Angiologia

# Sangramentos nasais: conceitos atuais em epistaxe

Postado em Atualizado em

 

Resultado de imagem para epistaxis

Dr. Gordon H. Sun

Pequeno sangramento nasal intermitente
Uma estudante de pós-doutorado de 28 anos deu entrada em um pronto-socorro com sangramento leve nas duas narinas, de forma intermitente, nas últimas duas semanas.
Ela negou ter sofrido traumatismo craniano antecedente ou doença respiratória superior. Ela não teve congestão nasal, coriza, problemas dentários ou dor e pressão nasofaciais, nem qualquer sangramento na parte de trás da garganta. Ela negou ter sofrido contusão ou menorragia. Além disso, ela negou ter sofrido déficits visuais ou otológicos.
O histórico médico e familiar da paciente foi negativo para distúrbios hemorrágicos. Ela não relatou qualquer uso de medicação ou alergias a medicamentos, era não fumante e não consumia bebida alcoólica. Ela não fez viagens recentes e viveu na mesma casa por muitos anos.
A paciente estava cooperativa, alerta e sem sofrimento aparente no exame. Os sinais vitais estavam dentro dos limites normais. Os exames oculares e otoscópicos não foram dignos de nota. Não foi evidenciada dor facial, inchaço ou fraqueza. A rinoscopia anterior demonstrou abrasões recentes no septo nasal anterior bilateralmente, mas sem sangramento ou coágulos ativos. O exame intraoral demonstrou boa dentição, nenhuma inflamação ou edema faríngeo, e nenhuma drenagem ou hemorragia da faringe posterior. O pescoço estava plano e flexível, com amplitude de movimento total e sem massas palpáveis.

Qual das seguintes é a causa mais provável de epistaxe
Trauma digital (rinotilexomania)
Corpo estranho nasal
Doença de von Willebrand
Perfuração septal

Trauma digital (rinotilexomania)
77%
Corpo estranho nasal
1%
Doença de von Willebrand
13%
Perfuração septal
9%

Epistaxe
A epistaxe (hemorragia nasal) tem uma prevalência estimada ao longo da vida de 60%, e cerca de 6% dos pacientes afetados procuram tratamento médico.[1] A incidência da epistaxe é bimodal, atingindo o pico em idades inferiores a 10 anos e superiores a 50 anos, e parece ser mais comum nos indivíduos do sexo masculino.[2]
As quatro opções acima compreendem apenas algumas das muitas causas locais e sistêmicas da epistaxe. No entanto, o trauma digital é considerado a etiologia mais comum da epistaxe, resultando no geral em abrasões e sangramento do septo anterior.[3]
Os corpos estranhos nasais são substancialmente mais comuns em crianças pequenas[4,5], mas também podem ser observados em adultos, em particular entre pessoas com atraso de desenvolvimento ou com doença psiquiátrica grave.[6,7] Um corpo estranho nasal normalmente apresenta coriza unilateral fétida e/ou epistaxe.
A doença de von Willebrand é a coagulopatia hereditária mais comum, com uma prevalência de 0,6% -1,3%.[8] Esta condição é no geral apresentada após um pequeno trauma nas superfícies mucosas (por exemplo, após procedimentos dentários).
A perfuração septal pode causar congestão nasal, sons de “assovio” do nariz, esmagamento e drenagem, e epistaxe periódica. As perfurações septais podem ser causadas por uma variedade de fatores, incluindo o uso de esteroides intranasais, uso de drogas ilícitas (por exemplo, cocaína) e várias condições autoimunes, como a granulomatose de Wegener[9,10]
Sangramentos nasais recorrentes e imprevisíveis
Uma gerente administrativa de 35 anos, em uma cidade de médio porte no sudoeste desértico, apresentou-se à sua enfermeira clínica de assistência básica com hemorragias nasais leves e esporádicas nos últimos dois anos.
Os sangramentos nasais geralmente não duravam mais de 10 minutos depois de aplicar pressão direta ao nariz, mas eram imprevisíveis e ocasionalmente perturbavam os colegas de trabalho quando ocorriam durante uma reunião. O nariz dela coçava às vezes mas, fora isso, ela negava apresentar congestão, dor e pressão nasofaciais, coriza e disosmia. A paciente não relatou problemas nos olhos ou nos ouvidos, dificuldades para respirar ou engolir, ou sintomas constitucionais.
O histórico médico e familiar da paciente não tinha qualquer coisa a ser notada. Ela não tomou qualquer medicamento nem tinha alergias a medicamentos. Ela fumava cigarros ocasionalmente, mas não fazia uso de bebidas alcoólicas.
A enfermeira clínica realizou um exame físico completo, que demonstrou sinais vitais normais e nenhum resultado positivo além de alguns pequenos coágulos de sangue nas narinas. Os coágulos foram aspirados com cuidado, revelando apenas alguma inflamação e irritação do septo nasal anteriormente. Não foi observado qualquer sangramento adicional.

Quais das seguintes medidas de autogestão podem ser úteis para a paciente na redução de episódios futuros de epistaxe?
Aplicação de vaselina levemente aos vestíbulos nasais
Obtenção de um umidificador de ambiente
Evitar fontes de inflamação e trauma local.
Estratégias para evitar o sangramento nasal
A maioria dos sangramentos nasais é leve e se resolve espontaneamente. Mais de 90% dos sangramentos nasais ocorrem dentro da área de Kiesselbach, uma região do septo anterior com vasculatura particularmente rica[1] (Figura). Apertar a parte anterior do nariz de 10 a 15 minutos enquanto está sentado e inclinar-se para frente para evitar aspiração acidental ou deglutição de sangue geralmente é efetivo como tratamento inicial. Os pacientes devem evitar pressionar a pirâmide óssea do nariz, o que não exerce pressão sobre a área de Kiesselbach. O uso de um descongestionante tópico, como a oximetazolina, pode ser eficaz na interrupção de um sangramento nasal leve.[11]

Várias estratégias conservadoras estão disponíveis para reduzir o risco de recorrência local. A hidratação das narinas previne a fissuração e o sangramento das superfícies mucosas, e promove a cicatrização do tecido friável. A hidratação pode ser realizada aplicando uma camada fina de vaselina ou pomada antibiótica sobre a mucosa do septo nasal anterior e do vestíbulo nasal, pulverizando as narinas com solução salina ou um emoliente solúvel em água ou o uso de máquinas umidificadoras domésticas. Finalmente, evitar o trauma nasal e a inflamação (por exemplo, parando de fumar) pode prevenir a ruptura mecânica da mucosa e o sangramento resultante dela.[1,3,12,13,14,15]
Hemorragia na clínica
Uma estudante de odontologia de 24 anos apresentou-se ao médico na clínica de saúde da universidade com episódios repetidos de epistaxe, ocorrendo várias vezes ao longo da semana anterior.
Os sangramentos nasais têm sido frequentes e graves o suficiente para prejudicar a capacidade de atender aos pacientes na clínica de ensino odontológico. Ela não relatou outros sintomas de cabeça e pescoço. O histórico médico e familiar foi benigno. Ela estava tomando uma pílula contraceptiva oral, mas nenhum outro medicamento. Ela negou apresentar alergias médicas ou ambientais. Ela não fumava e não bebia. A análise dos exames de sangue obtidos em um check-up realizado há 2 meses mostrou um nível de hemoglobina de 14,1 g/dL.
No exame, a paciente estava alerta, cooperativa e sem sofrimento agudo. Todos os sinais vitais pareciam estar normais. A paciente teve exames oculares, otoscópicos e intraorais normais. Nenhum sangue foi visto na faringe posterior. No entanto, a rinoscopia anterior demonstrou vários coágulos grandes nas abóbadas nasais. A médica usou cuidadosamente fórceps de baioneta e um espéculo nasal para remover os coágulos, o que resultou em gotejamento de sangue leve, mas constante, das duas narinas. Ao limpar o sangue fresco, a médica acreditou poder ver a fonte do sangramento em ambos lados do septo nasal.

