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Published on May 9, 2009

Author: deepak15

Source: slideshare.net

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lactic acidosis
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Lactic Acidosis Dr. tongjun Ma Emergency department of Tianjin Medical University General Hospital

Introduction LA are important in emergency medicine. common complication of many severe illness including sepsis , cardiac failure, respiratory failure, hepatic failure, cancer, AIDS, seizure, poisoning and drug therapy change into multiple organ dysfunction syndrome and the mortality rate is more than 75%

LA are important in emergency medicine.

common complication of many severe illness including sepsis , cardiac failure, respiratory failure, hepatic failure, cancer, AIDS, seizure, poisoning and drug therapy

change into multiple organ dysfunction syndrome and the mortality rate is more than 75%

Content Definition Pathophysiology Etiology and categories Manifestation Diagnosis Treatment Prognosis 8. D- Lactic Acidosis

Definition

Pathophysiology

Etiology and categories

Manifestation

Diagnosis

Treatment

Prognosis

8. D- Lactic Acidosis

1. Definition LA is a metabolic acidosis caused by lactic acid accumulation, pH ↓ + Lactate↑ plasma lactate concentration Normal: 0.5~1.5 mmol/L, average: 1 mmol/L Hyperlactatemia: 2~5 mmol/L Lactic acidosis: >5 mmol/L

LA is a metabolic acidosis caused by lactic acid accumulation, pH ↓ + Lactate↑

plasma lactate concentration

Normal: 0.5~1.5 mmol/L, average: 1 mmol/L

Hyperlactatemia: 2~5 mmol/L

Lactic acidosis: >5 mmol/L

2. Pathophysiology (1) Lactic acid production Lactate is a key substrate which is simultaneously produced and used by the body tissues All tissues can produce lactic acid, brain, erythrocytes and skeletal muscle are the main organs Basal lactate production is high, about 1 mmol/kg per hour(15~20 mmol/kg•d, or 1400 mmol per day for a 70 kg person) Under some conditions, the production rate can increase 50 times. In severe exercise, lactate levels can rise to very high levels eg up to 30 mmol/L.

Lactate is a key substrate which is simultaneously produced and used by the body tissues

All tissues can produce lactic acid, brain, erythrocytes and skeletal muscle are the main organs

Basal lactate production is high, about 1 mmol/kg per hour(15~20 mmol/kg•d, or 1400 mmol per day for a 70 kg person)

Under some conditions, the production rate can increase 50 times. In severe exercise, lactate levels can rise to very high levels eg up to 30 mmol/L.

Main pathways of lactate metabolism. lactic acid is a metabolic dead-end Pyruvate is the sole immediate precursor Pyruvate is the only route of metabolic transformation

Main pathways of lactate metabolism.

lactic acid is a metabolic dead-end

Pyruvate is the sole immediate precursor

Pyruvate is the only route of metabolic transformation

There is a balance between pyruvate and lactic acid catalyzed by LDH (lactate dehydrogenase) When concentration of pyruvate or NADH increase , the concentration of lactic acid will increase Under normal conditions, the lactate/pyruvate ratio ranges from 4:1 to 10:1

There is a balance between pyruvate and lactic acid

catalyzed by LDH (lactate dehydrogenase)

When concentration of pyruvate or NADH increase , the concentration of lactic acid will increase

Under normal conditions, the lactate/pyruvate ratio ranges from 4:1 to 10:1

From glucose and alanine The largest part originates from glucose (or glycogen) via the reactions of glycolysis A smaller part originates from transamination of alanine

From glucose and alanine

The largest part originates from glucose (or glycogen) via the reactions of glycolysis

A smaller part originates from transamination of alanine

Pyruvate can have several metabolic fates oxidation in the tricarboxylic acid cycle for energy production transformation into glucose via the gluconeogenesis pathways

Pyruvate can have several metabolic fates

oxidation in the tricarboxylic acid cycle for energy production

transformation into glucose via the gluconeogenesis pathways

Under aerobic conditions, pyruvate change into acetyl CoA. Acetyl CoA change into CO 2 and NADH through the tricarboxylic acid cycle in the matrix of the mitochondria. Under anaerobic conditions, pyruvate change into lactic acid in the cellular cytosol.

