AHPCO Spring Conference 05/23/2014

Transcription

1 Psychotropic Drug Use: Documentation and Consent Lisa Cheney, R.N., B.S.N. Hospice R.N. Case Manager Hospice of the West Andrew Barrett, PharmD, BCPS Clinical Pharmacist HospiScript, a Catamaran Company Session Overview This session will explore psychotropic drug use in an end of life setting and provide insight into the regulations and best practices regarding documentation and consent. Participants will take away information and strategies for assisting patients and families as well as guidance on documentation Learning Objectives Analyze regulations for Psychotropic Consents Identify documentation techniques for use and monitoring effectiveness of prescribed psychotropic medications Describe common and severe adverse effects and expected benefits for psychotropic medications used regularly in hospice 1

2 State Regulations for Use of Psychotropic Medication Lisa Cheney, R.N., B.S.N. Hospice R.N. Case Manager Hospice of the West What is Regulation C Arizona Department of Health Services Informed consent must be obtained from the person and/or legal guardian for each psychotropic medication prescribed The comprehensive clinical record must include documentation of the essential elements for obtaining informed consent for medication which are contained within the PM Form English & Spanish forms are located on the AZ Department of Health Services website Informed Consent Arizona Department of Health Services Article 1 R Informed Consent means advising a patient of a proposed treatment, surgical procedure, psychotropic drug, or diagnostic procedure; alternatives to the treatment, surgical procedure, psychotropic drug, or diagnostic procedure; associated risks and possible complications; and obtaining documented authorization for the proposed treatment, surgical procedure, psychotropic drug, or diagnostic procedure from the patient or the patient s representative. 2

3 Documentation in Medical Record Arizona Department of Health Services -Article 6 R Medical Records C5. Documentation of general consent, and if applicable informed consent, for treatment by the patient or the patient s representative except in an emergency Implementation of the Rule State licensing surveyors will cite after April 1, 2014 What does this mean for your hospice agency? Informed Consent must be obtained for any psychotropic medication, regardless of the indication or frequency of medication administration. A new informed consent must be obtained for changes in dosage/frequency to existing psychotropic medication orders Documentation Techniques for Use and Effectiveness of Psychotropic Medications Lisa Cheney, R.N., B.S.N. Hospice R.N. Case Manager Hospice of the West 3

4 Use of Psychotropic Medications Psychotropic medication should be used within a coordinated interdisciplinary care plan with emphasis on improvement of quality of life. The psychotropic medication plan should be part of the plan of care. The entire interdisciplinary team should document input on use and effectiveness of each psychotropic medication. Documentation for Use of Psychotropic Medications Medical Record should include: Mental Health History Medical Rational for use of medication Duration of time for use of medication Non pharmacological use Attempts for gradual dose reductions Documentation Guidelines Long Term Use of Psychotropic Medications Initial date of start of treatment Target behaviors Abnormal involuntary movements Clinical reviews should be conducted & documented on routine intervals for example; at each recertification visit for hospice patients 4

5 Documentation Guidelines PRN Use of Psychotropic Medications plan of the worst, hope for the best Document frequency of use & effectiveness of use Discontinue for non use Psychotropic Drug Use: Clinical Pearls Andrew Barrett, PharmD, BCPS Clinical Pharmacist HospiScript, a Catamaran Company Disclosures Andrew Barrett does not have any conflicts of interest. Off-label use of medications will be discussed during this presentation. This presentation will not cover all psychotropic medications currently available. 5

6 Definitions Drug ( 201(g);21 U.S.C. 321(g)) Recognized in official compendia (USP, NF, HPUS) Used in diagnosis, cure, mitigation, treatment, or prevention of disease Intended to affect the structure or function of the body Psychotropic drug Also known as psychoactive drugs or psychopharmaceuticals Primarily acts upon central nervous system function Primarily intended to alter consciousness, cognition, mood, and/or behavior Types of Psychotropic Drugs Antipsychotics Antidepressants Anxiolytics Sedative-hypnotics Mood stabilizers Others (not included in this presentation) Stimulants Euphoriants Hallucinogens Analgesics Introduction Discussing what to expect is part of the informed consent process Identifying target symptoms Time for onset of effects Common and severe adverse effects General knowledge of how psychotropic drugs work can help you: Anticipate effects, both intended and adverse Focus discussion with patients and families 6

