Although there is no definitive reporting on its incidence, acrocyanosis shows prevalence in children and young adults than in patients thirty years of age or older. Epidemiological data suggests that cold climate, outdoor occupation, and low body mass index are significant risk factors for developing acrocyanosis. As expected, acrocyanosis would be more prevalent in women than in men due to differences in BMI. However, the incidence rate of acrocyanosis often decreases with increasing age, regardless of regional climate. It completely resolves in many women after menopause implying significant hormonal influences.

Acrocyanosis is common initially after delivery in the preterm and full term newborn Intervention normally is not required, although hospitals opt to provide supplemental oxygen for precautionary measures.

Central cyanosis is often due to a circulatory or ventilatory problem that leads to poor blood oxygenation in the lungs. It develops when arterial oxygen saturation drops to ≤85% or ≤75%.

Acute cyanosis can be as a result of asphyxiation or choking, and is one of the definite signs that respiration is being blocked.

Central cyanosis may be due to the following causes:

1. Central nervous system (impairing normal ventilation):

- Intracranial hemorrhage

- Drug overdose (e.g. heroin)

- Tonic–clonic seizure (e.g. grand mal seizure)

2. Respiratory system:

- Pneumonia

- Bronchiolitis

- Bronchospasm (e.g. asthma)

- Pulmonary hypertension

- Pulmonary embolism

- Hypoventilation

- Chronic obstructive pulmonary disease, or COPD (emphysema)

3. Cardiovascular diseases:

- Congenital heart disease (e.g. Tetralogy of Fallot, right to left shunts in heart or great vessels)

- Heart failure

- Valvular heart disease

- Myocardial infarction

4. Blood:

- Methemoglobinemia * Note this causes "spurious" cyanosis, in that, since methemoglobin appears blue, the patient can appear cyanosed even in the presence of a normal arterial oxygen level.

- Polycythaemia

- Congenital cyanosis (HbM Boston) arises from a mutation in the α-codon which results in a change of primary sequence, H → Y. Tyrosine stabilises the Fe(III) form (oxyhaemoglobin) creating a permanent T-state of Hb.

5. Others:

- High altitude, cyanosis may develop in ascents to altitudes >2400 m.

- Hypothermia

- Obstructive sleep apnea

Peripheral cyanosis is the blue tint in fingers or extremities, due to an inadequate or obstructed circulation. The blood reaching the extremities is not oxygen-rich and when viewed through the skin a combination of factors can lead to the appearance of a blue color. All factors contributing to central cyanosis can also cause peripheral symptoms to appear but peripheral cyanosis can be observed in the absence of heart or lung failures. Small blood vessels may be restricted and can be treated by increasing the normal oxygenation level of the blood.

Peripheral cyanosis may be due to the following causes:

- All common causes of central cyanosis

- Reduced cardiac output (e.g. heart failure or hypovolaemia)

- Cold exposure

- Chronic obstructive pulmonary disease (COPD)

- Arterial obstruction (e.g. peripheral vascular disease, Raynaud phenomenon)

- Venous obstruction (e.g. deep vein thrombosis)

The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis.

Hepatic microvascular dysplasia (HMD or MVD) or portal atresia is a disorder where mixing of venous blood and arterial blood in the liver occurs at the microscopic level. It occurs most commonly in certain dog breeds such as the Cairn and Yorkshire terriers although any dog breed may be at risk.

This disease may also be found in cats.

HMD is sometimes misdiagnosed as Portosystemic vascular anomaly (PSVA) or a "Liver Shunt" (portosystemic shunt). HMD can be diagnosed with an MRI, using a tracing dye in the subject's blood, and observing the flow of blood through the subject's liver and surrounding areas (stomach, intestine) for anomalies. It can also be diagnosed using a bile-acid level test; or more accurately, a "fasting-blood ammonia levels" test. Symptoms include stunted growth in the first 6–9 months, vomiting, seizures, and hydro-encephalitic episodes (from ammonia concentrating in the blood). HMD is usually treated non-surgically with antibiotics (metronidazole) and stool-softeners (lactulose).

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%.

Several studies have attempted to predict the survival of patients with Budd–Chiari syndrome. In general, nearly 2/3 of patients with Budd–Chiari are alive at 10 years. Important negative prognostic indicators include ascites, encephalopathy, elevated Child-Pugh scores, elevated prothrombin time, and altered serum levels of various substances (sodium, creatinine, albumin, and bilirubin). Survival is also highly dependent on the underlying cause of the Budd–Chiari syndrome. For example, a patient with an underlying myeloproliferative disorder may progress to acute leukemia, independently of Budd–Chiari syndrome.

