Ten Years of Improving Acute Stroke Management in a Metropolitan Area: A Population-Based Quantification of Quality Indicators.

BACKGROUND AND PURPOSE: Rapid access to acute stroke treatment improves clinical outcomes in patients with ischemic stroke. We aimed to shorten the time to admission and to acute stroke treatment for patients with acute stroke in the Hamburg metropolitan area by collaborative multilevel measures involving all hospitals with stroke units, the Emergency Medical Services (EMS), and health-care authorities. METHODS: In 2007, an area-wide stroke care quality project was initiated. The project included mandatory admission of all stroke patients in Hamburg exclusively to hospitals with stroke units, harmonized acute treatment algorithms among all hospitals, repeated training of the EMS staff, a multimedia educational campaign, and a mandatory stroke care quality monitoring system based on structured data assessment and quality indicators for procedural measures. We analyzed data of all patients with acute stroke who received inhospital treatment in the city of Hamburg during the evaluation period from the quality assurance database data and evaluated trends of key quality indicators over time. RESULTS: From 2007 to 2016, a total of 83,395 patients with acute stroke were registered. During this period, the proportion of patients admitted within ≤3 h from symptom onset increased over time from 27.8% in 2007 to 35.2% in 2016 (p < 0.001). The proportion of patients who received rapid thrombolysis (within ≤30 min after admission) increased from 7.7 to 54.1% (p < 0.001). CONCLUSIONS: Collaborative stroke care quality projects are suitable and effective to improve acute stroke care.

[Quality of life and disability after severe stroke and early neurological rehabilitation]. / Lebensqualität und Behinderung nach schwerem Schlaganfall und neurologischer Frührehabilitation.

BACKGROUND: Data on the long-term effects on quality of life of patients after severe stroke and discharge from early institutional rehabilitation are important for guiding the early rehabilitation phase and the further outpatient care. OBJECTIVE: Analysis of the outcome of patients following severe stroke 3 and 12 months after discharge from early neurological rehabilitation. METHODS: Analysis of the Asklepios Hamburg multicenter early stroke rehabilitation registry (ICD 10: I61, I60, I63 and OPS 8­552). Structured interviews with documentation of disabilities using the early rehabilitation Barthel index (ERBI), modified Rankin scale (mRS) and quality of life (12-item short form health survey, SF-12). Assessment of further treatment and complications 3 and 12 months after discharge from the early rehabilitation departments by telephone interviews. RESULTS: Out of 1045 treated stroke patients 270 were enrolled between October 2015 and November 2017 and 200 and 151 patients could be followed up after 3 and 12 months, respectively. There was a significant improvement (p < 0.001) in the median ERBI (151 patients at 12 months). Factors influencing a poorer functional outcome (higher mRS) at 12 months were a higher mRS at discharge (OR 5.43 [1.18, 25.09], p = 0.03) and age (per decade OR 1.5 [1.09, 2.02]; p = 0.01). Female sex reduced the risk for a poorer outcome after 12 months (OR 0.49 [0.25, 0.96]; p = 0.04). Quality of life (SF-12) was not different over time. The mental quality of life showed no differences (p = 0.32) compared to a historical, significantly less (p<0.001) handicapped stroke collective. CONCLUSION: The surviving severe stroke patients recovered significantly up to 12 months after discharge. The mental quality of life did not differ from that of a historical less handicapped collective.

Anticoagulant reversal, blood pressure levels, and anticoagulant resumption in patients with anticoagulation-related intracerebral hemorrhage.

