Cherry & Merkatz’s Complications of Pregnancy
5th Edition

Ear, Nose, and Throat Disorders
William Lawson
Anthony J. Reino
Hugh F. Biller
W. Lawson, A.J. Reino, and H.F. Biller: Department of Otolaryngology, Mt. Sinai School of Medicine, New York, NY 10029.
The effects of pregnancy on head and neck structures are diverse. Relevant signs and symptoms that are encountered include nasal congestion and rhinorrhea, aural fullness and hearing loss, facial paralysis, hoarseness, neck swelling, and the production of tumors in the nose, oral cavity, and jaws. The pathogenesis of these clinical findings involves disturbances in fluid dynamics, increased protein synthesis and loss, and altered vascular proliferation and permeability induced by hormonal changes. The various head and neck disorders encountered are discussed according to the anatomic site involved.
Otosclerosis is a localized form of osteodystrophy involving the otic capsule of the temporal bone. Clinically, it is characterized by a hearing loss that is generally conductive in nature, secondary to fixation of the stapes footplate. Pregnancy has been traditionally considered to stimulate activity in otosclerosis, presumably by the increased concentration of circulating estrogens. These hormones act as stimulators of osteocytic activity and may play a dominant role during ossification of an otospongeotic bone lesion. This may explain the onset of a conductive hearing loss due to otosclerosis during pregnancy (1). In the premicrosurgical era it often was recommended that abortion be performed in otosclerotic women who became pregnant, in an attempt to preserve their hearing (2).
The concept that pregnancy activates otosclerosis and accelerates the hearing loss from the disease was based primarily on the subjective complaints of affected women. Nager (3) reported that 48% of 164 pregnant women surveyed claimed increased deafness with childbearing. In another survey of 194 otosclerotic women who became pregnant, House (4) found that 87 (45%) claimed increased loss of hearing. This occurred during the first pregnancy in 41 cases, during the second pregnancy in 23 cases, in the third pregnancy in 10 cases, and during one of several pregnancies in 10 other women. Walsh (5) surveyed 243 similar cases and found that 43% of the women stated that pregnancy worsened their hearing. Gristwood and Venables (6) conducted a retrospective study of 479 women who had otosclerosis to determine the effect of pregnancy on their hearing loss. They reported that the risk of a subjective sense of hearing loss was 33% in women who had bilateral otosclerosis after one pregnancy, which increased to 63% after six pregnancies. In women who had unilateral disease, the complaint of increased hearing loss was much less.
When the effect of pregnancy on otosclerosis was documented by audiometric testing, it became apparent that the actual incidence of hearing loss was much lower than subjectively reported by the patients. Day (7) tested 47 women undergoing 75 pregnancies and observed hearing loss in only three women. Sullivan (8) studied 25 otosclerotics who had undergone fenestration surgery and later became pregnant and noted hearing loss in the unoperated ear in three cases; however, this hearing loss occurred 3 to 5 years after the pregnancies. Walsh (5) similarly reviewed patients who became pregnant following fenestration surgery and found two who had hearing loss in the operated ear. Hearing loss was also observed in seven other patients; this also occurred 3 to 5 years following surgery. Walsh concluded that pregnancy had no significant effect on otosclerosis.
Lindsay (9) similarly doubted whether pregnancy had an adverse effect on otosclerosis. He considered the observed onset and increased severity of symptoms in pregnant women represented the coincidental peak incidence of this disorder during the childbearing years.

Meuniere Disease
Meuniere syndrome is characterized by vertigo, tinnitus, hearing loss, and aural fullness believed to be induced by endolymphatic hydrops. Although Lederer and Tardy (10) suggested that the retention of sodium and water occurring during pregnancy may aggravate labyrinthine dysfunction and result in the clinical manifestation of latent Meuniere disease, there are few reports on its course during pregnancy. Uchide and colleagues (11) noted a correlation between the patient’s serum osmolality and the frequency of Meuniere symptoms. Interestingly, they found that when the serum osmolality was significantly below normal (<270 mosm/kg) the attacks increased to 10 per month. However, as the pregnancy proceeded and the serum osmolality normalized, the attacks decreased in frequency. The vertigo in this study was treated with oral isosorbide and intramuscular injections of diazepam.
