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42. Riccardi VM: The genetic approach to human disease. New York, NY, Oxford University Press, 1977, pp 34. 43. Robert E: Treating depression in pregnancy. N Engl J Med 1996;335;1056-1058. 44. Roberts RJ, Blumer J, Gorman R, et al: Transfer of drugs and other chemicals into human milk. Pediatrics 84:924-936, 1989. 45. Robinson GE: The rational use of psychotropic drugs in pregnancy and postpartum. Can J Psychiatry 3 1 : 183-1 90, 1986. 46. Robinson L: Cognitive-behavioral treatment of panic disorder during pregnancy and lactation. Can J Psychiatry 37523-626, 1992. 47. Schou M: Lithium treatment during pregnancy, delivery and lactation: An update. J Clin Psychiatry 51:410412, 1990. 48. Sitland-Marken PA, Rickman L, Wells B, et al: Pharmacologic management of acute mania in pregnancy. J Clin Psychopharrn 9:78-87, 1989. 49. Spencer MJ: Fluoxetine hydrochloride (Prozac) toxicity in a neonate. Pediatrics 1993;92:721-722. so. Stewart DE, Raskin J, Garfinkel P, et al: Anorexia nervosa, bulimia and pregnancy. Am J Obstet Gynecol 157:1194-1198, 1987. 51. Susman VL, Katz JL: Weaning and depression: Another postpartum complication. Am J Psychiatry 145: 498-501, 1988. 52. Williams KE, Koran LM: Obsessive-compulsive disorder in pregnancy, the puerperium, and the premenstruum. J Clin Psychiatry 1997;58:33&334. 53. Willis DC, Rand CS: Pregnancy in bulimic women. Obstet Gynceol 71 :708-7 10, 1988. 54. Wisner KL, Perel JM: Serum levels of valproate and carbamazepine in breastfeeding mother-infant pairs. J Clin Psychopharmacol 1998;18:167-169. 55. Wisner KL, Perel JM, Blumer J: Serum sertraline and N-desmethylsertraline levels in breast-feeding motherinfant pairs. Am J Psychiatry 1998;155(5):690-692. 56. Wisner KL, Perel JM, Wheeler SB: Tricyclic dose requirements across pregnancy. Am J Psychiatry 1993;150(10):1541-1542.

64. POSTPARTUM PSYCHIATRIC DISORDERS

Doris C . Gundersm, M.D.

1. What psychiatric disorders are seen in the postpartum period? Maternity blues, postpartum psychosis, and postpartum depression are the psychiatric diagnoses most often made after delivery. 2. Define maternity blues. Maternity blues, or baby blues, is a term used to describe a self-limiting, relatively mild mood syndrome experienced by 30-80% of all postpartum women. Symptoms include lability of mood, anxiety, sadness, crying spells, insomnia, and fatigue. The onset of maternity blues is usually 3-10 days after parturition. The symptoms typically remit within 2 weeks.

3. Which risk factors predispose women to maternity blues? Many regard maternity blues as a normal postpartum phenomenon because of its frequency and
spontaneous remission. However, some women appear to be at higher risk. Major predictive factors include primiparous pregnancy, history of late luteal phase dysphoria (PMS), personal history of depression, or first-degree relative with depression.
4. What causes maternity blues? The precise cause of maternity blues is unknown. Because the condition is common in all cultures and races and appears to occur independently of psychosocial factors, a biologic cause is likely. Studies have demonstrated that estrogen and progesterone influence the sensitivity of neurotransmitter-binding sites much like chronic administration of antidepressant drugs. With the delivery of the

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placenta, the elevated estrogen and progesterone levels maintained throughout pregnancy fall precipitously, and pregravid serum concentrations are reached within 3 days, coinciding with peak symptoms of maternity blues. It is hypothesized that this rapid decline in reproductive hormones after delivery destabilizes neurotransmitter mechanisms involved in mood regulation.

5. Describe postpartum psychosis. Postpartum psychosis is sometimes called peurperal psychosis or postpartum psychotic depression. It develops in 1-2 per 1000 postpartum women worldwide. In the majority of cases, the symptoms are manifest within the first 2 weeks after delivery. However, a second peak has been observed 1-3 months after delivery. A common prodrome for postpartum psychosis is worsening insomnia in the absence of a crying infant or physical discomfort in the mother. Psychomotor agitation may precede the psychosis. Women experience confusion, memory impairment, irritability, and anxiety. Intrusive thoughts, usually about harming the infant, are not uncommon. Paranoid and religious delusions, auditory hallucinations, thought insertion, thought withdrawal, and thought broadcasting have been reported. Faulty interactions with the infant, either misreading cues or blatant disinterest, also may be manifestations. A unique feature of postpartum psychosis is the mercurial changeability of the symptoms.A brief period of elation characterized by incessant talking, increased energy, and euphoric mood may shift rapidly to profound, inexplicable sadness or rage. Lucid intervals are common and may give a deceptive impression of recovery. Abrupt episodes of floridly psychotic behavior may resurface after weeks of calm. Postpartum psychosis may resolve abruptly, but more often it evolves into serious, protracted depression. Postpartum psychosis frequently resembles mania and may prove to be a variant of bipolar affective disorder.

