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Infectious diseases
Unknown illness ... single infection ... community spread ... contagion ... epidemic ... pandemic. The recent year has demonstrated in full force that infectious diseases remain a major health concern. Infectious diseases jeopardize patient outcomes throughout the healthcare delivery system as well as in the perioperative sector. Additionally, new emerging infectious diseases stemming from special and novel pathogens pose great threats to the health and safety of persons in our local, national, and global communities, and new emerging pathogens can cause massive global disruption.
Multiple factors (i.e., overcrowding, poor sanitation, migration patterns, climate change, jet travel) in the past decade have led to fragile ecosystems that contribute to rapid disease spread. While many significant advances have been made in modern medicine in the treatment of cardiovascular disease and certain kinds of cancer, infectious organisms and their resultant diseases remain a major obstacle to worldwide health. The advent of antibiotics to treat some bacterial diseases was a major advance, as was the development of vaccines against a number of infectious diseases. But for every step forward, a substantial obstacle has appeared. For example, microorganisms have developed resistance to some antibiotic drugs, and they continue to mutate in ways that make their eradication ever more difficult. Development of vaccines to treat some of the most common and potentially deadly infectious diseases in the world have been stymied by the ability of some infectious agents to mutate much more quickly than lab personnel can change their vaccine formulations; malaria and human immunodeficiency virus (HIV) disease are examples of this. In addition, about one new infectious disease organism has been discovered annually over the past 50 years. Some have been discovered in regions far removed from our country, but easy travel has brought the opportunity for nearly anyone anywhere to become infected with what were formerly thought to be exotic diseases.
Healthcare facilities, long thought to be havens for the very ill, are now also reservoirs of multiple infectious diseases due to resistant microorganisms or to infection by microorganisms that can only manifest disease when other more virulent organisms have been reduced in number or eradicated. Thus the presence of infectious agents as a comorbid condition in patients presenting for surgery remains a significant issue for the perioperative physician. Additionally, the development of hospital-acquired infections remains a significant cause of morbidity and mortality in the perioperative period. Patients may have coexisting infectious diseases that impact perioperative care when they come for surgery; these infections may be explicitly manifest or occult. Preexisting infectious diseases may be the indication for surgery or they may impact the risks associated with the surgery. In addition, every patient undergoing surgery is at risk of acquiring an infectious disease during the perioperative period. Patients undergoing surgery are vulnerable to infection both at the surgical site and where natural defenses are breached (i.e., respiratory tract, urinary tract, bloodstream, and sites of invasive monitoring). These infectious diseases can be passed on to other patients and to health professionals in the perioperative period, and healthcare workers themselves may serve as active agents in transmitting infectious diseases to patients.
Infection prevention overview
Antibiotic resistance
Prior to the development of microscopic biology, humans had little understanding of infection and were subject to many devastating pandemics, such as the Black Death of the 14th century. Since the discovery of penicillin in 1928, bacteria have undergone thousands of mutations, resembling a Darwinian survival-of-the-fittest evolutionary response to antibiotic exposure that has perpetuated the need for ever-new antibiotics. Most classes of antibiotics were discovered in the 1940s and 1950s, and these drugs are directed at a few specific aspects of bacterial physiology: biosynthesis of the cell wall, DNA, and proteins. During the past 40 years, only two new chemical classes of antibiotics have been developed. One reason for the widespread drug resistance among bacterial pathogens is the limited choice of antibiotics that manipulate only a narrow range of bacterial functions. Another is overprescription and inappropriate use of current antibiotics.
Infectious diseases that were presumably eradicated (e.g., tuberculosis [TB]) are demonstrating a resurgence. Some reemerging pathogens, such as multidrug-resistant (MDR) TB and extensively drug-resistant (XDR) TB, have resistance to previously successful antimicrobial therapies. MDR organisms cause an increasing number of bacterial infections in hospitals, and bacteria are emerging with resistance to all available antibiotics. Much of the attention is presently focused on resistant gram-positive organisms, such as methicillin-resistant Staphylococcus aureus (MRSA). However, there is virtually no development of antibiotics active against resistant gram-negative pathogens. New antibiotic development has dramatically slowed owing to regulatory disincentives, market failures, and lack of profitability compared to other pharmacologic pursuits.
