80
Perioperative Management of a Case of Severe Peripartum Cardiomyopathy G. BROWN,· M. O'LEARy,t I. DOUGLASt AND R. HERKES§ Intensive Care Unit, Royal Prince Alfred Hospital, Sydney, New South Wales Key Words: INTENSIVE CARE: cardiomyopathy, peripartum
Peripartum cardiomyopathy was first described by Ritchie in 1849. 1 Since then it has become a recognised clinical entity and occurs in 0.005% of caucasian deliveries. A pregnant woman can develop any type of cardiomyopathy seen in the non-pregnant state, but there appears to be a distinct entity peculiar to pregnancy2 which Hughes et al. 3 have defined as 'primary myocardial disease occurring for the first time in the last trimester of pregnancy or the first trimester after delivery in the absence of preeclamptic toxaemia, hypertension or any other known heart disease'. We present the anaesthetic and intensive care management of a patient with peripartum cardiomyopathy presenting for caesarean section. CASE REPORT Preoperative management A thirty-year-old woman, parity 2012, at 33 weeks' gestation presented to Camden District Hospital with dyspnoea and orthopnoea. Her first pregnancy in 1984 had been complicated by hypertensive disease of pregnancy. Her second pregnancy was uncomplicated. She had displayed mild hypertension during this pregnancy with the highest reading 145/90 mmHg at 31 weeks but had neither proteinuria nor oedema at any of her regular antenatal visits. She was on no regular medications. On admission to Camden Hospital, clinical examination revealed an occasional wheeze, chest X-ray was clear and FEVllVC was 2.21/3.11. A diagnosis of bronchospasm due to bronchitis was made and she was treated with nebulised salbutamol and intravenous amoxicillin, and discharged after six days. ·M.B., B.S., Senior Registrar, ICU. tM.R.C.S., L.R.C.P., Registrar, ICU. iF.F.A.R.A.C.S., Deputy Director, Department of Anaesthetics. §F.R.A.C.P., Director, ICU. Address for Reprints: Dr. G. Brown E61CU, Royal Prince Alfred Hospital, Missenden Road, Camperdown, New South Wales 2050, Australia. Accepted for publication August 23, 1991
The patient was readmitted four days later at 34 + weeks gestation with dyspnoea at rest and orthopnoea. Her ECG on admission showed a sinus tachycardia of l50/min (there were no ST, T or QRS abnormalities) and a chest X-ray showed normal cardiac size but interstitial oedema. A diagnosis of cardiac failure was made. 'The patient was transferred to our institution fifteen days after her initial presentation. On admission she was afebrile with a resting sinus tachycardia of l40/min, blood pressure 110/80 mmHg, jugular venous pulse was raised to the jaw and there was pitting oedema to the knees. Auscultation revealed a third heart sound, a soft pan-systolic murmur at the apex and bi-basal pulmonary crepitations. She was treated with digoxin, frusemide, potassium supplements, subcutaneous heparin, and was placed on a 1200 ml/day fluid restriction. Haematologic and biochemical parameters were within normal limits, apart from a compensated mild metabolic acidosis (pH = 7.40, BE = -5, PaCo2 = 29 mmHg, P ao 2 = 104 on room air), an elevated plasma uric acid concentration (0.66 mmol/l) and tnidly deranged liver function tests (AST = 69 V/I, ALT = 65 V/I and GGT = 58 V/I). At no stage was the creatine kinase MB isoenzyme level elevated. An echocardiogram displayed a grossly dilated, diffusely hypokinetic left ventricle with fractional shortening of 