- Email: [email protected]
Autoimmune progesterone dermatitis in a parturient for emergency caesarean section
International Journal of Obstetric Anesthesia (2004) 13, 275–278 Ó 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2004.03.003
CASE REPORT
Autoimmune progesterone dermatitis in a parturient for emergency caesarean section J. O’Rourke, N. Khawaja, J. Loughrey, P. McKenna The Departments of Anaesthesia and Obstetrics, The Rotunda Hospital, Dublin, Ireland SUMMARY. A parturient with a 14-year history of autoimmune progesterone dermatitis presented in labour at 36 weeks’ gestation. She had suffered recurrent episodes of angioedema over a long period and had been scheduled for elective caesarean hysterectomy and bilateral oophorectomy at 37 weeks’ gestation. In most cases surgical oophorectomy provides prolonged relief from the recurrent angioedema and dermatological manifestations that are typical of autoimmune progesterone dermatitis. Spinal anaesthesia was chosen in order to avoid airway manipulation, a factor frequently implicated in the development of angioedema. Delivery was uneventful and the obstetricians proceeded to hysterectomy and oophorectomy. Forty minutes after delivery the patient experienced an attack of angioedema, she was markedly hypotensive and was given fluids, ephedrine and phenylephrine with good effect. As she remained normotensive, she was given intramuscular rather than intravenous epinephrine to provide a slower release. She recovered well and stabilised without the need for intubation or ventilation. This case reinforces the rationale for regional anaesthesia in these patients and demonstrates how intramuscular epinephrine contributed towards a positive outcome. Ó 2004 Elsevier Ltd. All rights reserved. Keywords: Autoimmune progesterone dermatitis; Cyclic anaphylaxis; Pregnancy
173 cm tall, weighed 105 kg and had an estimated body mass index of 35 kg/m2 (normal: 26-29). She was Cushingoid and markedly obese. Her past medical history included polycystic ovary disease and a 14-year history of autoimmune progesterone dermatitis. This was diagnosed clinically by the typical cyclic dermatological exacerbations coincident with the luteal phase of her menstrual cycle, together with a positive intradermal skin reaction to aqueous progesterone. Immunological analysis also revealed the presence of anti-progesterone antibodies. She had developed angioedema on three occasions within the previous year. On each occasion she described a prodromal period where she had complained of a lump in her throat followed shortly after by shortness of breath and generalised swelling. Each episode necessitated the use of an epinephrine self-administration syringe (Epipen 0.3 mg subcutaneously). Her medications included prednisolone (Deltacortril enteric) 20 mg daily, chlorpheniramine 24 mg daily and epinephrine for subcutaneous injection 0.3 mg as needed. Therapy for her autoimmune progesterone dermatitis had previously included antihistamines, systemic corticosteroids, luteinising hormone releasing hormone (LHRH) agonists, danazol and tamoxifen.
INTRODUCTION Autoimmune progesterone dermatitis is a rare cyclic premenstrual condition characterised by a rash and recurrent angioneurotic oedema. Characteristic periodic exacerbations have earned it the alternative title “cyclic anaphylaxis.” We describe the first such case of a parturient who developed intraoperative angioedema during caesarean hysterectomy.
