Evaluation and Management of Substance Use Disorders on the Inpatient Psychiatric Unit
Christine E. Yodelis-Flores
W. R. Murray Bennett
Jason P. Veitengruber
Richard K. Ries
The need to evaluate, diagnose, and manage substance use disorders (SUDs) in patients admitted to a psychiatric unit has become increasingly common for the inpatient psychiatrist over the last decade. Frequently, the attending psychiatrist will find half or more of his or her inpatient service to have ongoing or past substance use issues that may profoundly impact diagnosis, treatment, and discharge planning. The complex challenges that patients with SUDs or co-occurring disorders present might engender feelings of apprehension, helplessness, or therapeutic nihilism on the part of a psychiatrist not experienced in treating addictive disorders. The clinician may be unclear about how to assess and treat addiction, a chronic disorder that severely affects the course and prognosis of mental illness. Clinicians unprepared to treat addictive disorders may feel the temptation to avoid treating the patient, referring the individual to another treatment program, or alternatively making treatment demands that the individual cannot achieve. By not having a clear understanding of addiction and minimizing its impact on mental illness, or by not knowing the impact of mental illness on the course of addiction, the psychiatrist risks treatment failure and recidivism. On the other hand, with practical clinical approaches better outcomes are possible and rewarding for both the patient and the clinician. In this chapter, after defining the problem and its prevalence, the authors will primarily focus on the practical management of substance use and co-occurring disorders. They will provide a framework to proceed in the complex task of evaluation and treatment, as well as delineate the role of medications, inpatient staff, group therapies, and self-help groups commonly used in co-occurring treatment units to assist the clinician in the daunting task at hand.
Epidemiology
PREVALENCE OF CO-OCCURRING DISORDERS IN GENERAL POPULATIONS
According to Diagnostic and Statistic Manual of Mental Disorders, Fourth Edition (DSM-IV), substance-related disorders are divided into two groups: SUDs (abuse and dependence) and substance-induced disorders. The co-occurrence of a SUD with another psychiatric disorder is often referred to as dual diagnosis or co-occurring disorder. The term may also refer to substance-induced psychiatric disorders that occur in the context of substance abuse or dependence.
Several epidemiologic surveys have been done in the general population, looking at lifetime and 12-month prevalence rates of comorbid disorders: the Epidemiologic Catchment Area (ECA) survey;1 the National Comorbidity Survey (NCS);2 and the National Epidemiological Survey on Alcohol and Related Conditions (NESARC).3 Results from the ECA study found a lifetime prevalence rate of 29% for an addictive disorder in patients with mental disorders and a 61% lifetime prevalence rate for SUDs in those diagnosed with bipolar I. Conversely, those diagnosed with an alcohol disorder had a 37%
lifetime prevalence of mental disorders, and among those diagnosed with an addictive disorder other than alcoholism, 53% had a comorbid mental disorder. Among those diagnosed with schizophrenia there is a 34% prevalence rate of alcohol use disorders, and in those with bipolar disorder the prevalence rate is 46%. Of the individuals with affective disorder, the ECA study reported 32% also had a comorbid SUD.
lifetime prevalence of mental disorders, and among those diagnosed with an addictive disorder other than alcoholism, 53% had a comorbid mental disorder. Among those diagnosed with schizophrenia there is a 34% prevalence rate of alcohol use disorders, and in those with bipolar disorder the prevalence rate is 46%. Of the individuals with affective disorder, the ECA study reported 32% also had a comorbid SUD.
