A liver injury, also known as liver laceration, is some form of trauma sustained to the liver. This can occur through either a blunt force such as a car accident, or a penetrating foreign object such as a knife. Liver injuries constitute 5% of all traumas, making it the most common abdominal injury. Generally nonoperative management and observation is all that is required for a full recovery.

The initial management of liver trauma generally follows the same procedures for all traumas with a focus on maintaining airway, breathing, and circulation. A physical examination is a corner stone of the assessment of which there are various non-invasive means of diagnostic tools that can be utilized. An invasive diagnostic peritoneal lavage can also be used to diagnose and classify the extent of the damage. A large majority of liver injuries are minor and require only observation. Generally if there is estimated to be less than 300mL of free floating fluid, no injury to surrounding organs, and no need for blood transfusion, there is a low risk of complication from nonoperative management. In special cases where there is a higher risk with surgery, such as in the elderly, nonoperative management would include the infusion of packed red blood cells in an intensive care unit. Typically hepatic injuries resulting from stab wounds cause little damage unless a vital part of the liver is injured such as the hepatic portal vein, with gunshot wounds, the damage is worse.

When there is no pancreatic duct injury, typically hemostasis and surgical drainage are the main form of treatment. Surgical repair is undertaken when there is evidence or suspicion of ductal injury. The type of surgery depends on the degree of the injury and its proximity to the mesenteric blood vessels that serve the pancreas. When injuries are not close to the mesenteric vessels, a distal pancreatectomy may be done; this procedure preserves much of the pancreas and usually avoids loss of its endocrine and exocrine functions. In severe cases of pancreaticoduodenal injury, a pancreaticoduodenectomy can be used. Common complications after surgery include pancreatitis, pancreatic fistula, abscess, and pseudocyst formation. Initial management of hemorrhage includes controlling it by packing the wound.

Mild disease has a risk of death of about 10% while moderate disease has a risk of death of 20%. When it occurs as a result of bone marrow transplant and multiorgan failure is present, the risk of death is greater than 80%.

A pancreatic injury is some form of trauma sustained by the pancreas. The injury can be sustained through either blunt forces, such as a motor vehicle accident, or penetrative forces, such as that of a gunshot wound. The pancreas is one of the least commonly injured organs in abdominal trauma.

Diaphragmatic injuries are present in 1–7% of people with significant blunt trauma and an average of 3% of abdominal injuries.

A high body mass index may be associated with a higher risk of diaphragmatic rupture in people involved in vehicle accidents. It is rare for the diaphragm alone to be injured, especially in blunt trauma; other injuries are associated in as many as 80–100% of cases. In fact, if the diaphragm is injured, it is an indication that more severe injuries to organs may have occurred. Thus, the mortality after a diagnosis of diaphragmatic rupture is 17%, with most deaths due to lung complications. Common associated injuries include head injury, injuries to the aorta, fractures of the pelvis and long bones, and lacerations of the liver and spleen. Associated injuries occur in over three quarters of cases.

A significant complication of diaphragmatic rupture is traumatic diaphragmatic herniation: organs such as the stomach that herniate into the chest cavity and may be strangulated, losing their blood supply. Herniation of abdominal organs is present in 3–4% of people with abdominal trauma who present to a trauma center.

Exsanguination is a relatively uncommon cause of death in human beings. Traumatic injury can cause exsanguination if bleeding is not promptly controlled, and is the most common cause of death in military combat. Non-combat causes can include gunshot or stab wounds; motor vehicle crash injuries; suicide by severing arteries, typically those in the wrists; and partial or total limb amputation, such as via accidental contact with a circular or chain saw, or becoming entangled in operating machinery.

Patients can also develop catastrophic internal hemorrhages, such as from a bleeding peptic ulcer, postpartum bleeding or splenic hemorrhage, which can cause exsanguination without any external signs of distress. Another cause of exsanguination in the medical field is that of aneurysms. If a dissecting aortic aneurysm ruptures through the adventitia, massive hemorrhage and exsanguination can result in a matter of minutes.

Blunt force trauma to the liver, kidneys, and spleen can cause severe internal bleeding as well, though the abdominal cavity usually becomes visibly darkened as if bruised. Similarly, trauma to the lungs can cause bleeding out, though without medical attention, blood can fill the lungs causing the effect of drowning, or in the pleura causing suffocation, well before exsanguination would occur. In addition, serious trauma can cause tearing of major blood vessels without external trauma indicative of the damage.

