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Alcohol Withdrawal and Intoxication

JoAn Laes MD

Therapeutic Communication Includes Eye Contact

Introduction

In 2012, 71% of American adults reported that they drank alcohol at some point in the past year.1-3 Alcohol use is thought to be a factor in more than 2.6 million emergency room visits per year.4 Use of alcohol is common in the setting of trauma, including motor vehicle accidents. Attributed to 88,000 deaths annually between 2006 and 2010, it is the third-leading preventable cause of death in the U.S.5,6

More than 17 million Americans are considered to suffer from alcohol abuse or dependence, and many more engage in what is considered high-risk drinking patterns.7 The National Institute on Alcohol Abuse and Alcoholism considers at-risk drinking to be more than four drinks on any day or 14 drinks per week for men and more than three drinks per day or seven per week for women.8 Continuous long-term alcohol consumption leads to tolerance to the sedating effects of alcohol due to adaptive changes in inhibitory and excitatory neurotransmission. When a person who is tolerant to alcohol suddenly discontinues use, inhibitory effects on neurotransmission are lost, and the resulting symptoms are termed alcohol withdrawal syndrome. Alcohol withdrawal is thought to be a significant factor in 1.2 million emergency room visits per year, and develops in 8% of hospital admissions.9,10 The mortality associated with the most severe form of alcohol withdrawal is approximately 1–5%.11

Appropriate prehospital care is critical to the successful management of patients experiencing either alcohol intoxication or withdrawal. Complications related to these conditions are medical emergencies and require immediate intervention.

Alcohol Intoxication

Ethanol is an organic compound that is typically ingested in liquid form. Ethanol is only one of many types of alcohols, although in popular reference the term “alcohol” is synonymous with ethanol.

Once ingested, ethanol is quickly absorbed by the gastrointestinal tract and into the bloodstream. In a 70 kg person, one standard drink typically raises the blood ethanol concentration by 0.02% in males, and 0.03% in females.11 A standard alcoholic drink in the U.S. contains 0.6 fluid ounces of alcohol, such as 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of distilled spirits that are 40% ethanol by volume (80 proof).12 Although alcohol is typically ingested as a drink, it can be absorbed across mucous membranes, such as the rectum or vagina, or vaporized and inhaled. Many commercially available products contain ethanol, such as hand sanitizers and mouthwash (see Table 1 for the alcohol by volume percentage for common products). These methods are not advised and are, fortunately, not a popular route of intake. Routes of administration other than ingestion into the upper gastrointestinal tract result in rapid absorption of alcohol into the bloodstream, as initial metabolism in the stomach and liver is bypassed.

Table 1: Commercially Available Products Containing Ethanol

Product Alcohol by Volume
Beverages1
Beer 2–12%
Wine 9–6%
Distilled spirits > 20%
Personal Hygiene Products
Non-spray formulas < 10% (typically >5%)
Mouthwash > 22%
Spray formulas 30–70%
Colognes and perfumes 40–90%
Hand sanitizer 60–95%
Household Cleaning Products2
Non-spray formulas 1–5%
Spray disinfectants 40–60%
Over-the-Counter Medicine3
Cough and cold preparations 5–20%
Topical cold sprays 7%
Rubbing alcohol* 70%

Sources: 1. http://www.ttb.gov. Accessed August 13, 2015. 2.Chemical Information: Ethanol, Household Products Database. http://hpd.nlm.nih.gov/cgi-bin/household/brands?tbl=chem&id=25&query=eth.... Accessed December 29, 2014. 3.Medications Containing Alcohol | SDSU-DUIP. http://www.sdsuduip.com/medications-containing-alcohol/. Accessed December 29, 2014.

*Typically contains isopropyl alcohol, but may contain denatured ethanol.

