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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The review of the literature on Cheyne-Stokes respiratory periods reveals enormous variation of the opinions expressed. The original description concerned periodicity characterized by rhythmic changes of respiratory phases and respiratory pauses in a relation of 60 : 15 seconds. In the respiratory phase there were 30 respirations of increasing depths and frequency at the beginning of the phase and decreasing depths and frequency at the end of the phase. Literature data about Cheyne-Stokes respiration comprise a multiplicity of all rhythymic forms. The duration of respiratory cycles varies between 12 and 130 seconds. The relation of the respiratory phase and respiratory pause between 6 : 4 or 75 : 70 seconds, and the number of breaths between 3 and 30 during one respiratory phase. Cheyne-Stokes periods were observed in health subjects as well as in patients with neurological, neurosurgical, cardiac, pulmonary and paediatric diseases. Cheyne-Stokes periods were explained as sequel of prolongation of circulation time between pulmonary alveoli and respiratory centre, through increased sensitivity of the respiratory centre to CO2, diminished sensitivity of the respiratory centre to CO2 and O2-deficit, local blood flow disturbances, section of pathways in the brain stem with disinhibition of basic rhythms, brain immaturity, alterations of consciousness, and respiratory obstructions. Rhythmic changes of the heart beat, of excitability of the heart muscle, of blood pressure, of EEG and of neurological and mental signs were observed. In spite of numerous observations detailed analysis of the respiratory cycle was performed in only a few cases. Major studies are lacking.
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PMID:The definition of "Cheyne-Stokes rhythms". 36 Jul 80

Apgar scores are used routinely to assess early neonatal status, but are less accurate in the preterm neonate because of developmental immaturity. Attention has been directed to umbilical cord gases as a method of neonatal evaluation. Using a retrospective chart review of all viable preterm births (24-36 weeks' gestation) between January 1986 and December 1989, we tabulated the umbilical cord gas indices of these infants. Fetuses with lethal congenital anomalies and those with abnormal heart rate tracings on admission were excluded from the data base, leaving 1872 infants. Cord arterial blood gas values were available for analysis in 74.4% of cases and cord venous gas values in 81.8%. The mean (+/- standard deviation [SD]) arterial and venous umbilical cord blood gas values for the preterm infants, were, respectively: pH, 7.26 +/- 0.08 and 7.33 +/- 0.07; oxygen pressure, 19.0 +/- 7.9 and 29.2 +/- 9.7 mmHg; carbon dioxide pressure, 53.0 +/- 10.0 and 43.4 +/- 8.3 mmHg; bicarbonate, 24.0 +/- 2.3 and 22.8 +/- 2.1 mEq/L; and base excess, -3.2 +/- 2.9 and -2.6 +/- 2.5 mEq/L. Acidemia was defined statistically as 2 SDs or more below the population mean. The incidence of 5-minute Apgar scores below 7 in the preterm infants was 8.5% and within this group, 17.8% were acidemic (arterial pH 7.10 or lower). More than 82% of neonates with 5-minute Apgar scores less than 7 had normal umbilical cord blood gases. There was no significant difference in umbilical arterial blood gas values between preterm infants and 1924 term deliveries at our institution between 1986-1988.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of preterm birth on umbilical cord blood gases. 155 80

Nine of nineteen infants in this study exhibited two or more central apnea greater than or equal to 20 seconds when they were older than one week and between 32-36 weeks postconceptional age (PCA). We focused on the sequelae of these apneas. Apnea was separated from other morbidity associated with immaturity by the selection of consistently healthy infants. Following discharge, polygraphic tracings were obtained at 40, 44 and 52 weeks PCA in these non-apneic and previously apneic infants. Sleep states, minute by minute values for heart and respiratory rate, skin temperature and transcutaneous O2 (PtcO2) and CO2 (PtcCO2), apnea and transient decreases in PtcO2 were determined. Polygraphic measurements did not differentiate preterm infants with late apnea in the nursery from non-apneic ones. However, the apneic group exhibited a transient decrease in awakenings at 44 weeks PCA.
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PMID:Polygraphy after discharge in preterm infants with and without apnea in the nursery. 160 88

