American Journal of Emergency Medicine (2010) 28, 842.e1–842.
e4
Case Report
Massive atelectasis with acute respiratory failure in
postpartum misdiagnosed as pulmonary embolism
Abstract
Acute life-threatening complications can arise during
early postpartum period and result in maternal morbidity and
mortality. Prompt recognition of life-threatening conditions
and early effective management are essential to ensure
optimal maternal outcome. Thus, peripartum acute respira-
tory failure is an important cause of mortality, accounting for
30% of maternal deaths. We report a rare case of complete
left lung atelectasis, due to a massive fresh intrabronchial
clot, with respiratory failure, occurring in early postpartum
after cesarean delivery. The diagnosis was established by
direct flexible bronchoscopic evaluation. Therapy involved
lavage and clot aspiration. To the best of our knowledge,
there is no case report about this complication in the
early postpartum.
Peripartum acute respiratory failure is an important cause
of mortality, accounting for 30% of maternal deaths, with
pulmonary embolism being the leading cause of maternal
death [1]. Endobronchial blood clot is an unusual mechanism
of airway obstruction. The first confirmed case of endo-
bronchial obstruction from blood clot in a woman with
tuberculosis was reported by Wilson [2] in 1929. It has been
noted as a complication of bronchiectasis, tuberculosis,
mitral stenosis, pulmonary infarction, pulmonary arteriove-
nous malformation, sarcoidosis, bronchial carcinoma, or
intrathoracic trauma [3]. Mucosal damage from different
procedures has also led to airway blood clots [3].The
incidence of this complication is still not known. The impact
on respiratory function may be minimal or result in life-
threatening condition [3].
We report a rare case of complete left lung atelectasis with
respiratory failure due to a massive intrabronchial clot
occurring in early postpartum. It is important to consider this
condition to avoid unnecessary diagnostic test and to institute
prompt and proper therapy.
A 23-year-old overweight primigravida woman was
transferred to our emergency department 48 hours after the
cesarean delivery with general anesthesia. She suddenly
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developed dyspnea with anterior chest pain. On admission,
she was apyrexial and restless with central cyanosis. Cardiac
examination revealed tachycardia (120 beats per minute),
mild hypotension (80/60 mm Hg) without signs of
hypoperfusion, and no murmurs or gallop. Lungs were
clear, respiratory rate was 30 per minute, and oxygen
saturation was 78%, while receiving oxygen at a rate of 6 to
10 L/min by nasal cannula. Abdominal and gynecologic
examinations were as expected for postpartum stage. Arterial
blood gas measurements showed type I respiratory failure
(Table 1). Electrocardiogram showed sinus tachycardia with
diffuse flattened T waves. Transthoracic echocardiography
showed moderate tricuspid regurgitation with moderate
pulmonary hypertension (estimated systolic pulmonary
artery pressure of 50 mm Hg), without right chamber
dilation or paradoxical interventricular septal movement.
Left heart evaluation revealed no structural disease, with
preserved left ventricular systolic and diastolic functions, and
no signs of high left ventricular filling pressure (E/E′ ratio, 7;
E/Vp ratio, 1.6).
She was admitted on the cardiac intensive care unit where
empirical therapy for presumptive pulmonary embolism was
initiated with intravenous heparin and oxygen by nasal
cannula. After 6 hours, she repeated a new episode of
dyspnea, with oxygen saturation decreasing down to 70%. A
new clinical examination revealed diminished left chest wall
motion and reduction of vocal fremitus and flattening of the
percussion in the same area. Blood tests showed leukocytosis
with neutrophilia (26 120/mm3), inflammatory syndrome
(erythrocyte sedimentation rate, 74 mm/h; fibrinogen, 749
mg/dL), without other significant abnormalities (Table 1).
Chest x-ray (CxR) confirmed complete atelectasis of the
left lung (Fig. 1 A). Thoracic computed tomographic (CT)
scan showed complete collapse of the left lung, due to
obstructive material at the level of the proximal left main
stem bronchus (Fig. 2). Fiberoptic bronchoscopy revealed a
reddish giant fresh clot, obstructing the proximal left main
stem bronchus, without other abnormalities. Endobronchial
lavage and aspiration were successful in removal of the
entire clot.
After the clot removal, she remained apyrexial, without
dyspnea, and with normal oxygen saturation. Heart rate and
blood pressure returned to normal. After 24 hours, CxR
842.e2 Case Report

Table 1 Blood tests during admission

Admission 4th day Reference range
Biochemistry Glucose (mg/dL) 70 – 70-115
Urea (mg/dL) 15 20 10-40
Creatinine (mg/dL) 0.80 0.59 0.6-1.2
Sodium (mmol/L) 140 – 132-147
Potassium (mmol/L) 3.7 – 3.5-5.1
ALT (U/L) 17 – 5-37
AST (U/L) 22 – 5-40
PT (s) 11.5 – 11-13.2
ESR (mm/h) 74 64 5-10
Fibrinogen (mg/dL) 749 600 200-400
Hematology WCC (per mm3) 26 120 15 800 4000-9000
Neutrophils (%) 83.7 83 34-75
Hemoglobin (g/dL) 10.8 10.9 11-15.5
Hematocrit (%) 32.1 32.5 37-50
MCV (fL) 98 100 85-96
Platelets (×103/mm3) 310 326 150-350
Acid-base status pH 7.44 7.40 7.35-7.45
PO2 (mm Hg) 58 95 83-108
PCO2 (mm Hg) 21 33 32-48
SaO2 (%) 90 96 94-99
Lactate (mg/dL) 6 5 5-14
HCO−3 (mmol/L) 17.5 23 22-26
Base (mmol/L) −9 −1 −2 to + 2
ALT indicates alanine transaminase; AST, aspartate transaminase; PT, prothrombin time; ESR, erythrocyte sedimentation rate; WCC, white cell count;
MCV, mean corpuscular volume; SaO2, oxygen saturation; HCO−3 , bicarbonate.

