Management of alcohol-induced peripheral neuropathy : Nursing made Incredibly Easy

The sometimes-conflicting findings between biopsy findings may be representative of the complex interplay of pathological factors in alcohol-related peripheral neuropathy and is indicative of the need for further research in this area. Due to the breadth of the literature surrounding this topic, this review shall focus exclusively upon peripheral neuropathy, without discussing autonomic neuropathy. The damage may be the direct result of long periods where you drank too much alcohol. Nutritional problems linked to alcohol use, such as vitamin deficiency, can also cause nerve damage. Excessive, long-term consumption of alcohol can lead to malnutrition as well as nerve damage, and both contribute to the development of alcoholic neuropathy.

Treatment of Peripheral Neuropathy

Active denervation (presence of positive waves and fibrillations) was also present in the majority of patients. The prevalence of denervation findings on EMG ranged from muscle to muscle, with the highest being in the muscles of the lower limbs suggesting a length-dependent pattern [35, 45, 52, 59]. This could lead to disability, chronic pain, and damage to your arms alcohol neuropathy stages and legs. However, if caught early enough, you can minimize the damage from alcoholic neuropathy. Avoiding alcohol and improving your diet can sometimes lead to a moderate to full recovery. While peripheral neuropathy generally cannot be cured, there are several medical treatments that can be used to manage the pain of alcoholic neuropathy, aiding in your recovery.

Providing the Best Available Care for Patients with Neuropathy

• Ethanol is classified as a “depressant” because it has a generally slowing effect on brain activity through activation of γ-aminobutyric acid (GABA) pathways.
• Encourage patients to be active as tolerated to promote tissue oxygenation, mobility, and well-being.
• These treatments, in some cases, only suppress the symptoms but do not treat the underlying pathology.
• She is actively involved in research in chronic inflammatory demyelinating neuropathy at the Peripheral Neuropathy Center and supervises the general neurology resident clinic at NewYork-Presbyterian Hospital.
• Consumption of alcohol has and continues to serve major roles in religious and cultural ceremonies around the world.
• Chronic alcohol consumption leads to malnutrition with dysfunctions in protein and lipid metabolism which affect the metabolic pathways and progression of ALN symptoms within the central and peripheral nervous systems [89].

Ensuring patient safety and interprofessional collaboration are major frameworks for achieving these goals. Patients with neuropathic pain may be less mobile, predisposing them to conditions such as pneumonia, deep vein thrombosis, skin breakdown, muscle atrophy and weakness, and depression. Physical therapy should be included in the treatment plan to improve flexibility, strength, and balance. Occupational therapy can help the patient with self-care activities and safely navigating the home environment.

Want to protect your brain? Here’s what you need to know about alcohol consumption.

The prevalence of PN ranges from 2.4% to 8% per 100,000 individuals worldwide. The Foundation for Peripheral Neuropathy and the US Food and Drug Administration estimate that 20 million people in the US experience PN. Alcohol-induced peripheral neuropathy (PN) is a chronic and painful condition in which the neurotoxic effects of alcohol and nutritional deficiencies cause a pathologic response in nerve function. This article presents the pathophysiology, signs and symptoms, diagnostic approaches, treatment options, and nursing care of patients with alcohol-induced PN. The journal further reports that alcoholic polyneuropathy is likely caused by nutritional deficiencies and the depletion of thiamine that is caused by heavy and long-term drinking. It is most likely that drinking a lot of alcohol over several years causes direct damage to nerve cells and can also contribute to nutritional deficiencies in the body; these may both be factors in the onset of alcoholic polyneuropathy.

Topical Collection on The Pathobiology of Alcohol Consumption

• Multiple variables contribute to this painful neuropathic syndrome, including the toxic effects of alcohol on neurons and nutritional deficiencies.
• These two groups, however, were distinct from the standpoint that nerve conduction velocities were slower and sural nerve biopsy specimens revealed more segmental demyelination in the post gastrectomy group.

