Acuterenalfailure management in children

Acute Renal failure management

Moderator Dr Sudha Rudrappa

Dr. Vinayaka hegde

Clinical Approach to AKI: Pre-, Intra-, and Post-Renal

HistoryVolume status

UltrasoundUrinalysis US shows

Hydronephrosis

Post-Renal

Urinalysis Normal

UrinalysisAbnormal

Tubulointerstial Disorders

Glomerular and Vascular Disorders

Pre-renal

Lab Findings Anemia : Dilutional or hemolytic eg. SLE, renal vein

thrombosis, HUS Leukopenia : SLE, sepsis Thrombocytopenia :SLE, renal vein thrombosis, sepsis,

HUS Hyponatremia : dilutional Metabolic acidosis Elevated BUN, creatinine, uric acid, potassium, and

phosphate (diminished renal function); and hypocalcemia (hyperphosphatemia).

CXR : cardiomegaly, pulmonary congestion (fluid overload) or pleural effusions.

Renal USG :

Hydronephrosis /hydroureter,

Nephromegaly- s/o intrinsic renal disease.

Small kidney - Nephrosclerosis , CRF

Renal biopsy : who do not have clearly defined prerenal or postrenal ARF

Sensitivity and specificity of urine Na of <20 in differentiating prerenal azotemia from acute tubular necrosis are 90% and 82%, respectively.

Fractional excretion of sodium

= Urine:Plasma (U/P) ratio of sodium divided by U/P of creatinine × 100. (sensitivity and specificity of fractional excretion of

sodium of <1% in differentiating prerenal azotemia from acute tubular necrosis are 96% and 95%, respectively)

Other biomarkers:

- changes in plasma neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C levels

- urinary changes in NGAL, interleukin-18 (IL-18), and kidney injury molecule-1 (KIM-1).

Treatment of AKI

Aims of treatment:

1.Maintenance of Fluid and Electrolyte Homeostasis

2.Preventing Life-threatening Complications3.Avoiding Further Kidney Injury4.Providing Appropriate Nutrition5.RRT in most severe forms of AKI

The treatment of AKI divided into:

Nondialytic therapy (supportive therapy and medical management)

Dialytic therapy .

Management Catheterization - in newborn with suspected

posterior ureteral valves & nonambulatory older children.

The nondialytic therapy: to date the only effective nondialytic treatment of AKI entails:

1. Restoration of adequate renal blood flow

2. Avoidance of nephrotoxic medications or those that interfere with renal compensatory mechanisms

3. Assurance that renal perfusion has been maximized before exposure to nephrotoxic agents.

Creatinine clearance, GFR CrCl (ml/min/1.73m2)= K * lengh(cm)/Pcr

K = 0.35 fr preterm/LBW till 1 yr 0.45 fr term ,<1yr 0.55 fr children & adolescent girls 0.70 fr adolescent boys

Est Creatinine clearnce (U. creatinine/ S.creatinine )Urine

vol * 1.73/BSA in Ml/min/m2

Assessment of the patient for fluid balance Weight, BP, heart rate, skin turgor and

capillary refill are each used to assess the intravascular volume.

1- in children who are intravascular volume depleted, 10-20 ml / kg of normal saline can be infused to re-establish intravascular volume (dehydrated pt. generally void with in 2 hours) .

If U.O.P. does not increase and azotemia does not improve after fluid resuscitation, then catheterization of the blader and central venous pressure monitoring may be necessary to further guide fluid therapy.

the CVP normally between 2 and 12 cm H2O. If clinical and laboratory evaluations show that the patient is adequately hydrated, then aggressive diuretic therapy may be considered

2- for fluid overload, fluid restriction or fluid removal with dialysis or hemofiltration may be instituted if the child does not respond to diuretic therapy.

When intravascular volume normalized, euvoluemia can be maintained by providing the child with fluid to replace normal water losses from the skin, respiratory tract, and GIT (insensible losses, 400 ml / m2 / 24hr. + UOP)

Excess losses need to be accounted for as well and replaced with the appropriate fluid.In general, glucose containing solutions (10- 30%) with out electrolytes are used as maintenance fluids . The composition of the fluid may be modified in accordance with the state of electrolyte balance.

Daily weight measurements, BP, accurate fluid input & output records, physical examination and nutritional needs of the child guide on going fluid therapy.

