Infection in surgery II.

‘Every operation in surgery is

an experiment in bacteriology’.

Berkely Moynihan (1920)

Risk factors

Age

Obesity

Diabetes

Malnutrition

Prolonged

pre-

operative

stay

Infection at

a remote

site

PVD

Recent

operation

Skin

carriage of

S, aureus

Contaminated medications Inadequate disinfection/sterilization

Inadequate skin antisepsisInadequate ventilation

Drains Emergency procedures

HypothermiaInadequate antibiotics prophylaxis

Prolonged operative time

Intraabdominal infection is the most common infection as

the reason of hospitalisation on ICU in the world

-30% of patients with intraabdominal infection die because

of it

-if the reason of infection is previous operation, mortality is

more than 50 % !!!

Infection

Classification

Result of invasion and multiplication of

enteric bacteria in the wall of a hollow

viscus or beyond.

Intraperitoneal: peritonitis, abscess.

Visceral: liver, spleen, kidney, pancreas,

tuboovarian

Perivisceral: gallbladder, appendix, colon

Interloop

Peritoneal cavity

Peritonitis

Type Definition Microbiology

Primary Due to bacterial

translocation or

hematogenous seeding.

No break in integrity of

GI tract

Monomicrobial; coliforms

or streptococci

Secondary Microscopic or

macroscopic perforation

Polymicrobial; coliforms,

gram-positive cocci and

enteric anaerobes

Tertiary Persistent or recurrent

peritoneal infection

developing after

treatment of secondary

peritonitis

Nosocomial organisms;

enterococci,

staphylococci; resistant

gram negative bacilli and

yeast

Microbiology

Location Colony counts Flora

Stomach 1000 CFU/ml Gram positive, oral flora

Upper small gut Scant Same + coliforms

Distal small gut 1-100 million CFU/ml Coliforms +

enterococcus +

anaerobes

Colon 10-100 billion CFU/ml Coliforms +

enterococcus +

Anaerobes +

streptococci

Conditions which can change the

expected microflora

Hospitalization

Prior exposure to antibiotics

Obstruction and stasis of the gut

Think of: Pseudomonas, drug resistant

gram negatives, enterococcus, yeast,

staphylococcus

Role of enterococci and candida

Enterococci are present in 20% of

intraabdominal infections.

Important in setting of treatment failure

and nosocomial infections

Candida are important when present as

the sole or predominant isolate or when

accompanied by fungemia.

Management

Early diagnosis

Source control

Antimicrobial therapy

Diagnosis

Signs and symptoms

Lab tests: wbc, crp, cultures

Ultrasound: CT

Nuclear medicine.

Source control

1. Image guided drainage procedures

2. Minimally invasive surgery

3. Open laparotomy

Bowel decompression

Closure of perforation; resection of diseased

segment or organ

Drainage : drains; relaparotomy

Failure to achieve adequate source control is

associated with a worse clinical outcome.

Risks for failure of source control

Advanced age

High severity of illness (APACHE II score

>15)

Delay in initial intervention (>24H)

Comorbidity and degree of organ

dysfunction

Low albumin level

Poor nutritional status

Degree of peritoneal involvement

Underlying malignancy

post-operative infection

treataccordingly

if otherinfectionsfound

rule outotherinfections

accessiblebypercutaneousmethod

negative abdominal CTpositive abdominal CT

notaccessiblebypercutaneousmethodORseveresepsis

considerabdominalre-exploration

percutaneousaspirationor drainage

Drainage of abscessus

it is removing of infected with percutaneous drainage under

US, CT control

or by open laparotomy

Therapy of intraabdominal infection

Surgical principles on exploration

• do drain the “drainable” and leave drainage tubes behind (concept of controlled fistulation)

• do debride the obviously dead or ischaemic tissues

• do create stomas if anastomosis is risky

• do bear in mind the concept of “damage control surgery”

• do plan re-exploration if necessary

• don’t sit too tight on conservative or interventional radiological treatments

• don’t get into the theatre too late

Liver abscess

LiverAbscess

Gross specimen of a liver abscess

Severe necrotizing pancreatitis

Severe necrotizing pancreatitis

From the previous patient

Pancreatitis necrotisans

Lavage and laparostomy

- wound is not closed by

suture, it is covered only

with foil, or Ethizip

- Indication:

intraabdominal high

pressure- compartement

syndome, need for

repeated revision within

24-48 hours, huge defect

of abdominal wall after

necrectomy of fascia m.

