Aki in neonate

AKI in a neonate

Bharathi B

Sub headings

Definition

Classification – AKIN / RIFLE

Pathophysiology

Evaluation

Management

Medical

Dialysis

Definition

Acute kidney injury (AKI) - a sudden

impairment in kidney function, that

results in the retention of nitrogenous

waste products and alters the

regulation of extracellular fluid volume,

electrolytes, and acid-base

homeostasis.

“ recognize the injury , don’t wait for

the failure” ( Mehta 2007)

Creatinine based definition

Creatinine ≥1.5 mg/dL independent of day of life and regardless of the rate of urine output.

Problems of this approach1. Will not change till 25 – 50 % func loss2. Overestimates renal function3. Varies by muscle mass, age , sex, hydr4. Different methods of est ( Jaffe/

enzymatic)5. Easily dialysed

Avery diseases of the neonate – 9 th edition

P- RIFLE

Creatinine Urine output

Risk eCCl decrease by 25% <0.5 mL/kg/hr for 8 hr

Injury eCCl decrease by 50% <0.5 mL/kg/hr for

16 hr

Failure eCCl decrease by 75% or eCCl

<35 ml/min/1.73 m2

<0.3 mL/kg/hr for 24hr

or anuric for 12 hours

Loss Persistent failure >4 wk

End

stage

Persistent failure > 3 months

Proposed by bellomo et al ; modified by ackan - arikan

AKIN criteria ( Mehta et al ,

2007)Abrupt (within 48 h) reduction in

kidney function currently defined as an

absolute increase in serum creatinine

of 0.3 mg/dL or more or

A percentage increase in serum

creatinine of 50% or more (1.5-fold

from baseline) or

A reduction in urine output

(documented oliguria of < 0.5 mL/kg/h

for >6 h)

KDIGO staging for AKI severity

( Mehta et al 2007)Creatinine Urine output

Stage 1 1.5-1.9 times

baseline

or

≥0.3 mg/dL

increase

<0.5 mL/kg/hr for 6 hr

Stage 2 2- 2.9 times

baseline

<0.5 mL/kg/hr for 12 hr

Stage 3 3 times baseline

or

Increase in serum

creatinine to ≥4

mg/dL

or

Initiation of renal

< 0.3 mL/kg/h for 24 h

or

Anuria for ≥12 h

Problems

Delineation between the 1st week of life

and changes in SCr level after the 1st

week - needed in a neonatal AKI

classification system.

Despite these working classification

systems, the diagnosis of AKI is

problematic, because current diagnosis

relies on two functional abnormalities:

functional changes in SCr (marker of

GFR) and oliguria.

Avery diseases of the neonate – 9 th edition

Acute Renal Failure in the Neonate

Steven Alan Ringer Neoreviews

2010;11;e243

Etiopathogenesis


Steven Alan Ringer Neoreviews 2010;11;e243

Prerenal failure – pathophysio

Alteration in

plasma flow

Catecholami

ne surge

Prostagland

in & RAAS

activation

Dilation of

afferent

arteriole /

constric of

efferent



Intrinsic renal failure Increased

transcapillary

hydraulic pressure

Failure of

autoreg +-

renal

immaturity

Tubular damage

systemic

inflammatory

response



Post renal

Reversible with

reversal of

obstruction



Evaluation

Identify prerenal causes

Is there a volume contraction ?- Inadeq feeding- Dehydration- Large fetomaternal h’hage- Subgaleal bleeds- Warm shocks

Congestive cardiac failure



Investigations

Serum sodium, potassium, chloride,

bicarbonate, calcium, phosphorus,

magnesium, urea, creatinine, uric

acid, glucose, blood gases,

hemoglobin, and platelets

S.Cr often does not rise for days after

an injury, thus monitoring these values

for several days after the inciting event

is necessary to determine if AKI

occurred.

Intrinsic renal failure

Management

Supportive –

keep the kid

and kidney

alive


Steven Alan Ringer Neoreviews

2010;11;e243

Dopamine

Dopamine can increase renal

perfusion in the sick preterm and

term infant with prerenal azotemia

caused by hypoxemia, acidosis, or

indomethacin administration (Seri,

1995; Seri et al, 1998, 2002).

Compared with placebo, low-dose

dopamine does not improve survival,

shorten hospital stay, or limit dialysis

use.



Fenoldopam is a selective dopamine-1

receptor agonist whose effects include

vasodilation of renal and splanchnic

vasculature, increased renal blood

flow, and increased GFR.

Fenoldopam is approved to treat

severe hypertension in adults, but is

not clinically approved for the

treatment of AKI.

Avery ‘s diseases of newborn – 9th edition

Diuretic

No studies in neonates, children, or

adults have shown that diuretics are

effective in preventing AKI or

improving outcomes once AKI occurs

(Bellomo et al, 2000).

