Cyanosis

Cyanosis: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter

Janis F. Neuman

Cyanosis is a bluish discoloration of the skin and mucous membranes caused by increased amounts of unsaturated hemoglobin in the blood. For cyanosis to appear, 5 g/100 ml of reduced blood hemoglobin is required. An oxygen saturation (o₂ sat) less than 75% or a Pao₂ of 40 mm Hg will result in cyanosis (1). Cyanosis can be considered central or peripheral, based on the underlying abnormality. Central cyanosis includes conditions that lead to arterial desaturation such as decreased inspired oxygen tension, pulmonary disease, and conditions causing right to left shunts (e.g., congenital heart disease and intrapulmonary shunts). Abnormal hemoglobins are also considered central. Peripheral cyanosis is caused by reduced cardiac output, cold exposure, and arterial or venous obstruction.

Approach

When the patient is cyanotic, the objective is to determine the underlying cause and correct it. Oxygen delivery to the tissues depends on an intact respiratory system to provide oxygen for hemoglobin saturation, the concentration of hemoglobin, the cardiac output and regional microvasculature, and an oxyhemoglobin unloading mechanism (2).

 A. Decreased blood oxygenation (central cyanosis) is usually caused by one of the following:

1. Obstruction to the intake of oxygen (epiglottitis and acute laryngotracheobronchitis, asthma, chronic bronchitis or emphysema, and foreign body aspiration).

2. Decreased absorption of oxygen as occurs with an alveolar-capillary block (sarcoid, pulmonary fibrosis, pneumonia, pulmonary edema, or alveolar proteinosis). Ventilation-perfusion defects from emphysema, pneumoconioses, and sarcoid will also decrease o₂ absorption.

3. Decreased perfusion of the lung with blood (shock, septic or cardiogenic; pulmonary embolus; pulmonary vascular shunts from pulmonary hemangioma; or congenital heart disease).

4. Reduced intake of oxygen from an atmosphere with a decreased oxygen concentration.

5. A defective hemoglobin unable to attach to oxygen (methemoglobinemia, sulfhemoglobinemia, carbon monoxide poisoning, and other hemoglobinopathies).

B. Peripheral cyanosis will occur with:

1. Reduced cardiac output from acute myocardial infarction or other causes of pump failure.

2. Local or regional phenomenon from cold exposure, arterial obstruction from embolus or thrombosis, and venous stasis or obstruction.

3. Cold exposure (Raynauds’ phenomenon) (Chapter 7.11).

History

 A. When did the cyanosis appear? Is cyanosis of recent onset or has it been present since birth? A history of “squatting” episodes in childhood and congenital cyanosis suggest congenital heart disease. Chronic cyanosis caused by methemoglobinemia can be congenital or acquired. Other causes of chronic cyanosis include chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, and pulmonary atrioventricular fistula. Acute and subacute cyanosis is caused by acute myocardial infarct, pneumothorax, pulmonary embolus, pneumonia, or upper airway obstruction.

 B. Is the patient symptomatic or asymptomatic? Asymptomatic patients may have methemoglobinemia (congenital or drug-induced), or sulfhemoglobinemia. Exposure to drugs (prescribed and illicit) or environmental factors are important in these patients. Intermittent cyanosis, skin color changes, and pain with cold exposure suggests Raynaud’s phenomenon. Symptomatic patients, especially with chest pain and respiratory distress, are more likely to have a cardiac or pulmonary cause of cyanosis.

 C. Does the patient have known risk factors for cardiac or pulmonary disease, including smoking, hyperlipidemia, asthma, drug abuse (especially methamphetamines), severe obesity (sleep apnea), neuromuscular disease, or autoimmune disease? Does the patient have chest pain or intermittent cyanosis with exercise, suggesting angina? Chest pain can be present with acute pulmonary emboli or pneumothorax. Is there a cough and fever suggesting pneumonia? Has the patient had any occupational or environmental exposures that might cause pulmonary problems?

 D. Other. Is there a family history of abnormal hemoglobins or pulmonary disease? Has the patient suffered an episode of hypotension that could produce adult respiratory distress syndrome (ARDS), such as sepsis or heart failure?

Physical examination

A. Initial assessment. Vital signs are very important: tachycardia suggests cardiac arrhythmia, shock, volume depletion, anemia, or fever (Chapter 7.12). An increased or decreased respiratory rate and use of accessory musculature suggests hypoxia from any cause. Hypotension can signal vascular collapse from myocardial infarction, septic shock, or pulmonary embolus.

