What underlying conditions may have been masked by long-term alcohol (ethanol) consumption in a middle-aged adult who abruptly stopped drinking nearly two years ago and is now experiencing tachycardia, pain, fatigue, sensory issues, decreased sleep, and reduced heart rate variability (HRV)?

Alcohol Was Likely Masking Underlying Autonomic Dysfunction and Chronic Pain Conditions

The constellation of symptoms—tachycardia, decreased heart rate variability, pain, fatigue, sensory disturbances, and sleep disruption—emerging nearly two years after alcohol cessation suggests alcohol was suppressing underlying autonomic nervous system dysfunction, possibly dysautonomia or small fiber neuropathy, rather than causing acute withdrawal effects.

Understanding the Timeline

The critical distinction here is timing. Acute alcohol withdrawal follows a predictable sequence: mild symptoms within 6-24 hours, seizures within 48 hours, and delirium tremens peaking at 3-5 days after the last drink 1. Your patient stopped drinking nearly two years ago, placing them far beyond any withdrawal syndrome timeframe. The progressive worsening of symptoms over two years indicates unmasking of pre-existing conditions rather than withdrawal phenomena 1.

Primary Conditions to Investigate

Autonomic Dysfunction (Dysautonomia)

The combination of elevated resting heart rate and decreased HRV is pathognomonic for autonomic nervous system dysfunction. 2

• Chronic alcohol use can mask autonomic dysfunction through its depressant effects on the sympathetic nervous system 2
• Alcohol's GABAergic effects may have been compensating for underlying sympathetic hyperactivity 3
• Postural orthostatic tachycardia syndrome (POTS) or other forms of dysautonomia should be evaluated with tilt-table testing and autonomic function studies 2

Alcoholic Neuropathy or Small Fiber Neuropathy

The sensory disturbances and pain suggest peripheral nerve damage that alcohol may have been masking through its analgesic and sedative properties 4:

• Chronic heavy alcohol use (>90 grams daily for >5 years) causes peripheral neuropathy affecting sensory and autonomic fibers 2
• Small fiber neuropathy testing via skin biopsy should be performed to quantify nerve fiber density 4
• The pain may represent neuropathic pain that was previously suppressed by alcohol's analgesic effects 3

Alcoholic Cardiomyopathy

Chronic heavy drinking causes direct myocardial toxicity leading to cardiomyopathy with mortality rates of 40-50% within 3-6 years if drinking continues. 2

• The decreased HRV and tachycardia may indicate subclinical cardiac dysfunction 2
• Echocardiography and cardiac MRI should be obtained to assess left ventricular function and rule out structural heart disease 2
• Even after cessation, alcoholic cardiomyopathy can progress if other cardiovascular risk factors remain unaddressed 2

Underlying Psychiatric Conditions

Alcohol use disorders are strongly associated with depressive episodes, severe anxiety, and insomnia that may have been self-medicated with alcohol 4:

• The fatigue and sleep disturbances may represent major depressive disorder or generalized anxiety disorder that was masked by alcohol's sedative effects 4
• Formal psychiatric evaluation is warranted to assess for mood and anxiety disorders 5, 6

Diagnostic Workup Algorithm

Proceed systematically through the following evaluations:

1. Cardiovascular assessment:

   • Echocardiogram to evaluate for cardiomyopathy 2
   • 24-hour Holter monitor to quantify HRV and arrhythmias 2
   • Tilt-table testing for dysautonomia 2

2. Neurological evaluation:

   • Skin biopsy for small fiber neuropathy quantification 4
   • Nerve conduction studies if large fiber involvement suspected 4
   • Autonomic function testing (quantitative sudomotor axon reflex test, thermoregulatory sweat test) 2

3. Hepatic assessment:

   • Liver function tests and fibrosis assessment (FibroScan or equivalent) to evaluate for chronic liver disease 3
   • Chronic liver disease can cause autonomic dysfunction and fatigue 3

4. Psychiatric screening:

   • Formal evaluation for mood and anxiety disorders 5, 6
   • Sleep study if sleep architecture disruption suspected 4

5. Metabolic and endocrine screening:

   • Thyroid function, vitamin B12, folate, thiamine levels 1
   • Diabetes screening, as alcohol may have masked glucose dysregulation 4

Management Priorities

Total abstinence from alcohol must be maintained, as any return to drinking will worsen all underlying conditions. 2

• Refer to addiction specialist to ensure sustained abstinence with medications like naltrexone or acamprosate if relapse risk exists 5
• Thiamine supplementation (100-300 mg/day) should continue to support neurological and cardiac function 1, 2
• Treat identified autonomic dysfunction with beta-blockers (if tachycardia predominates) or midodrine/fludrocortisone (if hypotension present) 2
• Neuropathic pain requires gabapentinoids or tricyclic antidepressants rather than opioids 3
• If cardiomyopathy identified, initiate guideline-directed medical therapy with ACE inhibitors/ARBs, beta-blockers, mineralocorticoid receptor antagonists, and SGLT2 inhibitors 2

Critical Pitfall to Avoid

Do not attribute these symptoms to "post-acute withdrawal syndrome" (PAWS) at this timeline. While PAWS can cause mood and sleep disturbances for months, the specific pattern of autonomic dysfunction (tachycardia, decreased HRV) and progressive sensory symptoms over two years indicates structural organ damage rather than protracted withdrawal 1. Misattributing these symptoms to PAWS will delay diagnosis of potentially serious conditions like cardiomyopathy or dysautonomia that require specific treatment 2.

The alcohol was functioning as an inadvertent treatment for underlying autonomic hyperactivity and pain conditions, and its removal has unmasked these pathologies that now require targeted medical intervention 3, 2, 4.