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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
        <publisher-loc>S&#227;o Paulo, SP, Brazil</publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v3">x5nBSksd9kv5sMQpMsKysbj</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2013000200016</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(13)10000200016</article-id>
      <article-id pub-id-type="doi">10.5935/abc.20130037</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Correla&#231;&#227;o Anatomocl&#237;nica</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Caso 1/2013: homem de 69 anos com dor s&#250;bita em dorso e membro inferior direito e choque</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Espirito Santo</surname>
            <given-names>Carlos Vin&#237;cius Abreu do</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Franco</surname>
            <given-names>Rafael Alves</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Benvenuti</surname>
            <given-names>Luiz Alberto</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">S&#227;o Paulo</named-content>
        </addr-line>
        <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
        <institution content-type="orgdiv1">FM </institution>
        <institution content-type="orgdiv2">HC</institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>02</month>
        <year>2013</year>
      </pub-date>
      <volume>100</volume>
      <issue>2</issue>
      <fpage>e16</fpage>
      <lpage>e20</lpage>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/" xml:lang="en">
          <license-p>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>MSM, homem, 69 anos, procurou atendimento m&#233;dico por dor em dorso esquerdo e membro inferior direito. A radiografia de t&#243;rax revelou alargamento do mediastino. Estava em observa&#231;&#227;o quando apresentou rebaixamento da consci&#234;ncia e choque. Foi observado enfisema subcut&#226;neo em hemit&#243;rax esquerdo e aboli&#231;&#227;o do murm&#250;rio vesicular em base do mesmo pulm&#227;o. Foi feita a intuba&#231;&#227;o orotraqueal e realizada drenagem de hemit&#243;rax esquerdo, com sa&#237;da de l&#237;quido serossanguinolento. O ecocardiograma revelou ventr&#237;culo esquerdo (D/S): 44/29 mm; septo 12 mm; parede posterior 13 mm; discreta dilata&#231;&#227;o em raiz da aorta, presen&#231;a de l&#226;mina de dissec&#231;&#227;o e hematoma peria&#243;rtico. As valvas e peric&#225;rdio eram normais. O paciente foi transferido para o InCor. O exame f&#237;sico (21 out 2004: 10h45) revelou paciente sedado, com intuba&#231;&#227;o orotraqueal, com palidez cut&#226;nea, frequ&#234;ncia card&#237;aca 90 bpm, press&#227;o arterial 130 x 80 mmHg, drenagem tor&#225;cica sanguinolenta do dreno t&#243;rax. Eletrocardiograma - frequ&#234;ncia 90 bpm, ritmo sinusal, baixa voltagem no plano frontal e diminui&#231;&#227;o de voltagem em deriva&#231;&#245;es esquerdas (fig. 1). A tomografia revelou enfisema subcut&#226;neo bilateral, aorta tor&#225;cica com contornos imprecisos na sua por&#231;&#227;o descendente (da art&#233;ria subcl&#225;via at&#233; por&#231;&#227;o m&#233;dia), colapso do pulm&#227;o esquerdo e grande cole&#231;&#227;o de caracter&#237;sticas hem&#225;ticas em mesmo hemit&#243;rax e no mediastino m&#233;dio e posterior. Pequeno pneumot&#243;rax &#224; direita; pequeno derrame pleural &#224; direita com altera&#231;&#245;es do par&#234;nquima subjacente. A an&#225;lise do cora&#231;&#227;o foi prejudicada pela presen&#231;a do hemot&#243;rax. Durante a realiza&#231;&#227;o de tomografia apresentou aus&#234;ncia de pulsos, midr&#237;ase, com assistolia, sem resposta &#224;s manobras de ressuscita&#231;&#227;o e faleceu (21 out 2011; 15h).</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>S&#237;ndrome Coronariana Aguda</kwd>
        <kwd>Embolia Pulmonar</kwd>
        <kwd>Pneumot&#243;rax</kwd>
        <kwd>Aorta Tor&#225;cica</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>11</day>
        <month>03</month>
        <year>2013</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>CORRELA&#199;&#195;O ANATOMOCL&#205;NICA</bold>
    </p>
    <p>
      <bold>Caso 1/2013 - homem de 69 anos com dor s&#250;bita em dorso e membro inferior direito e choque</bold>
    </p>
    <p>
      <bold>Carlos Vin&#237;cius Abreu do Espirito Santo, Rafael Alves Franco, Luiz Alberto Benvenuti</bold>
    </p>
    <p>Instituto do Cora&#231;&#227;o (InCor), HC-FMUSP, S&#227;o Paulo, SP - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p>MSM, homem, 69 anos, procurou atendimento m&#233;dico por dor em dorso esquerdo e membro inferior direito. </p>
    <p> A radiografia de t&#243;rax revelou alargamento do mediastino. </p>
    <p> Estava em observa&#231;&#227;o quando apresentou rebaixamento da consci&#234;ncia e choque. Foi observado enfisema subcut&#226;neo em hemit&#243;rax esquerdo e aboli&#231;&#227;o do murm&#250;rio vesicular em base do mesmo pulm&#227;o. </p>
    <p> Foi feita a intuba&#231;&#227;o orotraqueal e realizada drenagem de hemit&#243;rax esquerdo, com sa&#237;da de l&#237;quido serossanguinolento. </p>
    <p> O ecocardiograma revelou ventr&#237;culo esquerdo (D/S): 44/29 mm; septo 12 mm; parede posterior 13 mm; discreta dilata&#231;&#227;o em raiz da aorta, presen&#231;a de l&#226;mina de dissec&#231;&#227;o e hematoma peria&#243;rtico. As valvas e peric&#225;rdio eram normais. </p>
    <p> O paciente foi transferido para o InCor. </p>
