Acidente isquêmico transitório (AIT): da história ao tratamento

Apresentação em tema: "Acidente isquêmico transitório (AIT): da história ao tratamento"— Transcrição da apresentação:

1 Acidente isquêmico transitório (AIT): da história ao tratamento
Medicina – Graduação Neurologia UFPR Curitiba 2014

2 Afonso Aragão Augusto Prado Luíz Gorski João Ventura Rafael Kayano Victor Souza Vitor Piseta Wagner Schiel

3 Este tema foi apresentado na forma de Seminário para os alunos do 7º Período do Curso de Medicina da Universidade Federal do Paraná, sob a orientação e coordenação do Prof Edison Matos Nóvak Novembro / 2014

4 Aspectos históricos Definição Epidemiologia Fisiopatologia Sinais e sintomas Diagnóstico Diagnóstico diferencial Manejo Prognóstico Conclusões

5 Ela [YOLANDA, esposa do presidente] disse que aquela noite, de madrugada, ouviu um barulho no banheiro. Levantou-se, ele estava de pijama, o cabelo meio revolto, e ela disse: 'O que é, Costa?'. Ele fez assim [aponta para a língua], não conseguia falar. Era o início do derrame. [...] Costa e Silva – segundo presidente do Regime Militar Brasileiro durante o período de 67-69 RELATO DE IVO ARZUA - Ela [YOLANDA, esposa do presidente] disse que aquela noite, de madrugada, ouviu um barulho no banheiro. Levantou-se, ele estava de pijama, o cabelo meio revolto, e ela disse: 'O que é, Costa?'. Ele fez assim [aponta para a língua], não conseguia falar. Era o início do derrame. [...] Eu estava repousando em Curitiba sob ordens médicas e o chefe da Casa Militar [Jayme Portella] telefonou pedindo minha presença porque o presidente ia descer no aeroporto militar no Rio, onde ia ser tratado. Foi a última vez que o vi em vida. Não deixavam a gente visitá-lo, só os militares. E dona Yolanda contou que ele, por não cumprir aquilo o que tinha prometido, de reabrir o Congresso, já não falava mais, só por gestos. Depois que morreu, levantaram o colchão... ele fingia que tomava os remédios. Ele estava tão profundamente desgostoso com o AI-5. Era um homem muito sério. Fonte: Fonte: Jornal do Brasil

6 Fonte: NYT Gerald Ford – presidente norte americano de 1974-77
Na convenção do partido nacional do partido republicano no ano 2000 sofreu 2 “minor strokes” Fonte: NYT

7 Aspectos históricos Apoplexia – Hipócrates (400a.C.)
“Stroke” – William Cole (1689) Fonte: Brief History of Definitions of Stroke and TIA The word “stroke” was likely first introduced into medicine in 1689 by William Cole in A Physico-Medical Essay Concerning the Late Frequencies of Apoplexies. Before Cole, the common term used to describe very acute nontraumatic brain injuries was “apoplexy.” Apoplexy was used by Hippocrates circa 400 BC.5 For >2000 years, physicians have struggled to define the term “stroke.” During the 1950s, physicians felt the need to also introduce a term for temporary vascular-related episodes of brain dysfunction that would not qualify as strokes, and “transient ischemic attack” came into use. Why the struggle to arrive at generally agreed on consensus definitions of stroke and TIA? Information about the brain and its anatomy, functions, and blood supply has advanced substantially during the past 200 years. Neurologists and other specialists in vascular diseases of the brain have proliferated during the past 50 years. The ability to safely and quickly image the brain and its blood-supplying vessels in patients has become a reality during the past 25 years. And, in the past 10 years, modern brain and vascular imaging has become generally available in community medical centers, although many still today do not have this capability. As knowledge, personnel, and technology evolve, we continue to learn about the nature, causes, and clinical and imaging findings in patients with cerebrovascular diseases. The current World Health Organization definition of stroke (introduced in 1970 and still used) is “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”6 During the 40 years since this definition was formulated, advances have been made in knowledge about the nature, timing, clinical recognition of stroke and its mimics, and imaging findings that require an updated definition. During the Second Princeton Cerebrovascular Disease Conference, C.M. Fisher presented an extensive characterization of what he termed “transient ischemic attacks,” which “may last from a few seconds up to several hours, the most common duration being a few seconds up to 5 or 10 minutes.”7 At the Fourth Princeton Cerebrovascular Disease Conference in 1965, the attendees agreed on “transient ischemic attack” as the preferred term for temporary episodes of brain and eye ischemia.8 In 1975, an Ad Hoc Committee on Cerebrovascular Disease published the following definition: “Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.”9 The 24-hour duration was arbitrarily chosen without data. When this definition was formulated, diagnostic techniques were unavailable that could determine the presence of brain infarction, and effective treatments of brain ischemia were not established. The definition of TIA that was used in the 1975 report was universally cited until the beginning of the 21st century, when data accumulated that prompted attempts at redefinition. These data fell into 2 categories: duration of TIAs and imaging findings. The new data ignited controversies, which remain to the present day, about redefining the duration of TIAs and the need for incorporating brain and vascular imaging data into the definition. In 2002, an expert committee proposed a new definition: “A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.”10 In 2009, an expert committee of the AHA/ASA published a scientific statement defining TIA and recommending evaluation. The definition proposed was “transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction.”1 The International Classification of Diseases (ICD) system aims to standardize diagnostic classification for most diseases. Recent iterations, including the 11th revision along with its clinical modification (ICD-11-CM) published in 2010,11 classified cerebrovascular disorders chiefly as TIA, cerebral ischemic stroke, ICH, or SAH. Biografiasyvidas.com

