J Extra Corpor Technol. 2005 Mar;37(1):43-7. 

Is platelet function as measured by Thrombelastograph monitoring in whole blood
affected by platelet inhibitors?

Bailey LA, Sistino JJ, Uber WE.

Department of Cardiovascular Perfusion, Medical University of South Carolina,
Charleston, South Carolina, USA. labailey@hotmail.com

Platelet inhibitors, especially the glycoprotein (GP) IIb/IIIa receptor
antagonists, have demonstrated their effectiveness in reducing the acute
ischemic complications of percutaneous coronary intervention (PCI) and in
improving clinical outcomes in patients with acute coronary crisis. Three common
platelet inhibitors observed in emergent cardiopulmonary bypass (CPB) for failed
PCI are abciximab, eptifibatide, and tirofiban. An in vitro model was
constructed in two parts to determine whether platelet aggregation inhibition
induced by platelet inhibitors would be demonstrated by the Thrombelastograph
(TEG) monitor when compared with baseline samples with no platelet inhibitor. In
part A, 20 mL of fresh whole blood was divided into four groups: group I =
baseline, group A = abcix-imab microg/mL, group E = eptifibatide ng/mL, and
group T = tirofiban ng/mL. Platelet inhibitor concentrations in whole blood were
derived starting with reported serum concentrations with escalation to achieve
80% platelet inhibition using the Medtronic hemoSTATUS and/or Lumi-aggregometer.
A concentration range determined by our in vitro tests were chosen for each drug
using concentrations achieving less than, equal to, or greater than 80% platelet
inhibition. In part B, TEG analysis was then performed using baseline and
concentrations for each drug derived in part A. Parameters measured were clot
formation reaction time (R), coagulation time (K), maximum amplitude (MA) and
alpha angle (A). Groups E1000 and E2000 extended R over control by 37% and 23%,
respectively (p = 0.01 and 0.03). Groups E1000 and E2000 increased K times by
45% and 58% (p = .02 and .04). T160 samples prolonged K by 20% (p = 0.01). The
angle or clot strength (A) was decreased in groups T160 and E1000 by 23% (+ 7.06
SD) and 18% (+ 11.23 SD), respectively (p = 0.001 and 0.01). The MA decrease was
statistically significant in the T160, E1000 and E2000 by 9%, 6% and 13%
respectively (p = 0.01). Samples treated with abciximab were comparable to
control values for all parameters measured. Although statistical significance
could be demonstrated with some parameters, sensitivity was only observed at
increased doses and was not seen with all agents tested. In our in vitro model,
the TEG monitor was unable to demonstrate clinically significant differences in
platelet function and may not be reflective of platelet function in samples
which have been treated with these GP IIb/IIIa inhibitors.

J Extra Corpor Technol. 2005 Mar;37(1):38-42. 

Temperature inaccuracies during cardiopulmonary bypass.

Salah M, Sutton R, Tsarovsky G, Djuric M.

Rush University, Perfusion Technology Program, Rush-Presbyterian-St Luke's
Medical Center, Chicago, Illinois 60612, USA.

Cerebral hyperthermia caused by perfusate temperature greater than 37 degrees C
during the rewarming phase of CPB has been linked to postoperative neurologic
deficits. The purpose of this study was to determine the accuracy of the coupled
temperature measurement system and the CDI 500 arterial temperature sensor.
Seventeen patients undergoing CPB were divided into four groups, each with a
different temperature probe coupled to the oxygenator. The coupled temperature
measurement system and CDI temperature sensors were compared with an indwelling
probe placed in direct contact with the arterial perfusate. Blood, bladder, room
and water temperatures, arterial line pressure, blood flow, and hemoglobin were
recorded while the patients were supported with CPB. The actual blood
temperature was significantly higher than the coupled temperature measurement
system for two of the four groups (mean = 1.61 degrees C and 0.91 degrees C, p <
0.0001). A significant positive correlation between the actual temperature and
the coupled temperature measurement system error was observed for the same two
groups (r = 0.44, p < 0.0001). The actual temperature was significantly higher
than the CDI temperature in all patients (mean = 1.2 degrees C, p < 0.0001). The
coupling mechanism on the oxygenator generates inconsistent temperature
readings. The perfusionist should consider these inconsistencies when using
coupled temperature measurements and may consider the use of a direct
temperature measurement system. The CDI temperature error is probably the result
of inadequate flow through the sensor. On the test circuit, the flow of 170
mL/min was inadequate for circuit temperature accuracy. The accuracy of the CDI
temperature drastically improved when the flow-through the sensor was increased
to approximately 400 mL/min. Thus, the perfusionist must ensure adequate flow
through the sensor in order for the temperature mechanism to function properly.
Finally, the perfusionist can prevent cerebral hyperthermia by not allowing
water temperature to exceed 37 degrees C, when using a coupled temperature
measurement system.

