In the past, OCD was categorized diagnostically as an anxiety disorder, but in the DSM V it has been separated into its own category. This is largely because research has shown that the genetics of OCD is different from the genetics of other anxiety disorder. OCD is defined as obsessions (intrusive, unwanted and excessive worries) and compulsions (rituals to relieve the anxiety) that are impairing to everyday life. The impairment can be defined by the amount of time spent on the obsessions and compulsions, its effect on preventing a patient from carrying out activities of daily living and work responsibilities, and its effect on alienating important people in the patient’s life. The obsessions and compulsions can involve the following: preoccupation with contamination, cleaning, checking, symmetry and order, preoccupation with sexual, violent or religious thoughts, and hoarding.

The diagnosis of OCD is primarily a clinical one. Two good screening questions to determine if further assessment is indicated are:

1. “Are bothered by unpleasant worries that repeatedly come into your mind about contamination, ordering things, etc?
2. “Are driven to perform certain acts over and over again like checking locks or washing your hands excessively?”

The YBOCs is a good diagnostic tool for delineating specific symptoms and determining the level of severity and the patient’s level of insight. The patient is typically aware that the obsessions and compulsions are irrational and excessive but are compelled to do them anyways. This egodystonic nature of the illness is partly what leads to the suffering from OCD and can lead to an increased risk of suicide.  In rare cases, when patients are not aware that their obsessions and compulsions are irrational and excessive, they are said to have “poor insight” and their OCD is typically more treatment-resistant. These cases can often be difficult to differentiate from true psychotic delusions.

OCD is frequently co-morbid with other anxiety disorders, depressive disorders, and eating disorders in adults and ADHD and tic disorders in children. Treatment options include exposure response prevention (a CBT specifically geared for OCD) and psychotropic medications. ERP involves repeated exposure to situations that trigger the obsessive thoughts and having the patient gradually learn to tolerate the anxiety and resist the urge to perform the compulsions. Medication options include the SSRIs (Prozac, Paxil, Lexapro, Celexa, Zoloft, Luvox) and Anafranil (an older tricyclic antidepressant, used primarily for treatment resistant cases). Medication treatment involves slow titration to avoid worsening the anxiety, and patients often need higher doses for longer periods of time for a full effect. It is important to make sure patients are aware that it can take up to 3 months to get to a full effective dose. Most patients do better with a combination of medication and ERP. There are adjunctive medication options available if full symptom relief is not achieved with an SSRI alone. These include the second-generation antipsychotic medications. Surgery and ECT vs deep brain stimulation can be used for refractory cases.

Given that OCD is more prevalent than previously thought, it is important that first line providers are comfortable with knowing when to assess for OCD and how to pursue with treatment recommendations.

Medication can be an important treatment for antepartum and postpartum depression (PPD), if the symptoms are moderate-severe and/or not responding to non-medication approaches. The selective serotonin reuptake inhibitors (SSRIs) are the first line agents, in particular sertraline because of its relatively short half-life and availability of low doses (can be dosed as low as 12.5 mg per day). Paroxetine is pregnancy category D because of there is evidence that it increases the risk of birth defects, including rare cardiac and CNS effects. While these birth defects are very serious, it is important to keep in mind that they are very rare at baseline and that the increase in absolute risk from SSRI use is very minimal and depends on the SSRI being considered. There is also a possible connection between SSRI use in the third trimester of pregnancy and development of persistent pulmonary hypertension of the newborn in infants. There have been reports of newborns experiencing temporary discontinuation symptoms at birth, including jitteriness and irritability when a woman is treated with antidepressants during pregnancy. Other antidepressants, like the SNRIs and tricyclic antidepressants, are not typically recommended during pregnancy.

