Transcript Septic Shock Definition Shock: a micro

Septic Shock
（感染性休克）
Peng Xiaomou
Department of Infectious Diseases
Third Affiliated Hospital
2015/7/7
1
Definition
Septic shock is only an important
type of shock
2015/7/7
2
Definition
Types of shock







2015/7/7
Hypovolemic shock (低容量休克)
Cardiogenic shock (心源性休克)
Neurogenic shock (神经性休克)
Anaphylactic shock (过敏性休克)
Psychogenic shock (精神性休克)
Metabolic shock (代谢性休克)
Septic shock
3
Definition
Shock

2015/7/7
“A form of acute failure of blood circulation”.
The inadequate tissue perfusion occurs,
which may lead to progressive organ
dysfunction that results in irreversible organ
damage and cell death.
4
Definition
Definition of septic shock


2015/7/7
Is the systemic responses to an infectious
process, caused directly or indirectly by
microorganisms or their toxins. Finally, “a
form of acute failure of blood circulation”
occurs.
In a word, septic shock is a shock that
begin with infection.
5
Definition
Key points of the definition

2015/7/7
Is a syndrome（综合症）, a general
pathogenic course of many different
infectious diseases or infections, or
septicemia (败血症). Most septic shock is
the complication of septicemia.
6
Definition
Key points of the definition


2015/7/7
Infection is the essential event for septic
shock.
Except for the pathogen of infection, the
host factors are equally important in
pathogenesis.
7
Definition
Incidence


2015/7/7
Septic shock is an important emergency in
the field of infectious diseases
Septic shock is the most common cause of
shock encountered by internists
8
Definition
Incidence

2015/7/7
Septic shock is a leading cause of death in
intensive care units (ICU) with preexisting
diseases as severe infectious diseases,
cirrhosis, diabetes, tumor, etc.
9
Definition
Special concerns



2015/7/7
The critical difference between septic shock
and other types of shock is in the etiology
or causes.
The clinical manifestations and treatment
are different too.
Thus, we have to study this syndrome
seriously
10
Definition
Special concerns

2015/7/7
Understanding how to deal with septic
shock may be helpful for your career in the
future, since there are severe infections in
almost every branch of modern medicine.
11
Etiology
Infection is critical for septic shock.
The pathogens of infection are bacteria,
viruses and fungi.
Bacterial infections are the most
common cause of septic shock, which is
responsible for 1/2 of total cases.
2015/7/7
12
Etiology
Gram-negative bacteria





2015/7/7
Enterobacteriaceae
 Escherichia coli, Klebsiella spp, Vibrio,
Yersinia, Salmonella, Shigellae spp
Haemophilus Influenzae
Neisseria Meningitidis
Pseudomonas spp
Bacteroides spp (anaerobe)
13
Etiology
Gram-negative bacteria





2015/7/7
Enterobacteriaceae
 Escherichia coli, Klebsiella spp, Vibrio,
Yersinia, Salmonella, Shigellae spp
Haemophilus Influenzae
Neisseria Meningitidis
Pseudomonas aeruginosa (绿脓杆菌)
Bacteroides spp (anaerobe)
14
Etiology
Gram-positive bacteria

Staphylococcus aureus
 Toxic shock syndrome, TSS




2015/7/7
Pneumococcus
Streptococcus, spp (TSS)
Enterococcus faecium (粪肠球菌)
Clostridium spp (anaerobe)
15
Etiology
Viruses, rickettsiae, fungi




2015/7/7
EHFV,
Dengue viruses
Rickettsia tsutsugamushi
Candida spp
16
Epidemiology
Source of infection


2015/7/7
Sometimes an exogenous source, some IDs,
nosocomial infection: instrumentation sites,
contaminated inhalation therapy equipment,
IV fluids
Usually an endogenous source, intestinal
tract, oropharynx
17
Epidemiology
Source of infection


2015/7/7
Septic shock is most likely to occur in
patients with nosocomial pneumonia.
Patients with intra-abdominal infection and
poly-microbial bacteremia (菌血症,
=septicemia) or postoperative wound
infections and bacteremia are at significant
risk for septic shock.
18
Epidemiology
Source of infection

