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A cesarean triggered by a steep drop in FHR reveals a surprising diagnosis.
by Shadi Rezai, MD, Gina Cavallo, BS, Dilfuza Nuritdinova, MD, and Cassandra E Henderson, MD
Dr Rezai is a resident in the Department of Obstetrics and Gynecology at Lincoln Medical and Mental Health Center, Bronx, NY.
Ms Cavallo is a medical student in Grenada, West Indies.
Dr Nuritdinova is an attending at the Department of Obstetrics and Gynecology at Lincoln Medical and Mental Health Center, Bronx, NY.
Dr Henderson is director of maternal and fetal medicine and professor of Obstetrics and Gynecology at Lincoln Medical and Mental Health Center, Bronx, NY.
The authors wish to thank Ray Mercado, DO, and Ruchi Upadhyay, MD, for editorial assistance and Ms Judith Wilkinson for providing the referenced articles.
A 36-year-old African-American G4P3003 presented with a complaint of lower abdominal pressure at 41 weeks’ gestation and was admitted for post-dates induction of labor. On arrival at the labor and delivery floor, her cervix was 2 cm dilated and she was not in labor.
The patient had had an unremarkable prenatal course, with no laboratory abnormalities, hypertension, or proteinuria. Her obstetric history was likewise uncomplicated, with 3 spontaneous vaginal deliveries at term. Her medical, surgical, and family histories were non-contributory.
Induction of labor was initiated with 50 μg buccal misoprostol. Three hours later, spontaneous rupture of membranes was noted and the patient progressed to 3-cm cervical dilatation and was having active contractions. The second dose of misoprostol, therefore, was withheld. For the next 4 hours, the patient’s condition was unchanged. Oxytocin augmentation was started and Pitocin was increased to 9 cc/hr. Within 2 hours, the woman’s cervix was fully dilated and the baby was in vertex position at 0 to +1 station. At that time the patient was experiencing contractions every 3 minutes. She started pushing while fully dilated at +1 station.
Several minutes into the second stage, the fetal heart rate (FHR) tracing was a category 2, with an FHR drop from 140 to 80 bpm, moderate variability and accelerations. Oxytocin was held and intrauterine resuscitation was attempted for 10 minutes, with neither further decline nor recovery of the FHR. The patient remained completely hemodynamically stable and the FHR tracing did not change. After 17 minutes, an emergency cesarean section for fetal bradycardia was called.
Differential diagnoses included uterine abruption, placenta previa, and vasa previa.1
The patient was taken to the operating room, whereupon entering the peritoneal cavity after a Pfannenstiel incision, the right fetal elbow was observed to be protruding from the uterus into the abdomen from the left side of the uterine rupture. A viable 3380-g male infant was delivered successfully. Cord gases at birth were as follows: arterial: PH: 6.948/ PCO2 93.1/PO2 14.5/ BE -14.3; venous: PH: 6.969/ PCO2 89.2/PO2 18.9/BE -13.7.
The uterus was exteriorized and a 5-cm left-sided extension was noted on the lower aspect of the uterine incision. The uterine extension and incision were repaired with good hemostasis. The total estimated blood loss was 800 mL. The patient and baby tolerated the procedure well. Two days after surgery, both mother and baby were discharged in stable condition.
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Spontaneous uterine rupture.
