44: Infections Acquired in the Intensive Care Unit
CHAPTER 44 Infections Acquired in the Intensive Care Unit
James S. Salonia1 and Andre Sotelo2
1 Icahn School of Medicine at Mount Sinai, New York, NY, USA
2 Hackensack University Medical Center, Hackensack, NJ, USA
General treatment rationale
When an ICU‐acquired infection is suspected, all devices should be removed when possible.
Antimicrobial agents are the primary treatment. These antibiotics should be administered promptly, as a delay in treatment may lead to increased mortality.
Choice of specific antibiotic agents should be determined by risk factors, local microbiology, and hospital‐based antibiograms.
Initial therapy should be administered intravenously with a transition to oral therapy in patients with appropriate clinical response. For C. difficile infection, oral treatment is preferred when possible.
General prevention
Hand hygiene (conventional soap and water or alcohol‐based hand sanitizer) and aseptic technique (maximal sterile barrier precautions with cap, mask, sterile gown, gloves, and full body drape).
Implementation of quality improvement programs and daily assessment of bundle adherence measures for all intravascular devices, indwelling urinary catheters, and endotracheal tubes.
All patients with suspected or laboratory confirmed C. difficile infections should be placed on contact precautions, utilizing barrier protection with gown, gloves, and disposable instruments (e.g. stethoscope). Hand hygiene with conventional soap and water is critical, as alcohol‐based hand rubs do not prevent the spread of C. difficile spores.
Simulation‐based training can be an effective tool to instruct health care providers in the proper technique of utilizing maximal sterile barrier precautions and on the proper placement of intravascular catheters and endotracheal intubation.
Central line‐associated bloodstream infections
Background
Definition of disease
CLABSI is a laboratory confirmed bloodstream infection where a central line was in place for >2 calendar days on the date of event, with the day of device placement designated as day 1. If the central line was in place for >2 calendar days and then removed, the date of laboratory confirmed bloodstream infection must be the day of discontinuation or the following day.
Etiology
Predominant organisms are:
Coagulase‐negative staphylococci.
Staphylococcus aureus.
Candida species.
Enteric Gram‐negative bacilli.
Pathology/pathogenesis
Pathogenic microbes are introduced through migration of skin organisms at the insertion site into the cutaneous catheter tract and along the surface of the catheter, with colonization of the catheter tip. This is the most common route of infection for short‐term catheters.
Direct contamination of the catheter or catheter hub, contact with hands or contaminated fluids or devices, hematogenously seeded infection from another focus of infection, and infusate contamination are less common methods of colonization and infection.
Predictive/risk factors
Prolonged central venous or arterial catheterization.
Skill of the operator.
Insertion site risk factors:
Chlorhexidine‐based solutions preferred.
Loss of skin integrity (e.g. burns, psoriasis).
Submaximal barrier precautions.
Non‐tunneled greater than tunneled catheters.
Type of catheter:
Number of lumens.
Lower risk with antibiotic impregnated catheters.
Greatest risk with pulmonary artery catheters.
Repeated catheterization and use.
Catheter site:
Femoral site has highest risk of infection.
Pre‐existing infection overlying insertion site.
Insertion circumstance:
Emergency greater than elective.
Severity of illness, chronic illness, and immune deficient state:
Granulocytopenia.
Immunosuppressive chemotherapy.
Total parenteral nutrition (TPN) administration.
Prevention
Utilize and maintain maximal sterile barrier precautions when inserting intravascular catheters.
Insertion site preparation:
2% chlorhexidine‐based solutions preferred.
Alternatives include iodine‐based solutions.
A subclavian or jugular site is the preferred location for central venous catheter placement. Avoid using the femoral vein for central venous access.
The use of antiseptic/antibiotic impregnated short‐term central venous catheters and chlorhexidine impregnated sponge dressings is recommended if the rate of infection is not decreasing despite adherence to other strategies.
Catheter stabilization with a sutureless securement device is preferred to avoid disruption around the catheter entry site.
If catheter site is bleeding or oozing, the use of sterile gauze is recommended until bleeding has resolved.
Prompt removal of intravascular catheter when no longer indicated.
