GOWINGO

COMPLICATIONS OF PREGNANCY.

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Abortion

Spontaneous abortion is the termination of pregnancy before 20 completed weeks of gestation (fetal weight < 500 g) and probably occurs with an incidence of 15% to 40%.

The interval may be divided with early abortion occurring before 12 weeks and late abortion at 12 to 20 weeks. Many other modifiers are utilized to describe the process. Inevitable abortion is when bleeding of intrauterine origin occurs with continuous and progressive dilatation of the cervix but without expulsion of the product of conception. Incomplete abortion is the expulsion of some but not all of the products of conception.

Complete abortion is an expulsion of all of the products of conception. Missed abortion is when the embryo or fetus dies in utero before the 20th week of gestation, but the products of conception are retained in utero for 8 or more weeks.
Approximately 75% of spontaneous abortions will occur before 16 weeks and 62% before 12 weeks of gestation. The incidence of abortion is influenced by age of the couple, previous full-term normal pregnancy, previous spontaneous abortions, previous stillbirth. previous infant with malformations or known genetic defects, and known parental influences (4.g., balanced translocation carrier, diabetes mellitus). Over 60% of first trimester spontaneous abortions have an abnormal karyotype. Other associations (listed in descending order of occurrence) include infection, anatomic defects, endocrine factors, immunologic factors, and maternal systemic diseases.
The symptomatology may vary from the simple slight bleeding and cramping with threatened abortion to pain, bleeding, cervical dilatation, and complete or incomplete expulsion of the products of conception. The differential diagnosis includes ectopic abortion, dysmenorrhea, unopposed estrogen stimulation of the endometrium, hydatidiform mole, pedunculated myomas, and cervical neoplasia.
Treatment for threatened abortion is generally no more than bed rest (including complete pelvic rest).
Inevitable, incomplete, and complete abortion may require intravenous fluids, oxytocics, and evacuation of the products of conception from the uterus.
Missed abortion may require evacuation of the uterus by either medical or surgical means; the most commonly used method is prostaglandin E suppositories.

Hyperemesis Gravidarum

Hyperemesis gravidarum represents a pernicious exaggeration of the nausea and vomiting that many pregnant women experience. Normally the height of nausea and vomiting coincides with the maximum peak of HCG production in the first trimester and, perhaps on this same basis, one can associate troublesome symptoms with the relatively higher levels found in molar and multiple pregnancy. Refractory vomiting leads to starvation, weight loss, marked dehydration, low-grade fever, hypokalemic alkalosis, extreme electrolyte imbalance, and finally acidosis. Most ominous signs include fever, tachycardia, jaundice, delirium, and retinal hemorrhages.
These grave cases are rare today, undoubtedly because of better emotional preparation and support of patients and because of appropriate family planning practices.
Among those with troublesome symptoms, the self-limiting nature of the problem together with simple measures, including reassurance, eliminating stressful commitments, adopting multiple small dry feedings, drinking only hot or very cold fluids between meals but often avoiding these altogether in the early morning, and use of an antiemetic drug, usually will be successful. Hospitalization is rarely necessary but may be useful for parenteral fluids and electrolyte adjustments as well as temporarily removing the patient from a stressful situation.
Psychiatric consultation may uncover an underlying disorder and aid in overall therapy. Nausea and vomiting appearing after the first trimester merit special investigation for an organic basis. The same is true of severe and refractory vomiting even in the first trimester. Possible underlying etiologic factors may include intestinal obstruction. gastrointestinal tumor or other disorders, hyperthyroidism, heavy metal poisoning. or other toxic states.

Hypertensive States of Pregnancy
Preeclampsia, eclampsia, chronic hypertension, chronic hypertension with superimposed preeclampsia, and transient hypertension are all included in the broad classification "hypertensive states of pregnancy." Preeclampsia is the presence of edema, hypertension, and proteinuria occurring primarily in nulliparas after the 20th week of gestation and has an increasing frequency near term. It occurs in approximately 8% of the general population and has the following predisposing associations: nulliparity, black race, maternal age less than 20 or over 35 years. multiple gestation, hydatidiform mole, low socioeconomic status, polyhydramnios. nonimmune fetal hydrops, diabetes.
chronic hypertension, and underlying renal disease.
Preeclampsia is divided into mild and severe categories. Mild preeclampsia is marked by a blood pressure of 140/90 mmHg or a 30 mmHg systolic or 15 mmHg diastolic increase above previous levels.
Other diagnostic criteria for preeclampsia include nondependent edema of the hands or face (dependent edema is considered a normal finding in pregnancy), weight gain in excess of 2 pounds per week, or a particularly sudden weight gain and proteinuria. Proteinuria is the last sign to develop in preeclampsia; indeed, nearly 30% of eclamptic patients do not have proteinuria. Edema is the least reliable sign. Indeed, nearly 40% of patients have no edema. The hemoglobin and hematocrit are elevated due to hemoconcentration, but severe cases may be marked by anemia due to hemolysis.
Thrombocytopenia may be present. Fibrin-split products and decreased coagulation factors may be detected. Uric acid is usually elevated above 6 mg/ml. Severe preeclampsia is marked by the following: systolic blood pressure more than 160 mmHg or diastolic blood pressure of 110 mmHg or more (recorded on two occasions at least 6 hours apart with the patient at bed rest), proteinuria exceeding 5 g in a 24-hour period or 3 to 4+ on dipstick testing, less than 500 ml of urine in a 24-hour period. cerebral or visual disturbances, epigastric pain, pulmonary edema, or cyanosis.
Many pathophysiologic alterations occur during this extraordinary process; however, a central factor appears to be an alteration in the sodium-potassium pump at the cellular membrane resulting in intracellular retention of sodium and. thus, water, Plasma volume is reduced materially with preeclampsia. Whereas normal pregnant patients are resistent to the vasopressor effects of angiotensin 11, women who develop preeclampsia lose their refractoriness many weeks prior to the onset of clinical symptomatology. In the kidney there is swelling in the glomerular capillary endothelium (glomerulo-endotheliosis) , which results in decreased glomerular perfusion and decreased GRF.
In some patients red blood cell disruption may occur along with disseminated intravascular coagulation (DIC) and Thrombocytopenia. In such cases elevated fibrin-split products: are usually found. The acronym "HELLP" syndrome has been used to describe patients with hemolytic anemia, elevated liver enzymes, and low platelet count. These stigmata are found in approximately 10% of patients with severe preeclampsia.
The complications of preeclampsia include early delivery with resultant fetal complications due to prematurity, acute uteroplacental insufficiency resulting in stillbirth, or intrapartum fetal distress or a small-for-gestationaI-age fetus.
The treatment of mild preeclampsia is bed rest and delivery. Patients are usually hospitalized, although occasionally mild preeclamptics who can be relied upon to follow instructions may be treated as outpatients. A typical regimen consists of bed rest, daily urine dipstick measurements for proteinuria, and blood pressure monitoring every 4 hours. Patients must be aware that severe headaches, epigastric pain, or visual disturbances constitute grave warning signals and should be reported immediately. Other danger signals include increasing blood pressure or increasing proteinuria. Patients should be weighed daily, and 24-hour urine studies for creatinine clearance and total protein obtained twice weekly. Other important laboratory considerations include liver function studies, uric acid, electrolytes, and serum albumin. Coagulation factors (prothrombin time [PT] and partial thromboplastin time [PTT], fibrinogen, platelet count) must be obtained in patients with severe preeclampsia. Antihypertensive medicines are not generally used unless the diastolic blood pressure exceeds 100 mmHg and the gestational age is 28 weeks or less.
Serial ultrasonography (every 2 to 4 weeks) and weekly NST and CST are used to determine fetal status. Amniocentesis assists in determining fetal pulmonary maturity, and corticosteroids may be used to accelerate fetal lung maturity in patients with increasing disease and an immature pulmonary maturity. When preeclampsia is rapidly worsening.
continuous fetal monitoring is advisable.
The overall goal of treatment of mild preeclampsia is to prolong the gestation to a point of fetal maturity for delivery. The goals of management of severe preeclampsia are to prevent eclampsia (convulsions), to control the maternal blood pressure, and to initiate delivery (definitive therapy). Some cases of mild preeclampsia and most cases of severe preeclampsia will be treated with magnesium sulfate. The exact mechanism by which it acts is unknown, but it decreases the amount of acetylcholine released at the myoneural junction, has a transient mild hypotensive effect. a transient mild decrease in uterine activity in labor, a tocolytic effect in premature labor, and potentiation of depolarizing muscle relaxants. The therapeutic level is 4.8 mg to 8.4 mg/ml. At a serum level of 10 mg/ml there is loss of deep tendon reflexes, and at IS mg/ml there is respiratory paralysis. At higher levels, cardiac arrest occurs in asystole. Magnesium sulfate is usually given intravenously with a loading dose of 2 to 4 g followed by constant infusion of 1.5 g to 2.0 g/hour after it is ascertained that urinary output is within normal limits (as magnesium sulfate is primarily excreted by the kidney). Magnesium sulfate should be administered only with an infusion pump, and the patient must be checked every 4 hours to ascertain that deep tendon reflexes are present, respirations are at least 12/minute, and urine output has been at least 25 mi/hour. Should overdosage with magnesium sulfate occur, the antidote is 10 ml of 10% calcium chloride or calcium gluconate given rapidly intravenously.
The goal of antihypertensive therapy is to bring the diastolic blood pressure to 90 to 100 mmHg. The drug of choice is hydralazine (a direct arteriolar vasodilator). which causes a secondary baroreceptor-mediated sympathetic discharge. It results in tachycardia and increased cardiac output and is metabolized by the liver. The dose is 5 mg given intravenously every 15 to 20 minutes, and the onset of action is 15 minutes. The peak effect occurs within 30 to 60 minutes, and duration is 4 to 6 hours.
In more than 95%c of cases hydralazine will be effective in controlling blood pressure. In some cases it may be necessary to go to labetalol. sodium nitroprusside, diazoxide, or trimethaphan. Once the patient is stabilized, a decision is reached as to whether delivery may be effected by induction of labor or whether cesarean is necessary.

