FUNDAMENTAL PRINCIPLES OF DESCRIPTIVE
ANATOMIC PATHOLOGY
(How to Describe and Interpret What You See)
Paul C. Stromberg DVM, PhD
Diplomate, American College of Veterinary Pathologists
Professor of Veterinary Pathology
Ohio State University
[email protected]
The Rosetta Stone
Descriptive pathology is the recognition, characterization and interpretation of pathologic
lesions or abnormalities. [ The proportions of each of these components may vary according to
the purpose of the reporting format i.e. autopsy report, surgical biopsy report, certification
examination, scientific publications or reports of new diseases and technical reports]. GROSS
PATHOLOGY concentrates on the organ or whole animal. Its value exists on several levels.
One, it provides a rapid determination of potential problems which could correlate with clinical
disease and support a presumptive diagnosis. The gross lesions of some diseases are sufficiently
distinct in their pattern to be presumptively diagnostic based upon autopsy alone. For many
disorders, the gross morbid anatomy is highly suggestive of a particular disease or class of related
diseases. Often the pattern of lesions suggests a pathogenesis or mechanisms of the clinical
disease. Related disease agents or mechanisms often display similar patterns and for comparative
biomedical scientists such as veterinarians who must deal with a wide spectrum of species,
learning to interpret these patterns can be extremely useful in arriving at diagnoses in rare or
unusual species. Commonly, the autopsy lesions are not distinct or specific and require additional
diagnostic modalities to confirm or establish a diagnosis definitively. In this regard, gross
pathology is the road map for what portions of the animal should be selected for histopathology,
bacterial and fungal culture, virus isolation or toxin identification. Thirdly, it provides a
permanent, written and legal record of the medical problems of the patient.
The role of the postmortem examination
(autopsy literally means “self examination” but
the context for this Latin phrase was intended to
mean “to examine for yourself”) is to identify,
characterize and record pathologic abnormalities
at the clinical level, arrive at a presumptive
diagnosis in light of the accompanying history
and serve as a spring board for additional
investigations if needed. This tradition is handed
down to us from 2 seminal works dating from the
Renaissance when dissecting human bodies
became acceptable practice. Andreas Vesalius,
the Flemish anatomist wrote De Humani Corporis Fabrica (known as “De Fabrica”) and
Giovanni Morgagni, an Italian pathologist began associating clinical signs with pathologic
1
changes in De Sedibus et Causis Morborum ( called “De Sedibus”). Performance of the autopsy
in veterinary medicine, (frequently called necropsy which means “death examination”) is
unique in its execution when compared to human medicine. Except for clinicians practicing in
training institutions where a resident staff of pathologists performs the autopsies, most private
veterinary practitioners must do the autopsy themselves. Thus, it is important to understand the
fundamentals of the autopsy to get the most out of it. The autopsy is an ephemeral event and
when it’s over, it’s over! This makes the accurate description and interpretation of the autopsy
findings critical because that is what remains in the permanent record as the basis for later
historical, medical and legal review and interpretation. A principal limitation of retrospective
clinical studies is the lack of or a poorly conducted autopsy with inconsistent or incomplete
characterization of the lesions. Although our human counterparts occasionally have the
opportunity to exhume a body for re-examination at a later date that option is rarely open to
veterinary pathologists.
Contrary to popular belief, the definitive diagnosis of disease is NOT always made at the
microscopic level. The microscopic examination evaluates a tiny fraction of the organs and
tissues. These histopathologic findings are integrated with the results of the autopsy and
interpreted in light of the signalment, history, clinical appearance and laboratory tests to arrive at
a diagnosis. What every histopathologist wants to know above all else is “What was the
gross appearance?” This is easy when the pathologist performs both the autopsy and
histopathologic examinations. However, the culture of veterinary medicine is such that most of
the time the autopsy is performed by a clinician and the tissues are sent to a pathologist (often far
away) for histopathology. To acquire precision and efficiency in the pathologic diagnosis of
disease and maximize the results of the autopsy, the clinician must accurately observe, describe,
record, interpret and communicate the results of the autopsy to the pathologist. When this is
done properly, pathologists can maximize their contribution to the process often by providing not
just a summary of the lesions they observe (called a “morphologic diagnosis”) but making a
specific clinical disease diagnosis. All too often veterinary students do not understand this.
Although trained to perform the autopsy, clinicians do not assign sufficient importance to it or
perform it often enough to reduce it to reliable practice and get the most out of it when needed.
The things the pathologist most wants to know, indeed frequently needs to know, for
definitive interpretation, are often out of his/her control. As a result communication between
clinician and pathologist breaks down leaving all parties dissatisfied, including the pet owners
who depend upon correct diagnosis for prognosis, decision making, grief counseling, absolution
of guilt and closure. Clinicians are frustrated because they are getting only morphologic
diagnoses which they cannot relate to clinical diseases instead of definitive clinical disease
diagnoses which they understand and know how to treat or explain to their clients. Pathologists
become frustrated because they know they can provide more but lack the information essential to
make a definitive diagnosis.
A post graduate continuing education effort for clinicians to rediscover the autopsy skills learned
in professional school would help considerably in this matter. An organized, systematic
approach to observation, description and interpretation of the lesions and changes found at
autopsy would provide clinicians with the means to fill in the gaps, deliver the information
2
pathologists most want to know, improve communication with the pathologist, assist in their own
knowledge of the case, provide immediate feedback to interested animal owners and maximize
the yield from the autopsy. In addition, the rules of gross pathology are easy to learn and apply
and with minimal guidance, the practitioner can improve their interpretation skills with feedback
from the pathologist. In short, continued learning and the satisfaction of professional growth at
minimal expense could result in the increased information flow to clients and better management
of clinical disease problems.
Although this discussion focuses upon interpreting autopsy lesions, the principals are exactly
the same for surgical pathology specimens. The skills learned here should be applied to the
submission of surgical biopsies with markedly improved results in a clinical setting where the
patient is still alive and treatment or therapeutic options may be significantly impacted by poor
communication. Often the difference between my making a specific disease diagnosis and a
generic pathologic process is determined by what the gross lesion looked like, where the lesion
occurred, how the lesions were distributed, the age, breed, sex of the patient and what the
clinician’s working diagnosis was. As incredible as it may seem, I frequently get surgical
biopsies in which I am not even told the species or the location of the sample much less the other
mentioned information. Some clinicians mistakenly believe you should not “bias” pathologists
by sharing information with them. Nothing could be further from the truth. I have often said that
if the object of the autopsy/biopsy is to see if you can fool me, I will tell you right now, You can
fool me. Easily! If, on the other hand, the object is to acquire a rapid, accurate, specific
diagnosis, share what you have observed and what you think with the pathologist. Do you think
physicians withhold information from human pathologists? Imagine what the malpractice
attorneys would do with THAT bit of information if they did? The most common reason biopsies
are returned to clinicians in some human medical centers is insufficient information. With the
heightened interest in animal rights and the uncontrolled proliferation of attorneys, it’s only a
matter of time before medical liability issues with pets are going to be tested in court. Delayed
treatment or misdiagnosis due to poor communication resulting in an “untoward outcome” may
elicit legal action in the near future.
Description versus Interpretation
Gross observations are objective and should never change. Interpretations are subjective, open to
discussion and can be altered retrospectively. Interpretation is always a guess but with proper
training and experience it can be a very, very good guess. Interpretation is what pathologists get
paid to do but they should always justify their interpretation by accurate descriptions.
Description:
The lung was diffuse dark
red to plum colored,
heavy, wet and
foamy fluid freely ran
from the cut surface.
It felt firmer than
normal and not
crepitant
Interpretation:
Describe first, then
interpret
3
Diffuse pulmonary
congestion and
edema
Diffuse acute
interstitial
pneumonia
ELEMENTS OF THE GROSS DESCRIPTION
The interpretation of gross lesions begins with the observation and
characterization of the abnormal findings. To do this one must know what
attributes are important and what they mean when observed. The following is a
list of those attributes which I believe form the elements of a good gross
description of abnormalities seen at autopsy, or surgical biopsy for that matter:
1.
DISTRIBUTION – What is the spatial arrangement of lesions?
2.
DEMARCATION – How clearly set off from the adjacent normal
tissue is it?
3.
CONTOUR - Are the lesions raised, flat or depressed
4.
SHAPE – Do the lesions have a geometric shape?
5.
COLOR - “Well, what color is it”? Pick one.
6.
SIZE – absolute vs. relative; lesion, whole organ, paired organs
7.
TEXTURE - What does the cut surface look like? Amorphous or solid
8.
CONSISTENCY - How does the lesion feel? Fluid, soft, firm, hard
9.
SPECIAL FEATURES - Odor, sound
10.
EXTENT – How much of the organ or tissue is affected?
11.
CHRONICITY
A subjective assessment; usually difficult to be precise.
What is the” real time” definition of chronic?
Often the following terms are used:
Acute – a change that can be produced in seconds to hours? Days?
Subacute – what are the gross criteria?
Acute and chronic – a mixture of acute and ongoing changes
Chronic-active – same as acute and chronic
Chronic - at least days.
4
GROSS HALLMARKS OF CHRONICITY
a. Proliferation of cells takes time. Thus evidence of cellular proliferation makes it
likely the lesion is chronic
b. Deposition of stroma or extra cellular matrix – Fibrosis, hyperostosis or Periosteal
new bone (PNB)
c. Size- large changes in organs either way (increased or decreased) imply a passage of
time. Hypertrophy, atrophy.
You can see fibrovascular proliferation (granulation tissue) microscopically as early as 35 days after the damage. So if you can see it grossly, the lesion must be at least 1-2 wks
old. Is that chronic?
THE LOGIC TEST: Ask yourself the question…
“Is the lesion…seconds, minutes, hours, days, weeks, months or years old?”
Arrive at an estimated range of the logical time you think it took to make the
lesion you observed.
12.
SEVERITY
Also a subjective assessment; a sliding scale that
is often relative and variable among pathologists.
Often a 5 point scale used:
Minimal
Mild
Moderate
Marked
Severe
A.
DISTRIBUTION = the spatial arrangement of the lesions in the organ or tissue.
Lesions or abnormalities may occur with distinct
distribution patterns which when recognized are
clues to the disease process and assist in
estimating severity or significance of the observed
findings. Among the attributes of gross lesions,
distribution is one of the most important and
should be included in nearly every morphologic
diagnosis. In many dermatopathies, the lesion
distribution is the key to diagnosis. Distribution
may reflect pathogenesis.
5
1. Random - the lesion occurs without reference to architecture or relationship to
particular organ or tissue structures. The scattering of abscesses or tumors
through out a lung or liver may be random.
2.
Symmetrical - a pattern with some degree of organization is apparent in the
abnormality.
Linear pattern
Suggests some
organization
Bilateral lesions may imply a metabolic or systemic disorder affecting a certain group of
related cells present in distinctly separated areas of the organ or tissue or the same
location in paired organs. Bilateral symmetrical flank alopecia in dogs;
polioencephalomalacia in ruminant brains. A symmetrical or organized appearance
occurs when a pathologic process highlights or outlines a certain anatomic or
physiological subunit; often it outlines a vascular unit or circulatory bed; airways in
the lung, portal tracts in the liver, glomeruli or tubules in kidney.
3.
Focal - a single defined lesion on a
background which is either normal or itself
abnormal but containing or reflecting a different
process than present in the focal lesion. i.e. a
6
solitary tumor in the liver; an abscess in a congested lung. One of the easiest
distributions to see but with little discriminative power as to pathogenesis.
4.
Multifocal - more than a single discrete lesion on a background.
Highly variable; several to many lesions. This may require a further
characterization such multifocal widespread to emphasize that the
abnormality was not just 2 or 3 foci. “Multifocality often suggests an
embolic shower” Also easy to appreciate.
5.
Multifocal to Coalescing - when there are
many lesions present that may appear to be
growing together or fusing. This reflects an
active process which is expanding or not
otherwise contained or limited by the host
defense mechanisms.
6. Miliary - a special case of”multifocal” in which there are numerous tiny foci present that
are too numerous to count The miliary pattern stems from miliarius which is the
7
Pale = necrosis or
exudate
Red = blood.
Platelets, DIC
Vascular damage
Latin word for millet seed. Miliary distributions may reflect a recent embolic shower to the
organ or tissue. Because the lesions are small, the implication is that the event is recent.
7.
Segmental - a well defined portion or segment of the tissue is abnormal; sometimes
a distinct geometric shape. This distribution implies that the pathologic process is
restricted by anatomic or physiologic factors and so occupies a discrete portion.
*Segmental lesions often define a vascular bed.
Distal “segment” of the tail
8.
