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Merlin B. Fausett is the chief of obstetrics/gynecology and a maternal-fetal medicine specialist at Landstuhl Regional Medical Center, Germany.
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In this article, we discuss the prevalence, pathophysiology, signs, symptoms, diagnosis, and management of anaphylactoid syndrome of pregnancy. General nursing considerations for postpartum patients are included because knowledge of puerperal care may be limited for some critical care nurses. The severity of the syndrome is illustrated by using a dramatic case study of a patient who survived.
Historical Context
Steiner and Lushbaugh6 were among the first who attempted to define a disease entity for unexplained obstetric mortality. In 1941, they described autopsy findings from 8 pregnant women in whom pulmonary edema and shock developed during labor. These researchers reported that powerful or tetanic contractions caused an embolism of squamous cells, mucin, and/or other amorphous debris, presumably from the fetus, to lodge in the patients’ pulmonary vasculature. They suggested that their findings identified a new disease, termed maternal pulmonary embolism by amniotic fluid, characterized by shock that developed during labor or shortly after delivery.
In a later study, Liban and Raz7 reported that cyanosis, respiratory distress, hypotension, and coagulopathy developed in 14 patients with amniotic fluid embolism. In addition, squamous cells were detected in the heart, liver, kidney, spleen, pancreas, and brain of several patients.
In 1993, Benson8 proposed a new clinical definition after summarizing 3 case reports of women who survived amniotic fluid embolism. The definition included sudden onset of cardiovascular collapse, sustained tachycardia, and the absence of other illnesses that could explain the signs and symptoms. Finally, Benson was one of the first investigators to raise doubts that amniotic fluid leakage into the maternal circulation was the primary cause of this abnormality and questioned whether this disease was associated with an immune response to a pregnancy-associated antigen.
Pathophysiology
Amniotic fluid surrounds the fetus during pregnancy and is produced by the fetal membranes and the fetus. The fluid has a neutral pH and increases in volume from 50 mL at 12 weeks to 1000 mL at 38 weeks.2 Amniotic fluid contains fetal components such as squamous cells from the skin, mucin, vernix, lanugo hairs, platelet activating factor, prostaglandins, complement- activating factors, procoagulants, and sometimes meconium.
Anaphylactoid syndrome of pregnancy seems to occur after maternal intravascular exposure to fetal tissue. This exposure routinely occurs during normal labor and delivery and can also take place after placement of an intrauterine catheter, after uterine rupture, during cesarean section, or during spontaneous or surgical abortion. Experts previously theorized that strong uterine contractions forced amniotic fluid into the maternal circulation; however, more recent research3,6 suggests that this theory is not correct. No ways to prevent this exposure are known.3
The exact pathophysiological mechanism by which anaphylactoid syndrome of pregnancy occurs is unknown. Under certain conditions, when amniotic fluid and its fetal components enter the maternal circulation, endogenous mediators (eg, prostaglandins, leukotrienes, histamine, bradykinin, cytokines, thromboxane, complement-activating factors, and platelet activating factor) are released and incite a striking maternal response. The pathological maternal response results in hypoxia, hemodynamic instability, and/or consumptive coagulopathy2,3 (see Figure
). These 3 characteristic clinical manifestations do not occur uniformly in all patients; any component may dominate or be entirely absent.9,10
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Clark et al3 formed a national registry of patients with amniotic fluid embolism. These investigators found a significant association between a male fetus and anaphylactoid syndrome of pregnancy. In the same study, 41% of patients with this syndrome had a history of allergy or atopy. Clark et al reported that the clinical, hemodynamic, hematologic, and laboratory manifestations in 46 patients with amniotic fluid embolism were similar to those in patients with septic and anaphylactic shock. They proposed the term anaphylactoid syndrome of pregnancy, suggesting that the signs and symptoms of the abnormality are not consistent with an embolic event, but rather, resemble septic and anaphylactic shock. Subsequent reports12–15 supported this hypothesis.
Tryptase, a mediator released during an anaphylactic reaction, is a laboratory marker for anaphylaxis.16 Farrar and Gherman15 published a case report of a patient who had severe hypoxia, cardiac arrest, coagulopathy, seizures, and facial erythema. A tryptase level measured 1.5 hours after the patient’s death was 4.7 ng/mL (normal is <1 ng/mL). These data also support the concept of anaphylactoid syndrome of pregnancy.
Maternal Signs and Symptoms
Table 1 lists maternal signs and symptoms of anaphylactoid syndrome of pregnancy. These signs and symptoms may commence during labor, after vaginal or cesarean delivery, or after pregnancy termination. Unexpected, rapid, and profound hypoxia, often the first indication of this syndrome, is most likely related to pulmonary vasospasm, pulmonary hypertension, and ventricular dysfunction.9 Hypoxia causes tetanic contractions and limits maternal-fetal exchange of blood.9 Bronchospasm, dyspnea, cough, pulmonary edema, acute respiratory distress syndrome, and cyanosis are sequelae of the initial lung injury.
