Neonatal Hemoperitoneum Secondary to Hemorrhage from Omental Venous Malformation.

Hemoperitoneum in the neonate is uncommon. We report our experience with a neonate who suddenly developed hemoperitoneum in late gestation. Ascites with right pleural effusion initially suggested fetal hydrops. However, a decrease in hemoglobin with bloody ascites from the paracentesis gave the impression of hemoperitoneum. Ultrasonography and computed tomography showed no abnormality in the solid organs. Using 3-mm laparoscopic exploration, we found the omental mass and excised it. It was histologically confirmed as a venous malformation. Venous malformation of the omentum with significant bleeding requiring exploration is a very rare condition in the neonate, but it should be considered as a cause of neonatal hemoperitoneum.

Congenital antral web in premature baby.

Antral web is a rare cause of gastric outlet obstruction in neonate. It is a 2-4 mm thin mucous membrane that can be found anywhere from 1 to 7 cm proximal to the pylorus. The baby was born at gestational age of 32(+1) weeks with 1,880 g as 2nd baby of dizygotic twin. After birth, the baby had constant non-bilious vomiting without feeding while he didn't show abdominal distension or discoloration. The infantogram showed distended stomach with distal small bowel gas. Upper gastrointestinal series revealed that the antrum was abruptly narrowed at 1 cm proximal to pylorus. We performed laparotomy at the 10th day after birth and excised the 2 mm-thick web circumferentially. He began milk feeding after 6 days and discharged uneventfully at postoperative 35 days with corrected age of 38(+4) weeks with body weight 2,420 g. The antral web should be considered in the case of non-bilious vomiting in neonate.

Swallowing dysfunction in very low birth weight infants with oral feeding desaturation.

BACKGROUND: We detected swallowing dysfunction by the modified barium swallow (MBS) test and determined risk factors for swallowing dysfunction in very low birth weight (VLBW) infants with oral feeding desaturation near discharge. METHODS: We retrospectively reviewed 41 VLBW infants referred for MBS test because of significant oral feeding desaturation at ≥ 35 weeks of postmenstrual age. Infants who showed impaired airway protection, including inadequate epiglottic closure, laryngeal penetration and/or tracheal aspiration by MBS test, were compared to those without impaired airway protection. RESULTS: Eleven infants (26.8%) showed impaired airway protection by MBS test. They had a significantly lower gestational age at birth but a similar postmenstrual age compared to those without impaired airway protection. All infants with impaired airway protection were born at ≤ 28 weeks of gestation. CONCLUSIONS: Swallowing dysfunction resulting in aspiration should be considered as a cause of significant oral feeding desaturation in infants born at ≤ 28 weeks of gestation regardless of postmenstrual age.

Granulocyte colony stimulating factor attenuates hyperoxia-induced lung injury by down-modulating inflammatory responses in neonatal rats.

PURPOSE: Granulocyte colony stimulating factor (G-CSF) has been known to increase neutrophil production and have anti-inflammatory properties, but the effect of G-CSF on pulmonary system is in controversy. We investigated whether G-CSF treatment could attenuate hyperoxia-induced lung injury, and whether this protective effect is mediated by the down-modulation of inflammatory responses in a neonatal rat model. MATERIALS AND METHODS: Newborn Sprague-Dawley rats (Orient Co., Seoul, Korea) were subjected to 14 days of hyperoxia (90% oxygen) beginning within 10 h after birth. G-CSF (20 µg/kg) was administered intraperitoneally on the fourth, fifth, and sixth postnatal days. RESULTS: This treatment significantly improved hyperoxia-induced reduction in body weight gain and lung pathology such as increased mean linear intercept, mean alveolar volume, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling positive cells. Hyperoxia- induced activation of nicotinamide adenine dinucleotide phosphate oxidase, which is responsible for superoxide anion production, as evidenced by upregulation and membrane translocation of p67(phox) was significantly attenuated after G-CSF treatment, as were inflammatory responses such as increased myeloperoxidase activity and mRNA expression of transforming growth factor-ß. However, the attenuation of other proinflammatory cytokines such as tumor necrosis factor-α and interleukin- 6 was not significant. CONCLUSION: In sum, G-CSF treatment significantly attenuated hyperoxia-induced lung injury by down-modulating the inflammatory responses in neonatal rats.

Erythropoietin attenuates hyperoxia-induced lung injury by down-modulating inflammation in neonatal rats.

