- Email: [email protected]
The use of a continuous infusion of epinephrine for anaphylactic shock during labor
CASE REPORT
The Use of a Continuous Infusion of Epinephrine for Anaphylactic Shock During Labor Alfredo F. Gei, MD, Luis D. Pacheco, MD, James W. Vanhook, MD, and Gary D. V. Hankins, MD Division of Maternal–Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, Galveston, Texas
BACKGROUND: Anaphylaxis is a potentially life threatening, acute, and severe systemic reaction that occurs after the reexposure to a specific antigen. This immunoglobulin E-mediated process is the result of the action of basophils and mast cell mediators, causing severe brochospasm, laringospasm, angioedema, urticaria, and cardiovascular collapse. CASE: We present a case of anaphylactic shock during labor secondary to administration of ampicillin for group B streptococcus prophylaxis. Generalized itching and hives were soon followed by severe maternal hypotension and tachycardia and prolonged fetal bradycardia. These symptoms responded partially to the administration of fluids and parenteral epinephrine. A continuous infusion of epinephrine was required for persistent maternal symptoms. The infusion did not result in further fetal compromise. The patient delivered a healthy fetus 4 hours after the start of the epinephrine infusion. CONCLUSION: This case supports the use of parenteral (intravenous) epinephrine for the treatment of anaphylactic reactions during pregnancy. (Obstet Gynecol 2003;102: 1332–5. © 2003 by The American College of Obstetricians and Gynecologists.)
CASE An 18-year-old secundigravida presented to the Labor and Delivery unit at 40 weeks’ gestation, complaining of leakage of amniotic fluid for the previous 15 hours. Her Address reprint requests to: Alfredo F. Gei, MD, Division of Maternal–Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, 3.400 John Sealy Annex, 301 University Boulevard, Galveston, TX 77555-0587; Email: [email protected].
1332
prenatal course was unremarkable. Past medical and surgical histories were noncontributory, and she denied any history of prior allergic reactions. At the time of presentation, she was taking prenatal vitamins, iron supplementation, and nitrofurantoin (for asymptomatic bacteriuria). On admission, the vital signs were as follows: blood pressure (BP), 122/46 mm Hg; heart rate, 81 beats per minute; respiratory rate, 18 per minute; and temperature, 37C. Her general physical examination was unremarkable. A single intrauterine pregnancy in cephalic presentation was documented. The fundal height was measured at 38 cm. Gross rupture of membranes was documented; her cervical examination was 4 cm dilated, 50% effaced, and the presentation noted to be at ⫺2 station. Electronic fetal monitoring showed a reactive electronic tracing with a baseline of 130 beats per minute and irregular contractions. The patient was admitted with diagnoses of term pregnancy, early labor, and rupture of membranes. An oxytocin infusion was started at 2 mIU per minute for augmentation of labor. Ampicillin was also started at a dose of 2 g intravenously (IV) for chemoprophylaxis against group B streptococcus 16 hours after the spontaneous rupture of membranes. During the infusion of the antibiotic, the patient complained of diffuse itching, and hives were noted by the nurse. Within seconds, the patient complained of shortness of breath, nausea, and dizziness. The patient was restless, her chest fields were clear to auscultation bilaterally, and a diffuse urticarial rash was noted. The antibiotic infusion was stopped, and 50 mg of diphenhydramine was given IV. Twenty-five minutes later, the patient became tachycardic (160 –170 beats per minute) and hypotensive (91/65), and the fetus developed a prolonged bradycardia (70s– 80s per minute). A vaginal examination showed the cervix to be 4 cm dilated, 75% effaced, and the cephalic presentation at ⫺2 station. A fetal scalp clip was placed. The patient was immediately placed in lateral decubitus and deep Trendelenburg position; oxygen was started via a face mask (10 L per minute); a second IV access (16 gauge) was obtained; and 2 L of crystalloids were administered IV as a bolus, with recovery of the fetal bradycardia within 5 minutes (Figure 1). At this time, the patient remained symptomatic (dizzy) and hypotensive (BP, 89/ 57; heart rate, 141 per minute). Three doses of epinephrine (100 g of a 1:1000 solution each) were given IV at 10-minute intervals, with transient improvement of BP and heart rate; however, the patient remained hypotensive (with diastolic BP as low as 17 mm Hg and pulse
VOL. 102, NO. 6, DECEMBER 2003 © 2003 by The American College of Obstetricians and Gynecologists. Published by Elsevier.
