INTENSIVE CARE

Nosocomial infections in the

intensive care unit

Learning objectives
After reading this article, you should be able to:
C
list the common pathogens that cause infections in the ICU
C
discuss strategies used to prevent antimicrobial resistance in
the ICU
C
name the steps in the WHO 5 moments of hand hygiene
campaign
C
discuss the risk factors for VAP, CLASBI and UTI in the ICU
C
list the components of the care bundles for VAP and CLASBI

Jason A Trubiano
Alexander A Padiglione

Abstract
Nosocomial infection in the intensive care unit (ICU) is associated with
increased mortality, morbidity and length of stay. It is defined as infection
that begins 48 hours after admission to hospital. The most common types
are ventilator-associated pneumonia (VAP), central line-associated bloodstream infection (CLABSI), urinary catheter-related infection and surgical
site infection. The common pathogens include Staphylococcus aureus,
Pseudomonas aeruginosa, Candida spp., Escherichia coli and Klebsiella
spp. Antimicrobial resistance is generally increasing, and has emerged
from selective pressure from antibiotic use and transmission via health
workers. Prevention of infection can be achieved through good antimicrobial use and infection control, including hand hygiene. Grouped, easy to
follow best practice activities called care bundles have been developed
to prevent VAP and CLABSI. Microbiological cultures are central to a rapid
and accurate diagnosis, which improves outcomes and reduces resistance. The principles of treatment include early antimicrobial therapy
(after appropriate specimens are taken) targeted to the local microbes,
then de-escalation according to culture and susceptibility results. This
article summarizes the pathogenesis, risk factors, microbiology, diagnosis, prevention and treatment of VAP, CLASI and nosocomial UTI in
the adult ICU.

related infection and surgical site infection. Other types of

nosocomial infection are also important, such as those in
immunocompromised hosts and neonates, but beyond the scope
of this article.

Microbiology and resistance

Colonization of critically ill patients with nosocomial organisms
usually occurs after 48e72 hours of admission; the most
important pathogens are displayed in Table 1. The spectrum of
nosocomial microorganisms is different from those in the community, with higher rates of resistant organisms. Antimicrobial
resistance emerges in ICU because of:
 evolution of resistance in existing bacteria, through selective pressure from antibiotic use
 nosocomial transmission especially through contact with
healthcare workers or via procedures.
Increasing incidence of resistant bacteria in ICUs is associated
with poorer outcomes. These include: methicillin-resistant
Staphylococcus aureus (MRSA), vancomycin-resistant Enterococci (VRE) and multi-drug resistant (MDR) Gram negatives.
There is a longer time to receipt of effective therapy; and the
agents used for treatment often have inferior efficacy, poor
pharmacokinetics/pharmacodynamics or increased toxicity (e.g.
vancomycin, linezolid, daptomycin, amikacin, colistin). More
recently, studies describe success in controlling some types of
resistant organisms (most notably reductions in MRSA, particularly attributed to better hand hygiene practices), but little impact
on MDR Gram negative and fungal resistance. Inappropriate
broad-spectrum antibiotic therapy increases the incidence of
MDR organisms, and is also an independent risk factor for
mortality.1
The emergence of resistant organisms tends to add to the total
burden of infections, rather than substituting for the more sensitive organisms previously present. For example, as MRSA becomes endemic in a unit, the total number of staphylococcal
infections increases; when MRSA is eliminated, the total number
of staphylococcal infections reduces.

Keywords Catheter related infections; cross infection; intensive care;

nosocomial infections; urinary tract infections; ventilator-associated
pneumonia
Royal College of Anaesthetists CPD Matrix: 2C00, 2C03

Introduction
Nosocomial infection (defined as onset more than 48 hours after
hospital admission) in the intensive care unit (ICU) is associated
with increased mortality, morbidity and length of stay. Prevalence rates of infection acquired in ICUs vary from 9% to 37%
when assessed in Europe and the USA. Timely diagnosis,
appropriate management and prevention improve patient outcomes and reduce antimicrobial resistance. The most common
types are ventilator-associated pneumonia (VAP), central lineassociated bloodstream infection (CLABSI), urinary catheter-

Jason A Trubiano BBiomedSci MBBS(Hons) FRACP is an Infectious Diseases

Physician at The Alfred Hospital, Austin Health and Peter MacCallum
Cancer Centre, Melbourne, Australia. Conflicts of interest: none
declared.

