Acute pancreatitis
(proteolysis)
Characteristic
 Acute
 Chemical inflammatory process: (an autodigestive process,
pancreatic enzyme)
 Mild and severe
 Mild: edema, self-limited
 Severe: bleeding and necrosis, complications, high
mortality
Cause & mechanism
 Most common causes
 Alcoholism (western country)
 Gallstone disease (China)
 Less common causes
 Hyperlipidemia (serum
triglyceride level)
 Hypercalcemia
(hyperparathyroidism,
calcification of pancreatic
duct, stricture)
 Pregnancy
(hyperlipidemia)
 Obstruction of pancreatic
duct (stone, tumor)
o Pancreatic cancer,
ampullary tumor
 Surgery (pancreas,
gallbladder, stomach)
 Abdominal trauma (blunt
or penetrating)
Mechanism
 Autodigestive process
 lipase, phospholipase A, kininase, elastase
o digest pancreatic & peripancreatic tissues
 ERCP (contrast medium,
pancreatic duct pressure)
 Infection (AIDS)
(ascariasis, clonorchiasis,
mumps, cytomegalo-
virus, cryptosporidiosis,
cryptococcosis,
toxoplasmosis)
 Sphincter of Oddi
dysfunction
 Medications
(azathioprine, thiazide
diuretics, sodium
valproate)
 Idiopathic acute
pancreatitis
Pathological & clinical classification
Pathological
Clinical
o digest cellular o edema
membranes
o hemorrhage
o vascular
damage
o fat necrosis
 Autodigestion theory
Common channel Hypersecretion & obstruction
Stones, roundworm, Hypersecretion
inflammation
(obstruction, sphincter o alcohol
of Oddi dysfunction,
bile and duodenal CCK, secretin￪→pancreatic juice￪
juice reflux)
o heavy meal
Vomit after heavy
alcohol (duodenal stimulate pancreatic juice secretion
juice reflux)
Obstruction
o heavy alcohol or meal
duodenal papilla edema
o heavy alcohol
more protein in pancreatic juice
o pancreatic stone or tumor
 Inflammatory media
 PAF (platelet active factor)
 PG (prostaglandin)
 IL-2,6,8; TNF (tumor necrosis factor)
 Abnormality in pancreatic microcirculation
 Severe pancreatitis
Edematous pancreatitis
Necrotizing pancreatitis
Mild (self-limited)
Severe (High mortality)
Clinical findings Chronic complication (3weeks later)

 Symptoms Abscesses (1-4%) Pseudocyst (1-8%) Chronic pancreatitis

(severe)
 Abdominal pain: constant, dull, & boring pain; epigastric
pain; radiate to back chest & flank; worse in supine, lessen
when sitting or fetal potiton. Diagnosis

 Nausea, vomiting Case history + PE findings + Laboratory test + Abdominal

imaging
 Abdominal distention: paralysis, hypopotassemia,
peritonitis
 Lab test
 Fever
WBC count  increases (leukocytosis)
 Shock (SAP): vomiting, blood vessels dilation, GI bleeding
 neutrophil counts increase
 Hypocalcaemia: fat necrosis, fat acid
Serum amylase  Start increasing: 6 hours after
 Hyperglycemia: DM and its complications onset

 Signs
 Abdominal tenderness
 Jaundice
 Severe acute pancreatitis:
o Muscular guarding
o Rebound tenderness
o mass (abscess, pseudocyst)
o ascites
 Peaks:12-48 hours
 Return to normal: within 7 days
 3 times above the normal
 Non-pancreatic conditions
(increase amylase levels)
o pleural effusion o serum amylase: less than 3 times
above the normal
o tachycardia
o cholangitis
o tachypnea
o gastrointestinal perforation or
o hypotension ischemia

o Grey Turner's sign (flank discoloration, due to catabolism o ruptured ectopic pregnancy
of Hb)
Urine amylase  Rise: later than serum amylase
o Cullen's sign (blue discoloration around the umbilicus)
 Remains elevated: for 7 to 10 days
Complication
Lipase (more specific  Increase peak: within 4 to 8 hours
Acute compliaction & sensitive of lipase of the onset
measurement to detect
MOF DM alcoholic pancreatitis)-  Decrease: 8-14 days (amylase: 7
rarely use (expensive) days)
Secondary infection Organ failure
Hepatic function  Hepatic transaminase and serum
GI bleeding (stress  Cardiovasculat complication (bleeding, studies bilirubin levels increase
ulcer) vascular resistance↓)
 Not sufficiently reliable for
Brain complications  Pulmonary complication (atelectasis, diagnosing acute biliary pancreatitis
(pancreatic ARDS)
encephalopathy) Serum calcium &  hypocalcemia
 Renal complication (acute renal failure: glucose
DIC secondary to cardiovascular collapse & o fat — fatty acid — fatty acid
hypotension → acute tubular necrosis) calcium

