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Amniotic fluid embolism
Department of Case Reports New Instruments, Etc. AMNIOTIC
FLUID
HERVEY K. GRAHAM, (From
the Department
of
Obstetrics
EMBOLISM
M.D., SAN DIEGO, CALIF. and
Gynecology,
Bees-Stealy
Clinic)
N 1941, Steiner and Lushbaugh’ described for the first time the entity of amniotic fluid embolism. Previous to this, sudden death in labor or in the immediate puerperium was ascribed to obstetric shock, postpartum hemorrhage, or acute pulmonary edema of pregnancy, in caseswhere no other definite pathology could be demonstrated as the cause. Since the original communication in 1941, a total of 57 cases has been reported. The incidence LISLLally has been reported as about one in 8,000 deliveries, although one survey shows no cases of this type in ten years’ experience in a teaching hospital. Amniotic fluid embolism usually develops in older multiparas with otherwise normal histories of past health and obstetrical experience. Their symptoms develop during labor or shortly following delivery. The labor is characteristically violent in nature, the membranes have ruptured, and meconium is present in the amniotic fluid. The individuals are frequently past term, and in a considerable number of cases the fetus has been dead for some time. It has been suggested that the character of the pains may be so violent because of the frequent associat,ion of some degree of placental separation. The chief symptoms of amniotic fluid embolism are those of restlessness, nausea, vomiting, chills, shortness of breath, and rapid or absent pulse. At the same time, the blood pressure is at shock levels or cannot be obtained. Cyanosis develops quickly, and coma and death occur immediately or within a few hours. The whole picture is similar to that of anaphylaxis and has often been described as an anaphylactoid type of reaction. The shock present in this kind of embolism often cannot be attributed to the amount of initial blood loss, as it is frequently manifested before the bleeding tendency has developed. It is more comparable to cardiovascular collapse. Pulmonary edema occasionally develops, and corresponding lung findings and frothy sputum may be present, with entirely normal heart findings. If a patient survives the initial shock reaction, an uncontrollable bleeding tendency soon develops from the uterus, gums, and at the sites of venipuncture or incision, Blood drawn for testing fails to clot, and at postmortem examination there is no evidence of clot formation in the large vessels or the heart. 657 I
When amniotic fluid enters the maternal circulation, it has a marked t hromboplast.ic action. 1.t producps rapid clot formation, followed by a fuj-t.hct- tlcfibrination of the blood, which results in the cscossivc bleeding tendency. This faulty clot formation can bc tlemonstr;tted in blood samples drawn. In addition, the blood serum c’xerts a lytic: action, so t.hat form4 clots tend to disintegrate. If the blood samplns taken from patients with amniotic iluid embolism are centrifuged or allowed t,o stand, they eventually show a lighter layer above the leukocytic layer. This layer contains amniotic fluid elements 01 squamous cells, mucusj meconium clcrivati\~cs. a,nd vernis caseosa. It has IWW suggested t,hat, in suspected cases of amniotic fluid embolism where ~C’SI. m~tIcm examination is refusc4, blood withdrawn from the right side of the. h(lart would show this layering chara.cterisit.ic. A tliagnosis ca.n be establishetl frolt~ study of the supc4Icia.l layer in srn~r or block. I’ossibly there have beeu a. nmnbrr- of unrecognized sublethal cases of amniotic fluid embolism. One cast cited. which was recognized, occurred in Bostoll. Sudden shock developed, followed by tliff’use lung pathology as found by physical examination ant1 s-ray. Shortly thcrcaftcr. hemorrhagic t~cndencics became ma,nifest and wer’c sucacssfully controlled by mult,iple transfusions of whole blood and administration of fibrinogen. Although the bleeding was controlled, there was complete suppression of kidney function fOllcJwing the multiple transfusions. After the patient, was transferred to Peter Bent Brigham Hospita,l, an artificial kidney wils rmployctl. Kidney fnncticm ultjmately retFurned, and t,he patient, was finally discharged. It remains to be sclcin whether or not she wil1 develop Sheehan’s syndrome at a. later date.
