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Ann Thorac Surg 2006;81:1401-1406
© 2006 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Cerebral Outcome in Adult Patients Treated With Extracorporeal Membrane Oxygenation

^a Department of Thoracic and Cardiovascular Surgery, Rikshospitalet University Hospital, Oslo, Norway
^b Department of Anaesthesiology, Rikshospitalet University Hospital, Oslo, Norway
^c Department of Radiology, Rikshospitalet University Hospital, Oslo, Norway
^d Department of Psychosomatic and Behavioural Medicine, Rikshospitalet University Hospital, Oslo, Norway
^e Department of Neurology, Rikshospitalet University Hospital, Oslo, Norway
^f Research Institute of Internal Medicine, Rikshospitalet University Hospital, Oslo, Norway
^g Institute of Immunology, Rikshospitalet University Hospital, Oslo, Norway
^h Institute of Psychology, Rikshospitalet University Hospital, Oslo, Norway

Accepted for publication October 10, 2005.

^_* Address correspondence to Dr Risnes, Department of Thoracic and Cardiovascular Surgery, Rikshospitalet University Hospital, Oslo N-0027, Norway (Email: ivar.risnes{at}rikshospitalet.no).

	Abstract

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BACKGROUND: Extracorporeal membrane oxygenation (ECMO) carries a high risk of brain injury. The aim of this study was to determine the cerebral status in 28 adult survivors on average 5.0 (range, 0.5 to 12) years after ECMO treatment for severe cardiorespiratory failure.

METHODS: All 28 patients were investigated at our institution. A comprehensive assessment protocol included a medical history, physical examination, neuropsychological assessment, electroencephalography, and neuroradiologic assessment.

RESULTS: All patients were ambulant unaided, and 43% were without any clinical findings. Impaired neuropsychological performance was found in 41%, neuroradiologic findings in 52%, and a pathologic electroencephalogram in 41% of the patients. There was a significant correlation between the cognitive outcome and neuroradiologic findings. The incidence of neuroradiologic findings (cerebral infarction, microemboli or hemorrhage) was significantly higher in the venoarterial group compared with the venovenous group (75% versus 17%). There was no correlation between the type of ECMO and neuropsychological impairment. Electroencephalography findings did not correlate with neuropsychological performance, nor with the neuroradiologic findings.

CONCLUSIONS: Late cerebral sequelae were frequently seen in patients treated on venoarterial ECMO. A significant correlation was found between cognitive impairment and neuroradiologic findings.

	Introduction

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Extracorporeal membrane oxygenation (ECMO) may be used in patients with respiratory or circulatory failure who are unresponsive to conventional therapy [1, 2]. The severity of illness that necessitates ECMO, as well as the risks associated with the procedure itself, have raised concerns about morbidity among the survivors. The major cause of death in ECMO-treated patients is not due to irreversible pulmonary and heart failure, but to cerebral injury caused by intracranial hemorrhage or infarction [3]. Futhermore, late sequelae in these patients may often be related to intracranial complications. Cerebral injury in ECMO patients can be due to several factors, including diseases before ECMO treatment. Changes in cerebral blood flow and the use of heparin may contribute to both hemorrhagic and nonhemorrhagic intracranial lesions. Thus, ECMO survivors carry a high risk of brain injury and subsequent functional deficit [4].

Case histories and clinical experience suggest that some patients may suffer cerebral sequelae after treatment and develop sensory deficit, motor disability, and cognitive impairment. Several studies have documented increased risk of neurologic complications among infants and children, whereas less is known of adult patients [5].

Little is known regarding the late status of adult ECMO-treated patients. The aim of the present paper is to report on the cerebral outcome in adult patients surviving ECMO treatment.

