NR 565 Week 4 Study Guide, Exams of Nursing

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NR 565 Week 4 Chapter 35: Chronic Migraine and Cluster Headache Chronic daily headache headaches 15 or more days a month for longer than 3 months e Chronic daily headaches (CDH) can be divided into five subtypes: o chronic tension-type headache o chronic migraine o hemicrania continua (Not in the study guide = not covered in depth) = rare disorder that responds completely to indomethacin and to nothing else. Indomethacin (Indocin) 75 to 150 mg is given daily; doses up to 200 mg daily may be needed. Referral to a neurologist is recommended. o medication-overuse headache o new daily persistent headache. e Use of drugs for acute headache treatment more than 9 days a month is associated with increased risk of chronic daily headaches. e Medication-overuse is addressed later Pathophysiology: Patho of CDH is often unclear and of mixed origin. e There is a clear difference between chronic migraine and hemicrania continua (Not in the study guide = not covered). ¢ The boundary between chronic tension-type headache and chronic migraine is less clear and may require a neurology referral for treatment. The term chronic migraine refers to CDH that starts as episodic migraine (less than 15 days a month) that transforms into a chronic pattern of greater than 15 days a month of migraine headache e It was formerly called “transformed migraine.” e The initial migraines have the pathogenesis of migraine discussed earlier. Chronic migraine is not well understood but is thought to be related to a combination of atypical pain processing, cortical hyperexcitability, neurologic inflammation, and central sensitization. e Risk factors for chronic migraine include female gender, history of head or neck injury, life stress, psychiatric disorders, and comorbid pain disorders Goals of Treatment The first goal of treatment for CDH is to break the pattern of daily headache. The patient is then stabilized on prophylactic or preventive therapy. Rational Drug Selection Chronic Migraine In most patients with chronic migraine, the daily headache cycle can be broken by using repeated doses of IV DHE (dihydroergotamine mesylate). e Approximately 70% to 80% of patients respond to DHE. o The patient is given a test dose of 0.33 mL of DHE (1 mg/mL solution) with 5 mg of metoclopramide or 10 mg of prochlorperazine (Compazine). o Followed by 0.5 mL of DHE and one of the anti-nausea medications every 6 hours for 48 to 72 hours. o This usually requires inpatient treatment. o DHE is contraindicated in coronary and peripheral vascular disease. Alternatives to DHE: ¢ Chlorpromazine (Thorazine) e Prochlorperazine. If the patient has medication-overuse headache due to misuse of analgesics, ergots, or combination medications, the patient has to be detoxified (Discussed later) Treatment of chronic migraine may require consultation with a neurologist. Preventive pharmacotherapy can be started after the headache cycle is broken. ¢ The patient usually responds to migraine-preventive medications such as propranolol, divalproex, or a tricyclic antidepressant. e Amitriptyline is a good choice if the patient is also depressed. ¢ The seizure medications topiramate or valproic acid may be used. e The patient is on preventive medication until the headache days are reduced by 50%, and then an additional 3 to 4 weeks, for a total of 6 to 12 weeks. The patient should also receive alternative therapy to treat CDH. Behavioral counseling, biofeedback therapy, relaxation therapy, physical exercise, and acupuncture are all valid alternative therapies for treatment of CDH. Monitoring Monitoring of patients with CDH who are on preventive therapy requires the patient to keep a diary of headache and medication use. e Patients’ blood pressure should be monitored if they are on a beta blocker e Liver function monitored if on divalproex, as per migraine therapy monitoring. e Ongoing monitoring of headache is necessary because 31% may have recurrence of headache in spite of preventive medication. Outcome Evaluation Patients with CDH are difficult to treat. Treatment success is determined by how effective it has been in breaking the cycle of daily headaches and how effective the preventive treatment is. The patient's headache diary is key in the evaluation of the success of treatment. Patient Education The acute attacks are severe and last only a short time-intervention must be fast-acting. The patient usually requires both acute and preventive medications to manage the headache. Acute Therapy ¢ Oxygen therapy administered via a 100% nonrebreather mask