rectus abdominis-

infection

Peritoneal lavage –

surgical washing out of

fluid

A silicon drains are

inserted towards the

focus of infections

(subphrenium,omental

bursa, paracolic, Douglas

space)

VAC

https://www.youtube.com/watch?v=4yPnW

IrLKhg

://www.youtube.com/watch?v=H_gwDrLw

9Yg

Prognosis

Age

Comorbidities

Duration of contamination

Presence of foreign material

Type of microorganisms

Site of contamination

Mortality is 3% in setting of early abdominal perforation. Increases to 60% in established peritonitis with organ failure

Inadequate antimicrobial therapy doubles mortality

Timing of source control

Diffuse peritonitis: immediate

Hemodynamically stable patient without

peritonitis: delay of up to 1d is acceptable

Antimicrobial therapy

1. Polymicrobial

2. Start soon

3. Use appropriate antibiotics

Uncomplicated: community acquired, normal host, no prior antibiotics: think E coli, streptococci and bacteroides (lower GI)

Complicated: nosocomial, prior antibiotics, immunocompromised host: also think of pseudomonas, enterococcus, yeast, staphylococcus

Duration of antimicrobials

1 day: early infection, no perforation, early

removal of source

5-7 days: perforation, but good source

control

7-14 days: perforation, delay in source

control

>14 days: abscess formation, inability to

properly control source, tertiary peritonitis

Primary wound healing

Wound surfaces opposed

Healing without complications

Minimal new tissue

Results optional

Primary healing wound

Secondary

Surfaces not approximated

Defect filled by granulation

Covered with epithelium

Less functional

More sensitive to thermal and mechanical

injury

Impaired Wound Healing

Infection

Decreased tissue PO2 and prolongs the

inflammatory phase

Impaired angiogenesis and

epithelialization

Increased collagenase activity

Nutrition

Low protein levels prolonged inflammatory phase

impaired fibroplasia

Of the essential amino

Methionine is critical

Hydration

A well hydrated wound will epithelialize faster than a dry one

Occlusive wound dressings hasten epithelial repair and control the proliferation of granulation tissue

Diabetes Mellitus

Larger arteries, rather than the arterioles, are typically affected

Sorbitol accumulation

Increased dermal vascular permeability and pericapillary albumin deposition

Impaired oxygen and nutrient delivery

Stiffened red blood cells and increased blood viscosity

affinity of glycosylated hemoglobin for oxygen contributing to low O2 delivery

impaired phagocytosis and bacterial killing

neuropathy

Radiation Therapy

Acute radiation injury

stasis and occlusion of small vessels

fibrosis and necrosis of capillaries

decrease in wound tensile strength

direct, permanent, adverse effect on fibroblast

may be progressive

fibroblast defects are the central problem in the healing of chronic radiation injury

The most common early postoperative

complications in wound healing

1.Haematoma - https://www.youtube.com/watch?v=SvHCfzn_h3s

2.Seroma -

https://www.youtube.com/watch?v=FzVbQNiLeF4&index=3&list=PLoYbFz

PqoFQoatj3jYb3Bh-

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eF4&index=3&list=PLoYbFzPqoFQoatj3jYb3Bh-KtyCHI7dbz

3.Infection of wound

4.Dehiscence of suture

Secondary Wound Healing

Secondary healing wound

Secondary Wound Healing

Secondary Wound Healing

Treatment with antibiotics

Should be used only when there is

obvious wound infection

Marks of infections: erythema, cellulitis,

swelling, purulent discharge

Indiscriminate use of antibiotics should be

avoided to prevent emergence of

multidrug resistant bacteria

Dressings

The main purpose of wound dressings is

to provide the ideal enviroment for wound

healing

The dressing should facilitate the major

changes taking place healing to produce

an optimally healed wound

Characteristics of wound dressings

Promote wound healing

Conformability

Pain control

Odor control

Nonallergic and nonirritating

Permeability to gas safety

Nontraumatic removal

Cost effectiveness

convenience

Characteristics of wound dressings

Are classified as primary or secondary.