	Material and Methods

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Patients and Procedures
Of 118 patients treated with ECMO at Rikshospitalet University Hospital in the period September 1990 to March 2004, 64 (54%) survived 30 days. During follow-up, 8 patients (7%) died. All survivors more than 18 years of age at follow-up were included in the present follow-up study (n = 28), with the exception of 1 previously mentally retarded patient. The mean age at follow-up was 37.9 years (range, 18.8 to 63.5). The patients, 15 men and 13 women, had been treated for respiratory (n = 12) or cardiac failure (n = 16). Five of the patients were younger than 18 years at the time of ECMO-treatment, but more than 18 years at the time of assessment, on average 5.0 (range, 0.5 to 12) years later. Of the 90 patients who were excluded from the study, 62 were not alive at follow-up, 22 have been followed up according to a protocol for children. Five children could not be evaluated because of age less than 3 years at follow-up. One child was mentally retarded.

Twelve patients had been treated for 15 (5 to 35) days on venovenous ECMO (VV-ECMO), whereas 16 patients had been treated for 6 (2 to 11) days on venoarterial ECMO (VA-ECMO). In 2 cases, the venoarterial ECMO served as a bridge to a long-term device (Thoratec; Thoratec Corporation, Stoneridge Drive Pleasanton, California). Both patients were successfully transplanted after 3 and 55 days, respectively. One patient had twice been on venoarterial ECMO (6 days on each occasion), whereas one venoarterial ECMO (5 days) had been converted to venovenous ECMO (6 days).

All patients were unconscious at the institution of ECMO, and on artificial ventilation. The indications for ECMO were acute respiratory distress syndrome or pneumonia (n = 11), postcardiotomy failure (n = 4), cardiomyopathy (bridge to transplant, n = 3), acute myocardial infarction (n = 3), pulmonary hypertension (n = 1), myocarditis (n = 1), meningococcal sepsis (n = 1), pulmonary emboli (n = 1), and intoxication with asystolia (n = 1). None of the patients underwent neurologic or neuroradiologic examination before ECMO. The majority of the complications occurred during ECMO treatment, and we are not aware of complications after ECMO.

The study was approved by the Regional Ethics Committee. All patients gave informed consent.

Surgical Technique
Details of the ECMO procedure have previously been reported [6]. Bio-Medicus wire reinforced arterial and venous cannulae, sized respectively F21 and F19 (Medtronics Bio-Medicus, Eden Prairie, Minnesota), were introduced by the percutaneous technique. In all cases, the venous cannula was introduced through the internal jugular or femoral vein by percutaneous technique, with the tip of the cannula located in the right atrium. The blood was returned into the femoral vein (VV-ECMO) or femoral artery (VA-ECMO) by cannulation through the femoral vessels. The flow rate could be kept at maximum 2.9 L/min, using a Bio-Medicus or Jostra (Rotaflow; Maquet Cardiopulmonary AG, Hirrlingen, Germany) centrifugal pumps. All surfaces of the ECMO circuit were heparin coated. While on ECMO, hemoglobin was maintained above 12 g/100 mL and platelets above 100,000 10⁹/L. Antitrombin III was kept above 60%. Negative pressure on the inlet side centrifugal pump input was not allowed to exceed 80 mm Hg to avoid hemolysis [6].

Data Collection and Analysis
Baseline data were obtained from our medical database (Datacor).

Methods
All patients were followed up at our institution. A comprehensive assessment protocol included a medical history, physical examination, neurospychological assessment, neuroradiologic assessment, and electroencephalography.

Neuropsychological Tests
The education level of the patients before ECMO was 12.0 (± 2.8) years. Mean IQ at follow-up was 98.6 (± 8.9) as estimated by subtests from the Wechsler Adult Intelligence Scale-Revised (WAIS-R) [7]. Standard neuropsychologic tests [7] were used to assess motor coordination (Grooved Pegboard), psychomotor speed (Digit Symbol, Trail Making Test part A and part B), attention (Digit Span, Stroop Color-Word Interference Test), verbal learning and memory (Rey Auditory Verbal Learning Test), visual memory (Rey Complex Figure Test), and verbal fluency (Controlled Oral Word Association Test). Based on available and widely used norms, raw scores for the selected 10 measures were converted toT scores with a mean of 50 and standard deviations of 10 (low score indicating poor performance). All T scores less than 40 (namely, more than 1 SD below mean) were defined as probably impaired. A composite impairment score was computed for each patient by counting the number of results below cut off. Patients who scored in the impaired range on at least 3 of the 10 subtests were classified as being neuropsychologically impaired.

