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Anesthesia: Essays and Researches
Case Report
Amniotic fluid embolism: A diagnostic dilemma Ashish Kulshrestha, Megha Mathur1 Department of Anaesthesia and Intensive Care GianSagar Medical College and Hospital, Ram Nagar, Banur, Patiala, Punjab, 1Department of Obstetrics and Gynecology, Govt. Medical College and Hospital, Chandigarh, India Corresponding author: Dr. Ashish Kulshrestha, H.No.401/GH-18, Sector-5, Mansa Devi Complex, Panchkula, Haryana, India. E-mail: [email protected]
Abstract Amniotic fluid embolism (AFE) is a rare obstetric catastrophe with an incidence of 7.7 per 100 000 deliveries and mortality as high as 60% to 80%. We describe a case of perioperative cardiac arrest in a young parturient undergoing an emergent cesarean section. Just after delivery of live healthy male baby, patient developed disseminated intravascular coagulation not responding to resuscitation with fluids and blood products. Her autopsy revealed edematous lungs with amniotic fluid debris within pulmonary vessels thus establishing the diagnosis of AFE. Amniotic fluid embolism is life threatening and difficult to predict or prevent condition, which should be always be kept in mind in a parturient with sudden cardiovascular collapse, so that resuscitation commences immediately, as early intervention is essential for a positive outcome. Key words: Amniotic fluid embolism, asystole, cesarean section, disseminated intravascular coagulation, fibrin-degradation products
INTRODUCTION Amniotic fluid embolism (AFE) is a rare catastrophe with an estimated frequency of approximately 7.7 per 100 000 deliveries.[1] This condition was originally described in 1941 by Steiner and Luschbaugh with evidence of fetal debris in pulmonary circulation in pregnant women.[2] Recently, a more descriptive term was suggested as “the anaphylactoid syndrome of pregnancy.”[3,4] This is a rare but important cause of peripartum death in the United States making up for 10% of all maternal deaths with an overall mortality rate as high as 60% to 80%.[1] More than 50% of patients die within first hour and about two-third Access this article online Website
DOI
www.aeronline.org
10.4103/0259-1162.94789
Quick Response Code
within 5 hour of the event with high incidence of severe and permanent neurological damage among survivors. We report a parturient who had cardiac arrest during emergency cesarean section culminating in disseminated intravascular coagulation (DIC).
Case report A 37-years old third gravida female presented with history of leaking per vaginum since 1 day and was admitted for further observation and management. She had regular antenatal checkups in the institution with no history of raised blood pressure anytime in the antenatal period and had uneventful previous two normal deliveries. She denied associated co-morbid illnesses or any allergies. Her obstetrical examination revealed a gestation period of 37 weeks and 3 days with vertex presentation and premature rupture of membranes. The patient was hospitalized and fetal monitoring established. She started having true labor pains 3h after admission along with the development of tachypnea and audible wheeze for which she was given 227
Anesthesia: Essays and Researches; 5(2); Jul-Dec 2011
supplemental oxygen through the face mask and was started on bronchodilator nebulizations. She showed improvement in her clinical condition with the treatment instituted. Her initial laboratory parameters showed Hb of 10.8 g/dL, platelet count of 109 000 cells/mm3, total leukocyte count of 9500 cells/mm3, normal coagulation parameters, liver function tests (including enzymes) were also within normal limits and her arterial blood gas on face mask oxygen at 5 l/min showed pH 7.37; pO2 92 mmHg; pCO2 31 mmHg; HCO3- 21.5 mmol/L; BE/BD−0.5; SaO2 96%.The cardiotocography showed a persistent fetal bradycardia indicating fetal distress and so a decision to proceed to emergency cesarean section was made by the obstetrician. After discussion with patient’s relatives about the implications of her worsening clinical condition, spinal anesthesia was planned. A quick but thorough pre anesthetic evaluation revealed an obese parturient with a weight of 85 kg and height of 140 cm with short neck but adequate mouth opening and modified Mallampati class of III. She was afebrile, comfortable in supine position and had occasional rhonchi on auscultation of chest. After transferring her to the operating room, she was preloaded with 500 mL of lactated ringer’s solution and monitoring included a five lead electrocardiogram, noninvasive blood pressure and pulse oximetry. The baseline recordings showed heart rate of 100 beats/min, blood pressure of 110/80 mmHg and spO2 of 94% on room air. Lumbar puncture was performed at L3–L4 interspace in sitting position in anticipation of technical difficulty and urgency of surgery and 2.4 mL of hyperbaric 0.5% bupivacaine was injected intrathecally and was immediately placed in the supine position with a wedge placed beneath her right buttock. A sensory level of T6 bilaterally (loss of sensation to pin