Sonographic Evaluation of Liver Cirrhosis: Causes and Pathophysiology _Juniper Publishers

 

ADVANCED RESEARCH IN GASTROENTEROLOGY & HEPATOLOGY JUNIPER PUBLISHERS

 

 

 

Authored by M Ayub Hussain 

Introduction

Liver cirrhosis existed since ancient times. It is widely speeded all over the world various causes:

    a. Known and unknown

    b. Signs and symptoms may be different for patients in

Biopsy is not the only and 100% positive test for Liver cirrhosis diagnosing. Clinical history, physical examination, signs and symptoms, blood works and Ultrasound evaluation can diagnose liver cirrhosis most of the time without the need of biopsy. Ultrasound is a helpful modality. Inexpensive, quick, available, noninvasive, portable, repeatable and more over non radiation. Elastography is a kind of ultrasonography recently started commercially.

Goals and Objectives

At the end of this session, we will learn the impact in details about:

    a. Patient history

    b. Details physical examination

    c. Selective blood works

    d. Sonography evaluation in order to diagnose the liver cirrhosis without biopsy (Figure 1-5).

Causes of Cirrhosis & Epidemiology

    a. Alcoholic cause is more prevalent in western countries 60-70%.

    b. Non Alcoholic viral causes: Hep B and C

    c. Higher in developing countries, especially Asia and Africa.

    d. Inadequate screening test for blood transfusion and contamination from dialysis machine.

    e. Unprotected sexual activity (Figure 6).

Non-Alcoholic Causes of Liver cirrhosis

    a. NASH (Non Alcoholic Steatohepatitis).

    b. Metabolic: Haemochromatosis, Wilson's disease, fatty infiltration and Alpha-1 antitrypsin deficiency

    c. Auto-Immune hepatitis.

    d. Biliary disease: primary sclerosing cholangitis and primary biliary cirrhosis.

    e. Vascular disease: congestive hepatopathy, Budd-chiari syndrome and hepatic veno-occlusive disease.

    f. Medications: Methotrexate.

    g. Cystic fibrosis: uncommon (Figure 7).

Pathophysiology

    Steps

    a. Fibrosis.

    b. Nodular regeneration.

    c. Distortion of liver architecture (Figure 8).

Signs, Symptoms & Physical Examination of Liver Cirrhosis

There’s no typical signs or symptoms of liver cirrhosis because depends on the stages and athophysiology of the disease.

    I. Early stage: Asymptomatic

    II. Late stage:

    a. Malaise

    b. Fatigue

    c. Lack of appetite

    d. Frequent loose motion after eating

    e. Distended and heaviness of abdomen

    f. Pain in left hypochondriac

    g. Muscle wasting

    h. Hemorrhoids

    i. Dizzy

    j. Jaundice

    k. Skin itchy

    l. Hepatic faces

    m. Caput medusa

    n. Disorientation: Dementia and amnetia (Figure 9).

Diagnosing Cirrhosis: Blood Works

    a. Blood tests to check liver functions: Albumin and Total serum protein.

    b. Prothrombin time/INR.

    c. Bilirubin

    d. Liver enzymes: AST, ALT and lactate dehydrogenase.

    e. Alkaline phosphatase.

    f. Hepatitis B and Hepatitis C antigen and antibody.

    g. Alpha 1-antitrypsin.

    h. Blood alcohol test.

    i. Antinuclear antibody (ANA), Anti- smooth muscle antibody (ASMA), Anti-mitochondrial antibody (AMA).

    j. Complete blood count (Figure 10-12).

Insult of Liver Cells

    A. Stellete cells

    a. Fibrin, collagen and intercellular matrix release.

    B. Hepatocytes

    a. Formation of regenetive nodules.

    C. Sinusoid compression

    a. Obstruction of blood flow.

    b. Results in portal HTN (Figure 13 & 14).

Portal Hypertension

PV dilation due to obstruction. Reverse flow to SMV, IMV, and SV. Blood that cannot enter into PV must return to systematic circulation via anatomotic sites. Results: Esophageal varices, rectal hemorrhoids, caput medusa, etc (Figure 15-29).

Complications

    a. Portal hypertension, liver failure and liver cancer

    b. Distended abdomen due to ascites.

    c. Wasting of muscles.

    d. Blood vomiting.

    e. Rectal bleeding.

    f. Defect in blood clotting.

    g. Gynecomastia.

    h. Spider angioma.

    i. Electrolyte imbalance.

    j. Caput medusa: Visible veins around the umbilicus.

    k. ETC (Figure 30-33).

