Click Here to Go Home
 
 
Current Issue

About
Critical Care Nurse

Career Guide

Join AACN

Free Product
Information





CC Nurse Journal Logo
FEBRUARY 1998 - VOLUME 18 - NUMBER 1
Protecting ICU Patients From Nosocomial Infections: Practical
Measures for Favorable Outcomes

Frederick J Tasota, Elaine M Fisher, Carolyn F Coulson, and Leslie A Hoffman

Appears in the printed version of the journal, "Critical Care Nurse" volume 18, number 1, p54-67.

About the Authors
Frederick J Tasota, RN, MSN is a pulmonary clinical specialist at the University of Pittsburgh School of Nursing, Pittsburgh, Pa.

Elaine M Fisher, RN, MSN is a doctoral student at the University of Pittsburgh School of Nursing and is employed as a critical care nursing instructor at the University of Akron, Akron, Ohio.

Carolyn F Coulson, RN, BSN is a student in the acute care nurse practitioner program, cardiopulmonary subspecialty, at the University of Pittsburgh School of Nursing and is employed as a cardiac catheter laboratory nurse at Mercy Hospital, Pittsburgh, Pa.

Leslie A Hoffman, RN, PhD is professor and chair of the department of acute-tertiary care nursing at the University of Pittsburgh School of Nursing.

Reprint requests: InnoVision Communications, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (714) 362-2050 (ext 532); fax, (714) 362-2022; e-mail, ivcReprint@aol.com.


Nosocomial infections continue to complicate the clinical course of critically ill patients and, consequently, to create substantial economic and human costs. In 1985, the Centers for Disease Control reported that 5.7% of all hospitalized patients acquired nosocomial infections, which were defined as infections not present or incubating before hospital admission. At that time, annual spending for the treatment of nosocomial infections was approximately $1 billion.1

Six years later, although the prevalence of nosocomial infections remained stable (about 6% of hospitalized patients), the estimated costs of treatment had escalated to between $5 billion and $10 billion.2 More than 80,000 deaths each year have been directly linked to the development of nosocomial infections.3 Subsequent reports are expected to report similar trends.

Although nurses are aware of infection control measures, inconsistent application of these measures continues to occur.4-6 Inadequate infection control is of particular concern because one third of nosocomial infections are preventable.1 In this article, we present up-to-date information on the risk of acquiring nosocomial infections, highlight the most common sites of these infections, and discuss strategies for preventing and controlling nosocomial infections in the ICU. The goals are to improve awareness and understanding of risks for infection and encourage consistent application of infection control measures by all ICU nurses to promote more favorable outcomes for patients.

PREVALENCE OF NOSOCOMIAL INFECTIONS
The prevalence of nosocomial infections in hospitalized patients is approximately 6%,1 and a disproportionate 20% of these occur in critically ill patients,6 even though ICUs account for only 5% of all hospital beds.7 The prevalence of nosocomial infections is 5 to 10 times greater in ICU patients than in patients on general units, and use of mechanical ventilation, urinary catheters, and intravascular devices (all routine in the ICU) are major factors contributing to this disparity.8

Kennedy9 describes the ICU as an "epidemiological jungle" because of the abundance of organisms that proliferate in these units. The predominant organisms responsible for nosocomial infections include Pseudomonas aeruginosa (13%), Staphylococcus aureus (12%), coagulase-negative staphylococci (10%), Candida (10%), enterococci (9%), and enterobacter (8%).10

CONTRIBUTING FACTORS
Factors common to ICU patients that contribute to the risk of nosocomial infections include acuity of illness, response to physiological and psychological stressors, age and associated comorbidity, indiscriminate use of antibiotics promoting the development of antibiotic-resistant organisms, drug therapies for stress ulcer, sleep deprivation, protein-energy malnutrition, and understaffing. With the exception of understaffing, each of these factors increases patients' risks of nosocomial infections by altering the patients' immune response or changing the response to infection.

Acuity of Illness
During acute illness, energy is diverted from normal body functions to meet increased metabolic needs. As the severity of an illness increases, energy stores needed to sustain normal body processes such as immune function become depleted, reducing the ability of the patient to resist colonization by exogenous organisms (originating outside the body). Critically ill patients are also more susceptible to overgrowth of resistant endogenous microbes (originating inside the body) such as staphylococci on skin and mucosal surfaces and enterococci in the gastrointestinal tract.11

Physiological and Psychological Stressors
Physiological stressors resulting from injury and illness and psychological stressors such as noise, pain, anxiety, and isolation are a few of the many stressors encountered daily by ICU patients. The stress response is the same whether the stressor is physical or psychological. The initial "fight or flight" response to a stressor includes neuroendocrine suppression of the function of lymphoid tissue. The goal at this stage is to redirect energy for use in the fight-or-flight response.12

Adrenocorticotropic hormone is released by the pituitary gland and stimulates the adrenal cortex to secrete cortisol. Cortisol, the primary hormone responsible for depressed immune function, suppresses synthesis of antibodies; reduces the number of lymphocytes and macrophages; and promotes stabilization of lysosomal membranes, inhibiting the release of hydrolases needed to destroy organisms.13 These changes culminate in the decreased ability of leukocytes to attack microorganisms.

