Alcohol-related illness - Clinical Tree

Essentials

1
Acute alcohol intoxication and withdrawal are responsible for many emergency department attendances and carry significant morbidity and mortality.
2
Chronic gastrointestinal and hepatic disease, mental illness, central nervous system disease and immunosuppression are common in alcohol-dependent persons, with complications that increase the morbidity and mortality further.
3
Wernicke encephalopathy is an uncommon but serious illness related to vitamin B1 deficiency. Treatment requires high-dose parenteral thiamine.
4
Many serious illnesses mimic alcohol intoxication or are masked by it. Maintain a high index of suspicion in the intoxicated patient with an altered state of consciousness.
5
Emergency physicians are uniquely placed to screen for high-risk drinking and other drug use as well as to offer brief advice or intervention to this group to reduce the burden of recurrent alcohol abuse.

Introduction

Alcohol use disorders, which include alcohol abuse and alcohol dependence, are common across the world and have a high prevalence in emergency department (ED) presentations. Alcohol misuse not only places the individual at risk of acute intoxication and injury but also poses significant long-term health issues.

Acute alcohol intoxication causes much morbidity and mortality from all forms of trauma, including falls, motor vehicle and other accidents, interpersonal violence and self-harm. Chronic alcohol use contributes to many hospitalizations and deaths due to alcohol-related medical conditions and injuries, resulting in both physical and psychosocial impairment.

Many acutely intoxicated patients have significant co-morbidities masked by alcohol.

Patient with alcohol use disorders may present in states of acute alcohol intoxication or withdrawal. Emergency physicians should not only recognize and treat alcohol-related emergencies but also intervene in patients at high risk from their alcohol intake who present with other conditions. Early opportunistic screening using recognized alcohol screening tools and standardized brief interventions reduce ‘at-risk’ drinking and the morbidity and mortality from alcohol-related illness.

Epidemiology

Australia was ranked second of 34 Organisation for Economic Co-operation and Development (OECD) countries in alcohol consumption per capita in 2015. Australian alcohol consumption per capita is estimated at 11.2 L of pure ethanol per person per annum. A study in five rural EDs in New South Wales found that the percentage of patients engaging in risky drinking ranged from 4% to 32%. A point prevalence survey of ED patients showed that 1 in 5 Australians and New Zealanders drank at levels that increased their lifetime risk of alcohol-related disease or injury and also that 17% to 35% of injury presentations to EDs involved alcohol consumption. One in seven of all patients presented for reasons related to alcohol consumption, and in certain departments the prevalence was as high as one in three. There are more alcohol-related presentations due to injury during weekends, but patients with alcohol-related conditions present to ED at all times throughout the week. The patients tend to be younger (age groups 18 to 29 and 30 to 39 years), male and brought to the ED either by ambulance or police.

Six percent of young persons (aged 12 to 19 years) attending city hospital EDs are there for alcohol-related reasons, with injury significantly more likely among alcohol users than among illicit drug users. Among young people attending the ED, nearly 38% may be drinking harmfully, 18% may have consumed alcohol in the previous 6 hours and 15% consider their attendance to be alcohol-related. Up to 45% of injured patients attending EDs may have consumed alcohol within the previous 24 hours and almost 30% in the previous 6 hours.

The natural history of alcohol dependence is to remit and relapse, with a relentless progression to early death. Risk factors for alcoholism include a family history of alcohol dependence or total abstention, parental divorce, youngest child, other substance misuse, availability of alcohol and extremes of income.

Pharmacology

Pharmacokinetics

Ethanol is passively absorbed from the entire gastrointestinal tract (GIT), with about 25% from the stomach. Absorption is rapid, within 60 to 120 minutes of intake, and may be slowed by food. Ethanol is distributed throughout the body water; females and obese people with lower ratios of body water to fat reach higher blood alcohol concentrations (BACs) sooner than their leaner counterparts. Hepatic oxidative metabolism occurs via alcohol dehydrogenase. Alcohol-tolerant people also utilize the hepatic microsomal ethanol oxidizing system, which is upregulated with increasing drinking. First-order elimination kinetics becomes saturated as the BAC increases, changing to zero-order kinetics and slower sobering at higher BACs.

