Problem 2 Flashcards
1
Q
What if the patient is old, allergic to penicillin with comorbidities
A
clarithromycine
2
Q
What is pneumonia
A
infection of the pulmonary parenchyma
3
Q
What is health-care associated pneumonia
A
CAP but the patient has multi-drug resistant pathogen associated with HAP
4
Q
Pneumonia results from…
A
Proliferation of microbial pathogens at the alveolar level and the host’s response to those pathogens.
5
Q
How does the pathogen get to the lower airways
A
The most common is by aspiration from the oropharynx. Small-volume aspiration occurs frequently during sleep (especially in the elderly) and in patients with decreased levels of consciousness.
Rarely, pneumonia occurs via hematogenous spread (e.g., from tricuspid endocarditis) or by contiguous extension from an infected pleural or mediastinal space.
6
Q
How does the body protect us from pneumonia
A
Mechanical factors:
-the hairs and turbinates of the nares capture larger inhaled particles before they reach the lower respiratory tract.
-The branching architecture of the tracheobronchial tree traps microbes on the airway lining, where mucociliary clearance and local antibacterial factors either clear or kill the potential pathogen.
-The gag and cough reflexes offer critical protection from aspiration.
In addition, the normal flora adhering to mucosal cells of the oropharynx, whose components are remarkably constant, prevents pathogenic bacteria from binding.
-When these barriers are overcome or when microorganisms are small enough to be inhaled to the alveolar level, resident alveolar macrophages are
extremely efficient at clearing and killing pathogens. Macrophages are assisted by proteins that are produced by the alveolar epithelial cells (e.g.,
surfactant proteins A and D) and that have intrinsic opsonizing properties or antibacterial or antiviral activity. Once engulfed by the macrophage, the
pathogens—even if they are not killed—are eliminated via either the mucociliary elevator or the lymphatics and no longer represent an infectious challenge.
7
Q
What triggers the clinical syndrome of pneumonia
A
The host inflammatory response
8
Q
What causes the fever
A
The release of inflammatory mediators, such as interleukin 1 and TNF
9
Q
What causes peripheral leukocytosis and increased purulent production
A
Chemokines, such as interleukin 8 and granulocyte colony-stimulating factor, stimulate the release of neutrophils and their attraction to the lung
10
Q
What causes hemoptysis
A
erythrocytes can cross the alveolar–capillary
membrane because of the capillary leaks
11
Q
What causes the radiographic infiltrate and rales detectable on auscultation
A
Capillary leaks
12
Q
Why does the patient have hypoxemia
A
alveolar filling
but also some bacterial pathogens appear to interfere with the hypoxemic vasoconstriction that would normally occur with fluid-filled alveoli
13
Q
What leads to dyspnea
A
Decreased compliance due to capillary leak
Hypoxemia
Increased respiratory drive
Increased secretions
Occasionally infection-related bronchospasm
14
Q
What happens if the changes in lung mechanics are severe enough
A
the changes in lung mechanics secondary to
reductions in lung volume and compliance and the intrapulmonary shunting of blood may cause respiratory failure and death.
15
Q
What is the alternative pathogenesis pathway
A
The alveolar microbiota is similar to the oropharyngeal microbiota; both are predominantly gram-positive in contrast to the gram-negative milieu of the normal gastrointestinal microbiota. Alterations in host defense may allow overgrowth of one or more components of the normal bacterial flora.
16
Q
What are the 2 most common causes to an altered alveolar microbiota
A
viral upper respiratory tract infections for CAP
and antibiotic therapy for HAP/VAP.
17
Q
What is the initial phase of pneumonia
A
The initial phase is one of edema, with the presence of a proteinaceous exudate— and often of bacteria—in the alveoli. This phase is rarely evident in clinical or autopsy specimens because of the rapid transition.
18
Q
What is the second phase of pneumonia
A
The red hepatization phase. The presence of erythrocytes in the cellular intra-alveolar exudate gives this second stage its name, but neutrophil influx is more important with regard to host defense. Bacteria are occasionally seen in pathologic specimens collected during this phase.
