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What you did was very, very wrong. Security Council resolution. They discussed the value of unity among the P5, and both felt it is important to act quickly," a U. The official spoke on condition of anonymity because they were not authorized to discuss the talks. Tracey wrote: Can you put it on the scales, please? Professor Usenko is an environmental forensic chemist who identifies contaminants from their unique chemical fingerprints.

Alphonse wrote: Can you hear me OK? The election ofyear-old opposition campaigner Ahmad Tumeh is meant to showit can fulfil that role. Murray wrote: Could I order a new chequebook, please? Bradicardia sinal tardio de falncia cardaca. Variabilidade da FC est descrita como um sinal precoce de choque sptico. Taquipneia Sinal muito inespecfico mas que pode traduzir tentativa de compensao respiratria de acidose metablica. Alteraes neurolgicas Inespecficas letargia incluindo recusa alimentar ou irritabilidade, hipotonia.

Isoladamente pode no ser indicador de compromisso circulatrio. Dada a dificuldade na caracterizao hemodinmica do RN, o tratamento baseia-se muitas vezes na identificao de hipotenso. No entanto, a teraputica da hipotenso, sem outros sinais sugestivos de FSS baixo em RN prematuro, provavelmente desnecessria, podendo ser prejudicial.

No recm-nascido no existe nenhum parmetro, que isoladamente, seja orientador, mas uma anamnese pormenorizada no sentido de definir o fator etiolgico e a combinao de diferentes indicadores clnicos e bioqumicos sugestivos de FSS baixo podem ajudar a identificar os recm- nascidos em risco. Se disponveis, podero ser teis outros instrumentos de monitorizao hemodinmica e da perfuso cerebral, nomeadamente a ecocardiografia, o NIRS e o aEEG.

O ecocardiograma funcional permite: excluso de cardiopatia congnita; avaliao da pr-carga cardaca, ou seja do grau de preenchimento vascular; avaliao da funo ventricular sistlica e diastlica; avaliao do canal arterial e da sua repercusso hemodinmica; determinao da ps-carga, nomeadamente clculo das presses pulmonares; clculo de dbitos- dbito do ventrculo direito e dbito da veia cava superior. Nas primeiras horas de vida, o shunt a nvel do foramen ovale geralmente menos significativo do que a nvel do CA, pelo que o dbito do VD mais representativo do FSS do que o dbito do VE.

Na prtica clnica, para avaliao do fluxo sanguneo sistmico durante o perodo de transio, a medio da velocidade de pico sistlico na artria pulmonar principal determinante do dbito do VD pode ser utilizada como rastreio, complementada com o clculo dos dbitos da VCS e do VD, de acordo com o organigrama.

Acidose metablica pH e EB so indicadores pouco fiveis de compromisso circulatrio. A hipoalbuminemia, frequente no RNEBP, pode mascarar a acidose tecidular existente, se o EB e o hiato aninico no forem corrigidos para a concentrao de albumina.

Saturao venosa central de O 2 SvcO 2 No RN a amostra de sangue colhida ao nvel da juno da veia cava inferior com a aurcula direita. Reflete a oxigenao tecidular global- valor normal no exclui hipxia de cada orgo individualmente.


A anlise da tendncia poder ser mais informativa do que o valor absoluto. Excluir pneumotrax. Acessos vasculares centrais venoso e arterial se possvel. Monitorizar FC; PA; SpO 2 ; SvcO 2 ; valores sricos de pH, lactato, glicose, hemoglobina, clcio ionizado; tempo de reperfuso capilar; diurese; fluxo na veia cava superior. Enquanto se procura caracterizar o estado hemodinmico global do recm-nascido, recorrendo a todos os sinais clnicos, laboratoriais e ao ecocardiograma funcional se disponvel , de forma a escolher a teraputica mais adequada, administrar: 1.

Escolha do frmaco dependendo dos efeitos cardiovasculares pretendidos e de acordo com etiologia mais provvel. Dopamina: fluxo sg renal. Adaptado de: Osborn DA: Diagnosis and treatment of preterm transitional circulatory compromise. Early Hum Dev. Clinical presentations of neonatal shock: the VLBW infant during de first postnatal day.

Philadelphia: Saunders Elsevier; O leito vascular pulmonar tem um desenvolvimento normal. Hipoplasia do leito vascular pulmonar RVP persistentemente elevada, com capacidade limitada de vasodilatao ps-natal. Hrnia diafragmtica congnita, malformao adenomatide qustica, agenesia renal, oligomnios, RCIU. Grupo com maior taxa de mortalidade.

Hipertrofia do msculo liso arteriolar pulmonar alterao do desenvolvimento vascular Designada como HTPP primria. O pulmo tem desenvolvimento normal, com normal diferenciao bronquolo-alveolar. Hipertrofia muscular das arterolas e capilares pulmonares. Fatores implicados no so totalmente conhecidos: predisposio gentica, hipxia crnica in utero insuficincia placentar, aumento da resistncia vascular placentar , condies que causam hiperfluxo pulmonar fetal: encerramento do canal arterial ou do foramen ovale in utero ex.

Labilidade de oxigenao: diminuio acentuada da SpO 2 com manipulao, estimulao, rudo. SDR: taquipneia, tiragem e gemido. Choque e falncia multiorgnica: nos casos mais graves. Auscultao cardaca: S 2 nico, de intensidade aumentada. Pode ter sopro sistlico rude, de regurgitao tricspide. A inexistncia de diferencial pr e ps-ductal no exclui HTPP. Se o canal arterial estiver encerrado, ou se o fluxo for pouco significativo no h diferencial de saturao.

Monitorizao da ventilao: pH e PaCO 2. Laboratrio Hemograma: hemoglobina e hematcrito; leucograma infeo ; plaquetas trombocitopenia frequentemente associada asfixia e sndrome de aspirao meconial. Eletrlitos: monitorizao frequente e contnua sobretudo da glicemia e calcemia. Radiografia de trax Padro varivel dependendo da patologia pulmonar SAM, pneumonia, dfice de surfatante, ar ectpico, hrnia diafragmtica congnita ; vascularizao pulmonar normal ou diminuda.

ICT geralmente normal ou ligeiramente aumentado. Excluso de cardiopatia congnita estrutural: ciantica; obstculos esquerdos crticos: contraindicao para vasodilatao pulmonar.

Acessos vasculares centrais: venoso e arterial, sempre que possvel. Oxignio Vasodilatador pulmonar. Ateno aos efeitos deletrios pulmonares. Ventilao assistida Otimizar a oxigenao e evitar a hiperinsuflao. Prevenir hipercapnia e acidose: PaCO 2 inicial mmHg. No parece ter eficcia em situaes de HTPP primria. Sedao A dor, a agitao e a assincronia com a ventilao, podem induzir a libertao de catecolaminas com consequente subida da RVP.