Interrupção do sangramento
A cauterização é geralmente considerada o melhor passo seguinte à pressão direta e se os vasoconstritores tópicos não conseguirem parar a epistaxe anterior.[1,2,3,6] A cauterização química com nitrato de prata (AgNO3) é de execução relativamente fácil e tem baixo custo; é, portanto, uma técnica frequentemente usada por não otorrinolaringologistas.[17] O nitrato de prata é o melhor para pequenos sangramentos nasais, porque um fluxo sanguíneo mais extenso eliminará o nitrato de prata antes que ele possa induzir a coagulação. A cauterização química tem uma taxa de sucesso inicial de 80% ou mais.[18,19,20] A oximetazolina demonstrou algum benefício adicional na interrupção dos sangramentos nasais quando pareada com cauterizador de AgNO3.[11]
A eletrocauterização é, em geral, reservada para casos mais graves de epistaxe anterior. Deve-se ter cuidado para evitar a eletrocauterização excessiva, que pode danificar facilmente o tecido saudável circundante. Para os dois tipos de cauterização é preferível realizar o procedimento em um lado do septo de cada vez, se possível, aguardando de quatro a seis semanas entre os tratamentos, para reduzir o risco de perfuração septal.[1,21] A anestesia tópica pode reduzir o desconforto associado à cauterização, em particular para o tratamento elétrico. Em geral, as técnicas de cauterização são melhor toleradas do que o tamponamento e a cirurgia.[22]
O tamponamento nasal anterior normalmente é considerado o procedimento seguinte a ser realizado caso a cauterização não interrompa a epistaxe. O tamponamento inclui produtos não absorvíveis e absorvíveis. As intervenções não absorvíveis incluem tampões infláveis, gaze de fita revestida com vaselina gelada, esponjas de álcool polivinílico e outros. Todos eles podem ser desconfortáveis para os pacientes, pois a colocação e a remoção podem ser difíceis e, comumente, eles são deixados no local por até cinco dias para confirmar a formação do coágulo. Além disso, esses pacientes necessitam de tratamento antibiótico oral para prevenir a síndrome do choque tóxico.[1,2,3] Outros efeitos adversos conhecidos do tamponamento nasal incluem hematomas septais e abscessos, rinossinusite, perfuração septal, necrose e até síncope.[2]
Os produtos absorvíveis, como a espuma de colágeno, o revestimento de celulose oxidado, ou a gelatina-trombina, tendem a ser melhor tolerados pelos pacientes devido à facilidade de administração e à falta de necessidade de remover o tamponamento em uma data posterior. Vários estudos prospectivos demonstraram que o uso de gelatina-trombina resultou em taxas de controle inicial para a epistaxe anterior acima de 80%.[23,24,25] Esses produtos tendem a ser mais caros do que o tamponamento não degradável, mas esses custos podem ser compensados pelo custo das visitas de acompanhamento e da remoção do tamponamento.[1]
O tamponamento nasal posterior e a ligadura da artéria esfenopalatina são técnicas substancialmente mais invasivas, cada uma associada a várias complicações potenciais graves, e reservada para casos muito graves de epistaxe posterior. Ambos são geralmente realizados por otorrinolaringologistas ou outros especialistas treinados.
Epistaxe que requer hospitalização
Um homem de 45 anos apresentou-se ao pronto-socorro local com sangramento contínuo das duas narinas, além de estar cuspindo sangue durante a última hora e meia.
Ele estava assistindo a um jogo de beisebol e terminando a terceira lata de cerveja quando o sangramento começou. O paciente relatou uma leve dor de cabeça ao início do sangramento. Ele negou ter sentido náuseas, tonturas, alterações de visão, falta de ar ou dor no peito. O histórico médico foi significativo para hipertensão, hiperlipidemia e diabetes tipo 2, e o histórico cirúrgico incluiu uma tonsilectomia e uma apendicectomia durante a infância. O paciente estava tomando hidroclorotiazida, lisinopril e aspirina. Ele negou ter alergias a medicamentos. Ele relatou beber de quatro a seis latas de cerveja diariamente, e fumar um maço de cigarros por dia por cerca de 30 anos.
No exame, o paciente estava ligeiramente ansioso e segurava um punhado de tecidos sangrentos sobre o nariz; fora isso, totalmente alerta e cooperativo com o exame. Ele estava sem febre e sua frequência cardíaca era de 85 batimentos/minuto, a frequência respiratória era de 16 respirações/min, e a pressão arterial era de 196/92 mm Hg. Sua saturação de oxigênio era de 97% no ar ambiente. O exame de cabeça e pescoço foi significativo para sangramentos intensos de ambas narinas, que persistiram apesar da sucção, bem como traços de sangue na parede orofaríngea posterior. Os sons do pulmão estavam limpos e o ritmo cardíaco estava regular. O exame do nervo craniano estava normal.
O médico irrigou de forma suave as passagens nasais do paciente com solução salina quente e pediu que ele gargarejasse água morna. O paciente então voltou a fazer pressão sobre as narinas. Uma enfermeira ajudou no fornecimento de ar umidificado com oxigênio suplementar por máscara facial. O médico então pediu exames de sangue, eletrocardiografia e TC da cabeça, e solicitou consulta tanto de um otorrinolaringologista quanto de um intensivista. O otorrinolaringologista avaliou o paciente e, com a assistência da enfermeira, tampou a nasofaringe com um cateter Foley 14-Fr e as narinas com gaze impregnada de vaselina, o que pareceu interromper o sangramento temporariamente. O intensivista então preparou-se para internar o paciente para tratamento médico e possível embolização arterial em conjunto com o radiologista intervencionista.

Fatores de risco para hospitalização devido à epistaxe
Demograficamente, os homens e os adultos mais velhos (idade > 60 anos) são mais propensos do que as mulheres e as pessoas mais jovens a serem internados devido à epistaxe.[26,27,28] Numerosas condições associadas à epistaxe como diagnóstico primário de admissão são conhecidas. A hipertensão e a coagulopatia são consideradas fatores de risco clássicos para a admissão hospitalar devido à epistaxe, embora não esteja claro se a hipertensão em si, ou as comorbidades relacionadas que requerem terapia antitrombótica, são a causa dessa associação.[29,30] Outras condições cardiovasculares, como fibrilação atrial, doença vascular periférica e doença cardíaca valvar, são prevalentes em pacientes admitidos devido à epistaxe. Abuso de álcool, doença hepática, insuficiência renal, artrite reumatoide, hipotireoidismo e linfoma são outros fatores de risco relatados.[28]
O custo das internações devido à epistaxe é bastante substancial. Uma análise da US National Inpatient Sample de 2008-2012 revelou que o custo médio de hospitalização para 16.828 pacientes admitidos devido à epistaxe foi de US$ 6.925 ou uma estimativa ponderada de mais de US$ 106 milhões por ano.[27] O período médio de permanência dos pacientes hospitalizados com diagnóstico primário de epistaxe é de cerca de três dias.[26,27,31] O abuso de álcool, a doença renal e a doença sinonasal em pacientes admitidos para epistaxe foram associados com custos significativamente maiores e maior tempo de permanência.[27]

MEDSCAPE

Anúncios

#No Signal for #Amputation With #Empagliflozin in #EMPA-REG

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Lisa Nainggolan

A post hoc analysis of the landmark EMPA-REG cardiovascular outcomes trial with the sodium glucose cotransporter 2 (SGLT2) empagliflozin (Jardiance, Boehringer Ingelheim) in patients with type 2 diabetes and established cardiovascular disease has found no evidence of an increased risk of lower-limb amputation with the drug vs placebo.

