Acta Anaesthesiol Taiwan 2008;46(4):187−190

C ASE R EPO RT

Application of Pulse Contour Cardiac Output

(PiCCO) System for Adequate Fluid
Management in a Patient with
Severe Reexpansion Pulmonary Edema
Ming-Hui Hung, Kuang-Cheng Chan, Chia-Ying Chang, Chuen-Shin Jeng,
Ya-Jung Cheng*
Department of Anesthesiology, National Taiwan University Hospital, Taipei, Taiwan, R.O.C.

Received: Dec 24, 2007
Revised: Apr 2, 2008
Accepted: Apr 8, 2008
KEY WORDS:
extravascular lung water;
fluid therapy;
pulmonary edema
We report a case of severe reexpansion pulmonary edema that occurred immediately
after reinflation of a collapsed lung by rapid negative pressure drainage of pro-
longed malignant pleural effusion and pneumohemothorax. Although hemodynamic
stability was difficult to maintain under aggressive treatment with inhalation of
nitric oxide, inotropics and prostacyclin infusion, conventional pulmonary artery
catheterization was not adequate for surveillance and adjustment of fluid therapy.
For balancing the preload and the extent of pulmonary edema, pulse contour car-
diac output monitoring using a single transpulmonary thermal dilution technique
was applied to achieve optimal cardiac preload for organ perfusion and to prevent
worsening of pulmonary edema from fluid overload.

1. Introduction pulmonary edema arising from fluid overload. We

Reexpansion pulmonary edema (RPE) is a rare but
well described complication that occurs when a
collapsed lung expands rapidly by evacuation of air
or fluid in the pleura.1 The onset of symptomatic
RPE can be rapid and dramatic after decompression
and mortality is estimated to be as high as 20%.2
If RPE is complicated with significant third spacing
in the lung,3,4 a rapid fluid shift could deplete the
intravascular volume and lead to cardiovascular
collapse.5 In such a condition, fluid management
can be challenging for physicians attempting to
achieve optimal organ perfusion without worsening
report a case of RPE complicated by hypovolemic
shock after operation and highlight that pulse con-
tour cardiac output (PiCCO) monitoring is useful in
functional hemodynamic monitoring to guide fluid
management in patients with pulmonary edema and
hypovolemia.
2. Case Report
A 29-year-old woman with a history of excision of right
thigh synovial sarcoma, followed by localized radio-
therapy 7 years previously, developed progressive

*Corresponding author. Department of Anesthesiology, National Taiwan University Hospital, 7 Chung-Shan South Road,
Taipei 100, Taiwan, R.O.C.
E-mail: chengyj@ntu.edu.tw

©2008 Taiwan Society of Anesthesiologists

188 M.H. Hung et al

dyspnea during her 24th gestational week. Chest

X-ray showed massive pleural effusion all over the
right lung. She repeatedly received thoracocentesis
to relieve the symptoms, but no further aggressive
intervention was made because of her strong desire
to keep the baby. As her symptoms worsened, emer-
gency cesarean section under general anesthesia was
performed in the 29th gestational week. As dyspnea
and generalized edema were aggravated within
a week after the delivery, she was transferred to
our hospital. Follow-up chest X-ray showed total
white-out of the right hemithorax with left medias-
tinal shift, and computed tomography findings were
compatible with right hemopneumothorax.
Emergency thoracotomy and decortication were
performed under general anesthesia with pressure-
control positive-pressure one-lung ventilation. The
peak inspiratory pressure of mechanical ventilation
was set at less than 30 cmH2O, with positive end-
expiratory pressure (PEEP) of 5−10 cmH2O to maintain
adequate oxygenation. More than 6 L of serosanguin-
ous pleural effusion and sustained blood loss were Figure 1 Reexpansion pulmonary edema over the right
drawn out during decortication. In addition, blood lung field shown on chest X-ray 12 hours after operation.
transfusion and medications were needed because
of persistent hypotension with tachycardia. One-
lung ventilation could barely maintain pulse oxi- In order to achieve a better guide for fluid man-
metry at 90−95% at an inspired O2 fraction (FiO2) of agement and a better method for surveying pulmo-
100% (30 cmH2O of peak inspiratory pressure; 250− nary edema, the PiCCO system (PiCCO Plus; Pulsion
300 mL of tidal volume delivered), even with addi- Medical Systems, Munich, Germany) was then estab-
tional application of high-frequency jet ventilation lished. Optimization of hemodynamics was achieved
at the rate of 150 per minute to the non-dependent according to a protocol-guided therapeutic strategy,
lung. Before closure of the right hemithorax, the including global end diastolic volume index (GEDVI;
collapsed right lung was reexpanded with manual 680−800 mL/m2) and extravascular lung water index
positive-pressure inflation with peak inspiratory pres- (EVLWI; < 10 mL/kg). During the stay in the ICU, the
sure less than 30 cmH2O to examine whether there data obtained by the PiCCO system, i.e. GEDVI,
was air leakage. Immediately after reexpansion of EVLWI, pulmonary vascular permeability index (PVPI)
the collapsed right lung, frothy, pink and blood- and LIS were as shown in Table 1, the lowest LIS being
stained sputa were found in the tracheal lumen of the on the 6th and 7th postoperative days. Under hemo-
left-sided double-lumen endotracheal tube (35 Fr, dynamic and volumetric monitoring by the PiCCO
Broncho-CathTM Left; Mallinckrodt Medical, Athlone, system, the cardiovascular circulation was optimized
Ireland). RPE of the right lung was suspected. for adequate organ perfusion and the respiratory
For monitoring the hemodynamics and fluid man- oxygenation improved from then on. She was extu-
agement, a pulmonary artery catheter was placed bated and discharged from the ICU on day 14 without
via the right internal jugular vein soon after the cardiac and renal complications.
operation. In the first 12 hours in the intensive care
unit (ICU), severe hypotension, diffuse pulmonary
edema over the right hemithorax on the chest X-ray 3. Discussion
(Figure 1) and poor lung injury score (LIS; PaO2/
FiO2: 105 mmHg) were noted, but the central venous Conventional treatments of pulmonary edema include
pressure (CVP; 8 mmHg) and pulmonary capillary water restriction, diuretics, increase of colloid on-
wedge pressure (PCWP; 11 mmHg) were acceptable. cotic pressure, and protective ventilatory strategy
Pulmonary hypertension (43/21 mmHg) persisted (low tidal volume, application of PEEP). Neverthe-
despite use of inhaled nitric oxide, inotropics and less, optimization of hemodynamics and fluid bal-
prostacyclin infusion. Transesophageal echocardiog- ance remain difficult in mechanically ventilated
raphy was performed, which revealed low ventricu- patients with pulmonary edema and hypovolemia.
lar filling without systolic or diastolic dysfunction Adequate cardiac preload is crucial to restore and
of the left ventricle. maintain organ perfusion but these patients are at
PiCCO system for reexpansion pulmonary edema 189

