6.lung abscess

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THE KURSK STATE MEDICAL UNIVERSITY
DEPARTMENT OF SURGICAL DISEASES № 1
LUNG ABSCESS
Information for self-training of English-speaking students
The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov)
BY ASS. PROFESSOR I.S. IVANOV
KURSK-2010
Anatomy
The respiratory system consists of the nose, nasal passages, nasopharynx, larynx,
trachea, bronchi, and lungs. The respiratory tree functions proximate to the thorax
and its bony and muscular components as well as to the pleura, pleural cavity, and
mediastinum. The influence of pathologic changes in associated structures on the
function of the respiratory system is important, and one should be familiar with
these anatomic relationships and the "topographic anatomy" of the thorax.
Chest wall and pleura
Beneath the skin and subcutaneous tissue, the chest wall is covered by the
pectoralis muscles anteriorly, and posterolaterally the latissimus dorsi and serratus
anterior muscles are encountered. In an anterior thoracotomy, the fibers of the
pectoralis major may be split, exposing the intercostal muscles. However, in the
standard posterolateral thoracotomy, the latissimus dorsi is divided, and then the
serratus anterior is divided or split.
Trachea
The entrance to the trachea is guarded by the larynx. It functions to prevent
aspiration and as the organ of phonation and has an important role in production of
the cough. The mucous membrane lining of the larynx is covered by ciliated
epithelial cells and a few goblet cells. The epithelial surfaces in contact with food
are covered by stratified squamous epithelium. Except for the cricothyroid muscle,
which is innervated by the external laryngeal branch of the superior laryngeal
nerve, the larynx receives both motor and sensory innervation by way of the vagal
accessory complex of nerve fibers. The intrinsic muscles of the larynx receive their
motor innervation by way of the inferior laryngeal branch of the recurrent vagus
nerve.
The trachea is a fibromuscular tube 10 to 12 cm. in length and varying from
13 to 22 mm. in width, supported laterally and ventrally by approximately 20 Ushaped hyaline cartilages. The trachea originates at the level of the cricoid cartilage
and descends through the superior aperture of the thorax and the superior
mediastinum to its bifurcation at the level of the stemal angle (lower border of the
fourth thoracic vertebra).
Bronchi
At its termination, the trachea divides into the right and left principal bronchi. The
right bronchus is 12 to 16 mm. in diameter; the left, 10 to 14 mm. The combined
cross-sectional area exceeds that of the trachea. The right main bronchus deviates
less from the axis of the trachea than does the left; this explains why foreign
objects entering the trachea more often lodge in the right bronchus or one of its
branches.
Within a primary lobe, the secondary bronchus soon divides into ternary branches,
which are remarkably constant in number and distribution.
Lung abscess
Lung abscess: A localized cavity with pus, resulting from necrosis of lung tissue,
with surrounding pneumonitis.
A lung abscess may be putrid (due to anaerobic bacteria) or nonputrid (due to
anaerobes or aerobes). "Gangrene of the lung" denotes a similar though more
diffuse and extensive process in which necrosis predominates.
Classifications
Etiology:
 Aerobic
 Anaerobic
 Mixed
2. Not bacterial
 The elementary organisms
 Funguses
Pathogenesis
1. Bronchogenic
 With aspiration
 With obtiration
 Metapneumonic
2. Hematogenous (embolic).
3 Traumatic
4. Lymphogenous.
5. Contact.
Localization:
1 Central
2 Peripheric
 cortical
 subpleural
Spreading:
Singular.
Multiple
 Unilateral
 Bilaterial
Character of the clinical features
Acute
Chronic:
 In phase of the remission
 In phase of the exacerbation
Connection with the bronchus:
1. It is not drained.
2. It is drained:
 There is enough
 There is not enough
Complications:
 Empyema of the pleura
 Bleeding.
 Defeat of another lung
 Phlegmon of the thoracal wall.
 Bacterial shock
 Sepsis
Etiology and Pathology
Lung abscesses are usually due to infected material from the upper airway
aspirated when a patient is unconscious or obtunded from alcohol, other drugs,
CNS disease, general anesthesia, coma, or excessive sedation. The causative
organisms are usually anaerobes. Lung abscesses are often associated with
periodontal disease, in which anaerobes are prevalent. Bacteria cultured from lung
abscesses include common and nasopharyngeal flora, particularly anaerobes, and
less often, aerobic bacteria or fungi. Bronchogenic carcinoma is an occasional
underlying cause in older smokers. Cavitary TB is not considered a lung abscess
