Zurab Kheladze & Zviad Kheladze Critical Care Medicine HAND BOOK

Transcription

1 Acute Pneumonias Is a severe infective-inflammatory disease, in this process all pulmonary element is involved. Pneumonia retains the fourth place between reasons of death, and lethality of patients during acute pneumonias complies 40-50%. Pathogenesis. The reasons that causes pneumonia without hospital are: streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Chlamidia pneumoniae, Legionella pneumoniae, Klebsiella pneumoniae, Staphylococcus aureus, Streptococcus hemilitikus. As for hospital pneumonias, it s considered to be pneumonia that is developed in 48 hours after hospitalization. According to the causing reasons of pneumonia there are distinguished the following etiologic peculiarities: in patients with broncho-pulmonary profile- Staphylococcus, aureus, pseudomonas, aeroginosa,klebsiella pneumoniae; with patients of urhologic profile-e. coli, Proteus, Enterococcus; with patients in post operational period- Staphilococcus aureus, E.coli, Proteus, Pseudomonas aeroginosa; hematologic patients- E.coli, Klebsiella pneumoniae, pseudomonas aeroginosa, staphylococcus aureus; with patients of dermatologic profile-staphilococcus aureus, E.coli, proteus, pseudomonas aeroginosa. earlier pneumonias associated with ventilation (pneumonias, which develop less than 7 days of controlled respiration) are caused from streptococcus pneumoniae, enterobacteriae, haemophilus influencae, staphylococcus aureus. later pneumonias related with ventilation is invoked by- Pseudomonas aeroginosa, enterobacteriae, staphiloccocus aureus. In the immunodeficiency condition pneumonia is caused by pneumocysts, cytomegalovirus, conditional-pathogenic fungus-aspergillus, criprococcus, and other pathogenic substrates. After entering a causing factor in pulmonary tissue( bronchogenous, hematogenic ways, spreading of microorganisms from neighbor organs), there is formed local inflammation of pulmonary tissue that includes the last one entirely (the inflammation is spread in the interalveolar area of bundle), there is developed sensibilization direct to the infective agent and immunoinflamatory reaction of pulmonary tissue (acute pneumonias are discussed as organism s hypererregic reaction); microcirculation in lungs is damaged that causes: *developing of ischemic centers in lungs; *formation of multiple micro thrombus; On the Russian pulmonologists congress in 1995 was collaborated the following classification of pneumonia: Critical Care Medicine HAND BOOK Page 1

2 1) groups distinguished by etiology: pneumococcus, streptococcus, staphylococcus; blue-green purulence s bacillus, hemophilic bacillus, Friedlander's bacillus, Chlamydia, legionellas, caused from viruses. 2) Groups distinguished by epidemiology: pneumonia apart from hospital, aspirational pneumonia, pneumonia, that is developed at the time of severe defect of immunity( congenital immunodeficiency, AID-infection, iatrogenic immunosuppression) 3) Groups distinguished by localization: One-sided (left- or right-sided), total, partial, segmental, central (near the root), doublesided. 4) groups differentiated by severity: weak, average, severe. 5) Groups distinguished by complications: Interpulmonary-parapneumonal pleurisy, pulmonary abscess and gangrene, syndrome of bronchial obstruction, acute respiratory failure. Apart from lung- acute pulmonary heart, inflectional-toxic shock, nonspecific myocarditis, meningitis, meningoencephalitis, syndrome of disseminate interblood-vessel coagulation, acute glomerulonephritis, toxic hepatitis. 6) groups distinguished by ongoing: periods of severity, ostentatious improvement, recovery, and processes of prolonged passing. During pneumonia the development od acute respiraotory failure is conditioned by: *lung s one or several part inflammatory injury; *lungs disseminate or mixed injury; *development of parapneumonial pleurisy; *generate destructive centers in pulmonary tissue. Partial pneumococcus pneumonia (crupous toxic pneumonia) is an inflammatory injury of lung s one or several part. the most often is developed at the time of pneumococcus pneumonia. The peculiarity is severe beginning with a single feverish and increasing of body s temperature until 39-40, the mostly is developed with healthy patients; pain in chest area is early symptom( the first-second days) that strengthens during respiration and cough (there is developed dry pneumonial pleurisy). The signs of acute respiratory failure are revealed in the first days. In the beginning of the disease tympanic sound is heard by percussion, that is changed by overhear. By means of auscultation breathe in the beginning is vesicular, after 2-3 days there is tender crepitating; after solidification of pulmonary tissue ( stage of awaking) is heard bronchial breathe, crepitating and friction of pleura is appeared. In the phase of exudate s liquefaction percussive sound is reduced, respiration is rough in the beginning, then vesicular, crepitating is appeared again that is louder than in the beginning of the disease thin-vesicle vocal wet wheeze, Critical Care Medicine HAND BOOK Page 2

