Purulent diseases of lungs and pleura

Lung abscess is defined as necrosis nof the pulmonary tissue and formation of cavities containing necrotic debris or nfluid caused by microbial infection. The formation of multiple small (< 2 cm) abscesses is occasionally nreferred to as necrotizing pneumonia or lung gangrene. Both lung abscess and nnecrotizing pneumonia are manifestations of a similar pathologic process. nFailure to recognize and treat lung abscess is associated with poor clinical noutcome.

Lung abscess was a devastating ndisease in the preantibiotic era, when one third of the patients died, another none third recovered, and the remainder developed debilitating illnesses such as nrecurrent abscesses, chronic empyema, bronchiectasis, or other consequences of nchronic pyogenic infections. In the early postantibiotic period, sulfonamides ndid not improve the outcome of patients with lung abscess until the penicillins nand tetracyclines were available. Although resectional surgery was ofteconsidered a treatment option in the past, the role of surgery has greatly ndiminished over time because most patients with uncomplicated lung abscess neventually respond to prolonged antibiotic therapy.

Lung abscesses can be classified nbased on the duration and the likely etiology. Acute abscesses are less tha4-6 weeks old, whereas chronic abscesses are of longer duration. Primary nabscess is infectious in origin, caused by aspiration or pneumonia in the nhealthy host; secondary abscess is caused by a preexisting condition (eg, nobstruction), spread from an extrapulmonary site, bronchiectasis, and/or aimmunocompromised state.

 

Most patients with primary lung nabscess improve with antibiotics, with cure rates documented at 90-95%

 Abscessing pneumonia nis characterized by the multiple destructive foci 0,3-0,5 cm in size within 1-2 nsegments of lungs, which are not disposed to progression. The destruction is naccompanied by expressed perifocal infiltration of a pulmonary tissue.

Abscess of nlungs – purulent or ichorous destruction of necrotic sites of pulmonary tissue nof one segment with formation of one or several cavities, filled by pus, and detached from adjacent parenchyma by a pyogenic ncapsule and expressed perifocal infiltration of surrounding pulmonary tissue. nIt arises at the persons with a maintained reactivity of the organism.

Gangrenous nabscess is a purulent, ichorous necrosis of a pulmonary tissue within 2-3 segments, ndetached from adjacent pulmonary parenchyma, with the liability to formation of nsequesters. Depending on reactivity of the organism it can transform into npurulent abscess (after the lysis of sequesters) or gangrene.

Gangrene of nlungs – a diffuse purulent, nichorous necrosis of the tissue without nthe tendency to defined demarcation with prompt dynamics of spreading of nnecrotic zone and destruction of the parenchyma. It is characterized by a grave nintoxication, liability to a pleural complications and pulmonary bleeding. If nonly the one lobe is affected the gangrene is considered to be limited, if naffected extensive areas of lungs the gangrene is wide-spread.

 

Etiology and pathogenesis

Lung abscesses have numerous infectious causes. nAnaerobic bacteria continue to be accountable for most cases. These bacteria npredominate in the upper respiratory tract and are heavily concentrated iareas of oral-gingival disease. Other bacteria involved in lung abscesses are ngram-positive and gram-negative organisms. However, lung cavities may not nalways be due to an underlying infection. Some evidence suggests that individuals nwith cyanotic heart disorders may also be more prone to lung abscess formation. nThe continuous hypoperfusion of the pulmonary tissues may predispose the nindividuals to chronic pulmonary infections.

The predominant factors which cause the disease:

·        ndisturbances of bronchial npatency with the development of atelectasis;

·        ninfectious inflammatory process nin a pulmonary tissue;

·        nregional disturbances of blood nsupply with a further necrosis of areas of pulmonary  parenchyma.

The embodiment of these factors occurs in condition of the changed nreactivity of the organism.

The states which result in the aspiration of contents of the upper parts nof alimentary tract (traumas of head, craniovascular disturbances, alcoholism, nnarcomania, narcoses, epilepsy etc.) contribute to the pulmonary nabscessing.  And also factors, which are ncapable to provoke secondary immunodeficiency and suppression of reactive nprocesses: diabetes mellitus, irradiation, long application of corticosteroids, nantineoplastic therapy, some hematological disease, AIDS favor the purulent nprocesses.

Factors contributing to lung abscess

Oral cavity disease

·        nPeriodontal ndisease

·        nGingivitis

Altered consciousness

·        nAlcoholism

·        nComa

·        nDrug nabuse

·        nAnesthesia

·        nSeizures

Immunocompromised host

·        nSteroid ntherapy

·        nChemotherapy

·        nMalnutrition

·        nMultiple ntrauma

Esophageal disease

·        nAchalasia

·        nReflux ndisease

·        nDepressed ncough and gag reflex

·        nEsophageal nobstruction

Bronchial obstruction

·        nTumor

·        nForeigbody

·        nStricture

Generalized sepsis

 

Pathology

The abscesses mainly develop in ІІ nand VІ segments of lungs. They may be single and multiple. The abscess is nconfined from adjacent pulmonary tissue by a capsule, which represents a ngranulating tissue and dense leukocytic rampart. Usually it is possible to find nout a draining bronchus. Later on in the wall of the abscess the amount of nconnective tissue fibers is enlarged.

In gangrene the pulmonary tissue is of black ncolor, swollen, with cavities, and in some places transfers into the sites with ndark green coloring. The macropreparatus is ncharacteristically fetid.

 

Classification

According to npathogenesis:

–         npostpneumonic;

–         naspirative;

–         nobturative;

–         nposttraumatic;

–         nhematogenous or septic;

–         nlymphogenous;

–         nthromboembolic.

 

According to nthe character of purulent process:

–         nsingle purulent abscesses;

–         nmultiple purulent abscesses;

–         nbilateral purulent abscesses;

–         ngangrenous abscesses (single, multiple, uni- and nbilateral);

–         nlimited gangrene;

–         nwide-spread gangrene.

 

According to nstages:

–         n1 stage – necrotic pneumonia;

–         n2 stages – destruction and rejection;

–         n3 stages – cleaning and cicatrization.

 

According to nthe term of existence:

–         nacute;

–         nchronic.

 

Complications:

–         npulmonary bleeding;

–         npyopneumothorax;

–         npleural empyema;

–         nsepsis;

–         nbronchogenic dissemination.

 

Symptomatology and clinical course

The clinical nmanifestations of acute purulent destruction of lungs depend on the size of the nfocus and character of destruction, reactivity of the organism and stage of the ndisease, peculiarities of the drainage of purulent cavities and complications.

 

At the first stage of acute abscess the patients complain of general nweakness, headache, malaise, suppressed appetite, moderate chest pain, dyspnea, nsubfebrile temperature.

At the second stage the nstate of the patients is worsened. The fever nrises to as high as 39-40°С and has a hectic character. At nthe same time the chest pain increases, which associates with a troubling cough nand dyspnea. The condition of the patients is worsened and the intoxicatioincreases. One can feel a foul-smelling from the mouth at cough. The amount of nsputum is small, with a rusty tone. With the beginning of the draining of ndestructive cavities through bronchus the daily quantity of the sputum reaches n500 ml and more. At this time is possible hemoptysis. The sputum is nfoul-smelling. At sedimentation it divides into three layers:

–         ninferior – resembling a grey nmass with detrites and flaps of a pulmonary tissue;

–         nmedial – purulent, turbid, nliquid;

–         nupper – mucous foamy layer.

Further in favourable ncases there is a considerable improvement of state of the patients. The body ntemperature falls, the signs of intoxication reduce and the appetite increases. n

The disease grades into nthe third stage, which is characterized by the regress of clinical nmanifestations, up to their complete disappearance.

The physical signs good nare well revealed at peripheral localization of the process. By palpation – nweakened vocal fremitus. At percussion – a blunted sound over the site of the npurulent focus and perifocal infiltration (at subpleural location of the nabscess). By auscultation – tubular sound with a moist rales in the zone of npurulent focus. Well-generated subpleural cavities of major sizes can be nrevealed by percussion by bandbox sound, on auscultation by moist rales on the nbackground of amphoric respiration.

At X-ray of the chest at the stage of necrotic pneumonia is nfound out a rounded lesion with irregular contour. For the second stage is characteristic nthe enlightenment of the shadow with a further developing of the rounded cavity nwith air-fluid level (Kordin’s symptom), gentle pyogenic sheath and the nperifocal infiltration. At the third stage on the place of suppuration observed nexpressed fibrosis, sometimes as a thin-walled annular formation.