    <p> O exame f&#237;sico (21 out 2004: 10h45) revelou paciente sedado, com intuba&#231;&#227;o orotraqueal, com palidez cut&#226;nea, frequ&#234;ncia card&#237;aca 90 bpm, press&#227;o arterial 130 x 80 mmHg, drenagem tor&#225;cica sanguinolenta do dreno t&#243;rax. </p>
    <p> Eletrocardiograma - frequ&#234;ncia 90 bpm, ritmo sinusal, baixa voltagem no plano frontal e diminui&#231;&#227;o de voltagem em deriva&#231;&#245;es esquerdas (fig. 1). </p>
    <p> A tomografia revelou enfisema subcut&#226;neo bilateral, aorta tor&#225;cica com contornos imprecisos na sua por&#231;&#227;o descendente (da art&#233;ria subcl&#225;via at&#233; por&#231;&#227;o m&#233;dia), colapso do pulm&#227;o esquerdo e grande cole&#231;&#227;o de caracter&#237;sticas hem&#225;ticas em mesmo hemit&#243;rax e no mediastino m&#233;dio e posterior. Pequeno pneumot&#243;rax &#224; direita; pequeno derrame pleural &#224; direita com altera&#231;&#245;es do par&#234;nquima subjacente. A an&#225;lise do cora&#231;&#227;o foi prejudicada pela presen&#231;a do hemot&#243;rax. </p>
    <p> Durante a realiza&#231;&#227;o de tomografia apresentou aus&#234;ncia de pulsos, midr&#237;ase, com assistolia, sem resposta &#224;s manobras de ressuscita&#231;&#227;o e faleceu (21 out 2011; 15h).</p>
    <p><bold>Palavras-chave:</bold> S&#237;ndrome Coronariana Aguda, Embolia Pulmonar, Pneumot&#243;rax, Aorta Tor&#225;cica / anormalidades.</p>
    <p>
      <bold>Aspectos cl&#237;nicos</bold>
    </p>
    <p>O caso descrito trata de um paciente do sexo masculino, de 69 anos de idade, sem antecedentes m&#243;rbidos, atendido em uma unidade hospitalar com dor em dorso &#224; esquerda e em membro inferior direito. Partindo dessa queixa, foi iniciado protocolo de investiga&#231;&#227;o da dor tor&#225;cica, sendo realizada radiografia de t&#243;rax, a qual evidenciou alargamento mediastinal, primeiro elemento sugestivo de uma etiologia espec&#237;fica para o caso (presente em 63% dos casos de dissec&#231;&#227;o de aorta ascendente e em 56% dos casos de acometimento da descendente)<sup>1</sup>. Cabe destacar ainda que, em rela&#231;&#227;o aos sintomas iniciais, a dor em membro inferior direito pode surgir no contexto da dissec&#231;&#227;o aguda de aorta com progress&#227;o para segmentos arteriais distais, n&#227;o sendo, por&#233;m, suficiente para confirmar o diagn&#243;stico para o caso, necessitando de investiga&#231;&#227;o complementar espec&#237;fica<sup>2</sup>.</p>
    <p>Durante o per&#237;odo de observa&#231;&#227;o houve piora s&#250;bita do quadro, caracterizada pelo rebaixamento do n&#237;vel de consci&#234;ncia, choque circulat&#243;rio, enfisema subcut&#226;neo e com proped&#234;utica pulmonar de derrame pleural &#224; esquerda, sendo necess&#225;rias medidas invasivas de suporte para estabiliza&#231;&#227;o do caso. Nesse momento, cabe rever as hip&#243;teses iniciais pertinentes quando a dor tor&#225;cica &#233; acompanhada de caracter&#237;sticas de alta letalidade, como a que se apresenta nesse caso (dor, associada a choque circulat&#243;rio):</p>
    <p>&#149; S&#237;ndrome Coronariana Aguda: o Infarto Agudo do Mioc&#225;rdio (IAM), seja pelo acometimento do ventr&#237;culo direito, de grandes &#225;reas do ventr&#237;culo esquerdo (IAM anterior extenso, por exemplo), seja pelo surgimento de complica&#231;&#245;es mec&#226;nicas, poderia justificar esse quadro. Por&#233;m, tal evolu&#231;&#227;o n&#227;o se associa aos achados como enfisema subcut&#226;neo, e seu diagn&#243;stico acompanha-se de achados eletrocardiogr&#225;ficos (supradesnivelamento de ST ou ondas q patol&#243;gicas, por exemplo).</p>
    <p>&#149; Tromboembolismo Pulmonar Maci&#231;o: Associa-se a derrame pleural, como descrito no caso, em at&#233; 40% dos casos, mas muito raramente vem acompanhado de pneumot&#243;rax e enfisema subcut&#226;neo<sup>3</sup>. A literatura traz, na forma de relatos de caso, publica&#231;&#245;es, destacando, por&#233;m, a caracter&#237;stica subaguda dessas complica&#231;&#245;es (dois a quatro dias ap&#243;s o evento). Destaca-se, ainda, a presen&#231;a de sinais eletrocardiogr&#225;ficos de sobrecarga de c&#226;maras direitas e desvio do eixo el&#233;trico, n&#227;o apresentados nesse caso<sup>4</sup>.</p>
    <p>
      <xref ref-type="fig" rid="a16fig01">Figura 1</xref>
    </p>
    <p content-type="asset">
      <fig id="a16fig01">
        <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf01.jpg"/></fig>
    </p>
    <p>&#149; Pneumot&#243;rax Hipertensivo Espont&#226;neo: A associa&#231;&#227;o dessa entidade com dor tor&#225;cica, choque e enfisema subcut&#226;neo &#233; bem descrita; por&#233;m, achados cl&#237;nicos importantes, n&#227;o descritos no caso, como desvio de traqueia, hipertimpanismo e redu&#231;&#227;o global da ausculta pulmonar s&#227;o marcantes. Al&#233;m disso, frequentemente acomente indiv&#237;duos longil&#237;neos e portadores de pneumopatia, e possivelmente j&#225; seria evidenciado &#224; radiografia inicial no pronto-socorro.</p>
    <p>&#149; Dissec&#231;&#227;o A&#243;rtica Complicada (ruptura e isquemia de membro inferior): Pode estar presente no contexto desse caso, apresentando-se com caracter&#237;sticas semelhantes, incluindo rebaixamento do n&#237;vel de consci&#234;ncia, seja por choque circulat&#243;rio (complica&#231;&#227;o de 13% dos casos), seja por extens&#227;o da dissec&#231;&#227;o para a circula&#231;&#227;o encef&#225;lica (8% - 15% dos casos). Al&#233;m disso, sua ruptura pode cursar n&#227;o s&#243; com derrame pleural (hemorr&#225;gico ou sero-hem&#225;tico, sendo esse atribu&#237;do &#224; presen&#231;a de processo inflamat&#243;rio pleural subjacente em 16% dos casos), como tamb&#233;m, ainda que raramente, com pneumot&#243;rax e enfisema subcut&#226;neo s&#250;bitos, relacionados &#224; sua expans&#227;o para par&#234;nquima pulmonar e cavidade pleural posteriormente<sup>5,6</sup>. Kurosaki e cols.6 descreveram um caso de um paciente de 79 anos, com antecedentes de fibrila&#231;&#227;o atrial e ataque isqu&#234;mico transit&#243;rio pr&#233;vios, v&#237;tima de morte s&#250;bita, em que um pneumot&#243;rax hipertensivo ocorreu como consequ&#234;ncia da ruptura de aneurisma de aorta tor&#225;cica.</p>