During the second stage of the stress response, the resistance phase, energy continues to be diverted to sustain the response until the host can reverse the process or until exhaustion of resources occurs and death ensues. The stage of exhaustion is often marked by overwhelming infections resulting in vascular collapse from a shock state.13

The stress response can also produce local changes that alter natural barriers to infection. For example, stress enhances secretion of salivary proteases, which decay fibronectin, a substance responsible for coating oral mucosal cells. The breakdown of fibronectin promotes adherence of gram-negative organisms to and colonization of structures in the upper part of the airway.14

Age and Comorbidity
Approximately 48% of all patients admitted to the ICU are more than 65 years old.15 Elderly patients are less resistant to infection than their younger counterparts are.16 Calianno17 reported that mortality from bacterial nosocomial pneumonia is five times more likely in patients more than 65 years old. One possible explanation for this increased susceptibility is the progressive atrophy of the thymus that occurs with age; the atrophy causes a decrease in cell-mediated immunity, as shown by depressed production of T lymphocytes.18

Also, natural defenses in the elderly are compromised. Respiratory ciliary action, respiratory excursion, and the cough reflex decrease, placing older patients at risk for nosocomial respiratory infections.19

The higher prevalence of chronic illnesses among the elderly also contributes to the risk for nosocomial infections.16 The types of infections that may develop are linked to the specific alterations in the host defense produced by the chronic illness (eg, chronic lung disease, chronic renal failure, diabetes).20 For example, elderly patients with chronic lung disease have a higher prevalence of bacterial nosocomial pneumonia caused by Streptococcus pneumoniae, Haemophilus influenzae, and Branhamella catarrhalis than do younger patients.21

Indiscriminate Use of Antibiotics and the Development of Resistant Organisms
Current practices for prescribing antibiotics are influenced by clinicians' preferences, marketing pressure from pharmaceutical companies, minimal adverse or toxic side effects with newer and more potent antibiotics, lack of precise methods for early identification of causative organisms, and concern over malpractice related to the potentially serious consequences of overwhelming infection in critically ill patients.22

Broad-spectrum antibiotics are often prescribed for critically ill patients when signs and symptoms consistent with infection are present, white blood cell counts are elevated, or invasive procedures are required. Broad-spectrum antibiotics are often given when narrow-spectrum or organism-specific agents would be sufficient to resolve the infection.
Indiscriminate use of antibiotics leads to the elimination of a greater number of normal flora, thus enabling modified and more virulent organisms to produce infection.22

These modified organisms have new characteristics against which standard agents are no longer effective. Traditionally, enterococcal infections were treatable with vancomycin. However, the development of multidrug-resistant enterococci that are resistant to vancomycin has resulted in bacteria that are now poorly controlled, despite the use of multiple, more potent antibiotics. The National Nosocomial Infection Surveillance System reported that the percentage of nosocomial infections caused by vancomycin-resistant enterococci increased from 0.4% to 13.6% between 1989 and 1993.23

Ultimately, patients infected with antibiotic-resistant pathogens have protracted hospitalizations, increased healthcare costs, and higher mortality rates.22 Additionally, lapses in infection control with these patients increase the transmission of resistant organisms from one patient to another.11 Thus, the discriminate use of organism-specific antibiotics is crucial to limiting the development of antibiotic-resistant organisms.

Prophylaxis for Stress Ulcers
Routine administration of antacids and histamine antagonists for prevention of stress ulcers in critically ill patients may increase the risk of infection.24 The increase in gastric pH produced by these agents may attenuate the bactericidal effect of an acidic pH, thus promoting gastric colonization not only by gram-negative and gram-positive bacteria but also by yeasts. Retrograde esophageal colonization by these organisms then increases the risk of aspiration of microbes and subsequent nosocomial pneumonia.24

In a meta-analysis,25 sucralfate was found to be associated with both a lower prevalence of pneumonia and a lower mortality rate than were other antacids and H2-receptor antagonists. Sucralfate has been recommended because it does not alter gastric pH but works by forming a mechanical barrier at the site of ulceration.26 Therefore, not only the primary effect of preventing stress ulcers but also the secondary effect of limiting bacterial growth, by maintaining a lower gastric pH, should be considered when prescribing prophylaxis for stress ulcers.

Sleep Deprivation
Krueger and Madge27 reported alterations in sleep patterns during infectious diseases. Lack of the usual quantity and quality of sleep, including loss of normal progression through sleep cycles, adds to the stress critically ill patients experience and may alter immune function.28

Interleukin-1, a protein known for its ability to amplify the immune response, has recently been linked with sleep regulation. During sleep deprivation, secretion of interleukin-1 is reduced, thus potentially limiting the cellular immune response.29,30 The reduction in other factors associated with immune function (eg, interleukin-2, natural killer cells, and lymphokine-activated cells) known to occur during sleep deprivation may similarly contribute to the decline in resistance to infection.31 However, further research is needed to describe the effects of sleep deprivation on immune function.

Malnutrition
Critically ill patients often experience hypermetabolic states as a consequence of physiological and psychological stressors, and these states lead to various degrees of malnutrition.32,33 Catabolism of protein, carbohydrate, and fat stores and changes in the use of micronutrients (vitamins and minerals) deplete energy sources and may compromise host defensive mechanisms by reducing the production of immune cells.34,35

Protein malnutrition has been linked with a breakdown of the intestinal mucosal lining that allows bacteria to move through the disrupted barrier into the lymph and bloodstream to produce infection.35 A second mechanism for bacterial movement from the bowel, bacterial translocation, the process of bacterial movement through an intact mucosal barrier, has also been linked to protein malnutrition.36

Understaffing
Recent data from an investigation by the Centers for Disease Control and Prevention indi-
cate that understaffing may be a risk factor for nosocomial infections.37,38 When the patient-
to-nurse ratio increases, the provision of routine nursing measures such as turning the patient, suctioning, and complying with aseptic technique may decline.

To determine risk factors associated with an increase in bloodstream infections associated with use of central venous catheters during a protracted outbreak of the infections, Fridkin et al38 analyzed multiple variables, including use of total parenteral nutrition, days of mechanical ventilation, and severity of illness. During the outbreak, patients' characteristics were unchanged, but patient-to-nurse ratios increased significantly.

