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Retinal Arteriolar Occlusions Following Amniotic Fluid Embolism
Retinal Arteriolar Occlusions
Following Amniotic
Fluid Embolism
MEIMEI CHANG, MD,* WILLIAM N. P. HERBERT, MDt
Abstract: Amniotic fluid embolism is a serious complication of pregnancy resulting in death in the majority of patients. Particulate matter originating in the amniotic fluid has been identified at autopsy in the lung, kidney, and brain. A patient is presented who survived amniotic fluid embolism and developed bilateral retinal arteriolar occlusions, presumably based on entrapment of particulate matter originating in amniotic fluid. Her clinical course and ophthalmic findings are reviewed, and the relationship between amniotic fluid embolism and retinal vascular occlusion is discussed.[Key words: Amniotic fluid embolism, intrapartum complication, particulate matter, retinal arteriolar occlusions.] Ophthalmology 91: 1634-1637, 1984
Amniotic fluid embolism (AFE) is a serious complication of pregnancy and represents a leading cause of intrapartum and early postpartum maternal death. Entry into maternal blood of sufficient quantities of amniotic fluid containing particulate matter causes sudden cardiopulmonary failure, usually accompanied by marked derangement of the coagulation mechanism. Death follows in 86% of cases. I Ocular manifestations with amniotic fluid embolism have rarely been published. In 1969, Fischbein2 described a patient who developed bilateral ischemic oculopathy following AFE. In 1978, Stromme and Fromke, 3 in reporting a patient who developed AFE following uterine evacuation for missed abortion, noted that she experienced field defects which were felt to be secondary to cerebral embolism. No ophthalmic findings were stated, however. We present a patient with amniotic fluid embolus who developed bilateral retinal arteriolar occlusions, presumably from particulate matter originating in amniotic fluid. The relationship between amniotic fluid embolus and these ocular findings is discussed.
From the Departments of Ophthalmology' and Obstetrics and Gynecology,t University of North Carolina School of Medicine, Chapel Hill. Supported in part by a grant from Research to Prevent Blindness, Inc. Reprint requests to Meimei Chang, MD, 617 Clinical Sciences Bldg. 229H, Chapel Hill, NC 27514.
1634
CASE REPORT A 28-year-old gravida three, para one, abortus one black woman was admitted to her local hospital at 42 weeks gestation for induction of labor. Her prenatal course had been benign except for one brief episode of vaginal bleeding at approximately 20 weeks gestation. The amniotic fluid was clear when the fetal membranes were artificially ruptured, and intravenous oxytocin infusion was begun. Three hours later, the patient suddenly developed shortness of breath and wheezing, followed moments later by loss of consciousness and cardiac arrest. Resuscitation was instituted, including tracheal intubation. Fetal bradycardia was noted and a pelvic examination was performed. The cervix was completely dilated. With the aid of low forceps, the patient delivered a 3000 gm depressed male infant who subsequently died. Immediately after delivery, marked uterine hemorrhage occurred, followed by tachycardia, hypotension, and bleeding from the nasopharynx and intravenous infusion sites. Coagulation studies were abnormal. Over the next two hours, multiple units of whole blood, platelets, cryoprecipitate, and fresh frozen plasma were administered and the bleeding diminished. The patient was transferred to North Carolina Memorial Hospital for further management. On arrival, she was obtunded, normotensive, but tachycardic. She responded to deep pain only. Pupils were equal and responded to light, and there were no lateralizing neurologic signs. Coagulation studies were normal. A computed tomography scan of the head was consistent with cerebral edema without evidence of intracranial hemorrhage. With intensive care and blood component therapy
CHANG AND HERBERT
•
AMNIOTIC FLUID EMBOLISM
~~ ~
~n
~~ ~ ~ ~0 ~ ~ ~
10~ ~ ~~~
".
~ ~~ ~ ~~ .....
-
Fig 2. Left eye. Goldmann perimetry demonstrates dense centroceal scotomata to V4e (cross-hatched area) and enlarged blind spot to he (diagonal lines).
