Chapter 5 - Hyponatremia

Question 1

Hyponatremia

Answer 1

Na < 135mEq/l

Question 2

Types of hyponatremia

Answer 2

1 - Hypovolemic hyponatremia - Sodium loss in excess of water
2 - Normovolemc Hyponatremia - Conditions that predispose to SIADH
3 - Hypervolemic Hyponatremia - Excess of free water retention

Question 3

Causes of Hypovolemic hyponatremia

Answer 3

sodium loss in excess of water 
A - Renal loss:
1 - Diuretics
2 - Osmotic Diuresis
3 - Renal salt wasting
4 - adrenal insufficiency
5 - pseudohypoaldosteronism

B- Extra renal loss
1 - Diarrhea
2 - vomiting
3 - drains
4 - Fistula
5 - sweat (cystic fibrosis)
6 - cerebral salt wasting syndrome
7 -  third spacing ( effusions, ascites)

Question 4

Normovolemic hyponatremia

Answer 4

Conditions that predisposes SIADH
1 - Inflammatory CNS disease - Meningitis, encephalitis
2 - Tumors
3 - Pulmonary diseases - Severe asthma, pneumonia
4 - Drugs - Cyclophosphamide, Vincritine
5 - Nausea
6 - Post operative

Question 5

Hypervolemic hyponatremia

Answer 5

excess free water retention
1 - congestive cardiac failure
2 - cirrhosis
3 - nephrotic syndrome
4 - acute or chronic renal failure

Question 6

SIADH - Syndrome of inappropriate antidiuretic hormone secretion

Answer 6

• Associated with pulmonary and cranial disorders and postoperatively.
• High levels of vadopressin or ADH is secreted despite low osmolality
• Diagnosis is made:
  1 - Presence of hyponatremia
  2 - Urine osmolality higher than maximal dilution
• SIADH should be differentiated from cerebral salt wasting disorder.
  SIADH :
  1 - Euvolemic or mild volume expansion
  2 - Relatively low urine output
  3 - High urine sodium
• Treatment - fluid restriction

Question 7

Difference between SIADH and salt wasting disorders

Answer 7

Salt wasting Disorders:
1 - Hypovolemic hyponatremia
2 - High urinary sodium (>80mEq/L)
1 & 2 is due to increase in blood levels of natriuretic factors
SIADH:
1 - Euvolemic or mild volume expansion
2 - Relatively low urine output
3 - High urine sodium

Treatment of salt wasting disorder: replacement of urinary salt water losses.

Question 8

Factitious Hyponatremia

Answer 8

• due to massive increase in blood trglyceride levels, extreme elevation of immunoglobulins as may occur in multiple myeloma, and very high level of blood glucose. ( wiki)
• observed mainly in adults with hyperproteinemia and hyperlipidemia, but it is very rare in children
• it was described in children who hd uncontrolled DM with hyperglycemia and hyperlipidemia, as well as in patients with nephrotic syndrome and hyperlipidemia .
• Large amounts of macro molecules (lipid and /or protein) reduce the percentage of water contained in a unit volume of serum
• a factitiously low value of plasma sodium concentration will be reported, even though the sodium concentration in plasma is normal.

Question 9

Patients are symptomatic when:

Answer 9

1 - Serum sodium concentration falls below 125mEq/l or

2 - Decline is acute ( <24hours)

Question 10

clinical manifestation of hyponatremia

Answer 10

1 - Early features: Headache, nausea, vomiting, lethargy, and confusion
2 - Advanced manifestation: Seizures, coma, decorticate posturing, dilated pupils, anisocoria (unequal size of the eyes’ pupils), papilledema, cardiac arrhythmias, myocardial ischemia, and central diabetes insipidus

Question 11

cerebral edema occurs when sodium concentration is:

Answer 11

125mEq/l or less

Question 12

Effect of hyponatremia on brain

Answer 12

• hypo osmolality cause influx of water into intracellular space causing cytotoxic cerebral edema and increased ICP –> brain ischemia, herniation and death
• ## to adapt brain get rid of intracellular electrolytes and osmolytes ( some osmolytes are excitatory amino acids such as glutamate and asparate that can produce seizures in the absence of detectable cerebral edema)