The liver is the main organ that metabolizes alcohol. It does so through hepatic oxidation and enzymatic processing, although there is some metabolism that occurs with enzymes located in the stomach.13 In adults, the average rate of ethanol metabolism is 0.1 g/kg per hour.14 In the normal-sized adult (70–100 kg), the blood-ethanol concentration falls by 0.01–0.02% per hour.15 However, chronic heavy use of alcohol may increase the rate of metabolism to almost double.16 There is a small amount of excretion of alcohol via the lungs.17 This accounts for the ability to measure alcohol concentrations by breath analyzer devices.

Pathophysiology

Alcohol is a central nervous system depressant, stimulating gamma-aminobutyric acid (GABA) receptors and acting as a blocker, or antagonist, of N-methyl-D-aspartate (NMDA) receptors.

GABA is the primary inhibitory neurotransmitter in the brain. Effects of GABA include decreased excitability in the brain leading to physical symptoms of sedation. Glutamate is one of the main excitatory neurotransmitters in the brain. Ethanol inhibits the binding of glutamate to NMDA receptors that, in addition to the effects of increased GABA, inhibits neuronal transmission and causes the appearance of lethargy.

With prolonged ethanol use, the GABA and NMDA receptors in the brain adapt to the effects of alcohol, requiring larger amounts of ethanol to produce the same level of inhibition.

Clinical Presentation

Alcohol causes significant impairment in memory, motor coordination, and mentation at 0.08% blood alcohol concentration, which is the legal limit set by many states for driving.18 Individuals with a marked tolerance to alcohol may not display the same degree of sedation as a non-tolerant individual, even at the same blood alcohol concentration. Depending on dose and tolerance, the patient may or may not present with slurred speech, ataxia, and impaired judgement. Severe alcohol intoxication can progress to central nervous system depression and coma. Table 2 describes the typical clinical presentation of a non-tolerant individual based on their blood alcohol level.

Table 2: Alcohol Intoxication by Blood Concentration19

Presentation Blood Alcohol Level
Sobriety 0.01–0.05%
Euphoria 0.03–0.12%
Excitement 0.09–0.25%
Confusion 0.18–0.30%
Stupor 0.25–0.40%
Coma 0.35–0.50%
Death 0.45% and higher
Other Complications

Dependence, coma and death are not the only complications of alcohol abuse. Other disease processes can develop with both acute and long-term alcohol use.

Metabolic disease processes: These include electrolyte disturbances, alcohol ketoacidosis, and hypoglycemia. Dehydration and electrolyte disturbances may develop during acute intoxication including hypokalemia, hypophosphatemia, hypocalcemia, and hyponatremia.20 These abnormalities are largely due to nausea, vomiting, diarrhea, or increased urination that occurs during acute alcohol intoxication.21,22 Muscle toxicity (rhabdomyolysis) may occur due to electrolyte disturbances, immobilization, or from direct toxicity of alcohol to muscle cells.23

Ethanol is metabolized by the enzymes alcohol dehydrogenase and aldehyde dehydrogenase to acetaldehyde and acetic acid. Acetic acid can undergo a variety of metabolic pathways in the body, such as oxidation through the Krebs cycle, conversion to fatty acid, and for use in the formation of ketone bodies. The conversion of acetaldehyde to acetic acid creates an increase in the ratio of NADH, which is an enzyme involved in oxidation and reduction reactions. With the increased amount of NADH, gluconeogenesis is suppressed. This potentially results in hypoglycemia, and formation of keto-acids (ketone bodies), such as beta-hydroxybutyrate, is increased. Physical complaints resulting from ketoacidosis are predominantly nausea, vomiting, and abdominal pain.

Wernicke’s encephalopathy: Wernicke’s encephalopathy (WE) is a nervous system condition due to deficiency of vitamin B1 (thiamine). The lack of vitamin B1 causes the symptoms of ataxia, which is a lack of coordination of muscle movements, confusion, and internuclear ophthalmoplegia, which is impaired horizontal movements of the eyes. Patients who chronically use alcohol may develop thiamine deficiency due to poor diet, changes in gastrointestinal absorption of nutrients due to effects of alcohol and changes in the storage and use of vitamins in the body.24 Symptoms can occur acutely to subacutely after consistent deficiency of thiamine. If not treated, the encephalopathy can progress. Both the prophylaxis and treatment of Wernicke’s encephalopathy involves administration of thiamine.25

