what is the liver essay

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The Liver and Its Functions

The liver is the largest solid organ in the body. It removes toxins from the body’s blood supply, maintains healthy blood sugar levels, regulates blood clotting, and performs hundreds of other vital functions. It is located beneath the rib cage in the right upper abdomen.

• The liver filters all of the blood in the body and breaks down poisonous substances, such as alcohol and drugs.
• The liver also produces bile, a fluid that helps digest fats and carry away waste.
• The liver consists of four lobes, which are each made up of eight sections and thousands of lobules (or small lobes).

Functions of the Liver

The liver is an essential organ of the body that performs over 500 vital functions. These include removing waste products and foreign substances from the bloodstream, regulating blood sugar levels, and creating essential nutrients. Here are some of its most important functions:

• Albumin Production : Albumin is a protein that keeps fluids in the bloodstream from leaking into surrounding tissue. It also carries hormones, vitamins, and enzymes through the body.
• Bile Production : Bile is a fluid that is critical to the digestion and absorption of fats in the small intestine.
• Filters Blood : All the blood leaving the stomach and intestines passes through the liver, which removes toxins, byproducts, and other harmful substances.
• Regulates Amino Acids : The production of proteins depend on amino acids. The liver makes sure amino acid levels in the bloodstream remain healthy.
• Regulates Blood Clotting : Blood clotting coagulants are created using vitamin K, which can only be absorbed with the help of bile, a fluid the liver produces.
• Resists Infections : As part of the filtering process, the liver also removes bacteria from the bloodstream. 
• Stores Vitamins and Minerals : The liver stores significant amounts of vitamins A, D, E, K, and B12, as well as iron and copper.
• Processes Glucose : The liver removes excess glucose (sugar) from the bloodstream and stores it as glycogen. As needed, it can convert glycogen back into glucose.

Anatomy of the Liver

The liver is reddish-brown and shaped approximately like a cone or a wedge, with the small end above the spleen and stomach and the large end above the small intestine. The entire organ is located below the lungs in the right upper abdomen. It weighs between 3 and 3.5 pounds.

The liver consists of four lobes: the larger right lobe and left lobe, and the smaller caudate lobe and quadrate lobe. The left and right lobe are divided by the falciform (“sickle-shaped” in Latin) ligament, which connects the liver to the abdominal wall. The liver’s lobes can be further divided into eight segments, which are made up of thousands of lobules (small lobes). Each of these lobules has a duct flowing toward the common hepatic duct, which drains bile from the liver.

The following are some of the most important individual parts of the liver:

• Common Hepatic Duct : A tube that carries bile out of the liver. It is formed from the intersection of the right and left hepatic ducts.
• Falciform Ligament : A thin, fibrous ligament that separates the two lobes of the liver and connects it to the abdominal wall.
• Glisson’s Capsule : A layer of loose connective tissue that surrounds the liver and its related arteries and ducts.
• Hepatic Artery : The main blood vessel that supplies the liver with oxygenated blood.
• Hepatic Portal Vein : The blood vessel that carries blood from the gastrointestinal tract, gallbladder, pancreas, and spleen to the liver. 
• Lobes : The anatomical sections of the liver.
• Lobules : Microscopic building blocks of the liver.
• Peritoneum : A membrane covering the liver that forms the exterior.

Maintaining a Healthy Liver

The best way to avoid liver disease is to take active steps toward a healthy life. The following are some recommendations that will help keep the liver functioning as it should:

• Avoid Illicit Drugs : Illicit drugs are toxins that the liver must filter out. Taking these drugs can cause long-term damage.
• Drink Alcohol Moderately : Alcohol must be broken down by the liver. While the liver can moderate amounts, excessive alcohol use can cause damage.
• Exercise Regularly : A regular exercise routine will help promote general health for every organ, including the liver.
• Eat Healthy Foods : Eating excessive fats can make it difficult for the liver to function and lead to fatty liver disease .
• Practice Safe Sex : Use protection to avoid sexually transmitted diseases such as hepatitis C .
• Vaccinate : Especially when traveling, get appropriate vaccinations against hepatitis A and B , as well as diseases such as malaria and yellow fever, which grow in the liver.

If you need help for a liver condition, give us a call at (877) LIVER MD/ (877) 548-3763 or get in touch using our online request form .

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The Many Vital Functions of the Liver

The liver is the heaviest organ in the body and one of the largest. It's located in the upper right portion of your belly under the ribs and is responsible for functions vital to life.

The liver primarily processes nutrients from food, makes bile, removes toxins from the body, and builds proteins. It metabolizes many drugs. It breaks down fat and produces cholesterol. It converts glycogen into glucose. It creates immune factors necessary to fight infection.

It's easy to see how inflammation of the liver , or hepatitis , interferes with these important functions and can lead to poor health. Fortunately, the liver is extremely resilient and most cases of liver inflammation don't even come to medical attention, but in cases of severe liver disease , there can be a serious interruption of these essential liver functions. Let's look at each of these functions a little closer.

Processing Nutrients from Food

The digestive system immediately begins to break down the food that we eat into smaller and smaller pieces. Eventually, these nutrients will enter the blood and travel to the liver through the hepatic portal system , the major pathway that blood takes from the ​ digestive system to the liver.

The liver will then process these nutrients in different ways, depending on the body's needs. It usually stores some of the nutrients in a form that the body can use for quick energy. The rest will be used to make other important chemicals the body needs.

When the liver is severely damaged, such as in liver failure , it can't continue to process nutrients from the blood that the body must have. Without aggressive medical care, the absence of these essential liver functions can result in signs of serious illness like brain damage and coma .

Making Bile

Bile is a thick, green-yellow fluid that the liver produces to help digest food, especially fat, as it passes from the stomach to the intestines. This fluid is made in the liver but is stored in a nearby sac called the gallbladder. When a person eats a meal heavy in fat, like a juicy steak, the body will use its store of bile to help break down the fats in the steak for digestion.

Removing Toxins From the Blood

All of the blood in the body will eventually pass through the liver. This is important because the liver needs to pull out any bad things in the blood, such as toxins, and remove them from the body. It metabolizes many drugs and alcohol and helps remove other toxins such as damaged cells, proteins, and old hormones.

The liver prepares all of these types of toxins to be removed from the body. However, when the liver is damaged, these toxins can't be removed and they start to accumulate creating problems.

Building Proteins

A protein is a complex chemical that is essential to living things, like plants, animals, and people. Proteins are everywhere in the body and need to be constantly produced to sustain life. The liver is in charge of building many kinds of proteins that the body uses every day.

For instance, there are many proteins produced by the liver that are responsible for blood clotting. When the liver is damaged , sometimes the body isn't able to clot blood effectively. In mild cases, it just takes a long time for bleeding to stop. However, in severe cases, the blood wouldn't be able to clot. A simple cut on the skin would lead to continued bleeding (though not necessarily a dangerous amount), and possibly bruises.

Gastrointestinal Society: Canadian Society of Intestinal Research. The liver - An amazing organ .

Centers for Disease Control and Prevention. What is viral hepatitis ?

Johns Hopkins Medicine. Liver: Anatomy and functions .

National Institute of Diabetes and Digestive and Kidney Diseases. Your digestive system and how it works .

American Liver Foundation. The progression of liver disease .

Johns Hopkins Medicine. Biliary system anatomy and functions .

Center for Liver Disease and Transplantation. The liver and its functions .

MedlinePlus. Loss of brain function - liver disease .

By Charles Daniel  Charles Daniel, MPH, CHES is an infectious disease epidemiologist, specializing in hepatitis.

• Patient Care & Health Information
• Diseases & Conditions
• Liver disease

The liver is the largest internal organ in the body. It's about the size of a football. It sits mainly in the upper right portion of the stomach area, above the stomach.

The liver is an organ that sits just under the rib cage on the right side of the abdomen. It can weigh up to 4 pounds (1.8 kilograms). The liver is needed to help digest food, rid the body of waste products and make substances, called clotting factors, that keep the blood flowing well, among other tasks.

Liver disease can be passed through families, called inherited. Anything that damages the liver also can cause liver problems, including viruses, alcohol use and obesity.

