Agenda Alcohol-related Emergencies 1. Background Blood and breath alcohol levels .2 ۃƱࢽூ ߍշጳ่ 3. ED evaluation and management 4. Alcohol withdrawal 5. Alcoholic ketoacidosis
Background Epidemiology
Alcohol tolerance Alcohol dependence or abuse over time, the person must consume more 40% ED patients alcohol to achieve the same intoxicating effects 25~40% trauma patients Alcohol dependence develops withdrawal symptoms with cessation of alcohol Alcohol addiction drastic behaviors used to maintain alcohol intake and often involves socially inappropriate behavior
Epidemiology Pharmacokinetics And Metabolism
Beneficial: 2~6 drinks per week Absorption: Harmful: > 2 drinks per day 20% in stomach, 80% in small intestine Metabolism: In general, one drink Liver (90%), kidneys, lungs = 1 ounce of hard liquor Alcohol dehydrogenase (ADH), = 1 beer Microsomal ethanol-oxidizing system = 1 glass of wine (MEOS) = 25 mg/dL blood alcohol level (BAL) Peroxidase-catalase system Rate of ethanol metabolism Alcoholism = risk factor
Non-tolerant adult: 20 mg/dL/h Trauma: Chronic drinkers: 30 mg/dL/h speeding, not wearing seatbelts (induction of the MEOS system) falling Rule of thumb: fighting 25 mg/dL/h (USA) 20 mg/dL/h (Taiwan) Alcohol hypersensitivity syndrome Asians Facial flushing – high aldehyde level
Alcoholism = risk factor Prehospital Care
Non-trauma : EMS transport pneumonia, lung abscess, meningitis If > 5 times: 71% alcoholics cardiomyopathy Refuse treatment or transport coagulopathy If altered mental status: suicide Check blood sugar Protect cervical spine Prevent aspiration
Initial evaluation in ED Initial evaluation in ED Secure ABCs - when in doubt, a Secure ABCs - when in doubt, a definitive airway should be secured definitive airway should be secured If AMS If AMS Protect and clear C-spine Protect and clear C-spine Monitor SpO2 Monitor SpO2 Check blood glucose (esp. children) Check blood glucose (esp. children) Give thiamine 100 mg (Wernicke’s Give thiamine 100 mg (Wernicke’s encephalopathy) encephalopathy) Naloxone [X], flumazenil [X] Differential diagnosis History ʍᾐI0ҧዔǑဇ1 ࠤɐᎹȝમᚳፗ̐⁄⊮ PHx: disulfiram, warfarin, phenytoin, sedatives Prior withdrawal seizure Abdominal pain, tachypnea Alternative drinks – wood / rubbing alcohols
PE Sobriety Tests
Complete secondary survey Field / boating sobriety test (> 100 Horizontal nystagmus mg/dL) Serial NE, esp. if multiple caretakers Horizontal gaze nystagmus Difficulty reciting alphabet from A to Z Chronic alcoholics: Difficulty with clapping hands while rhinophyma, palmar erythema, spider counting angiomata, hepatomegaly, testicular atrophy, “chipmunk cheeks” (parotid enlargement), gynecomastia, acne rosacea, Dupuytren’s contractures
Sobriety Tests Blood Alcohol Levels
Detect breath odors BALs correlate poorly with the degree Significant rate of false-negatives. of intoxication observed clinically (e.g. Failing to detect alcohol (false-negative), using Alcohol Symptom Checklist) not in overestimating its presence (false- positive)
