Infection Associated with Medical Devices

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Chapter 172 Infection Associated with Medical Devices

Patricia M. Flynn

Despite the therapeutic successes and convenience of the many synthetic devices used in pediatric patients, infectious complications are problematic. The pathogenesis of device-related infection is not completely defined, but many factors are important, including the susceptibility of the host, the composition of the device, the ability of microorganisms to adhere to the device itself or to the biofilm that quickly forms on it, and environmental factors that include the insertion technique and maintenance of the device.

Intravascular Access Devices

Intravascular access devices range from short stainless steel needles to multilumen implantable synthetic plastic catheters that are expected to remain in use for years. Infectious complications include localized infections and catheter-related bloodstream infections (CRBSI). Exit site infection denotes infection localized to the exit site often with purulent discharge. Tunnel tract infection indicates infection in the subcutaneous tissues tracking along the catheter, which may also include serous or serosanguineous discharge from a draining sinus along the catheter path and usually mandates removal of the catheter. Pocket infection indicates suppurative infection of a subcutaneous pocket containing a reservoir, usually of a totally implanted device. The source of catheter infection is usually contamination by bacteria on the skin rather than bacteremia from another focus seeding the intravascular device. Infection with the microbial skin flora at the insertion site may extend along the external surface of the catheter. This route of infection is most common in intravascular catheters in place for <30 days. Organisms may also gain access to the intraluminal portion of the catheter through improper handling of the catheter hub or contaminated infusate. This route of infection is thought to be more prevalent in catheters in place for >30 days. Gram-positive cocci predominate in both categories, with more than half caused by coagulase-negative staphylococci. Gram-negative enteric bacteria are isolated in approximately 20-30% of episodes, and fungi account for 5-10%.

The clinical manifestations of local infection include erythema, tenderness, and purulent discharge at the exit site or along the subcutaneous tunnel tract of the catheter. CRBSI may occur with or without local infection. Additional clinical findings include fever without an identifiable focus and rigors associated with catheter use.

The diagnosis of localized infection is established clinically. A Gram stain and culture of exit site drainage should be performed and may help elucidate the microbiologic cause. The diagnosis of CRBSI is confirmed by performing quantitative blood cultures simultaneously from the catheter and the peripheral vein. CRBSI is diagnosed when at least a 3-fold higher number of organisms are isolated from blood obtained via the catheter as compared to blood obtained via a peripheral vein. If quantitative blood cultures are not available, a catheter blood culture that becomes positive >2 hr before a peripheral culture, with equal amounts of blood using a radiometric detection system, may also be used for diagnosis. CRBSI can also be diagnosed by isolation of the same organism from the blood and the catheter tip. However, this method requires catheter removal and is not optimal for patients with long-term devices.

Short-term peripheral catheters are most commonly used in pediatric patients, and infectious complications occur infrequently. The rate of peripheral CRBSI is <0.15%. Patient age <1 yr, duration of use for >144 hr, and some infusates (e.g., total parenteral nutrition, lipids) are associated with increased risk for catheter-related infection.

Central venous catheters (CVCs) are widely used in both adult and pediatric patients and are responsible for the majority of catheter-related infections. They are commonly used in critically ill patients, including neonates, who often have many risk factors for the development of nosocomial infection. Patients who are in an intensive care unit and who have a CVC in place have a 5-fold greater risk for developing a nosocomial bloodstream infection than those without a CVC. The means for optimal maintenance of these catheters remains controversial. Although prevalence of infection increases with prolonged duration of catheter use, routine replacement of a CVC, either at a new site or over a guide wire, results in significant morbidity and should not be adopted. Catheters should be removed when they are no longer needed. The use of peripherally inserted central catheters (PICCs), which are inserted into a peripheral vein with the distal end in a central vein, has increased in pediatric patients. Published experience with these devices in children is scanty, but studies in adults document a life span of approximately 3 mo and infection rates of 1.9 episodes/1,000 catheter-days, significantly lower than for CVCs.

