Multiple organ dysfunction syndrome pathogenesis and care: a complex systems' theory perspective.

AIMS AND OBJECTIVES: To discuss multiple organ dysfunction syndrome (MODS) from a complex systems' theory perspective and to delineate a conceptual framework for the development and care of MODS. BACKGROUND: MODS is an intricate and devastating manifestation of critical illness characterized by widespread aberrant molecular, cellular and systemic responses. DESIGN AND METHODS: Narrative literature review (MEDLINE, CINAHL databases) and knowledge synthesis with the theoretical assertions of chaos and complex systems' theory. Cellular and systemic response paradoxes in MODS (including cellular hypoxia, cell death and signalling) are reviewed. RESULTS: The diseased person is depicted as a complex adaptive system. The relevancy of some of the principles of complex chaotic systems' theory to the proposed model is illustrated, including sensitive dependence on initial conditions, emergence, attractors, self-organization, self-organized criticality and emerging order. The transition from life-supporting to death-related organismic responses is illustrated as a critical event in MODS and care implications are drawn. CONCLUSIONS: Patient responses in MODS appear to conform to the principles of chaotic systems. Death is illustrated not as a consequence of homeostatic failure but as a 'deliberate' self-organized phenomenon entailing multiple dynamically evolving mechanisms. RELEVANCE TO CLINICAL PRACTICE: Some of the principles of chaotic complex systems may need to be taken into account to advance care in MODS. An alternative theoretical perspective may support nurses to conceptualize both MODS and their role in a way that will help them to cope better with this devastating syndrome and develop practice.

Association between subjective descriptors of coronary pain and disease characteristics: a pilot study in a Hellenic rural population.

PURPOSE: We explored whether the way Hellenic patients describe their cardiac chest pain (verbal descriptions of the nature, intensity, temporal quality, location and radiation) associates with the diagnosis [acute myocardial infarction (AMI) versus unstable angina (UA)] as well as with the location of the coronary lesions. METHODS: A cross-sectional correlational design was employed to study 80 consecutive coronary care patients (44 with AMI, 36 with UA) from northwestern Hellas. RESULTS: Pain intensity did not differ significantly between AMI and UA, in contrast to treatment-seeking behaviour and accompanying symptoms (p< or =0.03). Of AMI patients, women used more often the word "pain" (p=0.011), and indicated pain at the left shoulder (p=0.004). AMI patients used fewer words (p=0.03), and experienced pain at the back of the neck (p=0.03) and of the left arm (p=0.02) less often. The descriptions "knob", "constriction" and "drill" were more prevalent in UA patients (p<0.01). The description "drill" discriminated between diagnostic groups in a multivariate model (p=0.03). Associations between the infarct and pain location (p< or =0.03), and the use of some sensory descriptors (p< or =0.02) were detected. Pain locations associated with ECG findings (p< or =0.005). CONCLUSIONS: Subjective acute coronary pain descriptions and pain characteristics may associate with the pathophysiological processes in coronary syndromes.

Genomic variations and susceptibility to sepsis.

The considerable variability in septic patients' outcomes, which exceeds our understanding of the pathophysiology of sepsis and defies our current prognostic tools, has prompted investigation in the genetic variations that may predispose individuals for increased susceptibility to sepsis and adverse outcomes. This article aims to critically review current evidence from genetic association studies regarding the role of genetic polymorphisms in sepsis. Findings regarding polymorphisms in intercellular messenger mediators (cytokines), membrane-bound inflammatory receptors, intracellular signaling cascades, heat shock proteins, coagulation/fibrinolysis pathways, apoptotic mechanisms, and neuroendocrine axes are presented and discussed. Study results are often discrepant, whereas many methodological limitations, in terms of both study design and genotyping methods, may render the results difficult to generalize. Nonetheless, a role for genomic variations in sepsis outcomes has emerged. A theoretical framework for incorporation of genetic variations into individualized care planning based on complexity theory is proposed, and future prospects of microarray technology and systems modelling are discussed briefly.