8 Aspectos históricos “TIA” – Fisher (1958) – 2ª Conferência de Doença Cerebrovascular em Princeton Fonte: Brief History of Definitions of Stroke and TIA The word “stroke” was likely first introduced into medicine in 1689 by William Cole in A Physico-Medical Essay Concerning the Late Frequencies of Apoplexies. Before Cole, the common term used to describe very acute nontraumatic brain injuries was “apoplexy.” Apoplexy was used by Hippocrates circa 400 BC.5 For >2000 years, physicians have struggled to define the term “stroke.” During the 1950s, physicians felt the need to also introduce a term for temporary vascular-related episodes of brain dysfunction that would not qualify as strokes, and “transient ischemic attack” came into use. Why the struggle to arrive at generally agreed on consensus definitions of stroke and TIA? Information about the brain and its anatomy, functions, and blood supply has advanced substantially during the past 200 years. Neurologists and other specialists in vascular diseases of the brain have proliferated during the past 50 years. The ability to safely and quickly image the brain and its blood-supplying vessels in patients has become a reality during the past 25 years. And, in the past 10 years, modern brain and vascular imaging has become generally available in community medical centers, although many still today do not have this capability. As knowledge, personnel, and technology evolve, we continue to learn about the nature, causes, and clinical and imaging findings in patients with cerebrovascular diseases. The current World Health Organization definition of stroke (introduced in 1970 and still used) is “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”6 During the 40 years since this definition was formulated, advances have been made in knowledge about the nature, timing, clinical recognition of stroke and its mimics, and imaging findings that require an updated definition. During the Second Princeton Cerebrovascular Disease Conference, C.M. Fisher presented an extensive characterization of what he termed “transient ischemic attacks,” which “may last from a few seconds up to several hours, the most common duration being a few seconds up to 5 or 10 minutes.”7 At the Fourth Princeton Cerebrovascular Disease Conference in 1965, the attendees agreed on “transient ischemic attack” as the preferred term for temporary episodes of brain and eye ischemia.8 In 1975, an Ad Hoc Committee on Cerebrovascular Disease published the following definition: “Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.”9 The 24-hour duration was arbitrarily chosen without data. When this definition was formulated, diagnostic techniques were unavailable that could determine the presence of brain infarction, and effective treatments of brain ischemia were not established. The definition of TIA that was used in the 1975 report was universally cited until the beginning of the 21st century, when data accumulated that prompted attempts at redefinition. These data fell into 2 categories: duration of TIAs and imaging findings. The new data ignited controversies, which remain to the present day, about redefining the duration of TIAs and the need for incorporating brain and vascular imaging data into the definition. In 2002, an expert committee proposed a new definition: “A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.”10 In 2009, an expert committee of the AHA/ASA published a scientific statement defining TIA and recommending evaluation. The definition proposed was “transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction.”1 The International Classification of Diseases (ICD) system aims to standardize diagnostic classification for most diseases. Recent iterations, including the 11th revision along with its clinical modification (ICD-11-CM) published in 2010,11 classified cerebrovascular disorders chiefly as TIA, cerebral ischemic stroke, ICH, or SAH. Neurology.org

