Amniotic fluid embolism, shock, DIC - diagnosis, prevention, therapy

Amniotic fluid embolism
Amniotic fluid embolism is the penetration of amniotic fluid into the mother's circulation with subsequent blocking of the pulmonary canal and the development of pulmonary hypertension. This is a very serious birth complication that occurs rarely (1:80,000 births). The amniotic fluid enters the maternal circulation, where, similar to embolism of other etiology, shock develops. This condition requires immediate obstetric and anesthetic care. Different types of placental insertion – normal decidua, placenta accreta, placenta increta, placenta percreta

Causes

 * Premature separation of the placenta;
 * placenta accreta ;
 * insertio velamentosa umbilicalis with a short umbilical cord (tear in the membranes);
 * transplacental caesarean section ;
 * surgery in the third stage of labor ;
 * dead fetus ;
 * preeclampsia ;
 * throat injury.

Clinical picture
In the first stage, the symptoms of amniotic fluid embolism are the same as those of thromboembolism, namely cardiopulmonary failure in various ways. There is significant shortness of breath and hypotension with pO 2 falling below 80%. If the patient survives, DIC symptoms develop within 15 minutes. Respiratory distress syndrome and acute renal failure develop, and the patient usually succumbs to this. Based on the developing clinical picture, we try to terminate the pregnancy as quickly as possible. Amniotic fluid embolism description

Diagnosis
Definitively, amniotic fluid embolism is usually diagnosed post-mortem, based on findings in the lung tissue, where lanugo, fetal skin epithelium, and meconium bodies are typically found.

Prophylaxis and treatment
For prophylaxis, similar general principles are recommended as for thromboembolism (specific procedures are not known). The treatment is also similar to thromboembolism, complete DIC therapy as soon as possible, hypotension therapy, prophylaxis of renal failure and convulsions. In the case of an incipient clinical picture of DIC, we quickly provide a blood reserve.

Therapeutic procedure

 * 1) Presence of obstetrician, anesthetist.
 * 2) Blood sampling for hemocoagulation examination and lung amylase examination (statim), order a deleucotized erythrocyte mass.
 * 3) Sometimes necessary analgosedation/muscle relaxation with artificial pulmonary ventilation with immediate inclusion of PEEP (end-expiratory pressure up to 10 cmH 2 O (1.0 kPa)).
 * 4) Insertion of central venous catheter, pulmonary catheter and invasive measurement of arterial pressure.
 * 5) Management of hypotension: crystalloid solutions with dobutamine and norepinephrine titration.
 * 6) Nootropics – piracetam in a dose of 12 g/24 h.
 * 7) Neonatal intensive care for newborns.

shock
In obstetrics, we mainly encounter blood loss, which can lead to hypovolemic shock. In pregnancy, blood loss also conditions (in addition to other circulatory effects) a disorder of the uteroplacental circulation with the development of intrauterine fetal distress.

Obstetric causes of hypovolemic shock

 * In pregnancy
 * abortion ;
 * mole hydatidosa ;
 * ectopic pregnancy ;
 * placenta praevia ;
 * premature separation of the bed.


 * Intrapartum causes of hypovolemic shock
 * placenta praevia ;
 * premature separation of the bed;
 * uterine rupture.


 * In III. during labor and postpartum
 * birth injury;
 * bed separation disorder;
 * cotyledon retention;
 * Varicose veins of the vulva ;
 * uterine atony ;
 * coagulopathy.

All other extragenital sources of bleeding should be taken into account in the differential diagnosis.

Clinical stages of shock

 * 1st stage – compensation
 * The body compensates for losses of 500-1200 ml (10-25%) (by increasing cardiac output, centralizing volume, moving fluids into the intravascular space), the woman is pale, sleepy, sometimes restless. Tachycardia present, normal or slightly lower BP, diuresis is normal, shock index 1.


 * 2nd stage – decompensation (reversible)
 * Losses of 25-30%, organ flow decreases (mainly through the kidneys and liver), oliguria or anuria (acute renal insufficiency) occurs. Hypotension develops, rapid to thready pulse, shock index around 1.5.


 * 3rd stage – irreversible stage
 * Metabolic acidosis (lactate, acetoacetate, ...), MODS.

Therapy
General principles of stopping bleeding (operative, mediacamentous). Ensuring vital functions, possibly cardiopulmonary resuscitation, release of airways (or intubation), oxygen therapy , intravenous access, shock position, temperature maintenance, permanent monitoring.

Special measures – volume replacement with crystalloid, colloid or plasma expander (Haemaceel), always transfusion in the 2nd and 3rd stages.