Eclampsia, which includes the signs and symptoms of severe preeclampsia plus the addition of seizures, occurs in 0.2% to 0.5% of all deliveries.
Approximately 75% of eclamptic seizures occur before delivery. Approximately half of postpartum seizures will occur within the first 48 hours after delivery, but may occur as late as h weeks postpartum.
There may or may not be an aura preceding a seizure, and the seizures are of a tonic-clonic type.
Apnea is notable during the seizure and immediately postseizure hyperventilation occurs. Fever is a very poor prognostic sign. Complications of a seizure include tongue biting, broken bones, head trauma, aspiration of gastric contents, and retinal detachments. Pulmonary edema may occur following the seizures.
The treatment for seizures is usually magnesium sulfate given in the loading dose noted above. If the seizure occurs longer than 20 minutes after the loading dose, an additional 2 to 4 g of magnesium sulfite are given intravenously. If a seizure occurs despite a therapeutic level, diazepam 5 to 10 mg may be given intravenously or amylbarbitol up to 250 mg intravenously. Once the seizure is controlled and the mother is stabilized, the process for delivery is initiated using the same general guidelines as for severe preeclampsia. Preeclampsia and eclampsia contribute materially to both maternal and perinatal morbidity and mortality. Maternal complications include cerebral hemorrhage, aspiration pneumonia, hypoxic encephalopathy, thromboembolism, hepatic rupture, renal failure, or anesthetic accident.
In patients with just preeclampsia the risk of recurrence is only 1:3. but if there is chronic hypertension mistaken for preeclampsia the risk of recurrence is 70%.
There is only a 2% recurrence of eclampsia if the patient has had a previous hypertensive disorder not related to chronic hypertension.
Chronic hypertension complicating pregnancy varies according to the population. The average incidence is 1.5%. Of these patients, 80% have essential chronic hypertension, and 20% will have hypertension due to various renal diseases (e.g., interstitial nephritis, acute and chronic glomerulonephritis, systemic lupus erythematosus, and diabetic glomerulonephritis). Only a few cases will be due to endocrine diseases (e.g.., Cushing's disease.
primary hyperaldosteronism, thyrotoxicosis, pheochromocytoma) or coarctation of the aorta. Generally these patients are older (>30 years) obese, multiparous, and have associated medical problems (e.g., diabetes or renal disease). Black woman are at particular risk, as are women with a family history of hypertension. Typically, these patients have hypertension without other signs of preeclampsia, and the diagnosis is based on documented hypertension before conception, before 20 weeks of gestation, or persistence of hypertension longer than 6 weeks postpartum. Differentiating worsening hypertension from superimposed preeclampsia may be difficult.
The medical workup of these patients must include electrocardiography (left ventricular hypertrophy is found in 5% to 10%). Elevated serum creatinine, decreased creatinine clearance, and proteinuria are present in 5% to 10%. A chest x ray may reveal cardiomegaly.
Approximately one third of the patients with chronic hypertension in pregnancy will develop superimposed preeclampsia. These patients have an increased risk of abruptio placentae, DIC, acute tubular necrosis, or renal cortical necrosis. The fetus has a 20% to 30% a risk of prematurity and a 10% to 15% incidence of intrauterine growth retardation.
It is agreed that antihypertensive therapy will benefit the patient whose diastolic blood pressure exceeds 110 mmHg. Treatment of mild chronic hypertension remains controversial. If treatment of mild hypertension is utilized, methyldopa (a central alpha-adrenergic agonist) is the only antihypertensive drug whose long-term safety for mother and fetus has been adequately assessed. More severe hypertension may require hydralazine, B-blockers, labetalol, or the calcium channel blockers.
In the mildly chronic hypertensive patient there is little true maternal risk and perinatal survival should be 90% to 95%. The primary complications are superimposed preeclampsia, abruptio placentae, prematurity, and intrauterine growth retardation. In the more severe hypertensive who has onset of superimposed preeclampsia before 28 weeks of gestation, the addition of renal insufficiency prior to pregnancy, hypertensive cardiovascular disease, or congestive cardiomyopathy provide a more guarded prognosis for both mother and fetus.

Abruptio Placentae
Placental aborption refers to obstetric bleeding from the premature separation of a normally implanted placenta prior to the 20th gestational week.
Prior to this the mechanism may be similar but the process is referred to as an abortion. Whereas abruptio placenta occurs in approximately 11150 pregnancies. the severe form (which threatens maternal or perinatal survival) occurs in 1/500 pregnancies. Bleeding from this cause should be distinguished from placenta previa, uterine rupture, and nonobstetric causes of bleeding (such as infection, polyps, malignant lesions, etc.) and discharge of an endocervical mucous plug.
Although the etiology is unknown, placental abruption is found in association with maternal hypertension in about one half of cases. The predisposing factors may be vascular disease, preeclampsia, or chronic renal diseases. The previous occurrence of placental abruption is a risk factor.
Others include smoking, a uterine tumor, a hyperirritable or overdistended uterus, or the sudden reduction of uterine volume as in delivery of one twin, or membrane rupture and escape of a large quantity of amniotic fluid (polyhydramnios). Other possible causes that have been cited include multiparity, trauma, malnutrition (including folic acid deficiency and low vitamin C levels), vena caval compression, and short cord.
When the abrupted portion of the placenta is centrally located while peripheral attachments re main intact, the bleeding is internal or "concealed.'' An extension of the hematoma to the placental edge where peripheral disruption occurs or an abruption arising at the periphery give rise to visible or "external" bleeding. In the most severe cases there may be extensive hemorrhagic infiltration beneath the serosa of the uterus, the tubes and the adjacent ligaments, and also between the uterine muscle bundles. The latter occurrence is known as the uteroplacental apoplexy of Couvelaire; the additional complication of uterine atony and further hemorrhage postpartally sometimes occurs.
The classic signs and symptoms of abruptio placentae are (I) vaginal bleeding (usually dark red); (2) intense abdominal or lower back pain; (3) a tetanically contracted uterus (usually expressed as "boardlike"); and (4) symptoms of shock. Less than one half of cases present so dramatically and, often, minor disruptions involving only one or two central cotyledonJ may go unrecognized until the placenta is inspected after its removal. Ultrasonic scan assists in establishing the diagnosis. With profuse vaginal bleeding maternal hemodynamic instability becomes the primary concern and more rigorous intervention (usually cesarean) is necessary.

