Peyser and Kupferminc
with severe postpartum hemorrhage was derived from the well-established experience of induction of labor by extraamniotic prostaglandin F.a or E2 instillation. The continuous irrigation of the uterine cavity with small amounts of PGE 2 comparable to the physiologic levels at delivery apparently causes an immediate and uninterrupted tetanic contraction of the uterine musculature manifesting hemostasis. This method of drug administration is more effective than other routes that require absorption or delivery of the drug to the uterus from a distant site. Moreover, the minute dosage and bypassing of the systemic circulation avoids potentially complicating side effects. The direct application of prostaglandin to the placental site is a particularly efficient means to achieve myometrial tetany with occlusion of the afferent lacuna site arteries. The efficacy is apparent in cases with underlying chorioamnionitis or as a result of subinvolution of the placental site with late hemorrhage sequela. In conclusion, the continuous irrigation of the uterine cavity with a low concentration of PGE. presents a rapid and effective treatment of severe and uncontrollable atonic postpartum hemorrhage. The quick uterine hemostasis is gained regardless of the patient'S hemodynamic condition, thus allowing its prompt correction. This treatment does not cause any side effects. The achievement of an instantaneous hemostatic effect
March 1990
Am J Obstet Gynecol
in the case of subinvolution of the placental site with an uncontrollable hemorrhage bears a novel therapeutic means in the management of this entity; until now most cases required operation. REFERENCES I. Pritchard jA, MacDonald PC, Gant NF. Williams' obstetrics. Norwalk, Conn.: Appleton-Century-Crofts, 1985:707. 2. Hayashi RH, Castillo MS, Noah ML. Management of severe pospartum hemorrhage due to uterine atony using an analogue of prostaglandin Foa. Obstet Gynecol 1982;58: 426-9. 3. Sellers SM, Hodgson HT, Mitchel MD, et al. Raised prostaglandin levels in the third stage of labor. AM j OBSTET GVNECOL 1982;144:209-12. 4. Takagi S, Yoshida T. Togo Y, et al. The effect of intramyometrial injection of prostaglandin F'a on severe post partum hemorrhage. Prostaglandins 1976;12:565-79. 5. Henson G, Gough jD, Gillmer MDG. Control of persistent primary postpartum haemorrhage due to uterine atony with intravenous prostaglandin E •. Br j Obstet Gynaecol 1983;90:280-2. 6. Corson SL, Bolognese RL. Postpartum uterine atony treated with prostaglandin. AM j OBSTET GVNECOL 1977; 129:918-9. 7. Toppozada M, El-Bossaty M, El-Rahman HA, et al. Control of intractable atonic postpartum hemorrhage by 15-methyl prostaglandin F 2,. Obstet Gynecol 1981;58:327-30. 8. Hayashi RH, Castillo MS, Noah ML. Management of severe postpartum hemorrhage with prostaglandin FOa analogue. Obstet Gynecol 1984;63:806-8. 9. Hertz RH, Sokol Rj, Dierker LJ. Treatment of post partum uterine atony with prostaglandin E2 vaginal suppositories. Obstet Gynecol 1980;56: 129-30.
Postpartum pUlmonary embolus as an unusual cause of cortical blindness RobertJ. Stiller, MD, Sylvie Leone-Tomaschoff, MD,Joseph Cuteri, MD, and Lawrence Beck, MD Bridgeport, Connecticut A pregnant patient was delivered by cesarean section with blindness occurring in the postoperative period. Diagnostic evaluation revealed the presence of massive pulmonary embolus associated with cardiogenic shock. The differential diagnosis of blindness during pregnancy is discussed. (AM J OBSTET GVNECOL
1990;162:696-7.)
