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PubMed1995

Predictive value of early continuous amplitude integrated EEG recordings on outcome after severe birth asphyxia in full term infants.

The background pattern in single channel amplitude integrated EEG recordings (aEEG) was recorded in 47 infants within the first six hours after birth to see if this could predict outcome after birth asphyxia. The aEEG background pattern during the first six hours of life was continuous and of normal voltage in 26 infants. All these infants survived; 25 were healthy, one had delayed psychomotor development. A continuous but extremely low voltage pattern was present in two infants, both of whom survived with severe handicap. Five infants had flat (mainly isoelectric) tracings during the first six hours of life; four died in the neonatal period, and one survived with severe neurological handicap. Burst-suppression pattern was identified in 14 infants, of whom five died, six survived with severe handicap, and three were healthy at follow up. The type of background pattern recorded within the first six postnatal hours in the aEEG tracings predicted outcome correctly in 43 of 47 (91.5%) infants. Use of aEEG monitoring can predict outcome, with a high degree of accuracy, after birth asphyxia, within the first six hours after birth. The predictive value of a suppression-burst pattern was, however, somewhat lower than the other background patterns. The aEEG seems to be a feasible technique for identifying infants at high risk of subsequent brain damage who might benefit from interventionist treatment after asphyxia.

Asphyxia Neonatorum↗
PubMed1988

Clinical and biochemical assessments of damage due to perinatal asphyxia: a double blind trial of a quantitative method.

Using conventional criteria, a series of 26 infants was selected for intrapartum asphyxia from about 4000 deliveries over one year at a single hospital to assess the efficacy of a new biochemical method. Tissue damage was estimated from urinary excretion of hypoxanthine, an important and central intermediate in purine metabolism. The overall pattern showed agreement between the grading (by previously accepted methods) of asphyxia in the perinatal period and our new biochemical approach. The association with handicap at one year of age following asphyxia was complex. This biochemical technique could be used to exclude postasphyxial damage as a cause of clinical disturbances and to select a small group (0.1% of all births) who require further investigation for rarer disorders which may also cause long term handicap.

Asphyxia Neonatorum↗
PubMed1987

Vasopressin responses to asphyxia and hemorrhage in newborn pigs.

Vasopressin may be important in maintenance of arterial pressure and redistribution of cardiac output in hypotensive and asphyxiated newborns. We used chronically instrumented, unanesthetized, 4-day-old pigs to investigate the effects of hypotensive hemorrhage and asphyxia on plasma vasopressin concentration and to determine the effects of cyclooxygenase inhibition on these responses. Asphyxia [arterial O2 partial pressure (PaO2) = 40-50 Torr, arterial CO2 partial pressure (PaCO2) = 60-80 Torr) increases plasma lysine vasopressin (LVP) from 2.2 +/- 0.8 to 52.4 +/- 15.0 microU/ml. Neither the baseline nor stimulated plasma LVP was affected by indomethacin (5 mg/kg) or meclofenamate (5 mg/kg). Hemorrhage (30 ml/kg) increased plasma LVP from 2.8 +/- 0.8 to 163.4 +/- 28.1 (20 min) and 135.1 +/- 18.5 microU/ml (60 min). The effects of vehicle and indomethacin (5 mg/kg) 20 min after hemorrhage on plasma LVP 60 min after hemorrhage were not different. Changes in plasma vasopressin caused by asphyxia and hemorrhage in the unanesthetized newborn pig are similar to the responses observed in adults of other species. This study does not suggest that prostanoids are involved in these responses in newborn pigs.

Animals↗
PubMed1988

Pulmonary effects of acute prenatal asphyxia in ventilated premature lambs.

