Sepsis, shock

& MODS

Monika Grochova, MD, PhD.

Jozef Firment, MD, PhD.

Department of Anaesthesiology &

Intensive Care Medicine,

Medical faculty UPJŠ Košice

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DEFINITION OF SHOCK

• Complex syndrom developped by

insufficient capillary nutritional

perfusion of tissues

• Consequences: deficiency of oxygen &

energetical resources in tissues

= pathological metabolism

(anaerobic) & cummulation of toxic

products.

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SHOCK ACCORDING TO

PATOPHYSIOLOGY

• Hypovolemic

– (dehydration, haemorrhage)

• Distributive

– (spine laesion, high-level spinal anaesthesia, anaphylactic, septic)

• Obstructive

– (pulmonary embolism, hydropericard, pneumothorax)

• Cardiogenic

– (AMI)

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SHOCK ACCORDING

TO CLINICAL REASONS

• anaphylactic shock ( alergy to medicaments, to

venom, food, fruits )

• neurogenic shock spinal shock (spinal cord

laesion, high spinal anaesthesia...)

• haemorrhagic shock

• traumatic shock

• burn shock

• toxic shock (pancreatitis...)

• septic shock (sepsis...)

• cardiogenic shock (AMI...)

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DIFERENTIAL DG

Reason:

Anaphylactic response to allergen

Loos of 20% circul. blood volume

Traumat. laesion of cervical spine

Polytrauma

Burns (>20%, >10% children,

>5% newborns and babies)

Acute h.-necrot. pancreatitis

G- focus with bacteriaemia

Large diaphragmatic MI

Saqual:

• anafylactic

• haemorrhagic

• neurogenic

• traumatic

• burn

• toxic

• septic

• cardiogenic

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PREHOSPITAL PHASE –

FIRST SIGNS

Circulatory parameters:

• BP, P, circulatory centralisation, slow

capillary return, SpO2, cold sweat

• restlessness-lethargy, shivering...

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O2 supply

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The oxygen delivery cascade indicating the

potential role of current and future therapies to

optimize oxygen delivery to the tissues

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Rampal T, Jhanji S, Pearse R: Using oxygen delivery targets to optimize resuscitation in critically ill patients.

Current Opinion in Critical Care 2010, 16:244–249

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HYPOTENSION

Interpretation:

belove 0,5 = normal find out

above 1,0 = treatment is needed

Cave! Digitalis, beta-blockers, cardiostimulators...

Shock index =

Sh

ock s

ign

s

pulse rate

systolic BP

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LABORATORY SIGNS

MLAC > 2 mmol/l

SvO2 > 70% or < 70%

OLIGURIA

Diuresis < 0,5 ml/kg/hour

Sh

ock s

ign

s

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CARDIOGENIC SHOCK

• Early ventilatory support

• Oxygen inhalation, resp. artificial ventilation

• Analgesia (Fentanyl, Morfin)

Combination of vasoactive drugs

(nitroglycerin + DOB)

Trombolysis event. PCI

Intraaortal contrapulsation? Th

era

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l ste

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ANAPHYLACTIC SHOCK Disconnect alergen admin (infusion, blocking

absorbtion – infiltration by lidocain c. adren,

cooling...)

Oxygen inhalationa, resp. artificial ventil

Head-down position

Volume administration - colloids (HOHO),

crystalloids

Adrenalin slowly 1,0 mg/500 ml F1/1 i.v. or 0,5

mg i.m.

Glucocorticoid (Hydrocortison) 300 mg i.v.

Vasopressors ( DOP, NA in R1/1)

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HYPOVOLEMIC SHOCK

• Stoppage bleeding

Autotransfusion position (head-down)

Rapid iv volume replacement - colloids

(HO - HO, or isovolemic solution)

Oxygen, artificial ventilation.

