Identifying Withdrawal and Understanding Detoxification

Transcription

1 SECSAT-APRN Southeastern Consortium for Substance Abuse Training - Advanced Practice Registered Nurses Identifying Withdrawal and Understanding Detoxification Deborah Finnell, DNS, PMHNP-BC, CARN-AP, FAAN Susanne A. Fogger, DNP, CRNP, PMHNP-BC, FAAN Southeastern Consortium for Substance Abuse Training Advanced Practice Registered Nurses Funded by Grant 1U79T Substance Abuse and Mental Health Services Administration (SAMHSA) Last revised: May 15, 2014 Funded by: Funded by:

2 Key Contributors & SECSAT APRN Site Coordinators Mercer University, School of Medicine J. Paul Seale, MD Principal Investigator Annie Biers, LPC, Project Coordinator Sylvia Shellenberger, PhD Mercer University, Georgia Baptist College of Nursing Dr. Frieda Fuller Dr. Laura K. Baraona Armstrong Atlantic University Dr. Anita Nivens Dr. Linda Tuck Emory University, Nell Hodgson Woodson School of Nursing Dr. Carolyn Clevenger Dr. Ursula Kelly Dr. Phyllis Wright University of North Georgia Dr. Sharon Chalmers South University Dr. Doris Parrish Johns Hopkins University Dr. Christine Savage Dr. Deborah Finnell Georgia College & State University Dr. Deborah MacMillan Dr. Sallie Coke University of Alabama, Birmingham Dr. Susanne Fogger

3 Learning Objectives At the end of the session, you will be able to Understand basic physiological underpinnings for alcohol and other major drug withdrawal syndromes. Articulate assessment data to collect in assessing patients for potential withdrawal syndrome Identify substance-specific tools used in evaluating withdrawal severity. Recognize various levels of referral sources for detoxification. 3

4 The Toxicity of Drugs Gable, R. S. (2006). The toxicity of recreational drugs. American Scientist,94(3),

5 Cautionary Concerns Withdrawal from CNS depressants (alcohol, benzodiazepines & barbiturates) can be life threatening. Death has occurred in unsupervised withdrawal following uncontrolled seizures Withdrawal from opiates, cocaine, marijuana can range from minor to significant discomfort including risk for suicide. 5

6 Withdrawal Alcohol, Sedatives, Stimulants, Opiates 6

7 Processing of Alcohol Alcohol is metabolized by oxidation; that is, electrons are lost in the process. This results in oxidative stress. Alcohol acetaldehyde acetate 7

8 How is Alcohol Absorbed? First-pass Portal vein Second-pass Excreted in urine, bile, breath, perspiration 96% distributed in body fluid 4% diffused into body fat 8

9 Pharmacokinetics 10% - 20% of alcohol is absorbed in the stomach 80% - 90% of alcohol absorbed in the small intestine, especially the duodenum Absorption is considered to be complete 90 minutes after the end of a drinking period 9

10 Blood Alcohol Concentration Consequences 0.02 to 0.04% Lightheadedness - Relaxation; sensation of warmth, high; minor impairment of judgment 0.05 to 0.07% Euphoric - Relaxation, decreased inhibitions, minor impairment of reasoning and memory, exaggerated emotions (positive and negative) 0.08 to 0.10% Legally impaired Euphoria, fatigue, impairment in balance, speech, vision, reaction time and hearing, judgment and self-control are impaired 0.11 to 0.15% Intoxicated Reduced and depressive effects (anxiety, depression or unease) more pronounced, gross motor impairment, judgment and perception severely impaired Source: 10

11 Blood Alcohol Concentration Consequences 0.16 to 0.19% Highly intoxicated Strong state of depression, nausea, disorientation, dizziness, increased motor impairment, blurred vision, judgment further impaired 0.20 to 0.24% Dazed and confused Gross disorientation to time and place, increased nausea and vomiting, may need assistance to stand/walk, impervious to pain, blackout likely to 0.30% Stupor All mental, physical and sensory functions are severely impaired, accidents very likely, little comprehension, may pass out suddenly 0.31% and higher Coma Level of surgical amnesia, onset of coma, possibility of acute alcohol poisoning, death due to respiratory arrest is likely in 50% of those drinking at this level Source: 11