J Pediatr Surg. 2005 Mar;40(3):510-5. 

Does antegrade cerebral perfusion protect the brain during deep hypothermic
circulatory arrest?

Mahan VL, Ilangovan S, Cuison R, Patil J, Dockter S, Rizzo V, Ilbawi M.

Department of Pediatric Cardiothoracic Surgery, Heart Institute for Children at
Hope Children's Hospital, Oak Lawn, IL, USA. vmahan@kaleidahealth.org

PURPOSE: This study compares cerebral protection using no cerebroplegia and
using antegrade cerebroplegia with variable flow rates during deep hypothermic
circulatory arrest (DHCA). METHODS: Twenty healthy neonatal piglets (2.5-3.8 kg)
underwent 60 minutes of DHCA. No cerebroplegia was used in group 1 (n = 5). Cold
(16 degrees C) antegrade cerebral perfusate was administered through the
innominate artery at 10 mL/kg per minute in group 2 (n = 5), at 25 mL/kg per
minute in group 3 (n = 5), and at 50 mL/kg per minute in group 4 (n = 5). Venous
samples for lactate, pyruvate, S-100B protein, and creatine kinase BB (CKBB)
were drawn from the jugular vein before and after discontinuation of
cardiopulmonary bypass--lactate at 5 minutes postbypass, pyruvate at 5 minutes
postbypass, S-100B protein at 30 minutes postbypass, and CKBB at 6 hours
postbypass. Piglets were killed 6 hours postbypass and their brains were
harvested for histological/immunologic studies. Extent of damage was assessed
using a semiquantitative score of 0 to 4 based on a validated method. RESULTS:
Evidence for significant apoptosis and necrosis was apparent in all groups. The
mean H&E score was 2.2 for group 1, 2.3 for group 2, 2.5 for group 3, and 2.3
for group 4. The mean terminal deoxynucleotidyl transferase-mediated dUTP-biotin
nick end labeling score was 1.0 for group 1, 1.2 for group 2, 1.7 for group 3,
and 0.8 for group 4. Pathological changes were not greater in the piglets that
did not have antegrade cerebral perfusion. Serum lactate, pyruvate, S-100B
protein, and CKBB did not distinguish between perfusion strategies. CONCLUSIONS:
In neonates, unmodified antegrade cerebral perfusion at flow rates of 10, 25,
and 50 mL/kg per minute during DHCA does not provide additional protection of
the brain as determined by histology, immunology, serum lactate, pyruvate,
S-100B protein, and CKBB.

Chest. 2005 Mar;127(3):892-901. 

Pulmonary outcomes of off-pump vs on-pump coronary artery bypass surgery in a
randomized trial.

Staton GW, Williams WH, Mahoney EM, Hu J, Chu H, Duke PG, Puskas JD.

Department of Medicine, Division of Pulmonary and Critical Care Medicine, Emory
University School of Medicine, Medical Director, Wesley Woods Long Term
Hospital, 1821 Clifton Rd NE, Atlanta, GA 30329, USA.
gerald_staton@emoryhealthcare.org

