Suppurative Lung Diseases
DR. MOHAMED SEYAM PHD. PT.
ASSISTANT PROFESSOR OF PHYSICAL THERAPY
SUPPURATIVE LUNG DISEASES
SUPPURATIVE LUNG DISEASES is a syndrome characterized by cough and
expectoration that is usually excessive, purulent, paroxysmal and related to
posture.
Pulmonary Tuberculosis( TB)
Bronchiectasis
Cystic fibrosis
Lung abscess
Pneumonia
atelectasis
PT Management of SLD
1-Pulmonary Tuberculosis
One-third of the world's population is infected by the TB bacillus,
which may become active if the host's defense mechanisms are
compromised by poor living conditions, drug dependency or HIV
infection.
TB of the lung is the commonest form of the disease, causing 3
million deaths a year, more than any other infection.
Coughing disseminates infected aerosol, which can remain
suspended in the air for hours.
Symptoms
1.
2.
3.
4.
5.
6.
7.
Fever,
Night sweats
Cough
Chest wall pain
Weight loss
Hemoptysis
Dyspnea (breathlessness)
The X-ray shows cavitating lesions in the most stretched and poorly
perfused areas of lung, which are the apices in humans.
The tubercle bacillus is slow growing and tough, responding only to 6
months of treatment with a combination of powerful antibacterial drugs.
The patient is no longer infectious after 2 weeks' treatment, providing
sputum is clear of the bacillus.
The physiotherapist's role is usually confined to eliciting sputum
specimens in a negative pressure room and devising ways to
encourage exercise in an isolation cubicle.
A high-efficiency particulate air-filtering mask must be used throughout.
Patients in isolation need a window, a telephone and reassurance that they
are not stigmatized.
2-Bronchiectasis
It is an abnormal and
irreversible dilatation of the
bronchi result from chronic
airway infection and
inflammation.
Common in basal and
bilateral segments of lungs.
pathology
Pulmonary infection lead to destruction and dilatation of bronchial wall.
Bronchial obstruction lead to collapse.
Site of disease may be: bilateral, basal or patchy.
Shape may be: tubular, fusiform or saccular
Inside the lumen: pus
Outside the lumen: fibrosis
3-Cystic fibrosis
Developmental anomaly
of bronchial tree with
abnormally dilated
bronchial wall caliber with
bronchial cyst formation.
it is an autosomal
recessive disease of
chloride ion channels in
exocrine glands
4- LUNG ABSCESS
It is a necrotic, suppurative and cavitative lesion mainly due to
infection by pyogenic organisms.
It is almost caused by aspiration of oral secretion by impaired
conscious patients
Mode of infection
1. Infected teeth
2. Dental extraction
3. Tonsillectomy
4. Foreign body or vomitus may be inhale
5. Chest wall wound
6. Secondary to carcinoma
7. Associated with tuberculosis, fungal infections and necrosis in malignant tumors
and infected cysts
Clinical picture
1.
2.
3.
4.
5.
6.
Fever
Malaise
Cough
Pleuritic pain
Dyspnea
Expectoration and
excessive sputum
7- Hemoptysis
8- Tachypnea
9- Tachycardia
10- Tracheal shift
11- Anemic and weight loss
12- Clubbing finger
5- Atelectasis
Atelectasis is a state of lung tissue characterized by the collapse
of alveoli so they become airless.
Atelectasis occurs only if there is blood flow to the affected
alveoli, allowing absorption of gases.
It can occur as microatelectasis, which involves a diffuse area of
terminal lung units,
or as segmental or lobar atelectasis, which follows anatomic
distribution of a blocked airway.
CAUSES
It is associated with many pulmonary abnormalities, both pathological and
mechanical, and is caused by
1. obstruction of a bronchial airway (e.g., by mucus or tumor),
2. lung compression (e.g., by pleural effusion, pneumothorax, or
marked elevation of the diaphragm),
3. insufficient surfactant production,
4. inadequate inspiratory volume.
5. postoperative patients, particularly when there is an abdominal
or thoracic incision,
6. neurologic and musculoskeletal disorders that hinder proper
lung expansion.
Pathophysiology
Complete obstruction of an airway produces entrapment of air within the
alveoli distal to the obstruction; the slow absorption of gases into the
pulmonary capillary blood results in collapse of the alveoli, allowing
absorption of gases.
Collapsed, airless alveoli reduce lung compliance, which increases the work
of breathing.
If the atelectasis is localized, hypoxic vasoconstriction usually limits V/Q
mismatching and helps to maintain relatively normal gas exchange;
If atelectasis is extensive, the increase in pulmonary arterial pressure often
overrides the vasoconstriction, creating an intrapulmonary shunt (i.e., blood
flows past non-ventilated alveoli), and gas exchange deteriorates.
Diagram showing
atelectasis with
1- elevated hemidiaphragm
2- mediastinal shift toward
the affected side.
