Lung abscess is defined as necrosis
of the pulmonary tissue and formation of cavities containing necrotic debris or
fluid caused by microbial infection. The formation of multiple small (<
Lung abscess was a devastating disease in the preantibiotic era, when one third of the patients died, another one third recovered, and the remainder developed debilitating illnesses such as recurrent abscesses, chronic empyema, bronchiectasis, or other consequences of chronic pyogenic infections. In the early postantibiotic period, sulfonamides did not improve the outcome of patients with lung abscess until the penicillins and tetracyclines were available. Although resectional surgery was often considered a treatment option in the past, the role of surgery has greatly diminished over time because most patients with uncomplicated lung abscess eventually respond to prolonged antibiotic therapy.
Lung abscesses can be classified based on the duration and the likely etiology. Acute abscesses are less than 4-6 weeks old, whereas chronic abscesses are of longer duration. Primary abscess is infectious in origin, caused by aspiration or pneumonia in the healthy host; secondary abscess is caused by a preexisting condition (eg, obstruction), spread from an extrapulmonary site, bronchiectasis, and/or an immunocompromised state.
Most patients with primary lung abscess improve with antibiotics, with cure rates documented at 90-95%
is characterized by the multiple destructive foci 0,3-
Abscess of lungs - purulent or ichorous destruction of necrotic sites of pulmonary tissue of one segment with formation of one or several cavities, filled by pus, and detached from adjacent parenchyma by a pyogenic capsule and expressed perifocal infiltration of surrounding pulmonary tissue. It arises at the persons with a maintained reactivity of the organism.
Gangrenous abscess is a purulent, ichorous necrosis of a pulmonary tissue within 2-3 segments, detached from adjacent pulmonary parenchyma, with the liability to formation of sequesters. Depending on reactivity of the organism it can transform into purulent abscess (after the lysis of sequesters) or gangrene.
Gangrene of lungs a diffuse purulent, ichorous necrosis of the tissue without the tendency to defined demarcation with prompt dynamics of spreading of necrotic zone and destruction of the parenchyma. It is characterized by a grave intoxication, liability to a pleural complications and pulmonary bleeding. If only the one lobe is affected the gangrene is considered to be limited, if affected extensive areas of lungs the gangrene is wide-spread.
Lung abscesses have numerous infectious causes. Anaerobic bacteria continue to be accountable for most cases. These bacteria predominate in the upper respiratory tract and are heavily concentrated in areas of oral-gingival disease. Other bacteria involved in lung abscesses are gram-positive and gram-negative organisms. However, lung cavities may not always be due to an underlying infection. Some evidence suggests that individuals with cyanotic heart disorders may also be more prone to lung abscess formation. The continuous hypoperfusion of the pulmonary tissues may predispose the individuals to chronic pulmonary infections.
The predominant factors which cause the disease:
· disturbances of bronchial patency with the development of atelectasis;
· infectious inflammatory process in a pulmonary tissue;
· regional disturbances of blood supply with a further necrosis of areas of pulmonary parenchyma.
The embodiment of these factors occurs in condition of the changed reactivity of the organism.
The states which result in the aspiration of contents of the upper parts of alimentary tract (traumas of head, craniovascular disturbances, alcoholism, narcomania, narcoses, epilepsy etc.) contribute to the pulmonary abscessing. And also factors, which are capable to provoke secondary immunodeficiency and suppression of reactive processes: diabetes mellitus, irradiation, long application of corticosteroids, antineoplastic therapy, some hematological disease, AIDS favor the purulent processes.
Oral cavity disease
· Periodontal disease
· Drug abuse
· Steroid therapy
· Multiple trauma
· Reflux disease
· Depressed cough and gag reflex
· Esophageal obstruction
· Foreign body
The abscesses mainly develop in ²² and V² segments of lungs. They may be single and multiple. The abscess is confined from adjacent pulmonary tissue by a capsule, which represents a granulating tissue and dense leukocytic rampart. Usually it is possible to find out a draining bronchus. Later on in the wall of the abscess the amount of connective tissue fibers is enlarged.
In gangrene the pulmonary tissue is of black color, swollen, with cavities, and in some places transfers into the sites with dark green coloring. The macropreparatus is characteristically fetid.
According to pathogenesis:
- hematogenous or septic;
According to the character of purulent process:
- single purulent abscesses;
- multiple purulent abscesses;
- bilateral purulent abscesses;
- gangrenous abscesses (single, multiple, uni- and bilateral);
- limited gangrene;
- wide-spread gangrene.
According to stages:
- 1 stage - necrotic pneumonia;
- 2 stages - destruction and rejection;
- 3 stages - cleaning and cicatrization.
According to the term of existence:
- pulmonary bleeding;
- pleural empyema;
- bronchogenic dissemination.
The clinical manifestations of acute purulent destruction of lungs depend on the size of the focus and character of destruction, reactivity of the organism and stage of the disease, peculiarities of the drainage of purulent cavities and complications.
At the first stage of acute abscess the patients complain of general weakness, headache, malaise, suppressed appetite, moderate chest pain, dyspnea, subfebrile temperature.
At the second stage the state of the patients is worsened. The fever rises to as high as 39-40°Ñ and has a hectic character. At the same time the chest pain increases, which associates with a troubling cough and dyspnea. The condition of the patients is worsened and the intoxication increases. One can feel a foul-smelling from the mouth at cough. The amount of sputum is small, with a rusty tone. With the beginning of the draining of destructive cavities through bronchus the daily quantity of the sputum reaches 500 ml and more. At this time is possible hemoptysis. The sputum is foul-smelling. At sedimentation it divides into three layers:
- inferior resembling a grey mass with detrites and flaps of a pulmonary tissue;
- medial purulent, turbid, liquid;
- upper mucous foamy layer.
Further in favourable cases there is a considerable improvement of state of the patients. The body temperature falls, the signs of intoxication reduce and the appetite increases.
The disease grades into the third stage, which is characterized by the regress of clinical manifestations, up to their complete disappearance.
The physical signs good are well revealed at peripheral localization of the process. By palpation weakened vocal fremitus. At percussion a blunted sound over the site of the purulent focus and perifocal infiltration (at subpleural location of the abscess). By auscultation tubular sound with a moist rales in the zone of purulent focus. Well-generated subpleural cavities of major sizes can be revealed by percussion by bandbox sound, on auscultation by moist rales on the background of amphoric respiration.
At X-ray of the chest at the stage of necrotic pneumonia is found out a rounded lesion with irregular contour. For the second stage is characteristic the enlightenment of the shadow with a further developing of the rounded cavity with air-fluid level (Kordins symptom), gentle pyogenic sheath and the perifocal infiltration. At the third stage on the place of suppuration observed expressed fibrosis, sometimes as a thin-walled annular formation.
Acute abscess of the right lower lobe before draining
Acute abscess of the right lower lobe after draining
Gangrenous abscess is characterized by a grave state of the patient, expressed purulent intoxication, cough with expectoration of a great amount (500 ml and more) of grey-green sputum with a foul-smelling, hectic body temperature. Roentgenologically the inline of the cavity is poorly defined, it contains a visible sequesters that look as a polymorphous shadow. The adjacent pulmonary tissue is infiltrated.
