|
|
|
|
|
|
|
|
|
|
Absent |
Arms and Legs Flexed |
Active Movement |
|
|
Pulse |
Absent |
Below 100 bpm |
Above 100 bpm |
|
|
Grimace (Reflex Irritability) |
No Response |
Grimace |
Sneeze, cough, pulls away |
|
|
Appearance (Skin Colour) |
Blue-gray |
pale all over Normal, except for extremities |
Normal over entire body |
|
|
Respiration (Breathing) |
Absent |
Slow, irregular |
Good, crying |
A score of less than seven at the one-minute mark implies the baby may have experienced some stress during the labour and birth, resulting in lowered oxygen content. This is not necessarily and accurate assessment (see the section on How Accurate Are These Methods At Diagnosing Foetal Distress later in this paper). (Ref 5)
What Causes Foetal Distress?
The truth is that no one knows for sure. The actions of the uterus automatically mean that there will be some reduction of oxygen during contractions purely because there is less blood in the uterine muscle tissue during the contraction than when it is relaxed. In addition the contraction or the baby's position can cause pressure on the umbilical cord which can reduce the blood flow to the baby and therefore its oxygen supply.
There are also a number of conditions that can increase the risk of babies being affected by foetal distress. Some are to do with the condition of the mother or the baby, such as maternal pre-eclampsia (high blood pressure in the mother), prematurity (born before 37 weeks) and low birth weight (compared to other babies the same age). Others are created by the way the labour is managed such as induction and making the mother lay on her back.
It is known that foetal distress is more likely in certain mothers and babies because of conditions such as those described above, but there is no method of saying exactly which babies will or will not suffer foetal distress, and to what degree they will suffer it.
Why is Foetal Distress a Concern?
The main concerns when looking for indicators of foetal distress is the chance that the problem may lead to still birth or irreversible brain damage. Ref 6 states:
"Intrapartum foetal distress is an important cause of stillbirth and neonatal death. Although the exact incidence of foetal distress is uncertain, over 1100 infant deaths each year in the United States are attributed to intrauterine hypoxia and birth asphyxia. Although most foetuses tolerate intrauterine hypoxia during labour and are delivered without complication, some require resuscitation and other aggressive medical interventions for such complications as acidosis and seizures. Foetal distress during labour has also been implicated as a cause of cerebral palsy, which can be accompanied by mental retardation or epilepsy. "
Asphyxia, Brain Damage and Organ Damage. There are a number of terms used to express a lack of oxygen in the foetus. Some of them describe the medical result and others the event. These include asphyxia (lack of oxygen due to trouble with breathing or poor oxygen supply), Hypoxic-ischemic encephalopathy (HIE) (brain damage caused by poor blood flow or insufficient oxygen supply to the brain) and hypoxia (lack of oxygen in the tissues and organs). What they all basically describe is clinical (medically identified) symptoms that might correlate to some perinatal (before birth) oxygen deprivation. The oxygen deprivation can occur not only in the brain but in other parts of the body as well. (Ref 7 & 8)
Ref 6 noted 1100 foetal deaths associated with intrauterine hypoxia and birth asphyxia. It should be noted that in 2000 the USA had a birth rate of 3 912 990, the 1100 deaths represent a rate of 0.03% or 3 in 10,000. This is lower than the risk of uterine rupture - see my previous article.
The protocols from Royal Prince Alfred Hospital indicate that the incident of asphyxia (encephalopathy) 'probably' lies between 0.3% and 1.8%. They go on to indicate that the incident of deaths either during labour or shortly after was 4.2/1000 (0.42%) but do not indicate if these deaths can be directly attributed to asphyxia or some other cause. The identified consequences of asphyxia are that it:
"... may result in foetal demise (stillbirth), neonatal death, or a period of recovery during which there is organ dysfunction with possible long-term effects, particularly in neurological (brain) function." (Ref 9)
This reference goes on to identify a number of risks, not associated with normal pregnancies that increase the risk of asphyxia. These include: diminished placental reserve, as a result of maternal pre-eclampsia (high blood pressure), intrauterine growth restriction (unusually small babies), placental abruption (where the placenta partially detaches from the uterus before birth), foetal anaemia (eg rhesus incompatibility), postmaturity (past 41 weeks), unphysiological labour (eg induction), and malpresentation (baby lying in an odd position). It is important to be aware that these conditions increase the risk to the baby, but none of the documents and studies I reviewed indicated any effort to eliminate these conditions from their statistics. This means that for a normal pregnancy the statistics of adverse outcomes will be over inflated by the inclusion of adverse results from babies who were already at a greater risk even before the birth process commenced.
