Respiratory System Infections
The common cold
Several different viruses, (the
rhinoviruses) Shift
and drift
Virus damages epithelial cells causing
inflammation Watery
discharge
Condition abates in a few days as
cellular immunity develops
May lead to secondary bacterial
infection, eg. Staphylococci, Streptococci or Pneumococci.
Tonsillitis, pharyngitis,
laryngitis, tracheitis, otitis media.
Remember the respiratory tract is
continuous without boundaries.
Inflammation of the lining epithelium,
often with pus.
Acute Bronchitis
Bronchitis is inflammation of the
lining of the bronchi due to infection
This may lead to bronchopneumonia
Pneumonia
An acute inflammatory process of the
substance of lung tissue
An infection, involving the bronchial
passages and the alveoli
Consolidation of the alveolar spaces
with inflammatory exudates
Any lung condition in which the
alveoli become filled with fluid or blood cells
Pulmonary ventilation and diffusion
are impaired ----- hypoxia
Two forms occur broncho and lobar
pneumonia
Often classified by the causative
organism eg pneumococcal or streptococcal pneumonia
Bronchopneumonia
pus in many of the bronchi in both
lungs,
many small areas of infection and
inflammation, possible patchy consolidation
often more marked at the bases
many kinds of bacteria
mostly infants and old people
after viral infections, aspiration or
immobility
Often starts as a virus, especially in
the young and old.
Increased risk in immobility, pre-existing
reduced ventilatory function, excessive mucus production, and suppressed cough
reflex.
Common aetiological organisms include,
Staphylococci, Streptococci, and Pneumococci, viruses and fungi.
May also be caused by aspiration.
May be caused by immobility, referred
to as hypostatic pneumonia.
A common finding after death.
A common condition, often complicates
other conditions.
With Staphylococcal infection abscess
formation may occur, possibly leading to metastatic infection.
Signs and symptoms
sudden onset of chill followed by
fever, usually high 39.5`C
dyspnoea
increased respiratory rate, often
shallow
respiratory rate rises out of
proportion to temperature increased
pulse rate
cough - often unproductive initially
and very productive later crepitations
pallor malaise
cyanosis in severe hypoxaemia
colour and consistency of sputum will
vary with causative organism, usually tenacious, blood streaked and purulent
sputum weakness
headache and aching pains cold
sores around the mouth
Aetiology
Streptococcus pneumoniae
(Pneumococcus) Mycoplasma
pneumoniae
Influenza A virus Haemophilus
influenza
Chlamydia pneumoniae Staphylococcus
aureus
Pneumocystis carinii
Prevention
Vaccination of children against
measles and pertussis
Pneumococcal vaccine may be used in
"high risk" individuals
more common in:
Bronchial obstruction Aspiration
in oesophageal obstruction Bulbar
palsy
Cystic fibrosis "Ill"
patients Immunosuppression
Intravenous drug abuse Chronic
bronchitis Malnutrition
Alcoholism Smoking Cold
weather
Overcrowding Hot
dry indoor air Air
pollution
Nursing prevention
Mobilise nurse
upright
allow free chest movement fluids,
prevent dehydration
deep breathing expectoration,
coughing
no smoking physiotherapy
suction if unconscious antibiotics
in immunosuppressed individuals
Observations in pneumonia
TPR BP Tachycardia
may indicate increasing hypoxia
Progress or resolution of the
condition Possible
spread of the infection and shock
Listen to breathing sounds Observe
for symmetrical chest movements
Listen for areas of reduced or absent
air entry Colour
- pallor, cyanosis
Type and volume of sputum - culture
and sensitivity Fluid
balance chart
Disorientation or reduced levels of
consciousness Blood
tests eg white cell count and ESR
CXR to identify affected areas of lung
Management
Aim
Resolution of consolidation ie,
reabsorption and expectoration of fluids. Kill
infectious agents.
Prevention of spread
Droplet infections/disposal of
infected sputum
Possible barrier nursing, (pneumonic
plague Yersinia pestis)
Treat the infection
Broad spectrum antibiotics - as soon
as a sputum is taken for C and S
Mobilisation of secretions
A mucus plug may lead to atelectasis Nurse
propped up
Mobilisation of secretions Humidified
oxygen as required
Frequent positional changes Patients
should cough at least every hour
Physiotherapy
Improvement of overall condition
Physical and mental rest Nutrition
- concentrates if necessary
Reassurance Involve
family in care
Fluids 3 - 4 litres per day Comfort
changes of gown/washes due to sweating
Patient comfort
Initial painful unproductive cough -
linctus Later productive cough
- expectorant
Mouth care Prevent
harm during disorientation
Drug treatment
Mild
Amoxycillin Erythromycin Amoxycillin
and Erythromycin
Flucloxacillin Oral
cefaclor 250 mg 8 hourly and erythromycin 500 mg three times per day
Severe
Intravenous cefuroxime 1.5 g six hourly
and erythromycin
Convalescence
Gradually increase activity with
recovery Extra
rest for some weeks or even months
Patients may have lowered resistance
for some time
Nutrition Breathing
exercises for a few weeks
Lobar pneumonia
Aetiology
Pneumococcus, (Streptococcus
pneumoniae) almost always
Lobar pneumonia killed thousands of
young adults pre penicillin.
