Symptom Finder - Acidosis
ACIDOSIS (DECREASED pH)
Developing a list of possible causes of acidosis is also best approached by using the physiologic model of production, transport, excretion, or degradation.
Production: Acids are produced as the end products of metabolism; thus, sugar is broken down to water and carbon dioxide (CO2) (carbolic acid), fats are broken down to keto acids, and protein is broken down to sulfur-containing amino acids. In pathophysiologic states, there may be increased production of these acids. This should call to mind diabetic acidosis, lactic acidosis, and starvation as diagnostic possibilities when one is faced with a patient within acidosis.
Transport: If there is inadequate transport of acid to the kidney for excretion (as occurs in various forms of shock [prerenal azotemia]), acidosis may develop.
Excretion: Finally, these acids must be excreted by the lungs and the kidney. Thus, CO2 retention occurs in pulmonary emphysema leading to pulmonary acidosis, while retention of sulfates and phosphates occurs in uremia causing uremic acidosis. Primary diseases of the kidney that may cause uremia acidosis are glomerulonephritis, collagen disease, toxic nephritis from various drugs, and end-stage renal disease from a host of causes. Chronic obstructive uropathy from renal stones, bladder neck obstruction, and congenital anomalies may also lead to uremic acidosis. Acidosis is also produced by a decrease in production of bicarbonate by the kidney or an increased excretion of bicarbonate in the intestinal tract. Consequently, one must add to the differential list renal tubular acidosis and Fanconi syndrome, which are associated with decreased production of bicarbonate while not producing uremia at the same time. In addition, diarrhea of many causes must be added to the list because it is associated with increased excretion of bicarbonate.
Finally, the mechanism of regulation of bicarbonate production should bring to mind conditions with acidosis related to decreased production of bicarbonate. In Addison disease, there is little or no aldosterone hormone to induce the kidneys to produce bicarbonate; lack of this hormone leads to acidosis. Drugs such as acetazolamide diuretic also interfere with the kidney’s ability to produce bicarbonate, causing acidosis.
Approach to the Diagnosis
The laboratory will be of greatest assistance in determining the cause of acidosis. An elevated blood sugar and serum acetone level will help diagnose diabetic acidosis. An elevated blood urea nitrogen (BUN) level would point to uremia acidosis. Arterial blood gases may show an increased CO2, isolating pulmonary emphysema as the cause.
Other Useful Tests
1. CBC (shock, septicemia, lactic acidosis)
2. Urinalysis (renal tubular acidosis, uremia)
3. Chemistry panel (diabetes, uremia, Addison disease)
4. Serial electrolytes (diabetic acidosis, renal disease, Addison
disease)
5. Lactic acid (shock, lactic acidosis)
6. Pulmonary function tests (pulmonary emphysema)
7. ECG (CHF)
8. Pulmonology consult
9. Nephrology consult
Developing a list of possible causes of acidosis is also best approached by using the physiologic model of production, transport, excretion, or degradation.
Production: Acids are produced as the end products of metabolism; thus, sugar is broken down to water and carbon dioxide (CO2) (carbolic acid), fats are broken down to keto acids, and protein is broken down to sulfur-containing amino acids. In pathophysiologic states, there may be increased production of these acids. This should call to mind diabetic acidosis, lactic acidosis, and starvation as diagnostic possibilities when one is faced with a patient within acidosis.
Transport: If there is inadequate transport of acid to the kidney for excretion (as occurs in various forms of shock [prerenal azotemia]), acidosis may develop.
Excretion: Finally, these acids must be excreted by the lungs and the kidney. Thus, CO2 retention occurs in pulmonary emphysema leading to pulmonary acidosis, while retention of sulfates and phosphates occurs in uremia causing uremic acidosis. Primary diseases of the kidney that may cause uremia acidosis are glomerulonephritis, collagen disease, toxic nephritis from various drugs, and end-stage renal disease from a host of causes. Chronic obstructive uropathy from renal stones, bladder neck obstruction, and congenital anomalies may also lead to uremic acidosis. Acidosis is also produced by a decrease in production of bicarbonate by the kidney or an increased excretion of bicarbonate in the intestinal tract. Consequently, one must add to the differential list renal tubular acidosis and Fanconi syndrome, which are associated with decreased production of bicarbonate while not producing uremia at the same time. In addition, diarrhea of many causes must be added to the list because it is associated with increased excretion of bicarbonate.
Finally, the mechanism of regulation of bicarbonate production should bring to mind conditions with acidosis related to decreased production of bicarbonate. In Addison disease, there is little or no aldosterone hormone to induce the kidneys to produce bicarbonate; lack of this hormone leads to acidosis. Drugs such as acetazolamide diuretic also interfere with the kidney’s ability to produce bicarbonate, causing acidosis.
Approach to the Diagnosis
The laboratory will be of greatest assistance in determining the cause of acidosis. An elevated blood sugar and serum acetone level will help diagnose diabetic acidosis. An elevated blood urea nitrogen (BUN) level would point to uremia acidosis. Arterial blood gases may show an increased CO2, isolating pulmonary emphysema as the cause.
Other Useful Tests
1. CBC (shock, septicemia, lactic acidosis)
2. Urinalysis (renal tubular acidosis, uremia)
3. Chemistry panel (diabetes, uremia, Addison disease)
4. Serial electrolytes (diabetic acidosis, renal disease, Addison
disease)
5. Lactic acid (shock, lactic acidosis)
6. Pulmonary function tests (pulmonary emphysema)
7. ECG (CHF)
8. Pulmonology consult
9. Nephrology consult
