metabolik asidoz ve bikarbonat tedavisi

 

 

Akut metabolik asidoz

— We initiate bicarbonate therapy when acute metabolic acidosis has generated severe acidemia (ie, pH less than 7.1). We also generally suggest bicarbonate therapy for patients with less severe acidemia (eg, pH 7.1 to 7.2) who have severe acute kidney injury (ie, a twofold or greater increase in serum creatinine or oliguria); bicarbonate therapy in such patients can potentially prevent the need for dialysis and may improve survival  .

* Rapid infusions of sodyum bikarbonat may increase the partial pressure of carbon dioxide (PCO₂), lower the ionized calcium, expand the extracellular space, and raise the serum sodium concentration.

Ayrıca , paradoxical fall in intracellular pH, increased lactate production, and myocardial depression olabilir .

Thus, many clinicians initiate treatment of metabolic acidosis when the bicarbonate level is very low (eg, <5 mEq/L) and the pH is below 7.1.

We do not generally use bicarbonate therapy in patients with less severe acidosis (pH 7.1 or greater), unless the patient also has severe acute kidney injury. 

– In patients with acute metabolic acidosis, intravenous bicarbonate is given if the blood pH is <7.1 or, in some patients, <7.2. The initial goal is a pH >7.2 and/or serum bicarbonate concentration >16 mEq/L. (“Approach to the adult with metabolic acidosis” başlığı )

* “Overview of the management of acute kidney injury (AKI) in adults” başlığındaki öneriler :

Among patients with AKI and severe metabolic acidosis who are not volume overloaded and have no other indication for acute KRT, bicarbonate may be administered instead of KRT; diuretics can be used in nonoliguric patients to prevent hypervolemia and to enhance excretion of acid. The goal serum bicarbonate level is 20 to 22 mEq/L and the goal pH is >7.2

Oral sodium bicarbonate tablets or sodium citrate solution can also be used in patients who are able to tolerate oral administration of medications and who have mild acidosis (bicarbonate >18 mEq/L). We calculate the bicarbonate deficit as a guide to therapy and aim for 50 percent replacement of the deficit in the first 24 hours.

Bikarbonat açığı hesaplama  : bikarbonat açığı

Verilme Şekli :

- Infuse 2 ampules (100 mL)(türkiyede 50 ml lik ampul yok 10 mllik ampul var, yani 20 ampul gibi oluyor ?) of sodyum bikarbonat over 1 to 2 minutes and remeasure the blood pH and serum bicarbonate concentration (eg, after two hours).

•If the bicarbonate concentration does not increase by this level, then ongoing acid generation is probably expanding the apparent bicarbonate distribution space.

- An alternative approach to administering two additional ampules of hypertonic sodium bicarbonate is to add three ampules of 8.4 percent sodium bicarbonate to 1 liter of 5 percent dextrose to generate an intravenous solution containing approximately 150 mEq/L(türkiyede 1 ampul 10 meq ?)  of sodium bicarbonate; this is typically administered over 2 to 4 hours, and further treatment is determined based upon reassessment of the pH and serum bicarbonate.

Kronik metabolik asidoz :

The most common causes of chronic metabolic acidosis are diarrhea, advanced chronic kidney disease, and the various forms of RTA.

When chronic alkali treatment is required, options include the sodium or potassium salts of either bicarbonate or a metabolizable anion such as citrate or lactate . The potassium salts are indicated when hypokalemia and total body potassium deficits exist. In general, the initial dose is 50 to 100 mEq per day, which is then titrated up, or down, as required. If ongoing bicarbonate losses persist or accelerate, the dose will need to be adjusted accordingly.

Kronik Böbrek Yetmezliği :

KDIGO ve KDOQI kılavuzlarına göre , in patients with CKD and metabolic acidosis, alkali therapy (usually with sodyum bikarbonat) be used to maintain the serum bicarbonate concentration in the normal range (23 to 29 mEq/L or 24 to 26 mEq/L, respectively) . The upper bound of this target range is less clear than the lower bound .

Choice of therapy — Alkali therapy usually consists of sodyum bikarbonat or sodium citrate (citrate is rapidly metabolized to bicarbonate), typically in a dose of 0.5 to 1 mEq/kg per day . We generally prefer citrate, which does not produce the bloating associated with bicarbonate therapy. 

