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SIADH, DI, Cerebral Salt


By Tracy Merrill MD
Feb 24, 2003
Otak disuplai darah bersih oleh arteri utama. Ada 4 arteri
utama yang mensuplai darah ke otak al;
1. Right Common carotid arteri
2. Left common carotid artery
3. Right vertebral artery
4. Left vertebral artery
Dua cabang utama common carotid mensuplai kedaerah
otak bagian depan/anterior.
Dua vertebral arteri mensuplai ke daerah
Dalam pemeriksaan Radiography Neck vessel dan seluruh
peredaran darah otak dikenal dengan four vessel
angiogram sebab vessel tersebut secara bersamaan
dilakukan dengan memberikan suntikan kontras media.

Aorta adalah arteri utama yang darah

mengandung O2 dipompa oleh ventrikel kiri.
Dari Arcus aorta ada 3 cabang utama arteri:
1. Brachiocephalic artery
2. Left common carotid artery
3. Left subclavian artery
Pembuluh brachiocephalic pendek dan
bercabang dua yang terdiri dari
1. Right common carotid artery
2. Right subclavian artery
Right common carotid arteri naik ke atas setentang
dengan vertebrae cervicalis IV dan bercabang
menjadi pecabangan yaitu:
1.external carotid arteri
2.Internal carotid arteri
Bagian external mensuplai ke bagian depan leher,
bagian wajah,bagian kulit kepala dan meninges.
Bagian Internal carotid arteri mensuplai ke cerebral
hemispheres, pituitary gland, bagian orbita, hidung
bagian luar dan otak bagian depan.
Right vertebral arteri dibentuk dari arteri subclavian
kanan melalui foramen tranverse C6 menembus C1.
Cammon carotid arteriogram bagian kanan terdiri dari :
1. Right Internal Carotid
2. Right Extrenal Carotid
3. Right Common Carotid
External Carotid Arteri
Cabang External Carotid Arteri

Ada 4 Cabang dari Arteri Carotid External :

1. Facial artery/Wajah
2. Maxillary Artery
3. Superficial Temporal Artery
4. Occipital Artery
Vertebrobasilar Arteri

Kedua Vertebral arteri menuju kepala melalui Foramen Magnum dan

menjadi satu yang disebut BASILAR ATERI.

Merupakan penyatuan 5 buah arteri atau cabang yang dibentuk dari
Internal carotida dan Vertebral arteri.
Kelima (5) Cabang tersebut adalah :
1. Anterior Communicating artery
2. Anterior cerebral arteri
3. Cabang dari Internal Carotid Arteri
4. Posterior Communicating Artery
5. Posterior Cerebral Artery

= Syndrome of Inappropriate ADH

Definition: levels of ADH are
inappropriately elevated compared to
bodys 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 kidneys
medullary concentration gradient
SIADH: signs and symptoms

Decreased/low urine output

Signs of hyponatremia: lethargy, apathy,
disorientation, muscle cramps, anorexia,
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, maintenance

If symptomatic, may actually need to
replace NaCl, can use hypertonic saline for
example: 300cc/m2 of 1 % NS
Diuretics such as lasix
Treat underlying disorder, for example
usually resolves after removal of lung
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

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 wont get passively reabsorbed
Central DI: signs/symptoms

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
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

Wt loss
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

Volume for volume replacement of urine Na
When dcd from hospital, most will still need
oral Na supplementation for a period of time
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 high low
normal or