Symposium On PICU Protocols Of AIIMS

The Indian Journal of Pediatrics

June 2011, Volume 78, Issue 6, pp 718-725
First online: 17 December 2010

Management of Acute Renal Failure in the

Pediatric Intensive Care Unit

Ashima Gulati
, Arvind Bagga
10.1007/s12098-010-0306-8
Copyright information

Abstract
Pediatric acute renal failure (ARF) is a dynamic entity that has many causes. ARF is frequently seen in the
pediatric population and is associated with increased mortality and long-term morbidity rates. Of importance
is its early detection so as to allow interventions to either prevent or treat the disease timely during its
course. Recent developments in the definitions and classification schemes and the identification of new
biomarkers shall allow better predictive interventions for childhood ARF. ARF management in children
requires special considerations. Optimal care for the pediatric patient requiring renal replacement therapy
requires an understanding of the causes and patterns of pediatric ARF and recognition of the local expertise
with respect to the personnel and equipment resources. The aim of this article is to review pediatric ARF
management with an emphasis on emerging practice patterns and the modalities for renal replacement
therapy.
Keywords
Critically ill children Acute kidney injury Mortality

Introduction
Acute renal failure (ARF)/acute kidney injury (AKI) is a complex disorder having several etiologies and
occurs in a variety of settings with clinical features ranging from mild elevation of serum creatinine to
anuric renal failure [1]. ARF is a common complication in critically ill patients, affecting up to 3040% of
pediatric intensive care unit (PICU) admissions, and is associated with high mortality rates of 4050%
[2, 3]. ARF, severe enough to require renal replacement therapy (RRT), occurs in approximately 5% of
PICU patients [46]. This proportion may vary according to the PICU cohort described, e.g. cardiac surgery
versus medical ICU. Acute renal failure in the PICU frequently occurs as part of multiple organ failure [7].
In most instances, an acute decline in kidney function is secondary to tubular injury that leads to a
functional or structural change in the kidney.

Pre-Renal and Renalazotemia

The etiology of ARF has conventionally been classified as prerenal, intrinsic renal or postrenal. Prerenal
failure occurs due to inadequate systemic and/or renal circulation, due to either systemic hypovolemia or
renal hypoperfusion. The term pre-renal is used to emphasize the fact that there is no parenchymal
disease (e.g. glomerulonephritis or interstitial nephropathy) that is responsible for the decline in renal
function. However, pre-renal azotemia is a clinical entity which often progresses to become a
histopathological entity like acute tubular necrosis (ATN). It is often difficult to differentiate between prerenal and renal azotemia and more importantly to recognize the progression of pre-renal AKI to
structuralAKI or ATN.

The clinical usefulness of being able to accurately classify AKI into these two types is the implication for
fluid therapy and initiation of RRT. Prerenal failure is reversible if treated promptly. If hypovolemia
persists, sustained renal hypoperfusion results in ATN. The decision often relies on clinical judgment,
although urinary and blood indices might be useful (Table 1).
Table 1
Indices to differentiate prerenal azotemia from intrinsic renal failure

Pre-renal azotemia

Intrinsic Renal failure

Urinary sodium (mEq/L)

<20

>40

Urinary osmolality (mOsm/kg)

>500

<300

Blood urea-creatinine ratio

>20

<20

Urine-plasma osmolality ratio

>1.5

<1.0

Fractional excretion of sodiuma (%)

<l

>3

FeNa (%) = urine sodium x serum creatinine x 100

serum sodium x urine creatinine

The Concept of Acute Kidney Injury and the RIFLE Criteria

The term Acute renal failure (ARF) characterizes an abrupt and sustained decrease in kidney function.
There is a marked heterogeneity in the definition of ARF, with ensuing inability to compare data from
different centers and regions. Recognizing the need for uniform standards, the Acute Dialysis Quality
Initiative (ADQI) group in 2002 proposed consensus recommendations, the RIFLE criteria (acronym
for risk,injury, failure, loss and end stage renal disease) for the definition and staging of ARF [8]. In
September 2005, this group and representatives from nephrology and critical care societies formed the
Acute Kidney Injury Network and proposed the term acute kidney injury (AKI) to represent the spectrum of
acute renal dysfunction ranging from mild elevation in serum creatinine to severe forms requiring renal
replacement therapy [9]. The network also attempted to develop consensus on diagnostic criteria and staging
of AKI.