Thus, deficiency of these vitamins was felt to be unlikely in Danish beer drinkers at that time and, indeed, measured vitamin concentrations were mostly normal. Clinical features of neuropathies in the alcoholic and post gastrectomy patients were similar. These two groups, however, were distinct from the standpoint that nerve conduction velocities were slower and sural nerve biopsy specimens revealed more segmental demyelination in the post gastrectomy group. The authors concluded that malnutrition, including low blood concentrations of B vitamins, is not a prerequisite for the development of alcoholic neuropathy, and ethanol per se plays a role in the pathogenesis of alcoholic neuropathy. Coasting is a major feature of alcoholic neuropathy, largely due to chronic alcohol abuse. Even though much research was done in this area, still we do not have a full understanding of the mechanism of alcoholic neuropathy.

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Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition. A major treatment goal is for the patient to be involved in support groups or counseling that will help him or her reduce or abstain from alcohol use. Because support groups and counseling come in many forms, the patient, as an integral member of the team, will decide which group(s) and counseling formats are best for him or her. A more comprehensive EMG analysis may be conducted when the patient has lumbosacral radiculopathy. The primary findings in alcohol-induced PN are a positive sharp wave, fibrillation potentials, and complex repetitive charges—electrical measures indicating severely degenerative muscle function. It is important to supplement the diet with vitamins, including thiamine and folic acid.

Signs and Symptoms of Alcoholic Neuropathy

Treatment of ALN aims to reduce further damage to the peripheral nerves and restore their normal functioning. What is crucial during ALN treatment is the alleviation of the major causation of ALN which is alcohol abuse. Alcohol abuse treatment might lead to a resolution of neuropathic pain and alleviation of its symptoms. This can be achieved by complete alcohol abstinence and a balanced diet primarily supplemented by B6, B12, and E vitamins, as well as folate, thiamine, and niacin. Benzodiazepines are commonly used to reduce the symptoms of alcohol withdrawal syndrome; acamprosate and naltrexone are effective to treat alcohol dependence; however, the latter usually induces withdrawal symptoms [175]. Further, serotonin-norepinephrine reuptake inhibitors are prescribed to treat alcohol-induced neuropathic pain via exerting antinociceptive properties by increasing serotonergic and noradrenergic neurotransmissions [71].

• The majority of studies which investigate the relationship between malnutrition and neuropathy focus on thiamine deficiency as an aetiological factor, drawing upon existing knowledge of Beri Beri.
• Supplementation with benfotiamine significantly increased concentrations of TDP and total thiamine compared with supplementation with thiamine HCl [96].
• Pain seems to be consistent through the literature to be one of the most common complaints and can be the first clinical indication of the disease.
• The diagnosis of alcoholic neuropathy involves a combination of medical history, physical examination, and possibly blood tests or nerve tests such as electromyography (EMG) and nerve conduction studies (NCV).
• It results from damage to the peripheral nerves that span the body and connect the brain and spinal cord to the muscles, skin, joints and internal organs.

Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy. Chronic alcoholism can alter the intake, absorption and utilization of various nutrients (nicotinic acid, vitamin B2, vitamin B6, vitamin B12, folate or vitamin E). Thus, these vitamin deficiencies were not considered to be major causal factors of neuropathy [26]. Malnutrition has been implicated in the pathology of alcohol-related neuropathy by several authors. The majority of studies which investigate the relationship between malnutrition and neuropathy focus on thiamine deficiency as an aetiological factor, drawing upon existing knowledge of Beri Beri. A smaller number of publications do attribute thiamine deficiency, but generally speaking these studies were older or of lower quality evidence [4, 6, 30, 58, 76, 77].

Who does peripheral neuropathy affect?

Autonomic symptoms are among the most serious because they involve your body’s vital functions. When those don’t work correctly, it can have very severe — and sometimes dangerous — effects. Symptoms of AAN are non-specific; in the sympathetic division, these include impairments in perspiration, orthostatic hypotension, whereas in parasympathetic hoarseness, swallowing difficulties, or cardiac arrhythmias [111, 166].