- Email: [email protected]
Fatal hypertrophic cardiomyopathy in the fetus of a woman with diabetes
2. Carella M, Gossain V. Hyperparathyroidism and pregnancy: Case report and review. J Gen Intern Med 1992;7: 448 –53. 3. Fabrin B, Eldon K. Pregnancy complicated by concurrent hyperparathyroidism and pancreatitis. Acta Obstet Gynecol Scand 1986;65:651–2. 4. Rajala B, Abbasi RA, Hutchinson HT, Taylor T. Acute
Fatal Hypertrophic Cardiomyopathy in the Fetus of a Woman With Diabetes Maya G. Sardesai, Aileen A. Gray, MA, MD, Michael M. J. McGrath, MD, FRCSC, and Sally E. Ford, MBBS, FRCPC Queen’s University Medical School, Department of Family Medicine, Queen’s University, Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Queen’s University, and Department of Pathology, Queen’s University and Kingston General Hospital, Kingston, Ontario, Canada
BACKGROUND: Hypertrophic cardiomyopathy is recognized in infants of diabetic mothers, and when it occurs it is generally benign and transient. We describe a case of fetal cardiac death caused by hypertrophic cardiomyopathy in an infant of a diabetic mother. CASE: Hydrops fetalis caused by hypertrophic cardiomyopathy resulted in the death of a macrosomic male fetus of a young woman who had well-controlled diabetes mellitus and was treated with insulin therapy during pregnancy. CONCLUSION: It is important to monitor fetal heart function in macrosomic infants of diabetic mothers. Hypertrophic cardiomyopathy might explain otherwise unexplained fetal deaths in women with diabetes. (Obstet Gynecol 2001;98:925–7. © 2001 by the American College of Obstetricians and Gynecologists.)
Hypertrophic cardiomyopathy, which consists of cardiac enlargement and disproportionate septal hypertrophy, occurs in 30% of infants of diabetic mothers and likely reflects fetal hyperinsulinemia.1,2 With appropriate therapy (eg, propranolol or other -blockers), hypertrophic cardiomyopathy usually resolves without complications within 6 months after birth.3 There are very few documented cases of stillbirths of Address reprint requests to: Sally E. Ford, MBBS, FRCPC, Department of Pathology, Richardson Laboratory, Room 201, Queen’s University, Kingston, Ontario K7L 3N6, Canada; E-mail: ford@cliff. path.queensu.ca.
pancreatitis and primary hyperparathyroidism in pregnancy: Treatment of hypercalcemia with magnesium sulfate. Obstet Gynecol 1987;70:460 –2.
Received November 1, 2000. Received in revised form January 8, 2001. Accepted April 12, 2001.
infants of diabetic mothers with hypertrophic cardiomyopathy, and all but one of those cases have been attributed to noncardiac or unknown causes, although Leslie et al4 described a stillbirth where the infant had an enlarged heart.5,6 A MEDLINE search limited to English language for the period 1966 to the week of December 4, 2000, with subject and keyword search terms “cardiomyopathy,” “hypertrophic,” and “diabetes” or “fetal death” found no cases of death from hypertrophic cardiomyopathy-related cardiac failure in fetuses of mothers with diabetes, and very few in infants.7,8
CASE A 27-year-old woman, gravida 3, para 1, aborta 1, at 37 weeks’ gestation, presented to labor and delivery with spontaneous rupture of membranes and uterine contractions. She had noticed decreased fetal movement during the preceding 2 days; however, a biophysical profile approximately 12 hours before presentation to labor and delivery yielded a score of 8/8. Her medical history was significant for obesity and smoking five to seven cigarettes per day. She denied alcohol and drug use. Family history was positive for type II diabetes on her maternal side. Obstetric history included a first pregnancy that spontaneously aborted at 12 weeks and a second pregnancy complicated by gestational diabetes and fetal macrosomia (5305 g). She required cesarean delivery for failure to progress in labor. No blood glucose levels had been measured between her second and third pregnancies. Early in her third pregnancy, diabetes was identified, with a fasting blood glucose level of 180 mg/dL at 5 weeks. Her glycosylated hemoglobin was 6% at 9 weeks, consistent with optimal glycemic control. The diabetes was initially controlled by diet, but she was started on insulin at 26 weeks for escalating blood glucose measurements. No further glycosylated hemoglobin samples were drawn until the day of her delivery, at which point it measured 6.6%. She had reported good control based on frequent home monitoring. The patient had a normal anatomic scan at 18 weeks’
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01455-7
925
asymmetric hypertrophy (septum and inferior left-ventricular wall being 1.3 cm and 0.7 cm, respectively) and biventricular dilatation. Microscopically the myocardium showed extensive myofibrillar disarray in both the septum and the free wall. Microscopic mural thrombi were observed, and patchy early myocardial necrosis in association with occlusions of small intramural arteries was noted. These occlusions were probably emboli from the mural thrombi. Consistent with cardiac death, there was pulmonary congestion, massive centrilobular congestion, and necrosis of the liver, as well as hydrops fetalis, with peripheral edema, pleural effusions, and ascites.
