case 5 นศพ ปี 3

CASE VCASE V

Case study :

Case 5ชายอาย� 60 60 ปี�ปี� อาช�พทำ�านาอาการสำ�าคั�ญอาการสำ�าคั�ญ : อาเจี�ยนเปี�นเลื�อดอาเจี�ยนเปี�นเลื�อดประวั�ติ�ป�จจ�บั�นประวั�ติ�ป�จจ�บั�น :

• 1 ชม. ก่�อนมา รพ. ผู้��ปี�วยอาเจี�ยนเปี�นเลื�อดสดเลื�อดสด ปีระมาณ 2 2 ช�อนช�อนโต๊!ะโต๊!ะ ก่�อนหน�า น#$นอาเจี�ยนบ่�อย แต๊�ไม�เคยเปี�นเลื�อด

• 3 เด�อนก่�อนมา รพ. ร� �ส)ก่เหน�*อยง่�าย เบ่�*ออาหาร น�$าหน#ก่ต๊#วลืด ร� �ส)ก่เหน�*อยง่�าย เบ่�*ออาหาร น�$าหน#ก่ต๊#วลืด 8 8 ก่,โลืก่ร#มภายในเวลืา ก่,โลืก่ร#มภายในเวลืา 3 3 เด�อนเด�อน ส#ง่เก่ต๊ว�าทำ�อง่โต๊ทำ�อง่โต๊ ขึ้)$นมาก่ ไม�ม�อาก่ารไม�ม�อาก่าร

ปีวดทำ�อง่ ไม�ม�ถ่�ายอ�จีจีาระหร�อถ่�ายปี1สสาวะเปี�นเลื�อด ปีวดทำ�อง่ ไม�ม�ถ่�ายอ�จีจีาระหร�อถ่�ายปี1สสาวะเปี�นเลื�อดประวั�ติ�อดี�ติประวั�ติ�อดี�ติ :

• ด�*มส�ราด�*มส�รา ทำ�ก่ว#นว#นลืะ 2 แก่�วเปี�นเวลืานาน 30 ปี�• ก่,นยาช�ดแก่�ปีวดเม�*อยยาช�ดแก่�ปีวดเม�*อย ปีระมาณเด�อนลืะคร#$ง่• ไม�ส�บ่บ่�หร�*ไม�ส�บ่บ่�หร�* ไม�เคยม�ปีระว#ต๊,เจี2บ่ปี�วยร�นแรง่

ประวั�ติ�คัรอบัคัร�วัประวั�ติ�คัรอบัคัร�วั : ปีฏิ,เสธปีระว#ต๊,มะเร2ง่ในครอบ่คร#วปีฏิ,เสธปีระว#ต๊,มะเร2ง่ในครอบ่คร#ว ม�บ่�ต๊ร 3 คน หย�าก่#บ่ภรรยาได� 30 ปี� ปี1จีจี�บ่#นพ#ก่อาศั#ยอย��คนเด�ยว

Pertinent subjective data

• HematemesisHematemesis with no with no HematocheziaHematochezia and and MelenaMelena• Fatigue, Anorexia, Significant weight lossFatigue, Anorexia, Significant weight loss• Abdominal swelling with no painAbdominal swelling with no pain• Chronic alcoholismChronic alcoholism• NSAIDsNSAIDs

Ligament of Treitz

Upper GI Lower GI

Melena / Hematochezia

Bloody vomiting Coffee – ground apperance(RBC lyse by gastric acid)

No complain

40-50%

http://emedicine.medscape.com/article/196561-overview

Ligament of Treitz

• Peptic Ulcer Peptic Ulcer 35-62%35-62%• Esophageal VaricesEsophageal Varices 4-31%4-31%• Mallory – Weiss tearsMallory – Weiss tears 4-13%4-13%• Gastroduodenal erosionGastroduodenal erosion 3-11%3-11%• Erosive esophagitis Erosive esophagitis 2-8%2-8%• MalignancyMalignancy 1-4%1-4%

Ref : Harrison’s ed.16 page 235h

Chronic alcoholism and NSAIDsChronic alcoholism and NSAIDs

Causes of Upper GI bleeding

• Peptic Ulcer Peptic Ulcer • Esophageal VaricesEsophageal Varices• Mallory – Weiss tearsMallory – Weiss tears• Gastroduodenal erosionGastroduodenal erosion• Erosive esophagitisErosive esophagitis• MalignancyMalignancy

Harrison’s ed.16 page 235


No Massive vomitingNo Massive vomiting

No GERDNo GERD

High incidence + NSAIDs user High incidence + NSAIDs user

(Gastro esophageal reflux disease) Confirm?

