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Maternal and Perinatal Death Review Committee – Annual Report 2010

Office of the Chief Coroner for the Province of Ontario

September 2011

Print Version (PDF, 680 kb)


Table of Contents


Introduction
Committee Membership (2010)

Summary of Cases Reviewed in 2010

Case Summaries: Maternal Deaths
Case Summaries: Neonatal Deaths

Case Summaries: Stillbirths

APPENDIX A - Summary of Recommendations

APPENDIX B – Glossary of Terms



This report was prepared by Dr. Rick Mann, Chairperson of the Maternal and Perinatal Death Review Committee and Ms. Kathy Kerr, Executive Lead – Committee Management.


Introduction


Purpose

The purpose of the Maternal and Perinatal Death Review Committee (MPDRC) is to assist the Office of the Chief Coroner in the investigation, review and development of recommendations directed towards the prevention of future similar deaths relating to: all maternal deaths irrespective of cause. This includes all deaths during pregnancy and the post-natal period (which is considered to be up to 42 days after delivery).  Any deaths after 42 days and up to 365 days post delivery are reviewed if the cause of death is directly related to the pregnancy or a complication of the pregnancy.

The Committee reviews stillbirths and neonatal deaths where the family, coroner or regional coroner have concerns about the care that the mother or child received.

For the 2010 review, all cases of maternal deaths, stillbirths or neonatal deaths where care was provided by a midwife, were reviewed by the Committee.

Findings of legal responsibility or conclusions of law are not permitted.

Definition of Maternal, Stillborn and Neonate

The Maternal and Perinatal Death Review Committee reviews the deaths of all women who died “during pregnancy and following pregnancy in circumstances that could reasonably be attributed to pregnancy.” Deaths involving women who are pregnant, but where the pregnancy did not attribute to the death, are noted for statistical purposes only and no formal review is conducted.

The maternal deaths are classified by the following criteria:

  • Antepartum - >20 weeks gestation
  • Intrapartum - during delivery or immediately following delivery
  • Postpartum - < 42 days

This Committee does not review late maternal deaths occurring >42 days.

Stillbirth is defined as the complete expulsion or extraction from the mother of a product of conception either after the 20th week of pregnancy or after the product of conception has attained the weight of 500 grams or more, and where after such expulsion or extraction there is no breathing, beating of the heart, pulsation of the umbilical cord or movement of voluntary muscle.

Perinatal Death is defined as death during, at the time of, or shortly after birth, including home birth and death within the first seven days after birth.

Aims and Objectives

  1. To assist coroners in the Province of Ontario to investigate maternal and perinatal deaths and to make recommendations that would prevent similar deaths.
  2. To provide expert review of the care provided to women during pregnancy, labour and delivery, and the care provided to women and newborns in the immediate postpartum period.
  3. To provide expert review of the circumstances surrounding all maternal deaths in Ontario, in compliance with the recommendations of the Special Report on Maternal Mortality and Severe Morbidity in Canada.
  4. To inform doctors, midwives, nurses, institutions providing care to pregnant and postpartum women and newborns, and relevant agencies and Ministries of Government about hazardous practices and products identified during case reviews.
  5. To produce an annual report that can be made available to doctors, nurses and midwives providing care to mothers and infants, and hospital departments of obstetrics, midwifery, radiology/ultrasound, anaesthesia and emergency for the purpose of preventing future deaths.
  6. To help identify the presence or absence of systemic issues, problems, gaps, or shortcomings of each case to facilitate appropriate recommendations for prevention.
  7. To help identify trends, risk factors, and patterns from the cases reviewed to make recommendations for effective intervention and prevention strategies.
  8. To conduct and promote research where appropriate.
  9. To stimulate educational activities through the recognition of systemic issues or problems and/or:
  • referral to appropriate agencies for action;
  • where appropriate, to assist in the development of protocols with a view to prevention;
  • where appropriate, to disseminate educational information.

Note: All of the above described objectives and attendant committee activities are subject to the limitations imposed by the Coroners Act of Ontario Section 18(2) and the Freedom of Information and Protection of Privacy Act.

Structure and Size

The Committee membership consists of respected practitioners in the fields of specialty including: obstetrics, family practice, specialty neonatology, community pediatrics, pediatric and maternal pathology, midwifery and obstetrical nursing. The membership is balanced to reflect wide and practicable geographical representation as well as representation from all levels of institutions providing obstetrical care including teaching centers to the extent possible. The Chairperson will be a Deputy Chief Coroner or Regional Supervising Coroner or other person designated by the Chief Coroner.

Other individuals are invited to the Committee meetings as necessary on a case by case basis (e.g. investigating coroner, Regional Supervising Coroner, other specialty practitioner relevant to the facts of the case, etc.).

Methodology

Coroners and Regional Supervising Coroners refer cases to the Committee for review. At least one member of the Committee reviews the information submitted by the coroner and then presents the case to the other Committee members. After discussion by the Committee, a final case report is written consisting of a summary of events, discussion and recommendations (if any), intended to prevent deaths in similar circumstances. The report is then sent to the referring Regional Supervising Coroner who may conduct further investigation (if necessary). Recommendations made by the Committee are distributed by the Chief Coroner to agencies and organizations who may be in a position to effect the implementation of such recommendations.

Where a case presents a potential or real conflict of interest for a Committee member, a temporary member is named from another centre. Alternatively, the Committee reviews that case in the absence of the member with the conflict of interest.

When a case requires expertise from another discipline, an external expert reviews the case, attends the meeting and participates in the discussion and drafting of recommendations, if necessary.

Limitations

This Committee is advisory to the Coroner's system and will make recommendations to the Chief Coroner through the Chairperson.

The consensus report of the Committee is limited by the data provided. Efforts are made to obtain all relevant data.

The Maternal and Perinatal Death Review Committee case reports are prepared for the Office of the Chief Coroner and are therefore governed by the provisions of the Coroners Act, the Vital Statistics Act, the Freedom of Information and Protection of Privacy Act and the Personal Health Information and Protection of Privacy Act. As a result, each case review included in the annual report is a summary without identifying details. The recommendations made to the Regional Supervising Coroner and relevant organizations and agencies are included with each case.

It is important to acknowledge that these reports relied upon a review of the written records. The Coroner/Regional Supervising Coroner conducting the investigation may have received additional information that rendered one or more of the Committee's conclusions invalid. Where a fact was made known to the chair of the Committee prior to the production of the Annual Report, the case review was revised to reflect these findings.

Recommendations are made following a careful review of the circumstances of each death; they are not intended to be policy directives and should not be interpreted as such.

This report of the activities and recommendations of the Maternal and Perinatal Death Review Committee is intended to provoke thought and stimulate discussion about obstetrical care and maternal and perinatal deaths in general in the Province of Ontario.

Questions and comments regarding this report may be directed to:

Ms. Kathy Kerr
Executive Lead – Committee Management
Office of the Chief Coroner
26 Grenville Street
Toronto, Ontario
M7A 2G9
Kathy.M.Kerr@Ontario.ca



Committee Membership (2010)


Dr. Michael Dunn

Neonatologist (Level 3)

Dr. Karen Fleming

Family Physician (Level 3)

Dr. Robert Gratton

Maternal Foetal Medicine

Dr. Steven Halmo

Obstetrician (Level 2)

Ms. Susan Heideman

Perinatal Nurse

Dr. Robert Hutchison

Obstetrician (Level 3)

Dr. Sandra Katsiris

Anesthesiologist

Ms. Michelle Kryzanauskas

Midwife (Rural)

Dr. Catherine MacKinnon

Obstetrician (Level 2)

Dr. Dilipkumar Mehta

Paediatrician (Level 2)

Ms. Linda Moscovitch

Midwife (Urban)

Dr. Toby Rose

Forensic Pathologist

Dr. Roger Skinner
Dr. Rick Mann

Chairperson(s)
Regional Supervising Coroners

Ms. Kathy Kerr

Executive Lead



Summary of Cases Reviewed in 2010


This report includes reviews conducted by the Maternal and Perinatal Death Review Committee in 2010. Cases reviewed may involve deaths that occurred in previous years.

Total number of cases reviewed:

41

Total number of recommendations:

83

Number of maternal cases reviewed:

11

Number of maternal cases noted for statistical purposes only*:

6

Total number of maternal deaths:

17

Number of recommendations from the maternal deaths reviewed:

12

Number of neonatal cases reviewed:

19

Number of recommendations from the neonatal deaths:

48

Number of stillborn cases reviewed:

11

Number of recommendations from the stillborn cases:

20

* The Maternal and Perinatal Death Review Committee reviews the deaths of all women who died “during pregnancy and following pregnancy in circumstances that could reasonably be attributed to pregnancy.” Deaths involving women who are pregnant, but where the pregnancy did not attribute to the death, are noted for statistical purposes only and a formal review is not conducted.



Case Summaries: Maternal Deaths


Case: 2010-M-1

History

The deceased was a 29-year-old married immigrant from Sri Lanka. She lived with her husband, two- year-old child and her mother and father in-law. Her past medical history was significant for polycystic ovary syndrome (PCOS), allergic rhinitis, depression and adjustment disorder, gestational diabetes in her first pregnancy and hypothyroidism.

She was pregnant with her second child at the time of her death. She had conceived through the use of assistive reproductive technologies. Her dating ultrasound was done at 6 weeks 2 days with an estimated date of confinement of March 20, 2010. Her last documented visit to her family doctor was on August 13, 2009 for prenatal counseling and thyroid medication adjustment. She was to have ongoing prenatal care and her next visit was arranged for September 7, 2009 at 12 weeks gestational age. On August 31, 2009 she was found hanging in her basement by her mother in-law.   She was transported to hospital by EMS, but was pronounced dead in the Emergency Department.

The deceased had a history of a acetaminophen overdose in 2006 requiring Acetylcysteine and an assessment by psychiatry. This attempt was believed to have been triggered by familial stresses and she was diagnosed with an adjustment disorder. It was noted that she had a history of self cutting. She had disclosed to her family doctor that there were stressors living with her in-laws and issues of parenting styles had been raised. She had received both counseling and parenting classes together with her spouse. There was no mention in the last doctor’s note of August 13, 2009 of any issues with mood or concerns around pregnancy.

Post Mortem Findings

Autopsy confirmed the cause of death as hanging. There was an intrauterine pregnancy of 12-14 weeks gestation with a congenital anomaly in the form of a large cystic hygroma.

 

Discussion

The deceased had a history of a previous suicide attempt in 2006. It does not appear that she had ever been treated with antidepressants. There is no mention in the family doctor’s chart of depression at the time of the August 13, 2009 visit. The deceased apparently had a therapeutic relationship with a therapist who she saw on many occasions around family issues. Her spouse stated that he had not noted any change in her behaviour.  The deceased’s spouse was aware of conflict between his family and his wife, but was shocked by this outcome.

Psychiatric disease is a recognized complication of pregnancy and the post partum period and it is a recognized cause of both maternal morbidity and mortality. This case reminds us of the risks of depression and the importance of including screening questions when assessing both mental and physical well-being.

Recommendations

  1. Obstetrical care providers are reminded that psychiatric disease can complicate pregnancy and can be a cause of maternal mortality.
  2. Obstetrical care providers are reminded that women of certain cultural backgrounds can be at increased risk of social isolation. Screening should assess both the mental and physical well-being of the patient, and should include questions regarding family stressors. Referral to support services should be considered when such issues are identified.


Case: 2010-M-2

History

The deceased was a 39-year-old G7T4A2L2 who was admitted at 33 weeks and four days gestation as an inpatient to the hospital. Although she had apparently been followed in an out patient clinic, there were no clinic records or Ontario Prenatal Records I and II available for review. She had known hypertension as well as gestational diabetes and was on antihypertensive therapy and insulin. She was admitted to hospital because of her increasing blood pressure.

Her past obstetrical history included a term vaginal stillbirth, term live vaginal birth, two spontaneous early miscarriages, a preterm Caesarean section at 34 weeks for pregnancy induced hypertension (PIH) and another preterm Caesarean section at 33 weeks for PIH. This last child died at six weeks of age due to Sudden Infant Death Syndrome (SIDS). The deceased had a history of chronic hypertension, though it is unclear whether she was on medication between her pregnancies. She also had gestational diabetes and was on insulin at the time of admission. The deceased weighed 300 pounds on admission and was 5 foot 8 inches in height.

Her blood pressure was 210/140 on admission and her medications included nifedipine and methyldopa. She was on a diabetic diet having been in the Gestational Diabetes Management (GDM) class approximately 3 ½ months prior to admission. She was assessed by the dietician and she was “following her diet as closely as possible at home.” She was on 44 units NPH Insulin at bedtime (HS) at home until the time of admission with her sugars within normal limits.

She was continued on methyldopa 500 mg, by mouth, four times a day, and nifedipine XL 60 mg per day was added. Labetolol was subsequently added to this shortly after admission and increased to 400 mg three times a day by day three. Biophysical profile revealed a normally growing fetus with normal amniotic fluid volume and cord dopplers. The plan from this point was to monitor blood pressure and glycemic control in anticipation of allowing her to get closer to term before delivery.

Her blood pressure remained labile leading to a prolonged hospitalization though she continued to be asymptomatic and repeated blood and 24 hour urine tests were negative. She had four daytime leaves of absence during her hospital stay. Amniocentesis was done on October 26, November 2 and November 7. The plan was to do an elective Caesarean section as soon as fetal maturity was evident. A further amnio was planned for November 13, however a biophysical profile on that date revealed oligohydramnios, so an elective repeat Caesarean section was planned for the following day.

A low segment Caesarean section and tubal sterilization were performed on November 14 at 37 weeks and 3 days gestation. There is no dictated operative note. There were no apparent complications associated with the surgery or post operatively. The patient’s blood pressure remained in good control with continuation of her antihypertensive medications post delivery. She was discharged home on Day 3 with methyldopa 500 mg (every six hours), nifedipine XL 90 mg daily and labetolol 300 mg (every six hours). She was to follow up in the outpatient clinic the following week. There is no charting regarding the potential risks or prophylaxis for thromboembolic disease.

On the morning of November 14, ten days after delivery and seven days after discharge, the patient was found collapsed on the floor. 911 was called. Paramedics arrived and CPR was initiated however, it was unsuccessful. She was pronounced dead shortly after transfer to hospital.

Post Mortem Findings

Significant findings at autopsy:

  • Morbid Obesity - Body Mass Index (BMI) of 45
  • Thrombosis of left posterior tibial vein with recent thromboembolism to bilateral hilar pulmonary arteries.

The cause of death was attributed to bilateral pulmonary embolism.

Discussion

This 39-year-old patient with known chronic hypertension, which was further increased in pregnancy, had a prolonged hospitalization for approximately one month prior to delivery. She was not restricted to bed rest and had several passes to leave the hospital during her stay. She had appropriate treatment for managing her hypertension and gestational diabetes. She was appropriately followed for fetal well-being by biophysical profiles and non stress testing. There were repeated amniocenteses to determine fetal maturity with the plan of delivery as soon as maturity was evident. There does not appear to have been any compelling reason for delivery prior to the time of her elective Caesarean section on November 14. It was at that time that the biophysical profile first showed significant oligohydramnios. Her clinical status was otherwise stable. Her perioperative and post delivery care were appropriate.

This patient was at an increased risk for thromboembolic disease because she was pregnant, obese, had decreased physical activity and recently had delivered by Caesarean section. Among pregnant women, the highest risk period for venous thromboembolism and pulmonary embolus is postpartum. There was no documentation that this risk, or the use of thromboprophylaxis, was considered.

There is at present, inadequate evidence from randomized controlled trials (RCT’s) to confirm the best ways to prevent venous thromboembolism in pregnancy after Caesarean section. There is a clear need for well designed large scale RCT’s to assess the effects of thromboprophylaxis for rare outcomes such as thromboembolic events in pregnancy. There are guidelines from the Society of Obstetricians and Gynaecologists Canada (SOGC) that should be considered by caregivers regarding “Prevention and Treatment of Venous Thromboembolism (VTE) in Obstetrics.” No.95,-September 2000.

Recommendations

  1. . Obstetrical care providers are reminded that thromboprophylaxis in pregnant patients, particularly when there are increased risks (e.g. obesity, decreased activity and Caesarean delivery), should be considered. There is not however, adequate evidence from well designed trials to confirm the best management.


Case: 2010-M-3

History

The deceased was a 44-year-old G1 P1 who died 48 hours postpartum. Her prenatal care was provided by her family doctor with referral by 10 weeks to an obstetrician. She had dating established by her 11 week ultrasound. She underwent integrated prenatal screening (IPS) which gave a 1:72 risk of Down’s syndrome. Amniocentesis subsequently confirmed a normal baby. In late pregnancy, she had close follow up for late maternal age and post dates with ultrasounds and biophysical profiles.

Her labour was induced at 42 weeks gestation with artificial rupture of membranes (ARM) and intravenous oxytocin. There was meconium stained amniotic fluid.  External fetal heart rate monitoring was used and she received an epidural anaesthetic about three hours before the birth. Some decelerations were noted about one hour before the birth and she was found to be fully dilated. She was encouraged to start pushing.

The patient pushed with the obstetrician in attendance for one hour. The decelerations were then noted to be late, but with good beat to beat variability. The vertex was at spines +3 and right occipital anterior (ROA).  She was transferred to the operating room for a trial of forceps delivery. The anaesthesiologist was in attendance and the paediatrician was asked to attend. Delivery was accomplished with Tucker McLean forceps over two contractions with moderate traction and a right mediolateral episiotomy. The baby weighed 9 lbs 1 oz and was given Apgar scores of 8 and 8 at one and five minutes.

The mother was given five units of oxytocin IV push with the anterior shoulder and 20 more units were added to the IV bag for infusion. The placenta delivered spontaneously. A moderate amount of blood was noted by the obstetrician. The patient was found to have extensions of the episiotomy up the vaginal wall, but the cervix was intact. The obstetrician repaired the tears and the episiotomy. During the 15 minute repair procedure,  the nurses noted a large gush of blood and uterine “atony +++”. Hemabate© was given IM at nine minutes and the bleeding was still heavy. The obstetrician described the fundus as being firm, but the lower uterine segment boggy. After repairing the lacerations, repeated uterine massage was used to try to control the bleeding. A  balloon catheter was also placed, but it did not improve the bleeding, so it was removed. Misoprostol 800 ug per rectum was given at 24 minutes and a second dose of Hemabate© was given at 34 minutes after the birth.

Throughout the time from the birth, numerous attempts were made to start additional IVs. The Intensive Care Unit (ICU) nurse was called to assist and the anaesthesiologist was also present. Blood transfusion was commenced at 40 minutes after the birth. At this point, the obstetrician estimated the blood loss at 1500 ml, but the bleeding was still heavy.  A decision was made to perform a laparotomy and a second gynaecologist and vascular surgeon were called to assist.

The patient was given general anaesthesia approximately one hour after the birth by which time she was receiving her third unit of packed red cells. During the surgery, vascular access was a continued problem. She eventually had right femoral and right internal jugular lines established. A hysterectomy was performed without difficulty. At the completion, it was noted that all pedicles were hemostatic and the top of the vaginal vault had been oversewn. However, there was blood welling up from the vagina through the open vagina cuff.

Inspection of the vagina from below revealed a tear in the episiotomy repair which was sutured with a figure-eight stitch. Two other areas were noted to be bleeding on the vaginal tear, but the tissue was extremely friable so a decision was made to pack the vagina with two large lap sponges. With this done, the laparotomy was again inspected. Hemostasis was considered adequate and the vault was closed from above. The abdomen was closed with a Jackson Pratt drain left in place.

The abdominal closure and vaginal packs were noted to be soaked in blood. They were removed and the area was again inspected. The vaginal bleeding was noted to be coming from several places and the tissue was so raw that it could not be sutured. Three more packs were placed tightly against the now closed vaginal vault. The patient was noted to be bleeding from all her puncture sites. It was felt that she was now developing a disseminated intravascular coagulation (DIC) and that correction of her clotting was key to her recovery.

At this point, the patient had received 12 units of packed red cells, 500 ml of fresh frozen plasma (FFP) and one bag of platelets during the two hours of surgery. She did not receive any cryoprecipitate in the operating room. During the surgery, her blood pressure was recorded as 60-80/40-50, however several dictated notes indicated that her pressure was not obtainable for over an hour during the resuscitation and surgery. During the surgery, the patient’s pulse was 110 to 120 bpm and temperature was 34.5 C. A complete blood count (CBC) taken half way through the surgery (after 9 units of blood), showed a Hgb of 111 and platelets of 120. Coagulation screen done at the time was hemolysed and not reported. No arterial gases were taken during the surgery.

Post operatively, the patient was transferred to the ICU and her care was taken over by the ICU specialist. Over the next several hours, the patient continued to be hypotensive in spite of levophed, dopamine and vasopressin. She went on to develop a profound metabolic acidosis with high lactate levels. Her coagulopathy did not reverse with massive amounts of FFP, platelets and cryoprecipitate. The patient continued to drain large amounts from her abdominal drain. On the second day, the patient developed acute respiratory distress syndrome (ARDS) and became difficult to ventilate. Her inotrope requirements increased and she went on to have a cardiac arrest from which she could not be resuscitated.

Post Mortem Findings

No autopsy was performed.  The hysterectomy specimen showed changes consistent with a postpartum uterus.

Cause of death was noted as multi-system failure due to disseminated intravascular coagulation (DIC) due to postpartum hemorrhage complicating vaginal delivery by forceps.

Discussion

This woman died of multi-organ failure as a consequence of a massive postpartum hemorrhage from either uterine atony or from vaginal lacerations. In retrospect, it is impossible to determine the relative significance of the bleeding from her lacerations and uterine atony. An autopsy might have been of assistance in understanding what happened.

There was certainly a component of uterine atony and as such, more aggressive use of uterotonic medications could have been employed. The patient received two doses of Hemabate©, 26 minutes apart. The current recommendations are that this medication may be given as often as every 15 minutes, to a maximum of eight doses. The patient did not receive any ergonovine. It is impossible to know if more aggressive use of these medications would have changed the outcome.

The patient bled so much, so quickly, that she became hypotensive during her resuscitation. Vascular access was difficult immediately post partum. She was transfused and a hysterectomy was performed in an effort to stop the bleeding, but she developed a coagulopathy and acidosis that could not be corrected.

Recommendations

  1. This hospital should review their postpartum haemorrhage (PPH) management protocol.
  2. Coroners are reminded that post mortem examinations should be considered in all cases of maternal death.


Case: 2010-M-4

History

The deceased was a 40-year-old G2P1 with an estimated date of delivery of June 23, 2009. Her routine prenatal laboratory investigations were normal. Maternal serum screening (MSS) was negative and second trimester ultrasound was normal, other than a low-lying placenta. Repeat ultrasound on June 3 at 37 weeks gestation showed the placenta had moved up, estimated fetal weight in the 73 percentile and biophysical profile (BPP) 8/8. Glucose challenge test (GCT) at 28 weeks was 10.3. The patient was referred to an endocrinologist and was subsequently started on Insulin. Her blood sugars were well controlled.

 

On April 24, at 31 weeks 4 days gestation, the patient was admitted to hospital with E. coli urosepsis/pyelonephritis. She was discharged home on April 28 on oral antibiotics for two more weeks.  A Group B streptococcus (GBS) culture at 35 weeks was negative. Her past obstetric history was for one previous term pregnancy delivered vaginally of a 7 lb female infant in 1996.

The plan was to induce labour at 38 weeks gestation for gestational diabetes on Insulin. On June 19, at 39 weeks gestation, the cervix Bishop score was 4. The patient was given dinoprostone (Prostin©) gel 2mg at 1315 hours. She returned at 2100 hours and on re-assessment, the cervix Bishop score was 6. She was given further dinoprostone via Cervidil©. The fetal heart tracing was normal at the time of discharge.

Course in Labour and Delivery

The patient was admitted to hospital at 0355 hours with increasing contractions and bleeding. Membranes ruptured spontaneously for blood tinged fluid. The fetal heart rate tracing showed variable decelerations. On examination, the cervix was 2-3 cm dilated and dark red clots were noted. Due to concerns of placental abruption, the obstetrician recommended delivery by Caesarean section. Under a spinal anaesthetic, the patient was delivered of a 7 lb 14 oz female infant at 0453 hours. Apgars were 9 and 9 at one and five minutes. There were no intra-operative complications and estimated blood loss was within normal limits.

At 0517 hours, a heavy gush of bleeding was noted. The fundus was boggy, but firmed with massage. Twenty more units of oxytocin were ordered to the bag running. The obstetrician attended and two units of pack cells were ordered. Hemabate© 250mg was given IM at 0531 hours. At 0538 hours, 1000 mg of misoprostol was given as a rectal suppository.  A second dose of Hemabate© was given at 0556 hours and a third dose was given at 0610 hours. Bleeding continued and at 0625 hours, BP was 76/57 and pulse 123. At 0637 hours, a Bakri balloon was inserted. The hemoglobin at 0710 hours was 53 gm. APTT was >150 and INR >10. 

The patient was given six units of packed cells between 0706 hours and 0806 hours, but the bleeding continued. The interventional radiologist was paged for consideration of arterial embolization. This intervention could not be arranged.

A decision was made to proceed to a subtotal abdominal hysterectomy. The procedure was commenced at 0810 hours. On completion of the procedure at 0901 hours, the patient was transferred to the ICU where she was admitted at 0940 hours.

At 0945 hours, the patient became pulseless and CPR was started. Full resuscitation commenced. The patient was given further blood products and at 1020 hours, APTT was 52.6 and INR 1.2. Subsequently, her abdomen became distended from presumed intraperitoneal bleeding and hemoglobin dropped to 43 gm. She was taken back to the operating room at 1140 hours and at laparotomy, approximately five litres of blood was found. An attempt was made to cross-clamp the aorta at the epigastric level, but the surgeon felt that thoracotomy was necessary. While this was being performed, the abdominal cavity was systematically explored for the source of bleeding. There was diffuse oozing in the pelvis, but no obvious major source of bleeding. There was one small area from a pedicle which was over-sewn. The abdomen was packed off while blood product replacement continued. After some time, the packs were removed and again were soaked with blood. Again, only diffuse ooze was identified. A decision was made to pack off the abdomen and leave the abdomen open.

The patient returned to the ICU and continued to suffer ongoing bleeding, DIC and recurrent arrests. She developed multi-organ failure, renal failure and left ventricular dysfunction. The hemoglobin was stabilized, but over the course of June 21, she continued to experience progressive refractory shock. While investigations showed Grade 4 left ventricular dysfunction, the possibility of sepsis was also considered. Cefazolin was stopped and Tazocin© was started. A cardiology consult was obtained. Consideration was given to the insertion of a temporary impala device, but a medical surgical bed at  another hospital was not available. Blood culture report on the evening of June 21 showed multi-drug resistant Klebsiella oxytoca sensitive to levofloxacin which was then added to the antibiotic regimen.

The patient expired on June 22 at 2106 hours.

Post Mortem Findings

Autopsy findings showed multiple effects of massive blood loss and hypotension with diffuse alveolar injury of the lungs, acute tubular necrosis of the kidneys, acute centrilobular necrosis of the liver and diffuse anoxic/ischemic encephalopathy of the brain. There was extensive ischemic necrosis of the small and large intestine providing the site of origin for the terminal gram negative sepsis.

The cause of the blood loss could not be determined from examination of the uterus or placenta. There was no pathological evidence of placenta accreta, placental abruption or amniotic fluid embolism.

The cause of death was complications of massive peri-partum blood loss with multi-organ system failure. The cause for the peri-partum blood loss was not identified.

Discussion

The patient died from hemorrhagic shock, ensuing multi-organ failure and sepsis following delivery by Caesarean section for presumed abruption and a non-reassuring fetal heart rate tracing.

Given the grossly abnormal coagulation results that were detected, it is not clear why FFP and cryoprecipitate were not given sooner. It cannot be determined from this review whether earlier administration of blood coagulation products would have changed the outcome.

Recommendations

  1. Obstetrical care providers are reminded of the need to aggressively treat coagulopathies with appropriate blood components, particularly in the post-operative patient.
  2. The hospital should review the management of postpartum hemorrhage in this case and should develop a protocol for the management of post partum hemorrhage.


Case: 2010-M-5

History

The deceased was a 40-year-old G4P2 who had several risk factors including maternal age, previous pregnancy losses and obesity. She was counselled prior to pregnancy about her risks. In early pregnancy, her prenatal screening showed an increased alpha fetal protein, but the morphology USD was normal. At 13 weeks gestation, she developed edema, mild proteinuria, and renal dysfunction. She was seen by nephrology and was closely monitored by the Maternal Fetal Medicine Department.

In the third trimester, she developed mild gestational hypertension and thrombocytopenia and was admitted at 35 weeks gestation for assessment and close monitoring. She was induced at 35 weeks 6 days because of decreasing platelets (102). She did not have other signs or symptoms of pre eclampsia. She had a vaginal delivery of a male baby with Apgars 4 and 7 and weight 2464 kg, at 2220 hours on December 16, 2008.

On postpartum Day 1, she appeared to be unwell. Her creatinine increased and she was seen by internal medicine and nephrology. On Day 2, she developed hyperkalemia and acute renal failure. She was short of breath with ambulation. On Day 3, she started to improve, but had intermittent shortness of breath. Her oxygen saturation and gases were normal. Her EKG suggested right ventricular hypertrophy. Her health care providers were concerned about her edema and shortness of breath and wanted her to take deep vein thrombosis (DVT) prophylaxis. She declined, stating that she was up and about and thus felt she did not need heparin.

In the presence of her obstetrician and other healthcare providers, the patient suddenly became dyspneic and complained of chest pain. She suffered a cardiorespiratory arrest. Resuscitation was not successful.

Post Mortem Findings

Post mortem examination was carried out with the preliminary report revealing marked right ventricular hypertrophy and right heart failure. There appeared to be pre-existing pulmonary hypertension. There was no evidence of pulmonary embolism.

The main findings at post mortem revealed pulmonary plexogenic arteriopathy with Heath-Edwards Grade 5 pulmonary arterial hypertensive changes, pulmonary arterial atherosclerosis, marked right ventricular hypertrophy and stigmata of right sided heart failure. There is an association between pulmonary hypertension and sudden arrythmia leading to sudden death.

Discussion

The mortality of pulmonary hypertension is increased in the setting of pregnancy by approximately 50%. The etiology of the patient’s pulmonary hypertension could not be determined by this review. It should be noted that there is an association between appetite suppressing medications (i.e. “fenfen”) and pulmonary hypertension, however there was no indication that she had taken this type of medication in the material provided for this review.

No recommendations.



Case: 2010-M-6

History

The deceased was a 25-year-old G4T1A2L1 with an estimated date of confinement of March 4, 2009.

Her past medical history included an uncomplicated pregnancy and vaginal birth of a 7 lb 11 oz male infant in 2003.   There were subsequently two therapeutic abortions in 2005 and 2007.   The patient had a longstanding history of depression, including post partum depression after the last pregnancy.  She was well controlled on paroxetine, and was advised to continue usage throughout her pregnancy. She had a history of asthma, but was not on any medication.  The patient was allergic to penicillin and codeine, both of which had caused anaphylactic reactions.  

In the first trimester, the patient had spotting over several weeks.   At that time, she was also using crack cocaine. The patient was a smoker, was using drugs and alcohol and initially had not been planning to continue the pregnancy.   At approximately 16 weeks gestation, she decided to continue with the pregnancy and reportedly ceased using illicit drugs.

At the time of her assessment by the obstetrician consultant at 33½ weeks gestation, antenatal screening, including maternal serum screen (MSS) and second trimester ultrasound, were normal. She indicated that she had found an inpatient treatment program near where she lived. For the following 4-5 weeks, the patient was to go to that centre for concurrent care by an obstetrician, then return back to the larger tertiary centre for delivery.

The patient was admitted to the larger tertiary centre on the evening of March 5, 2009 at 40 weeks and 1 day gestation with a two day history of fluid leakage.  She was having uterine tightening at that time.   Prenatal testing had confirmed group B positive status.  Even though she was in early labour with a cervix 1 to 2 cm dilated, she was admitted for syntocinon augmentation.  Cefazolin was ordered for strep prophylaxis.  

At 1940 hours, the nurse spoke to the attending physician about the history of penicillin anaphylaxis and was advised to continue with the cefazolin order.  By 0315 hours on March 6, approximately nine hours after admission, the patient was still 2 to 3 cm dilated with a thick cervix, so an artificial rupture of membranes of forewaters was done.   At that time, the patient was on oxytocin 20 milliunits per minute and remained at that, or lower, until delivery.   Only one dose of cefazolin had been given at 1640 hours on March 5;  no subsequent doses were given. 

At approximately 0710 hours, the patient complained of nausea and vomiting.   She was subsequently given intravenous gravol. At approximately 0730 hours, the fetal heart was difficult to pick up with variable decelerations down to 90-100.  The patient was given fluids, the oxytocin was stopped and she was repositioned. The nurse recorded the patient’s cervix to be 6 cm dilated and the physician was notified. The fetal heart stabilized within the next few minutes. At approximately 0745 hours, the fetal heart decelerated and by that time, was an anterior lip.   The patient had been intermittently vomiting over the previous 30 to 40 minutes.

The physician attended at approximately 0751 hours and a fetal scalp electrode was applied. The patient was fully dilated with only a small anterior lip. As a multip with continued bradycardia, she was advised to begin pushing in order to initiate delivery of the newborn.  

