Nosocomial infections in a pediatric intensive care unit.

In a prospective 30-month study of nosocomial infections in a pediatric ICU (PICU), the incidence, sites, and causes of infection were determined. Factors associated with increased risk of infection were investigated. In 1,388 patients who remained in the PICU for a minimum of 72 h, 116 infections occurred (6.1 infections/100 admissions). Primary bacteremias comprised 38% of PICU infections and lower respiratory infections comprised 15%. The remaining infections were divided equally among GI, skin, eye, upper respiratory, postoperative wounds, and other sites. Coagulase-negative staphylococci, Pseudomonas aeruginosa, and Staphylococcus aureus were the most prevalent pathogens. Surgical patients had similar rates of infection to medical patients. Patients in the first 2 yr of life, particularly those between 7 and 30 days of age, had the highest rate of infection. Onset of infection was more common after the first week in the PICU with 11% of patients staying 14 to 20 days, 27% of patients staying 21 to 27 days, 48% of patients staying 28 to 34 days, and 52% of patients staying more than 35 days before the onset of infection. The risk of nosocomial infection increases with arterial and central line use, prolonged intubation, ventilation, intracranial pressure monitoring, and paralysis.

The effect of afterload on the cardiodepressor reflex response to coronary artery occlusion in dogs.

The acute hemodynamic responses to anterior and posterior wall ischemia were examined at different afterloads in 30 open-chest anaesthetized dogs. Regional and global left ventricular responses to acute ischemia were also measured before and following bilateral cervical vagotomy in 18 dogs. As the preocclusion afterload (mean aortic pressure) was progressively raised with intravenous methoxamine, a significant decrease in stroke volume occurred following circumflex artery occlusion, whereas no change in stroke volume occurred following occlusion of the left anterior descending artery. Bilateral cervical vagotomy completely inhibited the decrease in stroke volume during circumflex occlusion at high afterload. Vagotomy had no effect on the hemodynamic response to acute anterior wall ischemia. Reversible cold vagal block in paced hearts at high afterload unmasked compensatory inotropy in the nonischemic anterior myocardial segment during circumflex occlusion. Restoring vagal tone by rewarming attenuated the fractional shortening of the nonischemic segment. The results indicate that a relationship exists between myocardial wall tension and reflex cardioinhibition during acute posterior wall but not anterior wall ischemia in dogs.

The role of cardioplegic solution buffering in myocardial protection. A biochemical and histopathological assessment.

The advantages of buffering cardioplegic solutions to improve adenosine triphosphate preservation and postarrest hemodynamic function have been previously promoted. We evaluated the benefit of histidine buffering (195 mmol/L) in a low sodium (27 mEq/L) cardioplegic solution (Roe's) in a canine model of multidose cardioplegic arrest. Four solutions, two unbuffered (K+ = 10 mEq/L and K+ = 30 mEq/L) and two buffered (K+ = 10 mEq/L and K+ = 30 mEq/L), were tested in four groups of dogs for a 4 1/2 hour arrest period followed by 1 hour of reperfusion. Use of the unbuffered solution resulted in a drop in myocardial adenosine triphosphate from 29 +/- 1 mmol/kg (mean +/- standard error of the mean) (K+ = 30 mEq/L) and 28 +/- 2 mmol/kg (K+ = 10 mEq/L) to 8 +/- 2 mmol/kg and 7 +/- 2 mmol/kg, respectively, during the arrest period. In both buffered groups, adenosine triphosphate remained at preischemic levels during the entire arrest period. Myocardial glycogen followed the same pattern as adenosine triphosphate in the buffered groups. Lactate production was markedly elevated in all groups during ischemia. Postarrest hemodynamic function, as assessed by intraventricular isovolumic developed pressure measurements, was better (p less than 0.05) in the buffered low-potassium group than in the other three groups. The extent of myocardial necrosis, measured by triphenyl tetrazolium staining and confirmed by electron microscopy, was minimal (2% +/- 1% of biventricular mass) in the buffered low-potassium group, significantly greater (7% +/- 2% and 10% +/- 2%) in the unbuffered high-potassium and low-potassium groups, respectively, and highest (35% +/- 9%) in the buffered high-potassium group. These findings indicate that significant buffering capacity (similar to that of blood) in a crystalloid cardioplegic solution can be effective in preserving myocardial adenosine triphosphate stores, improving postarrest contractile function, and minimizing myocardial necrosis, provided the combination of high extracellular potassium and high pH levels is avoided.

Multidose blood versus crystalloid cardioplegia. Comparison by quantitative assessment of irreversible myocardial injury.

