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PubMed2001

Early markers of brain damage in premature low-birth-weight neonates who suffered from perinatal asphyxia and/or infection.

We studied 57 low-birth-weight premature neonates, of whom 29 suffered from perinatal asphyxia and/or infection, while the remaining 28 did not and served as controls. We measured peripheral nucleated red blood cell (NRBC) absolute numbers as well as interleukin (IL)-1beta, IL-6 and tumour necrosis factor (TNF)-alpha cytokine serum levels at 24 h postnatally and on days 3 and 7 following birth. Fourteen of the asphyxiated/infected neonates and 12 controls had neurologic assessments at the corrected postnatal age of 18 months. We found NRBC absolute numbers and serum IL-1beta and IL-6 cytokine levels at 24 h postnatally to be significantly higher in neonates with perinatal asphyxia/infection than in the controls (p = 0.022, p = 0.036 and p = 0.037, respectively). TNF-alpha levels did not differ. Neurologic examination at the corrected postnatal age of 18 months showed 8 out of the 14 children who had been asphyxiated/infected as neonates to have abnormal findings, while 12 children who were used as controls during their neonatal period were normal. Abnormal neurologic findings correlated with high NRBC counts and IL-1beta and IL-6 levels at 24 h postnatally. In conclusion, increased NRBC counts and proinflammatory cytokine levels in asphyxiated/infected neonates represent early markers for subsequent neurologic impairment.

Asphyxia Neonatorum↗
PubMed1985

Association between indicators of perinatal asphyxia and adverse outcome in the term infant: a methodological review.

There are conflicting opinions about the significance of 5 perinatal findings felt to be indicators of asphyxia (meconium staining of the amniotic fluid, abnormal fetal heart rate patterns, acidotic fetal scalp blood gases, low Apgar scores, and acidotic cord blood gases). A review of the literature was undertaken to determine the strength of association of each of these findings with adverse outcomes. Although all studies contained methodological problems, these indicators were found to have strong associations with one or more adverse outcomes such as perinatal death, low Apgar scores or cerebral palsy. The strength of the association (relative risk) was found to vary inversely with the prevalence of the outcome.

Acidosis↗
PubMed1975

Blood pressure response to both carotid occlucion and asphyxia, as influenced by intracerebroventricular injection of norepinephrine or epinephrine.

The carotid occlusion response (COR) in dogs was inhibited by 50 and 58% after intracerebroventricular injection of norepinephrine and hydrochloric acid, both at the pH 2.9. After norepinephrine at pH 7, this inhibition was 22%. The COR inhibition was 24% with epinephrine solution of pH 2.4 whereas the same solution at pH 7 produced no inhibition. The injection of drugs solved in acid solution, lead to a decrease in the pH of the cerebrospinal fluid. The response to asphyxia was inhibited by 50% after injection of norepinephrine at pH 2.9, but not after epinephrine at pH 2.4 or hydrochloric acid. Bradycardia was caused by epinephrine in neutral or acid solution and a decrease of arterial blood pressure was seen after epinephrine or norepinephrine in neutral or acid solution.

Animals↗
PubMed1976

Acetylcholinesterase activity in the erythrocytes of newborn infants with hyperbilirubinemia and asphyxia.

The authors measured erythrocyte acetylcholinesterase (ACHE) activity in 51 physiologic newborn infants, 35 pregnant women and 101 infants with hyperbilirubinemia caused by hemolytic diseases in the ABO and Rh systems, or of other origin (6 children). In total, 374 examinations of erythrocyte ACHE were performed. The normal values of physiologic infants during the first hours of life were 0.162 +/- 0.03, at the age of 3 days 0.104 +/- 0.04. The values in pregnant women were 0.206 +/- 0.07. The ACHE activity was considerably decreased in newborn infants affected by erythroblastosis-ABO, and its mean value, in the case of exsanguinotransfusion indicated by the Polácek scheme, amounted to 0.060 +/- 0.051. It raised after exsanguinotransfusion and was equal to the value of red cells transfused. In newborn infants affected by erythroblastosis-Rh, the value decreased in the cases complicated with asphyxia. Low values of ACHE are sometimes found in certain cases of IRDS or of septicemia. The determination of erythrocyte ACHE activity enables assessing the state of red blood cells.