When data were analyzed by using a logistic regression model, the occurrence of catheter-associated bloodstream infections was associated with a higher patient-to-nurse ratio. The investigators concluded that reductions in the number of nursing staff to less than a critical number during the outbreak may have contributed to the increase in the infections, because time constraints made adequate catheter care less likely.38

SITES OF INFECTION
The three major sites for nosocomial infections in the ICU are the respiratory system (31%), the urinary tract (24%), and the bloodstream (16%). Common diagnoses for infections at these sites are pneumonia, urinary tract infection, and septicemia.39

Respiratory System
The prevalence of hospital-acquired pneumonia, defined as a nosocomial pneumonia that occurs more than 48 hours after hospital admission but is not incubating at the time of admission, is not known, because this type of pneumonia is not a reportable illness.40 Current estimates suggest a prevalence of 5 to 10 cases per 1000 admissions, with a 6- to 20-fold increase for patients receiving mechanical ventilation.40 Hospital-acquired pneumonia is the second most common nosocomial infection but has the highest mortality (approximately 30%) and morbidity and prolongs the mean duration of hospitalization by an average of 7 to 9 days per patient.14,39,40,41 Endogenous and exogenous factors place critically ill patients at risk for nosocomial pneumonia (Table 1).

Table 1. Risk factors for nosocomial pneumonia
Endogenous
    • Age greater than 70 years
    • Alcoholism
    • Cardiopulmonary disease
    • Depressed level of consciousness
    • Diabetes
    • Malnutrition
    • Severe underlying disease
Exogenous
    • Abdominal or thoracic surgery
    • Conditions favoring aspiration
          Endotrachel intubation
          Nasogastric intubation
          Supine positioning
    • Immobility
    • Prolonged mechanical ventilation
    • Use of antibiotics
    • Use of H2 blockers or antacids
    • Use of immunosuppressive agents
xxx
Tracheal intubation is the most significant risk factor for the development of hospital-acquired pneumonia.39,42 An endotracheal tube compromises the natural barrier between the oropharynx and the trachea and impairs natural defenses such as coughing and mucociliary action. If healthcare personnel or respiratory equipment harbor pathogenic flora, these organisms can be directly inoculated into the tracheobronchial tree.40

The endotracheal tube can also become coated with a bacterial biofilm that may embolize into the airway.43 Instillation of normal saline, a common practice during suctioning, may also facilitate direct entry of bacteria into the respiratory tract. In an in vitro study, Hagler and Traver44 found that passing a suction catheter through an endotracheal tube dislodged up to 60,000 viable colonies of bacteria. When 5 mL of normal saline was instilled, as many as 310,000 colonies of bacteria were dislodged. In addition, as previously described, flora from the lower part of the intestine may colonize the stomach, be aspirated into the trachea, and contribute to the development of nosocomial infections.40,45

In addition, contaminated subglottic secretions, pooled above an inflated endotracheal cuff, may leak into the lower part of the respiratory tract. Two studies46,47 suggest that removal of pooled secretions by continuous aspiration may decrease the risk of hospital-acquired pneumonia. Valles et al46 compared continuous aspiration of subglottic secretions to routine care in a group of patients intubated for more than 3 days.

The prevalence of ventilator-associated pneumonia for the experimental group was half that for the control group. In a related study,47 researchers concluded that aspiration of subglottic secretions around the cuff of the endotracheal tube was the most important risk factor for the development of pneumonia during the first 8 days of intubation.

Additional factors associated with the risk of hospital-acquired pneumonia include the duration of mechanical ventilation, presence of chronic lung disease, use of a nasogastric tube, and bronchoscopy.14 Finally, poor nutritional status and immunosuppression increase the risk for pneumonia. Although use of broad-spectrum antibiotics has improved the prognosis for patients with hospital-acquired pneumonia, prevention continues to be the most important strategy. Critical care nurses can incorporate a number of strategies into routine practice to minimize the risk of hospital-acquired pneumonia (Table 2).


Table 2. Strategies for preventing nosocomial pneumonia
General
Educate staff members about characteristics and transmission modes of pathogens common to the unit or institution
Routinely assess patients for changes in lung sounds, sputum color or production, and redness or drainage around stoma sites.
Eliminate obtaining samples from patients and respiratory equipment for routine culturing of microorganisms.
Wash hands before and after providing mouth care and before and after coming in contact with respiratory equipment and tracheal tubes.
Use sterile water rather than tap water for mouth care of immunosuppressed patients or if waterborne organisms have been identified.
Vaccinate patients at high risk for pneumococcal pneumonia.
Suctioning
Provide a clean manual resuscitation bag for each patient.
Suction oropharyngeal secretions as needed to avoid accumulation of oral secretions
Use sterile technique when using open-suctioning techniques
Use sterile solutions to clear secretions from in-line suctioning devices.
Before deflating the cuff of the tracheal tube, suction secretions above the cuff by passing the catheter orotracheally, then provide a positive-pressure breath during deflation.
Monitor tracheal cuff pressure with a manometer, minimal seal, or minimal leak technique every 8 hours to ensure an adequate seal and avoid overpressurization.
Provide routine, meticulous mouth care.
Mechanical ventilation
Change ventilator circuits no more frequently than every 48 hours
Drain accumulated condensate in ventilator tubing into a fluid trap or other collection device, particularly before repositioning the patient.
Avoid backflow of condensate into tracheal tubes or humidification devices
Nasogastric tubes and enteral feedings
Assess patency and placement of nasogastric tubes routinely.
Elevate the head of the bed 30¡ or more to prevent gastric reflux of organisms into the lung.
Institute feeding as soon as possible to prevent breakdown of gut mucosa and possible bacterial translocation to the lung
Assess patients for signs of feeding intolerance: no bowel sounds, abdominal distension, increased residual volume, emesis.
Discontinue use of nasogastric tubes as soon as clinically feasible.
xxx
Urinary Tract
The genitourinary tract is the most common site of nosocomial infection in the acute care setting, accounting for 40% of all hospital-acquired infections. Catheterization and instrumentation of the urinary tract are implicated as precipitating factors in approximately 80% of the cases.48 Groups at high risk for urinary tract infection include patients who are female, elderly, diabetic, immunocompromised, critically ill, incontinent, malnourished, or who require extended hospitalization.49

