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Substance Abuse

I. Alcohol Detoxification

A. General Principles of Detoxification

1. Establish baseline vital signs; assess and follow with alcohol withdrawal scales such as the Clinical Institute Withdrawal Assessment (CIWA-Ar).

Each item graded 0 [not present] to 7 [most extreme]
1. Nausea and vomiting

2. Tremor

3. Paroxysmal Sweats

4. Anxiety

5. Agitation

6. Tactile disturbances

7. Auditory disturbances

8. Visual disturbances

9. Headaches, fullness in head

10. Orientation and clouding of sensorium alcoholism, cocaine, amphetamines, methamphetamines, stimulants, alcohol abuse, ampetamines, methamphetamine, how to make methamphetamine

Range: 0 to 67

<8: no medication needed

8 to 14: medication optional

15 to 20: must medicate

>20: impending DTs requires higher doses


2. Choose a cross-tolerant medication; orally effective drug. If using a short-acting drug, doses must be tapered to avoid

3. Adjust dose by monitoring Physical signs, and CIWA scale, not subjective complaints.

4. Titrate dose to avoid either intoxication or withdrawal.

B. Treatment of mild-to-moderate alcohol withdrawal (CIWA-Ar: 8 to 20)

1. Outpatient detoxification is possible for stable, compliant patients with no medical or psychiatric complications, and no concurrent abuse of other classes of drugs.

2. Long-acting benzodiazepines: The drugs of choice for most uncomplicated detox.

Provides slow, gradual detoxification (Mayo-Smith /ASAM, JAMA 2002). Drugs will self-taper if initial doses are high enough: >60 mg diazepam or >300mg chlordiazepoxide over 24 - 36 hours. Chlordiazepoxide (Librium) 50 to 100 mg po q 6-8 hrs.; taper over 3 days. Diazepam (Valium) 10 to 20 mg po q 6-8 hrs.; taper over 3 days, if necessary.

3. Short-acting benzodiazepine: requires closer patient monitoring and a drug taper Lorazepam (Ativan) 2 to 4 mg po q 4 hrs; or 1-2 mg IM q 2 hrs. prn; taper x 3 days

C. Treatment of severe withdrawal (ClWA-Ar: over 20

1. Diazepam is best for severe DTs, because it is effective IV and its rapid action: Diazepam 10 mg IV; then repeat 5 mg IV every 5 minutes until calm but still awake.

2. Lorazepam for patients with moderate-to-severe liver disease, or taking Cimetidine or Ranitidine (H2 receptor antagonists), or elderly, confused, or seriously ill medical patients. A short-acting benzodiazepine gives physician more immediate control over the patient's medication status. Use Lorazepam 4 mg po q l hr, up to 10 to 12 mg or 1-2 mg IM q 4hr, taper over 3 days.

For DTs plus hepatic dysfunction: Lorazepam 1-2 mg IV q 5 min until calm but awake.

D. Avoid These Medications for Detoxification:

- Thorazine: can lower the seizure threshold.

- Beta-blockers (propranolol, atenolol): may mask DTs.

- Alpha-adrenergic agonists (clonidine, lofexidine): may mask delirium tremens.


Pharmacotherapy of Alcohol Withdrawal
Three Components of Withdrawal Benzodiazepines

(all work)

Beta-blockers (Inderal) Alpha-2-adrenergic agonists (Clonidine)
Autonomic Nervous System Hyperactivity Yes Yes Yes
Neuronal Excitation (seizures) Yes No ?
Distorted Perceptions (hallucinations, delirium) Yes No ?


E. Valproic acid and newer anticonvulsants: Experimental detox protocols need more careful study to establish patient criteria, dose ranges, appropriate length of treatment and

F. Patients addicted to both alcohol & benzodiazepines: seizures are more likely; CBZ is an option for detoxification, IF liver function is adequate. However, protocols need

G. Supplemental Medication

1. Phenytoin (Dilantin)

- Needed only in patients with a history of grand real seizures unrelated to alcohol withdrawal.

- Give a loading dose (400 mg po q 4h x 3) followed by their routine daily dose (if off of reeds).

