Surgical Infections - Bast

prof.dr.D.Hompes, Surgical Oncology

(Based on Schwartz’s Principles of Surgery, 10th edition)

Surgical Infections

“All creatures great and small”

Historical background (1)

Ignaz Semmelweis

• Vienna, 1861

• Puerperal (“childbed”) fever:

training ward 9.1%

Midwives 3.4%

Chlorine water 1.5%


Louis Pasteur

• Paris, 1860

• “germ theory”

contagious disease = caused by

specific ‘microbes’, foreign to the

infected organism

Sterilization

Staphylococcus, streptococcus

pneumoniae


Joseph Lister• Glasgow, 1859

• >50% mortality due to infection

after amputation

Carbolic acid (phenol)

N=12 patients

- 10 no amputation

- 1 amputation

- 1 non-wound related death


Robert Koch• Wollstein, 1878

• “Koch’s postulates”

• Culture bacillus anthracis

• Cholera

• TBC


Charles McBurney

•New York, 1889

•Appendectomy

= “source control”

Treves

1902


Alexander Fleming

• London, 1928

• Inhibition of growth of

staphylococcus around

a mold colony

(penicillum notatum)

Penicillin


• F.Meleney, W.Altemeier, … (surgeons!)

Aerobes & anaerobes can synergize to cause serious soft tissue and intra-

abdominal infections

Concepts:

- resident microbes = non-pathogenic until they enter a sterile body cavity

at surgery

- Most surgical infections = polymicrobial

• William Osler (USA, 1904)

“Except on a few occasions, the patient appears to die from the body’s

response to infection than from it…”

Cytokines host inflammatory response

Pathogenesis of infection

HOST DEFENSES

• Prevent invasion

• Limit proliferation

• Contain/eradicate invading microbes

Site-specific defenses

Freely circulating components

CAVE: perturbation of 1 or more components

(e.g. Immunosuppressants, burns, …)

Host defenses

SKIN- Epithelial surface

- Chemicals from sebaceous glands

- Shedding of epithelial cells

- Endogenous / resident flora:

Gram positive: staphylococcus / streptococcus

corynebacterium / propionibacterium

Infra-umbilical region:

+ enterococcus faecalis & faecium

E.Coli

other enterobacteriaceae

yeast (e.g. candida albicans)

CAVE: skin disease overgrowth barrier breaches

introduction

Host defenses

RESPIRATORY TRACT

Upper- respiratory mucus- ciliated cells- coughing

Lower- alveaolar macrophages:

phagocytosis

Host defensesUROGENITAL TRACT BILIARY T TRACT &

PANCREATIC DUCTAL TRACT

DISTAL RESPIRATORY TRACT

No commensals!CAVE:

- barriers affected by disease

(e.g. malignancy)

- External source (e.g. catheter)

Oropharynx vast number microbes

highly acidic, low motilitygastric mucosa: 102-103 CFU/ml

microbial proliferationterminal ileum: 105-108 CFU/ml

low oxygen, staticexponential growthdistal colorectum: 1011-1012 CFU/mlanaerobic > aerobic (100:1)

Host defenses

GASTRO-INTESTINAL TRACT

Host defensesDistal colorectum

most extensive host endogenous flora

ANAEROBIC AEROBIC

Bacteroides fragilis

Bacteroides distasonis

Bacteroides thetaiomicron

Bifidobacterium

Clostridium

Eubacterium

Fusobacterium

Lactobacillus

Peptostreptococcus

species

E.Coli

Other enterobacteriaceae

Enterococcus faecalis &

faecium

Candida albicans

Others Candida species

Effective prevention of invasione.g. Shigella, Vibrio, Salmonella

BUT: CAVE perforation!

