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Objective To investigate the prevalence of nutritional risk (NRS2002) and malnutrition inhospitalized stroke patient and their nutritional intervention. Methods The stroke patients admitted to three de-partments of vascular neurology ward including cerebral hemorrhage, cerebral infarction and subarachnoid hemor-rhage in Beijing Tiantan Hospital from January 2018 to January 2019 were recruited using cluster sampling. Nutri-tional risk screening 2002 ( NRS 2002) was used to screen the nutritional risk of inpatients Malnutrition was as-sessed by criteria:(1) body mass index (BMI) <18. 5 kg/m2 with poorer general condition from January 2018 to January 2019;(2) Global leadership initiative on malnutrition ( GLIM) criteria were used except whole body muscle mass measurement from October 2018 to January 2019. The nutritional intervention for patients were closely observed during hospitalization. Results A total of 1532 patients were registered and1036 patients were included in the final analysis considering the inclusion and exclusion criteria. The prevalence of nutritional risk was 33. 0％ ( 342/1036) . The prevalence of malnutrition based on BMI and GLIM criteria was 0. 9％( 9/1036) and 2. 5％ (10/393) respectively. Among the 342 patients with nutritional risk, 112 patients received nutritional support therapy by tube feeding, but only 29 patients received nutritional support that met guideline standards. 81 patients received not standard nutritional support, and 2 patients received highly unregulated nutritional sup-port. No patients received sugar and electrolyte infusion, oral nutritional supplements ( ONS) , oral nutritional a-gents and compound nutrition intervention. The other 230 patients took hospital diet. Conclusion The prevalence of nutritional risk in hospitalized patients with cerebral hemorrhage, cerebral infarction or subarachnoid hemorrhage was high, and the prevalence of malnutrition was extremely low. There was a low proportion of nutri-tional support. High quality of large sample cohort studies will be conducted to show whether reasonable applica-tion of nutritional support therapy in patients with nutritional risk can improve patient outcome.
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ObjectiveToinvestigatetherelationshipbetweenserumcystatinC(CysC)leveland hypertensive intracerebral hemorrhage (HICH). Methods The patients w ith HICH and healthy controls w ere enroled. The demographic and clinical data were colected. Immunoturbidimetric assay was used to detect serum CysC level. Results A total of 94 consecutive patients w ith HICH and 131 healthy controls w ere enroled. The baseline systolic blood pressure ( 168.57 ±28.64 mmHg vs.128.13 ±16.23 mmHg; t=-13.442, P<0.001;1 mmHg=0.133 kPa), diastolic blood pressure ( 95.56 ±14.68 mmHg vs.76.80 ± 8.76 mmHg; t= -11.965, P<0.001 ), fasting plasma glucose ( 6.24 ±1.83 mmol/L vs.5.22 ± 1.13 mmol/L; t= -4.234, P<0.001), and serum CysC level (1.02 ±0.26 mg/L vs.0.91 ±0.13 mg/L, P<0.001) in the HICH group w ere significantly higher than those in the control group. Multivariable logistic regression analysis show ed that baseline systolic blood pressure≥140 mmHg ( odds ratio [ OR] 12.523, 95% confidence interval [CI] 5.353-29.299; P<0.01), diastolic blood pressure ≥90 mmHg (OR 3.968, 95%CI 1.792-8.784; P<0.01 ) and serum CysC level≥1.09 mg/L ( OR 3.279, 95%CI 1.336-8.050; P<0.05) w ere the independent risk factors for HICH. In patients w ith HICH, the CysC serum level (1.13 ±0.26 mg/L) in the bleeding ≥30 ml group w as higher than that in the bleeding <30 ml group (0.99 ±0.25 mg/L; P<0.001) and the control group ( 0.91 ±0.13 mg/L; P<0.001). The serum CysC level in the bleeding volume <30 ml w as higher than that in the control group ( P=0.004). There w ere positive correlations betw een serum CysC and age, creatinine, urea, and uric acid (al P<0.01);there w ere negative correlations betw een serum CysC level and the estimated glomerular filtration rate ( P<0.01). Multivariable linear regression analysis show ed that age, creatinine, urea and uric acid w ere independent associated w ith the serum CysC level ( al P<0.05 ). Conclusions The increased serum CysC level is correlated w ith the amount of bleeding in patients w ith HICH. The increased serum CysC level is an independent risk factor for HICH.
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Hemorrhagictransformation(HT)referstointracerebralhemorrhageoccurredwhenthe blood vessels restore blood flow after acute ischemic stroke. It is one of the common complications of ischemic stroke. HT may not have any clinical manifestations and can also be manifested as limb paralysis aggravation, decreased consciousness level, and other symptoms. The symptomatic HT may result in prolonged hospitalization, increased disability and fatality. Therefore, research on the mechanisms and risk factors for HT may be expected to provide the basis for clinical treatment, and thus improve the prognosis of patients. This article review s the formation mechanism of HT, risk factors, screening of high-risk patients, and prevention and treatment.
