scholarly journals The Solution of Discrepancy of Late Deceleration and the Prevention of Cerebral Palsy by the Hypoxia Index

Author(s):  
Kazuo Maeda

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.


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.


2010 ◽  
Vol 19 (1) ◽  
pp. 12-20 ◽  
Author(s):  
Guro Andersen ◽  
Tone R. Mjøen ◽  
Torstein Vik

Abstract This study describes the prevalence of speech problems and the use of augmentative and alternative communication (AAC) in children with cerebral palsy (CP) in Norway. Information on the communicative abilities of 564 children with CP born 1996–2003, recorded in the Norwegian CP Registry, was collected. A total of 270 children (48%) had normal speech, 90 (16%) had slightly indistinct speech, 52 (9%) had indistinct speech, 35 (6%) had very indistinct speech, 110 children (19%) had no speech, and 7 (1%) were unknown. Speech problems were most common in children with dyskinetic CP (92 %), in children with the most severe gross motor function impairments and among children being totally dependent on assistance in feeding or tube-fed children. A higher proportion of children born at term had speech problems when compared with children born before 32 weeks of gestational age 32 (p > 0.001). Among the 197 children with speech problems only, 106 (54%) used AAC in some form. Approximately 20% of children had no verbal speech, whereas ~15% had significant speech problems. Among children with either significant speech problems or no speech, only 54% used AAC in any form.


2007 ◽  
Vol 41 (10) ◽  
pp. 46
Author(s):  
ALEC HOON
Keyword(s):  

Author(s):  
Andrew M Gordon ◽  
Sarah R Lewis ◽  
Ann-Christin Eliasson ◽  
Susan V Duff

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