2015/7/7
Bacteremia associated with intravascular
catheters or indwelling urinary catheters
carries a lower risk of developing septic
shock.
19
Epidemiology
Sites of infections

2015/7/7
Lungs, abdomen, and urinary tract. Other
sites include the skin/soft tissue and the
CNS.
20
Epidemiology
Susceptibility of patients

Population
 Patients with nosocomial acquired
infections
 Aged group or neonatal baby
 Young menstruating women (TSS)
2015/7/7
21
Epidemiology
Susceptibility of patients

2015/7/7
Types of diseases
 Gram-negative bacterial septicemia
 Fulminant bacillary dysentery
 Fulminant meningococcal meningitis
 Fulminant pneumonia
 Peritoneal infections
 Epidemic hemorrhagic fever
 Dengue hemorrhagic fever
22
Epidemiology
Susceptibility of patients

Risk host factors
 Severe underlying diseases

2015/7/7
Neutropenia, cirrhosis, diabetes, cancer,
and transplantation
23
Epidemiology
Susceptibility of patients

Risk host factors
 Immune deficiency or suppression

2015/7/7
Steroids or other immuno-suppressive
drugs, or irradiation
24
Epidemiology
Susceptibility of patients

Risk host factors
 Antibiotic pressure

2015/7/7
broad-spectrum antibiotics
25
Epidemiology
Susceptibility of patients

Risk host factors
 Invasive devices

2015/7/7
Urinary catheter, cardiac
catheterization
26
Pathogenesis
Basic physiology of circulation
system


2015/7/7
The heart and blood vessels make up what
is called the “Vascular container.” The
body’s blood is contained with this system.
To function properly, this system must be
filled with blood and pumped efficiently.
27
Pathogenesis
The Heart
Blood
Blood Vessels
If the heart fails
to pump blood
efficiently
enough to keep
the vascular
container filled,
shock will
develop.
A serious loss
of blood
causing too
little to fill the
vascular
container will
lead to shock.
The vascular
container cannot be
too large for the
volume of blood.
Dilation of blood
vessels without
compensation of
other vessels can
cause shock.
2015/7/7
28
Pathogenesis
The mechanisms of septic shock are very
complicated.
They vary considerably in shocks with
different causes (infection and patient).
All three ways of shock may be involved
in septic shock.
2015/7/7
29
Pathogenesis
Septic shock often results from
bacteremia. However, bacteremia is
not necessary for the development of
septic shock.
Only 30-50 percent of patients with
septic shock have positive blood
culture results.
2015/7/7
30
Pathogenesis
Microbial triggers

Gram-negative bacteria: endotoxin,
exotoxins, and proteases
Gram-positive bacteria: exotoxins

Fungal cell wall material.

2015/7/7
31
Pathogenesis
From infection to septic shock

2015/7/7
There is a continuum of clinical
manifestations from infections to Systemic
Inflammatory Response Syndrome (SIRS，
全身炎症反应综合症) to sepsis (脓毒血症)
to severe sepsis to septic shock to Multiple
Organ Dysfunction Syndrome (MODS).
32
Pathogenesis
Endotoxin
Other components
GTSS
Cells
Complements
Hageman factor
Cytokines
Bradykinin,
Endorphins
2015/7/7
Exotoxins
Pathogen invasion
Immuno-pathogenesis
diphtheria
EHFV
cholera
Body fluid
Heart
Plasma
losses
damage exoleakage
33
Pathogenesis
Endotoxin
Exotoxins
Pathogen invasion
Other components
Immuno-pathogenesis
Gdiphtheria
TSS
EHF
Cells
cholera
Complements
Hageman factor
Body fluid Heart
Plasma
Cytokines
losses
damage exoleakage
Bradykinin,
Endorphins
2015/7/7
34
Pathogenesis
Endotoxin
Exotoxins
Pathogen invasion
Other components
Immuno-pathogenesis
Gdiphtheria
TSS
EHF
Cells
cholera
Complements
Hageman factor
Body fluid Heart
Plasma
Cytokines
losses
damage exoleakage
Bradykinin,
Endorphins
2015/7/7
35
Pathogenesis
cell activation
……
Body fluid
losses
Micro-circulation
disorder
Heart
damage
Plasma
exoleakage
Efficient intravascular
volume decrease
Inadequate tissue perfusion
Cell and organ damage
2015/7/7
36
Gram-negative
bacteria
2015/7/7
37
Clinical manifestations
Infection


