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PubMed1988

Fetal and neonatal cortical adrenal function in birth asphyxia.

Eighteen newborn infants, gestational age between 36 and 42 weeks with birth asphyxia were compared with 23 normal newborn infants to determine serum cortisol and dehydroepiandrosterone sulfate levels in cord blood and in venous blood samples collected 12-18 hours after birth. Both groups were similar in gestational age, birthweight, proportion of small for gestational age and large for gestational age infants, proportion of infants delivered by cesarean section with and without labor, and proportion of mothers with pre-eclampsia. There was no antenatal exposure to corticosteroid. The asphyxiated newborn infants had a significantly higher mean cord serum level of cortisol, and a significantly lower mean cord serum level of dehydroepiandrosterone sulfate than the control group. Mean serum cortisol and dehydroepiandrosterone sulfate levels collected 12-18 hours after birth were similar between both groups. It is suggested that elevated cord serum level of cortisol is related to birth asphyxia stress stimulating the adrenal definitive zone, and the low cord serum level of dehydroepiandrosterone sulfate is secondary to a transient hypoxemic-ischemic insult to the adrenal fetal zone.

Adrenal Cortex↗

PubMedDate not supplied

Myocardial dysfunction and cerebral blood flow velocity following birth asphyxia.

Birth asphyxia often leads to left ventricular myocardial dysfunction. To assess the effect of myocardial dysfunction on cerebral perfusion, we evaluated cardiac output and cerebral blood flow velocity in the anterior cerebral and internal carotid arteries in 20 asphyxiated term newborn infants during the first 4 days of life using 2-dimensional/pulsed Doppler ultrasound. In 8 infants with myocardial dysfunction cardiac output was reduced on days 1 and 2 and within normal limits thereafter. In these infants changes in mean cerebral blood flow velocity and pulsatility index were passively related to changes in mean arterial pressure and cardiac output. In 12 infants without myocardial dysfunction a stable cerebral blood flow velocity pattern was found, which was unaffected by changes in mean arterial pressure. We conclude that infants presenting with a reduced cardiac output after deliveries associated with severe asphyxia may be at risk for additional ischemic or hemorrhagic cerebral damage because of lack of autoregulation.

Asphyxia Neonatorum↗

PubMed1994

Cerebral function monitoring: a method of predicting outcome in term neonates after severe perinatal asphyxia.

The cerebral function monitor (CFM), a simplified one-channel EEG monitor, was evaluated in predicting outcome after severe perinatal asphyxia in 38 term infants. Survivors were followed until 1.5-2.5 years of age. All those 17 infants who survived without major neurological handicap showed continuous activity on the CFM trace during the first and/or second day of life. Twenty of the 21 infants who either died or developed severe neurological damage had burst suppression or paroxysmal activity on the first or second day of life. Thus cerebral function monitoring can be a valuable tool in predicting prognosis for infants with severe perinatal asphyxia.

Asphyxia Neonatorum↗

PubMed1996

Use of brain lactate levels to predict outcome after perinatal asphyxia.

Perinatal asphyxia is an important cause of neurological disability, but early prediction of outcome can be difficult. We performed proton magnetic resonance spectroscopy (MRS) and global cerebral blood flow measurements by xenon-133 clearance in 16 infants with evidence of perinatal asphyxia. Cerebral blood flow was determined daily in the first 3 days after birth in seven cases. Proton MRS was performed in 11 infants within the first week (mean 3.7 days), the rest within the first month (mean 22.2 days), and all had a scan around 3 months of age. Four infants died neonatally, three showed neurological deficits and the rest seemed to be progressing normally at neurodevelopmental follow-up at 1 year of age. A significant correlation was found between initial brain lactate levels and severe outcome (p = 0.0003) just as between cerebral hyperperfusion (mean cerebral blood flow (CBF) 86 ml(100 g)-1 min-1), (p = 0.02) and outcome. The diagnostic and prognostic implications of early MRS and CBF are predictive of poor outcome in severely asphyxiated infants.

Asphyxia Neonatorum↗

PubMed1997

Cholestasis in newborn infants with perinatal asphyxia.

