Pneumonia
Pneumonia
Pneumonia
1.Definition:
It is inflammation of the lung Parenchyma, i.e. of the alveoli rather than the bronchi or bronchioles, of infective origin & characterized by consolidation. Consolidation: It is a pathological process in which the alveoli are filled with a mixture of inflammatory exudate ,bacteria and WBCs that on chest X-ray appear as an opaque shadow in the normally clear lungs.
2-Etiology:
The main five causes of pneumonia are 1. 2. 3. 4. 5. Bacteria e.g. streptococcus pneumoniae Virus e.g. influenza virus Mycoplasmas fungi various chemicals e.g. sulphur dioxide exposure
3-Epideomology:
1. Approximately 450 million people are affected per year by pneumonia. 2. It is common in all parts of world and can occur to persons of all ages. However, the clinical manifestations are most severe in very young, the elderly and the chronically ill person.
4-Pathophysiology:
Alveoli are the basic functional units of lung which are responsible for gaseous exchange between atmosphere and RBCs.
GENERAL MECHANISM
1. Physical barriers: Normally the microbes can enter the lungs through nose and/or aspiration of gastric content. This can be prevented by physical barriers such as nostril hairs, muco-ciliary blanket, coughing and sneezing reflexes. Large size foreign particles are trapped and removed by muco-ciliary blanket. Coughing and sneezing reflexes also aid in foreign particles removal. However, particles having smaller size (0.5 micron) can sometime enter alveoli. 2. Humoral barriers:These include alveolar macrophages and certain protective chemicals such as "defensins" released by endothelial cells. Foreign particles are phagocytozed by the alevolar macrophages and removed. If macrophages cannot remove these foreign particles, they morph into giant cells and engulf them. Endothelial cells release defensins to protect against foreign particles.
PATHOLOGICAL CONDITIONS
When our immune system is weak (e.g. as in HIV), all of the infective agents cannot be phagocytised by alveolar macrphages. Then, these infective agents cause damage to the lung endothelium. Different causative agents shows different attack strategies. For example , influenza virus releases hemagglutin protein which bind with sialic acid on the endothelial cell and enter the endothelial cells where it replicates and then new generation of viruses rupture the cell when they move out. Sometimes, cells containing virus undergo apoptosis. The tissue damage leads to starting of inflammation pathway which include The alveolar macrophages release IL-1 and cytokines to call in neutrophils and other monocytes present in the body.
Meanwhile walling off of area occur to stop the spread of infection. Neutrophils invasion occurs. Together, macrophages and neutrophils fight with foreign agents leading to accumulation of cell debris (of WBCs, and bacteria ) in the alveoli . Thus, pus is formed which makes expanding and contracting of alveoli difficult. Also, due to damaging of membrane and pus coating gaseous exchange becomes difficult.
5-Symptoms
Fever sweating Chills Headache Muscle pain Fatigue Chest pain Shortness of breath
6-Classification
1- Anatomic 2-Clinical Anatomic classification includes 1. 2. 3. 4. Lobar pneumonia Multi-lobar pneumonia Bronchial pneumonia Interstitial pneumonia
1-LOBAR PNEUMONIA An infection involving a single lobe in which an exudate homogenously fill the lobe and this exudate can be visualized on radiograph.
2-Multilobar pneumonia It involves more than one lobe and often cause more severe illness. 3- Broncial pneumoia It implies a patchy distribution of inflammation involving more than one lobe. It is initial infection of bronchi with extension into adjacent alveoli. 4-Interstitial pneumonia It involves connective tissue between alveoli and it may be called interstitial pneumonitis. It also involves fibrosis and inflammation.
1.ACUTE PNEUMONIA a. COMMUNITY ACQUIRED ACUTE PNEUMONIA: It is a lower respiratory tract infection with abrupt onset. It evolves through four stages 1-Congestion:- it affected lobe is heavy, red and boggy 2-Red hepatization:- Lung lobe has liver like consistency, alveolar spaces are filled with neutrophils and fibrin. 3-Gray hepatization:- lung is dry, grey and firm Resoulution:- Alveolar exudate is enzymatically digested, granular, semifluid debris that is reabsorbed. Its symptoms are high fever,shaking chill, pleuritic chest pain, productive mucopurulent cough, and hemoptysis .
b-COMMUNITY ACQUIRED ATYPICAL PNEUMONIA The Term atypical denotes moderate amount of sputum. In this type, there is absence of physical finding of consolidation, and also lack of alveolar exudate. 1. Causative agents Virus : Influenza type A and B, Adenovirus, Rhinovirus and Rubella Mycoplasma pneumoniae Legionella pneumoniae 2. Pathogensis Attached to the respiratory epithelium and produce inflammatory response, necrosis of cells. This process extends to alveoli and produce interstitial inflammation. 3. Symptoms Acute, non specific febrile illness characterized by fever, headache, malaise, cough with minimal sputum.