Table 1 Data obtained from the PiCCO system, PEEP level and LIS during ICU stay

Day

1 2 3 4 5 6 7 8 9 10 11 12

CVP (mmHg) 6 8 7 10 9 10 9 7 6 5 6 7
GEDVI (mL/m2) 581 748 854 712 758 694 693 776 776 801 787
EVLWI (mL/kg) 11 9 9 11 13 13 12 11 11 12 12
PVPI 2 2 1.7 2.3 2.7 3 2.8 2.4 2 1.8 1.7
LIS (mmHg) 229 105 137 155 111 80 89 224 270 248 289 330
PEEP (cmH2O) 6 10 10 10 10 10 12 15 15 12 10 6

CVP = central venous pressure; GEDVI = global end-diastolic volume index; EVLWI = extravascular lung water index; PVPI = pulmonary
vascular permeability index; LIS = lung injury score (PaO2/FiO2); PEEP = positive end-expiratory pressure.

high risk of aggravation of pulmonary edema due
to potentially leaky capillaries.3 Hypotension often
follows RPE due to rapid massive effusion, contin-
uous surgical bleeding or fluid shift into the alveolar
space;4,5 even cardiovascular collapse may ensue
in severe cases.6 In this case of severe progressive
RPE, conventional monitoring with CVP and PCWP
was incapable of assessing adequate cardiac preload
because of mechanical ventilation with high PEEP
support to maintain respiratory stability. On the other
hand, GEDVI is reportedly a more sensitive guide
for fluid management than PCWP and CVP, espe-
cially under the influence of applied PEEP.6 Here,
we present the application of the PiCCO system for
adequate fluid management of severe RPE, using
parameters like GEDVI, PVPI and EVLWI to balance
the cardiac preload with the pulmonary condition.
Along with LIS and the clinical picture on chest
X-ray, EVLWI can serve as a surrogate for parame-
ters determined by pulmonary arterial catheter in
severe pulmonary edema.7 In combination with PVPI,
the causes of pulmonary edema can be further dif-
ferentiated between cardiogenic fluid overload,
congestive heart failure, or a noncardiogenic origin,
arising from a permeability change from capillary
membrane disruption, such as in acute respiratory
distress syndrome.8,9 In this case, the changes in
PVPI were correlated well with the changes in LIS
that increased from the 2nd day and peaked on the
6th to 7th day (Table 1). The delayed worsening of
LIS were considered to be mainly effected by per-
meability change, instead of hydrostatic pressure
from fluid overload, because EVLWI remained rela-
tively high and stable throughout the whole course
in the ICU, whereas the PVPI increased. It was dif-
ficult to maintain pulmonary oxygenation while the
increase in permeability continued. While permea-
bility change plays a major part in pulmonary edema
in sepsis and acute respiratory distress syndrome,
PVPI may be regarded as a better guide for fluid
management in pulmonary edema arising from cap-
illary membrane disruption. Prolonged higher EVLWI
than average may be the result of capillary mem-
brane disruption from prolonged pneumohemothorax
or physiological change during pregnancy.
The pathophysiology underlying the development
of RPE has not been well determined.10 For a perme-
ability change from reperfusion and reoxygenation
to cause damage of the endothelium,11−14 hydro-
static factors, such as pulmonary vascular flow re-
distribution, have been proposed to be involved.10
Although RPE is usually described in the treatment
of a chronically collapsed lung caused by pneumo-
thorax and pleural effusion, it can also occur imme-
diately following surgical procedures that employ
one-lung ventilation in operating theaters.15,16 It is
preferable that reexpansion of the collapsed lung
should be carried out gradually after the thoracic
procedures while the thoracotomy tube for drainage
should not be under excessive negative pressure
suction. Diagnosis should be mainly based on knowl-