The protocols identified that in an infant that demonstrated symptoms of asphyxia the speed with which resuscitation was achieved has a great effect on the long-term outcome of the baby. It was indicated the overall risk of death or handicap was 72% in a series of infants who took longer than 30 minutes to sustained spontaneous respiration (unaided breathing).
The conditions identified as being associated with babies that had a low apgar score, acidosis (a build up of acid in the blood from too little oxygen), hypoxic ischaemic encephalopathy (HIE) and multiorgan system dysfunction included kidney damage, heart damage, respiratory distress (breathing problems), liver failure and damage to the intestines. It was indicated in these instances that HIE was diagnosed 40% of babies would have kidney problems, 25% heart problems and 25% breathing problems. No figures were given for the other conditions, and no figures were given as to how prevalent HIE was overall.
The World Health Organisation (WHO) also indicates a number of symptoms and causal factors that can indicate hypoxic problems in the baby. Again no statistics are given that demonstrate how often these occur, however it is interesting to note in their table that there are other causes of the problems, most clearly identified being bacterial infection. It should also be noted that some conditions such as intracranial haemorrhage (bleeding in the brain) are more commonly associated with premature babies than full term babies.
|
|
|
|
Possible associated maternal complications |
|
Birth asphyxia Hypoxic-ischemic encephalopathy Intracranial haemorrhage |
Convulsions |
Hypoxic-ischemic encephalopathy
Severe bacterial infection |
Prolonged/obstructed labour |
You can start to see emerging that hypoxia in the baby is not just as a result of a "bad labour" there are a lot of other factors that increase the risks to the baby when it encounters some hypoxia, and these risks are not present in all labours. So with all the problems identified how significant is asphyxia in most infants. Schneider (in ref 11) indicates that sever cases of asphyxia are definitely associated with death and brain damage however in spite of this 90% of the survivors show normal development. He goes on to state:
"The association between perinatal asphyxia and neuromotor developmental disturbances does not provide proof of a causal connection. In addition to malformations, various forms of antenatal pathology like prematurity, intrauterine growth retardation and congenital infections are related to the development of brain damage. "
So we have identified that the injuries that some babies have suffered may be as a result of their increased risk to these factors in the first place, and that the majority of babies who suffer some form of asphyxia have no permanent injury. Ref 12 goes on to provide us some explanation as to why this is:
".... the foetus may tolerate an asphyxial insult (oxygen deprivation) without central nervous system injury (brain or nerve damage) because of the foetal cardiovascular (heart) adaptation to hypoxemia. Prediction of the significance of an asphyxial insult to the foetus requires a measure of both the duration and degree of the asphyxia as well as an expression of the foetal compensatory response to the asphyxia."
In lay terms it is important for the medical practitioner to look at the length and severity of the oxygen deprivation, as well as how the baby is coping with it or recovering from it in order to prevent unnecessary intervention that may put the baby at additional risks.
Cerebral Palsy. One of the brain injuries that we hear of most commonly associated with birth injuries is cerebral palsy. It affects approximately 0.2 - 0.32% of the total population. Many of these develop the condition later in life as a result of accidents or have the condition at birth with no evidence of hypoxia.
"Recent evidence suggests, however, that most cases of cerebral palsy occur in persons with no evidence of birth asphyxia or other Intrapartum events. Risk factors earlier in pregnancy, rather than Intrapartum events, are now considered the principal causes of cerebral palsy and mental retardation." (Ref 5)
The biggest problem associated with diagnosing the cause of cerebral palsy in infants is that the causes of cerebral palsy are not understood. As identified above a number of conditions can increase the risk of the condition but they do not mean the condition will or will not occur. MacDonald indicates:
'Preventative programmes will remain unsuccessful until the causation of cerebral palsy is more understood. What we are presently lacking is an understanding of the underlying conditions responsible for brain injury when asphyxia occurs despite our best efforts. While we have learned much about the causation and prevention of perinatal mortality very little has been established about the causation and prevention of cerebral palsy'.... 1. The incidence of cerebral palsy is not falling despite improved obstetrics. 2. The cause of more than 90% of cases of cerebral palsy remains unknown. 3. Asphyxia is hard to define and measure and is rarely the cause of cerebral palsy. " (Ref 7)
Ref 14 also supports this premise that 90% of cerebral palsy cannot be related to events during birth. This article also goes on to specify a number of measurement criteria that must be present in order to suggest that the cerebral palsy was as a result of hypoxia in labour.
