SIADH

Question 1

definition of SIADH

Answer 1

characterised by continued secretion of ADH, despite the abscence of normal stimuli for secretion (ie increased serum osmolarity or low blood vol)

Question 2

aetiology of SIADH

Answer 2

brain - subarachnoid/subdural haemorrhage/thrombosis, meningitis, meningoencephalitis, stroke, abscess, trauma, tumour, Guillain-Barre syndrome, neurosurgery, vasculitis, SLE

lung - pneumonia, TB, abscess, aspergillosis, small cell ca

tumour - small cell lung, lymphoma, leukaemia, pancreas, prostate, mestothelioma, sarcoma, thymoma. Ectopic ADH

drugs - vincristine, opiates, carbaemazepine, chlorpropamide, psychotropics, SSRI, cytotoxic

metabolic - porphyria, alcohol withdrawal

endo - hypothyroidism (not true SIADH, due to excess ADH relrase from carotid sinus baroreceptors triggered by low CO)

major abdo or thoracic surgery, symptomatic HIV

Question 3

epidemiology of SIADH

Answer 3

hyponatraemia most common electrolyte imbalance seen in hospitals

<50% of all severe hyponatraemia is due to SIADH

Question 4

symptoms of SIADH

Answer 4

mild hyponatraemia - may be asymptomatic

headache

nausea, vom

muscle cramp/weakness

irritability

confusion

drowsiness

convulsions

coma

symptoms of underlying cause

Question 5

signs of SIADG

Answer 5

mild hyponatraemia - no signs

severe hyponatraemia - low reflex, extensor plantar reflex

sign of underlying cause

the hyponatraemia in SIADH is dilutional from high body water and not low Na

Question 6

investigations into SIADH

Answer 6

low Na, creatinine, glucose, serum protein and lipids (exclude pseudohyponatraemia seen with high protein or lipids)

free T4 and TSH - exclude hypothyroidism

short ACTH stimulation test - exclude adrenal insufficiency

Question 7

diagnostic criteria for SIADH

Answer 7

low plasma osmolarity <260mosmol/Kg nad Na conc <125mmol/L|

high urine osmolarity >100mosmol/Kg and high Na >20mmol/L

presence of above and absence of the hypovolaemia/hypotension, oedema, renal failure, adrenal insufficiency and hypothyroidism needed for dx

Question 8

investigations to determine the cause of SIADH

Answer 8

CXR

CT chest abdo pelvis

MRI/CT head

Question 9

management of SIADH

Answer 9

treat the underlying cause

water restriction (0.5-1L/day)

if ineffective - demeclocycline (reduce responsiveness of the collectying tubule to ADH)

vasopressin (V2) receptor antagonists (VAPTANS) eg tolvaptan - likely to be useful in moderate chronic hyponatraemia if water restriction insufficient

in severe cases (seizures and reduced consciousness) - slow IV hypertonic 3% saline and furosemide with close monitoring - change in Na must not exceed 10mmol/L in the first 24hr and 18mmol/L in the 1st 48hr. Rapid correction can = central pontine myelinolysis

Question 10

complications of SIADH

Answer 10

convulsions

coma

death

central pontine myelinolysis (guadreparaesis, resp arrest, fits) with rapid correction

Question 11

prognosis of SIADH

Answer 11

depends on the underlying cause

high mobidity and mortality with Na <110mmol/L

up to 50% mortality with central pontine myelinolysis