Color Aflas of

Small Animal Necropsy

First Edition
by
Richard E. Moreland, BS, DVM
Necropsy Coordinator
Antech Diagnostics
lrvine, CA
REMSOTT PUBLISHING
w w u. retns oftpub li s hing. c om
2009
Table of Contents
CIIAPIER 1: BASIC PATHOLOGY DEFINITIONS
"
Importance of Necropsy........... 7
'
Basic Patholory Definitions ............. 7
*
Basic Pathological Changes.... ......... 8
CIIAPTER 2: Pre-Necropsy and General Considerations
n
When and Where To Do A Necropsy ..................10
.
Basic Equipment
. . .. ... .. . . 1 1
'
.
Protective C1othin9............... ..........L2
"
The Submission Form......... ............13
" Ancillary Specimen Submissions............... .......14
'
Common Postmortem Changes.... .....................15
-
Describing Gross Lesions..... ...........77
.
History...
......18
.
Routine vs. Cosmetic Necropsy ........19
CIIAPIER 3: THE NECROPT PROCEDURE
.
Overview.
,,., 2l
,
External Exam........ ......21
"
Limb and Skin Reflection.. ..............23
,
Icterus.... .................24
,
Opening and Examining the Abdominal Cavtty....... ........... 27
^
Feline Infectious Peitonitis.. .......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
.
lVecrosis.. .................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
'
AmAloidosis'..."....'.. .......'.........62
,
Removal and Examination of the Bladder..... .... 65
.
Removal and Examination of the 8rain........ .....66
CIIAPIER 4: THE NECROPSY RTPORT
.
Writing the Necropsy Report... ........7O
.
Writing the Necropsy Conclusion............ .........70
CHAPIER 5: COMPLBIE NECROPSY REPORT EI(AMPLE. ..,.... 7l
3
Chapter 1 Easia Patlrology Belinitions
THE IMPORTANCE O.F .IVECROPSjr
Necropsy is the animal analory 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 patholory. 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.
Obviously, a knowledge of the normal anatomy
is necessar5r 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.
Obtaining the maximum benefit and
information from a necropsy requires not only
knowledge of the proper necropsy dissection
procedure, but loeowledge of basic disease
processes. In particular an understanding of
basic pathologr processes is paramount,
starting with standard basic pathological
delinitions.
BASIC PATHOLOGY DEFINTTIO NS
Pathology is the study of disease.
Disease is any variation from the normal
morpholory or physiolory of a living organism.
Disease results from various causes, such as
infection, genetic defect, or environmental
stress, and is characterwed by an identifiable
group of lesions, clinical signs, and/or
sSrmptoms. Diagnosis of disease is important
for proper treatment.
Anatomical patholory 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
"s5rmptoms" are often used interchangeably,
although technically s5rmptoms 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:
.
Severit5r
'
Duration
"
Distribution
"
Anatomic site
"
Miscellaneous adjectives/modifiers
.
Lesion
Examples of a complete morphologic diagnosis:
,
Seaere, dc'ute, nrulttfocal" renaltubular
coagrulatlon necrosls"
,
Marked, chronlc,
focallg
esctenslae,
lgmphoplasmacgtlc, cholanglohepatltlso
7
*hxpt*r 1 Basi* ?at}a*Z<tgy t3*f?r:it!$&c
An etiolory is the cause of a disease or lesion.
Etiologies are numerous and diverse and
include infectious agents such as bacteria,
fungr, or parasites, and physical damage such
as blunt force trauma or thermal burns (to
name a very few). An etiologic diagnosis
names the etiologr (ex. Histoplasmosis).
Determining the etiolory when possible is very
important as it often dictates proper treatment.
Disease Names: When a condition features a
unique combination of lesions, clinical signs,
arrd/or s5rmptoms, that condition may be given
a narne. 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.
BAS.IC PATHOLAGICAL ?ISSUE
CHANGES
TTESTOJVS/
Broadly speaking, the primary lesions detectible
grossly and/or microscopically in body tissues
include degeneration, necrosis, infl ammation,
and neoplasia.
Degeneration represents the gradual
deterioration of cells or tissue due to tl:e loss of
specific cellular functions and manifested in
specifi c morphologic abnormalities.
Degeneration is usually reversible if the cause is
reversed. Examples include cloudy sutelllng
and hgdroplc ch.ange of hepatocytes, resulting
from the failure of plasma membranes sodium-
potassium pump to keep out water.
Necrosis is the morphologically recognizable
death of cells andlor tissue. Necrosis is not
reversible. In general, changes in the nucleus
of cells are the primary indicators of necrosis.
These changes include pgknosls,
karyon'hexlq and karyolysls. 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 appeararlce.
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 t5rpes of
inflammatory cells. The types of inflammatory
cells present usually give some indication of the
cause of the inflammation.
Neoplasia (tumor, cancer) is the abnormal and
uncontrolled proliferation of body cells. A11
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.
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/celI type (hepatoma, marnmary
adenoma). Those that arise from epithelial
tissue and determined to be malignant are
designated with the suffix <o,rcinoma
(hepatocellular carcinoma, marnmarJr
adenocarcinoma). T\rmors of non-epithelial
origin and determined to be benign also use the
suffix
-oma
(fibroma, osteoma). T\rmors of non-
epithelial origin and determined to be malignant
use the suffix
-sarcofltq.
(fibrosarcoma,
osteosarcoma). There are numerous exceptions
to these rules, with lymphoma and melanoma
being two glaring examples.
8
t"xapt*r 2 Fr*-S**r*gex3r axd *a:xeral *cacasid*rat9{}r:s
WHEN AND WHERE TO DO A
ivEcRoPsv
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 enz5rmatic reactions. If
possible, avoid freezing the carcass. For one
thing, it is impossible to necropsy afrozen
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 histopatholo$/ 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 exarn 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 prosector should have easy access to
their basic necropsy equipment, a lined
biohazard garbage can for excised tissue,
formalin containers, and toxicolory and
microbiolory collection materials.
Pre- and post storage ofthe 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 ald
necropsy table.
Figure 3: Specialized necropsy table with
downdraft ventilation and built-in disposal.
10
Chaptsr ? Fre-I$eerop*y arad &er:eral eonsi,derations
BASrC JVECROP,SY EQWPME NT
The choice of equipment for necropsy depends
in part on the size and type animal, t-he t5rpe of
examination requested, and the individual
preferences of the examiner. Most small animal
necropsies 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
'
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 temporaqr
viscera holding
'' A scale of some type for weighing organs
.
