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Background
Ethanol is a 2-carbon–chain alcohol; the chemical formula is CH2 CH3 OH. It is ubiquitous
throughout the world and is a leading cause of morbidity across cultures. Ethanol is the most
common psychoactive drug used by children and adolescents in the United States and is one of
the most commonly abused drugs in the world. In a 1995 questionnaire study of high-school
students, 88% admitted to using ethanol, and 37% admitted to consuming 5 or more drinks in
one night during the previous 2 weeks.
Pathophysiology
Ethanol has a volume of distribution (0.6 L/kg) and is readily distributed throughout the body.
The primary route of absorption is oral, although it can be absorbed by inhalation and even
percutaneously.
The pathway of ethanol metabolism. Disulfiram reduces the rate of oxidation of acetaldehyde by
competing with the cofactor nicotinamide adenine dinucleotide (NAD) for binding sites on aldehyde
dehydrogenase (ALDH).
Ethanol exerts its actions through several mechanisms. For instance, it binds directly to the
gamma-aminobutyric acid (GABA) receptor in the CNS and causes sedative effects similar to
those of benzodiazepines, which bind to the same GABA receptor. Furthermore, ethanol is also
an N -methyl-D-aspartate (NMDA) glutamate antagonist in the CNS. Ethanol also has direct
effects on cardiac muscle, thyroid tissue, and hepatic tissue. However, the exact molecular
targets of ethanol and the mechanism of action are still the subjects of ongoing research.1
Ethanol is rapidly absorbed, and peak serum concentrations typically occur 30-60 minutes after
ingestion. Its absorption into the body starts in the oral mucosa and continues in the stomach
and intestine. Both high and low concentrations of ethanol are slowly absorbed; the co-ingestion
of food also slows absorption.
In young children, ethanol causes hypoglycemia and hypoglycemic seizures; these
complications are not as common in older patients. Hypoglycemia occurs secondary to
ethanol's inhibition of gluconeogenesis and secondary to the relatively smaller glycogen stores
in the livers of young children. In toddlers who have not eaten for several hours, even small
quantities of ethanol can cause hypoglycemia.
Ethanol is primarily metabolized in the liver. Approximately 90% of an ethanol load is broken
down in the liver; the remainder is eliminated by the kidneys and lungs. In children, ethanol is
cleared by the liver at the rate of approximately 30 mg/dL/h, which is more rapid than the
clearance rate in adults.
In the liver, ethanol is broken down into acetaldehyde by alcohol dehydrogenase (ADH). Then, it
is further broken down to acetic acid by acetaldehyde dehydrogenase. Acetic acid is fed into the
Krebs cycle and is ultimately broken down into carbon dioxide and water. Also, a gastric
isozyme of ADH breaks down a significant amount of ethanol before it can be absorbed; sex
differences in ADH may, in part, account for differences in ethanol effects per given quantity
consumed between men and women.
Mortality/Morbidity
Trauma is the leading cause of mortality in children, and ethanol use is linked to a 3-fold to 7-
fold increased risk of trauma. Ethanol use is also strongly linked to other risk-taking behaviors
that can lead to minor trauma, assault, illicit drug use, and teenage pregnancy. Approximately
40% of the 10,000 annual nonautomotive pediatric deaths (usually drownings and falls) are
associated with ethanol.
The concomitant use of ethanol and other drugs is common, and combinations of ethanol with
other sedative-hypnotics or opioids may potentiate the sedative effects.
Ethanol greatly increases the risk of trauma, especially trauma due to motor vehicle collisions or
violent crimes. In a study of 295 pediatrics patients aged 10-21 years presenting to the
emergency department (ED) for treatment of any type of injury, Meropol et al found that 15
patients tested positive for alcohol; however, only 4 of these patients were tested upon initial ED
evaluation.4 Additionally, alcohol was linked with injuries secondary to assault and motor vehicle
crashes.
The intoxicated individual often engages in high-risk activities, even though his or her reflexes
are substantially slowed. Adolescent binge drinking has been linked with high-risk behaviors
such as riding in cars with intoxicated drivers, sexual activity, smoking cigarettes/cigars, suicide
attempts, and illicit drug use and may be the victim of dating violence.5 Early alcohol use has
been linked to dating violence victimization, suicidal ideation, and suicide attempts.6
Race
Data supporting a racial predilection in pediatric populations are limited. Studies of adult
patients suggest a lower tolerance in patients of Asian descent. This is most likely due to
differences in expression or enzyme activity of ADH.
