Opioid Utilization and Perception of Pain Control in Hospitalized Patients: A Cross-Sectional Study of 11 Sites in 8 Countries.

BACKGROUND: Hospitalized patients are frequently treated with opioids for pain control, and receipt of opioids at hospital discharge may increase the risk of future chronic opioid use. OBJECTIVE: To compare inpatient analgesic prescribing patterns and patients' perception of pain control in the United States and non-US hospitals. DESIGN: Cross-sectional observational study. SETTING: Four hospitals in the US and seven in seven other countries. PARTICIPANTS: Medical inpatients reporting pain. MEASUREMENTS: Opioid analgesics dispensed during the first 24-36 hours of hospitalization and at discharge; assessments and beliefs about pain. RESULTS: We acquired completed surveys for 981 patients, 503 of 719 patients in the US and 478 of 590 patients in other countries. After adjusting for confounding factors, we found that more US patients were given opioids during their hospitalization compared with patients in other countries, regardless of whether they did or did not report taking opioids prior to admission (92% vs 70% and 71% vs 41%, respectively; P < .05), and similar trends were seen for opioids prescribed at discharge. Patient satisfaction, beliefs, and expectations about pain control differed between patients in the US and other sites. LIMITATIONS: Limited number of sites and patients/country. CONCLUSIONS: In the hospitals we sampled, our data suggest that physicians in the US may prescribe opioids more frequently during patients' hospitalizations and at discharge than their colleagues in other countries, and patients have different beliefs and expectations about pain control. Efforts to curb the opioid epidemic likely need to include addressing inpatient analgesic prescribing practices and patients' expectations regarding pain control.

Where is this all leading?

The Future Hospital Commission acknowledges that the principal challenge for healthcare organisations and professionals is to accept the fundamental requirement that patients must be treated with compassion, kindness and respect while having their physical and emotional needs met at all times. The recognition that clinical outcomes alone are an insufficient guide to the adequacy of health service provision demands cultural, organisational and individual change. In the Future Hospital Forum we scan the world literature for papers on systems of care that might best ensure these principles are delivered, and to critically evaluate their potential impact. The theme in this edition is leadership.

Variation in iron homeostasis genes between patients with ARDS and healthy control subjects.

BACKGROUND: Abnormal plasma and lung iron mobilization is associated with the onset and progression of ARDS and is detectable in specific at-risk populations. Patients with ARDS also have pronounced oxidative and nitrosative stress that can be catalyzed and thereby aggravated by the bioavailability of redox active iron. ARDS of pulmonary and extrapulmonary origin may differ pathophysiologically and require different ventilatory strategies. Evidence suggests that genetic predisposition is relevant to the pathogenesis of ARDS. We therefore explored the hypothesis that polymorphisms from a panel of genes encoding iron-metabolizing proteins determine susceptibility to ARDS. METHODS: Retrospective case-control study conducted at the adult ICUs of two university hospitals. Patients with ARDS (n = 122) and healthy control subjects (n = 193) were genotyped. Sequence-specific primer polymerase chain reaction was used to genotype selected biallelic single-nucleotide polymorphisms. An audit of the patient database was conducted, and 104 of the 122 ARDS patients were eligible for the final data analysis. RESULTS: Preliminary analysis indicated differences between ARDS and healthy control subjects in the incidence of polymorphism of the gene encoding ferritin light chain. Subgroup analysis indicated the prevalence of ferritin light-chain gene -3381GG homozygotes was increased in patients with ARDS of extrapulmonary origin compared to healthy control subjects. Secondly, a common haplotype in the heme oxygenase 2 gene was reduced in patients with ARDS compared to healthy control subjects and was more evident in those with ARDS of direct or pulmonary etiology. CONCLUSIONS: These results provide preliminary evidence to suggest a distinction in the genetic background of the subpopulations studied, inferring that the ferritin light-chain gene genotype confers susceptibility to ARDS, while the heme oxygenase 2 haplotype is protective against the onset of the syndrome. Such data support further previous findings that suggest abnormalities in iron handling resulting in redox imbalance are implicated in the pathogenesis of ARDS.

Pathogenesis of the systemic inflammatory syndrome and acute lung injury: role of iron mobilization and decompartmentalization.