 

Acute abscess of the nright lower lobe before draining

 

 

Acute abscess of the nright lower lobe after draining

 

Gangrenous nabscess is ncharacterized by a grave state of the patient, expressed purulent intoxication, ncough with expectoration of a great amount (500 ml and more) of grey-greesputum with a foul-smelling, hectic body temperature. Roentgenologically the ninline of the cavity is poorly defined, it contains a visible sequesters that nlook as a polymorphous shadow. The adjacent pulmonary tissue is infiltrated.

 

 

Gangrenous abscess

 

 

The clinic of a pulmonary gangrene differs by a terminal expressioof signs. The state of the patients is critical. The patient is adynamic, exhausted, with edemas on legs. Dyspnea irest, hemodynamic disturbances are evident. Dirty-grey or brown sputum with ndetrites, pieces of necrotic parenchyma and threads of blood excretes out with nthe cough up to 1 l. nEarly pleural complications are usual and represent with pulmonary bleeding, nwhich may be profuse. Often it is associated with vital organ dysfunction and nloss of consciousness.

The intensive shadow which borrows a considerable area of lungs with a nvisible cavities, that contain sequesters, fluid levels, is roentgenologically nrevealed. The shadow outline is irregular, but could be well defined if the nprocess is within interlobar sulcus.

 

Pulmonary gangrene

 

Chronic abscess of lungs occurs at 12-15 % of cases. It is considered to be chronic at existence nof a pulmonary abscess more than 6-8 weeks. It is characterized by a cyclic ncourse. In the stage of remission the patients complain of a moderate dyspnea, ncough with expectoration of a mucous or mucopurulent discharge. The nexacerbation manifests by coughing up of 250-500 ml of a purulent foul sputum, nchest pain, dyspnea, hectic temperature with the difference in 1,5-2°С. Dizziness, suppression of appetite, general weakness nenlarges according to intoxication. The skin is pale with moderate cyanosis. nThe respiratory rate rises to 28-30 per min. In 6-8 months is noticed the nclubbing of the fingers and deformation of the chest. The vocal fremitus is a nlittle bit weakened on the side of lesion (particularly in peripheral nlocalization of the process). The percussion reveals a short sound iprojection of pathological process, the auscultation – a lot of moist rales othe background of amphoric respiration.

Roentgenologically chronic abscess is shown by one or several cavities of na spherical shape with a thick, dense pyogenic sheath. Exacerbation of the nprocess manifests by a cavity with horizontal air-fluid level. The size of nsurrounding perifocal infiltration depends on the phase of process.

 

Chronic abscess of nlungs

 

The blood analysis ipulmonary destruction is characterized by leukocytosis with deviation of the differential count to the left, nlymphocytopenia, elevation of the erythrocyte sedimentation rate. Gangrenous nchange of the process is accompanied by a progressing anemia, sometimes by nleukopenia. The hypoproteinemia arises from major losses of protein with npurulent sputum. Intoxication and toxic lesion of liver leads to ndisproteinemia. It is associated with the enlarged concentration of nmucoprotein, sialine acids, seromucoid, and fibrinogen.

The immunogram reveals nthe suppression of cellular and humoral immunity with na liability to hyperergy and autoaggression, depression of the mechanisms of nnonspecific protection.

The cytological bronchial water lavage is characterized by expressed nneutrocytosis, noncellular postdestructive insertions at lack or absence of nalveolar macrophages.

 

Variants of clinical course and complications

According to the clinical ncourse, there are such variants of the development of purulent diseases of nlungs:

1. Favorable ncourse. The adequate treatment results in prompt positive clinical, roentgenological and laboratory dynamics, and nterminates by recovery.

2. nNon-progressive course. A poor drainage of the suppurative focus and permanent npurulent intoxication result in transferring of the process in chronic form.

3. Progressing ncourse. Is predetermined by combination of a series of the unfavorable factors n(low resistance of the organism, autoimmune naggression, high virulence of the infecting agent etc.). Characterized by ndiffusion of the zone of necrosis and destruction with transferring igangrene.

4. Incapsulated process. Caused by the absence or complete obstruction of the draining bronchus nunder condition of satisfactory resistance of the organism.

5. Complicated course. Mostly is the result of progressive development of the pathological nprocess.

 

Pulmonary bleeding arise suddenly, are associated with coughing out of a nfoamy, red blood and clots by portions or continuous stream. The most oftesource of a pulmonary bleeding are the bronchial arteries and vessels of a npulmonary tissue. The clinical manifestations of a pulmonary suppuration are naccompanied by dizziness, weakness, dyspnea, chest pain. The hemodynamic ndisturbances depend on intensity of the bleeding. The auscultation of lungs nfrom both sides reveals the moist rales (aspiration). If the pulmonary ndestruction is present the plain film of the chest shows the localization of nthe source of bleeding. After hospitalization of the patient with this ncomplication the exclusive information is obtained with a fibrobronchoscopy.

According to degree the npulmonary bleedings are classified (V.Struchkov, n1985):

I degree – hemorrhage nup to 300 ml.

1.                 nSingle hemoptysis.

2.                 nMultiple hemoptysis.

ІІ degree – hemorrhage up to 700 ml.

1.     nSingle bleeding:

а) with fall in arterial pressure and decreasing of hemoglobin;

b) without fall in arterial pressure and decreasing of hemoglobin.

2.     nMultiple bleeding:

а) with fall in arterial pressure nand decreasing of hemoglobin;

b) without fall iarterial pressure and decreasing of hemoglobin.

ІІІ degree – hemorrhage exceeds 700 ml.

1.     nMassive bleeding.

2.     nFulminant, lethal bleeding.

The І degree of a pulmonary bleeding manifests by coughing nout the sputum tinged with blood, the hemodynamic disturbance usually absent. nAt bleeding of ІІ degree are observed decreasing of arterial pressure on 20-30 mm Hg, tachycardia to 100 nbeats/min, contents of hemoglobin within 60-80 g/l. The bleeding of ІІІ degree nare accompanied with sharp decreasing of arterial pressure, rapid (more tha100-120 beats/min), small, sometimes thread pulse, and even its disappearance non peripheral arteries, tachypnea to 40 per 1 min, hemoglobin to 50-60 g/l. nProbable the fulminant course up to the terminal state with prompt failure of ncardiac activity and asphyxia by blood.

Sepsis manifests by multisystem lesions with progressioof the syndrome of polyorganous failure, hematosepsis, npurulent metastasizing (frequently in brain).

Characteristic ncomplications for suppurative diseases of lungs such as pleural empyema and npyopneumothorax are described in separate parts.

 

The diagnostic program

1.     nComplaints and history of the disease.

Generally, most of the patients nadmitted to the hospital with a diagnosis of lung abscess have had symptoms for nat least 2 weeks. These patients typically have an intermittent febrile course, nproductive cough, weight loss, general malaise, and night sweats. Initially, nfoul sputum is not observed in the course of the infection; however, after ncavitation occurs, putrid expectorations are quite prevalent. The odor of the nbreath and sputum of a patient with an anaerobic lung abscess is often quite npronounced and noxious and may provide a clue to the diagnosis. Hemoptysis may noccasionally follow the expectoration of putrid sputum.

Symptoms depend on whether the nabscess is caused by anaerobic or other bacterial infection.

·                    nAnaerobic ninfection in lung abscess

o       nPatients noften present with indolent symptoms that evolve over a period of weeks to nmonths.

o       nThe nusual symptoms are fever, cough with sputum production, night sweats, anorexia, nand weight loss.

o       nThe nexpectorated sputum characteristically is foul smelling and bad tasting.

o       nPatients nmay develop hemoptysis or pleurisy

·                    nOther npathogens in lung abscess

o       nThese npatients generally present with conditions that are more emergent iature and nare usually treated while they have bacterial pneumonia.

o       nCavitatiooccurs subsequently as parenchymal necrosis ensues.

o       nAbscesses nfrom fungi, Nocardia species, and Mycobacteria species tend to have an indolent ncourse and gradually progressive symptoms.

2.     nPhysical findings.

The findings on physical examinatioof a patient with lung abscess are variable. Physical findings may be secondary nto associated conditions such as underlying pneumonia or pleural effusion. The nphysical examination findings may also vary depending on the organisms ninvolved, the severity and extent of the disease, and the patient’s health nstatus and comorbidities.

·                    nPatients nwith lung abscesses may have low-grade fever in anaerobic infections and ntemperatures higher than 38.5°C nin other infections.

