Liver cirrhosis (Causes, clinical manifestation, complications, diagnosis, treatment)
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Cirrhosis is a diffuse process characterized by liver necrosis and fibrosis that converts the normal liver architecture into abnormal nodules lacking lobular organization. It has many causes including alcohol, viral hepatitis, fatty liver disease, and genetic disorders. Clinically, it manifests as asymptomatic or symptoms like vomiting and weight loss. Complications arise from portal hypertension and include ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome. Diagnosis involves liver function tests, imaging, and biopsy. Treatment focuses on managing complications and the underlying cause. For end-stage disease, liver transplantation may be required.
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PORTAL HYPERTENSION
OUTLINE:
Definition
Causes
Pathogenesis
Clinical features
Investigations
Management
Complications
Prognosis
Approach
Definition:
Defined as:
Portal Pressure > 10-12 mm Hg, with diameter >10mm Or
Hepatic Venous Pressure Gradient > 4 mm Hg
increased portal resistance or increased portal venous blood flow
major cause of morbidity and mortality in chronic liver diseases
Portal Vein:
Causes of Portal HTN:
Extrahepatic/Pre-hepatic
Hepatic
Pre-Sinusoidal
Sinusoidal
Post-Sinusoidal
Post-hepatic
A. Extra-hepatic:
Portal Vein Thrombosis- Most common
Neonates: Omphalitis, Umbilical Vein Catheterization, Dehydration, Sepsis
Older Children: Intra-abdominal infections e.g., Appendicitis, IBD, PSC
Hypercoagulable states: Deficiencies of factor V Leiden, protein C, S
Blunt Abdominal Trauma
Portal vein agenesis, atresia, stenosis
Splenic vein thrombosis
Biliary tract disease
Extrahepatic biliary atresia
Choledochal cyst
B. Intra-hepatic:
C. Post-hepatic:
Budd-Chiari Syndrome
IVC Webs
Chronic Constrictive Pericarditis
Pathogenesis And Consequence of Portal HTN
Portosystemic collaterals:
Sites:
Lower part of esophagus
Lower part of rectum
Around Umbilicus
Clinical Features:
Bleeding:
Most common presentation
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rises to 38% in with known varices >5-yr period
Pattern of bleeding
Hematemesis/Malena: Most common
worsened by Stress / Intercurrent illness
Size of varices → Bleeding
Splenomegaly:
2nd Most common presentation
asymptomatic or associated with cytopenia
Ascites:
Seen in 7-21% patients
Less common but important manifestations
Portal Hypertensive Biliopathy
Growth Failure
Hepatopulmonary Syndrome
Porto-pulmonary HTN
Caput Medusae:
Abnormal, dilated venous network on anterior abdominal wall, radiating from the umbilicus
Not seen in extra-hepatic portal HTN
Seen in intra-hepatic portal HTN
Continuous murmur between umbilicus and lower sternum
Cruveilhier-Baumgarten Murmur
Investigations
USG with Doppler
portal vein diameter > 10 mm
hepatic diseases, masses, presence of varices and ascites
ascertain pattern of flow
Reversal of portal blood flow (Hepatofugal flow) - Associated with bleeding varices
Cavernous transformation of the portal vein in EHPVO
Increased thickness of lesser omentum
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GIT Endoscopy: Most reliable to detect varices
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CBC
LFT
Barium swallow
Portal angiogram
Percutaneous intrasplenic measurement of portal pressure
Venography
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1st Step (Initial resuscitation):
airway protection
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NG
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This document discusses several vascular disorders of the hepatobiliary system, including hepatic infarction, peliosis hepatis, veno-occlusive disease, portal hypertension, Budd-Chiari syndrome, ischemic hepatitis, and ischemic cholangiopathy. Hepatic infarction is a rare condition caused by compromise of both the hepatic artery and portal vein blood flows. Ischemic hepatitis results from impaired hepatic perfusion due to conditions like heart failure or sepsis. Ischemic cholangiopathy involves damage to the bile ducts from disruption of hepatic artery blood flow, such as after liver transplantation or tumors.
Portal hypertension
This document discusses portal hypertension and variceal bleeding. It begins by describing portal hemodynamics and defining clinically significant portal hypertension as a hepatic venous pressure gradient (HVPG) greater than 10-12 mm Hg.
The etiology of portal hypertension is categorized as prehepatic, hepatic, or posthepatic. Prehepatic causes include portal/splenic vein thrombosis. Hepatic causes include cirrhosis, which leads to fibrosis and increased production of vasoconstrictors. Posthepatic causes include Budd-Chiari syndrome.
Complications of portal hypertension include variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome. Investigations for diagnosis include ultrasound Doppler,
Cirrosis presentation
Cirrhosis is a serious chronic disease characterized by widespread disruption of the normal liver structure by fibrosis and regenerative nodules caused by conditions like long-term alcohol abuse or hepatitis. Common causes include alcohol abuse, hepatitis B/C, and certain drugs. Symptoms include enlarged liver, jaundice, fluid in the abdomen, and changes to circulation, hormones, and bleeding risk. Treatment depends on the cause but may include medications, procedures to control bleeding, antibiotics, dialysis, and liver transplantation in severe cases.