    <p>A partir da apresenta&#231;&#227;o clinica do caso e dos dados da literatura, as duas &#250;ltimas entidades cl&#237;nicas se colocariam como as principais hipoteses diagn&#243;sticas at&#233; essa fase da evolu&#231;&#227;o.</p>
    <p>O ecocardiograma (provavelmente transesof&#225;gico), bem indicado ante a instabilidade cl&#237;nica do caso, evidenciou a presen&#231;a de l&#226;mina de dissec&#231;&#227;o e hematoma peria&#243;rtico em raiz de aorta, al&#233;m de sinais de hipertrofia ventricular, estabelecendo n&#227;o s&#243; o diagn&#243;stico do caso, mas tamb&#233;m sendo suficiente para a defini&#231;&#227;o da conduta terap&#234;utica apropriada. A sensibilidade e a especificidade do ecocardiograma transesof&#225;gico, nesse contexto, s&#227;o, respectivamente, 98% e 95%7. Al&#233;m disso, a hipertens&#227;o arterial sist&#234;mica, presente em cerca de 72% dos casos de dissec&#231;&#227;o a&#243;rtica, surge como poss&#237;vel doen&#231;a de base e fator de risco para essa complica&#231;&#227;o a partir dos achados ecocardiogr&#225;ficos<sup>8</sup>.</p>
    <p>As dissec&#231;&#245;es de aorta tor&#225;cica s&#227;o mais frequentes no sexo masculino (2:1) e na faixa et&#225;ria entre 60 e 70 anos, sendo classificadas, especialmente pela dura&#231;&#227;o dos sintomas, em agudas e cr&#244;nicas, com o valor de corte de 15 dias para diferenci&#225;-las; e pela localiza&#231;&#227;o, em Stanford tipo A, quando acometem a por&#231;&#227;o ascendente da art&#233;ria, ou Stanford tipo B, quando poupam esse segmento.</p>
    <p>&#192; admiss&#227;o no InCor, chamavam a aten&#231;&#227;o a frequ&#234;ncia card&#237;aca e a press&#227;o arterial, que se encontravam fora das metas estabelecidas para o manejo cl&#237;nico efetivo da fase aguda da dissec&#231;&#227;o aguda de aorta. Entretanto, esses achados poderiam estar relacionados ao poss&#237;vel uso de agentes vasoativos<sup>9</sup>. Al&#233;m disso, o paciente encontrava-se sedado, o que, al&#233;m de dificultar a pesquisa de d&#233;ficits neurol&#243;gicos focais que contribuiriam para o diagn&#243;stico de complica&#231;&#245;es relacionadas &#224; doen&#231;a de base, impediriam a defini&#231;&#227;o de conduta terap&#234;utica cir&#250;rgica, j&#225; que o estado comatoso &#233; contraindica&#231;&#227;o formal para a abordagem invasiva.</p>
    <p>O eletrocardiograma inicial evidenciou ritmo sinusal e baixa voltagem no plano fontal e deriva&#231;&#245;es precordiais esquerdas. Tal achado pode sugerir evolu&#231;&#227;o do caso para uma das complica&#231;&#245;es poss&#237;veis da dissec&#231;&#227;o a&#243;rtica: derrame peric&#225;rdico, que ocorre em cerca de 2% dos casos. Ainda pela an&#225;lise do ECG, outras possibilidades diagn&#243;sticas tornam-se menos prov&#225;veis, como descrito anteriormente.</p>
    <p>A angiotomografia de t&#243;rax, elemento fundamental na investiga&#231;&#227;o diagn&#243;stica e avalia&#231;&#227;o anat&#244;mica da dissec&#231;&#227;o de aorta tor&#225;cica em pacientes com estabilidade hemodin&#226;mica, apresenta sensibilidade e especificidade respectivas de 98% e cerca de 100% nessa entidade. Nesse caso, al&#233;m da demonstra&#231;&#227;o da aorta com contornos imprecisos (sinal indireto de ruptura), evidenciou colapso pulmonar esquerdo, com hemot&#243;rax volumoso ipsilateral, al&#233;m de acometimento de mediastino m&#233;dio e posterior, que podem ser decorrentes da ruptura da aorta para o espa&#231;o pleural e mediastinal e corroboram a hip&#243;tese diagn&#243;stica de dissec&#231;&#227;o de aorta complicada. Deve-se ressaltar, nesse momento, a rara, por&#233;m bem descrita, associa&#231;&#227;o desses casos com pneumot&#243;rax e enfisema subcut&#226;neo<sup>7</sup>.</p>
    <p>A dissec&#231;&#227;o a&#243;rtica traz consigo m&#250;ltiplas associa&#231;&#245;es. Al&#233;m da idade avan&#231;ada e da hipertens&#227;o arterial sist&#234;mica (&#250;nicos fatores de risco suger&#237;veis para esse paciente), poderiamos citar, por exemplo, valva a&#243;rtica bivalvulada (5%-7% dos casos), manipula&#231;&#227;o cir&#250;rgica pr&#233;via, coarcta&#231;&#227;o de aorta e uso de coca&#237;na (1% dos casos), n&#227;o facilmente indentific&#225;veis nesse caso. Ainda, cabe citar a s&#237;ndrome de Marfan (5% dos casos), que pode contemplar, durante sua hist&#243;ria natural, a associa&#231;&#227;o de dissec&#231;&#227;o a&#243;rtica e acometimento pulmonar, na forma de pneumot&#243;rax, por&#233;m, muito dificilmente, em concomit&#226;ncia cl&#237;nica<sup>1,9,10</sup>.</p>
    <p>
      <bold>(Dr. Carlos Vin&#237;cius Abreu do Espirito Santo, Dr. Rafael Alves Franco)</bold>
    </p>
    <p>
      <bold>Hip&#243;tese diagn&#243;stica</bold>
    </p>
    <p>O paciente evoluiu, durante a TC de t&#243;rax, com Parada Cardiorrespirat&#243;ria (PCR) em assistolia. Tal evolu&#231;&#227;o nos remete a poss&#237;veis etiologias para o desfecho<sup>11</sup>:</p>
    <p>&#149; Hipovolemia: Por ruptura da aorta e sangramento maci&#231;o.</p>