for 15 to 30 minutes often provides immediate relief of cluster headache. ¢ Sumatriptan, administered SC, or intranasal sumatriptan or zolmitriptan may provide relief of acute cluster headaches e Intranasal lidocaine is thought to be effective in treating cluster headache. o The patient lies supine, hyperextends the head at 45 degrees, and rotates it 30 degrees to the side of the headache. o The lidocaine nasal solution is then dripped into the nostril on the affected side over 30 seconds. o The onset is approximately 5 minutes. ¢ Ergotamine derivatives are also effective for acute cluster headaches. o Sublingual 2 mg tablets are administered at the beginning of the cluster headache. o Ergotamine suppositories or DHE intranasally or IM may also be used o Ergotamine may also be administered in a 2 mg dose given before bed if nocturnal attacks occur frequently. Preventive Therapy ¢ Verapamil can prevent cluster headaches in some patients. ¢ Calcium channel blockers are thought to prevent cluster headache by inhibiting vasospasm of the cerebral arteries. ¢ Cluster headaches appear to need dosing in the high range to achieve headache reduction. ¢ Divalproex can be effective in preventing cluster headaches. The dosing is the same as for migraine prophylaxis e Lithium appears to have some effect on cluster headaches in some patients, and a trial of lithium is warranted if the patient does not respond to other preventive medications. o The dose for cluster headache prevention is 300 mg daily to a maximum of 300 mg 3 times a day. o The patient needs careful monitoring for adverse effects, including electrocardiogram (ECG), electrolytes, thyroid function, creatinine, and CBC studies. Nonpharmacological therapies include avoidance of all alcohol during the clustering of headaches because alcohol often precipitates a headache. ¢ Patients often are able to drink alcohol between headache clusters without adverse effects. ¢ Tobacco, stress, anger, and vigorous physical activity should be avoided. ¢ The patient needs to maintain a normal sleep pattern, if possible. Cluster headaches do not appear to respond to self-care measures such as massage and relaxation. Monitoring Cluster headaches can be severely disabling, and the intense pain and loss of sleep can significantly affect the patient's quality of life. The health-care provider needs to monitor the patient for suicidal thoughts during the headache. The headache diary helps to monitor the effectiveness of acute and preventive medications. A patient treated with lithium requires careful monitoring of ECG and chemistries throughout treatment. Outcome Evaluation Cluster headaches by definition are self-limiting and will eventually stop, regardless of treatment. The focus of care is to provide measures that shorten or prevent cluster headaches during the cluster. Evaluation of the effectiveness of acute and preventive therapy is accomplished by self-report with a headache diary. Modifications in pharmacological management of cluster headaches should be based on the headache diary. Patient Education Include a discussion of information related to the overall treatment plan as well as that specific to the drug therapy, reasons for taking the drug, drugs as part of the total treatment plan, and adherence issues. Patient education information specific to treating cluster headaches should focus on the following principles: 1. Educating the family about cluster headache, particularly the fact that itis a benign condition, in spite of the severe pain experienced during attacks. 2. Self-management of acute medications. The headache is usually brief, and therefore the patient must be able to self-medicate to provide relief. The pain may be gone by the time the patient can get transportation to a medical clinic. 3. Avoidance of alcohol is crucial during clusters of headaches. = Hamilton Rating scale for Anxiety — helps identify but not symptoms that are physically based 2. Generalized Anxiety Disorder (GAD) = Commonly seen in primary care but overlooked and undertreated = Excessive worry occurring more days than not, that is difficult to control, associated with restlessness, difficulty concentrating, fatigue, irritability and sleep disturbances. = Differentiate from: Hypoglycemia, hyperglycemia, asthma, COPD, sleep apnea. 