Adult: 10-80 mcg/dL or 6-47 μmol/L (SI units)
Child: 40-80 mcg/dL
Newborn: 90-150 mcg/dL
Ammonia: < 50 mcg/dL paracentesis fluid
Ammonia cerebrospinal fluid (CSF) level: 10-35 mg/dL (5.87-20.5 mmol/L) 
Conditions associated with “high” ammonia levels include the following  :
Hemolytic disease in infants (erythroblastosis fetalis)
Liver disease, cirrhosis
Hepatic coma (not reflective of degree of coma)
Gastrointestinal (GI) hemorrhage
HHH syndrome: hyperornithinemia, hyperammonemia, homocitrullinuria
Transient hyperammonemia of newborn
Certain inborn errors of metabolism of urea (which the exception of argininosuccinic aciduria)
Total parenteral nutrition (TPN)
GI tract infection with distention and stasis
Severe heart failure with congestive hepatomegaly
GI bleeding with mild liver disease
GI obstruction with mild liver disease 
Disseminated Ureaplasma bacteria 
Conditions associated with “low” ammonia levels include the following:
Essential or malignant hypertension
Use of certain antibiotics (eg, neomycin)
Hypothyroidism (rare) 
Other states that can affect ammonia levels include the following:
Excessive tourniquet use to collect blood samples
Cigarette smoking 
Cannabis intake 
Delays in transportation to the laboratory after collection or before completion of analysis 
Drugs that can increase ammonia levels include the following:
Drugs that may cause decreased levels include the following  :
Specifics regarding collection and panels are as follows:
Specimen type: Blood plasma; serum not acceptable, urine ammonia
Container: Vacutainer (chilled heparin tube)
Collection method: Venipuncture
Blood should be brought on ice within 10 minutes to the laboratory for testing.
Panels: Urine analysis
Related test: Liver panel
Ammonia is a compound produced by intestinal bacteria and cells during the digestion of protein. It is transported through the portal vein to the liver, where the ammonia is converted to glutamine that is then metabolized by the kidneys into the final product, urea, which is excreted. If the liver is diseased, the ammonia, instead of being broken down, will build up in the blood. It can pass through the blood-brain barrier, ultimately causing hepatic encephalopathy, a condition that produces mental and neurologic changes that manifest as confusion, disorientation, and sleeplessness. Untreated patients may experience seizures and breathing difficulty and may lapse into a coma. [7, 8, 9, 10]
Hyperammonemia causes hyperbilirubinemia, as it inhibits cell growth, induces apoptosis, and damages the mitochondria of the hepatocytes. This results in reduced energy synthesis, which in turn impacts the expression of enzymes associated with bilirubin metabolism. 
Moreover, hyperammonemia mediates increased skeletal muscle autophagy and may contribute to sarcopenia of cirrhosis. 
The test is used to help determine the cause of changes in behavior and consciousness, to confirm a diagnosis of Reye syndrome or hepatic encephalopathy caused by liver disease, to evaluate a urea cycle defect, or to investigate the cause of coma of unknown origin.
Indications for the test in newborns include the following:
Seizures in the first few days following birth
Indications for the test in children in whom Reye syndrome is suspected include the following:
Seizures following a viral illness
Indications for the test in adults include the following:
An acute change for the worse in patients with liver disease
TPN use (hyperalimentation)
Causes of problems in metabolizing/breaking down ammonia include the following:
Decreased blood flow to the liver
Reye syndrome (increased ammonia and decreased glucose)
Inherited defects in the urea cycle enzyme deficiency
Hemolytic disease of the newborn
Causes of increased ammonia levels in patients with advanced liver disease include the following:
High protein intake
Note: In hepatic encephalopathy, brain levels of ammonia may be much higher than blood ammonia levels.
The test measures the amount of ammonia in the blood. Patients should not smoke before collection of the sample.
Because other waste products can result in changes in mental and neurological performance, the ammonia level may not correlate accurately with the patient’s symptoms.
Hemolysis should be avoided and the specimen should be sent promptly to the laboratory. 
Glucose levels over 500 mg/dL may interfere with the test.
Deska Pagana K, Pagana TJ, Pagana TN. Ammonia. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis, Mo: Elsevier; 2017.
Talaska Fischbach F, Dunning MB III. Manual of Laboratory and Diagnostic Tests. 9th ed. Wolters Kluwer Health/Lippincott Williams & Wilkins; 2015.
Diaz-Fontenla F, Castillo-Pradillo M, Diaz-Gomez A, et al. Refractory hepatic encephalopathy in a patient with hypothyroidism: Another element in ammonia metabolism. World J Gastroenterol. 2017 Jul 28. 23 (28):5246-52. [Medline]. [Full Text].
