Major complications of cirrhosis
i) portal hypertension & its consequences(¿¹, GE varices & splenomegaly)
ii) ascites
iii) hepatic encephalopathy
iv) SBP
v) hepatorenal syndrome
vi) hepatocellular carcinoma
I. Portal hypertension
1. Á¤ÀÇ ¹× º´ÀÎ
* Á¤»ó portal vein pressure: 5-10 mmHg
* portal hypertension: >10 mmHg, portal blood flow¿¡¼ resistance°¡ Áõ°¡Çϱ⠶§¹®¿¡
»ý±ä´Ù.
portal veinÀº valve°¡ ¾ø±â ¶§¹®¿¡ heartÀÇ right side¿¡¼ºÎÅÍ splanchnic vessel »çÀÌÀÇ
¾îµð¿¡¼µç ÀúÇ×ÀÌ »ý±â¸é retrograde transmissionµÇ¾î ¾Ð·ÂÀÌ ¿Ã¶ó°¡°Ô µÈ´Ù. hepatic
sinusoids¸¦ ±âÁØÀ¸·Î ¼¼ level¿¡¼ ÀúÇ×ÀÇ Áõ°¡°¡ »ý±æ¼ö ÀÖ´Ù: presinusoidal, sinusoidal,
postsinusoidal
¨ç presinusoidal venous compartment obstructionÀº ÇØºÎÇÐÀûÀ¸·Î °£ ¹Û¿¡ Àְųª(¿¹,
PVT), °£³»¿¡ ÀÖ´õ¶óµµ ´ë°³ hepatic sinusoid proximal level¿¡ ÀÖ°Ô µÇ¾î °£½ÇÁúÀº
venous pressure Áõ°¡ÀÇ ¿µÇâÀ» ¹ÞÁö ¾Ê´Â´Ù(¿¹, schistosomiasis).
¨è postsinusoidal obstruction ¶ÇÇÑ °£¹ÛÀÇ hepatic vein level(¿¹, Budd-Chiari syndrome),
IVC ȤÀº ´ú ÈçÇϰԴ °£³»ºÎ(¿¹, VOD)¿¡¼ »ý±æ¼ö ÀÖ´Ù.
¨é cirrhosis°¡ portal hypertension¿¡ ÀÇÇØ »ý±æ ¶§ Áõ°¡µÈ ÀúÇ×Àº ÈçÈ÷ sinusoidal levelÀÌ´Ù.
pre-, post-, & sinusoidal process»çÀÌÀÇ ±¸ºÐÀº °³³äÀûÀÎ ±¸ºÐÀ̸ç, portal flow¿¡ ´ëÇÑ
±â´ÉÀû ÀúÇ×Àº ÇÑ level À̻󿡼 »ý±ä´Ù.
portal hypertensionÀÌ blood flowÁõ°¡(¿¹, massive splenomegaly or A-V fistula)·Î ÀÎÇØ¼
µµ »ý±æ¼ö ÀÖÁö¸¸ Á¤»ó °£¿¡¼ low outflow resistance°¡ ÀÓ»óÀû ¹®Á¦¸¦ ¾ß±âÇÏ´Â °æ¿ì´Â
µå¹°´Ù. cirrhosis´Â ¹Ì±¹¿¡¼ portal hypertensionÀÇ °¡Àå ÈçÇÑ ¿øÀÎÀÌ´Ù.
ÀÓ»óÀûÀ¸·Î ÀǹÌÀÖ´Â portal hypertensionÀº cirrhosisȯÀÚÀÇ 60%¿¡¼ ¹ß»ýÇÑ´Ù. portal vein
obstructionÀº 2¹øÂ°·Î ÈçÇÑ ¿øÀÎÀ̸ç idiopathic ȤÀº cirrhosis, infection, pancreatitis or
abdominal trauma¿Í °ü·ÃÇÏ¿© ¹ß»ýÇÑ´Ù.
* PVTÀÇ ¿øÀÎ: PVT´Â ´Ù¾çÇÑ hypercoagulable state¿¡¼µµ »ý±æ¼ö ÀÖ´Ù.
PV, ET, protein C, S deficiency, AT III deficiency, resistance to activated protein C
(factor V Leiden)¿¡ pathogenic gene mutation.
ºñ·Ï ȯÀÚµéÀÇ ÀϺΰ¡ subclinical myeloproliferative disorder¸¦ °¡Áö°í ÀÖÁö¸¸ Ư¹ß¼ºÀ¸·Î
»ý±æ¼ö ÀÖ´Ù.
hepatic vein thrombosis(Budd-Chiari syndrome) & hepatic VOD´Â ´Ù¼Ò µå¹® ¿øÀÎÀÌ´Ù.
portal vein occlusionÀº GE varix·Î ÀÎÇÏ¿© massive hematemesis¸¦ ¾ß±âÇÏÁö¸¸ ascites
´Â cirrhosis°¡ ÀÖÀ»¶§¸¸ »ý±ä´Ù. noncirrhotic portal fibrosis(Tab 299-2)´Â portal
hypertensionÀÇ µå¹® °æ¿ìÀÌ´Ù.
2. ÀÓ»óƯ¡
GE varix bleeding, splenomegaly with hypersplenism, ascites & acute & chronic hepatic
encephalopathy
portal-systemic collateral channelsÇü¼º°ú °ü·ÃÀÖ´Ù.
abdominal wall collaterals(caput medusae)
low-normal platelet count°¡ cirrhosisÁøÇàÀÇ Ã¹ ´Ü¼°¡ µÉ ¼ö ÀÖ´Ù. °á±¹ Ç÷¼ÒÆÇ ¹× ¹éÇ÷±¸ÀÇ
½ÉÇÑ °¨¼Ò(3¸¸-6¸¸)°¡ »ý±ä´Ù.
3. Áø´Ü
portal hypertensionÀÌ Àִ ȯÀÚ¿¡¼ splenomegaly, ascites, encephalopathy and/or
esophageal
varices°¡ Á¸ÀçÇÑ´Ù. ¹Ù²Ù¾î¸»Çϸé, ÀÌ·¯ÇÑ ¼Ò°ßÀÌ ÀÖÀ¸¸é Áï½Ã underlying portal
hypertension & liver diseaseÀÇ Á¸ÀçÀ¯¹«¸¦ Á¶»çÇØ¾ß ÇÑ´Ù.
