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    Were these infant’s delays secondary to fetal distress and hypoxia?



    Our MFM felt that the ongoing pattern of moderate and overwhelmingly minimal variability was ominous the longer it persisted. Accepting the fact that this was a 32+ week gestation, he stated that the BPP of 8/8 called for greater observation, earlier use of the MFM and the difficult decision as to whether to deliver several hours earlier. He had no problem with the fact that PGY-1 performed the first BPP. He stated that, because the FHR strips lacked significant variability, the test should have been repeated then or within 1 to 2 hours. That being said, he felt that the fetus had a significant infection throughout the 2 days before birth and that it was the competent producing cause of the significant neurological presentation virtually immediately after birth. He stated that the child was not hypoxic at birth and an earlier delivery would have confronted the same issues. 

    Our neonatal infectious disease expert said that the mother’s pneumonia had nothing to do with the outcome. This baby was born limp and so hospital staff immediately assumed that there was sepsis and the infant was treated clinically and given antibiotics. The drugs were important because he said that they would also treat chorioamnionitis, which was never pathologically proven. He noted that after 10 days of antibiotics, the infant had negative cultures. 

    The expert did not believe the infant had cytomegalovirus or toxoplasmosis because of the sudden onset of fetal inactivity, meaning she was kicking and moving as the mother testified and then suddenly not moving. Those infections don’t usually present with a sudden onset. The infant had a 7.37 cord blood gas recorded approximately 8 minutes after birth, which is not indicative of hypoxia. By 12:12 PM, approximately 24 minutes later, the infant’s arterial blood gas was 7.05, which is hypoxic.  Once damage is done to the brain, there is no chance of reversing it and in this case, the child was hypoxic within a short time of the cord being cut. By the time the arterial blood gas was taken 24 minutes later and registered at 7.05, she already had significant brain damage. However, he saw no signs of an infectious disease process causing neurologic injury.

    Our neonatologist stated that, at delivery, the child was not hypoxic. The maternal cord gas was a normal 7.37 pH. Apparently, as soon as the cord was cut, the child decompensated. He believed that some unidentified condition in utero caused the severe manifestations – gasping, poor heart rate, inability to initially ventilate. He believed that it was this undiagnosed condition that led to the poor outcome with profound neurological impairment. While he was critical of some of the initial treatment of the child upon delivery for causing or exacerbating bilateral pneumothoraxes, he said that did not cause the child’s neurological impairment, as within a relatively short time, parameters such as color, heart rate and blood gas values, and the pneumothoraxes began to improve. He opined that the profound ongoing nature of the neurological impairment goes back to the child’s condition in utero. He stated that this was not a case where “brain cooling” should have been employed.


    Plaintiff’s early demands were in the high 7- to low 8-figure range. After discovery and depositions, a series of mediations were held. Given the difficulties posed by the FHR strips, the lack of an alternative explanation for the child’s decompensation after birth beyond hypoxia and the significant exposure portended by a potential jury verdict, the matter was settled for $2.5 million.  


    1. 1992 twin, premature birth – Philippines – one child survived.  2009 birth; full term; preeclampsia; 7 lbs., 7 oz.; Apgars 9/9.

    2. Again, it should be noted that the post-delivery cord PH was an appropriate 7.37.

    Andrew I. Kaplan, Esq
    Mr. Kaplan is a partner at Aaronson, Rappaport, Feinstein & Deutsch, LLP, specializing in medical malpractice defense and healthcare ...

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    • UBM User
      No hypoxia at birth as documented by a cord gas and immediate neonatal examination essentially nullifies any theory of intrapartum asphyxia. Also, by deduction, and as commented by an expert, the neonatal behavior after cord clamping also suggests a preexisting metabolic or end-organ neurologic etiology. So, was the neurologic impairment CAUSED by the obstetrical team's failure to deliver the patient sooner? At what precise moment did this baby's intrauterine environment become hostile to sustain intrauterine hypoxic encephalopathy? Because this last question cannot be precisely answered, the case was understandably settled. The uncertainty principle favors the plaintiff's theory of causation rather than to provide for a defense. Most importantly is the theorem that our current tort law system fails miserably at any attempt to be reliable, therefore, it would be folly to present this case to a lay jury who, despite instructions to the contrary, would be totally overwhelmed with sympathy for this family. As a result, obstetricians are the default go-to payment mechanism for attempting to right the wrongs of nature.


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