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Ethanol Toxicity
 A colorless, odorless, volatile liquid. It is fully
miscible in water and is lipid soluble.
 Readily diffuses across lipid membranes,
accounting for its ubiquitous multiorgan effects.
 Heavily consumed in intoxicating beverages.
 Used as an additive in gasoline, as a diluent or
solvent, in many household products, and in
pharmaceuticals
 Its metabolism follows first-order, then after
saturation, Zero-order kinetics.
Introduction
 CNS depression.
 Malnutrition by decreasing intake or by
altering absorption, metabolism and/or
utilization of nutrients.
 Elevation of endotoxin in the bloodstream.
 Induction of microsomal enzymes.
 Change in the redox potential of the cell.
 Production of toxic metabolite
(acetaldehyde).
 Oxidative stress.
Ethanol toxicity
 The unfavorable change in redox potential as a
consequence of ethanol metabolism contributes to the
development of metabolic disorders, increased collagen
and scar tissue formation associated with alcoholism, and a
clinical syndrome of alcoholic ketoacidosis.
 Acetaldehyde directly affects cardiac function, interferes
with phosphorylation, causes structural and functional
alterations in mitochondria and hepatocytes, and
inactivates coenzyme A.
 Acetaldehyde can react with intracellular proteins to
generate adducts.
 Ethanol metabolism through the hepatic CYP2E1 pathway
generates highly reactive oxygen radicals.
 The induction of hepatic enzymes by ethanol may increase
the toxicity of some substances like CCl4.
 chronic ethanol consumption may promote carcinogenesis
by:
 Production of acetaldehyde, a weak mutagen and
carcinogen.
 Induction of CYP2E1 and its associated oxidative
stressors and conversion of procarcinogens to
carcinogens.
 Depletion of S-adenosylmethionine and, consequently,
induction of global DNA hypomethylation.
 Increased production of inhibitory guanine nucleotide
regulatory proteins and components of extracellular
signal-regulated kinase-mitogen-activated protein
kinase signaling.
 Accumulation of iron and associated oxidative stress.
 Inactivation of the tumor suppressor gene BRCA1 and
increased estrogen responsiveness (primarily in the
breast).
 Impairment of retinoic acid metabolism.
Clinical Features
 Inebriation with variable signs that differ
according to the degree of intoxication.
 Loss of respiratory reflexes with increased
intoxication, coma and maybe death.
 Flushed facies, hypothermia, diaphoresis,
vomiting and hypotension.
 Dysrhythmias .
 Diplopia, visual disturbances, and nystagmus.
 decreased serum ionized magnesium
concentrations.
 Myocardial ischemia in susceptible patients.
 Ethanol-induced seizures.
 Immunoassay or gas chromatography is
commonly used for determination of ethanol in
liquid specimens in most hospitals.
 The usual sample is serum, rarely plasma. Whole
blood is used in forensic determination of BAL.
 Breath ethanol analyzers make use of
electrochemical sensors for ethanol oxidation
or infrared spectral analysis for ethanol
determination.
 Ethanol-saliva testing is a promising alternative
to breath ethanol analysis in the rapid
assessment of blood ethanol levels in patients.
 Blood tests that should be considered for patients
with ethanol intoxication or alcoholic ketoacidosis:
 CBC.
 Electrolytes.
 BUN.
 Creatinine.
 Ketones.
 Acetone.
 Lipase.
 Liver enzymes.
 Prothrombin time.
 Ammonia.
 Calcium.
 Magnesium.
 gastrointestinal decontamination may be considered in
case of delayed absorption or recent ingestion.
 endotracheal intubation and ventilatory support in
case of severe respiratory depression.
 Abnormal vital signs should be addressed and
stabilized.
 Patients who are combative and violent should be both
physically and then chemically restrained with a
benzodiazepine.
 The patient's fluid and electrolyte status should be
assessed and abnormalities corrected.
 Hemodialysis is an effective means of enhancing the
systemic elimination of ethanol .
Indications for hospital admission:
 persistently abnormal vital signs.
 persistently abnormal mental status, with
or without an obvious cause.
 mixed overdose with other concerning
xenobiotics.
 concomitant serious trauma.
 consequential ethanol withdrawal.
 associated serious disease process, such
as pancreatitis or gastrointestinal
hemorrhage.
