Current Problems in Surgery
Volume 44, Issue 10 , Pages 628-633, October 2007

In Brief

  • Traci L. Hedrick, MD

      Affiliations

    • Resident in Surgery, University of Virginia School of Medicine, Charlottesville, Virginia
    • ,
  • Philip W. Smith, MD

      Affiliations

    • Resident in Surgery, University of Virginia School of Medicine, Charlottesville, Virginia
    • ,
  • Leo M. Gazoni, MD

      Affiliations

    • Resident in Surgery, University of Virginia School of Medicine, Charlottesville, Virginia
    • ,
  • Robert G. Sawyer, MD

      Affiliations

    • Professor of Surgery, Medical Co-Director, Surgical Trauma ICU, University of Virginia School of Medicine, Charlottesville, Virginia

Article Outline

 

For thousands of years, surgery was most commonly used as a desperate attempt to cure various advanced forms of infectious diseases. Boils were lanced, infected traumatized limbs were amputated, and malodorous, purulent tumors were excised. Elective or urgent procedures were generally limited to the rare Central American who underwent trephination to cure headaches or the unfortunate 16th century Frenchmen who underwent herniorrhaphy, complete with orchiectomy (before Paré). Yet, before the germ theory or improvements in surgical care that made elective operations practical, devastating perioperative infectious complications were described. Before the advent of antibiotics, an infected surgical site was tantamount to a death sentence. Consequently, even in those relatively prehistoric times, the broadest definition of surgical infectious diseases emerged: infections that required surgery or those caused by surgery.

In the past century, however, the capability to perform ever more complicated procedures safely has altered the relationship between surgery and infectious diseases. Series of surgical advances have inevitably led to the uncovering of new and unexpected infections. Certainly the problem of serious primary infections that require surgical intervention still remains. However, the most exciting, complicated, and vexing infectious disease problems faced by surgeons today relate instead to diseases and entire patient populations created by modern medicine. Overall, these iatrogenic conditions are the consequence of advances that have improved human wellness, but each has come at a cost.

One of the first examples of the infectious consequences attributable to modern medicine must be credited to Ignaz Semmelweis, who realized that puerperal infections and mortality after childbirth were associated with birthing in the hospital (a theoretical medical advance) rather than at home. Furthermore, he realized that the mortality rate was higher among women who were cared for by students undergoing formal medical training (another advance) than for women delivered by midwives. His conclusion that medical students transferred infection from the dissection suite to the women awaiting delivery and his subsequent use of a chlorinated lime solution for hand washing led to a significant decline in maternal mortality rates. Even more remarkably, Semmelweis made this connection before wide acceptance of the germ theory of disease.

Later in the 19th century, Joseph Lister was mortified that almost one half of his amputation patients died from postoperative infections, known at that time as the “hospital disease.” Influenced by the work of Louis Pasteur, Lister realized that living microorganisms could be the cause of these deaths and that an antiseptic agent might be used to alleviate this suffering. He started to use carbolic acid, previously used to treat sewage, to prepare his surgical sites and noted a remarkable decrease in the number of infections and deaths. Although the adoption of aseptic procedures came fairly rapidly, the underlying germ theory of disease took surprisingly longer to gain acceptance.

In 1928 Sir Alexander Fleming discovered the antibacterial properties of penicillin, perhaps the single greatest contribution to the evolution of modern medicine. The ability to mass produce penicillin, however, awaited World War II where the drug would be credited with saving thousands of lives from many combat-related infections, particularly in the amputated limb. In 1947, though, resistance to penicillin began to emerge and by the mid-1950s, penicillin-resistant Staphylococcus aureus was widespread and causing significant surgical morbidity and mortality, especially related to surgical site infections. The production of antibiotics from new classes was able to ameliorate this unexpected consequence, although the struggle to combat the negative effects of resistance using this strategy continues to this day.

The acute respiratory distress syndrome (ARDS) was first described by Ashbaugh in 1967.1 Although the mortality rate from ARDS initially was extraordinarily high due primarily to pulmonary failure, improvements in ventilatory strategies led to a significant new population of patients, those requiring long-term mechanical ventilation and intensive care support. The subsequent development of intensive care units with the ability to sustain patients with multisystem organ failure allowed the emergence of various iatrogenic septic or infectious conditions including ventilator-associated pneumonia (VAP), catheter-related sepsis, and bloodstream infection. These new and challenging infections have led to much of the current danger associated with hospitalization, and the optimal approach to treatment remains elusive; indeed, the basic definition and diagnosis of many of these infections stay in flux even to this day. Despite these new forms of “iatrogenic” disease, the overall survival rate for the underlying pathology leading to the need for intensive care has almost uniformly improved with time.

