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\title{Peripartum cardiomyopathy and massive transfusion due to postpartum
hemorrhage: was it associated with each other?~~~~}



\author[1]{Raissa Virgy Rianda}%
\author[1]{Amelya Armadani}%
\author[1]{Rama Azalix Rianda}%
\author[1]{Eka Prasetya Budi Mulia}%
\author[2]{M Sukmana}%
\affil[1]{Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia}%
\affil[2]{Dr. Sayidiman General Hospital, Magetan, Indonesia}%


\vspace{-1em}



  
  \date{May 01, 2026}


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\selectlanguage{english}
\begin{abstract}
\textbf{Background}: Peripartum cardiomyopathy (PPCM) is a potentially
life-threatening pregnancy-associated disease marked by left ventricular
dysfunction and heart failure (HF). Clinical findings of HF are often
masked by the normal physiological changes seen in pregnancy, making the
diagnosis challenging. Furthermore, postpartum hemorrhage followed by
massive blood transfusion may mask the diagnosis of PPCM or worsen the
decompensated HF.

\textbf{Case Description}: We report a 35-year-old postpartum gemelli
woman with a history of massive postpartum hemorrhage due to atonia
uteri and Disseminated Intravascular Coagulation, complain of shortness
of breath and fever. The patient received a massive blood transfusion
for her massive postpartum hemorrhage. Physical examination revealed
tachypnea and bilateral rales at lung bases. Chest radiographs showed
cardiomegaly, right pleural effusion, and early lung edema. The
echocardiography showed a decrease in left ventricular systolic function
with ejection fraction of 41\%, diastolic dysfunction, and global
hypokinetic. She was diagnosed with PPCM, acute lung edema, pleural
effusion, and pneumonia. Patient was treated with Furosemide continuous
pump, Spironolactone, Bisoprolol, Valsartan. Her dyspnea greatly
decrased with diuresis and antibiotic. She was discharged with HF
medication continued.

\textbf{Discussion}: Women with PPCM typically present with symptoms of
HF and signs of congestion. History of massive blood transfusion at
first can mask the diagnosis of PPCM due to the possibility of
Transfusion Associated Circulatory Overload, which also has signs of
congestion. Massive blood transfusion can increase preload and may
worsen the decompensated HF.

\textbf{Conclusion}: The presence of massive transfusion in a patient
with PPCM can be challenging in diagnosing PPCM itself and the
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.%
\end{abstract}%



\sloppy


\emph{*Corresponding author :~}
\href{https://authorea.com/users/417051}{\emph{Raissa Virgy Rianda}}
\emph{(}\href{mailto:raissa_rianda@yahoo.com}{\emph{raissa\_rianda@yahoo.com}}\emph{)}

\textbf{~}

\section*{Abstract}

{\label{283714}}

\textbf{Background}: Peripartum cardiomyopathy (PPCM) is a potentially
life-threatening pregnancy-associated disease marked by left ventricular
dysfunction and heart failure (HF). Clinical findings of HF are often
masked by the normal physiological changes seen in pregnancy, making the
diagnosis challenging. Furthermore, postpartum hemorrhage followed by
massive blood transfusion may mask the diagnosis of PPCM or worsen the
decompensated HF.

\textbf{Case Description}: We report a 35-year-old postpartum gemelli
woman with a history of massive postpartum hemorrhage due to atonia
uteri and Disseminated Intravascular Coagulation, complain of shortness
of breath and fever. The patient received a massive blood transfusion
for her massive postpartum hemorrhage. Physical examination revealed
tachypnea and bilateral rales at lung bases. Chest radiographs showed
cardiomegaly, right pleural effusion, and early lung edema. The
echocardiography showed a decrease in left ventricular systolic function
with ejection fraction of 41\%, diastolic dysfunction, and global
hypokinetic. She was diagnosed with PPCM, acute lung edema, pleural
effusion, and pneumonia. Patient was treated with Furosemide continuous
pump, Spironolactone, Bisoprolol, Valsartan. Her dyspnea greatly
decrased with diuresis and antibiotic. She was discharged with HF
medication continued.

\textbf{Discussion}: Women with PPCM typically present with symptoms of
HF and signs of congestion. History of massive blood transfusion at
first can mask the diagnosis of PPCM due to the possibility of
Transfusion Associated Circulatory Overload, which also has signs of
congestion. Massive blood transfusion can increase preload and may
worsen the decompensated HF.

\textbf{Conclusion}: The presence of massive transfusion in a patient
with PPCM can be challenging in diagnosing PPCM itself and the
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.

\textbf{Keywords}: Peripartum cardiomyopathy, postpartum hemorrhage,
massive transfusion, heart failure, pregnancy

\section*{}

{\label{638990}}

\section*{Introduction~}

{\label{638990}}

Peripartum cardiomyopathy (PPCM) is a possible life-threatening
pregnancy-associated condition characterized by left ventricular (LV)
dysfunction and heart failure (HF). Clinical findings of HF are
sometimes obscured by normal physiological observed during pregnancy
that renders the diagnosis complicated. Furthermore, postpartum
hemorrhage followed by massive blood transfusion may mask the diagnosis
of PPCM or worsen the decompensated HF The Risk factors for PPCM include
multiparity, black ethnicity, older maternal age, preeclampsia, and
gestational hypertension {[}1{]}. A case-control study in the United
States showed that African American women had a 15.7-fold higher
relative risk of PPCM than non -- African Americans {[}2{]}. The
prevalence of PPCM among black women was four times that of white women
(1:1087 versus 1:4266), and the 5-year follow-up fatality risk was
almost four times greater (24\% versus 6\%) {[}3{]}. The incidence of
PPCM was 1 in 1741 deliveries in South Korea. There were 1.384.449
deliveries in South Korea between 2010 and 2012, despite removing 20.102
patients with previous suspected HF. Of these, 795 cases had codes that
were specified as PPCM {[}4{]}.

