Written by Joshua Stein, MD

A common difficulty in the outpatient office is determining the steps needed to ensure the safety of a patient once they identify that they are suicidal. There are two known methods to ensure safety; mental health treatment at the appropriate level of care and means reduction. The need to determine level of care will be examined in a future post. The significant importance of the removal of means to suicide, or Means Reduction, is the focus of this article.

A common myth is that a suicidal person, who has identified a source for completion, will substitute an alternative method if his/her original method is taken away. This belief in almost all settings represents a fallacy. The lethal means, whether overdose, a firearm, a one car crash etc, will not be substituted for another. 

Given the opportunity, the removal of chosen lethal means, especially firearms, will greatly reduce the How people attempt: leading to time to determine the Why, and introduce treatment.

​Per NAMI, there are numerous examples from history where the removal of a lethal means has decreased the death rate. In 1960, lethal oven gas ingestion was the leading cause suicides in the UK. By 1970, the country had substituted non-poisonous gas, resulting in a one third decrease in the suicide rate. The entirety of the drop stemmed from the change in gas, and non-gas related suicides had only increased slightly. The entirety of the change stemmed from means reduction to lethal gas.

The Israeli Defense Force (IDF) struggled significantly with suicides off base on vacations and weekends. In 2006 soldiers were no longer allowed to carry firearms off base for breaks. The suicide rate dropped approximately 40 % with no change in the rate of suicides during the week. The entirety of the change appeared to be related to the means reduction to firearms off base.
Numerous studies demonstrate that the acute action phase towards suicide is commonly brief. By removing the means to attempt, people often reach a plateau of safety when support can be introduced. The most common method of suicide attempt is by intentional overdose. The most likely lethal attempt is by firearm. Practical steps are outlined below:

1. If a means is shared, it must be removed (substitutions are not likely)
2. Additional means to suicide should also be removed to improve safety
3. Remove all firearms
4. Lockup medications, including OTC (carry in car if needed)
5. Remove car keys
6. Remove Sharp objects/knives
7. Remove cords and ropes
8. Remove alcohol
9. Identify a family member or friend who can remove the means before a patient returns home
10. Have the person who is removing the means alert the treatment team by phone call that this has been completed
11. Document this step

At times, resistance to removing the means may occur from a friend/family member. A common desire to increase the difficulty of the attempt often is a practical point to reach agreement. As these are common objects in the home and firearms carry significant value, there is a time at which reintroduction should occur. Similar to the safety assessment in the medical office that led to removal of means, a safety assessment can take place to approve returning these objects to the home.

​In conclusion, removal of the means works in significantly improving safety. If a patient is deemed appropriate to return home, whether from a hospitalization or an outpatient appointment, steps towards means reduction need to take place. Finally, when a patient identifies a means, action should be taken, the fallacy to believe an alternative means will be substituted is incorrect.

SOURCES:

• NAMI MEANS REDUCTION LECTURE
• Shaffer D, Pfeffer CR, & the Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with suicidal behavior. JAACAP. 2001;40(7 Supplement):24S-51S.
• Shain BN. Suicide and suicide attempts in adolescents. Pediatrics. 2007;120(3):669-675.
• American Association of Suicidology. Youth Suicide Fact Sheet. January 28, 2008. Available at: http://suicidology.org/c/document_library/get_file?folderId=232&name=DLFE-24.pdf. Accessed April 19, 2009.
• American Psychiatric Association. Let’s Talk Facts About Teen Suicide. Available at: http://healthyminds.org/factsheets/LTF-TeenSuicide.pdf. Accessed April 19, 2009.

​Minnesota's Psychiatric Assistance Line (PAL) was honored by the American Psychiatric Association with the 2019 Community Gold Award🥇. Our state continues to be a leader in health care through creativity and collaboration. This transformative service is a partnership between Minnesota Department of Human Services, PrairieCare Medical Group, and the Minnesota Community Mental Heath Foundation.