0029-7844/03/$30.00 doi:10.1016/S0029-7844(03)00167-4
Figure 1. Electronic fetal monitoring at the beginning of the anaphylactic episode. Note simultaneous maternal tachycardia and fetal bradycardia. Gei. Anaphylaxis in Labor. Obstet Gynecol 2003.
pressures as large as 80 mm Hg), and a continuous infusion of epinephrine (1 mg in 250 mL of 0.9% sodium chloride) was started 30 minutes after the onset of the event at a dose of 1 g per minute. This infusion was rapidly titrated to 3.3 g per minute with hemodynamic and symptomatic improvement. Methylprednisolone (125 mg) and famotidine (20 mg) were also administered. During the event, maternal electrocardiogram monitoring showed sinus tachycardia and occasional premature ventricular contractions. One hour after the infusion was started, an attempt to wean the epinephrine (from 3 g per minute to 2.3 g per minute) resulted in recurrence of hypotension (BP, 128/56 to 92/26) establishing the need to continue it. Labor analgesia was achieved with IV boluses of fentanyl, followed by an epidural at 6 cm of dilation. Prophylaxis for group B streptococcus (GBS) was continued with clindamycin 900 mg IV every 8 hours. The epinephrine drip was weaned and eventually discontinued 3.5 hours after its start. During the remainder of the episode, the fetal heart tracing remained reassuring (Figure 2). Labor progressed spontaneously with stable maternal vital signs, and an uncomplicated vaginal delivery of a female infant with Apgar scores of 8 and 9 at 1 and 5 minutes, respectively, was achieved 4.5 hours after the onset of symptoms. The second stage lasted 25 minutes. The umbilical artery pH was 7.25. Methylprednisolone and famotidine were continued for 24 hours, and the patient and neonate were discharged on the second postpartum
VOL. 102, NO. 6, DECEMBER 2003
day in excellent condition. Upon discharge, the patient was warned about her allergy to -lactamase antibiotics.
COMMENT The incidence of anaphylaxis among inpatients has been reported to be three to five per 10,000.1 The incidence of anaphylaxis after penicillin administration has been estimated at 0.01% with a mortality rate of up to 9%.2 Penicillin anaphylaxis is responsible for 400 –500 deaths every year. Anaphylaxis has been described during pregnancy after laminaria insertion, the exposure of latex, with the administration of antibiotics (ampicillin and cefazolin), iron, ranitidine, snake antivenom, insect stings (ants and bees), local anesthetics, and induction of general anesthesia.3–17 The treatment of anaphylaxis is aimed towards aggressive cardiorespiratory support. The exposure of the suspected antigen should be recognized promptly and stopped immediately, and efforts should be made to maintain a patent airway.18,19 If the diagnosis is suspected, replacement of 1–2 L of crystalloids should be started.19 In pregnant patients, continuous electronic fetal monitoring is advocated during the event, as the fetus is very sensitive to maternal changes in BP. The patient should be placed on the left lateral position and given oxygen through a face mask.2,18 –20 Epinephrine is the mainstay of the treatment.1,2,4,6,7,17–21 It achieves vasoconstriction through
Gei et al
Anaphylaxis in Labor
1333
Figure 2. Typical heart tracing during epinephrine infusion. Note low diastolic blood pressure and large pulse pressure on the written additions to the strip. Gei. Anaphylaxis in Labor. Obstet Gynecol 2003.
