Amniotic fluid embolism (AFE) is a syndrome in which amniotic fluid enters the maternal circulation during labor and causes a series of severe symptoms such as pulmonary embolism, shock, and DIC. clark et al. suggested that AFE is more likely to be an allergic reaction of the mother to fetal components than embolism, and suggested the term anaphylactoid syndrome ofpregnancy. syndrome ofpregnancy). The most serious complication of cesarean delivery is amniotic fluid embolism, the incidence of which is not high, but when it occurs, the mortality rate is extremely high, and mastering the emergency treatment of amniotic fluid embolism is indeed a basic skill necessary for anesthesiologists.
Powder-stained keratinized epithelium in the lung capillaries at autopsy, this is the epidermal cells of the fetus shed in the amniotic fluid
I. Etiology
The tangible substances in the amniotic fluid enter the maternal blood circulation and cause a series of pathophysiological changes. The tangible substances in amniotic fluid include: flat epithelium, fine hair, fetal fat, meconium, mucin, etc.
The causative factors are as follows.
1)The majority of menstruating mothers;
2) Most of them have a history of premature rupture of membranes or artificial rupture of membranes;
3) Commonly caused by strong contractions or improper application of oxytocin
4) Early placental abruption, placenta praevia, uterine rupture or surgical delivery are prone to amniotic fluid embolism;
5) Stillbirth may increase the incidence of amniotic fluid embolism. The conditions for amniotic fluid to enter the maternal circulation are that the fetal membranes are broken; there are strong uterine contractions; and the blood vessels are open. The pathways of entry are endocervical veins and lower uterine veins; placental marginal venous sinuses; and injured uterine blood sinuses, such as uterine rupture and cervical laceration.
II. Pathophysiology
1.Anaphylactic shock and sudden death
Shock caused by amniotic fluid embolism can originate from two factors, one is allergic anaphylaxis, because the amniotic fluid contains tangible substances from the fetus, including epithelium, mucus, fetal fat and fetal stool, which is a kind of foreign body protein, as an antigen once it enters the maternal blood circulation, it can cause allergic reactions and anaphylaxis; the second is that there is a fraction of amniotic fluid into the blood can cause pulmonary vascular embolism. In addition, amniotic fluid still contains chemically active substances that can make vasospasm, such as prostaglandins, 5-hydroxytryptamine, etc., which can cause pulmonary vasospasm, thus causing pulmonary hypertension, so that the left atrial blood volume is significantly reduced, so the left ventricular blood discharge is also significantly reduced, causing peripheral circulatory failure, blood pressure drop, also known as this cardiogenic shock. At present, it is believed that these two types of shock are likely to exist simultaneously. In addition, the clinical also found a few patients in the onset, often in a shriek or convulsions after sudden death, the cause of sudden death more from cardiac arrest.
2.Acute respiratory and circulatory failure
1) Acute respiratory failure
After the amniotic fluid enters the maternal circulation, the contents of the amniotic fluid can lead to mechanical embolism of the pulmonary artery, but also stimulate the lung tissue to produce and release PGF2α, 5-hydroxytryptamine, leukotrienes and other vasoactive substances to cause pulmonary vasospasm, leading to acute pulmonary hypertension, pulmonary hypertension and pulmonary perfusion is significantly reduced, ventilation and blood flow disproportionate, lung tissue is severely hypoxic, pulmonary capillary permeability increases, fluid This leads to interstitial pulmonary edema and even pulmonary hemorrhage, resulting in clinical manifestations of acute respiratory failure such as cough, dyspnea and pulmonary rales.
2) Acute circulatory failure
In recent years, Clark analyzed the circulatory dynamics of patients with amniotic fluid embolism through pulmonary artery catheter and proposed a new concept of bidirectional pathophysiology. In the past, it was believed that the circulatory disturbance caused by amniotic fluid embolism was mainly pulmonary hypertension and deep hypoxemia due to impaired ventilation, which could lead to acute respiratory failure, but also acute right heart failure due to increased right heart load, but not left heart failure. This reaction is extremely dangerous but transient. If the patient can survive this acute phase, the second phase of hemodynamic disturbance may occur, which mainly includes left heart failure and various degrees of secondary pulmonary artery pressure elevation, usually only a mild increase and pulmonary edema. Therefore, the management principles are also different from the early stage.
3.Acute obstetric DIC
The amniotic fluid contains not only rich tissue thrombin, but also factor X-activating substances, lung surface active substances and trypsin in feces, which have pro-coagulant activity. As a result, a large amount of coagulation factors and platelets are consumed, leading to bleeding in many parts of the body, and bleeding does not stop and does not coagulate.