Diffuse - Everything in the frame of reference is abnormal or affected. This
generally implies greater severity and therefore significance than focal or multifocal
lesions. Also because it takes time for a process to affect the entire tissue, diffuse
lesions MAY (but not necessarily) be more chronic or older. **Often difficult to
appreciate because there is no contrast with normal.
8
Everything in the field of view looks pretty much the same
THE PARADOX OF DESCRIPTIVE PATHOLOGY
“The most severe lesion may be the easiest to overlook
because there is no normal for contrast”
Is this lung normal or not? You have to
remember what the normal post mortem variation
in color of the lung is to properly interpret your
observation
B.
DEMARCATION =The degree to which the lesion is set off or defined from the
adjacent tissue.
Iridium-rich
Cretaceous-Tertiary
boundary ~ extinction
of the dinosaurs
9
1. Well demarcated – The boundary between normal and abnormal is
abrupt, discrete and easily seen.
Implication = The lesion
represents a different tissue
or is well contained or
separated from the adjacent
normal tissue. Tumors,
abscesses with capsules,
pus, a rim of necrosis often
produce a well demarcated
lesion.
2. Poorly Demarcated – The
boundary between normal and
abnormal is blurred or not
easily seen.
Implication = the lesion
and adjacent tissue may be
similar; the process
gradually infiltrates into
normal or may be poorly
contained.
C.
CONTOUR = the degree to which the lesion is elevated or depressed with respect to
the adjacent tissue
10
1..
Raised - implies that “something is added” to the organ or tissue to cause
expansion.
Fluids - blood, transudates, exudates, effusions, edema, urine
Gas - emphysema
Cells - normal (= hyperplasia); abnormal (=
neoplasia) or exudates (=inflammation)
Stroma – fibrous tissue, cartilage, bone
Foreign Material – plant material, parasites
2. Depressed - implies that something is
removed or lost Most commonly this is related
to necrosis or atrophy but remember some
organs are physiologically dynamic like lung,
spleen, urinary bladder. The most common thing
taken away from the lung is air.
3.
Flat - the lesion is neither raised nor depressed with respect to the
surrounding tissues. This implies either a recent event which has not had sufficient time
to progress or a process that does not cause expansion or necrosis.
D.
SHAPE = beyond the contour, what geometric figure does the
lesion resemble.
Is the lesion circular, rectangular, triangular, spherical etc.
Because the vasculature of tissues is often laid out in geometric
patterns or distinct shapes this may reflect a pathologic process
highlighting or outlining a vascular bed. i.e. infarcts or segmental
11
lesions. Again, symmetrical shapes or patterns which appear somewhat organized
rather than random may reflect a unit of architecture such as lobes, lobules, septae,
hepatic portal tracts. Remember shape may also reflect the attribute of “segmental
distribution” and may inform us where the lesion is located.
E.
COLOR - one of the most obvious attributes of a lesion, especially when the lesion
differs from the normal color. Normal color of a tissue or organ is determined by:
1. The innate color or number of cells and stroma
in that tissue. Often this is colorless or white.
2. Special pigments or adipose tissue i.e. myelin,
myoglobin, steroids, bile
3. The amount of blood present in the vascular bed
Your eye sees the net effect of these 3 characteristics.
Dark Tissues - high pigment/tissue ratio; muscle,
spleen, liver
Light Tissues - low pigment/tissue ratio or high fat
content; lung, brain
4.
Red to Reddish Black - usually means blood or hemoglobin pigment. The
implication is congestion or hemorrhage. Differentiating between these two
requires additional attributes. Congestion tends to be a wider spread phenomenon
than hemorrhage and tends to be poorly demarcated.
5
White to Gray or Yellow - often ~ the lack of blood. Necrosis is often pale
because of the lack of blood.
Coagulation necrosis (necrosis with preservation of architecture) is an
acute event and therefore the foci are flat.
Exudates are also white to yellow and because Exudates add something,
foci of exudation are often raised.
Fibrosis is pale to white but because scar tissue fills in areas of necrosis
(something removed) and contracts as it matures, foci of fibrosis are often
depressed.
Hyperplasia often light to white or the normal tissue color; granulation
12
tissue is pink early when it has abundant capillaries; white as it matures.
Neoplasia is like hyperplasia; solid proliferating tissue but it may be a
different color or consistency
Meconium in tissue may be yellow.
Bilirubin stained tissues (icterus) may be yellow or even green
*Yellow discoloration in the CNS may indicate malacia
6.
Green – Often bile or bile pigments. Post mortem bile staining of tissue
is called Pseudomelanosis.
Coagulation necrosis may be various shades of green
Eosinophilic inflammation may impart a greenish discoloration to tissues
Aspiration pneumonia with plant material
Pigmented fungi can give a green color
7.
Green – Black
Pseudomelanosis = Artificial staining of tissues post mortem by bile from
the gall bladder and H2S pigments from the GI.
**usually limited penetration into organ adjacent to liver or bowel.
Aspiration pneumonia = saprophytic bacteria cause green black
discoloration.
8.
Black –Brown
Black usually means melanin
Melanosis = flat. Not enough to create contour
Melanoma = raised. Proliferating cells create contour
Pigmented fungi - Cladosporium, Curvularia
Brown = hemosiderin, pigmented fungi - Drechslera
13
“The Fine Arts 101 Rule of Colors”
“Processes producing a dark color (congestion, hemorrhage) can mask processes
producing a light color (necrosis, inflammation)”
F.
SIZE {LESIONS} - “Size Matters!” How big is the lesion or abnormal area?
Always measure or otherwise estimate the size of lesions as this directly impacts the
significance. What are the dimensions of masses, nodules, flat foci, depressions
etc?
Implication = small lesions are more recent events then large ones and may be
less important (but not always).
When there are multiple lesions, how does their size
vary?
Uniform Size - The lesions are all about the
same size. May mean the pathologic events
have occurred over a short period or at the
same time and are progressing at the same rate.
Non-uniform Size - The lesions are of
differing size. May mean the pathologic events
are separated in time or have different rates of
progression i.e. the small
lesions are more
recent, the larger lesions are older; recurring
pathologic process such as multiple
waves of metastasis.
G.
SIZE {WHOLE ORGANS} – “Size still matters!”
Unlike discrete lesions, organ size is often relative
and difficult to “see” because of the lack of contrast;
often a subjective opinion. Easiest to appreciate with
paired organs but small differences in organ size may
not be perceptible. i.e. hearts, livers, adrenal glands.
“The Organ Size Rule”
“Always give more weight to objective evaluations
than to subjective evaluation”
14
Rib impressions in lungs suggest the
lung was enlarged and pushed against
the ribs which left a series of
symmetrical linear depressions
Larger than normal = “something added”. Think hyperplasia, edema,
neoplasia, congestion, inflammation. Organs with capsules often bulge on cut
surface because the Asomething added@ increases pressure within capsule.
Smaller than normal = “something removed/lost”. Think hypoplasia, atrophy,
and necrosis. Organ may have a collapsed appearance. The organ may be
completely absent.
H.
SIZE {PAIRED ORGANS} – “Sorry Guys, but size
STILL matters!”
When paired organs or tissues are of different
sizes, which one is abnormal?
The large one or the small one? Fundamentally
different processes (addition/loss of something).
Must use additional attributes to properly interpret
such as shape, color, symmetry and contour.
?
?
Which kidney is the abnormal one?
SOMEBODY’s not normal. You
have to use other lesion attributes as
“corroborative testimony” to
support your conclusion
I.
J.
SIZE {DYNAMIC ORGANS} – “OK, so sometimes size DOESN’T matter”
Some organs and tissues are physiologically dynamic i.e. they change size and shape for
functional reasons or in response to physiologic demands.
1.
Rapidly dynamic (sec to min) - lungs, urinary bladder
Air and urine within the organs
2.
Moderately dynamic (min to hrs) - spleen, GI, brain
3.
Slowly dynamic (days to months) - heart, liver, LN=s, endocrine glands
Increased physiologic demands resulting in hyperplasia, hypertrophy
TEXTURE – “What does the cut surface look like?
1. Amorphous - semisolid, unorganized; no architecture;
can=t hold shape; not cohesive.
“You can spread it with a butter knife”= pus, exudates,
necrosis
15
2. Solid tissue - has apparent structure or architecture; holds together or maintains
shape; “Not spreadable with a butter knife”= usually means viable, living cells and
tissue or stroma. Hyperplasia, neoplasia, stromal deposition.
“The Texture Caveat”
“Sometimes granulomatous inflammation looks like neoplasia”
(Non-caseating granulomatous inflammation may be “cohesive”)
K.
1.
CONSISTENCY – “How does it feel?”
GAS - air trapped in tissue = emphysema
Bubbles in fluid
2. FLUID - the tissue looks or feels wet or Asquishy@,
like a water balloon. Usually means edema, blood, transudates, fluid rich exudates,
effusions, urine
16
3.
SOFT - the tissue is fluid rich/cell or stroma poor.
Exudates.
\
4. FIRM - the tissue is fluid poor/cell or stroma rich.
Exudates, hyperplasia, neoplasia, scar tissue or fibrosis.
5
HARD or GRITTY - usually means mineralized stroma or
matrix; cartilage,
bone, calcified tissues.
6. FLUID - “Takes the shape of its container and you can
pour it”
a. Serous – Clear. Extracellular fluid, water, urine,
transudates/. Edema
17
b. Serosanguinous – clear but blood tinged; common postmortem finding in body
cavities
c. Serofibrinous to fibrinous – Cloudy with strands of opaque white to yellow
d. Chylous - “milky white”. = lymph.
e. Purulent to seropurulent – Opaque, thin to thick. Contains degenerate
neutrophils (= “pus )
L.
SPECIAL FEATURES {WEIGHT} “Is the organ heavier or lighter than normal?”
Relative and subjective; often subtle and difficult to objectively determine.
Objective determination = weighing on scale. Common in rodents because we have well
established normographs; difficult for most domestic animals because of variable
organ/body weight ratio. But we should weigh some organs at autopsy such as hearts,
endocrine glands, livers, kidneys.
Heavy implies ‘something added’; use other attributes to fully interpret.
Light implies Asomething removed/taken away@
Feline Cardiomyopathy Hw/BW ratio > 6.4gm/Kg or >20gms. N = 4.8 and 1517gms

Most useful with lungs. The most common Asomething@ added to the lung is blood
and plasma (= congestion & edema). The
most
common “something lost is air (=
atelectasis).
“The Bucket Test”
“If the lung sinks in a bucket of water,
something heavier than water is added OR,
the air is removed (atelectasis is pretty common!) or both.”
M.
SPECIAL FEATURES {SOUND} “What does it sound like?”
18
1. Crepitant - the sound of popping air = emphysema, gas producing bacteria, normal
lung. Its absence in the lung = atelectasis.
2. Sloshing - the sound of fluid splashing = “Fluid where it shouldn’t be”
Edema, ascites, pleural effusion, diarrhea
3. Hard - sounds like a Arock@ when banged on a hard surface.
Bone, mineralized matrix.
SPECIAL FEATURES {ODOR} ”How does it smell?”
N.
1.
Foul - rotting smell; putrefactive necrosis,
saprophytic agents
2.
Ammonia = usually means uremia
3.
Apple cider - gastric hemorrhage or swallowed blood.
4.
O.
No odor - very common; many septic as well as aseptic processes.
SPECIAL FEATURES { TASTE} Well., How does it taste?
Hippocratic physicians used to routinely taste the blood, sweat, tears,
Urine, nasal mucus, sputum and ear wax of their patients.
P.
EXTENT - How much of the organ is affected?”
Estimate % of the total organ or tissue which is affected and potentially functionally
compromised. One measure of the severity and therefore the potential clinical
significance of the gross lesions. Most important in lungs and kidneys where we have
estimates of the physiologic reserve.
19
BLOOD LOSS Blood volume = 8% of body wt. Loss of at least 40%
of blood volume is critical 1cc of blood = 1 gm.
1. Weigh carcass. 2. Collect and measure vol of lost blood.
3. Calculate blood vol for animal. 4. Calculate % of total blood vol
that the collected hemorrhage represents.
Example:
10 kg dog has 0.8kg of blood volume ( 800 cc)
40% of 800cc = 320cc of hemorrhage
APPROACH TO GROSS DESCRIPTION AND INTERPRETATION
Step 2: Describe the abnormal part with respect to the above listed attributes which
are appropriate. Not all the attributes will be relevant to every lesion. However, most can
be described with respect to distribution, contour, color, size, consistency, extent of the
organ affected and any special features unique to it. A description doesn’t need to be a
dissertation. Adhere to the “KISS Principle”
“One or 2 sentences is enough”
20
Step 3: Interpret a pathologic process from what you have described based upon what
the attributes suggest. This is the fun part. It=s a chance to apply what you have learned
and when done in conjunction with submitting samples to a pathologist, you get feedback
about your interpretation.
