Mangement of sepsis and septic shock

Management of a child with sever
Sepsis and Septic Shock
Prof. Hamida Esahli
Head of PICU Elkhadra Hospital
Date: 12/09/2013
Event : World Sepsis Day in Libya

Title: This is the footer
Date: 13th September 2013
Slide no: 2
OBJECTIVE;
Identifying sepsis
•What do we look for in sepsis?
•Which patients get sepsis?
•What is sever sepsis?
•What is Septic Shock?
•What is Sepsis six?

Slide no: 3
SEPSIS
•Sepsis is one of the oldest and most elusive syndromes in
medicine.
•1.Hippocrates claimed that sepsis (σ ´ηψις) was the
process by which flesh rots, swamps generate foul airs, and
wounds fester. Galen later considered sepsis a laudable
event, necessary for wound healing.
•2 With the confirmation of germ theory by Semmelweis,
Pasteur, and others, sepsis was recast as a systemic
infection, often described as“bloodpoisoning,”and assumed
t be the result of the host's invasion by pathogenic
organisms that then spread in the bloodstream

Slide no: 4
Who are risk groups?
Old
Young
Ill
Infections
Malignancy
How many of your patients are
included?
 Compromised organs
 Immunocompromised
 Post chemotherapy
 Malnutrition
 Invasive lines

Slide no: 5
The Pathogenesis of Sepsis
Response to Stimulus
•Inflammation
•Immunosuppression
•Coagulopathy
•Mitochondrial dysfunction
Infectious Agents
•Endotoxin/LPS
•Lipopeptides
•Lipoteichoic acid
•DNA
•Flagellin
Susceptible Host
•Co-morbidities
•Age
•Genetic polymorphisms
SEP
SIS

Slide no: 6
Infectious or no ninfecectious
insult
Systemic inflammatory response
(SIRS)
Miocrovascular:
Endothelial function
Micro emboli
Gut mucosa ischemia
Hemodynamic:
vasodilatation Myocardial
depression
Redistribution/Shunting
O2 hypoxia
Organs
Cell
Mitochondria
Cellular damage/apoptosis
MODS
CNS –CVS-Renal-Hepatic-pulmonary-Hematology
Basic Pathophsiology

Slide no: 7
Definitions
 Infection
 Inflammatory response to
microorganisms, or
 Invasion of normally sterile
tissues
 Systemic Inflammatory
Response Syndrome (SIRS)
 Systemic response to a
variety of processes
 Sepsis
 Infection plus
 2 SIRS criteria
 Severe Sepsis
 Sepsis
 Organ dysfunction
 Septic shock
 Sepsis
 Hypotension despite fluid
resuscitation
Bone RC et al. Chest. 1992;101:1644-55.

Slide no: 8
Step 1: Is SIRS present?
A systemic response to a nonspecific insult
Infection, trauma, surgery, massive transfusion, etc
Defined as 2 of the following:
• Temperature > 38.3 or < 36 0C
• Heart rate in infant<90>160pmb
• in child<70>150bpm
• Respiratory rate >2SD above age
• AVPU V, P or U
• White cells < 4 or > 12
• If not diabetic, blood sugar >140mg/dl/l

Slide no: 9
Step 1: Is SIRS present?
Why do we see SIRS??
Temperature: ‘Pyrogens’ raise body temperature. Later, temperature drops
as we lose excess heat
HR: To stop B.P falling, heart rate rises
RR: The body needs more oxygen in sepsis, and tissues produce
more acid. RR increases to help with both.
AVPU: As B.P and cardiac output fall later in sepsis, blood flow
to the brain reduces
White cells: Rise to combat infection. As they are used up, if bone
marrow is exhausted WCC falls
Blood sugar: Rises as part of our ‘stress response’

Slide no: 10
Bacteria
Virus
Fungi
Parasite
Infection SIRS
Sepsis
Pancreatitis
Trauma
Infection
Other
Severe
Sepsis

Slide no: 11
SIRS = Systemic Inflammatory Response Syndrome
SepsisSIRSInfection/
Trauma
Severe Sepsis
, et al. Chest 1992;101:1644, Opal SM, et al. Crit Care Med 2000;28:S81
SIRS with a presumed or
confirmed infectious
process
Step 3 what is sepsis?