7 Introduction Most psychotropic drugs increase or decrease the effects of neurotransmitters and their targets Neurotransmitter Receptors Dopamine (DA) Serotonin (5HT) (5HT = 5-hydroxytryptamine) Norpepinephrine (NE) D 1,D 2, D 3, etc. 5HT 1,5HT 2, 5HT 3, etc. α, β Acetylcholine (ACh) M 1, M 2, M 3 Histamine (H) H 1, H 2, H 3 gamma-aminobutyric acid (GABA) GABA A, GABA B, GABA C Introduction Neurotransmitter Effectsif activity INCREASED Dopamine Mood, wakefulness, concentration Mania, psychosis Nausea/vomiting Serotonin Norepinephrine Acetylcholine Histamine GABA Mood Anxiety Insomnia, anorexia, nausea Mood, concentration, wakefulness Hypertension, sweating, anorexia Anxiety (short-term) cognition Cholinergic effects: salivation, urinary frequency, diarrhea, nausea/vomiting, bradycardia Itching, vasodilation, bronchoconstriction Wakefulness Nausea/vomiting Sedation, anxiety, anticonvulsant, muscle relaxation Introduction Neurotransmitter Effectsif activity DECREASED Dopamine Serotonin Norepinephrine Acetylcholine Histamine GABA Antipsychotic, antimanic Nausea/vomiting Extrapyramidal symptoms (EPS), tardive dyskinesia (TD) Antidepressant Sedation, weight gain Nausea/vomiting Anxiety Sedation Hypotension/orthostasis Nausea/vomiting Sedation Anticholinergic effects: Dry mouth, dry eyes, constipation,urinary retention, confusion, tachycardia, blurred vision Sedation, weight gain Nausea/vomiting and itching Stimulation, convulsions 7

8 Antipsychotic Agents Antipsychotics First generation antipsychotics (FGAs) A.K.A. typical or conventional antipsychotics Most common in hospice: Chlorpromazine (Thorazine ) Haloperidol (Haloperidol ) Second generation antipsychotics (SGAs) A.K.A. atypical antipsychotics Most common in hospice: Risperidone (Risperdal ) Quetiapine (Seroquel ) Olanzapine (Zyprexa ) Ziprasidone (Geodon ) Aripiprazole (Abilify ) Antipsychotics Psychosis ( Positivesymptoms ) Delusions Hallucinations Disorganized speech and behavior Agitation/aggression Negative symptoms Alogia(talks little) Affective flattening ( emotion) Asociality(socially withdrawn) Anhedonia ( pleasure) Avolition ( motivation) Target Symptoms Nausea/vomiting Mania Elevatedor irritable mood Self-esteem Agitation Risk taking Need for sleep Easily distracted More talkative Racing thoughts 8

9 Antipsychotics: Mechanisms of Action Receptor Effects Time to Onset (givenpo) Anti-D 2 Anti-5HT 2A Psychosis, mania Nausea/vomiting EPS, TD EPS and TD risk Negative symptoms Antipsychotic/antimanic: <1 week Antiemetic: min Negative symptoms: 4-6weeks or longer Antipsychotic (mostprominent) All antipsychotics (exceptaripiprazole) Especially haloperidol All SGAs Anti-H 1 Sedation Weight gain Nausea/vomiting Sedation/antiemetic: 30-60min Weight gain: 4-6 weeks Chlorpromazine Quetiapine Olanzapine Anti-M 1 Sedation Nausea/vomiting Anticholinergic effects Rapid (minutes to hours) Chlorpromazine Quetiapine Olanzapine Anti-α 1 Sedation Orthostatic hypotension Rapid (minutes to hours) Chlorpromazine Quetiapine Risperidone Antipsychotics: Comparison Drug Firstgeneration antipsychotics Sedation (H 1,M 1, α 1 ) Extrapyramidal Symptoms (D 2 ) Anticholinergic Effects (M 1 ) Orthostatic Hypotension (α 1 ) Chlorpromazine High Moderate Moderate Mod/High Haloperidol Low High Low Low Second generation antipsychotics Quetiapine Mod/High Very low Moderate Moderate Risperidone Low/Mod Low Very low Moderate Olanzapine Mod/High Low Moderate Moderate Ziprasidone Low/Mod Low Very low Low/Mod Aripiprazole Low Low Very low Very low Antipsychotics: EPS and TD Reaction Symptoms Period of Maximum Risk Acute dystonia Parkinsonism Akathisia Tardive dyskinesia Spasm of musclesof tongue, face, neck, back Bradykinesia Rigidity Tremor Shuffling gait Inner restlessness Unable to sit still Face/tongue movements Limb movements Management 1-5 days Benztropineor diphenhydramine (IM/IV preferred) 5-30 days (may persist) 5-60 days (commonly persists) Antiparkinsonagents Propranolol Dose or change drug Dose or change drug Benzodiazepines Antiparkinsonagents 6-24 months Discontinue drug Sometimes irreversible 9

