Di, siadh and cerebral salt wasting syndrome

DI, SIADH and Cerebral Salt
Wasting
Mohamad Soud

Similarities – What’s in
common?
Central neurogenic diabetes insipidus (CNDI), syndrome
of inappropriate secretion of
antidiuretic hormone (SIADH), and cerebral salt-wasting
syndrome (CSWS) ALL affect both sodium and water
balance; however, they have differences in
pathophysiology, diagnosis,
and treatment.

Antidiuretic hormone (ADH)
 A polypeptide
synthesized in the
supraoptic and
paraventricular nuclei in
the hypothalamus.
 Secretory granules
containing ADH migrate
down into the posterior
lobe of the pituitary,
where they are stored
and released after
appropriate stimuli.

Antidiuretic hormone (ADH)
 Most important
variable is osmotic
pressure of plasma
and ECF.
 = (2 x serum [Na]) + [glucose,
in mg/dL]/18 + [blood urea
nitrogen, in mg/dL]/2.8
 Largely a function of the
concentration of Na

Diabetes Insipidus
A hormone disorder that
occurs when the body
doesn’t produce enough
antidiuretic hormone (ADH)
or doesn't use the hormone
effectively >> excretion of
excessive quantities of very
dilute, but otherwise normal
urine.

Diabetes Insipidus – Types
Two types:
1. Central DI, a primary deficiency of ADH
2. Nephrogenic DI, caused by an inappropriate renal
response to ADH

Central DI
 The cause of central diabetes insipidus in adults is
usually damage to the pituitary gland or
hypothalamus
 Idiopathic - 30%
 Malignant or benign tumors of the brain or pituitary - 25%
 Cranial surgery - 20%
 Head trauma - 16%

Post Surgical Central DI
 Postsurgical diabetes insipidus results
from inflammatory edema around
the hypothalamus or posterior
pituitary and resolves with resolution
of the edema. It may also be
secondary to damage to the
supraoptic and paraventricular
neurons of the hypothalamus, the
pituitary stalk, or Pituitary
Vasculature
 The neurohypophysis is supplied
by the inferior hypophyseal
arteries terminal branches of
the meningohypophyseal trunk,
which arises from the
cavernous portion of the
internal carotid artery

Diabetes Insipidus -
Symptoms
Characterized by:
 Excessive thirst that may be intense or uncontrollable,
usually with the need to drink large amounts of water
 Excessive urine volume That is hypotonic, dilute and
tasteless (insipid)
 Versus the sweet urine of diabetes mellitus(honey).
 Excessive urination, often needing to urinate every hour
throughout the day and night.

Central DI – Treatments
 Desmopressin is the drug of choice.
 IV hypotonic solutions (0.45% saline) to replace urine
output.

Syndrome of Inappropriate Antidiuretic
Hormone Secretion (SIADH)
 Hyponatremia and hypo-osmolality resulting from
inappropriate, continued secretion or action of ADH
despite normal or increased plasma volume, which
results in impaired water excretion.

SIADH – Causes
 Any CNS disorder, including stroke,
hemorrhage (very common in SAH
population), infection, trauma, and
psychosis can enhance ADH release.
 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. Less common causes of
malignancy-associated SIADH include head
and neck cancer, olfactory neuroblastoma
(esthesioneuroblastoma), and
extrapulmonary small cell carcinomas.
 Certain drugs can enhance ADH release or
effect, including chlorpropamide,
carbazapine, oxcarbazepine (a derivative of
carbamazepine), high-dose intravenous
cyclophosphamide, and selective serotonin
reuptake inhibitors.
 Pulmonary diseases, particularly
pneumonia (viral, bacterial, tuberculous),
can lead to the SIADH, although the
mechanism by which this occurs is not
clear. A similar response may infrequently
be seen with asthma, atelectasis, acute
respiratory failure, and pneumothorax.

