Causes include

- Acute pancreatitis, whereby methemalbumin formed from digested blood tracks subcutaneously around the abdomen from the inflamed pancreas.

- Pancreatic hemorrhage

- Retroperitoneal hemorrhage

- Blunt abdominal trauma

- Ruptured / hemorrhagic ectopic pregnancy.

- Spontaneous bleeding secondary to coagulopathy (congenital or acquired)

- Aortic rupture, from ruptured abdominal aortic aneurysm or other causes.

Grey Turner's sign refers to bruising of the s, the part of the body between the last rib and the top of the hip. The bruising appears as a blue discoloration, and is a sign of retroperitoneal hemorrhage, or bleeding behind the peritoneum, which is a lining of the abdominal cavity. Grey Turner's sign takes 24–48 hours to develop, and can predict a severe attack of acute pancreatitis.

Grey Turner's sign may be accompanied by Cullen's sign. Both signs may be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding. Grey Turner's sign is named after British surgeon George Grey Turner.

Causes include:

- acute pancreatitis, where methemalbumin formed from digested blood tracks around the abdomen from the inflamed pancreas

- bleeding from blunt abdominal trauma

- bleeding from aortic rupture

- bleeding from ruptured ectopic pregnancy

Importance of the sign is on a decline since better diagnostic modalities are now available.

Cullen's sign is superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus.

It is named for gynecologist Thomas Stephen Cullen (1869–1953), who first described the sign in ruptured ectopic pregnancy in 1916.

This sign takes 24–48 hours to appear and can predict acute pancreatitis, with mortality rising from 8–10% to 40%. It may be accompanied by Grey Turner's sign (bruising of the flank), which may then be indicative of pancreatic necrosis with retroperitoneal or intraabdominal bleeding.

Gray baby syndrome (also termed Gray or Grey syndrome) is a rare but serious side effect that occurs in newborn infants (especially premature babies) following the accumulation of antibiotic chloramphenicol.

The exact causes of the degenerative process remain unclear. There are, however, some hypotheses and well-defined risk factors.

- Tobacco smoking: More than 90% of people who develop an AAA have smoked at some point in their lives.

- Alcohol and hypertension: The inflammation caused by prolonged use of alcohol and hypertensive effects from abdominal edema which leads to hemorrhoids, esophageal varices, and other conditions, is also considered a long-term cause of AAA.

- Genetic influences: The influence of genetic factors is high. AAA is four to six times more common in male siblings of known patients, with a risk of 20-30%. The high familial prevalence rate is most notable in male individuals. There are many hypotheses about the exact genetic disorder that could cause higher incidence of AAA among male members of the affected families. Some presumed that the influence of alpha 1-antitrypsin deficiency could be crucial, while other experimental works favored the hypothesis of X-linked mutation, which would explain the lower incidence in heterozygous females. Other hypotheses of genetic causes have also been formulated. Connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA. Both relapsing polychondritis and pseudoxanthoma elasticum may cause abdominal aortic aneurysm.

- Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA frequently carry an atherosclerotic burden. However, this hypothesis cannot be used to explain the initial defect and the development of occlusion, which is observed in the process.

- Other causes of the development of AAA include: infection, trauma, arteritis, and cystic medial necrosis.

A baby with a prenatally diagnosed cystic hygroma should be delivered in a major medical center equipped to deal with neonatal complications, such as a neonatal intensive care unit. An obstetrician usually decides the method of delivery. If the cystic hygroma is large, a cesarean section may be performed. After birth, infants with a persistent cystic hygroma must be monitored for airway obstruction. A thin needle may be used to reduce the volume of the cystic hygroma to prevent facial deformities and airway obstruction. Close observation of the baby by a neonatologist after birth is recommended. If resolution of the cystic hygroma does not occur before birth, a pediatric surgeon should be consulted.