When prolonged intravenous access is required, a cuffed silicone rubber (Silastic) catheter may be inserted into the right atrium through the subclavian, cephalic, or jugular vein. The extravascular segment of the catheter passes through a subcutaneous tunnel before exiting the skin, usually on the superior aspect of the chest (Broviac or Hickman catheters). Totally implanted devices consist of a reservoir or port placed in a subcutaneous pocket with a self-sealing silicone septum at the distal end that permits repeated percutaneous needle insertions for administration of drugs. The use of central venous devices has improved the quality of life of high-risk patients but has also increased the risk for various infections. The incidence of local (exit site, tunnel, and pocket) infection is 0.2-2.8/1,000 catheter-days. The incidence of Broviac or Hickman CRBSI is 0.5-6.8/1,000 catheter days, whereas that for implantable devices is 0.3-1.8/1,000 catheter-days. The risk for catheter infection is increased among premature infants, young children, and those receiving total parenteral nutrition.

If either localized infection or CRBSI is diagnosed in a short-term peripheral catheter or CVC, the device should be removed. Antibiotics should be administered in cases of systemic infection, with the exception of uncomplicated coagulase-negative staphylococcal bacteremia in normal hosts, for which catheter removal is sufficient.

For infections associated with long-term vascular access devices (Hickman, Broviac, totally implantable devices), antibiotic treatment is successful for most systemic bacterial infections without removal of the device. Antibiotic therapy should be directed to the isolated pathogen and given for a total of 7-14 days, depending on the organisms isolated. CRBSI caused by Staphylococcus aureus may require a longer duration of therapy. Until identification and susceptibility testing are available, empirical therapy, based on local antimicrobial susceptibility data and usually including a 3rd or 4th generation cephalosporin or aminoglycoside plus vancomycin is indicated. Antibiotic lock or dwell therapy, with administration of solutions of high concentrations of antibiotics or ethanol that remain in the catheter for up to 24 hr, may improve outcome when used as an adjuvant to systemic therapy. If blood cultures remain positive after 72 hr of appropriate therapy, as confirmed by susceptibility testing, or if a patient deteriorates clinically, the device should be removed. Although new evidence is emerging to support catheter retention, most experts advocate removal of the device as well as therapy with systemic antifungal therapy in cases of CRBSI caused by Candida spp. Exit site infections usually respond to local care or systemic antibiotics, but tunnel tract infections require removal of the catheter in approximately image of patients.

Prevention of Infection

Prevention of infections of long-term vascular access devices includes placement using meticulous surgical aseptic technique in an operating room–like environment, avoidance of bathing or swimming, and careful catheter care. The Centers for Disease Control and Prevention recommends that short-term peripheral catheters be replaced every 72-96 hr to prevent phlebitis. The use of antimicrobial-impregnated catheters may reduce the risk for catheter-associated bloodstream infections.

Cerebrospinal Fluid Shunts

Cerebrospinal fluid (CSF) shunting is required for the treatment of many children with hydrocephalus. The usual procedure uses a silicone rubber device with a proximal portion inserted into the ventricle, a unidirectional valve, and a distant segment that diverts the CSF from the ventricles to either the peritoneal cavity (ventriculoperitoneal [VP] shunt) or right atrium (ventriculoatrial [VA] shunt). The incidence of shunt infection ranges from 1 to 20%, with an average of 10%. The highest rates are reported in young infants, prior shunt infections, and certain etiologies of hydrocephalus. Most infections are a result of intraoperative contamination of the surgical wound by skin flora. Accordingly, coagulase-negative staphylococci are isolated in more than half of the cases. S. aureus is isolated in approximately 20% and gram-negative bacilli in 15% of cases.

Four distinct clinical syndromes have been described: colonization of the shunt, infection associated with wound infection, distal infection with peritonitis, and infection associated with meningitis.

The most common type of infection is colonization of the shunt, with symptoms that reflect shunt malfunction as opposed to frank infection. Symptoms associated with colonized VP shunts include lethargy, headache, vomiting, and a full fontanel. Low-grade fever is common. Symptoms usually occur within months of the surgical procedure. Colonization of a VA shunt results in more severe systemic symptoms and often without specific symptoms of shunt malfunction. Septic pulmonary emboli, pulmonary hypertension, and infective endocarditis are frequently reported complications of VA shunt colonization. Chronic VA shunt colonization may cause hypocomplementemic glomerulonephritis due to antigen-antibody complex deposition in the glomeruli, which is commonly called shunt nephritis; clinical findings include hypertension, microscopic hematuria, elevated blood urea nitrogen (BUN) and serum creatinine levels, and anemia. With shunt colonization, CSF obtained from either lumbar or ventricular puncture is often sterile, and the infecting organism is isolated only from the shunt reservoir. Accordingly, it is unusual to observe signs of ventriculitis, and CSF findings are only minimally abnormal. Blood culture results are usually negative in cases of VP colonization but positive in VA shunt colonization.

