K homeostasis

1. Hyperkalemia and Hypokalemia in Neonates
Presenter-DrBasantKumarPandey(JR)
Moderator-Dr.Poonam(AP,Neonatology)
Dr.Shantanu (SR,Neonatology)

2. TABLE OF CONTENTS
INTRODUCTION
PHYSIOLOGY OF K⁺
EXCRETION OF K⁺
DEFINITION OF HYPERKALEMIA, CLINICAL FEATURES,ETIOLOGY,TREATMENT
DEFINITION OF HYPOKALEMIA, CLINICAL FEATURES,ETIOLOGY,TREATMENT

3. Introduction
Potassium an essential cation for cellular functions, is widely distributed in
body. This is the most serious of electrolyte abnormalities because it can
cause fatal arrhythmias.
Normal potassium levels are generally between 3.5 and 5.5 mEq/L, with
a potassium >5.5 mEq/L indicating hyperkalemia.
Daily requirement of K is about 1-2 mEq/kg.
Potassium is needed for somatic growth.
Adults maintain a zero potassium balance,whereas in young children a
positive potassium balance is needed. This is reflected by higher serum
potassium levels in neonates.

4. Physiology
Nearly 98% of potassium is distributed in the ICS with a conc. Of 140-150 mEq/L.
Majority of extracellular potassium is in bones, <1% of total body potassium is in
plasma
The intercellular to extracellular potassium gradient is maintained by sodium
potassium triphosphatase and selective K⁺ channel.
Na-K-ATPase allows active transport of Potassium into cells whereas selective
channels allow passive diffusion of K⁺ out of cells.
Potassium homeostasis depends on a number of renal and extra renal factors like
intake , GI and Urinary losses and transcellular shift.

5. Normal distribution of potassium

7. After ingestion of a meal, approximately 80% of the potassium that is absorbed
by the gut is rapidly translocated into the intracellular space.
This rapid uptake of potassium is mainly induced by increased insulin
Insulin increases the activity of the Na+,K+-ATPase in hepatocytes,muscle cells, adipose
cells, and brain cells, thereby increasing their potassium uptake.
Meanwhile any rise in s. potassium levels will decrease the transmembrane potassium
gradient, thereby decreasing the passive efflux of potassium out of the cells.

8. Triiodothyronine (T3) increases Na+,K+- ATPase in muscle cells, increasing their
potassium uptake
hydrogen ions impair the activity of Na+,K+-ATPase, thus decreasing intracellular
potassium uptake
An increase in serum osmolality shifts water out of the cells, which
inevitably leads to an increase of intracellular potassium concentration

9. Excretion of K⁺
Kidney is the primary organ for excretion of K⁺ upto 90%
Nearly 90% of K⁺ is reabsorbed up to distal tubules and only 10-15% reaches cortical
and outer medullary collecting ducts, which is the principle site of regulation of
potassium excretion.
Potassium secretion in cortical collecting duct (CCD) is regulated by aldosterone
secreted from adrenal cortex.
Glucocorticoid, ADH, high urinary flow and Na delivery to distal nephron increases
urinary protein excreation

11. Hyperkalemia
DEFINITION
Serum K⁺ >5.5 mEq/L
Based on the Sr. K⁺ concentration, Hyperkalemia can be categorized as:
Serum potassium >6 mEq/L in full-term neonates.
Serum potassium >6.5 mEq/L in premature infants.
Moderate hyperkalemia: Serum potassium 6 to 7 mEq/L
Severe hyperkalemia: Serum potassium >7 mEq/L
The serum potassium level is 7.0 mEq/L in an extremely low birthweight
(ELBW) infant

12. Etiology
Spurious raised levels :
Release of K⁺ from Hemolysed RBC at the time of blood
sampling.
True Hyperkalemia :
Increased load
Impaired renal excretion
Transcellular shift of K⁺

13. Etiology
Increased Load
A)Exogenous Source :
Salt Supplements, Transfusion.
B)Endogenous Source :
Intravascular hemolysis
resolving hematoma
rhabdomyolysis
tumor lysis.

