Ethanol intoxication in children: Clinical features, evaluation, and management

INTRODUCTION — The evaluation and management of ethanol intoxication in children is discussed here.

Epidemiology, pharmacokinetics, estimation of toxicity, and toxic effects seen in pediatric ethanol exposure are discussed separately. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects".)

CLINICAL FEATURES — A rapid overview provides an approach to ethanol intoxication in children (table 1).

History — It is important to rapidly determine if the "alcohol" ingestion is ethanol or one of the toxic alcohols (eg, methanol, ethylene glycol). (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

Infants or young children who have ingested enough ethanol to cause a peak serum concentration ≥50 mg/dL (11 mmol/L) are at risk for profound hypoglycemia and require emergency evaluation. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Estimation of serum ethanol'.)

Other information should include the specific ethanol-containing substance, amount ingested, time of ingestion, and any co-ingestions. If the volume and concentration of ethanol ingested is known, then the serum ethanol concentration and degree of toxicity can be estimated (table 2) (calculator 1). (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Estimation of toxicity'.)

Witnesses of the ingestion and emergency medical services (EMS) personnel who may have recovered containers at the scene should be interviewed. In addition, caretakers should be questioned regarding medications in the house. The patient's or caretaker's pharmacy may provide valuable information regarding prescribed medications, the date of the most recent refill, and the total number of pills dispensed.

Parents or caregivers of intoxicated toddlers should be asked about ethanol-containing beverages or household products that may have been transferred from or left unsecured in their original containers. Common scenarios include the following:

●Exploratory ingestions of hand sanitizers [1-4]

●The early-rising toddler who discovers and drinks abandoned alcohol-containing beverages the morning after a party

●The young child who drinks mouthwash to imitate an adult's gargling

●The child who ingests a small amount of perfume or cologne

Older intoxicated children and adolescents often binge drink in a social setting that is outside of adult supervision (eg, parties, concerts). Key concerns include co-ingestion or exposure to other drugs, coexistence of trauma (particularly head trauma), and sexual assault. Often, EMS reports regarding the patient's environment or state of undress can assist in identifying physical or sexual assault.

Children and adolescents with depression or other mental illness are at high risk for intoxication. In some instances, ethanol may be ingested as part of a suicide attempt. In these circumstances, further mental health evaluation is indicated after the child recovers from intoxication. Ethanol is also a common substance used to facilitate sexual assault ("date rape"). (See "Evaluation and management of adult and adolescent sexual assault victims in the emergency department", section on 'Laboratory testing and diagnostic imaging'.)

Ethanol poisoning in infants less than one year of age raises the concern of intentional ethanol administration or serious neglect by a caretaker because infants usually lack the developmental skills, such as mobility and dexterity, to self-administer ethanol. Thus, this finding warrants involvement of social services [5].

Co-ingested sedative-hypnotic agents (eg, benzodiazepines, barbiturates, opioids, gamma hydroxybutyrate [GHB]) markedly increase the risk of deep coma with respiratory failure after ethanol ingestion.

Physical examination — Similar to other sedative-hypnotics, ethanol intoxication commonly manifests as altered behavior, lethargy, coma, ataxia, slurred speech, hypothermia, bradycardia, hypotension, and respiratory depression (table 3). A characteristic sickly sweet breath odor is often prominent. Degree of lethargy is highly correlated with serum ethanol concentration in older children and adolescents (table 4). Other important features include:

●Seizures caused by hypoglycemia (especially infants and young children). Ethanol intoxication typically masks the tachycardia, dilated pupils, and diaphoresis commonly associated with hypoglycemia [6]. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Ethanol-induced hypoglycemia'.)

●Nystagmus with variable pupil size on eye examination [7].

●Signs of hypovolemic dehydration due to vomiting and polyuria.

All patients warrant complete physical examination to identify associated injuries, especially head trauma, and findings that are the result of abuse (table 5), neglect, or physical or sexual assault. (See "Physical child abuse: Recognition" and "Child abuse: Eye findings in children with abusive head trauma (AHT)" and "Evaluation and management of adult and adolescent sexual assault victims in the emergency department" and "Severe traumatic brain injury (TBI) in children: Initial evaluation and management", section on 'Secondary survey'.)

