OBSTETRICS

OBSTETRICS

OBSTETRICS PHYSIOLOGIC CHANGES IN PREGNANT WOMEN Cardiovascular System Changes Changes in the cardiovascular system during pregnancy can be summarized as (I) an increase in intravascular fluid volume, (2) an increase in cardiac output, (3) a decrease in systemic vascular resistance

INTRAVASCULAR FLUID VOLUME Maternal intravascular fluid volume increases in the first trimester, and at term the plasma volume is increased about 45% and the erythrocyte volume about 20%. This disproportionate increase in plasma volume accounts for the relative anemia of pregnancy. The increased intravascular fluid volume offsets the 300 to 500 mL blood loss that accompanies vaginal delivery and the average 800 to 1000 mL blood loss that accompanies cesarean section. The total plasma protein concentration is decreased as a result of the dilutional effect of the increased intravascular fluid volume.

CARDIAC OUTPUT Cardiac output increases about 10% by the 10th week of gestation and increases 40% to 50% by the third trimester. This augmentation of cardiac output is due to an increased stroke volume (25% to 30%) and heart rate (15% to 25%). The onset of labor is associated with further increases in cardiac output, with the largest increase occurring immediately after delivery, when cardiac output is increased by as much as 80%. This presents a unique postpartum risk for patients with cardiac disease, such as fixed valvular stenosis. A regional anesthetic is capable of attenuating the release of catecholamines during painful labor and the resultant maternal tachycardia and systemic hypertension.

Cardiac output substantially returns toward prepregnant values by 2 weeks postpartum. SYSTEMIC VASCULAR RESISTANCE Systolic blood pressure decreases by as much as 15% during an uncomplicated pregnancy. Although there is an increase in cardiac output and plasma volume, systemic blood pressure does not increase because of a decrease in systemic vascular resistance (mean arterial pressure may decrease slightly). Furthermore, there is no change in central venous pressure during pregnancy despite the increased plasma volume because venous capacitance increases. Femoral venous pressure increases about 15%, presumably

reflecting compression of the inferior vena cava by the gravid uterus. AORTOCAVAL COMPRESSION (SUPINE HYPOTENSION SYNDROME) Decreases in maternal blood pressure because of aortocaval compression by the gravid utems are associated with the supine position. Significant aortoiliac artery compression occurs in 15% to 20% of pregnant women and vena cava compression in all such women. Vena cava compression may contribute to lower extremity venous stasis and thereby result in ankle edema and varices. Diaphoresis,

nausea, vomiting, and changes in cerebration may accompany this hypotension. These symptoms are termed the "supine hypotension syndrome." Mechanism and Compensatory Responses The mechanism of supine hypotension syndrome is decreased venous return as a result of compression of the inferior vena cava by the gravid uterus when the pregnant woman assumes the supine position. The resulting decrease in venous return leads to a decrease in cardiac output and a decline in systemic blood pressure.

compensatory responses that prevent hypotension despite aortocaval compression: One compensatory mechanism is increased venous pressure below the level of compression of the inferior vena cava, which serves to divert venous blood from the lower half of the body via the paravertebral venous plexuses to the azygos vein. Flow from the azygos vein enters the superior vena cava and venous return is maintained. Dilation of the epidural veins may make penetration of a vein more likely during attempted lumbar epidural anesthesia and thus could lead to accidental intravascular injection of the local anesthetic solution. This would result in a bolus delivery of local anesthetic to the heart

with potentially profound consequences on the central nervous and cardiovascular systems. Another compensatory response that prevents hypotension with aortocaval compression is a reflex increase in peripheral sympathetic nervous system activity. This results in increased systemic vascular resistance and permits systemic blood pressure to be maintained despite decreased cardiac output. It is important to recognize that compensatory increases in systemic vascular resistance are impaired by regional anesthetic techniques. Indeed, arterial hypotension is more common and profound during regional anesthesia administered to pregnant as compared with

nonpregnant women. In addition to compression of the inferior vena cava, the gravid uterus can compress the lower abdominal aorta . Such compression leads to arterial hypotension in the lower extremities, but maternal symptoms or decreases in systemic blood pressure as measured in the arms do not occur. RISKS: The significance of aortocaval compression is the associated decrease in uterine and placental blood flow. Even with a healthy uteroplacental unit,