2. Haloperidol Marked agitation or belligerence: 3 to 5 mg IM; rarely need more than one dose.

3. Magnesium Sulfate - do not use unless magnesium levels are low and the patient develops cardiac arrhythmias or neurologic complications (seizures).

4. Treatment of Vitamin Deficiency (See Appendix I)

II. Medications in the Long-Term Management of Alcoholism

A. Avoid minor tranquilizers and/or lithium in primary alcoholics; there is no proof they reduce drinking.

B. Disulfiram (Antabuse) inhibits ethanol metabolism

1. Works best for stable, employed, well supervised patients. Does not increase continuous abstinence but reduces days drinking & medical problems (Fuller, '86). Never use without regular counseling.

a. Dose: 500 mg po QD x 10 days, then 250 or 125 mg po QD.

b. Side effects: drowsiness, headache, metallic taste, diminished libido/potency; all dose related. 

c. Do serial LFTs: q 2 weeks x 4, repeat every 3 to 6 months. 

d. Rx for an Antabuse reaction: Benadryl 50 mg IM or IV.

2. Problems in the use of Antabuse

a. Amitriptyline potentiates the dose of Antabuse; may need to lower Antabuse dose.

b. Antabuse can be metabolized to a neurotoxin, carbon disulfide. Only seen in doses >500 mg. One in 200 patients reported numbness in the legs; Effects of drinking are far worse.

c. Antabuse does not work in cirrhotics; risk of drug induced hepatitis is increased (Wicht, 2002).

d. Antabuse inhibits the metabolism of:

Imipramine and Desipramine; need to use lower doses.

Dilantin; use lower doses and get Dilantin blood levels to avoid toxicity.

Diazepam and chlordiazepoxide; may need to use lower doses. Oxazepam and

Lorazepam are not affected since they are metabolized via glucuronide conjugation.

e. Antabuse-induced hepatitis: stop drug immediately; follow Liver Function Tests.

f. May exacerbate psychosis; it inhibits dopamine beta-hydroxylase, increases CNS Dopram. Use lower dose (125 mg) along with high potency dopamine blocking agent such as Haldol.

C. Naltrexone (ReVia), Reduces the frequency of serious relapse. It binds to mu opiate receptors and reduces alcohol craving and euphoria. (Volpicelli, 1992 & 1995, & O'Malley, 2002).

a. Dosing: 50 mg QD; Give with meals or antacids to reduce nausea.

b. Minimal side effects: nausea (10%), headache (7%), dizziness (4%), anxiety (4%).

c. Reversible hepatotoxicity at doses over 100rag daily, can be used safely with antidepressants.

d. Works best with highly compliant patients who complain of craving (Volpicelli, 2002). A positive response will be apparent within 7 to 10 days; if no response by 10 days, discontinue the drug.

e. do not prescribe with Antabuse (both are potentially hepatotoxic)

D. Fluoxetine, reduced daily drinking in non-depressed problem drinkers (Naranjo, '90); and reduced craving in some alcoholics (Tempesta, '91); effect lasts for only 1 week (Gorelick, '92). In recent trials, effect of SSRIs at 12 weeks was no better than placebo in reducing alcohol consumption (Naranjo, '94). Has no long term effect in preventing relapse (Kranzler, Am J Psychiatry 152:391-397, 1995).

E. Acamprosate (calcium acetyl homotaurinate): Approved in 12 countries to reduce drinking. Is being submitted for FDA approval. Mechanism of action is unknown, but alters both GABA and glutamate (NMDA) systems, and reduces craving and relapse. Alcohol + Acamprosate increases inhibitory effect on NMDA receptor. Causes no tolerance, withdrawal, sedation, or potentiation of alcohol. Has no serious side effects (Sass, 2002).

F. Nalmefene: New opioid antagonist, no hepatotoxicity and longer-acting than naltrexone; prevented relapse to heavy drinking in alcoholics (Mason, B J, ARCH GEN PSYCH 56:719-724, 2002).

III. Treatment of Anxiety Disorders in Alcoholics

Do not diagnose or treat unless symptoms last 2 to 4 weeks following detox (DSM-IV), and/or there is positive family history for anxiety disorders (Osser, 2002; Greist, 1986; Sellers, 2002).

