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 Table of Contents  
SYMPOSIUM
Year : 2018  |  Volume : 5  |  Issue : 2  |  Page : 60-63

Fluids in acute kidney injury


Consultant Pediatric Nephrologist, SRCC-NH Children's Hospital, Mumbai, Lilavati Hospital and Research Centre, Mumbai and Jupiter Hospital, Thane, India

Date of Submission27-Mar-2018
Date of Acceptance07-Apr-2018
Date of Web Publication30-Apr-2018

Correspondence Address:
Uma Ali
Consultant Pediatric Nephrologist, SRCC-NH Children's Hospital, Mumbai
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.21304/2018.0502.00375

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  Abstract 


Early restoration of euvolemia is the initial step in the management of critically ill children and is important for preventing acute kidney injury(AKI). Isotonic crystalloids are the preferred solutions for fluid resuscitation. Repeated boluses of normal saline may lead to hyperchloremia, renal vasoconstriction and renal injury. Balanced solutions have a physiological advantage and there is evidence to suggest that resuscitation with balanced solutions may be associated with lower incidence of AKI. Synthetic colloids such as starches cause renal injury and should be avoided. Albumin can be used judiciously along with crystalloids to limit fluid overload. Fluid resuscitation alone prevents AKI only in 50% of the critically ill patients. Fluid overload as well as rapid fluid administration may adversely affect the kidney through injury to the glycocalyx. It may lead to intrarenal edema and a compartment-like syndrome compromising renal perfusion. Repeat fluid bolus should only be given when there is evidence of ongoing hypoperfusion and the bedside hemodynamic assessment suggests fluid responsiveness, provided the patient is not at high risk for fluid overload. Moderate fluid resuscitation combined with pressors may restore renal perfusion better than fluids alone. In established AKI, diuretics have a limited role. Timely institution of renal replacement therapy leads to optimum fluid management. Overzealous fluid removal should be avoided to prevent hypovolemia and recurrent renal injury.

Keywords: crystalloids, colloids, balanced solutions, diuretics


How to cite this article:
Ali U. Fluids in acute kidney injury. J Pediatr Crit Care 2018;5:60-3

How to cite this URL:
Ali U. Fluids in acute kidney injury. J Pediatr Crit Care [serial online] 2018 [cited 2020 Mar 29];5:60-3. Available from: http://www.jpcc.org.in/text.asp?2018/5/2/60/281122



Fluid administration plays a central role in achieving hemodynamic stability in critically ill children as well as in the prevention and the management of acute kidney injury (AKI). The quantity and rate of fluid administered as well as the type of fluid given to prevent AKI has been the subject of several past and recent studies as well as a matter of considerable debate.

Prevention of AKI

How much fluid should be administered?

Fluid administration to correct prerenal failure and prevent its progression to intrinsic AKI has been an effective strategy when administered to patients with overt dehydration as in patients with diarrheal diseases. Its effectiveness is less clear when it is applied to children with critical illness such as sepsis where the pathophysiology of the AKI is far more complex. Although fluid resuscitation forms the cornerstone of the management of hemodynamic instability, restoration of volume may not always restore renal perfusion as it does not address the issues of systemic vasodilatation and issues beyond hemodynamics such as microvascular inflammation. It is therefore not surprising that fluid administration in critical illness prevents AKI in not more than 50% of the patients.[1]

The surviving sepsis guidelines recommends that at least 30 ml per kg of an isotonic crystalloid solution should be given within the first three hours in patients with sepsis associated hypoperfusion.[2] However, many critically ill children do not achieve hemodynamic stability with this initial therapy. To avoid the well-known ill effects of fluid overload, additional fluid challenge should be given only when hemodynamic assessment suggests fluid responsiveness.

