Disfagia no doente com AVC : prevalência e determinantes

Introdução: O acidente vascular cerebral (AVC) assume em Portugal elevadas taxas de morbilidade e reinternamento hospitalar. A disfagia surge como uma complicação frequente deste evento neurológico, com índices de morbilidade elevados pelo risco de desnutrição, desidratação e aspiração broncopulmonar. O diagnóstico e a sua monitorização no processo de reabilitação do doente são ações fundamentais na prevenção de aspirações alimentares, redução do internamento hospitalar e na eficácia da reabilitação do doente. Objetivo: Identificar e avaliar o grau de disfagia na pessoa com AVC e analisar a relação entre esta, e as variáveis socio-demográficas e clínicas no sentido de poder melhorar futuramente os cuidados de enfermagem de reabilitação. Métodos: Trata-se de um estudo não experimental, transversal, descritivo-correlacional de caráter quantitativo, que foi realizado numa amostra não probabilística por conveniência, constituída por 25 doentes com diagnóstico de AVC, internados na Rede Nacional Cuidados Continuados Integrados (RNCCI), em unidades de Convalescença e Reabilitação. O instrumento de colheita de dados integra uma seção de caracterização sócio-demográfica e clínica e duas escalas: Escala Gugging Swallowing Screen (GUSS) e Índice de Barthel, a fim de avaliar a disfagia e a funcionalidade, respetivamente. Resultados: A amostra apresenta uma média de idade de 76,8 anos, sendo 68% do sexo feminino e 32% do sexo masculino. Verificámos que 68% dos participantes apresenta mais de dois antecedentes clínicos e apenas 24% dos participantes não apresenta disfagia. Dos restantes, 12% apresenta disfagia grave, 36% moderada e 28% disfagia ligeira. A área de lesão parece influenciar a deglutição, demonstrando a Artéria Cerebral Média (ACM) e Artéria Cerebral Posterior (ACP) como áreas de maior sensibilidade. Denotou-se que quanto maior o grau de dependência, maior gravidade de disfagia. Conclusão: Doentes com AVC isquémico apresentam disfagia, com gravidade relacionada com a área vascular. A existência de vários antecedentes clínicos pode gerar perturbações na deglutição do doente. De igual modo, quanto maior for a dependência funcional do doente, maior é o grau de disfagia e o risco de aspiração pulmonar. Palavras-chave: AVC; Disfagia; Reabilitação.

Determinantes da incapacidade funcional em doentes com AVC

Introdução- O Acidente Vascular Cerebral continua a ser a primeira causa de morte em Portugal, sendo também responsável pelo elevado índice de incapacidade e dependência funcional da população adulta portuguesa, afetando significativamente os aspetos da vida física, económica e social. Os processos de reabilitação continuados têm-se mostrado bastante eficazes na recuperação da independência funcional destes doentes. Assim sendo o objetivo geral deste estudo consiste em avaliar o nível de independência funcional e os fatores determinantes nesses níveis, em doentes sujeitos a programas de reabilitação continuados e doentes sem reabilitação. Métodos- O presente estudo é de carácter quantitativo, enquadrando-se num desenho de estudo descritivo transversal e analítico, no qual participaram 60 indivíduos que sofreram AVC, pertencendo 36 ao grupo experimental e 24 ao grupo de controle. A recolha de dados foi efetuada através de um questionário composto por questões de caracterização sociodemográfica, de caracterização clinica, uma escala de APGAR Familiar e uma Escala de Medida de Independência funcional (MIF). Resultados- A análise por grupos mostra que o grupo experimental é mais independente que o grupo de controle, ou seja, o nível de independência funcional é mais elevado na sua generalidade na amostra de indivíduos sujeitos a processos de reabilitação. As variáveis que influenciaram significativamente a independência funcional foram: o género (no comportamento social no G.cont),o estado civil (solteiros/viúvo mais independentes aos níveis dos cuidados pessoais, controle dos esfíncteres, mobilidade e locomoção no G. exp), habilitações académicas (maior escolaridade maior independência no G. exp) fatores de risco (doentes sem fatores de risco no G. cont são mais independentes nos cuidados pessoais, controle de esfíncteres e locomoção), indivíduos com AVC isquémico são mais independentes nos cuidados pessoais e locomoção, e os que realizaram trombólise são mais independentes nas diferentes dimensões nos dois grupos. Conclusão- As variáveis sociodemográficas e clinicas exercem influência apenas em algumas dimensões da independência funcional dos utentes após o AVC e a reabilitação desenvolvida de forma continuada, aumenta o grau de independência dos doentes diminuindo o grau de incapacidade. Palavras-chave- Acidente Vascular Cerebral, Incapacidade, Independência Funcional, Reabilitação.