Host defensesMicrobes enter sterile body cavity additional host defenses

1. Primitive, non-specific

- Physical barriers

- Proteins (lactoferrin, transferrin) sequester Fe

- Fibrinogen polymerizes to fibrin: trapping

- Diaphragm, omentum, intestinal ileus

2. Tissue defense mechanisms

- Resident macrophages: cytokine synthesis (TNFα, Il1β, Il6, Il8, INFγ)

- Low levels of complement proteins en Ig

counterregulation response binding proteins (TNF-BP)

cytokine receptor antagonists (Il1ra)

anti-inflammatory cytokines (Il4 & Il10)

Host defenses3. Interaction with microbes

• opsonization (C1q, C3bi, IgFc)

phagocytosis

microbial destruction extracellular (C5b6-9 membrane attack complex)

intracellular (phagocytic vacuoles)

• Complement pathways

direct contact with/via IgM > IgG binding to microbes

release complement protein fragments (C3a, C4a, C5a)

enhance vascular permeability

• Bacterial cell wall components & enzymes from leukocyte phagocytic vacuoles

• C5a, microbial wall peptides, macrophage cytokines (e.g.Il8)

influx inflammatory fluid & diapedesis of PMN

Definitions

Initial number of microbes

Rate of microbial proliferation

Virulence

Potency of host defenses

Eradication

Containment

Locoregional infection

Distant spread (metastasic abscess)

Systemic infection

(bacteremia/fungemia)

= failure of local host defenses

Magnitude

of response

Definitions

Identification microorganisms

Inflammatory response

- Rubor

- Calor

- Dolor

Systemic manifestations-Elevated T°-Elevated WBC-Tachycardia-Tachypnea

Infection SIRS

Sepsis

Severesepsis

Septicshock

Polytrauma

Aspiration

Pancreatitis

Burn

Malignancy

Transfusion reaction

DefinitionsCriteria / Indicators for SIRS

General variables

- Fever (core T°>38,3°C)- Hypothermia (core T°<36°C)- Heart rate >90bpm- Tachypnea- Altered mental status- Significant edema or positive fluid balance (>20ml/kg over 24h)- Hyperglycemia in the abscence of diabetes

Inflammatory variables

- Leukocytosis (WBC>12.000)- Leukopenia (WBC<4000)- Bandemia (>10% band forms)- Plasma C-reactive protein >2 s.d. above normal value- Plasma protocalcitonin > 2 s.d. above normal value

Hemodynamic variables

- Arterial hypotension (SBP <90mmHg, MAP <70, or decrease SBP >40mmHg)- SvO2 <70%- Cardiac index >3,5L/min/m2

Organ dysfunction variables

Arterial hypoxemiaAcute oliguriaCreatinine increaseCoagulation abnormalitiesIleusThrombocytopeniaHyperbilirubinemia

Tissue perfusion variables

HyperlactemiaDecreased capillary filling

Microbial products:

- endotoxins (G-)

- Peptidoglycans/teichoic acids (G+)

- Cell wall components

Pro-inflammatory mediators

SEPSIS

=

SIRS

+

local or systemic source of infection

Definitions

• SEVERE SEPSIS= sepsis with new onset organ failure

- need for ventilatory support

- oliguria unresponsive to aggressive fluid resuscitation

- hypotension requiring vasopressors

Mortality = 51/100.000/year

• SEPTIC SHOCKacute circulatory failure

arterial hypotension (SBP <90mmHg) despite adequate fluidresuscitation

= most severe manifestation of infection

Mortality = 45-60%

40%

Microbiology of infectious agentsCommon pathogens in surgical patients

Microbiology of infectious agents

• Bacteria- Majority of surgical infections

- Classification:

- Gram-staining

- Morphology: cocci or bacilli

- Division: single, pairs (diplococci),

clusters (staphylococci),

chains (streptococci)

- Presence & location of spores

- Anaerobic organisms:

e.g. Propionibacterium acnes

unable to grow / divide poorly in air

skin, oropharynx, colorectum

- Mycobacterium

(M.Tuberculosis / M.avium-intracellulare / M.Leprae) & Nocardia

acid-fast bacilli, slow growing (DNA-based analysis)