Organ dysfunction: Alcohol can acutely (and chronically) affect many organs in the body. Extreme dehydration may occur, potentially leading to acute kidney failure.26 Alcohol is potentially toxic to the glands of the pancreas, and consumption of large amounts of alcohol can lead to alcohol-induced pancreatitis.19 Patients drinking large amounts of alcohol can develop gastritis, abnormal heart rhythms such as atrial fibrillation, and alcohol hepatitis, (inflammation of the liver).27–29 They are also susceptible to changes to the immune system.17–30

Assessment

Patients who are intoxicated exhibit variable signs and symptoms. A physical assessment must be rapidly obtained (see Table 3 for common physical exam findings in patients who are intoxicated). The general impression of the patient may be that they are off-balance or have slurred speech. Be prepared for unpredictable moods or behaviors—patients can become agitated or combative without warning. As always, steps should be taken for scene safety; this includes vigilance of cues for escalating behaviors, donning personal protective equipment to isolate from body fluids or environmental hazards, and law enforcement presence if available.

Table 3: Physical Exam Findings of Alcohol Intoxication

Exam Finding
General Variable, ranging from alert to somnotic
Eyes Horizontal nystagmus
Heart Regular rate and rhythm
Lungs Normal respirations to respiratory depression
Gastrointestinal Normal to nausea and vominting
Skin Normal to pale and clammy
Neurological condition Lack of coordination; inability to perform cognitive tasks (e.g., spelling backwards and counting backwards serially)
Psychiatric condition Loss of inhibition of emotions; wide range of presentations (e.g., may be tearful, agitated, or takative and friendly)

Vital signs are generally within the normal range; however, some depression of vital signs is possible with significant intoxications, typically when the blood alcohol level is greater than 0.30%. One of the first steps in assessment should be to evaluate whether the patient is able to protect their airway—note their alertness and ability to talk, as well as ability to handle their secretions (patients with decreased mental status have increased risk of aspiration). The mental status of intoxicated patients can rapidly deteriorate and must be frequently monitored. When assessing patients with altered mental status, there is a broad differential of emergent medical conditions (see Table 4, below) that may either present similarly (or in addition) to intoxication. Trauma is common in intoxicated individuals, and a high index of suspicion for other life threating disorders is critical to a thorough evaluation

A medical history should be obtained including signs/symptoms that the patient is experiencing, allergies, medications, past relevant medical history, and the events leading up to the clinical presentation. Collecting collateral information from the scene is important as the patient may not be able to contribute meaningfully to the medical history depending on their level of intoxication.

Table 4: Differential Diagnosis of Alcohol Intoxication

Diagnosis Type
Toxins
Neuroleptics Lithium, quetiapine, valproic acid, etc.
Opiods Hydrocodone, heroin, oxycodone, etc.
Other toxic alcohols
 
Isopropyl alcohol, methanol, and ethlyene glycol
 
Sedative-hypnotics Benzodiazepines, barbiturates, and gamma-hydroxybutyrate (GHB)
Diabetic Ketoacidosis
Central Nervous System Disorders
Infection Encephalitis and meningitis
Stroke  
Hemorrhage  
Seizure or other etiology Epilepsy or other toxins
Psychiatric Disorders
Depression  
Mania  
Psychoses  

Diagnostic testing: Typically, the diagnosis of alcohol intoxication is made by clinical assessment; however, there are a few point-of-care tests available in the field for use by law enforcement, such as breath alcohol concentration. Other diagnostic tests, including serum and whole blood alcohol, require laboratory capabilities.

  • Breath alcohol concentration: A rapid and commonly available method to determine alcohol level. This method can give slightly lower ethanol concentrations when directly compared to serum.31

  • Serum alcohol concentration: The test that provide most accurate determination of the patient’s alcohol level.