prolonged maternal hypotension (approximately 90 to 100 mm Hg systolic blood pressure for an average patient) for longer than 10 to 15 minutes will most likely significantly decrease uterine blood flow and lead to progressive fetal acidosis. Venous compression by the gravid uterus diverts some blood returning from the lower extremities through the internal vertebral venous plexus to the azygos and epidural veins, thereby increasing the likelihood of epidural venous puncture with epidural or spinal techniques. Supine positioning is avoided in pregnant women during anesthetic administration in the second and third trimesters. Anesthetic techniques that interfere with increased sympathetic nervous system tone will further compromise the compensatory mechanisms for vena cava compression induced by supine positioning and potentially cause profound hypotension

Treatment Displacing the gravid uterus can minimize the incidence of supine hypotension syndrome, which is important for patients undergoing regional or general anesthesia because their compensatory increases in systemic vascular resistance will be impaired. Displacement of the gravid uterus can be achieved by placing the pregnant woman in the lateral position or by moving the gravid uterus to the left and off the inferior vena cava or aorta. Displacement of the uterus to the left can be accomplished manually or by elevation of the right hip 10 to 15 cm with a blanket or wedge .

Pulmonary System Changes The most significant changes in the pulmonary system during pregnancy include alterations in (l) the upper airway, (2) minute ventilation, (3) lung volumes, (4) arterial oxygenation UPPER AIRWAY Capillary engorgement of the mucosal lining of the upper respiratory tract accompanies pregnancy, emphasizing

the need for careful instrumentation of the upper airway during suctioning, placement of airways (avoid nasal instrumentation if possible), and direct laryngoscopy. It may be prudent to select a smaller cuffed tracheal tube (6.5 to 7.0 mm internal diameter) because the vocal cords and arytenoids are often edematous. Weight gain associated with pregnancy, particularly in women of short stature or with coexisting obesity, can result in difficulty inserting the laryngoscope because of a short neck and large breasts. MINUTE VENTILATION Minute ventilation is increased about 50% above prepregnant levels during the first trimester and is maintained for

the remainder of the pregnancy. This increased minute ventilation is achieved primarily by an increased tidal volume, with small increases in the respiratory rate (see 1able 32-2). Increased circulating levels of progesterone are presumed to be the stimulus for increased minute ventilation. Resting maternal Paco2 decreases from 40 to about 32 mm Hg during the first trimester as a reflection of the increased minute ventilation. Arterial pH, however, remains near normal because of increased renal excretion of bicarbonate ions. The pain associated with labor and delivery results in further hyperventilation, which can be

attenuated by adequate analgesia, such as lumbar epidural analgesia. LUNG VOLUMES Lung volumes, in contrast to the early appearance of increased minute ventilation, do not begin to change until about the third month of pregnancy. With increasing enlargement of the uterus, the diaphragm is forced cephalad, which is primarily responsible for the 20% decrease in functional residual capacity (FRC) present at term. As a result, FRC can be less than closing capacity for many small airways and may give rise to atelectasis in the supine position. Vital capacity is not

significantly changed. The combination of increased minute ventilation and decreased FRC results in an increase in the rate at which changes in the alveolar concentration of inhaled anestheticcan be achieved. This affects induction of anesthesia, emergence from anesthesia, and changes in depth of anesthesia. ARTERIAL OXYGENATION

Early in gestation, maternal Pao2 while breathing room air is normally above 100 mm Hg because of the presence of hyperventilation. Later, Pao2 becomes normal or even slightly decreased, most likely reflecting airway closure. During induction of general anesthesia in a pregnant patient, Pao2 decreases more rapidly than in a nonpregnant patient because of decreased oxygen reserve (decreased FRC) and increased oxygen uptake (increased metabolic rate). For these reasons, the administration of supplemental oxygen during a regional anesthetic or "preoxygenation" (breathe oxygen for 3 minutes, four to five deep breaths, or eight maximal breaths over a I-minute period) before any anticipated period of apnea (such as induction of

general anesthesia) is recommended. Nervous System Changes Anesthetic requirements (minimum alveolar concentration [MAC]) for volatile anesthetics decrease during pregnancy as demonstrated in humans and animals.s The sedative effects produced by progesterone may be partially responsible. The important clinical implication of decreased MAC is that alveolar concentrations of inhaled drugs that would not produce unconsciousness in nonpregnant patients may approximate anesthetizing concentrations in pregnant women. This degree of central nervous system depression can impair protective upper airway reflexes

