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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.58 no.4 Campinas July/Aug. 2008

http://dx.doi.org/10.1590/S0034-70942008000400010 

CLINICAL REPORT

 

Amniotic fluid embolism during vaginal delivery under analgesia. Case report*

 

Embolia amniótica durante parto normal bajo analgesia. Relato de caso

 

 

José Fernando Amaral Meletti, TSAI; Reinaldo Vargas Bastos de Miranda, TSAII

IResponsável pelo CET/SBA da Disciplina de Anestesiologia da FMJ; Professor Adjunto da Disciplina de Anestesiologia da FMJ
IICo-Responsável do CET/SBA da Disciplina de Anestesiologia da FMJ, Professor Auxiliar da Disciplina de Anestesiologia da FMJ

Correspondence to

 

 


SUMMARY

BACKGROUND AND OBJECTIVES: Amniotic fluid embolism is a rare occurrence; it has a sudden onset and high morbidity. The objective of this report was to present a case of amniotic fluid embolism in a primipara undergoing analgesia for vaginal delivery.
CASE REPORT: This is a 38-year old pregnant woman with amniotic sac ruptured, cervix with 5-cm dilation, complaining of severe pain; the patient was agitated, diaphoretic, and with tachysystoly. After venipuncture, Ringer's lactate with 5 IU of oxytocin was infused slowly, blood pressure (BP) 110 × 70 mmHg, heart rate (HR) 115 bpm with sinus rhythm, and SpO2 98%. It was decided to use a combined technique: 2.5 mg of heavy bupivacaine and 20 µg of fentanyl were administered in the subarachnoid space and a catheter was inserted into the epidural space. Twenty minutes after the institution of analgesia, the patient complained of sudden onset of severe pruritus, she was agitated, with nausea and vomiting, pale, HR 160 bpm, tachypneic, SpO2 80%, and BP could not be detected. Normal saline (500 mL) associated with hydrocortisone, ephedrine (50 mg), and oxygen with a face mask at 10 L.min-1 were administered. At that moment, she presented BP 60 × 30 mmHg, HR 150 bpm, and SpO2 92%. Since BP tended to decrease, a total of 7 mg of metaraminol were administered divided in several doses. After vaginal delivery, the patient was transferred to the ICU with BP 90 × 60 mmHg, HR 110, and tachypnea. Two hours later, she developed bleeding and hypotension; disseminated intravascular coagulation (DIC) was diagnosed and the patient treated with crystalloid solutions, packed red blood cells and fresh frozen plasma. She was discharged from the ICU in the 3rd postoperative day (PO).
CONCLUSIONS: Due to the dramatic presentation, severity, and fast installation of the symptoms, the speed and objectivity of the measures instituted to maintain vital signs are fundamental and decisive for survival of pregnant patients. We alert for the importance of monitoring during labor analgesia.

Key Words: COMPLICATIONS: disseminated intravascular coagulation, amniotic fluid embolism; SURGERY, Obstetric: vaginal delivery.


RESUMEN

JUSTIFICATIVA Y OBJETIVOS: La embolia amniótica es rara siendo un cuadro clínico de inicio súbito y de elevada morbidez. El objetivo de este trabajo fue presentar un caso de embolia amniótica en paciente primigesta, sometida a la analgesia para parto normal.
RELATO DEL CASO: Embarazada de 38 años, bolsa rota y 5 cm de dilatación del cuello uterino. Se presentó con mucho dolor, agitación, sudoración, taquisistolia y venoclisis con Ringer con lactato asociado a 5 UI de ocitocina en goteo lento, presión arterial (PA) de 110 × 70 mmHg, frecuencia cardíaca (FC) 115 lpm, en ritmo sinusal y SpO2 de un 98%. Se optó por técnica combinada: empleando 2,5 mg de bupivacaína pesada y 20 µg de fentanil en el espacio subaracnoideo y catéter en el espacio epidural. Después de 20 minutos del inicio de la analgesia la paciente refirió prurito súbito e intenso, presentó agitación, vómito y palidez, FC 160 lpm, taquipnea, SpO2 80% y PA inaudible. Se administró una solución fisiológica a un 0,9% (500 mL) asociada a la hidrocortisona, efedrina (50 mg) y oxígeno bajo máscara facial con flujo de 10 L.min-1. En ese momento la PA era 60 × 30 mmHg, la FC 150 lpm y la SpO2 un 92%. Como la PA tendía a disminuir, se administró un total de 7 mg de metaraminol, divididos en varias dosis. Después del parto vaginal, la paciente se remitió a la UCI con PA 90 × 60 mmHg, FC 110 lpm y taquipnea. Dos horas después presentó sangramiento e hipotensión arterial, siendo diagnosticado coagulación intravascular diseminada (CIVD) y tratada con cristaloides, concentrado de glóbulos rojos y plasma fresco congelado. Alta de la UCI en el 3° PO.
CONCLUSIONES: Debido al dramatismo, a la gravedad e instalación abrupta del cuadro, la rapidez y objetividad de las medidas para mantener las señales vitales son fundamentales y decisivas para la sobrevida de las embarazadas. Se avisa sobre la importancia de la monitorización durante la analgesia de parto.