Cystic hygromas that develop in the third trimester, after thirty weeks gestation, or in the postnatal period are usually not associated with chromosome abnormalities. There is a chance of recurrence after surgical removal of the cystic hygroma. The chance of recurrence depends on the extent of the cystic hygroma and whether its wall was able to be completely removed.

Treatments for removal of cystic hygroma are surgery or sclerosing agents which include:

- Bleomycin

- Doxycycline

- Ethanol (pure)

- Picibanil (OK-432)

- Sodium tetradecyl sulfate

Two pathophysiologic mechanisms are thought to play a role in the development of gray baby syndrome after exposure to the anti-microbial drug chloramphenicol. This condition is due to a lack of glucuronidation reactions occurring in the baby, thus leading to an accumulation of toxic chloramphenicol metabolites. :

1. The UDP-glucuronyl transferase enzyme system of infants, especially premature infants, is immature and incapable of metabolizing the excessive drug load.

2. Insufficient renal excretion of the unconjugated drug.

Due to these two reasons the chloramphenicol level in blood is increased, at higher concentration chloramphenicol blocks electron transport in the liver, myocardium, and skeletal muscles, resulting the above symptoms.

Pyaemia (or pyemia) is a type of septicaemia that leads to widespread abscesses of a metastatic nature. It is usually caused by the staphylococcus bacteria by pus-forming organisms in the blood. Apart from the distinctive abscesses, pyaemia exhibits the same symptoms as other forms of septicaemia. It was almost universally fatal before the introduction of antibiotics.

Sir William Osler included a three-page discussion of pyaemia in his textbook "The Principles and Practice of Medicine", published in 1892. He defined pyaemia as follows:

Earlier still, Ignaz Semmelweis – who would later die of the disease – included a section titled "Childbed fever is a variety of pyaemia" in his treatise, "The Etiology of Childbed Fever" (1861). Jane Grey Swisshelm, in her autobiography titled "Half a Century", describes the treatment of pyaemia in 1862 during the American Civil War.

A cystic hygroma, also known as cystic lymphangioma and macrocystic lymphatic malformation, is an often congenital multiloculated lymphatic lesion that can arise anywhere, but is classically found in the left posterior triangle of the neck and armpits. This is the most common form of lymphangioma. It contains large cyst-like cavities containing lymph, a watery fluid that circulates throughout the lymphatic system. Microscopically, cystic hygroma consists of multiple locules filled with lymph. In the depth, the locules are quite big but they decrease in size towards the surface.

Cystic hygromas are benign, but can be disfiguring. It is a condition which usually affects children; very rarely it can present in adulthood.

Cystic hygroma is also known as lymphatic malformation. Currently, the medical field prefers to use the term lymphatic malformation because the term cystic hygroma means water tumor. Lymphatic malformation is more commonly used now because it is a sponge-like collection of abnormal growth that contains clear lymphatic fluid. The fluid collects within the cysts or channels, usually in the soft tissue. Cystic hygromas occur when the lymphatic vessels that make up the lymphatic system are not formed properly. There are two types of lymphatic malformations. They are macrocystic lymphatic malformations, large cysts, and microcystic, small cysts. A person may have only one kind of the malformation or can have a mixture of both macro and micro cysts.

Cystic hygroma can be associated with a nuchal lymphangioma or a fetal hydrops. Additionally, it can be associated with Turner syndrome or with Noonan syndrome.

A lethal version of this condition is known as Cowchock Wapner Kurtz syndrome that, in addition to cystic hygroma, includes cleft palate and lymphedema, a condition of localized edema and tissue swelling caused by a compromised lymphatic system.

Blue toe syndrome is a situation that may reflect atherothrombotic microembolism, causing transient focal ischaemia, occasionally with minor apparent tissue loss, but without diffuse forefoot ischemia. The development of blue or violaceous toes can also occur with trauma, cold-induced injury, disorders producing generalized cyanosis, decreased arterial flow, impaired venous outflow, and abnormal circulating blood.

The terms "blue toe syndrome", "grey toe syndrome" and "purple toe syndrome" are sometimes used interchangeably.

