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While rare, (1-2 per 1000), postpartum psychosis is a psychiatric emergency. It occurs most often within a few days to 2 weeks after delivery. Symptoms may include being detached or preoccupied, with an inability to sleep (Leibenluft et al, 1996). The mother may exhibit confusion, disorganized thought and/or behaviour, paranoia, hallucinations or delusions (Brockington et al, 1981). The latter may include beliefs about the safety of the baby, evils of the world or themselves and may include thoughts or attempts to harm the baby and or themselves. Psychosis commonly represents a bipolar episode. Women with bipolar disorder are at very high risk of recurrence, especially in the first two weeks postpartum (Kendell et al, 1987; Leibenluft, 1996). Adequate sleep may be preventive in some cases. Alternate causes include a psychotic depressive episode, an exacerbation of schizophrenia/schizoaffective disorder or a brief psychotic episode. While the risk of recurrence of postpartum psychosis with subsequent pregnancies, has been reported as high as 70%, it likely depends on the diagnosis. The most recent research suggests a 57% risk of recurrent postpartum psychosis when the diagnosis established is bipolar disorder (Robertson et al, 2005).
Questions: Start open-ended questions and maintain a nonjudgmental, non-reactive stance. Allow time for disorganized behaviour and thoughts to be revealed
Edinburgh Postnatal Depression Scale
The Edinburgh Postnatal Depression Scale (Cox et al, 1987) (see end of chapter) was developed to assist health professionals screen mothers for postnatal depression. The validation study revealed that of those who scored above threshold, 92.3% were likely to be suffering from a depressive illness. Clinical assessment and judgment are necessary to confirm the diagnosis and determine severity. The self-report scale consists of ten short statements about how she has been feeling in the past week. Most mothers are able to complete it in less than 5 minutes. It will not however, detect all anxiety disorders without accompanying depressive symptoms, phobias or personality disorders. The scale has also been validated for use in pregnancy, the first year postpartum, and fathers. It has been validated cross culturally, translated into many languages and may require a higher degree of suspicion if used with patients with English as a second language (Cox et al, 2003).
Comparison Postpartum, Blues and Depression
All anxiety disorders have been reported to be more common in women with peak incidence in the reproductive years (Kessler et al, 1994; Regier et al, 1990; Kessler et al, 1995). Pre-existing anxiety or antenatal anxiety may be a greater risk factor for PPD than a history of depression (Matthey et al, 2003). It is normal for new mothers to experience increased vigilance and have concern about their new baby whose life depends on their attentiveness. This may cross the line into an anxiety disorder in 4-6% of postpartum women. Although there is less literature regarding prevalence, new onset or course of perinatal anxiety disorders than mood disorders, there is increasing interest.
Generalized Anxiety Disorder
GAD presents as excessive worry about many things with difficulty sleeping, restlessness, poor concentration, fatigue and feeling keyed up or on edge. Women report an inability to sleep or relax. They may find themselves checking their baby more frequently than they think is necessary, and may have trouble leaving their baby even with a trusted caregiver. Domains of worry often include financial security, personal appearance and household responsibilities / hygiene (Wenzel et al, 2003). Anxiety disorders may be difficult to distinguish from PPD as they often represent the onset of PPD or co-occur. To distinguish anxiety from normal perinatal concern, anxiety must be widespread, be excessive and interfere with daily functioning. The DSM IV criteria of 6 months duration may not be met at initial presentation.
Panic attacks present as acute episodes of panic, with heart palpitations, shortness of breath, chest pain, dizziness and fear of impending doom or death. Panic Disorder has the additional feature of worry about having future panic attacks. It often occurs with generalised anxiety or MDD.
Post Traumatic Stress Disorder
PTSD may occur especially relating to labour and delivery due to anticipated pain, sexual exposure and lack of control. Re-experiencing (flashbacks, nightmares); avoidance (dissociation, numbing) and hyperarousal (difficulty sleeping, severe anticipatory anxiety) occur. Anxiety can feel so overwhelming that women may fear they are losing their minds and need reassurance. Trauma related to forthcoming delivery and traumatic birth experiences (invasive, poor pain control, life-threatening) are currently being researched as a source of PTSD.
