Perception of Patient Safety Culture among Health-care Providers in a Tertiary Care Hospital, South India.

Introduction: Patient safety is a global concern and is the most important domains of health-care quality. Medical error is a major patient safety concern, causing increase in health-care cost due to mortality, morbidity, or prolonged hospital stay.

Aim: The aim of the study was to assess the perceptions on patient safety culture among health-care providers (HCPs) at a public sector tertiary care hospital in South India.

A validated value-based model to improve hospital-wide perioperative outcomes: adaptability to combined medical/surgical inpatient cohorts.

Objectives: Authors hypothesized that building safe hospital systems to improve value-based surgical outcomes is predicated on workflow redesign for dynamic risk stratification, coupled with "real-time" mitigation of risk. We developed a comanagement model for hospitalized surgical cohort, and determined whether this iterative process redesign for surgery will be adaptable to disparate hospital systems and will be beneficial for combined medical/surgical adult inpatients.

Context: Concerns about preventable harm in hospitalized patients have generated a plethora of both, process-driven and outcome-based strategies in US Healthcare.

Milk fat globule epidermal growth factor 8 attenuates acute lung injury in mice after intestinal ischemia and reperfusion.

Rationale: Milk fat globule epidermal growth factor 8 (MFG-E8) is a potent opsonin for the clearance of apoptotic cells and is produced by mononuclear cells of immune competent organs including the spleen and lungs. It attenuates chronic and acute inflammation such as autoimmune glomerulonephritis and bacterial sepsis by enhancing apoptotic cell clearance. Ischemia-reperfusion (I/R) injury of the gut results in severe inflammation, apoptosis, and remote organ damage, including acute lung injury (ALI).

Immature dendritic cell-derived exosomes rescue septic animals via milk fat globule epidermal growth factor-factor VIII [corrected].

Sepsis, a highly lethal systemic inflammatory syndrome, is associated with increases of proinflammatory cytokines (e.g., TNF-alpha, HMGB1) and the accumulation of apoptotic cells that have the potential to be detrimental.

Human ghrelin ameliorates organ injury and improves survival after radiation injury combined with severe sepsis.

In the terrorist radiation exposure scenario, radiation victims are likely to suffer from additional injuries such as sepsis. Our previous studies have shown that ghrelin is protective in sepsis. However, it remains unknown whether ghrelin ameliorates sepsis-induced organ injury and mortality after radiation exposure.

Ghrelin hyporesponsiveness contributes to age-related hyperinflammation in septic shock.

Objective: To test the hypothesis that hyporesponsiveness to ghrelin due to reduced growth hormone (GH) contributes to the aging-related hyperinflammatory state in sepsis.

Summary Background Data: Sepsis and septic shock are a serious problem, particularly in the geriatric population. Ghrelin is an endogenous ligand for the GH secretagogue receptor 1a (GHSR1a, ie, ghrelin receptor).

Orexigenic hormone ghrelin ameliorates gut barrier dysfunction in sepsis in rats.

Objectives: We have recently shown that ghrelin, a novel orexigenic hormone, is reduced in sepsis. Ghrelin treatment, mediated through ghrelin receptors in the brain, attenuates sepsis-induced inflammation and mortality. Gut barrier dysfunction is common in sepsis.

Pivotal role of the alpha(2A)-adrenoceptor in producing inflammation and organ injury in a rat model of sepsis.

Background: Norepinephrine (NE) modulates the responsiveness of macrophages to proinflammatory stimuli through the activation of adrenergic receptors (ARs). Being part of the stress response, early increases of NE in sepsis sustain adverse systemic inflammatory responses. The intestine is an important source of NE release in the early stage of cecal ligation and puncture (CLP)-induced sepsis in rats, which then stimulates TNF-alpha production in Kupffer cells (KCs) through the activation of the alpha(2)-AR.

Human adrenomedullin and its binding protein attenuate organ injury and reduce mortality after hepatic ischemia-reperfusion.

Objective: To determine whether administration of a vasoactive peptide, human adrenomedullin (AM), in combination with its binding protein (ie, AMBP-1), prevents or minimizes hepatic ischemia-reperfusion (I/R) injury.

