Surgical Infections
Interuniversitair Postgraduaat Opleiding HEELKUNDE
2017-2018
Prof.dr.D.Hompes
Surgical Oncology
UZ Leuven
“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%
Historical background (2)
Louis Pasteur
•Paris, 1860
•“germ theory”
contagious disease = caused by
specific ‘microbes’, foreign to the
infected organism
Sterilization
Staphylococcus, streptococcus,
pneumococcus
Historical background (3)
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
Historical background (4)
Robert Koch
•Wollstein, 1878
•“Koch’s postulates”
•Culture bacillus anthracis
•Cholera
•TBC
Historical background (5)Charles McBurney
•New York, 1889
•Appendectomy
= “source control”
Treves
1902
Historical background (6)
Alexander Fleming
• London, 1928
• Inhibition of growth of
staphylococcus
around a mold colony
(penicillum notatum)
Penicillin
Historical background (7)• F.Meleney, W.Altemeier, … (surgeons!)
Aerobes & anaerobes can synergize to cause serious soft tissue and intra-
abd. Infections
Concept:
- 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 of from it…”
Cytokines host inflammatory response
Pathogenesis of infectionHOST 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 defensesSKIN
- Epithelial surface- Chemicals from sebaceous glands- Shedding of epithelial cells- Endogenous / resident flora:
Gram positive: staphylococcus / streptococcuscorynebacterium / propionibacterium
Infra-umbilical region:+ enterococcus faecalis & faecium
E.Coliother enterobacteriaceaeyeast (e.g. candida albicans)
CAVE: skin disease overgrowth barrier breachesintroduction
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 TRACTNo commensals!
CAVE:- barriers affected by disease
(e.g. malignancy)- External source (e.g. catheter)
Host defensesGASTRO-INTESTINAL TRACT
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 defensesDistal colorectum
most extensive host endogenous flora
ANAEROBIC AEROBIC
Bacteroides fragilisBacteroides distasonisBacteroides thetaiomicronBifidobacteriumClostridiumEubacteriumFusobacteriumLactobacillusPeptostreptococcus species
E.ColiOther enterobacteriaceaeEnterococcus faecalis & faecium
Candida albicansOthers 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
DefinitionsInitial 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 microorganismsInflammatory 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 SHOCK
acute circulatory failure
arterial hypotension (SBP <90mmHg) despite adequate fluid resuscitation
= most severe manifesation of infection
Mortality = 45-60%
40%
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 / 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
pyogenesSSI
(alone or in conjunctionwith other pathogens)
Most frequent: Enterobacteriaceae- E.Coli- Klebsiella pneumonieae- Serratia marcescens- Enterobacter- Citrobacter- AcinetobacterPseudomonas- Pseudomonas aeruginosa- Pseudomonas fluorescens- Pseudomonas xanthomonas
Enteric organisms- Enterococcus faecalis &
faeciumNosocomial infections
in immunocompromisedor chronically illpatients
(low virulence in healthyindividuals)
Microbiology of infectious agents• 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)
2. Rare causes of aggressive soft tissue infections
(e.g. Mucor)
3. Opportunisic pathogens immunocompromised host
(e.g. Aspergillus, Cryptococcus)
Microbiology of infectious agents
• 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. immunosuppression after Tx)
- adenoviruses, CMV, EBV, HSV, Varicella zoster virus
CAVE: HBV, HCV, HIV transmission to health care workers
Microbiology of infectious agentsCommon pathogens in surgical patients
Prevention and treatment of surgical infections
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)
Prevention and treatment of surgical infections
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
Prevention and treatment of surgical infections
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 ???
