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A Caucasian male infant was delivered vaginally at 34 4 7 weeks gestation to a 19-year-old mother of 2 who had a primary herpes simplex virus infection at 18 weeks and another probable outbreak at 26 4 7 weeks. She was treated with acyclovir for 7 days at both occurrences. Suppressive therapy was to be started at 36 weeks. Prenatal ultrasound at 25 1 7 weeks was unremarkable; however, at 32 2 7 weeks, prenatal ultrasound showed enlargement of the third ventricles and at 33 2 7 weeks showed severe ventriculomegaly.The infant was born limp and apneic. Tracheal suctioning was performed for light meconium, but no meconium was obtained. He was eventually intubated for a heart rate less than 100 beats/min and shallow respirations. Apgar scores were obtained at 1, 6, and 7 at 1, 5, and 10 minutes, respectively. Physical examination on admissions showed a preterm infant with minimal to absent spontaneous movement alternating with occasional focal clonic seizures of the right arm and rhythmic jerking movement of all four extremities. Birth weight and length were at the 50th percentile and the head circumference was at the 25th percentile for gestational age. He was normocephalic with open, soft anterior fontanelle. There were multiple raised hypopigmented lesions on his palm, chin, and arm, which resolved after 24 hours. The rest of the physical examination was unremarkable. He was placed under contact isolation. Laboratory samples were taken and the infant was started on ampicillin, gentamicin, and acyclovir. Phenobarbital and levetiracetam were given for the seizures.Initial complete blood count showed a white cell count of 8.7 with 37% neutrophils, 47% lymphocytes, 5% monocytes, and 65% eosinophil. Liver function tests and disseminated intravascular coagulolopathy panel were within normal limits. Blood cultures taken from 2 sites were negative. Antibodies to cytomegalovirus, toxoplasma, and herpes simplex virus type 1 (HSV-1) were negative, and Venereal Disease Research Laboratory was nonreactive. However, HSV-2 IgG was positive. Examination of the cerebrospinal fluid (CSF) showed 42 white blood cells/mm 3 , 2430 red blood cells/mm 3 , protein 772 mg/dL, and glucose 26 mg/dL (serum glucose 96 mg/dL). No organisms were seen on Gram stain. The urine, skin, and CSF polymerase chain reaction (PCR) for HSV-2 were all positive.A chest radiograph was suggestive of mild surfactant deficiency. A cranial ultrasound showed massive ventriculomegaly. A computed tomography scan, performed a few hours after birth to rule out an intracranial bleed, showed marked intracranial abnormality with ventriculomegaly in addition to an extensive area of brain destruction involving the frontal, temporal, and parietal lobes. Both cerebellar hemispheres were small in appearance. Marked atrophy was apparent in the brainstem. Intracranial calcifications were also seen. Magnetic resonance imaging showed similar findings with near complete absence of brain substance, with minimal residual brain identified in the occipital region. Magnetic resonance im...

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Objective: Preeclampsia (PreE) and diabetes mellitus (DM) in pregnancy share many risk factors and consequences. Thus, the interactions between these two disease-processes need to be further examined. We compared normal pregnancies to those complicated with preE, gestational diabetes (GDM), and/or pre-existing DM to assess the effect of DM on placental development and outcomes when this condition is complicated by preE. Methods: Chart reviews were performed in an IRB approved retrospective case-control design with pregnancies resulting in live born singletons. Total 178 subjects with preE with and without DM or GDM and live born singletons were selected from deliveries in 2008 through 2011 at Scott & White Memorial Hospital, Temple, Texas. These were compared to 443 without preE and with and without DM or GDM. Statistical analysis was performed using ANOVA and Duncan’s post-hoc test. Results: Patients who developed preE had higher systolic and diastolic pressures compared to groups without preE (p < 0.05). Patients with DM or GDM were older (p < 0.05). There was no difference among groups for gravidity (p = 0.21) with the average gravidity of 2.7 (1.8 SD) for 621 subjects having a range of 1 to 14 pregnancies. Patients with preE delivered earlier in pregnancy than those without preE regardless of diabetes status. However, those with preE and DM delivered earlier at 35.0 ± 0.4 weeks than the other two preE groups (p < 0.05), suggesting a more severe condition. Patients with DM who developed preE delivered smaller (p < 0.05) babies (correcting for gestational age at delivery) than those with DM without preE (1.00 ± 0.03 versus 1.16 ± 0.04, respectively). Development of GDM did not result in smaller babies for those pregnancies with preE (1.07 versus 1.09). Conclusions: The development of preE in those with pre-existing DM led to growth restriction and more severe disease as evidenced by lower birth weights corrected for gestational age and earlier gestational ages at delivery. These differences were not seen in GDM pregnancies. This observation supports the concept that elevated glucose levels during first trimester placental development may alter the placenta and lead to restriction later in pregnancy when a second stimulus triggers preE.