!! Understand each type of antimicrobial drug resistance that can. occur.!! Discuss the history and discovery of antimicrobials.

Transcription

1 CHAPTER 1 NURSES ROLE IN PREVENTING ANTIMICROBIAL RESISTANCE (10 Contact Hours) Learning objectives!! Define and distinguish between antimicrobial terms.!! Understand each type of antimicrobial drug resistance that can occur.!! Discuss the history and discovery of antimicrobials.!! Compare and contrast the antimicrobial drug classes.!! Understand the manner in which antimicrobial therapy can be managed successfully.!! List each of the hospital-acquired antimicrobial drug resistances that can occur (methicillin-resistant staphylococcus aureus, vancomycin-resistant enterococci and extended spectrum beta lactams).!! Compare and contrast the respiratory antimicrobial resistance noted in the hospital and community (streptococcus pneumonia, tuberculosis and pseudomonas aeruginosa).!! Discuss the most common sexually transmitted infection resistance (N. gonorrhoeae).!! Understand the antimicrobial resistance noted in clostridium difficile.!! Differentiate the antimicrobial resistance seen in viral infections (influenza, human immunodeficiency virus, herpes simplex virus and hepatitis).!! Understand the implication of agricultural effects on antimicrobial drug resistance globally.!! Discuss the general scope of preventing antimicrobial drug resistance.!! Discuss and differentiate the various types of isolation.!! Understand the specific manner for nurses to prevent antimicrobial drug resistance. Overview Throughout history, nurses have always been on the front line caring for patients to prevent infections and treat those battling various types of infections related to bacteria, fungus, viruses and parasites. Once a bacterial infection has developed, it is imperative that proper antibiotics be administered to eliminate the bacteria and to prevent it from spreading to other areas within the body. For the past half century, the discovery and use of antimicrobial agents has prevented serious complications posed by infectious diseases. The development and success of antimicrobial agents against diseases caused by various microbes has been one of modern medicine s greatest achievements. To this day, the use of antimicrobial agents continues to save the lives of people who have access to health care and the ability to complete the prescribed doses. Although antimicrobials are wonder drugs in fighting bacteria, viruses, fungus and parasites, many patients have developed resistance to the agents. Antimicrobial resistance is an adaptive response in which microbes tolerate the amount of medication that previously halted the growth of the organism [33]. The most resistance has emerged to antibiotics, chiefly because health care providers have written too many prescriptions for patients without a bacterial infection; organisms have shed sensitivity to the prescribed antibiotic class or dose; and patients have ingested antibiotics incorrectly. Many physicians and researchers have speculated that the widespread use of antibiotics has spurred an evolutionary adaptation that enables bacteria to survive these powerful drugs. The World Health Organization (WHO), Centers for Disease Control and Prevention (CDC), and Food and Drug Administration (FDA) have suggested that the bacterial infections that contribute the most to the emerging antimicrobial resistance are diarrheal diseases, respiratory tract infections, meningitis, sexually transmitted disease and hospital-acquired infections [41]. Antimicrobial resistance is a challenging, frustrating problem for health care providers, patients and the community. Unfortunately, a patient who has developed resistance to a certain antibiotic and/or a class of antibiotics may develop further complications or die. It is important that nurses understand their role to prevent patients from becoming resistant to antimicrobial agents, especially antibiotics that may potentially save their lives. Unless we collaborate to potentially eradicate and reduce the risk of resistance, we may encounter a society faced with previously treatable diseases that are untreatable again, as in the days before antibiotics were developed. Antibacterial definitions The term antimicrobial is a broad, general term that encompasses agents produced synthetically or from natural sources that are able to fight against bacteria, viruses, fungus and parasites. There is not one drug that will eradicate all four of the microbes. Since each microbe is unique in its own genetic makeup, development and replication, practitioners need to ensure that they prescribe the appropriate agent to eradicate or inhibit the specific microbe. The CDC, Mosby s and Stedman s medical dictionaries are congruent in the definitions for the following terminology [22, 25, 32]: Bacteria are small, unicellular microbes that are encased in a rigid cell wall, an envelope. The morphology of bacteria includes spheric (cocci), rod shaped (bacilli), spiral (spirochetes) or comma-shaped (vibrios). Therefore, if the offending microbe is speculated or confirmed to be bacterial in nature, the practitioner will prescribe the appropriate class of antibiotic to eradicate the specific bacteria and to break down the rigid cell wall. There are several classifications of drugs that will be explored, such as penicillins and cephalosporins that are capable of weakening the cell wall and promoting lysis of the bacteria (See classification of antimicrobial drugs). Viruses are minute parasitic microbes that are smaller than bacteria. The unique component of viruses is that they do not have independent metabolic activity and they can only replicate within a cell of a living plant or animal host. A virus consists of a core of nucleic acid deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) surrounded by a coat of antigenic protein that may be surrounded by an envelope of lipoprotein. Depending upon the type of virus, the practitioner will allow it to run the course and/or prescribe an antiviral agent. Antibiotics should never be prescribed for a viral illness. 1 Funguses are eukaryotic, thallus-forming organisms that feed by absorbing organic molecules from their surroundings. Fungi lack chlorophyll and therefore are not capable of photosynthesis. They are treated by antifungal agents. Parasites are organisms that live in or on a different organism. Parasites are treated by antiparisitic agents. Throughout this course, the term antimicrobials will be used to describe mechanisms to fight microbes. In some literature, the term anti-infective is used interchangeably with antimicrobials. Microbes are small microorganisms that are not visible to the naked eye and require a microscope to be detected. The terms microbes and microorganisms are used interchangeably, and microbes will be used here. Many times, the term antibiotic chemotherapy is used in the literature. As nurses, when we hear the word chemotherapy, we automatically think of drugs that suppress cancer cells. Although

2 that is accurate, antibiotic chemotherapy is defined as the use of chemicals against invading microbes, making the term applicable to the treatment of both cancer and infectious diseases. Types of drug resistance Microbes are living organisms that evolve over time by their ability to divide and proliferate efficiently and quickly. The unique component of microbes is that even if an antimicrobial ceases the microbe s ability to spread, genetic changes can evolve that will enable it to survive. The microbe s genetic versatility and adaptability make it difficult for practitioners to try to circumvent or inactivate the aggravating microbe. And when drug resistance occurs, it will render a previous treatment useless, creating a potential clinical crisis and an imminent need for a new medication [27, 33]: Intrinsic resistance occurs with an alteration in the structure and function of the microbe based upon the genome. Mutation. Microbes reproduce by dividing every few hours, allowing them to evolve rapidly and adapt to new environmental conditions that may potentially arise. In spontaneous DNA mutation, bacterial DNA may mutate spontaneously; drug-resistant tuberculosis arises this way. Microbes are very adaptable organisms. A key factor in the development of antibiotic resistance is the ability of infectious organisms to adapt quickly to new environmental conditions. Of all of the microbes, bacteria are more efficient in enhancing the effects of resistance secondary to their ability to multiply rapidly and transfer their resistance genes [41]. Microbes elaborate drug metabolizing enzymes. At this time, many bacteria have become resistant to penicillin G because of an increased production of penicillinase, an enzyme that converts penicillin to an inactive product. Because practitioners so often prescribe penicillin products in general, resistance may develop. Every time a patient takes penicillin or another antibiotic for a bacterial infection, the drug may kill most of the bacteria present. However, a few tenacious germs may survive by mutating or acquiring resistance genes from other bacteria. The surviving genes can multiply quickly, creating drug-resistant strains. The presence of these bacterium strains affects the next infection because the patient may not respond to the prescribed antibiotics. In addition, the resistant bacteria may be transmitted to others in the patient s community. Gene transfer. Microbes acquire genes from each other, including genes that make the microbe drug resistant. Chromosomal mutations or extra chromosomal DNA are transferred from a resistant species to a sensitive one. Microbial drugs receptors change. Sometimes bacteria become resistant to certain antibacterials, such as streptomycin. Unfortunately, streptomycin is losing its effectiveness because of structural changes in the ribosomes of bacteria. According to the Alliance for the Prudent Use of Antibiotics (APUA), intrinsic, genetic causes occur in about one in 10 million cells [1]. At any given point, there are numerous, distinct microbes present in any population, and a constant rate of mutations does occur. When resistance does occur, the end result will vary from a slight change in microbial sensitivity, which can be treated with larger doses of the medication, to complete loss of sensitivity. Acquired resistance occurs through random events that are increased by the use of the drug. Conjunction. Conjunction is the process by which an extrachromosomal DNA is transferred from one gram-negative bacterium to another. In order for this process to occur, the 2 donor organism must possess two unique DNA segments, one that codes for drug resistance and one that codes for sexual apparatus. Together, the two codes constitute the resistance (R) factor. A potentially dangerous scenario to contemplate is that a single plasmid can provide many different types of resistance. Research has demonstrated that plasmids encoded with drug resistance are naturally present in microbes before they have been exposed to the medication. The most common forms of bacteria that are affected by the (R) factor include gram-negative bacilli, such as pseudomonas and vibrio cholera; and gram-positive bacteria, such as bacillus and staphylococcus. In 1968, 12,500 people in Guatemala died in an epidemic of shigella diarrhea. The microbe harbored a plasmid that carried resistances to four antibiotics [40]. Selective pressure. In the presence of antimicrobials, microbes will cease existing or they will survive if resistance genes are present. To prevent selective pressure, it is imperative that a patient who has a bacterial infection be prescribed an antibiotic that is sensitive to the bacterium. Unfortunately, any microbes that survive will replicate, and then their progeny will become dominant. Selective pressure becomes a potential problem when antibiotics are prescribed when there are no bacteria present and the drugs provide no benefit to the patient. Once the bacterium is present and antibiotics are introduced, it will create selective pressure, favoring the overgrowth of microbes to become resistant. Spontaneous mutation. Spontaneous mutation produces random changes in the DNA of the microbe causing an increase in resistance. Initially, it will begin with a low-resistance, then with additional mutations (use) it will become high-resistance. The most common cause of spontaneous mutation is related to overuse of the medication due to societal pressures. Society as a whole has a misconceived notion that an antibiotic will improve the symptoms and eradicate the organism that causes a person to become ill. Unfortunately, antibiotics are too often inappropriately prescribed, leading to antimicrobial resistance such as in the following scenarios: Incorrect diagnosis. A provider assumes an illness is bacterial in origin when it is instead viral. A patient may develop resistance. Incorrect prescription. If a practitioner speculates the source of infection is one source of bacteria and it is another, then the bacteria will continue to proliferate. In addition, certain sources of bacteria require heavier doses of antibiotics in order to eradicate the infection. Misuse of antibiotics. There are various ways patients may abuse the use of antibiotics. Many times, patients will either not complete their prescribed antibiotics or they will take a leftover antibiotic for a subsequent illness. Patients who do not complete their prescribed antibiotics and/or they take a remnant dose may develop resistance. Some patients also illegally purchase antimicrobial therapy from other countries on the Web because their attending provider does not prescribe an antimicrobial; others shop around to find a provider who will prescribe an antibiotic. Hospital use. Critically ill patients are more susceptible to infections and thus require heavier use of antimicrobials. Often the complexity of the patient s condition and numerous, heavy doses of antibiotics predispose the patient to potential drug resistance. It is

3 estimated that approximately 70 percent of the bacteria that cause infections in the hospitals are resistant to at least one of the drugs most commonly used for the treatment and eradication of that bacteria [36]. Even more dangerous, some forms of bacteria are so resistant to antibiotics that previously eradicated them that only experimental toxic medications are being prescribed. In addition, the complexity of critically ill patients also predisposes other patients in hospitals and long-term care facilities to various bacteria and resistance. Hospitals also provide a fertile environment for antibiotic-resistant germs because of close contact among sick patients and extensive use of antibiotics. Community-acquired bacteria are also becoming resistant to bacteria at alarming rates, especially staphylococci and pneumococci (streptococcus pneumonia) infections. In a recent study, 25 percent of bacterial pneumonia cases were shown to be resistant to penicillin, and an additional 25 percent of cases were resistant to more than one antibiotic [36]. Agricultural use. Another much-publicized concern is the use of antibiotics in livestock, where the drugs are used to prevent disease in well animals that are later slaughtered for food. For over 50 years, farmers have administered antibiotics to their livestock to ensure the health of animals, sometimes placing low levels in livestock s food to increase the rate of weight gain and improve the efficiency of converting animal feed to units of animal production [40]. Scientists fear that certain bacteria that develop resistance in animals can then infect people who eat meat or other animal products. It is difficult to precisely measure the impact on human health, but experts believe that resistant strains of salmonella, campy-lobacter, enterococcus, and Escherichia coli (E.coli) have been transmitted from animals to people. (See the section on the impact of agriculture on antimicrobial resistance). As noted, there is a plethora of reasons antimicrobial resistance occurs. Antibiotics are designed to eradicate specific bacteria; they are not mutagenic and do not directly cause the genetic changes that underlie drug sensitivity. However, with continuous use, spontaneous mutation and conjunction will occur. The CDC reiterates the concept and estimates that the major factor in the emergence of antibiotic resistance bacteria is attributed to the overuse and misuse of antibiotics [7]. The more antibiotics are used, the faster drug resistance will emerge in our society. Antibiotics may be a double-edged sword when they are overused; although they can heal, they also can promote emergence of resistant pathogens and the overgrowth of normal flora that possess the ability to develop resistance [33]. It is important to understand this concept and to avoid prescribing antibiotics when they are not needed because normal flora can transfer resistance to potential pathogens. Due to the complexity and importance of certain contributing factors to the development of antimicrobial drug resistance, some causes will be further elaborated throughout this chapter. Remember, anytime antibiotics are used, one or more microorganisms may survive. As these bacteria reproduce, they pass this antibiotic resistance to subsequent generations. Stronger antibiotics are then used, which can escalate the cycle of antibiotic resistance. It is more likely to occur when antibiotics are stopped prematurely (before all bacteria are killed), or when prescribed inappropriately. Therefore, people must understand that if it is not bacterial in nature, they must let the viral infection run its course. The CDC speculates that many providers are sometimes quick to prescribe antibiotics for all sorts of symptoms, even though antibiotics work only against bacterial infections not viruses such as those that cause the flu or the common cold. Most biologists do not consider viruses to be living things, but instead as infectious particles. More than 50 million of the 150 million antibiotic prescriptions written each year for patients outside of hospitals are unnecessary, according to a recent CDC study (see chart) [39]. Source [38] History of antimicrobials During ancient times, researchers note that human cultures used alternative measures to control microbes, such as boiling water, burying wastes and burying or embalming the deceased. In addition, primitive medications, such as potions, poultices and mud plasters, were extracted from various plants, animals and mineral products with a trial-and-error approach [33]. Although their life expectancy was shorter, people attempted to halt the growth of microbes based upon the minimal opportunities that they had available to them at that time. It was not until the last century, a revolutionary time of technological growth, that physicians had the tools available to research and discover antimicrobial therapy. The first antimicrobials discovered were antibiotics. Interestingly, the first antibiotic, penicillin was initially discovered by a French medical student, Ernest Duchesne in 1896, and then rediscovered between the years of by Sir Alexander Fleming. Mr. Fleming discovered the antibiotic penicillin while observing the inhibition of staphylococci on an agar plate contaminated by a penicillium mold. Although he was able to slow the growth of the mold, he was unable to isolate it. Over a decade later, in 1939, Ernst Chain and Howard Florey developed a way to isolate the penicillin and used it to treat bacterial infections during World War II. Although penicillin began to be used to treat and eradicate horrendous wounds inflicted during the war by gram-positive bacteria, such as staphylococci and streptococci, within four years of use, microbes began appearing that could resist the drug. By the 1960s, as many as 80 percent of staphylococcus aureus (S. aureus), a gram-positive bacteria, was resistant to penicillin. With the discovery and implementation of penicillin, other physicians began to synthesize other classes of antibiotics. In the late 1930s, Gerhard Domagk, a German doctor, announced the discovery of a synthetic molecule with antibacterial properties that he named prontosil, a sulfonamide (sulfa) drug. Prontosil was introduced to clinical use in the 1930s and was used to combat 3

4 urinary tract infections, pneumonia and other conditions. Then, in the late 1940s and early 1950s, new antibiotics were introduced by different physicians, including streptomycin (an aminoglycoside), chloramphenicol (a bacteriostatic antimicrobial) and tetracycline (a broad-spectrum antibiotic), and the age of antibiotic chemotherapy came into full being. Once various classes of antibiotics were discovered and implemented, various forms of bacterial pathogens, such as gram-positive, gram-negative, intracellular parasites and the tuberculosis bacillus, were being eradicated, saving endless lives. Classification of antimicrobial drugs Regardless of the venue or specialty a nurse pursues in his or her career, each professional will be responsible for administering antimicrobials. Prior to implementing the order written by the provider, the nurse needs to be familiar with the classification, action and purpose for administering the antimicrobial. In general, antibiotics are chemical compounds that interfere with the specific bacteria s internal processes, inducing cell damage or death, thus eradicating it from the body. While not all antibiotics work the same way, the goal is to disrupt the cell process or structure of the microbe to prevent replication of the invading bacteria. [33]. Antibiotics are complex medications that require the nurse to be knowledgeable about the drug and to be diligent during the administration process. There are some antimicrobials that are active against only a few microbes called narrow-spectrum antibiotics; others are active against a wide variety and are broad-spectrum. To add to the complexity, there are over 260 different antimicrobial drugs that are currently classified in 20 drug families. The most commonly used classes will be explored as they relate to potential antimicrobial resistance [22, 33]: Antibacterial drugs that weaken the bacterial cell wall (penicillin, cephalosporins, carbapenem and vancomycin). 1. Penicillin antibiotics are a large and diverse group of compounds that end in the suffix -cillin. All penicillin drugs consist of three parts: a thiazolidine ring, a beta-lactam ring and a variable side chain that dictates its microbicidal activity. For a penicillin drug to be effective, the cell wall must be permeable with a mesh-like structure within it. Inside the cytoplasmic membrane the osmotic pressure is extremely high, creating an environment for the bacteria to absorb water and swell [33]. The penicillins weaken the cell wall, causing the bacteria to absorb the excess water and then rupture [22]. Penicillins are considered the drug of choice for infections by known sensitive, gram-positive cocci, such as streptococci and gram-negative bacteria (meningococci and the spirochete of syphilis). Synthetic penicillins, such as ampicillin, carbenicillin and amoxicillin are broader spectrum; therefore they can be used to treat infections by gram-negative enteric rods (haemophilus influenzae, Escherichia coli, salmonella and shigella) because they are able to penetrate the outer membrane. Extended-spectrum penicillins (antipseudomonal penicillins) consist of four drugs, ticarcillin, carbenicillin indanyl, mezloicillin and piperacillin. These drugs are susceptible to the aminopenicillins plus pseudomonas aeruginosa, enterobacter species, proteus, bacteriodes fragilis and klebsiella. All are susceptible to beta lactamases, hence ineffective against most strains of S. aureus. Penicillinase-resistant penicillins, such as methicillin, nafcillin and cloxacillin, are useful in treating infections caused by some penicillinase-producing bacteria. 4 The major problems with penicillins include: Allergic reactions. As many as 1 in 10 of all patients who receive penicillins will experience an allergic response. Reactions may appear as a mild rash to a life-threatening anaphylactic reaction. To date, there has been no direct relationship between the size of the dose and the intensity of the allergic response [22]. Resistant strains of pathogens, especially bacteria encapsulated by a beta-lactamase ring. Beta-lactamase activity can occur in gram-positive organisms (staphylococcus aureus and staphylococcus epidermidis); gram-negative organisms (haemophilus influenzae, neisseria gonorrhea, moraxella [formerly branhamella] catarrhalis, Escherichia coli, and proteus, serratia, pseudomonas and klebsiella species); and anaerobic organisms (bacteriodes species) [21]. Bacteria encapsulated by a beta-lactamase ring are eliminated by combining a penicillin or cephalosporin with a beta-lactamase inhibitor, such as one of the following combinations [33]: Ampicillin + sulbactam = unasyn. Amoxicillin + clavulanic acid = augmentin. Ticarcillin + clavulanic acid = timentin. Piperacillin + tazobactam = zosyn. Clavulanic acid is a chemical that inhibits beta-lactamase enzymes, thereby increasing the longevity of beta-lactamase antibiotics in the presence of penicillinase-producing bacteria. Beta-lactamase inhibitors have a minimal risk of toxicity and any adverse reactions that may occur with the combination drugs are related to the penicillin component. Bacterial resistance to penicillins develops by two factors [22]: 1. Inability of the penicillins to reach their targets. 2. Inactivation of penicillins by bacterial enzymes. It is important to note that although all bacteria are surrounded by a cell envelope, the envelopes differ in grampositive and gram-negative bacteria [22]: The cell envelope of gram-positive bacteria has only two layers, the cytoplasmic membrane plus a relatively thick cell wall. Although the membrane is thick, it can be easily penetrated by penicillins. The cell envelope of gram-negative bacteria has three layers; the cytoplasmic membrane, a thin cell wall and an additional outer membrane. The penicillins can penetrate the first two layers of the gram-negative wall, but have difficulty reaching and breaking through the outer layer. Therefore, penicillins are typically inactive against gramnegative organisms. 2. Cephalosporins are a newer group of antibiotics that currently account for the majority of all antibiotics administered today. Cephalosporins are similar to penicillins in their beta-lactamase structure, bactericidal and active against a broad spectrum of antibiotics. Similar to penicillins, cephalosporins bind to penicillin-binding proteins and activate enzymes that cleave to the cell wall, therefore damaging the cell wall. The generic names of cephalosporins have the root of cef-, ceph-, or kef-. Cephalosporins are versatile drugs that are relatively broad-spectrum and resistant to most penicillinase. Cephalosporins typically have fewer, less severe adverse reactions compared to penicillins, such as a maculopapular rash that develops in several days.

5 Although adverse reactions are lower in cephalosporins, research has provided ranges from a 5-30 percent risk of crossover sensitivity in patients who are allergic to penicillin [22].If a patient has suffered a severe, immediate hypersensitive penicillin reaction, a cephalosporin should never be administered [33]. There are four generations of cephalosporins that exist. Cephalosporins develop antimicrobial resistance due to the production of beta-lactamases, which is further discussed in the descriptions of each generation. [33] First-generation cephalosporins, such as cephalothin and cefazolin, are most effective against grampositive cocci but few gram-negative bacteria. Although all cephalosporins are capable of destroying the beta-lactamase, they are not all equally susceptible. For instance, most first-generation cephalosporins are destroyed by beta-lactamases. Second-generation cephalosporins, such as cefaclor and cefonicid, are more effective than the firstgeneration cephalosporins in treating infections induced by gram-negative bacteria, such as enterobacter, proteus and haemophilus. Third-generation cephalosporins, such as cephalexin (Keflex) and cefotaxime, are broad-spectrum antibiotics that are stable in the presence of bacteria with a beta lactamase ring. A newer semi-synthetic broad spectrum, ceftriaxone (rocephin) treats a wide variety of respiratory, skin, urinary and nervous system infections. The third- and fourth-generation cephalosporins are highly resistant to destroying beta lactamases. Although the third generations are stable in the presence of beta-lactamase, they should not be used routinely and instead used only when specific conditions arise to prevent the emergence of organisms to resist the antibiotic. Fourth-generation cephalosporins, such as cefepime, may be prescribed as needed. The majority of prescriptions written are the third-generation cephalosporins. Classification First generation. Second generation. Activity against gram-negative bacteria Low gram-negative activity, however, more active against grampositive bacteria (staphylococci, nonenterococcal streptococci) and prophylaxis for surgical patients. Higher, especially with pneumonia caused by haemophilus influenzae and klebsiella. Resistance to betalactamases Low. Higher. 5 Classification (continued) Activity against gram-negative bacteria Third generation. Higher, especially Higher. for meningitis because they are able to penetrate the cerebrospinal fluid (CSF). Fourth generation. Highest. Highest. Source [22] Resistance to beta lactamases 3. Carbapenems are beta-lactam antibiotics that have very broad antimicrobial spectrums. At this time, the three carbapenems available are only administered parentally. Imipenem. Meropenem. Ertapenem. 4. Vancomycin (vancocin, vancoled) is a potentially toxic drug that is used only for serious bacterial infections, such as antibiotic-associated pseudomembranous colitis (caused by C.difficile), infections with methicillin-resistant staphylococcus aureus (MRSA), and treatment of serious gram-positive infections in patients allergic to penicillins (i.e. staph epidermidis). The most common complications with vancomycin include reversible ototoxicity, flushing, tachycardia, hypotension and thrombophlebitis. Antibacterial drugs that inhibit protein synthesis (tetracyclines, macrolides, clindamycin, zyvox and aminoglycosides). These drugs suppress bacterial cell growth and replication, but do not kill the bacteria. The following drugs are considered secondline drugs due to emerging antimicrobial resistance. 1. Tetracyclines are broad-spectrum antibiotics that suppress bacterial growth by binding to ribosomes and blocking protein synthesis. Tetracyclines inhibit gram-positive and gram-negative rods and cocci, aerobic and anaerobic bacteria, mycoplasma, rickettsias and spirochetes. Tetracycline compounds include doxycycline and minocycline to primarily treat sexually transmitted infections (STI). Antimicrobial resistance occurs with tetracyclines because of reduced drug accumulation, increased drug inactivation, and decreased access by a drug to ribosomes. 2. Macrolides are big moleculer, broad-spectrum antibiotics that act by suppressing bacterial synthesis. Erythromycin (EES) is one of the oldest and safest members of the family. Other macrolides include azithromycin, clarithromycin, dirithromycin, derivatives of erythromycin. EES is the drug of choice for streptococcus pneumoniae, group A streptococcus pyogenes, legionella pneumonia, bordetella pertussis and chlamydial infections. 3. Others include clindamycin (cleocin), which is notorious for causing pseudomembranous colitis. Clindamycin is active against most gram-positive and gram-negative bacteria, although gram-negative bacterium are developing resistance (B. fragilis). At this time, clindamycin is preferred for abdominal and pelvic

6 infections caused by B. fragilis and/or as a substitute for penicillin G infections. Linezolid (zyvox) is a new member; at this time it has excellent activity against multidrug-resistant grampositive pathogens, including vancomycin-resistant enterococcus (VRE) and MRSA. Therefore, avoid using it unless needed for the treatment of VRE or MRSA. 4. Aminoglycoside drugs are composed of two or more amino sugars and an aminocyclitol (6-carbon) ring. Aminoglycoside drugs have a relatively broad antimicrobial spectrum because they inhibit protein synthesis (in the bacterial cell 30S ribosomal subunit). However, they are used more for narrowspectrum microbials, primarily against gram-negative bacilli. Sensitive organisms include Escherichia coli, klebsiella pneumoniae, serratia marcescens, proteus mirabilis and pseudomonas aeruginosa. Although aminoglycosides have low gastrointestinal absorption, the patient needs to be closely monitored due to the potential toxicities (nephrotoxicity, ototoxicity). Aminoglycosides are useful for treating infections induced by aerobic gram-negative rods and certain gram-positive bacteria. Aminoglycosides are typically prescribed for infections caused by enterobacteriaceae or P. aeruginosa. However, over the years, resistance has developed in P. aeruginosa. The most common aminoglycosides are streptomycin, gentamicin, tobramycin and amikacin. In the United States, gentamicin is the most commonly prescribed aminoglycoside. Aminoglycosides are typically prescribed in combination with beta lactamase agents. Over the years, aminoglycosides have developed resistance caused by the presence of one or more mechanisms: inactivation of the drug by the aminoglycoside modifying enzymes (AMEs) produced by bacteria, ribosomal alterations that prevent the drug from binding to the site of action, or loss of permeability of the bacterial cell to the drug [3]. On a positive note, although a patient may have developed a resistance to one aminoglycoside, it is not predictive of resistance to another because they vary in their drug specificity. Antibacterial drugs that disrupt the synthesis of tetrahydrofolic acid (sulfonamides) Bacterial growth is suppressed because the synthesis of folic acid (folate) is inhibited. Folate is a compound required by all cells for the biosynthesis of DNA, RNA and proteins. 1. Sulfonamides. Sulfonamides were the first drugs available for the systemic treatment of bacterial infections and are considered broad-spectrum antibiotics. Due to newer antimicrobial therapy and a high amount of drug resistance, sulfonamides are reserved for urinary tract infections (UTI). About 90 percent of UTIs are due to Escherichia coli, a bacterium that is highly sulfonamide sensitive. Sulfonamides have developed antimicrobial resistance by spontaneous mutation or by transfer of the R factor. Resistance is especially high among gonococci, meningococci, staphylococci, streptococci and shigellae. Miscellaneous antibacterial drugs (fluoroquinolones and metronidazole) 1. Fluoroquinolones include drugs that end in -oxacin, such as ciprofloxacin (cipro) and ofloxacin. Ciprofloxacin inhibits bacterial DNA gyrase, an enzyme 6 2. that converts closed circular DNA into a supercoiled configuration. To date, the precise mechanism of cell death is not completely understood. Ciprofloxacin has great broad-spectrum activity, including gram-negative and gram-positive bacterium. Many urinary tract infections are sensitive, such as Escherichia coli and klebsiella. Antimicrobial resistance has developed during treatment of staphylococcus aureus, serratia marcescens, C. jejuni and P. aeruginosa due to alterations in DNA gyrase and reduced ability of ciprofloxacin to cross bacterial membranes. Metronidazole (flagyl) is used for protozoal infections caused by anaerobic bacterium. In order for it to be effective, the drug must be taken up by the cells and then converted to its active form. Only anaerobes can perform this unique function. Metronidazole is active against many anaerobic bacterial infections. Other antimicrobial drugs include the following: 1. Anti-mycobacterial agents. Mycobacteriums are slowgrowing microbes that require prolonged treatments. Due to the prolonged therapy, patients typically develop drug toxicity, non-compliance and/or drug resistance. (See tuberculosis under respiratory. ) 2. Antifungal drugs. Fungi cells are eukaryotic and there are currently four main drug classifications to treat fungal infections. Systemic mycoses are used to treat opportunistic infections (candidiasis, aspergillosis, cryptococcosis and mucormycosis) and non-opportunistic infections that can occur in any host (sporotrichosis). 3. Anti-parisitic chemotherapy drugs. Due to the enormous diversity among protozoan and parasites, there are numerous approved and experimental drugs on the market. a. Antimalarial drugs. For over a hundred years, quinine has been utilized as the principle treatment for malaria. In past years, quinine was extracted from the bark of cinchona tree, but later replaced by the synthesized quinolones. b. Chemotherapy for other protozoan infections. The most common amebicide is metronidazole (flagyl), which is effective in treating mild and severe intestinal infections and hepatic disease. Quinicrine (a quinine-based drug), sulfonamides and tetracyclines also have antiprotozoan activities. c. Anti-helminthic drug therapy. Treating helminthic infections, such as flukes, tapeworms and roundworms, is accomplished by blocking the reproduction and inhibiting the metabolism of all stages of the life cycle. 4. Antiviral drugs. Viruses are unique because the infectious agent relies on the host cell for the majority of its metabolic functions. Therefore, in order to eradicate infections induced by certain viruses, the drug needs to disrupt the metabolism of the host cell. It should be noted, all viruses are not treated with antiviral agents; many resulting ailments typically run their course, such as colds, measles, and mumps. The majority of viral compounds need to exert their effects on the completion of the virus cycle by barring complete penetration of the virus into the host cell, blocking the transcription and translation of viral molecules and preventing the maturation of viral particles. The most common antiviral medications prescribed include but are not limited to the following:

7 Acyclovir (zovirax), which blocks DNA synthesis in a small group of viruses, especially the herpes virus. The herpes virus has developed resistance to acyclovir due to: Decreased production of thymidine kinase. Alteration of the thymidine kinase. Alteration of viral DNA polymerase that is less sensitive to inhibition. AZT (zidovudine) and others are administered for human immunodeficiency virus (HIV). (See HIV under the section on antimicrobial drug resistance and antiviral agents) Amantadine and rimantadine are used for the treatment of viruses restricted exclusively to the influenza A virus (flu). Whereas relenza and tamiflu are effective prophylactic and standard treatments against influenzas A and B, in order for the medication to be effective, it needs to be administered early in the virus infection to ensure that it can inhibit the fusion and uncoat the virus. Inhibit protein synthesis Aminoglycosides Amikacin Genamycin Streptomycin Macrolides Azithromycin Clarithromycin Erythromycin Quinolones Ciprofloxacin Enoxacin Lomefloxacin Levofloxacin Norfloxacin Ofloxacin Sparfloxacin Sulfonamides Acetyl sulfisoxazole Sulfamenthoxazole Sulfasalazine Trimethoprim/sulfamethoxazole Tetracyclines Demeclocycline Doxycycline Minocycline Oxytetracyclilne Tetracycline Table Source [18] Table 1: Actions of antibiotics Disrupt cell membrane Beta-lactamase inhibitors Aztreonam Cefotetan Cefoxitin Imipenem/cilastatin Loracarbef Cephalosporins Cefaclor Cefadroxil Cefamandole Cefazolin Cefixime Cefonicid Cefoperazone Cefotaxime Cefprozil Ceftazidime Ceftriaxone Ceftizoxime Cefuroxime Cephalexin Penicillins Amoxicillin Ampicillin Bacampicillin Carbenicillin Mezlocillin Penicillin G Penicillin V Piperacillin Ticarcillin Managing the success of antimicrobial therapy Prior to deciphering the most adequate antibiotic to give a patient, the practitioner must consider the patient s age, allergies, potential microbes based upon the diagnosis, drug sensitivity, host factors, bacteria with a beta lactamase ring and risk of drug resistance. There is a vast array of variables to contemplate to ensure the bacteria will be eradicated and potential complications for the patient and/or the community. They include: Patient s age. While caring for a young child, pregnant woman or an elderly patient, it is important to consider the body s ability to absorb, distribute, metabolize and excrete the medication. Young children, such as neonates and infants, have a difficult time in the following [8]: Absorbing drugs in their gastrointestinal system due to a variable and prolonged gastric emptying time, prolonged transit time and peristalsis. Gastric acidity reaches adult levels between 1 to 2 years of age, and the gastric emptying time once it reaches the adult level between 6 to 8 months. Peripheral circulation is poorly developed, leading to vasoconstriction, causing decreased absorption. Less muscle mass (25 percent of body weight versus 40 percent in adults) provides a smaller area for absorption of intramuscular (IM) medications. Therefore, IM and subcutaneous routes are not the best choices for the neonate. Immature enzymes systems (until 2 to 4 years of age), which affects drug metabolism. Smaller number of tubular cells, shorter tubules, decreased renal flow and a decreased glomelular filtration rate (GFR). Unfortunately, that results in a longer half life and increased absorption of drugs, especially penicillins and aminoglycosides. Pregnancy. In pregnancy, certain medications are passed through the blood-brain barrier (BBB) into the placenta, posing a risk to the developing fetus. Therefore, it is important to assess the efficacy of the drug for the patient and the unborn patient if it crosses the blood-brain barrier, increasing the risk of tetragenic complications. The FDA has developed a pregnancy risk classification table to help providers choose the appropriate medication for their patients. (See the table on the following page). Most providers will only prescribe antimicrobials classified in category B, and avoid prescribing any antimicrobials in category D. 7

