Comprehensive case study NUR 7202



Comprehensive Case Study NUR 7202Ashley PeczkowskiWright State UniversityNUR 7202Comprehensive case study NUR 7202Comprehensive Case StudyPatient InformationName: A. H., Age: 37, Race: Caucasian, Gender: MaleSource and ReliabilityChart review. Accuracy unknown. Chief ComplaintA 96% total surface body area (TSBA) burn patient with increased tachycardia, hyperthermia, and refractory hypotension. History of Present Illness Mr. Hill is a 37 year old male firefighter who entered a neighbor’s burning house while off duty and developed a flash burn with third degree burns on 96% TSBA. This patient has been treated with multiple skin grafts. On day 14 the patient developed increased tachycardia, hyperthermia, renal failure, acidosis, and hypotension refractory to intravenous fluid (IV) boluses. Past Medical History Childhood illness. UnknownImmunizations. DTAP 8/25/13Adult illness. UnknownPast Surgical HistoryTonsillectomy as a child. Right above the knee amputation (BKA) as a childFamily HistoryMother- HTN, smoker, COPD, alive; Father- smoker, MI, deceased; Brother- HTN, alive; Sister- negative history, alive; Maternal Aunt- HTN, CVA, aliveSocial History Birthplace and residence: Arlington, Kentucky. Education: High school and minimal college education. Relationship: Married for six years. Sexual History: Unknown.Family: Two children both boys age 4 and 7. Tobacco use: Current smoker one pack day for 19 years. Alcohol use: Six pack a day drinker for three years.Drugs: No illicit drug use. Work: Works as a lieutenant firefighter for ten years. Home MedicationsNoneAllergiesNo known allergies (NKA)Review of Systems General Health. Unable to assess secondary to mechanical ventilation, sedation, and minimally responsive state. Skin. Unable to assess secondary to mechanical ventilation and sedation.HEENT. Unable to assess secondary to mechanical ventilation and sedation. Neck.Unable to assess secondary to mechanical ventilation and sedation. Respiratory.Unable to assess secondary to mechanical ventilation and sedation. Cardiac.Unable to assess secondary to mechanical ventilation and sedation. Gastrointestinal. Unable to assess secondary to mechanical ventilation and sedation. Genitourinary.Unable to assess secondary to mechanical ventilation and sedation. Musculoskeletal. Unable to assess secondary to mechanical ventilation and sedation. History of right BKA from traumatic injury seven years ago. Neurological. Unable to assess secondary to mechanical ventilation and sedation. Physical Exam Vital signs.Temp: 101.8 rectal, HR: 132, BP: 152/76, O2: 96% on Ventilator AC mode Peep 10, TV 400ml, MV 4.4L, FiO2 60%, RR: 14. General.Young white male with deep second to third degree burns to all areas of the body except his right BKA stump and left foot. Well nourished. Skin. Second to third degree burns to the entire body except with BKA stump and left foot and partial ankle. Necrotic areas to nose, left neck, penis, scrotum, and left toes. Skin grafts to all parts of burnt body. Doppler pedal pulses bilaterally. Radial pulses 1+ bilaterally. Carotid pulses 2+ bilaterally. Fasciotomies to bilateral legs, bilateral arms, and chest box escharotomy. Dressing covering entire body and face. HEENT. Head: Normocephalic. Third degree burn to head, face, and neck. Necrotic area to left neck. Eyes: Eyelids sown shut to prevent damage and drying. Ears: Third degree burn to bilateral ears. Patient able to minimally turn head to strong voice stimuli when paralyzing agent are stopped. Nose: Third degree burn to nares. Throat: moist oral mucosa, no gag reflex, teeth present, inhalation injury present. Neck.Extensive third degree burns with necrotic area to left neck. Carotid pulses bilateral. Unable to assess for lymphadenopathy due to extensive inflammatory response and burn. No masses. Minimal ROM with greater movement to the left about one to two inches when paralyzing and sedating agents are held. Right subclavian triple lumen. Midline tracheostomy.Respiratory. Course rhonchi throughout all lung fields. Use of abdominal accessory muscles when not paralyzed. Cardiac. Sinus tachycardia on monitor, S1, S2, PMI at 6th intercostal space, 4cm lateral to midclavicular line. No heaves