The SSRIs are also the first line medication treatment in the postpartum period for patients for whom medication might be indicated. Of the SSRIs, sertraline and paroxetine are the least detectable in breast milk, because of their relatively short half-lives. Several case reports note an association between fluoxetine and citalopram use in lactating women and infant irritability, poor sleep, poor feeding, crying, and restlessness. This might be related to these medications’ relatively longer half-life. Other case reports have not noted any adverse effects in infants of mothers taking fluoxetine and citalopram.  If one is considering treating PPD with a medication, sertraline is a good first line agent because of its relatively shorter half-life and ability to dose in smaller doses, as low as 12.5 mg per day. The peak level of sertraline in breast milk is between 7-10 hours after taking the medication, which can be kept in mind to determine the optimal time for the patient to take the medication. If a woman is already on an antidepressant like fluoxetine with a good response, it is okay to continue with the medication and monitor closely for side effects in the mother and infant.

The important take home point for treating depression related to pregnancy is to first consider a non-medication treatment. If it is determined medication is needed, it is important to have a careful discussion about the risks and benefits and to try to use the smallest possible dose for the shortest length of time, with sertraline being a good first choice for both the antepartum and postpartum period. 

Website: www.pc2education.org

There are more complicated interactions between contraceptives and mood stabilizer medications, many of which are also used for epilepsy. Contraceptive medications can be affected by certain psychotropic medications. Carbamazepine, oxcarbazepine, and topiramate (mood stabilizers which induce the P450 3A4 pathway) can increase the metabolism of oral contraceptives (many of which are substrates of the P450 3A4 pathway), thereby reducing their effectiveness. This effect is also seen with vaginal contraceptive rings, because the hormones contained in these preparations are also metabolized by the liver. In these situations, the patient should either change her contraceptive method or change her mood stabilizer. Contraceptive alternatives include the birth control patch (which largely avoids liver metabolism) and barrier methods. Mood stabilizers like valproate and lamotrigine do not affect oral contraceptives, but lamotrigine clearance is increased with oral contraceptives that contain estrogen, thereby reducing the effectiveness of the medication. In patients who are taking a traditional mood stabilizer, including Lithium, highly effective contraception is important because these medications can have serious teratogenic effects if a patient accidently becomes pregnant. One option is a high-dose oral contraceptive, but because of the complexity of oral contraceptives and some traditional mood stabilizers as well as side effects of high-dose estrogen, it is important to consider non-hormonal approaches as a primary or adjunctive contraception. St. John’s Wort (an herbal supplement that many patients take for mild depression) can induce the P450 3A4 pathway, thereby inducing the metabolism of oral contraceptives, making them less effective.

There is some concern that progesterone-only pills and high-dose estrogen pills can lead to or worsen depression, although this has not been studied in a controlled fashion that clearly defines depression and addresses the confounding factor of natural fluctuations in mood symptom during various parts of the menstrual cycle. These hormones can increase the metabolism of serotonin in the brain, thereby lowering serotonin levels, which can contribute to depression. It is thought that low-dosed combined oral contraceptives have little risk for causing or worsening depression. However it is important to assess for changes in mood after a patient first starts contraception.

Here is a chart to summarize the interactions between BCP and psychotropic medications:

Risk factors for depression in older patients include:

1. Significant medical problems
2. Retirement and loss of professional identity
3. Decreased independence
4. Decreased physical mobility
5. Memory impairment
6. Loss of close loved ones

While depression is diagnosed in older adults using the same criteria used to diagnose younger and middle-aged adults, symptom presentation can vary slightly.  Older patients may not explicitly report symptoms of sadness. Other clues that depression may be present include: unexplained or aggravated aches and pains; sleep disturbance; feelings of hopelessness or helplessness; anxiety and worries; concentration problems; lack of motivation and energy; slowed movement and speech; irritability; loss of interest in socializing and hobbies; and neglecting personal care.

Both the number of symptoms and the level of impairment from these presenting symptoms are important features in determining whether a diagnosis of major depressive disorder is warranted.

