21.1 Death and dying

Initiation of the grieving process

Quality management of grief states can prevent significant morbidity, as pathological or unresolved grief can lead to later problems with physical and mental health. Emergency physicians have a duty of care to the survivors to play their part in the initiation of family grief.

Grief is not like an illness, to be fought and cured as so often is the case in Western medicine. Generalizations can be made about human behavioural tendencies and time lines can be drawn for predicted recovery, but each person’s grieving process is unique. Some people never get better and nobody survives grief unchanged.

All relatives need time to receive the clear message of death, which they may need to be given again and again. Some need to make meaning of the event and the clinical art of managing perceptions is paramount. For the families of the deceased, this time will be recalled with unrivalled clarity. It is a great privilege to be part of those memories and it carries the responsibility to manage the family in keeping with best practice principles for the initiation of grieving.

Breaking bad news

The interview with the family of the recently deceased can be more difficult than the resuscitation. Handled with sensitivity, however, it can be a positive start to successful grieving and recovery.

Viewing the body

Relatives and their invited friends should be encouraged to view the body. By seeing the body, by feeling and touching, the grieving process, separation and rebuilding can start. People should be encouraged to speak, touch, kiss, stroke, caress, even to argue, negotiate and cajole in private for as long as they wish. This facilitates natural grieving. The presence of a bereavement or viewing room can make this process much easier as, particularly with children, visiting can go on for several hours. A hospital morgue may be used, some have a purpose-built facility and appropriate staff support. Relatives should be informed of the necessity for police involvement if the matter has been referred to the coroner.

Cultural issues

Various ethnic and religious groups have differing practices for the handling and disposal of bodies. Emergency physicians should be able to manage different family requests in a sensitive manner while bearing in mind local statutory obligations.

For Australians of Aboriginal or Torres Strait Island descent, cultural practices and beliefs vary from region to region and families will guide practitioners. In larger hospitals, Aboriginal liaison services can help.

Death certificates

Doctors managing deaths in the ED must understand and have a sound knowledge of reporting requirements for the coroner’s court (see Chapter 25.2 The coroner). Any death suspected to be not entirely from natural causes or where the cause is unknown requires reporting. Local regulations stipulate the circumstances under which a death certificate may be issued and by whom. For instance, in some states, it is not necessary for the issuer to have seen the person while alive. Coroner’s courts are proactive in assisting medical practitioners to complete certificates where possible.

Organ donation

A thorough knowledge of local definitions is crucial for the emergency physician to participate in efforts to improve organ transplantation rates (see Chapter 21.7). Relatives can ask later why donation was not suggested and some really appreciate the opportunity to contribute to the welfare of others. All Australian states have access to professional transplant coordinators to facilitate the process once permission has been obtained.

Bereavement counselling

Most hospitals have qualified practitioners to support the recently bereaved. Referral should be arranged prior to departure if counsellors have not already made contact. Ministers of religion are trained in grief counselling and are usually available after hours. People can feel unprepared to ask for them and it is not necessary for the deceased to have had any religious affiliation to make use of such counsellors. The general practitioner is also a useful resource and should always be informed promptly of the death of a practice patient. Social workers are expert in grief counselling and many funeral companies and coroner’s offices now provide counselling services.

Subsequent issues

Permission to leave

Recently bereaved people are sometimes confused, frightened, stunned and at a loss as to what to do next. When forensic issues (identification and statements) and viewing have been completed, they can be given the dead person’s possessions and politely given permission to leave the hospital. ‘There is nothing more you can do’ or ‘Can I phone someone or get a taxi to take you home?’ may be usefully offered.

Information about contacting a funeral office to arrange for collection of the death certificate and the body and to discuss burial rites should be in an explanatory leaflet, readily available.

Professional issues

One of the important aspects of looking after survivors is caring for the carers, who are often overlooked. Patient death has been reported to lead to physical and emotional symptoms in emergency medicine practioners [4]. There is no evidence that psychological debriefing prevents or ameliorates post-traumatic stress disorder and it may cause harm to some. Often, after an unsuccessful resuscitation, professionals need to talk about the events within the team environment. This should be done to foster reflective practice around teamwork in crisis situations. It is uncertain whether this improves psychological outcome. There is, however, a distinct propensity for those who spend their lives among misery to become cynical and full of black humour. The cultural norms of emergency medicine can become so integrated into personal values that the physician does not even recognize their presence. We should regularly assess our own emotional fatigue and, if there is a significant divergence between our personal values and career activities, we may be motivated to seek support from a trusted source. This area awaits further research.

21.2 Sexual assault

Medical aftercare

The risk of genital infection after sexual assault

The risk of sexually transmitted infections (STIs) following rape is reported to be 4–56%, with infection reflecting those organisms that are locally prevalent. One study showed that with baseline testing, 43% of victims had evidence of pre-existing infection [17]. The finding of pre-existing infection is not admissible in court under Australian law. Most experts discourage testing for STIs in the emergency department unless symptomatic.

Baseline screening [18] for the following infections is recommended in follow up:

While the risk of acquiring an infection is difficult to define, antibiotic prophylaxis is not generally recommended for the victim unless the person committing the assault is known to be suffering from an STI, is at high risk for having an STI or it is thought unlikely to return for follow up. Poor follow-up rates are the norm and all patients should be offered prophylaxis in the emergency department if urgent follow up cannot be ensured. Intramuscular ceftriaxone 250 mg together with 1 g azithromycin orally plus either metronidazole 2 g or tinidazole 2 g as a single dose is the suggested antibiotic regimen [19].

Given the low prevalence of syphilis in the general community, it is reasonable not to give benzathine penicillin routinely but to have syphilis serology performed at 3 months, depending on the circumstances and whether follow up can be assured. Chlamydia trichomatis is the most common notifiable sexually transmitted infection in Australia. If the victim has a pre-existent infection and receives treatment with azithromycin without follow up or contact tracing there is a risk of re-infection and increased risk of serious morbidity, including infertility.