3. Obsessive Compulsive Disorder (OCD) = Often not diagnosed in primary care r/t shame and secrecy. = Yale-Brown Obsessive-Compulsive Scale (YBOCS) helps screen assess and measure = Refer to psychiatric provider (OCD — complex treatment) 4. Post-Traumatic Stress Disorder (PTSD) = Due to complex and different responses to exposure to stressful/traumatic situations- PTSD has been reclassified several times, now includes children and adolescents. = Other criteria: recurrent, involuntary and intrusive memories and nightmares, intense distress and physiological reactions to triggers, or cues from stressor. = Often not diagnosed in primary care- refer to psychiatric provider Key point= ALWAYS assess for presence of suicide ideation or the level of severity of risk. Neurobiology p. 899 Neurobiology of depression is evolving- classic theory deficiency of monoamines norepinephrine (NE), serotonin (5HT), and dopamine (DA). = corresponds with the current treatments, but little supporting data. = New more complex theory- involving neurotransmitter system regulates information processing in key areas of the brain correspond to symptoms of depression. = Another theory: dysregulation of brain circuits in different areas of the brain 0 Depression- dysfunction of amygdala and prefrontal cortex. oO Sleep and appetite- hypothalamus dysfunction oO Fatigue- NE and DA dysregulation in prefrontal cortex 0 Guilt, worthlessness, suicide- prefrontal cortex and amygdala = Continued genetic research: Brain-derived neurotropic factors (BDNF) and Vascular endothelial growth factor (VEGF) Neurobiology of Anxiety p. 900 Neurobiology for anxiety more complex and for each type. Worry is a core symptom = Worry and Obsession — dysfunction of cortico-striatal- thalamo-cortical (CSTC) loops in the brain. Specific dysfunction in these distinguish worry from panic and then from obsession. = GAD — dysfunction in circuits and amygdala are persistent = persistent worry. A repetitive loop may be involved in OCD Neurobiology of PTSD Neurobiology of PTSD is more complicated- dysfunction of the amygdala in interpretation of traumatic events and the hippocampus in the memory and re-experiencing of the events is also involved. = Malfunction of neurotransmitters (NT) that include monoamines as well as Gamma-aminobutyric acid (GABA), glutamate and other complex circuits involved in panic and phobias. NTs= GABA, glutamate, NE and 5HT- all involved in CSTC loops and information processing of the amygdala play roles in anxiety = more targeted medications for treatment. Evidence-Based Treatment of MDD and Anxiety Disorders (p. 900) National Institutes of Mental Health (NIMH) - study called Sequenced Treatment Alternatives to Relieve Depression (STAR*D) found that it is about 14 weeks on medication for remission of symptoms to be achieved. Those with remission had better outcomes. The American Psychiatric Association (APA) has clinical guidelines for treatment in adults of depression and anxiety. (Figure 29-1 and 29-2) General Algorithim for the Treatment of Depression Based on STAR’D Effectiveness Research 7 mental health p1 noncomp! chil potential, elderly patient, and for therapy. cultural issues, a ty [er] [ar —| General Algorithim for the Treatment of Adults With Anxiety Disorders isin] provider for therapy. substance comorbidities. Cognitive behavior therapy, exposure therapy, eye movement desensitization and reprocessing (EMDR) and short-term psychodynamic psychotherapy - found to be good therapies for adjuncts with depression and anxiety. Classes of Medication p. 901 = Nonselective norepinephrine-serotonin reuptake inhibitors (NNSRI) Vilazodone (Viibryd) - new antidepressant for MDD in adults. Serotonin partial agonist reuptake inhibitor (SPARI) 5HT, agonist - hypothesis is that it increases serotonin from several mechanisms. ¢ Little evidence for superiority with effectiveness within the drugs in this category. ¢ Toa significant degree SSRIs interact with many other drugs. ¢ Highly protein bound and INHIBIT CYP450 isoenzyme system = many potential drug interactions. e Patients benefit from a drug choice with fewer interactions if they are taking several other drugs. Table 29-2 CYP450 isoenzymes and potential drug interactions including grapefruit juice Isoenzyme | Substrates Inhibitors 1A2 Acetaminophen, caffeine, theophylline, Citalopram, fluoxetine, trimipramine, doxepin, clomipramine, fluvoxamine, amitriptyline, tacrine, propranolol, nefazodone, clozapine, trazodone, mirtazapine, fluoroquinolones, alprazolam grapefruit juice 2D6 Fluoxetine, sertraline, amitriptyline, Citalopram, fluoxetine, clomipramine, desipramine, imipramine, | fluvoxamine, nortriptyline, trimipramine, maprotiline, | paroxetine, sertraline, venlafaxine, nefazodone, trazodone, nefazodone, trazodone, paroxetine, bupropion, flurazepam venlafaxine, amitriptyline, Type I