HOSPITAL ACQUIRED PNEUMONIA

1. HOSPITAL ACQUIRED PNEUMONIA
DR SK HUMAYUN KABIR

2. • INTRODUCTION
• DEFINITION
• EPIDEMIOLOGY
• ETIOLOGY
• PATHOGENESIS
• DIAGNOSIS
• TREATMENT

3. Introduction.
• Hospital acquired pneumonia (HAP) remains
important cause of mortality despite of
advance antimicrobial therapy and better
preventive care . May be managed at ward or
icu.
• Ventilator associated pneumonia( VAP )
• Health care associated pneumonia.(HCAP)

4. Definition
• HAP- pneumonia that occurs 48 hours or more after
admission which was not incubating at the time of
admission.
• VAP- pneumonia that arises more than 48-72 after
endotracheal intubation.
• HCAP- pneumonia in a patient who was hospitalised in
acute care setting for two or more days within 90 days
of infection; residing in nursing homeor long term
facility; received recent iv antibiotic;
chemotherapy;wound care within 30 days of current
infection;attended a hospital or haemodylisis centre.

5. Cont..
• Most of the current DATA have collected from
VAP .
• Microbiological data from non intubated
patient is less accurate.
• Data can be applied to all patients of HAP

6. Epidimology
• 5 to 10 per 1000 hospital admission
• 6 -20 fold increased in mechanicaly ventilated
patients
• 25 % ofall ICU infections.
• 90 % of HAP occurs during mechanical
ventilation.
• Incidence of VAP highest in early days of hoispital
admission ( ≤ 5 days ).
• Early onset VAP or HAP (≤ 4 days ).
• Crude mortality rate 30- 50%

7. INCIDENCE IN INDIA :-
• Incidence of HAP in india is 53.9%.
• Incidence of VAP in india is 8.95/1000 ventilator
days.
• Mortality rate(attributable) is 37% - 47.3%
Park Es et al Am j inf control(2000)

8. Etiology
• Mostly wide spectrum of bacterial pathogens
• May be polymicrobial
• Viral or fungal pathogens in
immunocompromosed host.

9. Etiology
• P. areuginosa
• Escherichia coli
• Klebsiella pneumonie aerobic gram negetive
• Acinetobacter sp
• MRSA ( DM, head trauma,haemodylisis ,ICU patients)
• Streptococcus viridans
• Coagulase negetive staph immunocompr
• Fungal
• Viral (seasonal ,influenza A ,parainfluenza,adeno,rsv)
• Anerobic - occurs in non intubated patient following
aspiration,rare in patients with VAP.

10. Etiology for MDR infection
• Infection with multi drug resistant ( M D
R)strain is major concern in treating HAP.
• Frequency of MDR pathogens causing HAP
may vary by hospital ,patients population
,exposure to antibioticatype of ICU patient,
and changes over time, emphasizing the need.
• MRSA , pseudomonas, acinatobacter,
klebsiella are of main concern.

12. Risk factor and prevention.

13. Risk factor
• Non modifiable risk factor
I. male sex
II. Preexisting pulmonary disease
III. Multiple organ system failure

14. Modifiable risk factor
• Intubation and mechanical ventilation ( 6-21 %
increasd risk of HAP ).
1. TYPE OF ET TUBE
2. COLONISATION IN VENTILATOR
CIRCUIT
3. USE OF SEDATIVE OR PARALYTTIC
AGENTS
4. CUFF PRESSURE
5. COLONISATION IN PASSIVE
HUMIDIFIER

15. Aspiration ,body position ,enteral feeding
• Supine position
• Enteral feeding a risk factor ..?
• Colonisation of pathogen in oral cavity
• stress ulcer prophylaxis with H2 blocker.
• Blood transfusion .
• Hypo and hyper glycaemia.

16. - PREVENTIVE STRATEGIES FOR NOSOCOMIAL
PNEUMONIA :
1) Implementation ,as VAP bundle,of noso-
comial pneumonia preventive strategies
that have proven efficacy in reducing mo-
rbidity & mortality.

17. 2) Implementation of education programmes
(respiratory care physicians & nurses being
primary recepients),& frequent performance
feedbacks & compliance assesment.
3) Strict alcohol based hand hygiene.
4) Avoidance of tracheal intubation & use of NIV
when indicated(acute exacebn. of COPD,
acute hypoxemic resp failure,immunocomp.
with pulmonary infiltrates)
-Recent reports emphasize role of NIV in
preventing re-intubation in recently extubated
pts at risk for relapse & respiratory failure.

18. 5) Daily sedation vacation & implementation of weaning
protocols.
6) No ventilatory circuit tube changes unless soiled or
damaged.
7) Use of tracheal tubes with cuff made of novel
materials(polyurethane; & LVLP cuffs made of silicone
&latex) & shape(conical)
8)Application of low level PEEP(5-8cm H2O)during
tracheal intubation.
9) Use of silver coated ETT –
NASCENT trial concluded that silver coated
ETT has ↓ incidence of VAP,↓ mortality in pts
with VAP,is cost effective & has greatest
impact during first 10 days.