10 Antipsychotic Agents: Clinical Pearls Use in elderly patients with dementia Boxed Warning in labeling for all antipsychotics 1.6- to 1.7-fold increase in mortality vs. placebo (4.5% vs. 2.6%) Most common causes of death Cardiovascular (e.g., heart failure, sudden cardiac death) Infectious (e.g. pneumonia) Recommendations: Assess and treat reversible causes Use nonpharmacologic interventions when possible Reserve antipsychotics for psychosis or agitation causing significant distress to patient or danger to self/others Start at low doses, titrate slowly Consider reducing or withdrawing antipsychotic periodically (e.g., every several weeks) Antipsychotic Agents: Clinical Pearls Other potential adverse effects: QTc interval prolongation: Ziprasidone Haloperidol (especially when given IV and at high doses) Chlorpromazine Metabolic abnormalities Weight gain, obesity, dyslipidemia, diabetes, cardiovascular disease Long-term complications associated mainly with SGAs Relative risks: High: olanzapine Moderate: quetiapine, risperidone Low: ziprasidone, aripiprazole Antidepressant Agents 10

11 Antidepressants: Introduction In general, antidepressants increase the effects of one or more of the following: Serotonin Norepinephrine Dopamine SelectiveSerotonin Reuptake Inhibitors (SSRIs) Fluoxetine (Prozac ) Paroxetine(Paxil ) Sertraline(Zoloft ) Citalopram(Celexa ) Escitalopram(Lexapro ) Vilazodone (Viibryd ) Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) Venalafaxine(Effexor ) Desvenlafaxine(Pristiq ) Duloxteine (Cymbalta ) Antidepressants: Introduction Tricyclic Antidepressants (TCAs) TertiaryAmines Amitriptyline (Elavil ) Imipramine (Tofranil ) Doxepin (Sinequan ) Secondary Amines Nortriptyline (Pamelor ) Desipramine (Norpramin ) Norepinephrine-Dopamine Reuptake Inhibitor (NDRI) Bupropion(Wellbutrin, others) Novel Antidepressants Trazodone (Desyrel ) Mirtazapine (Remeron ) Core symptoms Depressed mood (most of the day) Apathy/loss of interest Target Symptoms Additional symptoms Sleepdisturbances Weight changes Psychomotor agitation or slowing Fatigue Guilt/worthlessness/suicidal ideation Antidepressants: Comparison Class Mechanism(s)of Action IntendedEffects Side Effects SSRIs SNRIs TCAs BlocksSERT Blocks SERT + NET Mood Anxiety Same as SSRIs + Pain (esp. neuropathy) Blocks SERT + NET Same as SNRIs + GI: Nausea, diarrhea, weight loss or gain CNS: insomnia,sedation, agitation, headache, tremor Sexual dysfunction Same as SSRIs + Sweating,hypertension Usually less GI upset than SSRIs or SNRIs Anti-H 1 Itching, sedation Sedation, weight gain Anti-M 1 (3 amines > 2 amines) Anti-α 1 Sedation Sedation Sedation, anticholinergic effects Sedation, orthostatic hypotension, dizziness Anti-Na + channel (esp. overdose) -- Arrhythmias,seizures SERT: Serotonin transporter, NET: Norepinephrine transporter 11

