Sodium Imbalance

Question 1

Both hypo- and hypernatremia are disorders of…

Answer 1

water balance or water distribution

Question 2

Sodium imbalance is due to what 2 things?

Answer 2

1. Both an initial challenge (change?) to water balance
2. As well as a failure of adaptive responses to compensate for this

Question 3

Hyponatremia is defined as a serum sodium of < ___ mEq/L

Answer 3

135

Question 4

True or False? Hyponatremia is the most common electrolyte abnormality

Answer 4

True

Question 5

Hyponatremia has many different causes and types, such as? (5)

Answer 5

1. Excess free water consumption
2. Hyperosmolar hyponatremia
3. Hypovolemic hyponatremia
4. Hypervolemic hyponatremia
5. Euvolemic hyponatremia e.g. SIADH

Question 6

Ingestion of too much “free” water is very rare, and a LOT of water must be consumed to overwhelm the kidney’s ability to excrete it. What are some potential causes of this overingestion? (5)

Answer 6

1. Usually seen in combination with a solute-poor diet (i.e. sodium-poor)
2. Psychogenic polydipsia
   - Compulsive water drinking, generally seen with concurrent psychiatric disorders, particularly schizophrenia
3. Water intoxication e.g. endurance athletes, hazing rituals
4. Beer potomia
   - Excessive intake of alcohol (usually beer) with poor dietary intake of solutes
5. “Tea and toast” diet

Question 7

Hyperosmolar hyponatremia occurs when?
What is the most commonly due to?

Answer 7

1. Occurs when an osmotically active agent OTHER than sodium accumulates in the ECF, drawing water into the ECF and diluting sodium
   - Actual sodium content is normal, but the concentration of sodium in water is reduced (dilutional hyponatremia)
2. Most commonly this is due to hyperglycemia
   - Excessive blood glucose draws water from ICF -> ECF
   - Increased water in ECF dilutes sodium -> relative hyponatremia

Question 8

Hypovolemic hyponatremia results from?

Answer 8

Net sodium loss

Question 9

True or False? Hyponatremia with loop diuretics is fairly common

Answer 9

False - relatively uncommon

Question 10

How do thiazide diuretics contribute to hypovolemic hyponatremia? (3)

Answer 10

1. Block sodium reabsorption from the distal tubule -> ↑ Na+ and water excretion -> ↓ blood volume -> ADH release -> ↑ water reabsorption in the collecting duct and ↑ thirst -> more sodium than water lost
2. Hyponatremia usually develops within 2 weeks of starting therapy or increasing dosage
3. ↑ age and females more vulnerable

Question 11

Hypervolemic hyponatremia occurs when?

Answer 11

Occurs during fluid-overloaded states such as HF, cirrhosis with ascites, and severe nephrotic syndrome

Question 12

What is dilutional hyponatremia?

Answer 12

Fluid shifts from the intravascular to the interstitial space

Question 13

The most common form of euvolemic hyponatremia is?

Answer 13

SIADH

Question 14

What is euvolemic hyponatremia?

Answer 14

Activation of water-conserving mechanisms (i.e. ADH) in the absence of osmotic- or volume-related stimuli
- Renal response to volume remains intact, so individuals are generally euvolemic
- However, due to increased total body water, serum sodium concentration is decreased

Question 15

What is SIADH?

Answer 15

Non-physiological release of ADH from the pituitary or an ectopic source

Question 16

There are many different possible causes of SIADH. What are they? (4)

Answer 16

1. Neurologic or psychiatric disorders (e.g. stroke, head trauma, acute psychosis, meningitis)
2. Pulmonary diseases (e.g. pneumonia, TB, acute respiratory failure)
3. Malignant tumors (most commonly small cell lung cancer)
4. Drugs (e.g. SSRIs, antipsychotics, narcotics, NSAIDs)

Question 17

Chronic hyponatremia is usually relatively asymptomatic. What to know/be aware of about it? (3)

Answer 17

1. Mild symptoms under-reported and under-recognized
2. Often detected on routine bloodwork
3. Has been associated with impaired attention, concentration, and gait -> increased fall risk

Question 18

Symptoms of hyponatremia are primarily ___________

Answer 18

neurologic
- Due to osmotic intracellular water shift –> cell swelling and cerebral edema

Question 19

Hyponatremia is proportional to: (2)

Answer 19

Magnitude and rapidity of sodium decline

Question 20

Acute hyponatremia develops over the course of ~__h

Answer 20

48

Question 21

What are the symptoms of acute hyponatremia? (3)

Answer 21

1. Symptoms may appear ~125 mEq/L and include nausea, malaise, headache
2. If [Na+] continues to ↓, symptoms progress to lethargy, confusion, decreased consciousness
3. Seizures, coma if [Na+] ~115 mEq/L

Question 22

What is chronic hyponatremia?

Answer 22

> 3 days’ duration
- Adaptive mechanisms kick in and help defend against cellular swelling, which minimizes symptoms

Question 23

How might hyponatremia be diagnosed? (3)

Answer 23

1. Plasma osmolality
   - Generally in hyponatremia, plasma osmolality should be LOW (< 275 mOsm/L)
   - If plasma osmolality is not low -> hyperosmolar hyponatremia (e.g. hyperglycemia)
2. Urine osmolality
   - Generally in hyponatremia, urine osmolality should be low (< 100 mOsm/L)
   - A urine sample that is not dilute suggests impaired free water excretion due to secretion of ADH (?SIADH)
3. Urine sodium concentration
   - Urine sodium > 20mEq/L suggests normal effective circulating volume or a sodium-wasting issue
   - Occasionally, excretion of a non-reabsorbed anion (e.g. ketonuria, bicarbonaturia) leads to sodium loss despite volume depletion

Question 24

It is important to treat hyponatremia ______. Why?