Studies may include echocardiography, thoracic and abdominal CT or MRI, peripheral arterial run off imaging studies, hypercoagulopathy labs, and interrogation of syndromes that lead to peripheral vascular pathology.

A callosity is another name for callus, a piece of skin that has become thickened as a result of repeated contact and friction.

The disease is characterized by intermittent high temperature with recurrent chills; metastatic processes in various parts of the body, especially in the lungs; septic pneumonia; empyema. It may be fatal.

Clinical sign and symptoms can be differ according to system it involves.

Abdominal aortic aneurysm (AAA or triple A) is a localized enlargement of the abdominal aorta such that the diameter is greater than 3 cm or more than 50% larger than normal diameter. They usually cause no symptoms except when ruptured. Occasionally, abdominal, back, or leg pain may occur. Large aneurysms can sometimes be felt by pushing on the abdomen. Rupture may result in pain in the abdomen or back, low blood pressure, or loss of consciousness, and often results in death.

AAAs occur most commonly in those over 50 years old, in men, and among those with a family history. Additional risk factors include smoking, high blood pressure, and other heart or blood vessel diseases. Genetic conditions with an increased risk include Marfan syndrome and Ehlers-Danlos syndrome. AAAs are the most common form of aortic aneurysm. About 85% occur below the kidneys with the rest either at the level of or above the kidneys. In the United States, screening with ultrasound is recommended for males between 65 and 75 years of age with a history of smoking. In the United Kingdom, screening all men over 65 is recommended. Once an aneurysm is found, further ultrasounds are typically done on a regular basis.

Not smoking is the single best way to prevent the disease. Other methods of prevention include treating high blood pressure, treating high blood cholesterol and not being overweight. Surgery is usually recommended when an AAA's diameter grows to >5.5 cm in males and >5.0 cm in females. Other reasons for repair include the presence of symptoms and a rapid increase in size (more than one centimeter per year). Repair may be either by open surgery or endovascular aneurysm repair (EVAR). As compared to open surgery, EVAR has a lower risk of death in the short term and a shorter hospital stay, but may not always be an option. There does not appear to be a difference in longer term outcomes between the two. With EVAR there is a higher need for repeat procedures.

AAAs affect between 2 and 8% of males over the age of 65. Rates among women are one-fourth as high. In those with an aneurysm less than 5.5 cm the risk of rupture in the next year is less than 1%. Among those with an aneurysm between 5.5 and 7 cm, the risk is about 10%, while for those with an aneurysm greater than 7 cm the risk is about 33%. Mortality if ruptured is 85% to 90%. During 2013, aortic aneurysms resulted in 168,200 deaths, up from 100,000 in 1990. In the United States AAAs resulted in between 10,000 and 18,000 deaths in 2009.

There has been no general recommendation for treatment of patients with Giant Platelet Disorders, as there are many different specific classifications to further categorize this disorder which each need differing treatments. Platelet transfusion is the main treatment for people presenting with bleeding symptoms. There have been experiments with DDAVP (1-deamino-8-arginine vasopressin) and splenectomy on people with Giant platelet disorders with mixed results, making this type of treatment contentious.

Symptoms usually present from the period of birth to early childhood as: nose bleeds, bruising, and/or gum bleeding. Problems later in life may arise from anything that can cause internal bleeding such as: stomach ulcers, surgery, trauma, or menstruation. Abnormality of the abdomen, Epistaxis, Menorrhagia, Purpura, Thrombocytopenia, and prolonged bleeding time have also been listed as symptoms of various Giant Platelet Disorders.

When occurring on an animal's buttocks, as with baboons, they are specifically called ischial callosities. Ischial relates to the ischium: it forms the lower and back part of the hip bone.

The pads enable the monkeys to sleep sitting upright on thin branches, beyond reach of predators, without falling.

The ischial callosities are one of the most distinctive pelvic features which separates Old World monkeys from New World monkeys.

