CURRENT REVIEW
Reexpansion Pulmonary Edema
Saade Mahfood, M.D., William R. Hix, M.D., Benjamin L. Aaron, M.D.,
Peter Blaes, M.D., and Donald C. Watson, M.D.
ABSTRACT Unilateral reexpansion pulmonary edema
(RPE) is a rare complication of the treatment of lung
collapse secondary to pneumothorax, pleural effusion, or
atelectasis. Although RPE generally is believed to occur
only when a chronically collapsed lung is rapidly reexpan-
ded by evacuation of large amounts of air or fluid, in this
review 15 of 47 cases of RPE available for assessment
occurred when the pulmonary collapse was of short dura-
tion or when the lung was reexpanded without suction.
The pathogenesis of RPE is unknown and is probably
multifactorial.Implicated in the etiological process of RPE
are chronicity of collapse, technique of reexpansion, in-
creased pulmonary vascular permeability, airway obstntc-
tion, loss of surfactant, and pulmonary artery pressure
changes. Since the outcome of RPE was fatal in 11 of 53
cases reviewed (20%), physicians treating lung collapse
must be aware of the possible causes and endeavor to
prevent the occurrence of this complication.
Although there are numerous noncardiac causes of
pulmonary edema [l], unilateral pulmonary edema fol-
lowing reexpansion of a collapsed lung is a rare compli-
cation [2,3]. We report a case of reexpansion pulmonary
edema (RPE)following pleural abrasion for spontaneous
pneumothorax and present a literature review on uni-
lateral pulmonary edema that occurs as a complication of
lung reexpansion following pneumothorax, pleural effu-
sion, and pulmonary atelectasis.
Case Report
A 24-year-old man suddenly experienced left-sided
chest pain and dyspnea on exertion. There was clinical
and roentgenographic evidence of complete pneumo-
thorax. A chest tube and 20 cm H,O underwater-seal
suction completely expanded the affected lung. Three
days later, the tube was removed and he was dis-
charged. Although the same complaints recurred the
following day, he did not seek medical attention until
one week later. There was again clinical and roentgen-
ographic evidence of complete left pneumothorax (Fig
1).Direct admission, lateral thoracotomy, inflation of the
lung by hand ventilation, and pleural abrasion were
performed. Two chest tubes were inserted and attached
to 20 cm H,O underwater-seal suction. The patient was
extubated and transferred to the recovery room breath-
From the Divisions of Cardiothoracic Surgery, The University of Ten-
nessee College of Medicine, Memphis, TN, and the George Washington
University Medical Center, Washington, DC.
Address reprint requests to Dr. Hix, The George Washington University
Medical Center, 2150 Pennsylvania Ave, NW, Washington, DC 20037.
340 Ann Thorac Surg 45:34@345, Mar 1988. Copyright 0 1988 by The Society of Thoracic Surgeons
ing 40% 0, administered by high-humidity face mask.
Five minutes later his clinical status deteriorated rapidly,
with severe coughing, foamy sputum, agitation, cyan-
osis, tachypnea (50/min), tachycardia (144/min), and
hypotension (systolic blood pressure, 84 mm Hg). Rales
could be heard over the entire left side of the chest.
Chest roentgenogram revealed unilateral pulmonary
edema of the left lung (Fig 2). Arterial blood gas analysis
revealed hypoxemia with hypercapnic respiratory acido-
sis. Following immediate reintubation and mechanical
ventilation with 10-cm positive end-expiratory pressure,
the hypoxemia abated. Over the next two hours his
hemodynamic and respiratory status stabilized. He was
extubated the following day. The remainder of his
hospital course was uneventful, and he was discharged
on the ninth postoperative day.
