Retransfusion Of Shed Blood Research Articles

Circulating particles during cardiac surgery

Shed blood is known to be a source of lipid micro-emboli in cardiac surgery. The aim of this study was to characterize the occurrence of these particles at different stages of the operation, and to study their occurrence in the circulation at multiple time-points after the retransfusion of shed blood. Forty-four patients undergoing routine surgery with cardiopulmonary bypass were included. Blood was sampled from the surgical field at different sampling locations during the operation. Shed blood was collected in a transfusion bag and retransfused. After which, blood was sampled from the arterial line of the heart-lung machine. A Coulter counter was used for particle determinion. The mean volume of shed blood collected was 340+/-215 ml. Particles in the size range 10-60 microm were found at varying concentrations, with the highest concentrations being found in blood collected after cannulation and from the pleura. After retransfusion of this blood, a biphasic response was seen in the blood drawn from the efferent line of the heart-lung machine. Particles are found in shed blood at all times during cardiac surgery, and when this blood was retransfused an increase was seen in particle concentration in the heart-lung machine.

Pre-operative injections of epoetin-α versus post-operative retransfusion of autologous shed blood in total hip and knee replacement

This prospective randomised clinical trial evaluated the effect of alternatives for allogeneic blood transfusions after total hip replacement and total knee replacement in patients with pre-operative haemoglobin levels between 10.0 g/dl and 13.0 g/dl. A total of 100 patients were randomly allocated to the Eprex (pre-operative injections of epoetin) or Bellovac groups (post-operative retransfusion of shed blood). Allogeneic blood transfusions were administered according to hospital policy. In the Eprex group, 4% of the patients (two patients) received at least one allogeneic blood transfusion. In the Bellovac group, where a mean 216 ml (0 to 700) shed blood was retransfused, 28% (14 patients) required the allogeneic transfusion (p = 0.002). When comparing Eprex with Bellovac in total hip replacement, the percentages were 7% (two of 30 patients) and 30% (nine of 30 patients) (p = 0.047) respectively, whereas in total knee replacement, the percentages were 0% (0 of 20 patients) and 25% (five of 20 patients) respectively (p = 0.042). Pre-operative epoetin injections are more effective but more costly in reducing the need for allogeneic blood transfusions in mildly anaemic patients than post-operative retransfusion of autologous blood.

Myocardial performance index during rapidly changing loading conditions

The myocardial performance index is a non-geometric, heart rate-independent echocardiography-derived index of left ventricular performance combining systolic and diastolic function. There is an ongoing debate whether the myocardial performance index is affected by preload or not. Moreover, a systematic evaluation of the effect of changing tidal volume ventilation on the myocardial performance index is still lacking. The aim of our study was to assess whether acute changes in preload and/or different depth of tidal volume ventilation affect the myocardial performance index. In all, 14 anesthetized pigs (35 +/- 2 kg) were studied during changing tidal volumes (VT 5, 10 and 15 mL kg(-1)) at baseline, after removal of 500 cm(3) of blood (haemorrhage) and after retransfusion of shed blood plus additional 500 cm(3) 6% hydroxyethyl starch (fluid loading). Echocardiographic measurements at each experimental stage included myocardial performance index, left ventricular end-diastolic area and fractional area change. Central venous pressure, pulmonary capillary wedge pressure, cardiac output and stroke volume index were obtained by a pulmonary artery catheter. Global end-diastolic volume was obtained by transpulmonary thermodilution. Comparing different loading conditions, we found significant changes in cardiac output, stroke volume index, central venous pressure, pulmonary capillary wedge pressure, global end diastolic volume and left ventricular end-diastolic area, indicating clinically relevant changes in preload. In the haemorrhage group, there was a significant reduction in the myocardial performance index (P < 0.05) independent of tidal volume applied and this was reversed after fluid loading. However, myocardial performance index was significantly impaired (P < 0.05) by high tidal volume ventilation (15 mL kg(-1)), while tidal volumes of 5 and 10 mL kg(-1) had no effect. The myocardial performance index is largely dependent on changes in preload. Moreover, high tidal volume ventilation significantly impaired the myocardial performance index.

The effect of hypovolaemia on colonic blood flow in the dog.

