Hemodynamic Risk Factors for Progression of Acute Kidney Injury in

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REDUCED OXYGEN DELIVERY AND LOWER BLOOD PRESSURE ARE RISK
FACTORS FOR PROGRESSION TO SEVERE AKI IN CRITICALLY ILL PATIENTS
WITH EARLY AKI
Raimundo, M1,2, Crichton, S1, Syed, Y1, Martin, J1, Whiteley, C1, Bennett, D1, Ostermann,
M1
1
King’s College London, Guy’s & St Thomas’ Hospital, Department of Critical Care,
London,
2
Hospital de Santa Maria, Department of Nephrology & Transplantation, Lisbon,
Portugal
BACKGROUND: Acute kidney injury (AKI) is common in critically ill patients and associated
with increased mortality, morbidity and financial costs. Research in high risk surgical patients
has shown that pre-emptive strategies of perioperative haemodynamic monitoring and
optimisation can reduce the incidence and mortality of postoperative AKI. Our objective was to
investigate the association between hemodynamic parameters at time of early AKI and risk of
progression to severe AKI in critically ill patients in the Intensive Care Unit (ICU).
METHOD: We retrospectively reviewed the electronic medical records of all patients admitted
to the ICU in a tertiary centre between June 2007 - June 2009 and identified patients with AKI
according to the AKI Network criteria who underwent advanced hemodynamic monitoring
within 12 hours of diagnosis of AKI stage I. Patients who died or were discharged on the day of
AKI diagnosis and patients with AKI stage III on admission to ICU were excluded.
Haemodynamic parameters were recorded on the day of AKI stage I and daily until progression
to AKI stage III or return to baseline renal function.
RESULTS: 205 patients (mean age: 66 years; 138 male) underwent haemodynamic monitoring
within 12 hours of the diagnosis of AKI I of whom 85 (41.46%) progressed to AKI III. Median
time to progression was 2 days (range 1-23). Patients who progressed to AKI III had a lower
cardiac index (2.82 vs 3.35 l/min/m2; p=0.004), lower indexed systemic oxygen delivery (DO2I)
(342.3 vs 405.0 ml/min/m2; p=0.006), lower mean arterial blood pressure (MAP) (71 vs 74
mmHg; p=0.011) and a higher central venous pressure (13 vs 11 mmH2O, p=0.043) on the day
of AKI I, compared to patients who did not develop AKI III. After adjusting for demographic
factors, severity scores on admission and other covariates, multivariate analysis showed that a
higher DO2I [Odds ratio (OR) per 50 ml/min/m2 increase 0.86 (95% CI 0.82 – 0.95)], and a
higher MAP (OR per 5 mmHg increase 0.80, 95% CI 0.66 – 0.985) on the day of AKI I were
independently associated with a reduced risk of progression to AKI III. Mean cumulative fluid
balance between day of AKI I and day of AKI III was +495ml/day (SD 910 ml) for nonprogressors and +1779ml/day (SD 616ml) for progressors (p <0.0001). Each 1000ml/day
increase in fluid balance after the diagnosis of AKI I was associated with 60% increase in the
risk of AKI progression in multivariate analysis including adjustment for urine output (p =
0.024). Rises in DO2I and MAP more than 12 hours after the diagnosis of AKI I were not
independently associated with reduced risk of progression to AKI III.
CONCLUSIONS: A higher DO2I and MAP on the day of AKI I are associated with a lower
risk of progression to AKI III. Once AKI is established, efforts to improve these hemodynamic
parameters may not be effective but may even be deleterious if associated with excessive fluid
administration.
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