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SEPSIS (Lecture 17/2/10) = systemic disease triggered by special kind of infectious, endogenic microorganisms and characterised by prolonged unrestricted hyperaemia with hemodynamic abnormalities and end-organ failure Main peculiarities : There is no cyclic course (dt unrestricted) Septicemia Triggered by special kind of infection, so called endogenic microorganism Char by unrestricted bacteremia, hemodynamic dist n organ F Cause by conditional pathogen, colonizing human body after procedure(abortion, skin abrasion) 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 and co-exist with microorganism – Play a great role -> Immunogenic readiness to defend organism against pathogenic microbes Causes: Bacteremia Isolation of bacteria from peripheral blood & mb transient or inconsequential May progress to septic shock if unRx Cause : absolute pathogenic microbe
Before fever, there are 3 types of changes of fever that is called pre-sepsis : 1° purulent focus
Short time 1-day ↑ of temperature during 1-2 weeks 2-3 days period of high fever during some weeks 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, it can 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
Gram –ve Proteus, Klebsiella, Enterobacter, Bacteriods (Cl. Perfringens) Gr. +ve Staphylococcus, Streptococcus
Sometimes the microbe associated may cause sepsis PATHOGENESIS Main factor : breakdown of defence mechanism against commensals & generalisation of endogenous infection Develop typical pathologic process ↓ Septic vasculitis
Secondary purulent foci = progressive disease Characterised by metastatic foci (abscess, phlegmona, meningitis, endocarditis) Sign of poor prognosis, will lead to multiple organfailure, which is the final stage with high autoimmune process and auto-aggression
Paresis of blood vessels and nerves which lead to fulminant sepsis and ITS permeability & output of fluid from blood to surrounding tissue. This lead to high doses of BAS, Inflammatory Cytokines, transformation of tissue protein to autoAg. Auto-aggression is triggered
Multiple Organ Failure is the final stage of the disease that often leads to death and is characterised by high autoimmune process and auto-aggression. It is associated with: Heart failure Renal failure Respiratory failure
Auto-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) (2) (3) (4) (5) (6) Fever Toxicosis Enlarged spleen Blood test changes Hv 1° and 2° foci Multi-organ failure & death Respiratory failure is dt lung damage and progressive acute respiratory failure or non-cardiac pulmonary edema (shock lung) Renal failure is characterised by oliguria, proteinuria and BUN. It develops in the first 3 days. SHOCK -variant of hypertoxicosis at the 1st 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 septic vasculitis There are 3 stages of shock according the mechanism of compensation :
Compensated - support BP - make up blood circulating volume - catecholamines lt spasm of pre-capillary sphincter - BP but ↓ in amount of capillaries. - centralization of blood circulation Subcompensated - paresis of pre-capillaries - ↓ of catecholamines - congestion of blood in venous part - ↓ venous return, ↓ systolic CO Decompensated - there is absence of perfusion - ↑ in lactate and leads to peripheral acidosis - in breathing (dyspnea, tachypnea) leads to central alkalosis - STOP in metabolism and death ensues
Positive result may be estimated in 5-7 days Negative results are in 10-14 days TREATMENT – Should be aggressive – Antimicrobial therapy ○ Best should be on result of sensitivity test but its not clinically responsible because it takes a long time ○ Odontogenous : Ampiox (Ampicillin + Oxacillin) 3rd generation Cephalosporin ○ Tonsillogenous Ampiox Aminoglycosides ○ All others Aminoglycoside Cephalosporin General rule is we should use a combination of 2 Antibiotics in maximal dose and one of the doses must be in IV form. We must estimate efficacy in 24hours. If there is no improvement, change the antibiotic. Anticoagulants – Max dose – Constantly during the day – 20 000 – 80 000 U of Heparin Protease inhibitor – Prevent auto-aggression ○ Octreatid ○ Gordox Immunotherapy Extracorporal detoxication – Not to be started during active phase because it ↓ concentration of antibiotic – Exception for septic shock or severe sepsis DDX Typhoid or Paratyphoid Epidemic typhus Malaria HIV If epidemic data of contact with animals, then suspect : – HFRS – Yersiniosis – Brucellosis Differential diagnosis with non-infectious disease – Collagenosis ○ Different temperature curve, in this case it is not ‘correct’ fever, for example high fever for 2 -3 days then no fever for a few 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 vaccine 10 – 15 days – Schizophrenia ○ Have hallucinations, thought echo, etc Chronic Sepsis must be differentiated with
CLASSIFICATION 1. Origin
a. b. c. d. e. f. 2.
Otogenic Staphylococcal Odontogenic Anaerobes Tonsillogenic Streptococcal Urinogenous Gram –ve bact Obstetrical origin Anaerobes Intestinal origin E.Coli
Modern classification, in use since 1991 +ve hemoculture without CM, revealed at special Ix w/o bacterial confirmation Fever >38.5 or <35.6, BP <90mmHg, PR > 90bpm dyspnea > 20/min, oliguria, leukocytosis > 12 CM + Lab confirmation CM + forming of 2° purulent foci, poor prognosis and risk of death
Syndrome of systemic inflammatory reaction
Sepsis Severe sepsis
Outcome = Septic Shock 3 types of Sepsis : 1. Fulminant 2. Acute ( >3 days) 3. Chronic (>1.5 months) DIAGNOSIS - Bacteria isolated from blood There are a few techniques on how to obtain blood specimen • 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 antibiotics administration The best period to take samples is during chills period because this means there is output of bacteria into the blood stream. The period of max temperature signifies the release of pyrogens after bacteria destruction.
– TB – Pathology of thyroid gland – Encephalic symptoms (febrile for months)
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