Diagnosis
Typical presentation
Unexplained fever, leukocytosis, and decompensation in a patient with central venous or arterial access.
Erythema, induration, and tenderness at the insertion site.
Clinical diagnosis
History
Prolonged intravascular catheterization in the presence of symptoms such as fever, chills, and rigors should increase suspicion for a catheter‐associated bloodstream infection.
Physical examination
Daily examination of all catheter insertion sites for erythema, purulent discharge, and tenderness.
Laboratory diagnosis
List of diagnostic tests
Paired aerobic and anaerobic blood cultures (at least one culture set from a peripheral vein), are collected in a sterile manner prior to the initiation of antibiotics. Skin preparation should be performed utilizing chlorhexidine.
Quantitative catheter tip cultures have been utilized for diagnosis of CLABSI, using growth of >15 colony forming units (cfu) as positive. A positive catheter tip culture itself, however, is not sufficient for diagnosis.
List of imaging techniques
Echocardiogram may be necessary in patients with CLABSI to evaluate for infective endocarditis.
Potential pitfalls/common errors made regarding diagnosis of disease
Failure to implement or adhere to central line insertion checklist or full compliance with central line maintenance bundle adherence measures.
Lack of aseptic technique in the collection of blood cultures may result in contamination and false positive cultures.
Treatment
Duration of antibiotic therapy is dependent on pathogenic organism. Duration of antibiotics is counted from the first day of negative blood cultures.
Vancomycin is recommended for empiric therapy due to prevalence of MRSA.
Empiric coverage for Gram‐negative organisms is recommended until cultures are available.
Empiric coverage for multidrug‐resistant (MDR) organisms is recommended for select patients:
Neutropenic patients.
Severely ill patients.
Known colonization with MDR pathogens.
Empiric coverage for Candida species with echinocandin may be recommended for patients with certain risk factors:
Total parenteral nutrition.
Prolonged duration of broad spectrum antibiotics.
Hematologic malignancy.
Transplant recipient.
Colonization due to Candida species.
Catheterized patients with a single positive blood culture growing coagulase‐negative Staphylococcus species may have additional cultures collected prior to considering catheter removal.
Prognosis
Mortality from CLABSI is approximately 12–25% and is influenced by the underlying acute illness and comorbidities.
Follow‐up tests and monitoring
Patients with CLABSI require close follow‐up with surveillance blood cultures to demonstrate clearance of bacteremia.
Persistent bacteremia and/or persistent symptoms 72 hours after catheter removal with appropriate antibiotics suggest complications such as infective endocarditis and/or metastatic infections.
Catheter‐associated urinary tract infections
Background
Definition of disease
CAUTI:
Laboratory confirmed infection where an indwelling urinary catheter was in place for >2 calendar days on the date of event, with the day of device placement designated as day 1 and was still present on or removed the day prior to the date of event and the patient has at least one of the following signs or symptoms:
Fever (>38°C).
Urinary urgency or frequency.
Dysuria.
Suprapubic or costovertebral pain or tenderness.
Altered metal status.
Plus, positive urine culture with no more than two species of organisms with at least one species of >100 000 cfu.
Incidence/prevalence
CAUTI is the most common healthcare‐associated infection.
Etiology
Predominant organisms are:
Escherichia coli.
Enterococcus.
Candida species.
Klebsiella species.
Pseudomonas aeruginosa.
Serratia species.
Citrobacter species.
Enterobacter species.
Long‐term catheterization usually results in polymicrobial infections.
Pathology/pathogenesis
Introduction of pathogenic microbes into the urinary system as a result of improper sterile technique with catheter placement, prolonged catheter insertion with migration of meatal, vaginal, or rectal microorganisms forming biofilms on the foreign catheter, and failure to maintain a closed drainage system are the most important mechanisms of CAUTI.
Biofilms protect the pathogenic organism from antimicrobials and host defense mechanisms.
Urinary stasis due to drainage failure and contamination of the urine collection bag can result in ascending infections.
Urinary catheterization disrupts host defense mechanisms and provides access of uropathogens to the urinary system.
Predictive/risk factors for CAUTI
Duration of catheterization is one of the most significant risk factors in the development of CAUTI.