Under aerobic conditions, pyruvate change into acetyl CoA. Acetyl CoA change into CO 2 and NADH through the tricarboxylic acid cycle in the matrix of the mitochondria.

Under anaerobic conditions, pyruvate change into lactic acid in the cellular cytosol.

2. Pathophysiology (1) Lactic acid production Pathological lactate production occurs when inadequate tissue oxygen supply defective pyruvate clearance increased pyruvate or NADH production

Pathological lactate production occurs when

inadequate tissue oxygen supply

defective pyruvate clearance

increased pyruvate or NADH production

2. Pathophysiology (2) Lactic acid destruction The half-life of serum lactate is about 60 minutes Cleared in three ways Gluconeogenesis Oxidation Excretion renal threshold is 6~10 mmol/L

The half-life of serum lactate is about 60 minutes

Cleared in three ways

Gluconeogenesis

Oxidation

Excretion

renal threshold is 6~10 mmol/L

2. Pathophysiology (2) Lactic acid destruction Lactate is utilized mainly by the liver and kidney. About 65% of lactate was cleared by liver. The kidneys can remove 10~20% of the total lactate.

Lactate is utilized mainly by the liver and kidney.

About 65% of lactate was cleared by liver.

The kidneys can remove 10~20% of the total lactate.

2. Pathophysiology (3) Mechanisms Lactic acidosis can occur due to excessive tissue lactate production impaired hepatic metabolism In most clinical cases both processes are contributing to the development of the acidosis.

Lactic acidosis can occur due to

excessive tissue lactate production

impaired hepatic metabolism

In most clinical cases both processes are contributing to the development of the acidosis.

3. Etiology and Categories Two types Type A obvious tissue hypoxia Common Type B tissue hypoxia is not apparent Rare Three subtypes: B1, B2, B3 developed by Cohen and Woods in 1976 and it is widely accepted now

Two types

Type A

obvious tissue hypoxia

Common

Type B

tissue hypoxia is not apparent

Rare

Three subtypes: B1, B2, B3

developed by Cohen and Woods in 1976 and it is widely accepted now

3. Etiology and Categories: type A Tissue hypoxaemia severe anemia carbon monoxide poisoning Tissue hypoperfusion with clinical evidence Hypotension cyanosis cool and clammy extremities

Tissue hypoxaemia

severe anemia

carbon monoxide poisoning

Tissue hypoperfusion

with clinical evidence

Hypotension

cyanosis

cool and clammy extremities

3.Etiology and Categories 76 years old, female chief complain: sudden severe pain across her mid-abdomen after dinner and moved to her left flank, vomiting past history: hypertension, kidney stone Laboratory data: WBC count 11000 , sodium 140 mEq/L, serum creatinine 1mg/dl, urine WBC +, urine ketones “trace” Ultrasound: hydronephrosis After admission, she developed shaking chills, T 39℃ , blood pressure became progressively lower and was hard to detect several hours later serum lactate level was 7.4 , pH 7.24 Diagnosis: Urinary tract infection, septic shock, LA

76 years old, female

chief complain: sudden severe pain across her mid-abdomen after dinner and moved to her left flank, vomiting

past history: hypertension, kidney stone

Laboratory data: WBC count 11000 , sodium 140 mEq/L, serum creatinine 1mg/dl, urine WBC +, urine ketones “trace”

Ultrasound: hydronephrosis

After admission, she developed shaking chills, T 39℃ , blood pressure became progressively lower and was hard to detect several hours later

serum lactate level was 7.4 , pH 7.24

Diagnosis: Urinary tract infection, septic shock, LA

3. Etiology and Categories (2) type B1 B1:with underlying disease liver diseases, renal failure ( glyconeogenesis) malignancy (eg, leukemia, lymphoma, lung cancer) Malignant cells produce more lactate Seizures, severe asthma (enhanced metabolic rate , increased Oxygen Consumption )

B1:with underlying disease

liver diseases, renal failure ( glyconeogenesis)

malignancy (eg, leukemia, lymphoma, lung cancer)

Malignant cells produce more lactate

Seizures, severe asthma (enhanced metabolic rate , increased Oxygen Consumption )