9 Aspectos históricos “Stroke” – OMS (1970)
Comitê Ad Hoc sobre a Doença Cerebrovascular (1975) Albers Working group (2002) “a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction” Brief History of Definitions of Stroke and TIA The word “stroke” was likely first introduced into medicine in 1689 by William Cole in A Physico-Medical Essay Concerning the Late Frequencies of Apoplexies. Before Cole, the common term used to describe very acute nontraumatic brain injuries was “apoplexy.” Apoplexy was used by Hippocrates circa 400 BC.5 For >2000 years, physicians have struggled to define the term “stroke.” During the 1950s, physicians felt the need to also introduce a term for temporary vascular-related episodes of brain dysfunction that would not qualify as strokes, and “transient ischemic attack” came into use. Why the struggle to arrive at generally agreed on consensus definitions of stroke and TIA? Information about the brain and its anatomy, functions, and blood supply has advanced substantially during the past 200 years. Neurologists and other specialists in vascular diseases of the brain have proliferated during the past 50 years. The ability to safely and quickly image the brain and its blood-supplying vessels in patients has become a reality during the past 25 years. And, in the past 10 years, modern brain and vascular imaging has become generally available in community medical centers, although many still today do not have this capability. As knowledge, personnel, and technology evolve, we continue to learn about the nature, causes, and clinical and imaging findings in patients with cerebrovascular diseases. The current World Health Organization definition of stroke (introduced in 1970 and still used) is “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”6 During the 40 years since this definition was formulated, advances have been made in knowledge about the nature, timing, clinical recognition of stroke and its mimics, and imaging findings that require an updated definition. During the Second Princeton Cerebrovascular Disease Conference, C.M. Fisher presented an extensive characterization of what he termed “transient ischemic attacks,” which “may last from a few seconds up to several hours, the most common duration being a few seconds up to 5 or 10 minutes.”7 At the Fourth Princeton Cerebrovascular Disease Conference in 1965, the attendees agreed on “transient ischemic attack” as the preferred term for temporary episodes of brain and eye ischemia.8 In 1975, an Ad Hoc Committee on Cerebrovascular Disease published the following definition: “Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.”9 The 24-hour duration was arbitrarily chosen without data. When this definition was formulated, diagnostic techniques were unavailable that could determine the presence of brain infarction, and effective treatments of brain ischemia were not established. The definition of TIA that was used in the 1975 report was universally cited until the beginning of the 21st century, when data accumulated that prompted attempts at redefinition. These data fell into 2 categories: duration of TIAs and imaging findings. The new data ignited controversies, which remain to the present day, about redefining the duration of TIAs and the need for incorporating brain and vascular imaging data into the definition. In 2002, an expert committee proposed a new definition: “A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.”10 In 2009, an expert committee of the AHA/ASA published a scientific statement defining TIA and recommending evaluation. The definition proposed was “transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction.”1 The International Classification of Diseases (ICD) system aims to standardize diagnostic classification for most diseases. Recent iterations, including the 11th revision along with its clinical modification (ICD-11-CM) published in 2010,11 classified cerebrovascular disorders chiefly as TIA, cerebral ischemic stroke, ICH, or SAH.

