Pneumocystis

Download Report

Transcript Pneumocystis

A case study of
Pneumocystis Pneumonia
9517
Objectives
 Definition
 Epidemiology
 Pathophysiology
 Clinical Manifestations
 Diagnosis
 Treatments
 Prognosis
 Case study
What is PCP?
 Pneumocystis Pneumonia is caused by the fungal
organism Pneumocystis carinii which was recently
renamed Pneumocystis jiroveci.
 PCP is found in many environments and does not
cause illness in healthy people, however in
immunosuppressed patients such as those with HIV
or AIDS, PCP is opportunistic and often fatal.
Current Opinion in Pulmonary Medicine
Emerging Infectious Diseases
Epidemiology
 PCP is thought to be spread by direct contact and has
been found in almost all mammalian species.
 PCP is the most prevalent opportunistic infection in
patients infected with the human immunodeficiency
virus.

It is the leading cause of death in HIV/AIDS patients and
up to 80% of AIDS patients contract PCP.
 Most children are exposed to PCP in the first few years
of life and it may contribute to SIDS
 Although PCP occurs all over the world, it is more of a
threat to underdeveloped nations.
Journal of Infectious Diseases
The New England Journal of Medicine
Pathophysiology
 Somewhat unclear since PCP cannot be
cultivated easily.
 Occurs most frequently when the CD4+ cell
count is less than 200 cells/mm3
 The trophic form of the organism attacks the
alveolar epithelium causing thickening of the
alveoli and inflammation.

Microscopically, the small predominantly haploid
trophic forms are 1-4 µm in diameter while the
cysts (up to 8 nuclei) are up to 8 µm in diameter.
 This decreases the alveolar-capillary membrane
permeability leading to significant hypoxia and
changes in lung capacities.
The New England Journal of Medicine
eMedicine
Pathophysiology cont.
 Glycoprotein A was the first molecule
identified from Pneumocystis and has an vital
role in the attachment of Pneumocystis to
host cells.
 Beta-1,3-glucan is part of the cyst wall
providing stability and is responsible for the
inflammatory response in the hosts lungs.
 Enhanced activity of the encoding gene
mitogen-activated protein kinase (PCM)
suggests trophic forms of Pneumocystis use
this pathway in the life cycle of PCP.
The New England Journal of Medicine
Pathophysiology cont
 Panel A shows the
trophic form adhering
to the alveolar epithelium
 Panel B shows trophic
forms attaching to each
other
which can be seen during
infection
 Panel C shows a cyst
The New England Journal of Medicine
Clinical Manifestations
 Symptoms include SOB, fever, and a dry non-
productive cough that may occur months
before clinical presentation.
 Tachycardia and tachypnea
 A significant drop in PaO2 along with bilateral
diffuse infiltrates originating in the perihilar
regions as seen on the CXR.
Seminars in respiratory and critical care medicine
Diagnosis
 The primary definitive diagnosis for PCP is direct
visualization through staining techniques

Grocott-Gomori methenamine silver is most used.
 Others are available including Wright-Giemsa,
calcoflour white, and the Papanicolaou.
 Immunoflourescent stains often produce false
positives.
 PCR
 Increased lactase dehydrogenase (LDH) levels often
associated with diagnosis.
Seminars in respiratory and critical care medicine
Treatments
 Although a fungus, PCP does not respond to
antifungal treatment.
 There is accumulating evidence of mutations of
certain genes in PCP arousing concern for
potential resistance to certain medications.
 Recommended duration of treatment for and
HIV/AIDS individual is 21 days and 14 days for
all other patients.
The New England Journal of Medicine
Current Opinion in Pulmonary Medicine
Treatments cont.
 Drugs to treat are TMP-SMX, Primaquine,
Clindamycin, Dapsone, Atovaquone,
Trimetraxate, and Pentamadine.
 Anti-inflammatory meds such as Prednisone
and Solu-medrol.
 Oxygen therapy and mechanical ventilation.
Current opinion in pulmonary medicine
Prognosis
 If left untreated may cause death.
 The prognosis depends on the extent of
infection and damage to lungs at time of
diagnosis.
 Those with suppressed immune systems take
longer to recover.
 Antibiotic treatment is about 80% effective.
Seminars in respiratory and critical care medicine
Case Study Objectives
 Source, reliability, and