8 FDA pregnancy risk classification in relation to antimicrobial therapy Category A Category B Category C Category D Category X Controlled studies in women fail to demonstrate a risk to the fetus in the first trimester. There is no evidence of risk in later trimesters. The possibility of fetal harm appears remote. Animal reproduction studies have not demonstrated a fetal risk, but there are no controlled studies in pregnant women. Or, animal reproduction studies have shown an adverse effect (other than a decrease in fertility), but which was not confirmed in controlled studies of women in the first trimester (and there is no evidence of risk in later trimesters). Either studies in animals have revealed adverse effects on the fetus (causing abnormalities or death) and there are no controlled studies in women or studies in women and animals are not available. Drugs in this category should be given only if the potential benefit justifies potential risk to the fetus. There is positive evidence of human fetal risk, but the benefits from the use in pregnant women may be acceptable despite the risk for example, if the drug is needed in a life-threatening situation or for a serious disease for which safer drugs cannot be used or are ineffective. Studies in animals or humans have demonstrated fetal abnormalities; there is evidence of fetal risk based on human experience, or both. The risk of use of the drug in pregnant women clearly outweighs any possible benefit. The drug should not be used by women who are or may become pregnant. No antimicrobials are in the category A. 1. Penicillins. 2. Beta-lactamase inhibitors (augmentin). 3. Macrolides (arythromycin, azithromycin). 4. Cephalosporins (all generations). 5. Metronidazole. 1. Macrolides (clarithromycin). 2. Sulfa (bactrim). 3. Aminoglycosides (gentamicin). 4. Other (vancomycin). 5. Fluroquinolones. 1. Tetracycline (doxycycline). Not related to antimicrobial therapy. Table Source [8] In addition, absorption is decreased due to a diminished gastric tone and motility, which may cause the drug to stay in the stomach longer. Elderly. Similar to the young, elderly patients have difficulty absorbing, distributing, metabolizing and excreting their medications [8]: Common conditions affecting the absorption process in the elderly include malabsorption, diarrhea or constipation. Many times, the elderly have heightened drug sensitivity due to the decreased rate of metabolism and drug excretion. There is a decrease in the liver mass, volume and blood flow, which affects the ability of the liver to eliminate the medication. As a rule of thumb, liver metabolic activity declines 1 percent every year after the age of 40. Allergies. The most common, severe drug allergy is with the penicillins. It is important to always ask the patient about any drug allergies. Asking the specifics: What has happened when you have taken the medication in the past? A true allergy results in a hypersensitive response due to immunoglobulin E (IgE) mediators. The symptoms include [22]: Respiratory: difficulty breathing and wheezing. Cardiac: tachycardia and rapid pulse. Skin: hives (urticaria) and rash. Swelling (edema) of the lips, tongue or face. Potential microbes. A list of the most common pathogens, based upon various literature, can be found on the next page [24]. 8

9 Site Most common bacteria identified Preferred antimicrobial Alternative treatment in resistant cases Otitis media (OM). S. pneumonia (+) 49 percent. Over 10 percent resolve spontaneously without treatment. H. influenzae (-) 29 percent. Over 50 percent resolve spontaneously without treatment. M. catarrhalis (-) 28 percent. Over 90 percent resolve spontaneously without treatment. Sinusitis. S. pneumonia 31 percent, (+). H. influenzae 21 percent (-). M. catarrhalis 2 percent (-). Virus 15 percent. Sore throat. Most common group A. B-hemolytic streptococci (+) If a virus is the contributing factor, no antibacterial should be prescribed. Other bacterial sources, neisseria gonorrhoeae, mycoplasma and chlamydia trachomatis. Bronchitis. Typically viral in nature, therefore no antibiotics for teenagers and young adults with acute bronchitis. For acute bronchitis exacerbation, viruses (20-50 percent), C.pneumonia 5 percent, M Pneumonia <1 percent. Pneumonia. Streptococcus pneumonia; (+). Haemophilus influenzae; ( -). Staphylococcus aureus; +. Moraxella catarrhalis; -. There are other sources, klebsiella pneumonia, Escherichia coli, legionella and chlamydia. Genital tract. Chlamydia. N. gonorrhoeae. If no previous antibiotics in the past month: Amoxicillin mg/kg/day or erythromycin 50 mg/kg/day plus sulfonamide (150 mg/kg/day) for 10 days. Reserve antibiotic treatment for symptoms that persists over 7 days with maxillary/facial pain, purulent nasal discharge and/or severe pain/fever. Same antibiotics as used in the treatment of OM. Penicillin V potassium 250 mg po three times/day or 500 mg twice day/ for 10 days. If there is a penicillin allergy, erythromycin is prescribed (also effective against mycoplasma and chlamydia). Amoxicillin, doxycycline, bactrim for mild to moderate disease. If severe, azithromycin, clarithromycin or a fluoroquinolones. Preferred penicillin G and amoxicillin. Cefotaxime, ceftriaxone, cefuroxime, doxycycline, azithromycin and bactrim. If methicillin-susceptible treat with penicillin with or without rifampin. Cephalosporin 2nd or 3rd generation or a fluoroquinolones. Doxycycline 100 mg po BID x7 days or azithromycin 1 gram as a single dose. Alternative: Erythromycin 500 mg po BID x 7days. Ceftriaxone 1 gram. No fluoroquinolones due to an enormous amount of antimicrobial resistance. Increase resistance, especially among S. pneumonia (50 percent are resistant to macrolides). Cefaclor 20-40mg/kg/day or amoxicillin-clavulanate 20-40mg/kg/day. Cephalosporins (cefuroxime), erythromycin or amoxicillin with clavulanate (augmentin). 25 percent are developing erythromycin resistance. Alternatives: Macrolides, cephalosporins, doxycycline, fluoroquinolones, clindamycin and bactrim. Alternatives: fluoroquinolones and clarithromycin. Alternatives: cephalosporin, clindamycin, bactrim, vancomycin or fluoroquinolones. If methicillin-resistant strains, treat with vancomycin with or without gentamicin or rifampin. Bactrim, amoxicillinclavulanic acid (augmentin) or a macrolides. 9

10 Drug sensitivity. Optimal antimicrobial therapy is based upon the identified infecting organism and sensitivity of the medications. In order to assess drug sensitivity, a culture should be done if applicable. There are certain conditions in which a culture may not be feasible due to the location of the infecting organism, cost and decreased risk of drug resistance. At that time the patient is treated empirically, based upon a guess, as a result of the patient s subjective complaints and the practitioner s objective findings. However, if a potential invading organism has an increased risk of drug resistance, a culture should be completed to assess for the sensitivity of the drug. Disk diffusion tests also known as the Kirby-Bauer test. It is performed by inoculating an agar plate with the infecting organism and then placing on that plate several small disks, each impregnated with a different antibiotic [22]. Broth dilution procedure is similar to the Kirby-Bauer, but the bacteria are grown in tubes containing different concentrations of antibiotics. Both tests measure the drug sensitivity, assessed in two clinical values [22]. Minimum inhibitory concentration (MIC), defined as the lowest concentration of antibiotic that produces complete inhibition of bacterial growth, but does not kill the bacteria. Minimum bactericidal concentration (MBC), defined as the lowest concentration of drug that produces a 99.9 percent decline in the number of bacterial colonies, indicating a bacterial kill. Host factors. In addition to matching the drug with the infecting bug and determining the drug sensitivity, the host factors (host defenses and site of infection) must be considered [22]. Host defenses consist primarily of the immune system and phagocytic cells (macrophages and neutrophils). In order for antimicrobial therapy to be successful, it requires collaboration of the host defense system to subdue the infection. To be effective, the antibiotic must be present at the site of the infection in a concentration greater than the MIC. It may pose a challenge if the bacteria are in a difficult area, such as the blood-brain barrier, endocarditis and infected abscesses. Bacteria with a beta-lactamase ring. Beta-lactamases (ß-lactam) are enzymes that cleave to a beta-lactam ring, thus rendering the prescribed antibiotics inactive. ß-lactam antibiotics include penicillins, cephalosporins, monobactams and carbapenams. (See previous discussion under penicillins). Risk of drug resistance. Unfortunately, antimicrobial drug resistance is prevailing globally. Every individual is at risk of developing resistance to antimicrobials. However, there are certain risk factors that increase the risk: [33]. Overuse of antibiotics. Overuse of broad-spectrum antibiotics. Use of higher doses of antibiotics. In combination with the use and high doses of antibiotics, the faster drug-resistant organisms will emerge. Not only do antibiotics eliminate the targeted bacterium, they also affect normal flora that possess mechanisms for resistance. However, all antimicrobial drugs are at risk of becoming resistant as they promote the emergence of drug-resistant organisms. Over time, organisms become less susceptible to previously effective prescribed antimicrobials. However, broad-spectrum antibiotics are more prone to induce this phenomenon because they kill off more organisms than narrow-spectrum antibiotics. At this time, the organisms for which drug resistance has the most serious clinical problem include the following [28, 33]: VRE vancomycin-resistant enterococci. MRSA methicillin/oxacillin-resistant staphylococcus aureus. ESBLs extended-spectrum beta-lactamases (which are resistant to cephalosporins and monobactams). PRSP penicillin-resistant streptococcus pneumoniae. According to the National Institute of Allergy and Infectious Diseases, the most dangerous, emerging microbes affecting the community at large include vancomycin-resistant enterococci (VRE) and methicillin-resistant staphylococcus aureus (MRSA) [20]. Because each organism can increase the patient s risk of complications and/or death, each will be explored in depth. In June 2008, the United States (U.S.) Department of Health and Human Services provided a testimony based upon unpublished data from the CDC s National Nosocomial Infection Surveillance System indicating that [37]: More than 90 percent of staphylococcus aureus strains are no longer treatable with penicillins (See the section on staphylococcus aureus under hospital acquired antimicrobial drug resistance). One third of streptococcus pneumoniae isolates, a common cause of ear infections, pneumonia and meningitis, are also no longer treatable with penicillin (See the section on streptococcus pneumonia under hospital acquired antimicrobial drug resistance). There are many penicillin-resistant strains that, in fact, multiply resistance to other commonly used drugs such as ceftriaxone, erythromycin and trimethoprimsulfamethoxazole (bactrim). On the rise, other resistant strains include: Strains of salmonella newport, which cause infections in food animals, such as dairy cows, and have been shown to be resistant to as many as seven antibiotics. Although still small, there is a growing subset of the gramnegative bacterial strains that cause health care-associated infections such as acinetobacter baumannii and pseudomonas aeruginosa, which have become resistant to all available antimicrobial agents. Worldwide, tuberculosis caused by strains resistant to the two most commonly used anti-tuberculosis agents, isoniazid and rifampin, was recently estimated to affect approximately half a million persons annually. Recently, in the upper Midwestern U.S. the first ciprofloxacin-resistant strains of neisseria meningitides was reported. Due to the prevalence and delicate matter of antimicrobial drug resistance, each of the major bacteria will be analyzed in the subsequent sections. Hospital-acquired antimicrobial drug resistance (enterococci, staphylococcus aureus, extended spectrum beta lactamases) According to the CDC (2008), antibiotic-resistant infections are a prevalent problem for hospitals and nursing homes because it can spread from one patient to another from open wounds and impaired immune systems. In 2007, the Journal of American Medical Association estimated that 94,360 patients in the U.S. developed an invasive infection from antibiotic resistant MRSA in 2005; nearly one in five, or 18,650 of them, died [7]. Failure to control and/or 10

11 eradicate MRSA leads to prolonged hospitalization stays and the possible risk of death. According to the CDC (2006), in American hospitals alone, health care-associated infections account for an estimated 1.7 million infections and 99,000 associated deaths each year. Of these infections [5]: 32 percent of all health care-associated infections are urinary tract infections. 22 percent are surgical site infections. 15 percent are pneumonia (lung infections). 14 percent are bloodstream infections. Anyone can be colonized with drug-resistant microorganisms. Environmental cultures have shown vancomycin-resistant enterococci (VRE) and methicillin-resistant staphylococcus aureus (MRSA) on linens as well as hard surfaces such as bedrails, bedside stands, and medical devices. For example, use techniques that avoid contamination when collecting wound cultures [5]: 1. Rinse wound with saline to expose wound bed. 2. Do not culture wound exudates/drainage. 3. Swab edges and base of the wound. 4. Use culture tube swab; do not substitute cotton swab. Postoperative wound infections may be the result of contamination of the surgical wound during the procedure or migration of an infection from another infection site. It could also be a reactivation of an infection that occurred previously. For example, a common site of hospital-acquired infection is the urinary tract, secondary to a procedure or catheterization. Infection can occur when a microorganism moves to a location where it is not normally found. Some people are more susceptible to infection. These same people are often patients in a clinic or hospital. At-risk populations include [18]: The elderly. Individuals with suppressed immune systems. Individuals with orthopedic implant surgery. Individuals with other infection sites. The morbidly obese. Those using IV, catheter, feeding tube or other invasive lines or tubes. A history of long-term and/or frequent use of antibiotics, multiple hospitalizations and long-term inpatient care. 1. Enterococci drug resistance Enterococci, previously called group D strep, can cause everything from urinary tract to heart valve infections. enterococci are typically colonized in the gastrointestinal tract and female genital tract, but in patients with poor hygiene, it may be found on the skin surfaces. The most common resistant Enterococci include E. faecalis and E. faecium [19]. Enterococci have become resistant to antimicrobials, especially penicillin, ampicillin, piperacillin, imipenem and vancomycin, which are among the few antibiotics that show consistent inhibitory, but not bactericidal, activity against E. faecalis [22]. E. faecium are less susceptible to ß-lactam antibiotics than E. faecalis because the penicillin-binding proteins of the former have markedly lower affinities for the antibiotics. Vancomycin, also known as vancomycin-resistant enterococci (VRE) is related to intrinsic and acquired variables. In the hospital setting, E. faecium is the most isolated species of VRE producing high vancomycin (more than 128 ug/ml) MIC [19].VRE is typically colonized in the gastrointestinal (GI) tract and occasionally in the urinary tract. It is important to note that a patient may colonize the 11 bacterium but not show any signs or symptoms of infection. Risk factors for VRE infection and colonization include [17, 19 20]: Previous vancomycin and/or multiantimicrobial therapy. Severe underlying disease or immunosuppression. Long-term intravenous lines or urinary catheters. Third-generation cephalosporin utilization. Anti-anaerobic antibiotics (such as clindamycin). Fluoroquinolones (such as ciprofloxacin). Intra-abdominal surgery. Since enterococcus is typically found in the normal gastrointestinal and female genital tracts, most infections have been attributed to endogenous sources within the individual patient. However, recent reports of outbreaks and endemic infections caused by enterococcus, including VRE, have indicated that patient-to-patient transmission of the microorganisms can occur either through direct contact or through indirect contact via [19]: Hands of personnel. Contaminated patient-care equipment and/or environmental surfaces. Therefore, the CDC recommends that health care facilities screen for VRE with all new admitted or high-risk patients (intensive care, oncology and surgical patients) [22]. Screening for VRE includes swabbing the perirectal/anal area or collecting a stool specimen. If any patient tests positive for VRE, the physician and infection control team need to be notified immediately. In 1995, the CDC provided recommendations for the Hospital Infection Control Practices Advisory Committee (HICPAC) to be implemented nationwide in order to reduce the spread of VRE [14]. To date, the CDC has not updated or revised its recommendations: 1. Situations in which the use of vancomycin is appropriate or acceptable: For treatment of serious infections caused by betalactam-resistant gram-positive microorganisms. Vancomycin may be less rapidly bactericidal than are beta-lactam agents for beta-lactam-susceptible staphylococci. For treatment of infections caused by gram-positive microbes in patients who have serious allergies to beta-lactam antimicrobials. When antibiotic-associated colitis fails to respond to metronidazole therapy or is severe and potentially life-threatening. Prophylaxis, as recommended by the American Heart Association (AHA), for endocarditis following certain procedures in patients at high risk for endocarditis. Prophylaxis for major surgical procedures involving implantation of prosthetic materials or devices (e.g., cardiac and vascular procedures and total hip replacement) at institutions that have a high rate of infections caused by MRSA or methicillinresistant S. epidermidis. A single dose of vancomycin administered immediately before surgery is sufficient unless the procedure lasts greater than six hours, in which case the dose should be repeated. Prophylaxis should be discontinued after a maximum of two doses. 2. Situations in which the use of vancomycin should be discouraged:

12 3. Routine surgical prophylaxis other than in a patient who has a life-threatening allergy to beta-lactam antibiotics. Empiric antimicrobial therapy for a febrile neutropenic patient, unless initial evidence indicates that the patient has an infection caused by grampositive microbes (i.e., at an inflamed exit site of Hickman catheter) and the prevalence of infections caused by MRSA in the hospital is substantial. Treatment in response to a single blood culture positive for coagulase-negative staphylococcus, if other blood cultures taken during the same time frame are negative (i.e., if contamination of the blood culture is likely). Because contamination of blood cultures with skin flora (i.e., S. epidermidis) could result in inappropriate administration of vancomycin, phlebotomists and other personnel who obtain blood cultures should be trained to minimize microbial contamination of specimens. Continued empiric use for presumed infections in patients whose cultures are negative for beta-lactamresistant gram-positive microbes. Systemic or local (i.e., antibiotic lock) prophylaxis for infection or colonization of indwelling central or peripheral intravascular catheters. Selective decontamination of the digestive tract. Eradication of MRSA colonization. Primary treatment of antibiotic-associated colitis. Routine prophylaxis for very low birth-weight infants (i.e., infants who weigh less than 1,500 grams, which is equivalent to 3 pounds 4 ounces.) Routine prophylaxis for patients on continuous ambulatory peritoneal dialysis or hemodialysis. Treatment (chosen for dosing convenience) of infections caused by beta-lactam-sensitive grampositive microbes in patients who have renal failure. Use of vancomycin solution for topical application or irrigation. Enhancing compliance with recommendations: Although several techniques may be useful, further study is required to determine the most effective methods for influencing the prescribing practices of physicians. Key parameters of vancomycin use can be monitored through the hospital s quality assurance/improvement process or as part of the drug-utilization review of the pharmacy and therapeutics committee and the medical staff. Preventing and controlling VRE transmission in all hospitals requires the following recommendations: 1. Initiate the following isolation precautions to prevent patient-to-patient transmission of VRE: Place VRE-infected or colonized patients in private rooms or in the same room as other patients who have VRE. Wear gloves (clean, nonsterile gloves are adequate) when entering the room of a VRE-infected or colonized patient because VRE can extensively contaminate such an environment. When caring for a patient, a change of gloves might be necessary after contact with material that could contain high concentrations of VRE (e.g., stool) Wear a gown (a clean, nonsterile gown is adequate) when entering the room of a VRE-infected or colonized patient a) if substantial contact with the patient or with environmental surfaces in the patient s room is anticipated, b) if the patient is incontinent, or c) if the patient has had an ileostomy or colostomy, has diarrhea, or has a wound drainage not contained by a dressing. Remove gloves and gown before leaving the patient s room and immediately wash hands with an antiseptic soap or a waterless antiseptic agent. Hands can be contaminated via glove leaks or during glove removal, and bland soap does not always completely remove VRE from the hands. Ensure that after glove and gown removal and hand washing that clothing and hands do not contact environmental surfaces in the patient s room that are potentially contaminated with VRE (e.g., a doorknob or curtain). 2. Dedicate the use of noncritical items (e.g., a stethoscope, sphygmomanometer, or rectal thermometer) to a single patient or cohort of patients infected or colonized with VRE. If such devices are to be used on other patients, adequately clean and disinfect these devices first. 3. Obtain a stool culture or rectal swab from roommates of patients newly found to be infected or colonized with VRE to determine their colonization status, and apply isolation precautions as necessary. Perform additional screening of patients on the ward at the discretion of the infection-control staff. 4. Adopt a policy for deciding when patients infected or colonized with VRE can be removed from isolation precautions. The optimal requirements remain unknown; however, because VRE colonization can persist indefinitely, stringent criteria might be appropriate, such as VRE-negative results on at least three consecutive occasions (greater than or equal to one week apart) for all cultures from multiple body sites (including stool or rectal swab, perineal area, axilla or umbilicus, and wound, Foley catheter and/or colostomy sites, if present). 5. Because patients with VRE can remain colonized for long periods after discharge from the hospital, establish a system for highlighting the records of infected or colonized patients so they can be promptly identified and placed on isolation precautions upon readmission to the hospital. This information should be computerized so that placement of colonized patients on isolation precautions will not be delayed because the patients medical records are unavailable. 6. Local and state health departments should be consulted when developing a plan regarding the discharge of VRE-infected or colonized patients to nursing homes, other hospitals, or home-health care. This plan should be part of a larger strategy for handling patients who have resolving infections and patients colonized with antimicrobial-resistant microorganisms [33]. Staphylococcus aureus Staphylococcus aureus has been prevalent for over a hundred years [24]. Staphylococcus normally resides on the skin and mucous membranes, including the linings of the respiratory, intestinal, and genitourinary tracts. Healthy individuals with intact skin are able to prevent infection caused by staphylococci; however any break in skin integrity may lead to staphylococcal

13 infection. Approximately 25 to 30 percent of the population is colonized with staphylococcus aureus, especially in the nose; however they do not have an infection. Staphylococcus aureus bacteria are one of the most common causes of skin infections in the United States. Once penicillin was discovered, many patients infected by staphylococcus aureus were prescribed penicillin and responded very well. Physicians were so impressed by the success that penicillins were being prescribed all the time, and unfortunately led to the resistance in the late 1940s. Methicillin, a form of penicillin, was introduced to counteract the penicillin resistant to staphylococcus aureus. In 1961, Methicillin developed resistance to staphylococcus aureus, leading to the birth of MRSA. The danger with MRSA is the bacterium is resistant to the entire class of penicillins, including the beta-lactamases. In 2002, there were outbreaks of vancomycin-resistant staphylococcus aureus (VRSE) in the U.S., presenting physicians with a serious problem. According to the National Institute of Allergy and Infectious Diseases, there have been few additional cases, all occurring in Michigan and reported to the CDC [29]. MRSA is prevalent within the community (CA) and hospitals (HA). According to the Association for Professionals in Infection Control (APIC), the risk of MRSA is 46.3 per 1,000 inpatients in the U.S., which includes infection or colonization. In 2007, the Journal of the American Medical Association estimated that 94,360 patients in the U.S. developed an invasive infection due to an antibiotic-resistant staphylococcus (MRSA) in 2005 and nearly one of every five, or 18,650, died [7]. The alarming statistics are approximately eight to 11 times higher than previous estimates [2]. Community-acquired MRSA has been around since the 1990s. The media has publicized CA-MRSA over the past few years, since so many healthy people have been infected, such as high-school athletes and young children. It just reiterates that MRSA can affect anybody, as the CDC implies even the strong. Transmission of CA-MRSA is elusive as it may occur in crowded settings, close skin-skin contact, areas where personal contact may be prevalent (razors, towels, sporting equipment) and with personal hygiene. The CDC has noted that CA-MRSA is increased among athletes, military recruits, children, Pacific Islanders, Alaskan Natives, Native Americans, men who have sex with men, and prisoners. Hospital-acquired MRSA has been prevalent for decades, especially in elderly patients with weakened immune systems and/or who have recently had surgery or implanted surgical medical devices. Other risk factors include patients with urinary tract infections, pneumonia caused by staphylococcus aureus or kidney failure. Patients admitted to the hospital typically are prescribed intravenous antibiotics, approximately 25 to 40 percent, increasing their chance of a resistant germ originating within their own bodies. According to the CDC, in 2005,1 percent of all hospital in-patient stays, or 292,045 patients a year, were associated with staphylococcus aureus based upon a study of 14 million discharges between 2000 and 2001 [7]. Patients infected with staphylococcus aureus had about three times the length of hospitalization, three times the cost and five times the risk of in-hospital death. Approximately, 14,000 patients died from staphylococcus aureus. Another growing population that may be community- or hospitalacquired MRSA includes our soldiers returning from Afghanistan and Iraq. Unfortunately, many soldiers have been burned by 13 explosions, bombings and/or gunshot wounds, leading to severe infections, including MRSA. Many also have also been affected by drug-resistant MRSA due to the complexity of their injuries and antimicrobials administered overseas. According to the CDC, nurses and health care providers can differentiate community-acquired MRSA and hospitalacquired MRSA by adhering to the following criteria to confirm community-acquired MRSA [8]: Diagnosis of MRSA was made in the outpatient setting or by a culture positive for MRSA within 48 hours after admission to the hospital. No medical history of MRSA infection or colonization. No medical history in the past year of: Hospitalization. Admission to a nursing home, skilled nursing facility or hospice. Dialysis. Surgery. No permanent indwelling catheters or medical devices that pass through the skin into the body. MRSA is diagnosed based upon the culture results obtained from the infection site and sent to the microbiology laboratory. Depending upon the potential site, the CDC recommends the cultures be taken in the following way [8]: Skin infection: Obtained by a small biopsy or the drainage cultured from the infected site. Pneumonia: Obtained by a sputum culture (expectorated purulent sputum, respiratory lavage or bronchoscopy). Bloodstream infection: Obtained by blood cultures using aseptic techniques. Urinary infection: Obtained by collecting urine cultures using aseptic techniques. Some states require mandatory reporting of all positive MRSA outbreaks; verify the recommendations of the local health department in the jurisdiction of employment. Once S. aureus and/or MRSA are speculated and/or identified, immediate treatment is required. Since 2006, the CDC recommends the following treatment protocol [16]: Clindamycin is FDA-approved for the treatment of S. aureus. Tetracyclines (e.g., tetracycline, doxycycline, and minocycline) are FDA approved for the treatment of S. aureus, but not specifically to MRSA. TMP-SMX (Bactrim) is not FDA-approved for the treatment of any form of staphylococcal infection. However, the medical literature contains several case reports of the successful use of TMP-SMX in the treatment of S. aureus infections, including MRSA. In a case-series of CA-MRSA skin infections in Los Angeles, prompt resolution of symptoms was achieved in six (50 percent) of 12 patients initially treated with double-strength TMP/SMX alone (in addition to incision and drainage of abscesses) and in all of six patients treated initially with a combination of TMP/SMX and rifampin. Rifampin (should not be used as a single agent): Resistant strains of S. aureus are observed rapidly when rifampin is used as a single agent. Rifampin has been used in combination with other antimicrobial agents that are active against S. aureus to treat staphylococcal infections. Linezolid (Consultation with an infectious disease specialist suggested): Linezolid is FDA-approved for the treatment of

14 3. complicated skin infections and hospital-acquired pneumonia due to MRSA in adults. If it is CA-MRSA and/or speculated to be resistant to antimicrobial According to the National Committee for Clinical Laboratory Standards (NCCLS), each isolate should be considered a potential ESBL-producer if the test results are as follows: therapy, the CDC recommends treating the infection with a fluoroquinolone or a macrolide. In addition to prescribing appropriate antimicrobial therapy, the CDC recommends enforcing standard infection control precautions for all patients in outpatient and inpatient health-care settings. The process includes performing hand hygiene (hand Disk diffusion cefpodoxime < 22 mm. ceftazidime < 22 mm. aztreonam < 27 mm. MICs cefpodoxime > 2 µg/ml. ceftazidime > 2 µg/ml. aztreonam > 2 µg/ml. washing or using alcohol hand gel) after touching body fluids or cefotaxime < 27 mm. cefotaxime > 2 µg/ml. contaminated items (whether or not gloves are worn), between ceftriaxone < 25 mm. ceftriaxone > 2 µg/ml. patients, and when moving from a contaminated body site to a clean site on the same patient; wearing gloves when managing wounds; and wearing gowns and eye protection as appropriate for procedures that are likely to generate splashes or sprays of body fluids. In addition, contact precautions, which involve The treatment of choice is typically a fourth-generation cephalosporin and/or an antimicrobial specific to the organism based upon the microbiological analysis. Therefore, it is customized in each patient. greater spatial separation of patients (through placing infected patients in private rooms or cohorting patients with similar Respiratory antimicrobial drug resistance infection status), use of gown and gloves for all contact with the Pneumonia is the second-most common nosocomial infection in the patient or their environment, and use of dedicated noncritical U.S. and is associated with substantial morbidity and mortality. The patient-care equipment, have been recommended for empiric use majority of patients who have nosocomial pneumonia include the in patients with abscesses or draining wounds in which wound following [10]: drainage cannot be contained. Infants. Young children. According to data per the CDC (2008), there has been a 60 percent reduction in the rate of MRSA infections since the implementation of a series of infection control procedures. In addition, new national data from CDC s National Healthcare Safety Network (NHSN), a surveillance tool for hospitals and Persons greater than 65 years of age. Persons who have severe underlying disease, immunosuppression, depressed sensorium, cardiopulmonary disease. Persons who have had thoracoabdominal surgery. state health departments that measures health care-associated infections (HAIs), show that there has been a significant drop Another potential risk factor includes patients receiving mechanically in the incidence of both MRSA and methicillin-susceptible S. assisted ventilation. Although they do not represent the majority of aureus (MSSA) central line-associated blood stream infections patients who have nosocomial pneumonia, they are the highest risk among intensive care unit patients in U.S. hospitals over the for acquiring the infection. Most bacterial nosocomial pneumonias last five years. The incidence of MRSA bloodstream infections occur by aspiration of bacteria colonizing the oropharynx or upper per 1,000 central line days (i.e., a measurement of infection gastrointestinal tract of the patient. Since intubation and mechanical burden derived from the number of patients who have a central ventilation alter first-line patient defenses, they greatly increase the line, or catheter, whether infected or not) decreased by 49.6 risk for nosocomial bacterial pneumonia. percent, while the incidence of central line-associated MSSA Traditional preventive measures for nosocomial pneumonia include infections decreased even more substantially, by 70.1 percent. decreasing aspiration by the patient, preventing cross-contamination Data on invasive MRSA infections from the Active Bacterial or colonization via hands of personnel, appropriate disinfection Core Surveillance system for also show a decrease or sterilization of respiratory-therapy devices, use of available in hospital-onset and health care-associated MRSA infections, vaccines to protect against particular infections, and education of confirming this downward trend. Thus, it appears that these hospital staff and patients. New measures being investigated involve practical efforts to reduce the transmission of MRSA in hospitals reducing oropharyngeal and gastric colonization by pathogenic are working, thereby further reducing the need for antibiotic microorganisms. Several large studies have examined the potential usage [34]. risk factors for nosocomial-acquired bacterial pneumonia related to ESBLs Extended-spectrum beta-lactamases mechanically assisted ventilation and endotracheal intubation [10]: ESBLs are enzymes that mediate resistance to extended-spectrum In many studies, the administration of antacids and H-2 blockers (third-generation) cephalosporins (e.g., ceftazidime, cefotaxime, for prevention of stress bleeding in critically ill, postoperative, and ceftriaxone) and monobactams (e.g., aztreonam), but do not and/or mechanically ventilated patients has been associated with affect cephamycins (e.g., cefoxitin and cefotetan) or carbapenems gastric bacterial overgrowth. Sucralfate, a cytoprotective agent (e.g., meropenem or imipenem) [12]. It is important to recognize that has little effect on gastric power of Hydrogen (ph) and the presence of ESBL-producing organisms in certain clinical may have bactericidal properties of its own, has been suggested infections (klebsiella pneumoniae, K. oxytoca, or Escherichia as a potential substitute for antacids and H-2 blockers. In most coli) to avoid treatment failure. According to the CDC, the choice randomized trials, intensive care unit (ICU) patients receiving of the antimicrobial agent to test is critical: mechanically assisted ventilation who were treated either with Actively hydrolyze ceftazidime, resulting in ceftazidime only antacids or with antacids and H-2 blockers had increased minimum inhibitory concentrations (MICs) of 256 µg/ml, but gastric ph, high bacteria counts in the gastric fluid and increased have poor activity on cefotaxime, producing MICs of only 4 risk for pneumonia in comparison with patients treated with µg/ml. If an ESBL is detected, all penicillins, cephalosporins, sucralfate. and aztreonam should be reported as resistant, even if in-vitro Patients receiving continuous, mechanically assisted ventilation test results indicate susceptibility. have six to 21 times the risk for acquiring nosocomial pneumonia 14

15 compared with patients not receiving ventilatory support. One study indicated that the risk for developing ventilator-associated pneumonia increased by 1 percent per day. The rationale for the increased risk was attributed partially to carriage of oropharyngeal organisms upon passage of the endotracheal tube into the trachea during intubation, as well as to depressed host defenses secondary to the patient s severe underlying illness. In addition, bacteria can aggregate on the surface of the tube over time and form a glycocalyx (i.e., a biofilm) that protects the bacteria from the action of antimicrobial agents or host defenses. Some researchers believe that these bacterial aggregates can become dislodged by ventilation flow, tube manipulation, or suctioning and subsequently embolize into the lower respiratory tract and cause focal pneumonia. Removing tracheal secretions by gentle suctioning and using aseptic techniques to reduce cross-contamination to patients from contaminated respiratory therapy equipment or contaminated or colonized hands of health care workers (HCWs) have been used traditionally to help prevent pneumonia in patients receiving mechanically assisted ventilation. Another risk for pneumonia also is increased by the direct access of bacteria to the lower respiratory tract, which often occurs because of leakage around the endotracheal cuff, thus enabling pooled secretions above the cuff to enter the trachea. In one study, the occurrence of nosocomial pneumonia was delayed and decreased in intubated patients whose endotracheal tubes had a separate dorsal lumen that allowed drainage (i.e., by suctioning) of secretions in the space above the endotracheal tube cuff and below the glottis. However, additional studies are needed to determine the cost-benefit ratio of using this device. Another factor to contemplate are the devices we use in the hospital that may be potential reservoirs and vehicles for harboring infectious microbes, such as: Nebulizers. They can allow the growth of hydrophilic bacteria that subsequently can be aerosolized during use of the device. Gram-negative bacilli (e.g., pseudomonas sp., xanthomonas sp., flavobacterium sp., legionella sp., and nontuberculous mycobacteria) can multiply to substantial concentrations in nebulizer fluid and increase the risk for pneumonia in patients using such devices. Diagnostic examinations (bronchoscopes and spirometers). Administration of anesthesia. The internal components of anesthesia machines, which include the gas sources and outlets, gas valves, pressure regulators, flow meters and vaporizers, are not considered an important source of bacterial contamination of inhaled gases. Thus, routine sterilization or high-level disinfection of the internal machinery is unnecessary. Mechanical ventilators. The potential risk for pneumonia in patients using mechanical ventilators that have heated bubble-through humidifiers stems primarily from the condensate that forms in the inspiratory-phase tubing of the ventilator circuit as a result of the difference in the temperatures of the inspiratory-phase gas and ambient air; condensate formation increases if the tubing is unheated. The tubing and condensate can rapidly become contaminated, usually with bacteria that originate in the patient s oropharynx. In one study, 33 percent of inspiratory circuits were colonized with bacteria via this route within two hours, and 80 percent within 24 hours, after initiation of mechanical ventilation. Spillage of the contaminated condensate into the patient s tracheobronchial tree, as can occur during procedures in which the tubing is moved (e.g., for suctioning, adjusting the ventilator setting, or feeding or caring for the patient), may increase the risk for pneumonia in the patient. Thus, in many hospitals, health care professionals are trained to prevent such spillage and to drain the fluid periodically. Breathing circuits, humidifiers, and heat-moisture exchangers. The Environmental Protection Agency (EPA) and FDA recommend sterilizing/disinfecting devices by steam autoclave, ethylene oxide or subjecting it to high-level disinfection by pasteurization at a temperature of 75 degrees Celsius (C) for 30 minutes or by use of liquid chemical disinfectants. There are many variables that may exacerbate and/or increase the vulnerable patient to nosocomial pneumonia while they are hospitalized. It is our duty as nurses to be conscious of each potential risk and to do our part in preventing nosocomial infections from occurring. Failure to prevent will only further exacerbate our antimicrobial resistance problem. Penicillin resistant streptococcus pneumoniae (PRSP or pneumococcus) Although streptococcus pneumonia (S. pneumonia) is prevalent in general, there is limited recent data available on penicillinresistant S. pneumonia. The majority of the literature is based upon data from the 1990s to the early turn of the century. It is speculated that the majority of health care professionals are aware of the risk of drug-resistant S. pneumonia with penicillins, perhaps abating the notion that they over-write prescriptions for high-risk patients. Researchers have discovered that the resistance of pneumococcus to penicillin and cephalosporins is through alteration in the cell wall penicillin-binding proteins (PBPs). By altering these sites (where the antibiotics bind), the antibiotic affinity is decreased, subsequently decreasing the susceptibilities. This type of resistance can be overcome if the serum or site levels of the antibiotic exceed the minimum inhibitory concentration (MIC) of the organism for percent of the dosing interval [26]. According to the CDC, for more than 25 years, isolates of S. pneumoniae were initially susceptible to penicillin. However, since 1967, there has been a gradual increase in penicillinresistant S. pneumoniae, on average a 25 percent risk. In certain areas of the U.S., PRSP strains become widespread during the 1990s; Alaska had the highest reported prevalence at 26 percent. According to the CDC and New England Journal of Medicine (NEJM), a study conducted in Atlanta found a 25 percent prevalence of PRSP in the community. In 2004, 21.4 percent of all isolates obtained showed intermediate or resistant susceptibility patterns to penicillin (up from 20 percent in 2003). Outside the United States, an even higher (33 to 58 percent) prevalence of PRSP has been reported [26]. Pneumococcal infections are a leading cause of morbidity and mortality in the U.S.; S. pneumoniae causes more than 500,000 cases of pneumonia, 55,000 cases of bacteremia and 6,000 cases of meningitis annually, which result in 40,000 deaths. The death rate from pneumococcal bacteremia approaches 30 percent, despite the use of appropriate antimicrobial therapy. Reports of refractory illness due to resistant pneumococci demonstrate the clinical relevance of these strains. Identifying risk factors in the development of PRSP infections is important for both the prevention and treatment of these infections [26]. Streptococcus pneumoniae, or pneumococcus, is a bacterium that causes many different kinds of infections in people, ranging