In those with cirrhosis, the risk of developing hepatic encephalopathy is 20% per year, and at any time about 30–45% of people with cirrhosis exhibit evidence of overt encephalopathy. The prevalence of minimal hepatic encephalopathy detectable on formal neuropsychological testing is 60–80%; this increases the likelihood of developing overt encephalopathy in the future. Once hepatic encephalopathy has developed, the prognosis is determined largely by other markers of liver failure, such as the levels of albumin (a protein produced by the liver), the prothrombin time (a test of coagulation, which relies on proteins produced in the liver), the presence of ascites and the level of bilirubin (a breakdown product of hemoglobin which is conjugated and excreted by the liver). Together with the severity of encephalopathy, these markers have been incorporated into the Child-Pugh score; this score determines the one- and two-year survival and may assist in a decision to offer liver transplantation.

In acute liver failure, the development of severe encephalopathy strongly predicts short-term mortality, and is almost as important as the nature of the underlying cause of the liver failure in determining the prognosis. Historically, widely used criteria for offering liver transplantation, such as King's College Criteria, are of limited use and recent guidelines discourage excessive reliance on these criteria. The occurrence of hepatic encephalopathy in people with Wilson's disease (hereditary copper accumulation) and mushroom poisoning indicates an urgent need for a liver transplant.

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.

Acute fatty liver of pregnancy is a rare condition and occurs in approximately one in 7,000 to one in 15,000 pregnancies. The mortality from acute fatty liver of pregnancy has been reduced significantly to 18%, and is now related primarily to complications, particularly DIC (Disseminated Intravascular Coagulation) and infections. After delivery, most mothers do well, as the stimulus for fatty acid overload is removed. The disease can recur in future pregnancies, with a calculated genetic chance of 25%; the actual rate is lower, however. Mortality of the foetus has also diminished significantly, but still remains 23%, and may be related to the need for premature delivery.

The risk may be reduced by administering a non-particulate antacid (e.g. Sodium Citrate) or an H-antagonist like Ranitidine.

Hyperdynamic circulation, with peripheral vasodilatation from low systemic vascular resistance, leads to hypotension. There is a compensatory increase in cardiac output. Adrenal insufficiency has been documented in 60% of ALF cases, and is likely to contribute in haemodynamic compromise. There is also abnormal oxygen transport and utilization. Although delivery of oxygen to the tissues is adequate, there is a decrease in tissue oxygen uptake, resulting in tissue hypoxia and lactic acidosis.

Pulmonary complications occur in up to 50% of patients. Severe lung injury and hypoxemia result in high mortality. Most cases of severe lung injury are due to ARDS, with or without sepsis. Pulmonary haemorrhage, pleural effusions, atelectasis, and intrapulmonary shunts also contribute to respiratory difficulty.

Historically it is said that a patient is at risk if they have:

- Residual gastric volume of greater than 25ml, with

- pH of less than 2.5

However these are indirect measurements and are not factors that directly influence aspiration risk.

Patients with a high risk should have a rapid sequence induction. High risk is defined as these factors:

1. Non-elective surgical procedure

2. Light anaesthesia/unexpected response to stimulation

3. Acute or chronic, upper or lower GI pathology

4. Obesity

5. Opioid medication

6. Neurological disease, impaired conscious level, or sedation

7. Lithotomy position

8. Difficult intubation/airway

9. Gastrointestinal reflux

10. Hiatal hernia

In a small proportion of cases, the encephalopathy is caused directly by liver failure; this is more likely in acute liver failure. More commonly, especially in chronic liver disease, hepatic encephalopathy is triggered by an additional cause, and identifying these triggers can be important to treat the episode effectively.

Hepatic encephalopathy may also occur after the creation of a transjugular intrahepatic portosystemic shunt (TIPS). This is used in the treatment of refractory ascites, bleeding from oesophageal varices and hepatorenal syndrome. TIPS-related encephalopathy occurs in about 30% of cases, with the risk being higher in those with previous episodes of encephalopathy, higher age, female sex and liver disease due to causes other than alcohol.

Very few risk factors for choanal atresia have been identified. While causes are unknown, both genetic and environmental triggers are suspected. One study suggests that chemicals that act as endocrine disrupters may put an unborn infant at risk. A 2012 epidemiological study looked at atrazine, a commonly used herbicide in the U.S., and found that women who lived in counties in Texas with the highest levels of this chemical being used to treat agricultural crops were 80 times more likely to give birth to infants with choanal atresia or stenosis compared to women who lived in the counties with the lowest levels. Another epidemiological report in 2010 found even higher associations between increased incidents of choanal atresia and exposure to second-hand-smoke, coffee consumption, high maternal zinc and B-12 intake and exposure to anti-infective urinary tract medications.

The cause can be found in more than 80% of patients.

