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AuthorsManu L. N. G. Malbrain, Pieter-Jan Hofkens, Ester Phillipse, Jelke De Vos, Patrick Verburgh, Niels Van Regenmortel, Inneke De Laet, Hilde Dits, Karen Schoonheydt
- Tags: abdominal pressure, cardio-abdominal-renal syndrome, fluid overload, fluids, kidney failure, nutrition
Recent studies suggest that fluid overload is related to endorgan dysfunction and even mortality. In sepsis the kidneys can get swollen especially in the setting of capillary leak and a direct relation has been demonstrated between the amount of fluid overload and the degree of acute kidney injury (AKI).
The aim of this review is to analyse the current evidence with regard to the impact of fluids and fluid overload on kidney function and AKI and intra-abdominal hypertension (IAH). In addition, this review will provide an update on the current knowledge on nutritional support in critically ill patients with sepsis and AKI. `
Review of the relevant literature on fluids and nutrition in AKI and IAH.
This review will give an overview on the current knowledge on the impact of different types of resuscitation fluids and fluid overload on kidney function. It will try to explain why fluid overload, IAH and AKI should be seen together and will give some suggestions on how to handle nutrition. Since IAH is often seen in relation to massive resuscitation, AKI and IAH go hand in hand and the kidneys are usually the canary in the coalmine for IAH. Since nutrition can only be administrated by providing extra fluid or volume to the patient, they should always be dealt with together. In patients with sepsis and AKI different metabolic alterations can be observed: energy expenditure changes due to the hypermetabolic state, carbohydrate metabolism is altered by the underlying critical illness and the loss of kidney function, stress diabetes can develop, malnutrition can develop and is related to a disease induced abnormal nutrient processing, glucose is preferentially metabolized to lactate, protein catabolism and negative nitrogen balance may occur. Nutritional support should be limited to patients with unmet nutrient requirements, documented inadequate oral intake, unpredictable return of gastrointestinal function or a prolonged period of bowel rest. Overfeeding should be avoided at all times and the clinician must be aware of the refeeding syndrome. The use of indirect calorimetry is recommended. Early enteral nutrition may have beneficial effects by triggering gut immunity while delay of enteral nutrition may promote a pro-inflammatory state.
The recommendations for nutritional support in AKI can at best be described as open for discussion and debate. Fluid accumulation should be avoided by all means and abdominal pressure needs to be measured in patients with sepsis, fluid overload and worsening kidney function.