7- Nutritional support

. AKI is associated with marked catabolism & malnutrition leading to delayed recovery from AKI

. if GIT is intact and functional, enteral feedings with formula (similac PM 60/40 for Newborns & infants) should be instituted .

. Dilute formula should be given initially and then feedings can be increase and concentrated to achieve optimal calories intake.

. In older children a diet of high-biologic-value protein, low-phosphorus& low-potassium foods can be used.

.Infants should receive maintenance calories (120 Kcal/kg/day) and older children appropriate maintenance calories plus 20% extra calories due to the catabolic state and malnutrition.

If enteral feeding are not possible, then hyperalimentation, usually through a central line, with high concentration of dextrose (25%), lipids (10-20%), andprotein (0.5-1.25g/kg/day) should be instituted .

If the child is oliguric or anuric and sufficient caloric intake cannot be achieved while appropriate fluid balance is maintained, dialysis should be initiated earlier than in the usual case.

Therapy to Decrease injury and promote Recovery

Recovery of Renal function after ATN requires a complex & not fully understood set of events that leads to restoration of renal blood flow and regeneration of renal tubular epithelial cells

1- Post-ischemic infusion of growth factors including IGF-1, epidermal GF & hepatocyte GF → accelerate

recovery of renal impairment .

2- Administration of melatonin-stimulating hormone, thyroxine, C5a receptor antagonist, selective inhibitors of inducible nitric oxide synthase, statins &Novel inhibitor of the Na / H exchange subtype 3 as well as inhibition of monocyte chemoattractant protein 1 by gene therapy has been shown to ameliorate AKI

3- Other studies demonstrate that anti-adhesion molecule therapy markedly decrease ischemic renal injury by preventing adhesion of activated neutrophils to renal cells.

Diuretic therapy : Only after the adequate hydration. Mannitol (0.5 g/kg) and furosemide (2-4 mg/kg) - as a

single IV dose. [Mannitol - effective in pigment (myoglobin, hemoglobin)-induced renal failure.]

Bumetanide (0.1 mg/kg)- an alternative to furosemide.

If urine output is not improved - continuous diuretic infusion may be considered.

Consider Dopamine (2-3 µg/kg/min) in conjunction with diuretic therapy.

There is little evidence that diuretics or dopamine can prevent ARF or hasten recovery.

Hyperkalemia Sr K >6 mEq/L - cardiac arrhythmia, cardiac arrest, and

death. Earliest ECG change - peaked T waves f/b widening of the

QRS intervals, ST segment depression, ventricular arrhythmias, and cardiac arrest.

Exogenous sources of K : dietary, intravenous fluids, total parenteral nutrition) should be eliminated.

Sodium polystyrene sulfonate resin (Kayexalate) : (1 g/kg) - orally or by retention enema when Sr K>6 mEq/L

- exchanges sodium for potassium

- can take several hours to take effect. A single dose of 1 g/kg can lower the sr K level by about 1 mEq/L.

- Resin therapy may be repeated every 2 hr, the frequency being limited primarily by the risk of sodium overload.

Table : Treatment of Hyperkalemia

Agent Mechanism Dose Onset of effect Complications

Sodium bicarbonate

Shifts K+ into cells 0.5-1 mEq/kg IV over 10-30 min.

15-30 min. Hypernatremia Change in ionized

calcium level

Calcium gluconate (10%)

Stabilizes membrane potential

0.5-1 mL/kg over 5-15 min.

Immediate Bradycardia Arrhythmias

Hypercalcemia

Glucose and insulin

Stimulates cellular uptake of K+

glucose50% 1ml/kg

insulin 0.1 U/kgIV over 60min.

30-120 min. Hypoglycemia

β – Agonists (albuterol)a

Stimulates cellular uptake of K+

5-10 mg nebulizer (adult dose)

30 min. Tachycardia Hypertension

Sodium polystyrene

sulfonate (Kayexalate)

Exchanges Na+ for K+ across colonic mucosa

1g/kg PO or PR in sorbitol

30-60 min. Hypernatremia Constipation

If Sr K >7 mEq/L : emergency measures in addition to Kayexalate.  

