comprehensive case study nur...

Running head: COMPREHENSIVE CASE STUDY NUR 7202 1

Comprehensive Case Study NUR 7202

Ashley Peczkowski

Wright State University

NUR 7202

COMPREHENSIVE CASE STUDY NUR 7202 2

Comprehensive case study NUR 7202

Comprehensive Case Study

Patient Information

Name: A. H., Age: 37, Race: Caucasian, Gender: Male

Source and Reliability

Chart review. Accuracy unknown.

Chief Complaint

A 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. Unknown

Immunizations. DTAP 8/25/13

Adult illness. Unknown

Past Surgical History

Tonsillectomy as a child. Right above the knee amputation (BKA) as a child

Family History


Mother- HTN, smoker, COPD, alive; Father- smoker, MI, deceased; Brother- HTN,

alive; Sister- negative history, alive; Maternal Aunt- HTN, CVA, alive

Social 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 Medications

None

Allergies

No 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.



Neck.


Respiratory.


Cardiac.


Gastrointestinal.


Genitourinary.


Musculoskeletal.

Unable to assess secondary to mechanical ventilation and sedation. History of right BKA

from traumatic injury seven years ago.

Neurological.


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.

Chemistry Current result Normal Range

Ph 7.21 7.35-7.45

PaCo2 45 38-42mmHg

PaO2 123 75-100mmHg

HCO3 35 22-28mEq/L

Base excess -2.2 -2-+2 mEq/L

SaO2 92% 90-100%

Lactate 4.1 0.5-2.2mmol/L

Albumin 2.1 3.4-5.4g/dL

Alkaline phosphatase 33 44-147IU/L

ALT 10 8-37 IU/L

AST 25 10-34 IU/L

Sodium 140 135-145mEq/L

Potassium 5.2 3.5-5 mEq/L

Co2 35 20-29 mmol/L

BUN 20 7-20 mg/dL

Creatinine 1.3 0.8-1.4 mg/dL

Glucose 102 70-100 mg/dL

Calcium 7.9 8.5-10.9 mg/dL


Magnesium 1.9 1.7-2.2mg/dL

Phosphorus 2.2 2.4-4.1 mg/dL

Chloride 111 96-106 mmol/L

WBC 26 3.5-10.5 billion/L

HGB 8.1 13.5-17.5 gram/L

HCT 24% 38.8-50.0%

PLT 32 150-450 billion/L

PTT 45 25-35 secs

INR 1.6 0.8-1.2

Cultures.

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 Fusarium

Chest 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 naïve 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 Tests

Diagnostic 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 Up

Follow 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 Promotion


Health 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.


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