Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Asphyxia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources
PubMed2006

Does early referral to tertiary care decrease the mortality related to birth asphyxia?

OBJECTIVE: To find the association of time of referral of asphyxiated newborns with the outcome. DESIGN: Observational study. PLACE AND DURATION OF STUDY: Neonatal Unit of Children's Hospital, Lahore, from August to December 2000. PATIENTS AND METHODS: One hundred fifty newborns with birth asphyxia were studied, who fulfilled four out of six Levene criteria. Exclusion criteria included age more than 48 hours at the time of admission, respiratory depression due to other causes, birth weight less than 1500 grams, gestational age less than 34 weeks, major congenital malformations, dysmorphism, severe hyperbilirubinemia, meningitis and bleeding disorders. Newborns were divided into two groups. Group A (n=78,52%) comprised of those newborns who reached our hospital within 12 hours after birth and group B (n=7, 48%) were those newborns who reached between 12-48 hours. Outcome was described either good outcome (newborns discharged from hospital in good clinical condition having normal vital signs, taking oral feed and not requiring medicine) or poor outcome (newborns expired during stay in neonatal unit). Chi-square test was applied and p-value was calculated. RESULTS: One hundred and seventeen (117) newborns (78%) were males and 33 (22%) were females. Thirty-five (35) mothers (23%) had proper antenatal visits to trained medical professionals. Majority of mothers (n=59, 39%) had their visits to untrained midwives, 56 mothers (37%) to semi-trained persons like a midwife, LHV or nurse. Majority (n =93, 61%) of study population were home delivered. Thirty-six newborns (24%) were delivered at private clinics and maternity homes while only 21 newborns (14%) came from tertiary care centers. Mortality was 24% in group A as compared to 76% in group B (p-value < 0.001). CONCLUSION: Those asphyxiated newborns who reached to a tertiary care hospital earlier had significantly better outcome as compared to those who arrived late. Early recognition of birth asphyxia and referral, therefore, reduces morbidity and mortality.

Age Factors↗
PubMed1998

An Apgar score of three or less at one minute is not diagnostic of birth asphyxia but is a useful screening test for neonatal encephalopathy.

OBJECTIVE: To evaluate the relationship between an Apgar score of three or less at one minute of life and the subsequent risk of developing neonatal encephalopathy (NE). DESIGN: Prospective. SETTING: The principal maternity hospital of Kathmandu, Nepal, a low income country, where over 50% of the local population deliver. METHODS: All liveborn infants over a 12 month period with a birthweight of 500 g or more were assessed by the Apgar scoring system at one minute of age. All term infants with neurological abnormalities presenting in the first day of life were systematically examined and described according to a conventionally defined encephalopathy grading system. Major congenital malformations and neonatal infections were excluded. RESULTS: Over 12 months there were 14,771 total births of a weight of 500 g or more of which 14,371 were live births and 400 were stillbirths. Of 734 infants with 1 min Apgar of three or less, 91 developed NE. The positive and negative predictive values of 1 min Apgar of three or less for NE were 11.4% and 99.9%, respectively. The probability of developing NE rose from 0.6% (amongst all infants born at this hospital) to 11.2% (amongst infants born with a one minute Apgar of three or less). CONCLUSIONS: An Apgar score of 3 or less at one minute is a useful screening test for clinically significant birth asphyxia (NE). It overestimates by eight fold the scale of the birth asphyxia problem, but identifies a high risk group requiring further observation of their neurological condition.

Apgar Score↗
PubMed1998

[Study on the mechanism for fetal asphyxia in intrahepatic cholestasis of pregnancy].

OBJECTIVE: To investigate the cause of fetal asphyxia of mothers with intrahepatic cholestasis of pregnancy (ICP). METHODS: The cord plasma erythropoietin (EPO) concentrations were measured in 37 infants of mothers with ICP and 46 control infants after elective cesarean section. Furthermore, the transfer of oxygen across the placental membranes in ICP group (n = 7) were compared with controls (n = 8) by dual perfusion of the human placental lobule in vitro. RESULTS: The oxygen transfer across the placental membrane in ICP was similar to the controls (P < 0.05). However cord venous EPO was lower in infants delivered by elective cesarean section from women with ICP (13.58 +/- 8.88 IU/L, P < 0.05) than that in control infants (20.43 +/- 14.15 IU/L). CONCLUSION: The transfer of oxygen across the placental membrane in ICP may be normal. The lower cord venous EPO value in ICP may be mainly responsible for the fetal asphyxia.