The effect of profound repetitive prenatal asphyxial insults on the cardiopulmonary function of premature ventilated lambs was studied. Twenty-nine fetal lambs (approximately 138 days gestational age) were exteriorized. In 16 of these lambs, the umbilical cord was occluded for 4 min then released for 10 min. This asphyxial episode was repeated until the arterial pH was approximately 7.00, and the mean arterial blood pressure was less than 40 mmHg and falling. The 13 control lambs were simply exteriorized with the umbilical circulation intact. The lambs were then ventilated for 3-4 h. There were no differences between the control vs. asphyxiated lambs in pulmonary compliances (0.57 and 0.58 ml.cmH2O-1.kg-1) wet-to-dry weight ratios (8.18 and 7.55), cardiac outputs (177.8 and 141.8 ml.kg-1.min-1), surfactant-saturated phosphatidylcholine pool sizes, or atrial and/or ductal shunts. Asphyxia did not interfere with the redirection of blood away from atelectatic lung segments created by bronchial obstruction with balloon catheters. Also, although the bidirectional flux of protein into and out of the airways of these preterm lambs was large relative to term lambs, there was no effect of asphyxia on this protein leak. In this animal model, prenatal asphyxia did not impact negatively on the severity of the respiratory failure.

Animals↗
PubMed1982

Brain prostaglandins E2 and F2 alpha following neonatal asphyxia in the guinea pig.

In this study, the effects of (1) asphyxia and (2) asphyxiation followed by resuscitation on brain levels of prostaglandins E2 and F2 alpha were evaluated in 2-day-old guinea pigs. Asphyxiation in a nitrogen atmosphere for either 3 min or 3 min 40 s did not alter brain PGF2 alpha levels but after 3 min 40 s of asphyxia, brain PGE2 levels were significantly elevated from control values. When asphyxiation was followed by resuscitation with 95% O2 and 5% CO2, brain PGF2 alpha levels rose significantly while PGE2 levels were not different from nonasphyxiated control values. Pretreatment of animals with indomethacin lowered brain levels of both prostaglandins below nonasphyxiated control levels and prevented any asphyxiation or resuscitation-induced rise in brain prostaglandin levels. Also, animals which were asphyxiated, resuscitated, and sacrificed 1 day after asphyxiation had brain prostaglandin levels which were not different from levels in nonasphyxiated control animals. These studies demonstrate a significant rise in brain PGF2 alpha levels following resuscitation from acute total asphyxia. We speculate that the resuscitation-induced rise in brain PGF2 alpha may contribute to restriction of cerebral blood flow in the postasphyxial period through its action as a vasoconstrictive agent.

Animals↗
PubMed1988

Naloxone potentiates the plasma catecholamine response to asphyxia in the fetus.

The effect of endogenous opioid peptide blockade with naloxone on the plasma catecholamine response to asphyxia (hypoxemia + acidemia) was investigated in 6 chronically catheterized late gestation (greater than or equal to 120 days) fetal lambs in utero. Animals were assigned randomly to receive either naloxone (1 mg/kg) or saline on alternate days. Hypoxemia was produced by gradual umbilical cord compression until arterial PO2 less than 15 Torr and maintained for 15 min. This resulted in the development of acidemia as pH decreased from a baseline of 7.41 +/- 0.02 to 7.25 +/- 0.01. Fetal heart rate declined initially from 183 +/- 5 to 113 +/- 7 beats/min and then increased progressively to approach, but not return, to baseline, whereas mean arterial pressure continued to rise from 45 +/- 2 Torr throughout the 15-min observation period to a peak of 61 +/- 5 Torr. No difference was noted between control and naloxone-treated fetuses in their blood pH, PO2, PCO, heart rate or blood pressure responses to asphyxia. Plasma epinephrine concentrations increased 10-fold from 143 +/- 45 to 1391 +/- 290 pg/ml in control fetuses and from 254 +/- 58 to 6944 +/- 847 pg/ml, a 27-fold increase, in naloxone-treated fetuses (p less than 0.05). Norepinephrine levels were not significantly altered by opioid receptor blockade, increasing from 525 +/- 121 to 4138 +/- 912 pg/ml in controls and from 719 +/- 186 to 6,958 +/- 1,439 pg/ml in naloxone-treated animals. Thus, naloxone potentiates the plasma epinephrine response to asphyxia. Endogenous opioid peptides may act as modulators of the sympathoadrenal response to severe stress in the fetus.

