Color Atlas of Small Animal Necropsy 1

.
Inasor
,
-
--
Color Atlas of
Small Animal Necropsy
First Edition
by
Richard E. Moreland, BS, DVM

Necropsy Coordinator
Antech Diagnostics
Irvine, CA
REMSOFT PUBLISHING
www.remsoftpublishing.com
2009
Statement of Copyright
Copyright 2009 by Remsoft Publishing. All rights reserved.
No part of this publication may be reproduced, stored in a retrieval

system, or transmitted in any form or by any means electronic,
mechanical, photocopying, recording or otherwise without the prior
permission of the publisher.
ISBN: 978-0-557-07597-3
102509V15
Table of Contents
CHAPTER 1: BASIC PATHOLOGY DEFINITIONS
Importance of Necropsy.. .... ......... ...... ................................... ............ .................. 7
Basic Pathology Definitions.. ........... . .. ................ ...... ..... .................. .................... 7
Basic Pathological Changes........... ....... ............................................................... 8
CHAPTER 2: Pre-Necropsy and General Considerations
When and Where To Do A Necropsy ........................................ ... .......................... 10
Basic Equipment ................................................................................................ 11
Protective Clothing ..................................... .......... ............................. .. ............... 12
The Submission Form ...................................................................... ... .... ............ 13
Ancillary Specimen Submissions ..... ... .............. ..... ................................. ......... .... 14
Common Postmortem Changes ............................................................................ 15
Describing Gross Lesions ......................................... .. ......................................... 17
History ............ .................... . .... ......... ............ ................................... ..... ............. 18
Routine vs. Cosmetic Necropsy ..................... ....... ... ............................. ................ 19
CHAPTER 3: THE NECROPV PROCEDURE
Overview ................... .. ................ . ............................................ ........ ....... .......... 21
External Exam .... .. ............................................................................................. 21
Limb and Skin Reflection .......................................................... .......................... 23
Icterus .. ..... .......... .. .......... .. ............. .... ..... ...... .. ................ ..... .... .................... 24
Removal of the Tongue and Trachea .................................................. ................ .. 25
Opening and Examining the Abdominal Cavity .................................................... 27
Feline Infectious Peritonitis ... '" ...... .......... ... ........ ..... .............. ..... ...... ....... ....... 29
Malpositions ........... .. ............................. .. ... .......... ...... ...... ........... ...... ......... .. 31
Opening and Examining the Thoracic Cavity .......................... ............................. 32
Removing the Heart and Lungs ........... ....... ............. ............................................ 34
Pneumonia ......................... ..... ....... ....... ................................. ........ .......... .... 37
Opening and Examining the Heart .......... .. .......................................................... 38
Thrombosis and Postmortem Clotting ...... ......................... ..... ............ ...... ... ...... 42
Removal and Examination of the Liver ............................ .... ... .. ............. ... .......... .. 44
Necrosis ................................... .. ................................................. ... ............... 46
Opening and Examining the Intestine .................................................................. 50
Examination of the Pancreas ........... .................................................................... 54
Removal and Examination of the Spleen .............................................................. 55
Hemangiosarcoma .......................................... ............................................... 57
Removal and Examination of the Adrenals ........................................................... 59
Removal and Examination of the Kidneys .................................................. .... ..... . 60
Amyloidosis ........................... ..... ........... ....... ................................................ 62
Removal and Examination of the Bladder ............................................................ 65
Removal and Examination of the Brain ................................................................ 66
CHAPTER 4: THE NECROPSY REPORT
Writing the Necropsy Report ........................ .......................... .......... ................... 70
Writing the Necropsy Conclusion ....................... .... ... ............................... ........... 70
CHAPTER 5: COMPLETE NECROPSY REPORT EXAMPLE.......................................... 71
Preface
Necropsy is the purest form of pathology. It involves the direct visualization of diseased organs and
tissues and can provide invaluable infortQation, not only about the animal being necropsied, but
about the cause, progression, and possible outcome of diseases in other patients. Necropsy results
can provide feedback on implemented therapies and confirm or deny clinical assumptions and
diagnoses.
(
Most people consider necropsy as just the gross dissection of a carcass. A complete necropsy,
however can be considered to be a 4 stage process.
The first stage is the pre-dissection preparation. Proper preparation includes consideration of
where and when the necropsy will be done, as well as the gathering of all necessary equipment
and supplies. Proper preparation significantly increases the efficiency of the dissection and the
prosector's ability to recognize and interpret lesions. Part of the pre-dissection stage is the
gathering and consideration of the history. History is of paramount importance, impacting-not
only the course of the dissection itself, but the final conclusions as well .
The second stage is the gross necropsy dissection itself. As with all diagnostic procedures, the
usefulness of a necropsy for drawing proper conclusions is only as good as the data (in the
case of necropsy, lesions) from which those conclusions are drawn. The primary goal of the
dissection stage of a necropsy is to dissect the carcass in a systematic manner to assure that
all important organs and tissues are visualized with maximal exposure to avoid overlooking
important lesions. Specimen collection for ancillary tests are also carried out during the
dissection stage.
.
The third stage is the handling of collected specimens taken during dissection for ancillary
testing. These specimens are submitted to the proper laboratories for processing, and the
results compiled on completion . The premier ancillary test associated with necropsy is
histopathology, however other tests such as microbiology, virology, and toxicoJogy may be very
important, even pivotal, in reaching proper conclusions.
The fourth stage is the writing of the necropsy report and the conclusions. The necropsy
report is the compilation of all of the data collected from the other three stages. The
conclusion is the comprehensive interpretation of all of the data, including the history, the
gross lesions, and the results of ancillary tests. The stronger the data from all stages, the more
accurate the conclusions.
The main goal of this book is to outline the proper standardized necropsy dissection procedure for
small companion animals . It is an attempt to increase the usefulness of necropsies in the clinical
setting by 1) insuring all gross lesions are visualized for interpretation, 2) familiarizing the
prosector with examples of common gross lesions, and 3) refreshing the understanding of basic
pathology concepts and pathogeneses important in the proper interpretation of necropsy findings.
Acknowledgements
First and foremost I would like to thank my family (Cynthia, Miles, Amber, and
Kristen) for their patience and understanding throughout this long and time
consuming process. Special thanks to my daughter Kristen for her help with
some of the book's graphics and cover art. I am very grateful to Dr. Earmie
Edwards of Lancaster Pet Clinic in Lancaster, CA for her invaluable help in
editing the manuscript. Lastly, I extend my appreciation to the professionals and
staff at Antech Diagnostic in Irvine, CA for their assistance, both direct and
indirect, on this project.
')
Chapter 1
Basic Pathology Definitions
THE IMPORTANCE OF NECROPSY

Necropsy is the animal analogy to human
autopsy. At its core, it is the systematic
dissection and examination of an animal
carcass to search for abnormal anatomical
changes (lesions) in the tissues. It is generally
used to determine the cause of death, but is
also used to chronicle disease progression.
Necropsy is the purest form of pathology. It
involves the direct visualization of diseased
organs and tissues (grossly and/ or
microscopically) and can provide a wealth of
information, not only about the animal being
necropsied, but about the cause, progression,
and possible outcome of diseases in other
patients. Necropsy results can provide feedback
on implemented therapies, and confirm or deny
clinical assumptions and diagnoses.
?bviously, a knowledge of the normal anatomy
necessary to make a distinction between
normal tissues and lesions. The proper,
standardized necropsy procedures are designed
to allow the prosector (the person doing the
necropsy) maximal exposure of organs for
maximum visualization of possible lesions.
IS
Obtaining the maximum benefit and

information from a necropsy requires not only
knowledge of the proper necropsy dissection
procedure, but knowledge of basic disease
processes. In particular an understandil).g of
basic pathology processes is paramount,
starting with standard basic pathological
definitions.
BASIC PATHOLOGY DEFINITIONS

Pathology is the study of disease .
Disease is any variation from the normal
morphology or physiology of a living organism.
Disease results from various causes, such as
infection, genetic defect, or environmental
stress, and is characterized by an identifiable
group of lesions, clinical signs, and/ or
symptoms. Diagnosis of disease is important
for proper treatment.
Anatomical pathology strives to diagnose
disease by concentrating on those anatomical
(morphological) changes in living tissue at the
gross and microscopic levels.
Clinical pathology strives to diagnose disease

by the use of tests on various body fluids and
body waste products. These include blood
plasma, urine, cerebrospinal fluid, sputum',
saliva, peritoneal fluid, thoracic fluid, and feces.
Lesions are recognizable morphologic
(anatomic) changes in tissues, either grossly or
microscopically.
Clinical signs are changes in behavior or
function that are observable by a third party
which indicates disease. Limping is an example
of a clinical sign which would suggest a broken
leg (a lesion). The terms "clinical signs" and
"symptoms" are often used interchangeably,
although technically symptoms are changes in
behavior or_function which cannot be observed
objectively by a third party. Symptoms can only
be detected by the individual (such as the pain
of a headache), however it may cause the
animal to behave in a way that is detectible as a
clinical sign (such as head pressing).
Morphologic diagnosis is a short phrase in
which the most important aspects of tissue
changes (either gross or microscopic) are
summed up and communicated.
The most important part of the morphologic
diagnosis is the naming of the lesion, with other
components giving specific information about
the lesion .
The elements of the morphologic diagnosis are:
Severity
Duration
Distribution
Anatomic site
Miscellaneous adjectives/modifiers
Lesion
Examples of a complete morphologic diagnosis:
Severe, acute, multifocal, renal tubular

coagulation necrosis"
Marked, chronic, focally extensive,
lymphoplasmacytic, cholangiohepatitis"
Chapter 1
Basic Pathology Definitions
An etiology is the cause of a disease or lesion.

Etiologies are numerous and diverse and
include infectious agents such as bacteria,
fungi, or parasites, and physical damage such
as blunt force trauma or thermal burns (to
name a very few). An etiologic diagnosis
names the etiology (ex. Histoplasmosis) .
Determining the etiology when possible is very
important as it often dictates proper treatment.
Inflammation is the vascular and cellular

response of the body to injury. Grossly,
inflammation is characterized by a swelling and
reddening of the affected tissue.
Microscopically, inflamed tissues feature the
presence of vascular congestion, edema, and
the presence of one or more types of
inflammatory cells. The types of inflammatory
cells present usually give some indication of the
cause of the inflammation.
Disease Names: When a condition features a

unique combination of lesions, clinical signs,
and/ or symptoms, that condition may be given
a name. For example, a disease of young
puppies caused by a morbillivirus that results
in pneumonia, encephalitis, and the formation
of eosinophilic inclusion bodies in epithelial
tissues has been named Canine Distemper.
Neoplasia (tumor, cancer) is the abnormal and

uncontrolled proliferation of body cells. All
tumors originate from some existing
tissue/body cell. Neoplastic cells usually try to
mimic their tissue of origin, which is an
important feature in helping to identify them.
Broadly, all body cells can be classified as
either epithelial or non-epithelial.
BASIC PATHOLOGICAL TISSUE

CHANGES (LESIC}NS)
Broadly speaking, the primary lesions detectib1e
grossly and/ or microscopically in body tissues
include degeneration, necrosis, inflammation,
and neoplasia.
Degeneration represents the gradual

deterioration of cells or tissue due to the loss of
specific cellular functions and manifested in
specific morphologic abnormalities.
Degeneration is usually reversible if the cause is
reversed. Examples include cloudy swelling
and hydropic change of hepatocytes, resulting
from the failure of plasma membranes sodiumpotassium pump to keep out water.
In naming tumors, those that arise from

epithelial cells and are determined to be benign
are designated with the suffIx -oma appended
to their tissue / cell type (hepatoma, mammary
adenoma). Those that arise from epithelial
tissue and determined to be malignant are
designated with the suffIx -carcinoma
(hepatocellular carcinoma, mammary
adenocarcinoma). Tumors of non-epithelial
origin and determined to be benign also use the
suffIx -oma (fibroma, osteoma). Tumors of nonepithelial origin and determined to be malignant
use the suffix -sarcoma (fibrosarcoma,
osteosarcoma). There are numerous exceptions
to these rules, with lymphoma and melanoma
being two glaring examples.
Necrosis is the morphologically recognizable

death of cells and/ or tissue. Necrosis is not
reversible. In general, changes in the nucleus
of cells are the primary indicators of necrosis.
These changes include pyknosis,
karyorrhexis, and karyolysis. A pyknotic
nucleus is one which has shrunken and
become very dense and dark, with little if any
recognizable chromatin. A karyorrhectic
nucleus is one which has fragmented into
several pieces. A karyolytic nucleus features a
slow loss of nuclear chromatin, resulting in a
very faded appearance.
Chapter 2
Pre-Necropsy and General Considerations
WHEN AND WHERE TO DO A

NECROPSY
The best time to do a necropsy is immediately
after the death of an animal to minimize
postmortem autolysis. When a necropsy has to
be delayed, the carcass should be refrigerated.
Refrigeration slows, but does not stop, autolysis
by slowing down enzymatic reactions. If
possible, avoid freezing the carcass. For one
thing, it is impossible to necropsy a frozen
carcass and thawing can take 24 hours or more
depending on the size of the carcass. More
importantly, however, ice crystals which form
during freezing damages the tissues at the
microscopic level making histopathology more
difficult~. However, if the necropsy is to be
delayed for a week or more, freezing is
preferable to the prolonged but continuing slow
autolysis of refrigeration,.
The necropsy location should have adequate
light, water, ventilation, drainage, and
provisions for cadaver storage and disposal. In
clinical settings, necropsies are often done on
an exam table, however these tables do not
provide for drainage of blood and fluids (except
over the side on to your shoes). Ideally, a
bathtub with a slatted grate or a wet prep table
should be used to allow drainage. Larger,
dedicated necropsy rooms may have a
customized stainless steel necropsy table.
Some feature downdraft ventilation in the table
to minimize odor. Wherever the necropsy is
done, the pro sectors should have easy access to
their basic necropsy equipment, a lined
biohazard garbage can for excised tissue,
formalin containers, and toxicology and
microbiology collection materials.
Pre- and post storage of the cadaver and
necropsy remains requires some form of
refrigeration. This can be problematic for large
animals. In larger dedicated necropsy rooms,
large walk-in coolers are often used. In smaller
necropsy rooms, an open top refrigerator may
suffice .
Figure 1: Wet prep table.
Figure 2 : Dedicated necropsy room and

necropsy table.
Figure 3: Specialized necropsy table with

downdraft ventilation and built-in disposal.
10
Chapter 2
BASIC NECROPSY EQUIPMENT