It was right at that time that the patient was found to be unresponsive. Immediately prior, the patient appeared to be conscious and behaving quite normally.  The nurse, as well as the patient’s partner and mother, attempted to rouse her.   Blood pressure was not detected and pulse oximetry was unable to pick up a heart rate or O2 saturation.   Narcan© was administered on the possibility that this was an overdose of medication. The patient remained unresponsive. At this time the fetal bradycardia continued in the 75 range. 

A “code blue” was called at 0757 hours.  Simultaneously, and due to an abnormal fetal heart rate, the baby was delivered by forceps. Apgars were 2, 6 and 8 at one, five and ten minutes and the baby weighed 4235 grams.   The placenta was left in place as initial resuscitative efforts were being made. There was no obvious vaginal bleeding or tear of the vagina.

The anesthesia consultant arrived with the code team at 0800 hours.  On arrival, the infant was being delivered by the obstetrician. The patient was observed to be initially in and out of consciousness and not breathing. She was assisted with a bag mask of ventilation at 100% oxygen and an oral airway.  

There was an initial response to epinephrine with a detectable pulse, but subsequently it was lost and never returned. The patient was intubated and multiple rounds of epinephrine/ bicarb/calcium/ magnesium/atropine were given as well as vasopressor and repeat defibrillation. The patient was also given multiple units of packed red blood cells and two units of fresh frozen plasma.

The anesthetist indicated that the patient had been given an epidural at 0500 hours and was running 0.125 % bupivicane with fentanyl at 10 cc’s per hour.  The patient had a 5 cc bolus approximately 20 minutes prior to her arrest.  It was felt that the events were extremely unlikely to be related to epidural, however Intralipid© was given as per dosing protocol to protect against bupivicane toxicity.   Blood gases determined the patient to be extremely acidotic and hypoxic and despite being ventilated with 100% oxygen and CPR maintained throughout, she did not recover.  The code was stopped after 1 hour and 10 minutes.

During the course of resuscitation, there appeared to be moderate vaginal bleeding and the uterus was atonic.  The patient was given intravenous oxytocin, ergometrine and  two doses of Hemabate©.   There appeared to be good uterine tone with this, however atony resumed without massage and therefore a foley balloon was placed for tamponade.   There did not appear to be any significant bleeding subsequent to that. 

Initial blood work revealed a hemoglobin of 120 and normal platelets. Subsequent tests at 0857 hours revealed a hemoglobin of 62, platelets of 29 (down from 124) and significantly elevated prothrombin time (PT) and partial thromboplastin time (PTT). The working diagnosis was an amniotic fluid embolus.  To rule out intra-abdominal bleeding, possibly from splenic artery or aorta, a real time ultrasound was done and showed no evidence of significant intra-abdominal free fluid.  The cardiac arrest team did not feel there was any evidence of cardiac anomaly such as tamponade or tension pneumothorax.   

Post Mortem Findings

The only significant finding on pathological examination was congestion of the lungs and  presence of squamous cells and keratin flakes in the vasculature.

The placental exam was normal.  

The cause of death was attributed to an anaphylactoid reaction caused by an amniotic fluid embolism.

Discussion

This 25 year old patient with a history of drug use in early pregnancy, went on to have an otherwise unremarkable pregnancy.   Her management in hospital up until when she was near fully dilated was unremarkable.   She developed a non reassuring fetal heart rate which was responded to by the attending nursing staff.  A physician was not immediately available, however the fetal heart recovered.  On arrival of the physician, the patient was having a sudden onset of altered consciousness. Concurrently, there was a persistent bradycardia.  A “code blue” was called at the same time as a forceps delivery of an infant. The infant subsequently did well.   

The resuscitation care appears to have been timely.  The patient developed a coagulopathy and became hypoxic and acidotic and could not be resuscitated despite a prolonged attempt. 

From the pathologic examination, toxicology testing, immunological assessments, and the notes from the attending physicians, including the obstetrician and anesthetist, it would appear that the cause of death was an amniotic fluid embolism.  

Amniotic fluid embolism has a high rate of mortality. There does not appear to have been anything further that could have been done to save this patient.  

Toxicological studies were done for the present/absence of drugs and/or poisons.   The only drugs detected were lidocaine and bupivacaine which were within the therapeutic range.   Toxicologic studies done on the day prior to delivery did not reveal evidence of any drug.

IgE testing for cefaclor and penicillin G were both less than 0.35 kU/L per litre. Detectable levels of allergen specific IgE are present in patients with allergic diseases as well as approximately 15 % of asymptomatic healthy individuals.  

Mature tryptase levels in the blood, which are a measure of mast cell activation, were measured.   Levels above 1 ng/ml indicate mast cell activation.  At post mortem, a triptase level greater than 10 increases the likelihood that systemic anaphlyaxis was involved in the terminal event.  Levels for this deceased patient were 3.9 ng/ml. 

According to these results, it is improbable that there was any penicillin related anaphylaxis from the administration of cefazolin 12 hours prior to arrest. 

No recommendations.



Case: 2010-M-7

History

The deceased was a 31-year-old G3P2. Ultrasounds on August 21 and September 23 were consistent with an estimated date of delivery of April 6, 2009. Routine prenatal laboratory investigations and integrated prenatal screening were normal. Routine second trimester ultrasound was done on November 18.

The patient’s past obstetrical history included two apparently uncomplicated term pregnancies. The first (1994), was a vaginal delivery of a 9 lb male infant and the second (1999), was a vaginal delivery of a 13+ lb male infant.

The patient previously had an abdominoplasty.

The patient’s medical history was significant for type II diabetes diagnosed in 2006. She was on metformin 500 mg, twice daily and glyburide 5 mg. The patient was not compliant with her medication. She was referred to an endocrinologist on August 12 at 6 weeks gestation.

On examination, the patient’s weight was 314 lb, height 5’11” and BMI was 44.  Her blood pressure was recorded as 110/70. She was known to have a neuropathy. HbA1C was 10.9%. She was started on insulin and a referral was made to the eye clinic. She was followed at the Gestational Diabetes Clinic and attended regularly up until October 28. She did not attend again until January 6 and did not monitor her blood sugars during that time. She also missed her appointment with the ophthalmologist.

Antenatal appointments were missed on a couple of occasions, but rescheduled appointments were attended. The patient was not hypertensive. Fetal growth was followed by ultrasound on January 20, at 30 weeks 5 days and February 24, at 34 weeks 3 days. Biophysical profile on March 20 was normal. The placenta was fundal and the estimated fetal weight was 4.55 kg (>90%ile for gestational age). The patient was booked for induction on March 23, 2009.

Course in Labour and Delivery

The patient was admitted to hospital at approximately 0930 hours on March 23. Difficulties were encountered auscultating the fetal heart due to the maternal body habitus. A bedside ultrasound at 1005 hours confirmed a fetal heart rate of 130 beats per minute (bpm). The cervix was 1 cm dilated, long and posterior. A Foley catheter was inserted for cervical ripening at 1030 hours. Tracing the fetal heart with the external monitor continued to be difficult and it was not clear whether there were fetal heart rate decelerations or whether the maternal heart rate was being picked up. A second bedside ultrasound was performed at 1047 hours and confirmed the fetal heart rate was 130 bpm. The ultrasound was completed at 1055 hours. During the course of this second scan, a fetal heart rate deceleration to 86 bpm was observed. This recovered quickly to 120 bpm. A decision was made to proceed to delivery by Caesarean section because of the presence of decelerations in the absence of labour.

The Foley catheter was removed and consent was obtained at 1100 hours. There was difficulty establishing an IV and the patient was eventually moved to the Caesarean section room at 1131 hours. The spinal anaesthetic was placed at 1149 hours. The on-call obstetrician was notified of the spinal placement at 1150 hours. Following insertion of the spinal, the patient became hypotensive. Blood pressure was restored with IV fluids and ephedrine. Fetal heart rate monitoring was not possible during this time because of the positioning for the spinal and the maternal body habitus. After insertion of the spinal, the fetal heart was auscultated at 50 bpm at 1152 hours. The patient was prepped and draped immediately. Caesarean section was started at 1203 hours by the obstetrical resident and the baby was delivered at 1208 hours with the obstetrician on call assisting.

Apgars were 0, 1 and 1 at one, five and ten minutes. The umbilical cord pH was 6.65. A large retroplacental clot was removed consistent with placental abruption. Resuscitation was commenced by the neonatal team, but was unsuccessful and the baby was pronounced dead at 1251 hours. The baby weighed 3812 g. The surgery was completed uneventfully, although several sutures were required at the left angle of the uterine incision for hemostasis. Estimated blood loss was 800cc.

Post-operative Course

The patient’s immediate post-operative course in hospital was uneventful. Prophylactic subcutaneous heparin 5,000U sc, twice daily, was started at 2200 hours on March 24. The last dose was given at 2200 hours on March 26. Her hemoglobin on the second day post-operatively was 99. She was started on glyburide and metformin and her blood sugars were monitored. She was discharged home on the fourth day, March 27. Heparin was not continued following discharge.

On the morning of March 29, the decedent began having some vaginal bleeding and went into the washroom at around 1045 hours. She began to feel unwell and asked for assistance. While being assisted, she collapsed. 911 was called and CPR was initiated. The ambulance arrived promptly and she was found to be in wide complex pulseless electrical activity. Despite resuscitation, the heart rhythm degenerated into asystole. Attempted intubation was unsuccessful and she was transferred to hospital where she was pronounced dead at 1210 hours.

Post Mortem Findings

At autopsy, there was evidence of a massive pulmonary embolism. There was also extensive pelvic deep vein thrombosis, likely the source of the pulmonary emboli. There were no signs of endometritis and no retained products in the uterus.

The cause of death was attributed to pulmonary thromboembolism due to pelvic deep vein thrombosis.

Discussion

The deceased died suddenly as a result of a massive pulmonary embolus six days following delivery by Caesarean section for an abnormal fetal heart rate. There was evidence of placental abruption at the time of Caesarean section resulting in fetal asphyxia and subsequent neonatal death. It was recognized by the patient’s caregivers that she was at risk for a thromboembolic event due to her morbid obesity, the postpartum state and the route of delivery. As a result, she was given prophylactic subcutaneous heparin 5,000U, twice daily, while in hospital. Despite this intervention, she developed pelvic deep vein thrombosis from which the fatal emboli originated.

At the present time, there is no consensus opinion on thromboprophylaxis in pregnancy and the puerperium. The most aggressive recommendations to date,  published by the Royal College of Obstetricians and Gynaecologists in November 2009, recommends at least 7 days of low molecular weight heparin (LMWH) prophylaxis for women with a BMI >40 and women who have had an emergency Caesarean section.

Recommendations

  1. The Society of Obstetricians and Gynaecologists of Canada should review and update its guidelines on thromboprophylaxis in pregnancy.


Case: 2010-M-8

History

The deceased was a 35-year -old G3P1 with an Estimated Date of Delivery (EDD) of September 8, 2010 by ultrasound for nuchal translucency on February 22, 2010. Routine prenatal laboratory investigations were normal and IPS was normal.

Her past obstetrical history included a spontaneous abortion in 2007 and an uneventful term pregnancy in 2008 when she delivered a 6 lb 6 oz baby boy.

Her past medical history included a left oophorocystectomy for a dermoid cyst in 2000 and a dilation and curettage procedure (D and C). She had been diagnosed with polycystic ovarian syndrome (PCOS). She was a carrier for Tay Sachs, but her husband was not. She was a non-smoker and was not on any medications.

On March 19, 2010 at 15 weeks 3 days gestation, the patient developed a viral-like illness with a low grade fever, fatigue, myalgia and upper respiratory symptoms. A complete blood count (CBC) on March 22, 2010 showed a low hemoglobin, platelet count 92,000 and low white blood cell (WBC) with atypical lymphocytes. Repeat CBC on March 26, 2010 was unchanged. On March 28, 2010, the WBC was normal and platelet count was up to 112,000. On April 6, 2010, the CBC continued to show atypical and reactive lymphocytes.

TORCH screen and Parvovirus B19 serologies were ordered. Cytomegalovirus (CMV) IgG and IgM were subsequently reported as reactive. CMV serology on March 22, 2010 was negative. Primary CMV infection was confirmed. After appropriate counselling of the risks of fetal infection, amniocentesis was arranged for May 6, 2010 for the detection of amniotic fluid CMV DNA.

The patient presented to obstetrical triage at the hospital on April 26, 2010 at 1650 hours with a four day history of flu-like symptoms. During the 24 hours prior to presentation, she had been experiencing vomiting and diarrhea. On the day of presentation, her temperature was 38.4 C. She had been unable to keep anything down and was quite dehydrated. On examination, she looked quite unwell. Vital signs showed temperature 37.5 C, pulse 147, RR 20 and BP 90/49. An IV was started and Ringer’s lactate was infused rapidly. CBC at 1813 hours showed a hemoglobin of 88gm, WBC 3.6 with toxic granulations and a left shift and platelet count 65,000.

The patient subsequently went to the washroom because of vaginal bleeding and while in the washroom, passed a stillborn fetus at 1910 hours. The placenta was retained. She was assisted back to bed and complained of feeling sore. She was given intravenous oxytocin and gentle traction was placed on the very thin umbilical cord in an attempt to deliver the placenta; this attempt was unsuccessful. Vital signs were BP 75/45, pulse 150 and temperature >39C. An order was received for intravenous Tazocin©.

The patient remained unstable and the Critical Care Response Team was called at 1954 hours. When the team arrived, she was found to have no detectable blood pressure, RR 47, pulse 147 and the SpO2 could not be measured. She was noted to have a rash on her arms and legs and her fingers and toes were cyanosed.

She was transferred to the ICU at approximately 2050 hours where she deteriorated rapidly with profound hypotension and hypoxia. A “Code Blue” was called, but after 45 minutes, she was pronounced dead.

Post Mortem Findings

An autopsy was not performed at the request of the family.

Blood cultures subsequently grew Group A Streptococcus.

Discussion

This patient died as the result of septic shock from a Group A Streptococcal infection at 20 weeks gestation. The most common portals of entry for streptococcal infections are the skin, pharynx and vagina. The portal of entry was not determined in this case. The literature indicates that in 45% of Group A Strep toxic shock syndrome cases, the portal of entry cannot be determined. The presentation can be variable, but influenza-like symptoms of fever, chills, myalgia, nausea, vomiting and diarrhea occur in 20% of the cases. Shock at the time of admission, or developing within 4-8 hours, is common. Complications are severe with rapid onset multi-organ failure and DIC. The mortality rate remains high.

No recommendations.



Case: 2010-M-9

History

The deceased was a 32-year-old previously healthy woman who was booked for a repeat Caesarean section at 39 weeks gestation. She had two previous Caesareans. Her prenatal care was by her family physician and a general surgeon was consulted for the Caesarean. The pregnancy was uncomplicated, except for a marginal placenta previa. She had one (or more) admissions with bleeding 10 days prior to delivery.

The Caesarean was commenced under spinal anaesthesia. The baby was a healthy girl, born at 0823 hours. Oxytocin was given by the anaesthesiologist. The surgeon noted the placenta to be densely adherent to the right side of the uterine cavity all the way down to the cervix. The surgeon dissected the placenta free with his fingers and felt the uterus was clean of placenta, but quite raw. There was considerable bleeding during this placenta removal. The surgeon estimated that 1500 ml of blood was lost during this time. The anaesthesiologist noted that 700 ml of blood was collected through suction within 2-3 minutes. Although the patient was stable at this point, due to the large blood loss, the anaesthesiologist requested four units of red cells to be sent stat. Shortly after this, the patient reported feeling nauseous, looked suddenly pale, and developed a bradycardia followed by a sinus cardiac arrest at 0835 hours. A “Code Blue” was called and the patient was intubated and given Atropine and Epinephrine. Chest compressions were commenced, however very soon after the medications were given, a sinus tachycardia was restored. Second and third IVs were started.

When the cardiac arrest occurred, the surgeon had just finished the first layer of closure of the uterine incision. After the patient was stabilized, the surgeon continued with closure of the uterus and abdomen. The blood arrived at 0845 hours and four units of packed red cells were given rapidly. The anaesthesiologist also gave several boluses of normal saline and phenylephrine and started a dopamine drip at 0900 hours. The surgery was completed at 0905 hours and the patient was transferred to the ICU at 0930 hours. The surgeon noted that when massaged, the uterus would firm and bleeding was minimal. When the massage was stopped, the uterus would fill up and bleeding would ensue. There is no mention in the medical notes of any uterotonic agents and no nursing notes were provided for the purposes of this review.

In the ICU, the patient had blood pressures of 40-90 mmHg and was noted by the ICU doctor to be pale and passing large amounts of blood per vagina. The patient was significantly shut down peripherally and attempts to start an arterial line were unsuccessful as no pulses could be palpated. A central subclavian line was however, started. The patient was placed on phenylephrine, dopamine and norepinephrine. She was given four more units of packed RBC and two units of FFP. An INR of 1.4 and PTT of 59 were drawn at 1018 hours, but it is unclear what time they were reported.

The surgeon called a colleague, another general surgeon, who routinely performs hysterectomies and Caesareans, but the other doctor was not available. The colleague suggested over the telephone, that the surgeon perform a hysterectomy. The patient was transferred back to the operating room at 1038 hours and a hysterectomy was performed. There was an inadvertent bladder entry which was repaired and a drain was left in the abdomen. The patient’s Hb at 1103 hours was 101 and platelets 69, with an INR of 1.4, calcium of 1.01 and magnesium of 0.36. The surgery took over 2.5 hours to complete, during which time the patient continued to receive the three vasopressors. She was also given ten units of packed RBC, four units of FFP and intravenous calcium and magnesium. Blood pressures in the operating room were 100/50, falling to 60/40 near the end. The patient’s pulse was 110 bpm, falling to 80 bpm and she was cold at 30 – 32 C.

The patient was transferred back to the ICU at 1340 hours. Lab tests taken at 1328 hours showed arterial blood gases of 6.89/50/205/9.6/11/-23.3, Hb 78, platelets 14, INR 2.3 and PTT >120. At this point, she continued to receive blood products and vasopressors. Attempts were made to correct her acidemia. Her abdominal drain produced one litre of bloody fluid and then her abdomen became distended. At 1415 hours, the obstetrician at a tertiary centre was contacted and consulted though Criticall. The primary centre was running out of blood products and already had platelets shipped in twice. In discussion with the tertiary ICU specialist, a decision was made to move the patient by air ambulance. At the time of her departure, she had received 22 units of packed RBC, two bags of platelets, eight units of FFP and 40 units/kg of Octaplex©.

The patient arrived at the tertiary ICU at 1719 hours. Lab tests at 1745 hours showed Hb 86, platelets 96, INR 1.5, PTT 82, lactate 5.5, troponin 0.67, calcium 1.15, fibrinogen 1.2 and arterial blood gases of 7.12/25/184/8/-20. Physical assessment determined she was brain dead. The patient died at 0140 hours on December 31, 2009.

Post Mortem Findings

The cause of death was recorded as “Multiple organ failure complicating intrapartum haemorrhage at elective repeat Caesarean due to retained products of conception (placenta increta).”

Findings included:

  • Extreme retroperitoneal haemorrhage and edema
  • Vascular pedicles secured
  • Retained placental tissue “just above the surgical incision”
  • Focal placenta increta
  • Surgical bladder injury repaired
  • No fetal tissue in uterine vessels
  • No evidence of amniotic fluid embolism in lungs

Discussion

This patient died of massive bleeding during Caesarean section. The section was performed in a primary care obstetrical unit by a general surgeon. The family doctor completed the prenatal care. She had an anterior placenta previa in the setting of two previous Caesarean sections. As this condition is associated with a high risk of abnormal placentation (acreta, increta or percreta), the patient should have been referred to an obstetrician for assessment of the placenta previa.

The risk of placenta accreta in the presence of placenta previa increases dramatically with the number of previous Caesarean sections with a 25% risk for one prior Caesarean section, and more than 40% risk for two prior Caesarean sections. If increta was diagnosed preoperatively or even just suspected, special arrangements could have been made to possibly improve the maternal outcome. The primary centre is unlikely to have access to all the products and procedures required to manage such cases.

It is not possible to determine from this review if transfer to a larger centre, or if staff preparation for situations involving large blood losses, would have changed the outcome for this patient.

The surgeon performing the Caesarean recognized the increta during the surgery, but failed to ensure hemostasis prior to transferring the patient out of the operating room. The patient suffered a cardiac arrest, likely secondary to massive blood loss, and was successfully revived. However, the DIC and the metabolic acidosis which subsequently developed, were not aggressively managed.

Recommendations

  1. The Chief of Staff for Hospital A should review the risk factors for postpartum hemorrhage (PPH) and the management of pregnancies with placenta previa with the obstetrical care providers in this case as per the SOGC Clinical Practice guideline: Diagnosis and Management of Placenta Previa. J Obstet Gynaecol Can 2007;29(3):261–266.
  2. The Chief of Staff for Hospital A should review the management of PPH with the obstetrical care providers in this case. This may include review of ALARM course material, the MORE obstetrical program and review of the following reference article:

Leduc, L. Active Management of the Third Stage of Labour: Prevention and Treatment of Postpartum Hemorrhage. J Obstet Gynaecol Can 2009;31(10):980–993.

  1. The obstetrical care staff of Hospital A should prepare a protocol for PPH and massive transfusion and ensure that all are educated on how and when to institute the protocol.

The following reference materials may be of assistance in developing this protocol:

Bormanis J. Development of a massive transfusion protocol. Transfus Apher Sci. 2008 Feb;38(1):57-63. Epub 2008 Mar 4.

Burtelow, M. How we treat: management of life-threatening primary postpartum hemorrhage with a standardized massive transfusion protocol TRANSFUSION Volume 47, September 2007.

  1. The Chief of Staff for Hospital A should review the guidelines for the selection of obstetrical cases to be delivered at this hospital.
  2. Obstetrical care providers should be reminded to utilize the assistance of CRITICALL early for facilitating expert advice in dealing with obstetrical emergencies.
  3. Obstetrical care providers and delivery centres should seriously consider establishing a mechanism to ensure that all ultrasound reports done in pregnancy be available at the birthing centre at the time the mother arrives.


Case: 2010-M-10

History

The deceased was a 37-year-old G3P1 with an EDD of April 26, 2009. A dating ultrasound on September 10 was consistent with the EDD. Her past obstetrical history included one previous term pregnancy and vaginal delivery of a 7 lb 10 oz male infant in 2007. The labour and delivery were precipitous and there was a postpartum hemorrhage. She had an uncomplicated spontaneous abortion at 8 weeks in 2008. In 1993, she underwent laser vaporization of the cervix for CIN 3. Subsequent Pap smears were normal.

She received midwifery prenatal care. At her first prenatal visit, her height was recorded at 5’7” and weight was 183 lbs with a BMI of 28.7. Routine prenatal laboratory investigations were normal. IPS was positive for Down Syndrome. Amniocentesis revealed a normal female chromosome analysis. Routine second trimester ultrasound at that time was normal.

A 75 gm Oral Glucose Tolerance Test (OGTT) on January 8, at 24 weeks 5 days was normal. She started wearing compression stockings at 25 weeks because of symptomatic varicose veins. A GBS culture at 35 weeks 4 days was negative.

On May 4, at 41 weeks 1 day, BPP was 8/8 and the estimated fetal weight was 10 lbs, 13 oz. Obstetrical consultation was obtained on May 5. She consented to undergo cervical ripening and induction of labour. A cervical balloon catheter was inserted, but fell out later that night. She presented to the local hospital the following morning at 1100 hours for induction.

Spontaneous rupture of membranes occurred at 1245 hours for “tinged” fluid. The cervix was 3 cm dilated with the vertex at spines -3. Contractions were irregular. Oxytocin was started at 1400 hours and was increased according to protocol. Contractions became regular at 2-3 minutes, lasting 40-60 seconds. She began feeling contractions at 1930 hours when the cervix was 5 cm dilated. At 2030 hours, she vomited, then appeared to have a seizure and collapsed at 2035 hours. The midwife called a code at 2042 hours. Response from hospital staff was prompt and resuscitation commenced immediately.

The initial attempt to intubate by the emergency physician was unsuccessful as the patient was clamped down. A laryngeal mask airway (LMA) was placed, followed by a second attempt to intubate as her oxygen saturation continued to drop. An anaesthetist arrived and intubation was successful at 2105 hours. A fetal scalp clip was placed. Fetal heart rate was in the 60-70’s. The patient remained pulseless and unresponsive. On advice from the general hospital, the patient was transferred to the operating room for Caesarean section. She was delivered of a stillborn female infant at 2125 hours. Resuscitation of the baby was unsuccessful. Birth weight was 10 lbs, 5 oz. Maternal death was pronounced at 2150 hours.

Post Mortem Findings

Cause of death: amniotic fluid embolus.

The stillbirth was due to intrapartum fetal demise following maternal death in labour. The fetus was large for gestational age with organomegaly, however there were no findings correlating to maternal diabetes.

The placenta was large, but there were no microscopic changes relating to maternal diabetes. There was no evidence of abruption.

Discussion

The mother died as a result of abrupt and total cardiovascular collapse in labour secondary to amniotic fluid embolus. Despite the immediate institution of resuscitative measures, she could not be revived. The resulting severe maternal hypoxemia was lethal for the fetus.

It cannot be ascertained from this review whether the hospital involved has a guideline or protocol for maternal cardiac arrest.

The decision to induce labour for post dates was appropriate. Despite the ultrasound report of fetal macrosomia with an estimated fetal weight of 10 lbs, 13 oz, it was appropriate to induce labour rather than deliver by Caesarean section. The benefits and risks of labour and delivery versus Caesarean section in the setting of macrosomia on ultrasound, should be discussed and documented in the antenatal record.

Recommendations

  1. All hospitals should consider developing a protocol for managing cardiac arrest in pregnancy.


Case: 2010-M-11

History

The deceased was a 34-year-old G3P0 with an EDD of April 10, 2007 based on first trimester ultrasound. Prenatal care was provided by her family doctor. Routine prenatal laboratory investigations were normal. IPS was negative. Routine second trimester ultrasound was normal and GCT was normal. She attended regular prenatal visits and all findings were normal. A 3-D ultrasound at 28 weeks showed the baby to be in breech presentation. Her last prenatal visit was on March 14 at 36 weeks 1 day. GBS test was negative. The baby was found to be in breech presentation and referral was made to an obstetrician for consideration of external cephalic version.

Her past medical history was unremarkable and she was a non-smoker.

On March 15, the patient developed a fever with associated aches and chills. She presented to a walk-in clinic that evening. The fetal heart was positive. She was diagnosed with a urinary tract infection (URTI) and given acetaminophen. She called the health centre (satellite location) obstetrical triage at 0600 hours on March 16 with contractions and pelvic pain. The triage record indicated that she was feeling fetal movement and the baby was in the breech presentation. She was instructed to come to the triage unit. She was seen at 0700 hours. She looked unwell and was sent to the emergency department at 0855 hours. Blood pressure was 73/33, pulse 136 and respiratory rate 30, temperature was 39.5C. She was given acetaminophen and a Foley catheter was inserted. Fetal heart was absent. IV crystalloids, Pentaspan© and cefazolin were given. Blood pressure improved to 128/52 and she was transferred to the health centre (primary site) emergency department by ambulance, attended by her family doctor and an emergency room nurse.

She arrived in the emergency department at 0910 hours. Heart rate was 138, respiratory rate 55, BP 123/88, SaO2 98%. There was blood in the catheter. The cervix was 2 cm dilated and 50% effaced. There were several clots in the cervix. Laboratory investigations from the satellite health centre showed an INR of 2.9, PTT >150 and fibrinogen .6 and platelets 22,000, consistent with DIC. She was given blood products including fresh frozen plasma, packed cells, cryoprecipitate and platelets in preparation for Caesarean section. Surgery started at 1100 hours.

She was administered a general anaesthetic and central lines were placed. The peritoneal cavity was entered through a lower midline incision. There was a volume of turbid fluid in the peritoneal cavity. The uterus was “almost black” and was consistent with a Couvelaire uterus. The fallopian tubes were also black. A low transverse uterine incision was made and a female stillborn infant was delivered. There was a large volume of blackish amniotic fluid in the uterine cavity with evidence of placental abruption. After closure of the uterine incision, the uterus was noted to be hypotonic. There was no response to massage and Hemabate©. A decision was made to proceed to subtotal hysterectomy. On completion of the procedure, the operative site appeared dry and drains were placed. Surgery was finished at 1135 hours.

Post operatively, the patient was transferred to the intensive care unit on vasopressors as she remained hypotensive. Laboratory investigations revealed an elevated serum lactate, liver function tests, creatinine and DIC consistent with multi-organ failure. Consults were obtained from infectious disease, hematology and nephrology. Despite resuscitative efforts, the patient continued to deteriorate and subsequently arrested. She was pronounced dead at 1945 hours.

Post Mortem Findings

Autopsy findings were consistent with DIC and multi-organ failure. The hysterectomy specimen showed extensive transmyometrial intravascular thrombosis and areas of hemorrhage. Placental weight was in the 75th percentile with a marginal infarct.

There was no evidence of chorioamnionitis or funisitis.

The cause of death was multi-organ failure due to, hemorrhagic shock due to, placental abruption and postpartum hemorrhage complicating Caesarean section and hysterectomy in a term pregnancy.

Discussion

The deceased died from hemorrhagic shock, DIC and multi-organ failure secondary to a massive concealed placental abruption resulting in fetal death and a Couvelaire uterus. Her antenatal course was uneventful until March 15 at 36 weeks 3 days when she presented to a walk-in clinic complaining of fever and chills. Medical records from the walk-in clinic were not available for review. Apparently, the fetal heart was auscultated. She was diagnosed with an URTI and given acetaminophen. Her condition deteriorated overnight and she called the obstetrical triage in the morning feeling unwell and having contractions. When seen in triage, fetal demise was confirmed and she was gravely ill. With hypotension and evidence of DIC, immediate evacuation of the uterus was indicated. She was transferred emergently by ambulance to the nearest site where this could be performed. She was given blood products and taken to the operating room where surgery confirmed placental abruption and a Couvelaire uterus. Hysterectomy was undertaken because of uterine atony which did not respond to intramyometrial Hemabate©. The operative report does not include whether other options for managing the uterine atony, such as the B-Lynch suture or Bakri balloon, were considered. Regardless, the true Couvelaire uterus would be unlikely to respond to such measures. Internal iliac artery ligation is another option, but requires a skilled surgeon. The hysterectomy was carried out expeditiously and the surgical site was dry upon completion. The profound shock and DIC resulted in multi-organ failure from which she could not recover.

No recommendations.



Case Summaries: Neonatal Deaths


Case: 2009-N-1

History

The mother of the deceased was a 33-year-old G2P1 with an EDD of November 13, 2007. An ultrasound on May 1 showed a diamniotic dichorionic twin pregnancy at 11 weeks 5 days. There was increased nuchal translucency on twin B and an IPS was positive. After appropriate counselling, the patient underwent an amniocentesis of both sacs at 15 weeks 1 day. Cytogenetics report showed normal 46XX karyotype for both. Routine prenatal laboratory investigations were normal.

The patient’s past obstetrical history was for one previous uneventful term pregnancy delivered vaginally for a 6 lb 5 oz male infant in 2005.

Ultrasound on June 25 showed both twins at 19 weeks and no placenta previa. Cervical length was 4.4 cm. The patient was referred to an obstetrician and was seen on July 17 at 23 weeks gestation.  Also on that day, an ultrasound showed normal growth and amniotic fluid volumes with no discordance. The ultrasound report from the scan done on July 17 did not comment on cervical length. The obstetrician’s plan was to see the patient every two weeks until 28 weeks, then every week thereafter with ultrasound assessment every four weeks and betamethasone at 28 weeks.  A glucose challenge test on August 10 was normal.

Course in Labour and Delivery

The patient presented to labour and delivery at Hospital A on August 19 at 27 weeks 4 days complaining of uterine contractions. The time cannot be determined from the records provided. The electronic fetal monitoring (EFM) strip was started at 1545 hours and the patient was seen and assessed by her obstetrician at 1640 hours.  EFM showed normal fetal heart patterns and mild uterine contractions every five minutes. The cervix was posterior, uneffaced and closed. She was admitted for observation.

At 1720 hours, an IV was started and the patient was given betamethasone and an indomethacin suppository. At 1840 hours, she reported stronger contractions every 2-3 minutes which “feel like labour.” She experienced diarrhea and informed hospital staff that her son and husband recently had the same. Contact precautions were instituted. The cervix was unchanged. EFM showed contractions every five minutes, lasting 30 seconds. The obstetrician was notified and morphine and Gravol© were given. At 1945 hours, contractions were every 2-3 minutes and were moderate on palpation. She was breathing with the contractions. The obstetrician was updated at 1948 hours.

At 1950 hours, the patient got up to use the washroom. While in the washroom at 1958 hours, spontaneous rupture of membranes (SROM) occurred and delivery of twin A shortly followed in the washroom. Twin A was pink and cried vigorously. The obstetrician attended and at 2010 hours, portable ultrasound confirmed twin B was also vertex. At 2012, artificial rupture of membranes (ARM) was carried out for clear fluid and twin B was spontaneously delivered at 2023 hours.

