Presentation on theme: "DR. HAMED SHAKHATREH NEPHROLOGIST CONSULTANT. Normal S. Sodium 135-148 mmol/L <135 = 22% of hospital patients <130 = 4% of hospital patient Hyponatremia."— Presentation transcript:
DR. HAMED SHAKHATREH NEPHROLOGIST CONSULTANT
Normal S. Sodium 135-148 mmol/L <135 = 22% of hospital patients <130 = 4% of hospital patient Hyponatremia important because: Acute hyponatremia cause morbidity & mortality Mild hyponatremia can progress to severe during treatment Rapid correction can produce severe neurological deficits and death. Hyponatremia and hypoosmolality are usually synonymous because the calculated osmolality. P osm = 2 Na + glucose mmol/L + BUN mmol/L
Hyponatremia = hypoosmolality except in 3 conditions: High proteins High glucose High Lipids Here the hyponatremia called pseudohyponatremia because the true sodium is normal if it measure by ion specific electrode not by photometry. For example: S. glucose 500mg/dl & S. Na 125mmol/L The true Na= 125 + (4x2.4) =135 mmol/L
Depletion (primary decrease in total body solute + secondary water retention) Renal solute loss Diuretic use Solute diuresis (Glucose, Mannitol) Solute wasting nephopathy Mineralocorticoid deficiency Non renal solute loss Gastro intestinal (diarrhea, vomiting, pancreatitis, bowel obstruction) Cutaneous (sweating, burns) Blood Loss
Decreased volume (hypovolemia) 20% orthostatic changes Decreased urine sodium <30 non renal cause: G/E Increase urine Na >30 renal cause Diuretic the most common cause & Thiazide the common. Low S.K indicate hypovolemia Chronic interstitial nephropathy PKD, Bartter’s Syndrome, Addison’s Disease.
Bp & Ps without orthostatic changes BUN & Uric Acid normal or low urine sodium <30 unlikely due to primary dilutional except in hypothyroidism. While Urine Na >30 = SIAD
Decreased osmolality P. <275 Inappropriate urine osmolality urine >100mo/kg. H2O with S. hypoosmolality Clinical Euvolemia Increased urine Na on normal salt & water intake Absence of causes of hypoosmolality such hypothyroidism, Addison’s disease and diuretics.
Abnormal water load 20ml/kg over 4 hours. Failure to dilute U osm <100 AVP inappropriately elevated relative to plasma hypo osmolality. S. Na improved with water restriction but not with volume expansion.
Increased ECF (Edema & Ascites 35%) Clinical edema or ascites Na <30 mmol Sometimes Na >30 mmol/L because of glucosuria, diuretic theraphy. Hyponatremia usually in advanced disease as CHF, Nephrotic syndrome and Cirrhosis.
Clinical picture depends on severity, speed of hyponatremia which means more than 48 hours or less. The picture reflect brain edema which presented from confusion to seizures to coma and the comorbilities. Special high incidence of morbidity & mortality in menstruating females & young children specially post operative.
Theraphy depends on severity of clinical situations, the level of S. Na, the period of which hyponatremia happened less than 48 hours or longer. Any correction not allowed more than 12 mmol/L in any 24 hours. Safe level >120 restrict water. Rapid correction induced pontine & extra poutine myelinolysis.
How to correct hyponatremia (infusate- actual)% (BW/2+1) or hypertonic saline 3%- 70ml/hr in 70kg patient increase S. Na by 1. SIAD – Demeclocyline 600mgx2 to induce NDI. Phenytoin, Opiates, Ethanol- decreased AVP.
Decreased in total body water, however total body Sodium maybe normal, increased or decreased. Hypernatremia happened in 2% of patients. Hypernatremia presented in two ways: Pre- Hospital or Intra-hospital.
This happened by the interaction of AVP in the Hypothalamus through posterior pituitary gland & the thirst centre in the anterior wall of third ventricle with the distal collecting duct in the kidney. Osmostat in the hypothaleum proportionally affected by osmolality decreased osmolality decreased AVP. Thirst center regulated with 5 mml/kg above osmostat.
Hypernatremia happened with thirst sense lost or unable to get water. Defects in Thirst: Primary- Hypodypsia Hypothalamic lesion Trauma Craniopharyngioma or Supracellular Tumor Metastatic Tumor Granulomas Vascular Lesion Essential Hypernatremia Geriatric Hypodypsia
Picture of hypernatremia mostly neurological and appear as confusion, seizures up to coma due to brain shrinkage & dehydration and also depends on the speed of appearance and state of hyperosmolality.
Classifications according to changes in extra cellular volume. Pure Water Deficit DI – hypothalamic Nephrogenic Hypotenic Fluid Loss Renal GastroIntestinal Cutaneous Hypertonic Sodium Gain Salt Ingestion Hypertonic Sodium Chloride Hypertonic Sodium Bicarbonate Total parenteral nutrition
Hypothalamic DI Nephrogenic DI - Pituitary Surgery- Drug Induced - Head Traum Lithium - NeoplasiaDemeclocycline - Vascular Lesion Amphotrecin B Sheehan’s syndrome - Electrolyte disturb - InfectionHypercalcemia - Granulomas Hypokalemia - Autoimmune - Obstructive uropathy - Congenital X-linked
The treatment of hypernatremia is water. Water deficit = 0.6 BW (Na/140-1) Rapid correction not allowed only 0.5 mmol/L S. Na reduced in hour. Rapid correction cause intra cranial hemorrhage CDI- treated by AVP NDI- treated by Thiazide Amiloride If hypernatremia with overload & comorbidity such as renal failure- hemodialysis is necessary.