The study, led by Silvio Inzucchi, MD, of Yale University, New Haven, Connecticut, has been published in Diabetes Care.

Concern about a possible association of SGLT2 inhibitors and increased risk of lower-limb amputation, primarily of the toe, first arose from interim data from a trial with a different agent in the class, canagliflozin (Invokana, Janssen Pharmaceuticals), from the Canagliflozin Cardiovascular Assessment Study (CANVAS) last year, which led to a warning on the labels of all SGLT2 inhibitors by the European Medicines Agency, as it determined that it wasn’t possible to exclude other SGLT2 inhibitors from the alert.

In contrast, the US Food and Drug Administration has mandated a boxed warning relating to the amputation risk only for canagliflozin specifically.

In the full presentation of the CANVAS data, at the ADA meeting in June this year, the results confirmed an overall doubling in the risk for amputations between those taking canagliflozin vs placebo (6.3 vs 3.4 cases per 1000 patient-years; hazard ratio [HR], 1.97).

But overall, canagliflozin still reduced cardiovascular events by 14% and cut the rate of renal decline by 40% in this large outcomes trial, and the investigators maintained that, even with the amputation signal, the benefit/risk profile of canagliflozin was favorable.

Yet doctors are clearly still concerned about this and whether it represents a class effect of SGLT2 inhibitors or is specific to canagliflozin.

Commenting on the topic in a recent perspective for Medscape Medical News, Harpreet Bajaj of Mount Sinai Hospital, University of Toronto, Ontario, said: “To reassure us of the benefit/harm balance with canagliflozin, we clinicians need more data-mining from CANVAS and additional long-term randomized controlled trials.”

Inherent Limitations in Manually Identifying Lower-Limb Amputations

EMPA-REG OUTCOMES randomized 7020 patients with type 2 diabetes and established cardiovascular disease to receive placebo or empagliflozin (10 mg/day or 25 mg/day) plus standard care for 3.1 years.

The results were the first to show, in 2015, that a diabetes drug offered cardiovascular benefit beyond mere glucose lowering, with empagliflozin producing a 38% relative risk reduction in cardiovascular mortality and a 32% risk reduction in all-cause mortality. The following year, the FDA approved the drug for the new indication of improving survival in adults with type 2 diabetes and cardiovascular disease.

When EMPA-REG was conducted, there was no inkling of any association of this SGLT2 inhibitor drug class with amputation, so these were not systematically reported.

And at the time of the presentation of the CANVAS data, Dr Inzucchi told Medscape Medical News that there was no signal for amputation in EMPA-REG with empagliflozin vs placebo.

Now he and his colleagues have published the details of their post hoc assessment of EMPA-REG for amputation.

They note in their new paper that “any hospital admission during EMPA-REG was to be reported as a serious adverse event [SAE],” with investigators asked to provide a detailed narrative in each case.

So they went back and identified lower-limb amputations via a systematic search of these SAEs, as well as looking for them in a number of other ways.

“All cases identified were medically reviewed to confirm a lower-limb–amputation event,” they note.

Overall, lower-limb amputations were identified in 131 patients: 88 patients treated with empagliflozin (1.9%) and 43 (1.8%) treated with placebo.

The incidence rate was 6.5 per 1000 patient-years in both groups.

In the analyses of time to first event, the risk of lower-limb amputation was similar between empagliflozin pooled and placebo (HR, 1.00).

And results were similar with empagliflozin 10 mg (HR, 0.96) and empagliflozin 25 mg (HR 1.04).

The findings were also consistent across subgroups by established amputation risk (such as history of smoking, diabetic foot, diabetic neuropathy, and peripheral artery disease).

“We acknowledge the inherent limitations of manually identifying lower-limb amputation and performing post hoc analyses. A dedicated case report form was not used in the EMPA-REG OUTCOME trial as there was no concern regarding an increased risk of amputation before or during the trial,” they explain.

Yet “we are confident that the reporting and systematic retrieval process employed were thorough. Empagliflozin was not associated with an increased risk of lower-limb amputation compared with placebo in EMPA-REG OUTCOME,” they reiterate.

EMPA-REG OUTCOME was funded by the Boehringer Ingelheim and Eli Lilly Alliance. Dr Inzucchi has consulted for Boehringer Ingelheim, AstraZeneca, Merck, Intarcia Therapeutics, Lexicon Pharmaceuticals, Janssen, Sanofi, Novo Nordisk, and vTv Therapeutics. Disclosures for the coauthors are listed in the paper.

Diabetes Care. Published online November 13, 2017. Article

# Coronary Calcium Helps Stratify 10-Year #Cardiac Risk in #Diabetes

Postado em

Coronary artery calcium (CAC) scores may be better at predicting the risk of a cardiovascular disease (CVD) event in patients with type 2 diabetes than traditional scores such as Framingham, even in those who’ve had diabetes for 10 years, researchers report[1].

This conclusion is based on a new analysis of participants in the Multi-Ethnic Study of Atherosclerosis (MESA) published online in JAMA Cardiology by Dr Shaista Malik (University of California, Irvine) and colleagues.

“When we consider how we want to treat a person with type 2 diabetes, how aggressive to be, most of the guidelines…consider having type 2 diabetes to be equivalent to having already had a heart attack,” Dr Malik told theheart.org | Medscape Cardiology.

However, the new findings indicate that people with diabetes or metabolic syndrome “are a rather heterogeneous group,” she stressed.

They suggest that “diabetes in particular may not be a coronary artery disease equivalent, and we should see whether a patient could benefit from additional screening such as a coronary calcium score to improve personalization of therapy.”

Asked for his thoughts, Dr Donald W Bowden (Wake Forest School of Medicine, Winston-Salem, NC), who was not involved in the study, told theheart.org | Medscape Cardiology that these new data add “to an extensive literature documenting the utility of CAC imaging to improve prediction and aid treatment of CVD in both people with and without diabetes.”

“It shows that inferences from shorter-term follow-up studies remain compelling over long periods,” he said in an email.

Moreover, this also demonstrates that “CAC reclassifies a significant percentage of [diabetes] patients,” he noted, pointing out that when CAC scores were compared with the Framingham risk or other scores, almost half the patients with diabetes were reclassified to a higher or lower CVD risk group.

Malik said that for patients with diabetes “the general thinking has been…they probably are going to have coronary calcium, so further risk stratification is not going to be more predictive. But what we’re showing is—even in those with diabetes—getting information on how calcified their coronary arteries are is helpful in distinguishing those at lower risk from those at higher risk.”

Low CAC Score Can Be Considered ‘Warranty’ For 10 Years in Diabetes

Malik and colleagues examined data from the MESA cohort of 6814 men and women aged 45–84 years without known CVD. Participants were ethnically diverse—White (38.5%), African American (27.5%), Hispanic (22%), and Chinese (12%)—and were enrolled in six US communities from July 2000 through August 2002.

The patients had a cardiac-gated electron-beam multidetector CT scan to determine CAC, and they were divided into four groups based on CAC scores from low to high: 0, 1–99, 100–399, and ≥400.

A total of 6751 participants with complete data were included in the current analysis. They had a mean age of 62 years and 47% were male.

Diabetes was defined as a fasting serum glucose ≥126 mg/dL.