Recognizing hypovolemia in a child who is not overtly dehydrated is a major clinical challenge. Static indices such as central venous pressure are poor indices of volume adequacy. Dynamic indices that capture the volume-exaggerated cardiorespiratory interactions such as pulse pressure variation and systolic pressure variation are better indicators of the volume status than static indices in mechanically ventilated patients. However, they are reliable only when strict conditions are met. Respiratory variations in inferior vena cava (IVC) diameter has similar restrictions.[3] A judicious assessment of the clinical status combined with ultrasound detected respiratory variations in the IVC diameter, functional echocardiography and lung ultrasound may help to decide whether fluids can be given safely or should be withheld. However, it does not tell us whether the child will respond to the administered fluid.

The increase in left ventricular output in response to passive leg raising in a spontaneously breathing patient or to end expiratory occlusion in a mechanically ventilated patient are good predictors of fluid responsiveness. The responsiveness however must be documented by measurement of cardiac output or aortic blood flow and not by observed blood pressure changes.[3]

There is no single, universally reliable bedside marker of fluid adequacy or responsiveness. The tests are complementary and should be chosen based on the physiological restrictions as well as the available measurement of cardiac output. Fluid responsiveness is not in itself an indication for fluid administration. Fluid should be given to a fluid responsive patient only if there is evidence of hypoperfusion and in the absence of high risk for fluid overload.

Which fluid to give?

Traditionally, for more than 50 years, normal saline has been the mainstay of resuscitation fluid. However, normal saline is neither normal nor physiological. It has an unphysiologically acidic pH of 5.4 and a sodium to chloride ratio of 1:1 when compared to plasma which has a ratio of 1.4:1. Repeated boluses of normal saline lead to hyperchloremia and metabolic acidosis. Hyperchloremia is known to cause renal vasoconstriction and has been shown to cause renal injury and AKI in animal studies and in several observational studies in humans. The metabolic acidosis may be misinterpreted to reflect under resuscitation and lead to erroneous administration of more saline.[4]

The alternative to normal saline is to use solutions that resemble plasma more closely in electrolyte composition. These are labelled as balanced solutions. The ideal balanced solution would have bicarbonate in addition to chloride to mimic plasma electrolyte composition. However, bicarbonate is relatively insoluble, has a poor shelf life and hence is not commercially available. The commercially available anions in so called balanced solutions are either lactate or acetate. Lactate is metabolized by the liver and in the presence of liver dysfunction or poor perfusion may not get converted to bicarbonate and may worsen the acidosis. Acetate is converted by both liver and muscle and is likely to be handled better. All balanced solutions also contain potassium. While this does not alter serum potassium levels when given in maintenance volumes, large volumes given for resuscitation in the face of already existing unrecognized AKI could lead to hyperkalaemia.[4],[5] Despite the favourable physiology, the SPLIT study, a randomized controlled trial (RCT) comparing saline vs balanced solutions failed to show a benefit of balanced solutions in reducing mortality, development of AKI or the need for renal replacement therapy (RRT).[6] However, the recent SMART study, a large RCT in critically ill adults showed that patients who received balanced solutions had lower mortality, lesser need for RRT and less rates of persistent renal dysfunction.[7]

Colloids versus crystalloids

Crystalloids have remained the mainstay of therapy due to their ease of availability, safety, and low cost. Their main disadvantage is their short stay in the intravascular compartment as they move out rapidly in the interstitial space. One hour after administration of 1 litre of normal saline only 250ml remains in the vascular compartment. This may be even less in the presence of capillary leak.

Colloids have attracted attention because of their higher oncotic pressure generating an expectation that they will remain longer in the intravascular compartment and draw in the interstitial fluid into the vasculature. A large systematic review of 42 RCTs involving 11399 adults showed a 59% increased risk of AKI , and a 32% increased need for RRT when hydroxy ethyl starch was used as resuscitaton fluid when compared to other fluids used for resuscitation and hence is not recommended.[8] Albumin when compared to saline has shown to be comparable but not superior in its efficacy and safety.[9],[10] The judicious use of albumin may help to limit the volume of crystalloids used in resuscitation and limit fluid overload.

