Dental Management of the Pregnant Patient

1

Ethical Issues in the Treatment of the Pregnant Patient

Christos A. Skouteris

Ethical principles and the rights of the mother and fetus for the provision of proper medical and dental care are closely intertwined. These principles are based on the fact that care is actually provided to two individuals. Since the mother is the life support of the fetus, the medical and dental status of the mother should be optimized during pregnancy. Therefore, necessary medical and dental treatment should not be denied to any female patient because of pregnancy.

Dental procedures, however minor, are associated with increased patient anxiety levels, the need for imaging, and the administration of medications. For these reasons, elective dental procedures should be postponed until postpartum. However, when a pregnant patient is in need of emergency, preventive, or restorative treatment, the aforementioned reasons may force the dentist to refuse treatment because of concern for the mother and the unborn child and the fear of liability and litigation if something happens to the pregnancy and the fetus. Denial of treatment, however, raises serious ethical issues. Thomas Raimann (2016), in response to the question whether it is ethical for dentists to refuse seeing pregnant women until after they give birth, laid out the ethical principles of the ADA Code of Ethics that particularly apply in the dental management of the pregnant patient (Box 1.1).

Box 1.1 Ethics in the dental management of the pregnant patient.

Applicable principles of the ADA Code of Ethics

Principle I: Autonomy, Involvement

Principle II: Nonmaleficence

Principle IV: Justice

Principle V: Veracity

The principle of patient Autonomy (self‐governance) and Involvement states that The dentist should inform the patient of the proposed treatment in a manner that allows the patient to become involved in treatment decisions. Patient involvement in treatment decisions is highly desirable and ethical; however, pregnant women who have medical needs during pregnancy should not be expected to weigh the risks and benefits when they have to decide whether to proceed with a proposed treatment whose impact on the fetus is unknown. This is an impossible demand; no one can weigh unknown risks and benefits. On the other hand, a straight denial of treatment by the dentist without patient involvement becomes a unilateral decision and thus ethically questionable.

The principle of Nonmaleficence (do no harm) expresses the concept that professionals have a duty to protect the patient from harm. Under this principle, the dentist’s primary obligations include keeping knowledge and skills current. Denying treatment to a pregnant patient violates this principle in the sense that it is evidence of lack of knowledge on the dentist’s part. Evidence‐based studies have shown that necessary dental procedures can be performed during the second trimester of pregnancy without an increased risk for serious medical adverse events, spontaneous abortions, preterm deliveries, and fetal malformations. The conservative approach of discouraging treatment because of lack of knowledge about the effects of a procedure and/or medication is not typically erring on the side of fetal safety; rather, it suggests a lack of knowledge about whether it is riskier for the fetus to be exposed to a medication or to the effects of untreated maternal morbidity. According to Lyerly et al. (2008), in the absence of information about the safety and efficacy of medications, pregnant women and their healthcare providers are left with two unsavory options: take a drug, with unknown safety and efficacy, or fail to treat the condition, thus leaving the woman and fetus vulnerable to the consequences of the underlying medical problems.

Under the principle of Justice (fairness), a dentist has a duty to treat people fairly. Moreover, the dentist’s primary obligations include dealing with people justly and delivering dental care without prejudice and dentists shall not refuse to accept patients into their practice or deny dental service to patients because of the patient’s sex. Refusing to treat a pregnant patient could be interpreted as discriminating against her unjustly and thus disregarding the ADA Code.

The Veracity principle (truthfulness) refers to the dentist’s primary obligations which include respecting the position of trust inherent in the dentist–patient relationship, communicating truthfully and without deception, and maintaining intellectual integrity. The dentist is not truthful if denying treatment to a pregnant patient on the grounds of potential harm to the mother and fetus, when scientific evidence does not support that the pregnancy and the fetus are at risk.