Question 13

Major risk factors for developing hyponatremic encephalopathy are

Answer 13

1 - young children –> due to relatively larger brain to intracranial volume ratio compared to adults.
2 - hypoxemia
3 - neurological disease

Question 14

Effects of asymptomatic hyponatremia in preterm neonates:

Answer 14

1 - poor growth and development
2 - sensorineural hearing loss
3 - its also a risk factor for mortality in neonates who suffered perinatal bith asphyxia

Question 15

acute and chronic hyponatremia

Answer 15

acute –> developed in less than 48 hours

chronic > 48 hours

Question 16

Treatment of hyponatremia is based on:

Answer 16

1- Acute or chronic
2 - symtomatic or asymptomatic
3 - on volume status

Question 17

Assessment of volume status

Answer 17

1 - Hypovolemia : TBW↓ and total body sodium ↓↓
2 - Euvolemia : TBW ↑ and total body sodium - normal
3 - Hypervolemia: TBW ↑↑ and total sodium ↑

Question 18

Causes of hyponatremia depending on urinary sodium

Answer 18

1 - hypovolemic : Renal losses –> Urinary sodium >20
Extra renal losses –> Urinary sodium <20
2 - Euvolemic : Urinary sodium > 20 mEq/L
3 - Hypervolemic : Acute, chronic renal failure –> Urinary sodium >20
NS, Cirrhosis, CHF –> Urinary sodium <20

Question 19

calculation of sodium deficit

Answer 19

Na deficit (mEq) = 0.6 x body wt(kg) x{ (desired Na) - (observed Na) }

Question 20

treatment of hyponatremia

Answer 20

1 - treat Hypotension first, regardless of serum sodium, using saline bolus, Ringer’s Lactate, 5% albumin. WHO oral re hydration salt is preferred for asymptomatic cases with hypovolemia

2 - Correct Deficit over 48 to 72 hours for chronic hyponatremia. Rapid decline is associated with rink of central pontine myelinosis. Recommended rate is 0.5mEq/L/hour (8-10mEq/L/day). Correction in first 48 hours should not exceed 15-20mEq/l. ( at first correct till sodium reaches 125 then correct at a slower rate)

3 - Acute and symptomatic hyponatremia can be corrected rapidly. For symptomatic cases, immediate increase in serum sodium by 5-6mEq/l with hypertonic saline (3% saline) is recommended. IV infusion at a dose of 3-5ml/kg over 1 - 2 hour will raise serum sodium by 5-6mEq/l. Alternatively 3% saline maybe given as 1-3 boluses at 2ml/kg/bolus over 10 minutes (maximum 100ml/bolus)

4 - Stop further therapy with 3% saline when patient is either symptom free and/ or acute rise in sodium of 10mEq/l is noted in first 5 hour.

5 - Increase in sodium can be estimated using Adrogue Madias formula:
▲Na = { (amount of Na in 1 litre of infusate) + (amount of K in 1 litre of infusate) - (serum Na) } / (TBW +1)
TBW = 0.6 x body weight

6 - Hypotonic infusate (0.45% dextrose normal saline) are used as maintenance fluid. Normal saline should be avoided except for correction of hypovolemia; can aggravate cerebral edema in those with impaired free water balance

7 - Fluid restriction alone is needed in SIADH; sodium and water restriction is required in hypervolemic hypernatremia. Diuretics ( loop diuretic such as Furosemide) maybe added in refractory cases. ( V2 receptor antagonists or vaptans that block binding of ADH to its V2 receptor are not yet recommended for treatment of hyponatremic encephalopathy. These might have role in treating euvolemia from SIADH and hypovolemia in CHF )

8 - Serum sodium should be monitored every 2 to 4 hour and appropriate adjustments made.

Question 21

Central Pontine myelinosis

Answer 21

• Aggressive therapy with hypertonic saline in chronic hyponatremia when brain has adjusted by extrution of electrolytes and osmoles leads to osmotic demylination called central pontine myrelinosis
• Often irreversible
• seen in patients with liver disease, severe malnutrition and hypoxia
• generally become symptomatic in 2 to 7 days following rapid correction ( > 25mEq/l in first 24- 48 hours)
• Clinical features : Mutism, dysarthria, spastic quadriplegia, ataxia, pseudobulbar palsy, altered menal status, seizures and hypotension.