ÇÊ¿äÇÑ °æ¿ì´Â µå¹°Áö¸¸, portal venous pressure´Â percutaneous transhepatic "skinny
needle" catheterizationÀ¸·Î Á÷Á¢ ÃøÁ¤Çϰųª transjugular cannulation of the hepatic vein
À¸·Î °£Á¢ÀûÀ¸·Î ÃøÁ¤ÇÒ¼öµµ ÀÖ´Ù. free & wedged hepatic vein pressure µÑ´Ù ÃøÁ¤Çؾß
ÇÑ´Ù.
ÈÄÀÚ(wedged hepatic vein pressure, WHVP)´Â sinusoidal & postsinusoidal portal
hypertension (cirrhosisÆ÷ÇÔ)¿¡¼ Áõ°¡µÇ¾î ÀÖÁö¸¸ presinusoidal portal hypertension¿¡¼
´Â ÈçÈ÷ Á¤»óÀÌ´Ù.
ºÎ°¡ÀûÀÎ Á¤º¸°¡ ÇÊ¿äÇÑ È¯ÀÚ(¿¹, portal-systemic shunt surgeryÀü) ȤÀº percutaneous
cathÀ̺Ұ¡´ÉÇÒ¶§´Â mesenteric & hepatic angiography°¡ µµ¿òÀÌ µÈ´Ù.
4. Ä¡·á
¨ç specific complicationÄ¡·á
¨è portal pressure°¨¼Ò
i) portal-systemic shunt surgery: »ýÁ¸·ü Çâ»óÀº ¾ø´Ù.
ii) TIPS
iii) ¥â-blocker(propranolol or nadolol) : resting pulse¸¦ 25% °¨¼Ò½ÃŰ´Â °ÍÀ» ±âÁØÀ¸·Î
¿ë·®Á¶Àý
¨é alcoholic hepatitis & cirrhosis, CAH, orther liver diseaseÀÇ Àû±ØÀû Ä¡·á
-> portal pressure¸¦ °¨¼Ò½Ã۰í variceal size¸¦ °¨¼Ò½ÃŰÁö¸¸ ÈçÈ÷ ºñ°¡¿ªÀûÀÌ´Ù.
¨ê hepatic transplantation
II. Variceal bleeding
1. º´ÀÎ
portal-systemic venous collaterals¿¡¼ ¹ß»ýÇÑ´Ù.
GE junction¿¡ À§Ä¡ÇÑ varix¿¡¼ °¡Àå ÈçÇÏ´Ù.
bleedingÀ» ÀÏÀ¸Å°´Â ÀÎÀÚ¿¡ ´ëÇØ ¿ÏÀüÈ÷ ¾ËÁö´Â ¸øÇÏÁö¸¸ portal hypertension(>12 mmHg)
¿Í varix size Á¤µµ¿Í °ü·ÃÀÖ´Ù.
2. ÀÓ»óƯ¡ ¹× Áø´Ü
ƯÁ¤À¯¹ß¿øÀξøÀÌ ÀÚÁÖ ¹ß»ýÇϸç ÈçÈ÷ ÅëÁõ¾øÀÌ massive hematemesisÇÑ´Ù.
µ¿¹ÝµÇ´Â signsÀ¸·Î´Â blood lossÁ¤µµ¿¡ µû¶ó mild postural tachycardiaºÎÅÍ profound
shock±îÁö ´Ù¾çÇÏ´Ù.
varixȯÀÚ´Â ´Ù¸¥ GI lesion(¿¹: peptic ulcer, gastritis)¿¡ ÀÇÇØ¼µµ ÀÚÁÖ ÃâÇ÷Çϱ⠶§¹®¿¡
ÀÌÀü¿¡ variceal bleedingÀÌ ÀÖ¾ú´ø ȯÀÚ¿¡¼µµ ´Ù¸¥ ÃâÇ÷¿øÀÎÀ» ¹èÁ¦ÇÏ´Â °ÍÀÌ Áß¿äÇÏ´Ù.
3. Ä¡·á(Fig 299-1)
¨ç ÀÀ±Þóġ
Ç÷¾×¼Ò½Ç¿¡ ´ëÇØ vigorous replacement¸¦ ÅëÇÑ intravascular volume À¯Áö°¡ Ä¡·á¿¡
ÇʼöÀûÀ̸ç Áø´ÜÀû °Ë»ç ¹× ÁöÇ÷½Ã۱âÀ§ÇÑ Ã³Ä¡º¸´Ù ¸ÕÀú ½ÃÇàÇÑ´Ù.
±×·¯³ª °ú´ÙÇÑ ¼ö¾×ÁÖÀÔÀº portal pressure¸¦ Áõ°¡½ÃÄÑ ÃâÇ÷À» ´õ¿í Á¶ÀåÇÒ¼ö ÀÖÀ¸¹Ç·Î
ÇÇÇØ¾ß ÇÑ´Ù. coagulopathy°¡ Àִ ȯÀÚ´Â clotting factor(FFP)ÀÇ ¼öÇ÷ÀÌ Áß¿äÇÏ´Ù.
ȯÀÚ°¡ hemodynamically stableÇØÁö¸é specific diagnostic study(endoscopy) ¹× recurrent
bleedingÀ» ¸·±âÀ§ÇÑ ´Ù¸¥ Ä¡·á¸¦ ½ÃÇàÇÑ´Ù.
variceal hemorrhageÀÇ ¹ÝÀº óġ¾øÀÌ ÀúÀý·Î ¸Ü´Â´Ù. ºñ·Ï ÀçÃâÇ÷ À§ÇèÀÌ ¾ÆÁÖ ³ôÁö¸¸..
