In the past, there has been considerable pessimism about our ability to identify the pregnant patient at risk. However, with the development of sophisticated diagnostic techniques these patients can be identified and with appropriate treatment their outcome can be improved. This paper presents the overall benefit of categorizing obstetrical patients, the method that has been developed at the Medical College of Virginia (MCV), and certain categories of high-risk obstetrical patients who continue to present problems and have unacceptably high complication rates

Coogan, Emily M.

Petres, Robert E.

VCU Scholars Compass

Identification of the High-Risk Gravida ROBERT E. PETRES, MD EMILY M. COOGAN, RN, MS, OGNP Department of Obstetrics and Gynecology, Medical College of Virginia, Health Sciences Division of Virginia Commonwealth University, Richmond, Virginia In the past, there has been considerable pessimism about our ability to identify the preg­nant patient at risk. However, with the develop­ment of sophisticated diagnostic techniques these patients can be identified and with appro­priate treatment their outcome can be im­proved. This paper presents the overall benefit of categorizing obstetrical patients, the method that has been developed at the Medical College of Virginia (MCV), and certain categories of high-risk obstetrical patients who continue to present problems and have unacceptably high complication rates. A variety of systems has recently ap­peared in the literature designed to categorize the high-risk obstetrical patient' To be success­ful such a system must be accurate and simple enough to understand. Some of the initial sys­tems of categorization were simply too com­plicated They involved the tabulation of mul­tiple factors drawn from virtually every aspect of the patient's lifestyle, physical examination, and laboratory assessment Consequently, they were too cumbersome to be practical The goal of any identification system should be to sepa­rate patients into groups which can then be managed according to the common require­ments of each group. The classification system used at MCV is based on the premise that a given pregnancy may represent a progressive risk to the fetus or the mother and that this risk can be attenuated by appropriate care. Not included in the system Correspondence and rep11nts requests to Dr. Robert E. Pel<es. Box 34. Medical College of Virg,n,a. Richmond. VA 23298 4 / PETRES AND COOGAN HIGH-RISK GRAVIDA are patients at risk for congenital anomalies. This group of patients undergoes comprehen­sive early antenatal evaluation. The results of this evaluation are then made available to the parents. who in turn determine what action is to be taken. On the other hand, there is a larger group of patients whose pregnancies are at pro­gressive risk in utero. Identification, classifica­tion and appropriate intervention can improve perinatal outcome in this larger group. The MCV identification system is divided into four categories. It was recognized at the outset that obstetrical patients could not simply be separated into normal patients and high-risk patients If this were done, 90% of the patients would be in the high-risk category and only 1 0% in the normal category Instead, it seemed more logical to group patients according to the severity of their problems. Class IV Critical care pregnancies Eclampsia Severe preeclampsia Chronic hypertension with superim­posed preeclampsia Chronic renal disease uncompensated (creatinine 1 .2 mg/% or greater) Organic heart disease uncompensated (early signs of failure) Hemoglobinopathies in crisis Pyelonephritis, acute Premature rupture of the membranes Premature dilatation of the cervix in the second half of pregnancy Diabetes (ketonuria) Placental accidents (abruptio placenta and placenta previa in the second half of pregnancy) Class Ill High-risk pregnancy Mild preeclampsia Diabetes without evidence of ketonuria Chronic hypertension Chronic renal disease compensated (creatinine less than 1 .2 mg/%) Organic heart disease compensated (no signs of failure) Hemoglobinopathy, disease stable (hemoglobin less than 1 0 gm%) Rhesus negative, sensitized Previous intrauterine fetal demise in second half of pregnancy Proven intrauterine growth retardation Maternal weight loss Gestational age documented greater than 4 2 weeks Multiple pregnancy Maternal weight greater than 300 pounds Deficiency anemias (hemoglobin less than 1 0 