Diagnosis of nosocomial infection

Rapid and accurate diagnosis of nosocomial infection both improves patient outcomes and decreases selection pressure for
resistance. It streamlines patients into the most effective treatment, allowing rapid cessation of unnecessary antibiotics and
minimizing unnecessary side effects. Correct timing is vital with

Alexander A Padiglione MBBS(Hons) FRACP PhD is an Infectious Diseases

Physician at The Alfred Hospital and Monash Medical Centre,
Melbourne, Australia. Conflicts of interest: none declared.

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INTENSIVE CARE

stewardship services can reduce broad-spectrum antibiotic usage,

adverse antimicrobial events and MDR bacteria resistance rates,
whilst improving antibiotic treatment in life-threatening bacterial
infections, improve antibiotic dosing and shorten antibiotic durations without effecting patient outcome.2 Elements of good
antibiotic use in ICU are given in Box 2. The role of combination
antibiotics in preventing resistance is controversial. It is usually
necessary to use combination empiric therapy for sepsis to ensure
adequate coverage of potential pathogens, but de-escalating to
narrower cover once cultures results are known or the patient
improves. Even pseudomonal infections do not require combination therapy once sensitivities are known, though some multidrug resistant organisms may have few alternatives to combination therapy. Cycling antibiotic use is poorly studied, and not
recommended.
Infection control minimizes cross transmission and prevents
colonizing bacteria from causing infection. One of the key elements is hand hygiene, which prevents cross transmission of
pathogens between patients by the hands of healthcare workers.
It is estimated that over 30% of healthcare associated infections
are preventable by hand hygiene. Multiple studies have shown a
reduction in healthcare-associated infection rates, specifically
reductions in MRSA and even elimination in some centres. The
WHO has recommended 5 moments for hand hygiene in
healthcare settings, both resource rich and poor.3 Alcohol-based
hand-rubs should be used before touching a patient, before a
procedure, after body fluid exposure, after touching a patient and
after touching patient surroundings. Other aspects of infection
control include surveillance for, and isolation of, patients with
multi-resistant organisms. Alternative infection control measures
such as chlorhexidine bathing and washcloths have in some
cohorts demonstrated reductions in MDR bacteria colonization/
infection and overall bacteraemia rates.4,5
Recent years have seen the widespread promotion of infection
control care bundles. These are groupings of best practices that
when applied together appear to result in greater improvement in
outcomes, based on the philosophy that the total may be greater
than the sum of the parts. They are simple, logical (mostly, but
evidence base can be variable) and easily evaluable (compliance

Common ICU nosocomial pathogens (EPIC II study)

Staphylococcus aureus
20%
Includes MRSAa (10%)
Pseudomonas aeruginosa
20%
Candida
17%
Escherichia coli
16%
Klebsiella species
13%
Enterococcus
11%
Includes VREb (4%)
Staphylococcus epidermidis
10%
Acinetobacter
9%
Enterobacter
7%
Important Gram negative resistance mechanisms include:
Extended-spectrum beta-lactamases (ESBLs): plasmid encoded
genes that confer resistance to penicillins and extended-spectrum
cephalosporins. Carbapenems are the treatment of choice.
AmpC-type beta-lactamases: Chromosomal or plasmid genes that
are similar to ESBLs.
Metallo-beta-lactamases (MBLs): Confer resistance to carbapenems,
inherent chromosomal (e.g Stenotrophomonas maltophilia) versus
plasmid acquired (e.g. New Delhi metallo-beta-lactamases (NDM)).
May be susceptible to colistin, tigecycline or fosfomycin.
Combination therapy including a carbapenems (even if resistant)
improves outcomes.
a
b

Methicillin-resistant Staphylococcus aureus.

Vancomycin-resistant Enterococcus faecium.

Table 1

all microbiologic tests: samples taken after new antibiotics are

started rapidly lose sensitivity.
The single most useful microbiologic test in ICU is correctly
performed blood cultures. A simple protocol is shown in Box 1.