19
Q
What is the third phase of pneumonia
A
In the third phase, gray hepatization, no new erythrocytes are extravasating, and those already present have been lysed and degraded. The neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared. This phase corresponds with successful containment of the infection and improvement in gas exchange.
20
Q
What is the final phase of pneumonia
A
In the final phase, resolution, the macrophage reappears as the dominant cell type in the alveolar space, and the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory response.
21
Q
akgdd
A
This pattern has been described best for lobar pneumococcal pneumonia and may not apply to pneumonia of all etiologies, especially viral or
Pneumocystis pneumonia. In VAP, respiratory bronchiolitis may precede the development of a radiologically apparent infiltrate. Because of the
microaspiration mechanism, a bronchopneumonia pattern is most common in nosocomial pneumonias, whereas a lobar pattern is more common in
bacterial CAP. Despite the radiographic appearance, viral and Pneumocystis pneumonias represent alveolar rather than interstitial processes.
22
Q
What is the most common pathogen causing CAP
A
Streptococcus pneumoniae
23
Q
Typical pathogens causing pneumonia
A
S. pneumoniae
Haemophilus influenzae
(in selected patients) S. aureus
Gram-negative bacilli such as Klebsiella pneumoniae and Pseudomonas aeruginosa.
24
Q
Atypical pathogens causing pneumonia
A
Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella species
Respiratory viruses such as influenza viruses, adenoviruses, human metapneumovirus, and respiratory syncytial viruses.
25
What are the caracteristics of atypical organisms
- Cannot be cultured on standard media or seen on Gram’s stain.
- They are intrinsically resistant to all β-lactam agents and must be treated with a macrolide, a fluoroquinolone, or a tetracycline
26
What makes anaerobic pneumonias so complicated
abscess formation and significant empyemas or parapneumonic effusions.
27
A serious consequence of MRSA
necrotizing pneumonia
28
Risk factors for CAP
alcoholism, asthma, immunosuppression, institutionalization, and an age of ≥70 years
In the elderly, factors such as decreased cough and gag
reflexes as well as reduced antibody and Toll-like receptor responses increase the likelihood of pneumonia
29
Risk factors for pneumococcal pneumonia
dementia, seizure disorders, heart failure, cerebrovascular disease, alcoholism, tobacco smoking, chronic obstructive pulmonary disease
(COPD), and HIV infection
30
Risk factors for Legionella infection
diabetes, hematologic malignancy, cancer, severe renal disease, HIV infection, smoking, male gender, and a recent hotel stay or ship cruise
31
Pneumonia clinical manifestations
febrile
tachycardia
or may have a history of chills and/or sweats
Cough may be either nonproductive or productive of
mucoid, purulent, or blood-tinged sputum.
Depending on severity, the patient may be able to
speak in full sentences or may be very short of breath.
If the pleura is involved, the patient may experience pleuritic chest pain.
Up to 20% of patients may have gastrointestinal symptoms such as nausea, vomiting, and/or diarrhea.
Other symptoms may include fatigue, headache, myalgias, and arthralgias.
Findings on physical examination vary with the degree of pulmonary consolidation and the presence or absence of a significant pleural effusion.
An increased respiratory rate and use of accessory muscles of respiration
Increased or decreased tactile fremitus
Percussion note can vary from dull to flat, reflecting underlying consolidated lung and pleural fluid, respectively.
Crackles, bronchial breath sounds, and possibly a pleural friction rub may be heard on auscultation.
The clinical presentation may not be so obvious in the elderly, who may initially display new-onset or worsening confusion and few other manifestations.
Severely ill patients may have septic shock and evidence of organ failure.
The risk of cardiac complications secondary to enhanced inflammation and procoagulant activity is increased. These complications include myocardial
infarction, congestive heart failure, and arrhythmias, particularly in the elderly. In pneumococcal CAP, the increased risk of acute coronary events may
be partially driven by pneumolysis, which increases platelet activation.
Up to 90% of acute coronary syndromes occur in the first week after onset of CAP, and the risk of new-onset congestive heart failure in elderly hospitalized CAP patients can extend up to 1 year.
