Keywords
acute otitis media - preterm - NICU - otorrhea
Acute otitis media (AOM) is one of the most common diagnoses among young children
in the primary care setting.[1] Though consensus on diagnosis may vary, in 2013 the American Academy of Pediatrics
released a clinical practice guideline on the management of AOM. However, this did
not address populations under 6 months, particularly those in the neonatal intensive
care unit (NICU).[2] Premature neonates have smaller eustachian tubes, distinct immune responses, and
a decreased level of secretory immunoglobulin A (IgA). Thus, prematurity is the most
common risk factor for recurrent otitis media with effusion (OME).[3]
Case Description
A premature baby girl was born at 26 weeks of gestation, weighing 790 g, to a 29-year-old,
Gravida 4 Para 0030. Perinatal history was significant for maternal abdominal pain
and vaginal bleeding. She was febrile with early cervical dilation one day prior to
delivery. Given the concern for preterm labor in the setting of chorioamnionitis,
the mother was started on ampicillin, gentamicin, given one dose of betamethasone
and induced. Prenatal lab results were negative for human immunodeficiency virus,
syphilis, chlamydia, gonorrhea, and hepatitis B virus. Group B Streptococcus was initially unknown and later positive. Maternal history was significant for sickle
cell trait and herpes simplex virus (HSV) prior to pregnancy with no active lesions
during pregnancy. The baby was delivered vaginally with APGAR scores of 6 and 8 at
1 and 5 minutes, respectively. She was intubated in the delivery room for poor respiratory
effort and admitted to the NICU for ongoing management related to her prematurity.
Maternal placental histopathology was consistent with a third trimester placenta with
acute chorioamnionitis and umbilical and chorionic vessels phlebitis.
Upon NICU admission, the patient received 48 hours of ampicillin and gentamicin for
suspected sepsis. Her other diagnoses included respiratory distress syndrome, slow
feeding, and apnea of prematurity. She required intubation for the first 2 days of
life (DOL). Total parental nutrition (TPN) and donor breast milk (DBM) began on DOL
0. Expressed breast milk (EBM) began on DOL 3. TPN was discontinued on DOL 11. The
infant received EBM (∼99.5%) and DBM (∼0.5%) until DOL 30.
The patient was hemodynamically stable on bubble continuous positive airway pressure
until DOL 30 when frequent and prolonged apneas led to reintubation. Due to the acute
change in clinical status, a partial sepsis evaluation was initiated with the following
laboratory results: complete blood count, basic metabolic panel, C-reactive protein,
and blood culture. Abdominal and chest radiographs were completed and nafcillin and
gentamicin were administered. Within 24 hours, bilateral purulent otorrhea was noted.
On physical exam, there was left-sided erythematous pre- and postauricular rash along
with postauricular desquamation. An otoscopic evaluation revealed bilateral purulent
drainage, left greater than right, the tympanic membranes (TM) could not be visualized,
and the external auditory canals were erythematous. Pediatric infectious disease consulted
and the following additional laboratory tests were sent: cerebrospinal fluid (CSF)
for HSV, culture, protein, glucose, and cell count, a urinalysis and urine culture;
and periauricular swabs for anaerobic, aerobic as well as HSV. Given concerns for
methicillin-resistant Staphylococcus
aureus (MRSA), pseudomonas and antibiotics were changed to linezolid, cefepime, acyclovir,
and fluconazole prophylaxis. See [Tables 1] and [2] for laboratory results. The aerobic ear culture grew: moderate Staphylococcus epidermidis, Klebsiella pneumoniae, and Enterococcus faecalis. Blood culture was negative, HSV swabs were negative, CSF culture was negative, urine
culture was negative, anaerobic culture was negative, and MRSA swabs were negative.
The chest and abdominal radiographs were unremarkable. On DOL 32, she was extubated.
She received a 7-day course of piperacillin/tazobactam. The drainage and desquamation
resolved within one week.
Table 1
Laboratory results
|
Test
|
DOL 30
|
DOL 32
|
|
WBC (k/µL)
|
19.6
|
11.4
|
|
Hb (g/dL)
|
8.6
|
10.6
|
|
Platelet (k/µL)
|
526
|
465
|
|
Absolute neutrophil count (cells/µL)
|
7,056
|
4,104
|
|
I/T ratio
|
0
|
0
|
|
C-reactive protein (mg/dL)
|
<0.5
|
1.5
|
|
HSV serum
|
Negative
|
|
BMP and urinalysis
|
Unremarkable
|
Abbreviations: BMP, basic metabolic panel; CSF, cerebrospinal fluid; DOL, day of life;
Hb, hemoglobin; HSV, herpes simplex virus; I/T ratio, immature/total neutrophil count;
WBC, white blood cell count.
