Documente Academic
Documente Profesional
Documente Cultură
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Infectious process is classically considered as a result of a
complex interaction of three factors: the presence of the
pathogen (its quantity and virulence), the state of the
primary focus and the body's resistance.
Consider these factors.
Pathogens NHS.
A characteristic feature of septic puerperal diseases is their
polymicrobial etiology.Pathogens can be both pathogenic and
opportunistic microorganisms.
Potentially disease pathogens include Gram-positive (enterococci,
Staphylococcus epidermidis and Staphylococcus, Streptococcus group A
and B), Gram-negative (Escherichia coli, Klebsiella, Proteus,
Enterobacteriaceae, Pseudomonas aeruginosa) aerobic bacteria.Among
the anaerobic bacteria are Bacteroides, peptokokki, peptostreptokokki.
Microbial associations have a more pronounced pathogenic properties
than monoculture, due to the synergism between them. This
phenomenon is called " Quorum sensing ", or" quorum sensing. "
Bacteria are able to communicate with each other via signals of protein
molecules, and the accumulation of a certain amount of bacterial
biomass allocation of pathogenicity factors increases.
Over the last decade has changed the species spectrum of
pathogens postpartum purulent-septic diseases. Along with leading
etiological your negative bacteria increases the importance of Grampositive flora. If before the main etiological factor is rightly considered
E. coli, at least - Pseudomonas aeruginosa and Proteus, now the leading
role belongs enterococci (up to 65% of all cases of postpartum purulentseptic diseases). This is especially important to know, because
enterococci sensitive to cephalosporins I and II generation and
aminoglycosides, which are often used in maternity hospitals.
Diagnostic criterion is the number of microbial bodies of more
than 10 4 CFU / ml.Bacteriological examination, indicating the
development of the infectious process.
It should be noted that increasing the number of diseases caused
by microorganisms, sexually transmitted infections (chlamydia,
mycoplasma, and viruses) It should be noted that mycoplasma (10%)
and chlamydia (2%) cause indolent forms of endometritis, often
connected to the primary causative agents of infection.
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Resistance of the host.
It is caused by the presence of the normal microflora (lactobacilli)
that competes with pathogens for adhesion to epithelial cells, and local
factors and systemic immunity female genital tract.
Causes changes in the composition of the vaginal flora in pregnant
women may be: unjustified and / or inconsistent antibacterial treatment,
as well as the use of surface disinfectants in otherwise healthy pregnant
women. Against this background, lactobacilli and die in their place
begins to develop opportunistic anaerobic flora, resulting in the
development of bacterial vaginosis in pregnant women. Bacterial
vaginosis - vaginal ecosystem pathology is caused mainly by increased
growth of obligate anaerobic bacteria.Bacterial vaginosis in pregnant
women is on average 14-20%. In 60% of postpartum women with
postoperative endometritis allocated the same microorganisms from the
vagina and of the uterus. In bacterial vaginosis in pregnant several times
increased risk of wound infection.
By the end of pregnancy in women noted significant change of
serum specific immunoglobulin classes (G, A, M), the absolute decrease
in the number of T-and B-lymphocytes (normal secondary
immunodeficiencies).
At birth there are additional factors contributing to the
development of postpartum infectious diseases. First of all, with a
discharge of mucus plug, which is a mechanical and immunological
barrier (secretory lgA) for microorganisms, lost one of the physiological
barriers antiinfective female genital tract. Amniorrhea causes an increase
in pH (decrease acidity) vaginal contents, and the study of vaginal
contents after the outpouring of water revealed important fact - the
complete absence of secretory immunoglobulin A. The reason for this
phenomenon is purely mechanical removal belkovosoderzhaschih
substrates with mucosal surfaces of the birth canal, drastically reducing
local secretory protection . Found that 6 hours after rupture of
membranes is not a single anti-infective barrier female genital tract, and
the degree of contamination and the nature of the microflora depend on
the duration of dry period. Against this background, dramatically
increase the risk of postpartum infectious complications of premature
rupture of water, prolonged labor, early amniotomy unreasonable,
multiple vaginal research, invasive methods of research status of the
fetus during labor, violation of sanitary-epidemiological regime. Clinical
manifestation of ascending infection in childbirth is chorioamnionitis. In
mothers, amid prolonged dry period or childbirth, general condition
worsens, the temperature rises, there is a fever, pulse quickens, amniotic
fluid become cloudy with odor, pus-like discharge sometimes appear, the
blood picture changes.Already a 12-hour dry interval 50% maternal
chorioamnionitis develops, and 24 hours later, this percentage is close to
100%.