Formalin-filled container for collection of
tissues for histopath
' Multiple, variably-sized Whirl-Pak or
Ziplock bags for fresh tissue collection
.
Digital carnera (optional)
.
Supplies and containers for collecting
specimens (formalin jars
and whirl-pak
bags)
Figure 3; lO%o 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
11
Figure 1: Basic necropsy equipment
Figure 5: Digital camera
Ciapter 2 Fr*-tr.cercps-'' =::d, General }qansiderati*&x
PROTECTIVE CLOTHING
The wearing of prc:e::-,-e ciothing is meant to
protect the exa=:::e:
=f=
contamination with
blood, tissues a:-: 3:cl- iluids from the
cadaver tha: a:e:::e::iaL carriers of infectious
panicies. T::e :es: ::otective clothing should
proride cc=:-?:: :c
-re
examiner while not
comDro-.' s=g ;:oiection against possible
co:::a-'-:ajc::. The primary clothing should be
e:=e: s-::3:cr- scrubs or cotton utility
cc;e::
's.
lqeali]', a second outer covering
s*c:: as a surgical gown or a plastic apron
s::o-*-c 3e \\-orn to give added protection. These
a:-:c-es must be washed clean and disinfected
a::e: each use.
Proper gloves are paramount when performing
a necropsy. Although latex surgery or
exarnination 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
ht the hands and fingers of the examiner
se*
Flgure 2: Plastic apron
Figure 3: Paper booties
Figure 4: Rubber boots
without interfering with manual dexterity and causing numbness. 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 performed in such a wet environment, rubber boots
should be worn.
F'igure 1: Scrubs
...r&\
_ffi
.dffiffi.s#',.
'*-ffi&ffi& f_qi*#r
%,
%,,
*,'
Figure 5: Gloves
t2
C&apter 2 Fre-ffieer**5:xy ax*3 *emaral e*rasideratien*
THE SUBMIS.SIOIV PORM
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 ldentification
-
Clinic name, lD#, address, phone number, doctor's name
Case ldentification - Assigned necropsy case number, clinical case number, and the date of submission
and examination
Owner's ldentification - Owner's name, address (optional), and phone number (optional)
' Specimen ldentification
-
Animal's name, species, breed, age, weight, and sex
Clinical History! - lncludes 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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A NCI LLARY SPECIME N S UBJIfJS,STOJVS
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:
Histopathology: Specimens should be
routlnely 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).
Histapathology
Histopathologr is the primary ancillary test
associated with necropsy and provides the
definitive answers in many cases. A1l gross
necropsies should involve the collection of
tissue samples from all of the major orgalls.
These include the heart, lung, liver, spleen,
kidneys, pancreas, stomach, small intestine,
large intestine, thyroids, adrenals, and brain.
Samples should be taken regardless of the
presence or absence ofgross lesions. Any
obvious lesions should of course be taken,
however, when no lesions are present, 7 or 2
random samples should be taken from each
tissue. These 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 pieces of
organs and tissues 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.
Microbiologg
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, abscess, 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.
Toxico'l.agy
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 toxicolory laboratory where the
samples will be sent to ensure that the right
specimens and amount are collected ald that
adequate precautions for handling and
preservation are observed.
It is important to note that most laboratories do
not have the capabilities to do "todcologr
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
toxicologr screening is not widely available,
toxicolory panels, in which a group of individual
tests are run together, are common. A common
toxicologr panel would include those
compounds commonly used in malicious
and/or accidental animal poisoning such as
strychnine, arsenic, metaldehyde, and warfarin.
t4
Chapter 2 Pre-}lecr*psy and GeEreral, Considerations
COMMO N POSTMORTEM CITA.NTGES
When an abnormality is found during
necropsy, it must be
judged whether it is an
antemortem leslon 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 cm be made.
Postmortem autolysis result from the
degradation of tissues associated with the
release of proteolytic lysosomal enz5rmes from
tissue cells when they die, as well as from the
action of postmortem bacterial enzJrrnes
(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 enArmes and bacterial enz5rmes are
temperature dependent, lower temperatures
slows (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, freezingis 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.
Hemoglobln tnhlbttton 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
oflarge arteries or in tl:e heart.
Blle tnblbitlon 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.
Pseudomelcnosis 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.
Lluor morals (hypostattc congestlon/ 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
orgrns and tissues on the down side of the
cadaver.
Figure 2: Hemoglobin imbibition of the
brain
15
ehapter 2 Fre-Saero3:sy and &eraera? Consideraticne
Figure 3: Pseudomelanosis of the kidneys. In
the anaerobic abdomen, pseudomelanosis has
a black to dark blue-green hue
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 gravit5r,
making them much darker than the right lobes
Figure 8: Though this looks like a myocardial
infarct, it is only an area of postmortem
autolysis
Figure 4: Pseudomelanosis of the pancreas
Figure 7: Pale pox-marking of the liver and
small gas bubbles due to bacterial putrefacation.
t6
Chapter 2 Fre-I$eeropsy and GeneraL Considerations
DESCRIBIIVG GROSS LESIOJVS
The general rule in recording necropsy findings is to be descriptive rather than interpretive.
Interpretation of lesions should be described in the diagnosis andlor 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, sponry, viscous, friable, etc.)
'...,,Color
(black, brown, mahogony, grey-green, red, tan, white, off-white, yellow)
.,.:Size (measured in centimeters)
*tDistribution and location (bilateral, unilateral, diffuse, focal, multiple, multifocal, patchy, etc.)
.lSurface appearance (bulging, ulcerated, eroded, rough, reticulated, smooth, pitted, umbilicated,
verrucous, etc.)
Figure L: "Lung and liuer lobes are
characterized bg firultifocal, coalescing dark
circular lesions in the parenchgma. These lesions
uary in size
from
.2 to .Scm, and haue a.firm
consistencg on palpation." (Metastatic
melanosarcoma)
Figure 3z "Both kidnegs
feafiire
similar
pathological changes. Both kidnegs are
enlarg e d uith slightlg distorted conformatio n.
There are multifocal, uariablg sized, pale,
firm
ma.sses present throughout the renal
parenchgma. Mang blood uessels contain large
occlusiue thrombi and scattered areas of the
parenchg ma are reddened.
Gross Diaqnosi.s: Bilateral, multifocal irregular
renal masses with uascular thrombosis and
hemorrhag e (fuing al infection - Phg comg co sis).
Figure 2z
oThe
kidneg
features
multifocal,
roughlg tiangula4 pale areas in the cortex.
Eachis bordered bg a thin zone of reddening
and are approximatelg 1 x 2 cm in size." (renal
cortical infarcts)
t7
Chapter * Fra-?6ecro3:s3r a:ad &erqeral ec::siderati&ns
HIs.TORY
The lmporAance of a good history cannot be oueremphaslzed. 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, warrant 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 (toxicolory,
microbiolory, 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 ofa dog. Subcutaneous
edema would be the most likely
interpretation. Subcutaneous edema
suggests many possible pathogenic scenarios
including heart failure andf 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
Ckapter 2 Fre-Ir{e*a'*psy *rad **vzera? e*cesideratit>xs
ROUfiNE YS. COSMETIC NECROPST
A routlne necropsy is the standardized, systemic gross dissection of the carcass whose goal is to
assure that all important organs and tissues are',risualized 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.
Co smetic Necrapsy Procedure
,
Make a single incision through the skin, muscles, and peritoneum in the ventral abdomen,
extending from the xiphoid process approximately the mid abdomen
Visuaiize tlne 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 a-llow 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.
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.
Using whichever bone cutting implement you have available, cut the calvarium to expose
the brain.
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.
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
The carcass should be returned to as near a pristine state as possible. Clean any blood and fluids
from the hair coat. Sutures should be continuous and as neat as possible.
t9
ekapt*r * ?h* IX**r*pe3r Fr*ec*;:r*
OVERWEW
The goal ofthe gross dissection phase ofthe
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.
In a routine necropsy, there is no generally a
detailed dissection of the musculoskeletal
system,
joints,
spine or spinal cord, the eyes,
sinus cavities, or the inner ears unless the
history, clinical signs, or obvious necropsy
changes warrant detailed attention.
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 exarn.
Figure 2: Alopecia and hyperpigmentation
(demodecosis)
Figure 4: Blood in the anterior chamber of
the eye (hyphema)
Figure 1: Traditionally,
with their left side down
recumbency)
animals are positioned
(left lateral
Figure 3: Severe emaciation (cruelty
starvation case)
21
Figure 5: Marked dental tartar
Figure 7: Severe fetal edema (anasarca)
("water puppy")
Figure 9: A large sublingual cystic mass full of
collected sa-liva resulting from a ruptured
salivary duct (a sublingual mucocele or ranulal
Figure 6: Severely worn teeth
Marked oral icterus
Figure 1O: Prior to the necropsy, x-rays can
be very useful in helping to localized broken
bones and finding small metal projectiles
22
Chapter S ?*le l$eeropsSr Procedure
STEP 2: LIMB AND S.IrriV
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.
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 3: Both left limbs have been reflected
along with the thoracic and flank skin to reveal
severe subcutaneous hemorrhage. This
hemorrhage resulted from the improper use of a
heating pad.
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.
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 2: Connect the exposed areas from
the two limb reflections and reflect the skin
off of the trunk and thorax dorsally and
ventrally.
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.
23
*tzaptxx 3 ?}:ln: l{*er*pe3, F*:a:*edaar*
ICTERUS
A distinctive yellowing is often noted in the
subcutaneous as well as 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
Figure 1: Icterus
unconjugated bilirubin within 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 bilirubtn. 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.
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 eventually stains the tissues yellow.
In liver 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 hepatocJrtes 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.
g:lururonk acld
l,
*-l-*l
free g6&J6*esA
Lrilit ubin
Hlir$bic
hepatosyte
I
lnto
{} sil.
ull.lulnin
/
t
* hrrile
-+
{*
phagocyte
Figure 1: Normal Heme Metabolism
24
Chapter 3 ?he lYeeropsy Prceedure
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).
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 1: Make a submandibular skin incision
then reflect the skin
Figure 3: Pull the tongue out through the
bottom of the mandible
Figure 4: Cut the hyoid bones at their
cartilaginous articulation (the "cornu")
Figure 2: Cut the muscles
along each side of the
mandible
Figure 4: Expose the retropharyngeal hyoid
bones
25
Chapter 3 The l{ecropsy ?roeedure
Figure 5: Dissect the tissues covering the
ventral neck to expose the ventral trachea
Figure 7: Identify and remove the thyroids and
the parathyroid glands.
Figure 9: Elongated soft palate (part of
Brachycephalic Syndrome).
Figure 6: Reflect the tongue, trachea, and
esophagus back to the thoracic inlet
Figure 8: Marked tracheal hypoplasia (part of
Brachycephalic Syndrome)
Figure 1O: Tracheal collapse (part of
Brachycephalic Syndrome)
*kap{ar S ?ke tr*er*g:"*y Fr*a:*eiaar*
S?EP 4; OPE"ItrIIIG A:VD .EJCAMIHruVG
TTT& ABDOMTNAT, CAWTY
The abdominal cavity is opened by removing
the abdominal (flank) wall along the ventral
midline, the curve of the last rib, and dorsally
at 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
sizes, and malpositions, however, no detailed
examination is done until all organs are
completely removed. Inflammation of the
peritoneal cavity (peritonitis) is generally
noted by the presence of reddening and
roughening ofthe serosal surfaces ofthe
visceral organs, along with the presence of
Iibrinous tags.
Any abdominal fluids should be collected and
quantified. Broadly, abdominal fluids can be
exudates, transudates, or blood. Blood in the
abdominal cavity is referred to as a
hemoabdomen. When large amounts of blood
are present, it is important to try and
determine the source of the bleed before
removing the abdominal viscera as this
generally makes it more difficult to determine
the origin. The presence of transudates and
exudates in the abdominal cavity is called
ascites. When transudates are
uncontaminated with blood they generally
have a clear yellowish (straw-colored)
appearance. When blood is present it tints the
fluid red and is referred to as serosanguinous.
Care must be taken to avoid confusing actual
(frank) blood with serosanguinous fluid.
Blood's higher opacity and viscosity are
generally the best features to distinguish it
from serosanguineous fluid.
The liver should be assessed in situ. Extension
well beyond the last rib is considered
hepatomegaly.
The thoracic cavity should be assessed for
negative pressure by inspection of the
diaphragm. It should be pulled taut toward the
thoracic cavity, and puncturing it should
produce an in-rush of air and a relaxation of
the muscle.