The effects of a minor degree of hypovolaemia on colonic blood flow and on systemic haemodynamics have been studied in nine greyhound dogs. A loss in blood volume of 10 per cent over 20 min produced no change in blood pressure and only a 7 per cent rise in heart rate. Cardiac output, however, fell by 26 per cent and central venous pressure also fell significantly. Colonic blood flow fell by 28 per cent and oxygen availability by 29 per cent. All these changes were statistically highly significant. Retransfusion of shed blood resulted in a slow and incomplete return to pre-bleed status. Since colonic blood flow and oxygen availability during and after surgery may be important for colonic healing, it is suggested that even the slightest degree of hypovolaemia should be avoided in cases involving colonic anastomosis. Systemic blood pressure may be an inadequate index of the need for transfusion in these cases.

Splanchnic metabolism during gut ischemia and short-term endotoxin and hemorrhagic shock as evaluated by intravasal microdialysis.

The splanchnic area is of considerable interest in different types of shock. To characterize the metabolic changes in the splanchnic region in response to different types of shock we used a model where shock-induced metabolic changes in the splanchnic region were studied by the use of intravasal microdialysis. 23 anesthetized domestic pigs were randomized into four groups: Group I, serving as controls (n = 5); Group II, mesenteric ischemia for 180 followed by 120 min of reperfusion (n = 5); Group III, endotoxin shock for 5 h (n = 5); and Group IV, hemorrhagic shock for 180 min followed by re-transfusion of shed blood (n = 8). Microdialysis catheters were placed in the left femoral artery, portal vein and a small ileal mesenteric vein. Samples of the perfusate were continuously collected in micro-vials and analyzed for glucose, lactate, pyruvate and glycerol. In gut ischemia and endotoxin shock the outflow-pattern of lactate, lactate/pyruvate ratio and glucose in the mesenteric vein differed significantly from controls and hemorrhage whereas an increase in glycerol was only noted in the ischemic group. The most prominent differences were detected in lactate/pyruvate ratio, a marker of tissue ischemia with the most pronounced changes during mesenteric ischemia/reperfusion. During endotoxin shock increases in microdialysate metabolites were only noted in the splanchnic region suggesting a specific vulnerability in the region. Studying the lactate/pyruvate ratio may provide additional information when interpreting increased blood lactate levels. In addition glycerol may prove to be a useful marker of splanchnic ischemia. Intravasal microdialysis represents a potentially useful method for monitoring regional metabolic events.

Low venular shear rates promote leukocyte-dependent recruitment of adherent platelets

The influence of reductions in venular shear rate on platelet-endothelial (P/E) cell adhesion has not been previously addressed. The objectives of this study were to define the effects of reductions in venular shear rate on P/E cell adhesion and to determine the interdependence of P/E cell adhesion and leukocyte-endothelial (L/E) cell adhesion at low shear rates. Intravital videomicroscopy was used to quantify P/E and L/E cell adhesion in rat mesenteric venules exposed to shear rates ranging between 118 +/- 9 and 835 +/- 44 s(-1). Shear rate was altered in postcapillary venules by rapid, graded blood withdrawal, without retransfusion of shed blood. Reducing shear rate from >600 s(-1) to <200 s(-1) resulted in an eightfold increase in L/E cell adhesion, whereas P/E cell adhesion increased 18-fold. A blocking antibody directed against P-selectin blunted both the P/E and L/E cell adhesion elicited by low shear rates. Immunoneutralization of CD11/CD18 on leukocytes or rendering animals neutropenic also blocked the shear rate-dependent recruitment of both platelets and leukocytes. These findings indicate that 1) low shear rates promote P/E and L/E cell adhesion in mesenteric venules, and 2) adherent neutrophils (mediated by CD11/CD18) create a platform onto which platelets can bind to the venular wall at low shear rates.

Perfusion method for thoracoabdominal aneurysm repair using the open distal technique.