Fig 1. Right eye. Amsler grid recording chart demonstrates focal scotomata.
as needed to maintain normal coagulation status, her condition became more stabilized over the following 24 hours, and she responded to her name. Over the next two weeks, she slowly began to ambulate with assistance, and her speech was slurred. She complained of partial loss of vision in the left eye. Ophthalmologic examination showed visual acuity of 20/60 in the right eye, 20/100 in the left eye, and extraocular motility and pupillary responses within normal limits. Amsler grid testing identified focal defects in her right eye (Fig 1) although Goldmann perimetry revealed a full field. There was a dense centrocecal scotoma in her left eye (Fig 2). The right macular area had perifoveal whitening with glial remnants on the optic disc (Fig 3). In the left eye, an inferotemporal macular retinal branch arteriolar occlusion by refractile bodies with distal edema involving fixation was present, along with cotton wool spots and superficial nerve fiber hemorrhages involving the superotemporal arcade (Fig 4). Fluorescein angiography delineated the areas of retinal vascular occlusion (Figs 5, 6). The remainder of the examination was normal. With both physical and speech therapy, she continued to progress and was discharged after 28 days of hospitalization. Over the ensuing five months, her ability to ambulate and articulate steadily improved. On subsequent ophthalmologic examinations at one, three, and five months, her visual acuity improved to 20/30 in the right eye, and 20170 in the left eye, and intraocular pressures remained stable at 18 mmHg in both eyes. In her right eye, the Amsler grid abnormalities decreased. In her left eye, the centrocecal scotoma shown by Goldmann perimetry became less dense (Fig 7) and corresponded to the areas of retinal ischemia (Figs 8, 9).
DISCUSSION Amniotic fluid embolism is a grave complication of pregnancy with death occurring in the majority of cases.
Cardinal signs include respiratory distress, cyanosis, cardiovascular collapse, hemorrhage, and coma. l ,4 Possible mechanisms for the clinical presentation include mechanical obstruction by the particulate matter in the amniotic fluid, anaphylaxis, and disseminated intravascular clotting. l •s Traditionally, definitive diagnosis has relied on postmortem examination of the lungs, where squamous cells, lanugo hair, fat, mucin, and bile have been found. 6 Identification of lanugo hair on cytologic examination of blood obtained through a Swan-Ganz catheter? and detection of squamous cells in maternal sputum8 have allowed definitive antemortem diagnosis in a few cases. Although neither blood nor sputum from this patient were examined for particulate matter, her clinical presentation was typical of AFE. On the basis of a complete clinical evaluation and the clinical course, other conditions in the differential diagnoses, including thrombotic pulmonary embolism, uterine rupture or inversion, eclampsia, aspiration syndrome, hemorrhagic shock, myocardial infarction, congestive heart failure, septicemia, bilateral pneumothorax, and toxic reaction to local anesthetics9 were eliminated. The retinal arteriolar occlusions are consistent with obstruction by particulate material, which presumably represents fetal squamous cells, lanugo hair, or other debris. In addition, the glistening nature of the material would also imply the presence of fat, mucin, or bile. The partial resolution of the visual field defects would suggest that there had been a reestablishment of blood flow or that the particulate material had passed on through the smaller retinal capillary bed into the venous circulation. These ocular findings are not completely unexpected, since these elements have been identified in the microvasculature of other organs, including the lung, kidney, and brain. 10. I I Based on these findings, we conclude that in patients with AFE, particulate matter can reach the ocular vas1635
Fig 3. Top left. right eye. Color fundus photograph. of posterior pole demonstrates parafoveal edema, and glial remnants on optic disc. Fig 4. Top righl. left eye. Color fundus photograph of posterior pole demonstrates macular branch retinal arteriolar occlusion by multiple glistening particles. Note diffuse, superficial retinal edema. Fig S. Second row left. right eye. Intravenous fluorescein angiography in arteriovenous phase demonstrates parafoveal capillary non perfusion, indicated by arrows. Fig 6. Second row righl. left eye. Intravenous fluorescein angiography delineates occluded vessels (arrows). Fig 7. Third row left. left eye. Goldmann perimetry five months postembolism demonstrates residual dense scotoma to V4e (cross-hatched areas). Fig 8. Third row righl. right eye. Color fundus photograph of posterior pole five months post-embolism. Note the absence of the minimal retinal reflex occurring secondary to retinal capillary occlusions. Fig 9. BOllom. left eye. Color fundus photograph of posterior pole five months post-embolism demonstrating residual sheathed arteriole.