Slide no: 12
• Sepsis with 1 sign of organ
failure
• Cardiovascular (refractory
hypotension)
• Renal
• Respiratory
• Hepatic
• Hematologic
• CNS
• Metabolic acidosis
SepsisSIRSInfection/
Trauma
Severe Sepsis
Bone et al. Chest 1992;101:1644; Wheeler and Bernard. N Engl J Med 1999;340:207

Slide no: 13
Step 4: what is Severe Sepsis?
Sepsis with organ dysfunction, including shock:
CNS: Acutely altered mental statusGCS<11
CVS: Syst <5th precentiaor mean <65 mmHg
Need for vasoactive drug to maintain BP
Unexplained metabolic acidosis: Base deicit>5mEq/L
Resp: Pao2/FiO2<300 OR Paco2>65mmHg OR>50%FiO2need
to maintain saturation>92%
Renal: Creatinine >2mg/dl
or UO <0.5 ml/kg/hr for 2 hrs
Hepatic: Bilirubin >4.0mg /dl ALT2 times upper limit for age
Bone marrow: Platelets <80,000mm3/l
Hypoperfusion: Lactate >above limits lab
Coagulopathy: INR>1.5 or aPTT >60secs

Slide no: 14
:Age specific upper and/lower limits of heart rate to define
tachycardia and bradycardia , respiratory rate, hypotension
Age group HR
Mean(range)
RR(breath/
min)
Systolic
BP,mmHg
Upto1
month
140[100-
190]
>60 <60mmHg
2months to 1
year
130[80-190] >50 <70mmHg
1-5 years 80[60-140] >40 <70+[2xage]
6-10 years 80[60-130] >30 <70+[2xage]
>10years 75[60-100] >30 <90
For heart rate lower values are approximately at 5th percentile and upper at 95
percentile for blood pressure, the heart rate values are at 5th percentile and for
respiratory rate the values are at95th percentile

Slide no: 15
What is Septic shock?
• Septic shock
• In a child with sepsis presence of : hypotension [ systolic BP< 70
mmHg in infant, <70+2 x age after 1 year of age ] or need for
vasoactive drug to maintain BP above fifth centile range
• or signs of hypoperfusion----any three of the following
• : decreased pulse volume [ weak or absent dorsalis pedis pulse] ,
• capillary refilling>2Sec
• , tachycardia heart rate as defined in [table] ,
• core [ rectal /oral ] to peripheral [skin –toe] temperature gap >3C ,
and
• urine output [<0.5ml/kg/h ] or sign of CVS dysfunction

Slide no: 16
Step 2: What counts as an infection?
RECOGNITATION: SCEERING FOR
INFECTION
i.e, if it sounds like an infection (history), or if
it looks like an infection (examination,
observations), then it probably is an infection!!

Slide no: 17
Step 2: What counts as an infection?
 Pneumonia 50%
 Urinary Tract infection
 Meningitis
 Endocarditis
 Device related
 Central line
 Cannula
• Abdominal 25%
• Pain
• Diarrhoea
• Distension
• Urgent laparotomy
• Soft tissue/ musculoskeletal
• Cellulitis
• Septic arthritis
• Fasciitis
• Wound infection

Slide no: 18
• Sepsis (documented or suspected infection plus ≥1 of the following)
• General Variables
• Fever.>38.3C
• Hypothermia(Core temperature <36C
• Heart rate > more than two SD above normal value for age
• Tachypnea
• Altered mental status
• Significant edema or positive fluid balance (>20ml/kg over 24 hr)
• Hyperglycaemia( plasma > 140mg/dl) in the absence of diabetes
• Inflammatory variables
• Leukocytosis (WBC count >12,000 mm3)
• Leukopenia( WBC count< 4000m3)
• Normal WBC count with >10% immature form
• Plasma C-reactive >two SD above normal value
• Plasma procalcitonin > TWO SD above normal
Diagnostic Criteria for Sepsis, Severe Sepsis, and
Septic Shock.

