Topic of the lecture:Topic of the lecture:

Pneumonias. Pleural syndrome. Pneumonias. Pleural syndrome. Ethiology. Clinical pattern. Ethiology. Clinical pattern.

Daignostics. Complications. Daignostics. Complications. Principles of treatmentPrinciples of treatment

Ass-prof. N. Bilkevych Ass-prof. N. Bilkevych

Acute inflammation of lung Acute inflammation of lung parenchyma with obvious parenchyma with obvious involvement of alveoli. involvement of alveoli. UUsually is caused by bacteria or sually is caused by bacteria or virusesviruses

Pneumonia (pneumonia)

Alveoli and lAlveoli and lung cells that produce ung cells that produce surfactant surfactant

• In up to 30% of patients no organism is identified, usually because of prior antibiotic administration. In many patients there is a preceding history of an upper respiratory virus infection. Most community acquired pneumonias can be managed at home, and have a low mortality; studies of such patients admitted to hospital have shown a mortality of 6—24% depending on the population studied and the presence or absence of such risk factors as old age and underlying disease.

EthiologyEthiology::

• Not specific pathogenic or obligate-pathogenic microbes

PathogenesisPathogenesis:: • Infection spread into the

organism through respiratory airways. Microbes appears and multiple on bronchial mucosa of upper airways and than spread down to bronchi and lung tissue

Acquired and congenital defects Acquired and congenital defects of bronchial clearanceof bronchial clearance

• disordered function of ciliated epithelium surfactant system defects

• infufficiency of alveolar makrophages

• Deranged bronchial patency

• disordered function of diaphragm and chest excursions

• changes of local and systemin immunity depressed coughing reflex

Pathogenetic differencePathogenetic difference

• Betveen croupous and focal pneumonia depends o the reaction of macroorganism on infectious agent

• In croupous pneumonia this reaction is hyperergic, in focal one – normo- or hypoergic

ClassificationClassification

• Community-acquired pneumonia.• Nosocomial (intrahospital) pneumonia – acute

infection of lower airways confirmed with X-ray, has being developed in 48 hrs after appearance of the patient in hospotal environment.

• Aspiration pneumonia.• Pneumonia in immunocompromizwd patients

Pneumonia: infecting organisms in Pneumonia: infecting organisms in approximate descending order of frequencyapproximate descending order of frequency

• Community acquired• Streptococcus pneumoniae• Mycoplasma pneumoniae• Influenza virus A• Haemophilus influenzae• Legionella pneumophila• Staphylococcus aureus• Coxiella burneti• Chlamydia psittaci• Hospital acquired• Gram-negative bacilli• Staphylococcus aureus• Streptococcus pneumoniae• Legionella pneumophila• Haemophilus influenzae• Pseudomonas spp

• Immunocompromised patients

• Pneumocystis carinii• Cytomegalovirus• Mycobacterium avium-

intracellulare• Mycobacterium tuberculosis• Streptococcus pneumoniae• Haemophilus influenzae• Legionella pneumophila• Actinomyces israelii• Aspergillus fumigatus• Nocardia asteroides

CourseCourseMild

RR – less than 25 per min, РS – less than 90 per min, t – less than 380C

signs of hypoxia and circulatory insufficiency are absent, volume of infiltrate – 1-2 segments unilaterally

ModerateModerate::

RR – less than 30 per min, РS – less than 100 per min, t – less than 390C

mild hypoxia, circulatory insufficiency is absent, volume of infiltrate – 1-2 segments bilaterally or entire lobe

SevereSevere::RR – till 40 per min, РS – more

than than 100 per min, t – till 400C

• signs of hypoxia and circulatory insufficiency are present, volume of infiltrate – several segments or more than 1 lobe

Very severeVery severe

RR – more than 40 per min, РS – more than 100 per min, t – more than 400C

• Marked signs of hypoxia and circulatory insufficiency, extensive damage

Croupous pneumoniaCroupous pneumonia• Acute inflammation of lungs, which in

most cases spreads on all pulmonary lobe. That is why it is called lobar pneumonia (pneumonia lobaris), but can be limited to the affection of segment or a few segments.

• Synonims fibrinous pneumonia, pleuropneumonia

• The usual clinical presentation in pneumonia caused by Streptococcus pneumoniae is acute, with the abrupt onset of malaise, fever, rigors, cough, pleuritic pain, tachycardia and tachypnoea, often accompanied by confusion, especially in the elderly. The signs in clude a high temperature, consolidation and pleural rubs, and herpetic lesions may appear on the lips. There may also be signs of pre-existing disease, especially chronic bronchitis and emphysema or heart failure in the elderly. The sputum becomes rust-coloured over the following 24 hours. The diagnosis is made on clinical grounds and confirmed by chest X-ray.

