MATERNAL DEATH DUE TO PULMONARY EMBOLISM :
AMNIOTIC FLUID EMBOLISM, A CASE REPORT.
Made Kornia Karkata
Division of Fetomaternal, Department of Obstetrics and Gynecology
Abstract:
Pulmonary embolism is a critical complication and life threatening disorder that result from venous thrombosis. Thromboembolism is rare in the Asian population. . The incidence averages about 1 in 7000 pregnancies. Pulmonary embolism in obstetrics may occur in the form of acute amniotic fluid embolism and pulmonary thromboemboli from deep venous thrombosis of the lower extremities. Predisposing factors commonly include tetanic uterine contraction, advanced maternal age, parity, obesity, traumatic delivery, abdominal delivery, thrombophlebitis , endometritis and history of previous pulmonary embolism or deep vein thrombosis. Diagnosis should be suspected if cardiac or pulmonary symptoms occur abruptly during labor or early post delivery. If possible, a serial of investigations should be done include laboratory findings and chest X-Ray, ECG, ventilation-perfusion (V/Q) scintigraphic lung scan, CT Pulmonary angiography , pulmonary angiography , MRI and MR angiography and post mortem clinical autopsy.
Management of cardiopulmonary resuscitation measures should be instituted immediately and under closed supervision in the intensive care unit by a team of experts. Closed monitoring is mandatory in particular related to treatment of acid base dysfunction and deep shock Because of the high mortality associated with pulmonary embolism it is better to start heparin therapy even in the absence of a definitive diagnosis if pulmonary embolism is likely. Management of anticoagulation follows the same protocol as for deep vein thrombosis. The number and size of emboli will influence the prognosis. High maternal mortality is high in amniotic fluid embolism, while a little lower in thromboembolism yet result in long term implications.
INTRODUCTION
Pulmonary embolism is a critical complication and life-threatening disorder that results from venous thrombosis . Although a rare complication of pregnancy (0.09%), it is a significant cause of maternal death (1). Pulmonary emboli consist of material that gains access to the venous system and subsequently to the pulmonary circulation.. The material might be in the form of amniotic fluid, fat, foreign body, oil parasite eggs, septic emboli, thrombus and tumor cell (2). Although it causes about 10% of maternal deaths, it is relatively uncommon during pregnancy and the puerperium. The incidence averages about 1 in 7000 pregnancies. The diagnosis is more commonly made (75% of cases) postpartum.(3). Predisposing factors commonly include advanced maternal age, obesity, traumatic delivery, abdominal delivery, thrombophlebitis and endometritis. and history of previous pulmonary embolism or deep vein thrombosis.
Pulmonary embolism in obstetrics may occur in the form of acute amniotic embolism and thromboemboli from deep venous thrombosis of the leg. Thrombo embolism is rare in the Asian population (4).
Amniotic fluid embolism is one of the most dangerous and challenging obstetric condition to treat and can occur during any stage of labor . It has been linked to mortality rate as high as 80% to 90% (5). Suspicion of pulmonary embolism as a cause of maternal death largely based on clinical appearance since in most Asian countries clinical autopsies cannot be performed readily(6). The most serious vascular complications to happen during pregnancy or early of the puerperium are venous thrombosis and pulmonary embolism. Besides the immediate threat to the mother thrombus is also potentially hazardous to the fetus due to the need for anticoagulant therapy.
PATHOPHYSIOLOGY
It was ten decades ago since Rudolf Virchow postulated the condition that predispose to the development of venous thrombosis namely: stasis, local trauma to the vessel wall and hypercoagulopathy, the risks that increase during normal pregnancy(7). Thromboemboli almost never originate from the pulmonary circulation; they arrive there by a venous route. The pathophysiology of amniotic fluid embolism is unclear. Amniotic fluid is thought to enter the circulation through a number of routes such as the endocervical veins, the normal placental site, through uterine tear during cesarean section or uterine rupture. Broken fetal membranes are needed for this condition to occur( ).
This condition leads to a systemic inflammatory response syndrome (SIRS), coagulopathy and disseminated intra vascular coagulation (DIC). Mechanical obstruction of the pulmonary microvasculature by amniotic debris or from prostaglandin mediated pulmonary arterial spasm results in acute pulmonary hypertension lead to left ventricular dysfunction( ).
Three primary acute events occur: 1. pulmonary vascular obstruction, leading to sudden decreases in left ventricular filling pressures and cardiac output; 2. pulmonary hypertension with acute cor pulmonale and 3, ventilation-perfusion inequality of lung tissue leading to arterial hypoxemia and its metabolic consequences.
