SERVING MARYLAND AND WASHINGTON DC

Case #4014 Delayed Cesarean Section Causing Hypoxic Brain Damage

$3,950,000

On January 10, at 39 weeks 5/7 days gestation, the Plaintiff, then a 35 year old, began to experience vaginal bleeding at home which began at approximately 12:00 p.m.  She called an ambulance, and was taken to Mercy Medical Center.  She reported a 25 minute history of abdominal pain and bleeding.  En route, EMS documented that she soaked two pads with frank bright red blood.  Her blood pressure was documented as 130/90 with a heart rate of 110.  According to the EMS records, the ambulance arrived at the hospital at 12:45 p.m.  There were no emergency room records documenting the Plaintiff’s arrival.  However, hospital notes indicate that the Plaintiff arrived in the labor and delivery department from the emergency department at 1:10 p.m.  Fetal heart monitoring was applied and an ultrasound revealed no placenta previa.  Speculum examination demonstrated brisk bleeding form the cervical os, 4-5 cm dilatation, 100% effacement, and the baby at the 0 station.  Fetal monitoring revealed a heart rate of 90s-60s.  A STAT cesarean section was called, and the patient was transferred to the operating room.  The senior resident reported that the time elapsed from his initial evaluation to skin incision (1:40 p.m.) was 15 minutes.

The Infant Plaintiff was delivered at 1:41 p.m. via emergent cesarean section for suspected placental abruption.  His APGAR scores were 1 / 4.  Operative diagnosis was large volume placental abruption with large retroplacental clot.  He demonstrated no respiratory effort at delivery, and was intubated in the delivery room (weaned to room air on DOL # 1).  The Infant Plaintiff’s initial cord gas revealed a pH of 6.8 and a base deficit of -30. Upon his arrival in the NICU, the Infant Plaintiff was observed to be seizing, and phenobarbital was started.  An MRI of the brain, performed on January 12, 2005, demonstrated findings worrisome for recent ischemia involving the bilateral basal ganglia, thalami, and cortex.  EEGs were indicative of encephalopathy.  The Infant Plaintiff sustained an hypoxic ischemic encephalopathy due to oxygen deprivation from the placental abruption and has been left with spastic diplegia as well as speech and language delays.

The Plaintiff alleged that the Defendants negligently delayed transferring the Plaintiff from the emergency room to labor and delivery, thereby delaying the necessary cesarean section and causing hypoxic brain damage.

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