For instance, The lungs were diffuse dark red, wet, heavy and fluid flowed freely
from the cut surface and airways@ (interpreted to be pulmonary congestion and
edema. There is a 3 cm white round mass in the liver which had a soft,
amorphous white cut surface, spreadable with a butter knife, and a thick fibrous
capsule@(interpreted to be an abscess). Both kidneys were diffuse, pale, wet and
bulged on cut surface (interpreted to be acute tubular necrosis or nephrosis). The
brain contained miliary 1 mm flat red foci on the surface@ (interpreted to be
petechiae, possibly DIC or acute meningitis). There was an anterior-ventral
distribution involving 40% of both lungs which were plum colored, had adherent
fibrinous material on the pleura, were firm and upon cut surface contained pus in
the airways@ (interpreted to be fibrinopurulent bronchopneumonia).
This interpretation of the pathologic process is summarized into a phrase or sentence
called the morphologic diagnosis. This is the stock in trade of pathologists. It is used as
a sort of short hand to document or denote pathologic processes. Skillful application of
accurate morphologic diagnoses is most important to pathologists and much time is spent
in training learning to do this properly. It is not necessarily important for clinicians to do
this but an accurate description of what they observe is so the pathologist may formulate a
presumptive morphologic diagnosis from the clinician=s description which can then be
verified from the histopathology.
LOOK FOR CORROBORATIVE TESTIMONY
“CORROBORATIVE TESTIMONY” = Additional information
from another source that supports your findings or conclusions.
i.e. in cases of pulpy kidney disease, there may be evidence of
glucosuria and fibrinous pericardial effusion; focal symmetrical
encephalomalacia?
21
Descriptive Pathology is….
“Painting with Words”
Style of writing should be
suited to the purpose and
needs of the reporting format
DESCRIPTIVE PATHOLOGY FOR AUTOPSY REPORTS
PURPOSE OF THE AUTOPSY REPORT
A) Explain the cause of death, establish or confirm the presence or absence of a disease
B) Create a permanent record of the ephemeral events found at autopsy
Its retrospective medicine
The autopsy is an ephemeral event. The only record of the findings is what YOU record during
the short period of time. It’s A Descriptive Exercise. Gross observations should dominate the
autopsy report. “Paint a picture with words” then apply the “Carpenter Test”. Close your eyes.
Can you see what you wrote? This is the permanent record of the gross findings. Thus provide
minute detail so that another pathologist reading your report could see in their mind the image
you described.
First and foremost gross pathology in the autopsy report is a descriptive exercise that forms a
rational basis for the interpretation of the observations. Interpretation is secondary to accurate
documentation of the lesions.
“Describe first, then interpret”
Description slows the process and opens the mind, making cognitive error in interpretation less
likely, and…..you generally time for this in the autopsy arena. Knowledge of the gross
22
appearance “Frames” the case and is extremely useful when reading microscopic. Together, the 2
make a powerful tool to get the correct diagnosis and interpretation and leaves a useful record.
Necropsies-in-a-jar = Clinician performed autopsy with tissues submitted to the diagnostic
lab as a surgical specimen. (“The Full Catastrophe”)
Often performed with poor or no documentation of the gross findings. The power of the autopsy
is the combination of both gross findings and the histopathology. If there is no gross,
interpretative power is list.
GROSS PATHOLOGY FOR CERTIFICATION EXAMS
“How to Play the Game to Win”
A.
EXAMINATION STRUCTURE &
COMPOSITION
The gross pathology portion of the examinations is a
projected gross image exam, not a practical.
1. Short answer, fill in the blank format.
2. Digital photographs not wet tissue.
3. One view of the organ; cannot manipulate specimen.
4. 1 ½ min time constraint
5. Species is the only given data; very limited framing
B.
GROSS PATHOLOGY EXAMINATION COMPOSITION
100 images selected from about 250 submitted. SOP requires diversity with respect to
species, organ, pathologic process so expect a wide variety. Emphasis on domestic
species; dog, cat, horse, cow, pig, sheep, goats, lab animals, wildlife, zoo and lower
vertebrates [fish, amphibians, reptiles, birds]. The examination is a subset of what images
are available to the examiners. There are only so many diseases of animals. There are
only so many images of these diseases. Images get recycled. Most of the examination will
consist of common diseases; don’t necessarily look for “zebras” 1st if you” hear hoof
beats”.
*** New Paradigm for the ACVP Phase Two Examination
Integrated examination structure. There will be a histopath section as there is now
23
but the Gross path and multiple choice will be integrated. So some questions will
have gross, histopath images and literature. This more closely resembles what we do
in the everyday world and wiil provide more clues or framing.
EXAMINATION CONDITIONS
It’s a short amount of time to see the image, get oriented, recognize the tissue and lesion,
make a diagnosis and answer the questions.
Lesion recognition, mental description and diagnosis must occur quickly, almost
intuitively. It’s “Shoot from the hip pathology” There is a premium on experience.
Specific preparation for this part of the examination is the key.
C.
GROSS PATHOLOGY EXAMINATION PHILOSOPHY
The gross pathology parts of the exams are intended to test your disease recognition skills
at the clinical, whole animal, organ and tissue level.
They are all about INTERPRETATION, not description. You do the description
subconsciously. Look at the lesion, collect the visual information, match the signalment
given, interpret the lesions and answer the questions.
Do Not Describe Lesions!!! The value of a pathologist is partly determined by his/her
ability to interpret and explain, generate and test hypotheses based upon what they see.
D.
THE TYPES OF INTERPRETATION
MORPHOLOGIC DIAGNOSIS (Mx) = A phrase or short sentence
summarizing the principal characteristic or dominant pathologic process present
in the organ or tissue. It should include an organ and distribution modifier and a
process. There is lots of latitude in Mx. Often there are many different correct
ways to say the same thing.
**Chronicity and severity modifiers are NOT needed in the examination arena.
Segmental renal cortical necrosis (infarct)
Bilaterally symmetrical hyperostotic maxillary fibrous osteodystrophy
Diffuse granulomatous enteritis
Osteochondrosis
Bilateral multinodular thyroid follicular adenomas
Leukoencephalomalacia
Serous atrophy of fat
Lymphoma
24
THE CARPENTER TEST
“Can you close your eyes and see what you said or wrote?”
It’s a good self evaluation for clarity and completeness
CAUSE = The specific cause of the lesion or disease depicted
in the
image. The same as “Etiology”.
Name a specific disease agent. A microbial agent, virus, bacteria, fungj, parasite,
toxin, genetic defect (deletion, recessive gene, mutation etc) or metabolic
disorder. Be specific as possible; genus and species for metazoans.
Canine adenovirus Type I
Metastrongylus apri
Sporodesmin or Pithomyces chartarum
Rhodococcus equi
Uroporphrynogen III cosynthetase deficiency
Nutritional Ca/P imbalance.
**Don’t name a disease when cause is requested.
NAME THE DISEASE OR CONDITION = the medical or common usage term
for the disease depicted in the image. Lots of latitude. Many different regional
names of diseases.
**Sometimes Mx and Name the Disease can be the same.
Leukoencephalomalacia
Osteopetrosis
Neoplasms – can be both
Fibrous osteodystrophy
Vesicular stomatitis
Pyometra
Palatoschisis
Cyclopia
STEP DOWN QUESTIONS = Questions outside of the “main sequence”
designed to test the depth of your knowledge about the disease or condition
depicted.
These are intended to add discrimination to the gross pathology portion of the
examination. How much more besides the obvious do you know about the
disease?
This relates to the concept of Integrative medicine. As a pathologist looking at
25
gross postmortem findings can you correlate other disease parameters, an
understanding of important mechanisms in the disease or that perhaps contributed
to the lesions and can you anticipate additional findings.
a. Name a Related Lesion = name another pathologic lesion in another
topographic location that may occur in this disease or condition. Once you
have made a Dx, what else is characteristically found in animals with this
lesion or disease? Not necessarily always but often or typically.
Pituitary adenoma in dogs – bilateral adrenal cortical hyperplasia
Chronic renal disease in cats – bilateral parathyroid hypertrophy
Bovine osteogenesis imperfecti – blue sclera, fractured teeth, intrauterine
rib fractures
White muscle disease in ruminants – aspiration pneumonia
b. Name a Related Clinical or Clinicopathologic Abnormality = name a related
clinical abnormality that is associated with the lesion or disease. Similar to
above but the abnormality is hematologic, biochemical, clinical etc rather than
an anatomic lesion.
K9 anal sac adenocarcinoma – hypercalcemia
Uroabdomen in foals – hypernatremia, hypochloroemia, hyperkalemia
Pars intermedia adenoma in horses – hyperhidrosis, hyperpyrexia,
polyuria/polydipsia, hirsutism
c. Differential Diagnosis = given the image, name the several diseases that
could present with this or a very similar lesion. **The lesion depicted is not
necessarily pathognomonic but falls within the range of several different
diseases. List the possible diseases. Generally you are asked for 2-3 other
diseases. There may be 10 others; give only how many others they ask for. The
committee has a list of acceptable responses. **Do not give more than is
asked!
Multifocal petecchia on the pig kidney –
DDx = 1) Erysipelas 2) Salmonellosis 3) Classical swine fever [hog
cholera] 4) African swine fever 5) Streptococcal septicemia
Bovine hemoglobinuria
DDx = 1) Leptospirosis 2) Bacillary hemoglobinuria 3) Cu toxicity
4) Onion poisoning (n-propyl disulfide toxicity) 5) hypophosphatemia 6)
26
Babesiosis 7) Brassica toxicity 8) Postparturient hemoglobinuria 9) Cold
water hemoglobinuria 10) Cu deficiency
Be sure to “Name a Disease” not a “Cause”
d. Pathogenesis = trace an outline for the events that cause the disease or lesion
This is generally written as a series or words or short phrases with arrows
separating them to show the progression of events from the initiation to the
end stage or lesion.
Deep Pectoral Myopathy of Broilers
Edema of supracoracoid muscle → swelling → Increased pressure within
the fascia → ischemia →coagulation necrosis
Atypical Interstitial Pneumonia of Cattle
Ingestion of excess L-tryptophane → circulation to lung → metabolism to
3-methyl indole by Clara cells → toxic intermediates → damage to Type I
cells → interstitial inflammation → diffuse pulmonary edema → hypoxia
→ dyspnea → interstitial emphysema
ETIOLOGIC DIAGNOSIS = a word or phrase that captures a pathologic process
with a reference of tissue and a cause or condition if possible. Not commonly
used anymore but seen occasionally. There are many different ways to formulate
these and no one way is correct. There is lots of latitude. This type of response to
diagnosis frees you from making a formal anatomic morphologic diagnosis. There
may be overlap with other forms of diagnosis. Etiologic diagnoses can be of
widely varying specificity.
*Because many answers are acceptable these tend to be low discrimination
answers and I think that is why they are not commonly used anymore.
Cutaneous acariasis
Verminous arteritis
Intestinal histoplasmosis (protozoal enteritis)
Toxic hepatopathy (hepatic mycotoxicosis)
Proliferative and exudative interstitial pneumonia (pulmonary
Toxoplasmosis)
Protozoal myelitis (Spinal sarcocystosis)
2. MAJOR HISTOPATHOLOGIC ALTERATION = what is the
histopathologic appearance of the gross lesion you are looking at grossly?
27
Used occasionally when the characteristic microscopic lesions for which the
Mx may not be obvious.
Hemomelasma ilei in horses – hemorrhage, hemosiderosis and
granulation tissue
Ostertagiosis (Morocco leather abomasums) – mucus neck cell metaplasia
and glandular hypertrophy
E. WHAT DETERMINES THE TYPE OF QUESTION ASKED?
Examiners ask the appropriate questions that are the most discriminating for that
image.
Mx, Causes, Name the Disease tend to be the most common.
Practice to be able to answer every type of question for every image you look at.
Remember if examiners cannot agree on an answer, how can they expect you to
answer correctly?
F. TESTMANSHIP
If you can not see a lesion, look in the center of the image.
Pathologists and photographers tend to center the item or interest in the
middle of the image. Remember that in situ images may have
multiple lesions in different areas NOT in the center.
If you can not get oriented as to organ to tissue, think about reproductive, endocrine
or lymphoid tissues. This portion of the examination is about interpreting what you
see, not formal description writing.
Read the question again and take your cue from what is
asked about the image. If the question asks for 3 Mx’s, that is
a tip off that there is more than one important Mx present in
the image. Look for them! If you do not see others, how can
you break up the Mx you do see into several.