16 from ear infections and sinus infections to pneumonia, meningitis and sepsis. Up to 30 percent of the strains of the bacterium are at least partially resistant to antibiotics in the penicillin family. Although the names (and bacterial genuses) are similar, S. pneumoniae is quite different from group A streptococcus (the bacteria that causes strep throat and rheumatic fever). S. pneumoniae infections are on average much more serious; pneumococcus is the most common cause of bacterial meningitis in the U.S., and about 8 percent of children with pneumococcal meningitis die of the infection. While one of four children will survive, they will suffer from neurologic damage including hearing loss after getting over the infection. Pneumococci are the most common cause of ear infections and sinus infections, as well as the most common bacteria found in the blood of children under 2 years old with fevers, many of whom have no obvious site of infection. Many people have pneumococci in their noses and throats but have no symptoms. The bacteria are transmitted from one person to another, usually by droplets. Like viral upper respiratory infections, pneumococcal infections are more common in winter. Infection can begin as little as one to three days after exposure. Studies of ear fluid cultures suggest that anywhere from 20 to 40 percent of ear infections are caused by pneumococcus. The signs of pneumococcal meningitis and sepsis can be the same as those of meningococcal meningitis. Often, however, pneumococcal infection can appear first as a high fever with a very high white blood cell count (where almost all of the white cells are neutrophils or bacteria-fighting cells) and no obvious site of infection. There are also some people who are more susceptible to pneumococcal infections than others. The risk factors include: Lack of a spleen due to injury or disease. Sickle-cell anemia because repeated sickle-cell crises cause damage to the red blood cells and destruction to the spleen tissue. Most doctors assume that the spleen of patients with sickle-cell disease will not be working by time they are in their 20s, at the latest. So sickle-cell patients are usually vaccinated against bacteria, such as pneumococcus and meningococcal, which the spleens of healthy people help kill. Immunodeficiencies, such as AIDS, decreased production of white blood cells and/or chronic illnesses. Although S. pneumonia is prevalent in various bacterial infections (upper, lower respiratory infections, meningitis, etc.) and a leading cause of death, it is highly resistant to not only penicillins, but also cephalosporins, sulfonamides, trimethoprimsulfamethoxazole (through amino acid changes), macrolides (through methylation or via an efflux pump), quinolones (through decreased permeability, efflux pumps, and alteration of enzymes), and chloramphenicol (through inactivating enzymes) [26]: Resistance rates of pneumococcal isolates in the United States to trimethoprim-sulfamethoxazole, doxycycline and the macrolides are relatively high. Some isolates (less than 10 percent in the United States) that are resistant to macrolides are also resistant to clindamycin. No vancomycin-resistant pneumococcal isolates have been reported to date. The phenomenon of tolerance (survival but not growth in the presence of a given antibiotic) has been observed, but its clinical relevance is unknown. Fortunately, in the U.S., most pneumococcal isolates remain susceptible to fluoroquinolones, but in certain countries and specific populations in whom the use of fluoroquinolones is more prevalent (e.g., nursing homes), an increase in resistance has 16 been seen. Although there is a 25 percent risk of penicillin drug resistance noted in streptococcus pneumonia, penicillin is still the mainstay drug of choice because 75 percent of the time it will work. Therefore, each patient is customized based upon his or her history and other risk factors. Depending upon the site and patient, the following guidelines are recommended [26]: Otitis media/sinusitis Amoxicillin mg/kg/day. If no improvement in hours, re-evaluate the patient and switch to amoxicillin-clavulanate or a second- or thirdgeneration oral cephalosporin, although highly resistant pneumococci may require treatment with parenteral ceftriax one in order to achieve adequate serum levels of antibiotics. Pneumonia Children Amoxicillin or amoxicillin-clavulanate at dosages used for the treatment of otitis media is recommended. In school-aged children (older than 5 years), the addition of a macrolide for coverage of atypical organisms is advised. In 2000, a new vaccine (prevnar) became available for children in the United States, and CDC began tracking the vaccine s impact on resistant pneumococcal infections. Since the vaccine was introduced into the routine childhood immunization program in the United States, penicillin-resistant pneumococcal infections declined by 35 percent. Not only has the vaccine been shown to prevent antibiotic-resistant infections, it has been shown to reduce the need for prescribing antibiotics for children with pneumococcal infection in the first place. CDC data also show that adults are getting fewer resistant pneumococcal infections because the vaccine is preventing spread of pneumococci from infected children to adult populations. Since 2001, it is estimated from CDC data that 170,000 severe pneumococcal infections and 10,000 deaths have been prevented by vaccine use. According to data published in the Archives of Pediatric Adolescent Medicine, the vaccine is highly cost-effective, saving an estimated $310 million in direct medical costs each year [50]. Adults Macrolide (or doxycycline) for outpatient therapy of previously healthy adults with no specific risk factors for resistant S. pneumoniae infection. Meningitis The recommended initial therapy of presumed bacterial meningitis in children is with vancomycin and ceftriaxone or cefotaxime at increased doses. If S. pneumoniae is isolated from the blood or cerebral spinal fluid (CSF) and is susceptible to penicillin or ceftriaxone/ cefotaxime, vancomycin should be stopped and therapy completed with penicillin G, ceftriaxone or cefotaxime as indicated. If the isolate is resistant to penicillin and cephalosporins, the regimen started initially should be continued through the completion of therapy, usually 10 days in uncomplicated cases. Most pneumococcal isolates in the United States remain susceptible to certain fluoroquinolones, including moxifloxacin (most effective), levofloxacin, gatifloxacin and gemifloxacin. Ciprofloxacin and ofloxacin have limited activity against pneumococcal infections. Fluoroquinolones provide broadspectrum treatment for CAP and achieve excellent serum drug levels and tissue penetration. Specific populations in whom the use of fluoroquinolones is traditionally increased (e.g., residents of nursing homes) have shown increased levels of pneumococcal

17 2. resistance to fluoroquinolones, and their empiric use in respiratory infections should also be tempered by the concern for rapid development of resistance to this class by many organisms [26]. Multiresistant pseudomonas aeruginosa Pseudomonas aeruginosa is noted for its environmental versatility, ability to cause disease in particularly susceptible individuals, and its resistance to antibiotics. The pathogens are widespread in nature, inhabiting soil, water, plants and animals, including humans. Pseudomonas aeruginosa has become an important cause of infection, especially in patients with compromised host defense mechanisms. It is the most common pathogen isolated from patients who have been hospitalized longer than one week, and is a frequent cause of nosocomial infections such as pneumonia, urinary tract infections (UTIs) and bacteremia. Pseudomonal infections are complicated and can be life-threatening. The bacterium is capable of utilizing a wide range of organic compounds as food sources, thus giving it an exceptional ability to colonize ecological niches where nutrients are limited. P. aeruginosa can produce a number of toxic proteins that not only cause extensive tissue damage, but also interfere with the human immune system s defense mechanisms. These proteins range from potent toxins that enter and kill host cells at or near the site of colonization to degradative enzymes that permanently disrupt the cell membranes and connective tissues in various organs. P. aeruginosa is an opportunistic pathogen. It rarely causes disease in healthy persons. In most cases of infection, the integrity of a physical barrier to infection (i.e., skin, mucous membrane) is lost or an underlying immune deficiency (i.e., neutropenia, immunosuppression) is present. Pseudomonas is both invasive and toxigenic. The three stages include: 1. Bacterial attachment and colonization. 2. Local infection. 3. Bloodstream dissemination and systemic disease. The importance of colonization and adherence is most evident when studied in the context of respiratory tract infection in patients with cystic fibrosis and in those that complicate mechanical ventilation. Production of extracellular proteases adds to the organism s virulence by assisting in bacterial adherence and invasion. According to Centers for Disease Control and Prevention data collected from , P. aeruginosa was the second-most common cause of nosocomial pneumonia (17 percent of the isolates), the third-most common cause of UTI (11 percent), the fourth-most common cause of surgical site infections (8 percent), the seventh-most common isolated pathogen from the bloodstream (3 percent), and the fifth-most common isolate overall (9 percent) obtained from all sites. Internationally, P. aeruginosa is common in patients with diabetes who are immunocompromised. Others at risk for P. aeruginosa include [1]: Cancer and burn patients, who also commonly suffer serious infections by this organism, as do certain other individuals with immune system deficiencies. Unlike many environmental bacteria, P. aeruginosa has a remarkable capacity to cause disease in susceptible hosts. It has the ability to adapt to and thrive in many ecological niches, from water and soil to plant and animal tissues. Elderly patients with vertebral osteomyelitis resulting from a pseudomonal infection Young people who experiment with intravenous (IV) drug abuse. All infections caused by P. aeruginosa are treatable and potentially curable. Acute fulminant infections, such as bacteremia pneumonia, sepsis, burn wound infections and meningitis, however, are associated with extremely high mortality. The clinical evaluation of the pneumococcal infections depends on the age and health of the patient, site and severity of the infection and the adequacy of the treatment. Penicillin was uniformly effective against pneumococcus until three decades ago, when the first reports of clinical resistance were published. Since then, there has been a rapid increase in the level and rates of resistance to penicillin, which parallels to beta lactamase and antimicrobials. Tuberculosis (TB) Tuberculosis (TB) is a disease that is spread from person to person through the air, and it is particularly dangerous for people infected with HIV. Worldwide, TB is the leading cause of death among people infected with HIV. According to the CDC, there are an estimated 10 million to 15 million Americans infected with the TB bacteria, with the potential to develop active TB disease in the future. About 10 percent of these infected individuals will develop TB at some point in their lives. The risk factors for developing TB include [35, 40]: Living in close proximity (i.e. incarcerated, group homes). Poverty (poor living conditions). Exposure to another with TB. HIV or acquired immunodeficiency diseases (AIDS). The risk of developing TB disease is much greater for those infected with HIV and living with AIDS. Because HIV infection so severely weakens the immune system, people dually infected with HIV and TB have a 100 times greater risk of developing active TB disease and becoming infectious compared to people not infected with HIV. CDC estimates that 10 to 15 percent of all TB cases and nearly 30 percent of cases among people ages 25 to 44 are occurring in HIVinfected individuals. Another problem with TB is the enormous resistance that has developed, called multidrug-resistant tuberculosis (MDR-TB). It is a form of tuberculosis that is resistant to two or more of the primary drugs used for the treatment of tuberculosis. Resistance to one or several forms of treatment occurs when the bacteria develop the ability to withstand antibiotic attack and relay that ability to their progeny. Since that entire strain of bacteria inherits this capacity to resist the effects of the various treatments, resistance can spread from one person to another. On an individual basis, however, inadequate treatment or improper use of anti-tuberculosis medications remains an important cause of drug-resistant tuberculosis [40]: In 2003, the CDC reported that 7.7 percent of tuberculosis cases in the U.S. were resistant to isoniazid, the first-line drug used to treat TB. The CDC also reported that 1.3 percent of tuberculosis cases in the U.S. were resistant to both isoniazid and rifampin. Rifampin is the drug most commonly used with isoniazid. The World Health Organization estimates that up to 50 million persons worldwide may be infected with drugresistant strains of TB. Also, 300,000 new cases of MDR-TB are diagnosed around the world each year, and 79 percent of the MDR-TB cases now show resistance to three or more drugs.

18 A strain of MDR-TB originally develops when a case of drug-susceptible tuberculosis is improperly or incompletely treated. This occurs when a physician does not prescribe proper treatment regimens or when a patient is unable to adhere to therapy. Improper treatment allows individual TB bacilli that have natural resistance to a drug to multiply. Eventually the majority of bacilli in the body are resistant. Once a strain of MDR-TB develops, it can be transmitted to others just like a normal drug-susceptible strain. Airborne transmission has been the cause of several well-publicized cases of nosocomial (hospital-based) outbreaks of MDR- TB in New York City and Florida. These outbreaks were responsible for the deaths of several patients and health care workers, a majority of whom were co-infected with HIV. MDR-TB has been a particular concern among HIV-infected persons. Some of the factors that have contributed to the number of cases of MDR-TB, both in general and among HIV-infected individuals, are: Delayed diagnosis and delayed determination of drug susceptibility, which may take several weeks. Susceptibility of immunosuppressed individuals for not only acquiring MDR-TB but also for rapid disease progression, which may result in rapid transmission of the disease to other immunosuppressed patients. Inadequate respiratory isolation procedures and other environmental safety conditions, especially in confined areas such as prisons. Noncompliance or intermittent compliance with antituberculosis drug therapy. MDR-TB is more difficult to treat than drug-susceptible strains of TB. The success of treatment depends upon how quickly a case of TB is identified as drug resistant and whether an effective drug therapy is available. The secondline drugs used in cases of MDR-TB are often less effective and more likely to cause side effects. FDA has approved rifater, a medication that combines the three main drugs (isoniazid, rifampin and pyrazinamide) used to treat tuberculosis into one pill. This reduces the number of pills a patient has to take each day and makes it impossible for the patient to take only one of the three medications, a common path to the development of MDR-TB. In June 1998, the FDA approved the first new drug for pulmonary tuberculosis in 25 years. The drug, rifapentine (Priftin), has been approved for use with other drugs to fight TB. One potential advantage of rifapentine is that it can be taken less often in the final four months of treatment once a week compared with twice a week for the standard regimen. Overall, the CDC s message is that resistance can be slowed if patients take medications correctly. Sexually transmitted infections (N. gonorrhoeae) 1. Neisseria gonorrhoeae Neisseria gonorrhoeae (N. gonorrhea) is the second-most common notifiable disease in the U.S with 339,593 cases documented in 2005[40]. Failure to control N. gonorrhea can lead to cervicitis, urethritis, proctitis and pelvic inflammatory disease (PID) with long-term sequels including infertility, ectopic pregnancy and chronic pelvic pain which all increase the risk of HIV. According to the Annals of Internal Medicine (1998), N. gonorrhea has developed resistance over the past 60 years to multiple antimicrobial classes [42]. In order to eradicate the infection and decrease transmission and complications to the 18 patient, it is imperative that effective treatment be initiated immediately. Initially, in 1936, sulfanilamides were used for treatment, but were short-lived due to the emergence of resistance in the 1940s. Over the next 40 years, penicillin was the drug of choice; however in the 1980s, penicillin developed resistance due to the spread of plasmid-containing genes. Therefore, ceftriaxone (a cephalosporin) was recommended for uncomplicated gonococcal infections. By 1989, penicillin was no longer used because resistance was widespread; therefore ceftriaxone became the recommended treatment, with ciprofloxacin as an alternative treatment option. In the early 1990s, quinolone-resistant N. gonorrhea emerged in the U.S., then spread worldwide by the turn of the century. Therefore, the CDC no longer recommends fluoroquinolones for the treatment of N. gonorrhea. Due to the epidemiology and significant antimicrobial resistance in the treatment of N. gonorrhea over the years, the CDC and WHO have recommended a change in the treatment when the prevalence of antimicrobial resistance exceeds 5 percent for a specific antibiotic [21]. The antimicrobial of choice requires a cure rate over 95 percent. In 2006, the CDC recommended cephalosporins as the primary treatment of choice [15, 42]: Ceftriaxone injection 125 milligrams (mg) intramuscular (IM) for uncomplicated urogenital and anorectal infection or cefixime 400 mg as a single dose. If a patient has a cephalosporin allergy: Azithromycin 2 grams orally. Spectinomycin 2 grams in a single dose IM initiated in History has proven that resistance eventually proliferates, especially in N. gonorrhea. To prevent and/or to prepare for the possible emergence of cephalosporin resistance, research studies are being implemented. Possible future treatments may include macrolides combined with either an aminoglycoside or the drug rifampin. In the interim, nurses can help the effort to control and prevent N. gonorrhea infection through proper education of patients and screening per the following recommendations [21, 42]: Primary screening. According to the U.S. Preventive Task Force (USPTF) and the American Academy of Family Physicians (AAFP), all sexually active men and women and any woman who is pregnant should be screened. The highest prevalence of N. gonorrhea occurs in sexually active individuals under the age of 25; people with prior gonorrheal infection or other sexually transmitted infections; those with new partners; and people who use drugs or are inconsistent about condom use. Secondary screening. All partners should be screened to prevent repeated infections and/or complications. Clostridium difficile (C. difficile) infections C. difficile disease can range from mild to debilitating diarrhea to more severe, life-threatening infections. The development of C. difficile infections among patients treated with antibiotics has long been considered an unintended consequence of antibiotic use. Recognized in the 1970s as a cause of antibiotic associated diarrhea in the 1980s and 1990s, these anaerobic bacteria species caused increasing numbers of outbreaks of diarrheal disease in hospitals and long-term care facilities. Recently, however, CDC and others have recognized the emergence of C. difficile disease, including more life-threatening forms of the disease, among otherwise healthy patients in the community.

19 A number of community patients had not taken antibiotics prior to their illness. Based on data from Ohio, estimates suggest that currently there may be as many as 500,000 cases of C. difficile infection occurring annually in the United States, contributing to between 15,000 and 30,000 deaths. Some antibiotic-resistant strains of C. difficile, including those resistant to macrolides and fluoroquinolones, are emerging. These strains appear to be more virulent due to increased toxin production and the presence of a novel virulence factor called the binary toxin. Surveillance data from other public health agencies around the world show such strains are spreading globally. While this antimicrobial resistance does not directly affect therapy for the C. difficile infection, since such infections are treated with other drugs, the resistance may allow C. difficile to spread more readily among patients who have received either a macrolide or fluoroquinolone antibiotic. This broadens even further the number of people at risk for acquiring disease [34]. Antimicrobial drug resistance and antiviral agents Antiviral drug resistance occurs due to a decrease in the susceptibility of the drug in a laboratory culture (a phenotype), change in the genetic makeup (genotype), and evolutionary changes over time (virus replicating over time) [11, 31]. The specific cause of antiviral drug resistance can be tested in the laboratory. At this time, the most prevalent antiviral resistance noted in the U.S. occurs with the following: Influenzae. According to the CDC (2008), amantadine and rimantadine were NOT recommended for use in the United States during the influenza season because many influenza viruses are resistant to these drugs. HIV. The primary reasons HIV treatment fails is due to poor drug compliance, pharmacological factors and drug resistance, but in many cases, failure occurs with resistant virus [46]. It is estimated that some HIV patients may be prescribed up to 30 tablets a day. Due to the significant prevalence of HIV-antiviral drug resistance, the National Institute of Health (NIH) (2007) recommends the following guidelines [30]: HIV drug-resistance testing is recommended for persons with HIV infection when they enter into care regardless of whether therapy will be initiated immediately. If therapy is deferred, repeat testing at the time of anti-retroviral therapy initiation should be considered. A genotypic assay is generally preferred for anti-retroviralnaïve persons. HIV drug-resistance testing should be performed to assist in selecting active drugs when changing anti-retroviral regimens in cases of virologic failure. Drug-resistance testing should also be performed when managing suboptimal viral load reduction. Drug-resistance testing in the setting of virologic failure should be performed while the patient is taking his/her antiretroviral drugs, or immediately (i.e., within four weeks) after discontinuing therapy. Genotypic-resistance testing is recommended for all pregnant women prior to initiation of therapy and for those entering pregnancy with detectable HIV RNA levels while on therapy. Drug-resistance testing is not advised for persons with HIV RNA less than 1,000 copies/ per milliliter (ml) because amplification of the virus is unreliable. Herpes virus. More than 45 million people nationwide have been infected by the genital herpes virus. The typical treatment for genital herpes includes drugs such as acyclovir, valaciclovir and famciclovir, which are widely used to treat infections with herpes simplex and varicella zoster. Researchers have noted drug resistance with acyclovir (5 to 10 percent), especially among patients with other immunocompromised disorders such as AIDS and recipients of bone marrow transplants [11]. Hepatitis virus. Although there are more than five types of hepatitis, researchers say hepatitis B has superseded as the one with the most-antiviral drug resistance. Drug resistance to lamivudine and famciclovir showed staggering increases over one year, 10 to 20 percent in patients with chronic hepatitis B [11]. It is speculated that the resistance occurs much like HIV because the viral polymerase catalytic site targeted by the drug is homologous between the two viruses. The impact of agriculture on antimicrobial resistance According to the United States Department of Agriculture (USDA) (2001), antimicrobial drugs have been fed to livestock at low levels to treat diseases, promote growth and to increase the efficiency of the feed [60]. However, many researchers and scientists question whether farmers should continue feeding their livestock antimicrobial therapy because many of the drugs they use are also used by humans. They fear the drugs can be passed from animals to humans through the handling of animals or ingestion of food. It is estimated that 10 percent of the overall antimicrobial resistance is attributed to livestock. Many countries in Europe have already banned the growth-promoting use of antimicrobial drugs in livestock as a precaution to prevent resistant microbes from passing to humans. Since the late 1990s, the U.S. has initiated the following steps [23]: In 1999, the Center for Science in the Public Interest, representing 37 health and consumer groups, petitioned the FDA to ban the use of penicillin, tetracycline, erythromycin, tylosin, lincomycin, virginiamycin and bacitracin in livestock production. In November 1999, the House of Representatives introduced a bill to ban subtherapeutic feeding of the same seven antimicrobials. However, to date, the U.S. has not banned the use of low-dose antimicrobials, primarily citing economic consequences. The 2001 USDA report lists these reasons [23] why the bans were rejected: Doing so would cause higher prices for meat because it would make less total meat available. Livestock fed antimicrobial therapy gain more weight, thus producing more meat. Cattle fed low levels of antimicrobial therapy have fewer diseases. The lack of low-dose antimicrobials could contribute to increased production risks. Death losses and reduced production from diseases that had been prevented by feeding low levels of antimicrobial drugs could be costly. Due to the ever-increasing antimicrobial resistance, the USDA and FDA are likely to re-evaluate the research and data to ensure humans are not exacerbating their risk of developing resistance to potential life-saving treatments. At this time, as implied earlier, the USDA and FDA believe there are numerous factors that contribute to overall antimicrobial drug resistance and that the overall economic stability of America is dependent upon livestock being healthy and prosperous. Preventing antimicrobial drug resistance Due to the prevalence of antimicrobial drug resistance, the CDC and various other prestigious organizations have been collaborating to work to eradicate antimicrobial resistance. The public health task force committee is co-chaired by the CDC, FDA, National Institute of Health (NIH) and Agency for Healthcare Research and Quality (AHRQ), Centers for Medicare Medicaid Services (CMS), the Health Resources and Services Administration (HRSA), 19

20 Department of Agriculture (USDA), the Department of Defense (DOD), Department of Veterans Affairs (VA) and the Environmental Protection Agency (EPA) [4]. The CDC s Campaign to Prevent Antimicrobial Resistance aims to prevent antimicrobial resistance in health care settings. The campaign centers on four main strategies: prevent infection, diagnose and treat infection, use antimicrobials wisely, and prevent transmission. Within the context of these strategies, multiple 12-step programs are being developed targeting clinicians who treat specialty-specific patient populations including hospitalized adults, dialysis patients, surgical patients, hospitalized children and long-term care patients. Educational tools and materials are being developed for each patient population. The 12-step program is available customized for various kinds of patients: those who are hospitalized, undergoing dialysis or surgeries, long-term patients, and children. The CDC s 12-step goals for hospitalized patients [13]: Step 1. Vaccinate staff and patients. Get the influenza vaccine. Give influenza and pneumococcal vaccine to patients in addition to routine vaccines (e.g. hepatitis B). Step 2. Get the catheters out. Hemodialysis Use catheters only when essential. Maximize use of fistulas/grafts. Remove catheters when they are no longer essential. Peritoneal dialysis Remove/replace infected catheters. Step 3. Optimize access care. Follow established KDOQI and CDC guidelines for access care. Use proper insertion and catheter-care protocols. Remove access device when infected. Use the correct catheter. Step 4. Target the pathogen. Obtain appropriate cultures. Target empiric therapy to likely pathogens. Target definitive therapy to known pathogens. Optimize timing, regimen, dose, route and duration. Step 5. Access the experts. Consult the appropriate expert for complicated infections. Step 6. Use local data. Know your local antibiogram (most common microbes and/or resistance in your area). Get previous microbiology results when patients transfer to your facility. Step 7. Know when to say no to vancomycin. Follow CDC guidelines for vancomycin use. Consider first-generation cephalosporins instead of vancomycin. Step 8. Treat infection, not contamination or colonization. Use proper antisepsis for drawing blood cultures. Get one peripheral vein blood culture, if possible. Avoid culturing vascular catheter tips. Treat bacteremia, not the catheter tip. Step 9. Stop antimicrobial treatment. When infection is treated. When infection is not diagnosed. The CDC s 12-step goals for hospitalized patients [13] (continued) Step 10: Follow infection control precautions. Use standard infection control precautions for dialysis centers. Consult local infection control expert. Step 11: Practice hand hygiene. Wash your hands or use an alcohol-based hand rub. Set an example. Step 12: Partner with your patients. Educate on access care and infection control measures. Re-educate regularly. Isolating the patient in the hospital setting Due to the prevalence and severity of various infections and antimicrobial drug resistance nationwide, the CDC has enforced stringent guidelines to prevent the spread of microbes in the hospital setting. As nurses, it is important to understand the implications for each precaution because nurses may be the ones initiating the recommendations, then collaborating with physicians. There are two tiers of HICPAC (Healthcare Infection Control Practices Advisory Committee) isolation precautions. In the first and most important tier, are those precautions designed for the care of all patients in hospitals, regardless of their diagnosis or presumed infection status, called standard precautions. It is important to always adhere to the standard precautions to prevent nosocomial infections. In the second tier are precautions designed only for the care of specified patients, called transmission-based precautions. These additional transmission-based precautions are for patients known or suspected to be infected by epidemiologically important pathogens spread by airborne or droplet transmission or by contact with dry skin or contaminated surfaces [32]. 1. Standard precautions Standard precautions synthesize the major features of universal precautions (UP, blood and body fluid precautions, designed to reduce the risk of transmission of blood-borne pathogens) and BSI (designed to reduce the risk of transmission of pathogens from moist body substances) and applies them to all patients receiving care in hospitals, regardless of their diagnosis or presumed infection status. Standard precautions apply to: Blood. All body fluids, secretions and excretions except sweat, regardless of whether they contain visible blood. Nonintact skin. Mucous membranes. Standard precautions are designed to reduce the risk of transmission of microorganisms from both recognized and unrecognized sources of infection in hospitals. The following are recommendations for standard precautions: Hand washing Wash hands after touching blood, body fluids, secretions, excretions and contaminated items, regardless of whether gloves are worn. Wash hands immediately after gloves are removed, between patient contacts, and when otherwise indicated to avoid transfer of microorganisms to other patients or environments. It may be necessary to wash hands between tasks and procedures on the same patient to prevent cross-contamination of different body sites. Gloves Wear gloves (clean, nonsterile gloves are adequate) when touching blood, body fluids, secretions, excretions and contaminated items. Put on clean gloves just before 20

21 touching mucous membranes and nonintact skin. Change gloves between tasks and procedures on the same patient after contact with material that may contain a high concentration of microorganisms. Remove gloves promptly after use, before touching noncontaminated items and environmental surfaces and before going to another patient, and wash hands immediately to avoid transfer of microorganisms to other patients or environments. Mask, eye protection, face shield Wear a mask and eye protection or a face shield to protect mucous membranes of the eyes, nose, and mouth during procedures and patient-care activities that are likely 2. to generate splashes or sprays of blood, body fluids, secretions and excretions. Gown Wear a gown (a clean, nonsterile gown is adequate) to protect skin and to prevent soiling of clothing during procedures and patient-care activities that are likely to generate splashes or sprays of blood, body fluids, secretions or excretions. Select a gown that is appropriate for the activity and amount of fluid likely to be encountered. Remove a soiled gown as promptly as possible and wash hands to avoid transfer of microorganisms to other patients or environments. Patient-care equipment Handle used patient-care equipment soiled with blood, body fluids, secretions and excretions in a manner that prevents skin and mucous membrane exposures, contamination of clothing and transfer of microorganisms to other patients and environments. Ensure that reusable equipment is not used for the care of another patient until it has been cleaned and reprocessed appropriately. Ensure that single-use items are discarded properly. Environmental control Ensure that the hospital has adequate procedures for the routine care, cleaning and disinfection of environmental surfaces, beds, bed rails, bedside equipment and other frequently touched surfaces and ensure that these procedures are being followed. Linen Handle, transport and process used linen soiled with blood, body fluids, secretions and excretions in a manner that prevents skin and mucous membrane exposures and contamination of clothing, and that avoids transfer of microorganisms to other patients and environments. Occupational health and blood-borne pathogens Take care to prevent injuries when using needles, scalpels and other sharp instruments or devices; when handling sharp instruments after procedures; when cleaning used instruments; and when disposing of used needles. Never recap used needles or otherwise manipulate them using both hands or use any other technique that involves directing the point of a needle toward any part of the body; rather, use either a one-handed scoop technique or a mechanical device designed for holding the needle sheath. Do not remove used needles from disposable syringes by hand, and do not bend, break or otherwise manipulate used needles by hand. Place used disposable syringes and needles, scalpel blades and other sharp items in appropriate puncture-resistant containers located as close as practical to the area in which the items were used, and place reusable syringes and needles 21 in a puncture-resistant container for transport to the reprocessing area. Use mouthpieces, resuscitation bags or other ventilation devices as an alternative to mouth-tomouth resuscitation methods in areas where the need for resuscitation is predictable. Patient placement Place a patient who contaminates the environment or who does not (or cannot be expected to) assist in maintaining appropriate hygiene or environmental control in a private room. If a private room is not available, consult with infection control professionals regarding patient placement or other alternatives. Transmission-based precautions Transmission-based precautions are designed for patients documented or suspected to be infected with highly transmissible or epidemiologically important pathogens for which additional precautions beyond standard precautions are needed to interrupt transmission in hospitals. There are three types of transmissionbased precautions: Airborne precautions, droplet precautions and contact precautions. They may be combined for diseases that have multiple routes of transmission. When used either singularly or in combination, they are to be used in addition to standard precautions. Airborne precautions are designed to reduce the risk of airborne transmission of infectious agents. Airborne transmission occurs by dissemination of either airborne droplet nuclei (small-particle residue {5 um or smaller in size} of evaporated droplets that may remain suspended in the air for long periods of time) or dust particles containing the infectious agent. Microorganisms carried in this manner can be dispersed widely by air currents and may become inhaled by or deposited on a susceptible host within the same room or over a longer distance from the source patient, depending on environmental factors; therefore, special air handling and ventilation are required to prevent airborne transmission. Airborne precautions apply to patients known or suspected to be infected with epidemiologically important pathogens that can be transmitted by the airborne route. In addition to the standard precautions, the following should be implemented to adhere to the airborne precautions: Patient placement Place the patient in a private room that has monitored negative air pressure in relation to the surrounding area, 6 to 12 air changes per hour, and appropriate discharge of air outdoors or monitored high-efficiency filtration of room air before the air is circulated to other areas in the hospital. Keep the room door closed and the patient in the room. When a private room is not available, place the patient in a room with a patient who has active infection with the same microorganism, unless otherwise recommended, but with no other infection. When a private room is not available and cohorting is not desirable, consultation with infection control professionals is advised before patient placement. Respiratory protection Wear respiratory protection when entering the room of a patient with known or suspected infectious pulmonary tuberculosis. Susceptible persons should not enter the room of patients known or suspected to have measles (rubeola) or varicella (chickenpox) if other immune caregivers are available. If susceptible persons must enter the room of a patient known or

22 suspected to have measles (rubeola) or varicella, they should wear respiratory protection. Persons immune to measles (rubeola) or varicella need not wear respiratory protection. Patient transport Limit the movement and transport of the patient from the room to essential purposes only. If transport or movement is necessary, minimize patient dispersal of droplet nuclei by placing a surgical mask on the patient, if possible. Droplet precautions are designed to reduce the risk of droplet transmission of infectious agents. Droplet transmission involves contact of the conjunctivae or the mucous membranes of the nose or mouth of a susceptible person with large-particle droplets (larger than 5 um in sizes) containing microorganisms generated from a person who has a clinical disease or who is a carrier of the microorganism. Droplets are generated from the source person primarily during coughing, sneezing or talking and during the performance of certain procedures such as suctioning and bronchoscopy. Transmission via large-particle droplets requires close contact between source and recipient persons, because droplets do not remain suspended in the air and generally travel only short distances, usually 3 feet or less, through the air. Because droplets do not remain suspended in the air, special air handling and ventilation are not required to prevent droplet transmission. Droplet precautions apply to any patient known or suspected to be infected with in a room with a patient(s) who has an active infection with the same microorganism but with no other infection (cohorting). When a private room is not available and cohorting is not achievable, maintain spatial separation of at least 3 feet between the infected patient and other patients and visitors. Special air handling and ventilation are not necessary, and the door may remain open. Mask In addition to standard precautions, wear a mask when working within 3 feet of the patient. (Logistically, some hospitals may want to implement the wearing of a mask to enter the room.) Patient transport Limit the movement and transport of the patient from the room to essential purposes only. If transport or movement is necessary, minimize patient dispersal of droplets by masking the patient, if possible. 3. Contact precautions are designed to reduce the risk of transmission of epidemiologically important microorganisms by direct or indirect contact. Direct-contact transmission involves skin-to-skin contact and physical transfer of microorganisms to a susceptible host from an infected or colonized person, such as occurs when personnel turn or bathe patients or perform other patient-care activities that require physical contact. Directcontact transmission also can occur between two patients (i.e., by hand contact), with one serving as the source of infectious microorganisms and the other as a susceptible host. Indirectcontact transmission involves contact of a susceptible host with a contaminated intermediate object, usually inanimate, in the patient s environment. Contact precautions apply to specified patients known or suspected to be infected or colonized (presence of microorganism in or on patient but without clinical signs and symptoms of infection) with epidemiologically important microorganisms that can be transmitted by direct or indirect contact. Patient placement Place the patient in a private room. When a private room is not available, place the patient in a room with a patient(s) who has active infection with the same microorganism but with no other infection (cohorting). When a private room is not available and cohorting is not achievable, consider the epidemiology of the microorganism and the patient population when determining patient placement. Consultation with infection control professionals is advised before patient placement. Gloves and hand washing In addition to wearing gloves as outlined under standard precautions, wear gloves (clean, nonsterile gloves are adequate) when entering the room. During the course of providing care for a patient, change gloves after having contact with infective material that may contain high concentrations of microorganisms (fecal material and wound drainage). Remove gloves before leaving the patient s environment and wash hands immediately with an antimicrobial agent or a waterless antiseptic agent. After glove removal and hand washing, ensure that hands do not touch potentially contaminated environmental surfaces or items in the patient s room to avoid transfer of microorganisms to other patients or environments. Gown In addition to wearing a gown as outlined under standard precautions, wear a gown (a clean, nonsterile gown is adequate) when entering the room if you anticipate that your clothing will have substantial contact with the patient, environmental surfaces, or items in the patient s room, or if the patient is incontinent or has diarrhea, an ileostomy, a colostomy, or wound drainage not contained by a dressing. Remove the gown before leaving the patient s environment. After gown removal, ensure that clothing does not contact potentially contaminated environmental surfaces to avoid transfer of microorganisms to other patients or environments. Patient transport Limit the movement and transport of the patient from the room to essential purposes only. If the patient is transported out of the room, ensure that precautions are maintained to minimize the risk of transmission of microorganisms to other patients and contamination of environmental surfaces or equipment. Patient care equipment When possible, dedicate the use of noncritical patient-care equipment to a single patient (or cohort of patients infected or colonized with the pathogen requiring precautions) to avoid sharing between patients. If use of common equipment or items is unavoidable, then adequately clean and disinfect them before use for another patient. In many instances, the risk of nosocomial transmission of infection may be highest before a definitive diagnosis can be made and before precautions based on that diagnosis can be implemented. The routine use of standard precautions for all patients should greatly reduce this risk for conditions other than those requiring airborne, droplet or 22