Surgical site infections
Surgical site infections (SSIs) have been the focus of much attention during the past 30 years, and the major emphasis has been on completely preventing the occurrence of surgery-related infections and their associated morbidity and mortality. In 2002, the Centers for Medicare and Medicaid Services (CMS), in collaboration with the Centers for Disease Control and Prevention (CDC), implemented the national Surgical Infection Prevention Project (SIPP). The key measures being monitored by this project are (1) the proportion of patients who receive parenterally administered antibiotics within 1 hour prior to incision (within 2 hours for vancomycin and fluoroquinolones), (2) the proportion of patients who receive prophylactic antimicrobial therapy consistent with published guidelines, and (3) the proportion of patients whose prophylactic antibiotic is discontinued within 24 hours after surgery.
Despite the implementation of numerous sets of drug and policy guidelines, SSIs continue to occur at a rate of 2% to 5% for extraabdominal surgery and up to 20% for intraabdominal surgery, and they affect approximately 500,000 patients annually. SSIs are among the most common causes of nosocomial infection, accounting for 14% to 16% of all nosocomial infections in hospitalized patients. SSIs are a major source of morbidity and mortality, rendering patients 60% more likely to spend time in the intensive care unit (ICU), five times more likely to require hospital readmission, and twice as likely to die. A recent resurgence in SSIs may be attributable to bacterial resistance, increased implantation of prosthetic and foreign materials, or the poor immune status of many patients undergoing surgery. Universal adoption of simple measures, including frequent handwashing and appropriate administration of prophylactic antibiotics, has been emphasized as a method of decreasing the incidence of SSIs.
SSIs are divided into superficial infections (involving skin and subcutaneous tissues), deep infections (involving fascial and muscle layers), and infections of organs or tissue spaces (any area opened or manipulated during surgery) ( Fig. 25.1 ). S. aureus, including MRSA, is the predominant cause of SSIs. The increased proportion of SSIs caused by resistant pathogens and Candida species may reflect the increasing numbers of severely ill and immunocompromised surgical patients and the impact of widespread use of broad-spectrum antimicrobial drugs.
Risk factors for surgical site infections
The risk of developing an SSI is affected by patient-related, microbe-related, and wound-related factors. Patient-related factors include chronic illness, extremes of age, baseline immunocompetence or inherent or acquired immunocompromise, diabetes mellitus, and corticosteroid therapy. These factors are associated with an increased risk of developing an SSI.
Microbial factors include pathogen enzyme production, possession of a polysaccharide capsule, and the ability to bind to fibronectin in blood clots. These are some of the mechanisms by which microorganisms exploit weakened host defenses and initiate infection. Biofilm formation is particularly important in the development of prosthetic material infections (i.e., prosthetic joint infection). Coagulase-negative staphylococci produce a glycocalyx and an associated component called slime that physically shield bacteria from phagocytes or inhibit antimicrobial agents from binding with or penetrating into the bacteria.
Devitalized tissue, dead space, and hematomas are wound-related features associated with the development of SSIs. Historically, wounds have been described as clean, contaminated, and dirty according to the expected number of bacteria entering the surgical site. The presence of a foreign body (i.e., sutures or mesh) reduces the number of organisms required to induce an SSI. Interestingly the implantation of major devices such as prosthetic joints and cardiac devices is not associated with a higher risk of SSIs. Risk factors for SSI are summarized in Table 25.1 .
TABLE 25.1
Risk Factors for Surgical Site Infection
| Patient-Related Factors | Microbial Factors | Wound-Related Factors |
|---|---|---|
| Extremes of age | Enzyme production | Devitalized tissue |
| Poor nutritional status | Polysaccharide capsule | Dead space |
| ASA physical status score >2 | Ability to bind to fibronectin | Hematoma |
| Diabetes mellitus | Biofilm and slime formation | Contaminated surgery |
| Smoking | Presence of foreign material | |
| Obesity | ||
| Coexisting infections | ||
| Colonization | ||
| Immunocompromise | ||
| Longer preoperative hospital stay |
ASA, American Society of Anesthesiologists.
Signs and symptoms
SSIs typically present within 30 days of surgery with localized inflammation at the surgical site and evidence of poor wound healing. Systemic features of infection, such as fever and malaise, may occur soon thereafter.