Figure Normal abdominal viscera
Figure 2: Enlarged liver, extending well beyond
the last rib
Figure 3: The diaphragm is checked to
confirm negative pressure in the thorax. The
diaphragm should be pulled tauted against the
thoracic cavity
27
Chapter 3 ?he Fleeropsy Proeed,ure
Figure 4: Marked abdominal hemorrhage
(hemoabdomen)
Figure 5: Serosanguinous ascitic fluid. Though
it looks like blood, its low viscosity as
judged
during the necropsy suggested it was in fact
blood-tinged fluid.
Figure 7'. An unknown intra-abdominal mass
turned out to be a granuloma formed around
gauze left from a previous surgery. This is
caused a gossiphiboma (it's scary that it occurs
often enough to have a name!)
Figure 6: Straw-colored ascitic fluid
28
Ckapt*r S ??ae i***r*p*y Frr***&zzx*
FELTNA TNFECTTOUS PERTTOJVr?IS (FrP)
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 tn6 effusive "wet" form, as well as organ damage due to imPaired blood flow. The wet
iorm 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 a92oh statistical chance the cat has FIP. If the
ratio is greater than 0.8 there is a 610/o 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 98oh acetic acid. Then, one drop of abdominal or pleura 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 [est is 97oh acourate in ruling out FIP. A positive test is 867o 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, cr5ptococcosis, blastomycosis, and
coccidiomycosis must be considered as part of the differential. To delinitively diagnosis FIP,
immunohistochemistry staining (IHC) of affected organs is necessar5r. 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, conlirming FIP
infection.
Figure 1: The abdomen is Iilled 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 The $ecropsy Procedure
FDLItte INFDCTIOUS PEP,ITOMTIS
(continued)
Figure 3: Small white nodular lesions cover the
serosal surfaces of the small intestine.
Microscopically these nodules feature
accumulations of macrophages and neutrophils
Figure 5: Small nodules and tags of clotted
fluid cling to the surface of the spleen
Figure 4: Small nodules and tags of clotted
fluid cling to the sudace of the liver
Figure 6: Small white raised nodular lesions
(pyogranulomas) are evident in the
parenchyma of both kidneys
30
Chapter 3 The $eeropsy Frocedure
MALPOSITIONS
Volrnrlus/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 dilationl 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 o:<ygen. Occasionally in
strbhg 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 3: Section of gut telescoped on itself
(intussusception). The telescoping cuts off
venous dralnage from the affected area and
the effect on the tissue is identical to a torsion
Figure 2: Gas-filled and hemorrhagic stomach
subsequent to gastric torsion/volvulus
3l
Figure 4z Localized intestinal torsion
Chapter 3 The l,{eeropsy Procedure
STEP 5: OPENING AND EXAMIMNG
THE THORACIC CAWTY
The thoracic cavity or the abdominal cavit5r 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 cavit5r, 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.
Figure 2: Normal heart and lungs exposed
after removing the rib cage
Rih Cage
Figure 1: The ribs are cut along the
costochondral
junction
and near their dorsal
spinal attachments
Figure 3: Blood accumulation in the thoracic
cavity (hemothorax)
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).
Chapter 3 The l$eeropsy Froeedure
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 actua,l blood.
Figure 6: Here the chest cavity is filled with a
very thick red exudate (often called a
"tomato
soup" exudate) consistent with blood-tinged
pus (pyothorax) caused by Nocardia.
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 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.
JJ
Chapter 3 ?he Necropsy Proeedure
STEP 6: REMOWNG THE HDART AND
.LUTVGS
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 into 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
unormal"
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: Tlrre heart and lungs (the "pIuck")
removed
Figure 4: Normal uncongested lungs
(microscopic)
Figure 3: Normal, uncongested lungs
Figure 5: Normal, irregularly congested lungs
Figure 7: Foamy tracheobronchial fluid
indicative of pulmonar5r edema
Figure 6: Normal congested lungs
(microscopic). The vasculature is distended \Mith
blood but the alveoli are clear
Figure 8: Pulmonar5r edema (microscopic).
Many alveoli contain eosinophilic staining fluid.
Figure 1O: Pulmonary atelectasis (microscopic).
The alveoli are devoid of air and collapsed.
35
Figure 9: Pulmonary atelectasis
Figure 11 : Pulmonar5r emphysema Figure 12 : Pulmonar5r emphysema
(microscopic). The alveoli are dilated, ruptured,
and coalescing.
Figure 14: Pulmonar5r hemorrhage
(microscopic). The alveoli are filled with blood
with no significant inflammation. Non-
inflammatory pulmonary hemorrhage may
result from pulmonar5r tJrromboembolism, lung
lobe torsion, or coagulopathy.
Figure 13: Pulmonar5r hemorrhage
CS.aapter S ?')a* 3**a*p*V ?r*';<,*taz::
PNEUMOMA
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
between inflammation from physiological or
passive congestion of the lungs since both
feature a reddening of the lung parenchyma.
Three gross characteristics of pneumonia can
help in distinguishing the two. First, since
pneumonia is usuaily caused by bacteria which
enter the lungs via the trachea
(bronchopneumonia), the inflammation starts
where the bacteria initially settle in the lungs.
Figure 1: Gross bronchopneumonia. Note the
pattern of reddening in the anterior and ventral
regions of the lung lobes
Figure 3: Pneumonia (microscopic). Note the
presence of inflammatory cells filling the
alveoli. Palpation of this tissue would result in
a firm feel, and there is no air to allow it to
float when placed in liquid.
This is usually the anterior and ventral regions
of the lungs, giving the reddening an
"antero-
ventral" distribution. Non-inflammatory
congestion is irregular and/or diffuse. Second,
because of the accumulation of inflammatory
cells in the alveoli, there is litfle 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 2: Gross bronchopneumonia. Note the
pattern of reddening in the anterior and ventral
regions of the lung lobes
Figure 4: Close-up of pneumonia lung. The
alveoli are filled with inflammatory cells and
devoid of air.
37
Chapter 3 ?he l{ecropsy Proeed,ure
STEP 7: OPENING AND EXAMINING
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 inter-
ventricular 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.
The left side of the heart is opened in a similar
way. A single incision is made through the left
atrial free wall, down ttrrough 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 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 1: Grossly normal heart. Note the
sharp apex.
Figure 2: Yery rounded apex indicating
either hypertrophy or dilation
Figure 4: Cut along the septum and exit the
right ventricle through the pulmonary artery.