Ganhos em independência funcional no doente com AVC

Introdução – O Acidente Vascular Cerebral (AVC) representa a principal causa de dependência funcional da população adulta portuguesa. Conhecer os fatores que possam aumentar os ganhos em independência funcional é crucial para uma melhoria na abordagem destes doentes. Objetivo – Analisar os ganhos em independência funcional no doente que sofreu AVC considerando a diferença no Índice de Barthel entre a admissão e a alta e desde a alta até à primeira consulta. Métodos – Estudo de coorte retrospetivo, utilizando a base de dados hospitalar para doentes admitidos numa unidade de AVC entre 2010 e 2014. O Índice de Barthel (IB) na admissão, alta e primeira consulta após alta foi usado para calcular ganhos em independência funcional por dia entre a admissão e a alta (diferença entre IB na alta e na admissão dividindo pelo número de dias de internamento) e por semana entre a alta e a primeira consulta (diferença entre IB na primeira consulta e na alta dividindo pelo número de semanas entre a alta e a consulta). Com modelos de regressão linear avaliou-se a influência de fatores demográficos, clínicos e o destino após a alta nos ganhos em independência funcional por dia e por semana, obtendo-se coeficientes de regressão e respetivo intervalo de confiança a 95% (IC95%). Resultados – Nos 483 doentes estudados, a idade mediana é 76 anos, 59,0% são homens, 84,3% têm AVC isquémico e 30,6% foram para o domicílio após a alta. A independência funcional por dia aumentou nos anos mais recentes, particularmente em 2013 em que este parâmetro aumentou 1,164 pontos (com IC95%: 0,192 e 2,135; p=0,019) em comparação com 2010. Também o diagnóstico influenciou os ganhos diários em independência funcional, com LACI e PACI apresentando um aumento estatisticamente significativo de 1,372 pontos (IC95%: 0,324 e 2,421; p=0,010) e de 1,275 pontos (IC95%: 0,037 e 2,514; p=0,044), respetivamente, em comparação com POCI. Relativamente à independência funcional por semana, idades mais avançada e score elevado do IB na alta estão associados a menos ganhos por semana (p<0,001 e p=0,002). Também o destino após alta influencia os ganhos por semana, doentes encaminhados para unidades de convalescença apresentam ganhos de 1,289 pontos (IC95%: 0,661 e 1,917; p<0,001) em comparação com os doentes que foram para o domicílio. iv Conclusões – Houve melhoria na evolução funcional entre a admissão e a alta dos doentes em anos mais recentes sugerindo melhorias nas unidades de AVC. Atenção particular deve ser dada a estes doentes após a alta, particularmente nos de idade mais avançada.

Behind Recurrent Thromboembolic Events

We describe the case of a 68-year-old man, who presented with an ischemic stroke due to cardiac embolization related to mitral valve endocarditis. Blood cultures were always negative and post-operative valve histology did not show microorganisms. The patient also presented further recurrent peripheral embolic events. These clinical aspects were the first sign of a pancreas adenocarcinoma, which was only diagnosed in the clinical autopsy. In conclusion, these clinical findings of recurrent thromboembolic events with no microorganisms isolated suggests the diagnostic of a marantic endocarditis.

