Sample Case Evaluation Reports - Obstetrics Expert Witness
 


Please click on the titles below to go to the corresponding sample Case Evaluation Reports.



Adrenal Gland Adrenalin-Like Secreting Tumor Not Detected in a Symptomatic Pregnant Women, Caused Death of Mother and Baby.

A pleochromocytoma is a tumor of the adrenal gland (next to the kidney) which usually secretes a catecholamine (adrenaline-like) chemical which stimulates the heart to beat faster and harder, causing hypertension which can fluctuate with the amount of catecholamine secreted during the day.

When suspected, it is common to obtain a 24-hour urine collection to measure the amount of catecholamine and its metabolic (breakdown) products. Also, an MRI examination of the upper abdomen is done to see if the tumor is present and its size and location so it can be surgically removed.

In her case, at age 33 she noted more frequent heart palpitations, her heart racing, her vision becoming black, and a severe pounding in the temporal areas of her head. These were worse with exercise. On 7/13 her blood pressure was low normal at 90/72 and she had a 24-hour cardiac monitor (Holter) test which showed episodes of rapid and irregular heartbeat that coincided with her symptoms. But no one had her check her blood pressure at home during the time she was symptomatic.

They never obtained the catecholamine urine test, despite symptoms consistent with episodic hypertension consistent with a pleochromocytoma. Even after they put her on the “beta blocker” drugs (atenolol and then inderal), which block the catecholamine effect, they were not always effective, when the amount of this chemical produced by her tumor exceeded the blocking effect of these drugs. And still no specific tests were done as noted above.

She was next seen on 10/12 and Dr. Rogers of the Hospital Clinic noted: “Since I last saw her, she has continued to experience palpitations on a frequent basis. …They can last for up to a minute in duration. They are frequently followed by some sharp pain in her face and nausea.” Her blood pressure in the office without symptoms was 90/50.

He focused on the arrhythmia, and not this potential cause in the differential diagnosis that he never noted. That, in my opinion, is a departure from the standards of care expected of an Assistant Professor of Medicine, a Cardiologist, affiliated with a medical school. He was part of the “electrophysiology service” and did not see the “big picture” beyond the electrical activity of her heart.

On 10/30 she had an echocardiogram (sound wave study of her heart) that found no anatomical or mechanical problems.

On 1/11 Dr. Rogers saw her again, and noted that the inderal was 80% to 90% effective. Her blood pressure was 114/70, which, for her, was a significant elevation, and he made no comment or follow up.

His last evaluation of her was on 5/10, and she was unchanged symptom wise and her blood pressure was 106/74. He never had her check her blood pressure at home, which is very easy to do manually, or with those semi-automatic devices. However, he did note that her symptoms lasted for 10 minutes (fatigue and lightheadedness) and concluded it was from her PUCs (premature ventricular contractions: arrhythmia), and not from the inderal. Again, he did not do the necessary tests.

Her Obstetricians would reply on the care given by the Cardiologist, and all of her blood pressure recordings on 5/22, 6/22, 7/31, 8/23, 9/22, 10/19, 11/3 and 11/20 were all “normal” between 100-120/70. On 12/1 it was 140/100. The second test of her blood pressure on 12/1 was 154/126 which is grossly abnormal and puts her and her fetus in danger. That is not a value from just rushing there, since it was the second value. Even if it was the first, it was alarming, and they should have contacted her Cardiologist that day. The third value was 140/84 and the fourth was 118/76.

Did she have an interpreter with her that day? Did she have her typical symptoms and did the doctor ask how she felt, and/or did she complain of any symptoms?

On 12/3 she arrived in the Emergency Room critically ill at 1135. She was shocky and had difficulty breathing. At 1157 she was intubated (breathing tube put into her windpipe), and at 1204 her baby was delivered by emergency caesarian section. His Apgar score was 0 out of 10 and eventually they were able to obtain a heartbeat, but he had severe effects of lack of oxygen from his mother’s severe compromised state, and died the next day.

If the Cardiologists were called on 12/1 and they obtained an emergency MRI, based on the 225 gram (7 ounce) size of this large tumor, it would have been found. Possibly urgent surgery (which could take place at the time of the C-section delivery since the fetus was almost 35 weeks [40 is “term”]), its survival would be 98%. Since this was a University Facility, such speed was possible.

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The Defense will contend that the collapse was brought about by the unanticipated hemorrhage into the adrenal gland tumor liberating a vast amount of catecholamine, which caused her collapse and death, despite excellent emergency room care. They will contend, that in their workup (testing), most likely it would take more than a few days, and she was stable and on inderal, which dose they could increase.

However, she was pregnant, and severe hypertension causes uterine arteries to go into spasm delivering less oxygen to the fetus, thus jeopardizing two patients, making the urgency even greater.

