You are on page 1of 20

Morning Report

Monday, 8/24/15
Mitch Peterson

CC: Sleepy, stopped breathing, turned blue

HPI: A 51 day old male with a history ofbirth at 30 weeks and discharge
from the NICU after a 45 day staypresents after he stopped breathing and
turned blue at home.He was acting like his normal self up until the morning
of presentation when his mother was holding him. She noticed that he
started looking up and then stopped breathing. He turned blue. His mother
gave him CPR and his color returned as he started to breathe again. They got
into the car and started driving to the emergency department. On the way,
he stopped breathing and turned blue again. They stopped the car and
administered CPR again. He again started to breathe and they were able to
make it to the University of Utah Emergency Department.
Course since arrival to the hospital: In the University of Utah Emergency
Department, he was found to be occasionally apneic with desaturations into
the 70s and 80s. He had a temperature of 38.7 celsius. Direct admission to

ROS: No prior fever, no rash, no cough, no congestion, no

increased work of breathing, somewhat decreased feeding,
several wet diapers the day of admit, emesis x 1, no diarrhea,
patient was with his mother all day, no sweating with feeds.
PMH: Born at 30 weeks because his mother had an infection.
He was not intubated, but needed a feeding tube. He was in
the NICU for 45 days or so. Discharged home on room air. His
family was told that he is remarkably healthy for a premature
infant. No surgeries. Got Hepatitis B vaccine prior to
Medications: NKDA, Multivitamin
Diet: Neosure 24 kcal/oz
FH/SH: No known inherited diseases of childhood. Lives with his 2
older sisters, 2 older brothers, mother and father. There are no
smokers or pets in the house.

T 37.0 HR 183 RR 28 BP 84/71 SpO2 98% on Nasal Cannula at1 LPM.

Wt -2.85 Kg, (~50%ile for CGA)Ht - 43 cm (~15%ile for CGA)
GENERAL: lethargic infant, lying in crib, moving occasionally, crying only
intermittently when stimulated
HEAD: small area of bruising on right anterior scalp, normocephalic, atraumatic,
anterior fontanelle open, soft, and flat.
EYES: normal red reflex and pupillary reflexes bilaterally, no conjunctival injection.
NOSE: nasal cannula in place without appreciable congestion
OROPHARYNX: moist mucus membranes, no cleft palate.
CARDIOVASCULAR: tachycardic, normal rhythm, normal S1/S2, no murmur, no
gallop, brachial/femoral pulses 2+ and symmetric, capillary refill time3 seconds.
LUNGS: clear to auscultation bilaterally, good air flow, no retractions.
ABDOMEN: soft, non-tender, non-distended with active bowel sounds and no
EXTREMITIES: all extremities warm and well perfused. No cyanosis, clubbing, or
GENITOURINARY: normal Male external genitalia, Tanner stage I, uncircumcised,
red birthmark near left inguinal canal area.
NEUROLOGIC: sleepy and arouses for short periods of time only with stimulation,
normal tone, weak suck
SKIN: No rashes, no mottling

Differential Diagnosis
51 day old male with history of prematurity who presents with
apnea and fever.

Differential Diagnosis
Urinary Tract Infection
Bronchiolitis vs Pneumonia
Non-accidental trauma
Chiari malformation
Apnea of prematurity
Foreign body aspiration
Aspiration Pneumonitis
Congenital pulmonary airway malformation (CPAM)

Work Up 1st tier

139 110




Protein 5.4


Albumin 3.7
Bilirubin 0.9


Alk. Phos. 186

ALT 11, AST 22



(11%B, 60%N, 20%L, 8%M,

Urinalysis: negative
RFA PCR: negative

Work Up - 2nd tier

CT Brain W/O Contrast: Normal noncontrast brain CT. Fluid in mastoid
air cells and left greater than right middle ears, which may represent
otitis media with mastoid effusions. Clinical correlation recommended.
CXR:Endotracheal tube overlies the low thoracic trachea. Scattered
subsegmental opacities suggest atelectasis. Marked gaseous distention
of the stomach.
Blood Culture: NGTD
Urine Culture: too young to read, re-incubating

Work Up - 3rd tier

CSF: WBC 3 (2%B, 72%N, 20%L, 6%M), RBC 134, Glucose 50, Protein
Brain MRI: Normal brain MRI. No Chiari one malformation or
other abnormal finding identified to explain lethargy and apnea.
EEG: This is a mildly abnormal EEG for age due to slight excess
discontinuity than might be expected for this child's postconceptional age. In addition, greater percentage of the EEG is spent
in a state where the EEG is discontinuous than might otherwise be
expected. However, there were no definite abnormalities otherwise,
no focal asymmetries and no epileptiform discharges. Finally, no
electrographic or electroclinical seizures were identified.