Hepatitis B virus can be transmitted by sexual intercourse but the risk of transmission is undefined. By comparison, the risk of infection following a percutaneous needle stick from an HBAg-positive individual to an HBAb-negative recipient is 5–43% [20]. Prophylaxis with hepatitis B vaccine 1 mL IM is indicated. HBV vaccination and hepatitis B immune globulin (HBIG) (400 IU IM) should be available where the assailant is either known to be HBV positive or the woman is considered to be particularly at risk of infection. Hepatitis B vaccination without HBIG is highly effective in preventing HBV infection in sexual contacts of persons who have chronic HBV infection. Persons exposed to an assailant with acute HBV infection additionally require HBIG which prevents 75% of such infections [21]. Unless victims have a reliable vaccination history and serological conversion, the full hepatitis B course should be initiated, even when the completion of the vaccine series cannot be ensured [22]. Hepatitis C is not efficiently transmitted sexually.

It is likely that the victim will be concerned about HIV or will become concerned at a later date. The offer of HIV testing should be made accompanied by the usual full explanation and written consent needs to be obtained if the test is done. HIV seroconversion has occurred in persons whose only known risk factor was sexual assault, although the frequency of this occurrence is thought to be low [22]. In consensual sex, the risk for HIV transmission from vaginal intercourse is 0.1–0.2% and for receptive anal intercourse 0.5–3.0%. The risk of transmission from oral intercourse is much lower. Specific circumstances of an assault that might increase risk for HIV transmission include the site of penetration, site of exposure to ejaculate and the presence of mucosal trauma, genital lesions or another STI.

Other factors that should be considered in the recommendation for post-exposure prophylaxis (PEP) include multiple assailants, the likelihood of an assailant having HIV given the local epidemiology for HIV and whether the assailant is from a high-risk group including men who have sex with men or use drugs by injection.

HIV PEP should be offered as soon as possible after the assault up to 72 hours post-exposure. PEP appears to be well tolerated. Local protocols for the initial 3–5-day medication supply, collection of baseline testing and prompt referral for specialist consultation must be in place. National guidelines [23] recommend the use of two and three antiretroviral drug regimens according to the calculated risk of HIV exposure, increased to a three-drug regimen using stavudine 40 mg twice daily when calculated exposure risk exceeds 1 in 1000. The full 28-day course must be undertaken with both regimens.

Tetanus prophylaxis must be considered as part of the management of any injuries in the usual way.

Pregnancy prophylaxis

The risk of pregnancy following a single unprotected episode of coitus has proven difficult to define. However, a large prospective study from North America rated the risk of pregnancy from rape as 5% [24]. Emergency contraception is readily available in Australian pharmacies and it is the responsibility of the medical practitioner to ensure the patient knows of the availability and has immediate access to the medication.

The progestagen levonorgestrel is used alone for emergency contraception in a dose of 1.5 mg and can be given up to 5 days from the time of unprotected intercourse. If this single dose is given within 72 hours, the proportion of pregnancies prevented was 85% in the WHO multicentre study [25]. The earlier it is given, the more effective it is.

The literature demonstrates that there is poor compliance with follow-up instructions in this setting. Arrangements for follow-up testing for pregnancy, sexually transmitted diseases, HIV and hepatitis B vaccination should be supplied as written instructions as victims may subsequently remember little of their interview.

Crisis intervention

Acute reactions to rape range from emotional numbing to shame, self-blame and severe emotional distress. The predominant reaction is a devastating sense of loss [26] based on the fear for survival and the gross invasion of bodily boundaries which removes the victim’s control over that which she finds most personal to her. Longitudinal data [27] suggest sexual assault survivors are at increased lifetime risk of post-traumatic stress disorder (30%) and major depression (30%). The input of sexual assault counsellors in evaluating the patient’s immediate and ongoing emotional and safety needs must be in place prior to discharge. The role of various psychological therapies in decreasing long-term sequelae is not yet clear.

It has been found that the greater support the doctor provides the victim, the better the outcome [28]. However, this study found doctors were the least supportive health professionals in this setting.

Children

Child sexual assault is ideally managed by a team with specific paediatric expertise. The circumstances regarding children who are the victims of sexual assault differ from those relating to adults. First, the child is likely to have been the victim of chronic abuse rather than an attack by a stranger. Second, almost always the offender will be a man known to the child, often in a position of authority and trust. This introduces the issue of protecting the child from further molestation. The injury pattern is highly variable. Chronic sexual abuse tends to develop as a pattern of behavior between the victim and the offender beginning with touching and possibly leading to penetrative intercourse. This escalation of activity may evolve over a lengthy period and physical trauma may not be a feature. If the child has been the victim of a stranger assault, the risk of physical injury is greater than for an adult victim [29].

Conclusion

A patient presenting for care after sexual assault should first be evaluated for acute traumatic injury and any intoxication issues. The victim should be assessed in order to offer appropriate post-exposure prophylaxis to pregnancy and sexually transmitted diseases including gonorrhoea, chlamydia, trichomoniasis, hepatitis B and HIV, plus routine tetanus prophylaxis. Specific informed consent must be obtained prior to forensic evaluation. The involvement of a multidisciplinary team with an experienced forensic examiner and sexual assault counsellor is of value. Discharge must not occur until the immediate safety of the victim is ensured. Follow up for medical issues and ongoing psychological support should be arranged prior to discharge. Maintaining a sympathetic non-judgemental approach by the physician improves the victim’s outcome.

21.3 Family violence

Risk factor identification

The identification of risk and contributory factors for family violence within intimate relationships has allowed for improved understanding of the nature, form and degree of danger to victims, as well as the conditions under which incidents of family violence are more likely to occur.

While the growing evidence base about risk factors has informed the development of a variety of tools and measures designed to improve and detect those at risk, the presence of these factors is not an infallible predictor of violence. For example, some victims with multiple risk factors will not experience escalating or severe violence, while fatal family violence can occur in the absence of clearly defined risk and contributory factors.

Despite this caveat, knowledge and recognition of these factors is an important step toward improved identification and intervention in violent behaviour. To this end, risk factors are generally classified at the level of the individual, relationship and social environment [13].

Individual level risk factors have been identified for both victims and perpetrators of violence. Individual characteristics associated with men having an increased risk of perpetrating violence are alcohol abuse, drug use, low education standards, unemployment and being a former rather than current partner [12]. Alcohol abuse is the most identifiable risk factor and the risk is proportional to the degree of abuse, although it is not necessarily causal. Pregnancy and new birth have been associated with both emerging and escalating violence [14]. There is some association between perpetrator mental health and violence, particularly conditions such as depression and psychosis [15].

