Norms and pathology criteria
In obstetric practice, the volume of permissible blood loss directly depends on the mode of delivery.
- Physiological blood loss: in vaginal delivery, it ranges from 300 to 500 ml.
- In cesarean section (CS): the norm increases to 750–1000 ml.
- In surgeries involving hysterectomy: elective CS with hysterectomy is accompanied by a loss of about 1500 ml, while emergency hysterectomy involves up to 3500 ml.
Massive bleeding is considered when a woman loses over 1000 ml of blood, more than 15% of the circulating blood volume (CBV), or over 1.5% of body weight.
Bleeding is recognized as life-threatening under the following conditions:
- Simultaneous loss of 1500–2000 ml (25–35% of CBV).
- Loss of 50% of CBV within 3 hours or complete loss (100% of CBV) within 24 hours.
- High rate of blood loss: 150 ml/min (or 1.5 ml/kg per minute) for 20 minutes or more.
Main causes
Massive obstetric hemorrhages rank 2nd to 3rd in the structure of maternal mortality. Their development is caused by:
- Placental abruption (both normally situated and placenta previa).
- Placenta accreta or partial morbid adherence of placental tissue.
- Uterine atony and hypotonia.
- Uterine rupture.
- Amniotic fluid embolism.
- Congenital or acquired defects of the hemostatic system.
Methods for estimating blood loss volume
Accurate calculation of lost blood is critically important for prescribing adequate infusion therapy. Relying solely on visual assessment is dangerous: the error reaches 30–50%.
To obtain objective data, the following methods are used:
- Graduated container. Allows collection of shed blood, but does not account for the volume remaining in the placenta (about 150 ml). Results can be distorted by admixtures of urine and amniotic fluid.
- Gravimetric method. Weighing surgical materials (pads, wipes) before and after use. The margin of error is up to 15% due to the absorption of amniotic fluid.
- Acid hematin method. Using radioactive isotopes (labeled red blood cells) to calculate plasma volume. This is the most accurate, but technically complex method requiring special equipment.
Important: Due to measurement errors of any kind, the physician's primary guide remains the patient's individual systemic response.
Hemorrhagic shock and its pathogenesis
Hemorrhagic shock is a state of multiple organ failure caused by low cardiac output syndrome and tissue hypoperfusion. In obstetrics, its clinical course is greatly aggravated by pain (in case of inadequate pain relief).
Several stages of shock development are distinguished:
- Compensation stage (loss > 15% of CBV). The sympathetic nervous system is activated: catecholamines, ADH, and angiotensin are released. This causes arteriolar spasm, increased heart rate and myocardial contractility, and sodium and water retention. Transcapillary fluid shift from tissues to blood vessels begins (lasts up to 40 hours). Due to lactate accumulation, the respiratory center is stimulated, resulting in hyperventilation.
- Decompensation stage (loss > 30% of CBV). Systolic blood pressure drops below 90 mm Hg. Prolonged stress triggers lipolysis and glycogenolysis, with escalating anaerobic metabolism and lactic acidosis. A drop in tissue pH blocks vascular spasm: arterioles dilate, and blood pools in the microvasculature. The endothelium is damaged, cardiac output drops, and DIC syndrome starts.
- Severe/irreversible stage (loss > 40% of CBV). Blood pressure drops below 50 mm Hg. A short-term rise in blood pressure ("second plateau") is possible due to CNS ischemia and a massive surge of hormones. Without intensive therapy, persistent vasodilation, generalized cell death, multiple organ failure, and asystole ensue.
- Reperfusion injury. Even if blood flow is restored, ischemic tissues release inflammatory mediators. Activated neutrophils and peroxide radicals destroy cell membranes, sustaining multiple organ failure.
Briefly: answers to topical questions
Which medications are used to treat uterine hypotonia and atony?
Uterine hypotonia and atony are treated with uterotonic drugs that stimulate myometrial contractile activity. These include:
- Oxytocin — administered intravenously or as an additional infusion.
- Carbetocin — administered intravenously after the delivery of the placenta or extraction of the fetus.
These medications are used for medical stimulation if uterine tone does not recover after placental delivery, as well as for the prevention of hemorrhages.
What is the algorithm for infusion and transfusion therapy in massive obstetric hemorrhage?
The algorithm for infusion and transfusion therapy in massive blood loss requires the immediate initiation of the massive transfusion protocol. Baseline therapy includes adequate administration of crystalloid and colloid solutions. In critical blood loss exceeding 1500–2000 ml, empirical administration includes:
- Fresh frozen plasma (FFP).
- Packed red blood cells.
- Platelets.
- Coagulation factor VIII.
It is recommended to follow the massive transfusion protocol using a 1:1:1 ratio, reflecting the proper proportion of red blood cells, FFP, and platelets. Administration exclusively of plasma expanders in volumes exceeding 30–40 ml/kg leads to dilutional coagulopathy and increased blood loss.
What surgical methods of hemostasis are used when conservative therapy is ineffective?
When conservative therapy is ineffective, staged surgical hemostasis is applied. The main methods include:
- Placement of an intrauterine hemostatic balloon — a temporary measure while preparing for laparotomy.
- Placement of hemostatic compression sutures — B-Lynch (B-Lynch), Pereira (Pereira) sutures, and mattress sutures are used.
- Vessel ligation — ligation of uterine or internal iliac arteries (a. iliaca interna).
- Endovascular surgery — uterine artery embolization.
If bleeding persists and all organ-preserving measures fail, a radical method is used — amputation or extirpation of the uterus (Hysterectomia).
What are the clinical and laboratory stages of DIC syndrome in obstetric hemorrhages?
There are 4 consecutive stages of DIC syndrome development, of which the initial ones are described in detail in the literature:
- Stage I (Hypercoagulation) — clinically corresponds to shock phenomena, characterized by the entry of thromboplastin into the bloodstream.
- Stage II (Consumption coagulopathy) — characterized by a decrease in the level of clotting factors.
General clinical and laboratory manifestations of progressive DIC syndrome include:
- Laboratory signs — hypofibrinogenemia, a critical drop in antithrombin III levels, significant thrombocytopenia, and a substantial increase in fibrin degradation products (FDP).
- Clinical signs — increasing bleeding, hemorrhages into undamaged tissues, and the development of multiple organ dysfunction syndrome (MODS).
Rule of visual error: "Small things seem large, and large things seem small." Physicians often overestimate scant bleeding and critically underestimate massive bleeding.
Class and exam questions
What is the main danger of the reperfusion period?
Even after cardiac output normalizes, tissues continue to release inflammatory mediators and free radicals. This leads to the destruction of cell membranes and the progression of multiple organ dysfunction.
Does the measuring container account for all the lost blood?
No, about 150 ml of blood remains in the placenta. In addition, the final volume in the container is often distorted due to admixture with urine and amniotic fluid.
What else to study on this topic
- Mechanisms of DIC syndrome development in obstetric hemorrhage
- The impact of inadequate analgesia on the rate of hemorrhagic shock development
- Pathogenesis of the arterial pressure "second plateau" phenomenon in severe shock
- Differential diagnosis of the causes of uterine hypotonia and atonia
- Principles of calculating infusion therapy depending on the stage of shock
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