In 1993 Schneider indicated that despite increased intervention and monitoring the rate of cerebral palsy has remained constant for the past 30 years. He states there is no clear correlation between asphyxia during labour and the development of cerebral palsy, and that less than 10% of all cerebral palsy cases showed any signs of severe asphyxia during labour. (Ref 11)
Some groups have indicated that mild oxygen deprivation during labour can result in problems developing as the child gets older. This concept was investigated by a paediatric research group and reported in ref 13. They found that children who had suffered from mild hypoxia during labour showed no signs of developmental deficits or brain damage when compared to an equivalent group of children who did not experience mild hypoxia, with comparison being done at 4 years and 6 - 8 years of age. (Ref 13)
The conclusions from the consensus statement issued by The Australian and New Zealand Perinatal Societies in 1995 indicate that further study is required in order to understand the causes of cerebral palsy and if birth injuries contribute to cerebral palsy, they state:
"There is no evidence that current obstetric practices can reduce the risk of cerebral palsy. The origins of many cases of cerebral palsy are likely to be antenatal. While obstetric interventions in the presence of signs of possible hypoxia may prevent foetal death, there is no evidence that they will limit the prevalence or severity of cerebral palsy. The antenatal signs of hypoxia and the methods to monitor hypoxia in labour are still imprecise. This can lead to over diagnosis of severe hypoxia and, even when correctly diagnosed, early delivery by caesarean section may not change the risk of cerebral palsy. All expert witnesses and the public should recognise that the belief that caesarean section will prevent many cases of cerebral palsy is incorrect. " (Ref 15.)
Lung Damage/ Meconium Aspiration Syndrome (MAS). Meconium staining is, in itself, not evidence that the foetus is suffering from oxygen deprivation in the uterus. There is suggestion that the foetus passes the meconium because it is under stress however the main concern is related to meconium aspiration syndrome, which is where the baby takes meconium contaminated fluid into its lungs either before or during birth. Although the baby does not breathe air before it is born it "practices" breathing in the uterus from about 20 weeks. This helps with the development of the lungs. In babies who are in distress these breathing movements increase and if meconium is present the risk of 'breathing' it in also increases. This is more common in post term babies (over 41 weeks) and is rare before 38 weeks. (Ref 17)
Ref 18 indicates that 12% of live births are complicated by meconium stained amniotic fluid and of these, 35% will develop MAS . That is 4% of all babies. MAS causes problems in breathing through two means; there is some evidence that indicates that meconium inhibits, or depletes, the function of the surfactant (a naturally produced soapy substance that stops the walls of the lung buds from sticking to each other) which makes breathing ineffective. The second problem caused is that the meconium can block the lungs thus reducing the amount of oxygen that can be taken in. The meconium also causes irritation in the lungs that can lead to inflammation and infection and potentially death of the affected areas of lung tissue. (Ref 18).
As indicated above MAS does not occur in all babies who are exposed to meconium. In a Singaporean study it was demonstrated that the incidence of MAS increased with the thickness of the meconium. In newborns with light, moderate and thick meconium in the amniotic fluid the instances of MAS were 0.3%, 5.8% and 61% respectively. Of those babies who did develop MAS 52% experienced metabolic acidosis, 2% had air leak syndrome, 2% had persistent pulmonary hypertension and 0.5% suffered hypoxic ischaemic encephalopathy (brain damage). The mortality rate of babies with MAS was 2%. Newborns with thick meconium were more likely to develop MAS if they were males, small-for- gestational-age, had foetal distress and meconium was sucked from the trachea at birth. (Ref 19).
Ref 14 indicates that it is difficult to distinguish between pre labour and during labour meconium staining of the amniotic fluid. However Ramin et al conducted amniocentesis on a number of women, who were booked for planned elective caesareans, to test for foetal lung maturity prior to surgery. They compared the blood pH of the meconium group with the non-meconium group. Their study indicated that meconium discovered prior to labour is not necessarily a marker for problems with the foetus. They found that 15% (6 babies) of the meconium group and 8% (3 babies) of the non-meconium group had some acidosis however none of the nine babies had a complications. They do go on to say, however, because all the meconium babies were delivered promptly they cannot say that intervention is not necessary. (Ref 15)
Death. Deaths of the foetus during labour are not all caused by hypoxia. Ref 7 indicates that:
"Further progress in eliminating antepartum and intrapartum deaths will only be made when it is accepted that, even with intense investigation by detailed autopsy, the cause of many deaths remains unknown. Many of these deaths may be ascribed to hypoxia. In the future, with more detailed non-invasive probing with CAT scanning and magnetic resonance imaging, other causes may be determined. "
References: