Transcript i. sepsis

SEPSE
History of sepsis
SEPSIOS – rotten, putrid
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2 thousand years BC – Egypt - abscess
5O years BC - Celsus – 4 signs of inflammation
1st century – Galen - + functio laesa
1752 – Pringle – antisepsis
187O-19OO – most bacterial causal organisms
1928 – Fleming PNC
ETIOLOGIC AGENTS
G-
G+
Mixed
YEASTS
50 - 80 %
20 - 40 %
15 - 20 %
MRSA
VISA
VRE
Sepsis is the most serious and
the most frequent complication
in surgery and traumatology
 Incidence rises every year by 8.7%
DEFINITION OF SEPSIS
1992 - C.C. USA
SEPSIS is systemic response to infection with aim to
eliminate the causal organism, to prevent spread
of infection and to repair the established tissue
Sepsis develops when infection overcomes local protective
barriers of an organism and mediators are washed out to
circulation from primary focus.
5 systems responsible for
inflammatory reaction
 Platelets
 Endothelial cells (NO, PGI2)
 Complement
 Leucocytes
 Plasmatic hemocoagulation system
Local inflammatory response
Symptoms of the local inflammation
 • rubor (color)
 • calor (temperature)
 • tumor (edema)
 • dolor (pain)
 • functio laesa (dysfunction)
Systemic inflammatory
response syndrome (SIRS)
 Definition
Delocalized and dysregulated inflammation process of high
intensity. It leads to disorders of microcirculation, organ
perfusion and finally to secondary organ dysfunction.
• This secondary dysfunction is not due to primary insult, but
due to auto-aggressive systemic inflammatory response of
the organism to the primary insult.
• This systemic inflammatory response syndrome (SIRS), leads
without therapeutic intervention to multiple organ
dysfunction syndrome (MODS) and death.
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CLASSIFICATION OF SEPSIS
(C.C. 1992)
I. SEPSIS
 body temperature above 38 oC
 heart rate above 90/min.
 respiratory rate above 20/min.
or
 PaCO2 less than 4,3 kPa (=32 mm Hg)
 leukocytes above 12 000/mm3 or 4 000 mm3
or
more than 10 % of rod forms
Peripheral vasodilatation
† 20 - 30 %
2<
2
Classification of sepsis
(C.C. 1992)
II. SEVERE SEPSIS
= sepsis +
 hypotension - 90/40 /-4Osyst./ > 2 hours
 signs of hypo-perfusion or organ dysfunction
Lactate acid , oliguria, thrombocytopenia, ARDS
lactate level 2,3 - 0,5ml/kg
† 40 - 50 %
3
Classification of sepsis
III. SEPTIC SHOCK
(C.C. 1992)
 hypotension which does not react to supplementation of volume /?/
 BP less than 9Osyst. or mean BP 6O-7O on support therapy with
catecholamine
 symptoms of organ hypo-perfusion
MODS …. MOFS>1
† 50 - 60 %
PROGNOSIS
 Multi-organ dysfunction causes 75% of deaths in
surgical intensive care
5 - 30 %
Number of malfunctioning
organs
1 organ
40 - 60 %
2 organs
60 - 80 %
3 organs
95 - 100 %
4 and more organs
Letality
MORTALITY
Sepsis
20 - 30 %
Severe sepsis
40 - 50 %
Septic shock
50 - 60 %
PREDISPOSITION
BARRIER FAILURE
- st. p. surgery, status post trauma
- i.v. cannula, shunts
- CVC
- urinary catheter
IMMUNITY REDUCTION
- decompensate diabetes, uremia
- therapy with corticosteroids, radiation, cytostatic drugs,
neutropenia
- st. p. splenectomy
- age lower than 6 years
- AIDS
PRIMARY LOWER VITALITY
- affection of vital organ (ICHD, cirrhosis, ...)
- high age
LOCALISATION OF SEPTIC FOCUS
I. In circulation
1) thrombophlebitis pelvic circulation
v. portae
v. jugularis
(metastatic spread is frequent,
persistent bacteriemia, severe course)
catheters
2) endocarditis - endarteritis = central sepsis
(metastatic spread, massive
bacteriemia is persistent, bad
prognosis)
LOCALIZATION OF SEPTIC FOCUS
II. Out of circulation
3) Hollow organs - abdominal cavity
billiary system
marrow cavity
otogenic
uropoetic
gynecologic
respiratory
CNS
4) Lymphatic propagation – wound sepsis
traumatic
surgical wounds
bed sores
burn injuries
(rare metastatic spread)
CLINICAL COURSE OF SEPSIS
1) Peracute (hours)
2) Acute (days)
3) Subacute (2 - 3 weeks)
4) Chronic with phases of exacerbation
Global state of organisms
Etiology agent (G -, meningococcus)
Inoculation dose
Localization of focus
PATHOPHYSIOLOGY OF SEPSIS
Infectious cause
Local wash out of inflammatory mediators
(histamine, heparin, serotonin, cytokines ...)