CASE REPORT A 37-year-old woman, para 1 gravida 2, presented to the obstetric service at 12 weeks’ gestation having become pregnant with the aid of clomiphene. She was
Accepted March 2004 Dr. James O’Rourke, Specialist Registrar in Anaesthesia; Dr. John Loughrey, Consultant Anaesthetist; Dr. Naveed Khawaja, Specialist Registrar in Obstetrics; Dr. Peter McKenna, Consultant Obstetrician, The Rotunda Hospital, Dublin, Ireland. Correspondence to: Dr. James O’Rourke, No. 38A Grace Park Road, Drumcondra, Dublin 9, Ireland. Tel.: +11 353 18844622/86 8761117. E-mail: [email protected], [email protected] 275
276 International Journal of Obstetric Anesthesia In view of the chronicity of the condition in this woman and following a period of counselling, it was decided to perform a hysterectomy and oophorectomy at the time of caesarean section. Elective caesarean hysterectomy and bilateral oophorectomy were planned at 37 weeks’ gestation. Her obstetric course was marked by recurrent short-lived urticarial reactions necessitating increasing doses of corticosteroids with steroid therapy peaking at 80 mg of prednisolone per day in the third trimester. She presented in labour 5 days before the planned delivery date with a cervical dilatation of 3 cm. She was experiencing contractions every 5 min and was in significant distress. Following premedication with hydrocortisone 200 mg, chlorpheniramine 20 mg and 0.3 M sodium citrate 30 mL orally, a 600-mL fluid bolus of compound sodium lactate solution was administered and an arterial line sited. Spinal anaesthesia was instituted with hyperbaric bupivacaine 15 mg and preservative-free morphine 100 lg via a 27-gauge pencil-point needle at L2/3 in the sitting position. Block of pinprick sensation to T4 and a dense lower-limb motor block were demonstrated. Surgery proceeded uneventfully and a 4.3-kg male infant was delivered with Apgar scores of 8 and 10 at 1 and 5 min respectively. Intra-operatively, the blood pressure remained fairly stable, falling from an initial mean arterial pressure (MAP) of 75 mmHg to 61 mmHg and remaining between 50 and 65 mmHg with boluses of ephedrine and fluids. Her heart rate varied from 110 to 120 beats/min throughout and her oxygen saturation remained at 100% on 40% supplemental oxygen. In total, she was given 2400 mL of crystalloid, 18 mg of ephedrine, Syntocinon 10 units and co-amoxiclav 1.2 g. Blood loss was estimated at 600 mL. The operation was concluded 40 min after delivery of the baby, but as the surgeon was closing the skin, the patient complained of a lump in her throat and shortness of breath. She had become markedly erythematous with pronounced facial oedema and her systolic blood pressure fell precipitously to 57 mmHg (MAP 33 mmHg) and her heart rate rose to 125 beats/min. Ephedrine 6 mg and phenylephrine 50 lg were administered, resulting in an immediate normalisation of her blood pressure to 110 mmHg systolic, MAP 70 mmHg. Epinephrine 1 mg was given intramuscularly and although the patient remained erythematous, she improved symptomatically and remained normotensive. When the surgical drapes were removed the full extent of the widespread urticaria could be appreciated. A femoral central venous line was inserted; this site was chosen due to the oedema of the head and neck together with dyspnoea and marked obesity. She was given an epinephrine infusion at 5 lg/min and was monitored in the high dependency unit. Analgesia was
provided with a morphine patient controlled analgesia (PCA) pump and regular paracetamol. The patient had tolerated morphine well in the past, so intrathecal morphine and a morphine PCA were chosen despite their associated histamine-releasing potential. The patient had no further sequelae and was discharged home on tapering doses of steroids eight days post partum. At follow-up her skin lesions had markedly improved and to date she has not had any further episodes of angioedema.
DISCUSSION Autoimmune progesterone dermatitis is characterised by luteal-phase exacerbations during the menstrual cycle. In mild cases there may be urticaria with a pruritic rash that may resemble erythema multiforme. The typical lesions are oedematous papules with two to three symmetrical concentric rings. In severe cases, recurrent angioedema may lead to laryngeal oedema resulting in significant morbidity.1 Autoimmune progesterone dermatitis may be diagnosed on the basis of the cyclic eruptions together with demonstration of anti-progesterone antibodies. Chronic urticaria and angioedema are manifestations of a number of conditions. Other autoimmune co-morbidities to consider in these patients include thyroid disease, Addison’s disease, diabetes, pernicious anaemia and vitiligo.2 Five percent of patients with chronic urticaria have an underlying vasculitic disorder, such as systemic lupus erythematosus, Sjçgren’s syndrome