Acetylcholinesterase↗
PubMed1981

Metabolic responses to severe perinatal asphyxia in term newborn infants with particular reference to the changes in plasma free amino acids.

Blood glucose, blood lactate, plasma FFA, plasma alpha-amino nitrogen and 17 individual amino acids were determined on admission, and at 24 and 48 h after admission in severely asphyxiated term newborn infants. The blood glucose value was widely scatterred and the plasma FFA level was low on admission. The total free plasma amino acid content correlated closely with the severity of asphyxia-induced lactic acidosis. Among the 17 amino acids determined, 11 turned out to be significantly increased. The increase of plasma free amino acids might be toxic for the central nervous system, therefore parenteral feeding of asphyxiated neonates with amino acid mixtures can be dangerous.

Acidosis↗
PubMed1992

Some animal models for the study of perinatal asphyxia.

Much of our current understanding concerning the pathophysiology of perinatal brain disorders has evolved from animal studies over the past three decades. Fetal and neonatal nonhuman primate, pregnant sheep, lamb, puppy, piglet and immature rodents, all have been important animal models for perinatal brain research. Although no model can be considered 'perfect' in reflecting the variety and complexity of human brain pathology, the investigator must assess the merits and limitations of each model within the framework of the research questions being asked. A variety of experimental designs have been used over the years and variations of particular interest are the animal age, the method of producing brain insult and the procedures used for evaluating outcomes. Most models relating to the study of intracranial hemorrhage, cerebral blood flow and cerebral energy metabolism have generally been acute preparations. Some important long-term survival models have also been developed in recent years for the study of hypoxic-ischemic encephalopathy. The latter include the nonhuman primate, piglet, sheep and immature rat models. In this article, I have reviewed some important animal models used in perinatal brain research with emphasis on those relating to perinatal asphyxia and intracranial hemorrhage.

Animals↗
PubMedDate not supplied

Beagle pup model of perinatal asphyxia: nimodipine studies.

Calcium antagonists may be of significant benefit in the pharmacotherapy of cerebral ischemia, possibly by improving postischemic cerebral blood flow (CBF). This study evaluated the effects of the calcium antagonist nimodipine on CBF in a newborn beagle pup model of perinatal asphyxia lasting 5 minutes. Immediately after the asphyxial episode, nimodipine (2 micrograms/kg/min) or saline was infused for 10 minutes, following which [14C]iodoantipyrine determinations of CBF were performed. In noninsulted pups, nimodipine caused both significant decreases in CBF to cortical and deep gray structures as well as a decrease in mean arterial blood pressure (MABP) (p less than 0.05). In insulted pups, nimodipine similarly decreased MABP (p less than 0.001) and CBF to cortical and deep gray matter regions. Nimodipine appeared to have no effect on arterial blood gases and EEG tracings in either insulted or noninsulted pups. Although nimodipine may be shown to improve neurologic outcome in asphyxiated newborn infants, the limits of this study do not show the mechanism to be that of improving CBF.

Animals↗
PubMed1988

Regulation of cerebral blood flow after asphyxia in neonatal lambs.

