Lung abscess

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* Concept

* Epidemiology

* Pathogenesis

* Pathology

* A clinical picture

* Supplementary examinations

* Evolution and complications

* Treatment

* Bibliography

CONCEPT

Lung abscess (AP) is an infectious lesion, necrotic and cavitated pulmonary parenchyma.

Some authors differentiate necrotizing pneumonia (small cavitated lesions limited to a specific region of the lung) by the number and size of the cavities within the lesion and talk about AP, when cavitation is unique and larger than 3 cm. Given the common pathogenesis, the majority makes no such differentiation.

EPIDEMIOLOGY

After the discovery of antibiotics, the frequency of primitive AP as well as decreased mortality. The incidence appears to be higher among patients with oral sepsis, in patients undergoing oropharyngeal surgery, among sinusitis sufferers, loss of consciousness seizures, anesthesia, alcohol abuse, drugs, etc.. situations occurring in some way, oropharyngeal aspiration.

From the point of view is useful to identify etiological if the disease is acquired in the community or in the hospital environment, as the causative agent in incidence differs depending on the condition, and this of course is important to determine the therapeutic

Varied germs can cause injury in the lung abscess (Table 1). Anaerobes, the most common germs, are those that typically cause a necrotizing lesion., Ie the so-called putrid or gangrenous abscess. While the most common cause aerobic called simple abscesses where pneumonic lesion is the predominant. The tubercle bacillus is not considered causal agent of AP and neither recognizes the fungal origin.

In most cases the injury is caused by more than one germ (polymicrobial).

Pathogenesis

Access roads to lung abscess producing germs are several:

1. – Aspiration for the airway of infected material from the upper respiratory tract, especially in people with poor oral hygiene, food or vomiting in anesthetized patients, foreign bodies, etc.. This is the most common and important in these cases the presence of oral sepsis (gingivitis, pyorrhea, etc..) Plays a key role in providing the infecting organism. Have been recognized as factors predisposing to aspiration, sepsis periodontal addition, alterations of consciousness for several reasons, the alterations of innervation and muscle control of the pharynx, larynx and esophagus, all individuals in the mechanism cough and other pulmonary defense system failed. The seed to reach the lungs causes pneumonitis is followed shortly necrosis. The site of the lesion and abscess formation depends on the position of the patient. Aspirativos abscesses are more common on the right side and are located toward the posterior segments of the lower lobe. If aspiration occurs lying then be located in the upper segments of the lower lobe or the posterior superior.

2. – Lung hematogenous dissemination. This form is the second most important path through her germs reach the lung from the right heart endocarditis, phlebitis, puerperal sepsis, etc.. The lung lesions that occur are multiple and may even be bilateral. A rare and hematogenous dissemination AP are presented in tonsillar infection by Fusobacterium nucleatum with phlebitis of the jugular. In pulmonary infarcts resulting from obstruction of the embolic via the blood, infection and secondary abscess formation sometimes occurs is bronchogenic aspiration.

3. – Bronchial obstruction stenosing tumors and lesions determined or promotes retention of secretions and bronchopulmonary suppuration corresponding segment. This type of abscess, which can occur in any part of the lung, requires finding tumor lesion especially when it comes to adult smokers or patients with unexplained a location other than the right lung base.

4. – Contiguity of chest wounds infected liver or subphrenic abscess, pleural empyema fistulizados the bronchi, esophageal perforation and mediastinal abscess. Thoracic contusions may become secondarily infected cavitate when, while chest wounds can become infected from the very beginning by the germ transit through the wound.

For transit or transabdominal transdiaphragmatic AP occurs amebic (complication of liver abscess) and other etiologies, originating in abdominal infections. Logically these lesions are located contiguous to the lung bases.

PATHOLOGICAL ANATOMY

The location and number of abscesses depends on the etiology. The diameter varies from a few millimeters to five or six inches.

From the viewpoint anatomoclinical consider the simple and gangrenosum.

Abscess simple.

In this type of abscess are three periods or stages:

1st Period: Characterized by a pneumonic congestion. The gross appearance of the abscess depends on its cause.

2nd Period: There parenchymal necrosis, liquefaction and sequestration.

3rd Period: Characterized by evacuation and cavitation. Once formed the cavity must be distinguished:

to Content pus is a greenish yellow, creamy, with remnants of necrotic parenchyma.

b: Wall: There tendency to limitation of the process. In abscesses short benign forms a very thin pyogenic membrane lining the cavity. In cases of long duration membrane is thick and sometimes reaches esclerosarse.

c: pericavitaria Zone: This consists of a region can also hepatization esclerosarse reach. The area adjacent to pleural abscess is attached and thickened, it may become perforated and lead to pneumothorax or empyema.

Gangrenous or putrid abscess.

