Respiratory function testing for guiding ventilator mode conversion in congenital diaphragmatic hernia.

INTRODUCTION: For patients with a congenital diaphragmatic hernia, conventional mechanical ventilation (CMV) and high-frequency oscillatory ventilation (HFOV) are used in initial ventilatory management. HFOV has recently been recommended as a rescue therapy; however, we use HFOV for initial ventilation management, with a preoperative challenge test for CMV conversion and respiratory function testing at the time of CMV conversion. We aimed to compare patient characteristics between CMV conversion- and HFOV-preferred treatment groups. METHODS: Ventilator settings and blood gases were retrospectively evaluated pre- and post-CMV conversion, and respiratory function tests for compliance of the respiratory system (Crs) and for resistance of the respiratory system (Rrs) were performed during the trial to CMV conversion. RESULTS: No differences were observed between the CMV conversion- and HFOV-preferred groups regarding gestational age, birth weight, and observed/expected lung area-to-head circumference ratios. The median Crs (ml/cmH2 O/kg) and Rrs (cmH2 Oï½¥kg/L/s) in the CMV conversion- and HFOV-preferred groups was 0.42 versus 0.53 (p = .44) and 467 versus 327 (p = .045), respectively. The pre and posttrial amount of change in blood gas levels and ventilator parameters in the CMV conversion- and HFOV-preferred groups were as follows: mean airway pressure, -2.0 versus 0 cmH2 O; partial pressure of carbon dioxide, 6.1 versus 2.9 Torr; alveolar-arterial oxygen difference, -39.5 versus -50 Torr; and oxygenation index, -1.0 versus -0.6; respectively. CONCLUSION: Respiratory function tests were useful in tailoring ventilator settings. Patients with high Rrs values responded better to CMV conversion.

Using airway resistance measurement to determine when to switch ventilator modes in congenital diaphragmatic hernia: a case report.

BACKGROUND: Congenital diaphragmatic hernia is a deficiency of the fetal diaphragm resulting in herniation of the abdominal viscera into the thoracic cavity. The best method of respiratory management of congenital diaphragmatic hernia is unclear, but high frequency oscillatory ventilation is often used as the initial ventilator mode for severe congenital diaphragmatic hernia. When it becomes impossible to maintain the pre-ductal saturations, the timing of successful switching of the ventilation mode from high frequency oscillatory ventilation to conventional mechanical ventilation remains unclear. Herein, we reported two cases in which airway resistance measurements based on pulmonary function tests were used for making the decision to switch the ventilator mode from high frequency oscillatory ventilation to conventional mechanical ventilation in patients with left isolated congenital diaphragmatic hernia. CASE PRESENTATION: Two 0-day-old infants with congenital diaphragmatic hernia were admitted to our hospital. In both patients, high frequency oscillatory ventilation was started initially, and the levels of saturation gradually rose within a few hours after birth. After 24 h of high frequency oscillatory ventilation, the level of saturation decreased, and the dissociation of pre-ductal and post-ductal saturation re-occurred. The respiratory-system resistance was 515 and 403 cmH2O·kg/L/s, respectively. Because the respiratory-system resistance was elevated, we decided to change the ventilator mode from high frequency oscillatory ventilation to conventional mechanical ventilation. After switching to conventional mechanical ventilation, the patients' heart rate and saturation increased immediately. CONCLUSIONS: In patients with congenital diaphragmatic hernia, resistance levels of > 400 cmH2O·kg/L/s may indicate high airway resistance and suggest greater alveolar vibration attenuation. When respiratory-system resistance reaches over 400 cmH2O·kg/L/s, it may be an optimal time for switching from high frequency oscillatory ventilation to conventional mechanical ventilation.

Temporal Relationship between Serum Levels of Interleukin-6 and C-Reactive Protein in Therapeutic Hypothermia for Neonatal Hypoxic-Ischemic Encephalopathy.

Objective C-reactive protein (CRP) is a useful marker of neonatal infection. Recent studies have shown that neonatal therapeutic hypothermia delays an elevation of CRP in infants with hypoxic-ischemic encephalopathy (HIE). This study investigated the time difference of peak levels of serum CRP and other inflammatory responses during therapeutic hypothermia. Study design We prospectively studied the serial serum data of CRP, interleukin-6 (IL-6), procalcitonin (PCT), and complete blood counts during the first week of life in HIE infants receiving therapeutic hypothermia. Results We identified 22 infants who received therapeutic hypothermia between August 2013 and July 2015. No infants developed clinically overt infections. The peak of serum levels of IL-6, PCT, and CRP were postnatal days 1, 2, and 4, respectively. White blood cells, neutrophils, and platelet counts gradually decreased from days 1 to 7. Early postnatal serum levels of IL-6 correlated with CRP on day 4 (IL-6 on day 2; r = 0.78, p < 0.001). Conclusion The peak value of CRP on day 4 might reflect the early production and secretion of IL-6 rather than an actual infection. Serial measurement of IL-6 might help avoid invasive sepsis workup and unnecessary change of antibiotics in infants.