Challenges related to perfusion support of thoracoabdominal aneurysm repair include maintenance of distal aortic perfusion, rapidity of fluid resuscitation, and avoidance of both hypothermia and excessive hemodilution. Using available technology, we have devised a circuit and protocol that addresses these issues. To accomplish such support a bypass circuit consisting of 3/8 inch tubing connected to a centrifugal pump and low-prime heat exchanger was constructed. The circuit was primed via 1/4 inch spiked connectors attached to a 3-liter bag of normal saline. After initial de-airing, the solution was recirculated through this bag. Patients were anticoagulated with 1 mg/kg of heparin prior to initiation of support. Left atrial-descending aorta bypass was used primarily. A cell salvage device was used for autotransfusion. All blood products were delivered via a rapid infusion device. During partial exsanguination, shed blood was not processed, but directed to the rapid infusor for immediate retransfusion. Any packed cells given were washed prior to transfusion. Citrate dextrose solution was used as an anticoagulant for the cell scavenger. This configuration was used successfully in 50 procedures during an 18-month period. Use of this low-prime, custom circuit reduced both hemodilution and cost. A connection off the cell salvage pump offers fast retransfusion of shed blood during partial exsanguination. Minimal heparinization and citrate anticoagulation appears to reduce coagulopathy.

Power spectral analysis of arterial and central venous pressure signals during graded hemorrhage in anesthetized rats.

Based on simultaneous power spectral analysis of systemic arterial pressure (SAP) and central venous pressure (CVP) signals in rats anesthetized with pentobarbital sodium, we assessed the hypotheses that subtle changes in the SAP spectrum exist during hemorrhagic shock, and that the CVP spectrum is a feasible index for central blood volume during acute graded blood loss. During Stage I hemorrhagic shock seen after reduction in 10% of total blood volume (TBV), there was a significant increase in the power of both the very low frequency (VLF, 0-.25 Hz) and low frequency (LF, .25-.8 Hz) components, along with a moderate decrease in the very high frequency (VHF, 5-9 Hz) component, of SAP signals. Substantial reduction in VLF, LF, and VHF components in the SAP spectrum occurred after a blood loss of 25% of TBV (Stage II), which persisted during Stage III hemorrhagic shock when the withdrawn blood reached 50% of TBV and the mean SAP maintained at 40 mm Hg. The depressed SAP-VLF and SAP-LF components sustained the period of spontaneous recovery and subsequent retransfusion of shed blood, although the power of SAP-VHF component gradually elevated during these two periods. The power of the high-frequency (HF, .8-2.4 Hz) component of SAP signals increased discernibly only during Stage III, became significant on spontaneous recovery, and declined during retransfusion. Although CVP and CVP-VHF component progressively declined, the power of the CVP-HF component manifested a gradual increase that was significantly and reversely correlated with the reduction in TBV. We conclude that differential changes in individual components of the SAP spectrum occur during hemorrhagic shock, and that the CVP-HF component may be a reliable indicator for central blood volume during acute graded blood loss.

Heterogeneous distribution of microcirculatory flow in the gastrointestinal tract during haemorrhage in anaesthetized pigs

O-9 Introduction: Hypoperfusion of splanchnic organs during haemorrhagic shock may lead to sepsis and multiple organ failure. Little is known about dynamic flow distribution within the splanchnic region in circulatory shock. Recently a multichannel laser Doppler flowmeter system (LDF) has become available that can measure microcirculatory flow (MBF) in multiple organs simultaneously and continuously. Objectives: The aim of this study was to compare systemic (cardiac index; CI), regional (superior mesenteric artery flow; SMA flow), and local flow (MBF) in multiple abdominal organs during haemorrhagic shock in anaesthetized pigs. Methods: Seven pigs (25 kg), anaesthetized with 0.6% halothane, N2O:O2(2:1), fentanyl and pancuronium, were bled to a MAP of 40 mmHg. After 180 min the shed blood was retransfused. MBF was measured in the intestinal mucosa (stomach, jejunum, colon), pancreas, liver and kidney by LDF, and SMA flow by ultrasonic transit time flowmetry. Data are presented as mean percentages of baseline. Results: During shock, MBF decreased by 15-30% in the stomach and colon mucosa, similar to the SMA flow, while the jejunal flow remained virtually unchanged. Flow in the liver and kidney decreased somewhat more (30-40%), but flow in the pancreas was most severely affected and decreased by 60%. After retransfusion of shed blood, SMA flow increased to 30% above baseline. Although microcirculatory flow in the pancreas increased slightly after retransfusion it remained 20% below baseline. Conclusion: 1. MBF in the intestinal mucosa of the stomach and colon decreased similarly to the SMA flow during shock and recovered promptly after retransfusion of shed blood. 2. In contrast, MBF in the jejunal mucosa did not decrease during shock, suggesting an intact autoregulation. 3. The pancreas appears to be particularly vulnerable to haemorrhage, since MBF decreased significantly more than CI and SMA flow.