chief complaint
History of present
illness
Past medical history
Home medications
Hospital medications
Review of systems
Social history
Family history
 Physical exam
 Lab data
 Echocardiogram and




chest x-ray
Assessment
Mechanical ventilation
daily summaries
Respiratory treatments
Summary of hospital
stay
The Case Study
 Source: The patient and the patients chart
 Reliability: Felt to be mostly accurate
 Chief complaint: DOE and a dry cough
getting progressively worse for 2-3 weeks.
History of Present Illness
 The patient is a 42 year old African American female
with AIDS complaining of DOE and worsening SOB
over the past two weeks.
 Her daughter asked her to go to the ER because she
looked sick, could not breath easy and kept
coughing.
 Her daughter took her to the ER where she was then
admitted to the floor and later the ICU.
Past Medical History





HIV/AIDS
 The patient was diagnosed in 1995 after the father of one of her children died.
 Starts antiretroviral meds, and is non-compliant.
 CD4 count went from 81 in 2000, to 24 in 2008 demonstrating very advanced AIDS
Hepatitis B
 Diagnosed 1995, non-compliant with all meds
Herpes S./Genital (HSV type 2)
 First diagnosed in mid 2007
 Started treatment with Valtrex, but as of January 2008 is no longer taking the meds and
has had no more outbreaks.
HTN
 Diagnosed in 2000 with her BP reading 180/118.
 Tried several different meds, however patient is non-compliant.
Chronic Anemia



The patient had first started these issues in 2001 following a very heavy
menstruation with a Hgb of 4.5, however asymptomatic.
From 2001 to 2006 she has received multiple blood transfusions.
She is non-compliant with all meds and refuses to go to her doctors
appointments.
Past Medical History cont.
 Cervical Malignancy and Menorrhagia




The bleeding first started in 2004 when the patient had 6 days of heavy
clots and was referred to a specialist whom she refused to see.
Diagnosed with squamous cell carcinoma in 2005 with more bleeding;
the patient claims to be getting a hysterectomy in two weeks.
The patient canceled surgery and has not shown up for three
appointments, states she is scared to schedule an appointment despite
lengthy discussions on the seriousness of this disease.
Finally had a total hysterectomy in 2007, ovaries remain intact.
 Thyroid Malignancy


Diagnosed in 2002
After several surgical cancellations, the patient had a subtotal
thyroidectomy in 2004 and continued on unithyroid irregularly.
 Hypothyroidism