Neuroradiologic Assessment
Twenty-five patients underwent a cerebral magnetic resonance (MR) examination. Two patients could not be examined owing to an implanted cardioverter-defibrillator, and 1 was excluded because of pregnancy.

The neuroradiologist was masked with regard to the patient and the technical details of the ECMO treatment. The MR investigations were performed with a Siemens Expert 1.0 T unit and a Siemens Harmony 1.0 T unit (Siemens, Erlangen, Germany).

The following sequences were obtained: sagittal T1 weighted spin-echo sequence with 5-mm slice thickness and 1.5-mm slice intergap, with 550 to 570 ms repetition time, and 14 to 15 ms in echo time; axial T2 weighted turbo spin-echo with 5-mm slice thickness and 1.5-mm slice intergap; repetition time 2200 to 2500 ms, echo time 14/85 ms (proton density/T2), or repetition time 4200 to 5000, echo time 96 ms (single echo T2). Coronal fluid-attenuated inversion recovery was performed with 5-mm slice thickness and 1.5-mm slice intergap, repetition time 9000 ms, echo time 105 to 110 ms.

The 2 patients with implanted cardioverter-defibrillators were examined with nonenhanced computed tomography (General Electric Medical Systems, Milwaukee, Wisconsin). White matter hyperintensities were graded as either within normal range or pathologic. Cerebral infarcts were defined as low signal intensity areas measuring more than 10 mm on T1 and fluid-attenuated inversion recovery, high signal on T2, and with signal changes consistent with perifocal gliosis on fluid-attenuated inversion recovery. Presence of blood products and widening of the cerebral fluid spaces were noted. The computed tomography investigations (n = 2) were evaluated with respect to infarctions, blood products, and cerebral fluid spaces. The images were interpreted retrospectively by one neuroradiologist on either hard copies, or on a PACS workstation (SECTRA AB, Linkoping, Sweden).

Electroencephalography Assessment
Resting 21-channel scalp electroencephalograms (the international 10 to 20 system) were obtained from all patients. One of the authors interpreted all the electroencephalograms.

Statistical Methods
The ² test was used to compare proportions. Continuous nonparametric distributed variables were evaluated using the Mann-Whitney test and the Spearman r correlation coefficient, and continuous parametric data using the Student t test. The level of statistical significance was p 0.05 or less. The statistical analysis was performed using the SPSS program version 11 (SPSS, Chicago, Illinois). The data are presented as mean values ± SD or range.

	Results

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Clinical Findings and Neurodevelopmental Outcome
Disabilities or sequelae were found in 16 patients (57%) at the clinical examination. Some patients had more than one complication. There were 12 patients (43%) without physical sequelae.

Half of the patients weaned from ECMO were able to continue full employment. Neurologic clinical sequels were seen in 11 patients (39%). Six patients (21%) had a motor disability with hemiplegia or polyneuropathy. All walked unaided. Sensory neural defects were found in 5 patients (18%). Three (11%) had vocal cord paralysis, and bilateral sensory loss of hearing was detected in 2 (7%) patients. One patient had cortical visual deficit and reduced vision.

Pulmonary failure in 2 patients (7%), renal impairment in 2 (7%), and lower limb ischemia in 1 patient represented the nonneurologic sequelae.