In a postasphyxia neonatal lamb model, the responses of the cerebral circulation to hypoxic hypoxia and changes in systemic arterial blood pressure were examined. Ventilated newborn lambs (n = 14) were subjected to a gradual asphyxial insult, resuscitated, and returned to control ventilator settings. During the time 2-5 hours after asphyxia, the responses of cerebral blood flow (CBF), cerebral oxygen delivery (OD), cerebral oxygen consumption (CMRO2), and cerebral fractional oxygen extraction (E) to changes in either arterial oxygen content (CaO2) or mean arterial blood pressure (MAP) were assessed. These data were compared with measurements from nonasphyxiated lambs (n = 7). With hypoxia (n = 7), cerebral blood flow increased (CBF = 646/CaO2 + 44) compared with nonasphyxiated lambs (CBF = 1121/CaO2 + 11). In asphyxiated lambs, cerebral oxygen delivery decreased (OD = 0.41 CaO2 + 6.87), but cerebral oxygen consumption remained stable due to a proportional increase in cerebral fractional oxygen extraction (E = -0.014 CaO2 + 0.65). In nonasphyxiated lambs, cerebral oxygen delivery, consumption, and fractional extraction were unchanged with hypoxia. In response to alterations in blood pressure, both cerebral blood flow (CBF = 0.84 MAP + 6.62) and oxygen delivery (OD = 0.13 MAP + 0.77) were pressure-passive. With hypotension, cerebral fractional oxygen extraction increased (E = -0.003 MAP + 0.69) but not enough to prevent a decrease in cerebral oxygen consumption (CMRO2 = 0.042 MAP + 1.79). In nonasphyxiated lambs, cerebral blood flow, oxygen delivery, consumption, and fractional extraction did not vary with blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Use of lithium carbonate in the treatment of autoerotic asphyxia.

We report the successful use of lithium carbonate to promptly extinguish life-threatening behavior in a case of autoerotic asphyxia occurring in a 26-year-old male. In addition to his paraphilia, the patient met the DSM-III-R criteria for dysthymia, and had an avoidant personality disorder secondary to verbal, physical and sexual abuse inflicted during childhood and adolescence.

Adult↗
PubMed1987

Renal function in full-term newborns following neonatal asphyxia. A prospective study.

A prospective study of full-term infants with neonatal asphyxia was performed to evaluate possible alterations in renal function. Twenty-one newborns with an Apgar score less than or equal to 3 at 1 minute after birth and a control group of 20 normal infants were included. Oliguria of 12 hours or more (less than 1 ml/Kg/h) during the first 24 hours after birth was considered indication for a volume challenge test and use of diuretic. The study of renal function was effected between 24 and 48 hours after birth for asphyxiated and control infants (Period I), and was repeated between 48 and 72 hours (Period II) for the asphyxiated group only. Intrinsic acute renal failure was diagnosed in two patients, one of whom died. In 10 cases, prerenal oliguria responded promptly to volume expansion with improvement of biochemical indices in Period II. In nine cases, urine volume was not altered, and all functional parameters were comparable with those of control.

Acute Kidney Injury↗
PubMed2002

Head injury with traumatic and postural asphyxia: a case report.

An autopsy was performed on a 22-year-old tractor driver who was found on a cliff, 20 feet down from the highway, trapped between the wheel of a tractor trolley and some stones in an inverted position, after sustaining a head injury. Post mortem lividity was present above the knee joints except where the left arm was firmly adducted on the chest and where the cloth folds were compressing on the chest and abdomen all round. Sub-mucosal ecchymoses and petechial hemorrhages were present in the pharyngeal walls, and on both surfaces of the epiglottis and larynx above the vestibular folds. Such hemorrhages were first noticed along with other findings of traumatic and postural asphyxia.

Accidents, Occupational↗
PubMed2000

Possible mechanisms in infants for selective basal ganglia damage from asphyxia, kernicterus, or mitochondrial encephalopathies.