    <p>&#149; Tamponamento card&#237;aco: Por dissec&#231;&#227;o retr&#243;grada para o saco peric&#225;rdico (n&#227;o evidenciado na avalia&#231;&#227;o ecocardiogr&#225;fica inicial).</p>
    <p>&#149; Infarto agudo do mioc&#225;rdio: Por dissec&#231;&#227;o retrograda dos &#243;stios coronarianos.</p>
    <p>&#149; Hip&#243;xia: Pelo colapso do pulm&#227;o esquerdo e derrame pleural &#224; direita evidenciados &#224; tomografia, associados aos riscos de transporte de pacientes.</p>
    <p>Finalmente, diante do quadro descrito, destacam-se como hip&#243;teses diagn&#243;ticas as seguintes condi&#231;&#245;es: dissec&#231;&#227;o aguda de aorta tor&#225;cica (Stanford tipo A), evoluindo com choque, decorrente de ruptura a&#243;rtica com hipovolemia e/ou pneumot&#243;rax hipertensivo. </p>
    <p>
      <bold>(Dr. Carlos Vin&#237;cius Abreu do Espirito Santo, Dr. Rafael Alves Franco)</bold>
    </p>
    <p>
      <bold>Necropsia</bold>
    </p>
    <p>&#192; abertura da cavidade tor&#225;cica foi detectado extenso hemot&#243;rax com co&#225;gulos do lado esquerdo, o que constituiu a causa terminal do &#243;bito. O cora&#231;&#227;o apresentava volume normal e pesou 320 g. Corte transversal dos ventr&#237;culos mostrou cavidades normais e discreta proemin&#234;ncia da massa ventricular esquerda; a parede livre desse ventr&#237;culo mediu 14 mm de espessura (<xref ref-type="fig" rid="a16fig02">fig. 2</xref>). A valva a&#243;rtica era trivalvulada, sem altera&#231;&#245;es anatomopatol&#243;gicas. Havia extensa hemorragia na advent&#237;cia do segmento inicial da aorta tor&#225;cica descendente. O exame interno da aorta evidenciou segmento ascendente preservado, com per&#237;metro de 70 mm, estreitamento abrupto na regi&#227;o do istmo, com per&#237;metro de 58 mm (coarcta&#231;&#227;o do arco a&#243;rtico) e discreta dilata&#231;&#227;o p&#243;s-esten&#243;tica do in&#237;cio do segmento tor&#225;cico descendente (per&#237;metro de 78 mm); nessa &#250;ltima regi&#227;o, e distando 25 mm da emerg&#234;ncia da art&#233;ria subcl&#225;via esquerda, havia rasgadura longitudinal da parede a&#243;rtica, medindo 20 mm de extens&#227;o, que constitu&#237;a orif&#237;cio de entrada de dissec&#231;&#227;o aguda da aorta (<xref ref-type="fig" rid="a16fig03">fig. 3</xref>). A dissec&#231;&#227;o da parede a&#243;rtica progredia por toda sua extens&#227;o, prolongando-se pelas art&#233;rias il&#237;acas e femorais, sem orif&#237;cio de reentrada; havia dissec&#231;&#227;o retr&#243;grada de pequena extens&#227;o da aorta tor&#225;cica descendente, mas n&#227;o do arco a&#243;rtico ou da aorta ascendente. O exame histol&#243;gico da aorta confirmou a dissec&#231;&#227;o aguda da parede e n&#227;o evidenciou processo inflamat&#243;rio. A aterosclerose da aorta era de grau discreto, com poucas placas calcificadas no segmento abdominal. Os rins apresentavam volume normal e pequenas depress&#245;es cicatriciais na superf&#237;cie, sendo evidente a presen&#231;a de arterioloesclerose hialina ao exame histol&#243;gico (<xref ref-type="fig" rid="a16fig04">fig. 4</xref>). Havia c&#225;lculo &#250;nico na ves&#237;cula biliar, enegrecido, medindo 4 mm.</p>
    <p content-type="asset">
      <fig id="a16fig02">
        <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf02.jpg"/></fig>
    </p>
    <p content-type="asset">
      <fig id="a16fig03">
        <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf03.jpg"/></fig>
    </p>
    <p content-type="asset">
      <fig id="a16fig04">
        <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf04.jpg"/></fig>
    </p>
    <p>
      <bold>(Dr. Luiz Alberto Benvenuti)</bold>
    </p>
    <p>
      <bold>Diagn&#243;sticos anatomopatol&#243;gicos</bold>
    </p>
    <p>Coarcta&#231;&#227;o do arco a&#243;rtico na regi&#227;o do istmo; dissec&#231;&#227;o aguda da aorta, rota; nefroesclerose benigna, discreta; calculose da ves&#237;cula biliar; hemot&#243;rax &#224; esquerda (causa do &#243;bito).</p>
    <p>
      <bold>(Dr. Luiz Alberto Benvenuti)</bold>
    </p>
    <p>
      <bold> Coment&#225;rios</bold>
    </p>
    <p>Caso de homem de 69 anos que apresentou dissec&#231;&#227;o aguda da aorta, confirmada pelo exame ecocardiogr&#225;fico, associada a enfisema subcut&#226;neo e hemot&#243;rax &#224; esquerda, evoluindo com rebaixamento da consci&#234;ncia e choque hemodin&#226;mico. N&#227;o &#233; referida na hist&#243;ria a presen&#231;a de hipertens&#227;o arterial sist&#234;mica, mas o paciente n&#227;o apresentava acompanhamento m&#233;dico conhecido. A necropsia confirmou o diagn&#243;stico de dissec&#231;&#227;o aguda da aorta, com ruptura para o hemit&#243;rax esquerdo. A dissec&#231;&#227;o originava-se na aorta tor&#225;cica descendente e n&#227;o acometia os segmentos proximais do vaso, sendo, portanto, classificada como tipo IIIb de DeBakey ou tipo B de Stanford. Foi ainda detectada coarcta&#231;&#227;o do arco a&#243;rtico, localizada na regi&#227;o do istmo, com estenose luminal de grau moderado. A valva a&#243;rtica era normal. Encontramos evid&#234;ncias anatomopatol&#243;gicas de hipertens&#227;o arterial sist&#234;mica, com arterioloesclerose hialina renal, mas como n&#227;o havia hipertrofia significativa do ventr&#237;culo esquerdo, com peso card&#237;aco dentro dos limites da normalidade, provavelmente a altera&#231;&#227;o press&#243;rica era de pequena monta.</p>