or cryoglobulinaemia (Tables 1 and 2). The cause of the angioedema and urticaria may remain elusive despite extensive investigations; a recent review failed to identify a precipitating cause in more than 60% of patients.3 The advice of a specialist immunologist should be sought in all patients with recurrent angioedema as the aetiology carries important management implications. The natural history of autoimmune progesterone dermatitis during pregnancy may vary, some patients report an improvement whilst the condition is worsened significantly in others.5 Autoimmune progesterone dermatitis may present for the first time during pregnancy and the rate of spontaneous abortion may be increased.4 Autoimmune progesterone dermatitis is difficult to treat; the evidence for this lies in the large number of treatments available, reflecting the poor efficacy of any individual therapy. It is prudent to avoid precipitants and medications known to cause histamine release. First-line therapies include the H1 antihistamines, while the addition of H2-receptor antagonists has been shown to speed the resolution of urticaria and angioedema.5 The tricyclic antidepressant doxepin also inhibits
Anaesthesia in autoimmune progesterone dermatitis 277 Table 1. Aetiology of angioedema Cause
Details
Percent of all cases
Drug induced
3%
Hereditary
Autosomal dominant Chromosome 11 C 1 esterase inhibitor deficiency
2% of total cases, Prevalence 1/50 000-1/150 000 of the population
Acquired
<1% - extremely rare
Autoimmune
Anti C1 esterase inhibitor autoantibodies Autoimmune progesterone dermatitis
Aspirin, NSAIDs ACE inhibitors {0.1-0.2%} Oral contraceptives Thrombolytic agents
Lymphoproliferative disorders Multiple myeloma Waldenstrçm’s macroglobulinaemia Myelofibrosis
Idiopathic
90% of all cases
Table 2. Aetiology of chronic urticaria Cause
Details
Percent of all cases
Physical
Solar Cholinergic, temperature Delayed pressure Vibration
35%
Autoimmune
Thyroiditis Addison’s disease Diabetes Vitiligo
25%
Urticarial vasculitis
Systemic lupus erythematosus Sjçgren’s syndrome Cryoglobulinaemia
Infection related Pseudoallergic Idiopathic
5%
2% 2% 30%
histamine release and has proved useful in some patients. Systemic corticosteroids are used as second-line agents. Agents that decrease serum progesterone and inhibit ovulation usually results in symptomatic improvement; varying degrees of success are reported with agents such as the LHRH agonists, androgens such as danazol, and the anti-oestrogen tamoxifen. Finally, autoimmune progesterone dermatitis has been successfully treated with oophorectomy with full resolution of symptoms in many patients.4,6–8 Chronic urticaria and angioedema are features of a number of other conditions apart from autoimmune progesterone dermatitis and authors have reported good results with cyclosporine. Other immunosuppressants such as azathioprine and methotrexate may have a future role. A growing body of evidence advocates the use of other modalities such as plasmapheresis and intravenous immunoglobulin.9,10
A history of angioedema presents the danger of laryngeal oedema, which may be triggered as a result of airway manipulation; most authors therefore advocate local or regional anaesthesia in these patients.11 Spinal anaesthesia was chosen in our case for its reliability and speed. One could argue that in an obese patient who was also scheduled for hysterectomy and oophorectomy an epidural catheter, alone or as part of a combined spinal epidural technique, would provide for a prolonged surgical procedure. However, as expected, the procedure was completed within the time-frame of the spinal anaesthetic. Intraoperative angioedema is the presenting feature of anaphylaxis in 88% of all cases. In this case intravenous epinephrine was considered but as the pressor effects of the phenylephrine and ephedrine had resulted in normotension, a depot intramuscular injection was chosen, ensuring a slower release to treat the angioedema. The intramuscular route is advocated for its safety by many authors.12,13 This approach has its merits, avoiding potential toxic effects of bolus intravenous epinephrine.14 This case highlights the importance of preoperative evaluation and planning when dealing with a patient who suffers from recurrent angioedema. In patients with hereditary angioedema and certain forms of drug-induced angioedema, the administration of C1-esterase inhibitor concentrate or fresh frozen plasma may prove more effective than epinephrine in the acute episode.15,16 Preoperative plasmapheresis or intravenous immunoglobulin may prove beneficial in patients with chronic urticaria refractory to other treatments. While anaphylaxis treatment is standard in the acute setting, other therapies are ideally planned in advance so that the patient’s condition may be optimised before she presents for surgery.