Pharmacodynamics

Alcohol is thought to act on γ-aminobutyric acid A (GABA _A ) inhibitory neuroreceptors in the brain, causing central nervous system (CNS) depression. The characteristic euphoria is thought to be related to the release of endogenous opioids (endorphins). A rapidly rising BAC causes quicker and more pronounced behavioural changes than the same level achieved over hours. A steady state of absorption to metabolism and excretion can be achieved at about one standard drink per hour. A standard drink is defined as containing 10 g or 12.5 mL of pure alcohol. Acute intoxication depends on factors such as habituation, food co-ingestion, body habitus and the concentration of alcohol in the drink.

Measurement of blood alcohol concentration

The blood alcohol concentration may be estimated using a Breathalyser that estimates BAC after measuring alcohol concentration in alveolar air. This is a useful non-invasive screening tool but relies on a cooperative and awake patient being able to exhale adequately for the reading. There is an approximate difference of 15% to 20% between breath alcohol readings and serum BAC. Readings are influenced by many factors, including temperature, hyper- or hypoventilation prior to exhalation, haematocrit level, other substances such as ketones, time since ingestion and machine error. A directly measured serum blood alcohol concentration is more reliable. The Australian legal limit for driving is 0.05%; in New Zealand it is 0.04%, whereas in the United States and the United Kingdom it is 0.08%.

Chronic alcohol-related illness

Gastrointestinal

Chronic alcohol use results in disease of the GIT, liver and pancreas. Morbidity most frequently arises from GIT bleeding, liver disease and pancreatopathy.

Gastrointestinal bleeding

The most common causes of alcohol-related GIT haemorrhage are peptic ulcer disease (PUD) and the consequences of portal hypertension, such as oesophagogastric varices or subepithelial gastropathy. Mallory-Weiss tears, oesophagitis and alcoholic gastropathy are less frequent causes of alcohol-related GIT haemorrhage. Heavy alcohol use may be a risk factor for the development of PUD, although the exact pathogenesis is poorly understood and the role of alcohol may be additive to the effects of Helicobacter pylori , non-steroidal anti-inflammatory drugs (NSAIDs) and tobacco.

Although Mallory-Weiss tears are less common, up to 44% are associated with alcohol use and may account for significant morbidity due to blood loss.

Alcoholic liver disease

Alcoholic liver disease (ALD) comprises a spectrum of disorders from alcoholic fatty liver (steatosis) and inflammation (hepatitis) to progressive fibrosis (cirrhosis) and hepatoma. These occur from chronic insult to the liver due to oxidative stress, damage from free radicals and the immunogenicity of alcohol metabolites. Many factors are involved in the aetiology of ALD, including genetic predisposition, gender, ethnicity, nutrition, ingestion of other hepatotoxic agents (i.e. drugs of abuse, weight-loss supplements, paracetamol), obesity and co-existent chronic viral hepatitis, non-alcoholic fatty liver and other liver diseases, such as autoimmune conditions.

The duration and amount of alcohol consumed play important roles; drinking at levels above the National Health & Medical Research Council (NHMRC), Australia recommendations (more than two standard drinks a day, both in men and women) is a defined risk for the development of alcohol-related injuries, ALD and eventual cirrhosis. The NHMRC also recommend drinking less than four standard drinks per occasion so as to reduce the short-term adverse effects of alcohol use, in particular alcohol-related injuries. Alcohol dependence does not inevitably lead to cirrhosis, which occurs in only 10% to 20% of heavy drinkers. Alcoholic fatty liver is a common finding among alcohol-dependent patients but is not a frequent cause for presentation to an ED.

Alcoholic hepatitis and cirrhosis

Alcoholic hepatitis may present as acute anorexia, nausea, vomiting, right-upper-quadrant pain and jaundice. Treatment is supportive and abstinence from alcohol is essential (see Chapter 9.6 ).