The clinic of a pulmonary gangrene differs by a terminal expression
of signs. The state of the patients is critical. The patient is adynamic, exhausted, with edemas on legs. Dyspnea in
rest, hemodynamic disturbances are evident. Dirty-grey or brown sputum with
detrites, pieces of necrotic parenchyma and threads of blood excretes out with
the cough up to
The intensive shadow which borrows a considerable area of lungs with a visible cavities, that contain sequesters, fluid levels, is roentgenologically revealed. The shadow outline is irregular, but could be well defined if the process is within interlobar sulcus.
Chronic abscess of lungs occurs at 12-15 % of cases. It is considered to be chronic at existence of a pulmonary abscess more than 6-8 weeks. It is characterized by a cyclic course. In the stage of remission the patients complain of a moderate dyspnea, cough with expectoration of a mucous or mucopurulent discharge. The exacerbation manifests by coughing up of 250-500 ml of a purulent foul sputum, chest pain, dyspnea, hectic temperature with the difference in 1,5-2°Ñ. Dizziness, suppression of appetite, general weakness enlarges according to intoxication. The skin is pale with moderate cyanosis. The respiratory rate rises to 28-30 per min. In 6-8 months is noticed the clubbing of the fingers and deformation of the chest. The vocal fremitus is a little bit weakened on the side of lesion (particularly in peripheral localization of the process). The percussion reveals a short sound in projection of pathological process, the auscultation - a lot of moist rales on the background of amphoric respiration.
Roentgenologically chronic abscess is shown by one or several cavities of a spherical shape with a thick, dense pyogenic sheath. Exacerbation of the process manifests by a cavity with horizontal air-fluid level. The size of surrounding perifocal infiltration depends on the phase of process.
Chronic abscess of lungs
The blood analysis in pulmonary destruction is characterized by leukocytosis with deviation of the differential count to the left, lymphocytopenia, elevation of the erythrocyte sedimentation rate. Gangrenous change of the process is accompanied by a progressing anemia, sometimes by leukopenia. The hypoproteinemia arises from major losses of protein with purulent sputum. Intoxication and toxic lesion of liver leads to disproteinemia. It is associated with the enlarged concentration of mucoprotein, sialine acids, seromucoid, and fibrinogen.
The immunogram reveals the suppression of cellular and humoral immunity with a liability to hyperergy and autoaggression, depression of the mechanisms of nonspecific protection.
The cytological bronchial water lavage is characterized by expressed neutrocytosis, noncellular postdestructive insertions at lack or absence of alveolar macrophages.
According to the clinical course, there are such variants of the development of purulent diseases of lungs:
1. Favorable course. The adequate treatment results in prompt positive clinical, roentgenological and laboratory dynamics, and terminates by recovery.
2. Non-progressive course. A poor drainage of the suppurative focus and permanent purulent intoxication result in transferring of the process in chronic form.
3. Progressing course. Is predetermined by combination of a series of the unfavorable factors (low resistance of the organism, autoimmune aggression, high virulence of the infecting agent etc.). Characterized by diffusion of the zone of necrosis and destruction with transferring in gangrene.
4. Incapsulated process. Caused by the absence or complete obstruction of the draining bronchus under condition of satisfactory resistance of the organism.
5. Complicated course. Mostly is the result of progressive development of the pathological process.
Pulmonary bleeding arise suddenly, are associated with coughing out of a foamy, red blood and clots by portions or continuous stream. The most often source of a pulmonary bleeding are the bronchial arteries and vessels of a pulmonary tissue. The clinical manifestations of a pulmonary suppuration are accompanied by dizziness, weakness, dyspnea, chest pain. The hemodynamic disturbances depend on intensity of the bleeding. The auscultation of lungs from both sides reveals the moist rales (aspiration). If the pulmonary destruction is present the plain film of the chest shows the localization of the source of bleeding. After hospitalization of the patient with this complication the exclusive information is obtained with a fibrobronchoscopy.
According to degree the pulmonary bleedings are classified (V.Struchkov, 1985):
I degree hemorrhage up to 300 ml.
1. Single hemoptysis.
2. Multiple hemoptysis.
²² degree hemorrhage up to 700 ml.
1. Single bleeding:
à) with fall in arterial pressure and decreasing of hemoglobin;
b) without fall in arterial pressure and decreasing of hemoglobin.
2. Multiple bleeding:
à) with fall in arterial pressure and decreasing of hemoglobin;
b) without fall in arterial pressure and decreasing of hemoglobin.
²²² degree - hemorrhage exceeds 700 ml.
1. Massive bleeding.
2. Fulminant, lethal bleeding.
The ² degree of a pulmonary bleeding manifests by coughing
out the sputum tinged with blood, the hemodynamic disturbance usually absent.
At bleeding of ²² degree are observed decreasing of arterial pressure on 20-
Sepsis manifests by multisystem lesions with progression of the syndrome of polyorganous failure, hematosepsis, purulent metastasizing (frequently in brain).
Characteristic complications for suppurative diseases of lungs such as pleural empyema and pyopneumothorax are described in separate parts.
1. Complaints and history of the disease.
Generally, most of the patients admitted to the hospital with a diagnosis of lung abscess have had symptoms for at least 2 weeks. These patients typically have an intermittent febrile course, productive cough, weight loss, general malaise, and night sweats. Initially, foul sputum is not observed in the course of the infection; however, after cavitation occurs, putrid expectorations are quite prevalent. The odor of the breath and sputum of a patient with an anaerobic lung abscess is often quite pronounced and noxious and may provide a clue to the diagnosis. Hemoptysis may occasionally follow the expectoration of putrid sputum.
Symptoms depend on whether the abscess is caused by anaerobic or other bacterial infection.
· Anaerobic infection in lung abscess
o Patients often present with indolent symptoms that evolve over a period of weeks to months.
o The usual symptoms are fever, cough with sputum production, night sweats, anorexia, and weight loss.
o The expectorated sputum characteristically is foul smelling and bad tasting.
o Patients may develop hemoptysis or pleurisy
· Other pathogens in lung abscess
o These patients generally present with conditions that are more emergent in nature and are usually treated while they have bacterial pneumonia.
o Cavitation occurs subsequently as parenchymal necrosis ensues.
o Abscesses from fungi, Nocardia species, and Mycobacteria species tend to have an indolent course and gradually progressive symptoms.
2. Physical findings.
The findings on physical examination of a patient with lung abscess are variable. Physical findings may be secondary to associated conditions such as underlying pneumonia or pleural effusion. The physical examination findings may also vary depending on the organisms involved, the severity and extent of the disease, and the patient's health status and comorbidities.
with lung abscesses may have low-grade fever in anaerobic infections and
temperatures higher than
· Generally, patients with in lung abscess have evidence of gingival disease.
· Clinical findings of concomitant consolidation may be present (eg, decreased breath sounds, dullness to percussion, bronchial breath sounds, course inspiratory crackles).
· The amphoric or cavernous breath sounds are only rarely elicited in modern practice.
· Evidence of pleural friction rub and signs of associated pleural effusion, empyema, and pyopneumothorax may be present. Signs include dullness to percussion, contralateral shift of the mediastinum, and absent breath sounds over the effusion.
· Digital clubbing may develop rapidly.
