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Amniotic Fluid Embolism
AMNIOTIC FLUID EMBOLISM Case Report JAMES
A.
BOWMAN, JR.,
M.D.,
CLEYELAXD, OHIO
( fi'rorn the Department of Obstetrics and Gynccolopy, Western Reserve University School Medicine, and MacDonald House of UnivGrsity Hospitals of Cleveland)
of
INCE Steiner and Lushbaugh first described the syndrome of maternal pulmonary embolism by amniotic fluid in 1941, some 30 cases of amniotic fluid embolism have been reported in the literature. The clinical picture of amniotic fluid embolism as described originally has remained largely unchanged. Several common factors are noted in a review of the individual case reports. The patient is generally a multipara in the older age group with an uncomplicated prenatal course and perhaps a postmature fetus or, at least, the fetus is larger than normal. The labor is short, with contractions that are described as being of greater intensity. The first sign or symptom may occur during labor or immediately after delivery. A subjective chilliness has been most commonly reported as the first symptom. Subsequently shock develops with a drop in the blood pressure and the patient then may show signs of anoxia with dyspnea and cyanosis developing. Death may occur in a matter of minutes or in hours. The fetus is usually stillborn or dies within hours after birth. The pathological diagnosis can be made only by the demonstration of amniotic fluid elements in the small arterioles and capillaries of the lungs. Among the amniotic fluid elements that can be demonstrated are squamous epithelial cells, mucus, and rarely lanugo hairs. In most sections demonstrating intravascular components, large numbers of polymorphonuclear leukocytes are seen. Gross and Benz centrifuged blood from the inferior vena cava and right side of the heart in one of their cases and demonstrated squamous cells of amniotic fluid origin. They recommend postmortem needle aspiration of the right side of the heart in those cases in which amniotic fluid embolus is suspected, in order to establish, the diagnosis when autopsy is denied. Examination of other organs shows minor changes consistent with anoxia. Gross examination of the uterus varies in the cases reported. About GO per cent of the uteri show breaks in the contiguity of the epithelium; either surgical incision or tears extending through the myometrium. Microscopic examination of folections of the uterus may show squamous cells and other amniotic fluid components in the uterine sinusoids or in the pelvic veins. In summary, the pathological diagnosis of amniotic fluid embolism is made on examination of tissue sections demonstrating amniotic fluid components in the pulmonary vascular system. Gross examination may often be normal or at least the only findings are those of anoxia.
S
905
906
BOWMAN
Am.
J. Obst. & Gynec.
April, 1955
Theories of the pathogenesis of fatal amniotic fluid embolism are concerned with two factors: the entrance of amniotic fluid elements into the maternal circulati
Volume 6q Nnmher 4
"DINIOTIC FLUID E1fBOLISM
!107
per minute and then ceased. The uterus was noted to be tonic. The peripheral pulses m~re thready. Artificial respiration with positive pressure oxygen was carried out. ~\. eut-down was attempted on the right leg at the ankle. When the \'cin was incised preparatory to in;
It has been proposed by Weiner and Reid that heparin be given intravenously as early as possible after recognition of the syndrome. It has been shown that large amounts of thromboplastin are inactivated by small amounts of heparin in vitro. The heparin may therefore prevent further intravascular clotting. In those patients who survive the mltlal emoollzation and who present hemorrhagic manifestations, intravenous fibrinogen in amounts of 4 to 12 Gm. and adequate blood replacement may result in recovery. Rcrently Reid, Weiner, and Roby reported upon 4 patients with presumptive amniotic fluid embolism and subsequent incoagulable blood who were succcssfnll~· tr·cated with fibrinogC'n replacement therapy and blood transfusions.
Conclusion 1. A case of fatal maternal pulmonary embolism by amniotic fluid IS presented in which intravascular clotting of hlood was (lf'monstrated prior to the patient's death. 2. A plan of therapy including heparin, fibrinog1•n, aJHl blood replac0ment is reviewed. 3. The literature IS briefly revie¥lCtl.
References Hross, P., and Benz, E. J.: Surg., Gyuec. & Obst. 85: :a:-;, J\J-1 I. Landing, B. H.: New England J. Med. 243: 590, 1950. Leary, 0. C., and Hertig, A. 'l'.: New England ,T. l\fed. 243: 588, 19ii0. Lu~hhaugh, C. C., and Steiner, P. E.: AM. J. 0BST. & GYNEC. 43: 833, lfl42. Mallory, G. K., Blackburn, N., Sparling, H ..T., and Nickerson, D. A.: New England .T. 243: 583, 1950. Ratnoff, 0. D., and Vosburgh, G. J.: New England .J. Med. 247: 970, 1952. Reid, D. E., Weiner, A. E., and Roby, C. C.: AM .•J. OBST. & GYNEn. 66: 465, Hl5:l. Steiner, P. 1~., and Lushbaugh, C. C.: J. A.M. A. ii7: 1245, 1941. W<>iner, A. K, and Reid, D. E.: New England J. Med. 243: 5!\7, 1!\50.