Eustachian Tube Dysfunction
Edema of the nose and upper aerodigestive tract during pregnancy may result in malfunction of the eustachian tube, with failure of equilibration of the pressure within the middle ear and mastoid and nasopharynx. Loss of patency of the eustachian tube produces the troublesome sensation of fullness in the ear that is unrelieved by swallowing. Persistent closure of the eustachian tube may result in the formation of a negative pressure in the middle ear space, secondary to resorption of air by the blood vessels of the lining mucosa. If this is sustained, a serous effusion results. The presence of fluid in the middle ear space produces a conductive hearing loss and carries the potential risk of secondary bacterial infection.
In a prospective study by Derkay (12) using tympanometry and anterior rhinomanometry, objective evidence of eustachian tube dysfunction and nasal obstruction was found in 80% of symptomatic third-trimester patients, compared with 45% of asymptomatic matched pregnant patients and with 30% of nonpregnant controls. Cigarette smoking was found to predispose women to this condition.
On otoscopy, the tympanic membrane may appear to be normal or slightly retracted and does not move on Valsalva’s maneuver. Impedance audiometry may reveal normal compliance, a persistent negative pressure in the middle ear, or evidence of fluid. If the condition progresses to serous otitis, a myringotomy and the insertion of a ventilating tube may be necessary. As in all adults with unilateral serous otitis, examination of the nasopharynx is mandatory in order to eliminate the possibility of a lesion obstructing the eustachian tube ostium. A limited trial of topical nasal decongestants (e.g., Neosynephrine) may be used. The symptoms usually subside spontaneously postpartum.
Facial Paralysis
The prevalence of Bell’s palsy appears to be greater in pregnant women than in the general population. Robinson and Pou (13) calculated an incidence of 1 case per 2,000 pregnancies over a 10-year period studied. Suggested causative factors include hormonal alterations, hypercoagulability, autoimmune disease, viral infection, vascular injury, and fluid retention (2), with the latter being generally favored, for although interstitial edema occurs in many body areas during pregnancy, swelling of the facial nerve within its bony canal causes direct mechanical injury to the nerve or obstruction to its blood supply. Powers (2) reviewed 46 reported cases of facial paralysis occurring in pregnancy. The mean age of the patients was 26 years. The right and left sides of the face were involved with equal frequency, with bilateral paralysis developing in only one case. There was a peak incidence in the third trimester (79% of the cases), with a small number of cases occurring in the second trimester (8%) and immediately postpartum (13%). Approximately half of the cases were associated with preeclampsia (13,14). The paralysis spontaneously resolved immediately after delivery in the majority of the patients, but persisted for 1 to 2 months in several cases (15). The loss of nerve excitability on electrical testing may be considered an indication for surgical decompression.
In 1995, Ben-David and colleagues (16) studied the effects of ovarian steroids on the brainstem during changes of estrogen and progesterone blood levels. They found, through the use of brainstem evoked response audiometry, that a significant delay in peak III occurred with an increased stimulus rate in the cohort with the highest estrogen level. They concluded that estrogen may cause a brainstem synaptic impairment, presumably because of ischemic changes, and therefore may also be responsible for a higher incidence of Bell’s palsy during pregnancy.
Drug Ototoxicity
Numerous chemical agents, including various antibiotics, diuretics, analgesics, and antineoplastic drugs, may produce sensorineural hearing loss, tinnitus, and vertigo from their deleterious effects on the inner ear. Prominent among these substances are the aminoglycoside antiobiotics (e.g., streptomycin, gentamicin, kanamycin, tobramycin, and amikacin), which are markedly cochleotoxic. The degree of placental transportation of these agents is unclear. Streptomycin is said to cross the placenta, whereas kanamycin was found to achieve only very low levels in the fetus (17). Consequently, these drugs should be administered with great caution to pregnant mothers to prevent the occurrence of ototoxicity in newborn infants.

The development of serous otitis from the increased tendency toward eustachian tube dysfunction during pregnancy may be complicated by secondary bacterial infection. Pain then supervenes on ear fullness and decreased hearing, with otoscopy revealing a reddened tympanic membrane with loss of landmarks. Antibiotic therapy is directed against Streptoccus pneumoniae and Hemophilus influenzae (including beta-lactamase–producing strains), which are the most commonly encountered pathogens. Presently, the drugs of choice are amoxicillin-clavulanic acid and the newer cephalosporins (e.g., cefuroxamine).
Naranbhai and colleagues (18) described the development of congenital tuberculous otis in two infants from two mothers who had miliary tuberculosis by infection in utero or at birth.
