Sodium Imbalance Flashcards
Both hypo- and hypernatremia are disorders of…
water balance or water distribution
Sodium imbalance is due to what 2 things?
- Both an initial challenge (change?) to water balance
- As well as a failure of adaptive responses to compensate for this
Hyponatremia is defined as a serum sodium of < ___ mEq/L
135
True or False? Hyponatremia is the most common electrolyte abnormality
True
Hyponatremia has many different causes and types, such as? (5)
- Excess free water consumption
- Hyperosmolar hyponatremia
- Hypovolemic hyponatremia
- Hypervolemic hyponatremia
- Euvolemic hyponatremia e.g. SIADH
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)
- Usually seen in combination with a solute-poor diet (i.e. sodium-poor)
- Psychogenic polydipsia
- Compulsive water drinking, generally seen with concurrent psychiatric disorders, particularly schizophrenia - Water intoxication e.g. endurance athletes, hazing rituals
- Beer potomia
- Excessive intake of alcohol (usually beer) with poor dietary intake of solutes - “Tea and toast” diet
Hyperosmolar hyponatremia occurs when?
What is the most commonly due to?
- 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) - Most commonly this is due to hyperglycemia
- Excessive blood glucose draws water from ICF -> ECF
- Increased water in ECF dilutes sodium -> relative hyponatremia
Hypovolemic hyponatremia results from?
Net sodium loss
True or False? Hyponatremia with loop diuretics is fairly common
False - relatively uncommon
How do thiazide diuretics contribute to hypovolemic hyponatremia? (3)
- 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
- Hyponatremia usually develops within 2 weeks of starting therapy or increasing dosage
- ↑ age and females more vulnerable
Hypervolemic hyponatremia occurs when?
Occurs during fluid-overloaded states such as HF, cirrhosis with ascites, and severe nephrotic syndrome
What is dilutional hyponatremia?
Fluid shifts from the intravascular to the interstitial space
The most common form of euvolemic hyponatremia is?
SIADH
What is euvolemic hyponatremia?
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
What is SIADH?
Non-physiological release of ADH from the pituitary or an ectopic source
There are many different possible causes of SIADH. What are they? (4)
- Neurologic or psychiatric disorders (e.g. stroke, head trauma, acute psychosis, meningitis)
- Pulmonary diseases (e.g. pneumonia, TB, acute respiratory failure)
- Malignant tumors (most commonly small cell lung cancer)
- Drugs (e.g. SSRIs, antipsychotics, narcotics, NSAIDs)
Chronic hyponatremia is usually relatively asymptomatic. What to know/be aware of about it? (3)
- Mild symptoms under-reported and under-recognized
- Often detected on routine bloodwork
- Has been associated with impaired attention, concentration, and gait -> increased fall risk
Symptoms of hyponatremia are primarily ___________
neurologic
- Due to osmotic intracellular water shift –> cell swelling and cerebral edema
Hyponatremia is proportional to: (2)
Magnitude and rapidity of sodium decline
Acute hyponatremia develops over the course of ~__h
48
What are the symptoms of acute hyponatremia? (3)
- Symptoms may appear ~125 mEq/L and include nausea, malaise, headache
- If [Na+] continues to ↓, symptoms progress to lethargy, confusion, decreased consciousness
- Seizures, coma if [Na+] ~115 mEq/L
What is chronic hyponatremia?
> 3 days’ duration
- Adaptive mechanisms kick in and help defend against cellular swelling, which minimizes symptoms
How might hyponatremia be diagnosed? (3)
- Plasma osmolality
- Generally in hyponatremia, plasma osmolality should be LOW (< 275 mOsm/L)
- If plasma osmolality is not low -> hyperosmolar hyponatremia (e.g. hyperglycemia) - 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) - 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
It is important to treat hyponatremia ______. Why?
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
Total daily sodium correction should not exceed _ mEq per day
8
Explain the treatment process of symptomatic hyponatremia (4)
- 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!)
- 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 - 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 - Frequent sodium rechecks to ensure appropriate correction, and adjust strategy as needed!
Explain the treatment process of asymptomatic hyponatremia (3)
- In asymptomatic hyponatremia, treatment may be targeted to the underlying cause
- Hypovolemic hyponatremia
- Use isotonic (0.9%) saline to restore the intravascular volume -> ↓ renal water retention (turn off ADH) -> normalize serum sodium concentration
- Avoid overcorrection! - 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
How is euvolemic hyponatremia (SIADH) treated? (2)
- Identify and correct underlying cause!
- 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+
What is hypernatremia?
- Plasma sodium > 145 mEq/L
- State of hyperosmolality -> cellular dehydration
- Usually results from a water deficit, rather than net sodium gain
Normally, the hyponatremia hyperosmolar state stimulates: (2)
Thirst and excretion of a maximally concentrated urine
For hypernatremia to persist, one or both of the compensatory mechanisms (thirst response, excretion) must not be working. How so? (2)
- Impaired thirst response:
- Limited access to water (e.g. infants and small children, institutionalized or intubated paients, delirium, dementia) - 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)
What is the clinical presentation of hypernatremia? (4)
- Hypernatremia -> movement of fluid from ICF to ECF -> brain cell shrinkage
- Presence and severity of symptoms depends on both the acuity and magnitude of hypernatremia
- Diabetes insipidus generally presents with polyuria and polydipsia
- Severe or acute hypernatremia may present with altered mental status, weakness, focal neurological deficits -> coma, seizures, death
Over-aggressive correction of hypernatremia can lead to?
Brain cell swelling –> seizures, permanent neurological damage, death
In symptomatic hypernatremia, sodium levels should be corrected by no more than __-__ mEq/L per day
10-12
In chronic (compensated) hypernatermia, sodium levels should be corrected even more slowly (_ to _ mEq/L per day)
5-8
If hypovolemic hypernatremia, ___ volume should be restored
ECF
How is central diabetes insipidus hypernatremia treated?
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)
How is nephrogenic diabetes insipidus hypernatremia treated? (3)
- Identify and correct concurrent hypercalcemia and hypokalemia
- Thiazide diuretic + Sodium restriction (< 2000 mg daily) decrease urine volume and normalize sodium levels
- Indomethacin 50 mg TID may also potentiate ADH activity in the kidney and decrease urine volume
How is sodium overload hypernatremia treated? (2)
- Usually iatrogenic (e.g.administration of too much sodium-containing fluids/medications in hospitalized patients)
- Administer D5W and loop diuretic (e.g. furosemide 20-40 mg) to facilitate sodium excretion
