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Electrolytes > Sodium > Flashcards

Sodium Flashcards

1
Q

Describe how sodium is distributed among the body compartments.

What is the major physiologic function of sodium?

A

Sodium is the major EXTRACELLULAR cation
Pumped out of cells by the Na/K-ATPase

Physiologic functions of sodium:

Flows into cells down its gradient during depolarization

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2
Q

What is the normal serum osmolality?

A

275-290

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3
Q

What is the pathophysiology that underlies the clinical manifestations of hyponatremia?

A

The symptoms directly attributable to hyponatremia primarily occur with acute and marked reductions in the serum sodium concentration and reflect neurologic dysfunction induced by cerebral edema

The associated fall in serum osmolality creates an osmolal gradient that favors water movement into the cells, leading to brain edema.

Basically the brain tissues swell because water flows into them down its osmotic gradient

Ultimately, ICP can increase and herniation can occur

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4
Q

What are the potential clinical manifestations of hyponatremia?

A

The major clinical manifestations of acute hyponatremia include:

Nausea and malaise, which are the earliest findings, may be seen when the serum sodium concentration falls below 125 to 130 mEq/L.

Headache, lethargy, obtundation and eventually seizures, coma, and respiratory arrest can occur if the serum sodium concentration falls below 115 to 120 mEq/L.

Noncardiogenic pulmonary edema has also been described.

The degree of cerebral edema and therefore the severity of neurologic symptoms are much less with chronic hyponatremia

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5
Q

Provide an approach to thinking about the causes of hyponatremia.

A

1) Fluid shifts
“Hyperosmolar hyponatremia”
“Pseudohyponatremia”
Non-specific term, in EMCrit refers to hyponatremia that is not hypoosmolar
Basically, check the serum glucose and correct sodium for glucose

2) Increased free water intake
Primary polydipsia and beer drinker’s potomania

3) Increased free water retention / decreased free water excretion
ADH-dependant hyponatremia, “hypoosmolar hyponatremia,” “true hyponatremia,” the meat and potatoes of hyponatremia
Usually divided into hypervolemic, euvolemic, and hypovolemic

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6
Q

What is the major cause of hyperosmolar or pseudohyponatremia?

A

Hyperglycemia

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7
Q

How do you correct the sodium for glucose?

A

The sodium concentration will fall by approximately 2 mEq/L for each 5.5 mmol/L increase in glucose concentration

Approximately 1:3

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8
Q

What are the major causes of increased free water intake?

A

Physiologic - decreased plasma tonicity (thirst stimulated)

Patholoic -

Psychogenic polydipsia (seen in schizophrenia)
Beer drinker's potomania
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9
Q

What are the causes of hypoosmolar or true hyponatremia?

A

Categorized by volume status

Hypervolemic with decreased effective circulating volume (heart failure, cirrhosis, nephrotic syndrome)

Euvolemic
SIADH

Hypovolemic

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10
Q

What are some causes of SIADH? Name 5.

A

CNS disease
Any CNS disorder, including stroke, hemorrhage, infection, trauma, and psychosis, can enhance ADH release

Lung cancer
Ectopic production of ADH by a tumor is most often due to a small cell carcinoma of the lung and is rarely seen with other lung tumors

Drugs
Anticonvulsants
SSRIs

Endocrinopathy
Hyper or hypothyroidism
Adrenal insufficiency

HIV infection

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11
Q

You discover hyponatremia. What further work-up would you order to determine the cause? Name 5 investigations.

A 
Serum osmolality
Urine osmolality
Urine electrolytes
TSH
Cortisol
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12
Q

What does urine osmolality tell you?

A

Tells you if the body is retaining or releasing free water.

Proxy marker of whether ADH is “on” or “off”

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13
Q

What is the significance of low urine osmolality?

A

Low urine osmolality = dilute urine = ADH “off” (body releasing free water)

Suggests excess free water intake, body responding appropriately

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14
Q

What is the significance of high urine osmolality?

A

High urine osmolality = concentrated urine = ADH “on” (body retaining free water)

Suggests hypoosmolar or “true” hyponatremia

May be appropriate or inappropriate

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15
Q

What does urine sodium tell you?

A

Tells you about the effective circulating volume

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16
Q

What is the significance of low serum sodium?

A

Body attempting to retain sodium to increase intravascular volume
Suggests decreased intravascular volume, either hyper or hypovolemic

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17
Q

What is the significance of high urine sodium?

