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Renal Week 1 > Lecture 12: Hypernatremia, Fluid and Electrolyte Homeostasis > Flashcards

Lecture 12: Hypernatremia, Fluid and Electrolyte Homeostasis Flashcards

1
Q

What is normal water distribution?

A

1/3 TBW ECF and 2/3 TBW ICF
Man = 60% TBW
Women = 50% TBW

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2
Q

What determines distribution of water between ICF and ECF?

A

The distribution of effective osmoles

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3
Q

What are examples of effective “impermeant” solutes?

A
  1. Na
  2. K
  3. Cl
  4. HCO3
  5. Glucose
  6. Mannitol
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4
Q

What are examples of ineffective “permeant” solutes”

A
  1. urea

2. ethanol

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5
Q

How does one calculate plasma osmolality?

A

Posm = 2Na + glucose/18 + 18/2.8
Normal range = 280-295 mOsm/kg H2O
Quick estimate = 2Na + 10

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6
Q

Why multiply Na by 2?

A

In order to account for Cl and HCO3

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7
Q

Why divide glucose and BUN by 18 and 2.8 respectively?

A

To convert from mg/dl to mmole/L

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8
Q

How does one calculate tonicity?

A

Tonicity = 2Na + glucose/18
Quick estimate = 2Na + 5
Normal range = 275-290 mOsm/kg H2O

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9
Q

What is the difference between tonicity and osmolality?

A

The former can only be calculated

The latter can be both measured and calculated

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10
Q

What are the basic characteristics of hypertonicity?

A
  1. Increased plasma concentration of one or more effective osmotic solutes
  2. ICF volume contraction (cellular dehydration) due to efflux of fluid towards side of osmotic pressure
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11
Q

What are the clinical manifestations of hypertonicity?

A
  1. Non-specific CNS symptoms
    i. agitation, restlessness, confusion, lethargy
    ii. seizures, stupor, coma
  2. Intracranial hemorrhage
    • intracerebral, subarachnoid, subdural
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12
Q

What are the severity of hypertonicity symptoms influenced by?

A
  1. age (very young and very old)
  2. magnitude of hypertonicity
  3. rate of development of hypertonicity
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13
Q

What is always in the DDx of abnormal CNS function?

A

Hypertonicity since the CNS symptoms are always so non-specific
Diagnosis is easily established by measuring plasma Na concentration

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14
Q

What does the brain do in response to hypertonicity?

A

Increase intracellular concentration of effective solutes such as Na
When you see too much intracellularly, you know there is some sort of dysfunction (Na/K pump is not working and the fact that there may be a hypertonic ECF)
Increasing intracellular concentration in response to hypertonicity so that not as much fluid leaks out
May be more indicator of damage rather than compensatory mechanism

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15
Q

What is the significance of organic osmolytes?

A

The term used to describe the effective solutes that brain cells generate in order to compensate for hypertonicity
Examples include Na and amino acids
(the compensatory mechanism mentioned a line above)

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16
Q

What are the therapeutic implications of organic osmolytes?

A
  1. Time course of organic osmolytes inactivation is unknown
  2. Danger of cerebral edema (with brain herniation) if correction is too rapid (since fluid would rush into the cell that has the presence of additional organic osmolytes)
  3. Thus, correct hypertonicity, especially chronic hypertonicity, SLOWLY
    • over days not hours
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17
Q

What are the physiologic responses to hypertension?

A
  1. ADH release

2. Thirsty

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18
Q

At what osmolarity of urine does one know that ADH is working?

A

Uosm > 500 mOsm/kg

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19
Q

How can you determine total body Na content?

A
  1. physical exam findings such as BP, orthostatic BP changes, pulse, jugular venous pressure (JVP), ascites, edema, neurological status
  2. urine (volume, specific gravity, osmolality, electrolytes)
  3. Blood (BUN) and creatinine (Cr)
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20
Q

How can you determine total body Na content?

