metabolic acidosis

1. METABOLIC ACIDOSIS
BY:
HarmanPreet Kaur
Harmanjit Kaur
Harmandeep Kaur
Harmanjit Singh
Harnoor Singh

2. INTRODUCTION
¢Metabolic acidosis is a condition that occurs
when the body produces excessive quantities of
acid or when the kidneys are not removing
enough acid from the body. If unchecked,
metabolic acidosis leads to acidemia, i.e., blood
pH is low (less than 7.35) due to increased
production of hydrogen ions by the body or the
inability of the body to form bicarbonate (HCO3
−
)
in the kidney. Its causes are diverse, and its
consequences can be serious, including coma and
death. Together with respiratory acidosis, it is
one of the two general causes of acidemia.

4. SIGNS AND SYMPTOMS:
¢Symptoms are not specific, and diagnosis can be
difficult unless the patient presents with clear
indications for arterial blood gas sampling. Symptoms
may include chest pain, palpitations, headache,
altered mental status such as severe anxiety due to
hypoxia, decreased visual acuity, nausea, vomiting,
abdominal pain, altered appetite and weight gain,
muscle weakness, bone pain and joint pain. Those in
metabolic acidosis may exhibit deep, rapid breathing
called Kussmaul respirations which is classically
associated with diabetic ketoacidosis. Rapid deep
breaths increase the amount of carbon dioxide
exhaled, thus lowering the serum carbon dioxide
levels, resulting in some degree of compensation.

5. ¢Extreme acidemia leads to neurological and
cardiac complications:
¢Neurological: lethargy, stupor, coma, seizures.
¢Cardiac: arrhythmias (ventricular tachycardia),
decreased response to epinephrine; both lead to
hypotension (low blood pressure).
¢Physical examination occasionally reveals signs
of disease, but is otherwise normal. Cranial nerve
abnormalities are reported in ethylene glycol
poisoning, and retinal edema can be a sign of
methanol (methyl alcohol) intoxication.
Longstanding chronic metabolic acidosis leads to
osteoporosis and can cause fractures.

7. ANION GAP
¢The anion gap is the difference in the measured cations
(positively charged ions) and the measured anions
(negatively charged ions) in serum, plasma, or urine.
The magnitude of this difference (i.e., "gap") in the
serum is often calculated in medicine when attempting
to identify the cause of metabolic acidosis, a lower than
normal pH in the blood. If the gap is greater than
normal, then high anion gap metabolic acidosis is
diagnosed.
¢The term "anion gap" usually implies "serum anion gap",
but the urine anion gap is also a clinically useful
measure.

9. NORMAL ANION GAP
¢In patients with a normal anion gap the drop in HCO3
−
is the primary pathology. Since there is only one other
major buffering anion, it must be compensated for
almost completely by an increase in Cl−
. This is
therefore also known as hyperchloremic acidosis.
¢The HCO3
−
lost is replaced by a chloride anion, and thus
there is a normal anion gap.

10. HIGH ANION GAP
¢The anion gap is affected by changes in unmeasured ions.
A high anion gap indicates acidosis. In uncontrolled
diabetes, there is an increase in ketoacids due to
metabolism of ketones. Ketoacids are unmeasured anions,
so there is a resulting increase in the anion gap. In these
conditions, bicarbonate concentrations decrease by acting
as a buffer against the increased presence of acids (as a
result of the underlying condition). The bicarbonate is
consumed by the unmeasured cation(H+) (via its action as
a buffer) resulting in a high anion gap.