3. X-ray examination of chest in two planes (direct and lateral).
· A typical chest radiographic appearance of a lung abscess is an irregularly shaped cavity with an air-fluid level inside. Lung abscesses as a result of aspiration most frequently occur in the posterior segments of the upper lobes or the superior segments of the lower lobes.
· The wall thickness of a lung abscess progresses from thick to thin and from ill-defined to well-circumscribed as the surrounding lung infection resolves. The cavity wall can be smooth or ragged but is less commonly nodular, which raises the possibility of cavitating carcinoma.
· The extent of the air-fluid level within a lung abscess is often the same in posteroanterior or lateral views. The abscess may extend to the pleural surface, in which case it forms acute angles with the pleural surface.
· Anaerobic infection may be suggested by cavitation within a dense segmental consolidation in the dependent lung zones.
· Lung infection with a virulent organism results in more widespread tissue necrosis, which facilitates progression of underlying infection to pulmonary gangrene.
4. Up to one third of lung
5. Tomogram of lungs.
6. Computed tomography
· CT scanning of the lungs may help visualize the anatomy better than chest radiography. CT scanning is very useful in the identification of concomitant empyema or lung infarction.
· On CT scans, an abscess often is a rounded radiolucent lesion with a thick wall and ill-defined irregular margins.
· The vessels and bronchi are not displaced by the lesion, as they are by an empyema.
· The lung abscess is located within the parenchyma compared with loculated empyema, which may be difficult to distinguish on chest radiographs.
· The lesion forms acute angles with the pleural surface chest wall.
7. Examination of the sputum (bacteriological, cytological).
8. General blood and urine analyses.
· A complete white blood cell count with differential may reveal leukocytosis and a left shift.
· Obtain sputum for Gram stain, culture, and sensitivity.
· If tuberculosis is suspected, acid-fast bacilli stain and mycobacterial culture is requested.
· Blood culture may be helpful in establishing the etiology.
· Obtain sputum for ova and parasite whenever a parasitic cause for lung abscess is suspected.
9. Biochemical blood analysis (protein and its fractions).
Primary bacterial pneumonias caused by single bacterial species other than the pneumococcus may account for up to 25% of community-acquired and 80% of hospital-acquired pneumonias. All of these pneumonias may have somewhat similar physical find- ings and x-ray evidence of pulmonary infiltration or consolidation. For proper treatment, it is crucial to identify the causative agent by blood culture and by sputum examination with stained smear and culture. Transtracheal aspiration, fiberoptic bronchoscopy, or even lung biopsy may be needed for specific diagnosis and treatment.
Pneumonia due to hemolytic streptococci occurs usually as a sequela to viral infection of the respiratory tract, especially influenza or measles, or in persons with underlying pulmonary disease. The patients are usually in a severely toxic condition and cyanotic. Pleural effusion develops frequently and early and progresses to empyema in one-third of untreated pa- tients. The diagnosis rests on finding large numbers of streptococci in smears of sputum and culturing hemolytic streptococci from blood and sputum.
The treatment of choice is with penicillin G in a dosage similar to that for pneumococcal pneumonia (see above). If treatment is started early, the prognosis is good.
Staphylococcal Pneumonia (picture 2)
Pneumonia caused by Staphylococcus aureus occurs as a sequela to viral infections of the respiratory tract (eg, influenza) and in debilitated (eg, postsurgical) patients or hospitalized infants, especially after antimicrobial drug administration. There is often a history of a mild illness with headache, cough, and generalized aches that abruptly changes to a very se- vere illness with high fever, chills, and exaggerated cough with purulent or blood-streaked sputum and deep cyanosis. There may be early signs of pleural effusion, empyema, or tension pneumothorax. X-ray examination reveals lung consolidation, pneumatoceles, abscesses, empyema, and pneumothorax. The demonstration of pyopneumothorax and of cavities with air-fluid levels by x-ray is highly suggestive of Staphylococcal pneumonia. The diagnosis must be confirmed by stained smear of sputum (masses of white cells and gram-positive cocci, many intra- cellular) and culture (predominantly S aureus), and
also by means of cultures of pleural fluid and blood. The white count is usually more than 20,000//zL.
Initial therapy (based on sputum smear) consists of nafcillin, 6-12 g/d, or vancomycin, 2 g/d, given intravenously in divided doses as a bolus. If the staphylococcus proves to be penicillin-sensitive by laboratory test, penicillin G, 20-60 million units/d intravenously, is the antibiotic of choice. Drugs should be continued for several weeks. If empyema develops, drainage must be established. The prognosis varies with the underlying condition of the patient and the drug susceptibility of the organism.
The eponym legionnaires' disease has been given to
a serious pneumonia that afflicted people attending the American Legion
Legionella pneumophila is a poorly staining
gram-negative bacterium that grows slowly on special media (eg, charcoal-yeast
Asymptomatic infection is evident only by a rise in specific antibodies. Symptomatic infection is ob- served mainly in elderly persons, smokers, and pa- tients undergoing hemodialysis or renal transplant.
The incubation period is estimated to be 2-10 days. Initial symptoms are malaise, diffuse myalgias, and headache, followed in 12-48 hours by high, non- remittent fever and chills. Nausea, vomiting, and diarrhea are frequent early in the illness. On the third day a dry cough begins that is nonproductive or produces scanty mucoid, sometimes blood-streaked sputum. Dyspnea and hypoxia become marked as signs of consolidation develop. Pleuritic chest pain occurs in one-third of patients. Severe confusion or delirium may occur.
There is leukocytosis with a shift to the left, hyponatremia, abnormal liver function tests, and, occasionally, microscopic hematuria. Chest x-rays reveal patchy, often multilobar pulmonary con- solidation, and, occasionally, small pleural effusions. The illness usually worsens for 4-7 days before im- provement begins in those who recover. During severe outbreaks, the mortality rate has been 10% in those with manifest disease. Death is attributed to respi- ratory or renal failure or shock, with disseminated intravascular coagulation.
The diagnosis is based on a clinical picture com- patible with the specific features of the disease and on negative results of bacteriologic laboratory tests for other pneumonias. The organism can be identified by immunofluorescence in cultures, lung biopsy, and, rarely, sputum specimens. A retrospective diagnosis is based on a significant rise in specific serum antibodies detected by immunofluorescence.
The treatment of choice is erythromycin, 0.5-
Pneumocystis carinii Pneumonia
This parasitic infection occurs in debilitated children or immunodeficient adults. It has been a prominent opportunistic infection in AIDS patients. The diagnosis is made by lung biopsy and the demonstration of typical cysts of P carinii in impression smears of lung tissue stained with methena- mine-silver. Early treatment with sulfamethoxazole- trimethoprim can cure the pneumonia. The same drug has been effective in prophylaxis during immunosuppression. An alternative, more toxic drug is pentamidine isethionate .
"MIXED" BACTERIAL PNEUMONIAS (Hypostatic Pneumonia, "Terminal" Pneumonia, Bronchopneumonia)
Essentials of Diagnosis
Variable onset of fever, cough, dyspnea, expectoration.
Symptoms and signs often masked by primary (debilitating) disease.
Greenish-yellow sputum (purulent) with mixed flora.
Leukocytosis (often absent in aged and debilitated patients).