Erythrocytes and Proinflammatory Mediators in Wound Drainage

Background and Objectives: Retransfusion of shed blood collected after operation has become popular, but recent reports of side effects led to a search for possible causes. Materials and Methods: In a randomized study of 28 patients undergoing total hip arthroplasty, shed blood was collected in Solcotrans, Orth-Evac, and ordinary Redon drainage. Osmotic fragility was measured and electron-microscopic pictures of erythrocytes from selective samples were taken. Serotonin, prostaglandin E₂ (PGE₂), and histamine were measured with enzyme-linked immunosorbent assays. Results: Higher osmotic fragility of erythrocytes collected with Solcotrans appeared to be due to ACD which was used only with that system. Serotonin concentrations did not differ significantly. However, there was a great increase in histamine (Solcotrans 477.7, Orth-Evac 344.0, Redon drainage 453.1 nmol/ml) and PGE₂ (Solcotrans 1,908.3, Orth-Evac 1,225.0, Redon drainage 2,666.7 μg/ml) in shed blood compared with venous blood (histamine 9.5 nmol/l, PGE₂ 4.2 μg/ml). Conclusion: Unwashed wound drainage blood collected after operation contains levels of proinflammatory mediators that can account for the reported side effects.

Erythrocytes and Proinflammatory Mediators in Wound Drainage

Abstract Background and Objectives: Retransfusion of shed blood collected after operation has become popular, but recent reports of side effects led to a search for possible causes. Materials and Methods: In a randomized study of 28 patients undergoing total hip arthroplasty, shed blood was collected in Solcotrans, Orth Evac, and ordinary Redon drainage. Osmotic fragility was measured and electron‐microscopic pictures of erythrocytes from selective samples were taken. Serotonin, prostaglandin E2 (PGE2), and histamine were measured with enzymelinked immunosorbent assays. Results: Higher osmotic fragility of erythrocytes collected with Solcotrans appeared to be due to ACD which was used only with that system. Serotonin concentrations did not differ significantly. However, there was a great increase in histamine (Solcotrans 477.7, Orth‐Evac 344.0, Redon drainage 453.1 nmol/ml) and PGE2 (Solcotrans 1,908.3, Orth‐Evac 1,225.0, Redon drainage 2,666.7 μg/ml) in shed blood compared with venous blood (histamine 9.5 nmol/l, PGE2 4.2 μg/ml). Conclusion:Unwashed wound drainage blood collected after operation contains levels of proinflammatory mediators that can account for the reported side effects.

Effect of sodium bicarbonate infusion on hepatocyte Ca2+ overload during resuscitation from hemorrhagic shock

Ischemia/reperfusion events alter the cellular ion homeostasis by intracellular acidosis and a subsequent rise of sodium and calcium concentrations. Since disturbance of intracellular Ca2+ signaling pathways impairs cellular function, we investigated the effect of sodium bicarbonate infusion on hepatocellular Ca2+ dysregulation induced by resuscitation from hemorrhagic shock. Anesthetized Sprague-Dawley rats were bled to a mean arterial blood pressure of 40 mmHg for 60 min. Rats were resuscitated by retransfusion of shed blood (60%) in 20 min and three-fold the bleed out volume as lactated Ringers' during 60 min and received either a bolus infusion of sodium bicarbonate (2 mval/kg body weight) or an equal volume of sodium chloride (0.9%). After hepatocyte isolation by portal collagenase perfusion, the rate of Ca2+ influx (Ca2+in) in the absence and presence of epinephrine (100 nM), cellular Ca2+ uptake (Ca2+up) and membrane Ca2+ flux (Ca2+flux) were determined using 45Ca2+ incubation techniques. Hemorrhage/resuscitation substantially increased hepatocyte Ca2+up (3.44±0.2 nmol/mg protein) and Ca2+flux (32.8±5 pmol/mg protein×min) compared to sham-operated controls (2.57±0.1 and 15.2±3.5; P<0.05). Resuscitation with sodium bicarbonate significantly prevented altered hepatocyte Ca2+ regulation (2.31±0.1 and 14.4±4.6; P<0.05). These findings suggested that postischemic hepatocyte Ca2+ overload could partly be due to enhanced membrane Ca2+ movements to correct for altered intracellular pH homeostasis.