3. Etiology and Categories (2) type B1 B1:with underlying disease thiamine deficiency coenzyme of pyruvate dehydrogenase, can lead to defective pyruvate metabolism Patients receiving total parenteral nutrition (TPN) without intravenous multivitamins (MVIs) supplementation are at risk for thiamine deficiency and life-threatening complications associated with severe deficiency of thiamine

B1:with underlying disease

thiamine deficiency

coenzyme of pyruvate dehydrogenase, can lead to defective pyruvate metabolism

Patients receiving total parenteral nutrition (TPN) without intravenous multivitamins (MVIs) supplementation are at risk for thiamine deficiency and life-threatening complications associated with severe deficiency of thiamine

3. Etiology and Categories (2) type B1 B1:with underlying disease thiamine deficiency a 32-year-old man underwent a total coloproctectomy with ileostomy as treatment for fulminant ulcerative colitis. TPN was initiated immediately postoperatively and included 2087 ml per day of amino acids (92 g) and dextrose (382.5 g) with 21 g fat emulsion, electrolytes, and minerals per day; however, no MVIs were added to the solution.

B1:with underlying disease

thiamine deficiency

a 32-year-old man underwent a total coloproctectomy with ileostomy as treatment for fulminant ulcerative colitis.

TPN was initiated immediately postoperatively and included 2087 ml per day of amino acids (92 g) and dextrose (382.5 g) with 21 g fat emulsion, electrolytes, and minerals per day; however, no MVIs were added to the solution.

3. Etiology and Categories (2) type B1 B1:with underlying disease thiamine deficiency Attempts to introduce clear liquids orally on 4th and fifth days after operation were unsuccessful because of persistent severe anorexia, nausea, and vomiting. 7 days after operation ,an upper gastrointestinal barium imaging study revealed delayed transit time, but no mechanical obstruction.

B1:with underlying disease

thiamine deficiency

Attempts to introduce clear liquids orally on 4th and fifth days after operation were unsuccessful because of persistent severe anorexia, nausea, and vomiting.

7 days after operation ,an upper gastrointestinal barium imaging study revealed delayed transit time, but no mechanical obstruction.

3. Etiology and Categories (2) type B1 B1:with underlying disease thiamine deficiency 19 days after operation, TPN was continued without MVIs. the patient was lethargic and weak, and abnormal laboratory findings included severe acidosis :pH 6.87 ; HCO3, 5 mEq/L ; pCO2, 28 mm Hg pO2, 131 mm Hg ; and serum lactic acid of 16 mmol/L serum ketones were negative. Lactic acidosis of unknown etiology was diagnosed.

B1:with underlying disease

thiamine deficiency

19 days after operation, TPN was continued without MVIs. the patient was lethargic and weak, and abnormal laboratory findings included severe acidosis :pH 6.87 ; HCO3, 5 mEq/L ; pCO2, 28 mm Hg pO2, 131 mm Hg ; and serum lactic acid of 16 mmol/L serum ketones were negative.

Lactic acidosis of unknown etiology was diagnosed.

3. Etiology and Categories (2) type B1 B1:with underlying disease thiamine deficiency During the next 8 hours, 600 mEq/L of bicarbonate was administered with only modest elevation of pH (to 7.20) . Because the patient's clinical condition continued to deteriorate, an exploratory laparotomy was performed; however, no focus of infection or bowel necrosis was found.

B1:with underlying disease

thiamine deficiency

During the next 8 hours, 600 mEq/L of bicarbonate was administered with only modest elevation of pH (to 7.20) .

Because the patient's clinical condition continued to deteriorate, an exploratory laparotomy was performed; however, no focus of infection or bowel necrosis was found.

3. Etiology and Categories (2) type B1 B1:with underlying disease thiamine deficiency An analysis for serum thiamine measured the lowest detectable level of 0.2 mg/dL (normal: 1.1-1.6 mg/dL), and 400 mg of thiamine was administered intravenously. Two hours later, a blood gas specimen contained a serum pH of 7.50 and an HCO3 of 11.3 mEq/L. Acid/base and clinical status improved; a second dose of 400 mg thiamine was administered intravenously, and pH, pCO2, and HCO3 levels returned to normal.