32
Gross hemoptysis is suggestive of
CA-MRSA pneumonia
33
Differential diagnosis
The differential diagnosis includes both infectious and noninfectious entities such as acute bronchitis, acute exacerbations of chronic bronchitis, heart failure, pulmonary embolism, hypersensitivity pneumonitis, and radiation pneumonitis.
34
What are the exams for etiology diagnosis
- gram stain and culture of sputum
- blood cultures
- urinary antigen test
- PCR
- serology
- biomarkers
35
What can urinary antigen tests detect
detect pneumococcal and Legionella antigen in urine
| can be used even after antibiotic treatment
36
What can PCR be used for
Standard for diagnosis of respiratory viral infection
| Can detect the nucleic acid of Legionella species, M. pneumoniae, C. pneumoniae, and mycobacteria
37
What are the 2 most used substances as markers for severe inflammation
C-reactive protein (CRP) and procalcitonin (PCT)
PCT may play a role in distinguishing bacterial from viral infection, determining the need for antibacterial therapy, or deciding when to discontinue treatment.
38
Treatment of CAP
- Use scores to determine whether to send the patient home or to the hospital (Pneumonia severity index PSI and CURB-65)
- Antibiotics
39
What are the criteria for CURB-65
The CURB-65 criteria include five variables:
confusion (C)
urea >7 mmol/L (U)
respiratory rate ≥30/min (R)
blood pressure, systolic ≤90 mmHg or diastolic ≤60 (B)
and age ≥65 years
With a score of 1 or 2, the patient should be hospitalized unless the score is entirely or in part attributable to an age of ≥65 years.
Among patients with scores of ≥3, mortality rates are 22% overall; these patients may require ICU admission.
40
The main resistance issues currently involve
S. pneumoniae and CA-MRSA.
41
Why do we have beta-lactam resistance
pneumococcal resistance is acquired by direct DNA incorporation and remodeling resulting from contact with closely related oral
commensal bacteria, by the process of natural transformation, or by mutation of certain genes.
Pneumococcal resistance to β-lactam drugs is due solely to low-affinity penicillin-binding proteins.
42
Resistance to macrolides mechanisms
Target-site modification caused by ribosomal methylation in 23S rRNA encoded by the ermB gene results in high-level resistance to macrolides, lincosamides, and streptogramin B–type antibiotics.
The efflux mechanism encoded by the mef gene (M phenotype) is usually associated with low-level resistance.
Pneumococcal resistance to fluoroquinolones (e.g., ciprofloxacin and levofloxacin) has been reported. Changes can occur in one or both target sites
(topoisomerases II and IV) from mutations in the gyrA and parC genes, respectively. In addition, an efflux pump may play a role in pneumococcal
resistance to fluoroquinolones.
43
What is the most important risk factor for antibiotic-resistant pneumococcal infection
the use of a specific antibiotic within the previous 3 months.
44
MRSA
Methicillin resistance in S. aureus is determined by the mecA gene, which encodes for resistance to all β-lactam drugs. At least five staphylococcal chromosomal cassette mec (SCCmec) types have been described. The typical hospital-acquired strain usually has type II or III,
whereas CA-MRSA has a type IV SCCmec element. CA-MRSA isolates tend to be less resistant than the older hospital-acquired strains and are often susceptible to trimethoprim-sulfamethoxazole, clindamycin, and tetracycline in addition to vancomycin and linezolid. However, the most important distinction is that CA-MRSA strains also carry genes for superantigens, such as enterotoxins B and C and Panton-Valentine leukocidin, a membranetropic toxin that can create cytolytic pores in polymorphonuclear neutrophils, monocytes, and macrophages.
45
Initial antibiotic management
Since the etiology of CAP is rarely known at the outset of treatment, initial therapy is usually empirical, designed to cover the most likely pathogens. In all cases, antibiotic treatment should be initiated as expeditiously as possible. Atypical pathogen coverage provided by the addition of a macrolide to a β-lactam or by the use of a fluoroquinolone alone has been consistently associated with a significant reduction in mortality rates compared with those for β-lactam coverage alone.
For the treatment of severe CAP, accumulating data continue to demonstrate the benefits of including a macrolide, such as reduced mortality.