23 contact precautions. While it is not possible to prospectively identify all patients needing these enhanced precautions, certain clinical syndromes and conditions carry a sufficiently high risk to warrant the empiric addition of enhanced precautions while a more definitive diagnosis is pursued. The organisms listed under the column potential pathogens are not intended to represent the complete or even most likely diagnoses, but rather possible etiologic agents that require additional precautions beyond standard precautions until they can be ruled out. Infection control professionals are encouraged to modify or adapt this table according to local conditions. To ensure that appropriate empiric precautions are implemented always, hospitals must have systems in place to evaluate patients routinely according to these criteria as part of their preadmission and admission care. In addition, the CDC has clarified some common terms in regards to the various types of transmission. Contact transmission, the most important and frequent mode of transmission of nosocomial infections, is divided into two subgroups: direct-contact transmission and indirect-contact transmission. Direct-contact transmission involves a direct body surface-to-body surface contact and physical transfer of microorganisms between a susceptible host and an infected or colonized person, such as occurs when a person turns a patient, gives a patient a bath, or performs other patient-care activities that require direct personal contact. Direct-contact transmission also can occur between two patients, with one serving as the source of the infectious microorganisms and the other as a susceptible host. Indirect-contact transmission involves contact of a susceptible host with a contaminated intermediate object, usually inanimate, such as contaminated instruments, needles or dressings, or contaminated hands that are not washed and gloves that are not changed between patients. Droplet transmission, theoretically, is a form of contact transmission. However, the mechanism of transfer of the pathogen to the host is quite distinct from either direct- or indirect-contact transmission. Therefore, droplet transmission will be considered a separate route of transmission in this guideline. Droplets are generated from the source person primarily during coughing, sneezing and talking, and during the performance of certain procedures such as suctioning and bronchoscopy. Transmission occurs when droplets containing microorganisms generated from the infected person are propelled a short distance through the air and deposited on the host s conjunctivae, nasal mucosa or mouth. Because droplets do not remain suspended in the air, special air handling and ventilation are not required to prevent droplet transmission; that is, droplet transmission must not be confused with airborne transmission. Airborne transmission occurs by dissemination of either airborne droplet nuclei (small-particle residue {5 um or smaller in size} of evaporated droplets containing microorganisms that remain suspended in the air for long periods of time) or dust particles containing the infectious agent. Microorganisms carried in this manner can be dispersed widely by air currents and may become inhaled by a susceptible host within the same room or over a longer distance from the source patient, depending on environmental factors; therefore, special air handling and ventilation are required to prevent airborne transmission. Microorganisms transmitted by airborne transmission include mycobacterium tuberculosis and the rubeola and varicella viruses. Common vehicle transmission applies to microorganisms transmitted by contaminated items such as food, water, medications, devices and equipment. Vectorborne transmission occurs when vectors such as mosquitoes, flies, rats and other vermin transmit microorganisms; this route of transmission is of less significance in hospitals in the United States than in other regions of the world. Nurses can help prevent the spread of infection in the hospital setting Even when used carefully, all organisms can develop some resistance to antibiotics over time. Therefore, preventing infection in the first place may be the best defense against an antibiotic-resistant infection [39]. Nurses, who are on the forefront, may hold a key to preventing the spread of infection and antimicrobial resistance. It is important to adhere to the following guidelines from the CDC [9]: Hand washing. Hand washing is frequently the single most important measure to reduce the risks of transmitting microorganisms from one person to another or from one site to another on the same patient. Washing hands for at least seconds as promptly and thoroughly as possible between patient contacts and after contact with blood, body fluids, secretions, excretions and equipment or articles contaminated by them is perhaps the primary component of infection control and isolation precautions. In addition to adherence by nurses and health care professionals to the simple basics of hand washing, the CDC also recommends: Use of alcohol-based hand rubs, which have been shown to terminate outbreaks in health care facilities to reduce transmission of antimicrobial resistant organisms (MRSA) and reduce overall infection rates. Proper use of alcohol-based hand rubs requires the application of the product to palm of one hand and rubbing hands together, covering all surfaces of hands and fingers, until hands are dry. Note that the volume needed to reduce the number of bacteria on hands varies by product. Alcohol-based hand rubs take less time to use than traditional hand washing. In an eight-hour shift, an estimated one hour of an ICU nurse s time will be saved by using an alcohol-based hand rub. Traditional hand washing with soap and water is considered the mainstream method, especially if hands are visibly soiled; always wash your hands with soap and water. Hand washing with soap and water remains a sensible strategy for hand hygiene in non-health care settings and is recommended by the CDC. Hand hygiene. Health care personnel should adhere to certain recommendations to avoid transmitting nosocomial infections and microorganisms from patient to patient. Those who care for patients at high risk of acquiring infections (e.g. patients in intensive care units or in transplant units) should avoid wearing artificial nails and keep natural nails less than one-quarter of an inch long. Gloves. The CDC recommends that in addition to hand washing, all health care personnel should wear gloves. Wearing gloves should never be in lieu of hand washing because gloves may have small, apparent defects or may be torn during use, and hands can become contaminated during removal of gloves. However, wearing gloves should be used in conjunction with hand washing to prevent the spread of microorganisms. Gloves reduce hand contamination by 70 percent to 80 percent, prevent 23

24 cross-contamination and protect patients and health care personnel from infection. Hand rubs should be used before and after each patient, just as gloves should be changed before and after each patient. Gloves are worn to provide a protective barrier and to prevent gross contamination of the hands when touching blood, body fluids, secretions, excretions, mucous membranes and nonintact skin; the wearing of gloves in specified circumstances to reduce the risk of exposures to blood-borne pathogens is mandated by the OSHA blood-borne pathogens final rule. Gloves are worn to reduce the likelihood that microorganisms present on the hands of personnel will be transmitted to patients during invasive or other patient-care procedures that involve touching a patient s mucous membranes and nonintact skin. Gloves are worn to reduce the likelihood that hands of personnel contaminated with microorganisms from a patient or a fomite can transmit these microorganisms to another patient. In this situation, gloves must be changed between patient contacts, and hands should be washed after gloves are removed. Isolating the patient. In hospitals and nursing homes, drug-resistant microorganisms require that the patient be placed in contact isolation, a transmission-based isolation strategy recommended by the Centers for Disease Control and Prevention. In 1996, the CDC presented guidelines for a two-level approach to infection isolation. Appropriate patient placement is a significant component of isolation precautions. A private room is important to prevent direct- or indirect-contact transmission when the source patient has poor hygienic habits, contaminates the environment or cannot be expected to assist in maintaining infection control precautions to limit transmission of microorganisms (e.g., infants, children and patients with altered mental status). When possible, a patient with highly transmissible or epidemiologically important microorganisms is placed in a private room with hand washing and toilet facilities to reduce opportunities for transmission of microorganisms. In addition to isolating the patient, it is important to consider the following: Linen and laundry. Although soiled linen may be contaminated with pathogenic microorganisms, the risk of disease transmission is negligible if it is handled, transported and laundered in a manner that avoids transfer of microorganisms to patients, personnel and environments. Rather than rigid rules and regulations, hygienic and common-sense storage and processing of clean and soiled linen are recommended. The methods for handling, transporting and laundering of soiled linen are determined by hospital policy and any applicable regulations. Dishes, glasses, cups and eating utensils. No special precautions are needed for dishes, glasses, cups or eating utensils. Either disposable or reusable dishes or utensils can be used for patients on isolation precautions. The combination of hot water and detergents used in hospital dishwashers is sufficient to decontaminate dishes, glasses, cups and eating utensils. Routine and terminal cleaning. The room or cubicle and bedside equipment of patients on transmission-based precautions are cleaned using the same procedures used for patients on standard precautions, unless the infecting microorganism(s) and the amount of environmental contamination indicate special cleaning. In addition to thorough cleaning, adequate disinfection of bedside 24 equipment and environmental surfaces (e.g., bed rails, bedside tables, carts, commodes, doorknobs, faucet handles) is indicated for certain pathogens, especially enterococci, which can survive in the inanimate environment for prolonged periods of time. Patients admitted to hospital rooms that previously were occupied by patients infected or colonized with such pathogens are at increased risk of infection from contaminated environmental surfaces and bedside equipment if they have not been cleaned and disinfected adequately. The methods, thoroughness and frequency of cleaning and the products used are determined by hospital policy [32]. If a private room is not available, an infected patient is placed with an appropriate roommate. Patients infected by the same microorganism usually can share a room, provided they are not infected with other potentially transmissible microorganisms and the likelihood of reinfection with the same organism is minimal. Such sharing of rooms, also referred to as cohorting patients, is useful especially during outbreaks or when there is a shortage of private rooms. When a private room is not available and cohorting is not achievable or recommended, it is very important to consider the epidemiology and mode of transmission of the infecting pathogen and the patient population being served in determining patient placement. Under these circumstances, consultation with infection control professionals is advised before patient placement. Moreover, when an infected patient shares a room with a noninfected patient, it also is important that patients, personnel and visitors take precautions to prevent the spread of infection. If the patient is placed into isolation, precautions are designed to prevent transmission of microorganisms by these routes in the hospital setting. The CDC has also recognized potential disadvantages for placing a patient in isolation. Isolation precautions may require specialized equipment and environmental modifications that add to the cost of hospitalization. Isolation precautions may make frequent visits by nurses, physicians and other personnel inconvenient, and they may make it more difficult for personnel to give the prompt and frequent care that sometimes is required. The use of a multipatient room for one patient uses valuable space that otherwise might accommodate several patients. Moreover, forced solitude deprives the patient of normal social relationships and may be psychologically harmful, especially to children. These disadvantages, however, must be weighed against the hospital s mission to prevent the spread of serious and epidemiologically important microorganisms within the hospital. Protective barriers. Dependent upon the type and location of the bacterium, the nurse may be required to wear protective gear, such as a mask, goggles, a face shield and/or gown to prevent the spread. Mask. A mask that covers both the nose and the mouth, and goggles or a face shield are worn by hospital personnel during procedures and patient-care activities that are likely to generate splashes or sprays of blood, body fluids, secretions or excretions to provide protection of the mucous membranes of the eyes, nose and mouth from contact transmission of pathogens. Use of masks, eye protection and face shields in specified circumstances to reduce the risk of exposures to blood-borne pathogens is mandated by the Occupational Safety and Health Administration (OSHA) blood-borne pathogens final rule. A surgical mask generally is worn by hospital personnel to provide protection against spread of infectious large-particle droplets that are transmitted by close

25 contact and generally travel only short distances (up to 3 feet) from infected patients who are coughing or sneezing [32]. Respiratory protection currently requires the use of a respirator with N95 or higher filtration to prevent inhalation of infectious particles. Respiratory protection is broadly regulated by OSHA under the general industry standard for respiratory protection, which requires U.S. employers in all employment settings to implement a program to protect employees from inhalation of toxic materials. OSHA program components include medical clearance to wear a respirator; provision and use of appropriate respirators, including fit-tested National Institute for Occupational Safety and Health (NIOSH)- certified N95 and higher particulate filtering respirators; education on respirator use and periodic re-evaluation of the respiratory protection program. The key is ensuring that the particular respirator is a good fit for the health care professional. The guidelines mandate that a user-seal check, formerly called a fit check, should be performed by the wearer of a respirator each time a respirator is donned to minimize air leakage around the face piece. The optimal frequency of fit-testing has not been determined [32]. Gowns are worn to prevent contamination of clothing and to protect the skin of personnel from blood and body fluid exposures. Gowns specially treated to make them impermeable to liquids, leg coverings, boots or shoe covers provide greater protection to the skin when splashes or large quantities of infective material are present or anticipated. The wearing of gowns and protective apparel under specified circumstances to reduce the risk of exposures to blood-borne pathogens is mandated by the OSHA blood-borne pathogens final rule. Gowns also are worn by personnel during the care of patients infected with epidemiologically important microorganisms to reduce the opportunity for transmission of pathogens from patients or items in their environment to other patients or environments; when gowns are worn for this purpose, they must be removed before leaving the patient s environment, and hands must be washed. Transporting infected patients. Limiting the movement and transport of patients infected with virulent or epidemiologically important microorganisms and ensuring that such patients leave their rooms only for essential purposes reduces opportunities for transmission of microorganisms in hospitals. When patient transport is necessary, it is important that: Appropriate barriers (i.e. masks, impervious dressings) are worn or used by the patient to reduce the opportunity for transmission of pertinent microorganisms to other patients, personnel and visitors and to reduce contamination of the environment. Personnel in the area to which the patient is to be taken are notified of the impending arrival of the patient and of the precautions to be used to reduce the risk of transmission of infectious microorganisms; and patients are informed of ways by which they can assist in preventing the transmission of their infectious microorganisms to others. Education. Nurses can help prevent the development of drugresistant microorganisms by explaining antibiotic misuse to each of their patients in the hospital and in the out-patient setting. When involved in the provision of prescriptions for antibiotics, nurses should [12]: Provide both the generic and trade name of the drug. Explain the purpose of the medication (to fight or prevent infection). Explain the dosage in easily understood terms, without abbreviations and/or medical jargon. Explain whether medication should be given around the clock or only during waking hours, how often it should be taken and whether it should be taken with food. Also, patients being discharged from the hospital should be informed about their last antimicrobial dose to ensure they continue the same administration cycle at home. Explain potential drug or food interactions and what to do if they miss a dose. Explain that the patient must continue to take all medication, even when he or she feels better. Confirm that the patient finished all of the prescribed medicine in appropriate dosages. In addition, nurses need to do the following when caring for a patient who has been prescribed antimicrobial therapy [18]: Carefully monitor antibiotic therapy, checking the peak and low levels, and reviewing the data and recommendations based on the cultures. Encourage the use of narrow-spectrum antibiotics until culture findings are known. Always check the cultures before antibiotics are started, and review all culture reports to ensure that bacteria are sensitive to the antibiotics used. Failure to comply will skew the results. Advocate for restrictions on the use of certain antibiotics, like vancomycin, empirically for preoperative prophylaxis. As implied, vancomycin should be reserved only for antimicrobial drug resistance. Monitor adherence to medical staff guidelines for antibiotic use. Research has demonstrated that although there are stringent guidelines in place to prevent the spread of microorganisms, the phenomenon is still occurring. Therefore, it is important to realize that each one of us can make a difference at all levels. If in doubt, ask the infection control team at the hospital. Never hesitate, as it is imperative that nurses diligently work together with all members of the health care team to prevent the spread of microorganisms that can further exacerbate the resistance to antimicrobial therapy. Closing It is inevitable that our society will continue to encounter antimicrobial drug resistance. Due to the prevalence and significance, it is imperative that everyone collaborates to prevent further resistance or to stall the process. Nurses need to be familiar with each classification of drugs, the manner in which they work and when they should be prescribed. It is also important to become aware of the most prevalent microbes within the community in which you reside by contacting your local health department. Nurses need to empower each of their patients and families with the knowledge of their prescribed antimicrobial drugs, the importance of taking the full dose as prescribed and when to return to their primary care provider. In addition, every nurse can do his or her part in educating patients and families about antimicrobial drug resistance and the importance of abating unnecessary antimicrobials for viral infections. According to the CDC [18]: On average, adults get three to five colds a year; children even more. Most colds last one week, but it is not unusual for symptoms to continue for as long as two to three weeks. We used to think that yellow or green mucus indicated a bacterial 25

26 infection. We now know this is not true. It is common to have yellow or green mucus with a viral infection, such as a cold. Colored mucus does not mean that you have a bacterial infection or need antibiotics. Each one of us holds the key to be knowledgeable about the reality and significance of antimicrobial drug resistance. We can make a difference. References 1. APUA (1999). About antibiotic resistance. Retrieved online August 24, 2008 at apua/q&a?a&a_ar.html 2. Association for Professionals in Infection Control & Epidemiology (2006). Summary of MRSA guidelines from (APIC). Retrieved online August 16, 2008 at ResearchFoundation/NationalMRSAPrevalenceStudy/APIC_MRSA_Prevention_Guidelines_Summary.pdf. 3. Centers for Disease Control and Prevention (1999). Aminoglycoside resistance in enter-obacteriaceae and pseudomonas aeruginosa. Retrieved online August 24, 2008 at 4. Centers for Disease Control and Prevention (2008). Antibiotic/Antimicrobial Resistance: The interagency task force on antimicrobial resistance and a public health action plan to combat antimicrobial resistance. Retrieved online August 23, 2008 at 5. Centers for Disease Control and Prevention (2006). Antimicrobial Resistance in Health care Settings (2006). Retrieved online September 28, 2008 at 6. Centers for Disease Control and Prevention. (1999). Vancomycin resistant Enterococcus (VRE) and the clinical laboratory. Retrieved online August 24, 2008 at 7. Centers for Disease Control and Prevention (2005). Foundation. Superbugs: Protecting the power of antibiotics. Retrieved online August 23, 2008 at AntibioticResistance.aspx 8. Centers for Disease Control and Prevention (2008). Community-Associated MRSA Information for the Public. Retrieved online September 19, 2008 at 9. Centers for Disease Control and Prevention. (2007). Guidelines for Isolation Precautions:Preventing Transmission of Infectious Agents in Health care Settings Retrieved online September 29, 2008 at Isolation 2007.pdf. 10. Centers for Disease Control and Prevention (1992). Guidelines for Prevention of Nosocomial Pneumonia. MMWR 46 (RR-1); Retrieved online October 3, 2008 at mmwrhtml/ htm 11. Centers for Disease Control and Prevention (2008). Influenza Antiviral drug resistance. Retrieved online October 3, 2008 at Centers for Disease Control and Prevention (1999). Laboratory detection of extended-spectrum beta lactamases. Retrieved online October 2, 2008 at Centers for Disease Control and Prevention (2005). Prevent antimicrobial resistance in health care settings. Retrieved online October 3, 2008 at care/ltc.htm 14. Centers for Disease Control and Prevention. (2008). Recommendations for Preventing the Spread of Vancomycin Resistance Recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC). Retrieved online September 23, 2008 at m asp 15. Centers for Disease Control and Prevention.(2006). Sexually Transmitted Diseases Treatment Guidelines for 2006: Fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR 56 (14); Retrieved online October 3, 2008 at htm?s_cid=mm5614a3_e 16. Centers for Disease Control and Prevention (2006) Strategies for Clinical Management of MRSA in the Community: Summary of an Experts Meeting Convened by the Centers fordisease Control and Prevention. Retrieved online October 3, 2008 at pdf 17. Centers for Disease Control and Prevention (2008). Vancomycin-resistant enterococci. Retrieved online September 28, 2008 at Glover, T. L. (2000). How Drug-Resistant Microorganisms Affect Nursing.Orthopaedic Nursing 19 (2) Gonzales, R. & Kutner, J. (2008). Current practice guidelines in primary care: 2008.McGraw-Hill: New York. 20. John Hopkins Medicine (no year) Vancomycin Resistant Enterococci. Retrieved online September 27, 2008 at Holten,K. & Onusko, E. (2001). Appropriate Prescribing of Oral Beta-Lactam Antibiotics. American Family Physician. Retrieved online September 10, 2008 at Lehne, R.A. (2004). Pharmacology for nursing care. Saunders: St. Louis 23. Mathews, K. (2001).United States Department of Agriculture: Antimicrobial drug use and veterinary costs in U.S livestock production. Retrieved online October 1, 2008 at aib766/aib766.pdf 24. McPhee, S.J., Papadakis, M. A. & Tierney, L.M (2007). Current medical diagnosis and treatment (46th ed). New York: McGraw-Hill. 25. Mosby s Dictionary of Medicine, Nursing and health professionals (2006).7th edition. Mosby: St Louis. 26. Muench, D. (2008). Pneumococcal infections. Retrieved online October 3, 2008 at com/med/topic1848.htm 27. National Institute of Allergy and Infectious Diseases (2008). Antimicrobial drug resistance. Retrieved online August 24, 2008 at Resistance/Understanding/causes/ htm. 28. National Institute of Allergy and Infectious Disease (2008). Antimicrobial Drug Resistance. Retrieved online August 24, 2008 at www3.niad.nih.gov/topics/antimicrobialresistance/understanding/healthissue.htm 29. National Institute of Allergy and Infectious Diseases (2008).National Institutes of Health. The Problem of Antimicrobial Resistance. Retrieved online August 19, 2008 at National Institute of Health (2007). Guidelines for the use of antiviral agents in infected adults and adolescents. Retrieved online October 1, 2008 at files/adultandadolescentgl. pdf 31. Pillay, D & Zambon, M. Antiviral drug resistance (no year) Retrieved online October 3, 2008 at Stedman s Medical Dictionary (2006). 27th edition. Lippincott: Baltimore. 33. Talaro, K.P (2005). Foundations in microbiology: basic principles. McGraw-Hill: New York. 34. Tenover,P. (2008). CDC s Role in Monitoring and Preventing Antimicrobial Resistance before Health, Education, Labor and Pensions Committee U.S. Senate. Retrieved online September 30, 2008 at hhs.gov/asl/testify/2008/06/t c.html 35. Tjaniadi, P.et al (2003). Antimicrobial resistance of bacterial pathogens associated with diarrheal patients in indonesia. Am. J. Trop. Med. Hyg., 68(6), pp Retrieved online August 30, 2008 at ajtmh.org/cgi/reprint/68/6/666.pdf 36. Todar, K. (2008). Bacterial resistance to antibiotics. Retrieved online August 31, 2008 at textbookofbacteriology.net/resantimicrobial.html 37. US Dept of Health and Human Services (2008). Testimony on CDC s Role in Monitoring and Preventing Antimicrobial Resistance. Retrieved online September 28, t c.html 38. U.S. Food and Drug Administration (no year) Graphics. Retrieved online September 1, 2008 at gov/fdac/graphics/1998graphics/unnantib.jpeg. 39. U.S. Food and Drug Administration (1998). Miracle Drugs vs. Superbugs. Retrieved online August 30, 2008 at U.S. Food and Drug Administration (1995). The Rise of Antibiotic-Resistant Infections. Retrieved online September 1, 2008 at World Health Organization (2002). Antimicrobial resistance. Retrieved online August 24, 2008 at Workowski, K., Berman, S., & Douglas, J. (2008). Emerging antimicrobial resistance in neisseria Gonorrhoeae: Urgent need to strengthen prevention strategies. Annals of Internal Medicine, 148 (8), Retrieved online August 24, 2008 at full/148/8/ Youngkin, E., Sawin, K., Kissinger, J., & Israel, D. (2005). Pharmacotherapeutics: A primary care clinical guide. (2nd ed). Pearson: New Jersey.

27 NURSES ROLE IN PREVENTING ANTIMICROBIAL RESISTANCE Self-evaluation Exercise Choose True or False for questions 1 through 10 and check your answers at the bottom of the page. NOTES 1. The CDC reiterates the concept and estimates that the major factor in the emergence of antibiotic resistance bacteria is attributed to the overuse and misuse of antibiotics. True False 2. All penicillin drugs consist of two parts: a thiazolidine ring and a beta-lactam ring. True False 3. Cephalosporins are a newer group of antibiotics that currently account for the majority of all antibiotics administered today. True False 4. The most common severe drug allergy is with the penicillins. True False 5. Less than 10 percent of staphylococcus aureus strains are no longer treatable with penicillins. True False 6. Vancomycin-resistant enterococci (VRE) is most typically colonized in the gastrointestinal tract; however it may be found in the urinary tract. True False 7. The danger with MRSA is the bacterium is resistant to the entire class of penicillins, including the beta-lactamases. True False 8. Neisseria gonorrhoeae (N. gonorrhea) is the most common notifiable disease in the U.S. with 339,593 cases documented in True False 9. Antiviral drug resistance occurs due to a decrease in the susceptibility of the drug in a laboratory culture (a phenotype), change in the genetic makeup (genotype), and evolutionary changes over time (virus replicating over time). True False 10. Nurses can help prevent the development of drug-resistant microorganisms by explaining antibiotic misuse with each of their patients in the hospital and in the out-patient setting. True False Answers: 1.T 2.F 3.T 4.T 5.F 6.T 7.T 8.F 9.T 10.T 27

28 CHAPTER 2 WOUND CARE (10 Contact Hours) Learning objectives!! Compare and contrast the various types of acute and chronic wounds.!! Identify the incidence and prevalence of acute and chronic wounds within the United States.!! Describe the normal anatomy and pathophysiology of the skin.!! List each of the phases required in order for the skin to heal normally.!! Compare and contrast the three ways wounds close.!! Identify the generalized factors that affect the normal healing process.!! Compare and contrast the different risk factors for each of the acute and chronic wounds.!! Describe the nurse s responsibility in completing the wound history and assessment.!! Describe treatment modalities for each of the wounds.!! Identify the nurse s responsibility in preventing acute and chronic wounds from occurring within the community and hospital.!! Identify the legal aspects for the nurse caring for a patient with a chronic wound. Introduction Wounds may be acquired from many different sources, such as bites, burns, punctures, scrapes, skin tears, surgically provoked and/ or chronic wounds, such as pressure ulcers typically induced from lack of mobility or leg ulcers that result from venous or arterial insufficiencies. Therefore, it may be difficult to assess the wound based upon the nature of origin, the patient s risk factors, and/or other co-morbidities that may affect the healing process. There are many wound-care dressings and products that may be prescribed by providers, and it may be difficult to understand the reason one product and/or type of dressing may be utilized over another for what a nurse may perceive as a similar wound. Ideally each facility should have a wound-care nurse to ensure that the proper dressings and/or products are being utilized appropriately for various types of wounds. However, realistically, a wound-care specialist may not be feasible or easily accessible. Therefore, it is imperative that nurses are enlightened and knowledgeable about the various products to ensure that wounds will be properly treated. There are many variables that intertwine and affect the healing process and capabilities. Therefore, throughout this educational offering the most common wounds will be analyzed and described to ensure that nurses and health care professionals are able to properly identify and treat the different types of wounds that may present on any shift assignment. In addition, it is important for the nurse to understand the mechanism behind the wound injury to prevent certain wounds, recognize the potential risk factors that predispose patients to various wounds and then to be able to properly identify and treat the wounds appropriately. Common skin injuries The definition of a wound is a breach in the external surface of the body [82]. Anytime there is a break in the outer layer of skin, also known as the epidermis, there is a wound. Depending upon the nature and degree of the wound, the overall well-being of the patient may be affected by the injury and/or complications of the wound. Therefore, nurses must be able to recognize the injury, then respond to it quickly to reduce the risk of complications, especially with wounds that are contaminated immediately due to the mechanism of the injury. The most common wounds will be explored. Acute wounds include but are not limited to abrasions, lacerations, puncture wounds, surgical wounds, burns and skin tears [3]. Chronic wounds consist of pressure ulcers, venous and arterial leg ulcers, diabetic foot ulcers and nonhealing surgical wounds [3]. 1. Abrasions, excoriations or scrapes These terms are typically used interchangeably as they are defined by superficial breaks in the epidermis of the skin due to friction, force or rubbing against an abrasive surface and/or a fall [78, 85]. Therefore, if there is an abrasion, excoriation or scrape, the deepest layers of the skin remain intact, such as the dermis and hypodermis. Thus bleeding is described as a slow oozing flow, and the skin injury will typically heal without antimicrobial ointment, unless there is a foreign body imbedded in it [78, 85]. According to the Association for Advancement of Wound Care (AAWC), the most common sites for abrasions, excoriations or scrapes occur in [78]: Upper extremities. Lower extremities. Buttocks. 2. Bites An animal or a human can inflict a bite, eliciting potential tissue and/or nerve damage, infection and rabies. A bite may be considered an abrasion, puncture wound, laceration, avulsion (the tissue separating from the body) or a combination of any of them depending upon the depth of the bite [85]. Typically, the presentation of the bite is specific to the particular source, such as: Dog bites appear as a laceration or avulsion and typically have components of a crush injury [31]. Cat bites, in contrast, typically induce a puncture wound in which bacterial organisms can be introduced [31]. 28 A human bite is no different than an animal bite; whether it was accidental or intentional will typically determine the severity of damage to the skin. There are three main types of human bites: a closed-fist injury, chomping injury to the finger, and puncture wound clashing with the head [4]. Each of the examples is elaborated upon as follows [4]: Closed fist injury occurs from striking an opponent s tooth during a fight. Chomping injury affects tendons, and their overlying sheaths are often affected by the bite. Head injury may appear as a mild wound, but deep bacterial contamination is possible. All bites are capable of inducing an infection, but human bites can also potentially transmit the hepatitis B and human immunodeficiency virus (HIV) during the bite [82]. In addition, cat and human bites are more likely to become infected than dog bites [7]. The unique component of a bite is the vast array of bacteria species found in the mouth, and there are usually more than just one present [51]. For instance, there are more than 64 species of bacteria found in the mouth of a dog or cat [51]. However the most common type of bacteria found in animal bites is the Pasteurella Multocida species, found in approximately 75 percent of cat bites and 50 percent of dog bites [44]. Other types of bacteria that may be found in animal bites include but are not limited to staphylococcus aureus, staphylococcus epidermidis, streptococcus and escherichia coli (E. coli) [51]. Human bites are typically composed of streptococcus, staphylococcus, or eikenella corrodens (found in 30 percent of all patients) [44]. The reason animal bites induce infection is

29 attributed to the normal aerobic flora of human skin coming in contact with anaerobic and aerobic oral flora of the biting animal, which is capable of inducing an infectious process[51]. 3. Bruises Bruising is a visible result or contusion caused by damaged blood vessels that are broken during an accident or trauma [73]. 4. Burns Burns are the leading cause of accidental death and are typically caused by the following [20]: Thermal Residential fires, automobile accidents, playing with matches, improper handling of fireworks, scalds. Chemical Contact, ingestion, inhalation or injection of acids, alkalies, or vesicants. Electrical Contact with faulty electrical wiring, electrical cords or high voltage power lines. Teenage boys have a higher incidence of suffering from an electrical burn due to their innate demeanor of being eager to experiment [50]. Friction or abrasion. Ultraviolet radiation Sunburn. Scald Water or grease. During a burn injury, collagen is lost, creating abnormal osmotic and hydrostatic pressure gradient, which causes the movement of intravascular fluid into the interstitial space [3]. During the cellular injury, mediators of inflammation are released. One of the most common forms of burns seen is scalding due to beverages, food and bath water [3]. According to the American Burn Association, a scald depends upon the temperature level one is exposed to and the length of time of exposure [3]. The American Burn Association provided the following examples [3]: The most common standard water temperature in a home is 120 degrees. If an individual is exposed to the maximum temperature for five minutes, he or she will suffer from a fullthickness injury. Typically, coffee, hot tea and hot chocolate are served at 160 degrees; at 140 degrees, it takes less than five seconds for one to suffer a burn injury. 5. Lacerations or cuts Lacerations or cuts typically go through all layers of the skin into the fat or deeper tissues, typically induced by a blow from a blunt object, a fall and/or contact with a sharp object. Most lacerations induce bleeding that is brisk or more severe due to various layers of tissues being torn [30]. A laceration (cut) may be defined as an incision or jagged [50]. It is important to note that how the laceration or abrasion was inflicted will determine how it will affect the normal healing process and the risk of infection to the injured area. The most common bacterial pathogens that affect lacerations or abrasions are staphylococcus aureus and B-hemolytic streptococcus [82]. 6. Perineal skin breakdown Research has demonstrated that incontinence, perineal skin breakdown and pressure ulcers typically coincide together [66]. The perineal skin breakdown occurs because of the moisture from incontinence, which alters the skin s normal protective ph, thus increasing the permeability of the stratum corneum (the outermost layer of the dermis) [66]. Perineal skin breakdown may be exacerbated by feces, which contains bacteria that will permeate the stratum corneum, allowing secondary infections to occur [66]. 7. Pressure ulcers are used interchangeably with decubitus ulcers and/or bedsores in the majority of the literature. The Agency for Healthcare Research and Quality (AHRQ) has endorsed the term pressure ulcers into its literature and research [41]. Since 2007, however, the Joint Commission (JCAHO) has provided definitions differentiating the terms decubitus ulcers and pressure ulcers [44]: Decubitus ulcers refer to the breakdown of the skin and subcutaneous tissue due to prolonged, unrelieved pressure over a bony prominence, often associated with malnutrition, paralysis, and/or physical deformity. The word decubitus means recumbent or horizontal posture. Pressure ulcer is a broader term that includes decubitus ulcers, but also includes ulcerations associated with prosthetic limbs or dental prosthesis. The ulcers that develop from dental prosthesis typically occur in the elderly. Unfortunately it can impact their nutritional status. The National Pressure Ulcer Advisory Panel (NPUAP) defines a pressure ulcer as a localized injury to the skin and/ or underlying tissue, usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/ or friction. A number of contributing or confounding factors are also associated with pressure ulcers; the significance of these factors is yet to be elucidated [94]. Pressure ulcers are caused by an impaired blood supply and tissue nutrition resulting from prolonged pressure over bony or cartilaginous prominences [57]. Pressure ulcers typically occur in localized areas that involve necrosis at the cellular level in the skin and subcutaneous tissue over the bony prominences [53]. Research has demonstrated that part of the injury related to pressure ulcers is caused by ischemia to the area followed by reperfusion (restoration of the blood flow) [39]. Once the oxygenation process has been activated, reactive oxygen species (ROS) causes an uncontrolled oxidation of vital cellular components, such as hydroxyl radical (HO) [39]. Therefore, ischemia-reperfusion (I-R) injury and reactive oxygen species (ROS) play an integral role in the pathogenesis of pressure ulcer development [39]. 8. Punctures Puncture wounds are inflicted by sharp objects entering the skin, such as stepping on a nail, getting stuck with a needle or being stabbed with a knife. Depending upon the depth and object utilized, the bleeding may be minimal, and the wound may not be very noticeable [30]. 9. Skin tears Defined as a traumatic wound resulting from separation of the epidermis from the dermis layer of the skin that occurs with friction or shearing [4]. The majority of skin tears, approximately 80 percent, occur on the upper extremities, especially the arms and hands [9]. 10. Surgical wounds A surgical wound is defined as a deliberate incision produced during a surgical procedure; it is the original incision [26]. 11. Ulcers An ulcer is a concave lesion with a sunken appearance that is the result of trauma and/or poor circulation. Ulcers extend from the epidermis into the dermis layer of the skin [18]. The most common chronic wound ulcers are pressure ulcers, diabetic foot ulcers and leg ulcers. However, due to the prevalence and wealth of information revolving around pressure ulcers, it will be addressed individually here. Diabetic foot ulcers Diabetic foot ulcers typically occur from consequences of diabetic neuropathy and can cause substantial morbidity [38]. The most common lesion found on a diabetic foot ulcer is an infected malperforans [38]. 29 Leg ulcers The most common cause of leg ulcers is venous or arterial (ischemia). Differentiating between the two types of ulcers can be very challenging for practitioners; therefore