Table 2
CSF studies on DOL 30
|
Test
|
Result
|
|
Appearance
|
Clear
|
|
Color
|
Colorless
|
|
RBC count
|
10
|
|
WBC count
|
3
|
|
Glucose
|
57
|
|
Total protein
|
116
|
|
CSF herpes simplex PCR
|
Not detected
|
Abbreviations: CSF, cerebrospinal fluid; DOL, day of life; RBC, red blood cell count;
PCR, polymerase chain reaction; WBC, white blood cell count.
On DOL 46 (postmenstrual age [PMA]: 32 weeks and 5 days), all respiratory support
was discontinued and on DOL 76 with PMA of 36 weeks and 6 days, she was discharged
home. Prior to discharge, the infant passed the hearing test bilaterally (evoked otoacoustic
emissions and auditory brainstem response). Due to extreme prematurity, the patient
had a head ultrasound and brain magnetic resonance imaging which were unremarkable.
Discussion
The etiology of the increased incidence of AOM in premature infants is multifactorial.
A study conducted on 86 preterm babies reported that the rate of AOM is inversely
related to the gestational age, and with every additional week of gestational age,
the odds ratio of AOM decreases by 0.7.[4] The study also determined that the frequency of finding abnormal ear exams in preterm
babies is 72.9%.[5] This in large part is influenced by intrinsic factors related to anatomical differences
with prematurity, such as smaller and straight eustachian tubes and lower level of
immunoglobins specifically secretory IgA.[3] Extrinsic factors that affect AOM incidence include mode of delivery, cesarean more
than vaginal, endotracheal intubation, and feeding tube insertion, which cause increased
pressure inside the eustachian tube, further contributing to dysfunction.[6] Additionally, proinflammatory mediators activated secondary to maternal chorioamnionitis
may lead to eustachian tube dysfunction with babies often presenting with OME.[7] Maternal chorioamnionitis, even when not histopathologically significant, has been
shown to be a significant factor in the development of OME in the first 3 years of
life.[7] Protective factors such as breast milk, which is rich in secretory IgA, are shown
to lower the incidence of AOM.[3]
Neonates rarely have specific signs and symptoms of AOM. Fortunately, ampicillin and
gentamicin are commonly used for neonatal sepsis and provide adequate antibiotic coverage
for AOM. Otitis media in infants can be difficult to diagnose as the TM is more horizontal
in shape; thus, a review article on OM in neonates concluded that OM is defined as
erythema/inflammation of TM and/or absent or minimal mobility of TM.[5]
[8] Inflammation of the ear mucosa can lead to watery, serosanguinous, or purulent discharge.
The infant in this case had purulent bilateral ear discharge along with some episodes
of apnea and bradycardia.
The most common pathogens isolated in AOM are gram-positive bacilli: S. pneumoniae and S. pyogenes, followed by gram-negative bacilli, nontypeable Haemophilus influenzae, Moraxella catarrhalis, which make up 10.5% of the cases.[9] A study published in 2005 reported that enteric bacteria such as Klebsiella pneumoniae is the pathogenic organism responsible for AOM in 6% of the cases in infants less
than 3 months of age.[10]
Klebsiella pneumoniae and Enterococcus faecalis were the isolated organisms in this patient, both of which are not common pathogenic
organisms of AOM. S. epidermidis was also isolated from the culture that is likely an organism from skin flora.
Antibiotic management was based on common pathogenic organisms known to cause AOM,
the neonatal risk factors, as well as the physical exam. Ampicillin was chosen for
gram-positive coverage, cefepime for gram-negative coverage, and CSF penetration and
acyclovir for HSV prophylaxis. HSV was a concern given the infant had postauricular
erythematous rash and maternal history of previous HSV.
When available, treatment is targeted to the sensitivities of the culture. Most literature
suggests ampicillin with or without clavulanic acid and a third-generation cephalosporin.[8]
[11] Literature showed debating data regarding hearing loss associated with recurrent
otitis media. A case–control study done on preterm infants demonstrated that cases
with tympanometry abnormality had a depressed hearing threshold.[12]
Conclusion
AOM should be considered on the list of differential diagnosis for preterm infants
who present with signs and symptoms of presumed sepsis. In addition to the routine
evaluation, an otoscopic exam should be utilized to rule out AOM.