Cirrhosis typically presents late, with subtle malaise, anorexia, weight loss, weakness and fatigue along with a combination of liver cell failure and the development of portal hypertension. Acute decompensation usually manifests as symptomatic ascites, jaundice, pruritus, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, variceal bleeding and/or coagulopathy.

Ascites

Ascites due to hypoalbuminaemia, secondary hyperaldosteronism and portal hypertension is usually recurrent. Sudden exacerbations may be caused by SBP, portal vein thrombosis, a hepatoma or medication non-compliance. Symptoms include abdominal discomfort, girth increase and anorexia. Fever, chills and abdominal pain occur with SBP or, conversely, signs of sepsis may be minimal but there is a sudden worsening of jaundice or encephalopathy.

Coagulopathy and encephalopathy

Coagulopathy results from the failure of hepatic synthesis of coagulation factors, thus parenteral administration of vitamin K and factor concentrate or fresh frozen plasma is required in the bleeding cirrhotic patient. GIT bleeding may also precipitate hepatic encephalopathy, with confusion and characteristic asterixis. This potentially reversible decrease in neuropsychiatric function must be distinguished from other causes of an altered level of consciousness in the cirrhotic patient.

Hepatic encephalopathy is associated with an increased nitrogenous GIT load (as from a gastrointestinal bleed), dehydration, sepsis, certain drugs, hyponatraemia or hypokalaemia, worsening liver function and increasing jaundice.

Thrombocytopaenia

Thrombocytopaenia is a common finding in. The aetiology is multifactorial: direct toxicity of the alcohol on the bone marrow, portal hypertension and platelet sequestration in the enlarged spleen, decreased thrombopoietin (TPO) synthesis in the liver, with a subsequent reduction in the proliferation and differentiation of megakaryocytes and platelet formation.

Alcoholic pancreatopathy

The term alcoholic pancreatopathy describes a group of pancreatic diseases caused by chronic heavy alcohol intake. It includes acute alcoholic pancreatitis, recurrent abdominal pain or GIT symptoms induced by alcohol, high serum levels of pancreatic enzymes or an abnormal pancreatic ultrasound. Recurrent bouts of acute alcoholic pancreatitis precede the development of pancreatic pseudocysts, chronic pancreatitis and pancreatic malignancies.

Alcohol is the most common aetiology of chronic pancreatitis (70% to 80%), although as few as 10% of heavy drinkers will develop it. Like cirrhosis, its aetiology is multifactorial; other risk factors include tobacco smoking and hyperlipidaemia, which should be addressed if early signs of pancreatopathy are recognized. Alcoholic pancreatitis, both acute and chronic, is managed conservatively with abstinence from alcohol as well as the administration of intravenous fluids, parenteral analgesia and, if pancreatic necrosis or an abscess is suspected, antibiotics (see Chapter 7.9 ).

Chronic pancreatitis can be debilitating, with recurrent cycles of pain and admissions to hospital. Progressive pancreatic calcification, failure of exocrine and endocrine function and chronic pain can all be mitigated if alcohol is avoided. Recurrent pancreatic insults and chronic pancreatitis increase the risk of pancreatic carcinoma by up to 16 times.

Mental health and mental state issues

Depression and suicidal intent

Alcohol is a recognized risk factor for suicide. Mood expression and intent of self-harm are often underestimated when intoxicated patients are seen in the ED. A Scandinavian study showed that 62% of 1207 ‘parasuicides’ who presented to an ED involved alcohol use, with even higher rates in young males. Psychiatric referral was less likely if alcohol was involved; yet, after 5.6 years, 3.3% of these individuals had completed suicide. This represented a 51-fold increased risk compared with the general population, with the risk of completed suicide being greatest in the first year.

Alcoholic hallucinosis

Alcohol misuse causes psychotic symptoms by several mechanisms, including direct intoxication, alcohol withdrawal, delirium tremens (DTs), Wernicke encephalopathy, Korsakoff psychosis and alcoholic dementia. Alcohol dependence doubles the risk of psychotic symptoms.