    <p>O fator de risco mais comum para a dissec&#231;&#227;o aguda da aorta &#233; a hipertens&#227;o arterial sist&#234;mica, mas tamb&#233;m deve ser lembrada a associa&#231;&#227;o com doen&#231;as do tecido conjuntivo, particularmente a s&#237;ndrome de Marfan, e a valva a&#243;rtica bivalvulada. Entretanto, quando se analisam apenas as dissec&#231;&#245;es de tipo III, ou seja, as que se originam na aorta tor&#225;cica descendente, a frequ&#234;ncia da hipertens&#227;o arterial sist&#234;mica &#233; ainda mais elevada e n&#227;o h&#225; associa&#231;&#227;o estat&#237;stica com valva a&#243;rtica bivalvulada<sup>12</sup>. Por outro lado, existem condi&#231;&#245;es mais raras que se associam &#224; dissec&#231;&#227;o aguda da aorta, como gravidez, cirurgia card&#237;aca pr&#233;via, trauma tor&#225;cico, aortite de c&#233;lulas gigantes, coarcta&#231;&#227;o da aorta e outras. De fato, existem v&#225;rias publica&#231;&#245;es pr&#233;vias relatando associa&#231;&#227;o de coarcta&#231;&#227;o da aorta com dissec&#231;&#227;o aguda da aorta, como no presente caso<sup>13-15</sup>. Obviamente a corre&#231;&#227;o da condi&#231;&#227;o (coarcta&#231;&#227;o da aorta e dissec&#231;&#227;o aguda) &#233; cir&#250;rgica, podendo ocorrer em dois tempos ou mesmo simultaneamente<sup>16</sup>. Finalmente, &#233; interessante comentar que no presente caso a valva a&#243;rtica n&#227;o era bivalvulada, altera&#231;&#227;o frequentemente associada &#224; coarcta&#231;&#227;o da aorta.</p>
    <p>
      <bold>(Dr. Luiz Alberto Benvenuti)</bold>
    </p>
    <p>
      <fn id="end" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Vera Demarchi Aiello </p>
        <p> Av. Dr En&#233;as C. Aguiar, 44, Sub-solo, bloco I, Cerqueira C&#233;sar </p>
        <p> CEP 05403-000, S&#227;o Paulo, SP - Brasil </p>
        <p> E-mail: </p>
        <p><email xlink:href="demarchi@cardiol.br">demarchi@cardiol.br</email>, </p>
        <p>
          <email xlink:href="vera.aiello@incor.usp.br">vera.aiello@incor.usp.br</email>
        </p>
      </fn>
    </p>
    <p><bold>Editor da Se&#231;&#227;o:</bold> Alfredo Jos&#233; Mansur (<email xlink:href="ajmansur@incor.usp.br">ajmansur@incor.usp.br</email>) </p>
    <p><bold>Editores Associados:</bold> Desid&#233;rio Favarato (<email xlink:href="dclfavarato@incor.usp.br">dclfavarato@incor.usp.br</email>). Vera Demarchi Aiello (<email xlink:href="anpvera@incor.usp.br">anpvera@incor.usp.br</email>)</p>
  </body>
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            </name>
            <name>
              <surname>Dodd</surname>
              <given-names>MJ</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B16">
        <mixed-citation>16. Cranfield KR, Brackenbury ET, Fraser SC. One-stage repair of an aortic dissection and aortic coarctation. Interact Cardiovasc Thorac Surg. 2008;7(1):170-2.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>One-stage repair of an aortic dissection and aortic coarctation</article-title>
          <source>Interact Cardiovasc Thorac Surg</source>
          <date>
            <year>2008</year>
          </date>
          <fpage>170</fpage>
          <lpage>2</lpage>
          <issue>1</issue>
          <volume>7</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Cranfield</surname>
              <given-names>KR</given-names>
            </name>
            <name>
              <surname>Brackenbury</surname>
              <given-names>ET</given-names>
            </name>
            <name>
              <surname>Fraser</surname>
              <given-names>SC</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
    </ref-list>
  </back>
  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Anatomopathological Session</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Case 1/2013: 69-year-old male patient with sudden back and lower right limb pain and shock</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>The patient, MSM, a 69-year-old man, sought medical care due to left dorsal and right lower limb pain. The chest x-ray showed mediastinal enlargement. He was undergoing examination when he lost consciousness and went into shock. Subcutaneous emphysema was observed in the left hemithorax, as well as abolition of breath sounds at auscultation. Tracheal intubation was performed with draining of blood-tinged fluid from the left hemithorax. Echocardiography showed left ventricle with 44/29 mm; septum, 12 mm; posterior wall, 13 mm; mild aortic root dilation, dissection of the lamina and periaortic hematoma. The valves and pericardium were normal. The patient was transferred to Instituto do Cora&#231;ao - InCor. Physical examination (21 Oct 2004: 10:45) showed that the patient was sedated with tracheal intubation, pale, heart rate at 90 bpm, blood pressure 130 x 80 mmHg, bloody drainage in the chest tube. Electrocardiogram - frequency 90 bpm, sinus rhythm, low voltage in the frontal plane and decreased voltage in left leads (Fig. 1). Computed tomography showed bilateral subcutaneous emphysema, thoracic aorta with inaccurate borders in its descending portion (from the subclavian artery to the middle portion), collapsed left lung and extensive collection of hematic characteristics in same hemithorax and middle and posterior mediastinum. Small right pneumothorax; small right pleural effusion with underlying parenchymal alterations. The analysis of the heart was impaired by the presence of hemothorax. While undergoing computed tomography, the patient showed no pulse, mydriasis, with asystole unresponsive to resuscitation and died (21 Oct 2011; 15:00 h).</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Acute Coronary Syndrome</kwd>
        <kwd>Pulmonary Embolism</kwd>
        <kwd>Pneumothorax</kwd>
        <kwd>Aorta, Thoracic</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ANATOMOPATHOLOGICAL SESSION</bold>
      </p>
      <p>
        <fn id="enda-body2">
