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PubMed1979

Auditory evoked potentials and auditory behavior following prenatal and perinatal asphyxia in rhesus monkeys.

Two types of asphyxia were studied in monkeys, total asphyxia during mid-pregnancy (94--98 days gestation) and combined partial and total axphyxia at term (165 days gestation). Auditory evoked potentials and the acquisition of 2 auditory discrimination tasks were studied in asphyxiated animals as well as in group of controls. The brains of all asphyxiates were examined histologically. No auditory discrimination deficit was found in the asphyxiated animals; however, the auditory evoked potentials differentiated between control and asphyxiated animals, especially those with verified inferior colliculus damage.

Animals↗
PubMed1984

Central monoamines and the death process time (antemortem time) during asphyxia. An experimental study in the mouse brain.

The changes of the brain monoamines, norepinephrine (NE), dopamine (DA), and serotonin (5-HT), during acute asphyxia, caused by strangulation, anoxia, and drowning, were studied in the mouse. In several asphyxiated animal groups significant linear correlation was found between the level of monoamines, NE, DA, and 5-HT, and the death process times or antemortem times were r = 0.50, 0.98 (P less than 0.05), and 0.57, respectively. It is concluded that the level of brain NE and DA increased in the mouse that died of asphyxia, and the level of 5-HT showed only an apparent decrease in anoxia groups as compared with the control group and showed a twice as high increase in drowning groups. Especially, there was a tendency that the longer the death process times or antemortem times, the higher was the level of DA.

Animals↗
PubMed1988

[Incidence and forensic value of liver cell hydrops in external asphyxia and sudden infant death].

A histological examination was carried out in 108 cases of asphyxia, 28 cases of SIDS, and 33 cases with other causes of death to assess the occurrence of liver-cell hydrops. In almost all cases of violent suffocation of newborns and children up to 10 years of age hydrops of the hepatocytes were found, whereas these results could be verified only exceptionally after violent suffocation of adults. Eighteen cases or 64.3% of SIDS showed a diffuse distribution of liver-cell hydrops over each liver lobule. Liver-cell hydrops seems to represent a frequent morphological equivalent of acute oxygen deficiency in asphyxia in childhood and is a common finding in SIDS.

Adult↗
PubMed1986

Dendritic development of cortical neurons of mice subjected to total asphyxia: a Golgi-Cox study.

The effect of total asphyxia on dendritic development of the pyramidal cells in the mouse cerebrum was investigated using the Golgi-Cox method. Although neonatal asphyxia did not alter the number of basal dendrites arising from the cell bodies, the dendrites in the 20-day-old treated animals were significantly shorter than those in the controls. Even at 60 days, the number of longer dendrites in the treated mice was significantly less than that in the controls.

Animals↗
PubMed2000

Cardiac abnormalities in birth asphyxia.

Cardiac abnormalities in birth asphyxia were first recognised in the 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the newborn (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and, therefore, requires treatment in the form of inotropic and ventilatory support (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses, especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required (v) persistent pulmonary hypertension of the newborn (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory tension and right ventricular failure with systolic murmur of tricuspid, and at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.

Asphyxia Neonatorum↗
PubMedDate not supplied

Newer concepts and approaches to neonatal brain asphyxia.

The asphyxial injury to neonate brain seems to be mediated through a cascade of biochemical events during ischaemia--reperfusion which includes excitatory amino acids, free radicals and accelerated programmed cell death (Apoptosis). The diagnosis of asphyxia requires rigorous approach based on background clinical information, certain diagnostic tests and exclusion of alternative diagnosis which may have similar clinical presentation. The treatment currently employed for the management of birth asphyxia controversial and requires critical appraisal. The future strategies for management include a number of approaches based on putative mechanism for asphyxial brain injury but they are still being evaluated as research and should not be used for clinical purposes in human newborns as yet.

Apoptosis↗
PubMed2002

Long-term sequelae of perinatal asphyxia in the aging rat.