¨è medical management: vasoconstrictors(somatostatin/octreotide or vasopressin)
i) vasopressin 0.1-0.4 U/mL : generalized vasoconstrictionÀ¸·Î portal venous blood flow
¸¦ °¨¼Ò½ÃÅ´. 80%¿¡¼ bleeding control½ÃŰÁö¸¸ ¾àÀ» ÁÙÀ̰ųª Áß´ÜÈÄ¿¡´Â ¹ÝÀ̻󿡼
´Ù½Ã ÀçÃâÇ÷Çϰí, ½ÉÇÑ ºÎÀÛ¿ë(cardiac, GI ischemia, ARF, hyponatremia)ÀÌ »ý±ä´Ù.
vasodilator(NTG)ÀÇ µ¿½Ã»ç¿ëÀ¸·Î vasopressinÀÇ È¿°ú¸¦ ³ôÀÌ°í ºÎÀÛ¿ëÀ» °¨¼Ò½Ãų¼ö
ÀÖ´Ù.
ii) somatostatin(its analogue octreotide): direct splanchnic vasoconstrictors
somatostatin: 250 ug bolus + 250 ug/h constant infusion
octreotide: 50-100 ug/h
¨é balloon tamponade: ÃâÇ÷ÀÌ ³Ê¹« ½ÉÇϰųª ³»½Ã°æÀ» ÇÒ¼ö ¾øÀ» ¶§ ½ÃµµÇÒ¼ö ÀÖ´Ù.
triple lumen(Sengstaken-Blackmore) or four-lumen(Minesota)
aspiration À§ÇèÀÌ ³ô±â ¶§¹®¿¡ tube¸¦ ³Ö±âÀü endotracheal intubationÀ» ½ÃÇàÇØ¾ß ÇÑ´Ù.
¨ê endoscopic intervention: acute bleeding controlÀÇ 1st line tx
i) sclerotherapy: 90%¿¡¼ bleeding control
¸ðµç varix°¡ obliterationµÉ¶§±îÁö repeated sclerotherapy¸¦ ½ÃÇàÇÒ¼ö ÀÖ´Ù.
±×·¯³ª »ýÁ¸·ü Çâ»óÀº ¾ø´Ù.
causative sclerosantÁÖÀÔÀ¸·Î ÀÎÇØ mucosal ulcerationÀÌ »ý±æ¼ö ÀÖÀ¸¸ç ÀÌ·Î ÀÎÇØ
´õ Å« ÃâÇ÷À̳ª ÇùÂøÀÌ »ý±æ¼ö ÀÖ´Ù.
ii) band ligation: ÃÖ±Ù¿¡´Â endoscopic band ligationÀÌ ÀÌ¿ëµÇ°í ÀÖ´Ù.
acute variceal bleeding control ¹× rebleeding ¿¹¹æ¿¡ ÀÖ¾î¼ Àû¾îµµ sclerotherapy¸¸Å
È¿°úÀûÀ̸ç Ä¡·á¿Í °ü·ÃÇÑ ÇÕº´Áõµµ Àû´Ù.
varixÀÇ long-term obliteration¿¡ recommendµÈ´Ù.
¨ë nonselective ¥â-blocker(propranolol)
hypovolemia·Î ÀÎÇÑ hypotensionÀÌ µ¿¹ÝµÇ¾î ÀÖÀ¸¹Ç·Î acute variceal bleedingÄ¡·á¿¡´Â
Á¦ÇÑÀûÀÌ´Ù. ±×·¯³ª recurrent variceal bleedingÀÇ 2ndary prevention¿¡´Â °¡Ä¡°¡ ÀÖ´Ù.
°Ô´Ù°¡ "high risk"(large varix)¿¡ ´ëÇØ prophylactic txÇÏ¿´À» ¶§ ÃâÇ÷ºóµµ¸¦ ³·Ãß°í »ýÁ¸·ü
À» Çâ»ó½ÃŲ´Ù. ±×·¯¹Ç·Î cirrhosis with varixȯÀÚ´Â endoscopic screeningÀÌ ÃßõµÈ´Ù.
±Ý±â°¡ ¾ø´Â portal hyeprtensionȯÀÚ´Â resting heart rate or hepatic venous pressure
gradient(HVPG)¸¦ 25% °¨¼Ò½ÃŰ´Â °ÍÀÌ À¯¿ëÇÏ´Ù.
propranololÀº ¶ÇÇÑ severe portal hypertensive gastropathy·Î ÀÎÇÑ recurrent bleedingÀ»
¿¹¹æÇÒ¼öµµ ÀÖ´Ù.
¨ì surgical treatment of portal hypertension & variceal bleeding
i) nonselective shunt: end-to-side or side-to-side portocaval and proximal splenorenal
shunt encephalopathy risk°¡ selective shuntº¸´Ù ³ô´Ù.
ii) selective shunt: distal splenorenal shunt
¨í TIPS
refractory bleeding¿¡¼ ¼ö¼úÀ» ´ë½ÅÇØ ½ÃÇàÇÑ´Ù.
±×·¯³ª ¼ö°³¿ùÈÄ stenosis or occlusionÀÌ ¹ß»ýÇØ 2nd TIPS°¡ ÇÊ¿äÇÏ´Ù.
³ëÀÎ, preexisting encephalopathyȯÀÚ¿¡¼ surgical shuntó·³ encephalopathy°¡ ¹®Á¦°¡
µÈ´Ù.
liver transplantation´ë±â¶§ "bridge"·Î À¯¿ëÇÏ´Ù.
¨î esophageal transection: È¿°ú´Â unproven
** Gastric fundal varix bleedingÄ¡·á´Â ¹®Á¦°¡ µÈ´Ù.
sclerotherapy¿Í band ligationµÑ´Ù È¿°ú°¡ ¾øÀ¸¹Ç·Î vasoactive parmacologic tx¸¦ ½Ãµµ
ÇØ¾ß ÇÏÁö¸¸ ½ÇÆÐÀ² ¹× ÀçÃâÇ÷ À§ÇèÀÌ ³ô±â¶§¹®¿¡ TIPS or "shunt surgery"¸¦ °í·ÁÇØ¾ß
ÇÑ´Ù.
isolated gastric varix°¡ ÀÖÀ»¶§´Â splenic vein thrombosis¸¦ »ý°¢ÇØ¾ß ÇÑ´Ù.
III. Splenomegaly
1. Á¤ÀÇ ¹× º´ÀÎ
severe portal hypertensionȯÀÚ¿¡¼ ÈçÇÏ´Ù.
µå¹°°Ô nonhepatic disease·Î ÀÎÇÑ massive splenomegaly¿¡¼ splenic veinÀ¸·ÎÀÇ
blood flow°¡ Áõ°¡µÇ¾î portal hypertensionÀ» ÀÏÀ¸Å³¼öµµ ÀÖ´Ù.
2. ÀÓ»óƯ¡
thrombocytopenia or pancytopenia, ÈçÈ÷ ¹«Áõ»ó
cirrhosis¾øÀÌ splenomegaly + variceal bleeding½Ã splenic vein thrombosis°¡´É¼ºÀ» »ý°¢
ÇØ¾ßÇÑ´Ù.