The 1980s were notable for the explosive increase in the numbers of immunosuppressed patients, due principally to the human immunodeficiency (HIV) virus, bone marrow transplants, ablative chemotherapy, and solid organ transplantation. Although the former 3 conditions only indirectly impact surgeons, solid organ transplantation, made feasible and widely available through advances in immunosuppression with the introduction of cyclosporine and tacrolimus, remains a solidly surgical field. Although the number of transplant surgeons who normally care for this population is small, the increasing number of organ recipients has already begun to impact specialists outside of the transplant field who might be asked to evaluate or treat a patient locally in the emergency department, clinic, or hospital. A good working knowledge of the infections related to the surgical aspects of transplantation that may arise acutely in these patients is useful for the practicing general surgeon in the community. This knowledge base should include not only simple technical concerns that frequently can be extrapolated from nonimmunosuppressed patients, such as draining an abscess or opening an infected wound, but also an idea of the pathogens that are found more frequently in these infections, such as fungi and vancomycin-resistant enterococci.

During the beginning of the new millennium, however, the most contentious topic related to the ongoing interaction between medical and surgical progress and the generation of new infectious diseases is the subject of antimicrobial resistance. Broadly speaking, resistant pathogens are generated in 1 of 2 ways. The first occurs when normally nonpathogenic organisms become pathogenic in the setting of an abnormal host response or the systematic suppression of other more common microorganisms via the administration of systemic antibiotics. The second mechanism is the induction of resistance in common pathogenic organisms and is strongly related to antimicrobial use and abuse, such as extended-spectrum β-lactamase producing Escherichia coli. In either case, surgeons must have a basic understanding of the relationship between the appropriate and inappropriate use of antibiotics and antimicrobial resistance. Two examples to illustrate these relationships include the emergence of Clostridium difficile colitis and community-acquired methicillin-resistant S. aureus.

Clostridium difficile is an organism that is often present in the normal human gastrointestinal flora without sequelae as long as balance is maintained between various classes of comensal bacteria. Over the past 25 years, however, C. difficile has become the most common identifiable bacterial cause of diarrhea after the administration of antibiotics.2 Although initially attributed to lincomycin and clindamycin use, all of the commonly used classes of antibiotics have now been associated with the overgrowth, toxin production, and morbidity associated with active C. difficile disease.2 Disturbingly for surgeons, significant C. difficile disease has been described frequently after the administration of prophylactic antibiotics, even when administered as a single dose.3 Traditionally, C. difficile-associated diarrhea has been considered mostly a nuisance, with short-term cure achieved with either metronidazole or oral vancomycin therapy. More recently, however, a particularly virulent strain of C. difficile has emerged. This strain, although best described in North America in reports from Pittsburgh and Quebec, shows striking similarities to strains from across the United States and Europe.4, 5, 6 The increased pathogenicity of these organisms is almost certainly due to an extraordinarily increased rate of production of both toxins A and B compared with other strains.7 This phenomenon appears to be on a per bacterium basis, because the growth kinetics of these strains do not appear to be different from less pathogenic strains. Many of these patients present in an atypical manner, with more severe systemic illness and the absence of diarrhea in a significant percentage of patients. The true pathogenic hallmark of this particular form of the disease, however, is rapidly progressive toxic megacolon frequently requiring emergent colectomy, sometimes within a day after presentation. Even with aggressive surgical treatment, the mortality rate is up to 50%. No specific therapy has yet been demonstrated to alter the incidence, endemicity, or mortality from this pathogen. Decreased rates of infection have been reported after the institution of strict hygiene procedures and isolation of infected patients.8 Simple measures, such as more thorough cleansing of rooms after the discharge of colonized patients and the use of soap and hand washing rather than alcohol-based hand rubs (C. difficile spores are resistant to alcohol) may be critical to stopping the spread of this complicated iatrogenic pathogen.8 However, ultimately cessation of the inappropriate use of antimicrobial therapy is paramount to prevention of this morbid, and sometimes mortal, infection.