30 it is imperative to properly assess the wound. Arterial ulcerations and mixed arteriovenous ulcers (a combination of venous and arterial disease) comprise 14 percent of all leg ulcers; 75 percent are related to venous ulcers [47]. Arterial/ischemia Arterial ulcers are the result of peripheral vascular disease due to atherosclerosis with micro vascular or macro vascular changes [47]. Venous The main culprit of venous ulcers is related to venous hypertension [25]. Chronic venous insufficiency is caused by high pressure in the veins that occurs due to abnormal blood flow [61]. Anatomy and pathophysiology of the skin In order to understand the various types of wounds that may occur, it is imperative to recognize the duty and purpose of each layer of skin because the affected portion during the wound injury may determine the effect on the healing process. The skin is the largest organ of the body and the primary mode of defense for the body. If there is a break or injury to the skin, it will affect homeostasis and can affect the overall health of the patient [41]. The total surface of the skin ranges from 15 to 20 square feet and accounts for 15 percent of the total body weight [72]. The majority of literature concludes that skin has four major functions [19, 28]: Acts as a barrier for protection of underlying structures against microorganisms and infectious agents. Protects and regulates the body temperature through conduction, convection and radiation. Aids in elimination of waste. Prevents dehydration. However, the skin has many additional functions in order to keep the body protected and functioning at an optimal level [41, 74]: Resistance to trauma and infection. The epidermis protects the body and skin from injury through [41]: Keratin, which provides protection to the epidermis layer. The epidermis, which inhibits proliferation of microorganisms because of its dry external surface. The epidermis, which protects the skin through intracellular bonds. The dermis protects the skin through the fibroblasts, which facilitate wound healing processes. In addition, the dermis provides mechanical strength through collagen, fibers, elastic fibers and ground substances such as fibroblasts. Vitamins The epidermis produces and regulates vitamin D synthesis. Sensation The dermis layer transmits sensations through the neuroreceptor system, enclosing an extensive network of nerve endings for relaying sensations to the brain. Thermoregulation The epidermis layer regulates the temperature through eccrine sweat glands as they dissipate heat through the evaporation of sweat secreted onto the skin surface. The dermis layer regulates the temperature through cutaneous vasculature dilation or constriction from the skin surface. Homeostasis The epidermis is able to regulate homeostasis through low permeability to water and electrolytes; in the dermis, the lymphatic and vasculature tissues respond to inflammation, injury, and infection. Although some texts disagree on the number of layers found in the skin, here we will explore each of the major layers because a wound injury may affect one or multiple layers of the skin. The majority of textbooks concur that the two major layers of the skin are the epidermis (a stratified squamous epithelium) and the dermis 30 (a deeper layer of connective tissue) [72]. The other two layers are important to mention because a breach in any aspect may affect the overall well-being of the patient: 1. Subcutaneous fat (adipose tissue) There is another layer of the skin that lies over the muscle and bones, the subcutaneous fat, also known as adipose tissue [41]. 2. Hypodermis Beneath the dermis, there is another layer of connective tissue, composed of subcutaneous tissue or superficial fascia that connects the overlying dermis to the underlying muscle [53]. The hypodermis (subcutis) is not typically alluded to as being part of the skin but is typically correlated in studies with the main two layers of the skin, the epidermis and dermis layers [72]. The skin is composed of two major layers [53, 72]: Epidermis The epidermis is the most important layer of the skin because it is on the outside, exposed to all of the external variables. The epidermis is composed of keratinized stratified squamous epithelium, which consists of dead cells packed with a tough protein keratin. The epidermis has a limited supply of blood to provide nutrients and thus depends upon the diffusion of nutrients from the underlying connective tissue, the dermis. The majority of the epidermis skin is very thick, approximately 1 to 2 millimeters (mm) in size; however the thickness varies depending upon the location, such as: Eyelids, less than 0.5 mm. Shoulders, up to 6 mm. It will thicken as needed from corns or calluses in areas of constant pressure or friction. The epidermis is composed of four to five layers of cells [72]: Stratum basale consists of a single layer of low columnar stem cells and keratinocytes on the basement membrane. Stratum spinosum consists of several layers of keratinocytes. Stratum granulosum consists of three to five layers of flat keratinocytes, typically in the thicker skin. Stratum lucidum consists of a thin translucent zone superficial to the stratum granulosum, typically seen only in the thick skin. Stratum corneum is the outermost layer of the dermis. It contains over 30 layers of dead, scaly, keratinized cells that make it waterproof. Keratinocytes are dead squamous cells that form the protective barrier of the skin. The average life of a keratinocyte is about 28 to 45 days in which it will shed (exfoliate) [41]. If the stratum corneum is not intact, the normal skin bacterium invades deeper into the skin, eventually accessing the bloodstream [19]. The epidermis is composed of five to six types of cells [72]: Stem cells are found in the deepest layer of the epidermis, called stratum basale. Keratinocytes are the most abundant of the epidermal cells. Melanocytes occur only in the stratum basale. Tactile (merkel) cells are relatively small in amount but are the receptors for the sense of touch. Dendritic (Langerhan) cells are found in two layers of the epidermis, called the stratum spinosum and stratum granulosum. The dendritic cells are macrophages that originate in the bone marrow, but migrate to the epidermis and other epithelial cells. The unique component of the dendritic cells is that they are the invaders during any injury or infection and they alert the

31 immune system to fight off the pathogens that penetrate into the skin. Dermis The dermis is a deeper layer, located above the adipose tissue (fat pad) [41]. The dermis is composed of irregular connective tissue with a rich blood, lymphatic and nerve supply; however it does not have any cells [41]. Therefore the dermis is rich in sensory nerves, which allows a patient to feel touch, pressure, temperature, pain and the urge to scratch/itch (pruritis) [41]. The dermis is composed mainly of collagen, but it has reticular fibers, fibroblasts and other fibrous connective tissue that allows it to be flexible [41]. Anytime there is an injury, collagen production increases as it forms scar tissue [41]. The dermis size varies from 1 to 4 mm in thickness [72] and is composed of two layers, the papillary and reticular layer [72]: Papillary layer is a thin zone of areolar tissue in and near the dermal papillae. Reticular layer of the dermis is deeper and much thicker. It consists of dense irregular connective tissue. Normal wound healing Ideally, the goal for all patients who present with a wound is for optimal healing at the cellular level. However, there are circumstances in which that doesn t happen. The depth of a wound determines whether the wound is at risk of becoming infected with bacteria, other substances, or whether it will leave a scar [28]. Wounds that do not penetrate the stratum germinativum, the basement layer of the skin, do not leave scars [28]. In order for wound healing to occur, two processes need to occur [86]: Regeneration to repair lost tissue with identical functional tissue. Connective tissue repair is lost tissue being replaced by formation of a scar. Once the skin has been broken, there are a few phases that need to occur simultaneously to ensure that wound healing occurs efficiently and the area reaches its optimal level of functioning [28]: Injury phase Once the injury occurs, the physiological aspects of the body are immediately working to restore a functional barrier to prevent further injury and/or damage to the skin. The injury phase is when the injury initially occurs, and involves the initiation and release of coagulating factors to halt the bleeding process by narrowing the blood vessels, thus forming a clot. In addition, platelets are initiated and released to facilitate the healing process. The explanation of platelets will be discussed in the inflammatory phase as they work simultaneously, typically overlapping phases. Epithelialization During this phase, the epithelial cells (keratinocytes) migrate across the wound surface providing new skin to act as a protective barrier and to protect against excessive water loss and bacteria [30]: The epithelialization phase typically begins its reconstructing within a few hours after the injury and it is complete within 24 to 48 hours in a clean, sutured wound. If it is an open wound, it may take seven to 10 days because the inflammatory process is prolonged, thus increasing the risk of the wound scarring. However, it may be delayed in dehydrated, deoxygenated skin [41]. Inflammatory phase The inflammatory phase is initiated immediately after any injury, thus occurring simultaneously with the injury phase. The inflammatory phase typically lasts two to five days [78]. During this phase, the damaged tissue will release chemical mediators, such as cytokines, which are responsible for initiating complex processes that cause homeostasis and begins the healing process [28]. During this inflammatory phase, there are other chemicals that are released to promote the healing process and clear the wound of debris [28]: Vasoconstriction occurs to reduce bleeding at the site of injury. Platelets aggregate, inducing bleeding, which is contradictory to it also releasing vasoconstriction methods, but with the combination of serotonin it activates the coagulation cascade. This process results in the conversion of fibrinogen into fibrin, which forms a platelet plug. The platelet plug activates vasodilatation and increases capillary permeability, which allows plasma to leak into the tissue surrounding the wounded area also known as the inflammatoryexudate. Thromboplastin Makes a clot. Once the homeostasis component is complete, monocytes and neutrophils are released to the site of injury. The monocytes activate the macrophages, which produce growth factors and cytokines. The monocytes are the immature white blood cells; the macrophages are the mature white blood cells. The macrophages are responsible for wound debridement [81]. The neutrophils trap and kill bacteria immediately. Once the wound becomes mononuclear, the neutrophils and macrophages will cease, signaling the end of the inflammatory phase and the initiation of the proliferative phase [18]. During the inflammatory process, the skin will exhibit the following appearance [81]: Redness due to the vasodilatation process per prostaglandins being released, such as prostacyclin (PG12). Edema due to the leakage of plasma proteins through gaps in the vascular endothelium. Edema is caused by prostaglandins, which also promote blood flow, contributing to the heat and edema around the wound. Once the wound is inflamed and warm to touch, it allows inflammatory cells to enter the wound due to increased vascular permeability. Heat as explained under edema. Pain is elicited by the effects of PG12 and other prostaglandins as they exert their effects on the sensory nerve endings. Proliferative phase The proliferative phase typically begins to work within two to three days after the injury; it is stimulated by the arrival of fibroblasts into the wound [81]. The proliferative phase is known as a matrix or latticework of formation of cells [30]. The proliferative phase is broken down into three stages [92]: Granulation During the granulation phase, new skin cells and blood vessels form to nourish the area as they supply and rebuild the cells with oxygen and nutrients to support the production of proteins, also known as collagen [30]. Collagen is the major component of acute wound healing, which takes approximately six weeks [81]. The major reason that collagen fibers work efficiently is that macrophages recruit fibroblasts [28]. The fibroblasts are driven by the macrophage that proliferate and synthesizes glycosaminoglycans and proteoglycans, the building blocks of the new extracellular matrix of granulated tissue and collagen [81]. Contraction consists of wound edges pulling together to reduce a defect in the wound healing process and potential scar formation [92]. Epithelialization crosses moist surfaces, and cells travel about three centimeters (cm) from the point of origin in all directions [92]. 31

32 During the inflammatory process, the skin will exhibit the following appearance [30]: The new small blood vessels, or capillaries, provide a pink and/or purple erythemic appearance. The proliferative phase typically lasts two days to three weeks [28]. Remodeling phase The remodeling phase is the final process. It typically begins two to three weeks after the injury to the skin. During this time, the collagen is more organized, ensuring that the tissue is stronger. Typically the blood vessels become less dense as demonstrated by the wound losing the pinkish appearance [30]. The appearance of the wound changes throughout this period, which is a reason many plastic surgeons wait six months before revising a scar [28]. In addition, the scar tissue is approximately 80 percent as strong as the original tissue [92]. Thus, if there is repeated injury and/or trauma to the area, scar tissue forms making the area harder and more difficult to treat if surgery is required. Methods of wound closure Another factor that contributes to the healing process is the type of method used to close the wound. The provider will choose the optimal manner to close the wound, dependent upon the patient s history, the amount of tissue damaged or lost during the injury and the potential for infection [86]. The primary methods of wound closure include primary, secondary and tertiary intentions [50, 86]: First intention healing involves the primary closure of the wound by mechanical mechanisms, such as tape, sutures, staples or glue. Steri-strips should be utilized if it is not over a hairy surface or joint. The method of first intention is preferred if there is minimal tissue loss and the skin edges are well approximated. The wound will repair through the normal phases of wound healing process. If the patient has no risk factors and/or comorbidities, the incision line is resurfaced and able to fight potential bacteria within 72 hours of closure. Although the external surface may appear as if it is healing adequately, the nurse and patient should not assume the integrity of the skin is functioning at the optimal level as it takes more time to heal. A healing ridge occurs along the incision line between days five and nine days after repair. The healing ridge is exhibited by firm edema or induration and it extends approximately 1 to 2 centimeters (cm) outside the incision line. It is important to assess for this ridge, as failure to notice may imply further treatment or intervention is needed to relieve stress on the wound. Therefore, the nurse should contact the doctor. The proliferative phase may take up to 21 days to heal. The advantage of first intention healing is that there is typically limited scar formation once the wound has healed. Examples of primary intention closure include surgical incisions. Secondary intention healing involves wounds that are left open to heal spontaneously or surgically due to significant tissue loss, damage and/or bacterial contamination. The healing process is typically extended due to the multiple layers of skin damage. Granulation occurs, and will induce bleeding in the wound. Deep and wide scars eventually form once the wound is healed. Examples of secondary intention include open abdominal wounds, dehisced wounds, stage three or four pressure ulcers, burn injuries, traumatic injuries and infected wounds. Tertiary intention healing involves a combination of primary and secondary intention. Typically the physician will leave the wound open for a short period of time to allow the edema and exudate to resolve and/or diminish. During this time, the nurse will be responsible for packing the wound with normal saline and dressings. Once this short period is over, the physician will close the wound by primary intention. The primary goal of treatment with tertiary intention is promoting the restoration of the skin and tissue integrity to the physiological optimal levels. In order for the wound to heal, multiple facets are considered. Factors that affect the healing process There are certain co-morbidities, lifestyles and/or medications that patients may be taking that can affect the ability of their skin to heal appropriately. The most common factors that contribute to the inability of the wound to heal properly are [78,81]: 1. Age Aging of the body affects the structure and function of the skin. During the aging process, everything slows down, including the phases of wound healing [86]. Functional changes in the skin include a decreased inflammatory response and thinning of the skin, which predisposes the elderly patient to fragility and injuries [19]. There are a few physical findings in the elderly that affect their ability to heal appropriately within the layers of the skin [41, 71]: Epidermis. Decreased thickness in the epidermal layer that causes an increased transparency and fragility. Delayed wound healing due to decrease in cell replacements. Decreased number of Langerhans cells. Change in the size and shape of the keratinocytes. Dermis. Decreased dermal blood flow, which causes an increased susceptibility to dry skin (xerosis). Decreased dermal thickness, which causes a paper-thin, transparent appearance increasing the risk of pressure ulcers. 2. Nutrition It is imperative that the patient has optimal nutritional intake to promote healing. If the patient lacks the necessary nutrients, the wound is unable to maintain adequate energy for collagen synthesis and is unable to heal appropriately [87]. 3. Obesity A patient who weighs greater than 20 percent of his or her ideal body weight is at greater risk of dehiscence, herniation and infection, thus exacerbating the wound healing process [86]. Obese patients have an abundant amount of adipose tissue, which is poorly vascular, thus increasing the incidence of ischemia. The nurse can reduce the risk of complications of dehiscence and herniation by encouraging the patient to utilize a binder or splint over the incision during straining or coughing [86]. 4. Presence of debris, necrotic tissue and infection Infection can cause collagen lysis. Tissue necrosis occurs from radiation treatments, which may increase the risk of local or systemic ischemia. 5. Repeated trauma If a patient has multiple wounds or surgeries, then the body s immediate defense mechanisms become limited due to the multiple requirements of the body at the same time. 6. Skin and moisture Skin must have an adequate amount of fluid to ensure adequate functioning and viability of the tissue. 32

33 Each of the layers of skin typically holds a certain amount of water [60]: Dermis contains about 80 percent. Stratum corneum about 30 percent, which is not uniformly distributed, varying from approximately 40 percent in the inner layers to 10 to 15 percent in the outermost layer. However, it can increase to approximately 60 percent when the skin is immersed or exposed to a very wet environment. If the moisture in the skin is altered in any format, even at a minimum level of 10 percent, the patient may exhibit dryness and scaling of the skin, thus predisposing the patient to further skin breakdown and potential infection [80]. In severe cases, total dehydration induced by death of the underlying dermal structures will lead to the formation of eschar, commonly associated with pressure ulcers [80]. According to World Wide Wounds (WWW) (2008), the effect of moisture on the skin can be described by a simple phenomenon that every individual can relate to on a daily basis [80]: After an individual takes a shower or bath, the skin will appear soft and wrinkled, which occurs from water permeating the intracellular spaces, crossing over the cell membranes then swelling the corneocytes. The same concept and phenomena is applicable if the integrity of the epidermis is seriously compromised by trauma, metabolic or physiologic disorders. The healing rate of the wound will be influenced by the moisture content of the surrounding skin and the local environment. If the skin is too dry, epithelialization will be delayed. If the skin is too wet, the patient is at risk for developing maceration and/or infections. 7. Systemic causes Common systemic disorders include diabetes mellitus (DM), malnourishment and immunodeficiency. DM plays an enormous role in the healing process of wounds and potentially predisposes the patient to wounds due to diminished sensation and poor arterial flow. The patient with DM is compromised due to the microvascular/macrovascular changes, poor glycemic control and loss of sensation (peripheral neuropathy). It is imperative to gain adequate control of the blood glucose in the diabetic patient to promote wound healing. Due to various systemic health conditions, the patient may be prescribed various drugs that may further exacerbate the healing ability of the skin. There are certain drugs that patients may take for other disease processes that may induce thinning of the skin, such as long-term steroids. Other diseases that may affect ability to heal include autoimmune disorders such as rheumatoid arthritis (RA) and systemic lupus (SLE). Typically, RA and SLE impair the healing process, and they require systemic steroids or immunosuppressive agents, which further exacerbate the wound s ability to heal [87]. 8. Tissue hypoxia The most common causes of tissue hypoxia are related to arterial occlusions or vasoconstrictions, hypotension, hypothermia and peripheral venous congestion. If there is a limited supply of oxygen to the wound, it inhibits the production of collagen. When the patient has an inadequate amount of oxygen circulating throughout the bloodstream, the patient will endure vasoconstriction. This may be the result of low blood volume, unrelieved pain or hypothermia. Any time a wound has excessive tension on the edges, it induces local tissue ischemia and necrosis of the area, thus impeding normal wound healing. Smoking also leads to tissue hypoxia. 9. Xerosis (dry skin) Individuals who endure dry skin, especially the elderly, are at risk for skin lesions, excoriations, infection and lichenification (thickening) due to scratching and rubbing the skin and thus further exacerbating the difficulty for the skin to heal adequately [41]. 10. Wound infection All wounds are contaminated with bacteria due to the injury process. However, the host s immune competence and the size of the bacterial inoculum determine whether the wound will become infected. If the patient has normal host defenses and adequate debridement, then a wound may have 100,000 microorganisms per gram of tissue and still heal effectively. It is important that nurses recognize that due to the lack of inflammatory response that occurs in the elderly, the geriatric population may not exhibit the typical signs and symptoms of infection such as fever, erythema and swelling at the site. However, in the elderly, the patient may have increasing pain, fatigue, anorexia and/or changes in the mental status [50]. Risk factors for developing various wounds Typical wounds that nurses care for in the hospital, out-patient and/ or home health settings are usually secondary lesions that are acute or chronic. However, collecting a thorough history and analyzing risk factors to assess the patient s co-morbidities will enable one to differentiate between acute and chronic wounds. The time frame of the wound being inflicted and the patient s risk factors and co-morbidities will help the nurse identify the anticipated healing process and make the differentiation. [98]: Acute wounds heal promptly, within three to 11 days with an adequate immune system and no other co-morbidities. Otherwise, an acute wound may heal in 30 days. However, a nurse can expect an acute wound in a diabetic to heal within 60 days. Chronic wounds take longer than 30 days if the patient is not diabetic. If the patient is diabetic, the healing process is affected tremendously because of the disease process of the DM and problems regulating blood sugars and further complications that develop, especially chronic wounds. 1. Abrasions, excoriations or scrapes Minor risky behavior can predispose an individual to a minor skin injury, such as: Bicycling. Playing ball. Skateboarding. In addition, abrasions may occur on a patient who is elderly, frail or confined to a wheelchair [4]. 2. Bites Children are more likely to be bitten, but individuals over 50 and those who are immunocompromised are more likely to develop an infection [6, 27]. 3. Bruising Anything can cause a bruise on the skin, but patients at the highest risk include the elderly and individuals at risk of falling. In addition, depending on the location of the bruising or whether a hematoma is present, the nurse should assess for a family history of any clotting disorders, hemophilia or whether the patient is taking any anticoagulants or nonsteroidal antiinflammatories (NSAIDS) that may exacerbate the problem or inflict bruises on the skin [4 ]. 4. Burns Everyone is at risk from suffering from a burn, but those with the highest risk factors are children, the elderly and individuals who have disabilities [3]. Research has determined that the following may affect the patient s mortality risk [57]: History of electrical injury. History of concomitant trauma (especially penetrating). Female sex. 33

34 Duration of stay in an intensive care unit (ICU). which include malnutrition, vitamin deficiencies and Presence of mechanical ventilation. obesity. Chronic diseases of the hematological system, such as 5. Lacerations or cuts Patients who use any tools or sharp anemia, polycythemia and myeloproliferative disorders. instruments in their profession or as a hobby have higher risks With sickle cell anemia, a patient may develop lower [4]. extremity ulcers that may resemble venous ulcers or other 6. Perineal skin breakdown The risk factors for perineal skin injuries to the lower extremities [48]. breakdown include incontinence of urine and/or feces. Chronic diseases of peripheral vascular pathology, such 7. Pressure ulcers Many of the numerous risk factors are as atherosclerotic disease, chronic venous insufficiency integrated, thus further exacerbating the risk of a pressure ulcer and lymphedema. developing, especially for the elderly. Chronic diseases of the renal system, such as renal failure Elderly The major risk factor is age; 60 to 90 percent of all or incontinence. pressure ulcers occur in the elderly [19] because of normal Other chronic disease processes, such as edema and physiological changes that occur in the aging process, such sepsis. as [41]: 8. Punctures Emedicine health has identified that most puncture Cognitive changes A patient with a memory deficit wounds are caused by risky behavior or an occupation that may not recognize the urge to shift or change position frequently and recognize or verbalize an area of erythema or pain in his or her skin. predisposes an individual to sharp items. The most common causes of puncture wounds are wood splinters, pins, nails, glass, scissors and knives [29]. Skin changes The skin goes through a vast array of changes during the aging process. A few of the specific 9. Skin tears The major risk factor for skin tears is fragile skin contributing factors are: in the elderly population [4]. In addition to the elderly, other Thinner skin (atrophy) due to the dermis decreasing individuals at risk for a skin tear include [4]: in size. Once the dermis begins to decrease in Individuals who are dependent upon caregivers for size, the skin becomes paper-thin and translucent maintaining their activities of daily living (ADL). in appearance. Atrophy is the shrinkage of tissue Individuals who use wheelchairs. through a loss in the cell size or number [72]. Individuals with visual, mental or sensory impairments. Dryer skin due to decreased vasculature. 10. Surgical wounds Although there is a risk of infection with Wrinkled skin due to the loss of elastin fibers. any surgical procedure, the Study of the Efficacy of Nosocomial Loss of muscle. Infection Control (SENIC) has identified four major risk factors Immobility Any patient who requires assistance in turning for a patient developing a postoperative wound infection [46]: or positioning and who cannot cognitively verbalize the urge Abdominal surgery. to shift their position is at high risk for an ulcer formation. Surgery lasting more than two hours. Incontinence Patients who are incontinent of their bowel Contaminated or dirty wound classification (See Treatment of or bladder functions are exposed to various chemicals surgical wound). that break the skin down, such as urea, bacteria, yeast and Patient with at least three medical diagnoses. enzymes [41]. Research has demonstrated that 56.7 percent of patients with pressure ulcers had fecal incontinence and The SENIC has suggested that patients with two or more of were 22 times more likely to have pressure ulcers than the four risk factors are at an increased risk of developing patients without fecal incontinence [66]. a postoperative surgical wound infection, and they should Nutritional deficits Poor nutrition and/or deficiencies play definitely receive prophylactic antimicrobial treatment [46]. an important role in a patient developing pressure ulcers. 11. Ulcers Intact skin and wound healing are dependent upon positive Diabetic foot ulcers The major risk factors include nitrogen balance and adequate serum protein levels [41]. diabetes and a diagnosis of it more than 10 years ago, having Disease processes There are certain disease processes that poor glucose control or having cardiovascular, renal or retinal may also predispose an individual to developing pressure complications or being a male. [19]. ulcers, such as [53, 78]: Leg ulcers: Hip fractures contribute to 66 percent of elderly adults Arterial ulcers While peripheral vascular disease with a pressure ulcer [19]. (PVD) is a major cause of developing arterial ulcers, Neurological disorders due to loss of sensation, rather patients with diabetes mellitus, trauma or advanced age than being immobile, such as spinal cord injuries (SCI), also are at risk [76]. dementia and cerebrovascular disease (CVA). Venous ulcers Venous ulcers are present in just 3.5 Chronic diseases of the cardiopulmonary system, such percent of all patients over 65 years of age. However their as chronic obstructive pulmonary disease (COPD), recurrence rate is more than 70 percent [19]. Patients are congestive heart failure (CHF). at risk of developing venous ulcers if they have a history Chronic diseases of the endocrine system, which of deep vein thrombophlebitis and thrombosis, a failed include DM and hypothyroidism. It is estimated that as calf pump, advanced age, pregnancy and/or a family many as 10 to 15 percent of the 20 million individuals history of venous ulcers [76]. Another risk factor is living with diabetes are at risk of developing diabetic immobility of the calf muscle, such as a paraplegic might ulcers [48]. Patients with diabetes may develop lower have [56]. extremity ulcers as a result of neuropathy with or without contributing factors [48]. Wound history and assessment Chronic diseases of the gastrointestinal system (GI), It is imperative to correctly identify any potential skin injuries to 34

35 prevent complications. Once a wound or break in the skin has been noted, nurses and practitioners need to properly assess the patient by gathering a complete history of present illness, current/past medical history, medications and a social history because each of these variables may affect the healing process. Once the history has been obtained, it is imperative to assess the patient completely, not just the wound. There are numerous organizations and guidelines to help reduce the incidence and prevalence of pressure ulcers nationwide. One of the organizations, the Institute for Healthcare Improvement (IHI), initiated and developed the 5 Million Lives campaign that sought a reduction of 5 million instances of harm from December 2006 through December To help do so, the IHI created stringent guidelines to reduce the incidence and prevalence of various disease processes, such as pressure ulcers, from occurring in health care facilities. Skin risk assessment tool Every patient admitted to a facility is required to have a skin risk assessment tool (such as the Braden scale) completed and a complete wound assessment upon admission according to the guidelines of JCAHO and the majority of hospitals. Nurses complete an initial skin assessment to reduce the risk of pressure ulcers or any skin breakdown from developing during the hospitalization. Depending upon the facility s policies and protocols, nurses may be required to complete the skin assessment more frequently on their patients. According to the guidelines of the Gerontological Nursing Interventions Research Center and summarized in the National Guideline Clearinghouse, facilities should abide by the following reassessment guidelines [16]: Acute-care patients should be assessed on admission, then reassessed at least every 48 hours. However, patients with risk factors or co-morbidities admitted in high-risk areas such as the intensive care unit (ICU) should be reassessed one to two times a day. Long-term care patients should be assessed on admission and then reassessed every 48 hours for the first week, then weekly for the first month, then quarterly or whenever their health status changes. Home health care patients should be assessed on admission, then reassessed at every visit. If the facility where a nurse is employed recommends more frequent skin assessment risk tools or reassessments to be completed, the nurse needs to adhere to the employer s protocol. The AHRQ (formerly Agency for Health Care Policy and Research) is an organization that works on providing clinical practice guidelines on pressure ulcer prevention. The AHRQ recommends an initial pressure ulcer risk assessment upon admission to a facility and then periodic reassessments [43]. The IHI recommends daily assessments on all patients at high risk or once their condition has changed [43]. In addition, if the patient is identified as high risk based upon the assessment, the patient should be properly identified with a visual cue, which could be placed on the patient s chart, arm band and in the patient s room to ensure all staff members are aware that the patient is at high-risk for developing a pressure ulcer [43]. Since February 2006, JCAHO has recommended in its national patient safety goals that all health care providers utilize one of the validated risk assessment tools, such as the Braden or Norton scales, to identify all patients at risk for developing a pressure ulcer, particularly long-term-care patients [44, 92]. Although the Braden and Norton scales are the most commonly used, there are other scales that may be used across the nation, such as the Gosnell, Knoll and/ or Waterlow scales. However, the Braden Scale developed in 1984 is the most widely used for predicting the development of pressure ulcers and any skin breakdown during the hospitalization admission. The Braden Scale measures skin areas for [7]: Sensory perception (the patient s ability to respond to meaningful pressure-related discomforts). Skin moisture (the degree to which the skin is exposed to moisture). Activity (the patient s degree of physical activity). Mobility (the patient s ability to change and control body position). Nutrition (food intake). Friction/shear. During the assessment of the Braden Scale, the nurse is required to rate each of the six categories objectively, then to document the risk with a number, one (highly impaired) to four (no impairment), based upon the patient s ability to demonstrate each of the listed categories. Each of the six categories is assigned a number based upon the description that best describes the patient. A patient s risk is based upon the total number of points [7]: Scores of 15 to 18 indicate the patient is at risk. Scores of 13 to 14 indicate the patient is at moderate risk. Scores of 10 to 12 indicate the patient is at high risk. Scores of 9 or less indicate the patient is at very high risk. Two retrospective studies on nursing homes and facilities that utilized and enforced the Braden scale showed an 87 percent decrease in the incidence of pressure ulcers [16]. Another study demonstrated that pressure ulcers in the most critically ill patients admitted to the intensive care unit decreased from 33 to 9 percent [16]. In addition to the patient s assigned risk, the overall patient is considered, including other major risk factors that may predispose the patient or skew the data, such as [7]: Fever. Diastolic pressure below 60. Hemodynamic instability. Advanced age. Collecting the history component of the assessment Nurses should collect a thorough history from the patient or any appropriate caregiver or emergency medical technician (EMT) to ensure all potential aspects are analyzed in caring for a patient who presents with a wound. Although a wound may initially appear minor or a patient presents with another complaint but has a large chronic pressure ulcer on the sacrum, it is vital that nurses are thorough in collecting the history. Patients may not be forthcoming with vital information because they don t consider the importance of the data or they may have forgotten it. Nurses who ask all of the appropriate questions could find the missing link in collecting the pieces to the puzzle. According to the Clinical Guidelines in Family Practice, a nurse should inquire and identify the following questions in their history about a wound. [82]: 1. What is the mechanism of injury? It is important to assess the mechanism of an injury because it helps to determine the presence of foreign bodies or the prognosis for developing an infection or scar [18]. The type and depth of injury may affect the healing process due to infection, tissue damage and/or other injury to the muscle and/or bone. 35

36 2. 3. Acute wounds. Bite wounds must be evaluated for associated injuries and risk of infection. Stab wounds should be evaluated for the depth of injury, because a surgeon may need to be consulted to protect the underlying structures if they have been penetrated or damaged in any way. Sharp objects often make smooth cuts that penetrate deep structures. However, a simple cut through the skin by a sharp object may cause minimal damage to the surrounding tissues, and it typically has a relatively low risk for infection or significant scarring [18]. Crushing injuries often damage underlying tissues and can result in fractures. In addition, they often need to be debrided in order to decrease the risk of infection. Tearing of the skin, as occurs when the chin strikes the floor, produces irregular wound margins and damage to the surrounding tissues; these lacerations have a moderate risk of infection and scarring [18]. Direct compression injuries, such as from a blow to the head, split the skin, injure the adjacent soft tissues and classically cause a satellite laceration; these wounds have the highest risk of infection [18]. Chronic wounds. Typically a patient with a chronic wound may present with complications from the chronic wound, or the patient may present with a complaint related to a comorbidity. Where is the location of the wound? The location and/or environment in which the wound occurred may determine other potential problems for the patient. Specific location of the wound needs to be identified. Where is the site of the injury? Are there any other injuries? Always inspect the entire body, not just one potential area and/or complaint. Environment in which the injury occurred may alert the nurse and practitioner to other risk factors or potential bacteria sources: Soil. If the injury and/or wound occurred in dirty soil, then the patient is at risk for being contaminated with spores of clostridium tetani (tetanus) Where is the site of the wound? The location of the wound may determine the ability of the wound to heal appropriately. Wounds that present contaminated ( dirty ) wounds are at a high risk for becoming infectious. Signs of infection include erythema, edema, purulent discharge; a fever may or may not be present. Typically, after a bite, signs of infection occur 24 to 72 hours after the bite [27]. Deep wounds are at risk of having underlying tissue destruction and a risk of contamination into the deeper tissues. Wounds with untidy edges typically heal slower and may heal with disfigurement. Wounds with tissue necrosis may be at risk for infection and delayed healing. It is also important to inspect the surrounding area of the wound. If the patient has any bruising on the head, face, abdomen, mid- or lower back with hematuria, the nurse needs to notify the doctor as it may imply a hematoma or thrombosis [4]. If a scab or eschar develops on or around the bruise, notify the doctor as it may imply a deeper injury that may require debridement [4]. What are the patient s risk factors? The specific risk factors for each wound are correlated to the specific type of wound as it is implied (See Risk factors). Wound assessment Once a history has been collected and the nurse is assessing the wound and any breaks in the skin, the nurse needs to note and record the size, length, depth and type of skin break. It is important to use sterile technique [82]. In order to properly assess and document the wound, the nurse should adhere to the following recommendations [78, 82, 86]: 1. Measure the size of the wound. It is important to assess and record the size, length, width and depth of the wound. The size is measured by multiplying the length by the width [10]. To ensure that each nurse and facility has standardized documentation, assess the wound as a clock face [41]: Example. Nurses should imagine a clock and think of 12 o clock as the patient s head and the 6 o clock as the patient s feet. Always measure the length from 12 o clock to 6 o clock and the width between 9 o clock and 3 o clock. The distance from the deepest portion of the wound base to the skin level should measure the depth. Document the depth of the wound, differentiating superficial and full thickness wounds. It is important that nurses do not cross-contaminate between wounds by using the same gloves, instruments or measuring devices [96]. When did the patient experience the injury and/or notice the break in the skin? (Essentially how old is the injury?) Research has demonstrated that if the injury occurred greater than six hours from the time the patient seeks medical care, bacteria has probably already multiplied, putting the patient at risk for sepsis. In addition, research has demonstrated the following [18]: Wounds that closed at up to 19 hours after the injury had a significantly higher rate of healing than those 2. Note any wound drainage that may be present. closed later (92 versus 77 percent). The nurse needs to assess for wound drainage, such as bleeding In contrast to wounds involving other body areas, the or exudate, and then document the precise amount with each healing of head wounds was virtually independent of assessment. It is important to document the color, amount, time from injury to repair: 42 of 44 (96 percent) of consistency and odor of the wound. wounds involving the head and repaired later than 19 Color The color of the wound drainage (exudate) needs to be hours after injury were healing compared with 47 of described. Exudate is the fluid produced by the wound, which 71 (66 percent) of all other wounds. In general, a consists of blood serum, serosanguineous fluid and leukocytes Facial wound can be closed up to 24 hours later with [86]. Exudate continuously bathes the wound, keeping it little risk of infection if it is reasonably clean. moist, supplying nutrients and providing the best condition for 36

37 3. migration and mitosis of epithelial cells and controlling the amount of bacteria in the wound [86]. Serosanguineous appears thin and blood-tinged with amber fluid. If the wound occurred in the previous 48 hours, this may be a normal process. If it occurs later, it may precede a wound dehiscence. Serous appears thin, watery and clear [10]. Purulent drainage is thin or thick in consistency and varies in color, depending upon the potential source. Creamy yellow implies a staphylococcus infection. Greenish blue pus with a fruity odor implies pseudomonas. Beige pus with a fishy odor implies proteus. Brownish pus with a fecal odor implies aerobic coliform and bacteroides that may occur as a complication after any intestinal surgeries. Bloody drainage is thin and bright red. Amount The nurse needs to measure any drainage by describing the amount that saturates the dressing and any amount that may be collected in a drain. The amount of drainage should be measured in milliliters (ml) at least every shift or more frequently, depending upon the amount of drainage. Consistency The consistency of the wound drainage should be assessed and documented. Is it thick, thin or tenacious? Odor If there are any signs of infection within the wound, it needs to be addressed before the wound can begin to heal [48, 96]: Fruity smells suggest a staphylococcus organism. Foul (fecal) odor suggests gram-negative bacteria (escherchia coli). Describe the appearance of the wound tissue, edges and color. The appearance of wound tissue depends upon the balance of granulated and necrotic tissue [86]: Wound tissue The surrounding tissue needs to be described as it may imply the patient needs a referral for a debridement to remove dead tissue [48]. Viable, healing wounds appear healthy when it is bright, beefy red, shiny and granular with a velvety appearance, implying the presence of granulated tissue. Granulation tissue is the growth of small blood vessels and connective tissue to fill in full thickness wounds [10]. Epithelialization is the process of epidermal resurfacing and appears as pink or red skin. In partial thickness wounds, it can occur throughout the wound bed as well as from the wound edges. In full thickness wounds, it occurs from the edges only [10]. Slough tissue is yellow or cream colored with a puslike consistency that occurs in the presence of moisture and bacteria (exudative or devitalized tissue) [10]: Non-adherent, yellow slough is a thin, mutinous substance that is scattered throughout the wound bed and is easily separated from wound tissue. Loosely adherent, yellow slough is thick, stringy, clumps of debris that are attached to wound tissue. Necrotic or eschar tissue is thick and it appears black or dark brown in color. Eschar tissue can be either [10]: Soft adherent and appear as soggy tissue that is firmly attached in the center or the base of the wound. Firmly adherent hard/black eschar, crusty tissue that is strongly attached to the wound base and edges (like a hard scab). Poorly healing wound tissue appears as pale pink or blanched to dull, dusky red color depending upon the source [10]. Poor arterial wounds appear pale with immature granulated tissues. Poor venous wounds appear with a deep red color, reflective of deoxygenated blood beneath the ulcer surface. If the patient has slough or necrotic tissue, the wound healing process is impeded because both conditions prevent granulation and epithelialization from occurring [86]. In order for the wound to begin healing, the patient needs to be free from slough and eschar, and the wound should be moist with red-pink budding granulated tissue [86]. Wound edges The wound edges should be inspected for contraction (gradual healing from the edges to the center of the wound) [86]. The edges may be described using the following terms recommended by Dr. Barbara Bates-Jensen (a doctoral prepared nurse who has implemented numerous research and clinical tools for practice to improve the quality of skin care). [10]: Indistinct, diffuse Unable to clearly distinguish wound outline. Attached Even or flush with wound base; no sides or walls present; flat. Not attached Sides or walls are present; floor or base of wound is deeper than edge. Rolled under, thickened Soft to firm and flexible to touch. Hyperkeratosis Callouslike tissue formation around wound and at edges. Fibrotic, scarred Hard, rigid to touch. Note if there is any erythema, tenderness, maceration or cellulitis. Maceration is exhibited when the wound appears pale or white in color. Maceration occurs when the drainage from the wound has extended contact with the healthy tissue around the wound [86]. Cellulitis may imply the patient s inability to resist infection if proper measures are not implemented to alleviate the pressure [48]. (See Complications: Cellulitis for treatment recommendations). Skin color Observe for any erythema or ecchymosis around the injured area by blanching the area. Assess and document the circulation, sensation and movement distal to the wound. It is important to assess for arterial disease, because it may actually be the cause of the wound and can impede the ability of the wound to heal [48]. A patient with arterial deficits should be referred to a surgical specialist immediately [48]. If there is a wound or skin breakdown noted on any of the patient s extremities, the nurse needs to assess the distal pulse and blanch the skin, then assess distal sensation [48]. Assess and document the range of motion (ROM) and strength of the affected and/or adjacent extremities. The ROM needs to be assessed against resistance on all parts surrounding the wound site [82]. Due to the complexity of wounds, the enormous complications