No existem ensaios clnicos de eficcia e segurana da curarizao no tratamento da HTPP. Suporte cardiovascular Manter volume intravascular adequado. A diminuio da presso arterial aumenta o shunt direito-esquerdo. Correo da acidose: acidose aumenta a RVP, deve ser sempre corrigida. No se recomenda induo de alcalose. Diminui a mortalidade e a necessidade de ECMO.

Contraindicaes cardiopatia congnita com obstculo esquerdo crtico; disfuno ventricular grave; hrnia diafragmtica congnita. Esquema teraputico Dose inicial- 20 ppm. A resposta geralmente rpida com subida da SpO 2 e da PaO 2 em minutos. Se no h resposta subir dose at 40 ppm. Doses superiores no demonstraram ser mais eficazes e associam-se a maior incidncia de efeitos secundrios.

Em RN que responde geralmente a durao do tratamento inferior a 5 dias. O aparelho e o circuito no devem ser desligados do doente at certeza de que no necessrio reiniciar. Monitorizao monitorizao contnua da dose administrada; NO 2 ; metahemoglobinemia.

Sildenafil Inibidor potente e seletivo da fosfodiesterase tipo 5, eficaz na diminuio da RVP, em doentes com hipertenso pulmonar; Parece diminuir o risco de rebound aps a suspenso do iNO; Aguardam-se estudos controlados randomizados sobre a sua utilizao na HTPP do RN. Risco de atraso de desenvolvimento psicomotor e de dfice auditivo.

Referenciao a consulta de Desenvolvimento e de ORL. Sobreviventes geralmente sem doena pulmonar ou cardaca. Confirmar com avaliao de SpO 2 e PaO 2.

Pode ou no ter sopro cardaco associado. O encerramento do canal condiciona hipoperfuso sistmica, compromisso da circulao coronria e aumento do dbito pulmonar. A apresentao clnica precoce, nas primeiras horas de vida com sinais de ICC SDR, taquipneia, fervores crepitantes, hepatomegalia, edema pulmonar e de m perfuso perifrica pele plida, suada, taquicardia, hipotenso arterial e acidose metablica.

Predominam, geralmente, os sinais de choque com m perfuso perifrica, acidose metablica progressiva, pulsos femorais dbeis, hipotonia, recusa alimentar diagnstico diferencial com choque sptico. Por outro lado, a intensidade do sopro no se correlaciona diretamente com a gravidade da cardiopatia. Teste da hiperxia: pode ser til, quando o ecocardiograma no for possvel, para diagnstico diferencial entre hipoxemia de causa cardaca e de causa respiratria.

Avaliao laboratorial: gasimetria avaliao de hipoxemia, acidose metablica e lactato ; hemograma, parmetros de infeo e, eventualmente, exames bacteriolgicos diagnstico diferencial com sepsis ; caritipo exceto na CIA, CIV muscular isolada e na TGA sem anomalias associadas. Ecocardiograma: diagnstico e caracterizao do tipo de cardiopatia. ECG: imprescindvel no caso de arritmia associada. A depresso cardiorrespiratria aps o nascimento geralmente secundria a doena pulmonar.

So excecionais as causas cardacas que condicionam m condio ao nascer: situaes de hidrpsia fetal no contexto de disritmias no controladas in utero, e de cardiopatia ductus-dependente com encerramento pr-natal do canal arterial. Cateterismo venoso umbilical. Iniciar alimentao entrica sempre que possvel. A ausncia de resposta sugestiva de foramen ovale restritivo. Evitar a hiperoxigenao. O oxignio diminui a RVP com consequente aumento do fluxo sanguneo pulmonar e diminuio do fluxo sanguneo sistmico.

Nas situaes de ventilao invasiva, manter parmetros mnimos, no hiperventilar. Se mantiver apneias- ventilao mecnica. Possvel a presena de foramen ovale com fluxo restritivo indicao para septostomia de Rashkind. Se agravamento clnico: aps excluso de outras causas, observao urgente por cardiologia peditrica. No h contraindicao para administrao de O 2. Estabilizao hemodinmica- expanso da volemia, eventual suporte inotrpico dopamina, dobutamina e correo da acidose metablica.

Se no h resposta: rever dose e permeabilidade do acesso vascular; observao emergente por cardiologia peditrica. Perante suspeita de cardiopatia ductus-dependente, na impossibilidade de confirmao diagnstica imediata, deve ser sempre iniciada perfuso de PgE 1 b RN com ICC progressiva aps a 2 semana de vida: restrio hdrica, furosemida, at avaliao por cardiologia peditrica, no emergente. O encerramento inicial funcional, por vasoconstrio da parede muscular, secundria diminuio sbita das prostaglandinas produzidas pela placenta e subida da PaO 2.

Nesta fase possvel a manuteno farmacolgica da permeabilidade do canal arterial em RN com cardiopatias congnitas ductus-dependente. Ao farmacolgica - vasodilatao arteriolar, por efeito direto no msculo liso vascular. Indicaes Manter a permeabilidade do canal arterial em cardiopatias congnitas ductus- dependente: 1. Cardiopatias com circulaes paralelas - necessidade de mistura de sangue arterial e venoso: transposio das grandes artrias. Contraindicaes No tem. Em todos os RN com hiptese diagnstica de cardiopatia congnita ductus- dependente, na impossibilidade de confirmao imediata do diagnstico deve ser sempre iniciada teraputica com PgE 1.

Ateno provvel necessidade de ventilao mecnica. Ajuste da dose de acordo com a resposta clnica: Restrio do fluxo pulmonar: melhoria da oxigenao geralmente em 30 minutos. Restrio do fluxo sistmico: subida da PA, melhoria da perfuso sistmica e da acidose resposta pode ser mais lenta. Doses superiores so excecionais e tm maior incidncia de efeitos secundrios. Ajustar de acordo com a evoluo clnica. Manter a dose mnima eficaz.

Taquicardia, precrdio hiperdinmico, pulsos amplos, diminuio da presso arterial diastlica, m perfuso perifrica, acidose metablica. Sopro cardaco sistlico ou contnuo, mais intenso no bordo esquerdo do esterno. Radiografia de trax: cardiomegalia, hipervascularizao pulmonar. Restantes prematuros: indicao para ecocardiograma sempre que o quadro clnico seja sugestivo. Monitorizao ecocardiogrfica seriada com periodicidade varivel, ajustada individualmente, de acordo com avaliao inicial, idade gestacional e evoluo clnica.

Objetivos Diagnstico: visualizao direta do canal arterial em modo bidimensional e com Doppler- cor. Excluso de hipertenso pulmonar e cardiopatia ductus-dependente. Avaliao do grau de repercusso hemodinmica Quadro Caractersticas do CA: dimetro transductal mm , avaliao da direo e velocidade do fluxo.

