Obstetrics and Gynecology - A.M. Gromova 2000

Obstetric Hemorrhage
Hemorrhage in the Placental and Early Postpartum Periods
Hemorrhage in the Early Postpartum Period Due to Uterine Hypotonicity or Atony

Postpartum hemostasis is a complex process maintained by multiple factors: muscular, hemocoagulative, vascular, and tissue-based, which accelerate thrombus formation under METABOLISM/18.html">The Influence of Amniotic Fluid, placental extracts, and other elements of the conceptus. From an obstetric clinical perspective, postpartum hemostasis relies on two primary mechanisms: myometrial retraction, which leads to the compression, twisting, and drawing of the spiral uterine Arteries into the Muscle thickness (the myogenic factor), and thrombus formation within the Vessels of the placental site, promoted by Blood clotting factors and accelerated by tissue activators (the hemocoagulative factor). Reliable hemostasis is achieved within 2–3 hours once firm fibrin thrombi bound to the vessel walls are formed. The formation of such thrombi significantly reduces the risk of Hemorrhage even if myometrial tone decreases. In the first hours following delivery, these clots are soft, loosely attached to the vessels, easily detached from the walls, and washed away by the blood flow if hypotonia develops.

Uterine bleeding in the early postpartum period, caused by impaired uterine contractility, occurs in 2–2.5% of all deliveries.

Uterine hypotonia is the insufficient ability of the uterine wall to contract.

Uterine atony is the complete loss of uterine contractile activity.

The causes of hypotonia and atony include:

- insufficiency of the neuromuscular apparatus of the Uterus associated with genetic factors, infantilism, ovarian hypofunction, and a deficiency of fetoplacental complex Hormones;

- congenital blood disorders (thrombocytopenic purpura, etc.);

- morphological inferiority of the uterus (dystrophic, cicatricial, and inflammatory Changes in the myometrium associated with abortions, complicated labor, tumors, or surgical interventions);

- uterine overdistension (macrosomia, polyhydramnios, Multiple Pregnancy, contracted pelvis);

- severe extragenital pathology leading to disorders of Homeostasis, vascular tone, and endocrine balance;

- hemostatic disorders associated with pregnancy complications (antenatal fetal death and retention in utero, Late gestosis, hemorrhagic Shock, Amniotic Fluid Embolism);

- Placenta Previa, premature detachment of a normally positioned placenta, morbidly adherent placenta (placenta accreta), and retention of the placenta or its parts in the uterine cavity;

- uterine inertia or labor discoordination, uncontrolled administration of medications (uterotonics), excessive pain, exhaustion, or agitation of the patient;

- retention of the placenta or its fragments within the uterine cavity.

The most favorable Location for the placenta is the body of the uterus. When it is localized in the fundus or the lower segment, increased bleeding during labor is observed. The more frequent occurrence of bleeding when the placenta is located in the uterine fundus is mainly due to a disruption of the myogenic factor of hemostasis. When the placenta is located in the lower segment of the uterus, hypercoagulation is observed with increased consumption of intrinsic Blood Coagulation factors, which leads to impaired microcirculation, hemodynamics, and The Development of "consumption coagulopathy," potentially causing excessive blood loss.

Pathomorphological and histological examination of a uterus removed due to hypotonic hemorrhage reveals marked leukocyte infiltration, foci of necrosis and muscular tissue dystrophy, and intramural hemorrhages. Edema of muscle fibers, along with Swelling and loosening of the Connective Tissue, are characteristic changes that impair uterine contractility. These changes may result from obstetric or extragenital pathology, or from prolonged and uncontrolled stimulation with uterotonics, which leads to the blockade of the neuromuscular apparatus of the uterus, promotes its atony, and subsequently causes unresponsiveness to uterotonic drugs.

The clinical picture of hypotonic hemorrhage consists of the following symptoms: uterine bleeding is intermittent, moderate or heavy, containing blood clots. The uterus is soft, contracts poorly, and increases in size due to the accumulation of blood clots in its cavity. Its spontaneous excitability and reactivity to all types of stimuli (pharmacological, chemical, thermal, and mechanical) are significantly reduced.