·                    nGenerally, npatients with in lung abscess have evidence of gingival disease.

·                    nClinical nfindings of concomitant consolidation may be present (eg, decreased breath nsounds, dullness to percussion, bronchial breath sounds, course inspiratory ncrackles).

·                    nThe namphoric or cavernous breath sounds are only rarely elicited in moderpractice.

·                    nEvidence nof pleural friction rub and signs of associated pleural effusion, empyema, and npyopneumothorax may be present. Signs include dullness to percussion, ncontralateral shift of the mediastinum, and absent breath sounds over the neffusion.

·                    nDigital nclubbing may develop rapidly.

3.     nX-ray examination of chest in two planes (direct and nlateral).

·                    nA ntypical chest radiographic appearance of a lung abscess is an irregularly nshaped cavity with an air-fluid level inside. Lung abscesses as a result of naspiration most frequently occur in the posterior segments of the upper lobes nor the superior segments of the lower lobes.

·                    nThe nwall thickness of a lung abscess progresses from thick to thin and from nill-defined to well-circumscribed as the surrounding lung infection resolves. nThe cavity wall can be smooth or ragged but is less commonly nodular, which nraises the possibility of cavitating carcinoma.

·                    nThe nextent of the air-fluid level within a lung abscess is often the same in posteroanterior nor lateral views. The abscess may extend to the pleural surface, in which case nit forms acute angles with the pleural surface.

·                    nAnaerobic ninfection may be suggested by cavitation within a dense segmental consolidatioin the dependent lung zones.

·                    nLung ninfection with a virulent organism results in more widespread tissue necrosis, nwhich facilitates progression of underlying infection to pulmonary gangrene.

4.     nUp nto one third of lung

5.     nTomogram of lungs.

6.     nComputed tomography

·                    nCT nscanning of the lungs may help visualize the anatomy better than chest nradiography. CT scanning is very useful in the identification of concomitant nempyema or lung infarction.

·                    nOCT scans, an abscess often is a rounded radiolucent lesion with a thick wall nand ill-defined irregular margins.

·                    nThe nvessels and bronchi are not displaced by the lesion, as they are by an empyema.

·                    nThe nlung abscess is located within the parenchyma compared with loculated empyema, nwhich may be difficult to distinguish on chest radiographs.

·                    nThe nlesion forms acute angles with the pleural surface chest wall.

7.     nExamination of the sputum (bacteriological, cytological).

8.     nGeneral blood and urine analyses.

·                    nA ncomplete white blood cell count with differential may reveal leukocytosis and a nleft shift.

·                    nObtaisputum for Gram stain, culture, and sensitivity.

·                    nIf ntuberculosis is suspected, acid-fast bacilli stain and mycobacterial culture is nrequested.

·                    nBlood nculture may be helpful in establishing the etiology.

·                    nObtaisputum for ova and parasite whenever a parasitic cause for lung abscess is nsuspected.

9.     nBiochemical blood analysis (protein and its fractions).

10.            nImmunogram.

11.            nFibrobronchoscopy.

 

Differential diagnostics

Pneumonia

Primary bacterial pneumonias caused by single bacterial nspecies other than the pneumococcus may account for up to 25% of ncommunity-acquired and 80% of hospital-acquired pneumonias. All of these npneumonias may have somewhat similar physical find- ings and x-ray evidence of npulmonary infiltration or •consolidation. For proper treatment, it is crucial nto identify the causative agent by blood culture and by sputum examination with nstained smear and culture. Transtracheal aspiration, fiberoptic bronchoscopy, nor even lung biopsy may be needed for specific diagnosis and treatment.

Streptococcal Pneumonia

Pneumonia due to hemolytic streptococci occurs nusually as a sequela to viral infection of the respiratory tract, especially ninfluenza or measles, or in persons with underlying pulmonary disease. The npatients are usually in a severely toxic condition and cyanotic. Pleural neffusion develops frequently and early and progresses to empyema in one-third nof untreated pa- tients. The diagnosis rests on finding large numbers of nstreptococci in smears of sputum and culturing hemolytic streptococci from nblood and sputum.

The treatment of choice is with penicillin G in a ndosage similar to that for pneumococcal pneumonia (see above). If treatment is nstarted early, the prognosis is good.

Staphylococcal Pneumonia (picture 2)

Pneumonia caused by Staphylococcus aureus occurs nas a sequela to viral infections of the respiratory tract (eg, influenza) and nin debilitated (eg, postsurgical) patients or hospitalized infants, especially nafter antimicrobial drug administration. There is often a history of a mild nillness with headache, cough, and generalized aches that abruptly changes to a nvery se- vere illness with high fever, chills, and exaggerated cough with npurulent or blood-streaked sputum and deep cyanosis. There may be early signs of npleural effusion, empyema, or tension pneumothorax. X-ray examination reveals nlung consolidation, pneumatoceles, abscesses, empyema, and pneumothorax. The ndemonstration of pyopneumothorax and of cavities with air-fluid levels by x-ray nis highly suggestive of Staphylococcal pneumonia. The diagnosis must be nconfirmed by stained smear of sputum (masses of white cells and gram-positive ncocci, many intra- cellular) and culture (predominantly S aureus), and

also by means of cultures of pleural fluid and nblood. The white count is usually more than 20,000//zL.

Initial therapy (based on sputum smear) consists nof nafcillin, 6-12 g/d, or vancomycin, 2 g/d, given intravenously in divided ndoses as a bolus. If the staphylococcus proves to be penicillin-sensitive by nlaboratory test, penicillin G, 20-60 million units/d intravenously, is the nantibiotic of choice. Drugs should be continued for several weeks. If empyema ndevelops, drainage must be established. The prognosis varies with the nunderlying condition of the patient and the drug susceptibility of the norganism.

Legionella Pneumonia

The eponym legionnaires’ disease has been given to na serious pneumonia that afflicted people attending the American LegioConvention in Philadelphia nin 1976. Other outbreaks have been diagnosed ret- rospectively at least since n1965, and sporadic infec- tions have occurred at least since 1947 in many nplaces.

Legionella pneumophila is a poorly staining ngram-negative bacterium that grows slowly on special media (eg, charcoal-yeast nextract) at 35 °C. nThere are at least 8 species of Legionella, some with multiple serotypes. These norganisms can be recovered in human disease from sputum, bronchial washings, npleural fluid, lung biopsies, or blood. Legionella species occur in the nenvironment and are acquired by humans from aerosols, dust from nair-conditioning systems, water, or soil. The infection is not usually communi- ncable from patient to contacts. Asymptomatic infec- tion is common at all ages, nwhereas symptomatic infection is most often an opportunistic pneumonia iimmunocompromised individuals.

Asymptomatic infection is evident only by a rise nin specific antibodies. Symptomatic infection is ob- served mainly in elderly npersons, smokers, and pa- tients undergoing hemodialysis or renal transplant.

The incubation period is estimated to be 2-10 ndays. Initial symptoms are malaise, diffuse myalgias, and headache, followed i12-48 hours by high, non- remittent fever and chills. Nausea, vomiting, and ndiarrhea are frequent early in the illness. On the third day a dry cough begins nthat is nonproductive or produces scanty mucoid, sometimes blood-streaked nsputum. Dyspnea and hypoxia become marked as signs of consolidation develop. nPleuritic chest pain occurs in one-third of patients. Severe confusion or delirium nmay occur.

There is leukocytosis with a shift to the left, nhyponatremia, abnormal liver function tests, and, occasionally, microscopic nhematuria. Chest x-rays reveal patchy, often multilobar pulmonary con- nsolidation, and, occasionally, small pleural effusions. The illness usually nworsens for 4-7 days before im- provement begins in those who recover. During nsevere outbreaks, the mortality rate has been 10% in those with manifest ndisease. Death is attributed to respi- ratory or renal failure or shock, with ndisseminated intravascular coagulation.

The diagnosis is based on a clinical picture com- npatible with the specific features of the disease and oegative results of nbacteriologic laboratory tests for other pneumonias. The organism can be nidentified by immunofluorescence in cultures, lung biopsy, and, rarely, sputum nspecimens. A retrospective diagnosis is based on a significant rise in specific nserum antibodies detected by immunofluorescence.

The treatment of choice is erythromycin, 0.5-1 g every 6 hours intravenously nor orally for 2-3 weeks. This usually results in improvement in 2-3 days. nRifampin, 10-20 mg/kg/d, has been suggested for patients who fail to respond to nerythromycin. Assisted ventilation and management of shock are essential.