On 12/1 in the obstetrical clinic she saw Eddie, a Health Care Proffesional. Was that person a Doctor (at what level of training), a Student, or a Nurse? Was her Obstetrician even notified of her blood pressure results that day? If not, they (that person, her or his employer, and the supervising Doctor) are all negligent.

The autopsy report I saw was the “preliminary anatomic diagnoses.” Obtain the final report which will include all the physical and microscopic findings, plus any laboratory reports.

The laboratory records showed the presence of some germs in the blood, but she had needles into her body, and its pre-mortem accuracy as causation, is in doubt.

The death certificate mentions the cause of death as “Amniotic fluid embolus” (this fluid can enter the bloodstream and cause death), but that death certificate box “#29B: If yes (autopsy), were findings used to determine cause of death” is not checked off for “No” or “Yes.” Therefore the death certificate’s accuracy is questionable. The Physicians are listed as Karen, M.D., S.M. Hospital and Anthony, M.D.

I would suggest Board Certified Experts in Cardiology, Obstetrics, General Surgery, Endocrinology, and Onocology to prepare opinions on negligence, causation and damages (longevity). The Medical Review Foundation, Inc. have these Medical Expert Witnesses on our Consulting Staff and would be happy to continue assisting you with this important case. We await your written authorization to proceed.

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Pulling the Uterus Inside–Out with the Removal of the Placenta.


At age 24 this patient came into the Hospital in labor at 37 weeks on 7/15. She previously had two children and two abortions.

Her condition was normal, except for premature labor at 32 weeks treated with steroids and tocolytic (labor stopping) drug therapy. She was also borderline anemic.

Dr. #1 was treating her in the hospital. He ruptured her membranes (AROM) and inserted a monitor for uterine contractions and for fetal monitoring. He checked her at 1952.

She was encouraged to push, and delivered a healthy male baby at 2003. Who delivered the baby? Who tried to remove the placenta? How much delay was there between the delivery and the attempt of removal of the placenta? Who did it? The “Labor and Delivery Summary” shows that the delivery was at 2003 but that the placenta was delivered at 20--. The Nurses were #1 and #2. The Attending Physician was Dr. #2. The assistants were Dr. #3 and Dr. #1.

At 2012 Dr. #3 was in the room an ordered a narcotic injection. At 2020 the Nurses notes show that the “placenta 90% out. Dr. #3 noted uterine inversion. Dr. #4 paged (who is he?). Anesthesia paged.” 

She was immediately taken to the Operating Room and placed under a light general anesthesia with the drug Ketamine at 2025. The operative report notes that the attending physician was Dr. #2. Was he there? He is responsible for supervising all her obstetrical care. Also noted were the Resident Surgeons Dr. #4 and Dr. #3.

They said: “We were called to see the patient in the third stage of labor (the “delivery” of the placenta), without the delivery of the placenta. The placenta was present in the vaginal vault (vagina). With gentle traction on the umbilical cord, the placenta was spontaneously delivered through the vaginal vault, at which time a uterine inversion was noted. 

Rapid pelvic replacement of the uterus was made, however, reinversion of the uterus could not be obtained.” Then she was taken to the Operating Room where “The surgeon’s hand was placed in the vagina. Gentle steady manipulation was performed until the uterus reinverted.”

The Pathologist noted that this 456 gram placenta was totally removed (“intact cotyledons”). 

The operative report is not accurate. Gentle traction would not invert the uterus. Excessive pulling would do it. Furthermore, the standard of care is to wait a few minutes between the delivery at 2003 until the pull on the umbilical cord is done, to allow the placenta to spontaneously separate. If it does not easily separate, a few more minutes delay should occur. If at that point it does not separate, the obstetrician uses their hand (covered by a sterile glove) to peel it off of the uterus.

Sometimes the placenta grows more deeply into the uterine muscle (placenta accreta) and when not recognized, and excessive (negligent) force is used to pull it loose, the uterus can invert (turn inside out like a sock). Since the placenta was removed intact in one piece, she most likely did not have placenta accreta. 

Either way, the uterine inversion was from negligently used excessive force. Who did it? What was their level of training at the time? Who was at their side (if anyone), supervising and protecting their patient?

They say she lost 1000 c.c. (two pints) of blood. Her hematocrit (packed red blood cell volume) dropped from 35.1 to 21.8. That is a critical level of anemia and consistent with three to four pints (units) of blood loss. Although she was not in documented shock, there may be some kidney damage. This is best assessed by the creatinine clearance test which is a 24 hour urine collection and one blood test. Her Physician can order that inexpensive study at any time.

Otherwise she recovered physically. On 8/23 she was counseled for a tubal ligation operation which took place on 8/26 with the use of Hulka clips, in the standard manner. No pathology was seen in her abdomen or pelvis. 

