Dr.shenawi Cons. general surgery M.G.H MBBch,Msc,MRCS(Ireland)

1. Dr.shenawi
Cons. general surgery
M.g.h
MBBCh,MsC,MrCs(irelanD)

2.  I,m not an intensivist &apologize for deficiency it
might encountered on the mini lecture.
 Thanks& greeting to all my colleagues& staff in
MGH,for their sympathy and support given to me
during my assignment in hajj duty.
 Accept my appology for any missbehave might
happen from me during my duty.
Dr.abdulfattah alshenawi

3.  It’s common and increasing in frequency as the
population ages
 It’s associated with high risk of death and long
length of stay
We could make a
 It’s expensive
difference
 AND…. The good new is:
 There are interventions proven to reduce
mortality & cost.
 However implementation of these interventions
are not routinely done in all hospitals!!

4.  35% diagnosed in hospital wards.
 52% diagnosed in ED.
 13 % diagnosed in ICU.
 Hospitalization for sepsis & sepsis related
illness has doubled in the states from year
2000 -2008.

5.  Sever sepsis & septic shock is the leading
cause of death in the non coronary care
with mortality rate of 20 -50%.
Ischemic stroke 1-2%
STEMI 3-5%

6. Cost 14-18 billion USD /y.
Cost 18.000 USD/case.

8.  Inflammation is a war!
 Non specific localized tissue response to injury.
 Purpose:
◦ Destroy
◦ Dilute
◦ Dam-off
 result is healing
◦ Regeneration (hyperplasia)
◦ Fibrosis (scarring)
 Collateral damage may occur(SIRS)

9.  1. Stimulus: Initiators of inflammation
 2. Local dilation of capillaries: increased blood
flow
 3. Microvascular structural changes: escape of
 plasma proteins from bloodstream
 4. Leukocyte transmigration through
endothelium
 and accumulation at injury site
 5. Phagocytosis / Oxygen burst: Cellular injury

11.  Leucocytic response.(organism specific)
 Margination&migration of neutrophils(90min)
 Phagocytosis .(physiologic debridment)
 Monocyte migration(24hrs)-macrophage.
 Release of cytokines.

12. Definition: Any messenger that acts on blood vessels,
inflammatory cells, or other cells to contribute to an
inflammatory response. (Pretty much anything...)

13.  Plasma proteins such as complement and
antibodies.
 Other proteins such as sPLA2 and acute phase
reactants.
 Cytokines and chemokines.
 Lipids such as prostaglandins and PAF.
 Amines such as histamine.
 ‘Gasses’ such as NO and O2-.
 Kinins such as bradykinin.
 Neuropeptides such as substance P.

14.  Systemic absorption of locally generated
inflamatory mediators.
 Non specific response!!!
 May be due to infectious or non infectious causes.

15.  Fever>100
 pulse.>100
 SBP<100
 leucocytosis
 RR>20
May be caused by infections(sepsis)
 Altered mental status
 Hyperglycemia
 or non
infections(burn,trauma,pancreatitis,
ischemia,reperfusion,chemical)

17. SIRS
SEPSIS
SEVER SEPSIS
SEPTIC SHOCK

18. SIRS+INFECTION(kn
own or suspected)
Infection may be
bacterial,viral ,fungal …
etc.

19. TRAUMA
BURNS
INFECTION SSEEPPSSIISS SIRS
PANCREAITIS
BACTEREMIA

20. SSEEPPSSIISS++22OORRGGAANN
ddyyssffuunnccttiioonn

21.  SEVER SEPSIS+ REFRACTORY
HYPOTENSION

22.  Normal response to infection.
Recognition of foreign antigen.
Immune system release inflammatory
mediators(PG,TNF,cytokines,interleuk)
Platlet activating factors.
Promote recovery of the affected
tissues.

23.  Uncontrolled response to
infection(sepsis syn)
 Flood of inflammatory mediators
Capillary leak.
 Activation of clotting cascade.
 Tissue hypoxia & hypoperfusion.
 Septic shock.
Microcirculatory failure is the key!!!

24. Figure B, page 948, reproduced with permission from Dellinger RP. Cardiovascular
management of septic shock. Crit Care Med 2003;31:946-955.

25.  Site of oxygen exchange.
Central role of the immune system.
During septic shock,it the first to go & late
to recover.
Rescue microcirculation is the
resuscitation end point.

26. Infection
Inflammatory
Mediators
Endothelial
Vasodilation Dysfunction
Hypotension Microvascular Plugging
Vasoconstriction Edema
Maldistribution of Microvascular Blood Flow
Ischemia
Cell Death
Organ Dysfunction

27. Oxygen won,t go where
blood don,t flow.
Early goal directed
therapy(EGDT) IS to restore
microcirculation before
mitochondia is permenantly
damaged.

