1.

Anionic gap=gaura anionica

= Na-(Cl+HCO3)

Ex.
[Na+] = 137 mEq/L;
[Cl−] = 102 mEq/L;
[HCO−3] = 24 mEq/L;
Anion Gap = [Na+] - ([Cl−] + [HCO−
3]) = 137 - (102 + 24) = 11 mEq/L.
NORMAL
• 8-16mEq/L-FARA K+

• 10-20mEq/L-CU K+

Daca e normala cu clorul normal atunci cauza e respiratorie!!!

HIGH ANION GAP= ACIDOZA
>11mEq/L

• DE CE?- SCADE HCO3 pentru ca e consumat- anion

The bicarbonate is consumed by the unmeasured cation(H+) (via its

action as a buffer) resulting in a high anion gap.
Lactic acidosis

Ketoacidosis

Diabetic ketoacidosis

Alcohol abuse

Toxins:
Methanol
Ethylene glycol
Propylene glycol
Lactic acid
Uremia
Aspirin
Phenformin (no longer on market in U.S. since 1978 due to severe lactic acidosis, but still a problem globally. "Old metformin")
Iron
Isoniazid
Cyanide, coupled with elevated venous oxygenation
Renal failure, causes high anion gap acidosis by decreased acid excretion and decreased HCO3−
reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap.
Normal anion gap

• In patients with a normal anion gap the drop in HCO−

3 is the primary pathology. Since there is only one other major
buffering anion, it must be compensated for almost completely by an
increase in Cl−. This is therefore also known as hyperchloremic
acidosis.

• The HCO−3 lost is replaced by a chloride anion, and thus there is a

normal anion gap.
CAUZE

Gastrointestinal loss of HCO−

3 (i.e., diarrhea) (note: vomiting causes hypochloraemic alkalosis)
•Renal loss of HCO−
3 (i.e., proximal renal tubular acidosis (RTA) also known as type 2 RTA)
•Renal dysfunction (i.e., distal renal tubular acidosis also known as type 1 RTA)
•Renal Hypoaldosterone (i.e., renal tubular acidosis also known as type IV RTA) characterized by elevated serum potassium.
There are three types.
1. Low Renin may be due to diabetic nephropathy or NSAIDS (and others causes).
2. Low aldosterone may be due to adrenal disorders or ACE inhibitors.
3. Low response to aldosterone maybe due to potassium sparing diuretics, Bactrim, or diabetes (and other causes). [13]
•Ingestions
•Ammonium chloride and acetazolamide, ifosfamide.
•Hyperalimentation fluids (i.e., total parenteral nutrition)
•Some cases of ketoacidosis, particularly during rehydration with Na+ containing IV solutions.
•Alcohol (such as ethanol) can cause a high anion gap acidosis in some patients, but a mixed picture in others due to concurrent metabolic alkalosis.
•Mineralocorticoid deficiency (Addison's disease)
Note: a useful mnemonic to remember this is FUSEDCARS (fistula (pancreatic), uretero-enterostomy, saline administration, endocrine (hyperparathyroidism),
diarrhea, carbonic anhydrase inhibitors (acetazolamide), ammonium chloride, renal tubular acidosis, spironolactone)
Low anion gap-RARE- CRESTE HCO3 si Cl

• A low anion gap is frequently caused by hypoalbuminemia. Albumin is

a negatively charged protein and its loss from the serum results in the
retention of other negatively charged ions such
as chloride and bicarbonate. As bicarbonate and chloride anions are
used to calculate the anion gap, there is a subsequent decrease in the
gap.
• The anion gap is sometimes reduced in multiple myeloma, where
there is an increase in plasma IgG (paraproteinaemia).
Correcting the anion gap for the albumin
concentration
• The calculated value of the anion gap should always be adjusted for variations in the serum albumin concentration.[15] For example, in cases of hypoalbuminemia the calculated
value of the anion gap should be increased by 2.3 to 2.5 mEq/L per each 1 g/dL decrease in serum albumin concentration (refer to Sample calculations, below).[16] Common
conditions that reduce serum albumin in the clinical setting are hemorrhage, nephrotic syndrome, intestinal obstruction and liver cirrhosis. Hypoalbuminemia is common in
critically ill patients.
• Hypoalbuminemia can mask a mild elevation of the anion gap, resulting in failure to detect an accumulation of unmeasured anions. Therefore, it is important to correct the
calculated value of the anion gap for the concentration of albumin, particularly in critically ill patients.[17][18][19] Corrections can be made for the albumin concentration using the
Figge-Jabor-Kazda-Fencl equation to give an accurate anion gap calculation as exemplified below.[20]
• Sample calculations[edit]
• Given the following data from a patient with severe hypoalbuminemia suffering from postoperative multiple organ failure,[21] calculate the anion gap and the albumin-corrected
anion gap.
• Data:
• [Na+] = 137 mEq/L;
• [Cl−] = 102 mEq/L;
• [HCO−
3] = 24 mEq/L;

• [Normal Albumin] = 4.4 g/dL;

• [Observed Albumin] = 0.6 g/dL.
• Calculations:
• Anion Gap = [Na+] - ([Cl−] + [HCO−
3]) = 137 - (102 + 24) = 11 mEq/L.

• Albumin-Corrected Anion Gap = Anion Gap + 2.5 x ([Normal Albumin] - [Observed Albumin]) = 11 + 2.5 x (4.4 - 0.6) = 20.5 mEq/L.
• In this example, the albumin-corrected anion gap reveals the presence of a significant quantity of unmeasured anions.[21]