Older children and adolescents may show signs of depression or other mental illness once their mental status allows for detailed psychiatric assessment. (See "Pediatric unipolar depression: Epidemiology, clinical features, assessment, and diagnosis".)

DIAGNOSIS — A history of ingestion from the caregiver or patient and characteristic physical findings, such as sickly sweet breath odor, altered mental status, and nystagmus with lateral gaze typically are sufficient to establish the diagnosis of ethanol intoxication. Detection of ethanol on the breath or in the serum provides additional confirmation.

DIFFERENTIAL DIAGNOSIS — There are many causes of coma that deserve consideration when evaluating the patient with suspected ethanol intoxication (table 6).

Other than toxicants, isolated or concomitant hypoglycemia or traumatic brain injury is the most likely cause of abrupt onset of lethargy of coma in children or adolescents. All children and adolescents with altered mental status should undergo measurement of rapid blood glucose and assessment for external signs of head trauma. In patients for whom traumatic brain injury is a strong possibility based upon clinical findings, computed tomography of the head may be warranted. Asymmetric structural lesions (eg, brain tumor, focal hemorrhage, or infection) are typically identified by focal findings on a careful neurologic examination followed by appropriate neuroimaging. Symmetrical structural lesions often have accompanying signs of increased intracranial pressure, especially headache. (See "Evaluation of stupor and coma in children" and "Severe traumatic brain injury (TBI) in children: Initial evaluation and management", section on 'Imaging'.)

Among toxic agents that may cause coma, other toxic alcohols (isopropyl alcohol, methanol), although chemically distinct, may mimic ethanol's toxic effects. Methanol and ethylene glycol, in particular, are important agents to consider since they have great toxic potential and frequently require antidotal therapy. They differ from ethanol in their inducement of profound metabolic acidosis, which typically takes hours to develop. In addition, ethanol may mask co-ingestion of other toxic alcohols. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

The combination of central nervous system depression and respiratory depression closely resembles the toxic syndrome seen with opioid intoxication (table 3). Many other sedative-hypnotic and psychoactive agents may also produce somnolence and respiratory depression and are often co-ingested with ethanol recreationally or with suicidal intent, especially in adolescents. Thus, even when serum or breath testing confirm ethanol ingestion, the possibility of sedative-hypnotic or opioid intoxication co-ingestion remains. An isolated ethanol overdose rarely causes profound respiratory depression requiring invasive airway management or cardiopulmonary instability. In such cases, the presence of co-ingestants should be investigated. (See 'Other studies' below.)

Administration of naloxone reverses the effects of opioid intoxication but will have minimal or no effect on central nervous system depression caused by ethanol or other sedative-hypnotic agents. However, naloxone may alleviate respiratory depression enough in patients with concomitant ethanol and opioid intoxication so that endotracheal intubation and mechanical ventilation can be avoided. Patients who respond to naloxone warrant close monitoring of respiratory status and frequently require redosing. (See "Opioid intoxication in children and adolescents", section on 'Naloxone'.)

Sedative-hypnotic intoxication is virtually indistinguishable clinically from ethanol intoxication. Rapid immunoassay screening of the urine can identify benzodiazepines and barbiturates, but a negative screen does not exclude exposure to benzodiazepines. (See "Benzodiazepine poisoning", section on 'Role of laboratory benzodiazepine testing'.)

Gamma hydroxybutyrate (GHB), an illicit sedative-hypnotic that is often ingested recreationally and has also been implicated in date rape, can cause psychomotor agitation and profound coma of short duration (several hours). GHB is commonly co-ingested with ethanol and is not detected on rapid immunoassay urine toxicology screens, although it can be detected in the urine by gas chromatography and mass spectrometry. Effects from GHB are not reversed by naloxone. Thus, diagnosis of GHB intoxication is primarily made by history or characteristic clinical findings of agitation prior to, following, or in abrupt alternation with coma of short duration. (See "Gamma hydroxybutyrate (GHB) intoxication", section on 'Diagnosis' and "Gamma hydroxybutyrate (GHB) intoxication", section on 'Laboratory evaluation'.)

Diabetic ketoacidosis may be mistaken for ethanol intoxication because of the presence of ketones on the breath. However, it is easily differentiated from ethanol poisoning by the typical history of polyuria, polydipsia, and polyphagia in patients with new-onset diabetes mellitus or past medical history of diabetes mellitus in combination with laboratory findings of hyperglycemia and metabolic acidosis. (See "Diabetic ketoacidosis in children: Clinical features and diagnosis", section on 'Clinical features'.)