- Primary Budd–Chiari syndrome (75%): thrombosis of the hepatic vein

- Hepatic vein thrombosis is associated with the following in decreasing order of frequency:

2. Polycythemia vera

1. Pregnancy

2. Postpartum state

3. Use of oral contraceptives

4. Paroxysmal nocturnal hemoglobinuria

5. Hepatocellular carcinoma

6. Lupus anticoagulants

- Secondary Budd–Chiari syndrome (25%): compression of the hepatic vein by an outside structure (e.g. a tumor)

Budd–Chiari syndrome is also seen in infections such as tuberculosis, congenital venous webs and occasionally in inferior vena caval stenosis.

Often, the patient is known to have a tendency towards thrombosis, although Budd–Chiari syndrome can also be the first symptom of such a tendency. Examples of genetic tendencies include protein C deficiency, protein S deficiency, the Factor V Leiden mutation, hereditary anti-thrombin deficiency and prothrombin mutation G20210A. An important non-genetic risk factor is the use of estrogen-containing (combined) forms of hormonal contraception. Other risk factors include the antiphospholipid syndrome, aspergillosis, Behçet's disease, dacarbazine, pregnancy, and trauma.

Many patients have Budd–Chiari syndrome as a complication of polycythemia vera (myeloproliferative disease of red blood cells). Patients suffering from paroxysmal nocturnal hemoglobinuria (PNH) appear to be especially at risk for Budd–Chiari syndrome, more than other forms of thrombophilia: up to 39% develop venous thromboses and 12% may acquire Budd-Chiari.

A related condition is veno-occlusive disease, which occurs in recipients of bone marrow transplants as a complication of their medication. Although its mechanism is similar, it is not considered a form of Budd–Chiari syndrome.

Other toxicologic causes of veno-occlusive disease include plant & herbal sources of pyrrolizidine alkaloids such as Borage, Boneset, Coltsfoot, T'u-san-chi, Comfrey, Heliotrope (sunflower seeds), Gordolobo, Germander, and Chaparral.

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.

Untreated, the disease has a mortality rate upwards of 90%. Cats treated in the early stages can have a recovery rate of 80–90%. Left untreated, the cats usually die from severe malnutrition or complications from liver failure. Treatment usually involves aggressive feeding through one of several methods.

Cats can have a feeding tube inserted by a veterinarian so that the owner can feed the cat a liquid diet several times a day. They can also be force-fed through the mouth with a syringe. If the cat stops vomiting and regains its appetite, it can be fed in a food dish normally. The key is aggressive feeding so the body stops converting fat in the liver. The cat liver has a high regeneration rate and the disease will eventually reverse assuming that irreparable damage has not been done to the liver.

The best method to combat feline hepatic lipidosis is prevention and early detection. Obesity increases the chances of onset. In addition, if a cat stops eating for 1–2 days, it should be taken to a vet immediately. The longer the disease goes untreated, the higher the mortality rate.

A portosystemic shunt (PSS), also known as a liver shunt, is a bypass of the liver by the body's circulatory system. It can be either a congenital (present at birth) or acquired condition.

Congenital PSS is a hereditary condition in dogs and cats, its frequency varying depending on the breed. The shunts found mainly in small dog breeds such as Shih Tzus, Tibetan Spaniels, Miniature Schnauzers and Yorkshire Terriers, and in cats such as Persians, British Shorthairs, Himalayans, and mixed breeds are usually extrahepatic (outside the liver), while the shunts found in large dog breeds such as Irish Wolfhounds and Labrador Retrievers tend to be intrahepatic (inside the liver).

Acquired PSS is uncommon and is found in dogs and cats with liver disease such as cirrhosis causing portal hypertension, which is high blood pressure in the portal vein.

The condition is usually congenital, but sporadic cases have also been reported. It may be associated with other congenital defects, commonly with autosomal recessive polycystic kidney disease, the most severe form of PKD. Some suggest that these two conditions are one disorder with different presentation.

"Acute on chronic liver failure" is said to exist when someone with chronic liver disease develops features of liver failure. A number of underlying causes may precipitate this, such as alcohol misuse or infection. People with ACLF can be critically ill and require intensive care treatment, and occasionally a liver transplant. Mortality with treatment is 50%.

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.

Hepatocellular carcinoma is a primary liver cancer that is more common in people with cirrhosis. People with known cirrhosis are often screened intermittently for early signs of this tumor, and screening has been shown to improve outcomes.

Anorexia always precedes liver disease, with the cat refusing to eat enough food for days, or weeks. This may be amplified by frequent vomiting when the cat does choose to eat. A lack of appetite causes the cat to refuse any food, even after it has purged its system of all stomach contents. Severe weight loss proceeds as the liver keeps the cat alive off body fat, causing a yellowing of the skin (jaundice). When the cat runs out of fat to process, severe muscle wasting (cachexia) takes place as the body converts protein into energy. Eventually the body cannot give the brain enough energy to function properly and the cat dies from malnutrition. In addition, an overworked liver can eventually fail causing total system collapse.