case study presentation on cirrhosis of the liver

CASE PRESENTATION ONCIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY.

A DETAIL CASE PRESENTATION ON CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. LIVER CIRRHOSIS AND ALL ITS COMPLICATION IN A PATIENT.

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• 1. AKHIL JOSEPH REG.NO : 13QO4O2
• 2.  Cirrhosis is a slowly progressing disease in which healthy liver tissue is replaced with scar tissue, eventually preventing the liver from functioning properly. The scar tissue blocks the flow of blood through the liver and slows the processing of nutrients, hormones, drugs, and naturally produced toxins.
• 3.  As the disease worsens, a person may become tired, weak, itchy, have swelling in the lower legs, develop yellow skin, bruise easily, have fluid build up in the abdomen, or develop spider-like blood vessels on the skin. The fluid build-up in the abdomen may become spontaneously infected. Other complications include hepatic encephalopathy, bleeding from dilated veins in the esophagus or dilated stomach veins, and liver cancer. Hepatic encephalopathy results in confusion and possibly unconsciousness.
• 5. EPIDEMIOLOGY  Cirrhosis is the ninth leading cause of death in the United States and is responsible for 1.2% of all US deaths • Many patients die in their fifth or sixth decade of life • The prevalence is higher in non-Hispanic blacks and Mexican Americans, those living below the poverty level, and those with less than a 12th grade education • Each year, 2000 additional deaths are attributed to fulminant hepatic failure (FHF), that may be caused viral hepatitis, drugs (e.g., acetaminophen), toxins (e.g., Amanita phalloides, the yellow deathcap mushroom), autoimmune hepatitis, Wilson disease, or a variety of less common etiologies. Cryptogenic causes are responsible for one third of fulminant cases.
• 6. ETIOLOGY  It has many possible causes; sometimes more than one cause is present in the same person. Globally, 57% of cirrhosis is attributable to either hepatitis B (30%) or hepatitis C (27%).Alcohol consumption is another important cause, accounting for about 20% of the cases.  Alcoholic liver disease (ALD). Alcoholic cirrhosis develops for 10–20% of individuals who drink heavily for a decade or more.  Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue.  Chronic hepatitis C.  Chronic hepatitis B.  Primary biliary cirrhosis. Damage of the bile ducts leading to secondary liver damage.
• 7.  Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat-soluble vitamin deficiencies, and metabolic bone disease.  Wilson's disease. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy and elevated 24-hour urine copper.  Cystic fibrosis  Hepatotoxic drugs or toxins  Autoimmune hepatitis. This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis.
• 9. PATHOPHYSIOLOGY
• 16. CLINICAL PRESENTATION SYMPTOMS  Gastrointestinal: bleeding, dark stool from digested blood, fluid in the abdomen, nausea, passing excessive amounts of gas, vomiting blood, or water retention  Whole body: fatigue, loss of appetite, or reduced hormone production  Skin: web of swollen blood vessels in the skin or yellow skin and eyes  Weight: weight gain or weight loss  Also common: swollen legs, yellow eyes, bleeding, breast enlargement, breast enlargement in men (Gynecomastia), bruising, dark urine, enlarged veins around belly button, flapping hand tremor, itching, mental confusion, Poor concentration and memory, muscle weakness, red palms, swelling, swelling in extremities, or swollen veins in the lower esophagus(Bleeding esophageal varices )
• 17. ASCITES WITH PORTAL HYPERTENSION
• 18. SIGNS  Jaundice  Scratch marks secondary to pruritus  Spider angiomata/naevi (mainly found on the trunk and face)  Skin telangiectasia's ('paper money skin')  Palmar erythema  Bruising  Petechia or purpura  Hair loss  White nails (sign of hypoalbuminemia)  Finger clubbing  Dupuytren's contracture
• 19. RISK FACTORS  Obesity/overweight increases the risk for liver disease. Obesity often results in the accumulation of fat cells in the liver. Acids that are secreted by these fat cells (called fatty acids) can cause a reaction in the body that destroys healthy liver cells and results in scarring (sclerosis) and liver damage.  The risk for developing liver disease varies, depending on the underlying cause and the particular condition. General risk factors for liver disease include alcoholism, exposure to industrial toxins, heredity (genetics), and long-term use of certain medications.  Age and gender also are risk factors for liver disease. These factors vary, depending on the particular type of disease. For example, women between the ages of 35 and 60 have the highest risk for primary biliary cirrhosis and men aged 30-40 are at higher risk for primary sclerosing cholangitis.
• 20. COMPLICATIONS  Anemia, thrombocytopenia and coagulopathy (folate deficiency, hemolysis, hypersplenism, cholestasis)  Esophageal varices (portal hypertension)  Ascites  Spontaneous bacterial peritonitis  Hepatocellular carcinoma  Cirrhotic cardiomyopathy  Hepatopulmonary syndrome  Portopulmonary hypertension.
• 21. DIAGNOSIS  The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous, transjugular, laparoscopic, or fine-needle approach. A biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis. Furthermore, there is a small but significant risk to liver biopsy, and cirrhosis itself predisposes for complications caused by liver biopsy.The best predictors of cirrhosis are ascites, platelet count <160,000/mm3, spider angiomata, and Bonacini cirrhosis discriminant score greater than 7.
• 22. normal liver tissue
• 23. The liver in this histologic picture has wide bands of fibrous connective tissue separating small islands of hepatic tissue.
• 24. LAB FINDINGS Thrombocytopenia - typically multifactorial. Due to alcoholic marrow suppression, sepsis, lack of folate, sequestering in the spleen as well as decreased thrombopoietin. However, this rarely results in platelet count < 50 000/mL.  Aminotransferases - AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferases do not preclude cirrhosis.  Alkaline phosphatase - slightly elevated but less than 2-3 times the upper limit of normal.  Gamma-glutamyl transferase – correlates with AP levels. Typically much higher in chronic liver disease from alcohol.  Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver
• 25.  Bilirubin - Levels normal when compensated but may elevate as cirrhosis progresses.  Prothrombin time - increases since the liver synthesizes clotting factors.  Globulins - increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.  Serum sodium - hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.  Leukopenia and neutropenia - due to splenomegaly with splenic margination.  Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.
• 26. IMAGING  Ultrasound is routinely used in the evaluation of cirrhosis. It may show a small and nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing areas. Other findings suggestive of cirrhosis in imaging are an enlarged caudate lobe, widening of the liver fissures and enlargement of the spleen. An enlarged spleen (splenomegaly), which normally measures less than 11–12 cm in adults, is suggestive of cirrhosis with portal hypertension in the right clinical setting. Ultrasound may also screen for hepatocellular carcinoma, portal hypertension, and Budd-Chiari syndrome (by assessing flow in the hepatic vein).  Computed tomography (CT) scanning and/or magnetic resonance imaging (MRI)
• 28. ENDOSCOPY  Gastroscopy (endoscopic examination of the esophagus, stomach, and duodenum) is performed in patients with established cirrhosis to exclude the possibility of esophageal varices. If these are found, prophylactic local therapy may be applied (sclerotherapy or banding)
• 29. GRADING OF DISEASE  The severity of cirrhosis is commonly classified with the Child-Pugh score. This score uses bilirubin, albumin, INR, presence and severity of ascites, and encephalopathy to classify patients in class A, B, or C. Class A has a favourable prognosis, while class C is at high risk of death. It was devised in 1964 by Child and Turcotte and modified in 1973 by Pugh and others. Although it was originally used to predict mortality during surgery, it is now used to determine the prognosis, as well as the required strength of treatment and the necessity of liver transplantation.  Modified Maddrey's discriminant function.  The modified Maddrey's discriminant function) was originally described by Maddrey and Boitnott to predict prognosis in alcoholic hepatitis. It is calculated by a simple formula: (4.6 x (PT test - control))+ S.Bilirubin in mg/dl  Prospective studies have shown that it is useful in predicting short term prognosis especially mortality within 30 days. A value more than 32 implies poor outcome with one month mortality ranging between 35% to 45%. Corticosteroid therapy or pentoxifylline have been used with mixed results for patients whose increased mortality is indicated with a value greater than 32.
• 30. SCORING Points Class One year survival Two year survival 5–6 A 100% 85% 7–9 B 81% 57% 10–15 C 45% 35% Measure 1 point 2 points 3 points Total bilirubin, μmol/L (mg/dL) <34 (<2) 34–50 (2–3) >50 (>3) Serum albumin, g/dL >3.5 2.8–3.5 <2.8 Prothrombin time, prolongation (s) <4.0 4.0–6.0 > 6.0 Ascites None Mild (or suppressed with medication) Moderate to Severe (or refractory) Hepatic encephalopathy None Grade I–II Grade III–IV The score employs five clinical measures of liver disease. Each measure is scored 1–3, with 3 indicating most severe derangement. Chronic liver disease is classified into Child–Pugh class A to C, employing the added score from above. INTERPRETATION
• 31. Modified Maddrey's discriminant function  to predict prognosis in alcoholic hepatitis. It is calculated by a simple formula:  (4.6 x (PT test - control))+ S.Bilirubin in mg/dl.  Prospective studies have shown that it is useful in predicting short term prognosis especially mortality within 30 days. A value more than 32 implies poor outcome with one month mortality ranging between 35% to 45%.