Read the article here: https://www.prnewswire.com/news-releases/minnesotas-psychiatric-assistance-line-receives-the-2019-community-gold-award-from-the-american-psychiatric-association-300928897.html

Psychiatric assessments for children continue to have both extensive wait times and geographic disparities. In the state of Minnesota the only county according to the American Academy of Child Adolescent Psychiatry (AACAP) to have an adequate child psychiatrist to patient ratio is Olmstead, due to presence of the Mayo Clinic. Given these issues, the burden to initiate care often falls on the pediatrician or family practitioner regardless of the complexity of the situation. The goal of PAL is to provide support for these providers with immediate phone consultations at the moment they are needed. 

The most common but also most difficult diagnostic patient is the irritable young child. The differential is extensive and includes learning disorders, social concerns, adverse childhood events, mental illness and medical considerations including absence seizures. A common question from primary care is, "can medications be used for treatment even if the differential outside of mental health cannot be exhausted?" 

There is no simple approach, however the outline below is beneficial:
 

1. Do these concerns happen in all environments or just one? (School vs home; mother’s vs. father’s home; summer camp and home). Although the diagnostic criteria for ADHD requires two environments, this can be a helpful clarifying questions for all diagnoses.
2. Is there a “Big T” or “Many little Ts?” Trauma comes in all sizes but the concern is the impact on the child. Stress hormones can be equally elevated at baseline in children who have had numerous small impactful trauma’s such as moves or bullying. Determining if trauma is present is an important first step.
3. Is there a learning or developmental disability? While psychological testing is an important tool to clarify diagnosis, especially in children struggling with agitation in school, it is not readily available. Treatment can often not wait the three to six months for testing. Clarify reading level and feedback parents have heard from teachers.
4. Does the child remind the parent of anyone? Often there is a similar pattern to parents that can be clarifying diagnostically.

 
After clarification of the details above, there is often treatment modalities that are non-pharmacologic that are primary. This is includes recommendation for an IEP, an occupational therapy eval, in home skills, family/individual therapy, tutors, glasses, social skills groups etc. These are primary, but medication initiation, especially those that palliate severe agitation symptoms can be an effective adjunct treatment. 

The goal is often to decrease agitation to the point that the above non-pharmacologic options can be started effectively rather than lead to further escalations. Hydroxyzine, clonidine and guanfacine often demonstrate benefit in the short term setting while the above treatments are initiated. 

In addition to psychiatric consult services with PAL, there is also a triage therapist available to assist with non-medical questions, referrals and concerns. They are available to help find services throughout the state of MN.

You can contact PAL by calling 855-431-6468, pal@prairie-care.com, or scheduling online!

As a practitioner in a partial hospital and inpatient setting the most common reason for adverse reaction to stimulants is incorrect diagnosis. In these support rich settings the ability to gain psychological testing helps to clarify the differential for hyperactivity and/or inattention. Often, learning disabilities (i.e. reading disorder, math disorder, and auditory processing disorder), anxiety or sensory concerns were missed. This is a common dilemma and a point of profound difficulty for the outpatient prescriber who doesn't have the assistance of formal testing in clinic. Despite these limitations, remembering that impairment must occur in two settings (most commonly home and school) to meet diagnostic criteria, is a helpful tool. Commonly, the absence of symptoms at home or school helps to clarify a need to deepen the differential. Additionally keep in mind that obstructive sleep apnea commonly can masquerade as ADHD. Questions about sleep are necessary as part of the initial workup.

Once the diagnosis of ADHD is made stimulants remain the most effective treatment for ADHD in children. Stimulant use remains the primary step in treatment, and non-stimulants are deferred in common cases until both classes of stimulants are failed. The vast majority of children will respond to either the methylphenidate class or amphetamine class. It is appropriate to build comfort with one or two medications in each class to support treatment. As a provider it is appropriate to choose either class first. If the initial class is failed then switching to the other class is warranted prior to a non-stimulant trial.