I suggest that the patient be evaluated by a local Clinical Psychologist with courtroom experience for any residual emotional (psychological) damages. Administration of standardized tests such as the M.M.P.I. (Minnesota Muliphasic Personality Inventory) which have been given to millions of people would further support that opinion before a jury. 

For the reasons stated above, I believe those Physicians and the Hospital which is responsible for its Resident (trainee) Doctor employees were negligent and caused preventable injury including her uterine inversion, massive blood loss, psychological damages as well as potential kidney impairment. It did not cause other problems. 

You may want to get a copy of the contracts between the Hospital and each Doctor, its existing published rules, regulations and standards regarding training and level of responsibility for patient care, particularly regarding obstetrical deliveries as they existed at the time of her delivery. Note that the Resident Doctor year begins on 7/1. How much delivery experience did each have after 15 days into their new year? Her Admitting (in charge) Physicians were Drs. #5 and #1. Dr. #4 (a Resident) was noted by the Anesthesiologist to be in the Operating Room although Dr. #2 was listed as the Attending Surgeon in the typed operative report. Dr. #3 dictated that report. Who was really there?

I would suggest that you authorize us to obtain an Expert review by a Board Certified Obstetrician now, or after you obtain answers to the questions I raised. We await your instructions. 

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Fetal demise at 37 weeks gestation after cervical cerclage suture was removed.

At age 17, she had a miscarriage at 20 weeks gestation. She was offered the option of a cervix cerclage procedure wherein a suture, like a noose, is inserted around the opening of her cervix (mouth of the womb), and she refused. She delivered a fetus which died at birth. It had only a weak heartbeat and was too premature to live.

She stated in that record that she had no previous abortion but when she came under her obstetrical care for the pregnancy in question, she noted she had a previous abortion. The D&C (dilatation and curettage: scraping) abortion procedure can damage the ability of the cervix to remain competently closed for holding in future pregnancies.

The office care was good. Because of a significant concern for an incompetent cervix, she underwent the cerclage procedure at 12 weeks gestation, the standard time to do that procedure. Some Obstetricians would require two previous miscarriages to do this operation, but that is a judgment call issue. In my opinion, it did not contribute to the fetal demise.

At 37? weeks, the cerclage suture was removed in the office, on September 16. That is good care.

On September 20, her blood pressure was normal at 122/82. It was normal in the hospital while in labor, in the operating room and afterward. She did not have pre-eclampsia (high blood pressure, abnormal reflexes and protein in her urine). That was not a cause of the fetal demise.

It is common for labor to begin soon after the cerclage suture is removed. That causes labor pains. It is acceptable for a midwife to assist with obstetrical care.

When she arrived in the Hospital, the Nurses and two Physicians could not identify a heartbeat. The ultrasound confirmed fetal demise. Labor was allowed to continue but she did not effectively progress. She had dystocia (failure of progression of labor). Then an epidural catheter was inserted for pain control and anesthesia.

During her labor, the membranes were ruptured and meconium (green/yellow) stained fluid was seen, consistent with prior fetal distress.

The C-section operation performed on 9/29 at 1505 (3:05 p.m.) by Dr. #1 was properly done, and also found a "heavy yellowish type of mucousy secretion that could possibly be meconium in the uterine cavity" (from a fetal bowel movement in utero from distress).

Her blood sugar was normal. She was not a diabetic out of control, which can cause fetal demise. Her other laboratory tests, looking for a medical cause of fetal demise, were normal.

The autopsy on this 6-pound 12-pounce still-born girl found an "angiomatous malformation" (blood vessel abnormality) of the umbilical cord with some hemorrhage (bleeding) into its flesh. The Pathologist concluded that it was the cause of death (cutting off the oxygen supply from the placenta/uterus). I agree.

The autopsy also noted: "The skin is peeling off over the face, ears, back and extremities." That term is called "maceration." After fetal demise, the dead fetus' skin in the amniotic fluid will become lose in layers and peel. That is a very common finding after hours of fetal demise. Also, the forces of labor (19 hours) will accelerate those changes, unfortunately.

The fetus was dead, and she could not push at the "wrong time." Her pushing only adds some extra force to the uterine muscle firmly compressing the fetus. In this case, she arrived at the hospital with fetal demise already present. They had to induce labor to extricate it because with excessive delay, toxic products could cause maternal demise.

When a patient is in pain and calls the Nurse for pain medication, it should be given in a reasonable amount of time. That delay did not cause any serious injury .

Having a "minister" who is on the Hospital Board Administer some Nursing care or be involved in confidential medical matters is not proper but did not cause injury to the mother.

No matter how incompetent her Obstetrician may have been alleged to be in other cases, in this case, there was a congenital anomaly in the umbilical cord, which unfortunately bled into its substance. It was not injured with the cerclage suture removal or the membranes would have to be ruptured (not possible with a closed cervix, and they were first ruptured in the hospital by Dr. #2 at 4:30 a.m. on 9/29). Furthermore, she had a congenital anomaly in the umbilical cord.