Non-specific: fever or hypothermia; chill;
malaise; anxiety or confusion
Specific: cough; diarrhea; bleeding; rush
Shock

2015/7/7
……
38
Clinical manifestations
Shock

Early stage

Shock developing stage

Dying (later) stage
2015/7/7
39
Clinical manifestations
Early stage


2015/7/7
Compensatory process for inadequate
intravascular volume of blood
Sympathetic(交感神经的) discharge
40
Clinical manifestations
Early stage

2015/7/7
Compensation
 Skin becomes pale, cyanotic, moist and
cool.
 Tachycardia, tachypnea,
 Blood pressure may be normal or slightly
depressed.
41
Clinical manifestations
Early stage

2015/7/7
Hypoperfusion of the tissues
 Restless, somnolence
 Decrease in urine,
 Nausea or vomiting
42
Clinical manifestations
“warm shock”
“cold shock”
2015/7/7
43
Clinical manifestations
Shock developing stage


Compensation
Skin mottled, pale, cyanotic, moist and
cool, tachycardia, tachypnea, fall in
systolic blood pressure, surface veins
collapse
Hypoperfusion
Agitation or unconsciousness, decrease in
urine or anuria
2015/7/7
44
Clinical manifestations
Dying stage





2015/7/7
Hypoperfusion is the main pathogenic
mechanism
Organ dysfunction become prominent
Previous symptom or signs are aggravated
further
Disseminated Intravascular Coagulation
(DIC) : extensively bleeding
Multiple system organ damage or failure
45
Multiple system organ damage or
failure
Brain: coma
Heart: thready pulses, cardiac failure, cardiac
arrhythmia
Lung: cyanosis, alkalosis, PO2<9.33 kPa Acute
Respiratory Distress Syndrome (ARDS)
Kidney: oliguria or anuria
Liver: jaundice, hepatic encephalopathy
Gastrointestinal damage: bleeding, abdominal
distension
2015/7/7
46
Laboratory findings
Blood routine



2015/7/7
leukocytosis, 10~30 G/L, neutrophil is
dominant
Hematocrit value and hemoglobin rise(血液
浓缩)
Thrombocytopenia(血小板减少症)
47
Laboratory findings
Urine routine and renal function
test


2015/7/7
Proteinuria
Density, osmole rise, sodium decrease in
early stage. They become fixed if acute
renal failure occurs
48
Laboratory findings
Blood biochemical examination






2015/7/7
BUN, creatinine levels
Arterial blood gas (PO2, PCO2, pH) analysis
Blood ions, CO2-CP
ALT, LDH
Prolongation of prothrombin time
fibrinogen decrease and secondary fibrin
lysis
49
Laboratory findings
Etiological examination

Smear and gram-stain

Blood or other body fluids and exudate
cultures

Serological examination

Endotoxin test
2015/7/7
50
Laboratory findings
Electron cardiac graph
Echocardiography
X-ray
Catheterization
 Central venous pressure
 Pulmonary arterial pressure
2015/7/7
51
Diagnosis
The diagnosis of septic shock requires a
high index of suspicion, the taking of an
excellent history, physical examination,
appropriate laboratory tests, and a close
follow-up of hemodynamic status.
2015/7/7
52
Diagnosis
Pay attentions to those populations who
are trend to suffer from septic shock,
and those diseases which often
complicated with septic shock.
Early recognition is very important to
surviving of the patients.
2015/7/7
53
Diagnosis
Clues to a septic shock





2015/7/7
Fever, hypothermia or unexplained signs
with malignancy or instrumentation
Hypotension, oliguria or anuria
Tachypnea or Hypoxemia without obvious
cause
Thrombocytopenia or bleeding
Altered mental status, restless or
somnolence
54
Diagnosis
From infection to septic shock

2015/7/7
There is a continuum of clinical
manifestations from infections to Systemic
Inflammatory Response Syndrome (SIRS，
全身炎症反应综合症) to sepsis (脓毒血症)
to severe sepsis to septic shock to Multiple
Organ Dysfunction Syndrome (MODS).
55
Diagnosis
Systemic inflammatory response
syndrome (SIRS)





