alcoholic neuropathy

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By: Millicent Gayle M. Villariza ALCOHOLIC NEUROPATHY Definition Neuropathy partly due to associated malnutrition esp. Vitamin B Peripheral neuropathy in alcohol abusers Axons die back Mixed motor & sensory Etiology Still debated Theories o Nutritional deficiencies and direct toxicity from prolonged alcohol consumption are the most likely causes o Direct toxic effect of ethanol Epidemiology Disease is uncommon in the US Chronic alcohol users are commonly affected Pathogenesis Nutritional deficiencies and direct toxicity from prolonged alcohol consumption are the most likely causes of the axonal neuropathies. Persons with alcoholism tend to have nutritional deficiencies due to deceased consumption and/or impaired gastrointestinal absorption. Thiamine is an essential vitamin in the breakdown of pyruvate and plays a role in the health of the peripheral nervous system. Some studies have also linked direct toxic effects of alcohol on peripheral nerves. The combination of nutritional deficiency and direct toxicity leads to wallerian degeneration of axons and reduced myelination in peripheral nerves, which results in neuropathy. Clinical Manifestations Sx first occur in LE (+) paresthesia Decreased sensation especially proprioception Distal muscle weakness & wasting Depressed distal reflexes As disorder worsens o Changes appear proximally in LE & begin in UE Common impairments o Numbness o Paresthesia o Pain o burning feet o muscle weakness (changes in sensation and muscle strength tend to be bilateral and affect the legs more than the arms) o heat intolerance o impotence (men) o incontinence o constipation o diarrhea o nausea/vomiting Common functional limitations o Difficulty ambulating o performing self care activities, o Driving

description

alcoholic neuropathy

Transcript of alcoholic neuropathy

Page 1: alcoholic neuropathy

By: Millicent Gayle M. Villariza

ALCOHOLIC NEUROPATHY Definition

Neuropathy partly due to associated malnutrition esp. Vitamin B

Peripheral neuropathy in alcohol abusers

Axons die back

Mixed motor & sensory Etiology

Still debated

Theories o Nutritional deficiencies and direct toxicity from prolonged alcohol

consumption are the most likely causes o Direct toxic effect of ethanol

Epidemiology

Disease is uncommon in the US

Chronic alcohol users are commonly affected Pathogenesis

Nutritional deficiencies and direct toxicity from prolonged alcohol consumption are the most likely causes of the axonal neuropathies.

Persons with alcoholism tend to have nutritional deficiencies due to deceased consumption and/or impaired gastrointestinal absorption.

Thiamine is an essential vitamin in the breakdown of pyruvate and plays a role in the health of the peripheral nervous system.

Some studies have also linked direct toxic effects of alcohol on peripheral nerves. The combination of nutritional deficiency and direct toxicity leads to wallerian degeneration of axons and reduced myelination in peripheral nerves, which results in neuropathy.

Clinical Manifestations

Sx first occur in LE

(+) paresthesia

Decreased sensation especially proprioception

Distal muscle weakness & wasting

Depressed distal reflexes

As disorder worsens o Changes appear proximally in LE & begin in UE

Common impairments

o Numbness

o Paresthesia

o Pain

o burning feet

o muscle weakness (changes in sensation and muscle strength tend to be bilateral and affect the legs more than the arms)

o heat intolerance

o impotence (men)

o incontinence

o constipation

o diarrhea

o nausea/vomiting

Common functional limitations

o Difficulty ambulating

o performing self care activities,

o Driving

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o etc.

Potential disabilities o Unable to

maintain employment personal relationships

o could become socially isolated o trouble reintegrating into community

Differential Diagnosis

Laboratory or imaging studies used to confirm or rule out diagnosis o Nutritional studies may show deficiencies

thiamine (vit B 1) pyridoxine (vit B6) vit B12 folic acid niacin (vit B3) vit A other deficiencies

o Nerve conduction tests and EMG may be used to determine the extent of neurological damage

Decreased sensory action potential amplitudes Minimal slowing of motor conduction velocity Distal latencies are minimally prolonged Positive sharp waves & fibrillation potentials in distal muscles

with polyphasic units of increase amplitude o Nerve biopsy may be used to rule out other causes o EGD, upper GI, and small bowel series may be used to r/o physical

obstruction as cause of vomiting and other GI symptoms o Voiding cystourethrogram (VCUG) may show decreased bladder

emptying caused by damaged nerves controlling the bladder o Chronic alcohol consumption may cause increased liver enzyme levels

as measured by AST and ALT tests o Elevated blood creatinine levels may implicate renal insuffiency as a

cause for peripheral neuropathy o An elevated erythrocyte sedimentation rate (ESR) may implicate an

inflammatory condition. o A screen for heavy metal toxicity since it can be a cause for neuropathy

