Transcript SEPSIS

SEPSIS
Sepsis is generalized infection, which forwards by
bacteremia on lowering of protective forces of organism.
This problem is not only surgical, but also generally
biological, because during the last years the new
approaches appeared to understanding of its
pathogenesis. They are in the new interpretation of
general mechanisms of violation of homeostasis and
inflammation.
The frequency of sepsis does not fall down though the
huge antibacterial therapy is used.
75000 patients die yearly in Germany. 50000 cases
registered in the USA every year. Mortality consist 3080%. Home statistics is absent to great regret.
TERMINOLOGY
The researches of the last years showed that a great
number of gangrenous tissues (pancreatonecrosis,
polytrauma, burns) are capable to change the
bacteriums in quality of starting mechanism of the
generalized reaction of the organism.
Clinically this stage is impossible to identification from
bacteremia.
At the coordinate conference of 1991 it was offered the
term – syndrome of systematized inflammatory
answer (SSIA).
This syndrome is caused by the microbial infection
determines as sepsis.
The most important achievement, which changed a
conception in pathogenesis of sepsis, was opening of
number of powerful mediators of systematical
inflammatory reaction.
It is informed that the starting moment in pathogenesis
of sepsis is fat-polysaccharide LPS of bacterium’s
membranes, in many cases, gram-negative. It is
determined as endogenous toxin. That’s why
reptodoglipans and teynon acid play the main role in
gram-positive sepsis. They surround membrane of the
gram-positive bacteriums. On the answer of the action
of endogenous toxin the organism produces a great
number of inflammation mediators, which bring on the
system answer hitting into general blood flow. These
matters – are mediators of sepsis one united under
one name – cytokines.
Today it’s known about 40 such matters. The most
significance among them has: swelling necrosis factor,
interleukins 1, 6, 8.
The considerable role in the pathogenesis of gramnegative sepsis plays the factor of activation of
thrombocytes. This phospholipid leads to the
freeing of considerable amount of cytokines.
The last stimulate production of prostaglandin, free
of radicals, oxide nitrogen, which changes in
membrane and in the cell’s nucleus.
If unspecific immune reaction gets along with
above-mentioned action, this so-called, mediate
phase is bought.
If no, the process goes into the phase of immuneparalysis and the final phase.
Clinically it is displayed by syndrome of poly-organ
insufficiency and septic shock.
The phases of the development of the generalized
infection
1.
Local inflectional focus
2.
Purulent resorptive fever
3.
Syndrome of the systematic inflammatory
answer
4.
Septicemia
5.
Lethal result
Septicopyemia
Chronic sepsis
Recovery
In according to coordinate conference on sepsis (Chicago, 1992) the
development of sepsis is interpreted something otherwise:
Local focus of infection
Syndrome on the systematic
inflammatory answer
Sepsis
Difficult (heavy) sepsis
Septic shock
Poly-organ insufficiency
Lethal result (fatal termination)
CLASSIFICATION
There is the primary and secondary
sepsis. The primary or cryptogenetic is
appeared under the lack of fixed primary
focus. The secondary is appeared on the
background of primary purulent focus.
CLASSIFICATION
On localization of primary focus
contradistinguish:
Surgical;
Obstetric-gynecological;
Urologic;
Otogenous;
Oral and others.
CLASSIFICATION
For exciter appearance:
Gram-positive (staphylococcal, streptococcal);
Gram-negative (intestinal, pyocyanogenetic,
proteus);
Anaerobic (clostridium and an clostridium).
For the phases of development:
Elementary (primary) phase (toxemia, toxicemia,
toxicohemia, toxinemia);
Septicemia (bacterioemia without purulent
metastases);
Septicopyemia (bacterioemia with metastases).
CLASSIFICATION
For clinical:
Lightning;
Acute;
Sub-acute;
Chronic;
Septic shock.
The dimensions and disposition of the primary focus
have the certain importance in the development of
disease. More frequently this is on the background of
purulent surgical diseases or vast wounds, ordinary
with crush and necrosis of soft tissues frequently after
insufficiently radical surgical treatment.
During the last years the cases of the beginning of
sepsis are established after various invasiveness
procedures: catheterization of the vessels, operations
with the use of apparatus of vasomotor system,
prosthetics of valves, etc.