Obsessive Compulsive Disorder
OCD is an anxiety disorder that may have its’ onset in pregnancy (Altshuler et al, 1998) or the postpartum period occurring in 1-3 % of postpartum women, often with PPD. OCD is characterized by obsessions (intrusive thoughts or images), which cause anxiety and/or compulsions repetitive or ritualistic behaviours or thought patterns) which transiently diminish anxiety. Intrusive, often sudden unwanted thoughts of harm coming to their baby or of doing harm to their baby are the most common phenomena. The thoughts are frightening, and experienced as not like themselves (ego-dystonic). Typically women with OCD alone do to not act on thoughts but one must make a careful assessment of impulsivity and co-occurring depression or anxiety. Women often find that being able to disclose these thoughts helps them feel more contained and in control. A calm non-judgmental approach assuring the mother that you will work with her to ensure both her and her baby’s safety is best.
Women with adjustment disorders have excessive reactions to stressful life circumstances. Adjustment Disorders may be difficult to distinguish from PPD due to the multi-factorial nature of PPD but they do not meet criteria for Minor Depressive Disorder, MDD, GAD or Panic Disorder and symptoms may be responsive to psychosocial interventions. A psychiatric assessment with past psychiatric and family psychiatric history or a trial intervention may assist with diagnosis.
Risks of Untreated Mood and Anxiety Disorders
The risks for the mother include poor self care, inadequate nutrition & weight gain, sleep disturbance, illicit drug use, smoking, alcohol abuse, emotional deterioration and increased anxiety. Interpersonal/family conflict may escalate especially if irritability is one of the symptoms. Depression in pregnancy confers a risk of PPD, which imparts independent risks for the child. There are some reports of an increased risk of pre-eclampsia (Kurki et al, 2000) and of operative delivery, epidurals and NICU admissions (Chung et al, 2001).
There are reports of preterm birth, lower birth weight, smaller head circumference, lower APGAR scores (Lou et al, 1994) and poor neonatal adaptation (Misri et al, 2004). Speculated mechanisms include increased cortisol, medications or lifestyle. There are many reports regarding the neurobiological impact of fetal exposure to MDD. There is evidence to suggest that at least some effects relate to the impact of MDD during pregnancy rather than inheritance.
Animal models of stress during pregnancy reveal adverse impact on growth (Schneider et al, 1999), adverse impact on learning (Weller et al, 1988), neuronal death and abnormal development of neuronal structure in fetal brain (Smith et al, 1981) and sustained dysfunction of the HPA axis in offspring (Maccari et al, 2003). It is also unknown whether these fetal effects are permanent; however some studies reveal the impact of prenatal stress in rodents and primates is endures into adulthood.
Postpartum risks for the mother are similar to antenatal risks.
A number of studies have revealed the negative impact on children (see also Psychology of Pregnancy chapter) of maternal depression. Reduced emotional and verbal responsivity, disengagement, intrusiveness, anger, irritability, frustration and impatience with the child are some of the possible manifestations of PPD. Abnormal infant attachment and behaviour (Murray, 1992; Stein et al, 1991) and cognitive development (Cogill et al, 1986; Hay et al, 2001; Sharp et al, 1995) have been associated with maternal depression. IQ was found to be significantly, negatively associated with duration of depression and language was negatively associated with number of depression episodes after delivery (Nulman et al, 2002). Although some mothers are able to interact positively in spite of depression and anxiety (Cohn & Tronick, 1989; Weinberg & Tronick, 1998a; Weinberg & Tronick, 1998b), the more severe and prolonged, with the greatest life adversity, the greater the impact (Grace et al, 2003; Suri et al, 2004). Thus it is inappropriate to lump all PPD together in terms of assessing risk to the infant and child. An individual assessment, including the severity and chronicity of depression and anxiety, and the mother’s ability to respond and parent her infant is more informative (Murray et al, 1996a; Murray et al, 1996b).
