SIADH, DI, Cerebral Salt Wasting

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 continued

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

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

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 s/s

Polyuria

Wt loss

Dehydration/hypovolemia

Hypotension

Low CVP

Cerebral Salt Wasting labs

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

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