cirrhosis complications

8/14/2019 Cirrhosis Complications

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CIRRHOSIS OF LIVERCIRRHOSIS OF LIVER


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Cirrhosis is a condition in which the liverslowly deteriorates and malfunctions due tochronic injury. Scar tissue replaces healthyliver tissue, partially blocking the flow of

blood through the liver. Scarring alsoimpairs the livers ability tocontrol infections, remove bacteria andtoxins from the blood and process nutrients,

hormones, drugs andmake proteins that regulate blood clotting.Liver produces bile to help absorb fatsincluding cholesteroland fat-solublevitaminsA healthy liver is able to regenerate mostof its own cells when they become damaged.With end-stage cirrhosis, the liver can nolonger effectively replace damaged cells. A

healthy liver is necessary for survival.


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VARICEAL HEMORRHAGEA type of varicose vein that develops inveins in the linings of the esophagus andupper stomach when these veins fill withblood as result of collateral circulationdue to portal hypertension. They get swollendue to an increase in blood pressure in theportal veins and tend to rupture. Bleeding

occurs in 1/3 patients with varices andtendency to bleed increases with largevarices, high pressure, more sever disease.Patients of variceal bleeding present withpainless but massive hematemesis with or

without melena. Proper history andexamination is required to exclude othercauses like peptic ulcer, portal hypertensivegastropathy and gastritis. In absence ofprevious history, the presence of

spleenomegaly, reduced liver span.


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Investigations include: Blood CP(to measureinitial level of hemoglobin and platelate

count), PT & APTT, LFT, Serum electrolytes,Endoscopy(for detection of varices).Prophylactic measures include administrationof non-selective beta-blocker as propranololand the patients who cannot tolerate beta

blockers should be administered isosorbidemononitrate. Prophylactic sclerotherapy isnot indicated because of increased mortality.however binding in high risk individuals can

reduce the incidence


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MANAGEMENT OF ACTIVEMANAGEMENT OF ACTIVE

BLEEDINGBLEEDING INITIAL RESUSCITATIONINITIAL RESUSCITATION monitor the blood pressure and pulsemonitor the blood pressure and pulse pass IV canula and give plasmapass IV canula and give plasmaexpander{gelafundin or haemaccel} to restoreexpander{gelafundin or haemaccel} to restorecirculation and arrange for blood and bloodcirculation and arrange for blood and bloodproducts such as fresh frozen plasmaproducts such as fresh frozen plasma

fresh frozen plasma is administered iffresh frozen plasma is administered ifpatents plasma PT is greater than 1.5 timespatents plasma PT is greater than 1.5 timesof normal.of normal.

Platelates should be infused if count isPlatelates should be infused if count is

less than 50,000 per microlitre.less than 50,000 per microlitre. Pass nasogastric tube to evacuate thePass nasogastric tube to evacuate thestomach to reduce nausea and vomiting and tostomach to reduce nausea and vomiting and tomonitor bleedingmonitor bleeding


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URGENT ENDOSCOPYURGENT ENDOSCOPY

Urgent endoscopy is performed after theUrgent endoscopy is performed after thepatient has become hemodynamically stablepatient has become hemodynamically stable

that usually takes 2-12 hours. Endoscopicthat usually takes 2-12 hours. Endoscopic

examination is performed toexamination is performed to

exclude other causes of GI bleeding asexclude other causes of GI bleeding aspeptic ulcer and congestive gastropathy.peptic ulcer and congestive gastropathy.

For endoscopic treatment of varices withFor endoscopic treatment of varices with

either banding or sclerotherapyeither banding or sclerotherapy


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BandingBanding Varices are sucked and rubber band isVarices are sucked and rubber band is

dislodged over the varicesdislodged over the varices Repeated banding sessions areRepeated banding sessions areperformed at interval of 1-2 weeksperformed at interval of 1-2 weeksuntil varices are oblitered.until varices are oblitered.

Banding varices lower the rate ofBanding varices lower the rate ofrebleeding and complications andrebleeding and complications anddeath than sclerotherapy, sodeath than sclerotherapy, so

therefore is treatment of choicetherefore is treatment of choice..


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Injection sclerotherapy:

Varices are injected with sclerosingagent ethanolamine tetradecyl sulfatethat arrests bleeding by producingvessel thrombosis. A needle is passeddown the biopsy channel of endoscopeand sclerosing agent is injected intovarices, and repeatedly the session isperformed at interval of 3-7 days

followed by 1-3 weeks until varices areobliterated. Complications includechest pain, fever, bacteremia,espophageal ulceration, perforation and

stricture.