278 International Journal of Obstetric Anesthesia REFERENCES 1. Hertzberg A J, Strohmeyer C R, Cirillo-Hyland V. Autoimmune progesterone dermatitis. J Am Acad Dermatol 1995; 2: 333–338. 2. Heymann W R. Chronic urticaria and angioedema associated with thyroid autoimmunity: review and therapeutic implications. J Am Acad Dermatol 1999; 40: 229–232. 3. Nettis E, Pannafino A, Aprile C D, Ferrannini A, Tursi A. Clinical and aetiological aspects in urticaria and angioedema. Br J Dermatol 2003; 148: 501–506. 4. Snyder J L, Krishnaswamy G. Autoimmune progesterone dermatitis and its manifestation as anaphylaxis: a case report and literature review. Ann Allergy Asthma Immunol 2003; 90: 469–477. 5. Lin R Y, Curry A, Pesola G R, et al. Improved outcomes in patients with allergic syndromes who are treated with combined H1 and H2 antagonists. Ann Emerg Med 2000; 36: 462–468. 6. Moody B R, Schatten S. Autoimmune progesterone dermatitis; onset in a woman without previous exogenous progesterone exposure. Mishell D R, editor. Yearbook of Obstetrics, Gynaecology and Women’s Health. St. Louis, MO: Mosby Inc., 1999: 12. 7. Rodenas J M, Herranz M T, Terchedor J. Autoimmune progesterone dermatitis: treatment with oophorectomy. Br J Dermatol 1998; 139: 508–511.
8. Mutasim D F, Baumbach J L. Bullous autoimmune oestrogen dermatitis. J Am Acad Dermatol 2003; 49: 130–132. 9. Kaplan A P. Chronic urticaria and angioedema. N Engl J Med 2002; 346: 175–179. 10. Grattan C E H, Sabroe E H, Greaves R A. Chronic urticaria. J Am Acad Dermatol 2002; 46: 645–657. 11. Poppers P J. Anaesthetic implications of hereditary angioneurotic oedema. Can J Anaesth 1987; 34: 76–78. 12. Hughes G, Fitzharris P. Managing acute anaphylaxis (new guidelines emphasising the importance of intramuscular adrenaline): editorial view. Br Med J 1999; 319: 1–2. 13. Douglas J A. Adrenaline and non-life threatening allergic reactions (intramuscular adrenaline is safe) letter. Br Med J 2003; 327: 226–227. 14. Johnston S L, Unsworth J, Gompets M M. Adrenaline given outside the context of life threatening reactions. Br Med J 2003; 326: 589–590. 15. Karim M Y, Masood A. Fresh frozen plasma as a treatment for life threatening ACE inhibitor angioedema. J Allergy Clin Immunol 2002; 109: 370–371. 16. Galan H L, Reedy M B, Starr J, Knight A B. Fresh frozen plasma prophylaxis for hereditary angioedema during pregnancy. A case report. J Reprod Med 1996; 41: 541–544.
CASE REPORT
Autoimmune progesterone dermatitis in a parturient for emergency caesarean section J. O’Rourke, N. Khawaja, J. Loughrey, P. McKenna The Departments of Anaesthesia and Obstetrics, The Rotunda Hospital, Dublin, Ireland SUMMARY. A parturient with a 14-year history of autoimmune progesterone dermatitis presented in labour at 36 weeks’ gestation. She had suffered recurrent episodes of angioedema over a long period and had been scheduled for elective caesarean hysterectomy and bilateral oophorectomy at 37 weeks’ gestation. In most cases surgical oophorectomy provides prolonged relief from the recurrent angioedema and dermatological manifestations that are typical of autoimmune progesterone dermatitis. Spinal anaesthesia was chosen in order to avoid airway manipulation, a factor frequently implicated in the development of angioedema. Delivery was uneventful and the obstetricians proceeded to hysterectomy and oophorectomy. Forty minutes after delivery the patient experienced an attack of angioedema, she was markedly hypotensive and was given fluids, ephedrine and phenylephrine with good effect. As she remained normotensive, she was given intramuscular rather than intravenous epinephrine to provide a slower release. She recovered well and stabilised without the need for intubation or ventilation. This case reinforces the rationale for regional anaesthesia in these patients and demonstrates how intramuscular epinephrine contributed towards a positive outcome. Ó 2004 Elsevier Ltd. All rights reserved. Keywords: Autoimmune progesterone dermatitis; Cyclic anaphylaxis; Pregnancy
173 cm tall, weighed 105 kg and had an estimated body mass index of 35 kg/m2 (normal: 26-29). She was Cushingoid and markedly obese. Her past medical history included polycystic ovary disease and a 14-year history of autoimmune progesterone dermatitis. This was diagnosed clinically by the typical cyclic dermatological exacerbations coincident with the luteal phase of her menstrual cycle, together with a positive intradermal skin reaction to aqueous progesterone. Immunological analysis also revealed the presence of anti-progesterone antibodies. She had developed angioedema on three occasions within the previous year. On each occasion she described a prodromal period where she had complained of a lump in her throat followed shortly after by shortness of breath and generalised swelling. Each episode necessitated the use of an epinephrine self-administration syringe (Epipen 0.3 mg subcutaneously). Her medications included prednisolone (Deltacortril enteric) 20 mg daily, chlorpheniramine 24 mg daily and epinephrine for subcutaneous injection 0.3 mg as needed. Therapy for her autoimmune progesterone dermatitis had previously included antihistamines, systemic corticosteroids, luteinising hormone releasing hormone (LHRH) agonists, danazol and tamoxifen.
