Indicaciones y contraindicaciones de la sonda vesical y sonda nasogastrica.pptx
Lesión renal aguda
1. Lesión Renal Aguda
Ana María Santos Arrieta
Medico Interno
Hospital Universitario del Caribe
2. Definición
FALLA RENAL AGUDA
Tradicionalmente se ha definido como el cese
abrupto de la función renal que resulta en la
retención de urea y otros productos nitrogenados
y en la desregulación del volumen extracelular y
electrolitos.
Definition of acute kidney injury (acute renal failure). Updated: Aug 01, 2013.
3. Creatinina Sérica
No refleja la TFG
• En estadios tempranos de LRA puede ser
normal aun con una reducción marcada en la
TFG
Es removida mediante la diálisis
• Una vez iniciada las diálisis no es posible
evaluar la función renal mediante la creatinina, a
menos que esta se reduzca los días que no se
realicen diálisis
Diferentes valores de corte
Definition of acute kidney injury (acute renal failure). Updated: Aug 01, 2013.
4. Acute Dialysis Quality Initiative
ADQI
Risk
Injury
Failure
Loss
End Stage
Incremento de 1.5 veces, Disminución de TFG >25%
o Gasto urinario <0,5 cc/Kg/h por 6 horas
Incremento de 2 veces, Disminución de TFG >50% o
Gasto urinario <0,5 cc/Kg/h por 12 horas
Incremento de 3 veces, Disminución de TFG >75% o
Gasto urinario <0,3 cc/Kg/h por 24 horas o anuria por
12 horas
Perdida completa de la función renal (necesidad de
terapia de remplazo renal) por mas de 4 semanas
Perdida completa de la función renal (necesidad de
terapia de remplazo renal) por mas de 3 meses
2,4
4,1
6,3
Definition of acute kidney injury (acute renal failure). Updated: Aug 01, 2013.
5. Limitaciones de los Criterios ADQI
• Los cambios en el gasto urinario y creatinina en
el mismo estrato no se basan en la evidencia.
LA creatinina sérica es un fuerte predictor de
mortalidad en UCI.
• Los cambios en la creatinina sérica no se
correlacionan con el cambio en la TFG actual
• Es imposible calcular el cambio en los niveles
de creatinina sérica en pacientes que no tengan
una medición previa
Definition of acute kidney injury (acute renal failure). Updated: Aug 01, 2013.
6. Acute Kidney Injury Network
AKIN
Incremento abrupto (48 horas) en la
concentración de creatinina sérica de 0,3mg/dl
o >50%, o oliguria <0,5ml/kg/h por mas de 6
horas
Consideraciones:
▫ Los criterios diagnósticos se deben aplicar
solo después que se ha optimizado la volemia
▫ Se necesita excluir obstrucción del tracto
urinario si se utiliza la oliguria como criterio
Definition of acute kidney injury (acute renal failure). Updated: Aug 01, 2013.
8. KDINGO
Incremento absoluto de creatinina sérica >0,3 mg/dl en 48
horas
Incremento porcentual de creatinina >50% en 7 días
Gasto urinario <0,5mL/Kg/h por mas de 6 horas
Estadio 1
• Incremento de 1,5 a
1,9 veces o 0,3mg/dl o
gasto urinario
<0,5cc/Kg/h por 6-12
horas
Estadio 2
• Incremento de 2 a 2,9
veces o gasto urinario
<0,5mg/dl por 12
horas
Estadio 3
• Incremento de 3
veces o creatinina
>4mg/dl o gasto
urinario <0,3mL7Kg/h
por 24 horas o anuria
por 12 horas o
iniciación de TRR
Definition of acute kidney injury (acute renal failure). Updated: Aug 01, 2013.