Reexpansion Pulmonary Edema following
Pneumothorax
RPE following pneumothorax was first reported in 1958
by Carlson and colleagues [4] and was comprehensively
reviewed by Ziskind and colleagues [5] in 1965. A search
of the literature disclosed 51 additional cases of unilat-
eral pulmonary edema following lung reexpansion in
pneumothorax. Clinical details were available for analy-
sis in 47 patients, including the present patient (Table 1)
[2-361. Of these patients, 38 were men and 9 were
women; average age was 42 years (age range, 18-84
years); 57% were under 50 years old. Pneumothorax was
present 3 days or longer in 39 of the 47 patients, or 83%
(average, 9 days; range, 0-81 days). Methods of lung
reexpansion included high negative suction with needle
aspiration, pump suction, chest tube with undenvater-
seal and suction, underwater-seal chest tube drainage
without suction, Heimlich valves, and reinflation by
positive-pressure ventilation. The onset of RPE was
immediate or within 1 hour in 30 of the 47 patients
(64%),and within 24 hours in the remainder. Almost all
cases of RPE were ipsilateral to the side of the pneumo-
thorax; contralateral pulmonary edema occurred in 3
patients, 2 of whom died. One patient had ipsilateral
and contralateral pulmonary edema sequentially and
recovered. The overall mortality was 19% (9 of 47
patients).
In the cases reviewed the clinical manifestations of
RPE varied from roentgenographic findings alone to
mild or severe cardiorespiratory insufficiency, shock,
coma, and death. Some patients received no specific
therapy; others were treated with a variety of modalities
and drugs, including oxygen, inotropic agents, digitalis,
steroids, diuretics, bronchodilators, and sedatives. In
severe cases, endotracheal intubation or tracheostomy
341 Current Review: Mahfood et al: Reexpansion Pulmonary Edema
Fig 1 . Spontaneous pneumothorax with complete collapse of left
lung.
Fig 2 . Unilateral reexpansion pulmonary edema of the left lung.
and mechanical ventilation with positive end-expiratory
pressure were required. Most patients who recovered
did so within a week.
Reexpansion Pulmona y Edema following Pleural
Effusion
In 1853, Pinault [37] described RPE following pleural
effusion in a patient who had a large volume of pleural
fluid rapidly removed by thoracentesis. RPE was not
unfamiliar in the late nineteenth and early twentieth
centuries when thoracentesis with high negative pres-
sure was often recommended for the aspiration of pleu-
ral effusions [38]. In 1905, Hartley [39] reviewed in detail
42 cases of "albuminous expectoration" following thora-
centesis. An analysis of these cases revealed a male-to-
female ratio of 30 : 12, with the condition mainly af-
fecting young patients (82% were 20-50 years old).
Pleurisy with serofibrinous effusion was the main indi-
cation for thoracentesis (28 patients). Three patients had
empyema, 7 had hydrothorax due to heart failure or
chronic renal disease, and 3 had malignant pleural
effusion. Pulmonary edema seldom occurred unless at
least 2 L (range, 30-5,500 ml) of effusion was rapidly
aspirated. Symptoms occurred several minutes to a few
hours following reexpansion. In most instances im-
provement occurred rapidly, usually within 24 to 48
hours; however, 7 patients (16%)died.
Recent reports of reexpansion pulmonary edema re-
lated to drainage of pleural effusion describe 7 patients,
6 in detail (Table 2) [6, 32,34, 40-421. Four were women,
2 were men; age ranged from 21 to 59 years; duration of
symptoms was 14 to 120 days; and an average of 2,600
ml was removed (range, 1,000-4,500 ml). The onset of
pulmonary edema was immediate in 3 patients and "a
few hours" in one instance. Four patients recovered,
and 2 died.
Reexpansion Pulmona y Edema following Atelectasis
Two instances of unilateral pulmonary edema following
rapid reexpansion of an atelectatic lung have been re-
ported [8]. In the case reported by Ravin and Dahmash
[49], total left lung atelectasis occurred during anesthesia
for abdominal surgery due to right bronchial intubation.
The malpositioned endotracheal tube was discovered in
the recovery room. Unilateral left pulmonary edema
followed rapid reexpansion of the lung after the endo-
tracheal tube was repositioned. There was no pleural
drainage in this patient.
Comment
RPE is generally considered a rare complication that
occurs when a chronically collapsed lung is rapidly
reexpanded by evacuation of large amounts of air or
fluid, usually with application of high negative intra-
pleural pressure. Although this is most often the case,
from this review it is clear that RPE can occur when the
pulmonary collapse has been of short duration or when
the lung is reexpanded without suction (15 of 47
patients).
That RPE is an unusual event is substantiated by two
large reviews in which 400 and 375 cases of spontaneous
pneumothorax (duration greater than one week in 10%)
were treated by tube thoracostomy and pleural suction
without this complication developing [44, 451. Some
observers believe that the true incidence of W E is
unknown because at times it is only a roentgenographic
phenomenon, without clinical manifestations [21, 281.
