The patient was transferred to the ICU and treated with diuretic Furosemide iv 40 mg initially, antibiotics Ceftriaxone iv 1 gram over 12 hours, and Bromhexin iv 4 mg over 12 hours, Combivent nebulizer 1 unit dose (2.5 ml), and Flixotide 2 mg over 8 hours. The patient was scheduled echocardiogram the day after.
The echocardiogram showed dilated left ventricle with decreased left ventricular ejection fraction of 41%, left ventricular global hypokinetic, and diastolic dysfunction. Normal right ventricle systolic function and low probability of PH were also found on echocardiogram. The patient had electrolyte imbalance hypokalemia potassium of 2.8 mmol/L and hypoalbuminemia 3.3 g/dL.
The patient was diagnosed with Postpartum Cardiomyopathy with Pleural Effusion, Acute Lung edema, and Pneumonia. She was treated in ICU for three days with continuous furosemide pump, Spironolactone 25 mg once daily, Bisoprolol 2.5 mg once daily, Valsartan 80 mg once daily.
The patient's signs and symptoms were significantly improved after 2 days of observation and treatment in the ICU. The patient was then transferred to the ward. Her dyspnea greatly decreased with diuresis and antibiotics administration. She was discharged from the hospital two days later and instructed to take Valsartan 80 mg, Spironolactone 25 mg, Bisoprolol 2.5 mg, and Furosemide 40 mg.
 

