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 ~ Amniotic Fluid Embolism ~   § Background: Recently, the term anaphylactoid syndrome of pregnancy 
has been proposed instead of AFE (amniotic fluid embolism), to better 
characterize this condition as a multisystemic reaction to toxins rather than an embolic 
phenomenon.   § Incidence: z True incidence of AFE: may 
not be known, 1/8000 to 1/83000 deliveries z Growing 
awareness of the syndrome, rather than a true increase in incidence or 
idiosyncrasies in obstetric practice, is responsible for these difference.s   § Mortality: z AFE constitute 
the leading cause of mortality during labor and the first few postpartum hours. Maternal death usually occurs because of sudden cardiac 
arrest, hemorrhage due to coagulopathy, or acute respiratory distress syndrome, and 
multiple organ failure z 5% to 18% of all maternal 
deaths are due to AFE. z 7.8 to 12 deaths per million 
births z For women diagnosed as having 
AFE, mortality rates ranging from 26% to 86% have been reported.   § Pathophysiology: z Anaphylaxis plays a role in 
the syndrome. z Clinically, the reaction to 
AFE comprises three distinct phases. Besides, the syndrome seems to have a logarithimic presentation with 
decreasing intensity, frequency, and mortality as time elapses from the 
onset of symptoms. If a patient survives with or without intervention, 
the morbidity and mortality are dramatically lower.   Amniotic fluid enters the venous systemic circulation, for reasons not completely known. z The first phase: Cardiogenic and noncardiogenic pulmonary edema Intrapulmonary shunting Bronchoconstriction Desaturation 1). Blue phase: respiratory, including respiratory 
distress and cyanosis Decreased coronary blood flow Decreased inotropism Decreased cardiac output Pulmonary congestion 2). White phase: hemodynamic, with pulmonary edema and 
shock 3). Neurologic, including seizures, confusion or coma ø These 
presentations can occur separately or in combination, and indifferent degrees Amniotic fluid enters the arterial systemic circulation z The second phase: Thromoplasins1). Intravascular coagulopathy 2). Red phase: hemorrhage ø Of patients who 
survive the initial acute cardiorespiratory insult, 40% to 50% enter 
  
    
      
        the second phase. In some women, this may be the 
        first and only clinical manifestation. z The third phase: Gray 
phase  The acute symptoms are 
over and tissue injury (brain, lung, or renal) is for 
  the most part already established.  During this 
convalescent period, which may last weeks, affected patients 
  can die as a result of severe lung or brain injury, 
  multisystemic organ failure, or infections.  Fetal hypoxia, fetal 
bradycardia, or fetal death may follow as a result of 
  systemic hypotension.   § Diagnosis: z Establishment of diagnosis of 
AFE: ~ by a pathologist Finding in maternal tissue of epithelial squamous cells, 
lanugo hair, fat 
  derived from vernix caseosa, mucin derived from infant’s 
  intestinal mucus, or bile derived from meconium. z Presumption of diagnosis of 
AFE: ? Symptoms/signs and their 
temporal relationship: Eg. sudden onset of respiratory distress, cardiac collapse, 
seizures, 
  
    
      
        unexplained fetal distress, and abnormal bleeding ‚ Clinical 
  conditions associated with AFE: - Onset of labor 
    
      - Rupture of membranes - Fetal death - Trauma - Uterine overdistension by multiple gestation, 
      polyhydramnios, or fetal macrosomia ƒ Aids for diagnosis 
  of AFE: (see table 2) z Differential diagnosis of AFE: 
  