A. Generalized Anxiety Disorder

1. GAD + Depression: Nefazodone or an SSRI

2. GAD, not depressed: Cognitive Behavior Therapy (CBT) or Relaxation Therapy. If no response, Buspirone, slowly build up to 60 mg QD (Kranzler, 1994).

3.Ninety percent GAD patients are co-morbid for Panic Disorder, PTSD, Social Phobia or OCD: if these conditions are present, treat as described below, for the co-morbid condition.

B. Panic Disorder

1. CBT + Nefazodone or SSRI

2. If no response: Altemative SSRI or Venlafaxine

C. Social Phobia

1. Specific type: CBT + beta-blocker (propranolol)

2. Generalized + depression: CBT + SSRI

3. Generalized, not depressed: Nefazodone or SSRI

D. PTSD: (Co-morbid alcoholism & PTSD are very difficult to treat and require specialized treatment units) 1. PTSD + depression: Nefazodone or SSRI; if no response, alternative SSRI 2. PTSD + related psychosis: atypical antipsychotics

3. PTSD + insomnia: Trazodone; if no response, sedating tricyclic

E. OCD: SSRI; if no response Clomipramine (if no seizures)

F. Attention deficit hyperactivity disorder (ADHD):

Triad: 1) inattention & distractibility, 2) impulsivity, 3) motoric hyperactivity

Incidence: 25% to 30% in adults with any Psychoactive Substance Abuse Disorder (Wilens '94)

Treatment: 

1) Methylphenidate (Ritalin) gradually increase dose up to 10 mg to 20 mg po TID

2) Desipramine; monitor blood levels (Wilens, 2002).

3) bupropion (Wellbutrin) 100 mg po TID (Wender, 1990).

If no other disease is present - assume the anxiety is a symptom of prolonged alcohol withdrawal. Symptoms can last for up to 12 months. Management: Supportive psychotherapy & CBT. Do not prescribe minor tranquilizers. However, the risk of benzodiazepine abuse in sober alcoholics with comorbid anxiety disorders is low and does not preclude benzodiazepine use in carefully selected cases (Uueller, J Clin Psychiatry 57(2):83-89, 2002).

IV. Pharmacologic Treatment of Depression in Alcoholics

Dysphoria and depression in alcoholics may continue for months or years after detox. Tools for differential diagnosis are inadequate and treatments are inadequate (Renner & Ciraulo, 1994). There are few reliable guidelines for the use of medication in the depressed alcoholic. Liskow and Goodwin (1987) reviewed the literature on the treatment of depression in alcoholics and felt that all of the studies had serious methodologic deficiencies. Except in manic depressive patients, it is not clear that treating dysphoric or depressive symptoms will alter drinking.

A. Serotonin reuptake inhibitors - CSF of alcoholics has lower 5-HIAA. Paroxetine may be the preferred SSRI for alcoholics, but well controlled comparative studies are lacking. Cornelius (2002) reported reduced drinking and depression in severely depressed alcoholics given fluoxetine. Supplemental Trazodone 25 mg QHS can be added if the patient complains of insomnia.

B. Nefazodone: efficacy is comparable to TCAs & SSRIs, but it has fewer side effects than TCAs, compliance is better, and it is less likely to interact with alcohol. Is very effective for depressed, anxious __ alcoholics, and helps normalize sleep pattems (Lader, J Clin Psychiatry 57(2):39-44, 2002). If patient  has a history of liver disease, monitor liver function tests.

C. Tricyclic antidepressants - no good controlled studies exist; alcoholics given 150 mg Imipramine had significantly lower blood levels and BDI scores got WORSE, as compared to controls given no meds. Lower plasma levels of Desipramine and Imipramine, lasting at least five weeks, have been documented in recently detoxified alcoholics. These TCA s are metabolized mainly by the hepatic microsomal drug oxidation system; this system is induced in chronic alcoholism. Desipramine clearance is less effected, suggesting this is the preferred TCA for use in depressed lcoholics (Ciraulo, 1988, Mason, 1991). In cirrhosis, the metabolism of TCA s is inhibited. Lower doses may be adequate in such cases, though plasma levels should always be monitored.