10 Aspectos históricos AHA/ ASA (2009)
Brief History of Definitions of Stroke and TIA The word “stroke” was likely first introduced into medicine in 1689 by William Cole in A Physico-Medical Essay Concerning the Late Frequencies of Apoplexies. Before Cole, the common term used to describe very acute nontraumatic brain injuries was “apoplexy.” Apoplexy was used by Hippocrates circa 400 BC.5 For >2000 years, physicians have struggled to define the term “stroke.” During the 1950s, physicians felt the need to also introduce a term for temporary vascular-related episodes of brain dysfunction that would not qualify as strokes, and “transient ischemic attack” came into use. Why the struggle to arrive at generally agreed on consensus definitions of stroke and TIA? Information about the brain and its anatomy, functions, and blood supply has advanced substantially during the past 200 years. Neurologists and other specialists in vascular diseases of the brain have proliferated during the past 50 years. The ability to safely and quickly image the brain and its blood-supplying vessels in patients has become a reality during the past 25 years. And, in the past 10 years, modern brain and vascular imaging has become generally available in community medical centers, although many still today do not have this capability. As knowledge, personnel, and technology evolve, we continue to learn about the nature, causes, and clinical and imaging findings in patients with cerebrovascular diseases. The current World Health Organization definition of stroke (introduced in 1970 and still used) is “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”6 During the 40 years since this definition was formulated, advances have been made in knowledge about the nature, timing, clinical recognition of stroke and its mimics, and imaging findings that require an updated definition. During the Second Princeton Cerebrovascular Disease Conference, C.M. Fisher presented an extensive characterization of what he termed “transient ischemic attacks,” which “may last from a few seconds up to several hours, the most common duration being a few seconds up to 5 or 10 minutes.”7 At the Fourth Princeton Cerebrovascular Disease Conference in 1965, the attendees agreed on “transient ischemic attack” as the preferred term for temporary episodes of brain and eye ischemia.8 In 1975, an Ad Hoc Committee on Cerebrovascular Disease published the following definition: “Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.”9 The 24-hour duration was arbitrarily chosen without data. When this definition was formulated, diagnostic techniques were unavailable that could determine the presence of brain infarction, and effective treatments of brain ischemia were not established. The definition of TIA that was used in the 1975 report was universally cited until the beginning of the 21st century, when data accumulated that prompted attempts at redefinition. These data fell into 2 categories: duration of TIAs and imaging findings. The new data ignited controversies, which remain to the present day, about redefining the duration of TIAs and the need for incorporating brain and vascular imaging data into the definition. In 2002, an expert committee proposed a new definition: “A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.”10 In 2009, an expert committee of the AHA/ASA published a scientific statement defining TIA and recommending evaluation. The definition proposed was “transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction.”1 The International Classification of Diseases (ICD) system aims to standardize diagnostic classification for most diseases. Recent iterations, including the 11th revision along with its clinical modification (ICD-11-CM) published in 2010,11 classified cerebrovascular disorders chiefly as TIA, cerebral ischemic stroke, ICH, or SAH.

11 Definição AHA/ ASA (2009) Brief History of Definitions of Stroke and TIA The word “stroke” was likely first introduced into medicine in 1689 by William Cole in A Physico-Medical Essay Concerning the Late Frequencies of Apoplexies. Before Cole, the common term used to describe very acute nontraumatic brain injuries was “apoplexy.” Apoplexy was used by Hippocrates circa 400 BC.5 For >2000 years, physicians have struggled to define the term “stroke.” During the 1950s, physicians felt the need to also introduce a term for temporary vascular-related episodes of brain dysfunction that would not qualify as strokes, and “transient ischemic attack” came into use. Why the struggle to arrive at generally agreed on consensus definitions of stroke and TIA? Information about the brain and its anatomy, functions, and blood supply has advanced substantially during the past 200 years. Neurologists and other specialists in vascular diseases of the brain have proliferated during the past 50 years. The ability to safely and quickly image the brain and its blood-supplying vessels in patients has become a reality during the past 25 years. And, in the past 10 years, modern brain and vascular imaging has become generally available in community medical centers, although many still today do not have this capability. As knowledge, personnel, and technology evolve, we continue to learn about the nature, causes, and clinical and imaging findings in patients with cerebrovascular diseases. The current World Health Organization definition of stroke (introduced in 1970 and still used) is “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”6 During the 40 years since this definition was formulated, advances have been made in knowledge about the nature, timing, clinical recognition of stroke and its mimics, and imaging findings that require an updated definition. During the Second Princeton Cerebrovascular Disease Conference, C.M. Fisher presented an extensive characterization of what he termed “transient ischemic attacks,” which “may last from a few seconds up to several hours, the most common duration being a few seconds up to 5 or 10 minutes.”7 At the Fourth Princeton Cerebrovascular Disease Conference in 1965, the attendees agreed on “transient ischemic attack” as the preferred term for temporary episodes of brain and eye ischemia.8 In 1975, an Ad Hoc Committee on Cerebrovascular Disease published the following definition: “Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.”9 The 24-hour duration was arbitrarily chosen without data. When this definition was formulated, diagnostic techniques were unavailable that could determine the presence of brain infarction, and effective treatments of brain ischemia were not established. The definition of TIA that was used in the 1975 report was universally cited until the beginning of the 21st century, when data accumulated that prompted attempts at redefinition. These data fell into 2 categories: duration of TIAs and imaging findings. The new data ignited controversies, which remain to the present day, about redefining the duration of TIAs and the need for incorporating brain and vascular imaging data into the definition. In 2002, an expert committee proposed a new definition: “A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.”10 In 2009, an expert committee of the AHA/ASA published a scientific statement defining TIA and recommending evaluation. The definition proposed was “transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction.”1 The International Classification of Diseases (ICD) system aims to standardize diagnostic classification for most diseases. Recent iterations, including the 11th revision along with its clinical modification (ICD-11-CM) published in 2010,11 classified cerebrovascular disorders chiefly as TIA, cerebral ischemic stroke, ICH, or SAH.