Gram-positive Gram-negative

Blue stain Red stain

Aerobic skin

commensals

- Staphylococcus

aureus & epidermidis

- Streptococcus

pyogenes

SSI

(alone or in conjunction

with other pathogens)

Most frequent:

Enterobacteriaceae

- E.Coli

- Klebsiella pneumonieae

- Serratia marcescens

- Enterobacter

- Citrobacter

- Acinetobacter

Pseudomonas

- Pseudomonas aeruginosa

- Pseudomonas fluorescens

- Pseudomonas xanthomonas

Enteric organisms

- Enterococcus faecalis

& faecium

Nosocomial infections

in

immunocompromised

or chronically ill

patients

(low virulence in healthy

individuals)


• Fungi

- Special stains (e.g. KOH, Giemsa, …)

- Observation form of branching and septation

- Growth characteristics in special media

- Growth at different temperature (25°C vs. 37°C)

1. Nosocomial infections as part of polymicrobial infections or fungemia

(e.g. C.Albicans)

1. Rare causes of aggressive soft tissue infections

(e.g. Mucor)

3. Opportunistic pathogens immunocompromised host

(e.g. Aspergillus, Cryptococcus)


• FungiANTIFUNGAL ADVANTAGES DISADVANTAGES

Amphotericin B Broad-spectrum, inexpensive Renal toxicity premeds, IV only

Liposomal Amphotericin B Broad-spectrum Extensive, IV only, renal toxicity

Azoles

Fluconazole IV and PO availibility Narrow-spectrum, drug interactions

Itraconazole IV and PO availibilty Narrow-spectrum, no CSF penetration

Drug interactions, decreased cardiac

contractility

Posaconazole Broad-spectrum, zygomycete activity PO only

Voriconazole IV and PO availibility, broad-spectrum IV diluent accumulates in renal failure (PO)

Visual disturbances

Echinocandins

Anidulafungin,

caspofungin, micafungin

Broad-spectrum IV only, poor CNS penetration


• Viruses

- Small size & necessity for growth within cells

difficult to culture: longer time than optimal

for clinical decision making

- Identification: host antibody response (indirect)

presence of viral DNA or RNA (e.g. PCR)

- Mostly in immunocompromised host (e.g. immunosuppressionafter Tx)

- adenoviruses, CMV, EBV, HSV, Varicella zoster virus

CAVE: HBV, HCV, HIV transmission to health care workers

Prevention and treatment

General principles

• “Prophylaxis”

= reduction of presence of endogenous & exogenous microbes

• Scrub OR personnel

• Desinfection operative site (+ hair removal)

• Intra-operative sterility

Reduction inoculum

• Antimicrobial agents?

- If ingress of high numbers of microbes (e.g. colonic resection)

- If infection would have high consequences (e.g. prosthetic graft)


Source control !!!I. “Ubi pus, ibi evacua”

• Drainage purulent material

(e.g. abscess drainage)

• Débridement of all infected/devitalized tissue

(e.g. necrotizing soft tissue infection)

• Removal of foreign bodies at infection site

• Remediate underlying cause of infection

(e.g. bowel perforation)

II. Antimicrobial agents

• Secondary importance to effective surgery

CAVE: delay in operative intervention increased morbidity (& mortality)


Appropriate use of antimicrobial agents

1. Prophylaxis

• = administration of antimicrobial agent(s) BEFORE surgery

number of microbes that enter soft tissue / body cavity

selection according to microbes likely to be present

• Limited to time before & during surgery

(≈ 1 dose, certain types of surgery)

• BUT: complex, prolonged procedures > serum t1/2!

(addtional dose)

• NB: Postoperative ???