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PHARMACOLOGICAL THERAPYPHARMACOLOGICAL THERAPY

Because of lack of facilities in our hospitalsBecause of lack of facilities in our hospitalsthe vasoconstrictor therapy is indicated tothe vasoconstrictor therapy is indicated toreduce the portal pressure. Octereotide isreduce the portal pressure. Octereotide istreatment of choice and vasopressin can alsotreatment of choice and vasopressin can also

be used. Octereotide reduces the splanchnicbe used. Octereotide reduces the splanchnicand hepatic blood flow and portal pressure inand hepatic blood flow and portal pressure incirrhosis patients and is comparable incirrhosis patients and is comparable inefficacy to sclerotherapy. It provides acuteefficacy to sclerotherapy. It provides acutecontrol of variceal bleeding. Vasopressin iscontrol of variceal bleeding. Vasopressin isnon selective vasoconstrictor and and reducesnon selective vasoconstrictor and and reduces

splanchnic blood flow but the complicationssplanchnic blood flow but the complicationsinclude angina, arrhythmia, and MI, so it isinclude angina, arrhythmia, and MI, so it iscontraindicated in patients with ischemiccontraindicated in patients with ischemicheart disease.heart disease.


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OTHER MEASURES TO STOP BLEEDINGOTHER MEASURES TO STOP BLEEDING

Ballon temponadeBallon temponade Transjugular intrahepatic portocaval shuntTransjugular intrahepatic portocaval shunt

Lactulose and vitamin KLactulose and vitamin K

Emergency surgeryEmergency surgery


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Ballon temponadeBallon temponade IT IS USED WHEN SCLEROTHERAPY HAS FAILED ORIT IS USED WHEN SCLEROTHERAPY HAS FAILED OR

UNAVAILABLE or vasoconstrictor therapy hasUNAVAILABLE or vasoconstrictor therapy has

failed or contraindicated. The sangstakenfailed or contraindicated. The sangstaken

blackmore tube is passed into stomach andblackmore tube is passed into stomach and

balloon is inflated with air and pulled backballoon is inflated with air and pulled back

which exerts pressure on lower esophagus andwhich exerts pressure on lower esophagus andgastric fundus to stop bleeding. Thegastric fundus to stop bleeding. The

complications include aspiration pneumonia,complications include aspiration pneumonia,

esophageal rupture and mucosal ulcerationesophageal rupture and mucosal ulceration..


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Transjugular intrahepaticTransjugular intrahepatic

portocaval shuntportocaval shunt

Is performed when when pharmacologic andIs performed when when pharmacologic and

endoscopic therapies are failed. A guidedendoscopic therapies are failed. A guided

wire is passed from jugular vein intowire is passed from jugular vein into

liver and an expandable metal stent isliver and an expandable metal stent isforced over it into the liver mass to formforced over it into the liver mass to form

post systemic shunt between portal andpost systemic shunt between portal and

hepatic vein. Complication include stenthepatic vein. Complication include stent

stenosis or thrombosisstenosis or thrombosis..


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Emergency surgeryEmergency surgery

PERFORMED WHEN OTHER MEASURES ARE FAILEDPERFORMED WHEN OTHER MEASURES ARE FAILED

or if tips is not available particularlyor if tips is not available particularly

if bleeding is from gastric fundalif bleeding is from gastric fundal

varices. The most common surgicalvarices. The most common surgicaltechnique is transaction of esophagus andtechnique is transaction of esophagus and

ligation of feeding vessel to bleedingligation of feeding vessel to bleeding

varices.varices.


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lactulose and vitamin Klactulose and vitamin K Lactulose management is to preventLactulose management is to prevent

encephalopathy precipitated by large bleed.encephalopathy precipitated by large bleed.Vitamin K should be administered inVitamin K should be administered in

patients with prolonged PTpatients with prolonged PT


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MEASURES TO STOP REBLEEDINGMEASURES TO STOP REBLEEDING

Repeated banding or scleropathy, betaRepeated banding or scleropathy, beta

blockers or nitrates and the shunts.blockers or nitrates and the shunts.


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ASCITES

ASCITES ARE PATHOLOGICAL ACCUMMULATION OFFLUID IN PERITONEAL CAVITY. Ascitic fluidmay be exudate or transudate. Ascites arecommon complication of cirhosis of liver.Assessment of ascites

Grade 1 mild; Detectable only by USGrade 2 moderate; Moderate symmetricaldistension of the abdomen

Grade 3 large or gross asites with markedabdominal distension


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Pathogenesis

oHypokalemia and Sodium and water retentiondue to stimulation of renin angiotensinsystem that develops as result of lowperfusion pressure of kidney in cirrhosis,

this retained fluid causes portalhypertension and ultimately the ascites.Nitric oxide is the vasodilator that causeslow perfusion pressure. Other agents areprostaglandins and natriuretic peptide.

oPortal hypertension that exerts localhydrostatic pressure causing transudation offluid in peritoneal cavity.


