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Sepsis

Sepsis

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Published by Maisarah Repin
Lecture Note from Infectious Disease rotation 5th year (NNSMA)
Lecture Note from Infectious Disease rotation 5th year (NNSMA)

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Published by: Maisarah Repin on Feb 18, 2010
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05/17/2012

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Maisarah Repin
SEPSIS (Lecture 17/2/10)= systemic disease triggered by special kind of infectious,endogenic microorganisms and characterised by prolongedunrestricted hyperaemia with hemodynamic abnormalitiesand end-organ failureMain peculiarities : There is no cyclic course (dt unrestricted)Septicemia BacteremiaTriggered by special kind of infection, so called endogenicmicroorganismIsolation of bacteria fromperipheral blood & mbtransient or inconsequentialChar by unrestrictedbacteremia, hemodynamicdist n organ FMay progress to septicshock if unRxCause by conditionalpathogen, colonizing humanbody after procedure(abortion,skin abrasion)Cause : absolutepathogenic microbe
ETIOLOGY 
 –Can be caused by a lot of commensals –They colonize human body since neonatal period,during which time immune mechanisms are absent.They colonize mucosa of the respiratory tract, GIT andco-exist with microorganism –Play a great role -> Immunogenic readiness to defendorganism against pathogenic microbesCauses:
Gram –ve
Proteus, Klebsiella, Enterobacter,Bacteriods (Cl. Perfringens)
Gr. +ve
Staphylococcus, StreptococcusSometimes the microbe associated may cause sepsis
PATHOGENESIS 
Main factor : breakdown of defence mechanism againstcommensals & generalisation of endogenous infectionDevelop typical pathologic process 
Septic vasculitis
Paresis of blood vessels and nerveswhich lead to fulminant sepsis and ITS
permeability & output of fluid fromblood to surrounding tissue. This lead tohigh doses of BAS, InflammatoryCytokines, transformation of tissueprotein to autoAg.
Auto-aggression is triggeredAuto-aggression = 2° inflammatory foci formed in diff organs
Progress and lead to development of multi-organ failure
They are reflected in main CM of sepsis (cardinal Sx) :(1)Feve(2)Toxicosis(3)Enlarged spleen(4)Blood test changes(5)Hv 1° and 2° foci(6)Multi-organ failure & deathBefore fever, there are 3 types of changes of fever that iscalled pre-sepsis :1° purulent focus
1.
Short time 1-day
of temperature during 1-2weeks2.2-3 days period of high fever during some weeks3.Undulant fever last 3-4 weeks
Fever 
- can be hectic or remittent- Hectic is a difference of temperature > 2 C- Remittent is a difference of temperature between 1 – 2 C
Toxicosis-
Shaking chills- HA- Prostration- n+v
Enlarged spleen-
HSM
early symptom. Develop in the first few days of disease- USE can reveal it in the beginning and after some time, itcan be revealed by palpation.- Structure of liver is soft, sagging and painless
Changes in blood
-
leukocytes- Neutrophils have toxic granularities- TCP-
ESR- anemia at later terms of disease
Hemorrhagic rash
 
symptom of generalized vasculitis 
range from point elements to extensive
Primary purulent foci
Not obligate sign of sepsis
Local inflammation
X always the SOI
Trigger factor 
Their sanation don’t lead to restriction of sepsis
Secondary purulent foci
= progressive disease
Characterised by metastatic foci (abscess,phlegmona, meningitis, endocarditis)
Sign of poor prognosis, will lead to multiple organ-failure, which is the final stage with high auto-immune process and auto-aggression
Multiple Organ Failure
is the final stage of the disease thatoften leads to death and is characterised by high auto-immune process and auto-aggression. It is associated with:
Heart failure
Renal failure
Respiratory failureRespiratory failure is dt lung damage and progressive acuterespiratory failure or non-cardiac pulmonary edema (shocklung)Renal failure is characterised by oliguria, proteinuria and
 BUN. It develops in the first 3 days.
SHOCK
-variant of hypertoxicosis at the 1
st
day/hours of sepsis-maybe as complication of a final stage of the disease-characterized by hemodynamic disorders as a result of toxin’s action(vasodilatation) & development of septicvasculitisThere are 3 stages of shock according the mechanism of compensation :
 