2. Empiric therapy

• When high risk of surgical infection e.g. ruptured appendicitis

• When significant contamination e.g. colonic spillage

Intra-operative findings: increased risk of infection

Prophylaxis Empiric therapy

• Critically ill patients with potential site of infection + sepsis

• Short: 3-5 days (cultures! clinical evolution!)

• Empiric therapy therapy if established infection

Prevention and treatment3. Therapy for established infection

MONOMICROBIAL

• Frequently nosocomial in postoperative patients

(e.g. UTI, pneumonia, bacteremia)

• SIRS + evidence of local infection

initiate empiric therapy: at first broadspectrum, based on

- initial evidence (Gram staining)

- institutional & unit-specific drug

sensitvity patterns

de-escalation / therapy refinement

Patient response

Culture & sensitivity

results (48-72h)

Prevention and treatment3. Therapy for established infection

POLYMICROBIAL

• Source controle (!!!) + antimicrobial agents

• Cultures: lesser importance:

Only limited cadre of microbes predominate

(<< large number present at initial contamination)

modification AB regimen: based on cultures & clinical

course!!!

• e.g. perforated appendicitis, bowel perforation

R/ agents directed against aerobes & anaerobes

during ≥3-5 days

• Failure? mostly due to inadequate source control !!!


4. Duration of therapy

• Decision at prescription

• Prophylaxis: single dose immediately prior to incision

• Empiric therapy: ≤ 3-5 days

curtail!

• CAVE: SIRS <50% of patients harbor infection

(Chest 1998)

Therapy duration

Monomicrobial

UTI

Pneumonia

Bacteremia

Osteomyelitis

Endocarditis

Prosthetic infection (when device removal = hazardous)

3-5 days

7-10 days

10-14 days

6-12 weeks

Serious / recrudescent infection

Multidrug-resistant pathogen

≥2 agents

1-2 weeks IV, then PO if:

- Clinical improvement

- High serum levels reached PO

Peritonitis

Penetrating GI trauma, no extensive contamination

Perforated / gangrenous appendicitis

Peritoneal soilage from perforated viscus

Moderate contamination

Extensive contamination

Immunosuppressed host

12-24 h

3-5 days

5-7 days

7-14 days

7-14 days



Later phases of postoperative AB treatment of serious intra-

abdominal infection:

• Lack of increased WBC Infection

• Lack of band forms of PMN on peripheral smear =

• Lack of fever [<38.6°C] eradicated

•Presence of indicators ≠ continuing / altering AB treatment

extra-abdominal infection?

residual / ongoing intra-abdominal infection? [source control !!!]

Prevention and treatmentALLERGY

• check medical history BEFORE prescription!

• “True” allergic symptoms: e.g. urticaria, bronchospasm, anaphylaxis

≠ indigestion, nausea

• Penicillin allergy incidence 0,7-10%

avoid any beta-lactam drugs

incidence of cross-reactivity low:

carbapenems 1%

cephalosporins 5-7%

monobactams extremely small

• Severe allergic reaction to certain AB preclude use of any agent

in that class, unless “lifesaving”

• (intradermal testing)

• (Desensitization)


MISUSE

• Increasing frequency

• Adverse events: toxicity, allergy

• Costs!

• °new infections e.g. Clostridium difficile colitis

• Multiagent drug resistance of nosocomial pathogens

“super bugs” !!!


RULES TO BE OBEYED…

• Limit prophylaxis to period of operative procedure

• Do not convert prophylaxis into empiric therapy, unless well-

defined conditions

• Set duration of AB treatment from the outset

• Curtail AB administration, when no clinical or microbiological

evidence of infection

• Limit therapy to short course whenever possible

Infections of significance in surgical patients

Surgical site infections (SSI) (30 days postop.)