prick) was achieved before starting the surgery and supplemental oxygen was given through face mask at 5 L/minute. The blood pressure showed a reading of 94/58 mmHg with a heart rate of 102 beats/min and spO2 of 97%. The sensory level of T6 was again confirmed before skin incision and a live 2.8 kg male baby was delivered with APGAR scores of 4 and 8 at 1 and 5 min, respectively. Just after delivery of baby and even before starting on oxytocin infusion, her blood pressure suddenly dropped to 60/40 mmHg with severe bradycardia (HR< 40 beats/min) culminating in asystole. Immediate tracheal intubation was performed and positive pressure ventilation was started with 100% oxygen and cardiopulmonary resuscitation with chest compressions at 100 compressions/min was commenced. Epinephrine 1 mg was given by intravenous push and was repeated twice (total 3 mg). The heart rate restored to 150 beats/min with the blood pressure of 60/30 mmHg with the total duration of cardiac arrest being less than a minute. The surgeons noticed abnormally increased oozing from the uterine incision site and suspected defective coagulation and closed uterus and abdomen after placing packs and abdominal drain. Immediately a 228
Kulshrestha and Mathur: Amniotic fluid embolism
bedside clotting test was performed using a capillary tube with blood from pin prick, which showed an abnormally increased clotting time. Resuscitation was continued with colloids (1000 mL) and inotropic support was started with infusions ofdopamine at 15 µg/kg/min and nor epinephrine at 0.1 µg/kg/min as blood pressure was not responding to intravenous fluids. A total of 1500 mL of crystalloids, 1000 mL colloid (hydroxyethyl starch), 2 units of packed red blood cells and 4 units of fresh frozen plasma were transfused in the operating room in anticipation of abnormal coagulation parameters and the blood loss was estimated at 1200 mL approximately. Arterial blood gas analyzed intraoperatively showed pH 7.05; pO2 363 mmHg; pCO2 37 mmHg; HCO -3 10 mmol; BE/BD −20; SaO2 100% on 100% oxygen suggesting severe metabolic acidosis which was corrected with 100 meq of soda bicarbonate infusion. She was quickly transferred to ICU for further management and monitoring. For hemodynamic monitoring and fluid status, a central venous line was placed in the right internal jugular vein and an arterial cannula was placed in the right radial artery that showed initial readings of 20 mmHg and a blood pressure of 80/42 mmHg, respectively. Mechanical ventilation was continued with the controlled mode of ventilation with 100% oxygen and an abnormal soakage of the dressing with collection of significant amount of blood in the abdominal drain was noticed. She remained hypotensive in the ICU inspite of inotropic supports with dopamine, nor epinephrine and epinephrine infusions. Her laboratory values showed Hb of 6 gm/dL, platelet count of 21 000 cells/mm3, prothrombin time of 14 s, activated partial thromboplastin time of 45.4 s with elevated D-dimer and fibrin degradation products thus raising suspicion of disseminated intravascular coagulation. A total of five units of packed red blood cells, 15 units of fresh frozen plasma and 10 units of platelet rich plasma were transfused. A repeat arterial blood gas analysis showed pH 7.20; pO2 162 mmHg; pCO2 29.5 mmHg; HCO3-16.2 mmol/L; BE/BD-12; SaO2 99%. Uterine artery embolization under radiological guidance was planned after discussing with the attending radiologist but the patient could not be transported to the x-ray department due to the hemodynamic instability. The resuscitation attempts were unsuccessful and the patient died 10h postoperatively. Autopsy was performed after taking consent from the patient’s relatives, which showed edema of lungs with debris in pulmonary vessels that on further microscopic examination showed fetal squamous epithelial cells, thus the diagnosis of AFE was considered most likely.
Discussion The various differential diagnoses in our patient with sudden cardiovascular collapse during an emergent cesarean section could have been
Anesthesia: Essays and Researches; 5(2); Jul-Dec 2011
• Total spinal coinciding with administration of oxytocics. • Drug anaphylaxis. • Venous air embolism. • Subclinical sepsis (chorioamnionitis) with Acute lung injury going in for systemic inflammatory response syndrome exaggerated with peak spinal effect. • Amniotic fluid embolism. Our patient developed cardiovascular collapse during cesarean section and also had few premonitory symptoms like tachypnea, audible wheeze and fetal bradycardia that could have pointed towards the possibility of AFE, but were not considered due to rarity of this condition and moreover the urgency of surgery was given more priority. Total spinal coinciding with administration of oxytocin was unlikely as the event occurred almost 15–20 min after intrathecal injection and also the sensory level was stable at T6 (checked twice) with stable hemodynamics and the oxytocics were not transfused till the episode occurred. Drug induced anaphylaxis was also unlikely as no antibiotic was given before the episode and local anesthetic was given intrathecally after ruling out any intravascular placement. Venous air embolism can occur in cesarean section under general anesthesia[5] and has also been reported with both epidural[6] and spinal anesthesia.