          <label>
            <bold>Case 1/2013 - 69-year-old male patient with sudden back and lower right limb pain and shock</bold>
          </label>
          <p>
            <bold>Carlos Vin&#237;cius Abreu do Espirito Santo; Rafael Alves Franco; Luiz Alberto Benvenuti</bold>
          </p>
        </fn>
      </p>
      <p>Instituto do Cora&#231;&#227;o (InCor), HC-FMUSP, S&#227;o Paulo, SP - Brazil</p>
      <p>Mailing Address</p>
      <p>
        <bold>ABSTRACT</bold>
      </p>
      <p>The patient, MSM, a 69-year-old man, sought medical care due to left dorsal and right lower limb pain.</p>
      <p> The chest x-ray showed mediastinal enlargement.</p>
      <p> He was undergoing examination when he lost consciousness and went into shock. Subcutaneous emphysema was observed in the left hemithorax, as well as abolition of breath sounds at auscultation. Tracheal intubation was performed with draining of blood-tinged fluid from the left hemithorax.</p>
      <p> Echocardiography showed left ventricle with 44/29 mm; septum, 12 mm; posterior wall, 13 mm; mild aortic root dilation, dissection of the lamina and periaortic hematoma. The valves and pericardium were normal.</p>
      <p> The patient was transferred to Instituto do Cora&#231;ao - InCor. </p>
      <p> Physical examination (21 Oct 2004: 10:45) showed that the patient was sedated with tracheal intubation, pale, heart rate at 90 bpm, blood pressure 130 x 80 mmHg, bloody drainage in the chest tube. Electrocardiogram - frequency 90 bpm, sinus rhythm, low voltage in the frontal plane and decreased voltage in left leads (Fig. 1).</p>
      <p> Computed tomography showed bilateral subcutaneous emphysema, thoracic aorta with inaccurate borders in its descending portion (from the subclavian artery to the middle portion), collapsed left lung and extensive collection of hematic characteristics in same hemithorax and middle and posterior mediastinum. Small right pneumothorax; small right pleural effusion with underlying parenchymal alterations. The analysis of the heart was impaired by the presence of hemothorax.</p>
      <p> While undergoing computed tomography, the patient showed no pulse, mydriasis, with asystole unresponsive to resuscitation and died (21 Oct 2011; 15:00 h).</p>
      <p><bold>Keywords:</bold> Acute Coronary Syndrome; Pulmonary Embolism; Pneumothorax; Aorta, Thoracic / abnormalities.</p>
      <p>
        <bold>Clinical aspects</bold>
      </p>
      <p>The case described is a previously healthy, 69-year-old male patient, treated in a hospital with pain in the left back region and right lower limb. Based on this complaint, chest pain protocol was initiated and a chest radiography was performed, which showed mediastinal enlargement, first element suggestive of a specific etiology for the case (present in 63% of cases of ascending aortic dissection and in 56 % of cases of descending aorta involvement)<sup>1</sup>. It is worth noting that, in relation to the initial symptoms, pain in the right lower limb may arise in the context of acute aortic dissection with progression to distal arterial segments, although not sufficient, however, to confirm the diagnosis for the case, requiring specific additional investigation<sup>2</sup>.</p>
      <p>During the observation period there was a sudden worsening of the picture, characterized by decreased level of consciousness, circulatory shock and subcutaneous emphysema, with pulmonary propedeutics of left pleural effusion, requiring invasive measures of support for stabilization. At this point, it is appropriate to review the initial hypotheses when chest pain is accompanied by high mortality characteristics, such as those presented in this case (pain associated with circulatory shock):</p>
      <p>&#149; Acute Coronary Syndrome: Acute Myocardial Infarction (AMI), either through the involvement of the right ventricle, large areas of the left ventricle (extensive anterior AMI, for instance), or the onset of mechanical complications, could justify this picture. However, this evolution is not associated with findings such as subcutaneous emphysema, and its diagnosis is accompanied by electrocardiographic findings (ST-segment elevation or pathological Q waves, for instance).</p>
      <p>&#149; Massive Pulmonary Thromboembolism: It is associated with pleural effusion, as described in this case, in up to 40% of cases, but is very rarely accompanied by pneumothorax and subcutaneous emphysema<sup>3</sup>. The literature has publications in the form of case reports; however, they stress the subacute characteristic of these complications (two to four days after the event). Noteworthy is also the presence of electrocardiographic signs of right chamber overload and electrical axis deviation, not shown in this case<sup>4</sup>.</p>
      <p>&#149; Spontaneous Hypertensive Pneumothorax: The association of this entity with chest pain, shock and subcutaneous emphysema is well described; however, important clinical findings not described in this case, such as tracheal deviation, hypertympanism and overall decreased pulmonary auscultation are striking. In addition, it often affects slim individuals with lung diseases and it possibly would have identified at the initial radiograph in the emergency room.</p>
      <p>
        <xref ref-type="fig" rid="en_a16fig01-body2">Figure 1</xref>
      </p>
      <p content-type="asset">
        <fig id="en_a16fig01-body2">
          <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf01-en.jpg"/></fig>
      </p>