This study was done to determine whether recombinant human erythropoietin (rhEPO) treatment could attenuate hyperoxia-induced lung injury, and if so, whether this protective effect is mediated by the down-modulation of inflammation in neonatal rats. Newborn Sprague Dawley rat pups were subjected to 14 days of hyperoxia (>95% oxygen) within 10 hr after birth. Treatment with rhEPO significantly attenuated the mortality and reduced body weight gain caused by hyperoxia. With rhEPO treatment, given 3 unit/gm intraperitoneally at 4th, 5th, and 6th postnatal day, hyperoxia- induced alterations in lung pathology such as decreased radial alveolar count, increased mean linear intercept, and fibrosis were significantly improved, and the inflammatory changes such as myeloperoxidase activity and tumor necrosis factor-alpha expression were also significantly attenuated. In summary, rhEPO treatment significantly attenuated hyperoxia-induced lung injury by down-modulating the inflammatory responses in neonatal rats.

A comparison of AmBisome to amphotericin B for treatment of systemic candidiasis in very low birth weight infants.

PURPOSE: Amphotericin B is considered the treatment of choice for systemic candidiasis, but adverse effects may limit its use. An alternative option for the treatment of candidiasis includes lipid preparations of amphotericin B. This study investigated the safety and efficacy of AmBisome, a lipid formulation of amphotericin B containing liposomal structures, for the treatment of systemic candidiasis in very low birth weight infants (VLBWI). MATERIALS AND METHODS: Data from 26 VLBWI treated with AmBisome in the study group (AmBisome group) from October 2003 to July 2006 were compared with data from 20 VLBWI treated with amphotericin B as a historical control (Amphotericin group). This study was a prospective, historical control, multi-center trial. RESULTS: Candida spp. was isolated in 73% (19/26) of the cases for the AmBisome group and 90% (18/20) of the cases for the Amphotericin group. The fungal eradication rate and the time to eradication was 84% (16/19) and 9+/-8 days in the AmBisome group, and 89% (16/18) and 10+/-9 days in the Amphotericin group, respectively (p=0.680 vs p=0.712). The major adverse effects were lower in the AmBisome group (renal toxicity, 21% vs 55%, p=0.029; hepatotoxity, 25% vs 65%, p=0.014, AmBisome group vs Amphotericin group, respectively). There was no significant difference in mortality attributed to systemic candidiasis (12% in the AmBisome group, 10% in the Amphotericin group, p=0.868). CONCLUSION: AmBisome is effective and safe for treating systemic fungal infections in VLBWI.

Therapeutic window for cycloheximide treatment after hypoxic-ischemic brain injury in neonatal rats.

We have previously shown that cycloheximide significantly inhibited apoptosis, and reduced ensuing cerebral infarction in a newborn rat model of cerebral hypoxiaischemia. This study was performed to determine the therapeutic window for cycloheximide therapy. Seven day-old newborn rat pups were subjected to 100 min of 8% oxygen following a unilateral carotid artery ligation, and cycloheximide was given at 0, 6, 12 and 24 hr after hypoxia-ischemia (HI). Apoptosis or necrosis was identified by performing flow cytometry with a combination of fluorescinated annexin V and propidium iodide, and the extent of cerebral infarction was evaluated with triphenyl tetrazolium chloride (TTC) at 48 hr and 72 hr after HI, respectively. With cycloheximide treatment at 0 hr after HI, both apoptotic and necrotic cells by flow cytometry were significantly reduced, only necrotic cells were significantly reduced at 6 and 12 hr, and no protective effect was seen if administration was delayed until 24 hr after HI compared to the HI control group. Infarct volume, measured by TTC, was significantly reduced by 92% and 61% when cycloheximide was given at 0 or 6 hr after HI respectively; however, there was an insignificant trend in infarct reduction if cycloheximide was administered 12 hr after HI, and no protective effect was observed when administration was delayed until 24 hr after HI. In summary, cycloheximide was neuroprotective when given within 6 hr after HI in the developing newborn rat brain.

Neuroprotective effect of cycloheximide on hypoxic-ischemic brain injury in neonatal rats.

This study was done to determine the neuroprotective effect of cycloheximide on neonatal hypoxic-ischemic brain injury. Seven day-old newborn rat pups were subjected to 90 min of 8% oxygen following a unilateral carotid artery ligation. The extent of cerebral infarction was evaluated at 1 and 4 week of recovery. Apoptosis was identified by performing terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining and flow cytometry with a combination of fluoresceinated annexin V and propidium iodide. Brain infarction area was significantly increased at 4 week compared to 1 week after hypoxia-ischemia in the control group. With cycloheximide treatment, the number of TUNEL positive cells in the ipsilateral cerebral cortex at 48 hr and peri-infarct area at 1 and 4 week of recovery was significantly reduced, both apoptotic and necrotic cells by flow cytometry 48 hr after the injury were significantly reduced, and the extent of cerebral infarction at 1 and 4 week of recovery was also significantly attenuated compared to the hypoxia-ischemia control group. In summary, our data suggest that apoptosis plays an important role in the development of delayed infarction, and inhibition of apoptosis with cycloheximide significantly reduces the ensuing cerebral infarction in a newborn rat pup model of cerebral hypoxia-ischemia.