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Related Concept Videos

Urea Cycle01:23

Urea Cycle

The urea cycle describes how liver cells convert ammonia to urea. Ammonia is a toxic waste product of protein catabolism. Land animals must convert ammonia into the less toxic urea which can be safely eliminated by the kidneys through urine. Marine animals excrete ammonia directly, and the surrounding water dilutes the ammonia to safe levels.
Titration of a Weak Base with a Strong Acid01:20

Titration of a Weak Base with a Strong Acid

The titration curve of a weak base like ammonia with a strong acid like hydrochloric acid is the mirror image of the titration curve of a weak acid with a strong base.
Using the ICE table and substituting the Kb value, we calculate the initial pH of 50 mL of 0.1 M ammonia to be 11.11. Addition of 25 mL of 0.1 M hydrochloric acid to this solution of ammonia results in a buffer with an equal concentration of ammonia and ammonium ions. The pH of this buffer can be calculated by substituting these...
Pharmacokinetics in Pediatric Patients: Drug Metabolism01:24

Pharmacokinetics in Pediatric Patients: Drug Metabolism

In pediatric care, understanding the nuances of hepatic drug metabolism is crucial, as it significantly differs from that of adults. This divergence is primarily due to the developmental stage of drug-metabolizing enzymes, which affects how medications are processed in the body. In neonates, for instance, the activity of Phase I enzymes—critical for the initial breakdown of drugs—is markedly reduced, functioning at just 20–40% of the levels seen in adults. This reduction poses a challenge in...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Pharmacokinetics in Pediatric Patients: Drug Excretion01:26

Pharmacokinetics in Pediatric Patients: Drug Excretion

In pediatric medicine, understanding the renal function and drug elimination nuances is crucial for administering safe and effective treatments. Newborns, in particular, display markedly slower renal functions than adults, profoundly affecting how drugs are cleared from their bodies. This slower drug clearance requires clinicians to extend the dosing intervals for many medications to prevent drug accumulation and toxicity while ensuring therapeutic efficacy.One key area where these adjustments...
Pharmacokinetics in Pediatric Patients: Overview and Drug Absorption01:23

Pharmacokinetics in Pediatric Patients: Overview and Drug Absorption

Understanding the physiological differences in the pediatric population is crucial for effective pharmacotherapy. Neonates, infants, and children exhibit significant variations in gastric pH, gastric emptying time, intestinal transit time, and biliary function. These variations profoundly affect oral drug absorption, necessitating a nuanced approach to pediatric dosing.Neonates present with a unique physiological profile, having a gastric pH greater than 4 and faster and more irregular gastric...

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Biochemical Measurement of Neonatal Hypoxia
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Published on: August 24, 2011

Threshold for toxicity from hyperammonemia in critically ill children.

Bruno Ozanne1, John Nelson, Jocelyne Cousineau

  • 1CHU Sainte-Justine, Soins Intensifs, 3175 Chemin de la Côte Sainte-Catherine, Montréal (QC), Canada H3T 1C5.

Journal of Hepatology
|June 28, 2011
PubMed
Summary

High ammonia levels (hyperammonemia) in children significantly increase mortality risk, especially in liver failure. A threshold of 200 μmol/L ammonia within 48 hours indicates a critical risk.

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Area of Science:

  • Pediatric critical care
  • Metabolic disorders
  • Toxicology

Background:

  • Hyperammonemia, caused by reduced liver function or urea cycle enzyme deficiency, can lead to severe cerebral edema and herniation.
  • The precise ammonia toxicity threshold and its impact on pediatric mortality remain incompletely understood.

Purpose of the Study:

  • To determine the ammonia toxicity threshold associated with mortality in critically ill children.
  • To identify risk factors for mortality in pediatric hyperammonemia.
  • To compare treatment patterns and outcomes between liver failure and urea cycle defects.

Main Methods:

  • Retrospective observational study of pediatric intensive care unit patients with hyperammonemia (January 2000 - April 2009).
  • Data collected included clinical and laboratory parameters, treatments, and ammonia levels within the first 7 days.
  • Logistic regression analysis was used to estimate the risk of 28-day mortality.

Main Results:

  • Ninety patients were included, primarily with liver failure (63.3%) or urea cycle defects (23.3%).
  • A 28-day mortality rate of 31.1% was observed.
  • Ammonemia ≥200 μmol/L within 48 hours was an independent risk factor for mortality (OR 3.3), with higher risk in liver failure compared to urea cycle defects. Ammonia scavengers were less frequently used in liver failure.

Conclusions:

  • An ammonia threshold of ≥200 μmol/L within 48 hours significantly increases mortality risk in pediatric hyperammonemia, particularly in cases of liver failure.
  • Timely and appropriate use of ammonia scavengers may be crucial, as they were underutilized in liver failure patients despite potential benefits.