Paediatric ventilation treatment of acute lung injury in Nordic intensive care units.

BACKGROUND: Treatment of acute respiratory distress syndrome (ARDS) in children is largely based on extrapolated knowledge obtained from adults and which varies between different hospitals. This study explores ventilation treatment strategies for children with ARDS in the Nordic countries, and compares these with international practice. METHODS: In October 2012, a questionnaire covering ventilation treatment strategies for children aged 1 month to 6 years of age with ARDS was sent to 21 large Nordic intensive care units that treat children with ARDS. Pre-terms and children with congenital conditions were excluded. RESULTS: Eighteen of the 21 (86%) targeted intensive care units responded to the questionnaire. Fifty per cent of these facilities were paediatric intensive care units. Written guidelines existed in 44% of the units. Fifty per cent of the units frequently used cuffed endotracheal tubes. Ventilation was achieved by pressure control for 89% vs. volume control for 11% of units. Bronchodilators were used by all units, whereas steroids usage was 83% and surfactant 39%. Inhaled nitric oxide and high frequency oscillation were available in 94% of the units. Neurally adjusted ventilator assist was used by 44% of the units. Extracorporeal membrane oxygenation could be started in 44% of the units. CONCLUSION: Ventilation treatment strategies for paediatric ARDS in the Nordic countries are relatively uniform and largely in accordance with international practice. The use of steroids and surfactant is more frequent than shown in other studies.

Does adding a dietician to the liaison team after discharge of geriatric patients improve nutritional outcome: a randomised controlled trial.

OBJECTIVES: The objective was to test whether adding a dietician to a discharge Liaison-Team after discharge of geriatric patients improves nutritional status, muscle strength and patient relevant outcomes. DESIGN: Twelve-week randomized controlled trial. SETTING AND SUBJECTS: Geriatric patients (70 + years and at nutritional risk) at discharge. INTERVENTIONS: Participants were randomly allocated to receive discharge Liaison-Team vs. discharge Liaison-Team in cooperation with a dietician. The dietician performed a total of three home visits with the aim of developing and implementing an individual nutritional care plan. The first visit took place at the day of discharge together with the discharge Liaison-Team while the remaining visits took place approximately three and eight weeks after discharge and were performed by a dietician alone. MAIN MEASURES: Nutritional status (weight, and dietary intake), muscle strength (hand grip strength, chair-stand), functional status (mobility, and activities of daily living), quality of life, use of social services, re-/hospitalization and mortality. RESULTS: Seventy-one patients were included (34 in the intervention group), and 63 (89%) completed the second data collection after 12 weeks (31 in the intervention group). Odds ratios for hospitalization and mortality 6 months after discharge were 0.367 (0.129; 1.042) and 0.323 (0.060; 1.724). Nutritional status improved and some positive tendencies in favour of the intervention group were observed for patient relevant outcomes, i.e. activities of daily living, and quality of life. Almost 100% of the intervention group received three home visits by a dietician. CONCLUSION: Adding a dietician to the discharge Liaison-Team after discharge of geriatric patients can improve nutritional status and may reduce the number of times hospitalized within 6 months. A larger study is necessary to see a significant effect on other patient relevant outcomes.

No morphine sparing effect of ketamine added to morphine for patient-controlled intravenous analgesia after uterine artery embolization.

BACKGROUND: Pain following embolization of the uterine arteries (UAEs) is variable and may be very severe requiring large doses of parenteral opioids for relief. The present study tested the hypothesis that the addition of ketamine to i.v. patient-controlled morphine reduces the amount of morphine required for pain-control during the first 24 h after UAE embolization. METHODS: Fifty-six patients undergoing UAE embolization for treatment of symptomatic uterine leiomyomata were randomized to receive either 2 mg/ml of morphine (Control group, n=30) or 2 mg/ml of both morphine and ketamine (Ketamine group, n=26) by i.v. patient-controlled analgesia (IV-PCA). Pump settings were bolus dose 1 ml, lockout 10 min, no background infusion. In addition, all patients received diclofenac and acetaminophen for pain relief. Pain scores, morphine consumption and adverse events like nausea, vomiting, itching, visual disturbances, anxiety, dreaming and hallucinations, if any, were recorded for 24 h after embolization. RESULTS: The mean +/- SD 24-h consumption of patient-controlled morphine was 38.3 +/- 21.0 mg in the Ketamine group vs. 33.3 +/- 18.3 mg in the Control group (NS). The difference between the means was 5.0 mg (95% confidence interval: -5.7; 15.6). One patient in the Ketamine group vs. none in the Control group experienced auditory hallucinations. CONCLUSION: Studying an unselected group of patients undergoing embolization of the UAEs for treatment of symptomatic uterine leiomyomata under conditions of basal analgesia with acetaminophen and diclofenac, we failed to demonstrate any morphine-sparing effect of IV-PCA ketamine and morphine compared with IV-PCA morphine alone.