Over time, conditions that damage the liver can lead to scarring, called cirrhosis. Cirrhosis can lead to liver failure, a life-threatening condition. But early treatment may give the liver time to heal.

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• Liver problems

Liver problems that can occur include fatty liver disease and cirrhosis. The liver and its cells, as seen through a microscope, change greatly when a liver becomes fatty or cirrhotic.

Liver disease doesn't always cause symptoms that can be seen or felt. If there are symptoms of liver disease, they may include:

• Yellowing of the skin and the whites of the eyes, called jaundice. Yellowing of the skin might be harder to see on Black or brown skin.
• Belly pain and swelling.
• Swelling in the legs and ankles.
• Itchy skin.
• Dark urine.
• Pale stool.
• Constant tiredness.
• Nausea or vomiting.
• Loss of appetite.
• Bruising easily.

When to see a doctor

Make an appointment with your healthcare professional if you have any lasting symptoms that worry you. Seek medical help right away if you have belly pain that is so bad that you can't stay still.

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Liver disease care at Mayo Clinic

• Liver cysts: A cause of stomach pain?

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Liver disease has many causes.

Parasites and viruses can infect the liver, causing swelling and irritation, called inflammation. Inflammation keeps the liver from working as it should. The viruses that cause liver damage can be spread through blood or semen, bad food or water, or close contact with a person who is infected.

The most common types of liver infection are hepatitis viruses, including:

• Hepatitis A.
• Hepatitis B.
• Hepatitis C.

Immune system condition

Diseases in which the immune system attacks certain parts of the body are called autoimmune diseases. Autoimmune liver diseases include:

• Autoimmune hepatitis.
• Primary biliary cholangitis.
• Primary sclerosing cholangitis.

A changed gene from one or both parents can cause substances to build up in the liver. This can cause liver damage. Genetic liver diseases include:

• Hemochromatosis.
• Wilson's disease.
• Alpha-1 antitrypsin deficiency.

Cancer and other growths

Examples include:

• Liver cancer.
• Bile duct cancer.
• Liver adenoma.

Other common causes of liver disease include:

• Long-term alcohol use.
• Fat that builds up in the liver, called nonalcoholic fatty liver disease or metabolic-associated steatotic liver disease.
• Certain prescription or other medicines.
• Certain herbal mixes.
• Being in contact often with toxic chemicals.

Risk factors

Factors that can increase the risk of liver disease include:

• Ongoing moderate or heavy alcohol use.
• Type 2 diabetes.
• Tattoos or body piercings.
• Shared needles to inject drugs.
• Blood transfusion before 1992.
• Contact with other people's blood and body fluids.
• Sex without protection.
• Contact with chemicals or toxins.
• Family history of liver disease.

Complications

Complications of liver disease depend on the cause of the liver problems. Without treatment, liver disease may progress to liver failure. Liver failure can be fatal.

To prevent liver disease:

• If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.
• Avoid risky behavior. Use a condom during sex. If you get tattoos or body piercings, pick a shop that's clean and safe. Seek help if you shoot illicit drugs. Don't share needles to shoot drugs.
• Get vaccinated. If you're at increased risk of getting hepatitis, talk with your healthcare professional about getting the hepatitis A and hepatitis B vaccines. This also is true if you've been infected with any form of the hepatitis virus.
• Be careful when taking medicines. Take prescription and other medicines only when needed. Take only as much as directed. Don't mix medicines and alcohol. Talk with your healthcare provider before mixing herbal supplements or prescription or other medicines.
• Stay away from other people's blood and body fluids. Hepatitis viruses can be spread by accidental needle sticks or poor cleanup of blood or body fluids.
• Keep your food safe. Wash your hands well before eating or making foods. If traveling in a resource-poor country, use bottled water to drink, wash your hands and brush your teeth.
• Take care with aerosol sprays. Make sure to use these products in an open area. Wear a mask when spraying insecticides, fungicides, paint and other toxic chemicals. Always follow the maker's instructions.
• Protect your skin. When using insecticides and other toxic chemicals, wear gloves, long sleeves, a hat and a mask so that chemicals don't get on your skin.
• Maintain a healthy weight. Obesity can cause nonalcoholic fatty liver disease, now called metabolic-associated steatotic liver disease.
• Loscalzo J, et al., eds. Approach to the patient with liver disease. In: Harrison's Principles of Internal Medicine. 21st ed. McGraw-Hill; 2022. https://accessmedicine.mhmedical.com. Accessed Nov. 8, 2023.
• How liver disease progresses. American Liver Foundation. https://liverfoundation.org/about-your-liver/how-liver-diseases-progress/. Accessed Nov. 14, 2023.
• AskMayoExpert. Metabolic and alcohol-associated liver disease (adult). Mayo Clinic; 2023.
• AskMayoExpert. Cirrhosis (adult). Mayo Clinic; 2023.
• Feldman M, et al. Liver disease caused by anesthetics, chemicals, toxins, and herbal and dietary supplements. In: Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. 11th ed. Elsevier; 2021. https://www.clinicalkey.com. Accessed Nov. 14, 2023.
• Elsevier Point of Care. Clinical Overview: Nonalcoholic fatty liver disease. https://www.clinicalkey.com. Accessed Nov. 14, 2023.
• Neshat SY, et al. Liver disease: Induction, progression, immunological mechanisms, and therapeutic interventions. International Journal of Molecular Sciences. 2021; doi:10.3390/ijms22136777.
• Malnick SDH, et al. Fatty liver disease — alcoholic and nonalcoholic: Similar but different. International Journal of Molecular Sciences. 2022; doi:10.3390/ijms232416226.
• Alcohol and public health: Frequently asked questions. Centers for Disease Control and Prevention. https://www.cdc.gov/alcohol/faqs.htm. Accessed Nov. 14, 2023.
• Fighting fatty liver: Steps against a silent disease. NIH News in Health. https://newsinhealth.nih.gov/2021/10/fighting-fatty-liver. Accessed Nov. 14, 2023.
• 13 ways to a healthy liver. American Liver Foundation. https://liverfoundation.org/resource-center/blog/13-ways-to-a-healthy-liver/. Nov. 14, 2023.
• Ami TR. Allscripts EPSi. Mayo Clinic. Nov. 14, 2023.

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The Organ Is Still Working. But It’s Not in a Body Anymore.

Perfusion keeps a donated organ alive outside the body, giving surgeons extra time and increasing the number of transplants possible.

By Ted Alcorn

On some level, the human liver in the operating room at Northwestern Memorial Hospital in Chicago was alive. Blood circulating through its tissues delivered oxygen and removed waste products, and the organ produced bile and proteins that are essential to the body.

But the donor had died a day earlier, and the liver lay inside a boxy plastic device. The organ owed its vitality to this machine, which was preserving it for transplantation into a needy patient.

“It’s a little bit science fiction,” said Dr. Daniel Borja-Cacho, a transplant surgeon at the hospital.

Surgeons are experimenting with organs from genetically modified animals , hinting at a future when they could be a source for transplants. But the field is already undergoing a paradigm shift, driven by technologies in widespread use that allow clinicians to temporarily store organs outside the body.

Perfusion, as its called, is changing every aspect of the organ transplant process, from the way surgeons operate, to the types of patients who can donate organs, to the outcomes for recipients.

Most significantly, surgical programs that have adopted perfusion are transplanting more organs.

Since 2020, Northwestern has had a 30 percent uptick in its volume of liver transplants. Nationally, the number of lung, liver and heart transplants each rose by more than 10 percent in 2023, one of the largest year-over-year increases in decades.

Without blood flow, organs rapidly deteriorate. That’s why clinicians have long considered the ideal organ donor to be someone who died under circumstances that ended brain activity but whose heart continued beating, keeping the organs viable until they could be matched with recipients.

To minimize injury to organs after their removal from a donor’s blood supply and before they are connected to a recipient’s, surgeons used to cool them to just above freezing, significantly slowing their metabolic processes.

This extends the window in which organs can be transplanted, but only briefly. Livers remain viable for no longer than 12 hours, and lungs and hearts closer to six.

