Electrolyte Disturbances



Electrolyte Disturbances


Christopher J. LaRosa



DIFFERENTIAL DIAGNOSIS LIST*

Sodium imbalance

Potassium imbalance

Calcium imbalance

Magnesium imbalance

Phosphate imbalance

Metabolic acidosis

Metabolic alkalosis

*Normal pediatric laboratory parameters vary according to age (Table 32-1)


DIFFERENTIAL DIAGNOSIS DISCUSSION


Hypernatremia


Etiology

Definition: Serum sodium >150 mEq/L.



  • Water loss



    • Unreplaced loss of solute-free water raises the serum sodium concentration and is the most common cause of hypernatremia. Concurrent sodium loss may occur, but with water loss in excess of sodium loss.


    • Major causes:



      • Gastrointestinal (diarrhea, vomiting, or both with inadequate fluid intake)


      • Insensible water loss (fevers, exposure to heat, exercise, infants with poor feeding)


      • Urinary water loss (central or nephrogenic diabetes insipidus, renal disease with urinary concentrating defect, therapy with loop diuretics)


      • Impaired thirst/hypodipsia (hypothalamic lesions, holoprosencephaly, osmoreceptor injury leading to essential hypernatremia)


      • Osmotic diuresis (glucose, urea, mannitol) in which urine is hypotonic to plasma due to nonreabsorbed osmotically active solute


  • Excess sodium



    • Exogenous sodium intake



      • Commonly iatrogenic (oral or intravenous sodium chloride or sodium bicarbonate)


      • Salt poisoning in infants and toddlers


    • Sodium retention



      • Mineralocorticoid excess can result in mild hypernatremia with reset osmostat



  • Intracellular water movement



    • Occurs during seizures or exercise due to transient intracellular increase in osmotically active molecules (lactic acid)








TABLE 32-1 Normal Serum Pediatric Laboratory Values (found at http://www.pediatriccareonline.org)





















Sodium (Na+)

136-145 mEq/L


Potassium (K+)

Newborns 4.5-7.2 mEq/L


2 d-3 mo 4.0-6.2 mEq/L


3 mo-1 yr 3.7-5.6 mEq/L


1-16 yr 3.5-5.0 mEq/L


Bicarbonate (HCO3–)

Newborns 17.2-23.6 mEq/L


2 mo-2 yr 19-24 mEq/L


Children 18-25 mEq/L


Calcium (Ca++)

Newborns 7.0-12.0 mg/dL


0-2 yr 8.8-11.2 mg/dL


>2 yr 9.0-11.0 mg/dL


Magnesium (Mg+)

1.5-2.5 mEq/L


Phosphorus (P)

Newborns 4.2-9.0 mg/dL


6 wk-19 mo 3.8-6.7 mg/dL


19 mo-3 yr 2.9-5.9 mg/dL


3-15 yr 3.6-5.6 mg/dL


>15 yr 2.5-5.0 mg/dL



Clinical Features



  • Variable and nonspecific


  • Depend on the magnitude of hypernatremia and the rate of change


  • Irritability, lethargy, weakness, MS changes, increased deep tendon reflexes, seizures, and cramping


  • Water loss can be accompanied by dehydration, volume depletion, and weight loss


  • Sodium excess can have weight gain, mild volume expansion, and edema


Evaluation

Hypernatremia associated with water loss can cause osmotic fluid shift from the intracellular to the extracellular space, with relative sparing of the extracellular fluid (ECF) volume.

Physical examination:



  • Assess weight change if possible. Weight loss may occur even in the absence of ECF volume depletion


  • Assess adequacy of ECF compartments



    • Intravascular compartment: peripheral pulses, perfusion, temperature, and capillary refill time


    • Interstitial compartment: skin turgor, tears, and mucous membrane appearance


Laboratory Studies



  • Basic metabolic panel


  • Urinalysis and urine osmolality, sodium, and creatinine









TABLE 32-2 Assessment of Hypernatremia





























Underlying Cause

ECF Volume

Urine Output

Urine Sodium

Specific Gravity


Sodium excess

Increased

Normal or increased

Increased

High


Water loss (DI)

Decreased*

Increased

Decreased

Low


Sodium and water loss (water more than sodium)

Decreased

Decreased

Increased

High


* In states of water loss alone, resulting hypernatremia results in intracellular to extracellular fluid shift, which may initially have relative sparing of ECF volume loss. DI, diabetes insipidus; ECF, extracellular fluid.


Table 32-2 summarizes the findings suggestive of the various underlying mechanisms of hypernatremia.