Primary dressing is placed directly on the

wound and may provide absortion of fluids

and prevent dessication, infection, and

adhesion of a secondary dressing

A secondary dressing is one that is placed

on the primary dressing for further

protection, absorption, compression and

occlusion

Dressings

Absorbent dressings

Non adherent dressings

Occlusive and semiocclusive dressings

Hydrophillic and hydrophobic dressings

Hydrocoloid and hydrogel dressings

Alginates absorbing dressings

Absorbent dressings

Accumulation of wound fluid can lead to

maceration and bacterial overgrowth

The dressing should absorb without

getting soaked through, as this would

permit bacteria from the outside the enter

the wound

The dressing must be designed to match

the exudative properties of the wound and

may include cotton, wool and sponge

Absorbent dressing

Nonadherent dressings

Are impregnated with paraffin, petroleum

jelly, or water-soluble jelly for use

nonadherent coverage

A secondary dressing must be placed on

top to seal the edges and prevent

desiccation and infection

Nonadherent dressing

Occlusive and semiocclusive dressings

Good enviroment for clean, minimally

exudative wounds

They are waterproof and impervious to

microbes, but permeable to water and

oxygen

Occlusive dressing

Hydrophyllic and hydrophobic dressings

Hydrophillic: The aim is absorption

Hydrophobic: is waterproof and prevents

absorption

Hydrocolloid and hydrogell dressings

It combinates benefits of occlusion and

absorbency

Absorption of exudates by the

hydrocolloid dressing leaves a yellowish-

brown gelatinous mass after dressing

removal that can be washed off

Hydrogels allow a high rate of evaporation

wihout compromising wound

hydratatation, which makes them useful in

burn treatment

Inflamatory

response

Hyperinflamatory

reaction

Antiinflamatory

response

Hypoinflamatory

reaction

SIRS

CARSCompensatory anti-

inflamatory

responce sy.

MARSmixed antagonist

response syndrome

MODS, MOF Imunosupresion

Definitions:

• Infection: A microbial phenomenon characterized by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms.

• Bacteremia: The presence of viable bacteria in the blood.

Definitions

• Systemic Inflamatory Response

Syndrome (SIRS): The systemic

inflammatory response to a variety of

severe clinical insults (For example,

infection).

• Sepsis:The systemic inflammatory

response to infection.

SIRS is manifested by two or

more of the following conditions:

• Temperature >38 degrees Celsius or

<36 degrees Celsius.

• Heart rate>90 beats per minute.

• Respiratory rate>20 breaths per minute

or PaCO2<32mmHg.

• White blood cell count > 12,000/cu mm,

<4,000/ cu mm, or >10% band forms.

Definitions

• Sepsis:

• Known or suspected infection, plus

• >2 SIRS Criteria.

• Severe Sepsis:

• Sepsis plus >1 organ dysfunction.

• MODS.

• Septic Shock.

Clinical Signs of Sepsis

• Fever.

• Leukocytosis.

• Tachypnea.

• Tachycardia.

• Reduced Vascular Tone.

• Organ Dysfunction.

Relationship Between Sepsis

and SIRS

TRAUMA

BURNS

PANCREATITIS

SEPSIS SIRSINFECTION SEPSIS

BACTEREMIA

Definitions :

• Septic Shock: Sepsis induced with

hypotension despite adequate

resuscitation along with the presence

of perfusion abnormalities which may

include, but are not limited to lactic

acidosis, oliguria, or an acute alteration

in mental status.

Definitions:

• Multiple Organ Dysfunction Syndrome

(MODS): The presence of altered organ

function in an acutely ill patient such

that homeostasis cannot be maintained

without intervention.

Clinical Signs of Septic Shock

• Hemodynamic Alterations

• Hyperdynamic State (“Warm Shock”)

• Tachycardia.

• Elevated or normal cardiac output.

• Decreased systemic vascular resistance.

• Hypodynamic State (“Cold Shock”)

• Low cardiac output.

Clinical Signs of Septic Shock

• Myocardial Depression.

• Altered Vasculature.

• Altered Organ Perfusion.

• Imbalance of O2 delivery and

Consumption.

• Metabolic (Lactic) Acidosis.

Stages In the Development of

SIRS

• Stage 1. In response to injury / infection, the

local environment produces cytokines.

• Stage 2. Small amounts of cytokines are

released into the circulation:

• Recruitment of inflammatory cells.

• Acute Phase Response.

• Normally kept in check by endogenous anti-

inflammatory mediators (IL-10, PGE2, Antibodies,

Cytokine receptor antagonists).

