manejo perioperatorio del paciente con fracaso …

SARTD-CHGUV Sesión de Formación ContinuadaValencia 18 de Junio de 2018

MANEJO PERIOPERATORIO DEL PACIENTE CON FRACASO RENAL

AGUDO

-Ruth Martínez Plumed ( FEA)-Clara Fernández Bardal ( R4)

Servicio de Anestesia Reanimación y Tratamiento del DolorConsorcio Hospital General Universitario de Valencia


ÍNDICE1. Introducción. 2. Definición LRA. 3. Estadificación LRA. 4. Evaluación de riesgo. 5. Diagnóstico. 6. Manejo perioperatorio.


INTRODUCCIÓN-LESIÓN RENAL AGUDA.

üIncidencia alta.üAumenta la morbimortalidad. üAumenta los costos en la atención del paciente. üSusceptible de detección temprana, prevención y

tratamiento.üAbordaje multidisciplinar en el paciente crítico.


GUÍA KDIGOGrupo de trabajoà expertos en diferentes materias ( nefrología, cuidados intensivos, medicina interna, pediatría, cardiología, radiología y enfermedades infecciosas y epidemiología).4 áreas principalesüDefinición y clasificación.üPrevención.üTratamiento farmacológico.üTerapia de reemplazo renal. Grados de recomendación

Nivel 1à FuerteNivel 2 à Débil

Aà respaldo alto.Bà moderado.Cà bajo.Dàmuy bajo


DEFINICIÓN LRA• GUIAS KDIGO DE LRA de 2012 unifican las

clasificaciones RIFLE y AKIN, para facilitar diagnóstico y seguimiento

• PROBLEMA• Solo tiene en cuenta la primera semana de evolución de LRA.• Dejan muchos pacientes fuera (no se identifican o no se siguen)

• Clasificación ADQI 2017---> COMPLEMENTARIO A KDIGO• LRA (lesión renal aguda): 1ª semana de evolución• ERA (enfermedad renal aguda): Días 7 a 90 • ERC (enfermedad renal crónica): > 90 días de evolución


DEFINICIÓN GUÍAS KDIGO: LRA

Disminución abrupta de la función renal, que incluye, pero no se limita a la insuficiencia renal aguda.

-Aumento de la Cr sérica ≥0.3 mg/dl en las primeras 48h.-Aumento de la Cr sérica ≥ 1,5 veces el valor inicial ocurrido

en los 7 días previos.

-Diuresis <0,5 ml/kg/h durante 6 horas.

-Clasificar la lesión renal aguda según gravedad.-Identificar la causa siempre que sea posible. Sin grado de

recomendación


ESTADIFICACIÓNESTADIO CR SÉRICA GASTO

URINARIO

1 1,5-1,9 veces ó aumento de > 0,3 mg/dl

< 0,5 ml/kg/h durante de 6 a 12h

2 2- 2,9 veces < 0,5 ml/kg/h durante > 12 h

3 > 3 veces óincremento de > 4 mg/dl ó inicio de TRR

< 0,3 ml/kg/h durante > 24 h o anuria > 12 h


CLASIFICACIÓN ADQI 2017ESTADIO CR SÉRICA

0 A0 B0 C0 B/C

Valor basal sin marcadores de daño renalValor basal con marcadores de daño renal1-1,5 veces valor basal sin marcadores daño renal1-1,5 veces valor basal con marcadores daño renal

1 1,5-1,9 veces ó aumento de > 0,3 mg/dl

2 2- 2,9 veces

3 > 3 veces ó incremento de > 4 mg/dl óinicio de TRR


LESIÓN RENAL AGUDA• Dificultad para diferenciar LRA,IRA, ERC o LRA sobre

ERC

• Hallazgos clínicos que sugieren proceso AGUDO:• Ausencia de historia clínica previa de enfermedad renal• Evento agudo precipitante documentado• Riñones de tamaño/morfología normal en ecografía• PTH< 170 pg/ml • Evolución hacia la recuperación de la función renal


Evaluación del riesgo LRAFACTOR DE EXPOSICIÓN + SUSCEPTIBILIDAD


Evaluación del riesgo LRAFACTOR DE EXPOSICIÓN + SUSCEPTIBILIDAD

àEstratificar el riesgo según exposiciones y susceptibilidades (Grado 1B).àMedir la producción de orina y la Cr sérica en los pacientes con más riesgo.


DIAGNÓSTICO1. Historia clínica minuciosa + examen físico.

-Medicaciones sin receta, remedios a base de hierbas, drogas…-Exposición a enfermedades tropicales.-Evaluación color orina, signos de IC agua y crónica e infección.

2 . Parámetros de laboratorio.-Cr y urea séricas.-Hemograma.-Análisis de orina.

3 . Pruebas de imagen: Ecografía.4 . Nuevos biomarcadores urinarios:

- Lipocalina + gelatinasa de neutrófilos.- Mol 1 de lesión renal y la IL-18.