[7] This diagnosis was also less likely as no air was detected in intravenous line and also at autopsy no evidence of air was found in pulmonary vessels. Subclinical sepsis due to chorioamnionitis usually has a history of premature rupture of membranes of longer duration and moreover patient had no fever preoperatively with a normal total leukocyte count and a normal arterial blood gas, so this possibility was also considered less likely. Our patient developed cardiovascular collapse during cesarean section and also had few symptoms preoperatively such as tachypnea, audible wheeze and fetal bradycardia that could have pointed toward the possibility of amniotic fluid embolism. The presence of hypoxia, cardiovascular collapse, high central venous pressure and severe metabolic acidosis in blood gas analysis pointed toward the diagnosis of pulmonary embolism and in our case as patient was pregnant and since venous air embolism was unlikely, possibility of AFE was considered as the likely diagnosis retrospectively. Transesophageal echocardiography can help in the diagnosis of AFE showing acute right ventricular strain with under filling of left ventricle but we were not able to perform it as bedside availability was not there and also the patient could not be shifted for same.[8,9] Amniotic fluid embolism, a rare obstetrical catastrophe, can present with constellation of signs and symptoms such as respiratory distress (57%), sudden hypotension (37%), coagulopathy (13%), and seizures (10%). More atypical presentations include abdominal pain, chest pain, and arrhythmias.[10] Most cases occur during
Kulshrestha and Mathur: Amniotic fluid embolism
labor (70%), during cesarean section (19%), or following vaginal delivery (11%). It has also been reported during early pregnancy, during second trimester abortions, amniocentesis or following abdominal injury.[11] The most recent CEMACH report shows an increase in number of deaths due to AFE (9 in 1985–1987 to 17 in 2003– 2005).[12] Although the pathophysiology of AFE is poorly understood, a biphasic response to amniotic fluid emboli has been suggested.[13,14] An initial transient phase, due to a reaction to vasoactive substances in amniotic fluid primarily arachidonic acid metabolites, causes intense pulmonary vasospasm, pulmonary hypertension and hypoxia leading to cardiovascular collapse. This stage usually lasts for 30 min and is responsible for about 50% of the mortality due to AFE within the first hour. The second phase then comprise of left ventricular failure, DIC and acute respiratory distress syndrome. Both the phases were probably present in our patient but due to rapid development of events, these were difficult to differentiate.[15] The definitive diagnosis is mostly histological on autopsy with demonstration of squamous cells, mucin and other fetal debris in pulmonary microvasculature of deceased women; however, fetal squamous cells have been found in the blood of laboring women aspirated from pulmonary artery due to other reasons also, thus reducing the diagnosing accuracy of this test.[16,17] The management of AFE comprises of prompt cardiopulmonary resuscitation without delay to achieve higher survival rate.[18] It is based on attempts at (a) maintaining maternal oxygenation, (b) optimizing the hemodynamic status, and (c) correcting the coagulopathy.[19] Newer modalities of management include selective pulmonary vasodilators in the setting of acute pulmonary hypertension seen in amniotic embolism.[20] If AFE is suspected at an early stage, measures that should be undertaken to prevent further cardiovascular collapse include maintaining maternal oxygenation by oxygen supplementation, prompt inotropic support if the hypotension persists and preparation of blood and blood products in anticipation of development of DIC. In the scenario of cardiovascular collapse due to suspected amniotic fluid embolism, successful use of hemodialysis with plasmapheresis and extracorporeal membrane oxygenation with intraaortic balloon counter pulsations have also been described in the literature.[21,22] In conclusion, AFE is a life threatening and difficult to predict or prevent condition that should be kept in mind in a parturient especially having risk factors such as known history of atopy or anaphylaxis, advanced gestational age at termination of pregnancy, rupture of membranes, or meconium staining of amniotic fluid.[23] The main aim to report this case is to stress on the difficulty in predicting and preventing this rare but fatal complication of pregnancy especially in centers with 229
Anesthesia: Essays and Researches; 5(2); Jul-Dec 2011
Kulshrestha and Mathur: Amniotic fluid embolism
limited resources where an algorithm for suspicion can be really helpful, as immediate resuscitation is essential for a positive outcome. It also stresses the importance of intensive care backup facilities for such cases.
REFERENCES 1.