TABLE 15.1 TWELVE-MONTH PREVALENCE OF DIAGNOSTIC AND STATISTICAL MANUAL OF MENTAL DISORDERS (DSM-IV) INDEPENDENT MOOD AND ANXIETY DISORDERS AMONG RESPONDENTS WITH A 12-MONTH SUBSTANCE USE DISORDER (SUD) | ||||||||||||||||||||||||||||||||||||||||||
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According to results from the NESARC, the 12-month prevalence of SUD, alcohol use disorder, and drug use disorder in the general population is 9.35%, 8.46%, and 2.0%. The 12-month prevalence of SUD among those diagnosed with a mood disorder is 20%. Among those with anxiety disorders 15% have a SUD4 (see Tables 15.1 and 15.2). The association of personality disorders and SUDs is also significant: the NESARC data report that among individuals with a personality disorder 16.4% reported a current alcohol use disorder and 6.5% had a drug use disorder. Conversely, among those with a current alcohol use disorder 28.6% had at least one personality disorder, and among those with a drug use disorder, 47.7% had a personality disorder.5
TABLE 15.2 TWELVE-MONTH PREVALENCE OF DIAGNOSTIC AND STATISTIC MANUAL (DSM-IV) SUBSTANCE USE DISORDERS AMONG RESPONDENTS WITH A 12-MONTH DSM-IV INDEPENDENT MOOD DISORDER | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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TABLE 15.3 PREVALENCE OF ACTIVE SUBSTANCE USE DISORDERS IN INPATIENT PSYCHIATRIC STUDIES | ||||||||||||||||
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PREVALENCE OF POLYSUBSTANCE DEPENDENCE
Results from the NESARC show an overwhelmingly positive correlation between alcohol use and drug use disorders. Persons with alcohol dependence have a 13%, 12-month prevalence of any drug use disorder. Those with cocaine dependence have an 89% prevalence of alcohol use disorder, and among those with opioid dependence the prevalence of alcohol use disorder is 74%. Among individuals with cannabis dependence and amphetamine dependence, the prevalence of alcohol use disorder is 68% and 78%, respectively.6
PREVALENCE OF SUBSTANCE USE DISORDERS IN INPATIENT PSYCHIATRIC POPULATIONS
Substance use worsens the course and complicates the treatment of mental illness. In patients with severe mental illness, substance use is associated with higher rates of medication noncompliance and increased relapse and readmission rates.7,8 It is linked to self-harm and suicide,9 poor health and self-care,10 increased episodes of violence and victimization,11,12 incarceration,13 and homelessness.14 Substance use can both cause and exacerbate mental illness, and it is associated with impulsivity and poor judgment.
For the reasons mentioned in the preceding text, it is no surprise that various inpatient psychiatric populations have a higher rate of concurrent SUDs than outpatient populations reported in surveys. Various studies report that 30% to 66% of psychiatric inpatients have an active SUD (see Table 15.3).
Diagnostic Considerations
The relationship between psychiatric illness and substance use is complex. Psychoactive drugs and alcohol both produce and exacerbate psychiatric symptoms through several pharmacologic mechanisms. Symptoms associated with acute and chronic intoxication and withdrawal may overlap with symptoms of psychiatric and cognitive disorders. Substance use also exacerbates coexisting psychiatric disorders, often being the primary reason for decompensation as well as causing psychosocial consequences that
contribute to the worsening of the psychiatric illness. Substance-induced psychiatric disorders may be misdiagnosed as primary depression, anxiety disorders, psychosis, and personality disorders. In diagnosing a co-occurring psychiatric disorder in a person with an active SUD, the physicians must often assign a provisional diagnosis and delay a more definitive diagnosis until a period of abstinence has been obtained. This is increasingly difficult to do in an inpatient setting as inpatient stays are becoming less frequent and of shorter duration. The length of abstinence necessary for diagnosis depends on the substance of abuse and the psychiatric diagnosis being assessed. To diagnose a substance-induced psychiatric disorder, DSM-IV criteria specify that the psychiatric symptoms arise within 1 month of substance intoxication or withdrawal. A co-occurring disorder rather than a substance-induced disorder is probable if the symptoms have been present during abstinence, if they are persistent despite the cessation of acute withdrawal or intoxication, or if symptoms are substantially in excess of what would be expected, given the amount and type of substance used.
contribute to the worsening of the psychiatric illness. Substance-induced psychiatric disorders may be misdiagnosed as primary depression, anxiety disorders, psychosis, and personality disorders. In diagnosing a co-occurring psychiatric disorder in a person with an active SUD, the physicians must often assign a provisional diagnosis and delay a more definitive diagnosis until a period of abstinence has been obtained. This is increasingly difficult to do in an inpatient setting as inpatient stays are becoming less frequent and of shorter duration. The length of abstinence necessary for diagnosis depends on the substance of abuse and the psychiatric diagnosis being assessed. To diagnose a substance-induced psychiatric disorder, DSM-IV criteria specify that the psychiatric symptoms arise within 1 month of substance intoxication or withdrawal. A co-occurring disorder rather than a substance-induced disorder is probable if the symptoms have been present during abstinence, if they are persistent despite the cessation of acute withdrawal or intoxication, or if symptoms are substantially in excess of what would be expected, given the amount and type of substance used.
Despite the high rates of dual diagnosis in the psychiatric inpatient populations, SUDs are frequently underdiagnosed.15,16 Treatment of addictive disorders may be ignored or mismanaged, in part because of the patients’ underreporting of substance use and denial or minimization, clinicians’ inexperience with dual diagnosis, low rates of reimbursement by insurance companies for treatment of substance-induced disorders, or the program’s lack of resources for appropriate treatment.