Treatment

Inadequate effective circulating volume (ECV) should be treated promptly and independently of the serum sodium.



  • Normal saline to restore ECV. Initial bolus of 20 mL/kg over about 30 minutes in children without known underlying cardiac or renal disease.


  • Close monitoring and reassessment is critical.


After Restoration of ECV



  • Reduce the serum sodium level slowly (approximately 0.5 mEq/L/hour and no greater than 15 mEq/L in a 24-hour period).


  • Assessment of the solute-free water deficit, maintenance needs, and ongoing losses of water ± sodium should be performed. The free water deficit is calculated as follows:



    • 4 mL/kg of free water decreases serum Na+ by 1 mEq/L


    • The free water deficit (L)= 4 mL/kg× wt(kg)× (observed Na+– desired Na+)


  • Hypotonic intravenous fluids at a concentration and rate determined by careful calculation and given over 48 hours is recommended.


  • Avoid rapid administration of very hypotonic fluids, which can lead to intracellular water shift, cell swelling, and cerebral edema.


  • Monitor serum sodium, fluid balance, and weight closely with any intravenous fluid therapy.


  • Patients with severe total body sodium excess require judicious use of fluids, with or without furosemide administration, dialysis, or both (under the guidance of a nephrologist).


Hyponatremia


Etiology

Definition: Serum sodium <130 mEq/L. All causes of hyponatremia can be considered to be dilutional, depletional, or both (Table 32-3).



  • Dilutional hyponatremia. The total body water is generally expanded and is increased relative to total body sodium.



  • Depletional hyponatremia. There is a decreased (or normal) amount of total body water and a deficit of sodium in excess of water.


  • Pseudohyponatremia. Sodium is not distributed throughout the serum and its concentration is artificially lowered. Causes of pseudohyponatremia include hyperlipidemia and hyperproteinemia. Na+ decrease = 0.002 × lipid concentration in mg/dL (hyperlipidemia) and 0.25 × (protein in g/dL -8) (hyperproteinemia).


  • Severe hyperglycemia. Hyponatremia may occur from osmotic movement of water out of cells. Na+ decreases by 1.6 mEq/L per 100 mg/dL rise in glucose.








TABLE 32-3 Causes of Hyponatremia



















































Dilutional Hyponatremia


Water intoxication (excess ingestion or iatrogenic administration)


Edema-associated states


Congestive heart failure


Nephrotic syndrome


Renal failure


Hepatic failure


Neuromuscular blockade (e.g., pancuronium-induced)


Excess antidiuretic hormone (ADH)* (nonedematous state)


Exogenous administration


Syndrome of inappropriate antidiuretic hormone (SIADH)


Hypothyroidism


Reset osmostat


Hyperglycemia


Depletional Hyponatremia


Renal sodium wasting (e.g., Fanconi syndrome, states of aldosterone


resistance)


Adrenal sodium wasting (e.g., adrenal insufficiency)


CAH (21-hydroxylase deficiency)


Diuretic therapy


Osmotic diuresis (e.g., glucosuria)


Gastrointestinal fluid losses with hypotonic replacement


Excessive perspiration associated with large sodium loss (e.g., cystic fibrosis)


* Conditions associated with increased ADH or an ADH-like effect and hyponatremia include pain, vomiting, central nervous system disorders (e.g., trauma, infection, neoplasia), intrathoracic conditions (e.g., infection, mechanical ventilation), and some drugs (e.g., narcotics, barbiturates, carbamazepine, nonsteroidal antiinflammatory agents [NSAIDs], cyclophosphamide, vincristine). CAH, congenital adrenal hyperplasia.



Clinical Features



  • Variable and nonspecific


  • Depend on the magnitude of hyponatremia and the rate of change


  • Lethargy, weakness, encephalopathy, and seizures


Evaluation

Physical examination:



  • Assess weight change and status of ECF volume as with hypernatremia.







FIGURE 32-1 Narrowing the differential diagnosis for the underlying cause of hyponatremia. ADH, antidiuretic hormone.


Laboratory Studies



  • Basic metabolic panel


  • Serum osmolality: Estimated by doubling the serum sodium level (mEq/L) and adding 10 or the following equation:

    Serum osm = 2 × Na+ (mEq/L) + Glucose/118 + BUN/2.8


  • Urine osmolality


  • Urine sodium


  • Serum and urine uric acid (helpful in SIADH)


  • Calculation of the fractional excretion of sodium (FE Na) can be useful when the urine sodium concentration is borderline (e.g., 19 to 21 mEq/L):

    FENa = (UNa × PCr)/(UCr × PNa) × 100%

Figure 32-1 demonstrates how the differential for the specific cause of the hyponatremia can be narrowed on the basis of urine output and urine sodium excretion.