Abenhaim HA, Azoulay L, Kramer MS, Ledue L. Incidence and risk factors of amniotic fluid embolisms: A population- based study on 3 million births in United States. Am J Obstet Gynecol 2008;199:49.el-8. 2. Steiner PE, Luschbaugh CC. Maternal Pulmonary Embolism by amniotic fluid as a cause of obstetric shock and unexpected deaths in obstetrics. JAMA 1941;117:1341-5. 3. Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF. Amniotic fluid embolism: analysis of the national registry. In: Transactions of the Thirteenth Annual Meeting of the American Gynecological and Obstetrical Society. Am J Obstet Gynecol 1995;172:1158-69. 4. Visconi CM, Clark SL. Amniotic fluid embolism. In: Norris MC, editor. Obstetric Anaesthesia 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 1999. p. 579-91. 5. Lew TW, Tay DH, Thomas E. Venous air embolism during Cesarean section more common than previously thought. Anesth Analg 1993;77:448-52. 6. Fong J, Gadalla F, Gimbel AA. Precordial Doppler diagnosis of haemodynamically compromising air embolism during caesarean section. Can J Anaesth 1990;37:262-4. 7. Nims M, Hallonquist H, Camann W. Coronary arterial air embolism occurring during cesarean delivery. Int J Obstet Anesth 2006;15:166-9. 8. James CF, Feinglass NG, Menke DM, Grinton SF, Papadimos TJ. Massive amniotic fluid embolism: Diagnosis aided by emergency transesophageal echocardiography. Int J Obstet Anesth 2004;13:279-83. 9. McDonnell NJ, Chan BO, Frengley RW. Rapid reversal of critical haemodynamic compromise with nitric oxide in a parturient with amniotic fluid embolism. Int JObstet Anesth 2007;16:269-73. 10. Visconi CM, Clark SL. Amniotic fluid embolism. In: Norris MC, editor. Obstetric Anaesthesia 2nd ed. Philadelphia: Lippincott Williams and Wilkins;
1999. p. 579-91. 11. Dedhia JD, Mushambi MC. Amniotic fluid embolism. Br J Anaesth 2007;7:152-6 12. Confidential Enquiry into Maternal and Child Health (CEMACH). Saving mother’s lives 2003-2005 Report: A Report of UK confidential enquiries into maternal deaths. London: RCOG Press; 2007. 13. Clark SL, Montz FJ, Phelan JP. Hemodynamic alterations associated with amniotic fluid embolism: A reappraisal. Am J Obstet Gynecol 1985;151:617-21. 14. Clark SL. Amniotic fluid embolism. Crit Care Clin 1991;7:877-82. 15. Howes LJ. Anaphylactoid reaction possibly caused by amniotic fluid embolism. Intl J Obstet Anesth 1995;4:51-4. 16. Aguilera LG, Fermandez D, Plaza A, Gracia J, Gomar C. Fatal amniotic fluid embolism diagnosed histologically. Acta Anaesthesiol Scand 2002;46:334-7. 17. Plauche WC. Amniotic fluid embolism. Am J Obstet Gynecol 1983;147:982. 18. Aziz ES. A successfully resuscitated case of amniotic fluid embolism. Eur J Anaesthesiol 2000;17:712-3. 19. Rodgers L, Dangel-Palmer MO, Berner N. Acute circulatory and respiratory collapse in obstetrical patients: A case report and review of literature. AANA J 2000;68:444-50. 20. Conde-Agudelo A, Romero R. Amniotic fluid embolism: An evidence- based review. Am J Obstet Gynecol 2010;202:92. 21. Kaneko Y, Ogihara T, Tajima H, Mochimaru F. Continuous hemodiafiltration for disseminated intravascular coagulation and shock due to amniotic fluid embolism: report of a dramatic response. Intern Med 2001;40:945-7. 22. Hsieh YY, Chang CC, Li PC, Tsai HD, Tsai CH. Successful application of extracorporeal membrane oxygenation and intra-aortic balloon counterpulsation as lifesaving therapy for a patient with amniotic fluid embolism. Am J Obstet Gynecol 2000;183:496-7. 23. Edwards GJ, Davies NJ. Amniotic fluid embolism following feticide- a cautionary tale. J Obstet Gynaecol 2000;20:191.
How to cite this article: Kulshrestha A, Mathur M. Amniotic fluid embolism: A diagnostic dilemma. Anesth Essays Res 2011;5:227-30. Source of Support: Nil, Conflict of Interest: None declared.