Liver disease
The document discusses the anatomy, histology, functions and common pathologies of the liver. Key points include:
- The liver has four lobes and receives dual blood supply from the hepatic artery and portal vein. It performs many metabolic and synthetic functions.
- Common liver diseases include viral hepatitis, alcoholic liver disease and cirrhosis. Cirrhosis results from chronic liver injury and scarring that disrupts the liver architecture.
- Primary liver cancers like hepatocellular carcinoma often arise in the setting of chronic liver disease and cirrhosis. Treatment options are limited but may include transplantation or resection in early stages.
Portal hypertension by Gowhar Ahmad
Portal hypertension occurs when there is increased resistance to blood flow through the portal vein, causing elevated pressure. It is usually caused by cirrhosis which damages the liver and increases vascular resistance. Common clinical signs include gastrointestinal bleeding, ascites, and an enlarged spleen. Treatment depends on the severity and includes pharmacotherapy, endoscopic procedures, transjugular intrahepatic portosystemic shunt placement, and liver transplantation for advanced disease. The goal is to reduce portal pressure and prevent complications.
Portal hypertension
This document discusses portal hypertension, including its definition, causes, clinical presentations, investigations, and management.
Portal hypertension is defined as elevated hepatic venous pressure gradient above 5 mmHg. It is clinically significant when the HVPG exceeds 10-12 mmHg. Common causes include cirrhosis, schistosomiasis, and portal or hepatic vein thrombosis.
The clinical triad of portal hypertension includes esophageal varices, splenomegaly, and ascites. Investigations include liver function tests, ultrasound, and endoscopy. Management involves general measures, treatment of varices with medications or endoscopic therapy, management of ascites and encephalopathy, and procedures to lower portal pressure such as T
Cirrhosis of liver
Cirrhosis is a diffuse process characterized by liver necrosis and fibrosis that converts the normal liver architecture into abnormal nodules. It has many causes including viral hepatitis, alcohol, autoimmune conditions, and genetic disorders. Cirrhosis can lead to complications from portal hypertension such as variceal bleeding and ascites. It is diagnosed based on clinical findings, lab tests, imaging, and may require liver biopsy. Treatment focuses on managing complications and potentially liver transplantation.
Gi bleed hegazy
This document discusses gastrointestinal bleeding (GIB). It is classified as upper GIB, arising above the ligament of Treitz, or lower GIB, arising below. Common causes of upper GIB include peptic ulcer disease, portal hypertension, Mallory-Weiss tears, and vascular anomalies. Initial management involves fluid resuscitation and endoscopy for diagnosis and treatment. Lower GIB causes include diverticulosis, angiodyplasia, and inflammatory bowel disease. The document provides details on evaluation, diagnosis, and management of GIB.
Renal manifestations of systemic disease(s).
Systemic diseases that commonly present with renal manifestations: diabetic and hypertensive nephropathy, lupus nephritis, congestive heart failure (Cardiorenal Syndromes), liver disease, and paraproteinemia , infections (HCV, HIV, COVID-19,..), other rheumatological disorders (Rhod A., Gout, SCL), HSP, Vasculitis, hereditary kidney diseases, Familial Mediterranean Fever (FMF), and Malignancy.
Cirrhosis of liver and complications
Cirrhosis and portal hypertension are defined. Cirrhosis is characterized by fibrosis and nodular regeneration of the liver. Portal hypertension is defined as a portal pressure greater than 5 mmHg and can occur before cirrhosis is established. Complications of cirrhosis and portal hypertension include ascites, variceal hemorrhage, hepatic encephalopathy, and hepatocellular carcinoma. The document discusses the mechanisms, diagnosis, and treatment of these complications.
Diseases of the liver
- Viral hepatitis can present asymptomatically, symptomatically before jaundice, or progress to fulminant hepatitis or chronic hepatitis. Diagnosis involves blood tests to check liver enzymes and serology or molecular testing to determine the virus.
- Liver abscesses can be pyogenic (most common), amebic, or fungal. Amebic abscesses are caused by Entamoeba histolytica and present with fever, abdominal pain, and hepatomegaly. Pyogenic abscesses require drainage if large or not improving with antibiotics.
- Hydatid cysts are caused by the tapeworm Echinococcus granulosus. Surgical removal is usually required for large or infected cysts while
Budd chiari syndrome
This document provides information on Budd-Chiari syndrome (BCS), including its definition, epidemiology, etiology, clinical features, diagnosis, pathophysiology, management, and role of medical and minimally invasive treatments. BCS is defined as obstruction of the hepatic veins or inferior vena cava, causing hepatic venous outflow obstruction. Common causes include infections, malignancies, and prothrombotic disorders. Clinical features include abdominal pain, ascites, hepatomegaly, and jaundice. Diagnosis involves imaging like ultrasound, CT, MRI and angiography. Management depends on the cause and includes anticoagulation, thrombolysis, angioplasty, stenting, TIPS, and
Complication of ascitis
Cirrhosis can lead to several serious complications including ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal hypertension, variceal bleeding, hepatorenal syndrome, and hepatocellular carcinoma. The document outlines the pathophysiology, clinical presentation, diagnostic approach, and treatment options for each of these common complications of cirrhosis. It provides detailed guidance on managing ascites, variceal bleeding, hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome.
