The effect of postoperative fasting on vomiting in children and their assessment of pain

Background:  Mandatory postoperative food intake has been shown to increase nausea and vomiting, and so postoperative fasting has become common practice even if patients request food or drink.
Objective:  We sought to investigate whether postoperative fasting reduces the incidence of postoperative vomiting in children when compared with a liberal regimen in which they are allowed to eat and drink upon request.
Methods:  One hundred forty-seven children scheduled for outpatient surgery were randomized to one of two groups. After anesthesia, patients in the 'fasting' group were expected to fast for 6 h. The children in the 'liberal' group were allowed to eat and drink according to their own needs. The incidence of vomiting and the children's well-being were recorded at several time points over a 24-hour period. Parents were also asked to rate, on a scale of 0–6, how much their children were bothered by fasting, pain, and nausea/vomiting.
Results:  Age (4.8 ± 2.6 years), weight (20 ± 9 kg) and gender (73% boys) were comparable between the groups. The incidence of vomiting was 15% in the liberal and 22% in the fasting group ( P  = 0.39) and, between 1 and 12 h after extubation, children in the liberal group were significantly happier ( P  < 0.001). Children in the liberal group were significantly less bothered by their pain than those in the fasting group ( P  < 0.001).
Conclusion:  Postoperative fasting did not reduce the incidence of vomiting after general anesthesia in children when compared with a liberal regimen. Furthermore, the ability to eat and drink at will decrease the bothersome aspects of pain and lead to happier patients.     

Coronary Stenting with the Sirolimus-Eluting Stent in Clinical Practice: Final Results from the Prospective Multicenter German Cypher Stent Registry

Aims: Drug-eluting coronary stents (DES) have gained widespread use for the treatment of coronary artery disease. However, because of safety concerns and frequent "off-label" use data from "real life," registries are necessary to monitor indications and outcome of DES in daily clinical practice.
Methods and Results: We evaluated data from the German Cypher Stent Registry. A total of 10,894 patients treated with at least one sirolimus-eluting stent (SES) at 152 hospitals were included. Follow-up at a median of 6.4 months was available in 10,006 patients (92%). Median age was 64.8 years and 75.5% were male. Per lesion a mean of 1.09 ± 0.41 SES were implanted with a mean length of 21.1 ± 11.5mm. During follow-up, death rate was 1.8% and the rates of myocardial infarction or stroke were 2.1% and 0.5%. Any target vessel revascularization (TVR) was performed in 8.0% of patients. Independent predictors for death, myocardial infarction, or stroke were: cardiogenic shock, acute coronary syndromes, reduced left ventricular function, renal insufficiency, diabetes mellitus, advanced age, three-vessel disease, degree of stenosis, and prior myocardial infarction. Predictors for a TVR were: two- or three-vessel disease, target vessel = coronary bypass, advanced age, stent diameter, ostial lesions, indication in-stent restenosis, renal failure, and target vessel = left anterior descended artery.
Conclusions: These results demonstrate that SES use in clinical practice is safe and effective. The main predictors of clinical events during follow-up are clinical parameters whereas as predictors of TVR mainly are angiographic parameters. (J Interven Cardiol 2010;23:18–25)     

Inappropriate Discharge of an Implantable Cardioverter Defibrillator During Atrial Flutter and Intermittent Ventricular Antibradycardia Pacing

Inappropriate Discharge of an ICD. Introduction : Inappropriate discharses of an implantable cardioverter defibrillator (ICD) are troublesome to the patient and sometimes a difficult task for the physician trying; to identify and treat the cause.
Methods and Results : For the first time, we report a mechanism of inappropriate ICD discharges during episodes of atrail flutter with a slow ventricular response and intermittent antibradycardia pacing. The episodes occurred in tow patients and were triggered by the unique sensing alogorithm of the Ventitex Cadence® V-100 in combination with the tripolar CPI Endotak® 072 transvenous defibrillation lead, which provides integrated bipolar sensing.
Conclusion : Besides treatment of the underlying arrhythmia, reprogramming of the device, an electrode position far away from the atria, and true bipolar sensing will enhance the performance of ICD systems with respect to the episodes described here. In addition, more flexible sensing algorithms may. in the future, prevent this overall rare complication.     

Body Surface Potentials During Discharge of the Implantable Cardioverter Defibrillator