3 bloody phlegm, that is conditioned by a large content of erythrocytes in blood, is seen on the 5-7 day of the disease. In the blood there is revealed high neutrophilous leukocytosis with leukocytic formula s deviation in the right before young forms, neutrophilouses toxic granularity; at the period of exacerbation of disease eosinophils dissaper, lymphocytes and thrombocytes are reduced. In the period of ostentatious improvement the norm of last mentioned ones becomes usual. ESR increases, the level of seromucoid, fibrinogen and alpha-2- globulin; on the saliva s medicament painted by Gram s method there are discovered grampositive lantseta-type lancet-type diplococi. The most characteristic alteration by X-ray is met in the phase of solidification in the form of pulmonary part s intensive covering. Pneumonia of Friedlender passes severely. In general lung s upper part s are injured. Frequently suffer patients who have diabetes, alcoholics, old people, breastfeed children; phlegm has color of currant jelly and smell of burnt meal; there occurs weakening of vesicular respiration sharply, bronchial respiration is heard (that is always sharply expressed because of bronchial exudate accumulated with a large amount); upper from the injured center there is overhear of percussive sound; pulmonary tissue s destruction is rapidly developed; often develop fibrin and exudative pleurisy with according clinical and rentgenologic expressions. Neuthrophenia is seen and when saliva is painted by Gram s method, this process reveals gram-negative bacillus. By x-ray, on the background of focal infiltration, on the 2-4 days we see cavities full of multiple liquid. Disseminate injury of lungs is disclosed because of staphylococcus pneumonias and pneumonias caused from blue-green purulence s bacillus. Staphylococcus pneumonia is frequently happen with breastfeed children, old persons, patients who overcome severe diseases, people with immunodeficiency, addicts; it s a revelation of sepsis in most cases. The disease is commenced rapidly, with recurrent fever, high temperature, unclear consciousness. On the background of overheard percussive sound and weakened respiratory there can be heard sonorous, wet, thin-vesicle wheeze. The laboratory data received from pneumococcal pneumonia is due to staphylococcal pneumonia. By means of x-ray, there is expressed wide multisegmental infiltration of pulmonary tissue, sometimes accompanied with pleurisy; on the 3-4 days of the disease bull s are formed, necrotic cavities with liquid s level, which configuration and amount change fast. Pneumonia caused by blue-green purulence s bacillus is ascribed to pneumonias of hospital, starts severely, patient s conditions immediately worsens, has high temperature of body (morning s peak of fever is characteristic). Symptoms of intoxication are clearly expressed, Critical Care Medicine HAND BOOK Page 3

4 shortness of breathe, cyanosis, tachycardia. This type of pneumonia is caused from burn, purulent wounds, infective-inflammatory diseases of urine-flowing way. The marking distinctness of pneumonia is fast formation of new inflammatory centers, frequent abscedity and earlier development of pleurisy (fibrin of exudative). also we see neutrophilic leukocytosis s formula with left deviation, and neuthropenia. On the medicament s painted with Gram s method is gram-negative bacillus. X-ray analysis represents central shadows ( centers of inflammatory infiltration), multiple (tend to dissemination is a marking point); when abscess exists we see cavities with horisontallevel, and when there is exudative pleurisy we can see intensive homogenous shadowing. Streptococcus pneumonia is developed after measles, chicken-pox, whooping-cough, flu, scarlet fever, streptococcus pharyngitis or infective disease. An acute beginning is characteristic, fever is seldom. Physical data are not always clearly expressed because of few pneumonic centers, at times they are localized in the posterior of medial parts of lungs but multiple centers of inflammation can be formed that gives a partial picture of pneumonia. Streptococcus pneumonia is marked by earlier development (2-3 days) of exudative pleurisy with purulent exudate (pleura s empyema). Also abscess formation of pneumonic centers, by means of laboratorial analyses there is revealed high leukocytosis ( /lit) with bending of leukocyte formula to the left. In the phlegm painted by gram s method chains of gram-positive kok s. X-ray analysis detects multiple centers, sometimes injure of pulmonary part s with developing of abscess ( cavities with horizontal level). Liquid received from pleural puncture is purulent, rarely serous, or serous- hemorrhagic. Pneumonia caused by hemophilic bacillus is often hospital-type. The risk groups include: *persons from low social level which are is negative sanitary-hygienic and economic conditions; * persons of black rasa. *patient who have carved spleen; *patients with lymphoproliterative diseases; * patients who suffer from disorder of creating antibodies; The disease begins severely, with fever, cough, discharge of mucous- purulent phlegm, overhear of percussive sound on the damage place, crepitating and thin-vesicle wheeze. May be complicated by pleurisy, arthritis, meningitis, and in addition by sepsis. laboratorial data is the same as pneumonia caused by blue-green purulence s bacillus. X-ray detects focal injure of lungs with signs of pleurisy. Treatment Oxygen therapy is conducted in case of acute respiratory failure; Critical Care Medicine HAND BOOK Page 4