Scientists have long experimented with techniques for keeping organs in more dynamic conditions, at a warmer temperature and perfused with blood or another oxygenated solution. After years of development, the first device for preserving lungs via perfusion won approval from the Food and Drug Administration in 2019. Devices for perfusing hearts and livers were approved in late 2021.

The devices essentially pump blood or an oxygenated fluid through tubes into the blood vessels of the donated organ. Because cells in a perfused organ continue to function, clinicians can better assess whether the organ will thrive in a recipient’s body.

Bolstered by that information, transplant surgeons have begun to use organs from older or sicker donors that they might otherwise have turned down, said Dr. Kris Croome, a professor of surgery at the Mayo Clinic in Florida. “We’re going after organs we never would have before, and we’re seeing good outcomes,” he said.

Perfusion also eases the grueling process of organ recovery and transplant, hourslong surgeries that doctors often conduct against the clock, beginning in the middle of the night and completed in back-to-back succession.

Now surgical teams can recover an organ, perfuse it overnight while they sleep and complete the transplant in the morning without fear that the delay will have damaged the organ.

Perhaps most important, perfusion has further opened the door to organ donation by comatose patients whose families have withdrawn life support, allowing their hearts to eventually stop. Each year, tens of thousands of people die this way, after the cessation of circulation, but they were rarely donor candidates because the dying process deprived their organs of oxygen.

Now, surgeons are perfusing these organs, either by removing them to a machine or, in a lower-tech manner, by recirculating blood in that region of the donor’s body . And that has made them much more appealing for transplant.

Since 2020, the number of livers transplanted after the circulatory death of the donor has doubled, according to an analysis of data from the United Network for Organ Sharing, the nonprofit that runs the United States’ transplant system.

Once, surgeons never used hearts from such donors because of that organ’s sensitivity to oxygen deprivation; in 2023, thanks to perfusion, they transplanted over 600.

By tapping this new cadre of donors, transplant centers said they could find organs more quickly for the excess of patients in urgent need. Dr. Shimul Shah said the organ transplant program he directs at the University of Cincinnati had essentially wiped out its waiting list for livers. “I never thought, in my career, I would ever say that,” he said.

One obstacle to the adoption of the technology may be cost. At the rates currently demanded by device makers, perfusing an organ outside the body can add more than $65,000 to the price of a transplant; smaller hospitals may not be able to justify the upfront expense.

One of the leading companies, TransMedics, raised its prices substantially after regulators approved its device, prompting a stern letter from Representative Paul Gosar, Republican of Arizona, who wrote: “What began as a promising medical equipment innovation and an opportunity to increase transplantation nationwide is now being held hostage by a public company that has lost its true north.”

But some surgeons said that the technology might nonetheless save money, since patients who receive perfused organs generally leave the hospital quicker and with fewer complications, and have better medium- and long-term outcomes .

Surgeons are still exploring the upper limits of how long perfused organs can survive outside the body, and as substantially as the technologies are already altering transplant, some say this is only the beginning.

Dr. Shaf Keshavjee, a surgeon at the University of Toronto whose lab was at the forefront of developing technologies to preserve lungs outside the body, said the devices could eventually allow doctors to remove, repair and return lungs to sick patients rather than replace them. “I think we can make organs that will outlive the recipient you put them in,” he said.

Dr. Ashish Shah, the chairman of cardiac surgery at Vanderbilt University, one of the busiest heart transplant programs in the country, agreed, calling that “the holy grail.”

“Your heart sucks,” he said. “I take it out. I put it on my apparatus. While you don’t have a heart, I can support you with an artificial heart for a little while. I then take your heart and fix it — cells, mitochondria, gene therapy, whatever — and then I sew it back in. Your own heart. That’s what we’re really working for.”

To revisit this article, visit My Profile, then View saved stories .

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Emily Mullin

This Bag of Cells Could Grow New Livers Inside of People

For the first time, scientists are attempting to grow a new, miniature liver inside of a person. It sounds like science fiction; in fact, the idea was the plot of a Grey’s Anatomy episode that aired in 2018. Now, biotech company LyGenesis is trying to turn the concept into reality.

Today, LyGenesis announced that an initial volunteer has received an injection of donor cells to turn one of their lymph nodes into a second liver. The procedure was carried out in Houston on March 25 as part of a clinical trial that will test the experimental treatment in 12 adults with end-stage liver disease.

These patients usually require a liver transplant, but donor organs are in short supply. LyGenesis is hoping to spur the growth of enough healthy liver tissue that patients don’t need a transplant. “We’re using the lymph node as a living bioreactor,” says Michael Hufford, cofounder and CEO of Pittsburgh-based LyGenesis. He says just 10 to 30 percent in additional liver mass could have meaningful effects for patients with end-stage liver disease.

About 10,000 people in the United States are on the transplant list for a liver, and many will wait months or years to get one. That number doesn’t include those who need a new liver but don’t qualify for a transplant because of other health problems.

Similarly, not all donor livers get matched to a patient awaiting a transplant. Sometimes they’re not the right blood type, or they may be too fatty for use. But they’re still viable for the LyGenesis process—and one donated liver has enough cells, Hufford says, to treat up to 75 people.

From those discarded organs, LyGenesis scientists isolate and purify hepatocytes—the most abundant cells in the liver—and collect them into an IV bag. The next step is getting the cells to the right place in the body.

Healthy donor cells can’t be injected directly into a diseased liver because they won’t survive, says Eric Lagasse, chief scientific officer of LyGenesis and a professor of pathology at the University of Pittsburgh. About a decade ago, he identified lymph nodes as a potential site for a new liver. These small, bean-shaped lumps of tissue help fight infection as part of the immune system. They also have the ability to expand and, like the liver, they filter blood. Because there are so many throughout the body—500 to 600 in adults—repurposing one shouldn’t affect how the rest do their job.

The LyGenesis treatment targets a cluster of abdominal lymph nodes involved in a vein system that’s connected to the liver. To dose the first volunteer, doctors threaded a thin, flexible tube with a camera on the end down the patient’s throat and through the digestive tract. Using ultrasound, they identified one of the target lymph nodes and injected 50 million hepatocytes into it.

LyGenesis chose lymph nodes close to the liver to take advantage of signals that it emits in an attempt to repair itself. The liver is the only organ with the ability to regenerate, and even when it’s damaged, it still releases growth factors and other molecules in an attempt to do so. The donor cells seem to pick up on those cues to form new liver structures.

David Kushner

Andy Greenberg

David Gilbert

In early experiments, Lagasse found that if he injected healthy liver cells into the lymph nodes of mice, the cells would flourish and form a second, smaller liver to take over the functions of the animal’s failing one. The new livers grew up to 70 percent of the size of a native liver. “What happened is that the liver grew to a certain size and then stopped growing when it reached the level necessary for normal function,” Lagasse says.

At the University of Pittsburgh, Lagasse and his colleagues also tested the approach in pigs. In a study published in 2020 , they found that pigs regained liver function after getting an injection of liver cells into an abdominal lymph node. When the scientists examined the lymph nodes with miniature livers, they found that a network of blood vessels and bile ducts had spontaneously formed. The more severe the damage in the pigs’ native liver, the bigger the second livers grew, suggesting the animals’ bodies may be able to recognize the healthy liver tissue and transfer responsibilities to it.

“It is remarkable to identify lymph nodes as a reproducible and fertile bed for the regeneration of a variety of tissues and organs in two different animal species,” Abla Creasey, vice president of therapeutics development at the California Institute for Regenerative Medicine, says of the company’s approach. “These findings suggest that such an approach could present an alternative tissue source for patients with failing organs,”

Elliot Tapper, a liver specialist at the University of Michigan, is also excited by the prospect of turning a lymph node into a new liver. “Even though it's not where the liver was intended to sit, it can still do some liver functions,” he says.

The most likely benefit of the LyGenesis treatment, he says, would be removing ammonia from the blood. In end-stage liver disease, ammonia can build up and travel to the brain, where it causes confusion, mood swings, falls, and sometimes comas. He doesn’t think the new mini organs could do all the jobs of a natural liver though, because they contain cell types other than hepatocytes.