Although there is no consensus on the precise distinctions between the terms bacteremia, sepsis, and septic shock, general agreement exists on the order in which these states occur. If bacterial infections in the urinary tract are not adequately treated, bacteria may enter the bloodstream, a condition called bacteremia. The point at which a systemic inflammatory response to this infection occurs is termed sepsis.50 Unchecked sepsis causes a state known as septic shock, characterized by profound hypotension and marked abnormalities in perfusion. Although most bacteremias are clinically insignificant, as many as 4% progress to septicemia, with mortality rates as high as 50%.48

With normal bladder function, urine flushes through the urethra, removing bacteria adhering to the urethral walls. The presence of an indwelling catheter hinders the cleansing action of this protective mechanism.51 The longer the catheter remains in the bladder, the greater is the risk of infection; the infection rate doubles from 50% at 2 weeks to 100% if the catheter remains in place for more than 4 weeks.9

Mechanisms involved in the development of nosocomial urinary tract infections include contamination with the patient's fecal flora and cross-contamination by hospital personnel. As a result, bacteria gain entry to the urinary tract via both the lumen and the external surface of the catheter.49

Critical care nurses are in an optimal position to prevent unnecessary catheterization and to monitor the length of time a catheter is in place. Several measures can be used to minimize the potential for nosocomial urinary tract infections (Table 3).



Table 3. Strategies to prevent nosocimial urinary tract infection
Use alternatives to indwelling catheters whenever possible (eg, external catheters, incontinence pads, bladder control techniques).
Anticipate patients' catheterization needs. For example, if excess sediment or clots are present in the urine, insert a three-way catheter to facilitate sterile irrigation.
Select smaller gauge urinary drainage catheters for insertion.
Use sterile technique to insert urinary drainage catheters
Maintain a closed catheter system.
Use universal precautions when emptying urine or obtaining specimens.
Avoid cross-contamination by using an individual container for each patient when emptying catheter drainage bags.
Change drainage bags that are leaking, contain excess sediment, or are malodorous.
Secure urinary drainage catheters to the patient's thigh.
Keep tubing and drainage bag below the level of the bladder at all times to prevent backflow of urine.
Prevent stasis of urine by assessing tubing for kinks and obstruction.
For male patients, cleanse the external meatus with soap and water and thoroughly dry the area twice a day and as needed.
For male patients, avoid use of powders because of potential irritation of the meatus.
Routinely assess patients for fecal incontinence, provide thorough cleansing, and use fecal incontinence bags as indicated.
Monitor intake and output to ensure adequate fluid balance.
xxx
Bloodstream
Intravascular devices provide access to the vascular system for administration of fluids and drugs and for hemodynamic monitoring. These devices bypass skin defenses, thus becoming direct portals of entry for microorganisms into the bloodstream. In the ICU, bloodstream infections occur at a rate two to seven times greater than the rate among the medical-surgical population and, in one study,7 accounted for double the length of stay in the unit. The average attributable mortality, defined as mortality directly related to the infection, apart from mortality that may be due to underlying conditions, is 26%.7

Infections associated with use of central venous catheters are most often due to colonization
of the insertion site by bacteria normally present on the skin (Staphylococcus epidermidis).52 Contamination of the lumen from frequent disconnection to administer medications or obtain blood samples is a second predisposing factor contributing to central venous catheter infections.9,53 Interestingly, the risk of infection associated with use of triple-lumen catheters is as much as three times greater than the risk associated with use of single-lumen catheters.54

Nonetheless, the most critical factor associated with the development of a catheter-related infection is the length of time the catheter remains in place.53 More than 40% of bloodstream infections in ICUs are associated with short-term use of central venous catheters.8 Although central venous catheters are considered short term, they are often left in place longer than necessary. Thus, consideration of the need for a catheter in each patient is essential for limiting infections associated with use of intravascular devices.

The rates of bloodstream infections associated with use of central venous and peripheral catheters vary.55 Jarvis et al10 reported rates of 2.1% to 30.2% per 1000 catheter days for central venous catheters and rates of 0% to 2% for peripheral catheters. Skin characteristics of the insertion site may account for differences in the prevalence of bloodstream infections between the two types of catheters, because temperature and moisture of the skin affect the rate of colonization.55

Skin in central locations is oilier and moister than skin in peripheral areas, thus enhancing conditions for bacterial colonization.56 Another factor is the proximity of central sites to sources of contamination: oral, nasal, and tracheal secretions for catheters in the neck or subclavian area; and feces and urine for femoral catheters.55 Patients with unexplained fever and signs and symptoms of localized infection most likely have a catheter-related infection. Their catheters should be removed and samples obtained for microbial culture.53

Two broad strategies to limit infections associated with use of intravascular devices are standardization of the procedures for care of the insertion site57 and improvement in catheter design58 and material.59 In a descriptive observational study of 116 episodes of site care, Roach et al57 found significant differences between two hospitals and within hospital units in the following practices: frequency of site care, use of ointment and skin adhesive, type of dressing, and duration of care. They concluded that well-defined site care protocols, familiar to all staff, and monitoring of care on a regular basis were needed to limit bloodstream infections.

Furthermore, periodic evaluation is necessary to assess the need for central devices according to the patient's unique risks. Several measures can be used to minimize the prevalence of catheter-related infections (Table 4).


