GIT Acute diarrheal diseases (ADD)1. Definition: Acute diarrhoea is passing more than 3 watery stools in a day of less than 14 days duration and without blood in stool; blood in stool is called dysentery. Diarrhea for > 14 days is called persistent diarrhoea2. WHO classification of Diarrhoea: 1. Acute watery diarrhea2. Persistent diarrhea3. Dysentery4. Diarrhea in severe malnutrition3. Etiological agents :1. Bacterial: 1. Enterotoxigenic e. Coli2. Shigellae 3. Salmonellae4. Vibrio cholerae 5. Campylobacter jejuni 6. Clostridium difficile2. Viral: Rotavirus important cause for diarrhea in infants3. Parasitic agents: Cryptosporidium4. Protozoans: Amoeba; Giardia4. Transmission:1. Rota virus, shigella and e.coli: person to person2. Cholera: food and water3. Salmonella and camphylobacter : food poison4. Clostridium difficile : antibody associated5. Pathogenesis:1. Toxin mediated2. Invasive3. Osmotic4. Increased motilityToxin: Eg.1. Rota virus:a. Activates intracellular signal transductionb. Inhibits Na, Cl coupled transportc. Eflux of Cl 2. E.coli:a. Activates adenylate cyclaseb. Increases intracellular cyclic AMPc. Pumps out Na and ClE.coli: types:a. ETEC: EnterotoxigenicFimbrial adherence; toxin mediated chloride shiftb. EPEC: EnteropathogenicAdherence and effacement; cell injuryc. EIEC: EnteroinvasiveShigella like toxin; invasion and cell necrosisd. EHEC: EnerohemolyticCan result in Hemolytic uremic syndromeInvasion:1. Shigella: Invasion, mucosal destruction and exudation2. E.Coli: EnteroinvasiveOsmotic:Eg: lactose intolerance; unabsorbed food produce osmotic pressure to water into lumenMotility disorder:Eg: irritable bowel syndrome6. Risk factorsfor diarrhea in infants:1. Age: infants for more susceptible for viral diarrheas2. Measles: direct infection and secondary bacterial infection3. Malnutrition: immune and vit.A deficiency 4. Breast feeding: lack of breast feeding leads to increased risk for ADD5. Formula feeding: bottle feeding is an important source of infection6. Vit.A deficiency: epithelium is defective to provide barrier of infection7. Zinc deficiency: leads to lack of local immunity 8. Race lactase deficiency common in Caucasians7. Role of Zinc: 1. Biochemical functions: 1. Component of enzymes like: carbonic unhydrase, alcohol dehydrogenase, alkaline Phosphatase, carboxy peptidase, superoxide dismutase etc.2. Essential for insulin storage and secretion by b cells.3. It is required for maintaining vit a level in serum.4. It is required for wound healing by unknown mechanism.5. Gusten is a zinc containing protein and is important for taste sensation.6. Zinc plays important roles in growth and development, the immune response, neurological function, and reproduction.2. Role of Zinc in diarrhoea 1. Improved absorption of water and electrolytes by the intestine,2. Faster regeneration of gut epithelium,3. Increased levels of enterocyte brush border enzymes,4. Enhanced immune response, 8. Behavioral factors: 1. Failure to breast-feed exclusively for the first 4-6 months of life2. Using infant bottles3. Unsafe water4. Improper hand washing5. Open air defecation 9. Malnutrition and diarrhea: Diarrhea produce malnutrition; malnutrition in turn produce immune deficiency and increases diarrheal episodes and hence a vicious cycle is set up.10. Signs and symptomsof ADD: Main symptom of diarrhoea is dehydration. The disease is classified by WHO according to degree of dehydration as follows:

CategoryGeneral conditionThirstEye signsSkin pinchUrine outputPulseFontanel

No dehydtrationPlan AAlert Absent Moist; not sunken; tears +Quick recoilNormalNormalAF normal

Some dehydrationPlan BIrritableIncresaed Dry; sunken;Tears lessSlow recoilreducedFast Depressed

Severe dehydrationPlan CLethargic Absent due to lethargyVery dry; deeply sunken; no tearsTenting on pinchNil Rapid and Thready Much depressed

Severe diseasePlan CIn addition to signs of severe dehydration child may have: unconsciousness; convulsions; cyanosis; no feeding; high fever etc

