infection in surgery ii. - upjs.sk
TRANSCRIPT
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
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://www.youtube.com/watch?v=H_gwDrLw
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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 -
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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.