A dilatao do VE e a regurgitao mitral so sinais tardios, de sobrecarga esquerda muito significativa. Sinais de hipoperfuso sistmica: padro de fluxo na Ao ps-ductal.

Evitar blus de volume e diurticos nos primeiros dias de vida. Oxigenao adequada. O encerramento farmacolgico deve ser o mais precoce possvel, aps o diagnstico ecogrfico de repercusso hemodinmica. Inibe a sntese de prostaglandinas. Ao farmacolgica: vasoconstrio arteriolar, encerramento do canal arterial. Risco de diminuio do fluxo sanguneo cerebral, renal e mesentrico. Farmacocintica: Metabolizao heptica. Tempo de semivida no RN prematuro muito varivel 43 h at D3, 21 h aps D3.

Eliminao renal, do frmaco e metabolitos. No est indicado para encerramento profiltico do canal arterial. Monitorizao: avaliao clnica contnua: diurese, sinais de insuficincia cardaca, sinais de hemorragia; avaliao laboratorial funo renal, hemograma, bilirrubina prvia ao tratamento e de acordo com evoluo; ecocardiogramas seriados- se encerramento do canal durante o tratamento ponderar interrupo do ciclo teraputico.

Deve ser realizado o mais rapidamente possvel. Em idade peditrica, a sua interpretao deve ter em conta variaes especficas da idade, relacionadas com alteraes na fisiologia ritmo, frequncia, conduo e anatomia dimenso corporal, posio e dimenso do corao e das suas cmaras. O perodo neonatal tem especificidades eletrocardiogrficas muito particulares. Hipertenso arterial.

Suspeita de doena metablica ou endocrinolgica neonatal. Relao com dimenso das aurculas e com a origem estmulo eltrico. Q: despolarizao do septo interventricular. R: despolarizao do pex. S: despolarizao das paredes ventriculares. Onda T Repolarizao ventricular; mecanicamente corresponde distole ventricular. Aumento da amplitude onda T: hipercaliemia. Mecanicamente corresponde sstole auricular. PR curto: Pr-excitao ventricular, doena de Fabry, doena de Pompe.

Grande variao com a FC: correo com a frmula de Bazett. QT curto: hipercalcemia, efeito digitlico, risco de morte sbita! QT longo: hipocalcemia, miocardite, sndrome de QT longo, enfarte do miocrdio, toxicidade de frmacos macrlidos, procinticos , mes com doena do tecido conjuntivo LES , leso do SNC. Causa gentica. Histria familiar. Surdez neurosensorial- importante para a suspeita diagnstica. Episdios de sncope por taquicardia ventricular tipo torsade de pointes, bradicardia, risco de morte sbita!

Durao: 0,,08 s. No 1 ano de vida pode haver elevao at 1 mm nas derivaes dos membros e 2 mm nas precordiais. Infradesnivelamento ST: hipocaliemia. Prolongamento ST: hipocalcemia.

Encurtamento ST: hipercalcemia. Diminuio da amplitude ondaT: hipocaliemia, hipomagnesemia. Embora as formas mais frequentes ocorram em RN sem doena cardaca, podem estar associadas a doena cardaca congnita, ou ser secundrias a frmacos, alteraes eletrolticas ou metablicas. A histria natural no recm nascido muito diferente da observada noutros grupos etrios. A arritmia mais frequente a extrassstolia supraventricular ESSV ou auricular. A taquicardia ventricular TV rara e geralmente secundria.

O bloqueio auriculoventricular BAV completo congnito a causa mais frequente de bradicardia mantida. Taquicardia: irritabilidade, letargia, intolerncia alimentar, palidez, cianose, SDR, diaforese, oligria. Bradicardia: intolerncia alimentar, SDR, m progresso ponderal. Etiologia: pode ocorrer em RN saudveis, com corao estruturalmente normal; aps cirurgia cardaca; CVC intracardacos; intoxicao por digitlicos.

Teraputica: no indicada, exceto se intoxicao digitlica. Evoluo: geralmente benigna, tem tendncia a desaparecer nos primeiros meses de vida. Etiologia: em coraes estruturalmente normais podem ser benignas, sobretudo se monomrficas maioria dos casos ; doena cardaca estrutural ou funcional; prolongamento do intervalo QT; leso isqumica do miocrdio; distrbios metablicos acidose ou eletrolticos hipocalimia ; frmacos digitlicos, simpaticomimticos ; infeo sistmica, CVC intracardacos.

Evoluo: geralmente benigna, com resoluo nos primeiros meses de vida.


Etiologia: idioptico; estimulao vagal; hipxia; aumento da presso intracraniana; frmacos digitlicos, bloqueantes. Teraputica: da causa subjacente. Quando isolada, geralmente no causa bradicardia nem sintomatogia. Etiologia: idioptico; doena cardaca congnita; frmacos digitlicos ; miocardite. O bloqueio ocorre normalmente em posio proximal ao ndulo AV. Etiologia: idioptico; frmacos; doena materna do tecido conjuntivo. O bloqueio ocorre normalmente em posio distal ao ndulo AV.

Teraputica: da causa subjacente; pode ser necessrio pacemaker. Etiologia: idioptico; doena materna do tecido conjuntivo exposio in utero a anticorpos anti-Ro e anti-La, mais frequentes no LES e sndrome de Sjogren ; cardiopatia congnita defeito do septo AV, transposio congenitamente corrigida das grandes artrias TCCGA, isomerismo esquerdo.

Etiologia: resposta fisiolgica a estmulos como dor; febre; anemia; hipovolemia; ICC; catecolaminas. Nota: Manobras vagais e adenosina EV quando acesso vascular disponvel podem ser usadas no doente instvel, mas apenas se no atrasarem a cardioverso eltrica. Antagonistas dos canais de clcio esto contra-indicados no recm nascido! Taquicardia recproca juncional permanente: forma rara de TSV de reentrada AV, geralmente incessante e difcil de controlar, apenas com resposta transitria adenosina e cardioverso.

Teraputica: bloqueante, amiodarona ou flecainida ; teraputica definitiva: ablao por radiofrequncia mais tarde. Etiologia: contexto de ps-operatrio cardaco. Teraputica: pode ser necessrio tratamento de curta durao com bloqueantes, antiarrtmicos classe IC e III.

Nota: frequentemente refratria ao tratamento eficaz para as arritmias de reentrada- importante para o diagnstico diferencial. Evoluo: habitualmente resoluo espontnea aos 6 meses de idade. ECG: incio e fim graduais, frequncia varivel, incessante, complexos QRS estreitos, dissociao AV, frequncia auricular inferior ventricular.