• Peptic UlcerPeptic Ulcer• Esophageal VaricesEsophageal Varices• Gastroduodenal erosion Gastroduodenal erosion • MalignancyMalignancy

Harrison’s ed.16 page 235


Differential DiagnosisDifferential Diagnosis

• Clinical presentation Clinical presentation

• Physical Examination Physical Examination

• Endoscopic resultsEndoscopic results

Causes of Fatigue, Anorexia Causes of Fatigue, Anorexia and Weight lossand Weight loss

• Fatigue : Hypothyroidism, Anemia, Depression, Hepatitis, Diabetes mellitus, Cancer, Alcoholism, Chronic fatigue syndrome, Autoimmune disease, Adrenal insufficiency,Aging

• Anorexia : Anorexia Nervosa, Severe Depression, Dementia, AIDS, CancerCancer, Chronic renal disease

• Weight loss : CancerCancer, GI disorder, Cardiac disorder, respiratory disorder, Renal insufficiency, Rheumatologic disease, Infection, NSAID MedicationInfection, NSAID Medication

Significant Weight Loss

• Loss of >5% of body weight over 6–12 months (Harrison Internal Medicine 17th Ed)

• Loss of >10% of ideal body weight over 3 months (Schwartz's Principles of Surgery, 8th Edition)

Abdominal swelling with no pain

• Heart Disease • Liver Disease• Renal Disease • Abdominal Cancer• Hypoalbuminemia

No complain of peripheral edemaNo complain of peripheral edema

No Hematuria and no facial swellingNo Hematuria and no facial swelling


Hematemesis

Upper GI Bleeding

Fatigue Anorexia Weight loss

•Cancer•Infection•Alcoholism•NSAIDs•Malnutrition

Abdominal Swelling with no pain

Alcoholic Liver Diseases ?Alcoholic Liver Diseases ?

Endoscopic results(confirmed)

•Liver Disease•Abdominal Cancer•Hypoalbuminemia

PE, Lab results

Clinical presentation + PE

Expected Physical Examination

• Vital sign : BP , PR , RR• Sclera : Jaundice• Skin : Ecchymoses• Stigmata of chronic liver disease : spider

nevi, liver palm, gynecomastia, testicular atrophy

• Liver : can’t be palpable• Spleen : palpable• PR : hemorrhoid with no rectal shelf• Ascites??

Physical Examination

System Results Interpretations

Vital sign

BT 37 °cPR 100 /min (80-100)

RR 20/min (12-20)

BP 100/60 mmHg (120/80)

Normal ( no infections )Baroreceptor reflex from blood

lossNormal

Blood loss

GA good consciousnessnot pale, mild jaundice

No Encephalopathy Liver damage/ Hemolytic Anemia/ Biliary Obstruction ( tumor/stone )

Skin Decrease Coagulation factor or plt and low Vit K absorption

ecchymosis both legs



HEENT mild icteric sclera

mild enlargement of both parotid glands

no lymphadenopathy, no injected pharynx

Pre/intra/Post -hepatic jaundice

Increase estrogen

No MetastasisNo infections

Chest spider nevi at anterior chest wall,

breast enlargement both sides

Increase estrogen


Lungs normal breast sound, no adventitious sound

No Infections

Heart normal S1 and S2, no murmur

-

Genitalia Testicular atrophy both sides

Increase estrogen

PR hemorrhoid, no rectal shelf

Inferior rectal vein dilatation from portal

hypertensionor no metastasis from

Abdominal cancer



Abdomen • markly distended abdomen with superficial vein dilatation • shifting dullness , fluid thrill • liver can’t be palpate• mildly enlarged spleen and hypoactive bowel sound • mild tender at RUQ