Key words: Pulmonary embolus, cortical blindness
From the Departments of Obstetrics and Gynecology and Neurology, Bridgeport Hospztal. Receivedfor publzcation September 7,1989; accepted September 13, 1989. Repnnt requests: Robert J. Stiller, MD, Director, Maternal-Fetal Medzczne, Department of Obstetncs and Gynecology, Bridgeport Hospztal, 267 Grant St., Bridgeport, CT 06610. 6/1/16660
696
Cortical blindness has been occasionally reported in obstetric complications such as severe preeclampsia and cerebral vein thrombosis. To the best of our knowledge, this disorder has not been reported to be associated with pulmonary embolus in the pregnant patient. We report a case in which cortical blindness was a major
Postpartum blindness
Volume 162 Number 3
sign in a postpartum patient found to have a pulmonary embolus. A discussion of the pathogenesis of cortical blindness in the pregnant patient is presented. Case report A 22-year-old, Hispanic woman, gravida 2, para 0, was admitted for induction of labor after spontaneous rupture of membranes. She underwent a primary cesarean section while under epidural anesthesia after a failed induction of labor. Her immediate postoperative course was uneventful. On the second postoperative day, the patient was found unconscious in her room. The patient regained consciousness and complained of severe back and occipital pain. She then also complained that she could not see. On physical examination she appeared cyanotic and anxious (heart rate, 130 beats/min; blood pressure, 70 mm Hg/palpable; respirations, 30/min). On neurologic examination, the pupils were equal and sluggishly reactive to light. There was no perception of light or movement. There was no evidence of paresis and no abnormal reflexes. The remainder of the physical examination appeared normal. The lungs were clear, and the heart had a regular rate and rhythm without audible murmurs. The abd~}Tlen was soft and no vaginal bleeding was noted. Extremities were not edematous and reflexes were normal. Oxygen was given by mask and initial arterial blood gas evaluation showed pH 7.39, Pco 2 30 mm Hg, Po, 200 mm Hg, and oxygen saturation 99%. Electrocardiogram showed sinus tachycardia and right axis deviation. A diagnosis of pulmonary embolus was considered, and ventilation-perfusion study revealed normal ventilation with multiple segmental perfusion defects in both lung fields unmatched by ventilatory or chest x-ray findings. Head computerized tomographic scan was reported as normal. Approximately 90 minutes after the initial event, the patient noted that her sight had returned. A diagnosis of massive pulmonary embolus was made and the patient was begun on a regimen of intravenous heparin. Pulmonary artery catheter inserted before heparinization revealed findings consistent with cardiogenic shock with a cardiac output of 2.6 Umin. Pulmonary artery pressure was elevated (41120 mm Hg) with a normal pulmonary artery wedge pressure (9 mm Hg). Subsequently, the patient improved and was discharged on the fifteenth hospital day to continue with oral anticoagulants for 3 months.
697
Comment
The reported causes of blindness during pregnancy include vasospasm or occlusion of the optic arteries, retinal edema and/or detachment, and cortical blindness. The diagnm;is of cortical blindness is characterized by blindness in patients with normal responses to light and normal ophthalmoscopic findings. l It is hypothesized that occipital poles of the cerebral cortex are more sensitive to generalized hypoxia because of their more distant location from the middle and posterior cerebral arteries. If hypoxia is severe or prolonged, there may be irreversible damage to the cortex and vision may not return. In less profound cases, full or partial recovery may occur. Although hypoxia is generally considered to be the most common etiologic factor in the development of cortical blindness, other diverse causes include trauma, meningitis, carbon monoxide, poisoning, neoplasm, embolism, and migraine. Cortical blindness during pregnancy usually has been associated with either severe preeclampsia or cerebral venous thrombosis." While the presenting signs of severe preeclampsia are well known to obstetricians, the diagnosis of cerebral vein thrombosis is usually characterized by headaches, convulsions, and focal neurologic signs. We hypothesize that the cardiogenic shock associated with massive pulmonary embolus in our patient did not permit adequate perfusion of the occipital poles, leading to transient cortical blindness. Therefore in the absence of signs of preeclampsia or cerebral venous thrombosis the possibility of cardiogenic shock that is secondary to pulmonary embolus should be considered in the evaluation of the pregnant or postoperative woman with cortical blindness. REFERENCES 1. Drymalski WG. Cortical blindness. The changing inCIdence and shifting etiology. Postgrad Med 1980;67:149-56. 2. Levavi H, Neri A, ZoldanJ. et al. pre-eclampsia, "HELLP" syndrome and postictal cortical blindness. Acta Obstet Gynecol Scand 1987;66:91-2.