9. Etiología
Múltiples etologías
• Hospitalizados
▫ Necrosis Tubular Aguda
▫ Exposición a nefrotoxinas
▫ Sepsis
• Hospitalizados o ambulatorios
▫ Disminución de la volemia
▫ Obstrucción urinaria
▫ Glomerulonefritis rápidamente progresiva
▫ Nefritis intersticial aguda
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
10. Categorización
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
11. Categorización
Prerrenal
• 60-70%
Renal
(Intrínseca)
• 20-30%
Posrrenal
• 10%
Diagnostic approach to the patient with acute kidney injury (acute renal failure) or chronic
kidney disease. Updated: Aug 14
12. LRA Prerrenal
1. Hipovolemia
Disminución TA
Disminución presión intraglomerular
Cese Filtración
2. Bajo GC FE del VI insuficiente (postcarga)
Precarga disminuida
3. Vasodilatación
Fracaso renal
Normotensive Ischemic Acute Renal Failure. NEJM 2007
17. Evaluación Inicial
CAUSAS
Electrolitos Gases arteriales BUN/Creatinina
Fosfato Calcio Albumina
COMPLICACIONES
HIPOTENSION
DEPLECION DE
VOLUMEN
OBSTRUCCION
HIPERKALEMIA
SOBRECARGA DE VOLUMEN
ACIDOSIS METABOLICA
HIPOCALCEMIA
HIPERFOSFATEMIA
HIPERURICEMIA
HIPERMAGNESEMIA
Acido úrico Magnesio Hemograma
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
18. ERC Vs LRA
ERC LRA
Inicio de los sintomas
Poco o Ninguno Gasto
Urinario
Imagenologicamente
riñones pequeños y con
Diagnostic approach to the patient with acute kidney injury (acute renal failure) or chronic
kidney disease. Updated: Aug 14
aumento de
ecogenicidad
Incremento diario de
creatinina
Anemia
NGAL
KIM-1
IL 18
20. Manejo
Sobrecarga de volumen
Hiperkalemia (>5,5mEq/L)
Signos de Uremia
Acidosis metabólica Severa
(pH<7,1)
DIALISIS
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
21. Manejo
MODIFICACIÓN DE LA DIETA:
• Ingestión calórica total de 35-50 Kcal/Kg/d
• Ingestión de sodio 2-4 g/d
• Ingestión de Fósforo se reduce a 800 mg/d
• Ingestión de potasio se restringe a 40 mEq/d
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
22. Manejo
DEPLECION DE VOLUMEN
Historia clínica de perdida de líquidos o examen físico concordante
con hipovolemia y/u oliguria = fluidoterapia intravenosa
La corrección de la depleción de la volemia puede prevenir o limitar
la lesión renal que lleva a necrosis tubular aguda
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
23. Manejo
Aumento de Volumen
Balance hídrico
positivo en pacientes
críticamente
enfermos, excesiva
fluidoterapia o
disfunción del VI
Los diuréticos se
utilizan como terapia
transitoria para aliviar
la hipervolemia.
Predilección por
diuréticos de asa que
proporcionan un
efecto natriuretico
importante.
Pacientes bajo terapia
diurética se les deben
monitorizar gasto
urinario, de no existir
un incremento se
deben utilizar terapias
adicionales como la
diálisis
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
24. Manejo
HIPERKALEMIA
Oliguria Catabolia
Daño Celular
Activo
Cambios EKG
Anormalidades
neuromasculares
• No se dializan hiperkalemia leve y LRA con
causa reversible, estos pacientes son tratados
con dieta, administración de volumen y cese de
IECA o ARA
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
25. Manejo
HIPERKALEMIA
• Disminución del aporte de potasio
• Intercambio de potasio en el tubo digestivo
utilizando resinas de unión a potasio
• Promover la entrada celular mediante
dextrosados, insulina y b-agonistas
• Dialisis
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
26. Manejo
ACIDOSIS
Excreción de Ácidos
Regeneración de
Bicarbonato
Inestabilidad hemodinámica relacionada con la disminución de
la contractilidad del VI, arritmias, vasodilatacion arterial y
venoconstriccion. Afecta la respuesta a catecolaminas.