6. How frequently do women with postpartum psychosis harm their infants?

The level of infant morbidity correlates well with the severity of psychiatric symptoms in the mother. Infants of mildly to moderately impaired mothers may demonstrate difficulty with feeding or bonding. Infants of more severely afflicted mothers present with failure to thrive or evidence of frank physical abuse. Infanticide occurs in an estimated 4% of cases. Approximately 80-120 infanticides are committed by psychotic new mothers in the United States each year. At least 50% of the infant deaths take place weeks to months after the acute symptoms have subsided, Such numbers emphasize the importance of continuous monitoring of the mothers behavior, well beyond the initial psychotic episode. The capacity for the psychosis to recur after lucid periods must always be kept in mind.

7. Are there specific risk factors for postpartum psychosis? Hereditary factors and prior history of affective episodes confer the greatest risk. A woman with a history of depression unrelated to pregnancy has a 20-25% risk of developing postpartum psychosis. This risk is higher for women with bipolar mood disorders than for women with a history of unipolar depression. If a bipolar woman develops postpartum psychosis, she carries a 50% risk for recurrence with subsequent deliveries. Women with a history of postpartum psychosis have a 1 in 3 chance of recurrence with future deliveries. The same women have a 38% risk for developing nonpsychotic postpartum depression. The need for careful prenatal screening and counseling is obvious. Other risk factors include single or primiparous women, cesarean section, or perinatal death. Postpartum psychosis peaks between ages 25-29 and 30-34 years, which coincide with vulnerable times for the development of PMS. A relationship between the two disorders has yet to be established.

8. What is the cause of postpartum psychosis? Postpartum psychosis is regarded as an organic syndrome. Psychological and social variables
are considered secondary to organic factors. After delivery of the placenta, a large source of hormone production is lost. As with maternity blues, the sudden and dramatic decline in serum estrogen may initiate a sequence of neuroendocrine events that produce serious psychiatric symptoms in susceptible women. Estrogen has antidopaminergic properties. It is hypothesized that the abrupt with-

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drawal of estrogen exposes sensitive postsynaptic receptors in the brain; this may be the triggering event for development of psychosis. The propensity for relapse at the time of menses further implicates sex hormones in development of this disorder. A decline in serum estrogen also leads to a fall in serum binding proteins, including transcortin. Cortisol levels are elevated during pregnancy. A surge of cortisol at labor is followed by an accelerated decline to second trimester levels within 72 hours. Acute psychotic reactions have been reported with adrenal insufficiency and/or steroid withdrawal. Small doses of the cortisol analog given to women with postpartum illness appear to decrease the severity and duration of symptoms. Unfortunately, no controlled studies of this regimen have been conducted. Finally, women with postpartum illness have a high incidence of thyroid abnormalities. T3 levels are significantly lowered in women with postpartum psychosis compared with controls. The absolute values often fall within the normal range, with no overt physical signs of hypothyroidism. Perhaps it is the slope of the T3 decline rather than the specific serum concentration that influences the development of psychosis.

9. Describe postpartum depression,

Between the extremes of maternity blues and postpartum psychosis lies postpartum depression, which develops in 10-20% of women after delivery. Unlike the blues or psychosis, postpartum depression tends to develop insidiously 3 or more weeks after delivery. The mood symptoms are more sustained, and the course of the illness is typically prolonged. Symptoms include crying spells, poor concentration, indecisiveness, and profound sadness. Thoughts are characterized by themes of failure and inadequacy. Suicidal ideation is common. Postpartum depression is characterized by physical signs and symptoms resembling moderate-to-severe hypothyroidism. Cold intolerance, fatigue, dry skin, slowed mentation, constipation, and fluid retention are commonly reported.

