What's new in emergencies, trauma and shock? Acute renal failure and intra-abdominal hypertension in acute compartment syndrome: Any corollaries with acute renal failure in cardiorenal syndrome?

Sir,

The authors describe their findings on abdominal compartment syndrome (ACS), a rare clinical entity that has been described in critically ill patients including medical, surgical, and trauma populations with high morbidity and mortality rates reported among those patients affected by it.[1] This was a 5-year retrospective chart review conducted at three level I trauma centers in the city of Chicago, IL, USA. ACS was defined as “sustained intra-abdominal pressure (IAP) exceeding 20 mmHg associated with new organ dysfunction or failure” with an estimated incidence 0.5-36% depending on the patient population studied and the definition used to describe the condition.[23]

One of the adverse effects of ACS attributed to the direct and indirect effects of increased IAP, was acute renal failure (ARF).[34] Regarding primary outcomes in this study, the incidence of ARF was 42.86%.[1] Furthermore, a lactic acid level >5 mmol/L on admission was strongly associated with transfusion requirements of >10 units of blood within the first 24 h of admission (r = 0.5, P = 0.04), and was moderately associated with the development of ARF (r = 0.4, P = 0.04) during hospital stay.[1] The authors further acknowledged that future areas of research include expanding the number of variables studied to identify the strength of association of additional markers to specific outcomes in trauma patients with intra-abdominal hypertension (IAH) in addition to those diagnosed with ACS.[1]

As a corollary, we had recently investigated the phenomenon of cardiorenal syndrome (CRS), with specific emphasis on current and possibly new management options to treat this syndrome.[5] Of note, among several suggested pathogenetic mechanisms for CRS, on titillating observation is that rennin angiotensin aldosterone system (RAAS) activation resulting from poor renal perfusion from heart failure (forward failure) or from increased renal venous hypertension due to venous congestion from congestive heart failure (backward failure) is a major contributor to renal failure in CRS.[6] Besides, new exciting frontiers for CRS therefore include therapeutic measures that directly target renal venous hypertension.[6] Ross, in a recent 2012 review, had examined the consequences of renal venous hypertension in producing what he referred to as “congestive renal failure”.[7] Moreover, the role of IAH in causing this “congestive renal failure” often goes unrecognized.[7] There is consequently the notion that targeted treatment of renal venous hypertension and congestion that would enable fluid removal and “decongestion” by extracorporeal ultrafiltration could be useful paradigms of care in CRS.[78] In addition, mechanical interventions for reducing IAH such as paracentesis, gastrointestinal decompression, wall musculature paralytics, decompressive abdominal wall surgery and dialytic therapy with ultrafiltration could become important and useful treatment options for the management of moderate to severe CRS.[78]

Thus, the recurring role of IAH in the causation of renal failure in ACS and in CRS raises interesting perspectives for possible therapeutic options for both syndromes.[123478] What, if any, is there a role for RAAS activation in the renal failure associated with posttraumatic ACS? Furthermore, what potential roles exist for mechanistic therapeutic interventions such as paracentesis, gastrointestinal decompression, wall musculature paralytics, decompressive abdominal wall surgery and peritoneal dialysis ultrafiltration, in the management of posttraumatic ACS, with or without ARF?[78] For example, would any of such “decompressive” therapies including dialytic ultrafiltration have a pre-emptive prophylactic role in preventing ARF in ACS? Clearly these questions are beyond the scope of the authors’ report.[1] But in our mind, the similarities between ACS and CRS, especially as it applies to the resulting ARF, lead to such tantalizing hypotheses as we have proffered here. These questions and hypotheses call for more studies into ACS and CRS.[15]

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