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Consumptive coagulopathy is evidenced by numerous signs ranging from petechiae to profuse hemorrhage that leads to rapid exsanguination. Evidence of hypovolemic shock develops in patients who have ongoing or excessive bleeding. Bleeding from the woman’s eyes, nose, gums, or vagina and from venipuncture, surgical, and episiotomy sites may occur. The patient’s stool or emesis may test positive for occult blood. Hematomas, flank pain, abdominal distention, swollen extremities, neurological abnormalities, hypotension, tachycardia, cool skin temperature, pallor, and diaphoresis may indicate internal bleeding.
Cerebral, cardiac, pulmonary, hepatic, and renal organ dysfunction may result from hypoperfusion or thrombosis-induced tissue ischemia. The prognosis for patients with multisystem organ failure is, at best, grim.
Fetal Signs and Symptoms
Profound fetal respiratory acidosis occurs as a result of maternal hypoxia and tetanic contractions. Although analysis of arterial blood from the umbilical cords of 11 neonates in the national registry study3 revealed a mean pH of 6.79, 9 of the 11 neonates survived without neurological impairment.
The low fetal pH results in fetal bradycardia, a heart rate less than 120/min. Prolonged bradycardia can result in hypotension and neurological injury. A short interval between cardiac arrest and delivery correlates positively with neonatal survival.9
Diagnosis
Anaphylactoid syndrome of pregnancy is diagnosed on the basis of its characteristic clinical features of acute hypoxia, acute hypotension, cardiac arrest, and/or coagulopathy that cannot be attributed to another cause.9,10,14 Differential diagnoses for the syndrome are outlined in Table 2.
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Management
Patients with signs and symptoms of anaphylactoid syndrome of pregnancy require immediate treatment. Therapies are supportive, because no specific therapies consistently improve outcomes for these women.3,5,10,14 The primary goals are providing oxygen, maintaining cardiac output and organ perfusion, correcting coagulopathy, and providing adjunctive therapies.
Providing Oxygen
Physicians, nurses, medical technicians, and respiratory therapy technicians must rapidly initiate cardiopulmonary resuscitation and Advanced Cardiac Life Support protocols for patients with cardiopulmonary arrest. The use of 100% oxygen is mandatory.14 Patients who lose consciousness or who are at risk for loss of a patent airway should be intubated by a qualified provider. The healthcare team should monitor results of pulse oximetry, arterial blood gases, and end-tidal carbon dioxide values and adjust oxygen and ventilator therapies as indicated. The goal is an arterial oxygen saturation greater than 90% and an arterial oxygen level greater than 60 mm Hg.14 A pregnant patient or recent postpartum patient is normally alkalotic because of a progesterone effect. Progesterone promotes a respiratory alkalosis with compensatory metabolic acidosis and a PaCO2 of 28 to 32 mm Hg, a mean pH of 7.42, and a mean bicarbonate level of 18 mmol/L. A PaCO2 greater than 32 to 34 mm Hg indicates hypoventilation.
Maintaining Cardiac Output and Organ Perfusion
Nursing measures to maintain cardiac output, blood pressure, cerebral blood flow, and kidney perfusion include the rapid administration of crystalloid solutions through a large-bore intravenous or central venous catheter. It is important to remember that these patients have a profound vascular leak. Because patients often require massive volumes of blood products to correct the coagulopathy and anemia due to ongoing hemorrhage, interstitial fluid overload can easily develop. As soon as blood products are available, crystalloid fluids should be used judiciously. Before delivery, the patient should be positioned on her side to maximize venous return. The skin should be assessed continually for color, temperature, and moisture. Nurses often administer and adjust doses of vasopressors and inotropic agents to treat hypotension and heart failure. Physicians and nurses routinely use hemodynamic monitoring data such as mixed venous oxygen saturation, cardiac output or index, pulmonary capillary wedge pressure, and central venous pressure to guide management. Table 3 lists target ranges for these variables; however, the appropriateness of each value and its current effect on the patient should always be evaluated.
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Nursing actions to treat coagulopathy and hemorrhage include the administration of packed red blood cells, platelets, fresh-frozen plasma, and cryoprecipitate as soon as these become available. Whole blood would be ideal; however, most institutions do not stock whole blood. If profound hemorrhage occurs, nurses must transfuse O-negative packed cells so that the transfusion is not delayed by waiting for type-specific and crossmatched blood. Use of a rapid volume infuser facilitates administration of massive amounts of fluids and blood products. Although controversial, low-dose heparin is sometimes used to inhibit the coagulation cascade and thus treat consumptive coagulopathy. Nurses should anticipate and prevent hypothermia, hyperkalemia, hypocalcemia, citrate intoxication, fever, hypersensitivity reactions, and tachycardia because these may be associated with largevolume blood transfusions.
Providing Adjunctive Therapies
Corticosteroids and/or epinephrine may be used to cause immunosuppression. 3,21 Clark et al3 recommend administration of hydrocortisone sodium succinate intravenously every 6 hours. Thus far, glucocorticoids have not been shown to improve patients’ outcomes. However, as with other specific therapies, because of the rarity of the syndrome, prospective evaluation of various treatment strategies is unlikely.