Definition and Staging of AKI

AKI is considered to be present when there is an abrupt (within 48-hr) reduction in kidney function, defined
as an absolute increase in serum creatinine of either 0.3 mg/dl or a percentage increase of
50% orreduction in urine output (documented oliguria of <0.5 ml/kg/hr for >6-hr) [9]. These criteria
include both an absolute and a percentage change in creatinine to accommodate variations related to age,
gender and body mass index and reduce the need for a baseline level of serum creatinine. It is however
necessary that the diagnosis be made following estimation of at least two creatinine values within 48-hr. If
the diagnosis of AKI is based on the urine output criterion alone, urinary tract obstruction and other
reversible causes of oliguria (hydration status and diuretic use), should be excluded.
Patients meeting the definition of AKI can be staged from stage 1 to 3 (Table 2). The new staging system
corresponds to the RIFLE stages. While the risk category has the same criteria as for stage 1 AKI, those
who are classified as having 'injury' and 'failure' match to stage 2 and 3 respectively. 'Loss' and 'end-stage

kidney disease' categories were removed from the staging system, since they represent outcomes. Given the
variability in indications and resources for commencing renal replacement therapy, patients receiving such
therapy are classified as stage 3 AKI.
Table 2
Staging of acute kidney injury [9]

Stage

Serum creatinine criteria

Urine output criteria

Increase in serum creatinine of 0.3 mg/dl or 150% to

200% (1.5- to 2-fold) from baseline

Less than 0.5 ml/kg per

hour for >6-hr

Increase in serum creatinine to more than 200% to 300%

(>2- to 3-fold) from baseline

Less than 0.5 ml/kg per

hour for >12-hr

3a

Increase in serum creatinine to more than 300% (>3-fold)

from baseline (or serum creatinine of 4.0 mg/dl with acute
increase of 0.5 mg/dl)

Less than 0.3 ml/kg per

hour for 24-hr, or anuria
for 12-hr

Only one criterion (creatinine or urine output) should be fulfilled to qualify for a stage
a

Patients receiving renal replacement therapy (RRT) are considered in stage 3

Etiology
The chief causes of ARF in children in developing countries include acute tubular necrosis secondary to
hypovolemia, sepsis and nephrotoxic agents, acute glomerulonephritis and hemolytic uremic syndrome
(Table 3). ARF related to overwhelming sepsis or following major surgery (especially cardiac) is common
in hospitalized children. Diarrhea associated hemolytic uremic syndrome (HUS) is an important cause of
intrinsic renal failure in young children in south Asia, though reduced incidence of dysentery and its
appropriate management has resulted in its decline during the last few years. Acute glomerulonephritis (GN)
is a significant cause of ARF in older children [10]. While appropriate use of antibiotics has resulted in
decline of post streptococcal GN, other infections may result in a similar clinical syndrome [11, 12]. ATN
due to snakebite and leptospirosis is frequent in coastal areas of Orissa, Tamilnadu and Kerala. Acute
intravascular hemolysis following exposure to oxidant drugs in G-6PD deficient subjects and falciparum
malaria is important in certain regions. Epidemics of severe ARF from diethylene glycol-contaminated
glycerine, used to manufacture expectorants and antipyretics, have occasionally been reported. Hantavirus
related hemorrhagic illness is important in Korea and China and has recently been reported from parts of
Europe.
Table 3
Important causes of acute renal failure

Prerenal failure
Hypovolemia (dehydration, blood loss, diabetic ketoacidosis)
Third space losses (septicemia, nephrotic syndrome)
Congestive heart failure

Perinatal asphyxia
Drugs (ACE inhibitors, NSAIDs, diuretics)
Intrinsic renal failure
Acute tubular necrosis
Prolonged prerenal insult (see above)
Medications: aminoglycoside, radiocontrast, NSAIDs
Exogenous toxins: diethylene glycol, methanol
Intravascular hemolysis, hemoglobinuria
Tumor lysis syndrome
Hemolytic uremic syndrome: diarrhea associated (D+) and atypical (D-) forms
Glomerulonephritis (GN)
Postinfectious GN
Systemic disorders: SLE, Henoch Schonlein syndrome, microscopic polyangiitis
Membranoproliferative GN
Interstitial nephritis (drug-induced, idiopathic)
Bilateral renal vessel occlusion (arterial, venous)
Postrenal failure
Posterior urethral valves, urethral stricture
Bilateral pelviureteric junction obstruction
Ureteral obstruction (stenosis, stone, ureterocele)