Intervertebral disc disease
Mx = Chondroid metaplasia and disc degeneration
1) With dorsal protrusion 2) Rupture into spinal canal 3) Focal myelomalacia
of the spinal cord.
28
Experience and practice pay huge dividends here. Experienced pathologists should
have no problem with this but learn how to play the game to ensure success.
Gross pathology images are readily available; personal collections, websites, CE courses
Try all questions for every image. Not all questions will be “appropriate” for each image.
It will be obvious which are and which are not.
*Be able to “Shoot from the hip” BEFORE to take the examination. The idea is to have
pre-formed Rx to images. Then is it only a matter of pattern recognition; you have already
decided how you will respond.
“It’s a funny profession, ours, you know. It offers
unparalleled opportunities for making a chump of
yourself. It helps to be good at the job, of course, but
even if you’re a positive genius humiliation and ridicule
are lurking just round the corner”…..Siegfried Farnon
( From “All Creatures Great and Small” by James Herriot)
“I pass, like night, from land to land;
I have strange power of speech;
That moment that his face I see,
I know the man who must hear me:
To him my tale I teach”
Samuel Taylor Coleridge
29
COGNITIVE ERRORS IN VETERINARY DIAGNOSTIC PATHOLOGY
Paul C. Stromberg DVM, PhD, Diplomate ACVP
Professor of Veterinary Pathology, Dept Veterinary Biosciences
1925 Coffey Road, Ohio State University
Columbus, Ohio 43210
[email protected]
Life is short, the art is long,
opportunity is fleeting, experience
delusive. Judgment difficult.
Hippocrates of Cos, 460 BC
“Every doctor is fallible. No doctor is right all the time.
Every physician, even the most brilliant, makes a
misdiagnosis or chooses the wrong therapy”
Jerome Groopman, MD
Recent studies in human medicine show that ~ 80% of the errors made by doctors are
caused by a cascade of cognitive errors, not ignorance of the clinical facts. As many as
15% of all diagnoses in human medicine are inaccurate. Because of the nature of what
veterinary pathologists do, we are “immune” to some of these errors.
1.
2.
3.
4.
5.
We are separated from our “patients”
We have little emotional involvement
We neither like or dislike them
We do not interact with or even elicit a history for the owners
We usually have little or no clinical data
The errors veterinary pathologists make are related to Perception and Analysis of gross
and microscopic visual patterns. Good research on errors in human radiology is highly
relevant to veterinary pathologists reading biopsies. Currently the average diagnostic
error rate in interpreting medical images is in the 20-30% range. No studies have been
done in veterinary pathology but there is every reason to believe the error rate is far
higher than any of us want to admit. The practice of veterinary pathology has two
components which are liable to error.
1.
2.
3.
Perception – we make an observation
Cognition – we analyze what we see, what it may mean and the possible
explanations for it.( Reading our “Rosetta Stone)
These processes are repeated over and over.
1
Perception
We teach our students to
1. Systematically inspect each component of the organ or tissue
2. Deconstruct the image pattern before them and
3. See the component parts.
Then by analysis of all the component parts, we make a judgment and arrive at a
diagnosis
The Observation
“It’s a smart phone”
Deconstructed iPhone 6s plus
The Interpretation
“It’s an iPhone 6s plus”
But with experience, we abandon this deliberate deconstruction of images and “see” at a
glance what is abnormal. This is called “Pattern Recognition” But different observers
may “see” different patterns.
We have already briefly discussed Visual Pattern
Recognition in pathology. It is an intuitive assessment
based on visual data that does not always occur in a linear,
step by step combination of clues. Yet that is how we
teach our students to approach diagnosis. Pattern
recognition is a very “soft” subconscious thing; that
psychologists call “Gestalt”. It is affected by the innate
variability of the image or pathologic process as well as technical aspects of
the slide. It is also impacted by our mental and physical state, our emotions
and fatigue.
2
Classic Lesion
Variations around the classic lesion
Pathologic lesions or
processes have a range
of expression.
Residents and
graduate students
learn the “Classic” or
“Protot ype” appearance and
then spend the rest of their
lives learning the variation
around the classic. With time,
they become comfortable with
the fuller range of expression.
It is the ability to operate
confidently in the ranges iof
variation that marks the
experienced pathology.
But the patterns of different
entities may overlap
at the margins of their
expression and this is
where experience
pays dividends in
sorting out the
diagnosis. This is also
where the variability in
diagnosis among pathologists
originates and is the area
where errors in cognitive
thinking originate as we sort
through the list of differential
diagnoses and try to settle on
Area of Diagnostic Overlap
one or another diagnosis. It is
the area of data collection that reinforces our bias for competing overlapping diagnostic
entities. The information found here by one pathologist may stimulate a diagnosis of
“histiocytoma” and another pathologist to say histiocytic sarcoma” Some of this may be
mitigated by proper framing of the case and additional testing results; the “Total Patient
Evaluation” concept.
3
Variation
Variation
“Prototype”
Range of Expression of Feline Renal Lymphoma
Pattern Overlap
LSA
FIP
What’s YOUR diagnosis?
4
K9 WD Nasal Carcinoma
Classic or “Prototypic” pattern
K9 WD Nasal Chondrosarcoma
Classic or “Prototypic” Pattern
In poorly differentiated nasal
neoplasia in the dog, the lesion
patterns of carcinomas and
sarcomas overlap and may
converge.
What’s YOUR Diagnosis?
5
P
6
Recognition is real and important and often right. It’s the mark of an
experienced pathologist that becomes refined over the years of practice
aided by remembering when you were wrong. Doctors (including
pathologists) achieve competence by recognizing their mistakes and
incorporating them into their memory.
“Identify your mistakes, analyze them,
keep them accessible at all times”
The problem in surgical pathology is that we get relatively little feedback about our
diagnoses. Clinicians at least see the patient again but often WE make a Dx and
never learn if it was correct or not. This is a critical issue in the profession.
Pathologists working in academic veterinary medical centers have far more
opportunity for this than those in the commercial or government diagnostic labs.
Labs with a single or small cadre of pathologists are too insular and have
insufficient diversity of opinion necessary to keep pathologists thinking about
their diagnoses. The pathology community needs to solve this problem and
promote more clinician-pathologist interaction.
“….Opportunity is fleeting”
Pattern recognition while extremely useful can also be dangerous. Research shows
that most medical judgment is made within seconds after perception. Experts
form an opinion on average in 20 seconds. The more seasoned and experienced
you are the greater is the temptation to rely on “Gestalt” alone.
“...Experience is delusive”
Cogent pathologic evaluation combines the 1st impression in pattern
recognition with deliberate analysis
“So its errors in thinking, not ignorance of facts.
Most of the errors we make are in “How we think about what we see”
7
COGNITIVE ERRORS IN VETERINARY PATHOLOGY
ANCHORING
One of the dangers of “Gestalt”. The observer does not consider the multiple
possibilities but quickly and firmly latches on to his or her “First Impression”
and ignores discrepancies that would argue to reject it. We see only the
landmarks we want to see and so become “anchored” in our opinion.
CONFIRMATION BIAS
The tendency to search for or interpret new information in a way that
confirms or reinforces your diagnosis and avoid or ignore information
that contradicts or would lead you away from prior belief. “Cognitive
Cherry Picking”. Usually follows “anchoring” in a “Gestalt” diagnosis.
We see in the data what we want to
see. We must stay uncommitted to a
diagnosis until we have seen or
considered all of the facts.
“Describe 1st, THEN interpret”
Ironically this is easier for students
than for experienced pathologists
because they lack “Gestalt”; they do
not have convictions generated by
the confidence of experience and so
delay their Dx. This not an uncommon problem on the histopathology section of the
certification examination. The candidate decides at the top of their essay what the
diagnosis is, then writes a description to that entity to fit their interpretation rather than
what is on their slide. That’s confirmation in action.
By ignoring data in the overlap that
would area that would point us toward
the other diagnosis, we force the Dx
into our “Gestalt” diagnosis.
8
SEARCH SATISFACTION
The natural cognitive tendency to stop thinking when
we make a major finding. The detection of one finding
interferes with that of others. This is a well known error
among human radiologists and is a major factor in false
negatives. So “Keep on truckin’” (We test this on the ACVP exam
with “Two-fors”
What’s a “Two-for”?
= A question, gross image or microscopic slide, that
contains more than one diagnostic entity or lesion.
“Oh
Thou who didst with Pitfall and with Gin,
Beset the Road I was to wander in,
Thou wilt not with Predestined Evil round
Enmesh me, and impute my fall to sin”
Well, I’m sorry but I’m afraid we will! Why?
Because it happens in the real world
Because, by testing for it, it teaches
“The Standard”
Because it’s highly discriminating
FALSE NEGATIVES
Our minds favor the perception of “positive” data over
“negative”. We are more likely to see lesions that are present than
lesions that result in the absence of something. Especially if the
lesion is symmetrical or diffuse. Remember
The Paradox of Anatomic Pathology
“Sometimes the most extensive, widespread or diffuse
lesion is the easiest to overlook because there is no normal
for comparison
9
FRAMING
Focusing on what is wrong and the cause of the problem. Often improper or lack
of framing leads to errors in thinking. Mostly for surgical pathologists the
clinician or surgeon “Frames” the case. **No or inadequate framing is a
serious problem for veterinary surgical pathologists. It is likely that concern
about improper framing or leading the pathologist astray is what motivates some
clinicians to say, “Don’t tell the pathologist anything, you will bias him”. I have
heard clinicians teach this to veterinary students. The reality is that without
some clinical clues, perception and cognition are significantly hampered. We
may be able to decrease errors in surgical pathology by at least some framing of
the case by clinicians. This is one of the values of working with clinicians and
providing a proper submission form that indicates what information is needed or
desired.
“Accept the “Frame” but be aware that it can mislead you”
AVAILABILITY
This is the tendency to judge the likelihood of an event (diagnosis) by the ease with which
relevant and recent examples come to mind. We teach our students to make the “most
likely diagnosis” given the image or facts. Indeed, we test for this on the certification
examination also.
“When you hear hoof beats,
think horses not zebras”
Is a good rule most of the time because common things occur
commonly. But if you get “anchored” to the idea, you will
miss some unusual diagnoses. But remember “Zebra” is a
“topographically relative” concept. While hoof beats in the
USA and Europe usually mean “Horses”, in Tanzania, most of
the time when you hear hoof beats, its actually zebras.
ZEBRA RETREAT
This is the shying away from a rare diagnosis. Powerful forces
discourage “zebra hunting”. Often “zebra hunters” are
considered to be “show boats” or arrogant. To verify the
occurrence of a Zebra diagnosis can cost money and time and
cost containment issues blunt this activity. Mostly the lack of
experience with the rare diagnosis fosters a lack of confidence
so the diagnosis is not pursued aggressively.
10
THE LAW OF PARSIMONY OR OCKHAM’S RAZOR
A bedrock principle of the scientific method that states that explanation of any
phenomenon should make as few assumptions as possible in the explanatory hypothesis.
“All things being equal, the simplest solution
tends to the best one”
Ockham’s Razor applies to decision making in descriptive pathology but should not
override thorough cogent analysis of the images and facts. Sometimes the correct answer
is complex
DIAGNOSIS MOMEMTUM
A ripple effect through a group of pathologists. A pathologist makes
an initial diagnosis that is accepted by peers and subordinates without
challenge. Subsequent opinions agree and soon the diagnosis is
universally agreed upon. This occurs especially when the first opinion
is made by an expert or senior experienced pathologist. I have seen
this many times in seminars when a senior resident gives a diagnosis
and all of the other residents follow suit even when the first diagnosis
is wrong. Soon the diagnosis gains enough force to crush all other
opinions.
UNCERTAINTY
All observers have characteristic ways they manage uncertainty which is common in
diagnostic pathology. Pathologists tend to be either “Risk Takers” that have more false
positive diagnoses or are “Risk Averse” who tend to have more false negatives.
11
Management of Risk
You manage this risk by being aware of the ramifications
of your diagnosis and what the consequences are if you are wrong.
I try to err on the side of least damage if I am wrong and this varies from
situation to situation. Remember to communicate your uncertainty to the clinician if it
impacts case management. Clinicians generally do not care of you called a tricholemoma
a trichoblastoma or sebaceous hyperplasia an adenoma. There is no clinical fallout.
Surgeons complain about pathologists who will not consistently commit to a firm
diagnosis and that is a danger as the threat of litigation becomes more frequent.