Commonly, a provider will start with a short acting stimulant such as Ritalin SA or Adderrall to test tolerance. Once tolerated, a long acting stimulant is preferred to avoid need for additional dosing. If trials in one class (i.e. methylphenidate) are not tolerated it is appropriate to switch to the alternate class (i.e amphetamine). There is significant individual details in finding dose and toleration. Stimulants have weight based indications but overall appear to be more individual based. It is appropriate to move to higher doses if tolerated to achieve symptomatic relief. Regular input from school is often needed as well.

Keep in mind cost and delivery methods when choosing medications. For example, Concerta (a long acting methylphenidate stimulant) is a pill that must be swallowed, while its analog Quillichew/Quillivent can be chewed or drank in liquid form. In small children delivery is often a concern. Vyvanse, a long acting amphetamine based stimulant, has the option of opening the tab and dissolving in liquid. Additionally it is a pro-drug, requiring digestion to promote action, decreasing the risk of diversion. For these reasons many providers prefer it to Adderall XR when it is affordable.

Some youth will require a second dose of a stimulant despite being on a long acting formulation. Short acting doses of Ritalin, Focalin, Metadate, Dexedrine or Adderall should be considered. This is where the regular check-ins become important. There is an art to prescribing these meds which includes determining how to cover a child for the duration needed with medication, while decreasing side effect risk. Over time, dosing needs and patterns will change. Clinic visits three times per year at the least are needed.

​Stimulant breaks are appropriate and often needed due to appetite suppression. At times, this can be on weekends, school breaks or summer break. For the hyperactive child this may not be a tolerable option for the family. Appetite suppression is often an issue for younger children as eating is related to hunger, while in teenagers it has gained social value similar to adults. If suppression is severe with a long acting stimulant consider returning to a short acting dosed after breakfast and lunch to support appetite.

There are numerous other considerations with stimulant use. Further blogs will provide additional information. I hope you find this initial dosing guide beneficial.

​An excellent resource for the diagnosis, treatment and use of stimulants in children is the American Academy of Pediatrics Clinical Practice Guideline. It can be found here https://pediatrics.aappublications.org/content/108/4/1033

​The use of second generation antipsychotics in the pediatric population is commonplace on inpatient psychiatric units and outpatient psychiatric clinics. Should this class of medications be in the primary care provider’s “toolbox” of medications for their patients with behavioral and/or mood symptoms when the first and second-line medications fail?

There are currently seven second generation, or atypical, antipsychotics approved for use in children and adolescents. These include risperidone (irritability associated with autism, schizophrenia, bipolar disorder), aripiprazole (irritability associated with autism, schizophrenia, bipolar disorder), quetiapine (schizophrenia and bipolar disorder), olanzapine (schizophrenia and bipolar disorder), lurasidone (schizophrenia and bipolar disorder), paliperidone (schizophrenia), and asenapine (bipolar disorder).

The child or adolescent with schizophrenia or bipolar disorder is typically having medications managed by a psychiatric provider. However, children with autism spectrum disorder and major depressive disorder are often managed by primary care. 

You may notice that augmentation of a SSRI medication with a second generation antipsychotic such as aripiprazole for major depression is not an FDA-approved use for adolescents. This use is only FDA approved for adults, so this would be off-label use, but also a reasonable strategy for augmenting treatment of depression in adolescent patients in the primary care clinic. I have found this to be helpful in adolescents who have partial benefit from SSRI or SNRI medication, but with residual symptoms of depression, especially irritability. A typical starting dose of aripiprazole for antidepressant augmentation is 1mg, which can be titrated to 2-5mg.

Both aripiprazole and risperidone can be quite helpful for managing behaviors and irritability in children with ASD. Aripiprazole can be started at 1mg daily, and titrated up to 5-10mg daily depending on tolerability. 1-2 mg is often a beneficial dose. Risperidone is started at 0.25mg daily, and titrated in increments of 0.25mg to max of 3mg total daily dose. Oftentimes 0.25mg BID is a beneficial dose.