Body Surface Potentials During ICD Discharge. Introduction: Little is known about the hazard for persons in contact with patients experiencing a high-voltage discharge of their implantable cardioverter defibrillator (ICD). Compared to epicardial systems, this risk may be increased with transvenous electrode systems and particularly in active can configurations. Methods and Results: In 23 patients with a transvenous active can ICD system, body surface potentials V_S and current through an external resistance were measured during 35 discharges. V_S was detected using skin electrodes positioned over the left subpectorally implanted pulse generator [C], apex of the heart [A], and the right pectoral region [RP]. Mean V_S during discharges without an external shunt resistance ranged between 13 and 63.8 V [C to A] and 12.5 to 47.3 V [C to RP] (ICD peak stored/output voltage V_cap= 183 to 606 V, n = 20). Mean current flow [C to A] was 8.2 to 46.8 mA (V_cap= 288 to 633 V. n = 10) and 42 to 120.7 mA (V_cap= 447 to 579 V, n = 5) across a resistance of 1.696 and 797 ω, respectively. Conclusion: During high-output shocks, a considerable potential difference is present on the hody surface of ICD patients that, according to the literature, may induce a single cardiac response in a bystander. Analogous to spontaneous extrasystoles, there is only a minimal chance of triggering a tachyarrhythmia by this stimulated extra beat. Direct induction of ventricular fibrillation is unlikely, since reported fibrillation threshold values are much higher than the ohserved magnitudes of current and voltage.     

Human endothelial cells bioactivate organic nitrates to nitric oxide: implications for the reinforcement of endothelial defence mechanisms

Abstract. Although in therapeutic use for more than a century, the mode of cellular action of organic nitrates remains incompletely understood. Despite ample experimental evidence from animal studies to show that nitrates are metabolized to NO in the vascular smooth muscle, direct demonstration of such an activity in human vascular cells is still lacking. Moreover, the role of the endothelium in modulating the pharmacodynamic action of nitrates is far from clear. We therefore aimed to investigate whether or not human endothelial cells are capable of bioactivating these drugs to NO and whether the amounts generated are sufficient to elicit any biological effects. Using cultured human umbilical vein endothelial cells (HUVECs) as an established model system a combination of three different methods was used to address this issue: (1) quantification of NO formation upon endothelial nitrate metabolism using the oxyhaemo-globin technique; (2) evaluation of the second messenger response using radioimmunoassay for cGMP; and (3) assessment of mechanism and extent of potentiation of the anti-aggregatory effect of nitrates in the presence of endothelial cells as a relevant bioassay. We now show that superfusion of cultured human endothelial cells on microcarrier beads with either glyceryl trinitrate (GTN) or isosorbide dinitrate (ISDN; both at 01.100 μmol L^-1) results in a concentration-dependent formation of NO. NO generation from isosorbide 5-mononitrate (IS-5-N) was below the detection limit. The amounts of NO produced (maximally 2–97 ± 0.98 pmoles NO min^-1 x mg protein with 100μmol L^-1 GTN; n= 8) were similar to those elicited upon challenge of the cells with 100nM bradykinin. NO formation from either organic nitrate was accompanied, in a concentration-dependent and methylene blue-inhibitable manner, by stimulation of endothelial soluble guany-lyl cyclase with consequent increases in the intracel-lular level of cGMP (maximally 32-fold over basal levels with ISDN), a significant portion of which was released into the extracellular space. Upon continuous 30 min superfusion or repeated application of high concentrations of GTN (100μmol L^-1) nitrate bioac-tivation to NO was subject to partial tachyphylaxis. Co-incubation of washed human platelets with HUVECs potentiated the anti-aggregatory action of nitrates in a cell number dependent and oxyhaemo-globin-sensitive manner and this effect, too, was accompanied by increases in intraplatelet cGMP levels. The potentiating effect was largely inhibited after blockade of sulfhydryl groups by pre-incubadon of HUVECs with N-ethylmaleimide and completely abrogated after pretreatment of cells with the tissue fixative glutaraldehyde. These results demonstrate that human endothelial cells are capable of bioactivating organic nitrates to NO by an enzymatic, apparently thiol-sensitive pathway, in quantities sufficient to influence endothelial and platelet function. Besides the well known vasorelaxant action of organic nitrates, which is mainly due to their metabolism in the smooth muscle compartment, these drugs may therefore be endowed with a hitherto underestimated potential to directly influence endothelial functions via the NO/ cGMP pathway. Through specific bioactivation in the endothelium itself organic nitrates can thus mimic and reinforce protective functions normally served by a functional endothelium such as the modulation of blood cell/vessel wall interactions and inhibition of cell proliferation.     

On the mechanism of renin release during experimental myocardial ischaemia

An increase in plasma renin activity (PRA) following experimental coronary occlusion has previously been demonstrated in anaesthetized and conscious dogs. The purpose of the present study was to analyse the mechanism of this renin release. In two distinct models of myocardial ischaemia in anaesthetized dogs--i.e. occlusion of the left-anterior descending coronary artery (model A, n = 21) and atrial pacing in the presence of stenosis of the left-anterior descending coronary artery (model B, n = 23), an increase in arterial PRA was found from 1.68 +/- 0.43 to 3.06 +/- 0.63 ng ml-1 h-1 (model A, mean +/- SEM, P less than 0.025) and from 9.87 +/- 3.59 to 14.96 +/- 4.06 ng ml-1 h-1 (model B, P less than 0.05), respectively. The increase in PRA following coronary occlusion was not blunted by adrenergic beta-receptor blockade with propranolol (3 mg kg-1 i.v.; n = 4). Coronary sinus PRA was lower than arterial PRA and the increase in PRA did not occur in nephrectomized dogs (n = 5). The data suggest that myocardial ischaemia induces a release of renin from the kidney which is not mediated by adrenergic beta receptors.     