One of the big questions is how many cells it will require for humans to grow a liver big enough to take over certain vital functions, such as filtering blood and producing bile. In the LyGenesis trial, three additional patients will get an injection of 50 million cells into a single lymph node—the lowest “dose.” If that seems safe, a second group of four will get 150 million cells into three different lymph nodes. A third group would get 250 million cells in five lymph nodes—meaning they could have five mini livers growing inside them.

The effects of the therapy won’t be immediate. Hufford says it will likely take two to three months for the new organ to grow big enough to take over some of the functions of the native liver. And like organ donor recipients, trial participants will need to go on immunosuppressant drugs for the rest of their lives to prevent their body from rejecting the donor cells.

If the approach works, it could provide a life-saving alternative to liver transplantation for some patients. “If they prove it’s effective and safe,” Tapper says, “there will definitely be candidates that are interested in this kind of intervention.”

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Typical imaging finding of hepatic infections: a pictorial essay

Sonaz malekzadeh.

1 Department of Diagnostic and Interventional Radiology, Fribourg Cantonal Hospital, Fribourg, Switzerland

2 Faculty of Medicine, University of Fribourg, Fribourg, Switzerland

Lucien Widmer

Faezeh salahshour.

3 Department of Diagnostic and Interventional Radiology, Imam Khomeini Hospital, Tehran, Iran

Bernhard Egger

4 Department of Surgery, Fribourg Cantonal Hospital, Fribourg, Switzerland

Maxime Ronot

5 Department of Radiology, AP-HP, HUPNVS, Beaujon Hospital, Clichy, France

Harriet C. Thoeny

Hepatic infections are frequent in clinical practice. Although epidemiological, clinical and laboratory data may suggest hepatic infection in certain cases, imaging is nearly always necessary to confirm the diagnosis, assess disease extension and its complications, evaluate the response to treatment, and sometimes to make differential diagnoses such as malignancies. Ultrasound (US) is usually the first-line investigation, while computed tomography (CT) and magnetic resonance imaging (MRI) provide better characterization and a more precise assessment of local extension, especially biliary and vascular. The purpose of this article is to describe the typical features and main complications of common hepatic infections. Familiarity with the radiological features of this entity can help suggest the correct diagnosis and the need for further studies as well as determine appropriate and timely treatment.

Introduction

Hepatic infections are relatively common. The prognosis varies and depends on the clinical context, the etiology of the underlying infection as well as when appropriate treatment is started. The clinical presentation ranges from chronic indolent forms to more aggressive lesions that are associated with a high mortality, especially in vulnerable or immunocompromised patients. The non-specific clinical symptoms of liver infections, including fever, abdominal discomfort, and nausea, highlight the importance of imaging with ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MRI) to obtain a correct and prompt diagnosis. Although the imaging features of liver infections may be characteristic and sometimes lead directly to a correct diagnosis, clinical, laboratory and imaging findings are usually needed to make a final diagnosis. Imaging-guided fine-needle aspiration may also occasionally be required. Besides its central diagnostic role, imaging is important during follow-up of hepatic infections to monitor response to treatment.

The aim of this pictorial review article is to describe the most common imaging features of hepatic infections, categorized into bacterial, fungal, viral, and parasitic infections (Table  1 ). We also describe typical radiological findings to differentiate infections from other pathologies. Typical imaging features are summarized in Table  2 . Chronic viral liver infection is beyond the scope of this article and will not be discussed.

Table 1

Overview of infectious agent, sub-classifications, and organisms

Table 2

Typical imaging findings of main acute hepatic infections

HIV Human immunodeficiency virus, EBV Epstein–Barr virus, US ultrasound, CT Computed tomography

Bacterial infections

Pyogenic liver abscess.

Although pyogenic abscesses are often polymicrobial, Escherichia coli and Klebsiellae pneumoniae are the most frequently isolated pathogens [ 1 , 2 ]. While the cause of pyogenic abscess can usually be determined, no obvious cause is found in up to 20% of cases, which are known as cryptogenic [ 3 , 4 ]. The most common cause of a cryptogenic pyogenic abscess is the hypervirulent K. pneumoniae, which is associated with aggressive inflammatory disease and additional sites of infection in other organs [ 5 , 6 ]. Surprisingly, it has a more favorable outcome than pyogenic abscesses, mainly because the former occur in immunocompetent patients [ 7 ]. Four main mechanisms can favor hepatic abscesses. First, they can be the result of hematogenous dissemination of gastrointestinal infections via the portal vein or disseminated sepsis via the hepatic artery. Bile infection, favored by duct obstruction from various etiologies including stones, neoplasms, and strictures (ascending cholangitis, pancreatic cancer, inflammatory bile duct diseases) is frequently observed. Moreover, biliary stents and bilio-digestive anastomosis are also iatrogenic predisposing factors for pyogenic liver abscesses [ 8 , 9 ]. Finally, hepatic infection by continuity, such as hepatic abscess from cholecystitis or direct introduction of bacteria into the liver parenchyma, such as during hepatic biopsy or surgery, and superinfection of pre-existing hepatic lesions, e.g., cysts or necrotic liver lesions, are other routes of liver abscesses [ 10 ]. Classically, pyogenic liver abscesses are pus-containing uni- or multilocular lesions surrounded by a fibrotic capsule.

Ultrasonography

On US, the appearance varies depending on the size and content of the abscess and ranges from a well or ill-defined tiny hypoechoic nodule to a large hypoechoic lesion with septa and debris [ 11 ].

Computed tomography

The same appearance may be observed on CT with the characteristic “double target sign,” defined as early arterial enhancement of the inner wall of the abscess and progressive enhancement of the outer layer [ 12 ]. The entire lesion is surrounded by segmental geographic or peripheral transient perfusion disorders, identified as regions with early arterial phase enhancement and iso-attenuation on portal venous and delayed phases [ 13 ]. These perfusion disorders are related to perilesional venule stenosis, due to edema and infiltration by inflammatory cells (Fig.  1 ). On CT pyogenic abscesses may also present as multiple tiny hypoattenuating lesions with peripheral rim enhancement that sometimes coalesce to form larger lesions, a feature referred to as the “cluster sign” [ 14 ] . This is a typical feature in abscesses of biliary origin.

Pyogenic abscess in a 60-year-old female patient with a history of chronic pancreatitis who presented with asthenia and fever. Axial arterial phase ( a ) and portal venous phase ( b ) contrast-enhanced CT show small clustering lesions with a dominant hypoattenuating lesion in segment V of the liver (white arrows) corresponding to pyogenic hepatic abscesses. Altered perfusion disorder is observed as geographic areas of hyperattenuation peripheral to the hepatic abscesses (white arrowheads), clearly visualized on arterial phase ( a )

Magnetic resonance imaging

On MRI, the central pus is hyperintense on T2-weighted images (T2WI) and hypointense on T1-weighted images (T1WI), with impeded diffusion due to pus accumulation and the increased viscosity of pus on Diffusion-weighted (DW MRI) imaging. The inner and outer layers of the wall appear hypo- and hyperintense on T2WI, respectively. Although pyogenic abscesses usually appear to be fluid collections, they may also have a more solid appearance, mimicking primary or secondary hepatic tumors. This is often found in association with K. pneumoniae [ 15 ].

Differential diagnosis

The main differential diagnosis of pyogenic abscesses includes primary or secondary hepatic tumors and amebic abscess. It is important to note that transient perilesional enhancement, which is more frequently associated with a pyogenic abscess, helps exclude hepatic tumors. Pyogenic liver abscesses may also be complicated by hepatic or portal vein thrombosis with a reported incidence of up to 42% [ 16 , 17 ]. Necrotic hepatocellular carcinoma associated with venous invasion can mimic a hepatic abscess complicated by cruoric venous thrombosis. However, venous thrombosis with luminal expansion, arterial phase intraluminal enhancement, and impeded diffusion of the venous structure suggests tumoral rather than cruoric venous thrombosis. Furthermore, the associated colon involvement supports amebic infection. However, the percutaneous approach is usually warranted for the diagnosis and therapeutic purposes.

