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NICU > Sodium homeostasis and osmolality > Flashcards

Sodium homeostasis and osmolality Flashcards

1
Q

What is SIADH?

A

Euvolem or Hypervolem Hypothonic Hyponatremia

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2
Q

Define hypotone

A

serum osmolality under 275mOsm/kg

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3
Q

What is a high urinary osmolality?

A

Over 100 mOSm/kg

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4
Q

What is Cerebral Salt Wasting?

A

SIADH but with ExtraCellular Fluid Depletion due to renal sodium loss.

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5
Q

What is abnormally high koncentrations of Na in urine?

A

More than 20 mEq/l

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6
Q

What disease is important to rule out when accessing suspected SIADH and/or cerebral salt wasting?

A

Hypotyreoidism. - Take an TSH.

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7
Q

Other than TSH, what is the minimum work up for suspected SIADH or cerebral salt wasting?

A
  • Serum Na, Urine Na, Serum osmolality, and clinical assessment of volume status.
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8
Q

What is the risk of overly rapid correction of low serum sodium?

A

Osmotic demyelination; Pontine myelinolysis

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9
Q

What is the treshold of severe hyponatremia?

A

under 125mEq/l

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10
Q

Normal range of serum osmolality

A

282-295.

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11
Q

Panic values of serum osmolality

A

under 240 and over 321.

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12
Q

Fatal range of serumosmolality

A

over 420.

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13
Q

serum osmolality that produces stupor?

A

over 384

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14
Q

What is the risk of treating SIADH patients with fluid restriction in a neurosurgical setting?

A

If the diagnosis is wrong and the real etiology is CSW, the patient is actually volume depleted and need volume replacement with Na.

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15
Q

What is the most common type of hyponatremia after neurosurgery?

A

SIADH - syndrome of inappropriate Antidiuretic hormone secretion.

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16
Q

SIADH is associated to different types of tumors and also to a specific type of surgery. Which?

A

Transsphenoidal

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17
Q

CSW is common after aneurysmal SAH. How common is it compared to SIADH?

A

CSW: 6-23%
SIADH: 35%

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18
Q

What endocrine disturbances might induce SIAD?

A
  • Hypothyreoidism
  • Adrenal insufficiency
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19
Q

What “miscellaneous” reasons might induce SIAD?

A
  1. Anemia
  2. Stimulation of ADH release:
    * Stress
    * Severe pain
    * Nausea
    * Hypotension
    * (postoperative state)
  3. Acute intermittent porphyria
20
Q

Name a common “neurosurgery-hormonal” drug that is an ADH analogue

A

Oxytocin - ADH cross activity.

21
Q

When can hypERtonic hyponatremia occur in a neurosurgical setting? 2 common scenarios

A
  1. Hyperglycemia - for every 100mg/dl increase of glucose, Na decrease by 1.6-2.4 mEq/dl.
  2. Mannitol
22
Q

Whats the difference between SIAD and SIADH?

A

SIADH = Release of ADH IN THE ABSCENCE of physiologic (osmotic) stimuli. In SIADH hypervolemic state is more common than euvolemic.

23
Q

What is the result of inappropriate ADH stimuli?

A
  • Urine koncentration and elevated urine osmolality
  • Expansion of extracellular fluid volume (as the Na konc is so low in the blood)
    For unclear reasons edema does not occur.
24
Q

How do we check for normal adrenal function?

A
  • No hypotension
  • No hyperkalemia
25
Q

What do we do if we suspect adrenal dysfunction in the setting of suspected SIADH?

A

Visst ger vi mineralkortikoider då? O vad heter det nu…….hrmmmm

26
Q

What do we do in case of suspected dehydration in patients where a SIADH was expected?

A

We then belive in CSW instead and treat with rehydration and Na.

27
Q

What is done if a patient with suspected SIADH has a serum Na of under 124 and/or clinical signs of hyponatremia

A

We give Na (konc dependent on how fast the hyponatremia occured) and measure arterial levels q2-4 hours.
If the patient is obvious hypervolemic and does not have hypotension or hyperkalemia, furosemide might also be given.

28
Q

What are signs of fast developing hyponatremia?

A
  • neuromuscular excitability
  • cerebral edema
  • muscle twitching and cramps
  • N/V
  • Confusion
  • Seizures
  • Resp arrest
  • Permanent neurologic injury/coma/death
29
Q

What are signs of gradually developing hyponatremia?

A
  • Anorexia
  • H/A
  • Concentration problems
  • Irritability
  • Dysgeusia
  • Muscle weakness
30
Q

What is hyperchloremic acidosis?

A

A metabolic acidosis caused by overuse of NaCl, due to Excess Cl-. Its hard to treat. May lead to hypocapnia.

31
Q

What causes Diabetes insipidus

A
  • Low levels of ADH.
  • Rarely - renal insensitivity to ADH.
32
Q

Signs of Diabetes insipidus and risks with diabetes insipidus?

A

Sign= watercraving and polyuria w low urine osmolality.
Risk= Severe dehydration

33
Q

What are the two etiologies of Diabetes insipidus?

A
  • Central or Neurogenic.
  • Nephrogenic
34
Q

Where in the brain is a damage situated that causes diabetes insipidus?

A

In the hypothalamic-pituitary axis

35
Q

What neurosurgical situations may involve diabetes insipidus?

A
  • Posttraumatic - incl surgery
  • Tumor ….craniopharyngeoma, lymphoma, mets
  • Granuloma; neurosarcoidosis, histiocytosis
    *Aneurysms
    (and non-neurosurgical like infection, autoimmune, familial, idiopathic)
36
Q

what is psycogenic diabetes insipidus?

A

Excessive water intake.

37
Q

When is transient diabetes insipidus seen?

A

After transsphenoidal surgery/removal of craniopharyngeoma

38
Q

What is typical for transient diabetes insipidus?

A

Supra-normal urine output and polydipsia that normalizes spontanious 12-36hours postoperatively.

39
Q

What is prolonged postoperative diabetes insipidus?

A

Stays for up to a year, and for 1/3 is permanent.

40
Q

What is triphasic diabetes insipidus?

A

1- injury to pituitary reduces ADH for 4-5 days (DI)
2. Cell death liberates ADH for the next 4-5 days. normalization or SIADH like water retention NB! - risk of continuing vasopressin treatment!
3. Reduced or absent ADH secretion with transient or prolonged DI following.

41
Q

What is the treatment of DI?

A

Desmopressin (Vasopressin analogue).

42
Q

How do I know its DI in the clinical setting?

A
  1. Typical clinical signs
  2. urine output more than 250cc/hour.
  3. Normal or above normal Na.
  4. Normal adrenal function
  5. Urine osmolality usually between 50-150mOsm/kg. Defined as below 200.
43
Q

What is normal urine osmolality?

A

between 500-800mOsm/kg

44
Q

WHY cannot DI occur in primary adrenal insufficiency?

A

Due to the need of the kidneys for at least minimum mineralcorticoid secretion to make free water.

45
Q

What might happen if mineralcorticoids are given to a deprived person after transsphenoidal surgery?

A

It might “bring out” Diabetes insipidus. So that the effect of the lack of ADH is seen when the mineralcorticoids allow the kidney to produce and get rid of H2O.

46
Q
A

NICU (7 decks)

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