There may be an apparent level of hypovolemic shock out of proportion to the observed blood loss.
since there may be considerable concealed hemorrhage associated with uterine enlargement, dysrhythmic myometrial contractility, and severe pain.
In the more severe grades of placental abruption associated.with classic findings and shock, there may be DIC. Fibrin obstruction occurring in periglomerular arterioles, hypotension, lack of adequate renal perfusion, and perhaps arteriolar spasm from the release of myoglobin from damaged tissues may give rise to acute renal failure in severe abruptio cases.
A suspicion of placental abruption is an indication for blood to be drawn for a clot observation test and baseline coagulation studies. Defective clotting begins to occur when the concentration of plasma fibrinogen falls below 150 mg/100 ml. There is no role for expectant management once the diagnosis of a major placental abruption has been made .
The hematologic problem in the severe cases involves a consumption coagulopathy characterized by a depression in platelet count and decline in circulating levels of fibrinogen; Factors V, VIII, XIII; and, to a lesser extent, prothrombin. Rarely, there may be primary activation of the fibrinolytic system resulting in the lysis of fibrinogen by fibrinolysins before fibrin can be formed. This possibility accentuates the consumption coagulopathy and exacerbates the hemorrhage. The suspicion of this complication calls for the determination of fibrinogen-split products in the blood. If possible, fresh whole blood should be administered. If that therapy is not available, then packed red cells, fresh frozen plasma, and platelet packs are preferred.
Success in eliminating the underlying problem (which usually means delivery) is evidenced by a decline in the concentration of fibrin-split products first and, subsequently, by a rise in plasma fibrinogen. It should be noted that subsequent postpartal hemorrhage, even involving uteri of the Couvelaire variety, seldom necessitates hysterectomy because the myometrium can be made to contract sufficiently to close off bleeding sites in most instances.
Even in the mild cases of placental abruption concern for the fetus will justify cesarean section as the preferred method of delivery. If labor has already commenced, the membranes may be artificially ruptured to hasten its progress, to ascertain if there is blood in the amniotic fluids, and so that appropriate fetal monitoring can be instituted. Placental abruption has a tendency to speed parturition. However, prompt delivery by cesarean section may be the best approach regardless of fetal status, if profuse bleeding, shock, and worrisome clinical signs are endangering the mother.
The prognosis for the mother varies with the severity of the placental abruption, but overall the maternal death rate in the United States is I% or less. Among women surviving major shock, there may be postpartal necrosis with resultant destruction of the anterior lobe of the pituitary, which may be associated with a depression of gonadotropic, adrenal, and thyroid functions, as well as the development of cachexia (Sheehan's syndrome). The perinatal risks also vary with the degree and type of placental separation and the underlying maternal complications, hypertension, for example malnutrition. In addition to the risks of hypoxia associated with maternal shock and placental disruption, the complications of premature birth impose additional grave hazards. More than 50% Of pregnancies with this complication result in infants weighing less than 2,500 g. Generally, the perinatal mortality rates are higher among black women than white women.
Among those with partial placental separations, the rate is 15% to 30%.
The risk is much lower when only a marginal sinus ruptures.
Contrariwise, in the presence of total placental abruption. perinatal mortality rates are about 80%. Long-term morbidities among survivors are higher than like-weight individuals from other complications (e.g., placenta previa). This is thought to be due to the additional risk of hypoxia from decreased placental transfer.

Placenta Previa
Placenta previa is encountered in about 1 in 200 deliveries. Placenta previa is defined as placental implantation in the lower uterine segment within the zone of cervical effacement and dilatation. About 20% will be total placenta previa where the placenta covers the entire cervix. The cause is not known.
but the abnormality of placentation occurs more often in multiparas. It has been suggested that alterations in endometrial blood supply, variations in depth and nidational quality of endometrium, alterations in the uterine cavity size or contour, uterine scars, and receptivity of the endometrium may play a role. Obviously, surface area and distribution of placenta (multiple gestation. placenta membranacea, etc.) have an impact upon area of attachment and anatomic relations in utero. The types are designed on the basis of the relationship of the placenta to the internal cervical os as follows: (I) complete, total, or central placenta previa (see above), (2) partial (the internal os is only partially covered by placenta), and (3) marginal (the edge of the placenta extends to the margin of the internal os).
The placental margin at or near the internal os is vulnerable, and a cleavage plane occurs in the decidua spongiosa. When separation occurs, particularly in response to increasing myometrial activity or cervical effacement, there may be external bleeding. The classic symptoms are recurrent episodes of bright red bleeding. usually painless, particularly in the earlier stages of pregnancy. With uterine contractions, bleeding may be accentuated and there may be discomfort. The Latter clinical condition may be quite similar to a partially separated placenta implanted normally in the fundus. generally.
the initial episode of bleeding ceases spontaneously or continues as only minimal drainage. The blood loss is ordinarily not life-threatening to the mother unless an internal examination has been performed.
However, recurrent episodes are the rule. In contrast with abruptio placenta, the bleeding is ordinarily entirely external and the degree of hypovolemia and anemia is proportional to observed blood loss. There should be no infiltrations of blood into the myometrium or other tissues and there is no tenderness or increase in the resting tone of the uterus.
Diagnosis. The most characteristic clinical presentation of painless, bright-red vaginal bleeding calls for the presumptive diagnosis. Since abnormal presentations are found in one quarter of the cases of placenta previa, the presence of a transverse lie or breech, particularly if the presenting part is high in the fundus, should provoke even more concern.
The definitive method of diagnosis is ultrasonic scan, maternal condition permitting. The technique is safe and carries an accuracy of more than 95%.
However, as pregnancy advances, due to variable placental growth relationship to uterine expansion, the relationship of the placenta to the lower uterine segment may change.
Active Treatment.
Definitive treatment (i.e.., delivery, usually by cesarean section) is indicated when labor ensues, when the amount of bleeding is hazardous to the life of the mother, or when the fetus is mature. Occasionally. late in pregnancy and with sufficient maternal blood loss to preclude a more leisurely evaluation, it will be necessary to go to a "double-setup vaginal examination." This examination must be performed with some rigid safeguards since manipulations may disrupt more placenta and create life-threatening hemorrhage. Thus, these potential risks can be tolerated only if the fetus is clearly viable or if delivery is required to stop heavy blood loss. An examination of this type can be undertaken only under sterile circumstances in the presence of a double-setup capability, which means that the operating room has been adequately prepared for immediate vaginal or abdominal delivery. There should be provisions for infusions, blood transfusions, oxygen, anesthesia, instruments, nursing and neonatal personnel to proceed with active intervention if necessary.
Expectant management is indicated if it is necessary to postpone delivery until the fetus becomes mature. Preferably, the patient should remain at bed rest in the hospital under close observation with blood readily available. Sometimes, spontaneous heavy bleeding makes it necessary to abandon this conservative approach under emergency conditions. If a conservative plan of management is followed, it may be terminated electively when fetal maturity occurs a measured by ultrasound studies or amniotic fluid studies (L/S ratio, etc.).
Adequate blood replacement and treatment of shock are basic considerations in any management.
All patients with total placenta previa should be delivered by cesarean section, and most who have even minor degrees of partial previa are better delivered by the abdominal route. The thinned out endometrium in the lower uterine segment predisposes not only to the possibility of previa but also to invasion of the myometrium by the trophoblast (e.g., placenta accreta, increta, and percreta).
Lower segment manipulations leading to partial placental disruption can lead to life-threatening hemorrhage .
Vaginal delivery may produce additional fetal hazards by compressing the placenta and creating partial obstruction of the fetal vessels or by enhancing placental separation. The additional hypoxia resulting from these vascular deficits may cause fetal compromise. The low-lying posteriorly implanted placenta may pose the additional risk of decreasing relative pelvic capacity to preclude pelvic entry of the presenting part.
Maternal risks involve primarily hemorrhage, shock, and puerperal infection, but the mortality rate in the United States is less than 0.25%. The perinatal risks are hypoxia, birth injury, and the consequences of premature birth, including respiratory distress syndrome and a slightly higher incidence of developmental defects. The perinatal mortality rate is in the range of 15% to 20%.