    | Coagulopathy/bleeding: Uterine atony Placental abruption Retained products of conception Urogenital tract laceration Sepsis |  
    | Fever: Sepsis Pulmonary thromboembolism Thyroid storm |    § Management: z Prompt and aggressive 
treatment of an acutely ill pregnant patient, regardless of the cause: · Write down the time. Call 
for help. Get code cart to the room. Ask relatives to step 
  outside the room or better yet, ask somebody to escort 
  them. · Airway patency. 
  Check and maintain patency. Start O2 via the quickest way avaliable · Breathing. Check 
  for spontaneous respiration. Evaluate breathing effort. Prepare for intubation. Proceed when possible. · Check pulse and blood 
  pressure. If none registered, begin CPR and order somebody to say the time out loud. Place defibrillator pads ASAP. 
  Obtain EKG tracing. Prepare for defibrillation. Call local Code Team. · Displacement of 
  the patient hips or the uterus to the left will improve venous return and uterine blood flow. · Endovascular access: - Place 2 large-bore (ideally 14 or 16) peripheral IV lines - Obtain at least 40 mL of blood for laboratory samples. (More if patient is febrile to touch, for cultures) - Do a bedside glucose if arrest not witnessed. Tell 
  glucose results out loud · Fluid, fetus, and 
  Foley: - Begin crystalloids in both sides, full open. - Monitor the fetus. - Place Foley catheter. Keep a urine sample. Quantify 
  amount. Notify others if blood 
    
      present. · Good or go: - Prepare the team caring for the patient for the 
  performance of a bedside C/S. - Ask for the time since arrest called and proceed if 
  deemed necessary. - If the situation is “good” (or improving) defer; if 
  “not good” go ahead and proceed 
    
      to deliver the infant. z Medications: ? To maintain systolic blood 
pressure ³ 90 mmHg, with acceptable 
  peripheral organ perfusion (manifested by urine output ³ 
  25 mL/hour) and to maintain patient’s sensorium:  Crystalloids 
  
    
       Inotropics (rapid 
      digitalization + b -adrenergics)  Pressors 
      (ephedrine, dopamine, dobutamine, norepinephrine infusions) ø After 
      hypotension has been corrected, fluid therapy should be restricted to maintenance levels, to minimize pulmonary edema due to 
      developing ARDS.  Corticosteroids 
      (hydrocortisone 500 mg iv q6h) ‚ To maintain arterial 
  PO2 > 60 mmHg or hemoglobin 
  saturation ³ 90%:  As in any other 
conditions when oxygenation and airway patency 
  
    
      may be compromised due to seizures, shock, or severe 
      respiratory distress, securing an airway through endotracheal 
      intubation is advisable. 1) Mechanical ventilation and high levels of fractional 
      inspired oxygen (FIO2) When still poor oxygenation despite of FIO2 > 
      0.6 2) Mechanical ventilation and positive end-expiratory 
      pressure (PEEP) ƒ To correct coagulation 
  abnormalities:  Packed red blood 
  cells 
    
       Fresh frozen 
      plasma  Cryoprecipitates: - Rich in both fibrinogen and fibronectin, the latter 
      facilitating the uptake of 
        cellular and particulate debris (such as amniotic 
        fluid contents) from the blood via the reticuloendothelial system  Platelets  Oxytocin and 
      other uterotonics for uterine atony ø The shock seen 
      in these patients is out of proportion to the amount of bleeding, so vasopressors are an indicated adjunct to blood 
      replacement. ø If the patient 
      has an epidural catheter, it is prudent to remove it as soon as possible. However, if bleeding occurs around the device, it may 
      be better to leave it in place to tamponade the site until further diagnostic testing. 
      After removal of the catheter, the patient should be monitored closely for any signs 
      of subarachnoid or epidural hemorrhage.   § Prognosis: z Data gathered from the 
  National AFE Registry: - Maternal mortality rate: 61% - Rate of survival without neurologic sequelae: 15% - Rate of survival in the presence of maternal cardiac 
arrest: 7.5% Only 8% of those survivors were without neurologic 
impairment. Neonatal survival rate: 68%, with only 32% having normal 
neurologic outcome - Neonatal survival rate: 79% Only 50% of the surviving infants were neurologically normal. The infant’s prognosis was adversely affected by maternal 
cardiac arrest. z Data from a recently 
published population-based study from California: - Maternal survival rate: 73.6% Intact maternal survival rate: 87% - Neonatal survival rate: 95% Intact neonatal survival rate: 72%   § References: 1. Amniotic fluid embolism: an update. Alfredo Gei, MD, and 
Gary DV Hankins, MD. Contemporary OB/GYN Jan. 2000: 53-62   Filename: Amniotic Fluid Embolism |