Presentation on theme: "This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division under the supervision and administration."— Presentation transcript:
This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Nephrology Consultant. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.
Disturbances in serum Na⁺ are generally due to changes in the body’s water balance, not sodium, i.e. changes in plasma osmolality. ↑ osmolality sensed by the osmo-receptors in the hypothalamus thirst & release of ADH ↑ water reabsorbtion from renal collecting ducts. Non-osmotic stimuli (hypovolemia, stress, nausea) can cause ADH release even if serum osmolality is normal or low.
Is the excess of water in relation to sodium ± concurrent sodium balance abnormality. Serum sodium < 135 mmol/L. Approach: (1) According to plasma osmolality. (2) According to extracellular volume.
1. Hypotonic hyponatremia (Dilutional hyponatremia): most common scenario true water excess relative to Na⁺ (± salt loss). 2. Hypertonic hyponatremia: excess of another effective osmole (glc, mannitol) that draws water intravenously. 3. Isotonic hyponatremia: *Pseudohyponatremia ; hyperlipidemia or hyperprotienemia results in low measured Na⁺ concentration (but osmolality is normal) it is a rare lab artifact *Artefactual hyponatremia; taking blood from a drip arm into which a low sodium fluid is being infused.
Once osmolality evaluation reveals hypo- osmotic hypoNa⁺, assess the extracellular volume. Classification According to Extracellular Volume: 1. Hypovolemic hypoNa⁺: deficit of both total body water & sodium, with the sodium deficit exceeding the water deficit. can be renal or extra-renal check the urinary sodium concentration to differentiate. ** diuretics are the most common cause of this with a high urine Na⁺ concentration. Clinical symptoms are due to the hypovolemia NOT the hyponatremia (rare why??) Management: give normal saline ( stimulus for ADH is removed kidneys will excrete excess water serum Na⁺ will normalized).
(3) Hypervolemic hypoNa⁺ (Dilutional hypoNa⁺): excess water relative to Na⁺ signs of volume overload (edema, ↑ JVP) ** most common mechanism of hypoNa⁺ in hospitalized ptns (overgenerous infusion of 5% glu in post op. ptns), and this is exacerbated by the stress-induced ↑ in ADH. Other causes: U[Na⁺] > 20: acute or chronic RF. U[Na⁺] < 20: CHF, cirrhosis, nephrotic synd. Clinical symptoms: occur when sodium is below 120 mmol/L more pronounced when developed rapidly (over hours) it is due to the water shift into the brain cells (cerebral edema) causes headache, confusion, convulsions, and coma.
Management: *in mild cases: water restriction. *in severe cases: medical emergency!! treat underlying cause Restrict water intake to 500 – 1000 ml/day Consider diuretic therapy Correct Mg⁺ and K⁺ defficiency If acute neurological symptoms present: infuse hypertonic saline 3%, 1-2 ml/kg/L aim to increase serum Na⁺ by 8-10 mmol/L in 1 st 4 hours then 15-20 mmol/L in 1 st 48 hours. give furosemide 40-80 mg I.V *Serum sodium should NOT be brough tup to more than 125-130 *hypertonic saline is contraindicated in fluid overloead. Give 100ml of 20% mannitol.
Why don’t we correct the hyponatremia rapidly?? It results in a severe neurological syndrome due to local areas of demyelination called “Central Pontine Myelinosis” or “Osmotic Demyelination Syndrome”. Symptoms include dysarthia, dysphagia, spastic quadriplegia, psuedobulbar palsy, and respiratory arrest. Occurs in the pons mostly, but also in the basal ganglia, internal capsule, and cerebral cortex.