Psychopharmacology and Pregnancy: Treatment Efficacy, Risks, and Guidelines 2014

11. Borderline Personality Disorder and the Eating Disorders in the Perinatal Period

Gaynor Blankley , Josephine Power1 and Andrew Chanen2, 3

(1)

Mercy Hospital for Women, Heidelberg, Australia

(2)

Orygen Youth Health Research Centre, Centre for Youth Mental Health, The University of Melbourne, Melbourne, Australia

(3)

Orygen Youth Health Clinical Program, Northwestern Mental Health, Melbourne, Australia

Gaynor Blankley

Email: gblankley@mercy.com.au

11.1 Borderline Personality Disorder

11.1.1 Brief Overview of Borderline Personality Disorder

11.1.2 Natural History of BPD in the Perinatal Period

11.1.3 Summary of Evidence for Treatment Improving the Course and Outcome of BPD

11.1.4 Risks of Not Treating BPD

11.1.5 Specific Pharmacological Treatment Options for BPD

11.1.6 Management Recommendations for BPD in the Perinatal Period

11.2 Eating Disorders

11.2.1 Brief Overview of the Key Features of the Eating Disorders

11.2.2 Natural History of Eating Disorders in the Perinatal Period

11.2.3 Summary of Evidence of Treatment Improving Eating Disorders

11.2.4 Risks of Not Treating Eating Disorders in Pregnancy

11.2.5 Specific Pharmacological Treatment Options for the Management of Eating Disorders

11.2.6 Management Recommendations for the Eating Disorders during the Perinatal Period

References

Abstract

Borderline Personality Disorder and the Eating Disorders are severe disorders that are associated with significant psychiatric and physical co-morbidity. Yet, there is limited research to draw upon regarding the natural history and risks associated with these disorders across pregnancy and the postnatal period. The risks to the mother and the infant of these conditions and their treatments require careful consideration and patients require individualised clinical care.

Keywords

Borderline Personality DisorderEating disordersPerinatalPsychopharmacological management

11.1 Borderline Personality Disorder

11.1.1 Brief Overview of Borderline Personality Disorder

Borderline Personality Disorder (BPD) is a severe mental disorder that is characterised by a pervasive pattern of impulsivity, emotional instability, interpersonal dysfunction, and disturbed self-image (Leichsenring et al. 2011), affecting 0.7–2.7 % of the general adult population (Coid et al. 2006; Trull et al. 2010), 9.3–22.5 % of psychiatric outpatients, and in some settings over 40 % of inpatients (Zimmerman et al. 2008). The outcome for BPD in American adults is now reliably characterised by attenuation of diagnostic criteria over time, with severe and continuing functional disability across a broad range of domains that is comparable to, or greater than, that associated with many mental state disorders (Gunderson et al. 2011; Zanarini et al. 2010). Patients with BPD also have continuing high rates of co-occurring conditions (Zanarini et al. 2004a), health service utilisation (Zanarini et al. 2004b; Horz et al 2010; Sansone et al. 2011), and a suicide rate of around 8 % (Pompili et al. 2005). Although effective interventions exist for adults with BPD (e.g. Bateman and Fonagy 2009; Giesen-Bloo et al. 2006; Linehan et al. 2006), the overall outcomes from such interventions are modest and their availability is limited.

BPD appears to arise from the interaction of biological and environmental risk and protective factors, but the developmental pathways remain unclear. Findings from prospective longitudinal studies of community samples and studies of young people with borderline pathology suggest a variety of genetic, neurobiological, psychopathological, and environmental risk factors (Chanen and Kaess 2012). However, these risk factors are common to other mental disorders and are generally not specific for BPD (Chanen and McCutcheon 2013).

Temperamental and mental state abnormalities that resemble aspects of the BPD phenotype emerge in childhood and adolescence and presage the BPD syndrome in adolescence or adulthood (Chanen and McCutcheon 2013). However, it is usually first identifiable during adolescence to early adulthood, which corresponds to the years when women are most fertile (De Genna et al. 2012).

11.1.2 Natural History of BPD in the Perinatal Period

Individuals with BPD are more likely to experience exacerbation of symptoms at times of interpersonal stress (Zanarini et al. 1997). Given that pregnancy and early parenthood are times of transition and for many a developmental crises (Cohen and Slade 2000), it could be expected that women with BPD might be more vulnerable to an exacerbation of mental health issues during these times. However, there are few studies that describe or quantify the mental health, obstetric, and early infant outcomes for women with this diagnosis across pregnancy and the postpartum period. There is some evidence that women with BPD might be less likely to have used contraception and to have teenage and unplanned pregnancies (Chen et al. 2007; De Genna et al. 20112012) and sexually transmitted infections (Chanen et al. 2007): factors that might contribute to an exacerbation of symptoms in the perinatal period.

Developmental trauma, including childhood sexual abuse, is common among women with BPD (Zanarini et al. 1997), and childbirth and parenting may reactivate past traumas for this group of women, such that they might be unable to focus and think about their new baby and its experiences and needs (Newman 2008). Shame and guilt-proneness is generally high among women with BPD (Rusch et al. 2007). These women frequently describe feelings such as anxiety, shame, ambivalence, loss of identity, depression, anger, and emptiness in the perinatal period and might struggle with their parenting, feel less satisfied, experience higher levels of parenting stress, and have difficulty with affect regulation and recognition of their infant’s cues (Newman and Stevenson 2005; Newman et al. 2007).

