Metabolic acidosis

SEMINAR

1. Metabolic Acidosis R.Anusha PharmD 5 th Year Roll No:07 1

2. Introduction 2 Acidosis : It is a process that increases [H+] Acidemia: When blood pH <7.35 Metabolic acidosis: When an acid other than carbonic acid accumulates in the body resulting in fall in HCO3- Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy.

3. 3 In body fluids, the concentration of hydrogen ions ([H + ]) is maintained within very narrow limits, with the normal physiologic concentration being 40 nEq /L. The concentration of HCO 3 -  (24 mEq /L) is 600,000 times that of [H + ]. The tight regulation of [H + ] at this low concentration is crucial for normal cellular activities because H +  at higher concentrations can bind strongly to negatively charged proteins, including enzymes, and impair their function.

4. 4 Under normal conditions, acids and, to a lesser extent, bases are being added constantly to the extracellular fluid compartment, and for the body to maintain a physiologic [H + ] of 40 nEq /L, the following three processes must take place: Buffering by extracellular and intracellular buffers Alveolar ventilation, which controls PaCO 2 Renal H +  excretion, which controls plasma HCO 3 -

5. 5 Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Decreased acid excretion GI or renal HCO3 − loss Results in: ↓pH (7.35) ↓HCO3- (<22mEq/L)

6. Signs and symptoms 6

7. Anion gap 7 Anion gap = ( [Na+ ] + [K+ ] ) − ( [Cl− ] + [HCO3 − ] ) Unmeasured anions subtracted by unmeasured cations (in ECF) Omission of potassium has become widely accepted, as potassium concentrations, being very low, usually have little effect on the calculated gap. Normal value: 3–11 mEq /L

8. High anion gap metabolic acidosis Causes include: 8 M-Methanol U- Uremia (chronic kidney failure) D- Diabetic ketoacidosis P-Propylene glycol I- Infection, Iron, Isoniazid, Inborn errors of metabolism L- Lactic acidosis E-Ethylene glycol

9. Normal anion gap acidosis Causes include 9 Longstanding diarrohea (bicarbonate loss) Bicarbonate loss due to taking topiramate Pancreatic fistula Uretero- sigmoidostomy Renal tubular acidosis Intoxication: ammonium chloride,acetazolamide,bile acid sequestrants, isopropyl alcohol Renal failure (occasionally) Inhalant abuse Toluene

10. 10 Some examples of specific treatments for underlying disorders: Fluid, insulin and electrolyte replacement is necessary for diabetic ketoacidosis Administration of bicarbonate and/or dialysis may be required for acidosis associated with renal failure Restoration of an adequate intravascular volume and peripheral perfusion is necessary in lactic acidosis.

11. Diabetic Keto Acidosis 11 Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: Correction of fluid loss with intravenous fluids Correction of hyperglycemia with insulin Correction of electrolyte disturbances, particularly potassium loss Correction of acid-base balance Treatment of concurrent infection, if present

12. Lactic Acidosis 12 Blood lactate concentrations >2mmol/L(20mg/dl) results lactic acidosis. Type 1 hypoxia + peripheral generation of Lactate in patient with circulatory failure+ shock. Type 2 impaired metabolism of Lactate in Liver disease and drug + toxin inhibit lactate metabolism( eg:Metformin ). Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery for type A lactic acidosis and the removal of the offending drug or toxin in type B lactic acidosis. Blood lactate concentrations >2mmol/L(20mg/dl) results lactic acidosis.

13. Renal tubular Acidosis 13 The treatment of type 1 and type 2 RTA is relatively simple, requiring the use of sodium bicarbonate or the slightly more palatable compound Shohl solution (or Bicitra ), which contains citric acid and sodium citrate, providing 1 mEq /mL of alkali. Polycitra K solutions contain potassium citrate to provide 2 mEq /mL of alkali and 2 mEq /mL of potassium,designed to correct both the acidosis and hypokalemia.

14. 14 Type 4 RTA may require treatment with fludrocortisone 0.1 to 0.3 mg/d (0.05 to 0.15 mg/m 2 per day). To reverse the hyperkalemia that characterizes the metabolic acidosis of type 4 RTA, dietary potassium restriction and orally administered potassium binders may be needed. Finally, to increase renal excretion of potassium, chlorothiazide and furosemide may be required to correct hyperkalemia. To neutralize the metabolic acidosis, bicarbonate therapy of 1.5 to 2.0 mEq /kg per day has been advocated.

15. The ECLS Approach to Management of Metabolic Acidosis 15 Emergency: intubation and ventilation for airway or ventilatory control; cardiopulmonary resuscitation; severe hyperkalaemia correction. Cause: Treat the underlying disorder as the primary therapeutic goal.Consequently,accurate diagnosis of the cause of the metabolic acidosis is very important. Losses: Replace losses (e.g. of fluids and electrolytes) where appropriate.Other supportive care (oxygen administration) is useful. In most cases, IV sodium bicarbonate is NOT necessary, NOT helpful, and may even be harmful so is not generally recommended.

16. 16 Specifics: There are often specific problems or complications associated with specific causes or specific cases which require specific management. For example: Ethanol blocking treatment with methanol ingestion; Rhabdomyolysis requires management for preventing acute renal failure; Haemodialysis can remove some toxins

17. Emergency <7.1(plasma bicarbonate of 8 mEq /L [mmol/L] 17 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 monitoring of the arterial blood gas readings. This intervention, however, has some serious complications in lactic acidosis and, in those cases, should be used with great care. 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.

18. REFERENCE 18 Medicine Update 2010 ; Vol. 20 ; Metabolic Acid Base Disorders ;690-694 https://emedicine.medscape.com/article/242975-overview