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BACKGROUND: The challenges of caring for stroke patients are growing due to population ageing and improved survival rates. Healthcare professionals' competence development in stroke care is a necessity to ensure high-quality patient care. OBJECTIVES: To identify and describe the competence areas of healthcare professionals working in the stroke patient care pathway and factors influencing these competences. DESIGN: A mixed-methods systematic review. METHODS: The review was conducted according to the JBI guidelines and registered in the PROSPERO database (CRD42020204062). PRISMA checklist guided the review process. Relevant original studies were identified by searching four databases-CINAHL (EBSCO), PubMed, Scopus and Medic. After researcher consensus was reached, 32 studies were selected for inclusion and subjected to content analysis and data tabulation. RESULTS: Competence in care processes, clinical competence, competence in using self-management strategies, interaction skills, skills in acknowledging family and competence in integrating the available evidence base into patient care were identified as key competence areas. Organisation of services, specialisation in stroke care, continuous development and education, family and carer and training in oral care and cognitive rehabilitation were identified as factors that influence healthcare professionals' competence. CONCLUSIONS: Diverse clinical and interaction competencies are needed throughout the stroke care pathway, and various factors affect healthcare professionals' competence. Further research on healthcare professionals' stroke care competence will be needed to respond to changing healthcare demand. RELEVANCE TO CLINICAL PRACTICE: We recommend organisational support and formulation of stroke care patient guidelines in line with healthcare competence requirements. Focus should be added for nursing professions in developing interactive communication competence since nurses spend the majority of the time providing individual patient care. Also, organisations should integrate continuing training in specialised stroke care for healthcare professionals' competence development.
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Health Personnel , Stroke , Clinical Competence , Delivery of Health Care , Health Personnel/education , Humans , Quality of Health Care , Stroke/therapyABSTRACT
AIM To determine the effect of L-arginin e on cerebral blood perfusion following subarachnoid hemorrhage(SAH) in rats. METHODS Endovascular perforating SAH models were replicated in Wista r rats, and animals were divided into sham-operated group, SAH group and SAH+ L-arginine group. Dynamic changes of regional cerebral blood flow (rCBF) with in 24 hours were measured and serum nitric oxide(NO, NO - 2/NO - 3)levels at different time points within 24 hours were detected. Mean arterial blood pre ssure and blood gas were monitored during the experiment. RESULTS No obvious change in physiological parameters in the three groups was observed . rCBF and serum nitric oxide level at every time point after operation in SAH g roup were lower than those in sham-operated group. Pathological alterations abo ve in SAH+L-arginine group were less obvious than those in SAH group. CONCLUSION L-arginine, by antagonizing the decrease of nitric oxi de, exerts protective effect on secondary cerebral ischemia following SAH.
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Objective To retrospectively analysis our experience of embolization of ruptured intracranial aneurysms during the period of cerebral vasospasm (CVS). Methods Thirty-seven patients with ruptured intracranial aneurysms were embolized with electrolytic detachable coils during the period of CVS (days 4 to 14). Group A included the 14 patients with angiographic CVS and group B included 23 patients without angiographic CVS. All except 2 patients were transferred to our department during the CVS period. Results Twelve patients in group A were successfully received the aneurysms embolization and treatment of the CVS with intraarterial papaverine injection and balloon angioplasty. The Glasgow Outcome Scales (GOS) in 3 months were good recovery in 7 patients, moderate disability in 2, severe disability in 1 and dead in 2. Two patients failed the embolization because the microcatheters can't pass the spasmatic parent arteries. All the aneurysms in group B were successfully embolized. The GOS were good recovery in 18 patients, moderate disability in 2, severe disability in 2 and dead in 1. There was no intraprocedural aneurysmal rupture but with 2 thromboembolic events. No rebleeding occurred during the mean 11 months follow-up.Conclusions The so-called “the period of CVS” isn't always associated with CVS in angiograpy. Embolization of ruptured intracranial aneurysms during the period of pure CVS doesn't carry an increased risk. Both the aneurysms and CVS can be treated during the single procedure. It can reduce the rebleeding rate in hospital and improved the prognosis of the patients with CVS.