Summary of Postnatal Course

Twin B was attended by an assigned medical team.  Her heart rate was greater than 100 bpm, but she had poor tone and reactivity with no respiratory effort.  Resuscitation was instituted with bag and mask ventilation and her condition improved. Apgar scores awarded were 3 at one minute, 5 at five minutes and 8 at 10 minutes of age.  Cord arterial blood gases revealed a pH=7.24, pCO2=43 mmHg, HCO3=18 mmol/L, BE=-9 mmol/L. The infant was intubated at 12 minutes of age and supported with bag ventilation.  An umbilical venous catheter was inserted and a normal saline bolus given followed by an infusion of D10W.  A call had been placed to the local tertiary perinatal centre and a transport team was dispatched.

The transport team arrived at 2133 hours when the baby was just over one hour of age.  The infant was being hand bagged through an endotracheal tube in 100% oxygen, but was dusky with arterial oxygen saturation of 80%.  Chest movement was poor, so the endotracheal tube was removed and bag and mask ventilation commenced to good effect.  She was successfully reintubated and a chest X-ray was performed.  The endotracheal tube was too deep and was pulled back 0.5 cm.  The infant was placed on the transport ventilator and the FIO2 was weaned.  Chest X-ray was consistent with respiratory distress syndrome (RDS), so surfactant was given via the endotracheal tube.  The baby’s temperature was low at 32.8 C, but she was described as “handling well.”  Warm towels were applied.  Bloodwork was drawn and she was started on antibiotics.  CBC was normal.  An arterial blood gas taken at 2315 hours, when the baby was three hours of age, showed pH=7.32, pCO2=39 mmHg, pO2=112 mmHg, HCO3=19 mmol/L and BE=-6 mmol/L.  Beds were not available in any of the NICUs in southern Ontario, so transfer to Hospital B in eastern Ontario was arranged.  The baby was transported via road ambulance to the airport, then by air ambulance to Hospital B.  The infant arrived at 0410 hours and the transport was described as “uneventful.”

On admission to Hospital B, the infant was still slightly hypothermic with a temperature of 35 C, but other vital signs were normal.  She was receiving assisted ventilation, but had weaned to room air.  She was described as “sleepy” but was reactive.  Initial weight taken in Hospital B was 976 g.  She was maintained on parenteral fluids and antibiotics.  Weaning of ventilatory support was planned.

The infant’s initial course in hospital was relatively uneventful.  Ventilatory support was weaned until she was successfully extubated to nasal continuous positive airflow pressure (CPAP) on Day 3.  She had intermittent apnoeic/bradycardic spells and remained CPAP dependent, but did not require reintubation until her terminal septic episode.  Feeds were commenced and advanced cautiously.  She had elevated blood glucose concentrations on several occasions that responded to a reduction in parenteral intake.  Antibiotics that were commenced shortly after birth were discontinued after four days when negative culture results from the initial blood culture were obtained.  Head ultrasounds revealed no evidence of haemorrhage or other abnormalities.  A persistent cardiac murmur was noted on Day 10 and an echocardiogram confirmed the presence of a large patent ductus arteriosus.  Treatment with a course of indomethacin was ordered, but stopped after one dose due to reduced urine output.  The murmur remained persistent but, since she was managing with non-invasive respiratory support, no further treatment was undertaken.

On day 11, the nurse caring for the baby noted a tender swelling with bluish discolouration in the baby’s left thigh.  X-rays revealed a displaced left femoral fracture. The orthopaedic service was consulted and recommended splinting for immobilization.  Some redness appeared on the skin of the left leg that was felt to be a possible cellulitis, so a course of Cloxacillin was commenced.  No etiology for the fracture was determined.  There was no evidence of congenital or metabolic bone disease, so it was felt that the fracture was most likely iatrogenic.  There were however, no recorded incidents of trauma or recent procedures that might have resulted in the application of significant force to the femur.

Over the next few days, the baby remained fairly stable, although there had been some hypoventilation associated with morphine treatment and some feeding intolerance with bilious aspirates.  Abdominal X-ray did not suggest necrotizing enterocolitis and feeds were cautiously reinstituted.  There was a loud murmur and the infant remained dependent upon CPAP for support.  A peripheral central catheter (PICC) line was inserted on September 5.  The infant was described as “stable and improving clinically.”

On the evening of September 6, at 18 days of age, the infant developed persistent tachycardia and some shallow breathing with intermittent apneic spells.  She was assessed by the resident who considered four possible causes in the differential diagnosis, including pain from the fracture, sepsis, anemia or hypovolemia.  Packed red blood cell transfusion was ordered for a haemoglobin concentration of 92 g/L.  A septic workup was performed and she was started on vancomycin and gentamicin.  A blood gas was performed that revealed a significant mixed acidosis with ph=7.08, pCO2=81 mmHg, HCO3=23.9 mmol/L and BE=-8 mmol/L.  The infant acutely deteriorated during a chest X-ray and was difficult to resuscitate.  After successful intubation, blood was suctioned from the endotracheal tube and she was difficult to ventilate with very stiff lungs.  She became and remained hypoxic and acidotic in spite of manipulations of the ventilator, sedation, inotropic support and transfusion therapy.  CBC showed that she had developed marked neutropenia.  She suffered from a severe bradycardic spell despite maximal support.  She was removed from the ventilator and passed away at 0503 hours on September 7, 2007. 

A blood culture subsequently came back growing E. coli, resistant to ampicillin, but sensitive to gentamicin. 

Post Mortem Findings

Significant findings at post mortem examination included:

  • Patent ductus arteriosus – 3mm
  • Large recent pulmonary haemorrhage
  • Complete spiral fracture of the left femur
  • Subacute meningitis, moderate to severe (no organisms seen on microscopy but no culture taken)
  • Positive aerobic blood culture – E. coli

Death was attributed to “complications of prematurity.”

Discussion

This infant (twin B), died at 19 days of age from E. coli sepsis as a complication of prematurity.  Premature labour is a well recognized risk factor in twin pregnancy. As interventions to prevent premature labour have not proven effective, management focuses on early identification to allow time for the administration of glucocorticoids (betamethasone or dexamethasone), antibiotics and transfer to a tertiary or secondary care unit as appropriate for gestational age. Assessment of the cervical length by ultrasound and fetal fibronectin testing have been studied as markers for the risk of premature labour. While the usefulness of these tests has not been clearly defined, abnormal results take on greater significance in the presence of significant uterine activity and may prompt earlier administration of steroids and antibiotics and/or transfer to a tertiary centre. 

In this case, the ultrasound done on June 25 at 19 weeks gestation reported normal cervical length of 4.4 cm. The ultrasound on July 17 was done at a different facility and the report did not comment on cervical length. It cannot be determined by this review if Hospital A had fetal fibronectin testing available. Nor can it be determined whether such testing would have allowed for safe and timely transfer to a tertiary care centre or whether the outcome would ultimately have been different.

At the time of presentation to Hospital A’s labour room, the contractions were regular, but were assessed to be mild. It appears from the progress note at 1640 hours that this was determined by the tocodynamometer and not by palpation. While the tocodynamometer can indicate the frequency of contractions, it cannot accurately assess the strength. Palpation of the uterus provides a better assessment of the quality of the contractions provided the patient is not obese and the care provider is experienced with this assessment. That the care providers in this case were concerned by the contractions is indicated by the fact that the patient was admitted and given an indomethacin suppository and steroids. The note at 1720 hours indicated that the patient was transferred from the labour room to another room. It cannot be determined by this review whether this was another bed within the labour and delivery area or an antenatal bed. It would have been appropriate to monitor such a patient within the labour and delivery area although there were also concerns about her diarrhea and contact precautions were taken because of this. There is no indication from the record that consideration was given to attempting transfer to a tertiary care center.

The severity of the contractions appeared to have changed at 1840 hours when the patient described them as “feeling like labour.” Although ultimately a change in the cervix is required to diagnose labour, this observation by a patient who has previously experienced labour is significant. Again a note is made referring to the frequency of contractions on the monitor, but there is no note as to whether an assessment was made by palpation. Despite the note at 1840 hours concluding with a comment to monitor closely for labour and contractions, there was no further note until 1930 hours after a shift change and assessment by a new care provider. That note did include an assessment by palpation and the contractions were every 2-3 minutes and moderate. By 1948 hours, the patient was breathing with the contractions, but was allowed up to the washroom at 1950 hours without the cervix being reassessed. At 1958 hours, membranes ruptured and twin A delivered in the washroom. Clinical palpation of uterine contractions may have alerted the care providers to the advanced stage of her labour and provided the opportunity for the delivery to occur in a more controlled fashion in the proper setting.

While twin A survived after a prolonged period of neonatal intensive care, twin B died at 19 days of age from E. coli sepsis.  Although she had been born significantly preterm at 27 5/7 weeks gestation, she had a relatively benign clinical course until the infection developed.  Her course had been complicated by respiratory distress syndrome, apnoea of prematurity, patent ductus arteriosus, feeding intolerance and a left femoral fracture.  In spite of this, she was described as “stable and improving” on the day before the septic episode and was managing with only non-invasive respiratory support.  The first clinical sign alerting the team to the possibility of sepsis was tachycardia which was investigated appropriately.  Sepsis was considered and antibiotics commenced after cultures were taken.  However, the infant deteriorated quickly with the development of pulmonary haemorrhage, respiratory failure and shock.  She died within 12 hours of her clinical presentation.  E. coli was grown from both the blood culture taken for the septic work-up and one taken post mortem.  There was also evidence of meningitis at autopsy, although no cerebrospinal fluid (CSF) samples were sent for culture. 

Nosocomial sepsis is a common complication of premature birth and NICU care.  Approximately 15% of infants born with birth weights of less than 1500 g will acquire at least one blood stream infection during their hospital stay.  Many of these infections are due to indwelling vascular devices and the most common isolate is coagulase-negative staphylococcus.  Bacteria can also gain entry from the respiratory tract, GI tract, urinary tract or skin.  In most cases, the baby will recover with supportive measures and treatment with antibiotics.  However, a significant proportion of septic episodes in preterm neonates are caused by gram-negative bacilli such as E. coli and a rapidly progressive, catastrophic clinical course is not uncommon. 

In this case, the source of the bacteria is not known. Although it is felt that a significant proportion of nosocomial infections in NICU patients are preventable, there is no evidence in this case to suggest that if the baby had been managed differently, the outcome would have been different.

Issues identified for review include the possible contribution of the need to have the baby transferred from southern Ontario to eastern Ontario for care and the cause and possible contribution of the femoral fracture.  With respect to the first issue, it is clearly undesirable and suboptimal to have a preterm infant born outside of a tertiary perinatal centre, but there are times when this cannot be avoided. Earlier recognition of preterm labour may have allowed for transfer to, and delivery at, a centre providing higher level perinatal care, but it not clear from this review that it would have been possible. 

When the infant was born at the community hospital in southern Ontario, the team appears to have managed the baby very effectively and she was in good condition when attended by the local transport team.  Lack of availability of a NICU bed for the baby at a nearby centre necessitated transport to a distant centre that had beds.  This is also suboptimal, but at times is the best approach to accessing the necessary care and maintaining patient safety.  Long distance transports should be avoided whenever possible for fragile, preterm neonates, but well-trained teams with advanced equipment can usually deliver the baby safely and intact.  In this case, the transport was described as “uneventful” and the baby was in good shape upon arrival at the receiving NICU.  There is no evidence that the need to transport the baby to eastern Ontario contributed to the infant’s demise.

With respect to the femoral fracture, fractures of the long bones in preterm infants are rare, but can result from birth trauma, post-natal trauma, congenital diseases of the bone such as osteogenesis imperfecta or metabolic bone disease.  The latter condition is not uncommon in tiny preterm infants but, with modern nutritional management and monitoring, it rarely progresses to the stage whereby fractures result. Severe metabolic bone disease most commonly occurs in a very preterm infant who is several weeks to months old and who has required a prolonged period of parenteral hyperalimentation. 

This infant was more mature and at a younger post-natal age than babies that are generally felt to be at risk.  In addition, the post mortem examination revealed “no metabolic bony deficiency” and there was nothing abnormal noted on X-ray, other than the fracture itself.  The etiology of the fracture is unknown. The fracture appears to have happened on, or around, the tenth day of age.  The first indication from the records that there might be something wrong was a mention by the nurse that the left leg appeared swollen and tender.  There was no documentation of a procedure in which excessive force may have been used or of any traumatic event.  It is possible that the fracture occurred during routine handling with the operator not appreciating what had happened.  In any event, it would not have contributed to a death from nosocomial sepsis.

Recommendations

  1. Obstetrical care providers are reminded that the external fetal monitor tocodynamometer does not accurately indicate the strength of uterine contractions and cannot be relied upon in lieu of palpation by an experienced obstetrical care provider.


Case: 2010-N-2

History

The mother of the deceased was a 25-year-old primigravid. She was a smoker and known to have polycystic ovarian syndrome for which she was treated with metformin prior to the pregnancy.  She did not have significant fertility difficulties.  She was cared for in the pregnancy by a family doctor. Her pregnancy appears to have been uneventful, although on her last two weekly visits, 7 and 14 days prior to her delivery, her blood pressure had been elevated to 142/86 and 156/90. There is no indication on the chart that any further investigations or treatments for this were undertaken. She was known to be GBS positive. There are no ultrasound reports in the hospital chart and none are recorded on the prenatal records aside from a note of May 26 that reads, “no previa.”

The patient presented to hospital at 2015 hours on August 3, 2009 at 40 weeks and 2 days gestation. She came to the hospital because of an episode of bright red vaginal bleeding which occurred during urination after swimming at approximately 1900 hours. She was attended by the nurses in the family practice birthing unit. She had been having irregular contractions for the past two days and now had constant lower backache.  When checked by the OBS triage nurse, she had a moderate amount of bright red vaginal bleeding.  Her blood pressure was elevated at 192/91 and 159/93.  Electronic foetal monitoring (EFM) was applied, however the date and time were not correct on the monitor.  A handwritten notation indicated the time of application.

The patient's physician was notified of her arrival.  A vaginal exam indicated that the cervix was 1 cm dilated, thick and posterior and the presenting part high.  Low backache and pressure continued.  The patient remained in triage on EFM and the physician was updated hourly.  No further active bleeding was noted.   The nurse notified the physician that the patient was GBS+ and that the non-stress test was “suspicious or equivocal.” 

At 2200 hours, the patient was experiencing Q10 minute contractions lasting 45 seconds.  These contractions palpated (with difficulty), as mild.  At 2215 hours, the physician had the patient admitted. 

On admission, the patient remained on EFM.  At 2240 hours, she was having tightening at Q 8-9 minutes, lasting 45 seconds. She continued to have constant lower backache and there was a small amount of blood on her peripad.  At 2330 hours, the patient's BP was 138/80.  A vaginal exam was done and the cervix remained unchanged with the presenting part high.  The physician was called and updated on the patient's status and EFM tracing.

At 0010 hours, the doctor was notified of contractions every four minutes and variable deceleration. The doctor came to assess the patient at 0105 hours. The doctor confirmed that the patient’s cervix was 1 cm and that the presenting part was not palpable. A bedside ultrasound was done and a transverse lie was diagnosed. As there was no surgical service at the hospital until 0800 hours, the doctor arranged transfer to a larger hospital. An IV and Penicillin G was started and the patient was transferred out by ambulance at 0250 hours.  A nurse did not accompany the patient during transport.

The patient arrived at the larger receiving hospital at 0332 hours on August 4. An EFM was instituted by the nurse and showed a baseline rate of 130 bpm with marked variability and accelerations. Contractions were noted every 2-5 minutes with coupling. The patient was assessed by the resident at 0350 hours and found to have a vertex presentation and  was in active labour. The patient’s cervix was 2-3 cm dilated. The vertex presentation was confirmed with a bedside ultrasound. EFM was continued until 0410 hours, at which time intermittent auscultation was undertaken. At 0430 hours, the resident performed an artificial rupture of membranes.

Intermittent auscultation was continued and the patient was up walking when a large gush of blood occurred at 0515 hours.  The resident attended at 0520 hours and a foetal scalp clip was applied. The tracing showed a baseline fluctuating between 135 and 150 bpm, with minimal to absent variability, and decelerations to 100 bpm.

At 0533 hours, the patient was transferred to the Caesarean section room. The anaesthesiologist on call was notified and the patient was given general anaesthesia. A male infant was born at 0552 hours, about 20 minutes after the decision was made to perform a Caesarean.  The baby was floppy and pale. Initial Apgar score was 0 and CPR and aggressive fluid resuscitation was undertaken. An Apt test taken prior to the Caesarean was reported after the delivery as positive for foetal blood.

It was noted that there were many clots found inside the uterus. This finding was consistent with an abruption.  Only small portions of the placenta were still attached to the uterine wall above the Caesarean incision. The patient had quite marked uterine atony and   intraoperative blood loss of 1000 ml. Oxytocin, uterine massage and intramyometrial Hemabate© were used to correct the atony. The patient’s hemoglobin dropped to 70, but otherwise she made an uneventful recovery.

The baby weighed 3790 grams. Apgar scores were 0, 0 and 0 at one, five and ten minutes. Full resuscitation was undertaken with CPR, intubation, umbilical line insertion, epinephrine administration, volume resuscitation and infusion of O negative uncrossed blood. The baby recovered a heart rate after 10 minutes and breathed spontaneously. The 15 minute Apgar was 3. A protocol of total body hypothermia was instituted, but his acidemia did not resolve. The baby had evidence of renal and hepatic damage as well as seizure activity and neurologic depression. By the second day of life, the baby was deteriorating and the parents were discussing withdrawal of care when the baby had a sudden significant further deterioration and ventilatory support was withdrawn as a terminal event. 

Post Mortem Findings

No autopsy was done.

Cause of neonatal death was noted as: Multisystem failure and hypoxic ischemic encephalopathy due to perinatal asphyxia and abruption and fetal blood loss.

Discussion

This baby died as a result of intrapartum abruption with asphyxia and foetal blood loss. The final abruptio event occurred suddenly during labour. Prior to this, there was some bleeding and uterine activity increased, but the foetal monitoring was normal.

The Caesarean section was done and the baby delivered 32 minutes after the abruption was detected. Although the baby was resuscitated, he remained profoundly acidemic and multi-organ failure was apparent.

Recommendations

  1. Obstetrical care providers are reminded that antepartum and intrapartum bleeding should heighten suspicion of the possibility of placental abruption.
  2. Obstetrical care providers are reminded that antepartum/intrapartum haemorrhage is an indication for continuous electronic fetal monitoring. (MOREOB Fetal Wellbeing and SOGC Clinical Practice Guideline – Fetal Health Surveillance in Labour, September 2007)
  3. Obstetrical care providers are reminded of the importance of complete and timely documentation.
  4. Obstetrical care providers are reminded of the importance of ensuring that the correct date and time is printed on the electronic foetal monitor (EFM) paper each time that a monitor is applied.   The print out should be verified and corrected as necessary.
  5. Obstetrical care providers are reminded of the importance of having transport personnel who have expertise, technical skills, and clinical judgement to provide proficient care for any emergency that may arise during transport.  (SOGC policy statement, October 2005)


Case: 2010-N-3

History

The mother of the deceased was a 33-year-old G2P1 with an EDD of August 28, 2009. This was a dichorionic, diamniotic twin pregnancy through in vitro fertilization (IVF). Routine prenatal laboratory investigations were normal. IPS was declined. The record does not indicate whether a glucose challenge test was done. She was GBS negative. Regular ultrasounds for fetal growth were normal. The last ultrasound prior to delivery showed both twins were vertex. The estimated fetal weight (EFW) of twin A was 2387 g and twin B was 2484 g.

The mother’s past obstetrical history included one previous term pregnancy for a 6 lb 6 oz girl delivered vaginally at 38 weeks gestation in 2007. Her past medical history was non-contributory. She was on sertraline 50 mg daily during the pregnancy.

She was admitted to hospital on August 10 at 37 weeks and 3 days for induction of labour.

At the time of admission, the patient’s cervix was 1cm dilated. A Foley catheter was inserted for cervical ripening around 1200 hours and oxytocin was started. The Foley catheter fell out around 1430 hours and membranes ruptured spontaneously. The patient reached full dilation at 1750 hours. The oxytocin infusion was stopped and she was transferred to the operating room for delivery.

Twin A, a male infant weighing 2560 g, was delivered spontaneously at 1814 hours.

Twin B was in the vertex presentation. An artificial rupture of membranes (ARM) was carried out for clear fluid at 1819 hours with the station at spines -2 and a fetal scalp electrode was placed. The oxytocin infusion was restarted and the patient was encouraged to push. The fetal heart rate pattern showed what were described as “variable decelerations down to 60-70 with recovery between contractions to a baseline of 150.” The oxytocin infusion increased at 1839 hours.

At 1845 hours, the vertex was at station 0 and at 1900 hours, at station spines +1. At 1906 hours, the oxytocin infusion was increased. The fetal heart rate deceleration pattern continued and at 1915 hours, the station remained at spines +1. At 1919 hours, the bladder was catheterized for 30cc of clear urine. Kiwi vacuum extractor was applied at 1922 hours. A pop off occurred at 1940 hours on the fifth application. The vacuum was applied a sixth time at 1945 hours, but an effective seal could not be obtained and the procedure was abandoned. Increasing caput was noted.  The vertex had been brought down to station +2. During the vacuum procedure the fetal heart rate tracing was discontinuous, but the baseline heart rate was 130-150. Forceps application was then attempted at 1950 hours with the station +2. The oxytocin infusion was stopped and a forceps application was attempted. After three unsuccessful attempts were made to apply the first blade, the procedure was abandoned at 1955 hours. Consent was obtained for Caesarean section.

The procedure began at 2005 hours and the baby was delivered at 2008 hours. The head was noted to be deflexed. Apgar scores were 0, 2 and 2 at one, five and ten minutes. The arterial umbilical cord blood gas showed a pH of 6.61 and bicarbonate of 14. Chest compressions were started and the baby was intubated. Despite resuscitative efforts, the baby remained severely acidotic. The children’s hospital was contacted and cooling was initiated at 30 minutes. When the team from the children’s hospital arrived, the baby was having seizure activity and the pupils were non-responsive. The baby was transferred to the children’s hospital with a clinical diagnosis of Stage III Encephalopathy. Electrophysiological testing confirmed absent cortical responses bilaterally and significant brain dysfunction. The baby was returned to the referring hospital where he died at 1611 hours.

Post Mortem Findings

Severe acute hypoxic-ischemic encephalopathy was confirmed at autopsy. There was evidence of birth injury with a left frontal scalp contusion 6 cm in diameter and a left frontal subaponeurotic hemorrhage.

The placental findings confirmed a diamniotic dichorionic placentation. There was evidence of a retroplacental clot consistent with placental abruption.

The cause of death was severe hypoxic-ischemic encephalopathy.

Discussion

This baby, twin B, died as a result of hypoxic-ischemic encephalopathy. Review of the fetal heart rate tracing shows an essentially normal tracing until approximately the time of ARM of twin B at 1819 hours. Thereafter, the tracing was atypical to abnormal. The tracing would appear to be the indication for proceeding with an operative delivery, although this cannot be determined with certainty by this review. That being the case, the objective would be to effect delivery within several minutes and failing that, to proceed to Caesarean section. Unfortunately, attempts at vaginal delivery with vacuum and then forceps were not only unsuccessful, but unduly prolonged. It cannot be determined from this review why the obstetrician persisted with this approach for this length of time.

There was evidence of birth injury in the form of a left frontal scalp contusion and subaponeurotic hemorrhage. The description is consistent with this being the site of the vacuum application and if so, this would indicate an incorrect application. This could occur if the position was misdiagnosed as occiput anterior (OA) when it was in fact, occiput posterior (OP). With such a misapplication, traction would result in further extension of the head rather than flexion, in effect adding to the cephalo-pelvic disproportion and failed operative vaginal delivery. The narrative of the delivery summary makes no mention of the position of the vertex.

Alternatively, rather than concerns about the fetal heart rate tracing, the decision for intervention may have been based on achieving a certain time interval between deliveries. If the fetal heart rate tracing had been normal, it would have been appropriate to restart labour with oxytocin and apply a fetal scalp clip for continuous electronic fetal monitoring. If descent did not occur readily after the delivery of twin A, as sometimes occurs with twins despite starting from a high station, labour could have been allowed to continue until such time that the presenting part came down to a station where maternal pushing efforts would have been more effective. Current guidelines for the delivery of twin B do not recognize a critical window of time for delivery of twin B provided fetal surveillance testing is normal.

Recommendations

  1. Obstetrical care providers are reminded of the criteria for an abnormal fetal heart rate tracing and the action required as outlined in JOGC September 2007.
  2. Obstetrical care providers are reminded of the importance of ascertaining and documenting in the delivery record, the fetal position prior to the application of the vacuum extractor or forceps.
  3. Obstetrical care providers are reminded of the SOGC ALARM guidelines for operative vaginal delivery and for limiting the number of pulls with the vacuum extractor to three pulls over three contractions with no progress.
  4. The hospital should conduct a review of the management of this case.


Case: 2010-N-4

History

The mother of the deceased was a 33-year-old G5P0A4. The infant was born on May 18, 2009 at 24 weeks gestation.  Obstetrical history revealed that the mother had two therapeutic and two spontaneous abortions in the past.  A dilation and curettage (D&C) had been required on two occasions and she had a cone biopsy in 2008.  The most recent pregnancy was spontaneously conceived.  Prenatal screening was normal. 

At 19 weeks gestation, an ultrasound showed a shortened cervix with mild dilatation, so a rescue cerclage was placed.  The pregnancy progressed satisfactorily until there was a spontaneous rupture of the membranes on May 15, 2009 at 23 3/7 weeks gestation.  The patient was admitted to the high-risk perinatal centre at Hospital A where the rupture of membranes was confirmed.  There were no available beds in the NICU, so transfer to Hospital B was arranged.  She was given indomethacin and betamethasone prior to transfer.  The transport was uneventful.

On arrival at Hospital B in the early hours of May 16, the patient was comfortable and in no acute distress.  Vital signs were normal.  Bedside ultrasound revealed a cephalic presentation, oligohydramnios and a cervical length of 1.7 cm.  She was placed on bedrest and closely monitored.  Over the next two days, she had intermittent cramping which increased in intensity and it became clear that she was going into active labour.  She was transferred to the labour and delivery unit and the cerclage was removed.  There were some variable decelerations and chorioamnionitis was suspected.  She progressed to a spontaneous vaginal delivery at 0103 hours on May 18, 2009.

The infant was born in reasonably good condition with a birth weight of 656 g.  Appearance was consistent with a normal neonate of 24 weeks gestation.  She was intubated and received positive pressure ventilation.  Apgar scores were 4 at one minute, 6 at five minutes and 7 at ten minutes.  Cord gases were normal.  Air entry was tight and it was difficult to oxygenate her, so the endotracheal tube was readjusted with improvement.  Surfactant was given via the endotracheal tube at 0122 hours.  Umbilical lines were inserted by the resident and secured.  Bloodwork was drawn and chest and abdominal X-rays were taken at 0210 hours.  The first arterial blood gas taken at 0150 hours revealed a mixed acidosis with pH=7.11, pCO2=60 mmHg, pO2=62 mmHg, HCO3=19 mmol/L and BE=-10.6 mmol/L.  There was a notation by the nurse that, prior to antibiotic administration via the umbilical vein catheter (UVC), line placement was confirmed by the resident.  The umbilical arterial catheter (UAC) was pulled back by 0.5 cm after the X-ray.  At 0300 hours, some discolouration of the baby’s toes was noted and the UAC was pulled back by an additional 0.5 cm.  Chest and abdominal X-rays were repeated to verify line placement again.  The UAC was withdrawn another 0.5 cm. There is no specific mention of the UVC position or any adjustments to it.

At 0450 hours, there was a sudden jump in heart rate to 259 beats per minute.  The resident was paged, but the heart rate had reverted to 160 before the page was answered.  No further investigation or adjustments were made at that time.  In retrospect, this was likely an episode of supraventricular tachycardia triggered by irritation from the intracardiac UVC.

The baby did well until the evening of May 18 with stable vital signs and improving blood gases.  A lumbar puncture was performed in the late afternoon in response to a reactive white blood cell count on the initial complete blood count.  Although several attempts were required, the baby appeared to tolerate the procedure well.

At 2030 hours, the nurse noticed that the blood pressure tracing from the UAC had become dampened.  Adjustments to the transducer failed to improve the tracing.  The mean blood pressure dropped to less than 22 mmHg and the baby’s heart rate began to drop.  Air entry and chest rise were felt to be good.  The respiratory therapist began to manually ventilate the baby and the doctor on call was paged and quickly attended.  The baby was described as pale and cyanotic.  Oxygen saturation and heart rate continued to drop so cardiac compressions were commenced.  The staff physician was paged and attended the baby.  In spite of ongoing full resuscitation with manual ventilation, cardiac compressions, intravenous administration of normal saline, three doses of epinephrine and a dose of calcium gluconate, the heart rate failed to respond and the baby was pronounced dead at 2056 hours. 

Upon review of the X-rays done earlier in the day, the attending physician noticed that the UVC was “in the heart” and had not been pulled back.  The doctor queried whether the cause of death might have been an arrhythmia or cardiac tamponade.

Post Mortem Findings

Post mortem examination confirmed that the UVC had passed through the foramen ovale and perforated the roof of the left atrium.  Approximately 6 ml of clear fluid was found in the pericardial sac. 

Death was attributed to “pericardial tamponade from UVC perforating roof of LA.” There were no other findings of significance that were felt to have contributed to the baby’s death.

Discussion

This infant died after an umbilical venous catheter that had been inserted for fluid therapy perforated the roof of the left atrium and caused pericardial tamponade.  The problem declared itself with a sudden acute cardiovascular deterioration and the baby did not respond to standard resuscitative measures.  The resuscitation team apparently did not consider pericardial tamponade as a possible cause for the baby’s condition and pericardiocentesis was not attempted.    

Although a rare event, there have been numerous reports of pericardial fluid accumulation and tamponade caused by intravascular central venous catheters in NICU patients.  This can occur when the tip of an umbilical venous catheter, PICC or surgically placed central venous line is located within the heart rather than an extracardiac great vessel.  It is felt that the tip can erode through the atrial wall and infused fluid gradually accumulates leading to an acute reduction in cardiac output.  Presentation is often sudden and dramatic with a rapidly fatal course unless prompt action is taken.  Many neonatal practitioners have never seen this complication and may not consider pericardiocentesis as a step to take when standard resuscitative measures are unsuccessful.  Knowledge of a suboptimally placed central venous catheter within the heart would certainly raise the index of suspicion.  However, in this case, the care providers that were present when the infant deteriorated were unaware that the UVC was malpositioned.

Umbilical vessel catheterization is one of the most frequently practiced procedures in neonatal patients.  Guidelines for placement of umbilical and other central venous catheters are widely available.  Included are recommendations for length of catheter insertion (based on a mathematical formula using external measurements or the baby’s weight) and optimal catheter tip position.  A central venous catheter that is intracardiac should be withdrawn until the tip is in one of the great vessels to remove the risk of tamponade.  Determination of exact catheter tip position can sometimes be difficult if it is very close to the junction of the vena cava and right atrium and there is a case report of fluid infusion into the pericardial sac even when the tip of the UVC appeared to be in optimal position on X-ray (J Perinatol 2007;27:317-319).  Bedside ultrasound has been proposed as a tool to help ensure optimal positioning.   However, in this infant’s case, it is clear from the radiologist’s report that the catheter tip was in the heart.  The main problem leading to the fatal complication was the failure to recognize that the UVC was malpositioned and to respond appropriately.

Although there is no detailed procedure note, the umbilical catheters were successfully and uneventfully inserted by the resident within the first hour after birth.  Two X-rays were performed thereafter to check catheter position, but the poor positioning of the UVC tip was not recognized.  It is unclear whether the resident did not appreciate the position or was unaware of the guidelines.  When the regular daytime clinical team took over care, it does not appear that the films from the night before were reviewed.  When a radiologist subsequently reported the malpositioned UVC tip and recommended readjustment, the information did not reach the clinical team in time to prevent the complication. 

There are a number of measures that could be applied to minimize the risk of such an event in the future.  Staff should ensure that anyone authorized to insert central venous catheters in neonates is certified to do so and has completed the necessary training.  A pre-insertion checklist that includes calculation of insertion distance should be used to ensure proper insertion technique.  Verification of catheter tip position by X-ray should be routinely performed and double-checked whenever possible.  Staff accepting transfer of care for an infant who has had a line inserted in the previous shift should routinely review the relevant X-rays to verify acceptable positioning.  Also, a method to expeditiously communicate critical findings detected by a radiologist (including sub-optimally place central lines) to the relevant members of the clinical team should be in place.

The staff at Hospital B recognized the medical error and quickly disclosed this information to the family.  There were several checks and balances that, had they been standard procedure at the hospital, could have detected the error in time to prevent the fatal complication.  This sentinel event should trigger a review and implementation of recommendations to avoid deaths in similar circumstances.

Recommendations

Neonatal health care providers are reminded that pericardial tamponade can be the cause of acute circulatory failure in a neonate with a central venous line and should be considered when standard resuscitative measures are unsuccessful in restoring output when ventilation is adequate.  Emergency pericardiocentesis can be life-saving.