• 32. DEMOGRAPHIC DETAILS OF PATIENT  NAME : XYZ  SEX : Male  DEPT : EICU  DOA : 15-01-2017  AGE : 56  I.P NO : 1624  UNIT :  DOD : 24-01-2017
• 33. REASON FOR ADMISSION:  C/O bleeding from gums after tooth extraction.  K/C/O alcoholic liver disease , admitted 6 months back.
• 34. HISTORY OF PRESENT ILLNESS:  Pt was apparently alright 2 days back the he had tooth extraction (3) following which he complains of bleeding from gums. He also had C/O abdominal distension and pedel edema.  Abdominal distension since 6 months.  K/C/O alcoholic liver disease, admitted for the same.  H/O pedal edema - pitting type, no h/o fever, no h/o pain in abdomen, no h/o vomiting of blood, no h/o passasge of dark coloured stools.
• 35. PAST MEDICAL HISTORY Admitted for ALD six months back. Not a K/C/O DM, HTN, TB, ASTHMA, EPILEPSY. No H/O previous surgeries.
• 36. Family history  Diet : veg  Sleep: disturbed  Appetite : normal and regular.  Habits : chronic alcoholic since 25 years, left 6 months back.
• 37. General physical examination.  Pt is moderatly built and nourished.  Not oriented to TPP. ON EXAMINATION  GC : fair  Afebrile  PR: 108 bpm  BP: 110/70 mmHg  SPO2 : 99% + + - - - +  P I C K L E
• 38. SYSTEMIC EXAMINATION  CVS : S1 S2 +, NO MURMUR  RS : B/L AE equal  CNS : pt. drowsy  P/A :palpation + no local rise in temperature non-tender hepatomegaly + inspection : distension +, umbilicus inverted.
• 39. INVESTIGATIONS  Complete hemogram with ESR  LFT  RBS  Blood urea  Serum electrolytes  BT  CT  PT  APTT  INR  Chest X-ray  USG abdomen and pelvis.
• 40. PROVISIONAL DIAGNOSIS LIVER CIRROSIS ?
• 41. LABORATORY FINDINGS HB : 6.9 g/dl ↓ ( 13.5- 17.5 g/dl )  WBC: 11,200 cells/µl. ↑  RBC: 2.07Million/µl. ↓  PLT: 1,12,000 cells/comm. ↓  DLC: polymorphs: 78% basophils: 00% eosinophils : 02% lymphocytes: 20% monocytes: 00% ESR : 120mm ↑ (<15mm) Complete hemogram  PCV : 17.2 % ( 40-50) ↓  MCH : 33.3 pg ( 27-32) ↑  MCHC : 40% ( 32- 46 )  MCV : 83.3 fl ( 82 - 101)
• 42.  ELECTROLYTES : Sodium : 138 (135-147 mEq / L ) Potassium :3.8( 3.5-5.2 mEq / L ) Chlorides : 105 ( 95-107 mEq / L ) RBS: 106 mg/dl (60-140 mg/dl ). HIV : Non-Reactive HBsAg : NEGATIVE HCV : NEGATIVE BT : 3 mnts. 30 sec (1-6 min ) CT : 5min. 30sec ( 5-10 min ) PT: test : 20 sec , control : 13sec ↑ INR : 1.5 (0.8-1.1) ↑ APTT : test : 40sec, control : 22sec. ↑
• 43.  PSS : normocytic normochromic anemia with neutrophilia.  Blood group : O+ve RFT  Sr. Urea : 32  Creatinine : 0.7
• 44. LFT  ALT : 24 U/L (6-38)  AST : 71 U/L ( 6-40) ↑  ALP : 63 U/L ( 35-140)  BILIRUBIN T : 7.3 MG% ( 0.2 – 1.0)↑ D : 2.8 MG% ( 0.1 - 0.4 ) ↑ I : 4.5 MG % ( 0.1 – 0.6)↑ Total protien : 6.7 ( 6.4-8.3 gm/dl) Albumin : 2.9 ( 3.5 – 5 gm/dl ) ↓ Globulin : 3.8 ( 2.3 – 3.5 gm/dl) ↑ A/G ratio : 1:1.3 Ammonia : 68mcg/dl ( 9.5-49) ↑
• 45. Ascitic fluid examination  Protien : 1.5 gm %  Chloride : 120mEq/L  Sugar : 173mg%  Gram stain : Few lymphocytes seen, no organisms.  ZN stain : No AFB
• 46. URINE ROUTINE  Pus cells : 1-2/ hpf  Epithelial cells : 1-2/hpf
• 47. USG ABDOMEN  1. CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION AS EVIDENCED BY SPLEENOMEGALYAND GROSS TENSE ASCITES.  2. CHOLELITHIASIS
• 49. TREATMENT CHART
• 50. BRAND NAME GENERIC NAME DOSE ROUTE FREQUENCY D A Y 1 D A Y 2 D A Y 3 D A Y 4 D A Y 5 D A Y 6 D A Y 7 D A Y 8 D A Y 9 D A Y 10 IVF NS DNS WITH 2 AMP OPTINEURON 2 PINT 1 PINT IV 1-0-0-1 √ √ √ √ √ √ √ √ √ √ √ √ √ INJ. XONE CEFTRIAXONE 1 GM IV 1-0-1 √ √ √ √ √ TAB OFLOX OFLOXACIN 400MG P/O 1-0-1 √ √ √ √ √ INJ. PAN PANTOPRAZOL E 40 MG IV 1-0-0 √ √ √ √ √ √ √ √ √ √ INJ. VITAMIN K VITAMIN K IM 1-0-1 √ √ √ √ √ √ INJ. HEPAMERZ L-ORNITHINE L-ASPARTATE I AMP IN 100 MLNS 1-1-1 2-2-2 (SACHET) √ √ √ √ √ 1- 1- 1 √ √ √ √ INJ. EMSET ONDANSTRON 4 MG IV 1-1-1 √ √ √ TAB. UDIBON URSODEOXYCH OLIC ACID SILYMARIN 300MG 140MG P/O 1-0-1 √ √ √ √ √ √ √ √ √ √ INJ. PAUSE TRANEXAMIC ACID I AMP IN 100 ML NS 1-0-1 √ √ √ √ √ T A B √ SYP.DUPHAL AC LACTULOSE 15ML P/O 1-1-1 √ √ √ √ √ √ √ √ √ √
• 51. BRAND NAME GENERIC NAME DOSE ROUTE FREQUENCY D A Y 1 D A Y 2 D A Y 3 D A Y 4 D A Y 5 D A Y 6 D A Y 7 D A Y 8 D A Y 9 D A Y 10 TAB. DYTOR PLUS TORASEMIDE SPIRONOLACTO NE 10 MG 50 MG P/O 1-0-0 √ √ √ √ √ INJ. 25% DEXTROSE DEXTROSE IV 1-1-1 √ √ √ √ TAB. RIFAGUT RIFAXIMIN 400MG P/O 1-1-1 √ √ √ √ √ √ √ √ √ INJ. OCTREOTID E OCTREOTIDE ACETATE 5 AMP IN 1OO ML NS IV @ 30ML / HR √ √ INJ.METRO GYL METRONIDAZO LE 100ML IV 1-1-1 √ √ √ √ T H. ALBUMIN HUMAN ALBUMIN 100 ML IV 1-0-0 √ SYP. POTKLOR KCL 2TSP P/O 2 TSP WITH WATER √ √ √ √ √ √ TAB. OROFER XT TOTAL ZN, FOLIC ACID,ELEMENT AL IRON, METHYLCOBAL AMIN 22.5MG 1.1MG 100MG1 .55MG P/O 0-1-0 √ √ √ Β- PROTIEN POWDER PROTIENS 2 TSP WITH MILK P/O 1-1-1 √
• 52. FOLLOW UP  DAY 1  PR : 120bpm  BP: 130/70 mmhg O/E  afebrile S/E  Pt is conscious and oriented.  CVS : S1S2 +  RS : B/L AEE  CNS : irritable and drowsy  P/A : hepatomegaly  1 PINT PCV TRANSFUSED
• 53. Abdominal Girth : 94cm Oral suctioning – hourly RT FEED : 100ML 1-1-1-1
• 54. ADVICE  INJ. METROGYL 100ML IV 1-1-1  INJ. XONE 1GM IV 1-0-1  INJ. PAN 40 MG IV 1-0-0  INJ. VITAMIN K 1 AMP IN 100ML NS IV 1-0-1  INJ. HEPAMERZ 2 AMP IN 100ML NS IV 1-1-1  INJ. EMSET 4MG IV 1-1-1  TAB. UDIBON 1-0-1  INJ. Pause 1 AMP IN 100ML NS 1-0-1  SYP. DUPHALAC 2 TSP √-√-√  INJ. 25% DEXTROSE 1-1-1  DUPHALAC BOWEL WASH 1-1-1-1-1-1  INJ. 1 PINT DNS WITH 2 AMP OPTINEURON 1-0-0-1  TAB. RFAGUT 400MG 1-1-1  INJ. OCTREOTIDE 5AMP IN 1 PINT NS @ 30ML/ HR
• 55. DAY 2 Pt on Mechanical Ventilation BP: 120/80 mmhg PR: 92 bpm Systemic examination CNS : conscious and oriented, B/L PERL + CVS : s1s2 + P/A : soft, distended. Spo2 : 98%
• 56. Investigations (17-01-2017)  Hb : 7.2  PT: T : 23.8 sec C: 13.5 sec INR: 1.86 APTT T: 28 sec C: 22 sec Creatinine : 1.0  Treatment As Per Chart.
• 57. Day 3  No fresh complaints.  PR: 72 bpm  BP: 110/80 mmhg  SPO2: 98%  CNS: conscious and oriented. Flaps +  RS: B/L AEE  CVS: s1s2 +  P/A: soft, distented. Free fluid +  Abdominal Girth : 91cm
• 58. Investigations HB : 6.6 g/dl ↓ ( 13.5- 17.5 g/dl )  WBC: 4800 cells/µl.  RBC: 2.04Million/µl. ↓  PLT: 73,000 cells/comm. ↓  DLC: polymorphs: 72% basophils: 00% eosinophils : 03% lymphocytes: 25% monocytes: 00%  ELECTROLYTES : Sodium : 144 (135-147 mEq / L ) Potassium :2.9 ( 3.5-5.2 mEq / L ) Treatment  As per chart
• 59. Day 4 No fresh complaints PR: 88bpm BP: 110/80 mmhg Spo2 : 96% CNS : conscious and oriented RS : B/L AEE CVS: s1 s2 + P/A: soft, distended.
• 60. Investigations  Potassium : 2.9 mEq/L CHILD PUGH SCORE  Score : 11  CLASS – C  1 YR MORTALITY – 55% , Two year survival – 35% Modified Maddrey's discriminant function – 54.7 TREATMENT  1 pint PCV transfused.  As per chart.
• 61. Day 5  Patient shifted to wards  No fresh complaints  PR: 86 bpm  BP: 114/76 mmhg  CNS: conscious and oriented RS: B/L AEE CVS: S1S2 + P/A: soft, distented.  Abdominal Girth : 90cm
• 62. Investigations  Potassium : 3.1 mEq/L TREATMENT  1 pint PCV transfused  As per chart.
• 63. Day 6  No fresh complaints  PR: 82 bpm  BP: 108/70 mmhg CNS: conscious and oriented RS: B/L AEE CVS: S1S2 + P/A: soft, distented, non-tender.
• 64. Investigations HB : 7.9 g/dl ↓ ( 13.5- 17.5 g/dl )  WBC: 5,100 cells/µl. ↓  RBC: 2.47Million/µl. ↓  PLT: 74,000 cells/comm. ↓  DLC: polymorphs: 60% basophils: 00% eosinophils : 04% lymphocytes: 34% monocytes: 02% RFT  Sr. Urea : 24  Creatinine : 1.0 TREATMENT  As per chart.
• 65. Day 7  No fresh complaints  PR: 88 bpm  BP: 110/70 mmhg CNS: conscious and oriented RS: B/L AEE CVS: S1S2 + P/A: soft, distented, non-tender. Abdominal Girth : 90cm
• 66. Investigations  ELECTROLYTES : Sodium : 136 (135-147 mEq / L ) Potassium :4.1( 3.5-5.2 mEq / L ) Chlorides : 101 ( 95-107 mEq / L ) LFT  ALT : 22 U/L (6-38)  AST : 57 U/L ( 6-40)  ALP : 49 U/L ( 35-140)  BILIRUBIN T : 4.6 MG% ( 0.2 – 1.0) D : 1.4 MG% ( 0.1 - 0.4 ) I : 3.2 MG % ( 0.1 – 0.6) Total protien : 5.9 Albumin : 2.0 Globulin : 3.9 A/G ratio : 1:1.9
• 67.  TREATMENT  1 pint PCV transfused  As per chart.
• 68. Day 8  No fresh complaints  PR: 86 bpm  BP: 108/74 mmhg CNS: conscious and oriented RS: B/L AEE CVS: S1S2 + P/A: soft, distented, non-tender. Abdominal Girth : 88cm
• 69. Treatment Advice  1 pint PCV transfused.  As per chart.
• 70. Day 9  No fresh complaints  PR: 84 bpm  BP: 130/90 mmhg CNS: conscious and oriented RS: B/L AEE CVS: S1S2 + P/A: soft, distented, non-tender. Abdominal Girth : 87cm
• 71. Investigations HB : 8.3 g/dl ( 13.5- 17.5 g/dl )  WBC: 5,300cells/µl.  RBC: 2.54Million/µl.  PLT: 1,50,000 cells/comm.  DLC: polymorphs: 70% basophils: 00% eosinophils : 02% lymphocytes: 208 monocytes: 00% ESR : 42 mm (<15mm) Complete hemogram  PCV : 23.3 % ( 40-50)  MCH : 32.5 pg ( 27-32) ↑  MCHC : 35.4% ( 32- 46 )  MCV : 92 fl ( 82 - 101)
• 72. PT test : 14 sec , control : 13sec INR : 1.0 (0.8-1.1) APTT test : 28sec, control : 22sec. Peripheral Smear Study Impression : NORMOCYTIC HYPOCHROMIC ANEMIA
• 73.  UPPER GI ENDOSCOPY Impression : GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY. Patient attendees are not willing for surgical intervention / banding.  TREATMENT AS PER CHART.
• 74. ESOPHAGEAL VARICES CONGESTIVE GASTROPATHY
• 75. Final Diagnosis  CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY.
• 76. DISCHARGE MEDICATION BRAND NAME GENERIC NAME DOSE ROUTE FREQUENC Y DURATION TAB. PAN PANTOPRAZOLE 40MG P/O 1-0-0 15 DAYS TAB. UDIBON URSEODEOXYCHOLIC ACID SILYMARIN 300MG 140MG P/O 1-0-1 15 DAYS TAB. RIFAGUT RIFAXIMIN 400MG P/O 1-1-1 15 DAYS HEPAMERZ SACHET WITH WATER L-ORNITHINE L-ASPARTATE 3 GM P/O 1-1-1 15 DAYS TAB. DYTOR PLUS TORASEMIDE SPIRONOLACTONE 10 MG 50MG P/O 1-1-0 15 DAYS SYP. DUPHALAC LACTULOSE 10ML P/O 1-1-1 15 DAYS B-PROTIEN POWDER WITH MILK PROTIEN 2 TSP P/O 1-1-1 15 DAYS TAB. OROFER XT TOTAL ZN, FOLIC ACID, ELEMENTAL IRON, METHYLCOBALAMIN 22.5MG 1.1MG 100MG 1.55MG P/O 0-1-0 15 DAYS
• 77. REVIEW  Review in medical OPD on WEDNESDAY after 15 days or incase of any emergencies.
• 78. PHARMACEUTICAL CARE PLAN
• 79. SUBJECTIVE EVIDENCES  C/O bleeding from gum after tooth extraction.  K/C/O alcoholic liver disease , admitted 6 months back.  Abdominal distension since 6 months.  B/L pedel edema – pitting type.
• 80. OBJECTIVE EVIDENCES HB : 6.9 g/dl ↓ ( 13.5- 17.5 g/dl )  WBC: 11,200 cells/µl. ↑  RBC: 2.07Million/µl. ↓  PLT: 1,12,000 cells/comm. ↓  ESR : 120mm ↑ (<15mm) PT: test : 20 sec , control : 13sec ↑ INR : 1.5 (0.8-1.1) ↑ APTT : test : 40sec, control : 22sec. ↑ PSS : normocytic normochromic anemia with neutrophilia.