38
elrapter S ?he l*earergrsy Froeedure
Figure 5: The flap
visualization of the
tricuspid valve.
produced allows
right atrium, ventricle, and
Figure 6: To open the left heart, cut into the
left atrium via the pulmonar5r veins and
continue the cut through the mitral valve and
along the free wall to the bottom of the left
ventricle.
Figure 8: 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 misconception.
Figure 7: Cut through the mitral valve to exit
the left ventricle through the aorta.
39
Figure 9: The nodular thickening noted in the
mitral valve of this partially fixed heart is
Valrmlar 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
m5n<omatous 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 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 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 hlrpertrophy or dilation
of the myocardium (Hypertrophic or Dilative
Cardiomyopathy). Secondar5r dilation or
hypertrophy (due to valvular defects, septal
defects, h5pertension, etc.) does not constitute
Cardiomyopathy.
Figure 12: Heart-based tumor
(chemodectoma)
40
Chapter 3 The Hecropsy Procedure
Figure 15: Small metal projectile (bb)
penetrated the heart and lungs causing marked
hemorrhage
Figure 14: Metastatic salivary gland
carcinoma
Figure 16: Subendocardial hemorrhage on
the papillary muscle
Figure 13: Metastatic thyroid carcinoma
4t
Ckapter S ?h.c ffe*r*psy Fr*cedare
THROMBOSIS as. POSTMORTDM
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 oftissue 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 botl:
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 well-
molded 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 friabilit5r, 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 t5pes of postmortem clots can
occur after death. The most common tSpe is
called a
ucurrantJellgu
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
"chlckenfat
clotl 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
jel$ 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
C?aapter 3 ?he ffi*er*pcy Fr*e*cluie
THROMBOSIS as. POSTMORTEM CLOTTING (continued)
Figure 4: TWo thrombi attached to the mitral
va-lve. 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 6: Microscopically, thrombi often have
alayered appearance (called
"Lines
ofZahrn").
Here, a thrombus nearly occludes a blood
vessel. The dark purple blobs are bacteria (this
is a "septic" thrombus)
Figure 7: Viewed here is an opened left
pulmonar5r artery containing one leg of a
saddle thrombus (arrows). The thrombus
started at the
junction
of the pulmonary trunk
then extended into the lungs along each
branch (pulmonary thromboembolism).
i
,,
rI
fi
I
43
Chapter 3 The llecropsy Procedtrre
STEP 8: REMOVAL AND DXAMINATION
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 mqjor
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.
Alternating pale and dark areas can produce a
areticulated"
or
ttnutmeg"
appearance.
Frominent fat infiltration can produce a very
yellowish liver. Obviously, uf,y masses or
nodules should be noted.
After assessing the surface, the liver should be
"bread-1oafed", cut into small l-2crl: slices
from end to end, to expose possible lesions
deep within the parenchyma that are not
visible on the surface. The gallbladder should
be opened to assess the character ofthe bile,
the presence of any stones or concretions, and
the possibility of hyperplasia or neoplasia of
the gallbladder epithelium.
Figure 1: The bile duct is checked for patency.
Rs the gallbladder is squeezed, note the stream
of bile from mqjor duodenal papilla (arrow)
Figure 2: Grossly normal liver
Figure 3: Focal area ofhepatic necrosis Figure 4: Severe hepatic lipidosis
Chapter 3 The llecropsy Procedure
Figure 6: Nutmeg liver (chronic passive
congestion)
Figure 5: Hepatic nodular hyperplasia
Figure 7: Gallstone in the gallbladder Figure 8: Hepatic biliary adenocarcinoma
F'igure 9: Metastatic hemangiosarcoma Figure 1O: Hepatocellular carcinoma
*iaaptcr 3 ?*:e ,S**rca;sy 3x*e*elur*
JVECROSIS
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 ofnecrosis. The types ofnecrosis are
coagulative, caseous, and liquefactlve.
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
characlerved 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 ofnecrosis due to hypoxia is called an
infarct. Microscopically, coagulative necrosis is
chxacterized by dead cells, recognizable due to
distinct nuclear changes. The nuclear changes
that represent undeniable cell death are
pyknosis, karyorrhexis, and karyolysis.
Sknotic
nuclei are shrunken, dense and dark.
Kar5rorrhectic nuclei are fragmented into several
pieces. Karyolytic nuclei have lost much of
their dark staining, resulting in either a pale
nucleus or no
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
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 ofbacteria are
often the cause of caseous necrosis including
Mgcobacteium ar.d some Corynebacteium
species.
Liquefactlve 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 t5rpe of necrosis in
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 enzyrnes 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.
Figure 2z TLre pale regions of this cow kidney
are necrotic. Since the gross tissue architecture
is still present, this represents coagulative
necrosis
i
I
I
{
i
$
{
{
Ji
i
ll
46
elaxpt*r * ?h* l{e*rcgrey Froeedure
JVECROSIS
(continued)
Figure 3: Coagulative necrosis. The cortex
features multiple infarcts, roughly triangular
pale regions bordered by a thin zone ofred
hemorrhage
Figure 5: Coagulative necrosis. Clear
evidence of cell death is apparent (pyknotic
and karyorrhectic nuclei), but the cellular
architecture is still intact
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 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
.IVECROSIS (continued)
fkap?-er 3 '{"hr }f **rr;px.y Frc**e9:.ar*
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
watled-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 1O: Microscopically liquefactive
necrosis features completely loss (liquefaction)
of the parenchymal tissue, with only
inflammatory cells (usually neutrophils)
remaining.
48
S?aapter 3 ?trae m*erclg:sy Fr**edure
AIECROSIS (continued)
The microscopic pattern of necrosis in an organ
can be helpful in determining the cause. In the
liver, necrosis can occur randomly throughout
the liver, or in one of three zones of the hepatic
lobule.
Random necrosis of the liver is usually
associated with infectious organs which gain
access to the liver via the vascular system. This
type of necrosis is usually associated with
inflammation, though some viral infection may
be non-inflammatory.
Patterns of necrosis of the hepatic lobule are
the result of its microanatomy and function.
The hepatic lobule is an irregular hexagonal
structure with a large vein at the center (the
central vein) and portal regions at the
periphery. The portal regions consist of the
hepatic artery
pringing
o>grgenated blood to the
liver), the hepatic vein (bring unoxygenated but
nutrient-rich blood from the GI tract), and a bile
duct. O>rygenated blood which enters via the
hepatic artery drains through the sinusoidal
spaces into the central vein, where it is
eventually dumped into the vena cava. Because
the hepatocytes around the central veins are
the last to receive o><ygenated blood, they are
extremely susceptible to hypoxia and anemia.