Supplementing newborn intrauterine growth restricted piglets with a bolus of porcine colostrum raises rectal temperatures one degree Celsius.

Hyperprolific sows have increased litter sizes but also result in more piglets that have been exposed to intrauterine growth restriction (IUGR). These IUGR piglets are likely to have a low rectal temperature and lower blood glucose levels compared with normal piglets at birth. Therefore, we hypothesized that a colostrum bolus at birth and/or heat from an external source would have a positive effect on blood glucose levels, rectal temperatures, and growth up to 8 h postpartum. In addition, liver glycogen and blood values at 8 h were investigated. Eighty-four piglets were classified at birth (time = 0) as IUGR based on their head morphology and randomly allocated to 1 of 4 treatments ( = 21) in a 2 × 2 factorial arrangement: 1) with or without a porcine colostrum bolus (12 mL/kg BW at birth) and 2) with sow or isolated from sow with external heat. Piglets were removed from the sow before they had suckled and were numbered and dried, and initial whole-blood glucose, rectal temperature, and BW were recorded. Piglets in the 2 treatments isolated from sow were placed under a heating lamp (150 W) with a temperature range of 35 to 39°C. Rectal temperatures, glucose, and BW were measured again at 1, 2, 4, 6, and 8 h after birth, and a final plasma sample and organs (liver and brain) were removed at 8 h. There was a time × colostrum bolus interaction ( = 0.026) and a time × sow interaction ( < 0.001) for whole-blood glucose. The piglets that were given a bolus had greater glucose levels after 1 h postpartum (time = 1 h) than piglets without a bolus at birth, but from time = 2 h and onward, there was no difference ( > 0.05). There was a time × colostrum bolus interaction ( < 0.001) and a time × sow interaction ( < 0.001) on rectal temperatures. One hour after birth, the piglets with a bolus had a greater rectal temperature compared with piglets without a bolus (37.5 vs. 36.6°C; < 0.001) and the piglets that had been isolated from the sow had a greater rectal temperature compared with the 2 treatments with sows (37.8 vs. 36.3°C; < 0.001). Four hours after birth, rectal temperature was not affected by treatments. In conclusion, both heat and a colostrum bolus increased rectal temperature by 1°C an hour after birth. However, after 4 h, no differences were found between the treatments. Interventions to help IUGR piglets postpartum most likely need to be frequent to have any effect on whole-blood glucose, rectal temperatures, and BW over the first 8 h.

Leucine aminopeptidase M-induced reductions in blood pressure in spontaneously hypertensive rats.

Leucine aminopeptidase M significantly reduced blood pressure for up to 40 minutes when infused intracerebroventricularly into anesthetized spontaneously hypertensive rats (SHR) from a mean +/- SEM of 190 +/- 4 to 94 +/- 7 mm Hg and also in normotensive Wistar-Kyoto (WKY) rats from 138 +/- 5 to 68 +/- 8 mm Hg. Cerebrospinal fluid levels of angiotensin II (Ang II) and III were measured by radioimmunoassay and indicated drops with leucine aminopeptidase M infusion in SHR (from 36 +/- 6 to 11 +/- 1 pg/100 microliters) and in WKY rats (from 33 +/- 9 to 13 +/- 1 pg/100 microliters). Pretreatment with the specific angiotensin receptor antagonist [Sar1, Thr8]Ang II (sarthran) significantly diminished the subsequent leucine aminopeptidase M-induced decreases in blood pressure in SHR and facilitated recovery to base level blood pressure and heart rate in blood strains. Thus, exogenous application of leucine aminopeptidase M into the brain lateral ventricles of SHR is temporarily effective at reducing blood pressure, and this effect appears dependent on the brain angiotensinergic system. This treatment also reduced blood pressure in WKY rats; however, pretreatment with sarthran was reasonably ineffective at preventing subsequent leucine aminopeptidase M-induced decreases in blood pressure.

Brain angiotensin: critical role in the ongoing regulation of body fluid homeostasis and cardiovascular function.

