SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
SIADH
• Syndrome of Inappropriate ADH Secretion
• Definition: levels of ADH are
inappropriately elevated compared to
body’s low osmolality, and ADH levels are
not suppressed by further decreases in
blood osmolality.
SIADH Causes
• Irritation of CNS
meningitis, encephalitis, brain tumors, brain
hemorrhage, hypoxic insult, trauma, brain
abscess, Guillain Barre, hydrocephalus
• Pulmonary disorders
pneumonia, asthma, positive end expiratory
pressure ventilation, CF, TB,
pneumothorax
SIADH causes
• Drugs: vincristine, vinblastine, opiates,
carbamazepime, cyclophosphamide
• Unregulated tumor production of ADH-like
peptides: oat cell lung carcinoma for
example, Ewings sarcoma, carcinoma of
duodenum, pancreas, thymus
SIADH function of ADH
• Antidiuretic hormone = vasopressin
• ADH is made in the supra-optic nuclei in the
hypothalamus, stored in the posterior
pituitary
• Normally released into the bloodstream
when osmo-receptors detect high plasma
osmolality
SIADH function of ADH
• At the kidney, attaches to receptors in
the collecting ducts, opens up water
channels
• Water is passively reabsorbed along
the kidney’s medullary concentration
gradient
SIADH
signs and symptoms
• Decreased / low urine output
• Signs of hyponatremia: lethargy, apathy,
disorientation, muscle cramps, anorexia,
agitation
• Signs of water toxicity: nausea, vomiting,
personality changes, confused, combative
• If Na < 110 mEq/L, seizures, bulbar palsies,
hypothermia, stupor, coma
SIADH
lab values
• Serum Na < 135 (Na is diluted by
excessive free water re-absorption)
• Serum osmolality low, normal is ~ 270
• Urine Na is inappropriately high, >20
mmol/L, actually losing Na in urine
instead of retaining it
SIADH
lab values
• Urine osmolality is inappropriately
high, can range b/t 300-1400
mosm/L
• CVP is high from free water retention
SIADH
Treatment
• Fluid restriction, ¾ maintenance
• If symptomatic, may actually need to replace
NaCl, can use hypertonic saline for example:
300cc/m2 of 1 ½ % NS
• Diuretics such as lasix
• Treat underlying disorder, for example usually
resolves after removal of lung carcinomas
SIADH
treatment cont…
• Demeclochlorotetracycline, blocks ADH
receptors in the renal collecting ducts
• In severe cases, hemodialysis
• Warning, if increase Na too fast, at risk
for pontine myelinolysis
• Max correction of 15mEq in 24 hours
DI = Diabetes Insipidus
• Definition: inability to effectively conserve urinary
water
• Central: ADH not made or not released in the
hypothalamic-pituitary axis
• Nephrogenic: ADH is released but not detected by the
receptors in the kidney collecting ducts, often a sex-
linked recessive condition, also due to renal pathology,
electrolyte disorders, drugs
Central DI
causes
• Head trauma
• Brain neoplasms
• Congenital CNS defects
• CNS infections
• CNS hypoxia
• ADH secretion also decreased by certain
drugs: EtOh, demerol, MSO4, dilantin,
barbiturates, glucocorticoids
DI
• Make sure distinguish DI from conditions in which
the presence of non-absorbable, osmotically active
solutes in the renal tubules prevent water re-
absorption.
• Example: glucose loss in the urine of diabetics will
decrease the tubule- medullary concentration
gradient and even though ADH is there, water won’t
get passively reabsorbed
Central DI
Signs/symptoms
• Polyuria
• Dehydration, may not be readily apparent b/c
of hyper-osmolarity, fluid shifts from cells to
intravascular spaces and maintains blood
pressure, CVP
• Weight loss is a better measure of fluid status
Central DI
Lab values
• Hypernatremia, Na >150-160
• High serum osmolality (normal 270)
• Urine Na < 20 mmol/L
• Low urine osmolality (very dilute urine)
Central DI
Treatment
• Increase po or IV free H20 consumption,
use hypotonic saline
• Volume replacement cc for cc
• Vasopressin/ ADH administration (bolus or
drip 1.5-2.5 mU/kg/hr)
• Of course, treat underlying cause
Cerebral Salt Wasting
Causes:
• CNS damage
• Closed head injury
• CNS surgery
• CNS tumors
• CNS infections, meningitis
Cerebral Salt Wasting
• Signs/symptoms:
–Polyuria
–Wt loss
–Dehydration/hypovolemia
–Hypotension
–Low CVP
Cerebral Salt Wasting
• Lab values:
– Hyponatremia due to excessive renal Na loss
– High urine Na, > 20 mmol/L
– Increased plasma ANP, atrial natriuretic peptide,
b/c of low volume status
– Inappropriately normal or low aldosterone and
ADH levels despite high ANP
Cerebral Salt Wasting
• Treatment:
–Volume for volume replacement of
urine Na losses
–When dc’d from hospital, most will still
need oral Na supplementation for a
period of time
DI SIADH CSW
Urine
Output
polyuric decreased polyuric
Serum Na high low low
Urine Na low high high
Serum osm high low Can be low
or normal
Urine osm low high Can be low
or normal
CVP Can be
normal or
low
high low
GOOD LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com

Cerebral salt wasting and siadh

  • 1.
    SAMIR EL ANSARY ICUPROFESSOR AIN SHAMS CAIRO
  • 2.