Clinical Model for Treatment
In the following section, division of the clinical model for treatment into acute and subacute phases is designed to assist the clinician develop a practical approach to initial and subsequent steps in assessment, diagnosis, and treatment of dual disorders. This approach also serves to underscore the therapeutic process of developing a treatment alliance with dual diagnosis patients, beginning with the initial interview and building on that foundation in subsequent interviews through motivational techniques and behavioral interventions designed to facilitate a patient’s understanding and acceptance of the complex association of addiction and mental illness.
ACUTE PHASE MEDICAL STABILIZATION: DAYS 1 TO 2 OF HOSPITALIZATION
At this initial point, questions the clinician should be asking him/herself include: Is the patient intoxicated and/or in danger of acute, possibly life-threatening substance withdrawal? Is this condition medically or psychiatrically substance-related? Are there emergent conditions such as head injury, toxic encephalopathy, overdose, infections, cardiac, hepatic or renal failure, and thiamine deficiency that will necessitate acute medical stabilization?
Given the high degree of substance-associated psychiatric illness in the acute care setting, it is important during the initial psychiatric evaluation to also focus on a substance use history by asking direct and detailed questions in a respectful and nonjudgmental manner regarding the patient’s substance use. Several screening instruments, such as the CAGE questionnaire,17 Alcohol Use Disorders Identification Test (AUDIT),18 the TWEAK questions,19 and the Brief Michigan Alcoholism Screening Test (Brief MAST),20 are available to assess SUDs. In the authors’ experience, however, it is preferable to conduct a detailed substance use history, as the clinician can utilize this interview process to engage the client, develop rapport, and underscore the importance of evaluating and treating SUDs during inpatient psychiatric evaluation and treatment.
The clinician should ascertain specific information such as doses and types of substances used, duration and frequency of use, time of last use, and a history of withdrawal symptoms and previous substance abuse treatment. This detailed questioning is important to determine the need for acute medical stabilization and detoxification as well as to determine if the psychiatric disorder is substance related. Of course, minimization, evasion, or denial may be present to some degree, and indeed is common not only in those with primary SUDs, but also in those with psychiatric disorders uncomplicated by substance use. The authors’ experience in an acute psychiatric inpatient service of an urban public hospital is that patients will often initially underreport or avoid discussions of addictive disorders, but they estimate that perhaps only 5% or 10% of psychiatric
patients with addictive disorders will deny their existence and refuse to participate in dual diagnosis treatment.
patients with addictive disorders will deny their existence and refuse to participate in dual diagnosis treatment.
CAGE Questionnaire
Have you ever:
1. Felt you should Cut down on your drinking?
2. Felt Annoyed by criticism of your drinking?
3. Felt bad or Guilty about your drinking?
4. Taken a drink in the morning (Eye-opener) to steady your nerves or get rid of a hangover?
(Reprinted with permission from Ewing JA. Detecting alcoholism. The CAGE questionnaire. JAMA 1984;252[14]:1905-1907. Copyright © 1984, American Medical Association. All rights reserved.)
“Dual CAGE” Questions
Have you ever:
1. Cut down (or stopped) Because mental symptoms worsened? Because mental health doctor or therapist suggested?
2. Felt Annoyed when your drug/alcohol use was discussed? Felt Annoyed, anxious or angry, or had fights when using? Been Admitted to emergency room (ER) or hospital for psychiatric problems, when using or not? ADHD as a child?
3. Felt Guilty about use? Felt Guilty, depressed, suicidal when using or not? Ever made a suicide attempt when using or not?
4. Taken an eye-opener drink or drug in the morning to feel better? Taken a drink or drug to blot out symptoms? Taken drink or drug with psychiatric medications? Not taken medications because of using drug/alcohol (forgot, avoid mixing, etc.)?
What are 2 or 3 reasons you use alcohol/drugs?
What are 2 or 3 reasons you might want to stop or cut down?
Case Vignette
Ms. S was admitted to the psychiatric unit for symptoms of depression and suicide attempt. She denied a drug or alcohol use disorder; however, she admitted that she had been drinking the night of her suicide attempt. The clinician provided education about depression and added information about the disinhibiting effects of alcohol and the dangers of drinking when depressed or suicidal. She asked Ms. S to attend the dual diagnosis therapy group to explore this issue, and although initially reluctant Ms. S agreed to do so.
