Skin surface carbon dioxide tension in sick infants

Skin surface PCO2 (PSCO2) was measured at 44 C in 17 sick infants using a Radiometer surface PCO2 electrode. Values obtained for PSCO2 were compared with simultaneous values for arterial PCO2 (PaCO2). PSCO2 was found to be linerarly related to PaCO2 by a regression line with a slope 1.37. PaCO2 could be predicted from PSCO2 to within 6 torr in all instances. The relationship was not affected by the patient's gestational age, postnatal age, weight, or blood pressure. This electrode is a valuable clinical tool in the management of sick infants.     

Cardiovascular effects of carbon dioxide in ventilated preterm infants

Sick preterm infants may, under certain conditions, demonstrate blood pressure passive cerebral blood flow in response to changes in arterial carbon dioxide tension. Blood pressure in turn depends on cardiac output and peripheral resistance. A Doppler technique for assessing cardiac output compared favourably in terms of reproducibility to a thermodilution technique in a group of infants undergoing cardiac catheterization for congenital heart disease. Doppler was subsequently used to monitor changes in cardiac output following an increase in arterial carbon dioxide tension of 1 kPa in 25 ventilated preterm infants. Blood pressure increased significantly (p = 0.006). However, heart rate did not change significantly (p = 0.16) and, in addition, both stroke and minute volume decreased (p = 0.023, p = 0.02, respectively). This suggests that accompanying changes in components of peripheral resistance exert important effects on blood pressure in the preterm neonate in response to changes in arterial carbon dioxide tension.     

Dysfunctional antithrombin III in sick premature infants

Antithrombin III, a major inhibitor of activated coagulation factors has low immunologic levels in the human infant. The objective of this study was to determine if the antithrombin III molecule is fully functional in sick premature infants. The populations studied included: adult controls (n = 20), full term healthy infants (n = 18), sick premature infants on day 1 (n = 16) and at greater than 7 days of age (n = 10), and infants with disseminated intravascular coagulation (n = 11). This was diagnosed in the presence of prolonged screening tests, decreased levels of fibrinogen, and platelets along with elevated fibrin degradation products. Plasma antithrombin III levels were measured biologically (chromogenic substrate S2238) and immunologically (radialimmunodiffusion), and expressed as a percent of adult pooled plasma. Crossed immunoelectrophoresis were performed in the presence and absence of heparin. The antithrombin III biologic/immunologic ratios for adults, healthy full term infants, and sick premature infants on day 1 of life were all near unity. In contrast sick premature infants beyond the 1st wk of life and infants with disseminated intravascular coagulation had lower biologic activity compared to immunologic (B/I = 0.77 +/- 0.28, 0.78 +/- 0.17, p less than 0.01), respectively. In all groups, the antithrombin III molecule was normal on crossed immunoelectrophoresis except for one infant with disseminated intravascular coagulation. Sick premature infants may acquire a dysfunctional antithrombin III molecule in the postnatal period.     

Carbon monoxide production in ventilated premature infants weighing less than 1500 g.

Mean pulmonary excretion rate of carbon monoxide in 13 premature babies on ventilators was significantly higher (p less than 0.001) than that of 19 healthy infants born at full term. This correlated with carboxyhaemoglobin concentrations in blood, indicating that the premature infants on ventilators produced abnormally large amounts of bilirubin.     

The efficacy of oral theophylline in ventilated premature infants

40 ventilated premature infants, with gestational ages of 24-34 weeks and a mean birthweight of 1422 g, were entered into a randomised controlled trial. 20 of the infants received orally 5 mg/ml anhydrous theophylline dissolved in 20% pure alcohol, with a loading dose of 5 mg/kg and then 1.25 mg/kg every 6 h. Plasma samples were assayed via an emit enzyme immunoassay, demonstrating satisfactory serum levels in all infants at 54 h after the loading dose. Possible side-effects were seen only in two infants, in one a tachycardia (220 beats/min) and the other became agitated during treatment.     

Dysfunction of pulmonary surfactant in chronically ventilated premature infants

Infants of <30 wk gestation often require respiratory support for several weeks and may develop bronchopulmonary dysplasia (BPD), which is associated with long-term pulmonary disability or death in severe cases. To examine the status of surfactant in infants at high risk for BPD, this prospective study analyzed 247 tracheal aspirate samples from 68 infants of 23-30 wk gestation who remained intubated for 7-84 d. Seventy-five percent of the infants had one or more surfactant samples with abnormal function (minimum surface tension 5.1-21.7 mN/m by pulsating bubble surfactometer), which were temporally associated with episodes of infection (p = 0.01) and respiratory deterioration (p = 0.005). Comparing normal and abnormal surfactant samples, there were no differences in amount of surfactant phospholipid, normalized to total protein that was recovered from tracheal aspirate, or in relative content of phosphatidylcholine and phosphatidylglycerol. Contents of surfactant proteins (SP) A, B, and C, measured in the surfactant pellet by immunoassay, were reduced by 50%, 80%, and 72%, respectively, in samples with abnormal surface tension (p < or = 0.001). On multivariable analysis of all samples, SP-B content (r = -0.58, p < 0.0001) and SP-C content (r = -0.32, p < 0.001) were correlated with surfactant function. We conclude that most premature infants requiring continued respiratory support after 7 d of age experience transient episodes of dysfunctional surfactant that are associated with a deficiency of SP-B and SP-C.     

