Pathology Scribes: Trey, Michael, Robert
Tuesday, 011601 Lecturer: Dr. Graham
9:00am
Announcement from Dr. Graham: if you missed small groups this morning, Wednesday (01/17/01) you really, really blew it. Be on time. On Thursday we will go over cases again. Included in our packet are diagrams of lung patterns, which we should be able to associate with particular diseases.
Beginning with review of complications of lung infection
I. Bronchopneumonia
-Classically occurs in a compromised host with a low-grade organism.
-Begins in the bronchi and can spread throughout the lobe and/or to other lobes of the lung
II. Lobar pneumonia
-Entire lobe is involved, “wall to wall” in a lobe
-Known as walking bacterial pneumonia
III. Lung abscess
Slide: AP view of cloudy abscess in lower lobe of right lung-“all whited out”
-Presents with fever, chills, elevated white count, shift to the left (immature white blood cells, -bands and immature granulocytes in the peripheral smear)
Indicative of a bacterial pneumonia
Slide: Later CXR of same patient
“Patient coughed up something,” leaving a clear space in the lung
Due to infectious process, patient has had necrosis in part of their lung
Ideally would see air-fluid level in CXR
Slide: Lateral view of same patient
Air-fluid level can now be seen in CXR: air is black, and pus is floating in water
Classic abscess with air fluid level in lobar pneumonia
Slide: Barium was place down into the lung of this individual
One could end up with a sequence of necrosis with an abscess cavity that can extend into the bronchioles and/or can communicate via a fistula into the pleural cavity. Giving the patient a bronchiolpleural fistula
Can also lead to air into the pleural cavity
Can get an abscess and the pleural cavity that will have to be drained due to poor blood flow
However, early antibiotic intervention can sometimes prevent this area from becoming septic and allowing the abscess to contain a sterile scar
Lung abscess can be focal or solitary which differ very little from a localized necrotizing pneumonia. Just the area of involvement is different
How does this usually occur? You inhale infectious material, other sites in the lung, from an infection elsewhere, or aspirate stomach material which are infective when they enter through the upper airway
Often this process complicates other types of necrotizing pneumonias (like in necrotizing bacterial pneumonia, bronchiectasis)
This same process of injury can give you necrotizing pneumonia, bronchiectasis, and/or abscess depending on the clinical situation. This makes it very difficult to tell sometimes between these. Presentation will show extreme crossover between clinical symptoms, bugs, and signs.
Septic embolization is a common side effect of abscess formation
Classic place of emboli form lung is brain which leads to a brain abscess which can be lethal Organisms are typically mixture of aerobes and anaerobes
Abscesses can be singular or multiple
Bronchiectasis is a common result of lung abscesses
On CXR may look like solid tumor or open space with air-fluid level
Slide: Lung with “hole” in it. Unable to determine what was in the hole during infection.
If during infection with anaerobic bacteria, sputum would be brown and foul smelling. Pus and brown smelly material. “I mean grody.”
Cavity that remains is then open to external influences, so fungi like aspergilus can grow there and form a fungus ball.
Slide: Lung of patient that had bronchopneumonia that spread to infect most of lung. Contains huge abscess cavity that has collapsed. White pus can be seen. Bronchiectasis and atelectasis can be seen as well.
Slide: AP CXR of overinflated lung (from emphysema patient) in which can be seen a gray area with an air cavity around it which is the fungus ball
Slide: Fungus ball that has been surgically removed
Complications of abscess infection include empyema, and fungus balls
If infection is chronic, secondary amyloidosis can result
Abscesses also contribute to early clubbing (changes of pulmonary osteoarthropathy)
Clubbing can been seen in some people idiopathically, but is also associated with intrathoracic disease like lung cancer, TB, and lung abscess
IV. Interstitial pneumonia a.k.a pneumonitis
Inflammation of the interstitium but not into the interalveolar fluid or exudate
In normal people most common cause is mycoplasma
viruses are also a cause
In compromised hosts, CMV, Herpes virus, p. carinii are causes
Slide: microscopic view of alveoli with inflammation in the interstitial wall
P. carinii is a little different because it “likes to live in the intraalveolar space” so one ends up with a foamy exudate in the alveolar space but the walls look “O.K.”
In our region, differential diagnosis would include a virus and histoplasmosis
Slide: CXR of interstitial pneumonia: interstitial markings in one region slightly more prominent. The presentation can be that subtle.
Slide: CXR of chronic interstitial pneumonia: increased markings
Slide: “normal lung” that’s really not. Important point is that some of the alveolar walls are expanded by infiltration by lymphocytes (remember that lymphocytes attack viruses). The air spaces are still clear. Slide of lung with thickened interstitial spaces.
V. Tuberculosis
Tuberculosis: if you don’t think about it, you won’t diagnose it because you won’t get the proper cultures. Our discussion right now will focus on classic M. tuberculosis, not some of the odd variants you might see in AIDS patients, etc.
Primary tuberculosis may be asymptomatic or mild, such that you usually don’t know when you get it. It may present like a common chest cold, leaving behind something called a Gohn’s complex.
A Gohn’s complex is the combination of calcified hilar lymph nodes along with a calcified primary site, and this may or may not be apparent on a CXR
The mediastinal lymph nodes will drain and enlarge with other bacterial infections of the lungs, but they don’t calcify because you don’t have the granulomatous reaction that you see with tuberculosis. It is this reaction that then calcifies and becomes visible on an x-ray
Another infectious disease that will give you an appearance similar to a Gohn’s complex is histoplasmosis. In Lubbock, we’ve seen more interstitial pneumonia from Histoplasma than from P. carinii at the autopsy table.
At some point later in life (usually age, although another disease may do it as well), the host becomes compromised and you will have reactivation of the primary tuberculosis
Reactivation tuberculosis can be in the lung and elsewhere, or it may just present in extrapulmonary sites such as the kidneys or bones
Classically, reactivation TB is a bilateral upper lobe lung disease, which is useful in its diagnosis. You will see a caseous center inside multiple, confluent granulomata. Sometimes these caseating granulomata will rupture into a bronchus and you will cough up the contents, resulting in a cavitary lesion that will scar down and may produce minor disease. Later in life, people will present with bilateral apical scarring without any recollection of a history of TB because it never came to clinical attention
Reactivation TB can spread throughout the lung and result in a pattern similar to bronchopneumonia, or may spread through the body by rupture into a vessel. The last pattern is called miliary TB, and results in numerous very small foci affecting multiple organs.
In TB, the pattern of inflammation is granulomatous. This usually happens when a strong host encounters a fairly weak organism that for some reason it can’t kill. So, the body will wall off the organism and keep it trapped for years, until something causes the host to become weak. When that happens you get bronchopulmonary and military TB, both a result of reactivation as the organism overwhelms the now weakened host.
Tuberculosis is an acid-fast bacillus, but culturing is still used for identification because there are other acid-fast bacilli it can be confused with.
Slide: lung with numerous acid-fast bacilli, but instead of macrophages and giant cells you see neutrophils. In this case, the body has been overwhelmed and is no longer even attempting to wall off the organisms. This was probably the result of AIDS or some other immunocompromising disease.