antiarrhythmics, clomipramine, dextromethorphan, oxycodone, codeine, | quinidine, fluphenazine, haloperidol, perphenazine, risperidone, | haloperidol, propranolol, alprenolol, timolol, perphenazine, metoprolol, indoramin, vilazodone methadone (Viibryd) 2C19 Citalopram, Citalopram, clomipramine, nortriptyline, | fluvoxamine, fluoxetine, desipramine, trimipramine, diazepam, paroxetine, sertraline, omeprazole, phenytoin, fluoxetine, venlafaxine, venlafaxine, phenelzine, vilazodone mirtazapine, (Viibryd) imipramine, tranylcypromine, diazepam, cimetidine, omeprazole 3A4 Loratadine, alprazolam, clonazepam, Fluvoxamine, diazepam, midazolam, triazolam, estazolam, flurazepam, carbamazepine, amitriptyline, imipramine, clomipramine, bupropion, nefazodone, sertraline, trazodone, venlafaxine, citalopram, calcium channel blockers, amiodarone, disopyramide, lidocaine, propafenone, quinidine, erythromycin, fluoxetine, paroxetine, sertraline, nefazodone, venlafaxine, mirtazapine, diltiazem, verapamil, clarithromycin, itraconazole, ketoconazole, acetaminophen, codeine, androgens, cimetidine, dexamethasone, estrogens dexamethasone, grapefruit juice SSRIs p.903 ¢ Commonly initial drug of choice for depression and anxiety e Equal efficacy to the nonspecific SNRIs with a safer and more tolerable SE profile ADRs: More common: dizziness, sexual dysfunction, nervousness, nausea, sleep disturbance and wt. changes. Serotonin Syndrome p. 903 Potentially life-threatening r/t excess serotonin agonist activity. Result of too rapid titration of medication, overdose, drug interaction, or ADR. More common than once thought Tramadol, Meperidine, St. John’s Wort and the OTCs dexomethorphan and decongestants often interact with SSRIs and cause Serotonin Syndrome. S/Sx: Diarrhea, diaphoresis -> can lead to mental status changes, autonomic dysfunction and neuromuscular abnormalities > death. e Treatment: discontinuing offending drug, supportive care, control of agitation and possible hospitalization Citalopram: 2011 FDA issued Drug Safety Communication- Doses no greater than 40mg/day due to possible dangerous electrical activity in the heart. ¢ Discourage in patients with prolonged QT intervals e 2012- FDA revised: precaution for those over 60 yoa 0 Periodic EKGs and electrolyte monitoring Discontinuation in patients found to have persistent QTc measurements greater than 500 ms. Limitation of the maximum recommended dose of citalopram to 20 mg per day for patients older than 60 years of age. e Patients with congenital long QT syndrome who are at particular risk of torsade de pointes, ventricular tachycardia, and sudden death when given drugs that prolong the QT interval has been changed from contraindicated to not recommended Discontinuation Syndrome p. 903 May occur when a patient takes an NNSRI or an SSRI for more than 5 weeks and the dose is sharply reduced or stopped suddenly. ¢ Symptoms include agitation, anxiety, balance problems, bad dreams, concentration issues, dizziness, diarrhea, nausea, vomiting, electric shock-like sensations and flu-like symptoms Can occur in up to 30% of patients anywhere from days to weeks after stopping or reducing the medication and is more common in medications with a shorter half-life. Gradual tapering may prevent discontinuation syndrome symptoms Fluoxetine has the lowest risk of causing these symptoms Discontinuation symptoms are more likely with paroxetine than with sertraline, citalopram, or escitalopram and all of the NNSRIs Serotonin-Agonist Reuptake Inhibitors p. 904 ¢ nefazadone ¢ trazadone Site of Action: Inhibit the reuptake of 5HT but also block the postsynaptic 5HT2 receptor subtype. Long-term usage: have the ability to increase serotonin release through the desensitization of 5HT1, receptors. Both of these drugs also have a mild to moderate a,-receptor antagonism. ADRs: Nefazadone- FDA Black-box Warning: Hepatotoxicity -available only in generic form. Benefits on sleep and minimal sexual SE. Trazadone: Priapism (persistent/painful erection) and anticholinergic side effects. Both drugs not typical 1* line anti-depressant r/t SE of sedation and orthostatic hypotension. Norepinephrine-and Serotonin-Specific Agonists p 904 © Mirtazapine (Remeron) — Unique addition — treats both anxiety and depression. Site of Action: 5HT agonist and reuptake inhibitor that blocks the reuptake of NE and the somato-dendritic reuptake of 5HT, resulting in an increase in 5HT available for release from the presynaptic neuron and more NE available in the synaptic cleft. Mirtazapine specifically blocks the 5HT, and 5HT; receptors. ADRs: ¢ Less sexual, gastrointestinal, and anxiogenic side effects. e Also blocks histamine, which contributes to the commonly observed side effects of