Metabolic syndrome was defined as having at least three of the following five conditions: waist circumference ≥102 cm in men or ≥88 cm in women; triglycerides ≥150 mg/dL; HDL-cholesterol <40 mg/dL in men or <50 mg/dL in women; blood pressure ≥130/85 mm Hg or use of antihypertensive medication; and fasting serum glucose 100–126 mg/dL.

At baseline, 13.0% of participants had diabetes, 26% had metabolic syndrome, and 61% had neither.

The primary end point was an incident CHD event (myocardial infarction, resuscitated cardiac arrest, or coronary heart disease [CHD] death). The secondary end point was an incident atherosclerotic CVD event (CHD event and fatal or nonfatal stroke).

During a mean follow-up of 11 years, among the 881 participants with diabetes there were 84 incident CHD events and 135 atherosclerotic CVD events. Among the 1738 participants with metabolic syndrome, there were 115 CHD events and 175 atherosclerotic CVD events.

The 4132 participants with neither condition had relatively fewer CHD (157) and atherosclerotic CVD events (250).

More than a third (37%) of patients with diabetes, 45% of those with metabolic syndrome, and 55% of the other patients had a baseline CAC score of 0, and this was associated with a low 10-year risk of CHD events.

Among patients without evidence of CAC at baseline, the 10-year CHD event rates were just 2.3% in patients with metabolic syndrome and 3.7% in patients with diabetes.

And this was independent of diabetes duration, insulin use, or glycemic control, even after adjusting for multiple confounders.

“Thus, the ‘warranty period’ of a CAC score of 0 can be extended to 10 years in those with metabolic syndrome or diabetes,” according to the researchers.

More Study Needed to Understand Resilience, Guide Individualized Care

“Although diabetes is known to accelerate the aging process, future studies need to focus on the factors that provide resilience among patients with lack of subclinical disease despite long-standing diabetes,” say Malik and colleagues.

“Maybe we do need to be aggressive in hyperglycemia management, or less aggressive in lipid management,” and further research may show that clinicians don’t need to put all patients with diabetes on a high-intensity statin, rather “they could get away with a moderate-intensity statin,” Malik suggested.

In addition, more work is needed to “examine whether newer antidiabetic medications, such as sodium glucose cotransporter 2 inhibitors or glucagonlike peptide 1 receptor agonists, that benefit patients with known [atherosclerotic CVD] could be considered for those at increased risk based on extent of CAC or other measures of subclinical atherosclerosis,” the group writes.

“Prospective studies that focus treatment intensity on objective measures of subclinical atherosclerosis may improve personalization of preventive therapies.”

The authors have reported no relevant financial disclosures.

#Pacientes con #penumbra posterior a #accidente cerebrovascular se benefician de # trombectomía tardía

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La trombectomía en pacientes con accidente cerebrovascular isquémico agudo todavía puede ser benéfica después de 6 horas de iniciados los síntomas en pacientes que tienen tejido cerebral salvable, identificado en los estudios por imágenes como un infarto con un núcleo pequeño, de acuerdo con los resultados del estudio DAWN.[1,2]

El estudio fue publicado en versión electrónica en The New England Journal of Medicine para coincidir con su presentación en el Congreso Anual de la Society of Vascular and Interventional Neurology (SVIN) 2017, en Boston, Estados Unidos. También fue presentado previamente en la 3rd. European Stroke Organisation Conference.

Los resultados demostraron que los desenlaces de discapacidad fueron mejores con la trombectomía más el tratamiento médico estándar que con solo el tratamiento médico estándar en pacientes con accidente cerebrovascular agudo que fueron tratados 6 a 24 horas después de haberse documentado que estaban bien y que tenían una discordancia entre la gravedad del déficit clínico y el volumen del infarto.

“Nuestro principal mensaje es que la selección del tratamiento endovascular en el accidente cerebrovascular isquémico agudo no debe basarse solo en el tiempo transcurrido. También es necesario considerar los criterios fisiológicos”, dijo a Medscape Noticias Médicas el Dr. Tudor Jovin, autor principal, del University of Pittsburgh Medical Center Stroke Institute, en Pensilvania, Estados Unidos.

El estudio DAWN reclutó a pacientes que acudieron después de 6 horas y en los que se identificó tejido cerebral salvable con base en la “discordancia entre los datos clínicos y el núcleo del infarto”, es decir, los pacientes que tenían un déficit clínico desproporcionado a lo esperado por las imágenes.

“El principio de la discordancia es simple”, explicó el Dr. Jovin. “Cuando se obstruye un vaso en el cerebro, una pequeña zona del cerebro muere inicialmente. Esto es lo que llamamos el núcleo. Pero se pone en riesgo una zona más grande irrigada por este vaso. A esta se le designa como la penumbra. En caso de que no haya tratamiento (reperfusión), la zona de penumbra también muere, pero puede sobrevivir durante varias horas si la circulación colateral es satisfactoria”.

“Para nuestro estudio definimos la discordancia como los pacientes con síntomas de accidente cerebrovascular grave que señalaban una considerable zona de tejido cerebral que no estaba funcionando adecuadamente, pero que en las imágenes resultaron con solo un núcleo pequeño de tejido que en realidad había muerto”, añadió el Dr. Jovin.

“En las primeras etapas, casi todos tienen discordancia, pero en la mayoría de los pacientes la zona completa de tejido ha muerto hacia las seis horas; estos son los que avanzan rápidamente. Sin embargo, algunos pacientes (los que evolucionan lentamente) todavía tienen tejido cerebral viable en la zona vulnerable muchas horas después de haber sufrido un infarto cerebrovascular de gran tamaño a juzgar por los síntomas”.

El Dr. Raul Nogueira, primer autor, del Marcus Stroke & Neuroscience Center y el Grady Memorial Hospital, en Atlanta, Estados Unidos, comentó a Medscape Noticias Médicas: “Todo es cuestión de la fisiología: qué tanto puede el flujo sanguíneo colateral compensar la isquemia causada por el coágulo en el vaso principal. El flujo colateral satisfactorio permite ganar tiempo para el tratamiento”.

“Pese a los periodos más prolongados hasta la presentación, la magnitud de efecto del tratamiento observada en el estudio DAWN es la más alta que la de cualquier estudio de accidente cerebrovascular realizado hasta la fecha”, añadió. “Esto indica que la discordancia entre las manifestaciones clínicas y el núcleo del infarto es un factor decisivo para pronosticar la respuesta al tratamiento, independientemente del tiempo transcurrido hasta la presentación. Por consiguiente, el tiempo por sí solo no debería ser un factor para descalificar una trombectomía”.

Estos resultados aumentarán el número de personas con accidente cerebrovascular agudo candidatos para trombectomía. Los investigadores señalan que aproximadamente un tercio de los pacientes con obstrucción de un vaso cerebral anterior proximal que se presentan en las primeras 6 a 24 horas después del inicio del accidente cerebrovascular pueden cumplir los criterios de elegibilidad basados en los estudios por imágenes que se utilizaron en este estudio.

La población reclutada en el estudio incluyó a pacientes con accidentes cerebrovasculares del despertar (en los que se descubrió un accidente cerebrovascular producido durante su sueño, de manera que no se conoce el tiempo de inicio real).

“Los accidentes cerebrovasculares del despertar son muy frecuentes (contribuyen con casi 25% a los accidentes cerebrovasculares) y estos pacientes no han sido elegibles para trombectomía con base en los criterios de tiempo, pero nuestros resultados abren la posibilidad de este tratamiento para este grupo, si resulta que tienen las características fisiológicas correctas”, comentó el Dr. Nogueira.