\par\null

\section*{Case Illustration}

{\label{393756}}

A 35-year-old multigravida
(G\textsubscript{4}P\textsubscript{3}A\textsubscript{0}) Indonesian
female referred to the Emergency Room (ER) by local midwifery and about
giving birth to her twin pregnancy. The first baby was born
spontaneously in her house one hour before admission. She had massive
and continued bleeding during delayed the second child labor. The
patient was observed to be lethargic during the ER examination and had
blood pressure (BP) 100/60 mmHg, heart rate 100 beats per minute,
respiratory rate of 24 breaths per minute, and oxygen saturation of
95\%. Hemoglobin from complete blood count shows 10.5 g/dL. The
gynecology examination was found uterine portio rupture and active
bleeding with three tampons attached. The second child was born in
hospital. She lost 750 ml of blood during labor and still had active
bleeding because of uterine atony and Disseminated Intravascular
Coagulation (DIC). The blood pressure decrease to 90/50 mmHg, a pulse
rate of 144 beats per minute, and the patient became agitated. She was
given 3000 ml of ringer lactate, four bags of whole blood transfusion,
and 1000 cc of HES solution. After the initial fluid resuscitation,
there was no sign of shortness of breath; however, the patient was still
agitated and disoriented. The patient was then scheduled for a
histerectomy right away.

During the hysterectomy, there was ongoing massive bleeding. She had a
transfusion of 750 ml of whole blood and 1000 ml of normal saline. After
the hysterectomy, the bleeding from vagina and drain was still active
(900 ml). Hemoglobin count showed 8 g/dL. The obstetrician decided to
reopen 3 hours after. After surgery, in the Intensive care unit (ICU),
the patient got five bags of fresh frozen plasma transfusion and five
bags of thrombocyte concentrate. The patient was noted to have DIC with
Prothrombin time (PT) 16.3 s (10-13 s), International Normalized Ratio
(INR) 1.22, Activated Partial Thromboplastin Time (aPTT) 35.5 s (25-35
s), Fibrinogen 319 g/L, D Dimer 7,777 ng/ml FEU. She was then observed
in ICU for 6 days and general ward for 9 days and then discharged with
no complaint.

Ten days after discharge from the hospital, the patient came to the ER
with shortness of breath, fever, and chest pain during cough for five
days and worsened in the last two days. The increased short of
breathness was associated with physical activity, and orthopnea was
noted.

On the ER examination, the patient was observed to be febrile and had a
normal BP (120/80mmHg), tachycardia (112 beats per minute), dyspnea (27
breaths per minute), and an oxygen saturation of 95\% while receiving
oxygen through 3 lpm nasal cannula. Her lungs were noted symmetrically
on inspection, dim on percussion in basal inferior, and bilateral rales
were found. Her heart rate was regular, without S3 gallop or murmur. Her
extremities were non-edematous. Compete blood count shows Hb 9.1 g/dL,
White blood cells 19,530 / \selectlanguage{greek}μ\selectlanguage{english}L, Thrombocyte 439,000 / \selectlanguage{greek}μ\selectlanguage{english}L. Blood gas
analysis showed partially compensated respiratory acidosis. An
electrocardiogram showed sinus tachycardia with a heart rate of 113
beats per minute with normal frontal axis and clockwise rotation on
horizontal axis (figure 1). Chest radiographs showed bilateral pleural
effusion, right paracardial infiltrate, and early lung edema (figure 2).

~\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/ecg/ecg}
\caption{{Sinus tachycardia on electrocardiogram.
{\label{553004}}%
}}
\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/WhatsApp-Image-2021-04-20-at-10-48-42/WhatsApp-Image-2021-04-20-at-10-48-42}
\caption{{Chest X-Ray on admission showing cardiomegaly, bilateral pleural
effusion, right paracardial infiltrate, and early lung edema.
{\label{702465}}%
}}
\end{center}
\end{figure}

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.

~

\section*{Discussion}

{\label{338952}}

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 \textgreater{}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 \textless{} 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 \selectlanguage{greek}β-\selectlanguage{english}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{]}.

~

\section*{Conclusion}

{\label{918739}}

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.

~

\textbf{Consent for publication:}~ Written informed consent was obtained
from the patient for publication of this case report and accompanying
images.

\textbf{Availability of data and material:} All data generated or
analysed during this study are included in this article.

\textbf{Competing interest:} Authors declare no conflict of interest for
this article.

\textbf{Funding:} No funding was received.

\textbf{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.

\textbf{Acknowledgements:} Not applicable

~

\section*{References}

{\label{354623}}

{[}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
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{[}8{]}~~~~~ Davis MB, Arany Z, McNamara DM, Goland S, Elkayam U.
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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
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https://doi.org/10.1186/s12884-017-1384-7.

{[}10{]}~~~ Senanayake HM, Patabendige M. Two potentially lethal
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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
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{[}15{]}~~~ Clevenger B, Kelleher A. Hazards of blood transfusion in
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