CHANG AND HERBERT
•
AMNIOTIC FLUID EMBOLISM
culature and cause occlusion. For this reason, we make the following recommendations:
REFERENCES
1. Careful ophthalmic examination should be performed on any patient suspected of having AFE. Since many patients are comatose, visual disturbances may go undiagnosed unless they are evaluated promptly. Otherwise, vision-threatening, potentially treatable conditions, such as central retinal artery occlusion, may escape detection. Moreover, documentation of less severe ocular insults may not be available for future reference. This aspect of care becomes increasingly important as improved techniques in critical care offer more hope for survival of these patients. 2. In patients with AFE who do not survive, postmortem examination of the ocular structures may provide histologic documentation of the precise nature of the particulate matter identified in our case. Pathologic confirmation of a relationship between ocular and systemic signs of AFE would expand our knowledge of the protean manifestations of this condition.
1. Courtney LD. Amniotic fluid embolism. Obstet Gynecol Surv 1974; 29:169-77. 2. Fischbein FI. Ischemic retinopathy following amniotic fluid embolization. Am J Ophthalmol 1969; 67:351-7. 3. Stromme WB, Fromke VL. Amniotic fluid embolism and disseminated intravascular coagulation after evacuation of missed abortion. Obstet Gynecol 1978; 52(Suppl 1):76S-80S. 4. Morgan M. Amniotic fluid embolism. Anaesthesia 1979; 34:20-32. 5. Phillips LL, Davidson EC Jr. Procoagulant properties of amniotic fluid. Am J Obstet Gynecol 1972; 113:911-9. 6. Lumley J, Owen R, Morgan M. Amniotic fluid embolism; a report of three cases. Anaesthesia 1979; 34:33-6. 7. Botero SO, Holmquist NO. Cytologic diagnosis of amniotic fluid embolus; report of a case. Acta Cytol 1979; 23:465-6. 8. Tuck CS. Anniotic fluid embolus. Proc R Soc Med 1972; 65:94-5. 9. Herbert WNP. Complications of the immediate puerperium. Clin Obstet Gynecol 1982; 25:219-32. 10. Meigs LC. Amniotic fluid embolism; pulmonary histopathologic findings in a rapidly fatal occurrence of amniotic fluid embolism. Am J Obstet Gynecol1971; 111:1069-74. 11. Attwood HD. Amniotic fluid embolism. Pathol Annu 1972; 7:14572.
1637
Following Amniotic
Fluid Embolism
MEIMEI CHANG, MD,* WILLIAM N. P. HERBERT, MDt
Abstract: Amniotic fluid embolism is a serious complication of pregnancy resulting in death in the majority of patients. Particulate matter originating in the amniotic fluid has been identified at autopsy in the lung, kidney, and brain. A patient is presented who survived amniotic fluid embolism and developed bilateral retinal arteriolar occlusions, presumably based on entrapment of particulate matter originating in amniotic fluid. Her clinical course and ophthalmic findings are reviewed, and the relationship between amniotic fluid embolism and retinal vascular occlusion is discussed.[Key words: Amniotic fluid embolism, intrapartum complication, particulate matter, retinal arteriolar occlusions.] Ophthalmology 91: 1634-1637, 1984
Amniotic fluid embolism (AFE) is a serious complication of pregnancy and represents a leading cause of intrapartum and early postpartum maternal death. Entry into maternal blood of sufficient quantities of amniotic fluid containing particulate matter causes sudden cardiopulmonary failure, usually accompanied by marked derangement of the coagulation mechanism. Death follows in 86% of cases. I Ocular manifestations with amniotic fluid embolism have rarely been published. In 1969, Fischbein2 described a patient who developed bilateral ischemic oculopathy following AFE. In 1978, Stromme and Fromke, 3 in reporting a patient who developed AFE following uterine evacuation for missed abortion, noted that she experienced field defects which were felt to be secondary to cerebral embolism. No ophthalmic findings were stated, however. We present a patient with amniotic fluid embolus who developed bilateral retinal arteriolar occlusions, presumably from particulate matter originating in amniotic fluid. The relationship between amniotic fluid embolus and these ocular findings is discussed.
From the Departments of Ophthalmology' and Obstetrics and Gynecology,t University of North Carolina School of Medicine, Chapel Hill. Supported in part by a grant from Research to Prevent Blindness, Inc. Reprint requests to Meimei Chang, MD, 617 Clinical Sciences Bldg. 229H, Chapel Hill, NC 27514.
