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Year : 2007  |  Volume : 51  |  Issue : 1  |  Page : 60-64 Table of Contents     

A rare case of peripartum cardiomyopathy posted for caesarean section

1 M.D., D.A., Asso. Prof , Department of Anesthesiology, J.S.S.MedicalCollege,RamanujaRoad,Mysore, India
2 M.D., D.A., Prof. & Head, Department of Anesthesiology, J.S.S.MedicalCollege,RamanujaRoad,Mysore, India
3 M.D., Resident, Department of Anesthesiology, J.S.S.MedicalCollege,RamanujaRoad,Mysore, India

Date of Acceptance15-Jan-2007
Date of Web Publication20-Mar-2010

Correspondence Address:
Nalini Kotekar
M.D., D.A., Asso. Prof , Department of Anesthesiology, J.S.S.MedicalCollege,RamanujaRoad,Mysore
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Source of Support: None, Conflict of Interest: None

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Post Partum Cardiomyopathy (PPCM) is a relatively rare form of heart failure associated with pregnancy. It was recognized first in the 19th century by Ritchie and is defined as the onset of acute heart failure in the last trimester or early post partum period in the absence of infections, metabolic, toxic, ischaemic or valvular causes of myocardial dysfunction. Prognosis depends on the degree of cardiomegaly at presentation and in the following 6 months. Initial high risk period carries a mortality of 25 to 50%. Keeping in mind the reduced contractility and ejection fraction with ventricular dilatation proceeding to cardiac failure, the anesthesiologist managing a case of PPCM faces the challenge of avoiding myocardial depression, hypovolemia and increased SVR, all of which may be hazardous

Keywords: Anaesthesia; Obstetric; Complications; Cardiomyopathy

How to cite this article:
Kotekar N, Nagalakshmi N V, Chandrashekar. A rare case of peripartum cardiomyopathy posted for caesarean section. Indian J Anaesth 2007;51:60-4

How to cite this URL:
Kotekar N, Nagalakshmi N V, Chandrashekar. A rare case of peripartum cardiomyopathy posted for caesarean section. Indian J Anaesth [serial online] 2007 [cited 2021 Feb 25];51:60-4. Available from: https://www.ijaweb.org/text.asp?2007/51/1/60/61119

   Introduction Top

Despite the advances in management of heart disease, pregnancy puts the mother at risk. The risk is so great with some cardiovascular abnormalities that a recommendation of interruption of pregnancy is supportable.

Peripartum cardiomyopathy is defined as the onset of acute heart failure without demonstrable cause in the last trimester of pregnancy or within the first 6 months after delivery. It occurs in about 1 in 4000 deliveries and is often unrecognized, as symptoms of normal pregnancy commonly mimic those of mild heart failure. [1]

In 1997, the National Heart, Lung and Blood Institute and the Office of rare diseases commenced the workshop that established the following diagnostic criteria for peripartum cardiomyopathy:

  1. Development of Cardiac failure in the last month of pregnancy or within 5 month after delivery.
  2. Absence of an identifiable cause for the cardiac failure.
  3. Absence of recognizable heart disease prior to the last month of pregnancy.
  4. Left ventricular systolic dysfunction demonstrated by classic echo cardio graphic criteria such as depressed shortening fraction or ejection fraction. [2],[3]

   Case Report Top

A 37 year old pregnant, physical training instructor was admitted to our hospital with 37 weeks of gestation for elective LSCS. Patient presented with complaints of increased fatigability with difficulty in breathing with PND since 1 week. Minimal physical activity made her dyspnoeic (some times even at rest) thereby, she could not perform her routine work.

Patient had been admitted with similar compliant 20 days earlier in our hospital ICCU. She was treated for cardiac failure with diuretics and digoxin and on improvement, was discharged with advice to continue digoxin 0.25 mg OD and lasix 40mg OD.

She never gave any history of chest pain or wheezing and was not a known case of diabetes, hypertension, IHD or bronchial asthma. Till her 8th month of pregnancy, she had been a very active physical training instructor at a school. Previous pregnancy 2 years back had ended in spontaneous abortion.

Diagnosis of Cardiomyopathy of pregnancy was made which is a very rare condition carrying a grave prognosis.