␣-receptor stimulation, with a concomitant increase in vascular systemic resistance and BP. The  effect increases myocardial contractibility and alleviates bronchospasm.18 It also has an antiinflammatory effect, inhibiting the release of mediators from mast cells and basophils via -2 stimulation.2–18 In mild cases, 0.3– 0.5 mg of a 1:1000 solution (0.3– 0.5 mL) may be administered through the subcutaneous route. Severe cases will require the IV route. Boluses of 0.1– 0.2 mL of a 1:1000 solution (100 –200 g) diluted in 10 mL of saline (or 1–2 mL of a 1:10,000 solution) may be given over a period of 10 minutes and repeated periodically as needed.2 If hemodynamic instability persists, a continuous drip of epinephrine may be needed. One mg of epinephrine is diluted in 250 mL of saline and started at 1 g per minute (15 mL per hour) and titrated according to clinical response.2 Because of its pharmacologic profile, the use of epinephrine during pregnancy can, at least theoretically, lead to decreased uterine blood flow. In a previously reported human case, epinephrine was thought to contribute to the anoxic injury on a 28-week old fetus from a hypotensive mother.12 For this reason, some authors have advocated ephedrine as the drug of choice because of its capacity of sparing uterine blood perfusion.6,7,9,10,13,20 Adamsons et al reported the induction of asphyxia to term rhesus fetuses when the mother was given catecholamines.22 Likewise, Greiss reported uterine artery constriction and subsequent decrease in uterine blood flow when epinephrine was administered in
1334
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Anaphylaxis in Labor
the aorta to sheep.23 He further demonstrated that 40fold doses of epinephrine were required to produce equivalent vasoconstrictive effects to those produced in the castrated ewe, suggesting that a protective effect for the fetus against adrenergic stimulation existed and evidenced by the relative insensitivity of the total uterine vasculature at term to ␣ adrenergic stimulation. We hypothesize that in the compromised mother, the increase in systemic vascular resistance (SVR) benefits the cardiac output and the uteroplacental perfusion, by causing arteriolar constriction of the relative larger splanchnic bed relative to the uteroplacental bed. The studies performed in animal models are not incongruous to this finding because they are starting with an intact circulation and stable hemodynamic state. The use of epinephrine in a low vascular resistance condition seems to spare (relatively or absolutely) the uterine flow enough to allow progression of labor and the delivery of an unaffected child. In our case, stabilization of the mother with a continuous infusion of epinephrine resulted in the delivery of a healthy infant via the vaginal route. Several reports in the literature have shown poor neonatal outcomes after an emergent cesarean delivery before stabilization of the mother.8 –10 Obstetricians should be familiar with the management of anaphylactic reactions. We advocate maternal stabilization of the mother before performing an emergent cesarean delivery and the use of epinephrine (even in a continuous infusion) to maintain an
OBSTETRICS & GYNECOLOGY
adequate cardiac output and uterine–placental–fetal perfusion. REFERENCES 1. Luskin AT, Luskin SS. Anaphylaxis and anaphylactoid reactions: Diagnosis and management. Am J Ther 1996;3: 515–20. 2. Haupt MT, Fujii TK, Carlson RW. Anaphylactic reactions. In: Grenvik A, Ayres SM, Holbrook PR, Schoemaker WC, eds. Textbook of critical care. Philadelphia, Pennsylvania: WB Saunders Company, 2000, 246 –58. 3. Cole DS, Bruck LR. Anaphylaxis after laminaria insertion. Obstet Gynecol 2000;95:1025. 4. Chanda M, Mackenzie P, Day JH. Hypersensitivity reactions following laminaria placement. Contraception 2000; 62:105–6. 5. Porter BJ, Acharya U, Ormerod AD, Herriot R. Latex/ chlorhexidine-induced anaphylaxis in pregnancy. Allergy 1998;53:455–7. 6. Eckhout GV, Ayad S. Anaphylaxis due to airborne exposure to latex in a primigravida. Anesthesiology 2001;95: 1034–5. 7. Gallagher JS. Anaphylaxis in pregnancy. Obstet Gynecol 1988;71:491–3. 8. Heim K, Alge A, Marth C. Anaphylactic reaction to ampicillin and severe complication in the fetus. Lancet 1991; 337:859–60. 9. Konno R, Nagase S. Anaphylactic reaction to cefazolin in pregnancy. J Obstet Gynaecol 1995;21:577–9. 10. Dunn AB, Blomquist J, Khouzami V. Anaphylaxis in labor secondary to prophylaxis against group B streptococcus. A case report. J Reprod Med 1999;44:381–4. 11. Luciano R, Zuppa AA, Maragliano G, Gallini F, Tortorolo G. Fetal encephalopathy after maternal anaphylaxis. Case report. Biol Neonate 1997;71:190–3.