o <1.75mmol/L (bad prognosis)

 hyperglycemia
  Radiologic (imaging) studies  Medications

 Abdominal plain radiographs (not specific) o decrease pancreatic secretion (atropine, somatostatin)

 Ultrasonography (suspect biliary disease) o reduce inflammation (indomethacin)

 CT  Nutritional management

o diffuse or segmental enlargement o Enteral feeding of an elemental diet into the jejunum ~
Total Parenteral Nutrition (TPN)
o necrosis
o Helping to maintain the integrity of the intestinal mucosa
o peripancreatic and retroperitoneal edema
o Preventing bacterial translocation across the intestine
o well-defined fluid collection (pseudocyst, abscess)
 Oral feedings should not be restarted until:
 ERCP (suspect biliary obstruction)
o major complications are treated
Treatment
o Free of pain & nausea
 Goals
o Serum amylase or lipase → returned to normal
 provide supportive care
 Management of gallstones
 decrease pancreatic inflammation and its results
o ERCP with sphincterectomy & stone extraction
 prevent and treat complications
o surgery
 Mild acute pancreatitis
 Management of pseudocysts
 bed rest
o Open internal surgical drainage of the cyst into the
 No oral intake (food, hydrochloric acid, cholecystokinin, stomach, duodenum, or a Roux loop of jejunum
secretin)
o New alternative treatment: minimally invasive
 Nasogastric suction (not as a routine treatment, but having (laparoscopic) surgery, percutaneous catheter drainage,
vomiting or obstruction) endoscopic drainage

 Intravenous hydration and electrolytes Chronic pancreatitis

 Analgesia (meperidine, morphine-not used) Characteristics

 Histamine receptor-2 blocker or PPI  irreversibly histological damage to pancreas

 Antibiotics (quinolones, antibiotics for anaerobe)  development of inflammation, fibrosis, and

destruction of exocrine and endocrine tissue
 Severe acute pancreatitis
 difficult to be diagnosed and classificated
 Same as MAP
Etiology & pathogenesis
 Vigorous iv hydration & electrolytes (critical)
 Most common: alcoholism & idiopathic
o Large volume, require careful attention to monitoring of
hemodynamics, urine output, renal and respiratory  Similar to AP: microlithiasis (implicated in some cases of
function chronic pancreatitis)

 Acute renal failure: dialysis  Rare: hereditary, hyperparathyroidism, autoimmune chronic

pancreatitis and obstruction of the main pancreatic duct
caused by stenosis, stones, or cancer
 Acute respiratory failure (ARDS): mechanical ventilation
 Rarely: SAP → sufficient pancreatic ductal stenosis → impair
drainage chronic pancreatitis
Symptoms (PMD) & Signs  H2 blocker or antacids (to reduce acid-stimulated
release of secretin, which can increase the flow of pancreatic
 P (pain): occasionally no pain, severe epigastric pain may last juice)
many hours or several days
 These do not relieve pain, requiring increased amounts of
 M (malabsorption): steatorrhea, passing greasy stools or even narcotics
oil droplets, and creatorrhea
 Medical treatment of CP pain (unsatisfactory), while
 D (DM): glucose intolerance or DM endoscopic or surgical treatment (drain persistent
pseudocysts, treat other complications or relieve pain)
Diagnosis
 Use of potent pancreatic enzymes recommended dose of
 Laboratory tests oral pancreatic enzymes: 30,000 U of lipase (eg, six tablets of
pancrelipase) with each meal
 amylase and lipase (frequently normal)
 Octreotide
 markers of inflammation: WBC count (generally
minimally elevated)  a long-acting somatostatin analogue