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State of the primary lesion.
In the postpartum period in the genital tract in childbed, not a
single anti-infective barrier. The inner surface of the postpartum uterus is
a wound surface, and the contents of the uterus (blood clots, epithelial
cells, land decidua) is a favorable environment for microbial growth.
The uterine cavity is easily infected by the ascent of pathogenic and
conditionally pathogenic flora of the vagina. As mentioned above, some
women in childbirth, postnatal infection is a continuation of
chorioamnionitis.
Postpartum infection - mostly wound. Development of infection in
the postpartum period contribute: subinvoljutcija uterus, placenta parts
delay, inflammatory diseases of the genital organs in history, the
presence of bacterial infection of extragenital lesions, anemia, endocrine
diseases, violation of sanitary-epidemiological regime.
Speaking of septic complications of caesarean section, the matter
is also the method by which it was made. Thus, the risk of postpartum
purulent-septic diseases is higher after cesarean corporal, because with
this method is difficult to compare the wound edges, formed more
hematomas, which are easily infected. If a cesarean section is performed
in the lower uterine segment, it is preferable to cut Derfleru when
incision is made acute by (with scissors), than Gusakov (when the
wound edges stupidly bred in hand with your fingers). This is due to the
fact that the incised wound healing better than jagged.
Persistence of wound infection also contributes to the phenomenon
of "bacterial film."This accumulation of microorganisms on the foreign
bodies that may be in obstetrics seam on the cervix or sutures in the
uterus after cesarean section. Microorganisms form clusters, covered
with a thick layer of mucopolysaccharides, preventing the penetration
of antibiotics, which reduces the effectiveness of antibiotic therapy.
Transmission path . In 9 out of 10 cases of postpartum infection
as such transmission route does not exist, since the activation of selfpathogenic flora (autozarazhenie). In other cases, infection occurs
outside hospital strains resistant in violation of the rules of asepsis and
antisepsis. Should be identified as a relatively new way of infection - the
intra-amniotic associated with the introduction of invasive obstetric
practice methods (amniocentesis Fetoscopy, cordocentesis).
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Concept of systemic inflammatory response syndrome.
The main mechanism of pathogenesis of postpartum purulentinflammatory diseases is a systemic inflammatory response syndrome,
which is the first stage of postpartum endometritis, and the last - septic
shock.
The basic starting point is the selection of phospholipase
microorganisms - enzyme that destroys cell membranes Phospholipids.
This starts a cascade of arachidonic acid, which is formed from
phospholipids. From the arachidonic acid produced prostacyclin and
thromboxane A 2. imbalance in favor of thromboxane
leading to
vasospasm and increased platelet aggregation, which leads to
generalized disturbance of microcirculation in tissue hypoxia and
metabolic acidosis.
Infection triggers cytokine release. Neutrophils, which fall into
the site of infection, also secrete biologically active substances: Nitric
oxide and superoxide contribute to the formation of oxygen radicals and
peroxides, which contributes to damage of the vascular endothelium. In
the process involves histamine, proteolytic enzymes. All this leads to
generalized endothelial defeat, hemostatic disorders and vascular tone,
impaired microcirculation, oozing liquid part of blood into the tissues,
which leads to a decrease in the bcc - comes hypovolemia. Increases the
risk of edema, especially the lungs, brain. Because of the deposit of
blood in the microvasculature open arteroivenoznye shunts. Because
hyperactivation of vascular-platelet
and plasma components of
hemostasis begins to develop DIC. Ultimately, it all leads to the
development of septic shock.
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CLASSIFICATION.
CLINICAL PICTURE.
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Postpartum endometritis.
In the structure of inflammatory diseases postpartum endometritis
retains its leading position. After normal delivery rate of postpartum
endometritis is 3-8%, after pathological births, this figure rises to 1020%. Chance of postpartum endometritis after cesarean increases 5-10
times compared with vaginal birth path. After repeated cesarean
delivery, it increases still 2.5 times. Caesarean section, making only 20%
of births, causes 80 - 90% of postpartum endometritis.
