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Pediatric emergency medicine trisk 646

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Symptoms Signs Respiratory Increased work of breathing Cough Cyanosis Cardiac Pallor Gastrointestinal Poor feeding Vomiting Diarrhea Skin and musculoskeletal Hypothermia Fever Jaundice Floppiness Neurologic Lethargy Irritability Seizures Laboratory abnormalities CBC High WBC count Low WBC count High ANC Tachypnea Desaturations Hyperventilation Respiratory distress (grunting, flaring, retractions) Apnea Tachycardia Bradycardia Hypotension Poor capillary refill Shock Abdominal distention Ileus Low temperature High temperature Hypotonia Petechiae Rash Full anterior fontanelle Hypertonia or hypotonia Meningismus (occasional) Electrolytes: metabolic acidosis, hypernatremia, hyponatremia Liver function tests: hyperbilirubinemia (direct or indirect) Low ANC (neutropenia) High immature to total WBC (>0.2) Thrombocytopenia CRP: elevated Blood sugar: hyperglycemia Hypoglycemia Coagulation studies: DIC WBC, white blood cells; DIC, disseminated intravascular coagulopathy; ANC, absolute neutrophil count Triage Considerations Any symptomatic neonate should be assessed for the possibility of neonatal sepsis Neonates should be triaged urgently due to the potential for rapid deterioration Shock and respiratory distress demand emergent treatment and initiation of resuscitation Rapid establishment of intravenous access and urgent antibiotic therapy are needed Meningitis can present in a similar fashion and could be part of the systemic infection Clinical Assessment History of GBS colonization in the mother, chorioamnionitis, prolonged rupture of membranes, maternal postpartum antibiotic use, or presence of maternal symptoms of infection (fever, rash, or URI) may raise clinicians’ suspicion of early infection Presence of sick contacts, CHD, and prematurity are risk factors that may be elicited in late-onset disease Physical examination may be notable for hypothermia or fever and may reveal a localized source of infection (e.g., pneumonia, meningitis, septic arthritis, herpetic rash, NEC, or omphalitis) However, examination findings are usually nonspecific ( Table 96.7 ) Neonates with signs of shock should be presumed to have neonatal sepsis but should also be evaluated for coarctation of the aorta and cardiogenic shock Clinicians can attempt to narrow diagnosis by history and physical examination to a specific cause, however, this can be very difficult Complete blood count with differential will reveal leukocytosis or leukopenia, and may also show neutropenia, elevated immature to total white blood cell (WBC) ratio above 0.20 (calculated as immature cells [bands + myelocytes + metamyelocytes] divided by total neutrophils) C-reactive protein (CRP) is an acute phase reactant that becomes elevated to hours after infection It reaches peak around 24 hours after initiation of infection and can be used to monitor response to treatment, and optimize duration of treatment Other acute phase reactants and cytokines are being studied as markers of disease including procalcitonin and interleukin (IL)-6, IL-8, tumor necrosis factor-alpha, and granulocyte colony–stimulating factor but are not commonly used clinically CBC, CRP, and other nonspecific markers are useful indicators of disease None of these tests alone or in combination are sensitive enough to be used solely to exclude the diagnosis of bacterial infection Definitive diagnosis is isolation of a specific pathogen from a normally sterile site, such as blood, urine, or CSF culture Blood samples for culture should be at least mL to allow for identification of low levels of bacteremia A catheterized urine specimen or suprapubic aspiration for urinalysis and urine culture is recommended for all infants since ascending infection can lead to bacteremia CSF will show elevation in WBC count (20 to 30 cells/μL definitive), high protein, and/or low glucose in bacterial infections HSV encephalitis may demonstrate elevated CSF protein only CSF Gram stain may show presence of bacteria Lumbar puncture prior to antibiotic administration is recommended for all neonates due to high incidence of meningitis (23%) in cases of bacteremia and up to 30% of neonates may have a negative blood culture even in the presence of bacterial meningitis Lumbar puncture can be deferred if the infant has hemodynamic instability but should be performed as soon as the infant is stable Infants should be placed on cardiorespiratory monitors during the lumbar puncture procedure Traumatic results should be interpreted with care Correction of CSF WBC count according to the RBC count in traumatic taps does not improve the ability to diagnose meningitis Clinicians should avoid this correction and presume meningitis until the CSF culture results are available Other specific testing can be done (e.g., HSV CSF PCR, liver function tests, and CSF enteroviral PCR) if specific pathogens are suspected CXR can be helpful if the neonate has respiratory or cardiac symptoms but is not routine Management Any neonate with concern for bacterial or serious viral infection should be admitted to the hospital Initial management should include placing the infant on cardiorespiratory monitoring, with vital sign monitoring and clinical reassessments Normal saline boluses may be given in cases of hypoperfusion and shock Blood pressure stabilization with pressors may be needed In some cases hydrocortisone may be required Hypothermia should be corrected by gradual warming of the baby Hypoglycemia and electrolyte abnormalities should also be corrected Oxygen, humidified nasal cannula, or other respiratory support may be needed for neonates with apnea or respiratory distress Antibiotics should be given as soon as possible Whenever feasible, cultures should be obtained before starting antibiotics Obtaining cultures and starting antibiotics are a priority Lumbar puncture may be delayed if the baby is unstable Intravenous ampicillin and an aminoglycoside are recommended for early-onset sepsis For full-term infants less than days of age, 200 to 300 mg/kg/day of ampicillin, intravenously, in three divided doses is the recommended dose; for newborns beyond days of age, 300 mg/kg/day, intravenously, in four divided doses is recommended Cefotaxime can be added for better CNS penetration if gram-negative meningitis is suspected or if renal dysfunction precludes the use of an aminoglycoside Ceftriaxone should be avoided in neonates due to possibility of exacerbating hyperbilirubinemia as a result of bilirubin displacement from albumin, and the possibility of precipitating sludging in the gall bladder Intravenous vancomycin should be considered in neonates who have been at home and exposed to community-acquired Staphylococci Intravenous vancomycin and an aminoglycoside are recommended for empiric therapy of lateonset sepsis until isolation of the specific pathogen occurs; at which time antibiotic therapy can be tailored accordingly Acyclovir should be considered if there is suspicion for herpes simplex infection (suspicious vesicular rash, transaminitis, or history of exposure) Doses and intervals of antibiotics and antivirals can vary according to postgestational age, renal function, and liver function For an expanded discussion on fever in children to months of age, please refer to Chapter 31 Fever Pneumonia in the Newborn Neonatal pneumonia, similar to neonatal sepsis, can occur early (within the first 72 hours of life) or late (after week of life) Early-onset pneumonia occurs as a result of vertical transmission during the perinatal period, possibly through aspiration of infected amniotic fluid or chorioamnionitis Although Group B streptococcal infection is the most common pathogen, other organisms similar to those causing early sepsis can be responsible for infection (bacteria, viruses, and fungi) Chlamydia trachomatis is also acquired perinatally The long incubation period in neonates causes infants to present around to weeks of age with an insidious onset of a staccato cough without fever or wheezing Infants who pass through a vaginal canal infected with C trachomatis have a 3% to 16% risk of developing pneumonia Tuberculosis and syphilis can also cross the placenta to infect the fetus Late-onset pneumonia occurs as a result of horizontal transmission from the infant’s surrounding environment; Streptococcus pneumoniae is the most common organism Other etiologic agents that cause late-onset sepsis are also implicated in development of pneumonia Acute respiratory failure and rapidly evolving pneumonia can occur as a result of Bordetella pertussis infection in

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