Slide no: 19
• Hemodynamic Variables
• Arterial hypotension SBP< 5TH Percentile or mean<65 mmHg
• Organ dysfunction Variables
• Arterial hypoxemia (Pao2/Fio2< 300)
• Acute oliguria (urine output <0.5ml/kg/hr for at least 2 hrs despite adequate
fluid resuscitation
• Creartinine increase >0.5mg/dl
• Coagulation abnormalities(INR >1.5 or aPT T>60s)
• Ileus
• Thrombocytopenia( platelet count <80,000mm3)
• Hperbilirubinemia (plasma total bilirubin >4mg/dl)
• Tissue perfusion variables
• Hyperlactaemia
• Decreased capillary refill or mottling skin
• Flash capillary refill
• Bounding peripheral pulses Warm Shock
• Wide pulse pressure(DPP< 1/3 of SBP)

Slide no: 20
Causes of organ failure
•Reduced delivery of oxygen to the tissues
•In sepsis, caused by any or all of:
• Hypoxia
• Hypotension
• Low cardiac output
• Redistribution of blood flow
• Oedema- further for oxygen to travel to cells
• Small blood clots (microthrombi)
• Mitochondria don’t work effectively
We need to correct these with interventions... And FAST

Slide no: 21
Mortality increases with increasing
organ failure
Hebert et al. Chest 1993;104:230-5

Slide no: 22
•For first 12 hours, 1% mortality per 5 minute delay
•Funk and Kumar, Crit Care Clinics 2011; 53-76

Slide no: 23
Sepsis Management
Time
Early diagnosis
Antibiotic administration
Hemodynamic stabilization
EGDT( A more definitive resuscitation strategy involves goal
oriented manipulation of cardiac preload ,after load and
contractility to achieve a balance between systemic oxygen
delivery and O2 demand River et al described steps
during the critical “GLODIN HOURS” (first 6 hours)
2012 Surviving Sepsis Campaign guidelines

Slide no: 24
N Engl J Med, Vol .354,No 19 November 2011
EGDT

Slide no: 25

Slide no: 26

Slide no: 27
Pre and post-discharge
Hospitalization
24 hours
6 hours
Recognition
Resuscitation
Initial Management
Maintenance
Recovery
RESUSCITATION
PHASE
GOAL: Keep him
alive for 24
hours
INITIAL
MANAGEMENT
PHASE
GOAL: Let’s get
him better
MAINTENANCE
PHASE
GOAL: Don’t kill
him

Slide no: 28
SEPSIS RESUSCTATION BUNDLE
• TO BE COMPLETWITHIN 3HOURS :
• Measure lactate level
• Obtain blood cultures prior to administration of antibiotics
• Administer broad sepectrum antibiotics
• Administer 20ml/kg crystalloid
• TO BE COMPLETED WITHIN 6 HOURS
• Apply vasopressors to maintain BP > 5th percentile for age
• In the event of persistent arterial hypotension despite volume
resuscitation:
• - Measure central venous pressure CVP>8mmHg
• - Measure central venous oxygen saturation(Scvo2)>70%
• Remeasure lactate if initial was elevated

Slide no: 29
Goal-directed therapy hemodynamic
target in septic shock
• Capillary refill <2Sec
• Urine out put>1ml/kg/h
• Heart rate: age approporiate
• Arterial O2 Sat >95%
• ScvO2 >70%
• Difference in preductal and postductal O2 <5%
• MAP Age appropriate

Slide no: 30
MANAGEMENT
•Maintain or restore airway, oxygenation and ventilation{up
to 40% of CO is used for work of breathing}
•Maintain or restore circulation: normal perfusion and blood
pressure; maintain or restore threshold HR
•MONITORING
•Pulse oximeter, ECG, BP, Pulse pressure, DBP,
Temperature, urine output, glucose, ionized calcium

