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

    Facts:

    The patient, age 43, presented to the emergency room at Defendant Hospital on 9/4/12 for confirmation of pregnancy diagnosed with an at-home test and for prenatal care. She already had 2 children1. Exam revealed a well-appearing, well-nourished female in no apparent distress with a closed os and no vaginal bleeding. A sonogram confirmed an intrauterine pregnancy, and lab work was positive for an early pregnancy and a urinary tract infection. The patient was discharged to home with antibiotics and Zantac (for acid reflux) and instructed to follow up in the high-risk clinic. 

    Screening by nursing staff on 9/5/12 documented the last menstrual period as 7/21/12 and an estimated date of confinement (EDC) of 4/27/13, with a current gestational age of 6w4d. Cervical length was normal. The patient’s pre-pregnancy weight was 142 lb. Urine HCG testing was positive and a maternal quad screen was positive for Down syndrome.2 The prenatal course was also noted to be significant for a low-lying placenta. The record stated that the patient wished to continue her pregnancy and declined amniocentesis.

    On 9/24/12, the patient was 9w2d pregnant, weighed 141.5 lb and her blood pressure (BP) was 103/64. Exam revealed a fundal height of 9 cm. Fetal well-being was reassuring. The patient was reported to be at risk due to hypertension and cholestasis (believed to be from previous pregnancy). Because of her advanced maternal age, she was again referred to the high-risk clinic. She was started on ferrous sulfate, folic acid and prenatal vitamins. Prenatal testing appeared to be within normal limits. 

    On 10/2/12, the patient’s chest x-ray was negative for active tuberculosis. She was evaluated by genetics on 10/13/12 and the age-related risk for fetal aneuploidy was 1 in 30. The benefits/limitations of the maternal serum screen and fetal anatomy ultrasound were reviewed with her and she again declined amniocentesis. 

    The patient was evaluated in the high-risk clinic on 10/18/12 by Dr. A. At 14w1d both fetal activity and fetal heart beat were present. The patient was scheduled for a follow-up sonogram in 1 week and re-dated by sonogram to 12 weeks.  

    On 10/20/12, a maternal quad screen was positive for Down syndrome and negative for open neural tube defects. On her return to the genetics clinic on 11/7/12, the risk of Down syndrome was noted to be more than 1 in 10.  Amniocentesis was again discussed and the woman declined.

    At 18w1d, the patient was evaluated in the high-risk clinic by Dr. B. A fetal heartbeat and good movement were noted, and cervical length was normal at 4 cm. Pregnancy-induced hypertension labs and 24-hour urine were reported to be normal. Urine testing revealed trace protein. Vaginal progesterone was started due to the woman’s history of preterm birth.

    On 11/29/12, 12/20/12 and 1/10/13, the patient was evaluated by MFM attending Dr. C in the high-risk clinic. On 11/29/12, her cervical length was reported as normal, with fetal and cardiac activity present and fundal height consistent with gestational age. On 1/10/13 Dr. C noted that the placenta was still low-lying and the patient was normotensive. Testing for syphilis was negative and a 1-hour glucose level was within normal limits. On 1/31/13, trace pedal edema and slightly decreased hemoglobin levels were noted by Dr. C and iron supplements were increased.

    Dr. E evaluated the patient in the prenatal clinic on 2/14/13. At 31w1d, the fundal height was 30 cm and maternal BP was 108/61. The visit was normal and without issue.

    NEXT: "On 2/25/13, the patient presented to labor and delivery triage"

    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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