Continuing Education Activity
Alcohol use disorder is a common condition that has been associated with severe impairments in social functioning and medical problems. As high as 20% of the population have been noted to exhibit alcohol overuse during their lifespan. More than 50% of those with a history of alcohol use disorder can exhibit alcohol withdrawal symptoms at discontinuing or decreasing their alcohol use. However, only a few (3% to 5%) exhibit symptoms of severe alcohol withdrawal with profound confusion, autonomic hyperactivity, and cardiovascular collapse. This is defined as alcohol withdrawal delirium, more commonly known as delirium tremens (DT). Delirium tremens was first recognized as a disorder attributed to excessive alcohol use in 1813. It is now commonly known to occur as early as 48 hours after abrupt cessation of alcohol in those with chronic use and can last up to 5 days. It has an anticipated mortality of up to 37% without appropriate treatment. It is crucial to identify early signs of withdrawal because it can become fatal. This activity examines when delirium tremens should be considered and how to evaluate it properly. This activity highlights the role of the interprofessional team in caring for patients with delirium tremens.
Objectives:
Review the cause of delirium tremens.
Describe the pathophysiology og delirium tremens.
Summarize the treatment of delirium tremens.
Outline the role of the interprofessional team in caring for patients with delirium tremens.
Introduction
Alcohol use disorder is a common condition that has been associated with severe impairments in social functioning and medical problems. As high as 20% of the population have been noted to exhibit alcohol overuse during their lifespan. More than 50% of those with a history of alcohol use disorder can exhibit alcohol withdrawal symptoms at discontinuing or decreasing their alcohol use. However, only a few (3% to 5%) exhibit symptoms of severe alcohol withdrawal with profound confusion, autonomic hyperactivity, and cardiovascular collapse. This is defined as alcohol withdrawal delirium, more commonly known as delirium tremens (DT).
Delirium tremens was first recognized as a disorder attributed to excessive alcohol use in 1813. It is now commonly known to occuras early as 48hours after abrupt cessation of alcohol in those with chronic useand can last up to 5 days. It has an anticipated mortality of up to 37% without appropriatetreatment. It is crucial to identify early signs of withdrawal because it can become fatal.[1][2][3]
Etiology
Delirium tremens occurs in chronic alcohol users who abruptly discontinue alcohol use, often as early as 48 hours.[4]
Epidemiology
The 12-month and lifetime prevalence is highest in adult men, with 17.6% and 36% respectively. There is a higher prevalence inthe White, younger population and in those who were never married or previously married. The lifetime risk for developing DT in the population with alcohol use disorder is approximately 5% to 10%.
Risk factors for DT includethe following:
a history of DT
prior history of seizures
the presence ofconcurrent illness with associated comorbidities
prior history of detoxification
the prolonged period prior to the last drink.[5][6]
Pathophysiology
Alcohol acts as a central nervous system depressant. It enhances the effect of inhibitory neurotransmitters while down-regulating excitatory neurotransmitters. Alcohol interacts with GABA receptors, chloride ion receptor acting as an inhibitory neurotransmitter, via several mechanisms to enhance its activity. Over time, through prolonged alcohol exposure, there is a decrease in GABA activity and alteration in the type ofGABA receptor and function. Abrupt cessation of alcohol causes a decrease in the inhibitory actions of the GABA neurotransmitter, resulting in overactivity of the central nervous system.
Alcohol also inhibits the action of NMDA receptors by acting as a receptor antagonist. It inhibits the action of glutamate, which is an excitatory amino acid. Prolonged alcohol use results in receptor up-regulation. Abrupt discontinuation of alcohol causes an increase in the action of glutamate, resulting in profound excitatory action. This may have a clinical manifestation of sympathetic overdrive, such as agitation, tremors, tachycardia, and hypertension.
Certain individuals are more vulnerable to developing withdrawal symptoms than others. Though the etiology remains unclear, there is a correlation between the duration of alcohol exposure and withdrawal symptoms.[7][8]
History and Physical
The initial history and physical examination are crucial to establish the diagnosis and evaluate the severity of alcohol withdrawal. Pertinent information in the medical history includes quantity and duration of alcohol use, duration since last drink, prior history and severity of alcohol withdrawal, and any additional drug use. Additional information should be identified regarding any complicating medical problems such as heart failure, coronary heart disease, and chronic liver disease, among others. Some of the symptoms may not beself-reported, and as a result, further evaluation is often needed. Physical examination and laboratory testing should be curtailed to identify underlying medical problems and identifying potential electrolyte abnormalities, renal and liver function, sources of infection, coronary ischemia, rhabdomyolysis, and other drug use.
