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
1:

BASIC PATHOLOGY DEFINITIONS

" Importance of Necropsy...........
'* Basic Patholory Definitions
Basic Pathological Changes....

CIIAPIER

CIIAPTER 2: Pre-Necropsy and General Considerations

n When and Where To Do A Necropsy
. Basic Equipment
' . Protective C1othin9...............
" The Submission Form.........
" Ancillary Specimen Submissions...............
' Common Postmortem Changes....
- Describing Gross Lesions.....

. History...
. Routine vs. Cosmetic Necropsy

3: THE NECROPT PROCEDURE

. Overview.
, External Exam........
, Icterus....

Opening and Examining the Abdominal

^ Feline Infectious Peitonitis..

Opening and Examining the Thoracic

Removing the Heart and Lungs.

'

Cavtty.......

Cavity.......

Pneumonia..............

Opening and Examining the Heart........

,' Thrombosis and Postmortem Clotting......
Removal and Examination of the Liver.........

' .
lVecrosis..

" Opening and Examining the Intestine....

" Examination of the Pancreas...............

Spleen.......
Hemangiosarcoma....
* Removal and Examination of the Adrenals...
. Removal and Examination of the Kidneys.....
' AmAloidosis'..."....'..
, Removal and Examination of the Bladder.....
. Removal and Examination of the 8rain........
Removal and Examination of the

"

CIIAPIER 4: THE NECROPSY RTPORT

. Writing the Necropsy Report...
. Writing the Necropsy Conclusion............
CHAPIER

5:

..

.. ... .. . . 1 1

..........L2
............13
.......14
.....................15
...........77

,,., 2l
......21
..............23
.................24

" Limb and Skin Reflection..

"

..................10

......18
........19

CIIAPIER

" Malpositions.............

............. 7
......... 8

COMPLBIE NECROPSY REPORT

EI(AMPLE.

........... 27
.......29
................31
.............. 32
......34
.................37
........... 38
......42
.....44
.................46
...........50
.............54
....55
.................57
..... 59

....60
.......'.........62
.... 65
.....66

........7O

.........70
..,.... 7l

Chapter

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

*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.

Inflammation is the vascular and cellular

response of the body to injury. Grossly,
inflammation is characterized by a swelling and

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.

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.

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 sodiumpotassium pump to keep out water.

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.

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 nonepithelial 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.

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.

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.

Figure 1: Wet prep table.

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.

Figure 2: Dedicated necropsy room ald

necropsy table.

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 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

'

Figure 1: Basic necropsy equipment

A plastic cutting board

,, Large syringes for collecting and measuring

fluids

Some means of cutting bone; either manual

hacksaw, bone shears, and/or a Stryker
saw.

, Plastic or metal containers for 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)

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.

Supplies and containers for collecting

specimens (formalin jars and whirl-pak
bags)

Figure 3; lO%o neutral

buffered formalin

Figure 4: Whirl-pak
bag

Figure 5: Digital camera

11

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.

se*

F'igure 1: Scrubs

Flgure

2:

Plastic apron

...r&\

_ffi

Proper gloves are paramount when performing

a necropsy. Although latex surgery or

exarnination gloves are often used, they

.dffiffi.s#',.
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
Figure 3: Paper booties Figure 4: Rubber boots
ht the hands and fingers of the examiner
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_qi*#r
'*-ffi&ffi&
%,

%,,

Figure

5:

Gloves

t2

C&apter

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

'

Specimen ldentification

Owner's name, address (optional), and phone number (optional)

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

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.

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.

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

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.

Postmortem autolysis can be slowed by

decreasing the animal's temperature via
refrigeration soon after death. Since most
lysosomal enArmes and bacterial enz5rmes are

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.

normal microbial flora in the intestine

proliferate soon after death. Invasion of
organs and tissue occurs primarily through
the vessels and lymphatics.

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

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
brain

2:

Hemoglobin imbibition of the

15

ehapter 2

Fre-Saero3:sy and &eraera? Consideraticne

4:

Figure 3: Pseudomelanosis of the kidneys. In

the anaerobic abdomen, pseudomelanosis has
a black to dark blue-green hue

Figure

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 7: Pale pox-marking of the liver and

small gas bubbles due to bacterial putrefacation.

Figure 8: Though this looks like a myocardial

infarct, it is only an area of postmortem
autolysis

Pseudomelanosis of the pancreas

t6

Chapter

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 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)

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).

