CASE PRESENTATION

History of Present Illness:

 A 50-year-old female presents after admission to the general medical/surgical hospital ward with a
chief complaint of shortness of breath on exertion. She reports that she was seen for similar
symptoms previously at her primary care physician’s office six months ago. At that time, she was
diagnosed with acute bronchitis and treated with bronchodilators, empiric antibiotics, and a short
course oral steroid taper. This management did not improve her symptoms, and she has gradually
worsened over six months. She reports a 20-pound intentional weight loss over the past year. She
denies any sick contacts. A brief review of systems is negative for fever, night sweats, palpitations,
chest pain, nausea, vomiting, diarrhea, constipation, abdominal pain, neural sensation changes,
muscular changes, and increased bruising or bleeding. She admits a cough, shortness of breath, and
shortness of breath on exertion.
Social History: Her tobacco use is 33 pack-years; however, she quit smoking shortly prior
to the onset of symptoms, six months ago. She denies alcohol and illicit drug use. She is married, in
a monogamous relationship, and has three children aged 15 months to 5 years. She is employed as
clinical instructor. She has two pet cats. She loves to travel.
Allergies: No known medicine, food, or environmental allergies.
Past Medical History: Essential Hypertension
Past Surgical History: Apendectomy and CS
Medications: Lisinopril 10mg by mouth every day
Physical Exam:
Vitals: Temperature, 105. F; heart rate 108; respiratory rate, 26; blood pressure 130/86; BMI 26.
General: She is well appearing but anxious, a pleasant female lying on a hospital stretcher. She is
conversing freely, with respiratory distress causing her to stop mid-sentence.
Respiratory: She has diffuse rales and mild wheezing; tachypneic.
Cardiovascular: She has an irregular rate and rhythm with PSVT
Gastrointestinal: Bowel sounds X4. No bruits or pulsatile mass.

Initial Evaluation
Laboratory Studies: Initial work-up from the emergency department revealed pancytopenia with a
platelet count of 74,000 per mm3; hemoglobin, 8.3 g per and mild transaminase elevation, AST 90
and ALT 112. Blood cultures were drawn and currently negative for bacterial growth or Gram
staining.
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I. NURSING HISTORY

A. History of Present Illness:

A 50-year-old female presents after admission to the general medical/surgical hospital ward
with a chief complaint of shortness of breath on exertion. She reports that she was seen for
similar symptoms previously at her primary care physician’s office six months ago. At that
time, she was diagnosed with acute bronchitis and treated with bronchodilators, empiric
antibiotics, and a short course oral steroid taper. This management did not improve her
symptoms, and she has gradually worsened over six months. She reports a 20-pound
intentional weight loss over the past year. She denies any sick contacts. A brief review of
systems is negative for fever, night sweats, palpitations, chest pain, nausea, vomiting,
diarrhea, constipation, abdominal pain, neural sensation changes, muscular changes, and
increased bruising or bleeding. She admits a cough, shortness of breath, and shortness of
breath on exertion.
B. Social History
Her tobacco use is 33 pack-years; however, she quit smoking shortly prior to the onset of
symptoms, six months ago. She denies alcohol and illicit drug use. She is married, in a
monogamous relationship, and has three children aged 15 months to 5 years. She is
employed as clinical instructor. She has two pet cats. She loves to travel.
C. Allergies: No known medicine, food, or environmental allergies.
D. Past Medical History: Essential Hypertension
E. Past Surgical History: Apendectomy and CS
F. Medications: Lisinopril 10mg by mouth every day
G. Physical Exam:
 Vitals: Temperature, 105. F; heart rate 108; respiratory rate, 26; blood
pressure 130/86; BMI 26.
 General: She is well appearing but anxious, a pleasant female lying on a
hospital stretcher. She is conversing freely, with respiratory distress causing
her to stop mid-sentence.
 Respiratory: She has diffuse rales and mild wheezing; tachypneic.
 Cardiovascular: She has an irregular rate and rhythm with PSVT
 Gastrointestinal: Bowel sounds X4. No bruits or pulsatile mass.
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ANATOMY OF THE AFFECTED ORGAN

