acute 2/ acute exacerbation of copd asthma 3 ... - · pdf file1/ acute asthma 2/ acute...

1/ Acute asthma

2/ Acute exacerbation of COPD

3/ Pneumonia

4/ Pneumothorax

Pascal Van BleyenberghDepartment of Pulmonology, UZ Leuven

AcuteAsthma

Pascal Van BleyenberghDepartment of Pulmonology, UZ KULeuven

allergensexercisecold airSO2 ,…

symptoms

hyperreactivityairflow

limitation

inflammationallergens

?

Asthma is a chronic inflammatory disorder of the airways

GINA 2015; www.ginasthma.org

Asthma in ER is not a frequent problem

prevalence of atopy 17–44%prevalence of asthma 5-6%<20% of asthmatics have been seen/admitted for an acute asthma exacerbation acute severe asthma ≤5% of all ER visits

ER & hospitalization >50% of total asthma costs

30% 4-7%

Asthma mortality rate is decreasing

mortality rate of 5,2/100.000 (US data)

rate decreasing: -8%status asthmaticus: 0-21% in hospital mortalityafter near-fatal attack: 26% 6-year mortality

Belgium<20pts/year

USA5.000/year

worldwide150.000/year

post-discharge management !!

Correct management- exposition- anti-inflammatorytreatment

- education

Risk factors of death from asthma attack - 1

60% female 45% age <25 years(chronic) Severe asthma

asthma history ≥15 years, ≥3 types of asthma medicationprevous use of systemic corticosteroids>2 canisters of SA β2-agonists / monthhigh degree of bronchial hyperresponsivenessprevious ER visits or ICU/hospital admissionsprior intubation for asthma

Smoking - illicit drug use - environmental factors

Co-morbidityobesity, cardiovascular, pulmonary, GERD,….

Alvarez GG et al. Can Respir J 2005; 12:265-270

Risk factors of death from asthma attack - 2

Medication: aspirin - β-blokker – NSAID - …Psychosocial problems

Low socioeconomical status Adherence and compliance with therapy inhaled steroids!

Blunted perception of airway obstruction

poor perception of dyspnea “underperceivers”

Genetic factors IgE, steroid responsiveness, TNFα in airways,

β-agonist responsivenes, …

Alvarez GG et al. Can Respir J 2005; 12:265-270

Phenotypes of acute asthma attack

Restrepo RD, Peters J. Curr Opin Pulm Med 2008; 14:13-23

Assessment of acute asthma

History/clinical examinationnonspecific – absence does not excude severe attack

O2sat, ABGtitration of O2therapy (94-98%)SpO2 >92%: hypercapnia rarehypercapnia severity of attack!

Laboratory datahypokalemia, leukocytosis (eos.), lactate,…

Chest radiographECGPulmonary function test

serial PEFR, FEV1 (bedside)

Assessment of acute asthma

GIN

A 20

15; w

ww.

gina

sthm

a.or

g

Assessment of acute asthmaseverity

BTS guidelines 2009; www.brit-thoracic.org.uk

Conditions mimicking an acute asthma attack

upper airway obstruction(VCD, tumor, stricture or foreign body)



AECOPD

patient characteristics

history of disease

Assessment of acute asthmadifferentiation with AECOPD…

ASTHMA

young age, sudden onset

atopy, familial history

episodic symptoms

reversible airway obstruction

serum IgE, airway inflammation (eosinophils, mastcells,

Th2 lymphocytes)

bronchial hyperresponsivenessidentifiable triggers

COPD

>40-60 years

smoking history

progressively worsening symptoms

not fully reversible airway obstruction

airway inflammation(macrophages, neutrophils)

chronic sputum expectoration, emphysema (parenchymal destruction)



AECOPDcongestive heart failurepulmonary embolismbronchopneumoniabronchiectasis vasculitis (Churg Strauss, ..)carcinoid syndromehyperventilation syndrome…

Management of acute asthma treatment

standard therapyoxygenbronchodilatorscorticosteroids (PO-IV-SC-inhalation)

additional therapy?MgSO4

-agonists SC or IVmethylxanthines...

(non)invasive ventilationprevention of future asthma attacks

Lazarus SC. New Engl J Med 2010; 363:755-764Papiris SA et al. Drugs 2009; 69(17):2363-2391

ALL PATIENTS!

Management of acute asthma:1/ oxygen

Hypoxemia= important cause of acute asthma-related death

supplemental oxygenO2 saturation ≥90-93%no RCT: "common sense" based medicineFiO2 28-32% is sufficient most of the timeshumidification recommended

hypoxemia may persist upon resolution of asthma attacknebulisation with oxygen! (10-12L/min)

Management of acute asthma:2/ inhaled 2-agonists

mechanism of action:bronchodilatation (+ other effects…)fast onset of action (5 min)

clinical benefit:acute symptoms of asthmamild, moderate & severe asthma attack

to be given immediately, on presentation!short-acting 2-agonists

salbutamol (= albuterol)formoterol(terbutaline), (fenoterol), R-enantiomer of albuterol (levalbuterol): improved bronchodilatation?adrenaline, isoprenaline: less selective!