OBJECTIVE: The aim of this study was to characterize the liver involvement in infants who have both neonatal asphyxia and neonatal cholestasis. METHODS: We describe four asphyctic newborn infants (three born at term) who developed early (age 3.8 +/- 2.1 days) intrahepatic neonatal cholestasis and in whom tests for causes of neonatal liver damage were negative. RESULTS: The clinical picture and course were benign and similar to that of sporadic "idiopathic" neonatal hepatitis. Clinical signs and abnormal liver function tests tended to normalize within the first year of life in all. Conjugated bilirubin became normal at 6 months after the onset of cholestasis, while liver enzymes tended towards normal values thereafter, within 1 year of follow-up. Liver biopsy (taken in one patient) showed a typical picture of giant cell hepatitis; ultrastructure was nonspecific. SIGNIFICANCE: Our results suggest that isolated asphyxia should be taken into account as a potential causal factor in term or pre-term asphyctic newborns who develop early "idiopathic" neonatal cholestasis.

Asphyxia Neonatorum↗

PubMed2005

Inflammatory chemokine expression in the peripheral blood of neonates with perinatal asphyxia and perinatal or nosocomial infections.

AIM: The inflammatory response induced by perinatal infections and asphyxia is considered to participate in neonatal brain damage. Inflammatory responses are characterized by the expression of chemokines. Although chemokine levels have been investigated in healthy newborns, their role during neonatal pathological conditions has not been studied. The aim of our study was to examine chemokine serum levels in asphyxiated and infected neonates. METHODS: Peripheral blood samples were obtained from perinatally asphyxiated and infected neonates during the first days of life and from neonates who developed nosocomial infections. Serum levels of interleukin-8 (IL-8), interferon-gamma-inducible protein-10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1alpha (MIP-1alpha), and regulated upon activation, normal T cells expressed and secreted (RANTES) were determined. RESULTS: In perinatally asphyxiated neonates, IL-8 levels were significantly elevated on the 1st day of life. In perinatally infected neonates, IL-8 and IP-10 levels were significantly increased on the 1st day of life, while RANTES levels were significantly lower and remained so until the 4th day. In nosocomially infected neonates, IL-8, IP-10 and MIP-1alpha levels were significantly increased on diagnosis of infection. CONCLUSION: The neonatal immune system is able to produce chemokines for the induction of an inflammatory response during perinatal asphyxia and perinatal or nosocomial infections. Blockade of inflammatory chemokines could possibly contribute to the prevention of brain damage.

Asphyxia Neonatorum↗

PubMed1990

Release of endothelin-like immunoreactivity in relation to neuropeptide Y and catecholamines during endotoxin shock and asphyxia in the pig.

The changes in endothelin-like immunoreactivity in plasma during various provocations in the pig were investigated and related to those of neuropeptide Y, noradrenaline and adrenaline. Release as revealed by overflow was determined in the spleen, kidney and femoral vascular bed (skeletal muscle) simultaneously by collecting local venous and arterial blood samples. Under basal conditions there was no net release of endothelin-like immunoreactivity from any region but a net removal (negative overflow) over the kidney. Endotoxin administration (20 micrograms kg-1 h-1 for 4 h) increased arterial endothelin-like immunoreactivity, neuropeptide Y-like immunoreactivity, noradrenaline and adrenaline seven-, 27-, 100- and 166-fold respectively, as well as splenic and renal vascular resistance. An increased overflow of endothelin-like immunoreactivity, neuropeptide Y-like immunoreactivity and noradrenaline, indicating local release, was observed in the spleen during endotoxin administration. The arterial plasma endothelin-like immunoreactivity during endotoxaemia correlated significantly with the splenic and renal vasoconstriction (r = 0.75 and 0.68 respectively). Chromatographic characterization revealed that the main portions of arterial plasma endothelin-like immunoreactivity collected during endotoxaemia corresponded to synthetic endothelin-1 and big endothelin. A similar uptake (50-90%) and plasma half-life (1-2 min) of exogenous endothelin-1-like immunoreactivity was observed both under control conditions and after endotoxin, suggesting that elevated plasma endothelin-like immunoreactivity after endotoxin was the result not of reduced clearance but rather of enhanced release. Asphyxia for 2 min did not increase arterial endothelin-like immunoreactivity but evoked an increased overflow of endothelin-like immunoreactivity, neuropeptide Y-like immunoreactivity and noradrenaline as well as vasoconstriction in the spleen. Capsaicin induced a release of neuropeptide Y-like immunoreactivity and noradrenaline from both the spleen and the kidney and of adrenaline from the adrenal, but no detectable overflow of endothelin-like immunoreactivity from any of the vascular regions. Renal nerve stimulation, renal artery occlusion for 30 min, haemorrhagic shock, hypotension induced by nitroprusside infusion or serotonin did not cause any detectable increase in arterial plasma levels or local overflow of endothelin-like immunoreactivity. It is concluded that plasma levels of endothelin-like immunoreactivity are increased, suggesting release in the pig in response to endotoxin administration and asphyxia. The possible involvement of endothelin as a mediator of the peripheral vasoconstrictor responses during these situations remains to be further established.