2015/7/7
Temperature > 38°C or < 36°C
Heart rate > 90 beats/minute
Respiration > 20/min or PaCO2 < 32mm Hg
Leukocyte count > 12,000/mm3, <
4,000/mm3 or > 10% immature (band) cells
Two or three criteria above
56
Diagnosis
Sepsis

2015/7/7
SIRS PLUS a documented infection site
57
Diagnosis
Severe sepsis

2015/7/7
Sepsis associated with organ
dysfunction
 Hypoperfusion abnormalities
 lactic acidosis, oliguria or an acute
alteration in mental status
 Hypotension
 One criteria above
58
Diagnosis
Septic shock

2015/7/7
Sepsis-induced hypotension despite fluid
resuscitation PLUS hypoperfusion
abnormalities.
59
Differential diagnosis
Differential diagnosis of Shock
Differential diagnosis of infection
2015/7/7
60
Differential diagnosis of Shock
With that results from bleeding or
cardiogenic shock


2015/7/7
bleeding: Sign of bleeding, amount>500ml
cardiogenic shock: heart enlarge, fullness of
surface vein
61
Differential diagnosis of infection
Bacteria, viruses or other pathogens







2015/7/7
Gram-negative bacterial septicemia
Fulminant bacillary dysentery
Fulminant pneumonia
Peritoneal infections or biliary tract infection
Fulminant meningococcal meningitis
Epidemic hemorrhagic fever
Dengue hemorrhagic fever
62
Prognosis
2015/7/7
63
Prognosis
Early recognition
Good reaction to treatment
Infection control
Complications:

Severe acidosis, high lactate, DIC,
multiple system organ failure
Severe underlying diseases
2015/7/7
64
Treatment
Always anticipate shock when a suitable
mechanism of injury or illness exists.
Early anticipation and care can prevent
the patient from later developing the
classic symptoms of shock.
Therapy should be initiated for high-risk
febrile (发热) patients in advance of
microbiologic confirmation of sepsis.
2015/7/7
65
Outlines of Treatment
Anti-shock treatment




General measure
Blood volume resuscitation (补充血容量)
Correct acidosis
Blood vessel activating drugs (血管活性药物)
Etiologic treatment


2015/7/7
Antibiotic therapy
Anti-toxemia therapy
66
Anti-shock treatment
General measures/Oxygen



Protection of airway, oxygen is given using
nasal cannula or face mask
Intubation may also be necessary to deliver
higher oxygen concentrations.
Mechanical ventilation may help lower
oxygen consumption by the respiratory
muscles and increase oxygen availability for
other tissues.
2015/7/7
67
Anti-shock treatment
General measures/Intravenous
access


2015/7/7
Circulation may be compromised and
significant decreases in blood pressure may
require aggressive fluid therapy (with
crystalloids or colloids)
Intravenous cannula is preferable
68
Anti-shock treatment
General measures/Shock position



2015/7/7
keep the patient supine with the lower
extremities elevated about twelve inches
a shock patient may also have lung
congestion
“Rothberg” position –raise patient’s upper
body at a 45 degree angle, and the lower
extremities about 15 degrees or bend the
knees as necessary
69
Anti-shock treatment
General measures/Monitoring




2015/7/7
Patients with severe sepsis should be in ICU.
Their vital signs (blood pressure, heart rate,
respiratory rate, and temperature) should
be monitored.
Urine output.
Central venous pressure; Pulmonary arterial
pressure
70
Anti-shock treatment
Blood volume resuscitation

Principles
 judge accurately and quickly
 combination of colloid and crystalloid
fluids
 faster, more in the beginning
 monitoring and adjustment
 take situations and heart, renal
functions into account
2015/7/7
71
Anti-shock treatment
Blood volume resuscitation
 Measures
 Crystalloid fluids (晶体液)
 Sodium bicarbonate; Ringer’s solution;
Normal saline ; 500-2000ml per day
2015/7/7
72
Anti-shock treatment
Blood volume resuscitation
 Measures
 Colloid fluids (胶体液)
 Low Polymer Dextran(低分子右旋糖酐)
500-1000ml iv by drip
 Albumin, plasma, Artificial plasma
 Blood
2015/7/7
73
Anti-shock treatment
Blood volume resuscitation

Standards for correct fluid resuscitation
Improve perfusion of tissues
Blood pressure
Pulse rate
Urine
Hemoglobin
2015/7/7
consciousness, no cyanosis
>12kPa; >4kPa
<100 pulses/min
>30ml/hr
normal
74
Anti-shock treatment
Correct acidosis

The essential measure to correct acidosis is
improve the perfusion of tissues.