10. What are the risk factors for postpartum depression? As with the blues and psychosis, hereditary factors and a history of previous psychiatric illness are identified as significant risk factors for postpartum depression. Women with previous episodes of depression unrelated to reproduction have a 1 0 4 0 % chance of developing postpartum depression. Women with a history of postpartum depression have a 50% rate of recurrence with subsequent pregnancies. Several psychosocial risk factors have been identified, including marital discord, stressful life events during pregnancy, ambivalence about motherhood, low socioeconomic status, isolation from extended family or friends, and single status. Unrealistic expectations or romanticized ideas about motherhood, which inevitably clash with reality, may predispose a woman to depression. High prenatal scores on neuroticism scales are associated with postpartum depression. 11. Is postpartum depression considered to be primarily a biologic illness? Not entirely. Ethnographic literature about childbirth suggests that the depressive reaction is at least partly attributable to cultural patterning of the postpartum period. Postpartum depression is not expressed globally; it appears rarely in non-Western cultures in which a new mother is absolved of all responsibilities beyond self-care and feeding her infant. Rituals practiced in third-world countries include provisions of social support for the new mother and clearly define her role. With modern birthing practices in Western society, there is less social structuring of postpartum events and a lack of clear role definition and social support for new mothers. 12. Are there endocrine or biologic correlates for postpartum depression? Postpartum depression often is accompanied by symptoms related to hypothyroidism, and research points to varying degrees of pituitary dysfunction and related thyroid abnormalities as contributing factors in development of the illness. After normal delivery, blood supply to the pituitary gland wanes. Trophic hormone secretion is reduced to prepregnancy quantities. If the delivery is complicated by shock (e.g., massive hemorrhage), the anterior pituitary may be damaged by infarction. In this scenario, secretion of trophic hormones ceases. Targeted endocrine glands fail. The patient develops profound apathy, cold sensi-

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tivity, loss of libido, memory impairment, lethargy, and thinning of axillary and pubic hair. Psychosis and eventually coma develop in untreated cases. This is known as Sheehan's syndrome. It is hypothesized that postpartum depression is an intermediate condition. A sluggish pituitary may compromise endocrine functioning. After delivery thyroxine levels tend to decline and remain at values below the nonpregnant average for up to 1 year. Although depressed, the thyroxine level tends to overlap with the normal range, possibly masking hypothyroidism. The level of thyroid-stimulating hormone (TSH) usually is normal in hypothyroidism of pituitary origin (secondary hypothyroidism). Case studies support the link between subclinical hypothyroidism of pituitary origin and postpartum illness. Antidepressant and antipsychotic medications, alone or in combination, frequently fail to treat adequately the symptoms of postpartum depression. With the addition of thyroid hormone, some patients experience rapid alleviation of psychiatric symptoms. Further support for partial pituitary dysfunction or damage is suggested by the heightened sensitivity to sunburn or diminished capacity to tan reported by several postpartum women. This finding suggests reduced or absent melanin production by the pituitary gland. Finally, 5-30% of postpartum cases become chronic, implying some degree of residual damage. Primary hypothyroidism, which originates in the thyroid gland, is also diagnosed in the postpartum period. Painless autoimmune thyroiditis, characterized by positive thyroid antibodies, occurs in 2-9% of postpartum women, surpassing the number observed in nonpregnant controls. Thyroxine may rise briefly with the inflammation. This rise is followed by a reduction in thyroid hormone and a corresponding rise in TSH. One study revealed persistent thyroid abnormalities 3 years after delivery in 50% of women. In summary, postpartum depression often includes symptoms identical to moderate-to-severe hypothyroidism. Routine laboratory screening may fail to identify the abnormality if it is of pituitary origin. Such subclinical hypothyroidism may render postpartum depression refractory to treatment.

13. Can postpartum disorders be prevented?

Postpartum illnesses are notoriously difficult to treat. For this reason, efforts should be made to prevent their onset by eliminating or at least reducing known risk factors. High-risk patients can be identified early in the course of pregnancy through the use of risk assessment checklists, ideally at the first prenatal visit. When significant vulnerability is identified, interventions may include reducing environmental stress, enlisting the aid of family members, and mobilizing additional sources of support. Prenatal anticipatory guidance prepares a new mother for maternity blues and helps her to distinguish the blues from more ominous symptoms that warrant professional attention. Women with past histories of depression or psychosis should be followed more closely. The earlier a postpartum illness is identified, the greater the opportunity for secondary prevention.