Cetoacidosis y Lactato
• Tratamiento dependiente de la volemia
• Diálisis: LRA oligurica-Anurica, sobrecarga de
volumen y pH<7,1 independiente de la causa de
acidosis
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
27. Manejo
• Dopamina
▫ Receptores adrenergicos y dopaminergicos
▫ 0,5 a 3,0 ug/Kg/min
▫ Vasodilatación renal y estimulación cardiaca
• Fenoldopam
▫ Agonista selectivo del receptor dopaminergico
▫ Vasodilatador de rápida acción
▫ 6 veces mas potente que la dopamina
▫ Hipertensión severa
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
28. Manejo
DIALISIS
• Expansión de volumen que no cede a manejo
diurético
• Hiperkalemia refractaria
• Corrección de trastorno acido-base refractario a
terapia medica
• Azoemia severa (BUN>80-100)
• Uremia
Overview of the management of acute kidney injury (acute renal failure) . Updated: Mar 04, 2013.
Editor's Notes
Acute renal failure (ARF) has traditionally been defined as the abrupt loss of kidney function that results in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes. The loss of kidney function is most easily detected by measurement of the serum creatinine which is used to estimate the glomerular filtration rate (GFR).
Three problems are associated with the use of the serum creatinine to quantitatively define ARF:
Serum creatinine does not accurately reflect the GFR in a patient who is not in steady state. In the early stages of severe acute renal failure, the serum creatinine may be low even though the actual (not estimated) GFR is markedly reduced since there may not have been sufficient time for the creatinine to accumulate. (See "Assessment of kidney function".)
Creatinine is removed by dialysis. As a result, it is usually not possible to assess kidney function by measuring the serum creatinine once dialysis is initiated. One exception is when the serum creatinine continues to fall on days when hemodialysis is not performed, indicating recovery of renal function.
Numerous epidemiologic studies and clinical trials have used different cut-off values for serum creatinine to quantitatively define ARF [1].
Recognizing the need for a uniform definition for ARF, the ADQI group proposed a consensus graded definition, called the RIFLE criteria [4]. A modification of the RIFLE criteria was subsequently proposed by the Acute Kidney Injury Network
RIFLE CRITERIA — The RIFLE criteria consists of three graded levels of injury (Risk, Injury, and Failure) based upon either the magnitude of elevation in serum creatinine or urine output, and two outcome measures (Loss and End-stage renal disease). The RIFLE strata are as follows [4]:
Risk — 1.5-fold increase in the serum creatinine or GFR decrease by 25 percent or urine output <0.5 mL/kg per hour for six hours
Injury — Twofold increase in the serum creatinine or GFR decrease by 50 percent or urine output <0.5 mL/kg per hour for 12 hours
Failure — Threefold increase in the serum creatinine or GFR decrease by 75 percent or urine output of <0.3 mL/kg per hour for 24 hours, or anuria for 12 hours
Loss — Complete loss of kidney function (eg, need for renal replacement therapy) for more than four weeks
ESRD — Complete loss of kidney function (eg, need for renal replacement therapy) for more than three months
Limitations — There are several important shortcomings to the RIFLE criteria:
The "risk," "injury," and "failure" strata are defined by either changes in serum creatinine or urine output. The assignment of the corresponding changes in serum creatinine and changes in urine output to the same strata are NOT based on evidence. In the one assessment of the RIFLE classification that compared the serum creatinine and urine output criteria, the serum creatinine criteria were strong predictors of ICU mortality, whereas the urine output criteria did not independently predict mortality [12]. Thus, if the RIFLE classification is used to stratify risk, it is important that the criteria that result in the least favorable RIFLE strata be used [4].
As mentioned above, the change in serum creatinine during acute renal failure does not directly correlate with the actual change in glomerular filtration rate, which alters the assignment of that patient to a particular RIFLE level. As an example, in a patient with an abrupt decline in renal function in the setting of severe ARF, the serum creatinine might rise from 1.0 to 1.5 mg/dL (88.4 to 133 micromol/L) on day one, 2.5 mg/dL (221 micromol/L) on day two, and 3.5 mg/dL (309 micromol/L) on day three. According to the RIFLE criteria, the patient would progress from "risk" on day one to "injury" on day two and "failure" on day three, even though the actual GFR has been <10 mL/min over the entire period. This issue is intrinsic to any assessment of acute renal failure based upon the serum creatinine level.
Even among patients in steady state, the change in serum creatinine concentrations do not correlate with the percent decrease in GFR that is cited in the RIFLE classification; a 1.5-fold increase in serum creatinine corresponds to a 33 rather than 25 percent decrease in GFR [15].