Table 4. Management of IV catheters to prevent nosocomial infection
Standardize insertion technique and care for all peripheral, central venous, and arterial catheters.
Select catheters with as few lumens as necessary for the patient's needs.
Avoid use of femoral catheters in patients with fecal or urinary incontinence.
Use aseptic technique to insert catheters.
Ensure that others inserting catheters use aseptic technique.
Stabilize cannula and tubing, and maintain a sterile occlusive dressing at the site of insertion.
Label insertion sites and all tubing with date and time of insertion.
Inspect insertion sites every 8 hours for signs of infection, and record the findings.
Replace nonocclusive dressings as specified by hospital policy (usually every 72 hours).
Replace peripheral catheters per hospital policy (usually every 48-72 hours), when indications for use are no longer present, fever of unknown origin develops, or catheters have been inserted under less than optimal circumstances such as IVs placed emergently outside the hospital or during cardiac arrest.
Change dressings per hospital policy. Cleanse the insertion site with povidone-iodine in a circular motion from inside to outside.
Avoid guidewire replacement of central venous catheters; use a different insertion site when possible.
xxx
Modifications in catheter design may assist in decreasing infection risk. Segura et al58 clinically tested a new hub design that significantly reduced catheter-related sepsis when compared with a control (4% vs 16%, respectively). In addition, catheters are being designed with the intention of preventing ascending infections by bonding antibiotics to the internal and external surfaces of the devices. Antimicrobial cuffs placed under the patient's skin at the insertion site are likewise being used to limit ascending infections.60

Studies on the efficacy of antibiotic-bonded catheters have produced mixed results. Both Greco and Harvey61 and Kamal et al62 reported a reduced prevalence in the rate of catheter infections when antibiotic-bonded catheters were used. In a randomized clinical trial of catheters bonded with silver sulfadiazine and chlorhexidine, Ciresi et al63 found no difference in the rates of catheter-induced infections or sepsis when catheters with or without bonding were used. One explanation for these mixed findings may be the use of different combinations of pharmacological agents for the treatment of gram-positive bacteria, gram-negative bacteria, and fungal organisms.

MINIMIZING RISK
The increased acuity of illness in ICU patients, the frequent use of invasive devices and procedures, and the frequent contact with staff members provide multiple opportunities for exposure to and transmission of pathogens.64 Successful prevention of nosocomial infections requires attention to their sources and to practices that promote their development.

Knowledge of situations that compromise infection control and promote contamination is a meaningful start, but recognition must be followed by actions directed toward changing the behavior of nurses and other healthcare professionals. It is not only appropriate but also ethically correct for a nurse to speak out when aseptic technique is not followed. Because critical care nurses are the primary advocates for each patient's well-being, it is their responsibility to ensure that each patient receives uncompromised care.65

The following are some basic, but important, examples that highlight appropriate infection control practices.

Hand Washing
Most preventable nosocomial infections are related to inappropriate infection control practices. Ignac Semmelweis recognized this fact in 1847.66 At that time, the Vienna General Hospital had two obstetrical divisions, both delivering approximately 3500 babies each year.

Obstetricians and medical students performed deliveries in division 1, and nurse midwives and their students delivered babies in division 2. Approximately 600 to 800 maternal deaths due to puerperal fever occurred annually on division 1 compared with 60 deaths per year on division 2. Seeking the reason for this discrepancy, Semmelweis discovered that physicians and medical students performed autopsies on a daily basis, whereas the midwives and the midwives' students did not.

He hypothesized that the fevers were caused by an unknown substance on the cadavers that was transmitted to the new mothers. A hand-washing policy was instituted that entailed using "a chlorine solution until the skin was slippery and the cadaver smell was gone."66 The following year, the death rate due to childbed fever did not differ between the two divisions. Several years later, Florence Nightingale requested scrub brushes and imposed sanitary regulations in field hospitals after observing that more soldiers died of fevers and infections than of battle wounds.67 These simple yet elegant illustrations exemplify the relationship between the simple act of hand washing and the prevention of nosocomial infections in the past and serve as reminders of its importance in the present.

Today, consistent and meticulous hand washing (Table 5) remains the most important contributing factor related to reduction of the frequency of nosocomial infections in the ICU.6 Because pathogens can survive on the hands for 30 minutes to several hours, hand washing significantly decreases the number of pathogens on the skin and contributes to decreases in patients' morbidity and mortality.6,68 Additionally, hand washing minimizes the chance that healthcare workers will themselves acquire infections.6,69

Table 5. Proper hand-washing technique
      • Wet hands under running water.
      • Dispense a minimum of 3-5 mL of soap or detergent, and thoroughly distribute it over all areas of both hands.
      • Vigorously wash all surfaces of hands and fingers for at least 10-15 seconds, including backs of hands and fingers and under the nails.
      • Rinse to remove soap, and thoroughly dry hands.
      • Use a paper towel to turn the faucet off.
xxx
Unfortunately, numerous studies have shown lack of adherence to the simple, inexpensive, and effective process of hand washing before and between contacts with patients in the ICU. In these studies, hand washing was carried out only 21% to 42% of the time.4,6 The most common reasons cited by healthcare providers for not complying were being too busy, having a limited exposure to infectious patients, and wishing to avoid skin irritation from cleansing agents.6 Although circumstances continue to improve (eg, sinks are closer to the patients, cleansing agents cause less irritation, and infection control education has become more accessible), noncompliance persists.4,6

Nails, Jewelry, and Lotion
Most microorganisms on the hands are under and around the nails. Short natural nails are preferable to artificial nails to minimize the number of bacteria and fungi around the nail and to prevent glove puncture. Clear nail polish is preferable for visual inspection during cleaning under the nails. However, optimally, healthcare professionals should avoid using any nail polish or artificial nails. Nail polish chips easily and can cause problems with infection.

Rings and other jewelry may increase the likelihood of tearing gloves and harboring microorganisms. Lotion may help decrease dermatitis and dryness related to hand washing and frequent use of gloves. Lotion can decrease the dispersal of bacteria on the hands. Small bottles are best, however, because with use, large containers can become contaminated.69

Gloves and Gowns
Gloves and gowns have been recognized as effective barriers against the transmission of microbes but are not 100% effective in protecting the wearer or patients. Universal precautions promote complacency, and gloves furnish yet another excuse not to wash the hands.70 Gloves are not a shield that makes hand washing unnecessary. Hand washing should be performed before and after each contact with patients regardless of what barriers are used. Gloves are not meant to be reused for the same patient or among different patients.