Unlike hypotonic hemorrhage, in cases of birth canal trauma, the uterus remains firm. Examination of the birth canal reveals tears in the cervix, Vagina, or Perineum.

In uterine atony, the organ completely loses its spontaneous excitability and pharmacological reactivity, signaling the onset of the parabiosic inhibitory phase in the uterine nervous apparatus.

The causes for the transition of uterine hypotonia to atony include: irrational Management of Labor, rough manipulations, overdose of uterotonic agents, prolonged hypoxemia, and the continued action of the factors that originally caused uterine hypotonia.

If the early stage of uterine hypotonia is treated belatedly or inadequately, and its contractile function remains impaired, blood loss volume increases. Hemocoagulation changes occur, indicating a significant depletion of clotting factors, which leads to thrombocytopenia, decreased fibrinogen concentration, reduced factor VIII activity, prolonged prothrombin and Thrombin times, alongside increased fibrinolytic activity and the appearance of fibrin and fibrinogen degradation products. All of this contributes to the rapid progression of disseminated intravascular coagulation (DIC) syndrome.

The condition of the parturient woman depends on the rate and volume of blood loss, her baseline physical status, hemodynamic stability, and the promptness of qualified care. If radical measures to stop the bleeding are applied too late, irreversible changes in vital Organs rapidly develop, leading to maternal death from acute blood loss and hemorrhagic shock.

Treatment of hypotonic hemorrhage aims at rapidly restoring normal uterine contractile function and combating acute anemia. If the placenta or its fragments are retained in the uterine cavity, or if placenta accreta is suspected, manual removal of the placenta and exploration of the uterine cavity must be performed. Repeated and rough attempts at placental expression must be avoided, as this disrupts uterine contractility and prolongs bleeding. In the presence of hypotonia, a bimanual external-internal uterine massage should be performed. The Procedure is carried out under anesthesia.

Surgical technique: using one hand (usually the left), the labia are parted; the right hand is formed into a cone, inserted into the uterus, clenched into a fist, and used to displace the uterus upward and forward. With the other hand, placed over a sterile sheet, a gentle massage is performed by stroking through the anterior abdominal wall. Rough mechanical irritation can cause hematomas, disrupt the coagulation system, and increase bleeding. When motor function is partially preserved, muscle contractions are noted; in atony, contractions are absent.

To treat hemorrhages resulting from uterine hypotonia, the following measures are applied sequentially:

1. Emptying of the Urinary Bladder;

2. Inspection of the placenta and birth canal;

3. External uterine massage;

4. Local hypothermia (applying cold to the lower abdomen);

5. Intravenous administration of 1 ml of methylergometrine or 1 ml of oxytocin, and restoration of BCC through intravenous infusion of rheopolyglucin, polyglucin, or blood.

6. Manual Exploration of the uterine cavity and bimanual compression/massage of the uterus (under anesthesia).

7. If bleeding persists, Methods aimed at enhancing uterine contractility by stimulating its receptors are applied: cold applied to the abdomen, placement of a suture on the posterior lip of the uterine cervix using V.A. Losytska's method or a circular suture using O.T. Mykhaylenko's method, an ether-soaked tampon in the posterior vaginal fornix, and clamping of the parametrium using Henkel-Tikanadze clamps (perpendicular to the edge of the uterine cervix) or M.S. Baksheyev's clamps (along the length of the cervix). The Use of an electrotonizer (Z.A. Chyladze's method) is also an option.

8. In the absence of an effect from the aforementioned measures and continued bleeding exceeding 1000 ml with signs of DIC syndrome, emergency laparotomy must be promptly performed for uterine vessel ligation, supravaginal amputation, or Hysterectomy.

For temporary hemostasis during the patient's transport to the operating room, the following techniques should be used:

— compression of the Abdominal Aorta;

— compression of the uterus against the Pubic Symphysis.

In cases of uterine atony, hysterectomy (complete removal of the uterus) is indicated.