Preterm or Premature Labor
Approximately 7% of deliveries in the United States are preterm (less than 37 weeks gestational age) and may or may not be small-for-dates. This is a very serious problem, for as a group the death rate of the low-birth-weight (LBW) neonate is 40-fold that of full-sized infants born at term, and both cerebral palsy (10-fold) and mental deficiency (5-fold) are increased in the LBW compared to the term neonate. Other sequelae of LBW include visual and hearing deficits, emotional disturbances, and social maladjustments. Preterm labor may be associated with many disorders or diseases; for example.
smoking, substance abuse, previous preterm birth.
incompetent cervix, uterine anomalies, multiple gestation, acute viral or bacterial infections, poor nutrition, and anemia. The clinical definition of premature labor involves four criteria: a gestation of more than 20 weeks but less than 36 weeks; regular, painful uterine contractions occurring at least twice every 10 minutes for at least 30 minutes; demonstrated cervical effacement or dilatation; and intact membranes. Other symptoms may include vaginal bleeding, increased vaginal discharge, and vaginal pressure.
When premature labor is being evaluated, it is necessary to ascertain that the membranes have not ruptured, that the fetus is truly premature, that fetal distress is not occurring, that cervical dilation has not exceeded 4 cm, and that there is not an abnormal fetal presentation (a frequent complication).
The necessary laboratory studies include blood for CBC with differential, serum electrolytes, and glucose; urine for analysis and culture and sensitivity; and ultrasonography for fetal size, position, and placental location. Amniocentesis may be necessary in borderline cases for fetal maturity (L/S ratio, phosphatidylglycerol) as well as to check for amniotic fluid bacteria (7%-26% of premature labors have intrauterine infection).
To ascertain if contractions are occurring (see above), 30 to 60 minutes of electronic fetal monitoring are performed and it is ultrasonically confirmed that the gestational age is 20 weeks to less than 36 weeks. A history, physical examination, and tests (see above) are used to rule out any contraindication to sedation-hydration therapy. The period of observation details whether labor is present and whether the cervix has changed. Thus; cases may be categorized as follows: (I) no contractions, no cervical changes (no labor); (2) contractions, no cervical change (false or early labor); (3) no contractions, cervical change (incompetent cervix); and (4) contractions, cervical change (labor). Of all cases originally presenting with presumed premature labor 75% will not be in labor, will have an incompetent cervix, or will have contraindications to tocolysis. Of those with false labor, early labor, or labor, sedation-hydration therapy is begun, if there are no contraindications, with morphine sulfate 8 to 12 mg intramuscularly and 5% dextrose lactated Ringer's solution intravenously. At the end of the hour, which of the three treatment groups the patient will enter is based on cervical effacement and dilatation as well as uterine contractions.
If contractions continue and the cervix is progressively changing (only a small percentage of cases), one should proceed to first-line tocolytics, the goal of therapy being to arrest labor until the fetus is mature enough to achieve intact survival in the atmosphere. If there is no cervical change but uterine contractions continue, the patient may benefit from first-line tocolytics. This group is usually less than one half of patients, and even if suppression is currently successful, they still have a risk of subsequent labor and delivery. When uterine contractions cease and there is no cervical change, observation should continue for 6 to 12 hours. More than half of patients will be in this group and here, too, there is a continued risk of labor and delivery, but the majority of these patients may be monitored by an outpatient regimen. Prior to the use of tocolytic drugs several items are important: serial measurement of blood pressure and pulse rate, baseline ECG, and establishment of a fluid intake and output chart. The fetal heart rate is monitored electronically throughout tocolysis. The safest tocolytic is magnesium sulfate. It may be given in a bolus followed by continuous intravenous infusion. The vital signs, deep tendon reflexes, urinary output, and ECG are monitored closely (every 30-60 minutes). With careful monitoring, serious adverse effects of magnesium administration, for example, hypotension, sinoatrial or atrioventricular block, or cardiac arrest, are exceptional. However, each time a magnesium level is drawn (every 6 hours) a calcium level should also be obtained to ascertain that acute hypocalcemia has not occurred. The fetus should be minimally affected by this regimen.
Intravenous Ritodrine, a more effective tocolytic than magnesium sulfate and FDA-approved for tocolysis, should be continued at effective dosage for at least 2 hours after cessation of contractions; then it should be slowly reduced over I to 2 hours.
A maintenance oral dose of Ritodrine may be used for weeks, if necessary. The adverse reactions of ritodrine are essentially those of all p-mimetic agents and are dose related. They include hyperglycemia, hypoinsulinemia, and hyperkalemia. Pulmonary edema may occur if ritodrine is given intravenously in saline solution, especially with excessive drug dosage or prolonged treatment, or when hyperhydration occurs. Unpleasant cardiovascular, gastrointestinal, or neurologic side effects must be expected but these are usually mild. Fetal tachycardia may occur with any B-adrenergic drug therapy.
However, with proper selection of patients, correct dosage, and cautiously maintained tocolysis, there should be no harm to the infant.

Disproportionate Fetal Growth Small-for-gestational-age (SGA) fetuses or neonate s, sometimes referred to as having 'intrauterine growth retardation," are less than the tenth percentile of weight, length, and head size for gestational age; while large-for-gestationaI-age (LGA) perinates are at or above the ninetieth percentile by the same criteria. Both SGA and LGA fetuses have altered body composition, altered distribution of organ weight, and altered body proportions. Both disproportionate growth perinates are at considerable risk for morbidity and mortality, although the risks are notably different.
Approximately 80% of SGA perinates are "asymmetrically" small, with relative sparing of brain, compared to other organs. The differential sparing is particularly prominent if deprivation occurs in the latter half of pregnancy. This form of SGA is caused by restricted growth potential and is usually caused by placental disorders (e.g., infarction, previa, villitis, partial separation, malformations. twin-to-twin transfusion syndrome), coexisting maternal disease (e.g., hypertensive states of pregnancy, anemia, renal diseases, malnutrition, pulmonary disease), or multiple pregnancy. The remainder of SGA perinates (20%) are symmetrically small and are said to have decreased growth potential. The most common causes of decreased growth potential are constitutional (small maternal stature, female fetus, certain races), genetic disorders (4%., autosomal [trisomy 21, trisomy 18, trisomy 13], sex chromesomal [Turner's syndrome], neural tube defects [anencephaly], dysmorphic syndromes--usually autosomal recessive [Meckel's, Smith-Lemli-Opitz] congenital anomalies [Potter's syndrome]), congenital infections (e.g., CMV, rubella, toxoplasmosis, malaria, listeriosis), substance abuse (opiates, cocaine, alcohol, tobacco), or drugs (warfarin, folic acid antagonists). Overall, the most common cause of SGA is decreased placental function as a result of placental abnormalities or the result of abnormal function of a normal placenta.
The pregnancy complicated by an SGA fetus may be marked by oligohydramnios, passage of meconium, enhanced pulmonary maturity for gestation, and ultrasonically detected fetal or placental abnormalities. It is crucial in any pregnancy at risk for SGA that baseline studies be established as early as possible. Critical points of diagnosis include accurate dating of the pregnancy, serial ultrasonography, genetic screening, maternal serum alpha-fetoprotein determinations, TORCH titers, specially indicated studies (e.g., umbilical blood sampling), biometric testing, assessment for delivery and maternal studies as indicated by each circumstance. Stillbirth is not uncommon and delivery is hazardous for the SGA because of hypoxia and acidosis. Cesarean section should be used liberally for delivery. The overall perinatal mortality rate for SGA is 1.4- to 3-fold higher than that of average for gestational age (AGA) perinates. Neonatally the SGA is more prone to hypoxia, acidosis, meconium aspiration syndrome, hypoglycemia, hypocalcemia, polycythemia, hypothermia, congenital malformations, and sudden infant death syndrome (SIDS). The longer-term sequelae of SGA include lower IQ, learning and behavior disorders, and major neurologic handicaps.
The LGA fetus is generally associated with maternal diabetes, maternal obesity, postdatism, multiparity, previous LGA infants, and large maternal stature. Rarely, genetic or congenital disorders will be associated with the LGA perinate. Screening for LGA risk is performed by history and physical examination (25%-50% will be discovered), maternal glucose screening, and liberal use of serial ultrasonography. Attempts to control fetal size are most influenced by the appropriate use of insulin, for example, in gestational diabetics. At term the LGA baby generally exceeds 4,000 g and is very prone to birth trauma (6%-24%) such as shoulder dystocia and operative delivery. Indeed, shoulder dystocia, which occurs in 0.3% to I% of AGA perinates, occurs with LGA at a frequency of 6% to 24%.
Therefore, as the EDC approaches, labor induction should be considered. The incidence of cesarean for the LGA is 2- to 2.5-fold higher than for AGA. The maternal risk of LGA delivery is considerable and includes hemorrhage, operative delivery, and perineal damage. Neonatally the LGA is more prone to low Apgar scores, hypoglycemia, hypocalcemia, polyçythemia, jaundice, birth injury, and feeding difficulties. Longer-term sequelae of LGA are obesity, Type II diabetes, and neurologic or behavior problems.