Management of acute asthma:2/ inhaled 2-agonists

administration:nebulized salbutamol

dosing: 2,5–5mg q 15-20min for 1h2,5–5mg salbutamol q 1 h for 4-5 h2,5–5mg salbutamol q 4 h or on demand(2,5mg 10 dr Ventolin®)

continuous better than repetitive? (FEV1<30%)MDI with spacer

as effective as nebulization !dosing: 400-600 µg salbutamol ( 4-6 puffs Ventolin®)

q 10min for 1 hq 1h for 4 h q 4h or on demand

patient coordination and supervision required!!

side effects: tremor, tachycardia, hypokalemia

Management of acute asthma:2/ 2-agonists SC - IV

2-agonists SC or IV (or PO)

conflicting evidence: no clear advantage of IV or SC administration over inhaled routeindications

inability to administer inhaled medicationinadequate response to inhaled therapy(severe refractory asthma?)

administrationIV salbutamol 0,5-30µg/kg/minSC epinephrine 0,3mg q20 min for 1h

more side effects !

Management of acute asthma:2/ inhaled anticholinergics

mechanism of action:bronchodilatation, less potent than 2-agonistsslower onset of actionadditive to 2-agonists (other mechanism!)

clinical benefit:improvement of FEV1 and PEFRreduction in admission rate

indication:adjunct to 2-agonists & steroidsmore severe disease (FEV1 <35%)

administration:nebulization

0,5 mg ipratropium bromide ( 20 dr or 1 MD Atrovent®)q 20 min for 1 h, continue q 4 h if improvement

MDI with spacer 80-160 µg ipratropium bromide ( 4-8 puffs Atrovent®) q 10-20 min for 1 h, continue q 4 h if improvement

no benefit of nebulized atropine

Rodrigo GJ et al.Thorax 2005; 60:740-746

Management of acute asthma:3/ corticosteroids - systemic

mechanism of action:anti-inflammatory effectimprovement of 2-induced bronchodilatationslow onset of action: improvement 6-12 h after first dose

clinical benefit:'common practice'more rapid improvement of lung function, fewer hospitalizations & lower rate of relapse (although only small RCT…)

indications:ALL moderate to severe attackspoor response to 2- agonistspts already on steroids (or need of steroid use in prior attacks)

administration:prednisone 50-100mg q 24 h or methylprednisolone 40-80mg q 24 horal therapy equivalent to IVcontinue steroids >5-10d (0,5-1mg/kg/d po, stop without tapering)

side effects: hyperglc, mood alteration, hypertension, …

Sherman MS et al. Clin Pulm Med 2006;13:315-320Krishnan JA et al. Am J Med 2009;122:977-991

Management of acute asthma:3/ corticosteroids - inhaled

rationaletopical anti-inflammatory effectquicker onset of action (<3h)

clinical benefitunequivocal study resultssmall benefit: slight improvement of FEV1 and reduction of admission rate (3 meta-analyses)

indications:treatment of chronic asthmaexacerbation & mild asthma attacksevere asthma attack ?post discharge

administration: high dose (250-500 µg fluticasone or 400 mg budesonide q10min for 3h)no severe side effects

NO SUBSTITUTE FOR SYSTEMIC STEROIDS !!

Management of acute asthma:4/ additional therapy

magnesium sulphatemechanism of action:

bronchodilationeffect on inflammation

resultssmall improvement of FEV1 for <4h reduction in admission rate

pts with severe asthma or FEV1<30%pred 2g MgSO4 IV over 20 minsingle or q30min? (max 12g/12h)nebulized MgSO4 (135-1152mg) : less evidence!

Rowe BH et al. Curr Opin Pulm Med 2008; 14:70-76


anti-leukotriene antagonist po - ivmechanism of action

anti-inflammatorybronchodilatation

clinical benefitweak but significant improvement of FEV1 -dyspneano reduction of admission rate (?)additive to 2-agonists & steroidsrapid onset of action (IV>>PO; <1-2hrs)

montelukast, zafirlukastno side effects

not recommended for routine useCamargo CA et al. J Allergy Clin Immunol 2010; 125:374-380


methylxanthinesbronchodilatation, anti-inflammmatoryinsufficient evidence of benefit

inferior to 2-agonists small effect on FEV1 & exacerbation rate?

side effects!!only for very severe refractory asthma?0,4 mg/kg/h IV (serum level 8-15µg/ml)

not recommended for routine use!

Parameswaran K et al. Cochrane Database Syst Rev 2000; 4:CD002742


helium-oxygen mixtures70-80% He & 20-30% O2 (density one third of air)mechanism of action

decrease airway resistance & hyperinflationimprove deposition of aerosolized bronchodilators

evidence of benefit in severe refractory attacks

experimental options: no routine useinhaled anesthetics: halothane, enflurane (case reports)nebulized lidocaïne(inhaled furosemide)

antibiotics: not routinely indicated!!contra-indicated

inhaled mucolyticssedation

Rodrigo G et al. Cochrane Database Syst Rev 2006; 4:CD002884

Management of acute asthma: treatment summary

Triage patient immediately- history of risk factors- vital signs and suymptoms

Oxygen(sat ≥90-94%)

Short-acting ß2-agonist +/- anticholinergic* nebulizer q20’ for 1h

*nebulizer q1hr or continuously

Oral/IV corticosteroids40mg methylprednisolone q12hrs

Continue treatmentfor 1-3 hrs

Discharge oradmission?

Consider magnesium sulfate2g IV once

Consider heliox

Consider NIPPVIntubation & ventilation

(bedside decision!!!)