The incidence of cerebral complications in adults who died on ECMO was documented in 25 of 32 patients. Cerebral infarction was found in 6 patients, hemorrhage in 6, astrocytehyperplasia was seen in patients with multiorgan failure in 2, astroglioma was found in medulla oblongata in 2, microemboli in 1, and cerebral contusion in 1. Seven patients had normal cerebral findings.

Neuroradiologic Findings
Neuroradiologic lesions were found in 14 patients (52%). The MR examination revealed cerebral injury in 12 patients (44%). Cerebral infarction was present in 6 patients (22%; Fig 1). White matter hyperintensities were found in 3 patients (11%; Fig 2). Brain hemorrhage was identified in 2 patients (7%; Fig 3), and cerebral contusion in 1. Sequelae of cerebral infarction were seen in both patients (7%) who underwent computed tomography scan. Cerebral injury was more often seen after VA-ECMO (75%) than after VV-ECMO (7%; p = 0.004; Fig 4). In the VA group, 8 patients had cerebral infarction, 3 white matter lesions, and 1 cerebral hemorrhage. Only 4 had normal findings. Ten of 12 patients were described as normal in the VV group. One patient had cerebral hemorrhage, and 1 had cerebral contusion with hemorrhage.

View larger version (189K): [in this window] [in a new window]   Fig 1. Coronal fluid attenuated inversion recovery shows an infarct in the left hemisphere with perifocal gliosis.

View larger version (154K): [in this window] [in a new window]   Fig 2. Coronal fluid attenuated inversion recovery shows white matter hyperintensities (arrows).

View larger version (127K): [in this window] [in a new window]   Fig 3. Axial T2-weighted turbo spin-echo image shows presence of blood products in both frontal lobes (arrows).

View larger version (22K): [in this window] [in a new window]   Fig 4. Neuroradiologic findings. The incidence of cerebral injury in venovenous (VV) extracorporeal membrane oxygenation (ECMO) and venoarterial (VA) ECMO. (Black bars = normal; hatched bars = pathologic; pts = patients.)

View larger version (20K): [in this window] [in a new window]   Fig 5. Neuropsychological findings. The incidence of cerebral injury in venovenous (VV) extracorporeal membrane oxygenation (ECMO) and venoarterial (VA) ECMO. (Black bars = normal; hatched bars = pathologic; n.s. = not significant; pts = patients.)

View larger version (22K): [in this window] [in a new window]   Fig 6. The correlation between magnetic resonance imaging findings and neuropsychological impairment. Neuropsychological test result on a scale from 0 to 7. Total more than 3 impaired test scores.

	Comment

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Cerebrovascular sequelae after ECMO treatment represent the potentially more serious risk factors for developing late effects. The use of ECMO in acute respiratory or cardiac failure increases survival, but may at the same time cause damage to the brain in the form of explicit or subclinical impairment [8, 9].

The major cause of death in ECMO patients is not due to irreversible pulmonary or cardiac failure, but to cerebral injury due to cerebral infarction or hemorrhage [10]. Nearly 50% of our original group of ECMO-treated patients were alive at follow-up, with a mean of 5 years after treatment. All patients aged 18 years or more (n = 28) consented to participate. The patients had been treated either on VA- or VV-ECMO, determined by their condition. Significantly more patients in the VA group showed cerebral MR pathology (75%) compared with the VV group (17%; Fig.4).

Cererbral injury may result from hypoxia, embolism, or bleeding. The ECMO-treated patients may suffer hypoxia for hours to days; thus, hypoxia is thought to be one of the most determining factors in developing cerebral injury [11]. The brain responds to hypoxia by increasing cerebral oxygen transport and cerebral oxygen extraction. A mild degree of hypoxia can be tolerated; however, prolonged periods of severe hypoxia may result in a loss of ability of the brain to maintain oxygen transport and cerebral oxygen metabolism, leading to inversible brain injury [12]. Low cardiac output may contribute to hypoxia.