Case Report The history
case here reported of Mercy Hospital.
is the first one diagnosed as amniotic fluid embolism This is an incidence of one in over 4n,OOO deliveries.
in
the
The patient was a 39-year-old woman, gravida iii, pars ii. The estimated date uf confinement was Feb. 1, 1954. On January 37, she was admitted to the hospital at 2:15 P.&I. Throughout the afternoon, she had irregular pains of poor quality. At 7 P.M., a sterile vaginal examination showed the cervix to be dilate11 to approximately 3 cm., with menibranes bulging. The membranes were ruptured to promote more rapid progress. The fluid that escaped was not meconium stained at thai time. At 7:40 P.M., the patient vomited. At i’:55 P.M., a convulsion was reported, followed by labored respiration, cyanosis, and unobtainable blood ~‘ressure. Oxygen was administered at the same timca. Illtr:l uuder pressure, and artificial respira.tion was used with an sirnx~venous glucose was started, caffeine sollium l~~nzoa tr IYRS allrniniatcretl into the intravearroll> :\llrenalin WP injected into thr hrert. tubing, anIl, when no heart sounds coultl IKB htwd. was At 8:09 P.M., the patient heard. A rapid postmortem cesarean infant in poor condition. The infant use of the Airlock, the infant survived not t,c evident for some time whether
pronounced &sad, 1 jut. fetal heart sounds could still be section was performed, with delivery of a living femalc responded to stimulation and oxygen, and, thanks to thr and is at present progressing satisfactorily. It will t.he anoxia has had a deleterious effect on the brain.
The autopsy done the following day disclosed no significant gross abnormality. The I)rain showed no abnormality or evidence of hemorrhage. The heart presented a normal (+rossly, the lungs showed slight congestion of myocardium, normal valves and vessels. tl~v lower lobes. The pulmonary vessels were grossly normal. The liver was normal, hut I Irma Iti~lneys sholred slight congestion.
Volume Number
70 3
AMNIOTIC
FLTJlB
(%!I
EMBOLlSM
The significant pathology was shown in microscopic study of the lung sections. Here, the small arterioles were plugged with epithelial cell R and amorphous material derived from the amniotic fluid. The same type of material plugged the capillaries of the alveolar There was no significant abnormality in the other tissues studied. These microwalls. scopic findings are diagnostic for amniotic fluid embolism.
Summary The occurrence of amniotic fluid embolism is most frequent among older multiparas with normal courses of pregnancy and normal past histories. In many cases, the delivery is of a known dead fetus, and often the fetus is lost because of coincidental disease. Frequently the fetus is quite large and postmature, and these factors lead to obstetrical difficulty. All of these conditions contribute to the presence of meconium in the amniot,ic fluid. When amniotic fluid embolism occurs, its onset is usually so rapid and so violent, with symptoms of such profound degree, that therapeutic measures are of no avail. In the case reported here, the infant survived because of excellent cooperaIn one other instance of a living tion and equipment immediately available. infant obtained by postmortem cesarean section following amniotic embolism, the infant is reported to have lived only twelve hours. References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.
Steiner, P. E., and Lushbaugh, C. C.: J. A. M. A. 117: 1245, 1340, 1941. Lushbaugh, C. C., and Steiner, P. E.: AM. J. OBST. & GYNEC. 43: 833, 19-K. Gross, P., and Benz, E. J.: Surg., Gynec. & Obst. 85: 315, 1947. Hemmings, C. T.: AM. J. OBST. & GYNEC. 53: 303, 1947. Seltzer, L. M., and Schuman, W.: AM. J. OBST. & GYNEC. 54: 1938, 1947. Jennings, E. R., and Stofer, B. E.: Arch. Path. 45: 616, 1948. Schneider, C. L.: Surg., Gynec. & Obst. 90: 613, 1950. Mallory, G. E., Blackburn, N., Sparling, H. J., and Nickerson, D. A.: New Med. 243: 583, 1950. Leary, 0. C., and Hertig, A. T.: New England J. Med. 243: 588, 1950. Landing, B. H.: New England J. Med. 243: 590, 1950. Weiner, A. E., and Reid, D. E.: New England J. Med. 243: 597, 1950. Ratnob, 0. D., and Vosburgh, G. J.: New England J. Med. 247: 970, 1952. Sluder, H. M., and Lock, F. R.: AM. J. OBST. & GYNEC. 64: 118? 1952. Editorial, J. A. M. A. 150: 943, 1952. Tunis, B.: AK J. OBST. & GYNEC. 64: 72, 1952. Reid, D. E., Weiner, A. E., and Roby, C. C.: J. A. M. A. 152: 227, 1953. Navori, C. A., and Wissler, R. W.: AM. J. OBST. & GYNEC. 67: 432, 1954.
