Chapter 72 Surgery in the Pregnant Patient
Physiologic Changes Of Pregnancy
Progesterone and estrogen, two of the principal hormones of pregnancy, mediate many of the maternal physiologic changes in pregnancy. Normal laboratory values differ in the gravid compared with the nonpregnant patient. The diaphragm can be elevated in pregnancy up to 4 cm and the lower chest wall can widen up to 7 cm.1 These changes may also mimic similar pathophysiology that occurs in nonpregnant women who have cardiac or liver disease. Elevated progesterone levels, as well as decreased serum motilin, result in smooth muscle relaxation, producing multiple effects on several organ systems. In the stomach, this decreased smooth muscle tone results in diminished gastric tone and motility. The lower esophageal sphincter tone is also decreased and, when combined with increased intra-abdominal pressure, results in an increase in the incidence of gastroesophageal reflux. Small bowel motility is reduced, increasing small bowel transit time. Absorption of nutrients, however, remains unchanged, with the exception of iron absorption, which is increased because of increased iron requirements. In the colon, pregnancy-related changes usually manifest as constipation. This is caused by a combination of increased colonic sodium and water absorption, decreased motility, and mechanical obstruction by the gravid uterus. An increase in portal venous pressure, and therefore an increase in the pressure in the collateral venous circulation, results in dilation of the veins at the gastroesophageal junction. This is of importance only if the patient had esophageal varices before becoming pregnant. The most common result of the increased portal venous pressure is dilation of the hemorrhoidal veins, leading to the well-known complaint of hemorrhoids.
In addition to alterations in smooth muscle tone and motility, other notable changes occur in the gastrointestinal tract. The function of the gallbladder is altered, as is the chemical composition of bile. During the second and third trimesters, the volume of the gallbladder may be twice that found in the nonpregnant state, and gallbladder emptying is markedly slower. Up to 4% of pregnant patients have gallstones on routine obstetric ultrasound.2 Still, only 1 of every 1000 pregnant patients develops symptoms. It is unknown whether the increased biliary stasis, changes in bile composition, or combination of these two factors results in an increased risk for gallstone formation, but the risk for developing gallstones increases with multiparity. However, the incidence of symptomatic cholelithiasis during pregnancy is similar to the incidence in age-related nonpregnant women.
Oxygen consumption increases during pregnancy. Minute ventilation increases by 50% because of an increase in tidal volume, which appears to be a result of an elevated serum progesterone level.1 Progesterone not only increases the sensitivity of the respiratory centers to CO2 but also acts as a direct stimulant to the respiratory centers. As a consequence of the increased minute ventilation, the maternal PaO2 level during late pregnancy ranges from 104 to 108 mm Hg and the maternal PaCO2 level ranges from 27 to 32 mm Hg. Renal compensation maintains a normal maternal pH. The decreased PaCO2 level increases the CO2 gradient from the fetus to the mother, facilitating CO2 transfer from the fetus to the mother. The oxygen-hemoglobin dissociation curve of maternal blood is shifted to the right; this, coupled with the increased affinity of fetal hemoglobin for oxygen, results in increased oxygen transfer to the fetus. Elevation of the diaphragm by as much as 4 cm results in a decrease in total lung volume by 5%. Diminished expiratory reserve volume and residual volume result in a functional residual capacity that is 20% lower than that in the nonpregnant woman. Vital capacity and inspiratory reserve volume remain stable.
In the kidney, there is an increase in the glomerular filtration rate by 50% that accompanies a 75% increase in renal plasma flow. Urinary glucose excretion increases as a direct consequence of the increased glomerular filtration rate. The blood urea nitrogen level decreases by 25% during the first trimester and is maintained at that level for the remainder of the pregnancy. The serum creatinine level also decreases by the end of the first trimester from a nonpregnant value of 0.8 to 0.7 mg/dL and may be as low as 0.5 mg/dL by term. A five- to tenfold increase in the serum renin level occurs, with a subsequent four- to fivefold increase in the angiotensin level. Although the pregnant patient is apparently less sensitive to the hypertensive effects of the increased angiotensin, elevated aldosterone levels result in an increase in sodium reabsorption, overcoming the natriuresis produced by elevated progesterone levels. Serum sodium levels are decreased, however, because the increase in sodium reabsorption is less than the increase in plasma volume. Serum osmolality is decreased to 270 to 280 mOsm/kg.1
The increase in plasma volume and red blood cell mass is accompanied by a progressive rise in the leukocyte count during pregnancy. During the first trimester, the white blood cell count ranges from 3,000 to 15,000 cells/mm3, increasing to a range of 6,000 to 16,000 cells/mm3 during the second and third trimesters.1 The platelet count progressively declines throughout pregnancy, whereas the mean platelet volume tends to increase after 28 weeks’ gestation. As noted, fibrinogen levels are elevated to a range of 400 to 500 mg/dL. Plasma levels of factors VII, VIII, IX, and X also rise progressively, whereas levels of factors XI and XIII decline, and levels of factors II, V, and XII remain unchanged. Despite these alterations in the coagulation cascade and platelet count, bleeding and clotting times are unchanged.