The duration since the last drink becomes critical in recognizing the severity of symptoms. The initial minor withdrawal symptoms are characterized by anxiety, insomnia, palpitations, headache, and gastrointestinal symptoms. These symptoms usually occur as early as 6 hours after cessation of alcohol use. After 12 hours, minor withdrawal symptoms can progress to alcohol hallucinosis, a condition characterized by visual hallucinations. It can typically resolve in 24 to 48 hours and may also be associated with auditory and tactile hallucinations. Alcohol withdrawal seizure is followed by alcohol hallucinosis, though it may presentas early as 6 hoursbeforealcohol hallucinosis. It can present as the only withdrawal symptoms but typically resolves 24 to 48 hours later. Seizures can recur, though rarely lead to status epilepticus. Uncharacteristic signs of seizure activity should warrant further workup. If withdrawal symptoms remain untreated, this can typically lead to DT. DT is characterized by visual hallucinations, profound confusion, tachycardia, hypertension, hyperthermia, agitation, and diaphoresis.
Evaluation
Clinicians needto evaluate the severity of alcohol withdrawal based on history and clinical presentation. The best-validated tool to assess the severity of alcohol withdrawal is the Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar). It is a 10-item questionnaire tool to evaluate, monitor, and treat alcohol withdrawal. It includes symptoms of withdrawal such as anxiety, nausea, and sweating, among others. A score of 8 points or lower corresponds to mild withdrawal, while a score of 9 to 15 corresponds to moderate withdrawal, and a score of 15 or greater corresponds to severe withdrawal symptoms, being at risk for seizures and DT.[9][10]CIWA-Ar is not recommended for withdrawal delirium due to its subjective nature and patients' inability to accurately report withdrawal symptoms.
Additional evaluation of a patient with DT involves identifying electrolyte, nutrition, and fluid abnormalities. Most of these patients present with severe dehydration (up to 10 L fluid deficit) and severe electrolyte abnormalities, including hypoglycemia, severe hypomagnesemia, and hypophosphatemia. Multivitamins and thiamine should be supplemented before glucose is given to prevent Wernicke encephalopathy.
Risk Factors
History of DTs
Concurrent illness
Advanced age
Hypokalemia
Prior withdrawal symptoms or detoxification
Treatment / Management
The treatment goals for alcohol withdrawal are to control agitation, decrease the risk of seizures, and decrease morbidity and mortality. The most common and validated treatment for alcohol withdrawal is benzodiazepine. Several benzodiazepines can be used, includinglorazepam, diazepam, and chlordiazepoxide, preferably administered via an intravenous route. This can be administered based on a symptom-triggered regimen or a fixed schedule. In a symptom-triggered regimen, medications are usually given when symptoms are present, sometimesusing a CIWA score greater than 8. In a fixed schedule regimen, the benzodiazepine is administered at fixed intervals, and additional doses are given based on the withdrawal symptoms.
Based on numerous trials, symptom triggered regimens have been shown to require less medication with a smaller duration of treatment. There is no clear consensus on the dosages of benzodiazepine, and this may variably change drastically from one patient to another. Those with substantial dosing requirements warrant intensive care unit monitoring, especially if there are associated comorbid conditions. In those patients with severe DT unresponsive to benzodiazepine, barbiturates such as phenobarbital in conjunctionwith benzodiazepine can be effective. Another alternative is the use of propofol in conjunctionwith benzodiazepine; this would, however, require mechanical ventilation.
