Alcohol related presentations to the emergency department
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This document provides an overview of alcohol-related presentations to the emergency department. It discusses statistics on alcohol use and related illnesses. It covers the pharmacology of ethanol and examines acute intoxication, alcohol in trauma, alcohol withdrawal, chronic alcoholism and associated health problems, toxic alcohols, and Wernicke-Korsakoff syndrome. Hepatic disease, encephalopathy, varices, and other issues related to long-term alcohol use are also reviewed.
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Alcohol related presentations to the emergency department
- 1. Alcohol Related Presentations to the ED DR CANDICE HANSON
- 2. Overview Some ED statistics Pharmacology of ethanol Acute Intoxication Alcohol in trauma Alcohol Withdrawal Chronic alcoholism – special problems Toxic Alcohols Summary Quiz
- 3. Some Statistics 3.3 million people world wide die from alcohol related illness p.a. (5.9%) Over 5% of annual burden of disease as DALYs is due to alcohol worldwide 25% of deaths in 20-39 yr olds world wide are attributable to ETOH ETOH is implicated in over 200 different health conditions 1 in 3 presentations to the ED in Australia are related to alcohol In 2010 estimates 3.5% Australian pop are dependent or use harmfully Australian men drink 20L per yr, women drink 9L per yr of pure alcohol
- 4. Pharmacology of Ethanol CNS depressant Potentiates action at GABA receptors and reduces NMDA activity (serotonin, NE) Absorbed 20% gastric 80% small intestine; metabolised at liver & excreted by kidney. 5% unchanged via lung. Water soluble. Zero order kinetics. Metabolism
- 5. Acute Intoxication Signs of acute intoxication Nystagmus, ataxia, slurred speech, CNS depression, respiratory depression Treatment – largely supportive. Aspiration risk – nurse on side. Patient must not be a danger to self or others before ED discharge (e.g. mobilise safely, responsible party will take home), passing urine No evidence that IVT improves recovery time / hastens metabolism, or BAL, but adds to cost of admission* If patient is not alcohol dependent, thiamine is not required
- 6. Alcohol in Trauma Higher suspicion for significant injuries e.g head trauma, c-spine If history / mechanism is unclear and patient has altered GCS, cannot assume it is due to alcohol. Lowered index to scan. If patient not improving or deteriorating during observation – look for alternate explanation Intoxication is a consideration in NEXUS c-spine rules, but not Canadian
- 7. Alcohol Withdrawal Minor withdrawal 6-24 hrs Tremor, anxiety, N&V, insomnia Major withdrawal 10-72 hrs Alcoholic hallucinosis, whole body tremor, vomiting, diaphoresis, HTN Seizures 6-48 hrs Brief and generalised, normal EEG, up to 60% not treated for withdrawal, up to 40% will progress to DT Delirium Tremens 3-10 days Medical emergency. Global confusion is hallmark; autonomic hyperactivity, risk of cardiovascular collapse, fluid / electrolyte disturbance. Large differential diagnosis.