Cystatin C and cardiovascular disease : A mendelian randomization study

BACKGROUND: Epidemiological studies show that high circulating cystatin C is associated with risk of cardiovascular disease (CVD), independent of creatinine-based renal function measurements. It is unclear whether this relationship is causal, arises from residual confounding, and/or is a consequence of reverse causation. OBJECTIVES: The aim of this study was to use Mendelian randomization to investigate whether cystatin C is causally related to CVD in the general population. METHODS We incorporated participant data from 16 prospective cohorts (n ¼ 76,481) with 37,126 measures of cystatin C and added genetic data from 43 studies (n ¼ 252,216) with 63,292 CVD events. We used the common variant rs911119 in CST3 as an instrumental variable to investigate the causal role of cystatin C in CVD, including coronary heart disease, ischemic stroke, and heart failure. RESULTS: Cystatin C concentrations were associated with CVD risk after adjusting for age, sex, and traditional risk factors (relative risk: 1.82 per doubling of cystatin C; 95% confidence interval [CI]: 1.56 to 2.13; p ¼ 2.12 1014). The minor allele of rs911119 was associated with decreased serum cystatin C (6.13% per allele; 95% CI: 5.75 to 6.50; p ¼ 5.95 10211), explaining 2.8% of the observed variation in cystatin C. Mendelian randomization analysis did not provide evidence for a causal role of cystatin C, with a causal relative risk for CVD of 1.00 per doubling cystatin C (95% CI: 0.82 to 1.22; p ¼ 0.994), which was statistically different from the observational estimate (p ¼ 1.6 105 ). A causal effect of cystatin C was not detected for any individual component of CVD. CONCLUSIONS: Mendelian randomization analyses did not support a causal role of cystatin C in the etiology of CVD. As such, therapeutics targeted at lowering circulating cystatin C are unlikely to be effective in preventing CVD. 

Antiplatelet therapy and clinical outcomes in cardiovascular diseases

Cardiovascular diseases (CVD) is a leading cause of death in the world. Despite effective treatment regimens for ischaemic heart disease (IHD) and ischaemic stroke, mortality and recurrence rates remain high. Antiplatelet therapy is on effective treatment and reduces the risk of recurrent heart attack and stroke. Nevertheless, there are patients who stopped or interrupted their antiplatelet therapy for certain reasons or some patients may be resistant or poor responders to antiplatelet therapy. Furthermore, there is evidence of rebound effect in platelet activity after antiplatelet cessation and this may associate with increased risk of cardiovascular event. This thesis is divided into five main chapters (chapters 3 to 7) which attempt to provide data to help resolve the uncertainty. Chapter 1 highlights the background of cardiovascular diseases and the global burden of cardiovascular and cerebrovascular diseases. The metabolism of platelets, antiplatelet therapy and current antiplatelet therapy guidelines are described, followed by discussion of the risk of cardiovascular event and changes in antiplatelet therapy. Chapter 2 describes the data source from Virtual International Stroke Trial Archive (VISTA) and National Health Service Greater Glasgow and Clyde (NHSGGC) Safe Haven, followed by definition of outcome measures. In chapter 3, Virtual International Stroke Trial Archive (VISTA) data was examined to test whether continue with the same antiplatelet therapy or changing to a new antiplatelet regimen reduces the risk of subsequent events in patients who experience a stroke whilst taking antiplatelet therapy. The findings indicate that subjects who switch to a new antiplatelet regimen after stroke did not have a lower early recurrence rate than subjects who continued with the same antiplatelet therapy. Observations on bleeding complications were similar in both groups. However, changing antiplatelet regimen after stroke was associated with more favourable functional outcome across a full scale modified Rankin Scale (mRS) at 90 days. In chapter 4, association between early or later initiation of antiplatelet with a recurrent ischaemic stroke and bleeding complications was assessed using VISTA data. The findings indicate that there was no association between a recurrent ischaemic stroke and timing of initiation of antiplatelet drug after stroke. However, early initiation was associated with increased risk of bleeding. In terms of functional outcomes, this study demonstrated that the mid-time and late initiation of antiplatelet therapy after acute stroke are associated with better functional outcomes compared with early initiation. In chapter 5, a nested case-control study was performed to explore the rate of antiplatelet cessation and interruption in a sample of patients with recent ischaemic stroke and to assess the risk of cardiovascular events associated with cessation and interruption of antiplatelet. It was found that there was no increased risk of cardiovascular event among patients who had early cessation or interrupted/stopped antiplatelet therapy within 90 days following acute ischaemic stroke. In chapter 6, the incidence and predictors of cardiovascular events after DAPT cessation were evaluated. The incidence of cardiovascular event while taking DAPT and following discontinuation of DAPT was 15.7% and 16.7% respectively. This study found that increasing age was associated with an increased risk of cardiovascular event, whereas, revascularization-treated patients and longer duration of DAPT, were each associated with a decreased risk. The duration of DAPT six months and less was associated a significantly higher risk for cardiovascular event. In chapter 7, an untargeted metabolomics analysis was performed while on DAPT (aspirin plus ticagrelor) and once they stopped ticagrelor to identify metabolite changes associated with cardiovascular events after stopping DAPT. Ten ACS patients were recruited in this study and data were analysed for seven patients. Three hundred eleven putative metabolites were identified. This study found 16 putative metabolites significantly altered following ticagrelor cessation. Of these, seven metabolites were from lipid pathway and down-regulated some up to 3-fold. On the other hand, adenosine, from nucleotide metabolism was upregulated up to 2.6-fold. It concluded that there are changes in numerous pathways following DAPT discontinuation and whether these changes differ in patients who have cardiovascular event after stopping DAPT warrant further investigation. In chapter 8, a summary of the findings of this thesis are presented as well as the future directions of research in this area.