11. LOW ANION GAP
¢A low anion gap is frequently caused by hypoalbuminemia.
Albumin is a negatively charged protein and its loss from the
serum results in the retention of other negatively charged ions
such as chloride and bicarbonate. As bicarbonate and chloride
anions are used to calculate the anion gap, there is a
subsequent decrease in the gap.
¢In hypoalbuminaemia the normal anion gap is decreased with
2.5 to 3 mmol/L per 1 g/dL decrease in serum
albumin.Common conditions that reduce serum albumin in the
clinical setting are hemorrhage nephrotic syndrome, intestinal
obstruction and liver cirrhosis.
¢The anion gap is sometimes reduced in multiple myeloma,
where there is an increase in plasma IgG (paraproteinaemia).
¢Corrections can be made for hypoalbuminemia to give an
accurate anion gap.

12. Causes of Metabolic Acidosis (classified by Anion Gap)
A: High Anion-Gap Acidosis
1. Ketoacidosis
•Diabetic ketoacidosis
•Alcoholic ketoacidosis
•Starvation ketoacidosis
2. Lactic Acidosis
•Type A Lactic acidosis (Impaired perfusion)
•Type B Lactic acidosis (Impaired carbohydrate metabolism)
3. Renal Failure
•Uraemic acidosis
•Acidosis with acute renal failure
4. Toxins
•Ethylene glycol
•Methanol
•Salicylates
CAUSES OF METABOLIC ACIDOSIS

13. B : Normal Anion-Gap Acidosis (or Hyperchloraemic acidosis)
1. Renal Causes
•Renal tubular acidosis
•Carbonic anhydrase inhibitors
2. GIT Causes
•Severe diarrhoea
•Uretero-enterostomy or Obstructed ileal conduit
•Drainage of pancreatic or biliary secretions
•Small bowel fistula
3. Other Causes
•Recovery from ketoacidosis
•Addition of HCl, NH4Cl

15. PATHOPHYSIOLOGY
¢Pathophysiology of Metabolic Acidosis
¢Metabolic acidosis occurs when either an increase in
the production of nonvolatile acids or a loss of
bicarbonate from the body overwhelms the
mechanisms of acid-base homeostasis or when renal
acidification mechanisms are compromised.
¢Acid Production
¢Under normal dietary and metabolic conditions,
average net acid production is 1 mmol/kg per day in
adults and 1-3 mmol/kg per day in infants and
children. Abnormalities in intermediary metabolism,
such as those that occur in lactic acid synthesis or
ketogenesis, and ingestion of substances that are
metabolized to organic acids, such as methanol or
ethylene glycol, can increase acid production
severalfold

16. COMPENSATORY MECHANISM:
¢Metabolic acidosis is either due to increased
generation of acid or an inability to generate
sufficient bicarbonate. The body regulates the
acidity of the blood by four buffering mechanisms.
¢bicarbonate buffering system
¢Intracellular buffering by absorption of hydrogen
atoms by various molecules, including proteins,
phosphates and carbonate in bone.
¢Respiratory compensation
¢Renal compensation

17. BICARBONATE BUFFERING SYSTEM
¢The bicarbonate buffering system is an important
buffer system in the acid-base homeostasis of living
things, including humans. As a buffer, it tends to
maintain a relatively constant plasma pH and
counteract any force that would alter. In this system,
carbon dioxide (CO2) combines with water (H2O) to
form carbonic acid (H2CO3), which in turn rapidly
dissociates to form hydrogen ions (H+
) and
bicarbonate (HCO3
−
) .
¢The carbon dioxide - carbonic acid equilibrium is
catalyzed by the enzyme carbonic anhydrase; the
carbonic acid - bicarbonate equilibrium is simple
proton dissociation/association and needs no catalyst

19. RESPIRATORY COMPENSATION
MECHANISM
¢Respiratory compensation is a mechanism by
which plasma pH can be altered by varying the
respiratory rate. It is faster than renal
compensation, but has less ability to restore
normal values.
¢In metabolic acidosis, chemoreceptors sense a
deranged acid-base system, and there is
increased breathing.
¢In metabolic alkalosis, the breathing rate is
decreased