11. Treatment: (WHO guidelines)Plan A: ADD with no dehydration:1. Mother care which consists of:1. Treat fever with paracetamol2. Continue breast feeding3. Give more foodthan usual to prevent malnutrition4. Give extra home available fluids- HAF a. Juices; Buttermilk; Rice water; coconut water; Rice, cereal, dhal; kanji.b. Do not give plain water, salt and water or glucose water5. Give Oral rehydration solution if available:Give as much as the child wants until diarrhoea stops. As a guide, after each loose stool, give:a. Children under 2 years of age: 50-100 ml per diarrheal episode (not per Kg)b. Children aged 2 up to 10 years: 100-200 ml c. Older children and adults: as much fluid as they want.6. Zinc supplementation: 10 mg for 6 mo for 14 days Plan B: Treatment of Some dehydration:Plan B is for child with some dehydration. It is a supervised management with ORT in a ORT corner of an health facility.ORT: 75 to 100 ml/kg to be given in 4 hours and then reassess the child; if the dehydration has been corrected continue as in Plan A; if dehydration remains same give one more Plan B treatment; If child has worsened to severe dehydration refer the child to hospital for Plan C management while continuing ORT.Plan C: Hospital management:a. Simplified IV management: Give Ringer Lactate 100 ml/kg as follows:Age First give 30 ml/kg in: Then give 70 ml/kg in:

Infants (under 12 months) 1 hour5 hours

Older 30 minutes21/2 hours

b. ElectrolytesHyponatremia:150 m.eq /l; continue ORS which will correct hypernatremia slowlyHypokalemia:6 meq/lAcidosis: correct by IV soda bicarb as per deficit 12. Other treatments:i. Zinc:1. 10 mg for 6 m for 14 daysii. Probiotics:1. Produce microbial lactase2. Competes with pathogenic bacteria3. Increase immune effect4. Provide acidity5. Protects cancer and allergy?iii. Drugs:1. No role of antibiotics as infantile diarrhea is mainly viral and self limiting.2. Give Co-trimoxazole if cholera is suspected; suspect cholera if there is large explosive rice water stools; effortless vomiting; severe dehydration in a short time; H/O > 3 admissions for severe diarrhea in the community or 1 death due to diarrhea.3. Give Nitazoxanide if giardiasis is foung in microscopy; Recently Nitazoxanide has been found to have some role role in treating Rota virus infection.4. If Shigella is found positive in stool culture: give quiolones or furazolidineiv. Vomiting:Ondensitran 2 mg stratumv. Anti secretary agents: Racecodotril:a. Enkephalinaze inhibitorb. Anti secretoryc. Under evaluation13. Complications15

1. 2. Shock kidney- ARF3. Intra cerebral thrombosis4. Hemolytic uremic syndrome5. Hypoglycemia6. Paralytic ileus 7. PEM14. Lab1. Electrolytes2. Stool microscopy3. Stool culture4. Stool reducing substance5. CBC

16. Prevention strategies 1. Breast feeding2. Improved weaning practices3. Proper use of water4. Hand washing5. Disposing feces properly6. Effectiveness of measles vaccination 17. New developmentssuper-ors: contains amino acid instead og glucose; rice based ORS contains rice powder instead of glucose; they try to more energy and nutrition; but increase the cost.Rotavirus vaccine: given at 2,4,6 months of age18. Note (WHO):a. Cholera should be suspected when a child older than 5 years or an adult develops severe dehydration from acute watery diarrhoea (usually with vomiting), or any patient older than 2 years has acute watery diarrhoea when cholera is known to be occurring in the area.

Oral Rehydration Therapy1. Oral rehydration takes advantage of glucose-coupled sodium transport, a process for sodium absorption which remains relatively intact in infective diarrheas due to viruses or to enteropathogenic bacteria, whether invasive or enterotoxigenic. Glucose enhances sodium, and secondarily, water transport across the mucosa of the upper intestine.For optimal absorption, the composition of the rehydration solution is critical. 2. Low Osmolality ORS:a. Studies have shown that the efficacy of ORS for treatment of children with acute diarrhoea is improved by reducing its sodium concentration to 75 mEq/l, its glucose concentration to 75 mmol/l, and its total osmolarity to 245 mOsm/l. This compares to the original solution which contained 90 mEq/l of sodium with a total osmolarity of 311 mOsm/l. There has been a concern that the original solution, which is slightly hyperosmolar when compared with plasma, may risk hypernatraemia (high plasma sodium concentration) or an increase in stool output, especially in infants and young childrenb. The formula for low osmolality ORS recommended by WHO and UNICEF contains:Reduced osmolarity ORSgrams/litreReduced osmolarity ORSmmol/litre