Nasal obstruction is a well-recognized accompaniment of pregnancy in some women. The experimental injection of estrogenic hormones has been shown to produce perivascular edema of the nasal mucosa in monkeys (19,20). Mabry (21) suggested that estrogen may produce nasal mucosal congestion through a cholinergic mechanism. Pooling of blood in the nasal tissues secondary to the increased circulating volume and a progesterone-induced smooth-muscle relaxation of blood vessels are other proposed causes of the observed nasal congestion (22,23).
The observation of nasal congestion in pregnancy, swelling of the nasal mucosa during menstruation, and the erectile property of the turbinates and septal mucosa led to the concept of a reciprocal nasogenital relationship in which there was postulated a physiologic association between the nose and the reproductive tract (24). MacKenzie (25) is credited with being the first to report the occurrence of nasal congestion and turbinate enlargement in pregnancy. Proetz (26) reported recurrent polyposis and nasal edema with successive pregnancies. The congested nasal mucosa manifests itself clinically by nasal stuffiness and obstruction, often with serous rhinorrhea or postnasal discharge.
During pregnancy, aggravation of nasal allergic symptoms is occasionally observed in patients with nasal allergy. Hamano and colleagues observed an increase in the expression of histamine (H1) receptor mRNA in patients with nasal allergy (27). Moreover, this study demonstrated that the female hormones beta-estradiol and progesterone significantly increased the expression of H1 receptor mRNA on human nasal epithelial cells and human mucosal microvascular endothelial cells. Because of this, they concluded that these sex hormones were related, at least partially, to symptoms of nasal hyperactivity during pregnancy.
Mabry (21) concluded in a study of 66 randomly selected pregnant women and 16 pregnant women under treatment for pregnancy rhinitis that rhinitis gravidarum may not be an isolated entity. Other causes of chronic nasal congestion in pregnant women also include allergic and bacterial rhinosinusitis and rhinitis medicamentosa (22,23).
Pharmacologic treatment of allergic diseases is often necessary during pregnancy. Drugs used should be safe and without serious side effects for either mother or fetus. Topical mucosal agents seem to be safest, due to their minimal or absent absorption. Preferred agents are topical anthihistamines and steroids (for rhinitis and conjunctivitis) and cromolyn with topical steroids (for asthma) because they are both safe and effective (28).
The congested and hyperemic mucosa may result in epistaxis from rupture of a superficial blood vessel. This is generally controlled by the application of a topical vasoconstrictor and chemical or electrocautery. Occasionally anterior nasal packing is required. The nasal edema of pregnancy is self-limiting and disappears after delivery. Derkay (12) noted that the rhinitis of pregnancy resolved spontaneously within 4 to 10 weeks following delivery on objective measuring with anterior rhinomanometry.
The prolonged use of topical nasal sprays containing sympathomimetic substances is to be avoided because of the rebound congestion they produce. In a long-term study by Settipane and colleagues (29) comparing mothers receiving allergy immunotherapy during pregnancy and untreated controls, no statistically significant difference was detectable in the offspring regarding the development of asthma, rhinitis, or positive skin tests.
The nasal hemangioma of pregnancy is a rare lesion. Ash and Old (30) on review of 3,000 benign nasal tumors, found only 23 nasal hemangiomas, one of which arose during pregnancy. Fu and Perzin (31) and Shalit and colleagues (32) each mentioned an additional case. The exact pathogenesis of these tumors is unknown, with suggested causes including hormonal alterations (especially during placentation), changes in blood volume, vessel growth in a preexisting vascular anomaly, or a combination of factors (33). Histologically, the majority of these lesions are of the capillary type. Clinically, these tumors generally arise on the anterior nasal septum and present with epistaxis. They tend to regress after delivery, and those that fail to involute should be excised.
It should be noted that hemangiomas arise at various cutaneous and mucosal sites during pregnancy. Barter and colleagues (33) reported such lesions appearing on the lips, tongue, cheek, and eyelid. They may require excision if they cause bleeding or produce deformity.
Nasal granuloma gravidarum is another rare entity occurring in pregnancy in which the patient rapidly develops an intranasal mass that produces obstruction and

bleeding. It generally develops in multiparous women. Whereas McShane and Walsh (34) were able to remove the lesions readily in their cases under local anesthesia, severe bleeding and recurrences were noted by other researchers (35).
The congestion of the nasal cavity commonly present during pregnancy may extend to the nasopharynx, producing the previously cited eustachian tube dysfunction. No distinct pathologic entity exists in the nasopharynx that is produced by or aggravated during pregnancy; however, Yan and colleagues (36) found that pregnant women who developed and underwent radiotherapy for nasopharyngeal carcinoma had a much poorer prognosis (5-year survival of 11%) than did women who became pregnant following completion of therapy.