Improving perfusional pressure with

vasopressors (DOP, NA in R1/1)

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era

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sh

ock

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PROGRESSION OF BLOOD LOSS

REPLACEMENT

0

10

20

30

40

50

60

70

80

90

100

Blo

od

lo

ss

in

%

CryCol Ery Alb, FFP Pt

HT

K <

25

%

Pro

tein

s <

50

g/l

Qu

ick <

35

%

Pt <

50

th

us/m

m3

3,5 3 1,5 1 Blood volume in liters

5

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SIRS - INFECTION - SEPSIS

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Recomendations for terminology

CCP/SCCM Consensus Conference (Chest, 101, 1992)

Recomended terminology

Infection

Bacteriemia viremia, fungemia, parazitemia

SIRS Sepsis

Severe sepsis

Septic shock

MODS

Nepoužívať termíny: Septikémia Septický syndrom Refraktéerny šok

• Systemic Inflammatory Response

Syndrome to severe insult

diagnostic criteria (for dg. SIRS minimally two

must be present) BT > 38 C or < 36 C

heart rate > 90/min

respiratory rate> 20

4000 > Leu > 12000

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Recomendations for terminology

CCP/SCCM Consensus Conference (Chest, 101, 1992)

Recomended terminology

Infection

Bacteriemia viremia, fungemia, parazitemia

SIRS

Sepsis Severe sepsis

Septic shock

MODS Nepoužívať termíny: Septikémia Septický syndrom Refraktéerny šok

• Systemic Inflammatory Response

Syndrome

•

BT > 38 C or< 36 C

heart rate > 90/min

respiratory rate >

20/min 4000 < Leu >12000

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Severe sepsis, septic shock

• Severe sepsis – sepsis + MOF

• Septic shock – persistent hypotension

despite of volume replacement therapy,

vasopressors must be added for increasing

mean arterial pressure to > 65 mm Hg

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Sepsis - mortality

• Mortality of severe sepsis comparable event.

higher than of cardiac failure, lung cancer,

breast cancer, colon cancer

• 28 days severe sepsis mortality 20% - 55%

• 45% patients after recovery from severe

sepsis die during 5 months after admision,

68% during 6 months and 72% during 1 year

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Risk factors of severe

sepsis • Pneumonia

• Abdominal

infections, stents

(biliary tract)

• Urinary tract

infections (PK)

• Neutropenic patients

- oncol.

• Imunosupression

• Pac. after

cardiosurgery

• Endokardititis

• Diabetes mellitus

• CVK, TPV

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Sepsis source identification

• Blood culture before start of ATB therapy – two or more samples

• CVC – new puncture + peripheral catheter > 48 hod.

• Samples from other parts of body

• Imaging methods - USG, CT, MRI

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Trzeciak S. et al: Serum lactate as a predictor of mortality in patients with infection.

Intensive Care Med (2007) 33:970–977

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CIRCULATORY

PARAMETERS

BP P SVR

Hypovolemic

Cardiogenic / /()

Septic hyperdyn.

Septic hypodyn.

Neurogenic

Anaphylactic /

= may not be,

/ = changes to both sides,

= increase, = dectrease, = marked increase

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INITIAL GENERAL

ANTI-SHOCK STEPS

Oxygen

Stoppage bleeding

Airway management (artificial ventil?)

Analgesia, tranquilisation

Anti-shock position (head-down)

Neutral temperature surroundings

Careful transport

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ock

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Infusion therapy

1 l loss of intravascular fluid

replacement:

4 l of crystaloids

1 l of coloid

12 – 14 l of 5% Glucose

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PROGRESSION OF BLOOD LOSS

REPLACEMENT

0

10

20

30

40

50

60

70

80

90

100

Blo

od

lo

ss

in

%

CryCol Ery Alb, FFP Pt

HT

K <

25

%

Pro

tein

s <

50

g/l

Qu

ick <

35

%

Pt <

50

th

us/m

m3

3,5 3 1,5 1 Blood volume in liters

5

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• Sepsis. Defined as SIRS in response to a confirmed infectious process. Infection can be suspected or proven (by culture, stain, or polymerase chain reaction (PCR)), or a clinical syndrome pathognomonic for infection. Specific evidence for infection includes WBCs in normally sterile fluid (such as urine or cerebrospinal fluid (CSF)); evidence of a perforated viscus (free air on abdominal x-ray or CT scan; signs of acute peritonitis); abnormal chest x-ray (CXR) consistent with pneumonia (with focal opacification); or petechiae, purpura, or purpura fulminans.