BLADDER DYSFUNCTION: AN INTEGRAL PART OF THE ECTOPIC URETEROCELE COMPLEX

Purpose

We evaluate whether bladder dysfunction is common in patients with ectopic ureterocele and, if so, whether it is an integral part of the ectopic ureterocele complex or a result of surgery.

Materials and Methods

From 1986 to 1995, 34 patients with a mean age of 10 months were treated for large or medium ectopic ureteroceles at our institution and 32 participated in postoperative followup. Bladder function was investigated by a careful history and repeat uroflowmetry, and residual urine estimation was assessed by ultrasound and cystometry.

Results

Of the 32 patients 19 had infrequent voiding and 3 had incontinence. Cystometric bladder capacity was increased to greater than 150% of the normal value for age in 15 of 27 patients (55%). Uroflowmetry revealed greater than 5 ml. residual urine in 15 patients (56%). Postoperatively no radiological signs of bladder neck obstruction were found. Increased bladder capacity and residual urine did not correlate with ureterocele size or location, or surgical procedure. There was no progression of bladder dysfunction with age.

Conclusions

Children with ectopic ureterocele are at high risk for a high capacity bladder with incomplete emptying. This bladder dysfunction associated with ectopic ureterocele does not seem to be the result of surgery but an integral part of the disorder.     

Preserved Autonomic Modulation of the Sinus and Atrioventricular Nodes Following Posteroseptal Ablation for Treatment of Atrioventricular Nodal Reentrant Tachycardia

Autonomic Control of the AV Node. Introduction : Following radiofrequency catheter ablation of AV nodal reentrant tachycardia (AVNRT), inappropriate sinus tachycardia may occur, possibly due to damage to autonomic cardiac nerve fibers. Furthermore, inducibility of AVNRT is often critically dependent on the autonomic balance. We investigated whether successful ablation of AVNRT is associated with an alteration of autonomic input to the sinus and AV nodes.
Methods and Results : To estimate changes in the automatic modulation of the sinus and AV nodes, power spectra of beat-to-beat PP and PR intervals were analyzed from high-quality nighttime ECG recordings of 11 patients before and after radiofrequency application. Normalized HF power (nHF) of PP and PR intervals was used as an index of efferent vagal modulation and the LF/HF ratio as an index of sympathovagal balance of the sinus node (PP) and AV node (PR). Before ablation, LF/HF_PP was 3.2 and nHF_PP was 0.3 in the sinus node, For the A/V node, LF/HF_PR was 1.2 and nHF^PR was 0.5. Following ablation. LF/HF_PP (3.5) and nHF_PP (0.3) of the PP intervals did not change. Similarly to the sinus node, there were no changes in the autonomic modulation of the AV node, as both LF/HF_PR (1.2) and nHF_PR (0.5) remained unchanged.
Conclusion : Our results indicate that autonomic control of the sinus und AV nodes is preserved following successful radiofrequency ablation of AVNRT. The effects of posteroseptal radiofrequency current application are not necessarily mediated by changes in the autonomic input to the AV node.     

Therapy with Renin‐Angiotensin System Blockers after Pulmonary Vein Isolation in Patients with Atrial Fibrillation: Who Is a Responder?

Aims: The data on anti‐arrhythmic effect of renin‐angiotensin‐aldesteron system blockers (RASB) in patients with atrial fibrillation (AF) are controversially discussed. The goal of this analysis was to identify cohort of patients with AF and hypertension, who may have benefit from RASB therapy after pulmonary vein isolation (PVI). Methods: A total of 284 patients with AF and hypertension (paroxysmal AF [PAF]= 218, male = 185, age = 61 years, left ventricular ejection fraction = 60%, coronary artery disease = 42) considered for PVI were included. The patients with PAF were stratified according to time spent in AF (AF burden) within 3 months prior to admission (</> 500 hours). Further patients were divided into two groups: (1) low‐burden AF; (2) high‐burden AF (PAF and persistent AF). In 195 patients, RASB therapy was administered. A 7‐day continuous Holter electrocardiogram was performed after discharge, every 3 months thereafter and by symptoms. Results: Preventive effect of RASB was revealed in whole group (112 out of 195 [57%] vs 36 out of 89 [40%]; P = 0.025) and was more pronounced in patients with low‐burden AF (79 out of 112 [71%] receiving RASB vs 27 out of 55 [49%] being on other drugs; P = 0.013). However, efficiency of RASB failed in patients with high‐burden AF (33 out of 83 on RASB [40%] vs nine out of 34 on other drugs [27%]; P = 0.328). Conclusions: Our data suggest that RASB appears to protect against AF recurrences after PVI in patients with low‐burden paroxysmal AF. These results should be tested in a prospective study. (PACE 2010; 33:1101–1111)