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, 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.

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.

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.

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.

Toxic levels of chloramphenicol after 2–9 days result in:

- Loss of appetite

- Vomiting

- Ashen gray color of the skin

- Hypotension (low blood pressure)

- Cyanosis (blue discolouration of lips and skin)

- Hypothermia

- Cardiovascular collapse

- Hypotonia

- Abdominal distension

- Irregular respiration

- Increased blood lactate

Cystic hygromas are increasingly diagnosed by prenatal ultrasonography. A common symptom is a neck growth. It may be found at birth, or discovered later in an infant after an upper respiratory tract infection. Cystic hygromas can grow very large and may affect breathing and swallowing. Some symptoms may include a mass or lump in the mouth, neck, cheek, or tongue. It feels like a large fluid-filled sac. In addition, cystic hygromas can be found in other body parts such as the arm, chest, legs, groin, and buttocks. Cystic hygromas are also often seen in Turner's syndrome, although a patient who does not have Turner's syndrome can present with this condition.

The signs and symptoms of a ruptured AAA may include severe pain in the lower back, flank, abdomen or groin. A mass that pulses with the heart beat may also be felt. The bleeding can lead to a hypovolemic shock with low blood pressure and a fast heart rate. This may lead to brief passing out.

The mortality of AAA rupture is as high as 90 percent. 65 to 75 percent of patients die before they arrive at the hospital and up to 90 percent die before they reach the operating room. The bleeding can be or into the abdominal cavity. Rupture can also create a connection between the aorta and intestine or inferior vena cava. Flank ecchymosis (appearance of a bruise) is a sign of retroperitoneal bleeding, and is also called Grey Turner's sign.

Aortic aneurysm rupture may be mistaken for the pain of kidney stones, or muscle related back pain.

The vast majority of aneurysms are asymptomatic. However, as abdominal aortic aneurysms expand, they may become painful and lead to pulsating sensations in the abdomen or pain in the chest, lower back, or scrotum. The risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery. The complications include rupture, peripheral embolization, acute aortic occlusion, and aortocaval (between the aorta and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination, a palpable and pulsatile abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.

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.

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.

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.

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.

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

Giant platelet disorders can be further categorized:

- caused by auto-immune disorders, for example Immune thrombocytopenic purpura (ITP), and characterized by low platelet count, but high MPV (Mean-Platelet Volume).

- Caused by glycoprotein abnormalities: Bernard-Soulier syndrome, Velocardiofacial syndrome

- Caused by calpain defect: Montreal platelet syndrome

- Caused by alpha granules defect: Gray platelet syndrome

- Characterized by abnormal neutrophil inclusions: May-Hegglin anomaly, Sebastian syndrome

- With systemic manifestations: Hereditary macrothrombocytopenia with hearing loss, Epstein syndrome, Fechtner syndrome

- With no specific abnormalities: Mediterranean macrothrombocytopenia

- Harris platelet syndrome

The skin lesions evolve through characteristic stages:

1. blistering (from birth to about four months of age),

2. a wart-like rash (for several months),

3. swirling macular hyperpigmentation (from about six months of age into adulthood), followed by

4. linear hypopigmentation.

Alopecia, hypodontia, abnormal tooth shape, and dystrophic nails are observed. Some patients have retinal vascular abnormalities predisposing to retinal detachment in early childhood. Cognitive delays/mental retardation are occasionally seen.

Discolored skin is caused by excessive deposits of melanin (normal skin pigment).

Most newborns with IP will develop discolored skin within the first two weeks.

The pigmentation involves the trunk and extremities, is slate-grey, blue or brown, and is distributed in irregular marbled or wavy lines.

The discoloration sometimes fades with age.

Neurological problems can include: cerebral atrophy, the formation of small cavities in the central white matter of the brain, and the loss of neurons in the cerebellar cortex.

About 20% of children with IP will have slow motor development, muscle weakness in one or both sides of the body, mental retardation, and seizures.

They are also likely to have visual problems, which can include: crossed eyes, cataracts, and severe visual loss.