• Severe sepsis. Defined as sepsis with organ dysfunction, hypoperfusion, or hypotension.

• Septic shock. Defined as sepsis with refractory arterial hypotension or hypoperfusion abnormalities in spite of adequate fluid resuscitation. Signs of systemic hypoperfusion may be either end-organ dysfunction or serum lactate greater than 4 mmol/dL. Other signs include oliguria and altered mental status. Patients are defined as having septic shock if they have sepsis plus hypotension after aggressive fluid resuscitation (typically upwards of 6 liters or 40 ml/kg of crystalloid). R

ec

om

me

nd

ati

on

s f

or

term

ino

log

y a

cc

ord

ing

to

AC

CP

/SC

CM

Co

ns

en

su

s C

on

fere

nce

(Ch

est,

10

1, 1

99

2)

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CLINICAL COURSE OF

SEPSIS

• SIGNS BP Oxygenation Oxygenation BP

Fluids O2 mask Artif ventil Vasopressors

Focus elimination, antibiotics

• TREATMENT

INFECTION SEPSIS SEVERE SEPSIS SEPT. SHOCK DEATH

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SOFA-score

Vincent JL, et al. Intensive Care Med 1996; 22: 707-710.

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INITIAL RESUSCITATION

OF SEPTIC SHOCK The resuscitation of a patient in severe sepsis or sepsis-induced tissue

hypoperfusion (hypotension or lactate acidosis) should begin as soon as the

syndrome is recognized and should not be delayed pending ICU admission. An

elevated serum lactate level identifies tissue hypoperfusion in patients at risk

who are not hypotensive. During the first 6 hours of resuscitation, the goals of

initial resuscitation of sepsis-induced hypoperfusion should include all of the

following as one part of a treatment protocol:

– Central venous pressure (CVP): 8-12 mm Hg (12-15 mm

Hg in mechanically ventilated patients)

– Mean arterial pressure (MAP) > 65 mm Hg

– Urine output > 0.5 ml/kg/hour

– Central venous (superior vena cava) [ScvO2] or mixed

venous O2 [SvO2] saturation 70%

Recommendation: Grade B

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Sepsis Bundles Sepsis Resuscitation Bundle:

1. Serum lactate measured

2. Blood cultures obtained prior to antibiotic administration

3. Broad-spectrum antibiotics administered

4. Deliver an initial minimum of 20 ml/kg of crystalloid (or colloid equivalent)

5. Apply vasopressors for hypotension not responding to initial fluid resuscitation

6. Achieve central venous pressure (CVP) of > 8 mm Hg

7. Achieve central venous oxygen saturation (ScvO2) of > 70%

Sepsis Management Bundle:

1. Low-dose steroids administered for septic shock

2. Drotrecogin alfa (activated) administered

3. Glucose control maintained > lower limit of normal, but < 150 mg/dl (8.3 mmol/L)

4. Inspiratory plateau pressures maintained < 30 cm H2O for mechanically ventilated patients

The key components of the Ventilator Bundle are:

1. Elevation of the Head of the Bed

2. Daily "Sedation Vacations" and Assessment of Readiness to Extubate

3. Peptic Ulcer Disease Prophylaxis

4. Deep Venous Thrombosis Prophylaxis

The key components of the Central Line Bundle are:

1. Hand Hygiene

2. Maximal Barrier Precautions Upon Insertion

3. Chlorhexidine Skin Antisepsis

4. Optimal Catheter Site Selection, with Subclavian Vein as the Preferred Site for Non-Tunneled Catheters

5. Daily Review of Line Necessity with Prompt Removal of Unnecessary Lines

http://www.ihi.org/IHI/Topics/CriticalCare/Sepsis/Changes

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Effects of hydrocortisone on microvascular

perfusion in patients with severe sepsis

Hydrocortisone improved the proportion of perfused capillaries in patients

with severe sepsis within 1 h of its administration. PSVD, perfused small

vessels density. P<0.05 compared with baseline.

