scholarly journals Cerebral Palsy is 25 or More of Hypoxia Index and No Cerebral Palsy is 24 or Less of Index in Fetal Monitoring

Author(s):  
Kazuo Maeda ◽  

Fetal outcome was ominous if fetal heart rate (FHR) was late deceleration (LD) in the past, while 3 connected typical LDs were normal, and repeated LDs for 50 min were heavy fetal brain damage. Also, LD is defined as LD when it is repeated for 15 minutes. As the fetus is damaged by repeated hypoxic decelerations followed by cerebral palsy, but not by its late appearing in LD, novel fetal hypoxia index (HI) is the sum of all deceleration durations (min) divided by the lowest FHR (bpm) and multiplied by 100 in fetal monitoring. The hypoxia index was 25 or more in all of 6 cerebral palsy cases, while it was 24 or less in all 16 cases of no cerebral palsy. As error probability is almost zero in the chi2 test of hypoxia index, no cerebral palsy is decided when the hypoxia index is 24 or less, while it is cerebral palsy, if hypoxia index is 25 or more. The hypoxia index is adopted to all FHR decelerations and bradycardia, as hypoxia index does not evaluate the late appearing of deceleration, instead of past subjective deceleration pattern diagnosis in fetal monitoring.

Author(s):  
Kazuo Maeda ◽  

Fetal outcome was ominous if fetal heart rate (FHR) was late deceleration (LD) in the past, while 3 connected typical LDs were normal, and repeated LDs for 50 min were heavy fetal brain damage. Also, LD is defined as LD when it is repeated for 15 minutes. As the fetus is damaged by repeated hypoxic decelerations followed by cerebral palsy, but not by its late appearing in LD, novel fetal hypoxia index (HI) is the sum of all deceleration durations (min) divided by the lowest FHR (bpm) and multiplied by 100 in fetal monitoring. The hypoxia index was 25 or more in all of 6 cerebral palsy cases, while it was 24 or less in all 16 cases of no cerebral palsy. As error probability is almost zero in the chi2 test of hypoxia index, no cerebral palsy is decided when the hypoxia index is 24 or less, while it is cerebral palsy, if hypoxia index is 25 or more. The hypoxia index is adopted to all FHR decelerations and bradycardia, as hypoxia index does not evaluate the late appearing of deceleration, instead of past subjective deceleration pattern diagnosis in fetal monitoring.


Fetal brain damage develops after the loss of FHR variability followed by infantile cerebral palsy due to severe hypoxia in frequently repeated fetal heart rate (FHR) decelerations (transient bradycardia) or prolonged fetal bradycardia, where novel hypxia index is 25 or more, and it is prevented if the hpoxia index is 24 or less. The hypoxia index (HI) is the sum of FHR deceleration durations (min) divided by the lowest FHR (bpm), and multiplied by 100 (Figure 1). The HI is calculated by visual measurement, while it is also suitably calculated by computerized FHR monitoring. Cerebral palsy is prevented when HI is 24 or less with almost zero error probability in the delivery. The cases whose HI was 25 or more will develop cerebral palsy, thus, it can receive early cerebral palsy trearments in neonatal stage. As late deceleration disappeared when the parturient woman changed her posture to lateral one from supine, a parturient woman is recommended to have lateral posture, when they notice the appearance of FHR deceleration during the delivery to disappear deceleration to prevent the increase of HI value. As the HI is adopted not only late deceleration, but also all decelerations and continuous bradycardia, fetal diagnosis will change to objective numeric FHR analysis from the monitoring with vague subjective FHR pattern classification.


2017 ◽  
Vol 17 (1-2) ◽  
pp. 43-64 ◽  
Author(s):  
Thomas P. Sartwelle ◽  
James C. Johnston ◽  
Berna Arda

Electronic fetal monitoring (EFM) was predicted by its inventors to be the long-sought cerebral palsy (CP) nemesis. Rather than prevent CP or any other birth problems, 40 years of EFM use has done substantial harm to mothers and babies and created a worldwide CP-EFM litigation industry that enriches only trial lawyers. Physicians, frightened by the ever-expanding and costly CP-EFM litigation crisis, and focused on avoiding lawsuits at all costs, embraced ethical relativism—charitably called defensive medicine—and continued EFM use even in the face of overwhelming evidence that EFM is merely junk science. In doing so, physicians completely abandoned the bedrock bioethics principles of autonomy, beneficence, and nonmaleficence. This daily ethical drama has played itself out for the past almost half century with little protest from obstetricians and no protest from ethicists. This article reviews EFM harms, the CP-EFM litigation crisis, and the resulting abandonment of bioethics principles and explores why the CP-EFM paradigm has failed utterly to follow the Kuhnian model of the scientific, technology, medical paradigm shift.


2020 ◽  
pp. 1-3
Author(s):  
Kazuo Maeda

Although fetal deaths was decreased by intrapartum Fetal Heart Rate (FHR) monitoring, infantile cerebral palsy was not decreased in Dublin trials of Electric Fetal Monitor (EFM), thus, an analysis to reduce cerebral palsy was studied, where cerebral palsy is prevented by setting the threshold of hypoxia index at 24 or less, in the analysis of FHR deceleration.