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

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.

Figure 1: Traditionally, animals are positioned

with their left side down (left lateral

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)

recumbency)

Figure 3: Severe emaciation (cruelty

starvation case)

Figure 4: Blood in the anterior chamber of

the eye (hyphema)

21

Figure

5:

Marked dental tartar

Figure 7: Severe fetal edema (anasarca)

("water puppy")

9: A large sublingual cystic mass full of

collected sa-liva resulting from a ruptured
salivary duct (a sublingual mucocele or ranulal

Figure

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

?*le l$eeropsSr Procedure

2:

LIMB AND S.IrriV

REFLECTION
Grasp and lift the right forelimb upward and
STEP

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.

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.

and abdomen. The subcutaneous tissues

should be inspected for hemorrhage, edema,
icterus, and other lesions.

Figure 1: Cut through the axillary region to

reflect the front limb, and through the
inguinal area to the coxofemoral joint to
reflect the hindlimb

Figure 2: Connect the exposed areas from

the two limb reflections and reflect the skin
off of the trunk and thorax dorsally and
ventrally.

Figure 3: Both left limbs have been reflected

along with the thoracic and flank skin to reveal
severe subcutaneous hemorrhage. This
hemorrhage resulted from the improper use of a
heating pad.

Figure 4: Exposed coxofemoral joint. This joint

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

Reflect the skin both dorsally and ventrally,

exposing the subcutaneous tissues of the thorax

23

*tzaptxx

?}: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
Figure 1: Icterus
be excreted. It is first converted to
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,
disease, and bile duct obstruction.

liver

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,

hrrile

-+

free
Lrilit

phagocyte

I lnto
{} sil.

*-l-*l

{*

ull.lulnin

ubin

g6&J6*esA

Hlir$bic

hepatosyte

Figure 1: Normal Heme Metabolism

24

Chapter

STEP

3:

?he lYeeropsy Prceedure

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
Figure 1: Make a submandibular skin incision
cartilaginous articulations (the cornu).
then reflect the skin
Once the tongue is reflected back, examine the palate, pharyngeal mucosa, and tonsillar tissues.
Continue dragging the tongue backward and dissect free the trachea and esophagus, cutting all
attachments back to the thoracic inlet. Identify and remove the thyroid glands and parathyroid
glands.

Figure

2:

Cut the muscles

along each side of the

mandible

Figure
bones

4:

Expose the retropharyngeal hyoid

Figure 3: Pull the tongue out through the

bottom of the mandible

Figure 4: Cut the hyoid bones at their

cartilaginous articulation (the "cornu")

25

Chapter

The l{ecropsy ?roeedure

6: Reflect the tongue, trachea, and

esophagus back to the thoracic inlet

Figure 5: Dissect the tissues covering the

ventral neck to expose the ventral trachea

Figure

Figure 7: Identify and remove the thyroids and

the parathyroid glands.

Figure 8: Marked tracheal hypoplasia (part of

Brachycephalic Syndrome)

Figure 9: Elongated soft palate (part of

Brachycephalic Syndrome).

Figure 1O: Tracheal collapse (part of

Brachycephalic Syndrome)

*kap{ar

S?EP

4;

?ke tr*er*g:"*y Fr*a:*eiaar*

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.

Figure

Normal abdominal viscera

Figure 2: Enlarged liver, extending well beyond

the last rib

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 3: The diaphragm is checked to

confirm negative pressure in the thorax. The
diaphragm should be pulled tauted against the
thoracic cavity

27

Chapter

?he Fleeropsy Proeed,ure

Figure 4: Marked abdominal hemorrhage

(hemoabdomen)

Figure

6:

Straw-colored ascitic fluid

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!)

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

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 4: Small nodules and tags of clotted

fluid cling to the sudace of the liver

Figure 5: Small nodules and tags of clotted

fluid cling to the surface of the spleen

Figure

6:

Small white raised nodular lesions

(pyogranulomas) are evident in the

parenchyma of both kidneys

30

Chapter

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

Figure 2: Gas-filled and hemorrhagic stomach

subsequent to gastric torsion/volvulus

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 4z Localized intestinal torsion

3l

Chapter

The l,{eeropsy Procedure

5:

OPENING AND EXAMIMNG

THE THORACIC CAWTY
The thoracic cavity or the abdominal cavit5r can

STEP

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.