38 De Backer D. et al: Coupling microcirculation to systemic hemodynamics. Current Opinion in Critical Care 2010, 16:250–254

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CAVH

CVVH

CAVHD

CVVHD

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Hypothesis: Gut as STARTER

of multiorgan failure

Neuroendocrine response

Splanchnic

blood flow

Gut ischaemia

Reperfusion

PLA2

PAF

Activation

of PMN

System

impact PMN MSOF

Initial

diagnosis

Kirton, Civetta, Critical Care 1997

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MODS – MSOF (Kerr, PGA55)

Organs – system

1. Lungs

2. Kidney

3. Cardiovascular

4. CNS

5. Periph. NS

6. Coagulation

7. Gastrointestinal

8. Liver

9. Suprarenal gland

10. Skeletal muscles

Clin. syndromme

1. ARDS

2. Acute tubul. necrosis

3. Hyperdyn hypotension

4. Metab encepahlopathy

5. Polyneuropathy

6. DIC

7. Gastroparesis, ileus

8. Non-inf hepatitis

9. Acute supraren insuf

10. Rhabdomyolysis

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Multiorgan dysfunction syndrom – MOF (Kerr,

PGA55)

Organ – system

1. Lungs

2. Kidneys

3. Cardiovasc. system

4. CNS

5. Perif. NS

6. Koagulation system

7. Gastrointest. tract

8. Liver

9. Suprarenal glands

10. Muscles

Clinical syndrom

1. ARDS

2. Acute tubul. necrosis

3. Hyperdyn. hypotenzia

4. Metab. encefalopathy

5. Polyneuropathy

6. DIC

7. Gastroparesis, ileus

8. Noninfection hepatitis

9. Acute suprarenal insuf.

10. Rhabdomyolysis

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ARDS

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Relationship between

organ failure and

mortality

Haas LEM et al: An introduction to sepsis. Lifelines in Critical Care and Anaesthesia. 2006, 10, 2-5.

Inflammation and homeostasis in

sepsis

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INITIAL

RESUSCITATION

OF SEPTIC

SHOCK

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Sepsis Bundle 6-Hour Severe Sepsis Bundle: Tasks that must be done within 6 hours for

patients with severe sepsis, severe sepsis with lactate >4 mmol/l, septic shock

Changes for Improvement

1. Serum lactate measured

2. Blood cultures obtained prior to antibiotic administration

3. Broad-spectrum antibiotics administered within 1 hour of presentation

4. In the event of hypotension (SBP <90, MAP < 65 - 70) or lactate >4 mmol/l, begin initial fluid resuscitation with 20-40 ml of crystalloid (or colloid equivalent) per estimated kg of body weight

5. Vasopressors employed for hypotension during and after initial fluid resuscitation

6. In the event of septic shock or lactate >4 mmol/l, CVP and ScvO2 or SvO2 measured

7. In the event of septic shock or lactate >4 mmol/l, CVP maintained 8-12 mmHg (12-15 in AV), i.e. 10-15 cmH2O (15-20 in AV)

8. Inotropes (and/or PRBCs if hematocrit 30%) delivered for ScvO2 <70% or SvO2 < 65% if CVP 8 mmHg

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Sepsis Bundle

24-Hour Severe Sepsis Bundle: Tasks that must be done within 24

hours for patients with severe sepsis, severe sepsis with lactate >4

mmol/l, septic shock.

Changes for Improvement

1. Glucose control maintained <150 mg/dl (8.3 mmol/l)

2. Drotrecogin alfa (activated) administered in accordance with

hospital guidelines ( meningitis due to Neisseria meningitis)

3. Steroids given for septic shock requiring continued use of

vasopressors for equal to or greater than 1 hour

4. Adoption of a lung protective strategy with plateau pressures 30

cmH2o for mechanically ventilated patients

Surviving Sepsis Campaign and the Institute for Healthcare Improvement, Boston, Massachusetts, USA

http://www.ihi.org/IHI/Topics/CriticalCare/Sepsis/Changes/

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INIT

IAL

RE

SU

SC

ITA

TIO

N

OF

SE

PT

IC S

HO

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Percentage of patients with severe sepsis

and different number of organ dysfunctions

Dombrovskiy VY et al: Rapid increase in hospitalization and mortality rates for severe sepsis in the United States:

A trend analysis from 1993 to 2003. Critical Care Medicine 2007, 35, 5, 1244-1250.

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