Sodium citrate should be avoided in patients also taking aluminum-containing antacids.Patients taking aluminum-containing antacids to control hyperphosphatemia are at increased risk of developing aluminum intoxication if they are treated with sodium citrate

Metabolic acidosis can also be treated using kalsiyum sitrat,kalsiyum asetat,kalsiyum karbonat, or a diet that is high in alkaline foods and low in dietary acid (ie, an alkaline-ash diet)

Laktik Asidoz :  

*We suggest that patients with lactic acidosis and severe acidemia (pH less than 7.1 and serum bicarbonate level 6 mEq/L or less) receive bicarbonate therapy.

We do not generally use bicarbonate therapy in patients with less severe acidosis (pH 7.1 or greater), unless the patient also has severe acute kidney injury.

When using bicarbonate therapy in patients with lactic acidosis and severe acidemia, we aim to maintain the arterial pH above 7.1 until the primary process causing the metabolic acidosis can be reversed. For the group of patients with severe acute kidney injury, the pH goal is 7.3 or higher.

If the patient's pH is 7.1 or lower and the serum bicarbonate level is greater than 6 mEq/L, then this indicates that the partial pressure of carbon dioxide (PCO₂) is greater than 20 mmHg, which signifies inadequate ventilation. Such patients have mixed metabolic and respiratory acidosis, and rapid infusion of sodyum bikarbonat may worsen the respiratory acidosis. Mechanical ventilation may be necessary to achieve a lower PCO₂ level and raise the pH in these patients with severe acidemia due to mixed acidosis.

APPROACH 

In critically ill patients with severe lactic acidosis, which has resulted in severe acidemia (pH less than 7.1 and serum bicarbonate concentration 6 mEq/L or less), we suggest the following approach in regard to bicarbonate therapy:

●Assure that the patient is adequately ventilated; this is a prerequisite to the effective use of exogenous bicarbonate in patients with lactic acidosis. In nonintubated patients with severe acidemia, an appropriate ventilatory response to the metabolic acidosis should reduce the partial pressure of carbon dioxide (PCO₂) to at least 15 mmHg and often to 10 to 12 mmHg.

●If bicarbonate administration raises the pH, this can reduce the ionized calcium concentration and have adverse hemodynamic consequences. Ideally, the ionized calcium should be measured and treated if it falls. However, in many facilities, this measurement may not be readily available within the required time frame. Under such circumstances, if the blood pressure falls or does not improve, and if the ionized calcium could be low, then empiric calcium infusion should be considered .

●If ventilation is adequate, the patient with severe lactic acidosis (pH less than 7.1) should be given an intravenous sodyum bikarbonat bolus of 1 to 2 mEq/kg body weight. The serum electrolytes and blood pH should be measured 30 to 60 minutes later, and the dose of sodium bicarbonate can be repeated if severe lactic acidosis (pH less than 7.1) persists.

●If several doses of NaHCO₃ do not increase the pH above 7.1 and all other appropriate therapeutic interventions have been undertaken, then further NaHCO₃ therapy should continue in the form of a near-isotonic solution of NaHCO₃. This can be prepared by adding 3 ampules of NaHCO₃ (8.4 percent) to a liter of 5% dextrose in water (D5W), which results in a solution of 150 mEq/L NaHCO₃ in D5W. This has the advantage of being relatively isotonic but does increase the volume given to the patient. If volume overload is an issue and kidney function is compromised, then dialytic therapy can be instituted.

Diyabetik Ketoasidoz

Hangi hastalara bikarbonat verilmeli:

●Patients with an arterial pH ≤6.9 in whom decreased cardiac contractility and vasodilatation can impair tissue perfusion . 7.0 üstünde vermeye gerek yok.

For patients with pH ≤6.9, we give 100 mEq of sodyum bikarbonat in 400 mL sterile water administered over two hours. If the serum potassium is less than 5.3 mEq/L, we add 20 mEq of KCl. When the bicarbonate concentration increases, the serum potassium may fall and more aggressive KCl replacement may be required.

●Patients with potentially life-threatening hyperkalemia, since bicarbonate administration in acidemic patients may drive potassium into cells, thereby lowering the serum potassium concentration. The exact potassium level that should trigger this intervention has not been defined; we administer sodyum bikarbonat if the serum potasyum is >6.4 mEq/L The venous pH and bicarbonate concentation should be monitored every two hours, and bicarbonate doses can be repeated until the pH rises above 7.0.

Renal Tübüler Asidoz (RTA)

Serum bikarbonat hedefi 22-24 dür. Ayrıntılı bilgi için :

Renal Tübüler Asidoz