3. Ä¡·á: no specfic tx
shunt surgery¾ø´Â splenectomy´Â portal pressure¸¦ ´õ¿í Áõ°¡½ÃÄÑ PVT¸¦ ÀÏÀ¸Å²´Ù.
splenomegaly°¡ portal hypertensionÀÌ¿ÜÀÇ ´Ù¸¥ ¿øÀÎÀ¸·Î »ý°å´Ù¸é(¿¹, splenic vein
thrombosis) splenectomy°¡ ÀûÀÀÀÌ µÉ ¼ö ÀÖ´Ù.
thrombocytopenia´Üµ¶Àº spleenÀ» Á¦°ÅÇØ¾ß ÇÒ ¸¸Å ½ÉÇÏÁö ¾Ê´Ù.
splenectomy´Â liver transplantation´ë»óÀΠȯÀÚ¿¡¼´Â ÇÇÇØ¾ß ÇÑ´Ù.
IV. Ascites
1. º´ÀÎ
1) three theories Fig 299-2
¨ç "underfilling" theory
* primary abnormality: portal hypertension & effective circulating blood volumeÀÇ °¨¼Ò·Î
splanchnic vascular bed³»¿¡¼ fluidÀÇ inappropriate sequestration
ÀÌ À̷п¡ µû¸£¸é, intravascular volumeÀÇ °¨¼Ò(underfilling)´Â ½ÅÀå¿¡¼ °¨ÁöµÇ¾î
salt & water retentionÀ» ÃÊ·¡ÇÏ°Ô µÈ´Ù.
¨è "overflow" theory
* primary abnormality: volume depletion¾øÀÌ salt & water retention
¨é peripheral arterial vasodilation hypothesis
arterial hypotension & C.O¡è + vasoconstrictor substance level¡è
cirrhosis & ascites ȯÀÚ¿¡¼ routineÀ¸·Î °üÂû
¶Ç sodium retentionÀº arterial vascular underfilling¿¡ 2Â÷ÀûÀ¸·Î »ý±ä °ÍÀ¸·Î »ý°¢µÈ´Ù.
ÀÌ À̷п¡ µû¸£¸é portal hypertensionÀº NO¿¡ ÀÇÇØ splanchnic arteriolar vasodilationÀ»
ÀÏÀ¸Å²´Ù. arterial vascular space underfilling & barotrauma-mediated renin-angiotensin,
sympathetic output, ADH release¸¦ ÀÚ±ØÇÑ´Ù.
initiating event¿¡µµ ºÒ±¸ÇÏ°í ¸¹Àº ÀÎÀÚ°¡ abdominal cavity¿¡ fluid°¡ ÃàÀûµÈ´Ù.
severe epigastric & norepinephrine levelÀÇ Áõ°¡°¡ Àß °üÂûµÈ´Ù.
2) ±â¿©ÀÎÀÚ
¨ç central sympathetic outflow¡è
cirrhosis & ascitesȯÀÚ¿¡¼ central sympathetic outflowÁõ°¡°¡ ¹ß°ßµÇÁö¸¸ cirrhosis
´Üµ¶À϶§´Â Áõ°¡°¡ ¾ø´Ù.
sympathetic outputÀÇ Áõ°¡, renin-angiotensin system activation & ANP¿¡ ´ëÇÑ
sensitivity °¨¼Ò·Î ÀÎÇØ natriuresis°¡ °¨¼ÒµÈ´Ù.
¨è portal hypertensionÀº splanchnic capillary bed³»¿¡ hydrostatic pressure¸¦ Áõ°¡½ÃÅ´
À¸·Î½á º¹¼öÇü¼º¿¡ ±â¿©ÇÑ´Ù.
¨é hypoalbuminemia & reduced plasma oncotic pressure
ÀÌ ¶ÇÇÑ peritoneal cavity·ÎÀÇ extravasationÀ» ÃÊ·¡ÇÑ´Ù.
±×·¯¹Ç·Î º¹¼ö´Â portal hypertension & hypoalbuminemia°¡ ¾ø´Ù¸é ÈçÄ¡ ¾Ê´Ù.
¨ê hepatic lymphatics
hepatic lymph´Â hepatic sinusoid & lymphatics distortion & obstructionÀ¸·Î ÀÎÇØ
cirrhotic liverÇ¥¸é¿¡¼ ÀÚÀ¯·ÎÀÌ Èê·¯ ascites Çü¼º¿¡ ±â¿©ÇÑ´Ù.
¨ë renal factors
ascites¸¦ À¯Áö½Ã۴µ¥ renal factor°¡ ¶ÇÇÑ Áß¿äÇÑ ¿ªÇÒÀ» ÇÑ´Ù.
º¹¼ö°¡ Àִ ȯÀÚ´Â Á¤»óÀûÀ¸·Î water load¸¦ extretionÇÏÁö ¸øÇÑ´Ù.
proximal & distal tubule¿¡¼ renal sodium reabsorptionÀÌ Áõ°¡ÇÑ´Ù.
distal tubule¿¡¼ÀÇ Áõ°¡´Â ÁÖ·Î plasma renin activityÁõ°¡ ¹× secondary
hyperaldosteronism¶§¹®¿¡ »ý±ä´Ù.
cirrhosis & ascitesȯÀÚ¿¡¼ circulating ANP°¡ Áõ°¡µÇ¾î Àִµ¥ ÀÌ circulating ANP¿¡
´ëÇÑ insensitivity°¡ Áß¿äÇÑ ±â¿©ÀÎÀÚÀÌ´Ù.
ÀÌ·¯ÇÑ insensitivity´Â ½ÉÇÑ sodium excretionÀå¾Ö¸¦ º¸ÀÌ´Â ´ëºÎºÐÀÇ È¯ÀÚ¿¡¼
°üÂûµÇ´Âµ¥ ±×µéÀº ¶ÇÇÑ ÀüÇüÀûÀ¸·Î low arterial pressure & marked renin-aldosterone
axis overactivity¸¦ º¸ÀδÙ.
serum PG or catecholamine levelÁõ°¡·Î ÀÎÇÑ renal vasoconstriction ¶ÇÇÑ sodium
retention¿¡ ±â¿©ÇÑ´Ù. ÃÖ±Ù¿¡ endothelin(=potent vasoconstrictor peptide)ÀÇ ¿ªÇÒÀÌ
Á¦½ÃµÇ°í ÀÖ´Ù.