The postnatal maturation and the adaptational ability of the sympathoadrenal system has been investigated in preterm neonates (n = 8), and in sick preterm neonates with respiratory disorders (n = 10). Plasma levels of dopamine (DA), norepinephrine (NE), epinephrine (E) and 3-4 dihydroxyphenylacetic acid (DOPAC) were evaluated at rest during the first month of life, and following an inhalation of a 5% carbon dioxide-21% oxygen mixture for 10 min. During the first month of life the sick preterm neonates exhibited similar NE, E, and DOPAC plasma levels but higher DA amounts than healthy infants. Plasma DA levels were inversely correlated with the transcutaneous oxygen tension (r = -0.636) indicating that hypoxemia was able to enhance the release of DA. Immediately following the hypercarbia test, there were no significant changes of plasma catecholamine levels in the sick preterms, but there was a significant increase of E plasma levels (+140%, p less than 0.05) and a moderate elevation of NE and DA amounts in the healthy preterms. It is concluded that preterm neonates who have had respiratory disorders did not exhibit an immaturity of the sympathoadrenal system at rest, but had a defect in the release of E following hypercarbia exposure, which may be secondary to an alteration in chemoreceptor function and/or reduced catecholamine stores.
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PMID:Plasma dopamine, norepinephrine, epinephrine and DOPAC levels in preterm infants prior to and immediately after a sleep ventilation hypercarbia test. 175 Mar 32

Intraventricular hemorrhage (IVH) in preterm infants is well known to be associated with the high morbidity and mortality of this group. Previous studies have suggested altered cerebral blood flow (CBF) as an important pathologic factor. We measured the CBF in near-term rabbit fetuses using the hydrogen clearance technique. The local CBF of the rabbit fetuses was significantly low compared with that of the maternal rabbits. The response of CBF to changes in PaCO2 was observed in rabbit fetuses. The CO2 reactivity index of the fetal rabbit was lower than that of the maternal rabbit. This low CO2 reactivity might reflect the immaturity of the fetal brain and its low CBF. We were unable to monitor the fetal blood pressure, but the fetal CBF remained stable when the maternal blood pressure was altered. It is well known that IVH in preterm infants originates from the subependymal germinal matrix and that this has many fragile vessels. Our observation suggests that even a small increase of CBF during hypercapnia might have a large effect towards producing hemorrhage.
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PMID:CO2 reactivity and autoregulation in fetal brain. 176 8

During the 4-year period, 1982-1986, 18 patients presented to the Children's Hospital, Camperdown, Sydney, with the following features: (1) Recurrent "absences" clinically indistinguishable from childhood absence epilepsy, (2) Normal clinical examination, (3) Electroencephalogram (EEG) demonstrating normal waking background and sleep activity. On hyperventilation, "absences" occurred, characterized on EEG by a marked build-up of paroxysmal slow-wave activity unassociated with evidence of epileptic activity. We designate these attacks "pseudoseizures caused by hyperventilation resembling absence epilepsy." Individual cases demonstrated a variety of other symptoms consistent with the hyperventilation syndrome. There was an identifiable environmental stress in 13 of the 18 cases. Follow-up of 13 patients after a mean period of 20 months revealed that only two children continued to have occasional absences, associated with a clear history of breathing up when upset. Treatment did not influence outcome. On repeat hyperventilation with EEG and respiratory monitoring, five of the 13 had pseudoseizures. There was no indication that susceptibility to these episodes was associated with an abnormal CO2 response. It is postulated that the occurrence of pseudoseizures is related to cerebrovascular immaturity and an excessive vasoconstrictor response to a given level of CO2.
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PMID:Pseudoseizures caused by hyperventilation resembling absence epilepsy. 212 20