It is impossible to calculate the change in serum creatinine in patients who present with ARF but without a baseline measurement of serum creatinine. The authors of the RIFLE criteria suggest back-calculating an estimated baseline serum creatinine concentration using the four-variable MDRD equation, assuming a baseline GFR of 75 mL/min per 1.73 m
2 [4]. However, this approach has been demonstrated to result in significant misclassification and is not recommended.
Diagnostic criteria — The proposed diagnostic criteria for ARF are an abrupt (within 48 hours) absolute increase in the serum creatinine concentration of =0.3mg/dL (26.4 micromol/L) from baseline, a percentage increase in the serum creatinine concentration of =50 percent, or oliguria of less than 0.5 mL/kg per hour for more than six hours (table 1).
The latter two of these criteria are identical to the RIFLE "risk" criteria. The addition of an absolute change in serum creatinine of =0.3 mg/dL is based on epidemiologic data that have demonstrated an 80 percent increase in mortality risk associated with changes in serum creatinine concentration of as little as 0.3 to 0.5 mg/dL [16]. Including a time constraint of 48 hours is based upon data that showed that poorer outcomes were associated with small changes in the creatinine when the rise in creatinine was observed within 24 to 48 hours
Two additional caveats were proposed by the AKIN group:
The diagnostic criteria should be applied only after volume status had been optimized.
Urinary tract obstruction needed to be excluded if oliguria was used as the sole diagnostic criterion.
A flaw with the last caveat is that, according to the current definition, AKI would still be used to describe the patient with acute urinary tract obstruction and an acute increase in serum creatinine. It is not clear whether the AKIN modifications to RIFLE have substantively changed the classification of patients with AKI or improved its ability to predict hospital mortality [19].
Staging system — The classification or staging system for ARF is comprised of three stages of increasing severity, which correspond to risk (stage 1), injury (stage 2), and failure (stage 3) of the RIFLE criteria. Loss and ESRD are removed from the staging system and defined as outcomes.
KDIGO MODIFICATIONS TO RIFLE AND AKIN — The KDIGO clinical practice guidelines included a revised definition of AKI while retaining the AKIN staging criteria [20]. In the KDIGO definition, the time frame for an absolute increase in serum creatinine of 0.3 mg/dL is retained from the AKIN definition (48 hours) while the time frame for a 50 percent increase in serum creatinine is the seven days, as originally suggested by the RIFLE criteria. The KDIGO criteria only utilize changes in serum creatinine and urine output ,and not changes in GFR for staging, with the exception of children under the age of 18 years, for whom an acute decrease in estimated GFR to <35 mL/min per 1.73m2 is included in the criteria for stage 3 AKI. As with the RIFLE and AKIN staging systems, patients should be classified according to criteria that result in the highest (ie, most severe) stage of injury. Using the KDIGO criteria, AKI is staged as follows:
Stage 1— 1.5 to 1.9 times baseline OR =0.3 mg/dL (=26.5 micromol/L) increase in the serum creatinine, OR urine output <0.5 mL/kg per hour for 6 to 12 hours.
Stage 2 — 2.0 to 2.9 times baseline increase in the serum creatinine OR urine output <0.5 mL/kg per hour for =12 hours.
Stage 3 — 3.0 times baseline increase in the serum creatinine OR increase in serum creatinine to =4.0 mg/dL (=353.6 micromol/L) OR urine output of <0.3mL/kg per hour for =24 hours, OR anuria for =12 hours OR the initiation of renal replacement therapy OR, in patients <18 years, decrease in estimated GFR to <35 mL/min per 1.73m
Among many patients, acute kidney injury (AKI) is mild and is manifested only by a transient increase in the serum creatinine or fall in urine output. However, AKI can cause life-threatening complications, even among those with relatively less-severe disease
All patients who present with AKI must be carefully evaluated both for reversible causes such as hypotension, volume depletion or obstruction, and for the presence of complications such as hyperkalemia and volume overload.
The patient with AKI is directed at determining the cause and identifying the complications that may require immediate attention.
