Sepse pediatrica

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Sepse Pediátrica 2017
Renato Barradas Rodrigues
Tipo: Artigo
Assunto/Tema: Educação Médica
Referências Bibliográficas: 
Pediatric Sepsis, 2017, Melanie K. Prusakowski, Audrey P. Chen.
Resumo/ Conteúdo de Interesse:
 A sepse pediátrica, assim como a sepse do adulto é uma condição grave, causada por uma reação inflamatória sistêmica e deletéria do organismo a um agente infeccioso. É uma grande fornecedora de estatísticas de morbidade e mortalidade em todo o mundo e também razão de altos gastos em saúde. Reconhecê-la precocemente no paciente e realizar o tratamento adequado, como a ressuscitação volêmica e o uso de antibióticos, é de fundamental importância para a diminuição desses números. 
 Em sua definição clínica,	tanto a Síndrome de Resposta Inflamatória Sistêmica (SIRS), quanto a sepse diferenciam-se dessas condições no adulto. A primeira envolve 4 critérios: temperatura retal ou anal maiores que 38,5ºC ou menores que 36ºC; taquicardia, bradicardia e Leucocitose, leucopenia ou “bandemia” (presença de células sanguíneas imaturas); sendo que o paciente precisa preencher 2 dos 4 critérios e um deles deve ser o da temperatura ou o de leucócitos. É importante ressaltar que esses parâmetros variam de acordo com a idade da criança. A sepse é caracterizada pela presença da SIRS com um foco conhecido ou suspeitado de infecção. A sepse grave é caracterizada ainda com o desenvolvimento ou de disfunção cardiovascular, ou de Síndrome do Desconforto Respiratório agudo (SDRA), ou como disfunção orgânica em 2 sistemas diferentes. Por último, o choque séptico é caracterizado pela sepse com alterações na frequência cardíaca (FC) e na perfusão capilar.
 No manejo inicial da sepse, os principais objetivos são garantir ventilação e oxigenação adequadas, dar suporte circulatório e restaurar a perfusão, assim como iniciar a antibioticoterapia. Esses fatores, além de serem fundamentais para a melhoria do prognostico do doente, se assemelham na sepse do adulto, mas não são os únicos. Condições crônicas como má formações cardíacas congênitas e doenças hepáticas ou neuromusculares são também agravantes do quadro. A acidose metabólica é um sinal de agravamento, assim como sinais de coagulação intravascular disseminada (CID), e é medida com o lactato sérico. A lesão renal aguda também é marcador importantíssimo no prognóstico.
 No entanto, a sepse pediátrica possui mais diferenças do que similaridades ao adulto. Possui menor mortalidade, assim como etiologias diferentes. Em crianças mais jovens, se torna muito mais comum a apresentação de um choque frio, devido à baixa compensação inotrópica desses pacientes, que desencadeia uma vasoconstricção periférica importante. Também possuem maior chance do colapso respiratório devido ao baixo volume residual, menor superfície alveolar, etc. Complicações hematológicas, glicêmicas, relacionadas ao cálcio e outros dados semiológicos, da mesma forma, são mais comuns nas crianças.
 Ao dar entrada em uma unidade de saúde o manejo inicial adequado, respeitando as regras citadas, é: suporte ventilatório com oxigênio de alto fluxo, garantir acessos venosos (idealmente 2) ou ósseo em 5 minutos, monitorização cardiorrespiratória e oximetria de pulso. É recomendado também monitorar a temperatura, PA e a produção urinária. A ressuscitação volêmica deve ser maior que 40ml/kg na primeira hora com alguns pacientes necessitando de até 200ml/kg. O correto é realizar bolus de 20ml/kg, nos primeiros 15 minutos para acelerar a recuperação volêmica. Deve-se prestar atenção para sinais de “encharcamento” do paciente. Gasometria, hemograma completo, cultura de sangue, urinálise com cultura e outras culturas pertinentes a casos específicos formam o grupo de primeiros exames laboratoriais. A intubação e ventilação mecânica também podem ser proveitosas e a droga de melhor escolha para a indução é a Ketamina. Em alguns casos de sangramentos, plaquetopenia e outros podem necessitar de transfusões de plasma fresco, plaquetas, etc.
 Os choques refratários a fluídos são aqueles que mesmo com ressuscitação volêmica adequada os sinais de hipoperfusão persistem. A dopamina começada a 5ug/kg/min e chegando aos 10ug/kg/min é a primeira linha de tratamento nesse caso. Os choques frios refratários a dopamina são tratados com Epinefrina 0,5-1,5ug/kg/min e os quentes, Norepinefrina de 0,3-1ug/kg/min. Nesses casos é sempre importante avaliar causas de choque refratário e como intervir nestas, caso presentes. O tratamento definitivo é a oxigenação por membrana extra-corpórea. Nessa fase deve-se pensar também na transferência do paciente a um hospital terciário.