Diagnosis
There may be nonspecific evidence of infection, such as an elevated white blood cell count, poor blood glucose control, and elevated levels of inflammatory markers such as C-reactive protein. However, surgery is a great confounder because surgery itself causes inflammation and thus renders surrogate markers of infection less reliable. Purulence at the wound site is highly suggestive of infection. The gold standard in documenting a wound infection is growth of organisms in an aseptically obtained culture specimen. Approximately one-third of organisms cultured are staphylococci ( S. aureus and S. epidermidis ); Enterococcus species make up more than 10%, and Enterobacteriaceae make up the bulk of the remaining culprits. Table 25.2 lists the criteria for diagnosing an SSI.
TABLE 25.2
Criteria for Diagnosis of Surgical Site Infection (SSI)
| Type of SSI | Time Course | Criteria (At Least One Must Be Present) |
|---|---|---|
| Superficial incisional SSI | Within 30 days of surgery | Superficial pus drainage Organisms cultured from superficial tissue or fluid Signs and symptoms (pain, redness, swelling, heat) |
| Deep incisional SSI | Within 30 days of surgery or within 1 yr if prosthetic implant present | Deep pus drainage Dehiscence or wound opened by surgeon (for temperature >38°C, pain, tenderness) Abscess (e.g., radiographically diagnosed) |
| Organ/space SSI | Within 30 days of surgery or within 1 yr if prosthetic implant present | Pus from a drain in the organ/space Organisms cultured from aseptically obtained specimen of fluid or tissue in the organ/space Abscess involving the organ/space |
Management of anesthesia
Preoperative.
Active infections should be treated aggressively before surgery; when possible, surgery should be postponed until infection has resolved. If a localized area of infection is present at the intended surgical site, surgery should be postponed until the localized infection is treated and/or resolves spontaneously. If a patient has clinical evidence of infection, such as fever, chills, or malaise, efforts should be made to identify the source of the infectious process. Several studies have shown that smoking may increase not only the incidence of respiratory tract infection but also the incidence of wound infections. Preoperative cessation of smoking for 4 to 8 weeks before orthopedic surgery decreases the incidence of wound-related complications. Significant preoperative alcohol consumption may result in generalized immunocompromise. One month of preoperative alcohol abstinence reduces postoperative morbidity in alcohol users.
Diabetes mellitus is an independent risk factor for infection, and optimization of preoperative diabetes treatment may decrease perioperative infection. Malnutrition, whether manifesting as cachexia or obesity, is associated with an increased perioperative infection rate. Appropriate diet and/or weight loss may be beneficial before major surgery.
S. aureus is the organism most commonly implicated in SSIs, and many individuals are carriers of S. aureus in the anterior nares. This carrier state has been identified as a risk factor for S. aureus wound infections. Topical mupirocin applied to the anterior nares has been successful in eliminating the carrier state of S. aureus and decreasing the risk of infection. However, there is concern that this practice may promote development of mupirocin-resistant S. aureus. Active surveillance programs to eliminate nasal colonization in hospital surgical personnel have controlled outbreaks of S. aureus SSIs.
Hair clipping at the planned surgical site is acceptable, but shaving increases the risk of SSI probably because microcuts serve as entry portals for microorganisms. Preoperative skin cleansing with chlorhexidine has been shown to reduce the incidence of SSIs.
Intraoperative
Prophylactic antibiotics.
It was recognized many years ago that prophylactic administration of antimicrobial agents prevents postoperative wound infections. This is particularly true when the inoculum of bacteria is high, such as in colon, rectal, or vaginal surgery, or when the procedure involves insertion of an artificial implant such as a hip prosthesis or heart valve. The organisms implicated in SSIs are usually those carried by the patient in the nose or on the skin. Unless the patient has been in the hospital for some time before surgery, these are usually community organisms that have not developed multiple drug resistance. Timing of antibiotic prophylaxis (within 1 hour of surgical incision) is important, since these organisms are introduced into the bloodstream at the time of incision. For most procedures a single dose of antibiotic is adequate. Prolonged surgery (>4 hours) may necessitate a second dose. Prophylaxis should be discontinued within 24 hours of the procedure. For cardiac surgery, The Joint Commission has recommended that the duration of prophylaxis be increased to 48 hours. A first-generation cephalosporin, such as cefazolin, is effective for many types of surgery. In general, the spectrum of bacteria against which cephalosporins are effective, their low incidence of side effects, and the tolerability of these drugs have made them an ideal choice for prophylaxis. For high-risk patients and procedures, selection of another appropriate antibiotic plays a critical role in decreasing the incidence of SSIs.