Patchy infiltration on chest x-ray.
Mixed bacterial pneumonias include those in which culture and smear reveal several organisms, not one of which can clearly be identified as the causative agent. These pneumonias usually appear as complica- tions of anesthesia, surgery, aspiration, trauma, or various chronic illnesses (cardiac failure, advanced carcinoma, uremia). They are common complications of chronic pulmonary diseases such as bronchiectasis and emphysema. Old people are most commonly affected ("terminal" pneumonia). Patients treated with intermittent positive pressure breathing apparatus or immunosuppressive drugs may develop pneumonia caused by gram-negative rods.
The following findings in a debilitated, chroni- cally ill, or aged person suggest a complicating pneumonia: (1) worsening of cough, dyspnea, cyanosis; (2) low-grade, irregular fever; (3) purulent sputum; and (4) patchy basal densities on a chest film (in addition to previously noted densities caused by a primary underlying disease, if any), sometimes with local necrosis and cavitation.
A. Symptoms and Signs: The onset is usually insidious, with low-grade fever, cough, expectoration, and dyspnea that may become marked and lead to cyanosis. Physical findings are extremely variable and may not be impressive against a background of cardiac or pulmonary disease. The signs listed under Other Bacterial Pneumonias may also be present.
B. Laboratory Findings: The appearance of a greenish or yellowish (purulent) sputum should suggest a complicating pneumonia. Smears and cul- tures reveal a mixed flora, often including anaerobes. Predominant types should be noted. Leukocytosis is often absent in the aged and debilitated patient present- ing with a mixed infection.
C. X-Ray Findings: X-ray (Picture 3) shows patchy, irregular infiltrations, most commonly posterior and basal (in bedridden patients). Abscess formation may be observed. Careful interpretation will avoid confusion with shadows due to preexisting heart or lung disease.
Mixed bacterial pneumonias must be differ- entiated from tuberculosis, carcinoma, and other spe- cific mycotic, bacterial, and viral pulmonary infec- tions (to which they may be secondary).
Clear the airway and correct hypoxia. Unless a probably significant etiologic agent can be identified, give one of the new cephalosporins (eg, cefotaxime, 12 g/d intravenously) as initial therapy. This will be modified according to clinical and laboratory results.
The prognosis depends upon the nature and sever- ity of the underlying pulmonary disease and varies with the predominating organism.
Aspiration pneumonia is an especially severe type of pneumonia, often with a high mortality rate. It results from the aspiration of gastric contents in addition to aspiration of upper respiratory flora in secretions. Important predisposing factors include impairment of the swallowing mechanism (eg, esopha- geal disease), inadequate cough reflex (eg, anesthesia, postoperative state, central nervous system disease, drug abuse), and impaired gastric emptying (eg, pyloric obstruction). Pulmonary injury is due in large part to the low pH (< 2.5) of gastric secretions.
Scattered areas of pulmonary edema and bron- chospasm occur, and the x-ray appearance (pictures 4-5) may be confused with that of pulmonary emboli, atelectasis, bronchopneumonia, and congestive heart failure.
Removal of aspirated material by catheter suction or bronchoscopy may be attempted, but this usually fails to remove all aspirate completely. Corticosteroids (eg, prednisone, 100 mg orally on the first or second day) may reduce the intensity of the inflammatory reaction to acidic gastric secretion, but the value of corticosteroids in the treatment of aspiration pneumo- nia is not proved, and they increase the risk of superinfection. Some aspiration pneumonias have no bacterial component, but in many others a mixed bacterial flora is involved. Antimicrobial drugs directed against the latter (eg, penicillin G plus an aminoglycoside or the best available cephalosporin) are sometimes adminis- tered without waiting for evidence of progressive pul- monary infection. In doing so, however, there is a risk of favoring the development of resistant mi- croorganisms. Therefore, administration of antimi- crobials should not continue without laboratory and clinical evidence of microbial infection. Assisted ventilation and supplementary oxygen are beneficial.
The cancer of the central location due to the obturation of bronchus results in atelectasis of a segment or lobe of lungs, with probable further abscessing. For the differentiation used tomography (reveals the obturation of bronchus by tumour, lesion of central lymph nodes), cytological examination of sputum and bronchial outwashes. The determinant role belongs to fibrobronchoscopy with a biopsy and verification of the diagnosis.
Central lung carcinoma
The peripheral cancer of lungs with destruction on tomograms is characterized by cavity with irregular inner surface, which external outline connects with root of the lung because of lymphatic metastatic spreading. The central lymph nodes frequently enlarged. The diagnosis is improved by results of transthoracic puncture or catheterizing biopsy with cytological investigation, fibrobronchoscopy. If it is impossible to confirm the diagnosis the thoracotomy is indicated.
The peripheral cancer of lungs
The tubercular cavern is mainly located in the upper lobes of lungs, roentgenologically revealed on the background of characteristic changes in adjacent pulmonary tissue (calcification, dissemination), sometimes detected a draining bronchus. In the sputum mycobacteria of tuberculosis are frequently found.
The tubercular cavern
The suppurative cyst of lungs differs by a gradual onset, slow course of the suppuration, less expressed intoxication. Roentgenologically its cavity has the oval or rounded shape with a thin sheath and regular contour. Perifocal infiltration is not characteristic.
The tactics in acute pulmonary destruction should be mainly conservative.
1. The adequate antibacterial, antiinflammatory therapy consists of intravenous introduction of antibiotics of a wide spectrum activity.
· First choice - Clindamycin (Cleocin 3)
· Alternative - Penicillin
· Oral therapy - Clindamycin, metronidazole (Flagyl), amoxicillin (Amoxil)
· First choices - Cephalosporins, aminoglycosides, quinolones
· Alternatives - Penicillins and cephalexin (Biocef)
· Oral therapy - Trimethoprim/sulfamethoxazole (Septra)
Pseudomonal organisms: First choices include aminoglycosides, quinolones, and cephalosporin.
· Gram-positive organisms
· First choices - Oxacillin (Bactocill), clindamycin, cephalexin, nafcillin (Nafcil), and amoxicillin
· Alternatives - Cefuroxime (Ceftin) and clindamycin
· Oral therapy - Vancomycin (Lyphocin)
Nocardial organisms: First choices include trimethoprim/sulfamethoxazole and tetracycline (Sumycin).
With the purpose of maximal concentration of drugs in the pathological focus applied:
- Injection of antibiotics in the vessels of a pulmonary circulation by means of catheterization of central veins, pulmonary artery;
- Introduction of medicinal agents into respiratory tracts (in the second stage) through the endotracheal microirrigator, nasogastric tube, during bronchoscopies, endoscopic catheterization of the abscess cavity through the draining bronchus, in aerosolic inhalations. The composition of medical admixtures includes: antibiotics, antiseptics (10 % dimexid, dioxydin, microcid etc.), enzymes;
The steps of microtraheostomia:
Tracheocentesis after local anesthesia
Insertion of the conductor
- Transcutaneous in the focus of destruction by means of puncture or draining with the usage of physical antiseptics (US, UVR, laser).
- By means of electrophoresis.