Adult↗
PubMed2000

Clinical value of a single postnatal lactate measurement after intrapartum asphyxia.

UNLABELLED: Our aim was to compare the respective values of base deficit and lactate in birth asphyxia. METHODS: Base deficit and lactate levels were measured from radial artery blood samples taken at 30 min of life in 115 term newborns suspected as having been asphyxiated during labour. Both base deficit and lactate levels were compared between patients who further developed moderate or severe encephalopathy and those who experienced no or only mild encephalopathy. Receiver operating characteristics curves and clinical values of both indicators were computed. RESULTS: The correlation between base deficit and lactate was significant (r2 = 0.51, p < 0.0001). Both indicators were significantly associated with neonatal outcome. Lactacidaemia lower than 5 mmol/l and/or base deficit level lower than 10 mEq/l were not followed by neurological complications. Plasma lactate concentration greater than 9 mmol/l was associated with moderate or severe encephalopathy with a sensitivity of 84% and a specificity of 67%. Base deficit and lactate had similar clinical values. CONCLUSIONS: Base deficit and lactate measurements in arterial blood at 30 min of life are equally valuable in assessing the severity of birth asphyxia.

Asphyxia Neonatorum↗
PubMed2000

Cardiac abnormalities in birth asphyxia.

Cardiac abnormalities in birth asphyxia were first recognised in 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 new born (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 new born (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 distress and cyanosis (sometimes differential). Clinical examination also reveals evidence of pulmonary arterial hypertension 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.

Apgar Score↗
PubMedDate not supplied

[Risk factors predictive of neurological sequelae in term newborn infants with perinatal asphyxia].

INTRODUCTION: Perinatal asphyxia (PA) and its neurologic manifestations are the most important cause of brain injury and neurologic sequelae in full-term infants. The objective of this study is to analyze the perinatal risk factors of neurologic sequelae in asphyctic term newborns. PATIENTS AND METHODS: One hundred and fifty-six consecutive asphyctic term infants were studied prospectively during 40 months. PA was graded in two stages (severe and non-severe), hypoxic-ischemic encephalopathy classification was based on Levene's criteria, and neurologic sequelae was based on Finer and Amiel-Tisson's criteria. The perinatal variables were graded as prenatal (gestational and obstetrics), neonatal (resuscitation, general data of the newborn, and organic manifestations of asphyxia) and postneonatal (neurologic sequelae with at least 24 months of follow-up). The relationships between these variables are studied by univariant and multivariant analysis (Cox's regression). RESULTS: PA was graded as severe in 31 cases and non-severe in 125. Neurologic manifestations (hypoxic-ischemic encephalopathy) during neonatal period were present in 25.6%, and extraneurologic manifestations (hypoxic-ischemic disease) in 41.7% cases. The incidence of neurologic sequelae, in 115 asphyxiated full-term infants follow-up at least 24 months, was 16.5% (19 cases). The perinatal variables associated to risk of neurologic sequelae on univariate analysis are variables of neonatal resuscitation (1 minute Apgar score < or = 4, 5 minute Apgar score < or = 6, endotracheal intubation, severity of PA) and variables of systemic manifestations (hypoxic-ischemic encephalopathy, cardiovascular and multi-systemic dysfunction, and mechanical ventilation). But only two variables are independently associated on multivariate analysis: severe PA (RR = 2.82; IC = 1.07-7.39) and hypoxic-ischemic encephalopathy (RR = 4.17; IC = 1.48-11.75). CONCLUSIONS: The best predictive risk factors for the neurological prognosis at follow-up are severe PA at birth and/or evidence of encephalopathy in neonatal period.

Acidosis↗
PubMed2001

[Cooling as treatment of birth asphyxia].

In about 10 per cent of children with cerebral palsy, the most probable cause is birth asphyxia. The brain injury following birth asphyxia evolves in part over hours or days--as a secondary process. This opens a 'window of opportunity' for intervention. Decreasing the temperature by as little as 3 degrees C appears to be effective. It is possible to identify babies with a 50 per cent risk of death or survival with cerebral palsy within 3 to 6 hours after birth. Pilot trials of cooling suggest that the side-effects of cooling can be managed. Randomized controlled trials are underway. Obtaining informed consent from the parents for these trials represents a particular challenge.

Asphyxia Neonatorum↗
PubMed1998

Ventilatory responsiveness to progressive asphyxia during sleep in newborn lambs: effects of maternal anemia during pregnancy.