Animals↗
PubMed1989

Thromboxane synthesis inhibitor in a beagle pup model of perinatal asphyxia.

During perinatal asphyxia, cerebral blood flow is markedly reduced in the gray and white matter of the telencephalon. Since previous work has implicated prostaglandins in the control of blood flow, we tested the hypothesis that a thromboxane synthesis inhibitor would improve cerebral blood flow and blunt the metabolic alterations that accompany asphyxia. Forty-three newborn beagles 2-7 days old were anesthetized, ventilated, and randomized to insult (5 minutes of asphyxia) or no insult and received treatment with either the thromboxane synthesis inhibitor CGS 13080 (CIBA-GEIGY Corp.) (0.06 mg/kg/hr i.v. infusion) or saline. Cerebral blood flow was measured in 25 pups. Pups received treatment 30 minutes before insult or no insult. In pups randomized to insult and receiving saline, cerebral blood flow increased during insult in the medulla but decreased elsewhere. Pups randomized to insult and treated with thromboxane synthesis inhibitor had increased cerebral blood flow during insult in all cerebral regions studied. In addition, these pups experienced a significantly higher incidence of intraventricular hemorrhage than did pups randomized to insult and receiving saline. In other experiments with 18 pups, brain extracts were prepared for proton nuclear magnetic resonance spectral analysis of high-energy phosphorylated compounds and lactate levels. In pups exposed to insult and receiving saline, mean +/- SD phosphocreatine concentration fell from 1.9 +/- 0.1 to 0.4 +/- 0.1 mmol/kg, lactate concentration increased from 2.0 +/- 0.5 to 3.3 +/- 0.4 mmol/kg, and the calculated pH fell 0.8 units. There were no differences between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1986

Plasma beta-endorphin in perinatal asphyxia and respiratory difficulties in newborn infants.

The effects of intrauterine stress and birth asphyxia on the plasma concentration of beta-endorphin (beta-E) in cord blood and in venous blood at the age of 2 h was investigated in newborn infants. Term infants with acute birth asphyxia (n = 11), infants born to mothers with preeclampsia (n = 15), and prematures with respiratory difficulties (n = 4) were entered into the study. Twenty control infants were studied; 12 were born after spontaneous delivery and eight after elective cesarean section. After normal spontaneous delivery, the plasma beta-E level decreased significantly, the median values being 17 pmol/liter at birth and 9.3 pmol/liter at the age of 2 h, whereas after elective cesarean section it remained unchanged (13 and 13 pmol/liter, respectively). In acute asphyxia the plasma beta-E level varied widely at birth, from 9.7 to 108 pmol/liter. At the age of 2 h, the beta-E level was high (26 to 83 pmol/liter) in those asphyctic infants who required prolonged mechanical ventilation, but it fell to the range of 1.6-13 pmol/liter when the infant recovered rapidly. The beta-E level was not increased in the preeclampsia group, not even in small for gestational age infants. In preterm newborn infants with respiratory difficulties, a significant postnatal rise of plasma beta-E level was found, the beta-E value varying from 7.3 to 16 pmol/liter at birth and from 61 to 168 pmol/liter at the age of 2 h. These results indicate that increased beta-E secretion is associated with respiratory difficulties in the newborn infant.

Apgar Score↗
PubMed1987

Indomethacin does not alter the circulating catecholamine response to asphyxia in the neonatal piglet.

The response of circulating catecholamines to asphyxia in unanesthetized, spontaneously breathing neonatal piglets was measured before and after treatment with indomethacin. Prior to treatment with indomethacin, baseline levels [geometric mean, pg/ml (95% confidence limits)] of D, E, and N were 162 (99-266), 174 (52-579), and 380 (286-506), respectively. Inhalation of 10% O2/9% CO2 for 20 min caused significant increases in arterial levels of all three catecholamines to 389 (230-659, 1514 (993-2306), and 3802 (2731-5293), respectively. Treatment with indomethacin (5 mg/kg, intravenous) did not significantly alter either baseline levels of the catecholamines or the levels after 20 min of the asphyxiating gas. In time control piglets, baseline levels and the response to asphyxia were similar before and after placebo. These results suggest that the circulating catecholamine response to asphyxia of the neonatal piglet is independent of the prostaglandin system.