Incisional SSI

» Superficial (skin, subcutis)

» Deep

Organ / space SSI

Factors:

1. Degree of microbial contamination of the wound during surgery

2. Duration of the procedure

2. Host factors e.g. DM, obesity, malnutrition, immune suppression, …


Risk Factors for SSI

Patient factors Older age

Immune suppression

Obesity

Diabetes mellitus

Chronic inflammatory process

Malnutrition

Smoking

Renal failure

Peripheral vascular disease

Anemia

Radiation

Chronic skin disease

Carrier state (e.g. chronic staphylococcus carriage)

Recent operation

Local factors Open compared to laparoscopic surgery

Poor skin preparation

Contamination of instruments

Inadequate antibiotic prophylaxis

Prolonged procedure

Local tissue necrosis

Blood transfusion

Hypoxia, hypothermia

Microbial factors Prolonged hospitalization (leading to nosocomial organisms)

Toxin secretion

Resistance to clearance (e.g. capsula formation)


Wound class Definition Expected

infection rates

Clean Class I No infection, only skin microflora potentially

contaminate the wound, no hollow viscus that

containes microbes is entered

1.0-5.4%

Class ID Class I in which a prosthetic device (e.g. mesh or

valve) is inserted

Clean/contaminated Class II Hollow viscus with indigenous bacterial flora is

opened under controlled circumstances, without

spillage

2.1-9.5%

Elective colorectal surgery 9-25%

Contaminated Class III Open accidental wounds encountered early after

injury, extensive introduction in normally sterile area

(due to major breaks in sterile techniques, gross

spillage of viscus content, incision through inflamed

tissue)

3.4-13.2%

Dirty Class IV Traumatic wounds with significant delay in treatment

and in which necrotic tissue is present, wounds

created in presence of overt infection (purulent

material) or created to access a perforated viscus

accompanied by a high degree of contamination

3.1-12.8%

Prophylaxis


• Surgical management

- Class I & II wounds: primary closure

- Class III & IV wounds: 25-50% SSI superficial part packed open

- heal by secondary intention

- delayed primary closure

BUT: Class III after appendectomy (gangrenous/perforated appendicitis):

primary closure if AB against aerobes & anaerobes 3-4% SSI


• Hyperglycemia

• Adverse effect on WBC function

• Diabetic patients increased SSI rates

e.g. hyperglycemia in cardiac surgery patients (bypass)

• Appropriate blood sugar control !!!

• Effective therapy for incisional SSIs?

• Incision & drainage without AB heal by secondary intention or VAC

• AB? if cellulitis, concurrent SIRS

culture results rarely direct treatment

• Topical AB & antiseptics? unproven


Intra-abdominal infections “PERITONITIS”

PRIMARY microbial peritonitis

• Cause > hematogenous dissemination from distant source or direct inoculation

• Patients Ascites +++ for medical reasons or peritoneal dialysis from renal failure

• S/ ascites, diffuse tenderness & guarding without localized findings,

no pneumoperitoneum, paracentesis: >100WBCs/ml,

microbes with single morphology on G stain (monomicrobial)

• Cultures dialysis patients: Gram-positive

others: E.Coli, K.Pneumoniae, pneumococci, others

• R/ AB (cultures!), 14-21 days,

removal of indwelling devices if necessary

Surgery = rarely required


SECONDARY microbial peritonitis

• Cause perforation / severe inflammation & infection of an intra-abdominal organ

(e.g.colonic perforation = most morbid)

• R/ Source control + AB directed against aerobes & anaerobes

conversion IV PO when ileus resolves

low failure rates (response 70-90%), mortality 5-6%

failure: - abscess

- leakage GI anastomosis postop.peritonitis

- tertiary persistent peritonitis

CAVE: inability to controle infection source mortality >40%


TERTIARY (persistent) peritonitis

• Poorly understood entity

1. More common in immunosuppressed patients

(i.e. inadequate host defenses*)

2. Microbes: E.faecalis & faecium, S.epidermidis, C.albicans, P.Aeruginosa, …

* Combination!

* Lack of responsiveness to initial AB? (resistance!)*

* Even with effective AB therapy: mortality >50% !!!