Summary Background Data: Hepatic I/R injury results from tissue hypoxia and subsequent inflammatory responses. Even though numerous pharmacological modalities and substances have been studied to reduce I/R-induced mortality, none have been entirely successful.

Maturation-induced down-regulation of MFG-E8 impairs apoptotic cell clearance and enhances endotoxin response.

In sepsis, phagocytosis and the killing of bacteria by phagocytes are important. Similarly, the clearance of accumulating apoptotic cells is critical in maintaining normal immunity. Upon maturation, peritoneal macrophages (PM) become a major source of proinflammatory cytokines, while losing their efficacy of phagocytosis.

Reversing established sepsis in rats with human vasoactive hormone adrenomedullin and its binding protein.

We recently demonstrated that early administration of rat adrenomedullin (AM), a vasoactive peptide, in combination with its binding protein (human AMBP-1) produces various beneficial effects in sepsis. Human AM is a 52-amino acid peptide, but rat AM differs from human AM, having only 50 amino acid residues, with two amino acid deletions and six substitutions. It remains unknown whether a combination of human AM and human AMBP-1 (AM/AMBP-1) is also beneficial in sepsis and, if so, whether human AM/AMBP-1 reverses established sepsis in rats.

Gut hyperpermiability after ischemia and reperfusion: attenuation with adrenomedullin and its binding protein treatment.

Ischemia bowel remains a critical problem resulting in up to 80% mortality. The loss of gut barrier function plays an important role. Our previous studies have shown that administration of adrenomedullin (AM), a novel vasoactive peptide, and its binding protein (AMBP-1), reduces the systemic inflammatory response and organ injury after systemic ischemia induced by hemorrhagic shock.

Orexigenic hormone ghrelin attenuates local and remote organ injury after intestinal ischemia-reperfusion.

Background: Gut ischemia/reperfusion (I/R) injury is a serious condition in intensive care patients. Activation of immune cells adjacent to the huge endothelial cell surface area of the intestinal microvasculature produces initially local and then systemic inflammatory responses. Stimulation of the vagus nerve can rapidly attenuate systemic inflammatory responses through inhibiting the activation of macrophages and endothelial cells.

Human vasoactive hormone adrenomedullin and its binding protein rescue experimental animals from shock.

We recently discovered that vascular responsiveness to adrenomedullin (AM), a vasoactive hormone, decreases after hemorrhage, which is markedly improved by the addition of its binding protein AMBP-1. One obstacle hampering the development of AM/AMBP-1 as resuscitation agents in trauma victims is the potential immunogenicity of rat proteins in humans. Although less potent than rat AM, human AM has been shown to increase organ perfusion in rats.

Fate of retained capsule: a pathognomonic for surgery.

Since its introduction in 2001, Wireless Video Capsule enteroscopy is gaining acceptance due to its high diagnostic potential and minimal risk. In some centers, it offers an alternative approach to visualize the small intestine and to evaluate patients with suspected small bowel disease. We present a series of known complications of this procedure and call for a more proactive role in the management of retained capsule.

Vasoactive hormone adrenomedullin and its binding protein: anti-inflammatory effects by up-regulating peroxisome proliferator-activated receptor-gamma.

Sepsis is a critical inflammatory condition from which numerous patients die due to multiple organ failure and septic shock. The vasoactive hormone adrenomedullin (AM) and its binding protein (AMBP-1) are beneficial in sepsis by abrogating the progression to irreversible shock and decreasing proinflammatory cytokine release. To investigate the anti-inflammatory mechanism, we studied to determine the effect of the AM/AMBP-1 complex on peroxisome proliferator-activated receptor-gamma (PPAR-gamma) expression and activation by using RAW264.

Ghrelin inhibits sympathetic nervous activity in sepsis.

Our previous studies have shown that norepinephrine (NE) upregulates proinflammatory cytokines by activating alpha(2)-adrenoceptor. Therefore, modulation of the sympathetic nervous system represents a novel treatment for sepsis. We have also shown that a novel stomach-derived peptide, ghrelin, is downregulated in sepsis and that its intravenous administration decreases proinflammatory cytokines and mitigates organ injury.

Fractalkine-induced MFG-E8 leads to enhanced apoptotic cell clearance by macrophages.