There are several reasons:
incision on the uterus during a cesarean section is accompanied by a
violation of the integrity of the blood and lymph vessels, which
contributes to direct bacterial invasion of the bloodstream and the
lymphatic system of the uterus;
operation performed on the background horionamnionita causes direct
spread of infection to the peritoneum with the emergence of early
peritonitis;
infectious agents in the zone of the uterine scar, acquire the ability to
proliferate, increased virulence, which leads to the spread of outside
wounds (myometrium, parameters);
Availability seam to slow uterine involution of the uterus in the
postpartum period, violating the normal flow of lochia, creating
favorable conditions for microbial growth.
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Metrotromboflebit.
Often observed after surgical delivery. Clinical symptoms usually
appear not earlier than 6 days post-partum period.
Runs hard, with high fever and intoxication. When vaginal study
determined enlarged, painful on palpation of the lateral surfaces of the
uterus, on the side surfaces Ingoda palpable tight, painful "cords." In
the clinical analysis of blood marked leukocytosis with a shift to the left
leykoformuly.
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Puerperal mastitis.
Puerperal mastitis is one of the most frequent complications of the
postpartum period.In recent years, according to domestic and foreign
authors, the incidence of mastitis varies widely - from 1% to 16%, with
an average of 3-5%. Among lactating women rate it has no tendency to
decrease.
In domestic obstetrics most widely found mastitis classification
proposed in 1975. BL Gurtovoy:
1. Purulent mastitis:
a.) serous (starting) mastitis;
b.) infiltrative mastitis.
purulent mastitis:
a). Infiltrative-purulent
b). Abscessed
abrasions areola
Abscess areola
abscess deep in the gland
abscess behind cancer (retromammary)
c). Phlegmonic
d). Gangrenous
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Etiology, pathogenesis, clinical manifestations, diagnosis.
Under modern conditions the major cause of lactation mastitis is
Staphylococcus aureus, which is characterized by a highly virulent
and resistant to many antibiotics.
Penetration of the pathogen in the breast tissue occurs
lymphogenous way through cracked nipples and galaktogennym way through dairy moves. Extremely rare inflammatory foci in the gland is
formed secondarily in generalizing postpartum infection localized in the
reproductive system.
Development of inflammation in the mammary gland promotes
lactostasis associated with occlusion of the ducts that bring milk, so
mastitis in 80-85% of cases occur in nulliparous.
For a typical clinical form of serous mastitis characterized by
acute onset usually 2-4 week postpartum period. Body temperature rises
rapidly to 38-39 C, often accompanied by chills. Develop general
weakness, fatigue, and headache. Pain arises in the mammary
gland.However there may be variants of the clinical course of mastitis in
which the general phenomena precede local. When inadequate therapy
beginning mastitis within 2-3 days goes into infiltrative form. In the
breast begin to palpate pretty tight painful infiltration. The skin over the
infiltration - always hyperemic.
Daylight purulent mastitis in form occurs within 2-4 days. The
temperature rises to 39 C, there is a fever, growing signs of
intoxication: lethargy, weakness, loss of appetite, headache. Growing
local signs of inflammation: swelling and soreness in the lesion, areas of
softening in the infiltrative-purulent form of mastitis occurring in about
half of patients with purulent mastitis.
In 20% of patients with purulent mastitis manifests as abscess
forms. When this dominant variants are abrasions and abscess halos rarer
and intramammary paramastitis representing purulent cavities defined
connective tissue capsule.
In 10-15% of patients with purulent mastitis occurs as a form of
abscess. Process captures most of the gland tissue and its melting
transition to the surrounding tissue and skin.General condition puerperal
in such cases - heavy. Temperature reaches 40 C, shaking chills
watching expressed intoxication. Mammary gland dramatically increases
in volume, her skin was swollen, flushed with a bluish tint, palpation of
the prostate - sharply painful. Gathered breast may be accompanied by
septic shock.
Sharp form gangrenous mastitis is extremely difficult for a
pronounced intoxication and necrosis of the breast. Gangrenous
mastitis outcome is unfavourable.
