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Treatment of severe hyperammonemia (serum ammonia levels greater than 1000 μmol/L) should begin with hemodialysis if it is otherwise medically appropriate and tolerated. [ 12 ] Continuous renal replacement therapy (CRRT) is a remarkably effective mode of therapy in neonatal hyperammonemia, particularly in severe cases of Urea cycle defects ...
Severe Transient Hyperammonemia is diagnosed when ammonia levels are above 50 μM up to as much as 4000 μM. Severe Transient Hyperammonemia causes neurological problems as ammonia levels in the brain are too high, which can cause infant hyptotonia as well as neonatal seizures. [5]
The treatment and recovery phases of diabetic ketoacidosis Volume resuscitation with 0.9% normal saline provides a chloride load, so that infusing more than 3–4L can cause acidosis Hyperalimentation ( i.e. , total parenteral nutrition )
Diagnosis is based mainly on clinical findings and laboratory test results. Plasma concentrations of ammonia (>150 μmol/L) and citrulline (200-300 μmol/L) are elevated. Elevated levels of argininosuccinic acid (5-110 μmol/L) in the plasma or urine are diagnostic. Molecular genetic testing confirms diagnosis.
In many cases, propionic acidemia can damage the brain, heart, kidney, liver, cause seizures and delays to normal development such as walking or talking. The accumulation of propionic acid is known to induce differential responses in different organs. The heart and liver are specific targets of the complication.
Laboratory tests may be obtained to rule out other causes of sudden amnesia such as a complete blood count, electrolytes, kidney function, liver function, inflammatory markers (such as C reactive protein and erythrocyte sedimentation rate), ammonia level (often elevated in hepatic encephalopathy), urine toxicology screening, alcohol level and ...
[1] [2] The delta ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether mixed acid base disorder (metabolic acidosis) is present. The list of agents that cause high anion gap metabolic acidosis is similar to but broader than the list of agents that cause a serum osmolal gap .
The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Hyperalimentation (e.g. from TPN containing ammonium chloride) Chloride administration, often from normal saline; Acetazolamide and other carbonic anhydrase inhibitors; Renal tubular acidosis [1]