Hyponatremia and Hypernatremia Study Notes

Hyponatremia

  • Pathophysiology and affected systems

    • Signs and symptoms are caused by effects on excitable cellular activity.
    • Major tissues involved: cerebral, neuromuscular, intestinal smooth muscle, and cardiovascular systems.
    • Intestinal changes: increased motility leading to nausea, diarrhea, and abdominal cramping.
    • GI assessment: listen to bowel sounds; bowel sounds are hyperactive; stools are frequent and watery.

  • Cardiovascular and volume status patterns

    • Hyponatremia with hypovolemia:
    • Cardiac changes: rapid, weak, thready pulse; peripheral pulses difficult to palpate and easily blocked.
    • Blood pressure: decreased; may have severe orthostatic hypotension, causing light-headedness or dizziness.
    • Central venous pressure (CVP): low.
    • Hyponatremia with hypervolemia (fluid overload):
    • Cardiac changes: full or bounding pulse with normal or high BP.
    • Peripheral pulses: full and difficult to block; may not be palpable if edema is present.

  • Assessment and priorities of care

    • Determine the cause of the low sodium to plan management.
    • Priorities: monitor response to therapy and prevent hypernatremia and fluid overload.
    • Monitor for signs of therapy-related issues (e.g., too-rapid correction).

  • Drug therapy considerations

    • Reduce doses of drugs that increase sodium loss (e.g., most diuretics).
    • If hyponatremia with a fluid deficit: administer IV saline infusions to restore both sodium and fluid volume.
    • Severe hyponatremia: small-volume infusions of hypertonic saline (3%  NaCl3\%\;\mathrm{NaCl}) with a controller to prevent accidental infusion-rate increases; monitor rate and patient response.
    • If hyponatremia with fluid excess: promote water excretion rather than sodium loss using vasopressin receptor antagonists (e.g., conivaptan\text{conivaptan} or tolvaptan\text{tolvaptan}). Reference: Sterns, 2022b\text{Sterns, 2022b}.
    • Hyponatremia due to inappropriate secretion of ADH (SIADH): may include lithium and demeclocycline.
    • Assess hourly for signs of excessive fluid loss, potassium loss, and rising sodium levels.

  • Nutrition therapy and fluid management

    • Mild hyponatremia: increase oral sodium intake; restrict oral fluid intake.
    • Collaborate with the Registered Dietitian Nutritionist (RDN) to identify foods to increase.
    • Fluid restriction may be needed long-term when chronic fluid overload or impaired kidney fluid excretion is present.

  • Nursing actions and patient safety

    • Nursing actions are similar to those for fluid overload: safety, skin protection, monitoring, and patient/family teaching.
    • Reassess the patient frequently to adjust therapy as the sodium level changes.

  • Treatment options by severity (summary)

    • Mild hyponatremia:
    • Oral sodium chloride tablets
    • Fluid restriction
    • Pronounced sodium depletion:
    • Intravenous normal saline (NS=0.9%NaCl\text{NS} = 0.9\%\mathrm{NaCl})
    • Lactated Ringer's solution
    • Severe hyponatremia:
    • Hypertonic saline (3% NaCl\text{3\% NaCl}) cautiously (risk of osmotic demyelination syndrome)
    • Vasopressin receptor antagonists: Conivaptan (Vaprisol)\text{Conivaptan (Vaprisol)} (IV) and Tolvatpan (Samsca)\text{Tolvatpan (Samsca)} (note: tolavaptan is spelled as tolvaptan; ensure correct product naming in practice)
    • Euvolemic hyponatremia:
    • Vasopressin receptor antagonists
    • SIADH:
    • Lithium
    • Demeclocycline
    • Nutritional interventions:
    • Increase oral sodium intake; restrict fluids
    • Address underlying causes:
    • Adjust medications contributing to sodium loss or fluid imbalance
    • Manage conditions leading to fluid imbalance
    • Monitoring during treatment:
    • Careful monitoring of serum sodium levels, infusion rates, and patient response to prevent complications such as fluid overload or overly rapid correction