  1. Centres providing neonatal intensive care services should ensure that anyone authorized to insert central venous catheters in neonates is certified to do so and has completed the necessary training.
  2. For insertion of umbilical catheters in neonates, use of a pre-insertion checklist that includes calculation of insertion distance should be considered to ensure proper technique and good positioning.
  3. Verification of catheter tip position by X-ray should be routinely performed and double-checked whenever possible.  Staff accepting transfer of care for an infant who has had a line inserted in the previous shift should routinely review the relevant X-rays to verify acceptable positioning.
  4. Hospitals providing intensive care services should ensure that there is a process in place to communicate critical findings detected by a radiologist (including sub-optimally place central lines) to the relevant members of the clinical team.


Case: 2010-N-5

History

The mother of the deceased was a 36-year-old G2P1 who had one previous Caesarean section for breech presentation at term. Her prenatal care was provided by an obstetrician. Her lab tests and four ultrasounds were normal. She declined genetics screening. The Caesarean was over 18 months previous and a two layer closure was employed. The obstetrician had discussed with her a trial of labour in the current pregnancy.

The patient was admitted for induction of labour at 40 weeks gestation due to ongoing back pain. Her obstetrician performed an artificial rupture of membranes at 0800 hours. Electronic fetal monitoring was implemented and was normal. Intravenous oxytocin was commenced at 0900 hours at 4 mu/min. The dose was increased by 4 mu/min every 15 minutes to 20 mu/min at 1000 hours. At 1000 hours, the contractions on external toco were every 2-3 minutes with many prolonged contractions. On several occasions, the uterine tone failed to return to baseline during 3 or 4 contractions.

The fetal heart rate however remained normal until 1145 hours when late decelerations appeared with virtually every contraction. By 1200 hours, there was no variability in the baseline which had increased from 150 to 160 bpm. The decelerations changed to complicated variable decelerations and persisted with each contraction. The patient was noted to be up to void and repositioned into a rocking chair. At 1215 hours, the nurse noted the decreased variability and decreased the oxytocin drip from 20 mu/min to 10. At 1222 hours, the nurse repositioned the patient into bed. She noted that the patient had a lot of pain and discussed an epidural with her. The fetal heart continued to have minimal to absent variability and deep decelerations with each contraction. At 1230 hours, the nurse performed a vaginal exam and found the cervix to be 3 cm.

At 1235 hours, the nurse paged the obstetrician who attended at 1241 hours and reviewed the tracing. After discussion with the parents, a Caesarean was planned. The oxytocin was discontinued at 1242 hours and the patient was prepared for surgery. At 1253 hours, as the preparations were underway, the mother had a sharp pain and the fetal heart dropped to 50 bpm. At this point, she was moved to the operating room urgently, arriving at 1302 hours. A spinal anaesthetic was placed and the surgery commenced at 1318 hours.

The obstetrician found the uterus had ruptured along the previous scar and the baby was partially expelled into the abdominal cavity. The baby was delivered at 1324 hours and given to the pediatrician. The infant was hypotonic with Apgar scores of 1, 1 and 2 at one, five and ten minutes. The arterial cord gases showed pH <6.8, pCO2 =113, pO2=17. The venous cord gases showed pH <6.8, pCO2 =125, pO2=8.

The baby was intubated and chest compressions began in the operating room. The baby was transferred to the special care nursery after six minutes. The baby began to have seizures at one hour of age. She was transferred to the tertiary care centre at six hours of age, where it was determined that the prognosis was very poor due to severe birth asphyxia.  The infant died after life support was withdrawn on the fourth day.

Post Mortem Findings

There was no autopsy or placental pathology.

Cause of Neonatal Death: Hypoxic ischemic encephalopathy

Discussion

This baby died of severe perinatal asphyxia secondary to uterine rupture during a trial of labour after previous Caesarean section. The mother’s labour was induced at term with ARM and intravenous oxytocin. The protocol for oxytocin induction in this hospital is not in keeping with the standard of care. The starting dose was high and the time between dose increases was too short. The nurse followed the protocol as ordered. The mother developed an extremely active labour pattern with tachysystole after only 60 minutes of IV oxytocin. At this point, the drip should have been stopped or decreased significantly. However, the fetal heart rate was not affected for another 90 minutes and no changes were made.

The baby then developed an increased baseline heart rate with loss of variability and late decelerations. With this abnormal fetal heart rate, the doctor should have been called 20-25 minutes earlier than he actually was. The oxytocin should have been stopped and intrauterine resuscitation begun. When the obstetrician did arrive, the decision was made to move to Caesarean section, but there did not seen to be any recognition of the urgency at the time. Ten minutes later, she was still in the labour room when the final bradycardia occurred and the mother noted a marked increase in her pain. This should have suggested uterine rupture to her caregivers.

Although the transfer to the operating room (on a different floor of this hospital) was then made urgently, the team still took time to place a spinal anaesthetic and perform a Pfannenstiel incision. The baby was delivered 22 minutes after the mother arrived in the operating room and 31 minutes after the uterine rupture likely occurred with a terminal bradycardia.

The baby had suffered severe asphyxia prior to the birth. It is impossible to know how different the outcome might have been if the signs of uterine tachysystole and hyperstimulation were recognized earlier and acted on appropriately. Uterine rupture is a known complication of trial of labour after Caesarean, and use of oxytocin to induce or augment the labour does increase the risk of uterine rupture. When rupture occurs, the outcome is often devastating for the fetus. The asphyxia is acute and so profound that even if the Caesarean can be done immediately, the results are often very poor.

Recommendations

  1. This hospital should review and revise its policy for oxytocin induction of labour.
  2. The nurse and obstetrician should review the interpretation of electronic fetal monitor tracings including definitions of excessive uterine activity.
  3. The hospital should review its policy for trial of labour after Caesarean.


Case: 2010-N-6

History

The mother of the deceased was a 33-year-old G2P0 with an EDD of May 9, 2009. Routine prenatal laboratory investigations and second trimester ultrasound were normal. Prenatal genetic screening was declined. Second trimester GCT was normal and she was GBS negative.

The mother’s past medical history included a spontaneous abortion at 5 weeks gestation in 2008 and a right pyeloplasty. At her first prenatal visit, her blood pressure was 120/90, weight 196 lbs and BMI 34. On April 23, at 37 weeks gestation, her blood pressure was 140/100 with trace protein. A repeat blood pressure four days later was 130/100, again with trace protein. She was started on labetolol 100mg, twice daily. On May 4, at 39 weeks gestation, her blood pressure was 120/80 and on May 11, it was 120/80. The labetolol was decreased to 50mg twice daily.  Foetal growth by SFH measurements was appropriate.

The patient was booked for induction on May 15 at 40 weeks, 6 days gestation. She underwent cervical ripening with prostaglandin gel on May 14.  At the time of cervical ripening, the cervix was 2 cm dilated and thick with the vertex at spines -3. Foetal heart rate tracing was normal.

Labour onset was at 0600 hours and the patient presented to the Labour Unit at the hospital at 0900 hours. On admission, she was 3-4 cm dilated. An epidural was to be started, but she quickly reached full dilation at 1100 hours. An artificial rupture of membranes was carried out at 1110 hours for clear fluid. On examination at 1300 hours, the position was determined to be occiput posterior. Because of the length of time in the second stage to that point and the position, the option of placing an epidural and assisted delivery were discussed. By 1330 hours however, progress had occurred and it was apparent that an unassisted vaginal birth would occur. The patient went on to a spontaneous delivery at 1402 hours of a 3460 g male infant in the occiput posterior position.

There were no cord complications. Apgars were 0, 0 and 3 at one, five and ten minutes. Chest compressions and bag and mask ventilation were begun within a minute and a “Code Pink” was called. The pediatrician attended at two minutes and the baby was intubated by three minutes. The baby was given a saline bolus 20cc IV and epinephrine 1cc of 1:10,000 at seven minutes. A second bolus of saline 10cc and 1cc of epinephrine was given at eight minutes and a heart rate was first detected at eight and a half minutes. Arterial blood gas drawn at twelve minutes showed a pH of 6.51. The pupils remained fixed and dilated and there was never any spontaneous respiration or movement. By thirty minutes, the heart rate started decreasing despite continuous bagging. The bagging was discontinued after which the baby had occasional agonal breaths. By one hour and 35 minutes, no heart rate could be detected and the baby was pronounced dead.

Cord blood gases were pH 6.66, pCO2 123, bicarb 13 and base excess -27.

Post Mortem Findings

Pertinent findings at autopsy related to the central nervous system. There was evidence of axonal injury in a pattern that can be associated with trauma, ischemic brain injury or a combination of the two. There was also evidence suggestive of brain swelling raising the possibility of early hypoxic-ischemic brain injury.

There were no significant placental findings.

The cause of death was stated as acute hypoxic-ischemic brain injury.

Discussion

This baby died as a result of hypoxic-ischemic encephalopathy. The changes at autopsy were early and in keeping with the insult occurring around the time of labour and delivery. Review of the fetal heart rate tracings indicated a normal tracing on the evening of May 14 at the time of insertion of prostaglandin gel. The following morning, the mother was admitted in labour around 0900 hours and continuous electronic fetal monitoring was started. The tracing was initially normal. Decelerations began to occur starting around 1053 hours, with late decelerations occurring at 1139 hours. The tracing for the most part thereafter meets the criteria for an abnormal tracing with repetitive decelerations and an erratic baseline. The concerning pattern does not appear to have been appreciated by the care providers.

Recommendations

Obstetrical care providers are reminded of the criteria for an abnormal fetal heart rate tracing and the action required as defined by SOGC Intrapartum Fetal Surveillance Guidelines published in September 2007.

Obstetrical care providers at the hospital should  review this case with attention to the application of the SOGC Intrapartum Fetal Surveillance Guidelines.



Case: 2010-N-7

History

The mother of the deceased was a 25-year-old G4T1P0A2 who was at 34.5 weeks gestation when she developed sudden vaginal bleeding. She was visiting family in a small Southwestern Ontario community at the time.

Her prenatal care had been provided by her family physician in her home community. There had been no complications in the pregnancy to date. She had two first trimester ultrasounds and a 20 week scan which showed no placenta previa. She had previously had a Caesarean section for failure to progress in labour at 40 weeks. She had a history of asthma, reflux, cervical dysplasia and depression. Her medications included salbutamol and fluoxetine. She was a smoker. She was to be transferred to an obstetrician for delivery.

When the patient experienced bleeding at 1226 hours, 911 was called. An ambulance was dispatched and arrived in 14 minutes with lights and sirens activated. She was assessed by the paramedics at the relative’s house that she was visiting. The ambulance departed after 11 minutes and she was transported to hospital. The ambulance arrived at the hospital in 20 minutes; this was 45 minutes after the initial 911 call was made. During the transfer, an IV was started and oxygen was given by nasal cannulas. The lights and sirens were not employed between the scene and the hospital.

On assessment in the triage area at 1312 hours, the patient was found to have bleeding and a fetal heart rate of 90 bpm was auscultated by the nurse. At 1317 hours, the obstetrician on call performed a bedside ultrasound and confirmed abruption and a fetal bradycardia. An emergency Caesarean was performed under general anaesthesia. The obstetrician noted that the placenta was abrupted on ¾ of its surface and found 1000 ml of clot and blood behind the placenta as well.

The baby was born at 27 minutes after arrival in the hospital at 1339 hours. The baby weighed 2145g and had Apgar scores of 1, 3 and 3 at one, five and ten minutes. The baby had no respiratory effort, tone or heart rate on delivery. The paediatrician, neonatal nurse and RT attended the birth. Positive pressure ventilation and compressions were given at zero and one minute of age. The baby was intubated at two minutes and PPV continued as he was transferred to the nursery.

Physical exam revealed no dysmorphic features. His chest was clear and cardiac exam normal. The pupils however were fixed and the baby had no response to pain. Cord gases showed arterial pH=6.59, PCO2=146, PO2=18, bicarbonate=13 and venous pH=6.75, PCO2=102, PO2=29, bicarbonate=13, base excess= -28. Arterial gases at 30 minutes of age showed pH=6.85, PCO2=48, PO2=98, bicarbonate=8, base excess=-29. The baby began to desaturate and was felt to be having seizures. He also demonstrated posturing that was quite concerning to the paediatrician. The paediatrician discussed withdrawal of support and the endotracheal tube was withdrawn at 39 minutes of age at 1417 hours. The baby died at 4 hours and 4 minutes of age.

Post Mortem Findings

An autopsy was not performed. Placental pathology was not done.

Cause of Neonatal Death: Perinatal asphyxia secondary to placental abruption.

Discussion

This baby died of severe perinatal asphyxia secondary to an acute abruption. The mother arrived at hospital by ambulance 45 minutes after the initial 911 call was made. An emergency Caesarean was undertaken and the baby was delivered 27 minutes after arrival in the hospital.

An abruption can occur suddenly without warning and although early presentation to the hospital and rapid delivery are desirable, it is impossible to know what difference, if any, delivery a few minutes earlier might have made in the baby’s prognosis.

The parents were concerned with the length of time it took the ambulance to arrive and transport the mother to the hospital. The case has been reviewed by the Director of Emergency Medical Services (EMS) for the area where ambulance services were provided. It was concluded that “the crew did not take into account the possible severity of the imminent birth and possible shock of the patient based on the incident history.” It was felt that this led to the patient being “inappropriately triaged” and led to a “slower transport time to hospital than would have been expected.” The paramedics involved have since attended and successfully completed a full day Obstetrical Emergency Training Session.

Recommendations

1. Obstetrical care providers should request placental pathology in cases where there are signs and symptoms of abnormal vaginal bleeding and/or evidence of abnormalities of fetal wellbeing.



Case: 2010-N-8

History

The mother of the deceased was a 34-year-old G2T1L1 with an EDD of September 6, 2008.   Her past history included the delivery of a 7 lb 13 oz infant at term by Caesarean section.  Sometime prior to that, she had a myomectomy, so the Caesarean had been elective. At that time, there was evidence of an occult dehiscence with only membrane covering the posterior portion of the uterus.  The patient was advised not to get pregnant.  She did not follow through on a request for a tubal sterilization.  She became pregnant and was booked for an elective repeat Caesarean section at 37 weeks and 2 days gestation on August 20, 2008.  

During this pregnancy she was on methyldopa 250 mg, to be taken orally, twice a day. Her blood pressure (BP) remained close to normal for most of the pregnancy. Her BP became slightly elevated at 35 weeks gestation at 140/80. 

On August 11, 2008 the patient visited her obstetrician’s office. Her BP was elevated at 180/120 and the patient was advised to go to the hospital that evening for consideration of an earlier delivery. The patient left the obstetrician’s office and was taking a transit bus home to get her belongings prior to going to the hospital.  Upon exiting the bus, the patient fell to the ground.  911 was called and the EMS responded.

The EMS report indicated that they were notified of the call at 1355 hours.  There are no other times on the report (i.e. when the patient was picked up or when vital signs were taken).  The assessment by EMS indicated a blood pressure of 114/62 and regular pulse of 80.  The patient stated to them that she had abdominal pain all over.  The EMS report noted that, “the patient not communicating/refusing to answer questions as she states too much pain to talk.”  The only injury documented was “minor abrasion to left elbow and left hand.”

The patient was transported to hospital.  The emergency record indicated that she was registered at the hospital at 1435 hours.  The patient appeared “out of it” and was “half in, half out of the wheelchair” and was complaining of abdominal pain.   Her vital signs at that time revealed a BP of 87/55, respirations 22, pulse 89, temperature 35.7. The attending obstetrician was contacted at 1455 hours and arrived at 1459 hours.

The patient was taken immediately to the operating theatre for an emergency Caesarean section.   The room was ready at 1500 hours and anesthetic care started at 1508 hours.  The procedure start time was 1518 hours. The initial anesthetic assessment indicated a blood pressure of 78/31 with pulse of 104. The anesthetist was “unable to take a history.  The patient uncontrollably irritable.”  Uncrossed blood was asked for as the blood bank estimated that greater than 30 minutes was required for a crossmatch.   A general anesthetic was administered.

A midline infraumbilical incision was made. There was considerable free blood in the peritoneal cavity. There were numerous intramural and subserosal fibroids and a high lower segment incision was made because of the fibroids.   The amniotic fluid was clear on entering the uterus. The baby was delivered as a vertex, but there were no vital signs present at the time of delivery.

The uterus was exteriorized and there was evidence of a large, fist-sized, rupture. Initial attempts were made to close the rupture site as well as the delivery site on the anterior wall. However, due to continued bleeding, a decision was made to proceed to a hysterectomy.  The patient had a hemoglobin of 55 prior to the surgery and had lost quite a lot of blood and was receiving packed cells intraoperatively.  A subtotal hysterectomy was performed as well as an appendectomy as the appendix was adhered onto the uterus.

The patient’s condition was stable during the operative procedure during which she received ten units of packed red cells, six units of fresh frozen plasma and 6400 cc’s crystalloid.  She had an estimated blood loss of 5½ liters. She was transferred to the intensive care unit and her subsequent postoperative course was unremarkable. She was discharged home on Day 10.

The infant was born at 1524 hours and weighed 3400 g. Apgars scores were 0 at one, five and ten minutes of age. The neonatal resuscitation record was not available for review, but information obtained in the Coroners Investigation Statement (Form 3) indicated that during the resuscitation, a spontaneous heart rate was obtained at 1640 hours. The initial arterial pH was reported as less than 6.8.  At 1642 hours, after a consultation with the children’s hospital, withdrawal of care was recommended due to a very poor prognosis.   Death was pronounced at 1915 hours.

Post Mortem Findings

Post mortem examination showed findings compatible with intrauterine asphyxia and an otherwise normally developed infant. The central nervous system showed normal development with congestion of the microvasculature.  

Placenta examination revealed mild meconium on the amnion.  There was patchy intravillous hemorrhage and suggestion of basal hematoma which raised the consideration of placental abruption.   However, no definite morphologic evidence of significant retroplacental hematoma was seen. On examination of the uterus, there was an area of focal placental acreta.   On the antenatal record, there was indication that the placenta was anterior. This was likely not relevant to the posterior wall uterine rupture.

The appendix that was adherent into the myometrial wall at the time of surgery showed fibrous adhesion with focal hemorrhage and chorionic villi present in the peri appendicial tissue.   The uterus had 10 fibroids measuring up to 10.5 cm in diameter.  

The final pathological diagnosis was consistent with the clinical history of intrauterine pregnancy with ruptured uterus.

Discussion

This newborn infant died within a few hours of being born due to intrauterine asphyxia secondary to maternal hemorrhage and hypotension due to uterine rupture.

This uterine rupture likely occurred at the time, or shortly before, the mother had a fall upon leaving the transit bus.  Her blood pressure was very elevated upon leaving her physician’s office.  When her blood pressure was checked by the EMS responding to her fall after leaving the bus, her blood pressure was significantly lower.  This abrupt change in blood pressure was likely due to the intra-abdominal hemorrhage.  This hemorrhage could have predisposed her to a fall. There was no information on the record to suggest that a blow to the abdominal wall sufficient to cause a uterine rupture occurred. As well, it was known from her previous pregnancy that she had an extremely thin posterior wall in the fundal portion of the uterus. This predisposed the patient to spontaneous uterine rupture and was the reason the patient was pre-booked for an elective Caesarean section at 37 weeks gestation.  

The family identified a concern regarding the length of time taken to transport the patient to hospital.  Records indicated that approximately 40 minutes had elapsed from the time 911 was contacted until the time EMS responded and the patient was transported and received at the hospital.   Although it is unclear whether a faster trip would have made a difference in this case, acute abdominal pain over a gravid uterus in a woman who has just had a fall should in itself alert the EMS crew to a highly probable diagnosis of acute placental abruption.  This potential diagnosis should warrant expedited transportation to the hospital, even if vital signs appear “normal.” This would suggest a learning opportunity for EMS crews relating to the acute assessment of injured pregnant patients under their care.

Closer surveillance and a plan for earlier delivery might have been warranted in this case. The patient had a known risk of uterine rupture, even spontaneous rupture without labour, from the recognition of an occult potential for a muscle rupture in her previous pregnancy.

Though ultrasound is often not helpful in determining the potential for rupture, where a previous significant defect has been seen, ultrasound surveillance may be warranted.   The posterior wall of the uterus may be difficult to assess by ultrasound, but MRI can be considered in such cases.

Recommendations

  1. Training of EMS crews in knowledge of obstetrical emergencies, and in particular an acute abdomen, should be reviewed.
  2. Obstetrical caregivers are reminded of the risk of spontaneous uterine rupture through a previous surgical scar in the uterine fundus.  Close ultrasound surveillance and timely delivery should be considered, particularly with previously documented uterine wall defects.


Case: 2010-N-9

History

The mother of the deceased was a 39-year-old G6 P4 with an EDD of September 4, 2008. Second trimester ultrasound done on April 4 was normal. Routine prenatal laboratory investigations were normal except for a hemoglobin of 86 gm. A second trimester GCT was abnormal at 9.5. A follow up Oral Glucose Tolerance Test (OGTT) was normal. Routine prenatal visits showed normal blood pressures and a symphysis fundal height (SFH) within normal limits. She was GBS negative.

The patient’s past obstetrical history was significant for delivery by Caesarean section in her first pregnancy of a 6 lb. female infant. She subsequently had three successful vaginal births after Caesarean (VBAC’s), two of which were spontaneous vaginal deliveries for 7 lb girls and the third a low vacuum extraction for a 7 lb boy.

Her past medical history was non-contributory and the plan was for her to have another VBAC.

The patient was admitted in labour to the hospital on August 31 at 2030 hours. Continuous external fetal heart rate tracing was commenced at 2040 hours. The cervix was 4 cm dilated. Consent was obtained for VBAC.

Oxytocin augmentation was started at 2200 hours at 1mU/min and was gradually increased to 5mU/min at 0245 hours. An artificial rupture of the membranes was performed at 2300 hours for clear fluid and an epidural was started at 2345 hours. At 2355 hours, she was 5 cm dilated and at 0125 hours she was 6 cm dilated. She was fully dilated at 0210 hours.

The obstetrician was notified of variable fetal heart rate decelerations at 0305 hours and the oxytocin infusion was stopped. The tracing was reviewed and a note was made that the fetal heart rate had recovered. Oxygen was given and she was encouraged to continue to push, however this was not effective and was stopped at 0310 hours. The oxytocin infusion was restarted at 0315 hours. Pushing restarted at 0400 hours. The tracing was again reviewed at 0410 hours and a note was made that it was satisfactory.

At 0430 hours, she had an episode of emesis. The fetal heart rate tracing subsequently became abnormal. She was assessed at 0505 hours for fetal bradycardia. The uterus was noted to be tender, but there was no vaginal bleeding. The cervix was fully dilated with the vertex at spines +2. Vacuum extraction was considered, but it was noted that the station of the presenting part was moving higher. Preparations were made for emergency Caesarean section. At this time, vaginal bleeding was noted and uterine rupture was suspected. She was delivered at 0530 hours of an approximately 2300g male infant. On opening the peritoneal cavity, it was confirmed that the uterus had ruptured and the baby had been extruded from the uterus. Apgars were 1, 3 and 4 at one, five and ten minutes. Arterial cord gas pH was 6.55.

The baby was intubated and started Positive Pressure Ventilation (PPV) and chest compressions. An umbilical venous catheter (UVC) was placed and two boluses of normal saline were given. Cultures were sent and antibiotics were given. By 2 hours and 30 minutes of age, seizure activity was noted. Phenobarbital 20mg/kg was given. The children’s hospital was contacted and the transport team arrived at approximately 0815 hours. The team was able to wean ventilation, but the baby remained unresponsive with fixed pupils. Blood gases showed persistent metabolic acidosis. Further seizure activity was noted and Phenobarbital 10mg/kg was given. A cooling protocol was started. The baby was transferred to the children’s hospital. During transport, another bolus of normal saline was given because of poor perfusion.

On admission to the children’s hospital, the infant remained unresponsive. Another seizure episode was noted. Blood work showed persistent metabolic acidosis. After discussions with the family, it was decided that end of life care would be provided. The infant was returned to the first hospital for continued end of life care and was pronounced dead at 0651 hours on September 2, the day following birth.

Post Mortem Findings

An autopsy was not performed.

Discussion

This infant died from severe hypoxic-ischemic encephalopathy resulting from intrapartum asphyxia as a complication of uterine rupture. While the mother of the deceased had three uncomplicated vaginal births following delivery of her first child by Caesarean section, the risk of uterine rupture was recognized and consent was obtained at the time of admission in labour.

The mother’s progress in labour was considered adequate, however progress was in fact slow, particularly during the second stage for a multiparous patient, despite oxytocin augmentation. Review of the progress notes suggested that progress was slow during the second stage due to ineffectual pushing as she did not feel any pressure.

Review of the fetal heart rate tracing showed an atypical pattern beginning at approximately 0340 hours. The pattern became decidedly abnormal following an episode of emesis at 0430 hours. The patient was not assessed until 0505 hours at which time delivery by vacuum extraction was considered, but abandoned as the station of the presenting part had moved higher. It cannot be determined by this review if earlier delivery by Caesarean section would have changed the outcome.

Recommendations

  1. Obstetrical care providers are reminded to have a high index of suspicion of uterine rupture in a patient with a previous Caesarean section who develops fetal heart rate changes.
  2. Obstetrical care providers are reminded of the need to proceed to immediate delivery in the presence of an abnormal fetal heart rate tracing.
  3. Obstetrical care providers are reminded of the guidelines for the management of the second stage of labour.


Case: 2010-N-10

History

The mother of the deceased was a 19-year-old G1P0 who was 5’3” with a body mass index of 24 at intake to midwifery care at 11 weeks and 2 days. Blood pressure and urinalysis for protein and glucose were normal throughout her pregnancy. She was HIV, Hepatitis B, syphilis and gonorrhea negative. The mother declined genetic screening and was rubella immune and GBS positive. A 75g OGTT was normal at 29 weeks and 3 days. She had her first ultrasound at 11 weeks and 5 days and an EDD of July 5, 2008 was established. The second ultrasound was done just after 19 weeks and showed an anterior placenta clear of the cervix and normal anatomy (limited cardiac views). The third ultrasound was done at 24 weeks and 3 days, confirming normal anatomy.

The fourth ultrasound was done at 35 weeks and 5 days because of a sudden increase in symphysis fundal height detected by the midwife. The ultrasound showed polyhydramnios with a large for gestational age (LGA) baby measuring 38 weeks size. The estimated fetal weight was 3423 g which is close to the 95th percentile. The midwife discussed the LGA with the mother and informed her of what to do if a rupture of membranes occurred.

On June 6 at 35 weeks and 5 days, the mother was seen in the hospital for possible preterm labour. She was assessed by her midwife at 0001 hours and her cervix was long and closed, with no evidence of ruptured membranes. Fetal monitoring showed irregular, but frequent, uterine activity on the toco, with a baseline fetal heart rate of 145 to 150 bpm and accelerations with no decelerations. A telephone consult was made with the obstetrician on call and orders for GBS prophylaxis and sedation were obtained. Four hours later, the obstetrician assessed the mother and noted clinically “marked” polyhydramnios. He also mentioned that a 75g OCTT was normal at 28 to 30 weeks. At this point, her contractions had settled and she was discharged home with recommendations for repeat ultrasound in a week or two. No further investigation or follow-up regarding the macrosomia was suggested.

On June 13, the fifth ultrasound, at 37 weeks, again showed a macrosomic 41 week size fetus with an estimated fetal weight (EFW) of 4313 g, with normal amniotic fluid volume. The sixth ultrasound was done on June 30, at 39 weeks and 2 days. This scan showed an estimated weight of 4758 g, amniotic fluid at the upper limits of normal and BPP 6/8.

On July 1, the mother presented to the hospital at 1417 hours with decreased fetal movement at 39 weeks and 3 days. She was assessed by her midwife and was noted to be 2-3 cm dilated with cervix 1 cm long and a ballotable presenting part at spines -3cm. The EFM record showed a baseline rate of 140-150 bpm with minimal variability, no accelerations and late decelerations. The toco picked up uterine activity every 2-4 minutes, but quite irregular. She was referred to the obstetrician on call due to concerns of decreased variability and possible early labour with polyhydramnios and macrosomia. The obstetrician noted the baseline to be “100” (possibly in error), with minimal variability. The obstetrician discharged the mother home at 1515 hours indicating to the patient that she was likely in early labour and to return immediately to hospital if there was any progress. If there was no progress, she should return in the morning and have an ultrasound and biophysical profile completed.

On July 2 at 0515 hours, the mother paged the midwife to report spontaneous rupture of membranes with greenish coloured fluid and some fetal movements with no cord in the vagina. The midwife advised the mother to go to hospital and arranged for monitoring of the fetus by a registered nurse when the mother arrived.

The mother arrived at the hospital at 0620 hours. EFM was commenced at 0626 hours. The tracing was very difficult to interpret, but was markedly different from 12 hours earlier and also from the June 6 tracing. Nurses’ notes indicated that the FHR was down to 105-115 bpm with normal variability, maternal pulse 90, pulse monitor reading 108 (palpated 90-100) and FHR 100-110 bpm. At 0630 hours, a vaginal exam by the nurse revealed that the mother was dilated 2-3 cm, -2 spines, 70% effaced and clear fluid.

At 0635 hours, the nurses attempted to contact the midwife. The midwife had been at another hospital delivering a baby, but was en route. The fetal heart continued to show marked abnormalities with variability between 105 and 120 bpm. Nursing notes showed the fetal heart to be 105-115 bpm with good variability and accelerations. The midwife arrived by 0655 hours and requested that the nurse place an IV. An IV was started at 0703 hours, O2 at 0705 hours and physicians were called at 0706 hours. The midwife attempted to attach the EFM spiral electrode and noted a large amount of meconium stained fluid. At 0711 hours, a Foley catheter was placed and the operating room was called to prepare for emergency Caesarean section. Further attempts to replace the scalp clip did not produce an interpretable tracing.

At 0718 hours, the obstetrician arrived and assumed care. Fetal heart tracing was unchanged and the scalp clip indicated 105 to 110 bpm with a very unusual pattern that was most likely maternal. There was an informed choice discussion with the parents regarding need and urgency with the abnormal fetal heart tracings. The obstetrician did not request or perform an ultrasound to rule out intrauterine demise. At 0740 hours, general anesthesia was started and at 0749 hours, surgery was commenced. At 0753 hours, an unresponsive male infant weighing 5476 g, with Apgar scores of 1, 1 and 0 at one, five and ten minutes was delivered.

Cord gases were ordered, but cord bloods could not be drawn. The placenta was delivered at 0756 hours with obvious meconium staining. The mother sustained a blood loss of 1100 ml and was treated with 30IU oxytocin IV 1000 RL, 200 mcg Hemabate© IV and misoprostol 800 mcg rectally.

There were many physicians, nurses, respiratory technologists and a midwife in attendance at the Caesarean section and immediate and appropriate resuscitation followed. The baby could not be resuscitated and was pronounced dead at 0824 hours.

Post Mortem Findings

No autopsy was performed and no placental pathology report was provided for review.

Discussion

This woman had clear evidence of marked polyhydramnios and macrosomia when she was seen at the hospital for possible preterm labour at 35 weeks and 6 days. She was attended both by her obstetrician and her midwife. Both were aware of the ultrasound result from the day before as well as a normal OGTT done 6 weeks previously. Her preterm labour settled and she was discharged. At that time, further investigations for gestational diabetes were indicated, but none were ordered.

At the 38 weeks and 4 days midwifery visit, a repeat ultrasound consultation with an obstetrician regarding a large for dates fetus and excessive fundal height increases was requested. There is no record to indicate that the consultation occurred. The ultrasound done five days later, at 39 weeks 2 days, confirmed an extremely large fetus of over 4700 g with BPP 8/8. Investigations for diabetes were still not ordered.

The day after this ultrasound, the mother came to the hospital with decreased fetal movement and cramping. The EFM showed irregular contractions and the fetal heart rate tracing was abnormal with absent variability and late decelerations. In addition, her cervix was found to be open at 2-3 cm with the presenting part still ballotable.

The patient was seen by her midwife who consulted the obstetrician about the fetal heart tracing. The obstetrician did not identify the tracing as abnormal. The obstetrician also did not identify the risks of an open cervix with an unengaged presenting part in early labour. The midwife may have recognized the tracing as requiring intervention and also the risks of cord prolapse, but failed to challenge the obstetrician on the management plan. Urgent delivery was indicated at that time although the mother was discharged home.

The mother returned a few hours later with what appears to have been fetal demise.

Recommendations

  1. The nurses, midwives and doctors involved with this patient should review EFM interpretation.
  2. Obstetrical care providers are reminded of their responsibility to question the care provided to patients they are attending. If they feel the care is below standard they should consult with other midwives, nurses, doctors and administration until satisfied.
  3. Obstetrical care providers are reminded of the risk of cord prolapse in early labour with a macrosomic unengaged baby and cervical dilation.
  4. Obstetrical care providers are reminded of the need for a thorough work up for women with polyhydramnios, macrosomia, or both.
  5. Obstetrical care providers are reminded of the need for repeated glucose testing in each trimester in pregnancies with risk factors for gestational diabetes.
  6. Obstetrical care providers are reminded that in all complicated deliveries, including neonatal death and stillbirth situations, the placenta should be sent to pathology for examination and reporting as per the coroner’s guidelines.
  7. Obstetrical care providers are reminded that it is recommended that all ultrasound reports should be sent to the place where the birth is planned. This should be done by either the obstetrical care provider or directly from the ultrasound department.