Based on all of the above, as well documented in these records, I do not find substandard care as the proximate cause of this unfortunate fetal demise.

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Ectopic pregnancy diagnosis delayed because of vaginal bleeding but surgery takes place before rupture and hemorrhage.

This patient was pregnant in her right fallopian tube (ectopic pregnancy), had persistent vaginal bleeding, an ultrasound (sound x-ray like study) that was consistent with an ectopic pregnancy and she had emergency surgery at which time the ectopic pregnancy was removed. It was a cornual ectopic (at the open end of the tube) and had not ruptured causing severe pelvic/abdominal hemorrhage and death.

On 4/30, at age 31, with a last normal period of 3/16, she was approximately four weeks pregnant and had vaginal bleeding for two weeks and heavy bleeding for two days. This is consistent with a spontaneous abortion, or a threatened abortion.

The ultrasound study of 4/30 found: "No visible intrauterine pregnancy and no gestational sac, fetal pole or heartbeat is detected." This is consistent with a spontaneous loss (abortion). At four weeks, it is very unusual for an ultrasound to detect an ectopic pregnancy. Sometimes it is seen at six to eight weeks, but by that time it usually erodes through the tube causing bleeding into the pelvis/abdomen and symptoms of severe pain, justifying surgery to remove it and save a woman's life.

On 4/30 the HCG (pregnancy hormone blood test) was 158. This is consistent with an approximate five-week pregnancy.

On 5/3 she came to the emergency room because of persistent vaginal bleeding. The HCG was 167 (no statistical difference) and they "correctly" diagnosed "threatened AB (abortion)." Nothing could be done to save the baby (or the tube to heal normally even if they operated on that date, for which there was no medical justification as viewed prospectively).

Because of persistent vaginal bleeding on 5/13 she was to have a "suction D&C" but because her uterus lining was misshapen by fibroids (benign smooth muscle uterine tumors), Dr. #1 performed the scrape out with the standard curette instrument. The pathologist found no fetus or fetal parts, no placenta (chorionic villi) and no decidua (changes of the uterine lining seen with a recent spontaneous abortion or ectopic pregnancy). Out of caution, the pathologist added: "Clinical correlation is therefore recommended to rule out an ectopic pregnancy." "The microscopic slides preparation, review and typing of the report was completed on 5/16."

On 5/16 she returned to the emergency room complaining of severe right lower abdominal plain and two episodes of vomiting. The HCG was 201. They concluded she had "abdominal cramps." That was a negligent diagnosis. An ectopic pregnancy should have been first on their differential diagnosis list, and an ultrasound study followed by surgery should have occurred without delay.

On 5/19 at her office visit she had "pink vaginal discharge." "Complaining of slight cramping." This was abnormal but not to the level where he would be negligent, and it would not have made any difference in any event.

On 5/23 she was worse, had an ultrasound that was suspicious for an ectopic pregnancy with fluid (blood) in her lower pelvis. The HCG was 106 and because of that ultrasound and her physical examination pain ("clinical correlation") emergency surgery took place, removing the cornual ectopic pregnancy by opening up the end of the fallopian tube (linear salpingostomy), and removing her appendix, which was inflamed at its tip (it was not appendicitis), and had to be excised.

The left fallopian tube was normal, as were both ovaries (cystic changes are normal findings), therefore, her fertility is 80% of before. There is a small risk of a recurrent ectopic pregnancy because Dr. #1, following the standard of care, did not remove the right fallopian tube.

She healed and did well except for her misplaced upset against Dr. #1.

Even if the surgery would have taken place on 5/16, or even two weeks earlier (for which there was no justification), there would be no provable (by reliable expert testimony) difference.

She was fortunate that she only had a small amount of internal bleeding, did not go into shock, develop kidney failure or die.

There was obvious hostility with her husband noted on the record, and a one-hour delay to remove her appendix, caused by his demand for it to be done by another Surgeon at that same ectopic pregnancy operation.

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Uterine bleeding and premature labor at 26 weeks not properly treated, fetal distress with delayed delivery, resulting in brain damage.

This patient delivered a baby boy on two years before and had no prenatal care. That delivery was uneventful. The placenta (after-birth) was normal.

She saw Dr. #1 at his clinic on 3/19. She was pregnant and wanted to know how far advanced she was. She bled for two days in October, November and December. That was abnormal. She was 16 years old. They concluded that based on the physical exam she was 16 to 18 weeks pregnant. An Obstetrical ultrasound (sonogram) was ordered to "get an exact size on the fetus". No further obstetrical care was done and should have begun in this high-risk (teenage, with earlier bleeding) pregnancy.