Meningitis and encephalitis can also present with altered mental status but are usually accompanied by fever and other signs of infection that help distinguish these entities from ethanol intoxication. (See "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Clinical features' and "Acute viral encephalitis in children: Clinical manifestations and diagnosis", section on 'Clinical features'.)

EVALUATION

Blood glucose — Rapid measurement of blood glucose should be performed in all patients, especially infants and young children, with altered mental status after ethanol ingestion.

If low, blood glucose should be corrected and then serially monitored, particularly in cases of younger children or others with limited glycogen stores who may be at risk for recurrent hypoglycemia. The specific clinical scenario, such as the time since ingestion and the age of the child, should determine the frequency of blood-glucose determinations, but these should be obtained until the patient demonstrates a pattern of stable blood sugars with normal oral glucose intake. (See "Approach to hypoglycemia in infants and children".)

Ethanol serum concentration — Measurement of serum ethanol concentration is an essential diagnostic step when evaluating symptomatic infants and young children after ethanol exposure. In adolescents with moderate to severe intoxication, who have ingested only ethanol, the concentration can help estimate duration of symptoms. In addition, degree of lethargy is highly correlated with serum ethanol concentrations in older children and adolescents (table 4). (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Duration of symptoms'.)

Asymptomatic patients over two years of age or minimally symptomatic adolescents do not usually require serum ethanol levels.

Quantitative and qualitative testing for ethanol is readily available in most hospitals. Headspace gas chromatography may be used to measure blood or serum ethanol. An enzymatic oxidation method also exists to measure serum ethanol levels. Most hospital laboratories use serum to perform the "blood" ethanol test. The serum-to-blood ethanol ratio varies from 1.12 to 1.18 depending upon ethanol concentration in the blood specimen [8].

●Serum ethanol levels are routine chemistry studies in most hospitals and identify ethanol exposure in the infant, young child, and obtunded or otherwise uncooperative older patient.

●Breath-alcohol meters rely on a relatively fixed partitioning (approximately 1 out of 2100) of ethanol between alveolar air and blood and provide an estimate of blood ethanol concentration at the bedside in the cooperative older child [9]. Carefully administer the test, as the use of alcohol-based hand sanitizers in the immediate vicinity of a breath-alcohol meter may cause falsely elevated readings [10]. A confirmatory blood ethanol, submitted to a hospital or reference laboratory, may be warranted as well, particularly if there are medical-legal issues surrounding the intoxication.

Other studies — Further laboratory evaluation of ethanol intoxication varies depending upon the circumstances of exposure. Other ancillary studies may be indicated in selected patients in whom ingestion of other toxic agents, trauma, child abuse, or sexual assault are suspected. (See "Evaluation of stupor and coma in children" and "Approach to the child with occult toxic exposure" and "Trauma management: Approach to the unstable child" and "Evaluation and management of adult and adolescent sexual assault victims in the emergency department".)

Other potentially helpful studies following ethanol ingestion include the following:

●Serum electrolyte determinations assess for electrolyte disturbance and allow for calculation of the anion gap in the setting of likely co-ingestants or evidence for metabolic acidosis. In addition, electrolytes may be altered by protracted vomiting and hypovolemia associated with acute ingestion. Associated laboratory findings may include hypokalemia and metabolic acidosis.

●Arterial or venous blood gas measurement combined with pulse oximetry determines adequacy of ventilation in patients with serious and persistent respiratory depression and characterizes acid-base disturbance after ethanol ingestion

●Plasma osmolality, if co-ingestion of toxic alcohols is suspected (see "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis", section on 'Plasma osmolal gap')

●Serum acetaminophen concentration in patients who ingest ethanol with suicidal intent

●Chest radiography if the history or exam suggests the possibility of pulmonary aspiration

●Computed tomography of the head in patients with clinical findings suggestive of significant head trauma

●Rapid urine drugs of abuse screen in older children and adolescents with significant signs of intoxication and in young children for whom intentional ethanol administration by the caretaker is suspected

●Rapid urine pregnancy test in postmenarchal women

MANAGEMENT — A rapid overview provides an approach to ethanol intoxication in children (table 1).