D. Bipolar disorder: BP h Lithium; BP Ih Valproic Acid

Brady, K.T., J Clin Psychiatry, 56:118-121, 1995.

V. Treatment of Dependence on Benzodiazepines and Other CNS Depressants

Benzodiazepines, barbiturates and other sedative/hypnotics are all cross tolerant medications and produce similar symptoms of intoxication, dependence, and withdrawal. All of these drugs inhibit CNS arousal by facilitating GABA binding to receptors and thus opening chloride ion channels.

A. Sedative/Hypnotic Overdoses

1. Benzodiazepines: Ipecac, (if alert); assisted respiration / 02. For acute overdoses in non-addicted patients: Flumazenil (Mazlcon) 0.2 mg IV per min; do not use in combination with tricyclics; it may cause seizures.

2. Barbiturates: activated charcoal or hemoperfusion

B. Benzodiazepine Discontinuation Syndromes

1. Return of original symptoms (may last indefinitely, or be recurrent)

2. Rebound (temporary intensification of original symptoms)

3. Benzodiazepine withdrawal symptoms (time limited)

C. Withdrawal of CNS Depressants: Onset and duration of withdrawal symptoms are related to dose, the length of consumption and the duration of action of the specific drug.

Withdrawal Short-Acting Barbiturates (secobarb, pentobarb, meprobamate) Long-Acting Barbiturates (phenobarb, benzodiazepines)
Onset 4 - 6 Hours 1 - 3 Days
Peak 1 - 5 Days 5 - 7 Days
Duration 3 - 15 Days 5- 20 Days
Seizures ++++ 11

 

Minor signs and symptoms: anxiety, postural faintness (orthostatic hypotension), profuse sweating, coarse rhythmic intention tremor, insomnia, anorexia, vomiting, muscular twitches.

Major signs and symptoms: Seizures of the clonic tonic grand mal type are the most common. Psychosis though less common are more variable, ranging from a DTs like syndrome (disorientation, agitation, tremor, delusions and hallucinations) to syndromes that may look like schizophrenia, because of a clear sensorium, or like Korsakoffs psychosis.

D. Benzodiazepine detoxification options: (Outpatient detox should be done VERY slowly).

1. Gradual taper of the primary sedative drug. Taper benzodiazepines more rapidly for 1st 50% of dose; slowly for each successive 25%. For short acting benzos, taper more slowly.

2. Clonazepam taper for persons addicted to short-acting benzodiazepines.

3. Transfer to a short-acting barbiturate (Pentobarbital) - See Appendix III

4. Transfer to a long-acting barbiturate (Phenobarbital) - See Appendix III

5. Experimental Benzo Detox with Valproic Acid: Substitute equivalent dose of chlordiazepoxide for other benzos; then taper over 3 to 5 days. Initiate Valproic Acid on day 1, increase to therapeutic level by day 3 (check levels); continue outpatient taper over 5-6 weeks (Apelt, 1990).

E. Special Problems with alprazolam (Xanax)

1. Seizures, delirium, severe anxiety, and paranoid reactions have been reported, even when the drug is withdrawn slowly (Bleich, 1987).

2. Xanax is not completely cross-tolerant with other benzos. It has at least one CNS receptor site that is not shared with any of the other benzos, except Clonazepam. Other benzodiazepines will not adequately "cover" Xanax withdrawal, causing a significant risk of seizures.

3. Options for Xanax Detoxification

• Gradually taper the Xanax; preferred for patients with history of anxiety disorder (Klein, 1994).

• Cover each mg Xanax with 0.6 mg Clonazepam; continue 1-3 weeks; taper not required.

• Add Buspirone 5 mg tid, two weeks before starting to taper Xanax. Taper Xanax 2-8 weeks; continue Buspirone alone another 2 weeks. (Udelman, 1990)

• Carbamazepine 400-800 mg daily; CBZ plus Xanax for 3 days, then CBZ alone, tapered over 3 weeks. (Ries, 1989); can be risky choice because of hepatoxicity.