During uterine hemorrhages in the placental and early postpartum periods, measures to stop the bleeding are conducted simultaneously with the Management of acute anemia. Blood loss is considered compensated if it does not exceed 1% of body weight, and the BCC deficit is no more than 15%. Blood loss reaching 1.5% of body weight with a BCC deficit greater than 15% is considered decompensated. Hemorrhagic shock is accompanied by a BCC deficit exceeding 25%, a drop in blood pressure, and the development of Hypoxia in all organs. Shock may develop with lesser blood loss in cases of exhaustion, overfatigue, and late pregnancy toxicosis.

The assessment of blood loss is based on determining pulse rate and volume, blood pressure, central venous pressure, hourly urine output, hematocrit, Hemoglobin, and the shock index. The latter is calculated by dividing the pulse rate by the maximum blood pressure; its normal value is 0.54.

Blood loss up to 500 ml is replaced solely with volume expanders (polyglucin, rheopolyglucin). Blood loss of 500–1000 ml is replaced with colloid solutions and blood in a 2:1 ratio. Blood loss of 1000–1500 ml is replaced with colloids and blood in a 1:1 ratio, and blood loss of 1500–3000 ml with colloids and blood/volume expanders in a 2:3 ratio. Massive blood loss must be restored exclusively using type-specific, preferably fresh, donor blood. Vasopressors (mesaton, adrenaline) are used only in the restored blood loss phase. Glucocorticoids are prescribed when adrenocortical insufficiency is suspected. Administration of cardiac Glycosides (strophanthinin), Oxygen therapy, and warming of the patient are advisable; in terminal states, endotracheal intubation, mechanical ventilation, closed-chest cardiac massage, and intracardiac administration of adrenaline are indicated.

Hemorrhagic shock (HS) is a critical bodily condition associated with acute blood loss, resulting in a macro- and microcirculation crisis and multiple organ and system dysfunction syndrome. From a pathophysiological standpoint, it is a microcirculation crisis characterized by the failure to provide adequate tissue exchange, meet tissue demands for oxygen and energy substrates, and remove toxic metabolic waste.

The body of a healthy woman can compensate for blood loss up to 20% of BCC (approximately 1000 ml) through autohemodilution and the redistribution of blood within the vascular bed. When blood loss exceeds 20–25%, these mechanisms are insufficient to eliminate the BCC deficit. In massive blood loss, persistent vasoconstriction remains the primary "protective" reaction of the body, thereby maintaining normal or near-normal blood pressure and ensuring Blood supply to the Brain and Heart (centralization of Circulation), albeit at the expense of diminished BLOOD FLOW IN Muscles and Internal Organs, including the Kidneys, Lungs, and Liver.

Prolonged sustained vasoconstriction, acting initially as a protective bodily response, maintains blood pressure within certain limits for some time; however, as shock progresses and in the absence of adequate therapy, it subsequently contributes to the sequential development of severe microcirculatory disorders, the formation of "shock organs," and the development of Acute Kidney Injury and other pathological states.

The severity and rate of deterioration in HS depend on the duration of arterial hypotension and the baseline condition of organs and systems. In the presence of baseline hypovolemia, short-term hypoxia during labor leads to shock, as it acts as a triggering mechanism for hemostatic disruption.

Clinical presentation

HS manifests as weakness, dizziness, nausea, dry Mouth, darkening before the eyes, and, with increasing blood loss, loss of consciousness. Due to the compensatory redistribution of blood, its volume decreases in the muscles and Skin, manifesting as pallor with a grayish tint; the extremities are cold and damp. Reduced renal blood flow is manifested by decreased urine output, followed by microcirculatory impairment in the kidneys accompanied by ischemia, hypoxia, and tubular necrosis. As the volume of blood loss increases, symptoms of respiratory failure mount: dyspnea, breathing pattern irregularities, agitation, and peripheral cyanosis.

Four degrees of hemorrhagic shock severity are distinguished:

Grade I severity is observed at a BCC deficit of 15%. The general condition is satisfactory, the skin is pale, with mild tachycardia (up to 80–90 bpm), blood pressure around 100 mmHg, Hb 90 g/L, and normal central venous pressure.

