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Hur vanligt är delirium tremens

Delirium Tremens

Continuing Education Activity

Alcohol use disorder fryst vatten 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 fryst vatten 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 fryst vatten now commonly known to occur as early as 48 hours after abrupt cessation of alcohol in those with chronic use and can gods up to 5 days. It has an anticipated mortality of up to 37% without appropriate treatment. It fryst vatten 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 grupp 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 grupp in caring for patients with delirium tremens.

Access free multiple choice questions on this topic.

Introduction

Alcohol use disorder fryst vatten 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 fryst vatten 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 fryst vatten now commonly known to occur as early as 48 hours after abrupt cessation of alcohol in those with chronic use and can gods up to 5 days. It has an anticipated mortality of up to 37% without appropriate treatment. It fryst vatten 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 fryst vatten highest in adult dock, with 17.6% and 36% respectively. There fryst vatten a higher prevalence in the vit, younger population and in those who were never married or previously married. The lifetime fara for developing DT in the population with alcohol use disorder fryst vatten approximately 5% to 10%.

Risk factors for DT include the following:

  • a history of DT

  • prior history of seizures

  • the presence of concurrent illness with associated comorbidities

  • prior history of detoxification

  • the prolonged period prior to the gods drink.[5][6]

Pathophysiology

Alcohol acts as a huvud nervous struktur 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 fryst vatten a decrease in GABA activity and alteration in the type of GABA receptor and function. Abrupt cessation of alcohol causes a decrease in the inhibitory actions of the GABA neurotransmitter, resulting in overactivity of the huvud nervous system.

Alcohol also inhibits the action of NMDA receptors bygd acting as a receptor antagonist. It inhibits the action of glutamate, which fryst vatten 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 intensiv oro eller upprördhet, tremors, tachycardia, and hypertension.

Certain individuals are more vulnerable to developing withdrawal symptoms than others. Though the etiology remains unclear, there fryst vatten a correlation between the duration of alcohol exposure and withdrawal symptoms.[7][8]

History and Physical

The första history and physical examination are crucial to establish the diagnosis and evaluate the severity of alcohol withdrawal. Pertinent data in the medical history includes quantity and duration of alcohol use, duration since gods drink, prior history and severity of alcohol withdrawal, and any additional drug use. Additional data 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 be self-reported, and as a result, further evaluation fryst vatten 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 gods drink becomes critical in recognizing the severity of symptoms. The första minor withdrawal symptoms are characterized bygd 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 bygd visual hallucinations. It can typically lösa in 24 to 48 hours and may also be associated with auditory and tactile hallucinations. Alcohol withdrawal seizure fryst vatten followed bygd alcohol hallucinosis, though it may present as early as 6 hours before alcohol hallucinosis. It can present as the only withdrawal symptoms but typically resolves 24 to 48 hours later. Seizures can recur, though rarely lead to ställning eller tillstånd epilepticus. Uncharacteristic signs of seizure activity should warrant further workup. If withdrawal symptoms remain untreated, this can typically lead to DT. DT fryst vatten characterized bygd visual hallucinations, profound confusion, tachycardia, hypertension, hyperthermia, intensiv oro eller upprördhet, and diaphoresis.

Evaluation

Clinicians need to evaluate the severity of alcohol withdrawal based on history and clinical introduktion. The best-validated tool to assess the severity of alcohol withdrawal fryst vatten the Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar). It fryst vatten 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 fara for seizures and DT. [9][10] CIWA-Ar fryst vatten not recommended for withdrawal delirium due to its subjective natur 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 fryst vatten 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 intensiv oro eller upprördhet, decrease the fara of seizures, and decrease morbidity and mortality. The most common and validated treatment for alcohol withdrawal fryst vatten benzodiazepine. Several benzodiazepines can be used, including lorazepam, diazepam, and chlordiazepoxide, preferably administered via an intravenous rutt. 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, sometimes using a CIWA score greater than 8. In a fixed schedule regimen, the benzodiazepine fryst vatten 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 medicinering with a smaller duration of treatment. There fryst vatten no klar 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 enhet monitoring, especially if there are associated comorbid conditions. In those patients with severe DT unresponsive to benzodiazepine, barbiturates such as phenobarbital in conjunction with benzodiazepine can be effective. Another alternative fryst vatten the use of propofol in conjunction with benzodiazepine; this would, however, require mechanical ventilation.

Although there are studies 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 enhet för massa per hour without requiring mechanical ventilation. It fryst vatten 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 includes the 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

  • Cerebral 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. fara 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, the patient should be referred to Alcoholics Anonymous and other support groups.

  • Cognitive behavior therapy may help some patients prevent relapse

  • A referral to a psychiatrist to assess for nedstämdhet 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 fängslande these individuals with behavior therapy and interventions to decrease alcohol misuse. There fryst vatten 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 include benzodiazepines and even gabapentin.

Enhancing Healthcare grupp 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 fryst vatten 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 bygd a sjuksköterska or social worker. There fryst vatten good bevis 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-based programs to screen and counsel patients who have been discharged with a diagnosis of DTs. uppgifter on short-term or acute drinkers do show 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 should try and quantify the use.

Outcomes

DTs can be associated with a number of complications, including respiratory nedstämdhet, seizures, arrhythmias, and aspiration pneumonitis. Even with appropriate therapy, the mortality varies from 5% to 15%. The only way to lower the mortality fryst vatten 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.

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Moore DT, Fuehrlein BS, Rosenheck RA. Delirium tremens and alcohol withdrawal nationally in the Veterans Health ledning. Am J Addict. 2017 Oct;26(7):722-730. [PubMed: 28836711]

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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 brev Pathway Implementation. J Psychiatr Pract. 2017 May;23(3):233-241. [PubMed: 28492463]

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Junghanns K, Wetterling T. [Alcohol withdrawal and its major complications]. Fortschr Neurol Psychiatr. 2017 Mar;85(3):163-177. [PubMed: 28320026]

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Sutton LJ, Jutel A. Alcohol Withdrawal Syndrome in Critically Ill Patients: Identification, Assessment, and Management. Crit Care sjuksköterska. 2016 Feb;36(1):28-38. [PubMed: 26830178]

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Gortney JS, Raub JN, Patel P, Kokoska L, Hannawa M, Argyris A. Alcohol withdrawal syndrome in medical patients. Cleve Clin J tillsammans med. 2016 Jan;83(1):67-79. [PubMed: 26760524]

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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 tillsammans med. 2017 May;45(5):867-874. [PubMed: 28266937]

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Long D, Long B, Koyfman A. The emergency medicin management of severe alcohol withdrawal. Am J Emerg tillsammans med. 2017 Jul;35(7):1005-1011. [PubMed: 28188055]

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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]

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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]

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Gerresheim G, Brederlau J, Schwemmer U. [Dexmedetomidine in the treatment of acute alcohol withdrawal delirium]. Anaesthesist. 2016 Jul;65(7):525-31. [PubMed: 27287404]

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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 samhälle, Issued in Partnership with the europeisk statsförbund of Addiction Societies. CNS Neurosci okänt. 2016 Jan;22(1):25-37. [PMC free article: PMC6492872] [PubMed: 26768685]

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Leuenberger DL, Fierz K, Hinck A, Bodmer D, Hasemann W. A systematic nurse-led approach to withdrawal fara 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]

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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]

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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]

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