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Transcript
SEPTICEMIA, SEPSIS,
SEPTIC SHOCK
Definition

An expert consensus conference of the American
College of Chest Physicians and the Society of
Critical Care coined the phrase systemic
inflammatory response syndrome (SIRS) to
describe a clinical syndrome believed to be the
result of an overly activated inflammatory
response.

This new definition recognized the important
role that endogenous mediators of systemic
inflammation play in sepsis, which was no longer
regarded as being caused by microbial
pathogenicity factors alone .

Septicemia is a dramatic clinical syndrome, which

Fever, chills, tachycardia, tachypnea and altered
mentation are common acute manifestations of
septicemia.

result from acute invasion of the bloodstream by certain
microorganism or their toxic products.
Bacteremia: is the presence of vivid bacteria in
bloodstream confirmed by the blood culture with the
isolation of a pathogen.
Systemic inflammatory response
syndrome (SIRS): contains two or
more of the following conditions:





fever, over the 38oC or hypothermia less than 36oC;
tachypneea more than 20 breaths/min;
tachycardia more than 90 beats/min.;
leucocytosis more than 12000/mmc;
leucopenia less than 4000/mmc or more than 10
percents immature forms.

Sepsis means: SIRS plus a documented
infection
 Severe sepsis
 Septic shock
Multiple organ dysfunction syndrome
(MODS)
Respiratory: PaO2<80 mmHg, PaCO2>50mmHg,
respiratory rate<5/min, or >50/min;
 Renal system: increased serum creatinine, oliguria
(<480ml/24h);
 Cardiovascular system: hypotension, heart rate<55/min,
ph<7.25;
 Hepatic system: serum bilirubin>60mg/l, TP<15%;
 Gastrointestinal system: bleedings, pancreatitis, ileus,
perforation;
 CNS: Glasgow coma score <6;
 Hematologic system: platelet count<20000/mmc,
leucocytes<1000/mmc, hematocrit<20%.

Etiology

Multiple components of the microbial structure
may initiate the systemic inflammatory response.
Gram positive:
 Streptococcus pneumoniae
 Staphylococcus aureus/epidermidis
 Streptococcus pyogenes
 Clostridium
Gram negative:
 Neisseria meningitidis
 Gram negative bacilli: E. coli, Salmonella, Klebsiella,
Pseudomonas, Yersinia pestis, Vibrio vulnificans,
Aeromonas species










Rickettsia rickettsii
Capnocytophaga canimorsus
Erlichia species
Bartonella species
Dengue viruses
Viruses - causes of the hantavirus pulmonary
syndrome
Plasmodium falciparum
Babesia microti
Anaerobes: peptococcus, microaerofili
streptococci, Actimomyces israelii.
Epidemiology
Predisposing factors include:
diabetes mellitus,
 cirrhosis,
 alcoholism,
 leukemia, lymphoma or disseminated carcinoma,
 cytotoxic chemotherapy and immunosuppresive drugs
which cause neutropenia,
 total parenteral nutrition,
 a variety of surgical procedures and infections arising
from the urinary, biliary or gastrointestinal tracts.


Pathogenesis and pathology
Most of the bacteria causing gram-negative sepsis are normal
commensals in the gastrointestinal tract. From there they may
spread to contiguous structures (as in peritonitis after appendiceal
perforation), or they may migrate from the perineum into the
urethra or bladder.







Gram-negative bacteremia follows infection in a primary forms,
usually the:
genitourinary tract,
biliary tree,
gastrointestinal tract or
lungs and
less commonly, the skin, bones and joints.
Metastatic abscess formation may complicate bacteremia.
The involved target organs are:


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lungs: pulmonary-edema, hemorrhage and hyaline membrane
formation, abscesses, bronchopneumonia
kidney: tubular or cortical necrosis,
myocardium: patchy necrosis, superficial ulceration or even
hemorrhage necrosis
gastrointestinal tract, superficial ulceration or even hemorrhage
necrosis
capillaries in many tissues: leukocyte-platelet or fibrin thrombus
formation
brain /meninges: abscesses, meningitis
Pathophysiology
Table 1: Virulence factors of Staphylococcus aureus and their proposed
pathogenic mechanism
VIRULENCE FACTORS OF STAPHYLOCOCCUS AUREUS AND THEIR PROPOSED
PATHOGENIC MECHANISM `
Twart host defenses
Microcapsule
Protein A
Coagulase
Fatty acid-metabolizing enzyme
Leukocidin and/or gama-toxin
Invade tissueProteases
NucleasesLipases
Hyaluronate lyase
StaphylokinaseElicit sepsis syndrome
Toxic shock syndrome toxin
Enterotoxins
Cytolytic toxins (alpha, beta, gama and delta)Induce specific toxinosis
Toxic shock syndrome toxin
EnterotoxinExfoliative toxin
Attach to endothelial cells and basement membrane
Binding proteins for fibrinogen, fibronectin, laminin, collagen, vitronectin and
Clinical manifestations
Clinical manifestations are related to the following
elements:
I.Portal of entry




Skin: erysipelas, staphylococcal skin infection,
trauma, burns;
Respiratory tract infections
Gastrointestinal tract lesions: stomatitis, gingivitis,
teeth extraction, enterocolitis;
Genito-urinary tract infections
II.Lymphangitis and primary sites of infection
III.Positive blood cultures: hematogenous dissemination is
manifested with fever, chills, headache;
IV.Metastatic foci of infection:

Cardiovascular system: infective endocarditis, myocarditis, pericarditis

Central nervous system: brain abscess, epidural abscess, purulent meningitis
(confusion, obtundation, coma);

Respiratory system: bronchopneumonia, pleural effusion (acute respiratory
distress syndrome, tachypnea, hypocapnea);

Gastrointestinal: liver and spleen abscess, impaired gastrointestinal motility,
sterss related mucosal disease, hyperbilirubinemia, elevation of liver enzymes.

Renal system: renal abscess, nephritis

Bone and joint involvement: osteitis, osteomyelitis, spondylodiscitis, arthritis
Cutaneous manifestations: cellulitis, flegmons, diffuse erythroderma (caused by
gram-positive organisms and by the action of pyrogenic or erythrogenic toxins);
colorful skin lesions such as ecthyma gangrenosum (associated with P.
aeruginosa septicemia), colorful vezicular or bullous lesions, cellulitis, petechial
lesions (may appear in gram negative septicemia)

Toxic shock syndrome
Clinical manifestations
1. Hemodynamic changes:
2. Dermatologic findings:
3. Severe myalgias, muscle tenderness, weakness
4. Diarrhea, nausea, vomiting]
5. Encephalopathy
6. Respiratory distress syndrome
7. Acute renal failure
8. Hepatic necrosis
9. Disseminated intravascular coagulation.
Table 4: Streptococcal Toxic Shock Syndrome
Streptococcal Toxic Shock Syndrome –
definition
An acute, febrile illness that begins with a mild viral-like
prodrome or minor soft-tissue infection and may
progress to shock, multiorgan failure and death
Symptoms
Early symptoms are vague:
Viral-like prodrome
Severe pain and erythema of an extremity
Mental confusion
Signs
Hypotension, systolic
Fever > 38 degree
Soft-tissue swelling
Tenderness
Respiratory failure, rales, cyanosis, tachypneea
Laboratory features
Hematologic:
Marked left shift
Decline in hematocrit
Thrombocytopenia
Renal azotemia (2,5 x normal on admission) and hematuria
Hypocalcemia
Hypoalbuminemia
Creatine phosphokinase elevation
Pulmonary abnormalities:
-Pulmonary infiltrate on chest x-ray
-Hypoxia
Table 5. Laboratory investigations in sepsis
Complete blood count
Blood chemistry
Urinalysis
Chest radiography
Erythrocyte sedimentation rate
Blood cultures (3 or more separate
specimens)
Cultures from other biologic fluids
(pus, pleural effusion, joint
effusion, catheter, etc)
Antinuclear antibodies
Rheumatoid factor
Computed tomography of
abdomen, pelvis, other sites
Radionuclide scansVenous duplex
imaging of lower limbs
Echocardiography

Differential diagnosis
Infectious diseases





Bacterial infections
Rickettsial infections
Viral infections:,
Parasitic infections:
Fungal infections:
Non-infectious diseases





