Regulating extracellular and vascular volume. Na+ and its attendant anions (Cl− and HCO3−) account for approximately 90% to 95% of the osmotic activity in the ECF.
Because sodium is part of the sodium bicarbonate molecule, it is important in regulating acid-base balance.
As a current-carryin...
Regulating extracellular and vascular volume. Na+ and its attendant anions (Cl− and HCO3−) account for approximately 90% to 95% of the osmotic activity in the ECF.
Because sodium is part of the sodium bicarbonate molecule, it is important in regulating acid-base balance.
As a current-carrying ion, Na+ contributes to the function of the nervous system and other excitable tissue.
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ELECTROLYTE IMBALANCE:SODIUM DR JESEE GICHURE MUNGA
INTRODUCTION The body of an adult man contains approximately 4000 mmol of sodium, 70% of which is freely exchangeable, the remainder being complexed in bone. Most of exchangeable sodium is extracellular: 135–145 mmol /L, while that in the ICF is only 4–10 mmol /L. Most cell membranes are relatively impermeable to sodium and the gradient is maintained by active pumping of sodium from the ICF to the ECF by Na+,K + ATPase.
SODIUM FUNCTIONS Regulating extracellular and vascular volume. Na+ and its attendant anions (Cl− and HCO3−) account for approximately 90% to 95% of the osmotic activity in the ECF. Because sodium is part of the sodium bicarbonate molecule, it is important in regulating acid-base balance. As a current-carrying ion, Na+ contributes to the function of the nervous system and other excitable tissue.
SODIUM DISTRIBUTION Sodium input and output normally are balanced. The sodium intake necessary to maintain sodium balance is much less than the normal intake; excess sodium is excreted in the urine. Note that there is a massive internal turnover of sodium. Sodium is secreted into the gut and filtered by the kidneys. Most of this sodium is regained by reabsorption in the gut and renal tubules and if there is failure of this reabsorption, sodium homoeostasis will be compromised.
SODIUM HOMEOSTASIS The volume of the ECF is directly dependent on the total body sodium content as water intake and loss are regulated to maintain a constant ECF osmolality, and hence sodium concentration, and because sodium is virtually confined to the ECF . Sodium balance is maintained by regulation of its renal excretion. Sodium excretion is dependent on glomerular filtration. Normally , approximately 70% of filtered sodium is actively reabsorbed in the proximal convoluted tubules, with further reabsorption in the loops of Henle. < 5% of filtered sodium reaches the distal convoluted tubules and this the major site for the fine control of sodium excretion.
Cont. : Aldosterone , released from the adrenal cortex in response to activation of the renin–angiotensin system, stimulates sodium reabsorption in the distal parts of the distal convoluted tubules and collecting ducts and is the major factor controlling renal sodium excretion . Renin secretion is stimulated primarily by a decrease in renal perfusion secondary to a decrease in blood volume. Atrial natriuretic peptide (ANP) is secreted by the cardiac atria in response to atrial stretch following a rise in atrial pressure. ANP acts by inhibiting distal tubular sodium reabsorption and through decreasing renin (and hence aldosterone) secretion.
HYPONATREMIA Plasma Na+ concentration <135mmol/l. Can be mild( 125-135 mmol /L),moderate(120-125 mmol /L) or severe( <120 mmol /L). The concentration of sodium in ECF is a reflection of the tonicity of body fluids ,not of total body sodium content. Hyponatremia is a common abnormality that leads to hospitalization. Mild hyponatremia is seen with a wide variety of illnesses and may be multifactorial in origin. It is a secondary phenomenon that reflects the presence of disease; treatment should be directed at the underlying cause and not at the hyponatremia Causes Hyponatremia should be associated with decreased osmolality therefore a finding of hyponatremia should be followed with osmolality measurements . Normal 280-295 , low <280 , high>295
Cont : True hyponatremia is always hypo- osmolar . The mechanisms primarily responsible for the development and maintenance of this hyponatremia are: sodium depletion (hypovolemic hyponatremia) water excess (euvolaemic hyponatremia) water and sodium excess ( hypervolemic hyponatremia).