• 81. LFT  ALT : 24 U/L (6-38)  AST : 71 U/L ( 6-40) ↑  ALP : 63 U/L ( 35-140)  BILIRUBIN T : 7.3 MG% ( 0.2 – 1.0)↑ D : 2.8 MG% ( 0.1 - 0.4 ) ↑ I : 4.5 MG % ( 0.1 – 0.6)↑ USG ABDOMEN  1. CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION AS EVIDENCED BY SPLEENOMEGALY AND GROSS TENSE ASCITES.  2. CHOLELITHIASIS UPPER GI ENDOSCOPY Impression : GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY.
• 82. ASSESSMENT  BY OBSERVING THE SUBJECTIVE AND OBJECTIVE EVIDENCES THE PATIENT WAS DIAGNOSED AS CIRRHOSIS OF LIVER WITH PORTAL HYPERTENSION, HEPATIC ENCEPHALOPATHY AND GRADE II OESOPHAGEAL VARICES WITH CONGESTIVE GASTROPATHY.
• 83. PLANNING GOALS TO BE ACHIEVED  To improve patients quality of life.  To prevent further progress of complications.  To reduce the gum bleeding.  To normalise the blood counts.  To reduce the ESR level.  To reduce the abdominal distension.  To reduce mortality rate.
• 84. GOALS ACHIEVED  Patients quality of life improved.  Minimised the further progress of complications.  Gum bleeding stopped.  Blood counts and levels are improving.  ESR level is decreased.  Abdominal distension reduced.
• 85. MONITORING PARAMETERS  CBC with complete hemogram.  ESR  LFT  Prothrombin time and INR  Ascites, abdominal distension, bleeding.  Sign and symptoms.
• 86. PHARMACIST INTERVENTION  Major drug-drug interactions.  POTASSIUM CHLORIDE – SPIRONOLACTONE Concurrent use of potassium and spironolactone may results in hyperkalemia.  METRONIDAZOLE-ONDANSETRON,  OCTREORIDE ACETATE- OFLOXACIN  ONDANSETRON- OCTREORIDE ACETATE  OFLOXACIN - ONDANSETRON  METRONIDAZOLE – OFLOXACIN  METRONIDAZOLE - OCTREORIDE ACETATE, all these maycauses QT interval prolongation.
• 87.  Moderate drug-drug interactions  ceftriaxone torsemide Cephalosporin antibiotics like cefTRIAXone can occasionally cause kidney problems, and using it with torsemide may increase that risk. The interaction is more likely to occur when the cephalosporin is given at high dosages by injection into the vein or when it is given to the elderly or individuals with preexisting kidney function impairment.  ofloxacin lactulose Ofloxacin can cause an irregular heart rhythm that may be serious and potentially lifethreatening, although it is a relatively rare side effect. The risk is increased if you have low blood levels of magnesium or potassium, which can occur with bowel cleansing preparations or excessive use of medications that have a laxative effect.
• 88.  Torsemide - Pantoprazole Using pantoprazole together with torsemide may cause a condition called hypomagnesemia, or low blood magnesium. Drugs known as proton pump inhibitors including pantoprazole can cause hypomagnesemia when used for a prolonged period. Banding has to be done to prevent the rupture of esophageal varices, rupture and bleeding further lead to more complications and increased mortality rate.
• 89. PATIENT COUNSELLING ABOUT DISEASE ;  Cirrhosis is a slowly progressing disease in which healthy liver tissue is replaced with scar tissue, eventually preventing the liver from functioning properly. The scar tissue blocks the flow of blood through the liver and slows the processing of nutrients, hormones, drugs, and naturally produced toxins.  Portal hypertension is an increase in the blood pressure within a system of veins called the portal venous system. Veins coming from the stomach, intestine, spleen, and pancreas merge into the portal vein, which then branches into smaller vessels and travels through the liver.
• 90.  Hepatic encephalopathy (HE) is the occurrence of confusion, altered level of consciousness, and coma as a result of liver failure. In the advanced stages it is called hepatic coma. It may ultimately lead to death. It is caused by accumulation in the bloodstream of toxic substances that are normally removed by the liver.  Esophageal varices are extremely dilated sub- mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.
• 91.  Portal hypertensive gastropathy ( congestive gastropathy ) refers to changes in the mucosa of the stomach in patients with portal hypertension ; by far the most common cause of this is cirrhosis of the liver. These changes in the mucosa include friability of the mucosa and the presence of ectatic blood vessels at the surface.
• 92. ABOUT MEDICATION  Take medications on time.  Don’t skip the medication.  Pantoprazole can be taken with or without food.  Rifaximin can be taken with or without food.  Udibon has to be taken with food.  Hepamerz sachet dissolved in a glass of water and taken after the meals.  Lactulose can be taken either with or without food. However, if you find it makes you feel sick this can be reduced by taking it with water, fruit juice or meals. You can take lactulose undiluted, or you can mix the required dose of lactulose into a drink of water or fruit juice.  Swallow each dose straight away. Don't keep it in your mouth as the sugar content may lead to tooth decay
• 93. LIFE STYLE MODIFICATIONS  Lifestyle changes cannot cure cirrhosis, but they can help to delay or stop progression of the disease, reduce the severity of symptoms, and help prevent complications.  Avoid drinking alcohol.  Eat a balanced diet.  Avoid raw seafood.  Discuss the appropriate amount of protein you need to eat, an adult who weighs 68 kilograms needs at least 54 grams of protein each day  Depending on your condition, you may either need to increase or decrease protein intake.  Take any vitamin or mineral supplements recommended by your doctor.  A low-salt diet may be needed to reduce fluid retention.  Get your doctor’s approval for all medicines. For example, acetaminophen (such as Tylenol) can speed up liver damage. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs)-for example, ibuprofen and naproxen -increase the risk of variceal bleeding if you have enlarged veins (varices) in the digestive tract.
• 94.  Get vaccines for flu, pneumonia, and hepatitis.  Put your feet up to reduce swelling.  Be careful with herbs and dietary supplements. Herbal remedies, herbal combinations and dietary supplements aren’t subject to the same approval process as medication and some may harm the liver. A few that have caused liver problems are cascara, chaparral, comfrey, kava and ephedra.  Stop smoking. Quitting tobacco use will improve your overall health, which may help make you a better candidate for a liver transplant if you need one.  Increased caffeine consumption is most beneficial for people who are at high risk for developing chronic liver disease, It's important to note if you already have cirrhosis, coffee isn’t powerful enough to reverse damage
• 95. STANDARD TREATMENT Complication Treatment Approach Monitoring Parameter Outcome Assessment Ascites Diet, diuretics, paracentesis, Daily assessment of weight Prevent or eliminate ascites and its secondary complications Variceal bleeding Pharmacologic prophylaxis Endoscopy, vasoactive drug therapy (octreotide), ligation or sclerotherapy, volume resuscitation, pharmacologic prophylaxis Child-Pugh score, endoscop, CBC, evidence of overt bleedingy, CBC Acute: control acute bleed Chronic: variceal obliteration, reduce portal pressures Hepatic encephalopathy Ammonia reduction (lactulose, cathartics), elimination of drugs causing CNS depression, limit excess protein in diet Grade of encephalopathy, EEG, psychological testing, mental status changes, concurrent drug therapy Maintain functional capacity, prevent hospitalization for encephalopathy, decrease ammonia levels, provide adequate nutrition
• 96. LIVER TRANSPLANTATION  The complications seen in patients with chronic liver disease are essentially functional as a secondary effect of the circulatory and metabolic changes that accompany liver failure. Consequently, liver transplantation is the only treatment that can offer a cure for complications of end-stage cirrhosis. However, patient selection, evaluation, and pre- and postsurgical management are beyond the scope of this review. The surgical procedure is very demanding and ranges from 4 to 18 hours depending on outcome. Numerous anastomoses and sutures, and many disconnections and reconnections of abdominal and liver tissue, must be made for the transplant to succeed, requiring an eligible recipient and a well-calibrated live or cadaveric donor match. The large majority of liver transplants use the entire liver from a non-living donor for the transplant, particularly for adult recipients. A major advance in pediatric liver transplantation was the development of reduced size liver transplantation, in which a portion of an adult liver is used for an infant or small child
• 97. Liver donor requirements  Any member of the family, parent, sibling, child, spouse or a volunteer can donate their liver. The criteria for a liver donation include:  Being in good health  Having a blood type that matches or is compatible with the recipient's, although some centres now perform blood group incompatible transplants with special immuno suppression protocols  Having a charitable desire of donation without financial motivation  Being between 18 and 60 years old  Being of similar or bigger size than the recipient  Before one becomes a living donor, the donor must undergo testing to ensure that the individual is physically fit. Sometimes CT scans or MRIs are done to image the liver. In most cases, the work up is done in 2–3 weeks.
• 98. Band Ligation / Banding  Endoscopy band ligation is used to treat enlarged veins in the esophagus, the tube connecting the throat to the stomach. If left untreated esophageal veins (varices) can spontaneously rupture and cause severe bleeding.  The procedure is performed during an upper gastrointestinal endoscopy. A local anesthetic is given to numb the throat and sedation medication will also be given through IV to help you relax/sleep through the procedure.  A scope is placed in the mouth down to the esophagus. When varices are found, tiny elastic bands are placed around the enlarged veins in the esophagus to tie them off so they can’t bleed. The banded varices are then eventually sloughed after a few days and the esophagus is much less likely to bleed after it’s healed.