gm/%) Class II At-risk pregnancy Maternal weight between 250 and 300 pounds Hemoglobinopathy, trait (hemoglobin 10 gm/% or greater) Deficiency anemias (hemoglobin 1 0 gm/% or greater) History of urinary tract infections Bacteriuria Rhesus negative, unsensitized Suspected intrauterine growth retarda-tion Inadequate maternal weight gain Previous cesarean section Previous premature baby Previous baby 1 0 pounds or greater Class I Normal pregnant patients Critical care pregnancies (Class IV) are those pregnancies in which there is an imminent possibility of decompensation. As is apparent from the diagnoses, there is a risk of death to the fetus or the mother. These patients should generally be cared for in the hospital. High-risk pregnancies (Class Ill) include those that are not quite as critical as the Class IV type but whose diagnoses carry an unaccep­tably high perinatal loss. This is the category at which all the "new" antepartum testing tech-niques and methods of management have been directed. Specialized high-risk obstetrical clinics have been developed in referral centers to eval­uate and closely follow patients in this category. The most substantial improvement in perinatal outcome can be realized in the Class Ill cate­gory. At-risk pregnancies (Class II) need to be identified but do not require specialized surveil­lance. From the nature of the diagnoses it is ap­parent that all these patients have the capacity to decompensate and therefore require close supervision. Low-risk pregnancies (Class I) include pa­tients with normal pregnancies Frequently, the least number of patients are found in this cate­gory. These are patients with normal histories, normal physical examinations and normal labo­ratory values. Their pregnancies follow the pro­jected course for fundal growth, maternal weight gain, blood pressure, and all other pa­rameters of normal pregnancy. It is important to note that the assignment of a classification does not mean that the pa­tient is necessarily going to remain in that classi­fication throughout the pregnancy. Patients may shift from one class to another as their status improves or worsens. For example, if a patient has an iron deficiency anemia with hemoglobin of 11 gm/% she is placed in the Class II cate­gory. She is counseled about nutrition and ap­propriate diet, and iron supplements are pre­scribed. If, however, her hemoglobin drops to 9 gm/% as her pregnancy progresses, she is then placed in the Class Ill category. This may mean that she is transferred from a routine ob­stetrical clinic to a high risk clinic with special­ized surveillance. There are several diagnoses contained in the classification system that are of special in­terest. One such diagnosis is maternal weight loss (Class Ill). In the past, not enough attention has been paid to adequate weight gain in pregnancy. A great deal of emphasis has been placed on ex­cessive weight gain yet poor weight gain or worse, weight loss, has not been so readily rec­ognized. It is important to realize that the corre­lation between low-birth-weight infants and lack of maternal weight gain is greater than with any other single factor. When charts are examined retrospectively for factors such as parity, so­cioeconomic status, maternal weight gain, lox-PETRES AND COOGAN: HIGH-RISK GRAVIDA / 5 emia, renal disease. cigarette smoking, and number of children, the greatest influence on fetal weight gain is maternal weight gain. Poor fetal weight gain is not necessarily due to the fact that the mother's nutritional status is inadequate. Maternal weight gain is predicted both on her nutritional status and on the size of her fetus. If there is a problem pre­venting the growth of the fetus, such as rubella, the mother will not gain weight. This mother can be fed an adequate diet. but the baby will not grow because of its limited potential. Decreased maternal weight may cause poor fetal growth, but the reverse is also true. Poor fetal growth may be responsible for limited maternal weight gain. Suspected intrauterine growth retardation (IUGR) is another category that deserves special attention because of the difficulty of diagnosis. Suspected intrauterine growth retardation, as measured by biparietal diameter with ul­trasound, is often an iatrogenic problem Er­roneous measurements. or studies done too fre­quently, may indicate that there is lack of growth in the biparietal diameter. This points to the possibility of