Electrolyte and Metabolic Disturbances

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Objectives
Review causes and clinical manifestations of severe electrolyte disturbances Outline emergent management of electrolyte disturbances Recognize acute adrenal insufficiency and appropriate treatment Describe management of severe hyperglycemic syndromes
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Principles of Electrolyte Disturbances

Implies an underlying disease process
Treat the electrolyte change, but seek the cause

Clinical manifestations usually not specific to a particular electrolyte change, e.g., seizures, arrhythmias

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Principles of Electrolyte Disturbances

Clinical manifestations determine urgency of treatment, not laboratory values
Speed and magnitude of correction dependent on clinical circumstances Frequent reassessment of electrolytes required

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Hypokalemia
Etiology renal loss, extrarenal loss, transcellular shift, decreased intake
Manifestations cardiac, neuromuscular, gastrointestinal Deficit poorly estimated by serum levels
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Hypokalemia
Titrate administration of K+ against serum level and manifestations Correct hypomagnesemia

ECG monitoring with emergent administration

Allowable maximum iv dose per hour controversial Treat hypokalemia urgently in acidosis
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Hyperkalemia
Etiology renal failure, transcellular shifts, cell death, drugs, pseudohyperkalemia Manifestations cardiac, neuromuscular

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Hyperkalemia Treatment
Stop intake
Give calcium for cardiac toxicity Shift K+ into cell glucose + insulin, NaHCO3, inhaled -agonist Remove from body diuretics, sodium polystyrene sulfonate, dialysis

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Pediatric Considerations Potassium

Replace at maximum iv rate <1.0 mmol/kg/hr; monitor ECG Hyperkalemia ECG abnormality: calcium gluconate or chloride Shift: NaHCO3, glucose + insulin, inhaled -agonists Removal: diuretic, sodium polystyrene sulfonate, dialysis
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Hyponatremia
Hypo-osmolar hyponatremia Euvolemic Hypovolemic Hypervolemic Normo- or hyperosmolar hyponatremia Pseudohyponatremia Manifestations neurologic, muscular, gastrointestinal
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Hyponatremia Treatment
Hypovolemic Na give normal saline, rule out adrenal insufficiency Hypervolemic Na increase free H2O loss Euvolemic hyponatremia

Restrict free water intake

Increase free water loss Normal or hypertonic saline

Correct slowly due to possibility of demyelinating syndromes

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Hypernatremia
Etiology H2O loss, H2O intake, Na intake Manifestations neurologic, muscular

H2O deficit (L) =

[ 0.6 wt (kg) ] [ obs Na - 1 ] 140

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Hypernatremia Treatment
Provide intravascular volume replacement Consider giving one-half of free H2O deficit initially Reduce Na cautiously: 0.5-1.0 mmol/L/hr Secondary neurologic syndromes with rapid correction

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Pediatric Considerations Sodium

Hyponatremia seizures: titrate 3% NaCl; usual dose 1.5-2.5 mmol/kg Hypernatremia calculate H2O deficit as 4 mL/kg for each 1 mmol/L serum Na >145 mmol/L Decrease serum Na no faster than 0.5 mmol/L/hr
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Other Electrolyte Deficits Ca, PO4, Mg

May produce serious but nonspecific cardiac, neuromuscular, respiratory, and other effects All are primarily intracellular ions, so deficits difficult to estimate Titrate replacement against clinical findings
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Other Electrolyte Disorders

Hypocalcemia Calcium chloride or gluconate Bolus + continuous infusion Hypercalcemia Rehydration with normal saline Loop diuretics
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Other Electrolyte Disorders

Hypophosphatemia Replacement iv for level < 1 mg/dL (0.32 mmol/L) Hypomagnesemia Emergent administration over 510 mins Less urgent administration over 1060 mins
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Acute Adrenal Insufficiency

Nonspecific manifestations Abdominal pain, nausea, emesis Orthostatic/refractory hypotension Laboratory findings Hyponatremia, hyperkalemia Hypoglycemia
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Acute Adrenal Insufficiency

Baseline blood samples
Volume and glucose infusion Dexamethasone or hydrocortisone

ACTH stimulation test if needed

Treat precipitating conditions

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Hyperglycemic Syndromes
Diabetic ketoacidosis (DKA) Hyperglycemic hyperosmolar state (HHS)

Manifestations dehydration, polyuria/ polydipsia, altered mental status, BP, nausea, emesis, abdominal pain

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Hyperglycemic Syndromes Laboratory

Hyperglycemia/hyperosmolality Ketonemia/ketonuria (DKA)

Increased anion gap metabolic acidosis (DKA)

Electrolyte changes (K, PO4, Na)
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Hyperglycemic Syndromes Treatment

Identify and treat precipitating factors
Restore fluid/electrolyte balance Insulin iv bolus and infusion

Add glucose to infusion when glucose <250-300 mg/dL (13.9-16.7 mmol/L)

Treat electrolyte changes (K, PO4) NaHCO3 rarely needed
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Pediatric Considerations DKA

Insulin bolus not used, titrate iv infusion Titrate fluid as serum Na increases; excessive hypotonic fluid may cause cerebral edema

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Thyroid Storm
Exaggerated manifestations of hyperthyroidism Supportive measures Specific measures

Propylthiouracil or methimazole
Propranolol Potassium or sodium iodide Dexamethasone, sodium ipodate
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Myxedema Coma
Manifestations of severe hypothyroidism Supportive measures airway, fluids, glucose, warming Treat precipitating cause Hydrocortisone L-thyroxine
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Please complete reading of metabolic and electrolyte disturbances covered in the FCCS textbook.

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Key Points

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