Excess vasopressin secretion and action - Hyponatremia
1. ÀÓ»óƯ¡
AVPÀÇ °úµµÇÑ ºÐºñ ȤÀº ÀÛ¿ëÀ¸·Î ÀÎÇÏ¿© ¼Òº¯·®ÀÌ °¨¼ÒÇÏ¸ç ¼Òº¯³óµµ°¡ ³óÃàµÈ´Ù.
fluid intake¸¦ °¨¼Ò½ÃŰÁö ¾ÊÀ¸¸é plasma osmolality/sodiumÀÌ °¨¼ÒÇÑ´Ù.
hyponatremia°¡ Á¡Â÷ ÁøÇàÇϰųª ¼öÀÏÀÌ»ó Áö¼ÓÇÏ¸é ¹«Áõ»óÀϼö ÀÖ´Ù. ±×·¯³ª
hyponatremia°¡ ±Þ°ÝÈ÷ ¹ß»ýÇϸé water intoxication symptom & signÀÌ ³ªÅ¸³ª´Âµ¥
mild headache, confusion, anorexia, nausea, vomiting, coma and convulsionÀÌ »ý±æ¼ö
ÀÖÀ¸¸ç severe hyponatremia´Â Ä¡¸íÀûÀϼö ÀÖ´Ù.
2. ¿øÀÎ Tab 329-3
1) primary defect in AVP secretion or action
= SIADH or euvolemic(type III) hyponatremia
i) AVP ectopic production(lung cancer or other neoplasms)
unregulated expression of the AVP-NP II gene¿¡ ÀÇÇØ »ý±è
ii) eutopic release by various disease or drug
-> osmoregulation disruption
: acute infections or strokes
chlorpropamide, carbamazepine, nicotine, phenothiazine, cyclophosphamide, TCA
MAO inhibitor, SSRI
iii) exogenous administrations of AVP, DDAVP, large dose of oxytocin
protracted nausea or isolated glucocorticoid deficiency¿¡ ÀÇÇÑ AVP secretionÀ¸·Î
¹ß»ýÇÑ acute or chronic hyponatremia´Â SIADH¿Í ¾ÆÁÖ À¯»çÇÏ´Ù.
2) secondary forms
type I(hypervolemic) hyponatremia
: sodium-retaining, edema-forming state(CHF, cirrhosis, or nephrosis)
effective blood volume°¨¼Ò·Î ÀÎÇÔ
type II(hypovolemic) hyponatremia
: sodium-depleted state
¿¹> severe gastroenteritis, diuretic abuse, or mineralocorticoid deficiency
blood volume and/or pressure°¨¼Ò·Î ÀÎÇÔ
3. º´Å»ý¸®
SIADH -> ADHÀÇ osmotic suppressionÀÌ ¾ÈµÊ
-> body fluidÀÇ significant expansion & dilution
SIADH¿¡¼ osmoregulation defect¿¡´Â 4°¡Áö ÇüŰ¡ ÀÖ´Ù(Fig 329-6 a-d)
i) plasma osmolality/sodium¿¡ ¿ÏÀüÈ÷ ¹ÝÀÀÇϳª osmoregulatory systemÀÇ threshold or
set point°¡ ºñÁ¤»óÀûÀ¸·Î ³·´Ù.
ii) ºÐ¸íÇÑ osmoregulation defect°¡ ÀÖÁö´Â ¾Ê´Ù.
ÀÌ·± ȯÀÚµéÀº low levels of AVPÀÇ antidiuretic effect¿¡ ´ëÇÑ renal sensitivity
Áõ°¡¿Í °°Àº ÀÌ»ó ȤÀº AVP, V2 receptor¿Í ¹«°üÇÑ ±âÀüÀ¸·Î aquaporin 2 water
channelÀÇ activation¿¡ ÀÇÇØ ¹ß»ýÇÑ´Ù.
SIADH¿¡¼ extracellular volume expansion -> ANP¡è, plasma renin activity¡é
compensatory urine sodium excretion¡è
-> hypervolemia°¨¼Ò, hyponatremia¿ÏÈ
hyponatremia: total-body waterÁõ°¡ »Ó¸¸ ¾Æ´Ï¶ó total-body sodium°¨¼Ò ¶§¹®¿¡ ¹ß»ý
acute water retention & plasma sodiumÀÌ °¨¼ÒµÇ¸é intracellular volumeÀÌ Áõ°¡ÇÏ¿©
brain swellingÀÌ »ý±â´Â µîÀÇ acute water intoxication sxÀÌ »ý±ä´Ù.
4. °¨º°Áø´Ü
water intoxication sx or signs°ú hyponatremia°¡ ÀÖÀ» ¶§ history, P/E, routine
chemistry¸¦ ÅëÇÏ¿© extracellular fluid volumeÀ» Æò°¡ÇÔÀ¸·Î½á hyponatremiaÀÇ Á¾·ù¸¦
°áÁ¤ÇÒ¼ö ÀÖ´Ù. À̰ÍÀÌ ¸ðÈ£ÇÏ´Ù¸é urinary sodium excretion or plasma renin activity°¡
µµ¿òÀÌ µÉ ¼ö ÀÖ´Ù. ±×·¯³ª À̰ÍÀº ȯÀÚ°¡ type II(hypovolemic) hyponatremia°¡ Àְųª
SIADH°¡ ¾ÈÁ¤»óÅ ȤÀº ȸº¹»óÅÂÀ϶§´Â À߸ø ÇØ¼®ÇÒ¼ö ÀÖ´Ù.