placental or fetal compromise. although, in fact. it may be nothing more than laboratory error. Intrauterine growth retardation diagnosed prior to 28 weeks gestation should be extremely suspect. Even in placental insufficiency syn­dromes. the fetal head usually continues to grow past 28 weeks, and it is extremely unlikely that the diagnosis of IUGR can be made from biparietal diameter data before that time. A biparietal diameter four or more weeks behind the dates prior to 28 weeks usually indicates "wrong dates." Hypertensive disorders in pregnancy are important because of their frequency and be­cause of the profound effects they have both on the mother and the fetus. They are divided into the toxemias (eclampsia and preeclampsia). chronic hypertension, gestational hypertension, and toxemia superimposed on hypertension. Gestational hypertension is hypertension that is unmasked in pregnancy but without the criteria for the diagnosis of toxemia. Making the appropriate diagnosis of hy­pertensive disorders in pregnancy can be con­fusing. However, high blood pressure, regard­less of etiology, has a deleterious effect on the end organs, be it the brain. the liver, the kidney, 6 / PETRES AND COOGAN HIGH-RISK GRAVIDA the cardiovascular system or the placenta. While it is important to establish a diagnosis, it ist more important to realize that the magnitude o� the blood pressure and the extent of end organ damage is directly proportional to fetal-maternal morbidity and mortality. In a series of hyperten" sives with proteinuria, the perinatal mortality, rate was 3 7. 9 per 1 000 births. This compared with a rate of 17.2 per 1000 for normotensive patients without proteinuria. 2 In patients with· diastolic blood pressure greater than 120, the perinatal mortality is 50%. 3 Hypertensive syndromes in pregnancy, continue to result in maternal mortality The out­come is compromised particularly if accelerated: hypertension occurs in the third trimester. Gen­erally this is categorized as chronic hyper­tension with superimposed toxemia.' Chesley reports that hypertension is rarely aggravated in pregnancy unless there is significant cardiac, renal, or retinal pathology.• What must be em­phasized. however, is that this type of pathol­ogy is fairly common in hypertensives and when these women become pregnant they are at in­creased risk. In the past several years much attention has been directed at predicting the patient who will develop hypertension in pregnancy. Dalton looked at weight gain as an indicator.6 She re­ported the incidence of preeclampsia to be 26% in patients who gained more than 1 % pounds per week after the 30th week of gesta­tion. The weight gain she is alluding to is not really caloric weight gain but rather fluid reten­tion which is one of the triad of symptoms asso­ciated with preeclampsia Edema. however. does not correlate well with increased perinatal morbidity and mortality. In fact, fluid retention is the least significant of the triad of hypertension, proteinuria and edema in relationship to peri­natal mortality. 3 Chesley has demonstrated that the diastolic blood pressure is the most signifi­cant factor in patients who will develop hyper­tension in pregnancy. 5 In his study, diastolic ele­vation occurred as the first symptom in 58% of patients whereas proteinuria occurred as the first symptom in only 34%. Proteinuria is only a reflection of the end organ damage to the kid­ney in hypertensives. In toxemia the vascular changes resulting in decreased perfusion of vi­tal organs is frequently long standing prior to a noticeable elevation in the diastolic blood pres­sure. Indeed, Gant and others' have demon-strated that the vascular changes typical of tox­emia occur as early as 24 weeks. Using 140/ 90 as a standard, the physician may not be able to appreciate an elevation until 35 or 36 weeks when end organ damage is already sub­stantial. If the diastolic blood pressure is 75-85 mm Hg, the perinatal mortality is about 7 per 1000. As the diastolic pressure increases to 85-90 mm Hg the rate is 10 per 1000. When the diastolic is 90-104 mm Hg, the perinatal mortality triples what it was at 7 5 mm Hg and there is a progressive linear increase in perinatal mortality as the diastolic blood pressure contin­ues to elevate.' A diastolic reading of 90 mm Hg at any point in pregnancy is distinctly abnor­mal. Calculation of the mean arterial pressure (MAP) is the most sensitive method of predicting impending hypertension in pregnancy. This measurement is obtained using the following formula. MAP = Systolic + 2 Diastolic 3 A MAP greater than 90 in the second trimester or greater than 105 in the third trimester is prognostic of hypertension, either gestational hypertension or toxemia.