Management of acute asthma: discharge or admission

discharge home

admit to hospital

admit to ICU

asthma action planmedical follow-up

• continue other treatment options

• possible intubation and ventilation

continue treatment

improvement no improvement

good responsePEF ≥70% for >1h

incompleteresponse

PEF 40-69%

poor responsePEF <40%

deteriorationpCO2 ≥42 mmHg

severe symptoms

Complications of asthma

mucous plugging and atelectasispneumonia (VAP!!)electrolyte disturbances (hypokalemia in 17%)hyperglycemialactic acidosisbarotrauma (≥4%): pneumothorax, pneumomediastinum, pneumopericardium, SC emphysemamyopathy (10-30%)myocardial infarct, arrhythmia,CV collapseanoxic brain injuryin hospital mortality 0-21%

Management of acute asthmapost ICU/ED care

(observe on ICU for >24h after extubation)course of oral steroids at dischargeadequate inhaled treatment:

= inh. steroids + long-acting 2-agonists + rescue therapy

check inhaler techniqueuse PEF meterformulate 'exacerbation action plan' with patient (cave ‘underperceivers’!)identification and avoidance of triggersregular follow-up care

COPDexacerbations

Pascal Van BleyenberghDepartment of Pneumology, UZ KULeuven

Sustained worsening of the patient’s symptoms (breathlessness, cough, sputum production, change in sputum colour) from his or her usual stable state that is beyond normal day-to-day variations, and acute in onset

AECOPD - definition

Rodriguez-Roisin Chest 2000; 117: 398 Burge et al. Eur Resp J 2003; 41: 46s

Celli et al. (ERS/ATS) Eur Resp J 2004; 23: 932GOLD guidelines, update 2015

AECOPD: significant events in natural history of COPD

Increased mortalitywith exacerbationhospitalizations

Accelerateddeclinein FEV1

Reducedhealth-relatedquality of life

Exacerbations

Increasedhealth resource utilization anddirect costs

• INFECTIOUS– Bacteria– Viruses– Mixed

AECOPD: etiology

35

• NON-INFECTIOUS– Pollution– Medication errors– …

The cause may be unidentifiablein up to 30% of exacerbations!

• “Frequent exacerbator” – phenotype(≥2 exacerbations per year)

Hurst JR et al. N Engl J Med 2010; 363: 1128-1138

AECOPD: bacterial pathogens

Balter et al. Can Med Assoc J. 1994;151,S5Eller et al. Eur Resp J. 1996;9, S107

Acutebronchitis

FEV

1 %

Acute exacerbations of COPD

Viruses, allergens, air pollution, smoking

M catarrhalisEnterobacteriaceae Pseudomonas sppGram - ,resistance

H influenzae, S pneumoniae, Gram + cocci

M pneumoniae, C pneumoniae

• Pneumonia• Pneumothorax• Pulmonary embolus• Lung cancer• Upper airway obstruction• Pleural effusion• Recurrent aspiration

• Left ventricular failure• Cardiac ischemia/myocardial infarction

• …

AECOPD: differential diagnosis

37

• Use of respiratory muscles• Paradoxical chest wall movement• Worsening or new central cyanosis• Development of peripheral edema• Hemodynamic instability• Deteriorated mental status

AECOPD: assessmentClinical signs of severity

38

• Inadequate respons to initial emergency therapy• Changes in mental status (confusion, lethargy, coma)• Persistent or worsening hypoxemia or respiratory

acidosis (pH <7,25mmHg)• Need for invasive mechanical ventilation• Hemodynamic instability - Need for vasopressors

• Full blood count & biochemistry (electrolytes, glycemia,…)

• Theophylline level (in pts on theophylline therapy)

• Arterial blood gases+ record inspired oxygen concentration!!

• Sputum for microscopy and culture (if purulent)

• Blood cultures (if pt is pyrexial)

• ECG• Chest X-ray

• Lung function tests not for routine use

AECOPD: assessmentUsefull diagnostic tests

39

A = Antibiotics

AECOPD: the A-B-C approach

40

AECOPD: antibiotics or not?

Saint et al. JAMA 1995; 273: 957

–1.0 1.0–0.5 1.50 0.5

Elmes et al. 1957Berry et al. 1960

Fear and Edwards. 1962Elmes et al. 1965

Petersen et al. 1967Pines et al. 1972

Nicotra et al. 1982Anthonisen et al. 1987Jorgensen et al. 1992

Overall

Pro placebo Pro antibiotica

Effect size

1. Anthonisen criteria Ann Intern Med 1987; 106: 196-204

a) dyspnea Bach Ann Intern Med 2001; 134: 600

b) increase in sputum productionc) increase in sputum purulence

2. Severity of underlying COPD Soler et al. Thorax 2007; 62: 29

FEV1 <50% antibiotics

3. Respiratory failure Nouira et al. Lancet 2001; 358: 2020

AECOPD: when antibiotics?

Difficult differential diagnosis 1/ infectious >< non-infectious

2/ bacterial >< viral

AECOPD: indications for antibiotics

FEV1 >80% FEV1 50-80% FEV1 <50%

Anthonisen 3/3 NO YES YES

Anthonisen 2/3(incl. sputum purulence)

NO YES YES

Anthonisen 1/3 NO NO YES

Acute respiratory failure YES YES YES

IDAB guidelines 2010Sanford guide, Belgian edition, 2013-2014

AECOPD: antibiotics

* Antibiotics almost always necessary in hospital

* Oral route is preferred

* Sequential therapy if intravenously started! (day 3)

1. Mild to moderate COPD (FEV1 <50%)

2. Severe to very severe COPD (FEV1 <50%),without risk-factors for P. aeruginosa

3. Severe to very severe COPD (FEV1 <50%),with risk-factors for P. aeruginosa

AECOPD: antibiotics

1/ Mild to moderate COPD (FEV1 >50%)

amoxicilline-clavulanic acid875/125 mg tid or 2000/125 mg bid ‘retard’ PO

first choice

moxifloxacine400 mg dd PO

first choice if allergic or intolerant to -lactams alternative in patients with frequent (≥3)

exacerbations: CYCLING !