      <p>&#149; Complicated Aortic Dissection (rupture and ischemia of lower limb): It may be present in the context of this case, presenting with similar characteristics, including decreased level of consciousness, either by circulatory shock (complication of 13% of cases), or by the extension of dissection to the brain circulation (8% - 15% cases). Moreover, its rupture can course not only with pleural effusion (hemorrhagic or serohematic, with this being attributed to the underlying presence of pleural inflammatory process in 16% of cases), but also, albeit rarely, with sudden pneumothorax and subcutaneous emphysema, related to its expansion into the lung parenchyma and subsequently, to the pleural cavity<sup>5,6</sup>. Kurosaki et al.<sup>6</sup> described the case of a 79-year-old patient with a history of atrial fibrillation and previous transient ischemic attack, who was a victim of sudden death, in whom a hypertensive pneumothorax occurred as a result of ruptured thoracic aortic aneurysm.</p>
      <p>Based on the clinical case presentation and literature data, the last two clinical entities would be the main diagnostic hypotheses until this phase of evolution.</p>
      <p>The echocardiogram (probably transesophageal), well indicated considering the clinical instability of the case, showed dissection of the lamina and periaortic hematoma and signs of ventricular hypertrophy, establishing not only the case diagnosis, but also being sufficient to define the appropriate therapeutic measures. The sensitivity and specificity of transesophageal echocardiography in this context are, respectively, 98% and 95%7. Furthermore, arterial hypertension, present in about 72% of cases of aortic dissection, emerges as a possible underlying disease and a risk factor for this complication based on the echocardiographic findings<sup>8</sup>.</p>
      <p>Thoracic aortic dissections are more common in males (2:1) and at the age range of 60 to 70 years, being classified, particularly by duration of symptoms, as acute or chronic, with a cutoff of 15 days to differentiate them; and by location as Stanford type A, when they involve the ascending portion of the artery, or Stanford type B when they spare this segment. </p>
      <p>At admission in InCor, the heart rate and blood pressure were noteworthy, which were outside the established targets for effective clinical management of acute aortic dissection. However, these findings could be related to the possible use of vasoactive agents<sup>9</sup>. Furthermore, the patient was sedated, which in addition to hindering the assessment of focal neurological deficits that would contribute to the diagnosis of complications related to the underlying disease, would also prevent the definition of the surgical therapeutic approach, as the comatose state is a formal contraindication to the invasive approach. </p>
      <p>The initial electrocardiogram showed sinus rhythm and low voltage in the frontal plane and left precordial leads. This finding may suggest evolution of the case to one of the possible complications of aortic dissection: pericardial effusion, which occurs in about 2% of cases. Also through the analysis of the ECG, other diagnostic possibilities become less likely, as described above.</p>
      <p>The chest angiotomography, a key element in the diagnostic investigation and anatomic evaluation of thoracic aortic dissection in patients with hemodynamic stability, has a respective sensitivity and specificity of 98% and approximately 100% in this entity. In this case, in addition to demonstrating the inaccurate borders of the aorta (indirect sign of rupture), it showed left lung collapse, with massive ipsilateral hemothorax, in addition to involvement of the middle and posterior mediastinum, which may be due to aortic rupture into the pleural and mediastinal space and corroborate the diagnosis of complicated aortic dissection. It should be noted, at this moment, the rare but well-described association of these cases with pneumothorax and subcutaneous emphysema<sup>7</sup>.</p>
      <p>Aortic dissection carries multiple associations. In addition to the advanced age and hypertension (the only risk factors suggested for this patient), we could cite, for example, bicuspid aortic valve (5%-7% of cases), previous surgical manipulation, aortic coarctation and cocaine use (1% of the cases), not easily identifiable in this case. Moreover, it is worth mentioning Marfan syndrome (5% of cases), which can contemplate during its natural history, the association of aortic dissection and pulmonary involvement in the form of pneumothorax, but which are very rarely clinically concomitant<sup>1,9,10</sup>.</p>
      <p>
        <bold>(Dr. Carlos Vin&#237;cius Abreu do Espirito Santo, Dr. Rafael Alves Franco)</bold>
      </p>
      <p>
        <bold>Diagnostic hypothesis</bold>
      </p>
      <p>The patient developed Cardiopulmonary Arrest (CPA) with asystole during chest CT. This evolution leads us to possible etiologies for the outcome<sup>11</sup>:</p>
      <p>&#149; Hypovolemia: due to aortic rupture and massive bleeding.</p>
      <p>&#149; Cardiac tamponade: due to retrograde dissection into the pericardial sac (not shown in the initial echocardiographic evaluation).</p>
      <p>&#149; Acute Myocardial Infarction: due to retrograde dissection of the coronary ostia.</p>
      <p>&#149; Hypoxia: due to left lung collapse and pleural effusion to the right demonstrated at the tomography, associated with risks of transporting patients.</p>
      <p>Finally, for the clinical picture described here, there are two diagnostic hypotheses to be considered: acute dissection of the thoracic aorta (Stanford type A), progressing to shock due to aortic rupture with hypovolemia and / or hypertensive pneumothorax.</p>
