Neurological deterioration under isovolemic hemodilution with hydroxyethyl starch in acute cerebral ischemia.

Background: Early neurological deterioration (END) is a feared complication of acute cerebral ischemia. However, estimates of END frequency vary widely, rates have not been systematically examined in hyperacute patients presenting within the first 2h of onset, nor separately in patients treated with and without thrombolysis, and risk factors for END have not been well delineated. Methods: We analyzed patients with a final diagnosis of acute cerebral ischemia in the NIH FAST-MAG Phase 3 multicenter clinical trial. END was defined as worsening post-admission by ≥ 4 NIHSS points up to Day 4. We separately analyzed patients who did and did not receive IV tPA. Results: Among 1245 acute cerebral ischemia patients transported by EMS to 55 stroke centers, time from last known well (LKW) to ED arrival was median 59 mins (IQR 80-46), and 36.1% received IV tPA. Overall, 211 (16.9%) experienced END by Day 4, with a greater proportion of END in tPA than non-tPA patients (21.2% vs 14.5%, p=0.003). In multivariate analysis, from 26 candidate variables, among tPA recipients, independent predictors of END were: age (OR 1.03/year, 95%CI 1.01-1.05), diastolic BP (OR 1.01/mm Hg, 95%CI 1.00-1.03), prior stroke (OR 1.65, 95%CI 0.98-2.77), glucose (OR 11.06/10 fold increase, 95%CI 1.90-64.44), and worse ASPECTS score (OR 0.85/point, 95%CI 0.78-0.92). Among non-tPA recipients, independent predictors of END were: more severe NIHSS (OR 1.08/point, 95%CI 1.05-1.11), glucose (OR 8.88/10 fold increase, 95%CI 1.83-43.12), and h/o hypertension (OR 2.62/mm Hg, 95%CI 1.25-5.48), with Akaike information criteria identifying SBP, shorter LKW-to-ED time, and absence of anticoagulant agents as additional contributors. C statistics for these models were 0.68 for tPA patients and 0.73 for non-tPA patients. Conclusions: Among hyperacute cerebral ischemia patients, END occurs in 1 in 5 who receive tPA, and 1 in 7 who do not receive tPA. Greater initial stroke severity (on neurologic exam or imaging), higher glucose, and hypertension increase risk of END for both lytic and non-lytic patients, with older age and prior stroke additionally increasing END risk with tPA. Models based on these risk factors show fair to good performance identifying patients who will experience END after hospital admission.

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Effects of isovolemic hemodilution in acute cerebral ischemia

Clinical Hemorheology and Microcirculation ◽

10.3233/ch-1986-6504 ◽

2016 ◽

Vol 6 (5) ◽

pp. 381-394

Author(s):

R. Cavestri ◽

A. Pelucchi ◽

B. Mastropasqua ◽

R. Agosti ◽

C. Le Grazie ◽

...

Keyword(s):

Cerebral Ischemia ◽

Isovolemic Hemodilution ◽

Acute Cerebral Ischemia

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Abstract TP233: Patterns, Determinants and Outcomes of Ultra-Early Neurological Deterioration (U-END) in Acute Ischemic Stroke

Stroke ◽

10.1161/str.48.suppl_1.tp233 ◽

2017 ◽

Vol 48 (suppl_1) ◽

Author(s):

Kristina Shkirkova ◽

Gregory Wong ◽

Julius Weng ◽

Jeffrey L Saver ◽

Sidney Starkman ◽

...

Keyword(s):