IV: amoxicilline-clavulanic acid 1 g qid

Sanford guide, Belgian edition, 2013-2014

AECOPD: antibiotics

2/ Severe or very severe COPD (FEV1 <50%),without risk-factors for P. aeruginosa

IV: amoxicilline-clavulanic acid 1 g qid

first choice

PO/IV moxifloxacine400 mg dd

first choice when oral therapy is possible first choice if allergy or intolerance to -lactams alternative in patients with frequent (≥3) exacerbations

(CYCLING !)


Risk factors for P. aeruginosa

1. Recent hospitalisation

2. Frequent use of antibiotics (>4 in past 12 months)

or recent use of antibiotics (last 3 months)

3. Very severe COPD (i.e. FEV1 <30%)

4. Isolation of P. aeruginosa during previous AECOPD

or colonisation during stable periods

5. Presence of bronchiectasis

Eller et al. Chest 1998; 157: 1542Miravitlles et al. Chest 1999; 116: 40

Woodhead et al. ERS Task force. Eur Resp J 2005; 26: 1138

AECOPD: antibiotics

3/ Severe or very severe COPD (FEV1 <50%),with risk factors for P. aeruginosa

ciprofloxacine400 mg tid IV - 750 mg bid PO

IV anti-pseudomonas -lactamsceftazidime 2 g tid – cefepime 2 g tid – piptazo 4 g qid

Combination therapy (with aminoglycoside or FQ) is to be considered with sepsis, invasive infection or mechanical ventilation!

GHB: levofloxacine(500mg bid PO)


B = Bronchodilators– Improve symptoms and FEV1

– MDI = nebuliser use (but…)– Nebuliser driven by compressed air, not oxygen– Increasing dose and/or frequency of short-acting BD– Combine β2-agonists and anticholinergics– Theophyllines only to be used as second-line therapy (significant

side effects, only modest and inconsistent beneficial effects)

AECOPD: the ABC approach

49

Celli BR et al. Eur Respir J 2004; 23: 932-946NICE Guidelines, 2010

GOLD Guidelines, 2015

Salbutamol 2,5mg + Ipratropium 0,5mg, qid (Combivent®)Fenoterol 1,25mg + Ipratropium 0,5mg, qid (Duovent®)

C = Corticosteroids– Improve symptoms, FEV1 and PaO2 in moderate/severe

AECOPD– Reduce treatment failure, relapse and LOS– Oral route is preferred– Induce possible side effects (hypoglycemia, …)

AECOPD: the ABC approach

50

Niewoehner DE et al. N Engl J Med 1999; 340: 1941-1947Aaron SD et al. N Engl J Med 2003; 348: 2618-2625

De Jong YP et al. Chest 2007; 132: 1741-1747Walters JA et al. Cochrane Database Syst Rev 2011; 10: CD006897


30-40mg prednisolonefor 5(-10) days

= 32mg methylprednisolone

Oxygen– Key component of therapy – CAVE hypercapnia!!– Titrated to target saturation of 88-92% ( 1-2 L/minute)– Check ABG after 30-60 minutes!

AECOPD: beyond ABC…

51

Austin MA ete al. BMJ 2010; 341: 5462

Noninvasive mechanical ventilation– Success rate of 80-85%– Improves respiratory acidosis– Decreases respiratory rate, work of breathing, severity of

breathlessness, complications of IPPV, LOS– Reduces mortality and intubation rates

Brochard L et al. N Engl J Med 1995; 333: 817-822Kramer N et al. Am J Respir Crit Care Med 1995; 151: 1799-1806

Plant PK et al. Lancet 2000; 355: 1931-1935

• Respiratory acidosis (pH ≤7,35 and/or PaCO2 ≥45mmHg)

• Severe dyspnea with clinical signs suggestive of respiratory muscle fatigue, increased work of breathing, or both(use of respiratory accesory muscles, paradoxical motion of the abdomen, retraction of intercostal spaces,…)

AECOPD: indications for NIPPV

52

Consensus report. Chest 1999; 116: 521-534Int Consensus Conference in Intens Care Med. Am J Respir Crit Care Med 2001; 163: 283-291

Lightowler JV et al. BMJ 2003; 326: 185GOLD Guidelines, 2015

Practical considerations

• Start as soon as needed• Experienced team• Dedicated setting• Settings:

– S/T (spontaneous/timed) with back-up rate 10-15/minute)– IPAP 10cmH2O, 16-20cmH2O– EPAP 4cmH2O (increase if problem of oxygenation)– Check PaCO2, pH, PaO2 and respiratory rate within 60min

• No success after 60-120min: intubation!

AECOPD: NIPPV

53

AECOPD: indications for IPPV

54

Conti G et al. Intensive Care Med 2002; 28: 1701-1707Esteban A et al. JAMA 2002; 287: 1450-1458


Unable to tolerate NIV or NIV failure Respiratory or cardiac arrest Respiratory pauses with loss of consciousness of gasping for

air Diminished consciousness, psychomotor agitation

inadequately controlled by sedation Massive aspiration Persistent inability to remove respiratory secretions Heart rate <50/miniute with loss of alertness Severe hemodynamic instability without response to fluids and

vasoactive drugs Severe ventricular arrythmias Life-threatening hypoxemia in patients unable to tolerate NIV

AECOPD: summary

55GOLD Guidelines, 2015

Pneumonia


Pneumonie

1. Community-acquired (CAP)

2. Health-care associated (HCAP)

3. Hospital-acquired (HAP)

* Ventilator associated (VAP)

CAP: definitie= pneumonie, ontstaan buiten het ziekenhuis (‘thuis ’) of 72uur

na ontslag uit ziekenhuis

frequente en ernstige ziekte, ondanksbeschikbaarheid van krachtige antibiotica en effectieve vaccins !