Commentary
Amniotic fluid embolism: A catastrophic problem in need of a prepared team with a plan There are few things more tragic than the death of a new mother – particularly one who was previously healthy and the cause of death is sudden and unpredictable. Amniotic fluid embolism (AFE) is one case catastrophic problem – as illustrated in the case and review by Kulshrestha and Mathur.[1] AFE is rare, occurring in less than 10 per 100 000 deliveries, but it has a mortality rate of 60–80% and accounts for 10% of maternal deaths.[2] Furthermore, it affects mothers worldwide and spares no culture, no demographic group, no society, and no corner of the world Access this article online Website www.aeronline.org
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– it affects the rich, as well as the poor. Fortunately, this problem is rare and few clinicians – even in busy delivery suites – will encounter this horrible problem. However, this very fact illustrates the challenges in diagnosis and management, particularly when even the slightest delay can mean the difference between life and death. With such a high mortality and the patient’s demise occurring suddenly, often within a few hours after delivery, Reviews such as this one presented by Kulshrestha, become critical in raising the level of awareness by helping clinicians recognize the signs and symptoms of AFE and provide adequate resuscitation. To improve survival, the clinical team must have a high suspicion and quickly work through a differential diagnoses in which many problems can be confused with AFE. But, more importantly, the team needs to be prepared. Even if the problem is recognized immediately, as with most disasters – medical and otherwise – if everyone is prepared and if there are
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Editor-in-Chief : Mohamad Said Maani Takrouri (KSA)
Open Access HTML Format
For entire Editorial Board visit : http://www.aeronline.org/editorialboard.asp
Anesthesia: Essays and Researches
Case Report
Amniotic fluid embolism: A diagnostic dilemma Ashish Kulshrestha, Megha Mathur1 Department of Anaesthesia and Intensive Care GianSagar Medical College and Hospital, Ram Nagar, Banur, Patiala, Punjab, 1Department of Obstetrics and Gynecology, Govt. Medical College and Hospital, Chandigarh, India Corresponding author: Dr. Ashish Kulshrestha, H.No.401/GH-18, Sector-5, Mansa Devi Complex, Panchkula, Haryana, India. E-mail: [email protected]
Abstract Amniotic fluid embolism (AFE) is a rare obstetric catastrophe with an incidence of 7.7 per 100 000 deliveries and mortality as high as 60% to 80%. We describe a case of perioperative cardiac arrest in a young parturient undergoing an emergent cesarean section. Just after delivery of live healthy male baby, patient developed disseminated intravascular coagulation not responding to resuscitation with fluids and blood products. Her autopsy revealed edematous lungs with amniotic fluid debris within pulmonary vessels thus establishing the diagnosis of AFE. Amniotic fluid embolism is life threatening and difficult to predict or prevent condition, which should be always be kept in mind in a parturient with sudden cardiovascular collapse, so that resuscitation commences immediately, as early intervention is essential for a positive outcome. Key words: Amniotic fluid embolism, asystole, cesarean section, disseminated intravascular coagulation, fibrin-degradation products
INTRODUCTION Amniotic fluid embolism (AFE) is a rare catastrophe with an estimated frequency of approximately 7.7 per 100 000 deliveries.[1] This condition was originally described in 1941 by Steiner and Luschbaugh with evidence of fetal debris in pulmonary circulation in pregnant women.[2] Recently, a more descriptive term was suggested as “the anaphylactoid syndrome of pregnancy.”[3,4] This is a rare but important cause of peripartum death in the United States making up for 10% of all maternal deaths with an overall mortality rate as high as 60% to 80%.[1] More than 50% of patients die within first hour and about two-third Access this article online Website
DOI
www.aeronline.org
10.4103/0259-1162.94789
Quick Response Code
within 5 hour of the event with high incidence of severe and permanent neurological damage among survivors. We report a parturient who had cardiac arrest during emergency cesarean section culminating in disseminated intravascular coagulation (DIC).
Case report A 37-years old third gravida female presented with history of leaking per vaginum since 1 day and was admitted for further observation and management. She had regular antenatal checkups in the institution with no history of raised blood pressure anytime in the antenatal period and had uneventful previous two normal deliveries. She denied associated co-morbid illnesses or any allergies. Her obstetrical examination revealed a gestation period of 37 weeks and 3 days with vertex presentation and premature rupture of membranes. The patient was hospitalized and fetal monitoring established. She started having true labor pains 3h after admission along with the development of tachypnea and audible wheeze for which she was given 227
Anesthesia: Essays and Researches; 5(2); Jul-Dec 2011