Remember our job is to help as much possible. I tend toward making a diagnosis
whenever possible but I am guided by the “First Rule of Medicine” (“Above all, do no
harm”). This is motivated by a desire to help clinicians, give the clinicians and pet
owners their money’s worth and the fact that for a long time we have been working with
impunity as to the legal consequences of our diagnoses. But I manage the risk by being
honest with clinicians
(“Nothing competes with honesty in the surgical biopsy report”)
and knowing the clinical consequences of a mistake for each diagnosis I give. Surgical
pathology today is a challenge and to work in this environment you have to accept that
and the risks and limitations. “Bring your “A” game to the microscope”
JUGGLING
The mark of the expert physician is the ability to keep seemingly
contradictory bits of data simultaneously in your mind then seeking
other information to make a decision one way or another
You must find a middle ground. Be aware of the cognitive
errors and traps. Recognize that certain patterns may not conform
to the prototype. The art of pathologic diagnosis is knowing
when you are outside the prototype range of lesion expression
and into which other overlapping lesion range you are in.
When the lesion is at the extreme limit,
opinions among pathologists may
12
differ remarkably and regardless of what they say, the certainty of each diagnosis is low.
Pathologists should communicate the unusual or atypical pattern that does not easily fit
into a diagnosis or that would likely elicit divergent opinions so the clinician can better
manage the uncertainty of the diagnosis and therefore the risk to the patient if the
diagnosis is wrong. Clinicians must understand the variable nature of disease patterns and
that it is a subjective opinion. This is why two board certified pathologists can look at the
same slide and render 2 often very different diagnoses
THE MANAGEMENT OF COGNITIVE ERRORS
1.
Be aware of the cognitive traps Other experienced
pathologists have similar mechanisms. “Man up”! You
make errors. We all do. Managing your cognitive errors
begins with “accepting your story”
2.
Slow the perception and analysis process. Time opens he
mind. However, time is the most precious commodity in
medicine. None of us has the luxury of making diagnoses with
unlimited time. Most difficult to do in surgical biopsy and on the
certification examination. Consultation with colleagues when
possible. Set the case aside and come back to it later. Often you
see the lesions with a more open mind.
“Most things are better by morning”
…………Lewis Thomas
This is the origin of the old medical axiom,
“Take 2 aspirin and call me in the morning”
3.
Deconstruct the pattern recognition image mentally or in writing just as we
teach our students to do. Use your Pattern Recognition skill (Gestalt), its
valuable and often correct but check it with a cogent analysis of all the facts if
possible (“Corroborative testimony”) . I always ask myself before I commit to
a diagnosis “Does it all add up” or “What else could this be”?
4.
“Describe uncertainty” because it forces you to slow
down and evaluate the separate parts of the “Gestalt
Image”.But employ a style that fits the purpose of the
task. Most critical in biopsy. Control fatigue by work
flow management and an efficient style that suits the
biopsy reports purpose.
13
“The amount written is inversely proportional to the certainty of the diagnosis.”
It’s different for everybody.
5. Make a mental list of DDx’s and work from that.
Again, the ACVP and ECVP certification examinations test
this skill for a good reason.
6. Use the Total Patient Evaluation Concept. Get all of
the pieces of the puzzle together before you interpret the
“picture”. “Read a slide but interpret a patient” Properly
framed cases often provide a lead or information that may
set off a DDx list or even stimulate a thought or idea that
you were not considering. Valuable but in some tasks
either purposely denied, as on the certification
examinations, or omitted by clinicians for whom you are
working. Always interpret framing cautiously because if
not accurate, it can lead you astray. “To examine for yourself”
PATHOLOGICAL MYOPIA
The tendency to over weight the data immediately in
front of you and ignore other information pertinent to
the diagnosis. Especially common in surgical biopsy
interpretation when the slide is all you have.
“Read a slide, but interpret a patient”
The Judgment of Competing Uncertainties
Sometimes the total patient evaluation helps to focus
you and assist in the decision. If not, “Take two
aspirin and look at it again in the morning” Then
seek another opinion from a colleague.
“Judgment is difficult”
14
THE MYTH OF INFALLIBILITY
The expectation of being perfect, while appealing to us, is unreasonable. There is a long
chain of events with multiple critical points before the pathologist even sees the case.
There are vagaries and subjectivity in pattern recognition. There are going to be mistakes
and some diagnoses cannot be reached by consensus. If this were not so, we would agree
on everything but we don’t. That is why the Greeks called medicine an “Art”. What is an
acceptable error rate? Who knows? 5%? The real rate is probably much higher. We do
know from human studies that the Interobserver variability is ~
20% and the Intraobserver variability is ~ 5-10%.
“And finally there is judgment. We try to teach it to our students,
but we wonder if we understand it ourselves. Sometimes the course
that seems right for this particular patient today is exactly the
opposite of what seemed right for someone with what seemed
to be exactly the same problem yesterday. If even statistics give
fuzzy answers, how much more unsteady must be judgment?
Were it infallible, doctors would never disagree. The problem
thus distills itself down to the first aphorism of Hippocrates;
judgment is difficult to learn, to apply and even to recognize;
medicine has few uncertainties….the ancients correctly called it the
Art.
(From “Doctors. The Illustrated History of Medical Pioneers”
By Sherwin B. Nuland MD)
15
THE MICROSCOPIC BASIS FOR MACROSCOPIC PATHOLOGY
or
(Why We See What We See at Autopsy)
Paul C. Stromberg DVM, PhD
Diplomate, American College of Veterinary Pathologists
Department of Veterinary Biosciences
Ohio State University
The descriptive attributes of gross lesions observed at post mortem examination may provide
information about the type of pathologic process, cause, parts of the organ or tissue affected or
involved and pathogenesis. As pathologists we can learn to read these lesions like
“hieroglyphics” interpret their meaning and by putting strings of lesion attributes together with
the patient signalment and history, arrive at a presumptive but often accurate diagnosis. A
carefully prepared postmortem examination with accurate description of the lesions can be a
valuable adjunct to the histopathologic examination if for no other reason than histopathology
examines such a tiny fraction of the patient. By establishing some guidelines for the significance
of the observed gross lesion attributes and interpreting them in the aggregate, we can often reach
logical conclusions about the nature of the pathologic process observed. The long term goal of
gross pathology is never to have to do histopathology. Of course this is a receding goal as we
always confirm by histopathology what we deduce from the post mortem. But histopathology is
relatively expensive (compared to visual observation at postmortem) and takes time.
I.
OBJECTIVE
Understand how microscopic lesions produce the macroscopic lesion attributes we see in
a variety of organs and tissues and shape the appearance of the lesions we see during the
1
port mortem examination. The approach will be to evaluate different types of lesion
attributes in pairs, observing the gross specimen and the sub-gross or microscopic lesion.
INTERPRETATIVE PATHOLOGY OF SPECIFIC ORGANS AND TISSUES
II.
LIVER - Dense solid organ normally dark, with symmetrical lobular microscopic
architecture defined by peripheral portal triads and a system of bile ducts. Provides good
contrast for pathologic processes causing a light or pale color
1.
Multifocal to miliary, well demarcated, random small foci = implies a recent embolic
shower. A common pattern in septicemia in many species which can look striking in
livers due to the high contrast between the necrotic foci that are often white or light and
the dark color of the background. The pattern is called military because it has the
appearance of millet seed (“Miliarius”; Latin for millet seed)
a.
Beaver with yersiniosis. The tiny foci are discrete because they consist of a
bacterial colony surrounded by a zone of degenerate or necrotic hepatocytes
Beaver liver w/ yersinosis
2.
b.
Horse with septicemic salmonellosis. A similar appearance to the beaver liver
c.
Snake with salmonellosis. In this case there is a peripheral layer of fibrosis that
contributes to the abrupt edge of the small granulomas.
Nonrandom well demarcated symmetrical nodules in linear array may indicate a
pathologic process which is highlighting the bile ducts. On a gross or subgross level, the
only structure in the liver that is symmetrically organized is the system of bile ducts. As
the ducts dilate, they assume a tortuous course and can cause a linear pattern of nodules
where the ducts bend and raise the hepatic surface. The nodules are well demarcated with
high contrast because there is a distinct histologic difference between the hepatic
parenchyma and the tissue of the bile ducts and the interface is abrupt.
2
a.
Rabbit with hepatic coccidiosis ( Eimeria stediae) - cystic biliary hyperplasia. If
you look carefully in this rabbit liver, you can discern a vague pattern of short
linear arrays of white nodules. Histologically they can be seen to be dilated
hyperplastic bile ducts with many coccidian organisms.
Cystic biliary hyperplasia
Rabbit liver w/ hepatic coccidosis
3
Multifocal poorly demarcated nodules = a process that tends to blend into the surrounding
normal tissue or the nodules are composed of altered normal tissue. Poorly demarcated
nodules may indicate the cellular or histological composition of the nodules is similar to
hepatic parenchyma and thus nodular proliferation of hepatocytes. Cirrhosis may be pale or
dark depending on the lipid content of the affected cells.
a.
Dog with cirrhosis ~ Porto
systemic shunt. In this case the
regenerative nodules are very
small giving an almost granular
appearance to the liver surface.
3
b.. Cat with chronic hepatitis and nodular regeneration (cirrhosis). The irregular
poor demarcation of nodules is created by the proliferating hepatocytes forming
nodules that are separated by zones of atrophy, mild inflammation and fibrosis.
There is also a nodular pattern in the spleen but as we will see later, it is another
and separate process.
c.
4.
Multifocal, random and red - can mask a process causing white foci.
a.
5.
Horse with chronic hepatitis and cirrhosis. In this case the regenerative nodules
are larger and a mixture of yellow (lipid) and green (bile). The histopathology
indicates substantial bile retention which imparts the green-yellow discoloration.
The trichrome stain reveals how much fibrosis there is in this liver that is not
appreciated on gross examination.
Puppy liver with hemorrhage masking necrosis ~ herpes viral septicemia. The
red hemorrhage can be seen easily on gross. Within these areas there is a barely
visible pale area what corresponds to hepatic necrosis but it is masked by the
sinusoidal congestion and hemorrhage.
Multifocal, well demarcated but random red depressed foci - depressed suggests
necrosis; we see the red color over the liver color because of hepatic necrosis or dilation
of sinusoids with pooling of blood similar to pigs with Vit E/Se deficiency.
a.
Dog with metatastic hemangiosarcoma in liver. In this liver we can see a miliary
organized symmetrical pattern that reflects congestion in lobules, a common pattern. The
4
real pattern is the blotchy discrete red depressed areas that correspond to tumor
infiltration that causes necrosis of hepatocytes, collapse of the architecture and pooling
of blood in the empty space. The pattern is the same for telangiectasis in cats and cattle.
6.
Diffuse pale liver usually means lipidosis. Systemic metabolic disorders usually
cause diffuse lipidosis. Actually, hepatocytes can be pale because of other
substances that produce vacuolated hepatocytes; intracellular fluid, glycogen.
a.
Cat with hepatic lipidosis. This liver also exhibits a symmetrical military
centrilobular pattern with a red center surrounded by pale areas that correspond to
vacuolated, swollen, lipid filled hepatocytes. The swollen hepatocytes squeeze
the sinusoids which likely impedes blood flow and may cause some
hypoperfusion and paleness of the liver.
b.
Cat with hepatic lipidosis, necrosis with hemorrhage. The depressed red
foci = something taken away are the areas of necrosis with pooling of
blood. These areas are depressed. The pale areas appear raised and
swollen and are filled with lipid
7.
Symmetry or organization to the lesion suggests process accentuating the normal
lobular architecture. Multifocal widespread symmetrical pale and red show high contrast but
what is the abnormal part? The architecture of the liver is laid out in a diffuse pattern of
symmetrical hexagonal lobules but because in most species (except swine) there is a minimal
or no border, we cannot see this pattern unless a pathologic process highlights it. That process
could be highlighting the central portion of the lobule or the portal triads or the periphery of the
lobules. When this happens it creates a fine almost military organized but evenly spaced pattern
we recognize as “symmetrical”. However, in many cases it is difficult at the gross level to
determine which part is abnormal. If the pattern looks more “irregular”, and not organized as tiny
round foci, it may be a cellular infiltrate, inflammatory or neoplastic, in the portal triads.
5
8.
a.
Cat with centrilobular hepatic lipidosis (pale) and periportal hepatic necrosis with
hemorrhage (red). Grossly it is often impossible to determine if the pale is
centrilobular or periportal.
b.
Llama with periportal LSA - In this case the white areas are the portal triads
which are filled with lymphoma and often spill out into adjacent hepatic lobules
giving the ramifying or branched appearance. This is a characteristic appearance
seen in diffuse hepatic lymphoma in many species
c.
Dog with histoplasmosis - cells fill portal tracts + random sinusoids
Pan lobular pattern - “massive” in the liver implies an entire lobule is affected. This
pattern is most easily appreciated when not every lobule is affected so you see affected
and normal lobules in an almost multifocal miliary but not regular distribution.
a.