Tuberculosis

Hepatic involvement in tuberculosis can occur from pulmonary or miliary tuberculosis or less frequently via portal vein from gastrointestinal lesions [ 18 ]. Hepatic tuberculosis can be local (tuberculous primary complex with caseous necrosis of the hepatic hilar lymph nodes) or miliary, a part of a generalized disease. The latter is the most common form of liver tuberculosis. [ 19 ]. Tuberculoma can also develop and correspond to the enlargement and confluence of miliary foci or nodular development of tuberculous foci.

On US, the presentation of miliary hepatic involvement includes hepatomegaly with a diffuse hyperechoic aspect to the liver parenchyma with or without small diffuse hypoechoic lesions [ 20 ]. In the macronodular tuberculosis, single or multiple focal lesions with variety of appearance ranging from hyper- to hypoechoic lesions can be observed (Fig.  2 a, b). Both hyper- and hypoechoic features are thought to represent different phases of disease corresponding to the degree of necrosis [ 21 ].

Liver tuberculosis in a 49-year-old female patient with asthenia and loss of weight without fever. Ultrasound a demonstrates a focal well-defined subcapsular hypoechoic lesion in segment III (white arrow). Enlarged lymph node (white arrowhead) is also observed in the porta hepatis ( b ) (Courtesy of Dr. Suzan Elhakiem, Ibn Sina Hospital, Khartoum, Sudan)

On CT, the miliary form is observed as the multiple small hypoattenuating foci with discrete enhancing rim after contrast administration [ 22 ]. The macronodular lesions are detected as hypoattenuating lesions ranging from 14 to 45 HU on unenhanced CT, with tiny peripheral enhancement after contrast administration while the central part remains unchanged [ 23 ]. Calcifications can be observed in both miliary and macronodular forms [ 19 ].

On MRI, the miliary form is detected as multiple tiny lesion which are hypointense on T1WI and hyperintense on T2WI. The macronodular form presents hypo- or hyperintense central area on T2WI, with a hypointense rim [ 22 , 24 ]. As observed with pyogenic abscess, liver tuberculosis can demonstrate impeded diffusion on DW MRI, making it difficult to differentiate from pyogenic abscess.

The main differential diagnosis of miliary form includes lymphoma, metastatic lesions, sarcoidosis, and fungal infections. For the macronodular form, primary and metastatic hepatic lesions as well as pyogenic abscesses constitute the main differentials. Imaging is usually insufficient to make the definitive diagnosis and percutaneous biopsy is needed.

Brucellosis

Hepatomegaly is a typical feature of hepatic abscess in brucellosis. A suppurative hepatic abscess is also a rare finding in these cases. Solitary abscesses normally present with a central calcification [ 25 ].

Hepatic abscesses from brucellosis may be solitary or miliary. Solitary lesions are seen as heterogeneous, well-delineated lesions, while miliary abscesses are seen as multiple hypoechoic hepatic subcentrimetric lesions which are difficult to be differentiated from tuberculosis, candidiasis or lymphoma.

Hepatic abscesses are hypoattenuating with thick peripheral enhancement on contrast-enhanced CT (Fig.  3 a). Perilesional transient perfusion disorder, like that found in pyogenic abscesses, may also occur with brucellosis.

Brucellosis in a 42-year-old male patient with evening fever and sweating. Contrast-enhanced axial CT image a shows a heterogeneous lesion with enhanced contours (black arrow), showing a central hypoechoic fluid component and a calcium deposit (white arrow). Axial contrast-enhanced T1-weighted image b shows enhancement of the peripheral tissular areola (black arrow) and central saccular formation with fluid, surrounded by an intermediary heterogeneous component.

Reprinted from Sisteron et al. [ 27 ], with permission from Elsevier

These abscesses are hyperintense on T2WI on MRI. It is important to note that thickened peripheral enhancement, up to 15 mm, has been described in these abscesses on after contrast administration (Fig.  3 b) [ 26 , 27 ].

When miliary, they should be differentiated from tuberculosis, candidiasis and lymphoma while pyogenic abscesses remain the differential diagnosis for solitary form.

Bartonellosis

Bartonellosis, also known as “cat-scratch disease”, is usually associated with painful lymphadenopathy near the cat bite or scratch site. In the presence of liver involvement, multiple necrotizing granulomas, measuring up to 3 cm, can be detected throughout the liver parenchyma.

Necrotizing granulomas are seen as non-specific hypoechoic nodules throughout the liver parenchyma.

These lesions are hypoattenuating on precontrast CT. These nodules may remain hypoattenuating after contrast administration (Fig.  4 ) or demonstrate iso-attenuation and sometimes rim enhancement [ 28 ].

Bartonellosis in a 65-year-old female patient treated for autoimmune hepatitis. Axial contrast-enhanced CT demonstrates hypoattenuating ill-defined lesions are scattered throughout the liver parenchyma (white arrowheads)

On MRI, they are hypointense on T1WI and hyperintense on T2WI with the same enhancement as that of CT [ 29 ].

Although it may be difficult to differentiate bartonellosis from lymphoma, fungal infection, sarcoidosis, tuberculosis or brucellosis on cross-sectional imaging, a history of cat contact in an immunocompetent child or young adult can be helpful.

Acute viral infection

Viral hepatitis.

Acute hepatic viral infections are mostly caused by hepatitis A, B, C, D, and E viruses [ 30 ]. Ingestion of contaminated food or water and contact with blood or other body fluid of infectious person are the common ways of transmission. Although the radiological features of acute hepatitis are non-specific, imaging is usually performed to exclude other diseases with the same clinical signs, such as biliary obstruction or diffuse liver metastases.

On US, acute hepatitis usually presents with hepatomegaly, decreased hepatic echogenicity, as well as a relative increase in portal wall echogenicity, known as the “starry sky” sign [ 11 ].

On CT, hepatomegaly, heterogeneous hepatic contrast enhancement on arterial phase images, well-defined parenchymal zones with low attenuation, periportal hypoattenuation, or hepatic hilum lymph node enlargement can be observed [ 31 ]. Gallbladder wall thickening may also be observed during acute hepatitis (Fig.  5 ) and should not be misinterpreted as acute cholecystitis [ 32 ]. Non-distended gallbladder and an absence of gallstones are the additional findings which suggest a diagnosis of acute hepatitis. Nevertheless, the liver may have a normal appearance on CT with serologically proven viral hepatitis.

Acute viral hepatitis in a 59-year-old male patient with jaundice and elevated liver enzymes due to hepatitis A infection. Axial contrast-enhanced CT shows a contracted gallbladder with a thick hypoattenuating edematous wall and an enhancing mucosal layer (white arrow)

The findings on MRI are the same as those on CT with a hyperintense periportal halo on T2WI and a hypointense T1WI image [ 33 ].

However, the diagnosis of viral hepatitis is mainly based on clinical and laboratory data rather than imaging findings.

The imaging findings of viral hepatitis such as hepatomegaly and periportal edema are non-specific and differential diagnosis includes metabolic disease, passive hepatic congestion, autoimmune hepatitis and drug-induced hepatitis.

Human Immunodeficiency Virus (HIV)

Liver involvement in patients with acquired immunodeficiency syndrome (AIDS) is not rare and frequently these patients suffer also from chronic viral infections such as hepatitis B and C.

On US, gallbladder wall thickening with biliary ducts wall thickening and dilatation can be encountered [ 11 ].

Hepatomegaly and periportal lymphadenopathy are usually observed which are non-specific. In rare cases, focal steatosis and acalculous cholecystitis can also be seen [ 34 ].

Because HIV hepatopathies are frequently associated with biliary and pancreatic disorders, contrast-enhanced MRI with Magnetic resonance cholangiopancreaticography (MRCP) has been proposed in a single session to evaluate biliary tract lesions as well as liver and pancreatic parenchymal anomalies [ 35 ]. Imaging findings include biliary stenosis involving long extrahepatic segments, papillary stenosis (Fig.  6 ), and acalculous cholecystitis [ 35 ].

HIV-related cholangiopathy in a 16-year-old female patient. Coronal T2-weighted image demonstrates intrahepatic and extrahepatic bile duct dilatation (white arrows) due to papillary stenosis (white arrowhead), a common finding in this disease

As for viral hepatitis, the imaging findings for liver involvement in HIV such as hepatomegaly and periportal lymphadenopathy are non-specific. However, the primary sclerosing cholangitis is considered to be the main differential diagnosis for HIV cholangiopathy.

