Pelvic Thrombophlebitis. Puerperal Progressing Thrombophlebitis

Puerperal thrombophlebitis is an inflammation of veins of pelvic wall, which spreads from the genitalia. Thrombophlebitis of the uterine veins (metrothrombophlebitis) develops from metroendometritis. The symptoms in general are similar to those at endometritis. But pain is more significant, irradiating to the loin and legs. On vaginal examination the inflamed veins may be palpated as enlarged, painful, with tight cords on the lateral side of the uterus.

Pelvic thrombophlebitis usually has similar symptoms: nagging, persistent pains in the lower abdomen, elevated temperature and pulse rate, enlarged painful uterus. On vaginal examination one can palpate the inflamed veins on the lateral side of the pelvis, enlarged, painful and hardened. The treatment is the same; spasmolytics and anticoagulative therapy should be added. The examination of blood clotting must be done every day to prevent thromboembolism.

Puerperal Progressing Thrombophlebitis. It is an inflammation which occurs in puerperium, extending to the external and internal iliac and femoral veins and then giving rise to obstruction to the venous return to the limb.

Clinical features. Usually during the second week after delivery shivering attack or actual rigor occurs or the temperature rises up to 39-40º C and is quickly followed by clinical evidence of femoral thrombosis, the vein becoming hard and tender, and the whole leg swells and becomes painful. In case of superficial thrombophlebitis the overlying skin looks red. In case of deep venous thrombosis the leg becomes enlarged, edematous, and painful. The pulse rate is absent in the area of ankles.

Treatment. The patient is prescribed bed rest with the foot end of the bed raised above the heart level. Pain in the affected area may be relieved with analgetics and antipyretics (baralgin, indometacin); appropriate antibiotics are to be administered. Anticoagulants should be also administered: heparin 15,000 units intravenously followed by 10.000 units, 4 to 6 hourly when the blood is likely to be depressed to the therapeutic levels. Breast feeding should be arrested during the period of therapy. Reopoliglukin 400 ml intravenously droppingly, trental 5 mg /kg/body weight are necessary. In case of high risk of embolism surgical treatment is indicated.

Puerperal Peritonitis. Obstetrical peritonitis is one of the severest and most dangerous situations in clinical practice. Commonly the incidence of puerperal peritonitis is 1-4.5%. The rate of maternal lethality due to peritonitis is 10-35%.

Most often the source of infection is the uterus (chorioamnionitis in labor, postpartum endometritis, endometritis after cesarean section, rupture of uterine sutures after cesarean section). There are a lot of contents in the uterine cavity after delivery and cesarean section: blood clots, elements of decidual membrane, elements of placental tissue; all these suggest a growth medium for microbes. Blood supply of the uterus, which is increased in pregnancy, facilitates the development of infectious process in the puerperal uterus (puerperal wound). The infectious–inflammatory development in this case happens against lowering immunity, general weakening of maternal organism after delivery, etc.

Thus uterus is an entry of infection in puerperal period.

Infectious agents: the most common type is mixed infection nowadays: Coli-bacillus, blue pus bacillus, staphylococcus, Bacillus proteus are of primary significance in development of puerperal peritonitis. Endogenous opportunistic infectious agents, which are resistant to antibiotics, take part in the development of the process. Anaerobic-aerobic colonies acquire greater significance in development and occurrence of puerperal peritonitis, as well as hospital infections.

Pathogenesis of Obstetrical Peritonitis. The following ways of contamination are distinguished:

· the most common type is ingress of contamination (of infectious agents) into the abdominal cavity during operation (cesarean section);

· spread of microbes from the uterine cavity due to its rupture or perforation;

· contamination through the tube canals.

· hematogenic way of contamination.

The main factors of development of peritonitis are:

· congestive hyperemia of peritoneum;

· hyperpermeability of blood vessels of the peritoneum;

· transudation.

While entering the abdominal cavity, the causative agents provoke reflex irritation of peritoneal receptors resulting in hyperemia of peritoneum and hyperpermeability of blood vessels of the peritoneum.

Plenty of fluids, albumins, electrolytes are lost because of transudation through the increased permeability of the intestinal walls. Due to leukocyte migration the exudation becomes purulent, due to fibrin production the adhesive processes develop, the intestinal motility decreases, and paralytic (adynamic) ileus develops. It is followed by production of toxic agents and metabolites (kinins, histamine), while the level of serotonin decreases in this process, which is a mediator of excitation of intestinal muscles.

Thus, due to paralytic condition the intestinal loops become overdistended, the intestinal walls become more permeable for fluids, microbes, toxins. Due to loss of albumin into intestinal space hypoproteinemia develops. The level of total protein decreases to 50-45 g/l, which is a threatening prognostic symptom. The colloid-oncotic pressure decreases, hypovolemia and hemoconcentration, DIC syndrome, thrombosis, multiple organ failure develop and death occurs.

Classification of Peritonitis. It is subdivided into:
- local peritonitis (pelvioperitonitis)
- diffuse peritonitis