In response to the hormonal influence of pregnancy and the local irritative effect of subgingival dental plaque or calculus, gingival hypertrophy occurs. It may progress to the development of a reddish-purple, friable, sessile, or pedunculated lobular mass involving one or several teeth. Lindhe and colleagues (37) demonstrated the ability of pregnancy hormones to cause increased vascular permeability and proliferation in the buccal mucosa of the hamster. Gridly (38) reported an incidence of gingivitis of 23% and of pregnancy tumor formation of 2.7% among 1,002 women studied.
The pregnancy tumor may arise anywhere in the oral cavity but has a predilection for the anterior teeth. The lesion is painless and may bleed spontaneously or from minimal trauma on mastication. It generally appears between the third and fifth months of pregnancy and progressively increases in size with gestation (39). Histologically, the lesion is composed of a vascular stroma containing infiltrates of acute and chronic inflammatory cells and is covered by a hyperplastic squamous epithelium. Consequently, these lesions frequently have been diagnosed microscopically as pyogenic granulomas or angiofibromas. Although some small tumors may regress postpartum, most persist and enlarge during subsequent pregnancies. Treatment is local excision; however, recurrence is not uncommon later in the pregnancy (40).
Maxilla and Mandible
McGowan (41) reported a patient who developed a central giant cell tumor of the mandible during pregnancy that reappeared during a subsequent pregnancy. On survey of the literature, he collected four other cases of giant cell tumors of the jaws that had enlarged during pregnancy. Based on review of the clinical histories of these cases, he proposed that a hormonal influence occurred during pregnancy that influenced the growth of these lesions. Additional reports of active enlargement of giant cell tumors were made in the mandible and the maxilla during pregnancy (42,43). Littler (43) reported reactivation of such a mandibular tumor in pregnancy after a quiescent period of 6 years. Fechner and colleagues (44) reported an unusual case of such a lesion of the maxilla that, in the last trimester of pregnancy, rapidly grew and extended intracranially, requiring a craniofacial resection for control.
Histologically these lesions consist of scattered multinucleated giant cells within a fibrous stroma containing focal areas of hemorrhage and osteoid formation. These lesions are considered reparative granulomas rather than true neoplasms, and they are treated by curettage. As with all giant cell lesions of the skeleton, hyperparathyroidism must be ruled out by appropriate biochemical tests.
Laryngopathia gravidarum is a temporary condition arising in some pregnant women in which edema, dryness, and crusting of the laryngeal mucosa produce hoarseness (45). The condition is innocuous, but probably has the potential to hinder endotracheal intubation.
Laryngeal edema is occasionally encountered in late pregnancy, which may complicate obstetric anesthesia. The congestion of the mucous membranes of the upper respiratory tract also may involve the false vocal cords (46). This can be aggravated by the increased venous pressure resulting from the strenuous bearing-down efforts of the second stage of labor (47). Jouppila and colleagues (48) reported difficult intubation in a patient requiring early postpartum anesthesia for a vaginal hematoma, and MacKenzie (47) described laryngeal edema complicating intubation in two patients with prolonged labor.
In patients who have preeclampsia with facial edema but no respiratory obstruction, unrecognized laryngeal edema may be present, which may render laryngeal intubation difficult. Several such cases have been reported (47,48 and 49). The presumed mechanism for this interstitial edema of the larynx is a decreased serum protein level secondary to the albuminuria of preeclampsia. Why it has a predilection for the larynx in some people is unknown.
Other unusual causes of airway obstruction in pregnancy are the occurrence of hereditary angioedema (50) and the development of necrotizing epiglottitis complicating infectious mononucleosis (51).
Supraglottic hemangiomas of the larynx that enlarged with pregnancy causing airway obstruction were reported by Brandwein and colleagues (52)

and Mugliston and Sanewan (53). In the case of Brandwein and colleagues (52) the lesion spontaneously involuted at 36 weeks of gestation; however, the patient in the study of Mugliston and Sangwan (53) required a tracheostomy because of the severe dyspnea.
Enlargement and increased vascularity of the thyroid gland is noted in more than 50% of normal pregnant patients (see Chapter 22) (54). Although a small amount of diffuse enlargement of the thyroid gland may be considered a normal physiologic response to pregnancy, the presence of a solitary nodule is a matter of greater concern. The reported incidence of autoimmune disease of the thyroid approaches 10% in women. This autoimmune state, which predisposes to the development of thyroid neoplasia, especially in patients with subclinical hypothyroidism, combined with tumor growth and immunologic factors that occur in pregnancy, account for the significant incidence of nodular thyroid disease in the pregnant state (52). Thyroid nodules that produce suspicious aspirates on cytologic examination should be managed with a certain degree of urgency (55). In a series of 30 patients with thyroid neoplasia arising during pregnancy, 43% were carcinoma and 37% adenoma. Given the results, surgical management of thyroid mass during pregnancy should be performed either in the second trimester or immediately after delivery (56).