Clinical features
sharp knife like pain on respiration pneumococci, (Streptococcus pneumoniae)
young adults mostly often
rust coloured or purulent sputum
rapid shallow respirations the
affected side moves less
dullness to percussion
Treatment
Antibiotics
Analgesia - do not suppress
respiration or depress cough reflex, eg pethidine 100 mg
Large amounts of inflammatory exudate
may completely fill one lobe of the lung
This process is described as
consolidation
The pleural surface of the lobe is
also inflamed and becomes covered with a shaggy thick layer of sticky fibrin,
ie. pleurisy
Death may occur but most recover - the
lung tissue recovers with little or no residual damage
Complications of pneumonia
Lung abscess
Severe localised suppuration
associated with cavity formation
Often secondary to aspiration Secondary
to obstruction
After septic pneumonia
Copious sputum often foul smelling due
to anaerobic activity
Swinging fever Ensure
complete treatment in pneumonia
Empyema
Pus in the pleural cavity Often
a complication of a ruptured abscess
Often anaerobic organisms Patients
are very ill with a high fever
Others
Cardiac failure Endocarditis Meningitis
Primary Atypical Pneumonia
Slow onset with a bronchopneumonia -
like pathology.
Often caused by mycoplasma, Mycoplasma
pneumoniae, (a type of organism like very small bacteria).
Tuberculosis
Approx. 10% of the worlds population
die from TB
"captain of the men of
death"
TB is reappearing in the west,
factors,
Aetiology
Mycobacterium tuberculosis
Transmission
Transmitted in milk
Inhalation of bacteria in to lungs
from an infected person
Diagnosis
AFBs CXR Positive
tuberculin test reaction Unexplained
cough
Clinical features
Influenza type symptoms or insidious
onset
Fatigue, malaise, weight loss, low
grade fever, anorexia etc.
Cough, mucoid or muco-purulent sputum
Haemoptysis, chest pain
Systemic involvement
Vaccination
BCG is a harmless form of tuberculosis
grown on potatoes.
It leaves a small tubercle in the skin
where it is injected, there will also be a tubercle in the armpit, and some
degree of immunity to subsequent infection.
Primary Infection
May be asymptomatic
Bacteria enter the lungs and divide,
(droplet infection)
A small knot called a tubercle,
composed of phagocytes
Some bacteria are usually carried to
local lymph nodes
Usually cellular immunity develops and
the infection subsides
If immunity does not develop, eg. due
to immune overload the tubercle bacilli divide and destroy some local cells.
Bacterial division and tissue
destruction leads to the release of some bacteria into a bronchus.
This may cause a rapidly spreading
bronchopneumonia, and also allow spread to any other part of the body.
Small tubercles may form anywhere and
may be seen in the back of the eye. These look like millet seeds giving rise to
the term miliary tuberculosis.
Tuberculosis bronchopneumonia and
miliary tuberculosis are both rapidly fatal without treatment.
Even with treatment there may be
residual damage to eyes, brain, bone and other organs.
Re-infection
A second infection will be different
due to the pre-existing cellular immunity
In most cases the immune cells rapidly
destroy the mycobacterium
However if the immunity is less
efficient inflammatory and fibrous cells move to the bacteria, however these
cells die without killing the bacteria and subsequently form a caseation,
(cheesy like material)
Fibrous cells form a fibro-caseous
lesion
This gives a situation of chronic
inflammation, the damage done by the bacterial balanced by the action of
inflammatory and fibrous cells
Inflammation and repair carry on
Local necrosis may occur resulting in cavitation
Mycobacteria may spread, eg. to
vertebrae or kidney forming a cold abscess, (so called because the fibrous
tissue on the outside shows no active inflammation).
Management
The aim of treatment is to improve the
overall health of the patient to tilt the balance in his or her favour.
Isolate active pulmonary cases
Bed rest does not help
In combination with drugs, compliance
is vital!!
Rifampicin, isoniazide, ethambutol,
pyrazinamide, streptomycin
Resistance may become a problem
Contact tracing
Mantoux test indicated an individuals
level of immunity.
Prevention
Promote vaccination
Promote good housing, prevent dampness
and overcrowding
Prevent poverty Screen
population movements
Teach disease awareness Promote
general physical and mental health
Avoid exposure to bacilli Maintain
degree of immunity
More common over age of 30
More common in presence of other
diseases, eg. diabetes, silicosis
More common after recent GI surgery Alcoholism
Pharyngitis
Influenza
Otitis media
Croup
Acute epiglottitis
Bronchitis
Bronchiolitis – respiratory
syncytial virus
Viral pneumonia
Atypical pneumonia
Bacterial pneumonia
Tuberculosis
Foreign bodies
Aspiration pneumonia
Heat and / or smoke inhalation