and subject pregnant women to pulmonary aspiration. Furthermore, the decreased FRC increases the rate at which potential excessive alveolar concentrations of anesthetics can be achieved. Engorgement of epidural veins as intra-abdominal pressure increases with progressive enlargement of the uterus results in a decrease in the size of the epidural space and decreased volume of cerebrospinal fluid (CSF) in the subarachnoid space. The decreased volume of these spaces facilitates the spread of local anesthetics. The observation of increased spread of local anesthetic solutions placed in the epidural space as early as the first trimester

suggests a role for biochemical as well as mechanical changes. Indeed, data from pregnant women demonstrate increased peripheral nerve sensitivity to lidocaine. These mechanical and biochemical changes are consistent with the decrease in dose requirements of local anesthetics necessary for epidural or spinal anesthesia in pregnant women at term gestation. Renal Changes Renal blood flow and the glomerular filtration rate are increased about 50% to 60% by the third month of

pregnancy. Therefore, the normal upper limits in blood urea nitrogen and serum creatinine concentrations are decreased about 50% in pregnant women. Hepatic Changes Plasma protein concentrations are reduced during pregnancy because of dilution, similar to the physiologic anemia of pregnancy. Decreased serum albumin levels can result in higher free blood levels of highly protein-bound drugs. Slightly elevated liver function test results do not necessarily indicate hepatic disease. Plasma cholinesterase (pseudocholinesterase) activity is decreased about 25%

from the 10th week of gestation to as long as 6 weeks postpartum. This decreased activity is unlikely to be associated with significant prolongation of the neuromuscular blocking effects of succinylcholine or mivacurium. As part of the hypercoagulable state of pregnancy, plasma concentrations of coagulation factors, including fibrinogen, are increased. Gastrointestinal Changes Gastrointestinal changes during pregnancy make pregnant women vulnerable to regurgitation of gastric contents and to the development of acid pneumonitis should pulmonary aspiration occur. Displacement of the pylorus

cephalad by the enlarged uterus retards gastric emptying, and progesterone decreases gastrointestinal motility. As a result, gastric fluid volume tends to be increased even in the fasting state. In addition, gastrin, which is secreted by the placenta, stimulates gastric hydrogen ion secretion such that the pH of gastric fluid is predictably low in pregnant women. The enlarging uterus changes the angle of the gastroesophageal junction and thereby leads to relative incompetence of the physiologic sphincter mechanism. For this reason, gastric fluid reflux into the esophagus with subsequent esophagitis (heartburn) is common in pregnant women.

RISK OF ASPIRATION Regardless of the time interval since the ingestion of food, women in labor must be treated as having a full stomach. Pain, anxiety, and drugs (especially opioids) administered during labor can all slow gastric emptying beyond an already prolonged transit time. The increased risk for pulmonary aspiration of gastric contents is the reason for recommending placement of a cuffed tube in the trachea of pregnant women rendered unconscious by anesthesia. The recognition that the pH of inhaled gastric fluid is important in the production and severity of acid pneumonitis is the basis for the administration of antacids to pregnant women before induction

of anesthesia. To obviate the hazards of inhalation of particulate antacids that can increase pulmonary damage, the use of a nonparticulate antacid such as sodium citrate is recommended. H2 receptor antagonists usually increase gastric fluid pH in pregnant women without producing adverse effects and are recommended by some. 1-12receptor antagonists, unlike antacids, do not alter the pl-l of gastric fluid already present in the stomach. Combinations of an 1-12receptor antagonist and sodium citrate may be more useful than an antacid alone for producing a persistent increase in gastric fluid pH. Metoclopramide can be useful for decreasing the gastric

fluid volume of pregnant women in active labor who require general anesthesia and are considered to be at high risk for increased gastric fluid volume (apprehension, systemic opioid analgesia, recent solid food ingestion). The gastric hypomotility associated with opioid administration, however, may be resistant to treatment with metoclopramide. PHYSIOLOGY OF THE UTEROPLACENTAL CIRCULATION The placenta is a union of maternal and fetal tissue for the purpose of physiologic exchange. Maternal blood is delivered to the placenta by the uterine arteries, and