Sex
Data supporting a sex predilection in pediatric populations are limited. Studies in adults have
reported that gastric ADH breaks down a significant amount of ethanol before it can be
absorbed, which may, in part, account for differences in tolerance between men and women.
Interestingly, one study found that among children aged 12-20, more drinking without binges
was reported among girls than among boys but that binge-drinking rates were still similar.5
Age
Ethanol intoxication can affect children and adults of all ages.
Clinical
History
Physical
Infants and toddlers have a clinical course significantly different from that of adolescents and
adults. Ethanol ingestion and intoxication can lead to a marked hypoglycemic state in infants
and young children. Ethanol has a CNS depressant action that can also lead to respiratory
depression and hypoxia. Ethanol has a sedative effect, producing general CNS depression,
respiratory depression, and often hypoglycemia. Young children often present to the ED after
drinking discarded alcoholic beverages left within their reach during and after parties or after
ingesting a fluid that contains ethanol. In older children and adolescents, ethanol intoxication
causes CNS depression, leading to respiratory depression. Hypoglycemia is less common in
this group.
As with all patients, a careful physical examination is warranted. In patients in whom ethanol
ingestion is suspected, carefully evaluate his or her mental status and perform a thorough
neurologic examination. Evaluate for signs of trauma, neglect, and illicit drug use. Ethanol
ingestion makes the patient more prone to trauma due to accidents or crime. The clinician's
most crucial clues to ethanol ingestion are a change in the patient's mental status and the smell
of alcohol on the patient's breath. The presence or absence of ethanol on breath cannot be
used to diagnose or exclude ethanol intoxication.
Compared with nonintoxicated teenagers, intoxicated teenagers are much more likely to be
affected by violence, even after drinking only one alcoholic beverage. Recent reports describe
the use of sedatives with alcohol to create date-rape drug combinations. Therefore, possible
sexual assault should be considered in teenaged patients.
Young children commonly ingest ethanol when they drink a liquid not meant for consumption,
such as perfume or cleaning agents. Frequently, other chemicals in the ingested substance are
more toxic than the ethanol. Therefore, a detailed physical examination is important to evaluate
for any signs and symptoms caused by these other toxins. Also, give special attention to the
examination of the oral cavity and airway because substances in cleaning agents can cause
chemical burns to these areas.
In children, the classic triad of signs of ethanol intoxication includes coma, hypoglycemia, and
hypothermia. These signs usually occur when the Ethanol level in the blood exceeds 50-100
mg/dL. However, hypoglycemia can be seen with serum Ethanol levels as low as 50 mg/dL.
Relatively small amounts of ethanol can produce hypoglycemia, especially in patients with low
glycogen stores, such as infants and small children who have not eaten for several hours.
Causes
Pediatric ethanol intoxication occurs in patterns that vary with the patient's age. Contributing
factors may include poor parenting habits or inadequate supervision.
Symptoms
Abdominal pain
Coma
Intestinal bleeding
Moving from side to side
Slowed breathing
Slurred speech
Stupor
Unable to walk normally
Vomiting
Home Care
If you can wake an adult who has drank too much alcohol, move the person to a comfortable
place to sleep off the effects. Make sure the person won't fall or get hurt.
Place the person on their side in case they throw up (vomit). DO NOT make the person throw up
unless told to do so by a health care professional or Poison Control.
Check the person frequently to make sure their condition does not get worse.
If the person is not alert (unconscious) or only somewhat alert (semi-conscious), emergency
assistance may be needed. When in doubt, call for medical help.
However, DO NOT delay calling for help if this information is not immediately available.
Poison Control
The National Poison Control Center (1-800-222-1222) can be called from anywhere in the
United States. This national hotline number will let you talk to experts in poisoning. They will
give you further instructions.
This is a free and confidential service. All local poison control centers in the United States use
this national number. You should call if you have any questions about poisoning or poison
prevention. It does NOT need to be an emergency. You can call for any reason, 24 hours a day, 7
days a week.
The health care provider will measure and monitor the patient's vital signs, including
temperature, pulse, breathing rate, and blood pressure. The patient may receive:
Serum glucose level: A bedside glucose finger stick is a quick and inexpensive method of assessing
hypoglycemia. Hypoglycemia in a common in young children with ethanol intoxication.