VOL. 102, NO. 6, DECEMBER 2003
12. Powell JA, Maycock EJ. Anaphylactoid reaction to ranitidine in an obstetric patient. Anaesth Intensive Care 1993; 21:702–3. 13. Entman SS, Moise KJ. Anaphylaxis in pregnancy. South Med J 1984;77:402–4. 14. Rizk DEE, Mensah-Brown E, Lukic M. Placental abruption and intrauterine death following an ant sting. Int J Gynaecol Obstet 1998;63:71–2. 15. Erasmus C, Blackwood W, Wilson J. Infantile multicystic encephalomalacia after maternal bee sting anaphylaxis during pregnancy. Arch Dis Child 1982;57:785–7. 16. Browne IM, Birnbach DJ. A pregnant woman with previous anaphylactic reaction to local anesthetics: A case report. Am J Obstet Gynecol 2001;185:1253–4. 17. Stannard L, Bellis A. Maternal anaphylactic reaction to a general anaesthetic at emergency caesarean section for fetal bradycardia. Br J Obstet Gynaecol 2001;108:539–40. 18. Levy JH, Yegin A. Anaphylaxis. What is monitored to make a diagnosis? How is therapy monitored? Anesthesiol Clin North America 2001;19:705–15. 19. Drain KL, Volcheck GW. Preventing and managing druginduced anaphylaxis. Drug Saf 2001;24:843–53. 20. Heinly TL, Lieberman P. Anaphylaxis in pregnancy. Immunol Allergy Clin North America 2000;20:831. 21. Edmondson WC, Skilton RWH. Anaphylaxis in pregnancy—The right treatment? Anaesthesia 1994;49:454–5. 22. Adamsons K, Mueller-Heubach E, Myers RE. Production of fetal asphyxia in the rhesus monkey by administration of catecholamines to the mother. Am J Obstet Gynecol 1971;109:248–62. 23. Greiss FC Jr. Differential reactivity of the myoendometrial and placental vasculatures: Adrenergic responses. Am J Obstet Gynecol 1972;112:20–30. Received October 22, 2002. Received in revised form January 6, 2003. Accepted January 23, 2003.
Gei et al
Anaphylaxis in Labor
1335
The Use of a Continuous Infusion of Epinephrine for Anaphylactic Shock During Labor Alfredo F. Gei, MD, Luis D. Pacheco, MD, James W. Vanhook, MD, and Gary D. V. Hankins, MD Division of Maternal–Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, Galveston, Texas
BACKGROUND: Anaphylaxis is a potentially life threatening, acute, and severe systemic reaction that occurs after the reexposure to a specific antigen. This immunoglobulin E-mediated process is the result of the action of basophils and mast cell mediators, causing severe brochospasm, laringospasm, angioedema, urticaria, and cardiovascular collapse. CASE: We present a case of anaphylactic shock during labor secondary to administration of ampicillin for group B streptococcus prophylaxis. Generalized itching and hives were soon followed by severe maternal hypotension and tachycardia and prolonged fetal bradycardia. These symptoms responded partially to the administration of fluids and parenteral epinephrine. A continuous infusion of epinephrine was required for persistent maternal symptoms. The infusion did not result in further fetal compromise. The patient delivered a healthy fetus 4 hours after the start of the epinephrine infusion. CONCLUSION: This case supports the use of parenteral (intravenous) epinephrine for the treatment of anaphylactic reactions during pregnancy. (Obstet Gynecol 2003;102: 1332–5. © 2003 by The American College of Obstetricians and Gynecologists.)
CASE An 18-year-old secundigravida presented to the Labor and Delivery unit at 40 weeks’ gestation, complaining of leakage of amniotic fluid for the previous 15 hours. Her Address reprint requests to: Alfredo F. Gei, MD, Division of Maternal–Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, 3.400 John Sealy Annex, 301 University Boulevard, Galveston, TX 77555-0587; Email: [email protected].