Etiologia: idioptico; cardiopatia congnita; CVC intracardaco. Teraputica: se hemodinamicamente estvel - sotalol, amiodarona ou pacing transesofgico. Etiologia: maior incidncia em RN nascidos por cesariana implicao potencial da anestesia na sua gnese ; parece ser um fenmeno do perodo neonatal com rpida resoluo ps-natal.

Teraputica: geralmente no necessria; em raros casos, sintomticos podem utilizar-se bloqueantes, flecainida ou amiodarona. Etiologia: miocardite; tumores hamartomas e rabdomiomas ; enfarte do miocrdio origem anmala da coronria esquerda a partir da artria pulmonar ; tromboembolismo; alteraes eletrolticas e metablicas hipocalimia-maior risco em associao digoxina; hipocalcmia e hipomagnesmia ; txicos; canalopatias sndrome de QT longo e sndrome de Brugada.

Sndrome de QT longo: Eletrofisiologia: Anomalia dos canais de potssio e de sdio com consequentes alteraes da repolarizao.

Etiologia: gentica; secundrio a frmacos. Teraputica: bloqueantes. Fluid and electrolyte management in the first week of life Perdas insensveis Relacionadas com: peso, idade gestacional, humidade, estabilidade clnica. Reduo das perdas transdrmicas em RN prematuros: humidade em incubadora fechada nos primeiros 2 a 3 dias de vida, uso de cobertor plstico e touca.

Estimativa diria das necessidades hdricas baseada na avaliao clnica e laboratorial. Exame objetivo: turgor cutneo, mucosas, fontanela anterior; avaliao dos pulsos. Densidade urinria: Ajuste de acordo com glicemia. Manifestaes clnicas Hipotonia, vmitos, hiperexcitabilidade, convulses. Alcalose redistribuio de K por aumento da captao celular. Perda superior na alcalose metablica. Etiologia Aporte insuficiente perda Frmacos: diurticos, anfotericina B, gentamicina, corticides, agonistas -adrenrgicos Gastrointestinal: diarreia, sonda gstrica ativa, vmitos - estenose pilrica mineralocorticide : estenose da artria renal Renal: poliria, excesso de administrao de bases, S.

Bartter 1 , hiperaldosteronismo 2 , S. Bartter: alterao dos canais de Cl poliria, hipocaliemia, hiponatremia, hipercalciria nefrocalcinose , aldosterona e renina aumentadas. T I C O potenciao da toxicidade digitlica. Confirmar as doses de correo dose elevada pode ser fatal. KCl 7. Manifestaes clnicas Situao potencialmente fatal sem tratamento arritmia e morte.

Alteraes cardacas: bradicardia, arritmia, choque; amplitude onda T, bloqueio cardaco com alargamento do complexo QRS, arritmia ventricular e paragem cardaca. ECG com alteraes Emergncia. Patologia do RN: Problemas de coordenao, hipotonia; sndrome de dificuldade respiratria; alteraes anatmicas - retrognatismo, fenda palatina. Pele: turgor cutneo diminudo, m perfuso perifrica, ictercia associao frequente com hiperbilirrubinemia.

Gastrointestinal: poucas dejees, fezes de transio tardias. SNC: alteraes do tnus hipertonia, reflexos vivos , fontanela anterior deprimida, suturas cavalgadas, convulses. Trombose do seio dural, veia renal ou perifrica risco de amputao hipercoagulabilidade. Maioria das complicaes resulta do tratamento inadequado sequelas neurolgicas, morte. Risco de edema cerebral pela correo rpida da hipernatrmia: Produo de osmis idiognicos como mecanismo protetor da perda de gua intracelular.

Incidncia dependente da causa. Alteraes da placenta ou do cordo umbilical: placenta previa, placenta anterior, descolamento de placenta; vasa previa, insero velamentosa, hematoma, aneurisma, prolapso ou rotura do cordo.

Clampagem precoce do cordo umbilical Ps-natal Hemorragia: traumatismo do parto: caput succedaneum, cefalohematoma; hemorragia subgaleal pode ser uma emergncia ; hemorragia intracraniana - subdural, subaracnoideia ou subependimria; hemorragia orgos internos - fgado, rins, bao ou suprarrenais.

Malformaes vasculares congnitas Alteraes da coagulao: deficincia congnita; coagulopatia de consumo sepsis. Trombocitopenia Iatrogenia: colheitas sanguneas RN prematuros. Anemia hemoltica autoimune rara : me com doena autoimune LES; frmacos - penicilina, cefalosporinas, -metildopa. Alteraes no imunolgicas Sepsis. Alteraes congnitas Alteraes da membrana: esferocitose, eliptocitose.

Alteraes enzimticas: deficincia de G6PD; deficincia de piruvato-quinase. Alteraes da hemoglobina: o-talassmia homozigtica perodo neonatal ; hemoglobinas instveis. Alteraes metablicas Galactosmia. Anemia hipoplsica ou baixa produo de GV raras, manifestaes para alm do perodo neonatal Congnitas: anemia de Fanconi: insuficincia medular; anemia de Diamond-Blackfan: insuficincia medular da linhagem eritride; atransferrinemia, disginesia reticular, leucemia congnita, anemia sideroblstica.

Adquiridas: infees parvovrus B19, rubola, sfilis; alteraes nutricionais deficincia de vitamina E; doenas metablicas.

Crnica: SDR ligeiro, anemia microctica hipocrmica, reticulocitose, hepatomegalia. Hemorragia de grande volume hipovolemia e choque, acidose metablica. Hemorragia intracraniana FA tensa, alteraes da conscincia, apneia, convulses. Hemorragia visceral distenso abdominal, tumefao abdominal, secrees hemticas.

Antecedentes familiares de anemia, esplenectomia, ictercia, litase biliar, grupo sanguneo me e RN, doena autoimune materna. Avaliao laboratorial 1 linha Hemograma com contagem de reticulcitos, esfregao sanguneo. Esfregao sanguneo: esferocitos - isoimunizao ABO, esferocitose; eliptocitos eliptocitose; picnocitos - dfice de G6PD; esquizocitos e corpos de Heinz - coagulopatia de consumo.

Bilirrubina total e conjugada. Teste de Coombs directo e tipagem sangunea. Estudos enzimticos, da membrana e das cadeias de Hb.


Exames imagiolgicos. Riscos transfusionais reduzidos, mas existentes. Limitao de colheitas sanguneas: Monitorizao no invasiva, micro-mtodos. Remoo precoce de vias centrais.

Critrios transfusionais restritivos. Excepo: RN que receberam mltiplas transfuses, que podem no necessitar de suplementos de ferro. Realizao de avaliao laboratorial aos M de I.

Estimulao da eritropoiese. Economia transfusional mas sem reduo dos riscos transfusionais, uma vez que no anula a necessidade de transfuses. Teraputica segura, sem efeitos adversos. Isoimunizao: produo de anticorpos maternos dirigidos contra antignios de eritrcitos fetais transmitidos pelo pai. Grau de sensibilizao materna proporcional ao volume de transfuso fetomaterna: aborto, gravidez ectpica, traumatismo abdominal, amniocentese, cordocentese, placenta prvia.

