Nosocomial Infections David M. Parenti, M.D.. Definitions u sterilization: use of physical...

Nosocomial Infections

David M. Parenti, M.D.

Definitions

sterilization: use of physical procedures or chemical agents to destroy all microbes, including spores, viruses, fungi

disinfection: use of physical procedures or chemical agents to destroy most microbes– high, intermediate, low level

antisepsis: use of chemical agents on skin or other tissue to inhibit or kill microbes

Nosocomial Infections Infection acquired in the hospital: > 48 hours after

admission $5 billion annually: increased hospital length of

stay, antibiotics, morbidity and mortality related to severity of underlying disease,

immunosuppression, invasive medical interventions frequently caused by antibiotic-resistant organisms:

MRSA, VRE, resistant Gram-negative bacilli, Candida

Sites of Nosocomial Infections

UTI

BSI

SSIPneum

Other

Klevens. Pub Health Rep 2007;122:160

36%

11%20%

22%

11%

Nosocomial InfectionTypes of Transmission

airborne

– tuberculosis, varicella, Aspergillus contact

– S. aureus, enterococci, Gram-negative bacilli

common vehicle

– food contamination

– Salmonella, hepatitis A

Patient 1 A 67 yo female with poorly controlled

hypertension was admitted because of a right-sided stroke. She had confusion, limitation of mobility of her left leg, and urinary incontinence. A urinary (Foley) catheter was placed and she was evaluated for rehabilitation.

4 days later she developed a temp to 103º F and blood pressure of 90/60 and was transferred to the ICU. Blood and urine cultures grew resistant Klebsiella.

Nosocomial UTI Up to 25% of hospitalized patients are

catheterized at some time during their hospital stay.

15% colonized (bacteruria)

– 5-10% per day of catheterization

– 50% after 14 days Gram-negative bacilli, VRE, Candida

– frequent antimicrobial resistance

Antibiotic-ResistantGram-Negative Bacilli increasingly a problem in the ICU: UTI, pneumonia selective pressure from high-level antibiotic usage in

hospital and community E. coli, Klebsiella, Enterobacter, Pseudomonas,

Serratia, Acinetobacter resistance to extended spectrum penicillins,

cephalosporins, aminoglycosides, quinolones colonization at multiple body sites: GI, skin, pharynx

Nosocomial UTI Pathogenesis

external

– most common

– colonization of urethral meatus

– movement of bacteria along fluid layer on external catheter surface

internal

– colonization of urine in bag, ascend through catheter lumen

Nosocomial UTI Prevention *avoid catheterization

– minimize duration of catheterization

– intermittent (“in and out”) catheterization aseptic insertion technique closed system dependent drainage silver-coated catheters

Patient 2 A 45 yo male is admitted for community-acquired

pneumonia. He has a long history of iv drug use, but has not used in several years. The intern has difficulty starting a peripheral iv so places a femoral venous catheter. His cough and fever begin to improve.

On hospital day 3 he has fever, chills and a WBC of 18,000. Blood cultures are positive for vancomycin-resistant Enterococcus.

Vascular Device-Associated Bacteremia

major cause of morbidity and mortality in hospitalized patients

150 million intravascular devices are purchased by hospitals yearly

estimated 50,000-100,000 intravascular device- related bacteremias in U.S./year

– non-cuffed central venous catheters account for 90% of vascular catheter-related bacteremias

CVC-Associated BacteremiasGWUH 2009

Staphylococcus aureus, MRSA, S. epidermidis Enterococcus faecalis, VRE Streptococcus agalactiae (group B strep)

Acinetobacter, Klebsiella pneumoniae, Enterobacter cloacae

Candida albicans, C. parapsilosis

Vascular Device-Associated Bacteremia: Pathogenesis initial step is colonization of the insertion or

access hub biofilm formation allows attachment of bacteria development of bacteremia

IV Catheter Biofilm 24 hours after Insertion

Coagulase Negative StaphylococciSlime-producing, Catheter Surface

Vascular Catheter InfectionsRisk Factors

type of catheter: plastic > steel

– multiple > single lumen location of catheter

– central > peripheral

– internal jugular, femoral > subclavian duration of placement: > 72 hours emergent placement > elective skill of venipuncturist: others > i.v. team

Vascular Catheter InfectionsClinical Clues local inflammation or phlebitis at catheter

insertion site bacteremia caused by associated organisms:

