Differences Between

Cerebral Salt Wasting and

Syndrome of Inappropriate
Antidiuretic Hormone

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Preceptor : dr. Martin Firman Suryo, Sp.S, FIPM
Clinical Clerkship Neurology Rotation
Royal Taruma Hospital
Period of 26 November – 30 December 2018
Definitions
Cerebral Salt Wasting (CSW)
• Defined by  the development of
extracellular volume depletion due to
a renal sodium transport abnormality
in patients with intracranial disease
and normal adrenal and thyroid
function
• Also can be called  renal salt wasting
Syndrome of Inappropriate Antidiuretic
Hormone Secretion (SIADH)
• Defined by  hyponatremia and hypo-
osmolality resulting from inappropriate,
continued secretion or action of the
antidiuretic hormone arginine vasopressin
(AVP) despite normal or increased plasma
volume, which results in impaired water
excretion
• Consists of  hyponatremia,
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inappropriately elevated urine osmolality
(>100 mOsm/kg), and decreased serum
osmolality in a euvolemic patient
What are the causes? (Etiology)
CSSW SIADH
 Head injury • Nervous system disorders (Stroke, Trauma,
Surgery, Meningitis, Cerebral SLE, Tumours,
 Brain tumour Cerebral Abscess, etc)

• Neoplasia (Small Cell Lung, Prostate,

 Intracranial surgery Thymic, Pancreatic, Lymphoma)
 Stroke • Pulmonary diseases (TB, Pneumonia, Lung
Abscess)
 Intracerebral haemorrhage

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• Drug induced (antineoplasmotic agents,
 Tuberculous meningitis SSRI, NSAID, etc)

 Craniosynostosis repair
 How does CSW happened?
(Pathophysiology)
• Exact mechanism is still unclear
• Defect in renal sodium transport 
extracellular volume depletion  cascade of
compensatory
• Abnormalities in the distal tubule  excessive
sodium losses  decreased effective
circulating volume  activates baroreceptors
 increase antidiuretic hormone (ADH)

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secretion  water conservation  return to
equilibrated state
Postulated Hypothesis
In the setting of cerebral injury :
• Increased activity of the sympathetic
nervous system & dopamine release 
exaggerated renal pressure–natriuresis
response  urinary sodium loss
• Injured brain  release of natriuretic
factors (possibly including brain natriuretic
peptide (C-type natriuretic peptide) or
urodilatin)

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Presentation of CSW
• Declining serum sodium concentration reduces serum osmolality developing
tonicity gradient across the blood-brain barrier  causes cerebral oedema
• Signs & symptoms  lethargy, agitation, headache, altered consciousness,
seizures, coma
• and also features suggesting hypovolemia  include thirst, abrupt weight
loss, decreasing urinary frequency, and negative fluid balance
• Usually develops in the first week following a brain insult
• Duration  usually brief (spontaneously resolves in 2-4 weeks) but can last for

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several months
How does SIADH happened?
(Pathophysiology)
• Non-physiological secretion of AVP (Arginine Vasopressin) / ADH  enhanced water
reabsorption  dilutional hyponatremia

• Extracellular fraction causes volume expansion  Volume receptors are activated and
natriuretic peptides are secreted  natriuresis and some degree of accompanying
potassium excretion (kaliuresis)

• Eventually, a steady state is reached because of unknown mechanism of Kidney

Adaptation  decreased in water reabsorption

• In addition to the inappropriate AVP secretion, persons with this syndrome may also
have an inappropriate thirst sensation, which leads to an intake of water that is in

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excess of free water excreted. This increase in water ingested may contribute to the
maintenance of hyponatremia
 RAAS ↓

↓Na reabsorption

Hyponatremia

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Presentation of SIADH
• Signs & symptoms of acute hyponatremia do not precisely correlate with the severity or the
acuity of the hyponatremia.
• Some patients with profound hyponatremia may be relatively asymptomatic
• Early symptoms when serum Na + level is less than 125 mEq/L  anorexia, nausea, and
malaise
• Further decrease  osmotic fluid shifts result in cerebral oedema and increased intracranial
pressure  headache, muscle cramps, irritability, drowsiness, confusion, weakness,
seizures, and coma
• Important to check for history of  CNS or pulmonary tumors (eg, hemoptysis, chronic
headaches), or head injury, and drug use, also excessive fluid intake because of
inappropriate thirst or psychogenic polydipsia or because hypotonic fluids were

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administered in a healthcare setting
• PE findings *may be seen only in severe or rapid-onset  Confusion, Disorientation,
Delirium, Generalized muscle weakness, Myoclonus, Tremor, Asterixis, Hyporeflexia, Ataxia,
Dysarthria, Cheyne-Stokes respiration, Pathologic reflexes, Generalized seizures, Coma
 SUMMARY

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 Work Up

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