Doena moderada a grave; morte in utero Kell. Abordagem clnica semelhante a isoimunizao Rh. Teraputicas adjuvantes Utilizao eletiva em situaes graves com indicao para exsanguneo-transfuso. Administrao precoce reduz necessidade de exsanguneo-transfuso. Objetivo Diminuio das complicaes neurolgicas da doena hemoltica imune. Ler atentamente as instrues de utilizao. Fase 2 Rodar 90 no sentido dos ponteiros do relgio e direcionar a torneira para o saco de recolha e injetar o sangue do RN. Fase 3 Rodar 90 no sentido dos ponteiros do relgio e direcionar a torneira para o sistema de transfuso e aspirar a mesma quantidade de sangue da fase 1.


Repetir fases Registo em papel de cada ciclo. Procedimento min, trocas lentas para evitar alteraes bruscas da PA. Agitar o saco a cada min para evitar sedimentao dos GV. No aplicar presso excessiva na extrao e infuso de sangue. Via perifrica para perfuso de soro glicosado e medicao. Retirar CVU aps realizao da tcnica. Monitorizao Monitorizao da temperatura e cardiorrespiratria. Pausa alimentar 4h, colocao de SNG.

Avaliao laboratorial: hemograma, ureia, creatinina, ionograma, calcemia, glicemia, coagulao, gasimetria. Reiniciar Fototerapia. Monitorizao bilirrubina pico horas depois. Complicaes Cardiorrespiratrias: apneia, bradicardia, hipo ou hipertenso. Infecciosas: onfalite, sepsis. Relacionadas com o cateter: vasoespasmo, trombose, embolia. Metablicas: hipocalcemia, hipo ou hiperglicemia, hipercaliemia. Hematolgicas: trombocitopenia, coagulopatia de diluio, CID.

Gastrointestinais: intolerncia alimentar, isqumia, NEC. Trombocitopenia moderada ou grave investigao. Falsa trombocitopenia aglutinao no tubo EDTA confirmao obrigatria em tubo de citrato. G I C O Exame objetivo: petquias generalizadas, aps traumatismos minor ou em locais de presso; equimoses, hemorragia; hepatoesplenomegalia infees congnitas ; dismorfismos, malformaes sndrome TAR, trissomias 13, 18, 21,sndrome de Turner; doenas hereditrias do metabolismo , hemangiomas Sndrome Kasabach-Merritt.

Esfregao de sangue perifrico. Imunes: anticorpos antiplaquetrios circulantes e ligados; Nota: pesquisa no RN pode ter resultado falso negativo. Fenotipagem plaquetria: contactar Servio de Imunohemoterapia; envio de amostras para o Instituto Portugus do Sangue; tubos no centrifugados nem congelados; me: 4 tubos de hemograma e 1 tubo seco de bioqumica; RN: 1 tubo de hemograma EDTA ; pai: 4 tubos de hemograma opcional.

Eventualmente: cariotipo, bipsia medular, outros estudos. Anticorpos antiplaquetrios classe IgG maternos atravessam a placenta e ligam-se s plaquetas fetais. As plaquetas fetais so destrudas pelo sistema reticuloendotelial fetal. Incidncia casos : 10 Seguimento Consulta 2 semanas aps IgEV com hemograma risco de agravamento de trombocitopenia por diminuio de imunoglobulinas circulantes ; Avaliao imagiolgica do SNC sempre ecografia cerebral; Repetir antes da alta se trombocitopenia grave.

Transfuso de concentrado de plaquetas CP : se hemorragia ativa; pouco eficaz porque anticorpos reagem com as plaquetas de qualquer dador. Seguimento: consulta 2 semanas aps IgEV com hemograma risco de agravamento de trombocitopenia por diminuio de imunoglobulinas circulantes. Dfice quantitativo: produo limitada at ao 2 trimestre de gravidez; menor reserva medular; menor capacidade de mobilizao da medula, resposta medular ao stress limitada; menor produo de GM-CSF em prematuros; Dfice qualitativo: limitao no reconhecimento de agentes patognicos, aderncia, quimiotaxia, fagocitose, diapedese e produo de superxidos.

Kostmann, S. Shwachman-Diamond, Disgenesia reticular, S. Barth, Neutropenia cclica Neutropenia induzida por frmacos B-lactmicos, diurticos tiazdicos, ranitidina, ganciclovir, indometacina, fenitona, clopromazina Doenas metablicas acidemias orgnicas, doena do armazenamento do glicognio 1b Neutropenia idioptica da prematuridade Dfice de vitaminas e micronutrientes cobre e folato Pseudoneutropenia Aloimune se associada a anticorpos anti-NB1 H E M A T O L.

G I C O Gravidade clnica e risco de infeo Neutropenia geralmente transitria, sem aumento de morbilidade e mortalidade. Neutropenia precoce em RN MBP - fator de risco de mortalidade independente de sepsis ; Risco de infeo e mortalidade dependente da gravidade e durao da neutropenia, situao clnica e doenas concomitantes: n total de neutrfilos condicionante de risco aumentado de infeo no est bem estabelecido para o RN: valores extrapolados de crianas com neutropenia crnica grave e sob quimioterapia.

Histria neonatal: sepsis bacteriana ou fngica, NEC, suspeita de infeo viral congnita ou ps- natal, anemia, trombocitopenia, imunodeficincia, cardiomiopatia dilatada sndrome de Barth , acidose metablica grave doena de armazenamento, acidrias orgnicas , nutrio parentrica dfice de cobre.

Exame objetivo RN LIG, hepatoesplenomegalia TORCHS ou doenas de armazenamento , exantema petequi al TORCHS , ictercia doena hemoltica ou colestase , displasia esqueltica, hipoplasia radial ou polegar, membros curtos sndrome de Shwachman-Diamond, hipoplasia cartilagem-cabelo , hiperpigmentao da pele com distrofia dos leitos ungueais disqueratose congnita. Parmetros hematolgicos permitem orientar a etiologia: monocitose no nadir dos neutrfilos aponta para causas de neutropenia no benignas ex.

Durao: dias; neutropenia imune: semanas. Transfuses de Neutrfilos: evidncia atual no recomenda o seu uso. Coagulao - processo dinmico: dependente de: plaquetas, endotlio vascular, fatores de coagulao, sistema de fibrinlise. Coagulao neonatal: fatores de coagulao dependentes da IG e idade do RN.