Alcohol Symptom Checklist (a clinical scoring tool) did not correlate with the blood alcohol in intoxicated patients ዚ╖ΨৈᙊǏἜᡛܾJǞҥ̊ᱜἜࠉᦇ ᕭଗ
ৈᙊዚ╖ᡛܾ üᒻዚ╖ᡛܾ ṟ᭘ ᭝᭣̊ᆺᒻጺᯟ⊛ዚ╖ᡛܾᑧǔί ǕΫƫͻۻmg/100mL) (mg/L) P˜ˤᒃƳ̵ɚ⊛ҟਲ਼ߝ่p) ╖⇶Ꮋࢃ⊛ᖀধ̃'ʌ๏̃ᚳΞ⊛ ʞ̃ഒҧ ɐִǑΫƫ̵ɚøᓸ⊛ḎÌ∙ᏺǞ᭝᭣⊛J 0.238~0.047 50~10 ΐȆમᔶᣤ⊛Ȕȑμేʅ̃Wಥ⊛ ૻ᭝᧿Ǖsྠ (ᇛཷ˴ᆢСǐଗʯ⏄ɐɐΩ͛ᄵJᇛཷ˴ 50~100 0.238~0.467 Mᇺ᎕ ᆢᲞߝøᄵϛ⏄əΩˤᄵଗв) ╖⇶ᒷ˒⊛܋৩ষWಥ⊛ஈ௦ɝ⊛ 150~300 0.714~1.428 в̃ᠤ↱⊛ষୂᠤ↱ ᭝᭣̊ᒻዚ╖ᡛܾᇜPˤˤᒃƳ̵ɚ⊛ ວÆ'࿀ŝ'ວΌ'Ȕȑljే᧷⊛ ᭝᭣̊ҟ̵ϙыǔǙСǐò⊛ߝɐ܌̵ɛྡ 250~400 1.190~1.904 ƿҧ'lj∙ ࠪɹ'୰ࠑમߝ̵əִƫ̵ɚἜøፙ (ɹᕭྷ ວᅿ⊛Фǐlj;ধೠ⊛ü¸ࡂᵈߣ ⏄ɐǓΩˤᄵʛə) 400~500 1.904~2.380 ʳ'ᐓ˱
ஐ⚌Ś ¹ᒻΏৈᙊɽዚ╖ᡛܾȚΥˢᾐ⊮
ᚉƴἔᶷ˴ᆢ˛ෝᆋᡪᲖÌ⊛ͻɚΰǕ üᒻዚ╖ᡛܾ x 200 = ৈᙊዚ╖ᡛܾ ఽW೮๑ዚ╖ጺᛄ⊛☫ᛄɢüᒻዚ╖ᡛ 0.25 mg/L x 200 = 50 mg/dL ܾᥒ 0.20 mg/L⊛Ǐ˛ෝἔᶷ⊛̦Ἔ 0.55 mg/L x 200 = 110 mg/dL ৈᙊዚ╖ᡛܾƲҩ⊮ ৈᙊዚ╖ప(̳ಥ)ᰟ ᑧҧ10~40 mg/dL zo᷀܋χ⊩20 mg/dL/hr
BAL and GCS
GCS is not statistically affected by the presence of alcohol until the BAL is 200 mg/dL or more Indications of head CT: BAL < 200 mg/dL and GCS ≤ 14 GCS ≤ 13 When to obtain BAL Laboratory Testing
Routine BAL: Glucose: F/S The American College of Surgeons’ K Committee on Trauma recommends Mg drug and alcohol screening as “essential” for level I and II and “desirable” for level Amylase, lipase III trauma centers Elevated Recommended if: Clinically diagnosis diagnosis of intoxication is uncertain clinical evidence of head injury
Head CT CT for alcoholics
Clinical evidence of skull fracture Either: Basilar skull fracture: periorbital ecchymosis (raccoon’s eyes), mastoid ecchymosis (Battle’s sign), 1. Liberal policy of CT (head, chest, CSF otorrhea or rhinorrhea, hemotympanum abdomen) Palpable skull fracture Major mechanism of injury and altered mental status 2. Admission for close observation or Level of consciousness more depressed than expected prolonged observation with frequent compared to the serum alcohol level serial re-examination / ultrasound Significantly altered mental status (GCS ≤ 13) and evidence or suspicion of head trauma Falling GCS Focal neurologic deficit
Cervical Spine Radiography ED management
NEXUS study: intoxicated patient can Physical or chemical restraints have asymptomatic CSI agitation Recommendation: disruptive to staff minimum of 3 views or be maintained in potentially threaten their own well-being spinal precautions until sober restless or combative – consider succinylcholine and intubation in high- risk patients (e.g. thrown through the windshield) Chemical restraints Alcohol withdrawal syndrome
Benzodiazepines AWS develops 6~24 hrs after a decrease in – combative / withdraw ethanol intake and lasts from 2~7 days Mild symptoms: irritability and Lorazepam sleeplessness Dormicum Major withdrawal: Butyrophenones Fever, diaphoresis, and hallucinations Autonomic hyperactivity - tremulousness, – behavioral emergencies sweating, nausea, vomiting, and agitation Haloperidol Vital signs - elevated HR and BP Droperidol Generalized seizures (rum fits), within 12~24 hrs of abstinence
Delirium tremens DDx of delirium tremens