12 Epidemiologia Incidência: 200.000-500.000 AIT/ ano[1,2]
Incidência de AIT’s aumenta com a idade[1] 1-3: (<35 anos) 1.500: (>85 anos) Incidência maior em negros e homens[3,4] 1 – Kleindorfer D and cols et al. Stroke. Apr 2005;36(4):720-3. 2 – Johnston SC and cols et al. Neurology. May ;60(9): 3 – Bots ML and cols et al. Stroke. Apr 1997;28(4): 4 – Albers and cols et al. N Engl J Med. Nov ;347(21): 1 – Kleindorfer D and cols et al. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. Apr 2005;36(4):720-3. 2 – Johnston SC and cols et al. Prevalence and knowledge of transient ischemic attack among US adults. Neurology. May ;60(9): 3 – Bots ML and cols et al. Transient neurological attacks in the general population. Prevalence, risk factors, and clinical relevance. Stroke. Apr 1997;28(4): 4 – Albers and cols et al. Transient ischemic attack--proposal for a new definition. N Engl J Med. Nov ;347(21):

13 Fatores de risco Não modificáveis
Idade avançada (2x – cada década após os 55a) Sexo (masculino) Negros (incidência 38% maior que os brancos) Baixo peso ao nascer (<2500g – 2x mais chances) HF+ (aumenta o risco de AVE em 30%) The risk of cerebrovascular disease increases with age and is higher in men14 and in blacks and Hispanics.15 The risk factors and clinical presentation do not differ between TIA and stroke, so the evaluation and treatment should not differ ei- ther. These two events represent a continuum of the same disease entity. Some risk factors for TIA are modifiable, others are not. Older age. The risk of ischemic stroke and intracranial hemorrhage doubles with each decade after age 55 in both sexes.16 Sex. Men have a significantly higher incidence of TIA than women,11 whereas the op- posite is true for stroke: women have a higher lifetime risk of stroke than men.17 African Americans have an incidence of stroke (all types) 38% higher than that of whites,and an incidence of TIA (inpatient and out-of-hospital) 40% higher than the overall age- and sex-adjusted rate in the white population. Low birth weight. The odds of stroke are more than twice as high in people who weighed less than 2,500 g at birth compared with those who weighed 4,000 g or more, probably because of a correlation between low birth weight and hypertension. A family history of stroke increases the risk of stroke by nearly 30%, the association being stronger with large-vessel and small- vessel stroke than with cardioembolic stroke.

14 Fatores de risco Modificáveis Tabagismo (2x) DM (2,5x)
Dislipidemia (LDL elevado/ HDL diminuído) FA (5x) Estenose carotídea Estilo de vida Cigarette smoking approximately doubles the risk of ischemic stroke.21–23 Hypertension has a relationship with stroke risk that is strong, continuous, graded, consistent, and significant.24 Diabetes increases stroke risk nearly six times.25 Lipid abnormalities. Most studies have found an association between lipid levels (to- tal cholesterol and low-density lipoprotein cholesterol) and the risk of death from isch- emic stroke,26–28 and an inverse relationship between high-density lipoprotein cholesterol levels and stroke risk.29 Atrial fibrillation increases the risk of isch- emic stroke up to fivefold, even in the absence of cardiac valvular disease. The mechanism is embolism of stasis-induced thrombi that form in the left atrial appendage.30 Carotid stenosis. Asymptomatic carotid atherosclerotic stenotic lesions in the extra- cranial internal carotid artery or carotid bulb are associated with a higher risk of stroke.24,31 Lifestyle factors. Diets that lower blood pressure have been found to decrease stroke risk.24 Exercise in men and women reduces the risk of stroke or death by 25% to 30% com- pared with inactive people.32 Weight reduc- tion has been found to lower blood pressure and reduce stroke risk.24

15 Fisiopatologia Causas de AIT’s e AVE: Trombose (aterosclerose)
Embolia (coração) Diminuição da perfusão sistêmica (IC ou hipotensão) Fonte: Acomete as artérias perfurantes Pode ocorrer por vasoespasmo, lipohialinose ou doença ateromatosa.

