Implementation and maintenance of a pain management quality assurance program at intensive care units: 360 degree feedback of physicians, nurses and patients.

BACKGROUND: Pain management quality assurance programs (PMQP) have been successfully implemented in numerous hospitals across Europe. We aimed to evaluate the medium-term sustainability of a PMQP implemented at intensive care units (ICUs). METHODS: Two surveys, the first in 2012, immediately after introduction of the PMQP, and the second in 2015, were carried out amongst patients, physicians and nurses. Demographic parameters of all participants were assessed. Patients were asked after their pain levels during ICU stay. Staff members answered a questionnaire regarding familiarity with standards and processes of PMQP and self-perception of their knowledge as well as contentment with interdisciplinary communication. RESULTS: In total (2012/2015), 267 (125/142) patients, 113 (65/48) physicians and 510 (264/246) members of the nursing staff participated. Minimum and maximum pain levels of patients did not differ between both surveys. Patients' tolerance of pain 24 hours before the survey was better (p = 0.023), and vomiting occurred less often (p = 0.037) in 2015. Physicians' and nurses' contentment with the own knowledge about pharmacological pain treatment had increased from 2012 to 2015 (p = 0.002 and 0.004). Satisfaction with communication between nurses and physicians was better in 2015 (p<0.001 and p = 0.002). Familiarity with PMQP standards and processes remained stable in both collectives. CONCLUSION: The implementation of our PMQP achieved a high standard of care, guarantying a high patient and staff member satisfaction. Continuous education, ongoing training, regular updates and implementation of feedback-loops ensure continuity, in some parameters even an increase in knowledge and competencies. This is mirrored in high patient and staff member satisfaction.

Standardized concept for the treatment of gastrointestinal dysmotility in critically ill patients--current status and future options.

Inhibition of gastrointestinal motility is a major problem in critically ill patients. Motor stasis gives rise to subsequent complications including intolerance to enteral feeding, enhanced permeability of the atrophic intestinal mucosa and conditions as severe as systemic inflammatory response syndrome, sepsis and multiple organ failure. Although the diagnosis of motility disturbances in critically ill patients is difficult, the type and site of the disturbance are important to consider in the analysis of the condition and in the choice of therapeutic approach. The pharmacological treatment of impaired gastrointestinal motility is difficult to handle for the clinician, because the underlying mechanisms are complex and not fully understood and the availability of pharmacological treatment options is limited. In addition, there is a lack of controlled studies on which to build an evidence-based treatment concept for critically ill patients. Notwithstanding this situation, there has been remarkable progress in the understanding of the integrated regulation of gastrointestinal motility in health and disease. These advances, which largely relate to the organization of the enteric nervous system and its signaling mechanisms, enable the intensivist to develop a standardized concept for the use of prokinetic agents in the treatment of impaired gastrointestinal motility in critically ill patients.

The enantiomers of tramadol and its major metabolite inhibit peristalsis in the guinea pig small intestine via differential mechanisms.

BACKGROUND: Inhibition of intestinal peristalsis is a major side effect of opioid analgesics. Although tramadol is an opioid-like analgesic, its effect on gut motility is little known. Therefore, the effect of (+)-tramadol, (-)-tramadol and the major metabolite O-desmethyltramadol on intestinal peristalsis in vitro and their mechanisms of action were examined. Distension-induced peristalsis was recorded in fluid-perfused segments of the guinea pig small intestine. The intraluminal peristaltic pressure threshold (PPT) was used to quantify the motor effects of extraserosally administered drugs. RESULTS: Racemic tramadol, its (+)- and (-)-enantiomers and the major metabolite O-desmethyltramadol (0.1-100 microM) concentration-dependently increased PPT until peristalsis was transiently or persistently abolished. The rank order of potency was (-)-tramadol < (+)-tramadol

Peristalsis in the Guinea pig small intestine in vitro is impaired by acetaminophen but not aspirin and dipyrone.

Inhibition of intestinal peristalsis is a major side effect of opioid analgesics. It is unknown whether non-opioid analgesics, such as acetaminophen, acetylsalicylic acid, and dipyrone, exert any effect on intestinal motility. In the current in vitro study we examined the effect of these analgesics on intestinal peristalsis and analyzed some of their mechanisms of action. In isolated segments of the guinea pig small intestine peristalsis was triggered by a perfusion-induced increase of the intraluminal pressure. The peristaltic pressure threshold (PPT) at which peristaltic waves were elicited was used to quantify drug effects on peristalsis. Vehicle (Tyrode's solution), acetaminophen (0.01-100 microM), acetylsalicylic acid (100-300 microM), and dipyrone (10-100 microM) were added extraserosally to the organ bath. Acetaminophen concentration-dependently increased PPT and abolished peristalsis in four of six segments at the concentration of 10 microM and in all segments tested at 100 microM (EC50=6.0 microM). The increase in PPT resulting from 3 microM acetaminophen was reduced by naloxone and apamin but not changed by L-nitro-arginine methylester (L-NAME), its inactive enantiomer D-NAME, acetylsalicylic acid, methysergide, or tropisetron. Acetylsalicylic acid and dipyrone did not affect peristalsis. The results reveal, for the first time, that acetaminophen concentration-dependently impairs intestinal peristalsis, whereas acetylsalicylic acid and dipyrone lacked such an effect. The inhibition caused by acetaminophen involves transmitters acting via small conductance Ca2+-activated potassium channels, endogenous opioidergic pathways, and presumably inhibition of cyclooxygenase-3.

Clonidine and dexmedetomidine potently inhibit peristalsis in the Guinea pig ileum in vitro.

BACKGROUND: Inhibition of intestinal peristalsis is a major side effect of drugs used for anesthesia or for analgesia and sedation of patients in the intensive care unit. This in vitro study examined the effect of clonidine and dexmedetomidine on intestinal peristalsis and analyzed some of their mechanisms of action. METHODS: In isolated segments of the guinea pig small intestine, peristalsis was triggered by a perfusion-induced rise of the intraluminal pressure. The peristaltic pressure threshold to elicit a peristaltic wave was used to quantify drug effects on peristalsis. Vehicle (Tyrode's solution), clonidine (10 nM-100 microm), or dexmedetomidine (0.1-100 nM) were added extraserosally to the organ bath. In other series of experiments, clonidine or dexmedetomidine was administered after pretreatment with yohimbine, prazosin, apamin, naloxone, or vehicle. Clonidine was also tested after blockade of NO synthase with L-NAME and in the presence of the inactive enantiomer D-NAME. RESULTS: Clonidine and dexmedetomidine concentration-dependently increased peristaltic pressure threshold and inhibited peristalsis (clonidine: EC50 = 19.6 microm; dexmedetomidine: EC50 = 12.0 nM). The inhibition caused by clonidine could be prevented by pretreatment with yohimbine, naloxone, and apamin, but not by prazosin, L-NAME, or D-NAME. Inhibition caused by dexmedetomidine was prevented by yohimbine only.(50) (50) CONCLUSIONS: The results reveal that clonidine and, much more potently, dexmedetomidine inhibit peristalsis of the guinea pig ileum. The inhibition is caused by interaction with alpha2 adrenoceptors and, in the case of clonidine, also involves activation of small conductance Ca2+ -activated potassium channels and endogenous opioidergic pathways.