Animals↗

PubMed1968

Vasomotor responses in the hind limbs of foetal and new-born lambs to asphyxia and aortic chemoreceptor stimulation.

1. Hind limb blood flow was measured in lambs of from 91 days gestation (delivered by Caesarean section) to 1 month after birth (term is about 147 days), under chloralose anaesthesia. Vascular resistance/100 g wet wt. increased progressively with age. There was reflex femoral vascular tone from the earliest age studied, as shown by vasodilatation on cutting the sciatic nerve.2. On asphyxia by cord occlusion reflex femoral vasoconstriction began earlier and was somewhat greater in older foetal lambs. At all ages, and after denervation of the hind limb, there was vasodilatation after local ischaemia, and a vasoconstriction of delayed onset during asphyxia attributed to release of noradrenaline into the circulation. The vasoconstrictor effect of noradrenaline in immature lambs was at least as great as at term or in the new-born.3. Injections of minimal effective doses of cyanide were used to localize possible chemoreceptor sites in foetal lambs. Injection into the left atrium caused a rise of arterial pressure, femoral vasoconstriction and a complex change in heart rate (usually bradycardia) but rarely any respiratory movement. After atropine, cyanide caused a large tachycardia. All responses were much reduced or abolished by cervical vagotomy.4. Injection of the same doses of cyanide into a jugular vein, the right ventricle, pulmonary or common carotid arteries of foetal lambs caused negligible cardiovascular or respiratory effects, whereas injection into the carotids of new-born lambs caused a profound hyperpnoea.5. It is concluded that the aortic chemoreceptors are active in the foetus, are supplied from the left heart, and that they probably represent the primary defence in blood gas homeostasis by their effects on the circulation.

Acetylcholine↗

PubMed1969

The oxygen uptake and pulmonary blood flow during resuscitation from asphyxia in foetal and adult sheep.

1. The foetuses of twenty-seven Welsh ewes and eight Clun Forest ewes were delivered by Caesarian section at an approximate gestational age of 140 days, maintaining the umbilical circulation. They were asphyxiated by clamping the umbilical cord, and resuscitated with IPPV. Oxygen consumption, heart rate, and blood pressures were recorded, and in one series of eight, blood flow through the left lung was recorded whilst IPPV was applied to this lung only.2. The hypothesis that oxygen consumption is abnormally low during resuscitation of the new-born from extreme asphyxia because of limited blood flow, was supported.3. Adult ewes were also asphyxiated and in a series of eight a quite different pattern of behaviour was observed, due to very rapid and complete recovery of the circulation.4. Observations on the pulmonary vascular resistance suggest that complete vasomotor paralysis occurs during extreme asphyxia, so that resistance falls to a near-minimum level for unexpanded lung. Expansion of the lung produced a large fall in resistance which appeared to be due to the introduction of gas into the alveolar spaces, lessening the resistance to flow of the capillaries.

Animals↗

PubMed2006

Therapeutic hypothermia following perinatal asphyxia.

Well constructed and carefully analysed trials of hypothermic neural rescue therapy for infants with neonatal encephalopathy have recently been reported. The data suggest that either selective head cooling or total body cooling reduces the combined chance of death or disability after birth asphyxia. However, as there are still unanswered questions about these treatments, many may still feel that further data are needed before health care policy can be changed to make cooling the standard of care for all babies with suspected birth asphyxia.

Asphyxia Neonatorum↗

PubMed1982

Brain-orientated intensive care treatment in severe neonatal asphyxia. Effects of phenobarbitone protection.

The effect of applying brain-orientated neonatal intensive care for term infants with severe neonatal asphyxia was studied. Such treatment included protective phenobarbitone administration together with assisted ventilation and other measures to counteract postasphyxial cerebral oedema and any abrupt changes in blood pressure and oxygenation. The mortality rate and incidence of long-term sequelae were reduced appreciably, resulting in a 0-1 year mortality rate of 14% (previously 50%) and an incidence of neurodevelopmental handicap at 18 months of 17% (previously 50%). It is important in the management of infants with severe asphyxia at birth to avoid blood pressure fluctuations and to control neuronal epileptic activity by the use of barbiturates and early ventilator treatment.

