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Lung Abscess (Des Jardins) Cheat Sheet by

Lung Abscess (Des Jardins)

Anatomic Altera­tions of the Lungs

Lung abscess
necrosis of lung tissue that in severe cases leads to a localized air- and fluid-­filled cavity
 
also known as “necrot­izing pneumonia” or “lung gangrene”
 
The fluid in the cavity is a collection of purulent exudate that is composed of liquefied white blood cell remains, proteins, and tissue debris.
Pyogenic membrane
encaps­ulates the air- and fluid-­filled cavity
 
consists of a layer of fibrin, inflam­matory cells, and granul­ation tissue
Early stages
pathology is indist­ing­uis­hable from that of any acute pneumonia
 
Polymo­rph­onu­clear leukocytes and macrop­hages move into the infected area to engulf any invading organisms. This action causes the pulmonary capill­aries to dilate, the inters­titium to fill with fluid, and the alveolar epithelium to swell from the edema fluid. In response to this inflam­matory reaction, the alveoli in the infected area become consol­idated
 
As the inflam­matory process progre­sses, tissue necrosis involving all the lung structures occurs.
 
In severe cases, tissue necrosis ruptures into a bronchus and allows a partial or total drainage of the liquefied contents from the cavity
 
An air- and fluid-­filled cavity also may rupture into the intrap­leural space via a bronch­opl­eural fistula and cause pleural effusion and empyema
After a period of time
fibrosis and calcif­ication of the tissues around the cavity encaps­ulate the abscess
Major pathologic or structural changes
• Alveolar consol­idation
• Alveol­ar-­cap­illary and bronchial wall destru­ction
• Tissue necrosis
• Cavity formation
• Fibrosis and calcif­ication of the lung parenchyma
• Bronch­opl­eural fistulas and empyema
• Atelec­tasis
• Excessive airway secretions

Etiology and Epidem­iology

Lung abscesses
most commonly occur as a compli­cation of aspiration pneumonia
 
—i.e., the pathologic events that follow shortly after aspirating either acidic gastric fluids or a variety of anaerobic organisms that are normally found in oropha­ryngeal secretions
 
Anaerobic organisms often colonize in the small grooves and spaces between the teeth and gums in patients with poor oral hygiene; they are frequently associated with gingivitis and dead or abscessed teeth.
Aspiration often occurs in the patient with a decreased level of consci­ous­ness.
Predis­posing factors
(1) alcohol abuse,
 
(2) seizure disorders,
 
(3) general anesth­esia,
 
(4) head trauma,
 
(5) cerebr­ova­scular accidents, and
 
(6) swallowing disorders.
Anatom­ically, lung abscesses most commonly develop in lung regions that are dependent in the recumbent position
e.g.
posterior segments of the upper lobes
 
superior segments of the lower lobes
The right lung is more commonly involved than the left.
Flash burn
aspiration of acidic gastric fluids is associated with immediate injury to the trache­obr­onchial tree and lung parenchyma
A lung abscess may also develop as a result of:
 
(1) bronchial obstru­ction with secondary cavitating infection (e.g., distal to bronch­ogenic carcinoma or an aspirated foreign body)
 
(2) vascular obstru­ction with tissue infarction (e.g., septic embolism, vascul­itis)
 
(3) inters­titial lung disease with cavity formation (e.g., pneumo­con­iosis [silic­osis], Wegener’s granul­oma­tosis, and rheumatoid nodules)
 
(4) bullae or cysts that become infected (e.g., congenital or bronch­ogenic cysts)
 
(5) penetr­ating chest wounds that lead to an infection (e.g., bullet wound)

Organisms Known to Cause Lung Abscess

Common Organisms Associated with Aspiration
Anaerobic gram-p­ositive cocci
Peptos­tre­pto­cocci
 
Peptococci
Anaerobic gram-n­egative bacilli
Bacter­oides fragilis
 
Prevotella melani­nog­enica
 
Fusoba­cterium species
Less Common Organisms
Klebsiella
Staphy­lococci
Mycoba­cterium tuberc­ulosis (plus atypical organisms Mycoba­cterium kansasii and Mycoba­cterium avium)
Histop­lasma capsulatum
Coccid­ioides immitis
Blasto­myces
Asperg­illus fumigatus
Parasites
Parago­nimus westermani
Echino­coccus
Entamoeba histol­ytica
Rare Causes
Strept­ococcus pneumoniae
Pseudo­monas aeruginosa
Legionella pneumo­phila
 