On examination, her pulse rate was 130 per minute and BP 110/70 mm of Hg with pitting type of pedal edema. Respiratory system showed bilaterally equal, normal vesicular breath sounds with no ronchi or crepitations. Haemoglobin was 8.5gm %. Her ECG showed sinus tachy cardia with ST depression. Chest X-ray showed massive cardiomegaly with basal haziness on the right side.

Echocardiography showed:

  1. Dilated LV
  2. Global hypokinesia
  3. LV systolic dysfunction
  4. Ejection Fraction 41% (N=60+6%)
  5. EDV = 170ml (N=96+20ml)

1. Cardiomyopathy

2. Myocarditis

She was on treatment with Injection Lasix 40 mg OD.

Tablet Digoxin 0.25 mg OD.

Tablet Cardace (ACE inhibitor) 2.5 mg OD

Tablet Omeprazole 20 mg BD.

She was admitted for safe confinement and for elective LSCS keeping in mind her poor cardiac status.

The patient and relatives were explained about the high risk and informed consent was taken.

Preoperatively injection Amoxicillin with clavulanic acid 1.2gm and injection Gentamycin 80 mg IV. was given.

Lumbar Epidural Anesthesia was administered between L 3 - L 4 inter space with injection Lignocaine 1% 20ml and injection Fentanyl 50micro gm. Adequate analgesia was seen till T 8 level.

Intra operative pulse rate ranged from 130-150 per minute, BP 110/80 to 90/60 mm of Hg. SpO 2 : 98-99%, ECG; sinus tachycardia. 800 ml of crystalloids was administered. A 3 kg male baby with APGAR score of 7 and 9 at 1& 5 minutes was extracted. 10 units of Oxytocin was given in infusion and injection midazolam 1mg was injected IV.

Procedure took 25 minutes and by the end of it her pulse rate was 120 per minute BP 90/60 mm of Hg with a sensory level of anesthesia at T 12 . Patient was shifted to ICU for observation and further management with instructions to keep the patient in propped up position and Oxygen through ventimask.

Four hours later, in the ICU patient developed excessive bleeding per vaginum. Uterus was well contracted and 10U of Oxytocin drip was started. Injection Carboprost 250mg IM was given. Repeat Hemoglobin was 8.5 gm%. Pulse rate 130 per minute BP 100/70 mm of Hg. On auscultation, bilateral basal crepts were heard. 2 units of packed cells were transfused along with injection Lasix 40mg. Injection Dobutamine 10micro gram per minute was started. After 6 hrs, BP fell to 80/60mm of Hg and Dobutamine drip was increased to 12.5 micro gm per minute. Another unit of Packed cells was transfused while Dobutamine, Lasix and Digoxin were continued.

48 hrs later patient developed dyspnoea and SpO 2 fell to 60% with HR at 130 per minute. Bilateral coarse crepitations were present. Diagnosis of acute pulmonary edema was made. Patient was treated with injection Morphine, Lasix, Steroids, Oxygen and propped up position but when she could not maintain her O 2 saturation, she was paralysed and put on the ventilator with PEEP.

Over the next 48 hrs. the patient showed marked improvement in all her vital parameters and was weaned to the spontaneous mode ventilation. By the 5th post operative day the patient showed a near normal ABG and electrolytes. Between 5 th -7 th postoperative day the patient was very comfortable on the spontaneous mode and we were even contemplating disconnecting ventilatory support. She was receiving Ryles tube feeding.

On the 8th post operative day the patient seemed comfortable but she suddenly complained of breathlessness and developed bradycardia and in no time arrested. All resuscitation measures proved futile and after 1 hr. efforts were abandoned and patient was declared dead.

   Discussion Top

PPCM is a form of Dilated Cardiomyopathy with left ventricular systolic dysfunction that results in signs and symptoms of heart failure. Symptoms usually occur in the last trimester and diagnosis is usually made in the peripartum period., [1],[3],[4]

The reported incidence in the USA and Europe ranges from 1 in 4000 deliveries, representing less than 1% of cardiovascular problems associated with pregnancy. Sixty percent present within the first 2 months postpartum but up to 7% may present in the last trimester of pregnancy. Geographic variations exist with a higher incidence reported in areas of Africa because of malnutrition and local customs in the puerperium. Etiology is still unknown. It may be postulated that it may be due to nutritional deficiencies, small vessel coronary artery abnormality, hormonal effects, toxaemia, maternal immulogic response to foetal antigen or mycarditis. [4] Predisposing factors include maternal age greater than 30 yr, multiparous or eclamptic patients, twinning, racial origin (black), hypertension and nutritional deficiencies. In the majority of cases there is no family history.