Animals↗
PubMed1991

Plasma immunoreactive endothelin-1 concentration in human fetal blood: its relation to asphyxia.

To elucidate the effects of birth stress on immunoreactive endothelin-1 (irET-1) concentrations in fetal blood, we determined irET-1 levels in cord plasma in different modes of delivery associated with or without complications such as asphyxia. The irET-1 concentrations in both the umbilical artery and vein were significantly higher than those found in maternal venous blood at delivery, although there was no significant difference between preterm and full-term infants. When plasma irET-1 concentrations of healthy infants born by vaginal delivery and by cesarean section without labor were compared, the former had significantly (p less than 0.05) higher levels than the latter (15.4 +/- 4.9 pg/mL versus 11.1 +/- 3.1 pg/mL). Furthermore, umbilical venous plasma obtained from vaginally delivered infants complicated by asphyxia showed significantly (p less than 0.001) higher irET-1 levels (28.2 +/- 9.4 pg/mL) than those of nonasphyxiated infants (14.2 +/- 4.5 pg/m). These data suggest that birth stress, especially asphyxia, may contribute to the increase in fetal circulating irET-1 levels.

Asphyxia Neonatorum↗
PubMed2003

Predictive value of brain-specific proteins in serum for neurodevelopmental outcome after birth asphyxia.

Brain-specific proteins have been used to detect cerebral injury after birth asphyxia. Previous investigations suggest that serum protein S-100beta, brain-specific creatine kinase (CK-BB), and neuron-specific enolase (NSE) are capable of identifying patients with a risk of developing hypoxic-ischemic encephalopathy. Whether detection of elevated serum concentrations of these proteins reflects long-term neurodevelopmental impairment remains to be investigated. We examined serum protein S-100beta, NSE, and CK-BB at 2, 6, 12, and 24 h after birth in 29 asphyxiated infants and 20 control infants. Neurodevelopmental follow-up examinations were performed at 20 mo of age using the German revision of the Griffiths scales for developmental assessment. Elevated concentrations of serum protein S-100beta, NSE, and CK-BB within 24 h after asphyxia did not correlate with long-term neurodevelopmental delay. We conclude that serum protein S-100beta, NSE, and CK-BB, sampled on the first day of life, is of limited value in predicting severe brain damage after birth asphyxia.

Asphyxia Neonatorum↗
PubMed1975

Central nervous system findings in the newborn monkey following severe in utero partial asphyxia.

Seizures, brain swelling, and cortical necrosis have been observed in the newborn rhesus monkey following a 2 to 4-hour period of intrauterine partial asphyxia produced by halothane-induced maternal hypotension. These clinical and neuropathologic findings are similar to those seen in human newborn infants who have experienced an episode of intrauterine asphyxia from such a cause as premature placental separation. The present study strongly indicates that fetal partial asphyxia, from any cause, in the absence of fetal circulatory collapse or fetal head compression, may be the primary event that sets in motion a vicious cycle of brain swelling and impaired cerebral blood flow, leading finally to cerebral necrosis.

Animals↗
PubMed1991

Delayed-onset dystonia due to perinatal or early childhood asphyxia.

We report 10 patients with delayed-onset dystonia associated with perinatal asphyxia and 2 associated with asphyxia in childhood. In the perinatal group, the mean age of onset was 12.9 years. Among these patients, dystonia continued to progress for a mean of 7 years, and as long as 28 years. These patients had moderate motor disability; none was wheelchair-bound, and thus their prognosis was better than that of the childhood-onset idiopathic torsion dystonias. The most frequently beneficial drugs were anticholinergics. Since some of these patients closely resembled cases of idiopathic torsion dystonia, the prior occurrence of asphyxia should be used as a criterion of exclusion for that diagnosis.

Aging↗
PubMed2003

Effects of chronic intermittent asphyxia on rat diaphragm and limb muscle contractility.

