Reconsidering electrophysiological markers of response inhibition in light of trigger failures in the stop-signal task.

This study investigates the neural correlates underpinning response inhibition using a parametric ex-Gaussian model of stop-signal task performance, fit with hierarchical Bayesian methods, in a large healthy sample (N = 156). The parametric model accounted for both stop-signal reaction time (SSRT) and trigger failure (i.e., failures to initiate the inhibition process). The returned SSRT estimate (SSRTEXG3 ) was attenuated by ≈65 ms compared to traditional nonparametric SSRT estimates (SSRTint ). The amplitude and latency of the N1 and P3 event-related potential components were derived for both stop-success and stop-failure trials and compared to behavioral estimates derived from traditional (SSRTint ) and parametric (SSRTEXG3 , trigger failure) models. Both the fronto-central N1 and P3 peaked earlier and were larger for stop-success than stop-failure trials. For stop-failure trials only, N1 peak latency correlated with both SSRT estimates as well as trigger failure and temporally coincided with SSRTEXG3 , but not SSRTint . In contrast, P3 peak and onset latency were not associated with any behavioral estimates of inhibition for either trial type. While the N1 peaked earlier for stop-success than stop-failure trials, this effect was not found in poor task performers (i.e., high trigger failure/slow SSRT). These findings are consistent with attentional modulation of both the speed and reliability of the inhibition process, but not for poor performers. Together with the absence of any P3 onset latency effect, our findings suggest that attentional mechanisms are important in supporting speeded and reliable inhibition processes required in the stop-signal task.

Diagnosis of postoperative arrhythmias following paediatric cardiac surgery.

Arrhythmias are commonly encountered in the paediatric intensive care unit setting, most frequently in the setting of postoperative congenital heart disease. Postoperative arrhythmias are an important cause of morbidity in children in the postoperative period following cardiac surgery for congenital cardiac lesions. It is important for all paediatric critical care physicians involved in the care of these children to understand the potential mechanisms involved and how to make an accurate diagnosis. The existing literature has focused on small groups and specific arrhythmias. There is a paucity of literature to guide the clinician in approaching arrhythmias in the paediatric intensive care unit setting. Our objective was to review the recognition and diagnosis of paediatric arrhythmias in the postoperative period following congenital cardiac surgery. Timely and accurate identification of the rhythm disturbance is mandatory and allows for the institution of effective, rhythm specific management strategies.

Abdominal compartment syndrome complicating paediatric extracorporeal life support: diagnostic and therapeutic challenges.

We report three paediatric cases, and summarise the reported experience in two others, with cardiorespiratory failure requiring extracorporeal life support for which supportive pump flows could not be maintained due to abdominal compartment syndrome. In two of our patients, the mechanism of abdominal compartment syndrome was massive intra-abdominal fluid extravasation secondary to sepsis, while in the third, the mechanism was post-traumatic intra-abdominal haemorrhage. Although all three children eventually died, decompressive laparotomy and arrest of haemorrhage in the trauma patient restored venous return and enabled technically adequate extracorporeal life support. In two previously reported cases of sepsis with massive fluid resuscitation resulting in abdominal compartment syndrome, one patient died without attempted decompression, while the other patient survived after peritoneal catheter placement restored venous return. Once correctable causes of inadequate venous cannula drainage have been excluded, abdominal compartment syndrome should be considered in any patient on extracorporeal life support with a taut abdomen and reduced venous return. If abdominal compartment syndrome can be proven or is strongly suspected, there may be a role for selective decompressive laparotomy.

Adjunct pharmacotherapy in acute lung disease in children.

Mechanical ventilation, while accepted as standard therapy for critically ill infants and children with respiratory failure, has significant morbidity and mortality. While recent emphasis on low tidal volume ventilation and low airway pressures may result in decreased lung stretch and limit lung disease, adjunctive therapies have been tried to reduce the stressors of mechanical ventilation. Therapies included inhaled nitric oxide, heliox and surfactant. There are compelling physiological reasons why these drugs may be of benefit in these patients. However, our understanding of their role is hindered by studies with small numbers of patients and its use in diseases with varied pulmonary pathology. Studies have shown potential for benefit of inhaled nitric oxide in newborns with hypoxemic respiratory failure and pulmonary hypertension, surfactant in respiratory distress syndrome in preterm neonates and heliox in severe upper airway obstruction. However, the use in other respiratory conditions has led to mixed results and hence paucity of firm recommendations.

Correlation of transcutaneous hepatic near-infrared spectroscopy readings with liver surface readings and perfusion parameters in a piglet endotoxemic shock model.