She returned on 3/25 and saw a Family Nurse Practitioner (FNP) #1. She was "complaining of lower abdominal pain that she describes as sharp and knife-like times 24 hours. This is relieved by fetal position and exacerbated by erect position. Patient denies difficulty with bowels and bladder". The patient was discussed with Dr. #1 and she was noted to be a "high risk pregnancy". The urinalysis test said "leukocytes (white blood cells) moderate". But the urine was discarded before any microscopic exam could be done. Was this a sterilely collected mid-stream clean catch specimen? She had no bladder symptoms and did have sharp pain relieved by position. This is not consistent with a bladder infection.

Pain in pregnancy is pathologic. This is consistent with an abruptio placenta: separation of the placenta from the uterus (womb). Dr. #1 should have seen and examined her under all these circumstances, and that failure is negligent. An urgent ultrasound should have been obtained and the patient should have been advised that if there was any bleeding, to go to the hospital without any delay. She was given an antibiotic for the presumed urinary tract infection, and prenatal vitamins. The ultrasound was scheduled for the next day.

That obstetrical ultrasound showed her pregnancy to be 24.4 + 1.8 weeks. The fetus including her brain was normal. There were no brain cysts.

She developed vaginal bleeding since 4/5 and went to the Hospital #1 Emergency Room where she was in labor, and uterine contraction (labor) preventing (tocolytic therapy) medication was begun (magnesium sulphate and terbutaline) without effect, and she was transferred by ambulance to the Hospital #2. On the way, her amniotic membranes (bag of water) broke. She was in active labor.

Tocolytic therapy medication is effective only in early labor before the cervix (mouth of the womb dilates more than 2 or 3 centimeters) and before its thickness thins out (effacement). The earlier the better.

I do not have the records from Hospital #1 on 4/7. Please obtain them. They began tocolytic therapy. When she arrived at the Hospital #2 they noted that there was a spontaneous rupture of membranes (SROM) at 1345, and she had contractions every 2 to 3 minutes. That is strong labor. Uterine contractions can cause abruptio placenta (the placenta separating from the uterine wall with clots beneath), or labor can be caused by abruptio placenta. Her cervix was dilated to 3 centimeters (one inch = 2.54 centimeters) and was 100% effaced.

The fetal heart rates were in the distress range (outside 120-160), especially low: it was below 80 to over 180 at 1412 (2:12 p.m.). This requires an emergency delivery, and since the fetus was in the breech (buttocks first) position, a C-section operation was safer, and with her consent was done at 1440 with the delivery of the premature baby at approximately 26 weeks gestation, weighing 915 grams, at 1447. The Pediatricians were in attendance and gave good care. The Apgar scores were 1 at one minute and 7 at five minutes. They are low, but are only valid for a full term (40 week) gestation.

Both the mother and baby received antibiotic therapy because at surgery they noted "purulent fluid," consistent with infection. They also noted "evidence of abruption behind the placenta."

Their obstetrical ultrasound just prior to delivery did not show any abruption. The amniotic fluid was severely decreased from the ruptured membranes. It also noted "fetal growth is not appropriate for this gestation," although the Pediatricians found this premature newborn to be normal (AGA = at gestational age).

The Pathologist confirmed the abruptio and presence of infection: "three vessel vasculitis" and "marked deciduitis and focal chorioamnionitis."

The premature baby had respiratory distress syndrome (RDS) from her immature lungs and was on a respirator for a few days.

Ultrasound studies of her brain and a MRI of June 9 found "Frank macrocystic encephalomalcia in the posterior right parietal and occipital lobes corresponding to the ultrasound report." In my opinion this loss of brain flesh replaced by fluid filled cysts was related to her fetal distress.

At 13 months of age there were substantial delays even when computed for her "corrected age." Adoptive and cognitive skills delay 7% -24%, and "may become more severe." Her gross motor delay was 60%, her fine motor skills were a 23% delay, language skills were a 32% delay, and her personal and social capability had 23% to 32% delay.

She received special education home care and made some progress, but still had major deficits.

The purulent fluid (pus) seen in the uterine cavity and infection of the placenta would be consistent with the amniotic fluid leaking for more than one day. The germs from her vagina would contaminate the uterus with the membrane sterile barrier broken. That infection would cause uterine irritability leading to premature labor. With only leakage the patient would be hospitalized, placed on bed rest, monitored, and given antibiotic therapy. That would increase the chance for sealing, not becoming infected, and allow the pregnancy to continue. The more weeks that pass, the greater the chance for an uncompromised baby being born.

With monitoring, if there was any fetal distress, urgent transfer to a high risk center (or transfer there initially for monitoring), and a timely C-section would take place without the fetus being subjected to the extremes it sustained which caused her brain damage.

Bleeding in pregnancy is not normal. It is consistent with an abruptio placenta. It is an obstetrical emergency.

According to the Statement of Facts, she began bleeding on 3/28, called Dr. #1 at his clinic and got an answering machine. They have a duty to be available to their patients. When no one returned her call she called Hospital #3 and they refused to see her without pre-approval from Dr. #1. All three health care providers are negligent.