38 and consequences to patients and indeed the health care system, it is imperative to properly document the wound completely to prevent further damage and to prevent lawsuits. Wound classification Over the years, various organizations have developed guidelines to ensure health care providers are able to describe and classify various wounds into specific categories. The classification of wounds is unique to the specific wound, but there are common terms that are used, depending upon the layers of skin that are involved [19, 41]: Superficial or partial thickness wounds involve only the epidermis layer, such as lacerations, skin tears, first-degree burns, abrasions and shallow ulcerations. Superficial/partial thickness wounds heal by re-epithelialization, the production of new cells into the basal layer of the dermis. The typical healing takes approximately five to seven days. Full-thickness wounds involve the epidermis and dermis layers of the skin and may even extend to the muscle and bone. Typical examples include deep lacerations, second- and third-degree burns, various types of ulcers and surgical and traumatic wounds. Full-thickness wounds heal through granulation by removing damaged tissue. Full thickness pressure ulcers are often covered by a layer of black, gray or brown nonviable, denatured collagen called eschar [41]. In the early stages of healing, eschar is dry, leathery and firmly attached to the wound surface. During the inflammatory process, the eschar begins to lifts and separates from the tissues beneath, which promotes a great site for bacteria to grow. If the bacteria proliferates, enzymes will be released, which softens necrotic tissue providing a softer, yellow appearance [41]. 1. Burns. Burns are classified according to the depth and thickness of the wound [19,72]: First-degree are superficial, localized injuries or destruction that involves the epidermis, typically by direct contact such as a chemical spill or an indirect cause, such as sunburn. Second-degree burns are partial thickness burns that involve the epidermis and part of the dermis. They typically leave part of the dermis intact. The degree of the burn is progressively deeper than first-degree, in which the hairs are easily extracted and/or absent, sweat glands are less visible, and the skin appears smoother [7]. Third- and fourth-degree burns are full thickness injuries that involve the epidermis and dermis and extend into the subcutaneous tissues. Another burn classification is the involvement of the burn injury based upon the percentage of the total body surface area that is damaged. This is estimated by the Rule of Nines chart to calculate the percentage of body surface area (BSA) [5]. Firstdegree burns are not analyzed for the percentage of total body surface because they do not represent significant injury [72]. Research has demonstrated that the majority of burns involve less than 10 percent of the total body surface area [7]. But the depth and involved area of injury determines the prognosis and mortality risks for the patient. Over the years, the three major risk factors for mortality from a burn include [57]: Age greater than 60. Percentage of total body surface area. Inhalation injury. The mortality calculation is based upon the Baux score formula [57]: Age plus percentage area burned equal the percent mortality Example: 50 years old plus 20 percent burned equals a 70 percent mortality risk. Pressure ulcers. In the 1980s, the National Pressure Ulcer Advisory Panel (NPUAP) developed a national staging system for pressure ulcers. In 2007, the NPUAP revised its guidelines, including the original four stages and adding two stages on deep tissue injury and unstageable pressure ulcers. The NPUAP s updated stages reflect an accumulation of research developed over six years [48, 67]. Pressure ulcers are classified in the following stages [19, 53, 67, 78] (See Table 1, at the end of this chapter): Suspected deep tissue injury: Presents as a purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. Stage 1 ulcers: Presents as a nonblanchable erythematous patch of skin. It is an observable pressure related to an alteration of the intact skin. The key is the skin remains intact, but once the pressure has been alleviated, the skin remains erythemic, pink, red and/or mottled in appearance [57]. The NPUAP convened a task force to review the definition of a Stage I pressure ulcer in At that time it elaborated on the definition to address individuals with darkly pigmented skin [65]: A Stage 1 pressure ulcer is an observable pressure-related alteration of intact skin whose indicators as compared to the adjacent or opposite area on the body may include changes in one or more of the following: Skin temperature (warmth or coolness), tissue consistency (firm or boggy feel) and/or sensation (pain, itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue or purple hues. Stage 1 pressure ulcers can be difficult to assess in patients with darkly pigmented skin [94]. Stage 1 pressure ulcers typically heal in 14 days. Stage 2 ulcers: A partial thickness skin loss that involves the epidermis, dermis layer and/or both. They are superficial ulcers that appear as a crack, abrasion, blister or shallow crater with an erythemic wound bed, without slough. Necrotic tissue may overlie the pressure ulcer [57]. The NPUAP (2007) provides further explanation on stage 2 because the organization wants to ensure that nurses do not confuse or describe skin tears, tape burns, perineal dermatitis, maceration or excoriation as a Stage 2 ulcer [67]. Typically, Stage 2 ulcers heal within a few weeks, or approximately 45 days. Stage 3 ulcers: A full thickness skin loss that involves damage or necrosis of the subcutaneous tissue. It may even extend to, but not through, the underlying fascia (tendons or bones). Appears as a distinct ulcer margin, a deep crater with or without undermining of adjacent tissue. Slough may be present, but should not obscure the depth of tissue loss and it may include tunneling. Typically they heal within a few months, or approximately 90 days.

39 3. Stage 4 ulcers: Presents as a full thickness skin loss with extensive destruction, tissue necrosis and/or damage to muscle, bone or support structures, such as the tendons or joint capsules. In addition, there may be tunneling, slough and eschar associated with stage 4 ulcers. Typically healing takes many months or longer depending upon the depth of destruction, necrosis and/or damage to the bones. During the third and fourth stages, the patient is at very high risk of enduring complicated infections that may cause sepsis. Actor Christopher Reeve died a few years ago related to complications from a pressure ulcer. Unstageable ulcers: Presents as a full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. The NPUAP states that an ulcer cannot be staged if there is slough and eschar on the top of the wound; it needs to be removed to expose the base of the wound to allow the nurse and practitioners to visualize the true depth and stage of the wound. However, if there is eschar (dry, adherent, intact and without erythema) on the heel, it should not be removed, according to the NPUAP guidelines, because it serves as the body s natural biological cover [67]. It should be noted, there are some sites that identify a Stage 5 as a closed cavity communicating through a small sinus [57]. However, nurses should adhere to the NPAUP staging system and their own employers policies to ensure compliance and unity in the profession. Once the wound has been staged, it needs to be reassessed frequently to monitor for any improvement or deterioration of the wound. Depending upon the venue in which the patient is being seen, this will determine the frequency in which the pressure ulcer is re-evaluated. If the patient is in the hospital setting, the patient will be reassessed preferably every shift, or a minimum of every day. It is important to adhere to the hospital policy as it may differ at each facility. If the patient is being followed and/or treated in the community, the wound needs to be reassessed at least weekly [94]. Although there are many variables that contribute to the risk of developing pressure ulcers, it can be alleviated with safe, diligent care. This involves recognizing the risk factors and turning all patients at a minimum of every two hours and the use of floatable devices and/or alternating pressure mattresses. Skin tears. Skin tears are classified based upon the Payne-Martin classification system for skin tears [19]: Category 1. Skin tear without tissue loss. Linear type: epidermis and dermis have been pulled apart. Flap type: epidermal flap completely covers the dermis to within one millimeter of the wound margin. Category 2. Skin tears with partial tissue loss. Scant tissue loss: 25 percent or less of the flap is lost. Moderate to large tissue loss: more than 25 percent of the epidermal flap is lost. Category 3. Skin tear with complete tissue loss. Epidermal flap is present. Signs and symptoms of the most common wounds Depending upon the type of wound, patients will present with symptoms that help practitioners and nurses differentiate between the diagnosis and treatment modalities. Therefore, it is imperative to ensure a thorough assessment is implemented, to avoid inappropriate and/or ineffective care. 1. Abrasions, excoriations, or scrapes. An abrasion typically presents as multiple lines of scraped skin with minuscule bleeding noted on and/or around the scratches. 2. Bites. The physical presentation of a bite will be dependent upon the extent and depth of the bite and can be a puncture, laceration or avulsion (tissue is torn away from the body). It is important to do further investigation depending upon the source of the bite and the appearance of the injury in order to prevent complications such as infection, bone and tissue injury and/or osteomyelitis. 3. Bruising. A bruise will present as ecchymosis that appears as a purplish, flat area that occurs when blood leaks out into the top layers of skin [73]. 4. Burns. Due to the various types of burns that may occur, there are various signs and symptoms that the patient may present with upon admission. Burn injuries are classified depending upon the depth of the tissue injury and involvement of the skin and surrounding organs [72]: Superficial partial thickness burns: First-degree burns The symptoms of a first-degree burn are erythema, slight edema and pain. In more severe first-degree burns, the patient may exhibit chills, headache, local edema, nausea and vomiting [5]. Firstdegree burns typically heal in a few days and rarely leave any scars, and they are nonlife-threatening. The most common first-degree burns are sunburns, which may cause blisters, although blisters do not occur initially [57]. If they do occur, then the wound is classified as a second-degree burn [57]. Second-degree burns are also known as superficial partial thickness burns. Second-degree burns appear erythemic, tan or white in color and are blistered. The blisters are typically thin-walled, fluid-filled blisters that develop within a few minutes of injury [5]. Once the blisters break, the nerve endings become exposed to the air, and pain and tactile responses remain intact [5]. Second-degree burns typically take two weeks to several months to heal and may leave scars. The most common second-degree burns are sunburns and scalds. Full thickness burns. Third- and fourth-degree burns involve the epidermis, dermis and often the deeper tissues are destroyed, including blood vessels. Because the dermis is completely destroyed, the skin regenerates only from the edges of the wound. The wound appears pale white, cherry red or black. The tissue is often dry with necrotic areas [19]. 5. Lacerations or cuts. Lacerations typically appear with bleeding, pain, numbness, and/ or swelling at the injured site. 39

40 6. Perineal skin breakdown may appear as one or all of the following symptoms: erythema, edema, oozing, vesiculation, crusting and/or scaling in the groin, perineum and buttocks [66]. 7. Pressure ulcers. Pressure ulcers typically develop over a bony prominence due to continuous pressure on the tissue, which occludes the blood supply [53]. The most common sites of pressure ulcers, which account for 95 percent of all pressure ulcers, include the following areas that are usually on the lower part of the body [51, 53, 94]: Sacrum (36 percent of cases, typically on the lower back). Greater trochanter. Ischial tuberosity. Heel (30 percent). Lateral malleolus. In addition, there are other areas to consider where pressure ulcers may occur, such as on the occiput, behind the ears, and on the elbows [57]. Anytime a patient is wearing oxygen, it is important to assess the back of the ears because if the oxygen apparatus is on too tight, pressure ulcers can occur behind the ears [41]. If the pressure is alleviated in a few hours, there will be erythema noted initially, which resolves without any lasting tissue damage [53]. If the pressure continues without relief and/or a change in position, then the endothelial lining becomes disrupted with platelet aggregation, forming micro thrombi that block the blood flow and cause anoxic necrosis of the surrounding tissues [53]. The NPUAP stage will determine the physical findings on the patient (See Wound classification). 8. Punctures. Puncture wounds usually present with mild bleeding and pain at the site. The source of injury may point to further problems and/ or damage, such as small pieces of glass in the skin [29]. 9. Skin tears. A skin tear presents as a tear, from no tissue loss to a flap depending upon the severity. (See Wound classification: Skin tears). 10. Surgical wounds. The majority of surgical wounds will close by primary intention in which the surgical site will demonstrate granulated tissue without signs and symptoms of infection. If the wound was closed by secondary or tertiary intention and/or infection prevails, the site may have erythema, drainage and odor. 11. Ulcers. Diabetic. Diabetic foot ulcers involve infectious symptoms of erythema, warmth, swelling or induration and/or pain or tenderness [38] (See Table 2, at the end of this chapter). Leg ulcers. Venous ulcers can be present anywhere between the knee and ankle, with the medial and lateral malleolus being the most common sites. Characteristics of venous wounds are as follows [76]: The wound margins tend to be large and irregular. The wounds are superficial. The wound beds vary in appearance from ruddy, beefy red to a superficial fibrinous gelatinous necrosis that may occur suddenly with healthy-appearing tissue underneath. The wound is painless. (See Table 3, at the end of this chapter) 40 Arterial ulcers are present anywhere on the leg, distal to the impaired arterial supply. Characteristics of arterial wounds are as follows [76]: The wound margins are even, sharply demarcated and punched out. The wound may be superficial or deep. The wound beds may be pale, gray or yellow with no evidence of new tissue growth. The wound is painful. (See Table 4, at the end of this chapter) Diagnosing wounds Proper diagnosis is the key to proper wound healing. If the specific wound is not properly diagnosed, then the patient may receive ineffective treatment modalities, thus exacerbating the injury and the potential ability of the wound to heal. In addition, the NPUAP has noted that the most challenging wounds to diagnose are chronic wounds on the lower extremities, as they may be related to neuropathy, ischemia, venous hypertension and/or pressure [48]. Once an injury or wound has been established, the primary care provider and/or provider responsible for the care of the wound may order certain labs and/or diagnostic tests to help determine the degree of damage and or underlying factors that may affect the healing process. The following laboratory, cultures and/or diagnostic tests may be implemented depending on the site and depth of injury, source of injury and ineffective healing modalities [78]: Laboratory. Basic metabolic profile (BMP) to assess the electrolytes and any renal insufficiency. The blood glucose level is important to monitor for all diabetics or undiagnosed diabetics since poor glucose control affects the wound healing. A coagulation study to evaluate for coagulation abnormalities, especially if a deep wound excision is required. Complete blood count (CBC) to assess for leukocytosis, anemia and thrombocytopenia. Leukocytosis is elevated white blood cells (WBC) and indicates an inflammatory response [19]. Anemia is exhibited by low hemoglobin and hematocrit, and depending upon the actual cause of the anemia, other factors such as the mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) may be altered. It is important to identify anemia in any patient with a wound because it will slow down the healing time due to the lack of oxygenation and perfusion [19]. Thrombocytopenia is exhibited by a low platelet count that may be caused by fever, infection and/or poor wound healing. C-reactive protein (CRP) to assess for any inflammation may be ordered as a baseline and to monitor the effectiveness of treatment [19]. However, the CRP is not a specific test for any certain disease, but a marker to evaluate an inflammatory process in the body. Protein, albumin, prealbumin, and transferrin to assess the patient s nutritional status. Serum prealbumin is sensitive for relatively acute malnutrition because the half-life is two to three days (rather than 21 days for albumin). If a patient has a serum prealbumin level less than seven grams per deciliter (dl) it indicates severe protein calorie malnutrition. Therefore, prealbumin reflects the recent protein consumption, whereas the albumin level reflects the long-term protein consumption [17]. If a patient is undernourished or malnourished, they should be referred to a dietician immediately because it is

41 associated with poor clinical outcomes, including mortality [17]. A combination of a low lymphocyte count, less than 1,500, coupled with an albumin count less than 3.5 grams per deciliter is indicative of malnutrition, which delays overall wound healing [71]. Cultures In order to assess for any fungi, bacteria or viral pathogens isolated in the skin area of concern, blood and wound cultures are taken to determine the most appropriate therapy. One should not assume that just because a wound is open that it is infected. But it would always be contaminated [23]. Contamination is defined as the presence of organisms without any clinical signs and/or symptoms of infection [23]. All chronic wounds are colonized with bacteria at varying degrees [33]. Wound infection is a contamination with a pathogenic organism that cannot be controlled by the body s immune defenses. It is exhibited by inflammation, induration, erythema, odor and exudate [21]. Therefore, a wound culture will be implemented to assess for various potential sources of the infection (bacterial or fungal). Fungal infections The skin area of concern should be gently scraped from the skin lesion then sent to the laboratory for analysis. If it is a deeper area of concern, then the patient will require a punch biopsy [23]. Pressure ulcers If the patient has a pressure ulcer, swab cultures will only demonstrate surface contaminants, rather than providing valid, reliable results on the specific bacteria colonized within the ulcer. Therefore, it is recommended that a needle aspiration should be utilized to identify the infecting organism [16]. Once the wound has been identified, it is imperative to assess the type of bacteria localized in the wound or found systemically in the body. Interestingly, a positive wound culture does not necessarily confirm a wound infection [78]. Diagnostic tests In addition to laboratory data and cultures, the following diagnostic tests may also be ordered [78]: Plain radiography (X-rays), CAT scan (CT) and magnetic resonance imaging (MRI) to assess for any underlying abnormalities and/or foreign bodies. It is important to obtain an X-ray with any accidental injury or a patient presenting with an incomplete history because a patient may have a wound infection or injury caused by a foreign body, which prevents the healing process because of debris and retained fragments [78]. Therefore, it is imperative to identify any foreign bodies before infection or injury occurs. In addition, X-rays may be ordered for any significant animal bite, such as a dog bite, since many dog bites induce crushing injuries and damage to the surrounding tissues [6]. Research has demonstrated that the jaw of a dog has the ability to exert 200 to 400 pounds per square inch (psi) during a bite [6]. If a diabetic foot ulcer is speculated, radiographs of the foot should be ordered to rule out osteomyelitis (bone infection) [38]. Vascular ultrasonography (US) to evaluate for aneurysmal disease or venous occlusion. Nuclear medicine (NM) bone scan to assess for osteomyelitis. Ankle/brachial index (ABI) is completed to evaluate the vascular system in a patient with a potential diagnosis of venous or arterial ulcers [57]. Once arterial disease is diagnosed, ABI should be implemented every three to seven months [30]. The ABI results are as follows [76]: 0.9 to 1 is normal to 0.9 is moderate disease. 0.5 to 0.75 is severe disease. If the results are between 0.6 and 0.8, the patient should be referred to an advanced wound clinician [30]. Below 0.5 implies limb-threatening disease, and the patient should be referred to a vascular lab for further investigation [85]. Biopsies They may be done to assess for potential complications of certain wound injuries. The most common type of biopsy is a punch biopsy in which a small, circular instrument punches a diameter from 2 to 6 millimeters (mm) [41]. For instance, a bone biopsy is the gold standard for diagnosing osteomyelitis [94]. Generalized treatment of wounds In order to properly treat a wound, it is imperative that the patient and the wound are properly assessed in their entirety. There are enormous variables that intertwine and may affect the healing process; this reiterates the important aspect of treating the patient holistically because individual patients may have various risk factors, co-morbidities and lifestyles that may affect the healing process. Due to the complexity of wound care, each of the treatment modalities are discussed and elaborated upon under each specific wound type in the next section, (Specific treatment of wounds). In order to maintain overall homeostasis and wound healing, the following factors, including tissue perfusion, nutrition, pain, wound cleaning, dressing changes, sutures and a tetanus shot need to be integrated and/or considered in the treatment plan for any wound. 1. Antimicrobials. There is a plethora of bacterial or fungal sources for causing infection, but one of the most prevalent and most dangerous is methicillin-resistant staphylococcus aureus (MRSA). The IHI has also added MRSA as among its goals to eradicate with its 5 Million Lives campaign [42] (See Wound complications). If the patient has a wound infection, it may require surgical debridement and appropriate systemic antibiotic therapy, depending on the type of bacteria [78]. Typically, topical antiseptics are avoided because they interfere with wound healing [78]. 2. Debridement. Debridement is a method of treatment to clean or remove necrotic, dead tissue so that granulation can occur to improve wound healing. There are various types of debridement [8,93]: Autolytic debridement involves the use of the body s own enzymes and WBCs to rehydrate, soften and finally liquify the eschar and slough. Achieved with the use of occlusive or semi-occlusive dressings that maintain fluid in contact with necrotic tissue. However, it can also be achieved with hydrocolloids, hydrogels and transparent films. Nurses should refrain from using an occlusive hydrocolloid as it may promote aerobic bacteria growth [95]. Best used in the treatment of stage 3 and 4 pressure ulcers. Enzymatic debridement involves the use of chemical enzymes as a fast-acting product to slough off necrotic tissue. Best used in the treatment of any wound with necrotic debris or eschar formation. Disadvantages to utilizing enzymatic debridement are the expense and that it may cause inflammation or discomfort at the site [95]. Mechanical debridement involves initial treatment with a 41

42 3. dressing, then manually removing the dressing mechanically. Hydrotherapy is an example of mechanical debridement. A disadvantage to using mechanical debridements is that it can traumatize healthy or healing tissue when the dressing is removed, therefore inducing further pain for the patient. Another side effect to mechanical debridement is the potential development of maceration [95]. Surgical debridement involves surgery under anesthesia to remove necrotic or infected tissues. After a patient undergoes debridement, the nurse should apply a moist sodium chloride dressing or isotonic sodium chloride gel (Normlgel, IntraSite gel) or a hydrocolloid paste (DuoDerm). In order to achieve optimal wound coverage, it is imperative to perform wet-to-dry dressings, which reinforce the autolytic debridement as it absorbs exudate and protects the surrounding healthy skin. A polyvinyl film dressing (Op-Site, Tegaderm) that is semipermeable to oxygen and moisture and impermeable to bacteria is a good choice for wounds that are neither very dry nor highly exudative [77]. Dressings. Nurses many times must ask: Do I apply a dressing to the wound? If so, what type of dressing do I apply? How often do I need to change the dressing? Nursing care for wounds is time-consuming because of the complexity of the wound and the frequency of dressing changes, especially if the wound requires a sterile field. In addition, there are numerous types of dressings that may be applied to a wound and various techniques that can cause confusion among nurses. The majority of dressings need to be changed daily and when they become wet or dirty to reduce the risk of infection and to promote the healing process [54]. Dressing changes are initiated and applied to accelerate the healing process by ensuring that unwanted debris stays away from the wound while creating a barrier between the body and environment [21]. On the flip side, many researchers recommend keeping a dressing in place for several days as it aides in the early healing process because the wound is left undisturbed and the wound remains moist. This helps regulate the body temperature, which in turn provides stability in the wound [23]. Dressing change techniques. It is important for a nurse to adhere to the appropriate dressing change technique to prevent cross-contamination and infection. Sterile technique involves stringent, diligent care from the nurse or health care providers to reduce exposure to microorganisms and keep the area as free from microorganisms as possible [33]. It is important to adhere to the 2005 Wound Ostomy Continence Nursing (WOCN) society s recommendations for sterile dressing change techniques [33]: Meticulous hand washing. Use a sterile field, including sterile gloves, when touching or using any equipment in or around the wound site and during the application of the dressing. Clean technique may also be referred to as a non-sterile procedure that involves strategies used in patient care to reduce the overall number of microorganisms or to prevent or to reduce the risk of transmitting microorganisms from one person to another [33]. The WOCN elaborates that clean technique involves [33]: 42 Meticulous hand washing. Maintaining a clean field with clean gloves and sterile instruments. Aseptic technique involves the prevention of the transfer of organisms from one person to another by keeping the microbe count to a minimum [33]. No-touch technique is a method of changing dressings on the surface without directly touching the wound or any surface that might come in contact with the wound [33]. Regardless of the type of wound, nurses are required to wash their hands before assessing or touching a wound and after any encounter with a patient to reduce the risk of nosocomial infections. Types of dressings It is important for the nurse to understand the types and purpose of dressings to ensure the ideal and most appropriate dressing is applied to a wound for adequate healing. It is important to refrain from using any dressing when a wound initially occurs as it may cause more harm than benefit to the wound. Another factor to contemplate, according to World Wide Wound (2008) [80]: A dressing that is ideally suited in the early stages of treatment of infected, malodorous or necrotic wounds may not be appropriate for the later stages of healing. For example, sterile maggots have proven to treat wounds rapidly and cost-effectively, but some researchers suggest maggots should not be applied to all types of wounds throughout the entire healing process. Similarly, a dressing that promotes angiogenesis and the production of granulation tissue may not be equally suitable for the final epithelialization stage of wound closure. To complicate matters further, there is no protocol for a specific dressing application for all wounds at specific stages. The ideal dressing is dependent upon the type and severity of the wound to promote adequate healing. Research has demonstrated that failure to utilize the most appropriate dressings will result in a delay in the healing process [23, 41, 50]. All absorbent combined dressings are large cotton-filled dressings that are typically used to cover the primary dressing, such as gauze or hydrophillic dressing for extra protection. It may also be used over an intact surgical wound. Examples include surgipad or an ABD dressing. Alginates are soft, nonwoven fibers that are derived from brown seaweeds that are available in a pad or rope form. Alginates are indicated for absorption and protection of the wound. The advantages of alginates are that they are highly absorbent, biodegradable, have easy application, can be used as a packing in deep wounds and can be used for infected wounds. Alginates are also beneficial for wounds with copious exudate. The disadvantage of alginates are that they require secondary dressings to keep them secure, and they can cause desiccation of the tissue if drainage is minimal. The frequency of dressing changes should be when the dressing is saturated or every three to five days. Examples of alginates are pads and ropes. Biological dressings are indicated after eschar removal, as a protector, to treat burns, assess skin grafts and for dormant, nonhealing wounds that do not respond to other topical therapies. The advantages of biological dressings are they are the most natural wound covering, they reduce pain, conform

43 to uneven wound surface, act as a catalyst for healing and they are an alternative option for autografts. The disadvantages of biological dressings are that they require secondary dressings for security, and they are very expensive. Cotton gauze dressings For years, cotton gauze has been the most common type of dressing used because it has impeccable abilities to absorb blood and tissue fluid during and after surgery. A disadvantage for cotton gauze dressings is the fiber in the gauze can be lost in the product, thus impairing the ability of the wound to heal appropriately [79]. Foams are indicated for absorption and protection. Foam dressings can absorb an abundance of fluid, and are useful in the earlier stages of healing when the drainage is the most abundant. Another advantage of the foam dressing is that they are comfortable and gentle to the skin and can be left in place for several days. In comparing foams and cotton gauze dressings, foam dressings are more attractive than the simple cellulosebased material in cotton gauze and eliminate the potential problem of fiber loss [79]. Examples of foam dressings: Allevyn adhesive dressings, Lyofoam and Polymen nonadhesive dressings. High bulk gauze bandages are primarily used for packing large wounds that are healing from secondary intention. Examples of high bulk gauze bandages are Fluffs. Hydrocolloidal wafers (adhesive wafer) dressings are indicated for debridement, absorption and protection. The hydrocolloidal dressings are formulated with elastic, adhesives and gelling agents that help keep the area moist to promote wound healing. Another advantage of the hydrocolloidal wafers is they only need to be changed every five to seven days. Examples of hydrocolloidal wafers are DuoDerm and Tegasorb. Hydrogel dressings are indicated for debridement, absorption and protection. In clinical practice, hydrogels usually are used to rehydrate eschar in order to promote autolytic debridement. The majority of hydrogels are applied directly to the wound, then a secondary dressing is applied over the hydrogel (such as a foam or gauze) to maintain the required moisture level for wound healing. Examples are DuoDerm Hydroactive wound gel and Tegagel. Hydrofiber is an absorptive textile fiber pad that is also available as a ribbon for packing of deep wounds. The unique component of hydrofiber is it is covered with secondary dressings. Hydrofiber works by combining with the wound exudate to produce a hydrophilic gel, such as Aquacel-AG that contains a 1.2 percent ionic silver solution that has strong antimicrobial components against many organisms, including methicillin-resistant staphylococcus aureus and vancomycinresistant enterococcus [77]. Hydrophobic occlusives are nonadhering dressings that protect the wound from air and moisture-borne contaminations. Examples are petrolatum gauze. Hydrophilic polyurethane films are very permeable to water vapor and thus permit the passage of a significant quantity of the aqueous component of exudate from the wound to the environment by evaporation. The advantages of hydrophilic dressings are they allow the drainage to penetrate the dressing. However they are nonadherent. An example is an oil-based gauze that is typically used on open ulcers or granulating wounds. Another example is a Telfa pad, which is optimal for simple, closed, stable wounds. Transparent films are indicated for debridement, protection (partial thickness lesions) and as a secondary dressing. These are useful for clean, dry wounds having minimal exudate, and they also are used to secure an underlying absorptive material. They are used for protection of high-friction areas and areas that are difficult to bandage such as heels (also used to secure IV catheters) [77]. The advantage of transparent films is that they are highly elastic dressings that adjust exceptionally well to the body. Examples include Tegaderm and Op-site. According to Medscape (2007), there were over 99 studies conducted between January 1990 and June 2006 monitoring the efficacy of modern dressings in healing acute and chronic wounds by secondary intention. The studies revealed the following [11]: The 99 studies were composed of 89 randomized controlled trials, three meta-analyses, seven systematic reviews and one cost-effectiveness study. Evidence demonstrated that hydrocolloid dressings were superior to saline gauze or paraffin gauze dressings for complete healing of chronic wounds, and alginates were better than other modern dressings for debriding necrotic wounds. When compared with other traditional dressings or a silver-coated dressing, respectively, hydrofiber and foam dressings reduced healing time of acute wounds. Types of dressing changes [50]. Dry-to-dry dressings are used for wounds closing by primary intention. The advantage is it provides good wound protection, absorbs any drainage and it provides pressure to the area if needed. The disadvantage is the dressing adheres to the wound surface once the drainage dries, thus impeding wound healing during the removal process because the granulated tissue is removed, and it causes pain for the patient. Wet-to-dry saline dressings are used for untidy or infected wounds that must be debrided or are closed by secondary intention. The advantage is it eliminates dead space because the gauze is saturated with sterile saline and/or an antimicrobial solution. The wet dressing is then covered with a dry dressing. Wet-to-wet dressings are used on clean, open wounds or on granulating surfaces. Similar to the wet-to-dry type of dressing change, sterile saline or antimicrobial agents may be used to saturate the dressing. The advantage is it provides a physiologic warm environment that enhances local healing and provides comfort to the patient. The disadvantage of this dressing is that the surrounding tissues can become macerated, thus increasing the risk of infection and frequent bed linen changes. 43

44 4. For years, dry-to-dry dressings were the mainstay therapy, but more recent research has demonstrated that local moisture is necessary to facilitate granulation and reepithelialization of the ulcer [87]. If a wound is moist (wetdry dressing), the wound healing process will be accelerated, and epithelialization will be rapid [87]. According to the Wound Healing Society (2006), the following guidelines are recommended [87]: Moist dressings are ideal to keep the area moist and to control any potential exudate. After a debridement, the wound should have a dry dressing to absorb any bleeding for the first eight to 24 hours. margarine, whole grains and green leafy vegetables. Zinc is a mineral that helps maintain the structure and function of the body and skin while it collaborates with other nutrients. It is in meat, fish, seafood, liver, eggs and beans [40]. 5. Pain. Depending upon the depth of injury and other co-morbidities, patients may endure a significant amount of pain during the dressing change. Therefore, it is important to assess the pain level according to the hospital policy as a baseline prior to any treatments and before/during/after administration of pain medications. In addition to administering pain medications, there are other treatment modalities that may help reduce the pain level Nutrition. [94]: Proper nourishment contributes to the support and growth of Cover the wound appropriately. granulation tissue [87], so patients should be encouraged to Adjust support surfaces for the patient. eat a well-balanced diet to maintain homeostasis. However, Reposition the patient. patients who are at the highest risk of inadequate wound healing 6. Sutures. are typically malnourished. Therefore, the nurse and health If sutures are required, typically the wound is open or longer care providers should encourage adequate calories, protein and than half an inch. The patient should seek care within six hours hydration based upon the patient s weight, nutritional goal and of the injury to avoid infection and to ensure sutures can be laboratory data, which are calculated by the consulting dietician implemented [54]. [40]. For the average healthy adult, the daily nutritional 7. Tetanus vaccination. requirements are approximately 1.25 to 1.5 grams of protein The CDC recommends that if a patient presents with any wound per kilogram (kg) of body weight and 30 to 35 calories per other than a clean, minor wound and does not have a clear history kg [78]. The patient s weight should be assessed whenever of at least three tetanus vaccinations, he or she should receive the there is a change in his or her condition. If the patient is tetanus immune globulin (TIG) and a tetanus vaccination [21]. malnourished or has a chronic illness, he or she will be The tetanus immune globulin takes effect immediately, whereas a deficient in protein, which is found in approximately 25 vaccination takes up to four weeks to be effective (See Table 5, at percent of all hospitalized patients [78]. Examples of foods the end of this chapter). high in protein include beef, chicken, pork, turkey, eggs, Tetanus is caused by the neurotoxin etanospasmin (clostridium liver, milk and cheese [15]. tetani), a spore of the tetani organism that is found in soil All patients should be encouraged to eat adequate [56]. The complication of tetani organisms interfering with servings of protein, carbohydrates, vitamins, minerals and the neurotransmitters is stiffness in the jaw and neck muscles, trace elements to ensure wound healing, especially with followed by uncontrolled spasms, exaggerated reflexes and any pressure ulcer [49]. painful convulsions [56]. Tetanus is most prevalent in the elderly, If a patient is unable to consume enough calories, especially older women (greater than 55 years of age), migrant protein or nutrients with his/her food intake, a workers, newborns, injection drug users, diabetics and those with physician should be notified to prescribe a dietary nonacute wounds (chronic ulcers, gangrene, abscesses/cellulitis) consult if not already ordered to ensure the patient [21, 56]. The CDC has released the following statistics [21]: receives the most appropriate nutritional supplement. Elderly In 2004, 71 percent of the 34 cases reported were In 2006, Medical Nutrition USA Inc., (MDNU) among persons more than 40 years of age, and 47 percent announced results of a clinical trial on its Pro-Stat(R) were among persons greater than 60 years of age. modular protein supplement and found that the use of Older women Research has demonstrated that women 55 Pro-Stat(R) improved the healing of pressure ulcers years of age and older do not have protective levels of tetanus among long-term care residents by 96 percent [58]. antibody. Patients who have vitamin or mineral deficiencies should Diabetics The CDC has reported that tetanus is about three receive supplemental treatment immediately to promote times more common in diabetics, and fatalities are about four the healing process [40, 78]. times more common. Vitamin A is a fat-soluble vitamin that increases Nonacute wounds Chronic ulcers, gangrene, abscess and fibronectin on the wound surface, thus increasing cell cellulitis account for one in six cases of reported tetanus; one chemotaxis, adhesions and tissue repair. Vitamin A is in 12 reported cases had no reported injury or lesion. necessary to maintain the integrity and function of the skin. It is found in milk, eggs, cheese, fish, dark green 8. Tissue perfusion/oxygenation. It is imperative to ensure vegetables, oranges and fresh fruits. that there is adequate oxygenation within the body as it is a Vitamin C is a water-soluble vitamin that promotes foundation for wound healing. Therefore, depending upon the collagen synthesis and serves in the formation mechanism in which the wound was inflicted, it is important to of connective tissue. It s found in citrus fruits, first address the adequacy of airway, breathing and circulation strawberries, tomatoes, potatoes, broccoli and (ABC) before initiating any other treatment modalities. If the cantaloupe. patient has any symptoms of shock due to extensive blood loss, Vitamin E is a fat-soluble antioxidant that facilitates the shock needs to be treated immediately. Signs and symptoms cell membrane function. It is found in vegetable oils, of shock include [50]: 44

45 9. Pale, mottled, diaphoretic skin. Tachycardia. Tachypnea. Hypotension (this is typically a late sign of shock). Once the shock has been stabilized and/or ruled out, there are other general factors that contribute to the body s inability to maintain adequate tissue perfusion and oxygenation [87]: Dehydration because it increases sympathetic tone such as cold, stress or pain, which will decrease tissue perfusion. Cigarette smoking decreases tissue oxygen by peripheral vasoconstriction. Hypovolemia will reduce the amount of circulating oxygenated blood, which may cause further problems for the patient. Therefore, if the patient is bleeding, it is important to stop the bleeding immediately. A small amount of bleeding may be cleansing to the wound and will stop within minutes [54]. However, with a patient who presents with a gushing, oozing gunshot or stabbing wound perfusing large amounts of blood, the following steps should be implemented to control the bleeding [54]: Apply firm pressure above the level of the heart with a gentle cloth. If the blood continues to soak, apply additional cloths on top of that cloth directly over the wound with pressure. In 2004, the Food and Drug Administration (FDA) approved a new solution to halt bleeding, QuikClot [35]. QuikClot is made from a zeolite material that occurs naturally in volcanic rock and is poured directly into a wound that will not stop bleeding [35]. Wound cleaning. It is imperative to cleanse wounds appropriately to remove foreign or necrotic matter, reduce odor and bacteria [15]. According to the Wound publication, numerous research studies were implemented to evaluate the effectiveness of woundcleansing products 15]: According to 11 randomized studies found on Medline, EM BASE, CINAHL, and Cochrane databases, there is no evidence that saline wound cleansing is more effective than tap water in reducing wound infection or improving healing. In order to ensure proper wound cleaning, there are certain measures that need to be implemented for adequate healing. Cleaning. The ideal method of irrigating all traumatic wounds is to attach a syringe and a 22-gauge angiocatheter to one liter of normal saline with IV tubing [19]. It is important to maintain pressure of 5 to 15 pounds per square inch to ensure effective cleaning [19]. In the latest 2008 research, a piston or bulb syringe is not recommended for irrigation because it does not generate the necessary pressure required to clean the wound efficiently [19]. Skin cleansers [23]. The skin around the wound contaminates should be cleansed with a skin cleanser to neutralize the drainage and to eliminate any odor. Anytime a wound is cleaned, it needs to be pat dried and not rubbed to prevent further skin breakdown. Moisturizers (emollients) are utilized for dry skin. It should be noted that dry skin is not attributed to the abnormal function of water intake, but to abnormal function of the epidermis [56]. According to the CMDT 2008, the best moisturizers include petroleum, mineral oil, Aquaphor and Eucerin [56]. The best way to apply a moisturizer is to apply it to wet skin in a thin layer with the grain of the hairs, rather than rubbing it up and down in order to avoid folliculitis (inflammation of hair follicles) [56]. Moisturizers should be implemented to provide hydration, soften and to protect the skin from breakdown. The Cleveland Clinic recommends using creams instead of lotions because they have less water, and research has shown that they provide intensive hydration for severely dry skin for 24 hours. Apply the moisturizing cream to all skin surfaces. Apply the moisturizing cream immediately after bathing while the pores are still open from the water. 10. Other treatment options for chronic wounds. Depending upon the severity and depth of the chronic wounds, such as pressure ulcers, diabetic foot ulcers and leg ulcers, there are other adjunctive therapies that are used in collaboration with the standard treatment modalities to promote wound healing and to prevent complications. Electrotherapy. Due to the prevalence of disvascular amputations and the costs associated with them, electrotherapy has been an effective adjunctive therapy for ischemic, chronic wounds [36]. Electrotherapy is intended to supplement surgical revascularization, which is the standard care for ischemic wounds. However, when vascular bypass is associated with minor amputation, such as with digits or at the transmetatarsal level, necrosis may still occur along the suture line, even with distal pulses present. Distal necrosis is more challenging to treat when a patient is a poor surgical candidate because of failing health or limited outflow arteries [36]. Grafts, skin substitutes or flap closures. There are times when chronic wounds have soft tissue visible but are not healing well. At that time the physician may contemplate a skin graft, application of bioengineered skin substitutes or flap closures [77]: Dermagrafts are a cryopreserved human fibroblastderived dermal substitute produced by seeding neonatal foreskin fibroblasts onto a bioabsorbable polyglactin mesh scaffold. Dermagraft is useful for managing fullthickness chronic diabetic foot ulcers. It is not appropriate for infected ulcers, those that involve bone or tendon, or those that have sinus tracts. A multicenter study of 314 patients demonstrated significantly improved 12- week healing rates with Dermagraft (30 percent) versus controls (17 percent). Apligraf (Organogenesis) is a living, bi-layered human skin substitute. It is not appropriate for infected ulcers, those that involve tendon or bone, or those that have sinus tracts. Bioengineered skin substitutes have been questioned because the mechanism of action is not clear, the efficacy is questionable, and the cost is high. 45 Hyperbaric therapy. Hyperbaric therapy involves placing the patient into a large chamber that promotes wound healing; it supports bacterial destruction by white blood cells, collagen growth via fibroblast proliferation, and assists in the development of new epithelial tissue [11]. Maggot debridement. Maggot debridement therapy (MDT) is an ancient woundcare modality that has been around since the battle of St.