DIAGNÓSTICO

• IMPORTANTE: cuando se evidencia elevación de Cr sérica: daño renal avanzado con implicaciones graves

en la morbimortalidad

• MARCADOR TARDÍO (24-48 h de evolución)

• Nuevos marcadores TEMPRANOS de daño renal

• Cistacina C, KIM1, IL 18, IGFBP7, TIMP2

• Importancia pruebas de imagenOriginal Article

The Association Between Pulsatile Portal Flowand Acute Kidney Injury after Cardiac Surgery:

A Retrospective Cohort Study

William Beaubien-Souligny, MDn,1, Roberto Eljaiek, MD, MScn,Annik Fortier, MSc†, Yoan Lamarche, MD, MSc‡,Mark Liszkowski, MD§, Josée Bouchard, MD||,

André Y. Denault, MD, PhDn

nDepartment of Anesthesiology and Intensive Care, Montreal Heart Institute, Montreal, Quebec, Canada†Montreal Health Innovations Coordinating Center, Montreal Heart Institute, Montreal, Quebec, Canada

‡Department of Cardiac Surgery, Montreal Heart Institute, Montreal, Quebec, Canada§Department of Cardiology, Montréal Heart Institute, Montreal, Quebec, Canada

||Department of Nephrology, Hôpital Sacré-Coeur de Montréal, Montreal, Quebec, Canada

Objective: Venous congestion is a possible mechanism leading to acute kidney injury (AKI) following cardiac surgery. Portal vein flowpulsatility is an echographic marker of cardiogenic portal hypertension and might identify clinically significant organ congestion. Thisexploratory study aims to assess if the presence of portal flow pulsatility measured by transthoracic echography in the postsurgical intensive careunit is associated with AKI after cardiac surgery.Design: Retrospective cohort study.Setting: Specialized care university hospital.Participants: Patients who underwent cardiac surgery between May 2015 and February 2016 and had at least 1 Doppler assessment of portalflow performed by the attending critical care physician during the week following cardiac surgery.Interventions: The association between portal flow pulsatility defined as a pulsatility fraction Z50% and the risk of subsequent AKI wasassessed using univariate and multivariate logistic regression analysis.Measurements and Main Results: The files of 132 consecutive patients were reviewed and 102 patients were included in the analysis. Significant portalflow pulsatility was detected in 38 patients (37.3%) in the week following surgery. During this period, 60.8% developed AKI and 13.7% progressed tosevere AKI. The detection of portal flow pulsatility was associated with an increased risk for the development of AKI (odds ration [OR] 4.31, confidenceinterval [CI] 1.50-12.35, p ¼ 0.007). After adjustment, portal flow pulsatility and AKI were independently associated (OR 4.88, CI 1.54-15.47, p ¼ 0.007).Conclusions: Assessment of portal flow using Doppler ultrasound at the bedside might be a promising tool to detect patients at risk for AKI dueto cardiogenic venous congestion.& 2017 Elsevier Inc. All rights reserved.

Key Words: cardiology and cardiac surgery; intensive care; heart failure; acute kidney injury; cardiorenal syndrome; point-of-care ultrasound

ACUTE KIDNEY INJURY (AKI) is a frequent complica-tion following cardiac surgery. Severe AKI, defined as aKidney Disease Improving Global Outcomes (KDIGO) stageZ2, is encountered in 4% to 9% of patients.1 AKI in thissetting is an independent risk factor for death and developmentof end-stage renal disease.2 The cardiorenal syndrome is a

Contents lists available at ScienceDirect

journal homepage: www.jcvaonline.com

https://doi.org/10.1053/j.jvca.2017.11.0301053-0770/& 2017 Elsevier Inc. All rights reserved.

André Y. Denault was the Speaker for Medtronic, Masimo and CAEHealthcare. The other authors have no conflict of interest to declare.This study was supported by the Richard I. Kaufman Endowment Fund in

Anesthesia and Critical Care and the Montreal Heart Institute Foundation. W.B.S. is supported by the Fonds de Recherche du Québec en Santé (FRQS).

1Address reprint requests to Dr William Beaubien-Souligny, Montreal HeartInstitute, 5000 Belanger St, Montreal, Quebec H1T 1C8, Canada.

E-mail address: [email protected] (W. Beaubien-Souligny).

Please cite this article as: Beaubien-Souligny W, et al. (2017), https://doi.org/10.1053/j.jvca.2017.11.030

Journal of Cardiothoracic and Vascular Anesthesia ] (]]]]) ]]]–]]]

ARTÍCULO JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA 2017


PULSATILIDAD DE VENA PORTA Y AKI

major mechanism leading to AKI in the perioperative period.3

While low cardiac output and low arterial pressure usually ispresumed to be the principal driving factor responsible for thealteration of renal function, venous hypertension has beenreported to be the most important predictor of worsening ofrenal function in congestive heart failure patients.4,5 It wasdemonstrated in animal studies that venous hypertensiondecreases renal blood flow and glomerular filtration.6–8 Inpatients undergoing cardiovascular surgery, high centralvenous pressure (CVP) after surgery has been associated withan increased risk of AKI.9,10

End-organ venous congestion is not easily measurable at thebedside. Absolute CVP measurements, beside jugular venouspressure estimation, peripheral edema, weight, and fluidbalance remain the most commonly used tools to assessvolume status. Point-of-care ultrasound is now enablingclinicians to perform Doppler assessments of the blood flowwithin intra-abdominal organs. Portal vein flow pulsatility is amarker of cardiogenic portal hypertension.11–16 Normal flowin the portal system continuous toward the liver does notusually exhibit a wide variation of velocities through thecardiac cycle, which results in a flat to slightly undulatingpattern on pulsed-wave Doppler.17 Portal vein flow pulsatilityoccurs following the distension of the inferior vena cava,which then becomes non-compliant, resulting in the transmis-sion of venous pressure variations during the cardiac cycle tointra-abdominal organs.18 The presence of portal vein flowpulsatility could be a surrogate marker of venous congestion ofother organs, such as the kidneys. In this exploratory study, thefollowing hypothesis was explored: the presence of portal veinflow pulsatility after cardiac surgery is a risk factor forsubsequent AKI.