OBJECTIVE: In obstructive sleep apnea (OSA), there is intermittent upper airway (UA) collapse due to an imbalance between the collapsing force generated by the diaphragm and the stabilizing force of the UA muscles. This results in chronic intermittent asphyxia (CIA). We have previously shown that CIA affects UA muscle fatigue, but little is known about the effects of chronic hypoxia on diaphragm or on limb muscle contractile properties and structure. DESIGN: Rats were exposed to asphyxia and normoxia twice per minute for 8 h/d for 5 weeks to simulate the intermittent asphyxia of OSA in humans. Isometric contractile properties were determined from strips of isolated diaphragm, extensor digitorum longus (EDL), and soleus muscles in Krebs solution at 30 degrees C. EDL and soleus type 1 (slow, fatigue resistant), type 2A (fast, fatigue resistant), and type 2B (fast, fatigable) fiber distribution was determined using adenosine triphosphatase staining. RESULTS: CIA caused a significant increase in diaphragm, EDL, and soleus fatigue, and reduced recovery from fatigue. Most of the other contractile properties were unaffected aside from a small reduction in diaphragm half-relaxation time and EDL twitch tension and a small shift to the left in the EDL force-frequency curve. There was no change in soleus fiber-type distribution and a small increase in EDL type 2A fibers (46.1 +/- 1.2% vs 49.9 +/- 1.4%, control vs CIA [mean +/- SD]). CONCLUSIONS: CIA increases diaphragm, EDL, and soleus muscle fatigue. We speculate that if this also occurs in OSA, it would contribute to the pathophysiology of the condition.

Animals↗
PubMed1988

Plasma free and sulfoconjugated catecholamines during acute asphyxia in the sheep fetus--relation to cardiovascular parameters.

Changes of free and sulfoconjugated catecholamines were measured radioenzymatically during a 5 minute period of acute asphyxia in chronically instrumented sheep fetuses (n = 5). Due to total reduction of uterine blood flow asphyxia as well as metabolic acidosis developed (pH = 6.94 +/- 0.02; Pco2 = 98 +/- 8 mmHG; lactate = 7.1 +/- 0.3 mmol/l). Peak concentrations of free catecholamines were reached after 3 minutes; free NE increased 60-fold, free E 370-fold and free DA 13-fold as compared to control values. Concomitantly, sulfoconjugated catecholamines rose markedly and were 40-fold (NE), 300-fold (E) and 10-fold (DA) higher when compared to the control period. Thus, the results reveal that the fetal sulfoconjugating system is very effective and able to match high concentrations of free catecholamines entering the circulation. After release of occlusion, free and sulfoconjugated catecholamines decreased with a half life time of 2.5 to 4.3 minutes during the initial 10 minutes. A close correlation could be demonstrated between free catecholamines and fetal arterial blood pressure, however, with interference of the effects of desoxygenation on the myocard. Moreover, fetal tachycardia is related to circulating catecholamines, especially E, during the postasphyxial period. Our results suggest, that in unstressed, normoxic fetuses the cardiovascular system is able to maintain basic functions (heart rate and blood pressure) during asphyxia for 5 minutes. In this context, a maximal sympathoadrenal stimulation with secretion of free catecholamines seems to be essential.

Acute Disease↗
PubMed2002

Adrenomedullin gene expression in human placental tIssue and leukocytes: a potential marker of severe tIssue hypoxia in neonates with birth asphyxia.

