A 2008 article appearing in the August edition of Prescrire International titled “SSRI antidepressants and persistent pulmonary hypertension in newborns.” further examines the adverse effects of exposure to selective serotonin reuptake inhibitor drugs (SSRIs) during pregnancy.  In recent decades, a number of prominent studies have linked heart defects to SSRIs, but many other negative consequences have been identified as well.

Here is the abstract of the aforementioned article in full, as available on PubMed Health, a service of the United States National Library of Medicine and The National Institutes of Health:

“(1) The list of adverse effects of selective serotonin reuptake inhibitor (SSRI) antidepressants in pregnant women and their newborns continues to grow; (2) It was already known that, when taken towards the end of pregnancy, SSRIs could cause spontaneously resolving neonatal disorders, particularly neurological problems; (3) A case-control study has shown an association between maternal exposure to SSRI antidepressants after the 20th week of pregnancy and neonatal persistent pulmonary hypertension, with a 6-fold increase in the risk. Another study has provided similar results; (4) Diagnosis of depression must be made with care during pregnancy, and it should be remembered that not all patients with depression require drug therapy.”

Citing a six-fold increased risk for persistent pulmonary hypertension of the newborn (PPHN), this study can be used in an SSRI birth defect lawsuit to illustrate that the manufacturers of drugs like Prozac, Paxil, and Zoloft knew, or should have known, the risks related to their products and failed to act.

PPHN is a birth defect wherein a newborn does not adapt to breathing outside the womb.  According to Medscape, a renowned medical information database, the disease is characterized as follows:

“Persistent pulmonary hypertension of the newborn (PPHN) is defined as the failure of the normal circulatory transition that occurs after birth. It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia and right-to-left intracardiac shunting of blood.

Signs and symptoms

PPHN is often associated with the following signs and symptoms of perinatal distress:

  • Asphyxia

  • Tachypnea, respiratory distress

  • Loud, single second heart sound (S2) or a harsh systolic murmur (secondary to tricuspid regurgitation)

  • Low Apgar scores

  • Meconium staining

  • Cyanosis; poor cardiac function and perfusion

  • Systemic hypotension

  • Symptoms of shock

Idiopathic persistent pulmonary hypertension of the newborn can present without signs of acute perinatal distress. Marked lability in oxygenation is frequently part of the clinical history.


Suspect PPHN whenever the level of hypoxemia is out of proportion to the level of pulmonary disease. Clinically, PPHN is most often recognized in term or near-term neonates, but it can occur in premature neonates, albeit infrequently.

In contrast to adult primary pulmonary hypertension, the newborn syndrome is not defined by a specific pressure of the pulmonary circulation. The diagnosis is confirmed regardless of the pulmonary arterial pressure, as long as it is accompanied by right-to-left shunt and absence of congenital heart disease.[1]

Echocardiography is considered the most reliable, convenient, and noninvasive test to establish the diagnosis, assess cardiac function, and exclude an associated structural heart disease.

Laboratory testing

  • Arterial blood gas levels (through indwelling line): To assess the pH, partial pressure of carbon dioxide in arterial gas (PaCO2), and the partial pressure of oxygen (PaO2)

  • Complete blood count with differential: To evaluate for high hematocrit level (polycythemia and hyperviscosity syndrome may lead to or exacerbate PPHN); to determine whether an underlying sepsis or pneumonia is present

  • Coagulation studies (eg, platelet count, prothrombin time, partial thromboplastin time, international normalized ratio): To assess for coagulopathy (increased disease severity)

  • Serum electrolytes (eg, calcium) and glucose levels

Imaging studies

  • Chest radiography: To assess for presence of underlying parenchymal lung disease (eg, meconium aspiration syndrome, pneumonia, surfactant deficiency) and/or to exclude underlying disorders (eg, congenital diaphragmatic hernia)

  • Echocardiography: To screen and assist in making the diagnosis of PPHN; assist in defining the anatomy of the pulmonary veins; and rule out associated partial/total anomalous pulmonary venous return before initiating extracorporeal membrane oxygenation therapy (ECMO)

  • Echocardiography with Doppler flow: To assess presence/direction of the intracardiac shunt at the ductus arteriosus and foramen ovale, as well as estimate the pulmonary arterial systolic/diastolic pressures

  • Cranial ultrasonography: To assess for intraventricular bleeding and for peripheral areas of hemorrhage or infarct before initiating (ECMO)

  • Cranial ultrasonography with Doppler flow: To assess whether a nonhemorrhagic infarct is present

  • Brain computed tomography scanning or magnetic resonance imaging: To evaluate for central nervous system injury


  • Cardiac catheterization: To exclude congenital heart disease (eg, obstructed anomalous pulmonary venous return, pulmonary vein stenosis) when echocardiographic findings are not definitive


The treatment strategy for PPHN is aimed at maintaining adequate systemic blood pressure, decreasing pulmonary vascular resistance, ensuring oxygen release to tissues, and minimizing lesions induced by high levels of inspired oxygen and ventilator high pressure settings.

General management principles include the following:

  • Continuous monitoring of oxygenation, blood pressure, and perfusion

  • Maintaining a normal body temperature

  • Correction of electrolytes/glucose abnormalities and metabolic acidosis

  • Nutritional support

  • Minimal stimulation/handling of the newborn

  • Minimal use of invasive procedures (eg, suctioning)

Medical therapy

PPHN treatment may consist of the following:

  • Inotropic support (eg, dopamine [first line], dobutamine, milrinone)

  • Surfactant administration: For newborns with parenchymal lung disease

  • High-frequency ventilation: Used in newborns with underlying parenchymal lung disease and low lung volumes; therapy is best in centers with clinicians experienced in achieving/maintaining optimal lung distention

  • ECMO: Used when optimal ventilatory support fails to maintain acceptable oxygenation and perfusion[2, 3]

  • Endotracheal intubation and mechanical ventilation: To maintain normal functional residual capacity by recruiting areas of atelectasis; to avoid overexpansion

  • Correction of acidosis and alkalosis

  • Induced paralysis: Controversial; paralytic agents are typically reserved for newborns who cannot be treated with sedatives alone (Note: paralysis, especially with pancuronium, may promote atelectasis of dependent lung regions and promote ventilation-perfusion mismatch.)

  • Hearing evaluation

  • Postdischarge neurologic evaluation by a neurologist or developmental pediatrician


  • Pulmonary vasodilators (eg, inhaled nitric oxide)

  • Vasodilators potentially beneficial for PPHN after the newborn period (eg, prostacyclin, phosphodiesterase inhibitors, endothelin receptor antagonists)”

This is by no means the first study to link PPHN with prenatal SSRI exposure.  If you or a loved one used SSRIs and gave birth to a child with PPHN or another congenital malformation, you may be entitled to significant financial compensation.  For a free, no-obligation case consultation, contact our team of SSRI birth defect lawyers at the information provided below.  We have the compassion, resources, and experience required to win the justice you deserve.  Call today and see how we can help.

(855) 452 – 5529


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