How best to treat perinatal depression: nurses and midwives need to be alert to the possibility of, and signs and symptoms of perinatal depression, so it can be effectively treated.

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Perinatal depression refers to minor and major depression occurring during pregnancy or up to 12 months postpartum. (1) It is estimated that 13 percent of women experience postpartum depression, with similar numbers occurring during the antenatal period. (2) The result of untreated perinatal depression has a potential negative flow-on effect, not only for the mother and child, but also the wh[??]nau and society as a whole.

Part of the difficulty in identifying perinatal depression is due to the sometimes subtle overlap of signs and symptoms with the normal adjustment and stresses associated with becalming a mother. Therefore, symptoms of depression are sometimes dismissed as merely "postpartum blues", (2) which can affect up to 50 percent of mothers but tends to be transient and of short duration. (3) Detection of depression through screening requires vigilance on the part of all health professionals, particularly during the perinatal period. It is important during the screening process to identify vulnerability factors, including previous affective disorder, especially a history of perinatal depression. Being a single parent with limited social supports, women with current substance abuse issues, domestic violence and unplanned pregnancies are all significant vulnerability factors. (4)

In the past, pregnancy was erroneously considered to be a psychologically protective time. More recent evidence suggests women are, in fact, more likely to develop depression during their child-bearing years than at any other time in their lives. (4) Furthermore, studies have shown that pregnant women experience at least the same incidence of depression as non-pregnant women, ie seven to 15 percent in economically developed countries, while the rate could be as high as 25 percent in poorer regions such as Pakistan, Goa and Rio de Janeiro. (4) The exact aetiology of perinatal depression is not completely understood but the theories have evolved over the centuries, from Hipprocrate's postulation that it was the suppressed lochial discharge being transported to the brain that caused agitation and labile affect in pregnant women. There is no significant sex difference prior to adolescence in the incidence of depression. However, multiple epidemiological studies in both developed and developing countries have consistently found that, from puberty, women are twice as likely to experience depression compared with males. Further-to-this, as with most other pathologies, depression is known to be multifactorial, including a genetic predisposition coupled with environmental and psychosocial factors. (4)

Currently, the favoured theory for depression is the monoamine hypothesis, which proposes that depression is primarily a consequence of decreased (or relatively decreased) noradrenaline (NA) and/or serotonin (5HT) neurotransmitter activity in the brain. (5) However, despite some support through the efficacy of such medications as tricyclic antidepressants (TCA) and selective serotonin re-uptake inhibitors (SSRIs), this theory remains at best incomplete. The treatment of depression, particularly in pregnancy, remains controversial. However, much of the literature appears to agree that the treatment choice for perinatal depression is based on the severity of presenting symptoms. Therefore, once diagnosis is made, treatment options need to be explored with the mother (and significant others), being ever mindful of the risk versus benefit ratio. (4,6,7)

Studies investigating the causation of postnatal depression have identified a number of risk factors, including the sudden decline in gonadal and stress steroid hormones within the first 48 hours postpartum. (3,4) It has been suggested that women susceptible to postnatal depression have an abnormal sensitivity to the hormonal milieu that precedes and follows child birth. (3) Also, from a physiological perspective, pregnancy can directly impact on mood, possibly due to the increasing levels of female sex hormones, corticosteroids and changes in thyroid function that occur during gestation. (4,8)

Pre-term delivery

The evidence is conflicting but it appears that untreated depression during the perinatal period can result in pre-term delivery and also increases the likelihood that women may smoke and drink alcohol, putting the baby at increased risk of low birth weight and deformity. (4) Other important considerations include the potential for the depression to become treatment-resistant, causing long-term morbidity.

Furthermore, despite the risk of suicide being relatively rare during the perinatal period, it is still the leading cause of maternal death in developed countries. (9) However, pregnancy is a known protective factor, as evidenced by the rate of suicide reducing from 3.4 per 100,000 in non-pregnant UK women to 2 per 100,000 in pregnant women. (4,9) Once identified and treated, perinatal depression has a good prognosis, with most cases resolving in three to six months, but relapse in the future, with or without pregnancy, is common. (3,4)

Impact of untreated depression

Untreated major depression has a negative impact on the mother, on her relationships, and is also associated with adverse outcomes for the infant, secondary to poor mother-baby bonding and a potentially unfavourable intrauterine environment due to maternal self-neglect. This in turn, can negatively affect the child's emotional and physical well-being, as well as subsequent development. However, as stated, major depression is a significant cause of morbidity in pregnant and post-partum women. Therefore, as health professionals, we need to identify those most at risk and determine the treatment, according to the degree of depression. But even after treatment has been initiated in pregnant and lactating women, it is paramount the risk versus benefit analysis be regularly revisited and reassessed to ensure the benefits always outweigh the risks for both mother and child. (4,6,7,10)