Slide no: 31
Airway
Breathing
Circulation
Disability
Exposure
Assessing any Critically Ill patient

Slide no: 32
Recognize decreased mental status and perfusion. Begin high
flow O2.Establish IV/IO access
• INTIAL RESUSCITATION
Push boluses of 20cc/kg isotonic saline up&over 40cc/kg then
3rd subsequent bolus 0.5g/kg 5% albumin until perfusion
improves or unless rales or hepatomegly develop.
Correct hypoglycaemia &hypocalcaemia . Begin antibiotics
• Shock not reversed: Fluid refractory shock Begin inotropes
0
min
15
min

Slide no: 33
becomes...

Slide no: 34
The Sepsis Six
1. Give high flow oxygen
2. IV fluid resuscitation
3. Give IV antibiotics
4. Take blood culture
5. Check haemoglobin and lactate
6. Accurate hourly urine output monitoring
may require catheter
... plus Critical Care support to complete EGDT
EARLY GOAL- DIRECTED THERAPY
Within one hour

Slide no: 35
Step 1: Oxygen
Oxygen delivery (DO2) is impaired
So, high flow oxygen maximises SaO2
‘Sats’ of 99% are better than 95% in sepsis!!
DO2 = CaO2 x CO
CaO2 = ([Hb] x SaO2)

Slide no: 36
Step 1: Is oxygen supply keeping up
with demand?
Central venous O2 saturation
Reflects oxygen extraction
by tissue, relative to
oxygen delivery
Lactate clearance
Reflects transition
from anaerobic to
aerobic metabolism
Oxygen delivery is determined by:
 Hemoglobin
 Cardiac output
 Arterial oxygen saturation

Slide no: 37
HEART
ARTERIESVEINS
ORGANS
O2
O2
O2
O2
O2
O2
O2
O2
STEP 1: Make sure
the pump is full
(volume depletion)

Slide no: 38
Step 2: Fluids
Why?
To reduce organ dysfunction and multi-organ failure
• By optimising tissue oxygen delivery
• By increasing organ perfusion

Slide no: 39
Fluid resuscitation
In the first hour:
• Fluids improve Cardiac Output (CO)
• Better Cardiac Output gives
•Higher delivery of O2
•Higher MAP
• This will reduce organ injury

Slide no: 40
Improving organ perfusion
• Organs have their own resistance to blood flow
• Perfusion depends therefore on pressure as well as flow
• Mean arterial pressure (MAP) is the key
MAP = CO x SVR
Where SVR is Systemic Vascular Resistance
Goal MAP > 65 or Systolic > 5th percentile
MAP = Diastolic + (systolic-diastolic)
3
An improved cardiac output gives a higher MAP

Slide no: 41
The C in the ABCs:
Volume Resuscitation
Assess for Volume Depletion
•History
•Exam - Organ perfusion – skin, brain, kidneys
•Measure intravascular pressures – arterial, central venous
Administer a “Fluid Challenge”
•20ml/kg cry stolid over 5-10 minutes up to over
60ml/kg until perfusion improves
Normalization of the heart rate
•Capillary refill of < 2sec
•Well felt dorsalis pedis pulses with no
differential between peripheral and
central pulses
•Warm extremities
•Normal of systolic pressure and pulse
pressure
•Urine output> 1 ml/kg/hour
•Return to baseline mental status tone
and posture
•Normal range respiratory rate

Slide no: 42
HEART
ARTERIESVEINS
ORGANS
O2
O2
O2
O2
O2
O2
O2
O2
STEP 2: Make the train is on
a fast track (vascular tone)
STEP 1: Make sure
the pump is full
(volume depletion)
STEP 3: See if supply is
keeping up with demand

Slide no: 43
How to fluid resuscitate
Judicious fluid challenges
• Up to 60ml/kg in divided boluses (min. 20ml/kg in shock)
Reassess for effect after each challenge
• HR, BP, capillary refill, urine output, RR
In patients with cardiac disease
• Use smaller volumes
• More frequent assessment
• Early CVC