Relactation by mothers of sick and premature infants

Relactation, the induction of lactation at any time beyond the immediate postpartum period, has received minimal scientific investigation. In this study, one adoptive mother and six mothers ten to 150 days postpartum, who for a variety of reasons did not initiate or maintain lactation after delivery, attempted relactation. Each suckled her infant at regular feeding intervals. Prior to milk production, formula was provided during suckling through an artificial device. Serum prolactin responses to thyrotropin-releasing hormone infusion and to suckling were measured at the start of the study and to suckling at approximately weekly intervals thereafter. All mothers produced milk; three completely nourished their infants and two others provided at least half of their infants' nutritional needs. The adoptive mother and one other failed to provide significant quantities of milk. Mothers reached their maximum potential for milk production in varying periods of time (eight to 58 days). Shorter postpartum interval and less postpartum breast involution correlated with the likelihood of successful relactation and the rapidity of the onset of lactation. Basal prolactin levels and stimulation tests were of no additional predictive value. Each mother, regardless of milk production, expressed positive feelings about nurturing her infants in this manner. We conclude that relactation frequently is possible and may offer the mother of a sick or premature infant who desires to breast-feed an alternative if she does not maintain lactation in the immediate postpartum period.     

Renal failure in sick hypertensive premature infants receiving captopril therapy

A retrospective study of nine sick premature infants with chronic lung disease who received captopril for control of systemic hypertension (systolic blood pressure (BP) greater than 113 mm Hg) was carried out to determine efficacy of therapy and associated complications. All nine infants had markedly elevated peripheral renin values, 134.3 +/- 128.1 ng/mL/hr (mean +/- SD). Five infants had abnormal renal sonographic and perfusion scans with evidence of renal artery thrombosis, parenchymal disease, or both. Captopril therapy (0.3 mg/kg) was instituted at a postnatal age of 123 +/- 108 days. After the initial dose, the systolic BP decreased significantly in all infants, the decrease ranging from 21% to 58% of the pretreatment value. Dosage was subsequently halved in all infants. Seventeen episodes of unpredictable decreases in BP more than 40% from baseline occurred during the reduced maintenance therapy. Four infants had a total of seven episodes during which the BP decreased by 57 +/- 10% from baseline; this decrease persisted for 17 +/- 6 hours and was unresponsive to volume reexpansion and inotropic therapy. All seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/hr) that persisted for 18 +/- 12 hours. These episodes were accompanied by neurologic signs (subtle seizures, lethargy, and/or apnea) within 18 +/- 6 hours after the onset of oliguria. The remaining five infants had a total of 13 episodes of decreased BP of 50 +/- 8% of baseline, which were of significantly shorter duration and responded to volume reexpanders, inotropic therapy, or both and were unaccompanied by oliguria. These data suggest the need for close observation of BP in infants receiving maintenance captopril therapy.     

新生儿机械通气时呼气末二氧化碳分压与动脉血二氧化碳分压相关性分析

目的 探讨新生儿机械通气时呼气末二氧化碳分压（PetCO2）和动脉血二氧化碳分压（PaCO2）的相关性。方法 对31例气管插管机械通气的新生儿进行持续主流PetCO2监测,并同时配对检测85例次动脉血血气分析,评估PetCO2与PaCO2的相关性和一致性。结果 31例机械通气新生儿PetCO2均值（41±10 mm Hg）低于PaCO2均值（46±11 mm Hg）（Pr=0.92,Pn=48）时,PetCO2和PaCO2具有显著正相关性（r=0.85,Pn=37）时,PetCO2和PaCO2也有显著正相关性（r=0.91,P结论 在机械通气的新生儿中,PetCO2和PaCO2有较好的相关性和一致性。     

Measurement of carbon dioxide production in very low birth weight babies

BACKGROUND: CO2 production is most commonly measured by using indirect calorimetry to quantify elimination of CO(2) in breath (VCO2). An alternative is to measure the rate at which CO2 appears in the body pool (RaCO2) by infusing a (13)C labelled bicarbonate tracer. VCO2 and RaCO2 generally differ but are related by c, a factor that adjusts for the incomplete recovery of infused tracer in the breath. The literature relating to human studies cites a wide range of values for c but the only neonatal study to determine c empirically estimated a mean value of 0.77. AIM: To estimate fractional recovery rate, c, in very low birthweight babies, and assess the feasibility of using the isotopic technique to measure CO2 production during mechanical ventilation. METHOD: Eleven spontaneously breathing, continuously fed, very low birthweight infants (median birth weight 1060 g, median gestational age 29 weeks) were studied. RESULTS: Mean (SD) VCO2 was 9.0 (2.0) ml/min (standard temperature and pressure dry, STPD) and mean (SD) RaCO2 was 9.6 (2.1) ml/min (STPD). The mean (SD) value of c was estimated as 0.95 (0.13). The 95% confidence intervals of the mean were 0.87-1.03. CONCLUSIONS: The results emphasise the importance of measuring c for a given study population rather than assuming a value based on adult studies. The close approximation of RaCO2 and VCO2 in this group of babies implies that the labelled bicarbonate infusion technique could be used to measure simply CO2 production during mechanical ventilation.     