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Objective To probe the application of CT cerebral perfusion imaging on transient ischemic attacks(TIA) Methods Conventional CT and CT cerebral perfusion imaging were performed on 5 normal adults and 20 patients with clinically diagnosed TIA After regular CT examination, dynamic scans of 40 seconds were performed on selected slice (usually on the basal ganglia slice), while 40 ml non ionic contrast material were bolus injected through antecubital vein with These dynamic images were processed with the "Perfusion CT" software package on a PC based workstation Cerebral blood flow (CBF) and time to peak (TP) enhancement were measured within specific regions of the brain on CT perfusion images Quantitative analysis was performed for these images Results A gradient of perfusion between gray matter and white matter was showed on CT perfusion images in normal adults and TIA patients CBF and TP for normal cortical and white matter were 378 2 ml?min -1 ?L -1 , 7 8 s and 112 5 ml?min -1 ?L -1 , 9 9 s, respectively In 20 cases with TIA, persisting abnormal perfusion changes corresponding to clinical symptoms were found in 15 cases with prolonged TP Other 5 cases showed normal results TP of affected side (11 8?4 4) s compared with that of the contralateral side (9 1?3 1) s was significantly prolonged ( t =5 277, P
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AIM: to study the change of glutamate(Glu) transport across blood brain barrier(BBB) in rat following forebrain ischemia/reperfusion. METHODS: BBB unidirectional transfer constant(K i) for [3H]-Glu in rat hippocampus, cerebral cortex and striatum were determined after rats were subjected to cerebral ischemia 10 min (two-carotid occlusion plus hypovolemic hypotension) followed by 0.17, 2, 6 and 24 h of reperfusion. The recovery of [3H]-Glu in cerebrum was also determined after intracerebral injection of [3H]-Glu in another experiment. RESULTS: Compared with control rat brain, K i for [3H]-Glu significantly(P
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AIM: To study the change of glutamate (Glu) transport across blood brain barrier ( BBB ) in rat following forebrain ischemia/reperfusion. METHODS: BBB unidirectional transfer constant ( Ki ) for [3H] - Glu in rat hippocampus, cerebral cortex and striatum were determined after rats were subjected to cerebral ischemia 10 min ( two - carotid occlusion plus hypovolemic hypotension) followed by 0.17, 2, 6 and 24 h of reperfusion. The recovery of [3H] - Glu in cerebrum was also determined after intracerebral injection of [3H] - Glu in another experiment. RESULTS: Compared with control rat brain, Ki for [3H] -Glu significantly( P < 0.05) decreased at 10 ain cerebral ischemia followed by 0.17, 2 and 6 h of reperfusion. At 5 min after intracerebrally injecting [3H] - Glu , recovery of [3H] - Glu in control rat brain was 23.83%. The result indicted that there is a Glu efflux mechanism on BBB. This efflux was not significantly inhibited by pretreatment of 200 mg/L probenecid. After 10 ain cerebral ischemia followed by 2 h of reperfusion, the recovery( 13.13 % ) was significantly lower than contro( P < 0.05), its recovery was only 55 % of the control. The result indicated that cerebral ischemia/reperfusion may enhanced the effiux of [3H] -Glu from brain. CONCLUSION: Cerebral ischemia/reperfusion significantly reduced Glu BBB transport from plasma to brain and enhanced effiux of Glu from brain.
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Objective To study the indications of carotid endarterectomy(CEA) and perioperative managements . Methods The clinical data of 11 patients with transient ischemia attack (TIA) and carotid artery stenosis who underwent CEA were reviewed retrospectively. Results After CEA, the TIA symptoms disappeared in all patients, and the chronic symptoms of cerebral ischemia had obvious improvement in 4 cases . There were no serious postoperative complications, such as cerebral hemorrhage, hemiplegia, etc. Conclusions CEA may be considered when one or both sides of carotid stenosis more than 50% is discovered by Duplex scanning, digital subtraction angiography or MRA in patients with TIA. Stage operation for bilateral carotid occlusive lesion is safer. Paying attention to perioperative managements is important for reducing operative complications.