Tailor-made circulatory management based on the stress-velocity relationship in preterm infants.

Preterm infants frequently experience pulmonary hemorrhage or cerebral intraventricular hemorrhage after birth. The immature myocardium of the left ventricle faces a high afterload after the baby is separated from the placenta. However, the preterm left ventricle has limited ability to respond to such an increase in afterload. This results in depressed cardiac function and a deterioration in hemodynamics. We speculated that the perinatal deterioration in cardiac performance would be closely related to serious hemorrhages. To prove our hypothesis, we studied the interrelationship between the perinatal changes in cardiac performance and the incidences of intraventricular and pulmonary hemorrhage. We obtained the stress-velocity relationship (rate-corrected mean fiber shortening velocity and end-systolic wall stress relationship) by M-mode echocardiography and arterial blood pressure measurement. We found that the incidences of intraventricular and/or pulmonary hemorrhages were higher in infants with an excessive afterload, which resulted in a decrease in the function of the left ventricle. We suggest that careful attention to keep the afterload at an acceptable level by vasodilator therapy and sedation may reduce or prevent these serious complications. In this review, we will discuss our data along with related literature.

TSH suppression after intravenous glucocorticosteroid administration in preterm infants.

BACKGROUND: Reports have described that, in adults, steroids suppress thyroid-stimulating hormone (TSH) and triiodothyronine (T3) and might suppress thyroxine (T4). No data have been reported for thyroid hormone changes before or after administration of glucocorticoid in preterm infants. AIMS: The aim of this study was to investigate short-term effects of thyroid hormones on preterm infants. INDEX CASES: We measured TSH, free T3 (FT3), and free T4 (FT4) before and after one or two doses of glucocorticoids administered to five infants at 29-37 weeks of corrected gestational age. RESULTS: Comparison of thyroid hormone levels before and 1 day after glucocorticoid administration showed that TSH significantly decreased by 76% (64%-87%), FT3 by 33% (10%-50%), and FT4 by 10% (3%-17%). The decline in TSH and FT3 was followed by an increase around the pretreatment level at 3-15 days after glucocorticoid administration. In two of the five infants, FT4 continued to decrease from 1 day after glucocorticoid administration. CONCLUSIONS: In preterm infants, assessing thyroid hormones after glucocorticoid therapy demands caution because very short-term administration causes marked changes.

Magnetic resonance imaging regional T1 abnormalities at term accurately predict motor outcome in preterm infants.

OBJECTIVE: The aim of this study was to assess whether periventricular leukomalacia findings are sufficiently sensitive for predicting the severity of motor prognosis by conventional MRI in the near term. METHODS: Preterm infants with T1 hyperintensity or cysts in the periventricular regions on term MRI were selected, and their gross motor functions were evaluated at the age of 3 to 5 years. Sixty-two infants had findings of T1 hyperintensity or cysts, and except for infants with these findings, none were diagnosed later as periventricular leukomalacia. RESULTS: All 37 patients with cerebral palsy had periventricular lesions with T1 hyperintensity or cysts in the corona radiata above the posterior limb of the internal capsule on coronal sections. Small T1 hyperintensity lesions were seen on coronal slices and were often difficult to detect on axial slices. All of the 17 infants with T1 hyperintensity findings sparing the corona radiata above the posterior limb of the internal capsule showed normal motor development, irrespective of findings of ventriculomegaly. There was a tendency for the presence of widespread lesions in corona radiata above the posterior limb of the internal capsule to be correlated with the severity of motor handicap. CONCLUSIONS: Lesions in the corona radiata above the posterior limb of the internal capsule on a coronal view by term MRI were useful for predicting motor prognosis in preterm infants with periventricular leukomalacia.

Congenital neuroblastoma in a patient with partial trisomy of 2p.

We report the fourth example of a patient with germline partial trisomy of 2p21-pter and congenital neuroblastoma. The male infant had a dysmorphic facial expression and presented with congenital heart disease, supernumerary nipples, hypospadias, shawl scrotum, hemilateral persistent hyperplastic primary vitreous, and neuroblastoma. His germline karyotype of 46,XY,der(8)t(2;8)(p21;p23.2) was inherited from a maternal-balanced translocation, which indicates that the proto-oncogene MYCN region of 2p24.3 is tripicated in germline cells. A cytogenetic study of the biopsied tumor cells did not show MYCN amplification, but the DNA index was 2.4 and histologic fluorescent in situ hybridization analysis indicated somatic mutation with near-pentaploidy of the tumor cells. This could be an alternative mechanism of MYCN activation in the process of the tumorigenesis of neuroblastoma.