One recently described organism that fulfills the concept of a common pathogen made more pathogenic after gaining antibiotic resistance is community-acquired methicillin-resistant S. aureus (CA-MRSA). CA-MRSA was originally described in patients from the upper Midwest United States.9 Many of the strains are genetically very similar, yet it is unclear how, when, or where this pathogen arose, and how its genesis was related to antibiotic usage. Several characteristics of CA-MRSA appear to differentiate it from the more common hospital- or health care-associated MRSA (HA-MRSA). First, unlike HA-MRSA, CA-MRSA tends to maintain sensitivity to clindamycin and trimethoprim-sulfamethoxazole.10 Second, CA-MRSA predominantly affects young healthy people, including children, soldiers, and athletes.11 Finally, under certain circumstances, CA-MRSA appears to be significantly more virulent than nonresistant strains, possibly related to the increased elaboration of the Panton-Valentine leukocidin (PVL), a pathogenicity molecule that may be associated with increased tissue destruction.12 Indeed, although the majority of patients with disease caused by CA-MRSA will have large skin and subcutaneous abscesses that can be treated with adequate incision and debridement followed by meticulous wound care, both highly lethal necrotizing fasciitis and pneumonitis have been described.13 Interestingly, the relationship between antibiotic resistance and virulence is far from clear, because skin lesions appear to heal frequently and equally well with active or inactive antibiotics.14 On the other hand, both necrotizing fasciitis and pneumonitis can be highly lethal even when active (as defined by in vitro susceptibility testing) antibiotics are promptly initiated.

In summary, the balance between medical progress and the generation of new vulnerable patient populations and infections can be expected to continue unabated for the foreseeable future. Some of the deleterious iatrogenic effects of medical care are inevitable and must be accepted (eg, the immunosuppression necessary for the maintenance of transplanted organs and the accompanying significant infectious morbidity). Despite the fact that some of these complications are unavoidable, surgeons and other physicians must attempt to prevent any unnecessary biologic cost of their interventions. Perhaps the simplest and cheapest way to improve surgical infectious disease outcomes is to strive for the appropriate, evidence-based use of antibiotics for the prophylaxis and treatment of infection. These interventions are the focus of the current manuscript.

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References 

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  2. Aslam S, Hamill RJ, Musher DM. Treatment of Clostridium difficile-associated disease: old therapies and new strategies. Lancet Infect Dis. 2005;5:549–557
  3. Privitera G, Scarpellini P, Ortisi G, Nicastro G, Nicolin R, de Lalla F. Prospective study of Clostridium difficile intestinal colonization and disease following single-dose antibiotic prophylaxis in surgery. Antimicrob Agents Chemother. 1991;35:208–210
  4. Hubert B, Loo VG, Bourgault AM, et al. A portrait of the geographic dissemination of the Clostridium difficile North American pulsed-field type 1 strain and the epidemiology of C. difficile-associated disease in Quebec. Clin Infect Dis. 2007;44:238–244
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  8. Cherifi S, Delmee M, Van Broeck J, Beyer I, Byl B, Mascart G. Management of an outbreak of Clostridium difficile-associated disease among geriatric patients. Infect Control Hosp Epidemiol. 2006;27:1200–1205
  9. Saravolatz LD, Pohlod DJ, Arking LM. Community-acquired methicillin-resistant Staphylococcus aureus infections: a new source for nosocomial outbreaks. Ann Intern Med. 1982;97:325–329
  10. Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med. 2006;355:666–674
  11. Elston DM. Community-acquired methicillin-resistant Staphylococcus aureus. J Am Acad Dermatol. 2007;56:1–16quiz 7-20.
  12. Chini V, Petinaki E, Foka A, Paratiras S, Dimitracopoulos G, Spiliopoulou I. Spread of Staphylococcus aureus clinical isolates carrying Panton-Valentine leukocidin genes during a 3-year period in Greece. Clin Microbiol Infect. 2006;12:29–34
  13. Frazee BW, Salz TO, Lambert L, Perdreau-Remington F. Fatal community-associated methicillin-resistant Staphylococcus aureus pneumonia in an immunocompetent young adult. Ann Emerg Med. 2005;46:401–404
  14. Paydar KZ, Hansen SL, Charlebois ED, Harris HW, Young DM. Inappropriate antibiotic use in soft tissue infections. Arch Surg. 2006;141:850–854discussion 5-6.

PII: S0011-3840(07)00106-2

doi:10.1067/j.cpsurg.2007.06.007

Current Problems in Surgery
Volume 44, Issue 10 , Pages 628-633, October 2007

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