Processo geralmente em equilbrio em RN saudveis: o maior risco de hemorragia equilibrado pelos efeitos protetores da deficincia fisiolgica de inibidores da coagulao e da capacidade fibrinoltica diminuda. Cascata da coagulao simplificada Vias intrnseca, extrnseca e final comum: a azul Via fibrinolitica: a cinzento; inibio: setas a tracejado. Alterao dos fatores de coagulao: congnitas: hemofilia; doena de von Willebrand; deficincia de outros factores de coagulao; insuficincia heptica atrsia das vias biliares; adquiridas: doena hemorrgica do RN deficincia de vitamina K; coagulao intravascular disseminada CID; insuficincia heptica colestase, hepatite.

CLNICA Hemorragia: intracraniana apneia, depresso do estado de conscincia, convulses; subgaleal, mucosas e pele, umbilical, gastrointestinal, vesical, locais de puno vascular anemia e ictercia. Histria obsttrica: doenas maternas, morte fetal in utero; frmacos. Recm-nascido: clinicamente bem: alterao das plaquetas; deficincia de vitamina K - confirmar profilaxia com vitamina K; deficincia congnita de fatores da coagulao; doente: coagulao intravascular disseminada - sepsis, asfixia ; insuficincia heptica: hepatite, colestase, atrsia das vias biliares.

Doseamento de fibrinognio, produtos degradao do fibrinognio e D-dmeros. Diagnstico Suspeita clnica Hemofilia: apresentao clnica diferente de crianas e adultos hamartroses raras ; hemorragia intracraniana; hematomas subgaleais, cefalohematomas extensos, hematomas retroperitoneais, hemorragia sucapsular heptica ou de outros orgos; hemorragia excessiva dos locais de puno venosa.

Afibrinogenemia ou hipofibrogenemia: hemorragia das mucosas clnica semelhante a trombocitopenia. Deficincia grave FXI: assintomtica a hemorragia grave. Diagnstico pr-natal - possvel nos casos com mutao identificada. Preveno via do parto: controversa; evico de monitorizaao invasiva fetal; evico injeces IM profilaxia vitamina K EV e vacinao.

Manifestaes clnicas Hemorragia cutnea, mucosas, cordo umbilical, gastrointestinal, intracraniana; formas de apresentao doena precoce, clssica ou tardia. Manifestaes clnicas Hemorragia fulminante e fatal, irreversvel se a funo heptica no normalizar: cutnea, gastrointestinal, intracraniana. G I C O aumento da sobrevida dos fatores de coagulao sem aumentar risco de hemorragia. Alteraes laboratoriais: TP e APTT aumentados, trombocitopenia, fibrinognio diminudo, produtos de degradao do fibrinognio e D-dmeros aumentados.

Tratamento: Orientado para a doena de base. Suporte transfusional: Concentrado de plaquetas ver Trombocitopenia. A bilirrubina livre o principal fator preditivo de neurotoxicidade: encefalopatia bilirrubnica: manifestaes agudas da toxicidade da bilirrubina: quadro neurolgico, consequncia da toxicidade da bilirrubina, observado nas 1s semanas de vida; kernicterus: alterao anatomopatolgica do crebro com morte neuronal por deposio do pigmento de bilirrubina; sequelas permanentes; M E T A B.

L I C O BIND Bilirubin induced neurologic dysfunction: largo espectro de doenas causadas por hiperbilirrubinemia grave, com leso neuronal ncleos da base, hipocampo, cerebelo, ncleos cerebrais oculomotores e da audio. A avaliao dos nveis de bilirrubina pela observao da colorao da pele no fivel e pode levar a erros.

O doseamento da bilirrubina transcutnea pode ser usado como mtodo de rastreio. O que mudou na nossa atitude nas ltimas dcadas? Altas precoces s h: antes de serem atingidos os valores mximos de bilirrubina; aleitamento materno ainda mal estabelecido. RN sem prematuridade tardia nos Berrios: RN com maior risco de ictercia grave por metabolizao mais lenta.

Maior nmero de RN amamentados. Menor preocupao com valores elevados de bilirrubina. Assegurar o seguimento aps a alta, de acordo com tempo de internamento e risco de hiperbilirrubinemia. Interveno rpida e tratamento aps confirmao de ictercia. Avaliar o risco do RN desenvolver hiperbilirrubinemia grave A Academia Americana de Pediatria tem em considerao no apenas o nvel de bilirrubina srica, mas tambm a idade gestacional, o nmero de horas de vida do RN e a presena ou ausncia de fatores de risco Avaliar o risco em todos os RN.

Efeitos adversos Relatos de toxicidade clinicamente significativa so raros: Desidratao: A FT no leva ao aumento do consumo de O 2 e no h aumento de perdas insensveis pela pele e aparelho respiratrio.

Monitorizar a hidratao do RN: peso dirio e eletrlitos. Actualmente no h indicao para aumentar o aporte hdrico por rotina em RN sob FT. RN com colestase: beb bronze.

Erupes purpricas e bolhosas so raras. Fatores de alto risco avaliao diria : asfixia, hipoxemia, acidose, hemlise com teste de Coombs positivo, agravamento clnico ou neurolgico sepsis, teraputica com aminas, meningite, hemorragia intracraniana Adaptado de D E van Imhoff et al.

Normogramas acessveis em www. Implementao de protocolos de diagnstico e tratamento especficos para cada servio incluindo critrios de avaliao da Bil T pela equipa de Enfermagem. Consultar www. Predio do risco Estratgia decisional na alta Aps a alta, avaliar: Peso e perda ponderal. Adaptao mama; necessidades hdricas asseguradas?

Padro de mices e dejees. Presena ou no de ictercia. Caratersticas fsicas dismrficas, exame neurolgico. Cataratas galactosemia, rubola congnita. Sopro cardaco atrsia das vias biliares, sndrome de Alagille, infees grupo TORCH, cromossomopatia ou sinais de insuficincia cardaca.

Exame abdominal: hepatomegalia todas as causas , esplenomegalia atrsia das vias biliares, sepsis, infees grupo TORCH, deficincia de 1 anti-tripsina, Niemann-Pick. Micropnis Hipopituitarismo congnito.

Petquias e equimoses Insuficincia heptica. Fitomenadiona Vitamina K1 2. A absoro intestinal deste grupo de vitaminas inferior da formulao AquADEKs, que absorvida a nvel da circulao enteroheptica. Doseamento srico de ferro, cido flico, vitamina B12, clcio, zinco. Iniciar a nutrio entrica o mais rapidamente possvel. Dieta deve incluir triglicridos de cadeia mdia absoro direta no sistema porta. Tratamento especfico da causa se existir Portoenterostomia de Kasai na atrsia das vias biliares deve ser realizado antes das 6 semanas de vida, est provado aumento da sobrevida aps a realizao precoce deste procedimento.

O objetivo da identificao de RNs com hipoglicemia a preveno de leses cerebrais irreversveis. No ps-parto 2 h vida observa-se descida da glicemia por perda da transferncia materno-fetal contnua de glicose, que estabiliza por volta das h de vida.

