Few crises shake a family like learning a newborn was deprived of oxygen at birth. As Baltimore birth injury attorneys at Schochor, Staton, Goldberg and Cardea, P.A., we, Jonathan Schochor and Kerry Staton, have stood with parents in that heartbreaking moment for more than four decades. Our downtown office at 1211 St Paul Street is five minutes from Johns Hopkins Hospital, yet our reach spans every delivery room in Maryland where preventable harm strikes.
We focus on severe birth injuries because meticulous legal work can change a child’s life trajectory. Multimillion-dollar recoveries we have secured for babies with cerebral palsy, hypoxic-ischemic encephalopathy (HIE), and fetal acidosis fund lifelong therapy, technology, and specialized education.
More importantly, they hold careless providers accountable so other infants stay safe. IIf you suspect medical negligence caused your child’s fetal acidosis, call us at (410) 234-1000 for a free, compassionate case review.
What Is Fetal Acidosis?
Fetal acidosis occurs when a baby’s blood becomes too acidic, typically a pH below 7.35, because oxygen levels fell during labor or immediately after delivery. Without oxygen, cells switch to anaerobic metabolism and flood the bloodstream with lactic acid. The longer this imbalance lasts, the more likely permanent brain or organ damage will follow.
How Does Fetal Acidosis Happen?
Fetal acidosis usually stems from an avoidable interruption in oxygen delivery:
- Umbilical cord compression, prolapse, or knot restricts blood flow.
- Placental insufficiency prevents adequate gas exchange.
- Excessive contractions from mismanaged Pitocin or a prolonged second stage squeeze the cord and uterus.
- Maternal complications such as severe hypotension or diabetes further limit fetal oxygen.
With continuous electronic fetal monitoring (EFM) and timely intervention, often an emergency Cesarean most cases are preventable. When doctors ignore unmistakable distress, families deserve answers.
Warning Signs of Fetal Distress
Abnormal heart tracings are the clearest red flag. Late decelerations, severe bradycardia, or loss of variability signal hypoxia. Reduced fetal movement, maternal bleeding, or meconium-stained fluid can also cause trouble. Labor teams must react within minutes; hesitation can push pH into the danger zone.
Injuries Caused by Fetal Acidosis
Oxygen deprivation during labor endangers every organ, but the brain is most vulnerable:
- Hypoxic-Ischemic Encephalopathy (HIE) may appear within hours and often predicts lifelong cognitive or motor deficits.
- Cerebral Palsy (CP), especially spastic or dyskinetic forms, develops in roughly two of every 1,000 U.S. births involving severe acidosis.
- Seizure disorders, developmental delays, and learning disabilities may surface in early childhood.
- Vision or hearing loss, speech impairment, and behavioral challenges frequently accompany HIE or CP.
Parents face skyrocketing costs—specialists, mobility aids, home modifications—that can exceed $1 million before adulthood.
Rare but Severe Complications
In extreme cases, metabolic acidosis triggers multi-organ failure, kidney injury, or neonatal stroke. Some infants suffer stillbirth or die shortly after delivery. Even when survival is possible, these catastrophic outcomes demand extensive medical and financial resources.
Diagnosing and Treating Fetal Acidosis
Continuous EFM provides the first clue. If tracings deteriorate, clinicians can confirm acidosis by sampling scalp blood in labor or umbilical cord blood at birth to measure pH, base deficit, and lactate. Immediate responses include:
- Giving the mother oxygen and IV fluids.
- Re-positioning to relieve cord compression.
- Halting Pitocin to slow contractions.
- Moving swiftly to operative delivery—often within 30 minutes of persistent Category III tracings.
After birth, babies receive NICU care, therapeutic hypothermia to limit brain injury, respiratory support, and seizure control as needed.
