Professional experience and wisdom have taught us that immobility is a risk factor for various adverse outcomes, such as deep vein thrombosis, joint contractures, pulmonary dysfunction, and bone demineralization to name a few. Balancing bed rest and mobility may improve both short- and long-term outcomes for our patients. Moreover, early, routine mobilization of critically ill patients is safe and reduces hospital length of stay, shortens the duration of mechanical ventilation, improves muscle strength, and functional independence. At the University of Michigan, we have turned the tides by creating a structured process to get our patients moving through the use of a standardized mobility protocol. Our protocol is simple and can easily be adapted for all patient populations by simply modifying some of the inclusion and exclusion criteria. The activities are grounded in the evidence and well thought out to prevent complications and promote mobilization. The purpose of this article was to present the science behind the development of a multidisciplinary protocol for early mobilization of critically ill patients that can be adapted to any intensive care unit patient with minor modifications.
Background: Regional citrate anticoagulation (RCA) is not recommended in patients with shock or severe liver failure. We designed a protocol with personalized pre-calculated flow settings for patients with absent citrate metabolism that abrogates risk of citrate toxicity, maintains neutral CKRT circuit calcium mass balance and normal systemic ionized calcium levels. Methods: Single center prospective cohort study of patients in five Adult Intensive Care Units triaged to the CVVHDF-RCA "Shock" protocol. Results: Of 31 patients included in the study, 30 (97%) had acute kidney injury, 16 (52%) had acute liver failure, and 5 (16%) had cirrhosis at the start of CKRT. The median (interquartile range (IQR)) lactate was 5 (3.2 to 10.7), AST 822 (122 to 2950), ALT 352 (41 to 2238), total bilirubin 2.7 (1.0 to 5.1), INR 2 (1.5 to 2.6). The median first hemofilter life censored for causes other than clotting exceeded 70 hours. The cumulative incidence of hypernatremia (Na >148 mM), metabolic alkalosis (HCO3- >30 mM) and hypophosphatemia (P< 2 mg/dL) were 1/26 (4%), 0/30 (0%), 1/30 (3%) respectively and were not clinically significant. Mild hypocalcemia occurred in the first 4 hours in 2/31 patients and corrected by hour 6 with no additional Ca-supplementation beyond the per-protocol administered Ca-infusion. The maximum systemic total Ca (tCa; mM)/ionized Ca (iCa; mM) ratio never exceeded 2.5. Conclusions: The "Shock" protocol can be used without contra-indications and is effective in maintaining circuit patency with a high, fixed ACDA infusion rate to blood flow ratio. Keeping single-pass citrate extraction on the dialyzer >0.75 minimizes the risk of citrate toxicity even in patients with absent citrate metabolism. Pre-calculated, personalized dosing of the initial Ca-infusion rate from a table based on the patient's albumin level and the filter effluent flow rate maintains neutral CKRT circuit calcium mass balance and a normal systemic iCa level.
Despite implementation of the early mobility protocol, we did not see an improvement in the PU rate overall or with time as protocol compliance improved.
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