“Baby Blues”: What Every Internist Should Know About Postpartum Psychiatric Dx

The postpartum period can be a chaotic time for many women. Right after birth, women experience an abrupt decline in their estrogen and progesterone levels which are known to help regulate mood states. As a result, many new mothers are susceptible to drastic mood changes during this period. Their risk for postpartum psychiatric issues can dramatically increase when dealing with stressful life events, interpersonal problems, an infant with health issues, a prior history of depression, family history of depression, an unplanned pregnancy, and/or poor social support.

Between 50 to 85% of new mothers experience a common and transient state of mood symptoms called the postpartum blues. Women often report mild symptoms of tearfulness, anxiety, irritability, moods swings, and sleep disturbances that usually start 3 days after delivery and spontaneously resolve by the second week. Most women suffering from postpartum blues get better. Validation and reassurance that they’re doing a great job and assistance in childcare during this stressful period can be very helpful.

If postpartum blues symptoms worsen or persist for more than two weeks, your patient may be developing postpartum depression which affects 20% of new mothers. It looks very similar to clinical depression with a depressed mood most of the day, loss of interest in activities, fatigue, high anxiety, poor concentration, poor sleep, and feelings of worthlessness. Some women may express thoughts of death or suicide. They may obsess over the health and well being of their baby despite constant reassurance by others. It can be common to have unwanted, intrusive thoughts and images of harming their infant such as throwing the baby out the window or drowning them. Make sure to check the thyroid level as 10% of postpartum women can develop hypothyroidism (which can lead to depression).

Rarely, new mothers can experience postpartum psychosis which occurs in 1-2 women per 1000 births. It is very rare but considered a serious psychiatric emergency. Women with a history of bipolar disorder or previous history of postpartum psychosis are at a higher risk for this illness. Studies report a recurrence rate as high as 30-50% with each subsequent delivery. Psychotic symptoms often appear within 3 weeks postpartum. Symptoms include mood swings, confusion, agitation, bizarre behavior, paranoia, and poor sleep. Women can have delusional thoughts such as the belief that someone is trying to kill their baby or their breast milk is poisoning the baby and hallucinations such as hearing voices telling them to kill their baby. Postpartum psychosis is important to identify and treat immediately because it can lead to suicide or infanticide if left untreated.

Of note, the diagnoses described above were extrapolated from DSM-IV TR. With the new DSM-V edition, all mood and psychotic symptoms occurring during pregnancy or within the first 4 weeks following delivery are referred to as peripartum mood or psychotic episodes (unless the patient meets full criteria for another diagnosis, e.g. major depressive disorder).

Though it is common for postpartum women to develop depressive symptoms, many of these women are improperly diagnosed and/or treated. Some women convince themselves they are just “stressed” or that their symptoms are “normal for women with babies”. Other women feel guilty for having such negative emotions during a time that is meant to be joyful and therefore are ashamed to seek help. What these mothers don’t realize is that their own mental health can significantly impact their baby’s short- and long-term physical and emotional development. Depressed or psychotic mothers have difficulty bonding with their baby, are less responsive to their baby’s needs, and can be indifferent or upset towards their child.

Treatment usually starts with increasing the mother’s support system and education about depression and/or psychosis. Increasing help around the house and getting adequate sleep and rest can significantly reduce the risk for such symptoms. Psychotherapy can be helpful in different forms- couples therapy for those having martial conflicts, individual therapy to work on personal issues, and group therapy to learn from other mothers dealing with the same problems. If medications are needed, anti-depressants such as Sertraline, Bupropion, Fluoxetine and Velaaxine can be very effective at treating depression. If a patient is suffering from psychotic symptoms, anti-psychotic medications such as Risperidone, Olanzapine or Haloperidol may be used to treat delusions and hallucinations.

When medications are indicated, it is crucial to provide education about the potential risks of breastfeeding as many of these medications can pass into the breast milk. The relative risk for harm or toxicity is low but should still be discussed. Some women may choose to substitute with formula milk during their pharmacologic treatment. Women with postpartum symptoms should continue treatment between 6-12 months and then be reassessed by their psychiatrist to see if treatment is still indicated. If therapy and medications are ineffective or one’s symptoms are severe enough (acute suicidality or psychosis) requiring immediate results, ECT (electroconvulsive therapy) can be a safe and successful option.

It’s important for primary care providers to encourage and empower their new mothers to seek mental health services if there are any signs or risk for postpartum mood or psychotic symptoms. Stigma and poor insight can be major barriers to seeking treatment. But with the help of primary care providers who have established rapport with their patients, we can help bridge the gap between medical and psychiatric care.

Internal Medicine Board Review: Ring-Enhancing and Non-Enhancing Lesions

A favorite of the USMLE Steps, NBME Internal Medicine Shelf, and ABIM Internal Medicine Board Exams seems to be those ring-shaped lesions picked up on imaging studies. Often, the scenario is a ring lesion identified on a CT head scan in an immunocompromised patient (particularly one with HIV or AIDS). These can be challenging because the clinical vignette focuses on the description of the lesion without providing detailed serologies. So let’s use an efficient approach to identifying the most commonly encountered ring lesion etiologies on medical exams.

