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Neonatal Withdrawal Syndrome caused by Prozac SSRI

Posted in Prozac Birth Defects, SSRI Birth Defects

Published in a 2000 edition of the Journal of Perinatology, Dr. Chandrakala Mohan and Dr. John Moore present a case review of an infant suffering from fluoxetine (Prozac®) intoxication at birth.  Prozac® is a type of antidepressant known as a selective serotonin reuptake inhibitor (SSRI) that regulates levels of serotonin in the brain, since serotonin is a chemical that plays a role in mood regulation.  It has also recently been shown that serotonin plays an important role in fetal development, and that SSRI drugs pass through the placenta and affect the developing brain of the fetus.

The presently discussed Mohan and Moore (2000) piece demonstrates the characteristics of a syndrome known as fluoxetine toxicity in a newborn.  This child, male, was born several weeks prematurely, at normal weight – 3270 grams,[1] to a mother who had used fluoxetine from the end of the first trimester to term.

When a baby is born, doctors perform a series of tests on the newborn to ensure that it stabilizes well after birth and adjusts to life outside the womb normally.  Doctors score a newborn on what is known as an “APGAR test,” with data taken at one, five, and occasionally ten minutes after birth.  MedlinePlus, a prominent online medical encyclopedia provided by the United States National Library of Medicine, explains the APGAR test as follows:

“The APGAR test is done by a doctor, midwife, or nurse. The health care provider will examine the baby’s:

  • Breathing effort
  • Heart rate
  • Muscle tone
  • Reflexes
  • Skin color

Each category is scored with 0, 1, or 2, depending on the observed condition.

Breathing effort:

  • If the infant is not breathing, the respiratory score is 0.
  • If the respirations are slow or irregular, the infant scores 1 for respiratory effort.
  • If the infant cries well, the respiratory score is 2.

Heart rate is evaluated by stethoscope. This is the most important assessment:

  • If there is no heartbeat, the infant scores 0 for heart rate.
  • If heart rate is less than 100 beats per minute, the infant scores 1 for heart rate.
  • If heart rate is greater than 100 beats per minute, the infant scores 2 for heart rate.

Muscle tone:

  • If muscles are loose and floppy, the infant scores 0 for muscle tone.
  • If there is some muscle tone, the infant scores 1.
  • If there is active motion, the infant scores 2 for muscle tone.

Grimace response or reflex irritability is a term describing response to stimulation such as a mild pinch:

  • If there is no reaction, the infant scores 0 for reflex irritability.
  • If there is grimacing, the infant scores 1 for reflex irritability.
  • If there is grimacing and a cough, sneeze, or vigorous cry, the infant scores 2 for reflex irritability.

Skin color:

  • If the skin color is pale blue, the infant scores 0 for color.
  • If the body is pink and the extremities are blue, the infant scores 1 for color.
  • If the entire body is pink, the infant scores 2 for color.”[2]

With five testing categories and a maximum score of 2 per category, the overall maximum APGAR score is ten.  A score of 10 indicates that the child is adjusting well to life outside the womb, and a score of 0 indicates that the newborn is not developing well after birth.

When the child discussed in the Mohan and Moore (2000) was born, his APGAR scores were “4, 7, and 9 at 1, 5, and 10 minutes, respectively,”[3] after birth.  This tells us that immediately after birth, the child’s condition was poor, but quickly improved in a ten-minute span.

Four hours after birth, doctors write that “the baby was tachypneic, with respiratory rate of 100/minute, and was in respiratory distress with grunting, flaring, and retractions.”[4]  Stating that a child is tachypneic simply means that the child has a high breathing rate, though this is made clear by noting that the child’s breath rate was 100/min, while the normal range for an infant is 30-60/min.[5]

Though the high breath rate subsided after 24 hours,[6] at about 36 hours after birth, the baby was found to be “increasingly jittery”[7] and “had three to four episodes of seizure-like activity… characterized by twitching of the face and eyebrows, grimacing, roving movements of eyes, and flailing movements of upper and lower extremities.”[8]  At 48 hours after birth, the child was transferred to a neonatal intensive care unit.[9]

At this point, the child had “petechiae on the abdomen, chest, and extremities”[10] and scleral icterus[11] (a yellowish hue of the skin).  Many tests, including an electroencephalogram did not show any clear reason for the child’s symptoms.[12]  “Skin manifestations resolved between 48 and 72 hours, but seizure-like activity peaked, with five to eight episodes per day.  By 144 hours, jitteriness and tremulousness decreased and feedings were started.  There was resolution of symptoms over the next 48 hours; feeding was advanced, and the infant was discharged from the hospital at 172 hours of age.[13]

Fortunately, a neurodevelopmental examination performed four months after birth showed that the child was developing normally.