Once the spores are inhaled in the lungs, Histoplasma spores starts its mycelial phase
(yeast budding) because of the ideal temperature in the host’s lung (37 C) that supports the
growth of the fungus. The disease can damage lungs to the point that the air sacs begin filling
with fluid. This prevents good air exchange and can deplete the oxygen in your blood.
Histoplasma yeast is also ingested by macrophages in the lungs. The macrophages travel into
the lymphatic system where the disease, if not contained, spreads to different organs in a linear
fashion following the lymphatic system and ultimately into systemic circulation. Once this
occurs, a full spectrum of disease is possible. The disease can cause inflammation of the sac
that surrounds the heart (pericardium). When the fluid in this sac increases, it can interfere
with the heart's ability to pump blood. It can also harm the adrenal glands, which produce
hormones that give instructions to virtually every organ and tissue in the body. Histoplasma
infection can resemble with pneumonia-like symptoms (fever, shortness of breath, productive
cough, chest pain).
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PATHOPHYSIOLOGY
Acute Pulmonary Histoplasmosis is caused by inhaling the microconidia of Histoplasma spp.
fungus into the lungs. The mycelial phase is present at ambient temperature in the
environment, and upon exposure to 37 C, such as in a host’s lungs, it changes into budding
yeast cells. This transition is an important determinant in the establishment of infection.
Inhalation from soil is a major route of transmission leading to infection. Human-to-human
transmission has not been reported. Infected individuals may harbor many yeast-forming
colonies chronically which remain viable for years after initial inoculation. The finding that
individuals who have moved or traveled from endemic to non-endemic areas may exhibit a
reactivated infection after many months to years supports this long-term viability. However, the
precise mechanism of reactivation in chronic carriers remains unknown.
Infection ranges from an asymptomatic illness to a life-threatening disease, depending on the
host’s immunological status, fungal inoculum size, and other factors. Histoplasma spp.
have grown particularly well in organic matter enriched with bird or bat excrement, leading to
the association that spelunking in bat-feces-rich caves increases the risk of infection. Likewise,
ownership of pet birds increases the rate of inoculation.
Non-immunocompromised patients present with a self-limited respiratory infection. However,
the infection in immunocompromised hosts disseminated histoplasmosis progresses very
aggressively. Within a few days, histoplasmosis can reach a fatality rate of 100% if not treated
aggressively and appropriately. Pulmonary histoplasmosis may progress to a systemic infection.
Like its pulmonary counterpart, the disseminated infection is related to an exposure to soil
containing infectious yeast. The disseminated disease progresses more slowly in
immunocompetent hosts compared to immunocompromised hosts. However, if the infection is
not treated, fatality rates are similar. The pathophysiology for a disseminated disease is that,
once inhaled, Histoplasma yeast are ingested by macrophages. The macrophages travel into the
lymphatic system where the disease, if not contained, spreads to different organs in a linear
fashion following the lymphatic system and ultimately into systemic circulation. Once this
occurs, a full spectrum of disease is possible. Inside the macrophage, this fungus is contained in
a phagosome. It requires thiamine for continued development and growth and will consume
systemic thiamine. In immunocompetent hosts, strong cellular immunity including
macrophages, epithelial, and lymphocytes surround the yeast buds to keep infection localized.
Eventually, it will become calcified as granulomatous tissue. In immunocompromised hosts, the
organisms disseminate to reticuloendothelial system, leading to progressive disseminated
histoplasmosis.
Symptoms of infection typically begin to show within three to17 days. Immunocompetent
individuals often have clinically silent manifestations with no apparent ill effects. The
acute phase of infection presents as nonspecific respiratory symptoms including a cough and
flu. A chest x-ray is read as normal in 40% to 70% cases. Chronic infection can resemble
tuberculosis with granulomatous changes or cavitation. The disseminated illness can lead
to hepatosplenomegaly, adrenal enlargement, and lymphadenopathy. The infected sites usually
 NCM 114 – CARE OF OLDER PERSON

calcify as they heal. Histoplasmosis is one of the most common causes of mediastinitis.
Presentation of the disease may vary as any other organ in the body may be affected by the
disseminated infection.

DIAGNOSTIC TESTS

Histoplasma antigen detection in urine and/or serum is the most widely used and most
sensitive method for diagnosing acute pulmonary histoplasmosis following exposure to a large
inoculum. Other methods include antibody tests, culture, and microscopy.  

