Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Low arterial pH and low HCO3.
B.Low pCO2 after respiratory compensation.
Incidence
A.Metabolic acidosis occurs frequently in acute and chronic renal disease and in patients with any type of poisoning from drugs or chemicals. It is a common finding in the hospital setting for a variety of reasons.
B.It is typically classified as having a normal anion gap (non-AG) or a high anion gap (AG).
Pathogenesis
A.Metabolic acidosis can be determined by calculating the AG, the first step in distinguishing the type of metabolic acidosis.
1.The equation to calculate the AG: AG = Na+ − (Cl- + HCO3).
2.The normal AG is 12 mEq/L.
B.The causes of metabolic acidosis can be a loss of bicarbonate or the addition of acid.
C.In metabolic acidosis caused by loss of bicarbonate, there is a non-AG.
1.Gastrointestinal (GI) losses.
a.Diarrhea.
b.Ileostomy.
c.Surgical drains.
2.Renal losses.
a.Proximal and distal renal tubular acidosis.
b.Hypoaldosteronism.
D.In metabolic acidosis caused by addition of acid, the AG is elevated above 12.
1.Renal failure or uremia.
2.Lactic acidosis.
3.Ketoacidosis.
a.Diabetes.
b.Ethanol.
c.Starvation.
4.Ingestion.
a.Ethylene glycol.
b.Methanol.
c.Paraldehyde.
d.Salicylate intoxication.
E.In metabolic acidosis, the PCO2 falls predictably depending on HCO3 concentration.
1.To calculate expected change, PCO2 = (1.5 HCO3-) + 8 + 2.
2.If the PCO2 is not as expected, there is a respiratory acid–base disturbance, too.
F.In AG metabolic acidosis, – can be used to discover a second metabolic acid–base disorder.
1.Gap/HCO3− = (measured AG – ideal AG)/(ideal HCO3 – measured HCO3-).
a.If less than 1 then there is a non-AG metabolic acidosis present.
b.If greater than 2 then there is a metabolic alkalosis present.
Predisposing Factors
A.There are none. Metabolic acidosis is dependent on cause, which determines the predisposing factors.
Subjective Data
A.Common complaints/symptoms.
1.Increased respiratory rate.
2.Drowsiness.
3.Nonspecific.
B.Family and social history.
1.Alcohol use or drug abuse.
2.Occupational history and potential exposure to metals or chemicals.
3.Genetic disorder associated with a family history of acidosis, typically discovered in childhood.
C.Review of systems.
1.Neurological: Blurred vision, vertigo, headache, confusion, generalized weakness.
2.Head, ear, eyes, nose, throat: Ringing in the ears, light bothering eyes, seeing floaters.
3.Respiratory—increased breathing.
4.Cardiovascular—chest pain, palpitations.
5.GI—diarrhea, vomiting, pain in the chest that feels like heartburn.
6.Renal—increased urination, increased thirst, urination at night.
7.Psychiatric: Any history of drug use or depression.
Physical Examination
A.Nonspecific physical examination that depends on the underlying cause.
1.Renal failure: Pallor, drowsiness, asterixis, pericardial rub.
2.Diabetic ketoacidosis: Reduced skin turgor, dry mucous membranes, fruity breath.
3.Sepsis—fever, confusion or coma, hypotension, Kussmaul respirations.
Diagnostic Tests
A.Serum electrolytes: Check serum bicarbonate.
B.Arterial blood gas (ABG): pH less than 7.40.
C.AG determination.
D.Base excess/deficit determination to determine the degree of acidosis.
E.CBC: Look for severe anemia which can affect oxygen delivery.
F.Urinalysis: Urine pH greater than 5.5 may be associated with certain renal diseases.
1.Calcium oxalate crystals seen in ethylene glycol toxicity.
G.Beta-hydroxybutyrate.
H.Lactate level.
I.Necessary in certain situations.
1.Salicylate levels.
2.Iron levels.
3.Aldosterone levels.
4.Ammonium levels.