Sodium chloride2.6Sodium75

Anhydrous Glucose13.5Anhydrous Glucose75

Potassium chloride1.5Chloride65

Trisodium citrate, dihydrate2.9Potassium20

Citrate10

Total Osmolarity245

3. How to prepare:i. Mix one full pocket of ORS in 1000 ml of safe water and use it in 24 hours4. Amount of ORS to be given:Plan A: No dehydration: Give as much fluid as the child wants until diarrhoea stops. As a guide, after each loose stool, give:II. Children under 2 years of age: 50-100 ml (a quarter to half a large cup) of fluid;III. Children aged 2 up to 10 years: 100-200 ml (a half to one large cup);IV. Older children and adults: as much fluid as they want. Plan B: Some dehydration: 75 to 100 ml/kg in 4 hours; after correcton of dehydration Continue as in no dehydration 5. Super ORS: To provide more energy without increasing osmolality trials are being done to use rise powder, amino acid in the place of glucose. They would be costlier routine ORS.6. Advantages of low osmolarity WHO Oral Rehydration Solution.a. Composites Standard ORS solutioni. Sodium90 (mEq or mmol/Lii. Chloride80iii. Potassium20iv. Citrate10v. Glucose111vi. Total osmolarity311b. Limitations of standard ORS:i. Does not decrease stool volumeii. Does not decrease frequencyiii. Does not decrease severityiv. Does not stop diarrhoea v. Potential risk of hypernatremia in children with noncholera diarrhoea vi. May provide too much Sodium to edematous childrenc. Advantage of new low osmolarity ORS:i. Reduction in need for unscheduled IV therapy ( 35% in metaanalysis)ii. Significant red in vomiting (30%)iii. Reduction in stool output (20%)iv. Reduction in duration of diarrhoea v. No risk of hyponatremia 7. Advantage of citrate over bicarbonate:1. The particular advantage of citrate containing ORS (over bicarbonate containing ORS) is its stability in tropical countries, where - up to temperatures of 60C - no discoloration occurs. A shelf-life of 2-3 years can be assumed without any particular storage precautions.2. Bircarbonate is hygroscopic and absorbs moisture and get spoiled on storage whereas citrate is less hygroscopic3. WHO has currently recommended citrate-based ORS to replace bicarbonate. Sodium citrate at 2.5 g/ltrs will give a concentration of 10meq/ltr of citrate. 4. Advantages of citrate-based ORS are: it increases shelf life, improves taste, cheaper, sodium absorption in high output diarrhoea and no soiling of pockets.

LACTOSE INTOLERANCE

a. Lactase a disccharidase is essential for digestion of lactose into monosacharides before absorption; b. Types:a. Secondary lactase deficiency is lactase deficiency that results from small bowel injury, such as acute gastroenteritis, persistent diarrhea,b. Congenital lactase deficiency is extremely rare and has a genetic origin.c. Clinical:a. Lactose containing milk feed produce abdominal distension, increased bowel sounds, abdominal colic and explosive watery stoolsb. Acidity of the stools produce perianal excopriationsc. Withdrawl of lactose containing feeds relieves the symptomsd. Challenge feed with lactose formula precipitates the symptoms d. Confirmatory tests:a. Measurement of carbohydrate in the stool using the Clinitest reagent for reducing substances is a simple screening test and can be performed at the bedside. b. The test is easily performed by combining 10 drops of water with 5 drops of stool and then adding a Clinitest tablet. The color change can be quantified as trace to 4+ using a color sheet provided by the manufacturer. Only 2+ or higher should raise the possibility of sugar malabsorption. Sucrose is not a reducing sugar and requires hydrolysis with hydrochloric acid before analysisc. Disaccharidase activities can be assayed in mucosal biopsy specimens. e. a. b. c. Stool pH, obtained easily with pH paper, lower than 5.6 is also suggestive of carbohydrate malabsorptiond. Osmotic diarrhea may be seen with carbohydrate malabsorption. e. The breath hydrogen test: A rise in hydrogen excretion of greater than 20 ppm from baseline is consistent with carbohydrate malabsorptione. Management:a. Lactose free formula from soy milk is an alternate feedb. Live-culture yogurt contains bacteria that produce lactase enzyme and is therefore tolerated by patients with lactase deficiencyc. A tablet with lactase activity can also be ingested with meals. ACUTE HEPATITIS:a. Hepatitis can be divided into two subgroups according to its duration: Acute hepatitis lasting less than six months Chronic hepatitis lasting longer than six months.b. Causes of acute hepatitis:a. Infectious viral hepatitis, such as hepatitis A, hepatitis B, hepatitis C, hepatitis D and hepatitis E.b. Other viral diseases, such as glandular fever and cytomegalovirus.c. Severe bacterial infections.d. Amoebic infections.e. Medicines, eg paracetamolpoisoning and halothane (an anaesthetic).f. Toxins: alcohol and fungal toxinsg. Parasites: Liver flukeh. Autoimmune: Reye sydrome i. Metabolic: hemochromatosis; Cystic fibrosis, Wilsons disease c. Investigations: Acute liver injury caused by the hepatotropic viruses manifests in three main functional liver biochemical profiles namely 1 . Cell injury and inflammation2. Cholestasis 3. Defecetive synthetic function 1. 1. Tests for Acute liver cell injury (parenchymal disease) in viral hepatitis: a. ALT alanine transaminase aminotransferasei. Normal value: 5-45 U/Lii. Can be raised up to 50 x normal. When they are this high it suggests viral hepatitis, iii. Normal levels in infants are 2 x that of adultsiv. During liver damage, ALT is released into serum causing raised levels that may remain high for weeks or months. Levels will be raised before jaundice appears.v. More specific for liver damage than AST.b. AST aspartate transaminase i. Normal: 5-45 U/Lii. Levels can go as high as 20 x normal.