The choice of equipment for necropsy depends
in part on the size and type animal, the type of
examination requested, and the individual
prefer ences of the examiner. Most small animal
necr opsies will require:
One or more sharp boning knives
Scalpel
One or more pairs of specialized scissors
One or more pairs of specialized forceps
A ruler (plastic or metal) and a tape
measure
An ink pen/marking pen and note paper
Figure 1: Basic necropsy equipment
A plastic cutting board

Large syringes for collecting and measuring
fluids
Some means of cutting bone; either manual
hacksaw, bone shears, and/or a Stryker
saw.
Plastic or metal containers for temporary
viscera holding
G
A scale of some type for weighing organs
Formalin-filled container for collection of

tissues for histopath
Multiple, variably-sized Whirl-Pak or Ziploc
bags for fresh tissue collection
Digital camera (optional)
Supplies and containers for collecting
specimens (formalin jars and whirl-pak
bags)
Figure 3: 10% neutral

buffered formalin
Figure 2: The Stryker saw is a special

motorized saw used for cutting bone.
Essentially the same as a cast cutter, it is used
primarily for cutting the flat bones of the skull to
remove the brain. The blade oscillates, so it only
cuts bone and not soft tissue.
Figure 4: Whirl-pak
bag
Figure 5: Digital camera
11
Chapter 2
:PROTECTIVE
CL9THI~G
The wearing of protective clothing is meant to

protect the examiner from contamination with
blood, tissues and body fluids from the cadaver
that are potential carriers of infectious particles.
The best protective clothing should provide comfort
to the examiner while not compromising protection
against possible contamination. The primary
clothing should be either surgical scrubs or cotton
utility coveralls.
Ideally, a second outer covering such as a surgical
gown or a plastic apron should be worn to give
added protection. Unless they are disposable,
these articles must be washed clean and
disinfected after each use.
Figure 1: Scrubs
Figure 2: Plastic apron
Figure 3: Paper booties
Figure 4: Rubber boots
Disposable paper booties are good for providing

protection for your footwear from contamination,
however, many formal necropsy rooms are often
wet environments. If the necropsy is done in such
a wet environment, rubber boots should be worn.
Proper gloves are paramount when performing a
necropsy. Although latex surgery or examination
gloves are often used, they generally are not hardy
enough for a full necropsy on animals larger than
small rodents, young kittens, or puppies. A pair of
ordinary garden or kitchen latex gloves of
appropriate size are best for performing a necropsy
on most dogs, cats, and large animals. Compared
with the latex glove, the latter are less expensive,
more durable and provide greater protection. The
gloves should fit the hands and fingers of the
examiner without interfering with manual
dexterity and causing numbness.
Facemasks, face shields, or goggles are generally
not used doing a routine necropsy unless a
contagious zoonotic disease is suspected and
additional protection is deemed necessary.
Disposable paper facemasks cleared by the FDA
for use as medical devices have been determined to
have specific levels of protection from penetration
of blood and body fluids, keeping unlikely splashes
or sprays from reaching the mouth and nose. They
are not designed to protect against breathing in
very small particle aerosols that may contain
viruses.
Contrary to popular belief, face masks do not mute
odors. Odors from a recently deceased or quickly
refrigerated carcass should be minimal. Obviously
the more autolytic the carcass, the worst the odor
will be. Most prosectors generally get use to even
strong odors within the first few minutes of the
necropsy. In particularly autolytic and rank
carcasses, practical techniques such as placing
Vicks VapoRub ointment underneath the nostrils
to mask the odor can be employed.
Figure 5: Gloves
Figure 6: Disposable
paper facemask
12
Chapter 2
THE SUBMISSION FORM

The style and type of necropsy submission forms vary from laboratory to laboratory, depending on the mode of
document storage and retrieval system in use,
At a minimum, submission forms should include the following information:
Clinic Identification - Clinic name, ID#, address, phone number, doctor's name
Case Identification - Assigned necropsy case number, clinical case number, and the date of submission
and examination
Owner's Identification - Owner's name, address (optional), and phone number (optional)
Specimen Identification - Animal's name, species, breed, age, weight, and sex
Clinical History! - Includes the details of clinical findings, signs and symptoms observed (especially
perimortem signs), and the clinical diagnosis, Use the back or additional sheets of paper if necessary,
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Chapter 2
pre-~opsy
-----_.-----------------------------------------
and General Considerations
ANCILLAl{Y SPECIMEN SUBMISSIONS

Obtaining a definitive diagnosis from gross
lesions alone is often not possible and may
require the use of other ancillary laboratory
diagnostic procedures. Specimens for those
diagnostic procedures may be collected during
the necropsy as deemed necessary. Specimens
are often collected for:
e
Histopathology: Specimens should be

routinely collected from every major
organs in all necropsies
Microbiology: Specimens are only

collected when the history, clinical
diagnosis, or necropsy lesions suggest a
causative infectious agent
Toxicology: Specimens are only collected
when the history, clinical diagnosis, or
necropsy lesions suggest a toxic agent
(poison).
Histopathology
Histopathology is the primary ancillary test
associated with necropsy and is often the test
which provides the definitive answers in many
cases. Collection of histopathology samples
should be a part of all gross necropsies.
What Specimens To Collect: Ideally, samples

for histopathology should be collected from all
of the major organs. These include the heart,
lung, liver, spleen, kidneys, bladder, pancreas,
stomach, small intestine, large intestine,
thyroids, mesenteric lymph nodes, adrenals, and
brain. When obvious lesions are present in
these tissues they should of course be sampled,

however, when no lesions are present, 1 or 2
random samples should be taken from each
tissue. When it is not feasible to take samples of
all major organs, and there are no obvious
lesions, priority should be given to those organs
and tissues which correlate most with the
primary clinical signs observed (i.e. GI for
vomiting, lung for dyspnea, etc.). All specimens
should be immediately fixed in 10% neutral
buffered formalin. Formalin stops all autolysis
and hardens the tissue in preparation for being
cut thinly for microscopic slides. The
specimens should be collected as soon as
possible and should not be more than 1.5 cm
thick. Collected tissue should be placed in a
volume of formalin that is 10 times the tissue
volume to ensure proper fixation .
Microbiology
Specimens intended for microbiological
examination should be collected aseptically as
possible. One technique is to sear the surface
of the organ or tissue With a hot spatula, then
incise and collect the required material from the

deeper portion of solid organs " a bscess, or
coagulated masses. From this incision, sterile
swabs, tissue fragments, and aspirates may
then be taken. Place sterile swabs and aspirates
in a special transport media, especially if the
suspect organism is a fastidious one . The
choice of transport media depends largely on
the microorganism suspected to be present in
the specimen. If cultures are required, sterile
swabs should be used immediately before fully
exposing body cavities or openings. Hollow
organs such as segments of the gastrointestinal
tract are best handled by obtaining a loop of
intestine tied at both ends and placing them in
a sterile petri dish.
Toxicology
Materials for toxicological examination should
be collected without contamination by
chemicals being used during necropsy.
Chemicals that may contaminate the specimen
include fixatives, detergents and disinfectants
routinely used during necropsy. Although
different toxicants require specific samples for
chemical analyses, in general certain tissue
samples are best. These include whole blood
and sera, tissue blocks (about 100 grams) of
both liver and kidneys, urine, and stomach and
intestinal contents.
Contact the toxicology laboratory where the
samples will be sent to ensure that the right
specimens and amount ar~ collected and that
adequate precautions for handling and
preservation are observed.
It is important to note that most laboratories do
not have the capabilities to do "toxicology

screening", i.e. checking a single sample for a
wide range of possible toxins (like they do on
CSI). In general, specific tests can be run for
specific toxins, each test having it's own
associated cost. Obviously, random testing is
impractical, so it is important to have some idea
of what toxin to test for. The problem is that
most toxins cause death without producing
significant (or any) gross or microscopic lesions
which might give clues to the cause . Generally,
the most important information on which toxin
to check for comes from the clinical history
and/ or antemortem clinical signs. While
toxicology screening is not widely available,
toxicology panels, in which a group of individual
tests are run together, are common. A common
toxicology panel would include those
compounds commonly used in malicious
and/ or accidental animal poisoning such as
strychnine, arsenic, metaldehyde, and warfarin.
14
Chapter 2
COMMON POSTMORTEM CHANGES

When an abnormality is found during
necropsy, it must be judged whether it is an
' antemortem lesion or a postmortem
change. Antemortem lesions occurred before
death and therefore may have contributed to
the death or disease of the animal;
postmortem changes occur only after death
and therefore cannot have contributed to the
death of the animal. Judging which is which
is very important so that a proper
interpretation can be made.
Postmortem autolysis result from the ,,\r~
degradation of tissues associated with the
release of proteolytic lysosomal enzymes from
tissue cells when they die, as well as from the
action of postmortem bacterial enzymes
(putrefaction). Bacteria that form part of the
normal microbial flora in the intestine
proliferate soon after death. Invasion of
organs and tissue occurs primarily through
the vessels and lymphatics.
Postmortem autolysis can be slowed by
decreasing the animal's temperature via
refrigeration soon after death. Since most
lysosomal enzymes and bacterial enzymes are
temperature dependent, lower temperatures
slow (but does 'not completely stop) the
degradation of the tissues. Lower temperature
also inhibits bacterial growth. Freezing is not,
however, recommended because the ice
crystals which form damage cells and can
make this histopath difficult to interpret.' Still,
if the necropsy must be delayed a week or
more, freezing is recommended since the
continued degradation of tissue refrigerated
longer than would have even more harmful
consequences.
Figure 1: Hemoglobin imbibition of the small

intestine
There are several tissue changes which can

occur after death however the more common
postmortem changes seen at necropsy include
hemoglobin imbibition, pseudomelanosis, and
livor mortis.
Hemoglobin imbibition is the pinkish to

reddish coloration imparted to tissues due to
the lysis of red blood cells. It is most evident on
the outer surfaces of light-colored organs like
the intestine or brain, or on the inner surfaces
of large arteries or in the heart.
Bile imbibition is the greenish-yellow
coloration imparted to tissues in contact with
the gallbladder after death. This is usually seen
on the surrounding liver tissue, as well as on
loops of gut.
Pseudomelanosis is a blue-green to blackish
discoloration imparted to tissues due to the
action of bacteria on hemoglobin, resulting in
the formation hydrogen sulfide and iron sulfide.
This discoloration is often black within the
anaerobic environment of the abdominal cavity,
but is often more greenish in the more aerobic
environment of the skin.
Livor mortis (hypostatic congestion) is
caused by the settling of blood to the down side
of the animal's body due to gravity. This
gravitational settling of blood and body fluids
results in a darker reddish coloration of the
orgahS and tissues on the down side of the
cadaver.
Figure 2: Hemoglobin imbibition of the

brain
15
Chapter 2
Figure 3: Pseudomelanosis of the kidneys . In

the anaerobic abdomen, pseudomelanosis has
a black to dark blue-green hue
Figure 4: Pseudomelanosis of the pancreas
Figure 5: Pseudomelanosis in the ventral

abdominal skin. In the more aerobic
environment of the skin, pseudomelanosis has
a lighter green hue.
Figure 6: Livor mortis in the lungs. Blood

has settled in the left lung lobes due to gravity,
making them much darker than the right lobes
Figure 7: Pale pox-marking of the liver and

small gas bubbles due to bacterial putrefacation.
Figure 8: Though this looks like a myocardial

infarct, it is only an area of postmortem
autolysis
16
Chapter 2
DESCRIBING GROSS LESIONS

The general rule in recording necropsy findings is to be descriptive rather than interpretive.
Interpretation of lesions should be described in the diagqosis and/ or conclusion section.
When applicable tissues/lesions should be described by:
Shape/margins (irregular, circular, ovoid, oblong, polypoid, botryoid, wedge-shaped, papillary,
pedunculated, indistinct, well-demarcated, infiltrative, etc.)
.:IConsistency (hard, firm, gritty, soft, rubbery, spongy, viscous, friable, etc.)
~ Color (black, brown, mahogany, grey-green, red, tan, white, off-white, yellow)
lJSize (measured in centimeters)
::JDistribution and location (bilateral, unilateral, diffuse, focal, multiple, multifocal, patchy, etc.)
u Surface appearance (bulging, ulcerated, eroded, rough, reticulated, smooth, pitted, umbilicated,
verrucous, etc.)
Figure 1: "Lung and liver lobes are

characterized by multifocal, coalescing dark
circular lesions in the parenchyma. These lesions
vary in size from .2 to . Scm, and have a firm
consistency on palpation." (Metastatic
melanosarcoma)
FigUre 2: "The kidney features multifocal,

roughly triangular, pale areas in the cortex.
Each is bordered by a thin zone of reddening
and are approximately 1 x 2 em in size. " (renal
cortical infarcts)
Figure 3: "Both kidneys feature similar

pathological changes. Both kidneys are
enlarged with slightly distorted conformation.
There are multifocal, variably sized, pale, firm
masses present throughout the renal
parenchyma. Many blood vessels contain large
occlusive thrombi and scattered areas of the
parenchyma are reddened.
Gross Diagnosis: Bilaterql, multifocal irregular
renal masses with vp.scular thrombosis and
hemorrhage (Fungal infection - Phycomycosis).
17
Chapter 2
HISTORY
The importance of a good history cannot be overemphasized. Arriving at a proper diagnosis
and/or cause of death often depends strongly on the information gathered from the clinical history.
The history gives the prosector clues about which organ systems might be more important in the
disease process, warranting greater scrutiny. The history may suggest the examination of tissues not
normally evaluated during the course of a routine necropsy (spinal cord, inner ear, sinus cavities,
etc.). The history may suggest the collection of certain tissues for ancillary tests (toxicology,
microbiology, etc.) which are not normally collected during a routine necropsy. While the history does
not affect what is seen at necropsy, it will affect the interpretation of what is seen. Consider the
following examples.
Figure 1: Edema fluid in tissues appears as

a clear translucent, almost gelatinous
material. It can be seen here in the
subcutaneous tissues of a dog's forearm.
This is a good example of subcutaneous
edema.
Figure 2: A similar clear translucent fluid

layer is present here in the skin taken from
the dorsal back of a dog. Subcutaneous
edema would be the most likely
interpretation. Subcutaneous edema
suggests many possible pathogenic scenarios
including heart failure and/ or
hypoproteinemia. However, the history
indicated the animal was being given
therapeutic subcutaneous fluids in this area.
This fluid is, in fact, the result of that therapy
and not from pathological edema. Without
that history, many erroneous interpretations
of this lesion could have been made.
18
Chapter 2
ROUTINE VS. COSMETIC NECROPSY

