Page 1358 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 97: Acute Kidney Injury 931

dopamine (≤5 µg/kg of body weight per minute) with placebo or no Patients who develop AKI, particularly in the ICU, are at risk of
therapy, which included 3359 patients at risk for ATN, concluded that protein-energy malnutrition. This occurs due to a number of factors
was no benefit in terms of overall mortality, need for renal replacement including inadequate nutritional support, preexisting poor nutritional
therapy or adverse effects. Consequently, there is no evidence to support status, superimposed catabolic illnesses (sepsis, trauma, surgery, che-
the use of dopamine to prevent AKI. 159 motherapy, etc), acidosis, blood losses, and nutrient losses during extra-
corporeal circulation. Nutritional status is a major prognostic factor in
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Fenoldopam: Fenoldopam is an agonist of dopamine type-1 receptors. patients with AKI; severe protein-energy malnutrition is associated with
It has similar hemodynamic effects as low-dose dopamine without an increased risk of complications, increased length of stay and hospital
adrenoceptor stimulation. A meta-analysis of 13 studies evaluated the mortality. Carbohydrate metabolism in AKI is characterized by hyper-
160
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effects of fenoldopam on the need for renal replacement therapy and glycemia due to peripheral insulin resistance and accelerated hepatic
mortality following cardiovascular surgery. One thousand and fifty-nine gluconeogenesis. The optimal energy-to-nitrogen ration has not been
7
patients were included in the meta-analysis, ten of the studies included determined in AKI. In a randomized trial in AKI patients comparing
patients at high risk for requiring RRT based on their baseline creatinine 30 and 40 kcal/kg per day energy provision, the higher energy allowance
or the presence of comorbidities. Treatment with fenoldopam reduced was associated with more hyperglycemia, hypertriglyceridemia, and a
the need for renal replacement therapy (OR 0.37 [95% CI 0.23-0.59], more positive fluid balance. Consequently a total energy intake of
168
p < 0.001) and in-hospital death (OR 0.46 [95% CI 0.29-0.75], p = 0.01). 20 to 30 kcal/kg per day is recommended in patients with AKI. 7
However, this meta-analysis included early treatment, prevention, and The optimal amount of protein supplementation in AKI patients is
case-matched studies. An RCT of fenoldopam versus placebo to prevent unknown. The protein catabolic rate (PCR) in AKI varies from 1.4 to
RRT postcardiac surgery was completed in 2013 and results are awaited. 1.8 g/kg per day and an intake of at least 0.25 g of nitrogen per day is
A prospective double-blind randomised pilot trial of fenoldopam infu- required to achieve less negative or nearly positive nitrogen balance. It
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sion versus placebo was conducted in 300 septic patients without renal is important that nutrition is optimised in critically ill patients, includ-
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impairment. The treatment group had a lower rate of AKI (OR 0.47, ing administration of sufficient protein to maintain metabolic balance.
p = 0.005) and shorter ICU stay. There was no difference between the Protein restriction to prevent need for RRT in patients with AKI should
groups in incidence of severe AKI (creatinine >300 µmol/L), need for therefore be avoided. Loss of protein and amino acids through extra-
dialysis or death. Larger confirmatory studies are required to confirm corporeal circulation has been estimated at 5 to 10 g/d of protein and
this finding.
10 to 15 g amino acids per day. Such losses should be included in
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Growth Factors: Insulin-like growth factor (IGF) is an anabolic peptide daily protein supplementation up to a maximum of 1.7 g/kg per day in
with renal vasodilatory properties. In animal models of AKI, rhIGH-1 patients on CRRT. 166
has accelerated recovery of renal function. A number of small ran- Protein restriction should not be used to limit urea generation and
162
domised studies have examined the role of IGF-1 in the prevention and decrease the need for RRT initiation or dose in AKI patients. If azote-
treatment of AKI. One study randomised 54 patients to receive rhIGF-1 mia is worsened by aggressive protein nutrition in critically ill, hyper-
every 12 hours for 6 doses or placebo following abdominal aortic catabolic AKI patients, then RRT should be initiated or intensified to
surgery. The incidence of post-operative AI was 22% in the interven- control azotemia, rather than choosing to limit protein intake instead.