Rih Cage
Figure 1: The ribs are cut along the
costochondral junction and near their dorsal
spinal attachments

When air is present in the thorax it is called a pneumothorax and the lungs will usually be partially
collapsed. If air builds to positive pressure inside the thorax, it is called a tension pneumothorax,
and the lungs are usually fully collapsed (atelectic).

Figure 2: Normal heart and lungs exposed

after removing the rib cage

Figure 3: Blood accumulation in the thoracic

cavity (hemothorax)

Chapter

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

STEP

6:

?he Necropsy Proeedure

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

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.

trachea indicates pulmonary edema.

Figure 1: The esophagus is separated from the

trachea back to the diaphragm

Figure

3:

Normal, uncongested lungs

Figure

2:

Tlrre

heart and lungs (the "pIuck")

removed

4: Normal uncongested lungs

(microscopic)

Figure

Figure

5:

Normal, irregularly congested lungs

6: Normal congested lungs

(microscopic). The vasculature is distended \Mith
blood but the alveoli are clear
Figure

Figure 7: Foamy tracheobronchial fluid

indicative of pulmonar5r edema

Figure 8: Pulmonar5r edema (microscopic).

Many alveoli contain eosinophilic staining fluid.

Figure 9: Pulmonary atelectasis

Figure 1O: Pulmonary atelectasis (microscopic).

The alveoli are devoid of air and collapsed.
35

Figure 11 : Pulmonar5r emphysema

Figure 12 : Pulmonar5r emphysema

Figure 13: Pulmonar5r hemorrhage

Figure 14: Pulmonar5r hemorrhage

(microscopic). The alveoli are filled with blood
with no significant inflammation. Noninflammatory pulmonary hemorrhage may
result from pulmonar5r tJrromboembolism, lung
lobe torsion, or coagulopathy.

(microscopic). The alveoli are dilated, ruptured,

and coalescing.

CS.aapter

?')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.

This is usually the anterior and ventral regions

of the lungs, giving the reddening an "anteroventral" distribution. Non-inflammatory
congestion is irregular and/or diffuse. Second,
because of the accumulation of inflammatory
cells in the alveoli, there is 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 1: Gross bronchopneumonia. Note the

pattern of reddening in the anterior and ventral
regions of the lung lobes

Figure 2: Gross bronchopneumonia. Note the

pattern of reddening in the anterior and ventral
regions of the lung lobes

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.

Figure

Figure

4: Close-up of pneumonia lung. The

alveoli are filled with inflammatory cells and
devoid of air.
37

Chapter

STEP

7:

?he l{ecropsy Proeed,ure

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 interventricular septum to the bottom of the ventricle,
then back to the base of the heart and out
through the pulmonary valve. This cut produces
a V-shaped flap which can be lifted to expose the
right ventricle, right atrium, and tricuspid valve.

Figure 1: Grossly normal heart. Note the

sharp apex.

The left side of the heart is opened in a similar

way. A single incision is made through the left
atrial free wall, down 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 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

?he l*earergrsy Froeedure

Figure 5: The flap produced allows

visualization of the right atrium, ventricle, and
tricuspid valve.

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 7: Cut through the mitral valve to exit

the left ventricle through the aorta.

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.

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 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 11: Severe left ventricular dilation.

Figure 12: Heart-based tumor

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.

(chemodectoma)

40

Chapter

The Hecropsy Procedure

Figure 13: Metastatic thyroid carcinoma

Figure 14: Metastatic salivary gland

carcinoma

Figure 15: Small metal projectile (bb)

penetrated the heart and lungs causing marked

Figure 16: Subendocardial hemorrhage on

the papillary muscle

hemorrhage

4t

Ckapter

?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 wellmolded to the shape of the vessel. Thrombi are
formed by the sequential deposition of platelets
and fibrin, forming a layered effect without the
incorporation of significant numbers of red
cells. Consequently thrombi have a friable
("crumbly like a cookie") consistency, and have
a paler, drier, rougher appearance. Because of
this 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.

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.

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 3: In this heart, both a currant jelly

clot and a chicken fat clot are evident. Both
are postmortem clots.

42

C?aapter

?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

Figure 5: A thrombus attached to the aortic

valve. Note the pale , dull and rough
appearance.

"vegetative endocarditis".

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).

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)

,,

rI

fi

43

Chapter

STEP

8:

The llecropsy Procedtrre

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.