2. Test for Cholestasis (obstructive disease) 1. The serum levels of total and conjugated bilirubin and serum bile acids are elevated 2. ALP alkaline phosphatise: Normal 25-110 U/L 3. Gamma-GT GGT: Normal: 6 mo7. Chronic infection is associated with the development of chronic liver disease, as well as hepatocellular carcinomaPATHOGENESIS 1. injury predominantly by immune-mediated processes2. Less cytopathic effect3. Immune-mediated mechanisms are also involved in the extrahepatic conditions CLINICAL MANIFESTATIONS 1. Prodrome marked by arthralgia or skin lesions, including urticarial, purpuric, macular, or maculopapular rashes2. Jaundice, in 25% of infected individuals, usually begins 8 wk after exposure and lasts for 4 wk3. Recovery in most people4. 10% become chronic carriers5. The liver is enlarged and tender 6. Splenomegaly and lymphadenopathy are common. 7. Clinical signs of altered sensorium and hyper-reflexivity mark the onset of encephalopathy and ALF DIAGNOSIS.1. HBs Ag is the 1st serologic marker of infection2. Anti-hbc Ig M also increase in acute phase3. Anti-hbc Ig G, appears months later and persists for years4. The development of anti-HBe marks improvement 5. Anti-HBs marks serologic recovery and protectionCOMPLICATIONS1. ALF with coagulopathy, encephalopathy, and cerebral edema 2. HBV infection can also result in:1. Chronic hepatitis, 2. Cirrhosis, 3. End-stage liver disease 4. Primary hepatocellular carcinoma.TREATMENT1. No available medical therapy is successful in the majority of persons infected with HBV. 2. Interferon--2b (IFN-2b) and lamivudine are the current therapies for treatment of chronic hepatitis B in adults older than 18 yr of age with compensated liver disease and HBV replication. 3. IFN-2b also has been used in children, with long-term eradication rates similar to the 25% rate reported in adults. 4. Recombinant interferons have immunomodulatory and antiviral effects whereas lamivudine, a nucleoside analog, inhibits the viral enzyme reverse transcriptase. 5. Liver transplantation also has been used to treat patients with end-stage HBV infection6. Peginterferon-2, adefovir dipivoxil and entecavir are approved for use only in adultsPREVENTIONUNIVERSAL PROPHYLAXIS Dose Schedule

