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Bai-Horng Su

Publications and source records attributed to Bai-Horng Su.

24 records · Page 2Linked to original sources

Medical treatment with atropine sulfate for hypertrophic pyloric stenosis.

We investigated whether atropine sulfate was an effective, non-surgical method for treating hypertrophic pyloric stenosis (HPS). The study group consisted of 5 patients, all of the patients presented with projectile vomiting. Hypertrophic pyloric stenosis was diagnosed based on abdominal sonographic findings. The age when symptom arose was 30.8 +/- 15.5 (mean +/- SD) days, the age upon admission was 43.2 +/- 9.6 days. The frequency of vomiting was 5.8 +/- 2.3 times per day. After admission, all patients received 10% atropine sulfate 0.01 mg/kg intravenous (i.v.) for 5 minutes q4H (every four hours) before each feeding. Formular milk was started and increased by 10 ml every feeding until full feeding (120 ml/kg/day) was achieved. When vomiting had ceased for a period of one day, i.v. atropine was changed to 0.02 mg/kg oral q4H before each feeding. The patient was hospitalized until full feeding was maintained for more than 2 days. Then oral atropine was tapered by half a dose every 2 weeks. Oral atropine was continued until the thickness of the pyloric muscle had normalized (< 3.5 mm). All five patients were successfully treated with atropine sulfate. The frequency of vomiting was reduced to less than two times per day (1.8 +/- 1.3 days). i.v. atropine was used for 6.4 +/- 3.4 days, and the oral form was used for 30 +/- 9 days. The total number of days of atropine sulfate treatment was 36.4 +/- 9.58 days. Full feeding was achieved at 8 +/- 5.3 days. The hospitalization was 14.6 +/- 6.2 days. The body weight when admitted was 4000 +/- 760.8 gm and the body weight when discharged was 4282 +/- 901 gm. The body weight one month after treatment was 5210 +/- 772.5 gm. The body weight gain one month after atropine treatment was 1262 +/- 441.4 gm. Body weigh range on admission was from <3rd to 25th percentile, and after one month of atropine treatment, the body weight range was from 10th to 75th percentile. Complications included transiently elevated heart rates (180-200 times/min) in two patients and facial flushing after the first dose of IV atropine in one patient. In conclusion, conservative treatment with initially IV atropine in the initial stages instead of oral atropine sulfate is an effective alternative to pyloromyotomy, particularly in infants with major concurrent disease or when parents are unwilling to let their infants undergo surgery. Surgical intervention is not always necessary.

Administration, Oral↗

Outcome of vocal cord paralysis in infants.

Although laryngomalacia is the leading cause of stridor in infancy, vocal cord paralysis, despite its low incidence, is still the second most common cause. However, the etiology of infant vocal cord paralysis is different from that of adults, and the management protocol is controversial. Therefore, we conducted this study to better characterize the cause and outcome of vocal cord paralysis in infants. From January 1997 to December 2003, we treated thirteen infants younger than one year for vocal cord paralysis. Seven infants were idiopathic (idiopathic group), two might be caused by prior surgery (iatrogenic group), two might be caused by central neuropathy (neurological group), and two were born after difficult delivery (obstetrical group). In the idiopathic group, six infants spontaneously recovered and one infant had right-side recovery, but the left side was still paralytic. All infants in the iatrogenic and obstetrical groups spontaneously recovered. However, no infant in the neurological group recovered. Spontaneous recovery occurred in 76.9% of affected infants. More than half (70%) of these spontaneous recoveries occurred within 6 months. In our experience, direct flexible laryngoscopy is mandatory for all infants younger than one year of age presenting with stridor. Except for extreme infants (e. g. bilateral vocal cord paralysis with severe respiratory distress and central neuropathy) who require a temporary tracheotomy to relieve the airway obstruction, we recommend waiting for at least 6 months before proceeding to invasive surgical interventions.

Dyspnea↗

No association of urokinase gene 3'-UTR polymorphism with bronchopulmonary dysplasia for ventilated preterm infants.