This type of abscess presents irregular cavities of variable size. The wall is thick. Inside there is a viscous, yellow-gray, foul-smelling. Pericavitaria area can be of two types: block neighborhood pneumonic and alveolitis.

The characteristic of gangrenous abscess is the great involvement and vascular necrosis. This is a sign that distinguishes outstanding single abscess. Also from the very early stages there is a pulmonary sclerosis develops dramatically and can cause deformities and bronchial dilation.

CLINICAL

You can find a history of oral sepsis, dental extractions, anesthesia sinusitis, tonsillectomy, history of coma, convulsions, neurological diseases etc. Please note that oropharyngeal aspiration can occur during sleep and that the above conditions are a must.

Classically discover three periods in the evolution of an abscess: Start, open and festering.

Period beginning:

It is characterized by moderate box, sometimes torpid, an acute lung disease lasts about a week and attends with general and local symptoms. General symptoms include fever, chills, anorexia and weakness. Among local symptoms is the initial dry cough, tip sideways and dyspnea and physical examination can detect signs of an inflammatory syndrome condensation. For anaerobic infection, the onset is subacute rather generally deteriorated state, weight loss, fever and sweating, this discomfort may extend for two or three weeks. The weight loss and anemia betray chronicity of the process.

. Or vomica Opening period:

It occurs in the second week of evolution. In this phase becomes productive cough, expectoration may be preceded or be downright hemoptysis hemoptysis. The progressively increasing amount of sputum is purulent and sometimes dark and fetid.

Sometimes expectoration occurs abruptly after a coughing fit, very filling and accompanied by nausea, is the classic vomica, rare in the era of routine use of antibiotic, it is more frequent and repeated moderate amount (vomica fractional Nummular vomica).

Seeping Period:

It is observed in untreated cases solely or in which the treatment has been ineffective. It begins when you open the abscess. If evolutionarily expectoration increases could be in progress of the abscess, if improvement is decreased or may have arisen because some difficulty in drainage in these cases the general symptoms become more evident, the fever is irregular, there are frequent sweating, weight loss, fatigue and sick airs of gravity.

Physical signs are variable dependent on the location and extent of the lesion often collected moist rales on auscultation. Can be found in very few cases a breath cavity. When pleural complications exist, were detected signs of pleural effusion.

SUPPLEMENTARY EXAMS

CBC: There leukocytosis in the initial stage can reach 20 to 30 x 109, with a predominance of polymorphonuclear cells, is frequently left shift. The AP can be chronic anemia.

ESR: Found accelerated.

Other blood chemistry studies: They can bring out diabetes mellitus or liver disorders due to alcoholism or malnutrition.

Blood cultures: Most of the time they are negative, because the way of acquiring the disease is bronchogenic and therefore no bacteremia. May be positive in patients infected with gram-negative bacilli and Staphylococcus aureus hematogenous dissemination.

Microbiological studies: Sputum is not very reliable in the AP because the germs that cause the disease are those of the oropharynx and make, of course, doubt diagnosed. However be practiced Gram stain and sputum culture for both aerobic and anaerobic bacteria.

Invasive methods for the sample of secretions such as transthoracic and transtracheal puncture, although they are much more reliable than the conventional sputum because they bypass the oropharyngeal flora, have the disadvantage of the complications that can occur, in addition to be contraindicated in certain situations are not therefore routine procedures. Fiberoptic bronchoscopy is also an invasive procedure, its use in this condition is given because it is the most reliable method to obtain the sample of secretions, also allows bronchial washing and brushing important for microbiology. Although it is still useful for identifying bronchial obstructions and take biopsy, bronchoscopy is not diagnostic of AP, which together with its invasiveness limits its indication to cases with poor outcome or where a tumor is suspected conditioning.

Radiology: The posteroanterior chest radiograph is the most important study for diagnosis. In the initial phase, the radiologic image is a pneumonic process. When properly defined, then you will appreciate a picture cavitated larger than three inches, with air-fluid level inside and perineumonitis area in the periphery (Figures 13.1 and 13.2). Sometimes what you see is a pulmonary parenchymal infiltrate multiple cavitary lesions less than 2 cm, which is called necrotizing pneumonia. The side view topographically helps locate the lesion. Computerized tomography supports the diagnosis and may provide additional data such as the presence of tumors and pleural complications.

DIAGNOSIS

Positive diagnosis:

Clinical elements as abundant and fetid expectoration, fever, generally deteriorated state of the patient, and sepsis periodontal us to suspect the entity, but only positive diagnosis is made by chest radiography.

Differential Diagnosis

In the initial period should be performed with acute lung diseases (pneumonia, tuberculosis, lung infarction) in addition to the infected lung bullae. In the period vomica and oozing with bronchiectasis, neoplasia abscess, cavitary tuberculosis and infected congenital cysts air.