- zesde doodsoorzaak ter wereld- meest lethale infectie

alle leeftijden 5-15/1000/jaar>65 jaar 20/1000/jaar>75 jaar 34/1000/jaar

21%-44% hospitalisatie

opname op ICU 5%-10%

CAP: epidemiologie

1900 1950 2000

Mortaliteit:- outpatients 1%- 5%- inpatients

- CAP III 6%-14%- CAP IV 36%-60%

- 18-44 jaar <1%- >65 jaar 12,5%

Gilbert K, Fine MJ. Semin Respir Infect 1994Marston et al, Arch Intern Med 1997

Gegevens van de ziekenhuizen in de VSPatiënten ≥12 jaar met bacteriële pneumonie

Gegevens van de ziekenhuizen in de VSPatiënten ≥12 jaar met bacteriële pneumonie

Meta-analyse

Gehospitaliseerde, ambulante en ICU, CAP

patiënten >18 jaar

Meta-analyse

Gehospitaliseerde, ambulante en ICU, CAP

patiënten >18 jaar

Gegevens van ziekenhuizen in de VS

CAP patiënten<2 jaar -> 65 jaar


CAP patiënten<2 jaar -> 65 jaar


CAP-patiënten >18 jaar


CAP-patiënten >18 jaar

12.3%MORTALITEIT

(N=4432)

12%MORTALITEIT

(N=5837)

~12%MORTALITEIT

(N=730)

12.2%MORTALITEIT

(N=1130)

1966 -1995

1995 -1997

1999 -2001

1952 -1962

Austrian R et al. Ann Intern Med 1964; 60: 759Fine MJ et al. JAMA 1996; 274: 134

Feikin DR et al. Am J Pub Health 2000; 90: 223Restrepo MI et al. Chest 2008; 133: 610

Mortaliteit CAP over tijd…

CAP: oorzaken

Welte T et al. Thorax 2012; 67: 71

Typische vs. atypische pneumonie

Mycoplasma pneumoniaeChlamydophila pneumoniaeLegionella species

Virussen

Streptococcus pneumoniaeHaemophilus influenzaeMoraxella catarrhalis

Enterobacteriaceae

Legionella species

…

β-lactam antibiotica macrolidenfluoroquinolones

Atypisch Typisch

Anamnese jonge patiënten oudere patiëntengeen co-morbiditeit productieve hoestdroge hoest hoge koorts, rillingenviraal syndroom dyspneegeen pleurale pijn pleurale pijninsidieus begin plots begin

Kliniek niet altijd crepitaties crepitatiesmineure klachten consolidatie

Labo lage leucocytose hoge leucocytose geen neutrofilie neutrofilie

Radiologie wazige infiltraten alveolair vullingsbeeldinterstitiële pneumonie lobair - multilobair

Atypisch Typisch

Anamnese jonge patiënten oudere patiëntengeen co-morbiditeit productieve hoestdroge hoest hoge koorts, rillingenviraal syndroom dyspneegeen pleurale pijn pleurale pijninsidieus begin plots begin

Kliniek niet altijd crepitaties crepitatiesmineure klachten consolidatie

Labo lage leucocytose hoge leucocytose geen neutrofilie neutrofilie

Radiologie wazige infiltraten alveolair vullingsbeeldinterstitiële pneumonie lobair - multilobair

Pneumonie: kliniek vaak atypisch!

koorts + dyspnee + hoesten: 30-50%

* koorts: 30%-60%* verwardheid en bewustzijnsstoornissen: 40%* vallen: 16%* achteruitgang van ADL-functies: 10%* incontinentie: 7%* hoest vaak minder productief (dehydratatie, spierzwakte, …)* anorexie, braken, tachypnee, thoracale pijn, hypotensie,

tachycardie…

vnl. bij oudere patiënten, co-morbiditeit,…

CAP: aanbevolen onderzoeken

* Anamnese en klinisch onderzoek

* Routine laboratorium(perifeer bloedbeeld, serum electrolyten, lever- en nierfunctie)

inschatten van ernst

* Bepaling van oxygenatie (oximetrie/arteriële bloedgassen)

* RX thorax- zekerheidsdiagnose van pneumonie (caveats!)- inschatten van ernst- onderliggende aandoeningen of complicaties- geen correlatie met etiologische kiem !!

* Sputum: kleuring en cultuur= controversieel (kolonisatie / contaminatie !!)

