Symptom Finder - Clubbing
CLUBBING AND PULMONARY OSTEOARTHROPATHY
Although there have been arguments in the past over whether clubbing and pulmonary osteoarthropathy are just two clinical manifestations of the same thing, I take the position that they are; their differential diagnosis, therefore, will be considered together.
When presented with a case of clubbing, one might simply use anatomy and think of all the major internal organs (except the kidney); one would then be closer to an accurate and reliable differential diagnosis. To be more scientific, apply basic physiology to provide an extensive and organized differential diagnosis. The important basic science, then, is physiology; according to Mauer,1 the principle common denominator is anoxia.. Anoxic anoxia or poor intake of oxygen would suggest the first category of disease, pulmonary; most significant among these are chronic diseases of the lung, including chronic bronchitis and emphysema, empyema, pulmonary tuberculosis, carcinoma of the lung, pneumoconiosis, bronchiectasis, and pulmonary fibrosis.
Acute pneumonia, pneumothorax, and bronchial asthma (where there may be many short episodes of anoxia) do not usually lead to clubbing.In the next group of disorders, the lungs may be normal but a significant amount of blood never reaches the alveoli; I call this shunt anoxia. Here are classified the tetralogy of Fallot and other congenital anomalies of the heart, recurrent pulmonary emboli, cirrhosis of the liver (associated with small pulmonary arteriovenous shunts), and pulmonary hemangiomas. Many conditions associated with anemia may present with clubbing. Thus, anemic anoxia may be a factor in portal cirrhosis, biliary cirrhosis, Banti disease, chronic malaria, and subacute bacterial endocarditis. It may also be a factor in disorders of the gastrointestinal tract, such as regional ileitis, ulcerative colitis, and carcinoma of the colon. Stagnant anoxia is not usually associated with clubbing, but this may be because severe anoxia in CHF and shock are usually transient.
Histotoxic anoxia is Mauer’s another explanation for clubbing in patients without low arterial oxygen saturation. The theory is hindered by chronic inflammatory diseases. This group includes subacute bacterial endocarditis, myxedema, ulcerative colitis, intestinal tuberculosis, and amebic dysentery. Of course, this is a regular occurrence in chronic methemoglobinemia or sulfhemoglobinemia.
Approach to the Diagnosis
The clinical approach to clubbing involves being certain that clubbing is present. A curved fingernail is not good evidence, and the “drumstick” appearance (which makes the finger look like a true club) does not occur until late. Early clubbing is determined by the angle between the nail covered portion and the skin-covered portion of the dorsal surface of the terminal phalanx. Normally this angle is 160 degrees. When the angle becomes 180 degrees and disappears, that is, when the terminal phalanx becomes flat, clubbing exists.
Careful examination for cyanosis and a thorough evaluation of the heart and lungs will determine the cause in most cases. Pulmonary function studies, and arterial blood gases before and after exercise and before and after 100% oxygen, will help confirm the diagnosis in many cases. Of course, lung scans and angiocardiography are frequently necessary. Blood cultures, stool culture and examination, and thorough radiologic studies of the gastrointestinal tract will be necessary in obscure cases.
Other Useful Tests
1. CBC (anemia)
2. Chemistry panel (liver disease)
3. Tuberculin test
4. Chest x-ray (neoplasm, bronchiectasis)
5. Sputum culture and sensitivity (lung abscess)
6. Sputum cytology (carcinoma of the lung)
7. Sputum for acid-fast bacillus (AFB) smear and culture
(tuberculosis)
8. Histoplasmin skin test
9. Coccidioidin skin test
10. Blastomycin skin test
11. Bronchoscopy (neoplasm, bronchiectasis)
12. Lung biopsy (neoplasm, silicosis)
13. Exploratory surgery
CLUBBING AND PULMONARY OSTEOARTHROPATHY
Although there have been arguments in the past over whether clubbing and pulmonary osteoarthropathy are just two clinical manifestations of the same thing, I take the position that they are; their differential diagnosis, therefore, will be considered together.
When presented with a case of clubbing, one might simply use anatomy and think of all the major internal organs (except the kidney); one would then be closer to an accurate and reliable differential diagnosis. To be more scientific, apply basic physiology to provide an extensive and organized differential diagnosis. The important basic science, then, is physiology; according to Mauer,1 the principle common denominator is anoxia.. Anoxic anoxia or poor intake of oxygen would suggest the first category of disease, pulmonary; most significant among these are chronic diseases of the lung, including chronic bronchitis and emphysema, empyema, pulmonary tuberculosis, carcinoma of the lung, pneumoconiosis, bronchiectasis, and pulmonary fibrosis.
Acute pneumonia, pneumothorax, and bronchial asthma (where there may be many short episodes of anoxia) do not usually lead to clubbing.In the next group of disorders, the lungs may be normal but a significant amount of blood never reaches the alveoli; I call this shunt anoxia. Here are classified the tetralogy of Fallot and other congenital anomalies of the heart, recurrent pulmonary emboli, cirrhosis of the liver (associated with small pulmonary arteriovenous shunts), and pulmonary hemangiomas. Many conditions associated with anemia may present with clubbing. Thus, anemic anoxia may be a factor in portal cirrhosis, biliary cirrhosis, Banti disease, chronic malaria, and subacute bacterial endocarditis. It may also be a factor in disorders of the gastrointestinal tract, such as regional ileitis, ulcerative colitis, and carcinoma of the colon. Stagnant anoxia is not usually associated with clubbing, but this may be because severe anoxia in CHF and shock are usually transient.
Histotoxic anoxia is Mauer’s another explanation for clubbing in patients without low arterial oxygen saturation. The theory is hindered by chronic inflammatory diseases. This group includes subacute bacterial endocarditis, myxedema, ulcerative colitis, intestinal tuberculosis, and amebic dysentery. Of course, this is a regular occurrence in chronic methemoglobinemia or sulfhemoglobinemia.
Approach to the Diagnosis
The clinical approach to clubbing involves being certain that clubbing is present. A curved fingernail is not good evidence, and the “drumstick” appearance (which makes the finger look like a true club) does not occur until late. Early clubbing is determined by the angle between the nail covered portion and the skin-covered portion of the dorsal surface of the terminal phalanx. Normally this angle is 160 degrees. When the angle becomes 180 degrees and disappears, that is, when the terminal phalanx becomes flat, clubbing exists.
Careful examination for cyanosis and a thorough evaluation of the heart and lungs will determine the cause in most cases. Pulmonary function studies, and arterial blood gases before and after exercise and before and after 100% oxygen, will help confirm the diagnosis in many cases. Of course, lung scans and angiocardiography are frequently necessary. Blood cultures, stool culture and examination, and thorough radiologic studies of the gastrointestinal tract will be necessary in obscure cases.
Other Useful Tests
1. CBC (anemia)
2. Chemistry panel (liver disease)
3. Tuberculin test
4. Chest x-ray (neoplasm, bronchiectasis)
5. Sputum culture and sensitivity (lung abscess)
6. Sputum cytology (carcinoma of the lung)
7. Sputum for acid-fast bacillus (AFB) smear and culture
(tuberculosis)
8. Histoplasmin skin test
9. Coccidioidin skin test
10. Blastomycin skin test
11. Bronchoscopy (neoplasm, bronchiectasis)
12. Lung biopsy (neoplasm, silicosis)
13. Exploratory surgery
