including high anion gap, lactic acidosis, renal tubular acidosis, keto acidosis, hyperchloremic Acidosis

1. METABOLIC ACIDOSIS
• YOGESH VISHWAKARMA.
• AKSHITA NAUTIYAL.
• CHANDANI KUMARI.
• NAZIYA INAMDAR.
• AAYUSHI PATEL.

2. METABOLIC ACIDOSIS
• 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.

3. CAUSES OF METABOLIC
ACIDOSIS
• There are 4 main causes of metabolic acidosis:
1. Lactic acidosis
2. Renal tubular acidosis
3. Keto acidosis
4. Diarrhea

4. ANION GAP
• Na+ + Unmeasured cations = Cl- + HCO3
- + Unmeasured anions.
• Or Unmeasured anions – Unmeasured cations = Na+ - Cl- + HCO3-
• Definition:
• Anion gap is quantity of anions not balanced by cations
• Usually due to negatively charged plasma proteins as the charges of the
other unmeasured cations and anions tend to balance out.

5. TESTS FOR METABOLIC ACIDOSIS
• Tests to diagnose metabolic acidosis :
• Arterial blood gas
• pH, pO2 , pCO2 , HCO3 (bicarbonate)
• Venous blood sample
• Sodium, potassium, chloride, bicarbonate
• Glucose
• Serum lactose
• Measured serum osmolarity
• Serum ketones
• Urine
• Urine pH, urine ketones
• Calculations
• Anion gap
• Sodium concentration minus the sum of chloride
concentration and bicarbonate concentration.
• Osmolar gap
• Measured osmolar gap minus calculated osmolar gap.
• Appropriate pCO2 change based on serum
bicarbonate.

6. DIAGNOSIS OF METABOLIC ACIDOSIS
• Determine the main acid – base problem.
1. pH lower than 7.35
• Acidosis
• Metabolic or Respiratory.
2. Bicarbonate lower than 20 meq/L
• Metabolic Acidosis
• Determine the main acid – base problem.
1. Calculate Anion Gap
• AG : Sodium – (Chloride +
Bicarbonate)
• Normal AG : 8 to 16 meq/L ( 5 to 7
meq/L using newer lab analyzers)
2. Determine if patients history and physical
fits the proposed diagnosis of type and
causes of metabolic acidosis.

7. HIGH ANION GAP
• High anion gap metabolic acidosis is a form of metabolic acidosis
characterized by a high anion gap.
• An anion gap is usually considered to be high if it is over 12 mEq/L.
• The most common cause for high anion gaps are:
Lactic Acidosis.
Ketoacidosis (diabetic ketoacidosis).

8. LACTIC ACIDOSIS.
• Lactic acidosis is a form of metabolic acidosis due to the inadequate
clearance of lactic acid from the blood.
• Lactic acidosis occurs when the body's buffering systems are
overloaded.
• Lactic acids are produced during anaerobic metabolism in the
muscle cells.
• Normally gets cleared from the blood through kidney.
• There are two types of lactic acid: L-lactate and D-lactate.
• Most forms of lactic acidosis are caused by too much L-lactate

10. CAUSES
• Lactic acidosis has a wide range of underlying causes.
Carbon monoxide poisoning.
Cholera.
Malaria.
Heart disease.
Cancer.
Intense exercise or physical activity.

11. PATHOPHYSIOLOGY

12. NORMAL CONDITION:
• In presence of oxygen. (Aerobic metabolism)
• Most of the cells use glucose for production of energy.
• In cytoplasm glucose is converted into 2 pyruvic acid through
Glycolysis.
• Then in the mitochondria pyruvic acids are converted into carbon
dioxide, water and ATP by the process of the Krebs cycle and
oxidative phosphorylation.
• The ATP produced by this process are used for muscle contraction or
other cellular activities.

13. ABNORMAL CONDITION:
• In absence of oxygen (anaerobic respiration)
• When the oxygen supply is inadequate this condition is
known as hypoxia.
• The mitochondria unable to produce ATP for body
functioning.
• In this condition glycolysis increased to produce ATP.
• So the pyruvic acid increases in the cytoplasm this pyruvic
acid converted into lactic acid, which diffuses into the
bloodstream which is causes lactic acidosis.

15. DIABETIC KETO ACIDOSIS
• Diabetic ketoacidosis is a serious complication of diabetes that occurs
when our body produces high levels of blood acids called ketones.
• Ketoacidosis is a high anion gap metabolic acidosis due to an excessive
blood concentration of ketone bodies (keto-anions).
• Ketone bodies released into the blood are acetoacetate, beta-
hydroxybutyrate, acetone.

