted magnetic resonance imaging: relation to neurocognitive function Eur J Cardiothorac Surg 2005;28:88-96.[Abstract/Free Full Text]
- Wityk RJ, Goldsborough MA, Hillis A, et al. Diffusion- and perfusion-weighted brain magnetic resonance imaging in patients with neurologic complications after cardiac surgery Arch Neurol 2001;58:571-576.[Abstract/Free Full Text]
- Mehall JR, Leach JL, Merrill WH. Posterior reversible encephalopathy syndrome after nontransplant cardiac surgery J Thorac Cardiovasc Surg 2005;130:1473-1474.[Free Full Text]
- McKinney AM, Short J, Truwit CL, et al. Posterior reversible encephalopathy syndrome: incidence of atypical regions of involvement and imaging findings AJR Am J Roentgenol 2007;189:904-912.[Abstract/Free Full Text]
- Bartynski WS, Boardman JF. Distinct imaging patterns and lesion distribution in posterior reversible encephalopathy syndrome AJNR Am J Neuroradiol 2007;28:1320-1327.[Abstract/Free Full Text]
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Abstract
Introduction