drowsiness and weight gain at some doses. e This may be an advantage for treatment in patients who are depressed with difficulty sleeping or patients with weight loss. © Mirtazapine does not have the anti-muscarinic side effects of NNSRIs. Monoamine Oxidase Inhibitors (MAOI) p.904 e Phenelzine ¢ Tranylcypromine e Isocarboxazid ¢ = selegiline Monoamine oxidase - enzyme found in nerve and other tissues such as liver and gut that contributes to degradation of the monoamines (DA, 5HT, and NE). This action allows for more of these NTs to be available for postsynaptic binding. Site of Action: e MAOIs block monoamine oxidase by binding to the enzyme and permanently inactivating it. ¢ Synthesis of replacement MAO requires about 2 weeks. e Allows for levels of the catecholamines (DA and NE) and 5HT to rise, but it also decreases MAO availability for two other amines found in human diets, tyramine and phenylethylamine. Dietary Concerns: MAO is a natural rate-limiting substance needed to detoxify tyramine in the human body before it causes such severe events as a sudden rise in pulse and blood pressure. Dietary restrictions of tyramine-containing foods, such as any aged meats and cheeses and fermented products (e.g., wine, beer, sauerkraut, soy sauce) 0 Ifneglected, can contribute to lethal side effects, these drugs are used less often than are other antidepressants and should only be prescribed by psychiatric providers Other ADRs: Hypertensive crisis (Potentially lethal) Occipital headache radiating frontally Sweating Photophobia Palpitations Stiffness in the neck Nausea or vomiting. MAOIs can have dangerous interactions with many medications, including over-the-counter medications and herbal remedies. After discontinuing an SSRI or other serotoninergic, MAOIs must not be administered for 2 to 5 weeks This is considered a “wash-out” period. Selegiline is available as a transdermal patch (Ensam) avoids first-pass metabolism and produces less inhibition of the liver and gut MAO. Associated with fewer food restrictions, but higher doses may cause an interaction with tyramine- containing foods and is a risk factor in elevated doses. Transdermal selegiline is not FDA approved for use in children less than 12 years of age Given the risks, in depression treatment this drug should be given only by a psychiatric provider. Benzodiazepines/GABA-ergics (BZDs) p. 904-905 Short-acting: oxazepam (Serax) triazolam (Halcion) Intermediate-acting: alprazolam (Xanax) lorazepam (Ativan) estazolam (Prosom) temazepam (Restoril) Long acting: diazepam (Valium) quazepam (Doral) clorazepate (Tranxene) chlordiazepoxide (Librium) flurazepam (Dalmane) BZDs: Controlled substance occasionally used to treat acute anxiety. BZDs are no longer considered first-line agents for the treatment of anxiety disorders and have been replaced by the SSRIs and SNRIs. Site of Action: Act on the chloride ion channel of GABA-A receptors when they are bound to their adjacent BZD receptor. This enhances GABA neurotransmission, which then lengthens hyperpolarization of the impulse, thus slowing down responses to successive impulses. The net effect is to decrease reactivity of the brain. e All the available SSRIs can bind with any SHT receptor subtype. ¢ = The binding of SHT to the SHT> receptor may be implicated in the adverse sexual reactions of the SSRIs. With 5HT, antagonists (e.g., {SARIs} nefazodone and trazodone) and the 5HT;, agonist buspirone (BuSpar), however, the sexual dysfunction effects are minimal. SSRIs have minimum to no effect on NE, DA, histamine, or acetylcholine, there are few adverse reactions associated with blockade of these receptors (e.g., anxiety, restlessness, drowsiness, constipation, and orthostasis). Serotonin syndrome, another adverse reaction. (Discussed earlier) SSRIs- Most common issue: Reduced sexual desire, delayed or absent orgasm, premature ejaculation, and erectile disturbance (can occur when taking any antidepressant) e These adverse reactions usually do not become evident for about a month, which may be more noticeable as the depressive symptoms are reduced. © The patient may also have a primary reason for sexual dysfunction that needs to be evaluated. e If the antidepressant is the cause of the sexual side effects, consider lowering the dose or changing to another antidepressant with less sexual side effects, such as bupropion. e If the patient does not want to try a different medication and the lowered dose does not help, other strategies for male patients might include adding sildenafil or tadalafil Educating patients about this possible side effect and informing them of other treatment options early can reduce the risk of patients decreasing their dosage or stopping treatment due to sexual dysfunction. As the advanced practice nurse treating the patient, it is important to ascertain that the patient is experiencing sexual side effects due to the medication and not a co-occurring medical disorder or other reason. Rational Rx selection. 