Or a Hypothesis. A very educated Guess. As I have mentioned previously, I sent Joshua's medical records to a Doctor in the US who specialises in HIE. It is all he does... he researches HIE. What causes it, possible treatments etc.
Now, he told me that he cannot be as conclusive as he would like to be, and that is basically because he is limited by the records that I have. Ideally, there would have been a placental pathology done that would have allowed him to rule out issues with the Placenta, but there wasn't, and ideally, he would have liked to see more regular blood gas analysis than what I had, but such is life, and we could only work with the picture that we have. But because of that, he can't guarantee 100% accuracy because there is not solid data for certain things, he can simply extrapolate and hypothesise from the information that he has and his knowledge of the subject.
We spent TWO HOURS on the phone this morning discussing it all. Firstly, he talked me through the results of the neuro-imaging reports.
Firstly, an Ultrasound of his head was done on the day he was born. The results of this were normal. Dr Hill said the main purpose of this ultrasound is to identify bleeds in the brain that would require immediate action. None were found, and that is about the scope of ultrasound imaging... it is not as detailed as other scans like CT and MRI. MRI is the best form of imaging.
Joshua's MRI was done at 5 days old, which, from a clinical point of view, allows enough time to see what damage has occurred. Basically, the explanation he gave me from Joshua's MRI results was that the scan showed abnormalities with the brain signals. They made reference in the report to the Peripheral brain, which he said that his interpretation of that would be the outer layers of the brain were where these signal abnormalities were at their worse, but although affected, the temporal/parietal regions showed less of a problem than the other areas. Overall though, the damage was all encompassing, which he believes is consistent with a generalised decrease in blood flow. Brain damage can also be focal, affecting only a specific area, but in Joshua's case, it was the whole lot.
A CT scan which was done at 5 months of age showed Encephalomalacia in the right parietal region and atrophy/hypoplasia of the frontoparietal regions of both cerebral hemispheres. Encephalomalcia basically looks like cysts in the brain... it occurs because brain tissue has died, and the pockets of dead cells are surrounded by healthy tissue.... the pockets fill with cerebral spinal fluid and appear like a cyst.
The CT report also mentions foci of calcification, some with linear appearances which can indicate brain damage as a result of perinatal intracranial infection. (For example, caused by the mother having Rubella, CMV etc) He said that the radiologist doing the scan is only looking at what he sees and does not take into account the patients medical history, so while this type of damage can be caused by a maternal infection, that was not indicated in my case and the damage is also consistent with a reduction in blood flow, so to disregard the comment regarding infection.
Reduced blood flow is called Ischemia, which is the 'Ichemic' part of the Hypoxic-Ischemic Encephalopathy diagnosis. It is difficult to have one without the other though, since blood carries oxygen, and a lack of blood in turn relates to a lack of oxygen. He believes in Joshua's case that Ischemia was the main problem.
As far as timing of the injury goes, he believes it happened during the labour and delivery period. The biggest indicator of that, is the fact that Joshua was born with a normal head circumference on the 50th percentile. If for example, the problem occurred a month before he was born, we would not expect to see a normal head circumference at birth. Joshua had a normal head circumference which then failed to grow normally in the neonatal period. Indicating that the problem occurred very close to the time of birth. He said it is *possible* for instance that the problem could have happened the day before he was born, but certainly not any greater time frame than that.
The Blood Biochemistry can tell us important things about the state of the newborn. We maintain a particular balance of oxygen and carbon dioxide in our blood all the time, and when something happens to disrupt the balance, the body will try and correct it. He says that the kidneys are actually part of the respiratory system for the fact that they produce bicarbonate or base. When there is a lack of oxygen, the blood becomes too acidic, so the body (kidneys) releases bi-carb or base to try and correct the balance. Base Excess is a number that refers to how much Base is being released to compensate for a lack of oxygen. The more negative the number, the worse it is.
A Base excess of -14 is considered to be a Severe Metabolic acidosis. Joshua's Base Excess at 90 mins of age was -7.2. He said that it depends who you are talking to as to how severe they would say that is. He said from an Obstetric point of view, they would consider -7.2 to be mild acidosis. But what would obstetricians know about brains? A Paediatric Neurologist on the other hand, would consider -7.2 to be a moderate acidosis. Because we do not have Blood gas analysis for anytime prior to 90 mins after birth, we are unable to say with any certainty what his levels would have been immediately after birth, but he believes it is quite likely that Joshua would have had Base Excess levels indicative of severe metabolic acidosis. Another commonly talked about measure is cord gas, or cord PH, which is taken from the blood of the umbilical cord immediately after birth. Anything below 7.0 is considered acidosis. Joshua's cord gas was 7.067. The problem with PH levels, is that they are extremely sensitive to Carbon Dioxide and PH levels fluctuate quickly and easily. So if there is a problem where the baby suffers from a lack of oxygen, but then the situation is resolved, the PH will change very quickly and doesn't give as accurate a picture as the Base Excess does, which is less sensitive to changes.