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ObjectiveToinvestigatetheclinicalfeatures,riskfactorsforbleedingandtreatment outcomes in moyamoya disease patients w ith intracranial aneurysms. Methods The clinical symptoms, location and size of aneurysm, treatment and the long-term folow-up results of the moyamoya disease patients w ith intracranial aneurysms w ere analyzed retrospectively. Results A total of 34 moyamoya disease patients w ith intracranial aneurysms (35 aneurysms) w ere enrol ed, including 22 (64.7%) in the intracranial hemorrhage group and 12 ( 35.3%) in the non-intracranial hemorrhage group. Of the 35 intracranial aneurysms, 23 (main artery type 11, peripheral artery type 12) w ere in the intracranial hemorrhage group and 12 (main artery type 11, peripheral artery type 1) w ere in the non-intracranial hemorrhage group. There w ere 29 smal aneurysms and 6 medium aneurysms (al w ere patients w ith hemorrhagic moyamoya disease). The aneurysms w ere mainly peripheral arterial type in the intracranial hemorrhage group, and the aneurysms w ere mainly artery type in the non-intracranial hemorrhage group. There w as significant difference in aneurysm typing betw een the tw o groups ( P= 0.013 ). Tw o patients did not perform encephalo-duro-arterio-synangiosis (EDAS) in the intracranial hemorrhage group, other patients and those of the non-intracranial hemorrhage group performed EDAS. Angiographical reexamination revealed that 3 patients w ith peripheral aneurysm disappeared, and 1 aneurysm recurred after aneurysm embolization, and the remaining aneurysms did not have any change. Long-term fol ow-up show ed that 1 patient died of sudden cerebral hemorrhage at 1 year after procedure in the intracranial hemorrhage group, and the others did not have ischemic or hemorrhagic stroke. The modified Rankin scale scores w ere improved in 21 patients. Conclusions There are differences in moyamoya disease patients w ith intracranial aneurysm typing w ith different clinical manifestations. Moyamoya disease patients w ith intracranial aneurysms are mostly smal aneurysms and they can not temporarily be treated directly and can perform EDAS directly. Intracranial aneurysms after procedure may remain long-term stability, and some peripheral aneurysms may disappear.
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Duetothepatientswithintracerebralhemorrhageusualypresenttheriskfactorsfor ischemic stroke, the survivors after intracerebral hemorrhage are usualy facing a high risk of recurrent intracerebral hemorrhage or ischemic stroke at the same time. There is alw ays controversy about w hether these patients should be treated w ith antiplatelet therapy. This article introduces the different point of view s of researchers.
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Objective Toinvestigatetheclinicalsignificanceofplasmamatrixmetalloproteinase9 (MMP-9)intheformationofdelayedcerebraledemaafterintracerebralhemorrhage.Methods The clinical data of 107 patients with spontaneous intracerebral hemorrhage treated with conservative medical treatment were analyzed retrospectively. According to the clinical features and imaging changes,they were divided into either a delayed cerebral edema group (case group n=39)or a non-delayed cerebral edema group (control group n =68 ). The plasma MMP-9 level was detected with enzyme-linked immunosorbent assay within 24 h after onset. The patients performed head CT scan again at day 7 and 14 after admission. The changes of hematoma and edema volume were detected. All the possible factors associated with the formation of delayed cerebral edema were firstly analyzed by the univariate analysis. Univariate analysis showed that the variables with significant differences were enrolled into multiple logistic regression analysis. Results TheplasmaMMP-9levelofthedelayedbrainedemagroupwassignificantlyhigherthanthatof the control group,they were 189 ± 51 and 118 ± 27 mg/L respectively (P<0. 01). The result of univariate analysis showed that age,history of smoking,blood glucose level,baseline hematoma volume,and National Institute of Health stroke scale (NIHSS )score on admission might be associated with the formation of delayed cerebral edema after intracerebral hemorrhage. Logistic regression analysis showed that MMP-9 level (OR,9. 745,95%CI 6. 754-15. 466,P<0. 01),baseline hematoma volume (OR,2. 411,95%CI 1. 190-2. 728,P =0. 018),blood glucose level on admission (OR,1. 327,95%CI 1. 133 -1. 850,P =0.004),and NIHSS score (OR,1. 867,95%CI 1. 272-2. 364,P=0. 020)were the independent risk factorsfortheformationofdelayedcerebraledemaafterintracerebralhemorrhage.Conclusion Theamount of bleeding,NIHSS score,and hyperglycemia are the risk factors for the formation of delayed cerebral edema in patients with spontaneous intracerebral hemorrhage,while high MMP-9 level on admission indicated that the risk of the formation of delayed cerebral edema is high.
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Objective To investigate the dynamic changes of serum insulin-like growth factor-1(IGF-1)levels in patients with acute cerebralhemorrhage.Methods Serum levels were determined with RIA in 40 patients with cerebralhemorrhage within 2 days and at 14 days and 20 healthy individuals serve as control groups.Results The serum IGF-1 levels in patients with cerebralhemorrhage were significantly lower than those in controls(P