Prevention and treatment of surgical infections
Site Antibiotic Alternative (e.g. penicillin
allergic)
Cardiovascular surgery cefazolin, cefuroxim vancomycin
Gastroduodenal area cefazolin, cefotetan, cefoxitin, ampicillin-sulbactam fluoroquinolone
Biliary tract with active infection (e.g. cholecytitis)
ampicillin-sulbactam, ticarcillin-clavulanate, piperacillin-tazobactam
fluoroquinoloneplus clindamycin or metronidazole
Colorectal surgery, obstructed small bowel
cefazolin plus metronidazole, ertapenem, ticarcillin-clavulanate, piperacillin-tazobactam
gentamycin or fluoroquinoloneplus clindamycin or metronidazole
Head and neck cefazolin aminoglyosideplus clindamycin
Neurosurgical procedures cefazolin vancomycin
Orthopedic surgery cefazolin, ceftriaxone vancomycin
Breast, Hernia cefazolin vancomycin
Prevention and treatment of surgical infections
Prevention and treatment of surgical infections
Prevention and treatment of surgical infections
2. Empiric therapy ( prophylaxis)
• When high risk of surgical infection e.g. ruptured appendicitis
• When significant contamination e.g. colonic spillage
• Critically ill patients with potential site of infection + sepsis
• Short: 3-5 days (cultures! clinical evolution!)
Prevention and treatment of surgical infections
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 !!!
Prevention and treatment of surgical infections
4. Duration of therapy
• Decision at prescription
• Empiric therapy ≤ 3-5 days
•Curtail!
•CAVE: SIRS <50% of patients harbor infection
(Chest 1998)
Therapy duration
MonomicrobialUTI
PneumoniaBacteremia
3-5 days7-10 days
10-14 days
OsteomyelitisEndocarditis
Prostethic infection(when device removal = hazardous)
6-12 weeks
Serious / recrudescent infectionMultidrug-resistant pathogen
≥2 agents1-2 weeks IV, then PO if:
-Clinical improvement-High serum levels reached PO
Peritonitis
Penetrating GI trauma, no extensive contamination
12-24h
Perforated / gangrenous appendicitis 3-5 days
Peritoneal soilage from perforated viscus- moderate contamination
-Extensive contamination-Immunosuppressed host
5-7 days7-14 days7-14 days
Prevention and treatment of surgical infections
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 treatment of surgical infections
MISUSE
• Increasing frequency
•Adverse events: toxicity, allergy
•Costs!
• New infections e.g. Clostridium difficile colitis
• Multiagent drug resistance of nosocomial pathogens
“super bugs” !!!
Prevention and treatment of surgical infections
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
3. Host factors e.g. DM, obesity, malnutrition, immune suppression, …
Infections of significance in surgical patients
• Risk Factors for SSI
Patient factors Older ageImmune suppressionObesityDiabetes mellitusChronic inflammatory processMalnutritionPeripheral vascular diseaseAnemiaRadiationChronic skin diseaseCarrier state (e.g. chronic staphylococcus carriage)Recent operation
Local factors Poor skin preparationContamination of instrumentsInadequate antibiotic prophylaxisProlonged procedureLocal tissue necrosisHypoxia, hypothermia
Microbial factors
Prolonged hospitalization (leading to nosocomial organisms)Toxin secretionResistance to clearance (e.g. capsula formation)
Infections of significance in surgical patients
Wound class Definition Expectedinfection
rates
Clean Class I No infection, only skin microflora potentiallycontaminate the wound, no hollow viscus thatcontaines microbes is entered
1,0-5,4%
Class ID Class I & Prosthetic device is entered
Clean/contaminated Class II Hollow viscus with indigenous bacterial flora is opened 2,1-9,5%
Elective colorectal surgery 9,4-25%
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
Infections of significance in surgical patients
• 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
Infections of significance in surgical patients
• 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
Infections of significance in surgical patients
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
Infections of significance in surgical patients
SECONDARY microbial peritonitis
• Cause perforation / severe inflammation & infection of an intra-
abdominal organ (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%
Infections of significance in surgical patients
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% !!!