Wound infection presents with obvious infection or dehiscence along the shunt tract and most often occurs within days to weeks of the surgical procedure. S. aureus is the most common isolate. In addition to the physical findings, fever is common, and no-signs of shunt malfunction eventually ensue in most cases.

Distal infection of VP shunts with peritonitis presents with abdominal symptoms, usually without evidence of shunt malfunction. The pathogenesis is likely related to perforation of bowel at the time of VP shunt placement or translocation of bacteria across the bowel wall. Thus, gram-negative isolates predominate, and mixed infection is common. The infecting organisms are often isolated from only the distal portion of the shunt.

The usual meningeal pathogens, Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b, can also cause bacterial meningitis in patients with shunts in place. The clinical presentation is similar to that for acute bacterial meningitis (Chapter 595.1).

Treatment of shunt colonization includes the use of antibiotics, systemically with or without the use of intraventricular antibiotics, against the specific organisms isolated and removal of the shunt. Intraventricular antibiotics may be indicated because of the poor penetration of most antibiotics into the central nervous system across uninflamed meninges. If the isolate is susceptible, a parenteral antistaphylococcal penicillin with or without intraventricular vancomycin is the treatment of choice. If the organism is resistant to the penicillins, systemic vancomycin and possibly intraventricular vancomycin is recommended. In cases of gram-negative infections, a combination of a 3rd generation cephalosporin with or without intraventricular aminoglycoside is optimal. When using intraventricular antibiotics, monitoring of CSF levels is necessary to avoid toxicity. The best treatment success occurs when removal of the colonized device and placement of an external ventricular drain to relieve intracranial pressure accompanies antibiotic therapy. Alternatively, some neurosurgeons opt to exteriorize the distal end of the shunt rather than completely remove the device. After CSF cultures remain sterile for at least 48 hr, shunt replacement can be performed. Distal shunt infection with peritonitis is best managed in a similar fashion. When wound infection is diagnosed, the shunt almost always needs to be removed. To allow for continued ventricular drainage, an external ventricular drain is often placed, with replacement of a new shunt after the wound infection has healed. Only systemic antibiotics are necessary for treatment of bacterial meningitis in patients with a shunt in place; the shunt itself does not need to be removed.

Prevention of Infection

Prevention of shunt infection includes meticulous cutaneous preparation and surgical technique. Systemic and intraventricular antibiotics, antibiotic-impregnated shunts, and soaking the shunt tubing in antibiotics have been used to reduce the incidence of infection, with varying success. A meta-analysis of 17 clinical trials using systemic prophylactic antibiotics or antibiotic-impregnated catheters involving 2,134 randomized patients showed that both strategies reduced the risk for infection.

Urethral Catheters

Urinary catheters are a frequent cause of nosocomial infection, with about 14 infections per 1,000 admissions. Like other devices, microorganisms adhere to the catheter surface and establish a biofilm that allows proliferation. The physical presence of the catheter reduces the normal host defenses by preventing complete emptying of the bladder, thus providing a medium for growth, distending the urethra, and blocking periurethral glands. Almost all patients catheterized for >30 days develop bacteriuria. The urinary tract is considered infected if specimens of urine obtained directly from an indwelling catheter harbor ≥100 colony-forming units/mL. Gram-negative bacilli and Enterococcus are the predominant organisms isolated in catheter-related urinary tract infection; coagulase-negative staphylococci are implicated in about 15% of cases. Symptomatic urinary tract infections should be treated with antibiotics and catheter removal. Asymptomatic infections can usually be managed with catheter removal alone.

Prevention of Infection

All urinary catheters introduce risk for infection, and their casual use should be avoided. When they are in place, their duration of use should be minimized. Technologic advances have led to development of silver- or antibiotic-impregnated urinary catheters that are associated with lower rates of infection. Prophylactic antibiotics do not reduce the infection rates for long-term indwelling urethral catheters.

