We present a 12-day-old newborn who came to the emergency department with a fever of 38.5oC of one hour of evolution and refusal to eat.
As antecedents stood out a controlled and normal pregnancy; negative serologies for hepatitis B and C virus, human immunodeficiency virus, syphilis and toxoplasma; negative vaginal smears for Streptococcus group B; spontaneous rupture of pregnancy g.
The Apgar test was at minute 8 and at 5 minutes 9, without requiring resuscitation.
She started her immunization schedule.
Allocation with exclusive breastfeeding.
Regarding family history, parents reported having suffered from arthritis the previous days.
Physical examination showed weakness and regular peripheral perfusion with normal vital signs, with no signs of focus.
The initial laboratory analysis showed a quantitative C-reactive protein (CRP) determination 133.4 mg/L, with a coagulated blood count and normal urine sediment.
Lumbar puncture was haemorrhagic.
She was admitted with a diagnosis of febrile syndrome without source and empirical antibiotic therapy with intravenous ampicillin and cefoxime was started after taking cultures.
The repeated blood count showed 5800 leukocytes/mm3, with normal formula, 13.4 g/dl hemoglobin, 32,000 platelets/mm3.
Eighteen hours after admission her general condition worsened and she developed generalized seizures that required treatment with fenobarbital and midazolam infusion.
The patient developed systemic involvement with hypotension, metabolic acidosis, hyponatremia, oliguria and severe platelet failure requiring conventional mechanical ventilation, transfusion of blood products, inotropic support with dopamine and diuretics.
On the third day of admission, Streptococcus pyogenes was isolated in the blood culture. Ampicillin was discontinued and treatment with intravenous cefuroxime was continued.
After stabilization, the patient presented clinical and laboratory improvement, which allowed suspension of the inotropic treatment after 48 h and extubation on the fourth day.
The clinical seizures were not repeated and the electroencephalogram was normal, so the anticonvulsant treatment was discontinued.
Lumbar puncture was repeated unsuccessfully.
Initial brain ultrasound and angioresonance showed intraventricular hemorrhage with mild ventriculomegaly and bilateral cortico-subcortical hemispheric lesions compatible with meningoencephalitis.
The auditory screening performed during admission using the brainstem auditory evoked potentials exploration technique (PEATC-A > 40 dB) was not exceeded.
Control cerebral ultrasound showed good evolution without increased ventricular dilatation.
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At 34 days of life, after completing 21 days of treatment with cefoxime, the patient was discharged with normal neurological examination, except for mild axis hypotonia.
A follow-up was carried out by specialists from the rehabilitation, otorhinolaryngology and neurology units. At one year of life, the patient did not present residual hearing or neurological pathology.