2. Evacuation of purulent content of the cavities:
- In natural way by an active sanation of tracheobronchial tree using repeated fibrobronchoscopies, aspirations through the endobronchial catheter, installations of medical agents through the microtracheostomy, aerosolic inhalations;
- Transthoracically by means of repeated punctures or external draining of peripheral cavities.
3. Detoxycation therapy (intra- and extracorporal).
4. Immune correction (under the control of immunogram):
- Active staphylococcal anatoxin according to the plan;
- Passive specific gamma-globulins, hyperimmune plasma;
- Non-specific (pirimidine and purine derivates, drugs of a thymus gland, splenin, levamisol,).
5. Homeostatic correction (oxygenotherapy, correction of anemia, hypoproteinemia, acidosis, microcirculatory disturbance).
6. Desensitizing, antiinflammatory therapy, regulation of activity of proteases: antihistamine, nonsteroid antiinflammatory agents, inhibitors of proteases, antioxidants.
7. Correction of dysfunction of the vital organs and systems, prevention of complications, symptomatic therapy.
Indications for operative management in acute destructive processes of lungs:
- Pulmonary bleeding of ²²- ²²² degree;
- Progression of the process on the background of active and appropriate therapy;
- Tense pyopneumothorax, which is failed to liquidate by the draining of pleural space;
- Impossibility to rule out the suspicion on a malignant tumour.
Contraindications: decompensation of the vital functions and systems in the terminal stage, bilateral purulent destruction of lungs, concomitant incurable malignant tumours.
Several important factors must be considered prior to undertaking surgery. Because of the high risk of spillage of the abscess into the contralateral lung, it is almost essential that a double-lumen tube be used to protect the airway. If this is not available, surgery poses a very high risk of abscess in the other lung and a risk of ARDS. In such cases, postponing the surgery is a wise decision. Another, less-satisfactory method to deal with this problem includes positioning the patient in the prone position. The surgeon must be skilled in resecting the abscess and in rapid clamping of the bronchus to prevent spillage into the trachea. These factors are extremely important when dealing with the surgical aspects of treating a lung abscess. If doubt persists, postponing the surgery is best.
Surgical treatment is now rarely necessary and is almost never the initial choice in the treatment of lung abscesses. In current practice, fewer than 15% of patients need surgical intervention for the unchecked disease and for complications that occur in both the acute and chronic stages of the disease.
Surgical management is reserved for specific indications such as little or no response to medical treatment, inability to eliminate a carcinoma as a cause, critical hemoptysis, and complications of lung abscess (eg, empyema, bronchopleural fistula). In addition, if after 4-6 weeks of medical treatment a notable residual cavity remains and the patient is symptomatic, surgical resection is advocated.
The results of surgery are difficult to assess because of the varying patient population and the tremendous increase in illicit drug abuse, alcoholism, AIDS, and infections by gram-negative and opportunistic organisms. These factors have increased the incidence of lung abscess and the associated morbidity.
A great deal of caution is needed during anesthesia when patients with lung abscess undergo surgery because spillage of the abscess material into the uninvolved lung can occur. Therefore, a double-lumen endotracheal tube is used in all cases.
A study by Nagasawa et al has shown that thoracoscopic surgery can lead to effective drainage of pediatric lung abscess without major complications. In addition, other benefits of thoracoscopy include rapid recovery, less pain, and minimal morbidity.
Operational incisions anterolateral, lateral and posterolateral thoracotomy. The operation suggests segmental, polysegmental resection, lobectomy, bilobectomy combined intervention (with the decortication, pleurectomy).
The patients with chronic abscesses should be undergone the operative treatment after complete liquidation of exacerbation.
In a pulmonary gangrene the stabilization of the process on the background of active conservative treatment allows in future to apply conservative tactics up to recovery or making optimal conditions for operation (liquidation of intoxication, aggressive panbronchitis, diffuse infiltration of the parenchyma, pleural complications). The headlong progression of the gangrene during first days, despite the active correction, occurrence of pulmonary bleeding requires urgent performance of operative management. Volume of the operation pneumonectomy, bilobectomy, lobectomy.
The pleural empyema is a purulent inflammation of its visceral and parietal membranes, which is associated with accumulation of pus in a pleural space.
The causes of occurrence of acute pleural empyema are inflammatory, or purulent and destructive processes of lungs, abscesses of abdominal cavity (secondary pleural empyema), open and closed damages of chest, and also, in some cases, operative approaches on thoracic organs (primary pleural empyema).
A secondary pleural empyema occurs in 88 % of the patients. Thus develops fibrinous, exsudative, and then purulent pleurisy.
In case of pulmonary gangrene, purulent mediastinitis, subphrenic abscess the stage of exsudative pleurisy extremely short. The progression of the process results in transferring of focal pleural empyema into wide-spread.
Macroscopically pleura is thickened, covered by pus with punctate hemorrhages. Microscopically it is diffusely oozed with neutrophils. In cases, when the empyema overcome into chronic course, the pleura deposits the calcareous salts, thick pus encapsulated, sometimes with the development of fistula.
². According to the etiological factor:
²². According to the pathogenic factor:
²²². According to the clinical course:
²V. According to extension of the process:
V. According to the presence of lung destruction:
1. Empyema with destruction of pulmonary tissue.
2. Empyema without destruction of pulmonary tissue.
VI. According to communication with environment:
1. Closed pleural empyema;
2. Open pleural empyema:
· bronchopleural fistula;
· thoracopleural fistula;
· thoracopleurobronchial fistula;
· cribrate lung.
The clinic of an acute pleural empyema depends on extension of the process, reactivity of organism and presence of complications.
The pain is the sign, which denote the involvement of pleural membranes in the process. Its intensity increases depending on depth of respiration and body position.
The dyspnea arises from accumulation of a purulent content in a pleural space and exception of particular volume of a pulmonary tissue from respiration. It's in direct ratio to amount of exudation in a pleural space.
The cough is manifestation of inflammation or purulent and destructive process in a pulmonary tissue.
Fever to 39-
The forced patient's position and restriction of breathing should be considered as outcomes of a pain syndrome. The extension of pleural empyema causes the swelling of thoracic wall, smoothing of intercostal spaces.
By palpation diminished vocal fremitus on the part of lesion.
The data of percussion and auscultation depend on extension of the process and amount of pus in a pleural space. At percussion over the exudate it is possible to reveal short sound with oblique upper contour. Above the exudate tympanic sound resulting from consolidation of pulmonary tissue. By auscultation diminished or absent sound in a great amount of exudate.
The predominant roentgenological sign of a focal or wide-spread empyema the presence of exudate. In localized acute pleural empyema observed a local intensive homogeneous shadow. Roentgenologically according to localization distinguished such types of a focal empyema:
The wide-spread pleural empyema manifests by intensive homogeneous shadow in a basal parts with oblique upper contour (Damuaso' line). The diaphragmatic dome is failed to observe. The more pus contents in a pleural space, the higher the upper measure of exudate.
Left-side pleural empyema
The clinic of a focal pleural empyema depends on the site of the process. The apical empyema, due to involvement in the process of a vascular-nervous fascicle, manifests by intensive pain. The soft tissues of supraclavicular region are swelled. The percussion and auscultation has no information.
The pain syndrome in parietal (paracostal) empyema is more expressed. Thoracic excursion is restricted. The diminishing of respiratory sound can be obtained over the exudate.