7%. There was no hypertrophy. Viral titres (influenza A and Band enteroviruses) were negative. Cardiolipin antibody, ANA and DNA antibody titres were all negative. Thyroid function tests were normal. Obstetric examination including cardiotocograph and ultrasound were unremarkable. Betamethasone was administered to promote foetal lung maturity. A provisional diagnosis of peripartum cardiomyopathy was made. Operative management An elective caesarean section was performed five days later (Day 0). We elected to use a general anaesthetic, as the patient's cardiac reserve was Anaesthesia and Intensive Care, Vol. 20. No. I. February, 1992
81
CASE REPORT TABLE 1 Operative data
Pre-induction Post-induction Delivery Skin closed
Cl
MAP
MPA
PAWP
Sv02
SVR
PVR
1.8 1.8 1.4 1.6
101 100 108 80
33 35 25 42
25 22 18 24
61 51 53 50
1936 1680 2576 1689
178 262 181 408
Description of terms and units: Cl = cardiac index (IIminlm2) MAP = mean arterial blood pressure (mmHg) MPA = mean pulmonary artery pressure (mmHg) P AWP = pulmonary artery wedge pressure (mmHg) Sv0 2 = mixed venous oxygen saturation (%) SVR = systemic vascular resistance (dyn.s.cm- 5) PVR = pulmonary vascular resistance (dyn.s.cm- 5)
considered so limited that any reduction in systemic vascular resistance due to epidural blockade could have been catastrophic. The patient was premedicated with morphine 10 mglM. Prior to induction, secure intravenous access and full monitoring were instituted, including ECG, pulse oximetry, invasive arterial pressure monitoring and an oximetric/thermodilution Swan-Ganz catheter. During the insertion of the lines 4% lignocaine 7 ml was nebulised via an oxygen facemask in an attempt to attenuate the stress response to laryngoscopy and tracheal intubation. The patient was pre-oxygenated for five minutes. During this period fentanyl was administered (with gentle application of cricoid pressure) in 50 )lg increments up to a dose of200 )lg (2 )lglkg). Sodium thiopentone (1 % solution) was then given in 10 mg
increments. The endpoint for induction was lack of eye-opening to command. A total of 70 mg of thiopentone was given. Muscle relaxation was then achieved with suxamethonium 100 mg. Laryngoscopy and intubation were uneventful. Muscle relaxation was continued with atracurium, and anaesthesia maintained with 100% oxygen and 1% isoflurane. Four units of oxytocinon were given after delivery and uterine contraction was adequate. Estimated blood loss was 600 ml and replacement consisted of 400 ml of normal saline. A further 150 )lg of fentanyl was given at the end of the procedure and the patient was transferred to the ICV. The haemodynamic changes throughout the different phases of the procedure are displayed in Table 1. A female infant weighing 2115 g was delivered. Apgar scores were 2, 6 and 10 at 1, 5 and 10 minutes
TABLE 2 Postoperative data
Admission +90 min + 3 hrs + 12 hrs + 24 hrs
Cl
MAP
MPA
PAWP
SVR
PVR
D02
1.7 2.9 3.6 4.2 4.4
90 76 71 86 82
47 24 28 28 30
20 18 20 16 14
1689 810 624 623 550
570 74 82 121 131
747 1285 1647 1945 2115
Description of terms and units: Cl = cardiac index (IIminlm2) MAP = mean arterial blood pressure (mmHg) MPA = mean pulmonary artery pressure (mmHg) P AWP = pulmonary artery wedge pressure (mmHg) SVR = systemic vascular resistance (dyn.s.cm- 5) PVR = pulmonary vascular resistance (dyn.s.cm- 5) D02 = oxygen delivery (mllmin) Anaesthesia and Intensive Care. Vol. 20. No. 1, February. 1992
82
G.
BROWN ET AL.