Diagnosed in 2005, the patient starts treatment (unithyroid) but takes
irregularly.
Home Medications
Brand
Generic
Type
Dose
Use
Bactrim
Sulfamethoxazole and
trimethoprim
Sulfonomide and
pyrimidine (to help
activity of sulfonomide)
DS QD (160 mg
tromethoprim, and 800
mg sulfa.)
To treat and prevent
PCP
Truvada
Tenofovir and
Emtricitabine
Anti-HIV Nucleoside
reverse transcriptase
inhibitor
200/300 mg QD
To treat HIV and HBV
Tenormin
Atenolol
Beta blocker
100 mg BID
To treat high blood
pressure
Valtrex
Valacyclovir
Antiviral
1 g QD
To treat/prevent
herpes
Lexiva
Fosamprenavir
Protease inhibitor
700 mg BID
Helps manage HIV
when taken with other
HIV meds
Synthroid
Levothyroxin Sodium
Hormone replacement
100 mcg QD
Thyroid replacement
therapy
In Hospital Medications
Brand
Generic
Type
Dose
Use
Zithromax
Azythromycin
Macrolide (inhibits
protein synthesis)
500 mg QD
To treat broad
spectrum bacteria
Cleocin
Clindamycin
Lincosamide (gram +
and anaerobic)
600 mg/4 ml Q6H
To treat PCP
Primiquine
phosphate
Primaquine
Antimalarial
26.3 mg QD
To treat PCP and
malaria
Valtrex
Valocyclovir
Antiviral
500 mg QD
To treat/prevent
herpes
Synthroid
Levothyroxin Sodium
Hormone
replacement
100 mcg QD
Thyroid replacement
therapy
Tenormin
Atenolol
Beta blocker
100 mg BID
To treat high blood
pressure
Prinivil
Lisinopril
ACE inhibitor
20 mg QD
To treat high blood
pressure
Cytovene
Ganciclovir
Guanine nucleoside
analog
400 mg Q12H
To treat CMV
In Hospital Medications cont.
Brand
Generic
Type
Dose
Use
Haldol
Haloperidol
Antipsychotic
5 mg IM PRN
To treat agitation
Versed
Midazolam
Benzodiazapine
2 mg PRN
To treat agitation
Fentanyl
Fentanyl
Narcotic
50 mcg/ml drip
To treat pain
associated with
ventilator
Nexium
Esomeprazole
Protein pump
inhibitor
40 mg PO QD
To prevent aspiration
Phenergran
Promethazine
Antiemetic
25 mg Q8H
To treat nausea
Solu-medrol
Methylprednisolone
Steroid
125 mg QD
DCd 8/16
To treat inflammation
Lasix
Furosemide
Loop diuretic
60 mg IV
To treat pulmonary
effusion
Combivent
Ipratropium and
Albuterol
Anticholinergic and
Adrenergic agents
4 puffs Q4H
To treat
bronchospasm
Review of Systems
 General: No fever/chills or night sweats
 Reproductive: No abnormal bleeding
 Respiratory: DOE, progressive for 2 weeks
with dry non-productive cough
 Neuromuscular: General weakness and
fatigue, no acute joint pain
 GI: No n/v/d, poor appetite for 2 months
 NKDA
 All other systems negative
Social History
 Long history of non-compliance with
medications, doctors appointments and
surgical procedures frequently canceled.
 Patient denied any alcohol or illegal drug use.
 The patient is a non-smoker.
 The patient has never traveled overseas.
 No occupational history
Family History
 Mother: Alive, overweight, arthritis, HTN
 Father: Died from lung cancer, smoker
 Brothers: The patient has 2 brothers that are
alive with HTN
 Sisters: The patient has 4 sisters that are
alive and well.
 Children: The patient has 3 children that are
alive and well

Father of children died in 1995 of AIDS
The Physical Exam
8/19/08
 General: An overweight AAF orally intubated
on mechanical ventilation.
 Vitals: Temp = 37, RR = 24,
BP = 124/82, P = 91, SaO2 = 95% on FiO2 of
65%.
 HEENT: No oral thrush, no oral herpes
 Chest: Normal to inspection with equal chest
rise. Bibasilar decreased BS with few
scattered crackles and rhonchi that clears
with suctioning.
The Physical Exam (cont.)
 Cardiovascular: No JVD.
 Abdomen: Soft and nontender with no
organomegaly detected.
 Skin: No significant lesions are noted.
 Extremities: no peripheral edema
 Neurological: Verbally arousable with a
distressed look, follows commands at times.
Lab Data
8/6/08 ER
Basic Metabolic Profile
Na+ (136-145) K+ (3.5-5.0)
Cl- (98-106)
Bicarb (22-26)
120 L
3.3 L
Complete Blood Count
87 L
26.2
BUN (3-20)
7
WBC (5-10)
Hgb (12-16)
HCT (37-47)
Platelets (150-450)
11.2 H
8.1 L
5.6 L
381
Cr (0.9-1.5)
Glucose (70-105)
LDH (135-214)
0.6 L
94
332 H
8/13/08 ICU
Basic Metabolic Profile
Na+
K+
125 L
4.7
Complete Blood Count
Cl-
Bicarb
BUN
Cr
97
19.5 L
11
0.6 L
WBC
Hgb
HCT
Platelets
19.8 H
12.2
36
157
Glucose
92
8/18/08
Basic Metabolic Profile
Na+
K+
Cl-
Bicarb
BUN
Cr
Glucose
137
4.1
92 L
34.6 H
33 H
0.7 L
102
Complete Blood Count
WBC
Hgb
HCT
Platelets
19.2 H
9.5 L
28.7 L
183
8/27/08
Basic Metabolic Profile
Na+
K+
Cl-
Bicarb
BUN
Cr
Glucose
146
5
110 H
25.3
63 H
0.8
146 H
Complete Blood Count
WBC
14.4 H
Hgb
9.2 L
HCT
28.5 L
Platelets
151
Lab Data
 Sputum Cultures