Case: 2010-N-11

History

The mother of the deceased was a 28-year-old healthy primigravida with an EDD of October 8, 2009. She had ultrasounds at 6, 12, 19, 20, 33 and 38 weeks and all showed normal growth and anatomy. Routine prenatal labs were all normal and a first trimester screen was negative for Down’s Syndrome. A glucose tolerance test at 25 weeks and GBS swab at 36 weeks were also negative. Her care was provided by an obstetrician from 13 weeks.

The mother came to the triage area of the hospital on October 1, 2009 with a question of possible spontaneous rupture of the membranes. This was ruled out and she was discharged after a normal non-stress test (NST) was completed. On October 12, she came to triage with pinkish spotting and decreased fetal movement. She was seen by the obstetrician on call and her cervix was found to be closed. An NST was performed and was normal. She was discharged home at 1140 hours with instructions on fetal movement counting and asked to call her obstetrician the following day for a bio physical profile.

Contractions began on the evening of October 13. Subsequent correspondence from the mother to the hospital indicated that she called the labour room at 2130 hours and was advised that if her contractions were every 3-5 minutes for 1-2 hours, she should come to the hospital. At 0320 hours, she came to the hospital with contractions every five minutes. The nurse noted her blood pressure to be 152/102 with a trace of protein in her urine. On commencing electronic fetal monitoring , the baseline was 115 to 120 bpm, with absent variability. A vaginal exam by the nurse revealed the patient’s cervix to be 1-2 cm. She had a prolonged deceleration after five minutes in the triage area.

At 0400 hours, the patient was moved from triage to the labour room and the obstetrician on call was notified, but was busy in another room with an urgent vacuum delivery. At 0418 hours, the nurses started an IV and a bolus of 500 ml was given. The tracing continued as a flat line around 120 bpm. At 0434 hours, oxygen was given and position change was tried by the nurses.

At 0449 hours, the obstetrician came to assess the mother. A vaginal exam was done and showed her cervix to be 3 cm dilated, 50% effaced with vertex at spines -3 cm. Artificial rupture of membranes was performed and no fluid was seen. A fetal scalp clip was applied, but the tracing remained the same. At 0456 hours, a Caesarean section was called and the anaesthesiologist, assistant and paediatrician were paged to attend urgently. The patient was moved to the operating room at 0501 hours. The anaesthesiologist began prepping for a spinal, but a fetal bradycardia began at 0510 hours and a general anaesthetic was requested by the obstetrician. The surgery began at 0520 hours and a baby girl with birth weight 3.25 kg was delivered at 0523 hours. Cord gases were obtained and the Caesarean was completed at 0548 hrs.

The baby was “flat” at birth with Apgars of 0, 0 and 4 at one, five and fifteen minutes. Meconium was present with staining of the umbilical cord.

The infant was intubated immediately and chest compressions were started. Meconium was noted below the vocal cords. The infant was given two doses of epinephrine and three boluses of normal saline, and the first audible heart sounds were noted at 10 minutes; respirations started at 11 minutes. Her blood sugar was low and perfusion was poor. The infant received glucose to normalize her sugar, but remained acidotic. She was placed on a ventilator.

The arterial cord gases were critical, with readings of pH 6.92, CO2 120, HC03 23, Base Excess -16.

The infant’s heart rate was 140 bpm, BP 85/56, MAP 64. Perfusion had improved. Respiratory rate was in the 60’s with O2 Sat >95% in 100% 02. There were spontaneous movements of the legs and eye opening.

Morphine was used to sedate and antibiotics were started. The infant was stabilized. Repeat venous gases showed improvement, but she was still acidotic, with serum lactate elevated at 16.9.

Transfer to the children’s hospital was requested and cooling was commenced as per protocol.

The infant developed generalized seizures just prior to the arrival of the transfer team at 0845 hours. She was given phenobarbitone, but also developed hypoglycemia (BS 1.5) and required dextrose infusion. The INR was elevated at 2.9 with a risk of developing DIC. Frothy pink tinged secretions were observed coming from the endotracheal tube. During treatment at the first hospital, venous blood gases began to show some improvement in the respiratory status.

Transfer to the children’s hospital was uneventful. On arrival, the infant had no spontaneous movements. Hypotonia was present, suck and gag reflexes were absent and pupils were small and sluggish to react to light. The diagnosis was severe hypoxic-ischemic encephalopathy (HIE).

The infant’s progress at the children’s hospital was unfavorable. Further seizures occurred, and a regimen of phenobarbitone, fosphenytoin and midazolam was started. An Electroencephalogram (EEG) was abnormal; a head ultrasound showed cerebral edema and an MRI showed restricted perfusion. The infant’s respiratory status was complicated by persistent pulmonary hypertension of the newborn and right pneumothorax. The infant required inspired nitrous oxide, high flow oxygen and thoracocentesis for respiratory support.

The infant’s cardiovascular status was also compromised with hypotension and low perfusion requiring dobutamine, epinephrine and milrinone infusions.

Further evidence of multiorgan failure included poor urine output, abnormal liver function and hyponatremia.

In view of severe HIE and multi-organ failure, the prognosis was very grim. The infant was extubated and died on October 18 at four days of age.

Post mortem examination showed changes of perinatal asphyxia in the liver, lungs, thymus and adrenals.

Discussion

This baby died of severe perinatal asphyxia. Evidence of abnormal fetal status was clear from the start of her admission. The on-call obstetrician was busy with another emergency and the nurses cared for the mother for almost 90 minutes. Although the nursing staff admitted the mother, appropriately started an IV and performed intrauterine resuscitation, they did not inform the on call obstetrician of the seriousness of the situation or attempt to find a second obstetrician to care for the mother. It took 27 minutes to deliver the baby after the decision to perform a Caesarean section. It is unclear if a Caesarean section performed any earlier would have changed the outcome.

Recommendations

The initial hospital involved in this case has undertaken a Quality of Care Information Protection Act (QCIPA) review. The following recommendations, together with the status of implementation of the recommendations, have been provided by the hospital:

  1. The obstetricians involved should have their documentation and communication skills reviewed and upgraded.

Status: Done. Courses completed. Documentation on personnel file. CPSO notified.

  1. There must be a more robust quality review process for the Women & Child Program.

Status: Done. An anonymous form drafted and available to all staff. This has lead to numerous case reviews, changes to process/practice, etc.

  1. There needs to be a more formal process for calling in a second obstetrician.

Status: Call schedule now in place, criteria for call established.

  1. There needs to be a procedure for calling an “Obstetrics Alert.”

Status: Done. Anyone on the team can initiate these calls in critical situations.

  1. There needs to be better communication among members of the obstetrics team.

Status: Ongoing. Both the new Department Chief, and the new manager for L&D, as well as the Operations Director for the entire program, are working with their staff to ensure there are open lines of communication both among and between provider groups. A memo has been sent to all relevant stakeholders that there must be a direct provider to provider communication in complex/critical situations.

  1. Our ultrasound equipment needs upgrading.

Status: On order. In the meantime, we have added two further Maternal Fetal Medicine specialists (one returning from sick leave) to ensure that we provide optimal antenatal care. We are in the process of expanding our current facility to a new area of the hospital as well.

  1. Biophysical profiles should be performed within 24 hours where clinically indicated.

Status: This is a standard of practice that all members of the Department of Obstetrics are expected to meet and they are aware.

  1. A cooling blanket should be available to be used as needed post-neonatal resuscitation.

Status: Discussed with the Hospital for Sick Children and their protocol requires passive cooling only, with active cooling in a tertiary centre only.

The MPDRC has no new recommendations in addition to those identified through the hospital’s review.



Case: 2010-N-12

History

The mother of the deceased was a 30-year-old woman at 40 weeks and 5 days gestation in her second pregnancy. Her first pregnancy was with twins delivered vaginally at 34.5 weeks. The current pregnancy was uneventful. She was a smoker, but stopped in the first trimester. Routine lab tests were normal and she had ultrasounds at 8 and 22 weeks, and an oral glucose tolerance test, which were normal. A GBS swab was negative. She was seen by an obstetrician for prenatal care, but the intrapartum care was by a family physician.

The patient presented to the labour room at 1220 hours with contractions every 2-3 minutes. Electronic fetal monitoring (EFM) was commenced and showed a normal pattern. EFM was discontinued at 1238 hours. The doctor attended at 1400 hours and found the patient’s cervix to be 4-5 cm and thin. The membranes were bulging and after a discussion, artificial rupture of membranes was performed for a small amount of clear fluid. EFM was recommenced at 1414 hours and was again normal. The doctor indicated that the EFM showed a baseline heart rate of 130’s to 150’s, however the EFM strips provided for review showed a baseline of 130 bpm. The labour record suggested EFM was done until 1530 hours, however the records provided for review only went until 1432 hours.

The patient used some nitrous oxide for pain control. At 1445 hours, she felt pressure and was reassessed by the doctor. The patient was found to be 6-7 cm dilated. At 1620 hours, she had a strong urge to push and her cervix was an anterior lip. The doctor attended and attempted to clear the anterior lip.

At 1655 hours, she was fully dilated and began pushing well at 1700 hours. The doctor noted that intermittent auscultation (IA) was used to assess the fetal heart “at least every 5 minutes after contractions and was 130’s to 150’s.” She also noted that fetal movement was noted between her pushing with movement of the fetal head as well.

The nursing documentation indicated EFM was done from 1400 to 1530 hours with baseline rates of 130 to 140 bpm and moderate variability. For the purposes of this review however, no strips were provided for the times between 1432 and 1530 hours.

From 1545 hours to the birth at 1808 hours, the fetal heart rate was recorded only by a dot on the labour record. These dots are recorded at 10 to 17 minute intervals and show an increasing rate from the original baseline of 130 bpm to between 150 and 160 bpm until 1740 hours when it dropped to 140 and 130 bpm. The last recorded fetal heart was 11 minutes prior to the birth at 1757 hours around 150 bpm.

At 1745 hours, the fetal head progressed to the perineum. The doctor consulted a colleague to attend the birth with her as she was anticipating shoulder dystocia. The baby was born spontaneously at 1808 hours. A loose nuchal cord was noted that slipped easily over the fetal head. The baby was female and weighed 4460g. Apgar scores were 1, 0, 0 and 0 at one, five, ten and twenty minutes.

The baby was flat at birth with a heart rate of 60 to 80 bpm and no respiratory effort. Bag and mask ventilation was commenced at 30 seconds of age and endotracheal intubation performed at two minutes of age. The heart rate initially increased to 80 to 100 bpm, but then fell to 60 bpm and cardiac compressions were given from 1.5 minutes. Epinephrine was given through the endotracheal tube, but the heart rate remained very low or absent. A UV line was placed and epinephrine, saline bolus and bicarbonate were each given twice. An orogastric tube was used to decompress the stomach. Cord arterial and venous pH were 6.93 and 7.24.

The situation was discussed with the parents and resuscitation was stopped. The infant was pronounced dead at 1850 hours, at less than one hour of age.

Post Mortem Report

Cause of neonatal death: Intrapartum Asphyxia

Findings at post mortem included:

  • Large for gestational age female.
  • No evidence of trauma.
  • No evidence of infection.
  • No congenital anomalies.
  • No definitive placental or cord abnormality.
  • Biochemistry of urine at autopsy was normal except for an elevated lactate.
  • Blood cultures at autopsy were consistent with post mortem contamination.
  • Cytogenetics failed to grow.
  • Tissue cultures of the brain heart and lung no virus.
  • Electron microscopy of the stool was negative for viruses.
  • Placental cultures negative.

Discussion

This baby died of severe intrapartum asphyxia, the cause of which has not been determined. Given her low risk pregnancy, monitoring by IA is appropriate, however the recording of the heart rates is less frequent (every 10-17 minutes) than recommended by most expert groups (e.g. the Society of Obstetricians and Gynaecologists of Canada recommends every 5 minutes).

A change in baseline heart rate did not appear to be identified by the nursing staff or the doctors although the rate did go as high as 160 bpm about 40 minutes prior to the birth (from admission baseline of 130 bpm). It is impossible to know if this actually signalled some compromise of the fetus and if there could have been an intervention to improve this outcome if EFM was implemented to assess the changing baseline.

Recommendations

  1. The hospital involved should review their intermittent auscultation protocols and indications for EFM, as well as the proper use of forms used for charting these observations.
  2. Obstetrical care providers are reminded of the importance of accurate and complete documentation.


Case: 2010-N-13

History

The mother of the deceased was a 39-year-old G3T0P0A2L0 with an estimated date of delivery of June 28, 2009. The prenatal 1 and 2 reports were available for review. The mother had two previous spontaneous first trimester miscarriages in 2005 and 2008. She had environmental allergens and was not on any medication other than prenatal vitamins. She required a general anesthetic for wisdom teeth extraction at 24 weeks gestation. On the prenatal 2 report, regular visits were recorded until 36 weeks gestation. At 30 weeks, an ultrasound revealed a large for gestational age infant. The formal ultrasound report was not available for review. The symphysis fundal height measurements throughout the prenatal visits were unremarkable. The patient was A positive without antibodies and the one hour glucose challenge test at 28 weeks gestation was normal.

The patient presented to labour and delivery at the hospital on the morning of June 29, 2009. She was in early labour with contractions for six hours, but was not dilated. She was GBS positive. She was instructed to go home and come back when in more active labour. She returned in active labour approximately 24 hours later on the morning of the June 30, 2009. She requested and received an epidural approximately one hour after admission. Antibiotics were started for Group B streptococcus prophylaxis.

The labour record indicates that continuous monitoring was initiated from the time of admission. The fetal heart strip in the chart that was provided for review only covered the time from 1154 hours until 1720 hours on June 30, 2009.

At the time of admission at 0620 hours, the patient was 4 cm dilated with membranes intact. At 0845 hours, the contractions spacing were up to Q 2-5 minutes apart and oxytocin was started as per protocol. At 1010 hours, the nursing notes indicated that the fetal heart rate showed variable decelerations with some contractions. At 1100 hours, the nursing notes indicated, “on hands and knees. Fetal heart down, repositioned, improved back to baseline.”

At 1200 hours, the resident was called because of decreased variability. The assessment revealed that the patient was 8 cm dilated and was showing “few early decels.” The fetal heart strips (FHS) available for review were commenced at this time. The FHS showed variable decelerations with good recovery occurring with most contractions. The patient was recorded as fully dilated at 1340 hours with a report of “variable decelerations with every contraction.” During the two hour span since fully dilated, the patient continued to have variable decelerations with most, but not all, contractions. There was always recovery to the baseline during this time, though some of these decelerations were wider and deeper than previously experienced. The patient felt an urge to push and proceeded to do so at 1550 hours.

From the time the patient started pushing, the decelerations appeared more prolonged and it was not clear if there was recovery with the stopping of the contraction. By 1645 hours when reassessed by the family medical resident, it was recorded that there had been “no significant decent since the previous exam - will give 20 minutes more pushing and see if progress - if no progress will C/S.” No comment was made pertaining to the fetal heart. At that time, and over the previous 30 minutes, there was significant change in the decelerations that were occurring with several that were very prolonged. At 1713 hours, it was recorded that the physicians were available and the plan was for a “double set up.” The last recorded fetal heart at 1722 hours had a baseline of 160 which was higher than the initial baseline of 140. The patient was transferred to the operating room (OR) at 1730 hours.

The obstetrical attending staff indicated that they were on the unit at 1720 hours during handover and advised that the patient was being transferred to the OR for double set up. On arrival into the OR to meet the patient, the obstetrical staff noted that there was difficulty determining the fetal heart. A scalp clip was applied with “few signals in the 80’s.”

An emergency Caesarean section was ordered and the anesthetist was already present. Despite topping up the epidural, it was inadequate, so a general anesthetic was instituted. A low segment Caesarean was performed. Meconium was found and the baby was delivered without incident. Apgars were 1, 1 and 5 at one, five and ten minutes. Arterial PH was 7.12 with a base deficit of 10.9. Venous gases were not reported and there was no “lab report” with the chart provided for review. There is a notation in the infant’s chart that the cord gas was 7.01 and 10.1 base deficit. The fetal weight was 4220g. There was no evidence of nuchal cord or abruption.

The Caesarean procedure was otherwise uncomplicated. The delivery was at 1755 hours - four hours after being fully dilated, two hours after initiation of pushing, 33 minutes after the external monitor was taken off in the room and 22 minutes after arriving in the operating theatre.

The neonatal team was available at the delivery. Initial assessment showed the infant to be centrally dusky with no spontaneous movement or breathing and an apex heart rate of less than 70. Mask with positive pressure ventilation was initiated for 15 seconds, and with no improvement, chest compressions were started.

The infant was intubated on the first attempt at 1758 hours. The apical heart rate was 100 by 1804 hours and compressions were stopped. At 1835 hours, 40 minutes after delivery, the infant’s condition with continued ventilation on 50% oxygen, was recorded as flat with no spontaneous movement and a flaccid tone.

The blood gases were recorded as:

Blood Gases

pH

BD

1847 hours

7.03

?

2015 hours

7.06

11.5

2355 hours

7.25

11.5

Seizure-like activity was reported at 2115 hours, approximately three hours after delivery. Seizure medications were given and request for transfer to a children’s hospital was initiated. The team arrived by 2230 hours and care was transferred. The baby was on the transport ventilator and was discharged at 0050 hours on July 1, 2009.

On admission to the NICU in the children’s hospital, the baby was described as being hemodynamically stable and was intubated and ventilated with 34 % oxygen. The pupils were 7 mm and fixed with no response. There was no gag or suck reflexes. There was poor tone (floppy) of the extremities. The assessment determined a level 3 status on the Sarnat scale. The parents had been informed by that time of a very guarded prognosis.

The infant was transferred to a palliative care area on the afternoon on July 3 and died later that evening.

Post Mortem Findings

Significant findings at autopsy revealed anoxic-ischemic encephalomyelopathy, generalized and very severe. Bacterial cultures were negative and there was no microscopic sign of infection.

Cause of death was attributed to perinatal asphyxia due to anoxic-ischemic brain damage and hemorrhagic necrosis of the adrenals.

Discussion

This pregnancy was normal and uncomplicated until the second stage of labour. The fetal heart monitoring indicated increasing depth and length of decelerations during this time for which it would have been reasonable to consider scalp gas testing or proceeding to delivery. The plan to transfer the patient for delivery appears to have been made because of a lack of descent with pushing, rather than for any significant concern about the fetal heart.

The “arterial pH” of 7.12 that was written in the chart may have been incorrect. There was no concurrent venous pH reported and there are no lab reports on the chart to confirm these numbers. The pH was not consistent with the clinical status of the newborn, nor the subsequent pathology findings. There was a written cord gas of 7.01 in the pediatric chart which appeared to be more consistent with the outcome and with the subsequent blood gases that were taken.

Recommendations

  1. Obstetrical care providers should recognize that an abnormal fetal heart tracing that worsens with pushing in the second stage of labour, without imminent delivery, warrants confirmation of normal scalp gases or urgent delivery. Caregivers should be mindful of this trap, and not assume that spontaneous delivery is close.


Case: 2010-N-14

History

The mother of the deceased was a 32 year old G2P1 who presented to hospital on November 29, 2009 at 38 weeks and 6 days gestation for her second pregnancy. Her antenatal course had been unremarkable and she had been found to be GBS positive. Her past obstetrical history included a forceps vaginal delivery in 1998 of a 7 lb 15 oz female infant. Her history was otherwise unremarkable.


She presented to hospital with spontaneous rupture of membranes at term. GBS prophylaxis was initiated and she received oxytocin augmentation of labour.

Fetal heart monitoring strips were available from 0431 hours until 0456 hours and again from 0804 hours until 1350 hours on that day. The timing of the obstetric activity is from these strips as no other documentation was available for review.

Decelerations were occurring with most contractions from approximately 0930 hours. There was always good recovery to the baseline until approximately 1140 hours and subsequent to that, there were an increasing number of contractions with prolonged recovery of the fetal heart to baseline. Obstetrics was consulted in the second stage of labour as she was fully dilated and pushing for greater than one hour without significant descent. The infant was at +1 station in a right occiput transverse presentation. The pubic arch was felt to be narrow, however it was thought to be adequate. There was a proven pelvis with a prior vaginal delivery of an 8 pound infant. Application of Kieland forceps was attempted at 1320 hours. This was unsuccessful. By that time, the fetal heart baseline had risen from approximately 130 at the start of monitoring, to 160 and there were recurrent and very deep, prolonged decelerations. They then proceeded with a vacuum assisted vaginal delivery. Between 1330 hours and 1350 hours, Kiwi vacuum was used over a series of eight contractions with four pop-offs. It was recorded that initially there was good progress with each contraction. However at station +3, progress decreased significantly secondary to a narrow pubic arch, so the decision was made to perform a Caesarean section. A low segment Caesarean was performed under epidural anesthesia and the infant delivered without difficulty. The infant was handed off to the waiting neonatal team. The remainder of the procedure was unremarkable.

The infant was born at 1412 hours and neonatal staff were available. The infant was limp at birth, with no spontaneous respiratory effort. Positive pressure ventilation was initiated at 30 seconds of life and the heart rate was approximately 150 beats per minute. The Apgar scores were 2, 3 and 5 at one, five and ten minutes. The infant was intubated at 13 minutes of life with 100% oxygen. On arrival at the NICU at 30 minutes of life, the infant was saturating 100% on 21% oxygen.

The initial examination revealed the newborn to be pale with poor capillary refill centrally and peripherally. There was bogginess and swelling over the posterior fontanel. Initial boluses of normal saline improved the blood pressure. Initial CBC revealed a hemoglobin of 117 and platelet count of 13. Cord bloods revealed an arterial pH of 7.05 with base excess of –11.5 and venous pH of 7.15 and base excess of –8.9. UVC access was obtained and platelets, packed cells and plasma were delivered. At approximately five hours of age, some posturing was noted and phenobarbital was started. At six hours of age, following transfusion, significant acidosis remained (pH of 6.5), though colour and blood pressure had been improved by blood products.

A head ultrasound at two hours of age was not helpful, however eventual interpretation revealed a large hematoma at the posterior aspect of the head appearing to be subgaleal. A CT scan at seven hours of age demonstrated, “a very large hematoma involving the majority of the soft tissue of the infant’s head” ; it was interpreted as a large subgaleal hematoma measuring a maximum of 2 cm in the coronal dimension over the posterior left parietal area. There was also a subdural hematoma over bilateral parietal lobes, anterior to the right transverse sinus, and along the posterior aspect of the falx and both temporal leaflets.

Neurology consultation on November 30 and December 1 revealed initial EEG findings that were consistent with diffuse brain dysfunction, cortical irritability and possible seizure activity. On December 1, while recognizing some intact brain activity and despite persistent acidosis and hypoprofusion, it was felt that there was no reasonable chance of intact neurological survival. The decision was made to withdraw care and the baby was pronounced dead at 1600 hours that day.

Post Mortem Findings

The primary finding at autopsy was a male infant born at term with a large subgaleal hemorrhage/hematoma measuring 20 x 20 x 2.5 cm.

The clinical cause of death was massive subgaleal hemorrhage and hypovolemic shock. There was clinical evidence of severe end organ asphyxial damage with renal failure, abnormal liver functions tests, DIC and significant brain injury.

Discussion

The course of this term pregnancy was unremarkable until the later stage of labour. There were fetal heart decelerations prior to initiating pushing. Over an hour had passed before the obstetrical staff attempted delivery. It was at that time that the fetal heart tracing revealed a worsening pattern of deep and prolonged decelerations of the fetal heart. By the time of consultation, it was prudent to proceed with delivery. The fetus was at station 1+, however the head was in a transverse position. With the inability to apply forceps, a decision was made to use a vacuum. There was reason to believe that the infant was in a transverse arrest and in mid pelvis. By the dictated operative note, the caregivers would appear to have been encouraged by initial “good progress with each contraction, however at the station of +3 progress, decreased significantly secondary to a narrow pubic arch.” Despite four pop-offs over a series of eight contractions, the attempted procedure appeared to have continued past what would normally be recommended.


It is well recognized that scalp and intracranial hemorrhage, in particular subgaleal hemorrhage, is a known serious potential complication of vacuum extraction and that the longer the vacuum is on, the more chance there is of fetal scalp trauma.

As there was already evidence of deep and prolonged fetal heart decelerations, it is not known what the outcome would have been without this prolonged attempt at operative vaginal delivery. The cord gases however, support the likelihood of intact survival.

Subsequent large subgaleal hemorrhage and ischemic brain injury compromised the likelihood of recovery from the time it occurred. It is extremely difficult to manage a hemorrhage of this size. It would appear that the neonatal and consulting staff performed appropriate attempts at resuscitation and management for this extremely ill newborn who subsequently died at two days of age.

Fetal heart monitoring, in particular abnormal fetal heart tracings, continue to be a concern in obstetrical care. All caregivers should be reminded to maintain their skills in interpretation and subsequent management of abnormal fetal heart tracings.

Vacuum extractor has again been shown to be an instrument that can cause significant fetal scalp injury. It is extremely important that the caregiver make a very critical decision about the appropriateness of using this instrument in the particular clinical situation and to limit time of its use and the number of pop-offs as soon as it becomes evident that a successful delivery is not imminent. The use of the vacuum extraction in the mid pelvis with a transverse position of the fetal head should alert the caregiver of the low probability of success.

Recommendations

  1. Obstetrical care providers are reminded that the presence of an abnormal fetal heart tracing requires confirmation of normal gases or urgent delivery.
  2. Obstetrical care providers are reminded of the limitations of the vacuum extractor, particularly for mid pelvic delivery and of the uncommon, though serious risk, of brain hemorrhage with its use. Adherence to guidelines for vacuum use is critical.


Case: 2010-N-15

History

The mother of the deceased was a 34-year-old gravida 1 at 40 weeks and 3 days gestation when she presented to hospital in early labour. She was cared for by an obstetrician from 11 weeks. Routine prenatal lab tests were normal. She had 12, 20 and 32 week ultrasounds which were normal. She had an IPS test that was negative and an OGCT that was normal. Her swab for GBS was negative.

The patient was assessed in triage at 2315 hours on July 29, 2008. A non-stress test was done and designated as “reactive.” The nurses and resident saw her and noted mild to moderate contractions every 3-4 minutes. Her cervix was 2 cm, 80% effaced and vertex at spines –2. She was given 15 mg of nalbuphine at 2355 hours and discharged to the “Early Labour Lounge” at 2358 hours. She returned to triage for reassessment at 0145 hours on July 30, 2008. At this assessment, another non-stress test was completed and designated again as reactive. She was found to be contracting every 2-3 minutes with moderate tone and her cervix was 3 cm, 90% effaced and vertex at spines –2. Membranes remained intact.

The patient was admitted to the birth unit after 10 minutes. After admission, she was monitored by intermittent auscultation. A fetal heart rate of 148 bpm was recorded at 0232 hours. She then entered the Jacuzzi tub. At 0305 hours, a fetal heart rate of 152 bpm was recorded while in the tub. At 0335 hours, the nurse had difficulty auscultating the fetal heart and the patient was asked to exit the tub. After she was in bed, the nurses still could not find a fetal heart rate and called the obstetrician on call. The obstetrician came to the room while the nurses started an IV and oxygen. An ultrasound was done by the obstetrician at 0347 hours. Fetal bradycardia was detected by ultrasound and an emergency Caesarean code was called.

An emergency Caesarean section was performed under general anaesthesia. The baby was born at 0358 hours. It was noted that there was thick meconium stained amniotic fluid and a nuchal cord, but that it was not tight. No evidence of abruption was seen.

The baby had Apgar scores of 0, 0 and 3 at one, five and ten minutes. The baby was male and weighed 3227g. The baby was resuscitated with intubation, chest compressions for nine minutes, two doses of endotracheal tube epinephrine, and a normal saline bolus through an umbilical venous catheter. The umbilical cord gases showed pH of 6.8, PaO2 of 34, PaCO2 of 81, bicarbonate of 13.7 and BE of –21.5.

Within a few hours, the baby began to have seizures and continued to have fixed dilated pupils and profound hypotonia with no spontaneous movement and no response to pain or gag reflex. A MRI of the baby’s head showed severe hypoxic ischemic changes throughout the brain. The prognosis was discussed with the parents. The baby was subsequently extubated and died at 38 hours of age.

Post Mortem Findings

The post mortem report revealed a male newborn with body weight and measurements in keeping with term gestation. The report noted:

  1. marked pulmonary congestion
  2. large amounts of mucous in trachea and main bronchi
  3. small hiatal hernia at the cardia
  4. urinary bladder markedly distended with clear urine
  5. cerebral vessels markedly congested
  6. vascular congestion in parenchymal organs (liver, kidneys, spleen)
  7. incidental finding of foamy enlarged cells in the outer zona fasiculata, no obvious storage disease

The neuropathology report indicated: anoxic-ischemic encephalomyelpathy, globally severe, associated with moderate to severe vascular congestion and early cerebral edema.

Bacterial cultures of a tracheal swab, cardiac blood, right and left lung as negative or non-contributory. Viral isolation from the right and left lung was negative.

Placental pathology: Mild to moderate acute umbilical arteritis and funisitis. Multifocal mild to moderate deciduitis and chorioamnionitis in the membranes. Mild to moderate chorionic vasculitis and chorioamnionitis in the disc.

Cause of Neonatal Death: Severe hypoxic ischemic encephalopathy due to perinatal asphyxia.

Discussion

This baby died of severe intrapartum asphyxia. His mother was healthy and the pregnancy was uncomplicated. The mother was appropriately monitored with intermittent auscultation in her labour. When the auscultation became difficult or abnormal, the team acted quickly to perform intrauterine resuscitation and delivered the baby by emergency Caesarean within 23 minutes. The baby was however, profoundly asphyxiated at birth and although resuscitation was performed, the ultimate prognosis was very poor.

Although requested, the fetal monitoring strips for this case were not provided by the hospital. A complete report would require the evaluation of these strips.

Recommendation

  1. The hospital should review its practices for the retention and storage of fetal monitoring strips.


Case: 2010-N-16 – deferred to 2011 for additional review



Case: 2010-N-17

History

The mother of the deceased was a 29-year-old gravida 1, with an estimated date of delivery of February 4, 2010. Her past medical history was unremarkable. The prenatal I and prenatal II records were completed and the documentation shows that she was followed in midwifery prenatal care from 16 weeks gestation. There were regular and appropriate number of visits and all documentation confirmed a normally developing pregnancy. All prenatal testing was normal, including a 50 gram glucose challenge test and second trimester ultrasound scan. She was Group B streptococcus (GBS) negative.


A biophysical profile (BPP) was performed on February 12, 2010 due to post dates at 41 weeks and one day. She was given a score of 6/8. It was recorded that there was “only one body roll noted, not sufficient for a full score” and so she was given a rating of 0 for fetal movement.

This finding was followed by a reactive non-stress test (NST) done at the obstetrical triage of the hospital. The obstetric consultant recommended induction of labour due to “concern re: fetal well being.” The parents wanted another ultrasound and then would make their decision. A second biophysical profile again had a score of 6/8 due to “sluggish movements.” After declining induction, the parents were advised by the midwife about fetal movement counting and reviewed when to call with regard to labour, bleeding, spontaneous rupture of membranes, decreased fetal movements or any other concerns.


A repeat NST on February 14, at 41 weeks and 3 days was documented as reactive. Mild contractions every 5 to 7 minutes were palpated and the midwife documented that the mother was likely in early labour.

A verbal consult was done with a second obstetrician. The second obstetrician did not feel that another BPP was necessary as the NST was normal and the patient was in early labour.

On February 15, 2010, around midnight, the midwife was paged. Documentation by the midwife started at approximately 0040 hours and indicated that the patient was progressing into early labour with normal fetal heart and no decelerations. The mother had reported fetal movements to be normal during the previous day and evening. The midwife stayed for approximately an hour as contractions were only four to seven minutes apart and the fetal heart had been checked on multiple occasions. The midwife left and advised the mother to call when she was in more active labour or membranes were ruptured.

Documentation from 0330 to 0552 hours confirmed increasing labour and cervical dilation with normal fetal heart. At 0552 hours, there was a spontaneous rupture of membranes with meconium noted. It was recommended that the mother be transferred to hospital for continuous fetal monitoring and pediatric attendance. At the time of arranging the transfer at 0555 hours, the mother was 8 cm dilated with normal fetal heart rate.

The documentation at the hospital started at 0630 hours. At that time, contractions were every three minutes, lasting for 45 to 60 seconds and continuing normal fetal heart. The mother was 9 cm dilated. As there was thick meconium, a pediatrician was contacted and was to be paged for attendance at delivery. At 0740 hours, initial late decelerations were noted on the fetal heart tracing. At 0810 hours, the obstetrician on call was contacted and was in attendance at 0818 hours. The obstetrical documentation indicated, “baseline good variability occasional late decels. Impression; no acute fetal concerns.”


On reviewing the fetal heart tracing, there appears to have been subtle late decelerations from approximately 0700 hours. The baseline had remained at 140 during this time, however these decelerations were persistent.

At the time the patient was requesting an epidural, she was under obstetrical care. At 0925 hours however, when she was fully dilated and no longer wanting an epidural, the care was transferred back to the midwives. Obstetrical documentation at that time was that the fetal heart was reassuring. There were however, subtle repeated depressions of the baseline after contractions continuing through that time.

The patient started pushing at 0926 hours. The midwife documented the repeated time of decelerations following a contraction.