STUDY OBJECTIVES: Comparison of pulmonary outcomes after off-pump coronary
artery bypass (OPCAB) vs on-pump coronary artery grafting with cardiopulmonary
bypass (CABG/CPB).Study design: We examined preoperative and postoperative
respiratory compliance, fluid balance, hemodynamics, arterial blood gases, chest
radiographs, spirometry, pulmonary complications, and time to extubation in a
prospective trial of 200 patients randomized to OPCAB vs CABG/CPB performed by
one surgeon. RESULTS: One CABG/CPB patient and two OPCAB patients required
mitral valve repair or replacement and were withdrawn. After three crossovers
from CABG/CBP to OPCAB and one crossover from OPCAB to CABG, 97 CABG/CPB
patients and 100 OPCAB patients remained. There were no significant preoperative
demographic differences between groups. Postoperative compliance was reduced
more after OPCAB than after CABG/CPB (- 15.4 +/- 10.7 mL/cm H(2)O vs - 11.2 +/-
10.1 mL/cm H(2)O [mean +/- SD]; p = 0.007), associated with rotation of the
heart into the right chest to perform posterolateral bypasses (p < 0.001) and
the concomitant increased fluid requirements necessary to maintain hemodynamic
stability during rotation of the heart. In addition to higher intraoperative
fluid intake (4,541 +/- 1,311 mL vs 3,585 +/- 1,033 mL, p < 0.0001), OPCAB
patients had higher intraoperative fluid balance (3,903 +/- 1,315 mL vs 1,772
+/- 1,373 mL, p < 0.0001), and higher postoperative pulmonary arterial diastolic
pressure (15.0 +/- 5.5 mm Hg vs 11.8 +/- 5.2 mm Hg, p < 0.0001) and central
venous pressure (10.4 +/- 4.5 mm Hg vs 8.4 +/- 4.7 mm Hg, p < 0.0001). Despite
lower compliance, immediate postoperative Pao(2) on fraction of inspired oxygen
of 1.0 (275 +/- 97 torr vs 221 +/- 92 torr, p = 0.001) was higher after OPCAB
and extubation was earlier (p = 0.001). Postoperative chest radiographs,
spirometry, mortality, reintubation, or readmission for pulmonary complications
were not different between groups. CONCLUSIONS: Compared to CABG/CPB, OPCAB was
associated with a greater reduction in postoperative respiratory compliance
associated with increased fluid administration and rotation of the heart into
the right chest to perform posterolateral grafts. OPCAB yielded better gas
exchange and earlier extubation but no difference in chest radiographs,
spirometry, or rates of death, pneumonia, pleural effusion, or pulmonary edema.

Cytokine. 2005 Mar 7;29(5):215-28. 

IL-10 and toll-like receptor-4 polymorphisms and the in vivo and ex vivo
response to endotoxin.

Schippers EF, van 't Veer C, van Voorden S, Martina CA, Huizinga TW, le Cessie
S, van Dissel JT.

Department of Infectious Diseases, C5-P42, Leiden University Medical Center, PO
Box 9600, 2300 RC Leiden, The Netherlands. e.f.schippers@lumc.nl

To determine to what extent lipopolysaccharide-induced IL-10 production capacity
is determined by polymorphisms in toll-like receptor-4 (TLR4) and the IL-10
promoter region, we measured in vivo IL-10 and TNF-alpha production in patients
undergoing elective cardiopulmonary bypass surgery, a major surgical trauma
associated with ischemia-reperfusion injury that triggers an endotoxemia and
profound inflammatory response in most patients. Ex vivo the IL-10 and TNF-alpha
production was measured in a whole blood stimulation assay, using 3 LPS
concentrations. Positive correlations were found between TNF-alpha and IL-10
production ex vivo, upon stimulation with each of the LPS concentrations. Also,
the estimated TNF-alpha and IL-10 EC50, and TNF-alpha(max) and IL-10max were
positively correlated (r = 0.203; p = 0.023 and r = 0.287; p = 0.001,
respectively), indicating that these parameters describing LPS sensitivity and
maximal production capacity, respectively, can be estimated by measuring either
TNF-alpha or IL-10. Interleukin-10 concentrations in patients experiencing
endotoxemia in vivo negatively correlated with the IL-10 levels produced upon
stimulation with 1000 ng/mL LPS as well as the estimated IL-10max ex vivo. In
vivo, a positive correlation between the TNF-alpha concentration at time-point 2
and the IL-10 concentration at time-point 3 was found, consistent with an
important contribution of the magnitude of TNF-alpha release upon the subsequent
IL-10 production. Carriers of the IL-10 promoter -1330G, -1082A, -819T, -592A
(GATA) haplotype had lower IL-10 production ex vivo upon stimulation with 10 and
100 ng/mL LPS and higher EC50 values (the estimated LPS concentration at which
50% of the maximal IL-10 response is reached) as compared to carriers of the
other haplotypes combined, indicating decreased LPS sensitivity ex vivo. These
individuals did not differ from the others in interleukin-10 production capacity
upon stimulation with a high LPS concentration (i.e., 1000 ng/mL) and the
estimated IL-10(max) values, were similar, indicating unimpaired maximal IL-10
production capacity ex vivo. Carriers of the IL-10 promoter AGCC haplotype had
lower EC50 values as compared to carriers of the other haplotypes combined,
indicating increased LPS sensitivity ex vivo. In accordance with this finding,
carriers of the AGCC haplotype had higher circulating IL-10 levels in vivo. The
common TLR4 polymorphisms (Asp299Gly and Thr399Ile) were associated with
slightly higher IL-10 production capacity ex vivo and in vivo, however, this was
not statistically significant. Our results indicate that polymorphisms in the
proximal IL-10 promoter region are associated with in vivo and ex vivo LPS
sensitivity. The contribution to the inter-individual variation, however, is
limited since the variation between individuals in LPS sensitivity and IL-10
production capacity can only partly be attributed to these IL-10 promoter
polymorphisms.