General prevention measures

Nosocomial infections are reduced by good antibiotic use and
strict infection control. Ongoing liaison between ICU, infectious
diseases (or clinical microbiology) and pharmacy personnel is
essential. This multidisciplinary approach is needed to develop
local guidelines (preferably guided by local microbiology data),
provide day-to-day advice, monitor usage and oversee control
measures for broad-spectrum antimicrobials, and provide feedback to the ICU staff in a useful manner. Antimicrobial

Good antibiotic use in ICU to reduce selection pressure

for resistance
C

Effective diagnosis of nosocomial infection: taking blood

cultures

C
C
C

C
C

Take three sets before starting or changing antibiotics

Fresh venepuncture, sterile technique (or from a new line inserted
in an aseptic manner)
Swab skin (70% alcohol with chlorhexidine), allow 30 seconds
before venepuncture
10 ml per blood culture bottle
No further BCs need be taken for 2e3 days unless clinical situation changes, or to demonstrate clearance of proven bacteraemia

Box 1

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Knowledge of local microbiological epidemiology to guide empiric

therapy
Prompt appropriate therapy for sepsis, including antifungals in
higher risk patients
Early source control, including changing of lines in a septic
patient
De-escalating broad-spectrum antibiotics early according to cultures and patient condition
Using shorter duration of antibiotics overall, e.g. 5e7 days is
adequate for most cases of VAP
Appropriate dosing will both maximize cure rates and minimize
selection of resistance. Unfortunately both under and over-dosing
are common in the ICU setting

Box 2

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INTENSIVE CARE

with each element in the bundle can be measured as a simple

yes/no). Not all possible proven therapies are included in the
bundle, as factors such as ease of implementation, adherence and
cost are considered. Examples of care bundles are given in Box 3.

consciousness and aspiration. The key modifiable factors

increasing risk of VAP are anti-acid therapy, previous antibiotic
exposure (particularly 3rd generation cephalosporins), use of
paralytic agents, re-intubation or prolonged intubation, frequent/
routine ventilator circuit changes, presence of a nasogastric tube
or intracranial pressure monitor.

Specific conditions
Ventilator-associated pneumonia
Hospital-acquired pneumonia (i.e. pneumonia that begins 48
hours or more after admission) is a leading cause of hospital
acquired infection leading to mortality.6 Ventilator-associated
pneumonia (VAP) is a subset of HAP, occurring 48 hours or
more after endotracheal intubation. Clinically diagnosed VAP has
a prevalence of 13e16%, though rates using stricter surveillance
definitions are much lower. Whilst crude mortality rates of 20
e30% are typically reported,7 most of these patients die not
because of their VAP but because of the underlying severity of
illness. The attributable mortality of treated VAP is commonly
said to be 10%, but may in fact be as low as 1% at day 30 if
careful adjustment for other patient factors in the course of their
ICU stay are taken into account.8 Some authors also describe
ventilator-associated tracheobronchitis (VAT) as a precursor
condition, differentiated from VAP by the absence of chest X-ray
infiltrates. It is unclear if VAT requires treatment; with studies
showing it increases duration of ventilation, length of ICU stay,
but not mortality rate.
The pathogenesis is thought to involve microaspiration of
oropharyngeal microorganisms, which enter into the lower respiratory tract via leakage around the endotracheal tube cuff or
directly through the tube. Aspiration of gastrointestinal microorganisms contributes to a lesser extent. Microbial virulence factors
and host defence factors then determine if pneumonia occurs.

