Sepsis and multiple organ failure are common causes of death in patients admitted to intensive care units. The incidence of sepsis and associated mortalities has been steadily increasing over the past 20 years. Sepsis is a complex inflammatory condition, the precise causes of which are still poorly understood. Animal models of sepsis have the potential to cause substantial suffering, and many of them have been poorly representative of the human syndrome. However, a number of non-animal approaches, including in vitro, in silico and clinical studies, show promise for addressing this situation. This report is based on discussions held at an expert workshop convened by Focus on Alternatives and held in 2004 at the Wellcome Trust, London. It provides an overview of some non-animal approaches to sepsis research, including their strengths and weaknesses, and argues that they should be prioritised for further development.

Bedside (or handheld) ultrasonography is being used in the ICU with increasing frequency, and areas of interest include echocardiography, vascular access, focussed abdominal ultrasound in trauma (FAST) and bladder scanning 1,2 .

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Objective: B-type natriuretic peptide (BNP) has been shown to be a sensitive marker of cardiac dysfunction and to increase in patients with septic shock. This study seeks to confirm these findings in a mixed group of critically ill patients. Design and setting: Prospective observational study in a general intensive care unit (ITU) of a university hospital. Patients and participants: Ninety-three consecutive admissions to the general ITU.Interventions: Measurement of NT-proBNP on admission and then daily thereafter. Collection of clinical and demographical data in relation to NT-proBNP over a period of 5 days and outcome data at 28 days and hospital discharge. Measurements and results: NT-proBNP levels were raised for the whole population at each time point. NT-proBNP levels were higher in non-survivors than in survivors from ITU (p 0/0.02), at 28 days (p 0/0.02) or hospital discharge (p 0/0.0004). NTproBNP was raised in patients with sepsis (11 688 (6140 Á/20 434) vs. 767 (472 Á/2267) ng/L, p 0/B/0.0001), cardiac dysfunction (7336 (3383 Á/14 906) vs. 757 (428 Á/1819) ng/L, p 0/ B/0.0001), requirement for vasoactive therapy (7151 (1089 Á/14 318) vs. 1257 (721 Á/3127) ng/L, p0/0.01) and renal support (12 128 (2693 Á/25 831) vs. 1687 (752 Á/3291) ng/L, p 0/ B/0.0001). Multiple regression analysis demonstrated that independent predictors of raised NT-proBNP levels were the diagnosis of sepsis (p B/0.0001) or ongoing cardiac dysfunction (p 0/0.006).Conclusions: NT-proBNP levels are raised in critically ill patients. The cause of these increases relates to either sepsis or cardiac dysfunction.