Information on the consequences of perinatal asphyxia (PA) on brain morphology and function in the aging rat is missing although several groups have hypothesized that PA may be responsible for neurological and psychiatric deficits in the adult. We therefore decided to study the effects of PA on the central nervous system (CNS) in terms of morphology, immunohistochemistry, neurology and behavior in the aging animal. Hippocampus and cerebellum were evaluated morphologically by histological, immunohistochemical and magnetic resonance imaging and cerebellum also by stereological tests. Neurological function was tested by an observational test battery and rota rod test. Cognitive functions were examined by multiple-T-maze and the Morris water maze (MWM). Increased serotonin transporter (SERT) immunoreactivity in the CA2 region of the hippocampus and a significant difference in the escape latency, when the platform of the MWM was moved to a new location, were observed in asphyxiated rats. We showed that deteriorated cognitive functions accompanied by aberrant expression of hippocampal SERT and impaired relearning are long-term sequelae of perinatal asphyxia, a finding that may form the basis for understanding CNS pathology in the aging subject, animal or human.

Aging↗
PubMed2000

Perirolandic hypoperfusion on single-photon emission computed tomography in term infants with perinatal asphyxia: comparison with MRI and clinical findings.

We describe the findings on single-photon emission computed tomography (SPECT) in patients with perinatal asphyxia at term, with perirolandic cortico-subcortical changes on MRI, and to correlate them with clinical features. SPECT of 7 patients was obtained after injection of 185-370 MBq of Tc-99m-ECD (ethyl cysteinate dimer). The patients had spastic quadriplegia (7/7) with perinatal asphyxia (6/7) at term (7/7). The results were correlated with the MRI findings. Hypoperfusion of the perirolandic cortex was clearly seen on SPECT in all patients, even in two with subtle changes on MRI. SPECT demonstrated a more extensive area of involvement than MRI, notably in the cerebellum (in 4), the thalamus (in 7) and basal ganglia (in 5), where MRI failed to show any abnormalities.

Asphyxia Neonatorum↗
PubMed2005

Prophylactic theophylline to prevent renal dysfunction in newborns exposed to perinatal asphyxia--a study in a developing country.

Renal damage frequently complicates perinatal asphyxia. Renal vasoconstriction due to adenosine metabolite leads to a fall in glomerular filtration rate (GFR) and filtration fraction. This might be inhibited by the nonspecific adenosine receptor antagonist, theophylline. This study was designed to determine whether theophylline could prevent and/or ameliorate renal dysfunction in term neonates with perinatal asphyxia. We randomized 40 severely asphyxiated term infants to receive intravenously a single dose of either theophylline (5 mg/kg; study group: n=20) or placebo (control group: n=20) during the first hour of life. Fluid intake, urine output, serum creatinine, creatinine clearance, GFR, urinary beta2 microglobulin (beta2 M) and sodium excretion were recorded during the first 5 days of life. The two groups were comparable. No significant difference was reported regarding mechanical ventilatory support, respiratory complications and seizures. Severe renal dysfunction was significantly higher in the control group. Serum creatinine values were less, and creatinine clearance and GFR were significantly higher in the theophylline group from the second day onwards. beta2 M excretion was significantly less in the theophylline group, while sodium excretion and hematuria showed no significant difference. Prophylactic theophylline treatment, given early after birth, has beneficial effects in reducing the renal involvement in asphyxiated full-term infants, with no significant changes in central nervous system involvement.

Asphyxia Neonatorum↗
PubMed2001

Perinatal asphyxia: timing and mechanisms of injury in neonatal encephalopathy.

This article summarizes the recent medical literature regarding perinatal asphyxia with respect to timing and mechanisms of injury for neonates who were clinically diagnosed with an encephalopathy in the newborn period. Multiple mechanisms of injury are reviewed, including genetic vulnerability, acquired inflammatory responses, and clotting defects that can lead to ischemic-induced brain damage. Before effective treatments for fetal and neonatal brain disorders can be developed, accurate and timely diagnoses of fetal or neonatal brain injury must be achieved. Specific subsets of children can then benefit from neuroprotective strategies that can target the specific developmental aspects of brain adaptation or plasticity relative to the specific etiology and timing of injury after asphyxia.

Apoptosis↗
PubMed1988

Motor and cognitive deficits after intrapartum asphyxia in the mature fetus.

The incidence of major and minor motor and/or cognitive deficits at 1 year of age, in 37 mature children who had experienced an intrapartum fetal asphyxial insult, was compared with the incidence of deficits at 1 year in 76 children of the control group. The incidence of both major and minor deficits was significantly greater in the group with intrapartum fetal asphyxia in relation to the control group. These findings support the concept that, beyond a critical threshold of fetal asphyxia, a continuum of casualty in the surviving newborn infants exists.