A 2007 study followed 112 individuals for a mean of 12 years (mean age 25.3, range 12–71). No patient died during follow-up, but several required medical interventions. The mean final heights were 167 and 153 cm for men and women, respectively, which is approximately 2 standard deviations below normal.

It results from cholesterol deposits in or hyalinosis of the corneal stroma, and may be associated with ocular defects or with familial hyperlipidemia. It is common in the apparently healthy middle aged and elderly; a prospective cohort study of 12,745 Danes followed up for a mean of 22 years found that it had no clinical value as a predictor of cardiovascular disease.

It can be a sign of disturbance in lipid metabolism, an indicator of conditions such as hypercholesterolemia, hyperlipoproteinemia or hyperlipidemia.

Unilateral arcus is a sign of decreased blood flow to the unaffected eye, due to carotid artery disease or ocular hypotony.

People over the age of 60 may present with a ring-shaped, grayish-white deposit of phospholipid and cholesterol near the peripheral edge of the cornea.

Younger people with the same abnormality at the edge of the cornea would be termed arcus juvenilis.

Since cerebral swelling presents a danger to the patient, treatment of cerebral contusion aims to prevent swelling. Measures to avoid swelling include prevention of hypotension (low blood pressure), hyponatremia (insufficient sodium), and hypercapnia (increased carbon dioxide in the blood). Due to the danger of increased intracranial pressure, surgery may be necessary to reduce it. People with cerebral contusion may require intensive care and close monitoring.

In some cases, the defect is linked to mutations of the EMX2, SIX3, and Collagen, type IV, alpha 1 genes. Because having a sibling with schizencephaly has been statistically shown to increase risk of the disorder, it is possible that there is a heritable genetic component to the disease.

Locoregional complications include pancreatic pseudocyst (Most common, occurring in up to 25% of all cases) and phlegmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis, pancreatic ascites, pleural effusion, sterile/infected pancreatic necrosis.

In the United States, the annual incidence is 18 cases of acute pancreatitis per 100,000 population, and it accounts for 220,000 hospitalizations in the US. In a European cross-sectional study, incidence of acute pancreatitis increased from 12.4 to 15.9 per 100,000 annually from 1985 to 1995; however, mortality remained stable as a result of better outcomes. Another study showed a lower incidence of 9.8 per 100,000 but a similar worsening trend (increasing from 4.9 in 1963-74) over time.

In Western countries, the most common cause is alcohol, accounting for 65 percent of acute pancreatitis cases in the US, 20 percent of cases in Sweden, and 5 percent of those in the United Kingdom. In Eastern countries, gallstones are the most common cause of acute pancreatitis. The causes of acute pancreatitis also varies across age groups, with trauma and systemic disease (such as infection) being more common in children. Mumps is a more common cause in adolescents and young adults than in other age groups.

It is also called "arcus adiposus", "arcus juvenilis" (when it occurs in younger individuals), "arcus lipoides corneae" or "arcus cornealis"; sometimes a "gerontoxon".

Recurrence in siblings and apparent transmission from parent to child has long suggested a genetic defect with autosomal dominant inheritance and variable expression. Mutations in the Ras/mitogen activated protein kinase signaling pathways are known to be responsible for ~70% of NS cases.

A person with NS has up to a 50% chance of transmitting it to their offspring. The fact that an affected parent is not always identified for children with NS suggests several possibilities:

1. Manifestations could be so subtle as to go unrecognized (variable expressivity)

2. NS is heterogeneous, comprising more than one similar condition of differing causes, and some of these may not be inherited.

3. A high proportion of cases may represent new, sporadic mutations.

Heterozygous mutations in "NRAS", "HRAS", "BRAF", "SHOC2", "MAP2K1", "MAP2K2", and "CBL" have also been associated with a smaller percentage of NS and related phenotypes.

A condition known as "neurofibromatosis-Noonan syndrome" is associated with neurofibromin.