respectively. Artificial ventilation was required but the infant established her own ventilation after naloxone and was extubated. She was discharged from the nursery after one day and has subsequently progressed well. Course in intensive care On admission to the ICU the patient had a sinus tachycardia of 140/min and blood pressure of 120/80 mmHg. Arterial blood gases demonstrated a P02 of 70 mmHg on an inspired oxygen of 100%. A chest X-ray showed cardiomegaly (even allowing for the AP projection) and gross pulmonary oedema. Presenting haemodynamic parameters are shown in Table 2 and on the basis of this data, dobutamine was commenced at 5 l1g/kg/min and dopamine at low dose, 3 l1g/kg/min. With this therapy both cardiac function and pulmonary gas exchange improved markedly (Table 2). A repeat chest X-ray confirmed reduction in heart size and clearing of the lung oedema. Formal anticoagulation with heparin was commenced several hours postoperatively. Improvement continued such that she was extubated on Day 2. On Day 3 a regular dose of captopril 2 mg bd was commenced and the dobutamine was carefully weaned. A gated heart pool scan demonstrated a left ventricular ejection fraction of 22%. On Day 4 the dopamine was ceased and the captropril dose was increased to 5 mg bd. The patient was discharged from the ICU on day 5. DISCUSSION
This patient satisfies the criteria of Hughes et al. for the diagnosis of peripartum cardiomyopathy. 3 As in this case, the haemodynamic manifestations of this condition are usually a low output, congestive pattern. 4 Recently, however, high output failure with well preserved ventricular function has been reported, suggesting that it is not an homogenous entity.s The fact that it is a specific entity at all is still open to some debate. Because the pathogenesis is not known, it has been suggested that the haemodynamic changes of pregnancy unmask a pre-existing cardiomyopathy. 6 Aetiological factors suggested by Hull et al. as early as 1937 7 were glomerulonephritis, toxaemia, beri-beri or other nutritional deficiencies or an infective process. None has subsequently been substantiated. Acute hypertensive heart failure has been proposed but as in our patient, hypertension is usually transient and not severe. 8 A toxic or immunological mechanism seems most likely but these again have not been proven. There have, however, been reported findings of anti-heart antibodies, 9 and several cases of myocarditis-induced peripartum cardiomyopathy have responded very well to
immunosuppressive therapy. The myocardial biopsy findings are, however, non-specific, involving lymphocytic infiltrate, myonecrosis, fibrosis and interstitial oedema. lo This is not supportive of a distinct immuno-pathological process. Cardiomyopathy may be seen in association with the gestosis syndrome, a syndrome encompassing the conditions known as preeclamptic toxaemia, pregnancy-induced hypertension, HELLP syndrome (hypertension, elevated liver enzymes and low platelets) and others. Electrocardiographic abnormalities are present in practically all patients with toxaemia of pregnancy, and cardiac arrhythmias may occur. Acute congestive cardiac failure may develop in these cases either due to excessive fluid therapy in the presence of impaired renal or cardiac function, or due to the development of a cardiomyopathy. 2 Despite her mildly elevated liver enzymes and raised uric acid concentration, we consider that this patient does not fit into this category since she only had hypertension early in the pregnancy, not requiring therapy, never had proteinuria, had a normal platelet count, and except for tachycardia a normal ECG. The prognosis of peripartum cardiomyopathy depends on whether the heart size returns to normal within six months of onset of the disease. 11 Patients who have cardiomegaly of greater than six months' duration have a very poor outlook without transplantation. The mortality in this group appears to be of the order of 75% with an average period of survival of 29 months l2 to 80% with an average survival of 4.7 years.13 These figures are similar to those for the other congestive cardiomyopathies. 14 The most frequent cause of death is congestive cardiac failure, complicated by pulmonary and systemic emboli.11 We elected to commence full heparinisation within 24 hours of surgery because we considered the risk of embolism to be sufficiently great to offset any risk of bleeding with anticoagulation so close to the time of surgery. If heart size returns to normal the prognosis is quite good. Twelve out of fourteen such patients followed up for an average of 10.7 years were found to return to a good level of function. The two deaths were from non-cardiac causes. I 1 The preoperative management of our patient was aimed at excluding any reversible cause, controlling her heart failure and attempting to optimize her condition for surgery with bed rest, fluid restriction, digitalis and diuretics. It was generally agreed that real improvement in her cardiac status would only be brought about by delivery via caesarean section. This patient presented quite an anaesthetic challenge due to her low cardiac output. However, Anaesthesia and Intensive Care, Vo!. 20, No. I, February, 1992
83
CASE REPORT
she tolerated a careful general anaesthetic well (Table 1). The cardiac index remained remarkably constant. The sinus tachycardia persisted but heart rate remained constant and there were no arrhythmias on intubation. The drop in pulmonary artery pressures related to delivery of the child was probably related to the small blood loss occurring at this time. It did not correspond to any change in cardiac output. We elected not to intervene with inotropes intraoperatively. With the institution of low-dose inotropic support guided by invasive haemodynamic monitoring, there was progressive postoperative improvement in cardiac function, confirmed both on clinical examination and by the radiological changes. This is also well demonstrated by the haemodynamic data in Table 2. The patient continued to improve clinically following discharge from ICV; however, a repeated gated heart pool scan three weeks later revealed a left ventricular ejection fraction unchanged from the day before ICV discharge, at 22%. This case is presented as an example of the perioperative management of a woman with severe heart failure presenting for caesarean section. REFERENCES
1. Ritchie C. Clinical contributions to the pathology, diagnosis, and treatment of certain chronic diseases of the heart. Edinburg Surg J 1849; 12:333. 2. Burch G. Heart disease and pregnancy. Am Heart J 1977; 93,1:104-116. 3. Hughes R, Kapur P, Sutton G, Honey M. A case of fatal peri-partum cardiomyopathy. Br Heart J 1970; 32:272-276.