The relative efficacy and safety of blood-based potassium cardioplegic solutions compared to crystalloid arresting solutions has been a major controversy in the field of intraoperative myocardial protection for cardiac operations. In this study multidose potassium (K+ = 30 mEq/L) blood cardioplegia was compared to multidose potassium crystalloid cardioplegia in a dog model in which hearts were arrested for periods of 4 1/2 and 6 hours. The cardioplegic solution was given as an initial bolus of 500 ml and then as 250 ml doses every 30 minutes of arrest. In the 4 1/2 hour arrest group, six animals received blood cardioplegia, six received a low-sodium crystalloid cardioplegia (modified Roe's solution), and 10 received a high sodium crystalloid cardioplegic solution of our own design. In the 6 hour arrest group, four animals received blood cardioplegia, four received the low-sodium solution, and four received the high-sodium solution. Myocardial temperature was precisely controlled at 27 degrees +/- 1 degree C in all groups. The hearts were reperfused for periods of 2 to 4 hours after the arrest periods and then examined morphologically for injury. The extent of myocardial damage was quantified in 5 mm thick transverse sections through the ventricles by using a tetrazolium enzyme-mapping technique. In the crystalloid groups the hearts arrested for 4 1/2 hours were significantly injured. The percentage (+/- SEM) of necrosis was 12.3 % +/- 5.6% in the low-sodium cardioplegic (modified Roe's) group and 9.3% +/- 3.4% in the high-sodium group. In the 6 hour arrest group the hearts were severely injured, with contracture occurring in all cases. The percentage of necrosis was 56.5% +/- 13% in the low-sodium cardioplegic group and 71.3% +/- 12% in the high-sodium group. In striking contrast all hearts protected with blood cardioplegia failed to show any evidence of tissue damage either on tetrazolium staining or on electron microscopic examination. We conclude that blood cardioplegia offers superior protection to the arrested heart at moderate hypothermia compared to crystalloid cardioplegia.

Myocardial pH during regional ischemia: evaluation of a fiber-optic photometric probe.

The relationship between the decrease in intramyocardial extracellular pH and the degree of stenosis of the left anterior descending (LAD) coronary artery was studied in eight dogs pretreated with propranolol. Intramyocardial pH was measured with a miniature glass pH electrode and with a new photometric pH probe that uses fiber-optic filaments to measure the color change of an indicator substance in a small permeable chamber. The LAD was cannulated and perfused from the axillary artery. Cannula flow was measured with an electromagnetic flow probe, and regional myocardial blood flow (RMBF) was measured with radioactive microspheres before and at the end of a period of critical stenosis, 2/3 reduction of flow, or total occlusion of the LAD cannula. In the region of the glass electrode, the mean RMBF (+/-SE) decreased by 16.3 +/- 3.3, 52.7 +/- 7.3, and 84.8 +/- 6.5% during the three levels of stenosis, and the pH correspondingly decreased by 0.05 +/- 0.01, 0.29 +/- 0.10, and 0.94 +/- 0.17 units. In the region of the photometric probe, the RMBF decreased 19.1 +/- 1.3, 47.2 +/- 6.7, and 84.3 +/- 6.0%, and the pH decreased by 0.05 +/- 0.02, 0.14 +/- 0.04, and 0.76 +/- 0.18 units. There was no statistically significant difference between the two types of pH sensor.

Intraoperative detection of spinal cord ischemia using somatosensory cortical evoked potentials during thoracic aortic occlusion.

Paraplegia remains a devastating and unpredictable complication of surgical procedures requiring temporary occlusion of the thoracic aorta, interruption of important spinal radicular vessels, or both. Intraoperative monitoring of the physiological integrity of the spinal cord should permit the early detection of spinal cord ischemia, the judicious and timely institution of corrective measures, including bypass or shunting, and the preservation of important intercostal arteries in appropriate circumstances. A model of spinal cord ischemia was created by temporary proximal and distal occlusion of the canine thoracic aorta. Serial measurement of somatosensory cortical evoked potentials (SCEP) generated by peripheral nerve stimulation, reflecting the status of long-tract neural conduction, was used to monitor alterations in spinal cord function during ischemia. Twelve animals subjected to aortic occlusion demonstrated a characteristic time-related deterioration of the SCEP with virtual extinction of the signal at a mean interval (+/- standard error of the mean) of 12.4 +/- 1.5 minutes. Six animals in which reperfusion was established immediately following the loss of the SCEP (Group 1) demonstrated complete recovery without neurological sequelae, as assessed by clinical and histological criteria. In 6 animals (Group 2), the period of aortic occlusion was extended for an additional 15 minutes following loss of the SCEP (27.3 +/- 2.3 minutes); postoperatively, 4 of 6 animals sustained major neurological lesions characterized by spastic paraplegia and histological evidence of spinal cord infarction (Group 1 versus Group 2, p less than 0.05). We conclude that distinctive alterations in the SCEP are indicative of reversible ischemic spinal cord dysfunction. On-line monitoring of spinal cord function using the technique of SCEP provides a rational basis for determining of SCEP provides a rational basis for determining operative strategy during surgical procedures on the thoracic aorta.