Ascites, Portal

Hypertension


Fluid thrill

Ref : http://images.google.co.th/imgres?imgurl=http://imgsrc.baidu.com/baike/pic/item/2e6fa7381ce2a7d6d462256c.jpg&imgrefurl=http://baike.baidu.com/view/1655994.htm&usg=__b1ewpP9C6zLmT5SKIsTjUdwQ8N8=&h=640&w=480&sz=35&hl=th&start=17&um=1&tbnid=PQG0l_FOfN8FBM:&tbnh=137&tbnw=103&prev=/images%3Fq%3Dfluid%2Bthrill%26um%3D1%26hl%3Dth%26lr%3Dlang_th%26sa%3DX

http://imgsrc.baidu.com/baike/pic/item/2e6fa7381ce2a7d6d462256c.jpg

Pertinent Pertinent subjective data subjective data

- Splenomegaly

- Caput Medusae

- Ascites

- Hemorrhoid

- Gynecomastia

- Jaundice

- Ascites

- Weight loss

- Anorexia

- fatigue

- Ecchymosis

- Salivary gland enlargement

Portal hypertensionPortal hypertension

Confirmed by endoscopic

Alcoholic cirrhosis Alcoholic cirrhosis

Suspected liver CASuspected liver CA

chachexiaAbdominal pain

(caused Esophageal varices?)

& Physical examination conclusions& Physical examination conclusions

Fatty liver, Alcoholic Fatty liver, Alcoholic hepatitis, hepatitis,

Alcoholic hepatitis

Hepatocyte injury charaterise by balloon degeneration, Spotty necrosis, PMN infiltration

Fibrosis in perivenular and perisinusoidal space of Disse

May develop to alcoholic cirrhosis

Fever

Spider nevi

Jaundice

Abdominal pain

anorexia

Alcoholic cirrhosis

Anorexia

Malnutrition

Weight loss

Reduction in skeletal muscle mass

Hepatocellular dysfunction

Portal hypertension

Progressive jaundice

GE varices

Ascites

Encephalopathy

Alcoholic cirrhosis Alcoholic cirrhosis and HCCand HCC

Fatty liver

RUQ discomfort

Nausea

Jaundice

Difficulty differentiate alcoholic/non alcoholic fatty liver unless an accurate drinking history is verified biopsy

Hepatocellular carcinoma

Abdominal pain with abdominal mass in RUQ

Blood – tinged ascites (rare)

Jaundice (rare)

Significant deterioration of liver function

AFP, ALP

May include paraneoplastic syndrome•EPO Erythrocytosis •PTH Hypercalcemia

LFT

Fatty liver, Alcoholic Fatty liver, Alcoholic hepatitis, hepatitis, Alcoholic cirrhosis Alcoholic cirrhosis

and HCCand HCC

Laboratory Laboratory InvestigationInvestigation

• CBC : Hct WBC Plt : Infection? Anemia? Thrombocytopenia?• Serum Electrolyte : Na K Cl HCO3

• Liver Function Test : – Direct bilirubin– Total bilirubin– AST– ALT– Alkaline Phosphatase– Serum albumin– Serum globulin– Prothrombin Time

• Serum AFP : Cancer?• Emergency endoscopic finding : Blood loss• Chest X-ray : Infection, Lung compression from hepatomegaly• Abdominal X-ray : Liver span, Spleen• CT upper abdomen : Liver span, Urolithiasis, Abdominal Fluid• Laparoscopy : For alternative management• Hepatic Angiography : CA liver?• Tissue biopsy : Hepatic Parenchyma

