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The physical element is an important part of a comprehensive approach to drinking problems. Helping services should be organized to cope effectively with diagnosis and treatment in the physical domain and, whatever the particular professional affiliation of the clinician who is working with the problem drinker, there is need for an alertness toward possible physical pathologies. Social workers in a counseling service are, of course, practising their own special types of skill, and no one would suggest that they should also cultivate highly specialized knowledge of liver pathology. It is, however, a reasonable expectation that they should know enough about the liver to understand the significance to their client of a diagnosis of cirrhosis, rather than their being mystified by this term and consequently deflecting that client from talking about something of vital importance. A polite conspiracy can be set up in which both parties pretend that the body does not exist.
Why physical complications matter
Excessive alcohol consumption is a major contributor to mortality and ill health, and “it is a causal factor in more than 60 major types of diseases and injuries and results in approximately 2.5 million deaths each year” (World Health Organization, 2011, p. 20) (Table 5.1). This translates into 4 percent of all deaths worldwide and to approximately 4.5 percent of the global burden of disease and injury attributable to alcohol.
| Men | Women | Both | |
|---|---|---|---|
| Malignant neoplasms | |||
| Mouth and oropharynx cancers | 22 | 9 | 19 |
| Oesophageal cancer | 37 | 15 | 29 |
| Liver cancer | 30 | 13 | 25 |
| Breast cancer | N/A | 7 | 7 |
| Neuropsychiatric disorders | |||
| Unipolar depressive disorders | 3 | 1 | 2 |
| Epilepsy | 23 | 12 | 18 |
| Alcohol use disorders | 100 | 100 | 100 |
| Diabetes mellitus | −1 | −1 | −1 |
| Cardiovascular diseases | |||
| Ischaemic heart disease | 4 | −1 | 2 |
| Haemorrhagic stroke | 18 | 1 | 10 |
| Ischaemic stroke | 3 | −6 | −1 |
| Gastrointestinal diseases | |||
| Cirrhosis of the liver | 39 | 18 | 32 |
| Unintentional injury | |||
| Motor vehicle accidents | 25 | 8 | 20 |
| Drownings | 12 | 6 | 10 |
| Falls | 9 | 3 | 7 |
| Poisonings | 23 | 9 | 18 |
| Intentional injury | |||
| Self-inflicted injuries | 15 | 5 | 11 |
| Homicide | 26 | 16 | 24 |
Burden of disease is quantified in terms of disability adjusted life years (DALYs), a summary measure that combines years of life lost to premature death with years of life lost due to disability. Males have a higher alcohol-related disease burden than do females. Alcohol is the world’s leading risk factor for deaths in males aged 15–59, and the deaths of young people in particular contribute to loss of many years of life (Whiteford et al., 2013).
There are large variations in the alcohol-attributable disease burden in different regions of the world, with injuries accounting for a higher proportion of the burden in lower income countries and cancers accounting for a higher proportion in higher income countries. For any given level of pattern of drinking, the harm is greater in poorer societies than in more affluent ones. In addition, homemade alcoholic beverages in some parts of the world may be contaminated with methanol or lead that also adversely affect health (World Health Organization, 2011).
Alcohol is the third largest risk factor for mortality in developed countries after tobacco and hypertension, and it accounts for 9.2 percent of DALYs lost. This compares with figures of 12.2 percent and 10.9 percent for tobacco and hypertension, respectively (Rehm et al., 2004; World Health Organization, 2007). The burden from liver cancer has increased between 1990 and 2010 by more than 45 percent, in part due to alcohol; cirrhosis accounted for 1.2 percent of global DALYs, with a nearly equal share related to hepatitis B, hepatitis C, and alcohol (Murray et al., 2012). Within mental and behavioural disorders that accounted for 7.4 percent of DALYs, alcohol use (0.7 percent) was in the top five after depressive disorder (2.5 percent), anxiety disorders (1.1 percent), and drug use disorders (0.8 percent). Notably, though, whereas the prevalence of alcohol, opioid, and cocaine dependence increased between 1990 and 2010, prevalence of other mental disorders did not (Whiteford et al., 2013).