Los 206 pacientes del estudio DAWN se presentaron con obstrucción de la arteria carótida interna intracraneal o la arteria cerebral media proximal, se contaba con el antecedente de estar clínicamente bien por lo menos 6 a 24 horas antes y al ingreso presentar un déficit clínico considerable (puntuaciones de 10 o más en la Escala de Accidente Cerebrovascular de NIH Normalizada). Los investigadores utilizaron imágenes de perfusión mediante resonancia magnética y tomografía computarizada para identificar a los pacientes que tenían un núcleo pequeño, y los criterios de inclusión basados en el tamaño del núcleo variaron con la edad. Fueron asignados de manera aleatoria a trombectomía más tratamiento estándar (el grupo con trombectomía) o a tratamiento estándar solo.

A los 31 meses, el reclutamiento en el estudio se suspendió a causa de los resultados de un análisis provisional especificado de antemano.

El estudio tuvo dos criterios de valoración principales utilizando la escala de Rankin modificada, ponderada en cuanto a utilidad, que fluctúa desde 0 (muerte) hasta 10 (ningún síntoma o discapacidad) y la tasa de independencia funcional (puntuaciones de 0, 1 o 2) en la escala de Rankin modificada más tradicional. Los dos criterios de valoración mostraron beneficios significativos para el grupo con trombectomía.

La puntuación media en la escala de Rankin modificada con utilidad ponderada a los 90 días fue 5,5 en el grupo con trombectomía, frente a 3,4 en el grupo de control, arrojando una diferencia ajustada (análisis bayesiano) de 2,0 puntos.
Y la tasa de independencia funcional a los 90 días fue 49% en el grupo con trombectomía frente a 13% en el grupo de control (diferencia ajustada: 33 puntos porcentuales).

Por cada 2 pacientes que se sometieron a trombectomía, un paciente adicional tuvo una mejor puntuación en cuanto a la discapacidad a los 90 días frente a los resultados en el grupo de control; por cada 2,8 pacientes que se sometieron a trombectomía, un paciente adicional tuvo independencia funcional a los 90 días.

Los investigadores señalan que la tasa de independencia funcional en el grupo con trombectomía en este estudio (49%) con una media de tiempo de tratamiento de 12 a 13 horas fue similar a la tasa comunicada en un análisis combinado de cinco estudios de trombectomía en el cual los pacientes se trataron dentro de las 6 horas (46%).

En contraste, la tasa de independencia funcional en el grupo de control en el presente estudio fue mucho más baja que en los estudios de pacientes previos (13% frente a 26%), lo cual, según los investigadores, puede deberse a los pacientes que recibieron tratamiento trombolítico en etapa más temprana.

“Incluimos a pacientes con síntomas iniciados 6 a 24 horas antes, y encontramos beneficio del tratamiento en toda la ventana de tiempo sin diferencia en el efecto del tratamiento”, dijo el Dr. Jovin.

Sin embargo, añadió que menos pacientes con los tiempos más tardíos habrían tenido discordancia y por tanto habrían reunido los requisitos para participar en el estudio. “Así que, desde luego, el tiempo transcurrido es lo más importante, pero una vez que se ha identificado al paciente y se ha determinado que tiene tejido cerebral salvable, tienen un beneficio similar independientemente del tiempo de presentación”.

“Consideramos que estos resultados serán muy relevantes para los países en vías de desarrollo donde los pacientes tienden a tardarse más en presentarse, pero estos países tienen menos probabilidades de contar con imagenología sofisticada, de manera que necesitamos encontrar formar más simples de medir el núcleo”, señaló. “Esto puede hacerse en una tomografía computarizada simple; esta simplemente podría ser lo suficientemente satisfactoria para hacer una estimación aceptable”.

El Dr. Nogueira hizo notar que los resultados de un estudio similar (DEFUSE-3) se presentarán a principios del próximo año.

“Sabemos que este estudio también ha demostrado un resultado positivo, y los resultados serán dados a conocer en la International Stroke Conference en enero. Los dos estudios se considerarán en conjunto para hacer recomendaciones sobre el tratamiento de los pacientes que acuden después de 6 horas”.

En un editorial que acompaña la publicación del estudio DAWN, el Dr. Werner Hacke, de la Heidelberg University, en Heidelberg, Alemania, dice que el estudio tiene “resultados extraordinariamente positivos”, pero advierte que solo una proporción limitada de los pacientes que acuden en etapa tardía cumplirán con todos los criterios para la realización de una trombectomía. Por consiguiente, “reducir el tiempo transcurrido desde el inicio del accidente cerebrovascular hasta el tratamiento sigue siendo fundamental y da lugar a los mejores resultados”.[3]

El estudio DAWN fue financiado por Stryker Neurovascular. El Dr. Jovin informa honorarios personales u otros apoyos de Silk Road Medical, Anconda Biomed, Route 92 Medical, Blockade Medical, FreeOx Biotech, Codman Neurovascular y Neuravi ajenos al estudio publicado. El Dr. Nogueira ha declarado no tener ningún conflicto de interés económico pertinente.

 

#How to Diagnose Aortic Dissection Without Breaking the Bank

Postado em

By Anton Helman | on November 13, 2017

Living Art Enterprises / Science Source

Living Art Enterprises / Science Source
It used to be said that missing the clinical diagnosis of aortic dissection was “the standard” as it is rare and often presents atypically. The diagnosis rate of aortic dissection changed with the landmark International Registry of Acute Aortic Dissection (IRAD) study in 2000, which deepened our understanding of the presentation.1 Nonetheless, aortic dissection remains difficult to diagnose, with one in six missed at the initial ED visit.

Herein lies the difficulty. Aortic dissection must be considered in all patients with chest, abdominal, or back pain; syncope; or stroke symptoms. Yet, we shouldn’t be working up every one of them, creating a resource utilization disaster. However, early, timely diagnosis is essential because each hour that passes from the onset of symptoms correlates with a 1 percent to 2 percent increase in mortality.

In this column, I’ll elucidate how to improve your diagnosis rate, without overimaging, by explaining five pain pearls, the concepts of “CP +1” and “1+ CP,” physical exam nuances, and how best to initially utilize tests.

The Five Pain Pearls of Aortic Dissection

Ask the following three things of all patients with torso pain:
What is the quality of pain? (The pain from aortic dissection is most commonly described as “sharp,” but the highest positive likelihood ratio [+LR] is for “tearing.”)
What was the pain intensity at onset? (It is abrupt in aortic dissection.)
What is the radiation of pain? (It is in the back and/or abdomen in aortic dissection.)
A 1998 study that reviewed a series of aortic dissection cases showed that for the 42 percent of physicians who asked about these three things, the diagnosis was suspected in 91 percent. When fewer than three questions were asked, dissection was suspected in only 49 percent.2

Think of aortic dissection as the subarachnoid hemorrhage of the torso. Just like a patient who presents with a new-onset, severe, abrupt headache should be suspected of having a subarachnoid hemorrhage, if a patient describes a truly abrupt onset of severe torso pain with maximal intensity at onset, think aortic dissection.
If you find yourself treating your chest pain patient with IV opioids to control severe colicky pain, think about aortic dissection.
Migrating pain has a +LR of 7.6.1 In addition to the old adage, “Pain above and below the diaphragm should heighten your suspicion for aortic dissection,” severe pain that progresses and moves in the same vector as the aorta significantly increases the likelihood of aortic dissection.
The pain can be intermittent as dissection of the aortic intima stops and starts. The combination of severe migrating and intermittent pain should raise the suspicion for aortic dissection.
Painless Aortic Dissection

While IRAD reported a painless aortic dissection rate of about 5 percent, a more recent study out of Japan reported that 17 percent of aortic dissection patients had no pain.3 These patients presented more frequently with a persistent disturbance of consciousness, syncope, or a focal neurological deficit. Cardiac tamponade was more frequent in the pain-free group as well.