The chief complaint in paramediastinal empyema is the heart pain. The location of the process in the upper mediastinum can cause the superior vena cava syndrome. The physical findings are vague.
In case of the basal (epiphrenic) empyema the patients complain of pain in subcostal area, which increases at respiration and irradiates in supraclavicular region. In some cases the pain irradiates in epigastric region. The palpation of intercostal spaces and hypochondrium is painful.
The clinical course of postoperative empyema depends on the character of operative approach (marginal resection of lung, lobectomy, pneumonectomy, operation on esophagus) and infection of the pleural space.
The clinical manifestations of posttraumatic empyema depend on the size of damage of the chest, lungs, mediastinal organs and complications (suppuration, hemothorax).
The involvement in the purulent process of a pulmonary tissue in acute empyema results in its fusion of membranes with formation of a bronchial or thoracopleural fistula (discharge of abscess through thoracic wall).
The inappropriate elimination of empyema results in chronic course, cribrate lung and pleurogenic cirrhosis of lungs.
1. Complaints and history of the disease.
2. Physical findings.
3. Data of chest X-ray (in two planes, if necessary laterography).
4. Pleural puncture.
5. The microbiological investigation of the exudate for its sensivity to antibiotics.
6. General blood and urine analyses.
7. Biochemical blood analysis.
8. Pleurography (in transferring of the process into chronic form).
Aspiration of the fluid
Localization of the needle:
1 the needle damaged the lung
2 the needle damaged the diaphragm
3 the needle locatedin pleural sinus
Pleuropneumonia complicated with exsudative pleurisy, in some cases resembles acute pleural empyema: a chest pain, fever, dyspnea, cough, and general weakness. The chest roentgenogram reveals hydrothorax (exsudative pleurisy, pleural empyema, hemothorax). The chief diagnostic method for differentiation is the thoracentesis. The presence of a serous (lucent, faint-yellow) exudate testifies about the pleuropneumonia, complicated with pleural effusion, and cloudy, foul-smelling exudate of white or greenish color about acute empyema.
The major difficulties in differential diagnostics cause the limited forms of empyema.
The Pancoast cancer clinically and roentgenologically in most cases has almost the similar course to apical form of empyema. The transthoracic biopsy permits to confirm the diagnosis.
The acute cholecystitis is necessary to differentiate with the epiphrenic empyema. The pain in the right hypochondrium, fever, phrenic symptom are common for both diseases. However the objective findings, X-radiography of chest and the thoracentesis allow to differentiate these pathological processes.
The tumour of anterior mediastinum complicated by superior vena cava syndrome is necessary to differentiate with paramediastinal empyema. Nevertheless the body temperature in such patients, as a rule, normal. The upper cavography is possible to find out the shift of cava vein and its irregular contours (filling defect) due to growth of the mediastinal tumour.
There are some difficulties in differential diagnostics of empyema with a posttraumatic diaphragmatic hernia. Such X-ray findings as deformation of diaphragm, additional shadows with a liquid level, intestinal loop suggest a diaphragmatic hernia. A laterography and contrast study of gastrointestinal tract is basic in differential diagnostics of this disease.
The atelectasis of a segment, and lobe of lung in some cases can cause misdiagnostics. Except X-ray chest examination (in two planes and tomography), these situations require necessity of diagnostic bronchoscopy, which reveals the cause of bronchial obturation (foreign body, endobronchial cancer etc.).
The presence of pus in a pleural space is the indication for its elimination. In the place of performed diagnostic thoracentesis carried out the draining of empyema's cavity, its sanation by means of antiseptic solutions. In a focal empyema the aspiration of pus is performed by thoracentesis and only in its inefficiency carried out a draining of pleural space.
Incertion of drainage tube
Passive drainage by Bulau
Intensive antibacterial and antiinflammatory therapy should be immediately instituted. For general improving used detoxication therapy (infusion of saline solutions, hemotransfusion, transfusion of proteins, solutions of dextran, haemodes, forced diuresis, hemosorption if necessary), therapy for rising up of immunological resistance of the organism.
During the empyema's sanation decreases the amount of pus which discharges out through the drainage. The optimal variant of such course is the liquidation of empyema's cavity, then the drainage must be removed.
Transferring of the process into the chronic form (10-12 weeks) results in formation of a residual empyema's cavity, which is possible is to reveal by means of pleurography introduction through the drainage of water-soluble contrast with the further X-radiography in 2 planes.
Operative approach is applied when the process has transferred into the chronic form, that is in case of residual empyema's cavity. Volume of the operation pleurectomy, decortication of lung.
In some cases, when a bronchial fistula and great empyema's cavity has been formed, there is the necessity of performance of resection of lung and corrective thoracoplasty.
The cysts of lungs are the thin-walled cavitary formations, filled with air or liquid contents.
Inherent and acquired cyst are distinguished.
Inherent cysts arise from the abnormalities of the development of lungs under influence of the multiple chemical, physical, biological factors. Whether they can develop from a bronchial tree (bronchial) of from alveolar tissue (alveolar). Their occurrence resulting from the delay of the development of peripheral parts of bronchus with their expansion or agenesia of alveoli with dilatation of terminal bronchioles. Congenital cysts at first develop and grow as secretory formations. After communication with bronchus they finally form as air or hydroair cavities.
The acquired cysts represent fibrous cavities, which remain after abscesses, tubercular caverns, echinococci, posttraumatic intrapulmonary hematomas. The degenerative changes in the wall of bronchus with obliteration of its lumen by a cloggy secret owing to repeated inflammatory processes result in occurrence of acquired retentional cysts.
Congenital cyst can be located in any part of lungs. The walls of bronchogenic cavities contain chaotically disposed elements of bronchus (cartilagous plates, muscle fibers, mucous glands), they are lined from inside by cylindrical or cubic epithelium. Squeezed alveolar cells line the walls of alveolar formations.
The acquired cyst are revealed in places of localization of previous diseases,. Their walls mainly consist of connective tissue. Epithelization is possible due to transferring of the epithelium from a draining bronchus at long existence.
The cysts could be uni- or multichamber, closed and open (depending on the presence of communication with bronchus).
According to parentage:
According to displacement:
- single, multiple;
- unilateral, bilateral.
- Appearance of the valvular mechanism;
- Discharge into a pleural space (pneumothorax, pyopneumothorax, pleural empyema);
Clinical manifestations of uncomplicated pulmonary cysts are vague. Sometimes patients complain of a chest pain, periodic cough, and inflammatory diseases of respiratory tract in history. In children the signs are much expressed, the dyspnea associates with the compression of airways.
In great, superficially disposed cysts revealed delayed respiratory movements on affected side during breathing.
By palpation - weakened vocal fremitus.
By percussion - short or bandbox sound, depending on contents.
By auscultation - weakened respiration, over the huge open cavities amphoric.
At routine chest films the closed congenital cyst forms a homogeneous shadow of the spherical or oval shape of average intensity with rather regular edge on the background of an intact pulmonary tissue. During roentgenoscopy sometimes observed the change of its shape depending on the phase of breathing elongation in inspiration (Escudero's syndrome). The character of the shadow is better to study on tomograms.
