Postpartum pulmonary edema 157

Acute Postpartum Pulmonary Edema: A Case Report

Min-Po Ho1, Wing-Keung Cheung2, Kaung-Chau Tsai1

Acute pulmonary edema after pregnancy is rare. Pulmonary emobolism, pneumonia, aspiration and
pulmonary edema are some of the potentially devastating causes that should be considered. We report a
case of a previously healthy 45 year-old woman had pulmonary edema 3 hours after a normal vaginal
delivery at a local clinic. Two days before admission, the patient had received tocolytic therapy to
suppress premature labor. After medical treatment, her symptoms subsided and a chest radiograph showed
resolution of pulmonary edema 12 hours later. She was discharged the next day in stable condition.

Key words: postpartum, acute pulmonary edema, tocolytic agent

Introduction or significant allergies. She had no family history

Postpartum pulmonary edema is a rare
clinical entity. Pulmonary edema of cardiac origin
is a common medical condition that can range in
severity from chronic, to subclinical to acute, with
accompanying severe respirstory compromise. In a
young, previously healthy postpartum patient, the
differential diagnosis must be expanded to include
some less prevalent casues, such as peripartum
cardiomyopathy and cardiac failure secondary to
tocolysis(1). Herein, we report a case of postpartum
noncardiogenic pulmonary edema with respiratory
distress after use of a tocolytic agent.
Case Report
A 45-year-old woman G2P1 presented to the
emergency department (ED) with progressive
dyspnea 3 hours after normal vaginal delivery
at a local clinic. She had no remarkable cardiac
disease, hypertension, respiratory tract infection
of cardiac or respiratory disease. Two days
previously, the patient had received tocolytic
therapy to suppress premature labor. Her baby had
been delivered by spontaneous vaginal delivery
at 37 weeks. The patient denied visual changes,
headache, and hand and face swelling. No lower
limb swelling was noted. On physical examination,
she had marked respiratory distress and chest
auscultation revealed basal crackles with reduced
breath sounds bilaterally. The rest of the physical
examination was unremarkable. Her blood pressure
was 110/68 mmHg, heart rate 120 beats/ minute,
respiratory rate 24 breaths/min, body temperature
37.4℃, and oxygen saturation on room air 89%.
Electrocardiography showed sinus tachycardia.
Her chest radiograph revealed increased
infiltration bilaterally (Fig. 1), compatible with
acute pulmonary edema. Laborotary data showed
mild leukocytosis and cardiac makers, C-reactive
protein and D-dimer were within the normal
range. A cardiologist was consulted and immediate

Received: November 25, 2009 Accepted for publication: January 11, 2010
From the 1Department of Emergency Medicine, 2Department of Medical Imaging, Far Eastern Memorial Hospital
Address reprint requests and correspondence: Dr. Kaung-Chau Tsai
Department of Emergency Medicine, Far Eastern Memorial Hospital
21 Section 2, Nanya South Road, Panchiao 220, Taipei County, Taiwan (R.O.C.)
Tel: (02)89667000 ext 1122 Fax: (02)89660454
E-mail: hikali@mail.femh.org.tw
158 J Emerg Crit Care Med. Vol. 21, No. 3, 2010
Fig. 1 Chest radiograph showing increased infiltration over both
lungs, compatible with acute pulmonary edema
echocardiography showed normal ventricular
function with an ejection fraction of 66%, trace
mitral and tricuspid regurgitation, normal wall
motion and no pericardial effusion, clots or shunt.
Arterial blood gas analysis showed the pH was
7.43, Pa CO2 38 mmHg, PaO2 59 mmHg and HCO2
28 mmol/L on 100% oxygen. Initial resuscitative
measures in the ED included oxygen administration
by nonrebreather mask, which increased her
oxygen saturation to 95%. Furosemide was
administered intravenously at a dose of 40 mg.
After aggressive medical treatment, her symptoms
gradually subsided and a repeat chest radiograph
(Fig. 2) taken 12 hours later showed resolution
of pulmonary edema. Urine output was 1700 mL
seven hours after initial treatment and she showed
considerable improvement in her symptoms.
Urinalysis revealed no evidence of urinary tract
infection. Blood cultures were negative. The patient
received close observation in the ED overnight
with monitoring of oxygen saturation, blood
pressure and electrocardiography. The next day,
12 hours after arrival in the ED, her pulmonary
edema was largely resolved and oxygen saturation
was 98% on room air. She was discharged in stable
condition. The patient was doing well at follow-up
9 months after discharge.
Discussion
It has been estimated that 0.08% of
pregnancies are complicated by acute pulmonary
edema. Despite the low rate of occurrence, there
is significant morbidity, and mortality has been
reported with this diagnosis(1). The most common
contributing factors include underlying cardiac
disease, the use of tocolytic agents, iatrogenic fluid
overload and preeclampsia(1,2).
According to Dunne et al 1, the differential
diagnosis for postpartum dyspnea includes the
following:
without pulmonary edema
• pulmonary embolism, amniotic fluid embolism,
pneumonia, foreign body aspiration, psychogenic
dyspnea
with pulmonary edema
• c a r d i o g e n i c : p e r i p a r t u m c a r d i o m y o p a t h y,
preecclampsia-related heart failure, underlying
cardiac disease, myocardial ischemia and sepsis
with poor cardiac output
• noncardiogenic: iatrogenic fluid overload, thyroid
disease, tocolytic therapy or medication related