3) SAAG(serum-ascites albumin gradient)
total protein or ´Ù¸¥ parameter¿¡ ÀÇÇÑ º¹¼ö ºÐ·ùº¸´Ù ´õ ÁÁÀº ºÐ·ù¹ýÀÌ´Ù.
cirrhosis¿¡¼ s-AlbÀº ÈçÈ÷ ascites fluidº¸´Ù 1g/dL ³ô±â ¶§¹®¿¡ high SAAG(¡Ã1.1 g/dL)´Â
°£Á¢ÀûÀ¸·Î portal bed¿Í ascites compartment»çÀÌÀÇ high hydrostatic pressrure gradient
ÀÌ»óÀ» ÀǹÌÇÑ´Ù.
¹Ý´ë·Î low SAAG(<1.1 g/dL)´Â cirrhosis & portal hypertensionÀ» ¹èÁ¦ÇÒ¼ö ÀÖ´Ù.
2. ÀÓ»óƯ¡ ¹× Áø´Ü
peritoneal fluid accumulationÀÌ 500mlÀÌ»óÀÏ ¶§ ÁøÂû¿¡¼ shifting dullness, fluid wave or
bulging flanks¸¦ °üÂûÇÒ¼ö ÀÖ´Ù.
3. Ä¡·á
¨ç ÃÖ±Ù¿¡ »ý°å°Å³ª ¾ÇÈµÈ È¯ÀÚ¿¡¼ À¯¹ßÀÎÀÚ¿¡ ´ëÇØ öÀúÇÑ Á¶»ç¸¦ ÇØ¾ß ÇÑ´Ù.
i) excessvie salt intake
ii) medication noncompliance
iii) superimposed infection
iv) worsening liver disease
v) PVT
vi) HCC¹ß»ý
¨è óÀ½ Áø´Ü¸ñÀûÀ¸·Î´Â small-gauged needleÀ» »ç¿ëÇÑ´Ù.
¼Ò·®(<200ml)À» »Ì¾Æ infection, tumor, ´Ù¸¥ °¡´ÉÇÑ ¿øÀÎ, ÇÕº´Áõ¿¡ ´ëÇØ °Ë»çÇϵµ·Ï ÇÑ´Ù.
therapeutic interventionÀº potential cxÀ§ÇèÀÌ Àְųª progressive ascites increase
(ȯÀÚ°¡ discomfort¸¦ ¾ß±âÇÒ Á¤µµ)¶§ ÀûÀÀÀÌ µÈ´Ù.
* ¸ñÇ¥: peripheral edema(+) ¡1.0 kg/d loss
ascites alone ¡0.5 kg/d
¨é salt restriction: cornerstone of treatment
800 mg sodium(2g NaCl)À̸é negative nitrogen balance¸¦ ÀÏÀ¸Å°´Âµ¥ ÃæºÐÇÏ´Ù.
salt restriction´Üµ¶À¸·Îµµ Àß ¹ÝÀÀÇÏ´Â °æ¿ì´Â
i) recent onset
ii) underlying disease°¡ °¡¿ªÀûÀÏ ¶§
iii) À¯¹ßÀÎÀÚ°¡ ±³Á¤µÉ¼ö ÀÖÀ» ¶§
iv) urine Na excretion(>25 mmol/d) & normal renal functionÀÏ ¶§ µîÀÌ´Ù.
¨ê fluid restriction 1000 mg/d
diuresis¸¦ °ÅÀÇ Áõ°¡½ÃŰÁö ¾ÊÀ¸³ª hyponatremia¸¦ ±³Á¤Çϱâ À§ÇØ ÇÊ¿äÇÏ´Ù.
sodium restriction´Üµ¶À¸·Î diuresis & wt loss¸¦ ÀÏÀ¸Å°±â¿¡ ÃæºÐÄ¡ ¾Ê´Ù¸é ÀÌ´¢Á¦¸¦
»ç¿ëÇÑ´Ù.
¨ë diuretics
salt retentionÀ» Áö¼ÓÇϴµ¥ hyperaldosteronismÀÌ ¿ªÇÒÀ» ÇϹǷΠspironolactone or other
distal tubule-acting diuretics(triamterene, amiloride)°¡ drug of choiceÀÌ´Ù.
ÀÌ·± Á¦Á¦µéÀº K+ sparing effect°¡ Àֱ⠶§¹®¿¡ ´õ¿í ÁÁ´Ù.
spironolactoneÀº óÀ½ 100 mg/d·Î ½ÃÀÛÇØ¼ ÇÊ¿ä½Ã ÃÖ°í 100 mg/d¾¿ Áõ·®ÇÑ´Ù. ÃÖ°í 400
mg/d´Â ³ÑÁö ¾Êµµ·Ï ÇÑ´Ù. ÃÖ¼Ò À¯È¿¿ë·®Àº urinary electrolyte concentrationÀ» º¸¸é¼
Á¤ÇÑ´Ù.
(urinary NaÁõ°¡¿Í K+ °¨¼ÒÁ¤µµ = effective competitive inhibition of aldosteroneÀ» ÀǹÌ)
¹Ý´ë·Î azotemic or hyperkalemia°¡ ÀÖ´Ù¸é ¿ë·®À» Á¦ÇÑÇϰųª °¨·®ÇÑ´Ù.
ÃÖ°í¿ë·®¿¡µµ ºÒ±¸Çϰí diuresis°¡ ½ÃÀÛµÇÁö ¾ÊÀ»¼ö Àִµ¥ ÀÌ´Â proximal tubular sodium
absorption ¶§¹®ÀÌ´Ù. À̶§´Â more potent & proximally acting diuretics(furosemide,
thiazide or ethacrynic acid)¸¦ Á¶½É½º·´°Ô Åõ¿©ÇÑ´Ù.
spironolactone + furosemide(40 or 80 mg/d) ´ëºÎºÐ ȯÀÚ¿¡¼ diuresis¸¦ ½ÃÀÛÇϱ⿡ ÃæºÐ
ÇÏ´Ù.