A

Body releasing sodium

Suggest SIADH

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18
Q

Provide an overview of the treatment of hyponatremia.

A

1) Send the work-up
2) Free water restrict all patients
3) Determine whether administration of a hypertonic solution is indicated

19
Q

What are the indications for the administration of a hypertonic solution?

A

Indicated in symptomatic hyponatremia, e.g.:
Seizure
Confusion
Headache, nausea, vomiting
Dizziness, gait instability, tremor, multifocal myoclonus

Clinical context is more important than the numeric value of sodium, for example:
Young woman with acute hyponatremia, Na of 125 mM, nausea and headache: This is an emergency, give hypertonic therapy immediately.
Elderly man with chronic hyponatremia, Na of 125 mM, asymptomatic: This might not even warrant hospital admission, don’t get too excited about it.

20
Q

What are the different hypertonic solutions that can be given in symptomatic hyponatremia?

A

Sodium bicarbonate

3% saline

21
Q

Describe the advantages and the administration of sodium bicarbonate in symptomatic hyponatremia.

A

Hypertonic bicarbonate is defined here as 1 mEq/ml sodium bicarbonate, which is generally found in ampules of bicarbonate in crash carts.

This solution of 1 mEq/ml sodium bicarbonate has the same tonicity as would 6% NaCl.

In the United States, each hypertonic bicarbonate ampule generally contains 50 ml

Hypertonic bicarbonate is usually the fastest medication to obtain in an emergency.

A typical dose is two ampules (100ml) of hypertonic bicarbonate

Ampules of bicarbonate should generally be infused slowly (e.g. each one over 5-10 minutes).

Bicarbonate is contraindicated in patients with metabolic alkalosis, which would be exacerbated by the bicarbonate.

2 amps of sodium bicarbonate is approximately the equivalent equivalent to giving ~200 ml of 3% saline, which will raise the serum sodium by ~3 mM).

22
Q

Describe disadvantages and the administration of 3% saline in symptomatic hyponatremia.

A

3% saline may be provided in a dose of 2 ml/kg body weight (e.g. ~150 ml)

This is the traditional therapy for hyponatremia.

The main drawback is that it often takes a long time to receive from the pharmacy.

Please note that 3% saline IS SAFE to administer through a peripheral line.

3% saline does NOT require placement of a central line

23
Q

How fast should the serum sodium be corrected?

A

Hourly rate:

No faster than 0.5 mEq/L in any given hour
Excludes the initial rise obtained from the administration of hypertonic saline, which may be about 3-5 mM

Daily rate:
No faster than 8 mEq/L in the first 24 hours
Note that this includes the initial rise if a hypertonic solution was provided

24
Q

What is the feared complication of raising the serum sodium too quickly?

A

Osmotic demyelination syndrome (ODS)

Previously called central pontine myelinolysis

25
Q

What is osmotic demyelination syndrome?

A

Syndrome of motor weakness that occurs when rapid a fall in brain volume leads to a demyelination of neurons

Caused by iatrogenic overcorrection of hyponatremia

Correction of chronic hyponatremia = higher risk than correction of acute hyponatremia

The brain begins to adapt to hypotonicity almost immediately after a fall in serum sodium, and the adaptation is complete within two days
Because the brain is able to adapt to hypotonicity, hyponatremia that develops over more than two to three days is not associated with severe brain swelling and is therefore much less likely to be complicated by seizures and coma; it is also extremely unlikely to produce brain herniation

26
Q

Describe the clinical presentation of ODS.

A

The clinical manifestations of ODS are typically delayed for two to six days after overly rapid elevation of the serum sodium concentration has occurred

Presents with motor weakness
The symptoms include dysarthria, dysphagia, paraparesis or quadriparesis, behavioral disturbances, movement disorders, seizures, lethargy, confusion, disorientation, obtundation, and coma

Symptoms are frequently irreversible.

27
Q

The sodium has risen too quickly. How can this be treated?

A

Administration of DDAVP

28
Q

What is an osmole?

A

A unit of measurement for solutes that exert osmotic pressure
An osmole = 1 mole of solute

29
Q

What is osmolarity?

A

Measure of solute concentration, defined as the number of osmoles (Osm) of solute per litre (L) of solution

30
Q

What is osmolality?

A

Measure of solute concentration, defined as the number of osmoles measured in osmoles of the solute per kilogram of water

31
Q

What is tonicity? What is the difference between osmolality and tonicity?