- 8. Chronic Alcoholism – Special Problems Alcohol effects every bodily system Cardiovascular – HTN, alcoholic cardiomyopathy (direct toxic effect) Haematological – anaemia, thrombocytopaenia, macrocytosis, risk of infections, bleeding risk Neurological – cerebral atrophy, ?alcohol dementia (loose criteria, in DSM-IV, often overlaps with other forms of dementia, distinct from Korsakoff), head injuries / bleeds, cerebellar atrophy Endocrine – hyperoestrogenism, hypoglycaemia, pancreatitis Reproductive– spontaneous abortion, foetal alcohol sy, infertility (men & women), low birth wt Misc – gout, Dupytreyn’s, myopathy Psychosocial – financial, marital, violence, risk of sexual assault, employment. Screening tools e.g. CAGE (cut down, annoyed, guilty, eye opener)
- 9. Thiamine Deficiency Water soluble essential nutrient – Vitamin B1 Thiamine is phosphorylated in the gut to active coenzyme form, important in ATP production, normal nerve conduction & maintenance of neural membranes Deficiency results from poor nutrition, decreased conversion to coenzyme, reduced storage in fatty liver, ethanol may inhibit intestinal transport, impaired absorption Deficiency causes beriberi* Dry beriberi – polyneuropathy (symmetrical, non-specific myelin degen, usually lower limbs, affects sensory, motor and reflexive arcs. Progressive) Wet beriberi – affects the heart, leading to high output cardiac failure Wernicke-Korsakoff Syndrome
- 10. Wernicke-Korsakoff Syndrome Spectrum of disease Wernicke typically precedes, reversible if identified early Ophthalmoplegia (esp. lateral recti), nystagmus, ataxia Deranged mental function, fluctuates. Confusion, apathy, sleep disturbance, disorientation, listlessness to coma Korsakoff mostly irreversible Retrograde (then anterograde) amnesia Confabulation
- 11. Hepatic Disease Fatty liver, hepatitis, cirrhosis, HCC Hepatitis can range from mild with non-specific symptoms through to jaundice and fulminant hepatic failure. Can also become chronic Portal HTN – in setting of cirrhosis Ascites, portosystemic shunts, congestive splenomegaly, hepatic encephalopathy Hepatic failure – low albumin, low clotting factors, high ammonia, peripheral stigmata, jaundice. Risk of SBP, hepatorenal & hepatopulmoary syndromes (high mortality)
- 12. Hepatic Encephalopathy Distinct from Wernicke’s; occurs in setting of pre-existing liver disease Liver cannot cope with nitrogenous load (normally metabolises ammonium ammonia urea, excreted via kidney). Ammonia XBBB into astrocytes for metabolism, osmotic load cerebral oedema Clinical features: hepatic flap, confusion, altered cognition / coma Prevention – minimise protein / nitrogen load e.g. low protein diet, enemas, Aims for 3-4 soft stools daily. Antibiotics *** Lactulose – decreases transit time through gut (less absorption) and reduces production of nitrogenous waste by gut flora. (PO or PR 30mls tds)
- 13. Varices Oesophageal varcies – lower 1/3 of oesophagus venous drainage via gastric vein vein to portal system. Develop in setting of portal HTN Treatment of acute bleed Careful resuscitation (Hb 70-80) Terlipressin on suspicion of varices (don’t wait for confirmation) 2mg IV (4 hrly up to 3-5 days) Endoscopy – banding ligation > sclerotherapy within 12 hrs presentation Antibiotic to prevent gram negative infection – quinolone or 3rd gen ceph Balloon tamponade with Blakemore tube (pt is intubated). Risk of oesophageal necrosis / rupture http://www.youtube.com/watch?v=imFCMWeWDpU TIPSS / surgery
- 14. Toxic Alcohols Methanol: >0.5ml/kg can be lethal metabolised to formic acid, toxic to ocular tissues; CNS effects; initially elevated osmolar gap, then HAGMA (although normal values don’t exclude significant toxicity) Chemical thinners, paints, wood spirits, varnishes (not found in methylated spirits in Australia) Ethylene glycol: >1mg/kg can be lethal Metabolised to oxalic acid; HAGMA & osmolar gap; rapid CNS depression; formation calcium oxalate crystals in tissues with hypoCa++ & renal failure, cardiorespiratory failure Solvents, coolants, anti-freeze, brake fluids * Treatments include ethanol, fomepizole (ADH inhibitor), NaHCO3, haemodialysis.
- 15. Summary Alcohol related illness is a huge part of the ED workload burden Management of acute intoxication is largely supportive Higher risk, higher suspicion in trauma with alcohol on board Acute withdrawal – manage with benzos and thiamine supplementation Disease associated with thiamine deficiency – may be reversible Chronic disease related to alcohol – every bodily system. Emergencies to consider include liver failure, encephalopathy, bleeding varices Toxic alcohol ingestions can be potentially lethal if not managed early
- 16. “ ” QUIZ HOORAY! WINNER TAKES ALL…
- 17. Question 1 Who coined the following phrase? “Alcohol – the cause and solution to all of life’s problems”
- 18. Question 2 & 3 2) What city was the bar from this TV show set it? 3) The theme song was Where Everybody Knows You Name. What was the name of the bar’s proprietor?