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Objective To evaluate the effect of lidocaine on delayed neuroal death after global cerebral ischemia. Methods Global cerebral ischemia was induced by the occlusions of bilateral commom carotid and vertebral arteries . Twenty-five rabbits were randomly divided into three groups:sham operative group (SH group,n=5) without the four-vessel occlusion; ischemia group(IS group,n=10) with intravenous normal saline of 15 ml followed by the four-vessel occlusion for 5 min; lidocaine group (LI group,n=10) with intravenous lidocaine of 10mg/kg followed by the four-vessel occlusion for 5 min. Three days later, every cerebrum was resected and stained using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and hematoxylin-eosin (HE) methods,to count the amount of the positive stained cells of hippocampus. Results The positive cell amount of HE staining (ischemic change cells) was correlated with that of TUNEL staining (apoptosis cells) (r=0.915).Compared with that in SH group, the amount of apoptosis cells increased significantly in IS and LI groups (P
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Objective To investigate the effect of glucocorticoid on ischemia-induced neuronal damage in gerbil hippocampus with forebrain ischemia model.Methods Twenty-one gerbils were randomly assigned to 3 groups (7 animals each). The animal was anesthetized and both common carotid arteries were exposed and separated. Silk threads were looped around these arteries. In group A and group B ,10 ?l saline was given and in group C dexamethasone-water soluble ( 3?g dissolved in 10 ?l saline ) was administered intracerebroventricularly. After a stabilization period of 60 min, transient forebrain ishcmia for 2.5 min was induced in group B and group C by pulling the arteries with 8g weights under the brain temperature of 37.5℃?0.2℃. Seven days after the ischemia, the brains were taken out and fixed with 10% buffered formalin. Brain slices, 5 ?m thick, were stained with hematoxylin and eosin. The numbers of preserved pyramidal cells in the hippocampal CA1 field per 1 mm length of stratum pyramidal were counted.Results (1) Compared with those in group A, the preserved pyramidal cells in hippocampal CA1 field were reduced in group B and group C (P
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Objective To investigate if isoflurane preconditioning induces ischemic tolerance against neuronal damage produced by middle cerebral artery occlusion (MCAO) in rats Methods Thirty male SD rats weighing 350 400g were randomly divided into three groups: control group (no pretreatment,n=10),isoflurane preconditioning group (ISO group) (inhalation of 2% isoflurane and 98% O 2 1h per day lasting 5d,n=10), oxygen preconditioning group (O 2 group) (inhalation of 98% O 2 1h per day lasting 5d ,n=10) Right MCAO was induced by a 3 0 nylon thread with round tip inserted cranially into right internal carotid artery under isoflurane anesthesia and maintained for 120 min The neurologic deficit score (NDS) was evaluated 1, 3, 6, 12, 16 and 24h after reperfusion and the infarct volume was calculated at 24th following reperfusion Results The NDS of ISO group was lower than that of other two groups at each time interval (P0 05) Conclusions Isoflurane pretreatment can induce ischemic tolerance against neuronal damage produced by transient MCAO in rats
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ObjectiveTo investigate preliminary applic ation values of intravascular ultrasound(IVUS)in the carotid artery narrowing of transient ischemia attack (TIA) patients. MethodsIVUS has been used to 4 TIA patients with carotid artery narrowing identified by carotid artery echo, following carotid stenting and completion angiogram to detect evidence of inappropriate stent deployment. ResultsIVUS revealed the vessel wall structure, plaque morphology, measured accurately the narrowing degree of carotid artery. The narrowing percent identified by IVUS was larger than angiogram, and IVUS was more sensitive in detecting plaque than digital subtraction angiography(DSA). Four patients accepted stent deployment successfully.ConclusionsDSA underestimated the severity of the lesion. IVUS more accurately evaluates the extent and characteristics of the lesions than DSA, it is an important and useful component of carotid artery stent procedures.
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The contents of amino acids in dorsal hippocampus were measured at themoment of 10-min transient forebrain ischemia by using amino acid autoanalyser, delayedneuronal death (DND) model was established by bilateral carotid arteries occlusion for10-min followed by 7-day reperfusion. Effect of monosodium glutamate, ketamine on DNDin the hippocampus was examined by counting neuronal density in CA_1 sector. The Ca~(2+)content in dorsal hippocampus was measured, and the effect of ketamine on Ca~(2+) concen- tration was examined. The results showed that the contents of glutamate and aspartate indorsal hippocampus were increased significantly at the moment of 10-min transient fore-brain ischemia (P0.05). These results suggested that excitatory amino acids (EAA)and Ca~(2+) played an important role directly or indirectly in the development of DND inhippocampus following transient forebrain ischemia in gerbils; ca~(2+) over-load may be ancommon final pathway of neuronal death.
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AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.