Placement of urinary catheter for inappropriate indications.
Repeated catheterization.
Improper sterile technique with catheter placement.
Failure to maintain a closed drainage system.
Prolonged urinary catheterization.
Advanced age.
Female gender.
Impaired immunity.
Diabetes mellitus.
Prevention
Alternative methods to internal urinary catheters such as intermittent catheterization or external catheters.
Perform and maintain sterile technique with internal urinary catheter placement.
Maintain a closed drainage system with unobstructed urine flow.
The use of antiseptic impregnated urinary catheters may be considered.
Prompt removal of internal urinary catheters when no longer indicated.
Diagnosis
Typical presentation
Unexplained fever, leukocytosis, and decompensation in a patient with indwelling urinary catheter, especially if prolonged, should trigger evaluation of a possible CAUTI.
Clinical diagnosis
History
Prolonged internal urinary catheterization in the presence of symptoms such as fever, chills, and rigors.
Physical examination
Visible erythema, tenderness, and purulent discharge from the urethral meatus, as well as purulent urine in the catheter collecting system suggest the urinary catheter as a source of infection.
Laboratory diagnosis
List of diagnostic tests
Specimens for urine culture should only be collected when CAUTI is suspected based on abnormal urinalysis.
Urine culture should be collected after removing the indwelling catheter and obtaining a midstream specimen.
If the catheter cannot be removed, specimens for urine culture should be collected through a catheter port using aseptic technique.
In patients with long‐term indwelling catheters, it is recommended that a new indwelling urinary catheter be placed prior to specimen collection for urine cultures.
Urine culture specimens should not be obtained from the urinary collecting bag.
List of imaging techniques
Ultrasound and/or CT scan of the kidneys may be considered in patients with CAUTI who present with clinical findings of acute pyelonephritis.
Potential pitfalls/common errors made regarding diagnosis of disease
Failure to implement or adhere to daily CAUTI prevention bundle adherence measures.
Lack of aseptic technique in the collection of urine specimen may result in contamination and false positive cultures.
Treatment
Prompt removal of indwelling urinary catheters.
Empiric coverage for Gram‐negative organisms is recommended until cultures are available.
Duration of antibiotic treatment is dependent on the patient’s response.
Prognosis
Mortality attributed to CAUTI is approximately 2.3% and is likely to be influenced by the underlying acute illness and comorbidities.
Follow‐up tests and monitoring
All patients diagnosed with hospital‐acquired infection should be closely monitored for clinical response to treatment.
Ventilator‐associated event and ventilator‐associated pneumonia
Background
Definition of disease
VAE is defined as worsening oxygenation following ≥2 days of stable or decreasing FiO2 or PEEP. There are three tiers within the VAE algorithm:
Ventilator‐associated condition (VAC): increase in daily FiO2 ≥20% over daily minimum FiO2 sustained for ≥2 days or increase in PEEP of ≥3 over daily minimum PEEP for ≥2 days.
Infection‐related ventilator‐associated complication (IVAC): ≥3 days of mechanical ventilation and within 2 days of worsening oxygenation, the patient develops a temperature >38°C or <36°C, or WBC ≥12 000 or ≤4000 and a new antibiotic is started and continued for ≥4 days.
Possible or probable ventilator‐associated pneumonia (VAP): above criteria for IVAC plus positive bacterial laboratory confirmation or lung histopathology.
Etiology
Predominant organisms are:
P. aeruginosa.
S. aureus.
Klebsiella pneumoniae.
Acinetobacter species.
E. coli.
Pathology/pathogenesis
Microaspiration of oropharyngeal contents and migration of bacteria around the endotracheal tube cuff is the primary method by which bacteria invade the lower respiratory tract.
Intubation procedure can introduce pathogenic organisms resulting in infection.
Colonization of the endotracheal tube or the ventilator circuit by bacteria with the formation of biofilm.
Natural host defense mechanism of secretion clearance is disrupted by the presence of an endotracheal tube and sedation.
Predictive/risk factors
Skill of the operator performing endotracheal intubation.
Prolonged mechanical ventilation.
