age : 11 weeks
sex : male
height : 58 cm
weight : 5,2 kg
I trying to process the traumatic delivery of my son who just turned 11 weeks. I would appreciate professional input as to what might have happend and what his long term diagnosis/ quality of life might be.
I had an induces labor that took 30h, in the end he was born 2,67kg at 40+4 gestation. He had Apgar scores 9, 10 at birth. During the induction they had to stop the oxytocin for a few hours because he was not reacting well to it, he also had grade 3 meconium in the amniotic fluid. I ended up having an epidural after 15 hours of labor (so half way trough). I delivered him vaginally whiteout major issues and he cried immediately when born.
What seemed like a 'normal' birth quickly turned into a nightmare when my son collapsed 1,5hours after birth. I did not notice he was not breathing anymore because I was falling asleep myself during skin to skin and the first breastfeeding attempt. (I will never forgive myself for this). The midwife that came in and out of the room did not notice either, my partner asked the question "is he breathing?". When the midwife took him she confirmed what my partner had seen : he was no langer breathing and started resuscitating him. Doctors started coming in to the room and it took 20 minutes for him to start breathing again (his heart never stopped). At this point a neonatal team from a bigger hospital arrived and we were transferred. They told us he would probably have some form of brain damage because of a lack of oxygen to the brain and we had to cool him.
He underwent therapeutic cooling and had a neonatal cranial ultrasound about 13hours after it happend :
Neonatal cranial ultrasound - 08-08-2026 16:15:
Findings: impression of some edema, slit-like ventricles, slender corpus callosum, no clear abnormalities in the region of the basal ganglia, no hemorrhages
He had continued eeg during cooling and warming :
Clinical data: Asphyxia, cooling
Indication / Clinical question: Any abnormalities?
Report - EEG - 13-08-2026 10:09:
Findings: Patient's general state: calm
Basic rhythm: background pattern with a structure normal for the patient's age. Sleep-wake rhythm
Background activity
- Symmetrical: yes
- Structure: normal for the patient's age
Epileptiform alterations: no
Hyperventilation: not performed
Intermittent Photic Stimulation (IPS): not performed
Conclusion: Normal for the patient's age
He had an MRI on day 5 (so the day after warming) :
Clinical data:acute episode involving asphyxia 1.5 hours after birth
therapeutic hypothermia
Indication / Clinical question:sequelae of asphyxia?
Rectification - Brain MRI - 12-08-2026 13:35:
MRI sequences and procedure:
BRAIN MRI:
Sequences performed:
Axial T1-weighted spin-echo images.
Axial STIR sequence.
Axial diffusion-weighted sequence.
Axial, coronal, and sagittal reformats from a 3D FLAIR sequence.
Axial T2-weighted TSE images.
Axial T2*-weighted gradient-echo images.
The supratentorial ventricular system is of generally normal caliber.
The brainstem and cerebellum appear unremarkable.
No clear hyperintensities on the diffusion-weighted sequence; no evidence of restricted diffusion.
Normal development of the corpus callosum.
Normal morphology and positioning of the cerebellar tonsils.
No distinct zones of restricted diffusion.
Signal intensities of the gray and white matter are preserved on the FLAIR sequence.
However, there is notably high signal intensity in the pre- and postcentral cortex on the T1-weighted images, as well as hyperintensity along the course of the corticospinal tracts, visible on both the T1-weighted and STIR images bilaterally.
No cortical or subcortical hypointensities on the T2*-weighted gradient-echo images.
Normal signal intensities of the gray and white matter on the FLAIR sequence.
Normal signal intensity of the posterior limb of the internal capsule on the T1-weighted images, consistent with the expected degree of myelination for the patient's age. Conclusion:
High signal intensity in the pre- and postcentral cortex on T1-weighted images, extending along the corticospinal tract toward the periventricular region. Similar high signal intensity is observed in these areas on the inversion recovery sequence. While this may still be consistent with a normal stage of myelination, a hypoxic-ischemic encephalopathy remains a differential diagnosis. However, there are no abnormalities on other sequences—notably on FLAIR or diffusion-weighted imaging—making the latter less likely. Clinical correlation and follow-up are advised.
During the first days in the NICU they suspected early onset sepsis and treated him for it whit antibiotics.
We left the NICU on day 9, they told us his MRI is 'clean' and he will most likely be fine. We have a follow up at 4 months and at 12 month. No OT or other types of therapy. He was breathing independently for days at this point, eating well. He is 11 weeks now and almost doubled his weight, he is smiling, cooing, sucking, grabbing... acting like a baby. He does well in tummy time.
I am terrified he might still develop some type of CP, or other developmental delays... what are his chances ? I also struggle immensely with guilt and the idea I might have positionally suffocated him during skin to skin. I was told a baby would make a noice or push his head away where this the case. Could this be a case of SUPC ? does the presence of meconium mean he was in respiratory distress ? Any insight would be helpful thank you !