Microbiology: a wide spectrum of organisms causes VAP,

including aerobic Gram negatives (Escherichia coli, Klebsiella,
Enterobacter etc), Gram positive cocci (Streptococci, Enterococci
etc), and oropharyngeal flora; some of these may be multiresistant. However the local epidemiology is important.
Diagnosis: the optimal diagnostic algorithm for VAP remains
unclear. Clinical plus radiological features only have moderate
sensitivity (69%) and specificity (75%). Positive microbiological
sampling alone cannot differentiate between colonization, VAT
or VAP; however negative cultures from good quality specimens
(before receipt of antibiotics) reasonably excludes VAP. Microbiology results need to be interpreted, especially in poorer quality
samples: isolation in sputum of Pseudomonas is usually significant, Staphylococci may not always be, Acinetobacter and Stenotrophomonas are most commonly just colonizers, and Candida
pneumonia probably does not exist. A combination of clinical,
microbiological and radiological criteria is required. Clinical risk
rules have shown promise in trials but have proved cumbersome
to implement in clinical practice. Biomarkers such as procalcitonin seem to be of most value in less sick patients, and only
some studies show benefit.
More reliable microbiology results translate into improved
outcomes in a number of studies, with less antibiotic use, less
development of resistance, better patient outcomes and increased
clinician confidence. Quantitative culture of good quality bronchoscopy specimens yields the most reliable microbiologic result,
but has variable application within units due to concerns around
cost, logistics and side effects. Invasive specimens may be risky
to obtain, whilst quantitative cultures did not reduce mortality,
time in ICU, time on mechanical ventilation or antibiotic usage.9
The most important factor is that a good quality specimen should
be collected before starting or changing antibiotics. Rapid pathogen detection technologies (for example nucleic acid amplification combined with mass spectrometry) are in late stage
development but clinical correlation and impact on management
will take longer to determine.

Risk factors: mechanical ventilation increases the risk of pneumonia 6e20 times. The most significant risk factors for VAP
include age >70 years, chronic lung disease, depressed

Care bundles in the ICU

VAP care bundle
C
C

C
C

Elevate the head of the bed 30e45 degrees

Daily sedative interruption and assessment of readiness to
extubate
Peptic ulcer disease prophylaxisa
Venous thromboembolism prophylaxisa

Management: the principles of treating VAP include early antimicrobial therapy (after appropriate specimens are taken) guided
by the local microbiology, then de-escalation according to culture
and sensitivity results. In many units this will result in empiric
combination therapy to cover multi-resistant organisms (MROs).
Aerosolized agents are not proven for routine use; this may
change with trials underway of newer technologies better able to
deliver the right droplet size to the site of infection. Streamlining treatment to the most effective narrow-spectrum agent
should occur once an organism is isolated, with a total duration
of 5e7 days of effective therapy adequate for most pathogens,
though most physicians would treat for 10e14 days for Pseudomonas spp., MDR Gram negatives or S. aureus pneumonia.

CLABSI care bundle

C
C
C
C
C
C

Hand hygiene
Avoid femoral insertion site in adults
Maximum barrier precautions
Alcoholic chlorhexadine skin antisepsis
Optimal catheter site selection
Daily review of line necessity & prompt removal

Not supported by good evidence, but commonly included in bundle.

Box 3

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Prevention: strategies to prevent VAP include reducing need for

ventilation, reducing colonization and reducing aspiration.
Sedation should be avoided or minimized, and interrupted daily
if possible, together with daily assessment of readiness to extubate. Non-invasive ventilation is preferred where possible. Early
mobilization is encouraged.
Methods to reduce aspiration include the use of semirecumbent patient positioning, subglottic drainage techniques
and ventilator circuits should not be routinely changed. Although
they may lower VAP rates, there is little evidence for improved
patient outcomes from acid-suppressants, early tracheostomy,
early TPN, prone positioning or antiseptic impregnated ETTs.10
Selective digestive decontamination (SDD) involves the
application of topical antimicrobials to the oropharynx and/or
oral antibiotics to the digestive system via nasogastric tube, with
or without systemic antibiotics. SDD has been shown in three
meta-analyses to reduce the rates of VAP, bacteraemia, MDR
bacteria colonization (e.g. MRSA, VRE) and mortality in certain
subgroups, though the most significant effect is seen in the
groups receiving systemic therapy. It is not accepted widely into
practice, due in part to concerns of selection of antimicrobial
resistance (e.g. colistin and aminoglycoside resistance increased
following one SDD program).11 It is probably most effective
where VAP rates are high but background resistance rates low.
Topical chlorhexidine along with good oral hygiene, such as
tooth brushing, may be a more acceptable way to stop microaspiration of oral flora into the respiratory tree, however further
studies are required.