Reintubation.
Position of endotracheal and gastric tubes. Orotracheal intubation and orogastric tubes are preferred over nasotracheal intubation and nasogastric tubes to reduce the risk of VAP.
Risk factors for MDR organisms:
Antibiotic therapy in previous 90 days.
Current hospitalization of 2 days or more.
High frequency of antibiotic resistance in the community or hospital.
Residence in nursing home.
Home infusion therapy.
Chronic dialysis.
Home wound care.
Family member with multidrug‐resistant organism.
Immunosuppressive disease and/or therapy.
Prevention
Non‐invasive ventilation in selected patients to prevent intubation.
Maintain semi‐recumbent position of 30–45° to prevent aspiration.
Oral chlorhexidine to prevent oropharyngeal colonization.
Continuous aspiration of subglottic secretions can reduce the risk of VAP.
Endotracheal tube cuff pressure should be maintained >20 cmH2O to prevent leakage of secretions around the cuff into the lower respiratory tract.
Remove contaminated condensate from the ventilator circuit and prevent condensate from entering the endotracheal tube.
Reduce the duration of mechanical ventilation and accelerate weaning through adherence to daily ventilator bundle measures.
Diagnosis
Differential diagnosis
Differential diagnosis
Features
Pulmonary embolism (PE)
Risk factors for PE No purulent secretions Negative cultures CT angiogram or V/Q scan showing PE
Congestive heart failure
Non‐purulent secretions Reduced ventricular function on echocardiogram Improvement with diuretics No response to antibiotics
Pulmonary hemorrhage
Bloody secretions No response to antibiotics Bronchoscopy with hemorrhagic lavage
Atelectasis
No purulent secretions No response to antibiotics Fleeting opacities on imaging
Typical presentation
Increase in purulent secretions, fever, and worsening hypoxemia suggest VAP.
Clinical diagnosis
Physical examination
Auscultation for the presence of crackles, wheezing, and/or egophony.
Dullness to percussion may indicate consolidated lung or the presence of a pleural effusion.
Daily assessment of the quality and quantity of endotracheal tube secretions
Laboratory diagnosis
List of diagnostic tests
Lower respiratory tract secretions should be sent for culture.
Bronchoscopic specimen collection may be considered.
Blood cultures should be collected prior to administration of antibiotics.
A diagnostic thoracentesis should be performed if a patient has a moderate or large pleural effusion to rule out parapneumonic effusion or empyema.
List of imaging techniques
Chest radiography should be performed in patients with suspected VAP to:
Define severity of pneumonia.
Identify presence of complications such as effusion or cavitation.
Chest ultrasonography may be obtained in institutions with appropriate ultrasound expertise.
Potential pitfalls/common errors made regarding diagnosis of disease
Failure to maintain accurate duration dates for mechanical ventilation.
Failure to implement or fully adhere to daily ventilator bundle measures.
Lack of proper technique in the collection of tracheal aspirate or bronchoscopic specimen may result in contamination and/or inadequate specimen.
Treatment
Antibiotic therapy is recommended in patients with no known risk factors for MDR pathogens (Table 44.1).
Combination antibiotic therapy is recommended in patients with suspected MDR pathogens (Table 44.2).
Duration of appropriate antibiotic treatment for VAP in a patient with appropriate clinical response is 7 days.
P. aeruginosa should be treated for at least 14 days.
Aerosolized antibiotics may be considered as adjunctive therapy in patients with VAP due to MDR Gram‐negative pathogens not responding to intravenous therapy.
Prognosis
Mortality attributed to VAP has been reported prior to the new VAE definition to be approximately 13% and is likely to be influenced by the underlying acute illness and comorbidities.
Table 44.1Initial empiric antibiotic therapy for suspected VAP in patients with no known risk factors for MDR pathogens.
Table 44.2Initial empiric antibiotic therapy for suspected VAP in patients with risk factors for MDR pathogens.