Currently there is only one guideline published for the management of BPD in the perinatal period (Government of South Australia, Maternity Care Guidelines 2006), which is based on clinical opinion, with no data available on the evaluation of its implementation. Issues described included the need to be aware of the risks for both mother and foetus, frequent requests for early delivery and issues associated with polypharmacy. However, the guidelines are for the management of patients with BPD as they access care within the maternity care setting and are not comprehensive guidelines for the management of BPD in the perinatal period.

11.1.3 Summary of Evidence for Treatment Improving the Course and Outcome of BPD

The most recently published national guidelines for BPD are the Clinical Practice Guidelines for the Management of BPD, developed by the Australian Government’s National Health and Medical Research Council (NHMRC) (National Health and Medical Research Council 2012). This systematic literature review supports interventions for people with BPD and found that the characteristics of effective treatments involved treatment that was founded on an explicit theory of BPD, delivered by an appropriately trained and supervised therapist regularly over a planned treatment course, whilst attending to the patient’s emotional state and focused on achieving change and the relationship between the clinician and the patient. It was further recommended that pharmacotherapy should not be routinely added to psychological interventions. They concluded that there is insufficient evidence to support that any one specific treatment has advantages over another in improving the outcomes for patients with BPD in the long term and that further research is required to clarify this.

11.1.4 Risks of Not Treating BPD

Whist there is evidence that a diagnosis of BPD carries significant risks for physical and psychiatric co-morbidity, including Substance Use Disorders (Zanarini et al. 2004b), risk of impulsive and risk taking behaviour, deliberate self-harm, suicide attempts, and suicide, all of which have known risks for mothers and infants across the perinatal period, there is no evidence currently that this diagnosis carries specific risks for the pregnancy or the foetus. However, there are risks associated with treating BPD, including the risks of polypharmacy, which in pregnancy would expose the unborn infant unnecessarily to medications that are unlikely to be helpful to the mother.

11.1.5 Specific Pharmacological Treatment Options for BPD

Whilst there is no specific pharmacological treatment for BPD, polypharmacy is common (Zanarini et al. 2004ab). The NH&MRC (2012) reviewed the evidence basis for the pharmacological treatments for BPD including a meta-analysis of RCTs for pharmacotherapy versus placebo. They found the studies to be difficult to interpret because of the small sample sizes and the different outcome measures across studies. They concluded that pharmacotherapy did not alter the course or outcome of BPD. Furthermore, they determined that specific recommendations could not be made about the use of a particular medication to target specific symptoms when less than 3 RCTs were available for the meta-analysis.

They found that SSRIs may have some effect on mood symptoms, but that they also needed to be prescribed with caution because overall they were less efficacious in treating depression in patients with BPD and they have potentially harmful side effects such as an increase in suicidal ideation, especially in patients under 25 years of age. Lithium was reviewed in four studies with findings that it had some benefits for mood symptoms and anger. Sodium valproate was found to help with mood symptoms, anger, aggression, and impulsivity, and lamotrigine and topiramate were found to have some benefits for impulsivity, mood lability, and anger. Antipsychotic medications were found to have been prescribed for cognitive and perceptual abnormalities, dysphoria, anxiety, anger, and depressive symptoms. Olanzapine was found to provide some benefits for the management of hostility, irritability, general psychopathology, and general functioning. Ariprazole was found in one study to be beneficial for anger, hostility, irritability, anxiety, depression, and interpersonal functioning, and quetiapine has been reported to provide benefits for affective symptoms and impulsivity.

However, it must be stressed that the findings from these studies are insufficient to recommend the routine or common use of psychotropic medications in BPD. Moreover, many of the agents studied pose significant risks to the developing foetus. The findings must be replicated before any of these medications are adopted and prescribed as ‘mainstay’ treatments.

The NHMRC (2012) recommendations are summarised below.

There is no evidence available to support the prescribing of benzodiazepines to patients with BPD, and as a class they are associated with issues of abuse and dependence, and in pregnancy they should be prescribed sparingly.

11.1.5.1 Prescribing for BPD in pregnancy

Given the lack of data to support the effectiveness of pharmacological treatments in patients with BPD clinicians should have an even higher threshold for prescribing during pregnancy and wherever possible avoided. There is insufficient evidence available to develop concise prescribing guidelines for patients with BPD. In addition, prescribing medication may result in a missed opportunity to engage the patient in an effective structured psychosocial treatment plan. If a decision is made to prescribe medications during pregnancy the risks of individual medications, both known and unknown, including teratogenic risks, risks during pregnancy, delivery and the postpartum period, risks for the newborn, and longer term risks for neurobehavioral development should be clearly discussed with the patient and documented.

11.1.6 Management Recommendations for BPD in the Perinatal Period

Management of BPD requires structured psychosocial interventions that are based upon a theory of BPD and delivered by appropriately trained and supervised clinical staff. This might occur intermittently or on a continuous basis, depending upon the patient’s needs. During the perinatal period, it is appropriate to follow recommendations of the NH&MRC’s recent guidelines (2012). Wherever possible management should include:

11.1.6.1 Preconception: Sexual and Reproductive Health

Sexual and reproductive health should be a focus of management for all women of childbearing age with BPD. As already noted, impulsivity may result in unsafe sex and unplanned pregnancies, many of which may remain undiagnosed well into the first trimester (Chanen et al. 2007; De Genna et al. 20112012; Chen et al. 2007; Henshaw and Protti 2010). Thus, it is ideal for female patients in their reproductive years to be referred to their general practitioner or family planning clinic for consultation regarding the management of their sexual and reproductive health and the risks associated with unplanned or planned pregnancy. Consideration should be given to a second opinion from a specialist perinatal psychiatrist when psychotropic medications are prescribed in pregnancy. Specific liaison with the patient’s general practitioner or gynaecologist about the patient’s anxieties accessing health care may be required.