4. Homans D. Current Concepts Peripartum Cardiomyopathy. N Eng J Med 1985; 312,22:1432-1437. 5. Marin-Neto J, Maciel B, Teran Urbanetz L et al. High output failure in patients with peripartum cardiomyopathy: A comparative study with dilated cardiomyopathy. Am Heart J 1991; 1,1:134-140. 6. de Swiet M. Heart disease in pregnancy. In: Michael de Swiet ed. Medical Disorders in Obstetric Practice, 1st Ed. Blackwell Scientific Publications, Melbourne 1984; 116-118, 137-138. 7. Hull E, Hidden E. Postpartal heart failure. South Med J 1938; 31 :265. 8. Davidson N, Parry EH. The etiology of peripartum heart failure. Am Heart J 1979; 97,4:535-536. 9. Kirsner A, Hess E, Fowler N. Immunological findings in idiopathic cardiomyopathy: a prospective serial study. Am Heart J 1973; 86:625. 10. Melvin K, Richardson P, Olsen E, Daly K, Jackson G. Peripartum cardiomyopathy due to myocarditis. N Engl J Med 1982; 307,12:731-734. 11. Demkakis J, Rahimtoo1a S, Sutton G. Natural course of peripartum cardiomyopathy. Circulation 1971; 44:1053-1061. 12. Walsh J, Burch G, Black W, Ferrans V, Hibbs R. Idiopathic myocardiopathy of the puerperium (postpartal heart disease). Circulation 1965; 32-1913. Demkakis J, Rahimtoola S. Peripartum cardiomyopathy. Circulation 1971; 44:964-968. 14. Wynne J, Braunwald E. The cardiomyopathies and myocarditides. In: Petersdorf R, Adams R, Braunwald E, Isselbacher K, Martin J, Wilson J. Harrison's Principles of Internal Medicine, 10th Ed. McGraw-Hill Book Company, Sydney 1982; 1450-1451.
Severe Localised Bronchospasm In A Young Asthmatic Patient During Thoracotomy A. w. Y. CHUA* AND N. SYMONSt Department of Anaesthesia, Royal Prince Alfred Hospital, Sydney, New South Wales Key Words: ANAESTHESIA COMPLICATIONS: asthma, bronchospasm
Patients with severe asthma may present a difficult challenge to any anaesthetist. Here we report an intraoperative management problem occurring during a thoracotomy in a young asthmatic patient. 'M.B.B.S., Anaesthetic Registrar. tF.F.A.R.A.C.S., Visiting Anaesthetist. Address for Reprints: Dr. N. Symons, Department of Anaesthesia, Royal Prince Alfred Hospital, Missenden Road, Camperdown, N.S.W. 2050, Australia. Accepted for publication August 20, 1991 Anaesthesia and Intensive Care. Vol. 20. No. I. February. 1992
CASE REPORT
A 26-year-old woman presented for elective right thoracotomy for excision of a superior mediastinal tumour. The asymptomatic lesion was discovered coincidentally on a routine chest X-ray. She had a past history of severe asthma from the age of two years and had previously been on extracorporeal membrane oxygenation (ECMO) for five days for an acute episode of asthma when she was seventeen. Her last hospital admission for
Perioperative Management of a Case of Severe Peripartum Cardiomyopathy G. BROWN,· M. O'LEARy,t I. DOUGLASt AND R. HERKES§ Intensive Care Unit, Royal Prince Alfred Hospital, Sydney, New South Wales Key Words: INTENSIVE CARE: cardiomyopathy, peripartum