A routine necropsy is the standardized, systemic gross dissection of the carcass whose goal is to
assure that all important organs and tissues are visualized with maximal exposure to avoid
overlooking important lesions . Since the aim of the technique is thoroughness, there is considerable
mutilation of the carcass.
A cosmetic necropsy is one where the dissection is not as extensive (or as mutilating) as in a routine
necropsy. It is commonly requested by owners who have a strong aversion to the mutilation of their
pet, and/or wish some post-necropsy viewing of the body. Such necropsies are not nearly complete
and may result in missed lesions, and, as such, are not recommended.
The cosmetic necropsy involves the bulk removal of the internal organs through a single ventral
midline incision. Visualization of organs and lesions can be difficult, and many of the cuts needed to
remove the organ have to be made blindly.
Cosmetic Necropsy Procedure
w
.J
.J
..J
..J
.J
.J
...l
.J
...l
...l
Make a single incision through the skin, muscles, and peritoneum in the ventral abdomen,
extending from the xiphoid process approximately the mid abdomen
Visualize the abdominal cavity through the incision and make note of any fluid accumulations.
Assess the orientation of the organs for possible malpositions .
Incise the diaphragm, making note of the presence or absence of negative pressure in the
thorax. Cut the diaphragm as completely as possible from its attachments .
Reaching as far as possible into the cranial mediastinum, cut the esophagus, trachea, and
cranial mediastinal vessels at the thoracic inlet
Remove the heart and lungs by pulling the esophageal-tracheal stump through the abdominal
incision, tearing or cutting them free from their dorsal attachments
Cutting the root of the mesentery will allow the liver, stomach, spleen, and small intestines to
be partially extracted through the skin incision . Cutting the colon as far caudally as possible
will allow full removal of the viscera .
Identify the kidneys and remove them. If visible, identify and remove the adrenal glands .
Identify and remove the bladder .
Drain any fluids remaining in the cavities. It is a good idea to place old newspapers in the
abdominal cavity so that it does not have a sunken appearance when closed .
Suture the abdominal incision to close the abdomen .
The brain is removed only if the history suggests a neurological problem.
o Make a midline incision between the eyes towards the level of the first cervical vertebra.
Dissect the skin and reflect all muscles covering the calvarium, cutting them towards the
sides.
u Using whichever bone cutting implement you have available, cut the calvarium to expose
the brain.
o Sever the spinal cord and lift the brain carefully. Cut all of the nerves at the base of the
brain. Tilt the head upward and backward to simplify removal of the brain from the cranial
cavity.
Q Replace the calvarium, reposition the muscles and skin, and suture the skin closed.
Examine the removed organs per the usual routine as normal and take whichever specimens
deemed necessary
~ e carcass should De returned to as near a pristine state as possible . Clean any blood and fluids
::-om the hair coat. Sutures should be continuous and as neat as possible.
19
Chapter 3
The Necropsy Procedure
OVERVIEW
STEP 1: EXTERNAL EXAM
The goal of the gross dissection phase of the

necropsy is the removal and close examination
of the major organs for lesions, and for the
collection of tissue samples for further ancillary
testing. In most animals this involves the
reflection of the front and hind limbs on one
side to get greater access to the thoracic and
abdominal cavities. Once the body cavities are
exposed, cursory examination of the organs is
performed prior to the complete removal of the
organs, with the more detailed organ
examinations performed outside of the body.
Position the carcass on the table in left lateral

recumbency. Carefully examine the animal's
exterior. Measure the carcass length from tail
base to nose-tip . Observe the eyes, ears, and
other body openings for the presence of
secretions or excretions, prolapse, and
abnormal coloring of mucus membranes.
Examine the hair coat, and note for the
presence of ectoparasites, areas of alopecia,
thickening of the skin, tumor masses, and
possible wounds. Palpate the continuity of bony
structures and look for evidences of fractures,
enlarged joints, and abnormal masses. Open
the mouth and examine the oral cavity (if rigor
permits). Many types of abnormalities are
evident from the external exam .
In a routine necropsy, there is not generally a

detailed dissection of the musculoskeletal
system, joints, spine or spinal cord, the eyes,
s inus cavities, or the inner ears unless the
history, clinical signs, or obvious necropsy
changes warrant detailed attention.
Figure 1: Traditionally, animals are positioned .

left lateral recumbency. This animal is
severely emaciated (cruelty starvation case).
Figure 2: Alopecia and hyperpigmentation

(demodecosis)
Figure 3: Sublingual oral fibrosarcoma
Figure 4: Blood in the anterior chamber of

the eye (hyphema)
21
Chapter 3
Figure 5: Glossal and gingival fungal lesions

(Cryptococcosis)
Figure 6: Glossal and gingival fungal lesions

(Cryptococcosis)
Figure 7: Corneal ulceration and

inflammation (ulcerative keratitis)
Figure 8: Marked oral, ocular, and nasal

planum icterus
Figure 9: A large sublingual cystic mass full of

collected saliva resulting from a ruptured
salivary duct (a sublingual mucocele or ranula)
Figure 10: Prior to the necropsy, x-rays of

the carcass can be very useful in helping to
localized broken bones and finding small
metal projectiles
22
Chapter 3
STEP 2: LIMB AND SKIN

REFLECTION
Grasp and lift the right forelimb upward and
cut all muscles between the subscapular area
and the rib cage to free the limb. Reflect the
leg dorsally. Hold the right hind limb up and
cut down to the hip joint. Cut the joint capsule
and the round ligament to free the head of the
femur. Continue cutting through the soft
tissue and reflect the freed hind limb to the
dorsum of the specimen. Inspect the hip joint
for signs of Degenerative Joint Disease or
other changes.
Reflect the skin both dorsally and ventrally,

exposing the subcutaneous tissues of the thorax
and abdomen. The subcutaneous tissues
should be inspected for hemorrhage, edema,
icterus, and other lesions.
Figure 1: Cut through the axillary region to

reflect the front limb, and through the
inguinal area to the coxofemoral joint to
reflect the hindlimb
Figure 2: Connect the exposed areas from

the two limb reflections and reflect the skin
off of the trunk and thorax dorsally and
ventrally.
Figure 3: Both left limbs have been reflected

along with the thoracic and flank skin to reveal
severe subcutaneous hemorrhage . This
i emorrhage resulted from the improper use of a
. eating pad.
Figure 4: Exposed coxofemoral joint. This joint

features a thickened capsule and eroded
femoral head cartilage with polishing of the
underlying bone (ebernation). These are all
signs of Degenerative Joint Disease .
Connect the skin opening made when reflecting

the front leg to the skin opening made when
reflecting the hind leg by cutting beneath the
skin along the right lateral thorax and abdomen.
23
..
Chapter 3
ICTERUS
A distinctive yellowing can occasionally be noted in the oral, ocular,

subcutaneous, or abdominal tissues on necropsy. This yellowing is
called icterus or jaundice and is caused by the deposition of the
compound bilirubin. Bilirubin is a normal breakdown product of
heme and icterus only occurs when it present in high amounts in the
blood stream. Normal heme metabolism starts with the phagocytosis
of old or damaged RBCs in the spleen by splenic macrophages.
Hemoglobin is removed and separated into its heme, globin, and iron
components. The iron is converted to ferritin and hemosiderin for
storage and recycling. The globin is broken down into amino acids for
recycling. The heme cannot be recycled and therefore must be
excreted. It is first converted to unconjugated bilirubin wtthin the
splenic macrophage, then transferred via the blood-stream to the liver
while attached to albumin. Within the liver cell it is conjugated with
glucoronic acid to become conjugated bilirubin. It is then put into
the bile via the bile caniculi, the small tracts between the hepatic
cords. Bilirubin is not a bile salt and does not aid in the breakdown
of fat; it is only in the biliary system as a means of disposal.
Figure 1: Oral, ocular, and
nasal planum icterus
The three primary mechanisms of icterus are
intravascular or extravascular hemolysis, liver
disease, and bile duct obstruction.
With hemolysis, the spleen is forced to deal with
an excessive amount of heme, either from
increased phagocytosis (extravascular hemolysis)
or hemoglobin released into the bloodstream from
lysed RBCs (intravascular hemolysis). With
intravascular hemolysis some of the heme in the
bloodstream (hemoglobinemia) will pass through
the kidneys and into the urine (hemoglobinuria).
Regardless of the type of hemolysis, the spleen
produces excessive amounts of unconjugated
bilirubin for processing by the liver. The liver is
unable to process all of this extra bilirubin which
consequently remains in the blood-stream and
Figure 2: Icterus of the subcutaneous and
eventually stains the tissues yellow. In liver
omental adipose tissue
disease, the liver is unable to process even the normal amounts of bilirubin resulting from normal
heme metabolism. The excess unconjugated bilirubin remains in the bloodstream and stains the
tissues yellow. In addition, the swelling of hepatocytes causes some obstruction of the bile caniculi,
resulting in a portion of the conjugated bilirubin gaining access to the blood-stream.
In biliary obstruction, the processed conjugated bilirubin from normal heme metabolism cannot gain
access to the biliary system, spills over into the bloodstream and stains the tissues yellow .
... .Ihto
8U""
Figure 1: Normal Heme Metabolism
24
Chapter 3
STEP 3: REMOVAL OF THE TONGUE,

TRACHEA, AND ESOPHAGUS
Make a skin incision from the mandibular
symphysis along the mid-ventral neck, to the
thoracic inlet. Reflect the skin as before to
expose the underlying structures .
The tongue must be removed to thoroughly
examine the buccal cavity. Cut the muscular
and tissue attachments of the tongue along the
inner surfaces of both sides of the mandible.
After cutting, the tongue can be pulled out
through the floor of mandible . Reflect the
tongue back to the pharyngeal hyoid bones,
continuing to cut all muscular attachments.
Cut through the hyoid bones by severing their
cartilaginous articulations (the cornu).
Figure 1: Make a submandibular skin incision

then reflect the skin
Once the tongue is reflected back, examine the palate, pharyngeal mucosa, and tonsillar tissues.
Continue dragging the tongue backward and dissect free the trachea and esophagus, cutting all
attachments back to the thoracic inlet. Identify and remove the thyroid glands and parathyroid
glands.
Figure 2: Cut the muscles

along each side of the
mandible
Figure 4: Expose the oretropharyngeal hyoid

b ones
Figure 3: Pull the tongue out through the

bottom of the mandible
Figure 4 : Cut the hyoid bones at their

cartilaginous articulation (the "cornu")
25

Chapter 3
Figure 5: Dissect the tissues covering the

ventral neck to expose the ventral trachea
Figure 6: Reflect the tongue, trachea, and

esophagus back to the thoracic inlet
Figure 7: Identify and remove the thyroids

and the parathyroid glands on the sides the
trachea.
Figure 8: Bilateral parathyroid hyperplasia due

to renal failure (renal secondary
hyperparathyroidism)
Figure 9: Marked tracheal hypoplasia (part of

Brachycephalic Syndrome)
Figure 10: Tracheal collapse (part of .

Brachycephalic Syndrome)
26
Chapter 3
STEP 4: OPENING AND EXAMINING

THE ABDOMINAL CA VITY
The abdominal cavity is opened by removing
the abdominal (flank) wall along the ventral
midline, the curve of the last rib, and dorsally
a t the level of the kidneys. Usually the
abdominal viscera is initially obscured by fatty
omentum which can be removed.
The viscera should be regarded in situ for
obvious lesions, fluid accumulations, relative
s izes, and malpositions, however, no detailed
examination is done until all organs are
completely removed. Inflammation of the
p eritoneal cavity (peritonitis) is generally
:1oted by the presence of reddening and
:-oughening of the serosal surfaces of the
n sceral organs, along with the presence of
~brinous tags.
_illy abdominal fluids should be collected and
~antified. Broadly, abdominal fluids can be
exudates, transudates, or btood. Blood in the
abdominal cavity is referred to as a
h emoabdomen. When large amounts of blood
are present, it is important to try and
:::etermine the source of the bleed before
:-emoving the abdominal viscera as this
~enerally makes it more difficult to determine
::"1e origin. The presence of transudates and
::"' rudates in the abdominal cavity is calleq
ascites. When transudates are
-..mcontaminated with blood they generally
:::'ave a clear yellowish (straw-colored)
2.flpearance. When blood is present it tints the
:::'uid red and is referred to as serosanguinous.
:are must be taken to avoid confusing actual
::-ank) blood with serosanguinous fluid.
3 ood's higher opacity and viscosity are
~en erally the best features to distinguish it
=:-om serosanguineous fluid.
Figure 1: Normal abdominal viscera
Figure 2: Enlarged liver (hepatomegaly),

extending well beyond the last rib
~e liver should be assessed in situ. Extension

- ell beyond the last rib is considered
~ep atomegaly.
-=-- e thoracic cavity should be assessed for

::egative pressure by inspection of the
.:.:aphragm. Normally it should be pulled taut
:.:ward the thoracic cavity. Puncturing it
"-""ould produce an in-rush of air and a
:=:axation of the musGle. If the muscle is
=--eady relaxed prior to puncturing it, it is
.=.dicative of pneumothorax..
Figure 3: Serosanguinous ascitic fluid.