[Management of transient ischemic attack (TIA) and acute stroke]

Patients with a transient ischemic attack and an acute stroke need urgent investigations and therapy in a stroke unit. Immediate investigation of the etiology and early secondary prevention measures reduce the likelihood of recurrent and other vascular events. In selected stroke patients intravenous thrombolysis and/or endovascular therapies lead to a significant reduction of long term disabilities.

Sleep deprivation before stroke is neuroprotective: A pre-ischemic conditioning related to sleep rebound

BACKGROUND AND AIM: We have previously shown in a rat model of focal cerebral ischemia that sleep deprivation after stroke onset aggravates brain damage. Others reported that sleep deprivation prior to stroke is neuroprotective. The main aim of this study was to test the hypothesis that the neuroprotection may be related to an increase in sleep (sleep rebound) during the acute phase of stroke. METHODS: Male Sprague Dawley rats (n=36) were subjected to continuous polygraphic recordings for baseline, total sleep deprivation (TSD), and 24h after ischemia. TSD for 6h was performed by gentle handling and immediately followed by ischemia. Focal cerebral ischemia was induced by permanent occlusion of distal branches of the middle cerebral artery. Control experiments included ischemia without SD (nSD) and sham surgery with TSD (n=6/group). RESULTS: Shortly after stroke, the amount of slow wave sleep (SWS) and paradoxical sleep (PS) increased significantly (p<0.05) in the TSD/ischemia, resulting in an increase in the total sleep time by 30% compared to baseline, or by 20% compared with the nSD/ischemia group. The infarct volume decreased significantly by 50% in the TSD/ischemia compared to nSD group (p<0.02). Removal of sleep rebound by allowing TSD-rats sleep for 24h before ischemia eliminated the reduction in the infarct size. CONCLUSION PRESTROKE: Sleep deprivation results in sleep rebound and reduces brain damage. Sleep rebound may be causally related to the neuroprotection.

Prodromal Transient Ischemic Attack or Minor Stroke and Outcome in Basilar Artery Occlusion

BACKGROUND The presence of prodromal transient ischemic attacks (TIAs) has been associated with a favorable outcome in anterior circulation stroke. We aimed to determine the association between prodromal TIAs or minor stroke and outcomes at 1 month, in the Basilar Artery International Cooperation Study, a registry of patients presenting with an acute symptomatic and radiologically confirmed basilar artery occlusion. METHODS A total of 619 patients were enrolled in the registry. Information on prodromal TIAs was available for 517 patients and on prodromal stroke for 487 patients. We calculated risk ratios and corresponding 95% confidence intervals (CIs) for poor clinical outcome (modified Rankin Scale score ≥4) according to the variables of interest. RESULTS Prodromal minor stroke was associated with poor outcome (crude risk ratio [cRR], 1.26; 95% CI, 1.12-1.42), but TIAs were not (cRR, .93; 95% CI, .79-1.09). These associations remained essentially the same after adjustment for confounding variables. CONCLUSIONS Prodromal minor stroke was associated with an unfavorable outcome in patients with basilar artery occlusion, whereas prodromal TIA was not.

