Does leukodepletion during elective cardiac surgery really influence the overall clinical outcome?

AIM: We examined the impact of leukocyte filtration during the entire bypass time on postoperative leukocytosis, perioperative hemorrhage and overall clinical outcome in patients undergoing elective cardiac surgery. METHODS: Eighty patients who electively underwent cardiac surgery were randomly allocated to a leukocyte depletion group (n=40) or a control group (n=40). In patients of the leukocyte depletion group an arterial line filter with leukocyte depleting capacity (Pall LG6) was applied instead of a standard arterial line filter. White blood cells and platelet count were estimated preoperatively and at various times postoperatively. Postoperative clinical outcomes were also recorded. RESULTS: Repeated measure analysis of variance between groups showed that leukocyte counts were significantly lower in the depletion group postoperatively (p=0.005) whereas no difference was found in the platelet counts (p=0.37). The catecholamine dose required at the time of weaning from cardiopulmonary bypass and during the first 12 postoperative hours was found to be lower in the leukodepletion group (p=0.027 and p=0.021, respectively). Furthermore leukodepleted patients showed a transient improvement in the oxygenation index (p=0.029) and a shorter period of mechanical ventilation (p<0.001). The incidences of postoperative complications were similar between the groups. No difference was observed in regard to postoperative blood loss (p=0.821) and amount of packed red blood cells required for transfusion during the first 24 hours (p=0.846). The duration of intensive care unit stay and of hospitalization were similar between the groups. CONCLUSION: Leukocyte depletion contributes to early postoperative improvement in heart and lung function but does not influence significantly the overall clinical outcome of patients undergoing elective cardiac surgery.

Effect of prostacyclin PGI2 on cardiopulmonary bypass-induced lung injury.

Lung injury produced by cardiopulmonary bypass (CPB) is clinically characterized as postperfusion pulmonary dysfunction syndrome. The roles of humoral factors, altered perfusion modes and the occurrence of diffuse microembolism have been subjects of a number of studies. This paper presents the effectiveness of a platelet inhibiting drug, PGI2 in preventing occlusive microaggregates in the pulmonary circulation. In a series of experimental dog studies using a PGI2 dosage protocol of 10 ng/kg/minute for 30 minutes prior to the onset of CPB followed by 20 mg/kg/minute during CPB, the following effects have been observed: 1) Preservation of platelet numbers during CPB (p < 0.01 versus controls; n = 16). 2) Significant reduction in platelet aggregation during CPB (p < 0.01; n = 16). 3) Insignificant hypotensive effect at normal levels of peripheral vascular resistance (n = 16). 4) Occlusive fibrin, leucocytes and small platelet-based microaggregates obstructing pulmonary arterioles in six of the seven control dogs but in none of the dogs receiving PGI2 infusion. 5) No evidence of perivascular or intra-alveolar oedema, interstitial inflammatory cell infiltrates or haemorrhage was seen in either group of dogs. The controversy existing in relation to the possible therapeutic role of PGI2 and, in particular, its ability to prevent occlusive microaggregates in the arterioles and capillaries of vital organs should encourage further clinical studies of PGI2 and its derivatives during cardiac surgery.

Brain damage after profoundly hypothermic circulatory arrest: correlations between neurophysiologic and neuropathologic findings. An experimental study in vertebrates.

Five groups of neonatal pigs were subjected to cardiopulmonary bypass with circulatory arrest periods that varied from 70 to 120 minutes for the investigation of brain changes in induced deep-core hypothermia (15 degrees C) with circulatory arrest. The parameters that were analyzed were (1) microscopy of the brain in animals at 6 hours after bypass procedures and (2) intraoperative monitoring of somatosensory evoked potentials. Microscopic cellular damage appeared in all animals with a circulatory arrest period of more than 70 minutes. These changes involved mainly Purkinje's cells of the cerebellum, and they affected particularly the inferior half of the cerebellum. The prolongation of latency in the cortical responses, which reflects a slowing of the neural transmission with hypothermia, occurred in all animals. The late evoked potentials remained absent in all piglets with circulatory arrest periods of 90, 105, and 120 minutes, but they were fully recovered in all piglets of the control group and those with 70-minute arrest times. We concluded that the cerebellar region is the most sensitive site in which ischemic lesions attain their maximal severity and extent, and the maximum time of circulatory arrest without histopathologic and neurophysiologic sequelae should not exceed 70 minutes.

Neuropathological features of profoundly hypothermic circulatory arrest: an experimental study in the pig.

Twenty-four neonatal pigs were exposed to periods of circulatory arrest of between 70 and 120 min under profound hypothermia at 15 degrees C. Brain tissue taken 6h after cardiopulmonary bypass was examined histologically and by electron microscopy for evidence of hypoxic damage. Specimens from control pigs and animals subjected to 70 min arrest showed no morphological changes in the cerebral or cerebellar neurones. The earliest changes were seen after 90-min arrest; these were highly significant after 120 min. The changes involved mainly the Purkinje cells of the cerebellum with vacuolation in the cytoplasm; the inferior half of the cerebellum was particularly affected. The frequency and pattern of selective vulnerability of the cerebellum may be related primarily to the nature of its blood supply.

Assessment of neurological injury due to circulatory arrest during profound hypothermia. An experimental study in vertebrates.

To investigate brain changes in induced deep core hypothermia (15 degrees C) with circulatory arrest, five groups of neonatal pigs were subjected to cardiopulmonary bypass (CPB), with circulatory arrest (CA) periods varying from 70-120 min. The parameters analysed were: 1. Histology and electron microscopy of the brain six hours post-CPB, 2. Creatinophosphokinase (CPK) from cerebrospinal fluid (CSF), 3. Vasointestinal neuropeptide (VIP) and 7B2 specific neuropeptide both in plasma and brain tissue. The earliest morphological changes were seen after 90 min CA and were highly significant after 120 min arrest. These changes involved mainly the Purkinje cells of the interior half of the cerebellum with vacuolation in their cytoplasm. A rise in CPK in CSF occurred in all piglet-groups. The differences among the various groups were highly significant at 2 and 5 h post-CPB. (P < 0.05). Statistically significant differences were not exhibited among the various groups both in serum and brain tissue total mean values of VIP and 7B2 neuropeptides. We suggest that 1. The cerebellar region is the most sensitive where ischemic lesions attain their maximal severity and extent; the frequency and pattern of selective vulnerability of the cerebellum may be related primarily to its pattern of blood supply 2. The maximum time of CA without histopathological sequelae should not exceed 70 min.

Thirteen years evaluation of the Bjork-Shiley isolated mitral valve prosthesis. The Wessex experience.

Between 1973 and 1985, 349 patients had isolated mitral valve replacement by a Bjork-Shiley prosthesis with an overall early (30 day) mortality of 5.1%. Of the 331 survivors, 294 patients have been traced and their clinical outcome was followed for up to 13 years in order to define the long term performance of the mitral Bjork-Shiley models MBRP-standard, MBRC-convexo concave and MMSM-monostrut. Cumulative follow-up extends to 6620 patient years (mean 5.75 years). The MBRP valve was implanted in 236 patients, the MBRC valve used in 44 patients and the MMSM valve inserted in 14 patients. The late mortality and morbidity was 0.8% and 0.6% per patient year at 13 years respectively. Actuarial survival rate for the whole group excluding operative deaths was 85% at 5 years, 66% at 10 years and 58.5% at 13 years. The freedom from all valve related complications at 13 years was 70.75%. Bjork-Shiley models MBRP, MBRC and MMSM mitral valve prosthesis show excellent durability with only one case of mechanical failure over a 13 year period.