Sodium homeostasis and osmolality Flashcards
What is SIADH?
Euvolem or Hypervolem Hypothonic Hyponatremia
Define hypotone
serum osmolality under 275mOsm/kg
What is a high urinary osmolality?
Over 100 mOSm/kg
What is Cerebral Salt Wasting?
SIADH but with ExtraCellular Fluid Depletion due to renal sodium loss.
What is abnormally high koncentrations of Na in urine?
More than 20 mEq/l
What disease is important to rule out when accessing suspected SIADH and/or cerebral salt wasting?
Hypotyreoidism. - Take an TSH.
Other than TSH, what is the minimum work up for suspected SIADH or cerebral salt wasting?
- Serum Na, Urine Na, Serum osmolality, and clinical assessment of volume status.
What is the risk of overly rapid correction of low serum sodium?
Osmotic demyelination; Pontine myelinolysis
What is the treshold of severe hyponatremia?
under 125mEq/l
Normal range of serum osmolality
282-295.
Panic values of serum osmolality
under 240 and over 321.
Fatal range of serumosmolality
over 420.
serum osmolality that produces stupor?
over 384
What is the risk of treating SIADH patients with fluid restriction in a neurosurgical setting?
If the diagnosis is wrong and the real etiology is CSW, the patient is actually volume depleted and need volume replacement with Na.
What is the most common type of hyponatremia after neurosurgery?
SIADH - syndrome of inappropriate Antidiuretic hormone secretion.
SIADH is associated to different types of tumors and also to a specific type of surgery. Which?
Transsphenoidal
CSW is common after aneurysmal SAH. How common is it compared to SIADH?
CSW: 6-23%
SIADH: 35%
What endocrine disturbances might induce SIAD?
- Hypothyreoidism
- Adrenal insufficiency
What “miscellaneous” reasons might induce SIAD?
- Anemia
- Stimulation of ADH release:
* Stress
* Severe pain
* Nausea
* Hypotension
* (postoperative state) - Acute intermittent porphyria
Name a common “neurosurgery-hormonal” drug that is an ADH analogue
Oxytocin - ADH cross activity.
When can hypERtonic hyponatremia occur in a neurosurgical setting? 2 common scenarios
- Hyperglycemia - for every 100mg/dl increase of glucose, Na decrease by 1.6-2.4 mEq/dl.
- Mannitol
Whats the difference between SIAD and SIADH?
SIADH = Release of ADH IN THE ABSCENCE of physiologic (osmotic) stimuli. In SIADH hypervolemic state is more common than euvolemic.
What is the result of inappropriate ADH stimuli?
- 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.
How do we check for normal adrenal function?
- No hypotension
- No hyperkalemia
What do we do if we suspect adrenal dysfunction in the setting of suspected SIADH?
Visst ger vi mineralkortikoider då? O vad heter det nu…….hrmmmm
What do we do in case of suspected dehydration in patients where a SIADH was expected?
We then belive in CSW instead and treat with rehydration and Na.
What is done if a patient with suspected SIADH has a serum Na of under 124 and/or clinical signs of hyponatremia
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.
What are signs of fast developing hyponatremia?
- neuromuscular excitability
- cerebral edema
- muscle twitching and cramps
- N/V
- Confusion
- Seizures
- Resp arrest
- Permanent neurologic injury/coma/death
What are signs of gradually developing hyponatremia?
- Anorexia
- H/A
- Concentration problems
- Irritability
- Dysgeusia
- Muscle weakness
What is hyperchloremic acidosis?
A metabolic acidosis caused by overuse of NaCl, due to Excess Cl-. Its hard to treat. May lead to hypocapnia.
What causes Diabetes insipidus
- Low levels of ADH.
- Rarely - renal insensitivity to ADH.
Signs of Diabetes insipidus and risks with diabetes insipidus?
Sign= watercraving and polyuria w low urine osmolality.
Risk= Severe dehydration
What are the two etiologies of Diabetes insipidus?
- Central or Neurogenic.
- Nephrogenic
Where in the brain is a damage situated that causes diabetes insipidus?
In the hypothalamic-pituitary axis
What neurosurgical situations may involve diabetes insipidus?
- Posttraumatic - incl surgery
- Tumor ….craniopharyngeoma, lymphoma, mets
- Granuloma; neurosarcoidosis, histiocytosis
*Aneurysms
(and non-neurosurgical like infection, autoimmune, familial, idiopathic)
what is psycogenic diabetes insipidus?
Excessive water intake.
When is transient diabetes insipidus seen?
After transsphenoidal surgery/removal of craniopharyngeoma
What is typical for transient diabetes insipidus?
Supra-normal urine output and polydipsia that normalizes spontanious 12-36hours postoperatively.
What is prolonged postoperative diabetes insipidus?
Stays for up to a year, and for 1/3 is permanent.
What is triphasic diabetes insipidus?
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.
What is the treatment of DI?
Desmopressin (Vasopressin analogue).
How do I know its DI in the clinical setting?
- Typical clinical signs
- urine output more than 250cc/hour.
- Normal or above normal Na.
- Normal adrenal function
- Urine osmolality usually between 50-150mOsm/kg. Defined as below 200.
What is normal urine osmolality?
between 500-800mOsm/kg
WHY cannot DI occur in primary adrenal insufficiency?
Due to the need of the kidneys for at least minimum mineralcorticoid secretion to make free water.
What might happen if mineralcorticoids are given to a deprived person after transsphenoidal surgery?
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.