14. Impaired Renal Excretion
A)↓ed Na & H20 delivery to distal cortical tubules : AKD or Volume Depletion
B) Functional Aldosterone :
Hypoaldosteronism with ed Renin levels – Primary Adrenal Disease(Addison, CAH),
Aldosterone synthase deficiency, use of drugs (ACE inhibitors, Angiotensin receptor
blocker)
Renal Tubular Diseases : Bartter syndrome –type II, Urinary Tract obstruction, Kidney
transplant
Potassium sparing diuretics & NSAIDS

15. Etiology
Transcellular shift
Acidosis
Hypertonicity
Diabetes
Myolysis
Drugs like Digoxin, Beta blockers &
Succinylcholine
Extensive Muscle/ Cellular Injury
Malignant hyperthermia

16. Clinical Presentation
Muscular or respiratory paralysis
Bradycardia
Ventricular arrhythmias(ventricular fibrillation/tachycardia)
Shock
Cardiac arrest
Tendon reflexes can be decreased

17. In neonates, serum potassium >6.7 mEq/L is associated with ECG changes.
Serum potassium of 5.5 to 6.5 mEq/L- Tall peaked T waves with a narrow base,
shortening of PR interval, normal or decreased QT.
Serum potassium of 6.5 to 8 mEq/L. Tall peaked T waves, prolonged PR interval,
loss or decreased P wave, amplified R wave, widening of QRS.
Serum potassium >8 mEq/L. Absent P wave, wide bizarre diphasic QRS, progressive
QRS widening merging with the T wave, bundle branch blocks, ventricular
fibrillation or asystole.

19. Lab studies
1. Immediate tests
a. Serum potassium level
b. Serum and urine electrolytes.
c. Complete blood count and differential-To rule out sepsis and hemolysis.
d. Serum ionized and total calcium levels. Hypocalcemia may potentiate the
effects of hyperkalemia. Maintain normal serum calcium concentrations.
e. Serum pH and bicarbonate. To rule out acidosis, which may potentiate
hyperkalemia.
f. Blood urea nitrogen and serum creatinine levels. May reveal renal
insufficiency.

20. g. Urine dipstick and specific gravity. To assess renal status and blood and
hemoglobin for tissue breakdown secondary to hemolysis.
2. Further testing- Serum renin, angiotensin, and aldosterone for hypoaldosteronism
and pseudohypoaldosteronism.
C. Imaging and other studies
1. Abdominal radiograph if NEC is suspected.
2. Electrocardiogram may reveal the cardiac changes characteristic of hyperkalemia
and provides a baseline study

21. TREATMENT
If plasma K⁺ >6.5 mEq/L or ECG abnormalities are detected, emergency treatment
should be initiated.
Priority of Rx
1. Withdrawl of Source if any; in case blood transfusion is urgently needed use of
fresh & washed RBC’s are recommended,
2. Stabilization of myocardial cells.
3. Rapid reduction of plasma K levels with transcellular shift.
4. Enhance K elimination from body
5. Treatement of underlying cause.

22. TREATMENT
Cardiac stabilization
10 % calcium gluconate 1-2 ml/kg 1 hour under cardiac monitoring.
Dilution and intracellular shifting of potassium
 Glucose insulin infusion :
Bolus of 0.05 unit/kg regular insulin with 2ml/kg of 10% Dextrose f/b continuous infusion
of D10 at 2-4ml/kg/hr and insulin @1 ml/kg/hr.Should be monitored for hypoglycemia.
Short acting beta agonist : Salbutamol Neb 2.5 -5 ml in 3ml NS over 20 mins
1-2mEq/kg/hr of Sodium bicarbonate may be used

23. Enhanced potassium excreation:
Ion exchange Resin : sodium polysterene sulfonate (Kayexalate) 1-2g/kg PO or PR
IV Furosemide 1-2 mg/kg if Kidney function is normal
Hemodialysis/ Peritoneal Dialysis with K free fluid.

26. Nonoliguric hyperkalemia (NOKH)
NOKH is hyperkalemia in the absence of oliguria and potassium intake.
NOKH is serum potassium ≥7 mmol/L in the presence of urine output of ≥1 mL/kg/h
during the first 72 hours of life
Incidence varies between 11% and 52%.
It occurs more commonly in ELBW infants than term infants, with 80% of NOHK cases in
ELBW infants <28 weeks’ gestation.
These infants usually did not have exposure to antenatal steroids, which seems to
protect some infants.
Due to the immature function of Na/K-ATPase activity in premature
neonates.