Neurogenic bladder
ACE Angiotensin converting enzyme, NSAIDs Non-steroidal anti-inflammatory drugs, SLE Systemic lupus erythematosus

Evaluation
A careful history provides useful clues to underlying cause of ARF. Conditions resulting in decreased
intravascular volume are associated with oliguria and prerenal failure. In a child having oligoanuria, it is
important to assess for prerenal factors that lead to renal hypoperfusion. A history of diarrhea, vomiting,
fluid or blood loss should be sought and an assessment of fluid intake in the previous 24 h made.
In prerenal ARF, renal blood flow and glomerular filtration rate decline, but tubular reabsorption of salt and
water continues. Thus, there is oliguria with low urine sodium, high urine osmolality, increased blood urea
to creatinine ratio and low fractional excretion of sodium. The rise in blood urea to creatinine ratio occurs
because oliguria with decreased tubular flow results in greatly increased urea reabsorption while that of
creatinine is not affected. The level of blood urea and urea to creatinine ratio is also elevated when there is
increased urea production (e.g., due to excessive breakdown, infections or high-dose steroid therapy). ATN
is characterized by diminished tubular function with high urine sodium and dilute urine. Of the several
indices (Table 1) that differentiate prerenal from established renal failure, fractional excretion of sodium is
the most sensitive and reliable. These indices are, however, not useful in patients with non-oliguric renal
failure and those receiving diuretics.
In prerenal ARF, expansion of the intravascular volume leads to improved renal perfusion and increase in
urine output. Dehydration is corrected by infusion of 2030 ml/kg of isotonic saline or Ringers lactate over
3045 min. During this period, the child's vital signs are monitored and care taken to avoid overhydration.
Central venous pressure (CVP) should be measured to determine the adequacy of fluid replacement if
clinical assessment of hypovolemia is difficult. If urine output increases and CVP is still low, infusion may
be continued. Once fluid replacement is accomplished, frusemide (2-3 mg/kg) may be given intravenously.
This should normally induce diuresis (urine flow of 24 ml/kg over the next 2-3 h if renal tubular function is
intact). If these measures fail to induce diuresis, a diagnosis of intrinsic ARF is made. Investigations
(Table 4) are aimed at identifying complications of ARF and the underlying etiology. Regular monitoring of
electrolytes, urea and creatinine is important.
Table 4
Investigations in patients with acute renal failure

Blood
Complete blood counts
Urea, creatinine, sodium, potassium, calcium, phosphate, pH, bicarbonate
Urine
Urinalysis; culture
Sodium, osmolality, fractional excretion of sodium
Chest X-ray (for fluid overload, cardiomegaly)

Abdominal ultrasonography (identify urinary tract dilatation, obstruction)

Investigations to determine cause
Peripheral smear examination, platelet and reticulocyte count, complement (C3), LDH levels; stool
culture (suspected hemolytic uremic syndrome)
Blood ASO, C3, antinuclear antibody, antineutrophil cytoplasmic antibody (suspected acute or
rapidly progressive GN)
Doppler ultrasonography (suspected arterial or venous thrombosis)
Renal biopsy (specific diagnosis feasible)

Kidney Biopsy
A kidney biopsy is not required in most patients with ARF and is rarely necessary in the first 2 weeks of
illness. A biopsy is indicated if the following conditions are suspected: Rapidly progressive GN; Nonresolving acute GN; Interstitial nephritis; Patients with a clinical diagnosis of ATN or HUS if significant
renal dysfunction persists beyond 2-3 weeks or; Patients with ARF where the underlying cause is not
apparent on clinical features and investigations.
Patients with severe azotemia (blood urea >150200 mg/dL, creatinine >3-4 mg/dL) are at risk of bleeding
following renal biopsy. These patients should be dialyzed, either peritoneally or by hemodialysis, to reduce
the severity of azotemia. Hypertension should be adequately controlled; platelet count and bleeding, clotting
and prothrombin time should be normal. Intravenous (0.3 g/kg) or nasal (2-3 g/kg) desmopressin,
administered 6090 min prior to the procedure, is useful in reducing the risk of bleeding.

