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Dr Sampurna Roy MD                                         January 2016


Toast to your health this festive season? 

Be careful !

         

                     

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Dangers of  "Holiday Heart Syndrome" and other complications of Chronic Alcoholism

 


Chronic alcoholism is defined as the regular intake of a quantity of alcohol that is enough to injure a person socially, psychologically, or physically.

Although this addiction is more common in men, the number of female alcoholics has been rapidly increasing.

While there are no firm rules for most people, a daily consumption of more than 40 gm alcohol should probably be discouraged. Intake of 100 gm or more a day may be dangerous. 

Sudden excessive drinking during holiday season can cause serious problems.

The following changes are noted in the major organs in alcoholics:

Heart:

Cardiac Path Online

Dilated cardiomyopathy is associated with heavy consumption over an extended period.  An association between the ingestion of acute alcohol and onset of cardiac arrhythmias was first reported in the early 70's.

Regular alcohol intake appears to increase blood pressure, leading to arterial hypertension, which is a risk factor for other cardiovascular diseases  and for sudden death.

There is also a higher risk of sudden cardiac death with alcohol abuse, which increases with the amount ingested, regardless of the presence of previous heart disease like ischemic heart disease or myocardial infarction.

Chronic consumption of large amounts of alcohol is associated with alcoholic cardiomyopathy, a subtype of secondary dilated cardiomyopathy, known to be associated with not only cardiac failure but also with atrial fibrillation  and other cardiac arrhythmia.

Alcohol appears to be able to cause cardiac arrhythmias in healthy people either following acute excessive alcohol ingestion, commonly known as "binge drinking," or chronic ingestion.

Arrhythmia due to chronic drinking appears to be significantly associated with consumption of >36 gm alcohol/day

"In 1978, Philip Ettinger described "Holiday heart syndrome" for the first time. This condition is characterized by cardiac arrhythmia in healthy people without heart disease. There is acute cardiac rhythm disturbance and atrial fibrillation, after binge drinking. The name is derived from the fact that episodes were initially observed more frequently after weekends or public holidays like Christmas or New Year's Eve.  This disturbance disappeared with subsequent abstinence, leaving no residual heart disease."

Holiday heart syndrome revisited after 34 years.

There are many types of alcholic beverages like beer, wine, and distilled drinks such as vodka and whisky. It is important to be aware if some of these types of drink cause increased risk of  "Holiday heart syndrome".

Beware of "holiday heart syndrome". Overdrinking may cause your heart rhythm to go haywire.

Brain:

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Acute Wernicke's encephalopathy and the Wernicke-Korsakoff syndrome are nutrition deficiency disorders due to brain damage caused by a lack of thiamine (vitamin B1). These disorders are often noted in alcoholic patients. There is mental confusion, ataxia, abnormal ocular motility, and polyneuropathy.

Severe impairment of cognitive functions which is known as the "alcohol-associated dementia" is present.

Thiamin is required for energy production and proper functioning of neurons. Thiamin deficiency can lead to damage or death of neurons.

Low levels of thiamine damage more severely some vulnerable regions of the brain.

i) Thalamus (the major relay station of the brain that serves many important functions) and

ii) Mammillary bodies, which are part of the hypothalamus, located just below the thalamus. The mammillary bodies receive many neural connections from the hippocampus, which appears to be the primary part of the brain involved in the formation of memories. Mammillary bodies neurons projects to the thalamus, which in turn makes connections with the cerebral cortex, where long-term memories are stored. These correlations may explain why lesions involving the thalamus and the mammillary bodies can lead to anterograde amnesia. Memories formed in the hippocampus cannot be stored since connections within the cortex are disrupted.

- Alcoholic cerebellar degeneration is differentiated from other forms of acquired or familial cerebellar degeneration by the uniformity of its manifestations. The cerebellar vermis shows shrinkage of the folia and widening of the sulci.

- Central pontine myelinolysis is another change in the brain of alcoholics. It is caused by electrolytic imbalance, usually after electrolyte therapy, after an alcoholic binge, or during withdrawal. The patient present with progressive weakness of bulbar muscles causing dysphagia and dysarthria. This is followed by inability to swallow. Quadriparesis and coma eventually end in respiratory paralysis. Microscopic examination reveals foci of demyelination in pons.

Liver:  

The effect of alcohol on the liver has been known for several thousand years, having been implied in the Ayurveda, the ancient medical text of India.