Lab investigation

Lab investigationLab investigation

คั�าปกติ� ผลการติรวัจCBC - Hct - WBC - Plt

42-525,000-10,000

145,000-450,000

38%10,000 cell/mm3

150,000 /mm3

Electrolyte - Na - K - Cl - HCO3

135-1453.6 – 4.896 – 109

21-29

142 mmol/L4.3 mmol/L109 mmol/L23.5 mmol/L

Ref : J.Wallach, Interpretation of Diagnotic Tests, ed 7,New York, 2000

คั�าปกติ� ผลการติรวัจLFT - SGOT(AST) - SGPT(ALT) - total bilirubin - direct bilirubin - ALP - total protein - albumin - PT - FBS

15 - 4510 - 40

0.3 - 1.00.1 - 0.335 - 1176.3 - 8.63.1 - 4.3

< 1275 – 115

300 U/L158 U/L

5.2 mg/dL4.2 mg/dL

95 U/L6.4 g/dL2.2 g/dL18 sec

60 mg/dL

Serum AFP 0 - 15 700 microgram/L


Ref : J.Wallach, Interpretation of Diagnotic Tests, ed 7,New York, 2000

• Emergency endoscopic findings: – Dilated and bleeding blood vessels in esophagus

• CT upper abdomen: – Enlarged, Irregular liver with larged hypodense mass

size 5 cm involving right lobe (segment 6,7,8) with large area of necrosis

• Tissue biopsy of liver: – multiple micronodular cirrhotic nodules, size 0.2-0.3

cm with mass. – The tumor cells resemble hepatocytes, containing

round nuclei with increased N/C ratio, prominent nucleoli, granular eosinophilic cytoplasm and well defined cell borders.

– The trabecular are more than three cell thick and are covered be a layer of flattented endothelial cells.


CBCCBC• Hct

• Hematemesis

• WBC ( normal ) • No infection

• Plt ( normal )• Not cause ecchymosis

AST & ALTAST & ALT• AST (Aspartate Aminotransferase)

liver, skeletal muscle, brain, and heart. • ALT (Alanine Aminotransferase)

liver, kidney

• Intracellular enzyme involved in amino acid metabolism. • Released into the bloodstream when tissue is damaged,

especially in liver injury. • The level of elevation depends on the length of time that the

blood is tested after the injury. • Serum AST levels become elevated eight hours after cell

injury, peak at 24-36 hours, and return to normal in 3-7 days. • If the cellular injury is chronic, AST levels will remain elevated.

• Increase in: – Alcoholic hepatitis (AST > ALT) – Cirrhosis (AST > ALT) – Acute viral hepatitis (ALT > AST) – Vascular: right-sided congestive heart failure, shock liver,

Budd-Chiari syndrome (AST & ALT > 500-1000)

– Biliary tract obstruction – Liver abscess – Hepatocellular or metastatic cancer – Drugs eg INH, statins

• AST/ALT ratio > 2:1 is suggestive of alcoholic liver disease.

Case : AST 300 U/L , ALT 158 U/L AST/ALT ratio = 1.9:1

AST & ALTAST & ALT

• Normal Total bilirubin 0.25-1.5 mg/dl ( 5.2 )

Direct bilirubin 0-0.3 mg/dl ( 4.2 )

Indirect bilirubin 0.3-0.7 mg/dl ( 1.0 )

Jaundice

BilirubinBilirubin

• Type of jaundiceType of jaundice

Type Hyperbilirubinemia Urine bilirubin

Pre hepatic

Hepatic

Post hepatic

Indirect bilirubin Absent

Indirect/direct bilirubin increase

BilirubinBilirubin

Direct bilirubin (+ALP ) increase

Alkaline Alkaline PhosphatasePhosphatase• ALP :

เอ2นไซม7ทำ�*จี#ดอย��ในพวก่ไฮโดรเลืส(hydrolase) ทำ�าหน�าทำ�*เร�ง่ปีฏิ,ก่,ร,ยา แยก่พ#นธะขึ้อง่เอซ,ลืเอสเธอร7 (Acyl ester) แลืะฟอสฟอร,ลื เอสเธอร7

(phosphoryl ester) • bone, liver, placenta, bile canal epithelium• ALP

- hepatociliary disease : cholestasis - increase osteoblastic activity : children,

paget’s disease- pregnancy

ALP normal= 39-117 U/l ( 95 )