Centrllobular necrosis is most commonly
associated with anemia of any cause, or
with passive congestion of the liver due to
right sided heart failure. Centrilobular
hepatocytes also contain the highest
concentrations of mixed function oxidases
(MFOs). MFOs are er:vjrmes 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
todcities (like hexacholorophene in cats).
Pet'tporaal 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 then the mid-zonal or
centrilobular regions.
Figure 11: Centrilobular hepatic necrosis Figure 12: Periportal hepatic necrosis
49
ekapter 3 ?lae l{**r*Xasy Fr*eedure
THE INTES?IIVE
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 pathologr 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.
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
intestine. Stomach and intestinal contents are
assessed, along with the surface mucosa. Any
foreign objects and/or parasites should be
identified and their possible impact on
gastrointestinal function assessed. The entire
tract should be assessed for inflammation,
ulceration, thickening, and
/
or neoplasia.
Flgure 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, h5peremic, and have a slightly
pitted surface, all evidence of inflammation.
Figure 2: When necessarJr, 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
Ckapt*r 3 ?*a* }Ic*ro;:sy Froecdarr*
Figure 5: The intestine and liver are knotted
together in a tight ball by fibrin (fibrinous
peritonitis)
Figure 7: Roundworms (?oxocara canls) in
the small intestine
Figure 9: Severely hemorrhagic intestine
(Panroviral Enteritis)
Figure 6: Multifocal petechial hemorrhaging
in the mucosa of the small intestine due to
hookworms
Figure 8: Whipworms (?Hcarls trulpls) rn
the large intestine
Figure 1O: Hemorrhagic mucosa surface of
jejunum (Panroviral Enteritis)
51
elaapter S ?k* Ieeronrsy Froeedure
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 hyphai fungal
organisms (Phycomycosis)
Figure 13: Thickened region of the
jejunum
with focal perforation and leakage of intestinal
contents.
Figure 12: Neurofibrosarcoma on the colon
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.
Figure 15: Severe esophageal inflammation
and ulceration from gastric reflux (Gastro-
esophageal Reflux Dlsease or GERD)
Figure 15: Multifocal gastric ulcerations and
hemorrhage (injudicious NSAIDS use)
Figure 18: This stomach was filled with
clearly recognizable pieces of sausage. This was
not deemed important until considered with
the history. The owner stated that she fed the
animal a strict commercial dog food diet. This
made the presence of sausage suspicious. The
animal had died acutely with no clinical signs.
Closer inspection of the sausage revealed small
pellets (see insert) consistent with Strychnine
pellets. Subsequent todcolory was positive for
Strychnine. The history was pivotal in this
case as it affected the consideration of a
seemingly benign finding.
Figure 17: Gastric foreign body
53
elaagpter 3 ?ia* S**r;*gr*y Fr*e*du.re
PAJVCR.EAS
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
enzJfines leaking from the parrcreas on the fat.
This generally appears as white plaques within
the fat. When pancreatitis is chronic, the
gland is generally very nodular in
Figure 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 to pancreatic acinar-cell injury
include obesity, high fat diets, and
hyperlipoproteinemia. Drugs are also suspected
of causing some cases of pancreatitis an these
include sulfonamides, 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)
Figure 4: Pancreatitis with fat saponification.
Note the white plaques in the adipose tissue.
Figure 3: Chronic pancreatitis
54
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 cal 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
qghir$an
appea-rance. 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 3: Cut surface of congested spleen
Figure 5: Cut surface of hyperplastic spleen
(Histoplasmosis)
Figure 1: Grossly normal contracted spleen
Figure 2: Grossly normal congested spleen
Figure 4: Hyperplastic spleen (Histoplasmosis)
55
Chapter 3 ?he *leeropsy Procedure
Figure 6: Incomplete contraction (irregular
congestion)
Figure 8: Multiple dark red hyperplastic
splenic nodules with tan llbrosiderotic
plaques along the splenic edges (arrow)
Figure 1O: Marked splenomegaly due to
l5rmphosarcoma
Figure 7: Ruptured and hemorrhaging
nodular splenic hyperplasia
Figure 9: Ruptured hemangiosarcoma with
blood clot
Figure 11: Focal splenic infarction
I
elaapter 3 ?he fifeeropsy Proeedure
HEMANGIOSARCOMA
Hemangiosarcoma is a tumor of neoplastic endothelial cells which often form vascular channels filled
with blood. It occurs most commonly in the spleen and right atrium of the heart, however, a primary
hemangiosarcoma can occur anywhere due to the ubiquitous nature of endothelium. Splenic
hemangiosarcomas are often as5rmptomatic until they rupture, with the resulting peracute abdominal
hemorrhaging causing h5povolemic shock and death. Atrial hemangiosarcomas may be
asymptomatic or may cause cardiopulmonary signs. They often rupture resulting in
hemopericardium, 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.
Hemangiosarcomas occur in the spleen and right atrium simultaneously (no metastasis) in about 25%
of the cases.
Asymptomatic splenic hemangiosarcoma may result in mild anemia, spherocytosis, and
schistocytosis due to red blood cell damage as they pass through the neoplastic blood channels of
the tumor (microangiopathy). The presence of acanthocytes (acanthocytosis) is an especially
important signal of possible hemangiosarcoma.
Figure 1: The pericardial sac
with blood after rupture of an
hemangiosarcoma
Figure 3: Ruptured hemangiosarcoma on the
right atrial auricle.
Figure 2: Opened pericardial sac revealing
hemopericardium
Figure 4: Marked hemoabdomen due to a
ruptured splenic hemangiosarcoma
is distended
atrial
57
*k*r:tcr 3 ?ke iSalar*ps3r Fr***ciur*
HEMA NGIO SARC OMA
(
c o ntinue d)
Figure 6: Metastatic foci of hemangiosarcoma
in the lungs
Figure 8: Microscopically, hemangiosarcomas
often form irregular and abnormal blood
vessels and vaicular passages filled with blood
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 histolory alone. In such cases,
immunohistochemistry staining (IHCf can be
very useful. IHC staining uses antibodies
directed against certain proteins that are
exclusive (or nearly exclusive) to a certain t5pe
of tissue. In the case of HSA, the antibodies are
directed against the endothelial cellprotein
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 stain is
positive, it is definitive for hemangiosarcoma,
regardless of the tumor's histologic appearance.