F. For patients addicted to both narcotics and CNS depressants, withdraw the DEPRESSANT FIRST while holding on a stable methadone dose; then withdraw on methadone. Clonazepam can be used to detox methadone patients from alprazolam and other benzodiazepines. (Wilens, 1993)

G. Trazodone (100 mg TID) eliminated all withdrawal symptoms during a four week benzo taper for benzodiazepine addicts, and also controlled anxiety during a 1-year follow-up (Ansseau, 1993).

VI. Management of Stimulant Abuse

A. Acute Cocaine Intoxication

1. May require life support: ventilation with airway & 02; lethal doses can be metabolized in 60 min.

2. Cardiac arrhythmias treated with calcium-channel blocker: Nitrendepine

3. Acute anxiety or panic: Diazepam po (5-10 mg); IV for seizures (5 mg/min)

4. Acute paranoia or manic-like states: Haldol 5 mg po BID (Haldol is a dopamine antagonist) (Differential Diagnosis: Cocaine, Amphetamine, or PCP intoxication vs. Mania)

B. Acute Cocaine Withdrawal (Crashing)

1. Withdrawal requires no specific treatment, but suicide can be a significant risk.

2. Initial agitation is followed by severe depression with tremors, muscle aches, and excessive sleep.

3. Depression clears in a few days; antidepressants not necessary and could aggravate cardiac arrhythmias due to acute cocaine intoxication.

C. Long-Term Management of Stimulant Abuse/Dependence

1. Abstinence from ALL drugs, including alcohol

2. CBT & Relapse Prevention (Sandberg & Marlatt, 1991)

3. Self-Help groups: A.A., N.A., Cocaine Anonymous

4. Combined alcohol & cocaine abuse: Antabuse reduces use of both drugs (Carroll, 1993)

5. Acupuncture

D. Pharmacotherapy of Stimulant Abuse (Kosten, 2002)

1. Drugs that enhance CNS catecholamine function may reduce Acute Craving: Amantadine, Bromocriptine, and Pergolide Mesylate have all failed to demonstrate efficacy in double blind placebo controlled clinical trials.

2. Drugs tried to date for primary Chronic Cocaine Abuse: Carbamazepine, Desipramine, Imipramine, Fluoxetine, Maprotiline, & Trazodone: No convincing evidence for efficacy.

3. Lithium, if there is a history of bi-polar disease. There is no evidence that it is of benefit to cocaine users with no history of mood swings (Gawin & Kleber, 1984.)

4. Methylphenidate, if there is co-morbid Attention Deficit Hyperactivity Disorder (Levin, 2002) NOTE: methylphenidate may stimulate cocaine use in cocaine addicts with no ADHD.

5. Buprenorphine -"some" reduction in cocaine use in opiate addicts treated in buprenorphine maintenance trials.

E. Methamphetamine Abuse (Ice, Speed, Crystal, Crank): Powdered "meth" is cooked to make a crystal that is smoked for a cheap, very potent instant hi.qh, lasting 6 to 24 hrs. Is highly addictive and can produce brain damage. Treatment is similar to cocaine intoxication and withdrawal.

VII. Treatment of Opiate Abuse and Dependence

A. Opiate Overdose

1. Signs: Coma, pinpoint pupils, depressed pulse and respirations

2. Treatment: Naloxone (Narcan) 0.4 mg (1 mL) IV, can be repeated at 4 minute intervals, PRN.

3. If patient does not respond, initiate treatment for a sedative/hypnotic overdose.

4. N.B. If patient has overdosed on Methadone, he or she may initially respond to Narcan and then lapse back into a coma after leaving the EW. Such patients must be monitored for 24 hours.

B. Opiate Withdrawal

1. Mechanism of opiate withdrawal: supersensitivity of NE receptors in the Locus Coeruleus. Withdrawal from narcotics is not a life threatening situation but can be extremely dysphoric; the addict may increase his manipulation to secure drugs, therefore:

- More credence should be placed in signs than symptoms

- Establish base-line vital signs; track signs carefully

- Obtain urine drug screen to verify current use

2. Signs and symptoms of opiate withdrawal:

Signs: lacrimation, rhinorrhea, yawning, perspiration, dilated pupils, increased respirations; then at the peak of withdrawal: goose-flesh, vomiting, diarrhea, tachycardia, increased blood pressure, tremor, muscle spasms, and kicking movements.