Infants of HBsAg-negative women0.5 ml Birth, 12, 618 mo

Children and adolescents (1119 yr)0.5 ml 0, 1, and 6 mo

Infants of HBsAg (+) women0.5 ml Birth 1 and 6 mo & 0.5 mL HBIG

Extra hepatic manifestation of Hepatitis B:1. Immune-mediated mechanisms are involved in the extrahepatic conditions 2. Circulating immune complexes containing HBsAg can occur in patients who may develop :a. Polyarteritis nodosa, b. Membranous or membranoproliferative glomerulonephritis, c. Polymyalgia rheumatica, d. Leukocytoclastic vasculitis, e. Guillain-Barr syndrome. 3. The illness may also be preceded in a few children by a serum sickness-like prodrome marked by:a. Arthralgia b. Skin lesions, including urticarial, purpuric, macular, or maculopapular rashes.c. Papular acrodermatitis, the Gianotti-Crosti syndrome 4. Other extrahepatic conditions associated with HBV infections in children can include aplastic anemia. HEPATITIS C1. Transfusion-related non-A, non-B hepatitis2. Single- stranded RNA virus, classified as a separate genus within the Flaviviridae family3. Mild and insidious in onset 4. Causes chronic infection5. Progress to cirrhosis, liver failure, and, occasionally, primary hepatocellular carcinoma (HCC) within 2030 yr of the acute infection.6. Diagnosis: aniti HCV antibody; PCR 7. Treatment: 1. Effective therapy to prevent the progression of HCV infection to cirrhosis, liver failure, or hepatocellular cancer is not yet available for the majority of patients. 2. Monotherapy with IFN-2b has resulted in sustained response in 10-15% of patients, defined as having normal ALT levels and negative PCR results 6 mo after completion of therapy. 3. Combination therapy with interferon and ribavirin has yielded sustained response in about one third of patients and is now considered first-line therapy. 4. Future treatment strategies are likely to include development of more effective protease and helicase inhibitors and drugs that can disrupt the HCV RNA genome.HEPATITIS D1. The smallest known animal virus, 2. It cannot produce infection without a concurrent hbv infection. 3. The 36 nm diameter virus is incapable of making its own coat protein; 4. Its outer coat is composed of excess hbsag from hbv. 5. The inner core of the virus is single-stranded circular RNA that expresses the HDV antigen.6. Transmission as HBV infection (co-infection), or those already infected with HBV (super-infection).7. Disease more severe than those of the other hepatotropic viruses8. chronic hepatitis & acute liver failure are common9. Diagnosis: IgM antibody to HDV10. The treatment:1. HDV superinfection of a person who has chronic HBV infection is more common2. Treatment is to as per management of HBV and is mostly based on controlling and treating HBV HEPATITIS E1. RNA virus ; a non-enveloped calicivirus 2. Transmission is fecal-oral 3. infection is similar to HAV but is often more severe4. ALF in pregnant women5. Diag: IgM and IgG assays 6. HEV is associated with a high prevalence of death in pregnant women.7. No specific treatment or prevention are available8. Child is to be manages as in Hepatitis A9. Vaccine not effective; pooled immunoglobulin can be given