There is a complicated relationship between depression and dementia in older patients. Dementia can be a risk factor for depression and depression can be a risk factor for dementia. Additionally, older patients with depression can have memory and concentration troubles without also having dementia. The cognitive problems seen in depression and dementia are different from each other. Persons with depression commonly report trouble concentrating and being motivated. Persons with dementia present with short-term memory loss and word finding difficulties, and often may not be aware of the cognitive challenges.

Depression is also common in patients with mild cognitive impairment (MCI), occurring in up to 1/3 of patients with MCI. It is therefore important to assess for depressive symptoms in an older patient presenting with early and generally mild signs of cognitive impairment.

It is also important to be aware that medical problems and medications can cause depression in older adults. Medical problems that can cause depression, either directly or as a psychological reaction to the illness, include Parkinson’s disease, stroke, heart disease, cancer, diabetes, thyroid disorders, vitamin B12 deficiency, dementia, lupus and multiple sclerosis.

Medications that can cause or worsen depression include: beta-blockers, sleeping medications, benzodiazepines, calcium-channel blockers, ulcer medications, steroids, cholesterol medications, and pain medications. While the mood-related side effects of prescription medication can affect anyone, older adults are more sensitive because of less efficient metabolism of medication.

The Geriatric Depression Scale is a validated screening tool for assessing for depression in older patients. It is a self-administered screen. A link and copy of the screening tool is included.

https://www.healthcare.uiowa.edu/igec/tools/depression/GDS.pdf

Next week’s e-weekly will address treatment of depression in older patients and how it is different than treatment of depression in younger adults.

Currently, six types of SSRIs are available for prescribing in the U.S.: fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), sertraline (Zoloft), and citalopram (Celexa), escitalopram (Lexapro). These drugs are subject to extensive oxidative metabolism in the liver. Because these antidepressants have a wide therapeutic index, inhibition or induction of their metabolism is unlikely to be of concern. However, SSRIs may cause a clinically relevant inhibition of CYP enzymes, and care must be exercised when an SSRI is being added to a multidrug regimen.

The potency of the SSRIs as inhibitors of the metabolism of the P450-P2-D6 varies and is reported in descending order of potency as paroxetine, fluoxetine, sertraline, citalopram, and fluvoxamine. Fluoxetine and paroxetine are more likely to cause P450 drug interactions than citalopram and sertraline, particularly in combination with medications metabolized by or inhibiting the cytochrome P450 2D6 isoenzyme (e.g., certain antidepressants, phenothiazines,antipsychotics type IC antiarrhythmics).

Drug interactions with clinical consequences usually involve combinations of an SSRI with other psychotropics, especially monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants. The interaction between MAOIs and SSRIs is the most important drug interaction limiting SSRI use. MAOI’s are infrequently prescribed due to other options available and the high risk of interaction with other drugs.

Sertraline, citalopram and escitalopram have the lowest potential for drug interactions among the SSRIs, and are to be preferred in patients on other drugs for general medical conditions or if consideration is given to adding an SSRI to other psychotropic medication.

With the drug interaction between fluoxetine and paroxetine and codeine-based pain medications, patients can experience reduced pain relief because the CYP2D6 inhibition will reduce conversion of codeine and related medications to the clinically effective metabolite (morphine, hydromorphone, oxymorphone).

It is also important to be aware of the risk of serotonin syndrome (increase heart rate, sweating, myoclonus, hyperthermia, and agitation) when combining certain medications with SSRIs because it can be life threatening. MAOIs are contraindicated with SSRIs for this and other reasons (the combination can also increase the risk of hypertensive crisis). Be cautious when combining SSRIs with Tramodol, Meperidine, St. John’s Wort (an herbal supplement used for mild depression) or dextromethorphan.

Some studies suggest that NSAIDs can reduce the efficacy of SSRI medications, although the overall data is inconclusive.  This combination may lead to increased gastrointestinal side effects.

It is our hope that this discussion is helpful for providers in the primary care setting as they are prescribing SSRIs in conjuction with other medications for their patients.

