Dr Abdullah Ansari JR 2 Medicine AMU, Aligarh Physiology of sodium imbalance and effect on Brain Symptoms of sodium imbalance Hyponatremia Pseudohyponatremia Hypertonic hyponatremia Hypotonic hypervolumic hyponatremia Hypotonic hypovolumic hyponatremia Hypotonic euvolumic hyponatremia : SIADH Managemant : symptomatic/acute vs asymptomatic/chronic Hypernatremia Hypovolumic or euvolumic hypernatremia : Diabetes insipidus Hypervolumic hypernatremia Management

1. Disorders Of Sodium
Approach & Management
Dr Abdullah Ansari
JR 2 Medicine
AMU, Aligarh

2. Introduction
 Major cation of ECF & determines its Osmolality
 Na+ maintains ECF volume and blood pressure
 Disorders of Na+ are primarily of water balance
(osmoregulation) or water distribution
Serum Osmolality = 2*Na+ + B.Sugar/18 + BUN/2.8

3. Effect on Brain
 Most osmotically sensitive organ
 Hyponatremia neurons swelling in fixed cranium
herniation
 Hypernatremia neurons shrinkage tearing of
brain away from meninges hemorrhage

4. Symptoms of Na+ imbalance
 Depends on acuity of disturbance & magnitude
 Neurons adapts to gradual changes over 48 hours
 Both present with similar symptomatology
 Headache, confusion, stupor, seizures or coma

5.  Measure serum osmolality to confirm hypotonic
state
 Hypotonic : patient's volume status for ADH from
true hypovolemia, or a perceived decrease in
effective circulating volume
 If euvolemic, either “inappropriate” ADH secretion
(nonosmotic, nonvolume mediated) or hypotonic
fluid loading (psychogenic polydipsia)
 If hypovolemic, check urine osmolality

6. Measure Serum Osmolality
Normal
(280-290 mOsm/kg)
Low
(<280 mOsm/kg)
Elevated
(>290 mOsm/kg)
Pseudohyponatremia
• Hyperlipidemia
• Hyperproteinemia
Asses Volume Status Hypertonic hyponatremia
• Hypeyglycemia
• Hypertonic infusions
(mannitol, glycerie)
Hypervolumic
• CHF
• Cirrhosis
• Nephrotic syndrome
Hypovolumic Euvolumic
• SIADH(Urine Osm >100)
• Psycogenic polydipsia
(Urine Osm <100)
• Hypothyroidism
• Cortisol deficiency
Check Urinary Na+
<15 mEq/L(Extrarenal loss)
• Vomitting, Diarrhea, fistulas
• Burns, sweating
• Pancreatitis, Peritonitis
>15 mEq/L(Renal loss)
• Recent diuretics
• Adrenal insufficiency
• Cerebral Salt wasting

7. Hyperglycemia (Hypertonic Hyponatremia)
 ECF hyperosmolarity withdraws water from ICF
 Dilutional hyponatremia occurs
 Na+ falls by 2.4 mEq/L for every 100 mg/dL rise in
BS above normal

8. Edematous States (Hypervolemic Hyponatremia)
 Heart failure and cirrhosis : decreased “effective
circulating volume”
 “nonosmotic” ADH release
 Hyponatremia if total body water exceeds total
body sodium
 Degree of hyponatremia correlates with severity of
underlying condition

9. Syndrome Of Inappropriate ADH (Euvolemic
Hyponatremia)
 Nonosmotic, nonvolume mediated release of ADH
 Source either from posterior pituitary or ectopic
 Patients euvolemic, a true or perceived volume
deficit is not the stimulus for ADH

10. SIADH is a clinical diagnosis
1. Hyponatremia
2. Decreased osmolality < 280 mosm/kg
3. Absence of heart, kidney, or liver disease
4. Normal thyroid and adrenal function
5. Urine sodium > 20 mEq/L

11. Causes of SIADH
Neuropsychiatric disorders • Meningitis
• Encephalitis
• Stroke
• Head injury
Pulmonary diseases • Pneumonia
• Tuberculosis
• Positive pressure ventilation
• Acute respiratory failure
Malignant tumors • Small cell lung cancer
Drugs • Antidepressants
• Anticancers
• Antipsychotics
• NSAIDs
• Oxytocin
• Desmopressin
Others • Physical/emotional stress
• Pain

12. Cerebral Salt Wasting (Hypovolemic Hyponatremia)
 Brain injury : Neurosurgery, trauma, SAH
 BNP release Excessive renal Na+ excretion
volume depletion ADH release

13.  Treat underlying causes
 Water restriction
 Hypertonic (3%) saline : correct @ 1-2 mEq/L/hr
until symptoms abate
 Calculate rate and composition of fluid by
Androgue Madias equation
Change in [Na+] per liter = (infusate Na+ + K+) — Serum Na+
estimated total body water (kg) + 1

14.  Symptoms improve : correct @ <0.5 mEq/L/hr or
12 mEq/L/day
 Add Tolvaptan PO 15 mg OD, Conivaptan 20 mg
in 100ml of D5% IV over 30 min
 Overly rapid correction central pontine
myelinolysis (CPM)
 CPM : flaccid paralysis, dysarthria, dysphagia,
and death

15.  No immediate correction if mild
 Treat underlying cause
 Water restriction
 Correct @ <0.5 mEq/L/hr or 12 mEq/L/day

16.  The 3 primary mechanisms
1. Decreased free water intake
2. Increased free water loss
3. Excessive gain of hypertonic fluid
 However, almost always result of relative water
deficit

17. Hypernatremia
Hypovolumia or euvolumia Hypervolumia
ADH present ?
Urine Osm>800
(ADH present)
Urine Osm<800
(ADH absent or ineffective)
Hypertonic Sodium load
Hyperaldosteronism
Urine Volume ? Response to vasopressin ?
<800 ml/day
Decreased water
intake
Increased
insensible loss
>1000 ml/day
Osmotic diuresis
Yes
Central DI
No
Nephrogenc DI

18. Decreased Water Intake
 Most common etiology in hospitalized patients
 Patients with dementia or sedated, intubated
patient in ICU
 Maximal ADH release & urine osmolality > 800
mOsm/kg, hypernatremia occurs

19. Insensible Free Water Loss
 400 to 500 mL/day each from skin and respiratory
tract in ambulatory adults at room temperature
 Depends on respiratory rate, body temperature,
ambient temperature, and humidity
 Difficult to predict in hospitalized, mechanically
ventilated patients

20. Diabetes Insipidus
Central DI : damage of neurohypophysis
 Trauma
 Neurosurgery
 Granulomatous disease
 Neoplasms
 Strokes
 Infections

21. Nephrogenic DI
 Intrinsic renal diseases of CD : sickle cell
nephropathy, polycystic kidney disease, obstructive
nephropathy
 Drugs : lithium, demeclocycline, amphotericin
 Electrolyte disorders : hypercalcemia and
hypokalemia
 Chronic diuretic use : reduced renal medullary
hypertonicity

22. Osmotic Diuresis
 Glycosuria
 IV mannitol
 Retained uremic toxins in recovering renal failure

23. Primary Na+ Gain
 Normal kidneys huge capacity for sodium
excretion
 Iatrogenic hypernatremia uncommon unless renal
insufficinecy

24.  Correct @ <0.5 mEq/L/hr unless acute symptoms
present or acute onset (<2 days), correct @ 1-2
mEq/L/hr until symptoms disappears
 The Adrogue Madias equation is used
 Rapid correction cerebral edema brain
herniation
 5% dextrose given
 If volume depletion, NS or half-NS initially used