Most patients become willing and even enthusiastic participants in dual diagnosis treatment if the addictive disorder in importance is elevated to the level of the psychiatric disorder in the authors’
subsequent discussions with the patient. To minimize denial, it is helpful to utilize an empathetic, respectful, and nonjudgmental style to engage the client, such as is demonstrated in the dialogue in Table 15.4.
subsequent discussions with the patient. To minimize denial, it is helpful to utilize an empathetic, respectful, and nonjudgmental style to engage the client, such as is demonstrated in the dialogue in Table 15.4.
TABLE 15.4 PATIENT ADMITTED FOR DEPRESSION AND SUICIDAL BEHAVIOR: CAGE STYLE INTERVIEW | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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A medical history and physical examination, as well as a review of symptoms, should be done, focusing on possible substance-related medical conditions such as recent falls or injuries; neurologic problems such as visual and balance difficulties, blackouts, seizures, and memory difficulties; infections and skin wounds or tracks; cardiac diseases such as cardiomyopathy, hypertension, or endocarditis; and liver and gastrointestinal problems such as hepatitis, ulcers, or pancreatitis. Laboratory tests include a urine toxicology screen, blood alcohol level, liver function tests, complete blood count (CBC), and comprehensive chemistry panel. If neuropsychological symptoms are present, a head computed tomography (CT) should be performed. As a rule, if alcohol abuse or dependence is suspected, patients should receive thiamine 50 mg IM or PO immediately and orally for the subsequent 3 days in addition to multivitamins as alcoholics are at risk for thiamine deficiency, which may lead to Wernicke disease and the Wernicke-Korsakoff syndrome.
Acute Phase: Detoxification
Management of polydrug detoxification is a common problem, and this potential should be determined during the initial evaluation of SUDs. Particularly difficult is a combined sedative-hypnotic, alcohol, and opioid withdrawal. In these cases, the substance that could potentially cause the most medically severe withdrawal sequelae (alcohol or sedative-hypnotic) should take precedence, and the clinician should focus primarily on managing that withdrawal rather than withdrawal from opiates.
Case Vignette
Mr. T was admitted for suicidal ideation in the context of heroin dependence and difficulty tolerating the symptoms of withdrawal. When questioned about the amount and types of substances used, he admitted to frequent heavy alcohol, cocaine, and benzodiazepine use to enhance his opiate “highs” and mitigate withdrawal effects. Because of concerns about alcohol and benzodiazepine withdrawal, the clinician decided against using buprenorphine for opiate detoxification and instead initiated an alcohol/benzodiazepine withdrawal protocol using chlordiazepoxide with a clonidine withdrawal protocol added when signs of opiate withdrawal emerged. After inpatient day 3, the patient was tolerating detoxification, but was still using an average of 300 mg of chlordiazepoxide daily and 0.2 mg of clonidine t.i.d. At this point it was decided to discontinue the protocols and begin a 3-day taper of chlordiazepoxide and continue the clonidine at 0.2 mg t.i.d. for an additional 2 days before tapering by 0.2 mg per day. On day 7, after discontinuing chlordiazepoxide, the patient endorsed worsening anxiety, restlessness, and insomnia as well as muscle twitching. Symptoms were managed by addition of gabapentin 300 mg t.i.d. and trazodone 50 mg at bedtime. By discharge on day 10, Mr. T denied withdrawal symptoms and was preparing to enter a residential addiction treatment program. He was instructed to continue gabapentin for an additional 2 weeks before tapering over a third week and to continue the trazodone as needed for insomnia over the subsequent month.