Although physical complications are common in any population of heavy drinkers, early detection and cessation of drinking can lead to recovery from the medical comorbidity. Continued drinking, on the other hand, is likely to exacerbate the alcohol-related problem and may seriously threaten life. Physical complications impinge on all aspects of the problem drinker’s life, and it is unrealistic to compartmentalize psychological, social, and physical disability. Therefore, any assessment, even if done by someone without medical training, should include questions about physical health. If there are any concerns or queries, these should be referred to an appropriate individual or service.
Often, physical complications are the main reason for seeking help. If information about the physical symptoms is imparted clearly, so that the patient can understand their significance, this information can be used to consider the patient’s position. Thus, an understanding of the physical symptoms may have the potential to influence drinking behaviour. As ever, the clinician is the informant, the person who brings up the issue, and who shares and reflects the patient’s feelings and concerns, rather than the disembodied pronouncer of facts. The way in which information on physical problems is presented to the patient can be part of treatment. Here are two dialogues that illustrate different ways in which the patient’s concern over his physical health can be met at interview. First, and very briefly, a dialogue that is not to be dismissed as caricature:
Second, and more constructively:
The vital question is what any information on physical consequences means to the patient. Patients and their families are concerned about their physical health and deserve to be given the facts. Explaining and talking through this information is an opportunity for the therapist to facilitate behavioural change in the patient.
Some patients stop drinking abruptly or greatly reduce their consumption when persuaded that alcohol is posing a tangible threat to their physical health. Even if the news of physical damage constitutes the turning point, in reality, this is only the final event to tip a decision when the moment for change has been set up by many previous occurrences. That said, using the results of the physical examination or the laboratory tests for crude scare tactics is likely to be counter productive. Patients may dismiss what they are being told simply because the information is too frightening to accept, or they may decide that all is lost and that they may as well drink themselves to death.
Physical complications
The medical conditions associated with alcohol consumption can be broken down into those directly due to alcohol and those due to acute and chronic conditions to which alcohol is a contributory factor (World Health Organization, 2011). Physical conditions directly attributable to alcohol include alcoholic polyneuropathy, alcoholic gastritis, alcoholic liver disease, and ethanol toxicity. Acute conditions to which alcohol is a contributory cause include road injuries (drivers and pedestrians), injuries from falls, fires, drownings, occupational injuries, other accidents, suicide, and assault. Whilst amount consumed is linked to ill-health, heavy drinking events are particularly linked with injuries, intentional and unintentional. Chronic alcohol-attributable conditions include various cancers, liver cirrhosis, acute and chronic pancreatitis, spontaneous abortion, and psoriasis (World Health Organization, 2011).
Heavy drinking in pregnancy can lead to foetal alcohol spectrum disorders. Heavy drinking in adolescents and young people is likely to affect brain development (see Chapter 2). In some conditions, both the toxic element and disturbance of nutritional status may be implicated as causes of damage. Less is known about the risks associated with different beverage types, although it has been suggested that the risk of developing certain physical disorders is higher for drinkers of spirits (Chou, Grant, & Dawson, 1998).
What level of alcohol intake constitutes a threshold for physical dangers? The answer must vary according to the particular condition, but, in general, the evidence points to a dose–response relationship, with higher consumption being associated with a higher risk of disease. Even individuals who drink “socially” but above the daily guidelines are at risk.
Binge drinking puts individuals at higher risk of developing alcohol dependence syndrome, injuries, and brain trauma. There is considerable individual variation in the effects of alcohol consumption: not every chronic heavy drinker develops liver cirrhosis.
However, whatever the risks at the relatively lower ranges of intake, by the time someone is drinking in the fashion characteristic of the dependence syndrome, the question of whether their level of intake carries dangers hardly needs to be asked. The answer is resoundingly “yes” for nearly every tissue of the body. And, quite apart from any specific tissue damage discussed in this chapter, it should be remembered that, as a consequence of heavy drinking and dietary neglect, almost every aspect of the body’s chemistry may in some circumstances be put out of balance; even such seemingly obscure aspects as serum zinc or magnesium levels may be disturbed.
The physical complications that can result from excessive drinking will now be described. As far as possible, technical language is explained, but, as noted in the Introduction, this is a chapter where the nonmedical reader will have to show some forbearance. However as stated before, at the very least, initial and continuing assessments should include questions about physical health, and, if there are any concerns or queries, these should be referred to an appropriate individual or service. Table 5.2 lists the major alcohol-related health conditions contributing to morbidity and mortality. The presence of these conditions should alert the clinician to the possibility of an underlying drinking problem. In any case, basic inquiry into the patient’s drinking history should be absolutely routine in medical practice.