However, two recent studies of patients hospitalized with moderate CAP yielded differing results. One study demonstrated a more rapid return to
clinical stability and fewer adverse events with a β-lactam–macrolide combination than with a β-lactam alone. Using cluster randomization, the second study reported no difference among three regimens—a β-lactam alone, a β-lactam–macrolide combination, and a fluoroquinolone—but had significant design flaws.
If concern exists about macrolide resistance, the patient is otherwise well and has not recently received antibiotics, and the local doxycycline resistance rate among pneumococcal isolates is <25%, doxycycline may be used instead of macrolide monotherapy. Otherwise, a fluoroquinolone or a β-lactam plus a macrolide should be used.
A meta-analysis found ceftaroline to be superior to ceftriaxone as the β-lactam component of IV empirical treatment of CAP in hospitalized patients
in PORT risk class III or IV who have not received prior antibiotics. Clinical response rates for patients infected with S. pneumoniae or S. aureus also
favored ceftaroline. If blood cultures yield S. pneumoniae sensitive to penicillin after 2 days of treatment with a macrolide plus a β-lactam or with a fluoroquinolone alone, should therapy be switched to penicillin alone? The concern here is that a β-lactam alone would not be effective in the
potential 15% of cases with atypical co-infection. No standard approach exists. Some experts think that 3 days of macrolide therapy is adequate for
Mycoplasma infection and that, unless the test for Legionella urinary antigen is positive, treatment can be continued with a β-lactam alone. In all
cases, the individual patient and the various risk factors must be considered.
Management of bacteremic pneumococcal pneumonia is also controversial. Data from nonrandomized studies suggest that combination therapy
(especially with a β-lactam–macrolide combination) is associated with a lower mortality rate than monotherapy, particularly in severely ill patients.
The exact reason is unknown, but possible explanations include an additive or synergistic antibacterial effect, antimicrobial tolerance, atypical coinfection,
or the immunomodulatory effects of the macrolides.
For CAP patients admitted to the ICU, the risk of infection with P. aeruginosa or CA-MRSA is increased. Empirical coverage should be considered
when a patient has risk factors or a Gram’s stain suggestive of these pathogens. If CA-MRSA is suspected, either linezolid or
vancomycin—with or without clindamycin to inhibit toxin production—can be added to the initial empirical regimen.
46
Concerns about vancomycin
vancomycin’s loss of potency against MRSA, poor penetration into epithelial lining fluid, and lack of effect on toxin production relative to linezolid.
47
What are adjunctive measures
In addition to appropriate antimicrobial therapy, certain adjunctive measures should be used. Adequate hydration, oxygen therapy for hypoxemia, vasopressors, and assisted ventilation when necessary are critical to successful treatment.
48
If the patient truly has CAP and empirical treatment is aimed at the correct pathogen, lack of response may be explained by
The pathogen may be resistant to the drug selected, or a sequestered focus (e.g., lung abscess or empyema) may be blocking access of the antibiotic(s) to the
pathogen.
The patient may be getting either the wrong drug or the correct drug at the wrong dose or frequency of administration.
Another possibility is that CAP is the correct diagnosis but an unsuspected pathogen (e.g., CA-MRSA, M. tuberculosis, or a fungus) is the cause.
Nosocomial superinfections—both pulmonary and extrapulmonary—are other possible explanations.
In all cases of delayed response or worsening condition, the patient must be carefully reassessed and appropriate studies initiated,
possibly including procedures such as CT or bronchoscopy.
COMPLICATIONS
Complications of severe CAP include respiratory failure, shock and multiorgan failure, coagulopathy, and exacerbation of comorbid illnesses. Three
particularly noteworthy conditions are metastatic infection, lung abscess, and complicated pleural effusion. Metastatic infection (e.g., brain abscess
or endocarditis) is very unusual and will require a high degree of suspicion and a detailed workup for proper treatment. Lung abscess may occur in
association with aspiration or with infection caused by a single CAP pathogen, such as CA-MRSA, P. aeruginosa, or (rarely) S. pneumoniae.
