Utilizing an electronic health record system to improve vaccination coverage in children.

BACKGROUND: Electronic Health Records (EHR) are widely believed to improve quality of care and effectiveness of service delivery. Use of EHR to improve childhood immunization rates has not been fully explored in an ambulatory setting. OBJECTIVE: To describe a pediatric practice's use of Electronic Health Records (EHR) in improving childhood immunization. METHODS: A multi-faceted EHR-based quality improvement initiative used electronic templates with pre-loaded immunization records, automatic diagnosis coding, and EHR alerts of missing or delayed vaccinations. An electronic patient tracking system was created to identify patients with missing vaccines. Barcode scanning technology was introduced to aid speed and accuracy of documentation of administered vaccines. Electronic reporting to a local health department immunization registry facilitated ordering of vaccines. RESULTS: Immunization completion rates captured in monthly patient reports showed a rise in the percentage of children receiving the recommended series of vaccination (65% to 76%) (p<0.000). Barcode technology reduced the time of immunization documentation (86 seconds to 26 seconds) (p<0.000). Use of barcode scanning showed increased accuracy of documentation of vaccine lot numbers (from 95% to 100%) (p<0.000). CONCLUSION: EHR-based quality improvement interventions were successfully implemented at a community health center. EHR systems have versatility in their ability to track patients in need of vaccines, identify patients who are delayed, facilitate ordering and coding of multiple vaccines and promote interdisciplinary communication among personnel involved in the vaccination process. EHR systems can be used to improve childhood vaccination rates.

Rat gastrointestinal motor responses mediated via activation of neurokinin receptors.

Natural neurokinins (NK) and their specific receptor agonists, including substance P (SP), neurokinin A (NKA), neurokinin B (NKB), septide, [NIe10]-NKA4-10 and senktide, were used to assess whether they could activate established NK receptors in rat gastrointestinal tract and central nervous system to alter gastric emptying or intestinal transit. Fasting rats were intubated with an orogastric catheter to feed them liquid radiochromium. Neurokinins and analogues (at 10(-10), 10(-9), 10(-8) and 10(-7) mol/kg) and vehicle (saline + 0.1% bovine serum albumin) were injected via an intraperitoneal route. Rats were killed 15 min later and the whole gut was removed. The radioactivity of the stomach and 10 equally divided small intestinal segments was counted to determine gastric emptying and the geometric centre of intestinal transit. Septide treatment at 10(-8) and 10(-7) mol/kg markedly delayed gastric emptying. All doses of NKA inhibited gastric emptying. However, other peptides did not influence gastric emptying. Both septide and NKB treatment at 10(-8) and 10(-7) mol/kg enhanced intestinal transit. Substance P or senktide treatment (10-(-7) mol/kg) also enhanced intestinal transit. Stasis of remaining radioactivity in the proximal intestine was found following SP, septide, NKA and NKB treatment, whereas accelerated transit in the distal intestine was induced following NKA, NKB and senktide treatment. In conclusion, the in vivo study of NK and their specific agonists manifests a selective influence of these compounds on rat gastrointestinal tract. This selective activation of stomach NK1 and NK2 receptors delays gastric emptying, whereas activation of intestinal NK1 and NK3 receptors enhances intestinal transit.

Disturbed small intestinal motility in the late rat pregnancy.

We investigated whether various periods of pregnancy might disturb rat gastrointestinal motility. When the proestrus of female rats occurred, they were housed with male rats. Motility studies were conducted on day 7 (first period), day 14 (second) and day 21 (third) of pregnancy, respectively. After the orogastric feeding of radiochromium marker, rats were sacrificed 15 min later. Gastric emptyings of pregnant rats measured at various periods did not differ from the nonpregnant diestrus controls. The geometric center represented intestinal transits in the first, second and third periods of pregnancy and controls were (mean+/-SEM) 4.54+/-0.25, 4.47+/-0.17, 3.61+/-0.27 and 4.98+/-0.13, respectively (p < 0.01) while their plasma progesterone levels were 15.6+/-2.6, 18+/-1.4, 7.1+/-0.5 and 8.6+/-0.4 ng/ml, respectively (p< 0.01). This shows that late pregnancy inhibits small intestinal transit, whereas gastric emptying remains unchanged. Altered progesterone during pregnancy is not a main mediator to disturb intestinal transit.

Influence of blood glucose levels on rat liquid gastric emptying.