1332
prenatal course was unremarkable. Past medical and surgical histories were noncontributory, and she denied any history of prior allergic reactions. At the time of presentation, she was taking prenatal vitamins, iron supplementation, and nitrofurantoin (for asymptomatic bacteriuria). On admission, the vital signs were as follows: blood pressure (BP), 122/46 mm Hg; heart rate, 81 beats per minute; respiratory rate, 18 per minute; and temperature, 37C. Her general physical examination was unremarkable. A single intrauterine pregnancy in cephalic presentation was documented. The fundal height was measured at 38 cm. Gross rupture of membranes was documented; her cervical examination was 4 cm dilated, 50% effaced, and the presentation noted to be at ⫺2 station. Electronic fetal monitoring showed a reactive electronic tracing with a baseline of 130 beats per minute and irregular contractions. The patient was admitted with diagnoses of term pregnancy, early labor, and rupture of membranes. An oxytocin infusion was started at 2 mIU per minute for augmentation of labor. Ampicillin was also started at a dose of 2 g intravenously (IV) for chemoprophylaxis against group B streptococcus 16 hours after the spontaneous rupture of membranes. During the infusion of the antibiotic, the patient complained of diffuse itching, and hives were noted by the nurse. Within seconds, the patient complained of shortness of breath, nausea, and dizziness. The patient was restless, her chest fields were clear to auscultation bilaterally, and a diffuse urticarial rash was noted. The antibiotic infusion was stopped, and 50 mg of diphenhydramine was given IV. Twenty-five minutes later, the patient became tachycardic (160 –170 beats per minute) and hypotensive (91/65), and the fetus developed a prolonged bradycardia (70s– 80s per minute). A vaginal examination showed the cervix to be 4 cm dilated, 75% effaced, and the cephalic presentation at ⫺2 station. A fetal scalp clip was placed. The patient was immediately placed in lateral decubitus and deep Trendelenburg position; oxygen was started via a face mask (10 L per minute); a second IV access (16 gauge) was obtained; and 2 L of crystalloids were administered IV as a bolus, with recovery of the fetal bradycardia within 5 minutes (Figure 1). At this time, the patient remained symptomatic (dizzy) and hypotensive (BP, 89/ 57; heart rate, 141 per minute). Three doses of epinephrine (100 g of a 1:1000 solution each) were given IV at 10-minute intervals, with transient improvement of BP and heart rate; however, the patient remained hypotensive (with diastolic BP as low as 17 mm Hg and pulse
VOL. 102, NO. 6, DECEMBER 2003 © 2003 by The American College of Obstetricians and Gynecologists. Published by Elsevier.
0029-7844/03/$30.00 doi:10.1016/S0029-7844(03)00167-4
Figure 1. Electronic fetal monitoring at the beginning of the anaphylactic episode. Note simultaneous maternal tachycardia and fetal bradycardia. Gei. Anaphylaxis in Labor. Obstet Gynecol 2003.
pressures as large as 80 mm Hg), and a continuous infusion of epinephrine (1 mg in 250 mL of 0.9% sodium chloride) was started 30 minutes after the onset of the event at a dose of 1 g per minute. This infusion was rapidly titrated to 3.3 g per minute with hemodynamic and symptomatic improvement. Methylprednisolone (125 mg) and famotidine (20 mg) were also administered. During the event, maternal electrocardiogram monitoring showed sinus tachycardia and occasional premature ventricular contractions. One hour after the infusion was started, an attempt to wean the epinephrine (from 3 g per minute to 2.3 g per minute) resulted in recurrence of hypotension (BP, 128/56 to 92/26) establishing the need to continue it. Labor analgesia was achieved with IV boluses of fentanyl, followed by an epidural at 6 cm of dilation. Prophylaxis for group B streptococcus (GBS) was continued with clindamycin 900 mg IV every 8 hours. The epinephrine drip was weaned and eventually discontinued 3.5 hours after its start. During the remainder of the episode, the fetal heart tracing remained reassuring (Figure 2). Labor progressed spontaneously with stable maternal vital signs, and an uncomplicated vaginal delivery of a female infant with Apgar scores of 8 and 9 at 1 and 5 minutes, respectively, was achieved 4.5 hours after the onset of symptoms. The second stage lasted 25 minutes. The umbilical artery pH was 7.25. Methylprednisolone and famotidine were continued for 24 hours, and the patient and neonate were discharged on the second postpartum
VOL. 102, NO. 6, DECEMBER 2003
day in excellent condition. Upon discharge, the patient was warned about her allergy to -lactamase antibiotics.