By 1034 hours, the patient was becoming very tired and there was minimal progress with pushing. There was a discussion about the need for an epidural and possible need for oxytocin augmentation as the contractions remained only 3 to 5 minutes apart. At that time, care was again transferred to an obstetrician and it would appear that this was done because of the plan for an epidural. The obstetrical fellow assessed the patient at 1050 hours and confirmed “baseline 160, reduced variability, no decelerations, contractions every 5 minutes.” It was noted that there were, “no signs of acute fetal compromise.”

The plan was for an epidural, oxytocin and continuous monitoring with consideration of assisted delivery according to head position and fetal monitoring. The attending obstetrician was notified.

The fetal heart tracings showed the baseline up to 160 by 1030 hours and then over the next hour, decreased down to 140 bpm. By 1230 hours, the rate was down to 120 bpm. During this time, there continued to be subtle depression of the baseline after contractions with slow recovery.

At 1235 hours, the obstetrical team was again called due to decreased baseline in the 110’s. Oxygen had already been started, oxytocin was stopped and the patient repositioned. An IV bolus was administered. The fetal scalp stimulation was attempted without acceleration and a scalp clip was applied. Since it was questionable whether she may be having tetanic contractions, two sprays of sublingual nitroglycerine were given. The fetal heart remained in the 90 to 100 bpm range. As the vertex was felt to be above spines, plans were made for an urgent Caesarean section.

The baby was delivered by Caesarean section at 1310 hours. The infant was cared for by pediatric staff that were in attendance at delivery. Cord bloods and cord gases were taken and the placenta was sent for pathology. The procedure was otherwise unremarkable.

The Apgar scores were 0 at one and five minutes, 1 at ten minutes and 3 at twenty minutes. The arterial cord gas showed a PH of 6.67 with a base deficient of –31.4. The umbilical vein had a PH of 6.73 and a base deficient of –28.7. Despite resuscitation, the first gas taken at 1 ½ hours of age revealed a PH of 6.8 and a base deficient of –33. Seizures first occurred at 2 ½ hours of age.

The resuscitation began immediately after delivery with intubation at 20 seconds of age. There was no meconium below the cords. Initial chest compressions were given for 12 minutes and 2 doses of epinephrine were given via the endotracheal tube. The first gasp occurred at 30 minutes and regular respirations were established at 45 minutes. Over the next 30 minutes, ventilation was weaned down to minimal and room air, but the baby was obtunded neurologically, although breathing regularly. Passive cooling was initiated. Phenobarbital was started due to seizures. Clinically, the baby was diagnosed with SAMAT stage 3 hypoxic-ischemic encephalopathy (HIE).

The attending physician recommended palliative care. Although the parents understood the seriousness of the baby’s condition, they wanted to give the infant more time. The baby was subsequently transferred to a children’s hospital for palliative care. The infant’s condition continued to deteriorate, including a severe coagulopathy, with no improvement of the neurological status. The infant died at 0955 hours on February 16, 2010 at less than 24 hours of age.

Post Mortem Findings

The major diagnoses on examination were meconium aspiration syndrome, and multi organ injury, secondary to severe, wide spread hypoxic ischemic encephalopathy due to perinatal asphyxia. The placenta was described as being mature, large for dates, (680 grams, greater than the 90 percentile), with meconium exposure effects. There was acute deciduitis and subchorionitis, but without established chorioamnioitis.

Discussion

This pregnancy progressed normally until after 41 weeks. The biophysical results indicated that the fetus may have been showing compromise, however the NST on the day prior to labour, was normal. It is not clear whether induction, when recommended, would have changed the outcome.

The mother went into spontaneous labour at home and was attended by her midwife soon after being called. The assessments and documentation in early labour appear to be appropriate. When she had spontaneous rupture of the membranes and meconium was found, plans were made for transfer to the hospital so pediatric staff would be available at the time of delivery.

During labour, there were a number of occasions where late decelerations were documented in the notes. There were two consultations with obstetrics at times when an epidural was being considered. The obstetrical consultants determined that there was no evidence of fetal compromise. In the second stage, due to failure of sufficient progress, the obstetrical consultant recommended oxytocin augmentation and again did not feel that the fetal heart monitoring revealed any concerns.

It was not until significant episodes of bradycardia occurred that there was a determination of fetal compromise and recommendation for urgent delivery by Caesarean section. At no point during labour was there consideration of fetal scalp gases.

When the newborn was delivered, it was severely depressed, with an extremely low PH. There was early evidence of severe HIE and acknowledgement that further attempts of aggressive care were not going to be successful. The pediatric care appears to have been appropriate as the baby was already significantly compromised at the time of delivery.

On a number of occasions, the midwife had documented that there were episodes of late decelerations. The obstetrical consultants did not determine any abnormality. Upon reviewing the continuous monitoring that was done, it is clear that there were repeated late decelerations with slow recovery throughout labour. These decelerations were not appreciated as the variability was felt to be normal and there was no significant bradycardia to raise the alarm.

There were several obstetric consultants involved in the care of this patient. Each assessment however, focused on the current condition and missed the pattern of compromise, thick meconium, and recurrent late decelerations.

Recommendations

  1. Obstetrical care providers are reminded of the Fetal Health Surveillance Guidelines of the SOCG (JOGC September 2007).
  2. Obstetrical care providers are reminded to consider the entire clinical picture when assessing fetal wellbeing.


Case: 2010-N-18

History

The mother was a 31-year-old G4P1A2 with two previous early spontaneous abortions and a 39 week vaginal delivery of a 5 lb 14 oz baby girl six years previously. She was 4’11” with a BMI of 30 at her first prenatal visit at 14 weeks, but she gained 30 more pounds in the pregnancy. She was followed by an obstetrician. There is no record of her initial prenatal blood work as the doctor used an old Prenatal I form and a new Prenatal II form and information was not transferred from one to the other. The mother was Rh negative and Rhogam was booked at 28 weeks. Hb was recorded as 114, but no date was recorded. It was assumed that glucose testing was done with the Oral Glucose Challenge Test which was recorded and was normal, but again no date was provided. The record ends at 29 weeks 6 days, so it was assumed that the glucose testing was prior to that. There was a suggestion on the Prenatal II form that an ultrasound was performed at 7 weeks, but no result was attached. The mother’s GBS status was negative.

Three ultrasound reports were included with the hospital chart. An ultrasound at 18 weeks was consistent with the menstrual dates and noted a low placenta and did not get good spine views. The next ultrasound was at 31 weeks 3 days and continued to show a low placenta at 1.6 cm from the cervix. Polyhydramnios and an oblique lie were noted on this scan. Measurements were consistent with her dates. There was no comment made on spinal anatomy. Another ultrasound at 35 weeks 4 days showed the placenta to now be clear at 3 cm from the cervix. There was no recorded comment on the amniotic fluid volume, spinal anatomy or fetal size or position.

The mother was booked for elective induction at 39 weeks and 6 days. Her cervix was 1 cm soft and long. Dinoprostone (Prostin) gel 1 mg was given vaginally by the obstetrician at 1015 hours on December 10, 2009. EFM was commenced prior to the gel and was normal. Monitoring was continued for two hours after the gel and again was normal, with only a few cramps reported by the mother. Between 1215 and 1715 hours, she was ambulating and the fetal heart was checked by auscultation hourly and was normal at 130 to 140 bpm.

At 1715 hours, the obstetrician performed an artificial rupture of membranes (ARM) for large amounts of clear amniotic fluid. The cervix was recorded as 2 cm and 50% effaced. EFM was instituted after the ARM and was normal. Irregular contractions were seen with the toco every 2-3 minutes. EFM was discontinued at 1800 hours. She was up walking and in the tub between 1800 and 2230 hours. Cervix was 4 cm and 85% effaced at 2100 hours and 6-7 cm at 2230 hours. At this point, she requested an epidural and was put in bed, EFM commenced and an IV started. The tracing remained normal with baseline 130 bpm, moderate variability and accelerations noted.

The epidural was placed by 2330 hours and she was re-examined at 2350 hours and was 7-8 cm dilated. The EFM continued to be normal with contractions every 2-4 minutes and a bit irregular. At 0140 hours, she had not changed her cervix in two hours. The obstetrician was contacted and ordered an oxytocin drip if she did not change in the next hour. There was a decrease in variability between 0150 and 0240 hours with no decelerations and no accelerations. However, this resolved at 0240 hours when she was examined and found to still be 8 cm dilated. Contractions were every three minutes and more regular.

Oxytocin was commenced at 2mU/min at 0240 hours. Between 0300 and 0700 hours, the drip was increased by 2mU/min every 30 minutes to 22mU/min. During this time, the nurses recorded contractions as q1.5-2 minutes and strong. Two hours later, at 0435 hours, her cervix was 9 cm. The tracing showed short periods of minimal variability and occasional variable decelerations. At 0535 hours, the obstetrician reviewed the tracing which was then normal.

At 0618 hours, the mother felt pressure and was found to be fully dilated. She then had an episode of vomiting and the tracing is difficult to interpret, but appears to be a bradycardia. She commenced pushing at 0624 hours. The tracing deteriorated with marked variability, erratic baseline and late decelerations with each contraction. At 0634 hours, an IV bolus was given and O2 started. The obstetrician was called to view the tracing.

The obstetrician examined the mother at 0640 hours and found the presentation to be “OP position at spines (caput).” While the tracing remained abnormal, the obstetrician noted that the fetal heart “seemed to recover” with oxygen and a fluid bolus. The obstetrician also noted that the contractions were “difficult to palpate.” The oxytocin was increased at 0650, 0720 and 0750 hours despite the abnormal fetal heart and contractions every three minutes. At 0700 hours, the tracing showed minimal variability with tachycardia around 160 bpm and decelerations with each contraction to 80-100 bpm and slow return to baseline. By 0730 hours, the baseline reached 180 bpm.

At 0750 hours, there was a change of nursing staff and the obstetrician was again noted to be present. The tracing showed a baseline of 180 bpm with minimal variability and late decelerations with each contraction to 100 bpm. At 0820 hours, the mother was repositioned to her right side to “try to make her pushing more effective.” The tracing did not improve.

At 0830 hours, after pushing for over two hours with an abnormal EFM, the obstetrician examined the mother and found the vertex at spines, but little movement was noted over 2-3 pushes. The obstetrician suggested a Kiwi vacuum delivery and the mother agreed as she was exhausted. The obstetrician explained the risk of “scalp laceration and bleeding and trauma to the baby.” Forceps were brought to the room in case the vacuum failed.

The bladder could not be emptied as the mother was too swollen. The vacuum was applied at 0841 hours. The obstetrician described checking the vagina for trapped tissue, but does not indicate the position of the cup on the fetal head. The head delivered at 0852 hours after four pulls in the “green zone.”

The baby weighed 3302 g, had a head circumference of 34 cm and command length of 49 cm. Apgars were 3 and 5 at one and five minutes. Cord gases were not obtained. There were no lacerations and the placenta delivered spontaneously.

The infant was pale, limp and not breathing. She was placed on the mother’s abdomen, dried and stimulated. Heart rate was palpated in the cord at 60/min. The cord was cut by the father and the baby had a gasp while being transferred to the warmer. Heart rate was still low at 80/min and positive pressure ventilation (PPV) was initiated with oxygen.

At one minute of age, colour was pale pink with onset of respirations, but still hypotonic and bradycardiac at 80/min.

At two minutes of age, spontaneous onset of respirations with nasal flaring was reported.

0857 hours, at five minutes of age, the heart rate was reportedly 150/min and colour and tone were improving. PPV was stopped and oxygen given by mask. At six minutes of age, deterioration of colour and tone was noticed and there were no audible heart sounds. Chest compressions and PPV was commenced. The infant was intubated at nine minutes of age and Epinephrine 0.5 ml of 1:10,000 was instilled via the ET tube, with no response. Repeat dose was given after a further four minutes, again with no response. A third dose of epinephrine (0.5 mls) was given three minutes later. Chest compressions were continued. An umbilical venous line was placed at 35 minutes of age and 5 ml of 4.2% Na HCO3 was infused.

As there was no response, resuscitation was stopped at 0938 hours, at 46 minutes of age.

Post Mortem Findings

A complete autopsy was done at the children’s hospital. Significant findings were noted in the scalp and the brain only. A subgaleal hemorrhage was noted under an area of the scalp showing a circular suction mark of 8 x 7 cm. An irregular area of abrasion and hemorrhage in the scalp measuring 3.5 x 1.2 cm, surrounded by erythema and edema, was also noted.

The brain showed cerebral edema. Blood and all tissue cultures were negative.

Umbilical cord was hyper-coiled; although a risk for adverse outcome, it was not the case here.

Cause of death was undetermined.

Discussion – Obstetrical Care

This woman had an apparently healthy pregnancy at term when she came for elective induction. As her cervix was unfavourable, this was accomplished with prostaglandin gel and artificial rupture of membranes and IV oxytocin. The indication given was maternal discomfort. There is no indication of prior discussion of the risks of elective induction.

The mother went on to develop a dystocia in her labour at 8 cm with an occiput posterior presentation. IV oxytocin was used to attempt to overcome the dystocia, but even with augmentation, six hours elapsed between 8 cm and full dilation. She did achieve full dilation, but the presenting part was still high at spines and occiput posterior. The woman then pushed for two hours in an attempt to deliver spontaneously. Eventually, it was clear that no progress was occurring and a vacuum was used to complete the birth from the mid-pelvis after a 2.5 hour second stage. No back up plans were in place for Caesarean section if the vaginal delivery failed. The vacuum resulted in considerable trauma to the infant, including a subgaleal hematoma.

There was clear evidence of cephalopelvic disproportion for several hours, yet the caregivers persisted through to a traumatic vaginal birth. There is little in the charting to indicate that it was recognized that the labour was not proceeding normally. There is no evidence that the woman was offered an alternative of Caesarean at any point when the labour progress became abnormal or when the mid station vacuum delivery was contemplated. There is no indication that the obstetrician recognized the risk of the use of vacuum at this station or considered the potential need for an urgent Caesarean.

In addition to the issues of not managing the dystocia, there appears to have been a lack of recognition of the abnormal fetal status present from shortly after full dilation. Few resuscitative measures were undertaken and the strip is misinterpreted as being normal by the obstetrician. The nursing staff may have recognized the abnormal fetal status, but did nothing beyond providing oxygen and IV bolus. In the two hour period where the fetal heart rate tracing was abnormal, the nurses did not appear to challenge the obstetrician’s interpretation of the fetal condition and they did not contact another obstetrician or the Chief of Medical Staff regarding this woman’s care. Cord gases were not obtained.

Discussion – Pediatric Care

It was somewhat difficult to do an adequate assessment of pediatric care since the information provided was very limited. In particular:

  1. There were inadequate records of vital signs such as respiratory rate, blood pressure and adequacy of perfusion;
  2. Neurological assessment did not include pupillary findings, gag reflex or any response to stimuli;
  3. No blood work was obtained, especially haemoglobin, cord gas or blood sugar.

With respect to treatment, chest compressions were started late and sodium bicarbonate and epinephrine were given in subtheraputic doses. No saline bolus was administered for volume expansion.

It is unusual in perinatal death to have an apparent rapid improvement in neonatal physiology over a few minutes followed just as rapidly, or more rapidly, by a profound decline.

Since there was no evidence of intrapartum asphyxia, the only finding that may offer an explanation for this unusual cause is a subgaleal hemorrhage (SGH) with significant blood loss.

SGH is a rare, but potentially lethal condition. The prevalence of moderate to severe SGH is approximately 1.5 per 10,000. In a term baby, the subaponeurotic space may hold as much as 260 ml of blood. 1 cm increase in the head circumference equals to about 40 cc of blood. SGH is most often associated with vacuum extraction and forceps delivery, but may also occur spontaneously.

In one large study of 42 newborns (Paediatrics International), 77% of the cases had instrumental delivery. The incidence was 0.6/1000 deliveries and 4.6/1000 vacuum assisted deliveries. 13 (31%) had poor outcome. Optimizing the outcome for SGH requires early diagnosis, careful monitoring and prompt treatment.

Recommendations

  1. The obstetrical care providers involved should upgrade their skills in labour management and fetal monitoring.
  2. Nurses are reminded of their responsibility to question the care provided to patients they are attending. If they feel the care is below standard, they should consult with other nurses, doctors and administration until satisfied.
  3. All hospitals that provide obstetrical care should have protocols in place to monitor infants whose delivery involve vacuum extraction for signs of subgaleal hemorrhage.
  4. Neonatal health care providers should review Neonatal Resuscitation (NRP) guidelines.
  5. Obstetrical care providers are reminded of the need to collect cord blood gases at all births.
  6. A Regional Supervising Coroners Review should be conducted on this case.


Case: 2010-N-19

History

The deceased infant was born at 32 weeks gestation following a premature rupture of membranes over 48 hours.

The mother of the deceased was a 30-year-old G2P1 who had a previous premature baby at 31 weeks gestation who subsequently did well. The mother’s GBS status was unknown and she received multiple doses of antibiotics prior to delivery. There were some psycho-social issues involving the mother’s partner and the Children’s Aid Society were involved.

The infant was born by spontaneous vaginal delivery. No resuscitation was required. Apgars were 9 at one minute and 10 at five minutes. There was mild respiratory distress which resolved spontaneously. Birth weight was 1766 g and physical examination was normal.

In view of the premature rupture of membranes, a partial septic work up was done and the infant was started on empiric ampicillin and gentamicin in the Neonatal Intensive Care Unit (NICU). Blood cultures grew E. coli. Seizures were noted on day 1 manifesting in tonic extensor posturing initiating with a cry and then associated with oxygen desaturation and an episode of bradycardia. A lumbar puncture was performed, the antibiotic doses were increased to the meningitic levels and cefotaxime was added. The cultures of the cerebrospinal fluid (CFS) were sterile, probably due to the prior antibiotic therapy. The E. coli was sensitive to all three antibiotics. A loading dose of phenobarbitone was given, but did not require any maintenance treatment as there were no further seizures. An ultrasound of the head showed a Gr. II intraventricular hemorrhage (IVH) and evidence of echogenic areas in the periventricular region suggestive of periventricular leukomalacia in the left parenchymal area. The longterm neuro-developmental sequelae were discussed with the parents. Serial weekly ultrasounds were done and although they did not show hydrocephalus, asymmetry of the ventricular size was noted with the left being larger than right.

The infant’s clinical neurological status remained normal. Her urinary output was satisfactory and the electrolytes were normal. She was in room air and had normal cardiovascular status. Caffeine was started for apnea of prematurity on March 31 and discontinued on April 14, 2010. The infant developed jaundice with a bilirubin of 212 and was started on phototherapy. Following a second bout of phototherapy, jaundice resolved.

The infant was started on dextrose infusion and was on total parenteral nutrition (TPN). Gavage feeds were commenced and well tolerated. Expressed breast milk (EBM) with fortifier was given and the infant’s weight gain was satisfactory.

The antibiotics were given for a total of three weeks as per recommended protocol.

Repeat blood cultures done on day 2 were sterile. The infant appeared to have made a full recovery and plans were made for discharge in three days after discontinuation of the antibiotics. However, the infant became ill on April 22; she was lethargic, not interested in feeds and hypotonic. A full septic work up was done.

The blood culture grew E. coli within six hours. Cerebrospinal fluid showed gram negative organisms and a white cell count was 1400. The infant was started on cloxacillin, cefotaxime and gentamicin. She also received phenobarbitone for reoccurrence of seizures.

The infant was placed on continuous positive airway pressure (CPAP) due to episodes of bradycardia and was stable initially. The initial venous gas on nasal CPAP was: pH 7.27, CO2 44, bicarbonate 20 and base excess -6.

The infant’s condition subsequently deteriorated with hypotonia, although reflexes could be elicited. The urine output was reduced and sodium dropped to 123. Diagnosis of Syndrome of Inappropriate Antidiuretic Hormone (SIADH) was made and the infant was placed on fluid restriction. Due to reduced urine output, she received two boluses of NaCl and showed some improvement.

The infant had further apneic spells and only a brief break from CPAP resulted in bradycardic spells. She was intubated on April 23 without difficulty and was easy to ventilate. Her rate was 40 with pressures 12/5. Her capillary gas showed a pH of 7.19, pCO2 of 53 and HC03 of 20.

Blood work showed significant neutropenia with a WCC of 1.3. Repeat CBC showed some improvement in the WCC.

The infant was transferred to the children’s hospital on April 23. She remained on full ventilatory support and the antibiotics were changed to meropenem and gentamicin. She had become unresponsive, with no eye opening or spontaneous movements and persistent seizure activity. She required further anticonvulsant therapy with additional phenobarbitone. However, more aggressive treatment was required with midozalam infusion for better seizure control.

Further ultrasounds showed left parietal cystic leukomalacia and an MRI on April 26 showed extensive patchy diffusion abnormalities in the cerebral and cerebellar hemispheres and the brainstem. An EEG showed continuous seizure activity despite aggressive treatment.

The infant was also hypotensive and was started on dobatamine infusion and multiple boluses of normal saline. Her postnatal course at the children’s hospital was stormy. Her urine output was poor with elevated creatinine level. Hyponatremia was also an issue due to sepsis/meningitis.

The infant had signs of disseminated intravascular coagulation (DIC) and electrolyte imbalance. Liver function was also abnormal with elevated enzymes. Fresh frozen plasma (FFP) infusion was given to correct some of the abnormalities.

The decision was made to withdraw intensive care support. The infant was extubated at 0120 hours on April 28 and expired at 1300 hours later that day.

Post Mortem Findings

No autopsy was performed.

Summary/ Comments.

This infant was managed well from the time of birth. In view of her prematurity and premature rupture of membranes, she had a septic work up and started on antibiotics. Due to transient seizure activity and positive blood culture at 24 hours of age, a lumbar puncture (LP) was done and appropriate antibiotics were given. The course of therapy was adequate and monitoring, including serial head ultrasound, was appropriate.

It appears that due to the central nervous system (CNS) complications, the E. coli meningitis relapsed and despite aggressive and appropriate therapy, her condition deteriorated. Diagnosis of multiorgan failure, coagulopathy, neutropenia, hypotension, metabolic acidosis and seizures was discussed. Care was withdrawn in view of a grave prognosis.

Discussion

Neonates are at great risk of sepsis and meningitis due to deficiencies in humoral and cellular immunity and in phagocytic function.

Infants younger than 32 weeks gestation receive little of the maternal immunoglobulins received by full term infants. Deficiency of complement pathway compromises their defense against capsulated bacteria. T-cell and B-cell activities are also compromised. The incidence of bacterial meningitis is 0.3 per 1000 live births (the incidence of HSV meningitis is 0.02 -0.5 per 1000 live births).

Although mortality has declined from 50% in the 70’s, to 10% in late 90’s, the morbidity remains a significant cause of disability.

In a term infant, Group B streptococcus is the main pathogen, but in a premature infant, E. coli is predominant .

No recommendations.



Case: 2010-N-20

History

The mother of the deceased was a G2P0A1, single, 16-year-old high school student with an estimated date of delivery (EDD) of September 11, 2009. By early ultrasound done at 10 weeks, her EDD was changed to September 16, 2009. She had an anatomic scan done at 21 weeks and full anatomic survey was carried out and normal anatomy was reported with a posterior placed placenta. Her family physician followed her throughout the pregnancy and delivery. She was A+ and her serology was unremarkable. Her Pap test showed low grade cervical squamous intraepithelial lesions (LSIL), but swabs for chlamydia and gonorrhea were negative. She was referred to public health and was seen at home initially and followed through pregnancy.

There was no documentation of non-invasive genetic screening being offered. She had a history of depression and was on citalopram 20mg commencing at 24 weeks. Her family physician induced labour with prostin gel on September 24, 2009 at 1645 hours at 41 weeks and one day gestation. She was admitted and oxytocin was started at 1030 hours on September 25, 2009. She was fully dilated at 0136 hours on September 26, 2009 and another doctor was consulted regarding abnormal fetal heart surveillance. The fetal heart was at 70 bpm on initial exam by the doctor. Vacuum was discussed and applied on and off from 0145 to 0211 hours when it was elected to move to the operating room for a trial of forceps.

The patient repeatedly declined Caesarean section. Epidural was topped up at 0235 hours and forceps applied at 0248 hours and removed at 0258 hours as no descent was noted. There was fetal tachycardia throughout this trial of forceps. The patient consented to Caesarean section at 0255 hours and meconium was now noted. A male infant weighing 3850 g, with Apgars of 2, 4 and 5 at one, five and ten minutes, was delivered by Caesarean section at 0316 hours. Arterial and venous gases were drawn, but were essentially the same at 7.07 (7.06), BE -17. NICU staff were in attendance and the baby was immediately resuscitated and intubated. The infant was flat at birth with severe respiratory metabolic acidosis and worsening cephalohematoma, so the decision was made to transfer the infant to a Level 3 facility at one hour of age.

Cooling was initiated while waiting transfer as the baby was felt to be at risk of hypoxic ischemic encephalopathy. The baby was transferred to the Level 3 facility via neonatal transport team. The mother was also transferred to be closer to the infant.

The baby died at seven days of age.

Post Mortem Findings

Cause of death was Hypoxic ischemic encephalopathy in a child with Arnold Chiari type 2 malformation.

Discussion

Initial concerns were noted by obstetrical care providers after the tracing was completed at 0136 hours on September 26. Upon review, abnormal findings were actually present following the tracing completed at 2230 hours on September 25.

While it is understood that there was a delay in performing the Caesarean section due to reluctance on the part of the patient, the end result was vacuum followed by forceps in the setting of an abnormal tracing with the vertex just below spines in a primiparous young woman. These conditions are associated with a reduced likelihood of success. The time from vacuum until delivery by Caesarean section was almost 1.5 hours with an abnormal tracing.

There were documented concerns in the nursing notes with respect to the interpretation of the tracings over the course of labour.

Recommendation

  1. Obstetrical care providers are reminded of the importance of being familiar with and implementing the SOGC Fetal Health Surveillance Guidelines. (JOGC, September 2007)


Case Summaries: Stillbirths



Case: 2009-S-1

History

The mother, age 37 years, had two previous spontaneous pregnancy losses and three previous therapeutic abortions. In October 2007, she was hit by a car while riding her bicycle.  She did not seek medical attention or see a doctor. She developed some bleeding in November and felt that she had miscarried, but did not see a doctor.  

On January 16, 2008, the mother attended a women’s medical clinic where an ultrasound showed a single viable fetus at 23 weeks gestation by BPD measurement. The doctor noted that the mother was “not ready for the responsibility” of a having a child and indicated that there were “financial concerns.” The mother signed consent for termination with laminaria, misoprostol and dilation and evacuation.

On the first visit, two laminaria were inserted. The patient returned to the clinic as instructed on the following day, January 17, 2008, and the two laminaria were removed and nine more were placed. The patient did not return to the clinic on January 18 for the booked dilation and evacuation procedure. The clinic tried unsuccessfully to reach the patient on that date.

On January 19, the patient reportedly felt fevered and on January 20, she had a large gush of fluid.  She did not seek medical attention until four days after her missed booking for pregnancy termination when she summoned an ambulance due to severe abdominal pains.

On January 22, the patient was brought by ambulance to the hospital with abdominal pain and fever. The EMS noted a temperature of 39.1C. At 1000 hours, her admission vital signs in the hospital showed a fever of 38.6C, pulse 110, respirations 20 and blood pressure of 96/58. No fetal heartbeat could be detected. The on-call obstetrician examined her and removed five foul smelling sponges and eight laminaria tents. The patient was noted to be contracting regularly and her cervix was 5-6 cm dilated. Ultrasound at the bedside confirmed intrauterine fetal demise and vertex presentation. The obstetrician ordered an IV and lab tests including blood cultures as well as cefazolin, gentamycin and metronidazole to be given intravenously. By 1335 hours, the patient was fully dilated and at 1408 hours, a stillborn female was spontaneously delivered.  

The patient remained in hospital for 28 hours postpartum, during which time her fever decreased to 37.7C. She was discharged home on oral cephalexin and metronidazole. Her blood cultures grew gram positive cocci in pairs and chains and gram negative bacilli. This report was received after her discharge and the emergency physician contacted her that evening by phone and confirmed that she was taking her antibiotics and was feeling better. The final blood cultures showed Streptococcus constellatus and Prevotella bivia in the anaerobic culture and Streptococcus viridans in the aerobic bottle. These results were called to the obstetrician on the morning after discharge.

Post Mortem Findings

Stillborn female

  • development consistent with 23 weeks gestation
  • no congenital anomalies
  • post mortem maceration, moderately advanced
  • blood and gastric cultures positive for multiple gram positive and gram negative bacteria

Placenta, immature singleton

  • chorionic villus development consistent with late second trimester
  • necrotizing chorioamnionitis, polymicrobial
  • necrotizing funisitis
  • chorionic surface vasculitis

Cause of Stillbirth: Amniotic infection syndrome with necrotizing chorioamnionitis secondary to incomplete termination of pregnancy.

Discussion

This baby died as a result of an infection secondary to incomplete termination of pregnancy at 23 weeks gestation. The mother failed to complete the termination procedure as planned and as a consequence, became infected and very ill herself.

No recommendations.



Case: 2010-S-2

History

This 35-year-old G1P0 had an estimated date of delivery (EDD) of August 23, 2008. An ultrasound on February 11, at 12 weeks and 2 days, gave a gestational age of 13 weeks and 1 day. The Antenatal Record II documented the discrepancy as being within the accepted range and confirmed an EDD of August 23.

Routine prenatal laboratory investigations were normal. An integrated pregnancy screening (IPS) was negative and a glucose challenge test (GCT) was declined. She was GBS negative and her past medical history included asthma and pericarditis (fluid on the heart) in 2003, laparoscopy for endometriosis in 2004, a longstanding history of migraine headaches and autoimmune hepatitis (AIH).

The patient’s care was provided by midwives. During the first trimester, she experienced nausea and vomiting (NVP) for which she took Diclectin©. She did not experience a significant weight loss and discontinued Diclectin© in the second trimester. On June 17, at 30 weeks and 3 days, an ultrasound showed fetal size consistent with 32 weeks and 5 days, with normal amniotic fluid index (AFI) and placenta.

On the June 20 prenatal visit at 30 weeks and 6 days, the patient’s midwife discussed a referral to a naturopath with regards to her auto-immune hepatitis. The referral was declined. A note dictated postpartum by the midwife indicated that an obstetrical consultation was also suggested, but was declined as her gastroenterologist had indicated that her liver condition should not impact on her pregnancy. The Antenatal Record 2 indicated that liver tests were done by the family doctor in early August (which equates to around 37 weeks), but the results were not sent to the midwife and were not included in the records provided. It does not appear from her clinical course that there was any problem with her liver function.

On September 2, at 41 weeks and 3 days, a biophysical profile scored 8/8. The report was not included in the records provided. On September 3, management of post dates pregnancy was discussed. A biophysical profile ultrasound was to be repeated on September 5.

Course in Labour and Delivery

The patient began having irregular contractions at 0730 hours on September 5, at 41 weeks and 6 days. She contacted her midwife at 1230 hours and informed her that the contractions were more regular. She was assessed at home at 1300 hours and the cervix was found to be 2 cm dilated, 50% effaced with the vertex at spines -2. The fetal heart was 152-157 bpm. She was advised to notify her midwife when the contractions became more intense.

The patient paged the midwife at 1730 hours to advise her that the contractions were more intense. The midwife attended at 1900 hours and on examination, the cervix was 2-3 cm dilated, 90% effaced with the vertex at spines -2. Contractions were every 2-5 minutes, lasting 30 seconds and the fetal heart was 150-160 bpm. Following the assessment, the patient decided to go to bed and rest while the midwife stayed in the home. The patient got up at 2230 hours and had a shower. She was assessed by the midwife at 2310 hours and the fetal heart could not be detected. At 2315 hours, the cervix was 5-6 cm dilated. A spontaneous rupture of membranes (SROM) occurred for meconium-stained fluid at 2317 hours. An ambulance was called at 2330 hours and arrived at 0020 hours. The hospital was also notified. The patient was assessed by the obstetrician on call and ultrasound confirmed fetal demise. The patient was afebrile and her admission CBC showed an elevated WBC of 19.8. An epidural was started at 0128 hours and oxytocin augmentation was started at 0250 hours. She complained of pruritus at 0330 hours and went on to delivery by vacuum extraction at 1237 hours of a 3560 g stillborn male infant.

Post Mortem Findings

Autopsy findings revealed a male fetus with no anatomical developmental malformation. The body surface showed meconium staining, but no evidence of meconium aspiration. The degree of autolysis of various organs ranged from mild to advanced. The major abnormality was the presence of extensive moderate to severe acute chorioamnionitis. Viral and bacterial cultures were negative. There were no fetal or placental features to suggest diabetes.

The placenta showed a small old infarct.

The cause of death was undetermined.

Discussion

This baby was stillborn as a result of fetal demise occurring in early labour at 41 weeks 6 days. Although post dates, a biophysical profile three days before was normal. There was no clinical evidence or findings at autopsy to indicate deterioration in placental function.

The autopsy found evidence of extensive moderate and severe acute chorioamnionitis. Clinically, there was no evidence of infection. Although the maternal WBC was elevated at 19.8 at the time of admission to hospital, this is a non-specific test and not an uncommon finding during labour. There was no maternal fever.

The patient developed pruritus after admission to hospital and the question arose as to whether this might have been a symptom of liver disease or new onset intrahepatic cholestasis of pregnancy (ICP). Both AIH and ICP are associated with adverse pregnancy outcome, but no laboratory investigations were done to assess these conditions.

