Approach to child with metabolic acidosis

by Dr.Anand Rauniyar

1. Approach to Metabolic Acidosis Moderator, Asst.Prof.Dr.Arun Giri Dr.Anand Rauniyar Jr-2 nd year

2. Normal Values of Arterial Blood Gases pH : 7.40 ± 0.05 [HCO3−] : 24 ± 4 mEq /L PCO2 : 35-40 mm Hg Hyperventilation of pregnancy : umbilical arterial blood gases have a normal pH range of 7.20 to 7.28

3. Acidosis : 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- .

4. Etiology occur via 3 basic mechanisms: Loss of bicarbonate from the body. Impaired ability to excrete acid by the kidney. Addition of acid to the body (exogenous or endogenous).

5. Homeostatic response to metabolic acidosis Respiratory compensation : Fall in PCO2 raises the pH toward normal but will not lead to overcorrection (simple metabolic acidosis). B egins in the first hour, and is complete by 12 to 24 hours. Acute compensation results in a 1.2 mmHg fall in the PCO2 for every 1 mEq /L reduction in the serum HCO 3- .

6. Differentiating between simple and mixed acidosis P atients with mixed acidosis have components of both metabolic and respiratory acidosis (inadequate compensation ). Winter's formula : PCO2 = (1.5 x [HCO3-]) + 8 ± 2 Example : An infant with gastroenteritis has a pH of 7.22, measured serum bicarbonate of 9 mEq /L, and a PCO2 of 22 mmHg ( torr ). According to Winter's formula, the appropriate respiratory compensation in this infant would result in a PCO2 of 22 mmHg ([1.5 x 9] + 8). In this case, the infant has simple metabolic acidosis with appropriate respiratory compensation

7. Renal response Increased reabsorption of filtered HCO3 - in the proximal tubule . Increased secretion of hydrogen ions (H+) as titratable acids ( eg , [H PO4 -]) or as (NH4 +) leads to regeneration of HCO3 - within the renal tubules.

8. Consequence of Acidemia O n V arious Organ System Organ System Effect Cardiovascular System Dec contractility, Arterial vasodilatation, Dec MAP, Dec CO, Dec response to Catecholamine, Inc risk of arrhythmias Respiratory System Hyperventilation(compensatory), Dec Respiratory Muscle Strength Metabolic Inc Potassium ( Due to H + /K + pump exchanging excess H + with Intracellular K + ) Neurological Altered Mental Status

9. Consequence

10. Anion Gap (AG) Represents the concentration of unmeasured anions in the plasma . AG = Unmeasured anions- Unmeasured cations To maintain electroneutrality, total number of cations should equal total number of anions . [Na+] + UC = ([Cl-] + [HCO3-]) + UA UA-UC= [Na+] - ([Cl-] + [HCO3-]) Normal: 12 ± 4 mmol/L

11. The normal range of the serum anion gap in newborns is 8 to 16 mEq /L. AG above 14 mEq /L in child and above 16 mEq /L in neonate is considered elevated .

12. Anion Gap and Albumin The normal AG is affected by patients plasma albumi n concentration . For every 1g/dl reduction in plasma albumin concentration the AG decreases by 2.5 . Corrected AG = Calculated AG + [2.5 × (4 – albumin )]

13. Classification approach INCREASED ANION GAP : Lactic acidosis caused by tissue hypoxia : Asphyxia, hypothermia, shock, Severe anemia Sepsis, respiratory distress syndrome. Inborn errors of metabolism Congenital lactic acidosis. Organic acidosis. Renal failure Late metabolic acidosis

14. Ketoacidosis Diabetic ketoacidosis Starvation ketoacidosis Poisoning Ethylene glycol Methanol Salicylate Toluene Paraldehyde

15. NORMAL ANION GAP : Renal bicarbonate loss : Bicarbonate wasting caused by immaturity. Renal tubular acidosis Carbonic anhydrase inhibitors Gastrointestinal bicarbonate loss : Small bowel drainage: ileostomy , fistula Diarrhea Extracellular volume expansion with bicarbonate dilution Aldosterone deficiency Excessive chloride in intravenous fluids

16. Mixed normal ( hyperchloremic ) and high AG metabolic acidosis Severe diarrhea .

17. Δ anion gap/ Δ HCO3- ratio Helpful in differentiating mixed AG from high AG metabolic acidosis. High AG metabolic acidosis ( eg , DKA, CKD, methanol poisoning), the ratio is usually between 1 and 1.6 Patients with a mixed high and normal AG metabolic acidosis, the ratio is less than 1.