England
J.
FLUID
HERVEY K. GRAHAM, (From
the Department
of
Obstetrics
EMBOLISM
M.D., SAN DIEGO, CALIF. and
Gynecology,
Bees-Stealy
Clinic)
N 1941, Steiner and Lushbaugh’ described for the first time the entity of amniotic fluid embolism. Previous to this, sudden death in labor or in the immediate puerperium was ascribed to obstetric shock, postpartum hemorrhage, or acute pulmonary edema of pregnancy, in caseswhere no other definite pathology could be demonstrated as the cause. Since the original communication in 1941, a total of 57 cases has been reported. The incidence LISLLally has been reported as about one in 8,000 deliveries, although one survey shows no cases of this type in ten years’ experience in a teaching hospital. Amniotic fluid embolism usually develops in older multiparas with otherwise normal histories of past health and obstetrical experience. Their symptoms develop during labor or shortly following delivery. The labor is characteristically violent in nature, the membranes have ruptured, and meconium is present in the amniotic fluid. The individuals are frequently past term, and in a considerable number of cases the fetus has been dead for some time. It has been suggested that the character of the pains may be so violent because of the frequent associat,ion of some degree of placental separation. The chief symptoms of amniotic fluid embolism are those of restlessness, nausea, vomiting, chills, shortness of breath, and rapid or absent pulse. At the same time, the blood pressure is at shock levels or cannot be obtained. Cyanosis develops quickly, and coma and death occur immediately or within a few hours. The whole picture is similar to that of anaphylaxis and has often been described as an anaphylactoid type of reaction. The shock present in this kind of embolism often cannot be attributed to the amount of initial blood loss, as it is frequently manifested before the bleeding tendency has developed. It is more comparable to cardiovascular collapse. Pulmonary edema occasionally develops, and corresponding lung findings and frothy sputum may be present, with entirely normal heart findings. If a patient survives the initial shock reaction, an uncontrollable bleeding tendency soon develops from the uterus, gums, and at the sites of venipuncture or incision, Blood drawn for testing fails to clot, and at postmortem examination there is no evidence of clot formation in the large vessels or the heart. 657 I
When amniotic fluid enters the maternal circulation, it has a marked t hromboplast.ic action. 1.t producps rapid clot formation, followed by a fuj-t.hct- tlcfibrination of the blood, which results in the cscossivc bleeding tendency. This faulty clot formation can bc tlemonstr;tted in blood samples drawn. In addition, the blood serum c’xerts a lytic: action, so t.hat form4 clots tend to disintegrate. If the blood samplns taken from patients with amniotic iluid embolism are centrifuged or allowed t,o stand, they eventually show a lighter layer above the leukocytic layer. This layer contains amniotic fluid elements 01 squamous cells, mucusj meconium clcrivati\~cs. a,nd vernis caseosa. It has IWW suggested t,hat, in suspected cases of amniotic fluid embolism where ~C’SI. m~tIcm examination is refusc4, blood withdrawn from the right side of the. h(lart would show this layering chara.cterisit.ic. A tliagnosis ca.n be establishetl frolt~ study of the supc4Icia.l layer in srn~r or block. I’ossibly there have beeu a. nmnbrr- of unrecognized sublethal cases of amniotic fluid embolism. One cast cited. which was recognized, occurred in Bostoll. Sudden shock developed, followed by tliff’use lung pathology as found by physical examination ant1 s-ray. Shortly thcrcaftcr. hemorrhagic t~cndencics became ma,nifest and wer’c sucacssfully controlled by mult,iple transfusions of whole blood and administration of fibrinogen. Although the bleeding was controlled, there was complete suppression of kidney function fOllcJwing the multiple transfusions. After the patient, was transferred to Peter Bent Brigham Hospita,l, an artificial kidney wils rmployctl. Kidney fnncticm ultjmately retFurned, and t,he patient, was finally discharged. It remains to be sclcin whether or not she wil1 develop Sheehan’s syndrome at a. later date.