5% sodium bicarbonate:400-800ml per day

sodium lactate

THAM
2015/7/7
75
Anti-shock treatment
Blood vessel activating drugs


2015/7/7
Vasodilators (扩血管药物)
Vasopressors (缩血管药物)
76
Anti-shock treatment
Blood vessel activating drugs

Vasodilators (扩血管药物)
 Principles
 blood volume are adequately
resuscitated, but shock is continued
 belonged
2015/7/7
to “cold shock”
77
Anti-shock treatment
Vasodilators

2015/7/7
 receptor antagonist (受体阻断剂):
Regtin 10~20mg in 100ml glucose
solution iv by drip
78
Anti-shock treatment
Vasodilators

2015/7/7
anti-cholinergic drugs (抗胆碱能药):
Anisodamin(654-2) 10~20mg
intravenous injection, repeat every 15~30
min, at most 10 times;
79
Anti-shock treatment
Vasodilators

2015/7/7
 receptor activator (受体兴奋剂):
Dopamine 10~20mg in 100ml glucose
solution iv by drip 2~5g/kg/min;
Isoprenaline 0.1 ~0.2mg in 100ml glucose
solution iv by drip
80
Anti-shock treatment
Blood vessel activating drugs

2015/7/7
Vasopressors (缩血管药物)
 Principles
 Blood pressure falls quickly, and
blood volume can not be completely
resuscitated in short time.
 No effect of vasodilator therapy
 “Cold shock” with cardiac failure,
combination with vasodilator
81
Anti-shock treatment

Vasopressors
 Aramine: 10~20mg, in 100ml glucose
solution iv by drip
 Noradrenaline: 0.5~1mg, in 100ml
glucose solution iv by drip
2015/7/7
82
Anti-shock treatment
Maintain vital organ functions

Cardiac failure: Cedilanid or strophanthin
K, vasodilator, steroids,

Prevent and treatment of ARDS:
Oxygen, Maintain air way smoothly, Artificial
respiration; Vasodilators, High-dose
corticosteroids, Anti-TNF
2015/7/7
83
Anti-shock treatment
Maintain vital organ functions


Kidney: 20% mannitol, Furosemide
Brain edema: 20% mannitol, High-dose
corticosteriods, Furosemide

Disseminated intravascular
coagulation: Heparin (1mg/kg, iv or iv by
drip, 4~6hr repeat)
2015/7/7
84
Anti-shock treatment
Use corticosteroids

Corticosteroids should be given when
severe toxemia, cardiac failure, ARDS and
brain edema occur.
Other drugs

2015/7/7
Naloxone and SOD are not popular
measures in China at present.
85
Etiologic treatment
Antibiotic therapy

2015/7/7
Antibiotic therapy is the major measure for
septic shock. Sometime, antiviral drugs
have to be used.
86
Etiologic treatment
Significance of antibiotic therapy


2015/7/7
Rapidly cleared of microorganisms from
blood
However, certain antimicrobial agents may
cause the patients to get worse. It is
believed that certain antimicrobials cause
more LPS to be released and then cause
more problems for the patient.
87
Etiologic treatment
Antibiotic therapy

2015/7/7
Principles for antibiotic choice
 Clinical findings
 Sites of infection (lung, biliary tract,
genitourinary tract)
 Smear and gram-stain
 Cultures and susceptibility tests
88
Etiologic treatment
Antibiotic therapy

2015/7/7
Principles to establish therapy
regimens
 As quickly as possible
 Combination, effective, wide spectrum,
bacteria-killing and of low side effect
 adequate, intravenously,
 Adjustment accounting to the effect and
susceptibility tests
89
Etiologic treatment
Anti-toxemia therapy



Steroids
Antiserum for endotoxin
Clarify infection sites (primary and
secondary)
 Clusis (灌肠) to fulminant bacillary dysentery
2015/7/7
90