If a woman with a pre-existing diagnosis of BPD is planning a pregnancy, then a discussion about the impact of pregnancy and parenting on her mental health and the impact that treatments may have on her unborn infant should be undertaken. Management options and their associated risks and benefits should also be discussed. Wherever possible, the partner/father of the baby should be involved in discussions.

Pregnancy may be the first time a patient presents for mental health assessment and therefore assessment and management may only begin at this time.

11.1.6.2 Management During Pregnancy

A comprehensive clinical assessment, diagnosis, and formulation including co-morbid psychiatric diagnoses, co-existing medical and obstetric conditions, assessment of the foetus, and the relationship developing between the mother and her infant should be undertaken during pregnancy. Management planning should include an understanding of the effect of pregnancy and parenting on the woman’s mental illness and its treatment and the impact that the illness and its treatment will have on the pregnancy, foetus, and neonate. The particular physical, psychological, social, and relationship changes associated with pregnancy need to be considered (Galbally et al. 2013). Particular attention should be paid to how anxiety, ‘affective storms’, impulsivity, suicidality, idealisation, and/or devaluation of the unborn infant as well as staff, family, and friends caring for her may affect maternal and infant care and how this can be best managed. The antenatal period may provide a good opportunity, and possibly an incentive, to provide supportive psychoeducation and preparatory psychotherapy for parenthood.

In more severe BPD, multiple health providers and agencies may be involved in patient care and there is a risk that there may be a lack of coordination between care providers. Staff may experience difficulties caring for patients with BPD, including powerful countertransference feelings, which might affect care decisions. It is recommended that a management plan be developed in collaboration with the patient and as many health professionals as possible, relevant to the patient’s care and that particular attention be paid to communication among these professionals.

The following specific issues as they arise within the obstetric care setting may require attention:

As pregnancy progresses, management plans should be reviewed, updated (in collaboration with the patient), and circulated to all relevant clinicians and kept in the patient’s obstetric file.

Throughout pregnancy, attention also needs to be given to the developing foetus. Specific issues include:

1.

2.

3.

4.

Longer term treatment options, as outlined in the NHMRC guidelines, should also be discussed with the patient, and wherever possible, liaison between health-care providers involved in the patients’ longer term care and those involved in perinatal care should occur.

11.2 Eating Disorders

11.2.1 Brief Overview of the Key Features of the Eating Disorders

Eating disorders (EDs) are severe psychiatric illnesses that are most common in women of childbearing age. Anorexia nervosa (AN) and bulimia nervosa (BN) are the two eating disorders specified in the DSM-IV; however, the most common diagnosis in clinical and community samples is the residual category ‘eating disorder not otherwise specified’ (EDNOS) (Smink et al. 2012). EDNOS is a poorly defined group in the DSM-IV that includes partial syndromes of AN and/or BN, purging disorder, and binge eating disorder (BED). The DSM-V contains a revised ED section with broadening of existing criteria and includes BED as a separate diagnosis (APA 2013), but hitherto research has been hampered by a lack of clear or consensus criteria. All EDs have serious physical, emotional, psychological, and social sequelae that greatly impact on pregnancy, transition to motherhood, and parenting.

AN mostly affects young women with 40 % of incident cases being girls aged 15–19 (Smink et al. 2012). It has a prevalence of 1.9–4.3 % depending on the population studied and criteria used (Wade et al. 2006). It is characterised by an intense fear of weight gain, disordered body image, and refusal to maintain normal weight through rigorous exercise, restricted eating, and sometimes bingeing and purging. Amenorrhea, either primary or secondary, may be present as a consequence of starvation and hormonal imbalance.

Psychiatric co-morbidities are common in AN, with depression present in 65 %, social phobia in 34 %, and OCD in 26 %. Medical co-morbidities are almost ubiquitous, with every major organ system potentially affected. AN has the highest rate of mortality among all mental disorders (Harris and Barraclough 1998) with a crude mortality rate of 0.51 % per year. In one study, one in five deaths was due to suicide (Arcelus et al. 2011). The natural history is of recovery in a third of patients, chronic relapsing and remitting illness in another third, and severe illness leading to premature death for the remainder.

BN has a mean age of onset at 17 years (Hoek and van Hoeken 2003) and a point prevalence of 1 % in young females (Keski-Rahkonen et al. 2009). It is characterised by episodes of binge eating during which there is a sense of loss of control over the amount and type of food eaten. Binges are typically followed by feelings of self-loathing, guilt, and disgust, with consequent frantic compensatory behaviour to reduce the amount of weight gained by purging or using laxatives, diuretics, or enemas. Despite this, weight may be normal. Psychiatric co-morbidities are common with substance abuse and depression being found most frequently. The medical consequences include hormonal, oral, and gastrointestinal complications and electrolyte imbalances that may lead to cardiac arrhythmias and potentially death. Relapse–remission is the most common pattern of illness, but overall the prognosis is better than for AN. Remission rates of 74 % have been quoted, but this same sample showed 42 % relapse over the study period (Grilo et al. 2007).