Is ultrasound perfusion imaging capable of detecting mismatch? A proof-of-concept study in acute stroke patients.

In this study, we compared contrast-enhanced ultrasound perfusion imaging with magnetic resonance perfusion-weighted imaging or perfusion computed tomography for detecting normo-, hypo-, and nonperfused brain areas in acute middle cerebral artery stroke. We performed high mechanical index contrast-enhanced ultrasound perfusion imaging in 30 patients. Time-to-peak intensity of 10 ischemic regions of interests was compared to four standardized nonischemic regions of interests of the same patient. A time-to-peak >3 s (ultrasound perfusion imaging) or >4 s (perfusion computed tomography and magnetic resonance perfusion) defined hypoperfusion. In 16 patients, 98 of 160 ultrasound perfusion imaging regions of interests of the ischemic hemisphere were classified as normal, and 52 as hypoperfused or nonperfused. Ten regions of interests were excluded due to artifacts. There was a significant correlation of the ultrasound perfusion imaging and magnetic resonance perfusion or perfusion computed tomography (Pearson`s chi-squared test 79.119, p < 0.001) (OR 0.1065, 95% CI 0.06-0.18). No perfusion in ultrasound perfusion imaging (18 regions of interests) correlated highly with diffusion restriction on magnetic resonance imaging (Pearson's chi-squared test 42.307, p < 0.001). Analysis of receiver operating characteristics proved a high sensitivity of ultrasound perfusion imaging in the diagnosis of hypoperfused area under the curve, (AUC = 0.917; p < 0.001) and nonperfused (AUC = 0.830; p < 0.001) tissue in comparison with perfusion computed tomography and magnetic resonance perfusion. We present a proof of concept in determining normo-, hypo-, and nonperfused tissue in acute stroke by advanced contrast-enhanced ultrasound perfusion imaging.

Advancing nursing practice: The role of the nurse practitioner in an acute stroke program

The Foothills Medical Centre in Calgary, AB, Canada, is a tertiarycare referral center for southern Alberta and southeastern British Columbia. The Calgary Stroke Program, which serves a population of 1.5 million people and a geographic territory of more than 114,233 square kilometers (44,622 square miles), annually offers acute and follow-up care to more than 1,000 people with stroke. Leading the team of healthcare professionals dedicated to providing excellence in stroke patient care is a stroke nurse practitioner (SNP). The nurse practitioner role in Canada, as in many healthcare settings, was initially developed in response to cutbacks in medical residency programs and increasing acuity levels of hospitalized patients (Irvine et al., 2000). This article describes the development of the SNP role and its impact on system and process changes and patient care and outcomes in an acute stroke program in the Calgary Health Region.

Canadian Stroke Best Practice Recommendations: Mood, Cognition and Fatigue Following Stroke practice guidelines, update 2015

Every year, approximately 62 000 people with stroke and transient ischemic attack are treated in Canadian hospitals, and the evidence suggests one-third or more will experience vascular-cognitive impairment, and/or intractable fatigue, either alone or in combination. The 2015 update of the Canadian Stroke Best Practice Recommendations: Mood, Cognition and Fatigue Module guideline is a comprehensive summary of current evidence-based recommendations for clinicians in a range of settings, who provide care to patients following stroke. The three consequences of stroke that are the focus of the this guideline (poststroke depression, vascular cognitive impairment, and fatigue) have high incidence rates and significant impact on the lives of people who have had a stroke, impede recovery, and result in worse long-term outcomes. Significant practice variations and gaps in the research evidence have been reported for initial screening and in-depth assessment of stroke patients for these conditions. Also of concern, an increased number of family members and informal caregivers may also experience depressive symptoms in the poststroke recovery phase which further impact patient recovery. These factors emphasize the need for a system of care that ensures screening occurs as a standard and consistent component of clinical practice across settings as stroke patients transition from acute care to active rehabilitation and reintegration into their community. Additionally, building system capacity to ensure access to appropriate specialists for treatment and ongoing management of stroke survivors with these conditions is another great challenge.