Peripartum cardiomyopathy was first described by Ritchie in 1849. 1 Since then it has become a recognised clinical entity and occurs in 0.005% of caucasian deliveries. A pregnant woman can develop any type of cardiomyopathy seen in the non-pregnant state, but there appears to be a distinct entity peculiar to pregnancy2 which Hughes et al. 3 have defined as 'primary myocardial disease occurring for the first time in the last trimester of pregnancy or the first trimester after delivery in the absence of preeclamptic toxaemia, hypertension or any other known heart disease'. We present the anaesthetic and intensive care management of a patient with peripartum cardiomyopathy presenting for caesarean section. CASE REPORT Preoperative management A thirty-year-old woman, parity 2012, at 33 weeks' gestation presented to Camden District Hospital with dyspnoea and orthopnoea. Her first pregnancy in 1984 had been complicated by hypertensive disease of pregnancy. Her second pregnancy was uncomplicated. She had displayed mild hypertension during this pregnancy with the highest reading 145/90 mmHg at 31 weeks but had neither proteinuria nor oedema at any of her regular antenatal visits. She was on no regular medications. On admission to Camden Hospital, clinical examination revealed an occasional wheeze, chest X-ray was clear and FEVllVC was 2.21/3.11. A diagnosis of bronchospasm due to bronchitis was made and she was treated with nebulised salbutamol and intravenous amoxicillin, and discharged after six days. ·M.B., B.S., Senior Registrar, ICU. tM.R.C.S., L.R.C.P., Registrar, ICU. iF.F.A.R.A.C.S., Deputy Director, Department of Anaesthetics. §F.R.A.C.P., Director, ICU. Address for Reprints: Dr. G. Brown E61CU, Royal Prince Alfred Hospital, Missenden Road, Camperdown, New South Wales 2050, Australia. Accepted for publication August 23, 1991
The patient was readmitted four days later at 34 + weeks gestation with dyspnoea at rest and orthopnoea. Her ECG on admission showed a sinus tachycardia of l50/min (there were no ST, T or QRS abnormalities) and a chest X-ray showed normal cardiac size but interstitial oedema. A diagnosis of cardiac failure was made. 'The patient was transferred to our institution fifteen days after her initial presentation. On admission she was afebrile with a resting sinus tachycardia of l40/min, blood pressure 110/80 mmHg, jugular venous pulse was raised to the jaw and there was pitting oedema to the knees. Auscultation revealed a third heart sound, a soft pan-systolic murmur at the apex and bi-basal pulmonary crepitations. She was treated with digoxin, frusemide, potassium supplements, subcutaneous heparin, and was placed on a 1200 ml/day fluid restriction. Haematologic and biochemical parameters were within normal limits, apart from a compensated mild metabolic acidosis (pH = 7.40, BE = -5, PaCo2 = 29 mmHg, P ao 2 = 104 on room air), an elevated plasma uric acid concentration (0.66 mmol/l) and tnidly deranged liver function tests (AST = 69 V/I, ALT = 65 V/I and GGT = 58 V/I). At no stage was the creatine kinase MB isoenzyme level elevated. An echocardiogram displayed a grossly dilated, diffusely hypokinetic left ventricle with fractional shortening of 7%. There was no hypertrophy. Viral titres (influenza A and Band enteroviruses) were negative. Cardiolipin antibody, ANA and DNA antibody titres were all negative. Thyroid function tests were normal. Obstetric examination including cardiotocograph and ultrasound were unremarkable. Betamethasone was administered to promote foetal lung maturity. A provisional diagnosis of peripartum cardiomyopathy was made. Operative management An elective caesarean section was performed five days later (Day 0). We elected to use a general anaesthetic, as the patient's cardiac reserve was Anaesthesia and Intensive Care, Vol. 20. No. I. February, 1992