but must be remembered in the differential diagnosis.
Pneumonia due to Klebsiella pneumoniae (Friedländer's bacillus), Staphylococcus
aureus, Actinomyces israelii, -hemolytic streptococcus, Streptococcus milleri (and
other aerobic or microaerophilic streptococci), Legionella sp, or Haemophilus
influenzae is sometimes complicated by abscess formation. Lung abscess in the
compromised host is usually due to Nocardia sp, Cryptococcus sp, Aspergillus sp,
Phycomycetes sp, atypical mycobacteria (primarily Mycobacterium aviumintracellulare or M. kansasii), or gram-negative bacilli. Blastomycosis,
histoplasmosis, and coccidioidomycosis may also cause acute or chronic lung
abscesses and should be suspected in a person who has nonputrid abscesses and
who lives in an endemic area. Less common causes of lung abscess include septic
pulmonary emboli, secondary infection of pulmonary infarcts, and direct extension
of amebic or bacterial abscesses from the liver through the diaphragm into the
lower lobe of the lung.
Single lung abscesses are most common. Multiple abscesses usually are unilateral;
they may develop simultaneously or spread from a single focus. In abscesses due
to aspiration, the superior segment of a lower lobe and the posterior segment of an
upper lobe are affected most often. A solitary abscess secondary to bronchial
obstruction or to an infected embolus starts as necrosis of a major portion of the
affected bronchopulmonary segment. The base of the segment is usually next to the
chest wall, and the pleural space in the area is often obliterated by inflammatory
adhesions. Embolic spread of infection, most often due to S. aureus with tricuspid
endocarditis in IV drug abusers, has become more common and is usually
characterized by multiple lung lesions in noncontiguous sites. Suppurative venous
thrombophlebitis due to aerobic or anaerobic bacteria may also cause embolic lung
abscesses.
An abscess usually ruptures into a bronchus, and its contents are expectorated,
leaving a cavity filled with fluid and air. Occasionally, an abscess ruptures into the
pleural cavity, resulting in an empyema, sometimes with bronchopleural fistula.
Similarly, the rupture of a large abscess into a bronchus or vigorous attempts at
drainage may cause widespread bronchial dissemination of pus with diffuse
pneumonia and a condition resembling adult respiratory distress syndrome.
Symptoms and Signs
There are two periods of development this disease.
The first period - before break of pus in the bronchi.
Signs:
Body temperature about 40 C
Stethalgias on the side of defeat
Backlog of the struck side in the act of respiration
Morbidity at the palpation of the struck side
The second period
The second period begins after break of an abscess in bronchus (draining
bronchus).
Main signs
Fast downstroke of temperature (37,5-38 C)
A plenty of the sputum. The sputum is parted on three layers
1. Bottom Layer - pus
2. Average Layer - serous liquid
3. Top Layer - foam.
Sometimes there is the impurity of blood.
Onset may be acute or insidious. Early symptoms are often those of pneumonia, ie,
malaise, anorexia, sputum-producing cough, sweats, and fever. Severe prostration
and a temperature of 39.4° C (103° F) or higher may be present. Fever, anorexia,
weakness, and debility are sometimes minimal if the infection is limited or
indolent. Unless the abscess is completely walled off, the sputum is purulent and
may be blood-streaked. An abscess may not be suspected until it perforates a
bronchus, when a large amount of purulent sputum, putrid or not, may be
expectorated over a few hours or several days. The sputum may contain
gangrenous lung tissue. A putrid (penetrating and foul) odor is diagnostic of
anaerobic bacterial causation. Putrid sputum occurs in 30 to 50% of all patients
with lung abscess, but about 40% of patients with abscesses due to anaerobes do
not have a putrid sputum, so its absence does not exclude this diagnosis. Chest
pain, if present, usually indicates pleural involvement.
Physical signs include a small area of dullness, indicating localized pneumonic
consolidation, and usually suppressed (rather than bronchial) breath sounds. Fine
or medium moist crackles may be present. If the cavity is large (unusual with
current therapy), there may be tympany and amphoric breath sounds.
Signs of pulmonary suppuration generally disappear with appropriate antibiotic
therapy, but this disappearance does not necessarily denote cure. If the abscess
becomes
chronic,
weight
loss,
anemia,
and
hypertrophic
pulmonary
osteoarthropathy may occur. Physical examination of the chest may be negative in
the chronic phase, but rales and rhonchi are usually present.
Diagnosis
Methods of Diagnostics
Chest Imaging