References:

Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). http://medicine.iupui.edu/clinpharm/ddis/table.aspx. Accessed 12/14/12.

Albers LJ, MD et al. Handbook of Psychiatric Drugs. 2008 Edition. University of California, Irvine.
https://www.uspharmacist.com/article/overview-of-drugdrug-interactions-with-ssris

This case leads nicely into a discussion about how to approach the treatment of an anxiety disorder. The first step is to determine a specific diagnosis and determine the level of impairment of the symptoms. If the impairment is mild-moderate, one could start with a therapy approach and determine if medication treatment is needed in the future.

If the impairment is moderate-severe, the standard of care is to begin therapy and medication treatment concurrently. Medication treatment should minimally involve an approach to treat the underlying anxiety – first line would be an SSRI medication.

Other options, if that doesn’t work, could include: SNRIs, Remeron, and Buspar. For many patients, it is helpful to initially prescribe an adjunctive medication to provide some relief for their anxiety while the primary medication is “kicking in”. These include: Buspar (which can be useful for the underlying anxiety management as well as for acute anxiety management), Vistaril, Propranolol, and the benzodiazepines.

Some providers may consider low doses of the atypical antipsychotics, but the concern about that practice is that the patient is still exposed to the possible metabolic side effects of that class of medications even at low doses, as many of the metabolic side effects of antipsychotics are dose-independent. For patients for whom they are effective, these adjunctive medications yield benefits more quickly than the traditional anti-anxiety medications.

In many cases, these medications can be tapered off once the base medication has fully “kicked in”.  Buspar is typically dosed 7.5 mg bid and increased by 5 mg every 2-3 days as tolerated up to 30 mg bid. Onset of action may take 2 weeks. It is relatively well tolerated with less cognitive impairment than benzodiazepines. Major side effects include dizziness, fatigue, and nausea. Vistaril is typically dosed 25-50 mg bid-tid on a prn basis. It is less sedating than Benadryl, therefore is better tolerated during the daytime. Propranolol is typically dosed 20-40 mg if used on a prn basis and 20 mg bid-tid titrated up to 40 mg bid-tid as tolerated and needed if used on a standing basis.

We hope this extensive discussion about this case and the thinking process that occurred in the background was helpful for other similar cases you might encounter in your practice.

Withdrawal from benzodiazepines is similar to withdrawal from alcohol—problems may include: feeling jittery, elevated blood pressure and heart rate, anxiety, insomnia and irritability. With more severe dependence, life-threatening effects like withdrawal seizures and delirium tremens may occur.  The longer a patient has been taking daily benzodiazepines, the longer the taper process should be. If a patient is using a short-acting benzodiazepine, the taper process is smoother and more successful if the patient is first transitioned to a long-acting benzodiazepine and then tapered off the long-acting medication.

Clonazepam is a good medication to use for tapering purposes, and it is helpful to dose it twice per day to establish a more even blood level and to give the patient psychological relief by taking the medication more frequently. Clonazepam has a 1:1 ratio dose equivalence to alprazolam (i.e. 1mg clonazepam = 1mg alprazolam) and a 1:2 ratio dose equivalence to lorazepam (i.e. 1 mg clonazepam = 2 mg lorazepam).  Care should be taken when the patient is taking high doses of a benzodiazepine medication and, in certain cases, dosing clonazepam more frequently during the tapering process may be more successful.

Diazepam can also be used in a similar fashion.  It has a 10:1 ratio dose equivalence to alprazolam and a 5:1 ratio dose equivalence to lorazepam.   Some advantages of diazepam are that it has an even longer half-life than clonazapam and is available in smaller effective doses, and so often allows a smoother taper with fewer withdrawal symptoms.  Some disadvantages are that diazepam has a relatively fast onset of action, causing many patients to experience an initial “high” when they take it, much like they may experience with shorter acting medications like alprazolam.  In addition, because of the extremely long half-life (up to 100 hours including its active metabolites), the drug can often accumulate, especially in elderly and patients with liver dysfunction.