COMMENT Figure 1. Cross section of the infant’s heart at autopsy showing asymmetric hypertrophy. RV ⫽ right ventricle; LV ⫽ left ventricle. Sardesai. Fatal Hypertrophic Cardiomyopathy. Obstet Gynecol 2001.
gestation but did not have fetal echocardiography in the second trimester because she was treated as having gestational diabetes. An ultrasound at 36 weeks identified fetal macrosomia with an estimated fetal weight above the 97.5th percentile. She had been scheduled for an elective repeat cesarean for the day after her actual presentation to labor and delivery. On presentation, an external fetal monitor was unable to identify fetal cardiac activity. Ultrasound was attempted but was difficult because of obesity and lack of amniotic fluid. No cardiac activity was seen. She was then examined, and rupture of membranes was confirmed with nitrazine. Her cervix was dilated 3 to 4 cm and 100% effaced. A scalp electrode was applied, and no cardiac signal was detected. A second electrode was applied, and fetal death was confirmed. A decision was made to go immediately to cesarean, and a stillborn, cyanotic, male infant weighing 5580 g was delivered. The placenta and umbilical cord appeared normal, and the amniotic fluid was clear. Autopsy showed a macerated and markedly macrosomic fetus (5550 g), with lungs, heart, liver, kidneys, spleen, and thymus all weighing greater than the 99th percentile for gestational age. The enlarged placenta showed meconium staining of the fetal surface. The infant was deeply cyanosed, and there were alveolar squamae and pleural and pericardial petechiae, all strongly suggestive of intrauterine hypoxia. The heart was particularly enlarged, weighing 56 g, at least double the expected size (Figure 1). There was
926
Sardesai et al
Fatal Hypertrophic Cardiomyopathy
Impaired maternal glucose tolerance has been associated with several morbidities, including maternal toxemia and fetal macrosomia, growth restriction, neonatal hypoglycemia, hypocalcemia, hypomagnesemia, polycythemia, hyperbilirubinemia, respiratory distress syndrome, congenital anomalies, and hypertrophic cardiomyopathy.2 Major long-term complications for the child include obesity and diabetes mellitus.3 Several complications (including macrosomia and hypertrophic cardiomyopathy) have been attributed to fetal hyperinsulinemia, which usually results from fetal hyperglycemia caused by poor maternal glycemic control, because fetal blood glucose concentrations are 70 – 80% of maternal levels.2 Common features of hypertrophic cardiomyopathy in infants of diabetic mothers include hypertrophy of the ventricular and septal walls, anterior motion of the mitral valve during mid-systole, and a shift in ventricular filling from ventricular diastole to atrial systole.2 One study showed that 5% of affected infants of diabetic mothers had congestive heart failure secondary to left ventricular outflow obstruction.3 With time, myocardial hypertrophy regresses and usually resolves within 6 months without complication. Unlike some forms of familial hypertrophic cardiomypathy, sudden death is rare.3 The pathologic findings in this case suggested that the fetus had intrauterine cardiac failure caused by the cardiomyopathy. Presumably ventricular dilatation and hypocontractility allowed the formation of mural thrombi, and embolization from that source caused myocardial necrosis, which in turn was sufficient to cause the fatal consequences. The ultrasounds were retrospectively reviewed in detail, specifically for signs of hydrops and for taking cardiac measurements. No signs of hydrops were identified. However, the 36-week ultrasound showed markedly increased intraventricular septal and ventricular wall measurements of 0.9 mm and 0.5 mm, respectively.