Higher brain neurons succumb to acute stroke-like insult while lower brain neurons strongly resist

Pyramidal neurons (PyNs) in ‘higher’ brain are highly susceptible to acute stroke injury yet ‘lower’ brain regions better survive global ischemia, presumably because of better residual blood flow. Here we show that projection neurons in ‘lower’ brain regions of hypothalamus and brainstem intrinsically resist acute stroke-like injury independent of blood flow in the brain slice. In contrast `higher` projection neurons in neocortex, hippocampus, striatum and thalamus are highly susceptible. In live brain slices from rat deprived of oxygen and glucose (OGD), we imaged anoxic depolarization (AD) as it propagates through these regions. AD, the initial electrophysiological event of stroke, is a depolarizing front that drains residual energy in compromised gray matter. The extent of AD reliably determines ensuing damage in higher brain, but using whole-cell recordings we found that all CNS neurons do not generate a robust AD. Higher neurons generate strong AD and show no functional recovery in contrast to neurons in hypothalamus and brainstem that generate a weak and gradual AD. Most dramatically, lower neurons recover their membrane potential, input resistance and spike amplitude when oxygen and glucose is restored, while higher neurons do not. Following OGD, new recordings could be acquired in all lower (but not higher) brain regions, with some neurons even withstanding multiple OGD exposure. Two-photon laser scanning microscopy confirmed neuroprotection in lower, but not higher gray matter. Specifically pyramidal neurons swell and lose their dendritic spines post-OGD, whereas neurons in hypothalamus and brainstem display no such injury. Exposure to the Na+/K+ ATPase inhibitor ouabain (100 μM), induces depolarization similar to OGD in all cell types tested. Moreover, elevated [K+]o evokes spreading depression (SD), a milder version of AD, in higher brain but not hypothalamus or brainstem so weak AD correlates with the inability to generate SD. In summary, overriding the Na+/K+ pump using OGD, ouabain or elevated [K+]o evokes steep and robust depolarization of higher gray matter. We show that this important regional difference can be largely accounted for by the intrinsic properties of the resident neurons and that Na+/K+ ATPase pump efficiency is a major determining factor generating strong or weak spreading depolarizations.

Ischemic preconditioning before lower limb ischemia-reperfusion protects against acute lung injury

Objective: Prolonged limb ischemia followed by reperfusion (I/R) is associated with a systemic inflammatory response syndrome and remote acute lung injury. Ischemic preconditioning (IPC), achieved with repeated brief periods of I/R before the prolonged ischemic period, has been shown to protect skeletal muscle against ischemic injury. The aim of this study was to ascertain whether IPC of the limb before I/R injury also attenuates systemic inflammation and acute lung injury in a fully resuscitated porcine model of hind limb I/R. Methods: This prospective, randomized, controlled, experimental animal study was performed in a university-based animal research facility with 18 male Landrace pigs that weighed from 30 to 35 kg. Anesthetized ventilated swine were randomized (n = 6 per group) to three groups: sham-operated control group, I/R group (2 hours of bilateral hind limb ischemia and 2.5 hours of reperfusion), and IPC group (three cycles of 5 minutes of ischemia/5 minutes of reperfusion immediately preceding I/R). Plasma was separated and stored at -70° C for later determination of plasma tumor necrosis factor-a and interleukin-6 with bioassay as markers of systemic inflammation. Circulating phagocytic cell priming was assessed with a whole blood chemiluminescence assay. Lung tissue wet-to-dry weight ratio and myeloperoxidase concentration were markers of edema and neutrophil sequestration, respectively. The alveolar-arterial oxygen gradient and pulmonary artery pressure were indices of lung function. Results: In a porcine model, bilateral hind limb (I/R) injury significantly increased plasma interleukin-6 concentrations, circulating phagocytic cell priming, and pulmonary leukosequestration, edema, and impaired gas exchange. Conversely, pigs treated with IPC before the onset of the ischemic period had significantly reduced interleukin-6 levels, circulating phagocytic cell priming, and experienced significantly less pulmonary edema, leukosequestration, and respiratory failure. Conclusion: Lower limb IPC protects against systemic inflammation and acute lung injury in lower limb I/R injury.