CME On UGIB and Management of Decompensated Liver.pptx

UGIB management and decompensated liver failure

1. CME On UGIB and Management of Decompensated Liver Cirrhosis Supervised by: Dr Sooi C Y ( Gastroenterology and Hepatology Specialist) Presented by: Ngew Kah Yih Malani Shubana Muraleetharan

2. INTRODUCTION Acute GI bleeding is a potentially life-threatening abdominal emergency that remains a common cause of hospitalization Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz. Hematemesis: bloody vomitus (bright red or coffee-grounds) Melena: black, tarry, foul-smelling stool Hematochezia: bright red or maroon blood per rectum Occult: positive stool occult test Symptoms of anemia: angina, dyspnea, or lightheadedness

3. Acute UGIB Differential Diagnosis Peptic ulcer disease Gastric ulcer Duodenal ulcer Mallory-Weiss tear Varices Esophagitis Dieulafoy’s lesion Vascular anomalies Malignancy Post-procedural Cameron’s lesions Hemobilia Hemorrhagic gastropathy Aortoenteric fistula Major Causes Minor Causes

4. Peptic ulcers

5. Forrest classification of Bleeding Peptic Ulcers Forrest Class Stigmata IA Arterial spurting IB Arterial oozing IIA Visible vessel IIB Adherent clot IIC Pigmented flat spot III Clean based

6. Endoscopic Procedure Bleeding/perforated ulcers Clean based ulcers

7. Mallory-Weiss tear Longitudinal tear in the mucosa at the gastroesophageal junction. Traumatic injury due to excessive vomiting, coughing, CPR, straining or direct blunt trauma. Iatrogenic

8. Oesophageal Varices Dilated submucosal distal esophageal veins connecting the portal and systemic circulations. Pathophysiology: Portal hypertension causes portocaval anastomosis to develop to decompress portal circulation. Since the portal venous system is valveless, resistance at any level between the splanchnic vessels and right side of the heart results in retrograde flow and elevated pressure. The collaterals slowly enlarge and connect the systemic circulation to the portal venous system. Over time, this leads to a congested submucosal venous plexus with tortuous dilated veins in the distal esophagus.

9. Grades for Esophageal Varices

10. Dieulafoy’s lesion ‘calibre persistent artery’ Congenital dilated tortuous submucosal artery that erodes overlying gastrointestinal mucosa

11. Clinical presentations • Confirm presence of bleeding → Hematemasis , melena, hematochezia → Complication: anemia , shock – dizziness, palpitation, SOB, syncope •Amount & rapidity of bleeding •Source & potential causes •Presence of serious associated disease Followed by the significant history

12. Physical Examination General assessment Alert , conscious Pale Nutritional status : cachexic Respiratory distress Vital signs Heart rate : tachycardia Respiratory rate : tachypnoea Blood pressure : hypotension Sp02 Temperature Abdomen Inspection Abdomen moving symmetrically with respiration Abdominal distension Scars Dilated veins/ caput medusae Visible gastric peristalsis Palpation Tenderness, guarding Mass : site , size, shape, margin, surface, consistency, mobility Organomegaly : splenomegaly, hepatomegaly Percussion Auscultation Bowel sounds Rectal examination Inspection Skin excoriations Skin tags Blood : malaena or fresh blood Mucus Masses Ulcers Anal fissures Prolapsed haemorrhoids Palpation Tenderness Mass or polyp Internal haemorrhoids

13. OGDS of bleeding ulcers Bleeding ulcers Post procedure – banding done

14. Decompensated Liver cirrhosis 

15. Definition. Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.

16. Causes of cirrhosis  Heavy alcohol consumption for a long period of time (alcoholic hepatitis)  Chronic hepatitis B and C Fatty build up in liver  Autoimmune disease Malformation of bile ducts  Injuries of bile duct  Certain drugs ( ETOH, NSAID , OPOIDS ) Hepatocellular carcinoma. Acute portal vein thrombosis Iron/ copper build up in liver 

17. Sign and symptoms   Jaundice  Ascites  GI bleeding  Easy bruising /bleeding Renal impairment  Sepsis/hypovolemia Hepatic encephalopathy  Unexplained itchiness  Spider nevi  Redness of palm 

18. Pathophysiology of liver cell failure  Liver:  • Hyper-bilirubinemia (due to ↓ secretory function of the liver).  • Hypo-albuminemia ( due to ↓ synthetic function) → tissue edema, ascites, pleural effusion.  • Elevated liver enzymes as a result of hepatocellular damage.