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Acute alcohol intoxication and coma
The effects of intoxication vary according to a number of factors including the amount of alcohol consumed, how rapidly it has been consumed, and whether the drinker has a degree of tolerance to alcohol or rarely drinks. A life-threatening overdose with alcohol is unlikely to occur in the alcohol dependent person, both because of their experience in handling their drinking and their raised tolerance. That is not to deny the possibility of such a patient at times getting very drunk or drinking to unconsciousness. Drinking to the point of collapse and “passing out” is more likely to be the result of a casual drinking binge or a Saturday night celebration, and it is this type of patient who is the familiar late-night visitor to the Emergency Room. Drug overdoses are often taken in the context of intoxication, intentionally or otherwise. Occasionally, a child will overdose accidentally with alcohol: this is discussed in relation to hypoglycaemia (see the section on Hypoglycaemia).
Intoxication can usually be dealt with on a sensibly conservative basis and patients left to sleep off their binge, with due care taken to ensure that they do not inhale their vomit: examination must of course also ensure that there is no other cause for unconsciousness. A stomach wash-out may sometimes be indicated. With higher levels of intoxication, there is a risk of respiratory depression and death. The blood alcohol concentration (BAC) likely to be associated with such a tragedy will vary with the individual, but a BAC of 400 mg/100 mL is usually quoted as the threshold for very serious danger. Because of the occasional risk of death from respiratory paralysis, the more common danger from inhaled vomit, and the many possibilities of being unwarily overwhelmed by some underlying or complicating condition (head injury, hypoglycaemia, ketoacidosis, systemic infection, overdose of other licit or illicit drugs, for example), the problem set by alcoholic overdose and by the often rather unwelcome visitor to the Emergency Room should not be too casually dismissed as “routine.” When coma is thought to be due to alcohol, it is important that a high alcohol concentration is shown by measurements of breath or blood alcohol. Skull radiography, neuroimaging, and urine toxicology are other fundamental investigations. Alcoholic coma has a mortality rate of approximately 5 percent.
Acute poisoning with methyl alcohol (methanol) is a rarer and a much more threatening condition than intoxication with ordinary beverage alcohol. There are substantial risks of blindness or death, and intensive emergency medical care will be required, possibly with dialysis.
Cancers
Evidence has mounted over recent years that the more alcohol an individual drinks over time, particularly regularly, increases the risk of developing a number of cancers (Bofetta & Hashibe, 2006; Department of Health, 2016; International Agency for Research on Cancer, 1998; World Cancer Research Fund/American Institute for Cancer Research, 2007). Greater alcohol consumption increases the risk of cancers of the mouth, pharynx, larynx, and oesophagus (gullet); liver cancer (either directly or indirectly via chronic infection with hepatitis B or C); and colo-rectal (men) and breast (women) cancers.
There appears to be “no safe threshold below which no effect on any cancer risk is observed” which influenced the recent changes to advice in the UK to drink no more than 14 units per week (Department of Health, 2016, p. 7). (British Medical Association Board of Science, 2008, p. 29). In addition, because many who drink alcohol excessively also smoke tobacco, this is an added risk, particularly for head and neck cancers. Genes involved in metabolizing (breaking down) alcohol likely moderate cancer risk. For instance, some forms of aldehyde dehydrogenase 2 (ALDH2) (see Chapter 2), which metabolizes toxic acetaldehyde to nontoxic substances, are associated with increased risk of head and neck cancers (Druesne-Pecollo et al., 2009).
Cardiovascular disease
The hypothesized protective or beneficial effects to the heart of one to two drinks per day have been the subject of much interest and debate about what contributes to this so-called J-shaped curve (Department of Health, 2016; O’Keefe et al., 2014; Thompson, 2013). Claims regarding this J-shaped relationship have often been oversimplified and oversold, as we explore in the next section. In any event, it should be remembered that because noncardiovascular adverse outcomes rise linearly with increased drinking, there is no case for nondrinkers to begin drinking in order to lower their overall risk of disease (Department of Health, 2016).
