No abstract

No abstract

Genetically determined obesities, involving leptin- and melanocortin-signaling pathways, have focused attention on the four medial hypothalamic nuclei as primary sources of feeding- and metabolically-based obesity. All four medial cell groups contain leptin receptors. To determine which of these cell groups normally mediates the effects of leptin on food intake and body weight gain, we injected colchicine bilaterally into each nucleus and determined the pathophysiological effects of disruption and responsivity to leptin injected intracerebroventricularly. Intracerebroventricular injections of leptin in sham-lesioned rats decreased food intake during the dark period, but not during the light period. Lesions of the arcuate (ARC), paraventricular (PVN), and ventromedial (VMN) nuclei all resulted in leptin insensitivity; by contrast, lesions of the dorsomedial nuclei (DMN) augmented sensitivity to leptin on feeding and body weight gain. Although rats with ARC and PVN lesions were obese, they were still capable of reducing caloric efficiency over the 5 days of study and increasing uncoupling protein content in interscapular brown adipose tissue. Caloric efficiency and uncoupling protein content were unchanged in rats with VMN and DMN lesions. Finally, the slope of the relationship between leptin and mesenteric white adipose tissue was increased in rats with VMN lesions and abolished in rats with ARC lesions. Thus, lesions of the ARC, PVN, and VMN produced obesity via separate pathways. We conclude that the medial hypothalamic cell groups, each with a different role in energy balance, are all necessary for normal leptin responsiveness.

BACKGROUND Low cardiac output syndrome is a transient constellation of signs and symptoms that indicate the heart’s inability to supply sufficient oxygen to tissues and end-organs to meet metabolic demand. Because the term lacks a standard clinical definition, the bedside diagnosis of this syndrome can be difficult. OBJECTIVE To evaluate concordance among pediatric cardiac intensive care unit nurses in their identification of low cardiac output syndrome in pediatric patients after cardiac surgery. METHODS An anonymous survey was distributed to 69 pediatric cardiac intensive care unit nurses. The survey described 10 randomly selected patients aged 6 months or younger who had undergone corrective or palliative cardiac surgery at a freestanding children’s hospital in a tertiary academic center. For each patient, data were presented corresponding to 5 time points (0, 6, 12, 18, and 24 hours postoperatively). The respondent was asked to indicate whether the patient had low cardiac output syndrome (yes or no) at each time point on the basis of the data presented. RESULTS The response rate was 46% (32 of 69 nurses). The overall Fleiss k value was 0.30, indicating fair agreement among raters. When the results were analyzed by years of experience, agreement remained only slight to fair. CONCLUSIONS Regardless of years of experience, nurses have difficulty agreeing on the presence of low cardiac output syndrome. Further research is needed to determine whether the development of objective guidelines could improve recognition and facilitate communication between the pediatric cardiac intensive care unit nurse and the medical team.

Continuous advances in pediatric cardiology, surgery, and critical care have significantly improved survival rates for children and adults with congenital heart disease. Paradoxically, the resulting increase in longevity has expanded the prevalence of both repaired and unrepaired congenital heart disease and has escalated the need for diagnostic and interventional procedures. Because of this expansion in prevalence, anesthesiologists, pediatricians, and other health care professionals increasingly encounter patients with congenital heart disease or other pediatric cardiac diseases who are presenting for surgical treatment of unrelated, noncardiac disease. Patients with congenital heart disease are at high risk for mortality, complications, and reoperation after noncardiac procedures. Rigorous study of risk factors and outcomes has identified subsets of patients with minor, major, and severe congenital heart disease who may have higher-than-baseline risk when undergoing noncardiac procedures, and this has led to the development of risk prediction scores specific to this population. This scientific statement reviews contemporary data on risk from noncardiac procedures, focusing on pediatric patients with congenital heart disease and describing current knowledge on the subject. This scientific statement also addresses preoperative evaluation and testing, perioperative considerations, and postoperative care in this unique patient population and highlights relevant aspects of the pathophysiology of selected conditions that can influence perioperative care and patient management.