12 Alcohol Tolerance People with little tolerance to alcohol tend to be more sensitive (less tolerant) to the acute and rebound effects of alcohol consumption. Other people may be able to tolerate a higher BAC. These individuals develop other types of tolerance: Metabolic (liver) Functional (cellular, tissue, brain) Neuroadaptation occurs with repeated intermittent alcohol use (i.e., sensitization) and with continued exposure (i.e., tolerance). Alcohol Adaptation 12

13 Alcohol Withdrawal (severity is related to amount and duration of use) Major Systems Affected Corticotropinreleasing factor Glutamate Gamma aminobutyric acid (GABA) Dopamine Norepinephrine Impact Hypofunction of neuronal GABA receptors Central Nervous System excitation Increased peripheral release of adrenaline (epinephrine) Adrenergic hyperactivity Hyperactivity of l-glutamaterelated neurotransmission Delirium 13

14 Alcohol/Sedative Withdrawal Clinical Institute Withdrawal Assessment Score seizures stage 3 delirium tremens long acting benzodiazepines stage 2: hallucinations stage Time in Days 14

15 Risk for Alcohol Withdrawal Syndrome (AWS) Heavy drinking for 8 years or more Alcohol intake is greater than 100 grams (1 standard drink=14 grams of pure alcohol) Has experienced withdrawal symptoms when abstinent Hepatic cirrhosis Lab abnormalities 2 or more abnormal biomarkers: GGT, AST, ALT, MCV 15

16 Urgent Attention for CNS Depressant Withdrawal Heightened deep tendon reflexes and ankle clonus indicates profound CNS irritability Significant increases/decreases in BP and HR Changes in mental status Hallucinations Abdominal pain Changes in responsiveness of pupils Temperature greater than F Suicidal ideation 16

17 Clinical Institute Withdrawal Assessment, revised (CIWA-Ar) Agitation Anxiety Auditory disturbances Clouding of sensorium Headache Nausea/vomiting Paroxysmal sweats Tactile disturbances Tremor Visual disturbances Sullivan, J. T., Sykora, K., Schneiderman, J., Naranjo, C. A., & Sellers, E. M. (1989). Assessment of alcohol withdrawal: The revised Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA Ar). British Journal of Addiction, 84(11),

18 Score: 8-10 (mild), usually some nausea, anxiety and headache (moderate) marked autonomic activity > 15 (severe) impending delirium tremens and urgency of pharmacological treatment 18

19 Stimulants Act primarily to increase synaptic dopamine by inhibition of dopamine reuptake or an increase in release. Stimulate hypothalamus-pituitary axis (HPA) activity. Elevate adrenocortiotropin hormone (ACTH) and cortisosteroid levels. Corticotropin releasing factor (CRF) activity is increased, explaining the anxiogenic and stress-like consequences of withdrawal. Kreek, M. J., Levran, O., Reed, B., Schlussman, S. D., Zhou, Y., & Butelman, E. R. (2012). Opiate addiction and cocaine addiction: Underlying molecular neurobiology and genetics. The Journal of Clinical Investigation, 122(10),

20 Stimulant Withdrawal (severity and profile is related to dosage and duration of use) Major Systems Affected Depletion of presynaptic monamine stores Down-regulation of receptors Dopaminergic and serotonergic axon damage (neurotoxicity) Impact Disturbed sleep (hypersomnolence to insomnia) Depressed mood Anxiety Agitation Reduced energy Vivid or unpleasant dreams 20

21 Stimulant Withdrawal systolic and diastolic blood pressure heart rate respiratory rate body temperature pupilary dilation heightened alertness motor activity appetite Fatigue Depression Anxiety Poor concentration Paranoia Irritability Hypersomnia or insomnia 21