      <p>
        <bold>(Dr. Carlos Vin&#237;cius Abreu do Espirito Santo, Dr. Rafael Alves Franco)</bold>
      </p>
      <p>
        <bold>Necropsy</bold>
      </p>
      <p>After opening the thoracic cavity, extensive hemothorax was detected with clots on the left side, which was the final cause of death. The heart had normal volume and weighed 320 g. Cross-section of the ventricles showed normal cavities and slight prominence of the left ventricular mass; the free wall of this ventricle measured 14 mm in thickness (<xref ref-type="fig" rid="en_a16fig02-body2">Fig. 2</xref>). The aortic valve presented three leaflets, with no pathological alterations. There was extensive hemorrhage in the adventitia of the initial segment of the descending thoracic aorta. The internal examination of the aorta showed the preserved ascending segment, with a perimeter of 70 mm, abrupt narrowing in the isthmus region, with a perimeter of 58 mm (coarctation of the aortic arch) and mild post-stenotic dilation in the beginning of descending thoracic segment (perimeter of 78 mm); in this latter region, and 25 mm distally from the emergence of the left subclavian artery there was a longitudinal tear in the aortic wall, measuring 20 mm long, which constituted the site of acute dissection of the aorta (<xref ref-type="fig" rid="en_a16fig03-body2">Fig. 3</xref>). The dissection of the aortic wall progressed throughout its length, extending through the femoral and iliac arteries without reentry; there was a small retrograde dissection in the descending thoracic aorta, but not of the aortic arch or ascending aorta.</p>
      <p content-type="asset">
        <fig id="en_a16fig02-body2">
          <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf02-en.jpg"/></fig>
      </p>
      <p content-type="asset">
        <fig id="en_a16fig03-body2">
          <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf03-en.jpg"/></fig>
      </p>
      <p>Histological examination confirmed the aortic wall dissection and showed no inflammatory process. Aorta atherosclerosis was mild, with few calcified plaques in the abdominal segment. The kidneys showed normal volume and small cicatricial depressions on the surface, showing the presence of hyaline arteriolosclerosis on histological examination (<xref ref-type="fig" rid="en_a16fig04-body2">Fig. 4</xref>). There was a single calculus in the gallbladder, blackened, measuring 4 mm.</p>
      <p content-type="asset">
        <fig id="en_a16fig04-body2">
          <graphic xlink:href="1678-4170-abc-100-02-0e16-30037-gf04-en.jpg"/></fig>
      </p>
      <p>
        <bold>(Dr. Luiz Alberto Benvenuti)</bold>
      </p>
      <p>
        <bold>Anatomopathological diagnoses</bold>
      </p>
      <p>Coarctation of the aortic arch at the isthmus region; ruptured acute aortic dissection; benign and mild nephrosclerosis; gallbladder calculosis; left hemothorax (cause of death). </p>
      <p>
        <bold>(Dr. Luiz Alberto Benvenuti)</bold>
      </p>
      <p>
        <bold>Comments</bold>
      </p>
      <p>This is the case of a 69-year-old man who presented with acute aortic dissection, confirmed by echocardiography, associated with subcutaneous emphysema and left hemothorax, evolving with loss of consciousness and hemodynamic shock. The presence of systemic arterial hypertension is not mentioned in the history, but the patient had no known medical follow-up.</p>
      <p>The necropsy confirmed the diagnosis of acute aortic dissection, with rupture into the left hemithorax. The dissection originated in the descending thoracic aorta and did not affect the proximal segments of the vessel, and was therefore classified as DeBakey type IIIb or Stanford type B. Coarctation of the aortic arch was also detected, located in the isthmus region, with moderate luminal stenosis. The aortic valve was normal. We found anatomopathological evidence of systemic arterial hypertension, with renal hyaline arteriolosclerosis, but there was no significant left ventricular hypertrophy, heart weight was within normal limits, and probably the blood pressure alteration was a minor one.</p>
      <p>The most common risk factor for acute aortic dissection is hypertension, but one should also remember the association with connective tissue diseases, particularly Marfan syndrome and bicuspid aortic valve. However, when considering only the type III dissections, i.e., those that originate in the descending thoracic aorta, the frequency of systemic arterial hypertension is even higher and there is no statistical association with bicuspid aortic valve<sup>12</sup>.</p>
      <p>On the other hand, there are even rarer conditions associated with acute aortic dissection, such as pregnancy, heart surgery, chest trauma, giant cell aortitis, coarctation of the aorta and others. In fact, there have been several previous publications that reported an association between coarctation of the aorta with acute aortic dissection, as in this case<sup>13-15</sup>. Obviously the correction of the condition (aortic coarctation and acute dissection) is surgical and may occur at different times or even simultaneously<sup>16</sup>. Finally, it is interesting to mention that in this case the aortic valve was not bicuspid, an alteration often associated with coarctation of the aorta. </p>
      <p>
        <bold>(Dr. Luiz Alberto Benvenuti)</bold>
      </p>
      <p>
        <bold>References</bold>
      </p>
    </body>
  </sub-article>
</article>