Symptoms: increasing irritability, insomnia, anorexia, feeling restless, weakness, depression, abdominal cramps, cramping in legs and back, nausea, and chills.

 

Comparison Between: Heroin Methadone
Onset of Withdrawal Symptoms 12-14 hours 24-48 hours
Peak Withdrawal Symptoms 36-72 hours 6 days
Duration of Acute Withdrawal 7-10 days 10-14 days


C. Opiate Detoxification

1. Methadone

a. Unless exact narcotic dose is known, initial dose of 20 mg meth. should not be exceeded. Begin after documenting withdrawal signs. Repeat dose in 2 hours if withdrawal signs increase.

b. Titrate dose to avoid intoxication or withdrawal.

c. Federal regulations permit a 180 day outpatient detox, if addict cannot handle a 30 day detox.

d. Inpatient Detox: Can usually be accomplished in 10 to 14 days (see Clonidine section below).

2. Clonidine an alpha-2-adrenergic agonist that suppresses firing of the Locus Coeruleus. (Lofexidine, which is approved in England for opiate detox, causes much less hypotension & sedation)

a. Methadone Maintenance Patient: Reduce methadone gradually to 20 mg/day; then initiate Clonidine 0.2 to 0.3 mg TID. Can be tapered over 10 days, or less, inpatient).

b. Street Heroin or Demerol: Clonidine 5 mcg/kg/day x 5 days, then decrease 0.2 to 0.4 mg/day. In outpatient treatment, don't exceed 0.3 mg TID.

c. Side Effects: Hypotension and sedation; monitor BP before each dose and hold dose for BP <90/60. May get Clonidine withdrawal symptoms if use extends beyond 2 weeks.

d. Clonidine may not suppress all subjective withdrawal symptoms.

3. Clonidine & Naloxone (IV) for 4 days, then continue on naltrexone (experimental)

4. Ultra Rapid Detox (URD): Opiate antagonist detox under anesthesia; no good follow-up data. (O'Connor, JAMA 279:229-234, 2002)

5. Buprenorphine ( 3 to 6 days, s.l., s.c., or IM) better results than clonidine (Experimental)

D. Opiate Substitution Therapy

1. Methadone Maintenance: 60 to 120 mg daily

2. LAAM (levo-alpha-acetylmethadol): can be dosed 2 or 3 times/week; no take homes permitted

3. Buprenorphine (partial opiate agonist): 8 to 20 mg/day; dose can last 48 hours; no risk of overdose; patients feel "normal," with no sense of opiate effect.

F. Methadone: Drug-Drug Interactions

1. Drugs that raise methadone levels: Ketoconazole, Fluconazole, Amitriptyline, Luvox, Diazepam, Halcion, Alprazolam, and Tagamet

2. Drugs that Lower Methadone Levels: Tegretol, dilantin (use valproic acid), Viramune (for HIV), INH Rifampin, and Vitamin C in large doses

3. Methadone raises potency of AZT by 50% (therefore reduce dose of AZT by 50%)

4. Alcohol initially increases methadone levels, chronic use decreases methadone levels.

5. Protease Inhibitors (ritonavir & indinavir) MAY decrease methadone levels

E. Improving Results in Opiate Substitution Therapy

1. Use adequate doses.

2. Provide skilled psychotherapists (Woody, '95) and good ancillary services.

3. Give patients more control, especially regarding doses.

4. Reward clean urines quickly and frequently; don't wait 90 days for "rewards."

5. Long-term/indefinite maintenance, especially for older addicts; don't push detoxification. (Caplehom, 1994)

F. Managing Dual Diagnosis Patients (Nunes, 1994):

1. Affective Disorders (lifetime incidence: males 11.4%, females 27.5%)

Doxepin has been shown effective in depressed maintenance patients. (Woody, 1975) Desipramine (175 mg QD) can be used in depressed methadone pts who also abuse cocaine. Lower doses can be used, because methadone may induce higher serum levels. (Manny, 1989) Depressed maintenance patient are at high risk for relapse if detoxified (Kanof, 1993) Nefazodone & SSE's appear to be effective in depressed methadone patients, but well-controlled studies are lacking.