supplemental oxygen through the face mask and was started on bronchodilator nebulizations. She showed improvement in her clinical condition with the treatment instituted. Her initial laboratory parameters showed Hb of 10.8 g/dL, platelet count of 109 000 cells/mm3, total leukocyte count of 9500 cells/mm3, normal coagulation parameters, liver function tests (including enzymes) were also within normal limits and her arterial blood gas on face mask oxygen at 5 l/min showed pH 7.37; pO2 92 mmHg; pCO2 31 mmHg; HCO3- 21.5 mmol/L; BE/BD−0.5; SaO2 96%.The cardiotocography showed a persistent fetal bradycardia indicating fetal distress and so a decision to proceed to emergency cesarean section was made by the obstetrician. After discussion with patient’s relatives about the implications of her worsening clinical condition, spinal anesthesia was planned. A quick but thorough pre anesthetic evaluation revealed an obese parturient with a weight of 85 kg and height of 140 cm with short neck but adequate mouth opening and modified Mallampati class of III. She was afebrile, comfortable in supine position and had occasional rhonchi on auscultation of chest. After transferring her to the operating room, she was preloaded with 500 mL of lactated ringer’s solution and monitoring included a five lead electrocardiogram, noninvasive blood pressure and pulse oximetry. The baseline recordings showed heart rate of 100 beats/min, blood pressure of 110/80 mmHg and spO2 of 94% on room air. Lumbar puncture was performed at L3–L4 interspace in sitting position in anticipation of technical difficulty and urgency of surgery and 2.4 mL of hyperbaric 0.5% bupivacaine was injected intrathecally and was immediately placed in the supine position with a wedge placed beneath her right buttock. A sensory level of T6 bilaterally (loss of sensation to pin prick) was achieved before starting the surgery and supplemental oxygen was given through face mask at 5 L/minute. The blood pressure showed a reading of 94/58 mmHg with a heart rate of 102 beats/min and spO2 of 97%. The sensory level of T6 was again confirmed before skin incision and a live 2.8 kg male baby was delivered with APGAR scores of 4 and 8 at 1 and 5 min, respectively. Just after delivery of baby and even before starting on oxytocin infusion, her blood pressure suddenly dropped to 60/40 mmHg with severe bradycardia (HR< 40 beats/min) culminating in asystole. Immediate tracheal intubation was performed and positive pressure ventilation was started with 100% oxygen and cardiopulmonary resuscitation with chest compressions at 100 compressions/min was commenced. Epinephrine 1 mg was given by intravenous push and was repeated twice (total 3 mg). The heart rate restored to 150 beats/min with the blood pressure of 60/30 mmHg with the total duration of cardiac arrest being less than a minute. The surgeons noticed abnormally increased oozing from the uterine incision site and suspected defective coagulation and closed uterus and abdomen after placing packs and abdominal drain. Immediately a 228
Kulshrestha and Mathur: Amniotic fluid embolism
bedside clotting test was performed using a capillary tube with blood from pin prick, which showed an abnormally increased clotting time. Resuscitation was continued with colloids (1000 mL) and inotropic support was started with infusions ofdopamine at 15 µg/kg/min and nor epinephrine at 0.1 µg/kg/min as blood pressure was not responding to intravenous fluids. A total of 1500 mL of crystalloids, 1000 mL colloid (hydroxyethyl starch), 2 units of packed red blood cells and 4 units of fresh frozen plasma were transfused in the operating room in anticipation of abnormal coagulation parameters and the blood loss was estimated at 1200 mL approximately. Arterial blood gas analyzed intraoperatively showed pH 7.05; pO2 363 mmHg; pCO2 37 mmHg; HCO -3 10 mmol; BE/BD −20; SaO2 100% on 100% oxygen suggesting severe metabolic acidosis which was corrected with 100 meq of soda bicarbonate infusion. She was quickly transferred to ICU for further management and monitoring. For hemodynamic monitoring and fluid status, a central venous line was placed in the right internal jugular vein and an arterial cannula was placed in the right radial artery that showed initial readings of 20 mmHg and a blood pressure of 80/42 mmHg, respectively. Mechanical ventilation was continued with the controlled mode of ventilation with 100% oxygen and an abnormal soakage of the dressing with collection of significant amount of blood in the abdominal drain was noticed. She remained hypotensive in the ICU inspite of inotropic supports with dopamine, nor epinephrine and epinephrine infusions. Her laboratory values showed Hb of 6 gm/dL, platelet count of 21 000 cells/mm3, prothrombin time of 14 s, activated partial thromboplastin time of 45.4 s with elevated D-dimer and fibrin degradation products thus raising suspicion of disseminated intravascular coagulation. A total of five units of packed red blood cells, 15 units of fresh frozen plasma and 10 units of platelet rich plasma were transfused. A repeat arterial blood gas analysis showed pH 7.20; pO2 162 mmHg; pCO2 29.5 mmHg; HCO3-16.2 mmol/L; BE/BD-12; SaO2 99%. Uterine artery embolization under radiological guidance was planned after discussing with the attending radiologist but the patient could not be transported to the x-ray department due to the hemodynamic instability. The resuscitation attempts were unsuccessful and the patient died 10h postoperatively. Autopsy was performed after taking consent from the patient’s relatives, which showed edema of lungs with debris in pulmonary vessels that on further microscopic examination showed fetal squamous epithelial cells, thus the diagnosis of AFE was considered most likely.
