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    Dr.P.santhosh Kumar Post Graduate

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    Srilakshmi Sathiya
    - The patient is a middle aged male with signs of liver failure including pallor, icterus, muscle wasting and distended abdomen. - Examination found the liver to be cirrhotic based on signs such as shifting dullness and a reduced liver span. - The most likely diagnosis is decompensated chronic liver disease/cirrhosis caused by conditions like alcoholism, viral hepatitis, or non-alcoholic fatty liver disease. Management includes treating complications and consideration for liver transplantation.

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    Dr.P.santhosh Kumar Post Graduate

    Uploaded by

    Srilakshmi Sathiya
    56 views22 pages
    - The patient is a middle aged male with signs of liver failure including pallor, icterus, muscle wasting and distended abdomen. - Examination found the liver to be cirrhotic based on signs such as shifting dullness and a reduced liver span. - The most likely diagnosis is decompensated chronic liver disease/cirrhosis caused by conditions like alcoholism, viral hepatitis, or non-alcoholic fatty liver disease. Management includes treating complications and consideration for liver transplantation.

    Original Description:

    Abdomen short case presentation

    Original Title

    Abd1

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    - The patient is a middle aged male with signs of liver failure including pallor, icterus, muscle wasting and distended abdomen. - Examination found the liver to be cirrhotic based on signs such as shifting dullness and a reduced liver span. - The most likely diagnosis is decompensated chronic liver disease/cirrhosis caused by conditions like alcoholism, viral hepatitis, or non-alcoholic fatty liver disease. Management includes treating complications and consideration for liver transplantation.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    56 views22 pages

    Dr.P.santhosh Kumar Post Graduate

    Uploaded by

    Srilakshmi Sathiya
    - The patient is a middle aged male with signs of liver failure including pallor, icterus, muscle wasting and distended abdomen. - Examination found the liver to be cirrhotic based on signs such as shifting dullness and a reduced liver span. - The most likely diagnosis is decompensated chronic liver disease/cirrhosis caused by conditions like alcoholism, viral hepatitis, or non-alcoholic fatty liver disease. Management includes treating complications and consideration for liver transplantation.

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    © All Rights Reserved
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    Abdomen system

    short case

    • Dr.P.santhosh Kumar post graduate


    General examination

    • Middle aged male individual

    • Conscious oriented , afebrile

    • Thin built and poorly nourished

    • Generalised muscle wasting present

    • BMI - 23.2 kg/m2

    • Pallor + icterus ++

    • No icterus clubbing cyanosis pedal edema and lymphadenopathy .


    SIGNS OF LIVER
    FAILURE
    KF RING ABSENT
    PREMATURE ARCUS ABSENT
    SUB CONJUCTIVAL BLEED ABSENT
    BITOT’S SPOT ABSENT
    LOSS OF STERNAL AND AXILLARY PRESENT
    HAIR
    PAROTID ENLARGEMENT ABSENT
    FETOR HEPATICUS ABSENT
    GYNAECOMASTIA ABSENT
    SPIDER NAEVI ABSENT
    DUPUYTREN’S CONTRACTURE ABSENT

    PALMAR ERYTHEMA ABSENT


    SPLINTER HAEMORRHAGES ABSENT
    KOILONYCHIA ABSENT
    LEUKONYCHIA ABSENT
    ASTERIXIS ABSENT
    Vitals
    • Afebrile - 98.4 F

    • Pulse - 66/min regular in rhythm , normal in


    volume and character , no vessel wall thickening ,
    no radioradial , no radiofemoral delay , all
    peripheral pulses felt

    • JVP- not elevated

    • B.P- 100/60 mm/Hg measured in right upper limb


    in sitting posture

    • R.R - 20/min
    Systemic
    examination
    • On inspection , abdomen examined in supine position

    • Abdomen distended and flanks are full , umbilicus is


    everted and pushed down.

    • Umbilical hernia present .

    • Divarication of recti present

    • All quadrants move equal with respiration

    • No dilated veins / no visible pulsation seen


    System examination

    • Skin : dry scaly skin


    present with multiple
    iatrogenic needle marks
    seen over the flanks .

    • Umbilical hernia with


    divarication of recti seen

    • Inguinal orifice , genitalia


    and left clavicular fossa
    appears normal .
    Palpation on supine
    position
    • Superficial palpation : no warmth no tenderness

    • Deep : liver and spleen not palpable .

    • Measurements :

    • From xiphysternum - umbilicus 24 cms

    • From umbilicus to pubic symphysis - 14 cms

    • Abdominal girth - 82 cms at the level of umbilicus


    Percussion
    • Liver span measures around 7.5 cms from right
    fifth intercostal space

    • Shifting dullness present and fluid thrill absent

    • AUSCULTATION:

    • Bowel sounds heard

    • No hepatic bruits , No renal artery bruit, No splenic


    rub
    Differential diagnosis

    • Decompensated chronic liver disease - cirrhosis


    with portal hypertension .
    Causes of cirrhosis ?
    • Alcoholic liver disease

    • Chronic viral hepatitis B &C

    • Hemochromatosis

    • Nonalcoholic fatty liver disease

    • Autoimmune hepatitis

    • Primary and secondary biliary cirrhosis

    • Primary sclerosis cholangitis

    • Medications ( methotrexate ,isoniazid )


    Causes of cirrhosis
    • Wilson disease

    • Alpha -1 anti trypsin deficiency

    • Celiac disease

    • Granulomatous liver disease

    • Idiopathic portal fibrosis

    • Polycystic liver disease

    • Infection ( brucellosis , sylphilis , echinococcosis)

    • Right sided heart failure

    • Hereditary hemorrhagic telangiectasia

    • Veno-ooclusive disease
    How to prevent
    superimposed insults on
    liver ?