Supportive care — Supportive care is the mainstay of managing ethanol intoxication in children. Treatment of respiratory depression, hypoglycemia, hypovolemia, and hypothermia are the key interventions to ensure good outcomes. Unlike adults, children rarely need thiamine supplementation during treatment. (See "Ethanol intoxication in adults".)

Management begins with assessment and stabilization of the airway, breathing, and circulation. The ethanol-intoxicated patient should be attached to monitors with cardiorespiratory and oxygen-saturation tracings.

●Basic airway interventions such as supplemental oxygen (via "blow-by," nasal cannula, or face mask) and nasopharyngeal airway usually suffice to maintain normal oxygen saturation. (See "Basic airway management in children".)

In patients requiring more than basic airway interventions to maintain the airway and breathing, administration of naloxone reverses the effects of possible opioid intoxication and empiric trial is warranted. (See 'Antidotes' below.)

However, the emergency provider should proceed with endotracheal intubation and mechanical ventilation if naloxone is ineffective and if significant respiratory compromise or risk of pulmonary aspiration (eg, coma with absent gag reflex) persists (table 7). (See "Technique of emergency endotracheal intubation in children".)

●Intravenous access should be obtained in patients with altered mental status and rapid blood glucose measurement determined. Blood should also be sent for serum ethanol concentration. Other laboratory studies should be obtained as clinically indicated. (See 'Other studies' above and "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies".)

●If seizures occur, airway and breathing should be supported, and evaluation for and treatment of possible hypoglycemia or traumatic injury should be high priorities. Seizures should be treated as outlined in the table with support of airway and breathing, treatment of hypoglycemia, if present, and followed by administration of benzodiazepines if seizures persist (table 8). (See "Management of convulsive status epilepticus in children".)

●Hypoglycemic patients should receive a rapid intravenous bolus of dextrose (0.25 g/kg) followed by a continuous infusion of dextrose (eg, D5W or D10W with one-fourth or one-half normal saline, depending upon sodium maintenance requirements) adequate to maintain serum glucose above 60 mg/dL (3.33 mmol/L). (See "Approach to hypoglycemia in infants and children".)

●Isotonic intravenous fluids (normal saline or Lactated Ringer) should be administered to correct hypovolemia. Potassium-containing solutions may also be needed to treat hypokalemia in the context of frequent vomiting. (See "Hypovolemic shock in children in resource-abundant settings: Initial evaluation and management" and "Clinical manifestations and treatment of hypokalemia in adults".)

●Attention should be paid to temperature, particularly in younger patients and those exposed to cool environments prior to arrival. Hypothermic patients merit active external warming with radiant heat, heat lamps, or warm blankets.

●Intoxicated patients with prolonged exposure to cold temperatures may develop profound hypothermia and frostbite involving the nose, ears, and extremities. (See "Hypothermia in children: Clinical manifestations and diagnosis", section on 'Clinical presentation' and "Frostbite: Emergency care and prevention".)

Gastrointestinal decontamination — Because ethanol is rapidly absorbed, often induces vomiting, and does not bind to activated charcoal, gastric emptying (eg, gastric lavage, syrup of ipecac administration) or gastrointestinal decontamination (administration of activated charcoal [AC]) do not prevent or lessen ethanol intoxication and pose a small but definite risk of pulmonary aspiration. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Pharmacokinetics'.)

●Multiple trials have shown minimal benefit and possible risk of pulmonary aspiration with progression to respiratory distress syndrome in patients undergoing gastric emptying after poisoning with many different agents, including ethanol. Thus, we recommend that children or adolescents with isolated ethanol intoxication not undergo gastric emptying procedures. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Gastric lavage' and "Gastrointestinal decontamination of the poisoned patient", section on 'Syrup of Ipecac'.)

●Activated charcoal cannot adsorb ethanol and should not be given after isolated ethanol ingestion. In patients who have ingested other substances, AC may be administered if the time from ingestion is less than one hour and if the benefit of AC for the treatment of the co-ingestants is expected to exceed the potential harm from aspiration. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Activated charcoal: Volunteer data'.)

Antidotes — No specific antidotes are available for treatment of ethanol intoxication. Dextrose-containing intravenous fluids may be necessary for documented and recurrent hypoglycemia, particularly for infants and younger children with limited glycogen stores and ethanol-induced inhibition of gluconeogenesis. (See "Approach to hypoglycemia in infants and children" and "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Ethanol-induced hypoglycemia'.)