SIADH – Pathophysiology
 ADH-induced water retention
 Dilutional hyponatremia
 Volume expansion >> secondary natriuresis (ANP)
 Sodium and water loss
 Result: Euvolemic hyponatremia
 Reduced serum osmolality
 Increased urine osmolality
 Increased urine sodium

SIADH – Symptoms
 Nausea or vomiting
 Cramps or tremors
 Depressed mood or memory impairment
 Irritability
 Personality changes, such as combativeness, confusion,
and hallucinations
 Seizures
 Stupor or coma

SIADH – Diagnosis
 Euvolemic hyponatremia <134 mEq/L,
 Serum Osm <275 mOsm/kg
 Urine osmolality >300 mOsm/kg
 Urine sodium concentration >40 mEq/L with normal
dietary salt intake

SIADH – Treatment
 Treat the underlying cause, if known
 Water restriction to about 500-1500 mL/d
 Correct Na+ deficit: no more than 10mEq/L in 24 hours, 18mEq/L in 48 hours
 0.9% NaCl
 3% NaCl
 NaCl enteral tablets – 2-3g TID
 Vasopressin receptor antagonists: inhibition of the AVP V2 receptor reduces the
number of aquaporin-2 water channels in the renal collecting duct and decreases the
water permeability of the collecting duct; There are 2 aquaretics that are currently
FDA approved:
• Conivaptan (Vaprisol)
• Tolvaptan
 loop diuretic: usually used in conjunction with normal saline to replenish the
Na+ excreted with the diuresis
 Demeclocycline.

Cerebral Salt Wasting Syndrome
(CSWS)
 Cerebral salt-wasting syndrome (CSWS) is a rare
endocrine condition featuring a low blood sodium
concentration and dehydration in response to
trauma/injury or the presence of tumors in or
surrounding the brain.

CSWS – Causes
Condition leading to CSW include the following:
 Head injury
 Brain tumor
 Intracranial surgery
 Stroke
 Intracerebral hemorrhage
 Tuberculous meningitis

CSWS – Pathophysiology
 Sympathetic Nervous System
Hypothesis: loss of adrenergic tone
to nephron >> decrease in renin
secretion by juxtaglomerular cells,
thereby causing decreased levels of
aldosterone and decreased sodium
reabsorption at PCT.
 Natriuretic Peptide Theory: a
release of natriuretic factors,
possibly including brain natriuretic
peptide (C-type natriuretic peptide)
by the injured brain , which
decreases sodium reabsorption and
inhibits renin.

CSWS – Symptoms
 As the decline in serum sodium concentration reduces
serum osmolality, a tonicity gradient develops across
the blood-brain barrier that causes cerebral edema.
 Symptoms include lethargy, agitation, headache, altered consciousness,
seizures, and coma.
 Intravascular volume depletion
 thirst, abrupt weight loss, decreasing urinary frequency, and negative fluid
balance.

CSWS – Diagnosis
 Hyponatremia < 135 meq/L with a low plasma
osmolality
 An inappropriately elevated urine osmolality >
100 mosmol/kg and > 300 mosmol/kg)
 A urine sodium concentration > 40 meq/L
 A low serum uric acid concentration due to urate
wasting in the urine

CSWS – Treatment
 IV hypertonic saline solutions are employed to correct
intravascular volume depletion and hyponatremia and to
replace ongoing urinary sodium loss.
 Mineralocorticoids enhance sodium reabsorption in the
kidney by direct action on distal tubule cells
 Fludrocortisone

Summary
Central DI is associated
with HYPERnatremia, whereas
SIADH and CSWS are associated
with HYPOnatremia.

Summary – SIADH vs. CSWS
vs. DI
SIADH CSWS DI
Serum Na+
Urine Na+
Serum Osm
Urine Osm

Summary – SIADH vs. CSWS
vs. DI
SIADH CSWS DI
Urine O/P oliguria polyuria polyuria
CVP normal/high low normal/low
Plasma ADH high normal low
Rx Fluid restrict, give
Na+, Conivaptan,
Demeclocycline
Give volume, give
Na+,
Fludrocortisone
Drink to thirst,
45% saline,
DDAVP
(central), HCTZ
(nephrogenic)

Di, siadh and cerebral salt wasting syndrome

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Di, siadh and cerebral salt wasting syndrome