Suspected MDR pathogen
Recommended combination antibiotic therapy
Pseudomonas aeruginosa Klebsiella pneumoniae Acinetobacter species Methicillin‐resistant Staphylococcus aureus (MRSA)
Antipseudomonal cephalosporin Or Antipseudomonal carbapenem Or Antipseudomonal β‐lactam/β‐lactamase inhibitor (piperacillin/tazobactam) Plus Vancomycin or linezolid
Clostridium difficile infection
Background
Definition of disease
CDI is one of the main causes of antibiotic‐associated diarrhea in hospitalized patients. Diagnosis is based on a combination of clinical and laboratory findings in patients with current or recent health care exposure.
The most common clinical finding is diarrhea:
≥3 unformed stools within a 24 hour period.
The Bristol stool scale can be used in the initial assessment: ≥3 stools is categorized as type 5 or greater within 48 hours or 1 stool is categorized as type 7 (watery) within the past 24 hours.
Laboratory confirmation with either a positive test on an unformed stool specimen for toxin‐producing C. difficile or direct colonoscopic visualization with findings revealing pseudomembranous colitis.
Etiology
Clostridium difficile is an anaerobic organism responsible for the majority of cases of antibiotic‐associated colitis.
Pathology/pathogenesis
CDI is the result of person‐to‐person spread through the fecal–oral route. The most important mechanism by which C. difficile is spread is through the hands of health care workers contaminated with C. difficile spores.
Antimicrobial therapy results in alteration of the normal intestinal flora, predisposing patients to the development of C. difficile colitis.
Pathogenic C. difficile produces two distinct toxins. Toxin A is an enterotoxin and toxin B is a cytotoxin. Both toxins bind to the intestinal mucosal cells resulting in mucosal inflammation and the development of pseudomembranous colitis. This mucosal inflammation leads to diarrhea (bloody or non‐bloody), and in severe cases, ileus with toxic megacolon.
NAP1 is a hypervirulent strain of C. difficile most commonly associated with severe and fulminant colitis.
Asymptomatic C. difficile colonization is common, with an estimated prevalence of 7–26% in acute care facilities.
Predictive/risk factors
Inappropriate use of antibiotics. Any antibiotic can predispose to CDI. The most frequently implicated antibiotics include clindamycin, fluoroquinolones, and cephalosporins.
Hospitalization.
Advanced age >70 years.
Severe illness and impaired immunity:
Chemotherapy.
Hematopoietic stem cell transplant.
Gastrointestinal surgery.
Use of proton pump inhibitors.
Failure to utilize appropriate contact precautions and disposable medical devices, as well as improper hand hygiene.
Improper sterilization of rooms and equipment after exposure.
Prevention
Screening
Stool culture, enzyme immunoassay (EIA) for C. difficile toxin, or PCR of liquid stool sample in patients with risk factors and new onset diarrhea.
Primary prevention
Antibiotic stewardship. Optimize the use and duration of antibiotic therapy to minimize unnecessary antibiotic exposure.
Early detection and contact isolation precautions:
Use of private rooms is recommended.
Gloves and gowns should be worn upon room entry and removed prior to exiting the room.
Strict adherence to hand hygiene with conventional soap and water. Instruct visitors on the necessity of hand hygiene.
Dedicated disposable medical equipment should be utilized.
Contact precautions should be maintained for the duration of diarrhea.
Environmental cleansing with chlorine‐based agents is recommended.
Secondary prevention
Antimicrobial therapy:
Prolonged course of oral vancomycin with a gradual taper in recurrent disease.
Fidaxomicin may be considered for recurrent disease.
Fecal microbiota therapy (FMT):
Indications:
Recurrent or relapsing infection:
≥3 episodes of mild–moderate CDI and failure of 6–8 week vancomycin taper.
≥2 episodes of severe CDI.
Persistent moderate (>1 week) or severe (>48 hours) CDI not responding to appropriate therapy.
Protracted CDI:
≥3 weeks of ongoing symptoms on appropriate antimicrobial therapy.
Absolute contraindications to FMT:
Decompensated liver cirrhosis.
HIV/AIDS.
Bone marrow transplant recipients.
Severe immunodeficiency.
Anaphylactic food allergy which was not excluded from donor diet.
FMT may be delivered by colonoscopy or flexible sigmoidoscopy.
Repeat FMT may be considered if inadequate response to initial FMT therapy.