The most serious ethical issues arise in cases of life‐threatening conditions, such as head and neck infections, severe maxillofacial trauma, and locally aggressive benign and malignant tumors. These conditions will be discussed later in the book. Under those circumstances, treatment decisions for a pregnant patient necessitate a choice between saving her life and that of the fetus, or other dramatic trade‐offs. In such cases, Puls et al. (1997) stated that there is general consensus (especially in the wake of the Angela Carder case; Box 1.2) that the primary consideration should be saving the life of the mother. Charles Weijer (1998) points out, however, that in some cases a pregnant patient’s decision to refuse treatment and sacrifice herself for her child should be counted as an autonomous decision worth respecting, and that it should not be assumed that only self‐interest decisions can be autonomous.

Box 1.2 The Angela Carder case.

Angela Carder (née Stoner) was diagnosed with Ewing’s sarcoma at the age of 13 years. Her prognosis was dismal but following chemotherapy and radiation, she managed to survive and remained in remission for several years. She got married and with her doctors’ approval she became pregnant.

In 1987, in her first week of the third trimester of pregnancy, she was found to have recurrence of her disease with lung metastases. She had already fought hard to survive and she requested to be treated again with chemotherapy and radiation which had contributed to her years in remission, in spite of the risks to the fetus. She was admitted to George Washington University Hospital, in Washington DC, where she was deemed a terminal case. As a result of her condition, there was disagreement as to whether she should be treated, exercising her right to save or prolong her life, at the expense of the life of the fetus. Although her condition deteriorated and she was running out of time, Angela did not elect to have an emergent C‐section.

This caused concern among the hospital risk managers who, fearing a lawsuit from pro‐life organizations, requested a court hearing on the issue, providing legal representation for Angela, the fetus, and the hospital. At the hearing, her family and her attending physicians all testified against performing a C‐section, based on low survivability for the patient and her expressed desire not to go through with the procedure. Angela was not able to testify during the hearing because of her very poor physical condition. The testimony that tipped the balance in favor of an emergent C‐section was that of a neonatologist, not familiar with her condition, who testified that the fetal survival rate was 60%. Interestingly, the same fetal survival rate applies also to pregnant women in good health who are at the same gestational age. Angela’s attending oncologist was not asked to testify, although he had expressed the view that the procedure was inadvisable for the patient and the fetus.

The court eventually issued an order for an emergent C‐section to be performed, although Angela strenuously objected to it. Only one of the hospital’s obstetricians reluctantly agreed to perform the procedure without an informed consent and against the will of the patient. Following the C‐section, the fetus is purported to have survived for 2 hours. Angela endured the procedure, was informed about the fate of the fetus, and died 2 days later.

Eventually, in April of 1990 after a legal battle, the US Appellate Court ruled that all previous decisions be annulled and that Angela Carder had the right to make her own decisions relative to her health and the health of her fetus. It was the first Appellate Court decision to take a stand against forced C‐sections. The case stands as a landmark in United States case law establishing the rights of pregnant women to determine their own healthcare.

Adapted from Thornton and Paltrow (1991) .

References

Lyerly AD, Little MO, and Faden RR. (2008) A critique of the fetus as patient. American Journal of Bioethics, 8, 42.

Puls L, Terry R, and Hunter J. (1997) Primary vaginal cancer in pregnancy: difficulty in the ethical management. Ethics and Medicine, 13, 56.

Raimann T. (2016) The ethics of dental treatment during pregnancy. Journal of the American Dental Association, 147, 689.

Thornton TE and Paltrow L (1991) The rights of pregnant patients. Carder case brings bold policy initiatives. HealthSpan, 8(5), 10–16.

Weijer C. (1998) Commentary: self‐interest is not the sole legitimate basis for making decisions. British Medical Journal, 316, 850.

Further Reading

Flyn TR and Susarla SM. (2007) Oral and maxillofacial surgery for the pregnant patient. Oral and Maxillofacial Surgical Clinics of North America, 19, 207.

Zalta EN, Nodelman U, Allen C, et al. (2011) Pregnancy, birth, and medicine. Stanford Encyclopedia of Philosophy. Available online at: https://plato.stanford.edu/entries/ethics‐pregnancy/ (accessed 15 October 2017).