- 19. Question 4 Who is this handsome fella, and what is his contribution to alcohol related medicine? (Hint: he produced a thesis entitled Alcoholic Paralysis)
- 20. Question 5 This unfortunately named singer famously sang about her refusal to enter rehab. What was her cause of death?
- 21. Question 6 This well loved Australian icon reportedly died from alcohol related dementia (or HIV according to Derryn Hinch). Who is he and why was he booted off Australian television in 1975? (I will give bonus points for an impression of the event)
- 22. Question 7 What are the alcoholic components of a traditional Long Island Iced Tea? (Hint: there are five)
- 23. Question 8 On September 19, 1975, the Star Hotel in Newcastle was closed down by police resulting in an infamous riot (ordinary fare in Newie, really). Which famous Australian band wrote the song ‘Star Hotel’ about this event?
- 24. Question 9 For Game of Thrones Fans… What type of drink does Tyrion Lannister like with his breakfast?
- 25. Question 10 Robert Downey Jnr is quoted as saying he has an allergy to alcohol. What does he break out in if he drinks?
- 26. Question 11 & 12 11) Tom Cruise starred in the 1988 movie Cocktail. What style of bartending did he help make famous? 12) Which Beach Boys song was the title track to the film?
- 27. Question 13 You can get it any old how, matter o’ fact, I’ve got it now! Which famous Aussie beer is this the advertising slogan for?
- 28. Question 14 On which day of the year is St Patrick’s Day celebrated? (Bonus point if you know why)
- 29. Question 15 What is Barney’s last name?
- 30. Quiz Answers 1 Homer Simpson 2 Boston, Massachusetts 3 Sam Malone 4 Sergei Korsakoff (Russian neuropsychaiatrist) 5 Amy Winehouse, acute alcohol poisoning 6 Graham Kennedy, crow impersonation “Faaarck” 7 Tequila, white rum, vodka, gin, triple sec 8 Cold Chisel 9 Black beer 10 Handcuffs 11 Flair or flairing 12 Kokomo 13 VB 14 March 17 (he died on this day) 15 Gumble
- 31. The Winner is… THANK YOU!
Editor's Notes
- WHO data: http://www.who.int/substance_abuse/publications/global_alcohol_report/profiles/aus.pdf?ua=1 http://www.who.int/mediacentre/factsheets/fs349/en/ ACEM https://acem.org.au/getmedia/3c816a16-f4c9-4e1c-a66a-7a25df114955/ACEM_Alcohol_Harm_Survey_Media_Release_AUS181213.pdf.aspx?ext=.pdf
- Article: *Intravenous 09% sodium chloride therapy does not reduce length of stay of alcohol-intoxicated patients in the emergency department: A randomised controlled trial. Perez, Keijers, Steele, Byrnes et al. J Em Med Aust; (2013) 25,527-34.
- Link to article: prospective study to determine superiority of NEXUS vs CCS rules in trauma in NEJM http://www.nejm.org/doi/full/10.1056/NEJMoa031375
- Screen using AWS – this is a validated tool Treat with long acting benzodiazepine e.g. PO/IV diazepam Replace thiamine e.g 100mg PO/IV daily DT is a medical emergency with a large differential diagnosis (stroke, sepsis, thyrotoxicosis, co-ingestion etc etc). Managed as inpatient. Other considerations – overall nutrition, social welfare Good chapter in Toxicology Handbook 2nd ed – Alcohol Abude, Dependence and Withdrawal p85 (Chapter 2.12)
- NB effects of thiamine deficiency e.g. wet beriberi / cardiac failure are distinct from the direct toxic effects of alcohol e.g. alcoholic cardiomyopathy
- Wernicke encephalopathy is distinct from hepatic encephalopathy. Wernicke’s is caused by deficiency of thiamine and can be improved or reversed with supplemental thiamine; Hepatic encephalopathy occurs where there is pre-existing liver disease (which may or may not be alcohol related). Usually nitrogenous waste build up which the diseased liver cannot process leads to cerebral oedema and features of encephalopathy. Mainstay of treatment is correcting underlying causes, and reducing nitrogenous load e.g. low protein diet, use of enemas and lactulose to reduce nitrogen absorption and waste formation by gut flora.