81
CASE REPORT TABLE 1 Operative data
Pre-induction Post-induction Delivery Skin closed
Cl
MAP
MPA
PAWP
Sv02
SVR
PVR
1.8 1.8 1.4 1.6
101 100 108 80
33 35 25 42
25 22 18 24
61 51 53 50
1936 1680 2576 1689
178 262 181 408
Description of terms and units: Cl = cardiac index (IIminlm2) MAP = mean arterial blood pressure (mmHg) MPA = mean pulmonary artery pressure (mmHg) P AWP = pulmonary artery wedge pressure (mmHg) Sv0 2 = mixed venous oxygen saturation (%) SVR = systemic vascular resistance (dyn.s.cm- 5) PVR = pulmonary vascular resistance (dyn.s.cm- 5)
considered so limited that any reduction in systemic vascular resistance due to epidural blockade could have been catastrophic. The patient was premedicated with morphine 10 mglM. Prior to induction, secure intravenous access and full monitoring were instituted, including ECG, pulse oximetry, invasive arterial pressure monitoring and an oximetric/thermodilution Swan-Ganz catheter. During the insertion of the lines 4% lignocaine 7 ml was nebulised via an oxygen facemask in an attempt to attenuate the stress response to laryngoscopy and tracheal intubation. The patient was pre-oxygenated for five minutes. During this period fentanyl was administered (with gentle application of cricoid pressure) in 50 )lg increments up to a dose of200 )lg (2 )lglkg). Sodium thiopentone (1 % solution) was then given in 10 mg
increments. The endpoint for induction was lack of eye-opening to command. A total of 70 mg of thiopentone was given. Muscle relaxation was then achieved with suxamethonium 100 mg. Laryngoscopy and intubation were uneventful. Muscle relaxation was continued with atracurium, and anaesthesia maintained with 100% oxygen and 1% isoflurane. Four units of oxytocinon were given after delivery and uterine contraction was adequate. Estimated blood loss was 600 ml and replacement consisted of 400 ml of normal saline. A further 150 )lg of fentanyl was given at the end of the procedure and the patient was transferred to the ICV. The haemodynamic changes throughout the different phases of the procedure are displayed in Table 1. A female infant weighing 2115 g was delivered. Apgar scores were 2, 6 and 10 at 1, 5 and 10 minutes
TABLE 2 Postoperative data
Admission +90 min + 3 hrs + 12 hrs + 24 hrs
Cl
MAP
MPA
PAWP
SVR
PVR
D02
1.7 2.9 3.6 4.2 4.4
90 76 71 86 82
47 24 28 28 30
20 18 20 16 14
1689 810 624 623 550
570 74 82 121 131
747 1285 1647 1945 2115
Description of terms and units: Cl = cardiac index (IIminlm2) MAP = mean arterial blood pressure (mmHg) MPA = mean pulmonary artery pressure (mmHg) P AWP = pulmonary artery wedge pressure (mmHg) SVR = systemic vascular resistance (dyn.s.cm- 5) PVR = pulmonary vascular resistance (dyn.s.cm- 5) D02 = oxygen delivery (mllmin) Anaesthesia and Intensive Care. Vol. 20. No. 1, February. 1992
82
G.
BROWN ET AL.