Benzodiazepine Dose Equivalents

Depending on how long the patient has been taking daily benzodiazepines, one can reduce the dose by 10% of the current dose every 4-7 days. For example if a patient has been taking 4mg of alprazolam per day in split doses for five years, one option is to change the patient over to clonazepam 2mg BID and then reduce the dose initially by 0.5 mg per week, slowing down the taper to 0.25mg at a time towards the end. This relatively slow taper would take about 2 months to complete. If a patient is having withdrawal symptoms at any point during a taper, consider slowing down the taper.

In certain circumstances, it may be appropriate for a patient to be on a long-term daily benzodiazepine. One example is a patient who has tried non-benzodiazepine medications as adjunctive to a sub-therapeutic response to an SSRI, but they do not work as well as a benzodiazepine medication and the patient is not misusing it. In this clinical situation, the provider could consider switching from a short-acting medication to a longer-acting medication like clonazepam for long-term use, with a decreased risk for dependence.

If it is determined that a patient needs a long term PRN medication for anxiety and long-term benzodiazepine use is deemed problematic, consider alternatives including propranolol or hydroxyzine.  Buspirone (Buspar) can be effective for anxiety, but must be taken daily.

We hope that this step-by-step review on tapering benzodiazepines has been helpful. The important take home point is to not rush a taper, otherwise the patient might give up if he feels uncomfortable in any way or, more seriously, there could be dangerous consequences.

While the intention behind prescribing a benzodiazepine for a patient is to help alleviate emotional or physical pain for the patient, many times the use of the medication gets out of hand. Generally, benzodiazepines, which work to enhance GABA, are helpful in treating anxiety, insomnia, agitation, seizures, muscle spasms, alcohol withdrawal and as a premedication for medical or dental procedures.

Here we will focus on its uses for anxiety disorders. Benzodiazepines can be useful in the short-term for 1-3 months for a variety of anxiety disorders, like Generalized Anxiety Disorder, Social Anxiety Disorder and Panic Disorder, while waiting for the SSRI or other antidepressant/anti-anxiety medication to “kick in”. Benzodiazepines are not particularly helpful for depressive disorders or Obsessive-Compulsive Disorder. When starting a benzodiazepine, it is important to inform the patient that it is a short-term intervention, explaining the reason is to avoid long-term side effects, like tolerance, cognitive effects, and physiological and psychological dependence. When choosing a benzodiazepine, it is important to try to avoid short-acting medications like alprazolam if possible, because patients can develop a quick dependence to it because they can experience a “high” with it, and it has a short half-life, which can lead to rebound anxiety and can make it very difficult to taper off the medication. Also alprazolam is not a good medication for insomnia because of its short half-life. Patients may complain of being able to fall asleep okay but then waking up in the middle of the night. Alternative benzodiazepines to consider on a short-term basis for sleep include: clonazepam and temazepam.

If a patient is requiring adjunctive medication on a long-term basis for anxiety, consider non-benzodiazepine alternatives like diphenhydramine, hydroxyzine, propranolol, or buspirone. In the rare case when a long-term daily benzodiazepine is indicated, for example with Generalized Anxiety Disorder which responds well to a combination of SSRI + benzodiazepine, consider clonazepam. If a patient has infrequent panic attacks and a daily SSRI is not indicated, one could consider lorazepam on a prn basis. Lorazepam works well as a prn medication for acute anxiety and panic attacks, because it works relatively quickly but does not build up in the bloodstream. If one is prescribing long-term benzodiazepines, it is important to make sure the use is not slowly escalating, because that is a sign of tolerance and dependence.  Also, when helping a patient taper off a medication after he has been on it for some time, it is important to conduct a slow taper to avoid serious withdrawal symptoms, and to provide an alternative to treat the ongoing anxiety symptoms. Guidelines for appropriately tapering off benzodiazepines are discussed in another e-Weekly.