22 Opiates Active metabolites of heroin and prescription opioids act primarily as mu opioid receptor agonists relieving of GABAergic inhibition of dopaminergic neurons release of dopamine rewarding effects Adrenocortiotropin hormone (ACTH) and cortisol levels are disrupted in individuals actively using opiates Corticotropin releasing factor (CRF) activity is increased, explaining the anxiogenic and stress-like consequences of withdrawal. Kreek, M. J., Levran, O., Reed, B., Schlussman, S. D., Zhou, Y., & Butelman, E. R. (2012). Opiate addiction and cocaine addiction: Underlying molecular neurobiology and genetics. The Journal of Clinical Investigation, 122(10),

23 Vital Signs Rapid pulse Opiate Withdrawal Elevated blood pressure Increase body temperature Increased respiratory rate ENT Dilated pupils Tearing of eyes Runny nose Anxiety Skin Sweating Gooseflesh Reflexes GI Heightened response Abdominal cramping Nausea and vomiting Diarrhea Bone and muscle Pain: Flu-like symptoms Spasms 23

24 Opiate Withdrawal (intensity is a function of the severity of physical dependence on opioids and the relative occupancy of the mu opiate receptor) Major Systems Affected Impact Hyperactivity in the locus coeruleus (provides the majority of noradrenergic input to the CNS) Stress Anxiety Gastrointestinal discomfort Pain Arousal Scavone, J. L., Sterling, R. C., & Van Bockstaele, E. J. (2013). Cannabinoid and opioid interactions: Implications for opiate dependence and withdrawal. Neuroscience,248,

25 Clinical Opiate Withdrawal Scale (COWS) Pulse rate Sweating Restlessness Pupil size Bone or joint aches Runny nose or tearing GI upset Tremor Yawning Anxiety or irritability Gooseflesh skin Wesson, D. R., & Ling, W. (2003). The clinical opiate withdrawal scale (COWS). Journal of Psychoactive Drugs, 35(2),

26 Score: 5-12 (mild) (moderate) (moderately severe) < 36 (severe) 26

27 Detoxification Set of interventions aimed at managing acute intoxication and withdrawal. Denotes a clearing of toxins from the body. Seeks to minimize the physical harm caused by the abuse of substances. Is not a substitute for treatment and rehabilitation but is required to begin the process. Center for Substance Abuse Treatment (2006). Detoxification and Substance Abuse Treatment. Treatment Improvement Protocol (TIP) Series 45. DHHS Publication No. (SMA) Rockville, MD: SAMHSA. 27

28 Levels of Care Level Treatment Setting 1. Outpatient treatment Outpatient care Methadone maintenance 2. Intensive outpatient or partial hospitalization 3. Medically monitored intensive inpatient treatment 4. Medically managed intensive inpatient treatment Intensive outpatient program Medical subacute hospital Chemical dependency program Psychiatric hospital Medical acute-care hospital Emergency room / department American Society of Addiction Medicine. (2013). The ASAM criteria : Treatment criteria for addictive, substance-related, and co-occurring conditions. Chevy Chase, MD: American Society of Addiction Medicine. 28

29 Inpatient Detoxification Where Offered Advantages Disadvantages Acute care hospitals Psychiatric hospitals Medically managed residential treatment centers Provides protected setting where access to substances of abuse is restricted. Intensive level of care that can provide close observation for serious withdrawal symptoms and ability to rapidly adjust treatment protocol. Expense Variability in care depending on number of appropriately credentialed personnel, implementation of evidence-based protocols. 29

30 Outpatient Detoxification Where Offered Advantages Disadvantages Emergency Departments Intensive Outpatient Programs Methadone Maintenance / Buprenorphine Clinics Office-Based Clinics Less expensive than inpatient treatment Patient s life is not as disrupted as during inpatient treatment Patient does not have abrupt transition from protected inpatient setting to the home / work settings. Available access to substances of abuse Less ability than inpatient to quickly adjust detoxification regimen 30

31 Take Home Points Assessment of withdrawal symptoms is critical for providing timely and appropriate treatment. Evidence-based measures can be feasibly administered in practice settings the symptoms and severity of alcohol- and opiate-related withdrawal. The severity of withdrawal symptoms is key for informing referral to treatment for detoxification. 31

32 QUESTIONS? 32