PURPOSE: To determine whether transcutaneous liver near-infrared spectrophotometry (NIRS) measurements correlate with NIRS measurements taken directly from the liver surface, and invasive blood flow measurements. PROCEDURE: Laparotomy was performed in 12 Yorkshire piglets, and ultrasound blood flow probes were placed on the hepatic artery and portal vein. Intravascular catheters were inserted into the hepatic and portal veins for intermittent blood sampling, and a pulmonary artery catheter was inserted via the jugular vein for cardiac output measurements. NIRS optodes were placed on skin overlying the liver and directly across the right hepatic lobe. Endotoxemic shock was induced by continuous infusion of Escherichia coli lipopolysaccharide O55:B5. Pearson's correlations were calculated between the NIRS readings and the perfusion parameters. FINDINGS: After endotoxemic shock induction, liver blood flow, and oxygen delivery decreased significantly. There were statistically significant correlations between the transcutaneous and liver-surface NIRS readings for oxyhemoglobin, deoxyhemoglobin, and cytochrome c oxidase concentrations. There were similar significant correlations of the transcutaneous oxyhemoglobin with both the mixed venous and hepatic vein saturation, and mixed venous and hepatic vein lactate. CONCLUSIONS: Transcutaneous NIRS readings of the liver, in an endotoxemic shock model, correlate with NIRS readings taking directly from the liver surface, as well as with global and specific organ-perfusion parameters.

Hypothermia pediatric head injury trial: the value of a pretrial clinical evaluation phase.

BACKGROUND: The utility of a pretrial clinical evaluation or run-in phase prior to conducting trials of complex interventions such as hypothermia therapy following severe traumatic brain injury in children and adolescents has not been established. METHODS: The primary objective of this study was to prospectively evaluate the ability of investigators to adhere to the clinical protocols of care including the cooling and rewarming procedures as well as management guidelines in patients with severe traumatic brain injury (Glasgow Coma Scale

Acute renal failure in children undergoing cardiopulmonary bypass.

OBJECTIVE: To investigate the incidence, implicating factors and outcome of acute renal failure after cardiopulmonary bypass in patients admitted to a paediatric intensive care unit. DESIGN: Prospective observational pilot study. SETTING: A 14 bed paediatric intensive care unit in a university affiliated, tertiary care referral children's hospital. PATIENTS: One hundred and one children (less than sixteen years of age) admitted to the Pediatric Intensive Care Unit following cardiopulmonary bypass between June 2003 and May 2004. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: PRISM-III score was calculated on admission. Baseline admission urea (mmol/L) and creatinine (micromol/L) serum levels and highest urea and creatinine levels were measured. Urine output (mL/kg/hour) and frusemide dose (mg/kg/day) were also noted. A baseline inotrope score was calculated on admission and the highest inotrope score was noted based on maximum infused doses of inotrope in the first 36 hours. The surgical procedure was used to determine a Jenkins score. Eleven (11%) children developed acute renal injury (doubling of creatinine), one child (1%) developed acute renal failure (tripling of creatinine) and one child died (1%). No child required dialysis for acute renal failure and none developed chronic renal impairment. Low cardiac output was the only significant risk factor identified for developing acute renal injury or failure. CONCLUSIONS: Acute renal injury is common and occurred in 11% of our children following congenital cardiac surgery, but acute renal failure requiring dialysis is uncommon.

Post-traumatic fat embolism in the inferior vena cava.

Histologically, pulmonary fat embolism is seen in up to 97% of traumatized patients, yet almost all of them are asymptomatic. Although clinically significant, fat embolism syndrome is not common; it is a frequent cause of death when it does occur. The authors report the computed tomographic demonstration of fat embolism in the inferior vena cava of a patient who sustained multiple fractures. To their knowledge, no similar case has ever been described.

Hyperbaric oxygen therapy for cerebral palsy: two complications of treatment.

There is growing interest in the use of hyperbaric oxygen therapy (HBO(2)) for children with cerebral palsy. Although there is no rigorous evidence to support this management, private hyperbaric centers have been established throughout the United States and Canada. There is likely to be increasing pressure on pediatricians and other health professionals to prescribe HBO(2). We describe 2 children with cerebral palsy who suffered significant morbidity immediately after treatment with hyperbaric oxygen. Both the temporal association and pathologic findings suggest that the hyperbaric treatment is likely to have been responsible for the resulting complications. As with any new therapy, we suggest waiting for the results of a randomized, controlled trial before recommending this treatment.

Effect of hyperventilation on regional cerebral blood flow in head-injured children.