Therefore, hands should not be washed while the gloves are on. While wearing gloves, healthcare providers should avoid actions that predispose patients to contamination, including emptying urine drainage bags before performing hands-on care. Gowns are indicated only when clothing may become soiled.69

INSTITUTIONAL STRATEGIES
The current focus on patients' outcomes is an excellent means of increasing awareness of problems related to nosocomial infections. Prevention of these infections is a win-win situation, simultaneously improving care and reducing costs. This concept can be included in critical pathways for high-risk groups and incorporated into continuous-quality-improvement designs to ensure that prevention of nosocomial infections maintains a prominent position. These strategies will increase the focus on infection control practices and on evaluation of the usefulness of the practices and, it is hoped, result in improved compliance.

Rather than direct attention to infrequent clusters of infection that represent only 2% to 3% of all nosocomial infections, nurses should focus their efforts on areas of highest risk, specific to the ICU population in the particular setting.71 Using a data-based approach, rather than guidelines, gives greater credence to recommendations. For example, having each ICU monitor the numbers and types of nosocomial infections and having the pharmacy monitor adherence to guidelines for use of antibiotics provides staff with valuable information related to everyday practices.72,73

The Joint Commission on Accreditation of Healthcare Organizations states that a hospital-wide approach, including a standing infection control committee, must be taken to coordinate infection control practices.74 A multidisciplinary approach is essential to guide and support these efforts, and nurses are critical to the success of this endeavor. Clinical specialists, case managers, and nurse practitioners are in excellent positions to detect areas for improvement and to influence practice. Even more important are bedside nurses, the most direct consumers of infection control recommendations.71

Successful infection control requires that each member of the healthcare team recognize that humans are the primary source of nosocomial infections. Successful control also mandates awareness that, both individually and collectively, all healthcare practitioners are pivotal to the prevention of nosocomial infections.69 Compliance can be increased by including nurses in decision making and in formulating directives.75 Nursing staff can play an integral role in relaying information to surveillance professionals, and, in turn, infection control professionals can directly interact with staff to share information. Encouraging nurses to participate in research activities related to infection control may also enhance willingness to accept and use infection control practices less casually.

Education is inherently linked to a comprehensive infection control strategy; it ties together individuals and groups of personnel directly and indirectly involved in infection control. Nurses' lack of sufficient knowledge of microbiology and inconsistent application of infection control measures continue to be issues.76 However, another inservice program is not the answer. Both knowledge and motivation are critical for effective infection control, and motivation to change behavior is not learned in an occasional class. Sustained unit-based education must be the vehicle for presenting data that convince staff that problems exist and persuade staff members to use optimal infection control practices.71

Feedback about infection control practices is another influential strategy to successfully reduce the number of nosocomial infections. Data on the number and type of infections in specific populations of patients and reports on infection control practices in the unit should be expressed in a manner that staff can understand. Establishing benchmarks for these data to improve compliance with infection control is an additional method of influencing practice.
Using performance feedback (providing information about past performance with educational instruction to promote improvement) provides an opportunity to correct behavior and move toward established benchmarks.77

This strategy can be made more personal, timely, and effective by direct observation of nurses and physicians. In one study,78 memos were used to alert staff members that their hand-washing technique was ineffective. This mechanism increased compliance to 98% in the experimental group compared with 26% in a control group not receiving feedback.78 A similar observational study79 found 97% compliance with performance feedback versus 37% with educational classes alone. Therefore, an integrated approach is essential to generate and maintain change.

CONCLUSION
Nosocomial infections in the ICU pose a significant problem today and will continue to do so. The ICU population will continue to grow older, and acuity will consistently escalate. As patients have comorbid conditions and receive more invasive care, practitioners will struggle with fewer antibiotics to offer as treatment for infection. Therefore, critical care nurses must become increasingly vigilant in attempts to use essential prophylactic techniques to minimize nosocomial pneumonia, nosocomial urinary tract infections, and catheter-related infections.

Basic though the strategies included in Tables 2 to 5 may be, they cannot be effective if ICU personnel do not heed them. Not all nosocomial infections can be prevented, but it is prudent for healthcare professionals to recognize, implement, and use appropriate comprehensive strategies to prevent these infections and optimize patients' outcomes. As Florence Nightingale observed, "The first responsibility to the patient is to do no harm."67