INTRODUCTION Autoimmune progesterone dermatitis is a rare cyclic premenstrual condition characterised by a rash and recurrent angioneurotic oedema. Characteristic periodic exacerbations have earned it the alternative title “cyclic anaphylaxis.” We describe the first such case of a parturient who developed intraoperative angioedema during caesarean hysterectomy.
CASE REPORT A 37-year-old woman, para 1 gravida 2, presented to the obstetric service at 12 weeks’ gestation having become pregnant with the aid of clomiphene. She was
Accepted March 2004 Dr. James O’Rourke, Specialist Registrar in Anaesthesia; Dr. John Loughrey, Consultant Anaesthetist; Dr. Naveed Khawaja, Specialist Registrar in Obstetrics; Dr. Peter McKenna, Consultant Obstetrician, The Rotunda Hospital, Dublin, Ireland. Correspondence to: Dr. James O’Rourke, No. 38A Grace Park Road, Drumcondra, Dublin 9, Ireland. Tel.: +11 353 18844622/86 8761117. E-mail: [email protected], [email protected] 275
276 International Journal of Obstetric Anesthesia In view of the chronicity of the condition in this woman and following a period of counselling, it was decided to perform a hysterectomy and oophorectomy at the time of caesarean section. Elective caesarean hysterectomy and bilateral oophorectomy were planned at 37 weeks’ gestation. Her obstetric course was marked by recurrent short-lived urticarial reactions necessitating increasing doses of corticosteroids with steroid therapy peaking at 80 mg of prednisolone per day in the third trimester. She presented in labour 5 days before the planned delivery date with a cervical dilatation of 3 cm. She was experiencing contractions every 5 min and was in significant distress. Following premedication with hydrocortisone 200 mg, chlorpheniramine 20 mg and 0.3 M sodium citrate 30 mL orally, a 600-mL fluid bolus of compound sodium lactate solution was administered and an arterial line sited. Spinal anaesthesia was instituted with hyperbaric bupivacaine 15 mg and preservative-free morphine 100 lg via a 27-gauge pencil-point needle at L2/3 in the sitting position. Block of pinprick sensation to T4 and a dense lower-limb motor block were demonstrated. Surgery proceeded uneventfully and a 4.3-kg male infant was delivered with Apgar scores of 8 and 10 at 1 and 5 min respectively. Intra-operatively, the blood pressure remained fairly stable, falling from an initial mean arterial pressure (MAP) of 75 mmHg to 61 mmHg and remaining between 50 and 65 mmHg with boluses of ephedrine and fluids. Her heart rate varied from 110 to 120 beats/min throughout and her oxygen saturation remained at 100% on 40% supplemental oxygen. In total, she was given 2400 mL of crystalloid, 18 mg of ephedrine, Syntocinon 10 units and co-amoxiclav 1.2 g. Blood loss was estimated at 600 mL. The operation was concluded 40 min after delivery of the baby, but as the surgeon was closing the skin, the patient complained of a lump in her throat and shortness of breath. She had become markedly erythematous with pronounced facial oedema and her systolic blood pressure fell precipitously to 57 mmHg (MAP 33 mmHg) and her heart rate rose to 125 beats/min. Ephedrine 6 mg and phenylephrine 50 lg were administered, resulting in an immediate normalisation of her blood pressure to 110 mmHg systolic, MAP 70 mmHg. Epinephrine 1 mg was given intramuscularly and although the patient remained erythematous, she improved symptomatically and remained normotensive. When the surgical drapes were removed the full extent of the widespread urticaria could be appreciated. A femoral central venous line was inserted; this site was chosen due to the oedema of the head and neck together with dyspnoea and marked obesity. She was given an epinephrine infusion at 5 lg/min and was monitored in the high dependency unit. Analgesia was
provided with a morphine patient controlled analgesia (PCA) pump and regular paracetamol. The patient had tolerated morphine well in the past, so intrathecal morphine and a morphine PCA were chosen despite their associated histamine-releasing potential. The patient had no further sequelae and was discharged home on tapering doses of steroids eight days post partum. At follow-up her skin lesions had markedly improved and to date she has not had any further episodes of angioedema.