Answer 24

slowly
- Cells gradually adapt to the hyponatremic state, and overly rapid correction can lead to rapid cell swelling and brain damage
- Overly rapid correction can lead to central pontine myelinosis – neuron damage from rapid osmotic shifts
– Hyperreflexia, parkinsonism, paralysis, locked-in syndrome, death

Question 25

Total daily sodium correction should not exceed _ mEq per day

Answer 25

8

Question 26

Explain the treatment process of symptomatic hyponatremia (4)

Answer 26

1. In symptomatic hyponatremia, hypertonic saline should be used to correct by 4-6 mEq/L in the first 6 hours (up to a maximum of 8mEq/L in the first 24 hours!) 2. Hypertonic saline can be given in 100 mL IV boluses (up to three times as needed) to limit the risk of overcorrection with sodium monitoring q hour in between - Generally sufficient to bring the patient out of the symptomatic range 3. Hypertonic saline may also be given as an IV infusion - Calculations to determine how much hypertonic saline to give per hour for the desired rate of correction - Generally start conservatively to prevent over-correction and titrate up as needed 4. Frequent sodium rechecks to ensure appropriate correction, and adjust strategy as needed!

Question 27

Explain the treatment process of asymptomatic hyponatremia (3)

Answer 27

1. In asymptomatic hyponatremia, treatment may be targeted to the underlying cause 2. Hypovolemic hyponatremia - Use isotonic (0.9%) saline to restore the intravascular volume -> ↓ renal water retention (turn off ADH) -> normalize serum sodium concentration - Avoid overcorrection! 3. Hypervolemic hyponatremia (HF, cirrhosis) - Manage underlying condition - Administration of fluids will worsen volume overload without changing serum sodium concentration - Restricting water intake (<1000 – 1200 mL/day) and salt intake (1000-2000 mg/day) - Diuretics (loop) may help attenuate hypervolemia

Question 28

How is euvolemic hyponatremia (SIADH) treated? (2)

Answer 28

1. Identify and correct underlying cause! 2. If not effective: - Water restriction (< 1000-1200 mL/day) - Salt tablets to ↑ water excretion - Loop diuretics impair urine-concentrating mechanisms and ↑ water excretion - If still refractory: Vasopressin antagonists e.g. conivaptan (IV) or tolvaptan (po) -- Promote water excretion -- Risk of overcorrection -> should be initiated in an inpatient setting with close monitoring of serum Na+

Question 29

What is hypernatremia?

Answer 29

1. Plasma sodium > 145 mEq/L 2. State of hyperosmolality -> cellular dehydration 3. Usually results from a water deficit, rather than net sodium gain

Question 30

Normally, the hyponatremia hyperosmolar state stimulates: (2)

Answer 30

Thirst and excretion of a maximally concentrated urine

Question 31

For hypernatremia to persist, one or both of the compensatory mechanisms (thirst response, excretion) must not be working. How so? (2)

Answer 31

1. Impaired thirst response: - Limited access to water (e.g. infants and small children, institutionalized or intubated paients, delirium, dementia) 2. Hypernatremia due to water loss in excess of electrolyte loss - Non-renal water loss is most commonly due to significant diarrhea - Renal water loss from osmotic diuresis or diabetes insipidus - Osmotic diuresis e.g. glucosuria - Diabetes insipidus – lack of secretion of ADH (central diabetes insipidus) or lack of renal response to ADH (nephrogenic diabetes insipidus)

Question 32

What is the clinical presentation of hypernatremia? (4)

Answer 32

1. Hypernatremia -> movement of fluid from ICF to ECF -> brain cell shrinkage 2. Presence and severity of symptoms depends on both the acuity and magnitude of hypernatremia 3. Diabetes insipidus generally presents with polyuria and polydipsia 4. Severe or acute hypernatremia may present with altered mental status, weakness, focal neurological deficits -> coma, seizures, death

Question 33

Over-aggressive correction of hypernatremia can lead to?

Answer 33

Brain cell swelling --> seizures, permanent neurological damage, death

Question 34

In symptomatic hypernatremia, sodium levels should be corrected by no more than __-__ mEq/L per day

Answer 34

10-12

Question 35

In chronic (compensated) hypernatermia, sodium levels should be corrected even more slowly (_ to _ mEq/L per day)

Answer 35

5-8

Question 36

If hypovolemic hypernatremia, ___ volume should be restored

Answer 36

ECF

Question 37

How is central diabetes insipidus hypernatremia treated?

Answer 37

Desmopressin is a synthetic analogue of vasopressin (ADH) - May be administered orally or intranasally (DDAVP) - Titrated to achieve high-normal sodium concentration, 1.5-2L urine output/day and minimal nocturia - Sodium levels should be monitored q1-3 days during initiation and titration, then every 1-2 months (risk for hyponatremia)

Question 38

How is nephrogenic diabetes insipidus hypernatremia treated? (3)

Answer 38

1. Identify and correct concurrent hypercalcemia and hypokalemia 2. Thiazide diuretic + Sodium restriction (< 2000 mg daily) decrease urine volume and normalize sodium levels 3. Indomethacin 50 mg TID may also potentiate ADH activity in the kidney and decrease urine volume

Question 39

How is sodium overload hypernatremia treated? (2)

Answer 39

1. Usually iatrogenic (e.g.administration of too much sodium-containing fluids/medications in hospitalized patients) 2. Administer D5W and loop diuretic (e.g. furosemide 20-40 mg) to facilitate sodium excretion