Collected via mini BAL on 8/14

Silver stain (+) PCP, (-) AFB, (+) CMV
EKG and CXR
 Regular sinus rhythm, no ectopy
 Chest X-ray




August 6th  Diffuse interstitial infiltrates, patchy airspace
infiltrates in the right lower lobe. (PA and lateral)
August 13th  Post intubation film confirmed proper tube
placement with tip at T3
August 15th Mild cardiomegaly, mild effusions in both
lungs, hypo-inflation in both lungs, interstitial reticularnodular changes in perihilar and lower lobes
August 23rd  No cardiomegaly, no effusions or edema.
Improvement in aeration in both lungs as well as decreased
infiltrates compared to previous studies.
Example CXR
Laurence Huang, MD
Assessment
 Pulmonary Assessment
 Pneumonia
 likely PCP
 CAP
 Malignancies
 Consider metastatic etiology
 Tuberculosis
 Cytomegalovirus-can cause interstitial pneumonia in
immunocompromised patients
 Cardiovascular Assessment
 Hypertension
Mechanical Ventilation Daily Summaries
Delivery
device
ER
8/6/2008
ICU
8/13/2008
ICU
8/13/2008
Vent day 1
ICU
8/14/2008
Vent day 2
PICC line
Art-line
10LPM via NRB
15LPM via NRB
Unable to saturate with NRB at
15LPM. Transferred to ICU for
elective intubation.
Avea mechanical ventilator
#8.0 ETT at 22cm at lip
Avea mechanical ventilator
Mode
Vt
Rate
FiO2
PEEP
PIP
MAP
Mode
Vent
Settings
ABG
ABG and
VS
VS
pH
PCO2
7.56
31
BP
HR
PaO2
40
RR
HCO3- 26
SpO2
ABG
202/104
114
VS
pH
PCO2
7.35 BP
33 HR
34
PaO2
49
85%
HCO3-
19
Temp 36.8o
ABG taken on room air
Volume A/C
550ml
12 (21 over)
1.0
10
29
18
ABG
193/113
72
RR
30
SpO2
83%
Temp
37o
On FiO2 1.0 and 15 LPM NRB
VS
PaO2
7.23
49
69
HCO3-
21
pH
PCO2
Volume A/C
Rate
↑ 600ml
↑ 14 (8 over)
FiO2
PEEP
PIP
MAP
1.0
10
38
13
Vt
ABG
BP
157/108
HR
91
RR
33
SpO2 90%
Temp 37.1o
This ABG was the basis for the
vent change on day 2
pH
PCO2
PaO2
HCO3-
VS
7.34
35
83
19
BP
165/110
HR
88
RR
22
SpO2 96%
Temp 37o
Taken after the vent change
Mechanical Ventilation Daily Summaries
ICU
8/16/2008
Vent day 4
ICU
8/19/2008
Vent day 7
ICU
8/21-8/22/2008
Vent day 8 and 9
ICU
8/24-8/26/2008
Vent day 11, 12, and 13
Arousable and following
commands, (+) cough reflex
Avea mechanical ventilator
#8.0 ETT at 22cm at lip
Avea mechanical ventilator
#8.0 ETT at 22cm at lip
Pressure A/C
580ml
14(10 over)
1.0
Mode
Volume A/C
Vt
↓ 500ml
Rate
14(15 over)
FiO2
600ml
14(8 over)
1.0
Mode
~Vt
Rate
FiO2
PEEP
↑ 12
PEEP
↑ 14
PIP
MAP
35
16
PIP
MAP
37
22
Pressure A/C
Arousable and following
commands, (+) cough reflex
Avea mechanical ventilator
#8.0 ETT at 22cm at lip
Mode
~Vt
Rate
FiO2
ICU
8/27/2008
Vent day 14 and 15
↓ .80 (in
increments)
PEEP
↓ 12
PIP
MAP
24
15
Avea mechanical ventilator
#8.0 ETT at 22cm at lip
Mode
~Vt
Rate
Avea mechanical ventilator
#8.0 ETT at 22cm at lip
Pressure A/C
Mode
PSV
500ml
12(8 over)
~Vt
~Rate
FiO2
500ml
25
.50
↓ .50 (in
increments)
FiO2
PEEP
PIP
MAP
12
30
18
16-8 (in
increments)
CPAP
12-10-5 (in
increments)
PS
MAP
ABG
VS
ABG
VS
ABG
VS
pH
7.42
PCO2 41
BP
HR
142/65
pH
7.41
PCO2 46
BP
HR
124/82
86
91
pH 7.38
PCO2 44
78
RR
22
PaO2
90
RR
24
PaO2
PaO2
HCO3- 26.4 SpO2 93%
Temp 36o
HCO3- 29
SpO2 97%
Temp 37o
Taken after vent change
Taken before vent change
95
HCO3- 26
BP
HR
RR
ABG
VS
pH
7.38
PCO2 45
BP
HR
122/81
103
29
PaO2
RR
20
118/89
SpO2 97%
Temp 36o
Taken after vent changes
105
HCO3- 26
ABG
82
SpO2 99%
Temp 36o
Taken after vent changes
7
VS
pH
7.39 BP
120/88
PCO2 44 HR
75
PaO2 109 RR
25
HCO3- 25 SpO2 99%
Temp 36o
Taken 30 minutes prior to
extubation
Respiratory Treatments
Date
Type
Intubation
8/13/08
ET tube size
8mm @ 22 cm at
the lip
Mechanical
Ventilation
8/13/08
Avea mechanical
ventilator
Bronchodilator
8/6-8/29/08
Combivent
Suctioning
Indications
Patient Data
Protection of the
airway and
impending failure
pH 7.35
PaCO2 33
PaO2 49
HCO3 19
Initially put on
Volume A/C with
an FiO2 of 100%
VOPS/Respiratory
Failure (impending
or acute)
pH 7.35
PaCO2 33
PaO2 49
HCO3 19
4 puffs QID
Bronchospasm
Prophylaxis
8/138/27/09
PRN
Secretions
~3 cc thick white
mucus
Incentive
Spirometry
8/278/29/08
10 times an hour,
every hour
patient is awake
To reverse and
prevent further
atelectasis from
being on the vent
Atelectasis
Oxygen (0n
floor)
8/278/29/08
10 LPM
Hypoxemia
SpO2 >90%
Oxymizer
Dose
Summary of hospital stay
 ER
 Floor
 ICU

