Placement of neonatal central venous catheter tips in the right atrium: a practice to be avoided?
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Biomedical subjects
Publications and source records attributed to P R Dear.
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AIMS: To describe the relation between oscillatory amplitude changes and arterial blood gas (ABG) changes in preterm infants receiving high frequency oscillatory ventilation, using a multiparameter intra-arterial sensor (MPIAS). METHODS: Continuous MPIAS ABG data were collected after amplitude changes and stratified according to FIO(2): high (> 0.4) or low (< 0.3). For each amplitude change, the maximum change (from baseline) in PaCO(2) and PaO(2) over the following 30 minutes was determined. In total, 64 oscillatory amplitude changes were measured in 21 infants (median birth weight 1040 g; gestation 27 weeks). RESULTS: All amplitude increases produced PaCO(2) falls (median -0.98 and -1.13 kPa for high and low FIO(2) groups respectively). All amplitude decreases produced PaCO(2) rises (median +0.94 and +1.24 kPa for high and low FIO(2) groups respectively). About 95% of the change in PaCO(2) was completed in 30 minutes. Amplitude changes did not affect PaO(2) when FIO(2) > 0.4. When FIO(2) < 0.3, amplitude increases produced a PaO(2) rise (median = +1.1 kPa; P < 0.001) and amplitude decreases a fall (median = -1.2 kPa; P < 0.001). CONCLUSIONS: After oscillatory amplitude changes, the speed but not the magnitude of the PaCO(2) change is predictable, and a rapid PaO(2) change accompanies the PaCO(2) change in infants with mild lung disease and a low FIO(2).
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It is well recognised that reducing positive end expiratory pressure (PEEP) leads to an increase in the tidal volume and minute volume in ventilated neonates. The magnitude of this effect is perhaps not commonly appreciated, however. Effectively, PEEP is four times as potent as peak inflation pressure (PIP) in bringing about changes in tidal volume. The influence of changes in PEEP and PIP on tidal volume and the relative magnitude of each are considered. Twenty one preterm infants were studied on 38 separate occasions. All were sedated, paralysed, and ventilated, 19 for hyaline membrane disease. A 1 cm H2O reduction in PEEP was twice as potent as a 2 cm H2O increase in PIP in achieving an increase in tidal volume (14 v 7%). Similarly, increasing PEEP by 1 cm H2O was twice as effective as a 2 cm H2O decrease in PIP in reducing tidal volume (13 v 6%). Small (0.5-1 cm H2O) changes in PEEP can often be used to improve ventilation and carbon dioxide elimination. Levels of PEEP of 4-5 cm H2O may, at times, impair gas exchange and contribute to overdistension.
Little is known about the ontogeny of gastric acid secretion in the very preterm infant. In order to study this we recorded intragastric pH continuously for 24 h on 71 occasions in 22 enterally starved preterm infants. Infants ranged from 24 to 29 weeks' gestation and were studied in the first 5 days, and in the third week, of life. As the infants became more mature, both in terms of gestation and postnatal age, there was a decrease in intragastric pH from median (range) 3.7, 2.5 (0.6-3.9) and 1.8 (1.3-2.6) for infants of 24-25, 26-27 and 28-29 weeks' gestation, respectively on the first day of life to 1.8 (1.7-1.9), 2.0 (1.8-2.3) and 1.7 (1.5-2.0) on day 16. All the infants were able to maintain a gastric pH of below 4 from the first day of life. Our data lay to rest the suggestion that the preterm infant is incapable of hydrogen ion secretion. Gastric acid secretion in the newborn preterm infant should allow normal proteolytic activity and the well recognised clinical problems of intragastric bleeding, gastritis or oesophagitis may be attributable to intragastric acid.
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Gastric perforation is a catastrophic, albeit uncommon, side effect of steroid treatment for premature infants with bronchopulmonary dysplasia (BPD). A reduction of intragastric acidity may protect against peptic ulceration. The effect of different doses of ranitidine, given as intravenous infusions, on intragastric acidity in premature neonates was therefore examined. Ten consecutive, enterally starved, infants receiving dexamethasone (0.6 mg/kg) for BPD were enrolled. Intragastric pH was continuously monitored on the day before steroid treatment and on the four following days, initially without H2 blockade and then using a continuous intravenous infusion of ranitidine at 0.031, 0.0625, and 0.125 mg/kg/hour. An infusion of 0.0625 mg/kg/hour of ranitidine was sufficient to increase and maintain gastric pH above 4; the authors therefore use this infusion during dexamethasone administration as possible prevention of gastric perforation.