Br J Haematol. 2005 Mar;128(6):837-41. 

Changes in platelet count after cardiac surgery can effectively predict the
development of pathogenic heparin-dependent antibodies.

Pouplard C, May MA, Regina S, Marchand M, Fusciardi J, Gruel Y.

Haematology-Haemostasis, Hopital Trousseau, 37044 Tours, France.

Cardiopulmonary bypass (CPB) induces the release of platelet factor 4 (PF4) and
patients are at risk of heparin-induced thrombocytopenia (HIT). This study was
aimed to determine whether an abnormal evolution in platelet count (PC) after
CPB is predictive of the development of HIT antibodies. Two abnormal PC patterns
were defined: pattern P1, characterized by a decrease in PC following previous
correction of thrombocytopenia occurring during CPB, and pattern P2, defined as
a persistent low PC in the days following CPB. PC was evaluated for 10 d in 305
consecutive patients before and after CPB. Serotonin release assay (SRA) was
carried out between days 8 and 10 to detect pathogenic heparin-dependent
antibodies. Moreover, antibodies to heparin-PF4 (H-PF4) complexes were assayed
by enzyme-linked immunosorbent assay. PC evolution after CPB was normal in 300
patients although antibodies to H-PF4 were frequently present (53.4%). Changes
in PC were abnormal in five patients with pattern P1 (n = 4) or P2 (n = 1). As
SRA was positive in four of the five cases, the positive predictive value of
abnormal PC pattern for pathogenic HIT antibodies was 80%. Careful follow-up of
PC after CPB makes it possible to predict with high specificity (99%) for those
patients who develop pathogenic HIT antibodies.

Crit Care Med. 2005 Mar;33(3):623-8. 

Calpain inhibition decreases endothelin-1 levels and pulmonary hypertension
after cardiopulmonary bypass with deep hypothermic circulatory arrest.

Duffy JY, Schwartz SM, Lyons JM, Bell JH, Wagner CJ, Zingarelli B, Pearl JM.

Pediatric Cardiothoracic Surgery, Cincinnati Children's Hospital Medical Center,
and the University of Cincinnati College of Medicine, Cincinnati, OH, USA.

