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Abstract

An association between abnormal gastrointestinal perfusion and critical illness has been suggested for a number of years. Much of the data to support this idea comes from studies using gastric tonometry. Although an attractive technology, the interpretation of tonometry data is complex. Furthermore, current understanding of the physiology of gastrointestinal perfusion in health and disease is incomplete. This review considers critically the striking clinical data and basic physiological investigations that support a key role for gastrointestinal hypoperfusion in initiating and/or perpetuating critical disease.

Bladder Mucosal CO2Compared with Gastric Mucosal CO2as a Marker for Low Perfusion States in Septic Shock

“…We observed, as expected, a decrease of tissue perfusion starting the first hour after the septic provocation, as measured by CO 2 in gastric mucosa, whose value was increased gradually over hours, reflecting the increase in hepato-esplachnic blood flow that occurs in sepsis, in concordance with that observed in other studies [13, 14]. This was accompanied by a compatible hemodynamic pattern coincident with that found in other studies of E. Coli -induced sepsis in animal models [15].…”

Physiology of Stress and Use of Skin-to-Skin Care as a Stress-Reducing Intervention in the NICU

“…Therefore, in response to stress, the infant's body diverts resources away from growth and toward meeting the immediate demands of the body (e.g., by increasing blood glucose to make it available to cardiac and respiratory muscles); this results in poor somatic growth. Simultaneously, the SNS diverts blood away from the gastrointestinal tract and toward the brain, heart, and lungs, which decreases motility, digestion, and absorption, further detracting from nutrient uptake and growth and contributing to symptoms of enteral feeding intolerance (Ackland, Grocott, & Mythen, 2000).…”

Evaluation of Multiple Modes of Oximetry Monitoring as an Index of Splanchnic Blood Flow in a Newborn Lamb Model of Hypoxic, Ischemic, and Hemorrhagic Stress

“…Decreases in splanchnic perfusion may accelerate critical illness and postoperative morbidity due to mucosal hypoperfusion and increased permeability to bacteria or toxins (10, 11). Thus, monitoring oxygenation of tissues supplied by the splanchnic circulation may enable earlier interventions to slow progression of morbidities related to hypoperfusion or sepsis.…”