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


    On 2/25/13, the patient presented to labor and delivery triage at 11:40 AM with complaints of a cough and sore throat. Her BP was 109/67, heart rate was 101, and fetal activity was present. At 32w5d her total pregnancy weight gain was 18 lb. At 12:35 PM a nurse noted that the patient’s temperature was 100.3° and the fetal heart rate (FHR) was 182 beats per minute (bpm) with moderate variability. Tylenol was given, an intravenous (IV) was started and observation continued. Lab work revealed a white blood cell count of 19, a potassium level of 3.1 and total protein of 6.3. Chest x-ray revealed mild right lower lobe pneumonia. A sonogram done on admission indicated decreased fetal activity. Antibiotics and dexamethasone were administered. Electronic fetal monitoring (EFM) revealed initial persistent tachycardia and minimal variability throughout the night. The patient was placed on her left side and oxygen and IV fluid boluses were given. Staff monitoring was active and charted.

    At 5:54 PM PGY 3 Dr. F reviewed prenatal labs and presenting symptoms and noted that the patient remained on vaginal progesterone. On exam, fetal tachycardia and a category II EFM tracing were noted. The patient continued to receive ceftriaxone and azithromycin for pneumonia.  An 8 PM nursing note said that the chief resident was notified of the tracing, and IV fluids and monitoring were to continue.

    Evaluation by attending Dr. G at 8:21 PM showed presence of fetal movement with persistent fetal tachycardia and no contractions, vaginal bleeding or loss of fluid. Report on a (presumed) sonogram revealed a vertex presentation, adequate amniotic fluid index and a posterior placenta. It was noted that the patient had a posterior complete placenta previa at 18 weeks, which resolved at 29 weeks. The plan was to admit to the MFM service, obtain a growth sonogram and continue antibiotics and monitoring. 

    A 2/26/13 nursing notes documented continued fetal tachycardia, 160-180s, with minimal to moderate variability. At 4 AM, the RN documented that Chief Resident was “notified the whole night about patient’s category II tracing of having minimal variability and very few accels <10.  At 2:30 AM, by nurse’s note and on the EFM “Remarks,” Chief Resident came to the patient’s bedside and shook patient’s stomach and assessed patient. No orders were given, but to continue to monitor patient including Fetal Heart Monitoring. IVF was in progress at 125 cc/hr.  Dr. G attending was notified as well.” 

    At 4:09 AM PGY1 documented the mother’s vital signs as BP 108/60, heart rate 82, respiratory rate 19 and temp 98.1. EFM indicated 150 bpm with minimal variability, no accelerations or decelerations. A BPP performed by PGY-1 was 8/8. The assessment was fetal well-being reassured in the setting of pneumonia. Nursing documented a category II tracing, and the patient remained on her left side with oxygen.

    At 5 AM an RN documented a FHR of 153 with minimal variability and that the Chief Resident and Dr. G were aware of the tracing. A second dose of dexamethasone was given. At 6 AM an RN documented that Chief Resident was made aware that the patient was having variable decelerations at that time; the “MD” (unknown) evaluated the tracing and no action was needed. At 6:54 AM an RN noted that resident Dr. F, the covering MFM, was at the bedside and assessed the patient and tracing. As per Dr. F, the patient was to have a second official sonogram that morning.

    NEXT: "The 'official' BPP performed at 9 AM scored 4/8"

    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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