Intervention for Perinatal Depression and Anxiety Disorders
Treatment should be tailored to the severity of depression/anxiety and individual needs of the mother and her family, including appropriate biological, psychological and social interventions.
Treatment should include validation of experience, patient education and recruitment of family and partners for assistance. Education of partners and family is essential, as they may feel helpless and overwhelmed or defensively dismissive. Ensuring adequate sleep is an important preventive and treatment measure. Mothers frequently regard their partner’s job as ‘work’ with an entitlement of sleep, while the work of caring for a baby is minimized. This stance is often supported by the partner, necessitating education of the couple. Partners or family may assist with night feeds and diaper changes. Overlapping shifts can be organized to maximize the sleep of each partner. Supplementing with formula may help women achieve extended hours. Breastfeeding may give the greatest nourishment and protection to newborns but can be associated with pain and difficulty (eg. latching difficulties, inverted or cracked nipples, mastitis) in great contradistinction to expectations. As difficulty with breastfeeding is often a source of diminished self-esteem, guilt and depression, a flexible non-judgemental stance by care providers is essential. Women experience enormous societal imposed pressures to breast feed, which is unhelpful in the context of postpartum depression and anxiety.
Respite care, visiting home assistance, public health, mental health nursing and other community agencies can be employed with great benefit. Reduction of stress such as the care of other children, housework and other domestic chores should be addressed. Women commonly feel they should be able to manage all the usual tasks of housework and may focus on it as a way of dealing with anxiety or failing self-esteem. Emotional support should be addressed and can be as or more important for depressed mothers than instrumental support. New mothers benefit from ample opportunity to talk about their feelings, anxieties and thoughts.
Treatment with psychotherapy, facilitated support groups, and supportive counselling may be effective in mild or moderate syndromes and is usually preferred over medication by both mothers and health care professionals (see chapters on Psychological Adaptations of Pregnancy and on IPT). Involvement with groups of well mothers is often reported to cause unfavourable comparisons and make depressed mothers feel worse. Nonetheless, social isolation can be severe and needs to be addressed with available resources.
A careful history will allow physicians to determine the individual risks and benefits of treating with medication. In more severe situations, wherein anxiety and /or depression is disabling, and has a profound negative impact (including risk of death) for the mother, baby, other children and marriage, medication should be encouraged. Mothers should participate in an informed decision and some may wish to try psychotherapy first. Many who have a chronic history, more severe depression, or in whom therapy has not been effective are relieved by the accumulated data and take medication with good response. Motherisk (www.motherisk.com) at the Hospital for Sick Children (Toronto) is an excellent international resource for data on the risk of medications in pregnancy and lactation.
Initiation of medication in pregnancy and postpartum especially in patients with severe anxiety or irritability requires close attention for the occurrence of side effects which might impair functioning further. Some patients will require an increase of antidepressant dose through the end of the second and third trimester due to changes of body volume and metabolism. This should be determined on an individual clinical basis. Patients should be followed carefully and treated for one year before a trial of weaning off antidepressants. Some PPD will be the first episode of chronic or recurrent mood disorders requiring longer-term treatment (Bell et al, 1994). Women with depression in pregnancy or postpartum should be educated to seek advice about prevention or treatment with respect to future pregnancies.
Exposure to antidepressants is greater for the fetus via placental passage than to the infant via breast milk. Case reports and case series are the sources of the bulk of data regarding lactation.