Alcohol-related arrhythmias
Arrhythmias, or disturbances of the normal heart rhythm, can occur as a result of episodic heavy drinking and heavy consistent alcohol use; these arrhythmias are often called “holiday heart” because of their association with binge drinking on weekends and holidays. The mildest presentation is that of palpitations caused by a few extra and irregular beats (extra-systoles). Palpitations can also be caused by an alcohol-induced tachycardia (fast heart rate): either atrial fibrillation or atrial flutter or a supraventricular tachycardia. Atrial fibrillation is the most common arrhythmia associated with alcohol use. These arrhythmias typically resolve with abstinence, but some individuals will require antiarrhythmic medication. Ventricular arrhythmias have also been reported.
Several studies have now documented an association between alcohol use and sudden coronary death in both heavy drinkers and occasional drinkers, even in people without any evidence of preexisting heart disease (Mukamal et al., 2005a).
Hypertension
Alcohol raises blood pressure and increases the risk of hypertension in a dose-dependent manner in both men and women, independent of age, body weight, and cigarette smoking (Corrao, Bagnardi, Zambon, & Arico, 1999). Consumption exceeding 30 g/d is associated with higher blood pressure, and binge drinking may be particularly implicated (Beilin & Puddey, 2006). A meta-analysis of 15 randomized controlled trials showed that reducing alcohol consumption was associated with reduced systolic and diastolic pressures (Xin et al., 2001). In addition, trials in alcohol dependent patients show that blood pressures are lower in those who cut down or abstain (Stewart et al., 2008). Individuals presenting with hypertension to a general practitioner or physician should always have an alcohol history taken, together with appropriate laboratory investigations, and should be advised to reduce their alcohol consumption.
In the absence of the possibility of conducting a randomized trial to understand the impact of alcohol consumption on cardiovascular health, an alternative approach, Mendelian randomization, has been used. This takes a large epidemiological population to compare those with and without a variant of an ALDH enzyme that is associated with alcohol-related flushing and lower levels of alcohol consumption (see Chapter 2). A meta-analysis of studies found that those individuals with the variant of ALDH2 associated with lower alcohol consumption also had lower blood pressure (Chen et al., 2008).
Stroke
There are two broad categories of stroke. These are haemorrhagic stroke, due to ruptured blood vessels on the surface of the brain (subarachnoid haemorrhage) and in the substance of the brain (intracranial haemorrhage), and ischaemic stroke, due to blockage of brain blood vessels by clot formation or emboli to the brain from the heart or elsewhere, or blockage of blood vessels outside the brain (mainly the carotid arteries). Alcohol increases the risk of haemorrhagic stroke in a dose-dependent fashion (Corrao et al., 1999). Episodic heavy drinking is a risk factor for both haemorrhagic and ischaemic stroke, particularly in adolescents and people under the age of 40 years. The risk of heavy drinking leading to ischaemic stroke is moderated by a gene that influences high density lipoprotein (HDL) cholesterol, one of the mediators of the cardioprotective effect. In the absence of this gene effect, there is no statistical relationship between alcohol consumption and risk of ischaemic stroke. When the gene is present, alcohol consumption increases the risk of ischaemic stroke (Mukamal et al., 2005b). Moderate drinking has been shown to have some beneficial effect in reducing the risk of ischaemic stroke; however, the effect is small and present only at lower levels compared with coronary heart disease (Klatsky, Armstrong, Friedman, & Sidney, 2001; O’Keefe et al., 2014)
Coronary heart disease
Observational data suggest that light to moderate alcohol consumption is associated with significant decreases in cardiovascular-related death, with maximum protection derived from ½ to 1 drink per day for women and 1–2 drinks for men (O’Keefe et al., 2014). Drinking more than 2½ drinks per day for women and 3 drinks for men is associated with higher death rates in a dose-dependent manner. However, the greatest benefits appear in middle-aged (>50 years) and older individuals (Hvidtfeldt et al., 2010). In addition, light to moderate alcohol consumption has been shown to improve outcomes in those with established coronary heart disease (Constanzo Di Castelnuovo, Donati, Iacoviello, & de Gaetano, 2010).
The “cardioprotective effect” has been proposed to derive from alcohol itself and frequency of drinking rather than from any specific beverage type. Alcohol may have a partial inhibitory effect on atherosclerosis by increasing levels of HDLs, which carry cholesterol to different parts of the body. This is because HDLs are associated with a reduced risk of coronary heart disease and are thought to protect the arteries from a build-up of cholesterol. However, the effect of alcohol on HDL appears small. Alcohol also reduces platelet stickiness and aggregation, lowers plasma fibrinogen, and increases fibrinolysis.