Sequelae of acquired cytomegalovirus infection in premature and sick term infants

To assess the risk of long-term sequelae after acquired cytomegalovirus (CMV) infection in premature and sick term infants, 55 CMV infected patients were matched prospectively with 55 control patients and these matched pairs were evaluated at 3 years of age. Sensorineural hearing losses were present in four of 43 CMV infected patients (all mild-moderate) and in two of 43 controls (one severe). The incidence of neurologic sequelae was not increased in CMV infected patients with birth weight greater than 2000 gm. Among patients with birth weight less than 2001 gm, moderately abnormal EEGs were found in four (17%) of 23 CMV infected patients and in one (4%) of 23 controls, and severe handicaps occurred in four (14%) of 29 CMV infected patients and in two (7%) of 29 controls. Severe handicaps in premature infants were significantly (P less than 0.05) associated with early onset of CMV excretion (less than 8 weeks of age) and severe cardiopulmonary disease. Among the premature infants who were documented early excretors, three of 13 had severe neuromuscular impairment, four of 13 had severe handicaps (DQ less than 70, severe neuromuscular impairment, or profound loss of vision or hearing), and an additional four had DQs of 70 to 79. Among their matched control subjects, none of 13 had severe neuromuscular impairment, two of 13 had severe handicaps, and an additional two had DQs between 70 and 79. None of the premature infants who were documented late excretors (greater than or equal to 8 weeks of age) had any neurologic sequelae. The risk of neurologic sequelae and handicap may be increased in premature infants with onset of CMV excretion in the first 2 months of life.     

Fluctuating pressure-passivity is common in the cerebral circulation of sick premature infants

Cerebral blood flow pressure-passivity results when pressure autoregulation is impaired, or overwhelmed, and is thought to underlie cerebrovascular injury in the premature infant. Earlier bedside observations suggested that transient periods of cerebral pressure-passivity occurred in premature infants. However, these transient events cannot be detected reliably by intermittent static measurements of pressure autoregulation. We therefore used continuous bedside recordings of mean arterial pressure (MAP; from an indwelling arterial catheter) and cerebral perfusion [using the near-infrared spectroscopy (NIRS) Hb difference (HbD) signal) to detect cerebral pressure-passivity in the first 5 d after birth in infants with birth weight <1500 g. Because the Hb difference (HbD) signal [HbD = oxyhemoglobin (HbO2) - Hb] correlates with cerebral blood flow (CBF), we used coherence between MAP and HbD to define pressure-passivity. We measured the prevalence of pressure-passivity using a pressure-passive index (PPI), defined as the percentage of 10-min epochs with significant low-frequency coherence between the MAP and HbD signals. Pressure-passivity occurred in 87 of 90 premature infants, with a mean PPI of 20.3%. Cerebral pressure-passivity was significantly associated with low gestational age and birth weight, systemic hypotension, and maternal hemodynamic factors, but not with markers of maternal infection. Future studies using consistent serial brain imaging are needed to define the relationship between PPI and cerebrovascular injury in the sick premature infant.     

Pulmonary function changes after nebulised and intravenous frusemide in ventilated premature infants

AIMS—To compare the effects of a single dose of frusemide administered either intravenously or by nebulisation on pulmonary mechanics in premature infants with evolving chronic lung disease.
METHODS—The effect of frusemide on pulmonary mechanics was studied at a median postnatal age of 23 (range 14-52) days in 19 premature infants at 24 to 30 weeks gestational age, who had been dependent on mechanical ventilation since birth. Frusemide (1 mg/kg/body weight) was administered, in random order, intravenously and by nebulisation, on two separate occasions 24 hours apart. Pulmonary function studies were performed before and at 30, 60, and 120 minutes after administration of frusemide. Urine was collected for six hours immediately before and for six hours after administration of frusemide.
RESULTS—Nebulised frusemide increased the tidal volume 31(SE 11.5)% and compliance 34 (SE 12)% after two hours, whereas no change in either was noted for up to two hours after intravenous frusemide administration. Neither intravenous nor nebulised frusemide had any effect on airway resistance. Six hour urine output increased from a mean (SE) of 3.3 (0.4) ml/kg/hour to 5.9 (0.8) ml/kg/hour following intravenous frusemide administration while nebulised frusemide had no effect on urine output. Urinary sodium, potassium, and chloride losses were also significantly higher after intravenous frusemide, whereas nebulised frusemide did not increase urinary electrolyte losses.
CONCLUSION—Single dose nebulised frusemide improves pulmonary function in premature infants with evolving chronic lung disease without adverse effects on fluid and electrolyte balance.