Pneumocystis carinii Pneumonia

This parasitic infection occurs in debilitated nchildren or immunodeficient adults. It has been a prominent opportunistic ninfection in AIDS patients. The diagnosis is made by lung biopsy and the ndemonstration of typical cysts of P carinii in impression smears of lung tissue nstained with methena- mine-silver. Early treatment with sulfamethoxazole- ntrimethoprim can cure the pneumonia. The same drug has been effective iprophylaxis during immunosuppression. An alternative, more toxic drug is npentamidine isethionate .

“MIXED” BACTERIAL PNEUMONIAS (Hypostatic nPneumonia, “Terminal” Pneumonia, Bronchopneumonia)

Essentials of Diagnosis

• Variable onset of fever, cough, dyspnea, nexpectoration.

• Symptoms and signs often masked by primary n(debilitating) disease.

• Greenish-yellow sputum (purulent) with mixed nflora.

• Leukocytosis (often absent in aged and ndebilitated patients).

• Patchy infiltration on chest x-ray.

General Considerations

Mixed bacterial pneumonias include those in which nculture and smear reveal several organisms, not one of which can clearly be nidentified as the causative agent. These pneumonias usually appear as complica- ntions of anesthesia, surgery, aspiration, trauma, or various chronic illnesses n(cardiac failure, advanced carcinoma, uremia). They are common complications of nchronic pulmonary diseases such as bronchiectasis and emphysema. Old people are nmost commonly affected (“terminal” pneumonia). Patients treated with nintermittent positive pressure breathing apparatus or immunosuppressive drugs nmay develop pneumonia caused by gram-negative rods.

The following findings in a debilitated, chroni- ncally ill, or aged person suggest a complicating pneumonia: (1) worsening of ncough, dyspnea, cyanosis; (2) low-grade, irregular fever; (3) purulent sputum; nand (4) patchy basal densities on a chest film (in addition to previously noted ndensities caused by a primary underlying disease, if any), sometimes with local nnecrosis and cavitation.

Clinical Findings

A. Symptoms and Signs: The onset is usually ninsidious, with low-grade fever, cough, expectoration, and dyspnea that may nbecome marked and lead to cyanosis. Physical findings are extremely variable nand may not be impressive against a background of cardiac or pulmonary disease. nThe signs listed under Other Bacterial Pneumonias may also be present.

B. Laboratory Findings: The appearance of a ngreenish or yellowish (purulent) sputum should suggest a complicating npneumonia. Smears and cul- tures reveal a mixed flora, often including nanaerobes. Predominant types should be noted. Leukocytosis is often absent ithe aged and debilitated patient present- ing with a mixed infection.

C. X-Ray Findings: X-ray (Picture 3) shows patchy, nirregular infiltrations, most commonly posterior and basal (in bedriddepatients). Abscess formation may be observed. Careful interpretation will avoid nconfusion with shadows due to preexisting heart or lung disease.

Differential Diagnosis

Mixed bacterial pneumonias must be differ- nentiated from tuberculosis, carcinoma, and other spe- cific mycotic, bacterial, nand viral pulmonary infec- tions (to which they may be secondary).

Treatment

Clear the airway and correct hypoxia. Unless a nprobably significant etiologic agent can be identified, give one of the new ncephalosporins (eg, cefotaxime, 12 g/d intravenously) as initial therapy. This nwill be modified according to clinical and laboratory results.

Prognosis

The prognosis depends upon the nature and sever- nity of the underlying pulmonary disease and varies with the predominating norganism.

ASPIRATION PNEUMONIA

Aspiration pneumonia is an especially severe type nof pneumonia, often with a high mortality rate. It results from the aspiratioof gastric contents in addition to aspiration of upper respiratory flora isecretions. Important predisposing factors include impairment of the swallowing nmechanism (eg, esopha- geal disease), inadequate cough reflex (eg, anesthesia, npostoperative state, central nervous system disease, drug abuse), and impaired ngastric emptying (eg, pyloric obstruction). Pulmonary injury is due in large npart to the low pH (< 2.5) of gastric secretions.

Scattered areas of pulmonary edema and bron- nchospasm occur, and the x-ray appearance (pictures 4-5) may be confused with nthat of pulmonary emboli, atelectasis, bronchopneumonia, and congestive heart nfailure.

 

Removal of aspirated material by catheter suction or bronchoscopy may be nattempted, but this usually fails to remove all aspirate completely. Corticosteroids (eg, prednisone, 100 mg orally on the first or second day) may nreduce the intensity of the inflammatory reaction to acidic gastric secretion, nbut the value of corticosteroids in the treatment of aspiration pneumo- nia is nnot proved, and they increase the risk of superinfection. Some aspiratiopneumonias have no bacterial component, but in many others a mixed bacterial nflora is involved. Antimicrobial drugs directed against the latter (eg, npenicillin G plus an aminoglycoside or the best available cephalosporin) are nsometimes adminis- tered without waiting for evidence of progressive pul- nmonary infection. In doing so, however, there is a risk of favoring the ndevelopment of resistant mi- croorganisms. Therefore, administration of antimi- ncrobials should not continue without laboratory and clinical evidence of nmicrobial infection. Assisted ventilation and supplementary oxygen are nbeneficial.

 

 

The cancer of the central nlocation due to the obturation of bronchus results in atelectasis of a segment nor lobe of lungs, with probable further abscessing. For the differentiation used tomography (reveals the nobturation of bronchus by tumour, lesion of central lymph nodes), cytological nexamination of sputum and bronchial outwashes. The determinant role belongs to nfibrobronchoscopy with a biopsy and verification of the diagnosis.

Central lung ncarcinoma

 

The peripheral cancer of nlungs with destruction on tomograms is characterized by cavity with irregular inner surface, which external outline connects nwith root of the lung because of lymphatic metastatic spreading. The central nlymph nodes frequently enlarged. The diagnosis is improved by results of ntransthoracic puncture or catheterizing biopsy with cytological investigation, nfibrobronchoscopy. If it is impossible to confirm the diagnosis the thoracotomy nis indicated.

The nperipheral cancer of lungs

 

The tubercular cavern is mainly nlocated in the upper lobes of lungs, roentgenologically revealed on the nbackground of characteristic changes in adjacent pulmonary tissue n(calcification, dissemination), sometimes detected a draining bronchus. In the nsputum mycobacteria of tuberculosis are frequently found.

The ntubercular cavern

 

The suppurative cyst of nlungs differs by a gradual onset, slow course of the suppuration, less nexpressed intoxication. Roentgenologically its cavity has the oval or rounded nshape with a thin sheath and regular contour. Perifocal infiltration is not ncharacteristic.

 

Tactics and choice of treatment

The tactics in acute npulmonary destruction should be mainly conservative.

1.     nThe adequate antibacterial, antiinflammatory therapy nconsists of intravenous introduction of antibiotics of a wide spectrum nactivity.

Antibiotics in lung nabscess

Anaerobic organisms[3]

·        nFirst nchoice – Clindamycin (Cleocin 3)

·        nAlternative n- Penicillin

·        nOral ntherapy – Clindamycin, metronidazole (Flagyl), amoxicillin (Amoxil)

Gram-negative organisms

·        nFirst nchoices – Cephalosporins, aminoglycosides, quinolones

·        nAlternatives n- Penicillins and cephalexin (Biocef)

·        nOral ntherapy – Trimethoprim/sulfamethoxazole (Septra)

Pseudomonal organisms: First choices include aminoglycosides, quinolones, nand cephalosporin.

·        nGram-positive norganisms

·        nFirst nchoices – Oxacillin (Bactocill), clindamycin, cephalexin, nafcillin (Nafcil), nand amoxicillin

·        nAlternatives n- Cefuroxime (Ceftin) and clindamycin

·        nOral ntherapy – Vancomycin (Lyphocin)

Nocardial organisms: First choices include trimethoprim/sulfamethoxazole nand tetracycline (Sumycin).

 

With the purpose of nmaximal concentration of drugs in the pathological focus applied:

–         nInjection of antibiotics in the nvessels of a pulmonary circulation by means of catheterization of central nveins, pulmonary artery;

–         nIntroduction of medicinal agents ninto respiratory tracts (in the second stage) – through the endotracheal nmicroirrigator, nasogastric tube, during bronchoscopies, endoscopic ncatheterization of the abscess cavity through the draining bronchus, iaerosolic inhalations. The composition of medical admixtures includes: nantibiotics, antiseptics (10 % dimexid, dioxydin, microcid etc.), enzymes;

 

The nsteps of microtraheostomia:

 

Tracheocentesis after local anesthesia

 

 

 

 

 

Insertion of the conductor

 

 

 

 

Incertion of the irrigator along the nconductor

 

 

 

 

Skin wound

 

–         nTranscutaneous in the focus of ndestruction by means of puncture or draining with the usage of physical nantiseptics (US, UVR, laser).

