An iliac artery rupture results in a patient's death. Was it caused by the cesarean delivery, the patient’s disease process, or the care she received following her delivery?
Mr. Kaplan is a partner at Aaronson, Rappaport, Feinstein & Deutsch, LLP, specializing in medical malpractice defense and healthcare litigation. He welcomes feedback on this column via email to email@example.com.
On December 18, 2009, at 7:19 am, a 28-year-old woman at 37 weeks’ gestation presented to a hospital by ambulance with ruptured membranes and right-upper-quadrant pain. The patient/plaintiff had received her prenatal care at another hospital and had a medical history of neurofibromatosis, a genetic disorder characterized by nerve tissue tumors that can grow rapidly during pregnancy and can cause complications such as hypertension.
On initial exam, no fetal heart rate (FHR) was detected. At 7:32 am, FHR monitoring was begun and revealed a FHR of 50 bpm. Co-defendant ob/gyn Dr. A was alerted and a STAT cesarean delivery was called at 7:44 am. The operative record reveals that the patient was in the OR at 7:45 am, anesthesia started at 7:47 am, skin incision was made at 7:50 am, and delivery was accomplished at 7:52 am. The infant had Apgars of 1 and 2. Cord blood PCO2 was 100 with a base excess of -32.
In his operative report for the cesarean delivery, Dr. A noted that the cul-de-sac was cleared of all clots and debris. After he confirmed hemostasis, the peritoneal membrane was closed. On presentation to the delivery room, the plaintiff’s blood pressure was low (82/59), with a heart rate of 127. At 8:45 am, when the defendant resident anesthesiologist Dr. B discharged the plaintiff to the recovery room and signed off to defendant attending anesthesiologist Dr. C, the patient’s blood pressure was documented at 100/50, with a heart rate of 130.
During the next 3 ½ hours, the plaintiff was monitored in the recovery room. Her blood pressure and pulse were labile, ranging from a low of 70/37 to a high of 146/103. Her heart rate was consistently tachycardic, ranging between 133 and 162. She was placed in the Trendelenburg position at 8:51 am. Approximately 3 L of IV fluid were administered. Bolusing began at 9:21 and fluid was given again at 10:44. However, the patient remained tachycardic and the exact amount of the boluses is not recorded.
At approximately 10:30 am the patient complained of cramping in her left leg; she had a history of left leg fracture as a child and had undergone reparative surgery. She was able to move all her extremities, pedal pulses were present, and capillary refill was felt to be adequate. Venodyne boots remained in place.
The chief ob/gyn resident, Dr. D, evaluated the patient and ordered Toradol for her discomfort. An hour later the plaintiff was noted to be drowsy, lethargic, and to have minimal verbal response. Internal hemorrhage was considered, and an abdominal ultrasound confirmed what looked like a pelvic collection. The medical emergency team was called and pressors, fluids, and 2 units of packed red blood cells were administered. A femoral line was placed and the patient was intubated and taken to the OR at 12:25 pm.
Dr. A performed an exploratory laparotomy because he suspected uterine artery bleeding. A supracervical hysterectomy was performed and no bleeding from the uterine vessels was found. Dr. A called for an intraoperative vascular consult, which was answered by nonparty vascular surgeon Dr. E, who noted a large hematoma in the retroperitoneum. Upon opening the retroperitoneum, he discovered a rupture in the iliac artery, which he described as friable and attempted to repair.
Despite administration of multiple blood products, fluids, and pressors, the plaintiff coded 5 times and expired at 3:58 pm. On autopsy, the cause of death was noted as retroperitoneal hemorrhage due to spontaneous rupture of the left iliac artery as a consequence of neurofibromatosis and pregnancy.
The plaintiff’s attorneys asserted that injury to the iliac artery occurred as a result of an improperly performed
cesarean delivery. They also asserted that there was a delay in appreciating and responding to the iliac artery injury, resulting in retroperitoneal hemorrhage, rupture of the common iliac artery and veins, cardiac arrest, and death.
Based on the records and the autopsy report, our obstetric expert felt that the iliac artery rupture was not caused by the cesarean delivery but rather, that it was a result of the patient’s disease process. He was critical, however, of the care in the recovery room. He felt that the patient was unstable throughout her time in the recovery room because she was tachycardic throughout and her blood pressures were remarkably low. He felt she was clearly bleeding while in the recovery room and there was a failure to react to it in a timely manner.
Our obstetric anesthesia expert was critical of the care in the recovery room as well. The fact that the plaintiff’s heart rate was elevated at all times meant that one had to consider that she might be bleeding. The tachycardia meant bleeding until proven otherwise. Despite the lack of documentation that bleeding was considered, the patient was placed in the Trendelenburg position for hypotension, and was given ongoing IV fluids. Although she was tachycardic, she had strong pulses and capillary refill and, as such, it appears that this was why she was thought not to be bleeding. Unfortunately, the IV boluses that were given did not serve to reduce the tachycardia and there was an obvious problem of lack of documentation by the recovery room staff.
Our vascular expert could not defend the care by our defendants and felt it was a departure from the standard of care not to obtain hemoglobin and hematocrit levels at least 1 hour after the prolonged tachycardia and hypotension in this postoperative patient. This is especially problematic in light of the fact that the recovery room staff were giving the patient fluid boluses and put her in Trendelenburg. She also had no urine output. This expert was also very critical of the nurses in the recovery room and felt that they did not do enough to bring the patient’s condition to the doctors’ attention. It was her opinion that earlier intervention could have changed the outcome.
The intraoperative vascular consultant further testified that the laceration he found was “ragged” and in his opinion was not a result of iatrogenic injury caused by the codefendant ob/gyn. The doctor also testified that the cause of the laceration was the patient’s underlying neurofibromatosis.
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The plaintiff’s demand for settlement was $3 million. Prior to depositions by the chief resident and the hospital’s recovery room staff, the case settled as to the defendant hospital only in the amount of $2.2 million. The case was discontinued against codefendant ob/gyn Dr. A.
The plaintiff’s initial focus in the case was the defendant ob/gyn, in the belief that he caused the injury to the artery and failed to follow up on or appreciate the patient’s downward spiral thereafter. It became apparent through the discovery process-record review and analysis, expert evaluation, and testimony of the defendant ob/gyn and the nonparty vascular surgeon-that, in fact, the cause of the patient’s rupture was her underlying disease process and not the technical aspects of the surgery itself.
Once it was confirmed that the defendant ob/gyn was not assigned to follow the patient in recovery but instead had other labor and delivery responsibilities thereafter, the focus became the staff’s reaction to the patient’s complaints and concerning vital signs in the recovery room.
For many reasons we felt that settling the case, rather than involving the staff members responsible for the patient’s care in the recovery room, was the proper course of action.