Treatment Risks with Antidepressant
SSRI’s, SNRI and TCA’s appear not to be associated with major malformation (Nonacs & Cohen, 2003; Addis et al, 1995; Wisner et al, 1993b; Kulin et al, 1998; Einarson et al, 2001) but may be associated with a clinically insignificant lower birth weight. Studies have been criticized for grouping data for each class of drug; however sufficient data for each medication alone is not available. Data is insufficient to assess increases in minor malformation. One study reported a nonstatistical increase in spontaneous abortion but this was not controlled for depression (Pastuszak et al, 1993). A recent advisory (GSK Advisory, 2005) regarding an increase of both cardiac and major malformations associated with first trimester paroxetine exposure vs. other SSRI’s was issued due to new data. The GSK report is an uncontrolled retrospective review in addition to two recently presented abstracts. Contradictory data has been reported in the literature. Publication and peer review is necessary to know how to interpret the conflicting data (Health Canada, 2005).
Neurobehavioural teratogenesis is concerned with the impact of exposure on variables such as cognition and behaviour. The data regarding TCA’s and SSRI’s are reassuring. A prospective study, controlled for depression & other variables with TCA (Kessler et al, 1995), fluoxetine (Leibenluft, 1996) found no effect of fetal exposure throughout gestation on children’s’ global IQ, language development, and behaviour (to age 71 months). A similar study found no developmental delay to age 2 [TCA(209), SSRI(185)] (Simon et al, 2002). Nulman’s earlier study found no difference up to 86 months of age of exposed compared to unexposed infants in language, mood, temperament, activity, distractibility, or behaviour problems [TCA (80), fluoxetine (55)] (Nulman et al, 1997). While this data is reassuring, longer-term studies are needed. Both TCA’s and SSRI’s are secreted in breast milk, but the exposure is less than in utero. The small studies on the impact due to exposure via breast milk are reassuring (Stowe et al, 1997; Rampono et al, 2000) but the long-term neurodevelopmental impact is unknown (Nulman et al, 2003). Some studies report preferences of one agent over another due to decreased passage into the breast milk and infant drug levels, however distinctions to date suggests the primacy of therapeutic impact on the mother.
SSRI’s and Neonatal Adaptation Syndrome
There are numerous reports of a “neonatal adaptation syndrome”. There may exist both a toxicity syndrome and a discontinuation syndrome, which has yet to be clearly distinguished (Haddad et al, 2005). While adaptation difficulties occur in unexposed children, the risk is higher in babies exposed to either untreated depression or antidepressants. The risk is ever higher in babies exposed to co-morbid psychiatric disorders and those treated with both antidepressants and clonazepam (Oberlander et al, 2004). Respiratory distress and CNS, motor and GI symptoms are most commonly observed (Chambers et al, 1996; Koren et al, 1998; Costei et al, 2002). Symptoms are usually mild and resolved within the first few days to 2 weeks. Authors of a literature review estimate the relative risk from third trimester exposure compared to first trimester or no exposure to be 3.0 (Moses-Kolko et al, 2005). A more severe but rare syndrome but no fatalities have also been reported. It may be possible to reduce the adaptation syndrome at birth by decreasing the dose close to term however research confirmation is pending. Such a technique must be considered carefully with respect to the individual’s history and risk of recurrence of depression. Polypharmacy should be avoided if possible.
Treatment Risks with Benzodiazepines
There have been contradictory reports regarding the risk for cleft palate with benzodiazepine exposure in the first trimester. A meta-analysis revealed increased rates of major malformation and of oral clefts but only in case control studies (Dolovich et al, 1998). Authors disagree on the likelihood of increased rate of oral clefts with first trimester exposure, but suggest the increase is in the range of 0.7% (Born & Steiner, 2003). Possible minor IUGR is a risk with diazepam, but not lorazepam or clonazepam. Neurobehavioural teratogenesis requires further study but the data thus far reveal no differences to minor motor developmental delays. If benzodiazepines are given near term neonatal adaptation may be impaired with symptoms of hypotonia, difficulty with temperature regulation, apnea, lower AGPAR scores, failure to feed, and withdrawal. Benzodiazepines are highly lipid soluble with long retention in neural tissues and thus it is recommended to use higher potency ones with lower accumulation, wherein high peak concentrations can be avoided. Lorazepam is recommended by some due to its lower rate of placental transfer.