Alcoholic hallucinosis is a schizophrenia-like syndrome that differs from the other causes in that it occurs at a younger age, in a setting of clear consciousness and unrelated to acute withdrawal. There are no associated physical symptoms of autonomic dysfunction, as in the DTs, and its duration is longer, with predominantly auditory hallucinations as opposed to visual ones. Its chronicity and the derogatory auditory hallucinations are similar to those occurring in schizophrenia, but thought disorder is not a feature.

Alcohol withdrawal states

The alcohol withdrawal syndrome follows prior alcohol dependence. Its clinical importance lies in the potential severity of the symptoms and signs, the need to consider alternative or concomitant pathology and the likelihood of seizures occurring. The principal symptoms are tremor, agitation, nausea and vomiting, sweating, anxiety and autonomic nervous system overactivity with tachycardia, tachypnoea and fever. Sleep disturbance, hallucinations and generalized tonic-clonic seizures often begin within 10 hours of reduced alcohol intake, with peak intensity by day 2; it may last up to 5 days.

Alcohol withdrawal scales

A number of scales measure alcohol withdrawal. One simple one is to rate symptoms as mild (tremulousness), moderate (agitation) and severe (confusion). Most EDs use an alcohol withdrawal scale (AWS) to measure symptoms, predict the likelihood of seizure and direct preventative management. The most commonly used AWS is the Clinical Institute Withdrawal Assessment—Alcohol, Revised (CIWA-R) scale. This scale measures 10 items and was primarily developed for planned detoxification or for use on general medical and psychiatric wards. Surprisingly, blood pressure and pulse, although often abnormal, are not included in the scale. A modified version that includes seizures in the AWS is also used. Patients with high scores have an increased risk of seizure if they remain untreated. The higher the score, the greater the relative risk.

Pharmacological therapy

Benzodiazepine (BZD) therapy reduces signs and symptoms of alcohol withdrawal and prevents complications. All BZDs appear to have similar efficacy, but diazepam, lorazepam and chlordiazepoxide have been studied most. Longer-acting agents, such as diazepam used with symptom-triggered dosing (as opposed to regular), decrease the total of drugs given and both shorten and smooth the clinical course. Early treatment is preferred to waiting for advanced withdrawal.

Published data on ideal doses are lacking. High-dose oral diazepam 20 mg q1–2h may be needed for symptom control and up to 160 mg/day may be required to allow for BZD tolerance, which is common in alcohol-dependent patients. Under-dosing for fear of over-sedation is common.

Antipsychotics such as droperidol, haloperidol and olanzapine are commonly used to manage the agitation and other behavioural disturbances induced by severe alcohol withdrawal. However, they lower the seizure threshold and can cause anticholinergic syndrome if given in excessive doses. They can also cause prolongation of the QT interval and increase the risk of torsade de pointes in alcoholic patients, who are often hypokalaemic, hypocalcaemic and hypomagnesaemic. Ethanol, of course, would ‘treat’ the symptoms of withdrawal; however, it has been shown to be inferior to BZDs.

Baclofen, a GABA _B agonist, is increasingly used in the management of alcohol withdrawal, with various studies showing efficacy in decreasing withdrawal symptoms.

Alcohol withdrawal seizures

Around 3% to 5% of those with severe alcohol use disorder experience withdrawal seizures within 48 hours of stopping drinking, and 15% will have a seizure within their lifetimes. Previous withdrawal seizure is the strongest predictor of recurrent seizure. Most alcohol withdrawal seizures are short-lived and self-terminating. They occur early (usually 7 to 24 hours after the last drink), are grand mal in type (i.e. generalised, not focal); they usually (though not always) occur as a single episode. Localizing signs or prolonged seizures should prompt a search for alternate pathology. Intravenous BZD are the first line treatment for seizures secondary to alcohol withdrawal using the same doses as for seizures of any other cause (see Chapter 8.5 ). Phenytoin is not recommended for alcohol withdrawal seizures unless there is a coexistent epileptic disorder.

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