Sodium depletion ( hypovolemic hyponatremia ) Excessive loss of sodium- See diagram following Reduced intake – extremely unlikely
Water excess ( Euvolaemic hyponatremia) Gives rise to a dilutional hyponatremia with reduced plasma osmolality . It can occur acutely purely due to excessive water intake, but this is rare: water intoxication and hyponatremia will be seen only when very large quantities of fluid are ingested rapidly. It can also occur in people who drink large quantities of weak beer . Far more frequently, however, the acute development of water excess and hyponatremia is a result of a combination of excessive hypotonic fluid intake and impairment of diuresis.
Water excess ( Euvolaemic hyponatremia The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) . The laboratory criteria for the diagnosis are: Plasma osmolality is low Urine less than maximally dilute (i.e. osmolality >50 mmol /kg ). Oedema is not a feature of SIADH: the excess of water is distributed throughout both the ICF and the ECF and the effect on ECF volume is insufficient to cause oedema .
Combined water and sodium excess – hypervolemic hyponatremia It underlies the hyponatremia of congestive cardiac failure, hypoproteinaemic states and some patients with liver failure. The fact that there is sodium excess is indicated by signs of increased ECF volume (e.g. peripheral edema). The logical treatment in these patients involves measures to treat the underlying cause and remove the excess sodium and water (e.g. with diuretics).
Investigation of hyponatremia In many instances, the cause of hyponatremia can often be recognized clinically and that additional investigation may add nothing to the management of the patient. Hyponatremia due to sodium depletion may be accompanied by physical signs of a decrease in ECF volume. ECF volume is normal in patients with water excess. In combined water and sodium excess the signs will be those of ECF expansion. An appreciation of the underlying principles is vital for correct interpretation of results.
TREATMENT: symptomatic acute hyponatremia(<24-48hrs) 3% NaCl is the fluid of choice, because It’s hypertonic – It has a much higher sodium concentration (513 mEq /L) than blood, which helps rapidly raise serum sodium levels. Precise correction – It's used in carefully controlled doses, to avoid osmotic demyelination syndrome, a risk from correcting sodium too fast. Increase serum Na+ by 4-6 mmol /L. Urgent correction goal, with aim of preventing brain herniation.
Osmotic Demyelination Syndrome Due to rapid correction of chronic hyponatremia . When serum [Na+] is rapidly raised, the plasma osmolality becomes hypertonic to the brain with resultant water movement from the brain. This cerebral dehydration probably causes myelinolysis and ODS. Risk factors of ODS: Serum sodium concentration ≤105 mmol /L Significant hypokalemia Alcohol use disorder Malnutrition Advanced liver disease Lower baseline starting serum sodium concentration Overly rapid correction of hyponatremia ( > 6-8 mmol /L at 24 hours or > 18 mmol /L at 48 hours)
CASE STUDY Ms AJ a 59yr old patient presented to the facility on 19/7/2025 as a referral from a peripheral facility and was reported to have had 4 episodes of convulsions (GTC ).Had earlier been evaluated for symptomatic UTI( dysuria, generalized body malaise)and discharged on Zulu MR and cefuroxime. Past Medical History: Known hypertensive on carditan AM(Losartan 50mg/Amlodipine 5mg).On follow up for long standing gastritis. UECs.Sodium levels 19/07/2025:115.38mmol/L 20/07/2025:116.91mmol/L 21/7/2025:117mmol/L Meds as per Tsheet : Amlodipine 5mg+Losartan 50mg OD Ceftriaxone 1g BD x 7/7 Esomeprazole 40mg Iv OD 5/7
Cont.. Hypertonic saline Iv TDS x 3/7 Levetiracetam 500mg IV BD x 5/7 Paracetamol 1g Iv TDS x 7/7 NS infusion