INTRA-ABDOMINAL ABSCESS

• Mostly: CT-guided percutaneous drainage

• Surgery? - multiple abscesses

- proximity to vital structures (at risk at percutaneous drainage)

- ongoing source of contamination

• AB? Short course (3-7 days), directed against aerobic & anaerobic activity

• Drain removal? Cavity collapse

<10-20ml/d.

no evidence of ongoing infection source

improved clinical condition


Organ-specific infectionsHepatic abscess• 15/100.000 admissions/year

• 80% pyogenic

20% parasitic and fungal– Manipulation biliary tract

– Pylephlebitis > neglegted appendicitis, diverticulitis

– <50% e causa ignota

• Aerobic: E.Coli, K.Pneumoniae, enteric bacilli, enterococci, Pseudomonas

Anaerobic: Bacteroides, anaerobic streptococci, Fusobacterium

• R/ small (<1cm), multiple: sampling, 4-6 weeks AB

larger: percutaneous drainage


Splenic abscess

• Extremely rare

• R/ cfr. Hepatic abscess

Recurrent hepatic or splenic abscess

• Surgical unroofing & marsupialization

• splenectomy


Secundary pancreatic infections• e.g. infected pancreatic necrosis, pancreatic abscess

• In 10-15% of patients with severe pancreatitis with necrosis

• ce CT at diagnosis (CT Severity Index (CTSI))

• > grade C Monitoring in ICU

(APACHE II / Ranson score)

• follow-up CTs

Infections of significance in surgical patientsSecundary pancreatic infections

• Prevention:

- Prophylactic AB???

- Enteral (+parenteral nutrition)

• Diagnosis of secondary infection:

- Persistent SIRS (fever, ↑WBC, organ dysfunction)

- Initial recuperation sepsis after 2-3 weeks

- CT-guided aspiration: Gram’s stain & cultures: positive

- Gas within pancreas on CT

• Surgery:

- Repeated débridement (median 4x) of infected pancreatic necrosis: timing: delay >2-4

weeks after onset ( maturation of fluid collection): transgastric vs retroperitoneal vs

endoscopic vs lumbar vs open approach (experience & multidisciplinarity!)

- + Jejunal feeding tube, gastrostomy, CCE (if indicated & condition permits)


Infections of the skin and soft tissue• Classification: according to need for surgery

• Superficial: Cellulitis, Erysipelas, Lymfangitis

– only AB (active against Gram+ skin microflora)

– Local source of infection?

• Furuncles or boils

– Spontaneous drainage or surgical I & D

– AB?

If significant cellulitis of if no rapid resolution after I & D

CAVE: MRSA

(if persistence after I & D and adequate AB)

http://www.huidziekten.nl/afbeeldingen/lymphangitis2.jpg


Aggressive soft tissue infections• Rare

• Difficult diagnosis

failure 80-100% mortality

rapid recognition 16-25% mortality

• Delineation based on involved soft tissue layers & pathogens

• At risk: - elderly BUT

- immunosuppressed also healthy

- diabetic individuals !!!

- peripheral vascular disease (streptococci)

• Compromise of fascial blood supply to some degree

+ introduction exogenous microbes


• Clinical findings

– Sepsis / septic shock eci

– “Dishwater pus” evecuation from entry site

(mostly extremities, perineum, torso)

– Skin changes (bronze hue, brawny induration), blebs, crepitus

– Pain at infection site, out of proportion to physical manifestations

IMMEDIATE SURGERY !!!

exposure / direct visualization potentially infected tissue (deep!)

+ radical resection infected areas (amputation, disfiguring surgery)

CAVE: incomplete higher rates of morbidity & mortality

• NO Imaging DELAY! confusing!