Mild to moderate depression

For mild to moderate depression, the first line of treatment is psychotherapy which can take the form of either interpersonal therapy or cognitive behavioural therapy. Interpersonal therapy aims at improving communication, coping strategies and establishing social interventions, whereas cognitive behavioural therapy focuses on reducing the perpetuating negative-self thought processes some women experience. Antenatal groups also appear to reduce the incidence of post-partum depression, most Likely because they provide a supportive affirming environment for mothers and families. (4,10,11,12) Unfortunately, "talk therapies" are not funded by the New Zealand health system, therefore, cost may be prohibitive to some women, as might the time commitment. Hence pharmacotherapy, which is subsidised and doesn't require an investment of time, is used more frequently.

Bright Light therapy has also shown promise as a therapeutic strategy, particularly in women with a history of seasonal affective disorder (needs at Least 30 minutes/day). (11)

Antidepressant pharmacotherapy, for moderate to major depression, aims to increase the amount of serotonin and/or noradrenaline at post-synaptic receptor sites and this, in turn, improves mood and hence Lends support to the monoamine hypothesis of depression. (4)

It is important to note that:

* ALL antidepressants, because they are lipophilic (ie, very fat soluble), readily cross the placental barrier and also appear in varying amounts in the breast milk.

* Because all antidepressants are lipophilic and therefore can readily permeate the blood-brain-barrier of the fetus, they can induce a serotonin-withdrawal syndrome in the neonate. (10)

* No randomised controlled prospective trials of antidepressant therapy have ever been performed on pregnant women (and rightly so!), hence the evidence available tends to be anecdotal and retrospective.

Tricyclic antidepressants are the most dangerous antidepressants in overdose, due to their potential for cardiotoxicity, but they are also considered to be the most favourable in pregnancy and Lactation because they have fewer adverse impacts on the newborn, compared to the other pharmacotherapies.

A study of the effects of mainly SSRIs on the foetus and neonates found that fluoxetine did not appear to cause foetal deformities. However, paroxetine has been linked to foetal abnormalities. (6) SSRIs, although generally well tolerated by pregnant women, should gradually be discontinued, as abrupt cessation can induce a SSRI withdrawal syndrome. This can include dizziness, anxiety, sleep disturbances, agitation, tremor, nausea, sweating and confusion. (13) However, it is not only the mother who experiences withdrawal from medication, as most drugs that enter the maternal system cross the placental barrier or are secreted in breast milk. Therefore, neonates, because they are exposed to SSRIs via their mother, are also at risk of SSRI-withdrawal syndrome. These effects, as with adults, appear to be self-limiting. (6,7)

Signs of SSRI-withdrawal in the newborn include irritability, tremors and convulsions. While SSRI-withdrawal syndromes are the most widely reported, TCA cessation is also implicated in serotonin-induced withdrawal. (7)

The role of Omega-3

Omega-3 fatty acid supplementation is showing promise as a positive mood enhancer. Studies have shown that lowered levels of Omega-3 fatty acids are associated with depression, while regular intake of these fatty acids is positively correlated with low levels of depression in the general population. (14,15) Omega-3 fatty acid levels are depleted in pregnancy, which may therefore increase risk for maternal depression. It has also been theorised that Omega-3 fatty acids may reduce the risk of pre-term delivery and preeclampsia, although the mechanism for this is not fully understood. Moreover, Omega-3 fatty acid is an important factor in foetal neurodevelopment, so supplementation could impact positively on the infant's neurological development. (16,17,18,19)

However, one of the richest sources of Omega-3 is cod-liver oil, which should be used judiciously in pregnancy due to the high levels of retinoic acid (the synthetic form of vitamin A), as this has been shown to cause birth defects. Also, Omega-3 alters plate/et function, therefore should be used with caution in those women taking anticoagulants such as Low-close aspirin or clexane. (16,17,18)

Perinatal depression is very common but needs to be detected early, as untreated or under-treated depression seriously affects the well-being of both the mother and child. In mild to moderate forms of depression, psychotherapy is a very effective first-Line treatment, as are some other non-pharmacological strategies such as bright Light therapy. Omega-3 fatty acid Literature shows promise in providing prophylaxis and possibly treatment for perinatal depression, while concomitantly improving health outcomes for the infant.

Antidepressant medication for more severe depression appears to be relatively safe. However, all medications reach the infant in varying quantities and this needs to be considered when prescribing or administering these drugs.