  • Whole blood alcohol: A test typically used in forensic settings. Alcohol concentration from whole blood is measured lower than serum concentration.32

Management

Patients who present with alcohol intoxication at high blood ethanol levels (see Table 2) may have difficulty maintaining their own airway. As with all patients, identifying airway patency is the first priority in management, followed by treatment of hypoglycemia and management of agitation.

Maintain the airway: Ensure an open airway and adequate tone to protect against aspiration. To open an airway in patients without suspicion of a cervical spine neck injury, perform a head-tilt chin lift. If there is suspicion of cervical spine trauma, use a jaw thrust maneuver. Next insert an oral or nasal airway. Perform a jaw thrust maneuver when the airway is in place to lift the jaw, and consequently the tongue, preventing airway occlusion.

Treat hypoglycemia and ketoacidosis: Check glucose. If <60 mg/dL, administer intravenous (IV) dextrose. Use caution with oral glucose if the patient is altered. Recheck the glucose in five minutes. If the glucose level remains <60 mg/dL, administer more intravenous (IV) dextrose. If unable to obtain IV access, dextrose can be administered via intraosseous routes or glucagon 1 mg intramuscular (IM) may be administered. Note that glucagon may have limited efficacy in reversing hypoglycemia due to alcohol intoxication. Administer IV fluids using isotonic solutions.

Manage agitation or disinhibited behaviors: Generally, reassurance and maintaining a calm environment is all that is needed to manage the behaviors of an intoxicated individual. However, occasionally extreme agitation may occur, requiring pharmacological management for sedation or physical restraint to protect both the patient and the provider. Options include IV/IM midazolam (Versed) 2-5 mg or lorazepam (Ativan) 2-4 mg, or IV diazepam (Valium) 5–10 mg.33 Midazolam can be administered intranasal (IN), though this is an off-label route.34 Ketamine IM has been increasingly used in management of excited delirium prehospital, and can be considered if available.

Alcohol Withdrawal

Pathophysiology

As exposure to alcohol persists, there is downregulation and decreased sensitivity of inhibitory GABA receptors to the effects of alcohol, and simultaneous upregulation of the excitatory NMDA (glutamate) receptors. These cellular changes are the basis of tolerance and dependence. The brain requires more alcohol to achieve the same level of inhibition with time. A consequence of this adaptation is neuronal excitement that occurs when alcohol is suddenly removed from the system, leading to symptoms of alcohol withdrawal. Without alcohol present, the downregulated and desensitized GABA receptors are not able to suppress neuronal activity as they should, and there is preponderance of excitatory glutamate neurotransmission pathways. This leads to the physical symptoms of withdrawal—central and autonomic nervous system hyperactivity including tachycardia, diaphoresis, hallucinations, and seizures.

Not everyone who drinks heavily for prolonged periods will experience alcohol withdrawal, and there is variability among the withdrawal symptoms that do occur among patients. However, withdrawal typically does not occur in those who only drink intermittently. Genetic predisposition and personal history of severe withdrawal appear to be major contributors to the development of alcohol withdrawal symptoms.35

Clinical Pesentation

Notably in some patients, a reduction in alcohol use even with measurable alcohol present in their blood may lead to onset of withdrawal symptoms. Minor alcohol withdrawal symptoms may start six to 24 hours after the last drink. Minor withdrawal symptoms include anxiety, nausea, headache, palpitations, tremor, and diaphoresis. As withdrawal progresses, moderate symptoms of hypertension, tachycardia, and increased diaphoresis may occur around twenty-four to thirty-six hours. If symptoms do not progress to more severe alcohol withdrawal, they tend to resolve in one to three days. Seizures related to alcohol withdrawal tend to occur six to forty-eight hours after the last drink, although they may occur as early as two hours and they may occur with normal vital signs.36 The seizures are usually generalized and singular, although a second or multiple seizures may occur in a short period of time following the initial seizure. If multiple seizures occur, other causes for seizures should be evaluated.