OBJECTIVE: Cardiopulmonary bypass in infants and children can result in
cardiopulmonary dysfunction through ischemia and reperfusion injury. Pulmonary
hypertension and injury are particularly common and morbid complications of
neonatal cardiac surgery. Inhibition of calpain, a cysteine protease, has been
shown to inhibit reperfusion injury in adult organ systems. The hypothesis is
that calpain inhibition can alleviate the cardiopulmonary dysfunction seen in
immature animals following ischemia and reperfusion with cardiopulmonary bypass.
DESIGN: Animal case study. SETTING: Medical laboratory. SUBJECTS: Crossbred
piglets (5-7 kg). INTERVENTIONS: Piglets were cooled with cardiopulmonary bypass
to 18 degrees C followed by deep hypothermic circulatory arrest for 120 mins.
Animals were rewarmed to 38 degrees C on cardiopulmonary bypass and maintained
for 120 mins. Six animals were administered calpain inhibitor
(Z-Leu-Leu-Tyr-fluoromethyl ketone; 1 mg/kg, intravenously) 60 mins before
cardiopulmonary bypass. Nine animals were administered saline as a control.
Plasma endothelin-1, pulmonary and hemodynamic function, and markers of
leukocyte activity and injury were measured. MEASUREMENTS AND MAIN RESULTS:
Calpain inhibition prevented the increased pulmonary vascular resistance seen in
control animals (95.7 +/- 39.4 vs. 325.3 +/- 83.6 dyne.sec/cm, respectively, 120
mins after cardiopulmonary bypass and deep hypothermic circulatory arrest, p =
.05). The attenuation in pulmonary vascular resistance was associated with a
blunted plasma endothelin-1 response (4.91 +/- 1.72 pg/mL with calpain
inhibition vs. 10.66 +/- 6.21 pg/mL in controls, p < .05). Pulmonary function
after cardiopulmonary bypass was better maintained after calpain inhibition
compared with controls: Po2/Fio2 ratio (507.2 +/- 46.5 vs. 344.7 +/- 140.5,
respectively, p < .05) and alveolar-arterial gradient (40.0 +/- 17.2 vs. 128.1
+/- 85.2 mm Hg, respectively, p < .05). Systemic oxygen delivery was higher
after calpain inhibition compared with controls (759 +/- 171 vs. 277 +/- 46
mL/min, respectively, p < .001). In addition, endothelial nitric oxide synthase
activity in lung tissue was maintained with calpain inhibition. CONCLUSIONS: The
reduction in plasma endothelin-1 and maintenance of lung endothelial nitric
oxide levels after cardiopulmonary bypass and deep hypothermic circulatory
arrest with calpain inhibition were associated with reduced pulmonary vascular
resistance. Improved gas exchange and higher systemic oxygen delivery suggest
that calpain inhibition may be advantageous for reducing postoperative
cardiopulmonary dysfunction commonly associated with pediatric heart surgery and
cardiopulmonary bypass.

J Thorac Cardiovasc Surg. 2005 Mar;129(3):645-51. 

Emergency endovascular interventions for acute thoracic aortic rupture:
four-year follow-up.

Doss M, Wood JP, Balzer J, Martens S, Deschka H, Moritz A.

Department of Thoracic and Cardiovascular Surgery, Johann Wolfgang Goethe
University Frankfurt/Main, Germany. mirkodoss@aol.com

OBJECTIVE: High mortality and paraplegia rates associated with the surgical
management of acute thoracic aortic ruptures limit its success. It was our
objective to evaluate whether emergency endovascular interventions would improve
the outcomes of these patients. METHODS: Sixty patients aged 28 to 83 years were
admitted to our institution with an acute rupture of the thoracic aorta (27
ruptured aneurysms, 15 perforated type B dissections, 18 traumatic ruptures).
Twenty-eight patients were treated surgically with cardiopulmonary bypass, and
32 patients were acutely treated with an endovascular stent graft. Medical
records were reviewed for prehospital and emergency department data, operative
findings, and outcomes. Patients were followed up at yearly intervals with
high-resolution multidetector computed tomographic angiography. RESULTS:
Perioperatively, there were 1 death (3.1%) among the 32 patients in the
endovascular group and 5 deaths (17.8%) among the 28 patients in the surgical
group. There were 4 late deaths in the endovascular group and 1 in the surgical
group. There were 2 access failures in the endovascular group. There were 1
stroke in the endovascular group and 1 case of paraplegia in the surgical group.
Three patients in the endovascular group had endovascular leaks develop that
required reintervention. Two patients in the endovascular group had late
thrombosis of the left subclavian artery. CONCLUSION: Despite encouraging early
outcomes, midterm results suggest a trend toward increased reintervention and
late complication rates in the endovascular group. Therefore continued
surveillance of patients treated with stent grafts is necessary.

J Thorac Cardiovasc Surg. 2005 Mar;129(3):599-606. 

Polarized arrest with warm or cold adenosine/lidocaine blood cardioplegia is
equivalent to hypothermic potassium blood cardioplegia.

Corvera JS, Kin H, Dobson GP, Kerendi F, Halkos ME, Katzmark S, Payne CS, Zhao
ZQ, Guyton RA, Vinten-Johansen J.

Cardiothoracic Research Laboratory and Carlyle Fraser Heart Center, Emory
University School of Medicine, Altanta, GA 30308, USA.