At the level of the relationship, a history of abusive and violent behaviour is one of the strongest predictors of further violence [16]. Separation or the announcement of an intention to end an intimate relationship is associated with an increased risk of violence. Separated or divorced women are four times more likely to be abused than women who have never married, are married or are widowed [17]. Men who are abused are commonly assaulted by the women whom they abuse [18].

Social environment factors affecting family violence include gender inequality supported by societal norms and economic or social policies that create or sustain inequalities [13].

Outcomes

Family violence affects health outcomes in a multitude of physical and psychological ways. Most presentations to health professionals by victims of violence are a complex mix of indirectly related physical and psychological problems and are not trauma related [9].

Physical injury and illness

Physical injuries resulting from family violence may have patterns similar to other forms of non-accidental injury, such as a history inconsistent with the injury, injuries of varying temporal stages or unreasonable delay in presentation. Non-accidental injuries are often in central compared with peripheral areas of the body. Injuries to defensive areas of the body or to the back, legs, buttocks, back of the head and soles of the feet reflect attempts at self-protection. Injuries inflicted on females are likely to be contusions, abrasions, lacerations, fractures and dislocations [19]. Women are more likely to be choked, beaten or sexually abused. Men have a greater risk of having objects thrown at them or weapons used against them. Although family violence-related injuries may follow certain patterns, injury pattern is of low positive predictive value in the identification of family violence [19].

Abuse before, during and after pregnancy represents a threat to the well-being of the mother and baby. Approximately 40% of women who are physically abused are forced into non-consensual sex at some stage. This results in high rates of sexually transmitted disease, unintended and adolescent pregnancy and termination of pregnancy. There is also an established complex link between family violence and preterm labour, low-birthweight babies and postnatal depression [20].

Prevention of access to or interference with general healthcare or antenatal care may occur with up to 17% of abused women reporting partner interference with accessing healthcare [21].

In Australia, homicide among intimate partners and other family members forms a substantial proportion of annual homicide incidents. Between 1989 and 2002, 38% of homicide victims were murdered by a family member [22]. Approximately 25% of USA female homicides are family violence related. Many homicide victims had presented to an ED in the 2 years preceding their death. Documentation of violence and intervention were rare [23].

Psychological impact

Family violence is an independent risk factor for mental illness. Women who have experienced family violence have an approximately 11-fold increase of dissociative disorders, 6-fold increase in somatization disorders, 5 times higher incidence of anxiety and are three times more likely to suffer depression, phobias and drug dependence [17,18]. Exposure to family violence has also been shown to be associated with the onset of post-traumatic stress disorder. Abused women have twice the rates of hazardous alcohol consumption and dependence [17]. Abuse occurring both in childhood and adulthood causes a further significant increase in the incidence of mental illness. The experience of psychological abuse, especially ridicule and humiliation, are particularly responsible for causing low self-esteem.

Impact on children

The impact of family violence on children includes potential victimization, witnessing violence, separations from family, foster care, risks of future mental illness and an increased potential to perpetrate violence in the future [6].

Children living in a home where violence is perpetrated against a parent are 15 times more likely to be a victim of abuse or neglect themselves [20]. Family violence is a risk factor for becoming a perpetrator of homicide in the pre-teenage group [24].

The outcome of the experience of violence is directly proportional to the duration and frequency of violent episodes. Overall, approximately one-third of the population risk for all mental illness is attributable to family violence [25].

Social

Control by the perpetrator who fears disclosure by the victim can lead to social isolation, prevention from paid employment or contact with medical practitioners.

Financial dependence and the responsibility of children increase isolation, loss of choices and difficulties of separation from the perpetrator. Poverty is prevalent and multifactorial. Separation from or incarceration of the perpetrator may lead to further loss of income.

Homelessness may be relative, where there is no sense of safety or security in the home, or absolute, where there is need for interim or emergency accommodation or families may be living on the streets. Children or elderly people living in violent circumstances may be institutionalized by authorities or carers.

Outcomes for male victims differ from female victims in several significant ways. Male victims typically express fewer feelings of fear and terror and less frequently feel trapped and controlled. Men are also generally less constrained by financial dependence. As fear, control, dependence and isolation contribute greatly to the psychological outcomes of family violence, women still suffer approximately 95% of the serious physical and psychological consequences of family violence [18].

Economic cost

The costs of family violence are vast. Costs include pain, suffering and premature mortality costs, health costs (victim, perpetrator and children), production-related costs (lost productivity), consumption-related costs (property replacement), second-generation costs (childcare, child protection), administrative (legal and forensic) and transfer costs (income support, lost taxes). The total annual cost of family violence in Australia in 2002–03 was AUD $8.1 billion. The lifetime cost per victim was AUD $224 470 [26]. The National Council to Reduce Violence Against Women and their Children has more recently projected that family violence will cost Australia $9.9 billion in the years 2021–22, if appropriate action is not taken [27]. International studies estimate costs in the billions of dollars annually [28].

Barriers to detection and reporting of family violence

Detection rates of family violence in EDs are low. Only 10% of those who present with acute family violence-related injuries or issues will be asked by the attending nurse or physician or volunteer information about the violence issue. Documentation of violence in the medical record is rare [9]. Barriers to detection may include system factors, such as inadequate privacy, health-practitioner’s lack of time and education, health-practitioner’s attitudes and cultural, social and gender issues.

Crime statistics in Australia show a general increase in reporting of family violence. Rates of women reporting physical and sexual assault to the police rose from 19% and 15% in 1996, respectively to 36% and 19%, respectively in 2005 [10,29].

A range of barriers can inhibit victims’ disclosure, including feelings of fear and shame, concerns about not being believed or about further victimization, anxiety about possible medical or legal processes, as well as familial, cultural or religious pressures. In some cases, individuals do not recognize themselves as victims of violence or may not have yet considered seeking assistance in respect to their violent partner.

Indigenous women in Australia report violence rarely. Historical interactions with police, such as forcible removal of children and high rates of Aboriginal death in custody, contribute to indigenous women fearing for the safety of themselves and their families when police or social services are involved [20] and the lack of accessible and culturally appropriate legal processes create further barriers to reporting. The elderly may be prevented from reporting by fear of further abuse, neglect or the threat of institutionalization [20].