Differential Diagnosis
A.For normal AG metabolic acidosis.
1.Abdomen.
a.Diarrhea.
b.Fistulas.
2.Renal.
a.Renal tubular acidosis: Addison’s disease.
b.Carbonic anhydrase inhibitors.
c.Post hypocapnia.
d.Excessive chloride (large volumes of saline).
B.For a high AG metabolic acidosis, use the mnemonic MUDPILES to remember the differential diagnosis.
1.Methanol.
2.Uremia.
3.Diabetic ketoacidosis.
4.Paraldehyde.
5.Infection, iron, isoniazid, ibuprofen.
6.Lactic acidosis.
7.Ethylene glycol.
8.Salicylates.
Evaluation and Management Plan
A.General plan.
1. Treat with an alkali therapy to raise plasma pH greater than 7.20.
2. Calculate the sodium bicarbonate deficit to determine how much must be administered intravenously to raise the serum bicarbonate level to increase the pH greater than 7.20.
3. Determine the underlying cause of the metabolic acidosis and treat appropriately.
B.Pharmacotherapy.
1.Metabolic acidosis of any type. Sodium bicarbonate can be used, but treating the underlying issue is critical.
a.Be cautious of volume overload; loop diuretics can be used to reduce volume as needed.
2.Methanol or ethylene glycol poisoning. Fomepizole can be used to treat ethylene glycol poisoning.
3.Uremia. Sodium bicarbonate can be used to keep serum bicarbonate levels above 20 mEq/L.
4.Diabetic ketoacidosis. Insulin can be used to treat ketoacidosis.
5.Paraldehyde poisoning. Alkali therapy can be used to correct metabolic acidosis during supportive care; no specific antidote exists.
6.Infection, iron, isoniazid, or ibuprofen. Antibiotics can be used to treat sepsis and activated charcoal can be used for the treatment of poisoning caused by drugs and chemicals.
7.Lactic acidosis. Alkali therapy such as sodium bicarbonate or tromethamine can be used.
a.The role of alkali therapy can be controversial.
8.Ethylene glycol—Fomepizole or ethanol can be used to treat cases of poisoning.
9.Salicylates—Acetazolamide can treat salicylate poisoning by inducing alkaline diuresis.
Follow-Up
A.The patient needs to follow-up with the primary care provider and any appropriate service providers involved in regulating the underlying disease process that causes the metabolic acidosis.
Consultation/Referral
A.Refer to the appropriate service provider related to the cause of the metabolic acidosis.
B.Consult nephrology as quickly as possible in cases that may require hemodialysis.
C.Consult endocrine for patients who present with diabetic ketoacidosis.
Special/Geriatric Considerations
A.Metabolic complications are common in the elderly and can be exacerbated in chronic kidney disease.
B.Special care to monitor and detect metabolic disturbances should be instituted.
Bibliography
Kraut, J. A., & Madias, N. E. (2015, October 15). Metabolic acidosis of CKD: An update. American Journal of Kidney Diseases, 67(2), 307–317. doi: 10.1053/j.ajkd.2015.08.028
Kraut, J. A., & Madias, N. E. (2016, September). Lactic acidosis: Current treatments and future directions. American Journal of Kidney Diseases, 68(3), 473–482. doi:10.1053/j.ajkd.2016.04.020
Rastegar, M., & G. T. Nagami (2017, February). Non-anion gap metabolic acidosis: A clinical approach to evaluation. American Journal of Kidney Diseases, 69(2), 296–301. doi:10.1053/j.ajkd.2016.09.013
Reddy, P., & Mooradian, A. D. (2009, October). Clinical utility of anion gap in deciphering acid-base disorders. International Journal of Clinical Practice, 63(10), 1516–1525. doi:10.1111/j.1742-1241.2009.02000.x
Thomas, C. P. (2018, October 10). Metabolic acidosis. In V. Batuman (Ed.), Medscape. Retrieved from https://emedicine.medscape.com/article/242975-overview