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Peripheral Edema, Central Venous Pressure, and Risk of AKI in Critical Illness

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Peripheral Edema, Central Venous Pressure, and Risk of AKI in Critical Illness Article Peripheral Edema, Central Venous Pressure, and Risk of AKI in Critical Illness Kenneth P. Chen,* Susan Cavender,† Joon Lee,†‡ Mengling Feng,†§ Roger G. Mark,† Leo Anthony Celi,*† Kenneth J. Mukamal,* and John Danziger* Abstract Background and objectives Although venous congestion has been linked to renal dysfunction in heart failure, its significance in a broader context has not been investigated. *Department of Medicine, Beth Israel Deaconess Medical Design, setting, participants, & measurements Using an inception cohort of 12,778 critically ill adult patients Center, Boston, admitted to an urban tertiary medical center between 2001 and 2008, we examined whether the presence of Massachusetts; † peripheral edema on admission physical examination was associated with an increased risk of AKI within the Division of Health Sciences and first 7 days of critical illness. In addition, in those with admission central venous pressure (CVP) measurements, fi Technology, Harvard- we examined the association of CVPs with subsequent AKI. AKI was de ned using the Kidney Disease Im- Massachusetts proving Global Outcomes criteria. Institute of Technology, Results Of the 18% (n=2338) of patients with peripheral edema on admission, 27% (n=631) developed AKI, Cambridge, n Massachusetts; compared with 16% ( =1713) of those without peripheral edema. In a model that included adjustment for ‡School of Public comorbidities, severity of illness, and the presence of pulmonary edema, peripheral edema was associated with a Health and Health 30% higher risk of AKI (95% confidence interval [95% CI], 1.15 to 1.46; P,0.001), whereas pulmonary edema Systems, University of was not significantly related to risk. Peripheral edema was also associated with a 13% higher adjusted risk of a Waterloo, Waterloo, P, Ontario, Canada; and higher AKI stage (95% CI, 1.07 to 1.20; 0.001). Furthermore, levels of trace, 1+, 2+, and 3+ edema were §Data Analytics associated with 34% (95% CI, 1.10 to 1.65), 17% (95% CI, 0.96 to 1.14), 47% (95% CI, 1.18 to 1.83), and 57% (95% CI, Department, Institute 1.07 to 2.31) higher adjusted risk of AKI, respectively, compared with edema-free patients. In the 4761 patients for Infocomm Research, Agency for with admission CVP measurements, each 1 cm H2O higher CVP was associated with a 2% higher adjusted risk of AKI (95% CI, 1.00 to 1.03; P=0.02). Science, Technology And Research, Singapore Conclusions Venous congestion, as manifested as either peripheral edema or increased CVP, is directly associated with AKI in critically ill patients. Whether treatment of venous congestion with diuretics can modify this risk will Correspondence: require further study. Dr. John Danziger, Clin J Am Soc Nephrol 11: 602–608, 2016. doi: 10.2215/CJN.08080715 185 Pilgrim Road, Farr 8, Boston, MA 02215. Email: jdanzige@ bidmc.harvard.edu Introduction Venous congestion manifests as peripheral edema The role of venous congestion as a determinant of on physical examination and by increased CVP. renal function was first described almost 85 years Although peripheral edema can also be seen in the ago. In early physiology experiments on dogs, F. R. setting of mechanical obstruction, it usually reflects an Winton showed that increasing renal venous pressure outward hydrostatic pressure that exceeds the inward decreased both urine and renal arterial flow (1), high- oncotic force, resulting in extravasation of intravas- lighting the importance of the “trans-renal pressure cular fluid into the interstitial compartments. The gradient,” a balance between mean arterial and venous clinical importance of peripheral edema is not well pressures (2). More recent clinical data have focused on described, and is typically considered cosmetic and venous congestion in heart failure (3), where central non-life threatening (11). Given the emerging impor- venous pressures (CVP), but not cardiac output or tance of venous congestion in renal function, we hy- pulmonary capillary wedge pressures, are associated pothesized that peripheral edema and increased CVP with renal dysfunction (4). Consequently, the current would be associated with a higher risk of AKI. concept of the cardiorenal syndrome, typically used to Using a large cohort of critically ill patients admitted describe renal injury in the setting of poor arterial to a tertiary medical center, we examined whether the flow due to left ventricular dysfunction, is being mod- presence and severity of peripheral edema on the hospital ified to include venous congestion (5–9) and right ven- admission physical examination was associated with AKI tricular function (10). Whether venous congestion is during the first 7 days of