Can you create a SOAP note with three differential diagnoses for a patient who presents with new symmetric distal peripheral neuropathy, reports about 10 standard alcoholic drinks per week, has no personal history of diabetes, autoimmune disease, or prior neuropathy, and has first-degree relatives with diabetes mellitus, chronic alcohol abuse, and rheumatoid arthritis?

SOAP Note: New Symmetric Distal Neuropathy with Alcohol Use and Family History

Subjective

Chief Concern: New onset symmetric distal neuropathy symptoms

History of Present Illness:

• Patient reports new symmetric distal sensory symptoms (specify: burning pain, tingling, numbness, "electrical shock" sensations, or altered temperature perception) 1
• Symptoms began distally in feet with potential proximal progression 2
• Pain characteristically worse at night, causing sleep disturbance 1
• May describe discomfort as "walking barefoot on marbles" or "walking barefoot on hot sand" 1
• Reports 10 standard alcoholic drinks per week (likely underestimated; actual consumption may be higher) 3

Past Medical History:

• No personal history of diabetes mellitus, autoimmune disease, or prior neuropathy
• Family history: First-degree relatives with diabetes mellitus, chronic alcohol abuse, and rheumatoid arthritis

Review of Systems:

• Assess for autonomic symptoms: orthostatic dizziness, erectile dysfunction, gastroparesis symptoms, bladder dysfunction 2
• Screen for depression and anxiety (present in >66% of patients with painful neuropathy) 1

Objective

Physical Examination:

Small Fiber Function:

• Pinprick sensation testing in distal lower extremities 2
• Temperature sensation assessment 2

Large Fiber Function:

• Vibration perception using 128-Hz tuning fork at great toes and malleoli 2, 4
• Ankle reflexes (diminished or absent suggests polyneuropathy) 5
• Joint position sense testing 5

Protective Sensation:

• 10-g monofilament testing at plantar surfaces to identify loss of protective sensation and ulceration risk 2, 4

Vascular Assessment:

• Pedal pulses and ankle-brachial index to exclude peripheral arterial disease 1

Gait and Motor:

• Assess for distal weakness or atrophy 2
• Evaluate gait abnormalities 5

Assessment

Differential Diagnoses:

1. Alcohol-Induced Peripheral Neuropathy (Most Likely)

Alcohol is the second most common cause of distal symmetric polyneuropathy after diabetes and is almost never adequately evaluated. 3

• Rationale: Patient reports 10 drinks/week, but alcohol intake is routinely underestimated by patient history 3. Family history of alcohol abuse increases suspicion. Alcohol causes axonal distal symmetric sensorimotor neuropathy identical to diabetic neuropathy 6.
• Key Point: Even without diabetes, alcohol at this level can cause neuropathy, and if alcohol consumption continues, neuropathy will not improve regardless of other interventions 3.
• Critical Testing: Urinary ethyl glucuronide (EtG) detects alcohol intake within previous 90 hours and is most likely to detect surreptitious alcohol use 3. Check markers of high alcohol intake: elevated liver enzymes (AST, ALT, GGT), elevated uric acid, elevated triglycerides, low magnesium, low folic acid 3.

2. Prediabetes or Early Diabetes Mellitus

Screen for diabetes in all patients with symmetric distal neuropathy, as it is the leading cause of burning feet syndrome. 4

• Rationale: Strong family history of diabetes mellitus in first-degree relative significantly increases risk. 10-15% of newly diagnosed type 2 diabetes patients already have distal symmetric polyneuropathy 7.
• Key Point: Diabetic neuropathy presents identically to alcohol-induced neuropathy with distal symmetric sensory loss, burning pain, and dysesthesias affecting small fibers first 4.
• Critical Testing: Fasting blood glucose and hemoglobin A1c are essential initial screening 4, 8. Even prediabetic states can cause neuropathy.

3. Vitamin B12 Deficiency

Vitamin B12 deficiency is a common and reversible cause that must be excluded in all patients with burning feet. 4

• Rationale: Alcohol consumption interferes with B12 absorption and metabolism 8. B12 deficiency causes both symptomatic and asymptomatic small fiber loss with reduced intraepidermal nerve fiber density 4.
• Key Point: This is a treatable cause that can prevent progression if identified early 8.
• Critical Testing: Serum vitamin B12 level (consider methylmalonic acid if B12 borderline) 4, 8.

