Fluid and Electrolytes

Fluid and Electrolytes

Introduction

  • Body water content:
    • Males: 60% of body weight
    • Females: 55% of body weight
  • Distribution:
    • Intracellular Fluid (ICF): 66%
    • Extracellular Fluid (ECF): 33%
    • Plasma: Only 8% of ECF
  • Water movement: Not actively transported, moves freely across compartments, determined by osmotic content.
  • Water source: Diet and oxidative metabolism
  • Water loss: Kidneys, gut, lungs, and skin
  • Kidney filtration: Approximately 170L of water is filtered daily.
  • Minimum urine volume: 500mL/24hrs for adequate waste excretion
  • Electrolyte composition: ICF and ECF have different compositions.
    • ECF: Na+ predominant
    • ICF: K+ predominant
  • Concentration maintenance: Energy-dependent Na^+/K^+-ATPase

Osmolality and Osmolarity

  • Osmolality:
    • Measured using an osmometer
    • Principle: Freezing point depression
  • Osmolarity:
    • Calculated: 2[Na^+] + [urea] + [glucose]
  • Osmolal Gap (OG):
    • Calculated: OG = Osmolality - Osmolarity
    • Increased OG indicates an increase in other osmoles.
    • Renal Failure (RF), Diabetic Ketoacidosis (DKA), lactic acidosis: OG > 10
    • Ethanol, ethylene glycol: OG > 15

Water and Sodium Homeostasis

  • Water intake: Varies greatly, influenced by availability, diet, habit, social factors, etc.
  • Kidneys: Able to vary urine output in volume and concentration; obligatory loss of about 500mL/24hrs.
  • Major homeostatic systems:
    • Renin-Angiotensin-Aldosterone (RAA) system
    • Antidiuretic Hormone (ADH)

Hyponatremia

  • Definition: Plasma concentration below reference limit (~135mmol/L)
  • Exclusion: First exclude pseudo hypoNa – excess lipid, protein
  • Common electrolyte abnormality: Clinical effects may not be apparent until plasma concentration reaches ≤ 125mmol/L.
  • Rate of decrease: Important factor
  • Chronic hyponatremia: May be present for months or years, may be asymptomatic (common in the elderly).
  • Acute hyponatremia: May be fatal if occurring rapidly (common in infants).

Cellular Response to Hyponatremia

  • Cells extrude organic and inorganic particles (osmolytes) to prevent intracellular volume increase.
  • Rapid decline in sodium levels: Adaptive mechanisms are not achieved, leading to cerebral edema and symptoms like nausea, vomiting, confusion, coma, and even death.
  • Acute hyponatremia: Medical emergency, requires early and aggressive treatment.
  • Chronic hyponatremia: Dangerous if treated aggressively.

Approach to Hyponatremia

  • Volume status: Provides approximation of Total Body Sodium (TBNa); treatment varies based on volume status.
    • Hypervolemia: ≈↑TBNa+ and ↑↑Total Body Water (TBW) – Lasix plus fluid restriction
    • Euvolemia: ≈↔TBNa+ and ↑TBW – Fluid restriction
    • Hypovolemia: ≈↓↓TBNa+ and ↓TBW – Saline rehydration

Syndrome of Inappropriate ADH (SIADH)

  • Excess antidiuretic hormone.
  • ADH measurement: Not practical, not routinely done by clinical labs.
  • SIADH: Diagnosis of exclusion (only considered when other causes of hyponatremia are excluded).
  • Diagnostic Criteria:
    • Hyponatremia and low serum osmolality
    • Urine osmolality > 100 mOsm/kg (urine not maximally diluted)
    • Normal ECF volume
    • Normal kidney, adrenal, and thyroid function
    • Patient not on drugs that may cause hyponatremia

Hypernatremia

  • Definition: Serum concentration > 145 mmol/L
  • Prerequisite: Inadequate water intake.
  • Rare occurrence in: Alert patients with intact thirst mechanism + access to water + ability to drink water.

Approach to Hypernatremia

  • First assess volume status to reflect potential cause and guide management.
    • Hypervolemia: ≈↑↑TBNa+ and ↑TBW – Furosemide and 5% dextrose IVI
    • Euvolemia: ≈↔TBNa+ and ↓TBW – 5% dextrose IVI or H2O orally or via n-g tube
    • Hypovolemia: ≈↓TBNa+ and ↓↓TBW – Isotonic saline and 5% dextrose IVI
  • Water loss: When water loss is the primary cause, ECF depletion occurs late due to buffering by the larger ICF volume.
  • Salt gain: ECF expansion occurs rapidly; symptoms appear quickly (e.g., primary or secondary mineralocorticoid excess).
  • Other causes: Impaired ADH secretion or inability of collecting tubules to concentrate urine (Diabetes insipidus – central or peripheral).

Cerebral Adaptation

  • Timeframe: Starts within hours, established by 2-3 days.
  • Adaptation to hyponatremia: Brain secretes idiogenic molecules (osmolytes) out of brain cells to ECF.
  • Adaptation to hypernatremia: Brain accumulates intracellular idiogenic molecules.
  • Overzealous correction: May be detrimental.

Potassium Homeostasis

  • Kidney reabsorption: Filtered potassium is mostly reabsorbed in the proximal tubules.
  • Distal tubule: Some active secretion takes place.
  • Urinary K excretion influenced by:
    • Circulating aldosterone levels
    • Amount of Na arriving at the distal tubules
    • Relative availability hydrogen and potassium levels of the cells at the distal tubules and collecting ducts
    • Capacity of the cells to secrete hydrogen ions
    • Dietary potassium intake
    • Intravascular volume (reduction stimulates aldosterone secretion)

Hypokalemia

  • Principal causes:
    • Transcellular K movement
      • Alkalosis
      • Insulin administration
      • Refeeding syndrome
    • Increased K excretion
      • Renal causes
        • Diuretics
        • AKI (diuretic phase)
        • RTA 1 and 2
        • Mineralocorticoid excess: Primary and secondary aldosteronism, Cushing syndrome
        • Tubular disorders: Batter syndrome, Liddle syndrome, Gitelman’s syndrome
      • Extra renal causes
        • Diarrhoea
        • Vomiting
    • Decreased intake

Hyperkalemia

  • Spurious:
    • Haemolysis
    • EDTA contamination
    • Old sample
    • Abnormal blood cells (leukaemia, thrombocytosis)
  • Transcellular movement:
    • Acidosis
    • Tissue damage (tumour lysis syndrome)
    • Vigorous exercise
  • Decreased K excretion:
    • AKI and CKD
    • K-sparing diuretics
    • Mineralocorticoid deficiency: e.g., Addison’s syndrome; adrenalectomy; hyporeninemic hypoaldosteronism
  • Excessive intake:
    • E.g., slow K
    • Parenteral infusion

Summary/Conclusions

  • Sodium, potassium, and water homeostasis are interlinked.
  • Na and K are transported actively.
  • H2O follows passive transport.
  • Hyponatremia is very common in inpatients and requires proper investigation for ideal management.
  • Electrolyte disorders can lead to devastating outcomes if not appropriately managed.