Alcohol
Alcohol withdrawal may occur after a heavy drinker stops or reduces the amount of alcohol intake. Symptoms of alcohol withdrawal include signs of autonomic hyperactivity such as tachycardia, hypertension, fever, and sweating. Other signs are anxiety, insomnia, psychomotor agitation, nausea or vomiting, and tremor. Rarely, transient visual, tactile, or auditory hallucinations can occur as well as withdrawal-associated seizures. Symptoms of withdrawal usually peak around the second day and improve after day 5, although prolonged subclinical withdrawal syndromes may take months to resolve. Approximately 5% of alcohol-dependent patients will develop severe withdrawal consisting of seizures or alcohol-induced delirium, commonly known as delirium tremens.21 Alcohol detoxification is done on the psychiatric unit using protocols for alcohol withdrawal, which include administering the Clinical Institute Withdrawal Assessment for Alcohol Scale-Revised (CIWA-Ar)22 every 2 hours while awake and giving chlordiazepoxide 50 to 100 mg or lorazepam 1 to 2 mg for scores >8-9. Chlordiazepoxide is less reinforcing than lorazepam and longer acting; however, lorazepam is preferred for patients with significant liver dysfunction. For patients at risk for withdrawal seizures, anticonvulsants such as divalproex sodium, carbamazepine, or gabapentin can be used as adjunctive agents. Gabapentin can also be used in place of benzodiazepines for withdrawal, starting at 300 mg three times a day and increasing if necessary to up to 600 mg every 6 hours.23, 24, 25
Opiates
Clinical manifestations of acute opioid withdrawal are due to noradrenergic hyperactivity and rebound effects and include tachycardia, hypertension, fever, mydriasis, lacrimation, rhinorrhea, piloerection, perspiration, nausea, vomiting, diarrhea, abdominal cramping, myalgia, muscle spasms, restlessness, irritability, insomnia, craving, and yawning. Onset of withdrawal symptoms depends on the half-life of the substance: as short as 4 to 6 hours for heroin and up to 36 hours for methadone. Severity of withdrawal varies with dose and duration of use. Duration of the withdrawal syndrome is shortest with
short-acting agents: heroin withdrawal generally peaks at 36 to 72 hours and lasts 7 to 14 days, while methadone withdrawal syndromes last approximately 4 to 8 weeks. Protracted withdrawal syndromes persisting for up to 6 months have been reported. Management of opioid detoxification depends on underlying medical conditions such as hepatitis C, hepatic disease, and pregnancy. Opioid withdrawal during pregnancy can lead to fetal distress and premature labor, so methadone maintenance during pregnancy is the treatment of choice, and pregnant women should be referred to a local methadone maintenance program.
short-acting agents: heroin withdrawal generally peaks at 36 to 72 hours and lasts 7 to 14 days, while methadone withdrawal syndromes last approximately 4 to 8 weeks. Protracted withdrawal syndromes persisting for up to 6 months have been reported. Management of opioid detoxification depends on underlying medical conditions such as hepatitis C, hepatic disease, and pregnancy. Opioid withdrawal during pregnancy can lead to fetal distress and premature labor, so methadone maintenance during pregnancy is the treatment of choice, and pregnant women should be referred to a local methadone maintenance program.
It can be extraordinarily difficult to manage opiate withdrawal in patients hospitalized with co-occurring psychiatric illness, and patients may abruptly leave the inpatient unit against medical advice if the withdrawal syndrome is not managed appropriately. The most common pharmacologic therapies used to manage opiate withdrawal include opioid agonist substitution with taper and clonidine detoxification. In patients who are withdrawing from alcohol or sedative-hypnotics as well as opiates, caution must be taken to avoid adverse drug interactions such as excessive respiratory suppression due to combining protocols using opioid agonists and benzodiazepines. In these cases, the clinician must primarily focus on the alcohol or sedative-hypnotic withdrawal (which can be far more medically serious than opioid withdrawal) and avoid or limit opioid doses used. Clonidine detoxification would be preferred over an opioid detoxification to avoid respiratory suppression.
Opiate Agonist Substitution with Taper
The most common opioids used for detoxification include methadone and buprenorphine. To use buprenorphine in detoxification, physicians must complete an 8-hour training, or be certified in Addiction Medicine, or boarded in Addiction Psychiatry and apply to the Drug Enforcement Administration (DEA) through a Notification of Intent (NOI) to use buprenorphine for the treatment of opioid treatment or detoxification.
Methadone detoxification.
Inpatient methadone substitution and taper with patients who illicitly use drugs can be difficult, as knowledge of the exact dosage of heroin or other narcotic is not usually available. Patients may over- or underestimate their use, and the purity of street drugs is notoriously variable. The physician must guess at the initial methadone dosage. As little as 40 mg of methadone could be fatal to someone who is nontolerant to opiates. To ensure safety, it is important to start with a methadone dose of 10 to 20 mg, and closely observe the patient to assess the effects of the dose. If the initial dose does not suppress withdrawal symptoms within 1 hour, an additional dose of 5 to 10 mg methadone can be given. No greater than 30 mg of methadone should be given within the first 24 hours of detoxification unless there is documented evidence that the patient uses >40 mg of methadone equivalents per day. On day 2 of detoxification, the initial dosage used to stabilize a patient in withdrawal should be repeated. Subsequently, the dosage can be adjusted by 5 mg every 2 days if the patient is having continued symptoms of withdrawal. Blood levels will continue to rise on the same daily dose of methadone for the next 4 days. Once the patient is stabilized, the methadone dosage can be decreased by 5 mg per day until a zero dosage is achieved. This method of methadone tapering can take anywhere from 5 to 10 days.