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

3: Focal area ofhepatic

necrosis

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

2:

Grossly normal liver

Figure

4:

Severe hepatic lipidosis

The llecropsy Procedure

Figure

5:

Hepatic nodular hyperplasia

Figure

Figure

7:

Gallstone in the gallbladder

Figure

F'igure

9:

Metastatic hemangiosarcoma

Figure 1O: Hepatocellular carcinoma

Chapter

6: Nutmeg liver (chronic passive

congestion)

8:

Hepatic biliary adenocarcinoma

*iaaptcr

?*: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.

I
I
{

i
$

{
{
Ji

i
ll

Figure 2z TLre pale regions of this cow kidney

are necrotic. Since the gross tissue architecture
is still present, this represents coagulative
necrosis

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 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.

5: Coagulative necrosis. Clear

evidence of cell death is apparent (pyknotic

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.

Figure

and karyorrhectic nuclei), but the cellular

architecture is still intact

47

fkap?-er 3

'{"hr }f **rr;px.y Frc**e9:.ar*

.IVECROSIS (continued)

Figure 7: Grossly, caseous necrosis has a dry,

granular, "cottage cheese-like" consistency.

Figure 9: Grossly liquefactive necrosis is

often characterized by a well-circumscribed
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

?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.

Figure 11: Centrilobular hepatic necrosis

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 12: Periportal hepatic necrosis

49

ekapter

?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.

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.

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.

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 6: Multifocal petechial hemorrhaging

in the mucosa of the small intestine due to
hookworms

Figure 7: Roundworms (?oxocara canls) in

the small intestine

Figure 8: Whipworms (?Hcarls trulpls) rn

the large intestine

Figure 9: Severely hemorrhagic intestine

(Panroviral Enteritis)

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

Figure 12: Neurofibrosarcoma on the colon

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 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 (Gastroesophageal Reflux Dlsease or GERD)

Figure 15: Multifocal gastric ulcerations and

hemorrhage (injudicious NSAIDS use)

Figure 17: Gastric foreign body

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.

53

elaagpter

?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

3:

Chronic pancreatitis

Figure 4: Pancreatitis with fat saponification.

Note the white plaques in the adipose tissue.

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
Figure 1: Grossly normal contracted spleen
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

2:

Grossly normal congested spleen

Figure

3:

Cut surface of congested spleen

Figure

4:

Hyperplastic spleen (Histoplasmosis)

Figure

5:

Cut surface of hyperplastic spleen

(Histoplasmosis)

55

Chapter

Figure

6:

?he *leeropsy Procedure

Incomplete contraction (irregular

congestion)

Figure 7: Ruptured and hemorrhaging

nodular splenic hyperplasia

Figure 8: Multiple dark red hyperplastic

splenic nodules with tan llbrosiderotic
plaques along the splenic edges (arrow)

Figure 9: Ruptured hemangiosarcoma with

blood clot

Figure 1O: Marked splenomegaly due to

Figure 11: Focal splenic infarction

l5rmphosarcoma

elaapter

?he fifeeropsy Proeedure

HEMANGIOSARCOMA
I

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 is distended

with blood after rupture of an atrial

Figure 2: Opened pericardial sac revealing

hemopericardium

hemangiosarcoma

Figure 3: Ruptured hemangiosarcoma on the

right atrial auricle.

Figure 4: Marked hemoabdomen due to a

ruptured splenic hemangiosarcoma

57

*k*r:tcr

?ke iSalar*ps3r Fr***ciur*

HEMA NGIO SARC OMA

(c o

ntinue d)

Figure 5: Two hemangiosarcoma masses on

the head and tail of the spleen. The larger
mass ruptured resulting in hemoperitoneum.

Figure 6: Metastatic foci of hemangiosarcoma

in the lungs

Figure 7: Metastatic foci of hemangiosarcoma

in the intestine and on the spleen

Figure 8: Microscopically, hemangiosarcomas

often form irregular and abnormal blood
vessels and 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

Figure 9: Undifferentiated spindle cell tumor

from the spleen. A hemangiosarcoma is
susoectedbut cannot be cdnfirmed because it
laclis the definitive vascular pattern.

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.