3rd~4th post-abstinence day Metabolic disorders 5% of AWS Hypoxia S/S Hypoglycemia Hallucinations – visual, tactile (formication) Hyperthyroidism Confusion, disorientation Hepatic encephalopathy Pronounced autonomic hyperactivity – Infectious disasters adrenergic storm Sepsis Tx = benzodiazepines Meningitis Mortality less than 15% Encephalitis
BZD for AWS AWS: adjunctive treatments
Drug of choice = lorazepam Haloperidol, droperidol Ease of administration, rapid onset of ß-blockers, clonidine, carbamazepine action, non-hepatic metabolism, and lack Alcohol detoxification units - only for of active metabolites those who have stable vital signs and IV dose: 2~5 mg bolus, 2~5 mg q20min are not hallucinating or confused When using BZDs, avoid switching agents but instead administer repeated doses of a single agent Rum fits Alcoholic ketoacidosis (AKA) Alcohol withdrawal seizures Chronic alcoholic + poor nutrition Onset: 12~48 hrs after a major decline in blood alcohol levels recent binge drinking & decreased 6.2% 1st-time seizure related to alcohol carbohydrate intake had intracranial lesions Tx: lorazepam depletion of glycogen stores Anticonvulsant duration: 15 min for diazepam vs 12 hrs for lorazepam & reduced insulin production If lorazepam not used, 8 times more likely to have 2nd seizure Lipolysis free fatty acids
AKA: symptoms AKA: signs Volume depletion – tachycardia, orthostatic hypotension Anorexia and nausea Odor of ketones Protracted vomiting Tachypnea and/or Kussmaul respirations (rapid and deep breathing) Diffuse abdominal pain Metabolic acidosis - anion gap Reduce oral intake Fever is generally absent Mental status usually normal Lipolysis unless co-existing sepsis or hypoglycemia Diffuse abdominal tenderness can mimic pancreatitis and peritonitis
AKA: DDx AKA: lab tests
Diabetic ketoacidosis Hypokalemia Methanol or ethylene glycol ingestion Hyponatremia Iron overdose Hypomagnesemia Salicylate poisoning Hypophosphatemia Severe pancreatitis Blood glucose variable Ischemic bowel Alcohol levels typically low or undetectable, however, AKA can occur high BALs AKA: ketones AKA: management
A negative nitroprusside reaction does not Cornerstones of therapy = volume repletion rule out ketoacidosis Fluid resuscitation in AKA should include nitroprusside reaction - sensitive for acetoacetate and acetone but not for ß- dextrose and saline hydroxybutyrate (BOHB, the major ketoacid in Patients in AKA do not need insulin AKA) Clinical response is the best way to follow An increasingly positive nitroprusside the patient’s response to intervention reaction is consistent with an improvement rather than a worsening of the ketoacidosis Supply potassium and magnesium nitroprusside reaction becomes more positive as Give thiamine the ß-hydroxybutyrate is metabolized to acetoacetate Bicarbonates not indicated
Take home message Summary 1. ዚ╖పᰟ
2. ¹ᒻΏৈᙊɽዚ╖ᡛܾȚΥˢᾐ⊮
3. ᕓỚ AWS Ἔ drug of choice
4. AKA ἜᜮᕓỚ
Take home message 1. ዚ╖పᰟ Thanks 20 mg/dL/h 2. ¹ᒻΏৈᙊɽዚ╖ᡛܾȚΥˢᾐ⊮ üᒻᡛܾ x 200 = ৈᙊᡛܾ 3. ᕓỚ AWS Ἔ drug of choice Lorazepam 2~5 mg 4. AKA ἜᜮᕓỚ Dextrose+saline; no insulin'no Jusomin