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Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find one of our health articles more useful.

Cyanosis is the abnormal blue discoloration of the skin and mucous membranes, caused by an increase in the deoxygenated haemoglobin level to above 5 g/dL. Patients with anaemia do not develop cyanosis until the oxygen saturation (SaO2) has fallen to lower levels than for patients with normal haemoglobin levels and patients with polycythaemia develop cyanosis at higher oxygen saturation levels. Cyanosis can be divided into either central or peripheral1.

Central cyanosis

  • Central cyanosis is caused by diseases of the heart or lungs, or abnormal haemoglobin (methaemoglobinaemia or sulfhaemoglobinaemia).

  • Cyanosis is seen in the tongue and lips and is due to desaturation of central arterial blood resulting from cardiac and respiratory disorders associated with shunting of deoxygenated venous blood into the systemic circulation.

  • Patients who are centrally cyanosed will usually also be peripherally cyanosed.

  • Associated features of central cyanosis depend on the underlying cause and include dyspnoea and tachypnoea, secondary polycythaemia and bluish or purple discolouration of the oral mucous membranes, fingers and toes. The hands and feet are usually normal temperature or warm but not cold unless there is an associated poor peripheral circulation.

Peripheral cyanosis

  • Peripheral cyanosis is caused by decreased local circulation and increased extraction of oxygen in the peripheral tissues.

  • Isolated peripheral cyanosis occurs in conditions associated with peripheral vasoconstriction and stasis of blood in the extremities, leading to increased peripheral oxygen extraction - eg, congestive heart failure, circulatory shock, exposure to cold temperatures and abnormalities of the peripheral circulation.

  • Features of peripheral cyanosis therefore include peripheral vasoconstriction and bluish or purple discolouration of the affected area, which is usually cold. Peripheral cyanosis is most intense in nail beds and may resolve with gentle warming of the extremity. The mucous membranes of the oral cavity are usually spared.

Unless the cause is already established, episodes of central cyanosis require urgent assessment, especially infants and young children, who require urgent admission.

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Differential diagnosis

Central cyanosis in neonates2

Central cyanosis in adults

Causes of peripheral cyanosis

  • All causes of central cyanosis cause peripheral cyanosis.

  • Reduced cardiac output - eg, heart failure, shock.

  • Peripheral arterial disease - eg, thrombosis, atheroma or embolism.

  • Vasoconstriction:

    • Cold exposure.

    • Raynaud's phenomenon.

    • Acrocyanosis: benign, caused by spasm of smaller skin arteries and arterioles, causing hands and feet to be cold and mottled4.

    • Erythrocyanosis: usually affects young women; blotches of cyanosis occur in the lower legs.

    • Beta-blocker drugs.

  • Venous obstruction (eg, lower limb deep vein thrombosis) can occasionally produce a painful blue leg (phlegmasia cerulea dolens). Obstruction of the superior vena cava can cause cyanosis, venous engorgement and oedema affecting the face.



  • Age and nature of onset:

    • Cyanosis due to congenital heart disease causing anatomical right-to-left shunts may have been present since birth or the first few years of life.

    • Acute onset of cyanosis may be due to pulmonary emboli, cardiac failure, pneumonia or asthma.

    • Patients with COPD develop cyanosis over many years and associated polycythaemia may exacerbate the degree of cyanosis.

    • The description may be typical of Raynaud's phenomenon.

  • Past history: cyanosis can result from any lung disease of sufficient severity.

  • Drug history: certain drugs may cause methaemoglobinaemia (eg, nitrates, dapsone) or sulfhaemoglobinaemia (eg, metoclopramide).

  • Associated symptoms:

    • Chest pain: cyanosis associated with pleuritic chest pains may be due to pulmonary emboli or pneumonia. Pulmonary oedema may cause dull, aching chest tightness.

    • Dyspnoea: sudden onset of dyspnoea can occur with pulmonary emboli, pulmonary oedema or asthma.


  • Temperature: pneumonia and pulmonary emboli may be associated with pyrexia.

  • Inspection:

    • Central cyanosis produces a blue discolouration of the mucous membranes of the lips and tongue as well as the extremities.

    • Peripheral cyanosis affects the extremities and the skin around the lips but not the mucous membranes.

    • The combination of clubbing and cyanosis is frequent in congenital heart disease and may also occur in pulmonary disease (lung abscess, bronchiectasis, cystic fibrosis) and pulmonary arteriovenous shunts.

    • The jugular venous pressure is elevated with congestive cardiac failure.

  • Respiratory examination:

    • Poor chest expansion occurs with chronic bronchitis, and asthma. Unilateral reduced chest expansion may occur with lobar pneumonia.

    • Dullness to percussion occurs over an area of consolidation.

    • Localised crepitation may be heard with lobar pneumonia. Crepitation is more widespread with bronchopneumonia and pulmonary oedema. Air entry may be poor with COPD and asthma. Bronchial breathing may be auscultated over an area of consolidation, and wheezing may be heard with asthma.

  • Heart sounds may be abnormal or added heart murmurs may suggest a cardiac origin.

  • Localised features suggesting an aetiology of peripheral cyanosis, such as oedema in venous insufficiency or absent peripheral pulses and ischaemia in arterial occlusion.

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  • Arterial blood gases: oxygen saturation for patients with central cyanosis is usually below 85%. If the oxygen saturation does not increase to above 95% while the patient inhales 100% oxygen then there is likely to be pulmonary intravascular shunting of blood bypassing the alveoli (eg, right-to-left intracardiac shunt or pulmonary arteriovenous fistulae).

  • FBC: haemoglobin level is increased with chronic cyanosis. White cell count is increased in pneumonia and pulmonary embolism.

  • ECG: features of myocardial infarction; nonspecific ST abnormalities with pulmonary emboli.

  • CXR: pneumonia, pulmonary infarction, cardiac failure.

  • Sputum and blood cultures: pneumonia.

  • Ventilation-perfusion scan - 'VQ scan', or pulmonary angiography: pulmonary embolus.

  • Echocardiography: cardiac defects.

  • Haemoglobin spectroscopy: methaemoglobinaemia, sulfhaemoglobinaemia.

  • Digital subtraction angiography: acute arterial occlusion.

  • Duplex Doppler or venography: acute venous occlusion.


  • Oxygen therapy for patients who are hypoxic.

  • Treatment of the underlying cause.

Further reading and references

  • Desai K, Rabinowitz EJ, Epstein S; Physiologic diagnosis of congenital heart disease in cyanotic neonates. Curr Opin Pediatr. 2019 Apr;31(2):274-283. doi: 10.1097/MOP.0000000000000742.
  1. Adeyinka A et al; Cyanosis. In: StatPearls, 2020.
  2. Dani C, Drovandi L, Bertini G, et al; Unexpected episodes of cyanosis in late preterm and term neonates prompted admission to a neonatal care unit. Ital J Pediatr. 2017 Apr 14;43(1):35. doi: 10.1186/s13052-017-0349-9.
  3. Trivedi DJ, Joshiraj B, Bidkar V, et al; Methemoglobinemia: Living with Dormant Devil. Indian J Clin Biochem. 2017 Jun;32(2):248-250. doi: 10.1007/s12291-016-0586-5. Epub 2016 Jun 13.
  4. Das S, Maiti A; Acrocyanosis: an overview. Indian J Dermatol. 2013 Nov;58(6):417-20. doi: 10.4103/0019-5154.119946.

Article history

The information on this page is written and peer reviewed by qualified clinicians.

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