Volume Hi2
Correspondence
:'\urnber 2
with the ultrasonographic diagnosis of cord presentation. In these cases the presence of variable decelerations or significant fetal bradycardia is highly suggestive of cord compromise (Fig. 3). The routine application of suprapubic and fundal pressure at the conclusion of the test (in an attempt to provoke fetal bradycardia, which may indicate decreased amniotic fluid volume and potential cord entrapment) is recommended (Fig. 4). 3. If the pregnancy remains uncomplicated, ultrasonography and nonstress test should be repeated at weekly intervals unless changes in maternal or fetal condition indicate closer evaluation. Gentle and sterile pelvic examinations should be done regularly to check the status of the cervix, membranes, presenting part, and umbilical cord. 4. In patients at term, prompt delivery by cesarean section in cases of persistent cord presentation seems logic. Surgical intervention in all other cases remains an individual clinical decision. Hospitalization of these patients for close observation is strongly recommended. It must be emphasized that in questionable cases the ultrasonographic examination should be repeated just before surge.'y because cord position may change even late in pregnancy. Until recently little could be done to prevent spontaneous prolapse of the cord. The combined prenatal use of ultrasound and electronic fetal monitoring may substantially reduce the incidence of this catastrophic obstetric complication. Marro A. Pel!J.Ii, MD Pelosi Women's Medical Center 350-360 Kennedy Blvd. Bayonne, NJ 07002 REFERENCES
not consider a patient's plasma volume or body hematocrit. ' Pregnant women with large fetuses have increased plasma volume and relatively low hematocrits. By contrast, gravid women with growth-retarded fetuses have decreased plasma volume and high hematocrits. Thus those with hematocrits <35% may have increased red cell masses or body hematocrits and the reverse applies to those pregnant women with high hematocrits.' \ After cesarean section in gravid women with relative hypovolemia, a 15% to 25% decrease in venous hematocrits may occur because of mobilization of extravascular fluid. Because the concept of body hematocrits and increased plasma volumes is ignored, I have seen such postpartum women overtransfused and adult respiratory distress syndrome develop. Venous hematocrits are not enough when evaluating an apparent anemia in the postpartum women or even the prenatal patient at term. Instead. one should estimate the plasma volume and perhaps obtain a ferritin level. \ As Sir Albert Liley said; "It is unfortunate that an estimation of hematocrit is one of the quickest, easiest and cheapest laboratory tests we can do and potentially one of the most difficult to interpret. This is especially true in pregnancy.'" Robert C. Goodlin, MD City and County of Denver Department of Health and Hospital., Obstetrics and Gynecology 777 Bannock St. Denver, CO 80204-4507 REFERENCES I. NIH consensus conference. PerioperatIve red blood cell transfusion . .lAMA 1988;260:2700-3. 2. Liley AW. Clinical and laboratory significance of maternal plasma volume in pregnancy. IntJ Gvnecol Obstet 1970; 8:358. 3. Goodlin RC. Why treat "physiologic" anemia of pregnancy. .I Reprod Med 1982;27:639-46. 4. Goodlin RC. Dobry CA. Anderson Je. et al. Clinical signs of normal plasma volume expan~ion during pregnancy. A \1 .I OBSIET GYNECOL 1983;145:1001-9.
l. PelOSI MA. The peril of a
2. 3. 4. 5.
prolap~ed cord. Emerg- !\fed 1981;13:213. Pelosi ~lA. Antepartum ultrasonog-raphic screening- for abnormal umbilical cord position. Perinatol Neonat 1985;9: 54. Pelosi MA. Prolapse of the umbilical cord. In: Perinatology case studies. Langer A. Iffy. L. eels. 2nd ed. New York: Medical Examination. 1985:478-90. Vintzileos AM. Nochimson DJ. Lillo NL. et al. Ultrasonic diagnosis of funic presentation. JCU 1983; II :510. Lange IR. Manning FA. Morrison I. et al. Cord prolapse: is antenatal diagnosis possible? A~I .I aBS lET GY'f( OL 1985;151:1083.