Magnetic resonance imaging and neuropathologic studies have demonstrated remarkably selective patterns of injury to subregions of the basal ganglia in children. Examples are kernicterus and certain mitochondrial encephalopathies, which cause selective injury to the globus pallidus, and near-total perinatal asphyxia, which causes lesions in the putamen and thalamus. To explain the differential vulnerability of nuclei within millimeters of each other, we hypothesize that their locations within the neurotransmitter-specific circuitry of the basal ganglia motor loop are important. In severe hypoxic-ischemic encephalopathy, excitatory glutamatergic pathways into the putamen and thalamus are overactive, but the globus pallidus might be protected because its activity is silenced by inhibitory neuronal activity. In contrast, the relatively high resting neuronal activity in the globus pallidus might make it more vulnerable to less intense, subacute oxidative stresses from mitochondrial toxins such as bilirubin or from genetic mitochondrial disorders. This hypothesis has implications for designing neuroprotective therapies and for treating associated chronic movement disorders.

Asphyxia Neonatorum↗
PubMed2006

Ictal nystagmus in a newborn baby after birth asphyxia.

Ictal nystagmus (IN) is an uncommon phenomenon characterized by rhythmic saccadic eye movements occurring during epileptic seizures. We report a newborn baby with severe birth asphyxia, undergoing long-term video EEG monitoring with electro-oculogram (EOG), who showed irregular IN when eye movements crossed the midline from left to right and vice versa, resulting in large amplitude of the nystagmoid movements. The nystagmus was followed 15 to 29 seconds later by ictal discharges in the occipital regions. MRI of the brain showed features suggestive of periventricular leukomalacia. This interesting combination of findings suggests a complex mechanism for IN of cortical or subcortical ictal rhythms, which results in (a) the generation of subcortical electrical discharges in the pons and midbrain, causing nystagmoid eye movements, and (b) subsequent occipital spiking. We conclude that this clinical manifestation supports the existence of functioning cortical-subcortical connections between the brainstem ocular motor centers and the occipital cortex at birth.

Asphyxia Neonatorum↗
PubMed2003

Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospital setting.

INTRODUCTION: There has been increased interest in the use of capnometry in recent years. During cardiopulmonary resuscitation (CPR), the partial pressure of end-tidal carbon dioxide (PetCO2) correlates with cardiac output and, consequently, it has a prognostic value in CPR. This study was undertaken to compare the initial PetCO2 and the PetCO2 after 1 min during CPR in asphyxial cardiac arrest versus primary cardiac arrest. METHODS: The prospective observational study included two groups of patients: cardiac arrest due to asphyxia with initial rhythm asystole or pulseless electrical activity, and cardiac arrest due to acute myocardial infarction or malignant arrhythmias with initial rhythm ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). The PetCO2 was measured for both groups immediately after intubation and then repeatedly every minute, both for patients with and without return of spontaneous circulation (ROSC). RESULTS: We analyzed 44 patients with asphyxial cardiac arrest and 141 patients with primary cardiac arrest. The first group showed no significant difference in the initial value of the PetCO2, even when we compared those with and without ROSC. There was a significant difference in the PetCO2 after 1 min of CPR between those patients with ROSC and those without ROSC. The mean value for all patients was significantly higher in the group with asphyxial arrest. In the group with VF/VT arrest there was a significant difference in the initial PetCO2 between patients without and with ROSC. In all patients with ROSC the initial PetCO2 was higher than 10 mmHg. CONCLUSIONS: The initial PetCO2 is significantly higher in asphyxial arrest than in VT/VF cardiac arrest. Regarding asphyxial arrest there is also no difference in values of initial PetCO2 between patients with and without ROSC. On the contrary, there is a significant difference in values of the initial PetCO2 in the VF/VT cardiac arrest between patients with and without ROSC. This difference could prove to be useful as one of the methods in prehospital diagnostic procedures and attendance of cardiac arrest. For this reason we should always include other clinical and laboratory tests.

Aged↗
PubMed1978

Effects of asphyxia on cardiac output and organ blood flow in the newborn piglet.

Experiments were performed on newborn piglets 6--96 hr of age. When the respiratory dead space was increased arterial pO2 decreased and pCO2 increased. During this time cardiac output was unchanged (Fig. 1), while heart rate, respiratory rate, and blood pressure increased (Figs. 2 and 3). After 90 min of asphyxia blood flow to the stomach and small and large intestines decreased. Changes in blood flow were associated with dilatation of segments of the small and large intestine with scattered areas of hemorrhage. Pathologic examination revealed scattered areas of mucosal necrosis (Fig. 6).

