¼±Åà - È­»ìǥŰ/¿£ÅÍŰ ´Ý±â - ESC

 

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¿¡ À־ 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 ȯÀÚ¿¡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/dLÀ̸鼭 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 ¾ÇÈ­µÈ´Ù(¿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.