Figure 5: Two hemangiosarcoma masses on
the head and tail of the spleen. The larger
mass ruptured resulting in hemoperitoneum.
Figure 7: Metastatic foci of hemangiosarcoma
in the intestine and on the spleen
Figure 9: Undifferentiated spindle cell tumor
from the spleen. A hemangiosarcoma is
susoectedbut cannot be cdnfirmed because it
laclis the definitive vascular pattern.
58
Chapter 3 ?he l{*cropsy Frecedure
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
ocomma',
"wedge", or "boomerang" shape.
The phrenicoabdominal vein course 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 and
pheochromoc5rtoma.
Figure 2z l,eft adrenal gland with pale
hyperplastic cortical foci
Figure 1: Grossly normal right adrenal gland
Figure 3: Adrenocortical nodular hyperplasia
Figure 4: Adrenal pheochromoc5rtoma
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 be be done.
Each kidney can be cut out of the perirenal fat
separately. The size and shape of each should
be noted, and evidence ofnecrosis,
hemorrhage, inflammation, and neoplasia
should be sought. The capsule should peel
easily off of each kidney; excessive adhesion
suggests inflammation. Inflammation of the
kidney may or may not be evident grossly.
Inflamed kidneys may have areas of petechial
hemorrhaging and congestion.
Figure 3: Bilateral polycystic kidneys on cut
surface
Necrosis is most often in the form of an infarct.
Infarcts are generally roughly trialgular 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 obvious as variably-sized masses
andlor diffuse infiltration in the parenchyma.
Figure 2: Polycystic cat kidneys (the pale
color and subcapsular veins are normal in
cats).
Figure 1: Normal dog kidneys
Figure 4: Focal renal abscess
60
Figure 5: Bilateral chronic renal infarcts. The
affected areas are markedly shrunken,
distorting the shape of the kidney
Figure 7: Hydronephrosis with dilation of the
renal pelvis
F'igure 9: Infiltrative neoplastic disease
(lyrnphosarcoma)
Figure 5: Bilateral chronic renal infarcts. The
affected areas are markedly shrunken,
distorting the shape of the kidneys
Figure 8: Severe unilateral hydronephrosts
and hydroureter
Figure 1O: To distinguish the left kidney from
the right kidney after removal, it is customar5r
to cut t}re right kidney at a right angle, and
the left longitudinally.
6l
ffuapter S ?&* Se*r*psy Pra:*edrxr*
AIYIYLOIDO,SIS
Amyloidosis is any disease entity characterized by the formation 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 identilied that can become
misfolded in this way and form amyloid. Regardless of which parent protein that causes amyloid,
microscopically, it all looks the same. Histologically it has a very pale bluish-red (amphophilic)
homogenous and amorphous appearance.
Of the numerous proteins that can form amyloid, there are only 3 which are common and important
in domestic animals. Amyloid associated (AA amyloid) is formed from a 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
(IAPP), 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 disease which, of course, produce
lots of the acute phase protein SAA. Normally, SAA should be degraded aJter 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 secondar5r to whatever is causing the
chronic inflammation, it is often called "secondarS/ or "reactive" amyloid.
Familial amyloidosis is seen as an inherited condition in some dogs (Shar pei) and cats
(Abyssinians). The type of amyloid is usually AA. The specific genetic defect which causes them to
be predisposed to amyloid formation has not been identified.
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 "primar5/ amyloidosis.
Figure 1: Molecular pattern of a b-pleated
sheet. The pleating refers to the "warf folding
(like drapery pleats) of the polypeptides.
62
Cfuapt*r 3 ?3re I{*er*3:s3r Frc**darr*
AlltY LOI DOSIS
(
c o ntinued)
In humans, a protein called amyloid precursor protein (APP) is an integral plasma membrane protein
which is found in highest concentrations in neurons nea.r s5mapses. Misfolding 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 s5n:drome 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 all looks
the same. The b-pleating of the proteins makes amyloid very resistant to normal degradation by
proteolytic enannes. 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 s5mdrome 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 filtration, 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
AIYIYLOI DOSIS (c o ntinue d)
Chapter S ?he l$eerogrsy Froeedure
Figure 4: Grossly, renal amyloidosis is
characterized by a nondescript paleness,
although it can cause tl:e tissue to have a wa.>ry
feel when severe.
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 an bright apple-green color.
Figure 5: Microscopically, amyloid has a pale
pinkish appearance. Here in the glomeruli it is
expanding and destroying the tuft
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
Ckx.pter 3 ?he $eer*psy Fro*ed*r*
S?EP 74: REMOVAL & EXAMINATION
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 urinar5r tract from naturally
occurring mineral saits 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".
Figure I : Large, distended, and hemorrhagic
bladder (blocked cat; FLUTD)
Uroliths may be smooth, jagged,
or "point5/. In
dogs and cats, bladder stones are more common
than kidney stones.
A serious problem in cats, especially males, is
called Feline Lower Urinaty Tract Disease
(FLUTD). It is sometimes also called by its
previous narne, 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 2: Severe hemorrhagic cystitis with
marked mucosal emphysema caused by gas-
forming bacteria
Figure 4z Large stone (urolith) in the lumen of
the bladder
65
Figure 3: Hemorrhagic cystitis (FLUTD)
Chapter 3 'lhe ltecropsy Procedure
STEP 75: 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-occtpttal
Jotnt.
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.
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 3: Assess the subcutaneous tissues,
muscles, and skull bones for signs of injury.
Here, fracture of the basisphenoid bone is
evident.
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 cm
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 histopathologr.
Figure 2z F,Jlter the head is removed, it should
be skinned dorsally and the temporalis
muscles cut away.
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
Figure 5: Removal of the ca-lvarium exposes
the brain.
Figure 7: Grossly normal dog brain removed
from cranial cavity
Figure 9: Multifocal leptomeningeaj
hemorrhaging.
Figure 5: Inverting the head and cutting the
cranial nerves will allow the brain to be
removed.
Figure 8: Subdural hematoma
1O: Focal cerebral malacia
67
elaapter i3 Yhe ffeer*grs3r Fre*edur*
Figure 13: Extensive intra-cerebral
hemorrhage
Figure 12: Multifocal metastatic
hemangiosarcoma
Figure 14: Hydrocephalus with enlargement
of the lateral ventricles and loss of the septum
pellucidum
68
Figure 11: Benign choroid plexus papilloma
Chaptcr 4 T'h.e ffieeropsy K,eport
STEP 76: WRITING THD NECROPST 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:
: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 s5rmptoms observed
(especially peri-mortem signs), and the clinical diagnosis.