CAP: aanbevolen onderzoeken

* Hemoculturen alle gehospitaliseerde patiënten met CAP (11% positief)

(S. pneumoniae, H. influenzae, S. aureus, K. pneumoniae)

* Serologische testen (Influenza, Para-influenza, Adeno, RSV, Mycoplasma, Chlamydia,…)

- patiënten met ernstige pneumonie- onvoldoende of geen respons op empirische therapie- specifieke epidemiologische omstandigheden

legionella antigeendetectie in urine patiënten met ernstige pneumonie alle patiënten met pneumonie bij epidemie

Scoresystemen/criteria voor beoordeling ernst CAP

BTS: CURB (1996) CURB-65 (2003)Fine: PSI (Pneumonia Severity Index) (1997)ATS: criteria for ‘severe pneumonia’Sepsis, severe sepsis, septic shockIDAB richtlijnen

Aangepaste BTS criteria“CURB-65”

Neill AM et al. Thorax 1996; 51(10):1010-6Lim WS et al. Thorax 2003;58:377-382

ConfusionUrea >7mmol/l (42 mg/dL)Respiratory rate ≥30/minBlood pressure: Psyst <90mmHg

Pdias ≤60mmHg

Age ≥65years

BTS Guidelines. Lim WS et al.Thorax 2009; 64(3); iii1-55

Resistentie in België

J. Verhaegen, referentie-laboratorium Leuven, 2014

Invasieve isolaten CAP: behandeling1. Ambulante patiënten zonder cardiopulmonaire ziekte en/of

andere risicofactoren

2. Ambulante patiënten met cardiopulmonaire ziekte en/of andere risicofactoren

3. Gehospitaliseerde patiënten, opgenomen op ‘gewone’ zaal

4. Gehospitaliseerde patiënten, opgenomen op eenheid voor Intensieve Zorgen

5. Gehospitaliseerde patiënten, opgenomen op eenheid voor Intensieve Zorgen mét risicofactoren voor infectie met P. aeruginosa

Sanford Guide to Antimicrobial Therapy 2013-2014Antibioticagids UZ Leuven 2014: www.uzleuven.be/antibioticagids

Ambulant, geen risicofactoren

Eerste keuze: amoxycilline 1 g 3x/d PO

Alternatieven:

* IgE-gemedieerde overgevoeligheid/ernstige intolerantie moxifloxacine 400 mg 1x/d PO

* Ongunstig klinisch verloop swith naar resp. FQ

of associeer neo-macrolide/azalide

Ambulant, met risicofactoren

Eerste keuze: amoxycilline-clavulaanzuur 2 g 2x/d POEerste keuze: amoxycilline-clavulaanzuur 2 g 2x/d POEerste keuze: amoxycilline-clavulaanzuur 2 g 2x/d PO

Alternatieven:

* IgE-gemedieerde overgevoeligheid/ernstige intolerantie moxifloxacine 400 mg 1x/d PO

* Ongunstig klinisch verloop swith naar resp. FQ

of associeer neo-macrolide/azalide

Opgenomen patiënten, ‘gewone zaal’

Orale behandeling mogelijk: moxifloxacine 400 mg 1x/d

Parenterale behandeling: amoxyclavulaanzuur 1 g 4x/d

IgE-gemedieerde overgevoeligheid/ernstige intolerantie moxifloxacine 400 mg 1x/d PO/IV

Ongunstig klinisch verloop switch naar resp. FQ IV

of associeer neo-macrolide IV

Opgenomen patiënten, ‘intensieve’

amoxyclavulaanzuur 1 g 4x/d IV

cefotaxime 2 g 3x/d IVceftriaxone 2 g 1x/d IV

plus

clarithromycin 500 mg 2x/d IV

moxifloxacine 400 mg 1x/d IV

ofof

clarithromycin 500 mg 2x/d IV

moxifloxacine 400 mg 1x/d IV

of

Opgenomen patiënten, P. aeruginosa

IV Antipseudomonas -lactam(cefepime, meropenem, pipera/tazobactam, ceftazidime)

IV Antipseudomonas fluoroquinolone plusplus

IV Antipseudomonas -lactam(cefepime, meropenem, pipera/tazobactam, ceftazidime)

IV Antipseudomonas fluoroquinolone plus

of

IV Antipseudomonas -lactam(cefepime, carbapenem, pipera/tazobactam, ceftazidime)

Aminoglycoside

IV clarithromycine of IV fluoroquinolone

plusplus

plusplus

IV Antipseudomonas -lactam(cefepime, carbapenem, pipera/tazobactam, ceftazidime)

Aminoglycoside

IV clarithromycine of IV fluoroquinolone

plus

plus

IV PO switch:criteria voor ‘klinische stabiliteit’

• Temperatuur ≤37,8°C• Hartritme ≤100/minuut• Bloeddruk systolisch ≥90mmHg• Ademhaling ≤24/minuut• PaO2 ≥60mmHg of SaO2 ≥90%• Normale mentale status• Orale route mogelijk

Halm EA, Fine MJ, Marrie TJ, et al. JAMA 1998; 279; 1452-1457

-lactam -lactamfluoroquinolone fluoroquinolone

cefalosporine fluoroquinolone

IV PO switch:Bio-equivalente antibiotica

Levofloxacine Tavanic®

Moxifloxacine Avelox®

Clarithromycine Biclar®

Clindamycine Dalacin®

Linezolide Zyvoxid®

Metronidazole Flagyl®

Ornidazole Tiberal®

Fluconazole Diflucan®

SMX/TMP Bactrim®, Eusaprim®

Duur van therapie met antibiotica Geen robuste data!

“tot 3 dagen koortsvrij”

Li JZ et al. Am J Med 1997; 120: 783-790BTS Guidelines. Lim WS et al. Thorax 2009; 64(3); iii1-55

5-7 dagen S. pneumoniae7-14 dagen Enterobacteriaceae

Pseudomonas aeruginosa14 dagen Staphylococci14-21 dagen Mycoplasma spp.

Chlamydophila spp.Legionella spp.