Bicarbonate reabsorption by the immature kidney in response to acute acid-base changes was assessed in 50 anesthetized newborn rabbits before the end of nephrogenesis. The normal newborn rabbit (age 5-12 days) is in a state of hypochloremic metabolic alkalosis (PHCO3-, 31.9 +/- 0.6 mmol/l; PCl-, 83.1 +/- 1.0) and excretes a hypertonic (Uosmol = 578 +/- 41 mosmol/kgH2O), alkaline (UpH = 7.40 +/- 0.15) urine containing 50 +/- 9 mmol/l Cl- and 13 +/- 4 mmol/l Na+. The alkalosis is probably generated by an alkaline load contained in the mother's milk and maintained by a state of chloride wasting and volume contraction. In this alkalotic model, bicarbonate reabsorption, expressed per milliliter glomerular filtration rate (GFR), correlates positively with arterial CO2 pressure (PaCO2). The ability of the immature kidney to reclaim filtered bicarbonate in response to an elevation of the plasma carbon dioxide tension remains unlimited up to PaCO2 of 110 mmHg (y = 20.7 + 0.15 x, r = 0.82, P less than 0.001). Hypercapnia is associated with a marked fall in GFR, so that the positive correlation between bicarbonate reabsorption and PaCO2 vanishes when the bicarbonate reabsorption rate is expressed in absolute terms. Bicarbonate reabsorption is strongly dependent on the filtered load during both acutely induced metabolic acidosis and alkalosis. The acid-base state of the newborn rabbit is in sharp contrast with that of most animal species, and the renal handling of bicarbonate as a function of GFR does not show signs of tubular immaturity.
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PMID:Bicarbonate reabsorption by the kidney of the newborn rabbit. 291 64

Continuous transcutaneous carbon dioxide partial pressure (tc PCO2) and continuous transcutaneous oxygen partial pressure (tc PO2) was monitored simultaneously in 10 consecutive neonatal intensive care patients treated for respiratory problems or immaturity. During measurement the electrode temperature was 44 degrees C while during the resting periods--with the electrodes left in situ--the electrode temperature was 37 degrees C. Measurements were performed for periods up to 31 hours. It was possible to discover changes in central blood gas partial pressures also at the lower electrode temperature. This was especially true for the tc PCO2 recording which was less influenced by the decrease in electrode temperature than the tc PO2 recording. In six patients an increased frequency of apnoea was diagnosed by the transcutaneous blood gas monitoring equipment previous to other clinical signs. A statistically highly significant correlation was found between transcutaneous and arterial blood gas values, the arterial samples obtained from umbilical artery catheters. tc PCO2 and tc PO2 very sensitively reacts to changes in the breathing pattern and to changes in activity of the neonate emphasizing the drawbacks of previous blood gas monitoring techniques. The technique for continuous transcutaneous carbon dioxide monitoring is ready for clinical use and is a valuable additional tool in all neonatal intensive care patients with the risk of alveolar hypoventilation.
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PMID:Simultaneous transcutaneous carbon dioxide and transcutaneous oxygen monitoring in neonatal intensive care. 640 25

A description is first given of respiratory activity in the fetus and its control. Evidence suggests that when the fetus makes respiratory movements, it is in a state comparable to REM sleep in the newborn and adult and that in the alternating periods of apnoea, it is in quiet sleep. It does not appear that the respiratory movements are normally regulated by chemical or reflex, e.g. Hering Breuer, inputs though they are enhanced by CO2 and depressed by hypoxia. In the apnoeic periods, breathing movements are virtually impossible to elicit by chemical or reflex means. Evidence from examination of peripheral inputs indicates that: the carotid body chemoreceptors are inhibited at receptor level, stimulation of the aortic chemoreceptors affects the circulation only and although pulmonary stretch receptors are active and are excited by inflation of the fetal lung, such inflation does not affect discharge in medullary respiratory units or phrenic nerve. Since there is no real evidence of immaturity of the respiratory system in late gestation and since chemical and most reflex inputs appear to provide an adequate stimulus, it is most probable that the periods of apnoea are caused by an inhibitory process, possibly of supra-pontine origin which acts close to medullary respiratory units and effectively inhibits the operation of the automatic component. This inhibitory process may operate periodically; or continuously and be periodically overridden in REM sleep. After birth, breathing is normally continuous and sensitive to lung inflation, CO2 and after a variable delay, to hypoxia. This may be due to the lifting of the inhibitory process allowing activation of the automatic component. However, there is evidence that even in normal, full term infants, full maturation of the automatic component is not complete until about three months of age and in the meanwhile, breathing tends to be imperfectly regulated and subject to damped oscillations when disturbed.
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PMID:Respiratory sensitivity before and after birth. 681 77

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2


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