27. Hypokalemia

28. Hypokalemia is defined as a serum potassium <3.5 mEq/L.
A. Mild hypokalemia is 3.0 to <3.5 mEq/L,
B. Moderate hypokalemia is 2.5 to 3.0 mEq/L,
C. Severe hypokalemia is <2.5 mEq/L.

29. Etiology
Spurious
High white blood cell count
Transcellular shifts
Alkalemia, Insulin, β-Adrenergic agonists, Drugs/toxins (theophylline, barium, toluene)
Hypokalemic periodic paralysis, Refeeding syndrome
Decreased intake

30. Extrarenal losses
Diarrhea,Sweating
metabolic acidosis
Ureterosigmoidostomy
Tubular toxins (amphotericin, cisplatin, aminoglycosides)
Hypomagnesemia
Adrenal adenoma or hyperplasia,Glucocorticoid-remediable aldosteronism,Renin-
secreting tumor
17α-Hydroxylase deficiency,11β-Hydroxylase deficiency

31. Presentation
Mild hypokalemia may not cause any signs or symptoms. There may be slight
muscle weakness.
Moderate hypokalemia
musculoskeletal symptoms (weakness,decreased tendon reflexes, myalgia, muscle
cramps, paresthesias, paralysis)
GI symptoms (nausea, vomiting, diarrhea, constipation, ileus)
central nervous system signs (lethargy). These are very difficult to evaluate in an infant.

32. Severe hypokalemia
lethargy, severe muscle weakness, paralysis,ileus (abdominal distension and hypoactive
bowel sounds)
cardiac arrhythmias (rare unless <2.5 mEq/L)
respiratory depression (flaccid or diaphragmatic paralysis), respiratory arrest, or
bradycardia with cardiovascular collapse.
Rhabdomyolysis (skeletal muscle destruction) and myoglobinuria (leakage of
muscle protein myoglobin in the urine) can occur. Muscle fasciculation and
tetany can occur.

33. ECG Changes
flattened T wave
depressed ST segment
Appearance of a U wave, which is located between the T wave (if still
visible) and P wave
increase in P wave amplitude
prolonged PR interval

34. Laboratory studies
1.serum potassium level
2.Spot check urinary electrolytes-
a. Urine potassium is <20 mmol/L: Suspect nonrenal losses.
b. Urine potassium is >20 mmol/L: Suspect renal losses and Bartter syndrome.
c. Urinary chloride level is low (<10 mEq/L): Consider GI losses
d. Urine chloride is normal in Bartter syndrome and diuretic therapy.

35. e. A low urine sodium level with a high urine potassium level is associated
with secondary hyperaldosteronism.
f. If urine magnesium is high, consider renal magnesium loss
3.Serum electrolytes and creatinine. To evaluate renal status and other electrolyte
abnormalities.
a. A low serum sodium suggests GI loss or thiazide diuretic use.

36. b. Urinary potassium-to-creatinine ratio-
If the ratio is <1.5, consider low potassium intake, GI losses, or thyrotoxicosis
If the ratio is ≥1.5, consider aldosteronism, Cushing syndrome, congenital adrenal
hyperplasia, renal tubular acidosis (RTA), diuretic use, Bartter/Gitelman syndrome, or
vomiting.
Blood gas levels. An alkalosis may cause or aggravate hypokalemia

37. Treatment
Emergency treatment
Limited to infants with life-threatening symptoms of hypokalemia or for a serum
potassium level <2.0 to 2.5 mEq/L
Never give a bolus of potassium
Give potassium chloride 0.5 to 1 mEq/kg/dose over 1 hour (some sources suggest 2
hours) with continuous ECG monitoring (maximum infusion rate: 1 mEq/kg/h).
.

38. Moderate symptomatic hypokalemia
1. Abnormal electrocardiogram:
ST-segment depression, T-wave depression,U-wave elevation:
Treat with potassium chloride 0.5 to 1 mEq/kg IV over 3
2. Normal electrocardiogram:
Add 20 mEq of potassium chloride per liter to peripheral vein IV fluids

39. Mild asymptomatic hypokalemia.
May resolve without treatment.
The majority of cases can be corrected by increasing the daily potassium intake by 1 to 2
mEq/kg
Hypokalemia with hypovolemia/polyuria. IV fluid with potassium chloride is indicated.

40. Thank you