The glycemic influence on liquid gastric emptying in rats was studied. Diabetic hyperglycemia was induced by streptozotocin-treated rats further received a daily insulin injection ( 2.5 or 10 IU/kg). Immediate hyperglycemia was induced in a separate group of rats by continuous intravenous glucose infusion (44 or 88 mg/kg/min) 10 min before the experiment. Rats were killed 15 min after radiochromium feeding; then the radioactivity of stomach and small intestine were counted to obtain the gastric emptying value. Emptying in diabetic rats was delayed compared with controls (mean +/- SE: 40.9 +/- 2.6% vs. 54.2 +/- 2.8%, P < 0.01). Low-dose insulin treatment reversed the impairment, while high-dose treatment even enhanced emptying. Immediate hyperglycemia induced with two glucose infusions also inhibited gastric emptying. Present results indicate that hyperglycemia elicited with any hyperglycemic model is at least one of the important mechanisms to delay liquid gastric emptying.

Hyperglycaemia is responsible for the inhibited gastrointestinal transit in the early diabetic rat.

The effect of plasma glucose levels on the gastrointestinal motility of the rat was studied. Chronic hyperglycaemia was induced by i.v. injection of streptozotocin 1 week before the motility experiment. Some rats received additional daily insulin therapy (1.25, 2.5 or 10 IU kg-1) after induction of diabetes mellitus. Acute hyperglycaemia was induced by the continuous i.v. infusion of glucose solution (11, 22, 44 or 88 mg kg-1 min-1) 10 min before the motility experiments. The rats were killed 15 min after successful orogastric feeding of a charcoal-contained suspension. Gastrointestinal transit was calculated as the percentage of the overall length of the small intestine to which the charcoal moved during this time period. The diabetic rats were found to have delayed transit compared with controls (mean +/- SEM: 32.2 +/- 2.1% vs. 42.9 +/- 4.2%, P < 0.05). Correction of hyperglycaemia with moderate doses of insulin therapy failed to inhibit transit, whereas hypoglycaemia induced by high-dose insulin treatment enhanced transit. High doses of glucose elicited acute hyperglycaemia and delayed transit when compared with saline infused non-diabetic rats. In early diabetes, hyperglycaemia probably mediates the inhibited gastrointestinal transit, since correction of hyperglycaemia usually restores the delayed transit.

Influence of pregnancy and uterine weight on rat gastrointestinal transit.

Orogastric feeding of a charcoal meal to rats was employed to measure whether the various stages of pregnancy could influence gastrointestinal transit. The oestrous cycle of female Sprague-Dawley rats was checked daily. If pro-oestrus occurred, the first day of pregnancy was defined to be on the next day after the copulation. Gastrointestinal transit studies were conducted on day 7 (first trimester), day 14 (second) and day 21 (third), respectively. The rats were killed 15 min after the successful feeding of a calorie-free, charcoal-containing test meal via a transiently placed orogastric catheter. Gastrointestinal transit was defined as the per cent of charcoal transit divided by the total length of the small intestine. These results were compared with the data obtained from non-pregnant female rats. Mean percentages of transit for the first, second and third trimester, and for controls were 42.8 +/- 1.9, 45.3 +/- 4.1, 35.7 +/- 1.7 and 42.6 +/- 1.4%, respectively (mean +/- s.e.). Late pregnancy elicited a marked inhibition of transit (P < 0.01). A significant negative correlation between transit and uterine weight of all pregnant rats was seen (r = -0.50, P < 0.05). The present study indicates that inhibited gastrointestinal transit occurs in the late pregnant rat.

Gastric inhibitory polypeptide and gastric acid secretion in pregnant rats.

The effects of pregnancy on the basal and pentagastrin-stimulated gastric acid secretion and the level of plasma gastric inhibitory polypeptide (GIP) in rats were studied on pentobarbital-anaesthetized non-pregnant rats and rats in the 1st, 2nd, or 3rd week of gestation. Acid output was determined by titration of the gastric perfusate. Basal secretion was collected for 45 min before a 30 min infusion of pentagastrin (8 micrograms/ml/300 g body weight). Concentration of plasma GIP was measured by a radioimmunoassay (RIA). The immunoreactivity of GIP-like substance in the extract of the rat placenta collected from the rat at day 21 of gestation was examined by RIA. The biological activity of GIP-like substance in the rat placenta extract was tested by the reduction of pentagastrin-stimulated gastric acid secretion in male rats. The basal level of gastric secretion was higher in late pregnancy as compared with the non-pregnant rats. Pentagastrin induced a greater increase of gastric acid secretion in early but not late pregnant rats as compared with the non-pregnant animals. The basal and post-pentagastrin level of plasma GIP was higher in rats in late pregnancy. Both immunoreactivity and biological activity of GIP exist in the rat placenta extract. These results suggest that the normalization of gastric acid secretion in late pregnant rats is at least in part due to the production of GIP-like substance from placenta.

