When a baby suffers a serious brain injury near the time of birth, his or her parents face significant challenges in their efforts to understand what happened to their newborn. One of the barriers to meaningful information for parents is the sheer number of complex medical terms that are associated with traumatic births and fetal health surveillance generally.
In most cases involving children diagnosed with cerebral palsy after a birth injury, parents will read or hear about the role of metabolic acidosis in the development of hypoxemia, but its meaning is not always readily apparent and can be confusing to parents struggling to meet the extensive care needs of a child diagnosed with a brain injury, such as hypoxic-ischemic encephalopathy.
In general terms, acidosis is an abnormal physiological process not specific to birth injuries that can happen to a fetus in the womb, child, or adult. The abnormal process (acidosis) can result in acidemia – an increased concentration of hydrogen ions in the body decreasing the buffering capacity. With this loss of buffering, blood can become too acidic (usually measured by looking at the pH of an arterial blood sample). While this may sound confusing, the basic idea is that there is a chemical imbalance in the blood rendering it more acidic than it should be.
Acidemia, increased blood acidity (measured as low blood pH), can be caused from respiratory acidosis (abnormal respiration processes) or metabolic acidosis (abnormal metabolic processes). Respiratory acidosis occurs when lungs are not removing enough of the carbon dioxide that the body produces. Metabolic acidosis is be caused metabolic processes not functioning properly, such as (1) increased acid generation (can be caused by respiratory acidosis); (2) loss of bicarbonate (acid buffering system), or (3) diminished renal acid excretion.
The bottom line is that metabolic acidosis results in an imbalance in the body’s acid-base balance that can cause acidemia (increased blood acidity). For the reasons outlined below, metabolic acidosis and resultant acidemia is strongly correlated with a type of brain injury common in cases of obstetrical negligence where the obstetrician does not intervene to expedite birth and the child is born with a pattern of brain damage referred to as hypoxic-ischemic encephalopathy.
Everyone produces carbon dioxide as a byproduct of metabolism (chemical reactions that occur in the body that make energy from nutrients). Most of the carbon dioxide in the body combines with water to form carbonic acid, a process which is essential for regulating the pH of extracellular fluid (acid-base homeostasis). A healthy person’s body transports carbonic acid to the lungs, where it is converted back to carbon dioxide and removed through exhalation.
A healthy fetus produces both carbonic and other acids. When placental circulation is functioning properly, carbon dioxide is rapidly cleared allowing for normal fetal acid-base maintenance. But if placental circulation is compromised, carbon dioxide is not cleared and the carbonic acid levels rise. This lack of clearance is respiratory acidosis, leading to acidemia (increased blood acidity). Since carbon dioxide is highly diffusible, its affect on the blood pH can often resolve very quickly without serious consequences.
Prolonged respiratory impairment can also lead to metabolic acidemia, increased blood acidity from acids other than carbon dioxide in the blood. When not enough oxygen is available for metabolism, the body uses alternative methods to produce energy (anaerobic respiration). This alternative method produces acidic by-products such as lactic acid and ketones. These other acids are cleared very slowly from the fetal blood, meaning that when they accumulate, a more sustained and usually more serious alteration in the fetal blood pH occurs compared to only respiratory acidemia.
There are a number of complications that can cause acidosis in a newborn including:
- an umbilical cord wrapped around a baby’s neck during pregnancy, labour or delivery, cutting off the oxygen supply;
- if the umbilical cord is compressed or twisted, blocking necessary nutrients and oxygen from reaching the fetus;
- if the baby’s shoulders become lodged under the mother’s pubic bone, causing a delay in delivery that could lead to a lack of oxygen;
- if the fetus becomes lodged in the birth canal or is unable to progress from the womb;
- abnormal positioning or presentation of the fetus during delivery.
How Does the Fetus Receive Oxygen?
The placenta functions as the lungs of the fetus. Oxygenated blood is delivered from the mother to the fetus through the placenta.
Sometimes, the delivery of oxygenated blood to the fetus is impaired or interrupted. For example, when the umbilical cord (connecting the fetus to the placenta) is compressed during the process of labour, oxygen supply is impaired. The healthy fetus will withstand some duration of oxygen impairment, but fetal reserves are not absolute. When subjected to severe or prolonged enough impairment of oxygenation, there is a build-up of carbon dioxide (respiratory acidemia) which can then lead to the production of lactic acid and ketones (metabolic acidemia). Remember, carbon dioxide build up can be quickly reversed with exhalation, but metabolic acidemia products are more sustained.
What Happens When the Fetus Doesn’t Get Enough Oxygen?
Babies are incredibly resilient. Even in the womb, the fetus responds to asphyxia (the impairment of oxygenated blood) with something called fetal cardiovascular compensation. In simple terms, when the fetus doesn’t get enough oxygen, it will compensate by redirecting the available oxygenated blood to the brain, heart, and adrenals. This is why, in many cases, obstetricians can intervene and prevent brain damage to a baby during a difficult labour when there is evidence of fetal distress.
If asphyxia persists, sadly, cardiovascular decompensation occurs. In other words, the fetus can withstand a disruption of oxygen, but not forever. This is where we see severe fetal metabolic acidemia with brain damage due to decreased cerebral oxygen consumption and increase in blood acidity.
Why is Acidosis Relevant in Medical Malpractice?
When parents of a baby with cerebral palsy sue the doctor who should have intervened earlier with a Caesarean-section, there will be evidence of metabolic acidemia because any brain injury caused by obstetrical negligence will be caused by oxygen debt that exceeded the fetal ability to withstand the asphyxial event.
In the vast majority of cases, blood samples are taken from the umbilical artery at delivery and are tested for the presence of acidemia (measured in pH). You will usually also see a value called “base excess” which is the amount of acid required to restore a liter of blood to its normal pH. Base excess values are decreased (more negative) when there is metabolic acidemia because of the increased amount of acid already in the blood.
Sometimes, there is a problem with the blood sample and there is no evidence of acidosis available. That does not mean you have no claim, but it does mean you should consult a birth injury lawyer if you are concerned that obstetrical negligence may have caused your baby to be born with a brain injury or with cerebral palsy.