The goal of this article is to help the primary care provider be more informed about the decision to prescribe a benzodiazepine to a patient in a safe and helpful way, because this class of medication has a role in treatment for anxiety disorders and can be helpful when used appropriately. It is therefore useful to look at some guidelines for appropriate prescribing practices for this class of medications.

Treatment options include therapy or a combination of therapy and medication:

• For patients with mild-moderate symptoms, a therapy approach is preferred, with the option incorporate medication if the therapy is not effective.
• For patients with moderate-severe symptoms with significant impairment in daily functioning, it may be warranted to consider starting with a combination of medication and therapy.

The key is that therapy is the important component to treatment of anxiety disorders in pediatrics, with medication used as an adjunctive treatment when needed. Therapy to address anxiety can easily be tailored to work with very young patients and is very effective. Types of therapy used include: cognitive behavioral therapy, exposure response prevention therapy, and relaxation techniques, among others.

Medications used to treat anxiety fall into two general categories: medications that treat the underlying anxiety and prevent future symptomatology and medications that treat acute symptoms, such as a panic attack. Medications in the first category include the selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), mirtazipine, and buspirone.  The SSRIs are the first line agents. This class includes: fluoxetine, citalopram, escitalopram, sertraline, fluvoxamine, and paroxetine.  Although prompt relief may result, just as with treating depression, the medication may take 4-6 weeks to have full impact, so patience is important.  Also of note, often a higher dose may be needed to fully treat anxiety symptoms as compared to depressive symptoms.

The motto to “start low and go slow” remains relevant to limit activation and thereby increase anxiety during the titration process. So, for example if one is considering prescribing citalopram for anxiety for a 10 year-old patient, consider starting at 5 mg q-day for one week then 10 mg q-day for 1 week then 20 mg q-day and assessing the response. Some patients experience akathisia (internal feeling of restlessness), which can feel like a worsening of their anxiety, if the dose is titrated too quickly. Other side effects include sleep disturbance, GI upset and headache but most of these symptoms are dose related and will resolve over time.

The treatment of anxiety disorders in pediatric patients is mostly off label. Only fluoxetine (ages 7+), sertraline (ages 6+) and fluvoxamine (ages 8+) have FDA approval for treatment of obsessive-compulsive disorder (OCD).

When prescribing any antidepressant medication to treat anxiety, it is appropriate to review the FDA black box warning about the increased risk of spontaneous reporting of suicidal thoughts, even if the medication is not being prescribed to treat depression per se.

When prescribing a medication, it is standard practice to first use an SSRI.  If a patient has 2 or more adequate (in terms of dose and length of treatment) trials of SSRIs that are ineffective, one could consider an alternative, either an SNRI (venlafaxine or duloxetine) or mirtazapine, but consultation or referral to psychiatry would be advised in such situations. If there is some benefit from the SSRI, one could consider augmentation with mirtazapine or buspirone. The primary side effects to be concerned with mirtazapine include sedation and increased appetite. Buspirone has an onset of action of about 2 weeks. The primary side effects to be concerned with include: dizziness, fatigue and GI upset. Occasionally the atypical antipsychotics are considered as adjunctive treatment to treatment-resistant OCD.

Benzodiazepines, are rarely used in this population. Pediatric patients can have a paradoxical reaction to them and exhibit behavioral disinhibition. Other side effects include: physiological and psychological addiction, confusion, sedation and impaired fine motor coordination. If a medication to treat acute anxiety is needed, for example for a teenager who has very occasional panic attacks, one could consider hydroxyzine 25-50 mg on a prn basis, which is not associated with dependence. Side effects include: sleepiness, dizziness, and dry mouth.