    SIADH • Syndrome ofInappropriate ADH Secretion • Definition: levels of ADH are inappropriately elevated compared to body’s low osmolality, and ADH levels are not suppressed by further decreases in blood osmolality.
  • 3.
    SIADH Causes • Irritationof CNS meningitis, encephalitis, brain tumors, brain hemorrhage, hypoxic insult, trauma, brain abscess, Guillain Barre, hydrocephalus • Pulmonary disorders pneumonia, asthma, positive end expiratory pressure ventilation, CF, TB, pneumothorax
  • 4.
    SIADH causes • Drugs:vincristine, vinblastine, opiates, carbamazepime, cyclophosphamide • Unregulated tumor production of ADH-like peptides: oat cell lung carcinoma for example, Ewings sarcoma, carcinoma of duodenum, pancreas, thymus
  • 5.
    SIADH function ofADH • Antidiuretic hormone = vasopressin • ADH is made in the supra-optic nuclei in the hypothalamus, stored in the posterior pituitary • Normally released into the bloodstream when osmo-receptors detect high plasma osmolality
  • 6.
    SIADH function ofADH • At the kidney, attaches to receptors in the collecting ducts, opens up water channels • Water is passively reabsorbed along the kidney’s medullary concentration gradient
  • 7.
    SIADH signs and symptoms •Decreased / low urine output • Signs of hyponatremia: lethargy, apathy, disorientation, muscle cramps, anorexia, agitation • Signs of water toxicity: nausea, vomiting, personality changes, confused, combative • If Na < 110 mEq/L, seizures, bulbar palsies, hypothermia, stupor, coma
  • 8.
    SIADH lab values • SerumNa < 135 (Na is diluted by excessive free water re-absorption) • Serum osmolality low, normal is ~ 270 • Urine Na is inappropriately high, >20 mmol/L, actually losing Na in urine instead of retaining it
  • 9.
    SIADH lab values • Urineosmolality is inappropriately high, can range b/t 300-1400 mosm/L • CVP is high from free water retention
  • 10.
    SIADH Treatment • Fluid restriction,¾ maintenance • If symptomatic, may actually need to replace NaCl, can use hypertonic saline for example: 300cc/m2 of 1 ½ % NS • Diuretics such as lasix • Treat underlying disorder, for example usually resolves after removal of lung carcinomas
  • 11.
    SIADH treatment cont… • Demeclochlorotetracycline,blocks ADH receptors in the renal collecting ducts • In severe cases, hemodialysis • Warning, if increase Na too fast, at risk for pontine myelinolysis • Max correction of 15mEq in 24 hours
  • 12.
    DI = DiabetesInsipidus • Definition: inability to effectively conserve urinary water • Central: ADH not made or not released in the hypothalamic-pituitary axis • Nephrogenic: ADH is released but not detected by the receptors in the kidney collecting ducts, often a sex- linked recessive condition, also due to renal pathology, electrolyte disorders, drugs
  • 13.
    Central DI causes • Headtrauma • Brain neoplasms • Congenital CNS defects • CNS infections • CNS hypoxia • ADH secretion also decreased by certain drugs: EtOh, demerol, MSO4, dilantin, barbiturates, glucocorticoids
  • 14.
    DI • Make suredistinguish DI from conditions in which the presence of non-absorbable, osmotically active solutes in the renal tubules prevent water re- absorption. • Example: glucose loss in the urine of diabetics will decrease the tubule- medullary concentration gradient and even though ADH is there, water won’t get passively reabsorbed
  • 15.
    Central DI Signs/symptoms • Polyuria •Dehydration, may not be readily apparent b/c of hyper-osmolarity, fluid shifts from cells to intravascular spaces and maintains blood pressure, CVP • Weight loss is a better measure of fluid status
  • 16.
    Central DI Lab values •Hypernatremia, Na >150-160 • High serum osmolality (normal 270) • Urine Na < 20 mmol/L • Low urine osmolality (very dilute urine)
  • 17.
    Central DI Treatment • Increasepo or IV free H20 consumption, use hypotonic saline • Volume replacement cc for cc • Vasopressin/ ADH administration (bolus or drip 1.5-2.5 mU/kg/hr) • Of course, treat underlying cause
  • 18.
    Cerebral Salt Wasting Causes: •CNS damage • Closed head injury • CNS surgery • CNS tumors • CNS infections, meningitis
  • 19.
    Cerebral Salt Wasting •Signs/symptoms: –Polyuria –Wt loss –Dehydration/hypovolemia –Hypotension –Low CVP
  • 20.
    Cerebral Salt Wasting •Lab values: – Hyponatremia due to excessive renal Na loss – High urine Na, > 20 mmol/L – Increased plasma ANP, atrial natriuretic peptide, b/c of low volume status – Inappropriately normal or low aldosterone and ADH levels despite high ANP
  • 21.
    Cerebral Salt Wasting •Treatment: –Volume for volume replacement of urine Na losses –When dc’d from hospital, most will still need oral Na supplementation for a period of time
  • 22.
    DI SIADH CSW Urine Output polyuricdecreased polyuric Serum Na high low low Urine Na low high high Serum osm high low Can be low or normal Urine osm low high Can be low or normal CVP Can be normal or low high low
  • 23.
    GOOD LUCK SAMIR ELANSARY ICU PROFESSOR AIN SHAMS CAIRO [email protected]