PneumococciPneumococci

пневмококпневмокок

Pneumococci are typically Pneumococci are typically asociated with pneumoniaasociated with pneumonia

Patalogoanatomical Patalogoanatomical stagesstages::

• inflow (12 hrs - 3 days)• red hepatisation (1 hr - 3 days)• grey hepatisation ( 2 - 6 days)• resolution

Clinical stagesClinical stages::

• initial• clinical manifestation

(corresponds to red and grey hepatisation

• resolution

Lobar pneumonia: stage of Lobar pneumonia: stage of onsetonset

• Morphology. Congestion stage — extensive serous exudation, vascular engorgement, rapid bacterial pro liferation.

• Inspection. An increased respiratory rate is usually evident. Pain is a frequent accompaniment, and with it the involved side shows a lag of respiratory motion.

• Palpation. Palpation confirms the findings on in spection. Tactile fremitus is normal or even slightly decreased, and a pleural friction rub may be present.

• Percussion. Impaired resonance may be elici ted with light percussion. This finding is extremely important.

• Auscultation. Although the breath sounds may be diminished, expiration is prolonged and crepitation (crepitus indux) is heard. With pleural involvement, a pleural friction sound is determined.

Lobar pneumonia: stage of Lobar pneumonia: stage of consolidationconsolidation

• Morphology. Red hepatization stage — airspaces are filled with PMN cells, vascular congestion, extravasa tion of RBC. Grey hepatization stage — accumulation of fibrin, inflammatory WBCs and RBCs in various stages of disintegration, alveolar spaces filled with in flammatory exudate.

• Complaints. Coughing may be associated with i sharp pain in the affected side. Mucoid sputum be comes rusty brown (prune juice color).

• General inspection. Cyanosis of the lips and fin gers. When the fever is high, the face may be flushed The patient's nostrils dilate on inspiration, and expi ration is often grunting.

• Inspection. Dyspnea is invariably present. Respi ratory movements are generally decreased on the af fected side.

• Palpation. Diminished respiratory excursions, i pleural friction rub may be felt. Tactile fremitus is in creased.

• Percussion. Dullness.• Auscultation. Bronchial breathing, bronchophony,

pectoriloquy and whispered bronchophony are evident with consolidation provided the bronchus to the in volved area is open. Rales are less numerous and dis tinct than in the stages of engorgement or resolution,

Forced positionForced position

Lobar pneumonia: stage of Lobar pneumonia: stage of resolutionresolution

• Morphology. Resolution stage — resorption of the exudate.

• Inspection. The patient looks more comfortable and the cyanosis disappears. The dyspnea disappears and the affected lung begins to expand again.

• Palpation. The previously increased tactile fremitus becomes less marked and gradually findings beco me normal.

• Percussion. The dullness gradually disappears and normal resonance returns.

• Auscultation. The bronchial breathing is gradually replaced by bronchovesicular breathing and later by normal vesicular breathing. Crepitation reappears (crepitus redux). Small and large moist rales are heard in increasing numbers.

Laboratory testsLaboratory tests• The white cell count and ESR are usually elevated.

Blood should be sent for culture before antibiotic ther apy is given and a baseline blood sample taken for se-rology. Sputum should be sent for culture. Direct Gram-staining of a fresh sputum sample may show the organism. Pneumococcal antigen can be identified in sputum, urine or serum. Antibiotic therapy should not be delayed while awaiting sputum culture results.

• The symptoms usually resolve rapidly over 7—10 days and the signs over a slightly longer period. Radio logical resolution should be complete by 12 weeks. Per sistence of changes in the X-ray after this, or recur rence of pneumonia, suggests some other pathological process and should trigger a search for underlying car cinoma. Careful examination should be made at pre sentation for clinical features of AIDS.

ComplicationsComplications

• Lung abscess or gangroene• Pleurisy• Toxic shock• Myocarditis• Acute respiratory insufficiency• Pneumosclerosis• Atelectasis• Sepsis• Meningitis, encefalitis

PleurisyPleurisy

Pleurisy with effusion: 1—Damoiseau's curve; 2—Garland's triangle;3—Rauchfuss-Grocco triangle.

Lung abscessLung abscess

Lung abscessLung abscess

Focal pneumoniaFocal pneumonia

Focal pneumoniaFocal pneumonia

Focal pneumoniaFocal pneumonia• The feature of these pneumonias is

an involvement of separate lobules or groups of lobules in the inflammatory process. Therefore it is named also lobular (pneumonia lobularis)

Synonim: bronchopneumonia

• Mycoplasma pneumoniae is the most common cause of the «atypical» pneumonias. Infection usually occurs in older children and young adults, who present with pharyngitis and bronchitis; pneumonia occurs in mi-nority and is rarely severe. Psittacosis is acquired from birds and Q-fever from animals, commonly farm live stock; they also cause «atypical pneumonia», although the Q-fever organism, Coxiella burnetti, may also cause endocarditis. The diagnosis of the atypical pneumonia is usually made by serology.

• Staphylococcal pneumonia typically occurs as a complication of influenza, especially in the elderly and, although uncommon, is important because of the at tendant high mortality. It is a destructive pneumonia, which frequently leads to the formation of cavities within the lung. Such cavitating pneumonia was most frequently caused by tuberculosis in the past but now Staphylococci, Klebsiella and anaerobic organisms are the most common causes.