The most common side effect from these two medications is weight gain. Also there is the risk of dyslipidemia and development of type 2 diabetes. Fasting lipids and glucose should be obtained at baseline, and again after three months of treatment, and every year thereafter. Weight should be checked at each appointment. Some psychiatrists obtain a baseline prolactin level prior to initiation of risperidone, though not necessarily the community standard of practice. The risk of gynocomastia should be discussed with the patient and guardian prior to initiation.

Extrapyramidal side effects are a risk with second generation antipsychotics. There continues to be a risk of tardive dyskinesia, though is relatively rare when compared with first generation antipsychotics. Second generation antipsychotics also carry the risk of dystonic reaction, akathisia, and rarely neuroleptic malignant syndrome.

EKG is not routinely obtained when starting aripiprazole or risperidone. This can be considered in a patient with a history of arrhythmia, or if used in combination with other potentially QT-prolonging medications (guanfacine/clonidine or stimulant medication, high dose (30-40mg) citalopram).
Another consideration with risperidone and aripiprazole specifically is their drug-drug interaction with fluoxetine (and paroxetine, though this is not routinely used in children). These SSRI medications inhibit the metabolism of both risperidone and aripiprazole, so lower starting doses are advised. Children with known deficiency of cytochrome 2D6 metabolism should start on lower doses as well.
Sources:

1. Prim Care Companion J Clin Psychiatry. 2002; 4(6): 233–241.
2. Atypical Antipsychotic Medications: Use in Pediatric Patients
3. UpToDate Neuroleptic Malignant Syndrome

The key feature of pediatric generalized anxiety disorder is excessive or uncontrollable worry lasting >6 months, with the worry being out of proportion to the situation. This article aims to briefly review the typical treatment algorithm for GAD, and also discuss newer pharmacologic interventions and alternative treatments.
 
The typical first line treatment for mild GAD is psychotherapy, specifically Cognitive Behavioral Therapy (CBT). For moderate and severe GAD, combination therapy and medication has demonstrated superior efficacy to either treatment alone. Interestingly, the only medication FDA approved for pediatric GAD is Duloxetine (Cymbalta), approved for ages 7-17. However, in practice, SSRI medication remains the typical first line pharmacologic intervention. There is no evidence that any SSRI is more effective than another. Fluoxetine (Prozac), Sertraline (Zoloft), and Escitalopram (Lexapro) are the most commonly prescribed, though Fluvoxamine (Luvox), Paroxetine (Paxil), and Venlafaxine (Effexor) have all shown efficacy in placebo-controlled trials. A typical algorithm (for medication intervention) is first SSRI, if not effective second SSRI, and if again not effective SNRI.
 
A typical PAL consult is what to do when the second SSRI is not effective or not tolerated. In a typical case, Duloxetine would be the recommendation, as this has shown efficacy in placebo-controlled trials, and has the FDA approval. Things become trickier if Duloxetine is not tolerated or not helpful. In this case, I would want to make sure Duloxetine is appropriately dosed. If there is no benefit at 60mg for 4-6 weeks, I would consider this a failed trial. However, if there is a partial response at 60mg, increasing to 90-120mg is reasonable, though doses above 60mg have not been found via placebo-controlled trial to provide additional benefit [5].
 
Benzodiazepines, while clearly efficacious and approved for adult GAD, have not shown clear benefit for the pediatric population [2]. For pre-pubertal children, these are known to have disinhibiting properties. I reserve benzodiazepine use for severe adolescent cases with clear functional impairment, active and trustworthy parents to help with administration, and no personal history of substance abuse. These should obviously be outlined as a short-term treatment to be used while the SSRI/SNRI are building up. I typically start with Clonazepam 0.25mg given bid-tid, either PRN or scheduled.
 
An alternative “PRN” medication for GAD is Hydroxyzine (Vistaril, Atarax). I have found 25mg to be sedating for many children, so usually start with a 10mg dose given tid PRN. This can be titrated up to 50mg per dose.
 