Methods

Study Design

The authors performed a retrospective study at a specializedtertiary care university hospital. All cardiac surgery patientsfrom May 2015 to February 2016 who had portal vein Dopplerimaging by the end of postoperative day (POD) 7 wereeligible. Screening was done in all patients who were underthe care of an experienced intensive care physician withNational Board Certification in critical care ultrasound fromthe American College of Chest Physicians during the studyperiod (consecutive patients). Patients with stage 5 chronickidney disease, AKI before surgery, with cirrhosis or portalvein thrombosis, who died within 12 hours after surgery, orwho had a critical preoperative state were excluded. The latterwas defined as aborted sudden death, preoperative cardiopul-monary resuscitation, preoperative positive-pressure ventila-tion, preoperative inotropes, or mechanical circulatory support.Portal vein flow Doppler assessment was performed at thebedside by the attending physician, and the difference betweenmaximal and minimal velocities during the cardiac cycle wassystematically documented. The medical team was not blindedto the Doppler results.

At the Montreal Heart Institute, informed consent forresearch purposes is obtained routinely from patients beforesurgery for data and ultrasound images recorded duringhospitalization. The ethics committee of the Montreal HeartInstitute approved the protocol of this study. Studies wereperformed in accordance with the Declaration of Helsinki andits later amendments.

Definitions

The technique of assessment of portal vein flow usingbedside transthoracic echography has been described pre-viously. The position of the probe and an example of thetwo-dimensional ultrasound image obtained is presented inFigures 1 and 2.19 The pulsatility fraction (PF) is defined as:

PF %ð Þ ¼ 100 n VMax−VMinð Þ=VMax! "

where VMax is the maximal velocity and VMin is the minimalvelocity during the cardiac cycle. Portal vein flow pulsatilitywas defined as a PF of Z50% based on the availableliterature.12–15,17 Examples of normal and pulsatile portal veinflow are presented in Figures 3 and 4. Among the studiedpatients, the PF was noted systematically in a specific portion

Fig 1. Portal vein position (black arrow) obtained from a posterior axillaryview using the Vimedix simulator (CAE Healthcare, St-Laurent, Canada).

Fig 2. Transthoracic ultrasound with color Doppler showing the relativeposition the portal vein (PV) and hepatic vein (HV).

W. Beaubien-Souligny et al. / Journal of Cardiothoracic and Vascular Anesthesia ] (]]]]) ]]]–]]]2


- Estudio de cohortes retrospectivo

detected at a median of 4 days (IQR 3-6 days). Detaileddata regarding ultrasound assessments are presented inTable 2.During the week following surgery, 62 patients (60.8%)

developed AKI. Severe AKI (KDIGO Z2) developed in 14patients (13.7%), and 5 patients (4.9%) required renal replace-ment therapy for a median of 3 days (IQR 2-5 days). Themajority developed AKI on POD 1 (50/62 patients), and serumcreatinine reached a peak after a median of 2 days (IQR 1-3).Clinical characteristics in relationship with the risk of AKI

and severe AKI are presented in Table 3. Patients’ character-istics associated with a higher risk to develop AKI were higherbaseline serum creatinine, lower baseline eGFR from theModified Diet in Renal Disease equation,27 and higher AKIprediction score by Thakar et al.22 During surgery, highersystolic and diastolic pulmonary artery pressures (PAP), as

well as use of vasopressin were associated with a higher risk ofdeveloping AKI. The use of epinephrine, amount of 5%albumin administered and the need for blood transfusions inthe first 24 hours after surgery were associated with anincreased risk of severe AKI. In the postoperative period,portal vein flow pulsatility, the cardiovascular component ofthe SOFA score, PAP, and mean cardiac index following ICUadmission (POD 0) were associated with a higher risk of AKI.In univariate analyses, after excluding 18 patients without

portal flow assessment before AKI diagnosis, there was anassociation between maximal PF Z50% and AKI (OR 4.31, CI1.50-12.35, p ¼ 0.007) (Table 3). In patients with AKI, 28.0%(7 out of 25 patients) of those with portal vein flow pulsatilitysubsequently progressed to severe AKI, while 13.3% (4 out of30 patients) of patients without portal vein flow pulsatilityprogressed to severe AKI (OR 2.53 [CI 0.64-9.92]).

Fig 5. Flow chart of patient inclusion.

Table 1Clinical Characteristics and Portal Flow PF after Cardiac Surgery

Total n ¼ 102 PF o50% n ¼ 64 (63%) PF Z50% n ¼ 38 (37%) p Value

Age (y) 69 7 11 68 7 12 70 7 11 0.35Female sex 32 (31%) 16 (25%) 16 (42%) 0.07Diabetes 29 (28%) 17 (27%) 12 (32%) 0.59Hypertension 85 (83%) 53 (83%) 32 (84%) 0.86Tobacco use 22 (22%) 13 (20%) 9 (24%) 0.69Peripheral artery disease 16 (16%) 12 (19%) 4 (11%) 0.27Previous coronary artery disease 24 (24%) 15 (23%) 9 (24%) 0.98EuroSCORE II24 (%) 2.8% (1.6-5.7) 2.7% (1.3-4.0) 2.9% (1.9-6.2) 0.15AKI risk score by Thakar et al25 3 (1-4) 2 (1-3) 4 (3-5) 0.0002Body mass index (kg/m2) 28.3 7 5.1 29.2 7 5.4 26.9 7 4.5 0.03NYHA functional class1 41 (40%) 25 (39%) 16 (42%)2 26 (26%) 19 (30%) 7 (18%) 0.483 25 (25%) 14 (22%) 11 (18%)4 5 (5%) 4 (6%) 1 (3%)Undetermined 5 (5%) 2 (3%) 3 (8%)Left ventricular ejection fraction (%) 52% (45%-60%) 54 (49%-64%) 50 (40%-60%) 0.10Tricuspid regurgitation grade 41 before surgery 9 (8.8%) 3 (4.7%) 6 (16%) 0.06Urgent surgery 17 (17%) 7 (11%) 10 (26%) 0.04Valvular surgery 53 (52%) 30 (47%) 23 (61%) 0.18Surgery on thoracic aorta 11 (10.8%) 8 (12.5%) 3 (7.9%) 0.53Cardiopulmonary bypass length (min) 80 (59-112) 77 (53-111) 81 (63-117) 0.38

NOTE. The maximal PF documented was considered.Abbreviations: AKI, acute kidney injury; NYHA, New York Heart Association; PF, portal flow pulsatility fraction.