–         nIntrapleural;

–         nBy means of electrophoresis.

2. Evacuation of purulent ncontent of the cavities:

–         nIatural way by aactive sanation of tracheobronchial tree using nrepeated fibrobronchoscopies, aspirations through the endobronchial catheter, ninstallations of medical agents through the microtracheostomy, aerosolic ninhalations;

–         nTransthoracically by means of nrepeated punctures or external draining of peripheral cavities.

3.     nDetoxycation therapy (intra- and extracorporal).

4.     nImmune correction (under the control nof immunogram):

–         nActive – staphylococcal anatoxiaccording to the plan;

–         nPassive – specific gamma-globulins, hyperimmune plasma;

–         nNon-specific (pirimidine nand purine derivates, drugs of a thymus gland, splenin, levamisol,).

5. Homeostatic correctio(oxygenotherapy, correction of anemia, hypoproteinemia, acidosis, microcirculatory disturbance).

6. Desensitizing, nantiinflammatory therapy, regulation of activity of proteases: antihistamine, nonsteroid antiinflammatory agents, inhibitors of proteases, antioxidants.

7. Correction of ndysfunction of the vital organs and systems, prevention of complications, nsymptomatic therapy.

Indications nfor operative management in acute destructive processes of lungs:

–         nPulmonary bleeding of ІІ- ІІІ degree;

–         nProgression of the process on the background of active nand appropriate therapy;

–         nTense pyopneumothorax, which is failed to liquidate by nthe draining of pleural space;

–         nImpossibility to rule out the suspicion on a malignant ntumour.

Contraindications: ndecompensation of the vital functions and systems in the terminal stage, nbilateral purulent destruction of lungs, concomitant incurable malignant ntumours.

Several important factors must be nconsidered prior to undertaking surgery. Because of the high risk of spillage nof the abscess into the contralateral lung, it is almost essential that a ndouble-lumen tube be used to protect the airway. If this is not available, nsurgery poses a very high risk of abscess in the other lung and a risk of ARDS. nIn such cases, postponing the surgery is a wise decision. Another, nless-satisfactory method to deal with this problem includes positioning the npatient in the prone position. The surgeon must be skilled in resecting the nabscess and in rapid clamping of the bronchus to prevent spillage into the ntrachea. These factors are extremely important when dealing with the surgical naspects of treating a lung abscess. If doubt persists, postponing the surgery nis best.

Surgical treatment is now rarely nnecessary and is almost never the initial choice in the treatment of lung nabscesses. In current practice, fewer than 15% of patients need surgical nintervention for the unchecked disease and for complications that occur in both nthe acute and chronic stages of the disease.

Surgical management is reserved for nspecific indications such as little or no response to medical treatment, ninability to eliminate a carcinoma as a cause, critical hemoptysis, and ncomplications of lung abscess (eg, empyema, bronchopleural fistula). Iaddition, if after 4-6 weeks of medical treatment a notable residual cavity nremains and the patient is symptomatic, surgical resection is advocated.

The results of surgery are difficult nto assess because of the varying patient population and the tremendous increase nin illicit drug abuse, alcoholism, AIDS, and infections by gram-negative and nopportunistic organisms. These factors have increased the incidence of lung nabscess and the associated morbidity.

A great deal of caution is needed nduring anesthesia when patients with lung abscess undergo surgery because nspillage of the abscess material into the uninvolved lung can occur. Therefore, na double-lumen endotracheal tube is used in all cases.

A study by Nagasawa et al has showthat thoracoscopic surgery can lead to effective drainage of pediatric lung nabscess without major complications. In addition, other benefits of nthoracoscopy include rapid recovery, less pain, and minimal morbidity.

 

Operational incisions – anterolateral, lateral and posterolateral thoracotomy. The operation suggests segmental, npolysegmental resection, lobectomy, bilobectomy combined intervention (with the ndecortication, pleurectomy).

 

 

Lateral access

 

 

 

 

Anterior access

 

 

 

 

Posterior access

 

 

The patients with chronic nabscesses should be undergone the operative treatment after complete nliquidation of exacerbation.

In a pulmonary gangrene nthe stabilization of the process on the background of active conservative ntreatment allows in future to apply conservative tactics up to recovery or nmaking optimal conditions for operation (liquidation of intoxication, naggressive panbronchitis, diffuse ninfiltration of the parenchyma, pleural complications). The headlong nprogression of the gangrene during first days, despite the active correction, noccurrence of pulmonary bleeding requires urgent performance of operative nmanagement. Volume of the operation – pneumonectomy, bilobectomy, lobectomy.

 

n

Pleural empyema

The pleural empyema is a purulent ninflammation of its visceral and parietal membranes, which is associated with naccumulation of pus in a pleural space.

 

Etiology and pathogenesis

The causes of occurrence nof acute pleural empyema are inflammatory, or purulent and destructive processes nof lungs, abscesses of abdominal cavity (secondary pleural empyema), open and nclosed damages of chest, and also, in some cases, operative approaches othoracic organs (primary pleural empyema).

A secondary pleural nempyema occurs in 88 % of the patients. Thus develops fibrinous, exsudative, nand then purulent pleurisy.

In case of pulmonary ngangrene, purulent mediastinitis, subphrenic nabscess the stage of exsudative pleurisy extremely short. The progression of nthe process results in transferring of focal pleural empyema into wide-spread.

 

Pathology

Macroscopically pleura is thickened, covered by npus with punctate hemorrhages. Microscopically it is diffusely oozed with neutrophils. In cases, when the empyema novercome into chronic course, the pleura deposits the calcareous salts, thick npus encapsulated, sometimes with the development of fistula.

 

Classification

І. According to the etiological factor:

1.     nSpecific.

2.     nNonspecific.

ІІ. According to the pathogenic factor:

1.     nPrimary.

2.     nSecondary.

ІІІ. According to the clinical course:

1.     nAcute.

2.     nChronic.

ІV. According to extension of the process:

1.     nFocal.

2.     nWide-spread.

V. According to the presence of lung ndestruction:

1.     nEmpyema with destruction of pulmonary tissue.

2.     nEmpyema without destruction of pulmonary tissue.

3.     nPyopneumothorax.

VI. According to communication with environment:

1.     nClosed pleural empyema;

2.     nOpen pleural empyema:

·        nbronchopleural fistula;

·        nthoracopleural fistula;

·        nthoracopleurobronchial fistula;

·        ncribrate lung.

 

Symptomatology and clinical course

The clinic of an acute npleural empyema depends on extension of the process, reactivity of organism and npresence of complications.

The pain is the sign, nwhich denote the involvement of pleural membranes in the process. Its intensity nincreases depending on depth of respiration and body position.

The dyspnea arises from naccumulation of a purulent content in a pleural space and exception of nparticular volume of a pulmonary tissue from respiration. It’s in direct ratio nto amount of exudation in a pleural space.

The cough is nmanifestation of inflammation or purulent and destructive process in a npulmonary tissue.

Fever to 39-40°C, headache, sleeplessness, general nmalaise, and anorexia – all these are manifestations of intoxication.

The forced patient’s nposition and restriction of breathing should be considered as outcomes of a npain syndrome. The extension of pleural empyema causes the swelling of thoracic wall, smoothing of intercostal spaces.

By palpation – diminished nvocal fremitus on the part of lesion.

The data of npercussion and auscultation depend on extension of the process and amount of npus in a pleural space. At percussion over the exudate it is possible to reveal nshort sound with oblique upper contour. Above the exudate – tympanic sound nresulting from consolidation of pulmonary tissue. By auscultation – diminished nor absent sound in a great amount of exudate.

The predominant roentgenological sign of a focal or wide-spread empyema – the presence of nexudate. In localized acute pleural empyema observed a local intensive homogeneous nshadow. Roentgenologically according to localization distinguished such types nof a focal empyema:

1)    napical;

2)    nparamediastinal;

3)    nparietal;

4)    ninterlobar;

5)    nepiphrenic.