 Antigen detection: Enzyme immunoassay (EIA) is typically performed on urine and/or

serum, but can also be used on cerebrospinal fluid or bronchoalveolar lavage fluid.
 Antibody tests: Because development of antibodies to Histoplasma can take two to six
weeks, antibody tests are not as useful as antigen detection tests in diagnosing acute
histoplasmosis or in immunosuppressed persons, who may not mount a strong immune
response.
o Immunodiffusion (ID): Tests for the presence of H (indicates chronic or severe
acute infection) and M (develops within weeks of acute infection and can persist
for months to years after the infection has resolved) precipitin bands; ~80%
sensitivity.
o Complement Fixation (CF): Complement-fixing antibodies may take up to 6
weeks to appear after infection. CF is more sensitive but less specific than
immunodiffusion.
 Culture: can be performed on tissue, blood, and other body fluids, but may take up to 6
weeks to become positive; most useful in the diagnosis of the severe forms of
histoplasmosis. A commercially available DNA probe (AccuProbe, GenProbe Inc.) can be
used to confirm.
 Microscopy: for detection of budding yeast in tissue or body fluids, low sensitivity, but
can provide a quick proven diagnosis if positive.
 Polymerase Chain Reaction (PCR): PCR for detection of Histoplasma directly from
clinical specimens is still experimental, but promising.
 MEDICATIONS

Pulmonary histoplasmosis in asymptomatic patients is self-resolving and requires no treatment.

However, once symptoms develop a decision to treat the patient needs to be made. In mild,
tolerable cases, no treatment other than close monitoring is necessary. However, once
symptoms progress to moderate or severe or if they are prolonged for greater than four weeks,
treatment with itraconazole is indicated. The anticipated duration is 6 to 12 weeks. The
patient's response should be monitored with a chest x-ray. Furthermore, observation for
recurrence is necessary for several years following the diagnosis. If the illness is determined to
be severe or does not respond to itraconazole, amphotericin B should be initiated for a
minimum of 2 weeks, but up to 1 year. Cotreatment with methylprednisolone is indicated to
 NCM 114 – CARE OF OLDER PERSON

improve pulmonary compliance and reduce inflammation, thus improving the work of
respiration.

ITRACONAZOLE

Itraconazole is the azole of choice in histoplasmosis and is administered 200 mg twice daily in
adults and 5-10 mg/kg not to exceed 400 mg daily in children daily for 6–12 weeks. Blood
concentrations of itraconazole obtained 2–4 h after administration of a dose could be
monitored in selected situations: suspected treatment failure, concern about compliance or
absorption, use of medications that may reduce the solubility of itraconazole or accelerate its
metabolism, and desire to reduce the dose from 200 mg twice daily to 200 mg once daily.

AMPHOTERICIN B
Amphotericin B, 50 mg daily, or about 0.7 mg/kg/d, is recommended for patients who are
judged to require hospitalization because of ventilatory insufficiency or general debilitation,
inability to take itraconazole because of drug interactions or allergies, inability to absorb
itraconazole, inability to achieve detectable concentrations of itraconazole in the blood, or
failure to improve clinically after at least 12 weeks of itraconazole therapy (AII). Some patients
may not be able to tolerate that dosage of amphotericin B, which justifies reducing the dosage
to 0.5–0.6 mg/kg/d or to use of 1 of the lipid formulations. If amphotericin B is administered for
the full course of therapy, at least 35 mg/kg should be given at doses of 50 mg 3 times weekly,
if tolerated. In most patients, however, treatment can be changed to itraconazole, 200 mg once
or twice daily.

METHYLPREDNISOLONE

Methylprednisolone is a synthetic corticosteroid with anti-inflammatory and

immunomodulating properties. Methylprednisolone binds to and activates specific nuclear
receptors, resulting in altered gene expression and inhibition of proinflammatory cytokine
production. This agent also decreases the number of circulating lymphocytes, induces cell
differentiation, and stimulates apoptosis in sensitive tumor cell populations. Cotreatment with
methylprednisolone is used together to treat acute pulmonary histoplasmosis to improve
pulmonary compliance and reduce inflammation, thus improving the work of respiration.
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DRUG STUDY

