The impact of implementing a preprinted order form for inpatient management of otherwise healthy children admitted to a tertiary care centre with a diagnosis of bronchiolitis.

OBJECTIVE: To examine the effect on length of stay (LOS) of a preprinted order (PPO) set for children admitted to hospital with a diagnosis of bronchiolitis, as well as on quality improvement measures, medical errors, and resource utilization. PATIENTS AND METHODS: A retrospective chart review was performed of children admitted to the inpatient units at the Children's Hospital of Eastern Ontario (CHEO) with a discharge diagnosis of bronchiolitis. Primary and secondary outcomes were compared between the pre-PPO (December 1, 2014 to June 30, 2015) and post-PPO (December 1, 2015 to June 30, 2016) periods. The primary outcome was LOS in days. Secondary outcomes included the proportion of quality improvement measures reached, the number of medical errors, and resource utilization. RESULTS: A total of 245 patients were included; 122 patients from the pre-PPO period (December 1, 2014 to June 30, 2015) and 123 patients from the post-PPO period (December 1, 2015 to June 30, 2016). Mean LOS was 3.1 days (2.7 to 3.5 days) and 2.8 days (2.4 to 3.2 days) in the pre- and post-PPO periods, respectively (multivariate analysis, P-value = 0.13). There were significant differences between the pre- and post-PPO periods in a number of quality improvement measures, although not in the number of medical errors. Significant reductions in oxygen, corticosteroid, antibiotic, and bronchodilator use were noted post-PPO implementation. CONCLUSION: Although our bronchiolitis PPO did not significantly shorten LOS, it led to important improvements in quality improvement measures and in resource utilization efficiency.

The epidemiology of intermittent and chronic ataxia in children in Manitoba, Canada.

AIM: To determine the epidemiology of chronic ataxia in children in Manitoba, Canada. METHOD: A retrospective study using multiple sources and disease codes identified children (age 0-16y) with chronic ataxia (>2mo duration or recurrent episodes of ataxia) seen at Winnipeg Children's Hospital from 1991 to 2008. Patients with isolated peripheral nerve diseases, vestibular disorders, or brain tumors were excluded. RESULTS: We identified 184 patients (males=females; mean age 15y, SD 7y 8mo) with chronic ataxia. Median age at the presenting symptom onset was 1 year 3 months and at ataxia onset 3 years 1 month. Median duration of follow-up was 6 years 5 months. During the study period, the crude incidence rate was 5.77 in 10,000; the crude prevalence rate was 6.59 in 10,000; and the crude mortality rate 0.446 in 10,000. The most common presenting symptoms were developmental delay, ataxia, or seizures. The most common diagnoses (known in 129) were Angelman syndrome (n=16), ataxia telangiectasia (n=13), mitochondrial disease (n=9), Friedreich ataxia (n=7), stroke (n=7), and familial/genetic episodic ataxia (n=7). INTERPRETATION: Chronic ataxia is a relatively common early-presenting symptom in childhood. A specific diagnosis is possible in 70% of patients after extensive investigations. The mortality rate is relatively low and the disease burden is high with significant comorbidities including developmental delay and epilepsy.

Possible mechanism of the vasodepressor effect of endokinin a/b in anesthetized rats.

We investigated the mechanism of the vasodepressor effect of endokinin A/B. An intravenous (IV) bolus of endokinin A/B (0.05-0.3 nmol/kg) dose-dependently decreased mean arterial pressure in thiobutabarbital-anesthetized rats. The magnitude of the response was unaffected by IV pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, inhibitor of nitric oxide synthase), methylene blue (inhibitor of soluble guanylyl cyclase), indomethacin (cyclooxygenase inhibitor), or tetraethylammonium (TEA, nonspecific K+ channel blocker). L-NAME reduced the half-recovery time of the vasodepressor effect of endokinin A/B relative to responses in rats pretreated with either saline or norepinephrine, which caused a similar pressor effect as did L-NAME. Methylene blue, but not TEA or indomethacin, reduced the recovery time of the vasodepressor effect of endokinin A/B. Therefore, the vasodepressor effect of endokinin A/B is mediated via the nitric oxide/L-arginine pathway and activation of soluble guanylyl cyclase but not by production of prostanoids or opening of TEA-sensitive K+ channels.

Analysis of the mechanism of the vasodepressor effect of urocortin in anesthetized rats.

The aim was to examine if the depressor effect of urocortin involves activation of the nitric oxide (NO)/L-arginine pathway, production of prostanoids or opening of K(+)-channels. I. v. bolus urocortin (0.1-3 nmol/kg) dose-dependently decreased mean arterial pressure in thiobutabarbital-anesthetized rats. The depressor effect of urocortin was unaffected by pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, inhibitor of NO synthase, i.v. bolus) or noradrenaline (i.v. infusion), which increased arterial pressure to a similar level as that produced by L-NAME. In addition, methylene blue (inhibitor of soluble guanylyl cyclase, i.v. infusion), indomethacin (cyclooxygenase inhibitor, i.v. bolus), glibenclamide (blocker of ATP-sensitive K(+)-channels, i.v. bolus) or tetraethylammonium (a non specific K(+)-channel blocker, i.v. bolus) did not affect the depressor effect of urocortin. In conclusion, the depressor effect of urocortin in anesthetized rats is not mediated via the NO/L-arginine pathway, activation of soluble guanylyl cyclase, production of prostanoids, opening of TEA sensitive K(+)-channels nor opening of ATP sensitive K(+)-channels.