2. Anxiety Disorders; (lifetime incidence: males 6.1%, females 10.7%) Imipramine & CBT ( also see Section III. Treatment of Anxiety Disorders in Alcoholics); try Clonazepam if no response to antidepressants.

3. Watch these patients carefully for concurrent alcohol & cocaine abuse. Antabuse may be helpful in methadone patients who abuse both alcohol and cocaine.

G. Naltrexone: (Narcotic Antagonist) 50 mg PO daily. Works best in motivated, married, employed patients who had a late onset of opiate use, and were never on maintenance treatment (Lemer, 2002).

VIII. Nicotine Dependence

A. Nicotine Inhaler: reduces daily nicotine by 70%, with no tar and no carbon monoxide

B. Bupropion (Zyban) 150 mg POx 3 days, then 150 mg PO BID for7 to 12 weeks

C. Also recommended: behavioral therapy, support groups, exercise, hypnosis, buspirone, nicotine gum, patches, antidepressants and anorectics (APA Practice Guideline, AM J Psychiatry (153): 2002).

D. Smoking cessation predicts depression in those with persistent withdrawal and prior depression history (Covey, 2002). Nortriptyline + CPT effective for depressed smokers wanting to quit (Hall, 2002).

Appendix I: - Management of Medical Problems in the Alcoholic

A. Treatment of vitamin deficiencies (continue vitamins for two months after detoxification).

1. Thiamine (Vitamin B-l) 100mg IU on admission then 100mg po BID for long-term treatment, give printed instructions.

2. Pyridoxine (Vitamin B-6), 500-100mg po BID.

3. B-complex vitamins with folic acid. (Folate 100 mg po QD)

B. Treatment of Korsakoff's disease (Alcohol amnestic syndrome). Use of a Serotonin Uptake inhibitor such as Fluvoxamine has been reported to be helpful {Martin, 1989)

C. Treatment of alcoholic liver disease

1. Propylthiouracil (PTU) 300mg QD reduced deaths 50% in alcoholics who continued moderate drinking despite liver disease (Orrego, H., NEJM, Dec. 12, 1987.)

2. Colchicine l mg 5 day/week doubled 5 year survival in Cirrhosis; interferes with scar tissue.

D. Treatment of alcohol-induced coma (Jeffery, DB. Lancet 1:308, 1980). Naloxone (Narcan) reversed coma in 10 rain. in 20 of 100 patients, using up to 1.2 mg.

E. Pain Management in Alcoholics: avoid the use of acetaminophen. Tylenol has caused fatal hepatic damage when used in large doses after heavy drinking.

Appendix I1: - Management of Insomnia

A. May last for months after detoxification: Do not treat with any sedative-hypnotics. Encourage good sleep habits, support patient while waiting for sleep patterns to return to normal.

B. If available, consider L-tryptophan, 3 gm po qhs; give 30 rain before sleep. Dose can be reduced if effective. A four-day-on, three-day-off schedule is recommended.

C. Zolpidem, an imidazopyridine (short-acting non-benzodiazepine hypnotic); use 10 mg po qhs.

Appendix Ill: - Techniques for Barbiturate Detoxification

A. Use of Short-Acting Barbiturates

Short-acting barbiturates may be given every hour, 100mg po, if possible, IU if required, until the patient is mildly intoxicated and showing no signs of withdrawal. Once mildly intoxicated, sufficient barbiturate is given every 2 hours to maintain this state. The amount required over 6 hours may be multiplied by 4 and the total used as the daily dose. This dose should be divided so that it may be administered every 4 to 6 hours. Once stabilized, begin slow detoxification by 100rag a day. If withdrawal occurs, dose should be held constant until signs are stabilized and then reduced 50mg/day.

B. Use of Long-Acting Barbiturates

The patient is first stabilized on a short-acting barbiturate, as described above. Once the stabilization dose is determined, the patient is then switched to phenobarb 30 mg according to the following schedule of equivalent doses: 

1. Secobarbital, 100 mg.

2. Pentobarbital, 100 mg.

3. Diazepam, 10 mg.

4. Chlordiazepoxide, 25 mg.

5. Meprobamate, 40 0mg.

Phenobarbital is then reduced 30 mg/day.