1634
CASE REPORT A 28-year-old gravida three, para one, abortus one black woman was admitted to her local hospital at 42 weeks gestation for induction of labor. Her prenatal course had been benign except for one brief episode of vaginal bleeding at approximately 20 weeks gestation. The amniotic fluid was clear when the fetal membranes were artificially ruptured, and intravenous oxytocin infusion was begun. Three hours later, the patient suddenly developed shortness of breath and wheezing, followed moments later by loss of consciousness and cardiac arrest. Resuscitation was instituted, including tracheal intubation. Fetal bradycardia was noted and a pelvic examination was performed. The cervix was completely dilated. With the aid of low forceps, the patient delivered a 3000 gm depressed male infant who subsequently died. Immediately after delivery, marked uterine hemorrhage occurred, followed by tachycardia, hypotension, and bleeding from the nasopharynx and intravenous infusion sites. Coagulation studies were abnormal. Over the next two hours, multiple units of whole blood, platelets, cryoprecipitate, and fresh frozen plasma were administered and the bleeding diminished. The patient was transferred to North Carolina Memorial Hospital for further management. On arrival, she was obtunded, normotensive, but tachycardic. She responded to deep pain only. Pupils were equal and responded to light, and there were no lateralizing neurologic signs. Coagulation studies were normal. A computed tomography scan of the head was consistent with cerebral edema without evidence of intracranial hemorrhage. With intensive care and blood component therapy
CHANG AND HERBERT
•
AMNIOTIC FLUID EMBOLISM
~~ ~
~n
~~ ~ ~ ~0 ~ ~ ~
10~ ~ ~~~
".
~ ~~ ~ ~~ .....
-
Fig 2. Left eye. Goldmann perimetry demonstrates dense centroceal scotomata to V4e (cross-hatched area) and enlarged blind spot to he (diagonal lines).
Fig 1. Right eye. Amsler grid recording chart demonstrates focal scotomata.
as needed to maintain normal coagulation status, her condition became more stabilized over the following 24 hours, and she responded to her name. Over the next two weeks, she slowly began to ambulate with assistance, and her speech was slurred. She complained of partial loss of vision in the left eye. Ophthalmologic examination showed visual acuity of 20/60 in the right eye, 20/100 in the left eye, and extraocular motility and pupillary responses within normal limits. Amsler grid testing identified focal defects in her right eye (Fig 1) although Goldmann perimetry revealed a full field. There was a dense centrocecal scotoma in her left eye (Fig 2). The right macular area had perifoveal whitening with glial remnants on the optic disc (Fig 3). In the left eye, an inferotemporal macular retinal branch arteriolar occlusion by refractile bodies with distal edema involving fixation was present, along with cotton wool spots and superficial nerve fiber hemorrhages involving the superotemporal arcade (Fig 4). Fluorescein angiography delineated the areas of retinal vascular occlusion (Figs 5, 6). The remainder of the examination was normal. With both physical and speech therapy, she continued to progress and was discharged after 28 days of hospitalization. Over the ensuing five months, her ability to ambulate and articulate steadily improved. On subsequent ophthalmologic examinations at one, three, and five months, her visual acuity improved to 20/30 in the right eye, and 20170 in the left eye, and intraocular pressures remained stable at 18 mmHg in both eyes. In her right eye, the Amsler grid abnormalities decreased. In her left eye, the centrocecal scotoma shown by Goldmann perimetry became less dense (Fig 7) and corresponded to the areas of retinal ischemia (Figs 8, 9).
DISCUSSION Amniotic fluid embolism is a grave complication of pregnancy with death occurring in the majority of cases.