• Gram’s stain (tissue fluid)

• AB directed against gram-positive & gram-negative aerobes and

anaerobes (e.g.Vanco+carbapenem) + high-dose aquaeous penicillin G

50% polymicrobial cfr.sec.peritonitis

(gram positive cocci more common)

50% monomicrobial S.Pyogenes, P.Aeruginosa,

C.Perfringens

• Repeat surgical exploration + additional resection

• Hyperbaric oxygen? Gas-forming organisms


Postoperative nosocomial infections

1. UTI

• US WBCs, bacteria, leukocyt esterase +

• UC symptomatic: >104 CFU/ml

asymptomatic: >105 CFU/ml

• AB: single agent, 3-5days

• Remove urinary catheter ASAP


2. Pneumonia• Pathogens common in nosocomial environment

• Prolonged mechanical ventilation

• Purulent sputum, ↑WBC, fever

• New chest X-ray abnormalities

• Sputum culture + Gram’s stain, (BAL)

• Weaning ASAP

• Postop. abdomino-thoracic surgery: respiratory physiotherapy !!!

• CAVE: aspiration pneumonia!!!


3. Bacteremia• Indwelling vascular catheters !

e.g. physiologic monitoring vascular access

drug delivery hyperalimentation

• 25% colonized, 5% associated with bacteremia

• Risk of infection:

– Duration of catheterization

– Insertion / manipulation under emergency / non-sterile

conditions

– Multilumen catheters

NB: peripherally inserted CVC: similar risk


• Diagnosis:

Often asymptomatic, only ↑ WBC

Blood cultures from peripheral site & through the catheter

• Catheter removal if:

– Obvious purulence at exit site of skin tunnel

– Severe sepsis without other obvious infection site

– Bacteremia Gram negative aerobes or fungi

• Low-virulence microbes (e.g.S.epidermidis):

• Can be treated in 50-60%

• 14-21 days of AB

• When no other vascular access site


Sepsis

• Increasing incidence, but mortality rates dropping to 30%

TREATMENT

• RESUSCITATION FLUIDS

CVP 8-12mmHg, MAP ≥ 65 mmHg,

urinary output ≥ 0.5ml/kg/h

early placement CVC!

Delay until ICU > 3 hours = poor outcome !


TREATMENT

• EARLY EMPIRIC AB

– ASAP broad-spectrum against most likely microbes

CAVE: delay = mortality !!!

– Cultures !

– Early identification & treatment of septic sources !


TREATMENT

• VASOPRESSORS AND INOTROPES

– e.g. norepinephrine, dopamine, vasopressin

– Monitoring SvO2, plasma lactate levels, MAP

reduce risk of vasopressor-induced perfusion deficits

• Pulmonary artery catheterization?

no clear benefit use


TREATMENT

• ADJUNCTIVE TREATMENTS

- Low-dose corticosteroids

if septic shock unresponsive to fluids & vasopressors

- Acute lung injury mechanical ventilation

TV 6-7 ml/kg

pulmonary airway plateau pressures ≤ 30cmH2O

- Red blood cell transfusion

if Hb < 7 mg/dl

sooner if severe CAD, ongoing blood loss, severe hypoxemia


RESISTANT ORGANISMS

• Drivers: genetic (e.g. receptors) + AB selection!

• > worldwide use of AB in people, agriculture and animals

• In all classes of AB

• Resistance mechanisms

• Intrinsic (natural resistance)

• Mutational and mediated by changes in chromosomal make-up of the organism

• Extrachromosomal transfer of genetic material via transposons and plasmids

• Important examples:

• MRSA CAVE: chronically ill, SSI

• ESBL-producing enterobacteraceae (Klebsiella, E.Coli)

• VRE (E.Faecium)

CAVE: co-infection!