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examin­ation
Vital Signs
Increased Respir­atory Rate (Tachy­pnea)
 
• Stimul­ation of peripheral chemor­ece­ptors (hypox­emia)
 
• Decreased lung compli­anc­e–i­ncr­eased ventil­atory rate relati­onship
 
• Stimul­ation of J receptors
 
• Pain, anxiety, fever
 
Increased Heart Rate (Pulse) and Blood Pressure
Pleuritic Chest Pain, Decreased Chest Expansion
Cyanosis
Cough, Sputum Produc­tion, and Hemoptysis
 
Early Stages: inflam­matory pneumo­nia­-like phase; nonpro­ductive barking or hacking cough
 
If the abscess progresses into an air- and fluid-­filled cavity and ruptures through a bronchus, the patient may suddenly cough up large amounts of sputum.
 
Foul-s­melling brown or gray sputum indicates a putrid infection that is caused by numerous organisms, including anaerobes.
 
An odorless green or yellow sputum indicates a nonputrid infection caused by a single aerobic organism.
 
Blood-­str­eaked sputum is common in patients with a lung abscess.
 
Occasi­onally, frank hemoptysis is seen
Chest Assessment Findings
 
Increased tactile and vocal fremitus
 
Crackles
The following may be heard directly over the abscess:
 
Dull percussion note
 
Bronchial breath sounds
 
Diminished breath sounds
 
Whispered pector­iloquy
 
Pleural friction rub (if abscess is near pleural surface)

Clinical Data from Lab Tests

ABNORMAL LAB TEST AND PROCEDURE RESULTS

Sputum Examin­ation
Many of these organisms are “slow growers” and may take some time to be identified completely on culture media.
Anaerobic Organisms
Anaerobic Gram-P­ositive Cocci
 
Peptos­tre­pto­cocci
 
Peptococci
Anaerobic Gram-N­egative Bacilli
 
Bacter­oides fragilis
 
Prevotella melani­nog­enica
 
Fusoba­cterium species

RADIOLOGIC FINDINGS

Chest Radiograph
 
Increased opacity
 
Cavity formation
 
Cavities with air-fluid levels
 
Fibrosis and calcif­ication
 
Pleural effusion
Early Stages
reveals localized consol­idation
Later, charac­ter­istic radiog­raphic appearance of a lung abscess appears after:
 
(1) the infection ruptures into a bronchus, and/or
 
(2) tissue destru­ction and necrosis have occurred, and/or
 
(3) partial evacuation of the purulent contents has occurred
The abscess usually appears on the radiograph as a circular radiol­ucency that contains an air-fluid level, surrounded by a dense wall of lung parenc­hyma.

General Management of Lung Abscess

Medica­tions and Procedures Commonly Prescribed by the Physician
Treatment varies based on the severity of the pneumonia and the lung abscess.
Treatment includes approp­riate (usually intrav­enous) antimi­crobial therapy coupled with prompt drainage and surgical debrid­ement.
Clinda­mycin
standard treatment for a lung abscess caused by an anaerobic pathogen
Other drugs that may be used are any combin­ation of:
 
beta-l­act­am–­bet­a-l­act­amase inhibitors (e.g., ampici­lli­n-s­ulb­actam)
 
penicillin plus metron­idazole
 
carbapenem
Linezolid
When the lung abscess is caused by methic­ill­in-­res­istant Staphy­loc­occus aureus (MRSA)
Altern­ative to linezolid
vancomycin
 
ceftar­oline, trimet­hop­rim­-su­lfa­met­hox­azole, and telavancin.
Respir­atory Care Treatment Protocols
Oxygen Therapy Protocol
 
treat hypoxemia, decrease the work of breathing, and decrease myocardial work
 
Hypoxemia caused by capillary shunting is often refractory to oxygen therapy.
Bronch­opu­lmonary Hygiene Therapy Protocol
 
e excessive production and accumu­lation of mucus associated with a ruptured lung abscess
Lung Expansion Therapy Protocol
 
alveolar consol­idation and atelec­tasis
When treated properly, most patients with a lung abscess show improv­ement. In acute cases, the size of the abscess quickly decreases and eventually closes altoge­ther. In severe or chronic cases, the patient’s improv­ement may be slow or insign­ifi­cant, even with approp­riate therapy.
       
 

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  • Published: 8th October, 2022

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