- CIRRHOSIS Severity can be graded using Child-Pugh classification system. Predicts prognosis, need for treatment and assessment for liver transplantation. Also used in chronic liver disease. Measures include: bilirubin, albumin, PT/INR, ascites, hepatic encephalopathy. Each is scored and then converted to a grade A/B/C HEPATITIS Mild, non specific Severe, jaundice with altered LFTs Fulminant hepatitis Also assoc coagulopathy, CVS instability, ARF, ARDS, acid base / electrolyte disturbances. Will not necessarily have chronic stigmata. Fulminant hepatitis – jaundice, encephalopathy, fetor hepaticus. Mortality approaches 90%. Chronic (>6/12 duration with LFT derangement, confirmed histologically) JAUNDICE Imbalance between bilirubin production and elimination Excessive production Reduced hepatocyte uptake Impaired conjugation Decreased hepatocellular excretion Impaired bile flow (intra & extra hepatic) PORTAL HYPERTENSION Resistance to flow through the portal system. May be prehepatic, intrahepatic, extrahepatic. Cirrhosis is the most common cause in Western cultures. Also cause by portal vein thrombosis, Budd Chiari, schistomiasis SPONTANEOUS BACTERIAL PERITONITIS High mortality if not recognised early Occurs in the setting of clinically appreciable ascites Fever (although can by mildly hypothermic) Abdominal pain / tenderness – although abdomen is rarely rigid. Altered mental status – can be very subtle Also – diarrhoea, paralytic ileus, hypotension Translocation of gram negative gut flora Rx – early resuscitation, gram negative antibiotic cover, asicitic tap (check plt and coags first!)
- Triggers include GI bleeds, TIPSS, dehydration, electrolyte imbalance, drugs/alcohol/analgesics, diuretics, renal failure Treatment also consists of correcting any underlying precipitants
- Primary prophylaxis – endoscopic ligation and non selective beta blocker. Repeat scopes until confirmation that varices are healed. Terlipressin Vasoconstrictor. Prodrug of vasopressin Use with caution in unstable angina / MI. Can cause bronchospasm Octreotide is an alternative Should be used in conjunction with endoscopic therapy Meta-analysis shows that use of vasoconstrictors decrease 7 day mortality, improve haemostasis, decrease transfusion requirement, decrease duration of hospitalisation. Banding ligation is superior to sclerotherapy Sclerotherapy may be tried if ligation fails or is not possible. PPI should then be given to prevent ulceration at injection site. Concomitant use of vasoconstrictor is superior than either method alone. If patient has early rebleed (<6/52) – consider use of Blakemore tube in an intubated patient (high risk aspiration) as temporising measure while preparing for TIPSS procedure (transjugular intrahepatic portosystemic shunt) or surgery.
- Toxic alcohols are often co-ingested with ethanol. Fantastic review article on toxicology of methanol: Barceloux DG, Bond R, Krenzelok EP et al. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. Journal of Toxicology – Clinical Toxicology 2002; 40(4):415-446 Fomepizole is an alcohol dehydrogenase inhibitor, not currently available in Australia. Used in methanol & ethylene glycol poisonings. Ethanol blocks formation of toxic metabolites in toxic alcohol ingestions as it has higher affinity for alcohol dehydrogenase (x50 in article above, x20 according to tox handbook). Loading dose ‘3x40ml shots of vodka in 70kg adult omit loading dose in already intoxicated patients, then 1x40ml shot every hr thereafter. Toxic alcohols are then not metabolised and are excreted unchanged by kidney.