 Imaging tests (may be normal in first few years of disease)  "rest" the pancreas

 Plain x-ray of the abdomen: calcification (intraductal  pain relief appears minimal
stones)
 Steatorrhea (excess fat in feces): with four to six tablets of
 Abdominal ultrasound or CT potent pancreatic extracts with meals (each contains lipase
≥5000 U)
o abnormalities in size and consistency of the pancreas
 If steatorrhea is particularly severe
o pancreatic pseudocyst
 medium chain triglycerides
o dilated pancreatic ducts
 provided as a source of fat absorbed without pancreatic
 ERCP or MRCP: abnormalities of the main pancreatic enzymes
duct and secondary branches
 reducing dietary fat proportionally
 EUS
 supplementation with fat-soluble vitamins (A, D, K)
 Pancreatic function tests(assess endocrine & exocrine
function)  DM

 Endocrine  Oral hypoglycemic drugs rarely used

o DM: 2-h PBG level > 11.1 mmol/L; FBG level > 6.66  Insulin
mmol/L
 Pancreatic cancer
 Exocrine
 CP: at increased risk for pancreatic cancer
o The secretin test: unavailable in most hospitals
 Examination for malignancy:
o 72-h test for stool fat: not sensitive for pancreatic
exocrine dysfunction o brushing of strictures for cytologic analysis

o More sensitive tests: serum trypsinogen, fecal o measurement of serum markers (eg, CA 19-9,
chymotrypsin carcinoembryonic antigen)

Treatment Liver Cirrhosis

 Relapse of CP: treatment similar to that of AP Characteristic

 Eschew alcohol  irreversible chronic injury at advanced-

 IV fluids and fasting (beneficial) – no diet
 Small feedings restricted in fat and protein (to reduce
secretion of pancreatic enzymes)
stage
 pathological character: pseudolobule
 clinical manifestations: abnormal liver
function, portal hypertension
  multiple complications Pathologic manifestation

Cause  gross appearance

Virus  hepatitis virus (HBV, o early stage: enlarged

HCV)
o advanced stage: shrink in size, hard nodular appearance
 EB virus,
cytomegalovirus  physiological change

Alcohol ethanol 80g/d, above 10 years: liver o pseudolobule

cirrhosis
Pathological classification
fatty liver→hepatitis→fibrosis→cirrhosis
 Micronodular cirrhosis: 3mm-1cm, slim, regular connective
Obstruction of  primary biliary tissue septa
biliary system cirrhosis
 Macronodular cirrhosis: 3mm-5cm, marked differences in
 primary sclerosing size, thick, irregular connective tissue septa
cholangitis
 Mixed cirrhosis
Cardiovascular  Budd-Chiari syndrome
disorder
 heart failure
Clinical manifestation

Industrial toxin or  amioradone Different degree of liver function

medication
 arsenicals Compensated liver cirrhosis Decompensated liver cirrhosis

 oral contraceptives
Compensated liver cirrhosis
other  inherited and metabolic disorders
 symptoms:
 immune items: autoimmune hepatitis
 asymptomatic (at autopsy or surgery)
No exact cause  no exact causes-
 Nonspecific symptoms: Fatigue, anorexia, nausea,
cryptogenic liver cirrhosis
vomiting, abdominal distention

o similar to those of chronic hepatitis

Pahtogenesis
o difficult to distinguish by the clinical features (biopsy)
 Formation of regenerative nodule: hepatocyte necrosis &
collapse of the supporting reticulin network → irregular  Signs: mild hepatomegaly & splenomegaly
nodular regeneration of remaining liver cells → subsequent
connective tissue deposition from portal triads to central  Tests:
veins → pseudolobule: the connective tissue network
surrounds small masses of remaining liver cells  liver function: normal or mildly abnormal

 Mechanism in hepatic fibrosis:  no specific changes in image tests

 stellate cell activation: from fat-storing cell into an Decompensated liver cirrhosis
myofibroblast-like cell, be able to synthesise collagen
matrix and inhibitors of collagen breakdown
Hepatic insufficiency Portal hypertension
 Cellular factors (cytokines): injured hepatocyte (IGF,
TGF- α), platelets and kupffer cell (EGF, TGF-β, PDGF)