Fungal infection

Hepatic candidiasis.

Invasive systemic candidiasis is a significant cause of morbidity and mortality in immunosuppressed patients, especially those receiving chemotherapy or with hematological malignancies.

Four US patterns of hepatosplenic candidiasis have been described [ 36 ]. The first pattern has a “wheel-within-a-wheel” appearance with a central hypoechoic area of necrosis and fungal debris, surrounded by a hyperechoic zone of inflammatory cells. A hypoechoic rim is found at the periphery, representing fibrosis. The second pattern is a bull’s eye configuration with a central hyperechoic nidus surrounded by a hypoechoic rim. In general, this pattern develops in patients with active fungal infection and a relatively normal white blood cell count. The third pattern is the most common and includes a uniformly hypoechoic nodule representing fibrosis that has developed in an area of prior inflammation, which is non-specific and can simulate metastases or lymphoma. The fourth pattern, which occurs in later stages of infection, consists of hyperechoic foci with different degrees of posterior acoustic shadowing, representing scars or calcifications.

On CT, the microabscesses are seen as small, round, hypoattenuating lesions, in a miliary pattern [ 37 ]. Also, a “wheel-within-a-wheel” pattern, as observed by US, can be detected.

On MRI, the untreated nodules are markedly hyperintense on T2WI and minimally hypointense on T1WI (Fig.  7 ) with moderate enhancement after contrast administration [ 38 ]. After treatment, the microabscesses develop to granuloma with various imaging patterns according to the phase after treatment.

Candidiasis in a 65-year-old male patient with acute myeloblastic leukemia. Axial contrast-enhanced T1-weighted image on hepatobiliary phase illustrates multiple tiny hypointense lesions throughout the liver parenchyma (white arrowheads) (Courtesy of Dr. Luisa Paulatto, Beaujon Hospital, Clichy, France)

Tuberculosis, sarcoidosis, metastases and lymphoma are the main diagnoses to be differentiated from hepatic candidiasis. A chest-X-ray may be conclusive to exclude tuberculosis and sarcoidosis. In patients with a known history of malignancy, the hepatic lesions can be likely metastases. However, a secondary fungal infection should also be considered in this group of patients. Lymphoma is usually associated with supra- and infra-diaphragmatic lymphadenopathies. Nonetheless, in some cases the percutaneous biopsy is conclusive for the diagnosis.

Hepatic histoplasmosis

Histoplasmosis is caused by inhalation of Histoplasma capsulatum spores. It usually develops in immunodeficient patients, such as HIV-positive patients and transplant recipients [ 39 ]. The liver is rarely the primary site of infection but it is often involved in the course of a progressive disseminated disease, which usually originates in the lungs or upper respiratory tract. Imaging lacks sensitivity and specificity, and findings are similar to those in tuberculosis, candidiasis or other disseminated fungal diseases, with multiple small nodules in the liver parenchyma.

Parasitic infections

Infection of the hepatic parenchyma, echinococcosis.

Echinococcus granulosus and Echinococcus multilocularis cause cystic echinococcosis (CE) and alveolar echinococcosis (AE), respectively. While E. granulosus is more common, E. multilocularis is more invasive [ 40 ]. Infections occur by either ingestion of food or plants containing the eggs from the Echinococcus tapeworm or by direct contact with the main hosts, which are dogs ( E. granulosus ) and foxes ( E. multilocularis ) [ 41 , 42 ]. The ingested embryos reach the portal venous system by invading the mucosal duodenal wall then embed the sinusoidal spaces and develop cysts.

Echinococcus granulosus

The mature cyst (i.e., hydatid cyst) of E. granulosus is composed of three layers. The outer layer or pericyst, mainly corresponds to the compressed adjacent hepatic parenchyma. The middle layer or ectocyst, is a translucent acellular layer allowing nutrition to pass to the endocyst, while the inner germinal layer produces the scolices, surrounding a fluid-filled central cavity [ 43 , 44 ].

The appearance of CE on imaging, which is best evaluated by US, depends on the stage of cyst growth, classified by WHO into the six following subgroups:

• CL (cystic lesions): are well-defined, unilocular, anechoic lesions with an imperceptible wall.
• CE1: is an anechoic lesion with a perceptible double-layer wall that contains dependent low-level echos called hydatid sand. Hydatid sand (free scolices produced by the endocyst) is mobile when the patient changes position, which is referred to as the “snowstorm” sign [ 11 , 42 , 45 ].
• CE2: is a cystic lesion that contains multiple septa or multiple cystic lesions involving nearly the entire cystic cavity so that the walls of the cysts are very close to each other, with a “rosette” appearance.
• CE3a: in these cases the germinal layer is detached from the pericyst, which remains intact and is seen floating in the cystic cavity, known as a “water-lily” sign [ 41 , 44 ].
• CE3b: is a cystic lesion that encases multiple daughter cysts. The daughter cysts are arranged peripherally in the cystic cavity which contains a solid-appearing matrix compared to the fluid in CE2.
• CE4: presents as a heterogeneous mass that ranges from hypoechoic to hyperechoic on US, with no identifiable daughter cyst.
• CE5: is a partially or entirely calcified cyst. When the cyst wall is calcified, it presents as a hyperechoic peripheral rim with acoustic shadow.

On precontrast CT, the cyst wall usually appears as a hyperattenuating capsule that is nearly isoattenuating compared to the adjacent hepatic parenchyma following contrast administration [ 46 ]. CL is visualized as a well-defined, unilocular hypoattenuating lesion with thin wall (Fig.  8 ). The debris, when visible, shows no obvious contrast enhancement. The detached germinal layers are visible as serpiginous hyperattenuating structures (Fig.  9 ). The daughter cysts present as the hypoattenuating lesions with a density lower than the matrix of the cyst (Fig.  10 ). When the wall is calcified, it is well appreciated on CT (Fig.  11 ).

Cystic echinococcosis type CL in a 32-year-old female patient with upper abdominal discomfort. Axial contrast-enhanced CT image shows two large cystic lesions with thin walls in segment VII and VIII of the liver (white arrow). Ultrasound (not shown) revealed an anechoic cyst with a double layered wall, no internal daughter cyst or detached membrane

Cystic echinococcosis type CE3a in a 27-year-old female patient with cough. Axial contrast-enhanced CT of the lower pulmonary parenchyma a reveals a pulmonary cyst in the middle lobe (white arrow) associated with a partial consolidation of the right lower lobe. Axial contrast-enhanced CT of the upper abdomen b shows two hepatic cystic lesions (white arrow) with internal detached membranes (“water-lily” sign) (white arrowhead)

Cystic echinococcosis type CE3b in a 54-year-old male patient with right upper quadrant pain. Axial contrast-enhanced CT reveals a large hepatic cyst in right hepatic lobe (black arrow) with solid matrix in the center (asterisk) and peripherally located daughter cysts (white arrow)

Cystic echinococcosis type CE5 in a 50-year-old female patient with an incidental solid mass reported on ultrasound. Axial precontrast CT shows a round highly calcified lesion in segment IV (white arrow)

On MRI the pericyst has a characteristic hypointense appearance, surrounding a markedly hyperintense T2WI and hypointense T1WI central cavity [ 44 , 47 , 48 ]. The daughter cysts are hyperintense and hypointense T2WI and T1WI, respectively, compared to the cyst matrix. The “ball of wool” sign, which is the characteristic feature of CE4, is a result of the detachment of the inner layer folding on itself so the lesion appears as a solid mass (Fig.  12 ). Calcifications are seen as the focal hypointense lesions on T2WI.

