Philip Moore DO, Toxicology Fellow, PinnacleHealth Toxicology Center Joanne Konick-McMahan RN MSRN, Staff RN, PinnacleHealth

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1 Philip Moore DO, Toxicology Fellow, PinnacleHealth Toxicology Center Joanne Konick-McMahan RN MSRN, Staff RN, PinnacleHealth I. II. Background A. AWS can occur in anyone who consumes alcohol B. Risk correlates with usage patterns C. Graded as mild, moderate or severe 1. Delirium tremors is severe AWS with confusion D. Occurs in 10-40% of hospitalized patients 1. Trauma patients may have a higher risk III. Physiology of intoxication and withdrawal A. Acute intoxication 1. Sedation, anxiolysis and/or disinhibition a) GABA: increases Cl channel conductance b) NMDA decreases Ca channel conductance c) Dopamine d) Opioid peptides e) Serotonin f) Adenosine B. Chronic intoxication 1. Tolerance is the result of continuous or repetitive intoxication a) Down regulation of GABA receptors with less ability to inhibit 1

2 b) Up regulation of glutamate receptors with more potential to excite C. Alcohol withdrawal c) Up regulation of NMDA receptors with more potential to excite d) Increase cellular calcium receptors 1. Results after an abrupt cessation of alcohol intake a) Abatement of the effects at GABA and NMDA receptors b) Disruption of homeostasis with rebound stimulatory effect and high autonomic sympathomimesis IV. Recognizing persons at risk for alcohol withdrawal A. Obtaining an alcohol history 1. Inquire about alcohol consumption (a passive or nonjudgmental approach is best) a) Recognize alcoholics may minimize usage patterns b) Find patients who drink >4 days per week for extended time periods c) When was their last drink? 2. Does the patient have symptoms of withdrawal on abstinent days? V. Signs and Symptoms A. Timing: 3. Any previous history of AWS while hospitalized? 4. An alcohol level from admission can be helpful 2

3 1. Symptoms usually begin 6-12 hrs after blood alcohol levels decrease 2. Symptoms peak around hours 3. Symptoms usually end by day 5 4. Rare cases can persist longer B. Symptoms 1. Symptoms can include tremor, anxiety, insomnia, nausea, paranoia, and hallucinations 2. Seizures occur during first 24 hrs 3. Confusion or agitated delirium gradually worsens and peaks around hours C. Physical exam 1. Vitals: fever, hypertension, and tachycardia 2. Mental Status: Riker >4, Anxious, poor registration and recall, oriented to self, and poor attention 3. Neurologic D. Laboratory VI. Treatment a) Tremor b) Chronic alcohol abusers may have B12 neuropathy or Wernicke s encephalopathy 1. Macrocytosis 2. Myelosuppression with thrombocytopenia 3. Alcoholic hepatitis (AST>ALT in classic 2:1 ratio) 4. Vitamin and electrolyte deficiencies: magnesium, potassium, phosphorus, sodium, and B vitamins A. Benzodiazepines 3

4 1. Benzodiazepines are first line treatment of AWS : increases chloride conductance through GABA complex resulting in sedation 3. Adverse effects: minimal decrease of HR and BP a) Benzodiazepines alone are not respiratory suppressants 4. Flumazenil available as reversal agent 5. Dosing and Pharmacokinetics B. Imidazolines a) No maximal dose (just like alcohol) b) Available IM? midazolam and lorazepam c) Benzodiazepine for cirrhosis? lorazepam d) Benzodiazepine for rapid sedation? diazepam or midazolam 1. Second line agents for patients with AWS and hyperadrenergic state (e.g. HTN and tachycardia) a) Reduced NE release b) Sympatholysis, anxiolysis, analgesia and sedation c) Adverse effects: hypotension and bradycardia (expected sympatholysis) 3. Dosing and Pharmacokinetics a) Clonidine (1) Available PO but can be administered SL 4

