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Practice EssentialsDelirium tremens (DTs) is the most severe form of ethanol withdrawal, manifested by altered mental status (global confusion) and sympathetic overdrive (autonomic hyperactivity), which can progress to cardiovascular collapse. Minor alcohol withdrawal is characterized by tremor, anxiety, nausea, vomiting, and insomnia. Major alcohol withdrawal signs and symptoms include visual hallucinations and auditory hallucinations, whole body tremor, vomiting, diaphoresis, and hypertension (high blood pressure). Signs and symptoms of delirium tremensSigns and symptoms can include the following:
See History and Physical Examination. Treatments for delirium tremensSee the list below:
See Treatment. Medications in delirium tremensVarious medications that may be used in the treatment and supportive care of delirium tremens include the following: See Medication. BackgroundDTs is the most severe manifestation of alcohol withdrawal and clinical manifestations include agitation, global confusion, disorientation, hallucinations, fever, hypertension, diaphoresis, and autonomic hyperactivity (tachycardia and hypertension). Profound global confusion is the hallmark of delirium tremens. DTs is a medical emergency with a high mortality rate, making early recognition and treatment essential. See Prognosis, Clinical Presentation, Differentials, Workup, and Treatment. PathophysiologyChronic intake of alcohol affects several neurotransmitter systems in the brain. These effects include (1) increased release of endogenous opiates; (2) activation of the inhibitory gamma-aminobutyric acid-A (GABA-A) receptor producing increased GABA inhibition, with a resultant influx of chloride ions; (3) up-regulation of the postsynaptic N-methyl-D-aspartate (NMDA) type of glutamate receptor, which mediates the postsynaptic excitatory effects of glutamate; and (4) interactions with serotonin and dopamine receptors. During withdrawal from alcohol, the loss of GABA-A receptor stimulation causes a reduction in chloride flux and is associated with tremors, diaphoresis, tachycardia, anxiety, and seizures. In addition, the lack of inhibition of the NMDA receptors may lead to seizures and delirium. Excessive nervous system excitability during periods of abstinence from alcohol is related to the effect of alcohol on the number and function of brain receptors. Etiology of Delirium TremensEthanol interacts with GABA receptors, enhancing activity. GABA receptors are a family of chloride ion channels that mediate inhibitory neurotransmission. They are pentameric complexes composed of several glycoprotein subunits. Chronic ethanol abuse seems to modify the GABA receptor via several mechanisms, leading to a decrease in GABA activity. Chronic ethanol exposure has been found to alter gene expression and to increase cellular internalization of certain subunits, affecting the type of GABA receptors that are available at the cell surface and the synapse. Chronic ethanol exposure has also been found to alter phosphorylation of GABA receptors, which may alter receptor function. When ethanol is withdrawn, a functional decrease in the inhibitory neurotransmitter GABA is seen. This leads to a loss of the inhibitory control of excitatory neurotransmitters such as norepinephrine, glutamate, and dopamine. Ethanol also acts as an NMDA receptor antagonist. Withdrawal of ethanol leads to increased activity of these excitatory neuroreceptors, resulting in the clinical manifestations of ethanol withdrawal: tremors, agitation, hallucinations, seizures, tachycardia, hyperthermia, and hypertension. The clinical manifestations of ethanol withdrawal are due to the combination of effects on the GABA and NMDA receptors. Past episodes of withdrawal lead to increased frequency and severity of future episodes. Risk factorsRisk factors for DTs are inconsistent among studies [1, 2] and include the following:
EpidemiologyUsing the diagnostic criteria for alcohol use disorder (AUD) listed in DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th edition), the 12-month and lifetime prevalences of AUD in US noninstitutionalized civilian adults is highest in men (17.6% and 36.0%, respectively), with higher prevalences in whites, Native Americans, younger adults, and previously married and never married adults, as compared with women, African Americans, Asian Americans, and older and married adults. [3] Less than 50% of alcohol-dependent persons develop any significant withdrawal symptoms that require pharmacologic treatment upon cessation of alcohol intake. The lifetime risk for developing delirium tremens (DTs) among individuals with chronic alcohol addiction is estimated at 5-10%. Only 5% of patients with ethanol withdrawal progress to DTs. White patients have a higher risk of developing severe alcohol withdrawal, while black patients have a lower risk. [4] Whether or not sex differences exist in the rates of development of severe alcohol withdrawal is not clear. In any particular alcohol-dependent person, symptoms of withdrawal can differ widely among different withdrawal episodes. Delirium tremens rarely occurs among pediatric patients, because the physiologic substrate for severe alcohol withdrawal takes time to develop. PrognosisDespite appropriate treatment, the current mortality for patients with DTs ranges from 5-15%, but should be closer to 5% with modern ICU management. Mortality was as high as 35% prior to the era of intensive care and advanced pharmacotherapy. The most common conditions leading to death in patients with DTs are respiratory failure and cardiac arrhythmias. Patients at greatest risk for death are those with extreme fever, fluid and electrolyte imbalance, or an intercurrent illness, such as occult trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis, or Wernicke-Korsakoff syndrome.