IMPORTANCE: Although use of oral anticoagulants (OACs) is increasing, there is a substantial lack of data on how to treat OAC-associated intracerebral hemorrhage (ICH). OBJECTIVE: To assess the association of anticoagulation reversal and blood pressure (BP) with hematoma enlargement and the effects of OAC resumption. DESIGN, SETTING, AND PARTICIPANTS: Retrospective cohort study at 19 German tertiary care centers (2006-2012) including 1176 individuals for analysis of long-term functional outcome, 853 for analysis of hematoma enlargement, and 719 for analysis of OAC resumption. EXPOSURES: Reversal of anticoagulation during acute phase, systolic BP at 4 hours, and reinitiation of OAC for long-term treatment. MAIN OUTCOMES AND MEASURES: Frequency of hematoma enlargement in relation to international normalized ratio (INR) and BP. Incidence analysis of ischemic and hemorrhagic events with or without OAC resumption. Factors associated with favorable (modified Rankin Scale score, 0-3) vs unfavorable functional outcome. RESULTS: Hemorrhage enlargement occurred in 307 of 853 patients (36.0%). Reduced rates of hematoma enlargement were associated with reversal of INR levels <1.3 within 4 hours after admission (43/217 [19.8%]) vs INR of ≥1.3 (264/636 [41.5%]; P < .001) and systolic BP <160 mm Hg at 4 hours (167/504 [33.1%]) vs ≥160 mm Hg (98/187 [52.4%]; P < .001). The combination of INR reversal <1.3 within 4 hours and systolic BP of <160 mm Hg at 4 hours was associated with lower rates of hematoma enlargement (35/193 [18.1%] vs 220/498 [44.2%] not achieving these values; OR, 0.28; 95% CI, 0.19-0.42; P < .001) and lower rates of in-hospital mortality (26/193 [13.5%] vs 103/498 [20.7%]; OR, 0.60; 95% CI, 0.37-0.95; P = .03). OAC was resumed in 172 of 719 survivors (23.9%). OAC resumption showed fewer ischemic complications (OAC: 9/172 [5.2%] vs no OAC: 82/547 [15.0%]; P < .001) and not significantly different hemorrhagic complications (OAC: 14/172 [8.1%] vs no OAC: 36/547 [6.6%]; P = .48). Propensity-matched survival analysis in patients with atrial fibrillation who restarted OAC showed a decreased HR of 0.258 (95% CI, 0.125-0.534; P < .001) for long-term mortality. Functional long-term outcome was unfavorable in 786 of 1083 patients (72.6%). CONCLUSIONS AND RELEVANCE: Among patients with OAC-associated ICH, reversal of INR <1.3 within 4 hours and systolic BP <160 mm Hg at 4 hours were associated with lower rates of hematoma enlargement, and resumption of OAC therapy was associated with lower risk of ischemic events. These findings require replication and assessment in prospective studies. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01829581.

Noninvasive assessment of cerebral perfusion and oxygenation in acute ischemic stroke by near-infrared spectroscopy.

BACKGROUND: In acute stroke patients, there is a need for noninvasive measurement to monitor blood flow-based therapies. We investigated the utility of near-infrared spectroscopy (NIRS) to determine cerebral perfusion in these patients. METHODS: Eleven patients were investigated within 1.4 +/- 2.2 days after onset of an ischemic middle cerebral artery infarction by monitoring the kinetics of an intravenous bolus of indocyanine green (ICG). For ICG kinetics, bolus peak time, time to peak (TTP = time between 0 and 100% ICG maximum), maximum ICG concentration, rise time (time between 10 and 90% ICG maximum), slope (maximum ICG/TTP), and blood flow index (BFI = maximum ICG/rise time) were obtained. Perfusion-weighted MRI (PWI) and NIRS measurements were performed within 24 h, and the interhemispherical differences of TTP values were compared. RESULTS: Stroke patients showed an increased bolus peak time (p < 0.02), TTP (p < 0.01), and rise time (p < 0.01), whereas slope (p < 0.01) and BFI (p < 0.01) were diminished at the site of infarction as compared to the unaffected hemisphere. The interhemispherical differences of TTP as measured by PWI and NIRS were closely correlated (r = 0.86). CONCLUSIONS: Noninvasive measurements of cerebral ICG kinetics by NIRS provide a useful means of detecting cerebral perfusion deficits in patients with acute stroke, which correlate well with those obtained by PWI.

