Hypernatremia

Hypovolemic

  Renal

    Nephrogenic diabetes insipidus

    Renal tubular dysfuntion

    Medications (e.g., thiazide, loop diuretics)

    Osmotic diuresis, including diabetic ketoacidosis, hyperosmolar hyperglycemic state

  Nonrenal

    Gastrointestinal (GI) fluid loss

    Cutaneous fluid loss (e.g., severe burns, fever, heat exposure, mechanical ventilation)

  Impaired thirst

    Altered mental status, physically impaired, limited access to water

Euvolemic

    Diabetes insipidus (neurogenic or nephrogenic)

Hypervolemic

    Exogenous sodium infusion

    Hyperaldosteronism

    Hypercortisolism

General

  Anorexia

  Fatigue

  Irritability

  Malaise

  Restlessness

  Fever

  Flushed skin

Neurologic

  Delirium

  Seizures

  Coma

  Hyperreflexia

  Cerebralhemorrhage

  Central pontine myelinolysis presenting with altered mental status, seizures, death

Respiratory

  Hyperventilation

Gastrointestinal

  Nausea/vomiting

Consult medicine for plasma [Na⁺] >145 mEq/L and presence of neurologic symptoms, mental status changes, hemodynamic instability, acute deterioration of renal function.

Perform complete history and physical examination.

Assess volume status, including vital signs, orthostatics, jugular venous distension, skin turgor, mucous membranes, edema.

Confirm why patient is not drinking water (e.g., paranoia, catatonia, impaired mobility).

Perform strict fluid intake/output measurements.

Laboratory studies may entail chemistry panel, uric acid, urinalysis, urine Na/K/Cl, urine and serum osmolalities.

Management as per medicine recommendations.

Management of lithium-induced nephrogenic diabetes insipidus (often reversible if lithium discontinued).

  Increase fluid intake.

  Consider K 10-20 mEq/day.

  Consider thiazide (caution), amiloride (nonthiazide and preferred) 5-10 mg p.o. BID.

  Discontinue lithium.

  Continue electrolyte monitoring.

If lithium must be continued:

  Decrease to lowest effective dose and QD if able.

    Monitor lithium level minimum q2mos.

Hyponatremia

Hypotonic

  Hypovolemic

    Renal losses (e.g., diuretics, hypoaldosteronism)

    Extrarenal losses including GI, cutaneous.

  Euvolemic

    Syndrome of inappropriate antidiuretic hormone (most common cause)

    Medications (e.g., antipsychotics, antidepressants, thiazides)

    Hypothyroidism

    Adrenal insufficiency

    Primary polydipsia

    Psychogenic polydipsia

  Hypervolemic

    Cirrhosis

    Congestive heart failure

    Nephrotic syndrome

    Advanced renal failure

  Isotonic

    Pseudohyponatremia

    Isotonic mannitol infusion

  Hypertonic

    Hyperglycemia

    Hypertonic solution infusions

General

  Anorexia

  Fatigue

  Malaise

  Agitation

Hypothermia

  Orthostatic hypotension

Neurologic

  Altered mental status

  Pseudobulbar palsy

  Cranial nerve palsies

  Hyporeflexia

  Positive

    Babinski sign

  Stupor

  Coma

  Seizures

  Death

  Lethargy

Respiratory

  Cheyne-Stokes respiration

Gastrointestinal

  Ileus

  Nausea/vomiting

  Hiccups

Musculoskeletal muscle cramps

Consult medicine for plasma [Na⁺] <130 mEq/L and/or rapid decrease in [Na⁺] as well as presence of neurologic symptoms, mental status changes, hemodynamic instability, acute deterioration of renal function.

Restrict fluid and perform close fluid intake/output measurements.

Consider 1:1 observation if psychogenic polydipsia suspected.

Perform complete history and physical examination.

Assess volume status, including vital signs, orthostatics, jugular venous distension, skin turgor, mucous membranes, edema.

Laboratory studies may entail chemistry panel, uric acid, urinalysis, urine Na/K/Cl, urine and serum osmolalities.

Management as per medicine recommendations.

Generally, this involves determination and correction of etiology, cautious replacement of sodium and potassium, and fluid restriction/loss.

Psychotropic-induced syndrome of inappropriate antidiuretic hormone secretion (SIADH):

Antidepressants (selective serotonin reuptake inhibitors [SSRIs], tricyclic antidepressants [TCAs], venlafaxine), antipsychotics, and carbamazepine have been observed to cause SIADH.

Symptoms include lethargy, headache, hyponatremia, elevated urinary sodium excretion, and hyperosmolar urine.