BACKGROUND: Hypothermic depolarizing hyperkalemic (K + 20 mEq/L) blood
cardioplegia is the "gold standard" in cardiac surgery. K + has been associated
with deleterious consequences, eg, intracellular calcium overload. This study
tested the hypothesis that elective arrest in a polarized state with adenosine
(400 micromol/L via adenosine triphosphate-sensitive potassium channel opening)
and the Na + channel blocker lidocaine (750 micromol/L) as the arresting agents
in blood cardioplegia provides cardioprotection comparable to standard
hypothermic K + -blood cardioplegia. METHODS: Anesthetized dogs were placed on
cardiopulmonary bypass and assigned to 1 of 3 groups receiving antegrade
cardioplegia delivered every 20 minutes for 1 hour of arrest: cold (10 degrees
C) K + -blood cardioplegia (n = 6), cold (10 degrees C) adenosine/lidocaine
blood cardioplegia (n = 6), or warm (37 degrees C) adenosine/lidocaine blood
cardioplegia (n = 6). After an hour of arrest, cardiopulmonary bypass was
discontinued, and reperfusion was continued for 120 minutes. RESULTS: Time to
arrest was longer with cold and warm adenosine/lidocaine blood cardioplegia (175
+/- 19 seconds and 143 +/- 19 seconds, respectively) compared with K + -blood
cardioplegia (27 +/- 2 seconds; P < .001). Postcardioplegia left ventricular
systolic function (slope of the end-systolic pressure/dimension relationship)
was comparable among the 3 groups (K + -blood cardioplegia, 15.2 +/- 2.1 mm
Hg/mm; cold adenosine/lidocaine blood cardioplegia, 15.9 +/- 3.4 mm Hg/mm; warm
adenosine/lidocaine blood cardioplegia, 14.1 +/- 2.8 mm Hg/mm; P = .90). Plasma
creatine kinase activity in cold and warm adenosine/lidocaine blood cardioplegia
was similar to that in K + -blood cardioplegia at 120 minutes of reperfusion
(cold adenosine/lidocaine blood cardioplegia, 11.5 +/- 2.1 IU/g protein; warm
adenosine/lidocaine blood cardioplegia, 10.1 +/- 0.9 IU/g protein; K + -blood
cardioplegia, 7.6 +/- 0.8 IU/g protein; P = .17). Postcardioplegia coronary
artery endothelial function was preserved in all groups. CONCLUSIONS:
Intermittent polarized arrest with warm or cold adenosine/lidocaine blood
cardioplegia provided the same degree of myocardial protection as intermittent
hypothermic K + -blood cardioplegia in normal hearts.

Paediatr Anaesth. 2005 Mar;15(3):235-40. 

Recombinant factor VIIa (NovoSeven) as a hemostatic agent after surgery for
congenital heart disease.

Razon Y, Erez E, Vidne B, Birk E, Katz J, Tamari H, Dagan O.

Cardiac Intensive Care Unit, Schneider Children's Medical Center of Israel,
Petah Tikva, Tel Aviv, Israel. yaronraz@clalit.org.il

BACKGROUND: Postoperative bleeding and blood product requirements can be
substantial in children undergoing open-heart surgery, and reexploration is
required in 1% of cases. Recombinant activated factor VII (rFVIIa, NovoSeven,
NovoNordisk, Denmark) is a hemostatic agent approved for the treatment of
hemophilic patients with inhibitors to factor VIII or factor IX. It has also
been used with success in other conditions. We present our experience with
rFVIIa treatment for uncontrolled bleeding after open-heart surgery in five
pediatric patients. METHODS: The study group consisted of five patients after
open-heart surgery with excessive blood loss. The patients were treated with
rFVIIa after failure of conventional treatment to control the bleeding. Blood
loss, blood product consumption, and coagulation test results were recorded
before and after rFVIIa administration. RESULTS: In all cases, blood loss
decreased considerably after rFVIIa administration (mean 7.8 ml x kg(-1) x
h(-1)), almost eliminating the need for additional blood products, and the
prolonged prothrombin time normalized. In two patients with thrombocytopathy,
rFVIIa helped to discriminate surgical bleeding from bleeding caused by a defect
in hemostasis. No side effects of rFVIIa treatment were noted. CONCLUSIONS:
These cases support the impression that RFVIIa is efficient and safe in
correcting hemostasis in children after cardiopulmonary bypass when other means
fail. However, the data are still limited, and more extensive research is
needed.