However, in most instances the onset of RPE is dra-
matic, and in our review the outcome was fatal in 11 of
53 recently reported cases (20%).
The exact cause of RPE is not known. Factors that
have been implicated in the pathogenesis of this com-
342 The Annals of Thoracic Surgery Vol45 No 3 March 1988

Table I. Recently Reported Cases of Reexpansion Pulmonary Edema Related to Pneurnothorax

No. of Age (yr)l Length of Reexpansion Onset of Affected
Reference, Year Patients Sex Collapse Method RPE Side Outcome

Carlson et a1 [4], 1958 5 (1)* 31lM 35d Hi-vol sxn 12 h I Recovered

Ziskind et a1 [5], 1965 1 19/F 5d Hi-vol sxn Immediate I Recovered
Trapnell and Thurston [6], 1970 2 55M 9d UWS; no sxn Immediate I Recovered
18lM 3d Hi-vol sxn 4 hr I Died
Humphreys and Berne [q,1970 2 67/F 14d C.T.; hi-vol sxn 45 min I Recovered
53M Few hours Needle aspiration 2 hr I Recovered
Sautter et a1 [8], 1971 1 69lM 81d C.T.; rapid 2 hr I Recovered
Childress et a1 [9], 1971 1 2#M 6d Hi-vol sxn Immediate I Recovered
RatIiff et a1 [lo], 1973 1 20M 3d C.T.; 15 cm sxn Immediate I Recovered
Steckell [ll],1973 2 8OlM Hours C.T.; rapid Immediate C Died
69M Hours C.T.; rapid Immediate C Died
Schwander et a1 [12], 1973 1 45lM 4d C.T.; UWS Immediate I Recovered
Martinez et a1 (131, 1973 2 23M 8d Needle aspiration Immediate I Recovered
25M 6d Needle aspiration Immediate I Recovered
Lopez et a1 [14], 1973 2 58lM 8d Needle aspiration 24 hr I Recovered
51M 5d Needle aspiration 24 hr I Recovered
Poulias and Prombonas (151, 1974 1 69M 1 hr C.T.; 15 cm sxn Immediate I Died
Grant [16], 1971 1 63/M 13d C.T. 4 hr I Died
Jaeschock [ l q , 1974 1 53M 74d Hi-vol sxn 5 hr I Died
Saini [MI,1974 1 21lM 7d C.T.; UWS Immediate I Recovered
Rogaly and Memtz [19], 1975 1 WM 8d C.T.; UWS 1 hr I Recovered
Shanahan et a1 [20], 1975 4 20lM 5d C.T.; 25 cm sxn Immediate I Recovered
18M 4d PPV Immediate I Recovered
23M 21d C.T.; 20 cm sxn Immediate I Recovered
84/M 10d No sxn 1 hr I Died
Waqaruddin and Bernstein [21], 1975 2 21M 35d Heimlich V Few minutes I Recovered
2#M 3d Heimlich V 3 hr I Recovered
Schaer and Roth [22], 1977 1 45lM 4d C.T. 5 hr I Recovered
Body et a1 [23], 1977 1 71lF 8d C.T.; 10 cm sxn 2 hr I Recovered
Mutz and Benzer [24], 1977 1 29M 8d C.T.; sxn 3 hr I Recovered
Sewell et a1 [ E l , 1978 1 28lM 6d C.T.; 20 cm sxn Immediate I Recovered
Gurman et a1 [26], 1978 1 5m 1 hr C.T.; Hi-vol sxn Immediate I Recovered
Brennan and Fitzgerald [27], 1979 1 3OlF 12 hr Heimlich V Few minutes I Recovered
Mahajan et a1 [28], 1979 1 181F 3d C.T.; 15 cm sxn 30 min I Recovered
Peatfield et a1 [29], 1979 1 19/F 1Od C.T.; UWS Immediate I Died
Miller [30], 1979 1 65M 5d Hi-vol sxn Immediate I Recovered
Sherman and Ravikrishna [31], 1980 1 79M Hours C.T.; 20 cm sxn Hours I Recovered
Kassis et a1 [3], 1981 2 63lM 7d Heimlich V Immediate I Recovered
72lM 7d Heimlich V Few hours I Recovered
Sprung et a1 [32], 1981 1 36M 3d C.T.; 15 cm sxn Immediate I Recovered
Karen et aI [33], 1983 1 58/M Od C.T.; sxn Immediate CII Recovered
Smith and Andersen (341, 1983 1 ... Long ... ... .. ...