or thrills. Pulses: Carotid: R-2+, L-2+, Brachial: R-2+, L-2+, Radial: R-1+, L-1+, Femoral: R-2+, L-2+, DP: R- Doppler, L- Doppler, PT: R- Doppler, L- Doppler. Gastrointestinal. Third degree burn to abdomen with escharotomy. Hypoactive bowel sounds in all four quadrants. Deep partial second degree burns to buttocks. Allograft skin grafts to all areas. Duo-tube with trickle feedings. No bruits, or masses felt. Unable to palpate liver, spleen, or kidneys. Genitourinary. Foley in place. Third degree burns to genitourinary. Necrotic areas to penis and scrotum. Rectal tube in place with liquid stool negative for C-Diff. Allograft skin grafts to buttocks and groin area. Musculoskeletal. No spontaneous movement in bilateral arms and legs. Able to move head to right one inch and left one to two inches when paralyzing and sedating agent are held. Able to blink to command however not consistent when awake. Arms and legs stiffened straight. Neurological. Unable to assess cranial nerves II-XII. Follows occasional commands to blink on command when awake. Extremities. Third degree burns to bilateral arms and legs except for right BKA stump and left foot and partial ankle. Allograft skin grafts to all extremities. Necrotic toes to left foot with absent capillary refill. Fasciotomies to bilateral arms and legs. Arm and leg stiffness noted. Data. Laboratory Findings. Blood work.ChemistryCurrent resultNormal RangePh7.217.35-7.45PaCo24538-42mmHgPaO212375-100mmHgHCO33522-28mEq/LBase excess -2.2-2-+2 mEq/LSaO292%90-100%Lactate4.10.5-2.2mmol/LAlbumin2.13.4-5.4g/dLAlkaline phosphatase3344-147IU/LALT108-37 IU/LAST2510-34 IU/LSodium140135-145mEq/LPotassium5.23.5-5 mEq/LCo23520-29 mmol/LBUN207-20 mg/dLCreatinine1.30.8-1.4 mg/dLGlucose10270-100 mg/dLCalcium7.98.5-10.9 mg/dLMagnesium1.91.7-2.2mg/dLPhosphorus 2.22.4-4.1 mg/dLChloride 11196-106 mmol/LWBC263.5-10.5 billion/LHGB8.113.5-17.5 gram/LHCT24%38.8-50.0%PLT32150-450 billion/LPTT4525-35 secsINR1.60.8-1.2Cultures.Central line 9/28: No growth after 48 hours. Arterial line 9/28: No growth after 48 hours. Peripheral 9/28: No growth after 48 hours. Foley 9/28: No growth after 48 hours. Acid fast culture plus stain 9/28: tissue- left thigh: No acid fast bacilli. Mycobacteria seen at two weeks. BAL 9/21: Normal respiratory flora Acinetobacter baumannii <1,000 cfu/ml.Fungus Culture 9/17: Mold Mucor Species. Tissue culture 9/17: Mucor and FusariumChest X-ray 9/28.Impression: Diffused patchy infiltrates constant with ARDS. Bilateral pleural effusions with the right greater than the left. DVT prophylaxis. Titratable heparin drip for right leg and arm DVT. Frequently stopped due to gastrointestinal bleeding developments. Antibiotics. Cefepime 2g Q8 hours, Vancomycin 1 gram Q24 hours, Amphotericin B 5mg/kg Q8 hours, Merrem 1gm Q8 hours, and topical amphotericin. Differential Diagnosis The most likely differential diagnosis for this patient is fungemia and bacterial sepsis. Fungal infections are a common source of infection in burn patients and can lead to fungemia sepsis. This in combination with positive blood cultures for fungi makes fungemia the most likely diagnosis. The differential diagnosis for fungemia is a bacterial infection, the second most likely differential, since most burn patients present with systemic inflammatory response syndrome (SIRS) often characteristic of a bacterial infection (Capoor, Sarabahi, Tiwari, & Narayanan, 2010). Fungemia.Fungemia caused by a burn wound infection require advantageous risk factors such as a “age of burns, total burn size, body surface area (BSA) (30–60%), full thickness burns, inhalational injury, prolonged hospital stay, late surgical excision, open dressing, artificial dermis, central venous catheters, antibiotics, steroid treatment, long-term artificial ventilation, fungal wound colonization (FWC), hyperglycemic episodes and other immunosuppressive disorders” (Capoor et al., 2010, p. 1).There is often a delay in diagnosis of many fungal infections in burn patients because of the similar presentation to that of bacterial infections and because blood cultures have poor sensitivity of up to only 50%. The importance of diagnosis and treatment in this sub group is extremely important because of the high mortality