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Background: Mortality is a basic measure for quality and safety in anesthesia. There are few anesthesia-related mortality data available for pediatric practice. Our objective for this study was to determine the incidence of 24-hour and 30-day mortality after anesthesia and to determine the incidence and nature of anesthesia-related mortality in pediatric practice at a large tertiary institution., Methods: Children ≤ 18 years old who had an anesthetic between January 1, 2003, and August 30, 2008, at the Royal Children's Hospital, Melbourne, Australia, were included for this study. Data were analyzed by merging a database for every anesthetic performed with an accurate electronic record of mortality of children who had ever been a Royal Children's Hospital patient. Cases of children dying within 30 days and 24 hours of an anesthetic were identified and the patient history and anesthetic record examined. Anesthesia-related death was defined as those cases whereby a panel of 3 senior anesthesiologists all agreed that anesthesia or factors under the control of the anesthesiologist more likely than not influenced the timing of death., Results: During this 68-month period, 101,885 anesthetics were administered to 56,263 children. The overall 24-hour mortality from any cause after anesthesia was 13.4 per 10,000 anesthetics delivered and 30-day mortality was 34.5 per 10,000 anesthetics delivered. The incidence of death was highest in children ≤ 30 days old. Patients undergoing cardiac surgery had a higher incidence of 24-hour and 30-day mortality than did those undergoing noncardiac surgery. From 101,885 anesthetics there were 10 anesthesia-related deaths. The incidence of anesthesia-related death was 1 in 10,188 or 0.98 cases per 10,000 anesthetics performed (95%confidence interval, 0.5 to 1.8). In all 10 cases, preexisting medical conditions were identified as being a significant factor in the patient's death. Five of these cases (50%) involved children with pulmonary hypertension., Conclusions: Anesthesia-related mortality is higher in children with heart disease and in particular those with pulmonary hypertension. The lack of anesthetic-related deaths in children who did not have major comorbidities reinforces the safety of pediatric anesthesia in healthy children.

Purpose: The aim of the present study was to test the hypothesis that adjunctive local anaesthesia decreases postoperative pain, vomiting or length of stay in children having strabismus repair, Method: A prospective, randomized, triple-armed clinical trial involving a treatment comparison between topical amethocaine, sub-conjunctival bupivacaine and, as a placebo, topical normal saline was performed. All treatments were given at the end of surgery before emergence from the anaesthetic., Results: Overall, there was no statistically significant difference between outcome measures in the three trial groups. Using post hoc analysis there was a statistically significant difference between the groups receiving amethocaine and bupivacaine compared with the saline group in terms of the pain score at 120 min postoperatively. This difference has little clinical significance., Conclusions: Neither topical amethocaine nor subconjunctival bupivacaine makes a clinically significant difference to postoperative pain, emesis or length of stay. Moderate dose paracetamol per rectum alone appears to be effective analgesia for strabismus surgery, although it probably masked any small adjunctive effect of the topical anaesthesia used in the present trial.

This study analysed the frequency of distress at induction (DAI) in 2122 paediatric patients. The data were analysed to assess predictors of DAI and to examine associations between predictors of DAI and recovery characteristics. Patient age, preoperative behaviour, premedication (oral midazolam, n = 480) and venue for anaesthesia induction were associated with changes in the incidence of DAI. Distressed preoperative behaviour was a good predictor of DAI in all age groups. Premedication reduced the incidence of DAI in children aged 0.5-2 years old, and in older children who were distressed preoperatively. Induction in the Day Surgery Unit was associated with a reduction of the incidence of DAI in younger children. Children with DAI were more likely to suffer from distress at arousal (P = 0.001). Average early recovery time was prolonged 4.4 minutes and average discharge time in day patients was delayed 36 minutes by the use of oral midazolam premedication. Premedication was not significantly associated with arousal distress. We conclude that a policy of optimizing nonpharmacological approaches for minimizing induction distress, combined with selective premedication with oral midazolam, can produce a low incidence of induction distress and adverse effects.

The mucopolysaccharidoses are a group of inherited disorders of metabolism, with varying clinical manifestations. A number of them present anaesthetic difficulties. This paper presents a summary table of the syndromes and reviews our experience over ten years with patients with these diagnoses. The clinical presentations, anaesthetic management, and complications are described. The effect of age and diagnosis on airway difficulties was studied. There were 31 patients, 28 of whom required anaesthesia, on a total of 99 occasions, for 115 procedures. The patients with Hunter, Hurler and Maroteaux-Lamy syndromes had significantly more airway difficulties as they grew older, and compared with patients in this group with other syndromes. Patients with Hurler's syndrome may have coronary artery involvement and one patient was given fentanyl and pancuronium for this reason. He proved impossible to intubate and an emergency tracheostomy was performed.