Hypernatremia

  • Definition and pathophysiology

    • Hypernatremia is a serum sodium level > 145\ \mathrm{mEq/L} (mmol/L).
    • It can be caused by, or can cause, changes in fluid volume.
    • As serum Na+ rises, the gradient between the extracellular fluid (ECF) and intracellular fluid (ICF) widens; irritability occurs because excitable tissues are more easily excited.
    • Water shifts from cells into the ECF, causing cellular dehydration and shrinkage; later, dehydrated excitable tissues may fail to respond to stimuli.
    • Principal consequence: irritability and impaired cellular function if not corrected.

  • Interprofessional assessment and cues

    • Neurologic changes: vary with severity and presence of fluid imbalance.
    • Normal or decreased fluid volume: short attention span, agitation, confusion.
    • Fluid overload: lethargy, stupor, or coma.
    • Skeletal muscle changes: twitching and irregular contractions early; as levels rise, reduced responsiveness; later, muscle weakness and reduced or absent deep tendon reflexes.
    • Assess muscle strength (e.g., handgrip, arm flexion) and deep tendon reflexes (knees and ankles).

  • Common causes (Box 13.5)

    • Actual Sodium Excesses:
    • Hyperaldosteronism
    • Kidney failure
    • Corticosteroids
    • Cushing syndrome or disease
    • Excessive oral sodium ingestion
    • Excessive administration of sodium-containing IV fluids
    • Relative Sodium Excesses:
    • Dehydration
    • Increased metabolic rate
    • Fever
    • Hyperventilation
    • Infection
    • Excessive diaphoresis
    • Watery diarrhea

  • Cardiovascular changes and signs

    • High Na+ can slow calcium entry into cardiac cells, reducing contractility.
    • Pulse: can be increased with hypernatremia and hypovolemia.
    • Peripheral pulses: difficult to palpate and easily blocked; may have hypotension and severe orthostatic hypotension; reduced pulse pressure.
    • In hypernatremia with hypervolemia: pulse may be slow to normal but bounding; peripheral pulses full and hard to block; neck veins distended even when upright; diastolic BP increased.

  • Interventions and management goals

    • Primary goals: prevent further sodium rise and restore normal serum Na+ levels.
    • Drug and nutrition therapies are used to address the hypernatremia etiology and sodium balance.
    • Fluid therapy:
    • Isotonic saline (0.9%NaCl0.9\%\mathrm{NaCl}) and dextrose 5% in 0.45% NaCl (D5W in 0.45% NaCl) are commonly used.
      • Note: D5W in the bag is hypertonic, but once infused and glucose is metabolized, the solution is effectively hypotonic.
    • Hypernatremia due to reduced renal sodium excretion:
    • Use diuretics that promote sodium loss (e.g., furosemide\mathrm{furosemide}, bumetanide\mathrm{bumetanide}).

  • Nursing considerations and monitoring

    • Assess hourly for signs of excessive losses of fluids, sodium, or potassium.
    • Nutrition therapy to prevent or correct mild hypernatremia:
    • Ensure adequate water intake, especially in older adults.
    • Consider dietary sodium restriction if kidney problems are present to prevent further sodium excess.
    • Collaborate with the RDN to help the patient determine sodium content in foods, beverages, and drugs.
    • Nursing actions: similar to those for fluid overload, with emphasis on safe fluid balance and monitoring for neurologic changes during correction.

  • Treatment considerations and monitoring during therapy

    • Careful monitoring of serum sodium and patient response is critical to avoid overly rapid correction, which can risk osmotic demyelination syndrome in severe cases.

  • References and notes

    • Guidelines and drug choices referenced include Jones et al., 2017; Sterns, 2022b for vaptans and hyponatremia management.
    • Throughout treatment, emphasize safety, prevention of fluid overload, and prevention of overly rapid correction of sodium levels.