Cyanosis

Cyanosis: Excerpt from Field Guide to Bedside Diagnosis

Differential Overview

❑ Asthma

❑ Chronic obstructive pulmonary disease

❑ Raynaud phenomenon

❑ Hypoventilation

❑ Pulmonary embolism

❑ Cardiac right-to-left shunt

❑ Pulmonary edema

❑ Low cardiac output/shock

❑ Polycythemia vera

❑ Arterial insufficiency

❑ Intrapulmonary shunts

❑ Tracheal obstruction

❑ Tricuspid insufficiency

❑ Superior vena cava obstruction

❑ Pneumonitis

❑ Methemoglobinemia

❑ Patent ductus arteriosus

❑ Pseudocyanosis

Diagnostic Approach

Central cyanosis is best seen in the nailbeds or mucous membranes in good natural light. Peripheral cyanosis (due to increased capillary oxygen extraction) is seen in exposed areas such as the fingers, earlobes, and the tip of the nose. Massage or heat, which increase blood flow, will abolish peripheral but not central cyanosis.

The minimal amount of deoxyhemoglobin to cause central cyanosis is 2.38 g/dL. This is an absolute amount, so is dependent upon the hemoglobin concentration. For example, at a hemoglobin of 12 g/dL, cyanosis appears at SaO₂ of 80%, while at a hemoglobin of 6 g/dL, cyanosis appears at SaO₂ of 60%.

“Harlequin cyanosis” with one arm pink and the other blue can occur with aortic dissection, embolic arterial occlusion, or patent ductus arteriosis with pulmonary hypertension. Blue fingers and pink toes suggest complete transposition of the great vessels, preductal coarctation with a patent ductus arteriosis, or pulmonary hypertension with reversed flow through a patent ductus.

Clinical Findings

Asthma  Episodic wheezing and a prolonged expiratory time are observed. By the time cyanosis is apparent, there will be marked retractions, a large pulsus paradoxus, and a rapidly failing patient. Acute worsening with a localized wheeze may be caused by an inspissated mucous plug.

Chronic obstructive pulmonary disease  There may be chronic hypoxemia and cor pulmonale in a “blue bloater.” An acute bronchospastic exacerbation can also cause cyanosis.

Raynaud phenomenon  Cold is the usual precipitant. A classic triphasic response begins with sharply demarcated blanching of the extremities, followed by cyanotic (slate-blue) discoloration with a dull aching caused by vascular stasis. With rewarming, the digits become livid purple, then deep red. The radial pulse remains normal throughout.

Hypoventilation  Hypoventilation can occur as a consequence of narcotic overdose, anterior horn cell disease (amyotrophic lateral sclerosis, polio), neuromuscular junction disease (myasthenia gravis, botulism), muscle weakness (muscular dystrophy, fatigue), or kyphoscoliosis.

Pulmonary embolism  The embolism is acute in onset and associated with pleuritic chest pain or hemoptysis. Cyanosis is caused by a combination of ventilation–perfusion mismatches and low cardiac output occurring with major hemodynamic compromise.

Cardiac right-to-left shunt  In adults, shunts occur with congenital or acquired atrial or ventricular septal defects, which are recognized by their prominent murmurs. Cyanosis occurs when more than one-third of the blood is shunted. There is little reduction in cyanosis with oxygen administration.

Pulmonary edema  Labored breathing, moist dependent rales, and a third heart sound are observed. There may be pink-tinged frothy sputum, especially with “flash” pulmonary edema.

Low cardiac output/shock  Cyanosis is caused by excessive oxygen extraction with a prolonged circulatory time and can occur regardless of the shock mechanism. Other signs of low output are present such as hypotension, vasoconstriction with cool skin, oliguria, and confusion.

Polycythemia vera  Ruddy plethora occurs with cyanosis due to slow flow with high viscosity. Heat-induced pruritus is common.

Arterial insufficiency  In severe atherosclerotic vascular disease, the distal pulses are thready or absent and the limb has dusky rubor when dependent and a waxy paleness when elevated.

Intrapulmonary shunts  Cyanosis due to intrapulmonary shunts can occur in cirrhosis and should be suspected when numerous cutaneous telangiectasias exist. With congenital pulmonary arteriovenous malformation, there will also be cutaneous telangiectasias and a continuous murmur over the AVM.

Tracheal obstruction  The patient presents acutely with stridor caused by foreign body aspiration or epiglottitis. The latter produces a severe sore throat out of proportion to pharyngeal findings. Cyanosis develops rapidly.

Tricuspid insufficiency  Advanced tricuspid insufficiency may produce icterocyanosis due to elevated venous pressure.

Superior vena cava obstruction  Facial plethora/cyanosis, swelling, and elevated jugular veins are telltale signs.

Pneumonitis  Alveolar hypoxemia may be caused by infectious (lobar pneumonia or Pneumocystis carinii), inflammatory (sarcoidosis or desquamative interstitial pneumonitis), or allergic (Loeffler) causes. Cyanosis may first appear on exertion. Cough is prominent.

Methemoglobinemia  Deoxyhemoglobin may be converted to methemoglobin by nitrates, sulfonamides, chlorates, aniline dyes, and phenacetin. The skin color is leaden.

Patent ductus arteriosus  Cyanosis and clubbing in the lower but not upper extremities is seen when reversed flow is present, due to severe pulmonary artery hypertension. At this point, the machinery murmur is usually absent.

Pseudocyanosis  Silver causes a blue discoloration in sun-exposed skin. Amiodarone deposits blue lipofuscin in the skin. Polymers of chlorpromazine oxidation give a blue-purple color.

Pictures

Book Source Details

• Book Title: Field Guide to Bedside Diagnosis
• Author(s): David S. Smith
• Year of Publication: 2007
• Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Field Guide to Bedside Diagnosis Authors: David S. Smith Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-78178-165-5

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