Screening

The high prevalence of family violence, low positive predictive values of demographic factors and clinical presentations, low detection rates and high incidence of subsequent physical and psychological illness have supported the argument for universal screening. Opportunistic screening may increase detection rates of family violence. Detection rates without screening are in the order of 0.4%. Rates of detection rise to approximately 14% with the use of simple direct questioning [30]. The use of a single screening question may be as effective as asking several questions. Screening questions should be simple and direct such as ‘Do you feel safe at home?’ or ‘Are you afraid of your partner?’ Explanation that these questions are routine may improve patient comfort.

Screening may indicate to the victim that channels of communication are open and that help will be available. It educates women about violence, its nature and prevalence. Screening may also be important in detection of perpetrators. Approximately 40% of family violence perpetrators have sought medical attention in the preceding 6 months with half having attended an ED [31].

Most women find screening an acceptable practice, however, up to two-thirds of medical practitioners and 50% of nurses are not in favour of performing screening. Reported barriers include a lack of education on how to ask questions about abuse, language barriers, a personal or family history of abuse and time constraints [32]. In the USA, the legal implications of mandatory reporting add to reluctance to screen.

Screening may improve detection rates and referral rates to external agencies. However, currently, no evidence exists that screening leads to improved health outcomes for victims [33].

Management

The management of family violence is complex. Leaving a violent relationship is no guarantee of safety and may precipitate increased levels of violence. Leaving a violent relationship is a process and not an event and requires support through all phases. Help may best be offered by validating the disclosure, expressing concern, listening, providing support, ensuring safety and offering a bridge to services.

Conclusion

Family violence is a pervasive social problem that does not discriminate across age, cultural background, religion or socioeconomic status. The implications of family violence are substantial, including physical injury, mental illness, economic and social costs and fatal outcomes. Despite the commonness of family violence, it frequently remains undetected and unreported. Identification of risk factors for violence and interventions aimed at increased identification and referral can be considered in the ED environment. When violence is disclosed, the expression of concern and a willingness to listen, risk assessment, safety planning, support and stage-appropriate referral are the mainstays of management.

21.4 Alcohol-related illness

Chronic alcohol-related illness

Gastrointestinal

Chronic alcohol use results in disease of the gastrointestinal tract (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 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 [9].

Variceal bleeding in portal hypertension results from raised portal blood flow and portal vascular resistance due to hepatic fibrosis. Fifty per cent of cirrhotic patients develop varices and, once present, variceal bleeding occurs in 10–30% per annum. Variceal bleeding may be catastrophic with a 30% mortality for a first bleed. The 5-year survival was estimated at 26% in one patient series of variceal bleeding, of which 80% were alcohol dependent [10].

While Mallory–Weiss tears are less common, up to 44% are associated with alcohol use and may have significant morbidity due to blood loss [11]. Alcohol-induced vomiting against a closed glottis can also result in oesophageal rupture (Boerhaave’s syndrome).

Management of GIT bleeding

Close attention to airway, breathing and circulation is the first priority. Aggressive initial fluid resuscitation is necessary in shock with an initial crystalloid bolus of 500–1000 mL, followed by transfusion of blood products if required. Vitamin K 10 mg IV is indicated in patients with known or suspected liver cell failure. Replacement of clotting factors with factor concentrate or fresh frozen plasma and platelets will also be required if the patient requires massive transfusion or has abnormal coagulation secondary to chronic liver disease or to major haemorrhage [12].

An intravenous proton pump inhibitor, such as omeprazole 80 mg stat, followed by an infusion at 8 mg/h is often initiated for bleeding from presumed PUD, oesophagitis, gastritis or duodenitis. This decreases hospital length of stay and the need for endoscopic therapy but does not reduce transfusion requirement, re-bleeding, the need for surgery or death at 30 days [13].

Variceal bleeding

After the initial resuscitation and replacement of clotting factors if needed, acute variceal bleeding should be managed with a bolus of octreotide or terlipressin, followed by an infusion, while urgent upper gastrointestinal endoscopy is arranged. Terlipressin is a synthetic analogue of vasopressin, that reduces splanchnic blood flow and portal pressure. It is the only agent that has been shown to improve mortality (34% relative risk reduction) in the setting of acute variceal bleeding [14]. Octreotide is a synthetic somatostatin analogue that reduces splanchnic blood flow. Endoscopy is diagnostic for the site of bleeding, as well as being both therapeutic and prognostic. Therapy is usually by banding ligation, sclerotherapy or tissue adhesive. Sclerotherapy with the injection of varices with sclerosant with octreotide is more effective than sclerotherapy alone at controlling bleeding but may not improve longer-term mortality. Gastroesophageal balloon tamponade with Sengstaken–Blakemore or Minnesota tube can provide temporary haemostasis when sclerotherapy is not available or is unsuccessful. It controls bleeding in up to 80% of cases, but it does not affect long-term mortality and it is associated with a high rate of complications, especially if it is performed by individuals who are not familiar with its use [15].

Early variceal surgery by oesophageal transection or selective portocaval shunt or interventional radiology, such as transjugular intrahepatic portosystemic shunting (TIPSS), may enhance short- and long-term survival, but both techniques are complicated by the risk of encephalopathy. TIPSS is preferred if liver transplantation is being considered. When the acute episode of variceal bleeding is over, oral propranolol and isosorbide mononitrate are used as maintenance therapy for portal hypertension.

Alcoholic liver disease

Alcoholic liver disease (ALD) comprises a spectrum of disorders from alcoholic fatty liver (steatosis), 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, obesity and co-existent chronic viral hepatitis, non-alcoholic fatty liver and other liver diseases, such as autoimmune.

The duration and amount of alcohol consumed play important roles; drinking at levels above the NHMRC 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. NHMRC also recommend drinking less than 4 standard drinks per occasion to reduce the short-term adverse effects of alcohol use, in particular alcohol-related injuries. Alcohol dependence does not inevitably lead to cirrhosis, as only 10–20% of heavy drinkers progress [16]. 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, with a combination of liver cell failure and the development of portal hypertension. Acute decompensation results in symptomatic ascites, jaundice, pruritus, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, variceal bleeding and coagulopathy.