46 Quentin in the 1500s [45]. However, MDT was not utilized in the United States until the 1930s, and then it lost popularity when antibiotics were introduced in the 1960s [45]. However, the effectiveness of MDT was not researched until 1989 in Long Beach, Calif. [93]. In 2004, the FDA approved production and marketing of maggots as a medical device under the brand name of Medical Maggots [45, 93]. MDT uses fly larvae, or immature flies that are hatched from eggs. Surprisingly, not all maggots are capable of feeding in necrotic, gangrenous tissue. The flies used most often in therapy are blow flies (calliphoridae); and the species used most commonly is phaenicia sericata, the green blowfly [93]. The Wound Care Network lists the following advantages and disadvantages of MDT [93]: It takes approximately minutes to apply a secure dressing to keep the maggots in place, with an excellent safety record. Medicinal maggots have three actions. They: Debride the wound by dissolving the dead (necrotic), infected tissue. Disinfect the wound by killing bacteria. Stimulate wound healing. Maggots are highly perishable and should be used within 24 hours of arrival. This treatment is simple enough that it can provide thorough debridement when surgery is not available or is not the optimal choice. Low cost of treatment. Clinical studies indicate that MDT accomplishes the same goal as other treatments in a shorter, cost-effective manner [45]. Dressing In order to keep the maggots isolated to the necrotic wound area, a porous, meshlike covering (i.e., nylon netting) should be placed over the wound border, then secured with tape, glue or a hydrocolloid pad. Remove the dressing and maggots 48 to 72 hours after the initiation of treatment [93]. Treatments The size of the wound and the goal of treatment will determine the necessary required treatment cycles of maggots. Typically the average patient receives two to four cycles [93]. Negative pressure wound therapy (NPWT). Vacuum-assisted closure (VAC) was cleared for use by the FDA in It is used to reduce colonization of bacteria and increase wound healing by [37]: Removing fluid from the extravascular space. Lowering capillary after-load. Improving blood supply during the inflammatory phase. Increasing the peripheral blood flow. VAC therapy was originally developed as an adjunct for pressure ulcers. However, in 2006, it gained approval for the treatment of other complex, chronic wounds, such as diabetic foot ulcers, flaps, grafts, traumatic wounds, dehisced wounds, in preparing wounds for closure and mainstay treatment of stage three and four pressure ulcers [84]. The suction in the VAC attaches to the wound edges toward the wound center to improve local oxygenation and prompts angiogenesis to deliver negative pressure ranging from 50 to 200 mm Hg [37] (See Table 6, at the end of this chapter). Surgery. Surgery is applicable if the wound is not healing after treatment or if the wound has failed to produce granulated tissue [8]. The most common surgeries completed to promote the growth of new tissue include [32]: Free tissue transfer flap, which involves moving tissue from one side of the body to another area. Myofasciocutaneous flap or rotation. Random flap. Specific treatment of wounds In order to properly treat each wound, it is important to adhere to the generalized care of wounds considering tissue perfusion, nutrition, pain, wound cleaning, dressing changes and the potential need for sutures or surgery. The ultimate goal in treating all acute wounds, such as abrasions, lacerations, bites, puncture and/or surgical wounds is to control the hemorrhage, protect the patient and the wound, and to provide comfort [19]. Treating chronic wounds is a little more complex as it requires specific interventions based upon other comorbidities of the patient. In addition, various research studies and guidelines provide the following specific treatment modalities for each type of wound. 1. Treatment of abrasions and scrapes. Typically, abrasions and scrapes do not require extensive treatment because they are only a superficial break in the skin. The primary treatment for abrasions and scrapes is [30]: Bleeding If there is any bleeding, stop it with firm pressure above the level of the heart for approximately 10 minutes. If debridement is required, remove any residual foreign material with forceps and/or pulsatile lavage with suction [4]. Cleaning Wash the abrasion and/or scrape four times a day for the first 48 hours, then keep the area covered with a sterile bandage. The AACW recommends cleaning the skin with NS or a noncytotoxic wound cleanser [4]. Cytotoxic products to avoid include all of the following [4]: Hydrogen peroxide. Iodine solutions. Merthiolate, Mercurochrome. It is important to ensure that all of the dirt and debris is removed from the abrasion and/or scrape. If the abrasion or scrape is due to a bite and/or a combination of a puncture or deeper wound, do not scrub the deep wound or bite; it is recommended that the area be just washed out. Dressing Once the area has been cleaned and the bleeding has stopped, protect the injury with a nonadherent dressing to promote a moist environment for optimal healing [4]. 2. Treatment of animal or human bites. Antimicrobials. Due to the prevalence and severe risk of infection, antibiotics are administered prophylactically and with any known infection depending upon the identified source. Most wounds do not develop signs and symptoms of infection until 24 to 72 hours after the bite [19]. Infections are caused by aerobes and anaerobes or anaerobes alone (36 percent) [56]: Aerobic. Pasteruella multicida, the most common isolate (75 percent of cat bites and 50 percent of dog bites) is a gram negative coccobaccillus that is usually resistant to the penicillinase-resistant penicillins, yet it is sensitive to penicillin [6, 56]. However, research has demonstrated that pasteruella multicoida is best treated with a 46

47 penicillin (PCN) or a tetracycline [56]. Cephalosporins administered orally do not reach blood concentrations high enough to eradicate the pasteurella multicoida infections effectively [6]. Staphylococcus aureus, another common aerobic bacteria, occurs in 30 percent of bites that are usually resistant to PCN, which may pose a potential problem for the efficacy of treatment [6]. Anaerobic. Fusobacterium. Bacteriodes. Porphyromonas. Prevotella. Empiric antibiotic therapy is most effective with Amoxicillinclavulanic acid 500 to 800 milligrams by mouth twice a day or Cefoxitin 500 milligrams IV twice a day for seven to fourteen days [19]. However, if the wound involves the bone and/or joints, antibiotic therapy should be prescribed for 21 days [19]. If a patient is allergic to PCN, then Doxycycline 100 milligrams by mouth twice a day or the combination of Clindamycin with Bactrim or Ciprofloxacin should be prescribed [19]. According to the CMDT (2008) guidelines, the antibiotic treatment recommendations for bites are as follows [56]: High-risk bites Typically in all high risk-bites, the patient will be treated prophylactically, such as a cat bite (30 to 50 percent risk). Therefore, the patient will be administered dicloxacillin 0.5 grams orally four times a day for three to five days. Dicloxacillin is a narrow spectrum beta-lactam antibiotic in the PCN family and is used to treat infections caused by susceptible gram-positive bacteria, such as staphylococcus aureaus, another common bacteria found in bites [25]. Hand bites If a patient presents with a bite to the hand, regardless of whether it is inflicted by an animal or a human, the patient will be administered PCN V 0.5 grams orally four times a day for three to five days [57]. Known bacteria If the wound has a known bacterial infection, the appropriate antibiotic will be administered based upon the type of bacteria, co-morbidities, risk factors and any allergies. The response to treatment may be slow and should be continued for at least two to three weeks. Human bites Typically human bites are prescribed intravenous (IV) therapy with a B-lactam plus B-lactamase inhibitor combination (such as Unasyn, Timentin, Zosyn) and/or a second-generation cephalosporin (cefoxitin, cefotetan, cefmetazole). If there is a PCN allergy, clindamycin plus a fluoroquinolone will be prescribed. Because of the variability of human bite wounds, a culture should always be taken to identify the exact bacteria source. Pregnant women Macrolides should be prescribed if the patient is allergic to B-lactamase PCNs [70]. It should be noted that dicloxacillin and PCN have been studied in their treatment of bite wounds. There has been concern about their use due to their narrow spectrum of activity (grampositive bacteria), especially since the most common bacteria is pasteruella (a gram-negative bacteria) [56]. The CMDT (2008) has implied that other agents that have not been studied for their efficacy of bite wounds may be more beneficial, such as [56]: Cefuroxime, a second-generation cephalosporin, has broad spectrum activity against anaerobes, gram-positive and gramnegative bacteria [46]. The typical adult dose is grams by mouth twice a day; in the pediatric patient, the dose 47 is grams twice a day [46]. Amoxicillin-clavulanic acid (Augmentin) is an extended spectrum PCN that has greater activity with gram-negative bacteria and has the ability to penetrate the outer membrane. It is inactivated by many of the B-lactamases [46].The typical adult dose is 500/125 by mouth three times a day to 875/125 by mouth twice a day. In the pediatric patient, the dose is 20 to 40 milligrams per kilogram by mouth three times a day [46]. Clindamycin plus a fluoroquinolone (ciprofloaxin or Levofloaxcin). Clindamycin is a chlorine-substitute that has coverage against anerobic and streptococci, staphylocci and pneumococcal [46]. The typical adult dose is grams every eight hours. The pediatric dose is 10 to 20 milligrams per kilogram a day [46]. Cleaning The most important component of treating an animal bite is wound cleaning and irrigation [13]. Because of the vast array of bacterial sources in a bite, it is imperative to irrigate the wound immediately to decrease the number of potential bacteria that may have been inoculated during the bite [6, 19]. The American Veterinary Medical Association (AVMA) recommends that all animal bites should be cleaned in the following way [6]: First, clean the wound with povidone-iodine solution. Second, irrigate the wound with normal saline (NS) 0.9 percent using an 18-gauge blunted needle on a 35 milliliter (ml) syringe. A liter of NS may be used at a pressure of 50 to 70 psi. If rabies is speculated, the wound needs to be cleaned immediately with soap and water or a 1 percent povidone-iodine solution to potentially lower the transmission rates [19]. Debridement Depending upon the depth of the injury and the surrounding skin, a debridement may be required to remove any devitalized tissue [27]. According to the AVMA research, infection developed in approximately 17 percent of wounds that were not debrided [6]. Other perks of debridement include easier surgical repair and a smaller scar at the site of the injury [6]. Sutures Over the years there has been controversy regarding suturing an animal wound. For many years, suturing was absolutely omitted in treatment guidelines because of reports that it can result in a loss of function of the area when bacteria are trapped under the sutures [57]. However, newer thought by the AVMA, emedicine and the CMDT of 2008 implies sutures may be used if the primary bite site has been meticulously cleaned and irrigated [27]: If the wound is capable of closing on its own; such as a fresh dog bite and a facial bite (if it does not require cosmetic surgery) [19]. Dependent upon the risk of infection in the bite wound. Dependent upon whether there are any cosmetic considerations. Hand wounds If a bite wound is infected or if the bite wound is on the hand, it should never be sutured because of the risk for loss of function, especially in the hand, because it may be a closed-space infection [56]. Hand wounds should be wrapped in sterile gauze, splinted in a position of slight wrist extension, then continuously elevated [13]. In addition, it should be noted that cat bites should never be sutured because of depth of the wound and higher risk of bacterial infection inside the wound [27]. Vaccinations Once the cleaning has been completed, there are other prophylactic vaccinations and/or medications that may

48 need to be administered depending upon the patient s previous vaccination history and/or risk factors. Tetanus toxoid is administered as advised in CDC guidelines (See the previous generalized treatment of wounds for guidelines of administering the tetanus vaccination and Table 6 at the end of this chapter). Hepatitis B is administered as a prophylaxis for patients who have been bitten by known carriers of hepatitis B. The patient will be given the hepatitis B immune globulin immediately at the time of injury because it will begin to work immediately; then the patient will be placed on a regimen based on CDC guidelines in 30 days [20]. Human immunodeficiency virus (HIV): Prophylaxis is not typically recommended, because it is a potential risk that is low [56]. Rabies shot (human diploid) is administered depending upon the risk of rabies exposure and the guidelines of the city or state public health departments, CDC and the Advisory Committee on Immunization Practices [19, 27]. If the patient has been exposed to rabies, the local health department and public authorities need to be notified immediately to decide whether the patient should be isolated, observed and/or quarantined [19]. The rabies vaccination is an inactivated form of the virus grown in primary cultures of chicken fibroblasts and it offers active immunity if it is used in combination with the human rabies immune globulin and local wound treatment [27]. The vaccination provides protection to a patient s post-exposure of a bite in all of the age groups, and the protocol is as follows [27]: Fourteen days after initiating the immunization series, anti-rabies antibody titers reach levels above minimal protective levels of 0.05 International Units (IU) per milliliter. Post exposure prophylaxis for previously unvaccinated patients is 20 IU per kilogram as soon as possible after exposure, with a total of five intramuscular (IM) doses on days 0, 3, 7, 14 and 28. Previously immunized patients will receive 1 milliter IM on day zero and day three. The rabies vaccine must be injected IM and never subcutaneous (SC), intradermal (ID), or intravenous (IV). In adults, the nurse should inject the vaccination into the deltoid muscle; small children should receive the vaccination into the anterolateral zone of the thigh. Follow-up The nurse should tell patients with a bite wound to inform their primary care provider (PCP) immediately if they experience any signs and symptoms of infection or a change in sensation of the area (numbness and/or tingling). In addition, patients treated on an outpatient basis and sent home after being seen in the ER should follow up with the PCP within 48 hours to reduce the risk of treatment failure and complications. Failure to identify and treat the bite appropriately and efficiently may result in complications such as cellulitis, tenosynovitis, septic arthritis, osteomyelitis, abscess and/or fatal sepsis [6]. In addition, cat bites may cause cat scratch fever, which results in adenopathy and which is typically self-limiting [27]. It is estimated that only 1 to 2 percent of all patients who present with a bite will be hospitalized. A patient should be hospitalized if he or she is experiencing any systemic symptoms (fever, chills), severe cellulitis, suspected noncompliance or infected bites [19] Treatment of bruising. The treatment of bruising is predominately superficial as it affects the epidermis of the skin. The initial treatment, according to the AACW, includes [4]: Apply cold compresses for 15 to 20 minutes per hour while awake for the first 48 hours. After the first 48 hours, apply warm compresses for comfort to the bruise. Avoid massaging the bruised area. Avoid taking any NSAIDS or aspirin (ASA) products for pain relief. Treatment of burns. It is crucial to ensure the patient receives safe, expert care when dealing with a burn. It is important that the patient is seen immediately to prevent long-term complications (such as cardiorespiratory distress and compromise) with major wounds and/or inflammation and infection that can occur in any burn patient. The type of injury will determine the primary skin treatment related to the burn injury [5]: Antibacterials Because of the complexity of bacteria, there is no ideal antimicrobial to prescribe for each scenario. Therefore, the most commonly prescribed topical antimicrobials are discussed, and they may be applied with Bacitracin ointment. The ideal antibacterials that are applied to the skin should cover broad spectrum bacterias and be nontoxic to the skin. The ideal anti-bacterial agents are [50]: Silver sulfadiazine (Silvadene, SSD) (1 percent solution). Silvadene is the most common agent utilized because of its excellent ability to fight gram-negative and grampositive bacteria. It is rarely toxic. Silvadene should be used with any open treatment or with a light or occlusive dressing. A major side effect of Silvadene is that it may induce transient leukopenia, low white blood cells (WBC). Therefore the nurse should monitor the WBC as ordered and notify the doctor if the patient s WBC is decreasing. According to Lippincott, Silvadene should be discontinued if the WBC is lower than 1,500 in adults or 2,000 in children. The nurse can anticipate the WBC to return to normal limits within two to four days of discontinuation of the product. Avoid with any sulfa allergies [19]. Mafenide acetate (Sulfamylon) (10 percent solution). Sulfamylon is effective against most gram-positive bacteria and gram-negative. Sulfamylon cream should be applied without dressing and re-applied every 12 hours. If a dressing is required, apply a bulky wet dressing and rewet it every two to four hours. The disadvantage of Sulfamylon is it causes pain during and immediately after the application. Silver nitrate (0.5 percent solution). Silver nitrate is a clear solution with low toxicity risk and has effective coverage against most common burn pathogens. Silver nitrate should be applied with a bulky dressing and rewet every two to four hours to maintain therapeutic concentration levels. Cleaning All burn wounds need to be cleansed initially and then daily with a mild antibacterial cleansing agent and saline solution or water [19]. Debridement If the burn has any blisters or eschar, it needs to be removed with natural, enzymatic, mechanical and/or surgical debridement [50]:

49 Natural manner involves the body s own ability to have the eschar attempt to separate from the underlying vulnerable tissue in combination with the nurse doing daily or twice daily (BID) dressing changes. Depending upon the hospital policy, forceps or scissors may be encouraged to attempt to remove the eschar. Enzymatic agents are applied to the wound and typically induce a more rapid debridement process of removing the eschar. Mechanical or surgical debridement involves removing nonviable tissue to the viable base. Dressings Prior to any dressing change and/or procedure, it is crucial that the nurse assesses the patient s pain level frequently and avoid waiting for complaints of pain to intervene. The typical dressing is 4 x 4 gauze pads or several layers of Kerlix bandages. All dressing changes should be under sterile technique. In addition, depending upon the depth of injury, other dressing covers may be more applicable to promote wound healing [50]: Minor burns need to be immersed in cool water at a temperature of 55 degrees Fahrenheit or application of cool compresses. The American Burn Association classifies a minor burn as one that involves less than 15 percent of total body surface area (TBSA) for those 10 to 50 years of age, or less than 10 percent of TBSA for those over 50 years of age [19]: The dressing should be a thin layer of antimicrobial cream or ointment, such as Silvadene. If the patient has a sulfa allergy, Bacitracin is a great alternative. Alternative dressings include DuoDerm, OpSite, Epigard, Epi-Lock, Biobrane or Tegaderm. These biosynthetic dressings are required to stay in place for one to two weeks until the wound heals. The wound should be cleaned and redressed twice a day for seven to 10 days until the wound is healed. If the patient has a burned extremity, it should be splinted and elevated. Major or severe burns The primary goals are to keep the patient s airway open, maintain cardiac output, adequate hydration and prevent infection. Partial thickness burns require DuoDerm, Op-site, or Vigilon to promote healing. A partial thickness burn over 30 percent TBSA or a full thickness burn over 5 percent TBSA needs to be covered with a clean, dry, sterile bed sheet to preserve the body temperature and to protect the skin. The DuoDerm covers the partial thickness burn and it prevents bacterial contamination. The Op-site covers clean partial thickness burns and/ or clean donor sites. Op-site also provides a moist environment for epithelization to occur. Vigilon is a suspension on a polymethylene mesh support that helps clean small partial thickness burns. Post surgical After a surgical procedure, the patient should have a wet-to-dry dressing change every four to six hours as ordered. Due to the frequency of the dressing change, provide warm blankets to the patient to prevent heat loss. In addition, a dry top layer of stockinette or a cotton bath blanket prevents evaporative heat loss. Other treatment modalities There are other treatment modalities with burns, depending upon the severity of the burn, the patient s health history and/or access to health care, such as: Hydrotherapy It involves the patient being immersed into a body of water to facilitate cleansing and debridement of the burned area [50]. The unique advantages of implementing hydrotherapy in the treatment plan are [50]: Topical medications, adherent dressings and eschar are more easily removed during the immersion in the water, which causes less pain to the patient. It encourages the patient to implement range of motion exercises (ROM) in the immersion of water to build up strength to the affected area. However, as with any treatment, there may be disadvantages [50]: The patient loses body heat and sodium each time he or she is immersed in the water. Therefore, it is recommended that if hydrotherapy is implemented, the time in the immersion of water should be limited to decrease the loss of body temperature and subsequent chilling. The immersion of water all over the body may induce generalized pain to the patient. The patient may experience more anxiety before the hydrotherapy treatment. Pain Minor burns are very painful, and the nurse should always make sure that prophylactic analgesics are provided to the patient before any dressing change and as needed. The most beneficial pain medication to administer is ibuprofen, an anti-prostaglandin that has a good anti-inflammatory and analgesic component [19]. Codeine may be another option. Vaccinations Tetanus prophylaxis if needed. Treatment of lacerations or cuts. The goal of treating lacerations includes prompt healing, minimizing the risk of infection and limiting cosmetic disfigurements [13]. The first mode of treatment is to ensure there are no other serious injuries present when a patient presents with a laceration [13]. Once other injuries have been ruled out, the bleeding should be controlled with direct pressure and elevation (if possible) [13]. Clamping should be avoided as it may damage adjacent nerves [13]. Based upon the Merck guidelines of 2006, the lacerated wound should be treated this way [13]: Cleansing Clean with NS and/or antibacterial soap with water and avoid any harsh chemicals, (such as povodine iodine or hydrogen peroxide) or products (brushes or rough materials) because the subdermal tissue of the wound is delicate. The lacerated wound may also be cleansed with an irrigation system using NS in a 20 to 35 milliliters syringe with a 20-gauge needle or an IV catheter. Povodine-iodine may be used around the injury, but not in the wound to reduce skin flora. Debridement All devitalized tissue should be removed to ensure adequate granulated tissue healing. Closure Individual patient care should be considered before deciding whether a wound should be closed based upon age, cause of the laceration, the degree of contamination and the patient s risk factors. However, a cat bite laceration should never be closed, nor should a bite to the hand, a puncture wound or a high-velocity missile wound. Primary closure. The majority of practitioners will close wounds on the face or scalp immediately if they are less

50 6. than six to eight hours old. Delayed primary closure. Other wounds can be closed after six to eight hours if there is any inflammation present. Sutures, staples, adhesive strips and liquid tissue adhesives may be used to close the wound. Dressings Change the dressing daily or if it becomes wet or soiled. In addition to the specific guidelines provided, additional measures may be implemented per the AACW dependent upon the depth and/or specific type of laceration [53]: Superficial lacerations. The goal of dressing superficial lacerations is to bring the wound edges together by securing it with a butterfly/skin tape, then applying a clean, nonadherent dressing. Deeper lacerations. In order for the wound to heal appropriately, sutures are typically required. Lacerations on the face require a plastic surgeon referral for potential cosmetic surgery. Tetanus Administer the vaccination, if necessary, according to CDC guidelines. Medications Antibiotics are not required, but there is no harm and it may be beneficial. If a wound infection occurs or if the patient is at risk of developing an infection, systemic antibiotics will be prescribed. The drug of choice that is effective against skin flora is cephalexin 500 milligrams twice a day or PCN 500 milligrams four times a day [53]. Other measures included in the treatment of lacerations include the following [53]: Avoid excessive movement of the affected area because it affects the healing process. Keep the wound clean and dry. Follow up with the PCP 48 hours after the injury occurred. After 48 hours, the wound can be cleaned with water or half-strength hydrogen peroxide. Treatment of perineal skin breakdown. According to the Ostomy Wound Management (OWM), the ultimate goal of perineal skin care is to properly manage the underlying incontinence through behavioral, pharmacological and/or surgical interventions [66]. Failure to manage the incontinence will precipitate further skin breakdown or complications. It is imperative that the wound be properly cleaned utilizing appropriate techniques and products, such as skin cleansers and moisturizers as needed [23, 66]: Perineal skin cleaners neutralize the drainage and eliminate any potential odors due to the incontinence. The OWM recommends that after each incontinent episode, the perineal area should be properly cleansed with a product specific for perineal skin cleansing. Ideal products should include any of the following humectin ingredients: Glycerin. Methyl glucose. Esters. Lanolin. Mineral oil. When a wound is cleansed, it needs to be pat-dried and not rubbed to prevent further skin breakdown [23]. Avoid no-rinse perineal cleansers, bar soaps, products specific for routine skin cleaning only or antibacterial hand washing as it can dry the skin, raise the ph and further erode the epidermis layer of skin Moisturizers protect and soften the skin. Perineal skin barriers, also referred to as moisturizers or skin protectants, protect the skin from exposure to irritants or moisture and hydrate, soften and protect the skin against breakdown [23]. The active ingredients in moisturizers include: Petrolatum. Dimethicone. Lanolin. Zinc oxide. There are two types of moisturizers, a basic moisturizer and a moisturizer barrier ointment [23]. Basic moisturizers Basic moisturizers should be used to provide hydration, soften and to protect the skin against breakdown. The Cleveland Clinic recommends using creams over lotions because they have less water, and research has shown that they provide intensive hydration for severely dry skin for 24 hours. Apply the moisturizer cream to all skin surfaces. Apply the moisturizer cream immediately after bathing while the pores are still open from the water. Moisturizer barrier ointment The moisturizer barrier ointment protects the skin from urine or stool if the patient is incontinent of either function. The main ingredients in moisturizer barrier ointments are dimethicone, zinc or petrolatum. Always clean the skin gently and thoroughly, then apply a layer of the product. In addition, there are instances when the moisturizer may be incorporated into the skin cleanser or it may be formulated separately as a cream (water based), ointment (oil based preparation) or paste. Ointment (oil based) products last longer on the skin. There are also liquid barrier films that are available that contain a polymer combined with a solvent. Ideally, the solvent evaporates and the polymer dries it to form a barrier for skin protection. It is important to avoid any liquid film barriers with barrier creams or pastes because of the incompatibility of the products [66]. The OWM also recommends that nurses incorporate the use of perineal devices, such as [66]: Underpads and/or absorbent pads may be used if they keep the moisture away, rather than trapping it in. External catheters are used to collect urine or a fecal incontinent collector to collect feces. If the external urinary Foley catheter and feces collectors are used appropriately, they can prevent and treat perineal skin breakdown. Rectal tubes should be avoided because they can perforate the bowel and damage the anal sphincter. Treatment of pressure ulcers. The ultimate goal of treatment is to remove any necrotic debris and to maintain a moist wound bed that will promote healing and the formation of granulated tissue [56]. All pressure ulcers should be treated in the following manner per the recommended Wound Care Information Network (WCIN) guidelines [94]: Enhance soft tissue viability and promote healing of the ulcer in the following steps [16]: Ensure proper positioning It is speculated and believed that pressure ulcers result from the compression of soft tissue against bony prominences [87]. Therefore, it is important to ensure that the patient who is at risk of a pressure ulcer or who already has been affected by one should be on a stringent repositioning schedule to avoid further damage and/or complications [87]. At this time,

51 the rule of thumb is to ensure that the patient is turned at a minimum of every two hours. However, it should be noted that skin breakdown and injury can occur in less time, so repositioning should be customized to the patient [41]. Keep the head of bed at the lowest degree depending on the patient s medical conditions, because levitation of the head produces shear and friction between the skin and the bed surface [87]. Keeping the head at the lowest position poses a challenge for certain patients, such as those in respiratory or cardiac distress or who have a feeding tubes. Therefore, the guidelines recommend that if possible, elevation of the head should be limited to certain increments [87]. During the time frame that the head of the bed needs to be at 90 degrees, the nurse can tilt the head forward more than 90 degrees with pillows to keep pressure off the sacral/coccyx area [41]. Ensure appropriate mattresses and/or devices Any patient who is at risk or who has an ulcer on admission should be ordered a pressure-reducing surface mattress. In order to alleviate pressure, consider the amount of pressure required to occlude the capillary blood flow, also known as the capillary closing pressure [41]. The normal capillary closing pressure ranges from 12 to 32 mm Hg. Therefore, any pressure device needs to be below the capillary closing pressure to prevent tissue ischemia [41]. Nurses can monitor this by observing skin color, the integrity of the skin and temperature to assess capillary flow adequacy because the device s reading may not be customized or accurate for each particular patient [41]. Research has demonstrated that pressure-reducing devices can reduce the risk of developing any ulcers by 60 percent compared to standard hospital beds [87]. If a patient has a stage 3 or 4 ulcer, he or she should be on an air mattress, although they may limit the ability of certain patients to reposition themselves [87]. Therefore, nurses and nursing assistants need to be attuned to this potential problem. They need to ensure the patient is turned frequently and that the call light is within reach of the patient. Use devices such as pillows or foam to keep heels off the bed and to keep knees and ankles from touching. Do not position the patient on the pressure ulcer. Avoid ring cushions (donut-type) devices and seat cushions that have the bottom out appearance. They increase venous congestion and edema [87]. If the patient has an ulcer in the area, sitting should be avoided or limited to less than an hour to avoid exacerbating the wound [87]. If possible, nurses should educate the patient and the families to have the patient shift his or her weight every 15 minutes while sitting to also avoid the risk of exacerbating the pressure ulcer [87]. Care of the ulcer. Cleaning the wound In order to properly clean a pressure ulcer, normal saline (NS) should be utilized. Do not use povodine iodine, iodophor, sodium hypochlorite solution, hydrogen peroxide, Dakin s (sodium hypochlorite solution) or acetic acid because they have been shown to be cytotoxic. NS is safe, and it is the preferred method [71]. Deep wounds If a patient has a deep wound that requires wound cleaning and/or irrigation, research has demonstrated that the nurse should use a 35-milliliter syringe [71]. In addition, the irrigation should be injected at a pressure of 4 to 15 pounds per square inch [71]. Eschar Notify the doctor immediately for removal. A pressure ulcer cannot heal appropriately if eschar is present because it prevents new granulation in the wound bed and it is an ideal source of bacterial growth [71]. Dressings The ideal dressing should protect the wound, be biocompatible and provide ideal hydration. According to the CMDT (2008), the recommended guidelines for treating specific pressure ulcers are [56]: Pressure ulcer stages: Stage 1. Polyurethane film. Hydrocolloid wafer. Semipermeable foam. Stage 2. Hydrocolloid wafer. Semipermeable foam dressing. Polyurethane film. Stage 3 and Stage 4. Exudate If there is an abundance of exudate, use a calcium alginate dressing or gauze packing as both have excellent absorptive capabilities. Shallow and clean Use a hydrocolloid wafer, semipermeable foam or a polyurethane. Location Certain locations, such as the ear, make it challenging and tedious for the nurse to apply a dressing properly and efficiently. Ear Apply a thin hydrocolloid dressing, approximately 5x7 centimeters to the wound. Cut the strip, fold it in half lengthways and then cut a fringe along one edge. The cuts should be approximately 0.5 centimeters apart. Apply the uncut edges of the dressing first and then use the cut edges to fold around the edge of the ear for stabilization. If there is any wound exudate, a small piece of alginate dressing should be applied underneath the hydrocolloid strip. Debridement Necrotic tissue is laden with bacteria. Devitalized tissue impairs the ability to fight infection. If the pressure ulcer wound has any eschar or if the wound is a stage 3 or 4, it requires debridement, wound cleansing, dressing application and possible adjunctive therapy to ensure wound healing [87]. Other treatment modalities There are other measures that the nurse should implement to prevent further progression of the pressure ulcer and to facilitate the healing process, including [71]: Avoid the use of incontinent pads or briefs with plastic liners because the plastic holds the moisture next to the skin and promotes the production of heat next to the skin. Avoid massaging over bony prominences to reduce the risk of ulcer formation from excessive friction. 51

