CPT Test code: 82140
|Minimum Volume:||0.5 mL|
|Container:||Lavender-top (EDTA) tube; EDTA is the only acceptable anticoagulant.|
|Special Instructions:||Date and time specimen was drawn must be written on tube of blood and request form.|
|Collection:||Tube must be filled completely and kept tightly stoppered at all times. Mix well. Specimen must be placed on ice immediately. Separate plasma from cells within 15 minutes of collection. Patient should not clench fist. Transfer specimen to a plastic transport tube before freezing. Avoid contamination of samples by ammonia from smoking or traffic in the laboratory or patient’s room, glassware, or water. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.|
|Storage Instructions:||Freeze. Ammonia is stable for several days at -20°C. Caution: Blood ammonia increases rapidly at room temperature.|
|Patient Preparation:||Patient should be fasting 12 to 14 hours to avoid lipemia, which interferes with the test.|
|Causes for Rejection:||Hemolysis which increases plasma ammonia; specimen not received frozen; anticoagulants such as citrate, oxalate, ammonium heparin, or sodium fluoride (may cause spuriously high results); lithium heparin may cause spuriously low results; serum specimen (ammonia values in serum are significantly but variably higher than their corresponding plasma values, as ammonia may be generated during clotting); lipemia.|
|Reference Interval:||Male: 27-102 μg/dL; female: 19-87 μg/dL|
|Use:||Ammonia is elevated in the following conditions: liver disease, urinary tract infection with distention and stasis, Reye syndrome, inborn errors of metabolism including deficiency of enzymes in the urea cycle, HHH syndrome (hyperammonemia-homocitrullinuria, hyperornithinemia), some normal neonates (usually returning to normal in 48 hours), total parenteral nutrition, ureterosigmoidostomy, and sodium valproate therapy. Ammonia determination is indicated in neonates with neurological deterioration, subjects with lethargy and/or emesis not explained, and in patients with possible encephalopathy.
Ammonia measurements are mainly of use in the diagnosis of urea cycle deficiencies (any neonate with unexplained nausea, vomiting, or neurological deterioration appearing after first feeding), and they play an important part in the detection of Reye syndrome.
In Reye syndrome threefold increases in AST, ALT and plasma ammonia are required for diagnosis with/or the diagnostic liver biopsy findings. Ammonia levels increase characteristically early; plasma ammonia ≥100 μg/dL reflects severe hepatic changes. Prothrombin time is increased in essentially all patients, prototypically three seconds longer than the control. Bilirubin is usually normal. Glucose should be monitored; hypoglycemia may develop. Hyperosmolality and acid-base imbalance may develop, lactate may increase, CK may increase and CK-MB may be elevated. Uric acid may increase.1,2 Increased ammonia and prolonged prothrombin time provide indicators of disease progression.3
|Limitations:||The correlation between blood ammonia levels and hepatic coma is poor. Ammonia determinations are not reliable predictors of impending hepatic coma.
Ammonia levels are not always high in all patients with urea cycle disorders. High protein diet may cause increased levels.4 Ammonia levels may also be elevated with gastrointestinal hemorrhage. If portal hypertension develops with cirrhosis, hepatic blood flow is altered, leading to elevated blood ammonia levels.
|Footnotes:||1. Bakerman S, Bakerman P, “Reye Syndrome: Laboratory and Clinical Features,” Lab Management, 1986, 25-8.
2. Meythaler JM, Varma RR, “Reye’s Syndrome in Adults: Diagnostic Considerations,” Arch Intern Med, 1987, 147(1):61-4. PubMed 3800531
3. Heubi JE, Daugherty CC, Partin JS, et al, “Grade 1 Reye’s Syndrome: Outcome and Predictors of Progression to Deeper Coma Grades,” N Engl J Med, 1984, 311(24):1539-42. PubMed 6504082
4. Glasgow AM, “Clinical Application of Blood Ammonia Determinations,” Lab Med, 1981, 12:151-7.