Ischemic Stroke ◽

Cerebral Ischemia ◽

Management Strategies ◽

Neurological Deterioration ◽

Effective Management ◽

Stroke Therapy ◽

Phase 3 ◽

Prehospital Treatment ◽

Acute Cerebral Ischemia ◽

Early Neurological Deterioration

Background: The patterns and outcomes of deterioration during prehospital transport and the first phase of ED care are important for planning for diversion of acute cerebral ischemia (ACI) patients to designated stroke centers and design of prehospital treatment trials. Methods: We analyzed patients enrolled in the NIH Phase 3 Field Administration of Stroke Therapy - Magnesium (FAST-MAG) trial within 2h of last known well (LKW). Deterioration was defined as worsening by ≥2 on the Glasgow Coma Scale (GCS), performed serially by paramedics in the field, upon ED arrival, and after the early ED course. Results: Among 713 acute cerebral ischemia patients, age was 65.4 (±13.4), 45% female. Times from LKW to GCS assessments were: paramedic, 25 mins (IQR 15-46); ED arrival, 60 mins (IQR 48-82); and after early ED course, 83 mins (IQR 60-106). Overall, 16.3% experienced neurological deterioration, including 9.0% in prehospital phase only, 7.3% in early ED phase only, and none in both phases. Granular patterns of deficit progression were: Prehospital Sustained - prehospital deterioration, then stable early ED phase, 2.2% (16); Dippers - prehospital deterioration, then early ED improvement, 6.7% (48); Delayed - stable prehospital, then ED deterioration, 3.0% (22); and Peakers - prehospital improvement, then early ED deterioration, 4.2% (30) (Figure). Ischemic stroke patients who experienced any U-END had higher age, 73.2 vs 69.8, p<0.01; lower prehospital GCS scores, 14 (IQR 11-15) vs 15 (IQR 14-15), p<0.001; and greater prehospital focal weakness, LAMS 4.2 vs 3.6, p<0.001. U-END was associated with higher rates of disability or death (mRS 2-6) at 90 days, 77.8% vs 53.8%, p<0.001. Conclusions: Ultra-early neurological deterioration occurs in one-sixth of EMS-transported acute cerebral ischemia patients, and is associated with less favorable outcome. Early identification and effective management strategies are needed to reduce its occurrence.

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Ebselen in the acute cerebral ischemia

Neuroscience Research ◽

10.1016/s0168-0102(00)80907-4 ◽

2000 ◽

Vol 38 ◽

pp. S10

Author(s):

M Suzuki

Keyword(s):

Cerebral Ischemia ◽

Acute Cerebral Ischemia

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Effect of carvedilol on the redox-status of plasma low-molecular-weight aminothyols in rats with acute cerebral ischemia

ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia» ◽

10.25557/0031-2991.2018.03.12-18 ◽

2018 ◽

pp. 12-18

Author(s):

К.А. Никифорова ◽

В.В. Александрин ◽

П.О. Булгакова ◽

А.В. Иванов ◽

Э.Д. Вирюс ◽

...

Keyword(s):

Molecular Weight ◽

Cerebral Ischemia ◽

Carotid Arteries ◽

Redox Status ◽

Global Cerebral Ischemia ◽

Low Molecular Weight ◽

Adrenergic Antagonist ◽

Acute Cerebral Ischemia ◽

Common Carotid Arteries ◽

Reduced Forms

Цель. Установить влияние неспецифического адреноблокатора карведилола на редокс-статус низкомолекулярных аминотиолов (цистеин, гомоцистеин, глутатион) в плазме крови при моделировании глобальной ишемии головного мозга у крыс. Методика. Нами была использована модель глобальной ишемии (пережатие общих сонных артерий с геморрагией длительностью 15 мин). Препарат вводили за 1 ч до операции. Уровни аминотиолов измеряли через 40 мин после начала реперфузии. Анализ уровня аминотиолов проводили методом жидкостной хроматографии. Результаты. Установлено, что у крыс, не подвергавшихся ишемии, карведилол в дозе 10 мг/кг вызывает рост редокс-статуса цистеина и глутатиона (в 3 и 3,5 раза соответственно по сравнению с контролем, p = 0,04 и p = 0,008) за счет увеличения их восстановленных форм. При ишемии данного эффекта не наблюдалось. Редокс-статус у крыс с ишемией на фоне карведилола (Цис = 0,85 ± 0,14%, Глн = 1,8 ± 0,7%, Гцис = 1,1 ± 0,8%) оставался таким же низким, как и у крыс с ишемией без введения карведилола (р > 0,8). Заключение. Полученный результат демонстрирует, что в условиях ишемии головного мозга карведилол не оказывает эффекта на гомеостаз аминотиолов плазмы крови, несмотря на выраженный антиоксидантный эффект в нормальных условиях. Aim. Effect of a nonspecific adrenergic antagonist carvedilol on the redox status of plasma low-molecular-weight aminothiols (cysteine, homocysteine, glutathione) was studied in rats with global cerebral ischemia (occlusion of common carotid arteries with hemorrhage). Methods. A model of global ischemia (occlusion of common carotid arteries with 15-min hemorrhage) was used. The drugs were administered one hour before the operation. Aminothiol levels were measured by HPLC with UV detection at 40 minutes after the onset of reperfusion. Results. Carvedilol 10 mg/kg increased the redox status of cysteine and glutathione in rats not exposed to ischemia (3 and 3.5 times, respectively, compared with the control, p = 0.04 and p = 0.008, respectively) but not of homocysteine, by increasing their reduced forms. However, this effect was not observed in ischemia. In rats with ischemia treated with carvedilol, the redox status (Cys = 0.85 ± 0.14%, GSH = 1.8 ± 0.7%, Hcys = 1.1 ± 0.8%) remained low similar to that in rats with ischemia not treated with carvedilol (p >0.8, 0.8, and 0.9, respectively). Conclusion. Carvedilol did not affect the homeostasis of blood plasma thiols in cerebral ischemia despite the pronounced antioxidant effect under the normal conditions.

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