First time onset of pruritus after the fetal demise makes ICP highly unlikely. There is not enough information provided about the patient’s initial presentation, diagnosis and treatment of AIH to comment on what level of risk this condition presented to her pregnancy. It would have been prudent for the midwife to have strongly recommended a consultation with a gastroenterologist/hepatologist (not a naturopath) during pregnancy and failing that, at least obtain the medical records and laboratory investigations for inclusion in her chart.

The records do not indicate whether an investigation of stillbirth protocol was initiated at the hospital. In a postpartum letter to the family doctor, the midwife indicated that these investigations had not been done and requested that the family doctor follow up on this. The records provided do not indicate whether any investigations were done.

Recommendations

  1. Obstetrical care providers are reminded that it has been recommended that a protocol should be used to investigate the possible cause of fetal death. (SOGC Clinical Practice Guideline No. 178 June 2006)
  2. Midwives are reminded that medical consultation is indicated when there is history of an illness that is associated with adverse perinatal outcome.


Case: 2010-S-3

History

The mother of the deceased was a 31-year-old gravida 1 with an EDD of August 18, 2008, confirmed by a 10 week ultrasound.   The patient was under midwifery care from week 12 of the pregnancy.   The antenatal records (I and II) showed appropriate visits and investigation for the duration of the pregnancy with the last recorded antenatal visit on August 14, 2008, three days prior to delivery.  

A urine culture in the first trimester on the last day of February revealed Hemolytic strep Group B.  A note was made that a consult was requested for antibiotics for urinary tract infection (UTI) on March 20.   Further positive cultures on April 21 and July 16 showed E. coli and Enterococus respectively.  The patient was sent for consultation for possible antibiotic treatment, although it is not clear whether any antibiotics were ever taken.  The patient did not have health insurance, did not speak English and required interpreters during the provision of care.

All other prenatal testing was completed and recorded as normal, including routine prenatal bloods, two hour glucose tolerance test and a second trimester ultrasound.   Fibroids were found on the uterus. Third trimester ultrasound scans were done at 29 and 34 weeks gestation and both of these showed appropriate growth and amniotic fluid volume. 

The patient paged the midwife on August 18, 2008 (time not documented) to report contractions.   She was assessed by the midwife as not in active labour at that time. There was no evidence of concern during this assessment. The midwife attended to the patient at 1040 hours on August 19 due to increasing contractions.   She was assessed to be in active labour with the cervix 4 to 5 cm with membranes intact.   The patient was advised to attend to the hospital for further management and consult for Group B streptococcus prophylaxis.  She arrived at the hospital by 1230 hours and by 1250 hours, she received her first dose of Penicillin G prophylaxis and was 8 to 9 cm dilated.  Fetal heart was taken by doptone at home and every 15 minutes thereafter until EFM was started in hospital just before 1400.  The readings appeared to be normal up until this time.  (Late entry notes were made from around 1400 hours and do not coincide with the electronic monitor readout or subsequent nursing and physician timing of events.)

Shortly after 1400 hours, EFM showed significant decelerations with slow recovery and subsequently, no discernable fetal heart. Nursing notes indicated that the initial request by the midwife did not suggest urgency.  The obstetrician’s note indicated that he was asked to go to the room for a scalp clip by one of the labour and delivery nurses and was not told of the indication.   He arrived in the room at 1421 hours.  Two scalp electrodes were tried, but did not pick up a fetal heart. The EFM strip confirmed this timing. Bedside ultrasound was done and confirmed that no fetal heart was detectable. An OBS alert -“code pink” - was initiated and a stat Caesarean section was ordered.

General anesthetic was instituted by the anesthetist and surgery was started at 1425 hours. The stillborn was delivered at 1430 hours.  The neonatal staff was in attendance.  The Apgars scores were 0 at one minute and continued to be so, with no signs of life, despite attempts at resuscitation.    


The resuscitation attempt included cardiac compression, intubation, epinephrine via ET tube on multiple attempts and intravenous fluids.   The code was stopped at 1455 hours, 32 minutes after birth with no return of the heart rate in this stillborn infant.  Cord gases revealed a venous PH of 7.20 and base excess of –11 and arterial PH of 6.97 with base excess of –14.

Post Mortem Findings

This stillborn female weighed 3700 g.  There was mild acute chorioamnioitis, but with negative microbiological cultures, as well as meconium staining of placental membranes.  

The examination of the brain revealed congestion and edema with normal CNS development and no evidence of infection.   

The cause of death was attributed to “perinatal asphyxia with no definitive cause identified.”

Discussion

This primiparous patient appeared to have a normal pregnancy except for lower tract urine infections.  Her early labour was unremarkable.  It was not until almost fully dilated, shortly after hospitalization and shortly after spontaneous rupturing of membranes, that there was difficulty in monitoring the fetal heart.  

There was communication between the midwife and nursing staff about a request for an obstetrical consultation, but there does not appear to have been an appreciation that this was urgent.  By the time of diagnosis of fetal compromise, approximately 20 minutes had elapsed since the first indication by electronic monitoring that there was an abnormal fetal heart rate. With the complete loss of fetal heart activity in this short time, there might have been undetected fetal heart abnormalities prior to that.

The subsequent emergency Caesarean section under general anesthesia was done as expediently as possible. It is not clear why Caesarean section was performed for fetal demise.  The baby was stillborn and could not be resuscitated despite the presence of the neonatal staff and initiation of attempted resuscitation right after birth.

The autopsy did not reveal any evidence of brain injury, so the final event was likely acute, with no known predisposing factors.  

Recommendations

  1. Health care providers are reminded of the need to clearly communicate clinical concerns when requesting consultation or assistance in the course of a developing emergency in labour.
  2. Health care providers are reminded of the importance of accurate documentation of the times of events in the course of clinical care in an emergency.


Case: 2010-S-4

History

The mother of the stillborn was a 26-year-old G1P0 with generally good health. She conceived following clomiphene and intrauterine insemination. Early ultrasound demonstrated a dichorionic twin gestation and confirmed her due date of May 10, 2009. The morphology ultrasound was normal. All her prenatal investigations were normal. She had no obstetrical risk factors.

Her prenatal care was consistent and well documented. She was Rh negative and received Rh immunoglobulin. She received celestone at 28 weeks. The GCT was normal. She was seen at 21, 25 and 27 weeks and no concerns were documented. At 28.5 weeks, an ultrasound was arranged for every two weeks.

On February 26, 2009, at 29 weeks, 3 days, the ultrasound revealed: twin A – 30 weeks, 1554 g, BPP 8/8, normal umbilical artery SD (systolic-diastolic) ratio; twin B – 29.5 weeks, 1349 g, BPP 8/8, no umbilical SD ratio reported.

On March 3, 2009, at 30 weeks, 3 days, the ultrasound revealed: twin A – 33 weeks, 2174 g, BBP 8/8, normal umbilical artery SD ratio; twin B – 32 weeks 1879 g, BPP 8/8, elevated SD ratio, “apparent absent” end diastolic flow. A verbal report was given to the doctor.

On March 4, 2009, weekly non-stress tests (NST), bi-weekly bio-physical profiles (BPP) were ordered.

On March 18, 2009, the mother’s blood pressure was mildly elevated at 140/90. She did not have any proteinuria or signs of preeclampsia. The increased SD ratio arising from twin B was documented.

The NST of twin B was non reactive and the doctor who reviewed the NST at the hospital ordered a BPP.

On March 18, 2009 at 32 weeks, 3 days, the ultrasound revealed: twin A- BBP 8/8, normal SD ratio twin B - BPP 4/8, S/D ratio significantly increased at 24.7, reversed flow in the umbilical artery, small amount of fluid in fetal abdomen.

The doctor was notified of these findings, and came to see the patient. He indicated that twin B was showing “evidence of compromise although there was no immediate distress.” The decision was made to deliver the twins. Anesthesia and pediatrics were notified, and the Caesarean section was scheduled for 2100 hours.

At 2100 hrs, however, anesthesia was not available as they were in the operating room. The second on call anesthetist had already gone home as he/she was feeling unwell. The Caesarean section was done as soon as anesthesia was available. Twin A was born at 2329 hours and was fine with Apgars of 8 and 8 and a birth weight of 2075 g.

Twin B was born at 2330 hours. The cord gases showed a severe metabolic acidosis with Arterial pH 6.81 and BE -25.3mmol/L. There was no heart rate or respiratory effort. The baby could not be resuscitated. The code was stopped at 2350 hours. There were no abnormalities seen in the cords or placenta at delivery. The baby’s weight was 1758 g, which was 15% discordance.

Autopsy indicated the cause of death was intrauterine asphyxia associated with fetal thrombotic vasculopathy of the placenta. These placental findings were localized primarily in the portion of the placenta of twin B.

Review of fetal heart rate tracings

The fetal heart rate (FHR) tracing begins at 1516 hours. Continuous monitoring until 1653 hours demonstrated a reactive tracing for twin A. Twin B’s FHR had a baseline of 140 bpm. There were no accelerations or decelerations. The short term variability was minimal. The fetal tracings were recorded from 1739 until 1828 hours and showed similar findings. There were no FHR recordings after 1828 hours.

Discussion

This is the case of the stillborn death of twin B following intrauterine asphyxia. The antenatal ultrasound findings of increased placental vascular resistance (abnormal umbilical artery Doppler) correlate with the pathologic findings in the placenta (fetal thrombotic vasculopathy). The umbilical artery Doppler demonstrated absent end diastolic flow two weeks prior to delivery, and reversed flow on the day of delivery.

It is difficult to determine whether the delay in completing the Caesarean section had any effect on the outcome. The baby was extremely acidotic with significant reverse end diastolic flow in the umbilical artery. It is difficult to determine if the delay of two hours impacted on the outcome. The fetal heart rates were not continuously recorded after 1828 hours, so it is impossible to determine if the fetal heart rate pattern of twin B deteriorated further prior to the Caesarean section. The baby’s FHR tracing was abnormal from 1516 – 1653 hours. The NST, the BPP and Doppler indicated there was fetal compromise. A decision to deliver could have been made immediately after either of these non-reassuring assessments.

The deterioration of twin B likely occurred gradually over a period of time. The ultrasound assessment performed on March 3 showed absent end diastolic flow in the umbilical artery. This indicated the presence of a significant increase in placental vascular resistance and placental insufficiency. At this time, the BPP was normal and the fetus was compensating despite the presence of abnormal placental function. A heightened level of surveillance may have provided an opportunity for delivery prior to the onset of severe placental insufficiency.

The reporting of the abnormal umbilical artery Doppler is confusing. The resistance is reported using the SD (systolic/diastolic) ratio. In the March 3 report, the SD ratio is reported as 6, but if there is no diastolic flow, the ratio should be infinity. The SD ratio is more problematic with reversed flow as evidenced by the report for March 18 (REDF and SD ratio of 24). For these reasons, the SD ratio has been replaced by the resistance index (SD)/S or the pulsatility index (SD)/mean in many centres.

Recommendations

  1. Obstetrical care providers are reminded of the importance of increased fetal surveillance in the presence of placental insufficiency. (Fetal Health Surveillance Antepartum and Intrapartum Consensus Guidelines, SOCC Clinical Practice Guideline, No.197, Sept 2007).
  2. Obstetrical care providers are reminded of the increased risks of perinatal morbidity and mortality in the presence of absent and reversed end diastolic flow in the umbilical artery. (Fetal Health Surveillance Antepartum and Intrapartum Consensus Guidelines, SOCC Clinical Practice Guideline, No.197, Sept 2007).


Case: 2010-S-5

History

The mother of the deceased was a 25-year-old G1P0 with an EDD of January 6, 2010.  She was transferred from an obstetrician to midwifery care at 14 weeks gestation.

The mother had an obstetrical and medical history that was normal, aside from a low initial hemoglobin of 100. The father of the deceased had thalassemia minor. A referral was made to see a hematologist. All other blood work and investigations were normal.

A nuchal translucency (NT) ultrasound was done at 12+5 weeks, which was normal and confirmed her due date of January 6, 2010. The anatomical scan done at 18+2 weeks revealed normal morphology.

On September 30, 2009, at 2040 hours, at 26 weeks gestation, the mother called her midwife to report bleeding. After a telephone assessment, it was decided that the pressure and spotting of bright red blood and fluid leaking was most likely due to the mother straining to have a bowel movement.  She was advised to rest and to call back if she experienced any further bleeding, regular contractions or fluid leaking.

A follow-up phone call was made an hour later. There was no pressure, but the mother reported some drops of blood and a rock hard uterus that was tender to touch. She indicated that she was generally feeling uncomfortable. She felt fetal movement and was uncertain about cramps.

The midwife reviewed the “warning signs of preterm labour” with the mother and made a plan for her to come to the clinic the next day to check her cervix and give her a requisition for an ultrasound.

The following morning, at 0545 hours, the mother woke up experiencing pain every 4-5 minutes, lasting 10-20 seconds. An hour later, she went to the washroom and passed the stillborn fetus into the toilet. EMS was called and efforts to revive the baby were futile. Intubation was performed and epinephrine given.

The baby was transported to hospital, but resuscitative efforts were unsuccessful.

The placenta was delivered intact and the postpartum course was normal.

Post Mortem Findings

The autopsy results indicate a stillborn female fetus following preterm delivery at 25-26 weeks.

The baby weighed 768 g. Length was 33 cm and was normal for gestation of 28+3 weeks.

There was a mark around the baby’s neck with congestion of face, neck and scalp above ligature mark possibly as a result of a tight nuchal cord. There was no air in the lungs.

Blood and lung cultures were negative. Placental studies were normal. The neuropathology exam revealed no anoxic-ischaemic changes, inflammation or infection.

Cause of death was intrauterine fetal demise from strangulation by the umbilical cord.

Discussion

The mother of the deceased reported bloody discharge, uterine tenderness and increased tone at 26 weeks gestation. A decision was made to assess her the following morning. At 26 weeks, there is a survival rate of 60-80%, especially if a corticosteroid injection is given to the woman to assist with lung maturation.

Bleeding in the second trimester is considered “Category 2” in the Indications for Mandatory Discussion, Consultation and Transfer of Care (IMDCTC) College of Midwives of Ontario (CMO) document.  Although this met the criteria for a “Category 2” notification, no action was taken by the midwife.

The autopsy report suggested that the cause of fetal demise was cord strangulation. It is uncertain whether earlier intervention would have altered the outcome of this pregnancy. However, hospital assessment would have allowed for monitoring, steroid administration and fetal fibronectin testing.

The mother was informed about “warning signs of preterm labour” and told to call with regular contractions. Unfortunately, she was already exhibiting signs of preterm labour at the time of this warning and these signs were not acknowledged.  Once frequent regular contractions are occurring at this early gestational period, it is often too late for any intervention.

Following delivery of the stillborn, the midwife was paged, but after two hours there was no response.  An additional page was made and the midwife responded and attended the hospital 50 minutes later.  It is unclear why there was not closer monitoring by the midwife.

Recommendations

Obstetrical care providers are reminded of the importance of careful education and assessment of women presenting with signs of possible preterm labour, so that measures such as fetal fibronectin testing, tocolytics and corticosteroids can be offered.

Midwives are reminded that the College of Midwives Indications for Mandatory Discussion, Consultation and Transfer of Care (IMCTC) document requires a level 2 consultation for a) bleeding in the second trimester and b) signs of preterm labour.



Case: 2010-S-6

History

The mother of this stillborn was a 34 year-old G2P1 with an EDD of November 16, 2008 based on her last menstrual period and an early second trimester ultrasound. Routine prenatal laboratory investigations and IPS were normal.  Routine second trimester ultrasound at 19 weeks 3 days gestation was normal. A GCT was normal. An ultrasound done on October 3 at 33 weeks 4 days gestation for fetal growth and assessment of cervical length, was normal.

Past obstetrical history was for one previous term pregnancy delivered vaginally of an 8 pound, 3 ounce male infant in 2005. The mother’s past medical history was unremarkable.

The mother presented to hospital on October 14, 2008 at 35 weeks 2 days gestation with a two day history of no fetal movement. A real time ultrasound scan confirmed fetal demise. After informing the parents, consent was obtained to induce labour.

Dinoprostone (Cervidil©) was inserted at 1225 hours on October 14.  Labour became established that evening and at 2230 hours, the cervix was 3 cm dilated. At 2300 hours, an epidural was placed. At 2330 hours, an artificial rupture of membranes was performed for lightly meconium stained fluid and oxytocin augmentation was started. She went on to a spontaneous delivery of a 2778 g male infant at 0040 hours. There was no cord accident noted at delivery, but the cord was noted to appear hemorrhagic and thrombosed. There was also a small clot delivered after the placenta.

Post Mortem Findings

Autopsy showed a normally-developed appropriate for gestational age male stillborn infant with maceration of the skin and visceral autolysis. There were no malformations. The placenta weighed 412 g and was accompanied by a 40 g blood clot, although there was no evidence of abruption. The only significant finding was a 0.8 cm length of cord which narrowed down to 0.6 cm in width at the site of insertion into the umbilicus. The rest of the cord was very congested and edematous. Microscopically, the cord vessels contained clotted blood. The umbilical vein in the baby was also distended and appeared to be clotted.

Although stricture of the umbilical cord is considered a controversial cause of stillbirth, the findings were considered supportive of this diagnosis.

Discussion

This infant was stillborn at 35 weeks gestation as a result of an apparent cord complication. The antenatal course was otherwise uncomplicated and an ultrasound done 12 days prior to delivery was normal.  Although stricture of the umbilical cord is a controversial cause of stillbirth, there were no other clinical or pathological explanations for the outcome.

No recommendations.



Case: 2010-S-7

History

The mother of the deceased was a 24-year-old primiparous woman with an EDD of November 22, 2008. She was being cared for by her family physician. Her prenatal care up until presentation to Hospital A on November 20, 2008, was unremarkable. She had been offered and declined IPS. She had an ultrasound at 18 4/7 weeks which was interpreted as normal with the caveat that all anatomy had not been seen. She was Group B streptococcus (GBS) negative and had a negative GTT. She had gained 47 pounds (21.5 kg) during the pregnancy. Her family history included diabetes and she had a brother with cerebral palsy (CP).

The patient presented to Hospital A on November 20, 2008 with intermittent abdominal pain. Her cervix was noted to be long and closed with station at spines -2, with no change over the course of six hours. She had a CBC drawn with a white count of 19, with left shift presumably felt to be in keeping with pregnancy and a urinalysis with a large amount of blood. She was afebrile with blood pressures from 115/76 -126/82 and pulse 97-110. She was initially on continuous monitoring, then intermittent auscultation prior to her discharge home around 0900 hours on November 20, 2008.

The fetal heart was abnormal throughout with no variability noted. It was recorded in the nursing note at 0600 hours that juice was given with no appreciable effect; the doctor was advised. The doctor wrote a late note on November 28, 2008 that fetal heart was “OK for IA” (intermittent auscultation) and that he felt she was in latent phase labour and fit to go home on pass to return in active labour.

The patient returned the next day with discomfort and the fetal heart was absent as confirmed by ultrasound by the doctor on call. The patient was transferred to Hospital B as Hospital A did not have Caesarean section or epidural capability on the weekend.

The patient was given Demerol© 75 mg and Gravol© 50 mg IM prior to transfer for "discomfort." She was transferred by car after arrangements had been confirmed through Criticall. Hospital B confirmed fetal demise by ultrasound and induction with misoprostol followed by artificial rupture of the membranes (ARM) and oxytocin was planned. It is unclear from the chart whether the patient received misoprostol which initiated labour or whether she started to labour spontaneously. There was thick meconium seen at ARM after her epidural at 5-6 cm. She had a spontaneous vaginal delivery of a stillborn girl on November 22, 2008 at 1645 hours with a nurse in attendance as the doctor was in the OR. The patient had first degree tears repaired with 3.0 Vicryl.

Post Mortem Finding

Autopsy revealed a normally developed female infant with moderate maceration consistent with death that occurred sometime prior to delivery. Neuropathological examination of the brain confirmed presence of mild anoxic-ischemic encephalopathy which would be consistent with asphyxia. Placenta showed deep green meconium staining consistent with fetal distress prior to death. The rest of the autopsy showed acute pneumonia and the placenta showed acute chorioamnionitis, but the post mortem blood culture was negative and the lungs yielded only light Lactobacillus.

Cause of death was reported as intrauterine asphyxia complicated by congenital pneumonia.

Discussion

The mother of this stillborn infant was assessed on November 20, 2008 for crampy abdominal pain felt to be early labour. The fetal monitoring was abnormal from admission. It appeared that this was not appreciated by the physician and therefore not acted upon. It is unclear what the outcome would have been had earlier intervention occurred. The cause of death was found to be intrauterine asphyxia complicated by congenital pneumonia. There were no clear indications of chorioamnionitis with the absence of fever and fetal tachycardia at admission November 20, 2008.

Recommendations

  1. Obstetrical care providers are reminded of the importance of confirming fetal well-being prior to discharge.
  2. Obstetrical care providers are reminded of the importance of asking mothers about fetal movements.
  3. A Regional Coroner’s Review should be conducted on this case.


Case: 2010-S-8

History

The mother of the deceased was a 16-year-old gravida 1 student with an EDD of June 14, 2010 confirmed by first trimester ultrasound.

She had a history of systemic lupus erythematosus (SLE), diagnosed at age 7 and was followed at the children’s hospital. She had previously had arthritis, rash, serositis and class 3 focal glomerulonephritis.

The mother was referred back to the rheumatology service at the children’s hospital at approximately 11 weeks gestation by her family doctor. She had not been seen there since April 2008 at which time she was supposed to have been on prednisone. However, she had already been demonstrating signs of noncompliance. Since that time, she had not contacted the clinic for any follow-up and had stopped all medications. The rheumatologist on this visit felt that she did not need any active treatment for her underlying disorder and that it was under control. She was confirmed to have positive ANA and anti-Ro antibody. Arrangements were made for fetal echo which was subsequently reported as normal.


The mother was referred to an immunologist in an obstetrical medicine service in Toronto and was seen there since the beginning of March at approximately 25 weeks gestation. The results of an ultrasound and the fetal echo were reviewed and her disease appeared stable. The immunologist assisted in coordinating efforts for an obstetrician in the patient’s home community outside of the city. The Toronto physician agreed to concurrently follow the patient for the potential of a lupus flare and would assist in transferring the patient to the appropriate hospital with specialized services if the patient had problems with the management of her SLE during the pregnancy.

The ultrasound scan at 25 weeks gestation was normal with an estimated fetal weight in the 27th percentile. At approximately 30 weeks gestation, she had her initial appointment with the obstetrician in her home community. On April 13, at 31 ½ weeks gestation, an ultrasound was done that gave the first indication of intrauterine growth restriction (IUGR) with a composite fetal age by ultrasound of 28 weeks. The abdominal circumference was equivalent to 26 weeks and 3 days and the estimated fetal weight of 1066 grams was in the 2nd percentile. The biophysical score was 8/8 and the amniotic fluid index was in the normal range. Doppler studies showed increased resistance, with normal ductus venosus and MCA PSV (middle cerebral artery peak systolic velocity) of 81.2 cm per second with a normal range of 30-60, MCA PI (middle cerebral artery pulsatility index) of 1.41 (normal 1.6-5).

The mother was seen in the office the following day, April 14, and found to be hypertensive for the first time with a B/P of 156/110 and 4 + protein. She was admitted directly to Hospital A in her home community. After admission, she was started on magnesium sulphate, labetolol for hypertension and given a first dose of celestone. Shortly after admission, arrangements were made for transfer to Hospital B in Toronto, where specialized services could be provided. The patient was very reluctant and expressed refusal to go to Toronto for social reasons. Subsequently, through discussion with a social worker, arrangements were made for a friend of the mother to accompany her to Hospital B in Toronto. She was transferred to Hospital B on the evening on April 14, 2010..

Early in the admission to Hospital B, the mother’s blood pressure was stable and did not require medication. Pregnancy induced hypertension (PIH) blood testing was normal. Ultrasound confirmed significant IUGR, with a very small placenta and increased umbilical artery resistance. By the following day, her blood pressure and other blood tests were stable. She was advised that it would be extremely important to stay in hospital for continued monitoring particularly because of significant IUGR of her infant. Over the next 24 hours, the mother continued to express a need to leave the hospital. Despite being advised that there was a high risk to the fetus for a poor outcome, she discharged herself from hospital against medical advice approximately 36 hours after admission to Hospital B.

On April 26, the mother was admitted to Hospital A in her home community. She had been sent in for a non stress test and there was no heart beat found. An ultrasound confirmed the fetal demise. She was admitted and given magnesium sulphate, an anti-hypertensive was started and labour was induced. She subsequently had the uncomplicated vaginal birth of a 1140 g stillborn male infant. The placenta was described as “extremely small” and was sent to pathology as per the obstetrician’s operative note and the nurse’s note. No report was submitted for the purposes of this review however. The request for an autopsy was declined.

The remainder of the mother’s hospital course was unremarkable. She was advised of the importance of care for her hypertension and subsequent follow up for SLE with the specialist in Toronto.

Discussion

This 33 week growth restricted stillborn infant was born to a teenage mother who had an underlying history of SLE which was stable clinically. Preeclampsia developed requiring hospitalization and subsequent referral to tertiary care due to prematurity.

The mother chose not stay at a hospital in Toronto despite being advised that there needed to be very close monitoring for herself and her fetus. She discharged herself and was not seen again in care again until ten days later at which time the fetal demise was diagnosed.

Upon readmission to the hospital in her home community, she had appropriate care for preeclampsia and labour induction of this stillborn infant.

The mother had been seen by the social services in both her home hospital and at the hospital in Toronto providing specialized services. She did not follow the advice of social services regarding provision of medical care. She had a history of non compliance of care that was initially noted by her rheumatologist in Toronto.

The mother’s challenging social situation and limited family support likely had an impact on her decision not to remain in hospital in Toronto.

No recommendations.



Case: 2010-S-9

History

The mother of the deceased was a 39-year-old G1P0 with an estimated date of delivery of February 17, 2010.

Ultrasound on August 9, 2009 showed a gestational age of 12 weeks 4 days. Routine prenatal laboratory investigations and IPS were normal. Routine second trimester ultrasound on September 26, 2009 was normal. HbA1C on August 4 at 12 weeks and September 12 at 17 weeks were .057 and .058 (normal <.060). A 75 gram oral glucose tolerance test done on November 21 at 27 weeks showed a fasting blood sugar of 5.5 (normal level is 3.3 - 5.3), with the one and two hour values in the normal range. The patient’s obstetrical care provider advised some changes in her diet, but a referral was not made to the Diabetic Education Center. No further blood sugar testing was performed.

Ultrasound on December 19 at 32 weeks and on January 23 at 37 weeks, showed normal growth, amniotic fluid volume and BPP scores. Symphysis fundal height (SFH) measurements on the Antenatal II are illegible. The GBS culture was positive.

The patient’s past medical history was unremarkable. Blood sugar testing was done coincidentally around the time of conception. Fasting blood sugar on May 9 was 5.7 (normal level is 3.3 - 6.0) and 6.3 on May 30 with HbA1C .059 (normal <.060).

On examination at her first prenatal visit, the patient’s height was 5’2” and weight 178 lbs. Her pre-pregnant weight was 156 lbs with a BMI of 28.6.

The patient presented to her family doctor for a routine prenatal visit on February 16, 2010 at 39 weeks 6 days. Blood pressure and fetal heart were normal. On February 20, she reported a 2-3 day history of decreased fetal movement. She was sent to the triage unit where fetal demise was confirmed by ultrasound. A decision was made to induce labour.

On examination, the cervix was 2-3 cm dilated, 80% effaced with the vertex at spines -2. Artificial rupture of membranes was carried out for thick meconium stained fluid. Oxytocin was started and labour became established. She reached full dilation approximately nine hours later. After two hours of pushing in the second stage, the vertex remained at spines -1. An epidural was placed and after another hour, there was no further descent. After obtaining consent, a vacuum extraction was attempted, but was unsuccessful. A subsequent forceps procedure was also unsuccessful. She then went on to Caesarean section for a 4200 g stillborn male infant. There were no findings at the time of Caesarean section to explain the stillbirth.

A haemoglobin A1C done on the morning of February 21 was .068.

The postpartum course was complicated by an immediate postpartum hemorrhage requiring use of the Bakri balloon and packed red cell transfusion. The patient then developed respiratory distress which was initially treated as a possible pulmonary embolus, but was subsequently diagnosed as more likely fluid overload. An endocrinology referral was made and she was started on metformin. Out patient follow up was arranged with the diabetes clinic.

Post Mortem Findings

Autopsy showed no evidence of congenital anomalies. There was extensive autolysis consistent with fetal demise occurring 4-5 days prior to delivery.

Examination of the placenta showed evidence of acute chorioamnionitis.

The Coroner’s Investigation Statement identified acute chorioamnionitis as the likely cause of the stillbirth and concluded that gestational diabetes did not appear to be related to the death.

Discussion

This infant was stillborn at term. Although the Coroner’s Investigation Statement identified acute chorioamnionitis as the likely cause, it is more likely that this developed during labour, rather than before.

The diagnosis and management of gestational diabetes remains controversial. The Canadian Diabetes Association guidelines require two abnormal blood sugars on oral glucose tolerance testing for the diagnosis of gestational diabetes. The glucose tolerance test done at 27 weeks had one abnormal value which is characterized as impaired glucose tolerance. This has been associated with increased risk, but not stillbirth.1

Recently, intervention with diet and blood sugar monitoring has been recommended for this diagnosis to reduce the recognized risks. The risk of stillbirth has been reported to be increased with gestational diabetes2 , but there was no further testing or monitoring during the third trimester. The ultrasounds done at 32 and 37 weeks did not show any parameters characteristic of poor glycemic control. Although this patient definitely had impaired glucose tolerance, it cannot be concluded that diabetes was the cause of the stillbirth. Therefore, although referral for management of impaired glucose tolerance may have been prudent, the outcome may have been the same.

Recommendations:

The Society of Obstetricians and Gynaecologists of Canada (SOGC) should review the current guidelines on Gestational Diabetes Mellitus in pregnancy.

References

  1. HAPO Study Cooperative Research Group. Hyperglycemia and Adverse Pregnancy Outcomes. N Engl J Med 2008; 358:1991-2002. May 8, 2008.
  2. Crowther, Caroline A. et al. Effect of Treatment of Gestational Diabetes Mellitus on Pregnancy Outcomes. N Engl J Med 2005; 352:2477-2486. June 16, 2005.


Case: 2010-S-10

History

The mother of the stillborn was a 32-year-old G2T0P0A1L0 who was AB positive with no antibodies. She was 5’7” and had a BMI of 28 at intake to midwifery care at 9 weeks 2 days. Her EDD was March 27, 2010. IPS was not done and she was rubella immune unknown. Hepatitis B, HIV, syphilis, chlamydia, gonorrhea and urine were negative at 17 weeks. Routine 50g oral glucose challenge test (OGCT) was declined at 26 plus weeks. BP was normal in prenatal period with +1 to trace protein on urinalysis. Multiple informed choice discussions were documented in the midwifery checklist and narrative notes. The first ultrasound at 12 weeks showed a single fetus consistent with last menstrual period. The second ultrasound at 18 weeks indicated normal morphology, except for the lack of a view of the spine with posterior placenta and no previa.

At the 33 week 4 day midwifery visit, the fundal heights exceed the 90th percentile for growth. The plan was to follow the growth with ultrasounds. The third ultrasound done on February 22 at 35 weeks and one day showed growth at the 75th percentile at 2860 g, complete breech, amniotic fluid index (AFI) of 28.4 (mild polyhydramnios), posterior placenta and a BPP of 8/8. The midwife had an informed choice discussion with the mother following detection of breech presentation. The patient decided on referral to another midwife for external cephalic version (ECV). The patient was also offered a referral to an obstetrician. A vaginal breech birth was also discussed if the ECV was not successful.

On March 1 at 36 weeks and one day, the fourth ultrasound was completed for position. AFI was normal at 22.3, posterior placenta grade I and II, no nuchal cord, sacrum anterior, complete breech and BPP was 8/8. Also on March 1, the first ECV was attempted by a consultant midwifery group and was not successful.

On March 5, at 36 weeks and five days, ultrasound number five for position confirmed still complete breech. Also on March 5, the second ECV was not successful by another midwife in the consulting group. The patient was offered and declined a non-stress test following the attempt.

On March 8, at 37 weeks and two days, the sixth ultrasound showed growth at close to the 90th percentile, a marked increase in abdominal circumference (AC) of 4 weeks size in 2 weeks, AFI 25.7, posterior placenta grade I, frank breech spine on maternal right and BPP 8/8. The same day, a referral was sent to an obstetrics group in an adjacent community regarding ECV. The consult note did not mention macrosomia. The obstetrician called the midwife to tell her she did not do ECV and gave the midwife the number for the hospital where ECV could be booked with an obstetrician. The obstetrician set up an appointment for the mother to be seen on March 16, for ongoing care if ECV was not successful.

On March 10, at 37 weeks and four days, the third ECV was attempted at a hospital by an obstetrician. It too was unsuccessful. There were no notes available, but an ultrasound report from this procedure showed that the AFV was normal, posterior placenta grade II, frank breech and BPP 8/8. The ultrasound report indicated that a non-stress test was suggested, but the patient declined.