Our aim was to determine the effects of intrauterine compromise, induced by maternal anemia, on ventilatory responsiveness of the sleeping newborn to progressive asphyxia. We induced anemia in 6 sheep for the final third of pregnancy and studied their offspring for 2-3 weeks after birth. Lambs from anemic ewes were growth-restricted at birth; they and 6 control lambs were chronically instrumented soon after birth and underwent studies during which we determined ventilatory and arousal responsiveness to a progressive asphyxic stimulus during sleep. During quiet wakefulness, active sleep and quiet sleep, lambs from anemic ewes had elevated end-tidal CO2 levels (FECO2,%) compared to controls. Ventilatory responsiveness (i.e., gradient of relationship between minute ventilation and FECO2) was greater in quiet sleep than in active sleep for both groups of lambs but did not differ between the two groups in either active or quiet sleep. Lambs from anemic ewes had significantly higher FECO2 values than controls before arousing from either active or quiet sleep. Other indices of arousability (time to arousal, percent hemoglobin saturation at arousal) were not different between the two groups. Our results indicate that prenatal exposure to maternal anemia induces fetal growth restriction and elevates the CO2 'set-point' for normal ventilation. It does not, however, produce significant abnormalities in ventilatory responsiveness to progressive asphyxia during sleep.

Anemia↗
PubMedDate not supplied

Perinatal asphyxia at Port Moresby General Hospital: a study of incidence, risk factors and outcome.

We investigated the incidence and outcome of perinatal asphyxia (PA) at Port Moresby General Hospital by a retrospective chart review and prospective collection of data, spanning a total of 2.5 years. 125 babies weighing more than 2000 g at birth with a gestation of 34 weeks or more and with no obvious congenital abnormalities were diagnosed to have PA. During the same time period 22,700 liveborn babies were delivered, a PA incidence of 5.5/1000 livebirths. There was a 31% mortality and considerable morbidity. Hospital records for 114 affected babies and 115 controls (the next baby born by normal delivery) were compared. Significant risk factors for PA were: previous stillbirth or neonatal death, fetal heart rate abnormalities, membranes ruptured for more than 12 hours prior to delivery, meconium staining, antepartum haemorrhage, maternal fever, prolonged first and second stages of labour, preterm or post-term delivery and operative delivery. In only 73 affected babies was the 5-minute Apgar score recorded as 6 or less. All 34 of the babies with grade 3 hypoxic ischaemic encephalopathy (HIE) either died (30) or had serious neurological impairment. The treatment of affected babies remains largely supportive and some causes of PA are currently unavoidable. It is, however, widely accepted that some cases of perinatal asphyxia may be prevented by the delivery of high-risk pregnancies in obstetric facilities with appropriate intervention and by good neonatal resuscitation. Sophisticated or expensive equipment is not a necessity.

Apgar Score↗
PubMed2001

[An autopsy case of an infant born with a caul who died due to asphyxia after live-birth].

We reported an autopsy case of a child born with a caul. The infant was a female and seemed to be full-term. No remarkable pathological findings for disease or anomalies were observed. The floating test of lungs was partially positive. And on the gastro-intestinal floating test, only stomach floated. In histological examination, the alveoli in the lungs were partially slightly open. We thought that those were due to the cardio-pulmonary resuscitation. Pulmonary surfactant was positive immunohistochemically. And the stable microbubble test on the liquid in her stomach was very strong. Even if a child is born alive, he or she will soon die due to asphyxia but for the production of surfactant in the lungs. We can evaluate more precisely the potential respiratory ability of a neonate died due to asphyxia by means of stable microbubble test on newborn gastric contents and immunohistochemical staining of surfactant in lungs.

Asphyxia Neonatorum↗
PubMed2002

[Perinatal asphyxia as incorrect explanation for mental retardation].

Three women, aged 21, 34 and 32 and with a family history of mental retardation said to be caused by perinatal asphyxia, each gave birth to a child with mental retardation. A chromosomal translocation, fragile X syndrome, and myotonic dystrophy could be diagnosed, respectively. In retrospect, the diagnosis of perinatal asphyxia in the family history had been too readily accepted. In reality the mental retardation was caused by a genetic disorder. Physicians are used to making a diagnosis, and when a diagnosis is not (yet) possible, they try to establish a working diagnosis or differential diagnosis. Too often such a working diagnosis becomes, through time, a definite diagnosis.

Adult↗
PubMedDate not supplied

[Definition of perinatal asphyxia in medical literature: the need of a consensus].