Patients may also have alcohol withdrawal hallucinations, which can occur with or without vital sign derangements; the patient tends to have a clear sensorium during the hallucinations, which differentiates this symptom from alcohol withdrawal delirium, the most severe form of alcohol withdrawal. Alcohol withdrawal delirium typically starts forty-eight to seventy-two hours after the cessation of alcohol; symptoms include many of the same as moderate withdrawal with additional changes in cognition, agitation, confusion, and disorientation. This stage can persist for several days. This is the stage of alcohol withdrawal that causes the most morbidity and mortality.37

Physiological consequences of severe withdrawal, such as hyperthermia, increased respiratory rate, vomiting, and extreme agitation, result in increased metabolism and oxygen requirements, hypovolemia, and electrolyte abnormalities. These alterations can lead to cardiac dysrhythmias and cardiac arrest. Improvements in supportive and intensive care have led to a decrease in the incidence and mortality of alcohol withdrawal delirium, but prompt recognition and management of the condition is required.

Other complications include hypoglycemia. This can be due to poor nutritional intake.

Table 5: Onset of Alcohol Withdrawal Symptoms

Symptoms Hours after Last Drink
Seizures 2–48
Minor withdrawal 6–36
Moderate withdrawal 24–36
Hallucinations 12–24
Severe withdrawal (delirium tremens) 48–96
Assessment

The general impression of the patient is that they may appear sick. Vital signs include a normal to elevated blood pressure, tachycardia, and normal to fast respiratory rate.

Table 6: Physical Exam Findings of Alcohol Withdrawal

Exam Finding
Eyes Nystagmus, gaze palsy (WE)
Heart Regular rhythm, tachycardia
Lungs Non-labored breathing but may have tachypnea
Skin May be normal or diaphoretic
Neurological Hyperreflexia, tremor
Psychiatric Anxios, may be hallucinating or confused

The Clinical Institute Withdrawal Assessment Scale revised (CIWA-Ar) is a scoring tool that many healthcare providers use to assess the severity of alcohol withdrawal in a patient and guide treatment. It evaluates nine criteria on a scale severity from zero to seven and a tenth on a scale of zero to four.

Table 7: Clinical Institute Withdrawal Assessment Scale

Criteria Rating
Nauseau and vomiting

0 = No nausea or vomiting
1 = Mild nausea with no vomiting
7= Constant nausea and frequent vomiting

Tremors 0 = No tremor
1 = Tremors not visible but can be felt fingertip to fingertip
7 = Severe even with arms not extended
Paroxysmal sweats 0 = No anxiety
1 = Barey perceptible sweating
7 = Drencing sweats
Anxiety

0 = Normal anxiety
1 = Somewhat more than normal
7 = Equivalent to panic attacks as seeen in severely acute schizophrenic reactions

Agitation 0 = Normal activity
1 = Somewhat more activity than normal
7 = Pacing back and forth during most of the interview or thrashing around
Tactile disturbances

0 = None
1 = Mild itching (e.g., pins and needles, burning, numbness)
7 = Continuous hallucinations

Auditory disturbances

0 = Not present
1 = Mild harshness or ability to frighten
7 = Continuous hallucinations

Visual disturbances

0 = Not present
1 = Mild sensitivity
2 = Continuous hallucinations

Headaches, fullness in the head

0 = Not present
1 = Mild
7 = Severe

Orientation and clouding sensorium

0 = Oriented and can do serial additions
1 = Cannot do serial additions or is uncertain about the date
7 = Disoriented for place or person

The above assessment is not typically used in the prehospital setting, but familiarity with the scale and scoring can help the prehospital provider to determine the presence and degree of withdrawal symptoms.

Differential diagnosis: The differential diagnoses for alcohol withdrawal include hypoglycemia; sepsis; trauma; central nervous system disorders—infection (e.g., encephalitis or meningitis), stroke, hemorrhage and seizures of other etiology (e.g., epilepsy and other toxins); psychiatric disorders (e.g., depression, mania, and psychoses); and toxins (e.g., stimulants and Serotonin Syndrome/Neuroleptic Malignant Syndrome).

