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SEPSIS
DEFINITIONS
microbes involves a
rapidly amplifying
polyphony of signals
and responses that
may spread beyond
the invaded tissue.
1.
1.
1.1
(systemic inflammatory response
syndromeSIRS)
1.2
1.2.1 38C36C
1.2.2 90
1.2.3 20
1.2.4 120004000
10(bands)
ETIOLOGY
gram-negative and gram-
positive bacteria
fungi,
mycobacteria,
rickettsiae,
viruses,
or protozoans
Fungemia :
immunosuppressed patients
neutropenia
broad-spectrum antimicrobial therapy
TPN
Intestinal perforation
PATHOPHYSIOLOGY
Endotoxin
S/S:
fever, chills, tachycardia, tachypnea, altered mental
status, and hypotension.
afebrile
common in neonates, in elderly patients
and in persons with uremia or alcoholism.
CLINICAL MANIFESTATIONS
Llaboratory finding:
C-reactive protein
fibrinogen
complement components
transferrin
inhibits albumin synthesis
Leukocytosis, left shift
LABORATORY FINDINGS
Early sepsis
leukocytosis with a left shift
Respiratory alkalosis
Thrombocytopenia
Hyperbilirubinemia
proteinuria.
neutrophils may contain toxic granulations, Dohle
bodies, or cytoplasmic vacuoles
LABORATORY FINDINGS
Progressing of sepsis:
thrombocytopenia worsens
prolongation of the thrombin time
decreased fibrinogen
presence of D-dimers, suggesting DIC)
Azotemia, hyperbilirubinemia become prominent
Elevated GOT GPT
LABORATORY FINDINGS
Progressing sepsis:
hyperventilation induces respiratory alkalosis.
accumulation of lactate,
metabolic acidosis (with increased anion gap)
hyperglycemia, severe infection may precipitate
diabetic ketoacidosis(DKA)
Multiple organ dysfunction
syndrome
MOF:
Dysfunction or failure of multiple organs
reflecting widespread vascular endothelial
injury
associated with high fatality rates.
Mortality and morbidity correlate with the
number of organs affected.
DIAGNOSIS
Definitive diagnosis
isolation of the microorganism from blood or a local
infected site
Gram's stain
culture of the primary site of infection.
TREATMENT
Successful management
urgent measures to treat the local site of infection,
hemodynamic and respiratory support
eliminate the offending microorganism
Therapy of acidosis and DIC, other complications
TREATMENT
Outcome
influenced by the patient's underlying disease
aggressively treated.
Antimicrobial agents
PROGNOSIS
Mortality:
More than 25 %
1/3 within the first 48 h
mortality can occur 14 or more days later.
Late deaths
poorly controlled infection
complications of intensive care
multiple organs failure
2.
2.1
2.1.1 8-12mmHg
2.1.2 65 mmHg
2.1.3 0.5
2.1.4 70
2.
2.2
2.2.123
2.2.2
2.2.3
2.2.4
2.
2.2
2.2.5
2.2.6
2.2.7
2.2.8
2.2.9
3.
3.1
3.2
()
3.3
(
)
3.3.1
3.3.2
3.3.3
3.
3.44872
3.4.1
3.4.2
3.4.3
3.4.47-10
3.4.5
4
4.1
4.1.1
4.1.2
5
5.1
5.1.1
5.1.2303001000
30300500
5.1.3
5.1.4
5.2
6
6.1
6.2
6.3 Nor-epinephrinedopamine
6.4
6.5 Nor-epinephrine0.010.04 units/
6.6 Cardiac index2.5 L.min-1.m2
7 (Dobutamine)
7.1
8
8.1
8.2 hydrocortisone20030034
7
8.3 ATCHdexamethasone
hydrocortisonecortisol
8.4
9 C
9.1
APACHEII score>=25
C(rhAPC)
10
10.1 7.0g/dl
10.2 7.09.0g/dl
10.3
10.4
5000/mm3(510-9/L)
11
11.1
12
12.1
12.2
13
13.1
13.2 200 mg/dl(
140 mg/dl)
13.3
14
14.1
14.2 pH7.3
14.3
14.4
15
15.1
15.2 H2 receptor
16
16.1
16.2
16.3
Epidemiology of Sepsis in the
United States from 1979-2000
Causative Organisms
(Grade C)
(Grade A)
(Grade E)
(Grade E)
Crit Care Med 2004; 32: 858-73.
Mechanical Ventilation of
Sepsis-induced ALI/ARDS
FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0
PEEP 5 5 8 8 8 10 10 12 14 14 14 16 18 20-24
(Grade B)
Crit Care Med 2004; 32: 858-73.
Intensive Insulin in Critical
Ill Patients
(Grade D)
(Grade E)
Crit Care Med 2004; 32: 858-73.
Intensive Insulin in Critical
Ill Patients
- prospective, randomized, controlled trial
- adults admitted to SICU (N= 1,548) who were receiving MV
adults admitted to MICU (N= 1,200) who were considered
to need ICU care for at least 3 days