There is evidence to support early screening for depression (perhaps at the antenatal booking). Screening involves identifying signs and symptoms of depression, along with potential vulnerability factors. It is also essential to educate mothers about the negative consequences of untreated or under-treated depression on the health and development of their infant. This, in turn, may encourage mothers to seek help at an earlier stage of their depression.

This article is dedicated to the memory of Sheryl Butcher who tragically died early last year. Sheryl was a mental health colleague who "moved mountains", not just in the nursing world, but in many people's lives.

References

(1) Freeman, M.P. (2006) Omega-3 fatty acids and perinatal depression: A review of the literature and recommendations for future research. Prostaglandins, Leukotrienes and Essential Fatty Adds; 75, 291-297.

(2) Rees, A-M., Austin, M-P. & and Parker, G. (2005) Role of omega-3 Fatty acids as a treatment for depression in the perinatal period. Australian and New Zealand Journal of Psychiatry; 39: 4, 274-280.

(3) Lusskin, S., PUnkia T.M. & Habib, S.M, (2007) Perinatal Depression: Hiding in Plain Sight. The Canadian Journal of Psychiatry; 52 8.

(4) O'Keane V & Marsh M. (2007) Depression during pregnancy. British Medical Journal; 334, 1003-3005.

(5) Hindmarch, I. (2002) Beyond the monoamine hypothesis: mechanisms, molecules and methods. European Psychiatry; 17, supplement 3, 294-299.

(6) Gentile S. (2005) The safety of newer antidepressants in pregnancy and breastfeeding, Drug Safety; 28: 2, 137-52.

(7) Sanz EJ, De-Las-Cuevas C, Kiuru A, Bate A, Edwards R. (2005) Selective serotonin reuptake inhibitors in pregnant women and neonatal withdrawal syndrome: a database analysis. The Lancet,;365: 9458, 482-7.

(8) Harris, B. (1994) Biological and hormonal aspects of pospartum depressed mood: Working towards strategies for prophylaxis and treatment. British Journal of Psychiatry; 164, 288-292.

(9) Oates M. (2003) Suicide: the Leading cause of maternal death. British Journal of Psychiatry; 18: 3, 279-281.

(10) National Institute for Clinical Excellence (2007) Antenatal and postnatal mental health: Clinical management and service guidance, Clinical Guideline No. 47. London, National Institute for Clinical Excellence.

(11) Jorm, A., Christensen, H., Griffiths, K. & Rodgers, B. (2002) Effectiveness of complementary and self-help treatments for depression. Med J Aust; 176.

(12) Pearlstein, T., Diaz, S., Howard, M., Zlotnick, C. & Neeta, J. (1999) Dysphoric Disorders in Women: A Case of Perinatal Depression: Medscape General Medicine; 1: 3. 1999. http://www.medscape.com/viewarticle/408888_print.

(13) Nordeng, H., Lindemann, R., Perminov, K.V. & Reikvam, A. (2001) Neonatal withdrawal syndrome after in utero exposure to selective serotonin reuptake inhibitors. Acta Paediatrica; 90: 3, 288-291.

(14) National Institute of Mental Health: http://www.nimh.nih.gov/health/ publications/suicide-in-the-us-statistics-and-prevention.shtml. Retrieved 06/06/08.

(15) Parker, G., Gibson, N.A., Brotchie, H., Heruc, G., Rees, A-M., & Dusan Hadzi-Pavlovic, D. (2006) Omega-3 Fatty Acids and Mood Disorders. American Journal of Psychiatry; 163, 969-978.

(16) Gallagher S. (2004) Omega 3 oils and pregnancy. Midwifery Today International Midwife; 69, 26-31.

(17) Haag M. (2003) Essential Fatty Acids and the Brain. Canadian Journal of Psychiatry; 48: 3.

(18) Raeder, M., Steen, V., Vollset, S., and Bjelland, I. (2007) Associations between cod river oil use and symptoms of depression: the Hordaland Health Study. 3 Affect Disord; 101: 1-3, 245-9.

(19) Robert K. McNamara, R.K. & Carlson, S. E. (2006) Role of omega-3 fatty acids in brain development and function: Potential implications for the pathogenesis and prevention of psychopathology. Prostaglandins, Leukotrienes and Essential Fatty Adds; 75, 329-349.

Jane Nugent, EN, RN, is studying medicine at Otago University. She is a trainee intern and her particular area of expertise is mental health. She also has a passion for teaching. This article has been developed from a presentation she gave to NZNO's EN conference in Christchurch in late May.