Serum proteinSerum protein• Total protein = albumin + globulin• In this case:

Total protein 6.4 (normal 6.0 - 8.0 g/dL) Albumin* 2.2 (normal 3.5 - 5.0 g/dL)Globulin 4.2 (normal 1.5 - 3.2 g/dL)

AlbuminAlbumin• The most important plasma protein• Synthesis by the liver • Albumin is tested to check how well the liv

er and kidney are working. • Decrease : malnutrition ( esp. protein) ,

liver dysfunction• Increase : intake food , drug (estrogen)

Prothrombin Prothrombin time ( PT )time ( PT )

• เปี�นก่ารต๊รวจีก่ารทำ�าง่านขึ้อง่• Normal 12s ( 18s )

Bleeding disorder

• Suspected chronic liver diseaseabnormal liver function

-Decrease coagulation factor-Decrease clearance of activated

coagulation factor and plasminogen activator

extrinsic pathway

Prothrombin Prothrombin time ( PT )time ( PT )

Fasting blood Fasting blood sugarsugar

• Normal80-100 mg/dl ( 60 )• Liver function

maintain blood glucose

abnormal function hypoglycemia

(glycogenolysis, gluconeogenesis)

SummarySummaryAST

ALT

Albumin

PT

(Plt normal)

Chronic Liver Disease

AST > ALT

Hepatic jaundice

FBS

Total bilirubinDirect bilirubinIndirect bilirubin

Alpha-Alpha-fetoproteinfetoprotein

• AFP is oncofetal glycoprotein• Synthesis by embryonic liver cells, fetal

yolk sac cells, alimentary canal• Tumor marker ( first stage of liver cancer )• Normal: 0-15 ng/ml

( increase in pregnancy )

• Germ-cell tumors of the testis• HCC & CCC• Metastatic carcinoma• Fetal malformations• Benign liver disease- Serum AFP > 500 ng/ml used to diagnosis

carcinoma of the liver

Alpha-Alpha-fetoproteinfetoprotein

Endoscopic Endoscopic findingsfindings

Emergency Emergency endoscopic findingsendoscopic findings

• Dilated and bleeding blood vessels in esophagus

Esophageal varices

CT SCANCT SCAN• CT upper abdomen:

Enlarged, irregular liver with larged hypodense mass size 5 cm involving right lobe (segment6,7,8) with large area of necrosis.

• http://www.wjgnet.com/1007-9327/11/200.asp

CT SCANCT SCAN

Diagnosis for Diagnosis for Liver MassLiver Mass • Trauma Causes • Infectious Disorders (Specific Agent )• Infected organ, Abscesses • Neoplastic Disorders • Congenital, Developmental Disorders • Anatomic, Foreign Body, Structural

Disorders • Arteriosclerotic, Vascular, Venous Disorders • Reference to Organ System • Pathophysiologic

Tissue Tissue BiopsyBiopsy

Micronodular cirrhotic noduleNormal hepatocytes

Liver BiopsyLiver BiopsyTumor cell resemble hepatocyte :-– round nuclei with increased N/C ratio – prominent nucleoli – granular eosinophilic cytoplasm – well defined cell borders – The trabecular are more than three cell thick

and are covered be a layer of flattented endothelial cells.

Liver tumor Liver tumor (epithelial tumor)(epithelial tumor)

• Hepatocellular tumor

• Cholangiocellular tumor

• Combined HCC/CCC

• Biliary cystadenocarcinoma

• Hepatoblastoma

Rare

(Common in female)

Common in child

No glandular structure

Normal hepatocytes Hepatocellular carcinoma

Tissue BiopsyTissue Biopsy

Ref : AASLD(American Associated Study of Liver Disease)

ElectrolyteElectrolyte• Na +

• K +

• Cl -

• HCO3-

Normal

Child-Pugh ClassificationChild-Pugh Classification

Ref. Harrison's Online

Note: Child-Pugh class is either A (a score of 5–6), B (7–9), or C (10 or above).

