Hap

HOSPITAL ACQUIRED PNEUMONIA

DR SK HUMAYUN KABIR

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

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)

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.

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

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%

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)

Etiology

• Mostly wide spectrum of bacterial pathogens• May be polymicrobial • Viral or fungal pathogens in

immunocompromosed host.

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.

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.

Risk factor and prevention.

Risk factor

• Non modifiable risk factorI. male sexII. Preexisting pulmonary diseaseIII. Multiple organ system failure

Modifiable risk factor

• Intubation and mechanical ventilation ( 6-21 % increasd risk of HAP ).

1. TYPE OF ET TUBE 2. COLONISATION IN VENTILATOR

CIRCUIT3. USE OF SEDATIVE OR PARALYTTIC

AGENTS4. CUFF PRESSURE5. COLONISATION IN PASSIVE

HUMIDIFIER

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.

- 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.

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.

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.

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

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 emptying17) Risk of VAP associated with early enteral feeding

didn`t translate into ↑ risk of death,so,early enteral feeding advised.

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

• Blood sugar controll 80-110mg• Decision of blood transfusion should defered

till hb% less than 7gm% instead of 9 gm%.

Pathogenesis

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

Pathogenesis

entry of microbial pathogens in LRT

colonisation

overcome the host mechanical ( cilia,mucus) humoral ( antibody ,complement) , cellular

(PMN,macrophages, lymphocytes)

infection

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.

Diagnosis

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

• - 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

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.

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.

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).

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.

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.

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.

strategy

• Clinical strategy• Bacteriological strategy

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

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

• 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 (-) (+)

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.

• 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.

TREATMENT

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.

Treatment

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.

• 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

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 pneumoniaNot improving with systemic therapy

Adjunct therapy with inhaled aminoglycoside or polymixin B.

Linezolid is an alternative to vancomycin for the treatment of MRSA VAP.

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.

• 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.

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.