Peritoneal Dialysis Catheters

During the 1st yr of peritoneal dialysis for end-stage renal disease, 65% of children will have 1 or more episodes of peritonitis. Bacterial entry comes from luminal or periluminal contamination of the catheter or by translocation across the intestinal wall. Hematogenous infection is rare. Infections can be localized at the exit site, associated with peritonitis, or both. Organisms responsible for peritonitis include coagulase-negative staphylococci (30-40%), S. aureus (10-20%), streptococci (10-15%), Escherichia coli (5-10%), Pseudomonas (5-10%), other gram-negative bacteria (5-15%), Enterococcus (3-6%), and fungi (2-10%). S. aureus is more common in localized exit or tunnel tract infections (42%). Most infectious episodes are due to a patient’s own flora, and carriers of S. aureus have been shown to have increased rates of infection as compared with noncarriers.

The clinical manifestations of peritonitis may be subtle and include low-grade fever, mild abdominal pain, and tenderness. Cloudy peritoneal dialysis fluid may be the 1st and predominant sign. With peritonitis, the peritoneal fluid cell count is usually >100 white blood cells/µL. When peritonitis is suspected, the effluent dialysate should be submitted for cell count, Gram stain, and culture. The Gram stain is positive in up to 40% of cases of peritonitis.

Patients with cloudy fluid and clinical symptoms should receive empirical therapy, preferably guided by results of a Gram stain. If no organisms are visualized, vancomycin and either an aminoglycoside or 3rd or 4th generation cephalosporin with antipseudomonal activity should be given via the intraperitoneal route. Patients without cloudy fluid and with minimal symptoms may have therapy withheld pending culture results. Once the cause is identified by culture, changes in the therapeutic regimen may be needed. Oral rifampin may be added for S. aureus infections. Fungal peritonitis should be treated with a combination of oral flucytosine and intraperitoneal or oral fluconazole alone. The duration of therapy is a minimum of 14 days, with longer treatment of 21-28 days for episodes of S. aureus and Pseudomonas and 28-42 days for fungi. Repeat episodes of peritonitis within 4 wk of previous therapy represent “apparently relapsing” peritonitis. If the patient responds to reinstitution of antimicrobial therapy, a course of up to 6 wk should be continued. In all cases, if the infection fails to clear on appropriate therapy or if a patient’s condition is deteriorating, the catheter should be removed. Exit site and tunnel infections may occur independently of peritonitis or may precede peritonitis. Appropriate antibiotics should be administered on the basis of Gram stain and culture findings. Some experts recommend that the peritoneal catheter be removed if Pseudomonas or fungal organisms are isolated.

Prevention of Infection

In addition to usual hygienic practices, mupirocin, applied either to the nares or at the exit site, reduces exit site infections and bacteremia caused by S. aureus.

Orthopedic Prostheses

Orthopedic prostheses are used infrequently in children. Infection most often follows introduction of microorganisms at surgery through airborne contamination or direct inoculation; via hematogenous spread; or contiguous spread from an adjacent infection. Early postoperative infection occurs within 2-4 wk of surgery, with typical manifestations that include fever, pain, and local symptoms of wound infection. Rapid assessment, including isolation of the infecting organism, best obtained by joint aspiration or intraoperative culture, and antimicrobial treatment may allow salvage of the implant if the duration of symptoms is less than 1 mo, the prosthesis is stable, and the pathogen is susceptible to antibiotics. Late chronic or delayed infections occur >1 mo after surgery and are often caused by organisms of low virulence that contaminated the implant at the time of surgery. Typical manifestations include pain and deterioration in function. Local symptoms such as erythema, swelling, or drainage may also occur. These infections respond poorly to antibiotic treatment and usually require removal of the implant in either 1 or 2 stages. Hematogenous infections are most often observed ≥2 yr after surgery. Retention of the prosthesis can be attempted. As with other long-term implanted devices, the most common organisms are about equally divided between coagulase-negative staphylococci and S. aureus.

The use of systemic antibiotic prophylaxis, antibiotic-containing bone cement, and operating rooms fitted with laminar airflow all have been proposed as beneficial in reducing infection. To date, results from clinical studies are conflicting.

Bibliography

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