2.2

5.2

18

of Cirrhosisof Cirrhosis

liver cells necrosis

Ischemia

Liver dysfunction

Coagulation factor Ecchymosis both legs

Abnormal carbohydrate metabolism FBS

Plasma protein

albumin

sex hormone binding protein

estrogen

spider neviTesticular atrophy gynecomastia

Cirrhosis

ดี��มเหล�า ดี��มเหล�า 3030 ป ป

AST ,ALT


CT & Biopsy

Caput madusae

portal hypertension

ascites

hypoactive bowel sound

Bilirubin

Jaundice

AFP

Enlarged spleen

Hemorrhoid

Esophageal varices

rupture

Hematemesis

Hct

Basic Science

Liver

lobe

lobule

acinar

Structural unit

functional unit

LiverLiver

BloodBlood SupplySupply

Abdominal aorta

Superior mesenteric artery

Celiac trunk Inferior

mesenteric artery

Celiac trunk

Celiac trunk

Common hepatic artery

Hepatic artery

BloodBlood supply to the supply to the liverliver

Esophagus

: esophageal varices

Umbilicus

: caput madusae

Rectum

: hemorrhoids

Portosystemic anastomoses

anterior

posterior

Hepatic lobule

Zone 1

Zone 2

Zone 3

Most affected by Viral hepatitis

CYP450

Sensitive to Ischemia

Sensitive to toxic

Alcoholic hepatitis

Intermediate zone

Pit cell

( liver specific NK cell)

(Ito cell)

Central vein

Portal vein

Hepatic artery

Bile duct

Hepatic lobule

Carbohydrate metabolism GlycogenesisGlycogenolysis Gluconeogenesis

Fat metabolismketogenesis

Protein metabolism anabolism deamination urea formation

Secretion of bile Detoxification Storage of vitamins

(A,D,K,B12) & minerals (iron,copper)

Metabolism

LIVER FUNCTIONSLIVER FUNCTIONS

Cholesterol

liver

Primary bile acids

Secondary bile acids

intestinal bacteria

Cholic acid

Chenodeoxycholic acid

Deoxycholic acid

Lithocholic acid

Carbohydrate metabolism GlycogenesisGlycogenolysis Gluconeogenesis

Fat metabolismketogenesis

Protein metabolism anabolism deamination urea formation

Secretion of bile Detoxification Storage of vitamins

(A,D,K,B12) & minerals (iron,copper)

Metabolism

LIVER FUNCTIONSLIVER FUNCTIONS

Metabolism of Metabolism of alcoholalcohol Metabolize in the liver via two pathways

• The alcohol dehydreogenase pathway

- mainly in moderate level alcohol consumption

- alcohol acetaldehyde acetate

• The microsomal ethanol-oxidizing system ( MEOS )

- mainly in high level alcohol consumption

- cytochrome P450 converts alcohol to acetaldehyde

ADH

NAD+ NADH + H+

ALDH

http://www.accessmedicine.com/resourceTOC.aspx?resourceID=4

albumin

Alcoholic Liver Diseases

AlcoholAlcohol

Hepatocellularcarcinoma

Hepatocellularcarcinoma

HepatocyteHepatocyte

ProliferationProliferation LipogenesisLipogenesis

Fatty liverFatty liver

Kupffer cell

Kupffer cell

Cell damageCell damage

HepatitisHepatitis

InflammationInflammation

ApoptosisApoptosis

PhagocytosisPhagocytosisStellate

cellStellate

cell

Endothelial cell

Endothelial cell

FibrosisFibrosis

CirrhosisCirrhosis

+

+

Pathogenesis

+

+

Zone 1

Zone 2

Zone 3

Most affected by Viral hepatitis

CYP450

Sensitive to Ischemia

Sensitive to toxic

Alcoholic hepatitis

Intermediate zone

Normal liverNormal liver

Fatty liverFatty liver

Alcoholic Alcoholic HepatitisHepatitis

CirrhosisCirrhosis

90-100%

8-20 %

(40 %)

10-35%

Percentage of heavy drinkers who have the different stages of alcoholic liver disease.