COMMENT The incidence of anaphylaxis among inpatients has been reported to be three to five per 10,000.1 The incidence of anaphylaxis after penicillin administration has been estimated at 0.01% with a mortality rate of up to 9%.2 Penicillin anaphylaxis is responsible for 400 –500 deaths every year. Anaphylaxis has been described during pregnancy after laminaria insertion, the exposure of latex, with the administration of antibiotics (ampicillin and cefazolin), iron, ranitidine, snake antivenom, insect stings (ants and bees), local anesthetics, and induction of general anesthesia.3–17 The treatment of anaphylaxis is aimed towards aggressive cardiorespiratory support. The exposure of the suspected antigen should be recognized promptly and stopped immediately, and efforts should be made to maintain a patent airway.18,19 If the diagnosis is suspected, replacement of 1–2 L of crystalloids should be started.19 In pregnant patients, continuous electronic fetal monitoring is advocated during the event, as the fetus is very sensitive to maternal changes in BP. The patient should be placed on the left lateral position and given oxygen through a face mask.2,18 –20 Epinephrine is the mainstay of the treatment.1,2,4,6,7,17–21 It achieves vasoconstriction through
Gei et al
Anaphylaxis in Labor
1333
Figure 2. Typical heart tracing during epinephrine infusion. Note low diastolic blood pressure and large pulse pressure on the written additions to the strip. Gei. Anaphylaxis in Labor. Obstet Gynecol 2003.
␣-receptor stimulation, with a concomitant increase in vascular systemic resistance and BP. The  effect increases myocardial contractibility and alleviates bronchospasm.18 It also has an antiinflammatory effect, inhibiting the release of mediators from mast cells and basophils via -2 stimulation.2–18 In mild cases, 0.3– 0.5 mg of a 1:1000 solution (0.3– 0.5 mL) may be administered through the subcutaneous route. Severe cases will require the IV route. Boluses of 0.1– 0.2 mL of a 1:1000 solution (100 –200 g) diluted in 10 mL of saline (or 1–2 mL of a 1:10,000 solution) may be given over a period of 10 minutes and repeated periodically as needed.2 If hemodynamic instability persists, a continuous drip of epinephrine may be needed. One mg of epinephrine is diluted in 250 mL of saline and started at 1 g per minute (15 mL per hour) and titrated according to clinical response.2 Because of its pharmacologic profile, the use of epinephrine during pregnancy can, at least theoretically, lead to decreased uterine blood flow. In a previously reported human case, epinephrine was thought to contribute to the anoxic injury on a 28-week old fetus from a hypotensive mother.12 For this reason, some authors have advocated ephedrine as the drug of choice because of its capacity of sparing uterine blood perfusion.6,7,9,10,13,20 Adamsons et al reported the induction of asphyxia to term rhesus fetuses when the mother was given catecholamines.22 Likewise, Greiss reported uterine artery constriction and subsequent decrease in uterine blood flow when epinephrine was administered in
1334
Gei et al
Anaphylaxis in Labor
the aorta to sheep.23 He further demonstrated that 40fold doses of epinephrine were required to produce equivalent vasoconstrictive effects to those produced in the castrated ewe, suggesting that a protective effect for the fetus against adrenergic stimulation existed and evidenced by the relative insensitivity of the total uterine vasculature at term to ␣ adrenergic stimulation. We hypothesize that in the compromised mother, the increase in systemic vascular resistance (SVR) benefits the cardiac output and the uteroplacental perfusion, by causing arteriolar constriction of the relative larger splanchnic bed relative to the uteroplacental bed. The studies performed in animal models are not incongruous to this finding because they are starting with an intact circulation and stable hemodynamic state. The use of epinephrine in a low vascular resistance condition seems