showed only a small degree of atelectasis in the left
pulmonary base (Fig. 1 B). Patient was discharged
uneventfully after 4 days. A 7-day broad-spectrum antibiotic
therapy with amoxicillin/clavulanate was recommended.
We report a rare case of complete left lung atelectasis,
with respiratory failure, due to a massive fresh intrabronchial
clot, occurring in early postpartum.
Pregnancy increases the risk of respiratory failure from
numerous causes, such as pulmonary embolism, cardiomy-
opathy, amniotic fluid embolism, adult respiratory distress
syndrome, pneumonia, and others [1,4-6].
Our case presented with sudden acute hypoxic respiratory
failure, the suspected diagnosis being of pulmonary
embolism. However, there were no electrocardiographic
findings of right heart pressure overload, and echocardiog-
raphy revealed only nonspecific right heart abnormalities
because mild-to-moderate pulmonary hypertension and
tricuspid regurgitation can be normal findings in early

Fig. 1 Chest x-ray at admission (left panel) shows opacification of the entire left hemithorax, ipsilateral shift of the mediastinum,
and elevation of the left diaphragm; after 24 hours from clot removal (right panel), regression of this opacification, with a small residual
atelectasis (arrow).
Case Report
Fig. 2 Thoracic CT scan shows opacification of the entire left hemithorax, left shift of the mediastinum, elevation of the left diaphragm,
crowding of the ribs, and a small left pleural effusion (5-6 mm), without thrombus in the pulmonary artery; compensatory hyperlucency of the
right lung.
postpartum. Because CxR showed complete left lung
atelectasis, a thoracic CT scan was performed, which was
essential to rule out pulmonary embolism; it confirmed a
massive atelectasis of the left lung due to a foreign body in
the proximal left main stem bronchus. The nature of this
foreign body was further clarified by flexible bronchoscopy.
The most common causes of acute atelectasis are
bronchial obstructions due to plugs, foreign bodies, endo-
bronchial tumors, or blood clots [7]. Airway obstruction
caused by blood clots has been reported as a complication of
bronchiectasis, tuberculosis, pulmonary infarction, pulmo-
nary arteriovenous malformation, and chest trauma [3].
Tracheobronchial mucosal damage from suctioning may also
result in endobronchial bleeding with clot formation [3].
Scarce data are available about the incidence of this severe
complication in relation with tracheobronchial intubation-
extubation procedures and general anesthesia [3,8].
Because no other disease was present in our case, we believe
that the mechanism of clot formation was a traumatic extubation.
Symptoms developed after 48 hours probably because of the
clot extension in the proximal main stem bronchus.
To the best of our knowledge, there is no case report
about this complication in the early postpartum. All reported
cases had a definite disease or trauma as a cause of clot
formation [3].
Any intervention to attempt removal of the clot may
induce further bleeding and result in more proximal
obstruction. Therefore, in a hemodynamically stable patient
with a normal gas exchange, the appropriate management is
careful follow-up [3]. In our case, repeated episodes of
dyspnea and arterial desaturation indicated the necessity of
clot removal. The initial strategy should involve flexible
bronchoscopic evaluation with lavage and aspiration. If
unsuccessful, the next step is forceps extraction, either en
bloc or in piecemeal fashion or Fogarty catheter dislodgment
of the clot [3]. Topical thrombolysis has been proposed,
under direct visualization of the clot via flexible bronchos-
copy [9,10]. Our case was successfully managed with lavage
and aspiration, without recurrence of symptoms. Because
secondary atelectasis usually becomes infected, regardless of
842.e3
the cause of obstruction, broad-spectrum antibiotics were
prescribed, marked inflammatory syndrome suggesting
associated infection [7].
Acute respiratory failure is an important problem in
peripartum. The emergency physicians should be made
aware of the rare causes, such as bronchial obstruction with
complete atelectasis due to blood clot. This diagnosis
should be taken into consideration, in the setting of general
anesthesia with intubation-extubation procedures. Any
delays in diagnosis and management could lead to maternal
death. The diagnosis is established by direct flexible
bronchoscopic evaluation. The next step is lavage and
clot aspiration.
Acknowledgments
We are grateful for participation in case diagnosis to
Dr Costica Balan, Dr Vlad Vintila, and Dr Andrea Ciobanu.
Roxana C. Sisu MD
Gabriela Bicescu MD, PhD
Dragos Vinereanu MD, PhD
Department of Cardiology
University and Emergency Hospital of Bucharest
169 Splaiul Independentei, sector 5, 050098
Bucharest, Romania
E-mail address: dvinereanu@yahoo.com
doi:10.1016/j.ajem.2009.11.012
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Case Report
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