Prolonged Pregnancy [Postdates)
Prolonged pregnancy has continued for 294 or more days, or 14 days beyond the EDC, as calculated from the first day of the last menses, and occurs in about 5% of all pregnancies. Most commonly the cause is never determined, but prolonged pregnancy is predisposed in those who have had it before (twice as common), in fetal anencephaly (due to adrenal hypoplasia and altered hormonal production), and in certain families. Among postdate fetuses, 30a/o to 40% are dysmature; that is, they have or have had fetal distress from placental insufficiency. These fetuses are underweight with reduced subçutaneous fat, appear wrinkled with peeling skin, and are often meconium-stained.
They are at increased perinatal risk, and oligohydramnios is frequently an associated finding.
However, the majority of postterm infants appear to be normal or are macrosomic, continuing to grow slightly even after the EDC. Accordingly, it is essential to ascertain which fetuses are jeopardized and which are not.
Evaluation of the postterm pregnancy involves accurately dating the pregnancy (the EDC may not yet have been reached). Accurate dating is best performed prospectively (during the course of pregnancy), but quite often that is not the case. Thus, if three of the following four clinical criteria are met, the patient should not be considered postdates: less than 36 weeks have elapsed since a positive pregnancy test; less than 32 weeks have elapsed since Doppler recording of fetal heart (FHTs); less than 24 weeks have elapsed since observed fetal movements; and less than 22 weeks have elapsed since FHTs were noted by auscultation. Two satisfactory ultrasonographic fetal biparietal (or other) measurements, at least one month apart, can establish gestational age by 1 week. The earlier in gestation the ultrasonic examinations were accomplished, the more accurate dating will be. The EDC cannot accurately be established or confirmed when the fetal biparietal diameter is greater than 9.5 cm by a single ultrasonography.
To affirm fetal well-being, fetal surveillance is essential after 294 days. Indeed, once the due date has passed and until week 42 it may be wise to implement all or part of the surveillance noted below (e.g., weekly instead of biweekly determinations). Clinical parameters include full maternal evaluation, a biweekly recording of fundal height and abdominal girth (decreasing uterine contents signal oligohydramnios), maternal fetal motion counting, and visualization of the membranes (if possible) through the cervix to determine if meconium has been passed. Meconium is a nonspecific reaction to stress and should not be taken as a sign of fetal distress, but a warning signal that the fetus may be near the limits of placental reserve. Twice weekly biophysical profile testing (or minimally nonstress testing) is a useful evaluation of fetal well being. At least one definitive (level III) ultrasonography, specifically examining fetal size parameters, fetal organ systems, and the placenta (including grading), should be obtained. Contraction stress testing should be performed if any parameter above is questionable. Amniocentesis is rarely indicated, but may be useful in the patient who has totally unknown dates and presents without any prospective monitoring. Analysis of the amniotic fluid does not assist in determining the gestational age but can definitively describe fetal pulmonary maturity, even when a sample is contaminated by blood or meconium.
The safest time for delivery is 39 to 41 weeks.
After week 41 there is steadily rising mortality (e.g., stillborn, uteroplacental insufficiency), and potential morbidity. The mortality is 5% to 7% in infants delivered at or after 44 weeks, and by week 42 the risk is equal to that at less than 35 weeks. The ideal time for delivery is when the minimal risk of induction is surpassed by the ever increasing risks of postdates gestation and must be individualized. By this criteria, delivery at or shortly after 290 days' gestation is indicated, which is generally accomplished by induction of labor. If the cervix is not effaced, not dilated, not soft, is posterior and the presenting part is high (i.e., a low Bishop score), it may be necessary to administer cervical prostaglandin E. Induction is most safely accomplished by rupture of the membranes, but if that cannot be accomplished, oxytocin may be administered.
Upon rupture of the membranes, observation for meconium staining is important. The fetus should be constantly monitored during induction because the dysmature fetuses are prone to fetal distress and withstand labor poorly, particularly when oxytocin stimulation is used. There is a real risk of intrapartum asphyxia. Should fetal distress occur, maternal complications intervene, or the serial induction of labor fail, cesarean should be undertaken immediately.