19. 10) Aspiration of subglottic secretions(every 4-6hrs)
11) Internal cuff pressure maintained within 25-30
cm H2O & carefully controlled during transport
of patients outside ICU.
12) Earlier tracheostomised pts (mean~7 days)
had shorter length of M/V & ICU stay,a ↓trend
towards pneumonia but no survival benefit as
compared to late tracheostomy(mean~14 days)
13) Routine saline instillation before tracheal
suctioning not recommended

20. 14) Intubated pts should be kept in semi-recumbent
position(30-45°),rather than supine to prevent
aspiration;especially when enterally fed.
15) Continuous lateral rotation of bed helps to reduce
extravascular lung water,improveV/Q
& enhance mobilization of secretions.
16) Post pyloric feeding in patients with impaired
gastric emptying
17) Risk of VAP associated with early enteral feeding
didn`t translate into ↑ risk of death,so,early enteral
feeding advised.

21. 18) Stress ulcer prophylaxis in high risk pts(coagulopathy,↑
duration of M/V,h/o
GI bleed.
19) Oral care with 2% chlorhexidine.
20) SELECTIVE CONTANINATION OF DIGESTIVE TRACT (SDD) :
- consists of nonabsorbable antibio. Against
gram – (tobramycin.polymyxin E) + nystatin/
ampho B for candida administered into GI to
prevent oropharyngeal & gastric colonization.
- SDD reduces incidence of VAP & it’s the only
strategy that has shown survival benefit

22. • Blood sugar controll 80-110mg
• Decision of blood transfusion should defered
till hb% less than 7gm% instead of 9 gm%.

24. Pathogenesis
• Shifting of delicate balance of host defence vs
colonisation and invasion in favour of
pathogens to persist and invade in lower
respiratory tract.

25. Pathogenesis
entry of microbial pathogens in LRT
colonisation
overcome the host mechanical ( cilia,mucus)
humoral ( antibody ,complement) , cellular
(PMN,macrophages, lymphocytes)
infection

26. Pathogenesis
• Source of pathogens include environment, transfer of
microbes.
• Colonisation fsvouring factor( prior surgery ,ivasive
respiratory device, immuno deficient state,prolong
antibiotic therapy)
• Aspiration f oropharyngeal pathogens ,leaking around ET
tube,.
• Direct inoculation of pathogens into lower
airway,haematogenous spread from infected catheter ,
microbial translocation from GI lumen.
• Infected biofilm in the ET tube.
• Stomach and sinus may act as potential reservior of
nosocomial pathogen by favouring colonisation.

28. Diagnosis
• To confirm the diagnosis of pneumonia.
• To identify the causative agent for pneumonia.

29. • - NON INFECTIOUS CAUSES OF
FEVER/INFILTRATES MIMICKING NOSOCOMIAL
PNEUMONIA :
- chemical pneumonitis
- atelectasis
- pulm embolism
- ARDS
- pulmomary hemorrhage
- lung contusion
- infiltrative tumour
- radiation pneumonitis
- drug reaction
- BOOP

30. Suspicion of HAP
• suspicion of HAP if fever ,purulent secretion
,leukocytosis,radiological infiltration in chest
xray.
• Tracheo bronchitis is associatd with negetive
xray finding.
• Unexplained haemodynamic instability or
deterioration of blood gases in ventilated
patient.

31. Diagnosis
• Confirmation of diagnosis with identifying the
causetive agent is very challenging.
• Main aim is to differentiated from colonisation
with infection.
• Etiological dignosis requires lower respiratory
secreation culture including endotracheal
aspirate, PSB (protracted brushing), BAL .
• Blood or pleural fluid culture.

32. Diagnosis
• Positive culture cannot always differentiate
from colonisation with infection.
• A sterile culture of LRTI of an intubated
patient in absent of recent change in antibiotic
is strong predictor of absence of pneumonia.(
negetive predictive value).

33. Recommendation for diagnosis
• All patient should undergo detailed clinical evaluation (
history and physical examination).
• Chest radiograph.
• Purulent tracheobroncitis should be properly
diagnosed ( negetive cxr finding)
• All routine blood investigation including ABG should be
done ( severity of ill ness and indicates other organ
involvement,need for oxygen)
• Blood culture and pleural fluid culture should be done.
• Samples of LRT should obtain in all suspected case of
HAP and should collected before antibiotic changes.

34. Recommendation for diagnosis
• Absence of clinical suspicion of HAP of TAB no
further workup necessary
• Sterile culture with no change of antibiotic
negetive for bacterial pneumonia but viral or
legionella pneumonia may presesnt.
• Search for extrapulmonary infection according
to clinical suspicion.

35. Diagnostic Strategy
• Clinical suspicion is over sensitive further
diagnostic approach needed for optimal
management.
• To ensure collection of appropiate sample.
• To promote use of early and effective
antibiotic therapy.
• Streamlinig or de esclation when possible.
• To identify extra pulmonary infections.