Animals↗
PubMed1980

Naloxone decreases the duration of primary apnea with neonatal asphyxia.

Naloxone, a specific opiate antagonist with no agonist properties, in doses of 0.4 and 4.0 mg/kg was found to markedly reduce the duration of primary apnea in asphyxiated newborn rabbits. There was no effect on the duration of the hyperpneic phase (time to primary apnea) or on survival time (time to last gasp). It is suggested that endogenous opiate-like peptides are released during asphyxia and are the major factor in the suppression of medullary inspiratory neuronal discharge during primary apnea.

Animals↗
PubMed1984

Thromboxane B2 production by fetal and neonatal platelets: effect of idiopathic respiratory distress syndrome and birth asphyxia.

To study the production of proaggregatory thromboxane A2 (TxA2) by fetal and neonatal platelets, blood specimens were collected from umbilical cords immediately after delivery at term (n = 22), from newborn infants during the first 10 days of life (n = 85), from infants between 1 and 3 months of age (n = 14), and from healthy adults (n = 18). The blood samples were allowed to clot spontaneously at +37 degrees C for 60 min, and the concentrations of thromboxane B2 (TxB2), a stable metabolite of TxA2, in the sera were measured by radioimmunoassay and expressed as nanograms of TxB2/10(6) platelets. Platelet TxB2 generation in term infants at the age of 1 day (1.344 +/- 0.253 ng/10(6) platelets, mean +/- SE, n = 9) was higher than that in cord blood (0.634 +/- 0.042 ng/10(6) platelets, n = 22), or in infants of 1-3 months of age (0.881 +/- 0.099 ng/10(6) platelets, n = 14), or in adults (0.869 +/- 0.062 ng/10(6) platelets, n = 18). Increase in TxB2 generation following birth was seen already at the age of 1 h (1.076 +/- 0.114 ng/10(6) platelets, n = 9). TxB2 synthesis in preterm infants (1.032 +/- 0.136 ng/10(6) platelets, n = 10) did not differ from that in term infants on the 1st day of life, and idiopathic respiratory distress syndrome had no effect on it (1.029 +/- 0.079 ng/10(6) platelets, n = 19). Severe birth asphyxia was accompanied by reduced TxB2 formation (0.564 +/- 0.201 ng/10(6) platelets, n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Effect of asphyxia on free thyroid hormone levels in full term newborns.

Alterations in the thyroid metabolism of hypoxic, fasted, and chronically ill adults and older children have been described. We evaluated the effects of asphyxia on thyroidal indices of term newborns and compared them to those of a control population. Blood was drawn from the cord and then serially at 5 min and 3, 24, and 48 h after delivery in all patients. Seven term healthy newborns (group 1)increased their free thyroxine (FT4) concentrations significantly after delivery from a mean +/- SD baseline of 0.94 +/- 0.13 ng/dl in cord blood to a mean +/- SD peak of 2.6 +/- 0.6 ng/dl 48 h after delivery (p less than 0.001 at 3, 24, and 48 h), while their free triiodothyronine (FT3) levels increased from a mean +/- SD baseline level of 2.3 +/- 0.5 pg/ml in cord blood to a mean +/- SD peak of 3.7 baseline level of 2.3 +/- 0.5 pg/ml 48 h after delivery (p less than 0.001 at 24 and 48 h). Seven term newborns with transient low Apgar scores at birth (group 2) and seven term neonates born to mothers with toxemia or hypertension (group 3) failed to increase their FT4 and FT3 concentrations above baseline during the first 48 h of life. FT4 and FT3 values at 3, 24, and 48 h were significantly higher in the control group than in groups 2 and 3. Cord blood thyroid-stimulating hormone, FT4, and FT3 levels were not statistically different in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