B1:with underlying disease

thiamine deficiency

An analysis for serum thiamine measured the lowest detectable level of 0.2 mg/dL (normal: 1.1-1.6 mg/dL), and 400 mg of thiamine was administered intravenously.

Two hours later, a blood gas specimen contained a serum pH of 7.50 and an HCO3 of 11.3 mEq/L. Acid/base and clinical status improved; a second dose of 400 mg thiamine was administered intravenously, and pH, pCO2, and HCO3 levels returned to normal.

3.Etiology and Categories (3)type B2 B2: drugs and toxins Biguanides phenformin, metformin Antihyperglycemic agent, used to treat type 2 diabetes (overweight, obesity) decrease gluconeogenesis probably interferes with mitochondrial function

B2: drugs and toxins

Biguanides

phenformin, metformin

Antihyperglycemic agent, used to treat type 2 diabetes (overweight, obesity)

decrease gluconeogenesis

probably interferes with mitochondrial function

3.Etiology and Categories (3)type B2 B2: drugs and toxins biguanides The estimated rate of phenformin-associated lactic acidosis ranged from 40 to 64 cases per 100,000 person-years, which has a 50% fatality rate. In 1977, phenformin was banned by the FDA. With the Cessation of phenformin therapy, lactic acidosis in diabetes become uncommon

B2: drugs and toxins

biguanides

The estimated rate of phenformin-associated lactic acidosis ranged from 40 to 64 cases per 100,000 person-years, which has a 50% fatality rate.

In 1977, phenformin was banned by the FDA.

With the Cessation of phenformin therapy, lactic acidosis in diabetes become uncommon

3.Etiology and Categories (3)type B2 B2: drugs and toxins biguanides The lactic acidosis rate in metformin users is much lower, 9 cases per 100,000 person-years. Metformin is contraindicated because of an increased risk of lactic acidosis : elevated serum creatinine levels (> 1.5 mg/dl for males and > 1.4 mg/dl for females) hepatic impairment hypoxic states (shock, severe heart failure) excessive alcohol intake

B2: drugs and toxins

biguanides

The lactic acidosis rate in metformin users is much lower, 9 cases per 100,000 person-years.

Metformin is contraindicated because of an increased risk of lactic acidosis :

elevated serum creatinine levels (> 1.5 mg/dl for males and > 1.4 mg/dl for females)

hepatic impairment

hypoxic states (shock, severe heart failure)

excessive alcohol intake

3.Etiology and Categories (3)type B2 B2: drugs and toxins biguanides Special X-ray tests that require the injection of contrast media often cause kidneys to be temporarily less efficient in clearing lactic acid To lessen the risk for lactic acidosis, metformin is stopped before the examination and restarted about 48 hours afterwards if the renal function is normal.

B2: drugs and toxins

biguanides

Special X-ray tests that require the injection of contrast media often cause kidneys to be temporarily less efficient in clearing lactic acid

To lessen the risk for lactic acidosis, metformin is stopped before the examination and restarted about 48 hours afterwards if the renal function is normal.

3.Etiology and Categories (3)type B2 B2: drugs and toxins anti-retrovirus drugs In 1996, AIDS patients were treat ed with anti-retrovirus drugs. s hortly thereafter, reports of fatal lactic acidosis began to appear .

B2: drugs and toxins

anti-retrovirus drugs

In 1996, AIDS patients were treat ed with anti-retrovirus drugs.

s hortly thereafter, reports of fatal lactic acidosis began to appear .

3.Etiology and Categories (3)type B2 B2: drugs and toxins anti-retrovirus drugs 20% ~ 80% of individuals develop some metabolic abnormalities Changes in body habitus ( Central obesity) increased plasma lipids glu cose intolerance and insulin resistance h yperlactatemia and lactic acidosis

B2: drugs and toxins

anti-retrovirus drugs

20% ~ 80% of individuals develop some metabolic abnormalities

Changes in body habitus ( Central obesity)

increased plasma lipids

glu cose intolerance and insulin resistance

h yperlactatemia and lactic acidosis

3.Etiology and Categories (3)type B2 B2: drugs and toxins anti-retrovirus drugs m itochondrial toxicity m itochondria has his own DNA and h ave their own DNA replicating enzyme incidence rate : Stavudine( d4T ) > zidovudine( AZT ) / didanosine ( ddI ) > lamivudine ( 3TC )