Although there arestudies that demonstrate the effectiveness of central-acting alpha-2 agonists such as clonidine and dexmedetomidine, these agents should not be used alone and as the primary treatment of alcohol withdrawal. Dexmedetomidine has been shown to work in conjunction with benzodiazepine with doses up to 0.7 micrograms per kilogram per hour without requiring mechanical ventilation. It is also recommended to avoid using alcohol, antipsychotics, anticonvulsants, beta-adrenergic receptor blockers, and baclofen for the treatment of alcohol withdrawal, as there are not enough studies to support the safety of these medications.[8][11][12]
Differential Diagnosis
The differential diagnosis for DT includesthe following:
Sepsis
Uremia
Stroke
Meningitis
Encephalitis
Wernicke encephalopathy
Neuroleptic malignant syndrome
Pheochromocytoma
Drug toxicity such as amphetamine, hallucinogens, cocaine, heroin, and phencyclidine
Electrolyte abnormalities such as hypocalcemia and hypomagnesemia
Thyrotoxicosis
See AlsoDelirium tremensCerebral hemorrhage
Cerebral embolism
Toxic ingestion or exposures (ethylene glycol)
Acute liver failure
Diabetic ketoacidosis
Brain abscess
Hypoglycemia
Prognosis
Mortality from DT has substantially decreased with early recognition and treatment. Early treatment has decreased the mortality rate to less than 5%. Complications from DTs include severe rhabdomyolysis, arrhythmia, and associated comorbid illness. Risk factors such as pneumonia, pancreatitis, older age, and a history of other medical problems can lead to increased mortality.
Complications
Seizures
Disorientation
Hypertension
Hyperthermia
Altered mental status
Global confusion
Arrhythmias
Aspiration pneumonitis
Respiratory failure
Death
Postoperative and Rehabilitation Care
To prevent relapse, thepatient should be referred to Alcoholics Anonymous and other support groups.
Cognitive behavior therapy may helpsomepatients prevent relapse
A referral to a psychiatrist to assess for depression and anxiety may help abstain from alcohol.
Pearls and Other Issues
Recognizing individuals with a history of alcohol use disorder can help prevent the progression of withdrawal symptoms. The US Preventative Services Task Force recommends screening individuals aged 18 or older involved with risky drinking and engaging these individuals with behavior therapy and interventions to decrease alcohol misuse. There is a lack of consensus on the prophylactic treatment of alcohol withdrawal. Variations in hospital-wide policies in treating alcohol withdrawal exist, and the medications used includebenzodiazepines and even gabapentin.
Enhancing Healthcare Team Outcomes
DTs are very common in hospitalized patients and can be difficult to manage. DTs also prolong hospital stays and result in a high cost of healthcare. Today, the emphasis is on the prevention of DTs. To prevent excessive use of alcohol, there are many screening tools available that should be performed in the emergency department or primary care settings. The screening tools are carried out by a nurse or social worker. There is good evidence showing that screening for alcohol use can result in a reduction of alcohol consumption, associated injuries, and a decreased rate of readmissions to hospitals. [13][14][15][Level 5] Nurses also run computer-basedprograms to screen and counsel patients who have been discharged with a diagnosis of DTs. Data on short-termor acute drinkers doshow that these screening protocols work, but whether they work in severe misusers of alcohol remains debatable. Anytime a patient presents with a history of alcohol use, one shouldtry and quantify the use.
Outcomes
DTs can be associated with a number of complications, including respiratory depression, seizures, arrhythmias, and aspiration pneumonitis. Even with appropriatetherapy, the mortality varies from 5% to 15%. The only way to lower the mortality is aggressive resuscitation and treatment of any concurrent illness. Failure to treat or delay in diagnosis always leads to high morbidity and mortality.[16][17] [Level 5]
References
- 1.
Sarkar S, Choudhury S, Ezhumalai G, Konthoujam J. Risk factors for the development of delirium in alcohol dependence syndrome: Clinical and neurobiological implications. Indian J Psychiatry. 2017 Jul-Sep;59(3):300-305. [PMC free article: PMC5659079] [PubMed: 29085088]
- 2.
Moore DT, Fuehrlein BS, Rosenheck RA. Delirium tremens and alcohol withdrawal nationally in the Veterans Health Administration. Am J Addict. 2017 Oct;26(7):722-730. [PubMed: 28836711]
- 3.
Muzyk AJ, Rogers RE, Dighe G, Hartung J, Musser RC, Stillwagon MJ, Rivelli S. Impact of an Alcohol Withdrawal Treatment Pathway on Hospital Length of Stay: A Retrospective Observational Study Comparing Pre and Post Pathway Implementation. J Psychiatr Pract. 2017 May;23(3):233-241. [PubMed: 28492463]
- 4.
Junghanns K, Wetterling T. [Alcohol withdrawal and its major complications]. Fortschr Neurol Psychiatr. 2017 Mar;85(3):163-177. [PubMed: 28320026]
- 5.