 Como os choques refratários ás catecolaminas não possuem muitos estudos randomizados que padronizam o uso de corticoides, seu uso deve ser reservado e cuidadoso.
 A terapia com antibióticos é geralmente seguida com ceftriaxona, cefepima ou vancomicina. Algumas exceções incluem um esquema de Penicilinas de amplo espectro ou cefalosporinas de 3°/4° gerações ou carbapenemes mais aminoglicosídeo e vancomicina. Deve-se prestar atenção para agentes não comuns como fungos e outros. Aos recém-nascidos, atenção especial a agentes aos quais este não é vacinado e a escolha é um esquema de ampicilina com gentamicina e vancomicina.
 A correção da hipoglicemia é feita com a administração de solução de dextrose apropriadas para a idade. A correção da hipocalcemia é feita com cálcio gluconato 50-100mg/kg ou 100 a 200mg/kg em casos de tetania.
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	Pediatric sepsis is life-threatening organ dysfunction caused by a deleterious host response to infection,1 and it continues to be a leading cause of death for children in the United States
	1
	2 Neonates, infants, and children with chronic medical conditions comprise a large percentage of those with morbidity and mortality from sepsis or septic shock.
	1
	The estimated annual health care expenditures for the treatment of pediatric severe sepsis is just under $5 billion in the United States.
	1
	The definition of pediatric SIRS differs from the adult definition in its requirement that at least 1 of the diagnostic criteria must be high or low core body temperature or a leukocyte count abnormality (Box 1).
	2
	Throughout pediatric development, vital signs and laboratory values change requiring, thoughtful attention to age-related norms (Table 1)11,12 for accurate and early SIRS and sepsis recognition.
	2
	Pediatric sepsis necessitates that the patient meet the SIRS criteria in the presence of a known or suspected infection (eg, bacterial, viral).
	2
	Severe sepsis in pediatrics is recognized as sepsis with the development of cardiovascular dysfunction or acute respiratory distress syndrome, or organ dysfunction in at least 2 systems (including renal, hematologic, neurologic, hepatic, or respiratory systems).
	3
	Septic shock is defined as sepsis with cardiovascular dysfunction manifesting as alterations in HR (tachycardia or bradycardia) and signs of impaired perfusion.
	3
	The International Pediatric Sepsis Consensus developed organ dysfunction definitions for cardiac, respiratory, hematologic, neurologic, renal, and hepatic systems (Box 4) that can guide the clinician’s diagnosis and trajectory of sepsis, severe sepsis, and septic shock.
	3
	Much like in adults, foundations of care include early recognition of sepsis, aggressive fluid resuscitation, timely administration of antibiotics, and source control.
	3
	Just as comorbid conditions drive the mortality of sepsis in adult patients, medical conditions such as prematurity, congenital heart disease, solid and hematopoietic cancers, and immune deficiencies significantly increase the mortality of pediatric sepsis.
	4
	The early investigation of sepsis in an infant or child includes source identification (eg, cultures and antigen testing) and inflammatory and biomarker marker evaluation (eg, white blood cell count, erythrocyte sedimentation rate, C-reactive protein analysis,lactate level).
	4
	In all populations, disseminated intravascular coagulation (DIC) impacts the likelihood of developing multisystem organ failure.
	4
	 The comorbid conditions most often observed in infants with sepsis are congenital heart disease and chronic lung disease, whereas cancer and neuromuscular disease emerge more often in childhood sepsis.
	4
	The site of infection is also age dependent
	4
	The pathology of illness in infants and young children is affected by their proportionally higher ratio of extracellular to intracellular fluid. The larger the percentage of extracellular fluid, the more likely decreased intake or increased losses will predispose them to rapid fluid losses
	4
	. Additionally, the younger the myocardium, the more likely it is functioning at a baseline high contractile state.
	4
	This pathophysiology explains the efficacy of inotropes as first-line therapy in fluid-refractory shock.
	4
	21 When increasing HR is no longer able to sustain adequate CO, vasoconstriction occurs in response to decreasing stroke volume and contractility
	4
	This mechanism makes cold shock more likely in the pediatric population
	6
	. Infants and children with sepsis are at greater risk for respiratory collapse than adults owing to a combination of proportionally lower alveolar surface area, lower functional residual capacity, more compliant chest wall dynamics, and relatively greater expenditure of energy to maintain respiratory drive when in distress.