The Concepts of “CP +1” and “1+ CP”

The intimal tear in the aorta can devascularize any organ from head to toe, including the brain, heart, kidneys, and spinal cord. Thus, 5 percent of dissections present as strokes, and these certainly are not the kind of stroke patients who should be receiving tPA! An objective focal neurologic deficit in the setting of acute, unexplained chest pain (CP) has +LR of 33 for aortic dissection, almost diagnostic. Some of the CP +1 phenomena to think about include torso pain, cerebrovascular accident, paralysis, hoarseness (recurrent laryngeal nerve), and limb ischemia.

These three coronal reconstructions from contrast enhanced CT angiograms of the chest show an extensive dissection of the thoracic aorta. This is a De Bakey type I or Standord A aortic dissection.

(click for larger image) These three coronal reconstructions from contrast enhanced CT angiograms of the chest show an extensive dissection of the thoracic aorta. This is a De Bakey type I or Standord A aortic dissection.
Source: Living Art Enterprises / Science Source
In addition to thinking of CP +1, it may help to think backwards in time (1+ CP) and ask patients who present with end-organ damage if they had torso pain prior to their symptoms of end organ damage. For example, ask patients who present with stroke symptoms if they had torso pain before the stroke symptoms.

Anyone under the age of 40 years who presents to the emergency department with unexplained torso pain should be asked if they have Marfan syndrome. In the IRAD analysis of those under 40 years, 50 percent of the aortic dissection patients had Marfan syndrome, representing 5 percent of all dissections.1

Look. The patient doesn’t always know they have Marfan syndrome, so you need to look for arachnodactyly (elongated fingers), pectus excavatum (sternal excavation), and lanky limbs.
Listen. A new aortic regurgitation murmur has a surprisingly high +LR of 5.
Feel. Feel for a pulse deficit, which has a +LR of 2.7, much higher than that of interarm blood pressure differences.
The patient’s blood pressure needs to be interpreted with caution and insight. Do not assume that the patient with a normal or low blood pressure does not have an aortic dissection. We know from the IRAD data that only about half of patients are hypertensive at initial presentation. Patients with aortic dissections that progress into the pericardium, resulting in cardiac tamponade, are often hypotensive. Patients with dissection who have a wide pulse pressure should be considered preterminal and usually require immediate surgery.

There is a lot more to chest radiograph interpretation for suspected aortic dissection than looking for a wide mediastinum. One-third of chest radiographs in aortic dissection are normal to the untrained eye, and a common pitfall is to assume that if the chest X-ray is normal, the patient does not have an aortic dissection. There are about a dozen X-ray findings associated with dissection, but two of them are especially important: loss of the aortic knob/aortopulmonary window and the calcium sign.

Look for a white line of calcium within the aortic knob, then measure the distance from there to the outer edge of the aortic knob. A distance >0.5 cm is considered a positive calcium sign, and a distance >1.0 cm is considered highly suspicious for aortic dissection. It is always wise to compare to an old film to see if there’s been an interval change.

Eighteen percent of patients with aortic dissection will have a positive troponin test, so if you suspect the diagnosis based on other clinical findings, don’t assume isolated acute coronary syndrome when the troponin comes back positive.5 Remember that fewer than one in 100 patients with a dissection will have associated coronary ischemia in any coronary distribution (most commonly inferior).

While D-dimer seems like it might be appealing to help rule out the diagnosis in low-risk patients, for such a rare diagnosis and poor test characteristics of D-dimer for dissection, guidelines do not recommend the use of D-dimer for the workup of aortic dissection.6

Aortic dissection can be considered the retinal detachment of the torso. While the sensitivity of point-of-care ultrasound (POCUS) by emergency physicians to detect an intimal flap is only 67 percent, the specificity has been shown to be 99 percent to 100 percent.7 For patients suspected of the diagnosis, look for an intimal flap that looks similar to a retinal detachment on POCUS and look for a pericardial effusion indicative of a retrograde dissection into the pericardium.8

Take-Home Points

Remember the big pain pearls when taking a history:
Ask the three important questions.
Aortic dissection should be considered the subarachnoid hemorrhage of the torso.
Migrating pain, colicky pain, plus need for IV opioids should raise your suspicion.
Intermittent pain can still be a dissection.
Look for Marfan syndrome, listen for an aortic regurgitation murmur, and feel for a pulse deficit.
Think not only about CP +1 but also 1+ CP.
Know the radiographic findings of loss or aortic knob/aortopulmonary window and the calcium sign, and use POCUS to look for an intimal flap and pericardial effusion.
Don’t be misled by a troponin or D-dimer.
Thanks to David Carr for his expert contributions to the EM Cases podcast that inspired this article.

 

References

Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903.
Rosman HS, Patel S, Borzak S, et al. Quality of history taking in patients with aortic dissection. Chest. 1998;114(3):793-795.
Imamura H, Sekiguchi Y, Iwashita T, et al. Painless acute aortic dissection: diagnostic, prognostic and clinical implications. Circ J. 2011;75(1):59-66.
Singer AJ, Hollander JE. Blood pressure: assessment of interarm differences. Arch Intern Med. 1996;156(17):2005-2008.
Leitman IM, Suzuki K, Wengrofsky AJ, et al. Early recognition of acute thoracic aortic dissection and aneurysm. World J Emerg Surg. 2013;8(1):47.
Diercks DB, Promes SB, Schuur JD, et al. Clinical policy: critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection. Ann Emerg Med. 2015;65(1):32-42.
Sobczyk D, Nycz K. Feasibility and accuracy of bedside transthoracic echocardiography in diagnosis of acute proximal aortic dissection. Cardiovasc Ultrasound. 2015;13:15.
Fojtik JP, Constantino TG, Dean AJ. The diagnosis of aortic dissection by emergency medicine ultrasound. J Emerg Med. 2007;32(2):191-96.

#Stroke: Causes, symptoms, diagnosis, and treatment

Postado em

Strokes occur due to problems with the blood supply to the brain: either the blood supply is blocked, or a blood vessel within the brain ruptures, causing brain tissue to die. A stroke is a medical emergency, and treatment must be sought as quickly as possible.

Stroke is the 5th leading cause of death in the United States, with one person dying every 4 minutes as a result. For black people, stroke is the 3rd leading cause of death.

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Approximately 800,000 people have a stroke each year; about one every 40 seconds. Only heart disease, cancer, chronic lower respiratory diseases, and accidents are more deadly.

There are three main kinds of stroke:

Ischemic strokes
Hemorrhagic strokes
Transient ischemic attacks (TIAs), also referred to as mini-strokes
In this article, we will explain why these types of stroke occur, and how they are treated and diagnosed.

Fast facts on stroke:

During a stroke, the brain does not receive enough oxygen or nutrients, causing brain cells to die.
Ischemic strokes are caused by a narrowing or blocking of arteries to the brain.
Hemorrhagic strokes are caused by blood vessels in and around the brain bursting or leaking.
Strokes need to be diagnosed and treated as quickly as possible to minimize brain damage.
Treatment depends on the type of stroke.
The most effective way to prevent strokes is through maintaining a healthy lifestyle and treating underlying conditions that are a risk factor.
What is stroke?
Stroke occurs when the supply of blood to the brain is either interrupted or reduced. When this happens, the brain does not get enough oxygen or nutrients, which causes brain cells to die.

There are three main kinds of stroke; ischemic, hemorrhagic, and TIA. This article will focus on ischemic and hemorrhagic strokes, as there is a separate Knowledge Center article for TIAs, which goes into specific detail about them.