A
  1. physical exam findings such as BP, orthostatic BP changes, pulse, jugular venous pressure (JVP), ascites, edema, neurological status
  2. urine (volume, specific gravity, osmolality, electrolytes)
  3. Blood (BUN) and creatinine (Cr)

Normal BP, normal JVP, no edema, no ascites = normal total body sodium
Low BP, orthostatic BP changes, tachycardia, no edema, no ascites = low total body Na content
Elevated BP, increased JVP, pulmonary rales, ascites, edema = elevated total body Na content
Basically hypovolemia vs hypervolemia

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21
Q

What is the pathogenesis for developing hypernatremia?

A
  1. Loss of H2O
  2. Loss of H2O and sodium, but lose more H2O than sodium
  3. Gain of sodium
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22
Q

What is the pathogenesis for EUvolemic hypernatremia?

A

A situation with normal total body Na content
Caused by:
i. electrolyte free water losses
ii. Inadequate water intake
Key point: euvolemic hypernatremia = a disorder of water intake rather than water excretion
Example: diabetes insipidus (patient can’t take up enough water to overcome the glucose concentration in blood)

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23
Q

What are defects that can lead to euvolemic hypernatremia (inability to intake water)?

A

What are defects that can lead to euvolemic hypernatremia (inability to intake water)

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24
Q

What is geriatric hypodipsia?

A

A condition where elderly patients develop euvolemic hypernatremia because of a decreased thirst sensation

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25
Q

What happens to maximal urinary concentrating ability as one ages?

A

Decreases with age

26
Q

What are the causes of euvolemic hypernatremia?

A
  1. Extrarenal water losses (insensible losses through skin and lungs…NOT sweat??)
    i. hyperthermia
    ii. high ambient temperature
    iii. hyperventilation
  2. Renal water losses
    i. Central diabetes insipidus (deficiency of vasopressin)
    - can be primary or secondary (from tumor, infection or trauma)
    ii. Nephrogenic diabetes insipidus (resistance to vasopressin)
    - can be congenital or acquired (kidney damage or drugs like lithium
  3. Primary hypodipsia (deficit in water intake)
27
Q

What types of body excretions contain very little solute?

A

Cutaneous and pulmonary losses

28
Q

What are the causes of central diabetes insipidus?

A

Caused by a lack of ADH

Can be due to CNS lesions or autoimmunity to hypothalamic AVP secreting cells

29
Q

What is Wolfram’s Syndrome?

A

A rare autosomal recessive disorder that can cause central diabetes insipidus

30
Q

What are the causes of nephrogenic diabetes insipidus?

A

Caused by a defect in ADH receptor (V2) or Genetic mutations of aquaporin 2

31
Q

For every liter of sweat, how much volume do you lose from your intravascular (aka plasma) compartment?

A

You only lose 83 ml (or 1/12 of 1 L)
That’s why losing just water does not do a whole lot to make you hypovolemic, and for the most part you would stay euvolemic

32
Q

Are electrolyte free water losses associated with circulatory instability? Why or why not?

A

No it is not usually
This is because the TBW in plasma makes up only a very small portion of TBW (ECF = 1/3 of TBW, and plasma is only ¼ of that 1/3 … or 1/12 of TBW)

33
Q

What is the clinical presentation of euvolemic hypernatremia?

A

History
i. CNS symptoms
ii. Source of excessive electrolyte free water loss
iii. limited access to water or hypodipsia
Physical exam
-euvolemia (normal BP; no edema)
Lab findings
i. Hypernatremia
ii. variable urine osmolality (indicative of source of water loss)

34
Q

What can urine osmolality tell us about the etiology of euvolemic hypernatremia?

A

If Uosm > 500 mOsm/kg OR Uosm/Posm&raquo_space; 1,
It is due to INSENSIBLE losses (such as non-sweat?? Cutaneous and pulmonary losses) or due to primary hypodipsia
-the urine is highly concentrated in this case because the loss of fluid is at least physiological
If Uosm < 100 mOsm/kg OR Uosm/Posm < 1
It is due to complete diabetes insipidus
-either central or nephrogenic
-this is because an inability to excrete concentrated urine EVEN THOUGH body is hypernatremic is indicative of renal pathology

35
Q

How does one calculate water deficit?