 

 

INTRODUCTION

Amniotic fluid embolism is a rare maternal complication, with an incidence that varies between 1:8,000 and 1:80,000 deliveries, with sudden presentation, and it is potentially fatal, with maternal mortality around 50% 1.

Among patients who survive, approximately 70% develop some neurologic deficit 2.

The present report focuses on a case of amniotic fluid embolism in a 38 years old primipara, on the 35th week of pregnancy, with ruptured amniotic sac, who underwent labor analgesia for vaginal delivery with combined spinal-epidural block.

 

CASE REPORT

A 38-year old female, physical status ASA II, approximately on the 35th week of pregnancy, was admitted to the hospital due to premature amniorrhexis. Labor analgesia was requested when the patient presented a 5-cm cervical dilation and uterine tachysystoly.

The patient presented with severe pain, agitated, and with difficulty to answer the questions of the pre-anesthetic evaluation; however, she did not present any contra-indication to conductive anesthesia. On physical exam, her blood pressure was (BP) 110 × 70 mmHg, heart rate (HR) 115 bpm, sinus rhythm, and SpO2 98%. The patient had a peripheral venous catheter with a slow infusion of Ringer's lactate associated with 5 units of oxytocin.

Combined spinal-epidural block was done, without intercurrences, between L3-L4, and 2.5 mg of 0.5% heavy bupivacaine and 20 µg of fentanyl were administered in the subarachnoid space, and a catheter was introduced into the epidural space. Approximately 3 minutes after the puncture the patient referred improvement of the pain; 1 g of cephalothin was administered upon request of the obstetrician. Her BP was 110 × 60 mmHg and HR 110 bpm.

Approximately 20 minutes after analgesia, the patient complained of severe pruritus, being treated with the slow administration of 10 mg of diphenidramine diluted in the maintenance crystalloid solution. She then complained of shortness of breath, became very agitated, and had one episode of vomiting. On physical exam, the patient was pale, with profuse diaphoresis, tachycardic (HR between 150 and 160 bpm), tachypneic, SpO2 between 80% and 85%, and BP was inaudible.

Ephedrine, 50 mg, was administered immediately, another venipuncture with a large bore catheter was done, and 500 mL of NS associated with 500 mg of hydrocortisone were infused rapidly. Oxygen 100% was also administered via a face mask at 10 L.min-1. A severe allergic reaction was the initial diagnosis.

At this moment, the patient presented BP 60 × 30 mmHg, HR 150 bpm, SpO2 92%, and her level of consciousness improved. Metaraminol, 7 mg divided in several doses, associated with Ringer's lactate, was administered for better blood pressure and heart rate control.

Five minutes after the beginning of the episode, the blood pressure was 90 × 40 mmHg, HR 110 bpm, the patient was awake and cooperative. The obstetrician decided to continue the vaginal delivery, which occurred 15 minutes later. The expulsive period was prolonged.

The male newborn had an Apgar of 0 in the first minute, 3 in the 5th minute, and 7 in the 10th minute. The patient developed uterine hypotonia and important bleeding; 15 IU of oxytocin and 0.2 mg of ergotrate intravenously associated with hydration with 1,500 mL of Ringer's lactate were administered.

The patient was unconscious when she was transferred to the ICU, BP 90 × 60 mmHg, HR 115 bpm, tachypneic, and pale. Two hours after her admission to the unit, she developed bleeding and severe hypotension; crystalloid solution and two units of packed red blood cells were administered. Blood was drawn for a coagulogram and CBC, and the patient was transferred to the operating room for revision of the delivery, but a site of severe bleeding was not determined.

Abdominal ultrasound showed an intact uterus with blood in the uterine cavity. Laboratorial exams showed: Ht 25%, Hb 8.2 g.dL-1, WBC 16,900, platelets 191,000 cel.mm3, PT 58.5 sec; AP 12%, INR 8.9, and aPTT 115 sec. The diagnosis of disseminated intravascular coagulation (DIC) and shock (anaphylactic, septic, hypovolemic) was made.

During her stay in the ICU, an echocardiogram showed a slight increase in the left chamber and discrete bilateral pleural effusion. Wide-spectrum antibiotics, a total of 6 units of packed red blood cells, and 6 units of fresh frozen plasma were administered. The patient was discharged from the unit on the 3rd day with normal CBC and coagulogram.

The patient was discharged from the hospital on the 5th post-delivery day without a clear cut diagnosis, only with the explanation of disseminated intravascular coagulation as a consequence of septic shock or allergic reaction. The newborn was discharged after 30 days without apparent neurologic abnormalities.