Though it looks like blood, its low viscosity as
judged during the necropsy suggested it was in
fact blood-tinged fluid.
27
Chapter 3
Figure 4: Straw-colored ascitic fluid
Figure 5: Marked abdominal hemorrhage

(hemoabdomen)
Figure 6: Partially clotted straw-colored

abdominal fluid with white nodular lesions on
the serosal surfaces of the small intestine and
mesentery (Feline Infectious Peritonitis - FIP).
Figure 7: An unknown intra-abdominal mass

turned out to be a granuloma formed around
gauze left from a previous surgery. This
"gauze granuloma" is called a gossypiboma.
Figure 8: The diaphragm is pulled taut

against the thoracic cavity, confirming negative
pressure within the thorax.
Figure 9: Here, the diaphragm is relaxed,

indicative of air in the thorax (pneumothorax)
and a lack of negative pressure.
28
Chapter 3
FELINE INFECTIOUS PERITONITIS lFIP)

FIP is a serious, fatal, infectious but non-contagious viral infection of cats. It is caused by a mutation
of the feline enteric coronavirus. FIP causes widespread pyogranulomatous inflammatory lesions
throughout the abdominal visceral and/ or thoracic organs, and often a thick viscous yellow ascitic or
pleural fluid . The widespread infection causes weight loss, anorexia, non-responsive fever, and
eventually organ failure and death.
The disease pathogenesis involves complement fIxation and the release of vasoactive amines that
causes increased vascular permeability and endothelial cell retraction. In addition, antigen-antibody
complexes result in systemic vasculitis. These changes lead to the exudation of fluid and plasma
proteins typical of the effusive "wet" form , as well as organ damage due to impaired blood flow. The wet
form generally causes death within a few weeks. The "dry" form is more insidious, leading to death
over a much longer period (often years) .
Testing for the disease clinically can be problematic. Exposure to the virus with the production of an
antibody titer does not mean the virus has mutated and will cause FIP. Higher titers could be more
suggestive, however some cats with fulminant FIP may have no titer. Most tests involve "statistical
probabilities" that the infection is present. The albumin to globulin ratio (A/G ratio) is one such
statistical method. If the ratio is less than 0.8, there is a 92% statistical chance the cat has FIP. If the
ratio is greater than 0.8 there is a 61 % statistical chance the cat does not have FIP. Another statistical
method is Rivalta's Test. This test is performed by taking a test tube that is fIlled with distilled water
and adding a single drop of 98% acetic acid. Then, one drop of abdominal or pleural effusion is added.
If the drop dissipates, the test is negative. If the drop retains its shape, the test is positive. A negative
Rivalta's test is 97% accurate in ruling out FIP. A positive test is 86% accurate in ruling in FIP. Lastly,
the pleural or ascitic fluid can be checked for protein, with FIP infectious fluid generally having a value
of 3.5 mg/ dl or higher.
At necropsy, the wet form of FIP is characterized by a viscous yellowish fluid which generally clots soon
after the abdomen is opened. The serosal surfaces of the intestine, kidneys, liver, and pancreas are
often covered to varying degrees with small white nodules. These nodules represent pyogranulomas,
accumulations of macrophages and neutrophils. This reaction is more common to fungal infections
than to viral ones. In fact, fungal infections such as histoplamosis, cryptococcosis, blastomycosis, and
coccidiomycosis must be considered as part of the differential. To defInitively diagnosis FIP,
immunohistochemistry staining (IHC) of affected organs is necessary. In IHC staining, antibodies
specifIc for the feline coronavirus are attached to a stain and exposed to the affected tissue. If
coronavirus is present in the lesion, the antibody will stick and so will the stain, confIrming FIP
infection.
.... ~
Figure 1: The abdomen is fIlled with copious

amounts of a clear but viscous yellowish fluid
with tags of fIbrin throughout.
Figure 2: Soon after opening the cavity, the

fluid has clotted.
29
Chapter 3
FELINE INFECTIOUS PERITONITIS
(continued)
Figure 3: Small white nodular lesions on the

serosal surfaces of the small intestine.
Microscopically these nodules feature
accumulations of macrophages and neutrophils.
Figure 4: Small nodules and tags of clotted

fluid cling to the surface of the liver.
Figure 5: Small nodules and tags of clotted

fluid cling to the surface of the spleen.
Figure 6: Small white raised nodular lesions

(pyogranulomas) are evident in the
parenchyma of both kidneys.
, ;
30
Chapter 3
MALPOSITIONS
Volvulus/torsion involves a twisting of the mesenteric attachments of the stomach and/ or intestines.
This twisting action cuts off the outflow of blood from the intestine and stomach, causing the tissues to
suffer from a buildup of carbon dioxide and, eventually, a lack of oxygen. A common consequence seen
is bloating (gaseous dilation) of the stomach. The twisting also pulls the spleen from the left side of the
body to the right side and causes it to be engorged with blood.
Sometimes the intestine will telescope in on itself. This is called an intussusception. The blood
supply draining the telescoped portion is cut off so the cells die from lack of oxygen. Occasionally in
strong trauma cases (such a hit by car) the diaphragm will rupture allowing the intestines to move up
into the chest cavity (diaphragmatic hernia). These abdominal organs interfere with the normal
functioning of the heart and lungs.
Figure 1: Large congested spleen evident on the

right side of the body caused by rotation of the
stomach.
.
Figure 2 : Gas-filled and hemorrhagic stomach

subsequent to gastric torsion/volvulus .
Figure 3: Section of gut telescoped on itself

:ntussusception) . The telescoping cuts off
- enous drainage from the affected area and
~e effect on the tissue is identical to a
:;)[sion.
Figure 4: Localized intestinal torsion.
31
r
Chapter 3

THE THORACIC CAVITY
The thoracic cavity or the abdominal cavity can
be opened next. When opening the thoracic
cavity, first cut the right ribs dorsally a few inches
below their vertebral attachments using bone
shears. Next, cut along the costo-chondral
junction. The rib cage can then be removed by
cutting any remaining muscle or soft tissues.
Removal of the rib cage exposes the thoracic
organs in situ.
Upon opening the thoracic cavity, make note of
any fluid in the chest or in the pericardial sac.
Blood in the thoracic cavity is called
hemothorax. If there is fluid in the chest cavity
that is not blood, the term is hydrothorax or
pleural effusion. If the fluid is not blood, but is
red because it is "blood-tinged", it is described as
serosanguinous.
Rib .cage
Figure 1: The ribs are cut along the
costochondral junction and near their dorsal
spinal attachments
When air is present in the thorax it is called a pneumothorax and the lungs will usually be partially
collapsed. If air builds to positive pressure inside the thorax, it is called a tension pneumothorax,
and the lungs are usually fully collapsed (atelectic).
Figure 2: Normal heart and lungs exposed

after removing the rib cage
Figure 3: Blood accumulation in the thoracic

cavity (hemothorax)
32
Chapter 3
Figure 4: Serosanguinous fluid in the thorax

(hydrothorax/pleural effusion). Though the
fluid is red, it is evident that it is translucent
and not thick enough to be actual blood.
Figure 5: Milky white fluid in the thoracic

cavity (chylothorax). This condition is usually
seen in association with cardiomyopathy, and
rarely, (although it is a common misconception)
due to thoracic duct rupture.
Figure 6: Here the chest cavity is filled with a

-;-ery thick red exudate (often called a "tomato
soup" exudate) consistent with blood-tinged
.!Jus (pyothorax) caused by Nocardia.
Figure 7: Much of the intestines have

migrated into the thoracic cavity via a hole in
the diaphragm (diaphragmatic hernia). The
negative pressure in the thorax facilitates the
movement of intestines into the thorax even
through very small openings .
33
jjO
Chapter 3
STEP 6: REMOVING THE HEART AND

LUNGS
The esophagus should be separated from the
trachea and is reflected to the point where it
goes through the diaphragm into the stomach.
The aorta and vena cava are cut and the
trachea, heart, and lungs ("the pluck") are
removed en masse. The trachea should be
opened and followed as far irito the bronchi as
possible. Foamy fluid in the bronchi or
trachea indicates pulmonary edema.
Figure 1: The esophagus is separated from the

trachea back to the diaphragm
The external color of the lungs should be

assessed and all lobes palpated for firmness
and/or nodular lesions. At necropsy, the
appearance of "normal" lungs can vary from an
uncongested pale light pink, to an irregular
splotchy reddened congestion. Other grossly
evident findings include hemorrhage, edema,
neoplasia, and pneumonia.
Figure 2: The heart and lungs (the "pluck")

removed
'.
"
', .. 'l""
,"
..l.. ....
"".....
4 ..
~;.; :,~ -::~!
.
;
'.
~;.... ~/' .~..f
Figure 3: Normal, uncongested lungs
"
Figure 4: Normal uncongested lungs

(microscopic)
34
.hapter 3
Figure 5: Normal, irregularly congested lungs
Figure 6: Normal congested lungs

(microscopic). The vasculature is distended with
blood but the alveoli are clear
Figure 7: Foamy tracheobronchial fluid

= dicative of pulmonary edema
Figure 8: Pulmonary edema (microscopic).

Many alveoli contain eosinophilic staining fluid.
Figure 9: Pulmonary atelectasis
Figure 10: Pulmonary atelectasis

(microscopic). The alveoli are devoid of air and
collapsed.
35
Figure 11: Pulmonary emphysema
Figure 12 : Pulmonary emphysema

(microscopic) . The alveoli are dilated, ruptured,
and coalescing.
.
Figure 13: Pulmonary hemorrhage
Figure 14: Pulmonary hemorrhage

(microscopic). The alveoli are filled with blood
with no significant inflammation. Noninflammatory pUlmonary hemorrhage may
result from pulmonary thromboembolism,
lung lobe torsion, or coagulopathy.
Figure 15: "The Float Test" is used to help

determine the presence of common lung
conditions at necropsy. When placed in fluid
(fixative or water), normal aerated lungs
(congested or non-congested) will float on the
surface. Lungs with pneumonia or that are
atelectic will sink to the bottom. Fluid-filled
lungs (pulmonary edema) will "float heavy",
suspended somewhere between the surface
and the bottom. This picture illustrates all
three examples .
36
1
Chapter 3
PNEUMONIA
Pneumonia is inflammation of the lungs. It is
characterized by the accumulation of
inflammatory cells and fluid within alveoli.
Grossly, it can be difficult to distinguish
':Jetween inflammation from physiological or
passive congestion of the lungs since both
::eature a reddening of the lung parenchyma.
hree gross characteristics of pneumonia can
~elp in distinguishing the two. First, since
pneumonia is usually caused by bacteria which
enter the lungs via the trachea
(bronchopneumonia), the inflammation starts
';1;'here the bacteria initially settle in the lungs.
This is usually the anterior and ventral regions

of the lungs, giving the reddening an "anteroventral" distribution. Non-inflammatory
congestion is irregular and/ or diffuse. Second,
because of the accumulation of inflammatory
cells in the alveoli, there is little or no air in the
alveoli, reSUlting in a firm feel to the
parenchyma (consolidation). Third, the lack of
air in the lungs in pneumonia causes the lungs
to sink when placed in water or fixative,
whereas congested lungs will still float.
Figure 1: Gross bronchopneumonia. Note

:he pattern of reddening in the anterior and
7entral regions of the lung lobes
Figure 2: Gross bronchopneumonia. Note

the pattern of reddening in the anterior and
ventral regions of the lung lobes
Figure 3: Pneumonia (microscopic). Note

:..'-1e presence of inflammatory cells filling the
" veoli. Palpation of this tissue would result in
?. firm feel, and there is no air to allow it to
::'oat when placed in liquid.
Figure 4: Close-up of pneumonia lung. The

alveoli are filled with inflammatory cells and
devoid of air.
37
---
..
.--
--------------------------------------------------------------------------------------------------~
Chapter 3

THE HEART
The outer surface of the heart should be
examined before opening. Assess the sharpness
of the apex; rounding may suggest hypertrophy
or dilation. If a scale is available, the heart
should be weighed. The normal heart weight (g)
to body weight (kg) ratio is 7.4 0.2 however,
care must be taken when interpreting this
number as certain factors can affect the formula.
In a fat or obese animal, the ratio will be skewed
low, where as in a thin or emaciated animal it
will be skewed high.
One of the most widely accepted methods of
opening the heart is by following the normal path
of blood flow. Beginning in the caudal vena cava
and/or entrance to the right atrium, a V-shaped
incision is made by cutting down through the
right atrio-ventricular valve, following the interventricular septum to the bottom of the ventricle,
then back to the base of the heart and out
through the pulmonary valve. This cut produces
a V-shaped flap which can be lifted to expose the
right ventricle, right atrium, and tricuspid valve.
Figure 1: Grossly normal heart. Note the

sharp apex.
The left side of the heart is opened in a similar

way. A single incision is made through the left
atrial free wall, down through the lateral border
of mitral valve and the left ventricular free wall
all the way down to the apex. A cut is then
made through the medial leaves of the mitral
valve into and out of the aorta.
Sometimes a better in situ visualization of the
valves, as well as an opportunity to compare the
relative thickness of the right and left ventricular
myocardium, can be determined by doing a
single longitudinal cut. The cut starts through
the middle of the right ventricle and proceeds
through the RV lumen, the interventricular
septum, the LV lumen, and finally through the
LV free wall.
Figure 2: Very rounded apex indicating

either hypertrophy or dilation
Figure 3: To open the right side of the heart,

cut into the right atrium via the vena cava,
then down through the tricuspid valve to the
bottom of the right ventricle.
Figure 4: Cut along the septum and exit the

right ventricle through the pulmonary artery.
38
hapte r 3
Figure 5: The flap produced allows

visualization of the right atrium, ventricle, and
rricuspid valve.
Figure 6 : To open the left heart, cut into the

left atrium via the pulmonary veins and
continue the cut through the mitral valve and
along the free wall to the bottom of the left
ventricle .
Figure 7: Cut through the mitral valve to exit

