Acidente Vascular Cerebral por dissecção carotídea bilateral pós-procedimento odontológico: relato de caso / Stroke from bilateral carotid dissection after dental procedure: case report

RESUMO: Introdução: A dissecção da artéria carótida (DAC) tem como uma das principais repercussões o Acidente Vascular Cerebral isquêmico (AVCi) em indivíduos jovens previamente saudáveis. É comum que nas DAC traumáticas, como em acidentes automobilísticos, o paciente seja submetido à investigação mais complexa com exames de imagem. Estes permitem um diagnóstico precoce e, portanto, um tratamento, reduzindo as chances de sequelas. Todavia, cau-sas não traumáticas com desfecho de DAC já foram relatadas, como as causas odontológicas. Objetivo: Contribuir para valorização diagnóstica da DAC não traumática e profilaxia de AVC subsequente. Métodos: Relatamos um caso de dissecção não aneurismática das artérias carótidas internas (ACI) pós-procedimento odontológico com desfecho de AVC bilateral em paciente de 52 anos. Resultados: Devido à forte associação de DAC a fatores traumáticos, em um primeiro contato com a paciente não foram levantadas suspeitas da ocorrência de DAC nem de AVC (ausência de déficit focal). Porém, tardiamente, foi identificada oclusão da ACI à esquerda e estenose na ACI direita, resultando em dois AVCs e incapacidade funcional severa na alta. Conclusão: O diagnóstico da DAC é um desafio, em especial por tratar-se de uma lesão de etiologia multifatorial. No entanto, seu reconhecimento precoce afetará diretamente o desfecho do paciente. Portanto, na presença de eventuais sintomas de alerta, faz-se necessário um meticuloso ques-tionamento sobre as últimas atividades do indivíduo. Este estudo alerta para a adoção de condutas profiláticas na ocorrência de fatores causais como hiperextensão cervical prolongada ou movimentos súbitos da cervical. (AU)

ABSTRACT: Introduction: Carotid artery dissection (CAD) has the ischemic stroke as one of the main repercussions in pre-viously healthy young individuals. It is common that in traumatic CAD, as in automobile accidents, the patient is subjected to a more complex investigation with imaging exams. These, allow an early diagnosis and, therefore, a treatment, reducing the chances of sequelae. However, non-traumatic causes with CAD outcomes have already been reported, such as dental causes. Objective: To contribute to the diagnostic valuation of non-traumatic CAD and subsequent stroke prophylaxis. Methods: We report a case of non-aneurysmatic dissection of the internal carotid arteries (ICA) after a dental procedure with evolution to bilateral stroke outcome in a 52-year-old patient. Results: Due to the strong association of CAD with traumatic factors, in a first contact with the patient there was no suspicion of CAD or stroke (absence of focal deficit). However, late, ICA occlusion on the left and stenosis on the right ICA were identified, resulting in two strokes and severe functional disability at discharge. Conclusion:The diagnosis of CAD is a challenge, especially since it is a multifactorial lesion. However, its early recognition will directly affect the patient's outcome. Therefore, in the presence of any warning symptoms, meticulous questioning about the individual's latest activities is necessary. This study alerts to the adoption of prophylactic conducts in the occurrence of causal factors such as prolonged cervical hyperextension or sudden movements of the cervical. (AU)

Hemostasis in Danio rerio: is the zebrafish a useful model for platelet research?

New scientific models have been established in the past few years to identify novel factors of hemostasis and thrombosis and to analyze their function in greater detail. One fairly new animal model is the zebrafish, Danio rerio, which shares most of the central factors of platelet adhesion, activation, aggregation and release reaction with humans. Examples include GPIIb-IIIa, many other integrins, coagulation factors, inflammatory and cytokine-like proteins as well as arachidonic acid metabolism enzymes. Yet the zebrafish genome has undergone a teleost-specific genome duplication, causing the existence of duplicated paralogues in some instances, and a few genes have not been identified in the zebrafish genome. Taken together the high fecundity of the zebrafish, the possibility to observe transparent developing embryos in real time, the availability of a large number of mutants and transgenics as well as the possibility to knock down gene function by microinjection of morpholino antisense oligonucleotides and the similarity of the hemostatic system are important assets of the zebrafish, promising that it will be an attractive model to study thrombocyte function, thrombosis and hemostasis. This review provides an overview of the central factors of thrombocyte function identified so far in the zebrafish genome and a compilation of methods and tools available for the study of thrombocyte development and function in zebrafish.

