metabolic acidosis

1. Metabolic acidosis
Dr.Fateh Akram
DTCD STUDENT
Medicine Unit VI
National Institute of Diseases of The Chest &
Hospital

3. 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 increased
generation of acid or an inability to generate
sufficient bicarbonate.

4. Clinical Calculator : Anion
Gap
Acidemia (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

5.  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.

6. High anion gap metabolic acidosis
Causes 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

7. Normal anion gap acidosis
Causes 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

8. 3
Acidosi
s
 Lactic acidosis
 Renal T acidosis
 Diabetic ketoacidosis
1
Electrolyte
K+

9. Signs and symptoms

10. Signs and symptoms

11. Compensatory
mechanism

12. Repair of the Bicarbonate Deficit
Correction 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

13. 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

14. Hyperventilation
To decrease the arterial PCO2.
Maximal compensation takes 12 to 24 hours

15. Investigation

16. 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 chloride
High anion gap•Total CO2 = [HCO3] + [H2CO3] + [carbamino CO2] + [dissolved CO2]

17.  ABG
In 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

18. Management

19. 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.

20. 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

21. 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.

22. 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)

23. Diabetic KetoA
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

24. Renal Tubular A

25. 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

26. 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.

27. 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.