Fig. 2 Twelve hours later, a chest radiograph shows resolution
of pulmonary edema
sepsis, acute respiratory distress syndrome
H o w e v e r, o u r i n v e s t i g a t i o n r u l e d o u t
pulmonary embolism, amniotic fluid embolism,
pneumonia and sepsis. Our patient was treated
with a tocolytic agent (β-adrenergic agonist) for
2 days. According to a physician from the local
clinic, iatrogenic fluid overload could be ruled out
because there was no history of administration of
large amounts of fluid before or during delivery.
Three hours after a normal vaginal delivery, our
patient suffered from progressive dyspnea. Cardiac
disease was ruled out as there was no evidence of
abnormal cardiac markers or abnormalities on the
echocardiogram. Tocolytic agents, which include
terbutaline, ritodrine, salbutamol, and isoxsuprine,
suppress premature uterine contractions during
pregnancy. These β-adrenergic agonists increase
intracellular cyclic adenosine monophosphate
levels, thus decreasing muscular contraction.
Pulmonary edema has been reported in association
with the short-term use of β-adrenergic agonists
(average 54 hours) in late pregnancy with
an incidence of approximately 0 to 4.4% (3,4) .
Pulmonary edema occurs during current or recent
(< 24 hours) usage or appears less than 12 hours
postpartum when tocolytic therapy has failed(5). In
Postpartum pulmonary edema 159
previous reports, using acute tocolysis therapy to
prolong pregnancy in patients hospitalized with
preterm labor at 32 to 34 weeks’ gestation was
associated with improved neonatal outcomes(6). At
32 weeks, tocolysis yielded the lowest total number
of adverse maternal and neonatal events. At 36
weeks it is probably better not to use tocolysis(7).
Generally, tocolytic therapy is not recommended
after 34 weeks’ gestation to avoid unnecessary
complications, such as noncardiogenic pulmonary
edema, as in our patient.
Clinical features and radiographic appearances
are generally indistinguishable from other causes
of pulmonary edema and adult respiratory distress
syndrome. Typical manifestations include dyspnea,
chest discomfort, tachypnea, and hypoxemia (5,8).
Unlike pulmonary edema due to congestive heart
failure, cardiomegaly and pulmonary vascular
redistribution are generally absent in cases that are
drug-related(8). Fluid overload purportendly occurs
in 70% of patients. Rapid clinical improvement
(< 24 hours) is normal, although a small percentage
of patients may need mechanical ventilatory
support. Mortality is low for both the mother
and fetus (5). These drugs may induce pulmonary
edema in pregnant women, although this effect
160 J Emerg Crit Care Med. Vol. 21, No. 3, 2010
has not been observed with treatment of asthma
in the nonpregnant state. This condition appears
to be a form of noncardiac pulmonary edema,
possibly caused by drug-induced fluid retention,
superimposed on that normally occurring in the
gravid state. This syndrome is unassociated with
evidence of myocardial dysfunction and responds
readily to diuretics and oxygen(9).
In conclusion, acute pulmonary edema in a
previously healthy woman who has recently given
birth is an uncommon clinical scenario with some
life-threatening complications. No matter what
the underlying pathology, prompt appropriate
resuscitation is always the first priority.
References
1. Dunne C, Meriano A. Acute postpartum
pulmonary edema in a 23-year-old woman
5 d a y s a f t e r c e s a r e a n d e l i v e r y. C J E M
2009;11:178-81.
2. Sciscione AC, Ivester T, Largoza M, Manley J,
Shlossman P, Colmorgen GH. Acute pulmonary
e d e m a i n p r e g n a n c y. O b s t e t G y n e c o l
2003;101:511-5.
3. Pisani RJ, Rosenow EC. Pulmonary edema
associated with tocolytic therapy. Ann Intern
Med 1989;110:714-8.
4. Russi EW, Spaetling L, Gmur J, Schneider H.
High permeability pulmonary edema (ARDS)
during tocolytic therapy: a case report. J
Perinat Med 1988;16:45-9.
5. R e e d C R, G l a u s e r F L. D r u g-i n d u c e d
noncardiogenic pulmonary edema. Chest
1991;100:1120-4.
6. Elliott JP, Istwan NB, Rhea DJ, Desch CN,
Stanziano GJ. The impact of acute tocolysis on
neonatal outcome in women hospitalized with
preterm labor at 32 to 34 weeks’ gestation. Am
J Perinatol 2009;2:123-8.
7. Macones GA, Bader TJ, Asch DA. Optimising
maternal-fetal outcomes in preterm labour:
a decision analysis. Br J Obstet Gynaecol
1998;5:541-50.
8. Lee-Chiong T Jr, Matthay RA. Drug-induced
pulmonary edema and acute respiratory distress
syndrome. Clin Chest Med. 2004;25:95-104.
9. Tavel ME, Le Jemtel TH. Differential diagnosis
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 產後發生急性肺水腫 161

產後發生急性肺水腫：病例報告

侯民波1　張永強2　蔡光超1

產後發生急性肺水腫是臨床上罕見的疾病。有關潛在性危險的肺栓塞，肺炎，肺水腫等原因也應該
要考慮的。我們報告一位45歲健康產婦自然生產後3小時發生急性肺水腫。該病患到院前2天在當地診所
接受安胎劑治療。經治療後症狀改善，12小時後追蹤胸部X光顯示肺水腫也消失。她第二天平安出院。

關鍵詞： 產後，急性肺水腫，安胎劑

收件：98年11月25日　接受刊載：99年1月11日
亞東紀念醫院1急診醫學部　2影像醫學科
通訊及抽印本索取：蔡光超醫師　台北縣板橋市南雅南路二段21號　亞東紀念醫院急診醫學部
電話：(02)89667000轉1122　傳真：(02)89660454
E-mail: hikali@mail.femh.org.tw