16. CAUSES
• Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated.
• In diabetic ketoacidosis, the body shifts from its normal metabolism (using
carbohydrates for fuel) to a fasting state (using fat for fuel).
• The resulting increase in blood sugar occurs, because insulin is unavailable to
transport sugar into cells for future use.
• As blood sugar levels rise, the kidneys cannot retain the extra sugar, thereby increasing
urination and causing dehydration.
• Causes may include such as diarrhea, vomiting, and/or high fever, heart
attack, stroke, trauma, stress, and surgery. A low percentage of cases have no
identifiable cause.

17. PATHOPHYSIOLOGY

18. HOW BODY PRODUCES KETONE
• Sugar is a main source of energy for the cells that helps muscles and
other tissues to do their work. Normally, insulin helps sugar enter our
cells.
• Without enough insulin, the body produces a stress response, hormones
begin to break down muscle, fat, and liver cells into glucose (sugar)
and fatty acids for use as fuel.
• These fatty acids are converted into ketones by a process called
oxidation.

19. • The excessive fatty acid release from fat stores with a resulting ketone body
synthesis in the liver.
• Under normal physiologic conditions, these fatty acids are converted to triglycerides
and very low density lipoproteins in the liver.
• However, in patients with diabetic ketoacidosis, excess glucagon alters hepatic
metabolism.
• An enzyme called, carnitinepalmitoyltransferase I is activated. This is the key
enzyme for fatty acid transport to the mitochondria, where in beta-oxidation and
ketone body formation occurs.

21. • The formation of ketone bodies and their utilization as an energy source is
initially a protective mechanism against cellular starvation.
• However, as the overproduction of ketone bodies continues and their
metabolism decreases due to limited cellular uptake mechanisms, ketone
bodies accumulate.
• Overproduction of ketones rather than decreased utilization, however,
appears to be the primary mechanism of ketone body accumulation in
diabetic ketoacidosis.

22. NORMAL ANION GAP
• Normal anion gap is when the number of bicarbonate ions (HCO3-)
decreases.
• To compensate the amount of lost bicarbonate ions our body starts
absorbing chloride ions (Cl-).
• As a result the anion gap remains normal but the amount of
chloride ions in our body increases.
• This is also known as hyperchloremic acidosis.

24. HYPERCHLOREMIC ACIDOSIS
• This occurs basically because of two major
diseases:
• 1: severe diarrhea
• 2: renal tubular acidosis

25. SEVERE DIARRHEA
• It is when the bowel movement occurs more than 5 times a day.
• The person loses a great amount of bicarbonate ions in the stool
and therefore the amount of anions decreases.
• Bicarbonate ions are important for the blood buffer system.
• Due loss of these ions the buffer system cannot work properly thus
making the blood acidic.

26. RENAL TUBULAR ACIDOSIS
• Renal tubular acidosis (RTA) is a condition charac
terized by too much acid in the body due to a defe
ct in kidney function.
• The person’s blood becomes too acidic.
• Leads to growth retardation, kidney stones, bone
disease, chronic kidney disease, and possibly total
kidney failure.

27. • Kidneys maintain acid-base balance by excreting the acid ions and
reabsorbing the bicarbonate ions (base) into the body.
• This base neutralizes the acid produced by the body for the
digestion of food.

28. TYPES OF RTA.
• RTA type 1: distal RTA
• RTA type 2: proximal RTA
• RTA type 3: combined proximal and distal RTA
• RTA type 4: hyperkalemic

29. RTA TYPE 1
• In type 1 or Classical Distal Renal Tubular Acidosis (RTA), the lower part of the kidney tubules is
affected. This part is involved in the secretion of acid. Decreased secretion of acid leads to acidosis.
• It could be inherited due to abnormal genes or it could occur as a part of other diseases like lupus, liver
disease, sickle cell anemia, thyroid or parathyroid disease, or certain kidney diseases.
• A major consequence of classical distal RTA is a low blood potassium level.

30. • Some patients with defective genes and Type 1 RTA may develop
deafness.
• The patients also suffer from low potassium level. This could
cause complications like muscle weakness and paralysis, and
abnormal heart rhythm.
• Other complications include growth retardation, kidney stones,
kidney failure and bone disease (rickets in children and
Osteomalacia in adults).