Blood-borne pathogens

General precautions against patient-to-healthcare worker

transmission:

1. Routine use of barriers when anticipating contact with blood & body

fluids

2. Washing of hands / other skin surfaces immediately after contact

with blood or body fluids

3. Careful handling and disposal of sharp instruments during and after

use


HIV• Risk of transmission patient-to-surgeon = low

• Risk of transmission after needlestick = 0,3%

• Postexposure prophylaxis ↓↓ risk of seroconversion after

occupational exposure to HIV

- within hours rather then days

- if significant exposure to HIV-positive patient, 2- or 3-drug regimen

- If patient’s HIV-status unknown, but high risk of HIV infection

• Risk = related to:

HIV prevalence in population being cared for

(number of) percutaneous lesions suffered during care

use of postoperative prophylaxis

NO: 1/200.000

YES: 1/10.000.000


HBV

• DNA virus

• Affects only humans

• Primary infection = generally self-limiting

• Can cause fulminant hepatitis or progress to chronic carrier

state

30% death of chronic liver disease or HCC

• Surgeons & other healthcare workers = at high risk

HBV vaccine!!!


HCV

• RNA flavivirus

• Confined to humans and chimpanzees

• 75-80% of infected patients chronic carrier state 75%

chronic liver disease

• Not transmitted efficiently through occupational exposures to

blood

seroconversion after accidental needlestick = 1.8%

• No vaccine available!

• No protective effect from HCV Ig

•R/ ribavirin en gamma-interferon

Biologic warfare agents

General remarks

• Definition:

Use of infectious organisms as potential biologic

weapons, as an alternative to nuclear weapons as

weapons of mass destruction

• Selection:

typical agent = selected for the ability to be spread via

inhalation route

(most efficient mode of mass exposure)

• US program involving biologic agents: halted in 1971, but...

Biologic warfare agentsBacillus anthracis (Anthrax)• Gram-positive rod

• Zoonotic disease, > domesticated & wild herbivores

• Inhalation anthrax: exposure history!, 1- to 6-day incubation period

malaise, myalgia, fever

after short period: worsening of S/

+ respiratory distress, chest pain, diaphoresis

chest X-ray: widened mediastinum + pleural effusions

• (rapid antigen tests under development)

• Postexposure prophylaxis: ciprofloxacin or doxocyclin (amoxicillin if

proven penicillin-sensitive)

• R/ ciprofloxacin + clindamycin (blocks toxin production) + rifampin

(penetrates CNS & intracellular locations)

exposure followed by symptoms

=high mortality


Yersinia pestis (Plague)• Gram-negative bacillus

• Naturally occuring: transmitted via flea bites from rodents

• Clinical manifestations:

* aerolized bacteria: epidemic pneumonia with blood-tinged sputum

* fleas as carriers: bubonic plague

Symptoms: painful lesions (bubo)

fever, severe malaise

exposure to fleas

• Diagnosis: aspirate of bubo + direct antibody stain

• Postexposure prophylaxis: doxocyclin

• R/ streptomycin, aminoglycosides, doxocyclin, ciprofloxacin, levofloxacin

or chloramphenicol

Biologic warfare agentsSmallpox• Variola virus

• Eradication in late 1970s

• CAVE: prolonged viability !

• Potential for reverse genetic engeneering (known sequence)

• US: vaccination program for key healthcare workers

• Highly infectious in aerolized form

• Clinical S/ incubation period 10-12 days

malaise, fever, vomiting, headache

centripetal rash (face extremities)

• Postexposure prophylaxis: smallpox vaccine, effective up to 4 days

postexposure

• R/ cidofovir (demonstrated activity in animal models)

Mortalityup to30%


Francisella tularensis (Tularemia)• Gram-negative aerobic

• Principal reservoir: tick

• Inoculation proliferates within macrophages

• Potential bioterrorist threat:

Very high infectivity after aerosolization

tularemia pneumonia: cough

pneumonia on chest X-ray

85%: enlarged lymph nodes

• Diagnosis: acute phase agglutination tests (cultures from tissue

samples = difficult)

• R/ aminoglycosides or second-line agents (e.g. doxocyclin &

ciprofloxacin)

Keypoints

Thank you !

Vragen?

[email protected]

mailto:[email protected]

Surgical Infections - Bast

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