The requirements for supplementary 3 ml epidural injections of bupivacaine 0.5% (top-ups) were used in a randomized double-blind study to compare the effects of five types of thoracic epidural infusions given at 2.5 ml h-1 for the first 24 h after major surgery to the upper abdomen in 99 patients and the lower abdomen in 72. The infusions were: bupivacaine 0.167% alone; diamorphine 0.167 mg ml-1 (0.417 mg h-1) in bupivacaine 0.167%; sufentanil 2 micrograms ml-1 (5 micrograms h-1) in 0.167% bupivacaine; sufentanil 4 micrograms ml-1 (10 micrograms h-1) in 0.167% bupivacaine; and sufentanil 4 micrograms ml-1 (10 micrograms h-1) in normal saline. The patients who had upper abdominal surgery were on average older than those having lower abdominal surgery and a larger proportion of them were female. They received on average fewer top-ups. After both upper and lower abdominal surgery, epidural infusions of bupivacaine alone required the most frequent supplementation (inter-quartile range 6-14 top-ups in 24 h) and the two sufentanil-bupivacaine mixtures required the fewest (interquartile range 0-12 top-ups in 24 h). The infusions of sufentanil without bupivacaine were significantly less effective than the sufentanil-bupivacaine mixtures after upper (but not lower) abdominal surgery. Although the two sufentanil-bupivacaine mixtures were indistinguishable in analgesic effectiveness after either upper or lower abdominal surgery, the lower (5 micrograms h-1) dose rate of sufentanil gave a significantly higher average breathing rate and lower average PaCO2 for the first 24 h after lower (but not upper) abdominal surgery. Blood samples were taken (as an afterthought) from 11 patients receiving sufentanil 10 micrograms h-1, just before the epidural infusion was stopped. The concentrations were mostly above the range for systemic analgesia, but below the values that would have been expected if a steady state had been achieved.

Three patients developed severe ovarian hyperstimulation syndrome (OHS) as a complication of ovarian hyperstimulation for in vitro fertilization. These patients presented with ovarian enlargement, vascular volume depletion, pleural effusions, and exudative ascites. A unique feature of the ascites in OHS was the markedly elevated renin concentration, the majority of which was prorenin. We speculate the renin-angiotensin system (RAS) may play a pathophysiologic role in the localized capillary leak that develops in OHS.

Isoelectric species of renin are physically heterogeneous. Recent evidence suggests that they may differ functionally, with some species producing natriuresis and diuresis, whereas others have no effect. A physiological function of secreted prorenin has not been documented in any species. The present study was designed to confirm and describe for the first time the renal effects of certain isoelectric species of prorenin. Anesthetized Sprague-Dawley rats were injected (0.1 ml) with trypsin-activated or nonactivated prorenin obtained from human ovarian follicular fluid. The dose chosen was calculated as sufficient to produce 2,300 ng angiotensin I.h-1.100 g rat body wt-1 in the presence of excess sheep substrate. Blood pressure, creatinine clearance, urine flow rate, and urine sodium, potassium, and osmolar excretion were measured. Activated prorenin from isoelectric peaks at isoelectric points (pI) 5.1, 5.2, 5.4, and 5.6 produced marked increases in urine volume (sixfold) and sodium excretion (7- to 10-fold) compared with the group receiving the vehicle (1% albumin in 0.9% saline). Activated prorenin from peaks at pI 4.9 and 5.8 produced no significant increase over the vehicle-only experiments. Captopril pretreatment (1 mg/kg iv) completely blocked the effects of peaks at pI 5.4 and 5.6. Interestingly, injection of nonactivated prorenin from peaks at pI 5.4 and 5.6 produced effects similar to the injection of activated prorenin from these peaks. Similarly, this effect was blocked by pretreatment with captopril. In summary, only certain isoelectric peaks of human prorenin whether activated, to active renin, or nonactivated produced a marked natriuresis and diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Active and inactive renin have been studied in peritoneal fluid and plasma of six patients with ascites and four patients on peritoneal dialysis (using concentrated dialysate). Acid-pepsin and trypsin activation gave similar results. In ascitic patients mean (+/- s.e.) plasma active renin was very high (0.31 +/- 0.99 pmol angiotensin l/l/s) compared with normal subjects (0.31 +/- 0.08 pmol ANG l/l/s). Plasma inactive renin (1.27 +/- 0.30 pmol ANG l/l/s) was similar to normal subjects (1.31 +/- 0.31 pmol ANG l/l/s) while the mean percentage of total renin which was inactive was 29.7 and 76.5. In ascitic fluid, active renin was very low (0.36 +/- 0.09 pmol ANG l/l/s) but inactive renin (2.15 +/- 0.28 pmol ANG l/l/s) was higher than plasma. Percentage of total renin inactive was 85.8. Peritoneal dialysate showed even smaller amounts of active renin but similar inactive renin with 95.4 per cent inactive (versus 73.8 in their plasma). Peritoneal fluid inactive renin was similar to that in plasma by affigel chromatography and gel filtration and showed, after activation, similar pH optima and Michaelis constants to plasma and peritoneal active renin.