When the small bowel is entered, coverage for gram-negative organisms is important; for procedures involving the large bowel and the female genital tract, the addition of coverage against anaerobic organisms is appropriate. Infections associated with clean surgery are caused by staphylococcal species, whereas infections associated with contaminated surgery are polymicrobial and involve the flora of the viscus entered. Guidelines for antimicrobial prophylaxis for those considered at risk of infective endocarditis are published by the American Heart Association. Additional treatment considerations are listed in Table 25.3 .
TABLE 25.3
Surgical Infection Prevention Guidelines
|
Physical and physiologic preventive measures.
Several simple physical measures have been studied to determine their effects on the incidence of postoperative infection. Much of the work has focused on the oxygen tension at the wound site. Destruction of organisms by oxidation (oxidative killing) is the most important defense against surgical pathogens and depends on the partial pressure of oxygen in contaminated tissue. In patients with normal peripheral perfusion, the subcutaneous oxygen tension is linearly related to the arterial oxygen tension. An inverse correlation has been demonstrated between subcutaneous tissue oxygen tension and the rate of wound infections. Tissue hypoxia appears to increase the vulnerability to infection.
Hypothermia has been shown to increase the incidence of SSI. In a study in which patients were randomly assigned to hypothermia and normothermia groups, SSI was found in 19% of patients in the hypothermia group but in only 6% of those in the normothermia group. Radiant heating to 38°C increases subcutaneous oxygen tension. This may be one of the mechanisms for the decreased infection risk associated with increased body temperature.
Oxygen.
An easy method of improving oxygen tension is to increase the concentration of inspired oxygen. Studies of patients undergoing colorectal resection have demonstrated that perioperative administration of 80% oxygen decreases the incidence of SSI in this patient group. It is unknown whether perioperative administration of 80% oxygen decreases the incidence of SSI in other surgical settings. Universal adoption of this treatment protocol remains controversial because a prolonged period of high inspired oxygen tension may cause pulmonary damage.
Analgesia.
Superior treatment of surgical pain is associated with increased postoperative subcutaneous oxygen partial pressures at wound sites. Adequate analgesia may therefore be associated with a decreased incidence of SSI.
Carbon dioxide.
Hypocapnia occurs frequently during anesthesia and can be deleterious for many reasons, particularly because of the vasoconstriction it causes. Such vasoconstriction could impair perfusion of vital organs. Hypercapnia causes vasodilation and increases skin perfusion. Intriguing research has shown that mild intraoperative hypercapnia increases the oxygen tension in subcutaneous tissue and the colon.
Glucose.
The results of studies to date suggest that in the perioperative period, the ideal blood glucose goal should be in the normal range with minimal variability. A high blood glucose concentration is thought to inhibit leukocyte function and provide a favorable environment for bacterial growth. Interestingly the therapy for hyperglycemia may itself have beneficial effects. Administration of glucose, insulin, and potassium stimulates lymphocytes to proliferate and attack pathogens. Glucose, insulin, and potassium may play an important role in restoring immunocompetence to patients with immunocompromise.
Wound-probing protocols.
Current studies suggest that infection of contaminated wounds can be decreased by following wound-probing protocols. Wound probing is a bedside technique that combines the benefits of primary and secondary wound closure. Use of this technique has been shown to decrease length of stay and SSIs, but the exact mechanism of its effect is not clearly understood.
Bloodborne infections
Bloodstream infections
Bloodstream infections (BSIs) are among the top three nosocomial infections in incidence. Anesthesiologists may play an important role in the prevention and often the treatment of BSIs. Although a 46% decrease in central line–associated bloodstream infections (CLABSIs) has occurred in hospitals across the United States from 2008 to 2013, an estimated 30,100 CLABSIs still occur in ICUs and wards of US acute care facilities each year. CLABSIs are serious infections typically causing a prolongation of hospital stay and increased cost and risk of mortality. CLABSIs are monitored by the National Healthcare Safety Network (NHSN) of the CDC. At every hospital, each institution should determine the CLABSI rate; this is calculated per 1000 central line days by dividing the number of CLABSIs by the number of central line days and multiplying the result by 1000. A central line utilization ratio is also calculated. Mortality risk related to these is estimated to be 12% to 25% for each bloodstream infection.