In the U.S., approximately 40 percent of stroke deaths are in males, with 60 percent in females. According to the American Heart Association(AHA), compared with white people, black people have nearly twice the risk of a first-ever stroke and a much higher death rate from stroke.

In 2009, stroke was listed as the underlying cause of death in 128,842 persons in the U.S., resulting in an age-adjusted rate of 38.9 deaths per 100,000 population. The rate was almost twice as high among non-Hispanic blacks (73.6 per 100,000), and the rate of premature death from stroke was also higher among non-Hispanic blacks than their white counterparts (25.0 versus 10.2).

Stroke is more likely to affect people if they are overweight, aged 55 or older, have a personal or family history of stroke, do not exercise much, drink heavily, smoke, or use illicit drugs.

What causes stroke?
The different forms of stroke have different specific causes.

Causes of ischemic stroke

Ischemic stroke is the most common form, accounting for around 85 percent of strokes. This type of stroke is caused by blockages or narrowing of the arteries that provide blood to the brain, resulting in ischemia – severely reduced blood flow that damages brain cells.

These blockages are often caused by blood clots, which can form either in the arteries within the brain, or in other blood vessels in the body before being swept through the bloodstream and into narrower arteries within the brain. Fatty deposits within the arteries called plaque can cause clots that result in ischemia.

Causes of hemorrhagic stroke

Hemorrhagic strokes are caused by arteries in the brain either leaking blood or bursting open. The leaked blood puts pressure on brain cells and damages them. It also reduces the blood supply reaching the brain tissue after the hemorrhage point. Blood vessels can burst and spill blood within the brain or near the surface of the brain, sending blood into the space between the brain and the skull.

The ruptures can be caused by conditions such as hypertension, trauma, blood-thinning medications, and aneurysms (weaknesses in blood vessel walls).

Intracerebral hemorrhage is the most common type of hemorrhagic stroke and occurs when brain tissue is flooded with blood after an artery in the brain bursts. Subarachnoid hemorrhage is the second type of hemorrhagic stroke and is less common. In this type of stroke, bleeding occurs in an artery in the subarachnoid space – the area between the brain and the thin tissues that cover it.

Causes of transient ischemic attack (TIA)

TIAs are different from the kinds above because the flow of blood to the brain is only briefly interrupted. TIAs are similar to ischemic strokes in that they are often caused by blood clots or other clots.

TIAs should be regarded as medical emergencies just like the other kinds of stroke, even if the blockage of the artery and symptoms are temporary. They serve as warning signs for future strokes and indicate that there is a partially blocked artery or clot source in the heart.

According to the Centers for Disease Control and Prevention (CDC), over a third of people who experience a TIA go on to have a major stroke within a year if they have not received any treatment. Between 10-15 percent will have a major stroke within 3 months of a TIA.

Symptoms of stroke
Strokes occur quickly, so symptoms often appear suddenly and without warning.

The main symptoms of stroke are:

Confusion– including trouble with speaking and understanding.
Headache– possibly with altered consciousness or vomiting.
Numbness or inability to move parts of the face, arm, or leg– particularly on one side of the body.
Trouble seeing– in one or both eyes.
Trouble walking– including dizziness and lack of co-ordination.
Strokes can lead to long-term problems. Depending on how quickly it is diagnosed and treated, the patient can experience temporary or permanent disabilities in the aftermath of a stroke. In addition to the persistence of the problems listed above, patients may also experience the following:

bladder or bowel control problems
depression
pain in the hands and feet that gets worse with movement and temperature changes
paralysis or weakness on one or both sides of the body
trouble controlling or expressing emotions
Symptoms vary among patients and may range in severity.

The acronym F.A.S.T. is a way to remember the signs of stroke, and can help identify the onset of stroke more quickly:

Face drooping– if the person tries to smile does one side of the face droop?
Arm weakness– if the person tries to raise both their arms does one arm drift downward?
Speech difficulty– if the person tries to repeat a simple phrase is their speech slurred or strange?
Time to call 911– if any of these signs are observed, contact the emergency services.
The faster a person with suspected stroke receives medical attention, the better their prognosis and the less likely they will be to experience lasting damage or death.

How is a stroke diagnosed?
Strokes happen fast and will often occur before an individual can be seen by a doctor for a proper diagnosis.

For a stroke patient to get the best diagnosis and treatment possible, they should be treated at a hospital within 3 hours of their symptoms first appearing.

Ischemic strokes and hemorrhagic strokes require different kinds of treatment.

Unfortunately, it is only possible to be sure of what type of stroke someone has had by giving them a brain scan in a hospital environment.

There are several different types of diagnostic tests that doctors can use to determine which type of stroke has occurred:

Physical examination– a doctor will ask about the patient’s symptoms and medical history. They may check blood pressure, listen to the carotid arteries in the neck, and examine the blood vessels at the back of the eyes, all to check for indications of clotting.
Blood tests– a doctor may perform blood tests to find out how quickly the patient’s blood clots, the levels of particular substances (including clotting factors) in the blood, and whether or not the patient has an infection.
CT scan– a series of X-rays that can show hemorrhages, strokes, tumors, and other conditions within the brain.
MRI scan– radio waves and magnets create an image of the brain to detect damaged brain tissue.
Carotid ultrasound– an ultrasound scan to check the blood flow in the carotid arteries and to see if there is any plaque present.
Cerebral angiogram– dyes are injected into the brain’s blood vessels to make them visible under X-ray, to give a detailed view of the brain and neck blood vessels.
Echocardiogram– a detailed image of the heart is created to check for any sources of clots that could have traveled to the brain to cause a stroke.
Treatments for stroke
As the ischemic and hemorrhagic strokes are caused by different factors, both require different forms of treatment. It is not only important that the type of stroke is diagnosed quickly to reduce the damage done to the brain, but also because treatment suitable for one kind of stroke can be harmful to someone who has had a different kind.

How is ischemic stroke treated?

Ischemic strokes are caused by arteries being blocked or narrowed, and so treatment focuses on restoring an adequate flow of blood to the brain.

Treatment can begin with drugs to break down clots and prevent others from forming. Aspirin can be given, as can an injection of a tissue plasminogen activator (TPA). TPA is very effective at dissolving clots but needs to be injected within 4.5 hours of stroke symptoms starting.

Emergency procedures include administering TPA directly into an artery in the brain or using a catheter to physically remove the clot. Recent studies have questioned the effectiveness of these methods, and so research is still ongoing as to how beneficial these procedures are.

There are other procedures that can be carried out to decrease the risk of strokes or TIAs. A carotid endarterectomy involves a surgeon opening the carotid artery and removing any plaque that might be blocking it.

Alternatively, an angioplasty involves a surgeon inflating a small balloon in a narrowed artery via catheter and then inserting a stent (a mesh tube) into the opening to prevent the artery from narrowing again.

How is hemorrhagic stroke treated?

Hemorrhagic strokes are caused by bleeding into the brain, so treatment focuses on controlling the bleeding and reducing the pressure on the brain.

Treatment can begin with drugs given to reduce the pressure in the brain, control overall blood pressure, prevent seizures and prevent sudden constrictions of blood vessels. If the patient is taking blood-thinning anti-coagulants or an anti-platelet medication like Warfarin or Clopidogrel, they can be given drugs to counter the medication’s effects or blood transfusions to make up for blood loss.

Surgery can be used to repair any problems with blood vessels that have led or could lead to hemorrhagic strokes. Surgeons can place small clamps at the base of aneurysms or fill them with detachable coils to stop blood flow and prevent rupture.