ÇöÀç plasma AVPÀÇ ÃøÁ¤Àº Áø´ÜÀû °¡Ä¡°¡ ¾ø´Ù.
SIADHÀÇ clinical criteria¸¦ ¸¸Á·Çϴ ȯÀÚ´Â plasma cortisolÀ» ¶ÇÇÑ ÃøÁ¤ÇÏ¿© ¿¹»óÄ¡
¸øÇß´ø secondary adrenal insufficiency¸¦ ¹èÁ¦ÇØ¾ß ÇÑ´Ù. adrenal functionÀÌ Á¤»óÀ̰í
SIADH¸¦ ÀÏÀ¸Å³¸¸ÇÑ ¶Ñ·ÇÇÑ ¿øÀÎÀÌ ¾ø´Ù¸é occult lung cancer¿¡ ´ëÇÑ Á¶»ç¸¦ ÇØ¾ß
ÇÑ´Ù.
5. Ä¡·á
1) total fluid intake restriction - the keystone to treatment of hyponatremia
insensible loss + urine outputº¸´Ù Àû°Ô intake Á¦ÇÑ
¼ºÀο¡¼ insensible loss°¡ 500 mL/dÁ¤µµ µÇ¹Ç·Î ¼·ÃëÇÏ´Â ¹°ÀÇ ¾çÀº
Àû¾îµµ 500 mL/d´Â ¼·ÃëÇØ¾ß ÇÑ´Ù. (urinary outputº¸´Ù´Â Àû°Ô)
2) hypertonic(3%) saline infusion
severe hyponatremia sx & signÀ» ¾ø¾Ö±â À§ÇØ hyponatremia¸¦ ºü¸£°Ô ±³Á¤Çؾß
ÇÒ Çʿ䰡 ÀÖÀ» ¶§ hypertonic salineÀ» IV infusionÇÑ´Ù. ±×·¯³ª 24-48½Ã°£ ÀÌ»ó
Áö¼ÓµÈ hyponatremia¸¦ ³Ê¹« ºü¸£°Ô ±³Á¤Çϸé central pontine myelinolysis¸¦ ÀÏÀ¸Å³¼ö
ÀÖ´Ù. ÀÌ·¯ÇÑ À§ÇèÀ» ÃÖ¼ÒÈÇϱâ À§ÇÏ¿© guidelinesÀÌ Á¦½ÃµÇ´Âµ¥
i) infusion rate ¡Â0.05 mL/kg/min (<40Gtt)
ii) serum Na+ monitoring
iii) serum Na+°¡ ÇÏ·ç 12 mmol/LÁõ°¡Çϰųª 130 mmol/L°¡ µÇ¸é ÁßÁö
3) demeclocylcine 150-300 mg tid or qid
È¿°ú´Â 7-14ÀÏ¿¡ ³ªÅ¸³ª¸ç nephrogenic DIÀÇ reversible formÀ» ¸¸µêÀ¸·Î½á
È¿°ú¸¦ ³ªÅ¸³½´Ù.
potential S/E : phototoxicity & azotemia
4) fludrocortisone 0.05 - 0.2 mg bid
1-2ÁÖ¿¡ È¿°ú°¡ ³ªÅ¸³ª°í ºÎºÐÀûÀ¸·Î´Â sodium retentionÀÇ Áõ°¡¿Í
thirst inhibitionÀÇ ÀÛ¿ëÀ¸·Î È¿°ú¸¦ ³ªÅ¸³½´Ù.
5) type I hyponatremia(CHF, cirrhosis, nephrosis) treatment
ÇöÀçÀÇ Ä¡·á´Â severe fluid restriction, urea or mannitolÅõ¿©·Î solute diuresisÀ¯¹ß,
effective hypovolemia¸¦ ±³Á¤Çϱâ À§ÇØ cardiotonics or serum albuminÀÇ Åõ¿©
µîÀÌ´Ù. À̵éÁß ¾î´À°Íµµ ƯÈ÷ È¿°úÀûÀÎ °ÍÀº ¾øÀ¸¸ç ÀϺÎ(mannitolÅõ¿© µî)´Â »ó´çÇÑ
À§ÇèÀÌ ÀÖ´Ù. hypertonic salineÀÇ Åõ¿©´Â sodium retention, edema¸¦ ¾ÇȽÃ۰í
cardiovascular decompensationÀ» Ã˹߽ÃŰ¹Ç·Î ±Ý±âÀÌ´Ù.
±×·¯³ª ¿¬±¸¿¡¼ AVP antagonist´Â type I hyponatremia¿¡¼ ¾ÈÀüÇϰí È¿°úÀ̶ó ÇÏ¿´
´Ù. ±×·¯¹Ç·Î AVP antagonist°¡ type I hyponatremiaÀÇ TOC°¡ µÉ ¼ö ÀÖÀ» °ÍÀÌ´Ù.
6) type II hyponatremia treatment
AVP secretion & water balance defect´Â ½±°Ô ±³Á¤ÇÒ¼ö ÀÖ°í sodium & water loss¸¦
Áß´ÜÇÏ°í °æ±¸ ȤÀº Á¤¸ÆÀ¸·Î normal or hypertonic salineÀ¸·Î ¼Õ½ÇºÐÀ» °ø±ÞÇÔÀ¸·Î½á
½±°Ô ±³Á¤ÇÒ¼ö ÀÖ´Ù.
fluid restriction or AVP antagonist´Â underlying volume depletionÀ» ¾ÇȽÃ۰í
cardiovascular decompensationÀ» ÀÏÀ¸Å³¼ö ÀÖÀ¸¹Ç·Î ±Ý±âÀÌ´Ù.