Work Up - 4th tier

Enterovirus PCR on CSF and Serum +
Blood, Urine, CSF cultures negative
HSV PCR on CSF negative

Enterovirus Classification
Old School:
Poliovirus, Coxsackie A, Coxsackie B, Echovirus, Numbered
New School:
Poliovirus, Enterovirus A, B, C, D
coxsackie A9, coxsackie B4, echovirus 6, and EV-69 are all listed
under the species human enterovirus B.

Enterovirus Diseases
Viral Exanthem and Fever
Herpangina (Coxsackie A)
Hand-Foot-Mouth Disease (Coxsackie A)
Myocarditis (Coxsackie B)
Respiratory Illness (Enterovirus D68 in Fall, 2014)

Febrile Infant
Enterovirus PCR
Note that we
recommend testing
seasonally (June through
November) and always
with a finding of CSF

Anticipated length of stay (LOS) for

high-risk and low-risk patients with
serious bacterial infection (SBI) ruled
Low risk anticipated LOS is 24 hours
High risk and positive viral studies
anticipated LOS is 24 hours
High risk and negative viral studies
anticipated LOS is 36 hours.

Enterovirus IVIG
Does IVIG administration improve neurological outcomes in
critically ill neonates with enterovirus meningitis?

Clin Infect Dis. 1995 May;20(5):1201-6.

Neonatal enterovirus infection: virology, serology,
and effects of intravenous immune globulin.
Abzug MJ1, Keyserling HL, Lee ML, Levin MJ, Rotbart HA.
Prospective study of 16 neonates and their mothers. IVIG
only helped with cessation of viremia and viruria if the
IVIG was high in neutralization titers specific to the
neonates virus.

Virology. 2011 Mar 15;411(2):288-305. doi:

10.1016/j.virol.2010.12.014. Epub 2011 Jan 20.
Enterovirus infections of the central nervous system.
Rhoades RE1, Tabor-Godwin JM, Tsueng G, Feuer R.
The standard therapy for aseptic meningitis caused by EV
infection continues to be intra-venous immunoglobulin (IVIg)
treatment, although the efficacy has not been proven (
Abzug, 2004).

Paediatr Drugs. 2004;6(1):1-10.

Presentation, diagnosis, and management of enterovirus infections in
Abzug MJ1.
The nonpoliovirus enteroviruses commonly infect newborns. . . Although most
illnesses are mild, severe disease develops in a subset of newborns infected
in the first 2 weeks of life. Severe disease may consist of sepsis,
meningoencephalitis, myocarditis, pneumonia, hepatitis, and/or coagulopathy.
Substantial mortality rates have been reported, and long-term sequelae may occur
among survivors. Risk factors and clinical features associated with severe
disease include absence of neutralizing antibody to the infecting serotype,
maternal illness prior to or at delivery, prematurity, illness onset within
the first few days of life, multiorgan disease, severe hepatitis, positive
serum viral culture, and specific infecting serotype (e.g. group B
coxsackieviruses and echovirus 11). . . . Immunoglobulin has been used as a
therapeutic agent for neonates with enterovirus disease; however, clinical
efficacy has not been proven.

Clin Microbiol Infect. 2000 Nov;6(11):630-2.

Enterovirus antibody titers after IVIG replacement
in agammaglobulinemic children.
Galama JM, Gielen M, Weemaes CM.
IVIG is used routinely in agammaglobulinemic children as
prophylaxis against, among other things, chronic
enteroviral infections.

Does IVIG administration improve

neurological outcomes in critically ill
neonates with enterovirus meningitis?
Maybe. Maybe not.