Murphy and Tomlanovich [2], 1983 1 24A4 6d C.T.; 20 cm sxn 3 min I Recovered
Shaw and Caterine [35], 1984 2 23lF 13d C.T.; 20 cm sxn 3 hr I Recovered
25/F 7d C.T.; UWS 2 hr I Recovered
Kernodle et a1 [36], 1984 2 50M 21d C.T.; 10 cm sxn 10 min I Died
58lM 17d C.T.; UWS 3 min I Recovered
Present report, 1985 1 24/M 7d PPV 5 min I Recovered

W E = reexpansion pulmonary edema; M = male; F = female; hi-vol pump sxn = high-volume pump suction; sxn = suction; UWS = underwater seal;
C.T. = chest tube; PPV = positive-pressureventilation; Heimlich V = Heimlich valve; I = ipsilateral; C = contralateral.
*Details only provided for 1 patient
343 Current Review: Mahfood et al: Reexpansion Pulmonary Edema
Table 2. Recently Reported Cases of Reexpansion Pulmonary Edema Caused by Drainage of Pleural Effusion
No. of Age (yr)/
Reference, Year Patients Sex
Trapnell and Thurston [6], 1970 2 56/M
58/M
Buczko et a1 [40], 1981 1 59/F
Sprung et a1 [32], 1981 1 22iF
Marland and Glauser [41], 1982 1 49/F
Smith and Andersen [34], 1983 1 ...
Milne et a1 [42], 1983 1 21/F
RPE = reexpansion pulmonary edema; M = male; F = female.
plication include chronicity of collapse, technique of
reexpansion, increased pulmonary vascular permeabil-
ity, airway obstruction, loss of surfactant, and pulmo-
nary artery pressure changes.
Most authorities cite as major contributing factors in
the development of RPE the chronicity of collapse (usu-
ally more than 3 days) and the rapidity of reexpansion
(using negative intrapleural pressure) [5, 6, 19, 21, 25,
28, 30, 36, 46, 471. This clinical impression has been
confirmed by animal experimental studies [45, 46, 48,
491. Therefore, it has been suggested that slow evacua-
tion of air or fluid from the pleural space by underwater-
seal drainage alone [48] or by repeated aspirations of less
than 1,000 ml of fluid or air [50] may aid in preventing;
RPE as well as the reexpansion hypotension that some-
times occurs concomitantly [51]. However, as noted in this
review and in the literature, RPE can develop regardless of
the duration of lung collapse [7,11,15,26,31,33,49]. The
rate of expansion appears to be more critical than the
method of lung inflation or the level of negative pressure
applied [7,52]. W E has occurred without suction and after
reinflation of the lung by positive-pressure ventilation, as
in the present case report.
Recent evidence from clinical and experimental obser-
vations supports increased pulmonary vascular perme-
ability as a major etiological factor in the development of
RPE [32, 36, 40, 41, 43, 47, 52-54]. The cause of the
increased permeability is unknown. Factors implicated
include hypoxic injury to the capillary and alveolar
membranes, increased pulmonary capillary pressure
and blood flow, decreased surfactant, and mechanical
damage. Rapid reexpansion of a collapsed lung or sud-
den increase in negative intrapleural pressure causes a
rapid increase in pulmonary capillary pressure and
blood flow [5]. This increase can lead to fluid transuda-
tion across the capillary and alveolar membranes, espe-
cially in the presence of hypoxic injury, and result in an
increase in pulmonary extravascular water [25]. Pulmo-
nary blood flow is reduced by atelectasis [7, 54, 551, and
the resulting hypoxia may cause vascular damage di-
rectly [56], or such damage may be due in part to
oxygen-derived free radicals generated by restoration of
perfusion and ventilation to previously hypoxic areas of
Duration of Volume
Symptoms Aspirated Onset of
(days) (mu RPE Outcome
90 3,000 Few hours Recovered
... 2,000 Immediate Recovered
14 3,000 5 min Recovered
42 1,300 2 hr Died
120 1,000 1 hr Died
... 3,500 ... ...