Clinical Manifestations
• Few or no symptoms if atelectasis evolves slowly; possible fever and cough
• If acute collapse of a large section of lung:
1. Profound dyspnea
2. Severe hypoxemia
3. Tracheal and mediastinal shift toward the affected side
4. Elevated diaphragm.
• Reduced or absent breath sounds, crackles and possible wheezes.
• Chest x-ray showing well-defined area of increased density, volume loss,
and tracheal and mediastinal shift toward the
affected side
Specific Treatment
• Prevention (e.g., airway clearance techniques, breathing exercises,
mobilization)
• Removal of obstruction
Vigorous chest physical therapy techniques to mobilize mucous obstructions.
Flexible bronchoscopy with lavage for removal of mucus plugs and retained
secretions.
Bronchoscopic or surgical removal of aspirated foreign object
Excision of tumor
• Treatment of underlying disorder if not obstructive atelectasis
Chest tube insertion for pneumothorax.
Pleurocentesis for drainage of pleural effusion.
6-Pneumonia
 Pneumonia is
an acute inflammation of the lung tissue - the
alveoli and adjacent airways.
 Streptococcus pneumonia is the most prevalent communityacquired pneumonia and affects all age groups.
Pathology
The invading organism causes inflammation in the bronchioles
and alveoli.
The exudates spreads into neighboring alveoli to provide a
medium for rapid spread of bacteria.
The alveoli become filled with red blood cells, leucocytes,
macrophages and fibrin and there is congestion throughout the
lobe.
Clinical features
1. Malaise,
2. pyrexia (temperature often >40°C), rigors, vomiting, confusion
due to hypoxemia (especially in the elderly), and tachycardia.
3. Cough
4. Breathlessness.
5. Pain - sharp pain aggravated by taking a deep breath or
coughing.
6. Mucus may be rusty or green or tinged with blood
(Hemoptysis)
Investigations
1. Hematology : This may reveal a raised white blood cell count.
2. Biochemistry : Arterial blood gases should be measured to reveal the
extent of arterial hypoxemia.
3. Microbiology : Sputum should be sent for Gram staining to identify the
causative organism.
4. Pleural aspiration for culture
5. Radiograph: Consolidation can be seen as an opacity especially in lobar
pneumonia. There may also be evidence of a pleural effusion.
6. Auscultation.
- Bronchial breathing
- Wheeze
Medical Management
1.
2.
3.
4.
Antibiotics are given to control infection.
Adequate fluids must be taken to ensure fluid balance.
Analgesics are given to relieve pleuritic pain.
Oxygen therapy may be necessary and blood gases
should be monitored regularly.
General management
High protein diet
Correction of anemia
Improvement of hygiene condition
Vaccination
Weight control and nutrition
Smoking cassation and control
Medication
Infection control
Physiotherapy Management
Physiotherapy is indicated when the inflammation has begun to resolve.
The aims of treatment are:
1.
2.
3.
4.
to clear lung fields of secretions
to gain full re-expansion of the lungs
to regain exercise tolerance and fitness.
to reduce Broncho spasm (if present)
Physical therapy goals for SLD
1-Maximize the patient quality of
life, general health and
physiological reverse capacity and
function
2- Facilitate mucociliary transport
3- Optimize secretions clear
4- Improve alveolar ventilation
5- Optimize lung volumes and
capacities
6-Improve ventilation perfusion
matching
7-reduce work of breathing
8- maximize aerobic capacity
9- Increase endurance and exercise
capacity
10-optimize general muscle
strength
Physical therapy modalities
1. Gentle diaphragmatic breathing
2. Localized basal expansion
3. Positional rotation program
4. Positive expiratory pressure(PEP)
5. high frequency chest wall oscillation
6. Active cycle of breathing
7. Percussion and vibration
8. Suction with caution
9. Autogenic drainage
10. Flutter
11. Posture drainage
Autogenic drainage (AD)
Autogenic drainage is breathing at different lung volumes and
an active expiration is used to mobilize the mucus.
It aims to
1. Maximize airflow within the airways.
2. Improve the clearance of mucus.
3. Improve ventilation.
Phases of Autogenic Drainage (AD)
THREE PHASES: 1- unstick
2- collect
3- evacuate.
1. Breathing at low lung volumes is said to mobilize peripheral mucus. This
is the first or 'unstick' phase.
2. It is followed by a period of tidal breathing which is said to 'collect'
mucus in the middle airways.
3. Then, by breathing at higher lung volumes, the 'evacuate' phase,
expectoration of secretions from the central airways is promoted.
4. A huff from high lung volume is now encouraged to clear the secretions
from the trachea .
5. Coughing is discouraged.
Surgical management
It is indicated in localized lesion with sever symptoms and
massive hemoptysis.
Types of operations are:
1. Lobectomy
2. Segmentectomy
3. Lung transplantation