601
Need for plasma volume estimation To the Editors: The publication by the Consensus Development Panel on perioperative red blood cell transfusion did
Pulmonary artery catheterization in severe preeclampsia To the Editor:.: Drs. Clark and Cotton (Clark SL, Cotton DB. Clinical indications for pulmonary artery catheterization in the patient with severe preeclampsia. AM J OB~"1 E'I Gyl'o:ECOL 1988; 158:453-8) have attempted to justify the use of the pulmonary artery catheter in patients with severe preeclampsia. More than a decade ago, we undertook studies in which we sought to demonstrate what the authors are proposing, mainly that with the Swan-Ganz catheter one could accurately interpret and safely administer colloid therapy in the hypovolemic, severely preeclamptic patient. I " Our studies then
602 Correspondence
showed, as has been recently e mphasized," that in these pr'e eclamptic patients the cardiac outputs may be increased, normal, or decreased and that their response to colloids is not necessarily predictable. Drs. Clark and Cotton further state that the hemodynamics are best described with reference to cardiac preload, afterload, and contractility. By contrast, Guyton· in his text, Arterial Pressure and Hypertension, devotes an entire chapter to "Fallacies in interpreting cardiac output, total peripheral resistance and blood volume data in hypertension studies: importance of mean circulatory filling pressure measurements." After our inability to interpret pregnant hypertensive patients' data from the Swan-Ganz catheter, we undertook estimates of the equivalent mean circulatory filling pressure (static pressure) measurements in normal and hypertensive pregnant patients!·7 It appears that Professor Guyton's and others'S pleas concerning the importance of venous reactivity have not been appreciated. I cannot accept Drs. Clark and Cotton's claim of precision in describing the hemodynamics of all patients with preeclampsia without venous measurements. Whil.e I do not now recommend the insertion of the pulmonary artery catheter in patients with severe preeclampsia, our anesthesiologists do. Just as we learned a decade ago, these preeclamptic patients now are often in overload after therapeutic response to the catheter's readings. Lasix (furosemide) is necessary to maintain the patient's good health. I continue to believe that a randomized trial is necessary in these patients with severe preeclampsia to demonstrate the value of the pulmonary artery catheter. If volume expansion appears indicated, it may be used safely without a pulmonary artery catheter and with only the stethoscope, chest x-ray film, and urine output monitoring. 9 Occasionally, furosemide will be necessary, but so will it be when the pulmonary artery catheter is used. The authors' condemn "therapeutic misadventure," but in my view they should first demonstrate that they are without error in their interpretation of the pulmonary artery catheter readings. Indeed, in a recent review, Dr. Cotton was much less emphatic about the value of the Swan-Ganz catheter lO than in this Clinical Opinion or in a second article with the same message in the same issue (Cotton DB, Lee W, Huhta JC, Dorman KF. Hemodynamic profile of severe pregnancy-induced hypertension. AM J OBSTET GVNECOL 1988; 158:523-9). Robert C. Goodlin, MD City and County of Denver Department of Health and Hospitals 777 Bannock St. Denver, CO 80204-4507 REFERENCES I . Goodlin RC, Cotton DB , Haesslein HC. Severe edemaproteinuria-hypertension gestosis. AM] OSSTET GYNECOL 1978; 132:595.
Februarv 1990 Am J Obstel C;ynecol
2. Goodlin RC. Volume expansio n in severe edemaproteinuria-hypertension gestosis. AM] OSSTET GYNt.COL 1979;135:276, 3. Mabie WC, Ratts TE, Sibai BM. The central hemodynamics of severe preeclampsia. AM] OBSTET GY:--ECOL 1989; 161: 1443-8. 4. Guyton AC. Arterial pressure and hypertension. Philadelphia: WB Saunders, 1980 :48-496. 5. Goodlin RC, Woods RE, McKinney ME, Hofschire Pl. Churchill GA. Elevated static pressure and pregnancy well-being. AM] OBSTET GYNECOL 1985; 152:462. 6. Goodlin RC. Leg static pressure values in pregnant women with iatrogenic pulmona ry edema. AM ] OBSTET GYNECOL 1986; 154:634. 7. Goodlin RC. Venous reactivity a nd pregnancy abnormalities. Acta Obstet Gynecol Scand 1986;65:345. 8. Stainer K, Morrison R, Pickles C, Cowley AJ. Abnormalities of peripheral venous tone in women with pregnancyinduced hypertension. Clin Sci 1986;70; ISS. 9. Goodlin RC. Heading off plasma volume problems of pregnancy. Contemp Ob/Gyn 1982 ;20;1?5. . . . 10. Wasserstrum N, Cotton DB . HemodynamiC momtormg 10 severe pregnancy-induced hypertensIon . Clin Perinatol 1986;13:781.
Reply To the Editors: We are surprised and dismayed by Dr. Goodlin's letter. We urge interested readers of this JOURNAL to examine carefully Dr. Goodlin's references 1 and 2, which he implies describe his experience with the pulmonary artery catheter in preeclampsia. On the basis of this supposed experience he attempts to refute our opinions as set forth in the AMERICA NJOURNAL. If one carefully examines Dr. Goodlin's references I and 2, it is evident that, despite his implications, neither actually contains data derived from invasive hemodynamic monitoring. In his first article Dr. Goodlin references a manuscript of his own dealing with cardiac output as "in preparation." In the intervening 10 years, these data have evidently never appeared in peer-review press. Dr. Goodlin's second "reference" is merely a reply to a letter to the editor critical of his first article, in which other investigators criticize the "potentially dangerous therapeutic concept" presented therein. Dr. Goodlin 's letter is misleading in that it misrepresents his own publications and references data that have never been published. His opinions must be viewed accordingly. If Dr. Goodlin does in fact have data derived from pulmonary artery catheterization that refute an expanding body of recently published data, we strongly urge that he publish them and reference the article directly so that we too may be enlightened. We also disagree strongly with Dr. Goodlin's statement that volume expansion can safely be given with "only the stethoscope, chest x-ray film, and urine output monitoring." Chest roentgenography is known to lag as much as 12 to 24 hours behind the clinical development of pulmonary edema. I The documentation of rales in the bases of the lungs means that pulmonary edema has already occurred and a "therapeutic mis-