Ascites

Ascites due to hypoalbuminaemia, secondary hyperaldosteronism and portal hypertension is usually recurrent. Sudden exacerbations may be caused by SBP, the development of 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 are minimal but there is sudden worsening of jaundice or encephalopathy.

The long-term treatment of ascites includes sodium restriction and diuretics, especially spironolactone and/or furosemide. Problematic ascites may require fluid restriction, recurrent abdominal paracentesis and albumin transfusion. It is important to exclude SBP by paracentesis and polymorphonuclear (PMN) cell count, with greater than 250 PMN cells/mm² being diagnostic. The treatment of SBP includes intravenous broad-spectrum antibiotics, such as ceftriaxone 1 g IV daily or timentin 3.1 g 6-hourly daily, followed by oral antibiotic prophylaxis with trimethoprim 160 mg and sulphamethoxazole 800 mg tablets once daily.

Coagulopathy and encephalopathy

Coagulopathy results from the failure of hepatic synthesis of coagulation factors, thus administration of vitamin K 10 mg IV 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 conscious level in the cirrhotic patient.

Hepatic encephalopathy is associated with an increased nitrogenous GIT load (such as from a gastrointestinal bleed), dehydration, sepsis, certain drugs, hyponatraemia or hypokalaemia, worsening liver function and increasing jaundice. The treatment includes supportive care, GIT cleansing with lactulose (oral and enema) and oral non-absorbable antibiotics, such as neomycin to reduce bacterial counts, although their efficacy is unclear [16].

Thrombocytopaenia

Thrombocytopaenia is a common finding in alcoholic liver disease and several factors contribute. 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 subsequent reduction in the proliferation and differentiation of megakaryocytes and platelet formation.

Alcoholic pancreatopathy

Alcoholic pancreatopathy is used to describe 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 (70–80%), 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. Acute and chronic alcoholic pancreatitis are managed conservatively, with abstinence from alcohol, intravenous fluids, parenteral analgesia and antibiotics if pancreatic necrosis or an abscess are suspected (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 self-harm intent are often underestimated in the ED intoxicated patient. 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% had completed suicide. This represented a 51-fold increased risk compared to the general population, with the risk of completed suicide being greatest in the first year [17].

Alcoholic hallucinosis

Alcohol misuse causes psychotic symptoms by several mechanisms, including direct intoxication, alcohol withdrawal, delirium tremens (DTs), Wernicke’s 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 not related 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. Its chronicity and derogatory auditory hallucinations are similar to 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 generally begin within 10 hours of reduced alcohol intake, with a peak intensity by day 2. The withdrawal syndrome may occur in an individual who usually drinks an ‘eye opener’ or ‘hair of the dog’ but is prevented from doing so.

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 and predict likelihood of seizure and direct preventative management. The most commonly used AWS is the Clinical Institute withdrawal assessment – alcohol, revised scale (CIWA-R). This scale measures 10 items and was primarily developed for planned detoxification or for use on general medical and psychiatric wards [18]. 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 [19]. Patients with high scores have an increased risk of seizure if they remain untreated. The higher the score, the greater the relative risk. However, some patients experience complicated withdrawal despite initial low scores.

Pharmacological therapy

Benzodiazepine (BZD) therapy reduces signs and symptoms of alcohol withdrawal and prevents complications [20]. All BZDs appear to have similar efficacy. 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 1- to 2-hourly may be needed for symptom control and up to 160 mg per 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.

Alcohol withdrawal seizures

Around 3–5% of those with severe alcohol use disorder experience withdrawal seizures within 48 hours of stopping drinking and 15% will have a seizure in their lifetime. Previous withdrawal seizure is the strongest predictor of recurrent seizure. Most alcohol withdrawal seizures are short lived and self-terminating. Localizing signs or prolonged seizure should prompt a search for alternate pathology. Intravenous BZD, such as midazolam 0.1–0.2 mg/kg, is given for prolonged seizure. Phenytoin is not recommended for alcohol withdrawal seizures, unless there is coexistent epileptic disorder.

Delirium tremens

DTs is characterized by confusion, altered conscious state and autonomic hyperactivity. The incidence of DTs has been reduced by effective early management of withdrawal and excluding intercurrent illness. DTs occur in less than 1% during any single withdrawal episode. The diagnosis is important, as the mortality approaches 15% if untreated. As symptoms usually manifest within 48 hours, DTs may be encountered in EDs experiencing access block or in short-stay observation units.

Risk factors for DTs: five risk factors are associated with the development of the DTs [21]. These include current infection, tachycardia greater than 120 beats/min, signs of alcohol withdrawal accompanied by BAC of more than 0.1%, seizure history and history of delirious episodes. DTs are rare in the absence of these factors. The treatment includes management in an intensive care with regular intravenous BZD, such as midazolam 0.1–0.2 mg/kg, and a search for underlying conditions, such as sepsis.

Wernicke’s encephalopathy

The classical features of Wernicke’s encephalopathy are ataxia, confusion and ophthalmoplegia, usually lateral rectus palsy. It is caused by thiamine deficiency, but severe deficiency may be present without these signs. In alcohol- dependent persons, oral thiamine absorption is poor. Malabsorption, reduced storage and impaired utilization of thiamine increase the risk of Wernicke’s encephalopathy.

Post-mortem studies suggest that thiamine deficiency sufficient to cause irreversible brain damage remains undiagnosed ante-mortem in 80–90% of alcohol-dependent persons. Wernicke’s encephalopathy should be considered in all patients in coma, as replacement of depleted brain thiamine is necessary. The mortality approaches 20% if left untreated.

Treatment of Wernicke’s encephalopathy

High-dose oral thiamine may be ineffective, thus parenteral therapy with thiamine 500 mg IV tds is recommended for at least 5 days. The risk of anaphylaxis is low with the current drug formulations [22,23]. The recommended prophylactic thiamine dosage has been increased to 200 mg parenterally tds.

Other alcohol-related neurological problems

Alcohol is a neurotoxin and chronic heavy use causes CNS damage, peripheral neuropathy, myopathy and movement disorders such as tremor, Parkinsonism, dyskinesias, cerebellar ataxia and asterixis.