Original Article

The Association Between Pulsatile Portal Flowand Acute Kidney Injury after Cardiac Surgery:

A Retrospective Cohort Study

William Beaubien-Souligny, MDn,1, Roberto Eljaiek, MD, MScn,Annik Fortier, MSc†, Yoan Lamarche, MD, MSc‡,Mark Liszkowski, MD§, Josée Bouchard, MD||,

André Y. Denault, MD, PhDn

nDepartment of Anesthesiology and Intensive Care, Montreal Heart Institute, Montreal, Quebec, Canada†Montreal Health Innovations Coordinating Center, Montreal Heart Institute, Montreal, Quebec, Canada

‡Department of Cardiac Surgery, Montreal Heart Institute, Montreal, Quebec, Canada§Department of Cardiology, Montréal Heart Institute, Montreal, Quebec, Canada

||Department of Nephrology, Hôpital Sacré-Coeur de Montréal, Montreal, Quebec, Canada

Objective: Venous congestion is a possible mechanism leading to acute kidney injury (AKI) following cardiac surgery. Portal vein flowpulsatility is an echographic marker of cardiogenic portal hypertension and might identify clinically significant organ congestion. Thisexploratory study aims to assess if the presence of portal flow pulsatility measured by transthoracic echography in the postsurgical intensive careunit is associated with AKI after cardiac surgery.Design: Retrospective cohort study.Setting: Specialized care university hospital.Participants: Patients who underwent cardiac surgery between May 2015 and February 2016 and had at least 1 Doppler assessment of portalflow performed by the attending critical care physician during the week following cardiac surgery.Interventions: The association between portal flow pulsatility defined as a pulsatility fraction Z50% and the risk of subsequent AKI wasassessed using univariate and multivariate logistic regression analysis.Measurements and Main Results: The files of 132 consecutive patients were reviewed and 102 patients were included in the analysis. Significant portalflow pulsatility was detected in 38 patients (37.3%) in the week following surgery. During this period, 60.8% developed AKI and 13.7% progressed tosevere AKI. The detection of portal flow pulsatility was associated with an increased risk for the development of AKI (odds ration [OR] 4.31, confidenceinterval [CI] 1.50-12.35, p ¼ 0.007). After adjustment, portal flow pulsatility and AKI were independently associated (OR 4.88, CI 1.54-15.47, p ¼ 0.007).Conclusions: Assessment of portal flow using Doppler ultrasound at the bedside might be a promising tool to detect patients at risk for AKI dueto cardiogenic venous congestion.& 2017 Elsevier Inc. All rights reserved.

Key Words: cardiology and cardiac surgery; intensive care; heart failure; acute kidney injury; cardiorenal syndrome; point-of-care ultrasound

ACUTE KIDNEY INJURY (AKI) is a frequent complica-tion following cardiac surgery. Severe AKI, defined as aKidney Disease Improving Global Outcomes (KDIGO) stageZ2, is encountered in 4% to 9% of patients.1 AKI in thissetting is an independent risk factor for death and developmentof end-stage renal disease.2 The cardiorenal syndrome is a

Contents lists available at ScienceDirect

journal homepage: www.jcvaonline.com

https://doi.org/10.1053/j.jvca.2017.11.0301053-0770/& 2017 Elsevier Inc. All rights reserved.

André Y. Denault was the Speaker for Medtronic, Masimo and CAEHealthcare. The other authors have no conflict of interest to declare.This study was supported by the Richard I. Kaufman Endowment Fund in

Anesthesia and Critical Care and the Montreal Heart Institute Foundation. W.B.S. is supported by the Fonds de Recherche du Québec en Santé (FRQS).

1Address reprint requests to Dr William Beaubien-Souligny, Montreal HeartInstitute, 5000 Belanger St, Montreal, Quebec H1T 1C8, Canada.

E-mail address: [email protected] (W. Beaubien-Souligny).


Journal of Cardiothoracic and Vascular Anesthesia ] (]]]]) ]]]–]]]


PULSATILIDAD VENA PORTA Y AKI

of daily medical record. AKI was defined according to theserum creatinine KDIGO criteria.20

Statistical Analyses

Descriptive data are presented as mean 7 standard devia-tion (SD) or median and interquartile range (IQR) andcompared using t test or Mann–Whitney U test, dependingon the distribution of data. Normality testing was performedby observing the distribution of data using the histogrammethod, comparing central distribution parameters (mean andmedian), and using the Shapiro–Wilk statistical test with a95% confidence level. Categorical variables are presented asfrequencies (percentages) and compared using the χ2 test.Potential predictors of AKI were identified using univariatelogistic regression analysis. Variables considered were predis-posing factors before surgery (age, context of surgery, renalfunction, diabetes, left ventricular ejection fraction, New YorkHeart Association functional class, EuroSCORE II,21 AKIprediction score by Thakar et al22), perioperative factors(procedure, cardiopulmonary bypass duration, fluid balance,administration of blood products and vasopressors), and post-operative factors (fluid balance, hemodynamic stability eval-uated by the cardiovascular component of the SequentialOrgan Function Assessment [SOFA] score23 during POD0 and 1, and cardiac index). The cardiovascular componentof the SOFA score is defined as the following: 0: mean arterialpressure Z70 mmHg; 1: mean arterial pressure o70 mmHg;2: dopamine r5 mg/kg/min or dobutamine (any dose);3: dopamine 45 mg/kg/min or epinephrine r0.1 mg/kg/min