905-906 Antidepressants © Clinical guidelines recommend that symptoms of depression and anxiety are best treated with a combination of medications and psychotherapy ¢ Many of the medications commonly used to treat anxiety are also used to treat depression oO Paroxetine is FDA approved to treat MDD, OCD, panic, GAD, and PTSD. 0 Escitalopram (Lexapro) {SSRI} is approved for the treatment of MDD and GAD. Sertraline is indicated for use in MDD, panic disorder, PTSD, and OCD. 0 Fluoxetine (Prozac) {SSRI} is approved to treat MDD for ages 8 and older, OCD for ages 7 and older, bulimia, and panic disorder. 0 Fluvoxamine (Prozac) {SSRI} has the approval to treat OCD and social anxiety disorder. O Venlafaxine XR (Effexor XR) {SNRI} is indicated for MDD, GAD, and panic disorder Research suggests that all antidepressants are equally effective; therefore, the most important considerations are differences in onset of action and adverse events. Escitalopram and sertraline were found to be the most effective The Agency for Healthcare Research and Quality (AHRQ, 2012) did a comparative analysis and did not find differences in outcomes between antidepressants. Continued research and systematic reviews are needed to give providers more assistance in better rationales for antidepressant choice. According to the APA practice guidelines (2010) for depression, the effectiveness of antidepressant medications is generally comparable between and within classes of medications. ¢ Acomprehensive psychiatric assessment be performed, and initial selection of an antidepressant be largely based on the preference and prior response of the patient, clinical features, safety and anticipated side effects, coexisting medical conditions (both physical and mental), the pharmacological properties of the medications, and cost. e For example, in an overweight individual, mirtazapine may not be the first choice because of the higher risks of weight gain. ¢ Mental disorders are often familial, it is helpful to know if anyone else in the family has similar symptoms and what medications have worked for them. @ When several choices are reasonable, select the medication that other blood relatives have had success with because they are likely to affect the patient in the same manner. All of the antidepressants discussed in this chapter usually take 2 to 4 weeks to produce the full therapeutic effect, with gradual improvement beginning with the vegetative symptoms, then arousal symptoms, before the relief of mood symptoms. Refer to the general treatment algorithm for depression (Fig. 29-1) Rational Rx Selection p. 906 Anxiety ¢ Normal emotion in response to threat or anticipation of harm. © The total body responds through the autonomic system by preparing the body to flee the situation, remain and fight, or remain and freeze. © Clearly, anxiety serves an adaptive purpose, and to automatically medicate anxiety may be countertherapeutic. @ When a patient maladaptively responds to stress and meets criteria for one of the anxiety disorders, the provider should consider medication and therapy Primary neural pathways involved in anxiety include 5HT, NE, and GABA. e Pharmacological intervention can use nonselective norepinephrine-serotonin reuptake inhibitors, SSRIs, and/or SNRIs, or serotonin agonists. e SSRIs and SNRIs can be used for GAD, PTSD, obsessive-compulsive disorders, and panic attacks. ¢ Take 2 to 4 weeks to provide the full therapeutic effect. e Anxiety symptoms often resolve earlier than depressive symptoms, and they usually require a much lower dosage. e For all anxiety disorders, starting low and going slow is the best way to avoid excessive serotonin adverse effects. Monitoring/Education: p. 906 Vital to build a trusting relationship and be optimistic when discussing treatment options with patients. Make sure that the patient knows that recovery is possible, and that confidentiality will be respected. Information about treatment and support groups should be provided ¢ Once treatment is initiated, the patient's status needs to be frequently monitored for response to treatment, possible side effects, safety, increased suicidal thinking, and adherence to treatment at least every 1 to 2 weeks. This should begin 1 or 2 weeks after the initiation of therapy e Frequency of