Sequence analysis of zebrafish chondromodulin-1 and expression profile in the notochord and chondrogenic regions during cartilage morphogenesis.

Chondromodulin-I (ChM-I) is suggested in higher vertebrate systems to function as a key regulatory protein for cartilage development. To further understand the process of chondrogenesis and the function of ChM-I, we have cloned the zebrafish cDNA for chondromodulin-1 (chm1) and have mapped the chm1 gene locus. The expression profile of chm1 was determined during zebrafish embryonic development and compared to that of type II collagen (col2a1). Maternal chm1 transcripts were detected before midblastula transition and zygotic expression of chm1 was first observed in the notochord at the 10-somite stage. At later developmental stages, chm1 expression was detected in areas surrounding the otic vesicles, in the developing craniofacial cartilage elements, and in the chondrogenic region of the pectoral fins.

Collagen content of alveolar wall tissue in emphysematous and non-emphysematous lungs.

BACKGROUND: Emphysema is currently defined as "a condition of the lung characterised by abnormal, permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls, and without obvious fibrosis." The functional and morphological changes that occur in emphysema have largely been attributed to changes in alveolar elastin rather than in collagen. A study was performed to determine whether the amount of collagen in the alveolar wall changes with age in the lungs of non-smokers and of smokers with different types of macroscopically defined emphysema in relation to a microscopic measurement of lung structure. METHODS: Total alveolar wall collagen was measured (as hydroxyproline) in known volumes of distended lung tissue (by reverse phase high pressure liquid chromatography) in the lungs of non-smokers (n = 23) and in regions sampled away from emphysematous lesions in the lungs of 36 smokers (four with no emphysema, 13 with centriacinar emphysema (CAE), nine with panacinar emphysema (PAE), and 10 with a mixture (MIX) of both PAE and CAE). Mean lung airspace wall surface area per unit volume (AWUV) was calculated from at least six random blocks per lung and on histological sections immediately adjacent to those prepared for collagen measurement with a rapid scanning device (fast interval processor). RESULTS: In non-smokers there was no significant correlation between the amount of collagen in the alveolar wall tissue and either mean lung AWUV or increasing patient age when amounts of collagen were expressed either per unit volume of distended lung (40 mm3 sample) or per unit surface area of airspace wall tissue. Smokers without emphysema had similar amounts of collagen to non-smokers. Lungs with PAE and MIX, but not CAE alone, contained significantly more collagen than normal when expressed per unit volume of airspace wall tissue whereas all groups, including CAE, contained significantly raised amounts of collagen when expressed per unit surface area. CONCLUSIONS: There is no significant age related change in the collagen content of the lungs of non-smokers which suggests that, as AWUV is lost with age, the main collagenous framework is maintained. However, in smokers with emphysema there is a loss of airspace wall tissue in regions remote from the macroscopic lesions that is accompanied by a net increase in collagen mass. The greater accumulation of collagen in MIX lungs than in CAE lungs suggests a greater degree of structural damage, indicative of an alternative pathogenetic mechanism operating between the different types of emphysema. Our results suggest an active alveolar wall fibrosis in emphysema as a consequence of cigarette smoking. It is suggested that the definition of emphysema may require further revision to include such change.

Quantitative studies of human lung airspace wall in relation to collagen and elastin content.

Biochemical determinations of the collagen and elastin content in 50 mm3 samples of human lung are presented in relation to morphometric measurements of lung structure, as the amount of alveolar wall surface area per unit volume (AWUV), on adjacent slices. There were no differences in AWUV values, collagen content (determined as hydroxyproline) or elastin content (determined as isodesmosine) between upper and lower lobes within a single lung. In a study of 102 samples from 9 smokers lungs with no evidence of macro- or microscopic emphysema (as estimated by AWUV measurement), there was a negative correlation between AWUV and the amounts of collagen or elastin per unit volume of inflated lung. The correlation was stronger when collagen and elastin content were expressed per unit area of alveolar wall. The negative correlation is interpreted as representing either the anatomical variation within the complex hierarchy of normal lung structure or possibly low levels of fibrosis in response to cigarette smoking.