Point prevalence of EDNOS is difficult to establish as there has been no consistent criteria for clinical diagnosis and research. BED, in which sufferers engage in binges with associated abnormal attitudes to food (APA 2013), has a lifetime prevalence of up to 10 % (Machado et al. 2007). Patients are usually obese, which leads to a range of other medical problems such as metabolic syndrome and cardiovascular disease. Studies suggest that it has a similar relapsing–remitting course to BN (Grilo et al. 2007).

11.2.2 Natural History of Eating Disorders in the Perinatal Period

Despite the significance of EDs in women of childbearing age, there has been limited research interest until recently. Early studies suggested that women with ED rarely became pregnant due to nutritional deficiency and hormone imbalance (Weinfeld et al. 1977). However, despite common menstrual irregularities, it would appear that fertility rates do not differ significantly from the general population (Kohmura et al. 1986; Bulik et al. 1999; Crow et al. 2002). In addition, women with AN may be more likely to have unplanned pregnancies (Bulik et al. 2010), potentially due to poor contraceptive advice based on the assumption of infertility. BN also appears to have little impact on later fertility (Crow et al. 2002). Studies are lacking in BED and fertility, but obesity is associated with reduced ability to conceive.

Most studies in this area are limited by being based on retrospective reports from clinical samples. The Norwegian Mother and Child Cohort Study is a large prospective population-based birth cohort study of 10,000 women (Bulik et al. 2007). It found that 0.1 % pregnant women met broad criteria for AN prior to pregnancy, 0.7 % reported BN, and 3.5 % reported BED. Rates of remission during pregnancy varied: 35 % BN remitted (higher in purging subtype) and 39 % BED with no data available for AN. Other studies have found remission of ED symptoms during pregnancy (Lacey and Smith 1987; Morgan et al. 1999), but only 23 % remain well postpartum and preoccupation with weight may recur acutely. Some women may deteriorate in comparison with pre-pregnancy symptoms (Morgan et al. 1999).

There is an increased rate of anxiety and depression in women with ED who become pregnant and fear of weight gain may lead to increased symptoms in pregnancy. When ED symptoms continue during pregnancy there is a higher risk of complications at all stages and into the postpartum period (Abraham 1998; Conti et al. 1998). A history of BN, active or not, raises the risk of hyperemesis, small head circumference, and SGA (Kouba et al. 2005), and active BN has been associated with lower birth weight, low Apgars, breech presentation, congenital malformations, smaller head circumference, miscarriage, gestational diabetes, and postpartum depression (Lacey and Smith 1987; Kouba et al. 2005; Mitchell et al. 1991; Franko et al. 2001; Morgan et al. 2006). Women with AN have higher rates of miscarriage and caesarean delivery (Bulik et al. 1999; Franko et al. 2001; Mitchell et al. 1991). Low pre-pregnancy weight and poor weight gain in pregnancy are associated with adverse outcomes such as stillbirth, IUGR, low Apgars, and breech presentation (Arbuckle and Sherman 1989; Wen et al. 1990), as well as congenital malformations such as cleft lip and palate. Intra-uterine growth retardation (IUGR) is itself associated with significant sequelae for the infant; in the short term there is a greater risk of neonatal asphyxia and neonatal adaptive problems such as meconium aspiration, pulmonary hypertension, failure of glucose regulation, and temperature instability necessitating increased medical attention and intervention (Rosenberg 2008). As the infant develops, there is an increased incidence of chronic lung disease, necrotising enterocolitis, and retinopathy with ongoing failure to thrive. Further-reaching consequences are still being investigated, but links have been established with IUGR and breast cancer risk and cardiovascular disease in adulthood (Kok et al. 1998; Michels et al. 1996; Rich-Edwards et al. 1997).

Women with BED and consequent obesity are at higher risk of miscarriage, thromboembolism, and pre-eclampsia (Yu et al. 2006). Obesity in pregnancy is a risk factor for gestational diabetes (Metzger et al. 2007). This in turn increases the risk of an infant being large for gestational age that has been linked to metabolic syndrome in childhood and future obesity (Boney et al. 2005). There is elevated perinatal mortality (Yu et al. 2006). Specific studies in this area are lacking.

Postpartum, the risk of depression is greater in women with ED (Abraham 1998). Even without depression, the physical disruption of ED symptoms may affect capacity to parent and interact with the infant. Ongoing ED symptoms may also increase the likelihood of marital instability and conflict, which further compromises the well-being of the child.

11.2.3 Summary of Evidence of Treatment Improving Eating Disorders

The 2006 APA guidelines recommend a combined approach including nutritional rehabilitation and psychological support for the management of AN and state that prescribing SSRIs to patients offers no advantage. For patients with severe resistance to weight gain the atypical antipsychotics may be useful for those with severe obsessional thinking and pro-motility agents may be useful for the treatment of abdominal pain and bloating. The SSRIs are recommended for the treatment of BN and BED.

Psychological interventions for EDs have been recommended for AN, BN, and EDNOS with Cognitive Behaviour Therapy (CBT) focusing on cognitive distortions and negative thinking patterns around body image and Interpersonal Therapy (IPT) focusing on addressing interpersonal issues that are associated with ED symptoms rather than the symptoms themselves.