Results of Liver Failure

    a. Accumulation of toxic materials in blood.

    b. Decreased production of clotting factors.

    c. Decreased production of plasma proteins.

    d. Poor metabolism of estrogen.

    e. Enzymes abnormalities.

    f. Increase Bilirubin.

    g. Platelets count decrease.

Conclusion

    A. Diagnostic procedures

    a. Patient history.

    b. Bedside physical exams.

    c. Blood works.

    d. Ultrasonography of liver (Figure 34).

    B. Sonographic characteristics of cirrhosis:

    a. Hyper echoic liver

    b. Course texture.

    c. Irregular/nodular surface.

    d. Small liver

    e. Caudate lobe hypertrophy and decrease echogenicity.

    f. Non visualization of hepatic veins.

    g. Portal vein dilation >13mm.

    h. Portal vein reverses flow.

    i. Portal vein hypertension.

    j. Dilation of splenic veins, SMV, IMV with reverse flow

    k. Splenomegaly.

    l. Ascites.

    m. Recanalization of umbilical vein [1-11].

     

For More open access Journals in Juniper Publishers Please click on: https://juniperpublishers.com/

For more articles in Advanced Research in Gastroenterology & Hepatology please click on https://juniperpublishers.com/argh/index.php

For more about Juniper Publishers please click on: https://juniperpublishers.com/video-articles.php

 

 

Comments

Post a Comment

Popular posts from this blog

Milk Curd Syndrome: A Forgotten Entity_Juniper Publishers

Image
ADVANCED RESEARCH IN GASTROENTEROLOGY & HEPATOLOGY JUNIPER PUBLISHERS   Authored by Kashish Khanna Abstract A full term neonatal baby girl presented with a lumbosacral meningomyelocele and underwent successful excision and repair. In the postoperative period, she developed abdominal distension, bilious vomiting and did not pass stools. Conservative management for ileus/intestinal obstruction failed. The abdominal exploration revealed milk curd syndrome (MCS) as a cause of intestinal obstruction. This article highlights the varied presentation of MCS and salient features to differentiate it from other causes of neonatal intestinal obstruction. Keywords: Neonatal intestinal obstruction; Milk curd syndrome; Inspissated milk syndrome; Milk plug syndrome Abbreviations: MCS: Milk Curd Syndrome; SBE: Small Bowel Obstruction; NEC: Necrotising Enterocolitis; MMC: Meningomyelocele; TCA: Total Colonic Aganglionosis ...
Read more

A Modified Sequential Regimen of Helicobacterpylori Treatment Enforced by Bacillus clausii and Zinc Carnosine Complex Yields High Eradication Rates_Juniper Publishers

Image
  ADVANCED RESEARCH IN GASTROENTEROLOGY & HEPATOLOGY JUNIPER PUBLISHERS   Authored by Dajani AI      Abstract Introduction: Over the past decade a worldwide trend of decline in the cure rates of Helicobacter pylori is observed. Current eradication rates achieved by the standard triple therapy are below 70%. Sequential therapy had provided a potential alternative that would compensate for the unmet performance of triple therapy. Despite its superiority to triple therapy, the excellent results reported initially were not reproduced by other investigators work. Adding adjuvant agents was also found to improve further the success rate of eradication. Probiotics emerged as a useful adjunct in treatment and prophylaxis of Helicobacter pylori infection. The nutritional supplement Zinc carnosine complex is another adjuvant which is believed to add value to the treatment. Patients and method: an open label randomized observational clinical study ...
Read more

Updating on Neuroendocrine Tumors New Clinical Evidence in the Search of the Ideal Treatment Sequence_Juniper Publishers

Image
ADVANCED RESEARCH IN GASTROENTEROLOGY & HEPATOLOGY JUNIPER PUBLISHERS Authored by Juan Manuel O'Connor   Introduction Neuroendocrine tumors (NETs) represent a heterogeneous clinical entity with an increasing incidence as shown by the different registers available. As opposed to other solid tumors, NETs represent a challenge, not only from the diagnostic standpoint but also in terms of treatment strategies. According to the data published by our Working group, ARGENTUM GROUP [ 1 ], with more than 600 patients assessed, roughly 60% of the cases present with metastatic disease from the onset. The reason why the incidence of advanced disease is high since early onset may be due to a bias, for most of the physicians in our Group are oncologists. Moreover, about 20% of the patients included present poorly differentiated NETs, a heterogeneous subgroup, with high risk and poor outcome according to the different series reported. G grading...
Read more