DISCUSSION Autoimmune progesterone dermatitis is characterised by luteal-phase exacerbations during the menstrual cycle. In mild cases there may be urticaria with a pruritic rash that may resemble erythema multiforme. The typical lesions are oedematous papules with two to three symmetrical concentric rings. In severe cases, recurrent angioedema may lead to laryngeal oedema resulting in significant morbidity.1 Autoimmune progesterone dermatitis may be diagnosed on the basis of the cyclic eruptions together with demonstration of anti-progesterone antibodies. Chronic urticaria and angioedema are manifestations of a number of conditions. Other autoimmune co-morbidities to consider in these patients include thyroid disease, Addison’s disease, diabetes, pernicious anaemia and vitiligo.2 Five percent of patients with chronic urticaria have an underlying vasculitic disorder, such as systemic lupus erythematosus, Sjçgren’s syndrome or cryoglobulinaemia (Tables 1 and 2). The cause of the angioedema and urticaria may remain elusive despite extensive investigations; a recent review failed to identify a precipitating cause in more than 60% of patients.3 The advice of a specialist immunologist should be sought in all patients with recurrent angioedema as the aetiology carries important management implications. The natural history of autoimmune progesterone dermatitis during pregnancy may vary, some patients report an improvement whilst the condition is worsened significantly in others.5 Autoimmune progesterone dermatitis may present for the first time during pregnancy and the rate of spontaneous abortion may be increased.4 Autoimmune progesterone dermatitis is difficult to treat; the evidence for this lies in the large number of treatments available, reflecting the poor efficacy of any individual therapy. It is prudent to avoid precipitants and medications known to cause histamine release. First-line therapies include the H1 antihistamines, while the addition of H2-receptor antagonists has been shown to speed the resolution of urticaria and angioedema.5 The tricyclic antidepressant doxepin also inhibits
Anaesthesia in autoimmune progesterone dermatitis 277 Table 1. Aetiology of angioedema Cause
Details
Percent of all cases
Drug induced
3%
Hereditary
Autosomal dominant Chromosome 11 C 1 esterase inhibitor deficiency
2% of total cases, Prevalence 1/50 000-1/150 000 of the population
Acquired
<1% - extremely rare
Autoimmune
Anti C1 esterase inhibitor autoantibodies Autoimmune progesterone dermatitis
Aspirin, NSAIDs ACE inhibitors {0.1-0.2%} Oral contraceptives Thrombolytic agents
Lymphoproliferative disorders Multiple myeloma Waldenstrçm’s macroglobulinaemia Myelofibrosis
Idiopathic
90% of all cases
Table 2. Aetiology of chronic urticaria Cause
Details
Percent of all cases
Physical
Solar Cholinergic, temperature Delayed pressure Vibration
35%
Autoimmune
Thyroiditis Addison’s disease Diabetes Vitiligo
25%
Urticarial vasculitis
Systemic lupus erythematosus Sjçgren’s syndrome Cryoglobulinaemia
Infection related Pseudoallergic Idiopathic
5%
2% 2% 30%
histamine release and has proved useful in some patients. Systemic corticosteroids are used as second-line agents. Agents that decrease serum progesterone and inhibit ovulation usually results in symptomatic improvement; varying degrees of success are reported with agents such as the LHRH agonists, androgens such as danazol, and the anti-oestrogen tamoxifen. Finally, autoimmune progesterone dermatitis has been successfully treated with oophorectomy with full resolution of symptoms in many patients.4,6–8 Chronic urticaria and angioedema are features of a number of other conditions apart from autoimmune progesterone dermatitis and authors have reported good results with cyclosporine. Other immunosuppressants such as azathioprine and methotrexate may have a future role. A growing body of evidence advocates the use of other modalities such as plasmapheresis and intravenous immunoglobulin.9,10