31. RTA TYPE 2
• Also known as proximal RTA.
• This form of RTA occurs most frequently in children as part of a disorder called Fanconi's syndrome.
• The features of Fanconi's syndrome include the abnormal excretion of glucose, amino acids, citrate,
and phosphate into the urine, as well as vitamin D deficiency and low blood-potassium.

32. RTA TYPE 3
• Type 3 is rarely used as a classification because it is now thought to
be a combination of type 1 and type 2.

33. RTA TYPE 4
• Type 4 is also called hyperkalemic RTA and is caused by a generalized transport abnormality of the distal
tubule.
• The transport of electrolytes such as sodium, chloride, and potassium that normally occurs in the distal
tubule is impaired.
• This form is distinguished from classical distal RTA and proximal RTA because it results in high levels of
potassium in the blood instead of low levels.
• Either low potassium—hypokalemia—or high potassium—hyperkalemia—can be a problem because
potassium is important in regulating heart rate.

34. • Type 4 RTA occurs when blood levels of the hormone aldosterone are
low or when the kidneys do not respond to it.
• Aldosterone directs the kidneys to regulate the levels of sodium,
potassium, and chloride in the blood.
• Type 4 RTA also occurs when the tubule transport of electrolytes such
as sodium, chloride, and potassium is impaired due to an inherited
disorder or the use of certain drugs.

37. SIGNS AND SYMPTOMS
• Most common symptoms for
metabolic acidosis:

38. SIGNS AND SYMPTOMS
Lactic Acidosis Renal tubular acidosis
• Back pain
• Lower abdominal pain
• Painful urination
• Cloudy urine
• Nausea/vomiting
• Muscle weakness
• Muscle cramping in the back and abdomen

39. SIGNS AND SYMPTOMS
Ketoacidosis Hyperchloremic acidosis
• Weakness
• Headache
• Nausea
• Severe dehydration
• Cardiac arrest

40. • A pH under 7.1 is an emergency, due to the risk of abnormal
heart rhythms, 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 intoxication may be
present, consultation with the nephrology team is considered
useful, as dialysis may clear both the intoxication and the
acidosis.
TREATMENT

41. • Intravenous fluid to promote circulation
• Oxygen, delivered with a face mask or another way
• positive pressure ventilation to deliver oxygen to the lungs
• Vitamin therapy
• Hemodialysis with bicarbonate
• Individuals who experience lactic acidosis while exercising can stop what
they are doing, rehydrate by drinking water, and rest.

42. TREATMENT FOR DIABETIC KETOACIDOSIS

43. Fluid replacement: You'll receive fluids — either by mouth or through a
vein (intravenously) — until you're rehydrated. The fluids will replace those
you've lost through excessive urination, as well as help dilute the excess
sugar in your blood.
Electrolyte replacement. Electrolytes are minerals in your blood that carry
an electric charge, such as sodium, potassium and chloride. The absence of
insulin can lower the level of several electrolytes in your blood. You'll
receive electrolytes through a vein to help keep your heart, muscles and nerve
cells functioning normally.
Insulin therapy. Insulin reverses the processes that cause diabetic
ketoacidosis. In addition to fluids and electrolytes, you'll receive insulin
therapy — usually through a vein. When your blood sugar level falls to about

44. TREATMENT FOR RENAL TUBULAR
ACIDOSIS
Treatment consists of correction of pH and electrolyte balance with
alkali therapy. Failure to treat RTA in children slows growth.
Alkaline agents such as sodium bicarbonate, potassium bicarbonate, or
sodium citrate help achieve a relatively normal plasma bicarbonate
concentration . Potassium citrate can be substituted when
persistent hypokalemia is present or, because sodium increases calcium
excretion, when calcium calculi are present. Vitamin D and oral
calcium supplements may also be needed to help reduce skeletal
deformities resulting from osteomalacia or rickets

45. You can't always prevent metabolic acidosis, but there are things you can
do to lessen the chance of it happening.
• Drink plenty of water and non-alcoholic fluids. Your pee should be clear
or pale yellow.
• Limit alcohol. It can increase acid build up. It can also dehydrate you.
• Manage your diabetes, if you have it.
• Follow directions when you take your medications.
PREVENTION

46. WHOS AT RISK FOR METABOLIC
ACIDOSIS ??
• A high-fat diet, low in carbohydrates
• Kidney failure
• Being obese (this can make it harder to breathe)
• Dehydration (drink plenty of water)
• Aspirin or methanol poisoning
• Having diabetes (make sure it is controlled, to avoid ketoacidosis)
• Smoking (damages the lungs and makes breathing less efficient)
• Chronic alcohol abuse (drinking increases the build-up of lactic acid)