Alcoholics and others with liver disease can also suffer from exsanguination. Thin-walled, normally low pressure dilated veins just below the lower esophageal mucosa called esophageal varices can become enlarged in conditions with portal hypertension. These may begin to bleed, which with the high pressure in the portal system can be fatal. The often causative impaired liver function also reduces the availability of clotting factors (many of which are made in the liver), making any rupture in vessels more likely to cause a fatal loss of blood.

Historically mortality has been high, being in excess of 80%. In recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly. At present overall short-term survival with transplant is more than 65%.

Several prognostic scoring systems have been devised to predict mortality and to identify who will require an early liver transplant. These include King's College Hospital criteria, MELD score, APACHE II, and Clichy criteria.

People with ascites due to cirrhosis are at risk of spontaneous bacterial peritonitis.

While some investigations suggest a possible beneficial effect of mesenchymal stem cells on heart and kidney reperfusion injury, to date, none have explored the role of stem cells in muscle tissue exposed to ischemia-reperfusion injury.

Stem cells have been implicated in the regeneration of skeletal muscle after traumatic and blast injuries, and have been shown to hone to muscle damaged after exercise.

This refers to changes in the mucosa of the stomach in people with portal hypertension, and is associated with cirrhosis severity.

Serum lactate level is a proxy measure of tissue oxygenation. When tissues do not have adequate oxygen delivery (i.e., are ischemic), they revert to less efficient metabolic processes, producing lactic acid.

Myoglobin is released from damaged muscle, as in the case of ischemia.

Serum creatinine and BUN may be elevated in the setting of Acute Kidney Injury.

Common causes for acute liver failure are paracetamol (acetaminophen) overdose, idiosyncratic reaction to medication (e.g. tetracycline, troglitazone), excessive alcohol consumption (severe alcoholic hepatitis), viral hepatitis (hepatitis A or B — it is extremely uncommon in hepatitis C), acute fatty liver of pregnancy, and idiopathic (without an obvious cause). Reye syndrome is acute liver failure in a child with a viral infection (e.g. chickenpox); it appears that aspirin use may play a significant role. Wilson's disease (hereditary copper accumulation) may infrequently present with acute liver failure.

The disease is typically progressive, leading to fulminant liver failure and death in childhood, in the absence of liver transplantation. Hepatocellular carcinoma may develop in PFIC-2 at a very early age; even toddlers have been affected.

In the BMT setting, VOD is felt to be due to injury to the hepatic venous endothelium from the conditioning regimen.

Toxic agents causing veno-occlusive disease include plants as well as the medication cyclophosphamide.

While any number of injuries may occur during the birthing process. A number of specific conditions are well described. Brachial plexus palsy occurs in 0.4 to 5.1 infants per 1000 live birth. Head trauma and brain damage during delivery can lead to a number of conditions include: caput succedaneum, cephalohematoma, subgaleal hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, epidural hemorrhage, and intraventricular hemorrhage.

The most common fracture during delivery is that of the clavicle (0.5%).

SSC is thought to develop as a consequence of known injuries or pathological processes of the biliary tree, such as biliary obstruction, surgical trauma to the bile duct, or ischemic injury to the biliary tree. Secondary causes of SSC include intraductal stone disease, surgical or blunt abdominal trauma, intra-arterial chemotherapy, and recurrent pancreatitis. It has been clearly demonstrated sclerosing cholangitis can develop after an episode of severe bacterial cholangitis. Also it was suggested that it can result from insult to the biliary tree by obstructive cholangitis secondary to choledocholithiasis, surgical damage, trauma, vascular insults, parasites, or congenital fibrocystic disorders. Additional causes of secondary SC are toxic, due to chemical agents or drugs.

The prognosis for people with ALD depends on the liver histology as well as cofactors, such as concomitant chronic viral hepatitis. Among patients with alcoholic hepatitis, progression to liver cirrhosis occurs at 10–20% per year, and 70% will eventually develop cirrhosis. Despite cessation of alcohol use, only 10% will have normalization of histology and serum liver enzyme levels. As previously noted, the MDF has been used to predict short-term mortality (i.e., MDF ≥ 32 associated with spontaneous survival of 50–65% without corticosteroid therapy, and MDF 11) and 90-day (MELD > 21) mortality. Liver cirrhosis develops in 6–14% of those who consume more than 60–80 g of alcohol daily for men and more than 20 g daily for women. Even in those who drink more than 120 g daily, only 13.5% will suffer serious alcohol-related liver injury. Nevertheless, alcohol-related mortality was the third leading cause of death in 2003 in the United States. Worldwide mortality is estimated to be 150,000 per year.