conventional chest x-rays

CT with or without contrast or high-resolution techniques

angiography of the pulmonary or bronchial circulation using contrast
materials or digital subtraction

ultrasonography

radionuclide scanning

MRI.
Diagnostic thoracentesis
Thoracoscopy
Bronchoscopy
Ancillary procedures:
 Bronchoalveolar lavage
 Transbronchial lung biopsy
 Submucosal and transbronchial needle aspiration
Percutaneous Transthoracic Needle Aspiration
Thoracotomy
Tracheal Aspiration
Lung abscess is suggested by the symptoms and signs described above. Chest xrays early in the course may show a segmental or lobar consolidation, which
sometimes becomes globular as pus distends it.
After an abscess ruptures into a bronchus, a cavity with a fluid level appears on xray. If chest x-rays suggest an underlying tumor or foreign body or if the
presentation is atypical, CT scanning may provide better anatomic definition.
Sputum should be examined by smear and culture for bacteria, fungi, and
mycobacteria. Expectorated sputum is not appropriate because the mouth normally
contains anaerobic organisms that contaminate the specimen during passage
through the upper airways. The attribution of disease to anaerobes usually requires
a specimen obtained by transtracheal aspiration, transthoracic aspiration, or
fiberoptic bronchoscopy with a protected brush and quantitative cultures, but these
procedures are not performed often. Such invasive procedures should be reserved
for cases that have an atypical presentation or that are unresponsive to antibiotics;
however, once antibiotics are initiated, there is no reliable method for obtaining
specimens useful for bacterial culture. Bronchoscopy is unnecessary if response to
antibiotics is adequate and if a foreign body or tumor is not suspected.
Lesions that simulate bacterial lung abscess include cavitating bronchogenic
carcinoma, bronchiectasis, empyema secondary to a bronchopleural fistula, TB,
coccidioidomycosis and other mycotic lung infections, infected pulmonary bulla or
air cyst, pulmonary sequestration, silicotic nodule with central necrosis, subphrenic
or hepatic (amebic or hydatid) abscess with perforation into a bronchus, and
Wegener's granulomatosis. Repeated clinical evaluation and the procedures
described above can usually differentiate these disorders from simple lung abscess.
Prognosis and Treatment
Prompt, complete healing of a lung abscess depends on adequate antibiotic
treatment. Most patients recover without surgery.
Antibiotics should be started as soon as sputum and blood have been collected for
culture and sensitivity. The preferred drug is clindamycin, initially 600 mg IV tid,
then 300 mg po qid. An alternative regimen is IV penicillin G 2 to 10 million
U/day, followed by oral penicillin V 500 to 750 mg qid. Antibiotics are changed to
oral when the patient is afebrile and subjectively improved. Some authorities prefer
to combine penicillin with oral metronidazole 500 mg qid. If a gram-negative
organism, S. aureus, or other aerobic pathogen is implicated, the antibiotic chosen
depends on the results of sensitivity tests. Treatment should be continued until the
pneumonitis has resolved and the cavity has disappeared, leaving only a small
stable residual lesion, a thin-walled cyst, or clear lung fields. Resolution usually
requires several weeks or months of treatment, much of which is given as oral
antibiotics on an outpatient basis.
Postural drainage may be a helpful adjunct, but it may also cause spillage of
infection into other bronchi with extension of the infection or acute obstruction. If
the patient is weak or paralyzed, tracheostomy and suctioning may be necessary.
Rarely, bronchoscopic aspiration may help facilitate drainage. Surgical drainage is
rarely necessary because lesions usually respond to antibiotics. Patients with large
cavities who do not respond to drugs may be candidates for percutaneous drainage;
patients with empyema require it.
Pulmonary resection is the procedure of choice for an abscess resistant to drugs,