INTRODUCTION: The pathophysiological definition of perinatal asphyxia (PA) is not operative in clinical practice; by this, several criteria have been proposed: abnormalities in electronic fetal monitoring, meconium stained amniotic fluid, metabolic acidemia, low Apgar score, postasphyctic neurologic and extraneurologic involvement, etc. AIMS. 1) To analyze the different definition criteria of PA in international medical literature; 2) to compare the studies in Spain about PA, and to know the epidemiological differences in relation with the definition of PA used. MATERIAL AND METHODS: Bibliographic searching in PubMed data base during the period 1994 1999, using the key word perinatal asphyxia . We review the articles published in these medical journals: Pediatrics, J Pediatrics, Eur J Pediatr, Pediatr Res, Am J Obstet Gynecol, Br Med J, N Engl J Med, An Esp Pediatr and Rev Neurol. INCLUSION CRITERIA: original articles with the definition of PA in term newborns; we excluded other types of articles (letters to editor, review.) and experimental models with animals. In a second part, we review 11 epidemiological studies about PA published in Spain. RESULTS: Twenty four articles meet the inclusion criteria: 5 in Pediatr Res, 4 in Pediatrics, 4 in J Pediatr, 3 in Eur J Pediatr, 3 in An Esp Pediatr, 3 in Rev Neurol, 1 in Am J Obstet Gynecol and 1 in N Engl J Med. Each study use a different definition: we found differences in the number and combination of criteria, and also in the cutt of points of quantitative variables (Apgar score and umbilical pH). It is not frequent to classify the severity of asphyctic event. We found important epidemiological differences in the 11 Spanish studies found in the literature about PA: the frequency of PA varies from 1.46 to 14.8% of alive newborns, the frequency of postasphyctic encephalopathy varies from 8.6 to 89%, and the frequency of neurologic sequelae varies from 11.2 to 30.5%. CONCLUSIONS: It is necessary to establish a common definition of PA (to differentiate between severe PA, the most important type, and non severe PA, the most frequent type), wich allow homogeneous comparisons in the epidemiological studies in relation to incidence and morbi mortality of PA

Asphyxia Neonatorum↗
PubMed2003

[Neurological prognosis of term infants with perinatal asphyxia].

Neonatal encephalopathies following birth asphyxia are the first features of cerebral insult. They never miss when asphyxia is directly involved in cerebral impairment. Mild encephalopathies have constantly a good prognosis. Conversely, moderate and severe encephalopathies are associated with poor outcome (death or severe handicap) in 25% to 100% of cases. Prognosis of these moderate and severe encephalopathies can be assessed during the first ten days of life by 3 complementary ways: clinical exam, electrophysiology and imaging. The most information is obtained from the EEG and MRI which together nearly reach 100% for both predictive positive and negative values for severe neurological sequelae.

Asphyxia Neonatorum↗
PubMedDate not supplied

[Blood ammonia and transaminases in full term infants suffering from perinatal asphyxia].

AIMS: To find hepatic markers of perinatal asphyxia. PATIENTS AND METHODS: Variations in blood ammonia during the first week of life and in transaminase in serum during the first 48 hours were analysed in four groups of newly born infants (NBI): Group I or control, in which 65 NBI were included, with suspected unconfirmed infection and no other pathologies; Group II, made up of 15 NBI with loss of foetal well being (LFW) with no posterior neurological clinical features; Group III, consisting of 27 NBI with LFW criteria and mild hypoxic ischemic encephalopathy (HIE); and Group IV, with 25 NBI with LFW criteria and mild HIE according to Amiel s criteria. RESULTS: The average blood ammonia values in full term infants remain steady during the first week of life (87.66 21.69 mg/dL), as occurs in infants with LFW but without HIE (89.08 24.69 mg/dL) and in those with mild HIE (89.08 20.75 mg/dL). In moderate HIE, the blood ammonia level rises until the third day (108.55 7.04 mg/dL) and then drops back to the initial values (p= 0.0045). When grouped by days, these values show significant differences (p= 0.04), with higher values in Group IV. The NBI with HIE presented higher levels of transaminases, especially of AST (GOT) (p= 0.000001), and this increase is proportional to its gravity. No relation was found between values of blood ammonia and transaminases. CONCLUSIONS: Both blood ammonia and transaminases can be considered to be perinatal asphyxia markers.

Alanine Transaminase↗
PubMed2003

Effect of perinatal asphyxia on thyroid-stimulating hormone and thyroid hormone levels.

