A Protective Kidney-Lung Approach to Improve Outcomes in Mechanically Ventilated Patients
* The predominant cause of death in ARDS is not hypoxemia, which is one of the defining criteria of ARDS, but multiorgan failure. It is well documented that acute kidney injury (AKI) is the most common organ dysfunction in ARDS patients and that in the presence of AKI the mortality rate increases to more than 40%, with the rate rising with AKI severity.
We review 4 disparate but complementary mechanisms that may contribute to the adverse outcome in ARDS patients with evidence of renal failure.
∎ Fluid Overload (FO)-
» Survivors can be separated from potential non-survivors simply by the degree of FO present on the day of admission and during intensive care unit stay.
» Bioelectrical impedance vector analysis is an emerging tool to assess total body water in critically ill patients, and recent literature encourages further testing and validation.
» Decrease in renal function can lead to acute lung injury via multiple biological mechanisms, including downregulation of lung water and salt channels.
∎ Cardiogenic Pulmonary Edema-
» Venous congestion, as a surrogate for right ventricular impairment, is one of the most important hemodynamic determinants of worsening renal function and is associated with higher mortality.
» Experimental models suggest that venous congestion is likely to decrease renal perfusion pressure and oxygen delivery by increasing intracapsular pressure due to the formation of renal edema, which aggravates the renal impairment.
∎ Noncardiogenic Pulmonary Edema-
» Patients with cardiogenic edema can theoretically improve rapidly with fluid removal, while patients with noncardiogenic pulmonary edema improve little, if at all.
» In clinical practice, however, most patients fall between the 2 categories, and the concept of keeping the patient ‘emptier’ is probably better than letting him be ‘overfilled’.
∎ Mechanical Ventilation and ARDS-
» Is there a kidney- lung protective strategy?
And if so, when does mechanical ventilation become injurious to the kidneys or to other organs?
For instance, is there an optimal positive end expiratory pressure level at which ventilation needs are met and renal function is preserved; will any deviation upset the balance?
» Ventilation with high tidal volumes may increase alveolar vascular permeability and thereby increase the risk of proinflammatory mediators translocating into the systemic circulation and causing end-organ damage.
█ To conclude, we believe that there is a kidney–lung protective strategy in mechanical ventilation, and only multidisciplinary care can address the unique needs of patients with ARDS.
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