• a. Hypochloremic, hypokalemic metabolic alkalosis.
• b. Moderate hypokalemia.
  • Classification of hypokalemia based on severity is as follows:
  • (Apart from numbers, any child with neuromuscular weakness or cardiac rhythm disturbances are considered as severe hypokalemia)

Serum potassium levels	Severity
3–3.5 mEq/L	Mild hypokalemia
2.5–3 mEq/L	Moderate hypokalemia
<2.5 mEq/L	Severe hypokalemia

• c. Prolonged PR interval, slightly peaked P wave, ST depression, shallow T wave, and prominent U wave.
• d. Hypokalemia is due to an increased potassium uptake by metabolically active cells like leukemic white blood cells (due to enhanced activity of sodium-potassium ATPase pump).
• e. Other gastrointestinal (GI) losses—gastroenteritis with predominant vomiting and renal losses—diuretic therapy.

• a. Salbutamol nebulization causing intracellular shift of potassium.
• b. Insulin administration in DKA, high insulin levels in refeeding syndrome, thyrotoxicosis, and familial periodic paralysis.
• c. Acidosis: The increase in H+ ion concentration reduces the activity of sodium-potassium ATPase (Na/K/ATPase) pump thereby reducing the cellular uptake of potassium resulting in high potassium levels in ECF.

Alkalosis has the opposite effect. Sodium-potassium ATPase pumps 3 sodium ions out of the cell and 2 potassium ions into the cell.

• a. TTKG is an index that measures or determines renal response to hypo/hyperkalemia. It is the reflection of potassium conservation by cortical collecting duct. It is calculated as:

TTKG values >4 indicates renal loss of potassium.

• b. FEK is the percentage of potassium filtered by kidney that is excreted in urine. It is calculated as:

FEK values >6% indicates renal loss of potassium.

• c. Urine potassium assessment helps to differentiate between GI and renal loss of potassium. Urine potassium >15 mEq/L indicates renal loss.
• d. Renal tubular acidosis (RTA), Bartter syndrome, Gitelman syndrome, drugs like thiazides, and loop diuretics (RTA—metabolic acidosis, Bartter and Gitelman syndrome—alkalosis). Remember mineralocorticoid excess can also lead to renal wasting of potassium but it will be associated with hypertension and metabolic alkalosis.

• a. Triad of hypertension, hypokalemia, and metabolic alkalosis—Liddle syndrome or pseudohyperaldosteronism (autosomal dominant inheritance) which mimics mineralocorticoid excess but has low renin and aldosterone levels.
  • Interpretations based on paired renin and aldosterone levels are as follows:

Paired renin and aldosterone	Interpretation
Raised renin and aldosterone	Renal artery stenosis
Raised aldosterone and low renin	Adrenal tumor and familial hyperaldosteronism
Low renin and aldosterone	Congenital adrenal hyperplasia (CAH), Liddle syndrome, and glucocorticoid excess

• b. Gain of function mutations of epithelial sodium channel (ENaC) located in collecting duct resulting in enhanced activity leading to excessive sodium reabsorption and potassium secretion.
• c. Syndrome of apparent mineralocorticoid excess.
• d. Oral amiloride or triamterene blocks the ENaC channels, correcting both hypertension and hypokalemia.

• a. This child is having severe hypokalemia due to GI loss which requires urgent correction by potassium infusion (never give potassium as IV bolus!). The dose is 0.3 mEq/kg/h over 1–3 hours through central line under cardiorespiratory monitoring preferably in an ICU. Here IV KCl is used, e.g., for a 20 kg child 6 mEq/h over 3 hours. This means KCl 9 mL (containing 18 mEq) mixed with 30 mL of NS and given over 3 hours in a syringe pump. The subsequent therapy is guided by repeat values of potassium after correction. Remember, mEq and mmol are same for Na+ and K+.
  • Treatment plan based on severity of hypokalemia is as follows:

Severity of hypokalemia	Treatment
Mild	Oral potassium supplement: 1–2 mEq/kg/day
Moderate	Increase the maintenance potassium to 40 mEq/L if given through peripheral line.
Severe	IV correction as mentioned above

• b. Normal Saline. Never infuse potassium with a glucose containing solution as it will cause release of insulin which will exaggerate hypokalemia by shifting the potassium inside the cells.
• c. RL—4 mEq/L
  • Potassium concentration in different IV fluids is as follows:

Fluid	Potassium concentration
RL and PlasmaLyte	4 mEq/L and 5 mEq/L
Isolyte P	20 mEq/L
KCl (15%)	2 mEq/mL
Normal saline and DNS	Nil

• a. Reduced renal excretion of potassium due to intrinsic renal disease.
• b. ECG changes: Tall T waves, prolonged PR interval, loss of P wave, prolonged QRS complex, and ST segment elevation.
• c. Urine potassium will be <15 mEq/L due to defective renal excretion.
• d. ACE inhibitors, angiotensin receptor blockers, potassium-sparing diuretics, and nonsteroidal anti-inflammatory drugs (NSAIDs).

• a. Hyperkalemia with low sodium suggests reduced mineralocorticoid activity. Low urine potassium and TTKG indicates defective mineralocorticoid action which is confirmed by low aldosterone level. Normal cortisol and 17 hydroxyprogesterone rules out CAH. Hence the diagnosis is isolated hypoaldosteronism.
• b.
  • Substituting the above indicates values, TTKG comes as 0.8
• c. TTKG values above 7 indicate appropriate aldosterone action while the levels <7 indicates aldosterone deficiency or resistance. Aldosterone resistance has high levels of aldosterone whereas deficiency state will have low or undetectable levels. Transtubular potassium gradient (TTKG) values are also used to find out the cause for defective renal excretion of potassium.
• d. Role of paired renin and aldosterone levels in a child with hyperkalemia is as follows:

Paired renin and aldosterone	Interpretation
Raised renin and aldosterone	Aldosterone resistance
Raised renin and low aldosterone	CAH and hypoaldosteronism
Low renin and aldosterone	Intrinsic renal disease

• e. Useful in the evaluation of hypokalemia due to renal loss and in the presence of hypertension. This evaluation helps one to decide (1) whether aldosterone secretion is secondary to reduced renal blood flow, renin secretion leading to aldosterone secretion or (2) increased aldosterone is because of autonomous secretion of aldosterone from adrenal gland which in turn suppresses rennin levels or (3) due to mineralocorticoid excess other than aldosterone.
  • Simplified concept of renin–angiotensin–aldosterone (RAA) axis is as follows:

• a. Tumor lysis syndrome.
• b. Hyperuricemia, hyperphosphatemia, and hypocalcemia.
• c. Thrombocytosis, hemolysis, tourniquet application, and cold storage
• d. Treatment for hyperkalemia is as follows:

Drug	Dose	Mechanism
Calcium gluconate (10%)	0.5–1 mL/kg with 5% dextrose	Cardiac stabilization
Sodium bicarbonate (7.5%)	1–2 mEq/kg IV	Intracellular shift
Insulin and glucose	0.1–0.2 U/kg of insulin with 0.5–1 g/kg glucose	Intracellular shift
Salbutamol nebulization	<1 year: 1.25 mg 1–5 years: 2.5 mg >5 years: 5 mg	Intracellular shift
Polystyrene sulfonate	1 g/kg/dose	Increased excretion

• a. Predominant cation in ECF—sodium; predominant cation in ICF—potassium (remember predominant anion in ECF is chloride and ICF is phosphate)
• b. The ECF volume is determined primarily by sodium ion
• c. 1 year of age
• d. 0.6 × body weight (BW)

Composition of total body water.

• a. Corrected sodium = Measured sodium +
  • In other words, for every 100 mg of sugar above 100 mg, sodium falls by 1.6 mEq. That means blood sugar rise is 200 mg above 100. 2 × 1.6 = 3.2 when added to 134, corrected sodium is 137.2
  • Substituting the above values, corrected sodium value comes as 137.2 mEq/L.
• b. Osmolality of plasma is 285–295 mOsm/kg. It is calculated as:
  • Osmolality = 2(Na) +
• c. Since urea is an ineffective osmole, only plasma glucose level is taken into consideration which is called as effective plasma osmolality.
  • Effective osmolality =
  • Ineffective osmoles are urea and ethanol.
• d. When the difference between the measured osmolality and calculated osmolality exceeds >10 mOsm/kg, it is called the Osmolal gap. It indicates the presence of unmeasured osmoles such as ethanol, methanol, ethylene glycol, etc. To quote an example, when a child with altered consciousness, also has high anion gap metabolic acidosis and osmolar gap, this indicates poisoning due to substances such as ethanol, methanol, or ethylene glycol.

