Cyanosis is defined as a bluish discoloration, especially of the skin and mucous membranes, due to excessive concentration of deoxyhemoglobin in the blood caused by deoxygenation.

Cyanosis is divided into two main types: Central (around the core, lips, and tongue) and Peripheral (only the extremities or fingers).

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)

If tissue is not being perfused properly, it may feel cold and appear pale; if severe, hypoxia can result in cyanosis, a blue discoloration of the skin. If hypoxia is very severe, a tissue may eventually become gangrenous.

Extreme pain may also be felt at or around the site.

The symptoms of generalized hypoxia depend on its severity and acceleration of onset.

In the case of altitude sickness, where hypoxia develops gradually, the symptoms include fatigue, numbness / tingling of extremities, nausea, and anoxia. In severe hypoxia, or hypoxia of very rapid onset, ataxia, confusion / disorientation / hallucinations / behavioral change, severe headaches / reduced level of consciousness, papilloedema, breathlessness, pallor, tachycardia, and pulmonary hypertension eventually leading to the late signs cyanosis, slow heart rate / cor pulmonale, and low blood pressure followed by death.

Because hemoglobin is a darker red when it is not bound to oxygen (deoxyhemoglobin), as opposed to the rich red color that it has when bound to oxygen (oxyhemoglobin), when seen through the skin it has an increased tendency to reflect blue light back to the eye. In cases where the oxygen is displaced by another molecule, such as carbon monoxide, the skin may appear 'cherry red' instead of cyanotic. Hypoxia can cause premature birth, and injure the liver, among other deleterious effects.

A living person can look deathly pale. This can happen when circumstances make the blood escape from the surface of the skin, as in deep shock. Also heart failure ("insufficientia cordis") can make the face look grey; the person then also has blue lips. Skin can also look deathly pale as a result of vasoconstriction as part of the body's homeostatic systems in cold conditions, or if the skin is deficient in vitamin D, as seen in people who spend most of the time indoors, away from sunlight.

Pallor mortis results from the cessation of capillary circulation throughout the body. Gravity then causes the blood to sink down into the lower parts of the body, creating livor mortis.

Acrocyanosis is characterized by peripheral cyanosis: persistent cyanosis of the hands or of the hands, feet, or face. The extremities often are cold and clammy and may exhibit some swelling (especially in the warmer weather). The palms and soles exhibit a wide range of sweating from moderately moist to profuse, but all peripheral pulses should have normal rate, rhythm, and quality. Exposure to cold temperatures worsens the cyanosis, while it often improves on warming. Aside from the color changes, patients normally are asymptomatic and therefore there is usually no associated pain. The most common sign, discoloration, usually is what prompts patients to seek medical care.

Acrocyanosis is persistent blue or cyanotic discoloration of the extremities, most commonly occurring in the hands, although it also occurs in the feet and distal parts of face.

The principal (primary) form of acrocyanosis is that of a benign cosmetic condition, sometimes caused by a relatively benign neurohormonal disorder. Regardless of its cause, the benign form typically does not require medical treatment. A medical emergency would ensue if the extremities experience prolonged periods of exposure to the cold, particularly in children and patients with poor general health. However, frostbite differs from acrocyanosis because pain (via thermal nociceptors) often accompanies the former condition, while the latter is very rarely associated with pain. There are also a number of other conditions that affect hands, feet, and parts of the face with associated skin color changes that need to be differentiated from acrocyanosis: Raynaud’s phenomenon, pernio, acrorygosis, erythromelalgia, blue finger syndrome. The diagnosis may be challenging in some cases, especially when these syndromes co-exist.

Acrocyanosis may be a sign of a more serious medical problem, such as connective tissue diseases and diseases associated with central cyanosis. Other causative conditions include infections, toxicities, antiphospholipid syndrome, cryoglobulinemia, neoplasms. In these cases, the observed cutaneous changes are known as "secondary acrocyanosis". They may have a less symmetric distribution and may be associated with pain and tissue loss.

Pallor is a pale color of the skin that can be caused by illness, emotional shock or stress, stimulant use, or anemia, and is the result of a reduced amount of oxyhaemoglobin and is visible in skin conjuctivae or mucous membrane.

Pallor is more evident on the face and palms. It can develop suddenly or gradually, depending on the cause. It is not usually clinically significant unless it is accompanied by a general pallor (pale lips, tongue, palms, mouth and other regions with mucous membranes). It is distinguished from similar presentations such as hypopigmentation (lack or loss of skin pigment) or simply a fair complexion.

Mendelson's syndrome is characterised by a bronchopulmonary reaction following aspiration of gastric contents during general anaesthesia due to abolition of the laryngeal reflexes. The main clinical features are signs of general hypoxia, two to five hours after anaesthesia. Such features may include cyanosis, dyspnea, fever, pulmonary wheeze, crepitant rales, rhonchi, and tachycardia with a low blood pressure. Decreased arterial oxygen tension is also likely to be evident. Pulmonary edema can cause sudden death or death may occur later from pulmonary complications.

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

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

One of the hallmarks of arterial claudication is that it occurs intermittently. It disappears after a very brief rest and the patient can start walking again until the pain recurs.