2

Physiologic Changes and Their Sequelae in Pregnancy

Christos A. Skouteris

The physiologic changes that occur during pregnancy are hormonal as well as anatomic, consequently affecting many organs and systems of the female body. These changes can occasionally present as subtle homeostatic alterations that can progress to serious, even life‐threatening situations, if they are not recognized early and preventive and management actions are not employed in a timely manner. Pregnancy induces cardiovascular, respiratory, hematologic, urinary, gastrointestinal, hepatobiliary, endocrine, immunologic, dermatologic, musculoskeletal, and psychologic changes that are more dramatic in multifetal than in single pregnancies. Most of these changes return to normal after delivery.

Cardiovascular

The cardiovascular system’s response to pregnancy is a dynamic process aiming at providing uteroplacental circulation for normal fetal growth and development. Changes in cardiovascular physiology involve the peripheral vascular resistance, cardiac output, heart rate, stroke volume, and blood pressure (Box 2.1).

Box 2.1 Most significant cardiovascular changes in pregnancy.

Peripheral vascular resistance decreases

Cardiac output increases

Heart rate increases

Stroke volume increases

Blood pressure decreases

Peripheral vascular resistance decreases by approximately 35–40% as a result of systemic vasodilation. Vasodilation is mostly the result of the action of increased concentrations of relaxin, progesterone, and estradiol. Relaxin is a peptide hormone produced by the corpus luteum of the ovary, the breast and, during pregnancy, also by the placenta, chorion, and decidua. This hormone has been shown to have an endothelium‐dependent vasodilatory role in pregnancy that can influence small arterial vessel resistance, thus causing an increase in arterial compliance. Nitric oxide was also thought to contribute to the decrease in peripheral vascular resistance through vasodilation, as studies of human hand flow suggested, but studies of forearm flow showed that it does not. The decrease in peripheral resistance starts in the first trimester, is more profound in the second trimester, with a slight upswing during the third trimester of pregnancy.

Cardiac output increases sharply in the first trimester, continues to increase into the second trimester and by the 24th week of gestation has reached a level of 30–50% above the baseline. There is no consensus as to whether any changes in cardiac output occur in the third trimester of pregnancy. The increase in cardiac output in early pregnancy is credited to increased stroke volume whereas the increase in cardiac output in late pregnancy is attributed to the increase in heart rate. Cardiac output falls to nonpregnant values in a few weeks after delivery. The physiologic increase in cardiac output is a compensatory mechanism to counteract the decreased oxygen capacity of maternal blood. Any event from any source that can cause a drop in cardiac output may result in maternal hypoxia and compromise the condition of the fetus.

Heart rate shows a progressive increase by 10–20 bpm during the first and second trimester with a peak in the third trimester. The overall increase in heart rate raises 10–20% above the baseline and remains increased for 2–5 days after delivery.

Stroke volume starts increasing from the eighth week and reaches a peak by the 20th week of pregnancy. It drops back to baseline by the second week post partum. Stroke volume is augmented by the increase in end‐diastolic volume and maintenance of ejection fraction through a possible increase in contractile force. The increase is the result of dramatic heart and vascular remodeling during the first few weeks of pregnancy. Heart remodeling is expressed throughout pregnancy by a left ventricular wall thickness and left ventricular wall mass increase by 28% and 52% above pre‐pregnancy values respectively, and by a 40% increase in right ventricular mass. Vascular remodeling is demonstrated by an increase in arterial compliance. A measure of increase in arterial compliance is provided by the aortic augmentation index, a marker of aortic stiffness, which decreases significantly early during pregnancy, reaching a lowest point in the second trimester and gradually increasing in the third trimester.