with severe postpartum hemorrhage was derived from the well-established experience of induction of labor by extraamniotic prostaglandin F.a or E2 instillation. The continuous irrigation of the uterine cavity with small amounts of PGE 2 comparable to the physiologic levels at delivery apparently causes an immediate and uninterrupted tetanic contraction of the uterine musculature manifesting hemostasis. This method of drug administration is more effective than other routes that require absorption or delivery of the drug to the uterus from a distant site. Moreover, the minute dosage and bypassing of the systemic circulation avoids potentially complicating side effects. The direct application of prostaglandin to the placental site is a particularly efficient means to achieve myometrial tetany with occlusion of the afferent lacuna site arteries. The efficacy is apparent in cases with underlying chorioamnionitis or as a result of subinvolution of the placental site with late hemorrhage sequela. In conclusion, the continuous irrigation of the uterine cavity with a low concentration of PGE. presents a rapid and effective treatment of severe and uncontrollable atonic postpartum hemorrhage. The quick uterine hemostasis is gained regardless of the patient'S hemodynamic condition, thus allowing its prompt correction. This treatment does not cause any side effects. The achievement of an instantaneous hemostatic effect
March 1990
Am J Obstet Gynecol
in the case of subinvolution of the placental site with an uncontrollable hemorrhage bears a novel therapeutic means in the management of this entity; until now most cases required operation. REFERENCES I. Pritchard jA, MacDonald PC, Gant NF. Williams' obstetrics. Norwalk, Conn.: Appleton-Century-Crofts, 1985:707. 2. Hayashi RH, Castillo MS, Noah ML. Management of severe pospartum hemorrhage due to uterine atony using an analogue of prostaglandin Foa. Obstet Gynecol 1982;58: 426-9. 3. Sellers SM, Hodgson HT, Mitchel MD, et al. Raised prostaglandin levels in the third stage of labor. AM j OBSTET GVNECOL 1982;144:209-12. 4. Takagi S, Yoshida T. Togo Y, et al. The effect of intramyometrial injection of prostaglandin F'a on severe post partum hemorrhage. Prostaglandins 1976;12:565-79. 5. Henson G, Gough jD, Gillmer MDG. Control of persistent primary postpartum haemorrhage due to uterine atony with intravenous prostaglandin E •. Br j Obstet Gynaecol 1983;90:280-2. 6. Corson SL, Bolognese RL. Postpartum uterine atony treated with prostaglandin. AM j OBSTET GVNECOL 1977; 129:918-9. 7. Toppozada M, El-Bossaty M, El-Rahman HA, et al. Control of intractable atonic postpartum hemorrhage by 15-methyl prostaglandin F 2,. Obstet Gynecol 1981;58:327-30. 8. Hayashi RH, Castillo MS, Noah ML. Management of severe postpartum hemorrhage with prostaglandin FOa analogue. Obstet Gynecol 1984;63:806-8. 9. Hertz RH, Sokol Rj, Dierker LJ. Treatment of post partum uterine atony with prostaglandin E2 vaginal suppositories. Obstet Gynecol 1980;56: 129-30.
Postpartum pUlmonary embolus as an unusual cause of cortical blindness RobertJ. Stiller, MD, Sylvie Leone-Tomaschoff, MD,Joseph Cuteri, MD, and Lawrence Beck, MD Bridgeport, Connecticut A pregnant patient was delivered by cesarean section with blindness occurring in the postoperative period. Diagnostic evaluation revealed the presence of massive pulmonary embolus associated with cardiogenic shock. The differential diagnosis of blindness during pregnancy is discussed. (AM J OBSTET GVNECOL
1990;162:696-7.)
