Pediatric Sessions Flashcards
36 week gestation, feeding difficulties, intermittent cyanosis, apneic spells. what ddx do you think of?
- Sepsis
- congenital heart defect
- respiratory distress syndrome
- inborn errors of metabolism (can be present from 6 hours-3 weeks)
- hypoxic/ischemic encephalopathy (compromise of O2 to the fetus)
- TORCH infections- toxoplasmosis, rubella, CMV, herpes infections
- seizures
- intracranial bleed
8-9 days after, infant appears ill, has moderate resp. distress with mild subcostal retractions, dusky blue color thats intermittent, tachycardia and tachypnea were present. auscultation of lungs shows crackles but no regions of consolidation, heart auscultation shows no murmurs. palpation of abdomen shows no masses. initial ddx and plan?
could be classic presentation of baby with neonatal sepsis
neonatal sepsis
definition: clinical syndrome in neonate characterized by systemic signs of infection with bacteriemia in first month of life
meningitis is usually a sequela of bacteremia and usually shares common cause and pathogenesis (thus need blood cultures and CSF tests)
typical organisms include both + and - organisms
two patterns of disease: early and late onset sepsis
early onset sepsis
first week of life
usually complications w/ pregnancy (mom had fever, strep screen suspect)
organism usually comes from mothers genital tract
clinical presentation: fulminant (kids get sick fast), **multisystem,
**pneumonia is frequent
mortality rate 3-50% (half of these babies could die) - must work baby up for sepsis immediately
Gram + organisms: Group B strep, listeria monocytongenes
Gram - organisms:
E. coli, H. influenza, citrobacter, candida
late onset sepsis
7-90 days out
- organism can come from mom or be post-natal environment
- presentation is slowly progressive but can be fulminant(severe/sudden) as well
- **focal meningitis is frequent
mortality rate: 2-40%
organisms:
Gram +: Group B strep, Staph aureus, coagulase negative staph, listeria monocytongenes (neonatal meningitis)
Gram - organisms:
E. coli, H. influenza, citrobacter, candida
+ organisms associated with bacterial sepsis
Group B strep - EOS/LOS
Staph aureus - LOS
Coagulase neg. staph - LOS
Listeria monocytogenes - LOS/EOS (hx of mom ingesting cheese and dairy products and canteloupe)
gram- associated with group B strep
E. coli (EOS and LOS)
Haemophilus influenza
Citrobacter
Candida albicans
what are clinical signs of bacterial sepsis
1/2 have hyperthermia - fever
15% have decreased temp
33% have resp. distress
apnea, cyanosis, jaundice, hepatomegaly, lethargy, irritability, anorexia, vomiting abdominal distension
clinical signs of bacterial meningitis?
62% have hypothermia/fever
50% with lethargy/irritability 48% anorexia and vomiting 41% resp. distress 35% bulging or full fontanelle 31% siezures 28% jaundice 16% nuchal rigidity diarrhea
how to make ddx of neonatal sepsis?
blood culture is gold standard
serum biomarkers can serve as adjunct to culture based ddx
Ideal marker:
- elevates early in infectious process
- stays elevated while sick
- has well defined values that differentiate infection from other entities
- a very high sensitivity and negative predictive value
CRP
most commonly used biomarker
synthesized 7 hours after exposure/infectious process
takes up to 24 hours after onset of infection to become abnormal
is also elevated w/ trauma and ischemia
good indicator for neonatal sepsis? probably not, so many resons it could be high
CRP does have high specificity - meaning if you have baby thats been sick for 48 hours and run CRP and its negative, it rules out neonatal sepsis
management of sepsis?
IV access, take blood cultures, CSF cultures, ABG, CXR, glucose electrolytes, BUN, CR, CRP levels
lab results of case: CSF shows mononuclear pleocytosis of 330 cells. EEG shows multifocal epileptic potentials consistent with encephalitis. CRP 5 (normal is less than 10)
mononuclear pleocytosis - significant for viral infection
Pleocytosis is an increased cell count {Gk. pleion more}, particularly an increase in white blood cell (WBC) count, in a bodily fluid, such as cerebrospinal fluid (CSF).[1] It is often defined specifically as an increased WBC count in CSF.[2]
empirical tx with amoxicillin/gent/acyclovir is started. despite antibiotics the baby continues to deteriorate with tachycardia and respiratory distress. new studies needed?
seems to have viral encephalitis
CXR shows pulmonary edema and infiltrates
EKG: shows ST depression and tachycardia (heart is becoming is ischmic) in V1-V4
Echo: shows normal anatomy with severely reduced LV EF of 20%
troponin levels are very high with newborn (10.2, should be less than 0.04)
this probably viral
final ddx of baby?
enterovirus coxsackie B3 myocarditis - this is one of the most common viruses causing disease in humans with 10-15 million infections yearly in US
infections occurs in summer and fall, and range from nonspecific febrile illness, mild URIs, myocarditis, hepatitis and encephalopathy.
transmission to neonate is antenatally, intrapartum and postnatally - it can occur in many different ways
clinical features of enterovirus infection?
wide spectrum of signs ranging from nonspecific febrile illness to fatal multisystem disease called “Neonatal Enterovirus Sepsis”
most common presents: fever, irritability, poor feeding and lethargy
hepatomegally may be present but splenomegaly is rare - half show evidence of hepatitis
nonspecific rash seen on half of infants
tx for neonatal enterovirus sepsis
VI IgG give
dopamine and milrinone started for decreased CO and developed arr.
extracorporeal membrane oxygen (ECMO) was started - heart and lung machine used for babies - allows for heart to be rested and sometimes the heart will improve
what does post-mortem exam show of viral myocarditis?
inflamm. infiltrate lymphocytes and extensive necrosis of myocardium - virus got into the heart and resulted in a myocarditis that was fatal
often these children need heart transplants
pediatric patients
<18 y/o
premature
<37 y/o
chlorampehenicol
- antibiotic that is strong and unable to be metabolized in children
“gray baby syndrome” - see abndominal distension, vomiting, diarrhea, characteristic gray color, resp. distress, hypotension, progressive shock
thalidomide
“phocomelia” - used for nausea in pregnant women
- inhibition of DNA synthesis/angiogenesis
saw congenital abnormalities, polynueuritis, nerve damage, mental retardation
Sulfonamide
“kernicterus”
- displaces billirubin from protein-binding sites on albumin, this bilirubin deposits in brain
- due to immature glucoronidation pathways
benzyl alcohol
used in many IV drips
- this has resulted in “caspean baby syndrome” - resp distress, metabolic problems,
drug absorption in GI tract
Gastric pH
- full term infant: pH 6-8 at birth
- pH drops to 1-3 within 24 hours
- premature infants have immature acid secretion adn pH remains elevated
- extrauterine factors most likely responsible for initiating acid production (nutrition)
Gastric emptying in neonatl period?
irregular and unpredictable
- gastric emptying is slowed/prolonged in premature infants, leads to prolonged contact time, increased absorption, can also delay absorption if drug is absorbed further down intestine
- this approaches adult values in first 6-8 months of life
- there is inverse relationship to gestation age and gastric retention: younger baby = increased gastric retention