Doherty and colleagues (56) retrospectively reviewed the records of 23 patients with thyroid nodules that were first detected during pregnancy. The incidence of malignancy in the series was 39%. Because of the apparent increased potential for malignancy in thyroid nodules during pregnancy, the author recommended the following management guidelines: fine-needle aspiration and biopsy to be performed for rapidly enlarging thyroid nodules before 20 weeks’ gestation; for nodules associated with palpable cervical adenopathy; for solid nodules larger than 2 cm; and for cystic nodules larger than 4 cm.
In contrast, Cunningham and Slaughter (57) studied 26 patients who underwent surgery for a solitary nodule that had arisen during, or was affected by, pregnancy. The majority were colloid nodules, with nine true adenomas found. Obstetrical parity did not influence the formation of the nodule. The nodules generally appeared in the first and second trimesters, or postpartum, and occurred infrequently during the last trimester. Medical management generally produced no effect. There were eight patients who had thyroid carcinoma, five of whom underwent surgery during pregnancy. Among these operated cases, there were three fetal deaths. In a comparative study of the incidence of carcinoma and adenoma in pregnant and nonpregnant women, the same relative frequency of both lesions was found in the two groups. Also, the number of pregnancies did not influence the development of carcinoma or alter its prognosis.
Rosvoll and Winship (58) studied 60 patients who had thyroid carcinoma: 38 had been treated for carcinoma 2 to 15 years before becoming pregnant and were clinically free of disease; 22 patients had residual and metastatic carcinoma and subsequently became pregnant. In the first group, pregnancy did not reactivate the carcinoma. In the second group it did not appear to accelerate tumor growth. Hill and colleagues (59) analyzed two groups of patients who had thyroid carcinoma: 70 patients had one or more pregnancies after the diagnosis of carcinoma was established, and 109 who had carcinoma did not subsequently become pregnant after it was diagnosed. They found no significant difference in the recurrence rate in both groups and no apparent effect on the clinical course of the disease by one or several pregnancies. There is considerable clinical evidence to support the conclusion that pregnancy does not increase the risk of thyroid malignancy or adversely influence the prognosis in patients who have thyroid carcinoma. Consequently, the decision to operate on a pregnant patient who has a solitary nodule should be based on the presence of clinical features suggesting malignancy, such as fixation of the gland, cervical lymphadenopathy, or the presence of a vocal cord paralysis.
Patients who have simple colloid goiters may experience enlargement, with pressure symptoms developing during pregnancy. This results from a decrease in the plasma iodine level secondary to increased renal clearance. Cunningham and Slaughter (57) noted enlargement during pregnancy in 13 of 18 patients with goiters.
In patients who have a multinodular goiter, a serum antithyroid antibody titer should be drawn to rule out Hashimoto’s disease. Thyroid function tests will identify the approximately 30% of patients who have this disease and who become hypothyroid (60).
Disorders of the head and neck arising in pregnancy have been reviewed according to the anatomic site of involvement.
In the ear there is an increased occurrence of eustachian tube dysfunction secondary to the edema of the mucosa of the upper respiratory tract. The incidence of facial paralysis is also greater in pregnant women; however, it carries a good prognosis, with spontaneous regression occurring postpartum in the majority of patients. No convincing evidence supports exacerbation of the hearing loss of otosclerosis or the vertigo of Meuniere’s disease by pregnancy. Caution must be exercised in administering potentially ototoxic drugs to pregnant women because of the risk of transplacental transfer to the fetus.
Nasal obstruction commonly arises from hormonally induced congestion of the mucosa lining (rhinitis gravidarum). Rarely, a hemangioma or granuloma of pregnancy develops in the nose.

In the oral cavity, angiofibromatous lesions arise from the gingiva (pregnancy tumor), and giant cell reparative granulomas of the jaws show a pattern of accelerated growth in response to pregnancy.
Hoarseness may occur from dryness and crusting of the larynx (laryngopathia gravidarum). Unsuspected laryngeal edema may complicate obstetrical anesthesia by rendering intubation difficult at the time of delivery or in the immediate postpartum period.
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