Signs and symptoms
Patients typically have nonspecific signs of infection with no obvious source. There is no cloudy urine, purulent sputum, pus drainage, or wound inflammation. There is only an indwelling catheter. Inflammation at the catheter insertion site is suggestive of infection. A sudden change in a patient’s condition, such as mental status changes, hemodynamic instability, altered tolerance for nutrition, and generalized malaise, can indicate a BSI.
Diagnosis
CLABSIs are defined as bacteremia or fungemia in a patient with an intravascular catheter with at least one blood culture positive for a recognized pathogen not related to another infection in that patient, clinical manifestations of infection, and no other apparent source for the BSI except the catheter. BSIs are considered to be associated with a central line if the line was in use during the 48-hour period before the development of the BSI. If the time interval between the onset of infection and device use is longer than 48 hours, other sources of infection must be considered. The diagnosis is more compelling if after catheter removal the same organisms that grew in the blood culture grow from the catheter tip. Table 25.4 lists pathogens commonly associated with BSI.
TABLE 25.4
Common Pathogens Associated With Bloodstream Infections
Adapted from Orsini J, Mainardi C, Muzylo E, et al. Microbiological profile of organisms causing bloodstream infection in critically ill patients. J Clin Med Res . 2012;4:371–377.
| Gram-positive bacteria (59%) |
| Coagulase-negative staphylococci |
| Staphylococcus aureus |
| Enterococci |
| Streptococcus pneumoniae |
| Gram-negative bacteria (31%) |
| Escherichia coli |
| Enterobacter species |
| Klebsiella pneumoniae |
| Acinetobacter baumannii |
| Fungi (10%) |
| Candida species |
Treatment
The best treatment for CLABSIs is prevention. However, if infection is suspected, the source of the infection should be removed as soon as possible, and broad-spectrum antimicrobial therapy should be initiated. Once culture results are available, antibiotic therapy can be targeted to the specific organism. Because of antibiotic resistance patterns, it is difficult to strike a compromise between providing appropriate initial empirical coverage and not exhausting the last-line antimicrobial agents with the first salvo of antibiotic therapy. Treatment of patients with BSIs is similar to treatment of patients with sepsis.
Management of anesthesia
Preoperative.
Many central venous catheters are placed by anesthesiologists who may not be informed about BSIs that develop days later. Preventing BSIs related to central venous catheter use can be minimized by implementing a series of evidence-based steps shown to reduce catheter-related infection. A recent interventional study targeted five evidence-based procedures recommended by the CDC and identified as having the greatest effect in reducing the rate of catheter-related BSIs and the fewest barriers to implementation. The five interventions are (1) healthcare professional will perform hand hygiene prior to insertion, (2) adhere to aseptic technique and utilize full-barrier precautions (hat, mask, sterile gown, sterile area covering) during central venous catheter insertion, (3) cleaning the skin with 0.5% chlorhexidine with alcohol, (4) avoiding the femoral site if possible, and (5) using sterile chlorhexidine-impregnated dressing over the site, conducting routine daily inspection of catheters and removing them as soon as deemed unnecessary. In this study, use of these evidence-based interventions resulted in a large and sustained reduction (up to 66%) in rates of CLABSIs that was maintained throughout the 18-month study period. The subclavian and internal jugular venous routes carry less risk of infection than the femoral route, but the decision regarding anatomic location also has to consider the higher risk of pneumothorax with a subclavian catheter. During insertion, catheter contamination rates can be further reduced by rinsing gloved hands in a solution of chlorhexidine in alcohol before handling the catheter. Sterility must be maintained with frequent hand decontamination and cleaning of catheter ports with alcohol before accessing them. The same high standards of sterility should be applied with regional anesthetic catheters. Central venous catheters may be coated or impregnated with antimicrobial or antiseptic agents. These catheters have been associated with a lower incidence of BSIs. Concerns about widespread adoption of drug-impregnated catheters are based on increased costs and promotion of antimicrobial resistance. However, use of such catheters may be indicated for the most vulnerable patients, such as those with severe immunocompromise.
Intraoperative.
Transfusion of red blood cells and blood components increases the incidence of postoperative infection via two mechanisms: direct transmission of organisms from the blood product and immunosuppression. Even autologous blood transfusion results in natural killer cell inhibition and is intrinsically immunosuppressive. The mechanism of immunosuppression may be related to infusion of donor leukocytes or their byproducts. Blood transfusion–associated immunosuppression may be decreased by leukodepletion.