rate, resistant fungi, and unusual yeasts and molds with few effective antifungals (Capoor et al., 2010). Even with effective antifungal treatment, the mortality rate for fungemia is greater than 30-80% of all patients (Unsinger et al., 2012). The risk of fungal infections increases drastically the longer the open wound is present. Those who are considered severely burned may benefit from rapid wound closer products, topical antifungals with mold cessation, and susceptible antifungal IV therapy. Fungal infection reported documentation varies tremendously from 6.3 to 44%. Studies have shown that on average 42% of burn patients are colonized while only 10% develop FWI. The mortality rate for fungal infection ranges from 21.6% to 76%. Fungal infections in burn patients with a TBSA of 30-60% are considered an independent risk factor for mortality; other variables play a larger impact on either side of this curve. It is for this reason burn size should be estimated on admission using the recommended Lund-Browder chart (Capoor et al., 2010). Fungaemia should be suspected in patients with physical findings of separated eschar, partial thickness burn which then convert to full thickness, tissue necrosis, and worsening burn with cellulitis or necrotizing fasciitis. The biggest indication for fungemia is a fever in patient with risk factors who continue to deteriorate despite treatment of broad spectrum antibiotics for greater than 7 to 15 days (Capoor et al., 2010). Commonly burned patients will develop a bacterial sepsis first that will allow opportunistic infections such as fungi to develop. The third most common cause of infection in the bloodstream and the most common secondary infection in a septic patient is the proliferation of Candida albicans (Unsinger et al., 2012). Treatment for fungal wound infection (FWI) or fungemia is initially started with amphotericin B or caspofungin until identification of fungi is made; at which time therapy can usually be lowered to voriconazole, itraconazole, or fluconazole depending of fungi susceptibility. Candida albicans is the most commonly seen fungal infection because, this is a normal flora seen on healthy individuals that reside in the mucosa and gastrointestinal tract. Once the patient becomes immunocompromised then saprophytic colonization overgrowth attacks the mucosa and internal organs (Capoor et al., 2010; Unsinger et al., 2012). Candida fungi can be treated with amphotericin B, voriconazole, and caspofungin; newer antimycotics echinocandins and traizoles; and in renal dysfunction liposomal amphotericin or caspofungin. It is important to note that a new sub-species of Candida have emerged with an azole resistance. Aspergillus fungi can be treated with amphotericin B alone or in with voriconazole, or caspofungin (Capoor et al., 2010). Aspergillus and mold were shown to have the highest mortality rate while Candida had the lowest mortality rate (Branski et al., 2009). Zygomycetes or fusarial fungi are treated with amphotericin B (Capoor et al., 2010). According to the Ohio Board of Nursing (2013) the acute care nurse practitioner may prescribe any antifungal via oral route and with a physician consult or initiated via intravenous route. While IV treatment with antifungals for fungemia is given topical treatment must also be initiated to suppress topical wound growth and prevent further development of new fungemia. Recommendations for combination of nystatin and mafenide acetate saturated dressings were given. The next step in treatment is surgical debridement with early wound coverage with either allografts (preferred) or xenografts. Skin grafts are recommended only after the patient has had negative culture swabs and skin biopsies without development of fungemia. This process may be unachievable in severely burned patients in which fungi become angioinvasive and proteolytic. In this case, surgery is still recommended to improve survival rate (Capoor et al., 2010). Newer forms of supportive treatment being study include the use of interleukin-7 as a means to restore immunity and decrease mortality. This interleukin does not induce a cytokine inflammatory response and has been shown in other studies against bacterial and viral infections