Ammonia arises during the deamination of proteins in the gut mainly renal and secondarily muscles.
It is immediately incorporated into glutamine, which provides transport to the liver. In the liver, glutamine is converted to urea (Krebs urea cycle).
The blood pH, the ammonia is 98% ionized form NH4 + and 2% as NH3.
• In a patient monitoring to hepatitis or cirrhosis, before the onset of headache, confusion or altered consciousness.
• In a newborn to lethargy, refusal to suck.
Collect blood, arterial or venous, EDTA, avoiding hemolysis.
Immediately send the sample to the laboratory on ice. The assay should be performed in the half-hour.
Avoid contact with tobacco smoke contains significant amounts of NH4 +.
• Venous blood:
– In children and adults: 0.3 to 0.9 mg / L (30 to 50 mmol / L)
– In the newborn: 1 to 1.5 mg / L (60 to 100 mmol / L)
• The values obtained on arterial or capillary blood are higher than those obtained with the venous blood (25%).
mg × 58 7 = ĩmol
ĩmol × 0.017 = mg
Hepatocellular deficiencies and portal hypertension:
The hyperammonemia is primarily due to large hepatocellular shortcomings of end-stage cirrhosis or severe hepatitis, viral or toxic.
The second cause is the existence of portacaval anastomoses, as is the case in portal hypertension.
When there is a gastrointestinal hemorrhage, blood proteins present in the gut are transformed into ammonia by the bacterial flora. Ammonia passes directly into the systemic circulation in favor of bypassing portacaval anastomoses liver and putting out of state to take the ammonia in the portal vein to detoxify. The hyperammonemia, which can be very high (200 to 300 mol / L), resulting in a hepatic encephalopathy, as ammonia is toxic to the brain.
Infants and children:
In the newborn, hyperammonemia results from a genetic deficiency in one of the six enzymes of the urea cycle, the most common (1 in 100 000 births) is the deficit ornithine transcarbamylase (OTC), which is revealed in the boy with a very serious neonatal hyperammonaemic coma, often fatal.