The existence of an endogenous brain-angiotensin system and its association with cardiovascular and body water regulation has been recognized for over a decade. Nevertheless, the importance of the brain-angiotensin system to the instantaneous regulation of these processes has not been firmly established. A 5-minute intracerebroventricular (ICV) infusion of the angiotensin antagonist, [Sar1,Thr8]-AII, effectively lowered the blood pressure in normotensive rats. Additionally, application of the selective aminopeptidase inhibitor, bestatin, given alone, resulted in a dramatic increase in blood pressure and a robust drinking response. Both effects were 100% blockable by [Sar1,Thr8]-AII pretreatment. Predictably, an aminopeptidase inhibitor, bestatin, greatly elongated the half-lives of AII and AIII in the cerebroventricles. Since neither of these treatments included the introduction of exogenous angiotensins, we have concluded that perturbations of the endogenous brain-angiotensin system are effective at rapidly influencing both cardiovascular and body fluid homeostasis, thus highlighting the paramount role played by brain angiotensin in their ongoing regulation.

Central effects of a specific angiotensin receptor antagonist, sarthran (Sar1, Thr8AII) in normotensive and spontaneously hypertensive rat strains.

The specific angiotensin receptor antagonist, Sar1, Thr8AII (sarthran), was infused intracerebroventricularly in alert spontaneously hypertensive rats (SHR), and Wistar-Kyoto (WKY) and Sprague-Dawley (SD) normotensive rat strains. This resulted in a mean decrease of 35 mm Hg in the SHR group by 25 min post-infusion, and corresponding decreases in the WKY and SD rats of 13 and 15 mm Hg, respectively. A prominent transient sarthran-induced elevation in blood pressure was noted in the SHR group during the 5-min infusion. This agonistic effect was not observed in members of the WKY and SD strains. These data encourage the use of sarthran as a valuable pharmacological probe in the examination of the role of the brain renin-angiotensin system in hypertension.

Increased blood pressure induced by central application of aminopeptidase inhibitors is angiotensinergic-dependent in normotensive and hypertensive rat strains.

Two aminopeptidase inhibitors, amastatin (AM) and bestatin (BE), were employed in 3 strains of rats, spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), and Sprague-Dawley (SD), to investigate the central angiotensinergic system. The results indicate that intracerebroventricular (i.c.v.) injections of AM and BE induced pressor elevations in all 3 strains of rats. In order to test for the possibility of spillage into peripheral vasculature, members from all 3 strains were peripherally infused with AM, BE, or 0.15 NaCl via jugular vein catheters. The SHRs were significantly more responsive to the aminopeptidases than the normotensive strains, however their overall pressor responses were only 33% of those to i.c.v. infusion. Next, in order to test the notion that these aminopeptidase inhibitors are having their effect via the central angiotensinergic system, and not some other peptidergic system, the specific angiotensin receptor antagonist, Sar1, Thr8-AII (sarthran) was employed. Intracerebroventricular pretreatment with sarthran prevented subsequent pressor responses to i.c.v. AM and BE in members of all 3 strains, thereby suggesting that these aminopeptidase inhibitors are having their effect via the central angiotensinergic system.

Intracerebroventricularly applied peptidase inhibitors increase endogenous angiotensin levels.

Rats received the aminopeptidase inhibitors amastatin (AM) and bestatin (BE), and carboxypeptidase inhibitor Plummer's (PL) via intracerebroventricular infusion in various combinations, i.e. PL alone, AM + BE, and a cocktail consisting of AM + BE + PL. Blood pressure responses were recorded and a postinfusion sample of cerebrospinal fluid (CSF) was radioimmunoassayed for endogenous angiotensin levels. Results indicate that CSF angiotensin was increased approximately 1.5x over control levels when PL was infused; a 2.5x increase accompanied AM + BE administration; and a 10.3x elevation was measured when all 3 inhibitors were infused as a cocktail. Concomitant elevations in blood pressure accompanied increased concentrations of angiotensin. We conclude that endogenous levels of angiotensin can be significantly increased in the ventricular space when a combination of these inhibitors is utilized to protect both the amino and carboxyl terminals of the angiotensin molecule from enzymatic degradation.

Microinfusion of aminopeptidase M into the paraventricular nucleus of the hypothalamus in normotensive and hypertensive rats.

Normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) received aminopeptidase M (AmM) delivered into the paraventricular nucleus of the hypothalamus (PVN). Resulting changes in blood pressure were recorded in both anesthetized and alert animals. The findings indicate significant dose-determined decreases in blood pressure in members of both strains with SHR more responsive than WKY rats. The respective drops in blood pressure for members within each strain were equivalent for the anesthetized and alert conditions. Pretreatment with the specific angiotensin receptor antagonist, sarthran, [Sar1, Thr2] Angll, into the PVN greatly diminished these responses, suggesting the involvement of the brain angiotensin system. Additionally, a sympathetic nervous system blocker, hexamethonium, and the arginine vasopressin antagonist, Pmp1, O-Me-Tyr2-[Arg] vasopressin, were peripherally administered to assess the potential contributions of these systems to cardiovascular regulation by the brain angiotensin system. The use of these blockers, individually and combined, attenuated responsiveness to infusion of AmM into the PVN. We conclude that AmM can act as a hypotensive agent in both SHR and WKY rats, and that this decrease in blood pressure is at least partially mediated via the brain angiotensin system although other systems may play a role.

