What is ETOH? Effects, risks, and addiction
While other important confounding factors, such as poor nutrition and hepatic impairment, play a role in individual patients, neither is necessary for myopathy development in clinical and animal studies. Type II atrophy is not specific for the effects of ethanol and is also a feature of glucocorticoid excess, disuse atrophy, hypothyroidism, hypophosphatemia with or without osteomalacia, and some cases of critical illness myopathy. Weakness ensues and is much more prominent than that for alcoholic neuropathy; reflexes are diminished or lost distally depending on severity. Neuropathy may progress quickly, especially at higher doses, and progression is typically more rapid than alcoholic polyneuropathy. The case highlights the often delayed nature of symptom reporting in alcoholic patients with profound neuropathy. Therefore, the need to establish a more effective control on ethanol consumption has been repeatedly claimed . Ondansetron has been studied in four blinded placebo-controlled trials comparing low doses for alcohol dependence. This suggests that a proportion of sudden unexpected deaths are due to alcohol related arrhythmia, but are still not being recognized as such. Several growth the effects of living with an alcoholic spouse factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage 119,133. The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed . Heart myocytes are relatively resistant to the toxic effect of ethanol, developing a functional and structural compensatory mechanism able to minimize or repair the ethanol-induced myocyte damage 20,31,39. In addition, contractile sarcomere proteins such as Myosin, Actin, and Troponin are also affected by ethanol, causing the functional progressive depression of myocyte contractility, inducing progression to heart failure 56,104,131. This damage first induces diastolic dysfunction, which is initially subclinical and later clinically apparent . What should I do if I think someone has EtOH addiction? Malnutrition and vitamin deficiency are common in chronic alcoholics, and thiamine has been the primary focus of investigation. Further clouding the clinical syndrome may be depression or apathy blamed on the alcoholism itself but which does not appreciably resolve once abstinence is achieved. Moreover, current neuropathologic criteria may bias patients with primarily alcohol-related dementia to be diagnosed with neurodegenerative disease when some changes of the latter are evident at autopsy. The syndrome has devastating effects, and up to 25% of patients require institutionalization.9 Korsakoff syndrome is another CNS syndrome resulting from thiamine deficiency in alcoholics. Gait disturbance due to sensory ataxia may be difficult to distinguish from, or be concomitant with, alcoholic cerebellar degeneration. When identified, alcoholic neuropathy is indistinguishable from other distal sensorimotor axonal processes. Patients with both alcohol exposure and thiamine deficiency demonstrate a mixture of findings that lead to similar treatment paradigms addressing both states.25 A 51-year-old man with a history of chronic alcoholism and colon adenocarcinoma with local intraabdominal metastases presented to the emergency department following several days of blurred vision followed by confusion and somnolence. A careful, open-ended alcohol history is very important, particularly among patients who may be unable to provide complete histories upon initial presentation. Alcohol withdrawal syndromes can be insidious and often ascribed to alternative diagnoses if alcohol histories are not fully divulged upon initial hospital presentation. Yale Medicine’s approach to alcohol use disorder is evidence-based, integrated, and individualized. This process, however, can bring about the unpleasant and potentially serious symptoms of alcohol withdrawal syndrome. Treatments for alcohol use disorder include medications as well as counseling and behavioral therapies. Along with developing heart damage, patients with ACM may also damage other organs, such as the liver, central and peripheral nervous system, skeletal muscle, pancreas, and digestive tract, and are exposed to an increased risk of cancer 24,63,64. The subject with excessive alcohol consumption, after more than 10 years of high ethanol consumption, usually develops subclinical heart functional changes before symptom appearance or signs of heart failure 55,56. In this review, we specifically describe and discuss the global effects that ethanol exerts on the heart myocytes, the so-called alcoholic cardiomyopathy (ACM). Similarly, patients suffering from other ethanol-related diseases such as liver cirrhosis or brain atrophy should completely suppress their ethanol consumption 47,48. Heart and Circulatory System Clinical trials in patients with uncontrolled comorbid psychiatric diagnoses are not included in this review but can be found in other publications.52,53 Naltrexone is available for oral or intramuscular administration to reduce the craving for alcohol. The degree of response to the disulfiram–alcohol reaction increases with the dose of disulfiram and blood alcohol concentration, but even small amounts of alcohol consumed with disulfiram can produce mild reactions.24 What makes Yale Medicine’s approach to alcohol use disorder unique? Out of end-stage cases, the majority of subjects affected by ACM who achieve complete ethanol abstinence functionally improve 33,82,135. Therefore, complete abstinence from ethanol is the most useful measure to control the natural course of ACM 51,56,135. Ethanol abstinence allows for recovery in the majority of cases, including in those with previous severe depression of LV EF 81,88,135. Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis 14,30,58. The sarcomere complex is early affected by ethanol, decreasing the titin content, a protein that is responsible for sarcomere relaxation and LV distensibility . The ryanodine L-type Ca2+ receptor at the sarcoplasmic reticulum (SR) is also significantly affected by ethanol in a dose-dependent manner 86,102. Alcohol’s Effects on the Body Although patients may initially present with hand dysesthesia, more commonly hand symptoms follow anesthesia in the legs, which may be otherwise unrecognized or overlooked until more bothersome symptoms evolve. This case underscores the often complex factors, including medical comorbidities and prolonged, obfuscated, or underappreciated histories, that may cloud or delay the diagnosis of Wernicke encephalopathy, which is easily treated once recognized. Brain MRI of a patient with Wernicke syndrome, as detailed in Case 7-2. His cognition gradually improved, and was unremarkable 1 month after thiamine repletion; however, fixed neuro-ophthalmic deficits, including right abducens paresis, remained at that time. ETOH Abuse Many published studies of non-approved medications included patients on psychotropic agents (eg,