fetal blood arrives via two umbilical arteries. Nutrient-rich and waste-free blood is delivered to the fetus through a single umbilical vein. Uterine Blood Flow Uterine blood flow increases to about 700 mUmin (about 10% of cardiac output) at term gestation, with about 80% of the uterine blood flow perfusing the intervillous space (placenta) and 20% the myometrium. The uterine vasculature is not autoregulated and remains essentially maximally

dilated under normal conditions during pregnancy. Though capable of marked vasoconstriction in response to a-adrenergic drugs, pregnancy is associated with reduced uterine artery response and sensitivity to vasoconstrictors. Uterine blood flow decreases because of decreased uterine perfusion pressure as a result of systemic hypotension (shock; general, epidural, or spinal anesthesia). Uterine blood flow also decreases with aortocaval compression or increased uterine venous pressure as a result of vena cava compression (supine position) or uterine contractions (particularly uterine hyperstimulation as may occur with oxytocin administration or abruption). Epidural or spinal

anesthesia does not alter uterine blood flow as long as maternal hypotension is avoided. ephedrine has been considered the drug of choice for the treatment of hypotension caused by the administration of regional anesthesia to pregnant women. Increased uterine vascular resistance with decreases in uterine blood flow can also result from maternal stress or pain that stimulates the endogenous release of catecholamines. This response suggests that a regional

or general anesthetic may be protective to the fetus in certain instances. Uterine contractions also decrease uterine blood flow secondary to increased uterine venous pressure. PLacentaL Exchange Placental exchange of substances occurs principally by diffusion from the maternal circulation to the fetus and vice versa. Diffusion of a substance across the placenta to the fetus depends on maternal-to-fetal concentration gradients, maternal protein binding, molecular weight, lipid solubility, and the degree of ionization of that substance. Minimizing the maternal blood concentration

of a drug is the most important method of limiting the amount that ultimately reaches the fetus. The high molecular weight and poor lipid solubility of nondepolarizing neuromuscular blocking drugs result in limited ability of these drugs to cross the placenta. Succinylcholine has a low molecular weight but is highly ionized and therefore does not readily cross the placenta. Thus, during administration of a general anesthetic for cesarean section, the fetus/neonate is not paralyzed. Placental transfer of barbiturates, local anesthetics, and opioids is facilitated by the relatively low molecular weights of these substances. Drugs that readily cross the blood-brain barrier

also cross the placenta. FETAL UPTAKE Fetal uptake of a substance that crosses the placenta is facilitated by the lower pH (0.1 unit) of fetal than maternal blood. The lower fetal pH means that weakly basic drugs (local anesthetics, opioids) that cross the placenta in the nonionized form will become ionized in the fetal circulation. Because an ionized drug cannot readily cross the placenta back to the maternal circulation, this drug will accumulate in the fetal blood against a concentration gradient. This phenomenon is known as ion trapping and may explain the higher concentrations of lidocaine found

in the fetus when acidosis secondary to fetal distress is present . Furthermore, conversion of lidocaine to the ionized fraction maintains the concentration gradient from the mother to the fetus for continued passage of nonionized lidocaine to the fetus. Despite decreased enzyme activity in comparison to adults, neonatal enzyme systems are adequately developed to metabolize most drugs, with the possible exception of mepivacaine. UNIQUE CHARACTERISTICS OF THE FETAL CIRCULATION The unique characteristics of the fetal circulation influence the distribution of drugs in the fetus and protect the vital

organs of the fetus from exposure to high concentrations of drugs initially present in umbilical venous blood. For example, about 75% of umbilical venous blood passes through the liver such that significant portions of drugscan be metabolized before reaching the fetal arterial circulation for delivery to the heart and brain. Moreover, drugs in the portion of umbilical venous blood that enters the inferior vena cava via the ductus venosus will be diluted by drug-free blood returning from the lower extremities and pelvic viscera of the fetus. ANESTHESIA FOR CESAREAN DELIVERY Although the majority of cesarean deliveries are performed

with regional anesthesia, sometimes the severity of the fetal condition (severe fetal heart rate deceleration) necessitates the use of general anesthesia for its rapidity, and at other times it is required when regional anesthesia is contraindicated. Regardless, in preparation for cesarean delivery, all pregnant women should receive an oral antacid (nonparticulate such as sodium citrate) to reduce gastric fluid pH. In addition, some anesthesiologists routinely administer a drug to accelerate gastric emptying (metoclopramide) or an H2 receptor antagonist (ranitidine), or both, to reduce gastric acid production. Spinal Anesthesia