Aspiration pneumonia is typically a polymicrobial infection involving both aerobes and anaerobes. A significant pleural effusion should be tapped
for both diagnostic and therapeutic purposes. If the fluid has a pH of <7, a glucose level of <2.2 mmol/L, and a lactate dehydrogenase concentration
of >1000 U/L or if bacteria are seen or cultured, it should be completely drained; a chest tube is often required, and video-assisted thoracoscopy
may be needed for late treatment or difficult cases.
FOLLOW-UP
Fever and leukocytosis usually resolve within 2–4 days in otherwise healthy patients with CAP, but physical findings may persist longer. Chest
radiographic abnormalities are slowest to resolve (4–12 weeks), with the speed of clearance depending on the patient’s age and underlying lung
disease. Patients may be discharged from the hospital once their clinical conditions, including comorbidities, are stable. The site of residence after
discharge (nursing home, home with family, home alone) is an important discharge consideration, particularly for elderly patients. For a
hospitalized patient, a follow-up radiograph ~4–6 weeks later is recommended. If relapse or recurrence is documented, particularly in the same lung
segment, the possibility of an underlying neoplasm must be considered.
49
How to prevent pneumonia
The main preventive measure is vaccination.
influenza and pneumococcal vaccines.
A pneumococcal polysaccharide vaccine (PPSV23) and a protein conjugate pneumococcal vaccine (PCV13)
Administration of this vaccine to children has led to an overall decrease in the prevalence of antimicrobial-resistant pneumococci and in the incidence of invasive pneumococcal disease among both children and adults.
The influenza vaccine is available in an inactivated or recombinant form. In the event of an influenza outbreak, unprotected patients at risk from complications should be vaccinated immediately and given
chemoprophylaxis with either oseltamivir or zanamivir for 2 weeks—i.e., until vaccine-induced antibody levels are sufficiently high.
50
What are the complications of severe CAP
Respiratory failure, shock and multiorgan failure, coagulopathy, and exacerbation of comorbid illnesses. Three particularly noteworthy conditions are metastatic infection, lung abscess, and complicated pleural effusion. Metastatic infection (e.g., brain abscess
or endocarditis) is very unusual.
Lung abscess may occur in association with aspiration or with infection caused by a single CAP pathogen, such as CA-MRSA, P. aeruginosa, or (rarely) S. pneumoniae.
Aspiration pneumonia is typically a polymicrobial infection involving both aerobes and anaerobes. A significant pleural effusion should be tapped for both diagnostic and therapeutic purposes. If the fluid has a pH of <7, a glucose level of <2.2 mmol/L, and a lactate dehydrogenase concentration of >1000 U/L or if bacteria are seen or cultured, it should be completely drained; a chest tube is often required, and video-assisted thoracoscopy may be needed for late treatment or difficult cases.
51
Follow up
Fever and leukocytosis usually resolve within 2–4 days in otherwise healthy patients with CAP, but physical findings may persist longer. Chest radiographic abnormalities are slowest to resolve (4–12 weeks), with the speed of clearance depending on the patient’s age and underlying lung disease. Patients may be discharged from the hospital once their clinical conditions, including comorbidities, are stable. The site of residence after discharge (nursing home, home with family, home alone) is an important discharge consideration, particularly for elderly patients. For a
hospitalized patient, a follow-up radiograph ~4–6 weeks later is recommended. If relapse or recurrence is documented, particularly in the same lung
segment, the possibility of an underlying neoplasm must be considered.
52
Antibiotique de choix pour PAC
amoxicilline
53
Si prise en charge en ambulatoire, reevaluation dans....
