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.