to increase proliferation of na?ve and memory T-cells (lymphocytes). The overall goal is to reverse sepsis-induced loss of the hypersensitivity response, prevent cell death, and improve overall cell function thus improving survival from fungemia (Unsinger et al., 2012).There are few research studies in the area of fungemia and minor research currently underway in fungal infections. More research is needed in these areas as more patients are able to live longer with more open, complicated wounds or immunocompromised. Understanding exact treatment and knowledge of fungi function will help improve treatment. Improved treatment is essential in light of few antifungal therapy and new fungal resistance development. Bacterial Sepsis. Bacterial sepsis is the leading cause of death in ICU patients. Sepsis can develop from any number of bacterial infections such as cellulitis, urinary tract infections, wound infection, and many other causes. The development of sepsis is a very complex and multi-faceted event characterized by an early hyperinflammatory phase which leads to immunosuppression and thus the inability to fight the present infection while also allowing for other opportunist infections to occur (Unsinger et al., 2012). Sepsis is the tenth leading cause of death and accounts for over 40% of all ICU admissions with a mortality rate of 10% (Stern, Cifu, & Altkorn, 2010). The stages of sepsis include SIRS, sepsis, severe sepsis, and septic shock. SIRS is characterized by fever, tachycardia, tachypnea, and abnormal white blood count. Sepsis follows with a characteristic of signs of SIRS with a documented or suspected infection (Edwards, 2012). Sepsis by definition is having infection and two or more: temperature greater than 38.5 degrees Celsius or less than 35.0 degree Celsius, pulse greater than 90 beats per minute, respirations greater than 20 per minute or PaO2 less than 32mmHg, and a white blood count greater than 12,000 or less than 4,000 or greater than 10% bands. Sepsis has a 16% mortality rate (Stern et al., 2010). Thirdly, severe sepsis is characterized by defined sepsis plus a minimum of one major organ dysfunction caused by sepsis. The most common organ failure seen in severe sepsis is renal failure which many times present as oliguria (Edwards, 2012). Severe sepsis by definition is the septic criteria and at least on sign of altered tissue perfusion such as altered mental status, oliguria, lactic acidosis, platelet count less than 100,000 and AIL/ARDS. Severe sepsis has the mortality rate of 20% (Stern et al., 2010). Finally septic shock characterized by all of the above plus impaired oxygen delivery, commonly also presenting with hypotension that is refractory to IV fluids (Edwards, 2012). By definition septic shock is the previous severe sepsis with a blood pressure less than 60 mmHg or less than 80 mmHg for a patient with history of hypertension even after fluid resuscitation or the need for vasopressors. Septic shock has the highest mortality rate of 46% (Stern et al., 2010).The actual pathology involved in developing sepsis and progressing to septic shock is still not fully understood. What is known is that pathogens release pathogen associated molecular patterns, like those of lipopolysaccharides, which then cause damage to the tissue. This damage results in release of the cells endogenous molecular trigger called damage-associated molecular patterns. These patterns are recognized by the body’s immune system such as lymphocytes that then trigger the inflammatory cascade. This system is a normal response to any infection. What makes sepsis different are the derangements in the immunity response where the T-cells active sub-sets leading to immune paralysis or unregulated inflammatory response. Cytokines and leukocyte activation results in endothelial damage and activation the clotting cascade. Microemboli then form and dislodge in the periphery blocking circulation the therefore altering the tissue perfusion ratio. Once the tissue is prevented from oxygenating, lactic acid production results until cellular death ensues. This causes further cytokines and leukocyte activation release thus increasing the clotting and inflammatory cascade. The ultimate result of the cellular