5 Infusive therapy is done with amount of ml under control of central venous pressure and diuresis. At the time of developing acute pulmonary failure and acute rightsided failure, the amount of infusion must be reduced till 1000ml. it s advisable to utilize rheological, mixture of glucose- potassium-insulin and detoxify means in the form of infusive therapy; Anticoagulants: heparin ( during injecting for four times per 24h) Broncholytic means: aminophylline, ml of 2,4% solution per 24h) Mucoregulator and expectorant means: intravenously injected ml of sodium-iodide s 10% solution per 24 hours, ambroxol 30 mg 2-3 times per days. Lowering of pressure in pulmonary artery: papaverine s hydrochloride 2 ml intravenously per 4 hours or drotaverine with the same dose. Treatment of complications. Antibacterial treatment. If causing is knowns then antibacterial therapy is conducted in consideration with sensibility of antibiotics. At the time of acute non-hospital pneumonias the medicament of choosing is cephalosporin of the third generation along with macrolides; alternative medicaments are: medicaments of fluroquinolones, pefloxacin, carbapenems. Hospital-type pneumonias which are developed without risk factors and at the time of earlier pneumonias associated with earlier ventilation are used the following choosing medicaments: cephalosporin with maximal doses of antipseudomonal effect along with aminoglycosides. Alternative medicaments are: fluroquinolone, pefloxacin, and medicaments of carbapenems group. Patients associated with pneumonias from ventilation risk must be prescribed to the following medicaments: cephalosporin of the third generation; with persons of severe defect of immunity choosing medicaments are: carbapenems; antipseudomonal cephalosporin+ aminoglycosides of the third generation; antipseudomonal penicillin+ aminoglycosides of the third generation; fluroquinolones. In the recent years atypical pneumonia is in the center of attention. The characteristics of this type of pneumonia is syndrome of intoxication and injury of other organs. False atypical pneumonia is marked by multiorganic injury s frequency. It s distinct from other pneumonias but this is not true atypical pneumonia caused by bird flu. Causing Microplasmic Chlamydial Legionella pneumonia pneumonia pneumonia Background Persons which are Persons which are Patients with chronically conditions of closely connected in the closely connected diseases: smokers, diabetics, patients same collective in the same patients of immunodeficiency collective conditions, alcoholics. Critical Care Medicine HAND BOOK Page 5

6 Age, gender Mostly men in average age Beginning of Starts with pharyngitis, Starts with 7 days are incubational period; the disease tracheitis, fever of 40 C, intoxication; on starts with weakness, myalgia, on the 4-6 days data of the 3-4 days signs arthralgia; fever- 40C. signs of pneumonia. of pneumonia. pneumonia on the 4-7 days. Pulmonary Showings of pneumonia Constant Bloody phlegm, in 50% of cases showings are weak prolonged cough exudative pleurisy with a little amount of liquid. x-ray signs Interstitional form -50%, Mostly Focal injury of posterior parta, focal injury of posterior interstitional sometimes right-sided or parts-30%, lobular alterations, double; in 5-25% interstitional pneumonia-20%. sometimes injury of posterior parts, pleural negative x-ray discharge exists, at timesvariant. abscess of lungs. Laboratorial May exist leukocytosis, Leucopenia, ESS s Neutrophilic leukocytosis with data or leucopenia (10-15); increasing. bending the formula to the left, hemolytic anemia, lymphopenia, thrombocytopenia. thrombocytopenia, lowering of sodium, phosphor, albumin; increasing of aminotransferase, alkali-phosphatase, bilirubin. Injury of other Myocarditis, pericarditis, Hepatosplenomeg Diarrhea, blurred consciousness organs and hepatitis, pancreatitis, aly, damage of (delirium, hallucinations), systems polyarthritis, nervous system nephritis. meningoencerebritis, (meningeal rash on the skin, syndrome). polylymphoadenophaty, septicopyemia. complications Shock, sepsis Shock, adult s respiratorydistress syndrome, acute kidney failure. Critical Care Medicine HAND BOOK Page 6

7 Treatment. Macrolides are effective. Less effective have medicaments of tetracycline and lincomycin and quinolones. Usage of penicillin and cephalosporin are not recommended. Critical Care Medicine HAND BOOK Page 7