Amniotic Fluid Embolism (AFE) Past Paper PDF

AMNIOTIC FLUID EMBOLISM NU3115 1 AIM & LEARNING OUTCOMES Learning outcomes: Students will be able to analyse AFE under the following headings: Incidence Pathophysiology Morbidity and Mortality Signs / Symptoms / Clinical Presentation and Progressio...

AMNIOTIC FLUID EMBOLISM NU3115 1 AIM & LEARNING OUTCOMES Learning outcomes: Students will be able to analyse AFE under the following headings: Incidence Pathophysiology Morbidity and Mortality Signs / Symptoms / Clinical Presentation and Progression Risk Factors Management Role of the Midwife - SD 2 INTRODUCTION Amniotic fluid embolism ranks as the 9th leading cause of direct maternal death in the most recent triennium (MBRRACE, 2015-18) Amniotic fluid embolism (AFE) remains a difficult condition to define, describe and understand, but it continues to be responsible for a significant proportion of maternal deaths (CMACE, 2011) 3 AFI REMAINS ONE THE LARGEST SINGLE CAUSE OF INDIRECT MATERNAL DEATHS IN THE UK / IRELAND ( MBRRACE 2015 - 17) INTRODUCTION Amniotic fluid embolism (AFE) https://www.youtube.com/watch?v=Ra-GtEDB2bQ https://www.uptodate.com/contents/amniotic-fluid-embolism AFE Foundation - https://afesupport.org/ The name of the condition is disputed Anaphylactoid syndrome of pregnancy -fetal tissue / amniotic fluid components -not always found in women who present with signs and symptoms attributable to AFE The term embolism almost implies an obstruction of the vessels as the mechanism of injury, when it is more complex than this, as will be discussed 5 ETIOLOGY Amniotic fluid embolism (AFE) is unpredictable –cause unknown Risk factors for the development of AFE are advanced maternal age, multiparity, male fetuses, and trauma. Induction of labour increases the risk of AFE. Fong (2015) found that women with cerebrovascular disorders and cardiac disease have 25 fold and 70 fold higher risk of AFE, respectively. Strong association of AFE with caesarean delivery, placenta preavia, eclampsia, placental abruption, polyhydramnios, dilatation and curettage, renal disease. Amniotic fluid and fetal components in the maternal circulation has been shown to create intense pulmonary vasoconstriction and bronco constriction. These effects are considered to be caused not only by physical obstruction but by the liberation of intense inflammatory cytokines reactant to the foreign material. Inflammatory mediators are also believed to trip the coagulation 6 and fibrinolytic pathways, creating a form of disseminated intravascular coagulation (DIC) syndrome EPIDEMIOLOGY The incidence of amniotic fluid embolism (AFE) is estimated at 1 case per 8000 to 30,000 pregnancies. Exact prevalence is not known due to inaccurate diagnosis and not reporting the nonfatal cases. Germany -AFE was the leading cause of death during parturition in 2011. AFE is identified as the leading direct cause of maternal mortality in Australia from 1 in 8000 to 1 in 80,000 deliveries. UK - estimated incidence is 1.9 per 10000 to 7.7 per 10000 births. USA AFE occurs in 2 to 8 per 100,000 deliveries and is the cause of maternal mortality between 7.5% to 10%. 7 PATHOPHYSIOLOGY Amniotic fluid is comprised of fetal urine and contains many cellular components, fetal hair, vernix and a variety of prostaglandins and leukotrienes. It may not be the actual presence of the amniotic fluid or its components, but the maternal (immune) response to these chemical mediators which ultimately determines whether the woman develops AFE It was initially proposed that there was a breach in the physical barrier between the maternal and fetal environments at the uterine trauma sites and the placental attachment site. However, these are unlikely sites of transfer if the uterus is well contracted. It is more plausible that small tears in the lower uterine segment and the veins in the endocervix are the entry sites during labour and birth. If the barrier between the amniotic fluid and 8 maternal circulation is broken, this causes amniotic fluid to enter the maternal circulation  PATHOPHYSIOLOGY The setting for amniotic fluid The hemodynamic result is acute embolism (AFE) - disruption of the pulmonary arterial obstruction, placenta-amniotic interface with dilatation of the right ventricle the subsequent entry of amniotic and the right atrium -significant fluid and fetal elements (such as tricuspid regurgitation. hair, meconium, squama, and mucin) into the maternal The right ventricular circulation. enlargement causes the Portals of entry may include intraventricular septum to bow placental attachment, into the left ventricle creating cervical veins, obstruction and systolic uterine surgical dysfunction, incisions. further raising pulmonary artery Upon entering - pulmonary arterial pressure and decreasing cardiac output. Hypoxemia and tree, intense pulmonary vasoconstriction occurs. May be hypotension lead to sudden associated with concomitant cardiovascular collapse 9 bronchoconstriction.  