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BACKGROUND: Diabetes mellitus is an established independent risk factor related to significant morbidity and mortality after cardiac surgical procedures. METHODS: Data on 16,184 patients undergoing cardiac surgery with and without cardiopulmonary bypass between April 1996 and August 2001 were prospectively evaluated. Diabetes mellitus as a patient related risk factor was subjected to univariate analysis to identify potential associations to 28 intra- and postoperative outcome variables. Outcome variables having a significant association with diabetes mellitus (p < 0.05) were then subjected to a stepwise logistic regression model to identify the influence of diabetes mellitus as compared to additional 30 different patient related risk factors and treatment variables. Diabetes mellitus was defined as glucose intolerance treated either dietary, with oral hypoglycemics or with insulin. RESULTS: Overall prevalence of diabetes mellitus was 33.3 %. Compared to non-diabetic patients the group with diabetes mellitus was older (p < 0.0001) and had a significantly lower ejection fraction (p < 0.0001). 15 outcome variables having a significant association with diabetes mellitus were identified. Furthermore, diabetes mellitus could be identified as an independent predictor for 7 postoperative outcome variables (prolonged ICU-stay, sternal instability and/or infection, sternal revision and refixation respiratory insufficiency, postoperative delirium, perioperative stroke, renal dysfunction, postoperative reintubation). CONCLUSION: Diabetes mellitus is a significant independent predictor for several postoperative outcome variables after cardiac surgery associated with higher postoperative morbidity and prolonged hospital stay.

Objectives: Recent studies suggest that myocardial reperfusion injury is exacerbated by free radicals when pure oxygen is used during cardiopulmonary bypass. Partial replacement of the oxygenator gas mixture with nitrogen, however, such as has already been adopted clinically in many centers, could increase the risk of gaseous nitrogen microembolus formation and therefore of brain damage because of the low solubility of nitrogen, particularly under conditions of hypothermia. Methods: Ten 7- to 10-kg piglets were cooled for 30 minutes to 15^oC on cardiopulmonary bypass and then rewarmed for 40 minutes to 37^oC. In 5 piglets cardiopulmonary bypass was normoxic and in 5 it was hyperoxic. In each group 3 bubble oxygenators without arterial filters and 2 membrane oxygenators with filters were used. Cerebral microemboli were monitored continuously by carotid Doppler ultrasonography (8 MHz) and intermittently by fluorescence retinography. Results: Embolus count was greater with lower rectal temperature (P < .001), use of a bubble oxygenator (P < .001), and lower oxygen concentration (P = .021) but was not affected by the temperature gradient between blood and body during cooling or rewarming. Conclusions: Gaseous microemboli are increased with normoxic perfusion, but this is only important if a bubble oxygenator without a filter is used. (J Thorac Cardiovasc Surg 1999; 117:1166-71)

Objectives: Laboratory studies suggest that myocardial reperfusion injury is exacerbated by free radicals when pure oxygen is used during cardiopulmonary bypass. In phase I of this study we demonstrated that normoxic perfusion during cardiopulmonary bypass does not increase the risk of microembolic brain injury so long as a membrane oxygenator with an arterial filter is used. In phase II of this study we studied the hypothesis that normoxic perfusion increases the risk of hypoxic brain injury after deep hypothermia with circulatory arrest. Methods: With membrane oxygenators with arterial filters, 10 piglets (8-10 kg) underwent 120 minutes of deep hypothermia and circulatory arrest at 15^oC, were rewarmed to 37^oC, and were weaned from bypass. In 5 piglets normoxia (PaO"2 64-181 mm Hg) was used during cardiopulmonary bypass and in 5 hyperoxia (PaO"2 400-900 mm Hg) was used. After 6 hours of reperfusion the brain was fixed for histologic evaluation. Near-infrared spectroscopy was used to monitor cerebral oxyhemoglobin and oxidized cytochrome a,a"3 concentrations. Results: Histologic examination revealed a significant increase in brain damage in the normoxia group (score 12.4 versus 8.6, P = .01), especially in the neocortex and hippocampal regions. Cytochrome a,a "3 and oxyhemoglobin concentrations tended to be lower during deep hypothermia and circulatory arrest in the normoxia group (P = .16). Conclusions: In the setting of prolonged deep hypothermia and circulatory arrest with membrane oxygenators, normoxic cardiopulmonary bypass significantly increases histologically graded brain damage with respect to hyperoxic cardiopulmonary bypass. Near-infrared spectroscopy suggests that the mechanism is hypoxic injury, which presumably overwhelms any injury caused by increased oxygen free radicals. (J Thorac Cardiovasc Surg 1999;117:1172-9)

Background: Aggressive surface warming is a common practice in the pediatric intensive care unit. However, recent rodent data emphasize the protective effect of mild (2^o-3^oC) hypothermia after cerebral ischemia. This study evaluates different temperature regulation strategies after deep hypothermic circulatory arrest with a survival piglet model. Methods: Fifteen piglets were randomly assigned to 3 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15^oC. Brain temperature was maintained at 34^oC for 24 hours after cardiopulmonary bypass in group I, 37^oC in group II, and 40^oC in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean +/- standard deviation. Recovery of neurologic deficit score (12.0 +/- 17.8, 47.0 +/- 49.95, 191.0 +/- 179.83; P = .05 for group I vs III), overall performance category (1.0 +/- 0.0, 1.4 +/- 0.6, 2.8 +/- 1.3; P < .05 for group I vs III), and histologic scores (0.0 +/- 0.0, 1.0 +/- 1.2, 2.8 +/- 1.8; P < .05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa"3 recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P < .05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided. (J Thorac Cardiovasc Surg 1998;116:780-92)