Metabolic acidosis

Dr.Fateh AkramDTCD STUDENTMedicine Unit VI

National Institute of Diseases of The Chest & Hospital

Metabolic acidosis? Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Decreased acid excretion GI or renal HCO3

− loss

Metabolic acidosis is either due to increasedgeneration of acid or an inability to generatesufficient bicarbonate.

Clinical Calculator : Anion GapAcidemia (arterial pH < 7.35) results when acid

load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap.

High anion gap Metabolic Acidosis Normal anion gap Metabolic Acidosis

Anion gap = ( [Na+] + [K+] ) − ( [Cl−] + [HCO3−] )

As sodium is the main extracellular cataion, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions. Normally, this concentration is about 8-16 mmol/l (12±4). An elevated anion gap (i.e. > 16 mmol/l) can indicate particular types of metabolic acidosis, particularly certain poisons, lactate acidosis and ketoacidosis.

High anion gap metabolic acidosisCauses include:

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

Normal anion gap acidosisCauses include longstanding diarrhea (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

3Acidosis

Lactic acidosis Renal T acidosis Diabetic ketoacidosis

1Electrolyte K+

Signs and symptoms

Signs and symptoms

Compensatory mechanism

Repair of the Bicarbonate DeficitCorrection involves repair of the bicarbonate deficit in the

body. So where does this bicarbonate come from?There are three usual sources: 1. Kidney: Renal generation of new bicarbonate

This usually occurs as a consequence of an increase in ammonium excretion.

2. Liver: Hepatic metabolism of acid anions to produce bicarbonate

3. Exogenous Administration of sodium bicarbonate

Compensatory mechanisms by four buffering mechanisms The body regulates the acidity of the blood by bicarbonate buffering system Intracellular buffering by absorption of hydrogen

atoms by various molecules, including proteins, phosphates and carbonate in bone.

Respiratory compensation by hyperventilation Renal compensation

HyperventilationTo decrease the arterial PCO2.

Maximal compensation takes 12 to 24 hours

Investigation

A metabolic acidosis is often strongly suspected because of the clinical presentation of the patient (eg diabetes, renal failure, severe diarrhoea). Three clues from a typical hospital automated biochemical profile are:Low ‘bicarbonate’ (or low ‘total CO2’)High chlorideHigh anion gap•Total CO2 = [HCO3] + [H2CO3] + [carbamino CO2] + [dissolved CO2]

ABGIn addition to arterial blood gases, some other investigations useful for indicating a metabolic

acidosis and for differentiating between the various major causes are:

Urine tests for glucose and ketones Electrolytes (incl chloride, anion gap,bicarbonate’) Plasma glucose Urea and creatinine Lactate

Management

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.

The ECLS Approach to Management of Metabolic Acidosis

Emergency: intubation and ventilation for airway or ventilatory control; cardiopulmonary resuscitation; severe hyperkalaemia 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.

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

Emergency <7.1 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, 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.

Lactic A Typte1 hypoxia+peripheral generation of

Lactate in patient with circulatory failure+ shock.

Type2 impaired metabolism of Lactate in Liver disease and drug+toxin inhibit lactate metabolism( eg:metformin)

>2mmol/l(20mg/dl)

Diabetic KetoAManaging 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

Renal Tubular A

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 ci-trate, 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

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.

Prognosis of Metabolic Acidosis

Recovery from Metabolic Acidosis is dependent on the cause. Appropriate and timely treatment goes a long way in helping speed up recovery. Some people totally recover from Metabolic Acidosis whereas others may end up with some form of organ dysfunction, respiratory issues, and renal failure. Extreme acidosis can also result in shock and rarely death.