or norepinephrine r0.1 mg/kg/min; or 4: dopamine415 mg/kg/min or epinephrine 40.1 mg/kg/min or norepi-nephrine 4 0.1 mg/kg/min. A multivariable analysis wasperformed using a stepwise selection method. Variables with ap value of o0.1 and o0.05 by univariate analysis wereintroduced in the stepwise selection process for models 1 and2, respectively.Model 3 was created by introducing baseline estimated

glomerular filtration rate (eGFR) in model 2 to account forpreoperative renal function. Because of the assumption thatportal vein flow pulsatility is a predictor of AKI, portal flowmeasurements performed after the diagnosis of AKI werecensored and patients without portal flow measurements beforethe day of AKI diagnosis were excluded from univariate andmultivariate models. Secondary outcomes included the inci-dence of severe AKI (KDIGO stage Z2), in-hospital mortal-ity, and hospital length of stay. Predictive factors of portal veinflow pulsatility were identified using univariate regressionanalysis. The relationship between serum creatinine changeand fluid balance at 48 hours and 72 hours after the discoveryof portal vein flow pulsatility was assessed using a generalizedestimating equations model. Statistical analyses were per-formed with SAS 9.4 (SAS Institute Inc, Cary, NC), andp o 0.05 was considered statistically significant.

Results

Between May 2015 and February 2016, 135 consecutivepatients were considered for inclusion. Among them, 108patients had at least 1 assessment of portal vein flow during theweek after cardiac surgery. After exclusion of 6 patients(2 with CKD stage 5, 2 patients with cirrhosis, and 2 deathswithin 12 hours of surgery), 102 patients with 216 portal veinflow assessments were included in the study as shown inFigure 5. Significant portal vein flow pulsatility (PF Z50%)was found in 38 patients (37.3%) during the week followingsurgery. Patient characteristics in relation to the presence ofportal vein flow pulsatility after cardiac surgery are presentedin Table 1. Patients who developed portal vein flow pulsatility(PF Z50%) had a lower body mass index (BMI) and a higherproportion of urgent surgery compared with patients withoutportal vein flow pulsatility (PF o50%).The first portal vein flow assessment was performed less

than 12 hours after surgery in 75% of patients and within 36hours (end of POD 1) in 89.2% of patients. The mediannumber of ultrasound assessments of portal vein flow perpatient was 2 (IQR 1-3) and in patients with multipleassessments, 90% of examinations were done within 24 hoursof each other. Forty-eight patients had consecutive examsperformed on POD 0 and POD 1. Among those, 34 (71%)patients had a consistent result. In 11 patients (22%), portalflow was pulsatile during POD 0 and non-pulsatile duringPOD 1. In 3 patients (6.3%), portal flow pulsatility was absenton POD 0 but appeared on POD 1. Portal vein flow pulsatilitywas detected in 38 patients, within 36 hours of intensive careunit (ICU) admission in 33 patients (86.8%). For the remainingpatients (5 patients; 13.2%), portal vein flow pulsatility was

Fig 3. Pulse-wave Doppler waveform of a normal portal flow (PoVF) showingminimal variation during the cardiac cycle.

Fig 4. Pulse-wave Doppler waveform of a pulsatile portal flow (PF: 66%).

W. Beaubien-Souligny et al. / Journal of Cardiothoracic and Vascular Anesthesia ] (]]]]) ]]]–]]] 3


of daily medical record. AKI was defined according to theserum creatinine KDIGO criteria.20

Statistical Analyses

Descriptive data are presented as mean 7 standard devia-tion (SD) or median and interquartile range (IQR) andcompared using t test or Mann–Whitney U test, dependingon the distribution of data. Normality testing was performedby observing the distribution of data using the histogrammethod, comparing central distribution parameters (mean andmedian), and using the Shapiro–Wilk statistical test with a95% confidence level. Categorical variables are presented asfrequencies (percentages) and compared using the χ2 test.Potential predictors of AKI were identified using univariatelogistic regression analysis. Variables considered were predis-posing factors before surgery (age, context of surgery, renalfunction, diabetes, left ventricular ejection fraction, New YorkHeart Association functional class, EuroSCORE II,21 AKIprediction score by Thakar et al22), perioperative factors(procedure, cardiopulmonary bypass duration, fluid balance,administration of blood products and vasopressors), and post-operative factors (fluid balance, hemodynamic stability eval-uated by the cardiovascular component of the SequentialOrgan Function Assessment [SOFA] score23 during POD0 and 1, and cardiac index). The cardiovascular componentof the SOFA score is defined as the following: 0: mean arterialpressure Z70 mmHg; 1: mean arterial pressure o70 mmHg;2: dopamine r5 mg/kg/min or dobutamine (any dose);3: dopamine 45 mg/kg/min or epinephrine r0.1 mg/kg/min

or norepinephrine r0.1 mg/kg/min; or 4: dopamine415 mg/kg/min or epinephrine 40.1 mg/kg/min or norepi-nephrine 4 0.1 mg/kg/min. A multivariable analysis wasperformed using a stepwise selection method. Variables with ap value of o0.1 and o0.05 by univariate analysis wereintroduced in the stepwise selection process for models 1 and2, respectively.Model 3 was created by introducing baseline estimated

glomerular filtration rate (eGFR) in model 2 to account forpreoperative renal function. Because of the assumption thatportal vein flow pulsatility is a predictor of AKI, portal flowmeasurements performed after the diagnosis of AKI werecensored and patients without portal flow measurements beforethe day of AKI diagnosis were excluded from univariate andmultivariate models. Secondary outcomes included the inci-dence of severe AKI (KDIGO stage Z2), in-hospital mortal-ity, and hospital length of stay. Predictive factors of portal veinflow pulsatility were identified using univariate regressionanalysis. The relationship between serum creatinine changeand fluid balance at 48 hours and 72 hours after the discoveryof portal vein flow pulsatility was assessed using a generalizedestimating equations model. Statistical analyses were per-formed with SAS 9.4 (SAS Institute Inc, Cary, NC), andp o 0.05 was considered statistically significant.