For a pregnant woman without an epidural catheter, spinal anesthesia is the most common regional anesthetic technique used for cesarean delivery (Table 32-6). The block is technically easier than an epidural anesthetic, more rapid in onset, and more reliable in providing surgical anesthesia from the mid thoracic level to the sacrum.The incidence of post-dural puncture headache has become low with the introduction of noncutting, "pencil-point" spinal needles. However, maternal hypotension is more likely and more profound with spinal anesthesia than with epidural anesthesia because the onset of sympathectomy is more rapid. Prehydration, avoidance of aortocaval compression, and aggressive use of ephedrine (even as a

prophylactic) may minimize the risk for hypotension. Spinal anesthesia can be safely used in patients with preeclampsia. Lumbar Epidural Anesthesia Epidural anesthesia is an excellent choice for surgical anesthesia when an indwelling, functioning epidural catheter has been placed for labor analgesia. It is also ideal for patients who cannot tolerate the sudden onset of sympathectomy or in some patients with cardiac disease. The volume and concentration of local anesthetic drugs used for surgical anesthesia are larger than those used for labor analgesia; however, the technique of catheter placement,

test dosing, and potential complications are similar. Typically, the anesthesiologist attempts to provide sensory anesthesia from the T4 level to the sacrum. This level of anesthesia may not always alleviate the visceral pain associated with peritoneal manipulation, and adjuvant drugs may be necessary (see Table 32-5). Local Anesthesia Although cesarean delivery can be performed by local infiltration, it is accompanied by considerable discomfort and risks the possibility of local anesthetic overdose; moreover, most obstetricians have not been trained to do this. However, in rare circumstances of acute fetal distress,

when a regional block is inadequate, and when induction of general anesthesia is considered dangerous (morbid obesity), local infiltration can be helpful to at least deliver the baby. General anesthesia can then be induced after securing the patient's airway with appropriate techniques, which may include awake fiberoptic tracheal innlbation. General Anesthesia General anesthesia is used in obstetric practice for cesarean section, typically when regional anesthesia is contraindicated (coagulopathy, certain cardiac lesions, hemorrhage) or for emergencies (placental abruption, uterine rupture, fetal bradycardia, prolapsed umbilical cord) because of its

rapid and predictable action (Table 32-7). After rapid-sequence induction of anesthesia and placement of a cuffed tracheal tube facilitated by the administration of succinylcholine or a nondepolarizing neuromuscular blocking drug, anesthesia is maintained by inhalation of nitrous oxide and a volatile anesthetic, often in combination with sedative-hypnotics or opioids (or both). Nondepolarizing neuromuscular blocking drugs are subsequently administered to facilitate surgery. INDUCTION DRUGS Thiopental Thiopental (4 to 6 mg/kg IV) is the most commonly used

drug for induction of general anesthesia in obstetrics because it renders the patient unconscious within 30 seconds of administration. This dose of thiopental has no significant clinical impact on neonatal well-being. Neonatal depression may, however, occur with higher doses of thiopental, and cardiorespiratory supportive techniques are necessary until the neonate can excrete the drug (may take up to 48 hours). Ketamine Ketamine produces a rapid onset of anesthesia and, unlike thiopental, increases systemic blood pressure, heart rate, and cardiac output by central stimulation of the sympathetic

nervous system. Increased uterine tone and decreased uterine blood flow can accompany excessively large doses of ketamine. In contrast to thiopental, low doses of ketamine (0.25 mglkg IV) have profound analgesic effects. The undesirable psychotomimetic side effects (hallucinations, bad dreams) associated with ketamine administrations can be lessened by coadministration of benzodiazepines . Many anesthesiologists consider ketamine the appropriate drug for induction of anesthesia in a pregnant woman who is actively hemorrhaging, has uncertain blood volume, and is at risk for profound hypotension in response to intravenous thiopental.