Naloxone administration is warranted for children and adolescents with marked coma and respiratory depression as empiric treatment for possible opioid poisoning. Although naloxone will have no effect on central nervous system depression caused by ethanol or other sedative-hypnotic agents, it may alleviate respiratory depression enough in patients with concomitant ethanol and opioid intoxication so that endotracheal intubation and mechanical ventilation can be avoided. Patients who respond to naloxone warrant close monitoring of respiratory status and frequently require redosing. (See "Approach to the child with occult toxic exposure", section on 'Altered mental status' and "Opioid intoxication in children and adolescents", section on 'Naloxone'.)

Extracorporeal removal — Severe ethanol intoxication may require a prolonged period of supportive care. Elimination of ethanol occurs three to four times faster with hemodialysis [11]. However, improvement in clinical outcome following hemodialysis for ethanol intoxication has not been demonstrated. Possible candidates for hemodialysis include patients with liver disease that significantly decreases ethanol metabolism or those with serum ethanol concentrations greater than 450 mg/dL (100 mmol/L) [12].

Child protection — A suspicion of intentional administration of ethanol to a child warrants involvement of an experienced child protection team (eg, social worker, nurse, physician with more extensive experience in the management of child abuse), if available. In many parts of the world (including the United States, United Kingdom, and Australia), a mandatory report to appropriate governmental authorities is also required. (See "Child abuse: Social and medicolegal issues", section on 'Reporting suspected abuse'.)

In addition, computed tomography of the head, funduscopic examination by an ophthalmologist to assess for retinal hemorrhages, and skeletal survey may be warranted once the patient's clinical status is stabilized. The safety of other children in the home must be ensured by local Child Protective Services. (See "Physical child abuse: Diagnostic evaluation and management" and "Child abuse: Eye findings in children with abusive head trauma (AHT)".)

Disposition — Further management depends upon presence of symptoms and circumstances surrounding the ingestion and is based on small observational studies.

Symptomatic patients — All children displaying major signs of ethanol intoxication (eg, coma, respiratory depression, and hypoglycemia) require hospital observation or admission. These patients typically fully recover within 12 to 24 hours.

Older children and adolescents with initial signs of inebriation who rapidly return to normal mental status within four to six hours and who are not suicidal may be discharged into the care of a competent adult.

Asymptomatic patients — We recommend that asymptomatic infants and young children with an ethanol ingestion sufficient in volume to produce a peak serum concentration greater than 50 mg/dL (11 mmol/L) undergo rapid blood glucose testing (calculator 1). Based upon the pharmacokinetics of ethanol and typical timing of hypoglycemia after its ingestion, these patients should be observed in a medical facility until six hours after ingestion and have at least one repeated rapid blood glucose measurement prior to discharge. Estimation of the ethanol volume that is ingested can be difficult. Thus, some clinicians may choose to evaluate all asymptomatic young children with ethanol exposure in this manner regardless of the reported amount. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Estimation of serum ethanol'.)

Initially asymptomatic patients who manifest altered mental status or hypoglycemia at any point during observation warrant inpatient admission [13]. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Ethanol-induced hypoglycemia'.)

Children who remain asymptomatic for six hours after a limited exposure to ethanol may be discharged home as long as close observation in a stable social setting and ability to rapidly return for medical care, if needed, are assured.

Intentional overdose — Patients who ingest ethanol with intent of self-harm should undergo mental health evaluation, measurement of serum acetaminophen concentration, and careful evaluation for other co-ingestants. (See 'Evaluation' above.)

Patients should be evaluated by the mental health provider before discharge from medical care. Psychiatric evaluation should be deferred in symptomatic patients until after they have recovered. (See "Approach to the child with occult toxic exposure" and "General approach to drug poisoning in adults".)

OUTCOME — Most ethanol exposures in young children involve small amounts of household products (eg, perfumes, colognes) and do not result in significant toxicity. In the US, many of these ingestions are observed at home with phone advice provided by experienced poison specialists when the expected peak ethanol concentration is <50 mg/dL (11 mmol/L) [13]. Life-threatening ethanol intoxication is unusual. Delay in seeking care with prolonged hypoglycemia is a prominent feature of the rare lethal cases of ethanol intoxication in young children [13,14]. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Estimation of serum ethanol' and 'Supportive care' above.)