Management

Patients who present with alcohol withdrawal syndrome or seizures related to alcohol withdrawal may have difficulty maintaining their own airway. As with all patients, identifying airway patency is the first priority. The following list orders the assessment and treatment of patients who present with alcohol withdrawal.

  • Maintain airway. Ensure an open airway and adequate tone to protect against aspiration. Please refer to the airway management concepts described in the section for management of alcohol intoxication.
  • Replace volume depletion. Patient should be administered an isotonic electrolyte solution such as normal saline.
  • Treat hypoglycemia. Check glucose. If <60 mg/dL, administer dextrose. Please refer to hypoglycemia management concepts in the section for management of alcohol intoxication.
  • Manage agitation or withdrawal. Always make sure the scene is safe prior to initiating care. Law enforcement presence to assist with scene safety, including that of the patient and the providers, is preferable if available. If agitation is causing danger to the patient or the healthcare providers, restraints may be necessary.

The first line of treatment for agitation in the setting of alcohol withdrawal is a benzodiazepine. Benzodiazepines commonly used in the prehospital setting are diazepam, lorazepam, and midazolam. Since the patient in alcohol withdrawal is considered to have a GABA deficient state, larger doses than expected are typically needed to control symptoms of severe alcohol withdrawal (symptoms comparable to a CIWA-Ar sore of >10).38 If the patient has alcohol withdrawal delirium, more frequent administration and possibly larger dosages than normal may be required.

Second-line agents to control agitation include neuroleptics, such as haloperidol (Haldol). Use of ketamine for symptoms of alcohol withdrawal has not been widely studied, and cannot be recommended at this time.39 Try to maintain a calm environment to prevent further agitation. Physical restraints should be padded. A risk of restraints is physical injury, hyperthermia, rhabdomyolysis, or metabolic acidosis caused by patient resistance against restraints.

Manage seizure activity: If the patient has alcohol withdrawal delirium, more frequent administration and possibly larger dosages than normal may be required. As mentioned under management of intoxication, midazolam can be administered intranasal and is thought to be effective for termination of seizures.40

Table 8: Benzodiazepine Comparison

Drug Route Equivalent Dose Onset of Action Duration of Effect Half Life
Diazepam
  PO (may be used PR with gel formation) 10 mg Minutes Hours (variable) 20–50 hour parent drug, 50–100 hour active metabolite
  IV 10 mg 2–5 minutes 1 hour  
  IM* 10 mg Erratic    
Lorazepam
  PO 1 mg 15–30 minutes 8 hours 12 hours
  IV 1 mg 5–15 minutes 6–8 hours  
  IM 1 mg      
Midazolam
  PO 10 mg 10––20 minutes 1–3 hours 2–6 hours
  IV (may be atomized for intranasal) 1–2 mg 3–5 minutes < 2 hours  
  IM 1–2 mg 15 minutes 6 hours  

*Indicates erratic absorption; this form is not recommended for use in treatment of alcohol withdrawal.

Treat nausea or vomiting: Appropriate medications for nausea include ondansetron IV/IM, prochlorperazine IV/IM, and promethazine IV/IM/PR (rectally). Potential side effects from prochlorperazine and promethazine include extrapyramidal symptoms. To prevent development of extrapyramidal symptoms, these medications are typically administered concurrently with diphenhydramine via IV or IM. For difficult-to-control nausea, lorazepam oral or IV may be given off-label.41

Treat or prevent Wernicke’s encephalopathy: Oral or IV thiamine can be given for prevention; higher doses of IV thiamine are recommended for treatment if symptoms are present.

Conclusion

The patient with alcohol intoxication has a presentation that is usually clinically identifiable. However, alcohol affects a lot of different body systems and masks symptoms of other diseases.  It should be a diagnosis of exclusion. There may be associated complications, such as hypoglycemia that the prehospital provider should be aware of and ready to manage. In contrast, alcohol withdrawal is a serious medical problem that should be promptly treated to prevent the complications of seizures and delirium.

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Published: December 2, 2016
Revised: January 5, 2017