Transfusion of cellular blood components has been implicated in transmission of viral, bacterial, and protozoal diseases. Over the past 20 years, reductions in the risk of viral infection from blood components have been achieved. Minipool nucleic acid amplification testing detects HIV and hepatitis B and C virus during the time before antibodies develop. This sensitive and specific test has decreased the risk of HIV-1 and hepatitis C virus transmission to 1 in 2 million blood transfusions.
Because of the success in detecting viral infection, bacterial contamination of blood products has emerged as the greatest residual source of transfusion-transmitted disease. Each year, approximately 9 million units of platelet concentrates are transfused in the United States. An estimated 1 in 1000 to 3000 platelet units is contaminated with bacteria. Platelets, to maintain viability and function, must be stored at room temperature, which creates an excellent growth environment for bacteria. The prevalence of episodes of transfusion-associated bacterial sepsis is approximately 1 in 50,000 for platelet units and 1 in 500,000 for red blood cell units. Implementation of bacterial detection methods will improve the safety and extend the shelf life of platelets. The best way to avoid infectious complications related to transfusion is simply to avoid or minimize the use of transfusions.
Postoperative.
Several postoperative management strategies can decrease the incidence of catheter-related BSI: (1) removal of central lines and pulmonary artery catheters as soon as possible, and (2) avoidance of unnecessary parenteral nutrition and dextrose-containing fluid, since these may be associated with an increased risk of BSI. Food and glucose can usually be withheld for a short period or delivered into the gut rather than into a vein.
Sepsis
Sepsis is an umbrella term encompassing those conditions in which there are pathogenic microorganisms in the body. Sepsis may be life threatening because of complications precipitated by an organism, its toxins, and the body’s own defensive inflammatory response. (A similar response may occur in the absence of infection, and this is sometimes called systemic inflammatory response syndrome [SIRS].) Sepsis is a spectrum of disorders on a continuum, with localized inflammation at one end and a severe generalized inflammatory response with multiorgan failure at the other ( Fig. 25.2 ). Severe sepsis is defined as acute organ dysfunction secondary to infection, and septic shock is severe sepsis with hypotension not reversed by fluid administration.
Surgery and anesthesia should be postponed until sepsis is at least partially treated. However, sometimes the underlying cause of sepsis requires urgent surgical intervention. Such surgery may be termed source control surgery . Examples of septic sources are abscesses, infective endocarditis, bowel perforation or infarction, infected prosthetic device (e.g., intravenous [IV] catheter, intrauterine device, or pacemaker), endometritis, and necrotizing fasciitis.
Bacterial components such as endotoxin, through their action on neutrophils and macrophages, can induce a wide range of proinflammatory factors and counterregulatory host responses that turn off production of proinflammatory cytokines. As a result the proinflammatory reaction (SIRS) can become exaggerated by associated activation of the complement system and coagulation cascade, widespread arterial vasodilation, and altered capillary permeability. This may result in multiorgan dysfunction and death.
Signs and symptoms
Signs and symptoms of sepsis are often nonspecific, and presentation varies according to the initial source of infection. SIRS is an important component of sepsis; however, sepsis is a continuum and can range from SIRS to septic shock ( Table 25.5 ). Sepsis may result in multiorgan failure. Features of infection include fever, altered mental status, and encephalopathy. Hyperglycemia may be present. Septic shock refers to hemodynamic instability that may accompany sepsis and the perfusion abnormalities that may include (but are not limited to) lactic acidosis, oliguria, or a change in mental status. Classically, hypotension, bounding pulses, and a wide pulse pressure are present. These are characteristic signs of high-output cardiac failure and distributive shock, both of which may occur with sepsis. Patients who are receiving inotropic drugs or vasopressor support may not be hypotensive.