Additional information to confirm diagnosis o thorough patient history to document any abuse of alcohol

Distinguishing characteristics of similar conditions o diabetic neuropathy

similar in its presentation of symptoms However, patients with this condition typically have a long-

standing history of diabetes Blood glucose tests are used to diagnose diabetes

Prognosis/Complications

GOOD prognosis if treated promptly

Medical factors impacting prognosis and outcome o current level of nerve damage is usually permanent and will progress if

Px continues to abuse alcohol o continued nutritional deficiencies could cause the condition to progress

Medical Management

Ensure good diet

Diet supplements including thiamine and folic acid, depending on individual's deficiencies

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Medication to treat pain, including OTC analgesics such as aspirin, ibuprofen, or acetaminophen.

Efforts to reduce orthostatic hypotension: eating extra salt, sleeping with the head elevated, medications.

Manual expression ofurine, catheterization, or medications to treat bladder dysfunction.

Referral to AA, medication, and Px education for treatment of alcoholism

PT INTERVENTION

PT Tests/Measures o Aerobic capacity and endurance

Patients with this disorder tend to have decreasing BP during sit to stand or supine to stand.

So BP should be assessed prior to activity. These patients may also have decrease endurance so baseline

endurance should also be recorded. o Arousal, attention, and cognition

Due to decreased neurological function these patients should be screened in this area

o Assistive and adaptive devices These patients can have balance and gait disorders and may

need to be assessed for the need to use assistive devices for safety purposes.

o Community and work integration or reintegration These patients may have still have emotional issues related to

alcoholism and may need help to reintegrate into the community or work place.

o Cranial nerve integrity This should be assessed to rule out other potential

neuromuscular disorders. o Environment, home and work

these patients may need assistance to reintegrate into their normal daily lives

o Gait, locomotion, and balance This can be a major impairment for this type of patient and

should be a major focus in the examination. This type of patient tends to present with ataxia and wide base of

support and can also present with bilateral foot drop. o Integumentary integrity

due to the decreased sensation to the lower extremities these patients should be screened for skin break down

o Motor function observe the patient's quality of movement (speed, smoothness)

and coordination o Orthotic, protective, and supportive devices

The decrease sensation in this disorder can lead to the need for protective shoes and socks.

These patients can also have decrease dorsiflexion and plantarflexion so these patients should be assessed for the need for AFOs.

o Pain These patients may or may not have pain a pain rating should be recorded as a baseline

o Range of motion Contractures may be present in this patient population due to

weakness in dorsiflexion and plantarflexion, length of gastroc should be assessed as the ROM in other joints

o Reflex integrity

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Tendon reflexes can be reduced in this population especially those in the lower extremity and should be assessed thoroughly

o Self-care and home management These patients may have trouble doing ADLs and IADLs so this

area should be assessed in order to determine appropriate intervention.

o Sensory integrity Sensation loss is very common in these patients

the loss usually starts in the lower extremities and in severe cases can include the upper extremities

Sensation loss is also usually found to be symmetrical these patients should also be assessed for vibration and

proprioception integrity

Additional Resources o These patients may benefit from

Psychiatric Nutritional and substance abuse support group resources These resources will depend on where the patient is at in their

rehabilitation program PT MANAGEMENT

Primary treatment is STOP DRINKING ALCOHOL BEVERAGES

Most likely outcome of PT o Comprehensive physical therapy for patients with alcoholic neuropathy

may include the following to address individual's impairments Gait and balance training, possibly with an assistive device

For safety ROM exercises and stretching, particularly for the gastroc-soleus

muscle

to prevent contracture and maintain normal gait mechanics

Strength training of weakened muscles Recommended activities

HEP to maintain LE strength and flexibility Education of Proper Foot Care

Feet should be washed each night with mild soap and warm water.

Wear clean socks daily.

Shoes should be loose fitting and custom fitted.

Cut the nails straight.

Do not cut corns or calluses.

Do not wear tight or constricting clothing.

Do not use tobacco in any form.