Management
Treatment of Complications
Immediate attention should be directed towards detection and management of life-threatening
complications. Clinical evaluation includes measurement of blood pressure, fundus examination and search
for signs of congestive heart failure, fluid overload, acidosis and anemia. Investigations include estimation
of blood levels of hemoglobin, urea, creatinine, sodium, potassium and bicarbonate. An electrocardiogram
(EKG) is done to detect potassium toxicity and an X-ray film of the chest for pulmonary edema.
Table 5 summarizes the management of complications that might be present.
Table 5
Management of complications

Complication

Fluid overload

Treatment

Fluid restriction Insensible losses

(400 ml/m/d); add urine output & other

Remarks

Monitor other losses and

replace as appropriate, consider
dialysis

Complication

Treatment

Remarks

losses; 5% dextrose for insensible

losses; N/5 saline for urine output

Pulmonary edema

Oxygen; frusemide 24 mg/kg iv

Symptomatic Sodium nitroprusside 0.5
8 g/kg/minute infusion; frusemide 2
4 mg/kg iv; nifedipine 0.30.5 mg/kg
oral/sublingual

Monitor using CVP; consider

dialysis

Hypertension

Asymptomatic Nifedipine, amlodipine,

prazosin or clonidine

In emergency, reduce blood

pressure by one-third of the
desired reduction during first
68 h, 1/3 over next 1224 h
and the final 1/3 slowly over 23 days

Metabolic acidosis

Sodium bicarbonate (IV or oral), if

bicarbonate levels <18 mEq/l

Watch for fluid overload,

hypernatremia, hypocalcemia;
consider dialysis

Calcium gluconate (10%) 0.51 ml/kg

over 510 min iv

Stabilizes cell membranes;

prevents arrhythmias

Salbutamol 510 mg nebulized

Shifts potassium into cells

Sodium bicarbonate (7.5%) 1-2 ml/kg

over 15 min

Shifts potassium into cells

Dextrose (10%) 0.51 g/kg and insulin

0.1-0.2 U/kg

Requires monitoring of blood

glucose

Hyperkalemia

Calcium or sodium resonium

(kayexalate) 1 g/kg per day

Given orally or rectally, can be

repeated every 4 h

Hyponatremia

Fluid restriction; if sensorial alteration

or seizures 3% saline 612 ml/kg over
3090 min

Hyponatremia is usually
dilutional; 12 ml/kg of 3%
saline raises sodium by
10 mEq/L

Severe anemia

Packed red cells 35 ml/kg; consider

exchange transfusion

Monitor blood pressure, fluid

overload

Complication

Treatment

Remarks

Hyperphosphatemia

Phosphate binders (calcium carbonate,

acetate; aluminum phosphate)

Avoid high phosphate products:

milk products, high protein
diets

Modified from Pediatric Nephrology; Fourth Edition, RN Srivastava, Arvind Bagga

Hyperkalemia is a serious emergency as the resultant cardiac toxicity may cause sudden death. Urgent
treatment is instituted depending on blood potassium levels and EKG changes. Concomitant metabolic
acidosis should be corrected. While sodium bicarbonate, glucose, insulin and salbutamol reduce the
extracellular concentration of potassium by moving the ion into the cells, calcium infusion decreases
membrane irritability without altering serum potassium levels. The action of kayexalate (sodium
polystyrene sulfonate) or calcium resonium, which exchange potassium for sodium or calcium ions, is slow
and not useful in emergencies. Peritoneal or hemodialysis is the most effective method to remove excess
potassium from the body.
Hypertension is commonly observed in cases of GN and HUS. The symptoms of hypertensive
encephalopathy are generally related to rapidity of rise rather than absolute value of the blood pressure.
They include headache, blurring of vision, convulsions, papilledema, cranial nerve palsies (especially
facial), vomiting and altered sensorium. Blood pressure should be reduced with appropriate medications
(Table 5).
Hyponatremia (sodium <130 mEq/L) is usually the result of excessive fluid administration rather than salt
loss. Patients with blood sodium concentration >125 mEq/L are rarely symptomatic. Hyponatremia is best
managed by fluid restriction; patients with resistant hyponatremia can be satisfactorily managed by dialysis.
Treatment with hypertonic saline (3%) is reserved for those with symptomatic hyponatremia
(encephalopathy, lethargy and seizures), but should be used cautiously because of potential complications of
fluid overload, hypertension and intraventricular hemorrhage.