to spare (relatively or absolutely) the uterine flow enough to allow progression of labor and the delivery of an unaffected child. In our case, stabilization of the mother with a continuous infusion of epinephrine resulted in the delivery of a healthy infant via the vaginal route. Several reports in the literature have shown poor neonatal outcomes after an emergent cesarean delivery before stabilization of the mother.8 –10 Obstetricians should be familiar with the management of anaphylactic reactions. We advocate maternal stabilization of the mother before performing an emergent cesarean delivery and the use of epinephrine (even in a continuous infusion) to maintain an
OBSTETRICS & GYNECOLOGY
adequate cardiac output and uterine–placental–fetal perfusion. REFERENCES 1. Luskin AT, Luskin SS. Anaphylaxis and anaphylactoid reactions: Diagnosis and management. Am J Ther 1996;3: 515–20. 2. Haupt MT, Fujii TK, Carlson RW. Anaphylactic reactions. In: Grenvik A, Ayres SM, Holbrook PR, Schoemaker WC, eds. Textbook of critical care. Philadelphia, Pennsylvania: WB Saunders Company, 2000, 246 –58. 3. Cole DS, Bruck LR. Anaphylaxis after laminaria insertion. Obstet Gynecol 2000;95:1025. 4. Chanda M, Mackenzie P, Day JH. Hypersensitivity reactions following laminaria placement. Contraception 2000; 62:105–6. 5. Porter BJ, Acharya U, Ormerod AD, Herriot R. Latex/ chlorhexidine-induced anaphylaxis in pregnancy. Allergy 1998;53:455–7. 6. Eckhout GV, Ayad S. Anaphylaxis due to airborne exposure to latex in a primigravida. Anesthesiology 2001;95: 1034–5. 7. Gallagher JS. Anaphylaxis in pregnancy. Obstet Gynecol 1988;71:491–3. 8. Heim K, Alge A, Marth C. Anaphylactic reaction to ampicillin and severe complication in the fetus. Lancet 1991; 337:859–60. 9. Konno R, Nagase S. Anaphylactic reaction to cefazolin in pregnancy. J Obstet Gynaecol 1995;21:577–9. 10. Dunn AB, Blomquist J, Khouzami V. Anaphylaxis in labor secondary to prophylaxis against group B streptococcus. A case report. J Reprod Med 1999;44:381–4. 11. Luciano R, Zuppa AA, Maragliano G, Gallini F, Tortorolo G. Fetal encephalopathy after maternal anaphylaxis. Case report. Biol Neonate 1997;71:190–3.
VOL. 102, NO. 6, DECEMBER 2003
12. Powell JA, Maycock EJ. Anaphylactoid reaction to ranitidine in an obstetric patient. Anaesth Intensive Care 1993; 21:702–3. 13. Entman SS, Moise KJ. Anaphylaxis in pregnancy. South Med J 1984;77:402–4. 14. Rizk DEE, Mensah-Brown E, Lukic M. Placental abruption and intrauterine death following an ant sting. Int J Gynaecol Obstet 1998;63:71–2. 15. Erasmus C, Blackwood W, Wilson J. Infantile multicystic encephalomalacia after maternal bee sting anaphylaxis during pregnancy. Arch Dis Child 1982;57:785–7. 16. Browne IM, Birnbach DJ. A pregnant woman with previous anaphylactic reaction to local anesthetics: A case report. Am J Obstet Gynecol 2001;185:1253–4. 17. Stannard L, Bellis A. Maternal anaphylactic reaction to a general anaesthetic at emergency caesarean section for fetal bradycardia. Br J Obstet Gynaecol 2001;108:539–40. 18. Levy JH, Yegin A. Anaphylaxis. What is monitored to make a diagnosis? How is therapy monitored? Anesthesiol Clin North America 2001;19:705–15. 19. Drain KL, Volcheck GW. Preventing and managing druginduced anaphylaxis. Drug Saf 2001;24:843–53. 20. Heinly TL, Lieberman P. Anaphylaxis in pregnancy. Immunol Allergy Clin North America 2000;20:831. 21. Edmondson WC, Skilton RWH. Anaphylaxis in pregnancy—The right treatment? Anaesthesia 1994;49:454–5. 22. Adamsons K, Mueller-Heubach E, Myers RE. Production of fetal asphyxia in the rhesus monkey by administration of catecholamines to the mother. Am J Obstet Gynecol 1971;109:248–62. 23. Greiss FC Jr. Differential reactivity of the myoendometrial and placental vasculatures: Adrenergic responses. Am J Obstet Gynecol 1972;112:20–30. Received October 22, 2002. Received in revised form January 6, 2003. Accepted January 23, 2003.
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Anaphylaxis in Labor
1335