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