AIM: To compare serum concentrations of thyroid hormones--T4, T3, free T4 (FT4) and reverse T3 (rT3)--and thyroid-stimulating hormone (TSH) found in the umbilical cord blood of term newborns with and without asphyxia and those found in their arterial blood collected between 18 and 24 h after birth. A further aim of the study was to assess the association between severity of hypoxic-ischemic encephalopathy and altered thyroid hormone and TSH levels, and between mortality and FT4 levels in the arterial blood of newborns between 18 and 24 h of life. METHODS: A case-control study was carried out. The case group comprised 17 term newborns (Apgar score < or = 3 and < or = 5 at the first and fifth minutes; umbilical cord blood pH < or = 7.15) who required bag and mask ventilation for at least one minute immediately after birth. The control group consisted of 17 normal, term newborns (Apgar score > or = 8 and > or = 9 at the first and fifth minutes; umbilical cord blood pH > or = 7.2). Cord blood and arterial blood samples were collected immediately after birth and 18 to 24 h after birth, respectively, and were used in the blood gas analysis and to determine serum concentrations of T4, T3, FT4, rT3 and TSH by radioimmunoassay. All newborns were followed-up until hospital discharge or death. RESULTS: Gestational age, birthweight, sex, size for gestational age, mode of delivery and skin color (white and non-white) were similar for both groups. No differences were found in mean levels of cord blood TSH, T4, T3 and FT4 between the groups. In the samples collected 18 to 24 h after birth, mean levels of TSH, T4, T3 and FT4 were significantly lower in the asphyxiated group than in the control group. Mean concentrations of arterial TSH, T4 and T3 between 18 and 24 h of life were lower than concentrations found in the cord blood analysis in asphyxiated newborns, but not in controls. In addition, asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy presented significantly lower mean levels of TSH, T4, T3 and FT4 than those of controls. None of the asphyxiated newborns with FT4 > or = 2.0 ng/dl died; 6 out of the 11 asphyxiated newborns with FT4 < 2.0 ng/dl died. CONCLUSIONS: Serum concentrations of TSH, T4, T3 and FT4 are lower in asphyxiated newborns than in normal newborns between 18 and 24 h of life; this suggests central hypothyroidism secondary to asphyxia. Asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy present a greater involvement of the thyroid function and consequently a greater risk of death.

Asphyxia Neonatorum↗
PubMed2003

[Perinatal asphyxia, known topic, new diagnostic prospects--advisability of troponin T in perinatal medicine].

Perinatal asphyxia is a major topic in neonatology. It has a high impact on neonatal mortality and morbidity and neurological and intellectual development of the infant. Hypoxia triggers compensatory mechanisms in the fetus and the newborn aimed to sustain adequate oxygen transport to the vital organs. Long periods of hypoxia and poor perfusion cause failure of mentioned compensative mechanisms and lead to irreversible damage in tissues. No clear-cut physiologic parameters exist which allow for an early identification of neonatal infants who are either at risk to develop brain damage or posthypoxic heart failure. In the above paper authors demonstrate new possibilities in diagnosis of perinatal asphyxia. They present cardiac troponin T, a thin filament contractile protein as a highly specific and sensitive marker of myocardial injury and hypoxia.

Asphyxia Neonatorum↗
PubMed1992

The course of respiration and circulation in death due to various types of asphyxia.

To investigate the course of respiration and circulation in death due to various types of asphyxia, dogs were asphyxiated by a method simulating typical hanging, by plastic-bag suffocation, by breathing pure nitrogen and low concentration of oxygen. Intrathoracic pressure, blood pressure in the femoral artery, electrocardiogram and electroencephalogram were registered and were compared with the course in death due to obstructive asphyxia.

Animals↗
PubMed1992

Application of hemoglobin analysis by CO-oximeter to medico-legal practice with special reference to diagnosis of asphyxia.

Hemoglobin analysis by CO-oximeter is more easily and rapidly available method than other spectrophotometric or GC methods. In the present study, the possibility of diagnosis of asphyxia by CO-oximeter was examined experimentally using rabbits. When measured value of oxyhemoglobin (O2Hb) was lower than about 20% and that of deoxyhemoglobin (HHb) was, on the other hand, higher than about 80%, being accompanied by low measured values of both methemoglobin (MetHb) and CO-hemoglobin (COHb) (< 5%), asphyxia should be firstly considered as the cause of death. To the corpses found at the scene of fire, three chief factors causing death such as burns, suffocation due to oxygen deficiency and intoxication by poisonous gases may have occurred simultaneously, and through measuring the values of O2Hb, COHb, MetHb and HHb, the main lethal factor could be selected out among these three factors above and the cause of death could be examined much more closely. Because of easy and rapid analysis, it could be considered that CO-oximeter was useful for forensic practices and police activities.

Animals↗