18. Inborn Errors of Metabolism Associated With Metabolic Acidosis Primary lactic acidosis. Organic acidemias Pyruvate carboxylase deficiency Pyruvate hydroxylase deficiency Galactosemia Hereditary fructose intolerance Type I glycogen storage disease

19. DIAGNOSIS Serum/plasma pH less than 7.35 . Abnormally low bicarbonate (HCO3 -) level In infants (<20 mEq /L) than in older children and adults (22 mEq /L). Decrease in the (PCO2 ); with respiration compensation, the decrease in PCO2 is typically about amounts 1 mmHg for every 1 mmol /l fall in serum HCO3 -.

20. Approach in neonate :

21. Urine Anion Gap

22. Urine electrolytes and anion gap UAG ( mEq /L) = Urine (Na + K - Cl ) Positive UAG : distal (type 1) RTA Negative (normal UAG) : proximal (type 2) RTA. Also helps in confirming non renal bicarbonate loss as a cause of metabolic acidosis, such as in patients with diarrhea. Renal ammonium generation in such patients is normal and the UAG is expected to be negative

23. Approach for normal AG metabolic acidosis

24. TREATMENT Treating underlying cause most effective therapeutic intervention in patients with metabolic acidosis

25. Acute metabolic acidosis The treatment remains controversial, Bicarbonate therapy: remains controversial the balance between the potential benefits and adverse effects of bicarbonate therapy in treatment of severe metabolic acidosis must be carefully weighed in pediatric patients, especially in newborns.

26. Guidelines to administer IV bicarbonate in children with severe metabolic acidosis : Conditions associated with bicarbonate loss, such as diarrhea and proximal (type 2) RTA, bicarbonate replacement therapy is generally beneficial. Patients with shock-induced lactic acidosis and a venous pH <7.1, cautious administration of bicarbonate can be considered along with adequate ventilation and restoration of tissue perfusion. Not recommended in patients with DKA, unless there is a potentially life-threatening condition.

27. The management of organic acidemias is varied, depending on the metabolic defect in the patient. Bicarbonate therapy may be used as adjunct therapy in the management of acute hyperkalemia. Used in pediatric patients after repair of complex congenital heart disease (CHD). Often utilized in patients with prolonged cardiac arrest, there is little evidence based data to support its use .

28. Bicarbonate use in neonates may be associated with increased mortality and morbidity ( eg , intraventricular hemorrhage [IVH], myocardial injury, deterioration of cardiac function, and worsening of intracellular acidosis. If indicated, sodium bicarbonate is given intravenously at a dose of 0.5 to 1 mEq /kg of body weight. The goal of the initial treatment is to raise and maintain the venous pH above 7.2

29. Dose of NaHCO3 ( mEq ) = Base deficit ( mEq /L) × Body weight (kg) × 0.3 Sodium bicarbonate should be administered slowly and in diluted form only to newborns with documented metabolic acidosis and adequate alveolar ventilation.

30. Adverse effects of bicarbonate Hypervolemia and hypernatremia Hypercarbia Development of hypokalemia in patients with diarrhea or DKA if metabolic acidosis is rapidly corrected Hypocalcemic tetany may result from aggressive treatment of metabolic acidosis, especially in patients with renal failure Potential tissue hypoxia, Increased risk of postnatal IVH in newborns.

31. THAM Tromethamine or tris-hydroxymethyl aminomethane (THAM) is an alternative alkalinizing agent that can be used to buffer pH. is a proton acceptor and does not generate excess CO2 and does not require the presence of an adequately ventilated patient. In general, THAM is preferred over bicarbonate in patients mixed acidosis and high PCO2

32. Oral base therapy : Is given to children with chronic metabolic acidosis. Available as sodium citrate, potassium citrate, and a 1 : 1 mix of sodium citrate and potassium citrate. Type I or type II RTA may have hypokalemia and may benefit from potassium supplements.

33. Hemodialysis : Appropriate choice in patients with renal insufficiency, especially if significant uremia or hyperkalemia is present. Hemodialysisis advantageous for correcting the metabolic acidosis caused by methanol or ethylene glycol intoxication.

34. Reference :