Peripartum cardiomyopathy usually presents with symptoms of worsening cardiac failure. These include dyspnoea on exertion, fatigue, ankle oedema, embolic phenomena, atypical chest pains and haemoptysis. Examination may reveal evidence of a raised CVP, tachycardia, cardiomegaly with a gallop rhythm (S3), mitral regurgitation, pulmonary crackles and peripheral oedema. Chest radiographs may show cardiomegaly with pulmonary oedema and pulmonary venous congestion. The electrocardiogram may show non­specific ST and T wave changes, atrial or ventricular arrhythmias and conduction defects. Echocardiographic / Doppler examination may reveal enlargement of all four chambers with marked reduction in left ventricular systolic function, small to moderate pericardial effusion and mitral, tricuspid and pulmonary regurgitation may be evident. Ventricular wall motion, ejection fraction and cardiac output are decreased and pulmonary wedge pressure is increased. [4],[5],[6]

Symptoms like decreased exercise capacity, tiredness, dyspnoea, orthopnoea and palpitations may occur even in normal pregnancy and can be mistaken for a diseased state. Physical signs like hyperventilation, edema, distended neck veins can be seen in normal pregnancy. On auscultation of the heart, one can hear loud first heart sound, exaggerated splitting, mid systolic murmur and continuous venous hum. These physical signs may confuse the anesthesiologist and there could be mistakes in the form of over diagnosis or disregarding of heart disease. [7],[8]

The clinical presentation and haemodynamic features in PPCM are indistinguishable from those of other forms of dilated cardiomyopathy. The clinical course of PPCM varies with approximately 50-60% patients showing complete or near complete recovering of clinical status and cardiac function, usually within the first 6 months postpartum. The remaining patients demonstrate either continued clinical deterioration leading to early death or persistent left ventricular dysfunction and chronic heart failure. There appears to be an initial high risk period with a mortality of 25-50% in the first 3 months postpartum. Patients with persistent cardiomegaly at 6 months have a reported mortality of 85% at 5 years. [1],[3],[5] Subsequent pregnancies in women with PPCM are often associated with relapses and high risk for maternal morbidity and mortality. For this reason subsequent pregnancy should be discouraged in women with PPCM who have persistent cardiac dysfunction. [1],[3],[4],[5]

Management of PPCM should include vigourous treatment of acute heart failure. [4],[7],[8]

  1. Oxygen, diuretics, digoxin and vasodilators.
  2. Use of ACE inhibitors in early pregnancy should be avoided as it has teratogenic effects on fetus
  3. Anticoagulant therapy is recommended because of high incidence of thromboembolic events in PPCM.
  4. Since the disease may be reversible, the temporary use of intra aortic balloon pump or LV assist device may help to stabilize the patient's condition pending improvement.
Dobutamine stress echocardiography may have a role in evaluating contractile reserve in women with recovered systolic function who are contemplating further pregnancies.

A high number of patients with PPCM show evidence of myocarditis in biopsy specimens. Necropsy shows cardiac enlargement, often with mural thrombi along with histological evidence of myocardial degeneration and fibrosis. [8]

The anesthetic considerations for a patient with heart failure presenting for caesarian section are similar regardless of etiology. Haemodynamic goals include maintenance of normal to low heart rate to decrease oxygen demand, and prevention of large swings in blood pressure. Achievement of these goals have been undertaken by giving general and regional anesthesia. During GA important factors to keep in mind are

  • Volatile agents that decrease LV contractility without dramatic vasodilatation is desirable.
  • Avoid agents that decease preload and after load, eg. hypovolemia, nitroglycerine, nitroprusside.
  • Avoid agents that directly or indirectly increase heart rate, and contractility eg. Pancuronium, atropine, epinephrine, ephedrine.
  • Blood loss to be replaced promptly.
  • Hypotension better treated with volume expansion and pure alpha adrenergic agonist.
  • Remember that insertion of CVP / PAC may induce atrial or ventricular dysarrhythmias. [9]
Our choice of epidural technique for this patient was to avoid the complications of endotracheal GA. GA carries with it the risks of sympathetic stimulation during laryngoscopy, use of a multi drug regime and doubts about extubating.