particularly if bronchogenic carcinoma is suspected. Lobectomy is the most
common procedure; segmental resection usually suffices for small lesions.
Pneumonectomy may be necessary for multiple abscesses or pulmonary gangrene
refractory to medical management. The mortality rate after pneumonectomy is 5 to
10%; after lesser resections, it is much lower.
CHRONIC PULMONARY ABSCESS
Pulmonary abscess which is not completed in two months (light weeks) is named
chronical. If during acute pulmonary abscess the main morphologic sign is
cavity with pus, walls of which consist from pulmonary tissue, during
chronical
abscess they are formed with connective tissue.
Forming of connective capsula may be noted to the end of sixth-eighth
week
from the beginning of the disease. Pulmonary tissue around destruction cavity also
concentrates. Pyogenic processin abscess cavity and complined inflammatory
process in surrounding parenchyma mutually support
each
other.
Gradually
purrulent infiltration of surrounding pulmonary tissue is taring place.
Opening into bronchial tree, singular a bscess promote generalization of
process to brochi. Disturbans of bronchial peristalsis, obstruction of their lumen
with pus lead to forming of focal atelectasis and secondary bronchiectasis.
There are some important components of chronic pyogenic process in the
lungs:
1) noneffective drainage
2) perypherical secondary bronchiectasis
3)changings in pulmonary tissue like sclerosis, deformation of bronchi
This
are the causes, promoting
transformation of acute abcsesse into
chronical:
1)unsatisfactory out flow of pus from cavity;
2)sequesters in abscess cavity;
3)hight pressure in the cavity;
4)forming of pleural commisures in defeated segments zone in lungs, which
prevent early lung collapse and obliteration of cavity;
5)epithelization of cavity
Treatment of acute abscess has been finishes with clinical convalescence.
Patient is discharged from hospital with residual cavity. It leads to chronical
purulent intoxication and othes complications.
CLINICAL PICTURE
The disease usually flows with aftern ation of aggravation and remission. The
most constant symptom is tussis with purulent sputum. Quontity of sputum grows
in aggravation period. During abundant expectoration the organism lose
much
protein, and it leads to inanition
The maun complaun of patients with cronic abscess
- asthenia (weakness);
- bad appetite;
- sleeplessness;
- pain in thorax.
- umpleasent smell from the mouth;
- edematous face;
- chement of ribs;
- falling behing of the "sick" half of thorax during breathing;
- fingers looking like "drum sticks" (may be seen in eighty five-ninty five per
cent of cases)
- deformation of nail plates like "watch glass".
Symptomatology, found during physical examination of thorax is variable, it
depends upon localisation of defeated zone, phaze of desease flow, availiability of
changes in pleural cavity.
In
blood count - leucocytosis, deviation
tothe left, anemia,
hypoproteinemia. Spirography - lowering of vital capacity. There are some
dystrophical changes in liver, heart.
Differential diagnosis:
1)pulmonary tuberculosis: availiadility of tuberculosis foci of various remoteness
in roentgenogram, sputum without any smell, but with typical bacteria.
2)Actinomycosis of lung - in sputum there are mycelium and drooze of radiant
fungus.
3)Cancer of lung (cavital form): is characterized with beginning without high
temperature, sputum without any smell with flood admixture, it includes "cancer"
cells.
Complications of
1) pulmonary hemorrhage
2) transformation into cancer
3) visceral amyloidosis
TREATMENT
Absolute depositions to operation are repeated pulmonary hemorrhage, quiqly
growing intoxication. Only radical operation is effective (resection of lobe of the
lung or pulmonectomy). Majority of patiens, who had lobecthomy, recover their
capacity for work in three – four months after operation. After pulmonectomy in
first six month patiens are transferred to invalidism.
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