Acquired retentional cyst is roentgenologically shown by a shadow of irregular shape (piriform, spindle-shaped etc.), that displays the shape of the distended bronchus. The adjacent tissue, as a rule, changed due to bronchiectases, pneumosclerosis, etc.
Cyst of the right lung
Open cysts are observed as thin-walled, good defined cavities of annular or oval shape.
On bronchograms congenital cysts are observed hypoplasia of segmental or lobar bronchus, lack of bronchial bifurcations, which tends to bone. Sometimes observed bronchiectases in the neighboring parts of lungs. A cystic cavity is infrequently defined.
The angiopulmonography reveals deformation of vascular branches, which circumflex the cyst.
The suppuration of the closed cysts resembles the development of a lung abscess with lesser expression of signs of intoxication (protective role of epithelial wall).
Infection of the open cysts is characterized by a gradual long course, moderate manifestation of suppuration and late intoxication.
The tension (valvular) cysts arise more often in children. They are characterized by severe respiratory and hemodynamic disturbances, up to terminal, owing to inflexion of venous trunks, shift of mediastinum and compression of lungs. The predominant signs are increased dyspnea, cyanosis, chest pain, respiratory lag on affected side, auscultatory absence or weakening of respiration, bandbox percussion sound over the cavity at mediastinal shift to the opposite side of the chest.
Pleural complications of pulmonary cysts, and also bleeding described in the relevant parts.
The malignant degeneration of pulmonary cysts occurs very rarely.
1. Complaints and history of the disease.
2. Physical methods of examination.
3. Routine chest film in two planes.
4. Lung tomography.
7. General blood and urine analyses.
The abscess of lungs, in contrast with a suppurative cyst, is characterized by prompt course, expressed purulent intoxication, roentgenologically its wall is irregular, with proper considerable perifocal infiltration.
The cancer with destruction differs by a thick wall with a tuberous inner surface, phenomena of lymphangitis in adjacent tissue. The determinant value has endoscopic examination or puncture with a biopsy and following morphological investigation.
The tubercular cavern displaced in the upper lobes, in adjacent tissue revealed fibrosis, petrifactions, dissemination, peribronchial lymphadenitis. In the sputum mycobacterium of tuberculosis.
Opposite to cyst, in termed diseases, the circumflex deformation of vascular branches never observed at angiopulmonography.
The considerable difficulties can arise at differentiation of the closed congenital cysts.
The tuberculoma differs from them by characteristic localization. At X-ray examination the heterogeneity of the shadow with calcifications, early excentric destruction, "tubercular" background is observed.
The benign tumours sometimes possible to differentiate only after the results of cytological investigation of punctate or after operation.
The echinococci cysts on tomogram can have a double contour of chitinous and fibrous sheaths. In blood analyses observed eosinophilia. The final decision is taken out after carrying out immunological (indirect microagglutination test) allergic (Cacconi's reaction) tests.
Huge cysts, in contrast with open air cysts, are characterized by a subpleural location.
The diagnostic doubts at suspicion on a diaphragmatic hernia are solved by radiopaque examination of a gastrointestinal tract.
The acquired cysts differ from congenital by roentgenological signs of the lesion of surrounding tissues (pneumofibrosis, deforming bronchitis, secondary bronchiectases, and calcifications). Postpneumonic cavities are of irregular shape, with grooves and pockets, their walls different thick. During bronchography they filled through some small bronchi. Sometimes the verification is possible only after postoperative morphological investigation.
The pulmonary cysts require the surgical treatment. In case of complications the indication for operation becomes absolute. Contraindications: the severe respiratory disturbance, concomitant malignant nonresectable tumors, vital organs dysfunction in the stage of permanent decompensation, elderly age of the patients.
The volume of the operation: if the adjacent pulmonary tissue is intact cystectomy, otherwise segmental or wedged resection, lobectomy.
The conservative therapy is applied in suppuration of cysts with the purpose of preoperative preparation. It is the similar, which applied for abscesses of lungs.
Spontaneous pneumothorax is the entry of air in a pleural space with the further lung collapse, which not associated with traumatic damage of chest or pulmonary tissue.
As a result of spontaneous disrupture of lung blebs and subpleural air cysts occurs the damage of pleural visceral membrane. It causes entry of air in pleural space. Owing to its leakage the elastic pulmonary tissue collapses. The degree of the collapse of lung depends on amount of air, that has penetrated a pleural space.
Morphologically in spontaneous pneumothorax found out a focal bullous emphysema with disrupture of blebs, subpleural air cyst, and also disorders, which have caused disturbances of ventilating ability of bronchi. It can be bronchitis, pneumosclerosis, tuberculosis and fibrous alveolitis.
The pneumothorax can be:
1. Unilateral or bilateral.
2. Partial (lung collapse to 1/3 of its volume).
3. Subtotal (lung collapse to 2/3 of its volume).
4. Total (lung collapse more than 2/3 of its volume).
5. Tension or valvular (complete collapse of lungs and shift of mediastinum in the opposite side).
6. Rigid (neglected pneumothorax with thickened visceral pleura).
Partial spontaneous pneumothorax
Subtotal spontaneous pneumothorax
Total spontaneous pneumothorax
The onset of the disease is sudden. A state of the patient and expression of clinical manifestations depends on amount of air, which has entered the pleural space. Usually in normal conditions, and sometimes after physical activity, the patients suddenly feel acute pain on the side of lesion, dyspnea, pain in the heart region and heartbeating. An available also Acrocyanosis or total cyanosis of skin is observed. The circulatory disturbance depends on degree of hypoxia. Intensity of pain and dyspnea gradually decrease, but a dry troublesome cough appears.
Examination of the chest allows to observe expansion of intercostal spaces and restriction of respiratory excursion. By palpation - diminishing of vocal fremitus on the affected side. At percussion a chief sign of pneumothorax is the tympanic sound. Auscultation reveals weakened or sharply weakened breathing sounds. The cardiac tones are muffled, tachycardia.
The diagnosis of a spontaneous pneumothorax is confirmed by X-ray examination. On the plain roentgenogram the air is present in pleural space, and the margins of collapsed lung are found out on its background.
pneumothorax possible to find out subpleural blebs of different sizes (0,5-
The atypical (asymptomatic) spontaneous pneumothorax occurs in 20 % of the patients, and mainly revealed at X-ray examination. In most cases it is the partial pneumothorax.
The expressed pain syndrome and dyspnea, which resulting from collapse of lung, characterize subtotal and total pneumothorax.
The tension spontaneous pneumothorax is the most severe form of pneumothorax. It manifests by sudden onset, progressive increase of dyspnea, expressed cyanosis. The breathing is superficial, rapid, with active participation of auxiliary muscles. Mediastinal shift and flexion of vessels result in disturbance of cardiac activity up to the cardiac arrest, and requires urgent management.
Rigid pneumothorax (rigid lung). The neglected pneumothorax causes fibrinous exsudative pleurisy. On the surface of lung (visceral pleura) commissures are formed, that give no opportunity for lung expansion. The presence of residual pleural cavity and progressive development of a purulent infection result in occurrence of acute pleural empyema. In such cases the patients complain of the fever up to 38-38,5°C, general weakness and increasing of dyspnea. The phenomena of intoxication increase. Thus such patients require the treatment of pleural empyema.