Electrolyte levels: The anion gap measurement should be determined. Acute ethanol intoxication
usually does not cause significant anion gap metabolic acidosis. The presence of a large anion gap or
severe acidosis should suggest the ingestion of another substance, such as methanol or ethylene
glycol. However, patients with multiple-trauma can also have marked metabolic acidosis, and ethanol
intoxication predisposes patients to trauma.
Ethanol level
o The serum ethanol concentration determined to obtain a starting level. Ethanol is metabolized
at a fixed rate in an individual; however, alcohol metabolism rates widely vary, and predicting
an individual's metabolism rate is impossible. If ethanol levels are obtained at two different
times, one can reliably predict what a patient's ethanol level would be at a given point in the
future. However, one cannot predict whether the patient would be "intoxicated" without
knowing the patient's tolerance to ethanol.
o A blood alcohol concentration (BAC) that could make one person apneic may be a level at
which another individual would suffer withdrawal. Also, a pharmacodynamic property, called
the Mellanby effect, is observed when neurological impairment is greater at a given BAC
when the BAC is increasing than the impairment observed at the same BAC when the BAC
isdecreasing.
o Most hospitals use ethanol assays that function by enzymatic methods that utilize ADH.
These assays detect ethanol only and do not have false-positive results when other toxic
alcohols are present. Therefore, these assays cannot detect other toxic alcohols, and
ingestion or co-ingestion of toxic alcohols or isopropanol may go unrecognized.
o If ingestion of toxic alcohols is suspected, a specific assay for those alcohols or gas
chromatography should be obtained.
o Clinical findings and ethanol concentrations may be categorized as follows (these are rough
estimates only and have not been validated in children):
Intoxication or inebriation - 100-150 mg/dL
Loss of muscle coordination - 150-200 mg/dL
Decreased level of consciousness - 200-300 mg/dL
Death - 300-500 mg/dL
o The effects widely vary based on the patient's BAC.
Human chorionic gonadotropin level: Urine pregnancy tests should be performed in all women of
childbearing age.
Serum salicylate and acetaminophen levels: In intentional suicidal ingestions, the presence of other
toxic substances must be determined, especially if the patient presents late or if he or she has
ingested a substance that has a significant risk of morbidity (eg, acetaminophen, salicylate).
Urine drug levels: Older patients may have ingested recreational drugs such as cocaine, marijuana,
benzodiazepines, amphetamines, and opiates.
ABG level
o A determination of the pH is important when polysubstance ingestion or ketoacidosis is
suspected. The partial pressure of carbon dioxide (pCO 2) can be helpful in assessing
respiratory depression.
o The pH also can help in ruling out the co-ingestion of methanol and ethylene glycol, because
significant academia is associated with those ingestions. However, reports in the literature
have documented that the co-ingestion of ethanol and methanol does not cause significant
acidosis.
Serum calcium and magnesium levels: High concentrations of ethanol and its chronic use can deplete
these cations.
Serum osmolality: The osmolar gap can provide information about the ethanol concentration in the
blood.
o The osmolar gap is calculated using the following equation: gap = measured osmolality - (2 X
[Na concentration]) + (glucose concentration/18) + (BUN concentration/2.8).
o An osmolar gap of 22-25 mOsm/kg results for every 100 mg/dL of ethanol in the serum. A
normal osmolar gap is 2 ± 6 mOsm/kg; 95% of the population have osmolar gaps between –
14 and +10 mOsm/kg.
o The predicted concentration of ethanol is calculated using the following equation: Ethanol
concentration = (osmolar gap - 10) X 4.6. This equation may provide a gross estimate of the
predicted level but varies based on the baseline osmolar gap.
Methanol levels: These results can be helpful if an ingestion of combined substances is suspected. A
positive methanol level can alert the physician to a co-ingestion.
Imaging Studies
Head CT scanning is warranted in patients with a change of mental status, focal neurologic findings,
or scalp bruises or lacerations and in patients in whom trauma cannot be excluded. C-spine
precautions should also be used if trauma is a suspected comorbidity until the neck is thoroughly
investigated.
If trauma is suspected, perform appropriate radiography
Treatment
Medical Care
The mainstay of medical treatment of patients with ethanol toxicity is supportive care. Many modalities for
treating ethanol intoxication and enhancing ethanol clearance have been attempted. In general, a conservative
approach is recommended.