as well as therapeutic. Culture of a catheter tip is only useful if

the catheter is thought to be infected. There is little evidence for
drawing cultures from every lumen of a central line.
Newer diagnostic methods such as direct nucleic acid amplification on blood, or markers of fungal infection such as 1e3
beta-D-glucan, show promise for earlier detection of bloodstream
infection, but low specificity, false positivity and cost currently
limit their widespread implementation.
Management: if CLABSI is suspected, the catheter should be
removed, cultures taken (peripheral, tip of CVC) and antimicrobial therapy initiated, most commonly a broad-spectrum betalactam antibiotic though extra gram negative (e.g. aminoglycoside) and/or Gram positive (e.g. glycopeptide) may be added
depending on the local microbiology. In patients at higher risk of
candidaemia (multi site colonization, immunosuppression, recent
abdominal surgery, recent receipt of broad-spectrum antibiotics,
TPN) empiric fluconazole is also appropriate whilst awaiting
culture results. Unfortunately most patients have at least some of
these risk factors and clinical prediction tools for candidaemia are
too imprecise for widespread implementation. Empiric use of an
echinocandin (e.g. micafungin, caspofungin, anidulafungin) over
fluconazole is preferred in patients with septic shock, prior azole
exposure or underlying immunosuppression.
Empirical therapy for S. aureus bacteraemia usually requires
the addition of a glycopeptide to an anti-staphylococcal beta-lactam (flucloxacillin, cephazolin, cephalothin) until the isolate is
confirmed as methicillin sensitive. Newer agents such as linezolid,
ceftaroline or daptomycin have no clear benefits over existing
agents. Staphylococcus aureus CLABSI requires a minimum of 14
days of intravenous therapy. Echocardiography is indicated in all
S. aureus bacteraemia, as endocarditis (or metastatic infection
such as endophthalmitis, osteomyelitis, septic thrombosis) or
tunnelled line infection requires prolonged therapy (4e6 weeks).
Coagulase-negative Staphylococcus can be treated for 3e5 days,
Gram negatives for 10e14 days, and Candida for 14 days, if
metastatic foci are not identified. Ophthalmology review in candidaemia is mandatory to exclude endophthalmitis.

Central line-associated bloodstream infection

Intravascular catheter-related infections are a major cause of
morbidity and mortality in the ICU. A meta-analysis showed a
case fatality rate of 19% of catheter related bloodstream infections.12 We will focus on central line associated bloodstream
infection (CLABSI).
Risk factors: host predisposing factors include immunosuppression, burns, malnutrition, use of TPN and extremes of age; however these are not modifiable. The risk of infection increases after
day 3. In adults higher rates of infection are seen with femoral
vein insertion sites, then jugular, and lowest with subclavian.

Prevention: simple practices to modify risk factors can eliminate

most CLABSI. Local protocols should reinforce: hand hygiene
practice and auditing, strict aseptic technique by an appropriately
qualified person, full barrier precautions, avoidance of femoral
placement, and use of 2% chlorhexidine for skin disinfection.
Vigilant catheter care is essential: all lines should be assessed
daily for infection, and unnecessary catheters removed. If
inserted under emergency conditions they should be removed/
replaced within 48 hours. Guide-wire exchange techniques result
in higher rates of associated bacteraemia and should be avoided.
Multi-modal strategies combining these strategies can virtually
eliminate CLABSI in large tertiary referral ICUs. Antibiotic
impregnated CVCs (e.g. minocycline/rifampicin) may be of
benefit in units with high rates of CLABSI, or selected patients at
high risk, whilst antiseptic coated CVCs appear less effective, but
have fewer concerns around selection pressure for resistance.

Microbiology: the pathogenesis of infection involves skin flora

colonizing the device. Infections in the first week after placement
are typically due to poor insertion technique, with skin organisms
travelling along the external surface of the catheter; infections
occurring later than 1 week after insertion are more typically
caused by intraluminal spread following contamination during
handling of the catheter. The pathogens involved are Staphylococci (coagulase-negative and aureus; 50%), Gram negative bacilli
(30%), Enterococci (10%) and Candida species (10%). Staphylococcus aureus has a significantly higher attributable mortality rate
than the other pathogens. Host factors play a role: for example,
gram negatives predominate in burns patients.
Diagnosis: this involves establishing bloodstream infection and
showing that the source is the catheter. Rapid removal or
replacement of all existing lines is necessary in undifferentiated
sepsis, and rapid response to removal of lines may be diagnostic

