Pneumonia pdf - D. Majeed

بسم هللا الرحمن الرحيم

a.c. 19/02/2020 1440 هجري

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

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.

Aetiology of lung abscess

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-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