Early disruption of the blood-brain barrier after thrombolytic therapy predicts hemorrhage in patients with acute stroke.

BACKGROUND AND PURPOSE: Leaks of the blood-brain barrier can be detected on postcontrast-enhanced T1-weighted MRIs. Although early disruptions of the blood-brain barrier appear to be an important risk factor for tissue plasminogen activator-related hemorrhages in rodents, little is known about their incidence and consequences in human stroke. METHODS: This is a retrospective analysis of a prospectively collected stroke database over the past 6 years. In 52 patients, multimodal MRI (including diffusion-weighted, perfusion-weighted, and postcontrast-enhanced T1-weighted MRI to detect blood-brain barrier changes) had been performed immediately before systemic thrombolysis and in 48 patients within a median of 30 minutes (interquartile range: 30 to 60 minutes) after recombinant tissue plasminogen activator treatment. The incidence of symptomatic hemorrhage (SICH), defined as any parenchymal hemorrhage leading to deterioration in the patient's clinical condition, was related to several clinical and imaging variables, including early blood-brain barrier changes. RESULTS: Overall, SICH was detected in 9 (9%) patients and among these, 2 died. Although no blood-brain barrier changes were detectable before thrombolysis, 3 of 48 patients (6.25%) had a parenchymal gadolinium enhancement in the areas of initial infarction after tissue plasminogen activator treatment. All 3 patients developed SICHs at sites corresponding to the areas of enhancement. The presence of a parenchymal enhancement was significantly associated with SICH (P<0.01), whereas other clinical and imaging variables did not predict SICH in this series. CONCLUSIONS: Early parenchymal enhancement after intravenous tissue plasminogen activator is significantly associated with subsequent SICH and could therefore become a useful imaging sign for the rapid initiation of preventive strategies in the future.

Influence of galantamine on vasomotor reactivity in Alzheimer's disease and vascular dementia due to cerebral microangiopathy.

BACKGROUND AND PURPOSE: Recent reports suggest that vascular factors play a crucial role in the development and progression of Alzheimer's disease. We aimed to assess vasomotor reactivity in patients with Alzheimer's disease and vascular dementia due to microangiopathy using transcranial Doppler sonography and near-infrared spectroscopy during a CO(2) exposition task. METHODS: The normalized CO(2) reactivity assessed at the middle cerebral artery and the oxygenated and deoxygenated hemoglobin of the frontal cortex were obtained. To investigate the impact of cholinergic deficiency known for Alzheimer's disease on vasomotor reactivity, both groups were reinvestigated during treatment with the acetylcholine esterase inhibitor galantamine. RESULTS: Transcranial Doppler analysis revealed significantly reduced normalized CO(2) reactivity for Alzheimer's disease and vascular dementia. Vasomotor reactivity assessed by near-infrared spectroscopy was decreased in patients with vascular dementia, but not in Alzheimer's disease. Galantamine treatment showed a beneficial effect, normalizing these parameters close to age-matched control levels. CONCLUSIONS: Our results suggest that Alzheimer's disease is associated with a lack of vasomotor reactivity, which might be associated with disturbed autoregulation indicating a potential risk for a decreased protection of brain tissue against blood pressure changes. Additionally, a diminished increase of cortical oxygenated hemoglobin during the CO(2) test was apparent in patients with vascular dementia. Galantamine treatment influenced vascular reactivity in the CO(2) test, thus providing evidence for the cholinergic deficiency, thereby adding to vascular dysregulation in Alzheimer's disease, but also indicating an important role of cholinergic system dysfunction for vascular dementia.

Autoantibodies against glutamate receptor δ2 after allogenic stem cell transplantation.

