Introduction to Liver Abscess

A liver abscess occurs when bacteria or protozoa destroy hepatic tissue, producing a cavity, which fills with infectious organisms, liquefied liver cells, and leukocytes. Necrotic tissue then walls off the cavity from the rest of the liver.

Liver abscess occurs equally in men and women, usually in those older than age 50. Death occurs in 15% of affected patients despite treatment.

Causes
Underlying causes of liver abscess include benign or malignant biliary obstruction along with cholangitis, extrahepatic abdominal sepsis, and trauma or surgery to the right upper quadrant. Liver abscesses also occur from intra-arterial chemoembolizations or cryosurgery in the liver, which causes necrosis of tumor cells and potential infection.

The method by which bacteria reach the liver reflects the underlying causes.

Biliary tract disease is the most common cause of liver abscess. Liver abscess after intra-abdominal sepsis (such as with diverticulitis) is most likely to be caused by hematogenous spread through the portal bloodstream. 

Hematogenous spread by hepatic arterial flow may occur in infectious endocarditis. 

Abscesses arising from hematogenous transmission are usually caused by a single organism; those arising from biliary obstruction, by mixed flora. 

Patients with metastatic cancer to the liver, diabetes mellitus, or alcoholism are more likely to develop a liver abscess. 

The organisms that predominate in liver abscess are gram-negative aerobic bacilli, enterococci, streptococci, and anaerobes. 

Amebic liver abscesses are caused by Entamoeba histolytica.

Introduction to Fatty liver

Steatosis, or fatty liver, is the accumulation of triglycerides and other fats in liver cells. In severe fatty liver, fat constitutes as much as 40% of the liver’s weight (as opposed to 5% in a normal liver); the liver’s weight may increase from 3.3 lb (1.5 kg) to as much as 11 lb (5 kg).
Minimal fatty changes are temporary and asymptomatic; severe or persistent changes may cause liver dysfunction. Fatty liver is usually reversible by simply eliminating the cause. This disorder may result in recurrent infection or sudden death from fat emboli in the lungs.

Causes
The most common cause of fatty liver in the United States and Europe is chronic alcoholism, with the severity of liver disease directly related to the amount of alcohol consumed. Other common, non-alcohol-related causes include acquired immunodeficiency syndrome, drug toxicity, and pregnancy.
Other causes include malnutrition (especially protein deficiency), obesity, diabetes mellitus, jejunoileal bypass surgery, Cushing’s syndrome, Reye’s syndrome, carbon tetrachloride intoxication, prolonged total parenteral nutrition (TPN), and DDT poisoning.
Whatever the cause, fatty infiltration of the liver probably results from mobilization of fatty acids from adipose tissues or from altered fat metabolism.

Signs and symptoms
Clinical features of fatty liver vary with the degree of lipid infiltration, and many patients are asymptomatic. The most typical sign is a large, tender liver (hepatomegaly). Common symptoms include right upper quadrant pain (with massive or rapid infiltration), ascites, edema, jaundice, and fever (all with hepatic necrosis or biliary stasis).
Nausea, vomiting, and anorexia are less common. Splenomegaly usually accompanies cirrhosis. Rarer changes are spider angiomas, varices, transient gynecomastia, and menstrual disorders.

Gallbladder and bile duct cancers

Introduction: Cancer of the gallbladder is rare, constituting less than 1% of all cancer cases. It’s usually found coincidentally in patients with cholecystitis; 1 in 400 cholecystectomies reveals cancer.
This disease is most prevalent in women over age 60. It’s rapidly progressive and usually fatal; patients seldom live 1 year after diagnosis. The poor prognosis is because of late diagnosis; gallbladder cancer usually isn’t diagnosed until after cholecystectomy, when it’s typically in an advanced, metastatic stage.
Extrahepatic bile duct cancer is the cause of about 3% of all cancer deaths in the United States. It occurs in both men and women between ages 60 and 70 (incidence is slightly higher in men). The usual site is at the bifurcation in the common duct.
Cancer at the distal end of the common duct is commonly confused with pancreatic cancer. Characteristically, metastasis occurs in local lymph nodes and in the liver, lungs, and peritoneum.