OBSTETRICS & GYNECOLOGY
No cardiac measurements could be obtained from earlier ultrasounds. The findings and outcome of this case indicate the importance of third-trimester echocardiographic monitoring of heart function in fetuses of mothers with diabetes. Although the incidence of fatal hypertrophic cardiomyopathy in infants of women with diabetes is believed to be rare, treatment, including early delivery and propranolol treatment of the neonate, might have improved the outcome in this case.3 Indeed it is possible that the unexplained fetal deaths described in previous reports6,7 might be attributable to hypertrophic cardiomyopathy. Diligent monitoring of fetal progress with special consideration of the possibility of hypertrophic cardiomyopathy could reveal additional cases, and could indicate more aggressive intervention than previously seemed appropriate.
3. Weintrob N, Karp M, Hod M. Short- and long-range complications in offspring of diabetic mothers. J Diabetes Complications 1996;10:294 –301. 4. Leslie J, Shen C, Strauss L. Hypertrophic cardiomyopathy in a midtrimester fetus born to a diabetic mother. J Pediatr 1982;100:631–2. 5. Maron BJ, Edwards JE, Henry WL, Clark CE, Bingle GJ, Epstein SE. Asymmetric septal hypertrophy (ASH) in infancy. Circulation 1974;50:809 –20. 6. Girz BA, Divon MY, Merkatz IR. Sudden fetal death in women with well-controlled, intensively monitored gestational diabetes. J Perinatol 1992;12:229 –33. 7. Gutgesell HP, Speer ME, Rosenberg HS. Characterization of the cardiomyopathy in infants of diabetic mothers. Circulation 1980;61:441–50.
REFERENCES
8. McMahon JN, Berry PJ, Joffe HS. Fatal hypertrophic cardiomyopathy in an infant of a diabetic mother. Pediatr Cardiol 1990;11:211–2.
1. Pildes, RS. Infants of diabetic mothers. N Engl J Med 1973;289:902– 4. 2. Tyrala EE. The infant of the diabetic mother. Obstet Gynecol Clin North Am 1996;23:221– 41.
Received December 15, 2000. Received in revised form March 9, 2001. Accepted April 19, 2001.
Placenta Percreta With Spontaneous Rupture of an Unscarred Uterus in the Second Trimester William J. LeMaire, MD, Claire Louisy, MD, Kathie Dalessandri, MD, and Frederick Muschenheim, MD Department of Obstetrics and Gynaecology, St. Jude Hospital, St. Lucia, West Indies; the Department of Obstetrics and Gynecology, University of Miami School of Medicine, Miami, Florida; and the Department of Surgery, Stanford University, Point Reyes Station, California
BACKGROUND: Rupture of a pregnant uterus occurs most often in a scarred uterus, and spontaneous rupture of a non-scarred uterus in the early second trimester is rare. CASE: A woman with two previous normal vaginal deliveries and no prior trauma to the uterus presented at 16 weeks’ gestation with an acute abdomen due to intraperitoneal hemorrhage. A large rupture of the fundus of the uterus was found. A supracervical hysterectomy was carAddress reprint requests to: William J. LeMaire, MD, PO Box 1672, Sitka, Alaska 99835; E-mail: [email protected].
ried out, with subsequent good recovery. The specimen showed placenta percreta. CONCLUSION: Spontaneous rupture of an unscarred uterus, due to placenta percreta, should be considered in cases of acute intraperitoneal hemorrhage, even in early pregnancy. (Obstet Gynecol 2001;98:927–9. © 2001 by the American College of Obstetricians and Gynecologists.)