Acute treatment generally involves discontinuation of drug and fluid restriction. If central nervous system (CNS) symptoms are present, refer to medicine for rapid correction of [Na⁺].

Patients not responding to water restriction and discontinuation of drug may require demeclocycline therapy.

Hyperkalemia

Pseudohyperkalemia

    Hemolysis

    Marked leukocytosis

    Repeated fist clenching

Transcellular shift

    Massive trauma, burns, neuromuscular disease

    Rhabdomyolysis

    Compartment syndrome (e.g., IV drug use)

    Massive blood transfusion

    Tumorlysis syndrome

    Metabolic acidosis

    Insulindeficiency

    Hypertonicity

    Exercise

    Beta-blockers

Decreased K⁺ excretion

    Renal failure

    Renal tubular dysfunction

    Hypoaldosteronism

    Medications including K⁺ sparing diuretics, trimethoprim, pentamidine, heparin, NSAIDs

    Diabetic nephropathy

Excessive K⁺ intake Iatrogenic

General

  Weakness

Cardiovascular

  Bradycardia

  Peaked T waves (K⁺ ≥5.5 mEq/L)

  AV conduction delay (K⁺ ≥6.0 mEq/L)

  PR prolongation (K⁺ >6.5 mEq/L)

  Widened QRS (K⁺ ≥7.0 mEq/L)

  Dysrhythmias

Gastrointestinal Nausea/vomiting Abdominal distention Diarrhea

Musculoskeletal

  Muscle weakness

  Rarely, flaccid paralysis, including respiratory muscles

Neurologic

  Hyporeflexia

  Paresthesias

Stat. EKG.

Consult medicine immediately in the event of severe hyperkalemia ([K⁺] ≥6.0 mEq/L), EKG changes, and/or cardiac toxicity, muscular paralysis (even in the absence of EKG changes).

Perform complete history (including medications and diet) and physical examination.

In the absence of EKG changes and symptoms, recheck serum K level to rule out pseudohyperkalemia.

Check chemistry panel, serum Ca, urine electrolytes, urine and serum osmolarities, creatine phosphokinase (CPK) level, urinalysis, urine toxicology screen, blood alcohol level.

Mild hyperkalemia ([K⁺] 5.0-5.5 mEq/L).

Consider Kayexalate 30-60 g p.o./pr q6h prn. Repeat if no bowel movement.

  Decreases [K⁺] by 0.5-1 mEq/L per dose.

Hypokalemia

Decreased K⁺ intake

    Dietary restriction

Transcellular shift

    Metabolic alkalosis

    Osmotic diuresis (e.g., hyperglycemia)

    Medications (e.g., betaadrenergic agonists, insulin, barium)

    Anabolic states (e.g., rapidly proliferating malignancy)

    Hypothermia

    Hypokalemic periodic paralysis

Renal loss

    Diuretic use/abuse

    Primary and secondary hyperaldosteronism

    Iatrogenic (e.g., loop and thiazide diuretics, antimicrobials, digoxin, licorice, tobacco, toluene, amphotericin B)

    Hypomagnesemia

    Renal tubular acidosis

    Cushing syndrome

    Diabetic ketoacidosis

    Vomiting

Nonrenal loss

    Gastrointestinal loss (e.g., diarrhea, laxative, vomiting, nasogastric suction, Zollinger-Ellison syndrome, villous adenoma)

    Excess sweating

Pseudohyperkalemia

    Lab error

    Leukocytosis

General

  Fatigue

Cardiovascular

  AV conduction delay

  T wave flattening and/or inversion

  Prominent U wave

  ST depression

  Prolonged PR and QT interval

  Prolonged QU interval

Gastrointestinal

  Nausea/vomiting

  Constipation/diarrhea

  Ileus

Musculoskeletal

  Myalgia

  Muscular weakness/cramps, particularly of lower extremities

Neurologic

  Hyporeflexia

  Paresthesias

Consult medicine for plasma [K⁺] <3mEq/L and presence of EKG changes, significant K⁺ loss not responding to oral therapy and/or unable to tolerate oral therapy, patients taking digoxin.

Perform complete history (including medications, past medical history, conditions predisposing to hypokalemia, such as bulimia and laxative abuse) and physical examination.

Laboratory studies may entail chemistry panel, serum Mg and Ca, urine Na/K/Cl.

Mild hypokalemia ([K⁺] 3.3-3.5 mEq/L) KCl 40-60 mEq/L p.o. in divided doses q2h.

Moderate hypokalemia ([K⁺] 3.0-3.2 mEq/L) KCl 60-80 mEq/L p.o. in divided doses q2h.

Continue monitoring serum K and serial EKGs until target serum [K⁺] 4-5 mEq/L. Replace serum Mg as needed.