DRUG NAME DOSAGES THERAPEUTIC INDICATIONS ADVERSE EFFECTS CONTRAINDICATIONS NURSING COSIDERATION
ACTIONS

Generic Name: Dosage: Block the activity of a Treatment for  GI: liver toxicity Contraindicated to patient Nursing Assessment
sterol in a fungal candidiasis,  Severe effects on with hypersensitivity to These are the important
Itraconazole 200 mg in adults wall. Therefore, they cryptococcal a fetus or a the drug. things the nurse should
and 5-10 mg/kg for may also block the nursing babies include in conducting
meningitis,
children. activity of human systemic mycoses, Pregnancy and lactation, assessment, history
taking, and examination:
steroids such as aspergillosis, known to cross the
Brand Name: Route: testosterone and among others placenta and enter breast
 Assess for the
cortisol. milk. mentioned cautions
Sporanox Oral and
contraindications
(e.g. known history
of allergy to
Drug Class: Frequency: antifungals, liver
and kidney
Antifungal BID dysfunction,
pregnancy and
lactation, etc.) to
prevent any
untoward
complications.
 Perform a thorough
physical assessment
(other medications
taken, orientation
and reflexes, skin
NCM 114 – CARE OF OLDER PERSON

color and lesions,

etc.) to establish
baseline data before
drug therapy begins,
to determine
effectiveness of
therapy, and to
evaluate for
occurrence of any
adverse effects
associated with
drug therapy.
 Obtain a culture of
the infected area to
make an accurate
determination of
the type and
responsiveness of
the fungus.
 Evaluate renal and
hepatic function
tests and complete
blood count to
determine baseline
function of these
organs and to assess
possible toxicity
during drug therapy.
 NCM 114 – CARE OF OLDER PERSON

DRUG NAME DOSAGES THERAPEUTIC INDICATIONS ADVERSE EFFECTS CONTRAINDICATIONS NURSING COSIDERATION
ACTIONS

Generic Name: Dose: Increased cell membrane Treatment of  CNS: headache  Hypersensitivity Monitor VS q15-30 min
permeability in severe, possibly and mild CNS  Severe bone during first inf; note
Amphotericin B 50 mg susceptible organisms by fatal fungal changes for marrow changes in pulse,BP.
griseofulvin depression - Monitor bloods tudies
binding sterols in fungal infection
Brand Name: Route:  GI and GU: - Monitor weight weekly;
membrane; decreases hepatic and renal if weight increases 2lb/wk,
potassium, sodium failure, nausea, edema is present; renal
Abelcet, Oral and nutrients in the cell vomiting, damage should be
Amphotec potentially considered.
Frequency: severe diarrhea, - Monitor for renal
anorexia, weight toxicity; increasing BUN and
OD loss serum creatinine
Drug Class:  Immunological: - Monitor for
bone marrow hepatotoxicity; I ncreasing
Antifungal suppression, AST,ALT, alkaline
rash, phophatase
dermatological - Monitor for allergic
changes reaction
 Local: pain at - Monitor for
injection site with hypokalemia
phlebitis or
thrombophlebitis

DRUG NAME DOSAGES THERAPEUTIC INDICATIONS ADVERSE EFFECTS CONTRAINDICATIONS NURSING COSIDERATION
 NCM 114 – CARE OF OLDER PERSON

ACTIONS

Generic Name: Dose: Methylprednisolone - Short-term Oedema, - Serious infections except

is a synthetic management of hypertension, septic shock or
Methylprednisolo 48 mg corticosteroid with various arrhythmia; CNS, tuberculous meningitis; Assessment
ne mainly glucocorticoid inflammatory and endocrine, metabolic viral, fungal and
activity and minimal allergic disorders, and GI effects; tubercular skin lesions; - History: Infections;
Route: kidney or liver disease,
mineralocorticoid such as hirsutism, acne, skin admin of live virus
Brand Name: hypothyroidism,
properties. It rheumatoid atrophy, bruising, vaccines. Preparations
Oral ulcerative colitis,
decreases arthritis, collagen hyperpigmentation; containing benzyl alcohol
Medrol inflammation by diseases (eg, SLE), transient leukocytosis; preservative are diverticulitis, active or
Frequency: suppression of dermatologic arthralgia, muscle contraindicated in infants. latent peptic ulcer,
Drug Class: migration of diseases (eg, weakness, inflammatory bowel
OD polymorphonuclear pemphigus), osteoporosis, disease, CHF,
Corticosteriod leukocytes and status fractures, cataracts, hypertension,
reversal of increased asthmaticus, and glaucoma; infections, thromboembolic
capillary autoimmune hypersensitivity disorders, osteoporosis,
permeability. disorders reactions, avascular seizure disorders,
- Hematologic necrosis, secondary diabetes mellitus;
disorders: malignancy, pregnancy; lactation
Thrombocytopeni intractable hiccups. - Physical: Weight, T,
a purpura, reflexes and grip
erythroblastopeni strength, affect and
a orientation, P, BP,
- Ulcerative colitis, peripheral perfusion
acute prominence of superficial
exacerbations of veins, R and adventitious
MS, and palliation sounds, serum
in some electrolytes, blood
leukemias and glucose
lymphomas Interventions
- Trichinosis with
- Use caution with the
neurologic or
24-mg tablets marketed
 NCM 114 – CARE OF OLDER PERSON