Results

Between May 2015 and February 2016, 135 consecutivepatients were considered for inclusion. Among them, 108patients had at least 1 assessment of portal vein flow during theweek after cardiac surgery. After exclusion of 6 patients(2 with CKD stage 5, 2 patients with cirrhosis, and 2 deathswithin 12 hours of surgery), 102 patients with 216 portal veinflow assessments were included in the study as shown inFigure 5. Significant portal vein flow pulsatility (PF Z50%)was found in 38 patients (37.3%) during the week followingsurgery. Patient characteristics in relation to the presence ofportal vein flow pulsatility after cardiac surgery are presentedin Table 1. Patients who developed portal vein flow pulsatility(PF Z50%) had a lower body mass index (BMI) and a higherproportion of urgent surgery compared with patients withoutportal vein flow pulsatility (PF o50%).The first portal vein flow assessment was performed less

than 12 hours after surgery in 75% of patients and within 36hours (end of POD 1) in 89.2% of patients. The mediannumber of ultrasound assessments of portal vein flow perpatient was 2 (IQR 1-3) and in patients with multipleassessments, 90% of examinations were done within 24 hoursof each other. Forty-eight patients had consecutive examsperformed on POD 0 and POD 1. Among those, 34 (71%)patients had a consistent result. In 11 patients (22%), portalflow was pulsatile during POD 0 and non-pulsatile duringPOD 1. In 3 patients (6.3%), portal flow pulsatility was absenton POD 0 but appeared on POD 1. Portal vein flow pulsatilitywas detected in 38 patients, within 36 hours of intensive careunit (ICU) admission in 33 patients (86.8%). For the remainingpatients (5 patients; 13.2%), portal vein flow pulsatility was

Fig 3. Pulse-wave Doppler waveform of a normal portal flow (PoVF) showingminimal variation during the cardiac cycle.

Fig 4. Pulse-wave Doppler waveform of a pulsatile portal flow (PF: 66%).

W. Beaubien-Souligny et al. / Journal of Cardiothoracic and Vascular Anesthesia ] (]]]]) ]]]–]]] 3





Methods

Study Design



Definitions








- Pusatilidad: PF> 50%

- 102 pacientes.

- 38 pacientesà pulsatilidad

significativa (37,3%) en la

semana posterior a la cirugía.

- 60.8% desarrollaron AKI y

13.7% progresaron a AKI

severa

- La detección de la pulsatibilidad

del flujo portal se asoció con un

mayor riesgo de desarrollo de

LRA (odds ratio [OR] 4,31, intervalo de confianza [IC] 1,50-12,35, p 1/4 0,007).


PULSATILIDAD DE VENA PORTA Y AKI




Methods

Study Design



Definitions








- CONCLUSIONES:

- Asociación independiente entre la detección de la pulsatilidad del flujo de la vena porta (PF >50%) y la AKI posterior en su cohorte retrospectiva.

- La presencia de pulsatilidaddel flujo de la vena porta después de la cirugía cardíaca se asoció con un mayor balance de fluidos positivo.


RECOMENDACIONES

-Evaluar a los pacientes con LRA con prontitud.-Medir Cr sérica y producción de orina. Grado A2-Clasificar según gravedad. Grado A2.-Manejar según gravedad y causa.-Valorar ERC preexistente.-Valorar riesgo de desarrollar ERC.


MANEJO PERIOPERTORIO


MANEJO PERIOPERTORIO

• MANEJO DE LÍQUIDOS.• USO DE VASOCONSTRICTORES.• AGENTES NEFROTÓXICOS.• CONTROL GLUCÉMICO Y NUTRICIONAL.• INTERVENCIONES FARMACOLÓGICAS.• TERAPIA DE REEMPLAZO RENAL.


PREVENCIÓN Y TRATAMIENTO

Uso de cristaloides isotónicos ( expansión

volumen IV)

Grado 2B

Uso asociado de vasopresores, Noradrenalina.

Grado 2C

Terapia guiada por objetivos

hemodinámicos en pacientes de alto

riesgo.

Grado 2C

1. MANEJO DE FLUIDOS Y VASOPRESORES


REPOSICIÓN DE VOLUMEN INTRAOEPRATORIO

TAM < 55 mmHg ( 10 minutos) àñ LRA postoperatoria. TAM< 60 mmHg ( 20 minutos) àñ LRA postoperatoria.

¿Qué hacemos ? -Reposición volumen IV. -Uso de fármacos inotropos y vasopresores.


REPOSICIÓN DE VOLUMEN

1. Valorar si el paciente es respondedor.-Marcadores dinámicos precarga à VVS y VPP. -Ver si el paciente es respondedor a volumen.

¿Problema?-Acumulación de líquidoà edema intersticialàHipoperfusión renal – aumento presión tubular à LRA.


¿QUÉ RECOMIENDAN?

-Utilizar una terapia guiada por objetivos ( menor riesgo de LRA).

- Asociar vasopresores y/o inotropos, para disminuir la cantidad de líquido infundida.

- Cristaloides à SSF 0.9% / soluciones balanceadas - Albúmina à no aumenta la incidencia de LRA.