PORTAL HYPERTENSIONDefinition:1. Portal hypertension, defined as an elevation of portal pressure >1012 mm Hg. The normal portal venous pressure is 7 mm HgCauses1. Portal hypertension is most commonly a result of cirrhosis. 2. Etiology:Prehepatic causes1. Umbilical infection (omphalitis) 2. Catheterization of the umbilical vein 3. Portal vein thrombosis due to neonatal dehydration and systemic infection. 4. Primary sclerosing cholangitis. 5. Hypercoagulable states such as deficiencies of factor V Leiden, protein C, or protein S. 6. Rare anomalies: agenesis, atresia, stenosis portal vein. The intrahepatic causes 1. Chronic hepatitis, 2. Congenital hepatic fibrosis3. Schistosomiasis4. Infiltration with malignant cells5. Idiopathic form of portal hypertension 6. Cirrhosis liver & its cause:1. Biliary atresia,2. Autoimmune hepatitis, 3. Chronic viral hepatitis, 4. Metabolic liver disease such as 1-antitrypsin deficiency, 5. Wilson disease, 6. Glycogen storage disease type iv, 7. Hereditary fructose intolerance, 8. Cystic fibrosis.9. Non alcoholic fatly liver diseasePosthepatic: 1. The Budd-Chiari syndrome; obstruction to hepatic vein due to thrombosis from hypercoagulable states2. Metastatic neoplasms, 3. Collagen vascular disease, 4. Veno occlusive disease:1. Cytotoxic drugs before bone marrow transplant; 2. Herbal teaPATHOPHYSIOLOGY1. Obstruction to portal blood flow2. Porto systemic shunt by collaterals 3. Hepatocellular dysfunction 4. Increase in plasma volume5. Congestive gastropathy- gastric varices6. Haemorrhoids CLINICAL MANIFESTATIONS1. Variable hepatosplenomegaly: enlarged slightly or shrunken 2. Digital clubbing occurs in 1015% of cases. 3. Pretibial edema due to hypoproteinemia. 4. In biliary cirrhosis, patients often have jaundice, dark urine, pruritus, hepatomegaly, and sometimes xanthomas 5. Bleeding from esophageal varices is the most common presentation; hematemesis or with melena during intercurrent illness. 6. Growth retardation7. Ascites in patients with intrahepatic causes 8. Collateral vessels carrying blood from the portal to systemic circulation in the periumbilical region9. Splenomegaly, with hypersplenism 9. Signs of Liver failure:a. PRURITUS. Intense generalized itching, often with skin excoriation, can occur in patients with cholestasis (conjugated hyperbilirubinemia). b. SPIDER ANGIOMAS: most prominent on the face and chest; reflective of altered estrogen metabolism c. PALMAR ERYTHEMA: This may be due to vasodilation and increased blood flow.d. XANTHOMAS: deposition of lipid in the dermis and subcutaneous tissue.e. ENDOCRINE ABNORMALITIES: reflect alterations in hepatic synthetic, storage, and metabolic functions.eg. amenorrhea, infertility, gynecomastia etcf. Hepatorenal syndrome (HRS) is defined as functional renal failure in patients with end-stage liver disease. The pathophysiology of HRS is poorly defined, but the hallmark is intense renal vasoconstriction g. Hepatopulmonary syndrome is characterized by the typical triad of hypoxemia, intrapulmonary vascular dilations, and liver disease. DIAGNOSIS1. Ultrasonography:a. presence of esophageal varices b. cavernous transformation of the portal veinc. Reversal of portal vein bloodflow2. Selective arteriography of the celiac axis, superior mesenteric artery, and splenic vein3. CT scan similar to ultrasonographyTREATMENT 1. No specific treatment for cirrhosis2. Bleeding managed by:a. fluid resuscitation, initially in the form of crystalloid infusionb. replacement of red blood cells c. Correction of coagulopathy by administration of vitamin K d. the infusion of platelets or fresh frozen plasma e. A nasogastric tube to monitor for ongoing bleeding. f. An H2 receptor blocker such as ranitidine should be given intravenously to reduce bleeding from gastric erosions.g. Vasopressin bolus of 0.33 U/kg over 20 min, followed by a continued infusion of 0.2 U/1.73 m2/minh. Nitroglycerin, usually given as a portion of a skin patch, has also been used to decrease portal pressure i. Endoscopic sclerosis or elastic band ligation of esophageal varicesj. Sengstaken-blakemore tube can be placed to stop hemorrhage by mechanically compressing esophageal and gastric varices.k. Portacaval, mesocaval or distal splenorenal shunt proceduresl. Transjugular intrahepatic portosystemic shunt (TIPS), in which a stent is placed between the right hepatic vein and the right or left branch of the portal vein3. blockers such as propranolol act by lowering cardiac output and portal perfusion in adults4. Liver transplantation Ascites1. Clinical examination (fluid wave, shifting dullness), abdominal ultrasonography.2. Sodium restriction (12 mEq/kg/d), spironolactone (35 mg/kg/d), 3. furosemide (12 mg/kg/d),4. intravenous albumin (0.51 g/kg per dose), 5. paracentesis, 6. peritoneovenous (LeVeen) shunt, 7. TIPS, surgical portosystemic shunt, 8. OLT- orthotopic liver transplantation Hepatic encephalopathy 1. Abnormal neurologic examination, elevated plasma ammonia2. Protein restriction (0.51 g/kg/d),3. intravenous glucose (68 mg/kg/min), 4. neomycin (24 g/m2 BSA PO in four doses),5. rifaximin (200 mg three times a day in children > 12 hry), 6. lactulose (1 mL/kg per dose [up to 30 mL] every 46 h PO), 7. Plasmapheresis, hemodialysis, OLT. Hypersplenism 1. Low WBC count, platelets, hemoglobin. Splenomegaly 2. No intervention, partial splenic embolization, surgical portosystemic shunt, TIPS, OLT. Splenectomy may worsen variceal bleeding.3. PROGNOSIS4. intrahepatic disease has a poor prognosis5. Patients with progressive liver disease and significant esophageal varices ultimately require liver transplantation.