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• v.9(1); 2022

Educational Case: Evaluating a patient with cirrhosis

The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see https://www.journals.elsevier.com/academic-pathology/news/pathology-competencies-for-medical-education-pcme . 1

Primary objective

Objective HB1.6: Cirrhosis. Classify types of cirrhosis, in terms of etiology, pathogenesis, morphologic pattern (gross and microscopic),and their relationship to neoplasia.

Competency 2: Organ system pathology; Topic: Hepatobiliary (HB); Learning goal 1: Hepatitis.

Secondary objectives

Objective HB3.4: Radiology of cirrhosis. Identify the major space occupying lesions that may be seen on radiographic imaging of the normal and cirrhotic liver, and discuss the complications of cirrhosis.

Competency 2: Organ system pathology; Topic: Hepatobiliary (HB); Learning goal 3: Hepatic neoplasms.

Objective CHEM1.4: Liver and gastrointestinal disease. Discuss the clinical presentation and the pathophysiologic bases of liver and gastrointestinal diseases including the efficient use of laboratory tests to make a definitive diagnosis and manage the disease.

Competency 3: Diagnostic medicine and therapeutic pathology; Topic: Chemistry (CHEM); Learning goal 1: Pathogenesis, diagnosis, and treatment of common disorders.

Patient presentation

A 56-year-old man accompanied by his wife presents to the clinic with chief concern of vague abdominal pain for the past two weeks. The patient has also experienced progressive shortness of breath, bloating, and fatigue during this time frame. His medical history is significant for obesity and lifestyle-controlled diabetes mellitus. Surgical history is significant for repair of a femoral fracture following a motor vehicle accident in 1990, which required a blood transfusion. The patient is unsure of his vaccination status. He takes no medications other than over-the-counter acetaminophen for a recent cold. He works as a marketing executive and recently traveled to several European and Southeast Asian countries on business. He does not report using tobacco products or illicit drugs. The patient states that he drinks occasionally, at which point his wife informs the physician that he consumes a six-pack of beer after work each day and more on the weekends.

Diagnostic findings, Part 1

Vital signs include a temperature of 97 ​°F, a heart rate of 87 beats per min, a respiratory rate of 18 breaths per min, an oxygen saturation of 94%, and a blood pressure of 137/86 ​mm Hg. Physical examination shows an uncomfortable-appearing male in no acute distress. The cardiac exam demonstrates regular rate and rhythm, with no rubs, or gallops. Lung auscultation demonstrates bilateral basilar crackles. Abdominal examination reveals a soft, protuberant abdomen with shifting dullness to percussion. There is pitting edema present to the mid-tibia bilaterally, with multiple bruises on the lower extremities.

Questions/discussion points, Part 1

What is the differential diagnosis for this patient's history and physical examination findings.

The differential diagnosis for abdominal pain with associated peripheral edema, fatigue, and shortness of breath is broad and includes heart failure, liver failure, renal failure, nephrotic syndrome, malnutrition, malabsorption, myxedema, lymphatic obstruction, and trauma. 2 The patient has specific risk factors for heart failure (obesity, diabetes mellitus, high alcohol consumption), liver disease (obesity, high alcohol consumption, hepatitis risk from travel or transfusion, and acetaminophen use), coagulopathy (bruises), and renal failure (diabetes mellitus).

Diagnostic findings, Part 2

Given the patient's broad differential, a comprehensive work-up is initiated including an electrocardiogram (EKG), B-type natriuretic peptide (BNP), complete blood count (CBC), coagulation panel, and complete metabolic panel (CMP). EKG findings are within normal limits, and the remaining laboratory results are displayed in Table 1 , Table 2 , Table 3 .

Table 1

Complete blood cell count with differential.

Table 2

Coagulation panel.

Table 3

Complete metabolic panel with B-type natriuretic peptide.

Questions/discussion points, Part 2

How do this patient's laboratory results help to differentiate between causes of coagulopathy.

The patient's elevated prothrombin time (PT), activated thromboplastin time (aPTT), and international normalized ratio (INR) are significant and suggestive of coagulopathy. These measurements are used to evaluate the integrity of the patient's clotting cascade. 2 , 3 PT is a measurement of clotting speed via the extrinsic or tissue factor and common pathways. 2 , 3 PT is used to assess the activity of clotting factors VII, V, X, II, and fibrinogen and can be prolonged if these are deficient or if there is an inhibitor. Deficiency could occur in the case of vitamin K deficiency, warfarin therapy, liver disease, and disseminated intravascular coagulation. 2 , 3 INR is a calculated standardization of the PT, used similarly to PT for assessment of extrinsic and common pathway clotting time and for monitoring the effects of warfarin pharmacotherapy. 2 aPTT measures the clotting time of the intrinsic and common pathways of the clotting cascade and is elevated in the setting of deficiencies in factors XII, XI, IX,VIII, V, X, II, or fibrinogen. aPTT can be elevated in some types of von Willebrand disease due to stabilization of factor VIII, antiphospholipid syndrome, in the presence of inhibitors, and in disseminated intravascular coagulation (DIC), severe vitamin K deficiency, or liver disease. 2 aPTT is also used in monitoring the effects of heparin pharmacotherapy. 2 Notably, vitamin K deficiency, DIC, and liver disease affect both PT and aPTT. 2 The presence of coagulopathy affecting both arms of the clotting cascade as reflected by the abnormal PT and aPTT measurements should be considered in context of the synthetic function of the liver.

The patient's CBC is also significant for low red blood cell count (RBC), low hemoglobin and hematocrit (Hgb and Hct, respectively), an elevated mean corpuscular volume (MCV), and an elevated red cell distribution width (RDW), all of which suggest megaloblastic anemia. Megaloblastic anemia can occur secondary to a micronutrient vitamin B 12 or folate deficiency. 4 , 5 , 6 In patients who consume large quantities of alcohol to the exclusion of more nutritious food may develop nutrient deficiencies. Folate and vitamin B 12 deficiencies impair hematopoiesis and primarily cause a decrease in number of RBCs. More severe cases can cause a significant decrease in WBCs and platelets as well, resulting in a pancytopenia. 4 It is likely that megaloblastic anemia is contributing to this patient's symptoms of fatigue and shortness of breath.