Discussion

Peripartum cardiomyopathy, a disease characterized by left ventricular dysfunction and heart failure, occurs during the last month of pregnancy or the first five months postpartum in the absence of any determinable heart disease. This is a potentially life-threatening disease that develops during the peripartum period and is idiopathic[3]. A higher incidence was correlated with factors such as black race, multiparity, maternal age >30 years, twin pregnancies, history of hypertension, preeclampsia, and eclampsia, although no causal association was identified [3–5]. In this case, the patient is multiparity (G4P3A0), age is 35-year-old and twin pregnancies. There is no history of hypertension and preeclampsia.
The diagnostic criteria used in clinical practice and research, consisting of the classical definition of PPCM and echocardiographic criteria, are as follows: (1) HF development during pregnancy in the last month of or within five months after delivery; (2) LV systolic dysfunction (LV EF < 45% by echocardiography); (3) no identifiable cause for HF; and (4) no identified heart disease previous to the last month of pregnancy. PPCM diagnosis must meet all four criteria. However, in patients with hemodynamic instability, emergency delivery irrespective of gestational age might be considered [6,7].
PPCM will present after 36 weeks of gestation, and the majority of cases are seen in the first month after delivery. An earlier presentation can occur in patients with underlying cardiac comorbidities as valvular or ischemic cardiomyopathy. Presentation of PPCM can vary depending on the degree of the disease at the moment of presentation. Symptoms related to heart failure and related to pregnancy are paroxysmal nocturnal dyspnea, pedal edema, orthopnea, and dyspnea on exertion. Other symptoms included dry cough, palpitations, an increase of abdominal girth, lightheadedness, and chest pain. Findings in the physical exam like jugular venous distentions, displaced apical impulse, third heart sound, and mitral regurgitation murmurs are common [8].
Postpartum hemorrhage (PPH) is the world's leading source of maternal morbidity and mortality. Several population-based trials have studied the epidemiology of massive transfusion for PPH. That is a four-fold occurrence recorded between 2012 and 2013 in the United Kingdom (23 per 100,000 deliveries), while the one-and-a-half times the recorded occurrence for New York state between 1998 and 2007 (60 per 100,000 deliveries). Uterine atony has become the leading cause of PPH with massive transfusion. One-fourth of all women who obtained massive transfusion performed hysterectomy to reduce bleeding[9]. Abrupting the placenta, uterine arterial embolization, and peripartum hysterectomy are related to blood loss during delivery. In these cases, massive transfusion or fluid resuscitation is typically needed in such circumstances, and such conditions may lead to HF at the time of delivery. Therefore, it is also not unexpected that an improvement in conditions correlated with peripartum hemorrhage in PPCM patients [4].
Senanayake et al. present a case of a 33-year-old Lankan primigravida giving birth to a caesarian section delivery at 38 weeks of gestation, a preliminary diagnosis of appendicitis. Immediate laparotomy revealed generalized oozing from the peritoneum contributing to hemoperitoneum and hemorrhage of the intestines. Her laboratory findings revealed microangiopathic hemolytic anemia and thrombocytopenia. It was diagnosed with thrombocytopenic purpura. After a stable recovery, on the 16th postoperative day, she was released from the hospital, but 12 hours later, she was readmitted from an acute-onset, gradually deteriorating shortness of breath. Echocardiography has confirmed peripartum cardiomyopathy. She was treated with a bromocriptine and heart failure regimen [10].
PPCM that may be correlated with anaphylaxis and epinephrine administration has never been published. Yesiler et al. reported a PPCM patient presented with pulmonary edema with anaphylaxis and epinephrine administration following blood transfusion [11].
Bosch et al. reported a case of a 27-year-old gravida 1 that was admitted to hospital at a 39+1 weeks of gestation with preeclampsia. Her blood pressure was 140/95 mmHg; postpartum, she had a blood loss of 1200 ml caused by an atonic uterus. She was provided blood transfusion with a cumulative blood loss of 3000 ml. Postoperatively acute respiratory failure was developed. She had a diagnosis of postpartum lung edema correlated with preeclampsia and probably a sulprostone effect. She recovered quickly and returned to the maternity ward two days later. However, five days later, the patient developed dyspnoea. She was referred to the ICU with a diagnosis of severe HF The chest X-ray revealed symptoms of pulmonary edema. Echocardiography revealed a dilated left ventricle with normal valves. The diagnosis of peripartum cardiomyopathy was rendered on the basic history, physical examination, and further examination. The sodium and fluid limitations, ACE inhibitor, and low-dose β-receptor antagonists were used in the treatment. She was discharged in eight days. The left ventricular ejection fraction was measured between 40 and 45%. The echocardiography revealed a normal right and left ventricular function with no valve anomalies seven weeks postpartum. The woman would like to get pregnant again [12].
Massive transfusion is defined as the transfusion of 10 units of packed red blood cells (PRBCs) within 24 hours. Massive transfusion is an effective life-saving treatment for patients with massive acute blood loss. Massive transfusion has been utilized in many healthcare environments, including obstetrics, gastroenterology, trauma, and surgery. Complications include hypothermia, acid/base derangements, electrolyte imbalance (hypocalcemia, hypomagnesemia, hypokalemia, hyperkalemia), citrate toxicity as well as severe lung damage associated with transfusion.[13,14]. Mild hypothermia (33.8C) is well tolerated and offers significant benefits, especially after cardiac arrest. However, more severe hypothermia might result in peripheral vasoconstriction, metabolic acidosis, cardiac failure, decreased citrate metabolism, decreased drug clearance and synthesis of acute phase proteins, and reduced tissue oxygen delivery by moving the Bohr curve to the left, and infection [15]. Hypocalcemia results in hypotension, small pulse pressure, flat ST-segments, and prolonged QT intervals on the ECG, which can contribute to myocardial depression that manifests earlier than hypocalcemia coagulopathy [14]. There is 250 mg of iron per unit of red cells. As the body has no successful iron excretion process other than by blood loss, the body is at risk for iron accumulation with the exposure of liver, heart, pancreas, and endocrine organ deposition due to recurring transfusions (e.g. sickle cell disease, beta Thalassemia, or myelodysplasia). It eventually results in cirrhosis, cardiomyopathy, diabetes, arthritis, and testicular failure. The use of repeated venesection or iron chelation therapy with deferoxamine can postpone or prevent the onset of iron overload in susceptible patients [15]
Monitoring before and 24 hours after delivery tracking is critical because it is the period of the most prominent hemodynamic changes. Understanding physiological hemodynamic changes during pregnancy are of considerable significance for the interpretation of hemodynamic parameters of PPCM. Autotransfusion due to uterine contractions and fluid postpartum fluid changes can alter the condition of patients with PPCM, augment the fluid load, and cause acute heart decomposition. PPCM shows reduced cardiac output and increased right and left heart filling [7].
Effective management of PPCM reduces mortality and improves the percentage of women who recover their left ventricular function entirely. Outcomes for subsequent pregnancies are better in women who have completely recovered cardiac function after PPCM. However, recurrence of cardiac failure is common in subsequent pregnancies [10].
 