Fat emboli occur in almost 90% of all people with severe injuries to bones, although only 10% of these are symptomatic. The risk of fat embolism syndrome is thought to be reduced by early immobilization of fractures and especially by early operative correction. There is also some evidence that steroid prophylaxis of high-risk individuals reduces the incidence. The mortality rate of fat-embolism syndrome is approximately 10–20%.

Fat emboli can be either traumatic (resulting from fracture of long bones, accidents, or trauma to soft tissue) or non-traumatic (resulting from burns or fatty liver).

A fat embolism (which via major trauma may progress to fat embolism syndrome) is a type of embolism in which the embolus consists of fatty material. They are often caused by physical trauma such as fracture of soft tissue trauma, and burns.Fat embolism syndrome is distinct from the presence of fat emboli, symptoms usually occur 1–3 days after a traumatic injury and are predominantly pulmonary (shortness of breath, hypoxemia), neurological (agitation, delirium, or coma), dermatological (petechial rash), and haematological (anaemia, low platelets). The syndrome manifests more frequently in closed fractures of the pelvis or long bones.

In most cases, liver function will return to normal if the offending drug is stopped early. Additionally, the patient may require supportive treatment. In acetaminophen toxicity, however, the initial insult can be fatal. Fulminant hepatic failure from drug-induced hepatotoxicity may require liver transplantation. In the past, glucocorticoids in allergic features and ursodeoxycholic acid in cholestatic cases had been used, but there is no good evidence to support their effectiveness.

An elevation in serum bilirubin level of more than 2 times ULN with associated transaminase rise is an ominous sign. This indicates severe hepatotoxicity and is likely to lead to mortality in 10% to 15% of patients, especially if the offending drug is not stopped (Hy's Law). This is because it requires significant damage to the liver to impair bilirubin excretion, hence minor impairment (in the absence of biliary obstruction or Gilbert syndrome) would not lead to jaundice. Other poor predictors of outcome are old age, female sex, high AST.

While needlestick injuries have the potential to transmit bacteria, protozoa, viruses and prions, the risk of contracting hepatitis B, hepatitis C, and HIV is the highest. The World Health Organization estimated that in 2000, 66,000 hepatitis B, 16,000 hepatitis C, and 1,000 HIV infections were caused by needlestick injuries. In places with higher rates of blood-borne diseases in the general population, healthcare workers are more susceptible to contracting these diseases from a needlestick injury.

Hepatitis B carries the greatest risk of transmission, with 10% of exposed workers eventually showing seroconversion and 10% having symptoms. Higher rates of hepatitis B vaccination among the general public and healthcare workers have reduced the risk of transmission; non-healthcare workers still have a lower HBV vaccine rate and therefore a higher risk. The hepatitis C transmission rate has been reported at 1.8%, but newer, larger surveys have shown only a 0.5% transmission rate. The overall risk of HIV infection after percutaneous exposure to HIV-infected material in the health care setting is 0.3%. Individualized risk of blood-borne infection from a used biomedical sharp is further dependent upon additional factors. Injuries with a hollow-bore needle, deep penetration, visible blood on the needle, a needle located in a deep artery or vein, or a biomedical device contaminated with blood from a terminally ill patient increase the risk for contracting a blood-borne infection.

After a needlestick injury, certain procedures must be followed to minimize the risk of infection. Lab tests of the recipient should be obtained for baseline studies, including HIV, acute hepatitis panel (HAV IgM, HBsAg, HB core IgM, HCV) and for immunized individuals, HB surface antibody. Unless already known, the infectious status of the source needs to be determined. Unless the source is known to be negative for HBV, HCV, and HIV, post-exposure prophylaxis (PEP) should be initiated, ideally within one hour of the injury.

Sequelae can occur in both the mother and the infant after a traumatic birth.

Birth trauma is uncommon in the Western world in relation to rates in the third world. In the West injury occurs in 1.1% of C-sections.

Secondary sclerosing cholangitis (SSC) is a chronic cholestatic liver disease. It is an aggressive and rare disease with complex and multiple causes. It is characterized by inflammation, fibrosis, destruction of the biliary tree and biliary cirrhosis. It can be treated with minor interventions, antibiotics, and monitoring, or with more serious cases, surgery, endoscopic intervention, and liver transplantation.