    • Vaccinations - against hepatitis A , B, influenza and


    pneumococcal.

    • Avoidance of hepatotoxins

    • Medication adjustments- non opioid , opioids, anti-


    convulsants, anti-microbial , cardiovascular and
    anti diabetes drugs.
    Can cirrhosis be
    reversed?

    • Significant reversibility documented in early


    fibrosis (<F2 ) , in hepatitis B, C , and NASH with
    advent of non invasive radiographic staging of
    early fibrosis along with anti-fibrotic therapies.
    How to manage
    refractory ascites ?
    1)An inability to mobilize ascites (manifested by minimal to no weight loss)
    despite confirmed adherence to the dietary sodium restriction (88 mEq [2000
    mg] per day) and the administration of maximum tolerable doses of oral
    diuretics (400 mg per day of spironolactone and 160 mg per day
    of furosemide.This dose is only infrequently reached because patients often
    develop side effects at much lower doses.

    2)Rapid reaccumulation of fluid after therapeutic paracentesis despite


    adherence to a sodium-restricted diet.

    3)The development of diuretic-related complications such as progressive


    azotemia, hepatic encephalopathy, or progressive electrolyte imbalances.
    Refractory ascites
    management
    • Continuing sodium restriction

    • Discontinuing beta blockers , ACE inhibitors and


    NSAIDS.

    • Liver transplantation

    • Therapeutic paracentesis

    • TIPS(Transjugular intrahepatic portosystemic


    shunt )
    MELD vs MELD -Na with
    exceptions ?

    • MODEL FOR END STAGE LIVER DISEASE

    • Incorporates serum bilirubin , serum creatinine and


    INR for prothrombin time and Indicates three
    month mortality risk based on the score .

    • Increasing score is associated with increasing


    mortality
    MELD-Na
    • Serum sodium indicates vasodilatory state in
    cirrhosis and predicts waitlist mortality
    independent of MELD score.

    • Linear increase in mortality by 5 percent for


    every m/mol drop of sodium between 125-140.

    • Addition of sodium to MELD score increases


    transplant priority by 12 percent for waitlist
    individuals and hence in 2016 jan organ
    procurement and transplantation network
    incorporated it .
    Exceptions

    Standard MELD exceptions include:


    Hepatocellular carcinoma
    Hepatopulmonary syndrome
    Portopulmonary hypertension
    Familial amyloid polyneuropathy
    Primary hyperoxaluria
    Cystic fibrosis
    Hilar cholangiocarcinoma
    Hepatic artery thrombosis
    Role of TIPS ?
    • Creation of low resistance channel between the hepatic vein
    and intrahepatic portion of portal vein

    • Absolute contraindications : Heart failure , severe tricuspid


    regurgitation , severe pulmonary hypertension,, multiple
    hepatic cysts, severe sepsis and unrelieved biliary
    obstruction.

    • Relative contraindication : Hepatoma especially if central,


    obstruction of all hepatic veins , portal vein thrombosis,
    severe coagulopathy , thrombocytepenia ( 20,000) .

    • Advantage : Buys time for waitlist individuals for liver


    transplantation

    • Common Limitation : Recurrent hepatic encephalopathy


    Liver transplantation
    indications and
    contraindications
    • INDICATIONS: Acute liver failure , cirrhosis , liver
    neoplasms, Liver based metabolic disorders.

    • Contraindications:Cardiopulmonary disease , AIDS,


    Malignancy outside of liver , hepatocellular
    carcinoma with metastasis , intrahepatic
    cholangiocarcinoma , hemangiosarcoma, severe
    sepsis, Acute liver failure with a sustained
    intracranial pressure >50mm/hg or a cerebral
    perfusion < 40mmHg.
    1.
    References
    Wong RJ, Aguilar M, Cheung R, et al. Nonalcoholic steatohepatitis is the second leading etiology of li
    ver disease among adults awaiting liver transplantation in the United States. Gastroenterology 2015; 1
    48:547.
    2.
    Heidelbaugh JJ, Bruderly M. Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation. Am
    Fam Physician 2006; 74:756.
    3.
    Anthony PP, Ishak KG, Nayak NC, et al. The morphology of cirrhosis. Recommendations on definition,
    nomenclature, and classification by a working group sponsored by the World Health Organization. J C
    lin Pathol 1978; 31:395.
    4.
    Fauerholdt L, Schlichting P, Christensen E, et al. Conversion of micronodular cirrhosis into macronodu
    lar cirrhosis. Hepatology 1983; 3:928.
    5.
    Van de Water J, Cooper A, Surh CD, et al. Detection of autoantibodies to recombinant mitochondrial pro
    teins in patients with primary biliary cirrhosis. N Engl J Med 1989; 320:1377.
    6.
    Abrams GA, Concato J, Fallon MB. Muscle cramps in patients with cirrhosis. Am J Gastroenterol 1996
    ; 91:1363.
    7.
    Baskol M, Ozbakir O, Coşkun R, et al. The role of serum zinc and other factors on the prevalence of mu
    scle cramps in non-alcoholic cirrhotic patients. J Clin Gastroenterol 2004; 38:524.
    8.
    Angeli P, Albino G, Carraro P, et al. Cirrhosis and muscle cramps: evidence of a causal relationship.
    Hepatology 1996; 23:264.
    9.
    Konikoff F, Theodor E. Painful muscle cramps. A symptom of liver cirrhosis? J Clin Gastroenterol 1986
    ; 8:669.

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