ABDOMEN CASE DISCUSSION Preeti thapar
ABDOMEN CASE DISCUSSION
Preeti thapar
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
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
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
Personal history
Married
Chronic alcohol intake present = 180ml of brandy per day for 10yrs
Occasional smoker
Denied history of exposure
Family history
Patient married
Has 2 children
Has 13 siblings
No similar complaints in family members
Treatment history
Patient has taken ayurvedic medication as a single dose for his jaundice 3 months back
No h/o taking siddha,unani medications
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 +
• 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
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
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
Percussion- liver dulness confirmed by percussion
Traube space is resonant, shifting dulness absent
Auscultation –no bruit heard
No venous hum
No rub
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
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
Is it a decompensated cirrhosis?
What suggests decompensated cirrhosis?
• The symptom triad of decompensated cirrhosis:
1. Abdominal distension (Ascites)
2. Internal / External bleeding
3. Behavioral/Mental changes
• What is Reitan Chart?
Reitan’s number connection chart
• The number connection chart used to assess Hepatic encephalopathy
• The maximum score is 24
• The maximum permitted time is 30 seconds
• What are the synonyms of asterixis ?
• What is the mechanism of asterixis ?
ASTERIXIS
SYNONYMHepatic flap, Metabolic tremor
MECHANISMNegative myoclonusImpaired inflow of joint position sense to
brainstem RAS resulting in brief lapse of posture
Why etiology is alcoholism? Other etiology?
11.Why decompensated liver disease due to alcohol?
• Convincing history
• Parotid enlargement- a sign common in alcoholism
• Signs of liver cell failure
• Ascites
Other etiology
a) Chronic viral hepatitis
b) Wilson’s disease
c) Auto-immune hepatitis
d) Haemochromatosis
Pre-hepatic etiology of PHT
Causes…..
Pre-hepatic etiology of PHT
1.Non-cirrhotic portal fibrosis [ NCPF]
2.Portal vein thrombosis
Non-hepatic intra-abdominal etiology of ascites
1.Malignancy
2.Tuberculosis peritonitis
3.Protein losing enteropathy, nephrotic syndrome
4.Pancreatic ascitis
5.Meigs syndrome
Acute decompensation of chronic liver disease
Reasons?
Acute decompensation of chronic liver disease
• Superadded hepatitis
• Sepsis including SBP
• Malignant tranformation
What is Non-cirrhotic portal vein obstruction ?
NCPF?
• Common among lower socioeconomic class
• Mean age of presentation 30 years
Symptoms of NCPF?
• Symptoms at diagnosis
GIT Bleed, 50% have multiple episodes
Mass in the abdomen
Pain abdomen
occasionally distension( ascites )
Jaundice rare
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
What are the different mechanisms of ascites?
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
Underfill theory,1963
Overflow theory, 1970
Lymph imbalance theory,1980
Vasodilation theory,1988
What is SAAG?
Why SAAG is elevated in PHT?
Can SAAG be elevated in non-PHT causes
Serum Ascitic Albumin Gradient
• Serum albumin- Ascitic fluid albumin
• Gives a clue about portal hydrostatic pressure
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
Non-PHT causes for ↑SAAG>1.1g/dL
• Cirrhosis
• Alcoholic hepatitis
• CCF
• Massive hepatic metastases
• Vascular occlusion
• Fatty liver disease of pregnancy
• Myxedema
Can you get exudative ascites in portal hypertension
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.
Thank you