 

The wide-spread pleural nempyema manifests by intensive homogeneous shadow in a basal parts with oblique nupper contour (Damuaso’ line). The diaphragmatic dome is nfailed to observe. The more pus contents in a pleural space, the higher the nupper measure of exudate.

 

Left-side pleural empyema

 

Pleural empyema

 

Pleural empyema

 

Pleural empyema

 

Pleural empyema

 

Variants of clinical course and complications

The clinic of a focal pleural nempyema depends on the site of the process. The apical empyema, due to involvement in the process of a vascular-nervous nfascicle, manifests by intensive pain. The soft tissues of supraclavicular nregion are swelled. The percussion and auscultation has no information.

The pain syndrome in parietal (paracostal) empyema is nmore expressed. Thoracic excursion is restricted. The diminishing of nrespiratory sound can be obtained over the exudate.

The chief complaint iparamediastinal empyema is the heart pain. The location of the process in the nupper mediastinum can cause the superior vena cava syndrome. The physical nfindings are vague.

In case of the basal n(epiphrenic) empyema the patients complain of pain in subcostal area, which nincreases at respiration and irradiates in supraclavicular region. In some ncases the pain irradiates in epigastric region. The palpation of intercostal nspaces and hypochondrium is painful.

The clinical course of npostoperative empyema depends on the character of operative approach (marginal nresection of lung, lobectomy, pneumonectomy, operation on esophagus) and infection of the pleural space.

The clinical nmanifestations of posttraumatic empyema depend on the size of damage of the nchest, lungs, mediastinal organs and complications (suppuration, hemothorax).

The involvement in the purulent process of a pulmonary tissue in acute nempyema results in its fusion of membranes with formation of a bronchial or nthoracopleural fistula (discharge of abscess through thoracic wall).

The inappropriate nelimination of empyema results in chronic course, cribrate lung and pleurogenic cirrhosis of lungs.

 

The diagnostic program

1. Complaints and history nof the disease.

2. Physical findings.

3. Data of chest X-ray (itwo planes, if necessary – laterography).

4. Pleural puncture.

5. The microbiological ninvestigation of the exudate for its sensivity to antibiotics.

6. General blood and nurine analyses.

7. Biochemical blood nanalysis.

8. Pleurography (itransferring of the process into chronic form).

 

Pleural puncture:

 

 

 

Local anesthesia

 

 

 

 

Thoracentesis

 

 

 

 

 

Aspiration of the fluid

 

 

 

 

Localization of the needle:

          1 the needle damaged the nlung

          2 the needle damaged the ndiaphragm

          3 the needle locatedin pleural nsinus

 

 

 

Differential diagnostics

Pleuropneumonia complicated nwith exsudative pleurisy, in some cases resembles acute pleural empyema: a nchest pain, fever, dyspnea, cough, and general weakness. The chest nroentgenogram reveals hydrothorax (exsudative pleurisy, pleural empyema, nhemothorax). The chief diagnostic method for ndifferentiation is the thoracentesis. The presence of a serous (lucent, nfaint-yellow) exudate testifies about the pleuropneumonia, complicated with npleural effusion, and cloudy, foul-smelling exudate of white or greenish color n– about acute empyema.

The major difficulties idifferential diagnostics cause the limited forms of empyema.

The Pancoast ncancer clinically and nroentgenologically in most cases has almost the similar course to apical form nof empyema. The transthoracic biopsy permits to confirm the diagnosis.

The acute ncholecystitis is necessary to differentiate with the epiphrenic nempyema. The pain in the right hypochondrium, fever, phrenic symptom are common for both diseases. However the objective findings, X-radiography of chest and the nthoracentesis allow to differentiate these pathological processes.

The tumour of nanterior mediastinum complicated by superior vena cava syndrome is necessary nto differentiate with paramediastinal empyema. Nevertheless the body ntemperature in such patients, as a rule, normal. The upper cavography is possible to find out the shift of cava nvein and its irregular contours (filling defect) due to growth of the nmediastinal tumour.

There are some ndifficulties in differential diagnostics of empyema with a posttraumatic diaphragmatic hernia. Such X-ray nfindings as deformation of diaphragm, additional shadows with a liquid level, nintestinal loop suggest a diaphragmatic hernia. A laterography and contrast study of gastrointestinal tract is basic idifferential diagnostics of this disease.

The atelectasis of a nsegment, and lobe of lung in some cases can cause misdiagnostics. Except X-ray chest nexamination (in two planes and tomography), these situations require necessity nof diagnostic bronchoscopy, which reveals the cause of bronchial obturatio(foreign body, endobronchial cancer etc.).

 

Tactics and choice of treatment

The presence of pus in a npleural space is the indication for its elimination. In the place of performed ndiagnostic thoracentesis carried out the draining of empyema’s cavity, its nsanation by means of antiseptic solutions. In a focal empyema the aspiration of npus is performed by thoracentesis and only iits inefficiency carried out a draining of pleural space.

 

Pleural drainage:

 

 

Trocar insertion

 

 

 

 

Incertion of drainage tube

 

 

 

 

 

 

Passive drainage by Bulau

 

 

 

 

 

Active aspiration

 

 

Intensive antibacterial and nantiinflammatory therapy should be immediately instituted. For general nimproving used detoxication therapy (infusion of saline solutions, nhemotransfusion, transfusion of proteins, solutions of dextran, haemodes, nforced diuresis, hemosorption if necessary), therapy for rising up of nimmunological resistance of the organism.

During the empyema’s nsanation decreases the amount of pus which discharges out through the drainage. nThe optimal variant of such course is the liquidation of empyema’s cavity, thethe drainage must be removed.

Transferring of the nprocess into the chronic form (10-12 weeks) results in formation of a residual nempyema’s cavity, which is possible is to reveal by means of pleurography – nintroduction through the drainage of water-soluble contrast with the further nX-radiography in 2 planes.

Operative approach is napplied when the process has transferred into the chronic form, that is in case nof residual empyema’s cavity. Volume of the operation – pleurectomy, ndecortication of lung.

In some cases, when a nbronchial fistula and great empyema’s cavity has been formed, there is the nnecessity of performance of resection of lung and corrective thoracoplasty.

n

lung Cysts

The cysts of lungs are nthe thin-walled cavitary formations, filled with air or liquid contents.

Inherent and acquired ncyst are distinguished.

 

Etiology and pathogenesis

Inherent cysts arise from nthe abnormalities of the development of lungs under ninfluence of the multiple chemical, physical, biological factors. Whether they ncan develop from a bronchial tree (bronchial) of from alveolar tissue n(alveolar). Their occurrence resulting from the delay of the development of nperipheral parts of bronchus with their expansion or agenesia of alveoli with ndilatation of terminal bronchioles. Congenital cysts at first develop and grow nas secretory formations. After communication with bronchus they finally form as nair or hydroair cavities.

The acquired cysts nrepresent fibrous cavities, which remain after abscesses, tubercular caverns, nechinococci, posttraumatic intrapulmonary hematomas. The ndegenerative changes in the wall of bronchus with obliteration of its lumen by na cloggy secret owing to repeated inflammatory processes result in occurrence nof acquired retentional cysts.

 

Pathology

Congenital cyst can be located in any part of nlungs. The walls of bronchogenic cavities contain chaotically disposed elements nof bronchus (cartilagous plates, muscle nfibers, mucous glands), they are lined from inside by cylindrical or cubic nepithelium. Squeezed alveolar cells line the walls of alveolar formations.

The acquired cyst are revealed in places of nlocalization of previous diseases,. Their nwalls mainly consist of connective tissue. Epithelization is possible due to ntransferring of the epithelium from a draining bronchus at long existence.

The cysts could be uni- or multichamber, closed nand open (depending on the presence of communication with bronchus).

 

Classification

According to nparentage:

–         ncongenital;

–         nacquired.

According to ndisplacement:

–         nsingle, multiple;

–         nunilateral, bilateral.

Complications: n

–         nSuppuration;

–         nAppearance of the valvular mechanism;

–         nBleeding;

–         nDischarge into a pleural space (pneumothorax, npyopneumothorax, pleural empyema);

–         nMalignancy.

 

Symptomatology and clinical course

Clinical manifestations nof uncomplicated pulmonary cysts are vague. Sometimes patients complain of a nchest pain, periodic cough, and inflammatory diseases of respiratory tract ihistory. In children the signs are much expressed, the dyspnea associates with nthe compression of airways.

In great, superficially ndisposed cysts revealed delayed respiratory movements on affected side during nbreathing.