Plan

Diagnostic Workup (Initial Laboratory Evaluation):

Mandatory Initial Tests:

• Fasting blood glucose and hemoglobin A1c (screen for diabetes/prediabetes) 4, 8
• Comprehensive metabolic profile (assess renal function, electrolytes) 4, 8
• Vitamin B12 level (exclude reversible deficiency) 4, 8
• Thyroid-stimulating hormone (TSH) (exclude hypothyroidism) 4, 8
• Complete blood count (assess for anemia, macrocytosis suggesting B12 deficiency or alcohol use) 8
• Serum protein electrophoresis with immunofixation (screen for monoclonal gammopathy, which occurs in up to 20% of neuropathy cases and fundamentally changes management) 9, 8

Alcohol-Specific Testing:

• Urinary ethyl glucuronide (EtG) (most sensitive for detecting recent alcohol use within 90 hours) 3
• Liver function tests (AST, ALT, GGT) (markers of chronic alcohol use) 3
• Uric acid, triglycerides (elevated with high alcohol intake) 3
• Magnesium, folic acid (low with chronic alcohol use) 3

If Initial Workup Inconclusive:

• Referral to neurology for electrodiagnostic studies (nerve conduction studies/EMG), though these may be normal in small fiber neuropathy 2, 4, 8
• Consider skin biopsy for intraepidermal nerve fiber density if small fiber neuropathy suspected with normal nerve conduction studies 2

Treatment Approach:

Address Underlying Etiology (Priority):

Alcohol Cessation (Critical):

• Counsel immediate and complete alcohol cessation 3. If alcohol consumption continues, distal symmetric polyneuropathy will not improve regardless of etiology 3.
• Do not prescribe neuropathic pain medications (tricyclics, gabapentinoids, SNRIs, analgesics) if alcohol use continues, as combination may excessively suppress respiration and cognitive function 3.
• Refer to addiction medicine or support services as needed.

Glycemic Control (If Diabetes/Prediabetes Identified):

• Target HbA1c <7% to prevent or delay neuropathy progression 2, 4. Tight glycemic control is the only strategy convincingly shown to prevent diabetic peripheral neuropathy in type 1 diabetes and slow progression in type 2 diabetes 4.

Vitamin Supplementation (If Deficient):

• Replace vitamin B12 if deficient (oral or intramuscular depending on severity) 4, 8

Symptomatic Pain Management (Only After Alcohol Cessation):

First-Line Pharmacologic Treatment:

• Pregabalin: Start 50 mg three times daily (150 mg/day), increase to 100 mg three times daily (300 mg/day) within 1 week based on efficacy and tolerability 4. Maximum recommended dose 300 mg/day 4. Pregabalin, duloxetine, and gabapentin achieve ≥50% pain reduction in 38% of patients at optimal dosing 1.
• Alternative: Duloxetine 30 mg daily, titrate to 60 mg daily after one week 1, 4
• Alternative: Gabapentin starting at 300 mg daily 1, 4

Second-Line Options (If First-Line Inadequate):

• Amitriptyline, nortriptyline, venlafaxine, topical lidocaine, topical capsaicin 4
• Caution with tricyclics: Risk of orthostatic hypotension, cardiac arrhythmias, anticholinergic effects 1

Non-Pharmacological Interventions:

• Supervised exercise therapy to improve symptoms and potentially slow neuropathy progression 1, 4
• Well-fitted walking shoes or athletic shoes with cushioning to redistribute plantar pressure 1
• Podiatry referral for custom orthotics if needed 1
• Avoid prolonged cold water immersion or ice application (risk of immersion foot, skin ulceration, infection) 1

Monitor for Complications:

• Screen for depression and anxiety (present in >66% of patients with painful neuropathy); addressing psychological comorbidities improves pain outcomes 1
• Annual 10-g monofilament testing to monitor for loss of protective sensation and ulceration risk 2
• Foot care education to prevent ulceration in patients with loss of protective sensation 2

Common Pitfalls to Avoid:

• Do not assume a single etiology: Multiple causes can coexist (alcohol + prediabetes + B12 deficiency) 9, 4
• Do not rely solely on patient-reported alcohol intake: Biochemical screening with urinary EtG is essential 3
• Do not rely solely on nerve conduction studies: Small fibers constitute 70-90% of peripheral nerve fibers and are damaged earliest, often before conventional electrophysiology shows abnormalities 4
• Do not prescribe neuropathic pain medications if alcohol use continues: Risk of respiratory and cognitive suppression 3
• Do not assume diabetic neuropathy without excluding other causes, even if diabetes is present 9, 4