TABLE 25.5
The Sepsis Continuum
| SIRS | Sepsis | Severe Sepsis | Septic Shock |
|---|---|---|---|
| Two or more SIRS criteria | Two or more SIRS criteria | Two or more SIRS criteria | Two or more SIRS criteria |
| Temperature: >100.4°F or <96.8°F (>38.0°C or <36.0°C) |
Source of infection: Presumed or documented infectious focus |
Source of infection | Source of infection |
| Tachycardia: Heart rate >90 beats/min |
Infiltrate on chest radiograph in patient with signs and symptoms consistent with pneumonia | Acute organ dysfunction: signs of microvascular compromise and poor perfusion | Acute organ dysfunction |
| Tachypnea: Respiratory rate >20 breaths per minute |
Infected fluid from a normally sterile site, including cerebrospinal fluid, joint fluid, and blood | Acute encephalopathy, presenting as altered mental status | Persistent hypotension: systolic blood pressure (SBP) <90 mm Hg or mean arterial blood pressure <65 mm Hg or a SBP reduction of >40 mm Hg from baseline, despite adequate fluid resuscitation (20–30 cc bolus over 30 min) |
| White blood cell count: >12,000/mm 3 ,<4000/mm 3 , or >10% immature cell |
Urinanalysis and microscopy consistent with infection Positive blood cultures Obvious cellulitis Purulent fluid drained from abnormal collection |
Renal dysfunction, presenting as oliguria Cardiac dysfunction, presenting as hypotension or myocardial depression Pulmonary dysfunction, presenting as severe hypoxia Tissue-level hypoperfusion, presenting as an elevated serum lactate level |
SIRS, Septic inflammatory reaction syndrome.
Diagnosis
A diagnosis of sepsis is surmised from history, signs, and symptoms. Confirmation is based on isolation of a specific causative pathogen. It is important to identify the culprit microbe to ensure that antimicrobial therapy is appropriate and targeted. Specimens for culture should be sent from all sources where organism growth is suspected. Blood, urine, and sputum specimens are a minimum. Tissue sampling from specific sources such as heart valves, bone marrow, and cerebrospinal fluid can also be important.
Treatment
Initial treatment of sepsis involves broad antimicrobial coverage coupled with supportive care of failing organs. The speed and appropriateness of therapy administered in the initial hours of sepsis can dramatically influence outcome. The replication of virulent bacteria can be so rapid that every minute may be crucial. As soon as specific microbiologic information is available, therapy should be tailored to the specific organism and its sensitivities. Choice of an antibiotic must also take into account the ability of the drug to penetrate various tissues, including bone, cerebrospinal fluid, lung tissue, and abscess cavities.
In addition to targeted antimicrobial therapy, supportive treatment relating to organ system dysfunction is essential. Early goal-directed optimization that targets oxygen delivery and cardiac output may improve outcome in sepsis.
Prognosis
Prognosis in sepsis depends on the virulence of the infecting pathogen(s), stage at which appropriate treatment is initiated, inflammatory response of the patient, immune status of the patient, and extent of organ system dysfunction. It is impossible to predict the outcome for any individual patient.
Management of anesthesia
Preoperative.
The most important considerations for a patient with sepsis requiring surgery are whether the surgery may be postponed pending treatment of sepsis and whether the patient’s condition may be improved before surgery. A treatment algorithm for septic patients ( Fig. 25.3 ) suggests goal-directed optimization of the patient’s condition. Resuscitation should be targeted to achieve mean arterial pressure above 65 mm Hg, central venous pressure of 8 to 12 mm Hg, adequate urine output, a pH without a metabolic (lactic) acidosis, and a mixed venous oxygen saturation above 70%.
Intraoperative.
Intraoperative management of patients with sepsis is challenging. Patients with sepsis may have limited physiologic reserve that renders them vulnerable to hypotension and hypoxemia with induction of anesthesia. Invasive monitoring, such as intraarterial blood pressure and central venous pressure monitoring, is usually indicated. Establishment of sufficient IV access to allow for volume resuscitation as well as transfusion of blood and blood components is essential. Antimicrobial prophylaxis appropriate for surgery is indicated. Ideally this would be combined with the treatment regimen for the pathogen thought to be responsible for the sepsis. Prophylactic antibiotics should be administered within 30 minutes of skin incision.
Postoperative.
Patients with sepsis invariably require ICU admission after surgery. In the ICU the priorities include support of failing organ systems, targeted antimicrobial therapy, and minimizing the likelihood of new infections such as a fungal infection, infection with Clostridium difficile, or the emergence of a resistant organism. Another important postoperative priority is continuation of antimicrobial therapy for only as long as it is indicated. Broad guidelines for treatment of patients with sepsis in the ICU have been published by the Society of Critical Care Medicine in the Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock.
Gastrointestinal infections
Clostridium difficile infection
C. difficile is an anaerobic, gram-positive, spore-forming bacterium that is the major identifiable cause of antibiotic-associated diarrhea and pseudomembranous colitis. It is clear today that most antibiotics can alter bowel flora, facilitating the growth of C. difficile. With the frequent use of broad-spectrum antibiotics, the incidence of C. difficile diarrhea has risen dramatically.
