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Pediatrics > Fetopathies > Flashcards

Fetopathies Flashcards

1
Q

Route of infection in Toxoplasmosis

A
  • fecal-oral (from cat feces)
  • contaminated water or soil, inadequatly cooked meat
  • transmission to embryo via placenta or during birth
  • mother can have acute infection or chronic if she is immunocompromised
  • The older the fetus, the higher the risk of fetal transmission
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2
Q

Clinical manifestations of congenital toxoplasmosis

A

FIRST TRIMESTER
- death, ophthalmologic and central nervous system consequences

SECOND TRIMESTER

  • Classic triad (hydrocephalus, intracranial calcifications, chorioretinitis)
  • rash (blueberry muffin)
  • hepatosplenomegaly
  • anemia
  • lymphadenopathy
  • microcephaly
  • developmental delay
  • visual problems and hearing loss
  • seizures

THIRD TRIMESTER
- common, but often asymtpomatic at birth

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3
Q

Diagnosis of toxoplasmosis

A

IN FETUS

  • Amniocentesis –> PCR
  • maternal ELISA

IN BORN CHILD

  • ophthalmologic examination
  • CT
  • Examine CSF for elevated protein and pleocytosis
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4
Q

Treatment of Toxoplasmosis

A

IN FETUS

  • if mother is infected, but not fetus –> spiramycin to prevent infection
  • when fetus is infected: give mother a combination of pyrimethamine, sulfadiazine, and folinic acid

BORN CHILD

  • Pyrimethamine, sulfadiazine and folinic acid for at least 1 year
  • if there is elevated protein concentration in CSF or severe chorioretinitis –> we can add corticosteroid like prednisolone
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5
Q

Congenital syphilis

- general information

A
  • caused by T. pallidum
  • transmitted via placenta
  • can lead to spontaneous abortion, stillborth or to congenital syphilis
  • can be infected at any developmental age
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6
Q

Classification of congenital syphilis

A

early congenital syphilis
–> develops in perinatal period, up to two years of age

Late congenital syphilis
–> develops after 2 years

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7
Q

Early congenital syphilis presentation

A
  • vesiculobulbous eruptions
  • maculopapular rash on palms, soles, nose, mouth and in diaper area
  • lymphadenopathy, hepatosplenomegaly
  • failure to thrive, fever, pneumonia
  • blood-stained nasal discharge
  • meningitis, choroiditis, hydrocephalus, seizures
  • ascites
  • within first 8 months: osteochondritis of the long bones and ribs can occur
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8
Q

Late congenital syphilis presentation

A
  • gummatous ulcers (nose and septum)
  • Hutchungton’s triad
    1- Syphilitic keratosis
    2- syphilitic conjunctivitis
    3- Hutchington’s teeth
  • clutton’s joints, saddle nose, saber shins, high palate, palate perforation, frontal bone protusion, short maxilla, mandible protrusion
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9
Q

Diagnosis of early congenital syphilis

A
  • clinical examination
  • dark-field microscope
  • lumbar puncture for CSF analysis
  • Long bone and cest X-ray –> wimberger sign (symmetric erosions of upper tibtia and long bones)
  • serologic testing
  • -> treponemal test
  • -> non-treponemal test

If NTT antibody titer >4 times the maternal titer, it indicates in most cases syphilis

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10
Q

Diagnosis of late congenital syphilis

A
  • clinical history and examination
  • positive serologic tests (same as in early CS)
  • Hutchington’s triad is indicative
  • poritive fluoroscent treponemal antibody absorption test
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11
Q

Treatment in early CS

A
  • benzathiene benzylpenicillin G (BPG)

- alternatives: doxycycline, ceftriaxone, azithromycin

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12
Q

Treatment in late CS

A
  • BPG

- if allergig: penicillin desensitization or doxycycline

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13
Q

Neurosyphilis treatment

A
  • Benzylpenicillin

- second choice: ceftriaxone, probenecid

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14
Q

Treatment of CS in pregnancy

A

for early syphilis

  • erythromycin
  • azitromycin
  • ceftriaxone

For late:
- erythromycin

DO NOT GIVE DOXYCYCLINE

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15
Q

Herpes simplex virus

- route of infection

A
  • direct contact with infected lesions or mucosa
  • neonates most oft4en thorugh an infected vaginal canal during birth
  • c-section reduces risk of infection if there is active maternal sheddign of HSV
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16
Q

Herpes simplex virus

- clinical manifestations

A
  • will present in firt 6 weeks of life
  • presents in one of three ways:
  1. Neurological symptoms: meningoencephalitis (mostly after 10-14 days)
  2. Systemic symptoms: major overwhelming illnes including shock, respiratory failure and severe haptitis and coagulation disorders, sometimes meningoencephalitis
  3. Cutaneous symptoms: rash, blisters and keratoconjunctivitis in second week of life
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17
Q