Standard Supportive Care

In a child with ARF in whom serious complications are absent or have been adequately treated, standard
supportive care is instituted. Management is based on close attention to the intake of fluid and electrolytes,
provision of proper nutrition, prevention and treatment of infections, careful monitoring and dialysis.

Fluid and Electrolyte Balance

Fluid and electrolyte intake in a patient with ARF should be regulated based on a clinical examination of
extracellular fluid volume status, urine output, and daily weights. The daily fluid requirement amounts to
insensible water losses (300400 ml/m2), urinary output and extra renal fluid losses. Insensible fluid losses
are replaced with 510% dextrose/glucose solution. Urine output should be measured without resorting to
catheterization. Urinary losses and those from extrarenal sources should have their composition analyzed
and replaced accordingly. It is preferable to administer the required amounts of fluid by mouth, whenever
feasible. If there is persistent vomiting, intravenous route may be necessary. Potassium containing fluids
should not be given to patients with oliguria.
Ongoing treatment is guided by intake-output analysis, daily weight, physical examination and serum
sodium. If fluid in an appropriate volume and composition has been given, the patient should lose 0.51% of
his weight every day. This weight loss is the result of caloric deprivation and not inadequate fluid therapy.
Serum sodium concentrations should be maintained within the normal range. A rapid weight loss and
increasing level of serum sodium suggest inadequate free water replacement. On the other hand, an absence
of weight loss and hyponatremia indicate excessive free water replacement.

Type of Fluid
The type of fluids used are mostly Crystalloids e,g. Saline, Ringers Lactate. The use of hypertonic
saline for resuscitation suggests a favourable effect but no randomized controlled trial in septic humans
using hypertonic saline has been done. There is no conclusive evidence whether crystalloids are better or
worse than colloids in resuscitating septic patients. However, the use of Colloids in the care of septic
patients to raise oncotic pressure has the rationale of minimizing edema formation. The three major subtypes
of colloid fluids are albumin, starches and gelatin. The use of albumin in intensive care setting is still
debated because many studies have failed to show an intrinsic advantage or disadvantage in terms of AKI
from using albumin or saline [13]. Starches are macromolecules metabolized by serum amylases and
excreted by the kidney. There is no conclusive evidence regarding the safety and efficacy of
hydroxyethylstarch in preventing alterations of renal function in septic patients. Gelatin in some case reports
has adversely affected kidney function, however, there is no controlled trial comparing gelatin solutions to
crystalloid.

Nutritional Management
Patients with ARF are usually catabolic and have increased metabolic needs. Adequate nutritional support is
desirable with maximization of caloric intake. However, volume restriction necessary during the oliguric
phase often imposes severe limits on the caloric intake. A diet containing 0.81.2 g/kg of protein in infants
and 0.60.8 g/kg in older children and a minimum of 5060 Cal/kg should be given. The latter requirement
can be met by adding liberal amounts of carbohydrates and fats to the diet. Once dialysis is initiated, dietary
fluid and electrolyte restrictions can be made more liberal. Vitamin and micronutrient supplements are
provided.
The use of the enteral route is recommended whenever possible. Hypermetabolic patients should be fed
early and a risk of renal failure should not delay the initiation of nutritional therapy. Parenteral nutrition is
indicated only after the acute phase of shock and severe metabolic disorders has been managed. Limitations
of the use of large volumes may be achieved with intermittent dialysis or continuous renal replacement
therapies.

Management of Infections
Patients with ARF are susceptible to develop infections because of depressed immunity induced by
azotemia, associated malnutrition and invasive procedures. Various infections (respiratory and urinary tract,
peritonitis and septicemia) are the immediate cause of death in many patients. All procedures must be
performed with aseptic techniques, intravenous lines carefully watched, and skin puncture sites cleaned and
dressed. Oral hygiene should be ensured.
Sepsis is suggested by hypothermia, persistent hypotension, hyperkalemia and a disproportionate rise of
blood urea compared to creatinine. The patient should be frequently examined to detect infection, which
may be present without fever. Once infection is suspected, appropriate specimens are cultured and
antibiotics started.

