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

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Presentation on theme: "Disturbances of Sodium in Critically Ill Adult Neurologic Patients R3 R3."— Presentation transcript:

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

2 Normal Physiology of Salt and Water 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 excretion –reabsorption : predominantly at proximal convoluted tubule

3 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

4 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

5 Changes in sodium and water balance 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

6 Dysnatremia

7 Hyponatremia epidemiology – defined as serum sodium <135mmol/L – 1~15% of hospital inpatients – 7~60% mortality increase – more common in neurologic patients : SAH, TBI, basilar meningitis causes – SIADH, CSWS, iatrogenic hyponatremia

8 Syndrome of Inappropriate Antidiuretic Hormone Secretion urinary sodium loss without corresponding loss of water fluid restriction : Tx lower threshold for thirst, loss of control of ADH release classified into 4 category – 1) neoplasia – 2) non-malignant lung disease – 3) drugs : antiepileptics – 4) neurologic disease : meningitis, SAH, TBI, tumor

9 Cerebral Salt Wasting Syndrome polyuria and natriuresis defined as renal loss of sodium d/t intracranial disease, leading to hyponatremia and hypovolemia inc. level od ANP, BNP mainly associated SAH

10 Investigation of Hyponatremic Neurologic Patient investigation to underlyng cause before management speed of onset : more important hypervolemia with normal total body sodium(SIADH) vs hypovolemia with low total body sodium(CSWS)

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

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

13 Treatment of Hyponatremia supportive management : asymptomatic patient gradual correction : target to Sx. rather than biochemically normality

14 Specific 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

15 Specific Treatment of CSWS fluid and sodium resuscitation : 0.9% solution used at first 3% as acute symptomatic pt. prophylactic fludrocortisone 0.1~0.4mg/da

16 Neurologic Complications of treatment of Hyponatremia rapid correction : dangerous myelinolysis : –pontine and extrapontine disorder –acute elevation of sodium –alcoholism, malnutrition, liver disease-risk factors –mutism, dysarthria, lethargy, spastic quadriparesis and pseudobulbar palsy –gradual correction <10mmol/L/24h

17 Hypernatremia serum sodium >145mmol/L 1% of all hospital patients in ICU, 9% of Patient water depletion and >15mmol/L

18 Central 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

19 Investigation of the Hypernatremic Neurologic Patient should be distinguished from simple dehydration by urine assessment, biochemical analysis thirst is often unreliable sign high serum osmolality(>305mmol/kg), serum sodium(>145mmol/L) with low urine osmolality(<350mmol/kg) urine SG : when urgent treatment is required(<1.005)

20 Management 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

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