Asphyxia Neonatorum↗
PubMed1995

Nucleated red blood cells: a marker for fetal asphyxia?

OBJECTIVE: Our purpose was to determine whether a relationship exists between the presence of nucleated red blood cells, hypoxic ischemic encephalopathy, and long-term neonatal neurologic impairment. STUDY DESIGN: Nucleated red blood cell data from 46 singleton term neurologically impaired neonates were compared with cord blood nucleated red blood cells of 83 term nonasphyxiated newborns. The neurologically impaired neonates group was also separated as follows: nonreactive, nonreactive fetal heart rate from admission to delivery; tachycardia, reactive fetal heart rate on admission followed by tachycardia with decelerations; rupture, uterine rupture. The first and highest nucleated red blood cells value and the time to nucleated red blood cells disappearance were assessed. RESULTS: The neurologically impaired neonates group exhibited a significantly higher number of nucleated red blood cells per 100 white blood cells (34.5 +/- 68) than did the control group (3.4 +/- 3.0) (p < 0.00001). When the neurologically impaired neonates are separated as to the basis for the neurologic impairment, distinct nucleated red blood cell patterns were observed. Overall, the nonreactive group exhibited the highest mean nucleated red blood cell (51.4 +/- 87.5) count and the longest clearance times (236 +/- 166 hours). CONCLUSION: In this limited population, nucleated red blood cell data appear to aid in identifying the presence of fetal asphyxia. When asphyxia was present, distinct nucleated red blood cells patterns were identified that were in keeping with the observed basis for the fetal injury. In general, the closer the birth was to the asphyxial event, the lower was the number of nucleated red blood cells. Thus our data suggest that cord blood nucleated red blood cells could assist in the timing of fetal neurologic injury.

Asphyxia Neonatorum↗
PubMed1989

Why is the lower torso protected in traumatic asphyxia? A new hypothesis.

Traumatic asphyxia secondary to a crush injury of the chest is characterized by craniocervical cyanosis, subconjunctival hemorrhage, and severe vascular engorgement of the head and neck. These signs are believed to be due to high venous pressures causing stasis and capillary rupture. A "fear response" that produces a strong Valsalva maneuver is thought to be necessary for their development. The lower torso seems to be protected, and previously this was thought to be due to its superior system of valves. We present here ultrasonographic evidence that the inferior vena cava is compressed or obliterated during a Valsalva maneuver, and propose that this compression protects the lower torso during traumatic asphyxia.

Abdomen↗
PubMed1991

Traumatic asphyxia.

During a 5-year period, we treated 14 cases of traumatic asphyxia. There were 12 male and 2 female patients ranging in age from 2 to 32 years. Most suffered crushing injuries at work or were run over by motor vehicles. Mild to severe cervicofacial cyanosis and petechiae developed in all patients. A fear response was reported by 12 of the patients. Subconjunctival hemorrhage was also found in 12 patients. Nine patients had tachypnea and 7 complained of dyspnea. Most of the patients suffered some associated injuries including 8 head injuries, 7 pulmonary contusions, and 6 cases of blunt abdominal trauma. Less-associated injuries were rib fractures, brachial and radial nerve injuries, hemothorax, and pneumothorax. The hospital stay ranged from 4 to 28 days (mean, 14 days) and follow-up from 10 to 60 months (mean, 32 months). Treatment for traumatic asphyxia included measurement of arterial blood gases, oxygen supplementation, and intubation with mechanical ventilation. The patients' recovery conditions were relative to the severity of injury and the associated injuries.

Adolescent↗
PubMed1990

Traumatic asphyxia.

Traumatic asphyxia is a distinctive clinical syndrome characterized by cervicofacial cyanosis and edema, multiple petechiae, and subconjunctival hemorrhage after a severe crush injury of the thorax or of the upper part of the abdomen. A case of traumatic asphyxia is reported, and its clinical and pathophysiologic features are discussed.

Abdominal Injuries↗
PubMed1984

Severe asphyxia and outcome of survivors.