Heightened blood pressure responsiveness to intracarotid infusion of angiotensins in the spontaneously hypertensive rat.

The purpose of this study was to test the hypothesis that intracarotid infusion of angiotensin via a brachial arterial catheter results in a heightened pressor response in the alert spontaneously hypertensive rat (SHR) as previously observed for intracerebroventricular (ICV) injection of angiotensin. We infused angiotensin II and III since these ligands are equivalently potent with respect to peak pressor effect when delivered ICV. We measured somewhat greater pressor responsiveness to AII than to AIII in the Wistar-Kyoto (WKY) normotensive control strain from a baselevel of 133.1 +/- 5.8 (mean +/- SEM) to 151.3 +/- 6.2 mmHg (+13.7%) at the 100 pmol/kg/min dose of AII, and from 132.5 +/- 5.8 to 146.0 +/- 6.1 mmHg (+10.2%) for AIII. The SHR revealed a heightened pressor sensitivity to AII, from a baselevel of 170.0 +/- 3.8 to 200.6 +/- 5.9 mmHg (+18%) while the response to AIII was less dramatic, from 171.3 +/- 2.1 to 189.8 +/- 2.4 mmHg (+10.8%). These findings suggest that a similar heightened pressor responsiveness occurs to peripheral infusion of angiotensin II in the SHR as previously observed to ICV injection.

Assessing and treating patients with complex fecal incontinence.

Fecal incontinence is the involuntary loss of gas, liquid, and/or solid stool. It affects 2.2% of the general population. Because fecal incontinence can be socially and psychologically devastating, and is not easily discussed, this figure is probably understated. Patients presenting with fecal incontinence need to be properly assessed, including physiological testing of the pelvic floor muscles and nerves. Identifying any abnormal anatomy or physiology in the pelvic floor helps the clinician develop a care plan that best suits the patient's etiology. Knowledge of the physiology of the pelvic floor musculature and its effects on continence is improving. Treatment options also have broadened. This article describes the current techniques of assessment and treatment, including the "gold standard," and newer investigational procedures offered to patients with complex fecal incontinence.

Fecal incontinence: evaluation and treatment.

Fecal incontinence, the involuntary passage of gas, liquid, or solid stool, is an underreported problem in our society. The evaluation of fecal incontinence includes a focused history, physical examination, and assessment of the pelvic floor musculature. This article describes the assessment of fecal incontinence, focusing on specific diagnostic tests designed to identify dysfunction of the anal sphincter and adjacent pelvic floor musculature and on the use of these tests in determining an appropriate treatment plan.

Biofeedback improves functional outcome after sphincteroplasty.

UNLABELLED: The primary treatment for obstetric sphincter injury is overlapping sphincteroplasty. However, despite restoration of the anatomy, only 65 percent of patients are fully continent. PURPOSE: This study was undertaken to determine if postoperative biofeedback improved continence in patients with poor functional outcomes after sphincteroplasty. METHOD: Outcomes of 28 patients who underwent electromyographic biofeedback training after sphincteroplasty for obstetric sphincter injury were reviewed. Nine patients had an accompanying levatorplasty. Average age was 34 (range, 23-57) years. Patients began biofeedback a mean of 32 (range, 2-192) months postoperatively. Before beginning biofeedback, patients completed an incontinence questionnaire, bowel diary, and scored their incontinence. At the end of treatment, they were again asked to score their incontinence and rate their improvement. Using an incontinence scale with a maximum score of 30, the average incontinence score before biofeedback was 20 (range, 13-30). Incontinent episodes per week ranged from one to nine. Sixteen patients were incontinent to solid stool. RESULTS: Overall, the average posttreatment incontinence score decreased from 20 to 3 (P < 0.0001). Average number of incontinent episodes per week decreased from 5.4 to 1.4 (P < 0.0001) Twenty-five patients (89 percent) reported improvement in their continence. All had a posttreatment incontinent score of less than three. Three patients noted no improvement. Of those, one subsequently had a colostomy, one is waiting the implant of an artificial anal sphincter, and one has sought no further treatment. There were no complications reported. CONCLUSION: Biofeedback improves functional outcome after sphincteroplasty and is a reasonable option for patients with less than optimum outcome after sphincteroplasty.