HCV infection

HCV infection

++ 8181%%

1919%%

Pathophysiology

1

2

3

4

5

Portal hypertension

Postsinusoidal

•Chronic hepatitis•Primary biliary cirrhosis•Granuloma in chistosomiasis•Tuberculosis•Leukemia•Etc.

•Acute hepatitis•Alcoholic liver disease•Toxins•Amyloidosis•Etc.

•Budd Chiari syndrome (obstruction of the large hepatic veins)

•Portal vein thrombosis

•Right heart failure•Constrictive pericarditis•Etc.

Prehepatic PosthepaticIntrahepatic

SinusoidalPresinusoidal

Cirrhosis


Stellate cell สำร�าง collagen

Fibrosis

Liver cell damaged

ROS

regeneration

liver cells necrosis

Ischemia

Liver dysfunction

Coagulation factor Ecchymosis both legs

Abnormal carbohydrate metabolism FBS

Plasma protein

albumin

sex hormone binding protein

estrogen

spider neviTesticular atrophy gynecomastia

Cirrhosis


AST ,ALT


CT & Biopsy

Caput madusae

portal hypertension

ascites

hypoactive bowel sound

Bilirubin

Jaundice

AFP

Enlarged spleen

Hemorrhoid

Esophageal varices

rupture

Hematemesis

Hct

Management

ManagementManagement• Cirrhosis

– Cirrhosis without complication• Adequate mixed diet and avoidance of alcohol

– Cirrhosis with complications• Variceal bleeding• Ascites• Hematologic problems : Coagulopathies• Hypoalbuminemia• Ectopic varices : Hemorrhoid • Hepatic encephalopathy• Hepatorenal syndrome

• Hepatocellular carcinoma

Management of variceal bleedingManagement of variceal bleeding

• Acute variceal bleeding- Medical treatment

:Vasopressin, Nitroglycerin, Somatostatin

- Endoscopic treatment

:Sclerotherapy, Endoscopic variceal band ligation

- Balloon temponade- Transjugular intrahepatic portosystemic shunt (TIPS)- Surgical treatment

: Surgical shunt & Devascularization

Endoscopic variceal Endoscopic variceal band ligationband ligation

Balloon temponadeBalloon temponade

Transjugular intrahepatic portosystemic shuntTransjugular intrahepatic portosystemic shunt ( (TIPSTIPS))

DevascularizationDevascularization

• Prophylaxis of variceal bleeding- Medical treatment

: Propanolol, Nadolol

- Endoscopic band ligation

Management of variceal bleedingManagement of variceal bleeding

Management of AscitesManagement of Ascites

• Sodium & Water restriction• Diuretics : Spinololactone,

Furosemide

• Paracentesis

Management of Management of Hematologic problemsHematologic problems

Prolonged PT

Vitamin K

Normal PT Prolonged PT

Hypofibrinogenemia Deficiency of factor V

Amicar cryoprecipitate FFP

Normal PT

and/or

สมเก่�ยรต๊, ว#ฒนศั,ร,ช#ยก่�ลื. Portal hypertension, ก่ร�ง่เทำพเวชสาร,ก่ร�ง่เทำพ, 2536

Management of Management of HypoalbuminemiaHypoalbuminemia

• A daily intake of 1 g protein/kg body weight

Management of Hemorrhoid

• Stool softener

• Steroid

• Rubber Band Ligation

• Surgical treatment

Management of Hepatocellular CarcinomaManagement of Hepatocellular Carcinoma

• Curative Treatments

• Palliative Treatments


– Surgical treatment

– Liver transplantation


Child-Pugh ClassificationChild-Pugh Classification

Ref. Harrison's Online

Note: Child-Pugh class is either A (a score of 5–6), B (7–9), or C (10 or above).