Hospital-acquired pneumonia (HAP)

= pneumonia die ontstaat ≥48u na hospitalisatie- geen incubatie op moment van opname- gewone afdeling/intensieve zorgen

Ventilator-associated pneumonia (VAP)= pneumonia die ontstaat ≥48-72u na

endotracheale intubatie

Niederman MS. Curr Opin Pulm Med 1996; 2:161-165

HAP: hoge morbiditeit en mortaliteit!

• 2de meest frequente oorzaak van nosocomiale infectie

• 5-10/1.000 hospitalisaties• 6-21voudige stijging bij geventileerde patiënten• 25% van alle ICU infecties

Chastre J. AJRCCM 2002; 163: 867-903Rello et al. Chest 2002; 122: 2121-2132

• VAP = 90% van alle HAP• incidentie stijgt met duur van ventilatie• risico is hoogst vroegtijdig in verloop van ventilatie• minder frequent bij niet-invasieve ventilatie

HAP: hoge morbiditeit en mortaliteit!

• ‘Globale’ mortaliteit voor HAP 30% - 70%

EN

‘specifieke’ mortaliteit = 33% - 50%- bacteriëmie (P. aeruginosa, Acinetobacter sp.)- medische eerder dan chirurgische pathologie- ernst van de onderliggende aandoening(en)- ‘inappropriate’ antibiotica-therapie

Heylandt et al. AJRCCM 1999; 159: 1249-1256Bregeon et al. Anesthesiology 2001; 94: 554-560

Papazian et al. AJRCCM 1996; 154: 91-97

CAP/HAP: microbiologie

HAP: microbiologie

Chastre J, Fagon JY. AJRCCM 2002; 165(7): 867–903

HAP: belang van tijdstip van ontstaan

• ‘Early-onset’ HAP/VAP= ontstaan binnen de eerste 7 dagen

na hospitalisatie/ventilatie

• ‘Late-onset’ HAP/VAP= ontstaan na 7 dagen na

hospitalisatie of ventilatie

≈ ‘early-onset’ HAP/VAP met voorafantibiotica/hospitalisatie (90d.)

HAP: belang van tijdstip van ontstaan HAP: diagnostische strategieHAP/VAP or HCAP suspectedHAP/VAP or HCAP suspected

Lower respiratory tract sample for culture and microscopyLower respiratory tract sample for culture and microscopy

Unless there is both a low clinical suspicion for pneumonia & negative microscopy of LRT sample, start empiric antimicrobial therapy

Unless there is both a low clinical suspicion for pneumonia & negative microscopy of LRT sample, start empiric antimicrobial therapy

Days 2-3: Check cultures & assess clinical response:(Temp., WBC, Chest X-ray, Oxygenation, Purulent sputum, Hemodynamic changes and Organ

function)

Days 2-3: Check cultures & assess clinical response:(Temp., WBC, Chest X-ray, Oxygenation, Purulent sputum, Hemodynamic changes and Organ

function)

Clincal improvement at 48-72 hoursClincal improvement at 48-72 hours

NONO

Adjust AB therapy, Search for other pathogens, Complications, Other diagnosies or Other sites of

infection

Adjust AB therapy, Search for other pathogens, Complications, Other diagnosies or Other sites of

infection

YESYES

Cultures -Cultures -

Stop ABStop AB

Cultures +Cultures +

De-escalalate AB if possible.

Treat selected pts for 7-8d.

De-escalalate AB if possible.

Treat selected pts for 7-8d.

HAP: behandeling

• Antibiotica zo snel mogelijk!• Vaak combinatietherapie• Cave multi-drugresistente kiemen (MDR)!• Duur: 7 dagen indien gunstige evolutie en geen

complicaties! (Uitz.: non-fermenters!!)

1. HAP: gewone afdeling, ‘early-onset’

2. HAP: gewone afdeling, late-onset’ / vooraf antibiotica

3. HAP: intensieve zorgen -- VAP

Risk factors for infection by multidrug resistant (MDR) pathogens

• Antibiotic therapy in previous 90 days• High frequency of resistance in community• Immunosuppression by disease or medication

• Risk factors for HCAP Hospitalisation for ≥2 days in previous 90 days Nursing home residence Home intravenous therapy Chronic dialysis within 30 days Chronic wound care Close contacts to MDR pathogens

Trouillet et al. AJRCCM 1998; 157: 531-539

HAP: gewone afdeling, early onset

amoxicillin-clavulaanzuur

4 x 1g/d IV

IgE-mediatedallergie/intolerantie:

moxifloxacine 1 x 400mg/d IV


HAP: gewone afdeling, late onset of vooraf AB

ceftriaxone 1 x 2g/d IV

cefotaxime 3 x 2g/d IV


HAP: intensieve zorgen -- VAP

cefepime 3 x 2g/d IV

meropenem 3 x 1g/d IV

piperacillin/tazobactam 4 x 4g/d IV

ceftazidim 3 x 2g/d IV

PLUS (MIN)

amikacine(of anti-Ps. fluoroquinolone)

1 x 1g/d IV

PLUS vancomycine (indien hoge prevalentie van MRSA)


Complicaties van pneumonie

• Pneumonie met abnormaal verloop- klinisch- radiologisch

• Ernstige pneumonie, leidend tot orgaanfalen

• Infectieuse complicaties van pneumonie

• Niet-infectieuse complicaties van pneumonie

Pneumonie met abnormaal verloop

Geen éénduidige definitie !! klinische evolutie

- koorts – CRP - Wbc 2- 4 dagen- respiratoire klachten 4- 9 dagen- auscultatoire tekens 3-14 dagen- radiologische afwijkingen 2- 4 weken

radiologische evolutie= meest gebruikte parameter in literatuur

‘slow’/’non-resolving’ pneumonia<50% of geen verbetering na één maand

Abnormaal verloop: oorzaken...