Herpes simplex virus

- complications

A
  • unctreated –> high morbidity and mortality
  • recurrent skin outbreaks despite treatment
  • neurologic outome for infants with CNS disease, even with treatment
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18
Q

Herpes simplex virus

- diagnosis

A
  • serum HSV IgM
  • HSV PCR
  • HSV culture of a lesion
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19
Q

Herpes simplex virus

- treatment

A
  • IV acyclovir
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20
Q

Rubella

- route of infection

A
  • contact wiht respiratory secretions and transplacentally
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21
Q

Rubella

- clinical manifestations

A
  • blueberry muffin rash
  • lymphadenopathy
  • hepatosplenomegaly
  • thrombocytopenia
  • interstitial pneumonitis
  • intrauterine growth restriction
  • infection after 12 weeks may have no clinical manifestations but is more likely to resilt in futre hearing loss and visual problems
  • eye problems: microphthalmos, pigmentary retinopathy, cataracts and congenital glaucoma
  • cardiac: pulmonic stenosis, patent ductus arteriosus
  • Endocrine: DM
  • Neurologic: developmental delay, encephalitis, hearing loss
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22
Q

Rubella

- diagnosis

A
  • virus can be isolated from blood, urine, CSF, oral and nasal secretions –> culture
  • serologic tseting for rubella-specific IgM and IgG in pregnant woman
  • rubella-specific IgG positive, considered immune
23
Q

Rubella

- treatment

A
  • prevented by maternal vaccination, 2 doses of MMR vaccine

- no treatment of rubella outside of supportive measures

24
Q

Varizella-Zoster Virus (VZV)

- route of infection

A
  • respiratory droplets
  • direct contact with skin lesions
  • congenital varicella: transplacentally
25
Q

VZV clinical manifestations

A
  • early symptoms: cold symptoms, fever, abdominal pain, headaches, general malaise
  • infection transmitted under 20 weeks: risk of fetus developing congenital varicella syndrome –> skin scarring, eye abnormalities, limb hypoplasia, cortical atrophy and microcephaly
  • infection a week beofre or up to 28 days: high risk of fatal varicella
  • Zoster immunoglobulin should be given immediatly to infants at high risk of congenital varicella
26
Q

VZV diagnosis

A
  • should be suspected in mother who presents with typical signs
  • in an infant who presnts with typical vesicular lesions –> PCR or direct fluoroscent antibody of the fluid
  • serology-speficic IgM and IgG antibodies in blood
27
Q

VZV treatment

A
  • pregnant women –> acyclovir
  • infants born with congenital varicella –> acyclovir and varizella-zoster immunoglobulin
  • vaccine (but not in pregnant women)
  • pregnant women who are exposed to VZV_ varizella-zoster immunoglobulin
28
Q

Cytomegalovirus (CMV)

- route of infection

A
  • saliva
  • genital secretions
  • breast milk
  • blood products
  • transplacentally
29
Q

CMV

- clinical presentation

A
  • most infants are asymptomatic at birth
  • petechiae
  • jaundice
  • hepatosplenomegaly
  • thrombocytopenia
  • small size
  • microcephaly
  • intracranial calcifications
  • sensironeural hearing loss
  • chorioretinitis
  • seizures
30
Q

CMV

- diagnosis

A

PRENATAL

  • Ultrasound
  • Amniocentesis
  • Fetal blood sampling for IgM

POSTNATAL

  • PCR or viral isolation in newborns under 3 weeks of age
  • clinical signs
  • liver panel: increased liver transaminases and bilirubin
  • Blood count: thrombocytopneia and decreased platelets
  • neuroimaging: calcifications, enlarged ventricles, polymicrogyria, lenticulostriate vasculopathy, white matter disease
31
Q

Long term consequences of CMV

A
  • hearing loss
  • neurodevelopmental disablities
  • cerebral palsy
  • intellectual disability
  • seizures
  • ocular damage
32
Q

CMV

- prevention and treatment

A
  • hygiene measures for mothers
  • pregnancy titers to identify at risk mothers
  • ganciclovir, valganciclovir (oral)
  • IV ganciclovir
  • no vaccine available
33
Q

Diabetic embryopathy

up to 9th week of gestation

A
  • heart defects, skeletal defects, neuronal tube defects

- can be improved with pre-conception glycemic control

34
Q

Diabetic fetopathy

from 9th week of gestation

A
  • macrosomia in the 3rd semester
  • birth weight over 4000g
  • increased risk for labor complications: shoulder dystocia, asphyxia, birth injury
  • transient hypoglycemia, congestive heart failure
35
Q

late onset neonatal sepsis

- diagnosis

A
  • blood culture
  • PCR
  • serum inflammatory biomarkers
  • monitoring of physiological data, heart rate
36
Q