C. difficile infection is the most common cause of diarrhea in healthcare settings, resulting in increased hospital stays and higher morbidity and mortality among patients. The prevalence of asymptomatic colonization in the hospital, especially in older people, is over 20%. It is transmitted by spores that are resistant to heat, acid, and antibiotics. C. difficile is extremely hardy, can survive in the environment for prolonged periods of time, and is resistant to common disinfectants, which leads to transmission from contaminated surfaces and airborne spores. In approximately one-third of those colonized, C. difficile produces toxins that cause diarrhea. The two principal toxins are toxin A and toxin B. Toxin B is approximately 1000 times more cytotoxic than toxin A. Toxin A activates macrophages and mast cells. Activation of these cells causes production of inflammatory mediators, which leads to loss of intestinal barrier function and neutrophilic colitis. Toxin A is also an enterotoxin in that it loosens the tight junctions between the epithelial cells that line the colon, which helps toxin B enter these colonic cells.
A number of risk factors for C. difficile –associated diarrhea have been identified: advanced age (>65 years), severe underlying disease, gastrointestinal (GI) surgery, presence of a nasogastric tube, use of antiulcer medications such as proton pump inhibitors, admission to an ICU, long duration of hospital stay, long duration of antibiotic administration (risk doubles after 3 days), use of multiple antibiotics, immunosuppressive therapy or general immunocompromise, recent surgery, and sharing of a hospital room with a C. difficile –infected patient. Some antibiotics are frequently associated with C. difficile infection ( Table 25.6 ).
TABLE 25.6
Antibiotic Therapy Most Commonly Associated With Clostridium Difficile Infection a
| Clindamycin |
| Fluoroquinolones |
| Cephalosporins, carbapenems, monobactams |
| Macrolides |
| Sulfonamides |
| Penicillins |
| Tetracyclines |
Signs and symptoms
The most frequent symptoms of C. difficile infection are diarrhea and abdominal pain. Patients may be febrile with abdominal tenderness and distention. With perforation, patients may have an acute abdomen.
Diagnosis
The gold standard for diagnosis C. difficile infection is detection of C. difficile toxins A and B in stool. The detection of C. difficile antibody does not indicate current infection.
Treatment
Therapy for patients with C. difficile –associated diarrhea consists of fluid and electrolyte replacement, withdrawal of current antibiotic therapy if possible, and institution of targeted antibiotic treatment to eradicate C. difficile. Antibiotic treatment should be given orally if possible. The first-line regimen is oral metronidazole 500 mg three times daily. An alternative is oral vancomycin 125 mg four times daily. Vancomycin has a theoretical advantage over metronidazole, since it is poorly absorbed and may therefore be present in higher concentrations at the site of infection. The major downside to vancomycin is that it may promote the growth of vancomycin-resistant enterococci. In 2011, fidaxomicin was approved by the US Food and Drug Administration (FDA) for treatment of C. difficile infection. It appears to be equivalent in effect to vancomycin in curing infection and is superior to vancomycin in reducing the risk of recurrent C. difficile infection. It is, however, even more expensive than vancomycin therapy. Fecal microbial transplantation is another treatment for C. difficile infection. Transplantation of feces from a healthy tested donor administered in a solution via a nasoduodenal tube and the cessation of all antibiotics are successful in treating over 90% of recurrent C. difficile infections.
Additional therapies might include probiotics to restore normal bowel flora, but their usefulness has yet to be defined.
Prognosis
C. difficile infection accounts for considerable increases in length of hospital stays and more than $1.1 billion in healthcare costs each year in the United States. The condition is a common cause of significant morbidity and even death in elderly, debilitated, and immunocompromised patients.
Management of anesthesia
Preoperative.
It is generally the sickest patients with C. difficile colitis, including those whose infection does not improve with conventional therapy, who come for surgery such as subtotal colectomy and ileostomy. If the patient is hemodynamically unstable, major surgery should be deferred and an ileostomy, cecostomy, or colostomy performed as a temporizing intervention. Surgery is associated with high mortality. Resuscitation and preoperative treatment of metabolic derangements may be needed. Patients with C. difficile infection should be scheduled for surgery at the end of the surgical day so the operating room can undergo additional cleaning to minimize the risk of transmission to subsequent patients.
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