At s h de vida a glicemia mantida pela glicogenlise, estimulada pelo aumento de epinefrina e glicagina, e diminuio insulina. Aps este perodo a glicemia fica dependente da neoglicognese. Estes valores so geralmente transitrios e assintomticos, sendo considerados uma fase da adaptao normal vida ps-natal. Neste perodo o mecanismo compensatrio a esta hipoglicemia fisiolgica consiste na produo de substratos energticos alternativos, como os corpos cetnicos. ETIOLOGIA A hipoglicemia pode surgir por diversos mecanismos: Diminuio da oferta de glicose: Reservas inadequadas de glicognio; diminuio da produo de glicose pela glicogenlise ou neoglicognese; Consumo excessivo de glicose: Hiperinsulinismo.

Doseamento de glicemia capilar, venosa ou arterial em tira reativa BMtest. Se hipoglicemia fazer colheita de sangue e iniciar teraputica. A hipoglicemia deve ser confirmada laboratorialmente sangue enviado de imediato para laboratrio e processado rapidamente.

Glicemia no sangue total incluindo aparelhos de gasimetria e BMtest. Manter doseamento de glicemia capilar antes de cada refeio: At s 24 h de vida: RN prematuro tardio e LIG; At s 12 h de vida: RN filho de me diabtica e GIG; Aps este perodo a monitorizao persiste em RN que mantenham nveis baixos de glicemia, at normalizao dos nveis glicmicos. Se hipoglicemia repetida ou persistente - investigar causas mais raras: SANGUE URINA Tubo Seco ml : Glicose, ionograma, funo heptica, cido rico, T4 livre, TSH, CK; Em hipoglicemia se possvel : insulina, pptido C, glicagina, hormona do crescimento e cortisol Tubo com EDTA: carnitina total e livre acilcarnitina transporte rpido em gelo ; cromatografia aminocidos Tubo com heparinato de ltio: amnia transporte rpido em gelo Tubo prprio Faculdade de Farmcia: estudo potencial redox Gasimetria com lactato Amostra nica: Corpos cetnicos Colheita de h colher cada mico e congelar : Substncias redutoras, cromatografia de aminocidos e cidos orgnicos Exames imagiolgicos se hipoglicmia grave ou sintomtica : Ecografia cerebral transfontanelar; Ressonncia magntica crnio-enceflica eventual.

L I C O A resposta transitria: elevao dos valores glicmicos ocorre 1 hora depois e persiste por 2 horas; Se a hipoglicemia persistir repetir a dose inicial. A ausncia de resposta glicagina pode indicar um defeito no armazenamento ou sntese do glicognio subjacente.

As sequelas neurolgicas mais frequentes so atraso no desenvolvimento psicomotor, alteraes do desenvolvimento cognitivo, paralisia cerebral e convulses recorrentes. Para a preveno de episdios de hipoglicemia essencial o incio precoce da alimentao com LM logo aps o parto horas de vida , e estabelecer intervalos de alimentao cada h.

Os RN alimentados com LM tm maiores concentraes de corpos cetnicos, o que lhes permite uma maior tolerncia a estados de hipoglicemia, sem presena de sintomas ou de sequelas neurolgicas. A hiperglicemia resulta habitualmente de intolerncia do RN a aportes endovenosos de glicose e inversamente proporcional idade gestacional e peso ao nascer.

Os mecanismos mais frequentes so uma resposta insulnica deficiente, produo excessiva endgena de glicose e uma elevao de hormonas de stress cortisol e epinefrina associadas a doena aguda. No entanto, estes valores so frequentemente encontrados em RN com aporte endovenoso de glicose e no requerem, habitualmente, cuidados especiais. ETIOLOGIA Aportes excessivos de glicose ou lpidos endovenosos; Prematuridade e extremo baixo peso intolerncia a aportes normais de glicose endovenosa ; Resposta ao stress ex: sepsis, ventilao mecnica, ps-operatrio, hemorragia intracraniana, convulses ; Frmacos ex: corticosteroides, fenitona, teofilina, cafena, uso materno de diazxido ; DM neonatal raro : hiperglicemia persistente durante mais de 2 semanas, que requer insulinoterapia transitria; permanente.

Sindrome de Wolcott-Rallison, Sindrome de Donohue e hipoplasia pancretica. Vestgios intermitentes de glicose na urina podem ser tolerados. Exames complementares dirigidos a eventuais causas secundrias e avaliao de repercusso sistmica: Hemograma com contagem diferencial de leuccitos e formas imaturas de neutrfilos; Protena C reativa, Exames culturais se suspeita de sepsis ver Risco infeccioso e Sepsis precoce e Sepsis tardia ; Funo renal e eletrlitos.

Insulina srica e pptido C srico e urinrio se suspeita de diabetes mellitus neonatal tubo seco : DM neonatal transitria nveis normais ou ligeiramente baixos de pptido C; DM neonatal permanente nveis extremamente baixos ou ausentes de pptido C. Exames imagiolgicos: Ecografia cerebral para avaliar a presena de hemorragia intraventricular. Dose inicial 0. Dose mxima 0. Aumentar intervalos quando a glicemia se encontrar estvel em determinaes subsequentes; Hipocaliemia iniciar, manter ou aumentar se necessrio aporte parentrico de potssio quando iniciar perfuso de insulina com monitorizao apertada da caliemia; Iniciar, assim que possvel, alimentao entrica com aumento progressivo da quantidade e decrscimo progressivo da alimentao parentrica.

A DM neonatal permanente persiste mantendo a necessidade de insulina exgena. A referenciao a consulta de Endocrinologia Peditrica mandatria em ambas as situaes. Componente fisiologicamente ativa.

Sinais inespecficos e no patognomnicos. Hipocalcemia precoce 1 semana : estridor; apneia, bradicardia, hipotenso; irritabilidade neuromuscular: tremores, hipertonia em extenso, hiperreflexia, sinal de Chvostek contrao facial aps percusso do nervo facial , sinal de Trousseau espasmo carpopedal ; clnus, tetania, convulses; arritmia, taquicardia, prolongamento do intervalo QT. Hipocalcemia tardia aps a 1 semana : letargia, apneia; intolerncia alimentar, distenso abdominal; desmineralizao ssea, fosfatase alcalina aumentada, fraturas sseas osteopenia da prematuridade.

Diagnstico Avaliao laboratorial: clcio total e ionizado, fosfato e magnsio, ionograma; albumina; gasimetria. Fosfatase alcalina.