By palpation – weakened nvocal fremitus.

By percussion – short or nbandbox sound, depending on contents.

By auscultation – nweakened respiration, over the huge open cavities – amphoric.

At routine chest films nthe closed congenital cyst forms a homogeneous shadow of the spherical or oval nshape of average intensity with rather regular edge on the background of aintact pulmonary tissue. During roentgenoscopy sometimes observed the change of nits shape depending on the phase of breathing – elongation in inspiratio(Escudero’s syndrome). The character of the shadow nis better to study on tomograms.

Acquired retentional cyst is roentgenologically shown by a shadow nof irregular shape (piriform, spindle-shaped etc.), that displays the shape of nthe distended bronchus. The adjacent tissue, as a rule, changed due to nbronchiectases, pneumosclerosis, etc.

 

Cyst of the right lung

 

 

Open cysts are observed nas thin-walled, good defined cavities of nannular or oval shape.

On bronchograms ncongenital cysts are observed hypoplasia of segmental or lobar bronchus, lack of bronchial bifurcations, which ntends to bone. Sometimes observed bronchiectases in the neighboring parts of nlungs. A cystic cavity is infrequently defined.

The angiopulmonography nreveals deformation of vascular branches, which circumflex the cyst.

 

Variants of clinical course and complications

The nsuppuration of the closed ncysts resembles the development of a lung abscess with lesser expression of nsigns of intoxication (protective role of epithelial wall).

Infection of the open cysts is characterized by a gradual long course, nmoderate manifestation of suppuration and late intoxication.

The tension (valvular) ncysts arise more often in children. They are characterized by severe nrespiratory and hemodynamic disturbances, up to terminal, owing to inflexion of nvenous trunks, shift of mediastinum and compression of lungs. The predominant nsigns are increased dyspnea, cyanosis, chest pain, respiratory lag on affected nside, auscultatory – absence or weakening of respiration, bandbox percussiosound over the cavity at mediastinal shift to the opposite side of the chest.

Pleural ncomplications of pulmonary cysts, and also bleeding described nin the relevant parts.

The malignant ndegeneration of pulmonary cysts occurs very rarely.

 

The diagnostic program

1. Complaints and history nof the disease.

2. Physical methods of nexamination.

3. Routine chest film itwo planes.

4. Lung tomography.

5. Bronchography.

6. Angiopulmonography.

7. General blood and nurine analyses.

 

Differential diagnostics

The abscess of nlungs, in contrast with a suppurative cyst, nis characterized by prompt course, expressed purulent intoxication, nroentgenologically its wall is irregular, with proper considerable perifocal ninfiltration.

The cancer nwith destruction differs by a thick wall with a tuberous inner surface, nphenomena of lymphangitis in adjacent tissue. The determinant value has endoscopic examination or puncture with a biopsy and nfollowing morphological investigation.

The tubercular ncavern displaced in the upper lobes, in adjacent tissue revealed fibrosis, npetrifactions, dissemination, peribronchial lymphadenitis. In the sputum – nmycobacterium of tuberculosis.

Opposite to cyst, itermed diseases, the circumflex deformation of vascular branches never observed nat angiopulmonography.

The considerable ndifficulties can arise at differentiation of the closed congenital cysts.

The ntuberculoma differs from them by characteristic localization. At X-ray examinatiothe heterogeneity of the shadow with calcifications, nearly excentric destruction, “tubercular” background is observed.

The benigtumours sometimes npossible to differentiate only after the results of cytological investigatioof punctate or after operation.

The nechinococci cysts on tomogram can have a double ncontour of chitinous and fibrous sheaths.  nIn blood analyses observed eosinophilia. The final decision is taken out nafter carrying out immunological (indirect microagglutination test) allergic n(Cacconi’s reaction) tests.

Huge cysts, in contrast with open air cysts, are ncharacterized by a subpleural location.

The diagnostic doubts at nsuspicion on a diaphragmatic hernia are solved nby radiopaque examination of a gastrointestinal tract.

The acquired ncysts differ from ncongenital by roentgenological signs of the lesion of surrounding tissues n(pneumofibrosis, deforming bronchitis, secondary bronchiectases, and ncalcifications). Postpneumonic cavities are of nirregular shape, with grooves and pockets, their walls different thick. During nbronchography they filled through some small bronchi. Sometimes the nverification is possible only after postoperative morphological investigation.

 

Tactics and choice of treatment

The pulmonary cysts nrequire the surgical treatment. In case of complications the indication for noperation becomes absolute. Contraindications: the severe respiratory ndisturbance, concomitant malignant nonresectable tumors, vital organs ndysfunction in the stage of permanent decompensation, elderly age of the patients.

The volume of the operation: if the adjacent pulmonary tissue is nintact – cystectomy, otherwise – segmental or wedged resection, lobectomy.

The conservative therapy nis applied in suppuration of cysts with the purpose of preoperative preparation. It is the similar, which applied for nabscesses of lungs.

n

Spontaneous npneumothorax

 

Spontaneous pneumothorax nis the entry of air in a pleural space with the further lung collapse, which nnot associated with traumatic damage of chest or pulmonary tissue.

 

Etiology and pathogenesis

As a result of spontaneous ndisrupture of lung blebs and subpleural air cysts occurs the damage of pleural nvisceral membrane. It causes entry of air in pleural space. Owing to its nleakage the elastic pulmonary tissue collapses. The degree of the collapse of nlung depends on amount of air, that has penetrated a pleural space.

 

Pathology

Morphologically in spontaneous npneumothorax found out a focal bullous emphysema with disrupture of blebs, subpleural air cyst, and also disorders, which have ncaused disturbances of ventilating ability of bronchi. It can be bronchitis, npneumosclerosis, tuberculosis and fibrous alveolitis.

 

Classification

The pneumothorax can be:

1.     nUnilateral or bilateral.

2.     nPartial (lung collapse to 1/3 of its volume).

3.     nSubtotal (lung collapse to 2/3 of its volume).

4.     nTotal (lung collapse more than 2/3 of its volume).

5.     nTension or valvular (complete collapse of lungs and nshift of mediastinum in the opposite side).

6. Rigid n(neglected pneumothorax with thickened visceral pleura).

 

 

Partial nspontaneous pneumothorax

 

 

 

Subtotal nspontaneous pneumothorax

 

 

 

 

Total nspontaneous pneumothorax

 

 

Manifestation and clinical course

The onset of the disease nis sudden. A state of the patient and expression of clinical manifestations depends non amount of air, which has entered the pleural space. Usually iormal nconditions, and sometimes after physical activity, the patients suddenly feel nacute pain on the side of lesion, dyspnea, pain in the heart region and nheartbeating. An available also Acrocyanosis or total cyanosis of skin is nobserved. The circulatory disturbance depends on degree of hypoxia. Intensity nof pain and dyspnea gradually decrease, but a dry troublesome cough appears.

Examination of the chest nallows to observe expansion of intercostal spaces and restriction of nrespiratory excursion. By palpation – diminishing of vocal fremitus on the naffected side. At percussion a chief sign of pneumothorax is the tympanic nsound. Auscultation reveals weakened or sharply weakened breathing sounds. The ncardiac tones are muffled, tachycardia.

The diagnosis of a nspontaneous pneumothorax is confirmed by X-ray examination. On the plairoentgenogram the air is present in pleural space, and the margins of collapsed lung are found out on its background.

Thoracoscopy ipneumothorax possible to find out subpleural blebs of different sizes (0,5-3 cm), which are mainly ndisposed on the apex of lung.

 

Variants of clinical course and complications

The atypical (asymptomatic) nspontaneous pneumothorax occurs in 20 % of the patients, and mainly revealed at nX-ray examination. In most cases it is the partial pneumothorax.

The expressed paisyndrome and dyspnea, which resulting from collapse of lung, characterize subtotal nand total pneumothorax.

The tension spontaneous npneumothorax is the most severe form of pneumothorax. It manifests by suddeonset, progressive increase of dyspnea, expressed cyanosis. The breathing is nsuperficial, rapid, with active participation of auxiliary muscles. Mediastinal nshift and flexion of vessels result in disturbance of cardiac activity up to the cardiac arrest, and requires urgent nmanagement.

Rigid pneumothorax (rigid lung). The neglected pneumothorax causes nfibrinous exsudative pleurisy. On the surface of lung (visceral pleura) ncommissures are formed, that give no opportunity for lung expansion. The npresence of residual pleural cavity and progressive development of a purulent ninfection result in occurrence of acute pleural empyema. In such cases the npatients complain of the fever up to 38-38,5°C, general weakness and increasing of dyspnea. The phenomena of nintoxication increase. Thus such patients require the treatment of pleural nempyema.