On 3/30 she spoke to FNP #1 and was told she was "OK." That is negligent care by FNP #1 and her employer.

Her mother called his clinic on 4/1 and was told that "bleeding is ok." Further negligent care.

Then she continued bleeding until the delivery. All this put the fetus at risk.

The Hospital #2 record confirms that she had a "history of (h/o) intermittent bleeding over the past 1 1/2 weeks." And that the "Patient presented to Hospital #1 at 0900 hour this AM with complaints (c/o) painful CTXs (contractions) q (every) 2 minutes which started early this AM."

Even if the tocolytic therapy would have failed, the fetus would have been delivered without being subjected to prolonged stress. But it had a chance of functioning if started very early, or, with bed rest and antibiotics, there would have been a chance that the leak would seal and the pregnancy continue.

For all the reasons stated above, it is my opinion that FNP #1, Dr. #1, his clinic and Hospital #3 were negligent, and their negligence was the proximate cause of the brain damage of this newborn baby.

Obtain the Hospital #1 records. Also obtain copies of the fetal monitor strips at both hospitals, and all the ambulance records.

Also obtain copies of both obstetrical ultrasounds for review by Obstetrical and Radiology Experts. After their review I recommend that we obtain a review of these records by a Pediatric Neurologist to comment on causation.

What is the specialty of Dr. #1? If he is not an Obstetrician I also suggest a review by an Expert in his specialty, even though he was functioning as an Obstetrician.

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Fetal distress with negligent delay in cesarean section delivery, causing increase of risk of premature newborn intra-cerebral hemorrhage.

There is no question that this child sustained severe brain damage. I reviewed all the documents and will give you my opinions below.

The office records reveal that she was a patient who in the past had received birth control pills. She delivered a healthy girl weighing 5 pounds 4-1/2 ounces four years earlier. She had routine office care and a normal delivery.

The next relevant records were from her delivery two years earlier when she delivered a healthy 5 pound 9-3/4 ounce girl. The diabetic screening was negative and the office care, hospital care and follow up was normal. The records reveal that she was a smoker both during this pregnancy and the previous one, as well as the one in question. Smoking does increase the risk of intrauterine growth retardation, which, in fact, was one of the problems with the previous pregnancy.

According to the office records, two years later, the patient had the injectable medication, Depo-Provera, on February 9, after the serum pregnancy test performed the day before was negative. The laboratory did positive and negative controls, according to the documents supplied.

Then, she had symptoms consistent with pregnancy and on March 14th had a positive urine pregnancy test. This was confirmed by a positive serum pregnancy test on that same date. Although it would be negligent to use Depo-Provera in a patient who was pregnant, having a negative serum pregnancy test would allow the physician to, in fact, assume the patient was not pregnant, and give her that birth control medication by injection form. In any event, in my opinion, that would not cause the type of brain damage that was found in this case.

The patient also had a history of chronic pelvic pain, but that is not relevant to the subsequent events. That might be a cause for infertility, which is not what this case is about.

That year, the record shows she was smoking one-half a pack of cigarettes per day. There were no other risk factors, and she had a benign pregnancy until August 22, when she was 31 weeks pregnant by dates. The records show that she fell down the steps the previous night, but there was no bleeding. The physician correctly ordered a nonstress test on a weekly basis.

On August 22, she underwent the first nonstress test. Her blood pressure was normal at 118/70. My review of the records is consistent with their interpretation showing good variability. Every few seconds the fetal heart rate would change. This is what is seen in a healthy fetus and is consistent with a healthy brain and no stress to the fetus. The nonstress test does not use any stimulation with the hormone drug, Pitocin, to cause uterine contractions. The nonstress test was ordered to be done weekly because the weight of the fetus was small for gestational age (SGA). In my opinion, this does meet the standard of care.

On August 30th there were some red flags. Her blood pressure had risen significantly to 130/90. This was not repeated in the obstetrical outpatient record at Hospital #1, and in my opinion, that would a departure from the accepted standards of care. The record also shows that the mother was upset and "states baby has not moved times two days."

Furthermore, the beat-to-beat variability was poor. I agree. It shows a very blunted, rather straight-line record at about 160-150 beats per minute. All this, in my opinion, is ominous. Even if her blood pressure would have returned to normal, the fact that this fetus had not moved for two days, and that the beat-to-beat variability was extremely poor, and the fact that Dr. #1 was notified, in my opinion would require immediate hospitalization and further intervention.

The nurses' notes show that the patient felt the baby kick twice and that there was some more fetal movement during this recording. However, the significant abnormality with regard to beat-to-beat variability, in my opinion, required some immediate investigations, which would include hospitalization.