	6
	In conjunction with a tendency to generate relatively higher systemic vascular resistance, a reduction in oxygen delivery, rather than a defect in oxygen extraction, can be the major determinant of oxygen consumption in pediatric sepsis.13
	6
	Neonates and young infants may be at increased risk for bleeding complications owing to lower circulating levels of vitamin K–dependent procoagulant factors, decreased thrombin production, lower circulating levels of coagulation inhibitors, and relatively hyporesponsive platelets.16 Hypocalcemia is a more frequent contributor to cardiac dysfunction in pediatric (especially neonatal) sepsis owing to a variety of developmental factors. Hypoglycemia is relatively common in neonates
	6
	Illness can be indolent and progressive or sudden and dramatic
	7
	Fever is a common presenting sign of sepsis in the pediatric populations, but is not specific to sepsis as a source of infection. Younger children and infants (much like the elderly) can also present with hypothermia as a manifestation of sepsis.
	8
	Signs of cold shock are more common in children because they use vasoconstriction to maintain blood pressure when stroke volume decreases. This phenomenon manifests as weak or absent distal pulses, prolonged capillary refill, cool extremities, and mottling of the skin.
	8
	Infants and children who present with sepsis may be described as fussy, sleepy, lethargic, irritable, not feeding well, or “just not looking right.”
	8
	Given the relative paucity of developmental abilities in neonates, this population is most likely to present with nonspecific, subtle signs of infection and are at greatest risk of having recognition delayed until more ominous mental status or vital sign changes occur.
	8
	Metabolic acidosis results when tissues and organ systems are hypoperfused with respect to their oxygen and substrate demands. Infants and children often become tachypneic in the setting of metabolic acidosis, even when the lungs are not the primary source of infection.
	8
	Similar to adults, the evaluation of sepsis focuses on source identification through cultures, laboratory studies, and imaging as appropriate. Inflammatory markers are less well-studied and supported than in adult sepsis
	9
	In the setting of pediatric sepsis, the first hour of resuscitation begins with initiating high-flow oxygen delivery by nasal cannula (nasopharyngeal continuous positive airway pressure is also acceptable) or 100% oxygen supplement by nonrebreather mask. Simultaneously, intravenous or intraosseous access should be established within 5 minutes.13,26,27 Continuous cardiorespiratory and pulse oximetry monitoring should be applied and are useful tools for assessing resuscitation progress. It is recommended to monitor temperature (eg, rectal, oral, bladder catheter), cycle a blood pressure at least every 15 minutes, and track urine output.
	9
	The goals within the first hour are to establish or maintain an airway, optimize oxygenation and ventilation, support circulation and restore adequate perfusion, and administer antibiotics early.13
	9
	Intravenous fluid resuscitation should begin with a 20 mL/kg rapid bolus of crystalloid.13 Initial laboratory studies should include peripheral blood culture, culture from indwelling central line or port if applicable, a complete blood count (with automated differential), coagulation studies, DIC studies, complete metabolic panel, ionized calcium, lactic acid, arterial blood gases or venous blood gases, urinalysis with culture, cerebrospinal fluid studies if meningitis is suspected, and other appropriate cultures (eg, wound, sputum).
	9
	Viral sources are common in pediatrics and targeted testing may be of significant value
	9
	Ideally, 2 intravenous lines should be established if possible to augment fluid administration and to ensure safe and timely administration of inotropes and antibiotics, because some of these medications must be given in separate intravenous lines
	9
	Fluid administration by gravity does not deliver resuscitation volume in a timely manner; therefore, it is recommended to give a 20 mL/kg (maximum 1000 mL per bolus) bolus over 5 minutes by syringe push or pressure bag.30 Repeat fluid boluses over the first 15 minutes while reassessing after each fluid bolus for response to treatment and signs of fluid overload. Often, resuscitation requires 40 to 60 mL/kg of crystalloids, with some children requiring upwards of 200 mL/kg.1 When sepsis resuscitation efforts in the ED fail to give more than 40 mL/kg within the first hour, the risk for mortality significantly increases.31
	10
	However, attention should also be given to signs of heart failure and fluid overload.13 Signs of heart failure or fluid overload include the development of rales, cardiomegaly on chest radiograph, increased work of breathing, hypoxemia owing to pulmonary edema, and hepatomegaly. Development of fluid-overload warrants cessation of fluid resuscitation and initiating diuretic therapy and inotropic support.