Stages In the Development of

SIRS

• Stage 3. Failure to control

inflammatory cascade:

• Loss of capillary integrity.

• Stimulation of Nitric Oxide Production.

• Maldistribution of microvascular blood

flow.

• Organ injury and dysfunction.

Severe Sepsis

• Major cause of morbidity and

mortality worldwide.

• Leading cause of death in noncoronary

ICU.

• 11th leading cause of death overall.

Severe Sepsis is deadly

34%

50%

28%

0%

5%

10%

15%

20%

25%

30%

35%

40%

45%

50%

Sands,et al Zeni, et al. Angus,et al

Mortality

Mechanisms of Sepsis - Induced

Organ Injury and Organ Failure

Question: Why do Septic Patients

Die?

• Answer: Organ Failure

Pathophysiology of Sepsis-

Induced Organ Injury

• Multiple Organ Dysfunction (MODS) and Multiple Organ Failure (MOF) result from diffuse cell injury / death resulting in compromised organ function.

• Mechanisms of cell injury / death:• Cellular Necrosis (ischemic injury).

• Apoptosis.

• Leukocyte-mediated tissue injury.

• Cytopathic Hypoxia

Pathophysiology of Sepsis-Induced

Ischemic Organ Injury

• Cytokine production leads to massive production of endogenous vasodilators.

• Structural changes in the endothelium result in extravasation of intravascular fluid into interstitium and subsequent tissue edema.

• Plugging of select microvascular beds with neutrophils, fibrin aggregates, and microthrombi impair microvascular perfusion.

• Organ-specific vasoconstriction.

Infection

Inflammatory

Mediators

Endothelial

DysfunctionVasodilation

Hypotension Vasoconstriction Edema

Maldistribution of Microvascular Blood Flow

Organ Dysfunction

Microvascular Plugging

Ischemia

Cell Death

Therapeutic Strategies in Sepsis

• Optimize Organ Perfusion

• Expand effective blood volume.

• Hemodynamic monitoring.

• Early goal-directed therapy.• 16% reduction in absolute risk of in-house

mortality.

• 39% reduction in relative risk of in-house mortality.

• Decreased 28 day and 60 day mortality.

• Less fluid volume, less blood transfusion, less vasopressor support, less hospital length of stay.

Therapeutic Strategies in Sepsis

• Optimize Organ Perfusion

• Pressors may be necessary.

• Compensated Septic Shock: Phenylephrine

Norepinephrine

Dopamine

Vasopressin

• Uncompensated Septic Shock: Epinephrine

Dobutamine + Phenylephrine / Norepinephrine

Therapeutic Strategies in Sepsis

• Control Infection Source

• Drainage

• Surgical

• Radiologically-guided

• Culture-directed antimicrobial therapy

• Support of reticuloendothelial system

• Enteral / parenteral nutritional support

• Minimize immunosuppressive therapies

Therapeutic Strategies in Sepsis

• Support Dysfunctional Organ Systems

• Renal replacement therapies (CVVHD, HD).

• Cardiovascular support (pressors, inotropes).

• Mechanical ventilation.

• Transfusion for hematologic dysfunction.

• Minimize exposure to hepatotoxic and nephrotoxic therapies.

Management strategies in patients

with severe sepsis

• Stop bacterial spillage into systemic circulation– correct surgical pathologies

– correct factors that would enhance bacterial translocation

– selective use of antibiotics (-)

– enteral nutrition (?) to keep the gut barrier intact

– probiotics, glutamine or anti-oxidants, dopexamine

• Organ support– aggressive monitoring of cardiac output, blood flow

and tissue oxygenation

– get the fluid, inotropes and ventilatory support right

– concept of “goal-directed” therapy

Acquired surgical infections

• The operative sites– Wounds

– Cavities

• In relation to a prosthesis

• Respiratory tract

• Gastrointestinal tract– pseudomembranous colitis

• Urinary tract

• Intravenous lines

• Cross infections

MRSA

Methicillin-resistant staphylococcus aureus (MRSA)

• It is a by-product of modern and advanced medical care

• Rapid rise in incidence all over the world since 1990

• Serious financial implications for the treatment of MRSA infection

• MRSA is around us silently and being “opportunistic”

Which organ did the MRSA affected?

Yap FH et al., Clin Infect Dis 2004; 39:511-516.