A history of angioedema presents the danger of laryngeal oedema, which may be triggered as a result of airway manipulation; most authors therefore advocate local or regional anaesthesia in these patients.11 Spinal anaesthesia was chosen in our case for its reliability and speed. One could argue that in an obese patient who was also scheduled for hysterectomy and oophorectomy an epidural catheter, alone or as part of a combined spinal epidural technique, would provide for a prolonged surgical procedure. However, as expected, the procedure was completed within the time-frame of the spinal anaesthetic. Intraoperative angioedema is the presenting feature of anaphylaxis in 88% of all cases. In this case intravenous epinephrine was considered but as the pressor effects of the phenylephrine and ephedrine had resulted in normotension, a depot intramuscular injection was chosen, ensuring a slower release to treat the angioedema. The intramuscular route is advocated for its safety by many authors.12,13 This approach has its merits, avoiding potential toxic effects of bolus intravenous epinephrine.14 This case highlights the importance of preoperative evaluation and planning when dealing with a patient who suffers from recurrent angioedema. In patients with hereditary angioedema and certain forms of drug-induced angioedema, the administration of C1-esterase inhibitor concentrate or fresh frozen plasma may prove more effective than epinephrine in the acute episode.15,16 Preoperative plasmapheresis or intravenous immunoglobulin may prove beneficial in patients with chronic urticaria refractory to other treatments. While anaphylaxis treatment is standard in the acute setting, other therapies are ideally planned in advance so that the patient’s condition may be optimised before she presents for surgery.
278 International Journal of Obstetric Anesthesia REFERENCES 1. Hertzberg A J, Strohmeyer C R, Cirillo-Hyland V. Autoimmune progesterone dermatitis. J Am Acad Dermatol 1995; 2: 333–338. 2. Heymann W R. Chronic urticaria and angioedema associated with thyroid autoimmunity: review and therapeutic implications. J Am Acad Dermatol 1999; 40: 229–232. 3. Nettis E, Pannafino A, Aprile C D, Ferrannini A, Tursi A. Clinical and aetiological aspects in urticaria and angioedema. Br J Dermatol 2003; 148: 501–506. 4. Snyder J L, Krishnaswamy G. Autoimmune progesterone dermatitis and its manifestation as anaphylaxis: a case report and literature review. Ann Allergy Asthma Immunol 2003; 90: 469–477. 5. Lin R Y, Curry A, Pesola G R, et al. Improved outcomes in patients with allergic syndromes who are treated with combined H1 and H2 antagonists. Ann Emerg Med 2000; 36: 462–468. 6. Moody B R, Schatten S. Autoimmune progesterone dermatitis; onset in a woman without previous exogenous progesterone exposure. Mishell D R, editor. Yearbook of Obstetrics, Gynaecology and Women’s Health. St. Louis, MO: Mosby Inc., 1999: 12. 7. Rodenas J M, Herranz M T, Terchedor J. Autoimmune progesterone dermatitis: treatment with oophorectomy. Br J Dermatol 1998; 139: 508–511.
8. Mutasim D F, Baumbach J L. Bullous autoimmune oestrogen dermatitis. J Am Acad Dermatol 2003; 49: 130–132. 9. Kaplan A P. Chronic urticaria and angioedema. N Engl J Med 2002; 346: 175–179. 10. Grattan C E H, Sabroe E H, Greaves R A. Chronic urticaria. J Am Acad Dermatol 2002; 46: 645–657. 11. Poppers P J. Anaesthetic implications of hereditary angioneurotic oedema. Can J Anaesth 1987; 34: 76–78. 12. Hughes G, Fitzharris P. Managing acute anaphylaxis (new guidelines emphasising the importance of intramuscular adrenaline): editorial view. Br Med J 1999; 319: 1–2. 13. Douglas J A. Adrenaline and non-life threatening allergic reactions (intramuscular adrenaline is safe) letter. Br Med J 2003; 327: 226–227. 14. Johnston S L, Unsworth J, Gompets M M. Adrenaline given outside the context of life threatening reactions. Br Med J 2003; 326: 589–590. 15. Karim M Y, Masood A. Fresh frozen plasma as a treatment for life threatening ACE inhibitor angioedema. J Allergy Clin Immunol 2002; 109: 370–371. 16. Galan H L, Reedy M B, Starr J, Knight A B. Fresh frozen plasma prophylaxis for hereditary angioedema during pregnancy. A case report. J Reprod Med 1996; 41: 541–544.