Key words: Pulmonary embolus, cortical blindness
From the Departments of Obstetrics and Gynecology and Neurology, Bridgeport Hospztal. Receivedfor publzcation September 7,1989; accepted September 13, 1989. Repnnt requests: Robert J. Stiller, MD, Director, Maternal-Fetal Medzczne, Department of Obstetncs and Gynecology, Bridgeport Hospztal, 267 Grant St., Bridgeport, CT 06610. 6/1/16660
696
Cortical blindness has been occasionally reported in obstetric complications such as severe preeclampsia and cerebral vein thrombosis. To the best of our knowledge, this disorder has not been reported to be associated with pulmonary embolus in the pregnant patient. We report a case in which cortical blindness was a major
Postpartum blindness
Volume 162 Number 3
sign in a postpartum patient found to have a pulmonary embolus. A discussion of the pathogenesis of cortical blindness in the pregnant patient is presented. Case report A 22-year-old, Hispanic woman, gravida 2, para 0, was admitted for induction of labor after spontaneous rupture of membranes. She underwent a primary cesarean section while under epidural anesthesia after a failed induction of labor. Her immediate postoperative course was uneventful. On the second postoperative day, the patient was found unconscious in her room. The patient regained consciousness and complained of severe back and occipital pain. She then also complained that she could not see. On physical examination she appeared cyanotic and anxious (heart rate, 130 beats/min; blood pressure, 70 mm Hg/palpable; respirations, 30/min). On neurologic examination, the pupils were equal and sluggishly reactive to light. There was no perception of light or movement. There was no evidence of paresis and no abnormal reflexes. The remainder of the physical examination appeared normal. The lungs were clear, and the heart had a regular rate and rhythm without audible murmurs. The abd~}Tlen was soft and no vaginal bleeding was noted. Extremities were not edematous and reflexes were normal. Oxygen was given by mask and initial arterial blood gas evaluation showed pH 7.39, Pco 2 30 mm Hg, Po, 200 mm Hg, and oxygen saturation 99%. Electrocardiogram showed sinus tachycardia and right axis deviation. A diagnosis of pulmonary embolus was considered, and ventilation-perfusion study revealed normal ventilation with multiple segmental perfusion defects in both lung fields unmatched by ventilatory or chest x-ray findings. Head computerized tomographic scan was reported as normal. Approximately 90 minutes after the initial event, the patient noted that her sight had returned. A diagnosis of massive pulmonary embolus was made and the patient was begun on a regimen of intravenous heparin. Pulmonary artery catheter inserted before heparinization revealed findings consistent with cardiogenic shock with a cardiac output of 2.6 Umin. Pulmonary artery pressure was elevated (41120 mm Hg) with a normal pulmonary artery wedge pressure (9 mm Hg). Subsequently, the patient improved and was discharged on the fifteenth hospital day to continue with oral anticoagulants for 3 months.
697
Comment
The reported causes of blindness during pregnancy include vasospasm or occlusion of the optic arteries, retinal edema and/or detachment, and cortical blindness. The diagnm;is of cortical blindness is characterized by blindness in patients with normal responses to light and normal ophthalmoscopic findings. l It is hypothesized that occipital poles of the cerebral cortex are more sensitive to generalized hypoxia because of their more distant location from the middle and posterior cerebral arteries. If hypoxia is severe or prolonged, there may be irreversible damage to the cortex and vision may not return. In less profound cases, full or partial recovery may occur. Although hypoxia is generally considered to be the most common etiologic factor in the development of cortical blindness, other diverse causes include trauma, meningitis, carbon monoxide, poisoning, neoplasm, embolism, and migraine. Cortical blindness during pregnancy usually has been associated with either severe preeclampsia or cerebral venous thrombosis." While the presenting signs of severe preeclampsia are well known to obstetricians, the diagnosis of cerebral vein thrombosis is usually characterized by headaches, convulsions, and focal neurologic signs. We hypothesize that the cardiogenic shock associated with massive pulmonary embolus in our patient did not permit adequate perfusion of the occipital poles, leading to transient cortical blindness. Therefore in the absence of signs of preeclampsia or cerebral venous thrombosis the possibility of cardiogenic shock that is secondary to pulmonary embolus should be considered in the evaluation of the pregnant or postoperative woman with cortical blindness. REFERENCES 1. Drymalski WG. Cortical blindness. The changing inCIdence and shifting etiology. Postgrad Med 1980;67:149-56. 2. Levavi H, Neri A, ZoldanJ. et al. pre-eclampsia, "HELLP" syndrome and postictal cortical blindness. Acta Obstet Gynecol Scand 1987;66:91-2.