The major complications of AKI include volume overload, hyperkalemia, metabolic acidosis, hypocalcemia, and hyperphosphatemia. With severe forms, mental status changes may be present. Hyperuricemia and hypermagnesemia may also occur. The initial assessment therefore should include the careful evaluation of volume status and measurement of serum electrolytes, particularly potassium and bicarbonate, and serum phosphate, calcium, and albumin. We also check serum uric acid, magnesium and a complete blood count.
Fluids may be either crystalloid or colloid. Crystalloid solutions, such as isotonic saline are preferred for initial therapy since studies have shown that colloid solutions provide no additional benefit and are more expensive. Potassium-containing crystalloid solutions, such as lactated Ringers solution, should be avoided since the kidney may not be able to excrete potassium and hyperkalemia may result. There continues to be much debate as to which intravenous fluid should be administered since large volumes of normal saline may result in hyperchloremic metabolic acidosis and a more pH-balanced solution may be of greater benefit
Fluids should be targeted to physiologic endpoints such as mean arterial pressure or urine output, or, among patients who in whom invasive monitoring is utilized, to dynamic changes in cardiac output. The optimal infusion rate varies depending on the clinical status and comorbidities of the patient. Overly aggressive volume repletion should be avoided as excessive volume expansion may lead to pulmonary congestion, especially in septic patients [3]. We suggest judicious administration beginning with one to three liters of fluid with careful and repeated clinical assessment to assess the patient's response to this therapy. In some cases additional fluid therapy may be necessary (severe burns, acute pancreatitis).
The total amount of administered volume depends upon the degree of volume depletion on presentation and on ongoing losses. The restoration of adequate urine flow and improvement in renal function with fluid resuscitation is consistent with a diagnosis of prerenal disease. Patients who do not respond to administered volume with an increase in urine output or decrease in the serum creatinine are unlikely to have prerenal disease and more likely to have established ATN or other forms of intrinsic AKI such as acute or rapidly progressive glomerulonephritis or acute interstitial nephritis. Some patients with relatively mild volume depletion may not have an obvious history of volume loss. In addition, less severe volume depletion is difficult to accurately detect on clinical examination especially in elderly patients. In this setting, AKI may still be reversed, at least in part, by fluid administration. Thus, in the absence of overt volume depletion, we frequently administer intravenous saline at a variable rate based upon clinical status. Although no consensus exists to guide therapy, among hemodynamically stable patients who do not have overt evidence of volume depletion, we administer 75 to 100 mL per hour. If this approach is undertaken, the patient's clinical status must be closely monitored to ensure that volume overload does not occur and that the rate of administration is sufficient to keep up with ongoing fluid losses. Once again, fluid therapy should be targeted to physiological endpoints.
Hypervolemia may be present upon initial evaluation or occur due to excessive fluid administration in the setting of impaired ability to excrete sodium and water. This is especially true for patients with sepsis who commonly receive aggressive intravenous fluid resuscitation.
Daily fluid balance is commonly positive in critically ill patients with ATN as a result of obligate fluid intake due to the administration of antibiotics, other intravenous medications, and nutritional support. This may result in progressive volume expansion and pulmonary edema, which may be especially poorly tolerated in patients with acute lung injury.
Less commonly, volume overload may result from primary left ventricular dysfunction and cause AKI, or type I cardiorenal syndrome.
Diuretics may be used to relieve hypervolemia among patients with AKI. However, we generally do not use diuretics for prolonged therapy to postpone the initiation of dialysis, since dialysis offers the most efficient method of volume removal in patients with AKI from any cause, and allows clinicians to optimize nutritional support and the use of intravenous medications. However, although several observational studies have demonstrated an association between the severity of volume overload at the time of initiation of dialysis [5-7], there are no studies that have demonstrated a benefit of early initiation of dialysis for volume management. If diuretics are used to treat volume overload, then the patient should be regularly assessed to see if urine output responds. If there is no increase in urine output then alternative therapies such as dialysis should be initiated. If diuretics are used as temporizing agents to relieve volume overload, loop diuretics are the preferred agents as they provide a greater natriuretic effect than thiazide diuretics. In patients who are refractory to high doses of loop diuretics, concomitant administration of a thiazide diuretic may achieve effective diuresis