Basically, acidosis triggers biochemical changes that damage neurons. Under ordinary circumstances, the brain is able to protect itself somewhat by producing enzymes that block the effects of these changes in blood biochemistry. Once a certain level is reached however, the brain is no longer able to protect itself and the enzymes produced by the acidosis begin to attack the brain.
These things can be present for long periods without causing death, however, if it was TOO prolonged then he would have died.
He believes the above is consistent with gradual, episodic reductions of blood flow over time.
A certain threshold is reached where brain damage is inevitable, but the clinical presentation can sometimes be delayed. This was the case with Joshua. He described it like a train leaving a station. When Joshua was born the train (brain damage) had already left the station and we can't bring it back, but we didn't know until we saw the signs.
Typically, the first sign is respiratory depression. Most HIE babies are born with very low apgars and require prolonged resuscitation. This wasn't Joshua. His Apgars were 5 and 8. He was breast feeding after he was born and appeared to be doing well. The next sign typically seen, is seizures. Joshua had his first seizure at about 5 hours old and it was not until this happened, that we knew there was something really not right. Initially, the seizures were explained by low blood sugar, and were not expected to continue after he was placed on a glucose drip. They DID continue. Dr Hill explained to me that as blood carries oxygen, it also carries glucose, so a reduction in blood flow would also cause the low blood sugar levels that Joshua had.
The other information we looked at was to do with Fetal Heart Rate monitoring during labour. It was a drop in heart rate that indicated that Joshua was in distress and prompted us to go to the hospital. At home, we had intermittent monitoring with a doppler, and then on arrival to the hospital, a period of continuous monitoring until he was born. His heart rate was extremely variable. He determined his baseline heart rate to be around 110-130 beats per minute, but it fluctuated greatly, dropping down to 80 beats per minute and staying there for 60 seconds and then shooting back up to 140 beats per minute. He says this variability is also consistent with an episodic pattern of blood flow.
So... What Caused this lack of blood flow? Dr Hill believes that the most likely cause is intermittent, transient umbilical cord compression. Basically, where the umbilical cord becomes lodged between the baby and for example, the mother's pelvis and prevents the flow of blood through the cord. The baby moves and the blood once again flows freely through the cord. The baby moves again, and the cord is once again compressed and blood flow is blocked.
There is one other possible explanation for this kind of episodic problems with blood flow, and that is utero-placental insufficiency. Where basically, the blood vessels connecting the uterus and the placenta are not as healthy as they should be and cause problems with blood flow. Some causes of this can be Maternal diabetes, or pregnancy hypertension. I DID have high blood pressure during my pregnancy, but Dr Hill does not believe that my blood pressure issues were significant enough to have caused a problem such as this. We cannot rule this out with 100% certainty, because there was no placental pathology report done. However Dr Hill believes that this is the least likely of the two scenarios.
The reason for this is to do with the types of heart decelerations observed. There are three different types. Late decelerations are when the baby's heart rate drops at the end of a contraction. Early decelerations are when the baby's heart rate drops at the beginning of a contraction. VARIABLE decelerations are when there is no clear pattern. It is random and the decelerations can be before, during or after contractions.
Joshua's heart rate decelerations were VARIABLE. Variable decelerations are highly associated with Umbilical cord compression, while placental issues are most commonly associated with LATE decelerations.
The other piece of information that supported this hypothesis, is the fact that it was noted in my records that the lowest fetal heart rate was 80 beats per minute with good pick up. He said although the words "good pick up" could be open to interpretation, his definition of good pick up is that the heart rate recovers quickly after a deceleration. This is common with cord compression, but when the problem is placental, a slow pick up is usually observed.
So although we are not able to get a 100% definite answer, he believes the cause to most likely have been Umbilical cord compression.
Umbilical Cord Compression is NOT preventable. Babies have umbilical cords, they do crazy things with them and they move all around everywhere. There is nothing we can do about it. It is quite likely that most babies suffer from a period of cord compression at some time while they are in utero. It is only a problem with the compression is repeated and/or prolonged. That is when brain damage can occur.
Cord Compression is a very common cause of HIE. However, in the general population, it is NOT a common occurrence. There is no way to detect a cord compression other than the suggestion of it by decelerations in heart rate. So essentially, the treatment for cord compression is delivery of the baby, and the only possible way to prevent it is to act appropriately to deliver as soon as possible after problems with the fetal heart rate is detected.
He basically said that the only real guarantee to prevent brain damage from a cord compression was if every woman was on continuous fetal monitoring for her entire labour and delivery and it was able to be detected immediately. This is not standard practice. Women are usually encouraged to labour at home for as long as possible before going into hospital for a hospital birth, so even if I was planning a hospital birth, by the time I went in to hospital, there would likely have already been problems with his heart rate which would have been unknown to me.
Most importantly, he said this is NOT something I have to worry about with a future pregnancy. I can't do anything to prevent cord compression from happening again, it really is just "one of those things". Bad luck if you will. I am at no greater risk of having a problem with a future baby than a woman who has never had a baby with this problem.