Kidney diseases by Harrison Mbohe
AKI, CKD, and ESRD are conditions involving the kidneys. AKI is a sudden loss of kidney function that develops over days or weeks and is often reversible. It is caused by prerenal factors like low blood pressure or intrinsic renal damage. Common causes include sepsis, low fluid intake, and medications. Diagnosis is based on increases in BUN and creatinine and decreased urine output. Treatment focuses on identifying and treating the underlying cause while managing fluid, electrolyte and acid-base imbalances. Long term kidney damage can progress to CKD or end stage renal disease requiring renal replacement therapies.
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- 1. Causes, clinical manifestation, complications, diagnosis, treatment Ilkin Bakirli
- 2. Introduction • WHO definition: a diffuse process characterised by liver necrosis and fibrosis and conversion of normal liver architecture into structurally abnormal nodules that lack lobular organisation • Chronic progressive disease of the liver characterised by extensive degeneration and destruction of parenchymal cells • The liver attempts to regenerate, but the process is disorganised, resulting in abnormal blood vessel and bile duct architecture, as well as regenerative nodules on the liver
- 3. Causes • Alcoholic • Viral: HBV, HCV • NAFLD (non-alcoholic fatty liver disease) • Primary sclerosing cholangitis • Autoimmune hepatitis • Biliary cirrhosis • Cystic fibrosis • Hemochromatosis • Wilson disease • Cryptogenic (idiopathic) • Alpha-antitrypsin deficiency
- 4. Pathophysiology • Extensive fibrosis (degeneration) and regeneration of the liver leading to nodules (hepatocellular hyperplasia and angiogenesis) • New vessels are formed between the hepatic artery, hepatic veins and the portal vein • These blood vessels are low volume, high pressure veins that cannot carry enough blood • This leads to portal hypertension
- 5. Clinical manifestations Symptoms Signs Asymptomatic Epistaxis Vomiting Hepatomegaly / atrophy Nausea Splenomegaly Alopecia in pubic areas Clubbing Gynecomastia Ascites Easy bruising Caput medusa Weight loss Spider telangiectasia Muscle cramps Hepatic encephalopathy Anorexia Testicular atrophy
- 6. Diagnosis 1. History, child-pugh score 2. Physical exam (hepatomegaly, ascites, clubbing, caput medusa) 3. Liver function tests: ↑ALT, ↑AST, normalALP, normal GGT, normal or ↑bilirubin, ↑PTT, ↓albumin 4. Coagulation tests: ↑PTT, increased bleeding time 5. CBC: microcytic and macrocytic anemia, hemolysis and hypersplenism, leukopenia, thrombocytopenia 6. Viral serology 7. Biopsy 8. USG, MRI,CT, ERCP/MRCP 9. Radionuclide technetium scan 10. Other: ↓iron and ↑ferritin in hemochromatosis, ↓alpha-antitrypsin
- 8. Treatment • Treat the underlying cause • Supportive therapy (coagulation factors, vitamin K, albumin) • Lifestyle changes • Treat the complications • Liver transplantation
- 9. Complications 1. Portal hypertension: prolonged elevated portal pressure (normal 2-5mmHg, HTN >12mmHg). Symptoms include splenomegaly, hypersplenism, thrombocytopenia, leukopenia, caput medusa, varices, fetor hepaticus. Diagnosis made by USG and venography Treatment: terlipressin + octreotide 2. Variceal bleeding: bleeding usually in the gastro-esophageal junction, 50% mortality Treatment: endoscopic banding, sclerotherapy, balloon tamponade,TIPSS (transjugular intrahepatic porto-systemic shunt), beta blockers
- 10. Complications 3. Ascites: accumulation of free fluid in the peritoneum Clinical: abdominal distention, shifting dullness on percussion, right side pleural effusion (10%). Diagnosis: USG, paracentesis (protein <25g/L). Risk of peritonitis Treatment: Na+ restriction, diuretics (spironolactone/furosemide), paracentesis, I.V albumin,TIPSS 4. Hepatorenal syndrome: in 10%, severe renal vasoconstriction due to extreme under filling of renal arterial circulation Type 1: oliguria, ↑↑↑↑creatinine, poor prognosis Type 2: in refractory ascites, ↑↑creatinine, better prognosis
- 11. Complications 5. Spontaneous bacterial peritonitis (SBP): sudden abdominal pain, rebound tenderness, absent peristalsis, fever, ascites, (usually) E.coli can be cultured from the fluid.Treatment: broad spectrum ATBs 6. Hepatopulmonary syndrome: intrapulomanry shunting through arteriovenous communications, causing resistant hypoxemia (Pa02 <70mmHg) due to pulmonary hypertension and pleural effusion 7. Congestive gastropathy: chronic gastric congestions, bleeding sites, can cause anemia.Treatment: propranolol,TIPSS