Hematologic scoring system (HSS)

A

Based on follwing severn criteria:

  • high values of total leukocyte count
  • high PMN level
  • elevated immature PMN count
  • Elevated immature to total PMN ratio
  • Immature to mature PMN ratio > 0.3
  • platelet count > 150.000/mm3
  • pronounced degenerative changes in PMNs

score > 2 –> likelyhood of sepsis

37
Q

IL6 and IL8 in late neonatal sepsis

A
  • they can be detected in blood early

- short half life

38
Q

CRP in late neonatal sepsis

A
  • best diagnostic marker
39
Q

Pro-calcitonin and presepson in late neonatal sepsis

A
  • more specific than CRP in bacterial infections
40
Q

Additional investigations in late neonatal sepsis

A
  • chest x-ray
  • blood gas
  • renal function test
  • liver function test
  • coagulation profile
41
Q

late neonatal sepsis

- clinical presentation

A
  • depends on virulence of pathogens
  • body temperature may be elevated or depressed
  • mtoro functions are reduced
  • delayed weight gain
  • pale skin
  • reduction of activity
  • cyanosis, apnea, tachycardia, bradycardia, hypotension
  • jaundice sometimes only symptom
  • CNS: drowsiness, irritability, lethargy, conculsions, increased tension at fontanelles
  • GI: vomiting, diarrhea, anorexia, abdominal distension
  • Cardiac: bradycardia, tachycardia, poor perfusion
  • oliguria and anuria
42
Q

late neonatal sepsis

- treatment

A
  • empiric therapy until identification of the casative therapy
  • usually vancomycin and an Aminoglycoside
  • duration from 7 to 21 days
  • supoortive therapy
43
Q

late neonatal sepsis

- prevention

A
  • universal GBS screening of all pregnant wimen at 35-37 weeks of gestation
  • penicillin, ampicillin, cezazolin or clindamycin at least 4 hours before delivery
  • breastfeeding
  • administration of lactoferrin
  • probiotics
44
Q

late neonatal sepsis

- definition

A
  • onset of manifestation after 72 hours of life
  • during first 3 months: innate immune system provides defence against pahtogens
  • Decreased function of neutrophils and lower concentration of immunoglobulins increase
    susceptibility of infections.
45
Q

late neonatal sepsis

- transmission

A
  • horizontla: postnatally from hospital environment or from community
  • hand contamination is most common
  • parturition
46
Q

late neonatal sepsis

- risk factors

A
  • poor hygiene
  • low birth weight
  • prematurity
  • invaisve ventilation
  • prolonged use of antibiotics
  • breakage of natural barriers
  • H2 receptor antagonists
47
Q

late neonatal sepsis

- microorganisms

A 
Group B streptococcus and coagulase negative staphylococcus (S.aureus, especially in
neonates with vascular access catheters)
• Gram negative organisms
• Gram positive organisms
• Acinetobacter spp
• Klebsiella
• E. coli
• Candida spp. (Candida parapsilosis)
• Herpes simplex virus
• Enterovirus
Infrequent
• Streptococcus pyogenes
• Neisseria gonorrhoeae
• Enterococcus faecalis
• Streptococcus pneumoniae
48
Q

Early onset neonatal sepsis

- definition

A
  • day 0-3
  • most present in first 24 hours
  • most rapid onset is in premature neonates
49
Q

Early onset neonatal sepsis

- route of infection

A
  • blood, placenta, ascending cervical infection
  • neonate bay be exposed to mother’s Genitourinary tract during birth (Group B streptococci, E. coli, coagulase negative staphylococci, H. influenza, L. monocytogenes)
50
Q

Early onset neonatal sepsis

- prophylaxis

A
  • intrapartum prophylactic antibiotic treatment in mothers
  • GBS screening in weeks 35 and 37
  • culture obtained with vaginal and anal swabs
  • delivering baby wihtin 12 to 24 hours of then membrane breaks
51
Q

Early onset neonatal sepsis

- treatment

A
  • combination of IV glycosides with expanded spectrum penicillin
  • specific antibiotics are chosen based on mothers history and trends of organism colonization and susceptibility
52
Q

Early onset neonatal sepsis

- diagnosis

A
  • blood tests: CBC, CPR, blood culture
  • skin and stool cultures
  • lumbar puncture (CSF)
53
Q

Early onset neonatal sepsis

- clinical presentatio

A
  • general: lethary, hypothermia, poor feeding
  • non-specific signs: anuria and acidosis
  • Respiratory symptoms: apnea, tachypnea, nasal flaring
  • Cardiac symtpoms: cyanosis, desaturation, bradycardia

preterm infants: apnea, bradycradia, cyanosis as first signs

Pediatrics (11 decks)

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