Asphyxia Neonatorum↗

PubMed1983

Multiple causes of asphyxia in infants at high risk for sudden infant death.

A wide range of clinical findings was present in 58 near-miss sudden infant death syndrome (SIDS) infants and 6 surviving twins of SIDS siblings. Specific investigations included: studies of gastro-oesophageal reflux and aspiration (24-hour oesophageal pH recordings, barium swallow, radionuclide 'milk-scan'); polygraphic studies of breathing, reflux, and sleep state; studies of upper airways disease (lateral airways radiography and endoscopy); detection of seizure activity by electroencephalography; evaluation of thiamine status by erythrocyte transketolase activity of venous blood. Thiamine deficiency was found in 12 of 43 tested infants; 5 of the deficient infants had a familial history of SIDS. Many potential mechanisms for asphyxia were found: idiopathic central apnoea (7 infants), tracheal obstruction from minimal tracheomalacia or aberrant innominate artery (4 infants), temporal lobe or generalised seizures (6 infants), gastro-oesophageal reflux (55 infants) with intrapulmonary aspiration (11 infants). The high incidence, severity, and timing of reflux were new findings. Reflux occurred in active and indeterminate sleep, but not in quiet sleep. The depression of respiratory reflexes by active sleep stresses the vulnerability to asphyxia. Two factors suggest that near-miss episodes are related to SIDS: the similar age distribution but earlier occurrence of near-miss episodes compared with age at death of SIDS infants, and the subsequent sudden death of 2 infants whose necropsies were consistent with SIDS.

Age Factors↗

PubMed1985

Effects of perinatal asphyxia and myoglobinuria on development of acute, neonatal renal failure.

Thirty four consecutive neonates with birth asphyxia or respiratory problems were examined in the first week of life to clarify the relation between neonatal myoglobinuria and acute renal failure. Investigations included determination of creatinine clearance, fractional sodium excretion, and N-acetyl-beta-D glucosaminidase index as an indicator of tubular injury. The infants' gestational ages ranged from 29 to 41 weeks (mean 36 weeks). Fifteen infants did not have myoglobinuria on the first day of life (group A); myoglobinuria was mild in eight infants (group B) and severe in eleven (group C). Two infants in group B and seven in group C developed acute renal failure (47%). Ten infants in group C (91%) had severe asphyxia, five of whom (45%) also suffered neonatal seizures and intracranial haemorrhage. We suggest that myoglobin derived from muscle breakdown in asphyxiated infants may lead to acute renal failure secondary to a reduction in renal blood flow, or to tubular damage.

Acute Kidney Injury↗

PubMed1991

Global and depth resolved phosphorus magnetic resonance spectroscopy to predict outcome after birth asphyxia.

Twelve normal and 32 asphyxiated neonates were studied using global and depth resolved phosphorus magnetic resonance spectroscopy (31PMRS). Eight of the asphyxiated group died or survived with major neurodevelopmental abnormalities. A global phosphocreatinine/inorganic phosphate (PCr/Pi) ratio below the range of values from normal infants predicted adverse outcome after asphyxia with a positive predictive value of 64%, sensitivity 88%, and specificity 83%. Corresponding values for global inorganic orthophosphate/adenosine triphosphate (Pi/ATP) ratios were positive predictive value 88%, sensitivity 96%, and specificity 88%. Spatially localised MRS data, obtained using phase modulated rotating frame imaging, showed cerebral energy metabolism to be more abnormal in deep than superficial regions after birth asphyxia. However, in this population of full term infants none of the regional metabolite concentrations were superior to global data for prediction of outcome.

Adenosine Triphosphate↗

PubMed1994

Potentially dangerous sleeping environments and accidental asphyxia in infancy and early childhood.