tion group compared to 33% in the control group. In a further study, If patients are unable to tolerate oral feed, enteral nutrition should be
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43 patients undergoing cadaveric transplant recipients were randomised instituted. Enteral nutrition in preferable to parenteral nutrition as deliv-
to receive rhIGF-1 or placebo. Patients were eligible if they were at ery of nutrients to the intestinal lumen helps maintain gut integrity. In
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high risk of developing delayed graft function with a GFR of <20 mL/min, general, feeds with lower K and Na concentrations are chosen. For the
+
+
as estimated by 2 hour posttransplant CrCl. There was no difference in patient who cannot tolerate enteral feeding, total parenteral nutrition
renal function at 7 days as measured by inulin clearance, or fractional (TPN) becomes necessary. Because of the volume of fluid required for
sodium excretion, urine flow or the nadir of serum creatinine after TPN, earlier institution of dialysis and ultrafiltration is often neces-
6 weeks or the proportion of patients requiring dialysis postoperatively. sary. A reasonable approach is to give sufficient calories to prevent
A multicenter study involving 72 patients with AKI were randomised negative nitrogen balance but not to overfeed patients to the point that
to receive either rhIGF-1 or placebo for up to 14 days. Sepsis and hepatic and platelet complications develop or that dialysis imposes
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hypovolemic shock were the commonest causes of AKI in both groups. additional risks.
There was no difference in mortality, need for RRT changes if GFR or The management of various electrolyte abnormalities often associ-
urine output. Consequently, despite promise in animal studies, there ated with AKI is described in greater detail in Chap. 99 and will only
is little supportive evidence for IGF-1 in the prevention or treatment be touched on here. Administration of excessive amounts of free water
of AKI. is the most common cause of hyponatremia in patients with AKI. Less
important causes of hyponatremia in this setting include water produc-
NONDIALYTIC SUPPORTIvE CARE tion from carbohydrate metabolism and water release from injured
tissue. Judicious fluid management will prevent any untoward com-
OF ACUTE RENAL FAILURE
plications from hyponatremia. Hyperkalemia is the most grave of the
When a diagnosis of intrinsic AKI has been firmly established and electrolyte perturbations that may complicate AKI. The clinical conse-
potentially reversible causes have been excluded or treated, the patient quences of hyperkalemia are largely confined to the cardiovascular and
is then monitored for early detection of complications. Conservative neuromuscular systems. The earliest hyperkalemic effects are manifest
measures consist of hospital observation with attention to blood pres- in the electrocardiogram (ECG). ECG changes are uniformly present
sure, volume status, neurologic function, and evidence of hemorrhagic above a potassium level of 8 mEq/L; below 7 mEq/L, changes may not be
or infectious complications. Electrolytes (Na , K , CI , HCO , Ca , evident. The treatment of hyperkalemia is summarized in Table 97-10.
2+
2−
+
+
−
3
and PO ), BUN, and creatinine should be monitored daily, although the Disturbances of divalent ion metabolism are common in AKI.
3−
4
hyperkalemic patient will require more frequent monitoring. Hyperphosphatemia is an almost universal accompaniment of oliguric
Fluid intake should be adjusted to replace urine and insensible losses, AKI. Acute severe hyperphosphatemia with symptomatic hypocalcemia
while Na and K are allowed in amounts to replace urine and GI losses. can be life-threatening. Hemodialysis may be required in patients with
+
+
Obviously, fluid and electrolyte restriction will be more substantial in symptomatic hypocalcemia, especially in the setting of AKI.
the oliguric patient. A small daily reduction in weight is expected in the Hypocalcemia is an expected complication of AKI but is generally
patient with AKI, but weight loss >1 kg daily indicates severe catabolism of no clinical significance and does not require intervention. However,
2+
or volume loss. On the other hand, it should be emphasized that mainte- severe depression of serum Ca may complicate rhabdomyolysis-
nance of weight or weight gain indicates volume expansion. induced AKI. Nevertheless, calcium salts are contraindicated except as
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