How do this patient's laboratory results help to differentiate between causes of liver disease?

CMP demonstrates low total protein and low albumin, both of which are indicators of the synthetic capacity of hepactocytes. 7 , 8 The major contributors to the total protein measurement are globulin and albumin fractions. 7 The globulin fraction includes enzymes, including clotting factors produced by hepatocytes, as well as immunoglobulins produced by plasma cells, and the albumin fraction consists exclusively of albumin produced by hepatocytes. 7 Damage to hepatocytes that results in decreased synthetic capacity is thus revealed by decreased albumin and total proteins measurements in the setting of coagulopathy. 7 , 8 Hepatocyte integrity can be further assessed with the measurement of serum levels of hepatocellular enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and should be considered in relation to biliary excretory function measured with alkaline phosphatase (ALP) and bilirubin levels. 8

This patient's metabolic laboratory studies demonstrate a hepatocellular pattern of liver injury as suggested by markedly elevated hepatocellular enzymes AST and ALT out of proportion to an also elevated ALP. 8 , 9 , 10 A cholestatic pattern of liver injury would be more likely if the ALP was elevated out of proportion to the AST and ALT, accompanied by a more severe hyperbilirubinemia. This pattern would warrant further consideration of biliary obstructive and non-hepatic etiologies. 8 , 9 , 10 The hepatocellular pattern of liver injury can be further characterized by the AST:ALT ratio, which is ​> ​1 in this case. 8 , 9 The AST:ALT ratio should be ​< ​1 in a normal person without elevations, and elevated values with an AST:ALT ratio > 1 are strongly suggestive of alcoholic liver disease, due to a variety of reasons related to alcohol metabolism in hepatocytes. 9 Hepatocellular patterns of liver injury closer to an AST:ALT ratio of < 1 are more suggestive of metabolic-associated fatty liver disease (MAFLD). 9 , 11 AST and ALT levels can decline in chronic liver disease as the severity progresses to end-stage liver disease and hepatocyte death removes the source of these enzymes. 12

How do this patient's laboratory studies help to differentiate between causes of hyponatremia?

The patient's CMP is also significant for low sodium, which in the context of physical exam findings of peripheral edema and shifting dullness to abdominal percussion indicating ascites, are suggestive of a hypervolemic state. This is consistent with hypervolemic hyponatremia, in which inappropriate water retention results in a dilutional hyponatremia, often secondary to renal failure, nephrotic syndrome, congestive heart failure, or cirrhosis. 13 , 14 , 15 In cirrhotic patients, the lack of oncotic pressure secondary to hypoalbuminemia results in a volume shift from intravascular spaces to extracellular compartments, as demonstrated by this patient's ascites and peripheral edema. 14 , 16 , 17 It is also significant that the patient's brain natriuretic peptide (BNP) is above normal limits. BNP is a hormone released in response to the increased cardiac ventricular wall stress experienced in a state of increased ventricular blood volume. It stimulates natriuresis, diuresis, and systemic vasodilation, while inhibiting the renin–angiotensin–aldosterone system to decrease blood pressure and increase cardiac ejection fraction. 18 , 19 This patient's slightly elevated BNP is evidence of hypervolemia, but is significantly less than would be expected in decompensated heart failure. 20 , 21 , 22 Thus, heart failure is unlikely to be the underlying etiology for this patient's hypervolemic hyponatremia. Renal failure is also made less likely by the patient's low creatinine, which is removed by the kidney and elevated in the setting of acute kidney injury and renal failure. 8 , 23 Creatinine is generated through the metabolism of creatine by hepatocytes, so chronic liver disease and loss of hepatocyte synthetic function is commonly associated with lower levels of creatinine. 16 , 24

Diagnostic findings, Part 3

It is concluded that the patient's symptoms are likely due to a hepatic disease process, and he is given a preliminary diagnosis of cryptogenic liver failure, with alcoholic liver disease as the most likely etiology. The remainder of the differential for liver disease includes the following: viral hepatitis, autoimmune hepatitis, drug- and toxin-induced liver injuries, metabolic-associated fatty liver disease, hemochromatosis, Wilson disease, and α1-antitrypsin deficiency. 8 Appropriate laboratory tests and an abdominal ultrasound with sonoelastography are ordered. The results are displayed Table 4 , Table 5 , Table 6 . 25 , 26 , 27 , 28

Table 4

Hepatitis panel.

Table 5

Ultrasonography findings.

Table 6

Sonoelastography.

Questions/discussion points, Part 3

How do this patient's additional laboratory results narrow the differential diagnosis.

The results of the hepatitis panel are significant for positivity for hepatitis B surface antibody (HBsAb) and negativity for the remainder of the tested antigens and antibodies. HBsAb positivity suggests previous exposure to the hepatitis B surface glycoproteins, which occurs during vaccination or infection. 29 During infection by the hepatitis B virus (HBV), the host's immune system is also exposed to the hepatitis B core proteins (HBc) and mounts an immune response that results in hepatitis B IgM core antibody (HBcAb-IgM) positivity during acute infection. This is followed by hepatitis B IgG core antibody (HBcAb-IgG) positivity later in the disease course and following resolution. 29 Hepatitis B type e antigen (HBeAg) detection is associated with a high level of active viral replication resulting in increased infectivity. 29 Detectable HBsAb with undetectable levels of other HBV antigens and antibodies suggests that the patient was successfully vaccinated against HBV and is unlikely to have been infected previously. 29 Undetectable levels of hepatitis A IgM, IgG, and hepatitis C antibodies (HA Ab-IgM, -IgG and, HC Ab, respectively) suggests that the patient has neither been nor is currently infected with the hepatitis A or C viruses. 29 Thus the patient's current presentation is unlikely to be related to a viral hepatitis.

What focal and diffuse liver lesions can be demonstrated with ultrasonography?

Abdominal ultrasound is a commonly utilized tool for detecting and characterizing lesions of the liver. 30 Normal liver parenchyma is echogenic with a homogenously porous appearance and visibly branching vasculature. 30 Abnormal ultrasonographic findings can be indicative of focal and diffuse liver disease depending on the morphologic pattern. 27 , 30 A hepatic cyst, the most common and often incidentally found space-occupying lesion of the liver, can be visualized as a round anechoic space with a variable degree of septation depending on lesion complexity. 30 , 31 A hepatic abscess secondary to infectious etiology can have a variable presentation on ultrasonography including but not limited to septations, debris, and the presence of gas demonstrated as bubbles or an air-fluid level. 32 Hemangiomas are the most common benign liver tumor and appear as well-defined hyperechoic lesions with vascular activity visible with use of color-Doppler. 33 Focal nodular hyperplasia (FNH) is the second most common benign liver tumor and is thought to result from a hyperplastic response to an arteriovenous malformation. 34 Ultrasonographic features of FNH are variable, but approximately 20% of cases demonstrate a central scar with disruption of surrounding vasculature. 35 A hepatocellular adenoma is a benign neoplasm of the liver associated with oral contraceptive use that is usually asymptomatic unless the neoplasm ruptures and bleeds. 36 This neoplasm is often characterized on ultrasonography as a solitary, well-circumscribed mass of variable echogenicity. 37

Diffuse liver disease includes etiologies such as the various viral and immune hepatitides, storage diseases, hepatic steatosis, fibrosis, and cirrhosis. 38 Ultrasonography findings are often non-specific in the case of diffuse liver disease, and biopsy is usually required to differentiate between the various etiologies. 38 In cases of acute hepatitis, the most common finding is hepatomegaly with diffusely decreased echogenicity. 38 Chronic hepatitis can be demonstrated by the presence of focal or diffuse hepatic steatosis and fibrosis developed in response to prolonged periods of parenchymal damage and regeneration. 38 Diffuse hepatic steatosis can also occur in cases of alcohol abuse, metabolic-associated steatohepatitis, chronic hepatitis, glycogen storage diseases, and various drug therapies. 39 Heterogenous or coarsened hepatic echotexture on ultrasonography is evidence of a loss of parenchymal uniformity as seen in cases of cirrhosis, metabolic storage diseases, and chronic hepatitis. 40 , 41 Surface nodularity can be a useful finding in differentiating cirrhosis from other forms of diffuse liver disease, as metastatic tumor nodules are the only other notable disease process that demonstrates this ultrasonographic finding. 38

A feared complication of diffuse liver disease, hepatocellular carcinoma (HCC) is the most common primary liver cancer in adults and can present as a focal, multifocal, or diffuse lesions on ultrasonography. 27 , 38 Over 80% of new cases of HCC occur in the setting of cirrhosis. 42 Thus cirrhotic patients are currently recommended to undergo biannual abdominal ultrasonography as a non-invasive and cost-effective screening modality. 42 In addition to cirrhosis, risk factors for HCC include any disease process which results in chronic hepatic injury, such as the immune and viral hepatitides, alcohol consumption, storage diseases, and metabolic-associated steatohepatitis. 43 , 44 Focal HCC lesions tend to be hypoechoic compared to surrounding hepatic parenchyma. As focal HCC lesions grow, they become increasingly heterogenous and echogenic, demonstrating features of fat accumulation, necrosis, and calcification, or development of a central scar that can be misinterpreted as FNH. 38 Advanced HCC usually presents in patients with underlying diffuse liver disease as multifocal lesions with variable echogenicity, and can appear similar to metastases on imaging. 38 , 43 , 44 HCC foci developing within regenerative nodules demonstrate a nodule-in-nodule appearance on magnetic resonance imaging. 45 Diffuse or infiltrative HCC presents with scattered hepatic nodularity, rather than distinct masses, that is difficult to differentiate from cirrhosis based on advanced imaging alone. 46

How do this patient's ultrasonography findings affect the differential diagnosis?

