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Page 1: Srmc abdomen

ABDOMEN CASE DISCUSSION

Preeti thapar

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Chief complaints

40 yrs old male patient presented to us with c/o

Jaundice-3months

High coloured urine-2months

Loss of appetite-2 months

Loss of weight (15kgs)-2 months

Blood stained vomitus -1month

Bleeding gums -1 month

Right sided abdominal pain -1month

h/o fever -1day

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HistoryNo h/o melena

No h/o abdominal distention

No h/o pedal oedema

No h/o oliguria

No h/o pruritis

No h/o rash

No h/o dyspnea

No h/o loose stools

No h/o cough with expectoration

No h/o altered sleep cycle

no h/o seizures/LOC

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PAST HISTORY

No h/o blood transfusion

No h/o iv drug abuse

No h/o surgeries in past

No h/o diabetes/TB/hypertension/CADin past

No h/o recent travel

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Personal history

Married

Chronic alcohol intake present = 180ml of brandy per day for 10yrs

Occasional smoker

Denied history of exposure

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Family history

Patient married

Has 2 children

Has 13 siblings

No similar complaints in family members

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Treatment history

Patient has taken ayurvedic medication as a single dose for his jaundice 3 months back

No h/o taking siddha,unani medications

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General examination

Patient is concious ,oriented to time place and person

Vitals ;BP -120/80 HR – 78/MIN

TEMP -98.4

No pallor,cynosis,pedal oedema,lymphadenopathy

Icterus present

Clubbing +

Alopecia +

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• Tatoo mark on rt arm

• Scar mark over right shoulder

• Lipoma over forehead

• Hyperpigmented patch over right popliteal fossa

• No KF ring

• No Bitot spot

• No xanthelasma

• B/l Parotid enlargement present

• Oral cavity –normal

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General physical exam

Fetor hepaticus absent

Gynaecomastia +

Loss of axillary hair,chest hair +

No scratch marks

No bruises/rash

No spider naevi

No palmar erythema

No dupuytrens contracture

No testicular atrophy

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Per abdomen

Inspection –normal shape, all quadrants move equally with respiration ,no visible veins,no scars, all hernial orifices intact

Palpation

Superficial palpation-normal ,no tenderness

Deep palpation -right hypochondrium tenderness present,liver enlarged 8 cm below costal margin, rounded borders,smooth surface ,firm in consistency

Liver span –17.5 cm

Spleen felt 5 cm below costal margin ,splenic notch felt surface smooth ,firm in consistency

No other mass felt

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Percussion- liver dulness confirmed by percussion

Traube space is resonant, shifting dulness absent

Auscultation –no bruit heard

No venous hum

No rub

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Other systems CVS –S1S2 heard,no murmur heard

Respiratory system – chest b/l symmetrical ,b/l air entry is equal ,no adventitious sounds heard

CNS –patient is concious ,oriented to time place and person

Higher functions normal

No flap or tremor seen

Trail making test – 18 sec

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Provisional diagnosis

Chronic decompensated parenchymal liver disease - cirrhosis with portal hypertension probably of alcoholic etiology with no ascites with no features of hepatic encephalopathy and coagulopathy

To rule out malignancy

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Is it a decompensated cirrhosis?

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What suggests decompensated cirrhosis?

• The symptom triad of decompensated cirrhosis:

1. Abdominal distension (Ascites)

2. Internal / External bleeding

3. Behavioral/Mental changes

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• What is Reitan Chart?

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Reitan’s number connection chart

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• The number connection chart used to assess Hepatic encephalopathy

• The maximum score is 24

• The maximum permitted time is 30 seconds

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• What are the synonyms of asterixis ?

• What is the mechanism of asterixis ?

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ASTERIXIS

SYNONYMHepatic flap, Metabolic tremor

MECHANISMNegative myoclonusImpaired inflow of joint position sense to

brainstem RAS resulting in brief lapse of posture

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Why etiology is alcoholism? Other etiology?

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11.Why decompensated liver disease due to alcohol?

• Convincing history

• Parotid enlargement- a sign common in alcoholism

• Signs of liver cell failure

• Ascites

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Other etiology

a) Chronic viral hepatitis

b) Wilson’s disease

c) Auto-immune hepatitis

d) Haemochromatosis

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Pre-hepatic etiology of PHT

Causes…..

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Pre-hepatic etiology of PHT

1.Non-cirrhotic portal fibrosis [ NCPF]

2.Portal vein thrombosis

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Non-hepatic intra-abdominal etiology of ascites

1.Malignancy

2.Tuberculosis peritonitis

3.Protein losing enteropathy, nephrotic syndrome

4.Pancreatic ascitis

5.Meigs syndrome

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Acute decompensation of chronic liver disease

Reasons?

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Acute decompensation of chronic liver disease

• Superadded hepatitis

• Sepsis including SBP

• Malignant tranformation

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What is Non-cirrhotic portal vein obstruction ?

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NCPF?

• Common among lower socioeconomic class

• Mean age of presentation 30 years

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Symptoms of NCPF?

• Symptoms at diagnosis

GIT Bleed, 50% have multiple episodes

Mass in the abdomen

Pain abdomen

occasionally distension( ascites )

Jaundice rare

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Signs in NCPF

• Splenomegaly is universal

• Two-thirds have massive spleen

• Mild or no ascites

• No anterior abdominal or back veins

• Liver occasionally enlarged

• No signs of liver cell failure

• Encephalopathy rare

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What are the different mechanisms of ascites?

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Mechanisms of ascitis

1. Underfill theory, S.Sherlock-1963

2. Overflow theory, Libermann-1970

3. Lymph Imbalance theory,Witt-1980

4. Vasodilation theory,Schrier-1988

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Underfill theory,1963

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Overflow theory, 1970

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Lymph imbalance theory,1980

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Vasodilation theory,1988

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What is SAAG?

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Why SAAG is elevated in PHT?

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Can SAAG be elevated in non-PHT causes

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Serum Ascitic Albumin Gradient

• Serum albumin- Ascitic fluid albumin

• Gives a clue about portal hydrostatic pressure

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SAAG

• A gradient >1.1 g/dl indicates PHT as the probable cause of ascitis

• High gradient due to ↑Portal hydrostatic pressure pushing the water to peritoneum leaving albumin in the vasculature

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Non-PHT causes for ↑SAAG>1.1g/dL

• Cirrhosis

• Alcoholic hepatitis

• CCF

• Massive hepatic metastases

• Vascular occlusion

• Fatty liver disease of pregnancy

• Myxedema

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Can you get exudative ascites in portal hypertension

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Exudative ascites in portal hypertension

• Cardiac ascites

• Acute Budd-Chiari syndrome

The concept of exudate and transudate in

the evaluation of ascites is no longer

recommended.

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Thank you