Appendix IV: Hallucinogens

A. Hallucinogens (Marijuana / LSD / Mescaline)

1.Bad trips (problems more likely in naive, inexperienced users)

a. Acute panic, fear, hallucinations

b. Psychotic-like reactions (with amphetamines or hallucinogens)

c. Delirium; disorientation, impaired cognition, combativeness (occurs with hallucinogens, anticholinergics, antihistamines)

2. Treatment: quiet, friends, reassurance, Diazepam

B. Phencyclidine (PCP)

1.Diagnosis: (R/O in any psychotic young person-serum & Urine analysis)

a. Effects: 1-5 mg » disinhibition; 5-15 mg » toxic psychosis, violence, paranoia;150mg » coma and death

b. Acute Physical Findings: Nystagmus, pin point pupils, ataxia and slurred speech

2. Treatment of PCP

a. Acute Intoxication: isolate, reduce external stimuli

b. Convulsions: Diazepam 5 to 10 mg IV

Do not give Phenothiazines, they may potentiate PCP and lower the seizure threshold.

c. Acute Psychosis: Lorazepam 2 to 3rag IM; if no response, try Haldol.

d. Persistent Psychosis: If patient has not responded to high dose Haldol, try 4 to 12 bilateral ECT.

Appendix V: - Clinical Problems in Methadone Maintenance Patients

A. Hospitalized Patients on Methadone Maintenance

1. Methadone can be continued until patient is discharged back to outpatient maintenance.

2. If patient is N.P.O., give 1/3 daily oral dose, IM BID. (60 mg po QD = 20 mg IM BID).

3. Hospitalized street addicts can be continued on Methadone until their medical or surgical problems are resolved. They should then be detoxed or transferred to a Methadone Clinic.

B. Management of Tuberculosis: INH & Rifampin increase the metabolism of methadone; may need to increase methadone dose for maintenance patients with tuberculosis.

C. Pain Management (JAMA 278:592-593, 2002)

1. OST patients are tolerant to analgesic effect of methadone and do experience acute & chronic pain.

2. They may require more frequent dosing with standard narcotics to control pain due to medical or surgical conditions, in addition to their daily methadone or LAAM dose.

3. Do not change or increase a Methadone Maintenance dose in a hospitalized addict in response to complaints of physical pain.

4. A single methadone dose controls withdrawal symptoms for 24 hours. The analgesic effect of methadone lasts only 6 or 8 hours; a single daily dose is inadequate for 

D. Anticonvulsant Medication in Methadone Maintenance Patients

1. Dilantin and Tegretol both induce hepatic enzymes leading to rapid metabolism of methadone and poor control of withdrawal symptoms.

2. Switch to valproic acid, a non-enzyme inducing anticonvulsant. Seizures are well controlled and patient will be comfortable on a lower dose of methadone. (Saxon, 1989)

Appendix VI: Alternative Alcohol Detoxification Protocols:

1. Symptom-triggered dosing: Diazepam 20 mg po or Chlordiazepoxide every 1-2 hrs while CIWA-Ar exceeds 10-15.

2. Front-loading: diazepam 20 mg po q 2hrs., up to 60 mg.; no taper needed.

3. Carbamazepine (CBZ) 200 mg po QID x 7 days - useful if patient has a history of seizures and/or medical complications (Malcolm '89). Patients are less sedated and have less memory impairment than with benzodiazepines. Do not use in patients with severe liver damage; CBZ can cause hepatocellular damage. Do not use in pregnant women; CBZ is teratogenic. Monitor CBC, platelets, & liver function tests on days 1, 3, and 6. Stop when CIWA drops <9; Do not use beyond 7 days. CBZ needs more evaluation to establish optimal dose ranges for detoxification.

4. Combination therapy: Lorazepam plus Clonidine (Clonidine 0.6 mg/day in 2 or 4 divided doses) permits faster withdrawal, with better control of autonomic nervous system symptoms.

5. Acupuncture (Renaud, J., Addiction and Recovery