The first step is to determine whether the lesion presented on the CT scan is ring-enhancing or non-enhancing.

If it is a ring-enhancing lesion, the most commonly seen etiologies are

• Cerebral toxoplasmosis (50%)
• Primary central nervous system (CNS) lymphoma (30%)
• Less commonly, Bacterial or Fungal abscess (e.g. Cryptococcosis, Histoplasmosis, Aspergillosis, Tuberculosis and Trypanosomiasis)

Cerebral Toxoplasmosis is the most common cause of ring-enhancing cerebral lesions. Often, multiple lesions are seen, usually located in the basal ganglia. It is unlikely to be seen in a patient who is already receiving prophylactic trimethoprim-sulfamethoxazole (TMP-SMX). Patients with AIDS and CD4 count less than 100/microL are at increased risk. It’s very important to remember that Toxoplasmosis serologies are non-specific but patients with cerebral toxoplasmosis are seropositive for T. gondii IgG antibody.

Primary CNS Lymphoma is the second most common cause of a ring-enhancing cerebral lesion. Unlike cerebral toxoplasmosis, primary CNS lymphoma may be solitary. Thus, if a solitary lesion is detected, even if toxoplasma serology is positive, CNS lymphoma is the more likely diagnosis than toxoplasmosis. The location of CNS lymphoma is more commonly in the periventricular areas. Lesions greater than 4cm in diameter are more likely to be primary CNS lymphoma rather than cerebral toxoplasmosis. Epstein-Barr virus (EBV) DNA in the cerebrospinal fluid (CSF) is quite specific for primary CNS lymphoma.

And the ring non-enhancing lesions are typically due to…

Progressive Multifocal Leukoencephalopathy (PML), which is attributed to the JC virus. It presents with multiple demyelinating lesions. It predominantly affects the white cerebral matter, in particular the brainstem and the cerebellum. Other patients at risk of developing PML are those receiving natalizumab therapy for relapsing-remitting multiple sclerosis, efalizumab for psoriasis, and brentuximab for Hogkin’s lymphoma.

I hope you find this review helpful in rapidly identifying the cause of each brain-ring lesion you may encounter on the USMLE Steps, NBME Internal Medicine Shelf, and ABIM Internal Medicine Board Exams.

Internal Medicine Board Review: Ring-Enhancing and Non-Enhancing Lesions

A favorite of the USMLE Steps, NBME Internal Medicine Shelf, and ABIM Internal Medicine Board Exams seems to be those ring-shaped lesions picked up on imaging studies. Often, the scenario is a ring lesion identified on a CT head scan in an immunocompromised patient (particularly one with HIV or AIDS). These can be challenging because the clinical vignette focuses on the description of the lesion without providing detailed serologies. So let’s use an efficient approach to identifying the most commonly encountered ring lesion etiologies on medical exams.

The first step is to determine whether the lesion presented on the CT scan is ring-enhancing or non-enhancing.

If it is a ring-enhancing lesion, the most commonly seen etiologies are

• Cerebral toxoplasmosis (50%)
• Primary central nervous system (CNS) lymphoma (30%)
• Less commonly, Bacterial or Fungal abscess (e.g. Cryptococcosis, Histoplasmosis, Aspergillosis, Tuberculosis and Trypanosomiasis)

Cerebral Toxoplasmosis is the most common cause of ring-enhancing cerebral lesions. Often, multiple lesions are seen, usually located in the basal ganglia. It is unlikely to be seen in a patient who is already receiving prophylactic trimethoprim-sulfamethoxazole (TMP-SMX). Patients with AIDS and CD4 count less than 100/microL are at increased risk. It’s very important to remember that Toxoplasmosis serologies are non-specific but patients with cerebral toxoplasmosis are seropositive for T. gondii IgG antibody.

Primary CNS Lymphoma is the second most common cause of a ring-enhancing cerebral lesion. Unlike cerebral toxoplasmosis, primary CNS lymphoma may be solitary. Thus, if a solitary lesion is detected, even if toxoplasma serology is positive, CNS lymphoma is the more likely diagnosis than toxoplasmosis. The location of CNS lymphoma is more commonly in the periventricular areas. Lesions greater than 4cm in diameter are more likely to be primary CNS lymphoma rather than cerebral toxoplasmosis. Epstein-Barr virus (EBV) DNA in the cerebrospinal fluid (CSF) is quite specific for primary CNS lymphoma.

And the ring non-enhancing lesions are typically due to…

Progressive Multifocal Leukoencephalopathy (PML), which is attributed to the JC virus. It presents with multiple demyelinating lesions. It predominantly affects the white cerebral matter, in particular the brainstem and the cerebellum. Other patients at risk of developing PML are those receiving natalizumab therapy for relapsing-remitting multiple sclerosis, efalizumab for psoriasis, and brentuximab for Hogkin’s lymphoma.

I hope you find this review helpful in rapidly identifying the cause of each brain-ring lesion you may encounter on the USMLE Steps, NBME Internal Medicine Shelf, and ABIM Internal Medicine Board Exams.