ANAESTHESIA AND INTENSIVE CARE MEDICINE 16:12

Nosocomial urinary tract infections

Catheter-associated urinary tract infection (CA-UTI) refers to
infection occurring in a person whose urinary tract is currently

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REFERENCES
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2 Kaki R, Elligsen M, Walker S, Simor A, Palmay L, Daneman N. Impact
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3 Pittet D, Allegranzi B, Boyce J, for the World Health Organization,
World Alliance for Patient Safety First Global Patient Safety Challenge
Core Group of Experts. The World Health Organization guidelines on
hand hygiene in health care and their consensus recommendations.
Infect Control Hosp Epidemiol 2009; 30: 611e22.
4 Septimus EJ, Hayden MK, Kleinman K, et al. Does chlorhexidine
bathing in adult intensive care units reduce blood culture contamination? A pragmatic cluster-randomized trial. Infect Control Hosp
Epidemiol 2014; 35(suppl 3): S17e22.
5 Climo MW, Yokoe DS, Warren DK, et al. Effect of daily chlorhexidine
bathing on hospital-acquired infection. N Engl J Med 2013; 368: 533e42.
6 American Thoracic Society, Infectious Diseases Society of America.
Guidelines for the management of adults with hospital-acquired,
ventilator-associated, and healthcare-associated pneumonia. Am J
Respir Crit Care Med 2005; 171: 388e416.
7 Craven DE, Hjalmarson KI. Ventilator-associated tracheobronchitis
and pneumonia: thinking outside the box. Clin Infect Dis 2010;
51(suppl 1): S59e66.
8 Bekaert M, Timsit JF, Vansteelandt S, et al. Attributable mortality of
ventilator-associated pneumonia: a reappraisal using causal analysis.
Am J Respir Crit Care Med 2011; 184: 1133e9.
9 Berton DC, Kalil AC, Teixeira PJ. Quantitative versus qualitative cultures of respiratory secretions for clinical outcomes in patients with
ventilator-associated pneumonia. Cochrane Database Syst Rev 2014.
Issue 10. Art. No.:CD006482.
10 Klompas M, Branson R, Eichenwald EC, et al. Strategies to prevent
ventilator-associated pneumonia in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol 2014; 35: 915e36.
11 Halaby T, Al Naiemi N, Kluytmans J, van der Palen J, VandenbrouckeGrauls CM. Emergence of colistin resistance in Enterobacteriaceae after
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catheterized (or catheterized within the previous 48 hours).

Catheter-associated asymptomatic bacteruria (CA-ASB) may also
occur in a patient without symptoms or signs attributable to the
urinary tract. Rates of CA-UTI and CA-ASB have declined
significantly in hospitals with active prevention programs.
Pathogens usually ascend from the urethral meatus on the
external surface of the tube. However, one-third ascend intraluminally (e.g. from a contaminated bag).
Microbiology: CA-UTI in the ICU may be caused by Staphylococci
and Pseudomonas, in addition to the usual community acquired
pathogens (Gram negatives, Enterococci). The presence of
Candida species is a common finding which normally represents
colonization in patients who have received broad-spectrum antibiotics, even in immunocompromised hosts. Rarely, it reflects
the presence of candidaemia (1.3% in one study).
Risk factors include prolonged catheterization and bacterial
colonization of the drainage bag.
Diagnosis: it can be difficult to distinguish true pathogens from
colonizing organisms, but presence of neutrophils, absence of
squamous epithelial cells and presence of organisms on Gram
stain all support true infection. Urine cultures should be obtained prior to antibiotic administration and not from the
drainage bag. A catheter change prior to sampling avoids
culturing colonizers.
Management: it is essential that a urine culture must be obtained prior to the initiation of treatment. Treatment duration
for patients who respond promptly to antibiotics is 7 days and
10e14 days for a delayed response or infection occurring in a
male. Asymptomatic candiduria usually resolves with catheter
change.
Prevention: the principles of prevention are avoiding catheterization where possible, aseptic technique and catheter
care, early removal and considering intermittent catheterization. Antibiotic-impregnated catheters are proven to be effective
and likely to be cost effective. It is unclear if they select for
resistant organisms. There is no evidence to support the use of
prophylactic antibiotics during catheter insertion and
removal.
A

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