:...'-1e left ventricle through the aorta.
Figure 8: Alternatively, by lining up on the

middle of the right ventricle, a single cut
through the right ventricle, interventricular
septum, and the left ventricle will allow a better
comparative visualization of the chambers . In
this normal heart, note the 3: 1 ratio of left
ventricular thickness to right ventricular
thickness. Also note the relatively tubular
shape of the left ventricular lumen, not a round
or bowl shape as is the popular miscoriception.
39
Chapter 3
Figure 9: The nodular thickening noted in the

mitral valve of this partially fIxed heart is
Valvular Endocardiosis (Degenerative Mitral
Valve Disease). In this condition, the heart
valve (usually the mitral) is thickened by the
proliferation of the valve's fIbrous and
myxomatous tissue. This proliferation distorts
the leaves of the valve, giving them a nodular
appearance. This change is usually mild and is
a common incidental fInding at necropsy of no
clinical consequence. It can get worse with age,
however, and can be signifIcant in older dogs.
When severe, the valves do not close properly
and blood regurgitates into the left atrium on
systole (causing a systolic murmur). The
eventual consequence of this regurgitation is
chronic heart failure . King Charles Cavalier
Spaniels have a very high genetic disposition to
develop this condition at an early age.
Figure 10: Severe left ventricular hypertrophy

is evident in this partially fIxed heart. The
lumen is extremely narrowed by the marked
thickening of the septum and free wall.
Cardiomyopathy (with a big C) refers to
primary cardiac disease in which some
inherent (and idiopathic) defect in the heart
muscle itself results in hypertrophy or dilation
of the myocardium (Hypertrophic or Dilative
Cardiomyopathy). Secondary dilation or
hypertrophy (due to valvular defects, septal
defects, hypertension, etc.) does not constitute
Cardiomyopathy.
Figure 11: Severe left ventricular dilation.

There is thinning of the free wall and septum
and smoothing of the endocardial surface. The
lumen shape is more bowl-like as opposed to a
more normal tubular shape.
Figure 12: Heart-based tumor

(chemodectoma)
40
a !UM
Chapter 3
Figure 13: Metastatic thyroid carcinoma
Figure 14: Metastatic salivary gland

carcinoma
Figure 15: Small metal projectile (bb)

?enetrated the heart and lungs causing marked
::::'emorrhage
Figure 16: Subendocardial hemorrhage on

the papillary muscle
41
..
,
Chapter 3
THROMBOSIS vs. POSTMORTEM

CLOTTING
During the necropsy examination,
differentiating postmortem clotting from
antemortem clotting is very important. Clots
are common in the heart and larger vessels.
Thrombi are always pathological and
significant, while postmortem clots hold no
significance.
The normal clotting mechanism in the living
animal leads to the formation of fibrin to plug
openings in blood vessels to prevent bleeding.
When clotting occurs within the vascular
system in response to endothelial injury, the
resulting clot is called a thrombus and can
block blood flow to tissues and cause necrosis
(infarction). Blood also clots after death in
response to the release of tissue factors. These
are called postmortem clots. Distinguishing
antemortem clots (thrombi) that are
important in causing disease from postmortem
clots that are of no significance is important
during necropsy. Even though they are both
clots, the mechanism of their formation makes
them physically distinguishable from each
other. Postmortem clots form as a solid net of
fibrin within the vessel, entrapping large
numbers of red blood cells. Consequently
postmortem clots are dark red in color, they
have a gelatinous consistency, and are smooth,
wet and shiny. They are also usually wellmolded to the shape of the vessel. Thrombi are
formed by the sequential deposition of platelets
and fibrin, forming a layered effect without the
incorporation of significant numbers of red
cells. Consequently thrombi have a friable
("crumbly like a cookie") consistency, and have
a paler, drier, rougher appearance. Because of
this friability, pieces easily break off the main
thrombi and float down the bloodstream as a
thromboembolus, and can lodge in smaller
vessels, block blood flow, and cause an infarct.
Two different types of postmortem clots can
occur after death. The most common type is
called a "currant jelly" clot. This is the very
common, red, shiny, and smooth gelatinous
clot. If clotting is delayed for some reason after
death, the stagnant blood will have a chance to
separate (the red cells settle to the bottom),
leaving a yellowish layer of plasma at the top.
When clotting ultimately occurs, a currant jelly
clot is formed at the bottom, and a plasma clot
(called a "chickenjat clot") is formed at the
top. The appearance of chicken fat clots in
most animals denotes a possible clotting
disorder since postmortem clotting was delayed.
Horse red blood cells, however, normally settle
rapidly due to rouleaux formation so chicken fat
clots in horse are inconsequential.
Figure 1: Two "currant jelly" postmortem clots

within the heart chambers. Note the smooth
dark red, shiny, and gelatinous appearance.
Figure 2: Microscopically, currant jelly

postmortem clots consists almost exclusively of
red blood cells with a few entrapped white blood
cells. Fibrin is usually not clearly recognizable.
Figure 3: In this heart, both a currant jelly

clot and a chicken fat clot are evident. -Both
are postmortem clots.
42
hapter 3
THROMBOSIS vs. POSTMORTEM CLOTTING (continued)
Figure 4: Two thrombi attached to the mitral

valve. Valvular thrombi are often caused by
bacterial endocardial damage and constitutes
"vegetative endocarditis".
Figure 5: A thrombus attached to the aortic

valve. Note the pale, dull and rough
appearance.
Figure 7: Viewed here is an opened left

pUlmonary artery containing one leg of a
s addle thrombus (arrows) . The thrombus
started at the junction of the pulmonary trunk
then extended into the lungs along each
branch (pulmonary thromboembolism).
Figure 6: Microscopically, thrombi often have

a layered appearance (called "Lines of Zahn").
Here, a thrombus nearly occludes a blood
vessel. The dark purple blobs are bacteria (this
is a "septic" thrombus)
43
Chapter 3
STEP 8: REMOVAL AND EXAMINATION

OF THE LIVER
After removal of heart, lungs, and the
diaphragm, the abdominal viscera can be
removed systematically, starting with the liver.
Before removal of the liver, the bile duct
connection to the duodenum should be
checked for patency. Make a small slit in the
proximal duodenum and identify the major
duodenal papilla. Squeeze the gallbladder to
see if bile can be easily expressed through the
duct and out the papilla. If not, the bile duct
should be opened and traced back up to the
gallbladder. The liver can then be removed by
cutting the bile duct and all diaphragmatic
and body wall connections.
After removal of the liver, the size,
conformation, and color should be assessed.
Figure 1: The bile duct is checked for patency.

As the gallbladder is squeezed, note the stream
of bile from major duodenal papilla (arrow)
Figure 3: Focal area of hepatic necrosis
Alternating pale and dark areas can produce a

"reticulated" or "nutmeg" appearance.
Prominent fat infiltration can produce a very
yellowish liver. Obviously, any masses or
nodules should be noted.
After assessing the surface, the liver should be
"bread-loafed", cut into small 1-2cm slices
from end to end, to expose possible lesions
deep within the pencltyma that are not
visible on ,the surf~c~,/fhe gallbladder should
be opened to assess the character of the bile,
the presence of any stones or concretions, and
the possibility of hyperplasia or neoplasia of
the gallbladder epithelium.
Figure 2: Grossly normal liver
Figure 4: Severe hepatic lipidosis
44
Chapter 3
Figure 5: Hepatic nodular hyperplasia
Figure 6: Nutdleg liver (chronic passive

congestion)
Figure 7: Gallstone in the gallbladder
Figure 8: Hepatic biliary adenocarcinoma
Figure 9: Metastatic hemangiosarcoma
Figure 10: Hepatocellular carcinoma
45
'f'
Chapter 3
NECROSIS
Necrosis is common in the liver and other
tissues and must be properly identified and
categorized when it occurs.
Necrosis is the death of cells within the body
that occurs prior to somatic death (death of the
animal). It can be recognized both grossly and
microscopically, and varies depending on the
type of necrosis. The types of necrosis are
coagulative, caseous, and liquefactive.
Coagulative necrosis is defined as necrosis

where cellular and/ or tissue architecture is
preserved (the cells still look like cells).
Grossly, coagulative necrosis is usually
characterized by a distinct paleness of the
tissue. Depending on the degree of hemorrhage
present, the tissue may be red or might have a
red border. One of the most common causes of
coagulative necrosis is hypoxia/ischemia, which
in turn is often due to loss of blood supply. An
area of necrosis due to hypoxia is called an
infarct. Microscopically, coagulative necrosis is
characterized by dead cells, recognizable due to
distinct nuclear changes. The nuclear changes
that represent undeniable cell death 'are
pyknosis, karyorrhexis, and karyolysis.
Pyknotic nuclei are shrunken, dense and dark.
Karyorrhectic nuclei are fragmented into several
pieces. Karyolytic nuclei have lost much of
their dark staining, resulting in either a pale
n ucleus or no nucleus at all. Caseous necrosis

is necrosis where the dead tissue is still present
but has degenerated into an unrecognizable
matrix. Grossly, caseous necrosis has a dry,
cottage cheese-like appearance and texture.
Microscopically, caseous necrosis is a
eosinophilic granular material with no
recognizable cells. Certain types of bacteria are
often the cause of caseous necrosis including
/:::
b
.
Myc~bacterium and somf Coryne actenum
speCles.
~/
Liquefactive necrosis is necrosis where the

tissue cells have been completely liquefied,
leaving only fluid, inflammatory cells, and
possibly the causative agent. Liquefactive . .
necrosis is the most common type of necrOS1S m
the brain due to the high water and lipid
content. In other tissues, liquefactive necrosis
usually only occurs due to infections by certain
bacteria with very powerful enzymes which can
liquefy tissue ("pyogenic" bacteria). Because of
these bacteria, neutrophils are generally
present in high numbers within the liquefied
tissue. Grossly, liquefactive necrosis is
characterized by a cavity filled with a creamy
white, viscous, and often foul-smelling fluid
(pus). When this cavity is well-defined and
walled off with connective tissue, it is referred to
as an abscess. Microscopically, no tissue cells
are present, only the neutrophils and the
bacteria.
nuclear changes
pyknosis
karyorrhexis
normal
karyolysis
Figure 1: The pale regions of this muscle are

necrotic. Aside from the color change, the
tissue architecture is still present (the affected
areas still look like muscle) so this would be
coagulative necrosis.
Figure 2: Microscopically, cell death in

coagulative necrosis is identified primarily by t~e
presence of particular nuclear changes (pyknOS1S,
karyorrhexis, and/or karyolysis). These changes
occur together but independently in the same
tissue and do not represent a continuum (ie.
karyorrhexis does not follow pyknosis, etc.).
46
vhapte r 3
.N ECROSIS (continued)
Figure 3: Coagulative necrosis. The cortex

:eatures mUltiple infarcts, roughly triangular
pale regions bordered by a thin zone of red
~ emorrhage
Figure 4: Microscopic coagulative necrosis of

the liver. Many necrotic cells have pyknotic
nuclei (white arrow) and karyolytic nuclei (green
arrow). There is also an increased cytoplasmic
eosinophilia and vacuolization, however cellular
architecture is still maintained .
Figure 5: Coagulative necrosis. Clear

3idence of cell death is apparent (pyknotic
",--'1 d karyorrhectic nuclei), but the cellular
:;:-chitecture is still intact
Figure 6: Coagulative necrosis can also

represent preservation of,tissue detaiL In this
kidney, renal tubular cells are unrecognizable
however the tissue/tubular shape
(architecture) is preserved.
47
Chapter 3
NECROSIS (continued)
Figure 7: Grossly, caseous necrosis has a

dry, granular, "cottage cheese-like"
consistency.
Figure 9: Grossly liquefactive necrosis is

often characterized by a well-circumscribed
walled-off cavity containing a creamy pale
foul-smelling viscous liquid (pus) forming an
abscess.
Figure 8: Microscopically, caseous necrosis

is generally a pink, amorphous matrix with no
recognizable cells or cellular structure
Figure 10: Microscopically liquefactive

necrosis features completely loss (liquefaction)
of the parenchymal tissue, with only
inflammatory cells (usually neutrophils)
remaining.
48
hapte r 3
NECROSIS (continued)
~e
microscopic pattern of necrosis in an organ

be helpful in determining the cause. In the
iver, necrosis can occur randomly throughout
::he liver, or in one of three zones of the hepatic
:;.an
~obule.
~andom necrosis of the liver is usually
a s sociated with infectious organs which gain
access to the liver via the vascular system. This
~7pe of necrosis is usually associated with
:""-illammation, though some viral infection may
':Je non-inflammatory.
?atterns of necrosis of the hepatic lobule are

