Hospital-Acquired Pneumonia: Epidemiology, Etiology, Diagnosis & Treatment
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a.c. 6/12/2018 1440
هجري
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To know the epidemiology ,etiology,
pathogenesis ,clinical presentation,
investigation ,diagnosis ,treatment
,complication ,prognosis
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Hospital-acquired or
nosocomial pneumonia
is a new episode of
pneumonia occurring at
least 2 days after
admission to hospital
It is the second most
common hospital-
acquired infection (HAI)
and the leading cause
of HAI-associated death.
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V
entilator-associated
pneumonia’ (VAP
)
Pneumonia occurred patients
in intensive care units,
especially when
mechanically ventilated;
Healthcare-associated
pneumonia (HCAP)
pneumonia in a person
who has spentat least 2
days in hospital within the
last 90 days,
has attended a
haemodialysis unit,
received intravenous
antibiotics .
been resident in a nursing
home or other long-term
care facility
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Reduced host defences against bacteria
• Reduced immune defences
(e.g.corticosteroid treatment, diabetes,
malignancy)
• Reduced cough reflex (e.g. post-operative)
• Disordered mucociliary clearance (e.g.
anaesthetic agents)
• Bulbar or vocal cord palsy
Aspiration of nasopharyngeal or gastric
secretions
• Immobility or reduced conscious level
• Vomiting, dysphagia (N.B. stroke disease),
achalasia or severe reflux
• Nasogastric intubation
Bacteria introduced into lower
respiratory tract
• Endotracheal
intubation/tracheostomy
• Infected
ventilators/nebulisers/bron-
choscopes
• Dental or sinus infection
Bacteraemia
• Abdominal sepsis
• IV cannula infection
• Infected emboli
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The early-onset HAP
(occurring within 4–5
days of admission) are
similar to those involved
in CAP.
Late onset HAP
Gram-negative bacteria
(e.g.
Escherichia,
Pseudomonas, Klebsiella
species and
Acinetobacterbaumannii),
Staph. aureus (including
the meticillinresistant
type (MRSA)) and anaerobes
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The hospitalised or ventilated patient
purulent sputum (or endotracheal secretions),
new radiological infiltrates,
unexplained increase in oxygen requirement,
a core temperature of more than 38.3°C,
a leucocytosis or leucopenia.
differential diagnosis
•
Venous thromboembolism .
•
ARDS .
•
pulmonary oedema.
•
Pulmonary haemorrhage.
•
drug toxicity.
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microbiological confirmation .
•
the full blood count (FBC).
•
urea and electrolytes (U&E),
•
Erythrocyte sedimentation rate (ESR) and C-
reactive protein (CRP).
•
arterial blood gas.
•
chest X-ray.
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adequate oxygenation,
•
Appropriate fluid balance
•
antibiotics.
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In early-onset HAP
,
1-If not received
antibiotics
treated with co-amoxiclav
or
cefuroxime.
2- Received antibiotics
piperacillin/tazobactam
or a third generation
Cephalosporin..
In late-onset HAP
,
the antibiotics must cover
the
1-Gram-negative bacteria
2-
Staph. aureus
(including MRSA)
3- anaerobes
.
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the mortality from HAP is approximately 30%,
Good hygie
regard to handwashing and any
equipment used.
The risk of aspiration
should be minimised,
ventilator associated pneumonia by
limiting use
of proton pump inhibitors.
decontaminate the upper airway
, by Oral
antiseptic (chlorhexidine 2%)
selective decontamination
of the digestive tract
.
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These conditions are considered together, as
their aetiology and clinical features overlap
Suppurative pneumonia
is characterised by
destruction of the lung parenchyma by the
inflammatory process .
Microabscess
formation is a characteristic
histological feature.
Pulmonary abscess’
is usually taken to refer
to lesions in which there is a large localised
collection of pus, or a cavity lined by chronic
inflammatory tissue, from which pus has
escaped by rupture into a bronchus.
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Inhalation
septic material
during operations on the nose, mouth or throat
under general anaesthesia,
vomitus during anaesthesia coma, particularly if oral hygiene is
poor.
bulbar palsy
vocal cord palsy,
stroke,
achalasia
oesophageal reflux,
alcoholism.
local bronchial obstruction
from a
neoplasm or foreign
body
.
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mixture of anaerobes and aerobes from
flora in the
mouth and upper respiratory tract.
in a previously healthy lung,
•
Staph. aureus
•
Klebsiella pneumoniae
.
pulmonary infarct or a collapsed
•
Strep. pneumoniae, Staph. aureus, Strep. pyogenes,
H. influenzae and, in some cases, anaerobic bacteria
.
In
many cases,
no pathogen
can be isolated,
particularly when antibiotics have been given
.