OBJECTIVE: To report on a Caucasian patient who developed steroid-responsive transverse myelitis, graft vs host disease of the gut, and anti-GluRδ2 after allogenic stem cell transplantation. METHODS: Histoimmunoprecipitation (HIP) with the patient's serum and cryosections of rat and porcine cerebellum followed by mass spectrometry was used to identify the autoantigen. Correct identification was verified by indirect immunofluorescence using recombinant GluRδ2 expressed in HEK293 cells. RESULTS: The patient's serum produced a granular staining of the cerebellar molecular layer (immunoglobulin G1 and immunoglobulin G3; endpoint titer: 1:1,000) but did not react with other CNS tissues or 28 established recombinant neural autoantigens. HIP revealed a unique protein band at ∼110 kDa that was identified as GluRδ2. The patient's serum also stained GluRδ2 transfected but not mock-transfected HEK293 cells. Control sera from 38 patients with multiple sclerosis, 85 patients with other neural autoantibodies, and 205 healthy blood donors were negative for anti-GluRδ2. Preadsorption with lysate from HEK293-GluRδ2 neutralized the patient's tissue reaction whereas control lysate had no effect. In addition to anti-GluRδ2, the patient's serum contained immunoglobulin G autoantibodies against the pancreatic glycoprotein CUZD1, which are known to be markers of Crohn disease. CONCLUSIONS: In the present case, the development of anti-GluRδ2 was associated with transverse myelitis, which was supposedly triggered by the stem cell transplantation. Similar to encephalitis in conjunction with anti-GluRδ2 reported in a few Japanese patients, the patient's neurologic symptoms ameliorated after steroid therapy.

Short-term effect of cigarette smoking on CO(2)-induced vasomotor reactivity in man: a study with near-infrared spectroscopy and tanscranial Doppler sonography.

Cigarette smoking is a major risk factor for stroke, and quitting reduces the stroke risk within a few years. The aim of our study was to clarify whether CO(2)-induced vasomotor reactivity (VMR) is impaired in smokers after smoking a cigarette as a possible factor of an increased stroke risk. We compared VMR of 23 healthy smokers assessed at baseline, immediately, and 30 min after smoking a cigarette (1.2 mg nicotine) with values from nonsmoking, age-matched controls (n=24), obtained at identical time intervals. Cerebral blood flow velocities (CBFV) of both middle cerebral arteries (transcranial Doppler sonography), changes in concentration of cerebral oxygenated, deoxygenated, and total hemoglobin (HbO(2), Hb, and HbT, near-infrared spectroscopy), mean arterial blood pressure (MAP), and skin blood flow were recorded during normo- and hypercapnia. VMR was calculated as percentage change in CBFV and as micromolar change in concentration of HbO(2), Hb, and HbT per 1% increase in endtidal CO(2). CBFV in smokers was increased at baseline (left, p<0.05; right, p=0.05), immediately (p<0.01), and 30 min after smoking (p<0.05) as compared with nonsmokers. MAP rose immediately after smoking (p<0.01) and declined after 30 min. VMR in smokers at baseline did not differ from controls, decreased immediately after smoking (p<0.05), and normalized after 30 min (p>0.05). Increased baseline CBFV in smokers after smoking might be due to arteriolar dilation, increased MAP, and possibly constriction of basal cerebral arteries. Impaired VMR for about 30 min after smoking reflects endothelial dysfunction. This might contribute to the enhanced stroke risk in smokers.

Acute effects of cigarette smoking on cerebral oxygenation and hemodynamics: a combined study with near-infrared spectroscopy and transcranial Doppler sonography.