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Basic principles of starting therapy (serous) mastitis. most
important component of a comprehensive treatment of lactation mastitis
is a complex application of antibiotics. Before starting antibiotic therapy
seeded milk from diseased and healthy breast flora. Currently
Staphylococcus aureus reveals the greatest sensitivity to semisynthetic
penicillins (methicillin, oxacillin, dicloxacillin), cephalosporins III - IV
generation, lincomycin and aminoglycosides (gentamicin, kanamycin).
While maintaining breastfeeding choice of antibiotics is associated with
the possibility of adverse effects on the newborn. Used penicillins and
cephalosporins.
In the initial stages of lactation mastitis antibiotic usually
administered intramuscularly.
In modern obstetrics indication for suppression of lactation
mastitis are:
rapidly progressing process, despite ongoing intensive therapy;
multifocal infiltrative-purulent and mammary abscess;
abscess and gangrenous forms of mastitis;
any form of mastitis in relapsing course;
5. Sluggish current mastitis is not amenable to complex therapy
including surgical opening of the hearth.
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Obstetric peritonitis.
This severe complication of the postpartum period, which occurs
on the background of endometritis, myoma node necrosis, torsion legs
ovarian tumor. However, the most common cause of obstetric peritonitis
is endometritis after cesarean section.
Peritonitis caused by diverse microflora and characterized early
occurring endogenous intoxication associated with systemic
inflammatory response syndrome. Disturbed microcirculation, there is
tissue hypoxia and metabolic acidosis. A special place in the
pathogenesis of peritonitis takes enteroplegia. Broken motor, secretory,
suction bowel function. In the lumen of the small intestine accumulate
significant amounts of fluid containing a large amount of protein and
electrolytes. Hyperextension and ischemia of the bowel wall is likely to
disrupt the intestinal barrier function and the further strengthening of
intoxication.
Obstetric peritonitis as surgical differs phasic flow.
The first phase - the initial or reactive (first 24 hours).
Compensatory mechanisms are preserved. No hypoxia. Patients few
euphoric, excited. Moderate enteroplegia, sluggish peristalsis.
Tachycardia is slightly ahead temperature reaction of the body. In the
blood, died leukocytosis with a shift to the left leykoformuly.
The second phase - toxic (24-72 h). In this period begin to dominate
the "general" response: developing hemodynamic disturbances,
microcirculatory changes liver and kidney function, gradually increasing
hypoxia and worsens tissue respiration. Patient sluggish, the color of the
skin, nausea, vomiting. Increases leukocytosis with toxic granulation
neutrophils. Distended belly.
The third phase - terminal (over 72 hours), is characterized by
decompensation syndromic disorders occurring in the toxic phase of
peritonitis. There is a complete absence of peristalsis, expressed
flatulence, diffuse tenderness throughout the abdomen. Formed
hypovolemic and septic shock with multiple organ failure. Patient
inhibited, arrhythmic heartbeat, shortness of breath, decreased blood
pressure.
Peritonitis caused after cesarean section, can be manifested in
three versions, depending on the route of infection.
Option 1 - against the background of horionamnionita . clinical picture
of peritonitis in this situation is characterized by an early start on the 1st
2 days after surgery, high body temperature to 38-39, tachycardia 120140 beats.
min., intestinal paresis.
allows Early Start eliminate
gapping in the uterus. May be a high leukocytosis (15,0-16,0 - 109 / l),
increasing the number of stab leukocytes. When monitoring for 12-24 h
the deterioration of the general condition. Rising enteroplegia takes
consistent, peristalsis is not defined, bowel stimulation measures are not
effective. Enhanced thirst, the tongue becomes dry, increases
tachycardia. Developed septic shock.
Option 2 - occurs when infection of the peritoneum associated with the
development of postoperative endometritis. The condition of patients
after surgery may remain relatively satisfactory. Body temperature
within 37,4-37,6 C, moderate tachycardia (90-100 beats. / Min.),
Appears early enteroplegia. Abdominal pain is not. Periodically is
nausea and vomiting. Abdomen is soft, no peritoneal signs. The most
characteristic symptom is recurrent. With the progression of the process,
despite ongoing medical therapy, with 3-4 days the patient's condition
worsens, growing signs of intoxication. It should be emphasized that the
differential diagnosis between normal postoperative intestinal paresis
and developing peritonitis is not simple.
The third option - the development of peritonitis in insolvency seams
on the uterus. This usually occurs due to an infection, at least - a
technical error sutures. At the wrong angle suturing wounds, where there
may be a bundle of muscles, separation of the uterus begins to flow into
the retroperitoneal space and the abdominal cavity. Clinical symptoms
usually appear early. From the earliest days growing signs of peritonitis.