c. NOSOCOMIAL INFECTION: It occur at least 2 days after admission to hospital. Mostly patients in ICU when mechanically ventilated are at high risk of developing infection. Clinical features and investigation Endotracheal secretions New radiological infiltrate Increase in O2 requirement A core temperature increased by 38.3C Leucocytosis
1. 2. 3. 4. 5.
d. ASPIRATION PNEUMONIA: Aspiration pneumonia is also known as anaerobic pneumonia. It is an inflammation of the bronchial tubes and lungs that is caused by inhaling foreign material, may lead to collection of pus in the lungs. Aspiration of foreign material into the lungs may occur with disorders that affect the esophagus or normal swallowing. Another cause is a decreased or absent gag reflex in people who are unconscious or semi-conscious. Aspiration pneumonia usually affects older people and those who are debilitated,
intoxicated by drugs or alcohol, unconscious from anesthesia or a medical condition. A healthy person, who inhales a large amount of material, can also develop this condition.Causative agents are given below
e- LUNG ABSCESS: Localized area of suppurative necrosis within pulmonary parenchyma resulting in formation of one or more large cavities . 2.CHRONIC PNEUMONIA It is an inflammation of the lungs that persists for an extended period of time at least 6 weeks, without a sudden onset. In Chronic pneumonia there is typically an inflammation caused by slow-growing organisms, such as fungi or mycobacteria. In immuno compromised, such as those with debilitating illness, on immuno suppressive therapy or with HIV infection there is usually systemic dissemination of causative organism accompanied by wide spread disease.
7.Risk Factors
For Hospital acquired pneumonia Elderly and very young Pt.'s with severe medical conditions
Pt.'s who had surgery Pt.'s in ICU, who are on mechanical ventilators & particular for new born. Pt.'s who have received sedatives (hospital patients received sedatives are at high risk of nosocomial pneumonia.
For Community Acquired Pneumonia COPD which includes chronic bronchitis and emphysema. This condition is a major risk for pneumonia Long term use of corticosteroid inhalers may increase the risk of pneumonia in COPD patients. Patients with other type of lung diseases like interstitial lung disease are also at high risk of getting pneumonia
8.Diagnosis:
Physical Examination: Heart Rate Temperature Breathing (Fast, Shallow, Shortness, Difficulty) Whether you have chest Pain Oxygen level
You doctor will listen to your chest for: Crackling or bubbling noises made by movement of fluid in the tiny air sacs of the lung. Sounds made by rubbing of swollen (inflamed) lung tissue on the lining of the lung cavity (pleural friction rub). Lack of breath sounds in a certain area of the chest, which may indicate air is not entering an area of the lung. Wheezing,(whistling sound) which usually indicates inflammation or spasm is present in the bronchial tubes. Severity is assessed according to clinical parameters & outcome by use of assessment tool called " CURB-65" which stands for
2.General Treatment: 1-Empiric Treatment 2-Targeted Treatment 1-EMPRIC TREATMENT All of the foregoing recommendations pre-suppose that the infecting organism is known before treatment is commenced .In practice, this is rarely the case and therapy will initially be empirical or best guess in nature. Most authoritative recommendations for the initial treatment of CAP are those produced by British Thoracic Society
2- TARGETED TREATMENT can be further classified as a- According to the severity of disease b- According to the common microorganisms a- According to the severity of disease
ALTERNATIVE TREATMENT STRATEGIES Penicillin + Ciprofloxacin (Pencillin to cover Streptococcus Pneumonia,Ciprofloxacin for H.Influenza and the atypical bacteria) Or even Moxifloxacillin alone but Quinolones use is emerging as an important independent risk factor for the acquisition of MRSA,much of which is quinolones resistant.
DOSES 1- Ciproxin (Ciprofloxacin) Orally 750mg (bid/ tid)Second line therapy for legionella spp for atypical pneumonia. 2-Tazocin (Piperacillin + tazobactam) Child over 12 years and adult IV injection over 3-5 min or by iv infusion 2.25-4.5g every 6-8 hrly; usually 4.5g every 8hrs 3- Amoxil (Amoxicillin) For streptococcus pneumonia 500mg 8hrly orally 4-Cefuroxime for mild to moderate lower respiratory tract infection 250mg bid daily 5-Tetracycline 250mg every 6 hr increase in severe infection to 500mg every 68hrs