Cigarette smoking has been shown to increase cerebral blood flow velocity (CBFV) and reduce vasomotor reactivity temporarily. The aim of our study was to clarify whether this results from dilation of resistance vessels alone with subsequent increase in regional cerebral blood flow (rCBF), or an additional constriction of basal cerebral arteries. In 24 healthy smokers (mean age+/-S.D., 32.7+/-10.5 years), cerebral oxygenation and hemodynamics were monitored by transcranial Doppler sonography and near-infrared spectroscopy before, during, and after smoking a cigarette (nicotine 0.9 mg). We simultaneously recorded CBFV of both middle cerebral arteries, mean arterial blood pressure, skin blood flow, end-tidal CO(2), changes in concentration of cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin (micromol/l), and a cerebral tissue oxygenation index. Smoking increased CBFV (p<0.01), oxyhemoglobin (p<0.01), and total hemoglobin (p<0.01). After smoking, the increase in CBFV and total hemoglobin persisted (p<0.01), while oxyhemoglobin returned to baseline. Deoxyhemoglobin and cerebral tissue oxygenation index did not change during the whole procedure. During, but not after smoking, CBFV increase was correlated to ipsilateral changes in oxyhemoglobin and total hemoglobin (p<0.05). The increase in oxyhemoglobin only during smoking and the lack of changes in deoxyhemoglobin and cerebral tissue oxygenation index indicate that smoking did not substantially increase rCBF. The smoking-induced elevation in CBFV might therefore be due to an additional constriction of the middle cerebral artery. The combined effects of smoking on basal cerebral arteries and arterioles might contribute to the increased stroke risk in smokers.

Evaluation of 5-fluorouracil pharmacokinetics in cancer patients with a c.1905+1G>A mutation in DPYD by means of a Bayesian limited sampling strategy.

BACKGROUND AND OBJECTIVE: Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme in the catabolism of 5-fluorouracil (5FU) and DPD deficiency is an important pharmacogenetic syndrome. So far, only very limited information is available regarding the pharmacokinetics of 5FU in patients with a (partial) DPD deficiency and no limited sampling models have been developed taking into account the non-linear pharmacokinetic behaviour of 5FU. The aim of this study was to evaluate the pharmacokinetics of 5FU and to develop a limited sampling strategy to detect decreased 5FU elimination in patients with a c.1905+1G>A-related DPD deficiency. METHODS: Thirty patients, heterozygous for the c.1905+1G>A mutation in DPYD, and 18 control patients received a dose of 5FU 300 mg/m2 and/or 5FU 450 mg/m2, followed by pharmacokinetic analysis of the 5FU plasma levels. A population pharmacokinetic analysis was performed in order to develop a compartmental pharmacokinetic model suitable for a limited sampling strategy. Clinical aspects of treating DPD-deficient patients with 5FU-based chemotherapy were assessed from the retrospectively collected clinical data. RESULTS: In a two-compartment model with Michaelis-Menten elimination, the mean maximum enzymatic conversion capacity (V(max)) value was 40% lower in DPD-deficient patients compared with controls (p < 0.001). Using a limited sampling strategy, with V(max) values calculated from 5FU concentrations at 30 or 60 minutes, significant differences were observed between DPD-deficient patients and controls at both dose levels (p < 0.001). The positive predictive value and negative predictive value for V(max), calculated from 5FU levels at 60 minutes, were 96% and 88%, respectively, in patients treated with a single dose of 5FU 300 mg/m2. All seven DPD-deficient patients (two males and five females) who had been genotyped prior to initiation of standard 5FU-containing chemotherapy developed grade 3-4 toxicity, with one case of lethal toxicity in a female patient. No grade 4 toxicity or lethal outcome was observed in 13 DPD-deficient patients treated with reduced doses of 5FU. The average dose of 5FU in DPD-deficient patients with mild toxicity (grade ≤2) was 61 ± 16% of the normal 5FU dose (n = 10). CONCLUSIONS: Profound differences in the elimination of 5FU could be detected between DPD-deficient patients and control patients. Pharmacokinetic 5FU profiling, using a single 5FU concentration at 60 minutes, may be useful for identification of DPD-deficient patients in order to reduce severe toxicity. Furthermore, treatment of DPD-deficient patients with standard 5FU-containing chemotherapy was associated with severe (lethal) toxicity.

Unilateral optic neuropathy following subdural hematoma: a case report.