When feasible, the use of rating scales can help in these efforts by documenting severity and monitoring clinical progress.   A good tool to review, the SCARED, is accessible at. http://www.pediatricbipolar.pitt.edu/content.asp?id=2333#3304 and a broader array of tools is listed at the following website http://www2.massgeneral.org/schoolpsychiatry/screening_anxiety.asp

Postpartum Blues: Symptoms of mood lability, irritability, interpersonal hypersensitivity and tearfulness are common in the postpartum period and are commonly known as the postpartum “blues”. The incidence is up to 75% and the symptoms typically arise and resolve within 7-14 days after the delivery.  The following conditions are of more concern:

Antepartum depression: The prevalence of depression during pregnancy ranges from 10-15% and it may persist into the first postpartum year. Depression during pregnancy is linked to birth complications like pre-eclampsia, low birth weight, premature delivery, and small for gestational age infants.

Postpartum depression: The prevalence of PPD is 10-15%. The postpartum year is one of the highest risk periods for first-onset depression for women with approximately 50% of women experiencing their first episode of depression during that time. In addition 25% of women with a history of Major Depressive Disorder will experience PPD and 50% of women who have had PPD will have a recurrence. The Edinburgh Postnatal Depression Scale and Postpartum Depression Screening Scale are useful screening tools. Women with PPD will typically present with prominent anxiety symptoms that involve distressing and intrusive thoughts about infant safety and feelings of guilt and inadequacy about mothering. Infants of depressed mothers have been found to be less responsive and more irritable than infants of non-depressed mothers. Infants of depressed mothers are also more likely to develop an insecure attachment because of (unintentional) maternal rejection of the baby. If one suspects PPD it is important to rule out medical conditions, like thyroid dysfunction and iron-deficiency anemia.

Postpartum psychosis: Postpartum psychosis is rare and occurs in 1-2 women per 1000. The onset is typically within 2 weeks of delivery. The psychotic symptoms typically accompany affective symptoms of depression and anxiety, rather than represent a psychotic first break. Postpartum psychosis is more common in women who have a history of bipolar disorder. In addition to auditory and visual hallucinations, patients may present with cognitive impairment, confusion, and olfactory and tactile hallucinations. Many mothers are distressed because they experience command hallucinations to harm their infants. If postpartum psychosis is suspected, it is important to seek immediate psychiatric attention and to consider psychiatric hospitalization. Antipsychotic medications are helpful, but it is more appropriate for the treatment to take place in a psychiatric hospital for the safety of mother and baby.

Treatment: Medication can be an important treatment for antepartum depression, if it is moderate-severe and/or not responding to non-medication approaches, like support groups and light therapy. SSRIs are the first line agents, in particular sertraline because of its relatively short half-life and availability of low doses (can be dosed as low as 12.5 mg per day). Paroxetine is pregnancy category D. There is evidence that it increases the risk of birth defects. There is also a possible connection between SSRI use in the 3rd trimester of pregnancy and development of persistent pulmonary hypertension of the newborn. While there are some reports of the risk of limb malformations with the tricyclic antidepressants, like amitriptyline and nortriptyline, these have not been confirmed. There have been reports of newborns experiencing temporary discontinuation symptoms at birth, including jitteriness and irritability when a woman is treated with antidepressants during pregnancy.

Currently, there are no FDA approved medications for PPD, mostly because it is difficult to conduct research. Of the SSRIs, sertraline and paroxetine are the least detectable in breast milk. Several case reports note an association between fluoxetine and citalopram use in lactating women and infant irritability, poor sleep, poor feeding, crying, and restlessness. This might be related to their relatively longer half-life. Other case reports have not noted any adverse effects in infants of mothers taking fluoxetine and citalopram.  If one is considering treating PPD with a medication, sertraline is a good first line agent because of its relatively short half-life and ability to dose in smaller doses, as low as 12.5 mg per day. If a woman is already on an antidepressant like fluoxetine with a good response, it is okay to continue with the medication and monitor closely for side effects in the mother and infant.

The important take home point for treating depression related to pregnancy is to first consider a non-medication treatment if that is a viable option. If it is determined medication is needed, it is important to have a careful discussion about the risks and benefits and to try to use the smallest possible dose for the shortest length of time.