The non-SSRI Buspirone (Buspar) was studied in an unpublished placebo-controlled trial (N=559). No statistically significant difference with Buspar and placebo was observed. There are case reports of successful treatment of GAD with Buspar, and it has been shown to be well-tolerated. In a primary care setting, I would reserve this for adolescents, starting dose of 7.5mg bid, increased by 5-10mg per week to max of 30mg bid [1].
 
For the child with comorbid ADHD, and/or “activation” with SSRI/SNRI treatments, Guanfacine extended-release (Intuniv), an alpha 2A –adrenergic receptor agonist, may be a reasonable alternative. Agents that decrease norepinephrine release may decrease the fear response, producing anxiolytic effects. A recent study by JR Strawn, et al. [4], aimed to demonstrate safety and tolerability, and potential efficacy of this medication. It was shown to be well-tolerated, with most common side effects of headache, fatigue/somnolence, abdominal pain, and dizziness. No significant difference was observed compared to placebo on the PARS (pediatric anxiety rating scale) or SCARED (screen for child anxiety related emotional disorders) scales. There was improvement in the Clinical Global Impression-Improvement (CGI-I) score with Intuniv versus placebo. Overall, this study was under-powered to show direct evidence of efficacy. Doses used in this trial were 1-6mg daily.
 
Sources:

1. Green’s Child and Adolescent Clinical Psychopharmocology, Fifth Edition. Pages 302-314.
2. Hussain FS, et al. Pharmacologic Treatment of Pediatric Anxiety Disorders. Curr Treat Options Psychiatry. 2016 Jun; 3(2): 151–160.
3. Strawn JR, et al. Efficacy and tolerability of antidepressants in pediatric anxiety disorders: a systematic review and meta-analysis. Depress Anxiety. 2015 Mar;32(3):149-57.
4. Strawn JR, et al. Extended Release Guanfacine in Pediatric Anxiety Disorders: A Pilot, Randomized, Placebo-Controlled Trial. Journal of Child and Adolexcent Psychopharmacology. 2017 Volume 27, Number 1: 29-37.
5. Strawn JR, et al. A randomized, placebo-controlled study of duloxetine for the treatment of children and adolescents with generalized anxiety disorder. J Am Acad Child Adolesc Psychiatry. 2015 Apr;54(4):283-93

Pharmacogenomic testing is becoming more commonplace in the world of psychiatry, leading to “guided treatment” and “precision medicine.” Genetic information can be helpful in choosing medication, choosing starting and target doses, and in predicting/explaining adverse events. The evidence base for this testing, as far as clinical outcomes, has gaps. This brief article aims to help the primary care provider decide when obtaining pharacogenomic testing is indicated, and how to interpret those results. This article will focus on guided antidepressant therapy.

There are multiple resources from which to obtain this testing, found in table 2 of this NIH paper. In my clinical practice, I tend to reserve pharmacogenomic testing for those who have failed at least two adequate medication trials for the same diagnosis, or has not tolerated typical therapeutic doses, though I do not necessarily always obtain testing in this situation. Some providers obtain a pharmacogenomic profile prior to initiation of the first medication. Though I do not personally advocate this for children and adolescents, this may have utility in achieving remission sooner.

For example, a 16 year old has had failed trials of both Fluoxetine and Escitalopram for depression and/or anxiety. Reasons for the failed trials include the possibility of this patient being a poor metabolizer at cytochrome 2D6, 2C19, and/or 3A4 and does not tolerate therapeutic doses, or an ultra-rapid metabolizer and is not achieving therapeutic plasma levels (though FDA label indicates Escitalopram should not be affected by a single cytochrome polymorphism or inhibition). SSRI medications may not be helpful or may not be tolerated due to a polymorphism in the serotonin transporter gene or the serotonin 2A receptor. At this point pharmacogenomic testing may help guide the next step in pharmacotherapy.