Normally, pregnancies are procoagulant, to begin with - increased levels of clotting factors X, IX, VIII, von Willebrand factor (VWF), and tissue factor pathway inhibitor (TFPI). The introduction of amniotic fluid and fetal elements trigger inflammatory mediators such as platelet-activating factor, tissue necrosis factor-alpha (TNF-alpha), interleukin-six, interleukin-one, phospholipase A2, endothelin, plasminogen activators, thromboplastins, and complement factors. The coagulation cascade and fibrinolytic systems are activated. Amniotic fluid in the maternal circulation activates platelet factor III, stimulates platelet aggregation, and activates clotting factor Xa. The superimposed pathologic activation of the coagulation and fibrinolytic pathways create severe coagulopathy. Disseminated intravascular coagulation (DIC) occurs in approximately 80% of patients with AFE. This may be immediate at the time of the cardiopulmonary collapse 10 or delayed. Bleeding may be severe, unrelenting, and fatal. 11 HISTORY AND EXAMINATION Classic history is -women in Medical history /history of late stages of labour become present illness of woman acutely short of breath + who sustains AFE may hypotension. reveal; Agitation / feeling of impending advanced maternal age, doom before onset of other multiple pregnancies, symptoms. placenta acreta, May experience seizures placenta abruption, followed by cardiac arrest. placenta praevia, Massive DIC-associated preeclampsia, haemorrhage follows /death. gestational Mostly die diabetes, polyhydramnios, within an hour of onset. 53% of amniocentesis, females -AFE present at time of amnioinfusion, delivery or even before it. mechanical rupture of 47% membranes, or surgery to present an average of nineteen the gravid uterus. 12 minutes after delivery.  The physical exam –show cardiovascular collapse with Haemorrhage may range from marked hypoxemia, hypotension and massive to minimal. cyanosis. Uterus frequently The classic triad of AFE is is atonic (83%) which further hypoxia, hypotension, and accentuates bleeding. Initial coagulopathy. Temperature bleeding -from vagina but may will be normal. also be first seen in surgical Funduscopic exam may reveal incisions. minute bubbles in the retinal Full-blown DIC -seen in approx arteries. 80% pts. Neurologic exam Tachypneic - classic usually reveals a dysphoric + holosystolic high-pitched encephalopathic patient. Tonic- murmur of tricuspid clonic seizures (10-50%) may regurgitation. Murmur is loudest at the complicate the picture. lower left sternal border and radiates to the right sternal 13 edge. ASSESSMENT No reliable definitive test for amniotic fluid embolism AFE Suspicion of AFE – suggested by sudden appearance of dyspnoea, dysphoria, hypotension, cardiovascular collapse, and coagulopathy following some action during the intrapartum period-, e.g., active labour, rupture of membranes, vaginal delivery, or caesarean section. AFE has also been seen during or after elective pregnancy terminations (induced or surgical). Initial evaluation for AFE is usually done during cardiopulmonary resuscitation. Evaluation is tailored to the two main system failures - hemodynamic and hematologic. Measurement of pulmonary wedge pressure, cardiac output, central venous pressure, pulse oximetry, arterial waveform, electrocardiography, and chest radiography should start the initial hemodynamic assessment.14  Coagulation screen to include Transthoracic echocardiography (TTE) or platelets, prothrombin time, partial transesophageal echocardiography (TEE) thromboplastin time, bleeding time, is essential to the diagnosis. fibrinogen, d-dimer, and fibrin Significant findings of AFE are right degradation products (FDPs). ventricle dilatation, hypokinesis, Metabolic and respiratory acidosis is tricuspid regurgitation, common. right atrial enlargement. Should be evaluated by an arterial blood gas – and end-tidal Early cardiac thrombi may be detected in carbon dioxide (etCO2) the enlarged right ventricle or right measurement. atrium. Highly associated with this syndrome is the bowing of the International society on thrombosis intraventricular septum into the left and haemostasis (ISTH) has a formal ventricle -creating left ventricular scoring system (10) determine the obstruction and systolic dysfunction. presence of DIC in pregnancy. The echocardiographic The score is appearance of this bowing resembles the based on platelet count, letter ‘D.’ international neutralization ratio Blood -obtained immediately for urgent (INR), and fibrinogen level. type and crossmatch, complete blood Scores of more than 3 count, metabolic screen, are indicative of DIC in pregnancy. 