Fluid overload

Whereas fluid resuscitation is essential, more is not always better. The challenge lies not only in giving timely adequate fluids but also in knowing when to stop. Fluid overload has been shown unequivocally to adversely affect the mortality, both in adults and in children.[11] Besides its effect on mortality it can adversely impact renal function through its effect on the lungs, the heart and the kidney itself. The adverse effects of fluid overload on the lungs is well known and may lead to the need for higher pressures on ventilator, longer duration of ventilation all of which may also cause AKI. Fluid overload also adversely impacts cardiac function. Cardiac dilatation secondary to volume overload causes ventricular wall stress, tricuspid insufficiency increases pulmonary pressures and diastolic dysfunction. Cardiac dysfunction is associated with delayed recovery from AKI.[11]

The kidney is an encapsulated organ and is acutely sensitive to fluid overload. Impairment of venous outflow due to increased abdominal pressure due to capillary leak or due to high intravascular volume and pressures impedes renal venous flow causing intrarenal venous congestion and interstitial renal edema that compromises renal blood flow and filtration akin to a compartment syndrome.[11],[12]

Effect of fluid overload on microvasculature. The aim of restoring global hemodynamics is to improve microcirculation and oxygen delivery to tissues. The integrity of the vasculature is maintained by a layer of glycoproteins that protects the vascular endothelium from injury. Disruption ofthis glycocalyx layer leads to capillary leak of fluids and proteins in the interstium which characterizes sepsis states. Large saline boluses may injure the glycocalyx directly. In addition, rapid fluid administration generates the release of atrial natriuretic peptide that is injurious to the glycocalyx.

Excessive crystalloid administration leads to interstitial fluid accumulation that increases the diffusion distance for oxygen from the capillaries to the tissues. Haemodilution with a large amount of crystalloid with low O2 carrying capacity reduces the oxygen carrying capacity in the capillaries and may worsen tissue hypoxia despite apparently normal hemodynamics.[12]

Non-invasive evaluation of the microcirculation to see regional hemodynamics and assessing tissue oxygenation in the kidneys may be important in evaluating the impact of fluid administration on the prevention of organ dysfunction and AKI. Moderate fluid administration along with the use of pressors may be more effective in restoring renal perfusion than giving fluids alone.[13]

Fluids in established AKI

Impairment of renal function poses a serious threat to the internal milieu and transfers the burden of maintaining fluid homeostasis to the disoriented physician who is a poor substitute for the highly organized renal tubule. The volume of fluid administered is generally equal to the insensible water losses plus the urine output. Patients who are ventilated and sedated may have negligible insensible water losses. Their fluid requirement would equal their urine output. Polyuric AKI will need more than normal fluid for maintenance equal to the urine output in volume and composition.

Fluid should preferably be given orally or enterally and should be incorporated in the nutrition of the patient. When enteral fluid is not feasible intravenous fluids may be given. In a child who has severe oliguria and is not yet on RRT, electrolyte free fluid is given. Where there is a moderate urine output, half normal saline may be given. Colloids, blood and blood products should be avoided in oliguric children who are not yet on RRT as they may increase blood pressure or cause respiratory distress due to pulmonary edema. Critically ill children with oliguric AKI cannot be manged without RRT as their needs for antibiotics, inotropes, nutrition, and blood products may greatly exceed the amount of fluid calculated based on urine output. However, overzealous fluid removal should be avoided to prevent hypovolemia and recurrent renal injury.

Diuretics in established AKI

The primary role of diuretics in an evolving AKI has been to kick start the urine output after volume repletion. In critical illness it may be safer as well as more effective to use furosemide infusions rather than bolus doses. A brisk and sustained urinary output response to furosemide at the early stage of AKI may indicate the presence of a mild AKI. As such, furosemide can be useful for reducing the severity of hyperkalaemia, acidosis, and fluid overload in mild AKI. However, the diuretic infusion should not be overstretched in a desperate attempt to avoid RRT. Diuretics do not prevent AKI, do not reduce the risk of RRT or improve outcomes.[13] In conclusion, we do not yet know the right amount, rate of administration or type of fluid to be given to a child with hemodynamic instability to prevent AKI. Adequacy of global hemodynamic markers does not always translate into adequate microcirculation, tissue perfusion and oxygenation. Monitoring of microcirculation at the bedside to assess response to fluid administration may be a good physiological marker.