INTRODUCTION: Unilateral optic neuropathy is commonly due to a prechiasmatic affliction of the anterior visual pathway, while losses in visual hemifields result from the damage to brain hemispheres. Here we report the unusual case of a patient who suffered from acute optic neuropathy following hemispherical subdural hematoma. Although confirmed up to now only through necropsy studies, our case strongly suggests a local, microcirculatory deficit identified through magnetic resonance imaging in vivo. CASE PRESENTATION: A 70-year-old Caucasian German who developed a massive left hemispheric subdural hematoma under oral anticoagulation presented with acute, severe visual impairment on his left eye, which was noticed after surgical decompression. Neurologic and ophthalmologic examinations indicated sinistral optic neuropathy with visual acuity reduced nearly to amaurosis. Ocular pathology such as vitreous body hemorrhage, papilledema, and central retinal artery occlusion were excluded. An orbital lesion was ruled out by means of orbital magnetic resonance imaging. However, cerebral diffusion-weighted imaging and T2 maps of magnetic resonance imaging revealed a circumscribed ischemic lesion within the edematous, slightly herniated temporomesial lobe within the immediate vicinity of the affected optic nerve. Thus, the clinical course and morphologic magnetic resonance imaging findings suggest the occurrence of pressure-induced posterior ischemic optic neuropathy due to microcirculatory compromise. CONCLUSION: Although lesions of the second cranial nerve following subdural hematoma have been reported individually, their pathogenesis was preferentially proposed from autopsy studies. Here we discuss a dual, pressure-induced and secondarily ischemic pathomechanism on the base of in vivo magnetic resonance imaging diagnostics which may remain unconsidered by computed tomography.

Hemispheric hypoperfusion in postictal paresis mimics early brain ischemia.

The clinical differentiation between stroke and seizure is usually straightforward but postictal neurological deficits can be mistaken for stroke in case no detailed medical history is available. Up to now, the imaging findings of Todd's paresis are not well described. This case report demonstrates that postictal paresis can be accompanied by a reversible global hemispheric hypoperfusion as measured with perfusion MRI indicating transient but profound cerebrovascular dysfunction in postictal paresis. Extensive postictal perfusion changes must be discriminated from emerging stroke to avoid potentially harmful therapy like thrombolysis. Further investigations are warranted to clarify the role of cerebrovascular dysfunction in the pathophysiology of postictal paresis.

Cerebral involvement in a patient with Goodpasture's disease due to shortened induction therapy: a case report.

INTRODUCTION: Goodpasture's disease is a rare immunological disease with formation of pathognomonic antibodies against renal and pulmonary basement membranes. Cerebral involvement has been reported in several cases in the literature, yet the pathogenetic mechanism is not entirely clear. CASE PRESENTATION: A 21-year-old Caucasian man with Goodpasture's disease and end-stage renal disease presented with two generalized seizures after a period of mild cognitive disturbance. Blood pressure and routine laboratory tests did not exceed the patient's usual values, and examination of cerebrospinal fluid was unremarkable. Cerebral magnetic resonance imaging (MRI) revealed multiple cortical and subcortical lesions on fluid-attenuated inversion recovery sequences. Since antiglomerular basement membrane antibodies were found to be positive with high titers, plasmapheresis was started. In addition, cyclophosphamide pulse therapy was given on day 13. Encephalopathy and MRI lesions disappeared during this therapy, and antiglomerular basement membrane antibodies were significantly reduced. Previous immunosuppressive therapy was performed without corticosteroids and terminated early after 3 months. The differential diagnostic considerations were cerebral vasculitis and posterior reversible encephalopathy syndrome. Vasculitis could be seen as an extrarenal manifestation of the underlying disease. Posterior reversible encephalopathy syndrome, on the other hand, can be triggered by immunosuppressive therapy and may appear without a hypertensive crisis. CONCLUSION: A combination of central nervous system symptoms with a positive antiglomerular basement membrane test in a patient with Goodpasture's disease should immediately be treated as an acute exacerbation of the disease with likely cross-reactivity of antibodies with the choroid plexus. In our patient, a discontinuous strategy of immunosuppressive therapy may have favored recurrence of Goodpasture's disease.