EVOLUTION

The AP evolves toward healing when treated properly. But sometimes this can be torpid evolution which has led to divide them into acute when the evolution time is up to 8 weeks and chronic when evolving for longer than this. This evolutionary approach, tracing the therapeutic in disease.

They may, in its evolution, complications arise.

COMPLICATIONS

The AP can be complications and extrapulmonary pleuropulmonary. The first is due to massive lung suppuration, empyema, pioneumtorax, bronchial fistula, mediastinitis, hemoptysis. Extrapulmonary complications are: septicopiemia, brain abscesses, splenic abscesses, endocarditis, amyloidosis and arthritis.

TREATMENT

Prophylactic treatment.

AP Prophylactic treatment comprises:

* Preoperative and postoperative oral sepsis, particularly in the speeches of the oropharynx, larynx, abdominal and chest that are most often complicated by abscesses aspirativos.

* Caution correct periodontal diseases in general.

* Strict compliance with the standards of anesthesia.

* Early and appropriate treatment of pneumonia.

Curative treatment

Two steps are basic and antimicrobial proper drainage, however must be given to the patient’s general condition. Medical treatment includes:

* Admission to hospital and rest until all symptoms disappear and signs of infection.

* E-calorie protein diet, remember that there is tissue destruction.

* Must relieve pain and reduce fever with antipyretic analgesics.

* If necessary the patient is transfused. They ensure fluid balance. Empirically, in patients who acquire the infection in the community Penicillin is the drug of choice.

It begins with crystalline penicillin, intravenously at 100 000 to 300 000 U. / Kg. / Day until fever subsides or developments dictate. It then passes procaine penicillin, intramuscularly at a dose of 50 000 to 100 000 U. / Kg. / Day in two doses until no injury radiology.

Clindamycin is presented as an alternative to the above treatment. It is the choice when you can not use penicillin, there is resistance to the same or the box is very severe, the dose is 600 mg IV every 6 to 8 hours until the fever drops, passing then to 300 mg every 6 hours until oral radiography advice. Other alternatives to penicillin, cephalosporins are the first and second generation such as cefazolin and cephalothin at a rate of 2 to 4 grams per day in two or three divided doses. The combination of penicillin and metronidazole latter at 2 gm daily in three oral doses, is another alternative to anaerobic pulmonary infection.

When the abscess is acquired in the hospital should be chosen as first-line drugs one antipseudomonal penicillin combined with an aminoglycoside, or the latter associated with a third generation cephalosporin. Clindamycin association with Aztreonam is a third alternative for these cases.

* Antibiotics should be considered if the abscess is acquired in the community or in the hospital and the incidence of anaerobic bacteria as the causative agent. Although it has been shown more than a germ responsible for the abscess (polymicrobial) in two thirds of cases are anaerobic bacteria.

* Physical therapy with postural drainage to promote drainage of secretions is a useful measure. The bronchial drainage can also be done through bronchoscopy.

Surgical Treatment

If despite treatment process no regression in a period not exceeding two months, will proceed to surgical treatment in order to prevent fibrosis pericavitaria prevents definitive healing of the abscess.

Having decided on the surgery it will be at least mutilating possible.

FORECAST

AP The forecast has improved with the use of antibiotics. Mortality of 35% has fallen to 5-10%. The prognosis depends on the type of germ, age and general condition of the patient, with factors of poor prognosis advanced age, malnutrition, associated diseases, bedridden, delays or deficiencies in treatment, the presence or absence of bronchial stenosis The extension of the process, etc..

REFERENCES

* Bendstrup KE, Jensen JL: Lung abscess with squamous epithelial lining. Respir.Med. 1998 May, 92 (5) :790-1

* Cecil. Treaty of Internal Medicine. 20th Edition, EDMED, Vol 1, 1996.

* The Internist. Internal Medicine for Internists. Internal Medicine Association of Mexico. First Edition in Spanish. McGraw-Hill. Mexico 1997.

* Escamilla J, J. Guerra Lung Abscess in Children. Rev. Colomb. Neumol. 8 (4) :177-82. November 1996

* Working SEPAR. Guidelines for the diagnosis and treatment of pneumonia. Barcelona. Doyma 1992.

* Harrison: Principles of Internal Medicine. 14th Edition McGraw-Hill. Madrid 1998.

* Mac Farlane JT. Community acquired pneumonia. In Mitchell DM, and recent advances in respiratory medicine no 5. London: Churchill Livingstone, 1991.

* Michael S. Niederman, MD. Respiratory Infections in the Eldenly Raven Press. New York. 1992

* Sancho L.M. Surgical treatment of lung abscesses. Rev. Hosp. Clin. Sao Paulo Med Fac Univ, 52 (5) 254-7. Sep 1997.