Slide no: 44
Before starting antibiotics, take at least one blood
culture:
• Percutaneously
• AND at least one from each vascular access device (if > 48 hrs)
Other cultures:
• Urine
• CSF
• Faeces
• Wound swabs
• Sputum
• other fluids from within cavities, e.g, intraperitoneal
Step 3: Blood Cultures

Slide no: 45
Within 6 hours source must be controlled
With cultures, consider:
Diagnostic imaging X ray
USS
CT
MRI
Discuss with radiologist/ surgeon if an enclosed
collection suspected
Step 3b: Source Control

Slide no: 46
Guidelines for obtaining cultures before
starting antibiotics
•Obtain two or more sets of BCs (both aerobic and anaerobic
bottles)
•One or more BCs should be Percutaneously
•One BC from each Vascular access device in place > 48hrs
•Culture other sites as clinically indicated (eg, urine, wound,
sputum, faecal, bronchial aspirate, CSF)

Slide no: 47
Start therapy as soon as possible and certainly in the first
hour...
...preferably after taking blood cultures!!
Choice should include one or more with activity against likely
pathogen
•Penetration of presumed source
•Guided by local pathogens
•Give broad spectrum till defined
Step 4: Give Antibiotics

Slide no: 48
• Antimicrobial regimen should be reassessed daily for potential de-
escalationto the most appropriate single therapy should be
performed as soon as the susceptibility profile is known .
• . Duration of therapy typically 7–10 days; longer courses may be
appropriate in patients who have a slow clinical response,
• Use of low procalcitonin levels or similar biomarkers to assist
the clinician in the discontinuation of empiric antibiotics in
patients who initially appeared septic, but have no subsequent
evidence of infection
• For patients with severe infections associated with respiratory failure
and septic shock, combination therapy with an extended spectrum
beta-lactam and either an aminoglycoside or a fluoroquinolone is for
P. aeruginosa bacteremia
• A combination of beta-lactam and macrolide for patients with septic
shock from bacteremic Streptococcus pneumoniae infections

Slide no: 49
Evidence!!
Cohort size Mortality % RRR %
(NNT)
Total 567 (100%) 34.7 -
No fluids in 1h 183 (32.3%) 44.8
Fluids in 1h 384 (67.7%) 30.0 33.0
(6.73)
© Ron Daniels 2010 Reproduction in part or whole not permitted

Slide no: 50
Evidence: fluids and antibiotics together
Cohort size Mortality % RRR %
(NNT)
Total 567 (100%) 34.7 -
Neither fluids
nor antibiotics
in 1hr
170 (30.0%) 45.3
Antibiotics after
BC and fluids
238 (42.0%) 24.0 47.0
(4.69)
© Ron Daniels 2010 Reproduction in part or whole not permitted

Slide no: 51
High lactate identifies tissue hypoperfusion in
patients at risk who have a normal BP
‘Cryptic shock’
Gives an overview of current tissue oxygen delivery
The Goal
Lactate to improve
as resuscitation
progresses
Step 5: Measure lactate

Slide no: 52
Risk stratification by lactate
0
5
10
15
20
25
30
35
40
%inhospitalMortality
Lactate threshold
Low (0 - 2.0)
Intermediate ( 2.1 - 3.9)
Severe (>4.0)
Trzeciak, S et al , Acad Emerg Med; 13, 1150-1151.