Regional techniques reduce after load with minimal effect on contractility, thus improving cardiac output and reducing myocardial work. [10],[11] Regional anaesthesia may minimize the incidence of venous stasis emboli, spinal and epidural narcotics are also useful for post operative analgesia prior to reimplementation of anticoagulant therapy, which should be with held before delivery.

McIndoe et al [12] described a previously asymptomatic patient who presented with a cardiac arrest at the induction of general anaesthesia for emergency caesarian section and subsequently developed acute heart failure. She had total absence of antecedent symptoms or signs of cardiac disease. She had history of previous three non obstetric surgeries under GA which were unremarkable. She was taken for emergency caesarian section in view of extremely poor CTG tracing. after intubating with injection Thiopentone 375 mg and injection Suxamethonium 100 mg I.V and confirming bilateral air entry, she was manually ventilated with 4lt. per minute N 2 O, 2lt. per min O 2 and 2% Isoflurane. Pulse oxymetry and capnography showed normal values. Suddenly patient developed bradycardia of 40 beats per minute and inspite of I.V. Atropine patient became asystolic. External cardiac massage with left lateral tilt was maintained with 100% oxygen along with inj. Adrenaline 1mg and further 2 mg Atropine. With active resuscitation, the obstetrician proceeded to deliver a 3.92 kg boy within two minutes. Cardiac electrical activity returned after 3 minutes but she had short lived, self terminating episodes of intermittent pulseless tachyarrhythmias. Rhythm disturbances settled over the next 30 minutes. Patient was electively ventilated in the post operative period. After initial improvement for the next 10 hrs she again desaturated and developed sinus tachycardia of 140 beats per minute and gallop rhythm. Echocardiogram revealed a dilated and poorly contractile left ventricle and global hypokinesia. She was anticoagulated and heart failure was treated with injection Frusamide and tablet Captopril. Idiosyncratic drug reaction because of I.V Ranitidine, Oxytocine and Midazolam was thought of since the patient had no subjective and objective signs of cardiac problems. Such a catastrophic reaction can pose a dilemma to the practicing anesthesiologist. Diagnosis of PPCM was made and patient was treated for cardiac failure.

Breen et al. [13] reports a successful outcome in a 14 year old parturient with pulmonary hypertension and PPCM and patent foramen ovale coming for caesarian section by giving lumbar epidural anaesthesia with Lidocaine and Fentanyl. Management goals included

  1. Maintaining right ventricular function.
  2. Avoiding haemodynamic effects of general endotracheal anaesthesia and
  3. Minimizing narcotic related neonatal respiratory depression.
Epidural was considered a safe alternative to GA.

Yahagi et al [14] reported a patient who showed acute heart failure caused by PPCM with persistent atrial tachycardia, followed by ventricular tachycardia, cardiac arrest, and successful treatment with vigorous multiple organ support including veno arterial bypass.

Ian Kaufman et al [15] describe a case of PPCM and thromboembolism in an obese and diabetic patient. They highlight the frequent occurrence of thrombo embolic morbidity in this group of parturients, emphasizing the need for early consideration of prophylactic anticoagulation.

Chan and Ngan Kee [16] presented a case of PPCM at 18 weeks gestation. She was managed medically with systemic anticoagulation, until 31 weeks, when fetal distress and maternal liver dysfunction forced an emergency caesarian section.

Patient had severe cardiac dysfunction and suffered a severe embolic stroke despite mo nitored Warfarin therapy. She died 5 months later.

Shrestha B.R. et al [17] reported a case of PPCM with ejection fraction of 18% brought for emergency caesarian section. It had a successful outcome using epidural with Lignocaine 2% and Adrenaline.

   Conclusion Top

PPCM is a severe from of heart failure that causes significant mortality. The diagnosis of PPCM remains a diagnosis of exclusion and cannot be made until underlying conditions, including chronic hypertension, valvular disease and viral myocardits, have been excluded. Once diagnosed, medical management must address the classical goals of heart failure therapy, and should include considerations of thrombo embolic prophylaxis.

Subarachnoid block can be hazardous as it can precipitate sudden and rapid reductions in systemic vascular resistance and there by preload. GA has its disadvantages of obnoxious stimulations and polypharmacy. Hence epidural anaesthesia appears to be the technique of choice for a patient with PPCM.

