SM 214a - Hypernatremia Flashcards

1
Q

Describe the changes in fluid compartments upon acute exposure to hypertonic Na solutions (Sea water).

What are the consequences?

A

Shift in total body water from ICF to ECF

  • -> Brain shrinkage
  • -> Cerebral blood vessel tears
  • -> Limbic demyelination
  • -> Elevation of EBV
  • -> Acute pulmonary edema
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2
Q

Hypertonic hypernatremia is recognized as a SNa above…

A

145 mEq/L

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3
Q

What two things can cause hypertonic hypernatremia (dehydration?)

A
  • Salt intake
  • Persistent H2O losses not replaced by H2O intake
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4
Q

If a patient has hypernatremia (Na+ >145) and ther urine osmolality is high, what is the cause?

A

Insensible losses or GI loses

+
Decreased H2O intake

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5
Q

What is the treatment for hypernatremia resulting from sweating, GI loss, or solute diuresis?

A

Need to replace Na+, K+, and H2O

Use 0.9% or 0.45% saline with potassium

Caution: Do not cause serum Na to fall too quickly!

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6
Q

What factors could impair H2O diuresis?

A
  • ADH release
    • -> Reabsorption of water
  • Decreased renal solute load
    • -> Decreased osmotic pressure in the tubule
    • -> Increased H2O reabsorption
  • Volume depletion
    • -> Decreased filtration
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7
Q

If a patient has hypernatremia and their urine osmolality is low, what is the most likely cause?

A

Diabetes Insipidus:
Renal H2O losses due to absent or ineffective ADH

  • Central diabetes insipidus
    • Low serum ADH
  • Nephrogenic diabetes insipidus
    • High serum ADH - the kidneys are resistant
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8
Q

Describe the general process of an H2O deprivation test in the setting of polyuria.

What do the results mean?

A

Evaluation of polydipsia vs. central DI vs. nephrogenic DI

  • Water deprivation to increased serum osm >298 mOsm/L
    • If urine osmolality increases, polydipsia is the cause of polyuria
    • ADH is working properly
  • Give desmopressin (ADH analog)
    • If urine osmolality increases significantly = central DI
      • Kidneys can resopnd to ADH
    • If urine osmolality does not increase = nephrogenic DI
      • Kidneys are resistant to AHD
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9
Q

What is the correction of SNa in the setting of high serum glucose?

A

Corrected SNa = SNa + [(Glucose – 100) ÷ 100 x 2 mEq/L]

Important to correct for glucose so hypernatremia in diabetes is not missed!

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10
Q

What is the treatment for nephrogenic DI?

A

Low sodium, low protein diet
+
Thiazide diuretics
+
NSAIDS

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11
Q

What is the treatment for central DI?

A
  • Acute: 2 mcg desmopressin IV every 12 hours
  • When polyuria resolves and patient is able, can switch to intranasal desmopressin
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12
Q

Gastrointestinal losses from vomiting or osmotic diarrhea are…

A. Hypertonic

B. Hypotonic

C. Isotonic

A

B. Hypotonic

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13
Q

Which patients are most likely to develop hypertonicity?

A

Elderly

Infirm

Infants

Intubuated

People with absent or decreased thirst drive, or who cannot freely respond to thirst

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14
Q

How do you estimate the water deficit in a patient with hypernatremia?

A

Current TBW x ( [SNa ÷ 140] – 1)

  • TBW in men is 0.6 * lean body weight (kg)
  • TBW in women is 0.5 * lean body weight (kg)
  • TBW in the elderly is 0.45 * lean body weight (kg)
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15
Q

What are the causes of polyuric hypertonic hypernatremia

(increased CefH2O)

A
  • Solute diuresis
    • Gluose (diabetics)
    • Mannitol
    • Urea
    • Diuretics
  • Pure H2O diuresis
    • Central Diabetes Insipidus
    • Nephrogenic Diabetes Insipidus
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16
Q

What additional pathologies do you worry about when you see a patient with persistent hypertonic hypernatremia?

A
  • Abnormal thirst drive
  • Decreased access to H2O
17
Q

What factors determine water reclamation?

A

Presence or absence of ADH

  • ADH released when plasma osmolality is high
  • ADH is not present when osmolality is low

Osmolality is sensed by osmoreceptors in the OLVT

Note: Volume depletion sensitizes the OLVT to release ADH in response to volume depletion - Severe volume depletion = lots of ADH released, even if osmolality is also low

18
Q

What is the mechanism of solute diuresis in diabetes melitus?

What electrolyte abnormalities does it cause?

A

Solute diuresis -> Hypernatremia, hypokalemia

  • Glucose in the urine draws more water into the urine
    • Increased osmotic pressure of tubular fluid
  • More water in the tubular fluid
    • -> Decreased concentration of Na+
    • -> Decreased reabsorption of Na+
  • Increased tubular flow rate, increased solute load
    • -> Washes out the interstitial gradient
    • -> Decreased concentrating power
  • ENaC is more active due to increased Na+ delivery to the collecting duct
    • -> Increased Na+ reabsorption
    • -> Increased K+ secretion
    • -> Hypokalemia
  • Hypotonic loss of water -> hypernatremia
    • -> Thirst
19
Q

How much water do we lose from insensible losses?

How?

A

~500 ml/day/m2 or 800 ml/day for a 70 Kg person

  • 60% is through the skin
  • 40% through respiration
20
Q

A diabetic with polyuria will be [hypo/hyper]kalemic

A

A diabetic with polyuria will be hypokalemic

  • Increased glucose in the tubule
  • -> Increased water in the tubule
  • -> Increased salt in the tubuel
  • -> Increased Na+ delivery to the collecting duct
  • -> Increased Na+ reabsorption
  • -> Increased K+ secretion
  • -> Hypokalemia