Ammonia is a natural byproduct formed in the body, primarily from the breakdown of proteins and other nitrogen-containing compounds. It is generated in various tissues, including the intestines by gut bacteria, and then transported to the liver. The concentration of ammonia in arterial blood, known as arterial ammonia, is a diagnostic marker for evaluating certain health conditions.
Understanding Ammonia and Arterial Measurement
Ammonia is continuously produced in the body, largely from the metabolism of amino acids and the action of urease-producing bacteria in the gut. The liver plays a primary role in detoxifying this ammonia by converting it into urea through the urea cycle. Urea, being less toxic, is then excreted by the kidneys through urine.
Arterial ammonia measurement is considered more accurate than venous ammonia for assessing levels impacting the brain. This is because skeletal muscles can consume ammonia, leading to lower concentrations in venous blood compared to arterial blood. Normal arterial ammonia levels in adults typically range from 20 to 50 micromoles per liter (µmol/L). Even slightly elevated concentrations can be harmful to the central nervous system.
Causes of Elevated Arterial Ammonia
Elevated arterial ammonia, known as hyperammonemia, most commonly results from liver dysfunction, such as cirrhosis or acute liver failure. The liver’s inability to convert ammonia into urea due to impaired function is a primary mechanism for its accumulation, leading to toxic ammonia levels in the bloodstream.
Other causes of hyperammonemia include genetic conditions, specifically urea cycle disorders (UCDs), which involve a defect in the enzymes required for the urea cycle. Severe infections, particularly those affecting the urinary tract, and certain medications like valproic acid, carbamazepine, or some chemotherapy drugs can also contribute to elevated ammonia levels by affecting liver function or ammonia metabolism.
Recognizing Symptoms and Complications
High arterial ammonia levels primarily affect the brain, leading to a range of neurological symptoms. These manifestations, often referred to as hepatic encephalopathy in the context of liver disease, can vary in severity. Early signs might include mild confusion, changes in sleep patterns, and reduced attention span.
As ammonia levels rise, symptoms can progress to lethargy, apathy, personality changes, and a characteristic flapping tremor of the hands known as asterixis. More severe cases can involve marked confusion, disorientation, seizures, and ultimately, coma. The severity of these neurological signs often correlates with the degree and rapidity of the ammonia increase.
Management and Treatment Approaches
Managing elevated arterial ammonia involves addressing the underlying cause and implementing strategies to reduce ammonia levels. For liver dysfunction, treatment focuses on supporting liver function and preventing further damage. Dietary protein restriction can help reduce ammonia production, as protein breakdown is a source of ammonia.
Medications like lactulose are commonly used to decrease ammonia production and absorption in the gut. Lactulose works by acidifying the colon, which traps ammonia ions and promotes their excretion through feces. Rifaximin, a non-absorbable antibiotic, is often added to lactulose therapy; it reduces ammonia-producing bacteria in the intestines. Treatment is individualized and requires careful medical supervision, with monitoring of ammonia levels to guide therapy.