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LIVER FAILURE

1. WHAT IS THE DIAGNOSIS OF THE DISEASE ?

DIAGNOSISThe diagnosis of the case is Liver

failure.The following conditions help

making the diagnosis:-JaundiceAbdominal enlargementPoor appetiteBloody vomitusFetor hepaticus

HepatomegalyHepatic encephalopathyCaput medusaeComa

2. WHAT ARE HbsAg, HbeAg, anti HBc IgM AND anti HBc IgG?

Hepatitis B

HbsAg

HBsAg  is the surface  antigen of the  hepatitis B virus (HBV).

It is present in the sera of patients with viral hepatitis B.

 Positive HBsAg tests can be due to recent vaccination against Hepatitis B virus but this positivity is unlikely to persist beyond 14 days post-vaccination.

Hepatitis B surface a ntigen (HBsAg) is the first serologic marker appearing in the serum at 6 to 16 weeks following exposure to HBV.

In acute infection, HBsAg usually disappears in 1 to 2 months after the onset of symptoms.

Persistence of HBsAg for >6 months in duration indicates development of either a chronic carrier state or chronic HBV infection

Hepatitis B Surface Antigen Serum Levels Help to Distinguish Active From Inactive Hepatitis B Virus Genotype D Carriers.

HBe Ag

This is a viral protein that is secreted by hepatitis B infected cells.

It is associated with chronic hepatitis B infections and is used as a marker of active viral disease and a patient's degree of infectiousness.

It is found in the early phase of hepatitis B infection soon after hepatitis B s antigen becomes detectable.

Serum levels of both antigens rise rapidly during the period of viral replication.

Positive HBeAg results usually indicate presence of active HBV replication and high infectivity.

• A negative HBeAg result indicates very minimal or lack of HBV replication.

• Often used as a marker of ability to spread the virus to other people (infectivity)

• It may also be used to monitor the effectiveness of treatment.

Anti HBc IgMIgM antibody to HBc (IgM anti-HBc) rise

rapidly in patients with acute infection and persists for several weeks to months.

During this stage of disease, the patient’s liver enzymes may be elevated.

The convalescent phase, anti-HBc IgM will persist after the disappearance of HBsAg and decreases slowly over time. 

Hepatitis B vaccination does not induce production of anti-HBc antibodies.

REACTIVE: indicates recent, acute infection of less than 6 month’s duration. It may be detectable in chronic carriers when moving from inactive to active HBV replication 

NON-REACTIVE: Excludes a recent, acute infection but does not rule out chronic infection.

Anti HBc IgG

A  'convalescent'  antibody  that  indicates  prior  HBV infection;

 It rises 4-6 months after infection.Occurs in patients with acute liver

diseasePartially protective anti HBc

antibody levels can be induced by recombinant vaccination ; but are short lived.

3. ENUMERATE THE MODE OF TRANSMISSION OF HEPATITIS B. HOW DID THE PATIENT ACQUIRE THE DISEASE?

MODE OF TRANSMISSION OF HEPATITIS BThe virus is transmitted by

exposure to infectious blood or body fluids.

 Infection around the time of birth or from contact with other people during childhood is the most frequent method by which hepatitis B is acquired in areas where the disease is common.

In areas where the disease is rare intravenous drug use and sexual intercourse are the most frequent routes of infection.

Other risk factors include: working in healthcare. blood transfusions. dialysis.living with an infected person. travel in countries where the

infection rate is high. living in an institution.

Tattooing and acupuncture lead to a significant number of cases

 The hepatitis B viruses cannot be spread by sharing eating utensils,coughing, sneezing, or breastfeeding.

The patient may have contracted hepatitis B due to infection around the time of his birth or due to contact with infected people during childhood.

4. EXPLAIN THE DIFFERENT LABORATORY DATA ON FIRST ADMISSION.

DATA LEVEL EXPLANATIONSGPT High Important enzyme of liver.

Released when damaged.

Alkaline phosphatase

High Liver congestion or cholestasis.

Prothrombine time

Increased Liver- major role in clotting factor release.Damaged- not released.

Total & direct bilirubin

Increased Damaged liver.

Total serum protein & serum globulin

Increased Indicate the presence of infection.

Serum albumin Decreased Produced by liver.Damage causes reduced production.

HbsAg, HbeAg, anti- HBcIgM

Positive Acute hepatitis B / high infectivity.