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Symptoms
•
Cough
with large amounts of sputum, sometimes fetid and blood-
stained
•
Pleural pain
common
•
Sudden expectoration of copious amounts
of foul sputum if abscess
ruptures into a bronchus
Clinical signs
•
High remittent pyrexia
• Profound systemic upset
• Digital clubbing may develop quickly
(10–14 days)
•
Consolidation
on chest examination; signs of cavitation rarely found
•
Pleural rub
common
• Rapid deterioration in general health, with marked
weight loss
if not
adequately treated
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Radiological features
Abscesses are characterised by cavitation and
fluid level.
Occasionally, a preexisting emphysematous
bulla becomes infected and appears as a
cavity containing an air–fluid level
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Intravenousco-amoxiclav 1.2 g 3 times daily.
Metronidazole 400 mg 3 times daily
If an anaerobic bacterial infection is
suspected (e.g. from fetor of the sputum), oral
CA-MRSA is
usually susceptible to a variety of oral non-β-lactam antibiotics,
such
as
trimethoprim/sulfamethoxazole,
clindamycin, others
Parenteral therapy with
vancomycin
or daptomycin and to metronidazole,
or clindamycin and third-generation cephalosporins
.
Prolonged treatment for 4–6 weeks
may be required in some patients
with lung abscess.
Physiotherapy
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In most patients, there is a
good response
to
treatment and, although residual fibrosis and
bronchiectasis
Surgery
may be required.
Pneumonia in the
immunocompromised patient
Patients immunocompromised by
drugs or
disease
are at high risk of pulmonary infection.
The majority of cases are caused by
the same
pathogens that cause pneumonia
Patients with more profound immunosuppression,
unusual organisms or those normally considered to
be of low virulence or non-pathogenic may become
‘opportunistic’pathogens
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fever,
cough
breathlessness,
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Invasive investigations, such as
Bronchoscopy.
BAL.
transbronchial biopsy.
surgical lung biopsy.
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Broad-spectrum antibiotic
a
third-generation cephalosporin or
aquinolone
,
plus an antistaphylococcal antibiotic
,
Or
an
antipseudomonal penicillin plus an
aminoglycoside
.
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Increased risk of and from respiratory
infection.
Predisposing factors: .
Atypical presentation .
Mortality
Influenza
TB
T
H
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N
K
Y
O
U
•
To know the epidemiology ,etiology,
pathogenesis ,clinical presentation,
investigation ,diagnosis ,treatment
,complication ,prognosis
Hospital-acquired pneumonia is a serious infection occurring at least 2 days after hospital admission, leading to complications and mortality. It can be classified into VAP and HCAP, with various predisposing factors and microbiological causes. Recognizing clinical features and prompt treatment are crucial for managing HAP.
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Presentation Transcript
Hospital-acquired pneumonia
OBJECTIVES To know the epidemiology ,etiology, pathogenesis ,clinical presentation, investigation ,diagnosis ,treatment ,complication ,prognosis
Hospital-acquired pneumonia Hospital-acquired or nosocomial pneumonia is a new episode of pneumonia occurring at least 2 days after admission to hospital It is the second most common hospital- acquired infection (HAI) and the leading cause of HAI-associated death.
Classification of HAP Ventilator-associated pneumonia (VAP) Pneumonia occurred patients in intensive care units, especially when mechanically ventilated; Healthcare-associated pneumonia (HCAP) pneumonia in a person who has spentat least 2 days in hospital within the last 90 days, has attended a haemodialysis unit, received intravenous antibiotics . been resident in a nursing home or other long-term care facility
Factors predisposing to hospital-acquired pneumonia Reduced host defences against bacteria Reduced immune defences (e.g.corticosteroid treatment, diabetes, malignancy) Reduced cough reflex (e.g. post-operative) Disordered mucociliary clearance (e.g. anaesthetic agents) Bulbar or vocal cord palsy Aspiration of nasopharyngeal or gastric secretions Immobility or reduced conscious level Vomiting, dysphagia (N.B. stroke disease), achalasia or severe reflux Nasogastric intubation Bacteria introduced into lower respiratory tract Endotracheal intubation/tracheostomy Infected ventilators/nebulisers/bron- choscopes Dental or sinus infection Bacteraemia Abdominal sepsis IV cannula infection Infected emboli
Microbiology The early-onset HAP (occurring within 4 5 days of admission) are similar to those involved in CAP. Late onset HAP Gram-negative bacteria (e.g. Escherichia, Pseudomonas, Klebsiella species and Acinetobacterbaumannii), Staph. aureus (including the meticillinresistant type (MRSA)) and anaerobes
Clinical features The hospitalised or ventilated patient purulent sputum (or endotracheal secretions), new radiological infiltrates, unexplained increase in oxygen requirement, a core temperature of more than 38.3 C, a leucocytosis or leucopenia. differential diagnosis Venous thromboembolism . ARDS . pulmonary oedema. Pulmonary haemorrhage. drug toxicity.