Yager et al. (2012) reviewed 342 articles that related to the evidence available supporting the key recommendations of the APA 2006 guidelines for the treatment of eating disorders. They found that there were few randomised controlled trials (RCTs) and that the studies available suffered from a range of methodological issues, such as small sample sizes, recruitment and retention issues, and poorly defined predictors of recovery across the different studies. However, their review supported hospital-based treatment in order to provide either tube feeding or nutritional rehabilitation in severely underweight patients with AN, but not in normal weight patients.

Whilst the theoretical underpinnings for psychological interventions appear sound, Yager et al. (2012) found that the research on psychotherapy for individuals with EDs was limited, with the methodology and outcome measures of studies being variable. They found some evidence that CBT and IPT are efficacious in the treatment of BN and that ‘guided self-help’ was more effective than being on a ‘wait list’ for treatment. Overall, they concluded that larger studies with more robust methodologies are required to substantiate evidence for the efficacy of psychotherapeutic treatments commonly prescribed.

11.2.4 Risks of Not Treating Eating Disorders in Pregnancy

Pregnancy is a time of great nutritional and metabolic strain on a woman’s body, as well as a period of potentially intense emotional upheaval. With compromise of physical or emotional reserves, there may be serious consequences for both mother and infant if EDs are left untreated.

During pregnancy, the developing foetus derives all nutrition from the mother. If stores of energy in the form of carbohydrates, protein, and fat are inadequate, or reserves of vitamins and minerals are low, they will be drained to support the growing foetus. Without adequate nutritional replacement, malnutrition is a real risk and this in turn may lead to physical illness in the mother.

The required weight gain in pregnancy can be extremely threatening for women who have been preoccupied with their weight and this may lead to avoidance of medical and obstetric care. Some women may be able to view the weight gain as a necessary sacrifice, but others can enter a crisis of their eating symptoms or develop serious mood disorder symptoms.

Women with untreated AN tend to have low weight gain during pregnancy and are at higher risk of having a baby with IUGR and its consequences. If purging is ongoing, the risks of dehydration, electrolyte imbalance, and cardiac arrhythmias are exacerbated during pregnancy. Those women who are overweight are at increased risk of elevated blood pressure and gestational diabetes.

In the postpartum period, untreated ED symptoms may escalate in response to the physical changes of pregnancy or as a means of coping with loss of control and other difficulties faced during the transition to motherhood. These symptoms can be a distraction for the mother and reduce her availability and responsiveness to her infant. This may lead to a failure of the attachment and bonding process, with potentially disastrous, long-lasting effects. Furthermore, women with a history of ED are more likely to experience difficulties in feeding their babies (Park et al. 2003).

11.2.5 Specific Pharmacological Treatment Options for the Management of Eating Disorders

Flament et al. (2012) reviewed the evidence for the efficacy and safety of pharmacological agents prescribed to treat EDs. They found that no single medication is indicated for the treatment of AN, although antipsychotics, antidepressants, mood stabilisers, gastric motility agents, appetite stimulants, and bi-phosphonates have all been prescribed. Their review found that high doses of the antidepressant fluoxetine (60 mg) were effective in relapse prevention in weight-restored patients with AN in 50 % of studies. Olanzapine was found to demonstrate an adjunctive effect for the treatment of underweight patients with an increase in weight gain and a decrease in obsessive ruminations about body size.

Tricyclic antidepressants (TCAs), mono-amine oxidase inhibitors (MAOIs), and SSRIs have been trialled for treating BN, all with positive results in the reduction of symptoms of bingeing and purging as well as ruminating about body image. However, given the potential toxicity of MAOIs and TCAs, the SSRIs are recommended as first line treatment.

The mood stabiliser’s and naltrexone have also been trialled for the treatment of AN and BN. However, given the potential for toxicity in patients who are already physically vulnerable, they are not recommended as part of treatment.

Eight RCTs were identified in which the SSRIs have been trialled for BED, with findings that they all resulted in a decrease in the frequency of bingeing.

Overall, there is insufficient evidence to provide the basis for developing prescribing guidelines for patients with EDs during the perinatal period. Prescribing needs to be considered in the context of each individual patient’s clinical presentation and with a clear understanding between clinician and patient of the goals of the medication and the risks to her if that medication is not prescribed. The specific risks of these medications, with respect to any increased risk of malformation, pregnancy and obstetric risks, neonatal risks, and longer term risks must also be considered. Monitoring recommendations have been described in previous chapters.

11.2.6 Management Recommendations for the Eating Disorders during the Perinatal Period

All the eating disorders require long-term psychiatric and medical care. AN is characterised by marked denial of the illness and noncompliance with treatment (McKnight and Park 2010), an issue that requires consideration during the perinatal period because of the additional risks of untreated illness on infant development. Management during the perinatal period should focus on encouraging appropriate weight gain/maintenance, monitoring for the particular medical, psychological, obstetric, and foetal growth and development issues that may emerge during this time. A multidisciplinary team approach is ideal, and wherever possible, consent should be obtained from the woman to enable close communication between herself, her partner/family (as appropriate), and all professionals involved in her care.