Multiple Gestation
Multiple pregnancy, more than one embryo or fetus in a gestation, may be caused by division of a single fertilized ovum (identical, monovular. or monozygotic) or fertilization of separate ova by different spermatozoa (fraternal, or dizygotic). Monozygotic multiple gestations share the same genetic features but may have phenotypic variation of considerable degree, while dizygotic gestations bear only the resemblance of brothers or sisters and may or may not have similar enough genetic features to serve as organ donors for each other. Monozygotism is constant (-2.3-4/1,000 deliveries), but dizygotism has a number of predispositions, including a recessive autosomal trait via the female descendants, race (greatest incidence in blacks. intermediate in white, orientals having the fewest), cessation of oral contraception, artificial ovulation induction, greater maternal height or weight, increasing maternal age (peaks at 35-45), and white mothers of blood group O or A. The incidence of the father's being a twin has little influence on his offspring's potential to be multiple gestations. In a heterogenous population (such as the United States), approximately 30% of twins are monozygotic and nearly 70% are dizygotic.
In heterogenous populations an estimate of the frequency of multiple gestation may be obtained by the knowledge that twinning occurs -12/1,000 births (1 : 88). Subsequent incidences may be estimated by raising the ratio 1 : 88 to the exponential of the birth number minus I. For example: triplets occur 1:88 (3-1=2) =1 : 7,744; quadruplets 1 :88 3 = 1 :681,472; and so forth.
Approximately 75% of twins are of the same sex, but in multiple births males predominate (45% compared to females 30%).
Maternal morbidity and mortality is higher in multiple, compared to singleton, pregnancies. The conditions associated with this risk include enhanced anemia, more urinary tract infections, increased incidence of preeclampsia-eclampsia, greater predisposition to hydramnios, more frequent uterine inertia (from overdistention), and greatly increased chances of hemorrhage (before, during, and after delivery).
The perinatal mortality rate of twins is also three to fourfold higher, and for each subsequent birth number much higher again, than for singletons. The two primary causes of this are prematurity and congenital anomalies. Considering both mono- and dizygotic fetuses congenital abnormalities of all organ systems are as high as 18%, compared to the 3% to 5% of singletons. As the number of fetuses rises, their average size and length of gestation falls; on the average, twins are delivered at about 36 weeks triplets at approximately 32 weeks, and quadruplets at less than 30 weeks. Intrauterine growth retardation (IUGR) is also more common in all multiple gestations, as opposed to singletons.
Other general perinatal risks of multiple gestations include abnormal presentation and position. hydramnios, hypoxia because of cord prolapse (approximately 4%), placenta previa, premature separation of the placenta after the first twin, or operative manipulation. Collision. impaction, and interlocking of twins are additional but uncommon complications.
Compared to dizygotic fetuses, monozygotic multiple fetuses are even more likely to be jeopardized from general congenital abnormalities (a further threefold increase), incomplete separation. enhanced early loss of one or both fetuses (probably two thirds of all implanted multiple gestations end up with a single birth), enhanced IUGR and possibility of death in utero (the monochorionic placenta is likely less efficient than a fused dichorionic placenta), or a parasitic fetus without a heart (fetus acardiacus). Another unique monozygotic complication is the "twin-to-twin transfusion syndrome" in which the smaller cardiomegalic twin pumps its arterial blood into the lower pressure venous system of the larger. plethoric, and macrosomic twin.
Cord problems are also enhanced in multiple gestation, including two vessel cords and velamentous cord insertion (7% incidence), and cord entanglement in a single monoamniotic sac (approximately 1% of all twins, but leads to about a 50% loss). The time of division is crucial to the outcome of monozygotic fetuses. Early separation, prior to the morula and trophoblastic differentiation (day 5), leads to separate or fused placentas, two chorions and two amnions. Division after trophoblastic differentiation but before amnion formation (5-10 days) is the pattern of two thirds of monozygotic twins and results in a single placenta, a common chorion, and two amnions. Later division (i.e., after amnion differentiation-days 10-14) leads to a single placenta, one chorion and one amnion. Division from day 8 to after day 14 results in conjoint ("Siamese") or incomplete twinning.
Early diagnosis of multiple gestation is desirable in order to provide the special care necessary for the mother as well as to prolong the gestation. The most precise method of diagnosis is ultrasonic imaging. Indeed, multiple pregnancy may be demonstrated by vaginal ultrasonography as early as the 8th week of gestation and should be routinely detected by other scanning methods by the IOth week. The clinical findings suggestive of multiple pregnancy include a uterus 4 cm or larger than expected for the length of pregnancy, uterine palpation of three or more large part or multiple small parts, simultaneous auscultation or recording of two fetal hearts varying more than 8 BPM and asynchronous to the maternal heart, unexplained excessive maternal weight gain, hydramnios, eclampsia-preeclampsia, and subjective maternal increased fetal activity. The laboratory findings suggestive of multiple pregnancy include elevations of maternal HCG and/or alphafetoprotein, moderate reductions in hematocrit (as well as hemoglobin and red blood cell count)l a blood volume increased over normal pregnancy values, and an increased incidence of glucose intolerance.
The differential diagnosis of multiple pregnancy includes single pregnancy, single pregnancy not compatible with gestation, hydramnios, hydatidiform mole, abdominal or pelvic tumors complicating singleton pregnancy, and complicated multiple gestation, Prevention of multiple pregnancy is possible by using barrier means of contraception for the first cycle off oral contraceptives and by more careful use of the ovulation induction agents. For example, clomiphene causes fewer multiple gestations, but dizygotic twins still occur in 5% to 10%.
A new and somewhat controversial technique is that of "selective reduction" (i.e., selective termination) of some of the fetuses. This technique employs ultrasonic guided techniques for reducing the number of fetuses with the rationale that intact survival of a few is better than nonintact survival of many. The initial reports support usage in certain Cases.
Maximizing nutrition and decreasing stress appear to assist in lengthening the gestation. Oral iron, high protein, high vitamin diet, and no weight gain limitation are all recommended in multiple gestations. Patients with multiple pregnancy are usually examined more often during pregnancy. Limiting physical activity may assist uterine blood flow.
Although not always necessary, frequent rest periods after the 24th week have been suggested as a method of lengthening gestation. Blood counts are usually obtained more frequently. Repeated ultrasonic examinations screen for fetal defects, IUGR, proper growth, fetus-to-fetus transfusion syndrome, and fetal well being. These are usually obtained monthly from diagnosis until the 32nd week, when both the examinations and biophysical profile of each fetus may be useful on a weekly basis. Anticipate delivery blood loss (hemorrhage is increased fivefold over singletons) and seek donors acceptable to the patient in advance. Delivery of multiple pregnancies is best conducted in a unit with adequate assistance and neonatology. Both cervical cerclage and/or tocolytic agents have been used to delay preterm birth in selected cases. Betamimetic agents should be used with caution because of possible maternal pulmonary edema. Individual testing for pulmonary maturity studies may necessitate sampling each amniotic cavity.
During labor a number of special precautions are necessary. A large bore intravenous with lactated Ringer's solution should be started. Blood work should include CBC and type and cross match for a minimum of 2 units packed RBC or whole blood.
The degree of aortocaval compression with subsequent hypotension may be profound; thus. it is prudent to keep the mother- from lying on her back.
Maternal oxygen therapy by mask (7 liters/minute) helps to guarantee proper maternal and fetal oxygenation. Each fetus is monitored electronically. Maternal analgesia and anesthesia is limited, with a preference for psychoprophylaxis or regional anesthesia.
Cesarean section is the preferred method of delivery for monoamniotic twins (10% delivery loss from cord entanglement), any birth number exceeding twins (e.g., triplets), twins <2,500 g, or if the first twin is any presentation except vertex. Indeed, even twin gestations are at such risk that they should be delivered in a cesarean section room with full preparation (including maternal abdominal prep), equipment, and personnel in attendance for cesarean section. The presentation of both twins is ascertained by ultrasound to plan the delivery method. Continuous electronic monitoring is used for both fetuses. When Twin A is vertex and Twin B is vertex (slightly more than 40% of cases) both are usually delivered by vertex vaginal delivery. When the first fetus is delivered, clamp the cord promptly to prevent the second of monozygotic twins from partially exsanguinating through the first cord. A vaginal examination immediately after the first delivery is used to identify a possible prolapsed cord and to ascertain fetal position. If the second fetus is anything but vertex, external version is utilized to attempt conversion of the second twin to vertex. If the external version is successful, the membranes may be cautiously ruptured (to avoid cord prolapse) and labor will proceed to vaginal vertex delivery.
However, if the external version is unsuccessful and the fetus is not a candidate for a vaginal breech delivery, cesarean should be performed immediately. When the external version is unsuccessful and the fetus is a candidate for a vaginal breech delivery (see Breech Presentation, below), that modality may be employed. When the first twin is nonvertex (approximately 20%), cesarean is used for delivery regardless of the second twin's position.
With all multiple gestations the three major preventable causes of morbidity are immaturity, trauma, and manipulative delivery (with associated asphyxia); thus, every effort is extended to prevent these problems. A second twin in distress and able to be delivered more quickly vaginally than abdominally may be an indication for the now rarely performed internal version; however, it is safer for the mother and baby if cesarean can be performed.
For example, if the first twin has been delivered and the second suffers fetal distress (severe cord compression or premature separation of the placenta) and cannot be delivered easily or immediately. an emergency cesarean should be performed. Both neonates must be attended by a team experienced in neonatal management and resuscitation.
After delivery of the last fetus oxytocin 5-10 units IV slowly but promptly after delivery, followed by an infusion of dilute oxytocin will decrease the possibility of uterine inertia. It is also useful to elevate (out of the pelvis) and gently massage the uterus. Inspection, as well as dissection and sectioning for microscopy, of the placenta(s) and membranes, particularly the membranous "T" septum between the fetuses, may be immediately useful in determining zygosity. Monozygotic twins have a thin septum made up of two amnionic membranes with no intervening chorion or decidua.
Dizygotic fetuses have a thick septum composed of two chorions, two amnions, and intervening decidua. In some circumstances it is necessary to resort to definitive genetic testing to determine mono- or dizygosity.
Coincidental Complications
Gravid women are naturally subject to all the diseases from which nonpregnant persons suffer. Most of these will not be aggravated by pregnancy, and the coincidental condition will not affect the normal course of gestation. The notable exceptions to this generalization are heart disease, diabetes mellitus, pyelonephritis, pneumonia, syphilis, and rubella.
Current opinion suggests that pregnancy exerts no deleterious effect on tuberculosis, and that therapeutic abortion is rarely indicated. As a rule, tuberculosis of the mother does not affect the infant.