With severe anxiety, symptom control sometimes necessitates the use of clonazepam, a benzodiazepine with a longer half-life.
There is a risk of sedation in exposed breast fed infants. Low doses of shorter acting benzodiazepines (lorazepam) are preferred.
Lithium is the safest of mood stabilizers during pregnancy. Nonetheless it is associated with organ dysgenesis, specifically Epstein’s anomaly, which increases from 1/20000 in unexposed to 1-2/1000 in exposed infants. This represents an increase of 20-40 times the norm. Growth may be affected with significantly more weight gain in a non-dose dependent fashion. In a small study there was no evidence of neurobehavioural teratogenesis. Neonatal toxicity including floppy baby, hypothyroidism, and nephrogenic diabetes is well known and requires anticipated intervention. Minimizing the impact is advised by using more frequent smaller dosing, increasing the dose through pregnancy as needed and decreasing before term.
Previously breast feeding was not recommended while taking Lithium (AAPCD, 2000) however the Academy of Pediatrics (AAPCD, 2001) has changed the classification to cautionary use. If breastfed, infants must be adequately hydrated, and be monitored for lithium levels, renal function and hypothyroidism.
Both valproic acid & carbamazepine are potential severe physical & neurobehavioural teratogens. If alternative agents are not an option, mothers should be maintained on folic acid (4 mg /day) and may be followed with level 2 ultrasounds and amniocentesis. Neural tube defects are increased twofold over baseline and the research on cognitive delay has yielded contradictory results thus far. In general anticonvulsants are associated with double the baseline rate of birth defects, with a predominance of orofacial clefts, neural tube defects, heart defects, microcephaly and IUGR (Boylan et al, 2003).
In preliminary studies, it is not clear whether lamotrigine increases organ dysgenesis (Vajda et al, 2003; Sabers et al, 2004; Costa et al, 2004). No details regarding impact on growth are available. The greatest risk of treatment of adults with lamotrigine is a life threatening rash (Stephen Johnson’s syndrome). Due to immature metabolic processes in infants, this side effect is a theoretical risk. There is a significantly increased clearance rate of lamotrigine in pregnancy with a rapid decrease postpartum, and both stages may require dosage adjustments (Pennell et al, 2004).
In breast feeding Valproic Acid is associated with a risk of hepatotoxicity in children under two. Carbamazepine is possibly associated with jaundice, and hepatic dysfunction but the risk overall to breastfed infants seems minimal (Burt et al, 2001).
First Generation Antipsychotics
Organ dysgenesis was initially not associated with chlorpromazine, trifluoperazine, perphenazine, and prochlorperazine, although a reanalysis of data questions these results (Zipursky et al, 2003). There is an increased risk of malformations in psychotic patients with or without chlorpromazine. Initial reports of limb reduction with haloperidol are not supported. Neonatal toxicity is possible with movement disorders seen with haloperidol, and extrapyramidal symptoms with phenothiazines mostly resolving within days. The risk may be less than with selected mood stabilizers, and thus a reasonable option for the treatment of acute mania or recurrence of symptoms while pregnant is to switch from lithium or an anticonvulsant for the entire pregnancy or first trimester. Concomitant anticholinergic and antihistaminergic agents are often needed.
Antipsychotics are secreted into breast milk and no clear guidelines are available. Infants should be monitored for sedation if exposed with lactation (Hallen, 2002).
Olanzapine has not been associated with malformations in several case reports and series. Data are limited regarding neonatal toxicity. Use of olanzapine necessitates monitoring for weight gain, insulin resistance, gestational diabetes, and preeclampsia. Thus far there have been no reports of adverse effects. Motherisk reports that for older atypical antipsychotics, 1-2% of the dose appears in the breast milk, far below the 10% limit considered safe. There is little data on newer antipsychotics.
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