Cardinal signs include respiratory distress, cyanosis, cardiovascular collapse, hemorrhage, and coma. l ,4 Possible mechanisms for the clinical presentation include mechanical obstruction by the particulate matter in the amniotic fluid, anaphylaxis, and disseminated intravascular clotting. l •s Traditionally, definitive diagnosis has relied on postmortem examination of the lungs, where squamous cells, lanugo hair, fat, mucin, and bile have been found. 6 Identification of lanugo hair on cytologic examination of blood obtained through a Swan-Ganz catheter? and detection of squamous cells in maternal sputum8 have allowed definitive antemortem diagnosis in a few cases. Although neither blood nor sputum from this patient were examined for particulate matter, her clinical presentation was typical of AFE. On the basis of a complete clinical evaluation and the clinical course, other conditions in the differential diagnoses, including thrombotic pulmonary embolism, uterine rupture or inversion, eclampsia, aspiration syndrome, hemorrhagic shock, myocardial infarction, congestive heart failure, septicemia, bilateral pneumothorax, and toxic reaction to local anesthetics9 were eliminated. The retinal arteriolar occlusions are consistent with obstruction by particulate material, which presumably represents fetal squamous cells, lanugo hair, or other debris. In addition, the glistening nature of the material would also imply the presence of fat, mucin, or bile. The partial resolution of the visual field defects would suggest that there had been a reestablishment of blood flow or that the particulate material had passed on through the smaller retinal capillary bed into the venous circulation. These ocular findings are not completely unexpected, since these elements have been identified in the microvasculature of other organs, including the lung, kidney, and brain. 10. I I Based on these findings, we conclude that in patients with AFE, particulate matter can reach the ocular vas1635
Fig 3. Top left. right eye. Color fundus photograph. of posterior pole demonstrates parafoveal edema, and glial remnants on optic disc. Fig 4. Top righl. left eye. Color fundus photograph of posterior pole demonstrates macular branch retinal arteriolar occlusion by multiple glistening particles. Note diffuse, superficial retinal edema. Fig S. Second row left. right eye. Intravenous fluorescein angiography in arteriovenous phase demonstrates parafoveal capillary non perfusion, indicated by arrows. Fig 6. Second row righl. left eye. Intravenous fluorescein angiography delineates occluded vessels (arrows). Fig 7. Third row left. left eye. Goldmann perimetry five months postembolism demonstrates residual dense scotoma to V4e (cross-hatched areas). Fig 8. Third row righl. right eye. Color fundus photograph of posterior pole five months post-embolism. Note the absence of the minimal retinal reflex occurring secondary to retinal capillary occlusions. Fig 9. BOllom. left eye. Color fundus photograph of posterior pole five months post-embolism demonstrating residual sheathed arteriole.
CHANG AND HERBERT
•
AMNIOTIC FLUID EMBOLISM
culature and cause occlusion. For this reason, we make the following recommendations:
REFERENCES
1. Careful ophthalmic examination should be performed on any patient suspected of having AFE. Since many patients are comatose, visual disturbances may go undiagnosed unless they are evaluated promptly. Otherwise, vision-threatening, potentially treatable conditions, such as central retinal artery occlusion, may escape detection. Moreover, documentation of less severe ocular insults may not be available for future reference. This aspect of care becomes increasingly important as improved techniques in critical care offer more hope for survival of these patients. 2. In patients with AFE who do not survive, postmortem examination of the ocular structures may provide histologic documentation of the precise nature of the particulate matter identified in our case. Pathologic confirmation of a relationship between ocular and systemic signs of AFE would expand our knowledge of the protean manifestations of this condition.
1. Courtney LD. Amniotic fluid embolism. Obstet Gynecol Surv 1974; 29:169-77. 2. Fischbein FI. Ischemic retinopathy following amniotic fluid embolization. Am J Ophthalmol 1969; 67:351-7. 3. Stromme WB, Fromke VL. Amniotic fluid embolism and disseminated intravascular coagulation after evacuation of missed abortion. Obstet Gynecol 1978; 52(Suppl 1):76S-80S. 4. Morgan M. Amniotic fluid embolism. Anaesthesia 1979; 34:20-32. 5. Phillips LL, Davidson EC Jr. Procoagulant properties of amniotic fluid. Am J Obstet Gynecol 1972; 113:911-9. 6. Lumley J, Owen R, Morgan M. Amniotic fluid embolism; a report of three cases. Anaesthesia 1979; 34:33-6. 7. Botero SO, Holmquist NO. Cytologic diagnosis of amniotic fluid embolus; report of a case. Acta Cytol 1979; 23:465-6. 8. Tuck CS. Anniotic fluid embolus. Proc R Soc Med 1972; 65:94-5. 9. Herbert WNP. Complications of the immediate puerperium. Clin Obstet Gynecol 1982; 25:219-32. 10. Meigs LC. Amniotic fluid embolism; pulmonary histopathologic findings in a rapidly fatal occurrence of amniotic fluid embolism. Am J Obstet Gynecol1971; 111:1069-74. 11. Attwood HD. Amniotic fluid embolism. Pathol Annu 1972; 7:14572.
1637