Abdominal ultrasound findings of mild hepatosplenomegaly, liver surface nodularity with heterogenous echotexture, and segmental hypertrophy and atrophy are consistent with cirrhosis. 26 Abnormal blood flow resultant from the disruption of normal hepatic cellular architecture results in segmental hypertrophy of the caudate lobe and lateral segments of the left lobe, with concurrent segmental atrophy of the right lobe and medial segments of the left lobe. 47 Nodule formation occurs secondary to fibrotic and regenerative processes involving both stromal and parenchymal hepatocytes, and is seen as the nodular surface and heterogenous texture on this patient's abdominal ultrasound. 8 , 47 Diffusely increased echogenicity of the hepatic parenchyma when compared to the right kidney is indicative of abnormal accumulation of lipids within hepatocytes, that occurs in response to chronic disease processes. 38 Hepatic echogenicity is normally similar to or greater than that of the renal cortex, which serves as a standard of comparison in determination of lipid accumulation. 38 Additional findings of an enlarged splenic vein and ascites are suggestive of portal hypertension and hypoalbuminemic edema, both of which are complications of cirrhosis. 26 Sonoelastography utilizes sonography and the application of mechanical pressure to evaluate tissue stiffness and elasticity, and it has been demonstrated to have a high negative predictive value when ruling out cirrhosis. 48 Stiffness and elasticity are measured in kilopascals (kPa), with increasing values correlating to higher stages of fibrosis. 48 , 49 Sonoelastography values over 10 ​kPa suggest advanced chronic liver disease, over 12.5 ​kPa suggest cirrhosis, and those exceeding 21 ​kPa suggest clinically significant portal hypertension. 49 , 50 This patient's sonoelastography findings suggest the presence of cirrhosis with clinically significant portal hypertension, which is further supported by previous physical exam, laboratory, and ultrasound findings. Despite recent and improved non-invasive modalities for assessment of liver fibrosis and cirrhosis, liver biopsy remains the gold standard for identification and classification of cirrhosis. 49

Diagnostic findings, Part 4

An ultrasound-guided liver biopsy is performed, and the results are in Fig. 1 , Fig. 2 , Fig. 3 .

Liver biopsy. At low power, the liver biopsy shows steatosis throughout, and inflammation (upper right and middle left). Bands of fibrosis are visible at low power (arrows). H&E, 40x.

Liver biopsy. At higher power, bands of fibrosis surrounding a nodule are seen (arrows). The hepatocytes contain numerous clear fat droplets, and there is predominantly lymphocytic portal inflammation in the upper right. H&E, 200x

Liver biopsy. Trichrome stain highlights in blue, the circumferential bands of fibrosis surrounding regenerative nodules. Trichrome stain, 100x.

Questions/discussion points, Part 4

What is the cellular architecture of the liver.

Hepatic micro-architecture is structured in terms of 1- to 2-mm diameter lobules composed of portal triads of hepatic arteries, portal veins, and bile ducts, surrounding plates of hepatocytes which radiate towards a central vein at the center. 8 , 51 Hepatocytic trabeculae are separated by intervening sinusoidal spaces in which a mixture of portal venous and hepatic arterial blood flows from the portal tract to the central vein. 8 , 51 Alternatively, the micro-architecture can be classified into acini made of three zones according to distance from the portal tract, which correlate to their respective degrees of oxygenation. 8 , 51 , 52 The area adjacent to the portal tract is zone 1, which is the most well-oxygenated region, the intermediate zone between the portal tract and the central vein is zone 2, and the area adjacent to the central vein is zone 3, which is the least oxygenated. 8 , 51 Non-parenchymal cells of the liver include liver sinusoidal endothelial cells (LSECs), Kupffer cells (KCs), and hepatic stellate cells (HSCs). 8 , 51 , 52 Fenestrated LSECs separate the sinusoidal spaces from the space of Disse which is occupied by hepatocytic microvilli responsible for transportation of nutrients from sinusoidal blood to the hepatocytes. 8 , 51 KCs are phagocytic monocytes present on the luminal aspect of LSECs. 8 , 51 , 52 HSCs occupy the space of Disse and are the primary mediators of hepatic fibrosis. 8 , 51 , 52 Bile canaliculi border hepatocytes and drain ultimately into the terminal bile ducts of the portal tracts. 8 , 51 , 52

What is the process of hepatocyte damage?

Irreversible injury to hepatocytes results in either apoptotic or necrotic cell death. 8 , 52 The former commonly occurs secondary to viral, autoimmune, or drug- and toxin-induced hepatitides, and the latter often occurs secondary to ischemic and hypoxic injury. 8 , 52 Hepatocyte apoptosis is a form of cell death whereby caspase cascades are activated, initiating an organized process of pyknosis, karyorrhexis, and cellular fragmentation into acidophil bodies, which appear intensely eosinophilic on staining. 8 Hepatocyte necrosis occurs when a hepatocyte is unable to maintain osmotic regulation, so it swells, and ruptures, releasing cytoplasmic contents, including pro-inflammatory cytokines, into the extracellular compartment. 8 Confluent necrosis is a phenomenon in which areas of necrosis are localized to one or more lobular acinar zones. Hepatocyte drop-out begins near the central vein in zone 3, where oxygenation is at its lowest within the acinus, and extends contiguously toward the penetrating hepatic vessels through zone 2 and zone 1. When necrosis involves multiple adjacent acini of multiple lobules it is described as bridging necrosis. 8 Confluent and bridging necrosis are the result of acute or severe chronic hepatocyte injury. 8

What is the response to hepatocyte apoptosis and necrosis?

KCs lining fenestrated LSECs are activated in response to hepatocyte injury. 8 , 17 , 52 KCs contribute to the cellular response to hepatocyte damage by producing the following cytokines: platelet-derived growth factor (PDGF), tumor necrosis factor alpha (TNF-a), endothelin-1 (ET-1), monocyte chemoattractant protein-1 (MCP-1), and transforming growth factor beta (TGF-b). PDGF and TNF-alpha stimulate HSC proliferation and activation of previously quiescent HSCs. ET-1 stimulates vasoconstriction, TGF-b stimulates fibrogenesis, and MCP-1 and PDGF stimulate chemotaxis of activated HSCs to the site of injury. 8 , 17 , 52 KCs further contribute to the activation of previously quiescent HSCs by degrading collagen type IV in the space of Disse. Additionally, KCs phagocytize hepatocyte apoptotic bodies and produce pro-apoptotic ligands, such as Fas. 8 , 17 , 52 The net effects of KC activation and function include hepatocyte dysfunction and death, HSC activation and chemotaxis, and stimulation of fibrogenesis. 8 , 17 , 52

Quiescent vitamin A-rich HSCs located in the space of Disse function as lipid-storing cells until they become active and convert to myofibroblasts. 8 , 17 , 52 Sources of activation include cytokines and chemokines produced by KCs and other non-parenchymal cells, pro-inflammatory cytokines associated with chronic inflammation, direct stimulation by toxins, and disruption of the extracellular matrix. 8 Myofibroblasts are highly fibrogenic and contribute significantly to the generation of types I and III collagen, which form fibrolysis-resistant collagen bundles through cross-linking and deposition of extracellular matrix within the space of Disse. 53 In a state of chronic liver disease, fibrogenesis is perpetuated and fibrous septa formed at the sites of parenchymal loss begin to surround regenerating hepatocytes, distorting the microarchitecture of the hepatic lobules and producing the nodularity of cirrhosis. 1 , 3 , 8 Fibrosis and fibrolysis are concurrent bidirectional processes, with active liver disease favoring the former and remitting liver disease favoring the latter. 8 , 17 , 52 Regression of cirrhotic nodularity with reversal of fibrotic scar formation has been demonstrated in cases where the insulting factor is removed before permanent microarchitectural change takes place. 54 Vascular architecture is also disrupted by this remodeling process, resulting in intralobular vascular shunts within the fibrous septa. 8 , 17 , 52

What are the types of cirrhosis and how can they be differentiated on histopathology?

Cirrhosis can be classified based on both the morphologic findings and the underlying etiology. 55 Morphological categories are separated into the following: micronodular, macronodular, and mixed. 55 In micronodular cirrhosis, nodules are uniform and less than 3 ​mm in diameter. 51 They are irregular and more than 3 ​mm in diameter in macronodular cirrhosis, and varied sizes with features of both in mixed cirrhosis. 51 Mixed cirrhosis is often an intermediate through which micronodular cirrhosis progresses to macronodular cirrhosis. 55 A micronodular pattern of cirrhosis can be seen in cases of cirrhosis secondary to alcoholic liver disease, hemochromatosis, and hepatic venous and biliary outflow obstructions. 55 Macronodular cirrhosis is more commonly seen in cases of chronic viral hepatitis, primary biliary cholangitis, Wilson disease, and α-1 antitrypsin deficiency. 8 , 55 Etiologies of cirrhosis can also be classified based on their pattern of hepatocyte damage and subsequent fibrosis. 55 For example, cirrhosis secondary to alcoholic liver disease and MAFLD demonstrate an initial centrilobular and perivenular pattern of fibrosis that advances toward the periportal acinar zones with progression of disease. Other etiologies of chronic liver disease that result in cirrhosis, including viral hepatitides, autoimmune hepatitis, chronic cholestatic disease, and metabolic and storage diseases, can be distinguished by a predominance of periportal fibrosis. 56

What are the histopathologic features of alcoholic liver disease?

Alcoholic liver disease is characterized by macrovesicular steatosis most prominent in acinar zone 3, or the perivenular area, continuing outward through acinar zones 2 and 1 in increasingly severe disease states. 57 Alcohol-metabolizing cytochromes are present in disproportionate amounts in the centrilobular hepatocytes when compared to the periportal hepatocytes. 56 Metabolism of alcohol and byproduct formation place additional stress on these centrilobular hepatocytes and are responsible for the hepatocellular ballooning pattern of hepatocellular injury seen on histopathological evaluation of alcoholic liver disease. 56 Hepatocellular ballooning and subsequent necrosis constitutes the primary mechanism of injury in alcoholic liver disease, which progresses to a micronodular cirrhosis with perivenular and pericellular fibrosis, visible as blue-stained collagen on Masson trichrome stain. 56 Mallory-Denk bodies are damaged filamentous inclusions in hepatocytes observable on hematoxylin and eosin (H&E) and chromotrope aniline stains in chronic liver disease, including alcoholic liver disease and cirrhosis. 56 The presence of centrilobular fibrosis accompanied by obliteration of the central vein, and perivenular necrosis with Mallory-Denk bodies constitutes sclerosing hyaline necrosis, a histopathological finding consistent with alcoholic cirrhosis. 58 Megamitochondria may also be seen on H&E stain in cases of alcoholic cirrhosis. 57 Metabolic-associated fatty liver disease demonstrates a similar histopathological pattern to that of alcoholic liver disease. Notable differences that exist between MAFLD and alcoholic liver disease include more significant steatosis in the former than the latter and more significant inflammation in latter than the former. 59 While also present in MAFLD, perivenular fibrosis tends to be more significant in alcoholic liver disease. 59 This patient's liver biopsy findings are consistent with alcoholic cirrhosis.