The intoxicated older child and adolescent typically do well with proper airway support and intravenous hydration, as needed. However, these patients are at heightened risk for major trauma, sexual assault, and significant mental illness. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Epidemiology' and 'Supportive care' above.)

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Treatment of acute poisoning caused by recreational drug or alcohol use" and "Society guideline links: Poisoning prevention".)

SUMMARY AND RECOMMENDATIONS

●Clinical assessment

•The clinician should rapidly determine if the "alcohol" ingestion is ethanol or one of the toxic alcohols (eg, methanol, ethylene glycol). If isolated ethanol ingestions is confirmed, the clinician should establish whether infants or young children have ingested enough ethanol to cause a peak serum concentration ≥50 mg/dL (11 mmol/L), the concentration at which profound hypoglycemia may occur. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Estimation of serum ethanol' and "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

•Ethanol intoxication commonly manifests as lethargy, coma, ataxia, slurred speech, hypothermia, bradycardia, hypotension, and respiratory depression (table 3). A characteristic sickly sweet breath odor is often prominent. (See 'Physical examination' above and 'Differential diagnosis' above.)

Other important features of ethanol intoxication include seizures caused by hypoglycemia (especially in infants and young children) and signs of hypovolemic dehydration due to vomiting and polyuria. (See "Ethanol intoxication in children: Epidemiology, estimation of toxicity, and toxic effects", section on 'Ethanol-induced hypoglycemia'.)

●Diagnosis – A history of ingestion from the caregiver or patient and characteristic physical findings, typically are sufficient to establish the diagnosis of ethanol intoxication. Detection of ethanol on the breath or in the serum provides additional confirmation and helps differentiate ethanol intoxication from other causes of altered mental status. (See 'Evaluation' above and 'Differential diagnosis' above.)

●Differential diagnosis – All children and adolescents with altered mental status should undergo measurement of rapid blood glucose and assessment for external signs of head trauma. In patients for whom traumatic brain injury is a strong possibility based upon clinical findings, computed tomography of the head may be warranted. Even when ethanol ingestion is confirmed by serum or breath testing, the possibility of sedative-hypnotic or opioid intoxication co-ingestion remains. (See 'Differential diagnosis' above.)

●Management

•Supportive care – Treatment of respiratory depression, hypoglycemia, hypovolemia, and hypothermia are the key interventions to ensure good outcomes in symptomatic children and adolescents with ethanol intoxication. (See 'Supportive care' above.)

All children displaying major signs of ethanol intoxication (eg, coma, respiratory depression, and hypoglycemia) require hospital observation or admission. (See 'Symptomatic patients' above.)

•Gastrointestinal decontamination – We recommend that children or adolescents who ingest ethanol not undergo gastric emptying procedures (gastric lavage or administration of syrup of ipecac) (Grade 1B). In addition, activated charcoal (AC) should not be administered to children who only ingest ethanol. The decision to administer AC to patients who co-ingest other substances depends upon the time since ingestion and potential efficacy of AC for preventing toxicity by the specific substance. (See 'Gastrointestinal decontamination' above.)

•Antidotes – Patients with profound respiratory depression requiring invasive airway management or with cardiopulmonary instability warrant further evaluation for co-ingestants and empiric administration of naloxone. (See 'Antidotes' above.)

•Asymptomatic patients – We recommend that asymptomatic infants and young children with an ethanol ingestion sufficient in volume to produce a peak serum concentration greater than 50 mg/dL (11 mmol/L) undergo rapid blood glucose testing (calculator 1). These patients should also be observed in a medical facility for at least six hours after ingestion and have at least one repeated rapid blood glucose measurement prior to discharge. Some clinicians may choose to evaluate all asymptomatic young children with ethanol exposure for hypoglycemia regardless of the ingestion history. (See 'Asymptomatic patients' above.)

Children who are asymptomatic for six hours after a limited exposure to ethanol may be discharged home if close observation in a stable social setting and ability to rapidly return for medical care, if needed, are assured. (See 'Asymptomatic patients' above.)

Patients who ingest ethanol with intent of self-harm should undergo mental health evaluation, measurement of serum acetaminophen concentration, and careful evaluation for other co-ingestants. (See 'Intentional overdose' above.)