Disorders in Potassium Balance

Disorders in Potassium

Balance

Melvin Bonilla-Felix, MD, FAAP

Chair,

Department of Pediatrics

University of Puerto Rico

Objectives



_{Review normal K}

+

_homeostasis



_{Discuss the most common causes of}

hypokalemia and hyperkalemia in

children

Clinical Case



You are asked to evaluate a 5 day old baby boy born after 34 weeks of

gestation, BW: 2200 grams. He is making urine, creatinine is up to 2.7

mg/dL,

serum K: 6.5 mEq/L

. The resident ordered Kayexelate 1

gm/Kg per rectum x 1 dose.

What is a normal serum K+ and creatinine for a 2.2 Kg baby born at 34 weeks of postmenstrual age? What would you do?

Potassium



Major Intracellular cation



42 mEq/Kg body weight



Almost all is in ICF and readily exchangeable



ICF concentration = 150-160 mEq/L



Lower in ECF (3.5 - 5 mEq/L)

 K+ concentration INSIDE cells approximates Na+ concentration OUTSIDE  Na+ concentration INSIDE cells approximates K+ concentration OUTSIDE

 Body keeps electrical charge constant in ICF and ECF, but uses different cations inside/outside cells

Total Body K

+

and Growth

Mortality and

serum K

+

K

+

Homeostasis

Youn JH et al. Annu Rev Physiol 2009; 71: 381

85-90% absorbed GI 90% excreted in urine 10% excreted in feces GI absorption Renal Excretion Distribution (ICF-ECF) Bone RBC Liver

Dietary K

+

and

Enteric

Regulation of

K

+

Renal K

+

Excretion

Tubular

Handling of K

+

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/nephrolo gy/hypokalemia-and-hyperkalemia/#figure1

K

+

Reabsorption

in the

Proximal

Tubule

K

+

Reabsorption

in the Loop of

Henle

K

+

Regulation

in DCT and

CCD

K

+

Absorption in

Collecting Duct

K

+

and GFR

Children with

CKD

Disorders of K

+

Balance



Clinical



Neuromuscular disorders



Cardiac arrest



REMEMBER: body maintains Na+/K+ gradient for

proper action potentials in neurons/muscles so

proper neuron/muscle function

Hyperkalemia



_Hyperkalemia

What is the

Most Common

Cause of

Hyperkalemia

in Infants?

Bad sample

–

Hemolyzed Sample

Assessment of hemolysis is subjective:

If it was a heelstick, fingertip or a just a

difficult stick (prolonged tourniquet) it is

Causes of

Hyperkalemia

•

❖_Diet

❖_{Blood transfusions} ❖_{Hemorrhages (GI, IVH)} ❖_Hemolysis

❖_{Tissue necrosis}



❖_{Decreased GFR}

❖_{Alteration in aldosterone-renin axis}  Hyporeninimic hypoaldosteronism  Obstructive uropathy ❖ _{Mineralocorticoid resistance} ❖_{Hyperkalemic RTA}  Redistribution ❖_{Acid-Base disturbances}

 Each ↑1 mEq/L serum [HCO3] -↓1.3 mEq/L serum [K+}

❖_{Non-oliguric hyperkalemia of the newborn}

 Drugs  Diuretics  β-blockers  Aldosterone antagonists  ENac blockers  Trimethoprim  Calcineurin inhibitors

Hyperkalemia:

EKG changes

❑

Increased amplitude of T

wave (peaked T waves) with

shortened Q-T interval (K: 6

meq/l

❑

Widening

of

the

QRS

complex

and

decreased

amplitude of P wave with

eventual

loss

of

P

wave (K:7-8 meq/l)

❑

Sine

wave

pattern

as

widened QRS merges with T

waves (K> 8 meq/l)

❑

Following these changes

ventricular fibrillation and

cardiac standstill

Management of

Acute

Hyperkalemia







❖_{Calcium gluconate 10%: 0.5 ml/kg over 5 mins}

o Effect in 1 -3 mins–lasts 30 –60 mins

▪ Dose may be repeated after 5 min if ECG changes persist



❖_{Insulin: 0.1–0.6 units/kg/h with glucose infusion of 0.5–1 g/kg/h (5–10}

ml/kg/h of glucose 10%

o Effect in 15 mins–lasts few hours



❖_{Rapid onset of action, no much data in neonates}

❖_{Dose Nebulised albuterol: 2.5 mg (under 25 kg) or 5 mg (over 25 kg).}

Intravenous albuetrolol

o Decreases K+ by 0.5–1 mmol/l

❖_{4 μg/kg given as an intravenous bolus over 5 min}

o Decreases K+ by 0.9–1.5 mmol/l



❖_{1 mmol/kg over 10–15 min – dilute 1:4 with H2O (hyperosmolality)}

❖Questionable efficacy in the absence of acidosis



❖_{1 g/Kg po or enemas}

❖_{Questionable efficacy in neonates}

Response to

Treatment of

Hyperkalemia

in ESRD

Causes of

Hypokalemia

• Poor intake

❖ _{Prolonged starvation}

❖ _{Insufficient K support in total parenteral nutrition}

• Increased renal losses

❖ _{Mineralocorticoid excess} ❖ _{Renal tubular acidosis}

❖ Bartter and Gitelman syndromes

❖ Mg Deficiency ❖ Diabetic ketoacidosis  GI Losses ❖ Vomiting ❖ _Diarrhea ❖ _{GI fistulas} ❖ _Ostomies  Drugs

❖ _{Anti-infectives (Amphotericin B and aminoglycosides)} ❖ Diuretics (Thiazides, Loop diuretics)

❖ Steroids  Redistribution ❖ Alkalosis ❖ Insulin ❖ Theophylline, caffeine ❖ _{Thyrotoxicosis} ❖ _{β agonists, epinephrine}

Hypokalemia:

EKG changes

❑

The amplitude of the T waves

decrease and flatten out.

❑

There is an increase in the

amplitude of the U wave

(normally there are no U

waves)

❑

Prolongation

of

the

Q-U

interval

❑

Increase in amplitude of the P

wave and prolongation of the

P-R interval

Management of

Hypokalemia



The safest treatment of K is via the oral/enteral route

❖_{KCl: 1–2 mEq/kg/day}



Severe symptomatic hypokalemia (K

≦

2.5 mEq/L) or GI problems

(ileus, NEC) use I.V.

❖_{KCL: 40 mEq/L}

❖_{If symptomatic, KCl: 0.5–1 mEq/kg over 1 –2 hours}

❖_{Higher concentrations (60–80 mEq/L) should be given through a}

central vein under ECG monitoring

❖_{Dextrose should not be used in initial fluids}

o Increases in insulin secretion, shifting K+ into the cells, lowering plasma K concentrations even further