• Uso muy debatido, beneficios muy contradictorios• De elección: diuréticos del asa (manejo hiperpotasemia y

acidosis metabólica)• LRA oligúrica, tras reposición adecuada de volumen:

• Prueba de diuresis:• Furosemida 1mg/kg si previamente no recibÍa diurético o 1,5 mg/kg si

recibÍa diurético.• Si diuresis a las 2 h:

• < 200 cc-à escasa respuesta, NO SE RECOMIENDA SU USO. Alta probabilidad de TRR

• > 200 cc-à adecuada respuesta. Uso en bolos o perfusión (menor ototoxicidad)

DIURÉTICOS



• Uso muy debatido, beneficios muy contradictorios• De elección: diuréticos del asa (manejo hiperpotasemia y

acidosis metabólica)• LRA oligúrica, tras reposición adecuada de volumen:

• Prueba de diuresis:• Furosemida 1mg/kg si previamente no recibÍa diurético o 1,5 mg/kg si

recibÍa diurético.• Si diuresis a las 2 h:

• < 200 cc-à escasa respuesta, NO SE RECOMIENDA SU USO. Alta probabilidad de TRR

• > 200 cc-à adecuada respuesta. Uso en bolos o perfusión (menor ototoxicidad)

DIURÉTICOS

àNo usarlos como terapia preventiva de la LRA ( Grado 1B)àNo usarlos como tratamiento, excepto en el manejo de la

sobrecarga de volumen (Grado 2C).


PREVENCIÓN Y TRATAMIENTO 2.NUTRICIÓN Y CONTROL GLUCÉMICO.

Estudio de normoglucemiainternacional Pacientes críticos médicoquirurgicos

Grupo de tratamiento intensivo con insulina. Rango objetivoà 81-108 mg/dl

Grupo control. Rango objetivo à < 180 mg/dl

-Mortalidad a los 90 días 27,5% vs 24,9%. -Sin diferencias significativas en la incidencia de la TRR.



àADULTOS• LRA estadio 1 y 2:

• Aporte calórico 30-35 kcal/kg/día• Aporte proteico 1-1,4 g/kg/día

• LRA estadio 3:• Mismo aporte calórico• Aporte proteico:

• SIN DIALISIS: 0,8- 1 g/kg/día• TRR INTERMITENTE: 1,5

g/kg/dia• TRR CONTINUAS: 1,7 g/kg/día

à NIÑOS

• 100- 130% del gasto energético basal.

• Ecuación Caldwell- Kennedy:Gasto energético en reposo (kcal / kg / día) = 22 + 31,05 × peso (kg) + 1,16 × edad • TRR-Aporte calórico: 21-53 kcal/kg/día.-Aporte protéico: <1 año: 2,4 g/Kg/día1-13 años: 1,9 g/kg/día>13 años: 1,3 g/kg/día

2. NUTRICIÓN Y CONTROL GLUCÉMICO



-Glucemia plasmática: 110-149 mg/dl. (Grado 2C)-Ingesta calórica total 20-30 kcal/kg/día en adultos en cualquier etapa de la LRA.(Grado 2C).

-Evitar la restricción proteica con el objetivo de retrasar la TRR. -Administrar: 0.8-1 g/kg/día (LRA sin diálisis); 1-1,5 g/kg/día con un máximo de 1,7g/kg/día ( LRA con diálisis). (Grado 2D).

-Nutrición vía enteral (Grado 2C).

2. NUTRICIÓN Y CONTROL GLUCÉMICO:

RECOMENDACIONES


PREVENCIÓN Y TRATAMIENTO 4. VASODILATADORES:

-Dopaminaü No aporta ningún beneficio. ü Taquiarritmias e isquemia miocárdica, reducción del flujo sanguíneo

intestinal, hipopitituarismo y supresión de las células T. ü No usar dopamina a dosis bajas para prevenir o tratar la LRA (

Grado 1 A)-Fenoldopam (análogo de la dopamina, sin estimulación adrenérgica)ü No está aprobada su indicación. ü No usar como prevención o tratamiento de la LRA ( Grado 2C). -PAN.ü No está recomendado usarlo de forma preventiva (Grado 2C) ni para

tratar (Grado 2B) la LRA.


PREVENCIÓN Y TRATAMIENTO 5. OTRAS TERAPIAS FARMACOLÓGICAS.

-Se recomienda no usar factores recombinantes humanos, para tratar o prevenir la lesión renal aguda. ( Grado 1B).

-Se recomienda una sola dosis de teofilina, en recién nacidos con insuficiencia respiratoria grave con alto riesgo de LRA ( Grado 2B).

-Evitar AINES.


PREVENCIÓN Y TRATAMIENTO 6. EVITAR AGENTES NEFROTÓXICOS.

AMINOGLUCÓSIDOS

-Riesgo atribuible LRAà hasta 25% (evitar su uso si es posible) Grado 2 A.-Evitar la sobredosificación (Régimen diario de dosis única) Grado 2B.-Monitorizar niveles, si > 24h ( nivel mínimo, indetectable 18-24 horas) Grado 1 A.

*Tobramicina inhalada: Mejora los niveles intrapulmonares y disminuye la nefrotoxicidad ( menor [sistémica]) à Utilizar cuando sea factible. Grado 2B.

ANFOTERICINA B

-Usa soluciones lipídicas. Grado 2 A.-Micosis sistémicas y/o infecciones parasitariasà azoles/equinocandinas ( si igual eficacia) Grado 1 A.


LESIÓN RENAL AGUDA INDUCIDA POR CONTRASTE (CI-AKI)

DEFINICIÓN:

• Cambios en la función renal tras la administración de medios de contraste intravasculares.

• A la espera de validación de nuevos biomarcadores, se recomienda el uso de los mismos criterios (cambios en la concentración de Cr y producción de orina) que en las otras formas de AKI.