21 4,500 Immediate Recovered
lung [57]. Mechanical stress to blood vessels during
reexpansion may contribute to increased vascular per-
meability.
Airway obstruction, with or without negative intra-
pleural pressure, increases the gradient between the
capillaries and the alveolar membranes, resulting in
transudation of fluid into the interstitial tissues and
alveoli [9, 271. However, in experimental RPE studies,
although microatelectasis was observed, bronchial ob-
struction was not demonstrated grossly or histologically
[4, 25, 481. Major bronchial occlusion has not been
demonstrated in RPE by bronchoscopic examination or
autopsy [15]; therefore, this is probably not a major
etiological factor.
Loss of tissue surfactant has been documented in
atelectatic lungs after 24 hours of induced pneumotho-
rax [25, 581. Although decreased surfactant is not the
cause of RPE, it probably contributes to the atelectasis
that accompanies pulmonary edema [4, 20, 251.
Although RPE is almost always ipsilateral to the side
of collapse, 3 instances of contralateral RPE have been
reported. Contralateral RPE occurred in 2 patients with
pneumothoraces following resuscitation from cardiac
arrest. Both patients were in severe left ventricular
failure. It was postulated that increased vascular resis-
tance and hypoperfusion in the collapsed lung pre-
vented development of pulmonary edema and that, by
the time the collapsed lung was reexpanded, measures
to treat pulmonary edema already had been instituted.
Both patients died [ll]. The third reported case of
contralateral RPE occurred in a patient who was cyanotic
from a left pneumothorax secondary to insertion of a
subclavian catheter. Initial roentgenograms showed
right-sided pulmonary edema. There was no evidence of
left ventricular failure, documented by low filling pres-
sures. However, there was marked increase in pulmo-
nary vascular resistance, associated with right-sided
heart failure, leading to reduced flow through the lungs
and a low-output state. It was believed that the causes of
contralateral pulmonary edema in this patient were the
acute, severe pulmonary hypertension and the associ-
ated capillary damage that was induced by systemic
hypotension and hypoxemia [33].
344 The Annals of Thoracic Surgery Vol 45 No 3 March 1988
It is not within the scope of this review to detail the
clinical management of RPE. Since RPE is generally
self-limited, the aim of treatment is to ensure that
adequate oxygenation and circulation are provided until
it resolves. The response of the lung to injury is edema
and alveolar collapse. The degree of resulting hypoxe-
mia depends on the extent of ventilation/perfusion mis-
match and the resultant intrapulmonary shunting. De-
creased pulmonary compliance and intraalveolar fluid
accumulation are additional factors contributing to hy-
poxemia [59]. If sufficient fluid volume is sequestered in
the lung, hypovolemia and hypotension occur. Roent-
genographic appearance and physical findings (in the
absence of frothy sputum and cyanosis) may not predict
the degree of physiological disturbance. The patient
must be closely monitored by arterial blood gas values
and, if necessary, with Swan-Ganz catheterization to
follow filling pressures and cardiac output. In the pa-
tient with only roentgenographic evidence of pulmonary
edema and no hypoxemia, no specific treatment is
necessary. Mild hypoxemia often is corrected by supple-
mental nasally administered oxygen. When severe hy-
poxemia is present, often accompanied by expectoration
of large amounts of frothy sputum, intubation and
mechanical ventilation with positive end-expiratory
pressure is required. Positive end-expiratory pressure
decreases intrapulmonary shunting and recruits col-
lapsed alveoli as it increases functional residual capacity.
Hypotension and low cardiac output must be managed
by volume replacement and inotropic agents, with care-
ful hemodynamic monitoring.
Physicians who are called on to treat hydrothorax or
pneumothorax must be aware of RPE. It usually occurs
unexpectedly and dramatically. RPE most often occurs
when a chronically collapsed lung is rapidly reexpanded
by increased negative intrapleural pressure, but as doc-
umented here, it can develop following reexpansion of
any collapsed lung, regardless of duration of collapse,
and in the absence of pleural suction. The rate of
reexpansion may be more critical than the amount of air
or fluid removed or the degree of suction applied.
Therefore, hydrothorax and pneumothorax, especially
when chronic, should be evacuated slowly, and pleural
suction only applied after the lung is mostly reexpan-
ded.
Despite increased awareness of this complication and
improved modalities for management, the mortality
from RPE remains notable and every effort must be
made to prevent its occurrence.
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