12 Antidepressants: Comparison Drug Mechanism(s)of Action Intended Effects Adverse Effects NDRIs (Bupropion) Trazodone Mirtazapine Blocks NET + DAT Low doses(25-150mg/day): Anti-H 1, anti-5ht 2A, anti-α 1 High doses ( mg/day): Sameas low dose + blocks SERT Anti-α 2 (high doses > low doses) ( release of 5HT and NE) Anti-H 1, anti-5ht 2C (low doses > high doses) Mood Sedation (not effective antidepressant) Sedation + Mood, Anxiety Mood, Anxiety Sedation, weight gain GI: nausea,anorexia, weight loss CNS: insomnia, anxiety, dizziness Seizures (rare) Sedation Orthostasis Priapism(rare) Sedation Weight gain Dry mouth Dizziness SERT: Serotonin transporter, NET: Norepinephrine transporter, DAT: Dopamine transporter Antidepressants: Clinical Pearls Time to Onset of Effects: Antidepressant, antianxiety: 2-6 weeks for full effects Neuropathic pain (TCAs, SNRIs): 1-2 weeks Sedation (TCAs, trazodone, mirtazapine): Usually immediate Weight gain (mirtazapine): Usually by week 6 Side effects: Usually immediate Most GI and CNS adverse effects of SSRIs, SNRIs, and NDRIs improve with continued use No clear evidence of superiority of one class or medication over another May respond differently to medications in the same class Anxiolyticsand Sedative-Hypnotics 12

13 Anxiolytics Coresymptoms Fear (panic, phobia) Excessive worry Target Symptoms Additional symptoms Sleep disturbances Impairedconcentration Fatigue Hyperarousal Irritability Muscle tension Avoidance Significant overlap of symptoms in anxiety and depression Most antidepressants can effectively reduce anxiety symptoms Delayed onset of effects (2-6 weeks) Drug Alprazolam (Xanax ) Clonazepam (Klonopin ) Diazepam (Valium ) Lorazepam (Ativan ) Anxiolytics: Benzodiazepines Mechanism of Action Effects of GABA via GABA A receptor Onset of Action (given PO) Elimination Half-Life (hr) Active metabolites? Relative potency (mg) Fast No 0.5 Intermediate No Very Fast > 100 Yes 5 Intermediate No 1 Adverse Effects Sedation, cognitive impairment,ataxia, paradoxical reactions, respiratory depression Other Effects Anticonvulsant Musclerelaxation Anxiolytics: Miscellaneous Drug Buspirone(Buspar ) Mechanism of Action 5HT 1A partial agonist ( effects of 5HT) Time to Onset Adverse Effects 2-4 weeks CNS: dizziness, headache, sedation, excitement GI: Nausea Hydroxyzine (Atarax, Vistaril ) H 1 receptor antagonist Rapid (15-20minutes) Sedation Anticholinergic effects 13

14 Sedative-Hypnotics Sedative: Activity, excitement Produces calming effect Hypnotic: Produces drowsiness Facilitates onset and maintenance of sleep Decreasing level of consciousness Sedative-Hypnotics: Benzodiazepines Drug Alprazolam (Xanax ) Clonazepam (Klonopin ) Diazepam (Valium ) Lorazepam (Ativan ) Temazepam (Restoril ) Triazolam (Halcion ) Onset of Action (given PO) Elimination Half-Life(hr) Active metabolites? Relative potency (mg) Fast No 0.5 Intermediate No Very Fast > 100 Yes 5 Intermediate No 1 Slow No 5 Intermediate 2-5 No 0.1 Sedative-Hypnotics: Nonbenzodiazepines Drug Zolpidem (Ambien ) Eszopiclone (Lunesta ) Diphenhydramine (Benadryl ) Phenobarbital (Luminal ) Mechanism of Action Effects of GABA at GABA A receptors specific for sleep Onset of Action (given PO) Elimination Half-Life (hr) 30 min min 6 Anti-H 1 15 min 7-12 Effects of GABA at GABA A receptors 20-60min Adverse Effects Dizziness/ataxia Amnesia Nervousness Sleepwalking Bittertaste (eszopiclone) Daytime sedation Anticholinergic effects Impairedcoordination Paradoxical excitement Rash Respiratory depression High potential for drug interactions 14