 B. Additional physical examination. Stridor suggests upper airway obstruction. Examine the pharynx for evidence of obstruction. If epiglottitis or foreign body is suspected, be prepared to intubate the patient. Check the neck for evidence of jugular venous distention (JVD). Auscultate the chest for rales, suggesting pulmonary edema; wheezing and rhonchi consistent with reactive airway disease; or absence of breath sounds, suggesting pneumonia or pneumothorax. Auscultate the heart for murmurs, arrhythmias, and abnormal heart sounds. Feel the pulses in the extremities to assess for arterial embolus or venous thrombosis, especially if cyanosis is localized to one extremity. Examine the abdomen for evidence of intraabdominal catastrophe or aneurysm. Examine the nails for evidence of clubbing, suggesting chronic pulmonary disease.

Testing

A. Pulse oximetry estimates oxygen saturation, but does not measure it directly. Direct measurements using arterial blood gases (ABGs) are necessary to assess a cyanotic patient. Patients with abnormal hemoglobins will have a normal Pao₂ but a decreased hemoglobin oxygen saturation. Cyanotic patients will have an o₂ sat. less than 75% and a Pao₂ less than 40 mm Hg if they have a normal hemoglobin concentration. A low Pao₂ is caused by respiratory or cardiac problems in most circumstances.

B. A chest radiograph helps assess heart size and lung parenchyma. Infiltrates suggest pneumonia, ARDS, or pulmonary edema. Exclude pneumothorax. Look for evidence of interstitial lung disease. Pleural effusion can represent infection, malignancy, or pulmonary edema (Chapter 8.4).

C. An electrocardiogram may demonstrate acute myocardial infarction, arrhythmia, or pericardial process. P-pulmonale, right ventricular hypertrophy (RVH), and R axis suggest chronic pulmonary disease.

D. Other tests. Ventilation-perfusion scans may demonstrate pulmonary embolus. Pulmonary artery catheterization and pressure measurements help distinguish cardiac from pulmonary causes of cyanosis. Pulmonary function testing can help in the diagnosis of various pulmonary diseases.

Diagnostic assessment

A focused history, physical examination, and diagnostic testing will elucidate the cause of cyanosis in affected patients. Response to supplemental o₂ can also help pinpoint the cause of cyanosis (2). Decreased oxygenation secondary to mild to moderate ·V/Q· mismatches caused by pneumonia, pulmonary embolus, and asthma may be reversible with supplemental oxygen. Severe ·V/Q· mismatch caused by intrapulmonary shunting from severe pulmonary edema or ARDS may be refractory to supplemental o₂. Moderate ·V/Q· mismatch associated with ventilatory failure (COPD) may respond to supplemental o₂, but be aware of increasing co₂ levels. ABGs directly measure Pao₂ and o₂ saturation. Abnormal hemoglobins will also be measured and help guide therapy. Hypoxia with an elevated co₂ suggests COPD or asthma, whereas hypoxia with a normal or decreased co₂ suggests pneumonia, ARDS, pulmonary edema, pulmonary emboli, or interstitial lung disease (1). Once the cause of the cyanosis is determined, the objective is to treat the underlying process. Causes of pseudocyanosis include argyria or bismuth poisoning (slate blue-gray color), hemochromatosis (brownish color), or polycythemia (ruddy red color). For peripheral cyanosis caused by decreased cardiac output, correct the causes of hypovolemia (e.g., dehydration, shock, heart failure from whatever cause). Surgical consultation may be required for acute embolization of an extremity, and anticoagulation for venous thrombosis.

References

1. Khan MG. Cardiac and pulmonary management. Philadelphia: Lee & Febiger, 1993:818–825.

2. Woodley M, Whelan A. Manual of medical therapeutics. Boston: Little, Brown and Company, 1993:179–181.

3. Hurst JW. Medicine for the practicing physician. Boston: Butterworth–Heineman, 1983:973–975.

4. Collins RD. Dynamic differential diagnosis. Philadelphia: JB Lippincott, 1981:
386–388.

Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

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More About This Book: Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter Authors: Robert B. Taylor (editor) Publisher: Lippincott Williams & Wilkins Copyright: 2000 ISBN: 0-78172-094-X

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