Pneumonia in the Pregnant Patient: A Synopsis

, and , Division of Pulmonary and Critical Care Medicine, Winthrop University Hospital, Mineola, NY


Medscape General Medicine. 1999;1(3) 

In This Article

Key Physiologic Changes in the Pregnant Host That Predispose to Pneumonia

Anatomic Changes

A number of anatomic changes occur in the chest during pregnancy, including outward flaring of the lower ribs, an increase in the subcostal angle, and an increased transverse diameter of the chest. The diaphragm also rises by 4cm.[2,4] Collectively, these alterations decrease the ability of the pregnant woman to clear respiratory secretions. The elevation of the diaphragm leads to a decreased functional residual capacity; this, coupled with the increase in oxygen consumption that occurs during pregnancy, reduces the pregnant patient's ability to tolerate even the briefest periods of hypoxia, particularly in the third trimester. Progesterone derived from the placenta stimulates the respiratory center centrally, leading to hyperventilation and the sensation of dyspnea that is commonly noted during a healthy pregnancy. Because the respiratory rate should remain "normal" during pregnancy, it is important that any evidence of tachypnea be recognized as pathologic. Incidence of tachypnea may therefore be used to evaluate the severity of illness when pneumonia is present.

Changes in Maternal Immune Status

The major factor predisposing pregnant women to severe pneumonic infections is an alteration in immune status.[5] These changes occur primarily in cell-mediated immunity, making viral, fungal, and tuberculous infections particularly pathogenic in these women.[2] Studies have documented a number of pregnancy-specific alterations in maternal immune status, including a decreased lymphocyte proliferative response, decreased natural killer cell activity, and a decreased absolute number of helper T4 cells. Maternal serum can also block lymphokine secretion and lymphoproliferative responses to alloantigens. Further, fetal lymphocytes may inhibit the maternal immune response by suppressing T-cell proliferation.[2,5] These immunologic adaptations which are in place to protect the growing fetus from its antigenically different mother, and clearly mandatory to support the fetus, increase maternal susceptibility to infection.

Hormonal Changes

The hormonal milieu in the pregnant state can also predispose to infection in several ways. Progesterone, human choriogonadotropin, alpha-fetoprotein, and cortisol all inhibit cell-mediated immunity. In addition, estrogens (the 17-estradiols), progesterones, and testosterone have been shown to enhance the growth of certain pathogens in vitro, such as Coccidioides immitis.[6] Finally, because of the physiologic adaptations to the pregnant state, changes in pulmonary water balance may occur. Pregnancy has been associated with a tendency to increase interstitial lung water, which increases the likelihood of lung injury.[7]


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