Cystic echinococcosis type CE4 in a 62-year-old female patient with upper abdominal pain. Axial fat-suppressed T2-weighted image shows a well-defined subcapsular moderately hyperintense lesion (white arrow) with a characteristic “ball of wool” sign. An adjacent dilated intrahepatic bile duct is also noted (white arrowhead)

CL, CE1, and CE2 are active lesions, while CE4 and CE5 are inactive lesions. CE3 corresponds to transitional lesions which are degenerating cysts but containing viable protoscoleces [ 49 , 50 ]. Hydatid cysts may be associated with complications including superinfection, communicating rupture, external rupture and the mass effect of large hydatid cysts. Superinfection is associated with a gas-fluid level or gas bubble in the hydatid cyst, frequently surrounded by areas of transient perfusion disorders in the surrounding hepatic parenchyma, such as in pyogenic abscesses [ 51 ]. Fistula with a hollow viscera or the tracheobronchial tree may also lead to gas-fluid levels which may be confounded with cyst superinfection [ 46 , 52 ]. Communicating rupture is a cystic rupture into the biliary tree which may result in the passage of hydatid sand, a floating membrane from the germinal layer or daughter cysts into the biliary ducts, as well as fluid-fluid levels containing bile in the hydatid cyst. The latter are seen as fat droplets in the cyst with marked hypoattenuation on CT, and signal dropout on opposed phased gradient echo T1WI. This feature in not entirely specific for cystic rupture, since fatty transformation may occur in old cysts.

External rupture is direct rupture of a cyst into the peritoneal or pleural cavity frequently via the bare area of the gastrohepatic ligament (Fig.  13 ). Finally, hydatid cysts can have a mass effect on the adjacent biliary or vascular structures. Chronic biliary obstruction and vascular compression, such as portal vein compression, can lead to hepatic segmental or lobar atrophy as well as secondary Budd-Chiari syndrome due to the mass effect on the hepatic veins (Fig.  14 ).

Peritonitis due to a ruptured hydatid cyst in a 45-year-old female patient with acute upper abdominal pain. Axial contrast-enhanced CT of the upper abdomen (a) demonstrates two hepatic cysts with irregular borders in the right and left liver lobe (white arrows); the latter reaches the anterior liver surface. Axial contrast-enhanced CT of lower abdomen (b) shows a significant amount of intraperitoneal fluid with a thickened enhancing peritoneum (white arrowheads)

Budd-Chiari syndrome secondary to compression of liver out-flow by the hydatid cyst in a 20-year-old female patient. Hypertrophy of the caudate lobe with inhomogeneous mottled liver appearance is indicative of Budd-Chiari syndrome. Axial delayed phase contrast-enhanced CT shows a deformed cystic lesion in the deep portion of segments VII and VIII of the liver (white arrow) associated with pneumobilia secondary to previous sphincterotomy (white arrowhead)

Various congenital, inflammatory, infectious, and neoplastic cystic lesions can mimic different stages of CE. However, the typical imaging features of CE along with the serological information are usually helpful to discriminate CE from its counterparts.

The treatment of the CE depends on the stage of the cyst, including medical treatment, percutaneous approach recognized as PAIR (puncture, aspiration, injection, and reaspiration), surgical strategy, and watch-and-wait [ 53 ]. Medical treatment, PAIR, and catheterization are usually reserved for CE1 and CE3a, whereas modified catheterization and surgery are preferred methods for CE2 and CE3b. CE4 and CE5 can be controlled by watch-and-wait as they are considered to be inactive [ 50 , 54 ].

Echinococcus multilocularis

AE includes small, multilocular confluent cysts associated with solid components that demonstrate exogenous growth invading the adjacent hepatic parenchyma. A large cystic component is also frequently observed. Small cysts include metacestodal vesicles, while large cysts are composed of liquefaction necrosis. Moreover, solid components encompass calcification and coagulation necrosis.

The two most frequent US findings of AE include a heterogeneous lesion with irregular borders and a large hypoechoic lesion. In the former, the heterogeneous lesion comprises the hypoechoic (necrosis and active parasitic tissue) and hyperechoic areas (fibrosis and calcification) with irregular borders indicating the invasive nature of the lesion while the latter is demonstrated as a central necrosis surrounded by hyperechoic fibrotic tissue [ 50 ].

On CT, AE is usually presented as heterogeneous lesion containing hypoattenuating areas of necrosis and active parasitic tissue with scattered calcification with no obvious enhancement after contrast administration (Fig.  15 a) [ 50 ].

Alveolar echinococcosis incidentally detected in a 75-year-old male patient. Axial contrast-enhanced CT a shows an ill-defined subcapsular hypoattenuating lesion in segment VII of the liver (black arrow). Axial fat-suppressed T2-weighted image b further characterizes this lesion as multiple tiny cystic lesions (white arrowhead) surrounding a solid component corresponding to type 3 of alveolar echinococcosis

Kodama et al. classified AE into five groups on MRI based on cystic and solid components, distribution and contrast enhancement (Table  2 ) [ 55 ]. Typical findings include peripheral arrangement of multilocular cysts and slight or no contrast enhancement of the solid component (Fig.  15 b). While cystic components are markedly hyperintense on T2WI, the solid component can range from hypo- to hyperintense on T2WI [ 55 , 56 ].

The heterogeneous form of AE can be misinterpreted as primary and secondary hepatic malignancies and the large necrotic AEs should be differentiated from pyogenic and amebic abscesses.

Amebic abscess

Liver amebic abscess is the most common site of extraintestinal involvement of amebiasis, the infection of the large bowel by Entamoeba histolytica . It occurs in less than 1% of patients with E. histolytica infection [ 11 , 57 ]. Amebic abscess is usually a solitary unilocular cyst that is frequently located in the right hepatic lobe, especially the posterior segment.

On US, it is demonstrated as a hypoechoic, well-delineated lesion containing low-level echoes that correspond to debris or hemorrhage (Fig.  16 a).

Amebic abscess in a 57-year-old male patient who presented with fever of unknown origin and right upper abdominal pain with a recent history of travel to Africa. Ultrasound a demonstrates a large relatively well-delineated lesion with a heterogeneous solid-appearing content (white arrow). Axial contrast-enhanced CT shows the “double target sign” (black arrow)

On precontrast CT, an amebic abscess is hypoattenuating but slightly more attenuating than water, and varies in density between 10 and 20 Hounsfield units [HU] with a thick peripheral capsule up to 1.5 mm in diameter [ 11 , 58 ]. The capsule is enhanced after contrast administration and surrounded by peripheral hypoattenuation, known as the “double target sign,” similar to that observed with pyogenic abscesses (Fig.  16 b) [ 43 , 44 ].

On MRI, the central area is hypointense and hyperintense on T1WI and T2WI, respectively. The peripheral capsule is enhanced after contrast administration, and the lesion is surrounded by a hyperintense T2WI peripheral area [ 59 ].

The appearance of an amebic abscess on imaging is nearly indistinguishable from that of a pyogenic abscess. However, a solitary abscess is more likely to be an amebic abscess compared to pyogenic abscess which is typically multiple. Also, the association of colon wall thickening that spares the ileum is highly suggestive of an amebic abscess. Furthermore, extrahepatic complications, such as pleural or pericardial effusion, and perihepatic collections, are more frequent with amebic than with pyogenic abscesses. Nonetheless, the definitive diagnosis is usually made through a combination of imaging, serological, microbial, and percutaneous aspiration data [ 60 ]. Metronidazole is the treatment of choice for amebic abscesses and aspiration or percutaneous drainage is considered for larger abscesses with high risk of rupture or in the case of failure to medical treatment [ 61 ].

Infection of hepatic vessels

Schistosomiasis.

Five species of S chistosoma cause human infection, and S. mansoni and S. japonicum are the most common causes of hepatic infection [ 62 ]. Schistosomes penetrate the skin to reach the bowel lumen where they lodge and release eggs into the mesenteric vein, gaining access to the portal system [ 44 ]. Schistosoma eggs cause a chronic inflammatory granulomatous reaction in the portal system, causing periportal fibrosis. Thus, the radiological features in the acute phase are non-specific, including hepatosplenomegaly and focal nodular liver lesions. In the chronic phase, fibrosis bands are observed surrounding the portal system. With S. mansoni , this is mainly observed when eggs are lodged in the proximal portion of the portal venous system while with S. japonicum , smaller eggs tend to lodge in the more distal portal veins [ 43 ].

On US, the fibrosis bands are defined as a hyperechoic mantle encompassing the anechoic portal vein called the “bull’s eye” sign (Fig.  17 ) [ 11 ]. Common hallmarks of the chronic phase are a cirrhosis-like appearance with heterogeneous parenchyma and irregular contours.