Abulseoud OA, Zuccoli ML, Zhang L, Barnes A, Huestis MA, Lin DT. The acute effect of cannabis on plasma, liver and brain ammonia dynamics, a translational study. Eur Neuropsychopharmacol. 2017 Jul. 27 (7):679-90. [Medline]. [Full Text].
Hashim IA, Cuthbert JA. Elevated ammonia concentrations: potential for pre-analytical and analytical contributing factors. Clin Biochem. 2014 Nov. 47 (16-17):233-6. [Medline].
Siracusa A, De Blay F, Folletti I, Moscato G, Olivieri M, Quirce S, et al. Asthma and exposure to cleaning products – a European Academy of Allergy and Clinical Immunology task force consensus statement. Allergy. 2013 Oct 16. [Medline].
Jazan E, Mirzaei H. Direct analysis of human breath ammonia using corona discharge ion mobility spectrometry. J Pharm Biomed Anal. 2013 Sep 10. 88C:315-320. [Medline].
Sathyamoorthy S, Chandran K, Ramsburg A. Biodegradation and Cometabolic Modeling of Selected Beta Blockers during Ammonia Oxidation. Environ Sci Technol. 2013 Oct 10. [Medline].
Zhang FY, Tang NH, Wang XQ, Li XJ, Chen YL. Simultaneous recovery of dual pathways for ammonia metabolism do not improve further detoxification of ammonia in HepG2 cells. Hepatobiliary Pancreat Dis Int. 2013 Oct. 12(5):525-32. [Medline].
Wang Q, Wang Y, Yu Z, et al. Ammonia-induced energy disorders interfere with bilirubin metabolism in hepatocytes. Arch Biochem Biophys. 2014 Aug. 555-6:16-22. [Medline].
Qiu J, Tsien C, Thapalaya S, et al. Hyperammonemia-mediated autophagy in skeletal muscle contributes to sarcopenia of cirrhosis. Am J Physiol Endocrinol Metab. 2012 Oct 15. 303 (8):E983-93. [Medline]. [Full Text].
Spinelli JB, Yoon H, Ringel AE, Jeanfavre S, Clish CB, Haigis MC. Metabolic recycling of ammonia via glutamate dehydrogenase supports breast cancer biomass. Science. 2017 Nov 17. 358 (6365):941-6. [Medline]. [Full Text].
Takeuchi Y, Nakayama Y, Fukusaki E, Irino Y. Glutamate production from ammonia via glutamate dehydrogenase 2 activity supports cancer cell proliferation under glutamine depletion. Biochem Biophys Res Commun. 2018 Jan 1. 495 (1):761-7. [Medline].
Noiret L, Baigent S, Jalan R. Arterial ammonia levels in cirrhosis are determined by systemic and hepatic hemodynamics, and organs function: a quantitative modelling study. Liver Int. 2013 Oct 17. [Medline].
Burtis CA, Ashwood ER, Bruns DE. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 5th edition. WB Saunders: Philadelphia, PA; 2012.
PDR: Physicians’ Desk Reference. 2018.
Sridevi Devaraj, PhD, DABCC, FACB Medical Director of Clinical Chemistry and POCT, Texas Children’s Hospital; Professor of Pathology and Immunology, Baylor College of Medicine; Associate Director of Translation, Texas Children’s Microbiome Center
Disclosure: Nothing to disclose.
Sameh Gomaa, MBBS Physician, Al-Tonsy Al-Hadary Family Medicine Unit, Egypt
Sameh Gomaa, MBBS is a member of the following medical societies: Egyptian Medical Syndicate
Disclosure: Nothing to disclose.
Catherine Anastasopoulou, MD, PhD, FACE Associate Professor of Medicine, Sidney Kimmel Medical College of Thomas Jefferson University; Attending Endocrinologist, Department of Medicine, Albert Einstein Medical Center
Catherine Anastasopoulou, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American Society for Bone and Mineral Research, Endocrine Society, Philadelphia Endocrine Society
Disclosure: Nothing to disclose.
Thomas M Wheeler, MD Chairman, Department of Pathology and Immunology, WL Moody, Jr, Professor of Pathology, Professor of Urology, Baylor College of Medicine
Thomas M Wheeler, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Cancer Research, American Medical Association, American Society for Clinical Pathology, American Society of Cytopathology, American Thyroid Association, American Urological Association, College of American Pathologists, United States and Canadian Academy of Pathology, International Society of Urological Pathology, Harris County Medical Society
Disclosure: Received stock from PathXL for medical advisory board. for: PathXL, Inc.
Research & References of Ammonia |A&C Accounting And Tax Services