14. What are the barriers to diagnosis? Early detection of postpartum illness is rare, in part as a result of modern obstetric practices. In the United States, postpartum women are discharged from the hospital within 48 hours. The symptoms of postpartum illnesses are usually manifest after the third postpartum day, when the expert observation of nursing staff and physicians is no longer available. Six weeks pass before the next professional contact is made, resulting in a window of extreme vulnerability for new mothers. The stigma placed by American culture on mental illness creates another barrier to early diagnosis. Patients and their families may conceal the severity of the problem out of shame, guilt, or embarrassment. Furthermore, depression after delivery contradicts the cultural expectation of "parental bliss.'' The prodrome for serious postpartum pathology often mimics the blues. Women who voice concerns about such symptoms may be reassured without further investigation. Finally, the focus of the first postnatal visit is the reproductive health of the mother; her emotional well-being is not routinely addressed. 15. What biologic treatment strategies are available? Maternity blues is a mild, transitory mood syndrome that typically resolves within a few days.

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Reassurance, observation, and occasionally a short-acting sedative are the primary interventions. It is important, however, to take the patients complaints seriously. This increases the likelihood of her reporting symptoms that linger or become more severe. Postpartum psychosis usually merits hospitalization because of the level of dysfunction and grave risk for both infanticide and suicide. The symptoms of postpartum psychosis are predominantly affective. Lithium or other mood-stabilizing medications are often helpful. Antipsychotic doses are typically lower than those required for other psychotic disorders. Electroconvulsive therapy (ECT) is indicated for severe, pharmacologically refractory cases. For postpartum depression antidepressants, especially those that are selective for serotonin, appear to have some efficacy in targeting symptoms. Low doses of antipsychotic medications should be included if symptoms of psychosis are present. As with postpartum psychosis, some women may respond preferentially to ECT. Thyroid screening should be performed routinely. For all postpartum cases, levels of serum thyroxine, TSH, and autoimmune antibodies should be assessed. Weekly thyroxine levels should be obtained. If a downward trend is identified, thyroxine replacement therapy should be initiated. A typical starting dose is 0.05 mg per day. In women at risk for recurrence, psychotropic drugs to prevent or mitigate serious psychiatric symptoms should be given serious consideration. Women with histories of postpartum psychosis should receive lithium immediately after delivery. Rapid achievement of therapeutic blood levels is the goal. Care must be exercised to prevent toxicity. Lithium excretion may be impaired by fluid and electrolyte changes in the immediate postpartum period. Low-dose antipsychotic medications are also recommended for at least 2-3 weeks after delivery. In women with previous nonpsychotic postpartum depressions, antidepressant medication may be initiated somewhat earlier than onset of the previous episode. Postpartum disorders that develop a more chronic course warrant endocrinology consultation to rule out more subtle disorders of the hypothalamic-pituitary-thyroid axis.

16. Which psychosocial interventions are effective? Psychotherapy is crucial for preventing psychological scarring. Most patients have not experienced prior mental illness and may have difficulty with accepting the need to participate in treatment. It is often helpful to emphasize the biologic aspects of postpartum illness, which should be considered a complication of pregnancy-a medical illness with psychiatric symptoms related to physiologic changes after childbirth. Opportunities for eliminating feelings of failure and guilt become obvious. Group therapy is particularly helpful for postpartum women. It is important to convey that postpartum illness has an excellent prognosis. New fathers are often the silent victims of postpartum disorders. They benefit from supportive outreach and education. Studies demonstrate that a fathers support positively influences his partners recovery. Extended family must be recruited to support a postpartum woman during recovery. Providing literature and directing them to local support groups are often helpful.

17. How may the infant be affected? Aggressive treatment of the mothers depression may prevent complications in the newborn. Studies show that depressed mothers demonstrate less positive attunement to their infants. They tend to be less affectionate and misread cues. Infants of depressed mothers are at risk for poorer mental and motor development, as well as emotional disturbances in childhood.

18. What areas are the focus of current research? Depressed levels of tryptophan and a slower than normal rise in tryptophan levels after delivery predict the blues. Attempts to avert the blues through tryptophan loading have failed, leading to speculation that a defect in metabolism rather than an absolute deficiency in tryptophan may be causally related to maternity blues. Pyridoxine is a cofactor required for neuronal utilization of tryptophan. With oral administra-

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tion for 28 days after delivery, an experimental group of high-risk women demonstrated a recurrence rate of the blues several times lower than the rate in a control group receiving placebo. A tryptophan study including pyridoxine supplementation may yield valuable information. Another highly experimental strategy for preventing more severe postpartum disorders involves administering long-acting estrogen to high-risk women at delivery. It is theorized that the supplementation of estrogen cushions the fall of the hormone after the placenta is delivered, In a series of 50 high-risk women receiving estrogen at delivery, none had recurrences. Because of concerns about the risk of thromboembolic phenomena, this strategy is not currently recommended for routine prophylactic treatment in women with histories of postpartum disorders.
8 1B LlOGRAPHY
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