Obstetrics and Gynecology - A. M. Gromova 2000

Postpartum Septic Infections
Fourth Stage

Sepsis

Sepsis belongs to the generalized forms of postpartum infection. Obstetric sepsis develops As a result of the spread of infection from a primary focus, namely the Uterus.

It has been established that bacteremia can be detected in only 45–48% of patients with clinical manifestations of sepsis. Furthermore, a large mass of necrotic and damaged Tissues can substitute for Bacteria as the triggering mechanism for the body's generalized reaction.

In 1991, at a conference of the American College of Chest Physicians and the Society of Critical Care Medicine, the term "Systemic Inflammatory Response Syndrome (SIRS)" was adopted.

SIRS can be triggered by various causes, including infection. A systemic inflammatory response caused by a proven infection is defined as sepsis.

A severe course of sepsis characterized by arterial hypotension and tissue hypoperfusion—even despite adequate fluid resuscitation—leading to organ and systemic dysfunctions, is defined as septic Shock.

The mere presence of an infection cannot account for the complex pathophysiological processes characteristic of sepsis. These processes are the result of the body’s response to the infection, driven by an increased production of various endogenous substances that initiate the pathological cascade in sepsis.

Sepsis should not be viewed as a consequence of the direct action of microorganisms on the macroorganism, but rather as the result of profound immune system dysfunctions that progress from a state of hyperactivation («hyper-inflammatory phase») to a state of immunodeficiency («immune paralysis phase»). Thus, The Immune System becomes an active participant in a destructive, or more precisely, auto-destructive process. Septic «autocannibalism» is a term introduced to describe the METABOLISM of a patient with sepsis.

The Pathogenesis of sepsis and its complications is driven primarily by endogenous mediators, impaired peripheral microcirculation, myocardial depression, and reduced Oxygen transport and tissue consumption.

Sepsis is always a «secondary» disease, meaning there is invariably a primary focus acting as the portal of entry for the infection.

Postpartum sepsis tends to follow a particularly severe course when preceded by a viral infection contracted during Pregnancy or immediately after childbirth.

The course of sepsis depends not only on the host's bodily response—largely determined by immune defense capabilities—but also on the CHARACTERISTICS OF THE causative microorganism. The predominance of staphylococci leads to a more torpid pathological process affecting multiple Internal Organs and exhibiting resistance to antibiotic therapy. Sepsis caused by Gram-negative flora is more frequently complicated by septic shock. Facultative anaerobes and Bacteroides as causative agents of postpartum sepsis tend to affect the hepatobiliary system and Kidneys, and cause hemolysis. Adenoviral sepsis is characterized by blockade of the woman's immune system, leading to a rapid clinical course, the absence of an inflammatory response in tissues, and multi-organ damage similar to that observed in disseminated intravascular coagulation (DIC).

Sepsis without metastasis represents an acute septic condition characterized by bacteremia and pronounced systemic intoxication.

A definitive Diagnosis can only be established through repeated Blood cultures yielding positive Microbial growth. When cultures are negative, the clinical manifestations of the disease must be taken into account.

Sepsis with metastasis is characterized by The formation of metastatic purulent foci in various organs, predominantly in the Lungs.

Postpartum sepsis clinically manifests as either septicemia or septicopyemia.

Septicemia is characterized by an early onset, high body Temperature (up to 40–41 °C), recurrent chills, rapidly escalating intoxication leading to altered mental status, tachycardia, tachypnea, cyanosis, and hypotension.

Additional diagnostic examinations reveal oliguria, proteinuria, elevated central venous pressure (CVP), electrocardiographic (ECG) signs of right Heart strain, leukocytosis (or leukopenia in severe cases) on the hemogram, accelerated ERYTHROCYTE SEDIMENTATION RATE (ESR), anemia, hyponatremia, hypo- and dysproteinemia, and moderate hypoglycemia.

Septicopyemia typically manifests later and is characterized by severe intoxication, where clinical deterioration is punctuated by brief remissions. It is accompanied by multiple organ dysfunction syndrome (MODS) and systemic failure.

Treatment

The management of sepsis combines targeted action against the infection source with comprehensive antimicrobial, infusion-transfusion, desensitizing, immunocorrective, and symptomatic therapy (for more details, see the section on Peritonitis treatment).

Recently, modern treatment modalities have been widely implemented in the management of obstetric sepsis, including ultraviolet blood irradiation (UVBI), laser therapy, hemosorption, lymphosorption, and plasmapheresis.

When selecting the management strategy for the primary focus, Hysterectomy is preferred if no clinical improvement is observed within 3–4 days of comprehensive therapy. In the event of uterine Hemorrhage, hysterectomy is performed immediately.

Postpartum Mastitis

Postpartum mastitis is an inflammatory disease of the Cytology/practical/135.html">Lactating mammary gland. The causative agent is most commonly coagulase-positive Staphylococcus aureus (hemolytic staphylococcus). The infection invades the breast via lymphatic pathways

and lactogenic pathway. The entry ports are nipple fissures. A crucial factor contributing to the onset and development of mastitis is milk stasis in the mammary gland (lactostasis).

The Clinical presentation of mastitis comprises three stages:

I. Serous (initial);

II. Infiltrative;

III. Purulent:

1. Infiltrative purulent:

a) diffuse;

b) nodular.

2. Abscessing:

a) furunculosis of the areola;

b) areolar abscess;

c) deep glandular abscess (intramammary);

d) retromammary abscess;

3. Phlegmonous:

a) purulent-necrotic;

4. Gangrenous.

Mastitis typically has an acute onset: body temperature rises to 39 C or higher, frequently accompanied by chills, malaise, headache, and breast pain, particularly during feeding. The affected breast enlarges and feels warmer to the Touch than the healthy one. Sometimes, tenderness in the axillary Lymph Nodes increases. As the condition progresses to suppuration, body temperature spikes, accompanied by chills, poor Sleep, and loss of appetite. The infiltrate rapidly increases in size, and fluctuation appears.

Therapy must be prompt. In the infiltrative stage, treatment includes emptying the mammary gland, Antibiotics, applying ice to the affected area during Swelling followed by oil compresses, retromammary blockade (novocaine + antibiotics), therapeutic ultrasound to the breast, and staphylococcal toxoid.

When the inflammatory process progresses to suppuration, surgical intervention is indicated—incision of the abscess with wide drainage of the purulent cavity, alongside management for a septic condition.

Breastfeeding is contraindicated in mastitis.

The issue of Lactation suppression should be addressed on an individual basis with the patient's consent. This is achieved using prolactin synthesis-inhibiting medications, such as bromocriptine (parlodel).

Prevention of postpartum mastitis should focus on three main directions: strict compliance with sanitary-hygienic and anti-epidemic measures, systematic prevention of staphylococcal infection, observance of personal hygiene, and effective treatment of lactostasis and nipple fissures.