Metabolic acidosis medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
A pH under 7.1 is an emergency, due to the risk of cardiac arrhythmias, and may warrant treatment with intravenous bicarbonate. Bicarbonate is given at 50-100 mmol at a time under scrupulous monitoring of the arterial blood gas readings. This intervention however, is not effective in case of lactic acidosis. If the acidosis is particularly severe and/or there may be intoxication, consultation with the nephrology team is considered useful, as dialysis may clear both the intoxication and the acidosis.
General Management
ECLS Approach to Management of Metabolic Acidosis
| ECLS Approach to Management of Metabolic Acidosis | |
|---|---|
| Emergency: | intubation and ventilation for airway or ventilatory control; Cardiopulmonary resuscitation: Severe hyperkalemia |
| Cause: | Treat the underlying disorder as the primary therapeutic goal. Consequently, an accurate diagnosis of the cause of metabolic acidosis is very important. |
| Losses: | Replace losses (e.g. fluids and electrolytes) where appropriate. Other supportive care (oxygen administration) is useful. In most cases, IV sodium bicarbonate is not necessary, and may even be harmful so is not generally recommended. |
| Specifics: | There are often specific problems or complications associated with specific causes or specific cases that require specific management. For example, Ethanol blocking treatment with methanol ingestion; rhabdomyolysis requires management by IV fluids and uricosurics agents for preventing acute renal failure; hemodialysis can remove some nephrotoxins |
Specific Treatment:
Administration of bicarbonates and dialysis is required for metabolic acidosis that is associated with Renal failure.[1]
Restoration of adequate intravascular volume and proper peripheral perfusion is necessary for metabolic acidosis caused by lactic acidosis.
| Base administration in the treatment of acute metabolic acidosis | Benefits | Description | side-effects |
|---|---|---|---|
| Intravenous sodium bicarbonate | Inexpensive
Simple to use bicarbonate |
It should be administered slowly as an isosmotic solution to avoid hyperosmolality and minimize the extent of intracellular acidosis | Might exacerbate intracellular acidosis; can provide large sodium load |
| Intravenous THAM | Buffers protons without generating CO;2 penetrates cells to buffer pH, | Given as 0.3M solution, best to give through a central vein; serum potassium and PCO2 should be monitored carefully during therapy | hyperkalaemia,
hypercapnia, liver necrosis in newborns |
| Intravenous carbicarb | It preserves cardiac contractility in animal studies, human practice not done. | Under-study | under-study |
| Dialysis | Can provide large quantities of base while preventing volume overload or hyperosmolality; CRRT can deliver base over 24 h period at low rate | Continuous renal replacement therapy is preferred over intermittent hemodialysis | Requires use of dialysis equipment and personnel;
hypotension can occur during procedure |
Treatment of Diabetic-ketoacidosis
- DKA is managed in an intensive care unit during the first day is always advisable
- Fluid, Insulin and electrolyte replacement are most crucial for DKA management.
- Correction of fluid loss with intravenous fluids only , Correction of hyperglycemia with insulin, Correction of electrolyte disturbances, particularly potassium loss is < 5.5, Correction of acid-base balance by bicarbonate if <7.1, Treatment of concurrent infection by antibiotics, if present.
| MANAGEMENT OF DKA AND HHS | ||
|---|---|---|
| IV fluids | Hight flow 0.9% normal saline is recommended and should be continued until corrected sodium is <135 mg/dl. Switch to .45% normal saline when Sodium >135 mg/dl.
Add dextrose into 0.45% normal saline when serum glucose <200 mg/dl and sodium <135. |
|
| Insulin | Initiate continuous IV regular insulin infusion
Switch to subcutaneous basal bolus insulin for the following :
Overlap subcutaneous and IV insulin by 1-2 hours. |
|
| Potassium | Add IV potassium if serum potassium <5.2 mEq/L
Hold insulin for serum potassium <3.3 mEq/L Nearly all patients are potassium depleted, even with hyperkalemia |
|
| Bicarbonates | Consider for patients with pH<6.9, Bicarbonate<5 and severe hyperkalemia. But mostly it is avoided as it is cause of cerebral edema in children. | |
| phosphate | Consider for serum phosphate <1 mg/dl, cardiac dysfunction, or respiratory depression
Monitor serum calcium frequently |
Experimental treatment:[2]
Small animal studies of various models of shock and lactic acidosis demonstrated improved cardiac function, reduced mortality, and decreased generation of pro-inflammatory cytokines; human studies yet to be performed, so options include as follows:[3]
- Dichloroacetate
- Administration of selective inhibitors Na+-H+ Exchanger 1 or amilonde analogues
- Administration of inhibitors of transient receptor potential vanilloid 1
- Administration of selective inhibitors acid sensing Ion channel la
- Administration of inhibitors of mitogen activated protein kinase
Contraindicated medications
Metabolic acidosis is considered an absolute contraindication to the use of the following medications:
References
- ↑ Kraut JA, Madias NE (2012). "Treatment of acute metabolic acidosis: a pathophysiologic approach". Nat Rev Nephrol. 8 (10): 589–601. doi:10.1038/nrneph.2012.186. PMID 22945490.
- ↑ Kraut JA, Madias NE (2012). "Treatment of acute metabolic acidosis: a pathophysiologic approach". Nat Rev Nephrol. 8 (10): 589–601. doi:10.1038/nrneph.2012.186. PMID 22945490.
- ↑ Kraut JA, Madias NE (2012). "Treatment of acute metabolic acidosis: a pathophysiologic approach". Nat Rev Nephrol. 8 (10): 589–601. doi:10.1038/nrneph.2012.186. PMID 22945490.