References
  1. Haley RW, Culver DH, White JW, et al. The efficacy of infection surveillance and control programs in preventing nosocomial infections in US hospitals. Am J Epidemiol. 1985;121:159-167.
  2. Wenzel RP. The economics of nosocomial infection. J Hosp Infect. 1995;31:79-87.
  3. Martone WJ, Jarvis WR, Culver DH, et al. Incidence and nature of endemic and epidemic nosocomial infections. In: Bennett JV, ed. Hospital Infections. 3rd ed. Boston, Mass: Little, Brown and Co; 1992:577-596.
  4. Kulow K, Stoller JK. Respiratory therapists' handwashing practices in medical intensive care unit: an observational study. Resp Care. 1996;41:S956. Abstract.
  5. Cohran J, Larson E, Roach H, et al. Effects of intravascular surveillance and relaxation program on rates of nosocomial bloodstream infection. Heart Lung. 1996;25:161-164.
  6. Turner J. Hand-washing behavior versus hand-washing guidelines in the ICU. Heart Lung. 1993;22:275-276.
  7. Pittet D, Tarara D, Wenzel RP. Nosocomial bloodstream infection in critically ill patients: excess length of stay, extra costs, and attributable mortality. JAMA. 994;271:1598-1601.
  8. Widmer AF. Infection control and prevention strategies in the ICU. Intensive Care Med. 1994;20:S7-S11.
  9. Kennedy KL. Special features: OBRA regulations and nosocomial infection. Ostomy Wound Manage. 1994;40:62-66.
  10. Jarvis WR, Edwards JR, Culver DH, et al. Nosocomial infection rates in adult and pediatric intensive care units in the United States. Am J Med. 1991;91(3B):185-191.
  11. Flaherty JP, Weinstein RA. Nosocomial infection caused by antibiotic-resistant organisms in the intensive-care unit. Infect Control Hosp Epidemiol. 1996;17:236-248.
  12. McCance KL, Shelby J. Stress and disease. In: Huether SE, McCance KL. Understanding Pathophysiology. St Louis, Mo: CV Mosby; 1996:215-228.
  13. Guyton AC, Hall JE. The adrenocortical hormones. In: Guyton AC, ed. Human Physiology and Mechanisms of Disease. 6th ed. Philadelphia, Pa: WB Saunders; 1997:616-624.
  14. George L. Epidemiology of pneumonia in intensive care unit patients. Clin Chest Med. 1995;16:29-44.
  15. Knaus WA, Wagner DP, Draper EA, et al. The APACHE III prognostic system: risk prediction of hospital mortality for critically ill hospitalized adults. Chest. 1991;100:1619-1636.
  16. Rottern GA, Rice D. Infection. In: Phipps WJ, Sands JS, Cassmeyer VL, et al, eds. Medical-Surgical Nursing: Concepts and Clinical Practice. 4th ed. St Louis, Mo: CV Mosby; 1991:273-295.
  17. Calianno C. Nosocomial pneumonia: repelling a deadly invader. Nursing 96. 1996;26(5):34-39.
  18. Bullock B. Normal immunologic response. In: Bullock B, Rosendahl P, eds. Pathophysiology: Adaptations and Alterations in Function. 3rd ed. Philadelphia, Pa: JB Lippincott; 1992:295-311.
  19. Durnbaugh T. Gerontologic considerations. In: Lewis SM, Collier IC, Heitkemper MM, eds. Medical-Surgical Nursing: Assessment and Management of Clinical Problems. 4th ed. St Louis, Mo: CV Mosby; 1996:32-55.
  20. Masur H, Fauci A. Infections in patients with inflammatory and immunologic defects. In: Isselbacher KJ, Braunwald E, Wilson JD, et al, eds. Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill Inc; 1994:494-498.
  21. Craven DE, Steger KA, Barber TW. Preventing nosocomial pneumonia: state of the art and perspectives for the 1990s. Am J Med. 1991;91(3B):44S-53S.
  22. Kollef MH. Antibiotic use and antibiotic resistance in the intensive care unit: are we curing or creating disease? Heart Lung. 1994;23:363-367.
  23. Hospital Infection Control Practices Advisory Committee (HICPAC). Recommendations for preventing the spread of vancomycin resistance. MMWR Morb Mortal Wkly Rep. 1995;44(RR-12):1-16.
  24. Tryba M. Risk of acute stress bleeding and nosocomial pneumonia in ventilated intensive care unit patients: sucralfate versus antacids. Am J Med. 1987;83:117-124.
  25. Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer prophylaxis in critically ill patients: resolving discordant meta-analysis. JAMA. 1996;275:24-31.
  26. Craven D. Prevention of hospital-acquired pneumonia: measuring effect in ounces, pounds and tons. Ann Intern Med. 1995;122:229-231.
  27. Krueger JM, Madge MA. Sleep as a host defense: its regulation by microbial products and cytokines. Clin Immunol Immunopathol. 1990;57:188-199.
  28. Beardsley T. Waking up. Sci Am. 1996;275:14, 18.
  29. Opp MR, Krueger JM. Anti-interleukin-1 beta reduces sleep and sleep rebound after sleep deprivation in rats. Am J Physiol. 1994;266(3)(pt 2):R688-R695.
  30. Opp MR, Krueger JM. Interleukin-1 is involved in responses to sleep deprivation in the rabbit. Brain Res. 1994;639:57-65.
  31. Irwin M, McClintick J, Costlow C, et al. Partial night sleep deprivation reduces natural killer and cellular immune responses in humans. FASEB J. 1996;10:643-653.
  32. Orme JF, Clemmer TP. Nutrition in the critical care unit. Med Clin North Am. 1983;67:1295-1303.
  33. Buckley S, Kudsk K. Metabolic response to critical illness and injury. AACN Clin Issues Crit Care Nurs. 1994;5:443-449.
  34. Lord L, Sax H. The role of the gut in critical illness. AACN Clin Issues Crit Care Nurs. 1994;5:450-458.
  35. Love AH. Metabolic response to malnutrition: its relevance to enteral feeding. Gut. 1986;27:9-13.
  36. Deitch EA, Wen-Jing MA, Berg RD, et al. Protein malnutrition predisposes to inflammatory-induced gut-origin septic status. Ann Surg. 1990;211:560-567.
  37. Farr BA. Understaffing: a risk factor for infection in the era of downsizing? Infect Control Hosp Epidemiol. 1996;17:147-149.
  38. Fridkin SK, Pear SM, Williamson TH, et al. The role of understaffing in central venous catheter-associated bloodstream infections. Infect Control Hosp Epidemiol. 1996;17:150-158.