• Page and Christianson calculated MAP in the second and third trimesters and correlated it with outcome.• They found that when the MAP went from 90 to 95 or greater, the incidence of preeclampsia tripled. It is important to note that a blood pressure of 140/90 yields a MAP of well over 1 00. A blood pressure reading that may appear grossly normal is often abnormal when calculating its mean arterial pressure. Diabetes in pregnancy, while it represents a much smaller proportion of patients than the hypertensives, continues to be a problem. Dia­betic pregnancies carry a perinatal death rate four to five times higher than normal preg­nancies.• The outcome depends largely on the severity of the diabetes and the amount of vas­cular disease present prior to pregnancy. Some of the common problems seen in these preg­nancies are congenital anomalies (6%), oligohy­dramnios, premature rupture of membranes, macrosomia, toxemia (13% to 50%), urinary tract infections, increased incidence of cesa­rean section, birth trauma and intrauterine deaths. In addition, babies of diabetic mothers experience many problems in the newborn nur-sery. They include hypoglycemia, respiratory distress syndrome, and hyperbilirubinemia. The key to improved outcome in diabetic pregnancies centers around early diagnosis and strict metabolic control. Patients with a family history of diabetes or macrosomic babies, (greater than 4000 grams) should have a glu­cose tolerance test to screen for diabetes. In women who have had a previous baby weighing more than 4000 grams, 10% have undiag­nosed diabetes. ' 0 These women have high blood sugars which stimulate the fetal pancreas to produce insulin. Insulin acts like growth hor­mones in the fetus resulting in macrosomia. Glycosuria in pregnancy is another indicator to screen for diabetes. It cannot be dismissed as a decreased renal threshold for glucose or as ga­lactosuria secondary to breast development. Any patient with glycosuria in pregnancy should be considered diabetic until proven otherwise. Finally, patients with a poor obstetrical his­tory should be screened for diabetes. This in­cludes previous congenital anomalies, stillbirth, and repeated pregnancy loss. In conclusion, the classification system developed at the Medical College of Virginia to identify the high-risk gravida has been pre­sented with a discussion of some of the prob­lems in pregnancy that carry a high perinatal mortality. The importance of classifying patients according to risk is emphasized so that appro­priate management can ensue. In this way, pregnancy outcome can be improved. REFERENCES 1. AUBRY RH, PENNINGTON JC: Identification and evalua­tion of high risk pregnancy: The perinatal concept. Clin Obstetr Gyn 16:3-27, 1973. 2. NAEYE RL, FRIEDMAN EA: Causes of perinatal death as­sociated with gestational hypertension and proteinuria. Am J Obstetr Gyn 133:8-10, 1979. 3. FRIEDMAN EA, NEFF RK: Hypertension-hypotension in pregnancy. JAMA 239:2249-2251, 1978. 4. CURET LB, OLSON RW: Evaluation of a program of bed­rest in the treatment of chronic hypertension in preg­nancy. Obstef Gyn 53:336-340, 1979. 5. CHESLEY LC: Hypertensive Disorders in Pregnancy. New York, Appleton-Century-Crofts, 1978, p 4 78. 6. DALTON K: Early symptoms of preeclamtic toxemia. lancef 1: 198-199, 1960. PETRES AND COOGAN: HIGH-RISK GRAVIDA / 7 7. GANT NF, CHAND S, WORLEY RJ, EL AL: A clinical test useful for predicting the development of acute hyper­tension in pregnancy. Am J Obstet Gyn 120:1-7, 1974. 8. PAGE EW, CHRISTIANSON R: The impact of mean arterial pressure in the middle trimester upon the outcome of pregnancy. Am J Obstet Gyn 125:740-746, 1976. 8 / PETRES ANO COOGAN: HIGH-RISK GRAVIOA 9. Report of the Workshop on Pregnancy. National Com: mission on Diabetes, 3(2): 179, 1976. 10. GYVES MT. RODMAN HM, LITTLE AB, ET AL: A moderr approach to management of pregnant diabetics: J two-year analysis of perinatal outcomes. Am J Obste� Gyn 128 606-612, 1977. 

Identification of the High-Risk Gravida

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Identification of the High-Risk Gravida

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