Peripheral neuropathy

Peripheral neuropathy is common in alcohol misuse and has multiple aetiologies, including direct toxic effect of ethanol and malnutrition with thiamine defficiency. The prevalence among chronic drinkers is unclear but is estimated at between 9 and 50%. Other contributing factors are increased age, total lifetime dose of alcohol, nutritional status (malnutrition and thiamine deficiency) and family history of alcohol misuse. Alcoholic peripheral neuropathy is most commonly sensory in the lower limbs.

Alcoholic autonomic neuropathy

Alcoholic autonomic neuropathy is uncommon. It is often asymptomatic or causes erectile dysfunction in males, postural hypotension and/or diarrhoea. It is related to different pathological processes than sensory peripheral neuropathy.

Ataxia

Ataxia is a common presenting symptom and sign and may be due to peripheral neuropathy affecting proprioception, cerebellar degeneration or a combination of both. Cerebellar ataxia is possibly an extension of the insult from thiamine deficiency as in Wernicke’s encephalopathy. Whereas in Wernicke’s encephalopathy the ataxia may be reversible by thiamine administration, full recovery is rare and permanent damage occurs affecting the superior cerebellar vermis.

Blackouts

Neuronal failure resulting in blackouts and amnesia is a direct toxic result of alcohol on the CNS. This is especially common in binge drinkers. Orthostatic hypotension from autonomic failure is differentiated on the clear relationship to posture.

Respiratory illness in alcohol-dependent persons

Chronic obstructive airways disease

Chronic obstructive airways disease (COAD) is common among alcohol-dependent persons, mostly due to the high prevalence of concurrent tobacco smoking (see Chapter 6.5).

Pneumonia

Alcohol dependence increases the risk of community-acquired pneumonia due to immunosuppression, as well as general lifestyle factors, such as hygiene and smoking. Typical organisms include Streptococcus pneumoniae and Haemophilus influenzae. There is also a higher frequency of cavitating disease, empyema and unusual pathogens. Anaerobic and Gram-negative organisms are frequent colonizers of the oropharynx and GIT and aspiration pneumonia is common. Opportunistic disease, such as tuberculosis, Pneumocystis carinii pneumonia, now known as Pneumocystis jiroveci, and Legionella are also more frequent in alcohol-dependent persons.

Metabolic problems with alcohol use

Alcohol use and metabolic acidosis

Alcoholic ketoacidosis

There is contention about the existence and frequency of alcoholic ketoacidosis. This refers to high anion-gap metabolic acidosis associated with the acute cessation of alcohol on a background of chronic alcohol abuse and relative starvation. Clinical features include nausea, vomiting, abdominal pain, tachycardia, tachypnoea and hypotension, all of which may occur in other alcohol-related emergency presentations.

Chronic alcohol intake can lead to depleted carbohydrate and protein stores in the body due to relative starvation. Reduced hepatic gluconeogenesis from substrates, such as lactic acid, glycerol and amino acids, can cause hypoglycaemia. In dehydrated states, the combination of hypotension and hypoglycaemia results in reduced insulin production and raised catecholamines, cortisol, glucagon and growth hormone. These hormones promote utilization of fatty acids for energy, resulting in ketogenesis.

Alcoholic ketoacidosis has been described as ‘a common reason for investigation and admission of alcohol-dependent patients’, although research data appear limited. There may be an increased frequency of sudden death among patients who present in this fashion [24].

Diabetic ketoacidosis

Acute alcohol intoxication can precipitate ketoacidosis in known insulin-dependent diabetics.

Acute alcohol ingestion can cause a state of acute insulin resistance. Alcohol-induced post-prandial hyperinsulinaemia occurs without significant decrease in blood glucose levels, consistent with impaired insulin sensitivity. Relative starvation may result in hypoglycaemia and reduced insulin release. Alcohol-induced insulin resistance is important in these patients to recover from hypoglycaemia. Conversely, there is a reduced risk of type II diabetes mellitus in moderate drinkers (18–48 g per day) compared to light or heavy drinkers.

Other metabolic acidosis

Metabolic acidosis is rare in alcohol intoxication alone. One study of 60 ED patients with BAC greater than 0.1% described seven patients with a raised serum lactate, all of whom had alternative reasons for this, such as seizure, hypoxia and sepsis [25]. The treatment of an alcohol-dependent patient with metabolic acidosis is symptomatic with intravenous crystalloid fluid resuscitation and rehydration, thiamine 200 mg IV, 5% or 10% dextrose for hypoglycaemia, electrolyte replacement (see below) and a search for and treatment of another underlying cause, such as sepsis.

Electrolyte disturbance

There are no direct correlations between acute or chronic use of alcohol with specific electrolyte disorders, although certain deficiencies are characteristic, such as hypokalaemia, hyponatraemia, hypomagnesaemia, hypophosphataemia and hypocalcaemia. The causes include poor intake, malabsorption, excessive losses from vomiting, diarrhoea and fluid diuresis, reduced renal tubular reabsorption and dilutional changes due to polydipsia.

Electrolyte imbalances result in disturbance of other endocrine systems. Thus, hypomagnesaemia suppresses parathyroid hormone release, resulting in hypocalcaemia. Electrolyte disturbances are also related to alcohol-induced illness, such as pancreatitis or pneumonia.

Cardiovascular

Coronary heart disease

There is a reduced mortality from coronary heart disease in diabetic moderate drinkers (approximately 28 g per day). However, alcohol use in diabetes increases the risk of retinopathy, peripheral neuropathy and foot ulcers. Coronary protective effects of alcohol are due to influences on increased high-density lipoprotein (HDL) cholesterol, platelet function and fibrinogen.

Hypertension

Acute alcohol intake is a vasodilator, whereas drinking alcohol over the longer term causes systolic hypertension and increased aortic stiffness. An assessment by the World Health Organization Global Burden of Disease 2000 Comparative Risk Analysis attributed 16% of all hypertensive disease to alcohol intake. These findings may be confounded by other lifestyle factors and there are many contrasting effects of alcohol at various intakes, depending on gender and body mass index (BMI). Thus, raising HDL cholesterol is cardioprotective, but developing central obesity ‘beer gut’ is not. Overall, any benefits of moderate alcohol consumption on coronary disease are likely to be outweighed by harmful effects.