Sutton LJ, Jutel A. Alcohol Withdrawal Syndrome in Critically Ill Patients: Identification, Assessment, and Management. Crit Care Nurse. 2016 Feb;36(1):28-38. [PubMed: 26830178]
- 6.
Gortney JS, Raub JN, Patel P, Kokoska L, Hannawa M, Argyris A. Alcohol withdrawal syndrome in medical patients. Cleve Clin J Med. 2016 Jan;83(1):67-79. [PubMed: 26760524]
- 7.
Salottolo K, McGuire E, Mains CW, van Doorn EC, Bar-Or D. Occurrence, Predictors, and Prognosis of Alcohol Withdrawal Syndrome and Delirium Tremens Following Traumatic Injury. Crit Care Med. 2017 May;45(5):867-874. [PubMed: 28266937]
- 8.
Long D, Long B, Koyfman A. The emergency medicine management of severe alcohol withdrawal. Am J Emerg Med. 2017 Jul;35(7):1005-1011. [PubMed: 28188055]
- 9.
Rastegar DA, Applewhite D, Alvanzo AAH, Welsh C, Niessen T, Chen ES. Development and implementation of an alcohol withdrawal protocol using a 5-item scale, the Brief Alcohol Withdrawal Scale (BAWS). Subst Abus. 2017 Oct-Dec;38(4):394-400. [PubMed: 28699845]
- 10.
Jesse S, Bråthen G, Ferrara M, Keindl M, Ben-Menachem E, Tanasescu R, Brodtkorb E, Hillbom M, Leone MA, Ludolph AC. Alcohol withdrawal syndrome: mechanisms, manifestations, and management. Acta Neurol Scand. 2017 Jan;135(1):4-16. [PMC free article: PMC6084325] [PubMed: 27586815]
- 11.
Gerresheim G, Brederlau J, Schwemmer U. [Dexmedetomidine in the treatment of acute alcohol withdrawal delirium]. Anaesthesist. 2016 Jul;65(7):525-31. [PubMed: 27287404]
- 12.
Rolland B, Paille F, Gillet C, Rigaud A, Moirand R, Dano C, Dematteis M, Mann K, Aubin HJ. Pharmacotherapy for Alcohol Dependence: The 2015 Recommendations of the French Alcohol Society, Issued in Partnership with the European Federation of Addiction Societies. CNS Neurosci Ther. 2016 Jan;22(1):25-37. [PMC free article: PMC6492872] [PubMed: 26768685]
- 13.
Leuenberger DL, Fierz K, Hinck A, Bodmer D, Hasemann W. A systematic nurse-led approach to withdrawal risk screening, prevention and treatment among inpatients with an alcohol use disorder in an ear, nose, throat and jaw surgery department-A formative evaluation. Appl Nurs Res. 2017 Feb;33:155-163. [PubMed: 28096011]
- 14.
Barrett J, Jansen M, Cooper A, Felbinger M, Waters F. Embracing a Nurse-Driven Alcohol Withdrawal Protocol Through Quality Improvement. J Addict Nurs. 2016 Oct/Dec;27(4):234-240. [PubMed: 27922474]
- 15.
Eads V, Maruzzella G. The Clinical Nurse as an Agent of Change. Medsurg Nurs. 2016 May-Jun;25(3):173-5. [PubMed: 27522845]
- 16.
Hammond DA, Rowe JM, Wong A, Wiley TL, Lee KC, Kane-Gill SL. Patient Outcomes Associated With Phenobarbital Use With or Without Benzodiazepines for Alcohol Withdrawal Syndrome: A Systematic Review. Hosp Pharm. 2017 Oct;52(9):607-616. [PMC free article: PMC5735736] [PubMed: 29276297]
- 17.
Baby S, Murthy P, Thennarasu K, Chand PK, Viswanath B. Comparative outcome in patients with delirium tremens receiving care in emergency services only versus those receiving comprehensive inpatient care. Indian J Psychiatry. 2017 Jul-Sep;59(3):293-299. [PMC free article: PMC5659078] [PubMed: 29085087]
Disclosure: Abdul Rahman declares no relevant financial relationships with ineligible companies.
Disclosure: Manju Paul declares no relevant financial relationships with ineligible companies.