¨ì paracentesis
½ÉÇÑ º¹¼ö¿¡¼ large-volume paracentesis°¡ prolonged bed rest + conventional diuretics
º¸´Ù È¿°úÀûÀÎ °ÍÀ¸·Î Áõ¸íµÇ¾ú´Ù.
concomitant albumin replacementÀÇ Çʿ伺Àº controversialÇÏÁö¸¸ peripheral edema°¡
¾ø´Â ȯÀÚ¿¡¼´Â intravascular volume depletion°ú hypotensionÀ» ÇÇÇϱâ À§ÇØ °í·ÁÇÒ¼ö
ÀÖ´Ù.
advanced cirrhosis ÀϺο¡¼ "refractory ascites" or rapidly accumulationµÈ´Ù.
¨í shunt operation
ÀÌ·± ȯÀÚ´Â side-to-side portacaval shunt°¡ º¹¼ö¸¦ È£Àü½Ãų¼ö ÀÖ´Ù. °ú°Å¿¡´Â plastic
peritoneo-venous shuntÀÇ surgical implantationÀ¸·Î Ä¡·áÇßÀ¸³ª ÀÌ ¹æ¹ýÀº infection, DIC,
thrombosis¿Í °°Àº ÇÕº´ÁõÀÌ ¸¹¾Æ¼ »ç¿ë¿¡ Á¦ÇÑÀûÀÌ´Ù.
º¸´Ù ÃÖ±Ù¿¡´Â ÀϺÎȯÀÚ¿¡¼ severe hepatic encephalopathy¸¦ ¾ß±âÇϱ⵵ ÇÏÁö¸¸ ¼±ÅÃÀû
À¸·Î TIPS°¡ refractory ascites control¿¡ È¿°úÀûÀ¸·Î »ç¿ëµÇ°í ÀÖ´Ù.
V. Spontaneous bacterial peritonitis(SBP)
1. °³¿ä
SBP º´ÀÎÀÇ key stepÀº ¿©ÀüÈ÷ ¹àÇôÁ®¾ßÇÒ ¹®Á¦·Î ³²¾ÆÀÖÁö¸¸ SBP¸¦ ÀÏÀ¸Å°´Â ´ëºÎºÐÀÇ
±ÕÀÌ bowel¿¡¼ ±â¿øÇÏ¿© hematogenous route & lymphatics¸¦ Ÿ°í º¹¼ö·Î ÆÛÁø´Ù´Â
»ç½ÇÀº ºÐ¸íÇÏ´Ù.
2. ÀÓ»óÁõ»ó
abrupt onset of fever, chills, generalized abdominal pain, µå¹°°Ô rebound abdominal
tenderness¸¦ º¸ÀÌÁö¸¸ ¼Ò¼ö¿¡¼ abdominal complaint¿Í °°Àº ÀÓ»óÀû Áõ»óÀº º¸ÀÌÁö ¾Ê°í
jaundice, encephalopathy¾ÇÈ·Î ³ªÅ¸³ª±âµµ ÇÑ´Ù.
3. Áø´Ü
¨ç typical SBP: WBC > 500 cells/L(poly ¡Ã50%) or poly ¡Ã 250 cells/L
fluid pH, lactate´Â ÀϹÝÀûÀ¸·Î Áø´Ü¿¡ ÇÊ¿äÄ¡ ¾Ê´Ù.
* 2ndary peritonitis¸¦ ½Ã»çÇÏ´Â °æ¿ì
> 10,000 /L, multiple organism, standard tx 48½Ã°£³» È£ÀüÀÌ ¾øÀ» ¶§
¨è SBP variant: monomicrobial nonneutrocytic bacterascites
neutrophil <250/LÀ̳ª culture(+) ÀÏ ¶§
¸¹Àº ȯÀÚ¿¡¼ subsequent paracentesis¶§ clearÇØÁöÁö¸¸ 40%´Â typical SBP·Î ¹ßÀüÇÑ´Ù.
±×·¯¹Ç·Î follow-up paracentesis°¡ ÇÊ¿äÇÏ´Ù.
cf. CNNA(culture negative neutrophilic ascites)
: neutrophil > 250 /LÀ̳ª culture negativeÀÎ °æ¿ì
4. Ä¡·á
¨ç empirical tx with cefotaxime or ampicillin + aminoglycoside(¡ñenteric GNB)
´ú ÈçÇÑ ±ÕÀ¸·Î´Â pneumococci, other G(+) bacteria
10-14ÀÏ Ä¡·á
ÀϺΠ¿¬±¸¿¡¼ 48½Ã°£ÈÄ repeat paracentesis¿¡¼ WBC°¡ 50%ÀÌ»ó °¨¼ÒÇϰí
negative culture¸¦ º¸ÀÏ ¶§ 5ÀÏÄ¡·á·Î ÃæºÐÇÏ´Ù°í ÇÏ¿´´Ù.
¨è prophylactic maintenance tx
norfloxacin(400mg/d), bactrim(5ÀÏ/week), ciprofloxacin 750mg/wk
variceal hemorrhageµ¿¾È SBP prophylaxisó·³ °íÀ§Ç豺¿¡¼ SBPÀÇ primary prevention
ÀÌ ÃßõµÉ¼ö ÀÖ´Ù.
cf. °íÀ§Ç豺À̶õ ascitic fluid albumin < 1.0 g/d
VI. Hepatorenal syndrome
1. Á¤ÀÇ ¹× º´ÀÎ
cirrhosis & ascitesȯÀÚÀÇ serious complicationÀ¸·Î azotemia¾ÇÈ, sodium retention &
oliguria°¡ “u»ýÇÏ´Â °ÍÀ» ¸»ÇÑ´Ù. renal dysfunctionÀ» ÀÏÀ¸Å³¸¸ÇÑ ¿øÀξøÀÌ kidney´Â ±¸Á¶
ÀûÀ¸·Î intactÇÏ´Ù(UA & pyelography Á¤»ó).
renal biopsy´Â ÇÊ¿ä¾øÀ¸¸ç Á¤»óÀÌ´Ù. arachidonic acid metabolites(PG & TX)ÀÇ ºÒ±ÕÇüÀÌ
pathogenic roleÀ» ÇÏ´Â °ÍÀ¸·Î »ý°¢µÈ´Ù.
2. ÀÓ»óƯ¡ ¹× Áø´Ü
¨ç hallmarks: azotemia¾ÇÈ, hyponatremia, progressive oliguria, hypotension
prerenal azotemia or ATNÀ» rule outÇØ¾ßÇÑ´Ù.
drug nephrotoxicity ¶ÇÇÑ °í·ÁÇØ¾ß ÇÑ´Ù(AG or contrast dye).