How does the pathophysiology of cirrhosis explain its clinical presentation and complications?

The symptomatic presentation of cirrhosis and its complications occurs secondary to increased intrahepatic vascular resistance, loss of synthetic and metabolic functions of hepatocytes, and prolonged regenerative processes. 60 Prolonged hepatocyte injury and subsequent fibrogenesis results in increased formation of collagen in the space of Disse and the loss of endothelial fenestration, a process which is referred to as sinusoidal capillarization. 60 Vascular reorganization is accompanied by fibrotic expansion of the portal tract and fibrosis of the central vein which results in portal hypertension. 60 Decreased synthetic capacity of the liver due to loss of functional hepatocytes results in diminished nitric oxide production and contributes to increased intrahepatic vascular resistance and portal hypertension. 61 This leads to the development of intrahepatic portal-systemic shunts that results in collateral circulation which bypasses normal liver flow. 17 , 52 , 60 While these shunts help to reduce portal hypertension, they enlarge over time and result in many serious and often life-threatening complications of cirrhosis. 17 , 52 , 60 Esophageal varices, a major complication of portal hypertension and vascular congestion, are abnormally enlarged veins in the esophagus that pose a significant bleeding risk to cirrhotic patients. 61

Intrahepatic shunting also leads to decreased metabolism of ammonia by functional hepatocytes and subsequently increased bioavailable ammonia in systemic circulation. 17 , 52 , 60 Increased flow of nitrogen-rich blood to the brain leads to the development of hepatic encephalopathy, a neuropsychiatric condition characterized by memory impairment, asterixis, myoclonus, and personality and behavioral changes. 62 Increased blood flow from portal-systemic shunting further contributes to the development of hepatopulmonary and hepatorenal syndromes. 17 , 52 , 60 In hepatopulmonary syndrome, pulmonary capillary dilation causes a ventilation–perfusion mismatch presenting with dyspnea, platypnea, and hypoxemia, such as in this patient's case. 63 Hepatorenal syndrome occurs when splanchnic vasodilation secondary to intrahepatic shunting leads to renal hypoperfusion and subsequent activation of the renin-angiotensin-aldosterone system, ultimately progressing to renal failure. 64 , 65 Vascular congestion secondary to portal hypertension and shunting also contributes to the development of splenomegaly and caput medusa, two prominent physical exam findings in cirrhotic patients. 60

Both portal hypertension and the decreased synthesis of albumin by hepatocytes contribute to the formation of ascites, the accumulation of protein-rich fluid in the abdominal cavity. 60 Ascites is a common finding in cirrhotic patients and can become complicated by infection resulting in spontaneous bacterial peritonitis. 66 This commonly presents with fever and altered mental status which can be accompanied by chills, abdominal pain, nausea, and vomiting. 66 Loss of hepatocytes contributes to decreased metabolic function, including bilirubin and estradiol metabolism. Reduced excretion of bilirubin results in intrahepatic cholestasis and jaundice, and reduced estradiol metabolism leads to hyperestrogenism and its effect of palmar erythema, gynecomastia, and spider angiomata, which are most prevalent on the upper trunk and face. 60

What are the next steps in management for this patient?

Management of this patient begins with determination of whether the cirrhosis is compensated or decompensated. 67 Compensated cirrhosis is an early asymptomatic stage of the disease process without complications of portal hypertension and liver dysfunction. 67 Decompensated cirrhosis is an acute deterioration in liver function with the presence of complications, and it can be precipitated by many etiologies such as medications, infections, hypovolemia, electrolyte imbalance, and alcohol use. 68 , 69 In this patient, the presence of complications suggests decompensated cirrhosis. 68 In the absence of life-threatening complications, such as variceal hemorrhage, management is directed toward symptomatic treatment, initiation of relevant surveillance programs, risk reduction, and patient education. 68 The presence of new-onset ascites warrants a diagnostic paracentesis with analysis of cell count, total protein, albumin, and bacterial culture with sensitivity testing. 69 Cirrhotic patients are effectively immunosuppressed and frequently decompensate due to infections such as spontaneous bacterial peritonitis. 68 In the absence of a known prior episode of spontaneous bacterial peritonitis, results from the diagnostic paracentesis will be used to determine if the patient requires oral antibiotic prophylaxis. 69 Reduction of ascites is accomplished with salt restriction and diuretic pharmacotherapy such as spironolactone with or without loop diuretics. 68 , 69 Hepatic encephalopathy, which is not present in this patient, is managed with the administration of lactulose with or without rifaximin to encourage stooling and elimination of nitrogen from the systemic circulation. 69

Health surveillance for this patient will include regular screenings for HCC and esophageal varices. 44 , 61 , 69 Screening for HCC is recommended every six months for cirrhotic patients and is performed via right upper quadrant ultrasonography. 69 Screening for esophageal varices via endoscopic gastroduodenoscopy (EGD) is indicated in newly diagnosed compensated cirrhosis, unless sonoelastography demonstrates a liver stiffness of at least 20 ​kPa and CBC demonstrates a platelet count of at least 150,000. 70 If no varices are detected on initial screening, EGD is repeated every three years in the absence of ongoing liver injury and every two years in the presence of ongoing liver injury. 70 For patients with decompensated cirrhosis, EGD is recommended at the time of diagnosis followed by repeat screening every year. 71 If present, esophageal varices are risk-stratified based on size and count. Primary prevention of variceal hemorrhage includes nonselective beta blockers and/or endoscopic band ligation depending on risk. 69 Acute variceal hemorrhage is a life-threatening emergency managed with vasoconstrictors, endoscopic band ligation, balloon tamponade, and surgical intervention. 72 Placement of a transjugular intrahepatic portosystemic shunt (TIPS) can be performed as a salvage treatment to reduce portal hypertension and variceal hemorrhage risk, but its use must be considered alongside potentially worsening hepatic encephalopathy secondary to increased intrahepatic shunting. 72

The model for end-stage liver disease (MELD) and Child–Pugh scores are two clinically useful calculations that use patient laboratory values and symptom severity to stratify risk and estimate disease severity in cirrhotic patients. 73 The MELD score is commonly used in transplant allocation. 74 Due to the progressive nature of chronic liver disease, liver transplant remains the definitive treatment option for advanced cirrhosis. 74 This patient's initial laboratory work-up demonstrates a MELD score of 20 and an estimated three-month mortality of 19.6%. 73 Patient education is an important intervention in the management of cirrhosis and includes counselling on alcohol reduction or abstinence, signs and symptoms of serious complications, and the importance of continued surveillance and long-term follow up. 67

Teaching points

• • Cirrhosis is characterized by hepatic fibrosis, prolonged hepatocellular regeneration, and disruption of hepatic microarchitecture that occurs secondary to chronic liver diseases. It is commonly classified by morphology or etiology.
• • Morphologic classifications include both macroscopic and microscopic patterns. Macroscopic patterns include micronodular, macronodular, and mixed types of cirrhosis. Microscopic patterns vary by etiology but can be categorized as biliary and nonbiliary types of cirrhosis.
• • Etiologies of cirrhosis include infectious (predominately viral) and autoimmune hepatitides, storage disorders, alcoholic and metabolic-associated steatohepatitides, and biliary dysfunction.
• • The loss of hepatocytes results in decreased metabolic and synthetic capacity of the liver leading to coagulopathies, jaundice, hepatic encephalopathy, hyperestrogenism, hypoalbuminemia, and ascites, which can be further complicated by spontaneous bacterial peritonitis.
• • Fibrosis and vascular reorganization in cirrhosis results in the development of portal hypertension and subsequent intrahepatic shunting leading to complications including hepatic encephalopathy, hepatopulmonary syndrome, hepatorenal syndrome, and esophageal varices.
• • Loss of hepatic parenchyma in the setting of cirrhosis is demonstrated by elevated liver enzymes (specifically AST ALT, ALP) in acute liver disease and declining levels in end-stage chronic liver disease. Interpretation of hepatocellular and cholestatic patterns of liver enzyme elevations can be used to differentiate liver disease etiology and direct further management.
• • Various identifiable patterns of AST, ALT, and ALP elevation are suggestive of different types of liver injury. A normal AST:ALT ratio is < 1 whereas an AST:ALT ratio > 1 is highly suggestive of liver injury. Predominant elevations of AST and ALT with or without notable ALP elevation suggest a hepatocellular pattern of liver injury. A hepatocellular pattern with an AST:ALT ratio >1 is strongly suggestive of an alcoholic etiology of liver damage while a ratio of < 1 suggests metabolic-associated fatty liver disease. Predominantly elevated ALP with or without significant AST and/or ALT elevations suggests a cholestatic pattern of liver injury.
• • Ultrasonography and sonoelastography are the most commonly used imaging modalities in the characterization of liver disease and cirrhosis. Ultrasonography characterizes hepatic parenchyma and can differentiate etiologies of focal and diffuse liver disease. Sonoelastography measures the stiffness and elasticity of hepatic tissue to determine the extent of hepatic fibrosis and can be used to risk stratify related complications.
• • Ultrasonographic evidence of cirrhosis includes heterogenous echotexture, nodularity, hepatosplenomegaly, segmental hypertrophy and atrophy, and vascular abnormalities.
• • Normal liver parenchyma appears homogenous and porous with an echogenic texture that is similar to that of the renal cortex. Abnormal ultrasonographic findings vary depending on the etiology of focal or diffuse liver disease.
• • Prolonged hepatocyte regeneration in the setting of chronic liver disease significantly increases the risk of developing hepatocellular carcinoma in cirrhotic patients.

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Authors’ note

The opinions expressed herein are those of the authors and are not necessarily representative of those of the Uniformed Services University of the Health Sciences (USUHS), the Department of Defense (DOD), or the United States Army, Navy, or Air Force, or the Henry M. Jackson Foundation.