52 Treating and managing bacterial colonization and infection within the pressure ulcer [16] Research has demonstrated that the majority of ulcers within stages 2 through 4 are colonized with bacteria. It is also important to prevent and treat any other potential forms of bacteria that may be colonized due to other sources, such as, but not limited to the following: Foley catheters (F/C), urinary tract infections (UTI), sinus and respiratory infections [87]. Research has demonstrated that a bacterium that enters the blood stream or lymphatic system can lodge into compressed tissue, denervated tissue, edematous tissue and/or any established wounds, thus further exacerbating multiple forms of bacteria in the body [87]. If there is any speculation of a bacterial infection within the debrided ulcer or if the epithelization phase is not progressing within two weeks, then it should be biopsied. Any ulcers that have more than 1 x 106 CFU/grams of bacteria following a debridement should be treated with topical antibiotics because research has demonstrated that systemic antibiotics are no longer effective to decrease bacterial levels in granulating wounds [87]. Early lesions should be treated with topical antibiotic powders and adhesive absorbent bandage (Gelfoam). Once clean, they can be treated with a hydrocolloid dressing such as a DuoDerm. Established lesions require surgical debridement, cleaning and dressings [57]. 8. Treatment of punctures. The treatment regimen for punctures is similar to the general recommendations for abrasions and lacerations. It is important to first stop any bleeding, then to clean the wound and apply an antibiotic ointment such as Neosporin or Polysporin. 9. Treatment of skin tears. Due to the delicate nature of the skin, it is imperative that nurses care for skin tears gently and professionally. According to the AACW, the following guidelines should be implemented when caring for a skin tear [4]: Cleaning Clean with NS and pat dry or leave to air dry. The skin should be as closely approximated as possible [19]. If there is a skin flap present on, over or around the skin tear: Cleanse the area gently with NS. Unroll the skin flap and approximate the edges with butterfly/skin tapes. Dressing Cover the skin tear with one of the following nonadherent dressings [19]. Transparent left in place for five to seven days. Hydrogel. Impregnated gauze (Xeroform). Ensure that the skin tear is secured with a gauze wrap or a stockinette to prevent the removal of additional frail skin around the area during dressing changes and avoid disturbing the wound unless exudate lifts the dressing, then use an absorptive dressing. Steri-strips may be useful in holding the wound edges together, especially in a grades 2 or 3 [19]. 10. Treatment of surgical wounds. Depending upon the type of surgery, various dressings may be applicable. However, one of the main treatment modalities is to administer antibiotics prophylactically to reduce the incidence of surgical wound infections, regardless of the type of procedure [90]. The most common side effect is postoperative wound infections, so antibiotics are administered. Antimicrobials On average, approximately 1 million patients develop wound infections after surgery each year, extending a hospital stay by one week while increasing the cost. The American Academy of Family Physicians has classified the risk of infection dependent upon the type of operative wound [90]: Clean wound An elective surgery that is not deemed an emergency surgery. The risk of postoperative infection is less than 2 percent. Clean-contaminated wound An urgent or emergency surgery. The risk of a post-operative infection is less than 10 percent. Contaminated wound A nonpurulent inflammation in which there is a gross spillage from the gastrointestinal tract, a major break in the sterile technique, a penetrating trauma of less than four hours or a chronic open wound that needs to be grafted or covered. The risk of postoperative infection is approximately 20 percent. Dirty wound A purulent inflammation that is typically the result of an abscess or a penetrating trauma greater than four hours old. The risk of postoperative infection is approximately 40 percent. For over a decade, the American Academy of Family Physicians has recommended the following protocol for administering antibiotics to reduce the risk of wound infections [90]: Administer the first dose of antibiotics 30 minutes before the procedure. The particular antibiotic and/or antibiotics chosen are dependent upon the surgical site, the most common organisms isolated in the vicinity of the surgery and the cost of the drug. Staphylococcus is the most common bacteria post-operatively. Therefore, the most commonly administered antibiotic is cefazolin (Ancef, Kefazol). If a patient has an allergy to cephalosporins, vancomycin should be administered at one gram intravenously (IV). Vancomycin should also be administered over cefazolin in hospitals with high rates of methicillin-resistant staphylococcus aureus or staphylococcus epidermis infections [46]. With gastrointestinal surgeries, gram-negative and anaerobic bacteria are isolated, so antibiotics that fight those particular organisms are administered. Cefazolin (Ancef) is the most common antibiotic administered, and it is the drug of choice for head and neck, gastroduodenal, biliary tract, gynecologic and/ or clean procedures [46]. Also administer the antibiotic at one to two half-lives of the drug during the procedure: Cefazolin (Ancef, Kefazol) has a half-life of 1.8 hours. Vancomycin has a half-life of three to nine hours. Aminoglycosides have a half-life of two hours. Metronidazole (Flagyl) has a half-life of eight hours. Postoperative administration is not indicated or recommended. Dressings According to Nursing Times (2003), the most commonly used surgical dressings are simple, low-adherent dressings. The following guidelines should be considered when physicians and nurses are applying the correct dressing after surgery [12]: 52

53 Consider the frequency of the dressing change and whether the patient is able to take a shower daily. If the patient is able to shower, use a shower-proof dressing. Research has demonstrated that dressings should only be changed if there are signs of infection, because the wound will heal better if the dressing is left undisturbed. If the patient has an open surgical wound that is healing by secondary intention, then the appropriate dressing should be based upon the size, depth and position of the wound. 11. Treatment of ulcers. Diabetic foot ulcers The diagnosis of diabetic foot ulcers is made based upon clinical appearance; if the patient exhibits pus or at least two of the following symptoms of infection [38]: Redness. Swelling or induration. Pain or tenderness. According to the research composed in Wounds (2008), it has been almost five years since there have been any alterations or enhancements in the treatment of diabetic foot ulcers [75]. In 2004, the Infectious Disease Society of America (IDSA) developed guidelines for the treatment of diabetic foot ulcers still used [38]: Antimicrobial The most common pathogen identified in diabetic foot ulcers are aerobic gram-positive cocci (staphylococcus aureus). However, if the patient has a chronic diabetic wound or other chronic wounds or if they have recently received antibiotics, they may be infected with gram-negative rods. Failure to treat diabetic foot ulcers adequately and efficiently may lead to further complications, such as osteomyelitis or cellulitis. The severity of the infection, the cause and the patient s co-morbidities should be considered when choosing the appropriate antibiotic. Outpatient mild to moderate cases The most commonly prescribed antibiotics are: Ofloxacin (Floxin), piperacillin-tazobactam (Zosyn), levofloxacin (Levaquin), clindamycin (Cleocin) and linezolid (Zyvox). Moderate to severe cases are typically prescribed parenteral therapy initially. The most challenging aspect of treating diabetic foot ulcers is the concern for osteomyelitis because it increases the risk of surgery, especially amputations; impairs wound healing; and predisposes the patient to further infection. (See Wound complications for further explanation of osteomyelitis). Cleaning The diabetic foot ulcer should be cleaned daily with NS to promote a moist environment. Debridement Once the ulcer is debrided, it is important to reduce the risk of infection, thus reducing the risk of an amputation. Dressings The dressing should be changed frequently, at least every 24 hours, and the ulcer should be checked often for infection because the patient may not be able to recognize it due to peripheral neuropathy. One of the biggest clues to infection is prolonged hyperglycemia. Leg ulcers. Factors that influence healing of leg ulcers include the size of the ulcer, other risk factors and co-morbidities, and the patient s willingness to comply with treatment modalities. An 53 estimated 65 to 70 percent of venous ulcers heal within six months of initiating treatment [47]. Venous If the wound is related to venous insufficiency, it should be managed with strategies to control the venous insufficiency, heal the wound and prevent recurrence. Cleaning The first priority in treating a venous ulcer is cleaning with saline or cleansers such as Saf-Clens [46]. If there is eschar present, the physician or practitioner may utilize a small curette or scissors to remove the yellow fibrin eschar under local anesthesia [56]. Compression stockings The majority of patients with venous leg ulcers benefit from utilization of compression bandages at the level appropriate to their vascular status. If the ulcer is the result of venous insufficiency, the external compression of the ulcer should be between 30 and 40 metric units of mercury (mm) (Hg) at the ankle to prevent capillary transudate [47]. However, the results of the ABI determines the compression therapy as follows [30]: ABI above 1.2 may indicate calcified arteries and should not be compressed. Do not compress until further vascular studies are completed. ABI between full compression. ABI between lower (mild to moderate) compression. ABI lower than 0.5 do not initiate compression, refer to vascular surgeon. Arterial/ischemic Arterial wounds should avoid compression therapy or debridement as it can result in necrosis or amputation [85]. The mainstay of treatment is surgery with revascularization to restore the blood supply to the compromised limbs. In order to improve the blood flow, other medical conditions need to be controlled, such as hyperlipidemia, hypertension and diabetes, and smoking cessation should be encouraged. Debridement One of the major mainstay treatment modalities is to debride the necrotic and fibrinous aspects of the wound to ensure healthy granulated tissue can develop [47]. Dressings Venous ulcers should be covered with one of the following dressings [56]: Occlusive dressing such as a DuoDerm, Hydrasorb or a Cutinova. Polyurethane foam (such as Allevyn). After the dressing is applied, the area is covered with a zinc paste boot that will be changed weekly [56]. Medications The patient may be prescribed metronidazole (Metrogel) to reduce bacterial growth and odor from the venous ulcer [56]. If the patient has any erythemic dermatitis of the skin, a medium-to-highpotency corticosteroid to decrease the inflammation will be prescribed [56]. There is insufficient evidence supporting the use of systemic antibiotics to improve the healing of venous ulcers [15]. But many researchers have speculated that topical antimicrobial cleansers or other formulations such as topical cadexomer iodine may be effective in treating venous ulcers. Further research is required [15]. Other treatments Other treatment guidelines to prevent the exacerbation of venous insufficiency and to prevent the development of other ulcers on the legs are [47]:

54 Elevate the legs above the level of the heart while sleeping. Avoid standing for long periods of time. Wound complications There are a variety of complications that may arise, depending upon the type of wound, injury, co-morbidities and/or lifestyle of the patient. In any acute wound, the biggest complication is infection, including MRSA. If the acute wound was induced by a laceration, abrasion or puncture, other complications may arise when foreign bodies are dislodged, exacerbating a potential infectious process, inflammation or tissue damage. The most common generalized complications that occur with any wound are cellulitis, contact dermatitis, MRSA and osteomyelitis. Cellulitis Cellulitis is an acute skin infection that spreads rapidly and deeply from the dermis to the subcutaneous tissue layers [19]. Soft tissue cellulitis prolongs the inflammatory phase by promoting tissue proteases, which inhibits the ability of granulated tissue formation and delays collagen deposits [81]. Cellulitis may occur after a bite or any wound due to a bacterial or fungal infection, especially Group A streptococcus and staphylococcus aureus [51]. The most common wounds that are prone to cellulitis include [6, 19]: Animal bites. Lacerations. Ulcers. Surgical wounds. If a patient has cellulitis, the offending organism invades the compromised area and overwhelms it with neutrophils, eosinophils, basophils and mast cells that break down the cellular components, leading to inflammation [51]. The patient will typically exhibit erythema, edema, warmth, pain, fever and lymphangitis. Erysipelas is a superficial form of cellulitis that involves the lymphatic system and it is characterized by streaking lines toward regional lymph nodes [19]. The most commonly affected sites include the lower area of the body, although it can occur anywhere [19]. Cellulitis is diagnosed by signs and symptoms that are clinical features, and by cultures. The laboratory data may demonstrate mild leukocytosis and an elevated erythrocyte sedimentation rate (ESR) demonstrating that there is an inflammatory process occurring [19]. Cellulitis is typically treated with oral or IV penicillin (PCN) to treat and eradicate the most common organism staphylococcus and streptococcus (gram-positive bacterias). The health of the patient and the extent of the cellulitis will determine the most effective course of treatment. Antimicrobial therapy. Healthy adults with an uncomplicated case of cellulitis should be prescribed dicloxacillin 500 milligrams by mouth four times a day or a cephalosporin, such as cephalexin 250 to 500 milligrams four times a day for seven to 10 days. If the patient has a PCN allergy, erythromycin (EES) should be prescribed, 250 to 500 milligrams by mouth four times a day. If the patient has any co-morbidities or is a complicated case (fever), he or she should be prescribed ceftriaxone IV for a few days, then an oral dose for seven to 10 days. Other recommendations. The patient should be encouraged to keep the area elevated to promote comfort and to decrease the edema [19]. Throughout the day, the patient should apply warm moist heat or soaks to 54 alleviate the pain and to decrease the edema by increasing the vasodilation process [51]. Contact dermatitis Contact dermatitis, also referred to as irritant dermatitis or nonallergic dermatitis, is a chronic inflammatory reaction that results from a substance coming in contact with the skin [19]. The majority of patients described are at risk of contact dermatitis caused by tape, cleansers, soaps or dressings applied to their skin during their treatment. The most common clinical presentation of contact dermatitis is a pruritic rash with erythema and/or vesicles, erosions or crusting that may form over the area [19]. Contact dermatitis is typically diagnosed based upon the clinical presentation and complaint of pruritis from the patient. If warranted, cultures and potassium hydroxide preparations can assess for infectious or fungal contributing factors [19]. The treatment of contact dermatitis is to remove and/or avoid the irritating, offending agent. Other measures that should be implemented include [19]: Cleaning Clean the area with mild soaps and cleaning creams followed by lubrication of the skin. Medications The patient should be prescribed an antiinflammatory to reduce the inflammatory process and alleviate the itching: Oral glucocorticoid 1 milliliter per kilogram tapered over two weeks. MRSA MRSA is a staphylococcus aureus infection that is resistant to treatment with methicillin and other similar drugs that typically and historically treated staphylococcus infections. MRSA has become prevalent in the community and hospitals nationwide. The IHI s 5 Million Lives campaign for reducing the incidence and prevalence of MRSA in the hospital and community settings stated that in 2005, the CDC composed research that demonstrated the following [42]: There were over 94,000 invasive MRSA infections in the United States population. About 19,000 of the patients died (18 percent) during their initial hospitalization. Approximately 75 percent were uncomplicated bacteremias; others include empyema, endocarditis and osteomyelitis. Most invasive MRSA disease (about 86 percent) occurs in patients who are exposed in hospitals or health care settings, while about 14 percent occurs in persons without recent hospitalization or other established MRSA risk factors. MRSA colonizes in the nares and skin and is spread by lack of hand washing in conjunction with altered immunity that may contribute to other co-morbidities and/or breaks in the skin. Patients at the highest risk of being affected by hospital acquired MRSA include [42]: Patients with other co-morbidities. Patients who reside in a long-term care facility or who have been hospitalized more than 14 days. The Mayo Clinic stated that in 2007, the Association for Professionals in Infection Control and Epidemiology estimated that 46 out of every 1,000 people hospitalized are infected or colonized with MRSA. Patients with invasive catheters, including but not limited to devices for dialysis, central lines, and foley catheters. Patients with recent antibiotic use. MRSA typically presents as a spontaneous appearance of a raised red lesion, surrounding erythema with potential streaks, abscess and/ or purulent drainage with a fever [22, 69]. In order to confirm the diagnosis, cultures are completed immediately if MRSA is suspected. The patient s overall health condition and whether hospitalization is

55 required will determine the treatment plan. If the patient is admitted to the hospital, he or she will typically be prescribed vancomycin. However, in 1997, a new strain of MRSA was discovered that is resistant to vancomycin, also known as vancomycin-resistant enterococcus (VRE) [22]. If the patient is in the community, the CDC recommends the patient be prescribed clindamycin, tetracyclines (doxycycline and minocycline), trimethoprim-sulfamethoxazole (TMP-SMX), rifampin (used only in combination with other agents), and linezolid. [69]. In order to prevent transmission, all health care workers should wash their hands, utilize sterile techniques, keep the patient in isolation and disinfect all materials that come in contact with the patient. Patients should have their own supplies while hospitalized, and they should never be shared. [59]. Osteomyelitis Osteomyelitis is a serious, potentially deadly infection that is difficult to treat and eradicate. Osteomyelitis is the spread of infection to the bone and is prevalent among chronic non-healing wounds. There are a few different types of osteomyelitis [57]: Hematogenous osteomyelitis is a bacteremia that occurs in patients with sickle cell disease, injection drug users and the elderly. The most common source of bacteria is staphylococcus aureus and P. aeruginosa. Osteomyelitis from an infection such as a prosthetic joint replacement, pressure ulcer, surgery and trauma. The most common source of bacteria is staphylococcus aureus or staphylococcus epidermis. Osteomyelitis associated with vascular insufficiency occurs in patients with DM and vascular insufficiency, especially in the foot and ankle. Patients are at risk of developing osteomyelitis if they have any of the following risk factors [82]: Bacteremia. Peripheral vascular disease (PVD). DM. Trauma. Surgery. Ulcers (pressure, diabetic, arterial/venous leg). The most common symptoms exhibited with osteomyelitis are sudden pain and swelling in one joint, fever or an associated ulcer or skin lesion with possible drainage [82]. According to the National Clearinghouse Guidelines, osteomyelitis should be suspected in a chronic wound if any of the following symptoms are exhibited [62]: Bone exposed (or easily probed). Tissue necrosis overlying bone. Gangrene. Persistent sinus tract. Underlying open fracture. Underlying internal fixation. Wound recurrence. If a patient has a diabetic foot ulcer, osteomyelitis should be considered if the patient has any of the following signs or symptoms [76]: Deep or extensive ulcer, especially one that is chronic or over a bony prominence. An ulcer that does not heal after at least six weeks of appropriate care. Bone that is visible or can be palpated with a metal probe. A swollen foot with a history of foot ulceration. A red, swollen toe. 55 An unexplained high WBC or other inflammatory markers such as CRP or ESR. X-rays showing bone destruction beneath an ulcer. X-rays and/ or MRIs confirm the diagnosis of osteomyelitis. If radiographic findings suggest osteomyelitis, a histologic evaluation and bone biopsy culture may be considered. The treatment of osteomyelitis includes surgery to remove the infection in the bone, debridement and prolonged systemic antibiotic therapy [38, 57]. Antibiotics usually are administered over a course of four to six weeks depending on the source of bacteria, extent of bone infection and any co-morbidities. The most common antibiotics to treat osteomyelitis are the following [82]: Quinolones (ciprofloaxin 750 milligrams twice a day). Quinolone combined with rifampin 300 milligrams twice daily orally if the bacteria source is staphylococcus aureus. Prevention of wounds Nurses can potentially reduce the incidence of illness through educating patients and their families about various dangers from their residence, occupation and hobbies. Depending on the social history of the individual; the patient should be told [30, 35]: To prevent abrasions, cuts, scrapes, lacerations and/or punctures: Avoid risky behaviors that can potentially end in a dangerous situation. Be careful with sharp objects, such as knives, scissors, saws and trimmers. Always carry knives, scissors and or any sharp object pointed downward. Avoid keeping sharp objects in areas in which children could access them. Always wear shoes to avoid stepping on something that may cause injury. Promote the use of helmets and knee pads when riding a bicycle, three/four wheelers, rollerblades and a motorcycle. The patient should be encouraged to wear the appropriate size helmet. Avoid picking up any broken glass or razor blades with bare hands. Children should always be in safe, size-appropriate car seats facing the right location and direction. According to the American Academy of Pediatrics, the following guidelines should be followed related to car safety [2]: Infants should be rear facing until they are 1 year of age and weigh at least 20 pounds. Toddlers should ride forward facing if they are at least 20 pounds. School-age children should be in a booster seat if they have outgrown their forward-facing car seats. Children should stay in a booster seat until the adult seat belts fit correctly (usually when a child reaches about 4 foot, 9 inches in height and is between 8 and 12 years of age). Older children who have outgrown their booster seats should ride in a lap and shoulder belt; they should ride in the back seat until 13 years of age. Bites It is important to teach parents with children common safe practices around animals and recommendations if they are bitten [19, 27]: The best preventive method is to avoid aggressive behavior with animals and to avoid unfamiliar animals. Teach young children to avoid provoking animals because it may lead to fewer incidents of animal bites.

56 Never leave children unattended in the presence of animals to potentially prevent attacks. Vaccinate all household animals for rabies. In the United States, it is mandatory for all domestic dogs and cats to be vaccinated against rabies [19]. If bitten, people should seek medical care immediately. Research has demonstrated that if the patient delays medical care for more than 24 hours, he or she is more likely to develop an infection [27]. In addition, patients who require sutures should seek care within six hours of the injury to prevent colonization of bacteria in the wound. Burns In order to prevent burns, the patient should be educated to [19]: Turn off all electrical currents before attempting any repairs. Keep protective covers in the outlets, especially with children in the home. Repair frayed electrical wires immediately. Lower the water temperature in the home. Avoid loose clothing when cooking. Keep children away from the burners and place all pans on the back burner with the handle turned away from the front of the stove. Pressure ulcers It cannot be stressed enough that pressure ulcers can be prevented. It is important for nurses to prevent pressure ulcers through good nursing care, good nutrition, and maintaining proper hygiene [57]: Keep the skin and the bed linens clean and dry at all times. Any patient who is immobile, bedfast, paralyzed, listless or incontinent should be turned frequently, at least hourly. Each time the patient is turned, his or her skin should be reassessed to ensure that there is no erythema or tenderness in any areas of the skin. Keep a written log to ensure accountability of the staff to turn the patient every hour. Use appropriate mattresses, pillows and pads to prevent patients at risk from developing pressure ulcers. Notify the doctor immediately if any breakdown occurs on the skin. Skin tears Nurses and nursing assistants hold the biggest key in preventing skin tears among the geriatric population when they care for them in a facility or at their home. In order to prevent skin tears, the following recommendations should be implemented, according to the National Guideline Clearinghouse (2008) [63]: Provide a safe environment. Encourage patients to wear long sleeves or pants to protect their extremities. Ensure the room has adequate light to reduce the risk of bumping into furniture or equipment and have the call light within reach. Educate staff or family caregivers in the correct way of handling patients to prevent skin tears. Maintain nutrition and hydration by offering fluids between meals, and use lotion on arms and legs twice a day. Protect from self-injury or injury during routine care by: Using a lift sheet to move and turn patients and to enforce transfer techniques that prevent friction or shear. Pad bedrails, wheelchair arms and leg supports. Support dangling arms and legs with pillows or blankets. Use non-adherent dressings on frail skin. Use gauze wraps, stockinettes or other wraps to secure dressings rather than tape. Use emollient antibacterial soap when cleaning the patient, and avoid any harsh chemicals that will exacerbate the effect on the elderly patient. Ulcers Diabetic foot ulcers According to the American Academy of Family Physicians (2005), patients can minimize their risk of developing a diabetic foot ulcer by [38]: Maintaining adequate blood glucose control by adhering to their diet, exercise regimen and taking any prescribed medications. In addition, patients should be instructed to see their PCP every three months or as recommended by their PCP. Performing daily self-inspections of the feet and reporting any changes to their health care professional. Leg ulcers. Venous ulcers Compression stockings are required to reduce the edema, thus preventing the development of pressure ulcers. Legal issues revolving around chronic wound care Unfortunately, we live in a society that thrives on finding errors by health care professionals to be medical malpractice. One of the most common lawsuits is related to chronic wounds, such as pressure ulcers, foot ulcers and leg ulcers. According to Medical News Today (2006) [58]: More than 17,000 lawsuits are related to pressure ulcers annually, the second-most common claim after wrongful death and more than those for falls or emotional distress. Individual settlements range from under $50,000 to as much as $4 million for each case. However, in 28 out of 30 plaintiff verdict settlements in pressure ulcer lawsuits, the average compensation was just less than $1 million. It is imperative that nurses recognize the risk factors and symptoms for wounds to ensure appropriate prevention and treatment modalities are initiated. They also must understand the importance of effective communication to ensure that their colleagues know the importance of turning a patient at least every two hours. Although it is the duty of the physician to order various diagnostic tests to potentially confirm a diagnosis rather than speculate, the nurse is held just as accountable to ensure the patient is safe at all times. Nurses have enormous responsibilities and expectations bestowed upon them every time they enter a facility and accept the responsibility of care. In order for a nurse to prevent litigation and potential harm to a patient, it is imperative that each nurse be familiar with the policies, procedures and laws that guide their practice. Nurses can take action by adhering to the following recommendations: Obtain a copy of your nurse practice act for the state or states in which you practice. Understand and review the policies and procedures at the facility to ensure compliance. Understand and review the standing protocols and/or preventive protocols at the facility in which you are employed to ensure that you are abiding by the protocols. Organizations As professionals, it is important to be involved in organizations that support the profession of nursing and to be affiliated with organizations based upon your areas of expertise. Nurses who work in areas in which they are responsible for caring for patients with wounds would benefit from becoming certified in wound care to 56

57 enhance their credibility and to ensure that the nurse is continuously receiving the latest guidelines and research. Due to the ever-changing medical field and the vast array of wounds that may be presented, being certified and affiliated with organizations will be beneficial to the nurse, the profession and the patients that we serve. Here are some organizations that are available for nurses to join [70]: American Academy of Wound Management (AAWM) is a national, voluntary, nonprofit, multidisciplinary certifying board for health care professionals involved in wound care. The purpose of AAWM is to establish and administer a certification process to elevate the standard of care across the continuum of wound management. The academy is dedicated to an interdisciplinary approach in promoting prevention, care, and treatment of acute and chronic wounds. The American College of Certified Wound Specialists (ACCWS) is a membership organization that serves as an educational resource. Wound, Ostomy and Continence Nursing Certification Board (WOCNCB) is the only organization that offers wound care certification exclusively to nurses. The goal of the WOCNCB is to set, maintain and evaluate national standards for certification and re-certification in wound, ostomy and continence nursing care. National Alliance of Wound Care (NAWC) is a nonprofit, national multidisciplinary wound-care certification board and a wound-care professional membership organization. The goal of the NAWC is dedicated to the advancement and promotion of wound care through the certification of wound-care practitioners in the United States. Closing Wound care remains a complex concept to grasp and understand because there are so many different types of wounds and treatment modalities. Nurses do not have control of the lifestyle choices that people make to put them at risk for acute wounds. However, we can control and prevent perineal skin breakdown, skin tears and pressure ulcers for any patient under our care or whom we are discharging home with a caregiver. It is imperative that nurses remain knowledgeable and attuned to evidence-based practice guidelines while caring for all patients to ensure that the care provided is efficient in preventing and managing any particular wound. There are many organizations researching and providing evidence-based practice guidelines and protocols; nurses need to ensure that they are adhering to guidelines of the facility where they are employed and credible sources alluded to throughout this continuing education. Table 1 Progression of decubitus ulcers [59] 68] Table 2 Diabetic foot ulcer Typical diabetic foot ulcer caused by high plantar pressures at the second metatarsal head. [34] Table 3 Venous ulcers [85] Table 4 Arterial ulcers 57 [85]

58 Table 5 CDC Tetanus schedule Vaccination history Unknown or less than 3 doses 3 or more doses and less than 5 years since last dose 3 or more doses and 6-10 years since last dose 3 or more doses and more than 10 years since last dose [21] Clean, minor wounds Td or Tdap (Tdap preferred for ages 11-18) Td or Tdap (Tdap preferred for ages 11-18) Table 6 Vacuum assisted closure mechanism All other wounds Td or Tdap (Tdap preferred for ages 11-18) Plus tetanus immune globulin (TIG) Td or Tdap (Tdap preferred for ages 11-18) Td or Tdap (Tdap preferred for ages 11-18) Figure 4: Principles of action of the VAC therapy device (with permission of KCI Europe). [31] Works Cited: 1. American Academy of Orthopaedic Surgeons. (2005). Most common ER visits. Retrieved online May 9, 2008 at percent20er%20visits.pdf 2. American Academy of Pediatrics (2008). Car seat safety: A guide for parents. Retrieved online June 3, 2008 at 3. American Burn Association (2000). Scald injury prevention: Educator s guide. Retrieved online April 20, 2008 at 4. Association for the Assessment of Wound Care (2006). The ABC s of skin and wound care. A guide for health care providers on the treatment of minor wounds. Retrieved online May 26, 2008 at aawconline.org/pdf/abc%20professional.pdf 5. Atlas of Pathophysiology: Anatomical Chart Company. (2002). Springhouse: Pennsylvania. 6. August, J. (2008). Dog and cat bites. Zoonosis Updates Initially published in December 1988, reviewed in 1995 and JAVMA. Retrieved online May 23, 2008 at zndogcat.asp 7. Ayello, Elizabeth (2007). Predicting pressure ulcer risk. Best practices in nursing care to older adults. Hartford Institute for Geriatric Nursing. Retrieved online May 26, 2008 at publications/trythis/issue05.pdf 8. Baharestani, M. & Leon, J. (2008). A practical guide for managing pressure ulcers with negative pressure wound therapy utilizing vacuum-assisted closure-understanding the treatment algorithm. Advances in Skin and Wound Care (21) 1, Baranoski, S. (2003). How to prevent and manage skin tears. Advances in Skin and Wound Care. Sept/ October Retrieved online May 25, 2008 at ai_n Bates (2001). Bates Jensen Wound Assessment Tool. Retrieved online June 1, 2008 at geronet.med.ucla.edu/centers/borun/modules/pressure_ulcer_prevention/pub WAT.pdf 11. Barclay, L. (2007). Consensus Statement Describes Dressings for Acute and Chronic Wound Management.Retrieved online June 1, 2008 at Baxter, H. (2003). Management of surgical wounds. Nursing Times (99), 13. Retrieved online May 30, 2008 at Beers, M., Porter, R., Jones, T., Kaplan, J., & Berwitz, M. (2006). The merck manual of diagnosis and treatment. Merck: NJ 14. BMJ (no year). Quantifying disease in populations. Retrieved online May 29, 2008 at htttp: com/epidem/epid.2.html 15. Bolton, L.(2008). Evidence corner: Safety and efficacy of wound cleansers. Wounds. Retrieved online May 9, 2008 at Braden, B., Maklebust, J. (2005). Preventing pressure ulcers with the Braden Scale. Wound Wise. American Journal of Nursing (105); 6; Braden Scale Risk (1988). Retrieved online May 25, 2008 at educationalstrategies/braden_scale_for_predicting_pres.htm 18. Brancato, J. (August 2004). Minor wound preparation and irrigation. Retrieved online June 1, 2008 at Buttaro, T. et al (2008). Primary Care: A collaborative practice. Mosby: St. Louis Buttaravoli & Stair (no year). Common simple emergencies: Bites. Retrieved online June 1, 2008 at CDC. (2005). Disaster Safety: Tetanus Prevention. Retrieved online May 9, 2008 at disasters/hurricanes/katrina/tetanus.asp 22. CDC. (March 2006). Strategies for Clinical Management of MRSA in the Community: Summary of an Experts Meeting Convened by the Centers for Disease Control and Prevention. Retrieved online June 1, 2008 at Cleveland Clinic (2008). Wound Dressings and other Accessory Products. Retrieved online May 9, 2008 at htttp: 24. DermNet. (2005). Synthetic wound dressings. Retrieved online May 25, 2008 at org/procedures/dressings.htm 25. Dicloxacillin. Retrieved online May 23, 2008 at Dictionary. Surgical wound. Retrieved May 8, 2008 at surgical+wound 27. Doud-Galli, S. K. (2006). Animal Bites. Retrieved online May 23, 2008 at ent/topic275.htm 28. Dunphy, L.M., Winland-Brown, J. E., Porter, B.O. & Thomas, D. J. (2007). Primary care: The art and science of advanced practice nursing. (2nd ed). F.A. Davis: Philadelphia. 29. emedicine Health (2005). Punctures. Retrieved online June 2, 2008 at puncture_wound/article_em.htm 30. emedicine Health (2005). Wound care. Retrieved online April 16, 2008 at com/script/main/art.asp?articlekey=58770&pf=3&page=1 31. European Pressure Ulcer Advisory Panel (no year). Retrieved online May 8, 2008 at google.com/imgres?imgurl= Fleck, C. (2003). Alternative and adjunctive therapies in wound management. ECPN (85) 1, Retrieved online May 20, 2008 at Fletcher, J (May 2007). Dressings: Cutting and application guide. World Wide Wounds. Retrieved online May 29, 2008 at Frykberg, R.G. (2002). Diabetic foot ulcers: Pathogenesis and management. American Family Physician. Retrieved online May 20, 2008 at afp/ /1655_f1.jpg&imgrefurl= 0&hl=en&start=3&um=1&tbnid=H0e2aUH8RxCuwM:&tbnh=95&tbnw=116&prev=/images%3Fq%3DDiab etic%2bfoot%2bulcer%2b%252b%2bpicture%26um%3d1%26hl%3den 35. Gale Encylcopedia of Medicine (2006). Wounds. Retrieved online May 29, 2008 at healthatoz.com/healthatoz/atoz/common/standard/transform.jsp?requesturi= 36. Goldman, R., Rosen, M., Brewley, B., & Golden, M. (2004). Advances in Skin and Wound Care. Retrieved online June 1, 2008 at Hampton,, S. (2005). Vacuum therapy. JCN (19); 3. Retrieved online May 20, 2008 at co.uk/journal.asp?monthnum=03&yearnum=2005&type=backissue&art 38. Hellekson, K. (2005). Practice Guidelines: ISDA release guidelines on the diagnosis and treatment of diabetic foot inspections. (April 2005). Retrieved online May 29, 2008 at AFPprinter/ /practice.html?print=yes 39. Houwing, R., Wilvan der Zwet, Sweder van Asbeck, Halfens, R., Wilem, J. (2008). An unexpected detrimental effect on the incidence of heel pressure ulcers after local 5% DMSO cream application: A randomized, double blind study in patients at risk for pressure ulcers. Wounds 20:4, Retrieved online May 9, 2008 at Hurd, T (2003). Nutrition wound care prevention and treatment. Wound Care Canada (2), 2, Ignatavicius, D., & Workman, M. L. (2006). Medical Surgical Nursing: Critical Thinking for Collaborative Care. (5th ed). Elsevier: St. Louis 42. Institute for Health care Improvement (2008). Getting Started Kit: Reduce Methicillin Resistant Staphylococcus aureus (MRSA) Infection. How to Guide. Retrieved online June 2, 2008 at Institute for Health care Improvement (2008). Pressure ulcer: How to guide. Retrieved online April 17, 2008 at Joint Commission (2008). National patient safety goals. Facts about the 2008 National Patient Safety Goals. Retrieved online May 26, 2008 at NationalPatientSafetyGoals/08_npsg_facts.htm 45. Jeske, H. (2007). Maggot debridement therapy. American Academy of Orthotists and Prosthetists. Retrieved online June 1, 2008 at Katzung, B.G. (2007). Basic and clinical pharmacology. 10th edition. McGraw: New York. 47. Khachemoune, A. & Kaufmann, C.L. (2002). Management of leg ulcers. The Internet Journal of Dermatology; 1:2. Retrieved online May 9, 2008 at Printer=true&xmlFile Path=journals/ijd/vol1n2/u 48. Kuehn, B. M (2007). Chronic wound care guidelines issued. Journal of American Medical Association. Vol 297. No9 (March 7, 2007). Retrieved online April 16, 2008 at full/297/9/938 *Permissions Requests: Lemone, P., & Burke, K. (2004). Medical Surgical Nursing: Critical Thinking for Client Care. (3rd ed). Pearson: New Jersey. 50. Lippincott. (2006). Manual of nursing practice. 8th ed. Wolters: Philadelphia. 51. Lippincott, Williams & Witkins (2007). Professional Guide to Pathophysiology. 2nd ed Wolters: Philadelphia. 52. Mayo Clinic (2008). MRSA. Retrieved online June 1, 2008 at DS00735/DSECTION=8 53. McCance, K. L., & Huether, S.J.(1994). Pathophysiology: The biologic basis for disease in adults and children (2nd ed). St Louis: Mosby. 54. McKinley Health Center. (2008). Wound care guidelines. Retrieved online May 9, 2008 at www. mckinley.uiuc.edu/handouts/pdfs/woundcare.pdf 55. McNamara, R. (2007). Bites, human. Retrieved online June 2, 2008 at EMERG/topic61.htm 56. McPhee, S.J., Papadakis, M. A. & Tierney, L.M (2008). Current medical diagnosis and treatment (47h ed). New York: McGraw-Hill. 57. McPhee, S.J., Papadakis, M. A. & Tierney, L.M (2007). Current medical diagnosis and treatment (46th ed). New York: McGraw-Hill. 58. Medical News Today (2006). Clinical Trial Shows 96% Improvement In Pressure Ulcer Healing Among Nursing Home Residents. Retrieved online June 1, 2008 at php 59. Medline Plus. (2007). Progression of decubitus ulcers. Retrieved online May 8, 2008 at nih.gov/medlineplus/ency/imagepages/19092.htm 60. MedMarket Diligence, LLC. (June 2008). Wound types and advanced wound products worldwide. Retrieved online June 3, 2008 at Mosquera, D.(2002). Chronic venous insufficiency and leg ulceration. Retrieved online May 8, 2008 at National Guideline Clearinghouse. (2008). Chronic wounds of the lower extremity. Retrieved online June 3, 2008 at National Guideline Clearinghouse (2008). Preventing pressure ulcers and skin tears. Retrieved online June 2, 2008 at National Pressure Ulcer Advisory Panel (2008). Home page. Retrieved online April 16, 2008 at