1. DR. HAMED SHAKHATREH NEPHROLOGIST CONSULTANT

2.  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

3.  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

4.  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

5.  Impaired renal free water excretion  Increased proximal reabsorption  Hypothyroidism  Impaired distal dilution  SIAD  Glucocorticoid deficiency  Combined increased proximal reabsorption and impaired distal dilution  CHF  Cirrhosis  Nephrotic syndrome  Decreased Urinary solute excretion  Beer Potomania   Excess water intake  Primary polydipsia  Dilute infant formula

6.  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.

7.  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

8.  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.

9.  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.

10.  Tumors  Pulmonary, GIT, Prostate Uterine Leukemia  Central NS disorders  Tumors, Abscess encephalitis, Meningitis  Drug Induced  Stimulated  Nicotine, Phenothiazine  Tricyclics and others  Pulmonary Disease  TB, Aspergillosis, COPD

11.  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.

12.  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.

13.  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.

14.  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.

15.  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.

16.  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.

17.  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

18.  Secondary- Cerebravascular Disease  Dementia  Delirium  Mental Status Changes

19.  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.

20.  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

21.  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

22.  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.