::he result of its microanatomy and function.
~e hepatic lobule is an irregular hexagonal
structure with a large vein at the center (the
~entral vein) and portal regions at the
:;>eriphery. The portal regions consist of the
::epatic artery (bringing oxygenated blood to the
iver), the hepatic vein (bring unoxygenated but
u trient-rich blood from the GI tract), and a bile
Qu ct. Oxygenated blood which enters via the
i epatic artery drains through the sinusoidal
sp aces into the central vein, where it is
eventually dumped into the vena cava. Because
:..~ e hepatocytes around the central veins are
::ne last to receive oxygenated blood, they are
extremely susceptible to hypoxia and anemia,
Figure 1 1: Centrilobular hepatic necrosis
Centrilobular necrosis is most commonly

associated with anemia of any cause, or with
passive congestion of the liver due to righ t sided
heart failure. Centrilobu lar hepatocytes a lso
contain the highest concentrations of mixed
function oxidases (MFOs). MFOs are enzymes
responsible for the metabolism of chemical
substances in the blood . Metabolism of some
substances may produce toxic metabolites
which may in turn cause degeneration and
necrosis of the centrilobular hepatocytes.
Substances which can cause this pattern of
necrosis include acetaminophen and aspirin.
Mid-zonal necrosis, necrosis in region of the
hepatic lobular between the centrilobular region
and the periportal region , is uncommon but is
seen in rare toxicities (like hexacholorophene in
cats).
Periportal necrosis occurs in toxicities where
the toxin does not require metabolism by MFOs,
but is already toxic when it enters the liver
through the hepatic artery or vein. Because the
periportal hepatocytes are the first affected,
they suffer more degeneration and necrosis
than the mid-zonal or centrilobular regions.
This pattern of necrosis can be seen in cer tain
poisonous, alkaloid-containing plants.
Figure 12: Periportal hepatic necrosis and

fibrosis .
49
Chapter 3
The Necropsy P r ocedure
STEP 9: OPENING AND EXAMINING OF

THE INTESTINE
The esophagus, stomach, small intestine, large
intestine, pancreas, and spleen are removed en
masse by cutting the diaphragm and the root of
the mesentery. The colon is typically cut as it
passes into the pelvic canal. If pathology is
suspected in the pelvic canal, it is opened by
cutting the pubic and ischial bones on both
sides, allowing the removal of the floor of the
pelvis.
Once the viscera is removed, the spleen is cut
away and set aside for later examination. The
pancreas is also examined, cut away from its
duodenal attachments and examined.
Figure 1: Remove the GI tract by cutting the

root of the mesentery (marked by the scissors)
Figure 3: Full GI tract. These small intestines

are thickened, hyperemic, and have a slightly
pitted surface, all evidence of inflammation .
To facilitate opening of the gastrointestinal (GI)

tract, all of the mesentery is cut away from the
bowel loops, thereby allowing the entire tract to
be laid out straight. Opening starts in the
esophagus, proceeds along the greater
curvature of the stomach, and extends
throughout the length of the small and large
intestiI}e. -Stomach and intestinal contents-are
assess~d, along with the surface mucosa. Any
foreign o,bjects and/ or parasites should be
identified -and their possible impact on
gastrointestinal function assessed. The entire
tr:act should be assessed for inflammation,
ulceration, thickening, and/or neoplasia.
Figure 2: When necessary, open the pelvis by

cutting the pubic (white arrow) and ischial
bones (green arrow) on each side to remove the
floor of the pelvic canal.
Figure 4: The mesentery has been cut away

to facilitate opening the intestines.
50
Chapter 3
Figure 5: The intestine and liver are knotted

together in a tight ball by fibrin (fibrinous
peritonitis)
Figure 6: Multifocal petechial hemorrhaging

in the mucosa of the small intestine due to
hookworms (Ancyclostoma caninum).
Figure 7: Roundworms (Toxocara canis) in

the small intestine
Figure 8: Whipworms (Tricuris vulpis) in

the large intestine
Figure 9: Severely hemorrhagic intestine

'Parvoviral Enteritis)
Figure 10: Hemorrhagic mucosal surface of

jejunum (Parvoviral Enteritis)
51
Chapter 3
Figure 11: Markedly thickened cross-section

of small intestine with multifocal pale yellow
necrotic regions . Microscopically, there was
prominent pyogranulomatous and necrotizing
enteritis with large numbers of hyphal fungal
organisms (Phycomycosis)
Figure 12: Neurofibrosarcoma on the colon
Figure 13: Thickened region of the jejunum

with focal perforation and leakage of intestinal
contents.
Figure 14: Section of intestine from Figure 13

opened up. Microscopically there was an
infiltration of neoplastic lymphocytes
(lymphosarcoma) which weakened the wall
and led to the perforation.
52
Chapter 3
Figure 15: Severe esophageal inflammation

and ulceration from gastric reflux (Gastroesophageal Re flux Disease or GERD)
Figure 16 : Multifocal gastric ulcerations and

hemorrhage (injudicious NSAIDS use)
Figure 17: Gastric foreign body
Figure 18: Gastric mucosal calcification due

to renal failure.
Figure 19: This stomach was filled with

clearly recognizable pieces of sausage. This was
:1ot deemed important until considered with
:he history. The owner stated that she fed the
animal a strict commercial dog food diet. This
~ ade the presence of sausage suspicious. The
animal had died acutely with no clinical signs.
Closer inspection of the sausage revealed small
:?ellets (see insert) consistent with Strychnine
:?ellets . Subsequent t~xicology was positive for
""'trychnine. The history was pivotal in this
::ase as it affected the consideration of a
seemingly benign finding .
53
Chapter 3
STEP 10: EXAMINATION OF THE

PANCREAS
Changes involving the pancreas include
inflammation, hemorrhage, and neoplasia.
When acute, pancreatitis is often hemorrhagic,
however hemorrhage can be an agonal change
so interpretation grossly is tentative unless
supported by accompanying lesions. Acute
pancreatitis is characterized by loss (necrosis)
of pancreatic tissue, as well as varying degrees
of necrosis of the surrounding tissues. The
peri-pancreatitic fat is commonly involved and
the result is saponification, the formation of
soap due to the action of the strongly alkaline
enzymes leaking from the pancreas on the fat .
This generally appears as white plaques within
the fat. When pancreatitis is chronic, the
gland is generally very nodular in
Figure 1: Grossly normal pancreas
appearance due to the formation of prominent

connective tissue, as well as due to regenerative
nodules.
There are numerous possible causes of
pancreatitis. Nutritional factors believed to
contribute tOiJancreatic acinar-cell injury
include obesity, h igh fat diets, and
hyper1ipoprotein~mia. Drugs are also suspected
of causing some cases of pancreatitis an these
include su1fonamides, tetracycline, and
corticosteroids. Surgical manipulation, blunt
abdominal trauma, and biliary tract diseases
have also been implicated.
Figure 2 : Marked pancreatic hemorrhage and

edema (acute pancreatitis)
(j
Figure 3 : Chronic pancreatitis
Figure 4: Pancreatitis with fat sap'onification.

Note the white plaques in the adipose tissue.
54
Chapter 3
STEP 11: REMOVAL & EXAMINATION

OF THE SPLEEN
The spleen should be examined for its size, shape
and conformation. A normal spleen can be either
contracted or congested at necropsy, although
contracted is most common. The contracted
spleen has a lightly brownish hue, often with
wrinkling of the capsule. The congested spleen is
very dark red, with a smooth taut outer surface
and a gelatinous cut surface. Sometimes the
spleen features irregular areas of congestion
which can be confused with hyperplastic nodules
or neoplasia. Hyperplastic nodules are usually
well circumscribed and sessile in appearance.
These masses are not neoplastic but can rupture
and bleed like malignant tumors. A common
finding on the edges of spleens are fibrosiderotic
(or just siderotic) plaques. These plaques have a
Figure 1: Grossly normal contracted spleen
grainy, light tan appearance. They represent small
areas of chronic degeneration with fibrous connective tissue proliferation and dystrophic calcium
deposits. The cause is unknown but they are of no clinical or pathological significance.
Figure 2: Grossly normal congested spleen
Figure 3: Cut surface of congested spleen
Figure 4: Hyperplastic spleen (Histoplasmosis)
Figure 5: Cut surface of hyperplastic spleen

(Histoplasmosis)
55
-Chapter 3
Figure 6: Incomplete contraction (irregular

congestion)
Figure 7: Ruptured and hemorrhaging

nodular splenic hyperplasia
Figure 8: MUltiple dark red hyperplastic

splenic nodules with tan fibrosiderotic
plaques along the splenic edges (arrow)
Figure 9: Ruptured hemangiosarcoma with

blood clot
, 1
Figure 10: Marked splenomegaly due to

lymphosarcoma
Figure 11: Focal splenic infarction
56
Chapter 3
HEMANGIOSARCOMA
::-Iemangiosarcoma is a tumor of neoplastic endothelial cells which often form vascular channels filled
-.vith blood. It occurs most commonly in the spleen and right atrium of the heart, however, a primary
::temangiosarcoma can occur anywhere due to the ubiquitous nature of endothelium. Splenic
::temangiosarcomas are often asymptomatic until they rupture, with the resulting peracute abdominal
. emorrhaging causing hypovolemic shock and death. Atrial hemangiosarcomas may be
asymptomatic or may cause cardiopulmonary signs. They often rupture resulting in
::temopericardium, cardiac tamponade, cardiogenic shock and peracute death. Metastasis usually
occurs very early in the course of the disease, often before the primary tumor is discovered.
:Iemangiosarcomas occur in the spleen and right atrium simultaneously (no metastasis) in about 25%
af the cases .
.\symptomatic splenic hemangiosarcoma may result in mild anemia, spherocytosis, and
s chistocytosis due to red blood cell damage as they pass through the neoplastic blood channels of
:he tumor (microangiopathy). The presence of acanthocytes (acanthocytosis) is an especially
::nportant signal of possible hemangiosarcoma.
Figure 1: The pericardial sac is distended

with blood after rupture of an atrial
hemangiosarcoma
Figure 2: Opened pericardial sac revealing

hemopericardium
Figure 3: Ruptured hemangiosarcoma on the

right atrial auricle.
Figure 4: Marked hemoabdomen due to a

ruptured splenic hemangiosarcoma
57
Chapter 3
HEMANGI0~ARCOMA
(cont.i1).ued)
Figure 5: Two hemangiosarcoma masses on

the head and tail of the spleen. The larger
mass ruptured resulting m hemoperitoneum.
Figure 6: Metastatic foci of hemangiosarcoma

in the lungs
Figure 7: Metastatic foci of hemangiosarcoma

in the intestine and on the spleen
Figure 8: Microscopically, hemangiosarcomas

often form irregular and abnormal blood
vessels and vascular passages filled with blood
Figure 9: Undifferentiated spindle cell tumor

from the spleen. A hemangiosarcoma is
suspected but cannot be confirmed because it
lacks the definitive vascular pattern.
The microscopic vascular appearance of

hemangiosarcomas (HSA) are very important for
the pathologist to make a definitive diagnosis.
When the tumor is undifferentiated and this
vascular pattern is not evident, it may not be
possible to make a definitive diagnosis with
H&E histology alone. In such cases,
immunohistochemistry staining (IHC) can be
very useful. IHe staining uses antibodies
directed against certain proteins that are
exclusive (or nearly exclusive) to a certain type
of tissue. In the case of HSA, the antibodies are
directed against the endothelial cell protein
Factor 8-related antigen. These antibodies are
conjugated with a stain so that if the antigens
are present and the antibodies stick to the
tissue, the tissue will stain. When this staip is
positive, it is definitive for hemangiosarcoma,
regardless of the tumor's histologic appearance.
58
Chapter 3
STEP 12: REMOVAL AND EXAMINATION OF THE ADRENALS

Before removal of the kidneys, the adrenal
glands should be identified and removed. The
adrenal glands are retroperitoneal structures.
The left adrenal gland is slightly craniomedial to
the left kidney, and ventrolateral to the aorta
between origins of the cranial mesenteric and
left renal arteries. It is centrally constricted with
enlarged extremities, having a "dumbbell" or
"peanut" shape.
The right adrenal is craniomedial to hilus of the
right kidney, dorsal or dorsolateral to the
caudal vena cava, and cranial to the right renal
artery and cranial mesenteric artery. It has a

"comma", "wedge", or "boomerang" shape.
The phrenicoabdominal vein courses across
the body of each gland slightly ventral to the
center. Adrenocortical hyperplasia is a
common finding in the adrenal glands. It may
be noted as a large nodular mass, or may
appear as multiple scattered pale yellowish
regions. Neoplastic masses include
adrenocortical adenoma and adrenocortical
carcinoma, both of which can cause Cushing's
Syndrome. Pheochromocytoma is neoplasia of
the medullary adrenal cells.
Figure 1: Grossly normal right adrenal gland
Figure 2: Left adrenal gland with pale

hyperplastic cortical foci
Figure 3: Adrenocortical nodular hyperplasia
Figure 4: Adrenal pheochromocytoma
59
Chapter 3

OF THE KIDNEYS
Both ureters should be identified and
examined for enlargements, strictures, stones,
or other abnormalities. If they are normal, en
masse removal of both kidneys, ureters, and
bladder together does not have to be done.
Each kidney can be cut out of the perirenal fat
separately. The size and shape of each should
be noted, and evidence of necrosis,
hemorrhage, inflammation, and neoplasia
should be sought. The capsule should peel
easily off of each kidney; excessive adhesion
suggests inflammation. Inflammation of the
kidney mayor may not be evident grossly.
Inflamed kidneys may have areas of petechial
hemorrhaging and congestion.
Necrosis is most often in the form of an infarct.