Author(s):  
Sunitha C. ◽  
P. S. Rao ◽  
Prajwal S. ◽  
Reema Kumar Bhat

Background: The importance of fetal monitoring during labour has been realized since long. The stress of uterine contractions may affect the fetus adversely especially if the fetus is already compromised, when the placental reserves are suboptimal, or when cord undergoes compression as in those associated with diminished liquor amnii or iatrogenic uterine hyperstimulation due to injudicious use of oxytocin. Even a fetus which is apparently normal in the antenatal period may develop distress during labour. Hence fetal monitoring during antepartum and intrapartum periods is of vital importance for timely detection of fetal distress so that appropriate management may be offered.Methods: This study was a prospective observational study included 100 patients of more than 34 weeks period of gestation were divided into two groups. Patients in labour were analyzed on an Electronic Monitor. Delivery conducted was either by vaginal route, instrumental or by caesarean section depending upon the fetal heart rate tracings and their interpretations as per the case. At the time of delivery umbilical cord blood was taken for the pH analysis. All new born babies were seen by the paediatrician immediately after the delivery and 1 and 5 minute APGAR score assessed for the delivered baby. The various EFM Patterns obtained were compared with the neonatal status at birth using the parameters already mentioned. The false positives and false negatives if any were tabulated. Data so obtained was analyzed statistically thereafter. Statistical Package for Social Sciences (SPSS) Version 13.0 was used for the purpose of analysis.Results: Results revealed that among the 50 subjects of the case group, 7 subjects showed the absence of the beat to beat variability, 12 subjects showed early deceleration, 32 subjects showed late deceleration, and 6 subjects showed the presence of variable deceleration. No significant association of beat to beat variability, early and variable deceleration could be established with meconium staining/NICU admissions/low APGAR. A significant positive association between persistent late deceleration with MSL, APGAR <7 at 1 min, and Instrumental/LSCS delivery was seen. A significant positive association between any CTG abnormality and APGAR at 1 min, type of delivery, and meconium staining was seen.Conclusions: EFM should be used judiciously. Cardiotocography machines are certainly required in the labour room. Equally important is the proper interpretation of the CTG tracings so that unjustified caesarean sections can be minimized, at the same time picking up cases of fetal distress in time which is likely to improve fetal outcome.


1981 ◽  
Author(s):  
H Ludwig ◽  
H J Genz

The treatment of occlusive deep vein thrombosis during pregnancy with fibrinolytic agents as streptokinase and urokinase is still controversial. The main points of controversy are retroplacental bleeding, fetal heart rate acceleration and malformations of the fetus. The main author conducted 122 therapeutic fibrinolytic treatments during pregnancy since 1961. The earliest beginning of treatment was the 14th week, the latest the 38th week of pregnancy. The indications to all treatments in these cases was an acute thrombotic occlusion of one or both ileofemoral veins in pregnant women. The diagnosis was established by clinical signs and, since 1975 by ultrasonography (n = 63). The treatment regimen was previously designed with the use of medium large doses of streptokinase in prolongation of an initially high dosage (1000,000 IU), later on 63 cases were treated by the following scheme: Initial dosage 1.5 - 1000,000 IU streptokinase within 30 minutes i.v. by monitored infusion, followed by an hourly dosage of not more than 250,000 IU streptokinase for 24 to 48 hours. An initial raise of body temperature occured in 28% of all cases. The fetal heart rate was watched by cardiotocography so far the pregnancy was beyond the 28th week. The success rate of all cases was 72%, indicating the complete restoration of the vessel's patency, 18% responded partially, 10% did not respond at all. 55% of all cases were examined by phlebography some days after delivery, the others were checked by clinical examination only or by ultrasonography respectively. The postfibrinolytic treatment in all cases consisted in the application of heparin in the dosage of 20,000 to 40,000 IU/24 hours for at least two weeks, approximately 60 percent of the cases received oral anticoagulants for further five weeks. Complications: One premature rupture of the membranes with healthy child, one premature separation of the well situated placenta with fatal fetal outcome, two severe bleedings during the treatment which made ar. emergency delivery by cesarean section necessary. Streptokinase was then neutralized by AM- CA. No fetal malformations were observed.


1995 ◽  
Vol 16 (11) ◽  
pp. 411-418
Author(s):  
Lawrence T. Taft

To be classified as cerebral palsy (CP), there must be difficulty in neuromotor control, a nonprogressive brain lesion, and an injury to the brain that occurred before it was fully mature. The term "cerebral palsy" should be used only if a static encephalopathy exists. If there is any question that a progressive central nervous system disorder exists, the term "cerebral palsy" should not be used diagnostically until the status of the lesion is clarified. Although the primary abnormality must be a motor deficit, often there are many associated symptoms of cerebral dysfunction present. Incidence and Prevalence The prevalence of CP has changed very little over the past 40 years, in spite of many technological advances that have decreased mortality in compromised preterm and full-term infants. The prevalence rate has been estimated to be between 2 and 5 per 1000 live births. At 12 months of age, the prevalence rate was estimated to be 5.2 per 1000, but at 7 years of age, the rate was estimated to be 2 per 1000 live births. This indicates that many children who showed signs or experienced symptoms suggesting a motor disorder did not have CP on follow-up. The past 3 decades have seen an increased survival rate of very small preterm infants, resulting in a change in the percentage rates of the different clinical types of motor disabilities among patients classified as having CP.


Sign in / Sign up

Export Citation Format

Share Document