Spontaneous rupture of a non-scarred uterus is a relatively rare occurrence. If it happens, it usually happens in the third trimester of pregnancy, during the process of labor and delivery. It’s occurrence in the early second trimester, without any predating injury or trauma, is very rare indeed. We report a case of spontaneous rupture of an unscarred uterus in the early second trimester of an otherwise uncomplicated pregnancy. CASE REPORT The patient is a gravida 3 with two previous healthy vaginal deliveries. She was seen in the emergency room at approximately 13 weeks’ gestation, calculated from her last menstrual period. She had a weeklong history of left lower abdominal pain. This pain had progressively increased, becoming diffuse throughout the abdomen, and was associated with vomiting. She had no vaginal
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01580-0
927
Fatal Hypertrophic Cardiomyopathy in the Fetus of a Woman With Diabetes Maya G. Sardesai, Aileen A. Gray, MA, MD, Michael M. J. McGrath, MD, FRCSC, and Sally E. Ford, MBBS, FRCPC Queen’s University Medical School, Department of Family Medicine, Queen’s University, Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Queen’s University, and Department of Pathology, Queen’s University and Kingston General Hospital, Kingston, Ontario, Canada
BACKGROUND: Hypertrophic cardiomyopathy is recognized in infants of diabetic mothers, and when it occurs it is generally benign and transient. We describe a case of fetal cardiac death caused by hypertrophic cardiomyopathy in an infant of a diabetic mother. CASE: Hydrops fetalis caused by hypertrophic cardiomyopathy resulted in the death of a macrosomic male fetus of a young woman who had well-controlled diabetes mellitus and was treated with insulin therapy during pregnancy. CONCLUSION: It is important to monitor fetal heart function in macrosomic infants of diabetic mothers. Hypertrophic cardiomyopathy might explain otherwise unexplained fetal deaths in women with diabetes. (Obstet Gynecol 2001;98:925–7. © 2001 by the American College of Obstetricians and Gynecologists.)
Hypertrophic cardiomyopathy, which consists of cardiac enlargement and disproportionate septal hypertrophy, occurs in 30% of infants of diabetic mothers and likely reflects fetal hyperinsulinemia.1,2 With appropriate therapy (eg, propranolol or other -blockers), hypertrophic cardiomyopathy usually resolves without complications within 6 months after birth.3 There are very few documented cases of stillbirths of Address reprint requests to: Sally E. Ford, MBBS, FRCPC, Department of Pathology, Richardson Laboratory, Room 201, Queen’s University, Kingston, Ontario K7L 3N6, Canada; E-mail: ford@cliff. path.queensu.ca.
pancreatitis and primary hyperparathyroidism in pregnancy: Treatment of hypercalcemia with magnesium sulfate. Obstet Gynecol 1987;70:460 –2.
Received November 1, 2000. Received in revised form January 8, 2001. Accepted April 12, 2001.
infants of diabetic mothers with hypertrophic cardiomyopathy, and all but one of those cases have been attributed to noncardiac or unknown causes, although Leslie et al4 described a stillbirth where the infant had an enlarged heart.5,6 A MEDLINE search limited to English language for the period 1966 to the week of December 4, 2000, with subject and keyword search terms “cardiomyopathy,” “hypertrophic,” and “diabetes” or “fetal death” found no cases of death from hypertrophic cardiomyopathy-related cardiac failure in fetuses of mothers with diabetes, and very few in infants.7,8
CASE A 27-year-old woman, gravida 3, para 1, aborta 1, at 37 weeks’ gestation, presented to labor and delivery with spontaneous rupture of membranes and uterine contractions. She had noticed decreased fetal movement during the preceding 2 days; however, a biophysical profile approximately 12 hours before presentation to labor and delivery yielded a score of 8/8. Her medical history was significant for obesity and smoking five to seven cigarettes per day. She denied alcohol and drug use. Family history was positive for type II diabetes on her maternal side. Obstetric history included a first pregnancy that spontaneously aborted at 12 weeks and a second pregnancy complicated by gestational diabetes and fetal macrosomia (5305 g). She required cesarean delivery for failure to progress in labor. No blood glucose levels had been measured between her second and third pregnancies. Early in her third pregnancy, diabetes was identified, with a fasting blood glucose level of 180 mg/dL at 5 weeks. Her glycosylated hemoglobin was 6% at 9 weeks, consistent with optimal glycemic control. The diabetes was initially controlled by diet, but she was started on insulin at 26 weeks for escalating blood glucose measurements. No further glycosylated hemoglobin samples were drawn until the day of her delivery, at which point it measured 6.6%. She had reported good control based on frequent home monitoring. The patient had a normal anatomic scan at 18 weeks’
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01455-7
925
asymmetric hypertrophy (septum and inferior left-ventricular wall being 1.3 cm and 0.7 cm, respectively) and biventricular dilatation. Microscopically the myocardium showed extensive myofibrillar disarray in both the septum and the free wall. Microscopic mural thrombi were observed, and patchy early myocardial necrosis in association with occlusions of small intramural arteries was noted. These occlusions were probably emboli from the mural thrombi. Consistent with cardiac death, there was pulmonary congestion, massive centrilobular congestion, and necrosis of the liver, as well as hydrops fetalis, with peripheral edema, pleural effusions, and ascites.