Characteristic pattern in pigs with Vit E/Se deficiency, cocklebur, coal tar pitch or
gossypol toxicity. We see the lighter colored hemorrhage over the darker color of
hepatocytes only because of the necrosis. “Fine Arts 101"
6
“Nutmeg” pattern = chronic passive congestion.
Differential retention of blood in sinusoids. Not every
sinus or lobule is equally affected, so the pattern is
“irregular” The contrast is enhanced if there is
concurrent hepatic lipidosis.
a.
III.
Cow with lipidosis and CPC secondary to
hardware disease
SPLEEN - a dark colored sinusoidal organ containing variable amount of blood and
multifocal white pulp. Size variation in the spleen can be physiological as well as
pathologic. Immunologically stimulated spleens have hyperplastic white pulp visible
grossly.
1.
Diffuse
infiltrations of the
spleen increase size and
may cause the color to be
light (= “raspberry
jam”) or dark (=
“blackberry jam”).
Enlarged light spleens
(raspberry jam spleens)
are light because they are
filled with cells that
contain no pigment or
hemoglobin. Almost
always this means diffuse
lymphoreticular
neoplasia (LSA or
Blackberry Jam
Raspberry Jam
leukemia). Enlarged dark
Spleen
Spleen
red spleens contain
abundant hemoglobin. This may be within RBC’s (congestion or hemorrhage) or free in
the parenchyma (hemolytic disease). Blackberry jam spleens may indicate shock,
septicemia or hemolysis. Because the agents that we use to perform euthanasia result in
vascular dilation and pooling of blood in the spleen, animals that have been euthanized
with these agents have blackberry jam spleens at post mortem examination. The spleens
in this panel are from a dog with LSA on the Lt and a dog that was euthanized on the Rt.
a.
K9 spleen w/ Lymphoma (“Raspberry jam” appearance)
b.
K9 with a “Blackberry jam” spleen due to hemolytic disease
7
2.
Well demarcated nodules with organized texture on cut surface (“Can’t spread it with
a butter knife”). = viable tissue and cells.
Dogs with nodular lymphoid hyperplasia (fibrohistiocytic nodule). Although the
cells in these nodules are no different than the lymphoreticular cells in the
adjacent red pulp the combination of cells and fibrous stroma make a dense mass
that has an abrupt edge from the red pulp sinusoids. The cells are viable and
connected which makes the cut surface cohesive and not friable.
b.
3.
Dog with metastatic histiocytic sarcoma
Multifocal well demarcated nodules without organized texture on cut surface
(“Spreadable with a butter knife”). = necrosis and suppurative exudate
Cow with Arcanobacterium pyogenes abscesses. As is common with abscesses
there is an abrupt margin between the red pulp and the lesion usually caused by a
band of necrosis ir a fibrous capsule. The center is friable because it is composed
of pus, dead or dying cells that are not cohesive or connected.
Dog with splenic HSA - “sampling is everything”. Hemangiosarcomas in the
spleen may be red or white and may have a discrete or blurred margin. The white
color is most often caused by fibrin but may be due to dense tumor cells with
minimal congestion of the vascular spaces. Often the tumor tissue is a minor part
of the volume of the mass with most being fibrin. This makes sampling for biopsy
a critical step in diagnosis because if the tumor tissue is not included, the
diagnosis will be missed. You should sample at least 4-6 pieces of splenic masses
that are suspected to be hemangiosarcomas.
b.
8
4.
5.
IV.
Poorly demarcated masses; blend into surrounding tissue. No abrupt transition from
lesion to normal.
a.
Equine spleen with EIA and lymphoid hyperplasia in white pulp. Hyperplastic
white pulp often is not as dense as neoplastic white pulp and can be blurred at the
margin. If the white pulp is diffusely affected as in a very reactive spleen, it can
give the spleen a “raspberry jam” appearance with a subtle multifocal widespread
pattern.
b.
Cat with splenic mast cell tumor ( mast cells are PAS +). Here you can see
anastomosing islands of neoplastic mast cells that are sufficiently dense to be seen
grossly
Diffuse pale spleen with prominent stroma. May = loss of blood and lymphoid tissue
a.
Dog with histoplasmosis - spleen filled with low contrast mixed granulomatous,
lymphoplasmacytic inflammation, fibrosis, amyloid and hemosiderin. This case is
somewhat unique in that there is inflammation added to the spleen but the overall
cross sectional area of the organ is not increased. Because the spleen is not
enlarged, the septal connective tissue and muscle are visible grossly
b.
Arab foal with CID and splenic lymphoid aplasia - the spleen is “empty” of
lymphocytes, somewhat collapsed so stroma is prominent. This is similar to the
dog with histoplasmosis. Because there is much less cellular content, the fibrous
connective tissue stands out.
LYMPH NODES - pale organs with a distinct cortex and medulla. Most significant
changes cause enlargement. “Immunologically dynamic” tissue.
Stromberg’s Law of Lymph Nodes
“If you can’t find them, they were not important”
Diffuse enlarged pale with effacement of architecture; organized cut surface (“Not
spreadable with a butter knife” = viable tissue). Always consider a “domestic” (primary)
neoplasm before an “imported” (metastatic) neoplasm.
Cow with LSA. This node has lost the distinction between cortex and medulla
indicating diffuse proliferation or infiltration of lymphoid cells that blurs the
normal architecture.
9
b.
Bovine bronchial lymph node with lymphadenitis, hyperplasia and edema
secondary to pneumonia. In this slide there is a clear boundary between the cortex
and medulla. The cut surface of the node is bulging (indicating something has
been added) but the intact architecture supports an interpretation of lymphoid
hyperplasia and inflammatory exudate rather than neoplasia. On gross appearance
the medulla is translucent, gelatinous typical of extracellular fluid (edema). On
histopath, it appears as clear space or separated fibers.
The Texture Caveat
“Sometimes granulomatous inflammation looks like neoplasia”
a.
2.
Dog with histoplasmosis - noncaseating granulomatous inflammation may
infiltrate but not cause necrosis; the texture may present with an organized
appearance because the cells are alive and adhering to each other. Chronic
inflammation may stimulate cytokine mediated fibrosis, amyloidosis etc that
adds organization and a “viable” appearance. This node is firm to the touch and
smooth. Histologically you can see a solid sheet of epithelioid macrophages
containing small organisms as well as fibrosis.
Diffuse enlarged pale lymph node with effacement of architecture; amorphous cut
surface (“spreadable with a butter knife”) = inflammation; suppurative or caseating.
a.
Sheep LN with caseous lymphadenitis abscess. The surface is amorphous because
of the pus and the distinction between cortex and medulla is lost because al of the
tissue is destroyed. This is readily apparent on histopathology where the field is
filled with degenerate, dying and dead neutrophils.
10
3.
Diffuse enlargement with retention of corticomedullary architecture = lymphoid
hyperplasia.
Goat intestinal LN with coccidiosis. This node is enlarged but the architecture is
intact with a hint of edema in the medulla. The histopathology clearly reveals
abundant follicular and paracortical lymphoid hyperplasia.
V.
KIDNEY - a complex organ with many subunits (glomeruli, tubules, lobules defined by
vasculature, interstitium) divided into cortex, medulla and pelvis. Complex lesion
patterns may highlight any of these.
1.
Lesions confined to or centered on the cortex likely = a vascular portal.
Multifocal well or poorly demarcated lesions.
RAISED = something added (cells).
DEPRESSED = something taken away (necrosis, fibrosis)
a.
Cat with septicemic Cryptococcus neoformans. Looks like FIP. Multifocality
implies embolic shower. The corroborative testimony is that the lesions are
centered on or predominately in the cortex which is the expected pattern for septic
lesions in the kidney. The lesions are well demarcated with an abrupt interface to
normal cortex and have a symmetrical shape suggesting they highlight a vascular
unit or lobule of the cortex.. There is no hemorrhage and very little inflammation.
The white color is caused by the organisms themselves
b.
11
Cat with FIP - multifocal immune complex vasculitis/interstitial nephritis.
Similar to the Cryptococcus case. Here the white color is caused by inflammation.
2.
c.
Puppy with septicemic herpesvirus - small hemorrhages mask the necrosis.
The military cortical lesions support a recent embolic shower and like the liver in
this case, the necrosis is masked by the hemorrhage.
d.
Horse with suppurative embolic nephritis (Actinobacillus sp). Abrupt transition
between pus and normal cortex. Vertical orientation ~ path of least resistance.
Discrete “almond shaped” cortical lesions. These foci are large enough that we
can see the pus on the cut surface.
e.
Cow with LSA - poorly demarcated = infiltrate without lytic necrosis. Unlike the
previous case of equine suppurative embolic nephritis, the white foci here are
poorly demarcated because the neoplastic lymphocytes “irregularly infiltrate”
into the adjacent renal tissue creating a blurred margin. There is little or no
necrosis to demarcate these foci.
Keystone pyramidal or wedge-shaped, flat, pale or red color in cortex = acute cortical
infarct
12
a.
3.
Mountain lion with septic embolization, thrombosis and infarct (Aspergillus).
Because vascular beds are often laid out in distinct geometric patterns, lesions that
exhibit such shapes may be outlining a pathologic process in such a vascular
segment or bed. In the kidney, the end arteries often describe triangles, keystones
or pyramidal shapes that follow lobular units.
Multifocal petecchia in the cortex = endothelial damage, septicemia, DIC
a.
“Turkey egg kidney” from a pig with erysipelas septicemia. This is the classic
expression of septicemic damage to small capillaries that is seen in a variety of
infectious diseases that have a septicemic component. Notice that the red foci of
petecchiae are irregular in size and larger than glomeruli which distinguishes
them from glomeruli.
13
4.
5.
Glomerulonephritis is often difficult to see grossly - pattern is multifocal, somewhat
symmetrical and should be confined to cortex. Glomeruli are less than 1mm in diameter
so details of pathologic processes that affect them are difficult to interpret with the naked
eye. Congestion and hemorrhage can be seen but if they do not accompany inflammation,
glomerulitis is hard to definitively appreciate with confidence. But any lesion interpreted
to be glomerulonephritis grossly should be confined to the renal cortex because there are
no glomeruli below the CM junction.
a.
Dog kidney with glomerular disease and markedly dilated Bowman’s spaces.
This dog’s glomerular disease is easier to see because the Bowman’s spaces are
markedly dilated
b.
Dog kidney w/ acute glomerulonephritis. This dog has acute glomeruloneophritis
which can only be seen because of the hemorrhage. This cannot be distinguished
grossly from glomerular congestion.
Diffuse dark colored = hemoglobinuria/myoglobinuria. “Port wine” colored
urine is classic. Think about hemolytic diseases and check in the bladder. Hemolytic
disease always causes a diffuse dark color to both kidneys because of the hemoglobin
deposited widely in tubules
Kidney
Diffuse dark colored kidney
hemoglobinuria
myoglobinuria.
“Port wine colored urine”
Hemoglobin looks like “Ruby
port”
Myoglobin looks like “Tawny
port”
Check the bladder! Think
hemolytic disease
14
Cow kidney w/ hemoglobinuria ~ leptospirosis
Cow urinary bladder w/ Port Wine colored urine ~ hemolytic anemia
c.
Sheep with Cu toxicity – The color of the kidney ranges from orange to dark red
with the classic color of “Gun Metal Grey”
*The “corroborative testimony” is in the urinary bladder. The urine should be
dark colored and translucent
**Dark colored urine which is turbid, is hematuria Histologically the dark color
is produced by hemoglobin in the tubules.
15
6.
Diffuse cortical dark greyish-brown color in goats = Cloisonné kidney. Pigmented
thickened b.m. of only proximal convoluted tubules. Suggests gold wire inlay around
porcelain seen in Cloisonné style jewelry. Don’t Dx hemoglobinuria!
a.
Cloisonné kidney from a goat. Only the cortex is discolored
16
7.
Diffuse “soft” kidney = “Pulpy Kidney” = autolysis unless evidence of reaction
a.
Sheep with enterotoxemia - flaccid, wet kidney with hemorrhage. If there is no
reaction, be careful of diagnosing “pulpy kidney disease”, it just may be autolysis
alone. You have to “feel” these kidneys!
Enterotoxemia
Autolysis
8.
Lesions confined to or centered in the medulla or pelvis likely = a urogenous portal
Exception = symmetrical lesions defining a vascular unit in the medulla may be ischemic.
Usually pyelonephritis is almost always due to ascending bacterial infection so it makes
sense the lesion is centered or most severe in the lower parts of the kidney
a.
