Cyanosis is the abnormal blue discoloration that occurs in the skin and mucous membrane by an increase in the deoxygenated hemoglobin levels to 5 g/dl. People with anemia do not develop Cyanosis until the oxygen saturation(SO2) has declined to lower levels than for a person with normal hemoglobin levels. People with polycythemia exhibit cyanosis at greater oxygen saturation levels, Cyanosis can be classified as either central or peripheral.
Central cyanosis is triggered by disease of the heart or lungs, or abnormal hemoglobin( methemoglobinemia, or sulfhaemoglobinaemia)
Cyanosis is visible on the lips and tongue due to desaturation of central arterial blood caused by cardio or respiratory disorder linked with shutting off deoxygenated venous blood into the systemic circulation.
People who are centrally cyanosed will usually be peripherally cyanosed as well.
Conditions related to central cyanosis depend on the underlying cause; these may include tachypnoea and dyspnoea, bluish or purple discoloration of the fingers, toes, and oral mucous membranes such as the lips and tongue, and secondary polycythemia. The hands and feet are typically standard temperatures or warm but not cold unless there is poor peripheral circulation.
Peripheral cyanosis is caused by decreased local circulation and enhanced oxygen extraction in the peripheral tissue.
Isolated peripheral cyanosis transpires in conditions associated with peripheral vasoconstriction and stasis of blood in the extremities. Causing an increase in peripheral oxygen extraction – e.g., Circulatory shock, abnormalities of the peripheral circulation, congestive heart failure, and exposure to cold temperatures.
Therefore, peripheral cyanosis features include peripheral vasoconstriction, blush or purple peripheral vasoconstriction, and bluish or purple discoloration of the affected area, which is commonly 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 spread.
Unless the cause is already established, episodes of central cyanosis require urgent attention, especially for infants and young children who need immediate admission.
Central cyanosis in neonates:
- Transient cyanosis after delivery – central cyanosis should clear within a few minutes of the birth. Peripheral cyanosis can clear within a few days. Increased sensitivity of the peripheral flow to cold temperature may persist well into infancy.
- Cardiac and circulatory causes include.
- Fallot’s tetralogy
- Transportation of the great arteries
- Huyplioastic left heart
- Total anomalous pulmonary venous return (consisting of all four pulmonary veins draining into systemic veins or the right atrium, linked with a right to left shunt through an atrial septal defect.
- Atresia or Stenosis of the tricuspid valve or pulmonary valve.
- Precessional fetal circulation ( blood continues to be shunted through the foramen ovale and a patent ductus arterioles)
Respiratory causes include:
- Respiratory distress syndrome
- Obstruction of the upper respiratory tract – an example is the Pierre Robin sequence.
- Pleural effusion
- Birth asphyxia, birth injury, or hemorrhage.
- Pulmonary edema
- Meconium aspiration
- Transient tachypnea or the newborn
There are other causes which include infection, and metabolic abnormalities, such as hypomagnesemia and hypoglycemia, and seizures.
Central cyanosis in adults:
Lung disease and severe respiratory disease, pulmonary edema, pulmonary emboli. Decreased PO2 of high altitude, severe pneumonia, chronic obstructive pulmonary disease (COPD), acute adult respiratory distress syndrome, severe acute asthma,
Right-to-left cardiac shunt. Pulmonary arteriovenous fistulas Eisenmenger’s syndrome, cyanotic congenital heart disease.
Abnormal hemoglobins (do not allow for enough oxygen level uptake)
sulfhaemoglobinaemia is commonly associated with certain drugs, especially sulfoxides
Methaemoglobinaemia – can be genetic or linked with certain drugs. Eg: quinones, sulfonamides, primaquine.
Polycythaemia Rubra Vera or any other cause of polycythemia may present with central cyanosis.
- Raynaud’s phenomenon
- Cold Exposure
- Beta-blocker drugs
- Erythrocytosis typically affects young women, with blotches of cyanosis that occur in the lower legs.
- Acrocyanosis – caused arterioles, and spasms of smaller skin arteries, leading to cold and mottled hands and feet.
- Venous obstruction ( also known as lower limb deep vein thrombosis) can periodically create a painful blue leg known as phlegmasia cerulea dolens). Interference of the superior vena cava can cause venous engorgement, cyanosis, and edema affecting the face.
Age and nature of Cyanosis onset.
Acute onset of cyanosis may be due to pneumonia, pulmonary emboli, asthma, cardiac failure
Cyanosis due to congenital heart disease triggering the anatomical right to left shunts may have been present since the birth of the first few years of life.
Acute onset of cyanosis may be due to pulmonary emboli, cardiac failure, asthma, and pneumonia.
Patients with COPD develop cyanosis over many years, and linked polycythemia may exacerbate the degree of cyanosis.
The description may be typical of Raynaud’s phenomenon
Health History: cyanosis can be caused by varying severity of lung disease.
Drug History: particular drugs may cause methemoglobinemia (e.g., nitrates, dapsone) and sulfhaemoglobinaemia (e.g., metoclopramide).
Dyspnoea – the immediate onset of dyspnoea can occur with pulmonary emboli, edema, or asthma.
Chest pain: cyanosis linked with pleuritic chest pain can be due to pneumonia or pulmonary emboli; pulmonary edema can result in chest tightness with dull achiness
Temperature: pneumonia and pulmonary emboli can result in pyrexia.
Central cyanosis generates a blue discoloration of the mucous membrane of the lips, tongue, and the libs.
Peripheral cyanosis affects the limbs and skin surrounding the lips, not the mucous membrane.
The jugular venous pressure is heightened with congestive cardiac failure
The combination of cyanosis and clubbing is frequent in congenital heart disease and can transpire in pulmonary disease ( cystic fibrosis, bronchiectasis, and lung abscess) and pulmonary arteriovenous shunts
Dulness to recursion occurs over consolidation
last chest caisson with asthma and chronic bronchitis. Unilateral drug chest expansion may take place with lobar pneumonia.
Located crepitation can be heard with lobar pneumonia. Crepitation is more extensive with bronchopneumonia and pulmonary edema. Air entry may be weak 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 irregular, or joined heart murmurs may suggest a cardiac origin.
Localized features imply a set of causes of peripheral cyanoses, such as edema in venous insufficiency or missing peripheral pulses and ischemia in arterial occlusion.