Blood pressure is decreased during pregnancy, including systolic blood pressure, diastolic blood pressure, mean arterial pressure, and central systolic blood pressure. Diastolic blood pressure and mean arterial pressure decrease more than systolic blood pressure. Arterial pressures decrease to a lowest point during the second trimester (dropping 5–10 mmHg below baseline), but the majority of the decrease occurs early in pregnancy (6–8‐week gestational age) compared with nonpregnancy values. This decrease in blood pressure during pregnancy is ascribed to vasodilation mainly caused by relaxin, progesterone, estradiol, prostacyclin, and potentially by nitric oxide.

Respiratory

Respiratory changes affect the condition of the upper airway tissues as much as the pulmonary and respiratory physiology (Boxes 2.2, 2.3). The upper airway undergoes significant mucosal changes. The mucosa becomes friable and edematous. Capillary engorgement causes hyperemia of the nasal and oropharyngeal mucosa and larynx which begins early in the first trimester and increases progressively throughout pregnancy. Up to one‐third of pregnant women experience severe rhinitis, which predisposes them to frequent episodes of epistaxis and upper respiratory tract infections. Polyposis of nose and sinuses may occur and regress after delivery. Airway conductance increases, indicating dilation of the respiratory tract below the larynx. This is mainly due to direct effects of progesterone, cortisone, and relaxin. Another potential mechanism is through enhanced beta‐adrenergic activity induced by progesterone.

Box 2.2 Respiratory changes in pregnancy: mucosal/anatomic.

Upper airway mucosa friable, edematous

Thoracic cage expands

Ribs flare

Diaphragm elevated

Intrathoracic pressure increases

Box 2.3 Respiratory changes in pregnancy: Pulmonary/respiratory.

Respiratory rate unchanged

Tidal volume increased

Minute ventilation increased

Total lung volume decreases

Vital capacity unchanged

Residual volume decreased

Inspiratory reserve volume unchanged

Expiratory reserve volume decreased

Forced expiratory volume 1 and ratio to forced vital capacity unchanged

Maternal/fetal O2 consumption increased

Functional residual capacity decreased

Hyperventilation

Compensatory respiratory alkalosis

Dyspnea

Respiratory changes in pregnancy: glossary of terms.

Tidal volume (TV): amount of air moving into lungs with each inspiration

Inspiratory reserve volume (IRV): air inspired with maximal inspiratory effort in excess of tidal volume

Expiratory reserve volume (ERV): volume expelled by active expiratory effort after passive expiration

Residual volume (RV): air left in lungs after maximal expiratory effort

Vital capacity (VC): greater amount of air that can be expired after maximal inspiratory effort

Forced vital capacity (FVC): the amount of air which can be forcibly exhaled after taking the deepest breath possible

Minute ventilation (MV): the total lung ventilation per minute

Functional residual capacity (FRC): volume of air present in the lungs at the end of passive expiration

Forced expiratory volume 1(FEV1): the maximum amount of air expired in 1 second

FEV1/FVC ratio: the proportion of vital capacity that can be expired in the first second of forced expiration

Anatomic and respiratory compensatory changes are commensurate with the increased oxygen demands of the mother and fetus and are mediated by biochemical and mechanical factors. These changes accommodate the progressive increase in oxygen consumption and the physical impact of the enlarging uterus. Normal oxygen consumption is 250 mL/min at rest and increases by 20% over the nonpregnant state in order to meet the 15% increase in the maternal metabolic rate.

As part of the anatomic adaptations to address these demands, the configuration of the thoracic cage changes early in pregnancy. The shape of the chest changes as diameters increase, by about 2 cm, resulting in a 5–7 cm expansion of the chest circumference. The flaring of the lower ribs causes the diaphragm to rise by up to 4 cm, its contribution to the respiratory effort increasing with no evidence of being impeded by the uterus. These changes are thought to be mediated by the effect of progesterone, which together with relaxin increases ribcage elasticity by relaxing ligaments. Flaring of the ribs results in an increase in the subcostal angle, transverse diameter, and chest circumference. As gestation advances, upward displacement of the diaphragm causes a total lung volume decrease of 5%.