DNR/Do not trach
 Floor

8/06/08
8/06 - 8/13/08
8/13 - 8/27/08
8/25/08
8/27 - 8/29/08
Discharged to Kindred 8/29/08

Plan is to send patient home in 1-2 weeks
References








.
D’Avignon LC, Schofield CM & Hospenthal DR (2008). Pneumocystis Pneumonia.
Seminars in respiratory and critical care medicine, 29(2), 132-140.
Fei M & Huang L (2008). HIV – associated pneumonias. Retrieved September 4, 2008
from http://img.thebody.com/sfaf/2008/winter08_pneumonia2.jpg
Kaplan JE, Hanson D, Dworkin MS, Frederick T, Bertolli J, Lindegren ML, et al (2000).
Epidemiology of human immunodeficiency virus-associated opportunistic infections
in the United States in the era of highly active antiretroviral therapy. Clinical of
Infectious Diseases; 30 1:S5–14.
Krajicek BJ, Limper AH, & Thomas CF (2008). Advances in the biology, pathogenesis and
identification of Pneumocystis pneumonia. Current Opinion in Pulmonary Medicine,
14, 228-234.
McLean J (2007). Pneumocystis (carinii) jiroveci Pneumonia. Retrieved August 27, 2008
from http://www.emedicine.com/med/topic1850.htm#section~AuthorsandEditors.
Morris A, Wei K, Afshar K, & Huang L (2008). Epidemiology and clinical significance of
Pneumocystis colonization. The Journal of Infectious Diseases, 197, 1-17.
Morris A, Lundgren J, Masur H, Walzer P, Hanson D, Frederick T et al (2008). Current
epidemiology of Pneumocystis pneumonia. Emerging Infectious Diseases, 10(10),
1713-1720.
Thomas CF & Limper AH (2004). Pneumocystis Pneumonia. The New England Journal of
Medicine, 350, 2487-2498.