 

DISCUSSION

Amniotic fluid embolism also known as amniotic caseous embolism or amniotic caseous fluid embolisms, and more recently as anaphylactic syndrome of pregnancy 3, is one of the causes of sudden death in obstetrics.

Described initially by Meyer 4 in 1926, it became notorious after the works of Steiner and Lushbaugh in 1941 5 and Liban and Ratz in 1969 6, who reported 14 deaths among pregnant women who presented fetal desquamation in the pulmonary circulation, kidney, liver, and brain 2,3.

Its incidence in the literature varies from 1:8,000 to 1:80,000; 70% of the cases of amniotic fluid embolism occur during labor, 11% after vaginal delivery, and 19% during cesarean section, and in those cases there was a significant correlation with the birth of males 2.

The clinical causes of amniotic fluid embolism include high rupture of the amniotic sac, premature placental separation, intrauterine maneuvers, accelerated labor associated with hypercontractility (oxytocics), the use of catheters for amnio-infusion, induced abortion, and fetal death 2. Advanced age and multiparity favor its development 1,7. In the case presented here, the patient was a 38-year old primiparous woman with ruptured amniotic sac, tachysystoly, and treated with slow dripping of oxytocin (without infusion pump).

The beginning of any case of amniotic fluid embolism is secondary to the entrance of variable amounts of amniotic fluid in the maternal circulation; in some pregnant women, especially those with allergies, it can cause the most common presentation: sudden onset of dyspnea, paleness, anguish, changes in the level of consciousness, severe hypotension, cardiovascular depression and shock, and, in 50% of the cases, it can lead to cardiac arrest and death 8,9. Other symptoms commonly present in amniotic fluid embolism include fever, chills, nausea, vomiting, headache, and evidence of acute fetal distress (deceleration and bradycardia) 10.

In the case presented here the patient developed: severe pruritus, agitation, vomiting, dyspnea, paleness, tachycardia, inaudible BP, and SpO2 85%.

This sequence of events would be originated by the exposure of the pulmonary vessels to an immunologically active fluid (arachidonic acid and its metabolites), resulting in severe vasoconstriction and the release of pulmonary proinflammatory factors, causing capillary changes, myocardial depression, hypotension, pulmonary edema secondary to left ventricular insufficiency, shock, and even death 2,11,12.

The diagnosis of amniotic fluid embolism is clinical, one of exclusion, and should always be suspected whenever a pregnant woman who, during labor of after delivery, develops the sudden and dramatic onset of hypotension, dyspnea, and cardiovascular collapse, which characterize the initial phase of this disorder.

Its management include life support with oxygen therapy, tracheal intubation if SpO2 < 90%, crystalloid solutions, vasoactive drugs, and possible catheterization of the pulmonary artery to evaluate cardiac output and pulmonary capillary wedge pressure to guide volemic reposition 13.

In this case, treatment included the administration of oxygen with a face mask without the need of tracheal intubation to maintain SpO2 of 92%, vasoactive drugs, crystalloid solution, corticosteroids, and diphenidramine. More than 50% of the patients die in this initial phase.

After this first stage amniotic fluid embolism can, through the release of pulmonary proinflammatory factors, lead to the immunological activation of coagulation pathways causing DIC in 83% of the cases. The presence of large amounts of thromboplastin in the amniotic fluid accelerates coagulation mechanisms, causes platelet aggregation, promotes the release of factor III, and activates directly factor X and the coagulation cascade 2.

The treatment of DIC should include packed red blood cells, fresh frozen plasma, platelets, and cryoprecipitate or fibrinogen, according to the symptomatology, and laboratorial exams should be followed.

Usually, DIC develops after the cardiovascular symptoms but in some cases can precede it. In severe cases of amniotic fluid embolism, the shock of the first stage is cardiogenic in origin, while in the second stage is more of the distributive type or hemorrhagic 14,15.

In approximately 55% of the cases, the baby has not been delivered yet, and fetal extraction or cesarean section are mandatory to prevent further damage to the fetus and facilitate resuscitation maneuvers 2.

A prophylactic method for amniotic fluid embolism does not exist. Only constant observation, monitoring the pulse oximetry, continuous electrocardiogram, and, if possible, capnography, can all help the detection and immediate institution of measures to save the patient.

Despite all those measures, the mortality rate continues to be high, and amniotic fluid embolism continues to be a catastrophic complication that demands a fast diagnosis and immediate and objective measures, and the importance of close monitoring and observation in rooms prepared for any emergency should be emphasized.

 

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Correspondence to:
Dr. José Fernando Amaral Meletti
Rua João Massagardi Filho, 98
Jardim Santa Tereza
13211-421 Jundiaí, SP
E-mail: dfmeletti@terra.com.br

Submitted em 31 de maio de 2007
Accepted para publicação em 22 de abril de 2008

 

 

* Received from Hospital Universitário da Faculdade de Medicina de Jundiaí (FMJ), SP