COMMENT Figure 1. Cross section of the infant’s heart at autopsy showing asymmetric hypertrophy. RV ⫽ right ventricle; LV ⫽ left ventricle. Sardesai. Fatal Hypertrophic Cardiomyopathy. Obstet Gynecol 2001.
gestation but did not have fetal echocardiography in the second trimester because she was treated as having gestational diabetes. An ultrasound at 36 weeks identified fetal macrosomia with an estimated fetal weight above the 97.5th percentile. She had been scheduled for an elective repeat cesarean for the day after her actual presentation to labor and delivery. On presentation, an external fetal monitor was unable to identify fetal cardiac activity. Ultrasound was attempted but was difficult because of obesity and lack of amniotic fluid. No cardiac activity was seen. She was then examined, and rupture of membranes was confirmed with nitrazine. Her cervix was dilated 3 to 4 cm and 100% effaced. A scalp electrode was applied, and no cardiac signal was detected. A second electrode was applied, and fetal death was confirmed. A decision was made to go immediately to cesarean, and a stillborn, cyanotic, male infant weighing 5580 g was delivered. The placenta and umbilical cord appeared normal, and the amniotic fluid was clear. Autopsy showed a macerated and markedly macrosomic fetus (5550 g), with lungs, heart, liver, kidneys, spleen, and thymus all weighing greater than the 99th percentile for gestational age. The enlarged placenta showed meconium staining of the fetal surface. The infant was deeply cyanosed, and there were alveolar squamae and pleural and pericardial petechiae, all strongly suggestive of intrauterine hypoxia. The heart was particularly enlarged, weighing 56 g, at least double the expected size (Figure 1). There was
926
Sardesai et al
Fatal Hypertrophic Cardiomyopathy
Impaired maternal glucose tolerance has been associated with several morbidities, including maternal toxemia and fetal macrosomia, growth restriction, neonatal hypoglycemia, hypocalcemia, hypomagnesemia, polycythemia, hyperbilirubinemia, respiratory distress syndrome, congenital anomalies, and hypertrophic cardiomyopathy.2 Major long-term complications for the child include obesity and diabetes mellitus.3 Several complications (including macrosomia and hypertrophic cardiomyopathy) have been attributed to fetal hyperinsulinemia, which usually results from fetal hyperglycemia caused by poor maternal glycemic control, because fetal blood glucose concentrations are 70 – 80% of maternal levels.2 Common features of hypertrophic cardiomyopathy in infants of diabetic mothers include hypertrophy of the ventricular and septal walls, anterior motion of the mitral valve during mid-systole, and a shift in ventricular filling from ventricular diastole to atrial systole.2 One study showed that 5% of affected infants of diabetic mothers had congestive heart failure secondary to left ventricular outflow obstruction.3 With time, myocardial hypertrophy regresses and usually resolves within 6 months without complication. Unlike some forms of familial hypertrophic cardiomypathy, sudden death is rare.3 The pathologic findings in this case suggested that the fetus had intrauterine cardiac failure caused by the cardiomyopathy. Presumably ventricular dilatation and hypocontractility allowed the formation of mural thrombi, and embolization from that source caused myocardial necrosis, which in turn was sufficient to cause the fatal consequences. The ultrasounds were retrospectively reviewed in detail, specifically for signs of hydrops and for taking cardiac measurements. No signs of hydrops were identified. However, the 36-week ultrasound showed markedly increased intraventricular septal and ventricular wall measurements of 0.9 mm and 0.5 mm, respectively.