Discussing the neonatal complications of this child in general, Mohan and Moore write that,

“Fluoxetine … may be responsible for the central nervous system side effects as described in reports of toxicity in adults; these side effects include nervousness, tremors, jitteriness, and occasionally seizures.  Bruising and bleeding disorders with increased hematoma frequency at birth have also been described with fluoxetine exposure in utero.[14][15]

Mohan and Moore also note that Chambers et al (1996) had found previously that developing children exposed to Prozac® late in gestation are more than three times as likely to have “poor neonatal adaptation, including jitteriness, cyanosis on feeding, and respiratory difficulties” as children who were exposed to Prozac® early in gestation.[16]

The report concludes by stating that “Although no life-threatening complications have been noted in infants exposed to maternal fluoxetine, the present report suggests that marked motor automatism, including seizure-like activity, can be expected in preterm infants.  Because [Prozac®] is metabolized primarily in the liver, the prematurity of the infant and the immaturity of the liver may account for the multisystem involvement and the protracted course.”[17]

This article may be used in a Prozac® birth defects lawsuit to illustrate to court that since at least the year 2000, and even before that – for the authors cite research illustrating the negative neonatal outcomes for children exposed to Prozac® in utero dating back to 1996 – the manufacturers of Prozac® knew, or should have known, the dangers of their product.

If you used Prozac® during pregnancy, unaware of the increased risk for birth defects and poor neonatal outcomes posed to your child by your use of Prozac® and your child was bone with Prozac® toxicity or a Prozac® birth defect, you may be entitled to compensation for your child’s injuries.  Please do not hesitate to contact our team of Prozac® birth defect lawyers for a free, no-obligation case consultation by phone at (855) 452-5529 or by e-mail at justinian@dangerousdrugs.us.

We are here to help you every step of the way.

Our SSRI Birth Defects Lawsuit Information page is a great place to start if you have any questions about SSRIs and Birth Defects.


[1] Mohan, C.G. & Moore, J.J. (2000) “Fluoxetine Toxicity in a Preterm Infant” Journal of Perinatology Vol. 20; pp. 445-446

[2] “APGAR: MedlinePlus Medical Encyclopedia” MedlinePlus. U.S. National Library of Medicine. National Institutes of Health. © 1997-2013 A.D.A.M., Inc. Available at <http://www.nlm.nih.gov/medlineplus/ency/article/003402.htm> Updated 24 January 2013, Accessed 18 February 2013.

[3] Mohan, C.G. & Moore, J.J. (2000) “Fluoxetine Toxicity in a Preterm Infant” Journal of Perinatology Vol. 20; pp. 445-446

[4] Ibid.

[5] “http://www.health.ny.gov/professionals/ems/pdf/assmttools.pdf” Department of Health. New York State. Available at <http://www.health.ny.gov/professionals/ems/pdf/assmttools.pdf> Accessed 18 February 2013

[6] Mohan, C.G. & Moore, J.J. (2000) “Fluoxetine Toxicity in a Preterm Infant” Journal of Perinatology Vol. 20; pp. 445-446

[7] Ibid.

[8] Ibid.

[9] Ibid.

[10] Ibid.

[11] Ibid.

[12] Ibid.

[13] Ibid.

[14] Stanford, MS., Patton, JH. (1993) “In utero exposure to fluoxetine HCl increases hematoma frequency at birth” Phamacol Biochem Behav Vol. 45; pp. 959-962

[15] Mohan, C.G. & Moore, J.J. (2000) “Fluoxetine Toxicity in a Preterm Infant” Journal of Perinatology Vol. 20; pp. 445-446

[16] Ibid.

[17] Ibid.