Suppurative Lung Diseases

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Presentation transcript:

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 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 Inside the lumen: pus Outside the lumen: fibrosis 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 Infected teeth Dental extraction Tonsillectomy Foreign body or vomitus may be inhale Chest wall wound Secondary to carcinoma Associated with tuberculosis, fungal infections and necrosis in malignant tumors and infected cysts

Clinical picture 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 obstruction of a bronchial airway (e.g., by mucus or tumor), It is associated with many pulmonary abnormalities, both pathological and mechanical, and is caused by obstruction of a bronchial airway (e.g., by mucus or tumor), lung compression (e.g., by pleural effusion, pneumothorax, or marked elevation of the diaphragm), insufficient surfactant production, inadequate inspiratory volume. postoperative patients, particularly when there is an abdominal or thoracic incision, 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: Profound dyspnea Severe hypoxemia Tracheal and mediastinal shift toward the affected side 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 • Removal of obstruction • 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 community- acquired 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 Malaise, pyrexia (temperature often >40°C), rigors, vomiting, confusion due to hypoxemia (especially in the elderly), and tachycardia. Cough Breathlessness. Pain - sharp pain aggravated by taking a deep breath or coughing. 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 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: 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 Gentle diaphragmatic breathing Localized basal expansion Positional rotation program Positive expiratory pressure(PEP) high frequency chest wall oscillation Active cycle of breathing Percussion and vibration Suction with caution Autogenic drainage Flutter 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 Maximize airflow within the airways. Improve the clearance of mucus. Improve ventilation.

Phases of Autogenic Drainage (AD) THREE PHASES: 1- unstick 2- collect 3- evacuate. Breathing at low lung volumes is said to mobilize peripheral mucus. This is the first or 'unstick' phase. It is followed by a period of tidal breathing which is said to 'collect' mucus in the middle airways. Then, by breathing at higher lung volumes, the 'evacuate' phase, expectoration of secretions from the central airways is promoted. A huff from high lung volume is now encouraged to clear the secretions from the trachea . Coughing is discouraged.

Surgical management It is indicated in localized lesion with sever symptoms and massive hemoptysis. Types of operations are: Lobectomy Segmentectomy Lung transplantation