Discussion The various differential diagnoses in our patient with sudden cardiovascular collapse during an emergent cesarean section could have been
Anesthesia: Essays and Researches; 5(2); Jul-Dec 2011
• Total spinal coinciding with administration of oxytocics. • Drug anaphylaxis. • Venous air embolism. • Subclinical sepsis (chorioamnionitis) with Acute lung injury going in for systemic inflammatory response syndrome exaggerated with peak spinal effect. • Amniotic fluid embolism. Our patient developed cardiovascular collapse during cesarean section and also had few premonitory symptoms like tachypnea, audible wheeze and fetal bradycardia that could have pointed towards the possibility of AFE, but were not considered due to rarity of this condition and moreover the urgency of surgery was given more priority. Total spinal coinciding with administration of oxytocin was unlikely as the event occurred almost 15–20 min after intrathecal injection and also the sensory level was stable at T6 (checked twice) with stable hemodynamics and the oxytocics were not transfused till the episode occurred. Drug induced anaphylaxis was also unlikely as no antibiotic was given before the episode and local anesthetic was given intrathecally after ruling out any intravascular placement. Venous air embolism can occur in cesarean section under general anesthesia[5] and has also been reported with both epidural[6] and spinal anesthesia.[7] This diagnosis was also less likely as no air was detected in intravenous line and also at autopsy no evidence of air was found in pulmonary vessels. Subclinical sepsis due to chorioamnionitis usually has a history of premature rupture of membranes of longer duration and moreover patient had no fever preoperatively with a normal total leukocyte count and a normal arterial blood gas, so this possibility was also considered less likely. Our patient developed cardiovascular collapse during cesarean section and also had few symptoms preoperatively such as tachypnea, audible wheeze and fetal bradycardia that could have pointed toward the possibility of amniotic fluid embolism. The presence of hypoxia, cardiovascular collapse, high central venous pressure and severe metabolic acidosis in blood gas analysis pointed toward the diagnosis of pulmonary embolism and in our case as patient was pregnant and since venous air embolism was unlikely, possibility of AFE was considered as the likely diagnosis retrospectively. Transesophageal echocardiography can help in the diagnosis of AFE showing acute right ventricular strain with under filling of left ventricle but we were not able to perform it as bedside availability was not there and also the patient could not be shifted for same.[8,9] Amniotic fluid embolism, a rare obstetrical catastrophe, can present with constellation of signs and symptoms such as respiratory distress (57%), sudden hypotension (37%), coagulopathy (13%), and seizures (10%). More atypical presentations include abdominal pain, chest pain, and arrhythmias.[10] Most cases occur during
Kulshrestha and Mathur: Amniotic fluid embolism
labor (70%), during cesarean section (19%), or following vaginal delivery (11%). It has also been reported during early pregnancy, during second trimester abortions, amniocentesis or following abdominal injury.[11] The most recent CEMACH report shows an increase in number of deaths due to AFE (9 in 1985–1987 to 17 in 2003– 2005).[12] Although the pathophysiology of AFE is poorly understood, a biphasic response to amniotic fluid emboli has been suggested.[13,14] An initial transient phase, due to a reaction to vasoactive substances in amniotic fluid primarily arachidonic acid metabolites, causes intense pulmonary vasospasm, pulmonary hypertension and hypoxia leading to cardiovascular collapse. This stage usually lasts for 30 min and is responsible for about 50% of the mortality due to AFE within the first hour. The second phase then comprise of left ventricular failure, DIC and acute respiratory distress syndrome. Both the phases were probably present in our patient but due to rapid development of events, these were difficult to differentiate.[15] The definitive diagnosis is mostly histological on autopsy with demonstration of squamous cells, mucin and other fetal debris in pulmonary microvasculature of deceased women; however, fetal squamous cells have been found in the blood of laboring women aspirated from pulmonary artery due to other reasons also, thus reducing the diagnosing accuracy of this test.[16,17] The management of AFE comprises of prompt cardiopulmonary resuscitation without delay to achieve higher survival rate.[18] It is based on attempts at (a) maintaining maternal oxygenation, (b) optimizing the hemodynamic status, and (c) correcting the coagulopathy.[19] Newer modalities of management include selective pulmonary vasodilators in the setting of acute pulmonary hypertension seen in amniotic embolism.[20] If AFE is suspected at an early stage, measures that should be undertaken to prevent further cardiovascular collapse include maintaining maternal oxygenation by oxygen supplementation, prompt inotropic support if the hypotension persists and preparation of blood and blood products in anticipation of development of DIC. In the scenario of cardiovascular collapse due to suspected amniotic fluid embolism, successful use of hemodialysis with plasmapheresis and extracorporeal membrane oxygenation with intraaortic balloon counter pulsations have also been described in the literature.[21,22] In conclusion, AFE is a life threatening and difficult to predict or prevent condition that should be kept in mind in a parturient especially having risk factors such as known history of atopy or anaphylaxis, advanced gestational age at termination of pregnancy, rupture of membranes, or meconium staining of amniotic fluid.[23] The main aim to report this case is to stress on the difficulty in predicting and preventing this rare but fatal complication of pregnancy especially in centers with 229
Anesthesia: Essays and Researches; 5(2); Jul-Dec 2011
Kulshrestha and Mathur: Amniotic fluid embolism
limited resources where an algorithm for suspicion can be really helpful, as immediate resuscitation is essential for a positive outcome. It also stresses the importance of intensive care backup facilities for such cases.
