Abdominal Perfusion Pressure as a Prognostic Marker in Intra-abdominal Hypertension
Elevated intra-abdominal pressure (IAP) is a continuum from intra-abdominal hypertension (IAH) to abdominal compartment syndrome (ACS) and has considerable impact on end-organ function [1]. However, no data are available on IAP from large prospective clin
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I Introduction Elevated intra-abdominal pressure (lAP) is a continuum from intra-abdominal hypertension (IAH) to abdominal compartment syndrome (ACS) and has considerable impact on end-organ function [1]. However, no data are available on lAP from large prospective clinical trials. Many thresholds have been proposed as the critical value for lAP in guiding decompression. Recent publications have improved our understanding of the pathophysiological mechanisms. We are now aware that even slight elevations in lAP of 10 mmHg may have a tremendous impact on end-organ function [1]. However, it is probably not the absolute value of lAP but the acuity of increase in lAP or the trend over time that is predictive for outcome. Most of the published studies relate to the hemodynamically stable patient or laboratory animal without prior insult. Extrapolation of these results to a critically ill patient or to a trauma patient who may have experienced episodes of shock and resuscitation and hence of ischemia-reperfusion (I/R) injury, may be incorrect. Co-morbidities play an important role in aggravating the effects of raised lAP such as pre-existing chronic renal failure, massive hemorrhage, hypovolemia, positive end-expiratory pressure (PEEP), or pre-existing cardiomyopathy, and these may reduce the threshold of IAH that causes clinical manifestations of ACS. Indeed, the critical lAP value differs from patient to patient and from time to time. A prognostic parameter that could help us in following these patients and guiding therapy would be very helpful. This chapter will focus on abdominal perfusion pressure (APP), defined as mean arterial pressure (MAP) minus lAP, as such a possible parameter.
I Rationale Many organs are capable of maintaining blood flow relatively constant over a wide range of perfusion pressures. The efficiency of this process differs from organ to organ and is greatest in the brain and kidneys. However, virtually all organs exhibit this sort of autoregulation. In most cases, blood flow is preserved within the mean pressure range of 60 to 160 mmHg. For the kidney, autoregulation has also been described in relation to the constant glomerular filtration rate (GFR) in response to variations in perfusion pressure. Adapting the renal vascular resistance of the preglomerular vasculature is the key-factor for autoregulation mediated by mechanisms intrinsic to the kidneys, which may reside in the vascular wall [2].
J.-L. Vincent (ed.), Yearbook of Intensive Care and Emergency Medicine 2002 © Springer-Verlag Berlin Heidelberg 2002
Abdominal Perfusion Pressure as a Prognostic Marker in Intra-abdominal Hypertension
The etiology of renal impairment in IAH with decreases in renal blood flow, GFR, urine output, and tubular dysfunction is probably multifactorial and due to endocrine, hemodynamic, and direct effects [1]. Figure 1 shows the different cardiovascular pathophysiologic mechanisms of IAH. An increase in antidiuretic hormone (ADH) production, and changes in the renin-angiotensin-aldosterone pathways with a ri
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