Fifty-four infants born severely asphyxiated with birth weights of more than 2500 g and gestational ages older than 37 weeks were studied with help of careful review of the case files. To establish a relationship between the time elapsed after birth to spontaneous regular active respiration and later outcome, the infants were divided into three groups: group A of 34 children, established spontaneous active respiration within 15 min; group B of 7 children recovered in 15-30 min, and group C of 13 children recovered 30 min after birth. The outcome in group C, in which the infants also had a history of prolonged intrapartum asphyxia, was uniformly bad. The absence or presence of an audible heart beat at birth was not a reliable clinical sign for a prognosis. The time that elapsed between the start of resuscitation and the first gasp had to be doubled to indicate the likely start of regular active respiration in one third of our babies. The results indicated that the combination of prolonged intrapartum asphyxia and a delay in onset of spontaneous regular respiration of more than 30 min following birth predicted a uniformly bad prognosis. Attempts at resuscitation after this interval did not appear to be warranted.

Acid-Base Equilibrium↗
PubMed1984

Asphyxia, cardiac arrest and resuscitation in rats. I. Short term recovery.

This study was conducted to investigate the degree of insult from asphyxia leading to total body circulatory arrest, as a model for brain resuscitation studies in rats. Of 78 male rats, 68 were anesthetized with halothane in O2/N2O, controlled ventilated, paralyzed with pancuronium and asphyxiated, 5, 7.5, 10, 12.5 and 15 min, respectively. Asphyxiation led to circulatory arrest in 244 +/- 22 s (mean +/- S.E.M.). Resuscitation was successful in 65% within 60 s using controlled ventilation with 100% O2, extrathoracic compressions and epinephrine intravenously. Subsequent intensive care to 6, 12 or 24 h was successful in 50% of resuscitated rats. At 6, 12 and 24 h of recovery, neurologic deficit scores and light microscopic neuropathology scores of the brain after in vivo fixation of the total body with intraventricular paraformaldehyde 3%, revealed a large scatter variability without a clear pattern. Lesions were located mostly in the frontal cortex and hippocampus (footplate) with ischemic neuronal change as the most frequent structural change. Brain cell necrosis was not seen after successful resuscitation. It seems that both scores were influenced by post-insult stress, as indicated by paroxysmal hypertension and motor activity, by complications, such as obstruction of the tracheotomy cannula by abundant sputum production, and by partial sedation with N2O and paralysis with pancuronium. This study indicates the feasibility of an asphyxial insult in rats for use in resuscitation studies of short duration. Although 24 h post-insult recovery is possible, up to 6 h seems most practical, with asphyxia of 7.5-10 min most successful and controllable. Questions are raised about the effects of irritation during the post-insult intensive care on both neurological deficit and neuropathology scores.

Animals↗
PubMed1984

Brain lactate and alanine-glutamate ratios during and after asphyxia in rats.

Recently, Conger, Garcia, Kauffman, Lust, Murakami and Passonneau, (1981) proposed the use of brain alanine-glutamate ratios (A:G) for the prediction of outcome after brain ischemia. This study evaluates this parameter and brain lactate concentration during and after asphyxial insults in rats. During the first 15 min of asphyxial death in rats (n = 37), lactate increased sharply from mean values of 1.48 to 18.06 mumol g-1 wet brain, and thereafter to 19.44 mumol g-1 wet brain at 180 min. During total body asphyxia (n = 38) and recovery after resuscitation, brain lactates increased to mean values of 15 and 17.5 mumol g-1 wet brain at 5 and 10 min, respectively, to recover after 30-60 min to baseline. The alanine-glutamate ratios did not rise during the insult; however, after restoration of circulation, the ratios rose to peak at about 15 min post-restoration of circulation and recovered slowly during the next 165 min to still slightly increased levels. During intermittent asphyxia (n = 15), lactate and alanine-glutamate ratios followed the same patterns as found before except at lower levels. The conclusions of this study are: (1) brain lactate concentrations had no value in predicting the potential of recovery; (2) increased lactate concentrations during recovery indicated secondary insult; (3) brain A:G's did not increase during asphyxiation; (4) brain alanine-glutamate ratios increased after restoration of circulation and may have reflected the quality of reflow; (5) increased ratios during recovery beyond 20 min indicated secondary insult. Brain alanine-glutamate ratios could not be used for prediction of outcome in asphyxial insults in rats.

Alanine↗