follow-up appointments, consider the severity of the illness, co-occurring medical conditions, available support systems, progression of symptom change, and the patients’ cooperation with treatment. If a patient needs closer monitoring, refer to a psychiatric provider All antidepressants have a Black-Box Warning regarding an increased risk of suicidal thinking and behavior in children, adolescents, and young adults to age 24. Because depression itself is associated with an increase in suicidal ideation, the chances of such ideation must be considered when making a choice about appropriate treatment. All patients who are prescribed an antidepressant and the parents of children or adolescents should be educated to monitor for an increase in suicidal ideation or behavior. It is especially important to assess for suicidality at the time of diagnosis, after initiating treatment, and as treatment progresses. The antidepressants begin to work on sleep, appetite, and energy, with mood as one of the last symptoms to remit. This puts all individuals being treated for depression and anxiety at risk for suicidal thinking. Table 29-1 SAFE-T Assessment of Suicide Risk Suicide Assessment Five-Step Evaluation and Triage Identify Risk Factors What can be modified to reduce risk? Identify Protective Factors What factors can be enhanced? Conduct Suicide Inquiry Ask about suicidal thoughts, plans, behavior, and intent Determine Risk/Level of Intervention Determine risk. Choose appropriate intervention to address and reduce risk Document Assessment of risk, rationale, intervention, and follow-up Assessment, Evaluation and Triage in Table 29-1 needs to be done Q 1-2 weeks in the first stages of treatment and dose changes. Immediate referral and possible hospitalization need to be considered if the patient persists in suicidal thinking. Some antidepressants, such as the NNSRIs and the SNRIs, can be lethal in overdose. When using these medications early on in treatment, consider dispensing weekly quantities and be aware of the possibility of hoarding. For patients who are having suicidal ideation, consider a safer medication in overdose, such as an SSRI Planning ahead for potential Suicide Ideation must ALWAYS be considered. Treatment plan for each individual is established. US Surgeon General: Support and treatment needs to be available at multiple points of entry. . Screening improves the likelihood that the person will receive appropriate evaluation and treatment . Training on recognition of risk and quality of care increases the likelihood of a good outcome . The care provider accurately diagnoses and records the problems and ensures that the appropriate public health surveillance systems are notified or made aware of the diagnoses . The implementation of trauma-informed policies and practices ensures that the person is treated with respect and in a way that promotes healing and recovery . Easy access to mental health-care referrals for individuals with suicide risk increases the likelihood of a better outcome . Education efforts by health-care providers increase knowledge of the warning signs of suicide risk among the individual and his or her family and/or support network . Continuous care and improved aftercare lead to better monitoring and follow-up of the at-risk individual over time Acute treatment phase: Important to monitor the patient's response to ensure the treatment has been given for a sufficient duration, frequency, or dose. ¢ A patient needs about 4 to 8 weeks of optimal dosing of medication treatment to appropriately evaluate whether or not there is a partial response or no response at all. ¢ Treatment should be modified if remission has not been obtained in at least a 14-week period of optimal dosing or there has been little symptomatic improvement. ¢ Mild-moderate response, increasing the dose or switching antidepressants or using of augmenting agents discussed earlier from the STAR*D results should be considered. Important to know when to refer someone who is not responding to treatment. Table 29-3 When to Refer Consider referring any individual with a poor response to two adequate trials of antidepressants, a chronic suikide, his ton Samael PTSD, &gmorbid eating disorders, or if this person shows indications of a more 8 payeniatite prov complicated mood disorder. * Bipolar disorder Refer ta,esyaajatric providers immediately those with any psychotic disorder and those who are dependent on substartsesnosis + Significant substance disorder comorbidities + Comorbid PTSD or OCD Comorbid eating disorder * Failure of two antidepressants + Possibility of a personality disorder