Infarcts are generally roughly: triangular in
shape, and when acute, are pale with a red
hemorrhagic rim. When chronic they can be
very pale and fibrotic, and cause considerable
distortion of the renal conformation. Renal
cysts are usually congenital and appear as
fluid-filled cavities of varying size. Degenerative
change such as hydronephrosis is
characterized by\ dilation of the pelvis and loss
of medullary or cortical parenchyma. In
extreme cases, the kidney can be greatly
enlarged and consist only of a fluid filled sac.
Neoplasia, either primary or metastatic, is
usually dbvious as variably-sized masses
and/ or diffuse infiltration in the parenchyma.
Figure 1: Normal dog kidneys
Figure 2: Polycystic cat kidneys (the pale

color and subcapsular veins are normal in
cats).
Figure 3: Bilateral polycystic kidneys on cut

surface
Figure 4: Focal renal abscess
60
Chapter 3
Figure 5: Unilateral renal hypoplasia
Figure 6: Bilateral chronic renal infarcts. The

affected areas are markedly shrunken,
distorting the shape of the kidneys
Figure 7: Hydronephrosis with dilation of

the renal pelvis
Figure 8: Severe unilateral hydronephrosis

and hydroureter
Figure 9: Infiltrative renal neoplastic disease

(lymphosarcoma)
Figure 10: To distinguish the left kidney from

the right kidney after removal, it is customary
to cut the right kidney at a right angle, and
the left longitudinally.
61
Chapter 3
AMYLOIDOSIS
Amyloidosis is any disease entity characterized
by the formation and deposition of amyloid.
Amyloid is a protein which is formed when a
protein or parts of a protein becomes misfolded
into an abnormal beta-pleated sheet
arrangement. There have been more than 15
proteins identified that can become misfolded in
this way and form amyloid. Regardless of which
parent protein causes amyloid, microscopically,
it all looks the same. Histologically it has a pale
bluish-red (amphophilic) homogenous and
amorphous appearance.
Of the numerous proteins that can form
amyloid, there are only 3 which are common
Figure 1: Molecular pattern of a b-pleated
and important in domestic animals. Amyloid
sheet. The pleating refers to the "wavy" folding
associated (AA amyloid) is formed from a
(like drapery pleats) of the polypeptides.
common acute phase protein called serum
amyloid (SAA), amyloid light chain (AL amyloid)
is formed from the light chains of immunoglobulins, and islet amyloid (IA amyloid) forms from a islet
amyloid polypeptide (lAPP), a protein synthesized by islet b-cells. IA amyloidosis is most commonly
seen in the pancreatic islets of old cats.
AA amyloid is commonly associated with chronic inflammatory diseases which, of course, produce
lots of the acute phase protein SAA. Normally, SAA should be degraded after it has performed its
function, however occasionally some component becomes (inexplicitly) folded in the b-pleated sheet
formation and becomes amyloid. Because the amyloidosis is secondary to whatever is causing the
chronic inflammation, it is often called "secondary" or "reactive" amyloid.
Familial amyloidosis is seen as an inherited condition in certain dogs (Shar peis) and cats
(Abyssinians) as an autosomal recessive condition. The type of amyloid is usually AA. In Shar peis it
is often (but not always) part of Familiar Shar pei Fever (FSF) syndrome, also referred to as Shar Pei
Fever and Swollen Hock Syndrome. It is characterized by recurrent, unexplained fever episodes
and is often accompanied by swollen hocks and/or joint inflammation (arthritis). Fevers are usually
105 - 107 degrees F, however it may go higher in rare cases. Shar-Peis with FSF have increased
levels of the cytokine Interleukin-6 (IL-6) which is involved with the fever response and is an integral
part of triggering the production of acute phase reactant proteins by the liver. The increased acute
phase proteins (particularly SAA) predisposes the animal to develop amyloidosis. About 25% of the
FSF dogs will develop renal failure due to renal glomerular amyloidosis. A smaller percentage will
develop hepatic amyloidosis as well.
AL amyloid is commonly associated with immunologic conditions resulting in the production of large
amounts of immunoglobulin. Occasionally (inexplicably) some of the light chains of the
.
immunoglobulins become folded in the b-pleated sheet formation and become amyloid. The most
common immunologic condition associated with AL amyloidosis is multiple myeloma or plasma cell
neoplasia. Neoplastic plasma cells produce very large amounts of immunoglobulins, some of which
become folded and form amyloid. AL amyloidosis is known as "primary" amyloidosis.
62
Chapter 3
AMYLOIDOSIS {continued}
In humans, a protein called amyloid precursor protein (APP) is an integral plasma membrane protein
which is found in highest concentrations in neurons near synapses. Misfo1ding of this protein forms
amyloid which commonly deposits in blood vessels of the brain and is associated with Alzheimer's
disease. Currently, no association of amyloid and Cognitive Dysfunction Syndrome, a syndrome in
animals analogous to Alzheimer's, has been established .
By far, however, the most common "form" of amyloidosis is idiopathic, when the condition cannot be
linked to any of the above stated conditions.
As previously stated, regardless of the parent protein that causes amyloid, microscopically it al1100ks
the same. The b-p1eating of the proteins makes amyloid very resistant to normal degradation by
proteolytic enzymes. Since it can't be broken down or excreted through the kidneys, the amyloid is
deposited in numerous extravascular sites. It can be deposited anywhere, however, common
extravascular sites of deposition include the hepatic sinusoids, renal glomeruli, and splenic
sinusoids. Amyloid is not toxic to the cells in these areas however its presence causes slow pressure
atrophy and eventual necrosis of the surrounding tissue . Obviously, the clinical syndrome associated
with amyloidosis has a lot to do with where it is deposited. In renal glomerular amyloidosis, the loss
of glomerular cells leads to a loss of proper fiitration, renal failure, and the presence of very
prominent proteinuria.
In the liver, severe amyloidosis can eventually cause chronic liver failure by its slow atrophy and
destruction of hepatocytes. More commonly, however, hepatic amyloidosis leads to fatal abdominal
hemorrhage. In severe cases, the presence of the amyloid markedly weakens the structural integrity
of the liver, making it very friable. Because of this friability, minor trauma to the liver can result in
fracturing/ cracking of the parenchyma, severe hemorrhage, and death from exsanguination.
Figure 2: Grossly, hepatic amyloidosis has

caused this liver to have a swollen, puffY
appearance, and there are several cracks and
fractures on the surface which have resulted
in fatal hemorrhage .
Figure 3: Microscopic hepatic amyloidosis.

Notice how the hepatic cords (white arrow) are
thin and atrophic, being separated an
compressed by the pale amorphous amyloid
(green arrow) in the sinusoids. This separation
and destruction of the hepatic cords weakens
the liver's structural integrity, predisposing it
to fracturing and hemorrhage.
63
Chapter 3
AMYLOIDOSIS (continued)
Figure 4: Grossly, renal amyloidosis is

characterized by a nondescript paleness,
although it can cause the tissue to have a waxy
feel when severe.
Figure 5: Microscopically, amyloid has a pale

pinkish appearance. Here in the glomeruli it is
expanding and destroying the tuft.
Figure 6: Amyloid can look similar to other

deposits (like fibrin and collagen) so Congo
Red staining is used to confirm. Under
polarized light it fluoresces a bright apple-green
color.
Figure 7: Amyloid can deposit in the white

pulp or the red pulp of the spleen. When the
deposits are in the white pulp they look like
grains of sand (or sago) and it is called a "sago
spleen" (the above picture). A "lardaceous
spleen" has its amyloid in the red pulp, and
usually indicates amyloid AL.
64
Chapte r 3

OF THE BLADDER
The bladder should be opened and the
character of the urine should be noted (red =>
hemoglobinuria; brown => myoglobinuria;
cloudy => cystitis). The bladder wall should be
checked for inflammation and/or hemorrhage,
and the lumen for the presence of uroliths.
A urolith is a rocklike body that can form
anywhere in the urinary tract from naturally
occurring mineral salts in the urine and which
can become lodged along the tract. Uroliths may
vary in size from sand-like particles, to larger,
sometimes radiographically visible "stones".
Uroliths may be smooth, jagged, or "pointy". In

dogs and cats, bladder stones are more common
than kidney stones.
A serious problem in cats, especially males, is
called Feline Lower Urinary Tract Disease
(FLUTD). It is sometimes also called by its
previous name, Feline Urologic Syndrome (FUS).
This is a disease of the urinary tract that is
often related to the buildup of crystals
(crystalluria) and/ or bladder stones, leading to
inflammation of the lining of the urinary bladder
and urethra.
Figure 1: Large, distended, and hemorrhagic

bladder (blocked cat; FLUTD)
Figure 2: Severe hemorrhagic cystitis with

marked mucosal emphysema caused by gasforming bacteria
Figure 3: Hemorrhagic cystitis (FLUTD)
Figure 4: Multiple variably-sized stones

(uroliths) in the lumen of the bladder
65
Chapter 3
STEP 15: REMOVAL OF THE BRAIN

The examination of the brain is most easily
facilitated by removal of the head from the rest
of the carcass, and opening the cranial cavity.
To remove the head, use your knife to sever all
attachments at the atlanto-occipital joint.
After removing the head, all muscle over the
calvarium (primarily the temporalis muscle)
should be removed. To open the cranial cavity
and expose the brain, a hacksaw or Stryker saw
may be used to saw through the flat bones.
After exposure, invert the head and cut all

attaching cranial nerves to remove the brain.
After removal, the brain should be cut
transversely at about lcm intervals to check for
hemorrhages, malacia, and masses in the inner
parenchyma. The brain's soft consistency can
make sectioning difficult while it is fresh, so it
is best to place the entire brain in formalin to
harden for 24 hours before cutting and taking
samples for histopathology.
Figure 1: Exposure of the atlanto-occipital

joint and foramen magnum. The spinal cord is
severed at the foramen, and the cutting of the
lateral and dorsal spinal ligaments at this
location will allow removal of the head.
Figure 2: After the head is removed, it should

be skinned dorsally and the temporalis
muscles cut away.
Figure 3: Assess the subcutaneous tissues,

muscles, and skull bones for signs of injury.
Here, fracture of the basisphenoid bone is
evident.
Figure 4: Starting just above the occipital

condyle, cut cranial to just behind the orbit,
then dorsally to the top of the skull. Repeat on
the other side. When the cuts are connected,
the calvarium can be removed.
66
Chapter 3
Figure 5: Removal of the calvarium exposes

the brain.
Figure 6: Inverting the head and cutting the

cranial nerves will allow the brain to be
removed .
Figure 7: Grossly normal dog brain removed

from cranial cavity
Figure 8: Subdural hematoma
Figure 9: Multifocalleptomeningeal
hemorrhaging.
Figure 10: Focal cerebral malacia
67

Chapter 3
Figure 11: Benign choroid plexus papilloma
Figure 12: Multifocal metastatic

hemangiosarcoma
Figure 13: Extensive intra-cerebral

hemorrhage
Figure 14: Hydrocephalus with enlargement

of the lateral ventricles and loss of the septum
pellucidum
Figure 15: Neoplastic pituitary
Figure 16: Neoplastic pituitary
58
Chapter 4
The Necropsy Report
STEP 16: WRITING THE NECROPSY REPORT

The necropsy report is the document which communicates the findings of the necropsy examination.
The report may be in narrative form or it may be a part of a specialized printed report form. If
ancillary tests are pending (especially histopath), a preliminary gross report may be written, however
its conclusions may be contradicted later by the microscopic findings. The final report should be a
compilation of all the gross and microscopic findings , as well as any ancillary tests, with comments
and conclusions representing these findings .
Whichever form the report takes, the following information should be included:
Q Case Identification - Assigned necropsy case number, clinical case number, and the date of
submission and examination
Q Owner's Identification - Owner's name, addJ ess (optional), and phone number (optional)
QSpecimen Identification - Animal's mh ne;{pecies, breed, age, weight, and sex
Q Clinical History - Includes the details of clinical findings , signs and symptoms observed
(especially peri-mortem signs) , and the clinical diagnosis.
Q Gross necropsy findings , often arranged by organs/system. This mayor may not include
pictures of the significant lesions and/ or major organs. For each organ, there should be a full
description followed by a morphologic diagnosis.
QThe microscopic findings (if this is the final report)
Q Necropsy Conclusions and Comments - The examiners final interpretation and diagnoses based
on the clinical history, the gross lesions, and the ancillary test findings , as well as any pertinent
and useful comments on the case.
STEP 17: WRITING THE NECROPSY CONCLUSION

The necropsy report conclusion is arguably the most important part of the report. It is where all of
the findings and information (the clinical history, gross findings, and the ancillary test findings) are
interpreted together and conclusions are drawn about the cause of death and/ or the clinical
syndrome. The conclusion should be written in narrative form and contain the following:
QA direct statement of the morphologic cause of death or the clinical syndrome (if it has been
determined) , including a statement about the etiology if determined
e .g. "This animal died from exsanguination (bleeding out) into the chest cavity subsequent to
traumatic injuries to the heart and lungs inflicted by a high powered projectile"
e .g. "The cause of death in this case was humane euthanasia"
QA brief pathogenesis for the cause of death or clinical syndrome, as well as any other significant
findings (whether or not they were related to the cause of death)
Important lesions can be restated (do not restate the entire report) to explain how the
findings inter-relate to each other
QIf a specific condition or neoplasia is found to be the cause of death (ex. lymphosarcoma), write a
brief, general description about the condition
Q If the specific cause of death could not be determined, speculations based on gross and/ or
microscopic lesions are permitted, after clearly stating that these are opinions and not facts
QAny other information or observations deemed pertinent or important to the case.
70
...
...
4I1r' 1IIIIr
D
c s
NECROPSY REPORT
Accession Number:
Hospital Name:
Hospital Address:
Doctor's Name:
Owner's Name:
Pet's Name:
Sex:
Age:
Species:
Weight:
Necropsy Date:
NA2005-55
Some Great Veterinary Hospital
5555 Main Street., Los Angeles, CA
Dr. Jones
John Smith
Gizmo
Male
5-6 months
Canine
-151bSJ
05105)0
HISTORY
Gizmo was at a local groomer for a grooming on 05-04-05. During the final brush out he
collapsed and died (no other details provided). He was delivered DOA to the veterinary
hospital. He has had a history of a distended abdomen.
GROSS EXAMINATION
The animal submitted for necropsy is Gizmo, a male Shih Tsu canine (Figures 1 - 2). He
measures approximately 18 inches from nose tip to tail-base. The hair coat is long with white,
tan, and black markings.
Integumentary System:
The carcass is in fairly good body condition with adequate fat stores. No significant gross
lesions are observed in the skin, subcutaneous, or musculoskeletal tissues.
72
JtIIIIIII . . .
41f111"' ,.,
D
c s
Digestive system and pancreas:

No significant lesions are noted in the oral cavity or the esophagus. The abdominal cavity
contains approximately 250ml of a yellowish, slightly blood tinged fluid (urine) (Figure 3). A
large fluid-filled sac, later determined to be the left kidney, is displacing the intestines
cranially, and there is very marked peri-renal accumulation of yellow fluid (urine) (Figures 4 5). The small intestinal bowel loops are pale and there is no evidence of inflammation,
rupture, or necrosis. The stomach contains only fluid and mucus, and no significant gross
lesions are observed. The left testicle is present in the abdominal cavity at the entrance to the
inguinal canal (Figure 6). The pancreas is pale with no inflammation, necrosis or masses
noted.
Gross Diagnosis:
1) Marked uro-abdomen
2) Prominent gastric and intestinal pal/or
3) Grossly normal pancreas
4) Left testicular cryptorchidism
73
c s
Figure 7
Liver:
The liver features relatively sharp edges and a
faint reticulated surface appearance. The
parenchyma has a reddish appearance with
several linear pale regions (postmortem rib
impressions), and the capsular surface is
smooth and glistening (Figure 7). There is no
significant oozing of blood on cut surface. No
masses, nodules, or evidence of inflammation
or necrosis is noted. The gallbladder is intact
with no stones or evidence of inflammation
Gross Diagnosis: Grossly normal liver and
gal/bladder
Spleen:
The spleen is normally contracted, measures approximately 9cm in length, and features no
elevated nodules or masses.
Gross Diagnosis: Grossly normal contracted spleen
Cardiopulmonary System:
All lobes of the lungs are inflated and have an irregular, dark red, mottled appearance (Figure
8). There is prominent foamy and bloody fluid in the trachea primarily at the tracheobronchial
bifurcation (Figure 9). There is approximately 2ml of clear, slightly red-tinged fluid in the
pericardial sac. The heart measures approximately 4.5 cm from its base to the apex (Figure
10). The left and right ventricular walls are of normal size and conformation, and the tricuspid
and mitral valves appear normal (Figure 11).
Gross Diagnosis:
1) Prominent pulmonary congestion, edema, and hemorrhage
2) Grossly normal heart
C
Figure 8
74
...
4111". . . . . .
D
Figure 10
c s
Figure 11
Urogenital System:
There is very marked enlargement of the left kidney, with normal size and conformation of the
right (Figure 12). There is complete atrophy of the left renal parenchyma, leaving only a
fluid-filled, dilated pelvis, fibrous calyxes, and capsule (Figures 13 - 14). No overt rupture
could be found, however there is very prominent leakage of fluid into the peri-renal tissues.
There is a double ureter exiting the pelvis, one of which is small and non-patent going to the
trigone of the bladder, and the other is patent, markedly dilated, and ends blindly in the region
of the prostate (Figure 15). There is mild to moderate vascular congestion of the cortex and
medulla of the right kidney. The bladder is empty with no significant gross lesions noted.
Gross Diagnoses:
1) Severe left renal atrophy with left renal hydronephrosis, non-patent ectopic double
ureters, and hydroureter
2) Moderate vascular congestion of the right kidney
3) Grossly normal bladder
75
.
. ..,.
~
~
Figure 14
c s
Figure 15
Adrenal glands and thyroid glands:

No significant gross lesions are noted in the adrenals or thyroid glands. 80th sets of glands
appear to be of normal size and conformation with no nodules or masses noted.
Gross Diagnosis: Grossly normal adrenals and thyroid glands
Brain:
The brain is characterized by moderate
congestion of the cerebral vessels (Figure 16).
It was serially sliced transversely at 5mm
intervals and no hemorrhage, malacia, or
neoplasia was observed.
Gross Diagnosis: Moderate
cerebrovascular congestion
'.
76
...
411/1f11'
,.,
A
c s
HISTOPATHOLOGY
STOMACH: Examined sections of gastric glandular mucosa features areas of
postmortem change but mostly an intact, columnar epithelial mucosal border without
evidence of erosion or ulceration. There are no significant inflammatory infiltrates
noted in the lamina propria, but there is mild edema.
Microscopic Diagnosis: Mildly edematous stomach
INTESTINE: In the small intestine there is mild autolysis of the villous tips but no
evidence of blunting, ulceration, necrosis, or inflammation. There is no evidence of
rupture of the bowel wall and no evidence of peritonitis, but there is mild edema. The
colon appears similarly normal histologically.
Microscopic Diagnosis: Mildly edematous small intestine with normal colon
PANCREAS: The pancreas featured normally arranged acini, and normal numbers of
well-spaced pancreatic islets. The interstitium is mildly expanded by edema fluid and
vascular congestion is prominent, but there is no evidence of hemorrhage,
inflammation, necrosis, or neoplasia.
Microscopic Diagnosis: Mild interstitial pancreatic congestion and edema
LIVER: Moderate sinusoidal and vascular congestion is evident. The accumulation is
most notable in the central veins and periacinar regions. The hepatic cords around the
central veins are attenuated and slightly pale, imparting a distinct reticulated
appearance to the section. Some hepatocytes feature vacuolar change.
Microscopic Diagnosis: Moderate hepatic passive hepatic congestion
LUNG: All of the pulmonary tissue vasculature is moderately congested. There are
extensive areas throughout the lung tissue characterized by prominent intra-alveolar
hemorrhage. No evidence of inflammation or necrosis are noted in association with
this hemorrhage. Pulmonary edema is also prominent, and scattered atelectic regions
are present.
Microscopic Diagnosis: Marked, focally extensive intra-alveolar pulmonary
hemorrhage, congestion, edema, and atelectasis
HEART: Examined sections of heart musculature feature variable fiber separation
characteristic of interstitial edema. Overall there were no significant histologic lesions
beyond mild vascular congestion. Myocardial fibers are intact, organized, and feature
no hyalinization, degeneration, or inflammatory changes.
Microscopic Diagnosis: Mild myocardial edema
77
~...
4111"" ,.,
D
-........
-}!A'
__ .-.,,-
AGNOS
SPLEEN: Examination of the splenic sections reveals contraction of the parenchyma

with prominence of the fibroleiomatous septae. Both the vascular red pulp and the
white pulp follicles are adequate with no evidence of inflammation, necrosis, or
neoplasia.
Microscopic Diagnosis: Histologically normal spleen
KIDNEYS: The right kidney featured well proportioned cortical and medullary tissue.
Glomeruli are adequate in number and are not distended or sclerotic. Bowman's
capsules are not thickened. There is moderate vascular congestion involving the
corticomedullary junction and the medulla. No crystaluria or proteinuria is noted in the
renal tubules. Almost no recognizable renal parenchyma was present in the left
kidney. The tissue featured tlfifly a connective tissue capsule with scant evidence of
atrophied tubules. No inflarlv!!ayon was noted.
Microscopic Diagnosis: Moderate right renal congestion with severe left renal
hydronephrosis and atrophy
BLADDER: Sections of bladder are characterized by mild to moderate mucosal and
submucosal congestion. There is no evidence of significant inflammation, necrosis, or
neoplasia.
Microscopic Diagnosis: Mild to moderate bladder congestion
LEFT AND RIGHT ADRENAL GLANDS: Examined sections from the left and right
adrenal glands features a normal cortical and medullary architecture. No hyperplastic
or neoplastic growth is observed. No evidence of inflammation or necrosis is noted.
Microscopic Diagnosis: Histologically normal adrenal glands
THYROID AND PARA THYROID GLANDS: Examined sections of thyroid glands featured
normal follicular developing with no hyperplastic or neoplastic growth observed.
There is no evidence of inflammation or necrosis. The observed parathyroid tissue is
normal.
,
Microscopic Diagnosis: Histologically normal thyroid and parathyroid glands
BRAIN: Examined are multiple sections of brain featuring no significant histologic
lesions beyond moderate vascular congestion. Neuronal fibers are intact, organized,
and feature no malacic, demyelination, degenerative, or inflammatory changes. No
viral inclusions are observed.
Microscopic Diagnosis: Moderate cerebrovascular congestion
78
~JIl.
411' '"
D
c s
COMMENTS AND CONCLUSIONS:

The gross and microscopic examinations rule out trauma and physical abuse as the cause of
death of this animal. Also eliminated are neoplasia, infection/inflammation, and ischemic
tissue necrosis (infarction). No foreign material was evident in the stomach or intestine to
suggest poisoning. While most of the findings noted were postmortem and/or nonspecific in
nature, several lesions do suggest a pathogenesis for the cause of death. Though the death
was acute, the lesions that led to the death were not, having been present since birth.
The most dramatic finding was the presence of severe hydronephrosis and hydroureter of the
left kidney. The lesion was congenital and due to the formation of double, non-patent ureters,
one of which was ectopic. The lack of a urine outlet for the left kidney led to dilation of the
ureter and pelvis and ultimately to slow pressure atrophy of the entire left renal parenchyma.
There was apparent adequate compensation by the right kidney as no signs of renal failure or
illness was reported previously by the owners. It appears, however, that there was some
sudden loss of integrity of the dilated, urine-filled kidney that resulted in significant urine
leakage into the surrounding tissues and the abdomen. This uroperitoneum led to peracute
azotemia, toxicity, and possibly hypovolemic shock. Finally, it appears there was severe
pulmonary hemorrhage and that death was ultimately due to respiratory failure.
Ectopic ureters are defined as ureters that empty at a site distal to the trigone. They may
empty at any point distal to this location, including the neck of the bladder, the proximal,
middle, or distal urethra, the uterus, or the vagina. The dilated left ureter in this case coursed
to the level of the proximal prostate, at which point it could no longer be identified. Ectopic
ureters are most commonly diagnosed in animals younger than one year of age, and more
commonly (20x) in female dogs. A familial predisposition has been found in Nordic breeds,
including the Siberian husky. Additional familial predispositions have been found in the golden
retrievers, Labrador retrievers, Newfoundland retrievers, West Highland White Terriers, Wire
Fox Terrier and the Poodle. Urinary tract infections are a common complication though this
was not present in this case.
Pathologist:
R.E. Moreland as, DVM
Antech Necropsy Coordinator
79
The Color Atlas of Small Animal Necropsy was written to serve

as a guide for veterinary students, technicians, and clinicians
on the important aspects of necropsy in dogs and cats. Using
over 230 vivid color photographs, it aims not only to show the
reader the proper standardized necropsy dissection technique,
but also to:
..:lRefresh the understanding of some of basic pathology
definitions and concepts important in the proper
interpretation of necropsy findings
r- Detail the im portan t preparatory pre-dissection
considerations of necropsy
OFamiliarize the prosector with examples of common gross
and microscopic lesions
[ Examine some common diseases and disease processes
which illustrate important pathological concepts
REMSOFT PUBUSHING
www.remsoftpublishing.com
2009
I5Bl ' 1810-557117597-3911

9 780 557
75973

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Basic Pathology Definitions

THE IMPORTANCE OF NECROPSY

Obtaining the maximum benefit and

BASIC PATHOLOGY DEFINITIONS

Clinical pathology strives to diagnose disease

Severe, acute, multifocal, renal tubular

Basic Pathology Definitions

An etiology is the cause of a disease or lesion.

Inflammation is the vascular and cellular

Disease Names: When a condition features a

Neoplasia (tumor, cancer) is the abnormal and

BASIC PATHOLOGICAL TISSUE

Degeneration represents the gradual

In naming tumors, those that arise from

Necrosis is the morphologically recognizable

Pre-Necropsy and General Considerations

WHEN AND WHERE TO DO A

Figure 1: Wet prep table.

Figure 2 : Dedicated necropsy room and

Figure 3: Specialized necropsy table with

Pre-Necropsy and General Considerations

BASIC NECROPSY EQUIPMENT

Figure 1: Basic necropsy equipment

A plastic cutting board

A scale of some type for weighing organs

Formalin-filled container for collection of

Figure 3: 10% neutral

Figure 2: The Stryker saw is a special

Figure 5: Digital camera

Pre-Necropsy and General Considerations

The wearing of protective clothing is meant to

Figure 2: Plastic apron

Figure 3: Paper booties

Figure 4: Rubber boots

Disposable paper booties are good for providing

Pre-Necropsy and General Considerations

THE SUBMISSION FORM

CSF "~h C'/flIC9Y_

Bonr) M';.nTO'\'Io' CytQIDgy

Bone Mam:r~'.. Cyt-nlogy wlCBC

o i>~F,:y 0 $l.\"", 8uffy Coal Smear - - SPECIAL STAINENG

Biopsy, Written (Inc:lL";'S

Prognosis. E'.. CotrnT~nt)

tJiOOS'l, Mit. (lt1;;llJdrr..; MjcKl:..~(lpic

Sooc Murrow Core BloPSY (Include:;

MiCfO'f'.copic: De~..cri plIDn, Micf\l~~c

AI[ riS$I,Ie{s) $uhmine4 '?

t\.'urroer ot Containers Submitted:

Ntl!'\'d)Cr' ot.sPCCirncM Subl'nit1d:

and General Considerations

ANCILLAl{Y SPECIMEN SUBMISSIONS

Histopathology: Specimens should be

Microbiology: Specimens are only

What Specimens To Collect: Ideally, samples

these tissues they should of course be sampled,

incise and collect the required material from the

not have the capabilities to do "toxicology

Pre-Necropsy and General Considerations

COMMON POSTMORTEM CHANGES

Figure 1: Hemoglobin imbibition of the small

There are several tissue changes which can