Hypoglycemia and respiratory depression are the 2 most immediate life-threatening complications that result
from ethanol intoxication in children.
Initial care
o Assess the airway. If necessary, secure the airway with an endotracheal (ET) tube if the
patient is not maintaining good ventilation or if a significant risk of aspiration is
observed. Provide respiratory support and mechanical ventilation if needed.
o Obtain intravenous (IV) access and replace any fluid deficit or use a maintenance fluid
infusion. Use plasma expanders and vasopressors to treat hypotension, if present.
o Ensure that the patient maintains a normal body temperature.
o Quickly correct hypoglycemia. In children, 2-4 mL/kg of 25% dextrose solution is usually
administered. A maintenance infusion of dextrose-containing IV fluids is often required.
Correct any electrolyte abnormalities found with laboratory studies. Routine empiric electrolyte
replacement is not helpful; only documented electrolytic abnormalities should be corrected.
o If the ingestion occurred within 1 hour of presentation, placing a nasogastric tube and
evacuating the stomach contents can be helpful.
o In patients with chronic ethanol abuse, administer thiamine 100 mg IV/intramuscularly (IM) to
prevent neurologic injury.
Additional care: If other substances have been co-ingested, initiate specific treatment for those
substances, if available. For instance, naloxone can be used to reverse respiratory depression if opiate
co-ingestion is suspected.
Other treatments
o The administration of medications to cause emesis is not recommended because of the rapid
onset of CNS depression and risk of aspiration.
o The administration of activated charcoal is not recommended for isolated alcohol ingestions
because it does not bind hydrocarbons or alcohols. If the clinician suspects a concomitant
ingestion of other toxic products, activated charcoal may be effective in absorbing these
toxins.
o Forced diuresis is not helpful because 90% of ethanol metabolism occurs in the liver, and only
10% of the ethanol load is secreted in the urine.
o GABA-receptor antagonists such as naloxone and flumazenil have little effect on the CNS or
respiratory depression caused by ethanol; their use is not recommended in isolated ethanol
intoxication.
o The effects of insulin, glucose, caffeine, and several other medications have been studied, but
none consistently increases ethanol metabolism or alleviate CNS depression.
o Glucose administration is important in patients who are hypoglycemic as a result of ethanol
intoxication; however, this treatment does not clear ethanol from the blood.
o Fructose infusion can increase the ethanol clearance by 25%. However, the use of fructose is
not recommended because significant adverse effects may occur. For instance, fructose
infusion can cause lactic acidosis, severe osmotic diuresis, and GI symptoms; therefore, it is
not routinely used in the treatment of ethanol intoxication.
o Hemodialysis efficiently clears ethanol from the blood but is an invasive procedure; thus, its
use is not routinely recommended. Hemodialysis can be used in patients whose clinical
condition is deteriorating or in patients whose CNS depression, respiratory depression, or
hypotension is refractory to standard therapy.
o Patients who have impaired hepatic function may require dialysis to clear an ethanol load.
Surgical Care
Consultations
Contact the regional or local poison control center for treatment guidance and reporting purposes.
Consider consulting social services personnel in all cases of ethanol intoxication in children.
Patients who chronically abuse alcohol may have serious nutritional deficiencies and may require a
consultation with a nutritionist.
Diet
If no specific electrolyte abnormalities are present, the patient should maintain a healthy well-balanced
diet.
All electrolytic disturbances should be corrected before their discharge from the hospital.
Activity
Medication
Vitamin and electrolyte replacement is recommended only for specific deficits detected by means of laboratory
testing. Thiamine replacement is an exception because it is the only vitamin for which routine administration is
recommended and it has been proved useful in patients with chronic alcohol abuse. Thiamine is given to
prevent Wernicke syndrome.
Vitamins
Vitamins are organic substances required in small amounts for various metabolic processes. In the body,
vitamins may be synthesized in small or insufficient amounts or not at all; thus, supplementation may be
required. Vitamins are used in patients with suspected chronic ethanol abuse to prevent serious neurologic
complications. If feasible, thiamine should be administered prior to glucose load to reduce risk of Wernicke
encephalopathy.
Emedicine.medscape.com
www.nlm.nih.gov/medlineplus/ency/article/002644.htm
emedicine.medscape.com/article/1010220-overview -