Etomidate Etomidate, like thiopental, has a rapid onset of action because of its high lipid solubility, and redistribution results in a relatively short duration of action. Although etomidate has minimal effects on the cardiovascular system, unlike thiopental and ketamine, it is painful on injection, induces extrapyramidal motor activity, and thus is rarely used in obstetrics. PropofoI The need to have syringes of induction drugs ready to

administer for rapid response to urgent situations requiring induction of general anesthesia (fetal distress) detracts from the value of preservative-free propofol in the obstetric suite. For an elective cesarean section, this highly lipid soluble drug results in rapid onset of action similar to thiopental and rapid and complete recovery with less residual sedative effect than is the case with thiopental. Nevertheless, propofol has not been demonstrated to be superior to thiopental in maternal or neonata] outcome. Furthermore, propofol has been associated with maternal bradycardia when administered with succinylcholine for induction of general anesthesia for cesarean section.

MAINTENANCE OF ANESTHESIA Maintenance of anesthesia for cesarean section often includes the inhalation of 50% nitrous oxide in combination with a low concentration of volatile anesthetic. A volatile anesthetic is an important component of general anesthesia for cesarean section because the incidence of maternal recall of intraoperative events without these drugs is unacceptably high. During a typical general anesthetic for cesarean delivery, opioids are administered after the baby is delivered to avoid the concern of placental transfer to the neonate. Placental transfer of volatile anesthetics is rapid because

they are nonionized, highly lipid-soluble substances of low molecular weight. Fetal concentrations depend on the concentration and duration of anesthetic administered to the mother. If excessive concentrations of volatile anesthetics are administered for prolonged periods, neonatal effects of these drugs, as evidenced by flaccidity, cardiorespiratory depression, and decreased tone, may be anticipated. It is important to recognize that if neonatal depression is due to transfer of anesthetic drugs, the infant is merely lightly anesthetized and should respond easily to simple treatment measures such as assisted ventilation of the lungs to facilitate excretion of the inhalation anesthetic. Rapid improvement of the infant should be expected,

and if it does not occur, it is important to search for other causes of depression. There may be confusion regarding the presence of fetal distress, the use of general anesthesia, and subsequent delivery of a depressed neonate. A depressed fetus is likely to be associated with a depressed neonate, and general anesthesia is selected because it is the most rapidly acting anesthetic technique to allow cesarean delivery. For a healthy fetus, the interval from induction to delivery is not as important to neonatal outcome as the interval from uterine incision to delivery, when uterine blood flow may be compromised and fetal asphyxia may occur. A long time from induction to delivery may result in a lightly

anesthetized neonate, but not an asphyxiated neonate. NEUROMUSCULAR BLOCKING DRUGS Succinylcholine remains the neuromuscular blocking drug of choice for obstetric anesthesia because of its rapid onset and short duration of action. This depolarizing neuromuscular blocking drug is normally hydrolyzed in maternal blood by the enzyme pseudocholinesterase and does not generally interfere with fetal neuromuscular activity. If the hydrolytic enzyme is present either in lowconcentration or in a genetically determined atypical form, prolonged maternal or neonatal respiratory depression secondary to muscular paralysis can occur

Nondepolarizing neuromuscular blocking drugs are titrated to response with the use of a peripheral nerve stimulator. Under normal circumstances, the poorly lipidsoluble, highly ionized, non depolarizing neuromuscular blocking drugs do not cross the placenta in amounts signifIcant enough to cause neonatal skeletal muscle weakness. This placental impermeability is only relative, however, and when large doses are given over long periods, as for the treatment of maternal tetanus or status epilepticus, neonatal neuromuscular blockade can occur. The diagnosis of neonatal depression secondary to drug-induced

neuromuscular blockade may be made on the basis of the maternal history (prolonged administration of neuromuscular blocking drugs, history of atypical pseudocholinesterase), the response of the mother to neuromuscular blocking drugs, and physical examination of the newborn. A paralyzed neonate will have normal cardiovascular function and good color, but no spontaneous ventilatory movements or reflex responses, and skeletal muscle flaccidity is present. The anesthesiologist can test the neonate with a peripheral nerve stimulator and demonstrate the classic signs of neuromuscular blockade. Treatment consists of respiratory support until the neonate excretes the drug (may take up to 48 hours). Antagonism of nondepolarizing neuromuscular blocking drugs with cholinesterase inhibitors (neostigmine, edrophonium) may be attempted, but adequate respiratory support is the mainstay of treatment.

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