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Abenhaim HA, Azoulay L, Kramer MS, Ledue L. Incidence and risk factors of amniotic fluid embolisms: A population- based study on 3 million births in United States. Am J Obstet Gynecol 2008;199:49.el-8. 2. Steiner PE, Luschbaugh CC. Maternal Pulmonary Embolism by amniotic fluid as a cause of obstetric shock and unexpected deaths in obstetrics. JAMA 1941;117:1341-5. 3. Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF. Amniotic fluid embolism: analysis of the national registry. In: Transactions of the Thirteenth Annual Meeting of the American Gynecological and Obstetrical Society. Am J Obstet Gynecol 1995;172:1158-69. 4. Visconi CM, Clark SL. Amniotic fluid embolism. In: Norris MC, editor. Obstetric Anaesthesia 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 1999. p. 579-91. 5. Lew TW, Tay DH, Thomas E. Venous air embolism during Cesarean section more common than previously thought. Anesth Analg 1993;77:448-52. 6. Fong J, Gadalla F, Gimbel AA. Precordial Doppler diagnosis of haemodynamically compromising air embolism during caesarean section. Can J Anaesth 1990;37:262-4. 7. Nims M, Hallonquist H, Camann W. Coronary arterial air embolism occurring during cesarean delivery. Int J Obstet Anesth 2006;15:166-9. 8. James CF, Feinglass NG, Menke DM, Grinton SF, Papadimos TJ. Massive amniotic fluid embolism: Diagnosis aided by emergency transesophageal echocardiography. Int J Obstet Anesth 2004;13:279-83. 9. McDonnell NJ, Chan BO, Frengley RW. Rapid reversal of critical haemodynamic compromise with nitric oxide in a parturient with amniotic fluid embolism. Int JObstet Anesth 2007;16:269-73. 10. Visconi CM, Clark SL. Amniotic fluid embolism. In: Norris MC, editor. Obstetric Anaesthesia 2nd ed. Philadelphia: Lippincott Williams and Wilkins;
1999. p. 579-91. 11. Dedhia JD, Mushambi MC. Amniotic fluid embolism. Br J Anaesth 2007;7:152-6 12. Confidential Enquiry into Maternal and Child Health (CEMACH). Saving mother’s lives 2003-2005 Report: A Report of UK confidential enquiries into maternal deaths. London: RCOG Press; 2007. 13. Clark SL, Montz FJ, Phelan JP. Hemodynamic alterations associated with amniotic fluid embolism: A reappraisal. Am J Obstet Gynecol 1985;151:617-21. 14. Clark SL. Amniotic fluid embolism. Crit Care Clin 1991;7:877-82. 15. Howes LJ. Anaphylactoid reaction possibly caused by amniotic fluid embolism. Intl J Obstet Anesth 1995;4:51-4. 16. Aguilera LG, Fermandez D, Plaza A, Gracia J, Gomar C. Fatal amniotic fluid embolism diagnosed histologically. Acta Anaesthesiol Scand 2002;46:334-7. 17. Plauche WC. Amniotic fluid embolism. Am J Obstet Gynecol 1983;147:982. 18. Aziz ES. A successfully resuscitated case of amniotic fluid embolism. Eur J Anaesthesiol 2000;17:712-3. 19. Rodgers L, Dangel-Palmer MO, Berner N. Acute circulatory and respiratory collapse in obstetrical patients: A case report and review of literature. AANA J 2000;68:444-50. 20. Conde-Agudelo A, Romero R. Amniotic fluid embolism: An evidence- based review. Am J Obstet Gynecol 2010;202:92. 21. Kaneko Y, Ogihara T, Tajima H, Mochimaru F. Continuous hemodiafiltration for disseminated intravascular coagulation and shock due to amniotic fluid embolism: report of a dramatic response. Intern Med 2001;40:945-7. 22. Hsieh YY, Chang CC, Li PC, Tsai HD, Tsai CH. Successful application of extracorporeal membrane oxygenation and intra-aortic balloon counterpulsation as lifesaving therapy for a patient with amniotic fluid embolism. Am J Obstet Gynecol 2000;183:496-7. 23. Edwards GJ, Davies NJ. Amniotic fluid embolism following feticide- a cautionary tale. J Obstet Gynaecol 2000;20:191.
How to cite this article: Kulshrestha A, Mathur M. Amniotic fluid embolism: A diagnostic dilemma. Anesth Essays Res 2011;5:227-30. Source of Support: Nil, Conflict of Interest: None declared.
Commentary
Amniotic fluid embolism: A catastrophic problem in need of a prepared team with a plan There are few things more tragic than the death of a new mother – particularly one who was previously healthy and the cause of death is sudden and unpredictable. Amniotic fluid embolism (AFE) is one case catastrophic problem – as illustrated in the case and review by Kulshrestha and Mathur.[1] AFE is rare, occurring in less than 10 per 100 000 deliveries, but it has a mortality rate of 60–80% and accounts for 10% of maternal deaths.[2] Furthermore, it affects mothers worldwide and spares no culture, no demographic group, no society, and no corner of the world Access this article online Website www.aeronline.org
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– it affects the rich, as well as the poor. Fortunately, this problem is rare and few clinicians – even in busy delivery suites – will encounter this horrible problem. However, this very fact illustrates the challenges in diagnosis and management, particularly when even the slightest delay can mean the difference between life and death. With such a high mortality and the patient’s demise occurring suddenly, often within a few hours after delivery, Reviews such as this one presented by Kulshrestha, become critical in raising the level of awareness by helping clinicians recognize the signs and symptoms of AFE and provide adequate resuscitation. To improve survival, the clinical team must have a high suspicion and quickly work through a differential diagnoses in which many problems can be confused with AFE. But, more importantly, the team needs to be prepared. Even if the problem is recognized immediately, as with most disasters – medical and otherwise – if everyone is prepared and if there are
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