Dental problems are common, and include missing or peg-shaped teeth - patients with IP often keep milk teeth into adult life.

Breast anomalies can occur in 1% of patients; anomalies can include hypoplasia and supernumerary nipples.

Skeletal and structural anomalies can occur in approximately 14% of patients, including:

- Somatic asymmetry,

- Hemivertebrae,

- Scoliosis,

- Spina bifida,

- Syndactyly,

- Acheiria (congenital absence of the hands - note: other limbs may be affected),

- Ear anomalies,

- Extra ribs,

- Skull deformities,

- Primary pulmonary hypertension,

- Cardiopulmonary failure

The symptoms of a cerebral contusion (bruising on the brain) depend on the severity of the injury, ranging from minor to severe. Individuals may experience a headache; confusion; sleepiness; dizziness; loss of consciousness; nausea and vomiting; seizures; and difficulty with coordination and movement. They may also have difficulty with memory, vision, speech, hearing, managing emotions, and thinking. Signs depend on the contusion's location in the brain.

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.

Up to ~85% of people with NS have one of the following heart defects:

- Pulmonary valvular stenosis (50–60%)

- Septal defects: atrial (10–25%) or ventricular (5–20%)

- Hypertrophic cardiomyopathy (12–35%)

Noonan syndrome (NS) is a relatively common autosomal dominant congenital disorder and is named after Jacqueline Noonan, a pediatric cardiologist. It is referred to as the male version of Turner's syndrome; however, the genetic causes of Noonan syndrome and Turner syndrome are distinct and both males and females are affected. The principal features include congenital heart defect (typicall pulmonary valve stenosis with dysplastic pulmonary valve also atrial septal defect and hypertrophic cardiomyopathy), short stature, learning problems, pectus excavatum, impaired blood clotting, and a characteristic configuration of facial features including a webbed neck and a flat nose bridge. NS is a RASopathy, and is one of several disorders that are caused by a disruption of RAS-MAPK signaling pathway.

It is believed that between approximately 1 in 1,000 and 1 in 2,500 children worldwide are born with NS. It is one of the most common genetic syndromes associated with congenital heart disease, similar in frequency to Down syndrome. However, the range and severity of features can vary greatly in patients with NS. Therefore, the syndrome is not always identified at an early age.

Incontinentia pigmenti (IP) is a rare genetic disorder that affects the skin, hair, teeth, nails, and central nervous system. It is named from its appearance under a microscope. It is also known as Bloch–Siemens syndrome, Bloch–Sulzberger disease, Bloch–Sulzberger syndrome, melanoblastosis cutis, and nevus pigmentosus systematicus.

It is characterized by skin abnormalities that begin in childhood, usually a blistering rash which heals, followed by the development of harder skin growths. The skin may develop grey or brown patches which fade with time. Other symptoms can include hair loss, dental abnormalities, eye abnormalities that can lead to vision loss, and lined or pitted fingernails and toenails. Associated problems can include delayed development, intellectual disability, seizures, and other neurological problems. There is no specific treatment, individual conditions must be managed by specialists.

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

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.

Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage), malabsorption due to exocrine failure

- Metabolic

- Respiratory

- Renal

- Renal artery or vein thrombosis

- Renal failure

- Circulatory

- Arrhythmias

- Hypovolemia and shock

- myocardial infarct

- Pericardial effusion

- vascular thrombosis

- Gastrointestinal

- Gastrointestinal hemorrhage from stress ulceration;

- gastric varices (secondary to splenic vein thrombosis)

- Gastrointestinal obstruction

- Hepatobiliary

- Jaundice

- Portal vein thrombosis

- Neurologic

- Psychosis or encephalopathy (confusion, delusion and coma)

- Cerebral Embolism

- Blindness (angiopathic retinopathy with hemorrhage)

- Hematologic

- Anemia

- DIC

- Leucocytosis

- Dermatologic

- Painful subcutaneous fat necrosis

- Miscellaneous

- Subcutaneous fat necrosis

- Arthalgia