In my opinion, they should have had the ultrasound biophysical profile study performed. However, Dr. #1 ordered that the nonstress test (NST) be repeated the next day on August 31st, and on that day, they should do a BPP (biophysical profile study).

When she returned on August 31st for that additional evaluation, the record says, "States still has felt no movement." Her blood pressure taken twice this visit was normal at 110/70 and 110/60. The X-ray Department called them and told them that there was no ultrasound available that day because the technician was ill. Certainly there must be one additional person capable of performing the study. This was a very serious problem because on August 31st, there was still no beat-to-beat variability. This puts great stress on the fetus and increases the risk of multiple complications, including that of intracerebral hemorrhage. The patient was admitted to the hospital that day.

Dr. #1 noted in the history, "The last nonstress test a week ago showed reactive patterns, but on nonstress test on August 30th, it showed straight line without much variability, no acceleration, with infrequent fetal movement. The plan was to repeat nonstress test the next day. The nonstress test on 8/31 showed the same findings, nonreactive. OCT (oxytocin: Pitocin) followed, which showed positive means, continuous late deceleration with uterine contraction. Biophysical came 2 of 8 from the amniotic fluid pocket, but generally the amniotic fluid itself was minimal. The fetal breathing or fetal tone were all negative. With all this fetal distress, emergency section was elected, after using steroids for the fetal lung maturity, the positive or negative side of this steroid use was fully discussed with the patient."

The above is not quite accurate. The biophysical profile was performed on September 1st, not August 31st, and it was on September 1st that the patient was taken to the operating room for the Cesarean section operation. And steroid use is controversial and not usually effective.

The placenta did not reveal any rupture, and had some changes consistent with some premature aging with fibrosis (scarring) and placental infarction (gangrene). In my opinion, the placenta was not that healthy, and it caused the intrauterine growth retardation. This fetus was in a very unhealthy environment, confirmed by the very abnormal nonstress test on August 30th. It was not until two days later that the Cesarean section operation took place.

With regard to the test performed on August 31st, Pitocin was begun at 11 a.m. Decelerations were noted. This is ominous. With uterine contractions, the fetal heart rate should not fall significantly. This is consistent with a stressed fetus. The nurses' notes clearly show, as does my interpretation of the fetal heart monitor, that there was consistently very poor variability.

Despite this, throughout the night being unchanged, including minimal variability and decelerations, it is only until 8:06 in the morning that the ultrasound biophysical profile was completed and the decision for a Cesarean section was made. The patient was taken to the operating room at 11:30 a.m.

Following Cesarean section, the mother initially did well. Unfortunately, she was rehospitalized from September 19-26 because of deep venous thrombosis involving her left leg. This was properly treated with anticoagulation (blood thinning medication), and the next year, the study for blood flow and venous thrombosis was negative. In my opinion, the negligent delay in performing the Cesarean section for the baby did not affect the risk for the mother developing the deep venous thrombosis.

The approximate gestational age by dates of the newborn delivered by Cesarean section was 32 weeks. The breathing was abnormal in that there was grunting and retractions (sucking in of the flesh secondary to difficulty in breathing in the air), and that, plus the x-ray findings consistent with granular-type changes in the lung, made the appropriate diagnosis of respiratory distress syndrome (RDS).

The baby's initial blood sugar when the transport team was called was approximately 90 mg percent; this is normal. However, in a stressed obstetrical delivery, the blood sugar can drop dramatically, and can cause diffuse brain damage. When he arrived at Hospital #2, the blood sugar (glucose) was 29, and they immediately gave the baby intravenous bolus (a large, quick dose) of sugar (D10W). This is proper care, and in my opinion, the blood sugar did not drop to that dangerous a low level (generally under 20) to cause diffuse brain damage, and this child did not have diffuse brain damage. Furthermore, the oxygen values reported are numerous arterial and capillary blood gases, and in my opinion, always were within the safe range. This child did not suffer brain damage, in my opinion, from low oxygen levels after birth.

During the Cesarean section operation, there was a very small amount of amniotic fluid, but there was no meconium staining. Often with fetal distress, the fetus will have a seizure in utero and have a bowel movement in the amniotic fluid, which turns it green (meconium). That was not found here.

The umbilical cord was not described as having any knots, neither by the obstetrician or the pathologist. In fact, the umbilical cord is described as normal with no knots or strictures within. In my opinion, the umbilical cord was not the cause of any problem to this fetus, but the placenta, as I described, was insufficient in its health, in my opinion, to fully sustain the pregnancy.

The newborn premature baby was described neurologically as "normal," and the Apgar score at one minute was 5, and at five minutes was 7. These are reasonably good values. The Apgar scores are for 40-week (full-term) babies and premature babies usually have a significantly reduced Apgar score. It was the examination by Dr. #2, at Hospital #2, that described the neurological exam as intact for age and the estimated gestational age at 32 weeks.

