Family of Boy with Permanent Brain Damage Recovers over $10 million – Substandard Care and Delay in the Treatment of Severe Neonatal Hypoglycemia by Negligent Doctors and Nurses
Mom became pregnant with her first child, a boy.
Following her pregnancy, mom went into labour and presented to hospital at around 02:10.
When mom presented at labour and delivery, she was examined by nursing staff who were also responsible for assessing the fetal heart rate (“FHR”), an important indicator of a baby’s overall wellbeing.
Upon conducting the FHR examination, Nurse F. noted periodic variable decelerations but failed to notify the doctor of these irregularities in the fetal heart tracing.
At 03:45 Nurse P. documented the continued presence of variable decelerations and minimal variability in the FHR. Nurse P. similarly did not notify the doctor of the non-reassuring tracing, nor did she perform any nursing interventions in an effort to restore normal oxygenation to the baby.
At 04:50, Nurse P. noted that decelerations were occurring more frequently and the doctor was finally informed. The doctor attended and performed a vaginal examination before rupturing the membrane, which revealed meconium (baby’s feces/stool). The doctor confirmed that there continued to be variable decelerations in the FHR and grew concerned that there may be fetal distress, subsequently recommending an emergency caesarean section. At 05:25, mom was transferred to the operating room.
Baby was delivered at 05:53 and was very depressed at birth. He was floppy, had no respiratory effort, and there was no cry.
There were no reported abnormal events during the pregnancy or with the fetus in utero.
At 06:10, baby was admitted to the Special Care Nursery for postpartum care where he would stay for 35 days.
On day 1, Nurse M. documented that baby’s initial glucometer reading was low and sent a sample to the lab for determination of the White Blood-Glucose. At 06:51, Nurse M. received the lab results and notified a doctor, who ordered treatment with intravenous dextrose (“D10W”) and Glucagon infusions. At 07:30, Nurse M. again documented a low glucometer reading. At 07:55, the lab advised Nurse M. that the results indicated a critically low glucometer reading. Nurse M. did not report this lab result to a physician.
Over a period of 2 days, Nurse Q. documented numerous low glucometer readings, a high-pitched cry, weak muscle tone, diaphoresis (sweating), lethargy, scalp edema, and jitteriness. Despite the various low glucometer readings, Nurse Q. failed to send any samples to the lab.
Until day 23, doctors continued treating baby with D10W and Glucagon infusions for persistent hypoglycemia.
The failure of nurses to apply the standard of care and promptly notify the doctor when the non-reassuring FHR patterns persisted caused a delay in medical treatment and contributed to baby’s hypoxic ischemic insult and stress, causing his neonatal hypoglycemia. As a result of this breach of the standard of care, baby was exposed to significant intrauterine hypoxia-ischemia (a reduced level of oxygen [hypoxia] and a decreased blood flow [ischemia] during fetal development) and acidosis (high amounts of acid levels in the blood). This breach was a contributing factor to the persistent neonatal stress hypoglycemia from which baby sustained irreversible brain damage.
More importantly, the doctors were negligent for failing to properly treat baby with the correct hypoglycemia medication, Diazoxide. In fact, it took 3 weeks for physicians to finally make the decision to treat baby with Diazoxide, the definitive and only treatment for hyperinsulinism (a condition that causes abnormally high levels of insulin and frequent episodes of low blood sugar [hypoglycemia]). During the time without the appropriate treatment, baby had multiple prolonged episodes of very severe hypoglycemia. The significant delay in starting the necessary Diazoxide treatment contributed to repeated episodes of hypoglycemia, and in turn, severe brain damage.
Had the doctors and nurses met the standard of care, baby’s hypoglycemia could have been prevented and/or controlled so as to avoid the extent, frequency and persistence of the metabolic dysfunction and associated biochemical abnormalities that occurred.