15 RISK FACTORS - TRANSMISSION Normally, the intact fetal membranes do not permit the entrance of the amniotic fluid in the maternal circulation. AFE occurs only when there is a breach in this barrier There are three routes where the normal barrier may breakdown. They include Endocervical veins, Uterine trauma sites Placental attachment site 16 17 CRITERIA FOR DIAGNOSING AFE Challenging - no single definitive test to clinch the diagnosis. Internationally - various standards have appeared defining AFE. American Society for Maternal-Fetal Medicine - a consensus symposium has created its criteria for AFE - requires the following: Sudden cardiopulmonary collapse, or hypotension (systolic blood pressure less than 90 mmHg) Presence of hypoxia (SpO2 less than 90%) DIC, according to ISTH definition Symptomatology either during labour or during placental delivery (or up to 30 minutes later) No fever 18 MANAGEMENT Management of acute AFE is -prompt and effective cardiopulmonary resuscitation of the mother + rapid evacuation of the fetus. The management of AFE still remains supportive rather than therapeutic with emphasis on 1. maintenance of oxygenation, 2. circulatory support 3. correcting coagulopathy 19 TREATMENT / MANAGEMENT Mother - securing the airway, effective ventilation, ideal fluid management, and the appropriate use of vasopressors. After intubation- large-bore intravenous catheters should be instituted for infusions. Pulmonary wedge catheters (Swan Ganz) measure left atrial and pulmonary artery pressures and cardiac output through thermal dilution. Pulmonary artery blood aspirants may reveal the presence of fetal components. Intra-arterial lines are useful to facilitate minute-to-minute pressure measurement and frequent arterial blood gas samplings. A central venous pressure line may assist in assessing right-sided preload. Urethral catheterization facilitates urine output documentation. Crystalloid fluids are generally given judiciously but must be limited 20 if coagulopathy ensues. MANAGEMENT 21  MANAGEMENT Copious fluid administration dilutes clotting factors making bleeding worse. So decision to move to vasopressors should be considered earlier as compared to significant bleeding from other etiologies. Vasopressors support - dopamine, dobutamine or epinephrine -may be switched to norepinephrine for persistent hypotension. Vasopressin may be added at this point to augment cardiac output. Ideally maintain mean arterial pressure (MAP) of more than 65 mmHg, a cardiac index of more than 2 L per meter square, an adequate urine output of 40-50 ml/hr, and a PaO2/FiO2 ratio of more than 250. Ventilation using inhaled nitric oxide assists in reducing RV afterload. 22 ITU Extracorporeal membrane oxygenation (ECMO) - used successfully for refractory cardiogenic shock secondary to amniotic fluid embolus. Patients may need to be transferred to tertiary facilities capable of ECMO. Red blood cells (pRBCs), fresh frozen plasma (FFP) platelets Cryoprecipitate contains concentrated clotting factors, including factor VIII, von Willebrand factor, and fibrinogen. Tranexamic acid is given for fibrinolysis. 23 OBSTETRIC MANAGEMENT Rapid birth of the fetus-caesarean section- over 23 weeks gestation. Ongoing resuscitation of the mother - anaesthetist / cardiac arrest team. CPR continues during emergency birth of the baby. Turn gravid uterus to the left - relieving aortocaval compression. Multidisciplinary team -initiate neonatal resuscitation - prepare SCBU -low Apgar score. Baby - rapid suctioning, intubation, and vascular access. Different procedures to alleviate the ongoing uterine haemorrhage - Uterine artery ligation or embolization has been documented with some success. Circumferential B-Lynch, Hayman, or Pereira compression sutures to compress the atonic uterus and staunch bleeding. Massive haemorrhage and atonic uterus - emergency hysterectomy 24 DIFFERENTIAL DIAGNOSIS Pulmonary embolism (PE) The differential diagnosis of a woman who sustains Peripartum cardiomyopathy complete cardiovascular Septic shock collapse during or close to Myocardial infarction the time of delivery and then subsequently develops Venous air embolism major haemorrhage should Eclampsia include: Anaphylaxis Cephalad spread of spinal anesthetic 25  Myocardial infarction, unless antecedent AFE can mimic pulmonary to the cardiac arrest would show typical embolus but an ongoing ST-T wave changes and elevation of serial coagulopathy is not seen in PE. cardiac enzymes. Postpartum cardiomyopathy would Bedside echocardiography would show likely have significant ST-T wave characteristic ventricular wall motion changes on electrocardiography, abnormalities of myocardial infarction. with left-sided congestive heart Venous air embolism usually presents with failure symptoms predominating. wheezing, gasping, and chest pain before Bedside echocardiography (TEE or the cardiovascular collapse. TTE) should make this differential Eclampsia would be suggested by with the classic right ventricular hypertension, oedema, proteinuria, dilatation and overload pattern headaches, or seizures before the and septal bowing into the left collapse. ventricle seen in AFE. Anaphylaxis -premonitory symptoms of Septic shock should show the wheezing, dyspnoea, rash, urticaria, and a classic systemic inflammatory period of hypotension before response syndrome (SIRS) picture cardiovascular decompensation. with - elevated or depressed body Cephalad distribution of spinal temperature and is unlikely to anaesthetic would present with elevated present with sudden sensory level, weakness of the upper 26 cardiovascular collapse. extremities, difficulty in speaking, dysphagia, bradycardia PROGNOSIS AFE is rare Mortality rate varies somewhere between 40 to 60% Maternal survival is uncommon, although the prognosis is improved with early recognition and prompt resuscitation. United Kingdom AFE registry has reported 37% mortality, and 7% of those who survived were neurologically impaired. Two-thirds of women surviving AFE are left with serious neurologic, pulmonary, cardiovascular deficits. Risk of recurrence is unknown. Successful subsequent pregnancies have been reported. The recommendations for elective caesarean delivery during future pregnancies to attempt to avoid labour are controversial. The mortality rate for the infant is slightly lower at approximately 30%. High risk of hypoxic-ischemic encephalopathy, cerebral palsy, 27 and other cognitive disabilities in survivors COMPLICATIONS The major complications for the mother who survive AFE are: Renal failure Infants delivered precipitously Prolonged respiratory failure with during maternal AFE frequently adult respiratory distress sustain hypoxic-ischemic encephalopathy (HIE). Myocardial infarction The usual result is a markedly Cardiomyopathy cognitively impaired child who Congestive heart failure may go on to have chronic Left ventricular systolic epilepsy, motor impairment, dysfunction and developmental delay. Prolonged coagulopathy Liver failure Seizures Anoxic encephalopathy Other cognitive impairments 28 PATIENT EDUCATION Amniotic fluid embolism is a very severe condition, Sudden onset although Few preventive measures that could be taken beforehand. To prevent AFE trauma to the uterus must be avoided during manoeuvres such as insertion of a pressure catheter or rupture of membranes. Incision of the placenta during caesarean delivery should also be avoided if possible 29 ENHANCING HEALTHCARE TEAM OUTCOMES Coordination between The very complicated nature obstetricians, maternal-fetal of the sudden onset of specialists, anaesthetists, cardiovascular collapse and midwives, neonatologists, subsequent severe haematologists, respiratory coagulopathy in the mother, therapists, and neonatal as well as the need for intensive care unit nurses is neonatal resuscitation of the mandatory for successful infant, make AFE challenging maternal and infant survival to any interdisciplinary team. outcomes 30  ROLE OF THE MIDWIFE IN AFE Individual activity: Now that you are aware of the medical management of AFE critically analyse the role of the midwife in caring for a woman presenting with this condition using the following headings: Aims of care Recognition of this scenario as an emergency – what to do? Reference to EC Directives/ABA Scope of practice Individualized care Rationale for all actions/observations Psychological care of woman and partner Debriefing 31 Reflection  SUMMARY OF KEY SIGNS AND SYMPTOMS Fetal compromise due to uterine hypoxia causing uterine hypertonia and in addition placental haemorrhage and maternal collapse Respiratory: cyanosis, dyspnoea, respiratory arrest Cardiovascular: tachycardia, hypotension,pale clammy skin/ shivering,cardiac arrest Haematological: haemorrhage from placental site, coagulation disorders, DIC Neurological: restlessness,panic, convulsions, pain less likely. 32 CONCLUSION AFE is a rare but potentially catastrophic syndrome Mortality is high (20–40%) but is improving with better management Classic presentation: acute severe hypoxia, cardiovascular collapse, mental status changes, and DIC. The pathophysiology of AFE remains controversial If AFE occurs while the mother is still pregnant, immediate birthing of the baby may result in survival 33  CONCLUSION There is clear evidence that amniotic fluid and its components enter the maternal venous circulation. This may result in mechanical obstruction in the pulmonary capillaries and/or incite a systemic response by the mother which is similar to anaphylaxis or sepsis. Every obstetric care provider should be familiar with this clinical syndrome and consider the diagnosis early in its presentation. Early diagnosis and initiation of treatment are paramount Treatment includes cardiovascular and respiratory resuscitation (with intubation/ventilation, crystalloids, vasopressors) in order to optimize cardiac output, and correction of coagulopathy. Practice emergency drills for maternal resuscitation in the 34 clinical area - recommended RESEARCH 35 REFERENCES 1Fong A, Chau CT, Pan D, Ogunyemi DA. 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