Declaration of competing interest

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

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CASE STUDY OF PATIENT WITH LIVER CIRRHOSIS

by Rashid Chaudhary

Livercirrhosisisadiseaseinwhichnormaltissueofliverreplacedwithscartissue,livercirrhosisisthe12thleadingcauseofdeathsbydiseaseintheworld.Livercirrhosisiscausedbyanyfactorthatcandamagelivertissues,mostlyfattyliverandchronicliverdiseasesarethemajorcauseoflivercirrhosis. WearepresentingherethecaseofanAsianmanwhowasthevictimoflivercirrhosisthatwascomplicatedbyuntreatedhepatitisc.Hewasexperiencinggeneralizedbodyweakness,brownishtintintheurine,andsuddenweightgainof8-kgswithinaperiodofthreeweeks.Bloodpressurecountwas100/60,pulseratefoundtobe76beats/min,temperature98F,andenlargedumbilical.Laboratorytestsincludingcompletebloodcount,liverfunctiontests,andureatestscameouttobesignificantlyabnormal,complicatingthecase.,ultrasoundreportrevealedthathisliverwasenlarged,urinarybladderpartiallyfilled,umbilicalherniagapereported,ascitespresent(retentionoffluidintheabdomen),Cirrhosisandsplenomegalywerereported.Hisliverwasdamagedandliverfunctioningtestswerenotreturningtonormal,hepatologistrecommendedlivertransplantationasthelastresortforhim. Thereistheneedofgoodclinicalevaluationbyaqualifiedtherapistanduseofappropriateinvestigativestudiestosecurepatientfromsuchacriticalhealthhazard. Keywords:chronicliverdisease,livertransplantation,

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1981, Human Pathology

IJAR Indexing

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Thiago Silva

2005, Jornal Brasileiro De Patologia E Medicina Laboratorial

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Andrés Cárdenas

2005, Journal of Hepatology

Rajiv Jalan

2011, Hepatology

Sanjiv Saigal

2010, Human Pathology

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tanuja manohar

Journal of Medical Science And clinical Research

International Journal of Contemporary Medical Research ijcmr

Introduction: Liver has got multiple functions and hence its insufficiency in a cirrhosis patient gives rise to involvement of various symptoms. The aim of the present study is to diagnose patients with clinical, oral and pathological test. Material and Methods: 60 cases of liver cirrhosis were selected irrespective of age and sex and were included in the study group.They were divided into group I and depending on the cause of cirrhosis and 40 normal patients as controls were observed with detailed clinical examination, liver function test, renalfunction test and oral manifestations. Result: In study group I and II liver function test like serum bilirubin, ALT,andprothrombin time as compared to control group were found to be significantly elevated whereas serum albumin was significantly reduced. More than 50% cases developed renal failure. Theoral hygiene was poor presenting with caries, extractions, calculus and periodontal problems with more in group I patients. Conclusion: These observation can elucidate in diagnosing hepatorenal disease and its outcome. Also the screening and management of oral manifestations prior to organ transplan-tation can overcome complications after transplantation like septicemia and others.

Josep Teres

1987, Hepatology

Servet Karagul

Rasit Yagci

2008, Pediatric Transplantation

Reza Malekzadeh

2013, Alimentary Pharmacology & Therapeutics

António De Figueiredo

2012, Critical Care Research and Practice

Liver cirrhosis (LC) can lead to a clinical state of liver failure, which can exacerbate through the course of the disease. New therapies aimed to control the diverse etiologies are now more effective, although the disease may result in advanced stages of liver failure, where liver transplantation (LT) remains the most effective treatment. The extended lifespan of these patients and the extended possibilities of liver support devices make their admission to an intensive care unit (ICU) more probable. In this paper the LC is approached from the point of view of the pathophysiological alterations present in LC patients previous to ICU admission, particularly cardiovascular, but also renal, coagulopathic, and encephalopathic. Infections and available liver detoxifications devices also deserve mentioning. We intend to contribute towards ICU physician readiness to the care for this particular type of patients, possibly in dedicated ICUs.

Carlos Terra

2005, Ascites and Renal Dysfunction in Liver Disease

Maximilian Schöniger-hekele

2003, Gastroenterology

IOSR Journals publish within 3 days

Objectives: The main objective is to study on management of comorbidity and complications in liver cirrhosis patients, to study the severity of liver cirrhosis at the time of admission and to identify the risk factors and complications of liver cirrhosis in various populations. Methods: A prospective observational study has been done in limited period of 1 year in inpatient department of gastroenterology and general medicine. We have excluded the patients who are non-cooperative and receiving less than 24hrs of emergency care. We have included the patients who are admitted in inpatient department of gastroenterology and general medicine and the cases with demographic details and with or without social habits. Results and Conclusion: In this study we found that male patients were 91out of 122 cases and were more prone to liver disease as alcohol is the main risk factor where alcoholic patients were 79 out 122 cases with 64.75%.The Pantoprazole PDD was 47.5 and ratio between PDD:DDD (47.5:40) was 1.1, Octreotide PDD was 0.171 and ratio between PDD:DDD (0.171:0.7) was 0.244, Ciprofloxacin PDD was 1000mg and ratio between PDD:DDD (1000:1000) was 1, Furosemide PDD was 49.33 and the ratio between PDD:DDD (49.33:40) was 1.23, PropanololPDD was 39.41 and the ratio between PDD:DDD (39.41:160) was 0.24, Metoclopramide PDD was 20.12 and the ratio between PDD:DDD (20.12:30) was 0.66, Ketorolac PDD was 60 and the ratio between PDD:DDD (60:30) was 2, Tramadol PDD was 32.57 and the ratio between PDD:DDD (328.57:300) was 1.09, Lactulose PDD was 523.5 and the ratio between PDD:DDD (523.5:670) was 0.78, Ranitidine PDD was 130 and the ratio between PDD:DDD (130:300) was 0.43, Hyoscinebutylbromide PDD was 96 and the ratio between PDD:DDD (96:100) was 0.96. The main complications in liver cirrhosis was found to be portal hypertension 35.94% and ascites 20.2% out of 122 cases. Conclusion: The complications of liver cirrhosis like portal hypertension and ascites are more common than other complications. Risk factors were common in males than females as alcohol is the established risk factor.

Zainab Safdar

Apurva Shah

Journal of Clinical and Experimental Hepatology

2012, Alimentary Pharmacology & Therapeutics

Prerna Goyal

2018, Journal of Gastrointestinal Infections

Ifemed Journal , Chukwuemeka A Obuekwe , Kolade J Adegoke

2022, Ifemed Journal

The natural history of liver cirrhosis begins with an asymptomatic phase of compensation. This is followed by a rapidly progressive phase of decompensation marked by clinical evidence of the complications of portal hypertension and/or impairment of liver function. The clinical prognosis of this decompensated phase is poor with reduced survival time. As a result, liver cirrhosis remains a leading cause of disability and mortality globally. To this end, the management of decompensated liver cirrhosis has evolved with the rationale of improving care and survival of the patient by managing individually the complications as they arise. This review discusses the stages of liver cirrhosis and details on interventions and improved therapeutic options for the complications of the decompensation phase-ascites, varices and variceal haemorrhage, hepatic encephalopathy, hyponatremia, hepato-renal syndrome, and infections in cirrhosis-while briefly discussing the pathogenesis of these complications and highlighting the pieces of evidence and rationale behind management options. This review also recognizes the gap in the prevention of these complications.

abdullah yousaf

Background:To determine the aetiology and complications of decompensated chronic liver disease (DCLD) Methods: In this cross-sectional descriptive study patients with DCLD were enrolled. Etiology, complications and other features were registered. Diagnosis was made on the basis of ultrasound and endoscopy findings. Lab investigation profile including serology for hepatitis, liver biopsy (to check for alcoholism and Wilson&#39;s disease) and serum & urinary copper and serum ceruloplasmin (to check for Wilson&#39;s disease) was taken into accountent. To determine complications, records of complete blood picture and liver function tests (for hepatic encephalopathy), renal function tests (for hepatorenal syndrome), chest X-ray, arterial blood gas, contrast-enhanced echocardiography and lung function tests (for hepatopulmonary syndrome), abdominal ultrasound (for portal hypertension and associated complications viz. ascites, splenomegaly, hepatomegaly, portosystemic shunts including esop...

beata gierej

2015, Gastroenterology Review

2009, Digestive Diseases and Sciences

Ifemed Journal

2021, Journal of the Obafemi Awolowo University Medical Students’ Association

We present Mr A.F, a 52-year-old married man of Christian faith and Yoruba Ethnicity. He is a known patient of the Gastroenterology Unit of the Department of Medicine, Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife who was being managed for Hepatitis B induced Liver Cirrhosis. The patient had defaulted regular clinic visits for one year prior to this presentation. He presented at the Accident and Emergency Department of this hospital with right upper abdominal pain of a week duration.

Lars Schmidt , Henning Grønbaek

Danish Medical Journal

National guidelines for treatment of ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, and hyponatremia have been approved by the Danish Society of Gastroenterology and Hepatology. Ascites develops in approximately 60% of patients with cirrhosis during a 10 year period and is frequently associated with complications that determine the course of the disease and the prognosis. These evidence-based guidelines are divided in two parts and consider definitions, pathophysiology, diagnostic aspects, treatment, and prophylaxis.

william ayibor

2018, The Journal of Medical Research

Introduction: Lifestyle and a variety of factors and conditions as well as genetics can cause damage to the liver, such as viruses and alcohol use which leads to end stage liver disease. Liver disorders be it inherited or due to lifestyle ranges from benign lesions and scarring (cirrhosis) to liver cancer. A retrospective review of post mortem cases with liver disorders in our center will give a clear picture of the trend and spectrum of such disorders to aid in review of clinical prognosis when dealing with patients. Methods: Information on cause of death as well as demographics were retrieved from the Autopsy Day Book of the department of pathology, Komfo Anokye Teaching Hospital where the clinical diagnoses, pathological findings and other relevant data were gathered. The data was entered into Microsoft Excel and analyzed using SPSS version 22. Results: Findings from the 445 autopsy cases revealed a total of ten (10) different diagnoses with some major disorders as well as complications. Males accounted for the most cases with 324 (72.81%) of cases with 121 (27.19%) for women. Liver cirrhosis accounted for more than half of all diagnoses made with 257 (57.75%) of cases, followed by liver cancer with 97(21.80%) of cases and both hepatic encephalopathy and hepatorenal disease recording a case each (0.22%). The age range is from 8 months to as high as 102 years with the 30-39 years group recording the highest number of cases, 124 (27.86%) and both the extremes of age groups recording the least with 7 (1.57%) each. Most of the cases recorded clustered around the middle age group with particularly high cases for ages 30 to 49. Conclusion: Liver cirrhosis is the commonest liver disorder in our center and young men are at more risk for liver diseases. Most of these liver complications are also more frequently overlooked by clinicians since they are usually asymptomatic.