5. HOW IS HEPATIC ENCEPHALOPATHY PRODUCED?

HEPATIC ENCEPHALOPATHY

Hepatic encephalopathy (also known as portosystemic encephalopathy) is a neuropsychiatric syndrome caused by hepatic in sufficiency.

It represents a reversible decrease in neurologic function based upon the disorder of metabolism caused by severe decompensated liver disease.

In the advanced stages it is called  hepatic coma  or  coma hepaticum

Cause: Accumulation in the bloodstream of toxic substances that are normally removed by the  liver. (Mostly ammonia)

It is seen in patients with severe acute or chronic liver dysfunction after exclution of other brain diseases.

6. HOW IS EDEMA PRODUCED IN LIVER FAILURE ?

EDEMA IN LIVER FAILURE

As a result of excessive accumulation of fluid in the abdominal cavity known as ascites

Complication of cirrhosis and liver failureAppears as abdominal bulgeAscites –bcoz of 2 factors-portal hypertension-hypoalbuminemia

Portal hypertension can also cause dilated veins in esophagus[varices]

Its due to increased pressure & accumulation of blood & excess fluid in abdominal blood vessels.

7. WHAT IS FETOR HEPATICUS? WHAT COMPOUNDS ARE RESPONSIBLE? HOW ARE THESE COMPOUNDS PRODUCED ?

Fetor hepaticus is a distinctive breath odor associated with hepatic encephalopathy a condition resulting from the accumulation of toxins in the blood stream that compromises brain function.

The breath of someone with hepatic encephalopathy is often characterized as musty and sometimes referred to as breath of the dead.

The liver is responsible for filtering and neutralizing toxic substances that enter the body. When liver not functions properly due to disease or injury, the filtration process can be disrupted.

Prolonged liver impairment can cause a buildup of toxins in the bloodstream placing vital organs, such as the brain, and nervous system at risk for hepatic encephalopathy.

When the liver fails to filter out toxins, such as ammonia, there is no place for the toxins to go but into the blood.

Significant toxin accumulation causes hepatic encephalopathy, or compromised brain function.

With hepatic encephalopathy, as the tainted blood moves through the lungs the toxins are expelled in breath, creating fetor hepaticus.

Fetor hepaticus is believed to be from a particular class of biological compounds called mercaptans that skip the liver via these porto-systemic shunts.

Normally the liver would chemically modify them into odourless compounds, but since it now doesn't get the chance to do this, the mercaptans reach the lungs (and urine) largely unadulterated. And when they are breathed (or urinated) out, they give off their distinctive odour.

8. WHAT IS CAPUT MEDUSAE? WHAT IS ITS SIGNIFICANCE?

CAPUT MEDUSAEThis is a medical term that is used to

describe the condition where you have engorged or swollen veins that appear on your abdomen. When you have caput medusae the veins will run outward from  umbilicus, in all direction.

They are twisted in shape. The veins that become engorged or swollen are called the paraumbilical veins.

The main cause of caput medusae is a medical condition called portal hypertension.

When a person has this medical condition there is an abnormally high pressure in your portal circulation, which is the flow of your blood from one organ to another without the blood going through your heart.

Portal hypertension is a term used to describe elevated pressures in the portal venous system

Normally, vascular channels are smooth, but liver cirrhosis can cause them to become irregular and tortuous with accompanying increased resistance to flow.

This resistance causes increased pressure, resulting in varices or dilations of the veins and tributaries.

Normally, portal vein pressure ranges between 1–4 mm Hg higher than the hepatic vein free pressure, and not more than 6 mm Hg higher than right atrial pressure.

Pressures that exceed these limits define portal hypertension

9. EXPLAIN THE DIFFERENT LABORATORY DATA ON SECOND ADMISSION.

DATA LEVEL

EXPLANATION

SGPT Normal Nothing much can be inferred

Alkaline phosphatase

High Liver damage, fuminant hepatitis

Prothombine time

Prolonged Liver damage- no release of clotting factors

Total & direct bilirubin

Increased Liver damage

Total serum protein & serum globulin

Decreased

InfectionAcute hepatitis- globulins

Serum albumin Decreased

Liver damage

BUN Decreased

Incapability of liver to convert ammonia to urea

RBS Low Liver failure- low insulin level-low bl. Sugar

HbsAg, anti-HBc IgG

Positive Chronic hepatitis B / high infectivity

10. WHY DID THE PATIENT VOMIT BLOODAND PASS OUT BLACKISH SOFT STOOLS?

BLOODY VOMITUS

PORTAL HYPERTENSION

BACKING UP OF BLOOD IN THE VEINS

VARICOSE VEINS

TEAR & BLEED

VOMITTING BLOOD

BLACKISH SOFT STOOLSDue to blood in stool.If the biliary duct is prevented from

secreting normal bile pigments into the intestine due to either a lack of bile production or duct blockage, the stool will lack pigmentation and appear lighter in color.