Role of paraventricular nucleus in control of blood pressure and drinking in rats.

The present investigation examined the abilities of angiotensin (ANG) II and III to produce increases in blood pressure and drinking when microinfused into the paraventricular nucleus (PVN) of the hypothalamus of the Sprague-Dawley rat. Dose-dependent elevations in systemic blood pressure and heart rate were measured to both ANG II and III in the anesthetized rat, with ANG II more potent than ANG III at the two highest doses examined. Pretreatment with the specific ANG receptor antagonist [Sar1,Thr8]ANG II (sarthran), blocked subsequent ANG II- and III-induced elevations in blood pressure, suggesting that these responses were dependent on the activation of ANG receptors. A similar analysis in awake rats yielded nearly equivalent results. A final experiment demonstrated that microinfusions of ANG II and III into the PVN produced drinking in a dose-dependent manner, with greater consumption to ANG II than ANG III. Again, sarthran was found to block the dipsogenic response. Histological examination revealed that the location of the injection site was linked to the character of the ANG-dependent response. These data suggest that the PVN may play a critical role in mediating central ANG effects on body water homeostasis and blood pressure regulation. Furthermore, it appears that subnuclei of the PVN may participate differentially in ANG-mediated actions.

Evaluation of an air-filled microballoon and mini-transducer in the clinical practice of anorectal manometry. Preliminary communication.

Anorectal manometry is becoming a commonly applied investigation in the field of colon and rectal surgery. Until now, however, most of this testing was performed in specialized units, which involved considerable expense and expertise to run. The authors assessed a commercially available mini-transducer and an air-filled microballoon catheter for their applicability to clinical anorectal manometry. This system is very accurate and is proving very useful in the ambulatory setting, on hospital wards, and in the operating room. It provides a simple alternative for areas where more sophisticated manometric systems are not available.

Artificial anal sphincter.

PURPOSE: This study was undertaken to evaluate the use of a fully implanted artificial anal sphincter for management of severe fecal incontinence. METHODS: An artificial anal sphincter was implanted in 12 patients who failed conventional management for severe fecal incontinence. Careful patient follow-up was recorded during a mean 58-month follow-up. Patients underwent preoperative and postoperative manometric assessment. Functional and patient satisfaction evaluations were obtained by mailed questionnaire. RESULTS: Three infections and three mechanical complications occurred in four patients (33 percent). A successful outcome was achieved in nine patients (75 percent). Postoperative manometric studies documented establishment of an elevated high-pressure zone compared with preoperative resting pressures. Seven patients returned a detailed functional assessment and patient satisfaction questionnaire at a mean of 40 months postsphincter activation. All seven patients reported continence to solid stool. Two patients had some problems with control of liquid stool, and three had occasional incontinence to flatus. Six of the seven patients rated their bowel control as good to excellent. All seven respondents were satisfied with their functional improvement. CONCLUSIONS: Early experience with an artificial anal sphincter has demonstrated that continence can be restored with acceptable morbidity in patients with severe fecal incontinence.

Neurogenic heterotopic ossification.

Neurogenic heterotopic ossification is a potential sequela of neurological disorders, especially spinal cord injury and head injury. The etiology is unknown. Clinical, radiologic, and bone scan findings are typical. Complications may threaten function. The differential diagnosis is crucial in its early stages. Treatment options include diphosphonates, non-steroidal anti-inflammatory drugs, and surgery. This article has reviewed the literature on neurogenic heterotopic ossification (HO), soft tissue ossification of neurologic disease, including pathogenesis, histology, presentation, diagnosis, natural history, complications, and current treatments.

Balloon topography. A simple method of evaluating anal function.

Balloon topography was developed to simultaneously measure anal canal pressure, anal canal length, and anorectal angle. It is performed using a cylindrical flexible balloon placed into the anal canal and rectum and filled with liquid radiopaque contrast dye under low pressure. The pressure of the dye inside the balloon is controlled by the investigator, and does not vary with changes in balloon volume. The shape of the balloon within the anal canal is recorded using fluoroscopy and plain radiopaques. The patient receives less radiation than he would receive during a single contrast barium enema. We have performed the test on 27 subjects including a normal control, rectal prolapse patients, and incontinent patients. Early results demonstrate the usefulness of the test in examining anal sphincter and pelvic floor function in maintaining fecal continence in health and disease. The test measures multiple aspects of anopelvic function simultaneously that previously required separate investigations.