Use of medical emergency team responses to reduce hospital cardiopulmonary arrests.

BACKGROUND: Medical emergency team (MET) responses have been implemented to reduce inpatient mortality, but data on their efficacy are sparse and there have been no reports to date from US hospitals. OBJECTIVES: To determine how the incidence and outcomes of cardiac arrests have changed following increased use of MET. METHODS: Objective criteria for MET activation were created and disseminated as part of a crisis management program, after which there was a rapid and sustained increase in the use of MET. A retrospective analysis of clinical outcomes was performed to compare the incidence and mortality of cardiopulmonary arrest before and after the increased use of MET. RESULTS: A retrospective analysis of 3269 MET responses and 1220 cardiopulmonary arrests over 6.8 years showed an increase in MET responses from 13.7 to 25.8 per 1000 admissions (p<0.0001) after instituting objective activation criteria. There was a coincident 17% decrease in the incidence of cardiopulmonary arrests from 6.5 to 5.4 per 1000 admissions (p = 0.016). The proportion of fatal arrests was similar before and after the increase in use of MET. CONCLUSIONS: Increased use of MET may be associated with fewer cardiopulmonary arrests.

Use of medical emergency team (MET) responses to detect medical errors.

BACKGROUND: No previous studies have investigated whether medical emergency team (MET) responses can be used to detect medical errors. OBJECTIVES: To determine whether review of MET responses can be used as a surveillance method for detecting medical errors. METHODS: Charts of all patients receiving MET responses during an 8 month period were reviewed by a hospital based Quality Improvement Committee to establish if the clinical deterioration that prompted the MET response was associated with a medical error (defined as an adverse event that was preventable with the current state of medical knowledge). Medical errors were categorized as diagnostic, treatment, or preventive errors using a descriptive typology based on previous published reports. RESULTS: Three hundred and sixty four consecutive MET responses underwent chart review and 114 (31.3%) were associated with medical errors: 77 (67.5%) were categorized as diagnostic errors, 68 (59.6%) as treatment errors, and 30 (26.3%) as prevention errors. Eighteen separate hospital care processes were identified and modified as a result of this review, 10 of which involved standardization. CONCLUSIONS: MET review may be used for surveillance to detect medical errors and to identify and modify processes of care that underlie those errors.

Apoptosis in sepsis.

Sepsis demonstrates a marked dysregulation of the immune system in its ability to fight infection. Previous models have focused on the mechanisms which upregulate and sustain the heightened immune response without addressing the role of down-regulation effectors. Attention has been drawn to these down-regulating mechanisms and their precise role in the pathophysiology of sepsis. Apoptosis is an evolutionarily conserved, energy-dependent mode of cell death requiring the initiation and regulation of complex genetic programs. It is the body's main method of getting rid of cells which are in excess, damaged, or no longer needed in a controlled manner. The role of this cellular phenomenon in physiology and pathophysiology has been the subject of intense scrutiny over the last decade. Much work has demonstrated that dysregulation of apoptosis does occur in immune and nonimmune cells in in vitro and in vivo models of sepsis. The difficulty has been in tying the phenomenology of apoptosis into the pathophysiology of sepsis. Further work is needed to make these connections to elucidate rational approaches for clinical applications of immunomodulation in sepsis.

The role of caspase-8 in resistance to cancer chemotherapy.

Toxicity of chemotherapeutic agents against cancer cells is mediated through the initiation of programmed cell death. Apoptosis is an evolutionarily conserved cascade of intracellular proteolytic events propagated by a family of cysteine proteases called caspases. Many receptor- and non-receptor-mediated death signals induce apoptosis via activation of caspase-8 (FLICE/MACH). Mechanisms of tumor resistance to cytotoxic drugs through decreased apoptosis may occur by altered expression of caspase-8, upregulation of caspase-8 inhibitors like FLIP (FLICE-like Inhibitory Protein), or sequestration of caspase-8 by Bcl-2. Modulation of caspase-8 and apoptosis may be a therapeutic strategy for sensitization of drug-resistant malignancies to radiation or combination chemotherapy.