Slide no: 53
STEP 6: Urine Output
Urine output is a direct measure of GFR
GFR= Glomerular Filtration Rate
GFR is directly proportional to CO
Kidneys receive 1/5 cardiac output (1 L/min)
CO falls UO falls
Therefore urine output in the early stages is a useful
assessment of cardiac output

Slide no: 54

Slide no: 55
Renal Blood Flow & Urine Output
In health, kidneys
autoregulate, so UO is
independent of BP over
a wide range
In sepsis, this is lost and
UO will fall as BP falls

Slide no: 56
Effects of fluid resuscitation
So…
Fluid resuscitation can improve
• Cardiac output (raises)
• Blood pressure (raises)
• Haematocrit (lowers)
… each of which will improve urine output

Slide no: 57
Goals for the first hour
Evidence of success:
•MAP >65mmHg
•Improving capillary refill
•Warming of extremities
•Urine output >1 ml/kg/hr
•Improving mental status
•Decreasing lactate

Slide no: 58
Pre and post-discharge
Hospitalization
24 hours
6 hours
Recognition
Resuscitation
Initial Management
Maintenance
Recovery
RESUSCITATION
PHASE
GOAL: Keep him
alive for 24
hours
INITIAL
MANAGEMENT
PHASE
GOAL: Let’s get
him better
MAINTENANCE
PHASE
GOAL: Don’t kill
him

Slide no: 59
INITIAL MANAGEMENT PHASE
GOAL: Let’s get him better
• Supportive care
• Identify organ failures
• Customize antibiotics based on
cultures/sensitivities
• Additional diagnostic testing
• Inotropes/Vasopressors/Vasodila
tors
• Corticosteroids
• Blood Products and plasma
Therapies
• Specific care
• Lung protective ventilation
• Conservative fluid management
• Sedation/Anlagesia/drug
Toxicities
• Glycemic control
• Deep Vein Thrombosis
Prophylaxis
• Stress Ulcer Prophylaxis
• Nutrition :enteral and iv glucose

Slide no: 60
Hydrocortisone Therapy
a child is at risk of absolute adrenal insufﬁciency or adrenal pituitary
axis failure (e.g., purpura fulminans, congenital adrenal hyperplasia,
prior recent steroid exposure, hypothalamic/pituitary abnormality)
and remains in shock despite epinephrine or norepinephrine
infusion,
• then hydrocortisone can be administered ideally after attaining a
blood sample for determination of baseline cortisol concentration.
Hydrocortisone may be administered as an intermittent
• or continuous infusion at a dosage which
• may range from 1–2 mg/kg/day for stress
• coverage to 50 mg/kg/day titrated to reverse the shock

Slide no: 61
Persistent Pulmonary Artery Hypertension
• Inhaled NO therapy is the treatment of choice for uncomplicated
PPHN However,
• metabolic alkalinization remains an important initial resuscitative
strategy during
• shock because PPHN can reverse when acidosis
• Milrinone or inamrinone may be added to improve heart function as
tolerated
• ECMO remains the therapy of choice for patients with refractory
• PPHN and sepsis
•New investigations:
• support use of inhaled iloprost (synthetic analog of prostacyclin) or
adenosine infusion as modes of therapy for PPHN

Slide no: 62
MAINTENANCE PHASE
GOAL: Don’t kill him
•Avoid nosocomial
complications
•Ventilator-induced lung
injury
•Get tubes and lines out
of him
•Clots and bleeding
•Avoid new infection
•Hand washing
•Semi-recumbent position
•Get tubes and lines out of
him
•Minimize transfusions

Slide no: 63
Long-term Cognitive Impairment and Functional Disability
Among Survivors of Severe Sepsis
• Compared 516 severe sepsis survivors with 4517 survivors of non-
sepsis hospitalization
• Prevalence of mod/severe cognitive impairment increased by 10.6%
after sepsis
• Severe sepsis associated with development of 1.5 new limitations in
ADLs
• 59% of sepsis survivors had worsened cognitive and/or physical
function Long-term Cognitive Impairment and Functional Disability
Among Survivors of Severe Sepsis
• Significantly worse than for non-sepsis hospitalizations
Iwashyna et al. JAMA 2010;304(16):1787-94

Slide no: 64
What is it?
•SIRS + Infection = Sepsis
•Sepsis + Organ Failure = Severe Sepsis
•Sepsis + Shock = Septic Shock
•Mortality increases with more organ failure
•GOLDEN HOURS definitive recognition and
treatment provide maximal benefit in term of outcome

Slide no: 65

Mangement of sepsis and septic shock

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