Pentobarbitone-anesthetized cats underwent peritoneal dialysis and had blood samples removed and kidneys deep frozen at sacrifice. Inactive renin is easily measurable in cat plasma and peritoneal dialysate fluid. Only small amounts are found after acid activation at pH 4.0, but large amounts after trypsin 2 mg/ml at 4 degrees C for 10 minutes. Mean active renin in pentobarbitone-anesthetized cats was 1.8 +/- 0.4 pmoles AI/ml/hr, while inactive renin was 2.3 +/- 0.5 pmoles AI/ml/hr. The increased angiotensin I producing activity after trypsin in peritoneal dialysate was most active at pH 7.0 (plasma and kidney active renin 7.25 and 7.85), and had an apparent molecular weight of 39-40,000. (Plasma active renin had an apparent MW of 33,500 and kidney active renin 36,000. Plasma inactive renin had an apparent MW of 35,500) Cat plasma after cibacron-blue affinity chromatography showed mainly active renin in the breakthrough buffer (30% of total renin eluted), and renin which is almost entirely inactive in the bound peak (70% of total renin eluted). Active renin from plasma and kidney, and activated inactive renin from concentrated peritoneal fluid, showed exactly similar inhibition by the renin inhibitor H77 (IC50 0.3 microM). Cat plasma angiotensinogen had an apparent MW of 53,000.

Active and inactive renin in plasma and peritoneal dialysate were studied in pentobarbitone anesthetized cats during 8 hours of peritoneal dialysis. In control cats, despite a significant rise in plasma active renin from 1.3 +/- 0.22 to 4.4 +/- 0.76 pmoles AI/ml/hr over 8 hours, plasma inactive renin was unchanged. Four-fold rises in plasma active renin after hemorrhage (15 ml/kg) and captopril (1 mg/Kg I.V.) were unaccompanied by significant change in inactive renin. Bilateral nephrectomy resulted in undetectable plasma active renin after 3 hours but plasma inactive renin was 25-30% of initial levels 6 hours post-nephrectomy. In peritoneal dialysate, active renin remained low in control cats but there was a ten-fold rise of inactive renin from 0.06 +/- 0.02 to 0.60 +/- 0.07 pmoles AI/ml/hr. After hemorrhage there was a slight rise of active renin after 3 and 4 hours. Inactive renin was lower than control 6 hours after nephrectomy and captopril, but higher than control 1 and 2 hours after hemorrhage. Dialysate inactive renin accumulation slopes were not different among treatments. Acute changes in plasma active renin have little effect on peritoneal dialysate renin.

Studies of plasma samples of 3 subjects with Bartter's syndrome were compared to 8 subjects with other conditions. Despite high levels of active renin initially, with low levels of inactive renin, addition of either human nephrectomized plasma or sheep substrate not only increased active renin (by at least 3-fold) but also led to the appearance of large quantities of inactive renin (10-20 times the concentration originally present, much greater than the small increase seen with other plasmas). The activated inactive renin after substrate addition possibly had a larger and more variable molecular size (42,000-48,000) than normal inactive renin (42,500-44,500). Renin substrate in Bartter's plasma was present in similar amounts and had a normal or supranormal angiotensin generation rate with exogenous human renin. Bartter's substrate had a similar molecular weight (55,000) to that found in normal human plasma. The agent in the exogenous substrate preparations causing the increase in apparent active and inactive renin was not ultrafiltrable. However, an acidification procedure that destroyed exogenous substrate also removed the renin-increasing effect. Captopril increased renin but not aldosterone, while amiloride increased aldosterone but not renin. Neither agent improved serum potassium significantly in these patients on indomethacin.