16 Fisiopatologia Causas de AIT’s e AVE: Trombose (aterosclerose)
Embolia (coração) Diminuição da perfusão sistêmica (IC ou hipotensão) Fonte: Mecanismo análogo ao do AVC isquêmico Há um desprendimento do êmbolo antes que ocorra sequela Déficit neurólógico pode durar mais de 1h

17 Fisiopatologia Causas de AIT’s e AVE: Trombose (aterosclerose)
Embolia (coração) Diminuição da perfusão sistêmica (IC ou hipotensão) Fonte: Ocorre quando há um baixo fluxo em um grande vaso. Duração de poucos minutos Associado a lesões ateroscleróticos nas artérias carótidas e a um baixo fluxo colateral pelo polígono de Willis.

18 Clínica do AIT M.C.G, mulher, 72 anos de idade, telefona para seu médico imediatamente após um episódio de dificuldade de fala e fraqueza do lado direito do rosto e braço direito que durou 30min. Nesto momento relata que está muito bem. Não há nada de relevante na história clínica. S. CLAIBORNE JOHNSTON, M.D., PH.D. TRANSIENT ISCHEMIC ATTACK. N Engl J Med, Vol. 347, No. 21 · November 21, 2002 S. CLAIBORNE JOHNSTON, M.D., PH.D. TRANSIENT ISCHEMIC ATTACK. N Engl J Med, Vol. 347, No. 21 · November 21, 2002

19 Clínica AIT Tratamento? TAC? RM? Doppler de carótidas?
Eletrocardiograma? Hemograma? Coagulograma? Eletrólitos? Glicemia capilar? AngioTC? AngioRM? Angiografia? Trombólise? Warfarina? Aspirina?

20 Clínica do AIT Até 60% das suspeitas de AIT na emergência  causa não isquêmica Prabhakaran S, Silver AJ, Warrior L, McClenathan B, Lee VH. Misdiagnosis of transient ischemic attacks in the emergency room. Cerebrovasc Dis 2008; 26:630–635

21 40% das suspeitas de AIT são realmente um AIT
Clínica do AIT Até 60% das suspeitas de AIT na emergência  causa não isquêmica 40% das suspeitas de AIT são realmente um AIT Prabhakaran S, Silver AJ, Warrior L, McClenathan B, Lee VH. Misdiagnosis of transient ischemic attacks in the emergency room. Cerebrovasc Dis 2008; 26:630–635 Prabhakaran S, Silver AJ, Warrior L, McClenathan B, Lee VH. Misdiagnosis of transient ischemic attacks in the emergency room. Cerebrovasc Dis 2008; 26:630–635

22 Como melhorar?

23 Clínica do AIT Sintomas são iguais ao de um AVEi
Segundos-minutos-horas Depende da área acometida Maioria dos casos dura <1h 14min no território carotídeo 8min no vertebrobasilar Déficit focal isquêmico estável há >1h  AVEi.

24 Sinais e Sintomas Perda de força Amaurose fugaz Cefaleia Tontura
Alteração de marcha e equilíbrio Alteração súbita da fala Alteração de sensibilidade Alteração de memória Confusão mental A amaurose fugaz ocorre devido a um embolo na arteria central da retina de um dos olhos, e isso pode indicar estenose carotida ou doenca local da arteria oftalmica (Harrison)

25 Apresentação clínica Anterior (ACI, ACM, ACA) – 80%
Posterior (AAVV, AB, ACP) – 20% 20% circulação anterior  ACP Sintomas negativos Hemiparesia/ plegia Hipoestesia Amaurose fugaz Transient Ischemic Attack: Definitions and Clinical Presentations Christopher A. Lewandowski, MD Chethan P. V. Rao, MD Brian Silver, MD Because transient ischemic attacks are vascular events, their presentation follows the vascular territory of the brain; this allows for classification according to the major arterial branches (Figures 2-7).24 The anterior circulation consists of the internal carotid arteries, the middle cerebral arteries, the anterior cerebral arteries, and their tributaries. It receives 80% of the cerebral blood flow and accounts for 80% of transient ischemic attacks and strokes.25-27 The posterior circulation consists of the vertebral arteries, basilar artery, posterior cerebral arteries, and their tributaries. The posterior circulation receives 20% of the cerebral blood flow, and 20% of transient ischemic attack or strokes occur in these vertebrobasilar territories.25-27 Approximately 20% of people have posterior cerebral artery flow from the anterior circulation.