Buprenorphine detoxification.
Buprenorphine is a partial μ-receptor agonist and antagonist approved by the U.S. Food and Drug Administration (FDA) in 2002 for detoxification and maintenance treatment of opioid dependence. Sublingual tablets are available both with and without naloxone added (Suboxone and Subutex). The addition of naloxone, a powerful opioid antagonist which is very poorly absorbed sublingually, is to reduce risks of buprenorphine abuse. Snorting or dissolving and injecting a crushed tablet containing naloxone will precipitate acute opiate withdrawal. In patients who are dependent on shorter-acting opioids, buprenorphine detoxification is effective, better tolerated, and safer than methadone detoxification on an inpatient unit.26 Because of the long half-life of methadone, however, it is much more difficult to use buprenorphine to detoxify methadone-dependent patients, and the authors do not recommend it for this purpose. Because of the partial agonist-antagonist effects, a precipitated opiate withdrawal syndrome can occur if buprenorphine is given to the patient before he or she is in clear opiate withdrawal. Therefore, the key to successful buprenorphine detoxification lies in waiting a sufficient time until mild to moderate symptoms of opiate withdrawal
are documented (usually 12 to 24 hours after the last dose of heroin). At that time, an initial 4 mg dose of buprenorphine is administered sublingually. If the patient is still in opiate withdrawal 2 hours after the buprenorphine is given, an additional 4 mg of sublingual buprenorphine can be administered. The following days the patient can be given 4 mg, 8 mg, or 12 mg sublingually to relieve withdrawal symptoms, and then on subsequent days the dose can be reduced by 2 to 4 mg per day until zero dosage is achieved. A buprenorphine detoxification taper usually takes from 3 to 7 days. The use of benzodiazepines is a relative contraindication in those being detoxified from opiates with buprenorphine, as there have been several reports of adverse events such as accidental overdose in those on this combination.27,28
are documented (usually 12 to 24 hours after the last dose of heroin). At that time, an initial 4 mg dose of buprenorphine is administered sublingually. If the patient is still in opiate withdrawal 2 hours after the buprenorphine is given, an additional 4 mg of sublingual buprenorphine can be administered. The following days the patient can be given 4 mg, 8 mg, or 12 mg sublingually to relieve withdrawal symptoms, and then on subsequent days the dose can be reduced by 2 to 4 mg per day until zero dosage is achieved. A buprenorphine detoxification taper usually takes from 3 to 7 days. The use of benzodiazepines is a relative contraindication in those being detoxified from opiates with buprenorphine, as there have been several reports of adverse events such as accidental overdose in those on this combination.27,28
Clonidine detoxification.
An α2 agonist and antihypertensive agent, clonidine ameliorates adrenergic-mediated symptoms by blocking activation of the locus ceruleus that shows increased activity during opioid withdrawal. It decreases opioid withdrawal symptoms; however, myalgias, craving, insomnia, and restlessness may still persist. The use of clonidine is limited by the hypotensive effects and it should be used with caution in patients with hypotension or on antihypertensive agents. Many inpatient psychiatric units have an opiate withdrawal protocol using clonidine. Inpatient detoxification can be accomplished with a 6- to 8-day scheduled clonidine taper, using 0.1 to 0.2 mg every 4 to 6 hours up to 1.0 mg total the first day and increasing as tolerated up to a maximum of 1.2 mg total in divided doses on days 2 to 4. For withdrawal from shorter-acting opiates, by day 5 clonidine can be tapered by 0.2 mg per day, to avoid hypertensive rebound, until zero dosage. For detoxification from longer-acting opiates such as methadone, clonidine should be maintained at a dose sufficient to ameliorate withdrawal symptoms for up to 5 additional days before a 0.2 mg per day taper. During detoxification, vital signs should be monitored before each dosing, and clonidine should be held for systolic blood pressures <100 mm Hg and diastolic readings <50 mm Hg.
Related posts:
The Ins and Outs of 200 Years of Psychiatric Hospitals in the United States
Psychosocial Approaches in Inpatient Psychiatry
Legal Issues in Inpatient Psychiatry
Psychiatric Education on the Inpatient Unit
Recurrently Readmitted Inpatient Psychiatric Patients: Characteristics and Care
The Patient with Borderline Personality Disorder
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