Infections of significance in surgical patients
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
Infections of significance in surgical patients
Organ-specific infections
Hepatic 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
Infections of significance in surgical patients
Splenic abscess
• Extremely rare
• R/ cfr. Hepatic abscess
Recurrent hepatic or splenic abscess
• Surgical unroofing & marsupialization
• splenectomy
Infections of significance in surgical patients
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 patients
Secundary pancreatic infections
•Prevention:
- 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
- Gas within pancreas on CT
•Surgery:
- Repeated débridement of infected pancreatic necrosis: remove infected inflammatory focus, pack
pancreatic bed with gauzes, closure abdomen on mesh, ∆ approach
- + Jejunal feeding tube, gastrostomy, CCE at index operation (if indicated & condition permits)
Infections of significance in surgical patients
Infections of the skin and soft tissue
• Classification: according to need for surgery
• Superficial: Cellulitis, erysipelas, lymfangitis
– only AB
– 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)
Infections of significance in surgical patients
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
Infections of significance in surgical patients
• 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 procedures)
CAVE: incomplete higher rates of morbidity & mortality
• NO Imaging DELAY! confusing!
Infections of significance in surgical patients
• 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
• IV Ig? Group A streptococcal infection + TSS
High risk of death: elderly, hypotension, bacteremia
Infections of significance in surgical patients
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
Infections of significance in surgical patients
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: repiratory physiotherapy !!!
•CAVE: aspiration pneumonia!!!
Infections of significance in surgical patients
3. Bacteremia
• Indwelling vascular catheters !
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
Infections of significance in surgical patients
• Diagnosis:
Often asymptomatic
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
Infections of significance in surgical patientsSepsis
• 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 !
•Vasopressors & inotropes
– e.g. norepinephrine, dopamine, vasopressin
– Effect on splanchnic perfusion!
– Monitoring SvO2, plasma lactate levels, MAP reduce risk of vasopressor-induced
perfusion deficits
• Pulmonary artery catheterization? no clear benefit use
Infections of significance in surgical patients
EARLY EMPIRIC AB
• ASAP broad-spectrum against most likely microbes
CAVE: delay =mortality !!!
• Cultures !
• Early identification & treatment of septic sources !
Infections of significance in surgical patients
ADJUNCTIVE TREATMENTS
• Low-dose corticosteroids
if septic shock unresponsive to fluids & vasopressors
(relative adrenal insufficiency)
• Recombinant human activated protein C (Xigris®)
survival benefit
in surgical patients: if septic shock sepsis and ≥ 2 organ failures
•Acute lung injury mechanical ventilation
TV 6ml/kg & pulmonary airway plateau pressures ≤30cmH2O
• Red blood cell transfusion if Hb < 7 mg/dl
sooner if severe CAD, ongoing blood loss, severe hypoxemia
Infections of significance in surgical patients
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
Infections of significance in surgical patientsHIV
• 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 is unknown but there’s 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
Infections of significance in surgical patients
HBV
• DNA virus
• Affects only humans
• Primary infection = generally self-limited (6% of infected are > 5 years of age)
• Can progress to chronic carrier state
30% death of chronic liver disease or HCC
• Surgeons & other healthcare workers = at high risk HBV vaccine!!!
• Postexposure: Hepatitis B immune globulin
+/-75% protection from HBV infection
Infections of significance in surgical patients
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 = 2%
CAVE: late conversion! (6 – 12m!!!)
CAVE: false positive testing (if + PCR testing!)
• No vaccine available!
• No protective effect from HCV Ig
• antiviral R/ directly acting agents (po), if fibroscan F2-F4
95% evolution to AS+, PCR-
Biologic warfare agentsGeneral 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: worse
+ respiratory distress, chest pain, diaphoresis
chest X-ray: widened mediastinum + pleural effusions
• (rapid antigen tests)
• Postexposure prophylaxis: ciprofloxacin or doxocyclin (amoxicillin if peni-sensitive)
• R/ ciprofloxacin + clindamycin (blocks toxin production) + rifampin (penetrates CNS & intracellular locations)
exposure followed by symptoms
=high mortality
Biologic warfare agentsYersinia 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/ aminoglycosides, doxocyclin, ciprofloxacin & 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: 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%
Biologic warfare agentsFrancisella 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: cultures from tissue samples (difficult), acute phase agglutination tests
• R/ aminoglycosides or second-line agents such as doxocyclin & ciprofloxacin
Key points
Thank you !