1. Complaint and anamnesis of disease.
2. Physical findings.
3. Routine chest film (direct and lateral projection).
6. Tomography of lungs.
Pleural effusion. This pathology manifests by more gradual onset. As opposite to pneumothorax, the complaints of chest pain predominate above the complaints of dyspnea. Frequently such patients specify on transferred undercooling.
As well as the spontaneous pneumothorax, the pleural effusion is characterized by diminishing of vocal fremitus, dullness of percussion sound, weakened of absent breathing sounds over the exudate. Nevertheless in the routine roentgenogram in such cases observed a homogeneous intensive shadow of a pleural space with oblique upper contour. The puncture of pleural space enables finally to confirm the diagnosis of pleural effusion.
Intercostal neuralgia. A predominant sign in clinical pattern is acute pain, which intensifies at physical activity, changes of body position and body movements, at deep breathing. The localization of pain coincides with zone of innervation of intercostal nerves.
Examination and chest X-radiography reveals no pathological changes.
Conservative treatment is applied in the patients with a partial pneumothorax. Thus thoracentesis in ²² intercostal space in the midclavicular line with aspiration of air is performed. The cases of its inefficiency, and also subtotal, total and tension pneumothorax require drainage of a pleural space with active aspiration of air.
The operative management is necessary, if there is no efficiency from active aspiration (in incomplete expansion of lung), recurrent of course of the process, presence of great subpleural blebs and rigid pneumothorax. Volume of operation depends on extension of the process: liquidation of alveolar fistula, wedged resection of lung or lobectomy.
Pyopneumothorax is the discharge of lung abscess of into pleural space, which is accompanied by purulent inflammation of pleural membranes with a collapse of lung.
Peripheral placement of the purulent focus in a pulmonary tissue results in destruction (fusion) of visceral membrane. As a result of, the pus and air penetrate into a pleural space that leads to a purulent inflammation of parietal and visceral membranes of pleura. The disorder of hermeticity of a pleural space results in a lung collapse.
Among other causes of pyopneumothorax are the chest trauma, which results in collapse of lung, infection and purulent inflammation of pleural membranes.
As the basic causes of pyopneumothorax are considered:
- acute abscess of lung;
- gangrenous abscess of lung;
- gangrene of lung;
- suppurative cyst of lung;
- abscessing pneumonia;
- bronchiectatic disease;
- subphrenic abscess, which has discharged into pleural space;
- damage of esophagus;
- chest trauma;
- operation and diagnostic manipulations on chest organs.
Morphologically in pyopneumothorax pus and air are present in pleural space. In the lungs subpleural disposed purulent or necrotic foci, which connected with a pleural space through a pleuro-pulmonary fistula. From the outside the zone of disrupture is confined by perifocal inflammation. In the draining bronchus it is possible to see manifestations of deforming, frequently polypous bronchitis.
². According to etiological factor:
²². According to pathogenic factor:
²²². According to clinical course:
1. Asymptomatic form.
2. Mild form.
3. Acute form.
²V. According to extension of the process:
1. Localized pyopneumothorax:
2. Subtotal pyopneumothorax.
3. Total pyopneumothorax.
4. Tension pyopneumothorax.
The clinic of pyopneumothorax depends on the size of the focus of destruction, which influences on degree of lung collapse, and on amount of purulent content in a pleural space.
The pain owing to discharge of the focus of destruction into pleural space often arises suddenly.
The dyspnea occurs as a result of collapse of lung owing to leakage of pus and air into pleural space. Its expression is in direct ratio to lung collapse. Therefore a dyspnea in rest observed in a subtotal and total pyopneumothorax. It sharply amplifies even at minor physical activity. Auxiliary muscles take part in order to force respiration.
The expectoration of sputum with ichorous smell is the outcome of destructive process in a pulmonary tissue. Its amount decreases after discharge of pus into pleural space.
Hectic fever with caused by enlargement of the area of resorption. The patients are adynamic, flaccid. Some of them are unconsciousness.
By objective examination the position of patients is forced, they sit in bed leaning upon the bed (subtotal, total pyopneumothorax). The affected hemithorax takes no part in respiration.
By palpation diminished vocal fremitus on the side of lesion.
Percussion reveals a sharp shortening of sound over the zone of exudate and bandbox sound above the region of collapsed lung.
By auscultation there are no breathing sounds on the affected side. In case of localized pyopneumothorax weakened or sharply weakened sound with a bronchial or amphoric tone.
The X-ray picture of pyopneumothorax depends on its form, but the obligatory sign is the air-fluid level in a pleural space with well-defined edge of collapsed lung on its background.
Left-side total pyopneumothorax
The clinical course of pyopneumothorax depends on adhesions between pleural membranes. It sometimes changes typical clinical course of a total lung collapse. The clinic of disease depends also on amount of a purulent exudate. Therefore according to extension of the process and size of destruction of lung distinguished acute, mild and asymptomatic forms of pyopneumothorax. Especially difficult for diagnostics is the asymptomatic form of localized pyopneumothorax. Dyspnea for such pathology not characteristic, as the adhesion of membranes prevents complete collapse of lung. Dyspnea is vague or absent at all in partial collapse. A diminished vocal fremitus on side of pathological process, shortening of percussion sound and weakened or sharply weakened breathing sounds over the collapsed lung and exudate are revealed. Roentgenological manifestations in localized pyopneumothorax not expressed and include horizontal fluid level, margin of partially collapsed lung and minor air in the pleural space.
In most cases after discharge of the destructive focus in a pleural space and collapse of lung observed the closure of bronchopleural fistula. Nevertheless the inflammatory process in a pulmonary tissue and pleural space is going on.
1. Complaint and history of disease.
2. Physical findings.
3. Chest X-radiography examination.
6. Bacterial culture and antibiotic sensitivity.
7. General blood, and urine analyses.
8. Biochemical blood analysis.
They're no special necessity for differential diagnostics of pyopneumothorax in the majority of patients. History (presence of the purulent focus in a pulmonary tissue), clinical course (acute pain and dyspnea at abscess discharge into pleural space), and also chest X-ray findings and thoracentesis frequently reliably permit to make the diagnosis.
In some cases a localized pyopneumothorax according to clinical course resembles a huge acute abscess of lungs. But the differences of roentgenological symptomatology permit to verify these pathological processes. In acute lung abscess the cavity of destruction localized in a pulmonary parenchyma, it is of rounded form with horizontal fluid level and expressed perifocal infiltration.
The purpose of treatment should include sanation of the destructive focus in pulmonary tissue and liquidation of complications; that means elimination of pus and air from a pleural space and prompt expanding of lung.
1. Active sanation of tracheobronchial tree by means of tracheocentesis.
2. Draining of pleural space, active aspiration of its content (air, pus) to expand the lungs.
3. Lavage of pleural space by antiseptic solutions.
4. Appropriate antibacterial, antiinflammatory and infusion therapy.
5. The therapy for rising up of immunological resistance of the organism (staphylococcal anatoxin according to scheme, antistaphylococcal gamma-globulin, antistaphylococcal plasma).
6. Endolymphatic introduction of immunity stimulators (thymalin, thymogen, Ò-activin).
The indications for operative management are the same, as in pleural empyema.