Hepatic schistosomiasis in a 20-year-old male patient with a history of gastrointestinal bleeding from 1 year ago. Ultrasound demonstrates a marked diffuse periportal thickening as a hyperechoic mantle encompassing the anechoic portal vein (white arrowheads) (Courtesy of Dr. Suzan Elhakiem, Ibn Sina Hospital, Khartoum, Sudan)

Periportal fibrosis presents as hypoattenuating bands on precontrast CT and with delayed phase contrast enhancement showing polygonal hypoattenuating structures surrounding areas of normal parenchyma [ 63 ]. The hypoattenuating peripheral septa observed with S. japonicum tend to calcify later in the disease and are seen as calcified septa, perpendicular to the hepatic capsule, called the “turtle back” sign or “tortoise shell” feature [ 63 ].

On MRI, periportal and polygonal fibrosis are hypointense on T1WI and hyperintense on T2WI with delayed contrast enhancement.

A cirrhosis-like appearance of chronic schistosomiasis should be differentiated from other causes of cirrhosis. However, calcification and periportal fibrosis, which are typical findings in schistosomiasis, are not common with other causes of cirrhosis.

Infection of bile ducts

Fascioliasis.

Fasciola hepatica and Fasciola gigantica are parasites that are responsible for fascioliasis infection [ 64 ]. Sheep and cattle are the definitive hosts, while humans may be infected by ingesting contaminated water or freshwater plants [ 65 ]. There are two phases to fascioliasis infection, including a parenchymal (migratory phase) and biliary phase. During the parenchymal phase, juvenile flukes reach the peritoneal space by invading the small bowel wall, then reach the hepatic parenchyma by penetrating the hepatic capsule. They migrate to the biliary tree from the subcapsular space in linear tracts, converging toward the portal triads. During the biliary phase, the flukes mature in the small biliary ducts and produce eggs. Although the imaging findings depend on the phase of infection, both phases can be present simultaneously.

During the hepatic phase, US shows confluent hypoechoic ill-defined subcapsular lesions [ 66 ]. In the biliary phase, intra and extrahepatic bile duct dilatation is observed. A mobile intraductal parasite, when visible, is characteristic [ 67 ].

On CT, ill-defined linear or patchy hypoattenuating subcapsular and periportal lesions that may converge from the hepatic capsule towards the hepatic hilum are observed (Fig.  18 a, b) [ 68 ]. As observed on US, biliary ducts dilatation, gallbladder wall thickening and hilar lymphadenopathy can be seen. Focal thickening and hyperenhancement of the Glisson capsule may also be observed [ 69 ].

Fascioliasis in a 42-year-old female patient with right upper abdominal pain and low-grade fever. Axial contrast-enhanced CT ( a, b ) show patchy ill-defined hypoattenuating lesions with subcapsular (white arrowheads) and periportal distribution (black arrow)

The lesions are hypointense on T1WI and hyperintense on T2WI, due to their inflammatory nature. Thickening and dilatation of the biliary tree similar to cholangitis can be observed during the biliary phase. The living, mobile parasite may sometimes be detected in the biliary tree as a biliary tree filling defect without contrast enhancement.

Confluent tiny hypoattenuating lesions can mimic primary and secondary liver malignancy or pyogenic abscess. In addition, the biliary ducts wall thickening and enhancement observed with fascioliasis should be discriminated from other causes of cholangitis such as biliary stone.

Ascariasis is a common infection caused by Ascaris lumbricoides in endemic areas. The adult worms mainly live in the jejunum, but may occasionally reach the ampulla of Vater due to altered small bowel motility [ 70 ]. Mechanical obstruction of the intrahepatic and common bile ducts by adult worms leads to cholangitis, cholecystitis, jaundice, and less frequently pancreatitis [ 71 ]. A hepatic abscess is also observed, although this is rare and thought to be due to a superinfection of the dead adult worm in the hepatic parenchyma [ 72 ].

On US, the radiological diagnosis of biliary involvement is mainly based on direct visualization of adult worms seen as a long tubular echogenic structure measuring up to 30 cm in the biliary tree. A longitudinal anechogenic line, representing the gastrointestinal tract of the worm in the center of the tubular structure, can also be seen [ 73 ]. A hepatic abscess presents as a non-specific hypoechoic focal lesion, usually with an ill-defined border [ 72 ].

Intra- and extrahepatic bile ducts dilatation can be depicted and the worm is seen as a linear filling defect in the bile duct (Fig.  19 a, b)

Ascariasis in a 36-year-old male patient. Axial and coronal reformatted contrast-enhanced CT ( a, b ) show intrahepatic and extrahepatic bile duct dilatation (black arrows). Note intrahepatic bile ducts filled with structures more attenuating than bile (black arrowhead), indicating adult worms. Oblique coronal single-shot fast spin-echo MR cholangiogram ( c ) shows adult worms as serpiginous and nodular filling defects in the left intrahepatic and extrahepatic bile ducts (white arrows)

As observed with other imaging modalities, the worm is seen as a linear filling defect in the bile duct on MRCP (Fig.  19 c). Liver abscess resembles abscess with other pathogenic agents: a focal lesion hyperintense T2 and hypointense T1.

Clonorchiasis

Clonorchiasis is caused by chronic infection of Clonorchis sinensis following ingestion of raw freshwater fish [ 74 ]. When ingested, the cyst is freed by gastric juices and then reaches the biliary tree via the ampulla of Vater. Larva mature and lodge in the intrahepatic biliary ducts, although they may also reside in the extrahepatic bile ducts and gallbladder [ 74 ]. Flukes are leaflike structures ranging from 8 to 15 mm long and may lodge sporadically or grouped in the biliary tree, causing obstruction and an inflammatory reaction of the biliary epithelium. This chronic inflammatory reaction results in adenomatous hyperplasia, lymphocyte infiltration, ductal stenosis, and periductal fibrosis [ 75 ]. The imaging features of clonorchiasis are mainly based on the obstructive and inflammatory-induced effects.

Mild diffuse peripheral intrahepatic bile duct dilatation reaching the subcapsular area, with relative sparing of the extrahepatic bile ducts, is characteristic [ 76 ]. Hyperechoic bundles surrounding the intrahepatic bile ducts are present, indicating thickening of the wall ducts. Mature flukes may be observed as elliptical or filamentous hyperechoic structures in the biliary tree [ 77 , 78 ]. Stenosis of the intrahepatic bile ducts can also be detected as the disease progresses.

A thickened biliary duct with increased periductal enhancement is usually seen.

As on US, intrahepatic bile ducts dilatation reaching the subcapsular area is observed (Fig.  20 ). MRCP shows elliptical or filamentous filling defects corresponding to mature flukes whose appearance can be differentiated from round or oval intraductal stones [ 76 ]. Cholangiocarcinoma is a well-known complication of clonorchiasis [ 78 ].

Clonorchiasis in a 74-year-old female patient with recurrent cholangitis. Axial contrast-enhanced fat-suppressed T1-weighted image shows intrahepatic bile ducts dilatation in segment VII reaching the subcapsular zone (white arrowheads)

It includes primary sclerosing cholangitis and recurrent pyogenic cholangitis.

Imaging plays a central role in the diagnosis of hepatic infectious diseases. Although hepatic infections may have typical imaging features, additional epidemiological, clinical, and laboratory information is frequently needed to confirm the diagnosis. However, in some cases, imaging-guided aspiration is the only diagnostic tool that can determine the causative agent or eliminate non-infectious pathologies. Although different imaging modalities, including US, CT, and MRI, may identify certain unique features of hepatic infections, US is the primary diagnostic tool due to its low cost, the absence of radiation exposure and optimal biliary tree evaluation. However, in the presence of non-specific clinical symptoms, CT is usually performed to characterize hepatic lesions as well as to evaluate extrahepatic expansion or the presence of calcifications. MRI has also become increasingly popular due to superior contrast resolution. Furthermore, the entire biliary tree, in particular the peripheral intrahepatic bile ducts and the distal part of the common bile duct, may be visualized on MRCP, while such visualization is difficult to see on US and CT.

Acknowledgements

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