HYPONATREMIA
&
HYPERNATREMIA
DR. HAMED SHAKHATREH
NEPHROLOGIST CONSULTANT
DR. HASSAN MANSOUR
NEPHROLOGIST
HYPONATREMIA
Normal S. Sodium 135-148 mmol/L
<135 = 22% of hospital patients
<130 = 4% of hospital patient
Hyponatremia important because:
1. Acute hyponatremia cause morbidity & mortality
2. Mild hyponatremia can progress to severe during treatment
3. 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
The normal range 275- 295
Hyponatremia = hypoosmolality except in 3 conditions:
1. High proteins
2. High glucose
3. 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
PATHOGENESIS:
Depletion (primary decrease in total body solute + secondary water retention)
1. Renal solute loss
Diuretic use
Solute diuresis (Glucose, Mannitol)
Solute wasting nephopathy
Mineralocorticoid deficiency
2. Non renal solute loss
Gastro intestinal (diarrhea, vomiting, pancreatitis, bowel obstruction)
Cutaneous (sweating, burns)
Blood Loss
Dilution (primary increase in total body water + secondary solute depletion).
1. Impaired renal free water excretion
a. Increased proximal reabsorption
Hypothyroidism
b. Impaired distal dilution
SIAD
Glucocorticoid deficiency
c. Combined increased proximal reabsorption and impaired distal dilution
CHF
Cirrhosis
Nephrotic syndrome
d. Decreased Urinary solute excretion
Beer Potomania
2. Excess water intake
Primary polydipsia
Dilute infant formula
Differential Diagnosis:
1. 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.
EUVOLEMIA 33%
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
Criteria to Diagnose SIAD:
Essential:
1. Decreased osmolality P. <275
2. Inappropriate urine osmolality urine >100mo/kg. H2O with S. hypoosmolality
3. Clinical Euvolemia
4. Increased urine Na on normal salt & water intake
5. Absence of causes of hypoosmolality such hypothyroidism, Addison’s disease
and diuretics.
SUPPLEMENTAL:
6. Abnormal water load 20ml/kg over 4 hours. Failure to dilute U osm <100
7. AVP inappropriately elevated relative to plasma hypo osmolality.
8. S. Na improved with water restriction but not with volume expansion.
COMMON CAUSES OF SIAD
-
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
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 MANIFESTATION
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.
THERAPY
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.
HYPERNATREMIA
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.
REGULATION OF WATER HOMOESTASIS:
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.
PATHOPHYSIOLOGY:
Hypernatremia happened with thirst sense lost or unable to get water.
Defects in Thirst:
1. Primary- Hypodypsia
Hypothalamic lesion
Trauma
Craniopharyngioma or Supracellular Tumor
Metastatic Tumor
Granulomas
Vascular Lesion
Essential Hypernatremia
Geriatric Hypodypsia
2. Secondary- Cerebravascular Disease
Dementia
Delirium
Mental Status Changes
CLINICAL MANIFESTATION:
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.
CLINICAL CLASSIFICATION:
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
- Pituitary Surgery
- Head Trauma
- Neoplasia
- Vascular Lesion
Sheehan’s syndrome
- Infection
- Granulomas
- Autoimmune
Nephrogenic DI
- Drug Induced
Lithium
Demeclocycline
Amphotrecin B
- Electrolyte disturb
Hypercalcemia
Hypokalemia
- Obstructive uropathy
- Congenital X-linked
TREATMENT
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 & comorbility such as renal failure- hemodialysis is
necessary.