Hipertension Intrabdominal

From American Journal of Kidney Diseases
Intra-abdominal Hypertension and Abdominal Compartment Syndrome
Jan J. De Waele, MD, PhD, Inneke De Laet, MD, Andrew W. Kirkpatrick, MD, FRCSC; Eric Hoste, MD, PhD
Authors and Disclosures
Posted: 01/12/2011; Am J Kidney Dis. 2011;57(1):159-169. © 2011 The National Kidney Foundation

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• Abstract and Introduction
• Definitionsand Etiology
• IAP Measurement
• Epidemiology
• IAH as a Risk Factor for Acute Kidney Injury
• Pathophysiology
• Effects of IAH and ACS on the Kidney
• IAH in Clinical Nephrology Practice: Summary Points
• Management of IAH and ACS
• Conclusions
• References
• Sidebar
Abstract and Introduction
Abstract
Increased intra-abdominal pressure (IAP), also referred to asintra-abdominal hypertension (IAH), affects organ function in critically ill patients and may lead to abdominal compartment syndrome (ACS). Although initially described in surgical patients, IAH and ACS also occur in medical patients without abdominal conditions. IAP can be measured easily and reliably in patients through the bladder using simple tools. The effects of increased IAP are multiple, but thekidney is especially vulnerable to increased IAP because of its anatomic position. Although the means by which kidney function is impaired in patients with ACS is incompletely elucidated, available evidence suggests that the most important factor involves alterations in renal blood flow. IAH should be considered as a potential cause of acute kidney injury in critically ill patients; its role inother conditions, such as hepatorenal syndrome, remains to be elucidated. Because several treatment options (both medical and surgical) are available, IAH and ACS should no longer be considered irrelevant epiphenomena of severe illness or critical care. An integrated approach targeting IAH may improve outcomes and decrease hospital costs, and IAP monitoring is a first step toward dedicated IAHmanagement. IAH prevention, most importantly during abdominal surgery but also during fluid resuscitation, may avoid ACS altogether. However, when ACS occurs and medical treatment fails, decompressive laparotomy is the only option.
Introduction
For several decades, increased IAP has been increasingly recognized as both cause and consequence of many adverse events in critically ill patients. IncreasedIAP within the closed anatomic volume of the abdominal cavity can lead to decreased perfusion and ischemia of intra-abdominal organs. In addition, increased IAP also leads to physiologic changes and organ dysfunction beyond the abdominal cavity because of the close anatomic relationships with contiguous cavities. Depending on the severity of increased IAP and organ function, the condition isdefined as intra-abdominal hypertension (IAH) or ACS (Box 1).
The harmful consequences of increased IAP initially were reported more than 100 years ago, and effects on the kidney were among the first described. In 1876, Wendt[3] reported that an increase in IAP was associated with a decrease in urine output, and in 1947, Bradley and Bradley[4] published a comprehensive experimental article describingthe effect of IAP on kidney perfusion and function. Several investigators have since noted similar effects in animal models[5] and clinical studies in the critically ill.[6,7] Presumably because measurement of IAP was cumbersome and clinicians were unaware of the dangers, clinical effects of IAP were not reported again until the early 1980s. It was not until the landmark report by Kron et al,[8]which reported that IAP could be monitored objectively and relatively easily through an indwelling intravesical catheter, that more clinical evidence was rapidly forthcoming concerning the deleterious effects of increased IAP on different organ systems.
Since then, the clinical importance of IAH andACS essentially has been rediscovered, largely by physicians and surgeons taking care of the...