Hepatic insufficiency

General symptoms: fatigue, weight loss, hepatic face, drying of

skin, edema

Digestive symptoms: anorexia, nausea, vomiting, diarrhea,

abdominal distention (hypokalemia, gastric congestion, flora
imbalance, constipation, ascites, enlargement of liver and spleen)
Bleeding trend and anemia: skin (ecchymosis and petechia),  subacute onset
epistaxis gingival bleeding, hypermenorrhea, GI bleeding
(decreasing of coagulation factors synthesis, hypersplenism),  fever, abdominal pain, distention, diarrhea, more
anemia (blood loss, hypersplenism) ascite, oliguria

 tenderness, positive result of ascites culture

Endocrinal disturbance:
 Hepatorenal syndrome (HRS)
 Inactivation of estrogen￬: estrogen￪ androgen￬
 Pathogenesis: (renal vasoconstriction)
 sexual hypoesthesia, testicular atrophy, amenorrhea,
sterility dilation of capillary vascular, palmar erythema, o disturbances in systemic hemodynamics
spider naevus, male mammary development)
o activation of vasoconstrictor systems (renin-angiotensin)
 Inactivation of aldosterone and antidiuretic hormone￬:
o reduction in activity of the vasodilator systems (nitrogen
 aldosterone and antidiuretic hormone ￪salt and water
monoxidum, NO)
retention
 Clinical manifestation:
 inactivation of insulin ￬: insulin ￪
o intractable ascites
 hepatogenic IGT or DM, hypoglycemia

Jaundice: (xanthochromia) o oliguria or anuria

 50～60% patients: mild or moderate jaundice o azotemia

 Intrahepatic biliary obstruction (compression of fiber) o dilutional hyponatremia and

 becoming more severe: bad prognosis o hyponatruria

Complication  Hepatopulmonary syndrome (HPS)

 Upper GI bleeding  Pathogenesis:

 common reasons: variceal bleeding, o inactivation of vasodilator ↓

portal hypertensive gastropathy
o nitrogen monoxidum, NO ↑
 precipitating reasons: hard or rough
food, drugs, cough, vomiting o pulmonary arteriovenous shunts → vasodilation →
hypoxaemia, reduction in arterial oxygen saturation
 clinical manifestations:
hematemesis, melena, hematochezia, shock  Clinical manifestation: clubbing finger, cyanosis (central)

 Infection  Hepatic encephalopathy

 common system: respiratory, urinary, biliary,  Primary liver cancer

digestive
Portal hypertension
 organisms: G－bacilli, anaerobe
Mechanism
 special infections: SBP, tuberculous peritonitis
 portal venous pressure > 10mmHg
 Spontaneous bacterial peritonitis (SBP)
 portal venous pressure = portal blood flow×portal vascular
o Definition: liver cirrhosis patients, no peritoneal resistance
organisms, bacterial infection of ascitic fluid
 portal vascular resistance ↑: initiative factor
o Clinical features：
 collagen fiber deposition in space of Disse
 G－ bacilli
 regenerative nodule compress hepatic sinus and hepatic
 always have large volume of ascites venous system
  portal blood flow ↑: accerlerating factor o portal vein pressure↑

 inactivation of noradrenaline ↓, sympathetic nerve excited, o salt and water retention

cardiac output ↑
o plasma oncotic pressure ↓
 low reaction on vasoconstrictors, visceral arteriole dilation,
visceral vascular congestion, portal blood flow↑, portal  Clinical features:
hypertension
o recurrent

o always have precipitating reasons

Classification
o dyspnea

Intrahepatic Extrahepatic o 5% pleura effusion, right pleura effusion

o normal: 50ml in peritoneal cavity

Intrahepatic pre-sinusoidal
Sinusoidal
Intrahepatic post-sinusoidal
Extrahepatic pre-sinusoidal: portal
vein thrombosis; splenic vein >200ml: ascites; >1000ml: shift dullness
thrombosis, superior mesenteric
vein thrombosis Test
Eextrahepatic post-sinusoidal: 1) Laboratory tests
Budd-Chiari syndrome (hepatic
vein, inferior vena cava),  Blood regular test & stool test
constrictive pericarditis)

Compensated Decompensated
Clinical manifestation

 Splenomegaly Normal Anaemia

 Congestion of spleen
WBC ↓
 Shrink after upper GI bleeding
Platelet↓
 Hypersplenism:
Urine bilirubin and
o splenomegaly urobilinogen↑

o blood cells ↓: platelet, WBC, RBC Positive stool occult blood test

o hyperplasia of bonemarrow hematopoiesis

 Liver function test

 Collateral circulation Aminotransferase ALT ↑: cytoplasm (more sensitive)