OBJECTIVE: The aim of the present study was to investigate the role of adrenomedullin (ADM) as a hypoxia-inducible marker of clinically relevant tIssue hypoxia in acute birth asphyxia of term newborn infants. METHODS: For this purpose, ADM mRNA was determined in human placental tIssue of 20 term pregnancies complicated by birth asphyxia (pH and base deficit values, clinical score). In addition, ADM mRNA was measured in leukocytes of the asphyxiated newborn infants during the first 12 h of life (n=12). Controls were available from ten healthy term pregnancies. In vitro, hypoxia-inducible expression of ADM mRNA was evaluated in human choriocarcinoma cells (BeWo) and human leukocytes exposed to hypoxia (1% O(2)) for 1-24 h. mRNA levels were measured by TaqMan real-time PCR. RESULTS: In vitro, ADM mRNA related to porphobilinogen deaminase (PBGD) mRNA levels significantly increased in response to hypoxia within a period of 4 h in leukocytes and 12 h in BeWo cells. In human placental tIssue, significantly higher levels of ADM/PBGD mRNA were present in asphyxiated newborn infants with severe hypoxic-ischemic encephalopathy (HIE) (n=5) compared with patients with mild or no HIE (n=15). Increased levels of ADM/PBGD mRNA levels were found during the first hours of life in leukocytes of neonates with severe HIE compared with controls. CONCLUSIONS: Our results indicate an upregulation of ADM gene expression in human placenta and leukocytes in clinically relevant hypoxic-ischemic birth complications and suggest ADM gene expression as a promising marker for severe complications due to perinatal asphyxia such as HIE.

Adrenomedullin↗
PubMed2006

Cerebral oxygenation and electrical activity after birth asphyxia: their relation to outcome.

OBJECTIVE: To determine the value of regional cerebral oxygen saturation (rSo2), fractional cerebral tissue oxygen extraction (FTOE) measured by near-infrared spectroscopy (NIRS), and amplitude integrated electroencephalogram (aEEG) after birth asphyxia in relation to neurodevelopmental outcome. METHODS: NIRS measured rSo2, FTOE, and aEEG were monitored simultaneously, together with arterial oxygen saturation (Sao2) and blood pressure during the first 48 hours after severe birth asphyxia in 18 term infants. FTOE was calculated as [Sao2-rSo2]/Sao2. Neurodevelopmental outcome was assessed at 3, 9, and 18 months and 3 and 5 years of age. At the time points 6, 12, 18, 24, 30, 36, 42, and 48 hours after birth, the mean values of Sao2, rSo2, FTOE, and mean arterial blood pressure were calculated over a 1-hour period. A stepwise-regression model was used to investigate the relative contribution of rSo2, FTOE, or aEEG to developmental outcome. RESULTS: Nine Infants died during the neonatal period as a result of neurologic deterioration, and 8 infants had a normal outcome at 5 years of age. One child developed learning disabilities and a mild diplegia. The rSo2 and FTOE remained stable in infants with a normal outcome. The rSo2 increased and the FTOE decreased after 24 hours in the infants with an adverse outcome. (rSo2: 65% vs 84% at 12 and 48 hours, respectively; FTOE: 0.32 vs 0.12 at 12 and 48 hours, respectively). aEEG showed the closest relationship with outcome, but also rSo2 showed a significant correlation 24 hours after birth. CONCLUSIONS: rSo2 and FTOE seem to reflect secondary energy failure. aEEG showed the closest relationship with outcome after severe birth asphyxia.

Asphyxia Neonatorum↗
PubMed2003

Asphyxia and diuretic-induced changes in the Ca2+ concentration of endolymph.

Using Ca2+ -selective microelectrodes based on the neutral carrier, ETH-1001 with polyvinyl chloride (PVC), we have measured changes in the free Ca2+ concentration of guinea pig cochlear endolymph ([Ca](e)) after transient asphyxia or intravenous administration of diuretics. Under the control conditions, the endocochlear potential (EP) was +80 mV, and the [Ca](e) was in the range 1.4 x 10(-7)-2.4 x 10(-6) M (n = 16). Transient asphyxia (1-1.5 min) produced an increase in the [Ca](e) with a fall in the EP, whereas the cessation of the asphyxia led to a quick recovery of both [Ca](e) and EP to their control levels. Intravenous administration of furosemide (60 mg/kg) or bumetanide (30 mg/kg) also caused an increase in the [Ca](e) with a fall in the EP, followed by a gradual recovery of both [Ca](e) and EP. From these results, we obtained a significant correlation between EP and p[Ca](e) (= -log[Ca](e)), and conclude that (1) the [Ca](e) is extremely low, around 10(-6) M or less, under normal conditions and (2) the [Ca](e) is directly correlated with EP under physiological conditions.

Animals↗