A

TBWnormal * PNaNormal = TBWpresent * PNaPresent
Take the difference between TBW normal and TBW present
Usually we are given TBW present
In order to get TBW present, take the person’s weight and multiply by 0.6 or 0.5 depending on male or female
Once you get TBW present, plug it into equation above to solve for TBW normal
Water deficit = TBW normal – TBW present
Water deficit = how much water you need to give back to the patient to correct hypernatremia (or the tonicity)

36
Q

What is the pathogenesis of HYPOvolemic hypernatremia?

A

Hypotonic fluid loss (loss of BOTH osmotic solutes and water in hypotonic proportion in which H2O loss&raquo_space; Na loss)
1. Loss of Na leads to ECF volume depletion
2. Loss of water in excess of Na leads to hypernatremia
3. Insufficient water intake often exacerbates hypernatremia
Most common cause of hypernatremia

37
Q

What is the characteristic of the fluid lost in hypovolemic hypernatremia?

A

The fluid LOST is HYPOTONIC because it contains more water than solute

38
Q

What are the etiologies of hypovolemic hypernatremia?

A

Renal losses from
A. Diuretics
B. Osmotic diuresis
-urea (high protein tube feedings, post-obstructive diuresis)
-glucose (uncontrolled diabetes mellitus
Urine contains more water than solute
Extra-Renal losses from
A. GI causes such as diarrhea, vomiting and nasogastric suction
B. Cutaneous losses like profuse sweating and extensive burns

39
Q

When you lose 2 L of 0.45% saline from body (or 150 mEq of Na), how much plasma volume do you lose?

A

You can split it up to 1 L of just water (as we saw from calculation above) and 1L of 0.9% saline (which is still 150 mEq of Na, but now in 1 L of solution)
For the 1 L of just water, plasma volume loses 1/12 of conent, or 83 ml (since volume loss is distributed)
For the 1 L of 0.9% saline, the 150 mEq of Na is lost ALL from the ECF (there is no ICF loss)
Therefore it is 1 L of ECF gone
-since plasma is ¼ of the ECF, that means plasma loses 250 mL of volume
Thus, losing salt takes away so much plasma volume because it only affects ECF

40
Q

Are hypotonic hypernatremic fluid losses associated with circulatory instability? How does that compare to euvolemic hypernatremic water loss?

A

Yes they are because salt is involved

Euvolemic hypernatremic water loss = only water involved = no salt involved = no circulatory instability

41
Q

What is the clinical presentation of hypovolemic hypernatremia?

A 
History
	i. CNS symptoms
	ii. Excessive hypotonic fluid losses
Physical Exam
	i. Hypovolemia (low BP; no edema)
Laboratory findings
	i. hypernatremia
	ii. urinary indices variable (indicative of source of hypotonic losses)
42
Q

What does urinary indices tell one about cause of hypovolemic hypernatremia?

A

If pathology of excessive hypotonic solution loss resides in kidney, then Uosm < 400 and UNa > 20 mEq/L since urine is excreting more than it should
If pathology of excessive hyptonic solution is not in the kidney, then you have a low volume of urine + Uosm > 500 mOsm/kg (concentrating mechanism work) + UNa < 10 mEq/L

43
Q

What are the clinical characteristics of hypervolemic hypernatremia?

A

Pathogenesis = “isolated” sodium excess
Etiology = iatrogenic (therefore known)
-hypertonic Na-containing fluids

44
Q

What are the consequences of hypervolemic hypernatremia?

A
  1. acute intravascular and ECF volume expansion
  2. Acute pulmonary edema (ventilation frequently significantly impared)
  3. acute ICF volume contraction (neurologic complications common)
  4. Life threatening emergency
45
Q

Why do you get edema in both hypernatremia and hyponatremia?

A

Hypernatremia has a hypervolemic variant; therefore you can have volume overload
Natremia does NOT equal volume
In hyponatremia, you can have a volume overload variant as well
Again, natremia says NOTHING about your volume

46
Q

What is the treatment for euvolemic hypernatremia?

A
  1. replace water deficit
    • oral
    • IV 5% D5W (dextrose in water)
  2. Correct about 50% of deficit in first 24-48 hours and remainder over the next several days (to prevent cerebral edema)
  3. Keep up with ongoing losses
  4. Treat underlying disorder if possible
47
Q

What is the treatment for hypovolemic hypernatremia?