If loop diuretics are to be used in

neonates, continuous doses of

furosemide may be superior to larger

intermittent doses

Volume & electrolyte / acidbase

imbalanceHyponatremia:

Na Required (mEq) =(Na Desired − Na + Actual) × Body weight (kg) × 0.7

Hypocalcemia -100 to 200 mg/kg of calcium gluconate should be infused over 10 to 20 minutes and repeated every 4 to 8 hours as necessary. Hyperphosphatemia - Breastmilk and Simi- lac 60/40 both contain low phosphorous and low potassium compared with other neonatal infant formulas .

Treatment of hyperkalemia

Vemgal and Olhson (2007) -no firm clinical practice recommendations on

which treatment modality was best to treat preterm infants with

hyperkalemia are available, except that insulin plus glucose may be better

in premature infants.

Nutrition & drugs

Nutritional goals in infants with AKI are similar to those of infants without AKI.

Feeds or parenteral nutrition will need to be concentrated to avoid excessive fluid

a neonate is receiving continuous peritoneal dialysis or hemodialysis, an additional 1 g/kg/day of protein is needed to supplement the protein losses that occur with these forms of dialysis (Zappitelli et al, 2008, 2009).

Indications For Renal Support

Severe electrolyte abnormalities that are

not correctable with medicalinterventions

Life-threatening intoxication by

medications that can be cleared with

dialysis

inborn errors of metabolism

fluid overload

Acidosis – refractory to medical

management

Coma Neonatal Peritoneal Dialysis

Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin Neoreviews 2005;6;e384

DOI: 10.1542/neo.6-8-e384

Renal replacement therapy

The timing of dialysis initiation in

infants with AKI is controversial.

Several observational studies show a

clear advantage in adults receiving

dialysis early versus late (Liu et al,

2006; Ronco et al, 1986).

Neonatal Peritoneal Dialysis

Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin

Neoreviews 2005;6;e384

DOI: 10.1542/neo.6-8-e384

Basic Physiology of Dialysis And

Ultrafiltration

Molecular movement across

semipermeable membrane

Basic mechanisms of water and

particle removal include

Diffusion

Convection

Ultrafiltration

Diffusion

Movement of dissolved particles

across semipermeable membrane

from area of high concentration to

area of low concentration

Favors movement of smaller particles

Stops when concentration gradient

achieves equilibrium

Convection

Dissolved particles pass across semi

permeable membrane due to effects

of pressure gradient

Ultrafiltration

Describes movement of water across

semipermeable due to pressure

3 modalities

Peritoneal dialysis

Intermittent Hemodialysis

Continuous Renal Replacement

Therapy

PERITONEAL DIALYSIS

Physiology

Peritoneum can be used as a dialysing membrane

Instillation of a dialysate into the peritoneal space permits diffusion of particles out of the blood across the peritoneum

Through the use of a hypertonic solution , water also passes across the membrane generating an ultrafiltrate

Water movement tends to drag particles across the peritoneum by convection

After the dwell is complete , the spent dialysate is drained from the abdomen and fresh dialysate may be introduced




DOI: 10.1542/neo.6-8-e384

Indications

Remove excess fluid and provide

volume control in the patient with

oligoanuria

Much slower than intermittent

hemodialysis

Preferable in the critically ill patient

Provides metabolic control




DOI: 10.1542/neo.6-8-e384

Technique

Instill sterile dialysate into peritoneal cavity

Allow it to dwell

End of dwell time the dialysate is removed

Dialysate contains base in the form of lactate

Ultrafiltration accomplished by osmotic pressure thro dextrose

Should be warmed to body temp

Start with 10 – ml/kg ( 500 ml/m2)

Dwell period of 30 - 60 minNeonatal Peritoneal Dialysis



DOI: 10.1542/neo.6-8-e384




DOI: 10.1542/neo.6-8-e384

Complications

Peritonitis

Leakage around the catheter exit site

Tunnel infection

Catheter malfunction, and obstruction by omentum (Coulthard and Vernon, 1995).

Fluid leakage into other compartments (including the chest in patients without an intact diaphragm) can occur and if suspected, the fluid composition will reveal high glucose levels if a leak is present Neonatal Peritoneal Dialysis



DOI: 10.1542/neo.6-8-e384

Issues

Loss of protein – supplement it

Hyperglycemia

GER – stomach comp

Critically ill – inc intra abd pressure

leading to dec Venous return and dec

diaphragm excursion




DOI: 10.1542/neo.6-8-e384

Poor candidates for PD

worsening respiratory status or

ventilatory

Diaphragmatic hernias

Abdominal wall defects




DOI: 10.1542/neo.6-8-e384

AKI to CKD

Adult studies – 3- 5 % go on to have

CKD

Stapleton – retrospective study – 40 –

88 % CKD prevalence

Preterms did worse than term babies

Aki in neonate

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