Grade II severity involves a BCC deficit of up to 30%. The general condition is moderate, with Complaints of weakness, dizziness, darkening before the eyes, nausea, and pale, cold skin. Blood pressure is 80–90 mmHg, central venous pressure is below 60 mm H₂O, tachycardia reaches 100–120 bpm, urine output is reduced, and Hb is 80 g/L or lower.

Grade III severity occurs with a BCC deficit of 30–40%. The general condition is severe. Marked lethargy, dizziness, pale skin, acrocyanosis, blood pressure below 60–70 mmHg, and a sharp drop in CVP (20–30 mm H₂O and lower) are observed. Hypothermia, a rapid pulse (130–140 bpm), and oliguria are present.

Grade IV severity occurs with a blood volume deficit exceeding 40%. The condition is extremely critical, and the patient is unconscious. Blood pressure and central venous pressure are undetectable, and pulses can be felt only in the carotid arteries. Respiration is shallow, rapid, and rhythmically disturbed, accompanied by motor agitation, hyporeflexia, and anuria.

Treatment

- rapid and reliable arrest of bleeding, taking into account the Etiology of obstetric hemorrhage;

- restoration of blood volume and maintenance of macro- and microcirculation as well as adequate tissue perfusion using controlled hemodilution, blood transfusion, rheological correctors, glucocorticoids, etc.;

- mechanical ventilation in a moderate hyperventilation mode with positive end-expiratory pressure (Prevention of "shock lung");

- management of disseminated intravascular coagulation (DIC), acid-base balance disorders, protein and Water-electrolyte metabolism, along with correction of metabolic acidosis;

- pain management, therapeutic anesthesia, and neuroprotective anti-hypoxic therapy;

- maintenance of adequate diuresis at 50–60 mL/h;

- support of cardiac and hepatic function;

- administration of broad-spectrum Antibiotics.

Elimination of the source of bleeding is the cornerstone of hemorrhagic shock management. The choice of hemostatic method depends on the underlying cause. In treating hemorrhagic shock, the speed of blood loss compensation and timely surgical intervention are of paramount importance. Grade II hemorrhagic shock is an absolute indication for surgical hemostasis.

Infusion therapy for hemorrhagic shock should be administered via 2–3 Veins: at a blood pressure of 40–50 mmHg, the infusion rate must be 300 mL/min; at 70–80 mmHg, 150–200 mL/min; once blood pressure stabilizes at 100–110 mmHg, the infusion is continued by drip under the monitoring of blood pressure and hourly diuresis.

The ratio of colloids to crystalloids should be 2:1. Infusion therapy includes: rheopolyglucukin, volecam, packed red Blood Cells, native or fresh frozen plasma (5–6 bottles), albumin, Ringer-Locke solution, glucose, pananghin, prednisolone, corglycone, and—for the correction of metabolic acidosis—4% sodium bicarbonate solution and trisamine. In cases of hypotensive syndrome, dopamine is administered. The infusion volume should exceed the estimated blood loss by 60–80%, accompanied by blood transfusion not exceeding 75% of the blood loss during immediate replacement, followed by delayed transfusion in smaller doses.

To relieve vasospasm after controlling the hemorrhage and correcting the blood volume deficit, ganglion blockers are used in combination with agents that improve blood rheology (rheopolyglucukin, trental, complamin, dipyridamole). High-dose glucocorticoids (30–50 mg/kg of hydrocortisone or 10–30 mg/kg of prednisolone), Diuretics, and mechanical ventilation must be employed in the management of hemorrhagic shock.

To treat DIC syndrome in hemorrhagic shock, fresh frozen plasma is administered, alongside protease inhibitors such as kontrikal (trasylol) at 60,000–80,000 IU and gordox at 500,000–600,000 IU. Dicynone, etamsylate, and androcton reduce capillary fragility and enhance platelet functional activity. Cardiac glycosides, immunomodulators, Vitamins, and—when indicated—antibacterial therapy, anabolic agents (nerobol, retabolil), and essential Phospholipids are also prescribed.

Rehabilitation therapy and Therapeutic Exercises are of great importance following intensive care.