Cow kidney w/ suppurative pyelonephritis ~ Corynebacterium renale
b.Dog with medullary necrosis, ascending pyelonephritis breaking out under capsule. The
discrete demarcation in the renal crest is caused by a acute necrosis and
mineralization with the pale color due to ischemia.
17
c.
9.
Dog with granulomatous nephritis ~ Prototheca; vascular or pelvic portal?
Sometimes the distribution of the renal lesion is impossible to interpret as in this
case. This dog has protochecosis which was likely acquired secondary to
immunosuppression and because the dog had similar lesions in multiple organs, it
likely arrived in the kidney by the vascular route and descended into the medulla.
Lesion defining tubules - well demarcated, linear in the cortex or medulla; could be
tubulointerstitial nephritis or deposits in tubules. Tubulointerstitial nephritis can be
hematogenous or urogenous.
a.
b.
Cow with suppurative tubulointerstitial nephritis. Ascending pyelonephritis or
descending embolic nephritis? This lesion is often attributed to ascending
pyelonephritis but this cow had no lesions in the medulla and no exudate in the
medulla.
Pig with nephrosis and urates in medullary tubules. Grossly the opaque white
linear streaks in the medulla are caused by the deposition of urates that outline
them giving symmetry to the lesion. But histologically the tubules appear only as
dilated tubules because the mineral dissolves out in processing of the tissue.
18
MEUTEN’S LAWS FOR PALE KIDNEYS
The 1st Law Swollen pale, wet kidneys = nephrosis. Necrosis and edema P within
capsule. When that P exceeds the renal arterial P, renal plasma flow stops, causing prerenal azotemia. BUN, Cr . The kidney is hypoperfused and becomes pale.
a.
Cat kidney with food associated acute renal
failure due to melamine and cyanuric acid
(Pet food nephrosis)
b.
Sheep with lead toxicity
c.Cow with oak bud nephrosis
19
d.
Cat with ethylene glycol toxicity
All of these cases appear similar grossly because of swelling, deceased perfusion and
some edema. The actual tubular necrosis is invisible grossly. If you look carefully, in
some cases of ethylene glycol toxicity, you can see minute faint opaque specks that = the
oxalate crystals. This is often overlooked on the autopsy room floor but can be seen in
well lighted photographs.
The 2nd Law Swollen pale, waxy kidneys = amyloidosis. Amyloid can make the
kidney very pale or less so but the amyloid is usually present only in the glomeruli. Some
or much of the paleness and waxy feeling to these kidneys is caused by the massive
proteinuria.
Cow kidneys with amyloidosis., Notice the massive protein deposition in the
tubules and visible grossly. Histologically it appears as eosinophilic material
distending the tubules.
The Color of the kidney varies from extremely pale to merely lighter than normal but
Almost always they have a distinct waxy feeling
20
Massive proteinuria. The amyloid is in the glomeruli
Not the tubules
The 3rd Law Small pale, irregular firm kidneys = fibrosis, atrophy, old infarcts
Dog with end stage kidney. This kidney is smaller and irregular in outline because of the
necrosis and loss of cortical tissue (mostly tubules). The white color and firmness is due
to the fibrosis which is easily seen on the Masson’s trichrome stain.
21
I.
BRAIN AND SPINAL CORD (CNS) Diffusely light colored tissues due to the high fat content. Some definition between grey
and white matter. Hemorrhage stands out, cellular infiltrates and edema can be indistinct.
Symmetry is very important in evaluation. The CNS lives in a closed space surrounded
by bone. There is no room for anything else.
Lesions with hemoglobin (hemorrhage, congestion) are most visible because of
contrast. The Distribution of the hemoglobin is the key to interpretation
1.
Multifocal lesions suggest embolic shower with/without blood.
Septicemia, DIC, platelet malfunction, endothelial damage.
a.Calf with septicemic meningitis ~ Colibacillosis. We do not see the
inflammatory exudate partly because the foci are very small and partly
there is poor contrast of the exudate with the white background of the
neuropil.
b.
Cow with TEME lesions ~ Hemophilus somnus. Similar to the
colibacillosis case. Although there is considerable inflammation and
infarction, all we see is the hemorrhage.
c.
Cat with soap bubble lesions of Cryptococcosis. The “soap bubbles” are
caused by the gelatinous capsular material of the yeast which provides
minimal contrast with the neuropil; only a faint translucent appearance.
Often there is no inflammation in these cases so no hemorrhage.
22
2.
3.
Diffuse red may = congestion or hemorrhage; distribution ~ where it is
a.
Cow with babesiosis – in this case the brain appears diffuse pink because
the vessels that are affected are capillaries, not larger vessels which might
standout. The affect is produced by RBC’s adhering to the vascular
endothelium because the Babesia organisms change the glycocalyx on the
RBC making them sticky. On histopathology y0ucan see all of the small
vessels are congested.
b.
Dog with submeningeal hemorrhage ~ spinal tap. There is regional severe
hemorrhage over the medulla. The subgross examination of the sections
reveals it is confined to the surface which is what we expect if a
superficial vessels were lacerated and bleeds into the subdural or
arachnoid space
Dilated ventricles = hydrocephalus
a.
Cat with high protein CSF in dilated ventricles = FIP; pyogranulomatous
periventricular encephalitis. In his case, the dilated ventricles contain
opaque fluid that is gelatinous (because otherwise it would flow out of the
coronal section). Much of the fluid has been removed during processing of
the slide but the adjacent periventricular inflammation, not apparent
grossly, is typical of FIP.
Any asymmetry in the brain is suggestive of an abnormality. Often subtle and easily
overlooked. Look at paired structures for size, shape, color. The horse brain with
the abscess clearly exhibits asymmetry. Notice that the midline is shifted to the Rt
and that the Lt hemisphere is swollen. Also the boundary between grey matter,
distinct in the Rt, is blurred on the Lt side because edema fluid .
4.
Asymmetrical cerebral hemispheres with collapse, missing grey matter =
polioencephalomalacia.
23
a.
5.
Dog with polio lesions. This brain is asymmetrical with los of grey matter
on the Rt side that is clearly evident in the histopathology image
Asymmetrical cerebral hemispheres with collapse, discoloration in white matter
- leukomalacia or inflammation
a.
Goat w/ leukoencephalitis ~ CAEV. Here the lost tissue is on the Lt side.
It is grossly apparent there is a discoloration in the white matter that
corresponds to the inflammation and loss of white matter
b.
Horse with moldy corn poisoning.. Only the white matter is affected. It is
slightly yellow in color and flecked with hemorrhage which is associated
with the malacia or pan necrosis. As a general rule, malacia appears
yellow although there is nothing microscopically that explains this.
6. Asymmetrical cerebrum with swelling, and a mass or masses - something
added.Abscess (amorphous cut surface) neoplasia (organized cut surface);
primary (solitary) or metastatic (multiple).
a.
b.
c.
Horse w/ Rhodococcus equi abscess in Rt cerebral hemisphere. Typical of
cerebral abscesses; the pus is well demarcated from the adjacent neuropil.
The texture of the surface is consistent with pus.
Dog with oligodendroglioma. Here the mass is gelatinous because of the
myelin component to oligos and it is clearly well demarcated in the
microscopic image because these tumor tend to grow by expansion and
not invade or infiltrate as astrocytomas do.
Dog with metastatic hemangiosarcoma. Hemangiosarcomas stand out
because of the blood they contain. The multifocal nature tends to support
an interpretation of a metastatic process.
24
.
Dog with metastatic pulmonary carcinoma. This metastatic pulmonary carcinoma
is difficult to interpret in isolation because of the texture of the surface and the
hemorrhage. But in the context of a radiographic lung mass, it raises the suspicion
of a metastatic tumor.
7.
Translucence in the CNS = malacia and edema. Can be masked by other
pigments. This horse brain with leukoencephalomalacia exhibits the typical
blurred boundary between grey and white matter that edema causes. The lesion is
confined to the white matter which helps to interpret the disease. The congestion
and hemorrhage obscures the pale color of the lesion
a.
VII.
Horse spinal cord with EPM lesion - hemorrhage masks the edema
and malacia, the severity of which can be seen in the
histopathologic section.
GASTROINTESTINAL SYSTEM - hollow tubular organ system separated into
distinct segments with mucous membrane and muscular tunics. Dense white color due to
musculature may mask color changes in the mucosa. “No evaluation of the GI is
complete without direct visualization of the mucosa”
Fibrinonecrotic inflammation (pseudomembraneous or diphtheritic) with ulceration
is a common response to necrosis on mucous membranes. It often signals lytic viral,
bacterial, fungal, parasitic or ischemic disease.
1.
Focal, multifocal, segmental and diffuse ulceration with fibrinonecrotic
inflammation may have different implications as to pathogenesis. Ulcers are
usually depressed (something missing).
a.
Cow with a focal ruminal ulcer ~ mycotic ruminitis. There is a discrete
circular lesion that appears off colored but not ulcerated yet consistent
with acute necrosis. The red rim of reaction is caused by peripheral
congestion and hemorrhage. With time this lesion will ulcerate
b..
Cow with focal abomasal ulcer. The lesion is sharply demarcated and
depressed. Ingesta adheres to the surface because of the fibrin exudation.
25
The depth of the ulcer and pseudomembrane can clearly be seen in the
histological section. The deep ulcer with extensive loss of tissue and
pesudomembrane is typical of an older lesion.
2.
or
c.
Cow with multifocal esophageal ulcers ~ BVD. Similar to the previous
abomasal ulcer. These multifocal lesions are hyperemic and have a
pseudomembrane. But the distinction is in there multifocal distribution,
their location in the esophagus. Microscopically you can see the vascular
congestion which imparts the hyperemic appearance and the adherent
pseudomembrane.
d.
Snake with diffuse fibrinonecrotic colitis ~ salmonellosis. Abundant
fibrinonecrotic exudate in the lumen and adhering to the colonic surface
e.
Chukar with diffuse fibrinonecrotic typhlitis ~ histomoniasis. Similar to
the snake colon with a thick fibrinonecrotic membrane but only
histologically do we appreciate that there is an amebia penetrating deeply
into the cecal wall accompanied by intense inflammation (which is not
generally visible grossly) and eventually spreading to the liver through the
portal vasculature.
Lesions that cause thickening without
mucosal ulceration and necrosis (“Morocco
Leather”) may be caused by epithelial proliferation
granulomatous inflammation. Granulomatous
inflammation infiltrates beneaththe surface but may not
cause necrosis; = “space occupying inflammation”.
Looks like “sulci and gyri”.
26
a.
Sheep abomasum with “Morocco leather” appearance from glandular
hyperplasia ~ chronic ostertagiosis. The glandular proliferation produces
confluent swellings of glandular groups incompletely divided from each
other which causes the sulci and gyri appearance grossly. There is often
less inflammation and fibrosis than you would think.
b.
Dog with hypertrophic pyloric gastropathy. A cluster of polypoid masses
in the pylorus caused by glandular proliferation with dilated lumens causes
the same sulci and gyri appearance on the surface. This can be a
challenging lesion to fully appreciate when looking at endoscopioc
fragments of the surface unless you know what the gross appearance looks
like. Although there is often inflammation present in this lesion, the gross
effect is nearly all caused by the increase in number and size of the glands.
c.
Cow with Johne’s Disease - “sulci and gyri” and submucosal edema.
Notice there is no ulceration or fibrinonecrotic inflammation because there
is no necrosis of the epithelium. The non-necrotizing inflammation is
beneath the surface filling the lamina propria. Submucosal edema
contributes to the thickening and the Morocco leather appearance. It is
clear from the histopathology that the effect is caused by the inflammation
and edema with little additive effect from epithelial hyperplasia. “Morocco
leather”
“Sulci &
gyri”
d.
Cat with granulomatous enteritis ~ histoplasmosis. Grossly similar to
other cases of the Morocco leather appearance. In this case there is diffuse
granulomatous inflammation in the lamina propria accompanied by many
macrophages filled with Histoplasma organisms which thickens the
mucosa and no epithelial proliferation
e.
Horse with idiopathic granulomatous enteritis. The inflammation almost
completely effaces the entire wall of the GI. The submucosa is markedly
thickened and it penetrates through the muscular tunics and accumulates
on the serosal surface. All of the thickening is caused by inflammation that
27
throws the mucosal surface into “sulci and gyri”. DDx = LSA
e.
3.
Pig with proliferative enteritis - Lawsonia sp. The surface looks the same
but in this case the thickening is caused by epithelial hyperplasia as well
as inflammation in the lamina propria.
Lesions on the serosal surface = peritonitis or serositis, not enteritis. For me,
if the lesion is peripheral to the submucosa and affects the outer muscular tunics
and serosa, it peritonitis as in this case of sheep intestine with Oesophagostmum
sp.
a.