20. RENAL COMPENSATION MECHANISM:
¢Renal compensation is a mechanism by which
the kidneys can regulate the plasma pH. It is
slower than respiratory compensation, but has a
greater ability to restore normal values.
¢In respiratory acidosis, the kidney produces and
excretes ammonium (NH4
+
) and monophosphate,
generating bicarbonate in the process while
clearing acid.
¢In respiratory alkalosis, less HCO3
−
is reabsorbed,
thus lowering the pH

21. ¢The decreased bicarbonate that distinguishes metabolic
acidosis is therefore due to two separate processes: the
buffer (from water and carbon dioxide) and additional
renal generation. The buffer reactions are:
¢The Henderson-Hasselbalch equation mathematically
describes the relationship between blood pH and the
components of the bicarbonate buffering system:
¢Using Henry's Law, we can say that [CO2]=0.03xPaCO2
(PaCO2 is the pressure of CO2 in arterial blood) Adding
the other normal values, we get

22. DIAGNOSIS
¢Arterial blood gas sampling is essential for the diagnosis. If
the pH is low (under 7.35) and the bicarbonate levels are
decreased (<24 mmol/l), metabolic acidemia is present, and
metabolic acidosis is presumed. Due to respiratory
compensation (hyperventilation), carbon dioxide is
decreased and conversely oxygen is increased. An ECG can
be useful to anticipate cardiac complications.
¢Other tests that are relevant in this context are
electrolytes (including chloride), glucose, renal function
and a full blood count. Urinalysis can reveal acidity
(salicylate poisoning) or alkalinity (renal tubular acidosis
type I). In addition, it can show ketones in ketoacidosis.
¢To distinguish between the main types of metabolic
acidosis, a clinical tool called the anion gap is considered
very useful. It is calculated by subtracting the chloride and
bicarbonate levels from the sodium.

23. ¢As sodium is the main extracellular cation, 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.
¢As the differential diagnosis is made, certain
other tests may be necessary, including
toxicological screening and imaging of the
kidneys. It is also important to differentiate
between acidosis-induced hyperventilation and
asthma; otherwise, treatment could lead to
inappropriate bronchodilatation.

24. TREATMENT PRINCIPLES
¢ The most important approach to managing a metabolic acidosis is to treat the
underlying disorder. Then with supportive management, the body will correct the
acid-base disorder. Accurate analysis & diagnosis is essential to ensure the correct
treatment is used. Fortunately, in most cases this is not particularly difficult in
principle. Remember though that a patient with a severe metabolic acidosis may
be very seriously ill and even with optimal management the patient may not
survive.
¢ The ECLS Approach to Management of Metabolic Acidosis
¢ 1. Emergency: Emergency management of immediately life-threatening conditions
always has the highest priority. For example, intubation and ventilation for airway
or ventilatory control; CPR ( cardiopulmonary resuscitation ); severe
hyperkalaemia
¢ 2. Cause: Treat the underlying disorder as the primary therapeutic goal.
Consequently, accurate diagnosis of the cause of the metabolic acidosis is very
important. I n some cases (e.g. methanol toxicity) there may be a substantial delay
become the diagnosis can be confirmed so management must be based on
suggestive evidence otherwise it will be too late.
¢ 3. Losses Replace losses (e.g. of fluids and electrolytes) where appropriate. Other
supportive care (oxygen administration) is useful. I n most cases, sodium
bicarbonate is NOT necessary, NOT helpful, and may even be harmful so is not
generally recommended.

25. ¢4. 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;
haemodialysis can remove some toxins.
¢Some examples of specific treatments for underlying
disorders:
¢Fluid, insulin and electrolyte replacement is necessary for
diabetic ketoacidosis
¢Administration of bicarbonate and 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 detailed treatment of the various specific disorders is
not considered here, but the important message is that
the treatment of each underlying disorder differs so an
accurate diagnosis is essential for selection of correct
treatment. Treatment of the underlying disorder will
result in correction of the metabolic acidosis (i.e. the
bicarbonate level will return to normal).