In general, what remains unchanged in the respiratory physiology of the pregnant patient is the respiratory rate, vital capacity (VC), inspiratory reserve volume (IRV), FEV1 or the ratio of FEV1 to forced vital capacity, and the arterial pH.

Gas exchange undergoes significant changes during pregnancy. Tidal volume (TV) and minute ventilation increase by 30–40%. Minute ventilation is increased (primarily an increase in tidal volume with a normal respiratory rate) for two reasons. First, oxygen consumption and carbon dioxide production increase 20–30% by the third trimester and up to 100% during labor, necessitating increased minute ventilation to maintain normal acid–base status. In addition, progesterone directly stimulates the central respiratory center, causing a further increase in minute ventilation. Expiratory reserve volume (ERV), residual volume (RV), and functional residual capacity (FRC) decrease by 20%. The decrease in FRC reaches 80% of nonpregnant value by term. The FRC reduction is further affected by obesity and postural changes. A pregnant woman in the supine position has an FRC 70% of that in the sitting position.

All of these changes in pregnancy result in overcompensation in an effort to meet the maternal and fetal respiratory demands. The resulting hyperventilation causes an increase in arterial oxygen tension (PaO2) and a decrease in arterial carbon dioxide tension (PaCO2). Hyperventilation also seems to be related to an increase in the sensitivity of brainstem respiratory centers to the combined action of PaCO2 and progesterone. The net effect is a mild respiratory alkalosis caused by a compensatory fall in serum bicarbonate (HCO3‐) through an increase of bicarbonate excretion via the kidneys.

Hyperventilation and elevation of the diaphragm are the most likely causes of the so‐called physiologic dyspnea of pregnancy which is a common complaint of 60–70% of pregnant women. It usually starts late in the first trimester, shows an increased frequency in the second trimester, and remains stable during the third trimester of pregnancy. The mechanism of dyspnea during normal pregnancy is not entirely clear. It occurs while the uterus is still relatively small, so it cannot be attributed solely to an increase in abdominal girth. Hyperventilation is likely to be at least partially responsible, perhaps due to the increase in ventilation above the level needed to meet the rise in metabolic demand. The presence of dyspnea during pregnancy has been found to correlate with a low PaCO2 and the women most likely to experience dyspnea are those who had relatively high baseline nonpregnant values for PaCO2. Although dyspnea in pregnancy is not usually associated with pathologic processes, care must be taken not to dismiss it lightly and miss a warning sign of cardiac or pulmonary disease.

Hematologic

There are a number of profound physiologic hematologic changes that result during normal pregnancy. Some of these, in addition to their clinical implications, can induce significant alterations in laboratory values that in a nonpregnant woman would be considered distinctly abnormal. The most significant hematologic changes are summarized in Box 2.4.

Box 2.4 Most significant hematologic changes in pregnancy.

Physiologic anemia

Leukocytosis (neutrophilia)

Gestational thrombocytopenia

Hypercoagulability

Decreased fibrinolysis

Plasma volume increases 45% at term as a result of the combined action of the renin‐angiotensin and aldosterone systems which promote an increase in fluid retention. Plasma volume increases progressively throughout normal pregnancy. Most of this increase occurs by the 34th week of gestation. Plasma volume expansion is required to address the increased maternal‐fetal‐placental circulatory demands. The red blood cell volume, however, does not show significant change. The net result is a dilutional anemia (physiologic anemia of pregnancy) and a decrease in the serum colloid osmotic pressure. (Figure 2.1, Table 2.1). The physiologic anemia of pregnancy starts in the first trimester, becoming more profound in the third trimester.

Figure 2.1 Physiologic anemia of pregnancy.

Table 2.1 Hemoglobin/hematocrit range includes references with and without iron supplementation.

Leukocytosis, occurring during pregnancy, is due to the physiologic stress induced by the pregnant state. Neutrophils are the major type of leukocytes on differential counts. This is likely due to impaired neutrophilic apoptosis in pregnancy and as a result of