However, associations identified in observational research may not be causal. The Mendelian randomization approach (explained earlier) has also been used to explore the relationship between alcohol consumption and coronary heart disease. Those with a variant of the ALDH 1B gene (ALDH1B) associated with alcohol-related flushing and lower levels of alcohol consumption (see Chapter 2) had a lower risk of coronary heart disease and a more favourable cardiovascular profile (Holmes et al., 2014).
Therefore, the latest evidence suggests that alcohol consumption increases coronary heart disease among all drinkers, including those who drink “moderately.” It is therefore no longer appropriate to advise drinking alcohol to improve cardiovascular health, particularly because heavy drinking episodes are associated with increased rates of heart attacks. The number of years of life lost attributable to drinking outweighs the years saved attributable to protective factors.
Cardiomyopathy
Chronic excessive alcohol consumption (more than 90 g/d for 5 years or more) can lead to cardiomyopathy and heart failure (Rubin & Urbano-Marquez, 1994). In the United States, alcohol accounts for about a third of nonischaemic dilated cardiomyopathy. In addition to the direct toxic action of alcohol on heart muscle, other consequences of heavy alcohol consumption such as hypertension, altered metabolism, and increased acetaldehyde also contribute to damage of the heart muscle (Walker et al., 2013), although a genetic predisposition may also be an important factor. Alcoholic cardiomyopathy was formerly attributed to thiamine deficiency, but this is probably not the case because it occurs in heavy drinkers who are well nourished. The disorder usually manifests itself between the ages of 30 and 60 years. Although more common in men because of their heavier consumption, women seem to be particularly vulnerable (Urbano-Marquez et al., 1995). Whilst complete abstinence improves outcomes, cardiomyopathy and heart failure are a common cause of death in heavy drinkers (O’Keefe et al., 2014).
Alcoholic cardiomyopathy is characterized by an enlarged, hypertrophied heart. The left ventricle is dilated, and there is dysfunction in cardiac contractility, leading to a depressed output (ejection fraction). In the early stages of hypertrophy and dilatation, there may be few symptoms. However, as the disorder progresses, patients develop arrhythmias, including atrial and ventricular tachyarrhythmias and atrioventricular conduction defects. Congestive cardiac failure (heart failure) is another typical form of presentation (breathlessness on exertion, breathlessness at night, and peripheral edema).
Subclinical forms of alcoholic cardiomyopathy can be identified in problem drinkers using noninvasive procedures such as echocardiography. Early detection and abstinence may halt or reverse the progress of this disorder.
Gastroenterological disorders
Alcoholic liver disease
Alcohol misuse is the commonest cause of liver damage in the United Kingdom, Europe, the United States, and Australia. Rates of liver disease vary enormously from country to country but appear to be highest where alcohol consumption is highest. Many studies suggest that women are at greater risk than men for a given level of alcohol consumption. In the UK, attention has recently been drawn to the fact that the improvements in other chronic disorders such as stroke, heart disease, and many cancers have not been seen in liver disease (Williams et al., 2014). Liver disease has become the third most common cause of premature death in the UK, and mortality rates have increased by 400 percent since 1970. The UK situation is worse than in other western European countries, where reductions in alcohol-related liver disease are evident. Chronic liver disease can be a silent killer (i.e., the individual is unaware of any difficulties until liver impairment is significant from hepatitis or cirrhosis and he or she presents with jaundice, gastric bleeding, or encephalopathy [confusion]).