Irritable bowels and irregular bowel movements may also be present. If the stools become a light color, it is a clear sign of either liver disease or gall bladder disease.

The natural dark color of stools comes almost exclusively from the bile.

Light colored stools are a clear sign that either not enough bile is being produced or secreted, or it is not making its way to the intestines due to blockage of the bile duct from stones, scarring, or inflammation.

Other descriptions of light colored stools include gray stools and pale stools.

Immunosuppression may lead to progression of hepatitis C virus-associated liver disease in hemophiliacs coinfected with HIV.

Department of Internal Medicine, Institute for Experimental Hematology, University of Bonn, Germany.Find all citations in this journal (default).Orfilter your current search The American Journal of Gastroenterology 1966 april 20

Objective

The aim of this study was to examine the interaction between HIV and hepatitis C virus (HCV) in hemophiliacs coinfected with the viruses and to investigate the possible relationship between immunosuppression and liver failure.

Method To identify risk factors for impending liver failure in

hemophiliacs coinfected with HIV and HCV, we analyzed clinical and laboratory parameters, including CD4 count, aminotransferases (ALT, AST), cholinesterase, alkaline phosphatase, bilirubin, and gamma-glutamyltransferase, during 3 yr of follow-up (1990-1993) in four groups of patients: hemophiliacs with progressive immunodeficiency who were coinfected with HCV and HIV (group A, n = 49)

; hemophiliacs with stable immune function who were seropositive for HIV and HCV (group B, n = 95);

hemophiliacs who were infected with HCV but not HIV (group C, n = 72);

and homosexuals with progressive immunodeficiency who were infected with HIV but not HCV (group D, n = 24

ResultUnivariate analysis of data for group A showed

a significant rise in gamma-glutamyltransferase and alkaline phosphatase (p < 0.01) that was not seen in groups B, C, and D.

In a multivariate Cox regression analysis, age (odds ratio, 1.054 per yr; 95% confidence interval, 1.014-1.096 per yr), decline in CD4 count (odds ratio, 1.063 per cell/microl;

95% confidence interval, 1.037-1.091 per cell/microl), and alkaline phosphatase level (odds ratio, 1.012 per U/L;

95% confidence interval, 1.002-1.021 per U/L) emerged as independent determinants of death

ConclusionsOur data suggest that progressive

immune dysfunction in hemophiliacs coinfected with HIV and HCV may influence progression of liver failure.

In these patients cholestasis is an additional prognostic marker for survival that may reflect both exhausted immunity and impaired liver function

Liver Failure and Death after Exposure to Microcystins at a Hemodialysis Center in Brazil

Background

Hemodialysis is a common but potentially hazardous procedure.

From February 17 to 20, 1996, 116 of 130 patients (89 percent) at a dialysis center (dialysis center A) in Caruaru, Brazil, had visual disturbances, nausea, and vomiting associated with hemodialysis.

By March 24, 26 of the patients had died of acute liver failure

MethodA case patient was defined as any patient

undergoing dialysis at dialysis center A or Caruaru's other dialysis center (dialysis center B) during February 1996 who had acute liver failure.

To determine the risk factors for and the source of the outbreak, we conducted a cohort study of the 130 patients at dialysis center A and the 47 patients at dialysis center B, reviewed the centers' water supplies, and collected water, patients' serum, and postmortem liver tissue for microcystin assays

ResultOne hundred one patients (all at dialysis center A)

met the case definition, and 50 died. Affected patients who died were older than those who

survived (median age, 47 vs. 35 years; P<0.001). Furthermore, all 17 patients undergoing dialysis on

the Tuesday-, Thursday-, and Saturday-night schedule became ill, and 13 of them (76 percent) died.

Both centers received water from a nearby reservoir. However, the water supplied to dialysis center B was treated, filtered, and chlorinated, whereas the water supplied to dialysis center A was not.

Microcystins produced by cyanobacteria were detected in water from the reservoir and from dialysis center A and in serum and liver tissue of case patients

Conclusion

Water used for hemodialysis can contain toxic materials, and its quality should therefore be carefully monitored