Investigations microbiological confirmation . the full blood count (FBC). urea and electrolytes (U&E), Erythrocyte sedimentation rate (ESR) and C- reactive protein (CRP). arterial blood gas. chest X-ray.
Management adequate oxygenation, Appropriate fluid balance antibiotics.
Treatment In early-onset HAP, 1-If not received antibiotics treated with co-amoxiclav or cefuroxime. 2- Received antibiotics piperacillin/tazobactam or a third generation Cephalosporin.. In late-onset HAP, the antibiotics must cover the 1-Gram-negative bacteria 2-Staph. aureus (including MRSA) 3- anaerobes.
Prevention the mortality from HAP is approximately 30%, Good hygie regard to handwashing and any equipment used. The risk of aspiration should be minimised, ventilator associated pneumonia by limiting use of proton pump inhibitors. decontaminate the upper airway, by Oral antiseptic (chlorhexidine 2%) selective decontamination of the digestive tract.
Suppurative pneumonia, aspiration pneumonia and pulmonary abscess These conditions are considered together, as their aetiology and clinical features overlap
Suppurative pneumonia is characterised by destruction of the lung parenchyma by the inflammatory process . Microabscess formation is a characteristic histological feature. Pulmonary abscess is usually taken to refer to lesions in which there is a large localised collection of pus, or a cavity lined by chronic inflammatory tissue, from which pus has escaped by rupture into a bronchus.
Risk Inhalation septic material during operations on the nose, mouth or throat under general anaesthesia, vomitus during anaesthesia coma, particularly if oral hygiene is poor. bulbar palsy vocal cord palsy, stroke, achalasia oesophageal reflux, alcoholism. local bronchial obstruction from a neoplasm or foreign body.
Microbilogy mixture of anaerobes and aerobes from flora in the mouth and upper respiratory tract. in a previously healthy lung, Staph. aureus Klebsiella pneumoniae. pulmonary infarct or a collapsed Strep. pneumoniae, Staph. aureus, Strep. pyogenes, H. influenzae and, in some cases, anaerobic bacteria. In many cases, no pathogen can be isolated, particularly when antibiotics have been given.
Clinical features of suppurative pneumonia Symptoms Cough with large amounts of sputum, sometimes fetid and blood- stained Pleural pain common Sudden expectoration of copious amounts of foul sputum if abscess ruptures into a bronchus Clinical signs High remittent pyrexia Profound systemic upset Digital clubbing may develop quickly (10 14 days) Consolidation on chest examination; signs of cavitation rarely found Pleural rub common Rapid deterioration in general health, with marked weight loss if not adequately treated
Investigations Radiological features Abscesses are characterised by cavitation and fluid level. Occasionally, a preexisting emphysematous bulla becomes infected and appears as a cavity containing an air fluid level
Managment Intravenousco-amoxiclav 1.2 g 3 times daily. Metronidazole 400 mg 3 times daily If an anaerobic bacterial infection is suspected (e.g. from fetor of the sputum), oral CA-MRSA is usually susceptible to a variety of oral non- -lactam antibiotics, such as trimethoprim/sulfamethoxazole, clindamycin, others Parenteral therapy with vancomycin or daptomycin and to metronidazole, or clindamycin and third-generation cephalosporins. Prolonged treatment for 4 6 weeks may be required in some patients with lung abscess. Physiotherapy
Prognosis In most patients, there is a good response to treatment and, although residual fibrosis and bronchiectasis Surgery may be required.
Pneumonia in the immunocompromised patient Patients immunocompromised by drugs or disease are at high risk of pulmonary infection. The majority of cases are caused by the same pathogens that cause pneumonia Patients with more profound immunosuppression, unusual organisms or those normally considered to be of low virulence or non-pathogenic may become opportunistic pathogens
Clinical features fever, cough breathlessness,
Diagnosis Invasive investigations, such as Bronchoscopy. BAL. transbronchial biopsy. surgical lung biopsy.
Management Broad-spectrum antibiotic a third-generation cephalosporin or aquinolone, plus an antistaphylococcal antibiotic, Or an antipseudomonal penicillin plus an aminoglycoside.
Respiratory infection in old age Increased risk of and from respiratory infection. Predisposing factors: . Atypical presentation . Mortality Influenza TB
THANK YOU To know the epidemiology ,etiology, pathogenesis ,clinical presentation, investigation ,diagnosis ,treatment ,complication ,prognosis