Disseminated intravascular coagulation
Disseminated intravascular coagulation is a coagulopathy, which in obstetrics is one of the most common causes of maternal death (after thromboembolic complications). DIC is one of the most serious syndromes in which coagulopathy manifests.

Pathogenesis
There are three key moments in the pathogenesis of disseminated intravascular coagulation:


 * 1) disruption of hemocoagulation balance ;
 * 2) excessive thrombin activity;
 * 3) dysregulation of plasmin activity.

In the fully developed state of DIC, there is uncontrolled activation of thrombin caused by the release of tissue factor into the circulation. Tissue factor is released from traumatized as well as non-traumatized tissues. In traumatized tissues, it is released from hematomas, exposed tissue, endothelium and leukocytes. In non-traumatized tissues, tissue factor is released from cells into the circulation under the influence of cytokines or endotoxin. In this case, DIC is part of SIRS, in sepsis. Systemic intravasal coagulation and numerous microthrombi occur. Subsequently, thrombolysis is activated (high D-dimers ), microthrombi damage platelets and they are absorbed in the spleen. Thrombocytopenia occurs. Hemorrhagic diathesis and MODS occur.

Classification of DIC in obstetrics

 * 1) Acute DIC :
 * 2) * the prothrombotic stage is short, goes unnoticed;
 * 3) * nausea, shortness of breath, cyanosis ;
 * 4) * usually manifests itself in unstoppable bleeding ;
 * 5) * if we do not intervene immediately, there will be a breakdown of the endothelium and uncontrollable bleeding into the mucous membranes and skin.
 * 6) Chronic DIC :
 * 7) * it can take place covertly, we can find it in the laboratory − ↓ platelets, ↓ fibrinogen, ↓ antithrombin, ↑ aPTT , ↑ D-dimers, ↑ FDP;
 * 8) * may arise as part of SIRS or manifest as MODS;
 * 9) * is the risk of thromboembolic complications;
 * 10) * bleeding starts more slowly;
 * 11) * if the cause persists ( abscess, infection), decompensation soon occurs and then acute DIC develops.

Risk factors
Risk factors mainly include:


 * eclampsia, thrombophlebitis in history;
 * HELLP syndrome ;
 * coagulation disorders, hemolytic states;
 * retention and stillbirth ;
 * repeated revisions of the uterine cavity;
 * septic birth (miscarriage), placenta accreta, amniotic fluid embolism;
 * mole hydatidosa ;
 * obesity.

Diagnostics
As a guide, we perform laboratory tests in the delivery room (Lee White, thrombin test) - if positive, we do not wait for the laboratory and deal with it.


 * Lee White test: roughly indicative, at the bedside – a coagulum forms in the test tube within 1−2 minutes.
 * Thrombin time: evidence of fibrinogen, it can also be done at the bedside - add 2 ml of blood to a tube with lyophilized thrombin, if there is fibrinogen in it, it will clot within 1 minute, if it is not, the blood will not clot.
 * Laboratory tests: INR, aPTT, antithrombin III, fibrinogen, platelets, FDP, D-dimers.


 * Differential diagnosis


 * Bleeding from a birth injury;
 * various types of thrombocytopenia;
 * von Willebrand's disease ;
 * coagulopathy in HELLP syndrome.

Prevention

 * 1) Primary prevention :
 * 2) * ambulatory detection of all conditions where there is a coagulation disorder - especially AT III deficiency, proteins C and S, Leiden mutation of factor V, homozygous MTHFR 677TT defect, etc., also, for example, antiphospholipid syndrome.
 * 3) Secondary prevention :
 * 4) * antenatal application of LMWH in pregnant women at higher risk (mainly in abortions and surgeries);
 * 5) * before sc, LMWH is routinely given to women in the following conditions: obesity, age over 30 years, hereditary thrombophilia, venous thrombosis in the anamnesis, preeclampsia, DM, previous abdominal surgery, placenta praevia, placental abruption, also during spontaneous stillbirth, maternal fever.

Therapy
If DIC is suspected, energetic intensive treatment is appropriate, if possible in a team (hematologist, anesthesiologist, internist, ...). The principle is to remove the provoking cause, regulate thrombin activity, maintain hemostasis.


 * Acute DIC


 * Order frozen plasma and erysma immediately ;
 * we will take blood for hemocoagulation examination;
 * first measure – we administer AT III – a bolus of 1,000 units IV and then a continuous infusion of another 1,000 units;
 * then we give heparin ;
 * circulating plasma replacement (dextrans and plasma expanders are contraindicated - they interfere with platelets);
 * we administer fibrinogen if its plasma level falls below 1 g/l.


 * Chronic DIC


 * Combination of AT III with heparin;
 * activated human protein C is newly used.