Use of warming lights, warmed intravenous fluids and blood products, and/or a heating blanket helps prevent hypothermia. Hypothermia may produce coagulopathy, thrombocytopenia, dysrhythmias, peripheral tissue ischemia, altered mentation, and increased hemoglobin affinity for oxygen.
Postpartum Care in the ICU
Critical postpartum nursing interventions are described in Table 4. Although details about all aspects of postpartum care cannot be included here, the basic information in Table 4 provides ICU nurses with a fundamental review of postpartum care. After the patient is in stable condition and transfers out of the ICU, the goals will be for her to perform self-care, demonstrate safe infant care, and prepare for discharge.
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Our patient was a 20-year-old primigravida at 39 weeks 1 day gestational age who underwent a low forceps vaginal delivery because of fetal bradycardia. A laceration of the left vaginal sidewall in combination with uterine atony resulted in an estimated blood loss of 800 mL. Approximately 30 minutes after the delivery of the infant and at the completion of the repair, the patient had sudden cardiopulmonary failure. Her blood pressure decreased to 60/20 mm Hg, she became unresponsive to verbal and tactile stimuli, and massive hemorrhage ensued. The presumptive diagnosis was anaphylactoid syndrome of pregnancy.
Resuscitative measures were initiated. The patient was intubated, multiple intravenous catheters were placed, and crystalloid boluses were begun pending the arrival of blood products. The initial hemoglobin level was 63 g/L (6.3 g/dL), and results of coagulation panels were consistent with the clinically diagnosed disseminated intravascular coagulation (partial thromboplastin time, 235 seconds; fibrinogen, <2.1 µmol/L [70 mg/dL]). Despite normal uterine tone, the patient continued to hemorrhage. Blood was evident in the Foley catheter, and large hematomas developed at the insertion sites of the central and peripheral catheters.
After the initial resuscitation, volume replacement was accomplished by using mostly blood products. Crystalloid fluids were limited because of the anticipated need for a massive transfusion of blood products and concern for potential fluid overload. During the first 10 hours, she received more than 60 units of blood products and was kept in the labor and delivery unit’s operating room because of her tenuous status. After 10 hours of treatment, her condition had stabilized to the point that she could be transferred to the ICU.
Six hours after the initial event, she had become anuric and soon after arrival in the ICU, an echocardiogram revealed significant cardiac contractility dysfunction. Inotropic agents were initiated, but only minimal improvement in hemodynamic parameters occurred. The patient’s blood pressure was moderately elevated, and hemodynamic parameters suggested volume overload (central venous pressure near 30 mm Hg). Nonetheless, because of persistent heavy bleeding, she continued to require large volumes of blood products to replace red blood cells and coagulation factors. Because of the nonfunctioning kidneys, we elected to initiate hemodialysis to help remove the excess fluid. Within 30 minutes after hemodialysis was started, cardiopulmonary function rapidly improved and inotropic agents were discontinued. During the first 21 hours after delivery, the patient received more than 100 L of fluids, including 10 L of crystalloid fluids, 53 units of packed red blood cells, 56 units of fresh-frozen plasma, 4 units of cryoprecipitate, and 7 sixpacks of platelets.
During the next 36 hours, the patient continued to receive blood products to correct the coagulopathy (final total was 80 units of packed red blood cells, 71 units of freshfrozen plasma, and 20 six-packs of platelets, exposing the patient to more than 200 blood donors). Hemodialysis was continued for the next week to maintain her fluid balance and possibly remove pathological proinflammatory mediators. Her pulmonary function remained good throughout the process, with only mild acute respiratory distress syndrome. Dilatation and curettage was performed in the ICU to evacuate large amounts of uterine clots. The patient was transferred from the ICU on postpartum day 12 and discharged home on day 27. Panhypopituitarism was diagnosed. We attributed this abnormality to hypotension-induced pituitary necrosis (Sheehan syndrome). The physiological pituitary hypertrophy that normally accompanies pregnancy leaves the pituitary gland susceptible to hypotension-induced injury. The patient also had vaginal reconstructive surgery but otherwise survived this catastrophic event without detectable renal, cardiac, pulmonary, or neurological impairment.
The patient’s husband was on active duty in the Navy aboard the USS Ticonderoga far from land in the Atlantic Ocean. We communicated with the ship’s captain and the patient’s husband. The captain changed the ship’s course, a step that allowed the ship’s helicopter to reach land safely in South America. The patient’s husband arrived nearly 48 hours after the infant was delivered.
We attribute this successful outcome to a patient-centered and multidisciplinary care approach, advanced clinical skills, flexible scheduling, open communication among caregivers, and coordination with the US Navy. For example, although several specialists were involved with the patient’s care, team members did not overstep their bounds, no panic occurred, and nurses and physicians stayed focused on a full-scale resuscitation that, in reality, lasted several days. The patient’s requirements for massive transfusions quickly depleted the blood supplies in our medical center and our community. Two Navy ships made unscheduled port visits so that sailors could donate blood. Additional Navy-sponsored blood drives ensured that we maintained an adequate blood reserve. A support group of Navy wives brought the patient’s family food, donated baby clothes, and helped the patient ’s husband arrange day care for the baby.
Acknowledgments
The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Air Force or the Department of Defense.
References
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