5 (2) Transdermal requires 24 hrs to effect (not ideal for AWS) C. Butyrophenones b) Dexmedetomidine (1) Available IV or IM (2) Expensive (3) Rapid onset and ability to titrate 1. 2 nd line agent for AWS and severe agitation a) Competitive receptor blockade (1) Dopamine, alpha, serotonin, muscarine, histamine b) Haloperidol has strong dopamine blockade with less effects on other receptors 3. Haloperidol D. Barbiturates a) IV has most rapid onset (5 min) b) Administered IM for agitated patients without IV access (delayed peak at 20 minutes) c) Max dose: unclear as there are case reports of ICU patients receiving ~300mg/day for sedation d) Adverse effects (1) Dose related prolongation of QTc: doses >2 mg IV require telemetry for monitoring (2) Akathisia associated with oral (pyridine metabolite) 5

6 1. 2 nd line agent for patients with AWS requiring high doses of benzodiazepines E. Propofol 2. Sometimes used as 1 st line agent given similarity to benzodiazepines 3. Mechanism: maintain chloride conductance through the GABA complex a) Different binding site on GABA complex than benzodiazepines 4. Adverse effects: associated with depression of all excitable tissues 1. 2 nd line agent for patients with very severe AWS : sedative hypnotic causing neural quiescence via sodium channel and NMDA receptor blockade 3. Rapid onset and titrateability 4. Adverse effects F. Alcohol infusion a) Propofol related infusion syndrome (mitochondrial toxin) b) Hypertriglyceridemia c) Seizures (many case reports) 1. Not recommended but can be occasionally encountered 2. Continuous IV infusion for 48 hrs then titrate off over next 48 hrs a) Requires frequent blood alcohol levels and dose adjustments 6

7 3. Adverse effects: injection site irritation, GI irritation, drug interactions 4. Clinical research G. Other therapies a) Average time to effect 14 hrs b) No advantage when compared to diazepam c) Risk for undersedation d) Risk for failing therapy (no failed patients in benzo group) 1. Baclofen: GABA-B agonist and muscle relaxant 2. Chlordiazepoxide: weak and long acting benzodiazepine 3. Carbamazapine: anticonvulsant 4. Gabapentin: inhibits GABA transmission 5. Pregabalin: agonist of alpha-2-delta reducing release of calcium dependent neurotransmitters 6. Valproate: inhibits reuptake of GABA, thereby increasing the concentration of GABA VII. Use of Order Set to Provide Best Care A. Provides application of evidenced based care. B. Appropriate doses of benzodiazepines to prevent withdrawal symptoms as well as treat symptoms C. Guides monitoring of symptoms and applies treatment based on symptoms D. Provides resources and guidelines for oversedation. E. Handout-Alcohol Withdrawal Order set F. Case study 1 G. Case study 2 7

8 References Goldstein. Atypical Antipsychotic Drugs: Beyond Acute Psychosis, New Directions. Emerging Drugs Gregoretti et al. Clonidine in Perioperative Medicine and ICU: More Than an Anti- Hypertensive Drug. Current Drug Targets Hendey et al. A prospective, Randomized Trial of Phenobarbital versus Benzodiazepines for Acute Alcohol Withdrawal. American Journal of Emergency Medicine Mayo-Smith, M.F. et al (2004) Management of Alcohol Withdrawal Delirium: An Evidence-based Practice Guideline. Archives of Internal Medicine: 164(13); Riddle et al, (2010). Alcohol Withdrawal: Development of a Standing Order Set. Critical Care Nurse: 3 (3); pp Riker et al. Prospective Evaluation of the Sedation-Agitation Scale for Adult Critically Ill Patients. Critical Care Medicine Riker, Fraser and Cox. Continuous Infusion of Haloperidol Controls Agitation in Critically Ill Patients. Critical Care Medicine 1994 Tetrault and O'Connor. Substance Abuse and Withdrawal in the Critical Care Setting. Critical Care Clinics Weinberg et al_comparison of IV Ethanol Versus Diazepam for Alcohol Withdrawal Prophylaxis in the Trauma ICU Results of a Randomized Trial. J. Trauma Young and Prielip. Benzodiazepines in the ICU. Critical Care Clinics

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