Patients with uterine rupture typically present with maternal tachycardia, sudden fetal distress followed by vaginal bleeding, and abdominal pain.2-6 However, whenever a patient has risk factors for rupture, a physician should remain vigilant regarding the possibility of the condition. The classic description of a loss of intrauterine pressure or cessation of labor may or may not be observed in patient with uterine rupture.7 The diagnosis of uterine rupture is primarily a clinical one, confirmed with laparotomy.1 The signs and symptoms previously listed should mobilize a physician to perform emergency laparotomy with cesarean delivery with the goal of saving both mother and baby. The importance of fluid resuscitation and hemostasis cannot be overemphasized. The life-threatening seriousness of uterine rupture is due to the fact that the maternal circulatory system delivers approximately 500 mL of blood to the term uterus per minute.8 Hemostasis may need to be attempted by performing aortic compression, administering oxytocin, and ligating the hypogastric, uterine or ovarian arteries.9
The most common risk factor of uterine rupture is the presence of a uterine scar.10 Short interpregnancy interval after cesarean delivery and misoprostol has additive risks for uterine rupture.11 The level of medical care and the presence of a previous scar affect the incidence of uterine rupture. Therefore, it is a very rare condition in the developed world and even more so in women with unscarred uteri.7 Gardil et al demonstrated that there were no cases of uterine rupture among 21,998 primigravidas, and only 2 occurred among 39,529 multigravidas with no uterine scar 12. The incidence of spontaneous rupture in a previously intact uterus is approximately 1 in 16,000 deliveries.13
Uterine rupture is typically classified as either complete or incomplete.14 Complete rupture occurs when all layers of the uterine wall are separated and incomplete rupture is when the uterine muscle is separated but the visceral peritoneum is intact.14 Uterine rupture is further divided into two main categories: rupture in a scarred uterus and rupture in an unscarred uterus. It is a rare and unexpected obstetrical emergency especially in women with unscarred uteri.7
Rupture of an unscarred uterus is most frequently encountered in patients of advanced age (> 35 years) and parity (> 4) whose obstructed labors were neglected, especially in the terminal first and second stages.3 Grand multiparity has been associated with an increased risk of uterine rupture.7 Ripley reported a 20-fold higher risk of uterine rupture in women with at least 7 previous deliveries.7 Fitzpatrick et al reported on a subpopulation of women with labor complicated by uterine rupture who had a parity of 3 or more.1 Any patient with mechanical dystocia should be considered as a candidate for uterine rupture. Thus suspected disproportion, arrest of dilatation, or prolonged active labor despite adequate forces, as well as abnormal presentation, may be precursors.5,6 Induction and augmentation with oxytocin are associated with serious adverse events, including intrapartum uterine rupture.1,7 Absence of hemorrhage and lack of a history of uterine surgery may give a false sense of security.15
According to the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists, a non-reassuring FHR pattern with variable heart rate decelerations that may evolve into late decelerations, bradycardia, and death is a sign of rupture.5 The most common FHR abnormality observed in uterine rupture is prolonged bradycardia but other observations noted include late decelerations, prolonged decelerations, variable decelerations, and a general diagnosis of "abnormalities" in the FHR.16 The most commonly cited FHR abnormality is prolonged bradycardia, which is seen in 33.3% to 70.3% of all cases of uterine rupture. The next most common abnormalities are late decelerations, which are reported in 19.0% to 87.5% of cases, and variable decelerations, which are reported in 5.1% to 19.0% of cases.16
Uterine rupture is associated with a 61% rate of infant mortality.1 If the fetus is partly or totally extruded from the site of uterine rupture, abdominal palpation or vaginal examination may be helpful to identify the presenting part.5 With rupture and expulsion of the fetus into the peritoneal cavity, the chances of intact fetal survival are dismal, and reported mortality rates range from 50% to 75%.8 Fetal condition depends on the degree to which the placental implantation remains intact, although that can change within minutes.5 With rupture, the only chance of fetal survival is afforded by immediate delivery, most often by laparotomy.5 Perinatal consequences are admission to the neonatal intensive care unit, fetal hypoxia or anoxia, and death.17 Best outcomes were noted when surgical delivery was accomplished within 17 minutes from the onset of fetal distress on electronic FHR monitors.8
The maternal mortality rate associated with uterine rupture is 5%.1,8 Maternal death from rupture is uncommon in North America, but in other areas of the world, rates of maternal death associated with rupture are much higher, such as the 30% reported in India.5 Maternal consequences are hemorrhage, hypovolemic shock, bladder injury, need for hysterectomy, and death.17 Overall, uterine rupture accounts for approximately 5% of all maternal death each year.7 Unhealthy tissues (such as necrotic, infected, injured, detached, damaged tissues) that remain after uterine repair may predispose a patient to complications such as infection, disseminated intravascular coagulation (DIC), abscess formation, and hemorrhage.2
Uterine rupture in an unscarred uterus is a rare phenomenon with significant morbidity and mortality for both mother and fetus.3 Although the patient in this case had no other significant risk factors for rupture, administration of misoprostol and oxytocin, although used appropriately, may have contributed. Physicians need to be vigilant for the signs and symptoms of uterine rupture because treatment must be prompt and aggressive. With immediate treatment, the complications of uterine rupture can be minimized.
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