myocardial as Medrol; these contain

involvement tartrazine, which may
- Prevention of cause allergic reactions,
nausea and especially in people who
vomiting are allergic to aspirin.
associated with - Give daily dose before 9
chemotherapy to mimic normal peak
- Unlabeled use: corticosteroid blood
Septic shock, levels.
respiratory - Increase dosage when
distress patient is subject to
syndrome, acute stress.
spinal cord injury - WARNING: Taper doses
when discontinuing high-
dose or long-term
therapy to allow adrenal
recovery.
- WARNING: Do not give
live virus vaccines with
immunosuppressive
doses of corticosteroids.

Teaching points

- Do not to stop taking

the oral drug without
consulting your health
care provider.
- Avoid exposure to
infections.
- Report unusual weight
gain, swelling of the
extremities, muscle
 NCM 114 – CARE OF OLDER PERSON

weakness, black or tarry

stools, fever, prolonged
sore throat, colds or
other infections,
worsening of disorder.

Name: AYEN, TRISHA NICOLE L.

Age: 50 y/o Gender: Female NURSING CARE PLAN Diagnosis: Acute Pulmonary Histoplasmosis
 NCM 114 – CARE OF OLDER PERSON

ASSESSMENT DIAGNOSIS PLANNING INTERVENTION RATIONALE EVALUATION

Subjective: Ineffective airway Short Term Goal: Independent: After 8 hours of nursing
clearance related to intervention, goal partially
“Nahihirapan akong increased production of After 8 hours of nursing 1.) Encourage deep 1.) Deep breathing met. The patient was able
huminga” as verbalized by respiratory secretions. intervention, secretions breathing exercises. promotes oxygenation to demonstrate coughing
the patient. will be mobilized, airway before controlled and deep breathing
patency will be 2.) Assist patient in coughing exercise very 1-2 hours
maintained free of coughing exercises.
during the day.
secretions as evidenced 2.) To improve
Objective: 3.) Increase fluid intake. productivity of cough
patient’s ability to Client respiratory rate is
- Shortness of Breath effectively cough out 4.) Monitor rate, rhythm, within normal range (RR =
3.) Adequate fluid intake
secretions, clear lung depth and effort of 19)
enhances liquefaction of
- Rapid breathing / sounds and respirations. pulmonary secretions and Inspiratory rales can still
Tachypnea uncompromised
facilitates expectoration be heard at the right
respiratory rate. 5.) Assist the patient into
Temp = 105 F of mucus. lower lobe.
moderate high back rest
position. 4.) Provides a basis for
HR = 108 bpm Cough continues to be
evaluating adequacy of productive.
6.) Auscultate lung fields,
RR = 26 cpm ventilation.
noting areas of decreased
BP = 130/86 mmHg of absent airflow and 5.) to promote drainage
adventitious breath of secretions and better
sounds. lung expansion

6.) Decreased airflow

occurs in areas
consolidated with fluid.
Bronchial breath sounds
(normal over bronchus)
can also occur in
consolidated areas.
Crackles, ronchi, wheezes
 NCM 114 – CARE OF OLDER PERSON

are heard on inspiration

and/or expiration in
response to fluid
accumulation, thick
secretions and airway
spasm/obstruction.

Dependent:

1.) Administer ordered

medications.

2.) Administer
nebulizations as needed.