4.Multi-organ damage
DIC and other pathological changes often involve multiple organs of the mother, with shock kidney, acute tubular necrosis, extensive hemorrhagic hepatic necrosis, lung and spleen hemorrhage, etc. being the most common. The clinical manifestation is acute hepatic and renal failure. When two or more important organs fail simultaneously or successively, it is called multi-system organ failure (MSOF), and its morbidity and mortality rate is almost 100%.
Clinical manifestations
The typical amniotic fluid embolism seen clinically can be divided into three periods.
First period Arterial hypertension and cardiopulmonary failure period (shock period)
Heart failure and acute respiratory failure due to pulmonary hypertension, and anaphylactic shock due to allergic reactions are newly considered. At the end of the first stage of labor or the second stage of labor when the contractions are strong, and a short time after the delivery of the fetus, the mother suddenly appears agitation, chills, nausea, vomiting, shortness of breath and other aura symptoms; followed by choking, cyanosis, dyspnea, increased heart rate and progressive aggravation, pale face, cold extremities, decreased blood pressure, coma and convulsions may occur. The lungs can be auscultated with wet mouth rales. In severe cases, the onset of the disease is rapid, with only a shriek or a yawn, blood pressure disappears, respiration and cardiac arrest, and death occurs rapidly in about 1/3 of cases, and the other 1/3 die of cardiopulmonary failure within about 1h.
The second period of coagulation dysfunction (bleeding)
When the mother has passed the stage of cardiopulmonary failure and shock, about 1/3 of the survivors develop coagulation dysfunction, the initial stage is rapid clotting of blood when blood is drawn, which can soon develop into the hypo-coagulation stage, with uncontrollable systemic extensive bleeding, massive vaginal bleeding, bleeding from surgical incisions and wounds, bleeding from the skin and mucous membranes all over the body, and even gastrointestinal hemorrhage. Some patients may also develop hemolysis, a rapid decline in hemoglobin, a progressive rise in fibrin and bilirubin, and hemoglobinuria.
In the third period of acute renal failure, due to circulatory failure causing renal ischemia, the thrombus formed in the first stage of DIC blocks the small blood vessels of the kidney, and in the later stage of maternity, oliguria, anuria and uremia may appear, causing renal ischemia and hypoxia, resulting in organic damage to the kidney. Eventually, multiple organ failure may occur, mainly in the brain, liver and other important organs within a short period of time.
In typical cases, the symptoms may appear in sequence, but due to individual differences in patients, they may not appear at the same time in each patient, nor do they have to appear in sequence, which should be taken seriously in the clinical treatment of patients. In atypical cases, the symptoms may only appear as shock or DIC.
Diagnosis
1.AFE National Clinical Diagnostic Criteria:
① Maternal acute hypotension or cardiac arrest;
(2) Acute maternal hypoxia, manifested as dyspnea, cyanosis or respiratory arrest;
③ Maternal coagulation disorder, laboratory data indicating intravascular fibrinolysis, or unexplained severe bleeding;
④The above symptoms occur during cervical dilatation, uterine muscle contraction, labor, cesarean delivery, or within 30 minutes after delivery;
⑤ Lack of other meaningful explanations for the above symptoms.
2. Laboratory tests.
1)The diagnosis can be confirmed by finding the amniotic fluid component by taking blood from the pulmonary artery or inferior vena cava;
2) Laboratory tests for DIC based on.
① Platelets <100×109/L or progressive decline;
②Fibrinogen <1.5g/L;
③Prothrombin time >15 seconds or more than 3 seconds for control group;
④Fisetin paraclotting (Triple P) test is positive;
⑤ Coagulation time >30 minutes by test tube method (normal 8-12 minutes);
⑥Blood smear with broken red blood cells. The diagnosis of DIC can be made only if three of the above tests are positive, and a simple blood clotting time observation test can be used if there is no condition to measure fibrinogen, which is positive if it is >16 minutes. The method is: take 5ml of venous blood in a test tube to observe, such as 6-10 minutes clotting, suggesting normal fibrinogen value; 11-15 minutes clotting, fibrinogen value > 1.5g/L; 16-30 minutes clotting, fibrinogen value of 1.0-1.5g/L; such as > 30 minutes, fibrinogen value < 1.0g/L.
3, X-ray radiographs: typically, bilateral diffuse dotted infiltrative shadows are seen, distributed along the periportal lung with right heart enlargement and mild pulmonary atelectasis.