As far as interpreting the results of pharmacogenomic testing, some of the reports are easier to digest than others. One of the local providers has a liaison who is typically available to discuss results. Also the psychiatrists staffing the PAL service are more than willing to go over these reports with you. The most commonly utilized test in the Twin Cities is arranged in a green, yellow, red format, which is based on drug-gene interactions. The yellow and red categories do not imply that these medications cannot be used, but have the possibility of drug-gene interactions, which can affect dosing considerations and increase risk of side effects. A common problem is the “green” category containing only medications that are not FDA approved for children, and oftentimes not covered by insurance. In these cases, more careful interpretation of the results is necessary than basing treatment decisions solely on the color status. The pharmacogenomic test results are however reasonable justification for obtaining a prior authorization for second tier or off-label medications, especially if there have been failed trials of first-line medications.
​
Sources:

1. Bousman, et al. Antidepressant prescribing in the precision medicine era: a prescriber's primer on pharmacogenetic tools. BMC Psychiatry. 2017; 17: 60.
2. Drozda et al. Pharmacogenomic Testing for Neuropsychiatric Drugs: Current Status of Drug Labeling, Guidelines for Using Genetic Information, and Test Options. Pharmacotherapy. 2014 Feb; 34(2): 166–184.
3. Tantisira et al. Review of pharmacogenomics. Uptodate.com
4. Lexapro FDA prescribing information. 

Recently the Psychiatric Assistance Line (PAL) team was asked about validated screening measure and scales for use within the primary care setting. Scales such as the PHQ-9 and the GAD-7 are routinely used in primary care settings, but are these sensitive/specific and validated for children and adolescents? This is a valid(ity) question.

There are multiple screening tools available to the primary care provider for several different mental health concerns and situations. The PHQ-9 does have a “modified” version for the teenager, the PHQ-A. After carefully comparing this with the PHQ-9, the only discernable difference is that the PHQ-A includes “irritability” as a possible symptom of depression, otherwise the two scales are identical. There are additional questions regarding suicidal symptoms on the PHQ-A. A 2012 study did find the PHQ-9 as valid for screening adolescents ages 12-18. Sensitivity and specificity each ranged from 85-88% depending on the source (1,4,7). Other “free” options for screening depression in a pediatric setting include the KADS, with 92% sensitivity and 71% specificity (4,7). Proprietary scales such as the Beck Depression inventory and the Child Depression Inventory are also validated child depression scales, the BDI with sensitivity and specificity of 91% (4,7).

Regarding generalized anxiety disorder, the GAD-7 is a well-validated scale for ages 13 and over (4). The Beck Anxiety Inventory, which is proprietary, has also shown validity and reliability for ages 14-18 (3). The Spence Children’s Anxiety Scale also is found to be valid from ages 8-18, and additionally has subscales for panic, social phobia, and OCD, as well as GAD (4).

As far as ADHD, the Vanderbilt assessment scale is a psychometrically reliable and valid scale using parent and teacher questionnaires. The VADPRS (parent Vanderbilt scale) produced a sensitivity of .80, and a specificity of .75 (2).

This summary of free assessment measures may be a useful tool to identify scales that may work well for your clinic. Also, this guideline for depression treatment of adolescents in primary care has information on screening, diagnosis, safety assessment, therapy, medication algorithms, and parent information, as well as a nice summary of the FDA black box warning on antidepressant medications.  

Sources:

1. Allgaier AK, et al. Screening for depression in adolescents: validity of the patient health questionnaire in pediatric care. Depress Anxiety. 2012 Oct;29(10):906-13.
2. Bard DE, et al. The psychometric properties of the Vanderbilt attention-deficit hyperactivity disorder diagnostic parent rating scale in a community population. J Dev Behav Pediatr. 2013 Feb;34(2):72-82
3. Grant MM. Beck Anxiety Inventory. See here.
4. Mental Health Screening and Assessment Tool For Primary Care.
5. Guidelines for Adolescent Depression in Primary Care Tool Kit
6. Center for School Mental Health Summary of Free Assessment Measures.
7. Adolescent Depression—enhancing the outcomes in primary care. http://www.acpm.org/?AdDepresTTClinRef