Comparison of two orogastric feeding markers for measuring gastrointestinal motor functions in rats.

Rat gastrointestinal (GI) transit parameters measured with charcoal and radiochromium were compared. Animals were fed with a calorie-free liquid test meal which contained 10% charcoal and radiochromium (0.5 microCi ml-1) via a transiently placed orogastric catheter. The rats were sacrificed at 1, 5, 15, 30, 60 and 120 min, respectively, since feeding. Various motor parameters were measured. Charcoal transit ratio, gastric emptying and geometric center were time dependent. Charcoal transit ratio occasionally showed a positive correlation with gastric emptying in the very late experimental periods. Concerning the correlation of charcoal transit ratio and geometric center, negative and positive correlations were seen in the very early and late periods, respectively. We conclude that the rat charcoal transit ratio has limited value to replace the GI transit parameters determined by feeding radiochromium.

The motor actions of natural neurokinins and their specific agonists on the gastrointestinal tract of the rat.

Neurokinins (NK) are a group of peptides that share a common C-terminal and play an important role in control of the motor functions of the mammalian gut. Neurokinin receptors such as NK1, NK2 are certainly present in any segment of gut, whereas the NK3 receptors are probably present in the ileum of the Guinea pig and duodenum of the rat. We measured gastrointestinal responses with natural NK and their very specific agonists to determine the probable receptors in the stomach and small intestine of Sprague-Dawley rats. After overnight fasting, the rats were intubated with a catheter to feed saline liquid meal that contained 10% charcoal. Simultaneously, various doses of NK ranged selected from 10(-10) and 10(-7) mol kg-1 included substance P (SP), neurokinin A (NKA), neurokinin B (NKB), septide, [Nle10]-NKA4-10, senktide, and vehicle were intraperitoneally injected. At 15 min after being fed test meal, the rats were sacrificed. Then we removed entire gut including the stomach to measure the total length of small intestine and transit length of the charcoal, from which the transit ratio was calculated. In comparison with ratios of rats treated with vehicle, the inhibited transit ratios for charcoal were seen among SP at 10(-10) mol kg-1, NKA at 10(-10) and 10(-7) mol kg-1, [Nle10]-NKA4-10 at 10(-7) mol kg-1, and senktide at all doses except 10(-8) mol kg-1. Enhanced transit ratios were seen for septide at the doses 10(-8) and 10(-7) mol kg-1. Likewise the mean total intestinal lengths of rats if they received various treatments of peptides except that rats treated with NKB had somewhat diminished length than those of vehicle-treated rats. Some natural NK and their very specific receptor agonists mainly inhibited rat gastrointestinal charcoal transits. We suggest the probable presence of NK1, NK2 and NK3 receptors in the small intestine and stomach including pylorus of the rat.

Gastric acid secretion in streptozotocin-diabetic female rats.

The secretion of gastric acid in normal and streptozotocin-induced diabetic rats was studied. Female rats were injected with streptozotocin (64 mg/kg BW, iv) or vehicle. Three days later, all rats were fasted overnight before anesthetization with pentobarbital (25 mg/kg BW, ip). The right jugular vein was catheterized. A PE-160 tubing was inserted into the esophagus and ligated at cervical level. A PE-320 cannula was introduced into the stomach through an incision in the duodenum and was ligated about 0.5 cm from the pylorus. The stomach was flushed through the esophagus cannula via a peristaltic pump with 10 ml saline at room temperature and then irrigated with saline. Acid output was determined by titration of the flushed perfusate with 0.01 N NaOH to pH 7.0. Basal secretions were collected for 45 min before infusion of pentagastrin (8 micrograms/ml/300 g BW) for 30 min, then for an additional 75 min. Blood samples were collected via jugular catheter at 0 min and 150 min following acid collection. Pentagastrin infusion stimulated gastric acid secretion in both diabetic and normal rats. The spontaneous gastric acid secretion in diabetic rats was not significantly different from that in normal animals. However, the secretion of gastric acid in response to pentagastrin was greater (p less than 0.05 to p less than 0.01) at 20, 30, and 35 min following pentagastrin infusion in diabetic rats than in normal females. Pentagastrin infusion stimulated gastric inhibitory polypeptide (GIP) secretion by 1.8-fold (p less than 0.05) in normal but not diabetic rats. The basal level of plasma GIP was higher (p less than 0.05) in diabetic than in normal rats. These results suggest that the increase of pentagastrin-induced gastric acid output in STZ-diabetic rats compared with normal controls is independent of GIP secretion.