Clearance of apoptotic cells is crucial to maintain cellular function under normal and pathological conditions. We have recently shown that administration of immature dendritic cell-derived exosomes to septic animals promotes phagocytosis of apoptotic cells and improves survival by providing milk fat globule epidermal growth factor-factor VIII (MFG-E8). MFG-E8 acts as an opsonin for apoptotic cells to be engulfed by phagocytosis.

Adrenomedullin and adrenomedullin binding protein-1 prevent acute lung injury after gut ischemia-reperfusion.

Background: Ischemic bowel remains a critical problem, resulting in up to 80% mortality. Acute lung injury, a common complication after intestinal ischemia/reperfusion (I/R), might be responsible for such a high mortality rate. Our previous studies have shown that administration of a novel vasoactive peptide adrenomedullin (AM) and its binding protein (AMBP-1) reduces the systemic inflammatory response in rat models of both hemorrhage and sepsis.

Ghrelin attenuates sepsis-induced acute lung injury and mortality in rats.

Rationale: Our study has shown that plasma levels of ghrelin, a stomach-derived peptide, are significantly reduced in sepsis, and that ghrelin administration improves organ blood flow via a nuclear factor (NF)-kappaB-dependent pathway. However, it remains unknown whether ghrelin has any protective effects on severe sepsis-induced acute lung injury (ALI) and, if so, whether inhibition of NF-kappaB plays any role in it.

Objectives: To test the hypothesis that ghrelin reduces severe sepsis-induced ALI and mortality through inhibition of NF-kappaB.

Pro-inflammatory cytokines from Kupffer cells downregulate hepatocyte expression of adrenomedullin binding protein-1.

Polymicrobial sepsis is characterized by an early, hyperdynamic phase followed by a late hypodynamic phase. Adrenomedullin (AM), a vasodilatory peptide, inhibits this transition from the early phase to the late phase. Adrenomedullin binding protein-1 (AMBP-1) enhances AM-mediated activities.

Ghrelin down-regulates proinflammatory cytokines in sepsis through activation of the vagus nerve.

Objective: To test the hypothesis that administration of ghrelin attenuates inflammatory responses in sepsis through vagal nerve stimulation.

Summary Background Data: Ghrelin has been demonstrated to possess multiple functions, including stimulation of the vagus nerve. Our recent study has shown that plasma levels of ghrelin were significantly reduced in sepsis; and ghrelin administration improved organ perfusion and function.

Adrenomedullin and adrenomedullin binding protein-1 prevent metabolic acidosis after uncontrolled hemorrhage in rats.

Objective: Management of trauma victims with uncontrolled hemorrhage remains a major problem in combat casualty care at the far-forward battlefield setting. The neuroendocrine response to hemorrhage is to maintain perfusion to the heart and brain, often at the expense of other organ systems. Decreased organ perfusion after hemorrhagic shock is associated with metabolic acidosis, in which the up-regulated endothelin-1 plays an important role.

Downregulation of hepatic cytochrome P-450 isoforms and PPAR-gamma: their role in hepatic injury and proinflammatory responses in a double-hit model of hemorrhage and sepsis.

Background: The "double-hit" model of hemorrhage and sepsis mimics the critically ill patient admitted to the surgical intensive care unit. Although the protein expression of a cytochrome (CYP) P-450 isoform CYP1A2 is reduced in the late stage of sepsis, the effect of hemorrhage on CYP isoforms and the anti-inflammatory nuclear receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma) has not been investigated. We hypothesized that hemorrhage down-regulates CYP isoforms and PPAR-gamma in the liver, which plays an important role in producing tissue injury and proinflammatory responses after the subsequent sepsis (i.

Combination tramadol plus acetaminophen for postsurgical pain.

Background: This multicenter, randomized, double-blind, active- and placebo-controlled trial evaluated tramadol plus acetaminophen (APAP) for orthopedic (n = 153) and abdominal (n = 152) postsurgical pain.

Methods: Patients with moderate pain or greater were randomized to an initial two tablets of 37.5 mg tramadol plus 325 mg APAP (n = 98), codeine 30 mg plus APAP 300 mg (n = 109), or placebo (n = 98); thereafter, they received 1 to 2 tablets every 4 to 6 hours as needed for pain for 6 days.