Cat with FIP. Although sometimes there is inflammation affecting the
mucosa in FIP in this case the histological section clearly demonstrates the
inflammation is primarily in the outer layers of the bowel wall
b.
Horse with hemomelasma ilei. Likewise this lesion typically affects only
the serosa. The hemorrhage and hemosiderin cause the dark color and the
firm adherent feel is caused by the granulation tissue component.
VIII. LUNG - a very complex organ with lobules, interstitium, many variably sized airways all
of which can reflect lesions. Symmetry and organization of lesions is important in
localizing disease. Physiologically dynamic size. A light pink color, light weight, dry
tissue.
King’s Law of Pneumonia
“If it’s not firm, it’s probably not pneumonia”
1.
Lesion distribution is important indicator of pathogenesis. Anterior ventral
patterns suggest an aerogenous portal and often = bronchopneumonia. If the
lesions look organized (symmetrical), they may be defining an architectural
subunit (lobule, airway etc).
a.
Rat with mycoplasmosis and a “symmetrical” (linearly arranged) AV
pattern of white “nodules” which are dilated airways filled with
suppurative exudate (= bonchiectasis/bronchiolitis).
28
Cow with suppurative bronchiolitis and necrosis ~ pasteurellosis. The pus shows
up well grossly as does the dilated septal lymphatics that are filled with fibrin.
Histologically the lunf field is very dense and filled with inflammatory cells,
hemorrhage and fibrin obscuring the open alveoli typical of normal lung.
2.
Multifocal poorly demarcated pale foci may be highlighting airways without
necrosis or pus; peribronchiolar and mucoid inflammation
a.
3.
Horse with heaves lesion - “mucoid or catarrhal bronchiolitis”. There is
no necrosis or pus but a distinct inflammatory reaction associated with
airways more in the wall and outside. The small airways are plugged with
mucus. The lack of necrosis blurs the distinction giving the poorly
demarcated appearance.
Hilar to diffuse patterns suggest a vascular portal and may indicate edema or
interstitial pneumonia. Interstitial pneumonia may be exudative or
nonexudative. The distinction between interstitial pneumonia and pulmonary
edema is extremely difficult to distinguish in a photograph. Interpretation depends
on how heavy the lung feels and is there clear fluid on the surface which cannot
be appreciated from just the gross appearance. Also low protein edema fluid may
be invisible in histopathology slides so your gross observations are very important
in making the final diagnosis.
a.
This lung from an okapi that died suddenly from an
anaphylactic react ion to an injection had extremely heavy and wet lungs
which may be appreciated grossly from the lights glistening on the surface
and the widened interlobular septae also had an enormous amount of clear
fluid run off the cut surface. Microscopically you do not see the edema
fluid. The alveolar septae are thickened with fibrin and perhaps fluid but
there is minimal cellular reaction.
29
b.
Sheep with lentiviral pneumonia - lungs are enlarged and were heavy and
the lung did not collapse which the rib impressions reinforce. The cut
surface was dry. That can be difficult to see in a photograph but easily
appreciated on the necropsy room. Microscopically the alveoli are free of
cellular exudate. Only lymphocytes around airways and in the alcveolar
septae are present. In this case and the last, there is no apparent fluid
present in the histopath section so you must rely on your gross
observations to confidently diagnose edema.
d.
Cow with acute bovine pulmonary edema and emphysema (“Fog Fever”).
Marked exudative interstitial pneumonia with edema. The emphysema is
caused by dyspnea due to edema and inflammation. The translucent
appearance is due to all of the emphysema but the lung was heavy and
dripped edema fluid when cut. Microscopically you can see the
emphysema as dilated interlobular lymphatics. The remainder of the lung
is dense with edema and acute inflammation with fibrin accumulating in
the alveoli.
30
4.
5.
Darker than normal lung can mean atelectasis. Diffuse or lobular
a.
Neonatal calf with incomplete inflation and interstitial edema due to
surfactant failure. Microscopically there are some lobules that are
relatively normally inflated but several that are dense with no apparent
open alveoli. Collapsed alveoli creates relatively more blood filled
capillaries together giving the dark color to atelectasis.
b.
Cow with irregular lobular atelectasis and edema of the interlobular
septae. In this case the microscopic sections exhibits suppurative exudate
in a small airway giving the reason for the atelectasis.
Diffuse dark red wet lung with miliary poorly demarcated white foci
(“Multifocality implies an embolic shower”)
a.Cat with FIP. The white foci are foci of immune complex vasculitis/interstitial
pneumonia on a background of congestion and edema ~ vascular leakage.
Microscopically the white foci are seen to be collections of fibrin and
lymphocytes consistent with a Type III immune complex vasculitis center
on the alveolar septae.
31
6.
Multifocal red lesions = petecchia; think vascular damage/septicemia, platelet
defect or DIC
b.
7.
Pig with erysipelas. What looks like a petecchia grossly is actually a small
localized focus of hemorrhage in the lung, likely centered on an alveolar
capillary likely caused by the bacteria
Multifocal white lesions (= embolic shower). Metastatic neoplasms or
abscesses. The multifocal lesions are easily seen grossly and well demarcated
because of the high contrast with the adjacent normal lung parenchyma
a.
Antelope with septicemic Aspergillosis and pyogranulomas.
Microscopically you can see discrete areas of pyogranuloma formation
with good contrast against the lung and on high power clearly visible are
the fungal hyphae typical of Aspergillus
b.
Rat with Corynebacterium kutcheri pyogranulomas
32
IX.
c.
Dog with Blastomyces dermatiditis. Here the foci appear to grow or blend
together as the process expands. High power histopathology bears out the
presence of the yeast organisms
d.
Dog w/ metastatic thyroid carcinoma
BONE - a dense white homogeneous hard tissue. Marrow cavities with active marrow,
vessels and hematopoietic elements provide good contrast but mostly there is poor
contrast among bone, cartilage, marrow fat and cellular infiltrate.
1.
Opaque white lesions could be necrosis (infarction), cellular infiltrate
(neoplastic or inflammatory) or bony proliferation; or all 3!
a.
2.
Cow rib with LSA - infiltrate of neoplastic cells, coagulation necrosis of
bone and hyperostosis. Architecture is preserved but there is opaque white
infiltration of tumor in the marrow as well as in the periosteum
Subphyseal lesions may indicate an embolic event ~ blood supply to the growth
plate. Capillaries fenestrated and turn back 180 degrees. Good site for septic
emboli/metastases
a.
Dog with metastatic carcinoma in proximal humerus. There is opaque
white-grey tissue with hemorrhage in the epiphysis which on
histopathological section resolves into mammary carcinoma with foci of
hemorrhage and necrosis that provide enough contrast to be seen grossly
b.
Foal with septicemic salmonellosis - multifocal phalangial subphyseal
infarction with osteomyelitis. Just beneath the growth plate there is a
distinct sequestrum with central necrosis that is rimmed by a fibrous
capsule. Although there is some residual inflammation, most has resolved.
The distinct white color is produced by ischemia in the sequestrum
33
d.Goat with CLA lesion in epiphysis and diaphysis - well demarcated exudate
bounded by a fibrous capsule. Similar to the sequestrum in the foal, the
opaque white area is caused by pus which on histopathology can be seen
to be laminated and surrounded by a capsule that was appreciated on the
gross.
d.
Foal metatarsus with linear ischemic necrosis below physis ~ septicemia
There is coagulation necrosis, microfracture and fibrosis. The narrow band of
subphyseal necrosis occurs in the classic location for a septic event. The zone is
pale and corresponds to the area on histopathology of necrotic bone and
inflammatory exudate. Below this there is a zone of microfractures and fibrosis
that is not as distinct on the gross but blends into the necrotic area. The periosteal
new bone on the lateral cortex can be seen gbrossly but is clearly distinctive in
histopath.
34
e.Foal metatarsus with wedge-shaped infarction and sequestrum~ vascular
thrombosis, infarction, necrotic trabeculae, fracture, fibrosis all from
septicemic salmonellosis. This infarct is also in the classic location for a
septic event hinting at the pathogenesis. However, this lesion is more
chronic as there has been time for the necrotic bone to separate from the
viable bone. The texture of the affected bone is similar to the surrounding
viable bone and is surrounded by a rim of reaction visible as a vague pale
area below the sequestrum that corresponds to the necrosis and fibrosis in
the histopath slide. The separation of the bone from the physis is nearly
complete and affects the entire growth plate.
3.
Fractured trabeculae may mask or distract you from the underlying problem
Always look for a process that may suggest a cause. In this photo of the bovine
vertebral body, the marrow cavity of the bone is discolored due to a combination
of necrosis and suppurative exudate characteristic of bacterial infection.
a.Horse with vertebral compression fracture and nutritional osteoporosis. Its easy
to see the shortened vertebral body and the disorganized trabeculae ~
compression fracture. It may be harder to appreciate that the trabecular of
bone are thinner than normal. This is partially due to “The Paradox” that
the bone is diffuse affected and there is no normal for comparison.
Histologically the problem of appreciating thin trabeculae is similar but in
this case there is no necrosis or exudate.
35
b.Dog with hypertrophic osteodystrophy (HOD) - which is really fracture
secondary to suppurative subphyseal osteomyelitis and hemorrhage. The
infraction and hemorrhage is visible both grossly as well as histologically
but the exudate is not easily seen on the gross specimen.
4.
Bony proliferation looks pretty much the same everywhere but the location
and characteristics can be instructive.
a.Cow humerus with growth retardation lattice (“The pause that refreshes”) subphyseal lateral trabecularization. (Longitudinal growth stops trabeculae
add bone laterally)
b.
Pig diaphyseal femur with cortical osteoporosis and nutritional fibrous
osteodystrophy (FOD). Improper Ca/P balance in feed ration. The details
of the linear band of cortex is difficult to see partly because the photo is
36
overexposed. Histopathology clearly reveals that the cortex is porotic but
accompanied by attempted hyperostosis that is poorly mineralized and
excessively fibrous (FOD)
c.
Pig distal femur with nutritional FOD. Fibrous stroma, few trabeculae
w/o mineralization. A distinct subphyseal white band is visible in the
femur but the details in the gross view are not clear. Histologically the
causae is clearly a zone of FOD where there is little or no marrow that
causes the white color.\
Horse maxilla with nutritional FOD (“Big Head”); abundant
unmineralized matrix is the “something added” that enlarges the maxillae.
Similar to the pig with FOD. The marrow cavity is pale because the
marrow elements are replaced by FOD. The maxilla is swollen because
something is added to the bone.
d.
e.
Cow humerus with diffuse symmetrical medullary hyperostosis
(osteopretosis) ; mineralized trabeculae replace and fill the marrow
cavity. The entire marrow is affected because normal remodeling does not
occur.
Cow rib with a fracture and callus. The outline of the fracture rib can be
seen grossly surrounded by pale dense white tissue. This is extensive
periosteal new bone induced by the fracture. In the context of the obvious
fracture, the pathogenesis of this bony proliferation is obvious
37
5.
Chondroid proliferation is a lot like bone but the location and how it grows is
instructive; its somewhat translucent though. The translucent retained cartilage
core in the metaphysis of a chicken is pathognomonic for tibial dyschondroplasia
a.
Dog femur with osteochrondroma - cartilage-capped polarized well
differentiated trabecular bone forming a mass. Dense white band under
cartilage is trabeculae and marrow elements. These zones can be easily
seen in both the gross and histoloic preparation with the translucent
cartilaginous nature of the tissue clear on gross examination. The
boundary between nolrmal cortical bone and the tumor is poorly
demarcated or blurred because both types of bone look similar.
c.Pig with osteochondrosis in the growth plate. This is similar to the lesion in the
chicken and indeed it is the same pathologic process. The distinct wedge
of growth plate cartilage is easily seen on both gross and histopathology.
38
Young horse with osteochondritis dessicans lesion on the articular facet and cervical instability
- the cartilage flap is separated from the subchondral bone by necrotic cartilage, plasma,
granulation tissue, new chondroid matrix all of which contribute to the discoloration. The lesion
stands out and is well demarcated from the adjacent healthy pure white articular cartilage
d.
Alpaca with ricketts ( = physeal osteodystrophy).
1.
2.
3.
4.
Elongated zone of hypertrophied cartilage
Retained cartilage core on the trabeculae
Trabecular microfractures
Wide osteoid seams
Notice how flared the rib is typical of rickets. This is a chronic lesion as
you can see there is much trabecular bone forming in the metaphysis
Alpaca costochondral
Healed rickets
39
Dense disorganized
trabeculae
Necrosis in the growth plate
Irregular thickening
Of the growth plate
40
Necrosis in the growth plate
Necrosis in the physis
41
42