Statin therapy at carotid angioplasty and stent placement: effect on procedure-related stroke, myocardial infarction, and death.

PURPOSE: To retrospectively determine if preprocedural statin treatment is associated with a reduction of cardiovascular events after carotid angioplasty and stent placement (CAS) in patients with symptomatic carotid stenosis. MATERIALS AND METHODS: A study resulting in a prospective database was approved by the institutional ethics review board; written informed consent was obtained. The approval and informed consent included future retrospective analysis. Consecutive patients (n = 180) from the prospective database underwent CAS for high-grade symptomatic carotid disease. The frequency of cardiovascular complications (composite of stroke, myocardial infarction, and death within 30 days after CAS) between 127 patients without preprocedural statin treatment and that of 53 patients with preprocedural statin treatment at CAS were compared with chi2 and multivariate logistic regression analysis. RESULTS: The overall 30-day myocardial infarction rate was two of 180 (1%) patients, the minor stroke rate was 16 of 180 (9%) patients, the major stroke rate was one of 180 (0.5%) patients, and the death rate was two of 180 (1%) patients. The incidence of cardiovascular events (composite of stroke, myocardial infarction, and death within 30 days after CAS) was significantly different between patients with preprocedural treatment (4%) and those without preprocedural statin treatment (15%) (P < .05). These higher complication rates among patients without preprocedural statin treatment were not mediated by adjustment for age, sex, other baseline characteristics, degree of carotid stenosis, use of cerebral protection devices, or the year in which CAS was performed. CONCLUSION: Preprocedural statin therapy appears to reduce the incidence of stroke, myocardial infarction, and death within 30 days after CAS. Future prospective randomized trials are warranted to further assess this potential protective effect of statin drugs during carotid interventions.

Incidence and risk factors for medical complications after carotid artery stenting.

OBJECTIVE: Carotid angioplasty and stenting (CAS) is being evaluated as an alternative to carotid endarterectomy for the treatment of carotid artery stenosis; however, to date little is known about the incidence of medical complications after CAS. The goal of this study was to determine the frequency of, and to identify potential clinical risk factors for, the development of medical complications after CAS. METHODS: Medical complications that occurred < or = 30 days after CAS in 327 consecutive patients (241 men, 86 women; mean age, 69 +/- 9 years; range, 45 to 90 years) treated for symptomatic (n = 182, 56%) or asymptomatic (n = 145, 44%) carotid artery stenosis were recorded. The effect of clinical characteristics on the subsequent development of medical complications was analyzed by logistic regression. RESULTS: Fifty-one patients (15%) had 62 medical complications: 3 (0.9%) myocardial infarctions, 3 (0.9%) cardiac arrhythmias, 4 (1.2%) episodes of angina pectoris, 3 (0.9%) episodes of symptomatic hypertension, 16 (4.9%) episodes of symptomatic hypotension, 10 (3.1%) chest infections, 9 (2.7%) had periods of confusion, 5 (1.5%) had urinary retention, and 9 (2.7%) urinary tract infections. One chest infection was fatal and 16 complications prolonged the intensive care unit monitoring period > 24 hours. Advanced age (odds ratio [OR], 1.1; 95% confidence interval [CI], 1.05 to 1.14) and a symptomatic carotid stenosis (OR, 2.1; 95% CI, 1.07 to 4.1) independently predicted the occurrence of medical complications. CONCLUSION: Although life-threatening or fatal non-neurologic events were uncommon in this series, the overall incidence of medical complications after CAS might be higher than currently anticipated. Older and symptomatic patients are at the highest risk, and these subgroups should be monitored closely.

Preserved CO(2) reactivity and increase in middle cerebral arterial blood flow velocity during laparoscopic surgery in children.