The liver involvement in alcoholic liver disease classically ranges from alcoholic steatosis, alcoholic hepatitis or steatohepatitis, alcoholic cirrhosis and even hepatocellular carcinoma.

Diagnosis of alcoholic liver disease can be made in persons with excessive alcohol intake  (20-40 gm/day for men and 20 gm/day for women) and evidence of liver injury.

The nature of the alcoholic beverage is largely irrelevant, only the total daily dose of alcohol is relevant.

Pancreas:

Pancreatic Pathology Online

Alcoholic pancreatitis is a major complication of alcohol abuse. 

The risk of developing pancreatitis increases with increasing doses of alcohol, suggesting that alcohol exerts dose-related toxic effects on the pancreas.

It has been suggested that only few alcoholics develop the disease, indicating that an additional trigger is needed to initiate clinically evident pancreatic injury.

It is now well established that alcohol is metabolized by the pancreas via both oxidative and non-oxidative metabolites.

Alcohol and its metabolites produce changes in the acinar cells,  which may promote premature intracellular digestive enzyme activation predisposing the gland to autodigestive injury.

Pancreatic stellate cells are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation.

Gastrointestinal Tract:

Acute and chronic alcohol ingestion causes a variety of pathological changes in the gastrointestinal tract, including gross morphological lesions and functional changes.

Reflux esophagitis may be particularly painful.

Peptic ulcers are also more common in the alcoholic.

Violent retching may lead to tears at the esophageal-gastric junction (Mallory-Weiss syndrome). In serious cases there is severe bleeding.

Chronic consumption of alcohol causes a significant increase in the risk for squamous carcinoma of the oesophagus.

Bone: 

 

Alcohol consumption is a risk factor for osteoporosis based on the frequent finding of a low bone mass, decreased bone formation rate, and increased fracture incidence in alcoholics. Alcohol also has been shown to reduce bone formation in healthy humans.

Skeletal Muscles:

Muscle weakness is extremely common in alcoholics and is often due to general debility and nutritional deficiency.

Clinically, even well-nourished alcoholics usually show some weakness, particularly of the proximal muscles.

A wide range of changes in skeletal muscle is seen in chronic alcoholics, varying from mild alterations in muscle fibers evident only by electron microscopy to a severe, debilitating chronic myopathy, with degeneration of muscle fibers and diffuse fibrosis.

On rare occasions, acute alcoholic rhabdomyolysis, acute necrosis of muscle fibers and release of myoglobin to the circulation is seen. This sudden event can be fatal, because of renal failure secondary to myoglobulinurea.

Blood:

Megaloblastic anemia secondary to a deficiency of folic acid can occur in malnourished alcoholics.

A nutritional deficiency of folic acid is the most important factor. Absorption of folate in the small intestine may be decreased in alcoholics.

Chronic alcohol intoxication can cause an increase in red blood cell volume.

In alcoholic cirrhosis the spleen is often enlarged by portal hypertension. In such cases hypersplenism often causes hemolytic anemia.

Acute transient thrombocytopenia is common after acute alcohol intoxication and may result in bleeding.

Alcohol also interferes with the aggregation of platelets, which may contribute to bleeding.

Cancer:

Alcohol increases risk of cancer of oral cavity and pharynx, oesophagus, colorectum, liver, larynx and female breast. 

There is also evidence that alcohol drinking is associated with some other cancers such as  pancreas and prostate cancer and melanoma.

Visit: As a doctor today I prescribe Thiamine (Vitamin B1) rich food:  Prevent Beriberi, Wernicke’s Encephalopathy, and Korsakoff’s Psychosis

 

Further reading:

Holiday heart syndrome.

Beer drinker's cardiomyopathy liver failure, hyponatraemia, hypo-osmolality, inappropriate secretion of antidiuretic hormone, lactic acidosis, venous gangrene and myoneuropathy.

Thiamine deficiency induced neurochemical, neuroanatomical, and neuropsychological alterations: a reappraisal.

Alcohol consumption and risk of cancer: a systematic literature review.

Pathology of alcoholic liver disease, can it be differentiated from nonalcoholic steatohepatitis?

Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis.

Mechanisms of alcoholic pancreatitis.

Alcohol and bone: review of dose effects and mechanisms.


 

 

Dr  Sampurna Roy  MD

Consultant Histopathologist (Kolkata - India)

 

 

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