Risk factors for amniotic fluid embolism are: difficult or prolonged labor, use of induction of labor , advanced maternal age, multiparity, intra uterine fetal death, trauma and abruption placentae. Severe dyspnea, cyanosis, circulatory collapse and seizures may developed suddenly. Pulmonary edema, DIC, hemorrhage, acute respiratory distress, convulsions and coma are serious complications that can lead to death within minutes in the first hour.
Pathophysiologic changes in pulmonary embolism(7)
| Basic Physiology | Effect of thromboembolism | Mechanism |
| Altered hemodynamics | Increased pulmonary vascular resistance | Vascular obstruction Vaso-constriction by serotonin , thromboxane A2 |
| Impaired gas exchange | Increase in alveolar dead space | Vascular obstruction Increased perfusion of lung units with high V/Q ratios |
| Hypoxemia | Increased perfusion of lung units with low V/Q ratios Right to left shunting Fall in cardiac output with fall in mixed venous Po2 | |
| Ventilatory control | Hyperventilation | Reflex stimulation of irritant receptors |
| Work of breathing | Increased airway resistance Decreased pulmonary compliance | Reflex bronchoconstriction Loss of surfactant with lung edema and hemorrhage |
DIAGNOSIS(3,4,5,8,9)
One should think about pulmonary embolism if cardiac or pulmonary symptoms occur abruptly during normal labor or early post delivery. For pulmonary amniotic fluid embolism, classically a woman in the late stages of labor or immediately post partum begins gasping for air, and then rapidly suffers seizure or cardiorespiratory arrest complicated by consumptive coagulopathy, uncontrolled bleeding, deep shock and death.
There is a sudden, unexplained peripartum respiratory distress, cardiovascular collapse and coagulopathy. Profuse bleeding follows secondary to coagulopathy or uterine atony. The most common symptoms are dyspnea (82%), chest pain (49%) , cough (20%), syncope (14%) and hemoptysis (7%) (3). Other clinical findings include tachypnea, apprehension and tachycardia. Diagnosis is confirmed by detection of squamous cells or other debris of fetal origin in the pulmonary circulation when clinical autopsy was applied (8,9).
Most cases of venous thrombosis during pregnancy are related to the deep veins disorders of the lower extremity. If the emboli are massive, sudden death may happen from acute cor-pulmonale. In cases with smaller emboli the diagnosis is suggested by the sudden onset of pleuritic pain , sometime with blood-streaked sputum and even a dry cough. Cardiopulmonary resuscitation should be first started immediately, meanwhile systematic investigation should be followed including laboratory findings, chest X-Ray, ECG , lung scan and pulmonary angiography.
MANAGEMENT (4,5,6,10)
Once the signs and symptoms are recognized and a presumptive diagnosis is made, supportive measures should be implemented promptly. The case should be managed jointly in an intensive care unit. In the event of cardiac arrest, resuscitation team should follow the standard of ACLS (Advanced Cardiac Life Support) protocols. The initial principles of dealing with obstetric emergencies are the same as for any emergency by keeping in order airway, breathing and circulation. There are several simultaneous interventions to maintain cardiac output and blood pressure.
Therapeutic measures are supportive and should be directed toward minimizing hypoxemia with supplemental oxygen, maintaining blood pressure and managing associated coagulopathies. Intubation and positive end-expiratory pressure should be applied Supportive measures include the initiation of fluid therapy, administration of pharmacological agents and electrocardiographic monitoring to detect and treat arrythmias. Circulatory support and blood component replacement are important. Pulmonary artery catheterization is highly recommended for monitoring cardiac output, central venous pressure, and pulmonary artery pressure and to control volume of fluid therapy. If invasive hemodynamic monitoring is not available, rapid digitalization should be administered. Management of anticoagulation follows the same protocol as for deep vein thrombosis Finally, the development of consumptive coagulopathy may require replacement of depleted hemostatic components in the case of uncontrolled bleeding or abnormal clotting parameters. If the baby is not yet delivered, the fetus should be monitored continuously for signs of compromise by expertise in electrical fetal monitoring. In women suffering cardiac arrest with undelivered baby consideration should be given to emergency perimortem cesarean delivery.
PROGNOSIS(3,4,5,6)
Amniotic fluid embolism is a catastrophic event and has been linked to high mortality which may be as high as 80% to 90% and estimated to account for 10% of all maternal death. Actually there are no data that any type of intervention improves maternal prognosis with amniotic fluid embolism. For pulmonary thromboembolism, maternal mortality is lower depending on size and number of emboli, yet may result in long term implications.
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