On March 15, at 38 weeks and one day, an ultrasound showed a large for gestational age fetus at 4480 g, well above the 95th percentile, with AC at 43 weeks size, amniotic fluid volume was normal, posterior placenta grade I, frank breech and BPP 8/8. The radiologist recommended obstetrical consultation and Caesarean section. That same day, the fourth ECV was attempted by the first midwifery consultant group and succeeded. There is no indication that a non-stress test was recommended on that day.

The following day, at 38 weeks and two days, the mother attended the previously arranged obstetrical consultation at the hospital. There was a discussion regarding breech vaginal birth if the fetus converted back to breech. There is no indication in the consultation note that the obstetrician examined the mother or that he was aware of the baby’s macrosomia identified on ultrasound the day before.

GBS was negative at term. One week later, at the next midwifery visit on March 22, at 39 weeks and two days, no fetal heart was detected and the patient went to the local hospital for ultrasound confirmation of fetal demise and consultation with an obstetrician.

Summary of Labour and Delivery

The obstetrician found the patient’s cervix to be unfavourable and dinoprostone (Cervidil©) was placed at 1545 hours. A CBC and group and type were done and arrangements were made for oxytocin induction the following day if the mother’s cervix had ripened. The patient was discharged home.

The patient returned at 2100 hours for pain relief. Morphine was provided routinely over the next 24 hours for pain control. At 0215 hours, there was a spontaneous rupture of membranes (SRM), with a large amount of meconium stained fluid. Cervidil© was removed by the nursing staff and the midwife was informed. Cervix was 1 cm and 100% effaced.

At 0520 hours, an epidural was placed and the midwife was called to come in at 0715 hours. After the epidural, the patient’s contractions were slow and oxytocin augmentation was commenced at 0745 hours. The midwife arrived at 0845 hours and appeared to have assumed care, but this was not clearly documented.

At 0933 hours, the cervix was 2 cm, -2 spines and oxytocin augmentation was increased per protocol to 14 mU/minute. At 1330 hours, the cervix was 5 cm, -2 spines and at 1600 hours, the cervix was 7-8 cm, dilated with some descent of the vertex to spines -1 cm. There were no narrative notations by nurses or midwifes, but it appears that there were some problems with pain control as the epidural was topped up at 1545, 1700, 1845, and 1930 hours, in addition to morphine doses at 1415, 1436, 1504 and 1600 hours. The anaesthesiologist attended to regulate the epidural several times between 1545 and 1930 hours.

The midwife contacted the obstetrician by phone at 1540 hours regarding the progress in labour. She informed the obstetrician about the mother’s blood pressure which was 148/93. She documented that the obstetrician asked to be called if the blood pressure was >105 diastolic.

No further vaginal exams are noted after 7-8 cm at 1600 hours. Contractions are not recorded after 1715 hours. Maternal vital signs are not recorded after 1830 hours. The second midwife documented the onset of pushing as the mother began to push at 2010 hours. The next notation is at 2115 hours when “plus, plus caput at introitis” was noted. At 2145 hours, the head to the eyes were delivered and at 2155 hours, the head was born and chin was out.

The midwives attempted to complete the delivery of the shoulders with Wood’s screw and Ruben’s maneuvers. They then attempted delivery of the posterior arm and delivery of anterior shoulder. The obstetrician was contacted at 2220 hours as the midwives had tried all manoeuvres for shoulder dystocia and sought consultant help for a vaginal extraction of the entrapped fetal shoulders.

The obstetrician asked the team to prepare the patient for the operating room, restart the epidural which had been closed by the midwife during the second stage, start a second IV and cross-match two units of blood as she was coming to the hospital. At 2230 hours, a second anaesthesiologist was passing by and aided with topping the epidural while the first anaesthesiologist came in. At 2235 hours, the midwives stopped attempting to deliver the baby. Another physician was called as an assistant and arrived at 2300 hours. The obstetrician arrived at 2305 hours and the anaesthesiologist at 2308. The doctors talked to the mother and agreed to go to the operating room where she could have general anaesthesia for further attempts at vaginal delivery or possible Caesarean section.

The patient was given a general anaesthesia at 2340 hours. The bladder was emptied and the baby’s head was noted to be protruding from the vagina with the anterior shoulder impacted behind the symphysis pubis. The McRobert’s manoeuvre was employed and a nurse was asked to attempt to dislodge the shoulder from above while the doctor tried from below. This attempt was not successful, so the obstetrician tried the Rubin and Wood’s screw maneuvers which helped move the angle by about 30 degrees. The posterior arm was then delivered. After this, the anterior shoulder remained impacted. Further rotational maneuvers allowed delivery of the other arm and the baby was completely delivered after approximately two hours, at 2345 hours. The stillborn male baby weighed 5056 g.

There was manual removal of placenta and a heart shaped uterus was noted. Perineal repairs were completed. The mother was given IV oxytocin and antibiotics. IPP blood loss was normal at 500cc. The patient was discharged from the hospital on March 26.

Post Mortem Findings

The fetus was large for gestation. Fetal tissues and organs showed variable, but advanced degrees of autolysis. There were no abnormalities in the fetus itself to explain the unexpected intra-uterine fetal demise (IUFD). Based on the degree and extent of autolytic change in fetus, both grossly and microscopically, the intrauterine fetal demise is estimated to have occurred within 48 to 96 hours prior to delivery, but not longer than this time frame. Under placental pathology it is noted: “very slight discordant villous maturation, mostly in villi in maternal floor, compatible with maternal diabetes.” Also noted was a velamentous insertion of the umbilical cord. There was no evidence of chorioamnionitis, villitis, viral infections or specific infections.

Cause of death: Stillborn associated with presumed maternal gestational diabetes.

Discussion

The mother declined a 50 gram glucose challenge at 26 weeks and 2 days. At 33 plus weeks, her fundal heights increased substantially and she was offered an ultrasound. An ultrasound was done at 35 weeks and one day and showed growth at the 75th percentile and mild polyhydramnios. It is also noted that the baby was in complete breech presentation. Subsequent ultrasounds at 37 and 38 weeks document the development of macrosomia to above the 95th percentile at 38 weeks. The woman does not appear to have been offered glucose screening again, when the large for gestational age (LGA) fetus was identified.

Although stillbirth is a risk of gestational diabetes, there is no way to confirm that this was indeed the cause of this baby’s demise. In fact, there is no firm evidence that the woman actually had gestational diabetes. No investigations were done to rule out other pregnancy complications or to confirm elevated blood sugars in this pregnancy. If glucose screening had been performed upon identifying the LGA fetus at 37 to 38 weeks gestation, management of the sugars would likely have had little effect on the birth weight of this baby. Depending on how well controlled her sugars were, this woman may have been offered induction of labour between 38 weeks and 40 weeks for her diabetes. The fetal demise occurred at about 39 weeks, so it is unclear whether the outcome would have been different. Also, if her sugars were abnormal, close fetal surveillance would have been recommended. She did however, have what amounted to twice weekly ultrasounds and BPP (but no NSTs) between 36 and 38 weeks. Unfortunately, the baby was not assessed after the last ECV for 7 days and during this time, the demise occurred. Even with close monitoring in the last week, the outcome could have been the same.

There was some concern raised regarding the LGA and ECV relevance to the stillbirth. It is the LGA fetus in the diabetic woman that was the risk that indicated the possible cause of the stillbirth. The fact that the baby was so large was apparent for about 7 days prior to the stillbirth. During this time, in addition to investigations for gestational diabetes mellitus (GDM), serious discussions should have occurred between the mother and her midwife as well as the consulting obstetricians regarding possible difficulties with the birth (e.g. vertex or breech). The obstetrician who saw the mother at the hospital and discussed the possibility of vaginal breech delivery if the baby reverted to breech, was clearly unaware of the weight over the 95th percentile. The obstetrician who consulted after the fetal demise was diagnosed also appeared to be unaware of the size of the baby until called to attend for the shoulder dystocia. The obstetrician’s notes indicated that the ultrasound reports were “unavailable” when she saw the woman and placed the Cervidil©. She later discussed the woman’s knowledge of the baby’s size with the mother and was informed that the woman and the midwife felt the ultrasound was inaccurate. All care providers, whether referring or seeing a pregnant woman in consultation, should ensure that all the investigations are available when the woman is assessed. However, even if all had been alerted to the size of this baby, without any other issues, it is unlikely that the baby would have been delivered by induction or Caesarean section before 39 weeks and the fetal demise would likely still have occurred.

The mother worked with her midwives and consultant midwives and physicians to turn her fetus from breech to cephalic at term. The ECVs were attempted by two different consultant midwives three times, and a physician once between 36 weeks 2 days and 38 weeks 2 days. The fourth and successful ECV attempt was performed after ultrasound had identified clear evidence of LGA above the 95th percentile with an estimated fetal weight of 4480 g at 38 weeks and one day. There is no available research documenting the added dangers of ECV in the LGA infant, however there are risks with any procedure and at a certain point, the risk may outweigh the benefits. These issues should have been discussed in detail with the mother before the procedure, however it may not have changed her determination to attempt a vaginal birth of her baby.

Evidence on the number of ECV attempts that would be considered reasonable does not appear to be in the literature, however standard practice indicates that two attempts should be the limit. The more procedures performed, the higher the risk of complications from the procedure. ECV in primips are difficult and have a high rate of no success. Failure of this procedure could have been predicted based on the woman’s primiparous status, the fetal size and the breech having been complete, then frank. It could not be determined from this review if the repeated ECV attempts, then success, were contributory to this fetal demise.

The three ECV attempts by the midwives were performed in the clinic setting. Research suggests that there is a possibility of bradycardia following ECV attempts and successes and recommends that NST monitoring follow the procedure. Should the NST reveal fetal compromise, the hospital setting is equipped to proceed with intrauterine resuscitation. If the problem does not resolve, Caesarean section may be needed urgently. ECV is therefore not recommended in the clinic setting.

In this case, the monitoring of the fetus was inadequate following all four attempts to turn the breech fetus to vertex. The three ECV attempts by the midwives were not followed by NSTs or ultrasound. In two of the attempts, NST and ultrasound were not documented as being offered. In one trial, they were recommended and the woman stated that she would follow up with the primary midwife. After the ECV in hospital by the obstetrician, the woman had an ultrasound, but clearly declined an NST. It is not possible to determine the role the ECVs may have had in the demise.

Recommendations:

  1. Obstetrical care providers are reminded of the indication for glucose screening in each trimester of a pregnancy with risk factors.
  2. Obstetrical care providers are reminded that a large for gestational age fetus is a contraindication to a vaginal breech delivery.
  3. Obstetrical care providers are reminded of the need to be prepared for a shoulder dystocia at any birth, but in particular with a macrosomic stillborn with labour dystocia.
  4. Obstetrical care providers offering External Cephalic Version (ECV) should do so in a hospital setting with protocols in place for selection of appropriate candidates for the procedure and for fetal assessment before, during and after, the attempt.
  5. Obstetrical care providers are reminded of the need to provide all ultrasound and lab test results to each care provider involved, as well as to provide such information to the labour room.
  6. The hospital involved should develop a protocol for investigation of unexplained stillbirth.
  7. The nurses and midwives involved should review their charting practices with particular attention to the use of narrative notes to supplement the partogram.


Case: 2010-S-11

History

The mother of the deceased was a 29-year-old G2P1 with an estimated date of delivery of September 6, 2010. Antenatal care was provided by a midwifery clinic. A routine prenatal laboratory investigations were normal. Her blood type was B positive and antibody screen was negative. She declined genetic screening testing. Routine second trimester ultrasound was normal, except for the finding of a marginal placenta previa. The plan was to recheck the placental location by repeat ultrasound at 32 weeks. Second trimester screening for gestational diabetes was negative. Her past obstetrical history included one previous term pregnancy delivered vaginally for an 8 lb male infant in 2008.

Her past medical history was significant for scoliosis. She was a non-smoker.

Her routine antenatal visits were uneventful until July 13 at 32 weeks 1 day, when she reported not feeling fetal movement for two days. The fetal heart could not be auscultated and an ultrasound confirmed fetal demise. The previously reported marginal placenta previa had resolved. There was soft tissue swelling “suggestive of evolving hydrops.”

Obstetrical consultation was obtained on July 13. The decision was made to proceed to induction of labour. She was discharged home with a prescription for misoprostol two tablets (200mcg) and instructions to insert the medication into the vagina in the morning and return when uncomfortable with contractions.

The mother was admitted to the local general hospital at 1115 hours on July 14. The cervix was 2 cm dilated, 80% effaced with the vertex at spines -2. She was having mild cramping. She was given nalbuphine 20mg IM for pain at 1452 hours. An epidural was placed at 1514 hours. Following epidural placement, she had difficulty moving her legs. Membranes ruptured spontaneously for blood stained fluid at 1535 hours (artificial rupture of membranes charted at midnight on July 15). Oxytocin augmentation was started at 1550 hours. After a long induction and labour process that was aggravated by problems with the epidural and poor pain control, she went on to a spontaneous vaginal delivery of a male infant weighing 5 lb 11 oz at 0016 hours. There was a tight nuchal cord.

The mother subsequently required a dilation and curettage for postpartum hemorrhage due to retained products of conception.

Post Mortem Findings

No autopsy was conducted.

The placental pathology report showed edema of the cord with thrombi in the vessels. There was no evidence of chorioamnionitis. There was no evidence of placental abruption.

Discussion

This infant was stillborn with a tight nuchal cord. TORCH screening ordered July 13 was negative. Result of a Kleihauer ordered the same day was not found in the medical records provided. It cannot be determined from this review if the ultrasound suggestion of developing hydrops and the large for dates status of the baby were included in the decision not to do an autopsy.

 

25% of all babies have nuchal cords. Short term morbidity may occur as a result of cord occlusion from a tight cord. Usually these babies are easily resuscitated. 1/2000 babies may die as a result of a tight nuchal cord. There appears to be some correlation between tight nuchal cords and decreased fetal movements proceeding intrauterine death. All pregnant women should be instructed on the importance of reporting decrease of perceived fetal movements. Any reports of decreased movement (e.g. less than 6-10 in two hours) should be followed up.

There is no documentation regarding any discussion about fetal movement awareness in the mother’s chart. The mother reported that there was reduced movement over the days prior to cessation. It is uncertain as to whether earlier intervention would have made a difference.

 

Recommendations

 

  1. Obstetrical health care providers are reminded of the importance of informing women to be aware of fetal movements.


APPENDIX A - Summary of Recommendations


Maternal Deaths


Case

Cause of Death

Recommendations

M-1

hanging

  1. Obstetrical care providers are reminded that psychiatric disease can complicate pregnancy and can be a cause of maternal mortality.
  2. Obstetrical care providers are reminded that women of certain cultural backgrounds can be at increased risk of social isolation. Screening should assess both the mental and physical well-being of the patient, and should include questions regarding family stressors. Referral to support services should be considered when such issues are identified.

M-2

bilateral pulmonary embolism

  1. Obstetrical care providers are reminded that thromboprophylaxis in pregnant patients, particularly when there are increased risks (e.g. obesity, decreased activity and Caesarean delivery), should be considered. There is not however, adequate evidence from well designed trials to confirm the best management.

M-3

multi-system failure due to disseminated intravascular coagulation due to postpartum hemorrhage complicating vaginal delivery by forceps

  1. This hospital should review their postpartum hemorrhage (PPH) management protocol.
  2. Coroners are reminded that post mortem examinations should be considered in all cases of maternal death.

M-4

complications of massive peri-partum blood loss with multi-organ system failure

  1. Obstetrical care providers are reminded of the need to aggressively treat coagulopathies with appropriate blood components, particularly in the post-operative patient.
  2. The hospital should review the management of post partum hemorrhage in this case and should develop a protocol for the management of postpartum hemorrhage.

M-5

Primary Pulmonary Hypertension

No recommendations.

M-6

anaphylactoid reaction caused by an amniotic fluid embolism

No recommendations.

M-7

pulmonary thromboembolism due to pelvic deep vein thrombosis.

  1. The Society of Obstetricians and Gynaecologists of Canada should review and update its guidelines on thromboprophylaxis in pregnancy.

M-8

septic shock from a Group A Streptococcal infection

No recommendations.

M-9

Multiple organ failure complicating intrapartum haemorrhage at elective repeat Caesarean due to retained products of conception (placenta increta)

  1. The Chief of Staff for Hospital A should review the risk factors for postpartum hemorrhage (PPH) and the management of pregnancies with placenta previa with the obstetrical care providers in this case as per the SOGC Clinical Practice guideline: Diagnosis and Management of Placenta Previa. J Obstet Gynaecol Can 2007;29(3):261–266.
  2. The Chief of Staff for Hospital A should review the management of PPH with the obstetrical care providers in this case. This may include review of ALARM course material, the MORE obstetrical program and review of the following reference article:

Leduc, L. Active Management of the Third Stage of Labour: Prevention and Treatment of Postpartum Hemorrhage. J Obstet Gynaecol Can 2009;31(10):980–993.

  1. The obstetrical care staff of Hospital A should prepare a protocol for PPH and massive transfusion and ensure that all are educated on how and when to institute the protocol.

The following reference materials may be of assistance in developing this protocol:

Bormanis J. Development of a massive transfusion protocol. Transfus Apher Sci. 2008 Feb;38(1):57-63. Epub 2008 Mar 4.

Burtelow, M. How we treat: management of life-threatening primary postpartum hemorrhage with a standardized massive transfusion protocol TRANSFUSION Volume 47, September 2007.

  1. The Chief of Staff for Hospital A should review the guidelines for the selection of obstetrical cases to be delivered at this hospital.
  2. Obstetrical care providers should be reminded to utilize the assistance of CRITICALL early for facilitating expert advice in dealing with obstetrical emergencies.
  3. Obstetrical care providers and delivery centres should seriously consider establishing a mechanism to ensure that all ultrasound reports done in pregnancy be available at the Birthing Centre at the time the mother arrives.

M-10

amniotic fluid embolus

  1. All hospitals should consider developing protocol for managing cardiac arrest in pregnancy.

M-11

multi-organ failure due to,

hemorrhagic shock due to,

placental abruption and postpartum hemorrhage complicating Caesarean section and hysterectomy in a term pregnancy.

No recommendations.



Neonatal Deaths


Case

Cause of Death

Recommendations

N-1

complications of prematurity

  1. Obstetrical care providers are reminded that the external fetal monitor tocodynamometer does not accurately indicate the strength of uterine contractions and cannot be relied upon in lieu of palpation by an experienced obstetrical care provider.

N-2

Multisystem failure and hypoxic ischemic encephalopathy due to perinatal asphyxia and abruption and fetal blood loss

  1. Obstetrical care providers are reminded that antepartum and intrapartum bleeding should heighten suspicion of the possibility of placental abruption.
  2. Obstetrical care providers are reminded that antepartum/intrapartum haemorrhage is an indication for continuous electronic fetal monitoring. (MOREOB Fetal Wellbeing and SOGC Clinical Practice Guideline – Fetal Health Surveillance in Labour, September 2007)
  3. Obstetrical care providers are reminded of the importance of complete and timely documentation.
  4. Obstetrical care providers are reminded of the importance of ensuring that the correct date and time is printing on the electronic foetal monitor (EFM) paper each time that a monitor is applied.   The print out should be verified and corrected as necessary.
  5. Obstetrical care providers are reminded of the importance of having transport personnel who have expertise, technical skills, and clinical judgement to provide proficient care for any emergency that may arise during transport.  (SOGC policy statement, October 2005)

N-3

severe hypoxic-ischemic encephalopathy

  1. Obstetrical care providers are reminded of the criteria for an abnormal fetal heart rate tracing and the action required as outlined in JOGC September 2007.
  2. Obstetrical care providers are reminded of the importance of ascertaining and documenting in the delivery record, the fetal position prior to the application of the vacuum extractor or forceps.
  3. Obstetrical care providers are reminded of the SOGC ALARM guidelines for operative vaginal delivery and for limiting the number of pulls with the vacuum extractor to three pulls over three contractions with no progress.
  4. The hospital should conduct a review of the management of this case.

N-4

pericardial tamponade from UVC perforating roof of LA

  1. Neonatal health care providers are reminded that pericardial tamponade can be the cause of acute circulatory failure in a neonate with a central venous line and should be considered when standard resuscitative measures are unsuccessful in restoring output when ventilation is adequate.  Emergency pericardiocentesis can be life-saving.
  2. Centres providing neonatal intensive care services should ensure that anyone authorized to insert central venous catheters in neonates is certified to do so and has completed the necessary training.
  3. For insertion of umbilical catheters in neonates, use of a pre-insertion checklist that includes calculation of insertion distance should be considered to ensure proper technique and good positioning.
  4. Verification of catheter tip position by X-ray should be routinely performed and double-checked whenever possible.  Staff accepting transfer of care for an infant who has had a line inserted in the previous shift should routinely review the relevant X-rays to verify acceptable positioning.
  5. Hospitals providing intensive care services should ensure that there is a process in place to communicate critical findings detected by a radiologist (including sub-optimally place central lines) to the relevant members of the clinical team.

N-5

Hypoxic ischemic encephalopathy

  1. This hospital should review and revise its policy for oxytocin induction of labour.
  2. The nurse and obstetrician should review the interpretation of electronic fetal monitor tracings including definitions of excessive uterine activity.
  3. The hospital should review its policy for trial of labour after Caesarean.

N-6

acute hypoxic-ischemic brain injury

  1. Obstetrical care providers are reminded of the criteria for an abnormal fetal heart rate tracing and the action required as defined by SOGC Intrapartum Fetal Surveillance Guidelines published in September 2007.
  2. Obstetrical care providers at the hospital should  review this case with attention to the application of the SOGC Intrapartum Fetal Surveillance Guidelines.

N-7

Perinatal asphyxia secondary to placental abruption

  1. Obstetrical care providers should request placental pathology in cases where there are signs and symptoms of abnormal vaginal bleeding and/or evidence of abnormalities of fetal wellbeing.

N-8

intrauterine asphyxia

  1. Training of EMS crews in knowledge of obstetrical emergencies, and in particular an acute abdomen, should be reviewed.
  2. Obstetrical caregivers are reminded of the risk of spontaneous uterine rupture through a previous surgical scar in the uterine fundus.  Close ultrasound surveillance and timely delivery should be considered, particularly with previously documented uterine wall defects.

N-9

severe hypoxic-ischemic encephalopathy

  1. Obstetrical care providers are reminded to have a high index of suspicion of uterine rupture in a patient with a previous Caesarean section who develops fetal heart rate changes.
  2. Obstetrical care providers are reminded of the need to proceed to immediate delivery in the presence of an abnormal fetal heart rate tracing.
  3. Obstetrical care providers are reminded of the guidelines for the management of the second stage of labour.

N-10

Perinatal death

  1. The nurses, midwives and doctors involved with this patient should review EFM interpretation.
  2. Obstetrical care providers are reminded of their responsibility to question the care provided to patients they are attending. If they feel the care is below standard they should consult with other midwives, nurses, doctors and administration until satisfied.
  3. Obstetrical care providers are reminded of the risk of cord prolapse in early labour with a macrosomic unengaged baby and cervical dilation.
  4. Obstetrical care providers are reminded of the need for a thorough work up for women with polyhydramnios, macrosomia, or both.
  5. Obstetrical care providers are reminded of the need for repeated glucose testing in each trimester in pregnancies with risk factors for gestational diabetes.
  6. Obstetrical care providers are reminded that in all complicated deliveries, including neonatal death and stillbirth situations, the placenta should be sent to pathology for examination and reporting as per the coroner’s guidelines.
  7. Obstetrical care providers are reminded that it is recommended that all ultrasound reports should be sent to the place where the birth is planned. This should be done by either the obstetrical care provider or directly from the ultrasound department.

N-11

Severe perinatal asphyxia

The initial hospital involved in this case has undertaken a Quality of Care Information Protection Act (QCIPA) review. The following recommendations, together with the status of implementation of the recommendations, have been provided by the hospital:

  1. The obstetricians involved should have their documentation and communication skills reviewed and upgraded.

Status: Done. Courses completed. Documentation on personnel file. CPSO notified.

  1. There must be a more robust quality review process for the Women & Child Program.

Status: Done. An anonymous form drafted and available to all staff. This has lead to numerous case reviews, changes to process/practice, etc.

  1. There needs to be a more formal process for calling in a second obstetrician.

Status: Call schedule now in place, criteria for call established.

  1. There needs to be a procedure for calling an “Obstetrics Alert.”

Status: Done. Anyone on the team can initiate these calls in critical situations.

  1. There needs to be better communication among members of the obstetrics team.

Status: Ongoing. Both our new Department Chief, and the new manager for L&D, as well as the Operations Director for the entire program, are working with their staff to ensure there are open lines of communication both among and between provider groups. A memo has been sent to all relevant stakeholders that there must be a direct provider to provider communication in complex/critical situations.

  1. Our ultrasound equipment needs upgrading.

Status: On order. In the meantime, we have added two further MFM specialists (one returning from sick leave) to ensure that we provide optimal antenatal care. We are in the process of expanding our current facility to a new area of the hospital as well.

  1. Biophysical profiles should be performed within 24 hours where clinically indicated.

Status: Standard of practice that all members of the Department of Obstetrics expected to meet and they are aware.

  1. A cooling blanket should be available to be used as needed post-neonatal resuscitation.

Status: Discussed with the Hospital for Sick Children and their protocol calls for passive cooling only, with active cooling in a tertiary centre only.

The MPDRC has no new recommendations in addition to those identified through the hospital’s review.

N-12

Intrapartum Asphyxia

  1. The hospital involved should review their intermittent auscultation (IA) protocols and indications for EFM, as well as the proper use of forms used for charting these observations.
  2. Obstetrical care providers are reminded of the importance of accurate and complete documentation.

N-13

perinatal asphyxia due to anoxic-ischemic brain damage and hemorrhagic necrosis of the adrenals.

  1. Obstetrical care providers should recognize that an abnormal fetal heart tracing that worsens with pushing in the second stage of labour, without imminent delivery, warrants confirmation of normal scalp gases or urgent delivery. Caregivers should be mindful of this trap, and not assume that spontaneous delivery is close.

N-14

Multi-system failure

  1. Obstetrical care providers are reminded that the presence of an abnormal fetal heart tracing requires confirmation of normal gases or urgent delivery.
  2. Obstetrical care providers are reminded of the limitations of the vacuum extractor, particularly for mid pelvic delivery and of the uncommon, though serious risk, of brain hemorrhage with its use. Adherence to guidelines for vacuum use is critical.

N-15

Severe hypoxic ischemic encephalopathy due to perinatal asphyxia

  1. The hospital should review its practices for the retention and storage of fetal monitoring strips.

N-16

Deferred to 2011 for review

 

N-17

Hypoxic Ischemic Complications of Resuscitated Perinatal Asphyxia

  1. Obstetrical care providers are reminded of the Fetal Health Surveillance Guidelines of the SOCG (JOGC September 2007).
  2. Obstetrical care providers are reminded to consider the entire clinical picture when assessing fetal wellbeing.

N-18

undetermined

  1. The obstetrical care providers involved should upgrade their skills in labour management and fetal monitoring.
  2. Nurses are reminded of their responsibility to question the care provided to patients they are attending. If they feel the care is below standard, they should consult with other nurses, doctors and administration until satisfied.
  3. All hospitals that provide obstetrical care should have protocols in place to monitor infants whose delivery involve vacuum extraction for signs of Subgaleal Hemorrhage.
  4. Neonatal health care providers should review Neonatal Resuscitation (NRP) guidelines.
  5. Obstetrical care providers are reminded of the need to collect cord blood gases at all births.
  6. A Regional Supervising Coroners Review should be conducted on this case.

N-19

E-coli menengitis

No recommendations.

N-20

Hypoxic ischemic encephalopathy in a child with Arnold Chiari type 2 malformation

  1. Obstetrical care providers are reminded of the importance of being familiar with and implementing the SOGC Fetal Health Surveillance Guidelines. (JOGC, September 2007)


Stillbirths


Case

Cause of Death

Recommendations

S-1

Amniotic Infection Syndrome with Necrotizing Chorioamnionitis

No recommendations.

S-2

Undetermined

  1. Obstetrical care providers are reminded that it has been recommended that a protocol should be used to investigate the possible cause of fetal death. (SOGC Clinical Practice Guideline No. 178 June 2006)
  2. Midwives are reminded that medical consultation is indicated when there is history of an illness that is associated with adverse perinatal outcome.

S-3

perinatal asphyxia with no definitive cause identified

  1. Health care providers are reminded of the need to clearly communicate clinical concerns when requesting consultation or assistance in the course of a developing emergency in labour.
  2. Health care providers are reminded of the importance of accurate documentation of the times of events in the course of clinical care in an emergency.

S-4

Intrauterine Asphyxis

  1. Obstetrical care providers are reminded of the importance of increased fetal surveillance in the presence of placental insufficiency. (Fetal Health Surveillance Antepartum and Intrapartum Consensus Guidelines, SOCC Clinical Practice Guideline, No.197, Sept 2007).
  2. Obstetrical care providers are reminded of the increased risks of perinatal morbidity and mortality in the presence of absent and reversed end diastolic flow in the umbilical artery. (Fetal Health Surveillance Antepartum and Intrapartum Consensus Guidelines, SOCC Clinical Practice Guideline, No.197, Sept 2007).

S-5

intrauterine fetal demise from strangulation by the umbilical cord

  1. Obstetrical care providers are reminded of the importance of careful education and assessment of women presenting with signs of possible preterm labour, so that measures such as fetal fibronectin testing, tocolytics and corticosteroids can be offered.
  2. Midwives are reminded that the College of Midwives Indications for Mandatory Discussion, Consultation and Transfer of Care (IMCTC) document requires a level 2 consultation for a) bleeding in the second trimester and b) signs of preterm labour.

S-6

Probable Umbilical Vein Thrombosis

No recommendations

S-7

intrauterine asphyxia complicated by congenital pneumonia

  1. Obstetrical care providers are reminded of the importance of confirming fetal well-being prior to discharge.
  2. Obstetrical care providers are reminded of the importance of asking mothers about fetal movements.
  3. A Regional Coroner’s Review should be conducted on this case.

S-8

stillbirth

No recommendations.

S-9

acute chorioamnionitis

  1. The Society of Obstetricians and Gynaecologists of Canada (SOGC) should review the current guidelines on Gestational Diabetes Mellitus in pregnancy.

S-10

Stillborn associated with presumed Maternal Gestational Diabetes

  1. Obstetrical care providers are reminded of the indication for glucose screening in each trimester of a pregnancy with risk factors.
  2. Obstetrical care providers are reminded that a large for gestational age fetus is a contraindication to a vaginal breech delivery.
  3. Obstetrical care providers are reminded of the need to be prepared for a shoulder dystocia at any birth, but in particular with a macrosomic stillborn with labour dystocia.
  4. Obstetrical care providers offering External Cephalic Version (ECV) should do so in a hospital setting with protocols in place for selection of appropriate candidates for the procedure and for fetal assessment before, during and after, the attempt.
  5. Obstetrical care providers are reminded of the need to provide all ultrasound and lab test results to each care provider involved, as well as to provide such information to the labour room.
  6. The hospital involved should develop a protocol for investigation of unexplained stillbirth.
  7. The nurses and midwives involved should review their charting practices with particular attention to the use of narrative notes to supplement the partogram.

S-11

stillbirth

  1. Obstetrical health care providers are reminded of the importance of informing women to be aware of fetal movements.


APPENDIX B – Glossary of Terms


AIH

autoimmune hepatitis

ARDS

acute respiratory distress syndrome

ARM

artificial rupture of membranes

BMI

body mass index

BPP

biophysical profile

CBC

complete blood count

CMV

cytomegalovirus

CNS

central nervous system

CPAP

continuous positive airway pressure

CPSO

College of Physicians and Surgeons of Ontario

CSF

cerebrolspinal fluid

D and C

dilation and curettage

DIC

disseminated intravascular coagulation

DVT

deep vein thrombosis

EBM

expressed breast milk

EDD

estimated date of delivery

EFM

electronic fetal monitoring

EMS

emergency medical services

FFP

fresh frozen plasma

GBS

Group B streptococcus

GCT

glucose challenge test

GDM

gestational diabetes management

HIE

hypoxic-ischemic encephalopathy

ICP

intraheptic cholestasis of pregnancy

ICU

intensive care unit

IPS

integrated pregnancy screening

IVF

in virtro fertilization

LMA

laryngeal mask airway

LMWH

low molecular weight heparin

LP

lumbar puncture

MFM

maternal fetal medicine

MPDRC

Maternal and Perinatal Death Review Committee

MSS

maternal serum screening

NICU

neonatal intensive care unit

NST

non-stress test

OGTT

oral glucose tolerance test

PCOS

polycystic ovary syndrome

PICC

peripheral central catheter

PIH

prenancy induced hypertension

PPV

positive pressure ventilation

PTT

partial thromboplastin time

QCIPA

Quality of Care Information Protection Act

RCT

randomized control trials

ROA

right occipital anterior

SFH

symphysis fundal height

SGH

subgaleal hemorrhage

SIADH

Syndrome of Inappropriate Antidiuretic Hormone

SIDS

sudden infant death syndrome

SOGC

Society of Obstetricians and Gynaecologists of Canada

SRM

spontaneous rupture of membranes

TPN

total parenteral nutrition

UAC

umbilical arterial catheter

URTI

urinary tract infection

UVC

umbilical vein catheter

VBAC

vaginal birth after Caesarean

VTE

venous thromembolism

WBC

white blood count