36. strategy
• Clinical strategy
• Bacteriological strategy

37. Clinical strategy
• Pneumonia = infiltrate in xray+ Two among three clinical criteria ( fever> 38
,leukocytosis or leukopaenia and purulent secretion) .
• Etiological cause is defined by semiquantative culture (light, moderate ,heavy) of
endo tracheal aspirate or sputum with initial microscopic examination.
• CPIS score used to increase accuracy in clinical strategy. CPIS > 6 then good co
relation with pneumonia.
• Intial gram stain to star empirical antibiotic therapy.
• Reevaluation of decision of using antibiotics done based on result of
semiquantetive culture report by day 3 or sooner

38. Bacteriological strategy
• Quantitative culture for lower respiratory tract done to
define presence of pneumonia and etiological
pathogen.
• Growth above thresold concentration required to
diagnose VAP/HAP
• Target is to avoid overtreatment antibiotic therapy
• Major concern is false negetive report may be lead to
failure to treat a specific pathogen .false negetive
reporty may be due to prior antibiot therapy.
• Endotracheal aspirate collected bronchoscopicaly and
non bronchoscopicaly and each technique has its
diagnostic threshold and methodological limitation

39. • CLINICAL PULMONARY INFECTION SCORE (CPIS) :
criterion 0 1 2
tracheal secn . (-) not purulent purulent
x- ray infiltrates NO DIFFUSE LOCALISED
temp °C ≥36.5&≤38.4 ≥38.5&≤38.9 ≥39or≤36
leucocytes ≥4000&≤11000 <4000or>11000 +immature
neutrophil >50%
microbio (-) (+)

41. Dignosis strategy final..
• Patient with suspected VAP LRT sample should sent for
culture and extra pulmonary infection should be
excluded before starting antibiotic therapy.
• If there high pre test probability and with sepsis
prompt therapy should started immidiately .
• Bronchoscopy sampling prefered if not available then
non bronchoscopic sampling to be done and
quantitavie culture should be priority over
semiquantitavie culture.
• Therapy should not be postponed for purpose of
diagnosis.

42. • isolation of candida albicans and other cadida
species in bronchoscopy is very common
mostly due to colonisationrather
pneumonia,and usuly no treatment is
required.
• Diagnosis of viral infection made by rapid
antigen testing and viral culture or serological
assays.

45. TREATMENT

46. Treatment
• Initial concern should be etiological pathogen
MDR or not.
• Evaluation of risk factor for MDR pathogen.
• Prompt initiation of therapy.
• Patient with HCAP considerd to be infected
with MDR.

47. Treatment

49. Treatment
• Choice of specific agent should dictated by local
microbiology,cost ,availability ,and formulatory restriction.
• Altarnate group of antibiotic should be selected if patient
received recent antibiotic therapy .
• On admission iv antibiotic therapy should be started .
• Combination therapy should be done if patients likely to
infected with MDR pathogens. Role is doubtful in comparison
to monotherapy except to enhance the likelyhood of initially
appropriate empiric therapy.

50. • Aminoglycosides can be stopped after 5-7 days if used with
combined therapy in a responding patients.
• Patient withh risk group should initialy receive combination
therapy until result of culture confirms that single agent can
be used
• If etiological agent is not p.aruginosa patient is having a good
response to intial antibiotic therapy , duration can be
shortened to 7 days in comparison to traditional 14 to 21 days

53. Important notes for specific pathogens
doccumented Pathogens Therapy recomendation
P aeruginosa Combined therapy. to avoid resistence (
weak evidence). Mojor concern is to avoid
inappropriate and ineffective treatment.
Acinetobacter spp. Carbapenem, sulbactum ,colistin, and
polymixin. No doccumented benefit in
combined therapy.
ESBL enterobacteriaceae Monotherapy with third generation
cephslosporin avoioded most active
MDR Gram negetive pneumonia
Not improving with systemic therapy
Adjunct therapy with inhaled
aminoglycoside or polymixin B.
Linezolid is an alternative to vancomycin for the treatment of MRSA VAP.

54. Response to therapy
• Clinical improvement usually takes 48-72 hours. Therapy
should not be changed during this window unless rapid
clinical decline.
• Non response to therapy usually evident on DAY 3 by
asesing clinical parameter.
• Serial respiratory tract culture can be used for defining
resolution , superinfections , recurrent infection or
microbiological persistense
• Chest radiography has limited value ,initial radiographic
deterioration is very much common.rapid deterioration or
multilobular involvement > 50% increase in size of lesion
,development of cavity ,significant pleural effusion, should
raise concern.

55. • WBC count, measures of oxygenation ,core
temperatue have used in several studies to
define normal pattern of resolution
• CPIS scoring can be used to predict resolution
at 3 days.

56. Reasons of non resolution
• Wrong diagnosis.
• Extrapulmonary infection not evluated.( UTI ,catheter
related infection,sinusitis,pseudomembrenos colitis.
• Resistant pathogen.
• Development of complication (lung abcess,empyema)
• complication during treatment.Drug fever ,sepsis with
MODS, pulmonary embolus with secondary infraction.
• Unusual pathogen not considered in emperical
therapy( m.tuberculosis ).
• Unrecognised immunosuppression , unrecognised
pneumocystis carini infection.