neonatal case conference Flashcards

1
Q

A 8 day old female infant born at 36 weeks gestation presented to the ED with feeding difficulties, intermittent cyanosis and apneic spells.

Initial Differential Diagnosis

A

see now

septic until proven otherwise

congenital heart defect

metabolic disease

  • Sepsis
  • Inborn error of metabolism (IEM)
  • TORCH infections
  • Congenital heart disease
  • Hypoxic ischemic encephalopathy (get hypoxic in utero or during birth)
  • Intracranial bleed
  • Seizures
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2
Q

want to see red reflex in eyes

A

cataracts

retinoblastoma

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3
Q

The infant appeared ill with moderate respiratory distress with mild subcostal retractions and a dusky blue color of the lips and nail beds that was intermittent. Episodic apneic spells were observed that responded to administration of O2and stimulation. Tachycardia and tachypnea were present. Auscultation of the lungs revealed crackles but no regions of consolidation. Heart auscultation revealed no murmurs. Palpation of the abdomen revealed no masses or organomegaly.

A

neonatal sepsis

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4
Q

apneic spells

A

chlamydia

lung infection

mycoplasma

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5
Q

neonatal sepsis

A

Definition-a clinical syndrome in the neonate characterized by systemic signs of infection with bacteremia (have to get cultures from blood) in the first month of life

  • Meningitis is usually a sequelaof bacteremia and usually shares a common cause and pathogenesis
  • Typical organisms include both gram (-) and gram (+) organisms
  • Two patterns of disease-early and late onset
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6
Q

early onset neonatal sepsis

A

Time of onset
0-6days

Complicationsof pregnancy or delivery
+

Source of organism
Mother’s genital tract

Usual clinical presentation
Fulminant
Multisystem
Pneumoniafrequent

Mortalityrate
3-50%
2-40%

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7
Q

late onset neonatal sepsis

A

Time of onset
7-90 days

Complicationsof pregnancy or delivery
±

Source of organism
Mother’s genital tract; postnatal environment

Usual clinical presentation
Slowly progressiveorfulminant
Focal
Meningitis frequent

Mortalityrate
2-40%

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8
Q

mortality rate in neonatal sepsis

A

dpends on how much they see this problem

not a black and white problem til you get labs

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9
Q

Organisms Associated with Bacterial Sepsis

•Gram Positive organisms

A

Group B strep (GBS) (EOS and LOS)

Staphylococci aureus (LOC)

Coagulase negative staphylococcus (CoNS) (LOS)

Listeria monocytongenes

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10
Q

Organisms Associated with Bacterial Sepsis

•Gram Negative organisms

A

–E. coli (EOS and LOS)

–Haemophilus influenza

–Citrobacter

Fungi
Candida albicans

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11
Q

Clinical Signs of Bacterial Sepsis

A
Hyperthermia
51
Hypothermia
15
Respiratory distress
33
Apnea
22
Cyanosis
24
Jaundice
35
Hepatomegaly
33
Lethargy
25
Irritability
16
Anorexia
28
Vomiting
25
Abdominal distention
17
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12
Q

Clinical Signs of Bacterial Meningitis

A
Hypothermia or fever
62
Lethargy or irritability
52
Anorexia or vomiting
48
Respiratory distress
41
Bulging or full fontanelle
35
Seizures
31
Jaundice
28
Nuchal rigidity
16
Diarrhea
14
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13
Q

Diagnosis of Neonatal Sepsis

A
  • Blood culture remains the gold standard
  • Serum biomarkers can serve as an adjunct to culture based diagnosis

•The ideal marker
–Elevates early in the infectious process
–Stays elevated to allow appropriate sampling
–Have well defined values that differentiate infection from other entities
–A very high sensitivity and negative predictive value

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14
Q

C-Reactive Protein (CRP)

A
  • Most commonly used biomarker
  • Synthesized within 6 hours of exposure to an infectious process
  • But takes up to 24 hours after onset of infection to become abnormal
  • Is also elevated with trauma and ischemia
  • A good indicator of neonatal sepsis??
  • CRP does have high specificity between 93-100% meaning what??
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15
Q

Initial Management

A
  • IV access (where?) (JUGULAR)
  • Cultures
  • Blood
  • CSF? (late onset or meningitis, but early probably not bc going to use antibiotics)
  • ABG
  • CXR
  • Glucose, electrolytes, BUN, creatinine (why?) (kidneys could ahve become damaged so dont want to put more on kidneys with abs)
  • CRP
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16
Q

Initial Positive Results in our case

A
  • CSF showed mononuclear pleocytosisof 330 cells/μL (shouldn’t have any)
  • EEG showed multifocal epileptic potentials consistent with encephalitis
  • CRP 5 mg/L (Normal
17
Q

Initial treatment

A
  • Empirical treatment with amoxicillin, gentamicin and acyclovir were started. A loading dose of phenobarbital was given. (bc of seizure)
  • Despite antibiotic therapy the baby continues to deteriorate with tachycardia and increasing respiratory distress requiring intubation.
18
Q

new studies in pt

A

varicella

herpes (neurologic problem with enephalitis with something in csf)

19
Q

Echo and EKG Findings

A
  • Echocardiography shows normal anatomy but severely reduced left ventricular contraction with an ejection fraction of 20%
  • EKG shows ST depression in leads V1-V4.
  • Troponin I level is reported at 10.2 μg/L with normal being less than 0.04
  • PCR confirms the diagnosis
20
Q

Final Diagnosis

A

Coxsackie B3 Myocarditis

21
Q

Enteroviral Infections in the Newborn

A
  • Among the most common viruses causing disease in humans with approximately 10-15 million symptomatic infections yearly in the USA
  • Infections tend to have a seasonal pattern during summer and fall
  • Illnesses range from a nonspecific febrile illness, mild URIs, self limiting gastroenteritis to myocarditis, hepatitis and encephalopathy
22
Q

Enterovirus Neonatal Transmission

A
  • Can be acquired antenatally, intrapartumand postnatally

* In-utero transmission can be by transplacentallyor by ascending infection

23
Q

Clinical Features of Enterovirus Infection

A
  • Associated with wide spectrum of signs and symptoms ranging from nonspecific febrile illness to fatal multisystem disease which is frequently called “Neonatal EnterovirusSepsis”
  • Most common presenting features include fever, irritability, poor feeding and lethargy
  • A nonspecific rash is seen in approximately half of infants infected

•Approximately half have evidence of hepatitis or jaundice. Hepatomegaly may be present but splenomegaly is rare
conjugated hyperbilirubinemia that doesnt go away

24
Q

Back to the Case

A
  • IV immunoglobulin was given
  • Because of the decreased cardiac output and developing arrhythmias dopamine and milrinonewere started
  • Over the next 48 hours the infant became refractory to amiodarone and electroconversionfor tachyarrhythmia
  • ECMO (Extracorporeal Membrane Oxygenation) was started
25
Q

ECMO was continued for 3 weeks with adequately decompressed heart chambers and without major bleeds or infection, however, left ventricular function did not improve and ECMO was withdrawn

A
Post-mortem examination
showed diffuse inflammatory
infiltrate of lymphocytes and
extensive necrosis of the
myocardium