¨è Áø´Ü: s-Cr > 1.5 g/dLÀÌ¸é¼ volume expansion¿¡ ¹ÝÀÀÇÏÁö ¾Ê°Å³ª diuresis withdrawal
¿¡ urine sodium retention
ÀüÇüÀûÀ¸·Î urine Na < 5mmol/L
3. Ä¡·á: unsuccessful
TOC = liver transplantation
VII. Hepatic encephalopathy
1. Á¤ÀÇ
ÀǽÄ, ÇൿÀå¾Ö, ÀΰÝÀÇ º¯È, ½Å°æÇÐÀû Áõ»ó, asterexis or "flapping tremor", ºÐ¸íÇÑ EEG
º¯È¸¦ Ư¡À¸·Î ÇÏ´Â complex neuropsychiatric syndromes
acute(reversible) or chronic(progressive)ÇÒ¼ö ÀÖÀ¸¸ç ½ÉÇÑ °æ¿ì´Â ºñ°¡¿ªÀû È¥¼ö ¹× »ç¸Á¿¡
À̸¦¼ö ÀÖ´Ù.
2. º´ÀÎ
º´Àο¡¼ °¡Àå Áß¿äÇÑ ÀÎÀÚ´Â severe hepatocellular dysfunction and/or intrahepatic and
extrahepatic shunting(portal blood -> systemic circulation)ÀÌ´Ù.
ÀÌ·Î ÀÎÇØ Àå¿¡¼ Èí¼öµÈ ¿©·¯ °¡Áö µ¶¼º¹°ÁúÀÌ °£¿¡¼ ÇØµ¶µÇÁö ¾Ê°í CNS¿¡ µµ´ÞÇÑ´Ù.
BBB permeabilityÀÇ Áõ°¡°¡ ¶ÇÇÑ º´Àο¡ ±â¿©ÇÑ´Ù.
(1) ¿øÀι°Áú
¨ç ammonia: °¡Àå ÈçÇÑ ¿øÀÎ ¹°ÁúÀÌ´Ù.
ÀüºÎ´Â ¾Æ´Ï´õ¶óµµ hepatic encephalopathyÀÇ ¸¹Àº ȯÀÚ°¡ blood ammonia levelÀÌ Áõ°¡
µÇ¾îÀÖÀ¸¸ç º¸Åë ȸº¹¶§ blood ammonia levelÀÌ °¨¼ÒÇÑ´Ù.
¨è other metabolites
i) mercaptans: intestinal metabolism¿¡ ÀÇÇØ methionineÀ¸·ÎºÎÅÍ »ý¼º
ii) short-acting fatty acids
iii) phenol
iv) false neurochemical transmitters(¿¹, octopamine): ºÎºÐÀûÀ¸·Î aromatic &
branched-chain amino acid¿¡¼ º¯ÈµÇ¾î »ý¼º
¨é GABA
GABA(inhibitory neurotransmitter)ÀÇ ³óµµÀÇ Áõ°¡°¡ hepatic encephalopathy¿¡¼ º¸ÀÌ´Â
ÀǽÄÀúÇÏ¿¡ Áß¿äÇÏ´Ù.
CNS¿¡¼ GABAÀÇ Áõ°¡´Â liver failure¸¦ ¹Ý¿µÇÑ´Ù. ¿©±â´Ù°¡ endogenous benzodiazepine
Àº GABA receptor¸¦ ÅëÇÏ¿© ÀÛ¿ëÇÏ¿© hepatic encephalopathy¹ß»ý¿¡ ±â¿©ÇÑ´Ù.
¨ê ¸Á°£(manganese)
°£°æº¯È¯ÀÚ¿¡¼ MRI»ó basal ganglia¿¡ hyeprintensity°¡ °üÂûµÇ´Âµ¥ ÀÌ´Â °ú´ÙÇÑ ¸Á°£
(manganese)ÀÌ º´Àο¡ ±â¿©ÇÔÀ» ÀǹÌÇÑ´Ù.
(2) À¯¹ßÀÎÀÚ Tab 299-3
stable cirrhosisȯÀÚ¿¡¼ hepatic encephalopathy´Â ºÐ¸íÇÑ precipitating eventÈÄ¿¡ ¹ß»ý
ÇÑ´Ù.
¨ç GI bleeding: mc predisposing factor
ammonia»ý»ê ¹× nitrogenous substance°¡ Áõ°¡ÇÏ¿© Àå³»Èí¼ö°¡ Áõ°¡ÇÑ´Ù.
¨è dietary protein¡è
¨é electrolyte disturbance: ƯÈ÷ hypokalemic alkalosis
°ú´ÙÇÑ ÀÌ´¢Á¦»ç¿ë, vigorous paracentesis or vomitingÀ¸·Î ÀÎÇØ ¹ß»ý
systemic alkalosis´Â nonionic ammonia(NH3)¸¦ Áõ°¡½ÃŲ´Ù.
nonionic(uncharged) ammonia¸¸ÀÌ BBB¸¦ ÀÚÀ¯·ÎÀÌ Åë°úÇÏ¿© CNS¿¡ ÃàÀûµÈ´Ù.
hypokalemia´Â ¶ÇÇÑ Á÷Á¢ renal ammonia»ý»êÀ» ÀÚ±ØÇÑ´Ù.
¨ê CNS depressing agent(¿¹, barbiturates, benzodiazepines)
¨ë acute infection
¨ì ±âŸ
superimposed acute viral hepatitis, alcoholic hepatitis, extrahepatic bile duct
obstruction, constipation, surgery, coincidental medical complication
acute encephalopathy´Â ¿øÀÎÀÌ ±³Á¤µÇ°Å³ª °£±â´ÉÀÌ È¸º¹µÇ¸é ½Å°æÇÐÀû °á¼ÕÀÌ ¿ÏÀüÈ÷
ȸº¹µÇÁö¸¸ chronic encephalopathy´Â ºñ°¡¿ªÀûÀ̰í ÁøÇàµÈ´Ù.
cerebral edema°¡ ÈçÇϸç À̶§ Àüü»ç¸Á·ü°ú °ü°èÀÖ´Ù.