Ethanol-induced
Hypoglycemia
 Occurs when ethanol metabolism
provides a high cellular reduction-to-
oxidation (redox) ratio. This redox state
favors the conversion of pyruvate to
lactate, diverting pyruvate from
gluconeogenesis.
 Hypoglycemia associated with ethanol
consumption usually occurs in
malnourished chronic alcoholics and
children
Ethanol toxicity
 Clinical features include: altered
consciousness, hypothermia and
tachypnea, positive blood ethanol
concentration, ketonuria without
glucosuria, and mild acidosis.
 Management of ethanol-induced
hypoglycemia is similar to other causes
of hypoglycemia.
Alcoholic Ketoacidosis
 Ethanol metabolism generates NADH, resulting
in an excess of reducing potential. This high
redox state favors the conversion of pyruvate
to lactate.
 The body increases fatty acid metabolism as
an alternative source of energy
 This response is mediated by a decrease in
insulin and an increased secretion of glucagon,
catecholamines, growth hormone, and cortisol.
 Most of the acetoacetate is reduced to
β-hydroxybutyrate as a consequence of
the excess reducing potential.
 Volume depletion contributes to the
acidosis.
 Lactic acidosis caused by hypoperfusion
or infection may coexist with the
underlying ketoacidosis.
Ethanol toxicity
 Patients are typically chronic ethanol
users, presenting after a few days of
“binge” drinking.
 starved because of cessation in oral
intake as a consequence of binging
itself, or because of:
Nausea.
 Vomiting.
 Abdominal pain from gastritis, hepatitis,
pancreatitis, or a concurrent acute illness.
 Underlying medical conditions may be present.
 Alcohol withdrawal may develop.
 Diagnosis of AKA is a diagnosis of exclusion.
 blood ethanol concentration is usually low or
undetectable.
 elevated anion gap metabolic acidosis with a
serum lactate concentration insufficient to
account for the gap.
 some patients will have a normal arterial pH or
be alkalemic.
 Reliance on the nitroprusside test alone may
underestimate the severity of ketoacidosis.
 Treatment should begin with adequate
crystalloid fluid replacement dextrose
and thiamine.
 Supplemental multivitamins, potassium,
and magnesium should be instituted on
an individual basis.
 During the recovery, β-hydroxybutyrate is
converted to acetoacetate.
 Mortality is rare from either ethanol-
induced ketoacidosis or hypoglycemia.

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Ethanol toxicity

  • 2.  A colorless, odorless, volatile liquid. It is fully miscible in water and is lipid soluble.  Readily diffuses across lipid membranes, accounting for its ubiquitous multiorgan effects.  Heavily consumed in intoxicating beverages.  Used as an additive in gasoline, as a diluent or solvent, in many household products, and in pharmaceuticals  Its metabolism follows first-order, then after saturation, Zero-order kinetics. Introduction
  • 3.  CNS depression.  Malnutrition by decreasing intake or by altering absorption, metabolism and/or utilization of nutrients.  Elevation of endotoxin in the bloodstream.  Induction of microsomal enzymes.  Change in the redox potential of the cell.  Production of toxic metabolite (acetaldehyde).  Oxidative stress.
  • 5.  The unfavorable change in redox potential as a consequence of ethanol metabolism contributes to the development of metabolic disorders, increased collagen and scar tissue formation associated with alcoholism, and a clinical syndrome of alcoholic ketoacidosis.  Acetaldehyde directly affects cardiac function, interferes with phosphorylation, causes structural and functional alterations in mitochondria and hepatocytes, and inactivates coenzyme A.  Acetaldehyde can react with intracellular proteins to generate adducts.  Ethanol metabolism through the hepatic CYP2E1 pathway generates highly reactive oxygen radicals.  The induction of hepatic enzymes by ethanol may increase the toxicity of some substances like CCl4.
  • 6.  chronic ethanol consumption may promote carcinogenesis by:  Production of acetaldehyde, a weak mutagen and carcinogen.  Induction of CYP2E1 and its associated oxidative stressors and conversion of procarcinogens to carcinogens.  Depletion of S-adenosylmethionine and, consequently, induction of global DNA hypomethylation.  Increased production of inhibitory guanine nucleotide regulatory proteins and components of extracellular signal-regulated kinase-mitogen-activated protein kinase signaling.  Accumulation of iron and associated oxidative stress.  Inactivation of the tumor suppressor gene BRCA1 and increased estrogen responsiveness (primarily in the breast).  Impairment of retinoic acid metabolism.