Therapy

In all cases of hyponatremia, therapy should aim to treat the underlying etiology. Management of fluid and sodium balance varies according to the category of hyponatremia.

Depletional hyponatremia: Associated with a water shift to the intracellular fluid (ICF) compartment. Therefore, careful assessment and prompt restoration of the ECF and intravascular volume are critical.



  • Compromised ECV. Restore promptly with the administration of isotonic saline, initially with an intravenous bolus of 20 mL/kg, given rapidly over about 30 minutes. Additional isotonic fluid boluses may be indicated after patient reassessment.



  • Sodium deficit. The sodium deficit should be calculated and measures taken to restore the sodium level. The sodium deficit can be calculated as follows:

    Na+ deficit (mEq) = 0.6 × wt (kg) × (desired Na+ – observed Na+)


  • Rapid increase in serum sodium with 3% saline is required in symptomatic patients (e.g., hyponatremia-induced seizures) 0.5 mEq/mL.



    • Volume of 3% (mEq) = (target Na+ – observed Na+) × wt (kg) × fD (fD – distribution factor, for Na+ 0.6-0.7 L/kg body weight).


    • In acute hyponatremia, the sodium level should be corrected to 125 mEq/L or to a level slightly higher than that associated with symptoms.


    • In chronic hyponatremia, rapid correction can lead to osmotic demyelinization syndrome or central pontine myelinolysis.


    • Target rate of Na+ rise in asymptomatic patients: 0.5-1 mEq/L/hour or 10-20 mEq/24 hour.


Dilutional hyponatremia:



  • General principle of treatment is restriction of fluid.


  • Exceptions include edematous states with hypoalbuminemia, where there is risk of intravascular volume depletion.



    • Restrict sodium, as it may contribute to worsening of associated edema.


  • SIADH: Treatment approach



    • Uncommon in pediatrics, usually transient. See Table 32-3 for medications causing SIADH.


    • ADH is fixed regardless of variation in intake, ECF volume, or serum osmolality.


    • Fluid restriction to approximately 2/3 of maintenance.



image HINT: Serum sodium concentration is maintained within a narrow range by adjustments in water intake and excretion in response to ADH secretion and thirst. Abnormalities in serum sodium are therefore predominantly a result of abnormalities in water balance, with or without a significant contribution from sodium itself; however, sodium may be a predominant factor in certain specific sodium derangements.


Hyperkalemia


Etiology



  • Transcellular potassium shifts are the most common cause of hyperkalemia in childhood. Potassium shifts from the ICF to the ECF in the following conditions:



    • Metabolic acidosis


    • Beta-adrenergic blockade


    • Strenuous exercise


    • Insulin deficiency, hyperglycemia, and hyperosmolality


    • Hyperkalemic periodic paralysis



  • Increased potassium intake



    • Potassium supplements, drugs containing potassium (e.g., potassium penicillins), salt substitute use, and blood transfusions (stored blood). Hyperkalemia usually occurs in the context of impaired renal potassium excretion.


  • Decreased renal excretion of potassium



    • Renal failure


    • Medications (Table 32-4)


    • Renal tubular acidosis (RTA) – Type IV or voltage-dependent distal (Type I) RTA


    • Mineralocorticoid deficiency (adrenal insufficiency, congenital adrenal hyperplasia (CAH), hyporeninemic hypoaldosteronism, and primary mineralocorticoid deficiency).


    • Mineralocorticoid resistance (transient condition in newborn, associated with renal injury, or due to pseudohypoaldosteronism).


  • Increased endogenous cellular release of potassium is associated with hypoxic or toxic cell death, burns, intravascular hemolysis, rhabdomyolysis, and acute tumor lysis syndrome.


  • Pseudohyperkalemia – Movement of potassium out of cells during or after specimen collection.



    • Hemolysis


    • Leukocytosis or thrombocytosis


    • Familial pseudohyperkalemia (temperature-dependent leakage of potassium out of cells)



image HINT: The presence of acidosis does not always account for the hyperkalemia and may lead to failure to recognize and treat another cause.








TABLE 32-4 Drugs Associated with Hyperkalemia























Potassium-sparing diuretics (spironolactone, triamterene, amiloride)


Potassium supplements (e.g., potassium chloride)


Potassium-containing penicillins


Stored blood


Calcineurin inhibitors (cyclosporine, tacrolimus)


Nonsteroidal anti-inflammatory drugs (NSAIDs)


Heparin


Angiotensin-converting enzyme (ACE) inhibitors


Beta-adrenergic blockers


Chemotherapeutic agents



Clinical Features

Symptoms of hyperkalemia are neither predictably present nor specific. They include muscle weakness, decreased deep tendon reflexes, ileus, anorexia, tingling of the mouth and extremities, malaise, and tetany.