OBJECTIVES: To study cerebral blood flow and cerebral oxygen consumption in severe head-injured children and also to assess the effect of hyperventilation on regional cerebral blood flow. DESIGN: Prospective cohort study. SETTING: Pediatric intensive care unit at a tertiary-level university children's hospital. PATIENTS: Twenty-three children with isolated severe brain injury, whose admission Glasgow Coma Scores were <8. INTERVENTIONS: PaCO2 was adjusted by altering minute ventilation. Cerebral metabolic measurements were made at three levels of PaCO2 (>35, 25 to 35, and <25 torr [>4.7, 3.3 to 4.7, and <3.3 kPa]) after allowing 15 mins for equilibrium. MEASUREMENTS AND MAIN RESULTS: Thirty-eight studies (each study consisting of three sets of measurements at different levels of PaCO2) were performed on 23 patients. At each level of PaCO2, the following measurements were made: xenon-enhanced computed tomography scans; cerebral blood flow; intracranial pressure; jugular venous bulb oxygen saturation; mean arterial pressure; and arterial oxygen saturation. Derived variables included: cerebral oxygen consumption; cerebral perfusion pressure; and oxygen extraction ratio. Cerebral blood flow decreased below normal after head injury (mean 49.6 +/- 14.6 mL/min/100 g). Cerebral oxygen consumption decreased out of proportion to the decrease in cerebral blood flow; cerebral oxygen consumption was only a third of the normal range (mean 1.02 +/- 0.59 mL/min/100 g). Neither cerebral blood flow nor cerebral oxygen consumption showed any relationship to time after injury, Glasgow Coma Score at the time of presentation, or intracranial pressure. The frequency of one or more regions of ischemia (defined as cerebral blood flow of <18 mL/min/100 g) was 28.9% during normocapnia. This value increased to 73.1% for PaCO2 at <25 torr. CONCLUSIONS: Severe head injury in children produced a modest decrease in cerebral blood flow but a much larger decrease in cerebral oxygen consumption. Absolute hyperemia was uncommon at any time, but measured cerebral blood flow rates were still above the metabolic requirements of most children. The clear relationship between the frequency of cerebral ischemia and hypocarbia, combined with the rarity of hyperemia, suggests that hyperventilation should be used with caution and monitored carefully in children with severe head injuries.

Evaluation of a mathematical model to predict intrapulmonary shunt non-invasively.

PURPOSE: We have previously published a mathematical model of oxygen transport. Using several physiological assumptions, the model provides a non-invasive estimate of intrapulmonary shunt. During a larger study of lung injury in a pig model, we had the opportunity to check the validity of our assumptions and the accuracy of the model's predictions. METHODS: We used six female pigs, average weight 12.8 kg. Following general anesthesia, tracheostomy and insertion of pulmonary venous and arterial lines, lung injury was induced by repeated saline lung lavage. Using hemodynamic measurements made at different levels of inspired oxygen, intrapulmonary shunt was calculated both by the traditional shunt equation and also by our mathematical model based on non-invasive measurements of FIO2 and SaO2. RESULTS: There was good agreement between the two methods of shunt calculation. Using linear regression the correlation coefficient was 0.95. Bland and Altman analysis showed a bias of -0.8 and precision of 12%. CONCLUSION: In a controlled setting, intrapulmonary shunt can be estimated from non-invasive measurements to a reasonable degree of accuracy. However, the calculation requires too many assumptions to be of general clinical value. The equations used provide a validated physiological model that acts as a useful tool for teaching cardiorespiratory physiology.

Partial liquid ventilation with perfluorocarbon in acute lung injury: light and transmission electron microscopy studies.

Liquid ventilation using perfluorocarbon has been shown to improve gas exchange in animal models of acute lung injury as well as in children with acute respiratory distress syndrome. This study was designed to define structural features of lung injury following partial liquid ventilation (PLV) using light and transmission electron microscopy in a rabbit model of acute respiratory distress. Animals were treated with either conventional mechanical ventilation (CMV-gas) (n = 6) or PLV (n = 5) for 4 h after the induction of acute lung injury with saline lavage. Control animals were killed after the lung injury. PLV significantly improved alveolar-arterial oxygen tension and the oxygen index compared with CMV (P < 0.05). Morphometric studies using light microscopy show less alveolar hemorrhage, less edema, and fewer hyaline membranes in the PLV group (P < 0.05). Polymorphonuclear leukocyte sequestration in lung capillaries (11.4 +/- 1.5 versus 19.2 +/- 3 x 10(8)/ml, P < 0.05, PLV versus CMV) and migration into airspaces (3.1 +/- 1.2 versus 4.5 +/- 1.1 x 10(8)/ml, P < 0.05, PLV versus CMV) were lower in the gravity-dependent lung regions. There were fewer alveolar macrophages in the PLV group compared with other groups (P < 0.05). Fluorescence microscopy analysis shows fewer type II alveolar epithelial cells in the CMV group and brighter type II cells in the PLV group. Transmission electron microscopy studies show more alveolar wall damage in the CMV group, with type II cells detached from their basement membrane with fewer surfactant-containing lamellar bodies. We conclude that quantitative histologic analysis shows less lung damage and inflammation when perfluorocarbon is combined with CMV in the management of acute respiratory distress syndrome.