A

First priority = restore intravascular volume
-if hypotensive, use isotonic fluids initially
-if stable, increase dietary Na intake
Second priority = correction of hypernatremia
-oral/IV electrolyte free water
-correct slowly over several days
Keep up with ongoing losses
Treat underlying disorder

48
Q

What is the treatment for hypervolemic hypernatremia patients?

A

First priority = stabilize ventilation by treating pulmonary edema
i. diuretics
ii. extracorporeal ultrafiltration (if renal function is significantly compromised)
iii. artificial ventilation
Second priority = turn to correction of hypernatremia
-administration of electrolyte-free water

49
Q

What is hyperosmolar hyperglycemic non-ketosis?

A

A complication of uncontrolled diabetes mellitus
Several unique “fluid and electrolyte” features
Relatively high morbidity and mortality
One of two major fluid and electrolyte syndromes seen in patients with uncontrolled diabetes mellitus
-the other is diabetic ketoacidosis (DKA)

50
Q

What are the clinical features of hyperosomolar hyperglycemic non-ketosis (HHNK)?

A
  1. older patients
  2. relatively prolonged period of polyuria and secondary polydipsia
  3. May have no history of diabetes
  4. precipitated by infection, pancreatitis, steroids, diuretics, etc
51
Q

What are the lab findings of HHNK?

A

Severe hyperglycemia
No ketosis (blood and urine ketones negative)
-this rules out DKA

52
Q

What is severe hyperglycemia defined as?

A

Severe hyperglycemia > 500 mg/dl

53
Q

What is the pathophysiology of HHNK?

A

Phase 1 = hyperglycemia
Phase 2 = osmotic diuresis
Phase 3 = Continued Na and H2O depletion

54
Q

What are the characteristics of the hyperglycemic phase of HHNK?

A

Phase 1 of HHNK
Hypertonicity and ICF volume contraction
Hyponatremia initially!
It is hypertonic despite being hyponatermia because of the glucose!

55
Q

What are the characteristics of the osmotic diuresis phase of HHNK?

A

Phase 2 of HHNK
Hypertonicity and ICF volume contration
Variable ECF volume
Variable plasma Na concentration

56
Q

What are the characteristics of continued Na and H2O depletion phase of HHNK?

A

Phase 3 of HHNK
Hypertonicity and ICF volume contraction
Decreased ECF volume
Hyper natremia

57
Q

What is the primary cause of HHNK?

A

Lack of insulin

Peripheral insulin insensitivity that leads to hyperglycemia

58
Q

What are points to remember for HHNK?

A

Since glucose is rapidly metabolized when insulin is given and since hyperglycemia may represent an important component of osmotic maintenance of ECF volume, in Na depleted patients, insulin therapy may

i. lead to vascular collapse
ii. lead to rapid correction of ECF hypertonicity and thus brain edema (with ICF rehydration)
59
Q

Why is the blood pressure normal in HHNK if patient has Loss of Na for phase 3? Significance?

A

Because the glucose maintains the BP
If you give insulin, you take away glucose, thus taking away solute that stabilizes BP
-this will kill the patient
Thus, for HHNK patients MUST GIVE SODIUM FIRST
-giving insulin first will kill them

60
Q

How do you treat HHNK?

A
  1. restore ECF volume deficits with isotonic saline
    • restoring GFR with saline = enhanced glucose excretion = amelioration of hyperglycemia
  2. employ low dose insulin therapy to avoid ECF volume depletion and cerebral edema
    • forestalls ECF volume depletion before Na deficits are fully corrected (what does that mean?)
  3. correct water deficits slowly over several days to avoid cerebral edema
  4. Replete K and PO4 deficits (since K is lost in osmotic diuresis)
61
Q

How do you estimate water deficit in HHNK?

A

Pna is lowered by hyperglycemia
Pna decreases 2.4 mEq/L for each 100 mg/dl increase in plasma glucose concentration
Use “corrected” Pna when calculating water deficits in HHNK
-correction takes into account redistribution of water back into ICF during treatment

Renal Week 1 (15 decks)

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