Pathological findings pertaining to bronchopulmonary dysplasia (BPD) are consistent with a process of prolonged lung inflammation and impaired healing. The balance of the competing activities of coagulation and fibrinolysis may contribute to the premature lung's response to acute injury. We investigated the association of the urokinase gene polymorphism with BPD in ventilated preterm infants whose gestational age was below 30 weeks. BPD is defined as infants remaining dependent upon active respiratory support and/or oxygen supplementation and featuring characteristic radiographic changes in the lung fields on the 28th postnatal day (BPD-28d) and at a corrected age of 36 weeks of gestation (BPD-36w). Two hundred and four ventilated preterm infants were enrolled in the study. The typing of each specific genotype polymorphism was performed by polymerase chain reaction (PCR) and restriction analysis. Perinatal risk factors for BPD, genotype distribution, and allelic frequencies were compared between infants suffering from BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. The genotype proportions of the urokinase 3'-UTR polymorphism for BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD did not differ significantly. There was no difference in allelic frequency for the urokinase 3'-UTR polymorphism between BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. We concluded that urokinase gene 3'-UTR C/T polymorphism is not a suitable marker for predicting susceptibility and severity to BPD for preterm infants of Taiwanese.

3' Flanking Region↗

System-based strategy for the management of meconium aspiration syndrome: 198 consecutive cases observations.

To evaluate whether the system-based strategy for management of meconium aspiration syndrome (MAS) could reduce the morbidity and mortality rate of MAS in our institute, a prospective consecutive clinical observation was conducted. System-based strategy including appropriately trained the relevant medical staff to familiar with neonatal resuscitation program, early surfactant replacement or lavage following with high-frequency ventilator (HFV) and/or inhaled nitric oxide (iNO). Outcome measurements were the morbidity and mortality rates of MAS. All infants of MAS in the study period were included except cases of congenital malformations or cyanotic congenital heart disease (CHD). Oxygen, nasal continuous positive airway pressure (CPAP), and intermittent mandatory ventilation (IMV) were applied as clinically indicated. Surfactant was used as replacement or lavage therapy for MAS infants whose oxygen index (OI) exceeded 20 or value for AaDO2 exceeded 400 within 6 hours of age. High-frequency oscillator ventilation (HFO) was applied for infants of MAS that demonstrated intractable respiratory failure with conventional mechanical ventilation and 100% oxygen. Inhaled nitric oxide (iNO) was used with IMV or HFO for infants of persistent pulmonary hypertension (PPHN) when it was unresponsive to conventional therapy. Dexamethasone was prescribed in infants of severe hypotension that did not respond to dopamine and epinephrine. A series of 198 consecutive infants of MAS born in this hospital during 9 years were analyzed. There was no mortality. Fourteen infants developed PPHN, 11 had pneumothorax, 1 had pulmonary hemorrhage, 2 had neurologic sequelae because of severe asphyxia, and 2 developed bronchopulmonary dysplasia. Our results indicated that appropriately trained relevant medical staff with neonatal resuscitation program to avoid complicated MAS and early surfactant replacement or lavage following with HFO and/or iNO could reduce the morbidity and mortality rate of MAS even without extracorporeal membrane oxygenation (ECMO).

Administration, Inhalation↗

No association between TAP1 DpnII polymorphism and bronchopulmonary dysplasia.

The possibility that a family history of asthma may have a role in susceptibility to bronchopulmonary dysplasia (BPD) had been raised in several reports, and there was evidence of a strong association between transporter associated with antigen processing (TAP1) polymorphism and asthma in Taiwanese population. To test whether TAP polymorphism has a role in the BPD, we investigated the association between TAP1 polymorphism and BPD by analyzing the results of genotype distribution. The study included 224 ventilated preterm infants (<30 weeks) who had respiratory distress syndrome (RDS) and needed intermittent mandatory ventilation (IMV) during Jan. 1999 to July 2003. The typing of TAP1 polymorphism was performed by polymerase chain reaction (PCR)-based restriction analysis. The demography between two groups of these ventilated preterm infants was not different. We observed no significant differences in genotype distribution or allele frequency of the TAPI polymorphisms between BPD and their respective control infants. There was also no significant difference in genotype distribution of the TAP1 polymorphism with duration of IMV. Therefor, we conclude that TAP1 polymorphism is not a useful marker for predicting the susceptibility or severity to BPD for Taiwanese.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Vein of Galen aneurysm complicated with pulmonary hypertension: report of one newborn case.

The vein of Galen aneurysm is a rarely seen congenital intracranial vascular malformation with abnormal aneurysmal dilation of the vein of Galen in neonatal stage. We report a full- term female newborn presented with intractable heart failure, pulmonary artery hypertension, and respiratory distress soon after birth, in whom persistent pulmonary hypertension of newborn was suspected initially. Further study by ultrasound revealed turbulent blood flow in the cerebral vascular lesion in the region of vein of Galen; therefore, secondary pulmonary artery hypertension complicated with 'steal' phenomenon was impressed. With the advancement of diagnostic technique, ultrasound provides a rapid and noninvasive method for diagnosing the condition.

Cerebral Veins↗