The right type of fluid is not yet there. It will probably be an artificial blood substitute, isotonic, balanced, remaining only in the vascular compartment with good oxygen carrying capacity without the risks of infections and antigen exposure associated with blood transfusion. Until then avoiding fluid overload by limiting the volume and rate of fluid administration remains more important than the type of fluid used to prevent AKI.

Source of Funding - Nil

Conflict of Interest - Nil



 
  References Top

1.
Marik PE, Cavallazzi R, Vasu T, Hirani A: Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med 2009; 37: 2642-47.   Back to cited text no. 1
    
2.
Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R et al; Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock Critical Care Medicine. 2017; 45(3):486-552.  Back to cited text no. 2
    
3.
Monnet X, Marik PE, Teboul JL. Prediction of fluid responsiveness: an update Ann Intensive Care. 2016;6:111-22.  Back to cited text no. 3
    
4.
Ince C, Groeneveld A B J; The case for 0.9% NaCl: is the undefendable, defensible? Kidney International 2014; 86:1087-95.  Back to cited text no. 4
    
5.
Godin M, Bouchard J, Mehta RL. Fluid Balance in Patients with Acute Kidney Injury: Emerging Concepts. Nephron Clin Pract 2013; 123:238-45.  Back to cited text no. 5
    
6.
Young P, Bailey M, Beasley R, Henderson S, Mackle D, McArthur C, et al. Effect of a buffered crystalloid solution vs saline on acute kidney injury among patients in the intensive care unit: the SPLIT randomized clinical trial. JAMA 2015; 7:1-10.  Back to cited text no. 6
    
7.
Semler MW, Self WH, Wanderer JP, Ehrenfeld J M, Wang L, Byrne DW, Stollings JL et al; for the SMART Investigators and the Pragmatic Critical Care Research Group* Balanced; Crystalloids versus Saline in Critically Ill Adults N Engl J Med 2018; 378:829-39.  Back to cited text no. 7
    
8.
Mutter TC, Ruth CA, Dart AB. Hydroxy ethyl starch (HES) versus other fluid therapies: effects on kidney function. Cochrane Database Syst Rev. 2013; 23.  Back to cited text no. 8
    
9.
Mutter TC, Ruth CA,Dart AB.Hydroxy ethyl starch (HES) versus other fluid therapies: effects on kidney function 2013; Issue 7. Art. No.: CD007594. DOI: 10.1002/14651858. CD007594.pub3.  Back to cited text no. 9
    
10.
Finfer S, McEvoy S, Bellomo R, McArthur C, Myburgh J, Norton R. SAFE Study Investigators, Impact of albumin compared to saline on organ function and mortality of patients with severe sepsis. Intensive Care Med 2011; 37:86-96  Back to cited text no. 10
    
11.
Caironi P, Tognoni G, Masson S, Fumagalli R, Pesenti A, Romero M, ALBIOS Study Investigators, et al. Albumin replacement in patients with severe sepsis or septic shock. N Engl J Med 2014; 370:1412-21.  Back to cited text no. 11
    
12.
Schreier RW. Fluid administration in critically ill patients with acute kidney injury Clin J Am Soc Nephrol 2010; 5:733-39.  Back to cited text no. 12
    
13.
Prowle JR. Clinical review. Volume of fluid resuscitation and the incidence of acute kidney injury-a systematic review. Crit Care 2012; 16: 230-45.  Back to cited text no. 13
    
14.
Ho KM, Power BM; Benefits and risks of furosemide in acute kidney injury. Anaesthesia 2010; 65 (3): 283-93.  Back to cited text no. 14
    




 

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