I have written about it more times than I care to count.
VBA3C homebirth: ruptured uterus, brain damaged babVBA3C homebirth: ruptured uterus, brain damaged baby
You risked your baby’s brain function for this?
Another homebirth, another brain injured baby, but the midwife was awesome
Unassisted birth: surprise second twin suffers brain damage
Conflicted: successful VBAC, brain damaged baby
He’s a spastic quadriplegic as a result, but she’s glad she had a homebirth
Another unassisted birth, another brain damaged baby
Lest you think that brain damage at homebirth is merely an anecdotal experience, consider that investigators have found that homebirth increases the risk of hypoxic brain injury by more than 1700%.
I read about another such “beautiful birth” just yesterday:
[pullquote align=”right” color=”#e3b03e”]No one can possibly care more about the microbiome or breastmilk than about brain damage, can they?[/pullquote]
The midwife quickly realised Poppy hadn’t turned herself and was shoulder dystocia …
They had to do an episiotomy (with no pain relief..!) Luckily it worked and nearly 4 minutes after her head was born the rest of her came out. She was blue, floppy and unresponsive but had a strong heart rate…
Poppy suffered birth asphyxiation and HIE (Hypoxic ischemic encephalopathy) she was taken to neonatal intensive care where she was placed onto a 72 hour cooling treatment where they wrap a fluid filled mat around the baby and keep them at 34 degrees to give the brain and organs time to repair themselves after being starved of oxygen. She had probes and wires just about everywhere monitoring every aspect of her.
Does Poppy’s mother have any regrets? Of course not. What’s a little brain damage (HIE) compared to a birth experience!
People often ask me if I regret my homebirth because of the circumstances but it has only made me feel like the homebirth was even more right for us. I laboured well at home and was relaxed and in my own environment, I think the panic that would have happened at the hospital would have freaked me out and I’d not have been so productive in pushing. The shoulder dystocia could have happened anywhere and the outcome of treatment would have been the same.
What happened to baby Poppy’s brain when she was deprived of oxygen?
As her brain sensed a decrease in oxygen and an increase in carbon dioxide, she tried to raise her blood pressure to get more blood to her brain. Epinephrine flooded her bloodstream and blood was diverted from inessential organs to the brain, heart and adrenal glands.
A baby can do this for only a limited amount of time and blood pressure begins to fall.
This leads to intracellular energy failure. During the early phases of brain injury, brain temperature drops, and local release of neurotransmitters, such as gamma-aminobutyric acid transaminase (GABA), increase. These changes reduce cerebral oxygen demand, transiently minimizing the impact of asphyxia.
What happens at the level of individual brain cells?
… During cerebral hypoxia-ischemia, the uptake of glutamate the major excitatory neurotransmitter of the mammalian brain is impaired. This results in high synaptic levels of glutamate and EAA receptor overactivation … and kainate receptors… Accumulation of Na+ coupled with the failure of energy dependent enzymes such as Na+/ K+ -ATPase leads to rapid cytotoxic edema and necrotic cell death…
EAAs accumulation also contributes to increasing the pace and extent of programmed cell death through secondary Ca++ intake into the nucleus. The pattern of injury seen after hypoxia-ischemia demonstrate regional susceptibility that can be largely explained by the excitatory circuity at this age (putamen, thalamus, perirolandic cerebral cortex). Finally, developing oligodendroglia is uniquely susceptible to hypoxia-ischemia, specifically excitotoxicity and free radical damage. This white matter injury may be the basis for the disruption of long-term learning and memory faculties in infants with hypoxic-ischemic encephalopathy.
The damage doesn’t end when oxygen levels are restored to normal.
During the reperfusion period, free radical production increases due to activation of enzymes such as cyclooxygenase, xanthine oxidase, and lipoxygenase. Free radicals can lead to lipid peroxidation as well as DNA and protein damage and can trigger apoptosis. Finally, free radicals can combine with nitric oxide (NO) to form peroxynitrite a highly toxic oxidant.
…[A] second wave of NO overproduction that can be prolonged for up to 4-7 days after the insult.
This excessive NO production plays an important role in the pathophysiology of perinatal hypoxic-ischemic brain injury. NO neurotoxicity depends in large part on rapid reaction with superoxide to form peroxynitrite.[11] This, in turn, leads to peroxynitrite-induced neurotoxicity, including lipid peroxidation, protein nitration and oxidation, mitochondrial damage and remodeling, depletion of antioxidant reserve, and DNA damage.
In other words, even a limited period of oxygen deprivation can lead to a cascade of cell death and further brain damage from the extremely toxic products of cell destruction.
What does that mean for the baby?
In severe HIE it can mean:
- Stupor or coma is typical; the infant may not respond to any physical stimulus except the most noxious.
- Breathing may be irregular, and the infant often requires ventilatory support
- Generalized hypotonia and depressed deep tendon reflexes are common
- Neonatal reflexes (eg, sucking, swallowing, grasping, Moro) are absent
- Disturbances of ocular motion, such as a skewed deviation of the eyes, nystagmus, bobbing, and loss of “doll’s eye” (ie, conjugate) movements may be revealed by cranial nerve examination
- Pupils may be dilated, fixed, or poorly reactive to light
- Irregularities of heart rate and blood pressure are common during the period of reperfusion injury, as is death from cardiorespiratory failure
Less severe HIE has less severe consequences, but no one should think that a baby who appears to recover has emerged unscathed.
What does infant cooling therapy do? By lowering the metabolism of brain cells it appears to limit cell death and the release of the toxic products of cell death. It can’t reverse brain damage that has already occurred, but it can limit the continuing damage that inevitably occurs when oxygen levels return to normal.
That’s what happened to baby Poppy, yet her mother seems to think that this is a trivial outcome.
Here’s what I want to know, and perhaps homebirth advocates can explain it to me:
You’re the folks who worry about C-section changing the infant gut microbiome and you are horrified if a baby deprived of the antibodies in colostrum because her mother does not want to breastfeed. Why do you think that is important but oxygen deprivation and brain damage are no big deal?
This raises the ugly possibility that homebirth isn’t about babies and what’s beneficial for them, but about mothers and their bragging right and midwives and their autonomy.
No one can possibly care more about the infant gut microbiome or breastmilk antibodies than about infant brain damage, can they?