The liver is vulnerable to alcohol-related injury because it is the primary site of alcohol metabolism. Three types of alcoholic liver disease have been described: fatty liver, alcoholic hepatitis, and alcoholic cirrhosis (see Table 5.3). All three may coexist. Fatty liver is present in up to 90 percent of persistent heavy drinkers at some time. Alcoholic hepatitis is seen in approximately 40 percent of individuals with a history of persistent heavy drinking. About a third of patients with alcohol-related liver disease are alcohol dependent, and about a third of lifelong heavy drinkers will develop cirrhosis (Williams et al., 2014). Important contributing factors to greater severity of liver disease with excess alcohol consumption include genetic and environmental factors such as obesity and viral hepatitis (e.g., hepatitis B and C). Genetic factors that increase the oxidation of alcohol to acetaldehyde or reduce the rate of acetaldehyde clearance will increase acetaldehyde levels in the liver and cause greater injury. Women develop cirrhosis at lower levels of alcohol consumption than men. In women, a reduced “first pass” metabolism of alcohol in the stomach by gastric alcohol dehydrogenase (ADH) leads to increased blood alcohol levels. The ratio of water to fat is lower in women than in men. Alcohol is distributed in water, so, for a given body weight, the concentration of ethanol in water and thus in the bloodstream tends to be higher in women than in men. Alcohol dependent individuals with hepatitis C infection develop liver injury at a younger age and at a lower cumulative dose of alcohol than do those without hepatitis C. Continuing heavy alcohol consumption is associated with accelerated progression of liver disease associated with cirrhosis and a higher risk of hepatocellular carcinoma in patients with hepatitis B and C. Cigarette smoking and coffee consumption also appear to increase the risk of developing cirrhosis in alcohol dependent individuals, although the reasons for this are not known. Smoking more than 20 cigarettes per day and drinking four or more cups of coffee per day is associated with a greater risk.
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Fatty liver
The first histological change seen in persistent heavy drinkers is deposition of fat in the liver. Although this is usually asymptomatic, patients may present with nonspecific symptoms such as malaise, tiredness, nausea, an enlarged and tender liver, or abnormal liver function tests. Occasionally, very severe fatty liver can lead to jaundice (obstructive jaundice), liver failure, or death due to a fatty embolism (globules of fat getting into the circulation and obstructing arteries to the brain). Fatty liver is reversible with abstinence.
Alcoholic hepatitis
Minor degrees of alcoholic hepatitis may be asymptomatic and clinically indistinguishable from fatty liver. More severe episodes reflect inflammation and destruction of liver tissue. Inflammation underpins alcoholic liver disease either from the direct impact of alcohol and withdrawal, as well as from indirect responses to gut microflora (bacteria). Scar tissue may begin to replace liver tissue. This process is called fibrosis. Symptoms of alcoholic hepatitis include loss of appetite, abdominal pain, nausea, weight loss, jaundice, and fever. Severe alcoholic hepatitis has a mortality rate of around 30–40 percent after 28 days (Hazeldine & Sheron, 2014). Corticosteroids, which suppress the inflammation process, may improve survival rate in the early stages, but abstinence is the best treatment and is essential for long-term survival. Abstinence leads to reversal of the histological changes, but alcoholic hepatitis almost always progresses to cirrhosis in women, even following abstinence.
Alcoholic cirrhosis
Cirrhosis may arise de novo in some cases, without passing through the intermediate state of hepatitis. Here, liver tissue becomes scarred by the development of fibrous septa that link the hepatic veins to portal tracts. This scarring, together with the regeneration of liver tissue, disturbs the normal liver architecture, and the consequences are twofold. First, the actual loss of functioning liver tissue causes a range of metabolic disturbances, and, ultimately, liver failure may occur. Second, and very importantly, the scarring and disorganization lead to the squeezing and blocking off of blood vessels. This physical damming causes a build-up of pressure in the portal venous system (the veins that carry blood from the gastrointestinal tract to the liver), a condition called portal hypertension. This can, in turn, cause bleeding from veins at the lower end of the oesophagus (oesophageal varices), and this bleeding can be severe and fatal.
Cirrhosis can exist in degrees. If the condition is not too advanced, abstinence may lead to stabilization and enhance life expectancy. From the patient’s point of view, they may know nothing of this insidious condition until they suddenly become jaundiced, find their abdomen swelling up with fluid (ascites), or have a massive bleed. More often, the diagnosis is picked up at an earlier stage on clinical examination and liver toxicity tests, with confirmation coming from various special investigations. Ultrasound scanning is a relatively easy and noninvasive investigation.