• a. 17 cal/100 mL. This provides approximately 20% of the normal calorie needs in a day which is enough to inhibit ketones production and protein degradation.
• b. As per Holliday-Segar formula, this child requires 1,250 mL of maintenance fluid per day (100% TFI) which comes as 50 mL/h. There are two types of IV infusion sets—micro and macro sets. In a micro drip set, each mL is made up of 60 drops/min. Here if the rate is set at 10 drops/min, it will provide 10 mL/h. 50 mL/h means we have to set up 50 drops/min. In macro drip sets, approximately 15 drops make 1 mL. Using a macro drip set divide mL/h by 4 to get number of drops/min. Here substituting the values, considering 15 kg—total fluid requirement is 50 mL/h—when using a macro drip set, 13 drops/min to be used. But one should remember that critical medications like insulin, adrenaline or dopamine cannot be given through micro or macro sets. It should be infused only in syringe pump or infusion pump.
• c. Composition of various fluids is as follows:

Fluid	Na (mEq/L)	Cl (mEq/L)	K (mEq/L)	Lactate	Dextrose
NS	154	154	—	—	—
DNS	154	154	—	—	5%
1/2 DNS	77	77	—	—	5%
1/2 NS	77	77	—	—	—
RL	130	109	4	28	—
Isolyte P	25	22	20	—	5%

• Remember, DNS, ½ DNS, and Isolyte P contains 5 g of glucose in 100 mL.
• d. When hypotonic fluids are used for IV infusions it will result in hyponatremia which will push water into red blood cells (RBCs) resulting in hemolysis.

• a. In a child with severe acute malnutrition (SAM), there will be an increase in cellular sodium and depletion of total body potassium and hence their diet should be low in sodium with supplemented potassium and magnesium for the first 2 weeks of rehabilitation.
• b. Oral or nasogastric tube feeding using ReSoMal. IV fluids are used only when a child is having shock, altered sensorium, or unable to drink orally. IV fluid of choice is 0.45% of NS with 5% glucose or RL with 5% glucose.
• c. Lethargy, thirst, cold clammy skin, weak or absent pulses, and reduced urine output.
• d. Sodium and potassium content in ReSoMal versus low osmolarity ORS is as follows:

Parameter	ReSoMal	Low osmolarity ORS
Sodium	45 mEq/L	75 mEq/L
Potassium	40 mEq/L	20 mEq/L

• e. Preparation of ReSoMal:
  • Step 1: Take one sachet of WHO standard ORS and mix in two litres of water
  • Step 2: Add 50 g of glucose to that
  • Step 3: Add 60 mEq of potassium in either of the following way:
    • a. Potclor syrup 45 mL or
    • b. IV KCl solution 30 mL to be mixed with this solution for oral use

• a. Composition of low osmolarity ORS is as follows:

Electrolyte	Concentration (mmol/L)
Sodium	75
Potassium	20
Glucose	75
Chloride	65
Citrate	10
Total osmolarity	245

• b. Acts through sodium glucose cotransporter 1 protein (SGLT1) in jejunum which actively transports both the sodium and glucose which results in improved water reabsorption from the gut into the body to maintain the osmotic balance.
• c. ORS fortified with amino acids such as L-alanine, glycine, glutamine, or addition of oligopeptides enriched starch from rice powder (instead of glucose).
• d. Green banana has high content of amylase-rich starch which is fermented by the colonic bacteria into short chain fatty acids which stimulate salt and water absorption from the gut.

• a. Pseudohyponatremia is due to hypercholesterolemia.
• b. Improper sampling, hyperglycemia, hyperproteinemia, and increased osmolar agents like mannitol. In these conditions, these substances reduce the water fraction of plasma. In other words, the total plasma volume raises hence sodium value is erroneously measured as low (remember total body sodium is normal in these conditions).
• c. Serum osmolarity is low in true hyponatremia whereas it is normal or high in pseudohyponatremia.
• d. By using direct ion-selective electrode (ISE) method which measures the sodium in total serum.