In my opinion, the care at Hospital #2 was good. This newborn baby did have abnormalities with its clotting studies, with an elevated prothrombin time and activated partial thromboplastin time (PT and APTT). Also, the platelet count and fibrinogen was depressed, and because of that, he did receive proper blood transfusions with the use of platelets, cryo-precipitate (blood clotting components) and plasma.

In my opinion, the newborn had sustained fetal distress of a moderate degree secondary to the impairment of the placenta as confirmed by the nonstress test and the oxytocin challenge stress test, significantly increased the risk for this newborn baby having a bleeding dysfunction.

Because of that bleeding problem, there was hemorrhage into the brain. This was confirmed by cerebral ultrasound studies.

On September 6th, there is a mention that there was an abnormal wrist position, etc., and they were going to ask the occupational therapist to evaluate the patient's tone of movement in the morning. That is the first note that I can find of any neurologic abnormality.

On September 6th, there was an ultrasound of the brain which says, "Five-day-old male who had tension pneumothorax (a collapsed lung that was timely recognized and treated with a chest tube) this morning and now has developed sluggish and asymmetric pupils and right upper extremity seizure-like activity." Therefore, it would appear that something happened on September 6, which was an acute neurologic change. This ultrasound of the brain revealed hemorrhages within the brain. There was blood clot and hemorrhage within the substance of the brain, including both frontal regions, and more extensive on the right, which would cause the seizures and neurlolgical changes. There were some cystic (fluid-filled) changes within those areas, and it says, "The findings are worrisome for extensive periventricular leukoencephalomalacia."

A repeat ultrasound of the brain on September 8th showed the previous hemorrhage with no additional changes. On September 11th, another ultrasound showed "continued evolution of bilateral periventricular leukomalacia with interval formation of several cysts."

On September 18th, another ultrasound compared to September 11th showed further progression. In the frontal lobes, there were areas of necrosis (gangrene) developing. There was further progression on the ultrasound on September 28th.

On November 27, the ultrasound showed "extensive bilateral periventricular leukomalacia, right greater than left and more marked in the frontal regions." This was at three months of age.

An MRI of the brain with no contrast on at 11 months of age confirmed all the findings of the previous ultrasound. All this was related to the hemorrhage within the brain.

In my opinion, the substantial brain damage of this child is related to the hemorrhage within the brain. In my opinion, there was negligence by Dr. #1 in not interceding on August 30th, and certainly by August 31st. He waited an additional two days from the first significant evidence of a severe problem to perform a Cesarean section operation.

If he was relying upon the ultrasound technician who was ill that day to perform the biophysical profile, and if the hospital was unable to supply an alternate technician, then in my opinion, the hospital would also be negligent.

This was a fetus that was in a very stressful situation. The mother also noted the absence of fetal movement, which is pathologic, and despite all of that, there were substantial delays in performing this Cesarean section operation. In my opinion, the fetus kept in that stressful environment for those extra two days was placed at greater risk for further complications developing, which would include the intracerebral hemorrhage, despite proper care at the Hospital #2.

At birth, on September 1st, it notes that the baby was given "Aquamephyton 1 mg." This is the correct medication to give a newborn to decrease the risk of hemorrhage. This is vitamin K, and it helps the liver produce the clotting substances. But in a stressed fetus, there are biophysical changes in the body that do increase the risk of intracerebral hemorrhage.

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Post-partum (after delivery) bleeding and question of a retained placenta (after-birth).

This 18-year-old girl previously had a vaginal delivery and became pregnant again. The obstetrical sonogram (ultrasound) on 3/3 showed a viable fetus estimated to weigh 264 grams and the placenta (afterbirth) was unremarkable.

She miscarried and delivered a non-viable fetus at home seven minutes before the ambulance arrived. In the hospital they described the fetus as otherwise normal and "the fetus and placenta were intact."

The Pathologist examined the specimens and noted the fetus weighed 225 grams and the placenta weighed 195 grams and measured 12.5x11.5x2 cm (one inch = 2.54 centimeters). The "placenta is ragged and torn". However, the normal appearance of a placenta has very irregular borders.

She stopped significant bleeding and appeared otherwise normal during her hospital stay.

Because, after she went home, bleeding persisted, there was concern for some fragments of retained placenta (products of conception). An ultrasound on 4/22 was consistent with that diagnosis, so she underwent a D&C (dilatation and curettage: scraping of the uterine lining) on 4/22.

At surgery they found "a moderate amount of blood with minimal amount of products of conception". The pathologist who found only 4x3.5x0.6 cm flesh also confirmed this and microscopically there were "focal areas suggestive of retained products of conception".

She did well and was sent home.

I find no departures from the standards of care.

The placenta was evaluated and found "intact".

When bleeding persisted she had an indicated D&C which found only minimal areas suggestive of small pieces of placenta. This was not a large piece missed, which would be negligent. There will probably be no damages for her future fertility.

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