Use of Medications
Drugs that increase severity of renal damage or delay recovery of renal function (e.g., aminoglycosides,
radiocontrast media, NSAIDs, amphotericin B) should be avoided. Medications that reduce renal perfusion
e.g., ACE inhibitors and indomethacin also should be used cautiously. The dose and dosing interval of
antibiotics particularly those, which are nephrotoxic, is modified depending on the severity of renal failure.

Role of Diuretics, Mannitol and Dopamine

Diuretics may be useful in instances where a high urine flow is required to prevent intratubular precipitation
as with intravascular hemolysis, hyperuricemia and myoglobinuria. There is no evidence that treatment with
diuretics improves renal function or the long-term outcome in patients with intrinsic renal failure. Mannitol
has been used, as a diuretic, but no clear benefits of its use are demonstrated. Intravenous administration of
mannitol, in patients with volume overload and oliguria, might be detrimental and result in congestive heart
failure. Dopamine, at low doses (13 g/kg) has traditionally been used to promote renal perfusion. Review
of data, however, suggests that the use of dopamine does not improve renal function, need for dialysis and
outcome. Rather, it may be detrimental and cause complications like arrhythmias and gastrointestinal
bleeds. Based on available evidence, its use is not recommended either for prevention or treatment of ARF.
Other experimental therapies including calcium channel blockers, antioxidants, thyroxin, peptide growth
factors and cytokines have been used in order to attenuate renal injury or enhance recovery of renal
function.

Specific Therapy
Intensive immunosuppression with high dose intravenous methylprednisolone followed by oral or
intravenous cyclophosphamide is indicated in patients with crescentic GN, lupus nephritis and vasculitis. A
short course of treatment with oral corticosteroids is useful in patients with acute interstitial nephritis.
Treatment in patients with D + HUS is chiefly supportive. Intensive plasmapheresis has been used in
patients with D- (atypical) HUS, and selected patients of crescentic GN and severe lupus nephritis.

Postrenal ARF
Postrenal failure occurs as a consequence of mechanical obstruction in the urinary collecting system. The
ideal management is to bypass the obstruction e.g., catheterization or vesicostomy in posterior urethral
valves or percutaneous nephrostomy in bilateral pelviureteric junction. If the patient is sick or the diagnosis
of obstruction unclear, intermittent peritoneal dialysis is done initially and nephrostomy performed later.
Both pre- and postrenal categories can, if prolonged, lead to parenchymal injury to the kidneys (intrinsic
renal failure).

Renal Replacement Therapy

ARF requiring dialysis can be managed with a variety of modalities, including peritoneal dialysis,
intermittent hemodialysis, and continuous hemofiltration or hemodiafiltration [14, 15]. The choice of
dialysis modality to be used in managing a specific patient is influenced by several factors, including the
goals of dialysis, the unique advantages and disadvantages of each modality and institutional resources.
Indications for initiating renal replacement therapy include severe or persistent hyperkalemia (>7 mEq/L),
fluid overload (pulmonary edema, severe hypertension), uremic encephalopathy, and severe metabolic
acidosis (TCO2 <1012 mEq/L), hyponatremia (120 mEq/L or symptomatic) or hypernatremia. The decision
to institute dialysis should be based on an overall assessment of the patient keeping in view the likely course
of ARF.

Intermittent Peritoneal Dialysis (IPD)

The initial renal replacement therapy of choice in sick and unstable patients is often IPD. It is popular
because of the ease of initiation and effectiveness in children of all ages, including neonates. Peritoneal
access, in most centers in India, is obtained using a stiff catheter and trocar. While peritoneal dialysis can be
effectively performed with these catheters, these should be removed after 4872 h, beyond which the risk of
infection is very high. Risk of injury to the viscera and infections is considerably less with soft silastic
(Tenckhoff or Cooks) catheters, which therefore can be used for repeated dialysis for prolonged periods.

While the standard Tenckhoff catheter needs to be placed surgically, a temporary (peel away) catheter can
be inserted bedside. The Cooks catheter is inserted using a guide wire by the Seldinger technique.
The dialysis prescription depends upon the clinical condition of the patient. The fill volume varies from 30
50 ml/kg (8001,200 ml/m). Commercially available dialysates are lactate based and with a dextrose
concentration of 1.7%. In patients with fluid overload, the concentration of dextrose is increased to 2.53%
to facilitate ultrafiltration.The initial dialysis cycles are of short duration (2030 min). Patients who are sick
and have severe lactic acidosis are dialyzed using a bicarbonate dialysate.
If the duration of ARF is prolonged and a need for renal replacement therapy arises, chronic PD may be
performed, either manually (continuous ambulatory peritoneal dialysis; CAPD) or with the use of an
automated device (continuous cycling peritoneal dialysis; CCPD).