11.2.6.1 Preconception: Reproductive and Sexual Health

Women with EDs may have menstrual irregularities and may assume that they cannot conceive which can lead to inadequate use of contraception and the risk of an unplanned pregnancy. Thus a referral to the patient’s GP or a family planning clinic should be considered in order to discuss reproductive health.

Pre conception planning should include:

1.

2.

3.

4.

5.

11.2.6.2 Pregnancy

Whether pregnancy is the first time the patient presents for psychiatric assessment and management, or the patient is already engaged in active treatment, a comprehensive clinical assessment, diagnosis, and formulation including co-morbid psychiatric diagnoses, co-existing medical and obstetrical conditions, assessment of her unborn infant, and the relationship developing between the mother and her infant are essential.

Throughout pregnancy and the early postpartum period the severity of the ED should be monitored and liaison between the treating psychiatric, medical, and obstetric teams is essential in order to ensure that adequate monitoring of maternal and infant physical health occurs and that appropriate treatment can begin if required. Developing a management plan, together with the patient, which includes both short- and long-term management goals and plans, is recommended.

Specific issues that may require focus during the perinatal period include:

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

(j)

(k)

(l)

11.2.6.3 Early Postpartum

Postnatal monitoring and support are essential as there is a risk of relapse of EDs postnatally. Continued consultation with a dietician, physician, and psychiatrist is recommended to ensure that education and advice around healthy eating and nutrition can be ongoing and that maternal physical and mental health can be monitored and early treatment (including physical investigations) initiated if required. Drugs such as laxatives, diuretics, and appetite suppressants may be used in an effort to lose weight quickly without realising the effect on the infant if breastfeeding.

Additional support and planning, particularly around the developing mother–infant relationship and breastfeeding, and admission to an inpatient mother baby unit to support this should be considered. There should be a low threshold for early referral to a paediatrician for infant assessment and monitoring throughout development.

References

Abraham S. Disordered eating and pregnancy, part 1. Eur Eat Disord Rev. 1998;9:1–4.

American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Arlington, VA: American Psychiatric Publishing; 2013.

Arcelus J, Mitchell AJ, Wales J, Nielsen S. Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Arch Gen Psychiatry. 2011;68(7):724–31.PubMedCrossRef

Arbuckle TE, Sherman GJ. Comparison of the risk factors for preterm delivery and intrauterine growth retardation. Paediatr Perinat Epidemiol. 1989;3:115–29.PubMedCrossRef

Bateman A, Fonagy P. Randomized controlled trial of outpatient mentalization-based treatment versus structured clinical management for borderline personality disorder. Am J Psychiatry. 2009;166(12):1355–64.PubMedCrossRef

Boney CM, Verma A, Tucker R, Vohr BR. Metabolic syndrome in childhood: associations with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics. 2005;115:290–6.CrossRef

Bulik C, Sullivan P, Fear J, Pickering A, Dawn A, McCullin M. Fertility and reproduction in women with a history of anorexia nervosa: a controlled study. J Clin Psychiatry. 1999;60:130–5.PubMedCrossRef

Bulik CM, von Holle A, Hamer R, Berg CK, Torgersen L, Magnus P, et al. Patterns of remission, continuation, and incidence of broadly defined eating disorders during early pregnancy in the Norwegian Mother and Child Cohort Study. Psychol Med. 2007;37(8):1109–18.PubMedCentralPubMedCrossRef

Bulik CM, Hoffman ER, Von Holle A, Torgersen L, Stoltenberg C, Reichborn-Kjennerud T. Unplanned pregnancy in women with anorexia nervosa. Obstet Gynecol. 2010;116(5):1136–40.PubMedCentralPubMedCrossRef

Chanen A, Jovev M, Jackson HJ. Adaptive functioning and psychiatric symptoms in adolescents with borderline personality disorder. J Clin Psychiatry. 2007;68(2):297–306.PubMedCrossRef

Chanen AM, Kaess M. Developmental pathways toward borderline personality disorder. Curr Psychiatry Rep. 2012;14(1):45–53.PubMedCrossRef

Chanen AM, McCutcheon LK. Prevention and early intervention for borderline personality disorder: current status and recent evidence. Br J Psychiatry. 2013;202(S54):s24–9.CrossRef

Chen EY, Brown MZ, Lo TY, Linehan MM. Sexually transmitted disease rates and high-risk sexual behaviours in borderline personality disorder versus borderline personality disorder with substance use disorder. J Nerv Ment Dis. 2007;195:125–9.PubMedCrossRef

Cohen LJ, Slade A. The psychology and psychopathology of pregnancy: reorganization and transformation. In: Jr. Zeanah CH, editor. Handbook of infant mental health. 2nd ed. New York, NY: Guildford; 2000.