V. First-aid treatment
1.Resuscitation organization procedure
1) 3 sets of intravenous channels must be maintained
①Fast transfusion of fresh blood;
②Infusion of dobutamine and interhydroxylamine.
2) Dedicated person to host resuscitation.
① a group of personnel around the patient for record-keeping;
② a group of close observation of the condition;
③ telephone contact test results;
④Tell the family.
3) Urgent hysterectomy in case of emergency or hemorrhage
2.Emergency measures
The key to successful rescue of amniotic fluid embolism lies in early diagnosis and early treatment, which is summarized as follows.
1) Anti-allergy: high-dose corticosteroids should be applied in case of anaphylactic shock, often hydrocortisone is used, 500mg instantly, generally 1000-2000mg daily, intravenously. However, hormone can inhibit the function of reticuloendothelial system, so that the activated coagulation factors can not be cleared in time and aggravate DIC, so repeated application should be noted that it is better to apply this drug on the basis of treatment with heparin.
2) Oxygenation: should strive to line positive pressure continuous oxygen, at least with mask oxygen, nasal catheter oxygen administration is not effective. When available, artificial ventilator can be used. Oxygen supply can reduce pulmonary edema and improve cerebral hypoxia and other tissue hypoxia.
3) Relief of pulmonary hypertension: oxygen supply can only solve alveolar oxygen pressure, but not pulmonary blood flow hypoperfusion. Pulmonary hypertension must be relieved as early as possible to fundamentally improve hypoxia and prevent acute right heart failure, peripheral circulation failure and acute respiratory failure. Commonly used drugs include the following.
(1) Aminophylline: It has the effect of relieving pulmonary vasospasm, dilating coronary artery and diuretic, and also relieving bronchial smooth muscle spasm. The dose is 0.25~0.5g added to 20ml of 10%~25% glucose solution and injected intravenously.
(2) poppy bases: the coronary vessels and pulmonary and cerebral vessels are dilated, is the ideal drug to lift pulmonary hypertension. The dose is 30-60mg added to 20ml of 25% glucose solution and injected intravenously.
(3) Atropine: relieves pulmonary vasospasm, also inhibits the secretory function of bronchus and improves microcirculation. The dose is 0.5~1mg, intravenous injection, every 10~15 minutes until the symptoms improve.
(4) Phentolamine: release pulmonary vasospasm, the dose is 20mg added to 250ml of 10% glucose solution, intravenous.
(4) Anti-shock: Shock caused by amniotic fluid embolism is complicated and related to various factors such as allergy, pulmonary origin, cardiogenic origin and DIC. Therefore, the treatment must be considered comprehensively.
(1) Expansion of blood volume: Insufficient effective blood volume exists in shock, and blood volume should be expanded as early as possible and as soon as possible, but improper application is very likely to induce heart failure. If possible, it is best to use a pulmonary artery float catheter to measure the pulmonary capillary wedge pressure (PCWP) and monitor the cardiac load while replenishing blood volume. If PCWP measurement is not available, fluids can be directed according to central venous pressure. Regardless of the monitoring method used, 5 ml of blood should be drawn while intubating for a blood sedimentation test, smear staining to look for amniotic fluid components, and relevant DIC laboratory tests. The choice of volume expansion fluid should start with more dextran-40 500-1000ml, intravenous drip, and those with blood loss should be supplemented with fresh blood and balance fluid.
(2) Correction of acidosis: For the first time, 100-200ml of 5% sodium bicarbonate can be given, or according to the formula: sodium bicarbonate (g)=(55-measured CO2CP)×0.026×kg body weight, first inject 1/2 to 2/3 of the calculated amount. it is better to do arterial blood gas and acid-base determination, and give the drug according to the imbalance.
(3) Adjust the vascular tension: shock symptoms are acute and serious or blood volume has been replenished but blood pressure is still unstable, vasoactive drugs can be used, commonly used dopamine 20-40mg added to glucose solution within 500ml, intravenous drip, can ensure the blood supply of important organs.
Prevention
Strictly grasp the indications for cesarean delivery In recent years, the rate of cesarean delivery has been high in hospitals all over the country, but obstetricians should still try their best to grasp the indications for surgery. During cesarean section, the surgical procedure should be standardized and gentle to prevent laceration of the uterus. After cutting the uterus and exposing the amniotic sac, a small incision should be made and as much amniotic fluid as possible should be sucked out before delivering the fetus. This can reduce the chance of amniotic fluid entering the open blood sinus.