15 Mood Stabilizers Mood Stabilizers Used to treat and prevent recurrences of mania and depression Most commonly used in treatment of bipolar disorder May also be used in treatment of: Dementia Personality disorders Brain injury Complex or unknown mechanisms of action Mood Stabilizers Mania Core symptoms Elevated mood Irritability Target Symptoms Depression Core symptoms Depressed mood (most of the day) Apathy/loss of interest Additional symptoms Self-esteem Agitation Risk taking Need for sleep Easily distracted More talkative Racing thoughts Additional symptoms Sleepdisturbances Weight changes Psychomotor agitation or slowing Fatigue Guilt/worthlessness Suicidalideation Most mood stabilizers will work primarily on either mania or depression symptoms Combinations of medications may be necessary 15

16 Mood Stabilizers Types of mood stabilizers Lithium (Eskalith, Lithobid ) Anticonvulsants Valproate(Depakene, Depakote ) Carbamazepine(Tegretol ) Lamotrigine (Lamictal ) Second-generation antipsychotics Most approved for treatment of mania Quetiapine also approved for treatment of bipolar depression Mood Stabilizers Drug PrimaryUse Time to Onset Adverse Effects Drug Monitoring Lithium Mania 1-3 weeks Valproate Mania Several days Lithium toxicity: tremor, ataxia, diarrhea, vomiting, sedation, arrhythmia Weight gain Diabetes insipidus Hypothyroidism CNS: Sedation, dizziness, ataxia GI: nausea, vomiting, abdominal pain, weight gain Alopecia Hepatotoxicityand pancreatitis (rare) Lithium levels Renal function Thyroid function High risk of drug-drug interactions Liver function CBC+ platelets Valproate levels Other Uses Treatment resistant depression (adjunct) Episodic rage, anger, violence Seizures Migraine prevention Mood Stabilizers Drug Primary Use Carbamazepine Mania Several weeks Time to Onset Adverse Effects Drug Monitoring CNS: sedation, dizziness, ataxia, confusion GI: nausea, vomiting, diarrhea Rash Leukopenia CBC Liver function Renal function Thyroid function High risk of drug-drug interactions Other Uses Seizures Neuropathic pain Lamotrigine Depression Several weeks to months Rash (most are benign) CNS: sedation, vision changes, dizziness,ataxia GI: nausea, vomiting, dyspepsia Stevens Johnson syndrome (rare) None required Seizures 16

17 Summary Psychotropic drugs are commonly used to manage a variety of end-of-life symptoms. Identifying target symptoms and usual onset of effects is important for establishing goals and expectations of drug therapy. Many psychotropic drugs affect the same neurotransmitters and their receptors. Common effects (beneficial or adverse) can often be predicted. References 1. APA Work Group on Alzheimer s Disease and other Dementias. American Psychiatric Association practice guideline for the treatment of patients with Alzheimer s disease and other dementias. Second edition. Am J Psychiatry 2007;164(12 Suppl): Brunton LB, LazoJS, Parker KL, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 11th ed. New York: McGraw-Hill; Koda-Kimble MA, Young LY, Alldredge BK, Corelli RL, GuglielmoBJ, KradjanWA, Williams BR, eds. Applied Therapeutics: The Clinical Use of Drugs. 9th ed. Baltimore, MD: Lippincott Williams & Wilkins; Lacy CF, Armstrong LL, Goldman MP, Lance LL, eds. Drug Information Handbook With International Trade Names Index. 20th ed. Hudson, OH: Lexi-Comp Inc.; Smith KM, Riche DM, HenyanNN, eds. Clinical Drug Data. 11th ed. New York: McGraw-Hill; Stahl, SM. Stahl s Essential Psychopharmacology: NeuroscientificBasis and Practical Applications. 4th ed. New York: Cambridge University Press; Stahl, SM. Stahl s Essential Psychopharmacology: the Prescriber s Guide. 4th ed. New York: Cambridge University Press;