Conclusion

The presence of massive transfusion in a patient with PPCM can be challenging in diagnosing PPCM itself and unpredictable course of decompensated HF in peripartum mothers. Due to its high mortality rate without proper treatment, prompt investigation is essential in improving maternal survival.
 
Consent for publication:  Written informed consent was obtained from the patient for publication of this case report and accompanying images.
Availability of data and material: All data generated or analysed during this study are included in this article.
Competing interest: Authors declare no conflict of interest for this article.
Funding: No funding was received.
Authors' contributions: RVR and AA equally contributed to data collection, analysis, and interpretation, and revised manuscript. RAR and EPBM contributed to data interpretation, literature review of the case, and manuscript drafting. MS contributed to literature review of the case and manuscript drafting. all authors have read and approved the manuscript.
Acknowledgements: Not applicable
 

References

[1]      Wang M. Peripartum Cardiomyopathy : Case Reports. Fam Med 2009;13:42–5.
[2]      Gentry MB, Dias JK, Luis A, Patel R, Thornton J, Reed GL. African-American Women Have a Higher Risk for Developing Peripartum Cardiomyopathy. J Am Coll Cardiol 2010;55:654–9. https://doi.org/10.1016/j.jacc.2009.09.043.
[3]      Begum SA, Chowdhury S, Nasrin B, Ferdous J, Bhuiyan ZR. Peripartum cardiomyopathy. Bangladesh J Obstet Gynecol 2009;24:67–70.
[4]      Lee S, Cho GJ, Park GU, Kim LY, Lee TS, Kim DY, et al. Incidence, Risk Factors, and Clinical Characteristics of Peripartum Cardiomyopathy in South Korea. Circ Hear Fail 2018;11:1–8. https://doi.org/10.1161/CIRCHEARTFAILURE.117.004134.
[5]      Huang GY, Zhang LY, Long-Le MA, Wang LX. Clinical characteristics and risk factors for peripartum cardiomyopathy. Afr Health Sci 2012;12:26–31.
[6]      Kim MJ, Shin MS. Practical management of peripartum cardiomyopathy. Korean J Intern Med 2017;32:393–403. https://doi.org/10.3904/kjim.2016.360.
[7]      Dinic V, Markovic D, Savic N, Kutlesic M, Jankovic RJ. Peripartum Cardiomyopathy in Intensive Care Unit: An Update. Front Med 2015;2:1–6. https://doi.org/10.3389/fmed.2015.00082.
[8]      Davis MB, Arany Z, McNamara DM, Goland S, Elkayam U. Peripartum Cardiomyopathy: JACC State-of-the-Art Review. J Am Coll Cardiol 2020;75:207–21. https://doi.org/10.1016/j.jacc.2019.11.014.
[9]      Ramler PI, van den Akker T, Henriquez DDCA, Zwart JJ, van Roosmalen J. Incidence, management and outcome of women requiring massive transfusion after childbirth in the Netherlands: Secondary analysis of a nationwide cohort study between 2004 and 2006. BMC Pregnancy Childbirth 2017;17:1–8. https://doi.org/10.1186/s12884-017-1384-7.
[10]    Senanayake HM, Patabendige M. Two potentially lethal conditions of probable immune origin occurring in a pregnant woman: A case report. J Med Case Rep 2018;12:10–3. https://doi.org/10.1186/s13256-018-1701-4.
[11]    Irem Yesiler F, Tosun V, Behram Kandemir Y, Guntekin U. Is Cardiomyopathy Associated with Peripartum or Anaphylactic Reaction? Which One? J Cardiol Curr Res 2018;10:40–2. https://doi.org/10.15406/jccr.2017.10.00355.
[12]    Bosch MGE, Santema JG, Van Der Voort PHJ, Bams JL. A serious complication in the puerperium: Peripartum cardiomyopathy. Netherlands Hear J 2008;16:415–8. https://doi.org/10.1007/BF03086189.
[13]    Jennings LK, Watson S. Massive Transfusion. StatPearls Publishing; 2020.
[14]    Patil V, Shetmahajan M. Massive transfusion and massive transfusion protocol. Indian J Anaesth 2014;58:590–5. https://doi.org/10.4103/0019-5049.144662.
[15]    Clevenger B, Kelleher A. Hazards of blood transfusion in adults and children. Contin Educ Anaesthesia, Crit Care Pain 2014;14:112–8. https://doi.org/10.1093/bjaceaccp/mkt042.