Moreover, the ECMO therapy itself can cause cerebral injury. When patients are cannulated for ECMO, there is a period of hypoxia before and during cannulation [13]. The cannulation itself, together with creation of solid and gaseous microemboli during perfusion, may cause cerebral injury. Arterial emboli may occur in connection with retrograde arterial cannulation [10, 13]. All the VA-ECMO patients in the study were percutanously cannulated in the femoral artery and vein, and treated on ECMO with a Biomedicus or Jostra centrifugal pump. Even careful cannulation with Seldinger technique may cause of thrombus formation [6].

Injuries were mainly observed in patients treated with VA-ECMO, where the blood is returned directly into the artery. The lungs function as a filter in VV-ECMO. There was a significant correlation between the radiologic findings, the neuropsychological findings, and neuroclinical outcome.

Hemodynamic instability and hypotension during ECMO may represent another risk factor for brain injury. Venoarterial ECMO may increase this risk, indicating that stabilization of patients who need cardiac assist is difficult [14, 15].

Cerebral autoregulation is an important homeostatic mechanism that maintains cerebral blood flow over a wide range of cerebral perfusion pressures. Systemic insults and hypoxia can disrupt cerebral autoregulation, leaving the cerebral microcirculation vulnerable to changes in systemic blood pressure. Hypotension can result in ischemic cerebral damage [16]. Hypertension can cause cerebral hyperemia and increase the risk of cerebral hemorrhage. Loss of autoregulation in an already injured brain, combined with systemic heparin therapy, can result in cerebral hemorrhage [8]. During VA-ECMO, cerebral perfusion is mainly nonpulsatile, unless combined with intra-aortic balloon pump. Nonpulsatile cerebral perfusion may lead to diffuse brain edema. The risk is reduced in VV-ECMO, in which the cerebral perfusion is pulsative [17].

There was no significant difference in neuropsychological impairment between the groups. In the VA group, 50% of the patients were classified as being neuropsychologically impaired compared with 33% in the VV group (Fig 5).

Our main finding was that approximately half of the group showed evidence of cerebral injury, either in the form of MR pathology or in the form of impaired neuropsychological performance on standard assessment. The strength of this finding is evidenced by the significant correspondence between these two types of assessment (Fig 6). Traditional coronary artery bypass graft surgery and ECMO treatment introduces several potential sources and maneuvers that may cause microemboli [18, 19]. Lund and coworkers [20] found significantly fewer cerebral microemboli during off-pump compared with on-pump coronary artery bypass graft surgery. However, there were no differences regarding cognitive outcome, and there were no associations between the number of cerebral microemboli and evidence of cognitive decline [20]. In contrast, our study demonstrates a significant correlation between the cerebral injury and cognitive deficit, possibly due to the length of treatment.

As in on-pump surgery, ECMO treatment may induce systemic inflammation with cerebral microembolization. Brain metabolism is changed owing to sedation and anesthesia. Furthermore, the cerebral blood flow pattern may be severely altered. The blood components are continuously exposed to the synthetic surfaces of the extracorporeal circuit [21, 22]. The systemic response may lead to cerebral injury and posttreatment morbidity. Extracorporeal membrane oxygenation differs from cardiac surgery in duration for days to weeks rather than hours.

Numerous degenerative disorders diffusely affect cerebral function and cause generalized changes in the electroencephalogram. The electroencephalographic abnormality usually consists of diffuse slowing, and the degree of the abnormality is often related to the rapidity of progression of the disease process and the severity of involvement. Cerebrovascular impairment is one of the most common causes of cerebral degeneration in the adult, and the electroencephalogram may show diffuse or focal changes depending on the area involved. These changes are nonspecific [23]. There was, however, no association between pathologic electroencephalography registration and the clinical neurologic outcome, and cerebral findings.

In summary, our study shows that ECMO treatment frequently resulted in cerebral sequelae such as infarction and hemorrhage. Cerebral findings were significantly associated with cognitive impairment. Signs of cerebral injury were mainly seen in patients treated with venoarterial ECMO.

	References

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