28. Acute organ dysfunction is
the marker of sever sepsis.
One organ damage lead to
20% increase mortality&
double thereafter.

29. A clinician, armed with the sepsis bundles,
attacks the three heads of severe sepsis:
hypotension, hypoperfusion and organ
dysfunction
.

30.  Recognition& screening for sepsis.
 ivf
 Early antibiotics.
 Transfer trigger tool.
 Emergency dept. initiation of 6hs bundle.

31.  Non specific symptoms in elderly pt.
 Fever may be absent.13% in pt>65y& 4% in
pt<65y
 Tachycardia may be absent.
 Presentation may be of M.O.D initially.

32. Pt. presented with.
Weakness
Confusion
Vomiting
Syncope
early recognition of sepsis &
implementation of evidence based tools
improves outcome & reduce mortality.

33.  Sepsis screening tools should be
practiced in all hospitals&
wards(ER,ICU,& GENERAL WARDS)

34. 2 or more of the following
 Temp>100 F
 Pulse>100/min
 SBP<100mmHg.
RR>20/min
 Spo2<90%
 Altered LOC

35.  Initiate evaluation for sever sepsis &
septic shock.
 Order S. lactate(result within 30min)
 Order CBC,ABG,U/cr/E,& metabolic
profile.
 Attach monitors.
 Start IVF & antibiotics.
 Notify consultant.

36.  Lactate is a surrogate marker of global tissue
hypoxia.
 Normal is<2mmol/l
 More >4mmol/l indicate tissue hypoperfusion
 Lactate elevation above normal associated with
increased mortality.
 Marker of (OCCULT )sepsis before
hypoperfusion or altered LOC happen.

37.  Arterial or venous, no tourniquet
 Normal lactate do not rule out severe
sepsis.
 Lactate may be elevated with seizures,
liver cell failure, ischemic bowels,&
drugs

38.  Decrease by> 10% every hour.
 Normalisation within 6 hs.
Associated with reduced mortality.
 Half life of lactate is 20 min.

40. 20 -30 ml /kg initial fluid
bolus.
Minimum 1 L bolus.
Minimum of 30ml/kg in the first
3hrs.

41.  Each 1 h delay in effective antibiotics is
associated with decrease in survival by
7.6%.
 Triage time to appropriate
antibiotics<1hr
_____mortality 19.5 vs 32.2%

42. Don,t let a prolonged search for the
source delay antibiotic administration.
Brief search &best guess ABX.
consider blood culture & empiric
antibiotics pending further evaluation
Stop antibiotics when no longer needed.

43.  Follow your own hospital protocol.
 Pipracillin / tazocin. 4.5gm/6h.+
 Vancomycin 2gm iv stat then adjust
according to pharmacy.
 Penicillin allergy
 meropenem 1gm iv/8h
 Community acquired pneumonia
 Levofloxacin 750mg iv/24h
 Azithromycin 500mgiv/24h

44.  For hospital without ICU. any of the
following
PROGRESSIVE SYMPTOMS DESPITE
TREATMENT
PERSISTENT ELEVATED LACT.>4mmol/l
PERSISTENT HYPOTENSION DESPITE
FLUID CHALLENGE
MORE THAN TWO ORGAN
DYSFUNCTION

45.  To be completed within 3 hs!!
Measure lactate.
Bl. Culture prior to antibiotics.
Antibiotics.
 Infusion of 30ml/kg crystalloids in
hypotension or lactate >4mmol/l

46.  Apply vasopressors for those not
responding to fluid challenge to maintain
MAP>65 mmhg.
 Persistent hypotension despit fluids,
measure
CVP
ScvO2
 Re measure lactate if initially elevated.

48. 1. CVP of 10mmhg for
unventilated &12-15 mmhg for
the ventilated
2. MAP >65mmhg
3. Hemoglobin > 9 gm/dL
4. ScvO2 > 70%
5. UOP>0.5ml/h

50. 3 hs bundle
 (culture, crystalloid, lactate,&
antibiotic.)
6 hs bundle
Continue resuscitation
Cvp,monitor,follow lactate.
Consider inotropes

51.  Screen pt . For sepsis. In ED
&wards.
 Evaluate all pt. with sepsis for
organ dysfunction to identify sever
sepsis.
 Implement sepsis bundles for all
pts with sever sepsis & septic
shock.

52.  Obtain lactate when 2 SIRS or suspected
infection.
 Begin 3hrs bundle when screen is +ve.
 For ED pt. u have 3 hrs from arrival to
determine pt has an infection, find the
likely source,& begin the appropriate
therapy.
 Clock is not your friend!