Cardiac arrhythmias

Heavy alcohol use is associated with an increased risk of sudden cardiac death, most commonly due to ventricular arrhythmias. Atrial arrhythmias including atrial fibrillation occur commonly after heavy binge drinking, ‘holiday heart’, in both acute and chronic drinkers. They are not necessarily associated with cardiomyopathy. The risk of a cardiac arrhythmia is increased by electrolyte abnormalities, such as hypokalaemia, hypomagnesaemia and hypocalcaemia.

The treatment of arrhythmias is as recommended by the current Advanced Cardiovascular Life Support guidelines.

Cardiomyopathy

Concentric left ventricular hypertrophy is common in chronic alcohol users. Dilated cardiomyopathy may ensue with progressive dilatation and fibrosis, leading to congestive cardiac failure. This myotoxic process has a worse prognosis than idiopathic dilated cardiomyopathy, particularly if drinking continues. Myocyte function can improve with total abstention.

Aggressive anti-failure therapy should be implemented with dietary measures, such as reduced sodium intake, an angiotensin converting-enzyme inhibitor and other pharmacotherapy, even if total abstention cannot be achieved.

The so-called ‘wet beri-beri’ cardiomyopathy is caused by severe thiamine deficiency that leads to myocardial dysfunction and peripheral vasodilation. Thiamine absorption is impaired by alcohol and long-term use of frusemide depletes the body of water-soluble vitamins, including thiamine. Changes in myocardial function occur within 1 hour of starting parenteral thiamine therapy and are back to normal within 1 week of treatment [26].

Malignancy

Alcohol has been causally linked to many types of neoplasia, most commonly those of the GIT. Oropharyngeal and other head and neck cancers have a direct link to alcohol. Drinking more than 1.5 bottles of wine daily elevates the risk of oesophageal cancer 100 times. Hepatocellular carcinoma (HCC) is usually preceded by alcoholic cirrhosis in the Western world, although other causes include hepatitis B and C viruses. Progression of cirrhosis to HCC is more rapid if drinking continues. Chronic alcohol consumption is also related to laryngeal, breast, pancreatic and colorectal carcinomas.

Important illnesses to be excluded that mimic alcohol intoxication

It is hard to know when to look for another cause for altered conscious state in the habitual drinker or intoxicated person, as many alternative conditions must be considered that mimic apparent alcohol intoxication (Table 21.4.1). The mean length of altered conscious state in an ED for intoxication alone has been reported at 3.2 hours with a wide standard deviation of 3.6 hours, with the likelihood of another pathology being present increasing rapidly after 4 hours. Close observation looking for trends in autonomic responses and neurological signs and detailed examination looking for other pathology are more appropriate than waiting for, or intervening after, a certain period of time.

Metabolic disturbance

There is little evidence that hypoglycaemia occurs in adults with simple alcohol intoxication alone; with one large study of ED patients screened for alcohol use and serum blood glucose finding no linear relation between blood alcohol and glucose levels. The incidence of hypoglycaemia is not increased in alcohol- related ED attendances compared to sober patients. Intravenous glucose administration has not been shown to be useful in changing rates of alcohol elimination or decreasing periods of intoxication. However, it is essential in each patient with an altered mental state to measure the blood glucose and treat if it is low. Chronic alcoholics have limited hepatic glycogen stores due to malnutrition, so administering glucagon is not effective as it cannot initiate gluconeogenesis. In the intoxicated or alcohol-dependent patient, an alternative cause for hypoglycaemia should still be sought.

Hyponatraemia may occur with sepsis and general debility. Diabetic ketoacidosis or hyperglycaemic, hyperosmolar non-ketotic syndrome should also be excluded (see Chapter 11.2).

Head injury

Head injuries are not only more common in intoxicated and alcohol-dependent patients, they are easily missed due to a presumption that intoxication is the main cause of the altered conscious state. Head injuries may be complicated by coexisting coagulopathy and thrombocytopaenia from liver disease, cerebral atrophy and underlying metabolic problems. A computed tomography (CT) brain scan is essential to rule out intracranial pathology, particularly cerebral contusion, extradural haematoma, subdural haematoma and base of skull fracture.

Close neurological observation in a monitored resuscitation area is necessary in the intoxicated person with an altered conscious level and a possible head injury. Worsening confusion, deteriorating level of consciousness or focal neurology necessitate an urgent CT brain scan, which may be challenging in a poorly compliant patient. Intravenous sedation or even endotracheal intubation may be necessary to obtain a CT scan safely.

Other intracranial pathology

Altered conscious state: differential diagnosis

A patient with any significant intracranial pathology may present with an altered conscious state mimicking alcohol intoxication. The chronic alcohol-dependent patient may present with an unusual cerebral infection, such as cryptococcal meningitis, cerebral abscess or herpes encephalitis. Also a cerebrovascular accident, either embolic or haemorrhagic, is more likely in the habitual drinker, due to co-morbid vascular disease and smoking, hypertension and coagulopathy.

An altered conscious state may be due to a seizure from alcohol excess or withdrawal, status epilepticus or a post-ictal state. Cerebral neoplasia, particularly metastases, may present late in this population. Again a CT scan is usually indicated in the alcohol-dependent patient following a seizure, particularly if there is persisting or deteriorating confusion or focal neurology. A lumbar puncture may be needed to exclude meningitis or a subarachnoid haemorrhage if there is clinical suspicion, even if the CT brain scan was normal.

Other toxicological states in the alcohol-dependent patient

Multiple drug ingestion

Multiple drug ingestion, whether prescription or illicit, is common in regular drinkers for recreational reasons, due to dependence, to ‘come down’ from other drug effects, in accidental overdose or in deliberate self-harm. The most common and important ingested drugs to consider include BZDs, opiates, paracetamol, often as over-the-counter analgesics, antidepressants including tricyclics and selective serotonin reuptake inhibitors, γ-hydroxybutyrate, ecstasy and other sympathomimetics, such as cocaine and ketamine.

Other alcohols

Other alcohols, such as methanol, ethylene glycol and isopropyl alcohol, although rare, should be considered in the significantly intoxicated, self-harm patient. ‘Methylated spirits’ bought over the counter in Australia only contains 95% ethanol v/w with no methanol at all and, in New Zealand, the methanol content has been reduced to 2% or less, due to deaths attributed to chronic misuse and methanol poisoning there.