48 heures
54
Top 5 most common pneumonia pathogens
1. Streptococcus pneumoniae
2. Virale
3. Heamophilus influenzae
4. Staphylococcus aureus
5. Moraxella catarallis
intracellular: mycoplasma pneumoniae, legionella, chlamydia
55
Quel score est recommande en ambulatoire
CRB-65
56
Quel score est recommande en ambulatoire
CRB-65
| 1 ou plus sauf si age seul critere
57
Quel score est recommande en hospitalier
CRUB-65
| 2 ou plus pour hopital
58
Comment distinguer une pneumonie d'une bronchite
radio du thorax
59
ttt pour pneumonie non severe SANS comorbidites
amoxicilline
60
ttt pour pneumonie non severe AVEC comorbidites
amoxicilline-clavulanate
| meilleure couverture sur MSSA, enterobacteries et anaerobes
61
En cas d'epidemie de grippe et PAC confirmee, quel est le ttt
ttt empirique d'oseltavimir
| pour personnes immunosupprimes et femmes enceintes
62
Are corticoides recommended ?
not in ambulatoire (faible a moderee)
63
Arret de travail ?
Oui, 5-7 jours
64
deux aspects dans la validation interne
discrimination: capacité du test à séparer les sujets qui présentent ou non la maladie. Elle a évidemment un lien avec la sensibilité (la proportion d’individus malades avec un test positif) et la spécificité (la proportion d’individus non malades avec un test négatif) du test. La discrimination est donc une qualité fondamentale des scores diagnostiques, puisqu’ils visent à
déterminer l’absence ou la présence d’une maladie.
On peut ensuite exprimer la discrimination de deux façons : graphiquement ou statistiquement, le lien entre les deux méthodes étant «l’aire sous la courbe».
L’expression graphique de la discrimination d’un score
se fait par la courbe ROC (Receiver operating characteristic), qui est le tracé des valeurs de la sensibilité en fonction du complément de la spécificité (= 1- spécificité).
L'expression statistique de la discrimination est la statistique c. Elle représente la probabilité que lorsqu’une paire d’individus avec et sans maladie est tirée au hasard, les individus réellement malades
présentent une probabilité de maladie plus élevée
que les individus non malades.
La statistique c correspond globalement à l’aire sous la
courbe ROC. Elle est au minimum de 0,5 (dans le cas d’une droite à 45°) et au maximum de 1 (droite verticale).
Calibration:
Principes théoriques
Avec la discrimination, vous savez si votre score distribue dichotomiquement (malades/pas malades) vos patients de façon correcte.
L’étape suivante consiste à déterminer dans quelle mesure le risque prédit est proche du risque réel. Par exemple, lorsque le seuil est fixé à une probabilité de 60% (les individus avec probabilité L 60% d’avoir la maladie sont classés comme malades), vous souhaitez savoir si votre score prédit un risque proche de 80, 90 et 100% aux individus dont le risque réel est, effectivement, de 80, 90, et 100% : c’est la calibration.
Pour évaluer cette calibration, on compare le nombre
d’événements prédits et le nombre réellement observé. Il y a là aussi deux moyens d’exprimer la calibration : graphique et statistique.
Le diagramme en barre (histogramme) est la représentation graphique la plus courante de la calibration d’un SC.
En général, on divise le risque prédit en dix catégories égales (ou déciles) que l’on reporte sur l’abscisse. Pour chacun des dix groupes de risques, on reporte en ordonnée le risque prédit et le risque observé. Si, pour chaque groupe, les barres prédites sont proches des barres observées et si la taille des barres augmente avec les groupes de risques, alors le score est bien calibre.
L’expression statistique de la calibration est le test d’Hosmer-Lemeshow qui suit une distribution de X2. Pour la calibration, on souhaite que la distance entre les risques prédits et les risques observés soit suffisamment proche pour conclure qu’il n’y a pas de différence.
65
Validation externe
reproductibilite(meme population) et transportabilite (population differente)
66
What if the patient is allergic to penicillin
Ceftriaxone
67
What are the 2 anatomic patterns for bacterial pneumonia
- lobar bronchopneumonia: patchy
| - lobar pneumonia: the whole lobe
68
Complications of pneumonia
- dissemination to the heart, liver....
- tissue destruction and necrosis and formation of absess
- spread to the pleural cavity causing an empyema
69
Is the radiology enough to say that the patient has persistant pneumonia ?
No, because radio does not get better until a few weeks later
70
Role de quelle imagerie dans le diagnostic d'une pneumonie persistante
CT scan
71
Causes infectieuses de pneumonie persistante
- Germes resistants (Les Haemophilus influenzae et Pseudomonas aeruginosa multirésistants ainsi que les staphylocoques dorés résistant à la méticilline (SARM) sont de plus en plus fréquemment rencontrés.)