death causes further oxygen tissue impairment, organ dysfunction, and death (Edwards, 2012). Diagnostic TestsDiagnostic tests for fungal infection vary widely with different degrees of sensitivity and specificity (Edwards, 2012). For this patient the most useful diagnostic tests include skin biopsies and blood cultures. It is extremely important of determine if the fungal infection is topical or systemic as treatment for both vary. Those with FWC need debridement with topical antifungal drugs while those with FWI need aggressive debridement, topical antifungal drugs, and powerful intravenous (IV) antifungal drugs such as amphotericin B and caspofungin (Capoor et al., 2010). Skin biopsies.Skin biopsies of direct tissues are rarely performed and are used to justify a suspicion. Full thickness burns are recommended to be excised every 7, 14, 21, and greater than 28 days. During this process skin biopsies are usually retrieved if fungemia is suspected. Current recommendations for diagnosis of FWI through skin biopsy are to obtain a tissue biopsy containing living tissue from dermis from under the eschar. At least three different areas are needed and tissue samples need to be collected at least three different time. This tissue is then gram stained, KOH, and cultured. If fungus is present on the KOH or gram stain then a periodic acid Schiff’s stain is completed (Capoor et al., 2010). Blood cultures. Blood cultures are main source of identification for fungemia but are often unreliable and results often take a considerable amount of time. This can be a common cause of delayed treatment in these types of patients, increasing the mortality rate. Duplicate tubes should be obtained and incubated at 25-37 degrees Celsius (Capoor et al., 2010). Bacterial infections are ruled out in twenty four hours; however, fungal infection can take up to six weeks before they are considered negative. To increase the sensitivity of the blood culture a lysis-centrifugation used be used (Edwards, 2012). Once the culture is positive for fungi then identification is performed for yeast through germ tube testing and mold through lactophenol cotton blue mount so that conidiogenesis, pattern, and arrangement can be evaluated (Capoor et al., 2010). Other. Other miscellaneous testing depends on the patient’s condition and are used more so to test for FWI which can then lead to fungemia. These tests are: fine needle aspirate if subeschar exudate, swabbed purulent drainage, urine culture, and throat swab culture (Capoor et al., 2010; Edwards, 2012). Plan Treatment of fungemia is indicated in this patient based on clinical presentation and laboratory findings of mucor and fusarium. This patient must also be treated for bacterial sepsis even without positive blood cultures based on the clinical deterioration seen when Vancomycin and Merrem were discontinue. Improvement was seen within 24s hour when antibiotics were added back on the patient’s pharmacy list. Antifungal treatment was initially started with voriconazole dosed at 12mg/kg loading dose for two days followed by six mg/kg/d daily. This drug is indicated for a total of four doses however, this patient continue to develop fungal growth so the drug was continued (Shelburne & Hamill, 2013). Voriconazole was discontinue when the patient developed kidney failure and had to be placed on continue dialysis. At this time he was place on amphotericin B liposomal because this drug not only covered the mucor and fusarium but was also not renal cleared. Amphotericin B liposomal is administered 3-6mg/kg daily (Shelburne & Hamill, 2013). Once the patient regains renal function, his antifungal was changed to amphotericin B because it was less expensive and was also not as renal cleared. Amphotericin B is dosed at 0.3-1.5 mg/kg daily (Shelburne & Hamill, 2013). The patient will remain on this antifungal because covers both the fungi and mold growth until the patient either develops negative blood cultures or experiences death. Along with the systemic antifungals, topical antifungals will be placed on dressings with each daily dressing change to reduce colonization. Other considerations for this patient include insensible fluid loss, nutrition, protein loss, and