Activation of Pyruvate Dehydrogenase Improves Heart Function and Metabolism after Hemorrhagic Shock

This study was designed to test the hypothesis that activation of myocardial pyruvate dehydrogenase (PDH) would improve recovery of heart function after brief, severe hemorrhagic shock. Pentobarbital-anesthetized rats were instrumented to monitor arterial blood pressure and right ventricular pressures. Rats were hemorrhaged via femoral artery to 25–30 mmHg mean arterial pressure (MAP) for 60 min, followed by retransfusion of shed blood with either 1.0 cc saline with no dichloroacetate (−DCA) or 1.0 cc saline containing 150 mg/kg sodium dichloroacetate (+DCA). Rats were observed for 3 h after retransfusion. Hearts were freeze-clampedin situfor analysis of adenosine triphosphate (ATP), creatine phosphate (CrP), lactate and pyruvate content as well as PDH activity (PDHa) and total PDH activity (PDHt). Three h after retransfusion, the rate pressure product (RPP=HR×PSP) was 23 000±2733 with no DCA treatmentv36 2769 mmHg/min with DCA treatment (P<0.05, ANOVA). Treatment with DCA also increased myocardial tissue content of high energy phosphates (ATP=10.1±1.1 and CrP=5.8±1.0μmol/g weight−DCA,v15.1±0.9 and 14.7±1.0μmol/g dry weight+DCA,P<0.05, both measurements). DCA administration also significantly reduced myocardial lactate contents (14.6±2.7μmol/g dry weight−DCAv5.9±1.0+DCA). Hemorrhagic shock did not change PDHa or PDHt compared to hearts obtained during the pre-hemorrhage period. Retransfusion with DCA significantly increased PDHa activity (6.8±1.1μmol/g dry weight/min−DCAv29.7±2.0μmol/g dry weight/min+DCA). PDHt was not different between controls and DCA-treated groups. These data indicate that activation of myocardial PDH by adding DCA to retransfused blood improved heart function and metabolism after severe hemorrhagic shock.

Nitric oxide in the brain increases during a short period of hemorrhagic shock in the rabbit.

We investigated the changes in nitric oxide (NO) concentration in the brain of the rabbit by measuring NO-related electrical current. Seventeen Japanese white rabbits were anesthetized with pentobarbital sodium and mechanically ventilated with tracheotomy tubes. An NO-selective electrode was used for the detection of NO. After a round craniotomy in the left parietal lobe, an NO-sensitive electrode was placed in the brain. Rabbits were hemorrhaged to a mean arterial blood pressure of 35 +/- 7 mmHg, from a baseline of 112 +/- 12 mmHg (mean +/- SD). The shock was maintained for 5 min. The mean extracted blood volume was 77 +/- 17 mL. Then, retransfusion of shed blood caused a rapid restoration of mean arterial blood pressure. The amount of time required to induce hemorrhagic shock was 261 +/- 34 s. The time required to retransfuse the extracted blood was 233 +/- 43 s (p > .05). During shock, the NO-selective electrode produced an extensive increase in current, from 110 +/- 94.5 pA to 1010 +/- 543 pA (mean +/- SD, p < .001). The current continued to increase for a few minutes after the recovery from shock, with a maximal increase reaching 1245 +/- 515 pA (p < .001). This enhanced release of NO-related current (1,132%) recovered to the baseline level at 44 +/- 7 min after retransfusion. When the same investigation was performed on the same animals on which had been placed the same electrode pretreated with NG-nitro-L-arginine methylester (L-NAME) 30 mg/kg intravenously, NO-related current increased from 101 +/- 158 to a maximum of 860 +/- 406 pA (752%). Our results suggest that NO may play an important role in the brain during the early period of hemorrhagic shock, and that L-NAME 30 mg/kg intravenously might not inhibit the NO production in the parietal lobe, probably due to a blood-brain barrier to the nitric oxide synthase-inhibiting drug.