If the hemorrhage was caused by arteriovenous malformations (AVMs), surgery can also be used to remove small them if they are not too big and not too deep within the brain. AVMs are tangled connections between arteries and veins that are weaker and burst more easily than other normal blood vessels.

Rehabilitation
Strokes are life-changing events that can affect a person both physically and emotionally, temporarily or permanently. After a stroke, successful recovery will often involve specific rehabilitative activities such as:

  Speech therapy – to help with problems producing or understanding speech. Practice, relaxation, and changing communication style, using gestures or different tones for example, all help.

  Physical therapy – to help a person relearn movement and co-ordination. It is important to get out and about, even if it is difficult at first.

  Occupational therapy – to help a person to improve their ability to carry out routine daily activities, such as bathing, cooking, dressing, eating, reading, and writing.

  Joining a support group – to help with common mental health problems such as depression that can occur after a stroke. Many find it useful to share common experiences and exchange information.

  Support from friends and family – to provide practical support and comfort. Letting friends and family know what can be done to help is very important.

Rehabilitation is an important and long part of treatment. With the right help, rehabilitation to a normal quality of life is possible, depending on the severity of the stroke.

 

In Doctors-Online

#Pacientes con #úlceras por pie diabético infectadas necesitan remisión rápida

Postado em

Liam Davenport

Los pacientes con una úlcera infectada por pie diabético tienen un pronóstico mucho peor de lo que se pensaba hasta ahora, de manera que 15% fallecen al cabo de un año, menos de la mitad de las úlceras cicatrizan en el mismo periodo y uno de cada siete individuos es sometido a amputación de todo un pie o parte del mismo, según los resultados de un nuevo estudio realizado en Reino Unido.[1]

El análisis de casi 300 pacientes con úlceras por pie diabético también demostró que aun cuando cicatrizara la úlcera, casi 10% presentaban una recidiva al cabo de 12 meses y más de 25% se sometían a alguna clase de procedimiento.

Por consiguiente, es crucial que estos pacientes sean examinados rápidamente y remitidos para atención especializada si es necesario, afirmaron Mwidimi Ndosi, PhD, de la University of West Bristol, Reino Unido, y sus colaboradores en su artículo publicado el 20 de noviembre en la versión electrónica de Diabetic Medicine.

“El aspecto fundamental es que las personas necesitan ser atendidas rápidamente si se comienza a formar una úlcera; esto brinda a los profesionales de la salud la máxima probabilidad de intentar tratar el trastorno”, resalta el coautor Michael Backhouse, PhD, un podiatra y becario de investigación sénior en la University of Leeds, Reino Unido, en un comunicado de prensa de esta institución.[2]

Estos últimos datos “deberían ser útiles a los profesionales clínicos en contextos de asistencia diversos para ayudar a identificar a las personas con más riesgo de desenlaces desfavorables que pueden necesitar priorización de más intervenciones o remisión a centros especializados”, dicen los científicos.

Isquemia, muchas úlceras y duración más prolongada de la úlcera pronostican resultados desfavorables

Para el análisis, los investigadores llevaron a cabo una evaluación observacional prospectiva de 12 meses, por medio de un análisis detallado de notas de casos de 250 pacientes con diabetes que habían participado en el estudio CODIFI (Concordance in Diabetic Foot Ulcer Infection ―Concordancia en la infección de úlcera por pie diabético―) y todavía estaban vivos al final de éste, en mayo de 2013. También incluyeron a 49 participantes del estudio que habían fallecido, de los cuales se contaba con datos clínicos.

La media de edad de los pacientes fue 64,3 años y 233 (77,9%) eran del género masculino.

Después de 12 meses de seguimiento adicional, la úlcera índice había cicatrizado en un total de 136 (45,5%) de los 299 pacientes, mientras que 13 (9,6) tenían una recidiva.

Cincuenta y dos (17,4%) se sometieron a amputación de una parte del pie durante el seguimiento, 18 (6,0) a revascularización periférica y 10 (3,3%) a los dos procedimientos.

Y otros 45 pacientes (15,1%) habían fallecido hacia la fecha límite de los 12 meses.

La mediana de tiempo transcurrido hasta la cicatrización de la úlcera índice fue de 4,5 meses, mientras que la mediana de tiempo transcurrido hasta la amputación, si ésta se llevó a cabo, fue de 2,0 meses, y para la revascularización fue de 3,0 meses.

En el caso de los que no sobrevivieron, el tiempo promedio transcurrido hasta el fallecimiento fue 5,6 meses.

Los factores que más pronosticaron resultados desfavorables a 12 meses fueron isquemia de la extremidad, múltiples úlceras en el pie y una duración de la úlcera más prolongada.

Por ejemplo, los pacientes con una úlcera presente durante 2 meses o más antes del reclutamiento en CODIFI tenían una menor probabilidad de cicatrización, con un hazard ratio (HR) de 0,55, lo mismo que aquellos con un grado de flujo sanguíneo, extensión, profundidad, infección y sensación (PEDIS) en la úlcera índice de ≥2, lo que indicó arteriopatía periférica; esto redujo 63% el riesgo de cicatrización (HR: 0,37)

Por el contrario, la presentación de sólo una úlcera en el pie índice se relacionó con un aumento en el riesgo de cicatrización de 90% [HR: 1,90], lo mismo que la identificación de estafilococos no productores de coagulasa en el cultivo de la úlcera (HR: 1,53); es muy probable, dicen los investigadores, que esto se deba a que la presencia de este microorganismo se relacionó inversamente con la de MRSA (Staphylococcus aureus resistente a meticilina) más virulento.

Se han de evitar las amputaciones cuando sea posible

Puede ser difícil diagnosticar si una úlcera por pie diabético está o no está infectada, sobre todo en caso de isquemia de la extremidad o neuropatía periférica, hacen notar los investigadores, pero en general se está de acuerdo en que esta decisión debe basarse en los signos o síntomas de inflamación o secreción purulenta.

La autora principal, E. Andrea Nelson, PhD, RGN, jefa de la School of Healthcare en la Facultad de Medicina y Salud, University of Leeds, Reino Unido, dijo a Medscape Noticias Médicas que la cohorte que reclutaron era representativa de la población general de pacientes del National Health Service en Inglaterra, y que el estudio tuvo pocos criterios de exclusión, de manera que considera que los datos serán ampliamente aplicables a las poblaciones con úlceras por pie diabético en otros países occidentales.

La Dra. Nelson resaltó que los pacientes que se someten a amputaciones generalmente tienen una calidad de vida inferior a la de los que evitan este desenlace y que someterse a una amputación indica una mayor probabilidad de una amputación subsiguiente pues significa una vascularización deficiente.

Además, hizo notar que las amputaciones son costosas por lo que respecta al tiempo que los pacientes tienen que hospitalizarse, el costo de la atención hospitalaria, la rehabilitación y las prótesis, etcétera, así como los cuidados necesarios después de la amputación.

Afirmó que lo ideal es proporcionar una atención que minimice la tasa de amputación en personas con úlceras por pie diabético.

No obstante, la amputación “no es algo que se evitaría a toda costa, pues someterse, por ejemplo, a la amputación de un dedo del pie, podría evitar un daño más considerable para el paciente”.

Los nuevos hallazgos no sólo ayudan a los médicos en diversos contextos a identificar a quienes puede ser necesario dar prioridad, sino también “deberían ser útiles para orientar respecto al diseño y el análisis de estudios clínicos futuros”, concluyen los investigadores.

La investigación fue financiada por el programa de Health Technology Assessment (HTA) del National Institute for Health Research (NIHR). La Dra. Nelson fue miembro de la HTA Commissioning Board. Los coautores no tienen ningún conflicto de interés económico pertinente.