• a. Diabetes insipidus and psychogenic polydipsia.
• b. Craniopharyngioma, Langerhans cell histiocytosis, sarcoidosis, lymphocytic infundibulo-hypophysitis, trauma, congenital malformation, and familial/genetic central DI. Central DI of unknown etiology is classified as idiopathic.
• c. Triple response is due to pituitary stalk injury from traumatic brain injury or in a neurosurgical procedure. Initially there is a central DI followed by SIADH and finally established central DI. The initial phase of central DI is due to stunning of arginine vasopressin (AVP) neurons and severing of downstream nerve terminals in the posterior pituitary followed by SIADH due to unregulated release of vasopressin from the remaining degenerating neurons followed by an established DI as the damaged neurons can no longer produce AVP.
• d. Water deprivation test.

• a. This child, with a background of meningitis, has hyponatremia with euvolemia (urine output is normal). Serum osmolarity is low hence it is true hyponatremia, urine osmolarity is more than serum osmolarity, and urine sodium is 50 mEq/L which indicates natriuresis despite low serum osmolarity—fits into SIADH.
• b. This child is symptomatic for >48 hours, hence chronic hyponatremia. This child should be corrected slowly (6–8 mEq/day correction) as rapid correction will result in osmotic demyelination.
• c. Vasopressin (v2) receptor antagonist.
• d. DI—hypernatremia and SIADH—hyponatremia.

• a. Acute hyponatremia—hypervolemic hyponatremia due to low intravascular volume.
• b. Cerebral edema.
• c. 3–5 mL/kg of 3% saline in euvolemic and hypervolemic hyponatremia. In hypovolemic hyponatremia 20 mL/kg of NS over 30–60 minutes. The goal is to increase the sodium up to 5 mEq/L from the baseline values which is enough to correct the symptoms. This is done in addition to stabilize the A, B, C, and control of seizures.
• d. Adrogué–Madias formula, Barsoum–Levine formula, electrolyte free water clearance, and Nguyen–Kurtz equation.

• a. Polyuria with hypovolemia hyponatremia, low serum osmolarity, and high urinary sodium excretion—cerebral salt wasting.
• b. Increased atrial natriuretic peptide (ANP) which inhibits AVP and aldosterone causing natriuresis.
• c. Sodium and water replacement using isotonic saline and fludrocortisone.
• d. 1 mL of 3% saline = 0.5 mEq sodium.

• a. Hypovolemic hypernatremia as evidenced by the presence of dehydration and high sodium levels.
• b. Intracranial bleed, venous sinus thrombosis, and hypocalcemia.
• c. Stabilize airway breathing and circulation. Give oxygen. Since this child is in compensated shock, give bolus with NS at 10–20 mL/kg over 30–60 minutes and further boluses if needed to be decided as per clinical status. This should be followed by fluid infusion consisting of deficit correction plus ongoing loss replacement plus daily maintenance. Free water deficit can be calculated as 4 mL/kg × (current sodium − desired sodium). In other words, deficit and maintenance together can be given as 1.25–1.5 times the maintenance. Fluid of choice is 1/4 − 1/2 NS or 1/5 NS.
• d. Serum sodium persistently >180 mEq/L, multiple electrolyte abnormalities, and acute kidney injury.
• e. 8–12 mEq/day. The rate of fall should not exceed beyond 0.5 mEq/h.

• a. This child has features of rickets with low serum calcium and phosphorus, high alkaline phosphatase, high PTH and normal 25-hydroxyvitamin D3, and a very low 1,25-dihydroxyvitamin D3—Vitamin D dependent rickets type 1 (VDDR type 1).
• b. Molecular testing for CYP27B1 gene mutation.
• c. Active vitamin D3 (1,25-dihydroxyvitamin D3) at a dose of 0.25 µg/day along with calcium with or without phosphorus.
• d. Vitamin D dependent rickets type 2 (VDDR type 2).

• a. This child has clinical and biochemical findings of rickets with a normal 25-hydroxyvitamin D level—suggestive of calcium deficiency. There are two reasons, if a child with rickets show normal serum 25 OH vitamin D levels—1) VDDR type 1. 2) Dietary calcium deficiency. In very low calcium intake groups in tropical population dietary calcium deficiency may play a synergistic role by accentuating the need for vitamin D.
• b. When the dietary intake of calcium is <200 mg/day.
• c. Celiac disease, intestinal abetalipoproteinemia, and small bowel resection.
• d. Low urine calcium and high urine phosphorus due to secondary hyperparathyroidism.