19.  Portal hypertension  Defined as a pressure gradient of > 10 mmHg between the portal vein and IVC.  It is a major contributory factor for ascites, esophageal varices, 

20. ASCITES  • Ascites as a result of portal HTN.  - It is a transudate in nature with protein concentration less than 2.5 mg/dL.  Total protein >1g/dL LDH > upper limit of normal for serum  Glucose <50 mg/dL Complication :  'SBP : appears to be caused by the translocation of GI tract bacteria across the gut wall and also by the hematogenous spread of bacteria. The most common causative organisms are Escherichia coli, Streptococcus pneumoniae, Klebsiella, and other gram-negative enteric organisms. 

21. Management of ASCITES  Abdominal paracentesis as therapeutic and diagnostic method • An area of percussion dullness in the left lower quadrant (2 cm cephalad and anterior to the anterior superior iliac spine) has a greater likelihood of ascites present than the midline. • Ultrasound guidance should be utilized if ascites is difficult to localize and to avoid venous collaterals, intestine. • An indwelling drainage catheter can be left for 3-5 days if therapeutic drainage is required

22. ASCITES TAP  Send fluid for :  1.CBC  2.Fluid culture 3.Fluid albumin If   PMN count 250 cells/mm3( white cell multiple with neurtrophil )  , to start antibiotics immediately. ( spontaneous bacterial peritonitis )  Choices of abx :  IV Tazocin 4.5mg QID   IV Ciprofloxacin 400mg if penicillin allergic 

23. Variceal Hemorrhage   Incidence and Outcome Gastroesophageal varices in 40%-60% cirrhotics • Variceal hemorrhage occurs in 25%-35% cirrhotics • 30% of the initial bleeding episodes are fatal • 70% have recurrent bleeding with a 1-year survival ranging from 30% to 80% • Non-variceal pathology (ulcers, gastritis, mucosal tear) may cause bleeding in patients with known liver disease and portal hypertension.

24. Hierachy treatment 

25. Treatment of  Varices Medical approach  Octreotide - Synthetic analogue of somatostatin  FX -Decreases portal pressure and azygos blood flow  -Stops variceal bleeding in 80% of the cases -Efficacy is similar to endoscopic sclerotherapy and better than vasopressin  -5-day course reduces bleeding after endoscopic therapy   • Terlipressin  (Vasopressin ) -Efficacy similar to endoscopic sclerotherapy and as effective as balloon tamponade when used with nitroglycerin

26. Treatment of Varices Hemorrhage  Surgical approach  1) Esophageal varices  -Primary approach is endoscopic banding or sclerotherapy - TIPSS, surgical shunts are alternatives 2) Gastric varices   Primary approach is TIPSS or surgery Reason : Diffuse, deep submucosal anatomy                  Endoscopic  tx  difficult, dangerous 

27. ENDOSCOPIC THERAPY  Endoscopic Band Ligation   - Controls bleeding in 80%-90% of cases - Lower complication rates than sclerotherapy • Endoscopic Sclerotherapy -  Intravariceal or paravariceal injection of a sclerosing agent - Stops bleeding in 80%-90% of the cases  Cyanoacrylate Injection  -Used to control bleeding from gastric varices -Superior to EBL for treatment of bleeding gastric varices

28. Transjugular Intrahepatic Portosystemic Shunt (TIPSS)  

29. Hepatic Encephalopathy  Hepatic encephalopathy is a syndrome marked by personality changes, intellectual impairment, and a depressed level of consciousness occurring as a result of diversion of portal blood into the systemic circulation ( porto -systemic shunting).  It is believed to be caused by the passage of neurotoxins which bypass hepatic detoxification and reach the brain via porto -systemic shunting.  Neurotoxins include short-chain fatty acids, mercaptans, false neurotransmitters ( eg , tyramine, octopamine), ammonia (NH3), and gamma-aminobutyric acid (GABA). Patients may have altered brain energy metabolism and increased permeability of the blood-brain barrier

30. ENCEPHALOPATHY SCALE  Grade 1- Mild psychological disturbances,  Trivial lack of awareness,  Euphoria or anxiety,  Shortened attention span Grade 2-  Lethargy or apathy, Minimal disorientation for time or place Subtle personality change , Inappropriate behavior , Impaired performance of subtraction,  Asterixis Grade 3- stupor, nystagmus, clonus  Grade 4- Coma , unresponsive to verbal or noxious stimuli 

31. Treatment of Hepatic encephalopathy • Treatment of the precipitanting factors of hepatic encephalopathy ( eg. metabolic disturbances, GI bleeding, infection, constipation)  • Lactulose - has multiple actions including cathartic, acidification of the colon to “ion-trap” ammonia as NH4+, and reduction of inoculum of urea-splitting bacteria. • Neomycin - non-absorbed aminoglycoside . -Decreasing the colonic concentration of ammoniagenic bacteria.  -Neomycin dosing is 250-1000 mg orally 2-4 times daily. • Rifaximin - non-absorbed antimicrobial 400 mg TDS  orally  • Metronidazole - oral dosing at 800 mg/day. • Flumazenil - benzodiazepine receptor (GABA) antagonist.

