A prospective observational study of human factors, adverse events, and patient outcomes in surgery for pediatric cardiac disease.

OBJECTIVE: To explore the impact of human factors on intraoperative adverse events and compensation mechanisms in pediatric cardiac surgery. METHODS: Prospective observations of pediatric cardiac surgical procedures were conducted. Patient complexity scores were calculated and outcomes recorded. The process of care was divided into epochs. Events were extracted and coded into compensated or uncompensated major and minor adverse events. Linear regression and analysis of variance were used to analyze the relationships between epochs, complexity, adverse events, and outcome. Patient-specific and procedure-specific variables were tested in a forward stepwise logistic regression as predictors of cases with 1 or more major adverse events. RESULTS: One hundred two patients undergoing pediatric cardiac surgery were observed. An average of 1.2 (range 0-6) major adverse events occurred per case. The most common type of major adverse event was cardiovascular, and most occurred during the surgery/postbypass epoch. Cognitive compensation was the most common compensation mechanism for major adverse events. An average of 15.3 minor adverse events occurred per case. Minor adverse events occurred frequently during the surgery/bypass epoch and related to communication and coordination failures. Higher case complexity, longer surgery duration, and higher number of major adverse events per patient correlated with death compared with other outcome groups (P < .01). Case complexity (P < .01) and surgery duration (P < .05) were both significant predictors of major adverse events. CONCLUSIONS: Pediatric cardiac surgery is an ideal model to study the coordinated efforts of team members in a complex organizational structure. Adverse events occurred routinely during pediatric cardiac surgery and were mostly compensated. Case complexity was a significant predictor of major adverse events. The number of major adverse events per patient correlated with clinical outcomes.

Postsynaptic contributions to hippocampal network hyperexcitability induced by chronic activity blockade in vivo.

Neuronal activity is thought to play an important role in refining patterns of synaptic connectivity during development and in the molecular maturation of synapses. In experiments reported here, a 2-week infusion of tetrodotoxin (TTX) into rat hippocampus beginning on postnatal day 12 produced abnormal synchronized network discharges in in vitro slices. Discharges recorded upon TTX washout were called 'minibursts', owing to their small amplitude. They were routinely recorded in area CA3 and abolished by CNQX, an AMPA receptor antagonist. Because recurrent excitatory axon collaterals remodel and glutamate receptor subunit composition changes after postnatal day 12, experiments examined possible TTX-induced alterations in recurrent excitation that could be responsible for network hyperexcitability. In biocytin-labelled pyramidal cells, recurrent axon arbors were neither longer nor more highly branched in the TTX infusion site compared with saline-infused controls. However, varicosity size and density were increased. Whereas most varicosities contained synaptophysin and synaptic vesicles, many were not adjacent to postsynaptic specializations, and thus failed to form anatomically identifiable synapses. An increased pattern of excitatory connectivity does not appear to explain network hyperexcitability. Quantitative immunoblots also indicated that presynaptic markers were unaltered in the TTX infusion site. However, the postsynaptic AMPA and NMDA receptor subunits, GluR1, NR1 and NR2B, were increased. In electrophysiological studies EPSPs recorded in slices from TTX-infused hippocampus had an enhanced sensitivity to the NR2B containing NMDA receptor antagonist, ifenprodil. Thus, increases in subunit protein result in alterations in the composition of synaptic NMDA receptors. Postsynaptic changes are likely to be the major contributors to the hippocampal network hyperexcitability and should enhance both excitatory synaptic efficacy and plasticity.