58

Chapter

?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

Figure 1: Grossly normal right adrenal gland

Figure

3: Adrenocortical

nodular hyperplasia

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

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 1: Normal dog kidneys

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
surface

3: Bilateral polycystic

kidneys on cut

Figure

4:

Focal renal abscess

60

Figure

5: Bilateral chronic

renal infarcts. The

Figure

5:

Bilateral chronic renal infarcts. The

affected areas are markedly shrunken,

distorting the shape of the kidney

affected areas are markedly shrunken,

distorting the shape of the kidneys

Figure 7: Hydronephrosis with dilation of the

renal pelvis

Figure 8: Severe unilateral hydronephrosts

and hydroureter

F'igure 9: Infiltrative neoplastic disease

(lyrnphosarcoma)

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

?&* 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 betapleated 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

?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

Chapter

?he l$eerogrsy Froeedure

AIYIYLOI DOSIS (c o ntinue d)

Figure

4:

Grossly, renal amyloidosis is

characterized by a nondescript paleness,

although it can cause tl:e tissue to have a
feel when severe.

wa.>ry

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

S?EP

74:

?he $eer*psy Fro*ed*r*

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.

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".
A

Figure I : Large, distended, and hemorrhagic

bladder (blocked cat; FLUTD)

Figure

3:

Hemorrhagic cystitis (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 gasforming bacteria

Figure 4z Large stone (urolith) in the lumen of

the bladder

65

Chapter

'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.

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 1: Exposure of the atlanto-occipital

joint and foramen magnum. The spinal cord is

Figure 2z F,Jlter the head is removed, it should

be skinned dorsally and the temporalis
muscles cut away.

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.

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 5: Inverting the head and cutting the

cranial nerves will allow the brain to be
removed.

Figure 7: Grossly normal dog brain removed

from cranial cavity

Figure 9: Multifocal leptomeningeaj

hemorrhaging.

Figure

8:

Subdural hematoma

1O: Focal cerebral malacia

67

elaapter

i3

Yhe ffeer*grs3r Fre*edur*

Figure 11: Benign choroid plexus papilloma

Figure 12: Multifocal metastatic

hemangiosarcoma

Figure 13: Extensive intra-cerebral

hemorrhage

Figure 14: Hydrocephalus with enlargement

of the lateral ventricles and loss of the septum
pellucidum

68

Chaptcr

STEP

T'h.e ffieeropsy K,eport

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

..Specimen Identification

Owner's name, address (optional), and phone number (optional)

- 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:

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

..iA

'.

e.g. "This animat diedfrom exsanguination (bleeding out) into the chest cauitg subseqrtent
traumatic injuies to the heart and lungs inflicted bg a high powered projectile"

'

e.g.

"The cause of death

to

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

.-),r-E^aDJJJU J EV't

DIAGNOSTICS

NECROPSY REPORT
Accession Number:
Hospital Name:
Hospital Address:
Doctor's Name:
Owner's Name:
Pet's Name:
Sex:
Age:
Species:
Weight:
Necropsy Date:

NA2005-55
Some Great Veterinary Hospital
5555 Main Street., Los Angeles, CA
Dr. Jones
John Smith
Gizmo
Male
5-6 months
Canine

-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

^-)^,

'JJUDIA

alEantt

GNOSTICS
-V'T

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
laier determined to be the left kidney, is displacilO the intestines
large fluid-hiled
"ac,
.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 -

GNOSTICS
-Vr-

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

Figure 7

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 8

Figure 9

.J),'

,UJU

DIA

Figure 10

flEan^p

GNOSTICS
-VrFigure

11

Urogenital System:
There is very marked enlargement of the left kidney, with normal size and conformation of the
right (Figure 12). There is complete atrophy of the left renal parenchyma, leaving only a
fluid-filled, dilated pelvis, fibrous calyxes, and capsule (Figures 13 - 14). No overt rupture
could be found, however there is very prominent leakage of fluid into the peri-renal tissues.
There is a double ureter exiting the pelvis, one of which is small and non-patent going to the
trigone of the bladder, and the other is patent, markedly dilated, and ends blindly in the region
of the prostate (Figure 15). There is mild to moderate vascular congestion of the cortex and
medulla of the right kidney. The bladder is empty with no significant gross lesions noted.
Gross 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

^-),rrGc.an,D
J EV'T
JJJU

DIAGNOST!CS

Figure 15

Figure 14

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

76

Figure 16

.-),ru--tt-JDIAGNOSTICS
-v-

--

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

z-]-aF\J

GNOSTICS
-V'T

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
SPLEEN: Examination

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,
neoplasia.
Microscopic Diagnosis: Mild to moderate bladder congestion

or

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

78

^s)^rz-aJ E1J7,_
JJJU

- -

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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