Disturbances of Sodium in Critically Ill Adult Neurologic Patients R3 R3.

Disturbances of Sodium in CriDisturbances of Sodium in Critically Ill Adult Neurologic Patitically Ill Adult Neurologic Pati

entsents

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Normal Physiology of Salt and Normal Physiology of Salt and Water RegulationWater Regulation

• Sodium– major extracellular cation in the body– most important osmotically active solutes– maintained by Na-K ATPase pump– total body sodium : controlled by renal excretio

n– reabsorption : predominantly at proximal convo

luted tubule

• affected by – 1) sympathetic innervation– 2) atrial natriuretic peptide(ANP)– 3) brain natriuretic peptide(BNP)– cause natriuresis via direct effect on the inner

medullary collecting duct, inhibiting renin and aldosterone

• Total body water– controlled by renal manipulation of body sodium

• water balance monitoring by– 1) osmoreceptors in the hypothalamus – 2) low pressure baroreceptors in Rt atrium – 3) high pressure in the carotid sinus

• water balance controlling by – 1) antidiuretic hormone(ADH) – 2) thirst

• ADH : increase of ECF tonicity, hypovolemia

Changes in sodium and water Changes in sodium and water balancebalance

• in acute hyperosmolar states : loss of intracellular water with cell shrinkage with gradual restoration of brain volume via the generation of nonelectrolyte osmotically active intracellular solute

• in hypoosmolar state : cellular expansion, corrected by loss of intracellular solute

DysnatremiaDysnatremia

HyponatremiaHyponatremia

• epidemiology– defined as serum sodium

<135mmol/L– 1~15% of hospital inpatien

ts– 7~60% mortality increase– more common in neurologi

c patients : SAH, TBI, basilar meningitis

• causes– SIADH, CSWS, iatrogenic h

yponatremia

Syndrome of Inappropriate AntidiureSyndrome of Inappropriate Antidiuretic Hormone Secretiontic Hormone Secretion

• urinary sodium loss without corresponding loss of water

• fluid restriction : Tx• lower threshold for thirst, loss of control of ADH r

elease• classified into 4 category

– 1) neoplasia– 2) non-malignant lung disease– 3) drugs : antiepileptics– 4) neurologic disease : meningitis, SAH, TBI, tumor

Cerebral Salt Wasting Cerebral Salt Wasting SyndromeSyndrome

• polyuria and natriuresis• defined as renal loss of sodium d/t intracr

anial disease, leading to hyponatremia and hypovolemia

• inc. level od ANP, BNP• mainly associated SAH

Investigation of Hyponatremic NeuroInvestigation of Hyponatremic Neurologic Patientlogic Patient

• investigation to underlyng cause before management

• speed of onset : more important• hypervolemia with normal total body sodiu

m(SIADH) vs hypovolemia with low total body sodium(CSWS)

• in SIADH– high free water absorption– low fractional water and sodium excretion– low or normal urine output– inc. ADH

• in CSWS– normal free water absorption– inc. fractional water and sodium excretion– high urine output– inc. ADH– volume depletion in CSWS : key difference

Treatment of HyponatremiaTreatment of Hyponatremia

• supportive management : asymptomatic patient

• gradual correction : target to Sx. rather than biochemically normality

Specific treatment of SIADHSpecific treatment of SIADH

• fluid restriction to 1L/day-> slow inc. of sodium 1.5mmol/L/day• furosemide• lithium :

– beneficial in pt. with SIADH after brain trauma– blocker of 3,5-adenosine monophosphatase – inhibits the action of ADH on the renal tubule- maintain plasma con as 1mmol/L

• demeclocycline : ADH antagonist, less toxic but taks long time

Specific Treatment of CSWSSpecific Treatment of CSWS

• fluid and sodium resuscitation : 0.9% solution used at first

• 3% as acute symptomatic pt.• prophylactic fludrocortisone 0.1~0.4mg/d

a

Neurologic Complications of treatmNeurologic Complications of treatment of Hyponatremiaent of Hyponatremia

• rapid correction : dangerous• myelinolysis :

– pontine and extrapontine disorder– acute elevation of sodium– alcoholism, malnutrition, liver disease-risk fact

ors– mutism, dysarthria, lethargy, spastic quadripar

esis and pseudobulbar palsy– gradual correction <10mmol/L/24h

HypernatremiaHypernatremia

• serum sodium >145mmol/L

• 1% of all hospital patients

• in ICU, 9% of Patient water depletion and >15mmol/L

Central Diabetic InsipidusCentral Diabetic Insipidus

• failure of homeostatic release od ADH from the hypothalamopituitary axis

• associated with pituitary surgery, TBI, Ant. comm. a aneurysmal SAH

• ADH : released from fiber ending in the median eminence

• 3.7% of neurosurgical unit : 1/3 SAH, 1/3 TBI, 1/6 pituitary surgery, 1/6 ICH

Investigation of the Hypernatremic Investigation of the Hypernatremic Neurologic PatientNeurologic Patient

• should be distinguished from simple dehydration by urine assessment, biochemical analysis

• thirst is often unreliable sign• high serum osmolality(>305mmol/kg), ser

um sodium(>145mmol/L) with low urine osmolality(<350mmol/kg)

• urine SG : when urgent treatment is required(<1.005)

Management of hypernatremiaManagement of hypernatremia

• invariably water replacement and retention

• vasopressin : 0.4ug iv or 100~200ug intranasally

• overrapid correction : can cause cerebral, pulmonary edema-10mmol/L/day