No one doubts that good nutrition is an important component of neonatal intensive care, nor that this can only be accomplished by the use of intravenous fat. With regard to the effects of nutrition on bronchopulmonary dysplasia, however, we are facing a dilemma. On the one hand there is the suggestion that inadequate nutrition increases the severity of bronchopulmonary dysplasia and on the other that the use of intravenous fat predisposes to it. In an attempt to narrow the area of uncertainty we randomly allocated 129 infants of less than 1750 g birth weight to receive either early or late lipid containing parenteral nutrition. The median duration of ventilation support in the 'early' group was 8.5 days and in the 'late' group eight days; this was not significantly different.
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A substantial increase in the plasma concentration of most amino acids was observed in 59 preterm infants with chronic lung disease soon after the initiation of dexamethasone therapy. The size of increase appeared to be dose related. This phenomenon is likely to be the result of steroid induced protein catabolism. Interestingly, neither phenylalanine nor tyrosine concentrations were significantly increased.
Most babies treated with dexamethasone for bronchopulmonary dysplasia exhibit an appreciable rise in the blood urea concentration, from a mean of 2.3 mmol/l before steroid to a mean of 7.1 mmol/l after. In order to discover whether this was primarily the result of increased protein catabolism, nitrogen balance studies before and after the start of dexamethasone were performed and a mean deficit in nitrogen retention of 158 mg/kg/24 hours was found. Similarly the urinary 3-methylhistidine (3MH):creatinine ratio before and after the commencement of dexamethasone treatment in a group of preterm babies was measured. It was found that there was a substantial increase in 3MH excretion after dexamethasone: from a mean 3MH:creatinine ratio of 46 in the week before steroids to a mean ratio of 77 in the week after. As 3MH emanates almost exclusively from the breakdown of actin in skeletal muscle cell, this finding implies the loss of muscle tissue. It was also found that the babies were in less positive nitrogen balance after dexamethasone, to a degree which is significant relative to their protein reserves. The long term consequences of a period of increased catabolism are not yet known but the authors suggest caution in the use of dexamethasone, at least in babies with milder degrees of bronchopulmonary dysplasia in whom the ratio of benefit to risk may be less favourable.
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Three cases of gastroduodenal perforation and one case of ulceration and extreme thinning of the gastric wall occurred in preterm babies treated with dexamethasone for bronchopulmonary dysplasia. This complication of treatment with steroids has not to our knowledge previously been described in preterm infants. Urgent abdominal paracentesis was an essential part of the resuscitation in these cases, and this potentially serious side effect should be considered in all babies treated with steroids.
In order to test the hypothesis suggested in a recent report that the birthweight ratio might be a useful predictor of several important clinical outcome measures in babies of less than 31 weeks' gestation, we examined the association between the birthweight ratio and aspects of both short and long term outcome in 436 Leeds babies of less than 31 weeks' gestation. Unlike the report, and contrary to what we had expected, we were unable to find any significant association between birthweight ratio and length of time on the ventilator, mortality, neurological outcome, or intellectual outcome.
Interpretation of the prognostic value of cranial ultrasound abnormalities in preterm infants has been hampered by the lack of a uniform approach to research, especially in the definition and classification of the abnormal appearances. Defining normality should be less controversial, but from a selected reading of the literature it is possible to gain quite varied impressions as to the prognostic value of normal ultrasound appearances. In order to determine the predictive value for normal development of consistently normal cranial ultrasound scans in the preterm baby, we have performed a meta-analysis on all the published reports in the English language which provide follow-up data on such cases. The overall prevalence of major disability among 1,604, mainly very low birthweight, babies was 15%. The predictive value of a normal scan for freedom from major disability was 93% and the predictive value for an entirely normal outcome was 88%. The value of this information in the counselling of parents is discussed.
To find out if the use of steroids affected the incidence of infection in babies who were nursed in the neonatal intensive care unit for nine weeks or more, 24 preterm babies who had received a three weeks course of dexamethasone (0.6 mg/kg/day, reducing to 0.3 mg/kg/day after a week, and 0.15 mg/kg/day after two weeks) were compared with 18 preterm babies who had not been so treated. No differences were found in the incidence or pattern of septicaemia or other bacteriologically proved infections between the groups. Of 57 episodes of septicaemia, 44 (77%) were caused by coagulase negative staphylococci.