Proton pump inhibitors (PPIs). Recently, utilization of H2 blockers has given way to the newer class of PPIs, including lansoprazole (Prevacid), pantoprazole (Protonix), and esomeprazole (Nexium). These drugs target the parietal cell hydrogen potassium ATPase, reducing acid secretion by 80% to 90%. Treatment is typically once daily for uncomplicated GERD and twice daily for LPR. Patients who have LPR also require higher dosages to achieve complete acid suppression and heal the delicate laryngeal tissue. Tissue injury in LPR may take 6 months to reverse once adequate therapy has been initiated. Severe, complicated cases may require the addition of an H2 blocker or even a third daily dose of the PPI.
Patients should not discontinue a PPI abruptly because of the risk of rebound hypersecretion of gastric acid. Rather, these drugs should be stopped gradually over several weeks. They are best taken 30 minutes before a meal, as that is when they reach maximum blood concentration.
PPIs are generally considered safe for use after the first trimester of pregnancy. All are Category B drugs, except for omeprazole (Prilosec), which is a Category C drug.
Doctor, will I ever sing again?
The human voice is extremely sensitive to the endocrinologic changes of pregnancy. Many of these changes manifest as alterations in fluid content of the lamina propria just beneath the laryngeal mucosa.27 Collectively, the voice changes of pregnancy are known as laryngopathia gravidarum. Abdominal distension during pregnancy also interferes with abdominal muscle function, altering the mechanics of phonation and creating overuse injuries.
Symptoms include hoarseness and voice loss. Singers, in particular, notice a deeper voice and a diminished range of pitch.28 Treatment is largely supportive, with hydration, and singers should be advised to refrain from singing until abdominal muscle function resolves.
Laryngopathia gravidarum typically resolves postpartum as endocrinologic alterations return to baseline and abdominal support returns.
Eustachian tube dysfunction usually resolves postpartum
This disorder affects between 5% and 30% of pregnant women. Symptoms usually begin after the first trimester and consist of tubal obstruction or patulous Eustachian tubes. Women who have tubal obstruction report a clogged or popping sensation in their ears, with muffling of sounds. In severe cases, serous effusion may develop.
Tubal obstruction is related to edema of the respiratory mucosa. In cases in which symptoms are more distressing to the patient, increased humidity, treatment of rhinitis, and frequent Valsalva maneuvers have had variable success in providing relief. For recalcitrant cases, pressure-equalization tubes can be placed (in an otolaryngology clinic).
Women who have patulous tubes usually report intermittent symptoms that consist of autophony and a roaring sensation in their ears that is synchronous with breathing and is worse when they are in an upright position or exercising (or both). The cause of patulous Eustachian tubes is not well defined. Weight loss and hormonal variables are believed to play a role.
This condition typically resolves postpartum.
Treatment is largely supportive, including humidification, reassurance, and instructions on how to perform a forceful inspiratory nasal sniff.
Incidence of Bell’s palsy in pregnancy is uncertain
A possible association between pregnancy and idiopathic facial paralysis (Bell’s palsy) was first noted by Sir Charles Bell in 1830. Retrospective literature at first suggested a 3.3-fold increased risk of Bell’s palsy during pregnancy, with the incidence peaking during the third trimester of gestation.10 Subsequent re-analysis found no significant difference in the incidence of Bell’s palsy between pregnant and nonpregnant women of childbearing age.11 Prospective studies are sorely needed to definitively establish the incidence of Bell’s palsy in pregnancy.
Bell’s palsy typically appears during the third trimester
A unique aspect of Bell’s palsy in pregnancy is its tendency to manifest during the third trimester and postpartum. The most widely accepted theory for this phenomenon is the reactivation of latent herpes simplex virus within the geniculate ganglion.12 A large body of scientific work supports this theory.
The maternal immune system undergoes complex alterations during pregnancy, although the mechanisms for these changes are not completely understood. The most pronounced change is a shift from cell-mediated immune responses toward humoral and innate immune responses as pregnancy progresses.13 Such a shift likely reduces the maternal cytotoxic potential against fetal antigens.14 Clinically, the decrease in cellular immunity manifests as an increased susceptibility to intracellular pathogens such as herpes simplex virus later in pregnancy.15
Sudden facial weakness is the usual presenting symptom
This weakness develops over 24 to 48 hours, progressing to complete or near-complete paralysis within 1 week. Associated symptoms often include pain, fever, dry eye, a change in taste and salivation, and sensitivity to noise.11