MRSA, CNS, VRE, Candida

above waist 38%

inguinal area 86%

hand or arm 29%

Bonten MJM . Lancet 1996; 348:1615

Vascular Catheter InfectionsDiagnosis

Maki rollplate technique catheter tip or intracutaneous segment is rolled on

agar plate colonies are counted > 15 colonies correlates with colonization and

potential source of bacteremia

Maki DG. NEJM 1977;296:1305

Semipermanent Tunneled Catheters (Groshong, Hickman, Mediport)

long term i.v. therapy much lower rate of infection dacron cuff incites inflammatory response, fibrosis

at insertion site prevents bacteria from migrating along external

catheter surface locations of infection: exit site, tunnel, tip

– tunnel infection always requires catheter removal septic thrombophlebitis/pulmonary emboli

Groshong catheter

CVC-Associated BacteremiaPrevention (Bundles) *minimize duration of catheterization use single vs multiple lumen catheters site placement meticulous insertion technique

– drapes, gown/gloves/mask antibiotic impregnated catheters impregnated dressing (Biopatch) outbreak/cluster control

Chlorhexidine/Silver Sulfadiazine-Coated CVCs 158 hospitalized patients with 403 triple-

lumen, polyurethane venous catheters chlorhexidine/silver sulfadiazine-coated vs

uncoated catheters-external surface

uncoated coated p colonization 24.1% 13.5% < 0.005 bacteremia 4.7% 1% < 0.03

Maki DG; Ann Intern Med 1997;127:257

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VRE RFLP GWUH 2004

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Patient 3 A 52 yo male is admitted with a severe headache

and is found to have a subarachnoid hemorrhage from a ruptured aneurysm. The neurosurgeons evacuate the hematoma and clip his aneurysm. Post-op he remains on a ventilator.

On hospital day 5 he spikes a fever to 102º F and is noted to have copious secretions from his endotracheal tube. Increasing amounts of inspired O2 are required. Blood and sputum cultures grow highly resistant Enterobacter cloacae.

Nosocomial Pneumonia 300,000 cases/year in U.S.

– 10-15% of nosocomial infections leading cause of death from nosocomial

infection– crude mortality 35-50%

ventilator-associated pneumonias occur 48-72 h post endotracheal intubation

organisms may originate from endogenous flora, other patients, visitors, or environmental sources

Ventilator Associated Pneumonia GWUH 2009

Staphylococcus aureus, MRSA

Proteus mirabilis, Serratia marcescens, Pseudomonas aeruginosa, Stenotrophomonas maltophilia

Nosocomial PneumoniaEpisodes Mortality

Klebsiella, 30% 40%

Enterobacter

S. aureus 27% 33%

P. aeruginosa 15% 72%

S. pneumoniae 12% 43%

E. coli 10% 31%

anaerobes 2% 0%

Bryan CS. Am Rev Resp Dis 1984;129:668-671

Gram-Negative Bacilli ColonizationRisk Factors

severity of underlying illness duration of hospitalization prior or concurrent use of antibiotics advanced age intubation major surgery achlorhydria ?

Ventilator-Associated PneumoniaPrevention

*limit duration of ventilation handwashing/gloves closed ventilator circuits semi-recumbent positioning

– avoid large gastric volumes avoid prolonged nasal intubation

– prevent sinusitis ? maintain gastric acidity

Patient 4 A 73 yo male is admitted with chest pain and

severe coronary artery disease. He has emergent 3-vessel coronary artery bypass grafting. He recovers fairly well from the surgery but on post-op day 10 develops fever and purulent drainage from the inferior aspect of the wound.

He returns to the operating room for extensive debridement of sternal osteomyelitis. Cultures grow methicillin-resistant Staphylococcus aureus.

Patient 4

Surgical Site Infection (SSI) usually introduction of skin organisms into the

wound– S. aureus, Gram-negative bacilli

risk factors– underlying disease– skill of the operator– duration of operative procedure

may not become clinically apparent until after discharge

risk may be decreased by appropriately timed pre-operative antibiotics

MRSA 1960 methicillin-resistant S. aureus identified MRSA 60% of S. aureus isolates at GW are MRSA

(2007) Community-acquired: recent increase in incidence Hospital-acquired: > 48 h after admission Healthcare-associated community-onset:

– previous positive MRSA culture– history of hospitalization, surgery, dialysis or

residence in long term care facility in the last year– indwelling catheter/percutanous device