~fed.
A.
BOWMAN, JR.,
M.D.,
CLEYELAXD, OHIO
( fi'rorn the Department of Obstetrics and Gynccolopy, Western Reserve University School Medicine, and MacDonald House of UnivGrsity Hospitals of Cleveland)
of
INCE Steiner and Lushbaugh first described the syndrome of maternal pulmonary embolism by amniotic fluid in 1941, some 30 cases of amniotic fluid embolism have been reported in the literature. The clinical picture of amniotic fluid embolism as described originally has remained largely unchanged. Several common factors are noted in a review of the individual case reports. The patient is generally a multipara in the older age group with an uncomplicated prenatal course and perhaps a postmature fetus or, at least, the fetus is larger than normal. The labor is short, with contractions that are described as being of greater intensity. The first sign or symptom may occur during labor or immediately after delivery. A subjective chilliness has been most commonly reported as the first symptom. Subsequently shock develops with a drop in the blood pressure and the patient then may show signs of anoxia with dyspnea and cyanosis developing. Death may occur in a matter of minutes or in hours. The fetus is usually stillborn or dies within hours after birth. The pathological diagnosis can be made only by the demonstration of amniotic fluid elements in the small arterioles and capillaries of the lungs. Among the amniotic fluid elements that can be demonstrated are squamous epithelial cells, mucus, and rarely lanugo hairs. In most sections demonstrating intravascular components, large numbers of polymorphonuclear leukocytes are seen. Gross and Benz centrifuged blood from the inferior vena cava and right side of the heart in one of their cases and demonstrated squamous cells of amniotic fluid origin. They recommend postmortem needle aspiration of the right side of the heart in those cases in which amniotic fluid embolus is suspected, in order to establish, the diagnosis when autopsy is denied. Examination of other organs shows minor changes consistent with anoxia. Gross examination of the uterus varies in the cases reported. About GO per cent of the uteri show breaks in the contiguity of the epithelium; either surgical incision or tears extending through the myometrium. Microscopic examination of folections of the uterus may show squamous cells and other amniotic fluid components in the uterine sinusoids or in the pelvic veins. In summary, the pathological diagnosis of amniotic fluid embolism is made on examination of tissue sections demonstrating amniotic fluid components in the pulmonary vascular system. Gross examination may often be normal or at least the only findings are those of anoxia.
S
905
906
BOWMAN
Am.
J. Obst. & Gynec.
April, 1955
Theories of the pathogenesis of fatal amniotic fluid embolism are concerned with two factors: the entrance of amniotic fluid elements into the maternal circulati
Volume 6q Nnmher 4
"DINIOTIC FLUID E1fBOLISM
!107
per minute and then ceased. The uterus was noted to be tonic. The peripheral pulses m~re thready. Artificial respiration with positive pressure oxygen was carried out. ~\. eut-down was attempted on the right leg at the ankle. When the \'cin was incised preparatory to in;
It has been proposed by Weiner and Reid that heparin be given intravenously as early as possible after recognition of the syndrome. It has been shown that large amounts of thromboplastin are inactivated by small amounts of heparin in vitro. The heparin may therefore prevent further intravascular clotting. In those patients who survive the mltlal emoollzation and who present hemorrhagic manifestations, intravenous fibrinogen in amounts of 4 to 12 Gm. and adequate blood replacement may result in recovery. Rcrently Reid, Weiner, and Roby reported upon 4 patients with presumptive amniotic fluid embolism and subsequent incoagulable blood who were succcssfnll~· tr·cated with fibrinogC'n replacement therapy and blood transfusions.
Conclusion 1. A case of fatal maternal pulmonary embolism by amniotic fluid IS presented in which intravascular clotting of hlood was (lf'monstrated prior to the patient's death. 2. A plan of therapy including heparin, fibrinog1•n, aJHl blood replac0ment is reviewed. 3. The literature IS briefly revie¥lCtl.
References Hross, P., and Benz, E. J.: Surg., Gyuec. & Obst. 85: :a:-;, J\J-1 I. Landing, B. H.: New England J. Med. 243: 590, 1950. Leary, 0. C., and Hertig, A. 'l'.: New England ,T. l\fed. 243: 588, 19ii0. Lu~hhaugh, C. C., and Steiner, P. E.: AM. J. 0BST. & GYNEC. 43: 833, lfl42. Mallory, G. K., Blackburn, N., Sparling, H ..T., and Nickerson, D. A.: New England .T. 243: 583, 1950. Ratnoff, 0. D., and Vosburgh, G. J.: New England .J. Med. 247: 970, 1952. Reid, D. E., Weiner, A. E., and Roby, C. C.: AM .•J. OBST. & GYNEn. 66: 465, Hl5:l. Steiner, P. 1~., and Lushbaugh, C. C.: J. A.M. A. ii7: 1245, 1941. W<>iner, A. K, and Reid, D. E.: New England J. Med. 243: 5!\7, 1!\50.
~fed.