Diagnosis
Differential diagnosis
Differential diagnosis
Features
Acalculous cholecystitis
Right upper quadrant (RUQ) tenderness Hepatic function panel with cholestatic profile RUQ ultrasound or HIDA scan showing cholecystitis
Infectious diarrhea (not due to C. difficile)
Negative C. difficile testing Stool culture positive for other organism May have bloody or non‐bloody diarrhea No significant antibiotic exposure or recent hospitalization
Ischemic colitis
Patient risk factors for ischemia Acute onset No significant antibiotic exposure or recent hospitalization May have bloody or non‐bloody diarrhea Elevated lactate Negative C. difficile testing
In CDI, diarrhea (mucus, bloody, or non‐bloody) remains the most common clinical presentation, especially in the setting of antibiotic use or recurrent hospitalization. Ileus due to CDI may present as abdominal pain and distension without associated diarrhea.
Clinical diagnosis
History
Patient reports of bloody or non‐bloody diarrhea with recent hospitalization, antibiotic exposure, or contact with an individual known to have C. difficile should raise awareness regarding possible CDI.
Physical examination
Observation for bloody or mucus/non‐bloody diarrhea. Auscultation for bowel sounds should be performed to assess for ileus. Examination and palpation of the abdomen for distension and tenderness to evaluate for progression to ileus and megacolon.
Disease severity classification
Mild to moderate:
White blood cell count <15 000/mm3.
Serum creatinine <1.5 times baseline.
Severe:
White blood cell count ≥15 000/mm3.
Serum creatinine ≥1.5 times baseline.
Severe and complicated:
White blood cell count ≥15 000/mm3.
Serum creatinine ≥1.5 times baseline.
Hypotension or shock.
Ileus or megacolon.
Laboratory diagnosis
List of diagnostic tests
Testing for C. difficile should be performed only on unformed stool, unless ileus from C. difficile is suspected.
Stool culture is the most sensitive test to detect CDI. It is limited by a slow turnaround time.
EIA testing for C. difficile toxins A and B is rapid, but is less sensitive than stool culture.
PCR testing is rapid, sensitive, and specific.
Two‐step testing may be considered to increase diagnostic accuracy.
Colonoscopy with biopsy may be performed to identify pseudomembranous colitis.
List of imaging techniques
Abdominal radiography (X‐ray or CT scan) should be obtained if complications of CDI such as ileus, megacolon, or perforation are suspected.
Potential pitfalls/common errors made regarding diagnosis of disease
Lack of consideration for CDI. Delay in testing and diagnosis can result in significant delay in treatment and spread of infection.
CDI is a clinical diagnosis with confirmatory laboratory findings. Sending C. difficile stool specimens without appropriate clinical symptoms may result in identification of C. difficile carrier state, which does not require treatment.
Treatment
CDI is characterized as non‐severe, severe, fulminant or recurrent.
A surgical consultation should be obtained in patients with severe CDI.
Clinical definition
Clinical data
Treatment
Initial episode, non‐severe disease
Inital episode, severe
Inital episode, fulminant
First recurrence
Second recurrence
WBC < 15 000/mm3 and serum creatinine level < 1.5 times baseline
WBC ≥ 15 000/mm3 or serum creatinine level ≥ 1.5 times baseline
Hypotension or shock, ileus, megacolon
Oral vancomycin 125 mg four times per day or oral fidaxomicin 200 mg twice daily, 10 days
Oral vancomycin 125 mg four times per day or oral fidaxomicin 200 mg twice daily, 10 days
Oral vancomycin 500 mg four times per day, plus intravenous metronidazole 500 mg every 8 hours. If ileus, consider adding rectal vancomycin
Same as initial treatment
Vancomycin in tapered or pulsed regimen
Prognosis
Mortality attributed to health care‐associated CDI ranges from 6% to 30%.
Infection with hypervirulent strain NAP1/BI/027 may result in more severe disease and higher mortality.
Natural history of untreated disease
The course of untreated CDI is dependent on the severity of disease, strain of C. difficile, and the underlying immune function of the patient.