Hemodialysis (HD)
HD is more efficient for correction of fluid and electrolyte abnormalities. However, it is expensive to
institute, requires expertise and skilled nursing and is not available at most centers in our country. It is not
suited for patients with hemodynamic instability, bleeding tendency and in very young children where
vascular access might be difficult.
The equipment required is the HD machine, pediatric dialyzer with tubings and dialysate fluid. The
semipermeable fibers, used in current dialyzers, are made of cellophane, cuprophane or cellulose acetate.
These dialyzers are available in different sizes varying between 0.51.5 m. Selection of the dialyzer
depends upon patients body size and its ultrafiltrate properties. An appropriate vascular access is necessary
for removing and returning large quantities of blood required for the procedure. This is usually achieved
using a double lumen venous catheter inserted into the internal jugular, femoral vein or subclavian vein.
The dialysis machine has a blood pump, which regulates the outflow of blood from the patient and delivers
it to the dialyzer. The heparinized blood flows on one side of the semipermeable membrane of the dialyzer,
while a concentrate of dialysate mixed in a fixed proportion with pre-treated water flows at a rate of at least
1.52 times the blood pump rate on the other side. After dialysis the blood is returned back to the patient's
circulation. The hemodialysis machine has a programmable ultra filtrate controller, which determines
removal of free water. Most children are maintained on a hemodialysis regimen of 3-4 h, three times a
week. Sick patients with fluid overload often benefit from daily dialysis initially.

Continuous Renal Replacement Therapies (CRRT) and Other Newer

Modalities
CRRT is any extracorporeal blood purification therapy intended to substitute for impaired renal function
over an extended period of time and applied for, or aimed at being applied for, 24-hr a day. These therapies
are gaining increasing popularity for the treatment of critically ill patients with ARF in developed countries.
Various modalities include CAVH (continuous arteriovenous hemofiltration), CVVH (continuous
venovenous hemofiltration), continuous venovenous hemodiafiltration (CVVHD) and slow continuous
ultrafiltration (SCUF). These therapies are useful when large amount of fluids have to be removed in sick
and unstable patients. CVVH is also preferred in ARF secondary to major surgical procedures, burns, heart
failure and septic shock especially when conventional HD or IPD are not possible.
Continuous hemofiltration provides smoother control of ultra filtered volume and gradual correction of
metabolic abnormalities in unstable patients. Special equipment (PRISMA system, modified hemodialysis
machine) and trained staff is necessary to provide CCRT in children.
The necessity of daily dialysis emphasizes the need for flexible treatments combining the advantages of
CRRT and the feasibility of IHD. One such hybrid therapy is a slow long extended daily dialysis (SLEDD)
done daily for an extended but limited period (810 h) using lower dialysate flow rates and at the same time
minimizing the cost and technical complexities associated with CRRT.

The outcome for patients needing RRT in the ICU is perhaps not influenced by the modality used. IHD is
however, much cheaper than CRRT, and therefore, it should be the first RRT of choice in centers where it is
available. It is likely that newer hybrid techniques (SLEDD) offer an additional advantage but this remains
to be proven.

Outcome of ARF and AKI

Length of Stay
Patients with AKI or ARF are amongst the most severely ill in the PICU. Therefore, PICU patients with
AKI or ARF have a longer length of stay in the ICU and in the hospital compared to ICU patients without
these conditions. Patients with less severe forms of AKI have an increased length of in-hospital stay
compared to patients without AKI, and there is a stepwise increase of length of stay depending on the
severity of AKI according to RIFLE criteria.

End-Stage Kidney Disease

Although the majority of survivors regain kidney function, some patients (1320%) do not recover from
ARF and evolve to end-stage kidney disease (ESKD) with permanent need for RRT [5].

Mortality
Mortality rate for PICU patients with ARF will depend upon the severity of AKI, and the cohort being
observed. Despite advances in treatment, the published mortality rates for ARF patients in individual studies
remain more or less constant at 50%.

Conflicts of Interest
None.

Role of Funding Source

None.

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