Maisarah Repin
1.
Compensated- support BP- make up blood circulating volume- catecholamines lt spasm of pre-capillarysphincter -
BP but
in amount of capillaries.- centralization of blood circulation
2.
Subcompensated- paresis of pre-capillaries-
of catecholamines- congestion of blood in venous part-
venous return,
systolic CO
3.
Decompensated- there is absence of perfusion-
in lactate and leads to peripheral acidosis-
in breathing (dyspnea, tachypnea) leads tocentral alkalosis- STOP in metabolism and death ensues
CLASSIFICATION 
1.Origin
a.
Otogenic
Staphylococcal
b.
Odontogenic
Anaerobes
c.
Tonsillogenic
Streptococcal
d.
Urinogenous
Gram –ve bact
e.
Obstetrical origin
Anaerobes
f.
Intestinal origin
E.Coli
2.
Modern classification, in use since 1991Bacteremia+ve hemoculture without CM,revealed at special IxSyndrome of systemicinflammatory reactionw/o bacterial confirmationFever >38.5 or <35.6, BP<90mmHg, PR > 90bpmdyspnea > 20/min, oliguria,leukocytosis > 12SepsisCM + Lab confirmationSevere sepsisCM + forming of 2° purulent foci,poor prognosis and
risk of deathOutcome = Septic Shock3 types of Sepsis :1.Fulminant2.Acute ( >3 days)3.Chronic (>1.5 months)
DIAGNOSIS 
- Bacteria isolated from bloodThere are a few techniques on how to obtain bloodspecimen
Site of venopuncture must be disinfected
Blood should be drawn at 2 different sites
Multiple samples should be drawn (3 samples over a 24h period)
Blood should be drawn before antibioticsadministrationThe best period to take samples is during chills periodbecause this means there is output of bacteria into the bloodstream. The period of max temperature signifies the releaseof pyrogens after bacteria destruction.Positive result may be estimated in 5-7 daysNegative results are in 10-14 days
TREATMENT 
 –Should be aggressive –Antimicrobial therapy
Best should be on result of sensitivitytest but its not clinically responsiblebecause it takes a long time
Odontogenous :
Ampiox (Ampicillin +Oxacillin)
3
rd
generation Cephalosporin
Tonsillogenous
Ampiox
Aminoglycosides
All others
Aminoglycoside
CephalosporinGeneral rule is we should use a combination of 2 Antibioticsin maximal dose and one of the doses must be in IV form.We must estimate efficacy in 24hours. If there is noimprovement, change the antibiotic.Anticoagulants –Max dose –Constantly during the day –20 000 – 80 000 U of HeparinProtease inhibitor  –Prevent auto-aggression
Octreatid
GordoxImmunotherapyExtracorporal detoxication
 –
Not to be started during active phase because it
concentration of antibiotic –Exception for septic shock or severe sepsis
DDX 
Typhoid or ParatyphoidEpidemic typhusMalariaHIVIf 
epidemic data of contact with animals, then suspect : HFRS –Yersiniosis –BrucellosisDifferential diagnosis with non-infectious disease –Collagenosis
Different temperature curve, in this caseit is not ‘correct’ fever, for example highfever for 2 -3 days then no fever for afew days then again fever…
In spite of high fever,
leukocytes
Oral steroids are effective –Tuberculosis
Fever, x like sepsis
We don’t see typical changes of blood
+ve skin test (Mantoux test)
APR –Pathology of blood
Myeloleucosis
Fever + hemorrhagic syndrome –Tumors with metastasis –Post-vaccination reaction
Difficult because fever precede vaccine10 – 15 days –Schizophrenia
Have hallucinations, thought echo, etcChronic Sepsis must be differentiated with

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