UNLABELLED: In adult patients, the creation of pneumoperitoneum (PP) by means of carbon dioxide (CO(2)) insufflation leads to an increase in cerebral blood flow velocity (CBFV), which is thought to be caused by hypercapnia. We evaluated whether PP leads to an increase of CBFV in children, and whether this increase is directly related to PP. The effects of PP on middle cerebral artery blood flow velocity were investigated in 12 children (mean age 3 yr, range 15-63 mo) undergoing laparoscopic herniorrhaphy under general anesthesia with sevoflurane and nitrous oxide/oxygen. CBFV was measured by using transcranial Doppler ultrasonography. During CO(2) insufflation, the end-tidal CO(2) concentration was kept constant by adjustment of ventilation by increasing minute volume. The CBFV increased significantly at an intraabdominal pressure of 12 mm Hg compared with baseline from 68 +/- 11 cm/s to 81 +/- 12 cm/s (P < 0.05). CO(2) reactivity remained in the normal range (4.0% +/- 1.9%/mm Hg) during PP. We conclude that the induction of PP leads to an increase in middle cerebral artery blood flow velocity in young children independent from hypercapnia, whereas CO(2) reactivity remains normal. IMPLICATIONS: Laparoscopic surgery is performed frequently in pediatric patients. Cerebral blood flow velocities increase during insufflation of the intraperitoneal cavity for minimally invasive surgery in children. The vasoreactivity as part of the cerebral autoregulation remains unaffected.

Noninvasive monitoring of cerebral oxygenation during vasomotor reactivity tests by a new near-infrared spectroscopy device.

BACKGROUND: Spatially resolved spectroscopy is a recently developed technique for noninvasive monitoring of cerebral tissue oxygenation using the photon diffusion theory. METHODS: We studied this technique with a new, commercial near-infrared spectroscopy (NIRS) device during vasomotor reactivity tests in 28 healthy volunteers (mean age 31.0 years; SD 10.6 years) and compared it with values assessed by the modified Beer-Lambert law and indices from simultaneous transcranial Doppler sonography of both middle cerebral arteries. We measured O(2) reactivity as percentage change of cerebral blood flow velocity (CBFV), as absolute change in the concentrations (measured in micromol/l) of oxygenated (HbO(2)), deoxygenated (Hb) and total hemoglobin (HbT), and as change in the tissue oxygenation index (TOI) during inhalation of 100% oxygen. CO(2) reactivity was calculated as percentage change of CBFV (NCR), as absolute change in the concentrations of HbO(2), Hb, and HbT (micromol/l), and as change in TOI (%) per 1% increase in end-tidal CO(2). RESULTS: One hundred percent oxygen inhalation lead to a decrease in CBFV (mean +/- SD: left -8.0 +/- 7.0%, p = 0.000; right -9.6 +/- 7.6%, p = 0.000), an increase in HbO(2) (0.99 +/- 1.07 micromol/l), Hbdiff (2.23 +/- 1.72 micromol/l), and TOI (3.1 +/- 1.5%), and a decrease in Hb (-1.22 +/- 0.74 micromol/l), significant from baseline values (p = 0.0000). CO(2) reactivity was: NCR left 25.4 +/- 14.7%; NCR right 25.9 +/- 13.4%; HbO(2) 1.99 +/- 0.97 micromol/l; Hb -1.24 +/- 0.81 micromol/l; HbT 0.81 +/- 1.0 micromol/l, and TOI 3.7 +/- 2.2%. O(2) reactivity in TCD did not correlate with NIRS reactivities (Pearson p > 0.05), but NCR did correlate with changes in HbO(2), Hb, and TOI (Pearson p < 0.01). TOI was closely related to indices derived from the Beer-Lambert law (Pearson p < 0.03), but not with mean arterial blood pressure or skin blood flow during vasomotor reactivity tests. CONCLUSION: Spatially resolved spectroscopy provides an encouraging, noninvasive new tool to study cerebral tissue oxygenation during vasomotor reactivity tests consistent with physiological changes.