Con: Shed mediastinal blood should not be reinfused after cardiac surgery

HE PREVENTION and treatment of postoperative bleeding after cardiac surgery are important both to reduce perioperative complications and to reduce the exposure of panents to homologous blood products. Postoperative reinfusion of shed mediastinal blood is one of a large array of interventions that have been studied to achieve these goals. In this technique, blood is collected from the chest tubes Into a reservoir under gentle suction and then retransfused into the patient after being passed through a filter. The average retransfuslon volume as approximately 400 to 500 mL but may range from a few hundred milliliters to several hters. The routine use of postoperative autotransfuslon was advocated by Schaff and colleagues x.2 They randomized 114 adult cardiac surgical patients to receive either retransfusion of shed medmstinal blood using a Sorenson autotransfusion system (Sorenson Research Corp., Salt Lake City, UT) or homologous blood only (control group). Total postoperative blood loss and total blood replacement were similar between the two groups, but the autotransfusion group received sigmficantly less banked blood (2.4 _+ 0.3 units v 4.8 - 0.6 units for the control group). They also reported data with the routine use of reinfusion of shed mediastinal blood m 700 adult and pediatric patients. 2 They suggested that autotransfusion reduced the need for postoperative homologous blood transfusions by 50% compared with a historical control group from 2 years previously. However, other studies have failed to demonstrate benefit with postoperative autotransfusion. 3-8 Thurer et al performed a randomazed prospective study of autotransfusion in 113 patients in whom additional techniques also were used to reduce the requirement for homologous transfusion? These techmques included intraoperatwe blood withdrawal and retransfusion after cardiopulmonary bypass (CPB), normovolemic hemodilution, intraoperatlve retransfusion of shed blood, and meticulous surgical hemostasis Use of these techniques alone had reduced their average blood product usage from 8 units per paUent in 1972 to 2.5 units an 1978. The investigators found no statistical difference in postoperatwe chest tube drainage, the number of patients requiring homologous blood, and average blood product replacement or hematocrit at any time postoperatively between patients who had postoperative autotransfusion and those who did not 9 Similarly, subgroup analysis of pataents wath large blood loss ( > 25 mL/kg) also showed no dafference in saving of banked blood in the autotransfusaon

EFFECT OF ANTI-TUMOR NECROSIS FACTOR α ON LEUKOCYTE ADHESION IN THE LIVER AFTER HEMORRHAGIC SHOCK: AN INTRAVITAL MICROSCOPIC STUDY IN THE RAT

Tumor necrosis factor (TNF) plays a well known role during the development of multiple organ failure, in part due to its role for the expression of adhesion molecules on endothelial cells, thereby contributing to inflammatory reactions. The purpose of this study was to investigate the effects of TNF on leukocyte-endothelial interactions in the liver as a key organ during the systemic inflammatory response syndrome. In Sprague-Dawley rats (n = 6/group) hemorrhagic shock was induced by reduction of the mean arterial blood pressure (MAP) to 40 mmHg for 45 min; resuscitation was initiated by retransfusion of shed blood (60%) and Ringer's lactate. At 1 and 5 h after resuscitation, intravital microscopy of the liver was performed after injection of acridine orange as marker of leukocytes in sham-control animals and in shock animals pretreated with anti-TNF monoclonal antibody (2 mg/kg b.w. TN3; Celltech, Slough, UK) or NaCl .9% 2 h prior to shock induction, respectively. At constant systemic hemodynamic conditions in all groups (e.g., normal MAP), sinusoidal diameters and sinusoidal blood flow were comparably decreased to approximately 75% of control values in all shock groups. Significant differences were observed particularly in respect to permanent adherent leukocytes with 31.8 +/- 4.7% in the shock/NaCl group and 20.7 +/- 2.6% (mean +/- S.E., p < .05) in the shock/TN3 group 5 h after resuscitation following hemorrhagic shock. Consistently higher adhesion rates were observed in the portal regions compared to pericentral regions of the liver lobules.(ABSTRACT TRUNCATED AT 250 WORDS)

Tissue-type plasminogen activator and fibrin monomers synergistically cause platelet dysfunction during retransfusion of shed blood after cardiopulmonary bypassde : de Haan J, Schonberger J, Haan J, et al: J Thorac Cardiovasc Surg 106:1017–1023, 1993