Effect of multidose cardioplegia and cardioplegic solution buffering on myocardial tissue acidosis.

Multidose administration of cardioplegic solution during cardiac operation is intended to maintain both electromechanical arrest of the heart and myocardial hypothermia as well as to remove accumulated metabolites of anaerobic glycolysis. This study was conducted to assess the effect of multidose infusion of three different types of cardioplegic solution on tissue acidosis during global myocardial ischemia. Three groups of five dogs each were placed on cardiopulmonary bypass and the aorta was cross-clamped for 3 hours. The hearts were maintained at a constant temperature (20 degrees C) and cardioplegic solution was infused at an initial dose of 500 ml and five supplementary doses of 250 ml administered every 30 minutes. Group 1 received a crystalloid solution weakly buffered with sodium bicarbonate, Group 2 received a blood-based solution, and Group 3 received a crystalloid solution strongly buffered with histidine (Bretschneider's solution). The buffering capacities of the solutions used in Groups 2 and 3 were 40 and 60 times, respectively, that of the solution used in Group 1. The average myocardial tissue pH at the end of 3 hours of ischemia was 6.54 +/- 0.07 in Group 1, 7.23 +/- 0.05 in Group 2, and 7.19 +/- 0.06 in Group 3 (Group 1 significantly lower than Groups 2 and 3). Multidose infusion of a cardioplegic solution with low buffering capacity was unable to prevent the progressive development of tissue acidosis during 3 hours of ischemia. However, the multidose infusion of either blood-based or crystalloid solutions with high buffering capacity completely prevented any further reduction of tissue pH after the first 30 minutes of ischemia.

Cardioplegia for severe coronary artery disease: an improved technique using direct coronary artery infusion.

Conventional techniques of cardioplegic solution administration result in regional disparities in the level of myocardial protection in patients with severe coronary artery disease. This report describes a simple adjunct to conventional transaortic administration of cardioplegic solution, in which additional solution is introduced directly through the coronary arteriotomy used for the vein graft anastomosis. The supplemental infusate is delivered through s small-caliber flexible catheter. This technique permits effective perfusion of the coronary vascular bed distal to severely stenotic and occlusive lesions. Using an experimental model of physiologically significant coronary arterial stenosis, we compared the effectiveness of this technique with that of conventional techniques of cardioplegia.

Afterload as a predeterminant of haemodynamics and segmental wall motion following coronary artery occlusion.

Maximal changes in haemodynamics and segmental wall motion were seen 2 min after coronary occlusion and were examined in relation to the loading conditions of the left ventricle before occlusion in 20 open chest dogs. There was a significant inverse relationship between the preligation mean aortic pressure and the percentage decrease in stroke volume following ligation. This relationship was observed whether afterload was distributed randomly (mean aortic pressure ranging from 9.7 to 17.6 kPa [73 to 132 mmHg]) between all dogs (r = 0.65; P less than 0.001) or altered by methoxamine (+4 kPa [+30 mmHg]) and nitroprusside (-3.2 kPa [-24 mmHg]) within the same dog (r = 0.82; P less than 0.001; n = 8). Although occlusion of the anterior descending artery caused a small (+5.5%) but significant increase in end-diastolic length of the non-ischaemic epicardial segment, the capacity for compensatory ventricular dilatation was not dependent on preligation afterload. However, the capacity of the ischaemic segment to undergo systolic expansion was significantly greater (+30.2% of end-systolic segment length) in those dogs with the lowest preligation MAP (8 to 12 kPa [60 to 90 mmHg]) compared with systolic lengthening of only 15.8% in the high afterload group (15 to 18 kPa [112 to 135 mmHg]). These data indicate that the loading conditions of the left ventricle predetermine the extent of global and segmental left ventricular dysfunction during the early phase of acute ischaemic injury.

Alpha and the eye.

It has been suggested by Lippold that the alpha rhythm is the result of a modulation of the corneo-retinal potential by translational eye tremor. We have attempted to replicate a critical test of the ocular origin of the alpha rhythm, altering the magnitude of the corneo-retinal potential while concomitantly measuring alpha amplitude. No changes in alpha amplitude related to changes in corneo-retinal potential could be seen. We are thus unable to confirm Lippold's hypothesis.