|Contributed by Robert Hevner, MD, PhD and Raymond A. Sobel, MD|
|Department of Pathology (Neuropathology), Stanford University Medical Center|
An 18-year-old primigravid mother with preeclampsia gave birth by Cesarean section to a premature male baby (28 weeks gestational age). Apgar scores were 6 at 1 minute, and 8 at 5 minutes. During the first postnatal week, the neonate required artificial ventilation for respiratory distress syndrome, and phototherapy for hyperbilirubinemia, but he did well and his condition stabilized. Two weeks postnatally, the baby was re-intubated for recurrent respiratory distress. At about that time, he also developed a rash (presumed candidal dermatitis) which was treated with topical miconazole and systemic amphotericin B. Multiple blood cultures were negative for bacteria or fungi. Four weeks postnatally, he had an episode of transient renal failure with acidosis, hyperkalemia, and hypernatremia, followed by neurologic deterioration with lethargy leading to coma, prompting ultrasound examinations. An ultrasound examination of the head (coronal plane) performed two days after the onset of renal failure revealed high signal intensity in the germinal matrix bilaterally (arrow); this was interpreted by the radiologist as intraventricular hemorrhage, grade 2. Three days later, a repeat ultrasound exam showed hyperintensity bilaterally in the periventricular white matter, germinal matrix, thalamus, and ventricle interpreted as intraventricular hemorrhage, grade 4. Despite aggressive treatment of fluid and electrolyte disorders, the baby died 31 days after birth, without any improvement in neurologic status.