HEART DISEASE
Heart disease complicating pregnancy may be indicated by any of the following criteria: a diastolic, presystolic, or continuous heart murmur; cardiac enlargement; a loud, harsh systolic murmur (especially with an associated thrill); and severe arrhythmia. In determining the prognosis of cardiac patients, emphasis should be given to the functional classification, the age of the patient, signs or history of heart failure, atrial fibrillation, and complicating serious disease. Generally speaking, the prognosis is most serious in aortic or mitral stenosis, either alone or in association with insufficiency. Judging the severity of the heart condition by these several criteria, the unfavorable group of cases comprises about 20% of the total, yet these women with poor prognostic signs account for about 85% of the deaths attributable to heart disease.
Heart disease complicates pregnancy in about I% of pregnant patients. The preponderance were rheumatic in etiology; however, in recent years, congenital cardiovascular lesions are being diagnosed more commonly and now the ratio of rheumatic to congenital disorders is <3 : I. The success of cardiac surgery may decrease additional risks for patients who subsequently become pregnant (e.g., correction of patent ductus arteriosus, atrial septal defect, aortic stenosis, or simple coarctation of the aorta). In other circumstances surgical intervention may be more palliative, and pregnancy would impose prohibitive maternal risks (e.g., corrected pulmonary hypertension, partially repaired cyanotic lesions, Marfan's syndrome, complicated coarctation of the aorta).
Another consideration in the advisability or safety of pregnancy pertains to the ill effects upon the fetus of drugs used in treatment of cardiovascular diseases. The coumarins are teratogenic, and long-term heparin seems to increase premature births and perinatal deaths. Beta-adrenergic blocking agents given to patients with certain cardiac arrhythmias have the potential of initiating premature labor. Digitalis increases myometrial tone, and thiazide diuretics reduce plasma volume during pregnancy.
A further consideration is the risk in some types of heart disease of infection, particularly in those who have undergone valvuloplasty for rheumatic heart disease and those with prostheses, grafts, and residual defects postsurgery. Antibiotic prophylaxis in these cases is mandatory. Overall, congenital anomalies are noted in the newborns of mothers with significant heart disease about six times more often than the normal population.
The considerable physiologic burdens imposed upon the cardiovascular system during pregnancy have been previously reviewed. Most cardiac decompensations occur after the 7th month, and cardiac stress is accentuated even more during labor and delivery when the output increases to 60% to 80% over nonpregnant states. The early puerperium, in contrast to supine prelabor, may show a 15% to 20% drop in heart rate and a 5% to 15% reduction in blood volume.
In addition to the deaths that bear a relationship to the functional classification, especially classes III and IV of the New York Heart Association classification, certain cardiovascular complications, such as vascular accidents and bacterial endocarditis, may take an additional toll.
The principles of management are adequate rest, reduced emotional strain, prevention or correction of anemia, proper diet to avoid excess weight and fluid retention, avoidance of infection, recognition of early signs of heart failure, allowing labor to ensue spontaneously, meticulous care in labor, and allaying decompensation. The ideal delivery has the objective of avoiding great exertion on the part of the mother (minimize bearing-down efforts) while achieving a simple vaginal delivery (perhaps outlet forceps) under local or possibly carefully administered regional anesthetic. These patients are very vulnerable to trauma, shock, hemorrhage, and sepsis. Warning signs of early cardiac failure are decreased vital capacity, fatigue, orthopnea, resting tachypnea, rales at lung bases, and pulmonary congestion on a chest film. In the presence of heart failure, delivery by any known method carries with it a maternal mortality of more than 50%. Should frank heart failure develop, digitalis and bed rest in the hospital are required throughout the remainder of the pregnancy. During pregnancy, cardiac: failure constitutes a grave hazard, since 15% or more of patients die. Valvotomy in pregnancy may be accomplished if necessary with relative safety for both mother and fetus. Recent reports dealing with large series of women undergoing pregnancy after placement of a prosthetic heart valve reveal a good perinatal outcome in about 72%; however, salvage is excellent (perhaps 95%) if oral anticoagulation therapy is not required. Uneventful pregnancies have been reported following insertion of a permanent pacemaker for complete heart block.
The early puerperium is a time of potential de compensation, collapse and death, since the cardiac output rises significantly and over a number of days fluid will be mobilizing. Bed rest and antibiotics are continued for I week postpartally.
The presence of heart disease must be identified at the onset of pregnancy to initiate appropriate therapy. Gestational disturbances making the diagnosis difficult include edema, fatigue, dyspnea, cardiac enlargement, left axis deviation, and occasional T-wave inversion on ECG, and apical or left sternal border systolic ejection-type murmurs.
Of special concern are those patients who have had cardiac failure previously, because repeated cardiac decompensation in pregnancy is very likely.
Another grave category is represented by women with congenital cyanotic heart disease. Here, not only are the perinatal risks great but the maternal mortality rate is very high. In some instances, patients may be suitable surgical candidates even during pregnancy; however, in general, all women, particularly older women, classified as having class III and IV heart disease are extremely serious risks and should be considered for elective abortion prior to the eighth gestational week. Otherwise, hospitalization and bed rest through pregnancy is required, along with the closest supervision.
One of the most serious complications of cardiac disease in pregnancy is bacterial endocarditis, usually by Streptococcus viridans , enterococci, or Staphylococcus aureus. A combination prophylactic drug therapy has become popular (e.g., penicillin, vancomycin, or ampicillin plus gentamycin, possibly alternatives of cephalothin, nafcillin, Keflin, or streptomycin). Such prophylaxis is indicated in any patient with a heart lesion, including mitral valve prolapse, although in the latter circumstances it is recommended only for delivery not during the entire course of pregnancy. In postsurgical patients, the prognosis depends upon any residual pulmonary hypertension or myocardial deterioration. Patients with repaired tetralogy of Fallot fare reasonably well in pregnancy if there is no pulmonary hypertension. Successful pregnancy has followed a cardiac bypass operation.

DIABETES MELLITUS
This is the most common and the most serious metabolic disease in pregnant women. The overall incidence of this maternal complication is <1%, although the incidence will be considerably higher in tertiary care centers (perhaps 2%-3%). Prior to the advent of insulin, about one half of diabetic patients were amenorrheic. When pregnancy did occur, maternal mortality was in the range of 25%.