AST ↑: mitochondrion (more severe)

70% ALP ↑; 90% GGT ↑:

intrahepatic biliary obstruction

complicated with liver cancer

Bilirubin Different degree, more severe means

(invove esophagus, fundus of stomach, anterior abdominal wall, rectum)
bad prognosis
 Consequences: Upper GI bleeding, PHG, Hepatic
encephalopathy Albumin & ALB↓ GLO↑ A/G <1
globumin
Severe decreasing: ALB<28g/L
 Ascites

 Mechanism: Prothrombin time Predict hepatic reservation

  d: dilation of collateral veins

End stage: apparently prolonged  e: enlargement of spleen

Vit K: cannot make PT less prolonged  w: widen interlobar fissure

bad prognosis
 s: shrink of liver
Fat metabolism Compensated: normal level of
cholesterol  w: waved surface of liver

Decompensated: decreased level of 3) Special tests

cholesterol
 Gastroendoscopic test: location and degree of the esophageal
and gastric varices

 Items for liver fibrosis:

 type Ⅲ procollagen, type Ⅳ collagen

Diagnosis
 hyaluronic acid (HA), fibronectin (FN),
laminar (LN) History + clinical manifestation + test + biopsy

 Immune test:
History HBV/HCV infection, alcoholic abuse,
 AFP ↑: active liver cirrhosis or liver cancer medications, stasis of bile (PBC), etc

 Antimitochondrial Ab, antinuclear Ab, smooth

muscle Ab: primary biliary cirrhosis
 Ascitic fluid test:
 SBP: routine tests (WBC), culture
 Tuberculous peritonitis: TB-Ab in blood or
fluid
 Cancerous ascites: cancer cells in fluid
Clinical Symptoms: symptoms of liver cells’ necrosis and
manifestation portal hypertension
Sign: hepatic face, spider naevus, palmar
erythema, splenomegaly, edema, shifting dullness
Test liver functions(A/G ↓, PT ↑; PBC: ALP ↑,GGT ↑)
, B ultrasound, barium meal test, gastric
endoscope, CT scanning, etc

Biopsy Pseudolobule

Diagnosis of complication

 Upper GI bleeding

2) Image tests  Infection: SBP

 B ultrasound:  HRS:

 cheap and no damage  plasma creatinine >132.6;

 size of liver and spleen, appearance of liver, diameters of  24h creatinine clearance rate < 40ml/min
portal vein and splenic vein
 Other criterias: Urine volume<500ml/d, osmotic pressure:
 ascites urine>plasma, Urine sodium<10mmol/L, plasma
sodium<130mmol/L
 Barium meal tests:
 Primary liver cancer
 esophageal varices: vermiform filling defect
 Hepatic encepholopathy
 CT (a-d-e-w-s-w)
 HPS: oxygen partial pressure < 70mmHg; pulmonary
 a: ascites scanning: positive
Treatment acid inhibitors: H2RA, PPI tube

1) Principle  sclerotherapy or banding

 early stage: (reversible)  advanced stage: (irreversible)

 SBP
 avoid the causes  recovery of necrotic liver
cells  early, enough dose, combined antibiotics, duration of 2
 recovery of necrotic weeks
liver cells  prevention and treatment of
complications  G－bacilli: quinolones, cephalosporins
 reverse liver
fibrosis  liver transplantation  HRS

 bad prognosis
2) General therapy
 avoiding precipitating reasons (heavily diuresis)
 Rest
 correct the electrolyte disturbance
 Diet
 albumin or plasma supply
o high vitamin and easy to be digested food
 Liver transplantation
o no hepatic coma: 1-1.5g protein/kg.d, less protein with
hepatic coma

o restrict salty diet

 Support therapy: vitamin, amino acid, albumin, plasma

3) Medication

 no alcohol, avoid some drugs

 reverse liver fibrosis

 protect liver cells: reduced glutathione sodium

Hepatic encephalopathy
 decrease the level of aminotransferase: diammonium
glycyrrhizinate, bifendate Characteristic

4) Treatment on ascities  Definition

 salt and water restriction  Severe liver diseases

 proper usage of diuretic drugs  Metabolic disturbance

 Neuropsychiatric syndrome
 increase oncotic pressure
 Clinical manifestations
 paracentesis
 Changes of intellect, personality, emotions and
5) Surgery for portal hypertension consciousness; finally coma