edge of this potentially life-threatening complication
(history of collapsed lung with rapid reinflation or
evacuation, prominent unilateral increased infiltrate
on chest X-ray), while at the same time excluding
cardiogenic or other factors such as transfusion-
related acute lung injury, pneumonia, or fluid excess
as the cause of pulmonary edema. If RPE occurs, the
treatment is supportive, including positive-pressure
ventilation. Diuresis and inotropic support should
be considered in individual cases.
In conclusion, it is very important that physicians
who take care of a patient with a collapsed lung
should be aware of RPE. This will facilitate pre-
vention of RPE and offer timely and appropriate
treatment if it does occur. The balancing of fluid
management on preload and extravascular lung
water remains difficult in severe cases of RPE. For
better management of optimal preload for organ
perfusion and prevention of worsening of pulmonary
edema, we suggest that PiCCO monitoring could
offer a more rational guide than pulmonary artery
catheterization in patient management. Its role in
this aspect warrants further investigation.
190
References
1. Mahfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Reexpansion
pulmonary edema. Ann Thorac Surg 1988;45:340−5.
2. Trachiotis GD, Vricella LA, Aaron BL, Hix WR. As originally
published in 1988: reexpansion pulmonary edema. Updated
in 1997. Ann Thorac Surg 1997;63:1206−7.
3. Sakka SG, Klein M, Reinhart K, Meier-Hellmann A. Prognostic
value of extravascular lung water in critically ill patients.
Chest 2002;122:2080−6.
4. Cinnella G, Dambrosio M, Brienza N, Ranieri VM. Reexpansion
pulmonary edema with acute hypovolemia. Intensive Care
Med 1998;24:1117.
5. Sherman SC. Reexpansion pulmonary edema: a case report
and review of the current literature. J Emerg Med 2003;
24:23−7.
6. Kinasewitz GT, Keddissi JI. Hepatic hydrothorax. Curr Opin
Pulm Med 2003;9:261−5.
7. Boussat S, Jacques T, Levy B, Laurent E, Gache A, Capellier G,
Neidhardt A. Intravascular volume monitoring and extravas-
cular lung water in septic patients with pulmonary edema.
Intensive Care Med 2002;28:712−8.
8. Kuzkov VV, Kirov MY, Sovershaev MA, Kuklin VN, Suborov EV,
Waerhaug K, Bjertnaes LJ. Extravascular lung water deter-
mined with single transpulmonary thermodilution corre-
lates with the severity of sepsis-induced acute lung injury.
Crit Care Med 2006;34:1647−53.
M.H. Hung et al
9. Monnet X, Anguel N, Osman D, Hamzaoui O, Richard C,
Teboul JL. Assessing pulmonary permeability by transpulmo-
nary thermodilution allows differentiation of hydrostatic
pulmonary edema from ALI/ARDS. Intensive Care Med 2007;
33:448−53.
10. Neustein SM. Reexpansion pulmonary edema. J Cardiothorac
Vasc Anesth 2007;21:887−91.
11. Sivrikoz MC, Tuncozgur B, Cekmen M, Bakir K, Meram I,
Kocer E, Cengiz B, et al. The role of tissue reperfusion in
the reexpansion injury of the lungs. Eur J Cardiothorac Surg
2002;22:721−7.
12. Jackson RM, Veal CF, Alexander CB, Brannen AL, Fulmer JD.
Re-expansion pulmonary edema. A potential role for free
radicals in its pathogenesis. Am Rev Respir Dis 1988;137:
1165−71.
13. Suzuki S, Tanita T, Koike K, Fujimura S. Evidence of acute
inflammatory response in reexpansion pulmonary edema.
Chest 1992;101:275−6.
14. Sprung CL, Loewenherz JW, Baier H, Hauser MJ. Evidence
for increased permeability in reexpansion pulmonary edema.
Am J Med 1981;71:497−500.
15. Yanagidate F, Dohi S, Hamaya Y, Tsujito T. Reexpansion pul-
monary edema after thoracoscopic mediastinal tumor resec-
tion. Anesth Analg 2001;92:1416−7.
16. Critchley LA, Au HK, Yim AP. Reexpansion pulmonary edema
occurring after thoracoscopic drainage of a pleural effusion.
J Clin Anesth 1996;8:591−4.