B2: drugs and toxins

anti-retrovirus drugs

m itochondrial toxicity

m itochondria has his own DNA and h ave their own DNA replicating enzyme

incidence rate : Stavudine( d4T ) > zidovudine( AZT ) / didanosine ( ddI ) > lamivudine ( 3TC )

3.Etiology and Categories (3)type B2 B2: drugs and toxins alcohols and glycols (methanol, propylene glycol) Overproduction of NADH in the liver Acetaminophen intoxication inhibiting mitochondrial respiration Cocaine intoxication seizures or other violent muscle activity , systemic hypoxia

B2: drugs and toxins

alcohols and glycols (methanol, propylene glycol)

Overproduction of NADH in the liver

Acetaminophen intoxication

inhibiting mitochondrial respiration

Cocaine intoxication

seizures or other violent muscle activity , systemic hypoxia

3.Etiology and Categories (4)type B3 B3: inborn errors of metabolism Glyconeogenesis enzyme deficiency glucose-6-phosphatase fructose-1,6-diphosphatase pyruvate carboxylase pyruvate dehydrogenase MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes) mutation in mitochondrial DNA gene

B3: inborn errors of metabolism

Glyconeogenesis enzyme deficiency

glucose-6-phosphatase

fructose-1,6-diphosphatase

pyruvate carboxylase

pyruvate dehydrogenase

MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes)

mutation in mitochondrial DNA gene

4.Manifestation Hyperventilation ,dyspnea Cardiovascular compromise is a frequent finding explaining many of the associated signs, which include cyanosis, cold extremities, tachycardia, hypotension, lethargy, stupor or coma pH , HC0 3 - ,AG , lactate

Hyperventilation ,dyspnea

Cardiovascular compromise is a frequent finding explaining many of the associated signs, which include cyanosis, cold extremities, tachycardia, hypotension,

lethargy, stupor or coma

pH , HC0 3 - ,AG , lactate

5.Diagnosis History Manifestation Laboratory test Exclude: DKA Uremia Intoxication: such as salicylates , by toxicology screen

History

Manifestation

Laboratory test

Exclude:

DKA

Uremia

Intoxication: such as salicylates , by toxicology screen

5.Diagnosis- Laboratory test In critically ill patients, arterial lactate concentrations are essentially equivalent to those measured in blood sampled from central venous or from pulmonary artery catheter. This is however not true for lactate measurements performed during cardiopulmonary resuscitation, where arterial concentrations are less than venous concentrations.

In critically ill patients, arterial lactate concentrations are essentially equivalent to those measured in blood sampled from central venous or from pulmonary artery catheter.

This is however not true for lactate measurements performed during cardiopulmonary resuscitation, where arterial concentrations are less than venous concentrations.

5.Diagnosis- Laboratory test Serial determinations of lactate plasma concentration give useful information on the evolution of the metabolic processes more powerful predictors of clinical outcome than a single determination of lactatemia. blood lactate must be measured as quickly as possible should be brought to the lab on ice

Serial determinations of lactate plasma concentration

give useful information on the evolution of the metabolic processes

more powerful predictors of clinical outcome than a single determination of lactatemia.

blood lactate must be measured as quickly as possible

should be brought to the lab on ice

6.Treatment (1) type A improve tissue oxygenation is the only effective treatment Maintenance of airway patency and oxygen delivery 100% oxygen by mask Intubate if the patient is unconscious, in severe shock, or otherwise in unstable condition.

improve tissue oxygenation is the only effective treatment

Maintenance of airway patency and oxygen delivery

100% oxygen by mask

Intubate if the patient is unconscious, in severe shock, or otherwise in unstable condition.