MRSA IsolatesPulse Field Gel Electrophoresis (PFGE)

MRSAMechanism of Resistance chromosomal mecA

gene *altered PBP 2´ or 2a

in cell wall low affinity for all ß-

lactam antibiotics

Hospital-acquired MRSA BSI 76% pneumonia 13% osteomyelitis 6% endocarditis 3% cellulitis 4% skin abscess/necrosis 1%

mortality 2.5%

www.cdc.gov/abcs

Hospital-acquired MRSA Risk factors:

– prolonged hospitalization

– prolonged antimicrobial therapy

– location in an intensive care unit

– proximity to a known MRSA case Persistent colonization up to 4 years: nares Contamination of environmental surfaces

– up to 30%: bed rails, table, BP cuff

SSI Prevention no shaving of operative site: clippers or no hair

removal hand hygiene; fastidious aseptic technique surgical site antisepsis with chlorhexidine prophylactic antibiotics

– single dose 30-60 minutes prior to incision– second dose for prolonged surgeries

laminar air flow or HEPA filtration; limit traffic in the operating room

pre-operative screening for S. aureus

Patient 5 A 26 yo medical student draws blood from

a patient for a classmate. He is in a hurry and sticks his thumb while recapping (?) the needle. The patient has been tested positive for HIV and hepatitis C. The student has received the hepatitis B immunization series.

HCW Blood/Body Fluid ExposureRisk Factors

needlestick/sharp>>mucosal>>non-intact skin inoculum: viral titer, volume of blood needle type

– hollow-bore needles > solid-bore– large bore > small bore

decreased risk with glove use

GWU Health Care WorkersPercutaneous Exposures: 2007-09

Occupation– Hospital staff 38-49%*

– Residents 39-56%*

– Students 6-11% Location

– ER 7-14%– ICU 7-21%*

– OR 31-52%*

– other floors 24-27%*

– Pathology 3-8%

Risk of Transmission following Percutaneous Exposure

HIV 0.3% Hepatitis C 1.9% HBeAg - < 6% HBeAg + 30% estimated US transmission for yr 2000*

– 390 cases of HCV– 40 cases of HBV– 5 cases of HIV

Henderson DK. Clin Microbiol Rev.2003;16:546* Prüss-Üstün A. Am J Ind Med 2005;48:482

HCW Blood/Body Fluid ExposureManagement

baseline serologies, including the patient if necessary

assessment of risk HIV: antiretroviral therapy hepatitis B: hepatitis B immune globulin

and hepatitis B vaccine if non-immune hepatitis C: close follow up

HCW Blood/Body Fluid ExposurePrevention

SLOW DOWN do not recap needles dispose of sharps in the proper receptacle use needleless systems whenever possible heptitis B immunization

Isolation to protect both patients and personnel Standard Precautions

– routinely consider all body fluids and moist surfaces as potentially infectious

airborne precautions droplet precautions contact precautions

IsolationAirborne Precautions transmission of pathogen via inhalation of

droplet nuclei

– tuberculosis, varicella, ? influenza private room negative pressure > 10 air exchanges per hour Staff: particulate respirators

IsolationDroplet Precautions

respiratory secretions via close personal contact

group A strep, influenza private room particulate respirator do not need negative pressure or increased

air exchanges

IsolationContact Precautions

transmitted via hands of personnel, inanimate surfaces

MRSA, VRE, highly resistant GN rods private room gloves with patient contact handwashing

Michael Jackson Approach

Handwashing

most important means to prevent spread of nosocomial pathogens

hand cultures of medical personnel

GN bacilli S. aureus

random sample 45% 11%

serial sample 100% 64%

persistent carrier 16% 16%

Puerpural SepsisIgnaz Semmelweis

Ignaz Semmelweis (1847) observed differences in the incidence of puerpural sepsis (group A strep) on 2 different wards

one ward was staffed by obstetricians, medical students: mortality 8%

one ward was staffed by midwives: mortality 2%

Puerpural SepsisIgnaz Semmelweis

Observation #1: lower mortality when students were on vacation

Observation #2: pathologist cut during autopsy developed similar illness

Solution: HAND HYGIENE in the autopsy room prevented transmission of organisms to the delivery suite

Ignaz SemmelweisDecreased Mortality with Improved Hand Hygiene

Ignaz Semmelweis(1818-65)

Chlorinated lime hand antisepsis