..,Gross necropsy findings, often arranged by organs/system. This may or may not include
pictures of the significant lesions and/or mqjor organs. For each organ, there should be a full
description followed by a morphologic diagnosis.
;The microscopic findings (if this is the final report)
..: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 77: WRITING THE NECROPST CO.IICLUSIOff
The necropsy report conclusion is arguably the most important part of the report. It is where all of
the lindings 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
s5rndrome. The conclusion should be written in narrative form and contain the following:
..iA direct statement of the morphologic cause of death or the clinical s5rndrome (if it has been
determined), including a statement about the etiolory if determined
'.
e.g. "This animat diedfrom exsanguination (bleeding out) into the chest cauitg subseqrtent to
traumatic injuies to the heart and lungs inflicted bg a high powered projectile"
' e.g. "The cause of death in this case u)as humane euthanasia"
.;A brief patJrogenesis for the cause of death or clinical sSmdrome, 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 reportl to explain how the
findings inter-relate to each other
.,:If a specific condition or neoplasia is found to be the cause of death (ex. lgmphosarcomal, write a
brtef, general description about the condition
,.,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
. ,Any other information or observations deemed pertinent or important to the case.
70
Accession Number:
Hospital Name:
Hospital Address:
Doctor's Name:
Owner's Name:
Pet's Name:
Sex:
Age:
Species:
Weight:
Necropsy Date:
.-),r-E^aD-
JJJU J EV't
DIAGNOSTICS
NECROPSY REPORT
NA2005-55
Some Great Veterinary Hospital
5555 Main Street., Los Angeles, CA
Dr. Jones
John Smith
Gizmo
Male
5-6 months
Canine
-15lbs
05/05/05
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.
lntegumentary 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
^-)^,
'JJU
DIA
alEantt
-
J
-V'T
GNOSTICS
Digestive system and
pancreas:
No-significait lesions are noted in the oral cavity or the esophagus. The abdominal cavity
contains approximately 250m1 of a yellowish, slightly blood tinged fluid (urine) (Figure 3). A
large fluid-hiled
"ac,
laier determined to be the left kidney, is displacilO the intestines
.r"iirlly, and there is very marked
peri-renal accumulation of yellow fluid (urine) (Figures 4 -
S). 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 Dia-qnosis.'
1) Illlarked uro-abdomen
2) Prominent
gastric and intestinal
pallor
3) Grossly normal pancreas
4) Left testicular cryptorchidism
Figure 4
.-),,
JJJU
DIA
r---
D
-
J
-Vr-
GNOSTICS
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 Dta-onosis: Grossly normal liver and
gallbladder
Spleen:
The spleen is normally contracted, measures approximately 9cm in length, and features no
elevated nodules or masses.
Gross Dragnosis: 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 Dia-onosls.'
1) Prominent pulmonary congestion, edema, and hemorrhage
2) Grossly normal heart
Figure 7
Figure 8
Figure 9
.J),'
,UJU
DIA
flEan^p
-
J
-Vr-
GNOSTICS
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 Dlagnoses;
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
Figure 10
Figure 11
Figure 14
^-),rrGc.an,D
f
JJJU J EV'T
DIAGNOST!CS
Adrenal glands and thyroid
glands:
No significant
gross lesions are noted in the adrenals or thyroid glands. Both sets of glands
appear to be of normal size and conformation with no nodules or masses noted.
Gross Dragnosrs: 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 Smm
intervals and no hemorrhage, malacia, or
neoplasia was observed.
Gross Dra-qnosr1s.' Moderate
ce reb rov asc u I ar co n gesti o n
Figure 15
Figure 16
76
.-),ru--
- -
-tt-J
-
-v-
DIAGNOSTICS
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 Diasnosis: Mildly edematous stomach
INTESTINE: ln 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 Diasnosis: Mildly edematous small intestine with normal colon
PANCREAS.' Ihe 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, butthere is no evidence of hemorrhage,
i nfl am m ati o n, n ec rosrls, or neop I as i a.
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 Diasnosis: Moderate hepatic passive hepatic congestion
LUNG: All of the pulmonary tissue vasculature is moderately congested. There are
extensive areas throughout the lung fissue characterized by prominent intra-alveolar
hemorrhage. No evidence of inflammation or necrosis are noted in association with
this hemorrhage. Pulmonary edema rs also prominent, and scattered atelectic regions
are present.
Microscopic Diagnosis: Marked, focally ertensive intra-alveolar pulmonary
he m o rrh ag e, co n g esti o n, ede m a, a n d ate I ectasis
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 Diasnosis: Mild myocardial edema
77
.-),,
,JJU
DIA
SPLEEN: Examination of the splenic secfions reveals contraction of the parenchyma
with prominence of the fibroleiomatous sepfae. 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 proporlioned 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
corticomedultary
junction
and the medulla. No crystaluria or proteinuria is noted in the
renal tubules. Atmost no recognizable renal parenchyma was present in the left
kidney. The tissue featured only a connective fissue capsule with scant evidence of
atrophied tubules. No inflammation was noted.
Micioscopic Diagnosis: Moderate right renal congestion with severe left renal
hydronephrosis a nd atrophy
BLADDER.' Sectrons of btadder 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 RTGHT ADRENAL GLANDS; Examined sectrons from the left and right
adrenal
glands features a normal cortical and medullary architecture. No hyperplastic
or neopkstic
grovtrth is observed. No evidence of inflammation or necrosis is noted.
Microscopic Diagnosis: Histologically normal adrenal
glands
THYROID AND PARATHYROTD GLANDS: Examined sections of thyroid
glands featured
normal follicular developing with no hyperplastic or neoplastic
growth obserued.
There is no evidence of inflammation or necrosis. The obserued
parathyrotd fissue ts
normal.
Microscopic Diasnosis: 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 obserued.
M i c roscopic D i ag nosis : Moderate cereb rovasc u I ar congestion
z-]-aF\-
-
J
-V'T
GNOSTICS
78
^s)^rz-a- - -
JJJU J E1J7,_
DIAGNOSTICS
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 bifth.
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. lt 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 distalto 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 BS, DVM
Antech Necropsy Coordinator
79
Small Animal Necropsy
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