Gastrointestinal (GI) tonometry, the only clinically available method for the accurate diagnosis of compromised GI blood flow, has been shown to be a sensitive predictor of increased morbidity, mortality and prolonged hospitalization. The recent introduction of the Tonocap, as a means of performing automated air tonometry, has simplified the application of GI tonometry in the clinical setting. Despite this the utility of GI tonometry remains controversial. The GI Tonometry: State of the Art meeting brought together a group of clinicians with a proven track record of research, clinical interest and expertise in this field. The aim of the meeting was to come to a consensus regarding certain issues such as the past and future roles of GI tonometry and standards for its correct usage and interpretation. Finally suggestions as to further research and clinical evaluation were made within a broader discussion regarding the complexities of applying the principles of evidence-based medicine to the introduction of a new piece of medical technology.

Non-operative management of traumatic pancreatitis in the absence of complete duct transection is safe in children and does not appear to be associated with adverse sequelae.

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Anesthetized lambs were subjected to epidural cord compression at T13 by means of an epidural balloon distended to 200 mmHg for 80 minutes. Determinations of spinal cord blood flow (SCBF) were made by labelled microspheres prior to and during compression, and then 1/2, 1 1/2, and 2 1/2 hours after compression. Twelve control animals received saline (80 ml/h). Nine animals received hetastarch (a 20 ml/kg bolus followed by an 80 ml/h infusion) and 8 animals received mannitol (a 1 g/kg bolus followed by 1 g/kg/hr). An additional 10 animals received phenylephrine to raise mean arterial pressure by 20 to 40%. Somatosensory evoked potentials (SEPs) were recorded following each determination of SCBF. Animals were killed following determination of the 2 1/2 hour postcompressive flow. The animals treated with either hetastarch or phenylephrine had a postcompressive mean arterial pressure that was significantly greater than that of the controls (P less than 0.01). During treatment, cardiac output in the hetastarch and mannitol animals was significantly greater and hematocrit significantly less than in the controls (P less than 0.05). In spite of these changes, postcompressive SCBF was significantly increased only in those animals treated with phenylephrine (P less than 0.05). Statistical analysis of the relationship between mean arterial pressure and postcompressive SCBF revealed that autoregulation is indeed lost with this experimental model of spinal cord injury. Histological examination of the injured site failed to demonstrate any difference in the area of hemorrhagic necrosis among the four groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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