3. Áø´Ü
4°¡Áö ÁÖ¿ä ÀÎÀÚ°¡ ÀÖÀ» ¶§ °í·ÁÇÒ¼ö ÀÖ´Ù.
i) acute or chronic hepatocellular disease and/or extensive portal-systemic collateral
shunts
ii) awareness & mentationÀå¾Ö
iii) neurologic signs: asterexis, rigidity, hyperreflexia, extensor plantar signs, µå¹° °Ô
seizures
iv) EEG patterns: Ư¡ÀûÀÌÁö¸¸ ºñƯÀÌÀû. symmetric, high-voltage, triphasic
slow-wave(25%)
* asterexis("liver flap", "flapping tremor"): nonrhythmic symmetric lapse in voluntary
sustained position of the extremities, heads, and trunk
* fetor hepaticus: È£Èí ¶Ç´Â ¼Òº¯¿¡¼ °õÆÎÀÌ ³¿»õ°¡ ³²(mercaptan¶§¹®)
acute & chronic alcoholism¿¡¼ ÀÓ»óÁõ»óÀÌ hepatic encephalopathy°¡ À¯»çÇϹǷΠ°¨º°ÀÌ
ÇÊ¿äÇÏ´Ù.
** DDx
acute alcohol intoxication, sedative overdose, delirum trimens, Wernicke's
encephalopathy Korsakoff's psychosis, SDH, meningitis, hypoglycemia, other metabolic
encephalopathy
4. Ä¡·á
Á¶±âÀÎÁö ¹× Áï°¢Àû Ä¡·á°¡ ÇʼöÀûÀÌ´Ù.
acute, severe hepatic encephalpathy(stage IV)´Â comaȯÀÚ¿¡ ÁØÇÑ º¸Á¸Ä¡·á¸¦ ÇÑ´Ù.
¨ç À¯¹ßÀÎÀÚ Á¦°Å
¨è blood ammonia & other toxinÀ» °¨¼Ò½Ã۱â À§ÇÑ Ä¡·á
i) protein-free diet
ii) lactulose 30-60mg q 1hr -> ¼³»çÇÒ¶§±îÁö -> ±×ÈÄ 15-30mg tid(2-4ȸ soft stool/day
À¯Áö)
iii) oral "nonabsorbable" antibiotics
neomycin(0.5g-1.0 g qid) or metronidazole (250mg tid)
bacteria¿¡ ÀÇÇÑ ammonia»ý»êÀ» °¨¼Ò½ÃÅ´.
neomycinÀº Èí¼öµÇ¾î renal toxicity¸¦ ÀÏÀ¸Å²´Ù.
¨élevodopa, bromocriptine, keto analogues of essential amino acids, branched-chain a. a
unproven benefit
¨ê flumazenil: benzodiazepine¿¡ ÀÇÇØ À¯¹ßµÈ encephalopathy¿¡¼ »ç¿ë
¨ë chronic encephalopathy
lactulose, dietary protein restriction(60g/d), low dose of lactulose or neomycin
½Ä¹°¼º ´Ü¹éÀÌ µ¿¹°¼º ´Ü¹éº¸´Ù ³´´Ù.
VIII. Coagulopathy
1) thrombocytopenia: hypersplenismÀ¸·Î ÀÎÇØ ¹ß»ý
alcoholic patient¿¡¼´Â ethanolÀÇ direct BM suppression¿¡ ÀÇÇØ¼µµ ÀϾ.
2) protein ÇÕ¼º °¨¼Ò·Î fibrinogen(factor I), prothrombin(factor II), factor V, VII, IX, X°¨¼Ò
¸ðµç factor°¡ °¨¼ÒÇϸç cholestasis·Î ÀÎÇÑ fat-soluble cofactor vitamin KÈí¼öÀå¾Ö°¡
µ¿¹ÝµÇ¾î ¾ÇȵȴÙ(¿¹¿Ü: factor V). ÀÌÁß factor VIIÀÌ Áß½ÉÀÌ´Ù.
À̵éÀÇ ¹Ý°¨±â°¡ ª±â ¶§¹®¿¡ °£°æº¯È¯ÀÚ¿¡¼ plasma replacement·Î PT¸¦ ±³Á¤ÇÏÁö
¸øÇÑ´Ù.
factor VIIÀÇ selective replacement·Î PT¸¦ ±³Á¤ÇÒ¼ö ÀÖ´Ù´Â ¿¬±¸°¡ Á¦½ÃµÇ¾ú´Ù.
IX. Hypoxemia & hepatopulmonary syndromes
1. Á¤ÀÇ ¹× º´ÀÎ
¸¸¼º°£Áúȯ ȯÀÚÀÇ 1/3¿¡¼ mild hypoxemia°¡ ¹ß»ýÇÑ´Ù.
hepatopulmonary syndromeÀº ÀüÇüÀûÀ¸·Î hypoxemia, platypnea, orthodeoxia·Î ³ªÅ¸
³´Ù.
hypoxemia´Â intrapulonary vessel dilatationÀ» ÅëÇÑ right-to-left intrapulmonary shunts·Î
¹ß»ýÇϸç contrast-enhanced echocardiography or macroaggregated albumin lung
perfusion scanÀ¸·Î Áø´ÜÇÒ¼ö ÀÖ´Ù.
shunt Çü¼ºÀÇ ±âÀüÀº ºÐ¸íÄ¡ ¾ÊÀ¸³ª µ¿¹°½ÇÇè¿¡¼ endothelin-1 level & pulmonary NO°¡
°£°æº¯ÀÌ ÀÖÀ» ¶§ Áõ°¡µÇ¾î ÀÖ°í shuntÁ¤µµ¿Í °ü·ÃÀÖÀ½ÀÌ Á¦½ÃµÇ¾ú´Ù.
2. Ä¡·á
large A-V shuntÀÇ °æ¿ì »öÀü¼úÀ» ½ÃÇàÇϱ⵵ ÇÏÁö¸¸ Áö¼ÓÀûÀ¸·Î È¿°úÀûÀÎ Ä¡·á´Â ¾ø´Ù.
advanced pulmonary hypertensionÀÌ ¹ß»ýÇÏÁö ¾ÊÀº °æ¿ì¿¡ liver transplantationÀÌ ±Ã±ØÀû
À¸·Î hepatopulmonary syndromeÀ» °³¼±½Ãų¼ö ÀÖ´Â ¹æ¹ýÀÌ´Ù.