26 Clínica do AIT Transient Ischemic Attack: Definitions and Clinical Presentations Christopher A. Lewandowski, MD Chethan P. V. Rao, MD Brian Silver, MD Christopher and cols. Transient Ischemic Attack: Definitions and Clinical Presentations

27 Clínica do AIT USP emergências médicas

28 Clínica do AIT USP emergências médicas

29 Como fazer o DX? Anamnese + EF + Exames complementares
Déficit neurológico focal temporário Descartar outras condições (mimics TIA) História Laboratório Imagem Complemetares Diagnóstico estabelecido através de uma clínica compatível, afastamento de outras condições que cursam com os sintomas, e análise dos exames complementares de imagem e laboratoriais. Investigação Etiológica de acordo com a história e sintomas do paciente. Ruling out metabolic or drug-induced causes of symptoms consistent with a transient ischemic attack (TIA) is important. Initial assessment is aimed at excluding emergency conditions that can mimic a TIA (eg, hypoglycemia, seizure, or intracranial hemorrhage). A fingerstick blood glucose test should be performed and blood drawn for a complete blood count (CBC), coagulation studies, and serum electrolyte levels. Obtain a 12-lead electrocardiogram (ECG) with rhythm strip, and evaluate for symptomatic arrhythmias or evidence of ischemia. Brain imaging is recommended within 24 hours of symptom onset. Although magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) is preferred, noncontrast computed tomography (CT) of the head is a reasonable first choice when MRI is not readily available.[3, 7, 4] Christopher and cols. Transient Ischemic Attack: Definitions and Clinical Presentations

30 Exames laboratoriais Glicemia HMG Eletrólitos Coagulação VHS
Perfil lipídico Enzimas cardíacas Líquor É importante descartar outras condições que cursam com os sintomas apresentados. Os mais urgentes são glicemia, hemograma, eletrólitos, coagulação e ecg. VHS, perfil lipídico e enzimas cardíacas podem ajudar na investigação e diagnóstico diferencial De acordo com a história do paciente, outros exames podem ser solicitados, como o rastreamento de estados de hipercoagulabilidade, serologia compatível com sífilis, anticorpo antifosfolípide, exames toxicológicos, análise do liquor, entre outros. Punção Liquórica – HSA, Infecção SNC, doenças desmielinizantes; The following tests are considered on an emergency basis: Serum chemistry profile, including creatinine Screening coagulation studies CBC The following tests may be helpful and often can be performed on an urgent basis: Erythrocyte sedimentation rate (ESR) Cardiac enzymes Lipid profile Screening for hypercoagulable states (particularly in younger patients with no known vascular risk factors) may be performed, dditional laboratory tests, ordered as needed and on the basis of the history and examination, include the following: Syphilis serology Antiphospholipid antibodies Toxicology screens Hemoglobin electrophoresis Serum protein electrophoresis Cerebrospinal fluid examination

31 O que perguntar na anamnese?
“CAST” C omorbidities A ge S ymptoms T ime Transient Ischemic Attack: Definitions and Clinical Presentations Christopher A. Lewandowski, MD Chethan P. V. Rao, MD Brian Silver, MD Christopher and cols. Transient Ischemic Attack: Definitions and Clinical Presentations

32 O que não esquecer no EF? Maioria sem sinais ao EF Desvio do olhar
Força muscular (paresias/ paralisias) Sensibilidade Fundoscopia Ausculta de carótidas Palpação de artéria temporal Transient Ischemic Attack: Definitions and Clinical Presentations Christopher A. Lewandowski, MD Chethan P. V. Rao, MD Brian Silver, MD Christopher and cols. Transient Ischemic Attack: Definitions and Clinical Presentations