These complications, which arise by reason of hospital
procedures, were accorded name “nazokomial
hospital sepsis” or “disease of medical progress”.
Some immunologists and physicians consider that
sepsis is developed in those cases when the immunedeficiency states arise until the invasion of
microorganisms into focus (AIDS, the drug habit,
diabetes, cancer).
CLINIC
The basic complaints are feeling of heat
and fever, associated with high
temperature. During sepsis with metastases
is observed, more frequently high-fever
heat, during the sepsis without metastases
sweeps of the temperature is less than 1°
C. Besides a general weakness, the loss of
appetite, insomnia, sometimes - diarrhea
disturb. Some patients have euphoria; some
are found into state of prostration.
Objectively:
The skin is of earthily gray color, with
icterychnum hue, sometimes there is petechia
break out. Tachycardia, hypotension, frequent
breathing, sometimes – the wheezes are missed.
Augmentation size of liver and spleen are. During
the sepsis with metastases there are the second
purulent focuses. The primary focus is determined
by the pallor of granulations, the delay of necrosis
of tissue, scantiness of secret, which is of
putrefactive – hemorrhagic character.
DIAGNOSTIC
The laboratory markers of sepsis are:
The progressing anemia;
Leukocytosis and deviation of the differential count to
the left. Lymphopenia – is prognostic unfavorable sign;
Augmentation of intoxication indexes (differential
blood index of intoxication, the level of middle
molecules);
T-lymphocytopenia;
Thrombocytopenia;
Elevation of erythrocyte sedimentation rate;
The fall of the level of inorganic phosphor more than
30% brings the depression of the phagocytic
bactericidal activity of granulocytes;
The growth of the level of tsytokines that testily about
the progressing pathologies.
The PGD-syndrome includes:
Respirator distress-syndrome.
Acute renal insufficiency.
Acute hepatic insufficiency.
Syndrome of disseminated intravascular
coagulation (DIC).
Violation of the function of central nervous
system.
CURE PRINCIPLES
1. Timely (right) diagnosis (take into account not
only clinical indexes but such criteria as acidbasic equilibrium, water-electrolyte balance,
activity indexes of the inflammatory process
and degree of oppression of the immune
system).
2. Cure (treatment) in the department of the
intensive therapy.
3. Radical surgical hearth treatment (adequate
drainage, timely closing).
4. Adequate antibacterial therapy. It is necessary
to take empiric antibacterial therapy before the
identification of stimulus, taking into account
the focus of infection, the state of kidneys,
liver, the immune system.
CURE PRINCIPLES
5.
Antitsitokinotherapy. Got and made the approbation the
specific monoclonial antibodies to endotoxin LPS.
The antibodies to the factor of tumors of swelling are
elaborated.
For blocking of tsitokines it is regarded the perspective the
use of ibuprophenum and trental (pentoxifillin), which
brake the formation of the factor of tumors of swelling
and predecessors of violation of the vascular
perspicacity of the lungs. It is perspective is the use of
preparation interleikin-2 – roncoleikin.
CURE PRINCIPLES
6.
7.
8.
Detoxication, which induces therapy in volume 3 – 6 litres
for day, the amount of shown out liquid more than 1000 ml,
forced diuresis (urine excretion) and the methods extra
corporal detoxication, among which the priority has
plazmapharez and limphosorbtion.
Immunocorrection depends on diagnostics displacements
in the immune system. It is better to make
hemotransfusion, transfusion of native and hiperimmune
plasmadestination of the preparations of thymus and
gamma globulins.
The feeding questions take an important place. Especially
the early enteral feeding, which improves the bloody
circulation in abdominal cavity, liver, mucous of the
stomach, warns acidosis. An important role in the
stimulation of the immune system of the bowels plays
feeding in small intestinum.
CURE PRINCIPLES
9. Hormonal therapy.
Corticosteroids used in the threat of
septic shock and also in the
augmentation of amount of T-killers and
T-supressors.
10. The correction of the system of blood
coagulation.
Heparin or lower-molecules heparins
(fraxiparin, calciparin, lavenox);
desagrigents (aspirin, tiklid); proteases
inhibitors (kontrikal, trasilol, gordox) are
used.