  39. Weinstein RA. Epidemiology and control of nosocomial infections in adult intensive care units. Am J Med. 1991;91(3B):179S-184S.
  40. American Thoracic Society. Hospital-acquired pneumonia in adults: diagnosis, assessment of severity, initial antimicrobial therapy and preventative strategies (consensus statement). Am J Respir Crit Care Med. 1995;153:1711-1725.
  41. Thompson CL. Critical care-acquired pneumonia. Crit Care Nurs Clin North Am. 1995;7:695-700.
  42. Craven DE, Steger KA. Epidemiology of nosocomial pneumonia: new perspectives on an old disease. Chest. 1995;108:1S-12S.
  43. Inglis TJ, Millar MR, Jones G, et al. Tracheal tube biofilm as a source of bacterial colonization of the lung. J Clin Microbiol. 1989;27:2014-2018.
  44. Hagler DA, Traver GA. Endotracheal saline and suction catheters: sources of lower airway contamination. Am J Crit Care. 1994;3:444-447.
  45. McCraney S, Rapp RP. Antibiotic agents in critical care. Crit Care Nurs Clin North Am. 1993;5:313-323.
  46. Vall s J, Artonio A, Rello J, et al. Continuous aspiration of subglottic secretions in preventing ventilator-associated pneumonia. Ann Intern Med. 1995;122:179-186.
  47. Rello J, Sonora R, Jubert P, et al. Pneumonia in intubated patients: role of respiratory airway care. Am J Respir Crit Care Med. 1996;154:111-115.
  48. Stamm WE, Martin SM, Bennett JV. Epidemiology of nosocomial infections due to gram-negative bacilli: aspects relevant to development and use of vaccines. J Infect Dis. 1977;136:151S-160S.
  49. Meares EM. Current patterns in nosocomial urinary tract infections. Urology. 1991;3:9S-12S.
  50. Nathens A, Marshall J. Sepsis, SIRS, and MODS: what's in a name? World J Surg. 1996;20:386-391.
  51. Falkiner FR. The insertion and management of indwelling ureteral catheters: minimizing the risks of infection. J Hosp Infect. 1993;25:79-90.
  52. Spencer RC. Epidemiology of infection in ICUs. Intensive Care Med. 1994;20:2S-6S.
  53. Cunha BA. Diagnosis and prevention of intravenous central line-associated infections. Heart Lung. 1995;24:261-262.
  54. Yeung C, May J, Hughes R. Infection rate for single lumen vs triple lumen subclavian catheters. Infect Control Hosp Epidemiol. 1988;9:154-158.
  55. Ryder M. Peripherally inserted central venous catheters. Nurs Clin North Am. 1993;28:937-965.
  56. Callahan J, Wesorick B. Bacterial growth under a transparent dressing. Am J Infect Control. 1987;15:231-237.
  57. Roach H, Larson E, Bartlett B. Intravascular site care: are critical care nurses practicing according to written protocols? Heart Lung. 1996;25:401-408.
  58. Segura M, Alvarez-Lerma F, Tellado J, et al. A clinical trial on the prevention of catheter-related sepsis using a new hub model. Ann Surg. 1996;223:363-369.
  59. Gilsdorf J, Wilson K, Beals T. Bacterial colonization of intravenous catheter materials in vitro and in vivo. Surgery. 1989;106:37-44.
  60. Flowers R, Schwenzer K, Kopel R, et al. Efficacy of an attachable subcutaneous cuff for prevention of intravascular catheter infection. JAMA. 1989;261:878-883.
  61. Greco R, Harvey R. The role of antibiotic bonding in the prevention of vascular prosthetic infections. Ann Surg. 1982;195:168-171.
  62. Kamal G, Pfaller M, Rempe L, et al. Reduced intravascular catheter infection by antibiotic bonding. JAMA. 1991;265:2364-2368.
  63. Ciresi D, Albrecht R, Volkers P. Failure of antiseptic bonding to prevent central venous catheter-related infection and sepsis. Am Surg. 1996;62:641-646.
  64. Maloney SA, Jarvis WR. Epidemic nosocomial pneumonia in the intensive care unit. Clin Chest Med. 1995;16:209-223.
  65. Crow S. Asepsis: an indispensable part of the patient's care plan. Crit Care Nurs Q. 1989;11:11-16.
  66. Sanford JP. Foreword. In: Bennett JV, Brachman PS. Hospital Infections. 3rd ed. Boston, Mass: Little, Brown, and Co; 1992:ix-xiv.
  67. Nightingale F. Notes on Nursing: What It Is and What It Is Not. London, England: Harrison and Sons; 1859.
  68. Ayliffe GAJ, Babb JR, Davies JG, et al. Hand disinfection: a comparison of various agents in laboratory and ward studies. J Hosp Infect. 1988;11:226-243.
  69. Larson EL. APIC guidelines for handwashing and hand antisepsis in health care settings. Am J Infect Control. 1995;23:251-269.
  70. Tasota FJ, Hoffman LA. Nosocomial infections in the ICU: back to basics. Crit Care Alert. 1995;8:61-63.
  71. Baker OG. Understanding parameters of risk and risk measurement in critical care. Crit Care Nurs Clin North Am. 1995;7:713-718.
  72. Evans ME, Kortas KJ. Vancomycin use in a university medical center: comparison with hospital infection control practices advisory committee guidelines. Infect Control Hosp Epidemiol. 1996;17:356-359.
  73. Goldman MP. Antibiotic prophylaxis in the critical care setting. Crit Care Nurs Clin North Am. 1995;7:667-674.
  74. Joint Commission on Accreditation of Healthcare Organizations. 1996 Accreditation Manual. Oaktree Terrace, Ill; 1996: vol 1, sec 2.
  75. Sproat LJ, Inglis TJ. A multicenter survey of hand hygiene practice in intensive care units. J Hosp Infect. 1994;26:137-148.
  76. Gould D. Nurses' hands as vectors of hospital-acquired infection: a review. J Adv Nurs. 1991;16:1216-1225.
  77. Weiner N. The Human Use of Human Beings: Cybernetics and Society. Boston, Mass: Houghton Mifflin; 1950.
  78. Mayer JA, Dubbert PM, Miller M, et al. Increasing handwashing in an intensive care unit. Infect Control. 1986;7:259-262.
  79. Dubbert PA, Dolce J, Richter W, et al. Increasing intensive care unit staff handwashing: effects of education and group feedback. Infect Control Hosp Epidemiol. 1990;11:191-193.

Please click here to see the entire article