 

The diagnostic program

1.     nComplaint and anamnesis of disease.

2.     nPhysical findings.

3.     nRoutine chest film (direct and lateral projection).

4.     nThoracentesis

5.     nThoracoscopy.

6.     nTomography of lungs.

 

Differential diagnostics

Pleural effusion. This pathology manifests by more gradual onset. As opposite to npneumothorax, the complaints of chest pain predominate above the complaints of ndyspnea. Frequently such patients specify on transferred undercooling.

As well as the nspontaneous pneumothorax, the pleural effusion is characterized by diminishing nof vocal fremitus, dullness of percussion sound, weakened of absent breathing nsounds over the exudate. Nevertheless in the routine roentgenogram in such ncases observed a homogeneous intensive nshadow of a pleural space with oblique upper contour. The puncture of pleural nspace enables finally to confirm the diagnosis of pleural effusion.

Intercostal neuralgia. A predominant sign iclinical pattern is acute pain, which intensifies at physical activity, changes nof body position and body movements, at deep breathing. The localization of npain coincides with zone of innervation of intercostal nnerves.

Examination and chest X-radiography reveals no pathological nchanges.

 

Tactics and choice of treatment

Conservative treatment is napplied in the patients with a partial pneumothorax. Thus thoracentesis in ІІ nintercostal space in the midclavicular line with aspiration of air is nperformed. The cases of its inefficiency, and also subtotal, total and tensiopneumothorax require drainage of a pleural space with active aspiration of air. n

The operative management nis necessary, if there is no efficiency from active aspiration (in incomplete expansion of lung), recurrent of course of the process, npresence of great subpleural blebs and rigid pneumothorax. Volume of operatiodepends on extension of the process: liquidation of alveolar fistula, wedged nresection of lung or lobectomy.

 

n

Pyopneumothorax n

Pyopneumothorax is the discharge of lung abscess of into pleural space, which nis accompanied by purulent inflammation of pleural membranes with a collapse of nlung.

 

Etiology and pathogenesis

Peripheral placement of nthe purulent focus in a pulmonary tissue results in destruction (fusion) of nvisceral membrane. As a result of, the pus and air penetrate into a pleural nspace that leads to a purulent inflammation of parietal and visceral membranes nof pleura. The disorder of hermeticity of a pleural space results in a lung ncollapse.

Among other causes of npyopneumothorax are the chest trauma, which nresults in collapse of lung, infection and purulent inflammation of pleural nmembranes.

As the basic causes of npyopneumothorax are considered:

–         nacute abscess of lung;

–         ngangrenous abscess of lung;

–         ngangrene of lung;

–         nsuppurative cyst of lung;

–         nabscessing pneumonia;

–         nbronchiectatic disease;

–         nsubphrenic abscess, which has ndischarged into pleural space;

–         ndamage of esophagus;

–         nmediastinitis;

–         nchest trauma;

–         noperation and diagnostic manipulations on chest organs.

 

Pathology

Morphologically ipyopneumothorax pus and air are present in pleural space. In the lungs nsubpleural disposed purulent or necrotic foci, which connected with a pleural nspace through a pleuro-pulmonary fistula. From the outside the zone of ndisrupture is confined by perifocal inflammation. In the draining bronchus it nis possible to see manifestations of deforming, frequently polypous bronchitis. n

 

Classificatio

І. According to etiological nfactor:

1.     nSpecific.

2.     nNonspecific.

ІІ. According to pathogenic factor: n

1.     nPrimary.

2.     nSecondary.

ІІІ. According to clinical ncourse:

1.     nAsymptomatic form.

2.     nMild form.

3.     nAcute form.

ІV. According to extension of nthe process:

1. Localized pyopneumothorax:

a)     nparietal;

b)    napical;

c)     nepiphrenic;

d)    nparamediastinal;

e)     npolychamber.

2. Subtotal pyopneumothorax.

3. Total pyopneumothorax.

4. Tension pyopneumothorax.

 

Manifestation and clinical course

The clinic of npyopneumothorax depends on the size of the focus of destruction, which ninfluences on degree of lung collapse, and on amount nof purulent content in a pleural space.

The pain owing to ndischarge of the focus of destruction into pleural space often arises suddenly. n

The dyspnea occurs as a nresult of collapse of lung owing to leakage of pus and air into pleural space. Its nexpression is in direct ratio to lung collapse. Therefore a dyspnea in rest nobserved in a subtotal and total pyopneumothorax. It sharply amplifies even at nminor physical activity. Auxiliary muscles take part in order to force nrespiration.

The expectoratioof sputum with ichorous smell is the outcome of destructive process in a pulmonary ntissue. Its amount decreases after discharge of pus into pleural space.

Hectic fever with caused by enlargement of the area of resorption. The npatients are adynamic, flaccid. Some of them are unconsciousness.

By objective nexamination the position of patients is forced, they sit in bed leaning upon the bed (subtotal, total pyopneumothorax). The affected nhemithorax takes no part in respiration.

By palpation – diminished nvocal fremitus on the side of lesion.

Percussion reveals a sharp shortening of sound over the zone of nexudate and bandbox sound above the region of collapsed lung.

By nauscultation there are no breathing sounds on the affected side. In case of localized pyopneumothorax n– weakened or sharply weakened sound with a bronchial or amphoric tone.

The X-ray npicture of pyopneumothorax depends on its form, but the obligatory sign is the nair-fluid level in a pleural space with well-defined edge of collapsed lung on its background.

 

Left-side total pyopneumothorax

 

Pyopneumothorax

 

Pyopneumothorax

 

Variants of clinical course and complications

The clinical course of npyopneumothorax depends on adhesions between pleural membranes. It sometimes changes typical clinical course of a total lung ncollapse. The clinic of disease depends also on amount of a purulent exudate. nTherefore according to extension of the process and size of destruction of lung ndistinguished acute, mild and asymptomatic forms of pyopneumothorax. Especially ndifficult for diagnostics is the asymptomatic form of localized npyopneumothorax. Dyspnea for such pathology not characteristic, as the adhesioof membranes prevents complete collapse of lung. Dyspnea is vague or absent at nall in partial collapse. A diminished vocal fremitus on side of pathological nprocess, shortening of percussion sound and weakened or sharply weakened nbreathing sounds over the collapsed lung and exudate are revealed. nRoentgenological manifestations in localized pyopneumothorax not expressed and ninclude horizontal fluid level, margin of partially collapsed lung and minor nair in the pleural space.

In most cases after ndischarge of the destructive focus in a pleural space and collapse of lung nobserved the closure of bronchopleural fistula. Nevertheless the inflammatory process in a pulmonary tissue and npleural space is going on.

 

The diagnostic program

1. Complaint and history nof disease.

2. Physical findings.

3. Chest X-radiography nexamination.

4. Thoracentesis.

5. Pleurography.

6. Bacterial culture and nantibiotic sensitivity.

7. General blood, and nurine analyses.

8. Biochemical blood nanalysis.

 

Differential diagnostics

They’re no special necessity nfor differential diagnostics of pyopneumothorax in the majority of patients. nHistory (presence of the purulent focus in a pulmonary tissue), clinical course n(acute pain and dyspnea at abscess discharge into pleural space), and also nchest X-ray findings and thoracentesis frequently reliably permit to make the ndiagnosis.

In some cases a localized npyopneumothorax according to clinical course resembles a huge acute abscess of nlungs. But the differences of roentgenological symptomatology permit to verify nthese pathological processes. In acute lung abscess the cavity of destructiolocalized in a pulmonary parenchyma, it is of rounded form with horizontal nfluid level and expressed perifocal infiltration.

 

Tactics and choice of treatment

The purpose of treatment nshould include sanation of the destructive focus in pulmonary tissue and nliquidation 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. n

2. Draining of pleural space, active aspiration of its content n(air, pus) to expand the lungs.

3. Lavage of pleural space by antiseptic solutions.

4. Appropriate antibacterial, nantiinflammatory and infusion therapy.

5. The therapy for rising nup of immunological resistance of the organism (staphylococcal anatoxiaccording to scheme, antistaphylococcal gamma-globulin, antistaphylococcal nplasma).

6. Endolymphatic introduction of immunity stimulators n(thymalin, thymogen, Т-activin).

The indications for noperative management are the same, as in pleural empyema.