Calcium gluconate 10% solution : 1.0 mL/kg IV, over 3-5 min

Sodium bicarbonate :1-2 mEq/kg IV, over 5-10 min

Regular insulin : 0.1 U/kg, with glucose 50% solution, 1 mL/kg, over 1 hr

Mild metabolic acidosis:common in ARF - rarely requires

treatment.

If severe (arterial pH < 7.15;

serum bicarbonate < 8 mEq/L) or contributes to hyperkalemia it should be corrected.

Hypocalcemia :

- Primarily treated by lowering the serum phosphorus level.

- Calcium should not be given IV except in cases of tetany, to avoid deposition of calcium salts into tissues.

- Follow a low-phosphorus diet,

Hyponatremia 

- most commonly a dilutional

- must be corrected by fluid restriction.

- hypertonic (3%) saline - limited to symptomatic hyponatremia (seizures, lethargy) or

those with a serum sodium level <120 mEq/L.

GI bleeding  because of uremic platelet dysfunction,

increased stress, and heparin exposure in hemodialysis.

Oral or intravenous H2 blocker-Ranitidine.

Hypertension  Common in ARF patients with acute

glomerulonephritis or HUS. Salt and water restriction, diuretics

Isradipine (0.05-0.15 mg/kg/dose,

amlodipine, 0.1-0.6 mg/kg/24 hr qd or divided bid

propranolol, 0.5-8 mg/kg/24 hr divided bid or tid;

labetalol, 4-40 mg/kg/24 hr divided bid or tid

severe symptomatic hypertension - continuous infusions of sodium nitroprusside or esmolol

Neurologic symptoms  Headache, seizures, lethargy, and confusion

(encephalopathy). Potential etiologic factors - hyponatremia,

hypocalcemia, hypertension, cerebral hemorrhage, cerebral vasculitis, and the uremic state.

Diazepam - most effective in controlling seizures, Treat the underlying cause.

Anemia of ARF generally mild packed red blood cells if Hb < 7 g/dL Slow (4-6 hr) transfusion with packed red

blood cells (10 mL/kg) diminishes the risk of hypervolemia.

Nutrition

 In most cases, sodium, potassium, and phosphorus should be restricted.

Protein – restricted & caloric intake maximised to minimize the accumulation of nitrogenous wastes.

Critically ill patients with ARF - parenteral

essential amino acids given

Protein : enough protein for growth - limiting high protein intake. Protein needs increase on dialysis. Foods with protein include

Eggs

Milk

Cheese

Chicken

Fish

Red meats

Beans

Yogurt

Cottage cheese

Sodium. Depend on stage of their kidney disease,

their age, and sometimes other factors. Foods high in sodium include canned foods some frozen foods most processed foods some snack foods, such as chips

Potassium. Low-potassium High-potassium

- Apples––cranberries––strawberries––blueberries––raspberries––pineapple––cabbage––boiled cauliflower––mustard greens

- Oranges––melons––apricots––bananas––potatoes––tomatoes––sweet potatoes––cooked spinach

Dialysis Indications  Volume overload with evidence of hypertension or

pulmonary edema refractory to diuretic therapy  Persistent hyperkalemia Severe metabolic acidosis unresponsive to

medical management Neurologic symptoms (altered mental status,

seizures) Blood urea nitrogen >100-150 mg/dL (or lower if

rapidly rising) Calcium:phosphorus imbalance, with

hypocalcemic tetany

Types of Dialysis

Peritoneal dialysis Intermittent hemodialysis Continuous renal replacement therapy

Choice of procedure depends on

1. Age &size 2. Cardiovascular status 3. Availability of vascular acess 4. Integrity of peritoneal membrane &

abdominal cavity 5. Expertise available

Take Home Points Management of a patient with ARF involves:

Treating potentially life-threatening complications Reversing pre-renal and post-renal causes Minimizing further hemodynamic and toxic insults to the

kidney stoppage of offending agent Admission and appropriate consultation in time Lack of evidence for converting oliguric to non-oliguric ARF Features of the history and physical examination in

addition to relevant lab and radiologic investigations help to determine the most likely cause(s) of ARF in a given patient and appropriate Rx for the same

Referances Nelson Textbook of pediatrics 19 th

edition Treatment Methods for Kidney Failure in

Children (National instt. of Diabetes & Kidney disease)

Bagga’s nephrology

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