2.2

5.2

18

of Cirrhosisof Cirrhosis


– Surgical treatment

– Liver transplantation


• Palliative Treatments– Systemic Chemotherapy : Mitoxantrone, 5-FU,

Doxorubicin, Mitomycin C, Cyclophosphamide– Transarterial Chemoembolization(TACE)

: Lipiodol + Chemotherapy– Percutaneous Ethanol Injection– Radiofrequency Ablation (RFA)– Immunotherapy


ReferencesReferences• Harrison Internal Medicine 16thed 2007• L.Schiff,E R.Schiff.Disease of the liver Ed 7, Philadephia,1993• S.Silbernagl,S.Lang.Color atlas of pathophysiology ,Newyork,2006

Robbin’s Basic Pathologic Disease 8thed 2008

• Willium F.Ganong:Review of medical physiology, 17th ed.USA,Connecticutt,Appleton & Lange, 1995

• http://www.nyp.org/health/liver_chronic.html• http://www.mdconsult.com/das/book/body/114745804-2/0/1249/

I4-u1.0-B0-7216-0187-1..50022-5--f5.fig?tocnode=51156723www.accessmedical.com

http://www.nyp.org/health/liver_chronic.html

http://www.nyp.org/health/liver_chronic.html

http://www.mdconsult.com/das/book/body/114745804-2/0/1249/I4-u1.0-B0-7216-0187-1..50022-5--f5.fig?tocnode=51156723























http://www.accessmedical.com/

• Anthony S. Fauci, Eugene Braunwald, Dennis L. Kasper, Stephen L. Hauser, Dan L. Longo, J. Larry Jameson, and Joseph Loscalzo, eds. Harrison's Principles of Internal Medicine, 17th ed. New Jersey :McGraw-Hill, 2008.

• Erwin Kuntz and Hans-Dieter Kuntz. Hepatology principle and practice,2th ed. Wetzlar :Springer,2006.

• Eugene R. Schiff, Michael F. Sorrell, Willis C. Maddrey, eds. Schiff's diseases of the liver, 9th ed. Philadelphia : Lippincott, Williams & Wilkins,2003.

• Kumar V, Abbas AK, Fausto N, Robbins SL, Cotran RS,eds. Robbins and Cotran pathologic basis of disease, 7th ed. Philadelphia:Elsevier Saunders; 2005.

• MacSween RNM, Burt AD,Portmann BC, Ishak KG, Scheuer PJ, AnthonyPP, eds. Pathology of the Liver. 4th ed. New York: Churchill Livingstone,2002.

• Robert K. Murray, Daryl K. Granner, Victor W. Rodwell ,eds. Harper's Illustrated Biochemistry, 27th ed. New Jersey :McGraw-Hill, 2006.

• http://www.niaaa.nih.gov/ResearchInformation/ExtramuralResearch/ResourcesAppGrantees/R21liver.htm

• https://atlases.muni.cz/atlases/stud/atl_en/main+jatra+jattum.html

ReferencesReferences

• พ,น,จี ก่�ลืลืะวณ,ชย7, อ�ดม คช,นทำร, วโรชา มหาช#ย.ว,ว#ฒนาก่ารในโรค ระบ่บ่ทำาง่เด,นอาหาร 7,สมาคมแพทำย7ระบ่บ่ทำาง่เด,นอาหารแห�ง่

ปีระเทำศัไทำย,ก่ร�ง่เทำพ,2540• เฟ<* อง่เพชร เก่�ยรต๊,เสว�.มะเร2ง่ต๊#บ่,ก่ร�ง่เทำพเวชสาร,ก่ร�ง่เทำพ,2544• เต๊,มช#ย ไชยน�ว#ต๊,. โรคต๊#บ่แลืะทำาง่เด,นน�$าด�. ส�าน#ก่พ,มพ7ก่ร�ง่เทำพเวช

สาร. 2529.• ช�วเคม�ทำาง่ก่ารแพทำย7: เมต๊าบ่อลื,สมขึ้อง่สารอาหารเช,ง่บ่�รณา

ก่าร. ก่ร�ง่เทำพ : บ่�!คเนทำ, 2546• สมเก่�ยรต๊, ว#ฒนศั,ร,ช#ยก่�ลื. Portal hypertension, ก่ร�ง่เทำพเวช

สาร,ก่ร�ง่เทำพ, 2536

ReferencesReferences

Thank you Thank you

for for

your attentionyour attention

case 5 นศพ ปี 3

Documents