critical illness. We also exam- similarly associated with poor renal outcomes in other ined whether CVP measurements taken on intensive populations is not known. care unit (ICU) admission were associated with AKI. 602 Copyright © 2016 by the American Society of Nephrology www.cjasn.org Vol 11 April, 2016 Clin J Am Soc Nephrol 11: 602–608, April, 2016 Peripheral Edema and AKI, Chen et al. 603 Materials and Methods We identified congestive heart failure patients through NLP Study Population searching of the past medical history section of the admission We used the Multiparameter Intelligent Monitoring in examination or Elixhauser discharge coding (14). We also Intensive Care (MIMIC‑II) database, a joint venture man- used oral diabetes medication or insulin usage, along with aged by the Laboratory for Computational Physiology at Elixhauser discharge coding, to identify diabetic patients. All Massachusetts Institute of Technology (MIT) and the De- additional 27 Elixhauser discharge coding comorbidities partment of Medicine at the Beth Israel Deaconess Medical were included as separate variables. ICU types included car- Center (BIDMC). MIMIC‑II contains data from 23,455 diac, surgical, cardiothoracic, and medical units. Sequential unique critical care admissions between 2001 and 2008 at Organ Failure Assessment scores were used to indicate se- BIDMC, a 700-bed urban academic medical center with 77 verity of illness. Because of the effect of hemodynamics on adult ICU beds. The database contains high temporal res- renal function, we also included systolic and diastolic BP, olution data from clinical systems, including lab results, heart rate, and temperature as independent continuous var- electronic documentation, and bedside monitor trends iables. Admission creatinine, defined as the first available and waveforms. Use of the MIMIC‑II database has been creatinine 24 hours prior to, or 6 hours after, ICU admission approved by the institutional review boards of BIDMC wasusedasadeterminantof“baseline” kidney function. and MIT. A total of 13,986 patients had complete admis- We used NLP searches of prehospital medication lists to sion history and physical examination as part of the hos- identify angiotensin-converting enzyme inhibitor (ACE-I), pital discharge summary. We excluded 270 prevalent angiotensin receptor blocker (ARB), statin (15), calcium ESRD patients. Another 930 were missing documentation channel blocker, and diuretic usage. of admission laboratory studies, leaving 12,778 unique in- dividuals for primary analysis. Analyses We present descriptive baseline characteristics stratified Primary Exposures by peripheral edema. We used logistic regression to In order to describe the effect of venous congestion examine the association between admission peripheral independently of pulmonary congestion, we developed a edema and the subsequent risk of AKI. We adjusted for age, Natural Language Processing (NLP) code based on standard gender, race, ICU type, Sequential Organ Failure Assess- clinical descriptors to identify both peripheral edema and ment score, history of diabetes, congestive heart failure, pulmonary edema as documented in the admission physical hypertension, chronic pulmonary disease, peripheral vas- examination (Supplemental Table 1). The developed code cular disease, and 24 additional Elixhauser comorbidities, was “trained” by manual review of eight sequential sets of admission systolic and diastolic BP, heart rate, temperature, randomly selected discharge summaries, ranging from 50 to admission creatinine, and preillness medication usage, in- 100 in number. Once the code consistently achieved an ac- cluding diuretic, ACE-I, ARB, calcium channel blocker, or curacy rate of .90% (Supplemental Figure 1), all reviewed statin use. In order to determine the effect of peripheral discharge summaries were combined, and the code was edema independently of pulmonary congestion, pulmonary tested on 10,000 random resamples (with replacement) of edema was included as a separate variable in all analyses. 100 discharge summaries. The histogram of bootstrap accu- We describe the incidence of AKI severity according to racy is provided (Supplemental Figure 2). We also examined admission peripheral edema, and used cumulative ordinal severity of peripheral edema, categorizing patients as having logistic regression to describe the adjusted risk of peripheral trace, 1+, 2+, and 3+ peripheral edema. We used CVP mea- edema with a one-step higher AKI stage using the same surements obtained within 6 hours of ICU admission as a variables as above. secondary primary exposure. In those patients with quantifiable edema, we created indicator variables for trace, 1+, 2+, and 3+ edema, and used Primary Outcomes logistic regression to describe the adjusted risk of peripheral The primary outcome was AKI during the first 7 days of edema severity with AKI.
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