Tissue-type plasminogen activator and fibrin monomers synergistically cause platelet dysfunction during retransfusion of shed blood after cardiopulmonary bypassde : de Haan J, Schonberger J, Haan J, et al: J Thorac Cardiovasc Surg 106:1017–1023, 1993

Tissue-type plasminogen activator and fibrin monomers synergistically cause platelet dysfunction during retransfusion of shed blood after cardiopulmonary bypass

Reduced hemostasis and bleeding tendency after cardiopulmonary bypass results from platelet dysfunction induced by the bypass procedure. The causes of this acquired platelet dysfunction are still subject to discussion, although, recently, greater emphasis has been placed on an overstimulated fibrinolytic system as a probable cause. In the first part of this study we assessed the effects of postoperative retransfusion of shed blood on blood loss to patients undergoing cardiopulmonary bypass. We observed that increasing concentrations of fibrinogen degradation products and tissue-type plasminogen activator stimulating activity in shed blood correlated significantly with a higher postoperative bleeding tendency (p < 0.05 for both). We further noted that retransfusion of shed blood increased the total postoperative blood loss by 43% (925 versus 1320 ml, p < 0.05). On the basis of these clinical observations, we hypothesized that the increased bleeding tendency was caused by fibrinolysis. In the second part of this study we collected evidence in support of this hypothesis by an in vitro study, in which we introduced similar (pro)fibrinolytic activity to platelet-rich plasma and measured the influence of this treatment on platelet function indicated by ristocetin agglutination. Tissue-type plasminogen activator and fibrin monomers (tissue-type plasminogen activator stimulator) together induced severe platelet damage, resulting in a decreased ristocetin agglutination response. Therefore, we propose a fibrinolysis-related mechanism for platelet dysfunction during cardiopulmonary bypass, dependent on fibrinolytic factors such as fibrin monomers, D-dimers, and tissue-type plasminogen activator.

A study of autologous blood collected after joint replacement surgery.

Blood from the surgical drains of 11 patients undergoing joint replacement was collected in the Solcotrans Orthopaedic autologous transfusion device and analysed for microparticulate matter before and after micro-aggregate filtration and for its effect on the coagulation of paired venous blood samples. An average of 165 ml (range 0-260 ml) was collected into the Solcotrans during the first hour. Using a Coulter Counter Zm particle counter, particulate matter of diameter 10-20 microns was found in only 2 of 10 collections at an average concentration of 33 x 10(3)/l. All units contained acoagulable blood [kaolin partial thromboplastin time (KPTT) greater than 600 s] but when mixed with paired post-operative venous samples exhibited the ability to shorten the KPTT by an average of 4.3 s inspite of the marked dilutional effect of mixing. Retransfusion of blood collected in the Solcotrans Orthopaedic device appears to be a suitable method to supplement or substitute pre-deposit and reduce exposure to homologous blood. Given the low incidence and concentration of microparticles detected, retransfusion of shed blood by this method is unlikely to cause significant pulmonary vascular occlusion resulting directly from deposition of microparticles.

A Study of Autologous Blood Collected after Joint Replacement Surgery

Blood from the surgical drains of 11 patients undergoing joint replacement was collected in the Solcotrans Orthopaedic autologous transfusion device and analysed for microparticulate matter before and after micro-aggregate filtration and for its effect on the coagulation of paired venous blood samples. An average of 165 ml (range 0-260 ml) was collected into the Solcotrans during the first hour. Using a Coulter Counter Zm particle counter, particulate matter of diameter 10-20 µm was found in only 2 of 10 collections at an average concentration of 33 x 10^3/l. All units contained acoagulable blood [kaolin partial thromboplastin time (KPTT) >600 s] but when mixed with paired post-operative venous samples exhibited the ability to shorten the KPTT by an average of 4.3 s inspite of the marked dilutional effect of mixing. Retransfusion of blood collected in the Solcotrans Orthopaedic device appears to be a suitable method to supplement or substitute pre-deposit and reduce exposure to homologous blood. Given the low incidence and concentration of microparticles detected, retransfusion of shed blood by this method is unlikely to cause significant pulmonary vascular occlusion resulting directly from deposition of microparticles.