 Author Shannon Toohey, MD, MAEd Residency Program Director, HS Assistant Clinical Professor, Department of Emergency Medicine, University of California, Irvine, School of Medicine Shannon Toohey, MD, MAEd is a member of the following medical societies: American College of Emergency Physicians, California American College of Emergency Physicians (ACEP), Council of Residency Directors in Emergency Medicine, Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Chief Editor David A Kaufman, MD Associate Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, New York University Grossman School of Medicine; Attending Physician, NYU-Langone Medical Center David A Kaufman, MD is a member of the following medical societies: American Thoracic Society, Society of Critical Care Medicine Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Pulsion Medical Systems (now Getinge/Maquet)<br/>Serve(d) as a speaker or a member of a speakers bureau for: Pulsion Medical Systems (now Getinge/Maquet)<br/>Received research grant from: National Institutes of Health (NIH); Cheetah Medical (now Baxter); Fisher and Paykel. Additional Contributors James B Price, MD Attending Emergency Physician, Mission Hospital; Clinical Faculty, Department of Emergency Medicine, Harbor-UCLA Medical Center James B Price, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians Disclosure: Nothing to disclose. Michael James Burns, MD, FACEP, FACP, FIDSA Health Science Clinical Professor, Department of Emergency Medicine, Department of Internal Medicine, Division of Infectious Diseases, University of California Irvine School of Medicine Michael James Burns, MD, FACEP, FACP, FIDSA is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Physicians, American Geriatrics Society, American Society of Tropical Medicine and Hygiene, California Medical Association, Infectious Diseases Society of America, Phi Beta Kappa, Royal Society of Tropical Medicine and Hygiene, Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Michael E Lekawa, MD, FACS Professor of Surgery, University of California, Irvine School of Medicine; Chief, Department of Surgery, Division of Trauma and Critical Care, Director of Trauma Services, Director of Surgical Intensive Care Unit, Director of Student Critical Care Teaching Program, Medical Director of Surgery Clinics, University of California, Irvine Medical Center Michael E Lekawa, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Society of Critical Care Medicine Disclosure: Nothing to disclose. Acknowledgements Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. William G Gossman, MD Associate Clinical Professor of Emergency Medicine, Creighton University School of Medicine; Consulting Staff, Department of Emergency Medicine, Creighton University Medical Center William G Gossman, MD is a member of the following medical societies: American Academy of Emergency Medicine Disclosure: Nothing to disclose. J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Lisa Kirkland, MD, FACP, CNSP, MSHA Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine Disclosure: Nothing to disclose. Harold L Manning, MD Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists Disclosure: Nothing to disclose. Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Assistant Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Anne Yim, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital and State University of New York Downstate Medical Center Anne Yim, MD is a member of the following medical societies: American College of Emergency Physicians Disclosure: Nothing to disclose. What is the effect of alcohol on the sympathetic nervous system?Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol.
Does alcohol activate the sympathetic nervous system?Among its many physiological effects, alcohol robustly activates the sympathetic nervous system. Our laboratory has reported that simulated binge alcohol consumption increases muscle sympathetic nerve activity (MSNA) (5), a finding consistent with several other alcohol and microneurographic studies (6–12).
How does alcohol stimulate the nervous system?Alcohol's Core Effects
Alcohol is classified as a central nervous system depressant. When consumed even in small amounts, it increases the number of neurotransmitters in the brain responsible for slowing down neuron-to-neuron communications. Under the influence of this change, brain activity decreases.
How does alcohol affect dysautonomia?ABSTRACT. Dysautonomia is a dysfunction of the autonomic nervous system, which mediates both sympathetic and parasympathetic functions of the human body. Alcohol has been established to affect the autonomic function through liver injury and accumulation of vasodilators.
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Which condition is associated with sympathetic system stimulation because of alcohol intake?
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