Treatment for cirrhosis is largely directed at relieving symptoms and complications. Liver transplantation can be used as a treatment for end-stage alcoholic cirrhosis. Outcomes are as good as for other liver disease and superior to those with hepatitis C, although worse survival is seen with combined hepatitis C and alcohol-related liver disease (Lucey, 2014). Psychiatric and specialist alcohol assessment has become an important element of the screening process in many transplant centres, because of the risks of anxiety, depression, and relapse to drinking in the postoperative period. If individuals do drink alcohol, the majority (~80 percent) only consume small amounts. If the individual relapses (as opposed to lapses), survival is reduced with progressive episodes of hepatitis.
Acute pancreatitis
Alcohol misuse and biliary disease are the two main causative factors in acute pancreatitis. As with the liver, more recently, a contribution from an inflammatory response to gut bacteria has been recognized. Individuals with acute alcoholic pancreatitis are likely to be young men drinking in excess of 80 g of alcohol per day. About 5–15 percent of alcoholics will ever experience pancreatitis. The most common form of presentation is a sudden onset of severe upper abdominal pain, typically penetrating through to the back and associated with vomiting. The pain lessens in severity over the first 72 hours. Patients with severe acute pancreatitis may be feverish, hypotensive, have rapid breathing, and suffer with acute ascites, pleural effusions, and paralytic ileus (paralysis of the intestines). The diagnosis is usually made from the clinical presentation and confirmed by gross elevations of amylase and lipase in the blood. The mortality rate is between 10 and 40 percent.
A businessman, aged 52, had a long history of alcohol dependence. On occasion, he would stop drinking for a few months, but he was never willing to consider long-term abstinence as the goal. One weekend, he relapsed once more into drinking with a very heavy binge. On Sunday night, he was admitted as an emergency to his local hospital with appalling abdominal pain radiating through to the back. A raised serum amylase confirmed the diagnosis of acute pancreatitis. Despite the hospital’s best efforts, he died in shock 36 hours later. Postmortem examination showed extensive necrosis of the pancreas and some old scarring. There was also evidence of early liver cirrhosis.
Chronic pancreatitis
Heavy drinking is the most frequent contributor to chronic pancreatitis in adults in the Western world, particularly the calcifying form. However, it is now thought that alcohol alone is not a sufficient cause, but rather sensitizes the pancreas to other insults. Smoking is an independent risk factor for chronic pancreatitis, and genetic (e.g., variants of enzymes) and environmental factors also modify the disease (Brock, Nielsen, Lelic, & Drewes, 2013). It mainly affects men who have been drinking heavily. Although the quantity and duration of alcohol consumption are related to the development of this condition, it rarely occurs alongside cirrhosis. The main presenting symptom is severe dull epigastric (abdominal) pain radiating to the back, which may be partly relieved by leaning forward. The pain is often associated with nausea and vomiting. Steatorrhoea (fat in the faeces making them pale, loose and difficult to flush away), diarrhoea, and weight loss also occur. These symptoms occur when more than 90 percent of the functioning exocrine tissue (the tissue that secretes digestive enzymes) is destroyed. Damage to the Islets of Langerhans, with consequent failure of insulin secretion and diabetes mellitus, occurs more slowly. Treatment is focused on the management of acute attacks of pain and other complications, such as diabetes mellitus and fat malabsorption. Abstinence from alcohol is the mainstay of treatment and is essential if attacks of pain are to be stopped. Managing chronic severe and intractable pain may be challenging and involve long-term opiate use, which carries its own risks.
Gastritis, peptic ulceration, and intestinal symptoms
Alcohol alters the tone of the sphincter between the oesophagus (gullet) and stomach, stimulates gastric juice secretion, and increases mucosal permeability. This combination leads to increased risk of oesophageal reflux (i.e., acidic stomach contents in the oesophagus that is experienced as heartburn or indigestion). It can also cause acute erosive ulcers in the stomach and duodenum (first part of small bowel). Studies of the interaction between alcohol consumption and Helicobacter pylori, another cause of gastritis, have shown that heavy consumption may sustain infection but moderate consumption (e.g., <75 g/week) may be protective (Franke, Teyssen, & Singer, 2005).
Patients presenting to alcohol services commonly suffer from intestinal symptoms, such as diarrhoea and malabsorption. The general malnutrition and weight loss seen in these patients are usually due to dietary neglect. Alcohol dependent individuals are therefore at risk of vitamin deficiencies (especially of folic acid, B1/thiamine, and B12). Deficiencies of minerals and trace elements (zinc, selenium) are also possible, again as a result of malabsorption and malnutrition.
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