SIADH, DI, Cerebral Salt Wasting

SIADH also known as

Syndrome of Inappropriate ADH Secretion

SIADH occurs when the

levels of ADH are inappropriately elevated

compared to body's low osmolality, and ADH levels are

not suppressed by further decreases in blood osmolality.

For whatever reason to much adh

Adh holds onto fluid

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

uDrugs: vincristine, vinblastine, opiates, carbamazepime, cyclophosphamide

uUnregulated tumor production of ADH-like peptides: oat cell lung carcinoma for example, Ewings sarcoma, carcinoma of duodenum, pancreas, thymus

antidiuretic hormone =

vasopressin

ADH is made in the

supra-optic nuclei in the

hypothalamus, stored in the posterior pituitary

ADH is normally released into the bloodstream when

osmo-receptors detect high plasma osmolality

adh at the kidneys attaches to

receptors in the

collecting ducts, opens up water channels

Water is passively

reabsorbed along the

kidney's medullary concentration gradient

siadh s/s

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

Can cause siadh by giving to much

vasopressin

SIADH: lab values

uSerum Na < 135 (Na is diluted by excessive free water re-absorption)

uSerum osmolality low, normal is ~ 270

uUrine Na is inappropriately high, >20 mmol/L, actually losing Na in urine instead of retaining it

uUrine osmolality is inappropriately high, can range b/t 300-1400 mosm/L

uCVP is high from free water retention

SIADH: treatment

uFluid restriction, ¾ maintenance

uIf symptomatic, may actually need to replace NaCl, can use hypertonic saline for example: 300cc/m2 of 1 ½ % NS or salt pills

uDiuretics such as lasix

uTreat underlying disorder, for example usually resolves after removal of lung carcinomas

uDemeclochlorotetracycline, blocks ADH receptors in the renal collecting ducts

uIn severe cases, hemodialysis

SIadh if pt has a feeding tube no

no water flush

things to remember abt soiudm replacemnt

cant do it quickly, can't do no more than 8 IN 24HRS, giving too much too quickly, causes demyelination syndrome- cant send signals form mylin sheath, effects rr, hr

DI is the

inability to effectively conserve urinary water,

pee liters

DI central

ADH not made or not released in the hypothalamic-pituitary axis

DI 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

uHead trauma

uBrain neoplasms

uCongenital CNS defects

uCNS infections

uCNS hypoxia

uADH 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.

uExample: 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

uPolyuria

uDehydration, may not be readily apparent b/c of hyper-osmolarity, fluid shifts from cells to intravascular spaces and maintains blood pressure, CVP

uWeight loss is a better measure of fluid status

uhypovolemic

Central DI: Lab values

uHypernatremia, Na >150-160

uHigh serum osmolality (normal 270)

uUrine Na < 20 mmol/L

uLow urine osmolality (very dilute urine)

Central DI: treatment

uIncrease po or IV free H20 consumption, use hypotonic saline, whatever they put out in an hour we put in in an hour

uVolume replacement cc for cc

uVasopressin/ ADH administration (bolus or drip 1.5-2.5 mU/kg/hr) (desmopressin, sub q)

uOf course, treat underlying cause

Cerebral Salt Wasting

For some reason your body can no longer hold onto sodium, Na helps to control water fluid levels, if ur putting out sodium it is take the water with it

Cerebral Salt Wasting causes

uCNS damage

uClosed head injury

uCNS surgery

uCNS tumors

uCNS infections, meningitis

Cerebral Salt Wasting S/S

uPolyuria

uWt loss

uDehydration/hypovolemia

uHypotension

uLow CVP

Cerebral Salt Wasting lsab value

uHyponatremia due to excessive renal Na loss

uHigh urine Na, > 20 mmol/L

uIncreased plasma ANP, atrial natriuretic peptide, b/c of low volume status

uInappropriately normal or low aldosterone and ADH levels despite high ANP

Cerebral Salt Wasting treatment

uVolume for volume replacement of urine Na losses

uWhen dc'd from hospital, most will still need oral Na supplementation for a period of time

look at table