Safety Concerns In Pregnancy
Radiologic Concerns
Radiographic studies remain useful diagnostic tools for the pregnant patient. Of greatest concern with radiation exposure is the risk to the fetus from the exposure. The accepted maximum dose of ionizing radiation during the entire pregnancy is 5 cGy. The fetus is at the highest risk from radiation exposure from the preimplantation period to approximately 15 weeks’ gestation. Primary organogenesis occurs during this time and the teratogenic effects of radiation, particularly to the developing central nervous system, are at their highest. Perinatal radiation exposure has also been associated with childhood leukemia and certain childhood malignancies. The radiation dose that has been associated with congenital malformation is higher than 10 cGy. As shown in Table 72-1, radiation exposure to the fetus with the doses from the more common radiology procedures is well below that threshold. Nonetheless, prudence on the part of the clinician is required to avoid unnecessary fetal exposure to ionizing radiation, especially during the first and early second trimesters, when the risk from exposure is greatest.
Table 72-1 Fetal Radiation Exposure With Radiographic Imaging
| EXAMINATION TYPE | ESTIMATED FETAL RADIATION EXPOSURE (cGy) |
|---|---|
| Two-view chest radiography | 0.00007 |
| Cervical spine radiography | 0.002 |
| Pelvis radiography | 0.04 |
| Head CT | <0.050 |
| Abdomen CT | 2.60 |
| Upper GI series | 0.056 |
| Barium enema | 3.986 |
| Hepatobiliary (HIDA) scanning | 0.150 |
GI, Gastrointestinal; HIDA, hepatobiliary iminodiacetic acid.
Magnetic resonance imaging (MRI) avoids exposure to ionizing radiation but poses an unknown risk to the fetus. Animal studies have shown no teratogenic effect or increased incidence of fetal death or congenital malformations from the electromagnetic radiation, static magnetic field, radiofrequency magnetic fields, or IV contrast agents used during MRI. Theoretically, the gradient magnetic fields may produce electric currents in the patient and the high-frequency currents induced by radiofrequency fields may cause local generation of heat. The long-term effect of exposure is not known.3 The National Radiological Protection Board has advised against the use of MRI during the first trimester of pregnancy.
Medication Concerns
Antibiotics
Quinolones
Ciprofloxacin
The use of ciprofloxacin during human gestation does not appear to be associated with an increased risk of major congenital malformations. Although a number of birth defects have occurred in the offspring of women who had taken this drug during pregnancy, the lack of a pattern among the anomalies is reassuring. In addition, a meta-analysis has shown that the use of quinolones during the first trimester of pregnancy does not appear to represent an increased risk for major malformations after birth, stillbirths, preterm births, or low birth weight.4
Anesthesia Concerns
The effects of anesthesia during pregnancy can be divided into direct, or active, and indirect, or passive, effects. The direct effects relate to the possible teratogenic or embryotoxic properties of the drugs used for anesthesia, some of which cross the placenta. The indirect effects are those mechanisms whereby an anesthetic agent or surgical procedure may interfere with maternal or fetal physiology and, in doing so, harm the fetus. For the most part, the fetus experiences indirect effects as a consequence of anesthetic agents administered to the mother and hemodynamic changes in the mother from blood loss or anesthetic agents. The most profound effects on the fetus are related to decreased uterine blood flow or decreased oxygen content of uterine blood. Unlike circulation to other vital organs, most notably the brain, the uterine circulation is not autoregulated. During the third trimester, uterine circulation represents almost 10% of cardiac output. When treating maternal hypotension, vasopressors such as dopamine and epinephrine, although increasing the maternal systemic pressure, have little or no effect on uterine circulation. Phenylephrine and metaraminol are alpha agonists that are effective in maintaining maternal blood pressure and preventing fetal acidosis.5 Other maneuvers, such as fluid bolus, Trendelenburg position, compression stockings, and leg elevation, have a larger impact on increasing uterine blood flow.
Postoperative pain control in the pregnant patient needs to be monitored closely. NSAIDs are not used in pregnancy because of the risk for premature closure of the ductus arteriosis.6 Morphine and fentanyl are both good IV choices postoperatively. Morphine has a higher associated incidence of nausea and vomiting, but most surgeons have extensive experience with it. A patient-controlled analgesia pump after surgery may be the best choice because of the associated low incidence of maternal respiratory depression and drug transfer to the fetus.
Abdominal Pain And The Acute Abdomen In Pregnancy
When the pregnant patient presents with abdominal pain, it may be difficult to distinguish a pathophysiologic cause from normal pregnancy-associated symptoms. Changes in the position and orientation of abdominal viscera from the enlarging uterus, and the alterations in physiology already described, may modify the perception or manifestation of an intra-abdominal process. If it is early in the pregnancy, the woman may not know that she is pregnant. Also, some intra-abdominal processes are exclusive to pregnancy, such as ectopic pregnancy, HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome, or acute fatty liver of pregnancy. Both patient and physician may attribute the patient’s complaints to normal pregnancy, resulting in a delay in evaluation and treatment. These delays in diagnosis and definitive intervention are the most serious adverse events affecting maternal and fetal outcome. It is usually not the treatment but the delay in diagnosis and severity of the primary disease process that affects outcomes poorly. Box 72-1 lists the more common causes of abdominal pain in the pregnant patient, classified according to location.