Doseamento de clcio urinrio. Estudos radiolgicos: desmineralizao ssea, hipertransparncia das metfises, fraturas sseas. Teraputica Atitude expectante se hipocalcemia precoce assintomtica. Tratar hipomagnesiemia. Suplementao com vitamina D. Efeitos secundrios arritmia, bradicardia, paragem cardaca; litase renal, calcificaes cerebrais em RN em estado grave. L I C O Manifestaes clnicas pode ser assintomtica. Imagiologia: ecografia renal calcificaes renais; radiografia de ossos longos desmineralizao dos ossos longos hiperparatiroidismo , leses osteoesclerticas hipervitaminose.

Associada a hipercalcemia. Efeitos secundrios: hiperfosfatemia, hipocalcemia, hipotenso, intolerncia gastrointestinal; a administrao rpida pode provocar arritmia. Teraputica Dependente da gravidade e da etiologia. Associada a hipocalcemia. Afeta sobretudo leon terminal regio ileo-cecal, zona de circulao terminal da artria mesentrica superior, associada a maior sofrimento em caso de alteraes hemodinmicas ou a totalidade do intestino nos casos mais graves.

Therapeutic decisions based upon clinical staging. Alteraes do crescimento e neurodesenvolvimento. J Pediatr Gastroenterol Nutr. Raleigh, North Carolina: Acorn Publishing, A escolha deve ser fundamentada de acordo com o quadro. Particularidades no RN Mecanismos excitatrios predominantes; Incapacidade de sustentar e propagar uma convulso generalizada imaturidade das estruturas ; Descargas mais profundas no se propagam at superfcie no so detetadas por EEG dissociao eletroclnica: Convulso eletroclnica crise clnica com traduo eletrogrfica; Convulso clnica crise clnica sem traduo eletrogrfica; Convulso eletrogrfica crise detetada no EEG sem traduo clnica.

Tnica: Focais contrao mantida de um membro ou postura assimtrica do tronco ou pescoo; Generalizadas postura em extenso descerebrao ou flexo descorticao dos membros superiores ou inferiores; frequente na hemorragia intraventricular catastrfica. Dependncia de piridoxina Dependncia de fosfato de piridoxal Convulses com resposta ao c.

Eletroencefalograma: Importante para determinao do padro intercrise; a teraputica no deve ser diferida para realizao de EEG; Se possvel vdeo-EEG gold standard ; EEG de amplitude integrada sinal EEG processado, em escala semilogartmica e traado comprimido. Material para intubao e ventilao disponvel risco de depresso respiratria pela convulso e pelos anticonvulsivantes. Corrigir eventual hipoglicemia ou desequilbrio hidroeletroltico 3. Tratar infeo: a.

Antibiticos meningite, sepsis ; b. Aciclovir suspeita de encefalite herptica. Fenobarbital: a. Efeitos secundrios sedao, letargia. Preferir fosfenitona pela facilidade e segurana de administrao prescrio em equivalentes de fenitona - EF ; e. Efeitos secundrios: depresso cardaca, cardiotoxicidade agravada pela hipotermia. Midazolam: a. Convulses refratrias ao fenobarbital e fenitona; b.

Manter fenobarbital e suspender fenitona; c. No RN sem diagnstico com crises refratrias ao fenobarbital e fenitona deve fazer-se prova teraputica com piridoxina; d. Efeitos secundrios: hipotenso, agravamento do prognstico neurolgico no RNPT; f. Nota: doses anticonvulsivantes superiores s doses de sedao.

Convulses refratrias Neuropediatria: a. Encefalopatia hipxico-isqumica: encefalopatia neonatal em que possvel documentar um evento hipxico-isqumico recente na etiologia do quadro clnico. Numa primeira fase ocorre morte celular por falncia energtica secundria a depleo de adenosina trifosfato por hipxia, com disfuno membranar, acumulao intracelular de clcio, sdio, gua e edema citotxico. A hipxia e isquemia cerebrais resultam da hipxia sistmica e da reduo do fluxo cerebral.

Numa segunda fase, a morte celular envolve processos bioqumicos que incluem a libertao excessiva de neurotransmissores excitatrios, a leso oxidativa por radicais livres, a inflamao e a apoptose. O intervalo entre a primeira e segunda fase representa uma fase latente de durao aproximada de 6 horas e corresponde a um perodo de janela teraputica.

Idealmente dever ser enviada a placenta para estudo anatomopatolgico. ABORDAGEM INICIAL deve ser sistemtica, de suporte e adaptada disfuno de orgo - Reanimao adequada de acordo com protocolo; suspenso das medidas de aquecimento aos dez minutos de vida, quando se considera indicao para hipotermia teraputica; - Procedimentos: cateterismo venoso umbilical idealmente duplo lmen , arterial se indicado e acesso venoso perifrico; considerar cateterizao vesical; - Monitorizao: somatometria entrada, temperatura, presso arterial, frequncia cardaca, diurese, variao ponderal e balano hdrico, exame neurolgico, escala neurolgica anexo , monitorizao da funo cerebral, near infrared spectroscopy; - Avaliao laboratorial entrada : gasimetria na primeira hora de vida com lactato , hemograma com bastonetes, protena C reativa, ionograma, clcio, fsforo, magnsio, glucose, ureia, creatinina, LDH, AST, ALT, -GT, albumina, bilirrubina total e direta, fosfatase alcalina, CK, CK-MB, Troponina I e T, grupo sanguneo, hemocultura, estudo coagulao TP, aPTT, fibrinognio.

Aps estabilizao, deve ser contactado o centro de tratamento para discusso da situao, mesmo que o RN no cumpra todos os critrios indicados. Confirmada a indicao para tratamento, desligar todas as fontes de aquecimento ativo vide Temperatura e ativar o sistema de transporte INEM-RN. Se oligria mantida superior a 8h: administrao de blus de volume: NaCl a 0. ALIMENTAO - Alimentao parentrica depois das h, aps estabilizao da funo renal e eletrlitos; - Iniciar alimentao entrica mnima no segundo dia de vida se hemodinamicamente estvel, preferencialmente com leite materno.

Aumento lento e progressivo nos dias subsequentes de acordo com gravidade do quadro clnica e tolerncia alimentar. Nota: a semi-vida do fenobarbital prolongada durante a hipotermia, pelo que no devem ser prescritas doses de manuteno antes de doseamento srico. No entanto, no sendo este facto consensual, deve ficar ao critrio de cada unidade de tratamento.

A presena de qualquer alterao sugere a presena de encefalopatia moderada a grave, com indicao para tratamento com hipotermia. Normal - margem superior acima dos 10 V; - margem inferior acima dos 5 V; - pode haver evidncia de ciclos sono-viglia. Moderadamente alterado - margem superior acima dos 10V; - margem inferior abaixo dos 5V: isto significa que o EEG descontnuo.

Convulses: mudana sbita de amplitude; se convulses sucessivas, aspeto de dente de serra. Artefacto: pode ser por interferncia eltrica ECG ou de movimento.