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oLow serum albumin as result of poorsynthesis by liver causing reduced plasmaosmotic pressure and resulting in intransudation of fluids in peritoneal cavity

clinical features

abdominal distension wih fullness in flank

diffuse abdominal pain

features of the cause(commonly the chronicliver disease)

Dehydration


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INVESTIGATION OF ASCITES

investigation of ascitic fluid

cirrhosis-----clear straw coloured orlight green

malignant disease-----bloody

infections-----cloudy

biliary communication-----heavy bilestating

lymnphatic obstruction-----milky white


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cell count

neutrophil count is more than 250 per mm cube

albumin and total protein

SAAG is best is best single test toclassify the ascites according to their

cause by portal hypertenion and non-portalhypertension

SAAG more than 1.1 g/dl suggests thatunderlying portal hypertension and lessthan it suggests non-portal hypertension

SAAG


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in 4% of patients High SAAG is due tomixed ascites(portal hypertension andmalignancy), so high SAAG indicated portal

hypertension but donot excludes malignancy

ascitic fluid protein level less than 1g/dl predispose the patient toward

spontaneous bacterial peritoniti


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culture and gram stainperformed to identify infection of asciticfluidneutrophil count is more tha 250/mm cube

Other testRBC greater than 50000/micro litre denoteshemorrhaic ascites which is due tomalignancy, TB, and traumaGlucose is low in TB peritonitis

amylase is high in pancreatic ascites


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ULTRASOUND ABDOMEN

confirms the presence of ascites

distinguishes between portal and non portal

cause of ascites.

shows the liver architecture and size ofportal vein


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SPECIFIC MEASURES

DIURESIS

Spironolactone and furesimideL:spironolactone is diuretic of choice , itantagonizes aldosterone and prevents salt andwater reabsorption from kidney as secondary

hyperaldosteronism is major factor in saltand water retention in cirrhosis. Sideeffects are gynecomastia and hyperkalemia.Furesimide is high potency loop diuretic andshould be added to spironolactone if response

to spironolactone high doses is poor.


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Therapeutic paracentesisin patients with massive ascites causingrespiratory distress or ascites refractory todiuretic therapy large volume paracentesisover 1-2 hours is effective. However there isrisk of hypovolumoa as ascitic fluidreaccumulates at expanse of circulating volume

leading to shock. This problem can be overcomeby administration of salt free albuminconcomitantly at dosage of 10g/l of asciticfluid removed to protect intravascular volume.

If the patient is non affording then useplasma expanders such as gelatin infusion125ml/l of ascitic fluid removed.


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LeVeen Shunt and TIPSits a procedure in which a catheter isintroduced from peritoneal cavity intointernal jugular vein incorporating a one wayvalve and allowing the passage of asciticfluid directly into circulation. COMPLICATIONSARE superior vena caval thrombosis, pulmonary

edema, and bleeding from esophageal varices.TIPS is better than LeVeen shunt.

HEPATORENAL FAILURE


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HEPATORENAL FAILURE

PATHOGENESIS

Hepatorenal syndrome is renal failure in absence of shock withend stage liver disease.

Occurs typically in patients with advanced cirrhosis with

jaundice and ascites. It presents as low urine output, raised urea

and creatinine. Low urinary sodium and hypotension.This is pre-renal type renal failure in which kidneys remain

histologically normal and if transplanted to non-cirrhotic patient

then they function normally.

Types of hepatorenal failure:

Type 1:doubling of serum creatinine to a level greater than

2.5mg/dl in less than 2 weeks

Type 2: is more slowly progressive and chronic


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Hepatorenal syndrome develops due toreduced blood flow as result of lowperipheral resistance which leads toincreased secretion of vasoconstrictors

such as nor adrenaline, angiotensin,aldosterone and vasopressin that causevasoconstriction of renal vasculatureresulting in reduced GFR that leads to

extremely low sodium excretion andthere may be decreased production ofrenal vasodilators prostaglandinE2

PATHOGENESIS


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PRECIPITATING FACTORS

Overvigrous diuretic therapy

DiarrheaGI bleedingSepsisLarge paracentesis

MANAGEMENT

The patient should be treated for pre renalfailure, the diuretic should be stopped and

intravascular hypovolemia is corrected withsalt free albumin. The dopamine infusion isineffective. TIPS may improve thecondition.

HEPATOPULMONARY SYNDROME


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HEPATOPULMONARY SYNDROME

Hepatopulmonary syndrome occurs occurs

due to chronic liver disease and manifestas dyspnea in upright position(orthodeoxia) that is relieved byrecumbency.

PATHOGENESIS

Hypoxia and dyspnea develops due to right

to left intrapulmonary shunt because theliver is unable to clear the circulatorypulmonary vasodilators.


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INVESTIGATION

Pulse oximetry shows oxygen saturation less

than 92%

Contrast echocardiography is sensitivescreening test for detecting intrapulmonary

shunts.

Macroaggregated albumin lung perfusionscanning is more specific and used to confirm

the diagnosis.

High resolution CT scan of chest showsdilated pulmonary vessels


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MANAGEMENT

No specific treatment is available howeverIV methylene blue may improve oxygenation inpatients by inhibiting nitric oxide inducedvasodilation. TIPS may provide palliation in

patients awaiting liver transplantation.

cirrhosis complications

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