- Complications infectieuses: epanchement parapneumonique, abces pulmonaire, infection metastatique
- Germes inhabituels: mycobacteries, Pneumocystis jirovecii, pneumonies fongiques
- Pneumonies virales: CMV chez immunosupprimes
72
Causes non infectieuses
-Neoplasie: cause une obstruction bronchique
-Causes inflammatoires: La pneumonie organisée (cryptogénique = COP) est une inflammation à prédominance intra-alvéolaire avec un remplissage des alvéoles et des bronchioles terminales par du tissu conjonctif.
Les vasculites systémiques avec atteinte pulmonaire peuvent mimer une pneumonie. Les plus fréquentes sont la granulomatose avec polyangéite (Wegener) et le syndrome hémorragique alvéolaire.
Une pneumonie à éosinophiles, dans sa forme aiguë avec infiltrats diffus ou dans sa forme chronique avec infiltrats à prédominance périphérique sous-pleurale.
Une sarcoïdose peut être identifiée comme une pneumonie, en cas d’atteinte parenchymateuse surtout si l’atteinte ganglionnaire est absente ou minime.
Parmi les pneumopathies interstitielles, la pneumonie interstitielle aiguë (diffuse alveolar damage) entre dans le diagnostic différentiel, devant un infiltrat en verre dépoli diffus ou pavimenteux. Le pronostic de cette entité est sombre.
La protéinose alvéolaire pulmonaire, traduisant une accumulation de substance lipoprotéinique dans les alvéoles, est associée à un infiltrat de type crazy paving.
-Pneumopathie medicamenteuse: amiodarone, le méthotrexate, la nitrofurantoïne et la bléomycine. inhibiteurs tyrosine kinase
-embolie pulmonaire, oedeme pulmonaire cardiogene,, pneumopathie postradique
73
When to do a radio
after 6 weeks
74
Place de la bronchoscopie dans diagnostic pneumonie persistante
pour examen microbiologique
Une prédominance neutrophilique > 50 % oriente vers une pneumonie bactérienne ou un dommage alvéolaire
diffus. Une lymphocytose alvéolaire > 25 % fait suggérer
une pneumopathie interstitielle, médicamenteuse ou
virale.
75
Pleural injury is associated with
fibrin deposition
76
The injection of... can stimulate pleural fluid production
t-PA
| plasminogen activator
77
The pleural milieu favours the flourishing of which organisms
anaerobic organisms as well as the facultative anaerobic Viridans streptococci
78
What is the most powerful clinical indicator to chest tube drainage
pleural fluid pH < 7.2
79
How to treat pleural effusion
- Antibiotics
- good nutrition
- chest drain
- intrapleural fibrinolytic therapy
- thoracoscopy
- surgery
80
What is transudative pleural effusion
occurs when systemic factors that influence the formation and absorption of pleural fluid are altered. The leading causes of transudative pleural effusions in the United States are left ventricular failure and cirrhosis.
81
What is exudative pleural effusion
An exudative pleural effusion occurs when local factors
that influence the formation and absorption of pleural fluid are altered. The leading causes are bacterial pneumonia, malignancy, viral infection, and pulmonary embolism.
82
How do we distinguish clinically between transudative and exudative
measuring LDH and protein levels in the pleural fluids
83
What are the criteria for exudative pleural effusion
Exudative pleural effusions meet at least one of the following criteria, whereas transudative pleural effusions meet none:
1. Pleural fluid protein/serum protein >0.5
2. Pleural fluid LDH/serum LDH >0.6
3. Pleural fluid LDH more than two-thirds the normal upper limit for serum
These criteria misidentify ~25% of transudates as exudates. If one or more of the exudative criteria are met and the patient is clinically thought to have
a condition producing a transudative effusion, the difference between the protein levels in the serum and the pleural fluid should be measured. If this
gradient is >31 g/L (3.1 g/dL), the exudative categorization by these criteria can be ignored because almost all such patients have a transudative pleural
effusion.