Localized (organ) inflammatory reaction
/T,D,R,C,FL /
Conversion of inflammatory mediators into circulation = SIRS
Endothelial damage
Generalized
inflammatory response
Sepsis /SIRS/
Persisting
damage of at least
1 organ,
hypotension
Septic shock
(MODS)
Refractory hypotension
and damage of more
organs
Multiorgan failure
/MOFS/
Pathophysiology of septic shock
Distribution form of circulatory failure
 Vasculature
1)
2)
3)
4)
Generalized vasodilaton
Toxic damage of endothelium
Evasion of plasma and inflammatory mediators in interstitial spce
Absolute insufficiency of circulatory volume
 Myocardium
MDF + TNF + O2
TRANSLOCATION OF BACTERIA
Hypo-perfusion and intestinal hypoxia
8O% IgA
translocation of physiology intestinal flora in organism
a) portal blood
b) splanchnic lymphatic system
c) directly in abdominal cavity
* G- bacteria
continuous pathology activation of immune system
MODS, MOFS
Practical precautions:
 restriction of multiplication G- bacteria in the intestine
(ATB, obstruction, bowel movement)
 maintenance of intestinal barrier
(enteral nutrition, glutamine + pulp material, prevent hypoperfusion of splanchnic region – circulation + adrenalin)
 prevent consequences of bacteria translocation
(ATB, hemodynamics)
SEPSIS THERAPY POSSIBILITIES
symptomatic therapy
- support of malfunctioning organs and systems
- energy supply
- restoration of inner environment
- retardation of cytokine cascade
causal therapy
- removal of primary cause
- liquidation of focus
- chemotherapy – liquidation of etiologic agent
Effects of
corticosteroids in sepsis
 High doses = more than 500 mg=
immunosuppressant effect
 Low doses = up to 300mg
increase of receptor sensitivity to
norepinephrine
inhibition of NO formation
increase of vascular tone
Administration of
corticosteroids in course of
septic shock
 200- 300mg/day
 3 - 4 doses
 For 7 days
 Reduction of mortality by 15%
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SUPPORT OF MALFUNCTIONING SYSTEMS
AND ORGANS
1) Removal of hypoxia
(RR>30, pO2 under 90, pCO2 above 8kPa)
2) Haemodynamic stability
CVP 12 -15 mm Hg
3) Elimination methods
4) Substitution of adrenal glands
cortisol 25O-6OO (Synacten)-ACTH
Dexamethasone
2
5) Blood coagulation - DIC
heparin 3x5 thousands units sc
x continuously.
antitrombin III pod 8O-5O%
thrombocytes substitution
fibrinogen under O,5-l g l
6) CNS
symptomatic therapy
7) Immune system
IgG + IgM
8) GIT
H2 blockers
 proton pump blockers
 antacids
ENERGY SUPPLY
enteral
x
parenteral
PARANTERAL THERAPY
1) Peracute phase = immediately after attack
= fluids + E, C vitamin + glucose
2) Acute phase
= hypermetabolic phase
= 3. – 7. day
= 80 % coverage
= G + AC + gradually lipids
3) Subacute phase
= 7. day and onwards
= 100 % coverage
+ lipids + enteral nutrition
PARENTERAL THERAPY IN SEPSIS
ALL - IN - ONE
Required energy supply ... 25 - 30/kJ/kg/day
(2100kcal - 8300 kJ/70 kg )
80 %
Higher calories supply reduces negative N balance but does not reduce
catabolism
Long term complete parenteral nutrition = more than 3-5 days
20 % amino acids - (10 - 40 %) lipids - (40 - 70 %) carbohydrates
SHOCK = 12 - 24 hours – contraindication of complete parenteral nutritio
Therapy of septic shock
 1. Volume therapy
Crystalloids 5OO-1OOOml /3Omin
Colloids 3OO-5OO ml /3O min
To be repeated according to response and tolerance every
24 hours
 2. Vasopressors
from BP 65-7O syst.BP NOREPINEPHRIN
in case of cardiac insufficiency Dobutamine
AMINO ACIDS: 20%
max. 1 g/kg/day ................. 70 g/day
Nutramin U ............................. Renal insufficiency
LIPIDS: 10 -
40%
max. 1 - 2 g/kg/day ............ 70 - 140 g/day
optimal supply of energy 30 - 50 %,
for optimal utilization of amino acids
Nutrolipid, Elolipid, Intralipid = LTC/ MTC
Lipofundin - MTC 50 g/l
Contraindication:
= 500 ml 20% emulsion
?shock?, decompensate diabetes, fat
embolism
?pancreatitis? TAG
DIC
severe liver failure
hyperglyceridemia> 4 mm/l
GLUCOSE:
max. 7 - 10 g/kg/day
(150 - 200 g/day) CNS
Sorbitol, Fructose - not suitable
G - infection, Candida, osmotic diuresis
CRYSTALLOIDS:
up to 7 liters ...................... diuresis 2 - 3 l/day
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Colloids ……. .. 1:2 /?/
VITAMINS:
TRACE ELEMENTS:
Causal therapy
1) Removal of primary cause
UC, CVC, DM .............
2) Liquidation of focus
a) diagnosis – abdominal x-ray, US, CT, MRI, SCINTI
b) removal - surgical
X-ray or US
punction
drainage
3) Liquidation of etiologic agent
a) Dg microscopic
culturing
serology
proof of toxins
b) ATB + CHT
empiric
targeted x
ATB
prevention