The patient's condition worsens, concerned about pain in the lower
abdomen on the right or left. Noteworthy is the paucity of discharge
from the uterus. Steadfastly held tachycardia, vomiting, bloating. When
percussion define exudate in the abdominal cavity, the number of which
is increasing.Intoxication comes quickly.
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Infusion and detoxification therapy. To eliminate hypovolemia,
and detoxification of the correction of underlying colloid osmotic state
spend multicomponent fluid therapy.Infusion using crystalloid, colloid
solutions, according to testimony - protein solutions.
Infusion volume varies depending upon the forms of the disease
from 1,500 ml. (At endometritis) 3 000 - 3500 ml. (With peritonitis).
Maintenance
Mode
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normalize
microcirculation and rheological characteristics of blood coagulation.
The most commonly used plasma expanders (reopoliklyukin,
polyglukin), synthetic colloids (gemodez, hydroxyethylated starches
(Infukoll, Refortan, stabizol)), protein drugs (Albumin, polyamine),
gelatin (zhelatinol) saline.
Fresh frozen plasma is introduced in peritonitis, when to use its
main value: the presence of procoagulants, anticoagulants, and
plasminogen. Indication for transfusion er.massy serves only decreased
hemoglobin below 70 g / l and hematocrit less than 0.2%.
Ratio of colloidal and crystalloid solution should be an average 1:2
ratio of protein and non-protein drugs -1:3.
For the purpose of infusion should be used infusion antihypoxants
mafusol and reamberin that cropped symptoms of systemic
inflammatory response.
In marked metabolic acidosis use
bicarbonate.
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Anti-infective treatment is a major component in the complex
treatment of inflammatory diseases postpartum.
Antibiotic therapy is started on a background infusion therapy as
antibiotics with bacteriolytic action (penicillins, cephalosporins) may
cause the release of large doses of endotoxin that will lead to greater
systemic inflammatory response syndrome and septic shock.
If at the time the therapy we have no evidence of bacteriological
tests with the definition of sensitivity to antibiotics, we prescribe
antibiotics empirically based is polymicrobial disease.
Currently, using a combination of cephalosporins I and II
generation aminoglycosides impractical because most microorganisms
insensitive to these drugs.
By means of first-line combination refers
(lincomycin, clindamycin) with aminoglycosides.
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Immunotherapy.
In order to use the immune preparations for passive
immunotherapy
- interferons (genferon, viferon), human
immunoglobulin and antistaphylococcal, pentaglobin, Intraglobin; and
immunomodulators (taktivin, timalin, timogen, roncoleukin). It should
be emphasized that the immunomodulators used only under the
supervision immunograms agreeing appointment with the immunologist.
In the course of treatment necessarily include sedatives,
desensitizing, painkillers.
To enhance the effectiveness of therapy in treatment sessions using
quantum therapy, ultraviolet blood irradiation in combination with
hyperbaric oxygenation. Hyperbaric oxygen promotes the relief of
bacterial infections, particularly anaerobic,
improves tissue
oxygenation, reduces or eliminates metabolic acidosis.
Very effective methods of efferent therapy , which include
plasmapheresis, hemofiltration, enterosorption. They contribute to the
elimination of biologically active substances (histamine, reactive oxygen
species, arachidonic acid metabolites) and eliminate systemic
inflammatory response syndrome. It is proved that for background use
efferent therapies mortality from septic shock is reduced by 4 times.
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Anticoagulant and antiaggregantnaya therapy conducted in
order to improve the microcirculation as well as prevention of
thromboembolic complications. Antiaggregantov use of Trental
and chimes of anticoagulants is preferable to use low molecular
weight heparins (fraksiparin, Clexane). Especially shows how to
use the presence of low molecular weight heparins
metrotromboflebita (high risk of pulmonary embolism) and
peritonitis (due to massive tissue destruction develops DIC).
Prevention enteroparesis women with postoperative peritonitis
held neostigmine methylsulfate, tserukalom assigned enema.
Symptomatic therapy - uterotonics with endometritis, with
peritonitis - means supporting the function of the heart (strofantin,
koglikon), liver (essentiale, Syrepar).
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