respectively. Artificial ventilation was required but the infant established her own ventilation after naloxone and was extubated. She was discharged from the nursery after one day and has subsequently progressed well. Course in intensive care On admission to the ICU the patient had a sinus tachycardia of 140/min and blood pressure of 120/80 mmHg. Arterial blood gases demonstrated a P02 of 70 mmHg on an inspired oxygen of 100%. A chest X-ray showed cardiomegaly (even allowing for the AP projection) and gross pulmonary oedema. Presenting haemodynamic parameters are shown in Table 2 and on the basis of this data, dobutamine was commenced at 5 l1g/kg/min and dopamine at low dose, 3 l1g/kg/min. With this therapy both cardiac function and pulmonary gas exchange improved markedly (Table 2). A repeat chest X-ray confirmed reduction in heart size and clearing of the lung oedema. Formal anticoagulation with heparin was commenced several hours postoperatively. Improvement continued such that she was extubated on Day 2. On Day 3 a regular dose of captopril 2 mg bd was commenced and the dobutamine was carefully weaned. A gated heart pool scan demonstrated a left ventricular ejection fraction of 22%. On Day 4 the dopamine was ceased and the captropril dose was increased to 5 mg bd. The patient was discharged from the ICU on day 5. DISCUSSION
This patient satisfies the criteria of Hughes et al. for the diagnosis of peripartum cardiomyopathy. 3 As in this case, the haemodynamic manifestations of this condition are usually a low output, congestive pattern. 4 Recently, however, high output failure with well preserved ventricular function has been reported, suggesting that it is not an homogenous entity.s The fact that it is a specific entity at all is still open to some debate. Because the pathogenesis is not known, it has been suggested that the haemodynamic changes of pregnancy unmask a pre-existing cardiomyopathy. 6 Aetiological factors suggested by Hull et al. as early as 1937 7 were glomerulonephritis, toxaemia, beri-beri or other nutritional deficiencies or an infective process. None has subsequently been substantiated. Acute hypertensive heart failure has been proposed but as in our patient, hypertension is usually transient and not severe. 8 A toxic or immunological mechanism seems most likely but these again have not been proven. There have, however, been reported findings of anti-heart antibodies, 9 and several cases of myocarditis-induced peripartum cardiomyopathy have responded very well to
immunosuppressive therapy. The myocardial biopsy findings are, however, non-specific, involving lymphocytic infiltrate, myonecrosis, fibrosis and interstitial oedema. lo This is not supportive of a distinct immuno-pathological process. Cardiomyopathy may be seen in association with the gestosis syndrome, a syndrome encompassing the conditions known as preeclamptic toxaemia, pregnancy-induced hypertension, HELLP syndrome (hypertension, elevated liver enzymes and low platelets) and others. Electrocardiographic abnormalities are present in practically all patients with toxaemia of pregnancy, and cardiac arrhythmias may occur. Acute congestive cardiac failure may develop in these cases either due to excessive fluid therapy in the presence of impaired renal or cardiac function, or due to the development of a cardiomyopathy. 2 Despite her mildly elevated liver enzymes and raised uric acid concentration, we consider that this patient does not fit into this category since she only had hypertension early in the pregnancy, not requiring therapy, never had proteinuria, had a normal platelet count, and except for tachycardia a normal ECG. The prognosis of peripartum cardiomyopathy depends on whether the heart size returns to normal within six months of onset of the disease. 11 Patients who have cardiomegaly of greater than six months' duration have a very poor outlook without transplantation. The mortality in this group appears to be of the order of 75% with an average period of survival of 29 months l2 to 80% with an average survival of 4.7 years.13 These figures are similar to those for the other congestive cardiomyopathies. 14 The most frequent cause of death is congestive cardiac failure, complicated by pulmonary and systemic emboli.11 We elected to commence full heparinisation within 24 hours of surgery because we considered the risk of embolism to be sufficiently great to offset any risk of bleeding with anticoagulation so close to the time of surgery. If heart size returns to normal the prognosis is quite good. Twelve out of fourteen such patients followed up for an average of 10.7 years were found to return to a good level of function. The two deaths were from non-cardiac causes. I 1 The preoperative management of our patient was aimed at excluding any reversible cause, controlling her heart failure and attempting to optimize her condition for surgery with bed rest, fluid restriction, digitalis and diuretics. It was generally agreed that real improvement in her cardiac status would only be brought about by delivery via caesarean section. This patient presented quite an anaesthetic challenge due to her low cardiac output. However, Anaesthesia and Intensive Care, Vo!. 20, No. I, February, 1992
83
CASE REPORT
she tolerated a careful general anaesthetic well (Table 1). The cardiac index remained remarkably constant. The sinus tachycardia persisted but heart rate remained constant and there were no arrhythmias on intubation. The drop in pulmonary artery pressures related to delivery of the child was probably related to the small blood loss occurring at this time. It did not correspond to any change in cardiac output. We elected not to intervene with inotropes intraoperatively. With the institution of low-dose inotropic support guided by invasive haemodynamic monitoring, there was progressive postoperative improvement in cardiac function, confirmed both on clinical examination and by the radiological changes. This is also well demonstrated by the haemodynamic data in Table 2. The patient continued to improve clinically following discharge from ICV; however, a repeated gated heart pool scan three weeks later revealed a left ventricular ejection fraction unchanged from the day before ICV discharge, at 22%. This case is presented as an example of the perioperative management of a woman with severe heart failure presenting for caesarean section. REFERENCES
1. Ritchie C. Clinical contributions to the pathology, diagnosis, and treatment of certain chronic diseases of the heart. Edinburg Surg J 1849; 12:333. 2. Burch G. Heart disease and pregnancy. Am Heart J 1977; 93,1:104-116. 3. Hughes R, Kapur P, Sutton G, Honey M. A case of fatal peri-partum cardiomyopathy. Br Heart J 1970; 32:272-276.