Infants and young children may be exposed to a variety of dangerous situations when left sleeping in cots, chairs, or beds. A review of 30 cases of accidental asphyxia occurring in infants and young children who had been left to sleep unattended was undertaken from the necropsy and consultation files of the Adelaide Children's Hospital. Causes of death included hanging from loose restrainers, clothing, or a curtain cord (12 cases), positional asphyxia/wedging from slipping between a mattress and bed/cot sides or wall, or from moving into a position where the face was covered and the upper airway occluded (16 cases), and suffocation from plastic bed covers (two cases). Cases of co-sleeping in bed with an adult and of non-accidental asphyxia were not included in this review. As the pathological findings were on occasion identical to those that are typically found in sudden infant death syndrome, adequate death scene examination was vital in several cases to allow identification of lethal sleeping environments and to enable steps to be taken to minimise the risk of future deaths due to similar situations. For example, two cases in which infants asphyxiated in rocking cradles led to the investigation of the cradles and to formulation of specific safety recommendations regarding the angle of tilt. Two infants who died after becoming wedged between the back of a couch and a co-sleeping parent in one case and cushions in the other, would indicate that this also represents a potentially lethal sleeping position. Other dangerous situations involved infant car seat restraints, seats with loose harnesses, cots with movable sides or projecting pieces, thin plastic mattress/pillow coverings, and beds with spaces between the mattress and cot side or wall. Lack of supervision at the time of death was a feature of each case.

Accidents, Home↗

PubMed1997

Traumatic asphyxia in children.

Two cases of traumatic asphyxia in young children are reported. The first was a 2 year old child run over at low speed by the front wheels of a delivery van. He made an uncomplicated recovery. The second child was pinned to the floor by an empty chest of drawers in an unwitnessed accident. He was discovered in cardiac arrest and resuscitation was unsuccessful. The outcome following traumatic asphyxia is a product of duration of compression and the weight involved. Considerable weight can be tolerated for a short period, whereas a comparatively modest weight applied for a longer period may result in death.

Accidents, Home↗

PubMed2002

Prediction of adverse outcome with cerebral lactate level and apparent diffusion coefficient in infants with perinatal asphyxia.

PURPOSE: To compare the predictive value for adverse outcome of quantitative cerebral lactate level and of apparent diffusion coefficient (ADC) in infants with perinatal asphyxia in the early postnatal period. MATERIALS AND METHODS: Lactate-choline ratios determined with proton magnetic resonance (MR) spectroscopy and ADC determined with diffusion MR imaging in basal ganglia and thalami in 26 full-term neonates (age range, 1-10 days) were compared with severity of acute hypoxic-ischemic encephalopathy and long-term clinical outcome. Differences in metabolites between outcome groups were evaluated with the nonparametric Kruskal-Wallis test and the Dunn test. Logistic regression was performed to examine the predictive value of each metabolite for differentiating normal from abnormal or fatal clinical outcome. The likelihood ratio test was used to assess the statistical significance of each metabolite. RESULTS: Logistic regression confirmed that lactate-choline ratio could be used to differentiate normal (n = 5) from abnormal (n = 14) or fatal (n = 6) outcome (P <.001). The probability of an adverse outcome exceeded 95% for a lactate-choline ratio of 1.0. Even when analyses were restricted to the early postnatal period, lactate-choline ratio was still a significant predictor of adverse outcome (P =.001). Although ADC images were useful in clinical examination of these infants, quantitative ADCs were not predictive of outcome (P =.82). CONCLUSION: Higher lactate-choline ratios in basal ganglia and thalami of infants with perinatal asphyxia were predictive of worse clinical outcomes. Absolute ADC in the same brain regions did not indicate a statistically significant relationship with clinical outcome. Cerebral lactate level is useful in identifying infants who would benefit from early therapeutic intervention.

Asphyxia Neonatorum↗

PubMed1976

Vascular response to short-term systemic hypoxia, hypercapnia, and asphyxia in the cat.

Acute systemic hypoxia, hypercapnia, or asphyxia was produced in ketamine-anesthetized, paralyzed cats by ventilating them for 2-4 min with appropriate gas mixtures. A sustained rise in arterial pressure occurred in all cases. Vascular responses to hypoxia (7% O2, 10% 02, or 14% O2) included muscle constriction, cutaneous (hindpaw) dilatation (no change with 14% O2), renal constriction (unchanged flow), and unchanged intestinal resistance. Asphyxia (hypoxia + 10% CO2) produced a similar pattern, except that intestinal dilatation occurred. Hypercapnia (10% CO2 + 21% O2) produced muscle constriction, renal constriction (unchanged flow), intestinal dilatation, and no change in cutaneous resistance. Intestinal dilatation seemed in all cases a response to elevated CO2 only. Hypercapnia augmented the effects of hypoxia in skin and skeletal muscle. The variation of responses in different vascular beds suggests a patterning of sympathetic discharge, and varying responsivity to local and humoral factors.

Animals↗