Causes
Many consider gallbladder cancer a complication of gallstones. This inference rests on circumstantial evidence from postmortem examinations: 60% to 90% of all gallbladder cancer patients also have gallstones. Postmortem data from patients with gallstones show gallbladder cancer in only 0.5%.
Adenocarcinoma accounts for 85% to 95% of all cases of gallbladder cancer; squamous cell carcinoma accounts for 5% to 15%. Mixed-tissue types are rare.
Lymph node metastasis is present in 25% to 70% of patients at diagnosis. Direct extension to the liver is common (46% to 89% of patients); direct extension to the cystic and the common bile ducts as well as the stomach, colon, duodenum, and jejunum produces obstructions. Metastasis also occurs through the portal or hepatic veins to the peritoneum, ovaries, and lower lung lobes.
The cause of extrahepatic bile duct cancer isn’t known, but statistics reveal an unexplained increased incidence of this cancer in patients with ulcerative colitis. This association may be attributed to a common cause —perhaps an immune mechanism or chronic use of certain drugs by the patient with colitis.

Signs and symptoms
Clinically, gallbladder cancer is almost indistinguishable from cholecystitis. The signs and symptoms of both disorders include pain in the epigastrium or right upper quadrant, weight loss, anorexia, nausea, vomiting, and jaundice. Chronic, progressively severe pain in an afebrile patient suggests cancer.

With simple gallstones, the pain is sporadic.
Another telling clue to cancer is a palpable gallbladder (in the right upper quadrant) with obstructive jaundice. Some patients may also have hepatosplenomegaly.

Brief Summary Of Hepatic Encephalopathy

Hepatic encephalopathy which is also known as portosystemic encephalopathy may be defined as a condition in which there is worsening of normal brain functioning as the liver is not able to detoxify the harmful substance in the blood and is characterized by altered level of consciousness and disorientation.

Pathology
The blood bypasses the liver via the collaterals and the toxic metabolities (e.g ammonia, free fatty acids and mercapts ) pass directly to the brain to produce the encephalopathy. There is also an increased sensitivity of CNS neurons to the inhibitory neurotransmittor (GABA) and an increase in circulating levels of endogenous benzodiazepines. Cerebral edema is frequently present and contributes to the development of clinical features.

Precipitating Factors

• Increased Nitrogen Load
• Gastrointestinal bleeding
• Excess dietray protein
• Azotemia
• Constipation
• Electrolyte and Metabolic Imbalance
• Hypokalemia
• Alkalosis
• Hypoxia
• Hyponatremia
• Drugs
• Narcotics, Tranquilizers. sedatives
• Diuretics
• Miscellaneous
• Infection
• Surgery
• Portosystemic shunt
• Superimposed acute liver failure
• Progressive liver disease

Clinical Manifestations
Symptoms

• Disturbance of sleep with sleeping during day and awaking in night is one of the earliest features.
• Alteration in personality, mood disturbances, confusion, deterioration of self care and deterioration of hand writing, slurring of speech, disorientation, drowsiness and eventually coma develop.
• Convulsions also sometimes develops.
• Hyperventilation, fever, nausea and vomiting are also common

Investigations Required In Patients With Ascites

Ascites is defined as collection of excess free fluid in the peritoneal cavity and it could be due to a number of different medical conditions. A proper history and clinical examination may reveal the underlying cause but still certain general and specific investigation are to be carried out in order to confirm or find out the possible etiology.

General Investigations

1. Urine Dipstick: It is a simple and cheap procedure that will be strongly positive for protein in nephrotic syndrome. If so, a 24 hour urine collection for protein should be undertaken; more than 3.5gm is indicative of nephrotic syndrome.

2. Complete Blood Count: Raised white cell count may indicate an infective etiology but a differential white count is more specific.

3. Urea and Electrolytes: Elevated urea and creatinine may indicate a renal etiology; however , it may also be a component of hepatorenal syndrome, which is renal impairment secondary to liver failure.

4. LFT’s : May be deranged in the presence of liver disease. The serum albumin will be able to indicate hypoalbuminaemia but the underlying cause must still be sought.

5. Chest X-ray: Findings suggestive of cardiac failure are cardiomegaly, upper venous diversion of blood, the presence of Kerley B lines, pulmonary edema and pleural effusion. Occasionally the presence of carcinoma may be suggested by a mass in the lung.

6. Ultrasound Abdomen: In addition to confirming the presence of ascites ultrasound will detect any intra abdominal masses that are not palpable on clinical examination. It may also indicate the presence of fatty deposits in the liver in the presence of cirrhosis. Dilated collateral veins may be visualized in conditions that cause obstruction of the venous outflow of the liver, including cirrhosis and Budd-Chiari syndrome.

7. Abdominal Paracentesis: Aspiration of the ascitic fluid is very useful to help determine the underlying cause. A sample should be sent to microbiology clinical chemistry and pathology.

Ascitic fluid Examinations