LESIÓN RENAL AGUDA INDUCIDA POR CONTRASTE (CI-AKI)• Evaluar el riesgo de CI-AKI.• Detectar el deterioro renal preexistente en todo paciente

que se vaya a someter a un procedimiento que requiera administración intravascular de contraste yodado.• Incremento de riesgo de CI-AKI si:

àCr > 1,3 mg/dl en hombresàCr> 1 mg/dl en mujeres

• Discutir riesgo – beneficio de prueba con contraste yodado con Radiología• La RNM con gadolinio como alternativa NO ES SEGURA

• Riesgo de fibrosis nefrogénica en pacientes con TFG < 30 ml/min


LESIÓN RENAL AGUDA INDUCIDA POR CONTRASTE (CI-AKI)

• Estrategias de prevención no farmacológicas.

• Usar dosis mas baja posible de contraste • Contraste yodado ISO-HIPOOSMOLAR> Hiperosmolar (grado 1 B)

Revisión de Goldfarb + metaanálisis de Barret y Carlisle

àRiesgo de CI-AKI similar con medios de contraste iso/hipo/hiperosmolaresen pacientes sanosàMedios de contraste hipoosmolares menos nefrotóxicos en pacientes con

deterioro de función renal preexistente


LESIÓN RENAL AGUDA INDUCIDA POR CONTRASTE (CI-AKI)• Estrategias de prevención farmacológicas

• Expansión de volumen con soluciones isotónicas (SF 0,9% o bicarbonato sódico). Grado 1A• Inicio 1 h antes y continuar 3-6 h tras administración de contraste

• No recomendada fluidoterapia oral de manera aislada (grado 1 C)• Uso de N-Acetil-Cisteina oral junto con cristaloides isotónicos iv

(grado 2 D)• No se recomienda el uso de teofilina (grado 2 C) ni fenoldopam (

grado 1 B)• No se recomienda el uso de TRR de manera profiláctica para

eliminación de los medios de contraste (grado 2C)


5. TRR en ERA. Timing• Pacientes estadio 3

• No recomendación de inicio temprano de TRR en estadio 2 de LRA, salvo situaciones especiales:

• Intoxicación por sustancias dializables.• Hiperpotasemia grave• Acidosis grave

• Inicio urgente: cambios potencialmente mortales en equilibrio hídroelectrolítico

• Uremia grave• Hiperpotasemia grave (> 6,5 mmol/L) o con cambios ECG• Acidosis metabólica grave (pH< 7,15 ó HCO3 < 12 mmol/L)• Oliguria con sobrecarga hídrica y compromiso pulmonar.• Oliguria/anuria > 24-48 h sin respuesta a tratamiento diurético.• Intoxicación sustancias dializables (metanol/ etilenglicol/litio/metformina)• HTA maligna refractaria a tratamiento médico.• Disnatremia aguda con compromiso cerebral sin respuesta a tratamiento

médico.


TRR en ERA. Timing

• Interrumpir TRR una vez alcanzado en objetivo por el que se empezó la terapia

• No se recomienda el uso de diuréticos para mejorar la recuperación de la función renal o para reducir la duración/frecuencia de TRR (grado 2B)


TRR en ERA. Tipo de terapias• No evidencia que soporte que tipo de TRR

(intermitente/continua) o con que frecuencia (diaria/interdiaria) mejore los desenlaces de mayor gravedad (mortalidad/ estancia UCI/ recuperación renal)

• Individualizar según características clínicas de cada paciente• Hemodinámicamente estable: HDI/SLED (6-12 h) • Hemodinámicamente inestable: Terapias continuas

• HDVVC (DIFUSIÓN, moléculas de pequeño tamaño < 500 D)• HFVVC (CONVECCIÓN, moléculas de tamaño medio)

• HDFVVC ( DIFUSIÓN + CONVECCIÓN, moléculas tamaño pequeño + grande > 1000D)

• SCUF (sobrecarga hídrica)


TRR en ERA. Dosis

• Evaluación frecuente de la dosis real administrada para reajuste de tratamiento (grado 1B)

• Dosis de tratamiento TRRC recomendada: 20 – 25 ml/kg/h (grado 1 A)

• Administrar una Kt/V de 3,9 por semana cuando se utilicen TRRI o SLED (grado 1 A)


TRR en ERA. Accesos vasculares• Catéter no tunelizado (grado 2D)

• Inserción ecoguiada (grado 1 A)

• Vías de acceso:• 1ª elección: vena yugular derecha• 2ª elección: vena femoral• 3ª elección: vena yugular izquierda• Última elección: vena subclavia, lado dominante


TRR en ERA. Anticoagulación

- Valorar beneficio- riesgo del uso de anticoagulación

- Uso UNICAMENTE en pacientes: (grado 1B)

- No aumento de riesgo de sangrado

- Coagulación normal- No reciben

anticoagulación sistémica


Para TRR intermitente: HNF/HBPM (grado 1 C)

Para la TRR continua:- Anticoagulación regional

con citrato (grado 2B)- SI contraindicación para

uso de citrato: HNF/HBPM (grado 2 C)


CONCLUSIONES

NEFROPROTECCIÓN: mejor tratamiento de LRA• Rápida administración de ATB en infecciones graves.• Mantener estado hemodinámico.• Hidratación adecuada, evitando balance hídrico positivo.• Uso racional de diuréticos.• Limitar uso de nefrotóxicos.• Monitorización periódica de función renal.

5 R: Risk Assessment, Recognition, Response, Renal support, Rehabilitation

VOLUME 2 | ISSUE 1 | MARCH 2012

http://www.kidney-international.org

OFFICIAL JOURNAL OF THE INTERNATIONAL SOCIETY OF NEPHROLOGY

KDIGO Clinical Practice Guideline for Acute Kidney Injury

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