Changes in iron homeostatic responses routinely accompany infectious or proinflammatory insults. The systemic inflammatory response syndrome (SIRS) and the development of acute lung injury (ALI) feature pronounced systemic and lung-specific alterations in iron/heme mobilization and decompartmentalization; such responses may be of pathological significance for both the onset and progression of acute inflammation. The potential for excessive iron-catalyzed oxidative stress, altered proinflammatory redox signaling, and provision of iron as a microbial growth factor represent obvious adverse aspects of altered in vivo iron handling. The release of hemoglobin during hemolytic disease or surgical procedures such as those utilizing cardiopulmonary bypass procedures further impacts on iron mobilization, turnover, and storage with associated implications. Genetic predisposition may ultimately determine the extent to which SIRS and related syndromes develop in response to such changes. The design of specific therapeutic interventions based on endogenous stratagems to limit adverse aspects of altered iron handling may prove of therapeutic benefit for the treatment of SIRS and ALI.

Arterial carboxyhemoglobin level and outcome in critically ill patients.

OBJECTIVE: Arterial carboxyhemoglobin is elevated in patients with critical illness. It is an indicator of the endogenous production of carbon monoxide by the enzyme heme oxygenase, which modulates the response to oxidant stress. The objective was to explore the hypothesis that arterial carboxyhemoglobin level is associated with inflammation and survival in patients requiring cardiothoracic intensive care. DESIGN: Prospective, observational study. SETTING: A cardiothoracic intensive care unit. PATIENTS: All patients admitted over a 15-month period. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Arterial carboxyhemoglobin, bilirubin, and standard biochemical, hematologic, and physiologic markers of inflammation were measured in 1,267 patients. Associations were sought between levels of arterial carboxyhemoglobin, markers of the inflammatory response, and clinical outcome. Intensive care unit mortality was associated with lower minimum and greater maximal carboxyhemoglobin levels (p < .0001 and p < .001, respectively). After adjustment for age, gender, illness severity, and other relevant variables, a lower minimum arterial carboxyhemoglobin was associated with an increased risk of death from all causes (odds risk of death, 0.391; 95% confidence interval, 0.190-0.807; p = .011). Arterial carboxyhemoglobin correlated with markers of the inflammatory response. CONCLUSIONS: Both low minimum and high maximum levels of arterial carboxyhemoglobin were associated with increased intensive care mortality. Although the heme oxygenase system is protective, excessive induction may be deleterious. This suggests that there may be an optimal range for heme oxygenase-1 induction.

Incidence, duration and causes of intensive care unit admission following pulmonary resection for malignancy.

BACKGROUND: We assessed the overall incidence and duration of ICU admission following pulmonary resection and attempted to identify patients requiring prolonged ICU stay. METHODS: Analysis of prospectively collected data on all patients undergoing pulmonary resection for suspected malignant disease that subsequently required ICU admission between March 2002 and October 2003. RESULTS: Of 170 patients 52 (30%) needed intensive care post-operatively: 21 (12%) for less than 24 h and 31 (18%) for more, for which group the average length of stay was 11.3 days. There was no significant difference between the patient groups at ICU admission in terms of median APACHE II scores (12 vs. 14), gas exchange (PaO2/FIO2, 441 vs. 364 mmHg), estimated post-operative absolute FEV1 (1.62 vs. 1.31 l) or predicted percentage FEV1 (61.8% vs. 44.3%). Mean ICU cost was 1,838 sterling pounds vs. 25,974 sterling pounds per admission, respectively. CONCLUSIONS: Following pulmonary resection some 18% of patients need a protracted ICU stay at considerable cost. Neither severity of illness scoring, indices of gas exchange at ICU admission, nor predicted post-operative FEV1 identifies such patients.

Redox regulation of neutrophil apoptosis and the systemic inflammatory response syndrome.

SIRS (systemic inflammatory response syndrome) may result from a wide variety of non-infective insults. Surgery is a recognized cause of SIRS, the onset of which can have adverse prognostic significance. Neutrophil activation is a key histopathological feature of SIRS, and neutrophil clearance through programmed cell death or apoptosis is an essential step in its resolution. Increasingly, it is recognized that ROS (reactive oxygen species), such as those generated by activated neutrophils during cardiac surgery, may have a regulatory role, influencing neutrophil lifespan and thus inflammation. In this review, we discuss the continuing importance of SIRS as a herald of inflammation and the role of neutrophil longevity in the resolution of inflammation, and we consider recent evidence for the regulation of neutrophil apoptosis by ROS.