Dr.shenawiCons. general surgery

M.G.HMBBch,Msc,MRCS(Ireland)

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

It’s common and increasing in frequency as the population ages

It’s associated with high risk of death and long length of stay

It’s expensive 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!!

We could make a difference

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.

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%

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

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)

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

Leucocytic response.(organism specific) Margination&migration of

neutrophils(90min) Phagocytosis .(physiologic debridment) Monocyte migration(24hrs)-macrophage. Release of cytokines.

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

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.

Systemic absorption of locally generated inflamatory mediators.

Non specific response!!! May be due to infectious or non infectious

causes.

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)

SIRSSEPSISSEVER SEPSISSEPTIC SHOCK

SIRS+INFECTION(known or suspected)

Infection may be bacterial,viral ,fungal …etc.

TRAUMA

BURNS

PANCREAITIS

SEPSIS SIRSINFECTION SEPSIS

BACTEREMIA

SEPSIS+2ORGAN SEPSIS+2ORGAN dysfunctiondysfunction

SEVER SEPSIS+ REFRACTORY HYPOTENSION

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.

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!!!

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

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.

Infection

InflammatoryMediators

Endothelial Dysfunction

Vasodilation

Hypotension Vasoconstriction Edema

Maldistribution of Microvascular Blood Flow

Organ Dysfunction

Microvascular Plugging

Ischemia

Cell Death

Oxygen won,t go where blood don,t flow.

Early goal directed therapy(EGDT) IS to restore microcirculation before mitochondia is permenantly damaged.

Acute organ dysfunction is the marker of sever sepsis.

One organ damage lead to 20% increase mortality& double thereafter.

A clinician, armed with the sepsis bundles, attacks the three heads of

severe sepsis: hypotension, hypoperfusion and organ dysfunction

.

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

bundle.

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.

Pt. presented with.WeaknessConfusionVomitingSyncopeearly recognition of sepsis &

implementation of evidence based tools improves outcome & reduce mortality.

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

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

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.

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.

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

Decrease by> 10% every hour. Normalisation within 6 hs. Associated with reduced mortality.

Half life of lactate is 20 min.

20 -30 ml /kg initial fluid bolus.

Minimum 1 L bolus.Minimum of 30ml/kg in the first 3hrs.

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%

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.

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

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

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

Apply vasopressors for those not responding to fluid challenge to maintain MAP>65 mmhg.

Persistent hypotension despit fluids, measure

CVPScvO2 Re measure lactate if initially

elevated.

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

3 hs bundle (culture, crystalloid, lactate,& antibiotic.)

6 hs bundleContinue resuscitationCvp,monitor,follow lactate.Consider inotropes

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.

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!