32. HEPATORENAL SYNDROME  Definition :  It is the occurrence of acute renal dysfunction in patients with preexisitng liver failure in the absence of primary renal disease. MODIFIED RIFLE CRITERIA  1. CR rises >1.5mg/dl  in 48 hours or > 50 % rise in 1/52 2. CR clearance less than 40 ml /min  3. Oliguria UO < 0.5mls/kg/ hr  for >6 hours / less than 500 ml perday 4. Clinically dehydrate 5. Urine Na <10mlEq/L If baseline unknown , follow  belows   CR >90 / eGFR <60

33. HEPATORENAL SYNDROME HRS 1 –  Rapid and progressive impairment in renal function (increase in serum creatinine of ≥100% compared to baseline to a level higher than 2.5mg/dl in <2 weeks)   >>> lead to encephalopathy/ edema / azotemia  HRS 2- Gradual decrease renal  fx  .Associated with building up ASCITES    >>>precipitate Spontaneous bacteria peritonitis  

34. Pathophysiology  Splanchnic vasodilation Activation of sympathetic nervous system and renal-angiotensin-aldosterone-system (RAAS) Cirrhotic cardiomyopathy- HF caused by humoral and nervous dysregulation  Increased vasoactive mediators –NO, TNF , endothelins,endotoxin , glucagon. Spontaenous bacterial peritonitis (SBP) is the most important risk factor for HRS. 30% patients with SBP may go in HRS.

35. Management of HRS  Optimal treatment  : Liver Transplant Suboptimal treatment : Transjugular intrahepatic portosystemic shunt – >>> solve portal hpt   Terlipressin (vasoconstrictor): 1-2 mg IV every 4-6 hours  Norepinephrine 0.5-3.0 mg/h intravenously • Midodrine 7.5 mg three times daily increased to 12.5 mg three times daily >>> [For splanchnic vasodilation ] Albumin: 1 gm/kg (to 100 mg) on day 1 then 20-40 mg daily >>> Volume expander  Alternative treatment : - Dialysis   - Maintaining electrolytes balances eg , magnesium, phosphate, calcium, sodium, potassium. - Promtly treat infection 

36. INVESTIGATION FBC LFT  CLOTTING PROFILE  Consider- VBG , CRP, Electrolytes ,Blood culture /septic screen 

37. US ABDOMEN  Suspicious portal vein thrombosis  Ascites fluid tap  Determine filling status  Renal tract ( determine prerenal / post renal AKI )  

38. Liver transplant  Liver Transplant- Can be transplant partially or full in view of regeneration ability of liver  Evaluation :  1.stage of liver disease by CTP  2.medical history  3.Psychological status  4.willingness for tx 5.chances of surviving surgery

39. MELD SCORE If MELD >15 – 95 % survive chance for 3 months  If MELD <15 – 30-65% survive chance for 3 months 

40. CHILD-TURCOTTE-PUGH 

41. Mo'emen modified classification of liver disease

42. Clinical case U/L: -Liver cirrhosis likely due to chronic alcohol consumption (Child's pugh C) - Stopped drinking several months ago - AFP: 3.2 - Hep B/C: non-reactive  Presents with worsening abdominal distension for the past week Associated with SOB and bilateral LL swelling for 3 days No fever at home Also been having a cough for the past 3-4 days , non productive Denies abdominal pain No Nausea and vomiting On examination, -Alert - GCS 15/15 - No liver flap - Lungs - Clear - CVS - S1S2 - Abdomen - Distended but not tense ascites, shifting dullness - Pedal oedema up to mid shins

43. Issues: Decompensated alcoholic liver disease (Child's pugh C11) Maddrey's score 31.1 Plan: Peritoneal tappin g (diagnostic and therapeutic) – drained hemoserous fluid Pe ritoneal fluid sent for fluid analysis and cytology ( SAAG: 10 / RBC 4400 / WC - ve Cytology: Pending ) Medications: Furosemide to IV 40mg BD, spironolactone 50mg OD, thiamine 100mg OD, albumin human 20% infusion 100mls TDS Peritoneal pigtail insertion done under IR – drained approximately 12litres hemoserous Daily RP,LFT,FBC