Evaluation


Laboratory Studies



  • Serum electrolyte panel; serum calcium, magnesium, and glucose


  • Urinalysis, urine potassium, and creatinine (to calculate the transtubular potassium gradient or TTKG)



  • Other tests (e.g., imaging, endocrine, or genetic studies) based upon clinical suspicion


  • ECG


  • Peaked T waves (especially in precordial leads) and prolonged PR intervals or a widened, prolonged QRS complex


  • Late life-threatening ECG changes include flattened P or T waves (or both) with ST segment depression, a sine wave pattern, and tachyarrhythmias or bradyarrhythmias



Treatment

If the verified potassium level is high or there are hyperkalemic signs and symptoms, emergency measures should be initiated. Table 32-5 summarizes the options for the management of hyperkalemia. Indications for urgent or emergent treatment include the following:



  • A potassium value above 7.0 mEq/L


  • A rapidly increasing potassium concentration


  • A clinical state in which the potassium level is expected to continue to increase (e.g., rhabdomyolysis)


  • Renal failure


  • Symptoms of hyperkalemia



image HINT: Avoidance of hyperkalemia is critical in patients with kidney disease and reduced glomerular filtration rate (GFR). These patients require frequent lab monitoring. Some may require restriction of potassium intake, avoidance of certain medications (e.g., renin-angiotensin system blockade), and use of potassium-free solutions for intravenous fluid therapy. All patients receiving intravenous fluids with potassium should have renal function assessed prior to administration.


Hypokalemia


Etiology



  • Severely limited nutrition (e.g., anorexia nervosa, renal excretion can adjust to more moderate limitations in potassium intake)


  • Increased gastrointestinal losses (e.g., vomiting, diarrhea, cathartic abuse)


  • Increased skin losses (e.g., excessive sweating, burns)


  • Increased renal losses— Fanconi syndrome, RTA, Bartter syndrome, diuretic therapy, osmotic diuresis (e.g., glucosuria), hyperaldosteronism, CAH, 11-b-hydroxysteroid dehydrogenase deficiency (or inhibition with natural licorice ingestion), Liddle syndrome, Gitelman syndrome (magnesium-losing tubulopathy), salt-wasting nephropathies, excess adrenocorticotropic hormone (ACTH), drugs (Table 32-6), magnesium depletion, chloride depletion, loss of gastric secretions, and polyuria


  • Transcellular potassium shifts— alkalosis (metabolic and respiratory), excess insulin, beta-adrenergic activity, hypokalemic periodic paralysis, and certain drugs (Table 32-6)









TABLE 32-5 Treatment of Hyperkalemia



























































Agent

Indication

Mechanism of Action

Dose

Side Effects/Potential Problems


10% calcium gluconate

ECG changes

Stabilizes membranes

1 mg/kg IV over 5-10 min

Hypercalcemia


Sodium bicarbonate*

ECG changes or very high K+ level

Shifts K+ to intracellular compartment

1 mg/kg IV over 5-10 min

Sodium load


Glucose plus insulin

ECG changes or very high K+ level

Shifts K+ to intracellular compartment

0.25-0.5 g/kg glucose plus 0.3 U insulin/g glucose over 30-60 min

Hyper- or hypoglycemia


Albuterol (Betaagonist)

ECG changes or very high K+ level

Shifts K+ to intracellular compartment

1.25-2.5 mg by nebulizer

Tachycardia


Kayexalate resin

To remove K+ from body

K+ binds to resin in gut

1 g/kg PO or PR in 50%-70% sorbitol

Constipation


Furosemide

Symptomatic hyperkalemia

Enhances urinary K+ excretion

1-2 mg/kg IV

May not be enough renal function to be effective


Hemodialysis or peritoneal dialysis

Decreased renal function

Removes K+ in dialysate

—

Risks associated with dialysis


Exchange transfusion

ECG changes or very high K+ level

Donor blood must be washed and have had most K+ removed

Double volume

Risks associated with exchange transfusion


* Sodium bicarbonate and calcium salts are incompatible in intravenous solutions. ECG, electrocardiogram; IV, intravenous; K+, potassium; PO, oral; PR, rectal.

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Sep 14, 2016 | Posted by in PEDIATRICS | Comments Off on Electrolyte Disturbances

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