Coid J, Yang M, Tyrer P, Roberts A, Ullrich S. Prevalence and correlates of personality disorder in Great Britain. Br J Psychiatry. 2006;188:423–31.PubMedCrossRef

Conti J, Abraham S, Taylor A. Eating behavior and pregnancy outcome. J Psychosom Res. 1998;44:465–77.PubMedCrossRef

Crow S, Thuras P, Keel PK, Mitchell JE. Long-term menstrual and reproductive function in patients with bulimia nervosa. Am J Psychiatry. 2002;159:1048–50.PubMedCrossRef

De Genna NM, Feske U, Angiolieri T, Gold MA. Race and sexually transmitted diseases in women with and without borderline personality disorder. J Womens Health. 2011;20:333–40.CrossRef

De Genna N, Feske U, Larkby C, Angilieri T, Gold M. Pregnancies, abortions and births among women with and without borderline personality disorder. Women’s Health Isuues. 2012;22–4:e371–7.CrossRef

Flament MF, Bissada H, Spettigue W. Evidence-based pharmacotherapy of eating disorders. J Neuropsychopharmacol. 2012;15:189–207.CrossRef

Franko D, Blais M, Becker A, Delinsky S, Greenwood DN, Flores AT, et al. Pregnancy complications and neonatal outcomes in women with eating disorders. Am J Psychiatry. 2001;158:1461–6.PubMedCrossRef

Galbally M, Blankley G, Power J, Snellen M. Perinatal mental health services: What are they and why do we need them? Australas Psychiatry. 2013;21(2):165–70.PubMedCrossRef

Giesen-Bloo J, van Dyck R, Spinhoven P, van Tilburg W, Dirksen C, van Asselt T, et al. Outpatient psychotherapy for borderline personality disorder: randomized trial of schema-focused therapy vs transference-focused psychotherapy. Arch Gen Psychiatry. 2006;63(6):649–58.PubMedCrossRef

Grilo CM, Pagano ME, Skodol AE, Sanislow CA, McGlashan TH, Gunderson JG, et al. Natural course of bulimia nervosa and eating disorder not otherwise specified: 5-year prospective study of remissions, relapses, and the effects of personality disorder psychopathology. J Clin Psychiatry. 2007;68(5):738–46.PubMedCentralPubMedCrossRef

Government of South Australia. Personality Disorders in Pregnancy, Ch 146. South Australian Perinatal Practice Guidelines. Maternity care in South Australia; 2006.

Gunderson JG, Stout RL, McGlashan TH, Shea MT, Morey LC, Grilo CM, et al. Ten-year course of borderline personality disorder: psychopathology and function from the collaborative longitudinal personality disorders study. Arch Gen Psychiatry. 2011;68(8):827–37.PubMedCentralPubMedCrossRef

Harris EC, Barraclough B. Excess mortality of mental disorder. Br J Psychiatry. 1998;173:11–53.PubMedCrossRef

Henshaw C, Protti O. Addressing the Sexual and reproductive health needs of women who use mental health services. Adv Psychiatr Treat. 2010;16:272–8.CrossRef

Hoek HW, van Hoeken D. Review of the prevalence and incidence of eating disorders. Int J Eat Disord. 2003;34(4):383–96.PubMedCrossRef

Horz S, Zanarini MC, Frankenburg FR, Reich DB, Fitzmaurice G. Ten-year use of mental health services by patients with borderline personality disorder and with other axis II disorders. Psychiatr Serv. 2010;61(6):612–6.PubMedCentralPubMedCrossRef

Keski-Rahkonen A, Hoek HW, Linna MS, Raevuori A, Sihvola E, Bulik CM, et al. Incidence and outcomes of bulimia nervosa: a nationwide population-based study. Psychol Med. 2009;39(5):823–31.PubMedCrossRef

Kohmura H, Miyake A, Aono T, Tanizawa O. Recovery of reproductive function in patients with anorexia nervosa: a 10-year follow-up study. Eur J Obstet Gynecol Reprod Biol. 1986;22:293–6.PubMedCrossRef

Kok JH, den Ouden LA, Verloove-Vanhorick SP, Brand R. Outcome of very preterm small for gestational age infants: the first nine years of life. Br J Obstet Gynaecol. 1998;105:162–8.PubMedCrossRef

Kouba S, Hallstrom T, Lindholm C, Hirschberg A. Pregnancy and neonatal outcomes in women with eating disorders. Obstet Gynecol. 2005;105:255–60.PubMedCrossRef

Lacey J, Smith G. Bulimia nervosa: the impact of pregnancy on mother and baby. Br J Psychiatry. 1987;50:777–81.CrossRef

Leichsenring F, Leibing E, Kruse J, New AS, Leweke F. Borderline personality disorder. Lancet. 2011;377(9759):74–84.PubMedCrossRef

Linehan MM, Comtois KA, Murray AM, Brown MZ, Gallop RJ, Heard HL, et al. Two-year randomized controlled trial and follow-up of dialectical behavior therapy vs therapy by experts for suicidal behaviors and borderline personality disorder. Arch Gen Psychiatry. 2006;63(7):57–766.CrossRef

Machado PP, Machado BC, Gonçalves S, Hoek HW. The prevalence of eating disorders not otherwise specified. Int J Eat Disord. 2007;40(3):212–7.PubMedCrossRef

McKnight RF, Park RJ. Atypical antipsychotics and anorexia nervosa: a review. Eur Eat Disord Rev. 2010;18(1):10–21.PubMedCrossRef

Metzger BE, Buchanan TA, Coustan DR, de Leiva A, Dunger DB, Hadden DR, et al. Summary and recommendations of the fifth international workshop-conference on gestational diabetes mellitus. Diabetes Care. 2007;30:S251–60.PubMedCrossRef

Michels KB, Trichopoulos D, Robins JM, Rosner BA, Manson JE, Hunter DJ, et al. Birthweight as a risk factor for breast cancer. Lancet. 1996;348:1542–6.PubMedCrossRef

Mitchell JE, Seim HC, Glotter D, Soll EA, Pyle RL. A retrospective study of pregnancy in bulmia nervosa. Int J Eat Disord. 1991;10:209–14.CrossRef

Morgan J, Lacey J, Sedgwick P. Impact of pregnancy on bulimia nervosa. Br J Psychiatry. 1999;174:135–40.PubMedCrossRef

Morgan JF, Lacey JH, Chung E. Risk of postnatal depression, miscarriage and preterm birth in bulimia nervosa: Retrospective controlled study. Psychosom Med. 2006;68:487–92.PubMedCrossRef

National Health and Medical Research Council. Clinical practice guideline for the management of borderline personality disorder. Melbourne: National Health and Medical Research Council; 2012.