Serum drug levels

The only clinically useful screening serum drug levels are paracetamol and ethanol. Other drug levels take hours to days to perform (institution dependent); thus they are not of use at the time and should only be requested if there are specific indications. The only safe antidotes to consider are naloxone, thiamine and glucose. Flumazenil is not recommended due to the risk of inducing seizures and then not being able to manage them effectively.

Other sepsis

Sepsis must be considered in any person with an altered conscious state potentially masked by alcohol intoxication and a directed septic work-up carried out.

Treatment of alcohol-related illness

Alcohol intoxication

Intoxication starts with a feeling of well-being and an increasing sense of relaxation, followed by impairment of judgement and incoordination. At BAC of 0.1%, dysarthria, ataxia and disinhibition are common. At BAC of 0.2%, confusion occurs and new memories are not formed. At BAC of 0.25%, cortical depression is seen with the onset of stupor. At BAC of 0.4%, most are unconscious and at risk of respiratory depression and death. The mean BAC found in fatal alcohol intoxication is 0.45%.

‘Pathological intoxication’

Some people have idiosyncratic responses to alcohol, the so-called ‘pathological intoxication’, which is more common among certain ethnic groups. A clear indicator of alcohol tolerance and neuroadaptation is the recording of high BAC in a person functioning at an otherwise reasonable level, for example the patient capable of normal conversation and gait with a BAC 0.3%. This may follow a continuous prolonged drinking binge.

Treatment of the acutely intoxicated person

The treatment of an acutely intoxicated person is supportive, protecting the at-risk airway and placing in the semi-prone position to reduce the risk of gastric aspiration. Gastric emptying procedures are not recommended under any circumstances. Intravenous fluids in simple alcohol intoxication do not increase the elimination or decrease the BAC. Likewise, IV 5% dextrose administration has not been shown to be useful in changing the rates of alcohol elimination or decreasing periods of intoxication.

There remains no antidote to alcohol intoxication. As alcohol affects endogenous opiate GABA receptors, both naloxone and flumazenil have been tried with no effect. Flumazenil use in the alcohol-intoxicated patient is dangerous as it renders benzodiazepines ineffective in the treatment of seizures for about 45 minutes after its use. It can also precipitate seizures if the patient is a chronic benzodiazepine user. Various substances have been tried in animals, but none so far is safe and/or effective. There has been interest in pyridoxine and, more recently, its analogue metadoxine in hastening alcohol metabolism and reversing both the biochemical and the clinical symptoms of intoxication, but studies are small [27].

‘Hangover’

It was estimated in the UK in 2003 that £2 billion in lost work value was due to post-alcohol-related headache and malaise ‘hangover’, which may be a greater economic problem than habitual intoxication. Paradoxically, light or binge drinkers’ hangovers cause the most lost work time as the hangover is more common and the sufferer is more commonly in regular employment than the heavy drinker.

Diagnosis and management

A hangover is distinguished from the alcohol withdrawal syndrome as it follows a defined single episode of intoxication. Symptoms include headache, feeling generally unwell, diarrhoea, anorexia, nausea, tremulousness and fatigue. The presence of two or more of these symptoms following alcohol intake has been used to define a hangover [27]. Acetaldehyde, the dehydrogenated metabolite of alcohol, has been implicated. Alcohol alters cytokine production and thromboxane B2 is increased, an effect blocked by prostaglandin inhibitors. This may explain why prostaglandin inhibitors, such as NSAIDs, including aspirin, may have some limited prophylactic effect on hangover development.

Hangover is not solely dose related. Hangovers are worse with dehydration, no food intake, decreased sleep, increased physical activity while intoxicated and poor general physical condition. Congener byproducts of some alcohols including aldehydes, esters, histamine, phenols, tannins, iron, lead and cobalt are found, especially in darker liquors, which are associated with an increased severity and incidence of hangover. Clear liquors, such as gin, vodka and rum, may lead to fewer hangovers. The evidence for hangover treatment and prevention is minimal [28,29].

The habitual alcohol-dependent emergency attender

Most EDs, particularly in metropolitan areas, have a group of recurrent ED attenders who keep presenting with alcohol intoxication and chronic alcohol-rela ted disease. Such people are usually male, aged 30–40 years and often have no fixed place of abode. They usually are well known to neighbouring EDs, community services and police. They tend to attend in cycles and an absence of attendance may indicate a prison term, a medical illness and/or hospital admission, an attempt at sobriety, use of an adjacent ED or sudden death. Over a year they may accumulate multiple investigations, especially CT scans of the head. This group has an increased mortality over time from assault and other trauma, as well as alcohol-related illness associated with neglect.

The ED as a temporary refuge

The ED provides a temporary refuge in an otherwise chaotic lifestyle and an opportunity for a health assessment and intervention. It is important to realize that providing care for this group of people is core business for every ED, despite any frustrations felt. Interventions to alter lifestyle and prevent recurrent attendances are successful. ED initiated case management involving community linkages and assistance with accommodation improves health outcomes but may increase ED utilization. Serial inebriate programmes may target this group, often commencing with socialization skills, such as personal hygiene and nutrition management [30]. Acceptance to such programmes is often precipitated by the threat of imprisonment. Such programmes have been demonstrated to be cost-effective.

Assessment of alcohol misuse

Alcohol screening tools

Emergency physicians witness daily the effects of lifestyle abuse on ED presentations and thus may find many opportunities to intervene opportunistically to affect the long-term health of the patient, as well as treating the immediate presentation. This is particularly valuable for patients with irregular contact with other medical services, such as the itinerant and the homeless [31].

Screening for chronic alcohol abuse or dependence

Any screening tool to be of value must have adequate sensitivity and specificity for detecting the illness involved and there should be an effective, cost-effective intervention available. Many screening tools for chronic alcohol abuse or dependence have been developed for primary care, with the best known being the CAGE questionnaire [32]. This poses four questions on behaviour and a positive answer to two or more indicates probable chronic alcohol abuse (Table 21.4.2).

Paddington alcohol test

An effective and quick alternative in the time-pressured setting of an ED is the Paddington alcohol test (PAT), which includes ‘routine’ focused selective screening combined with education, audit and feedback [32]. PAT has reduced screening time to 1 minute, simply quantifying the amount of alcohol consumed, how often and whether in the opinion of the patient the reason for ED attendance is due to alcohol.