hypermetabolic-catabolic states. Insensible fluid loss is extreme in this patient because of the 96% TBSA burn with the majority being third degree burns. During physical assessment the practitioner can see fluid ooze out of the patient’s fascia and drip on to the bed or floor. While this amount of fluid loss is extensive, even more is lost by evaporation. IV fluid bolus of crystalloids are needed daily, about 2-3 boluses, along with a total fluid volume of about 1500ml per hour continuously. Even with this amount of fluid intake there is still a negative net loss. Insensible fluid loss remains elevated until the final wound is closed and many patients need anywhere from two to four liters of crystalloids per day. Along with fluid loss, protein also escapes from the skin, either from wound exudate or bleeding, creating a negative protein balance. Albumin is given not only to help with fluid loss but also to help correct the protein loss (Demling & Desanti, 2005). Once the fluid loss is replaced the focus should shift to the hypermetabolic-catabolic state. Because of the inflammatory response from the burn catecholamines are release, which doubles the metabolic state, increasing oxygen consumption to almost double the normal body needs. The liver then kicks in and induces gluconeogenesis and breaks down muscle/ protein to meet the bodies’ demands. Unlike starvation where the body will breakdown fat before needing to break down muscle; burn patient’s bodies immediately start to breakdown muscle first in order to meet metabolic demands. The burn wound will obtain all of the patients caloric needs until the body has broken down 20% of the patients total body muscle. At this point both the muscle and burn wound will compete for caloric energy needed. After a 30% loss of total body muscle the body will shunt caloric availability away from the burn wound to the muscle in attempt to maintain life. Despite adequate nutrition the body will still break down muscle. The goal is to provide enough nutrition that the body will reduce muscle break down by 70%. This will provide the patient with more reserve for a longer period of time to allow for prolonged healing. In a patient with inhalation injury who has a tracheostomy, a duo-tube placed pyloric is preferred. Tube feeding should contain about 60% calories from carbohydrates, 30% from fat, and have 1.5-2.2 grams of protein per kg. Calculating the patient’s caloric needs during the acute crisis phase consists of 35cal/kg with the sum doubled. Enteric tube feeding should be started as soon as possible post resuscitation phase to reduce muscle breakdown (Posluszny, Conrad, Halerz, Shankar, & Gamelli, 2011).Follow UpFollow up for fungemia is recommended like any other infection with a follow up visit with a pre-visit CBC in one month with the primary care physician. At that time a full set a vital signs should be obtain and the patient should be assessed for any continuing signs of infection. The patient should also be instructed to call if he or she should start to show any signs of infection at home such as wound infection, purulent drainage, fever, shortness of breath, malaise, or any other concern (Reinhart et al., 2010). As for follow up for burn, this should be completed by a primary care physician if the burn is minor or by a burn specialist if the burn required hospitalization, surgery, or specialized treatment. Simple burns should be followed up the day after the injury to reassess and readjust pain medications. After the initial follow up the patient should return once weekly for continued monitoring of the burn until epithialization has occurred. During the first follow up visit the patient should be assess for ability to complete wound changes or ability of family to complete daily wound changes. If the patient or family is unable to perform dressing changes then the patient should be instructed to follow up daily for wound changes until epithiliazation has occurred (Selig et al., 2012). Epithiliazation usually occurs in about seven to ten days. If epithiliazation has not occurred in two weeks in pediatrics or African Americans, or three weeks in older persons or other races, then scarring will most likely occur. Hospitalized patients may follow