Now, under optimal conditions the maternal mortality is less than 0.5% with nearly all in the more severe groups. Diabetes' deleterious effect on pregnancy has several manifestations: an abortion rate twice the non diabetic, a rate of congenital abnormality two to threefold more than the non diabetic, and perinatal death rate fivefold that of the non diabetic. Other potential fetal sequelae include macrosomia, organomegaly, enhanced rates of respiratory distress syndrome, polycythemia, hyperbilirubinemia, hypocalcemia, hypomagnesemia, and neurologic instability. In the absence of adequate prenatal care, the perinatal mortality will be 40%, but it can be reduced to 3% to 5% under optimal conditions. Deaths increase towards term.
In the presence of severe maternal vascular disease, the perinatal death rate may rise to as high as 50%.
Pregnancy is diabetegenic; that is, insulin demands are increased during the gestational state.
This is due to a number of insulin antagonists, including chorionic somatomammotropin, which induces lipolysis, increases free fatty acids, and inhibits the cellular uptake of glucose and gluconeogenesis. In this biochemical process, glucose and protein are spared, presumably for fetal growth. As a consequence, there are increased maternal insulin requirements, especially after the first trimester.
Estrogens also play a role by exerting a peripheral antagonism to maternal insulin, especially in the latter part of pregnancy. The placenta may contribute to the diabetic picture by producing insulinase.
In normal pregnancy, plasma insulin levels are low in the fasting state but are elevated after a carbohydrate challenge.
First identification of the gravida at risk for diabetes is usually based on the medical history, physical findings, gynecologic background, past obstetric performance, and laboratory data. Obviously there are risk factors that make some individuals more vulnerable than others. A family history of diabetes in one close relative or two distant relatives should be taken into consideration. A gynecologic history of wound healing problems, resistance to infection, recurrent urinary tract infections, and refractory monilial vaginitis should be noteworthy. Obstetrically, a history of macrosoma, diabetes in a prior pregnancy, an unexplained fetal death, neonatal respiratory death, a child with anomalies, recurrent toxemia, gestational obesity, and polyhydramnios should be viewed with concern.
A screening procedure for diabetes is a routine procedure usually performed in early pregnancy and repeated in the third trimester. A common screen is accomplished by administering a 50-g glucose load to the gravida. A I-hour blood sugar of more than 150 mg/100 ml has a high correlation with diabetes and requires further investigation. A 2-hour postprandial blood sugar level of 140 mgl 100 ml is indicative of diabetes mellitus (or similar level 2 hours following ingestion of a solution containing 100 g of glucose). A sugar level in the 120 mg to 140 mg/100 ml range may suggest gestational diabetes. During pregnancy, postprandial glycosuria may be observed because the glomerular filtration rate is increased while there is no change in maximal tubular reabsorption, and the net effect is a decrease in the renal threshold for glucose.
However, glycosuria with the pregnant woman in the fasting state may be a clue to abnormal glucose intolerance. A patient may have a normal fasting serum glucose and yet have an abnormal glucose tolerance test (GTT). A 3-hour oral GTT is indicated when the family or postobstetric (gynecologic) histories are suggestive or screening tests are positive, as well as in older obese patients, particularly if there is glycosuria. These screening and diagnostic procedures in an obstetric population at a medical center will uncover the 2% or 3% of women with overt diabetes who will require special attention. According to O'Sullivan's criteria, two of the four venous blood sugar levels should be elevated above the following baseline figures: fasting of 90 mgl 100 ml; 1 hour = 165 mgl 100 ml; 2 hours = 145 mg/100 ml; and 3 hours = 125 mg/100 ml. If plasma sugar is determined, the values are approximately 15% higher. If the fasting blood sugar is above 140 mg/100 ml, the diagnosis is established, and the GTT should not be performed because it could be dangerous. On the other hand, a negative study in early pregnancy in a high-risk or suspect patient calls for a repeat GTT after the 28th week of gestation.
Once the diagnosis is established, the disease should be classified because this will bear on the pregnancy outcome and prospects for perinatal survival. Class A, Priscilla White Classification, 1965, is associated with the best perinatal survival, above 95%. At the other end of the spectrum, patients with hypertension, proteinuria, and nephropathy have a survival rate of only 50% to 65/10.
Generally, perinatal mortality rates are less than 5% for all cases throughout the United States.
Among patients with gestational diabetes, approximately 25% to 30% will progress to chemical diabetes mellitus within 5 years. In pregnancy.
there may be a rapid onset of diabetic symptoms even among previously undiagnosed patients.
There is enhanced tendency for acidosis in pregnancy, and the presence of vomiting may create a confusing disturbance in the chemical balance. Maternal acidosis is the most ominous association with perinatal mortality. Other adverse factors are hyperglycemia, water imbalance, hypertensive disorders (up to 50%), excessively sized fetus (somatic and splanchnic growth), and hydramnios (10%).
Monitoring the fetus should reveal several adverse findings with fetal jeopardy. Signs that are indicative of a deteriorating fetal status include deterioration of biophysical parameters of fetal well-being.
The risk of fetal death rises substantially after the 36th week. Regardless of the initial classification according to White, Pedersen's poor prognostic signs in diabetic pregnancy include (I)pyelonephritis (premature labor), (2) ketoacidosis, (3) toxemia (25% incidence creating a 25% likelihood of fetal loss), and (4) "neglectors" who do not cooperate in the plan of clinical management. With respect to the classification, the complicated insulin-dependent diabetics who suffer the most guarded prognosis fall into classes D, E, F, and R (White's classification), for example, juvenile onset, proliferative retinitis, calcified vessels, coronary artery disease, nephropathy, and so forth, probably representing about 10% of the clinical diabetics.
The prime target in medical management is adequate blood sugar control prior to and throughout pregnancy. Preconceptual control(at least 3 months before pregnancy) decreases abortions and anomalies. Careful control throughout minimizes fetal macrosomia and newborn problems (potential for hypoxia, delayed pulmonary maturation, hypoglycemia, and hyperbilirubinemia) . The daily amount of exercise should be maintained at a constant level.
Diet must be rigidly controlled and insulin therapy precisely based on blood glucose levels. The daily calorie intake (30 to 35 calories/kg of body weight), which is achieved by consuming three meals and one to three snacks per day, is intended to permit a total weight gain of about 25 pounds, emphasizing a progressive linear gain of 350 g to 400 g/week after the first trimester. About 1.5 g protein/kg of body weight (higher for adolescents) is desirable, and about one half of the total calories should be provided by carbohydrate consumption, while avoiding concentrated sugars. A diet too low in calories will give rise to ketonuria. Ketoacidosis should be avoided meticulously by keeping fasting plasma glucose levels 100 mg + 10 mg/100 and 2-hour postprandial levels below 120 mg/100 ml.
Oral hypoglycemics are contraindicated in pregnancy due to their teratic potential. The insulin regimen is usually two injections daily of both NPH and regular insulin (2: 1 ratio in the morning and I : I ratio in the evening) augmented in 20% increments to achieve better control as necessary.
Currently, even insulin-dependent diabetics are usually managed on an outpatient basis. Ideally, pregnancy assessment and control starts prior to gestation. It is only with impeccable control (as may be determined by normal hemoglobin Alc measurements) that the diabetic sequelae in pregnancy can be avoided.
For an outpatient diabetic program to be successful, it requires careful initial assessment, a reliable patient, frequent blood sugar determinations by the patient, open communications frequent outpatient visits, and a careful fetal-monitoring program. The initial assessment usually includes (in addition to the standard obstetric laboratory studies) a biochemical profile (SMA 6 and 12), electrolytes, creatinine clearance, urine culture, EKG, chest x ray, and in the more advanced classifications, retinal photography. Additionally, hemoglobin Alc determinations afford an indication of integrated control in the weeks preceding the analysis. For the first few days the patient takes finger stick blood glucose measurements: fasting (before breakfast), preprandial at noon, at 2:00 P.M., and at 8:00 P.M.
after the initial control is established, these may be taken one a day in a rotating pattern so that in 4 days values are available for each of the times noted. Frequent communication and visits assure that the maternal-monitoring program is comprehensive and affords the opportunities to assess the fetus. A schedule of fetal assessment includes ultrasonic examination: early in gestation, at 20 to 24 weeks, and every 4 to 6 weeks after 26 weeks.
Maternal assessment of fetal movements may be determined every day and NST employed weekly from 30 to 34 weeks, biweekly at 34 to 36 weeks, triweekly at 35 to 37 weeks, and more frequently (as indicated) after the 37th week. CSTs and biophysical profiles may assist if the NST is equivocal.
When appropriate (individualized for each patient), the fetal maturity is determined (usually by amniocentesis), and if the fetus is mature the labor is induced or cesarean section performed.
Definitive management of gestational (class A) diabetes is slightly controversial. However, at the present time it seems clear that only by the use of ADA diet and prophylactic insulin (25 U NPH in the morning) may macrosomia, operative delivery, and birth trauma be controlled. Women in the class A category who previously have experienced pregnancy-induced hypertension, overt diabetes in gestation or a fetal loss are best managed the same as an overt diabetic. In these, antepartal fetal monitoring is also required. Delivery is achieved by or beyond the 38th week of gestation once euglycemia and fetal maturity are achieved. Labor may be induced as required. Hemoglobin Alc levels, which are elevated in the presence of chronic hyperglycemia, can be used in series to roughly determine the quality of diabetic control. Preterm delivery before the 37th week by the vaginal route or cesarean section (if necessary) is dictated by bouts of acidosis, hypertension, worsening diabetic state, or fetal compromise. To avoid injury of these fragile infants, abdominal delivery is used liberally.
Intensive neonatal evaluation and impeccable care are mandatory.