The following signs are general signs of atherosclerosis of the lower extremity arteries:

- cyanosis

- atrophic changes like loss of hair, shiny skin

- decreased temperature

- decreased pulse

- redness when limb is returned to a "dependent" position (part of Buerger's test)

All the "P"s

- Pallor increase

- Pulses decreased

- Perishing cold

- Pain

- Paraesthesia

- Paralysis

The symptomatic patient may present with dyspnea, cyanosis, chest pain, pulsus paradoxus, bradycardia or tachycardia. On physical examination, the patient may have the classic “Beck’s triad” – hypotension, raised JVP and distant heart sounds, when complicated by cardiac tamponade. Extension of the mediastinal air to the subcutaneous tissues via the fascial planes may lead to subcutaneous emphysema. When air and fluid mix together in the pericardial sac, a tinkling sound superimposed over a succussion splash is heard. This is known as a “Bruit de Moulin”, which is French for “Mill–wheel” murmur. Air between the anterior parietal pericardium and the thoracic cage may also give rise to the “Hamman’s Sign” – which is a crunching sound typically heard on auscultation of the chest, but may sometimes be heard even with the unaided ear.

Symptoms can include:

- pallor

- tachycardia

- decreased activity

Pneumopericardium is a medical condition where air enters the pericardial cavity. This condition has been recognized in preterm neonates, in which it is associated with severe lung pathology, after vigorous resuscitation, or in the presence of assisted ventilation. This is a serious complication, which if untreated may lead to cardiac tamponade and death. Pneumomediastinum, which is the presence of air in the mediastinum, may mimic and also coexist with pneumopericardium.

It can be congenital, or introduced by a wound.

Sulfhemoglobinemia (or sulfhaemoglobinaemia) is a rare condition in which there is excess sulfhemoglobin (SulfHb) in the blood. The pigment is a greenish derivative of hemoglobin which cannot be converted back to normal, functional hemoglobin. It causes cyanosis even at low blood levels.

It is a rare blood condition that occurs when a sulfur atom is incorporated into the hemoglobin molecule. When hydrogen sulfide (HS) (or sulfide ions) and ferric ions combine in the blood, the blood is incapable of carrying oxygen.

The condition generally resolves itself with erythrocyte (red blood cell) turnover, although blood transfusions can be necessary in extreme cases.

Pure red cell aplasia (PRCA) or erythroblastopenia refers to a type of anemia affecting the precursors to red blood cells but not to white blood cells. In PRCA, the bone marrow ceases to produce red blood cells. The condition has been first described by Paul Kaznelson in 1922.

The condition can cause pain within the affected extremities, discoloration (paleness), and sensations of cold and/or numbness. This can often be distressing to those who are undiagnosed, and sometimes it can be obstructive. If someone with Raynaud's is placed into a cold climate, it could potentially become dangerous.

1. When exposed to cold temperatures, the blood supply to the fingers or toes, and in some cases the nose or earlobes, is markedly reduced; the skin turns pale or white (called pallor) and becomes cold and numb.

2. When the oxygen supply is depleted, the skin color turns blue (called cyanosis).

3. These events are episodic, and when the episode subsides or the area is warmed, the blood flow returns, and the skin color first turns red (rubor), and then back to normal, often accompanied by swelling, tingling, and a painful "pins and needles" sensation.

All three color changes are observed in classic Raynaud's. However, not all patients see all of the aforementioned color changes in all episodes, especially in milder cases of the condition. Symptoms are thought to be due to reactive hyperemias of the areas deprived of blood flow.

In pregnancy, this sign normally disappears owing to increased surface blood flow. Raynaud's has also occurred in breastfeeding mothers, causing nipples to turn white and become extremely painful. Nifedipine, a calcium channel blocker and vasodilator, was recommended to increase blood flow to the extremities and noticeably relieved pain in the breast in an extremely small study group.

Since oxygen is carried to tissues in the blood, insufficient blood supply causes tissue to become starved of oxygen. In the highly aerobic tissues of the heart and brain, irreversible damage to tissues can occur in as little as 3–4 minutes at body temperature. The kidneys are also quickly damaged by loss of blood flow (renal ischemia). Tissues with slower metabolic rates may undergo irreversible damage after 20 minutes.

Clinical manifestations of acute limb ischemia (which can be summarized as the "six P's") include pain, pallor, pulseless, paresthesia, paralysis, and poikilothermia.

Without immediate intervention, ischemia may progress quickly to tissue necrosis and gangrene within a few hours. Paralysis is a very late sign of acute arterial ischemia and signals the death of nerves supplying the extremity. Foot drop may occur as a result of nerve damage. Because nerves are extremely sensitive to hypoxia, limb paralysis or ischemic neuropathy may persist after revascularization and may be permanent.

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.

Cardiac ischemia may be asymptomatic or may cause chest pain, known as angina pectoris. It occurs when the heart muscle, or myocardium, receives insufficient blood flow. This most frequently results from atherosclerosis, which is the long-term accumulation of cholesterol-rich plaques in the coronary arteries. Ischemic heart disease is the most common cause of death in most Western countries and a major cause of hospital admissions.

Individuals with TEC have a median age of presentation of 18–26 months; however, the disorder may occur in infants younger than 6 months and in children as old as age 10 years.

Because of the gradual onset of the anemia, children are often healthier than expected from their low hemoglobin levels.

Phlegmasia cerulea dolens (literally: "painful blue edema") is an uncommon severe form of deep venous thrombosis which results from extensive thrombotic occlusion (blockage by a thrombus) of the major and the collateral veins of an extremity. It is characterized by sudden severe pain, swelling, cyanosis and edema of the affected limb. There is a high risk of massive pulmonary embolism, even under anticoagulation. Foot gangrene may also occur. An underlying malignancy is found in 50% of cases. Usually, it occurs in those afflicted by a life-threatening illness.

This phenomenon was discovered by Jonathan Towne, a vascular surgeon in Milwaukee, who was also the first to report the "white clot syndrome" (now called heparin induced thrombocytopenia [HIT]). Two of their HIT patients developed phlegmasia cerulea dolens that went on to become gangrenous.

Treatment by Catheter directed thrombolytic therapy.