   Acknowledgement Top

I acknowledge with thanks the support extended by Dr. Anjali Siddesh, Professor of O.B.G and Dr.Srinivas H.T. Post graduate student of Anesthesiology, J.S.S Medical College, Mysore.

   References Top

1.Michael de swiet. Heart disease in pregnancy. In: Michael de swiet. Editor.Medical disorders in obstetric practice. 4t h edition,Blackwell Scientific Publication 2002; 144-46.  Back to cited text no. 1      
2.Pearson GD, et al. Peripartum cardiomyopathy. National Heart, Lungs& Blood Institute& Office of Rare Diseases; Workshop recommendations& Review. JAMA 2000; 283; 1183-88.  Back to cited text no. 2      
3.F Garry Cunningham, Kenneth J Leveno, Steven L Bloom et al. Cardiovascular diseases.In: Dwight Rause, Bill Rainey, Cathy Spong, George Vendel Jr, editors. Williams Obsterics. 22 nd edition. Mc Graw Hill 2005: 1030-32.  Back to cited text no. 3      
4.Vinod Sharma. Peripartum Cardiomyopathy. Cardiology Today; May-June 2004; 8(3): 127-29.  Back to cited text no. 4      
5.Carvallo A, Brandao A et al. Prognosis in peripartum cardiomyopathy. Am J Cardiol; 1989; 64; 540-42.  Back to cited text no. 5      
6.Midei Mg et al. Peripartum myocarditis and cardiomyopathy, Circulation 1990; 81: 922-28.  Back to cited text no. 6      
7.Uri Elkayam. Pregnancy and cardiovascular diseases. In: Braunwald, Zipes, Libby,editors. A text book of cardiovascular medicine. 7 th edition. Saunders 2005: 1973-74.  Back to cited text no. 7      
8.Joshua Wynne. Eugene Braunwald.cardiomyopathy and myocarditis. In: Kasper, Braunwald,Fauci et al editors. Harrison's Principles of Internal medicine. 16 th edition,Mc Graw Hill 2005: 1408-14.  Back to cited text no. 8      
9.Maron BJ et al. Hypertropic cardiomyopathy. Inter relation of clinical manifestations, pathophysiology and therapy. N Engl J Med 1987; 316; 780-789, 844-51.  Back to cited text no. 9      
10.Shnaider R, Efri T,Sjmuk P, Larson S et al. combined spinal - epidural anaesthesia for cesarean section in a patient withperipartum dialated cardiomyopathy. Can J Anaesth 2001; 48; 681-83.  Back to cited text no. 10      
11.Pirlet M, Baird M, Jones Ritson M, Kinsella SM. Low dose combined spinal epidural anaesthesia for cesarean section in a patient withperipartum cardiomyopathy. Inter J Obstet Anaesth 2000; 9: 189-92.  Back to cited text no. 11      
12.McIndoe AK, Hammond EJ, Babington PCB. Peripartum cardiomyopaty presenting as cardiac arrest at induction of anaesthesia for emergency caeserian section. Br J Anaesth 1995; 75: 97-101.  Back to cited text no. 12      
13.Breen Terrance W, Janzen James A. Pulmonary hypertension and cariomyopathy:anaesthetic management for caesarian section. Can J Anaesth 1991; 38: 895-99.  Back to cited text no. 13      
14.Yahagi Naoki, Kumon Keiji, Nakatani Takeshi et al. Peripartum cardiomyopathy and tachycaria followed by multi organ failure… Anesth Analg 1994; 79: 581-82.  Back to cited text no. 14      
15.Ian Kaufman, Richard Bondy, Alice Benjamin. Peripartum cardiomyopathy and thromboembolism; anesthetic management and clinical course of an obese, diabetic patient,Can J Anaesth 2003; 50:1 61-65 .  Back to cited text no. 15      
16.Chan F, Ngan Kee WD. Idiopathic dilated cardiomyopathy presenting in pregnancy. Can J Anesth 1999; 46: 1146-49.  Back to cited text no. 16  [PUBMED]    
17.Shrestha B R, Thapa C, Peripartum cardiomyopathy undergoing caesarean section under epidural anaesthesia. Katmandu University Medical Journal 2006; 4: 503-05.  Back to cited text no. 17      


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