6.Treatment (1) type A restoration of the circulating fluid volume Establish an intravenous line, Give a fluid bolus if the patient has tachycardia, hypotension or other signs of poor tissue perfusion improve cardiac function, such dobutamine Monitor the cardiac rhythm Acidosis may predisposes to dysrhythmias Empirical antibiotic

restoration of the circulating fluid volume

Establish an intravenous line, Give a fluid bolus if the patient has tachycardia, hypotension or other signs of poor tissue perfusion

improve cardiac function, such dobutamine

Monitor the cardiac rhythm

Acidosis may predisposes to dysrhythmias

Empirical antibiotic

6. Treatment (2) Type B B1: identification of the primary illness and correction thiamine (50~100 mg IV followed by 50 mg/d orally for 1~2 wk) may be dramatic and potentially life saving chemotherapy for malignant disorders B2: discontinuation of causative drugs

B1: identification of the primary illness and correction

thiamine (50~100 mg IV followed by 50 mg/d orally for 1~2 wk) may be dramatic and potentially life saving

chemotherapy for malignant disorders

B2: discontinuation of causative drugs

6.Treatment (3) Alkalinization Controversial No Prospective studies have shown improved hemodynamics or outcomes The hydrogen ion may be produced at 72 mmol/ min, alkaline therapy ’s value is doubtful (need 120ml/min 5%HCO 3 ) Most studies show no change or decrease in intracellular pH Carbon dioxide leads to subsequent intracellular acidosis

Controversial

No Prospective studies have shown improved hemodynamics or outcomes

The hydrogen ion may be produced at 72 mmol/ min, alkaline therapy ’s value is doubtful (need 120ml/min 5%HCO 3 )

Most studies show no change or decrease in intracellular pH

Carbon dioxide leads to subsequent intracellular acidosis

6.Treatment (3) Alkalinization Controversial may cause respiratory failure Metabolic alkalosis The administration of HCO 3 - has been observed to reduce cardiac performance in patients with cardiac arrest, CHF, and AMI.

Controversial

may cause respiratory failure

Metabolic alkalosis

The administration of HCO 3 - has been observed to reduce cardiac performance in patients with cardiac arrest, CHF, and AMI.

6.Treatment (3) Alkalinization Conclusion In cardiopulmonary resuscitation, sodium bicarbonate generally is not recommended Toxic etiologies of lactic acidosis may use intravenous NaHCO 3 - to keep the pH above 7.2

Conclusion

In cardiopulmonary resuscitation, sodium bicarbonate generally is not recommended

Toxic etiologies of lactic acidosis may use

intravenous NaHCO 3 - to keep the pH above 7.2

6.Treatment (4) Hemodialysis Dialysis or continuous hemofiltration Consider hemodialysis in association with ethylene glycol and methanol poisoning. useful mode of therapy when severe lactic acidosis exists in conjunction with renal failure or congestive heart failure.

Dialysis or continuous hemofiltration

Consider hemodialysis in association with ethylene glycol and methanol poisoning.

useful mode of therapy when severe lactic acidosis exists in conjunction with renal failure or congestive heart failure.

7. Prognosis the primary disorder is determinant mortality rates may be 60%~80%,. arterial lactate values of more than 5 mmlo/l on admission to ICU were associated with a mortality rate exceeding 80% at 30 days lactate concentration >15 mmol/l, patients rarely survive

the primary disorder is determinant

mortality rates may be 60%~80%,.

arterial lactate values of more than 5 mmlo/l on admission to ICU were associated with a mortality rate exceeding 80% at 30 days

lactate concentration >15 mmol/l, patients rarely survive

8. D- Lactic Acidosi s Rare D-Lactate made by bacteria from glucose and carbohydrate L-Lactate normally produced in human beings Lactate dehydrogenase can effectively metabolize only L-lactate, so if D-Lactate was absorbed, it will accumulate in blood occur in patients with small bowel resections Unexplained metabolic acidosis , AG increased Treatment fluid resuscitation restriction of simple sugars NaHCO 3 administration as necessary

Rare

D-Lactate made by bacteria from glucose and carbohydrate

L-Lactate normally produced in human beings

Lactate dehydrogenase can effectively metabolize only L-lactate, so if D-Lactate was absorbed, it will accumulate in blood

occur in patients with small bowel resections

Unexplained metabolic acidosis , AG increased

Treatment

fluid resuscitation

restriction of simple sugars

NaHCO 3 administration as necessary

Thank you

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