Newman L, Stevenson C. Parenting and borderline personality disorder: ghosts in the nursery. Clin Child Psychol Psychiatry. 2005;10:385–90.CrossRef

Newman L, Stevenson CS, Bergman LR, Boyce P. Borderline personality disorder, mother–infant interaction and parenting perceptions: preliminary findings. Aust N Z J Psychiatry. 2007;41(7):598–605.PubMedCrossRef

Newman L. Trauma and ghosts in the nursery: parenting and borderline personality disorder. In: Sved-Williams A, Cowling V, editors. Infants of parents with mental illness: developmental, clinical, cultural and personal perspectives. Bowen Hills: Australian Academic; 2008. p. 212–27.

Park R, Senior R, Stein A. The offspring of mothers with eating disorders. Eur Child Adolesc Psychiatry. 2003;12:110–9.CrossRef

Pompili M, Girardi P, Ruberto A, Tatarelli R. Suicide in borderline personality disorder: a meta-analysis. Nord J Psychiatry. 2005;59(5):319–24.PubMedCrossRef

Rich-Edwards JW, Stampfer MJ, Manson JE, Rosner B, Hankinson SE, Colditz GA, et al. Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. Br Med J. 1997;315:396–400.CrossRef

Rosenberg A. The IUGR newborn. Semin Perinatol. 2008;32(3):219–24.PubMedCrossRef

Rusch N, Lieb K, Gottler I, Hermann C, Schramm E, Richter H, et al. Shame and implicit self-concept in women with borderline personality disorder. Am J Psychiatry. 2007;164(3):500–8.PubMedCrossRef

Sansone RA, Farukhi S, Wiederman MW. Utilization of primary care physicians in borderline personality. Gen Hosp Psychiatry. 2011;33(4):343–6.PubMedCrossRef

Smink FE, van Hoeken D, Hoek HW. Epidemiology of eating disorders: incidence, prevalence and mortality rates. Curr Psychiatry Rep. 2012;14(4):406–14.PubMedCentralPubMedCrossRef

Trull TJ, Jahng S, Tomko RL, Wood PK, Sher KJ. Revised NESARC personality disorder diagnoses: gender, prevalence, and comorbidity with substance dependence disorders. J Pers Disord. 2010;24(4):412–26.PubMedCentralPubMedCrossRef

Wade TD, Bergin JL, Tiggemann M, Bulik CM, Fairburn CG. Prevalence and long-term course of lifetime eating disorders in an adult Australian twin cohort. Aust N Z J Psychiatry. 2006;40(2):121–8.PubMedCrossRef

Wen SW, Goldenberg RL, Cutter GR, Hoffman HJ, Cliver SP. Intrauterine growth retardation and preterm delivery: prenatal risk factors in an indigent population. Am J Obstet Gynecol. 1990;162(1):213–8.PubMedCrossRef

Weinfeld R, Dubay M, Burchell R, Mellerick J, Kennedy A. Pregnancy associated with anorexia and starvation. Am J Obstet Gynecol. 1977;15:698–9.

Yager J, Devlin MJ, Halmi KA, Herzog DB, Mitchell III JE, Powers P, Zerbe KJ. Guideline watch (August 2012): Practice guideline for the treatment of patients with eating disorders. 3rd ed. Washington, DC: American Psychiatric Association (APA); 2006. 128 p [765 references].

Yu CKH, Teoh TG, Robinson S. Review article: obesity in pregnancy. Br J Obstet Gynaecol. 2006;113:1117–25.CrossRef

Zanarini MC, Williams AA, Lewis RE, Reich RB, Vera SC, Marino MF, et al. Reported pathological childhood experiences associated with the development of borderline personality disorder. Am J Psychiatry. 1997;54:1101–6.

Zanarini MC, Frankenburg J, Hennen J, Silk KR. Mental Health service utilization by borderline personality disorder patients and Axis II comparison subjects followed prospectively for 6 years. J Clin Psychiatry. 2004a;65(1):28–36.PubMedCrossRef

Zanarini MC, Frankenburg FR, Hennen J, Reich DB, Silk KR. Axis I comorbidity in patients with borderline personality disorder: 6-year follow-up and prediction of time to remission. Am J Psychiatry. 2004b;161(11):2108–14.PubMedCrossRef

Zanarini MC, Frankenburg FR, Reich DB, Fitzmaurice G. The 10-year course of psychosocial functioning among patients with borderline personality disorder and axis II comparison subjects. Acta Psychiatr Scand. 2010;122(2):103–9.PubMedCrossRef

Zimmerman M, Chelminski I, Young D. The frequency of personality disorders in psychiatric patients. Psychiatr Clin North Am. 2008;31(3):405–20.PubMedCrossRef



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