  • 7. Clinical Features  Inebriation with variable signs that differ according to the degree of intoxication.  Loss of respiratory reflexes with increased intoxication, coma and maybe death.  Flushed facies, hypothermia, diaphoresis, vomiting and hypotension.  Dysrhythmias .  Diplopia, visual disturbances, and nystagmus.  decreased serum ionized magnesium concentrations.  Myocardial ischemia in susceptible patients.  Ethanol-induced seizures.
  • 8.  Immunoassay or gas chromatography is commonly used for determination of ethanol in liquid specimens in most hospitals.  The usual sample is serum, rarely plasma. Whole blood is used in forensic determination of BAL.  Breath ethanol analyzers make use of electrochemical sensors for ethanol oxidation or infrared spectral analysis for ethanol determination.  Ethanol-saliva testing is a promising alternative to breath ethanol analysis in the rapid assessment of blood ethanol levels in patients.
  • 9.  Blood tests that should be considered for patients with ethanol intoxication or alcoholic ketoacidosis:  CBC.  Electrolytes.  BUN.  Creatinine.  Ketones.  Acetone.  Lipase.  Liver enzymes.  Prothrombin time.  Ammonia.  Calcium.  Magnesium.
  • 10.  gastrointestinal decontamination may be considered in case of delayed absorption or recent ingestion.  endotracheal intubation and ventilatory support in case of severe respiratory depression.  Abnormal vital signs should be addressed and stabilized.  Patients who are combative and violent should be both physically and then chemically restrained with a benzodiazepine.  The patient's fluid and electrolyte status should be assessed and abnormalities corrected.  Hemodialysis is an effective means of enhancing the systemic elimination of ethanol .
  • 11. Indications for hospital admission:  persistently abnormal vital signs.  persistently abnormal mental status, with or without an obvious cause.  mixed overdose with other concerning xenobiotics.  concomitant serious trauma.  consequential ethanol withdrawal.  associated serious disease process, such as pancreatitis or gastrointestinal hemorrhage.
  • 12. Ethanol-induced Hypoglycemia  Occurs when ethanol metabolism provides a high cellular reduction-to- oxidation (redox) ratio. This redox state favors the conversion of pyruvate to lactate, diverting pyruvate from gluconeogenesis.  Hypoglycemia associated with ethanol consumption usually occurs in malnourished chronic alcoholics and children
  • 14.  Clinical features include: altered consciousness, hypothermia and tachypnea, positive blood ethanol concentration, ketonuria without glucosuria, and mild acidosis.  Management of ethanol-induced hypoglycemia is similar to other causes of hypoglycemia.
  • 15. Alcoholic Ketoacidosis  Ethanol metabolism generates NADH, resulting in an excess of reducing potential. This high redox state favors the conversion of pyruvate to lactate.  The body increases fatty acid metabolism as an alternative source of energy  This response is mediated by a decrease in insulin and an increased secretion of glucagon, catecholamines, growth hormone, and cortisol.
  • 16.  Most of the acetoacetate is reduced to β-hydroxybutyrate as a consequence of the excess reducing potential.  Volume depletion contributes to the acidosis.  Lactic acidosis caused by hypoperfusion or infection may coexist with the underlying ketoacidosis.
  • 18.  Patients are typically chronic ethanol users, presenting after a few days of “binge” drinking.  starved because of cessation in oral intake as a consequence of binging itself, or because of: Nausea.  Vomiting.  Abdominal pain from gastritis, hepatitis, pancreatitis, or a concurrent acute illness.
  • 19.  Underlying medical conditions may be present.  Alcohol withdrawal may develop.  Diagnosis of AKA is a diagnosis of exclusion.  blood ethanol concentration is usually low or undetectable.  elevated anion gap metabolic acidosis with a serum lactate concentration insufficient to account for the gap.  some patients will have a normal arterial pH or be alkalemic.  Reliance on the nitroprusside test alone may underestimate the severity of ketoacidosis.
  • 20.  Treatment should begin with adequate crystalloid fluid replacement dextrose and thiamine.  Supplemental multivitamins, potassium, and magnesium should be instituted on an individual basis.  During the recovery, β-hydroxybutyrate is converted to acetoacetate.  Mortality is rare from either ethanol- induced ketoacidosis or hypoglycemia.