OBSTETRICS & GYNECOLOGY
No cardiac measurements could be obtained from earlier ultrasounds. The findings and outcome of this case indicate the importance of third-trimester echocardiographic monitoring of heart function in fetuses of mothers with diabetes. Although the incidence of fatal hypertrophic cardiomyopathy in infants of women with diabetes is believed to be rare, treatment, including early delivery and propranolol treatment of the neonate, might have improved the outcome in this case.3 Indeed it is possible that the unexplained fetal deaths described in previous reports6,7 might be attributable to hypertrophic cardiomyopathy. Diligent monitoring of fetal progress with special consideration of the possibility of hypertrophic cardiomyopathy could reveal additional cases, and could indicate more aggressive intervention than previously seemed appropriate.
3. Weintrob N, Karp M, Hod M. Short- and long-range complications in offspring of diabetic mothers. J Diabetes Complications 1996;10:294 –301. 4. Leslie J, Shen C, Strauss L. Hypertrophic cardiomyopathy in a midtrimester fetus born to a diabetic mother. J Pediatr 1982;100:631–2. 5. Maron BJ, Edwards JE, Henry WL, Clark CE, Bingle GJ, Epstein SE. Asymmetric septal hypertrophy (ASH) in infancy. Circulation 1974;50:809 –20. 6. Girz BA, Divon MY, Merkatz IR. Sudden fetal death in women with well-controlled, intensively monitored gestational diabetes. J Perinatol 1992;12:229 –33. 7. Gutgesell HP, Speer ME, Rosenberg HS. Characterization of the cardiomyopathy in infants of diabetic mothers. Circulation 1980;61:441–50.
REFERENCES
8. McMahon JN, Berry PJ, Joffe HS. Fatal hypertrophic cardiomyopathy in an infant of a diabetic mother. Pediatr Cardiol 1990;11:211–2.
1. Pildes, RS. Infants of diabetic mothers. N Engl J Med 1973;289:902– 4. 2. Tyrala EE. The infant of the diabetic mother. Obstet Gynecol Clin North Am 1996;23:221– 41.
Received December 15, 2000. Received in revised form March 9, 2001. Accepted April 19, 2001.
Placenta Percreta With Spontaneous Rupture of an Unscarred Uterus in the Second Trimester William J. LeMaire, MD, Claire Louisy, MD, Kathie Dalessandri, MD, and Frederick Muschenheim, MD Department of Obstetrics and Gynaecology, St. Jude Hospital, St. Lucia, West Indies; the Department of Obstetrics and Gynecology, University of Miami School of Medicine, Miami, Florida; and the Department of Surgery, Stanford University, Point Reyes Station, California
BACKGROUND: Rupture of a pregnant uterus occurs most often in a scarred uterus, and spontaneous rupture of a non-scarred uterus in the early second trimester is rare. CASE: A woman with two previous normal vaginal deliveries and no prior trauma to the uterus presented at 16 weeks’ gestation with an acute abdomen due to intraperitoneal hemorrhage. A large rupture of the fundus of the uterus was found. A supracervical hysterectomy was carAddress reprint requests to: William J. LeMaire, MD, PO Box 1672, Sitka, Alaska 99835; E-mail: [email protected].
ried out, with subsequent good recovery. The specimen showed placenta percreta. CONCLUSION: Spontaneous rupture of an unscarred uterus, due to placenta percreta, should be considered in cases of acute intraperitoneal hemorrhage, even in early pregnancy. (Obstet Gynecol 2001;98:927–9. © 2001 by the American College of Obstetricians and Gynecologists.)
Spontaneous rupture of a non-scarred uterus is a relatively rare occurrence. If it happens, it usually happens in the third trimester of pregnancy, during the process of labor and delivery. It’s occurrence in the early second trimester, without any predating injury or trauma, is very rare indeed. We report a case of spontaneous rupture of an unscarred uterus in the early second trimester of an otherwise uncomplicated pregnancy. CASE REPORT The patient is a gravida 3 with two previous healthy vaginal deliveries. She was seen in the emergency room at approximately 13 weeks’ gestation, calculated from her last menstrual period. She had a weeklong history of left lower abdominal pain. This pain had progressively increased, becoming diffuse throughout the abdomen, and was associated with vomiting. She had no vaginal
VOL. 98, NO. 5, PART 2, NOVEMBER 2001 © 2001 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
0029-7844/01/$20.00 PII S0029-7844(01)01580-0
927