up weekly until burn wound are completely healed. Treatment of scars can be reduced by applying a bandage with slight pressure while healing and increased pressure once the scar has formed. This process of reducing the scar is not well understood and the exact amount of pressure needed is not known. Once the scar has formed then lotions or silicone inserts can be applied to minimize and reduce scar formation (Morgan, Bledsoe, & Barker, 2000). Other follow up concerns involve complications of the burn such as contractures and depression. The patient should be assessed at each visit for depression and psychosocial support should be offered. Contracture can be a common event after a severe burn depending on burn size and location. A burn specialist will need to be consulted for appropriate management and possible surgery. Other reduction methods include implantation of silicone inserts and having the patient wear long term splints (Morgan, Bledsoe, & Barker, 2000). Health PromotionHealth promotion for fungemia is similar to bacterial infection prevention. Hand washing is the single most important step in preventing transmission to the patient. While fungi, yeast, and mold are all known to be spore forming which can linger in the air and be transported miles away, hand washing still can prevent a large percentage of transmission from person to patient (Allegranzi & Pittet, 2009). Other preventative measures include stand care infection control with addition to gown wearing. Gowns, gloves, masks, and occasionally protective foot wear should be used when changing the patient’s burn wound dressings. The not only protects the staff from body fluids but also help prevent transmission of fungi off the staff clothing to the patient. Many fungi are native to this region resulting in an elevated spore count compared to the many parts of the nation. Has fungi linger in the air we walk into them and the fungi become attached to our clothing only to be jostled off near the patient. By wearing protective clothing while the patients wound are exposed we can essentially entrap the fungi and prevent them from being dislodged into the patient’s wounds (Reinhard, 2008). Other health promotion techniques include ventilator assisted pneumonia (VAP) protocols and sterile dressing changes. By using the VAP protocol pneumonia can be prevented and health can be optimized. Because VAP can lead to sepsis which will allow opportunistic infection from fungi to grow, VAP protocols can reduce the risk for fungemia development. This protocol consists of cleaning the patient’s mouth frequently with a chloraxedine swab, using a tooth brush multiple times a day, subglottic suctioning, tracheal suctioning, having the head of bed 30 degrees at all times, and placing a post-pyloric feeding tube to prevent aspiration pneumonia (Chastre & Fagon, 2002). Sterile dressing changes are needed to prevent not only bacterial infections but also fungal infections. Dressing changes with an amphotericin B solution are indicated in burn wounds as an added protectant and fungal colonization reducer (Edwards, 2012; Reinhard, 2008). The main transport method of fungi into the blood stream is through invasive lines. For this reason maintaining a sterile line is imperative. Because the patient has no skin, amphotericin B soaked sterile gauze in loosely placed over the line insertion site. While this can provide some protection, soaked dressings can easily fall off or be removed once again exposing the site. Due to this a line changing schedule was devised to help prevent infection development (Patel et al., 2012). For this particular patient his invasive lines were rewired every three days with a new insertion site every week. His foley was also changed out weekly. Keeping this patient line sterile was extremely difficult and needed extra preventative measures such as more frequent line changes compared to other types of patients (Reinhard, 2008). While health promotion for fungemia is often directed at the acute phase, burn health promotion is focused more on the preventative phase. According to the World Health Organization (2013) fire prevention is focused on closing all doors to the fire to reduce flame height, use safer stoves, use