• Legionnaires' disease is pneumonia caused by Le-gionella pneumophila. Infection is most common in debilitated or immunocompromised patients. Most cases are sporadic, but outbreaks occur from contami nated water droplet sources. Patients may present with a wide spectrum of additional symptoms, such as head ache, cerebellar ataxia, renal failure or hepatic involve ment. Special medium is necessary for the culture of the organism and the diagnosis is usually made by serology.

• Aspiration pneumonia results from the aspiration of gastric contents into the lung and is associated with impaired consciousness {e.g. anaesthesia; epilepsy, al coholism) or dysphagia. Multiple organisms may be isolated.

• Nosocomial pneumonia occurs when infection takes place in hospital; patients may be debilitated, immunocompromised or have just undergone a major operation. The causative organism(s) are often Gram-negative or Gram-positive coccus, Staphylococcus au-reus. The high mortality is usually related to the sever ity of the underlying disease. Lung abscess or empye-ma (a collection of pus within the thoracic cavity), or both, may be caused by specific organisms or may com plicate any aspiration pneumonia. Septic pulmonary emboti can lead to multiple lung abscesses, pulmonary infarcts may become infected cavities and abscesses can develop distal to lesions obstructing a bronchus.

• Treatment of all pneumonias should be started im mediately and the antibiotic chosen should be the «best guess» (decided on by the origin of the pneumonia and its clinical severity). If community-acquired, then semisynthetic penicillins (or macrolids) will usually be effective, in severe cases – cefalosporines. The reserve drugs are pthorchynolones. Combinations such as macrolids with cephalosporin may be used.

•

• If legionnaires'disease is suspect ed on epidemiological grounds, rifampicin should be given with erythromycin. In hos pital-acquired pneumonia, combination therapy is required to cover the range of possible pathogenic or ganisms (especially Gram-negative bacilli).

• In aspiration pneumonia, in which anaerobes may be present, metronidasole should be added to these combinations. Supportive measures should include oxygen, intravenous fluids, inotropic agents when necessary, bronchial suction and assisted ventilation.

• Physiotherapy and bronchod-ilators are of value in pneumonia complicating chron ic bronchitis and emphysema.

Infection in the Infection in the immunocompromised hostimmunocompromised host

• There has been a steady increase in the number of patients whose immune system has been damaged by malignancy, organ failure, drugs or the HIV vi rus. In such immunocompromised patients, infections of the lung are common and may be caused by or ganisms that are not usually pathogenic in the nor mal host. Invasive fungal infections tend to occur in neutropenic patients, whereas T-cell defects of ten lead to infection with viruses, mycobacteria and protozoa such as Pneumocystis carinii. The tempo of infection in the immunocompromised patients can be extremely rapid; it is important to take steps to identify the pathogen and to start therapy as soon as possible.

• Pneumocystis carinii is the most important cause of fatal pneumonia in immunosuppressed patients. It is believed that the infection is acquired in early child hood, and that reactivation occurs when immune sys tem becomes damaged. The incubation period is ap proximately 1-2 months before the insidious appear ance of a low-grade progressive pneumonia, which manifest itself as severe dyspnoea with, at first, only minimal chest signs and X-ray changes.

• In Pneumocystis carinii pneumonia the changes on X-ray may be very minor, but the patient is markedly hypoxic and a transbronchial biopsy usually reveals P. carinii. Unless the infection is treated promptly, most severe pneumonic changes follow.

• The pneumonia progresses rapidly, and within a few days obvious pneumonic changes may be seen on the chest X-ray. Diagnosis depends on demonstrating the organism in sputum, bronchial lavage or lung tissue, which may require a lung biopsy. Treatment is with cotrimoxazole or pentamidine; both of these may be used in prophylaxis. Mortality remains high despite treatment.

Principles of treatmentPrinciples of treatment

• Antibiotics• Expectorants• Desintoxication• Oxygen• Antigistamine agents• Symptomatic therapy

ССorrect regimenorrect regimenBed mode

Care of patients: • proper lighting and ventilation

(fresh air improve patient’s sleep and bronchial clearance)

• Care of oral cavity

DietDietabout 2,5-3 litres of loquid per day (water with lemon juice, mineral or

boiled water • Fruit juices • chicken clear soups• food should be easly assimilable• in some days – diet № 10 or 15.

Diet enriched with vitaminsDiet enriched with vitamins

КліматотераКліматотерапіяпія

ClimatotherapyClimatotherapy mild dry warm mild dry warm

climatclimat

ПРИМОРСЬКІ КУРОРТИ З НИЗЬКИМ ПРИМОРСЬКІ КУРОРТИ З НИЗЬКИМ РІВНЕМ ВОЛОГОСТІРІВНЕМ ВОЛОГОСТІ

Symptomatic meansSymptomatic means• antitussives• antipyretics• Pain killers• antiinflammmatory

(nonsteroidal in pleural pain)• cardiotonics