 Transjugular intrahepatic portosystemic stent shunts (TIPSS)  Subclinical or latent HE

6) Treatment on complication  No abnormalities in clinical manifestations or biochemical

 Upper GI bleeding
 no ingestion
 blood volume supply
tests
 Abnormal number connection test and
electroencephalogram (EEG)
 decrease portal venous
blood flow: somatostatin Cause
 Sengstaken-Blakemore
 Main cause:
  liver cirrhosis (posthepatic cirrhosis)  GABA level is parallel to the severity of encephalopathy

 portosystemic connection surgery (portosystemic  Benzodiazepine antagonist (flumazenil): relieve neuronal

encephalopathy) depression

Porto-systemic shunting → portal blood directly flow into  Amino acid imbalance
systemic circulation → toxin not detoxified by liver → HE
 decompensated liver cirrhosis:
aromatic aa↑, branched-chain aa↓
 Less common:
 Manganese (Mn) deposition
 acute fulminant hepatitis  fatty liver in preganancy
 80% liver cirrhosis patients: MRI show high signal in
 hepatic failure  severe biliary infection
globus pallidus
primary hepatic carcinoma  Physiological tests confirm it manganese (Mn) deposition

 Precipitants: Clinical features

 upper GI bleeding  anesthetic agents  Acute & chronic manifestation

 uraemia  constipation

 infection  somnifacient (diazepam)  hepatic failure

 high-protein diet  surgery Acute  no apparent perticipants

 paracentesis (>3-5 liters)  electrolyte imbalance  suffer from coma or even die
just several days after onset

 porto - systemic
encephalopathy
Chronic
 chronic, recurrent
consciousness disorders or coma
Pathogenesis
 always have perticipants
 Ammonia (↑ammonia in blood)
 fetor hepaticus
 More synthesis
*Fetor hepaticus: a unique musty (zymotic apple) odor of the
o Exogenous: high-nitrogen food or drugs breath and urine

o Endogenous: GI bleeding, azotemia  Flapping tremor (asterixis, liver flap)

 Less clearence  have the patient extend the arms and dorsiflex the hands

o Hepatic failure, less urea synthesis  nonrhythmic asymmetric lapse of the extremities, head and
trunk
o Porto-systemic shunts, directly into systemic circulation
Clinical stages
 False neurotransmitters
Stage Mental status Asterixis EEG
 Result in part from plasma alterations of aromatic and
branched-chain amino acids 1 euphoria or depression, mild +/- Tripastic waves
confusion, slurred speech,
 Same structure as noradrenaline disorder sleep

 Can’t transmiss nerve impulse 2 lethargy, moderate confusion + Tripastic waves

 Consciousness disorder, coma 3 marked confusion,incoherent + Tripastic waves

speech, sleeping but arousable
 γ-aminobutyric acid
4 coma, initially responsive to - Delta activity
noxious stimuli, later
 Inhibitory neurotransmitter → neuronal depression unresponsive

 ↑GABA level in patients with liver cirrhosis

Lab test  Branched-chain aa

 Blood ammonia:  Treatment for cerebral edema

 chronic HE: ↑  dehydrant, ice cap

 acute HE: normal  Prevention for bleeding

 EEG: early diagonosis  vitK1, fresh blood transfusion

 Number connection test: valuable for subclinical HE  Dialysis

Diagnosis  uremia

 severe liver diseases or porto-systemic shunts

 changes of intellect, personality, emotions and consciousness;

finally coma

 perticipants

 abnormal liver function, blood ammonia ↑

 positive flapping tremor, abnormal EEG

 abnormal number connecting tests for subclinical HE

Differential diagnosis

 psychological diseases

 coma resulting from other diseases:

 DM, hypoglycemia, uremia

 cerebrovascular accident

 brain infection, over-dose somnifacient

Treatment (early recognition, prompt treatment)

 elimination of precipitators

 lowering of blood ammonia:

 dietary protein restriction

 enema or laxatives: acetic acid

 inhibit bacterial growth: lactulose (osmotic laxative);

neomycin, metronidazole

 medications for ammonia reducing　

 glutamate

 arginine

 sodium benzoate

 phenylacetic acid

 ornithine- α-ketoglutaric acid

 Benzodiazepine antagonist

 flumazenil