less dangerous fuels, have house inspections for safety regulations, use safe housing designs and materials, perform fire safety education, be compliant with industrial safety regulations, use fire-retardant material in all child’s clothing and instruct persons to avoid loose fitting clothing, do not smoke in bed, use child safer lighters, develop fire safer smoking material, and improve epilepsy treatment. ReferencesAllegranzi, B., & Pittet, D. (2009). Role of hand hygiene in healthcare-associated infection prevention. Journal of Hospital Infection, 73(4), 305-315. , L., Al-Mousawi, A., Rivero, H., Jeschke, M., Sanford, A., & Herndon, D. (2009). Emerging infections in burns. Surgical Infections, 10(5), 389-397. , M., Sarabahi, S., Tiwari, V., & Narayanan, R. (2010). Fungal infections in burns: Diagnosis and management. Indian Journal of Plastic Surgery, 43, 37-42. , J., & Fagon, J. (2002). Ventilator-associated pneumonia. American Journal of Respiratory and Critical Care Medicine, 165(7), 867-903. doi: 10.1164/ajrccm.165.7.2105078 Demling, R., & Desanti, L. (2005). Chapter 100. Burns: Inflammation-infection phase (Day 7 to wound closure). In J. Hall, G. Schmidt, & L. Woods (Eds.), Principles of Critical Care (3 ed. Retrieved from , J. (2012). Chapter 198. Diagnosis and treatment of fungal infections. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s Principles of Internal Medicine (18 ed. New York: McGraw-Hill.Micek, S., Welch, E., & Kollef, M. (2010). Empiric combination antibiotic therapy is associated with improved outcome against sepsis due to gram-negative bacteria: A retrospective analysis. Antimicrobial Agents and Chemotherapy, 54(5), 1742-1748. , E., Bledsoe, S., & Barker, J. (2000). Ambulatory management of burns. American Family Physicians, 62(9), 2015-2026. Retrieved from Board of Nursing. (2013). The Formulary Developed by the Committee on Prescriptive Governance. Retrieved from nursing.,PDFA/AdvPractice/Formulary_11-19-12.pfdPatel, B., Paratz, J., Mallet, A., Lipman, J., Rudd, M., Muller, M., ... Roberts, J. (2012). Characteristics of bloodstream infections in burn patients: An 11-year retrospective study. Burns, 38(5), 685-690. , J., Conrad, P., Halerz, M., Shankar, R., & Gamelli, R. (2011). Surgical burn wound infections and their clinical implications. Journal of Burn Care & Research, 32(2), 324-333. , K. (2008). The role of the acute care nurse practitioner in the early identification and management of sepsis (Doctoral dissertation). Retrieved from , K., Brunkhorst, F., Bone, H., Bardutzky, J., Dempfle, C., Forst, H., ... Welte, T. (2010). Prevention, diagnosis, therapy and follow-up care of sepsis: 1st revision of S-2k guidelines of the German Sepsis Society and the German Interdisciplinary Association of Intensive Care and Emergency Medicine. German Medical Science, 8(14). , L. (2011). Defining medical futility and improving medical care. Journal of Bioethical Inquiry. , H., Lumenta, D., Giretzlehner, M., Jeschke, M., Upton, D., & Kamolz, L. (2012). The properties of an “ideal” burn wound dressing- What do we need in daily clinical practice? Results of a worldwide online survey among burn care specialists. Burns, 38(7), 960-966. , S., & Hamill, R. (2013). Chapter 36. Mycotic infections. In M. Papadakis, S. McPhee, M. Rabow, & T. Berger (Eds.), CURRENT Medical Diagnosis & Treatment 2014. Retrieved from , S., Cifu, A., & Altkorn, D. (2010). Chapter 4. I have a patient with an acid-base abnormality. How do I determine the cause? In S. Stern, A. Cifu, & D. Altkorn (Eds.), Symptoms of Diagnosis: An Evidence-Based Guide (2 ed.) New York: McGraw-Hill.Unsinger, J., Burnham, C., McDonough, J., Morre, M., Prakas, P., Caldwell, C., ... Hotchkiss, R. (2012). Interleukin-7 ameliorates immune dysfunction and improves survival in a 2-hit model of fungal sepsis. The Journal of Infectious Disease, 206, 606-616. University Medical Center (n.d.). Clinical management guidelines: Treatment of fungal infections in surgical patients. Multidisciplinary Surgical Critical Care & Emergency General Surgery Service. Abstract retrieved from Health Organization. (2012). Facts about injuries: Burns. Retrieved from ................
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