1. Niet-bacteriële etiologie- mycobacteriën (m. tuberculosis, NTM)- schimmels (Aspergillus spp., …)- nocardia/actinomyces- viraal, …

2. Resistente kiemen- S. pneumoniae (DRSP)- MRSA, P. aeruginosa, aërobe Gram- bacillen,…

3. Infectieuze complicaties- gecompliceerde parapneumonische effusie, empyeem- abcedatie- metastatische infecties, …

Abnormaal verloop: oorzaken...

4. Gastheerfactoren- structurele longaandoeningen (bronchiëctasieën, tumor,…)- immuunsuppressie, …

5. Niet-infectieuze etiologie (20%)- maligniteit- collageen-vasculaire ziekten- BOOP- hypersensitiviteitspneumonitis- medicamenteus of toxisch longlijden- longembolie, longinfarct, longbloeding- longoedeem- radiatie-pneumonitis- ARDS

Abnormaal verloop: diagnostiek

* grondige heranamnese en klinisch onderzoek

* aanvullende biochemische testen inflammatoire parameters, auto-immuunserologie,…

* beeldvorming RX thorax – (HR)CT thorax – Echo thorax

* bronchoscopie washing, broncho-alveolaire lavage, biopsies

* pleurapunctie

* longbiopsie

* V/Q-scan, arteriografie, zweettest, …

Ernstige pneumonie orgaanfalen

Opname op intensieve zorgen

* kunstmatige ventilatie 50%-88%

* septische shock 10%-42%

* acuut nierfalen 30%-42%

* andere mentale verwardheid metastatische infectie acuut hartfalen ...

Pleuravocht punctie!

Stages Macroscopicappearance

Pleural fluidcharacteristics

Comments

Simpleparapneumonic

Clear fluid pH>7.2LDH<1000Glucose>30

Antibiotics(Drain if requiredon symptomatic

grounds)

Complicatedparapneumonic(fibrinopurulent)

Clear fluid

Cloudy/turbid

pH<7.2LDH>1000Glucose<30

Gram/cult. +/-

Chest tube drainage (+ …)

Empyema Frank pus Gram/cult. +/-

No other tests required

Chest tube drainage (+ …)

Surgery

Davies CWH. Thorax 2003

Pleuravocht/empyeem: behandeling

• Antibiotica- intraveneus / empyeem: langere duur (cf. longabces)

• Thoraxdrainage etter pH < 7,2 aanwezigheid van micro-organismen

bij etter best brede drain (Ch.28-32), in suctie spoeling noodzakelijk bij dunne drains

• GEEN NUT: seriële puncties, fibrinolytica (tenzij…!!!)

• Chirurgie zo onvoldoende effect na 3(-5) dagen!

Pulmonaryembolism


103

Asymptomatic

Epidemiology difficult to determine

104

Sudden death

• Increased risk if >40years (risk x2 with each decade)

• Deaths 34% sudden fatal PE 59% PE undiagnosed during life

• Provoked >< unprovoked

• Risk factors - patient-related- setting-related

Cohen AT et al. Thromb Haemost 2007; 98: 756-764

Risk factors are all around us…

105

• Data mostly from studies in orthopedic surgery

• Mostly proximal DVT PE in 40-50%

• Mortality: 30d 9-11%90d 9-17%

• Lung perfusion defects: 30-35% (one year)

• CTEPH: 1,5% (within 24months)

Natural history of PE

106

Goldhaber SZ et al. Lancet 1999; 353: 1386-1389Pengo V et al. N Engl J Med 2004; 350: 2257-2264

Laporte S et al. Circulation 2008; 117: 1711-1716Cosmi B et al. Intern Emerg Med 2011; 6: 521-528

The clinical signs and symptomsare non-specific!!

107Pollack CV et al. J Am Coll Cardiol 2011; 57: 700-706

• Predisposing factors!!!

• Up to 30%: no provoking factors detected!

• Arterial blood gasses:- up to 40% normal oxygen saturation- up to 20% normal A-a oxygen gradient

• Chest X-ray normal-abnormal (non-specific)

• ECG: up to 40% only sinus tachycardia

The clinical signs and symptomsare non-specific!!

108

Rodger MA et al. Am J Resp Crit Care Med 2000; 162: 2105-2108Elliott CG et al. Chest 2000; 118: 33-38

Geibel A et al. Eur Resp J 2005; 25: 843-848

Initial assessment: early mortality?

109

Key step in all diagnostic algorithms

Clinical or pre-test probability

110

Clinical judgement

Clinical prediction rules1. WELLS2. GENEVA

Clinical prediction rule: WELLS

111Wells PS et al. Thromb Haemost 2000; 83: 416-420

Gibson NS et al. Thromb Haemost 2008; 99: 229-234

Clinical prediction rule: GENEVA

112Le Gal G et al. Ann Intern Med 2006; 144: 135-171

Klok FA et al. Ann Intern Med 2008; 168: 2131-2136

Diagnostic algorithm “high-risk”

113

Diagnostic algorithm “low-risk”

114

Prognostic assessment: PESI score

115

Aujesky D et al. Am J Resp Crit Care Med 2005; 172: 1041-1046

Jimenez D et al. Arch Intern Med2010; 170: 1383-1389

Classification of pts with acute PE based on early mortality risk

116

Risk-adjusted management strategies

117 118

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