Untreated patients may have increasingly voluminous diarrhea, develop ileus, and progress to toxic megacolon with potential perforation and development of an overwhelming septic state.
Follow‐up tests and monitoring
Repeat testing during the same episodes of diarrhea is not recommended.
Test of cure following treatment of C. difficile is not recommended.
Pressure ulcer infection
Background
Definition of disease
A laboratory confirmed superficial or deep skin or soft tissue infection with at least two of the following signs or symptoms with identifiable risk factor(s): erythema, edema, or tenderness of the wound edges.
Plus, organisms identified from tissue biopsy or aspiration of fluid from the ulcer margin.
Etiology
Predominant organisms are:
Enterobacter species.
Staphylococci.
Enterococcus faecalis.
Pathology/pathogenesis
Pressure ulcers develop due to localized injury to the skin and/or soft tissue. These injuries typically occur over bony prominences as a result of sustained pressure and/or friction.
Breakdown of the skin barrier from a combination of pressure, friction, shearing forces, and moisture predisposes to bacterial colonization and the development of skin and soft tissue infections.
Externally applied pressure on body surfaces exceeds the capillary perfusion pressure within the tissue. This disrupts the microcirculation resulting in inflammation, free radical generation, and hypoxic tissue necrosis.
Predictive/risk factors
Immobility.
Malnutrition.
Reduced perfusion:
Peripheral arterial disease.
Congestive heart failure.
Sensory loss:
Spinal cord injury.
Neuropathy.
Moisture.
Prevention
Screening
Risk assessment and a complete skin assessment should be conducted on all patients admitted to the ICU and repeated as required based on risk factors and patient acuity.
Primary prevention
Cushion dressings should be applied to areas of high risk to protect the skin.
Daily skin inspection.
Frequent repositioning of immobile, bedbound patients with maintenance of dry skin environment.
Diagnosis
Typical presentation
Pressure ulcer infections typically present with erythema, edema, and tenderness with or without purulent discharge, on an area of the body vulnerable to pressure ulcers.
Clinical diagnosis
History
Prolonged immobility and infectious symptoms should raise concern for pressure ulcer infection.
Physical examination
Daily assessment of pressure ulcers for depth, visible erythema, edema, purulent discharge, or visible bone.
Disease severity classification
Pressure ulcers are categorized into stages:
Stage I: non‐blanchable erythema with intact skin.
Stage II: partial thickness loss of dermis with red‐pink wound bed.
Stage III: full thickness skin loss. Subcutaneous fat may be visible in areas of adipose tissue.
Stage IV: full thickness tissue loss with exposed tendon, muscle, and/or bone.
Unstageable: full thickness skin or tissue loss with depth unknown.
Laboratory diagnosis
Cultures should be collected either by tissue biopsy or aspirate of fluid at the ulcer margin.
MRI, CT scan, and/or bone scans are recommended in patients with infected pressure ulcers with high clinical suspicion for osteomyelitis.
Potential pitfalls/common errors made regarding diagnosis of disease
Failure to perform a thorough daily skin assessment in patients at high risk for pressure ulcers or with existing pressure ulcers
Treatment
Pain control.
Local wound care.
Consultation of wound care professional.
Intravenous antibiotics.
Patients with pressure ulcer infections and evidence of tissue necrosis should have surgical consultation and debridement.
Prognosis
Natural history of untreated disease
Neglected pressure ulcers will progress in severity.
Bone involvement may result in osteomyelitis. Secondary bacteremia may develop and can progress to a potentially lethal septic state.
Follow‐up tests and monitoring
Patients treated for pressure ulcer infections should have frequent skin examinations to ensure appropriate healing.
Reading list
Dudeck MA, et al. National Healthcare Safety Network report, data summary for 2013, device‐associated module. Am J Infect Control 2015; 43(3):206–21.
Yokoe DS, et al. A compendium of strategies to prevent healthcare‐associated infections in acute care hospitals: 2014 updates. Infect Control Hosp Epidemiol 2014; 35(8):967–77.
Zimlichman E, et al. Health care‐associated infections. A meta‐analysis of costs and financial impact on the US health care system. JAMA Intern Med 2013; 173(22):2039–46.