	10
	Resuscitation endpoints in the first hour include goals to (1) normalize vital signs for age, (2) normalize mental status, (3) achieve capillary refill of 2 seconds or less, and (4) produce urine output of greater than 1 mL/kg/h. Admission for pediatric sepsis should be to the pediatric intensive care unit.
	10
	Roughly 40% of CO is required to sustain respiratory efforts for a child during septic shock.13 Intubation and mechanical ventilation can help to reverse shock by maximizing CO through reduction in cardiac effort required to maintain work of breathing
	10
	Ketamine is a useful potential alternative induction and sedation agent owing to its favorable hemodynamic profile.
	10
	The ACCM guidelines recommend that fluid-refractory shock should be considered if after giving 40 to 60 mL/kg of isotonic fluids, hypotension or signs of poor perfusion are present. Once fluid refractory shock is recognized, the next step is to consider whether cold shock or warm shock (see Table 2) is present.
	10
	Dopamine (started at 5 mg/kg/min and titrated up to 10 mg/ kg/min) is first line for treating fluid-refractory shock
	11
	Those who remain in shock despite greater than 10 mg/kg/min of dopamine usually respond to continuous infusions of norepinephrine (0.05–1.5 mg/kg/min)34 for warm shock, or epinephrine (0.05–0.3 mg/kg/min, maximum of 1 mg/kg/min) for cold shock.
	11
	Finally, patientswith refractory shock should be evaluated for potentially reversible underlying causes of shock
	11
	Extracorporeal membrane oxygenation remains the definitive treatment for patients with refractory septic shock. This treatment should be taken into account when considering transfer options to a tertiary hospital.
	11
	Steroid use in pediatric sepsis remains a controversial topic because there are very limited randomized controlled trials to guide recommendations.
	11
	The ACCM guidelines reserve recommendation for steroid use only in children who do not respond to epinephrine or norepinephrine infusions (eg, catecholamine-resistant shock) and are suspected to be at risk for adrenal insufficiency or hypothalamic–pituitary–adrenal axis failure. For these patients, a baseline cortisol level should be drawn before administering hydrocortisone stress dose.
	11
	Antibiotics should be given within the first hour of sepsis and septic shock.13,27,35 Common choices include ceftriaxone, cefipime, and vancomycin. Factors such as local antibiotic resistance patterns, recent antibiotic use, existing immunosuppression, and drug allergies may factor importantly when choosing antibiotic therapy.
	11
	Glucose derangements are common in critically ill children and infants and require prompt recognition and correction by the emergency physician.
	12
	 Acute hypoglycemia is treated by correcting deficit to normal glucose levels by giving appropriate dextrose-containing solutions for age.
	12
	13 Hyperglycemia, after initial stress response, can be complicated by impaired insulin production and insulin resistance in sepsis.
	12
	Similarly, the ACCM guidelines recommend correcting hypocalcemia (defined as ionized calcium <1.1 mmol/L), because it may contribute to cardiac dysfunction. Intravenous calcium gluconate (50–100 mg/kg) given over 3 to 5 minutes is the treatment for hypocalcemia with cardiac manifestations and a dose of 100 to 200 mg/kg/dose over 20 minutes is recommended for patients with tetany.
	13
	There are, however, some pediatric patient groups with characteristics that put them at risk of sepsis from other unique pathogens
	13
	The risk of sepsis after splenectomy is especially high in children younger than 5 years of age at the time of surgery. Pneumococcus accounts for 50% of sepsis after splenectomy, but patients are at risk of invasive infection from all encapsulated microorganisms.
	13
	Compromised innate or adaptive immunity places patients at greater risk of bacterial sepsis than the average population.
	13
	Burns compromise the innate immunity of the skin and result in neutrophil dysfunction and abnormal antibody response. Necrotic tissue can be a nidus of infection. Burn victims are at increased risk of sepsis, particularly from P aeruginosa, S aureus, and coagulase-negative staphylococci.
	13
	The neonate is a special pediatric patient in whom deficits in innate and adaptive immune responses are particularly pronounced.16 Additionally, this population is not immunized against many common organisms that cause significant morbidity and mortality in infants. Newborns are at risk for infection from Escherichia coli, Group B streptococcus, and Listeria.
	14
	Neonatal sepsis is more often associated with hypothermia than fever.41 Apnea is a common presenting sign. Severe neonatal sepsis is more likely to be associated with neutropenia than leukocytosis.41 These features are particularly pronounced in the premature neonate, who is also at particularly high risk for complicated sepsis related to deficiencies in the thyroid and parathyroid axes
	14
	Newborn sepsis can be complicated by cardiac and circulatory factors that are unique to the neonatal period.
	14