Case Report The history
case here reported of Mercy Hospital.
is the first one diagnosed as amniotic fluid embolism This is an incidence of one in over 4n,OOO deliveries.
in
the
The patient was a 39-year-old woman, gravida iii, pars ii. The estimated date uf confinement was Feb. 1, 1954. On January 37, she was admitted to the hospital at 2:15 P.&I. Throughout the afternoon, she had irregular pains of poor quality. At 7 P.M., a sterile vaginal examination showed the cervix to be dilate11 to approximately 3 cm., with menibranes bulging. The membranes were ruptured to promote more rapid progress. The fluid that escaped was not meconium stained at thai time. At 7:40 P.M., the patient vomited. At i’:55 P.M., a convulsion was reported, followed by labored respiration, cyanosis, and unobtainable blood ~‘ressure. Oxygen was administered at the same timca. Illtr:l uuder pressure, and artificial respira.tion was used with an sirnx~venous glucose was started, caffeine sollium l~~nzoa tr IYRS allrniniatcretl into the intravearroll> :\llrenalin WP injected into thr hrert. tubing, anIl, when no heart sounds coultl IKB htwd. was At 8:09 P.M., the patient heard. A rapid postmortem cesarean infant in poor condition. The infant use of the Airlock, the infant survived not t,c evident for some time whether
pronounced &sad, 1 jut. fetal heart sounds could still be section was performed, with delivery of a living femalc responded to stimulation and oxygen, and, thanks to thr and is at present progressing satisfactorily. It will t.he anoxia has had a deleterious effect on the brain.
The autopsy done the following day disclosed no significant gross abnormality. The I)rain showed no abnormality or evidence of hemorrhage. The heart presented a normal (+rossly, the lungs showed slight congestion of myocardium, normal valves and vessels. tl~v lower lobes. The pulmonary vessels were grossly normal. The liver was normal, hut I Irma Iti~lneys sholred slight congestion.
Volume Number
70 3
AMNIOTIC
FLTJlB
(%!I
EMBOLlSM
The significant pathology was shown in microscopic study of the lung sections. Here, the small arterioles were plugged with epithelial cell R and amorphous material derived from the amniotic fluid. The same type of material plugged the capillaries of the alveolar There was no significant abnormality in the other tissues studied. These microwalls. scopic findings are diagnostic for amniotic fluid embolism.
Summary The occurrence of amniotic fluid embolism is most frequent among older multiparas with normal courses of pregnancy and normal past histories. In many cases, the delivery is of a known dead fetus, and often the fetus is lost because of coincidental disease. Frequently the fetus is quite large and postmature, and these factors lead to obstetrical difficulty. All of these conditions contribute to the presence of meconium in the amniot,ic fluid. When amniotic fluid embolism occurs, its onset is usually so rapid and so violent, with symptoms of such profound degree, that therapeutic measures are of no avail. In the case reported here, the infant survived because of excellent cooperaIn one other instance of a living tion and equipment immediately available. infant obtained by postmortem cesarean section following amniotic embolism, the infant is reported to have lived only twelve hours. References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.
Steiner, P. E., and Lushbaugh, C. C.: J. A. M. A. 117: 1245, 1340, 1941. Lushbaugh, C. C., and Steiner, P. E.: AM. J. OBST. & GYNEC. 43: 833, 19-K. Gross, P., and Benz, E. J.: Surg., Gynec. & Obst. 85: 315, 1947. Hemmings, C. T.: AM. J. OBST. & GYNEC. 53: 303, 1947. Seltzer, L. M., and Schuman, W.: AM. J. OBST. & GYNEC. 54: 1938, 1947. Jennings, E. R., and Stofer, B. E.: Arch. Path. 45: 616, 1948. Schneider, C. L.: Surg., Gynec. & Obst. 90: 613, 1950. Mallory, G. E., Blackburn, N., Sparling, H. J., and Nickerson, D. A.: New Med. 243: 583, 1950. Leary, 0. C., and Hertig, A. T.: New England J. Med. 243: 588, 1950. Landing, B. H.: New England J. Med. 243: 590, 1950. Weiner, A. E., and Reid, D. E.: New England J. Med. 243: 597, 1950. Ratnob, 0. D., and Vosburgh, G. J.: New England J. Med. 247: 970, 1952. Sluder, H. M., and Lock, F. R.: AM. J. OBST. & GYNEC. 64: 118? 1952. Editorial, J. A. M. A. 150: 943, 1952. Tunis, B.: AK J. OBST. & GYNEC. 64: 72, 1952. Reid, D. E., Weiner, A. E., and Roby, C. C.: J. A. M. A. 152: 227, 1953. Navori, C. A., and Wissler, R. W.: AM. J. OBST. & GYNEC. 67: 432, 1954.
England
J.