A

Tonicity = effective osmolality

The main difference between plasma tonicity and plasma osmolality is that plasma tonicity reflects the concentration of solutes that do not easily cross cell membranes (mostly sodium salts) and therefore affect the distribution of water between the cells and the ECF.

By contrast, the plasma osmolality also includes the osmotic contribution of urea, which is considered an “ineffective” osmole since it can equilibrate across the cell membrane and therefore has little effect on water movement across the cell membrane.

Ethanol is another osmole that rapidly enters cells and therefore has no tonicity.

32
Q

How can plasma osmolality be calculated?

A

Posm = 2 x [Na] + [Glucose] + [Urea]

“A bun with two salties and a sweet”

33
Q

Describe the regulation of plasma tonicity.

A

Changes in plasma tonicity are sensed by osmoreceptors in the hypothalamus.

These receptors affect both water intake and water excretion by influencing thirst and the release of ADH, respectively

Increased tonicity → thirst stimulated, ADH released, free water retained

Decreased tonicity → thirst suppressed, ADH suppressed, free water excreted

34
Q

How does ADH work?

A

Released from the posterior pituitary gland when plasma tonicity is high

Oxytocin is also released from the posterior pituitary, most other pituitary hormones released by the anterior pituitary

Instructs the kidneys to reabsorb free water

Its major renal effect is to augment the water permeability of the luminal membranes of principal cells in the cortical and medullary collecting tubules, thereby promoting water reabsorption via osmotic equilibration with the hypertonic interstitium.

35
Q

What are the potential clinical manifestations of hypernatremia?

A

The clinical manifestations of acute hypernatremia begin with lethargy, weakness, and irritability, and can progress to twitching, seizures, and coma.

36
Q

Describe the pathophysiology of hypernatremia.

A

Hypernatremia is basically a mirror image of hyponatremia

A rise in the serum sodium concentration and osmolality causes water movement out of the brain.

Brain shrinkage

With acute hypernatremia, the rapid decrease in brain volume can cause rupture of the cerebral veins, leading to focal intracerebral and subarachnoid hemorrhages and possibly irreversible neurologic damage

Acute hypernatremia can also result in demyelinating brain lesions similar to those associated with overly rapid correction of chronic hyponatremia

37
Q

What is the primary problem in hypernatremia?

A

Think of hypernatremia as a deficit rather than an excess of sodium

In other words, hypernatremia is a water problem, not a sodium problem.

38
Q

What i the primary problem in hyponatremia?

A

Water problem, not a sodium problem

Hyponatremia = too much water

39
Q

What are the principle causes of hypernatremia?

A

Remember, hypernatremia = too little water

1) Reduced free water intake
Inability to experience or respond to thirst
In general, hypernatremia develops only in those who are unable to experience thirst or access free water
Examples: elderly, infants, disabled, comatose, intubated
Patients who present with hypernatremia usually have a serious underlying condition that impairs either their ability to respond to thirst or to experience thirst. As a result, such patients usually require hospitalization to correct the hypernatremia.

2) Excessive free water elimination
Endocrinopathy - diabetes insipidus
Central - impaired release of ADH
Nephrogenic - impaired sensitivity to ADH

40
Q

What are the causes of central diabetes insipidus?

A

The most common causes of central diabetes insipidus (CDI), accounting for the vast majority of cases, are idiopathic diabetes insipidus (DI), primary or secondary tumors or infiltrative diseases, neurosurgery, and trauma.

41
Q

Describe the treatment options for hypernatremia.

A

Give free water

In patients with central diabetes insipidus, give desmopressin

42
Q

Describe how to give free water to the patient with hypernatremia?

A

Nearly all patients with hypernatremia will have chronic hypernatremia

Basically, give D5W at 100 cc/h

Five percent dextrose in water, intravenously, at a rate of (approximately 1.35 mL/hour x patient’s weight in kg) or approximately 70 mL/hour in a 50 kg patient and 100 mL/hour in a 70 kg patient

The rationale for treatment is complicated and requires calculating the free water deficit, which is a fraught and imprecise enterprise.

43
Q

What is the goal of correction in hypernatremia?

A

The goal of water repletion in patients with chronic hypernatremia is to lower the serum sodium by approximately 10 mEq/L in 24 hours but to avoid correcting the serum sodium by more than 12 mEq/L in 24 hours.

44
Q

What is the treatment for patients with central diabetes insipidus?

A

Desmopressin therapy

Electrolytes (1 decks)

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