4. Homans D. Current Concepts Peripartum Cardiomyopathy. N Eng J Med 1985; 312,22:1432-1437. 5. Marin-Neto J, Maciel B, Teran Urbanetz L et al. High output failure in patients with peripartum cardiomyopathy: A comparative study with dilated cardiomyopathy. Am Heart J 1991; 1,1:134-140. 6. de Swiet M. Heart disease in pregnancy. In: Michael de Swiet ed. Medical Disorders in Obstetric Practice, 1st Ed. Blackwell Scientific Publications, Melbourne 1984; 116-118, 137-138. 7. Hull E, Hidden E. Postpartal heart failure. South Med J 1938; 31 :265. 8. Davidson N, Parry EH. The etiology of peripartum heart failure. Am Heart J 1979; 97,4:535-536. 9. Kirsner A, Hess E, Fowler N. Immunological findings in idiopathic cardiomyopathy: a prospective serial study. Am Heart J 1973; 86:625. 10. Melvin K, Richardson P, Olsen E, Daly K, Jackson G. Peripartum cardiomyopathy due to myocarditis. N Engl J Med 1982; 307,12:731-734. 11. Demkakis J, Rahimtoo1a S, Sutton G. Natural course of peripartum cardiomyopathy. Circulation 1971; 44:1053-1061. 12. Walsh J, Burch G, Black W, Ferrans V, Hibbs R. Idiopathic myocardiopathy of the puerperium (postpartal heart disease). Circulation 1965; 32-1913. Demkakis J, Rahimtoola S. Peripartum cardiomyopathy. Circulation 1971; 44:964-968. 14. Wynne J, Braunwald E. The cardiomyopathies and myocarditides. In: Petersdorf R, Adams R, Braunwald E, Isselbacher K, Martin J, Wilson J. Harrison's Principles of Internal Medicine, 10th Ed. McGraw-Hill Book Company, Sydney 1982; 1450-1451.
Severe Localised Bronchospasm In A Young Asthmatic Patient During Thoracotomy A. w. Y. CHUA* AND N. SYMONSt Department of Anaesthesia, Royal Prince Alfred Hospital, Sydney, New South Wales Key Words: ANAESTHESIA COMPLICATIONS: asthma, bronchospasm
Patients with severe asthma may present a difficult challenge to any anaesthetist. Here we report an intraoperative management problem occurring during a thoracotomy in a young asthmatic patient. 'M.B.B.S., Anaesthetic Registrar. tF.F.A.R.A.C.S., Visiting Anaesthetist. Address for Reprints: Dr. N. Symons, Department of Anaesthesia, Royal Prince Alfred Hospital, Missenden Road, Camperdown, N.S.W. 2050, Australia. Accepted for publication August 20, 1991 Anaesthesia and Intensive Care. Vol. 20. No. I. February. 1992
CASE REPORT
A 26-year-old woman presented for elective right thoracotomy for excision of a superior mediastinal tumour. The asymptomatic lesion was discovered coincidentally on a routine chest X-ray. She had a past history of severe asthma from the age of two years and had previously been on extracorporeal membrane oxygenation (ECMO) for five days for an acute episode of asthma when she was seventeen. Her last hospital admission for
