FLUID AND ELECTROLYTE FLUID AND ELECTROLYTE IMBALANCEIMBALANCE

Hooman NAssociate professorAssociate professor

TUMS20122012

Na <135

P osmHigh NrLow

PseudoHyperosmolar

True

DehydrateEdematous

UNaEuvolemic

UNa

UNa

<

<10variable

<10

Extra‐renal

>20

renal

SIADHGCD

Hypothyroid.

CHFLiver

Capillary l k

RFyp yWater 

intoxication

leak syndrom.

Mechanisms underlying hyponatremiaMechanisms underlying hyponatremia(Intracranial disorder)

Pediatr Nephrol (2012) 27:733–739

h h f d lThe characteristic of ECF depletion, SIADH, CSW

Proximal tubule defect

Diagnostic criteria SIADHDiagnostic criteria SIADH

C di i   i i  CSW i  i   i l di dConditions mimic CSW in intra cranial disorders

Time elapsed pbetween onset of CSWS & of CSWS & intracranial event

Treatment

S i  ?   O    N   /L?Symptomatic ?   Or   Na<120 meq/L?

Nacl 3%4‐6 ml/kg /30‐60 min

Persist?

3‐4ml/kg

Persist?

3 4ml/kg

Neurologic sign?

CNS imaging

g g

CNS imaging

Asymptomatic?Asymptomatic?

Edematous?Na restrictionNa restrictionLoop diuretic pV2‐reseptor antagonist(Convaptan)

SIADHSIADH

Fl id  i i  (IWL UO)1. Fluid restriction (IWL+UO)

2. Furosemide + oral NaCl 

3. Lithium 4. Dimeclocyclin4. Dimeclocyclin

5 Conevaptan/Tolvaptan5. Conevaptan/Tolvaptan

Dehydrate?Dehydrate?

R id Fl id  h  (NS/RL)Rapid Fluid therapy (NS/RL)

Main (+ Deficit (Na+Fluid)

( 130‐Pna)0.6WT

Renal salt wasting syndrome?Renal salt wasting syndrome?

Fl id  lFluid replacement

Na<125?     Or Large volume required?Nacl 1.5% IVAdult NaCl 1.5% ‐50‐150ml/h

Fludrocortisone:0.1‐0.2 mg PO ‐BD

Pediatr Nephrol (2012) 27:733–739

Ri k F t   f d l i   b l d li tiRisk Factors of developing cerebral demylinationin hyponatremic patients

Complication Hyponatremia

Clin J Am Soc Nephrol 5: 167–168, 2010

Pediatr Nephrol (2010) 25:1225–1238

Non‐cardiogenic pulmonary edema

ImportantImportant

T   di   /LTarget sodium 130 meq/L

Rate of Na increment  <0.6 meq/L

Max Rise Na in 48 H  25meq/L

HypernatremiaHypernatremia

Na>150a 50

Volume status HypervolemichypovolemicVolume status Hypervolemicyp

UO , SG Na excess

High UO  Highdilute

Oliguricconcentrate

Renal failure

Osmotic iuresis

DDAVP test

Sosm

ExtrarenallossSosm

Uosm

>50%>50%9‐50%<9%

TreatmentTreatment

HTN  / d ?HTN +/‐ edematous?

Diuretic (Furosemide)

Dialysis

Dehydrate (water + Na deficit)Dehydrate (water   Na deficit)

Maint   (2/3 )Maint.  (2/3 )

Deficit  correction rateNa 150‐160 in 24 H

160‐170 in 48H7 4

170‐180 in 72 H180‐190 94 H180‐190 94 H

Reduce P Na <12 meq/L /daySubtract water deficit from water+Na deficitSubtract water deficit from water+Na deficit

Water deficit?

Water deficit =NBW –CBW

)1140

P[Na] (BW x 0.4 −140

Treatment of cerebral edemaTreatment of cerebral edema

C b l  d   i   h ld b   d  i h Cerebral edema, seizures should be treated with 3% NS

6 l kDose: 4‐6 ml/kg1ml/kg of 3% NS will change Na concentration by 1 meq/L

DyskalemiaDyskalemia

HypokalemiaHypokalemia

Am J Kidney Dis. 2012;60(3):492‐497

K<3.5 Cellular uptake

UK , TTKG<15,<4 >15, >4Extra‐renal

Blood gas

MetabolicAlk l i

MetabolicAlkalosis Acid

UclLow/Nr

Barter,Gittelman

>15 <15BP

HTNPRALow

HTNPRAHigh

Ald  DOCAld, DOC17‐OHP, Cortisol,ACTH

3.5-5.5 >2

2

11

Am J Kidney Dis. 2012;60(3):492‐497

Pediatric dosagePediatric dosage

l d  oral dose: 2‐4mEq/kg/day (max. 120‐240 mEq/day in divided doses) divided doses) 

The dose of IV (emergent) :0.5‐1 mEq/kg, usually given over 1 hr.

Potassium saltsPotassium salts

KCl    KHCO  / K  i  ?KCl  vs KHCO3 / K citrate ?

KK↓Cl

K↓K↑

↓HCO3

Rate of replacement

Nonemergent :20‐40 meq of K is added to 1 L Dw / salineMaximum rate 10‐20meq/h

Emergent: 20meq in 100ml saline  (200meq/l) , femoral vein Maximum rate 40‐100meq/h

HYPERKALEMIAHYPERKALEMIA

K>5.5 RedistributiveSpuriouspTrue

GFR

<10 >20

J Am Soc Nephrol 19: 424–426, 2008.

<6 adult<5 infant<4 child

increase<4 child

Low aldosteronebioavailability

0.2  mgFludrocortisone

TTKGLow

The goals of therapy, in chronologic order

1. Antagonize the effect of K on excitable cell

bmembranes.

2 R di t ib t t ll l K i t ll2. Redistribute extracellular K into cells.

3 E h li i ti f K f th b d3. Enhance elimination of K from the body.

ECGECGpoor sensitivity and specificityTh  i     t f  th i    i   idi  There is no support for their use in guiding treatment of stable patients Wi h  id ifi bl   l di hi  Without identifiable electrocardiographic markers of the risk for complications, management of hyperkalemia should be management of hyperkalemia should be guided by the clinical scenario and serial potassium measurementspotassium measurements.

Clin J Am Soc Nephrol 3: 324-330, 2008.

Rapid treatmentRapid treatment

EliminationElimination

Cli J A S N h l 5 1723 1726 2010

J Am Soc Nephrol 21: 733–735, 2010.

Clin J Am Soc Nephrol 5: 1723–1726, 2010

Conclusion

El  di b  i    i      

Conclusion

Elyte disturbance is common in acute or chronic ill childC d h d l dConsider the underlying diseaseTreat the emergenciesAppropriate  work upApropriate chronic treatmentp p