Neoplastic diseases:;
Autoimmune diseases:
Hypersensitivity;
Granulomatous diseases:
Other: CNS hemorrhage, CNS degenerative diseases, familial
Mediteranean fever, cholangitis.
Treatment

A. Initial therapy for the sepsis syndrome
Community-acquired infections
Suspected staphyloccocal etiology: oxacillin+aminoglycoside
Suspected genito-urinary source: a third generation cephalosporin (3GC); a
quinolone; ticarcillin/piperacillin with/without an aminoglycoside;
Non-urinary tract source: 3GC or ampicillin/ticarcillin/piperacillin – beta
lactamase-inhibitor (BLI)
Hospital-acquired infections:
Non-neutropenic patients: 3GC with/without metronidazole, cefepime, a beta
lactam drug-BLI/imipenem with/without an aminoglycoside
Neutropenic patients: ceftazidime + an aminoglycoside; ticarcillinclavulanat/piperacillin-tazobactam + an aminoglycoside;
imipenem/meropenem + an aminoglycoside.
Tabel 6.First intention treatment and alternative therapy for
infective endocarditis on native valve
Etiology
S.aureus metiSS.aureus meti-RS.viridans, S.
bovis- sensitive to Pen.
G(CMI<o,1microg/ml)
S.viridans, S.bovis with CMI
PenG:0,1-0,5microg/ml.
S viridans, S.bovis (CMI
PenG>1),
enterococi sensitive to
ampi/Pen G, vanco, genta
Enterococi (CMI Pen G
>16ng/ml)
Enterococi pen/ampi R, high
resistance to genta, vancoR
Difteroizi sensitive to genta
(MIC<4/ml)Difteroizi
resistent to genta (>4/ml)
gram-negative cocobacili
from the group HACEK*
BartonellaCandida
EI on valvular prothesis with
negative bloodcultures
First intention treatment
Alternative
(oxaciline 8g/d iv, every 4h)x4-6wks
+gentax3-5days
(Vanco 2g/d iv, every 12h)x4-6wks
Pen.G 12-18milU/d, iv, cont/4hx2 wks +
genta 3mg/kg/d x2wks or
Pen G x4wks or
Ceftriaxone 4g/d x4wks
Pen G 18mil U/d x4wks+genta 3mg/kg/d
x 2wks,
Pen G 18milU/24h, 4-6spt+genta 46wks, or (AMP12g/zi iv cont or
every 4h+genta)x4-6wks
Vanco+gentax4-6wks
Quinupristin/dalfopristin or linezolid
1200mg/zi iv
PenG+gentax6wks
Vancox6wks
Ceftriaxone 2-3g iv or cefotaxime 3g
ivx6wks
Fluoroquinolone or RIF or macrolide
Amfotericine B+/-an azol (fluconazole)
Vanco+RIF+gentax6wks
1. Cefazolin 6g ivx46weeks+genta3mg/kgx
3-5d, OR 2. Vanco 46wks
3. (Ceftriaxone +
genta)x2wks
4. vanco 30mg/kgc/d
until la 2g/dx4wks
5. (vanco+genta) x46wks
7.Vancox6wks
Ampi 12g/d+(strepto
15mg/kg-1g/d or
genta)x6wks
Table 7. Infective endocarditis on prosthetic valve
Etiology
S. epidermidis
S.aureus meti-R
S.aureus meti-S
EI on valvular prothesis with
negative bloodcultures
For the other etiology
First intention
treatment
(Vanco 2g/d iv, every
12h+RIF 900mg/d, every
8h)x6wks +genta*
240mg/d every 8 hx2wks
“ “
“
(oxaciline 8g/d iv, every
4h+RIF)x6wks
+gentax2wks
Vanco+RIF+gentax6wks
As for the native valve
endocarditis.
Alternative
Vanco+Fluoroquinolone+RI
F
“
“ “
B. Adjunctive measures in the treatment of
sepsis syndrome

Maintenance of adequate tissue perfusion with volume
replacement: normal saline solution, fresh frozen
plasma, albumin, dextran, crystaloid solutions.

Sympatomimetic amines: dopamine, dobutamine

Corticosteroids for gram-negative rod septicemia-is
controversed.

Diuretics for the early oliguric phases of schock.