Color Aflas ofSmall Animal Necropsy

First Edition

by

Richard E. Moreland, BS, DVM

Necropsy Coordinator

Antech Diagnostics

lrvine, CA

REMSOTT PUBLISHINGw w u. retns oftpub li s hing. c om

2009

Table of ContentsCIIAPIER 1: BASIC PATHOLOGY DEFINITIONS

" Importance of Necropsy........... 7

' Basic Patholory Definitions ............. 7* Basic Pathological Changes.... ......... 8

CIIAPTER 2: Pre-Necropsy and General Considerationsn When and Where To Do A Necropsy ..................10. Basic Equipment . . .. ... .. . . 1 1' . Protective C1othin9............... ..........L2" The Submission Form......... ............13" Ancillary Specimen Submissions............... .......14' Common Postmortem Changes.... .....................15- Describing Gross Lesions..... ...........77. History... ......18. Routine vs. Cosmetic Necropsy ........19

CIIAPIER 3: THE NECROPT PROCEDURE. Overview. ,,., 2l, External Exam........ ......21" Limb and Skin Reflection.. ..............23

, Icterus.... .................24

, Opening and Examining the Abdominal Cavtty....... ........... 27^ Feline Infectious Peitonitis.. .......29" Malpositions............. ................31

, Opening and Examining the Thoracic Cavity....... .............. 32" Removing the Heart and Lungs. ......34

* Pneumonia.............. .................37' Opening and Examining the Heart........ ........... 38

,' Thrombosis and Postmortem Clotting...... ......42' Removal and Examination of the Liver......... .....44

. lVecrosis.. .................46" Opening and Examining the Intestine.... ...........50" Examination of the Pancreas............... .............54. Removal and Examination of the Spleen....... ....55

" Hemangiosarcoma.... .................57* Removal and Examination of the Adrenals... ..... 59. Removal and Examination of the Kidneys..... ....60

' AmAloidosis'..."....'.. .......'.........62, Removal and Examination of the Bladder..... .... 65. Removal and Examination of the 8rain........ .....66

CIIAPIER 4: THE NECROPSY RTPORT. Writing the Necropsy Report... ........7O. Writing the Necropsy Conclusion............ .........70

CHAPIER 5: COMPLBIE NECROPSY REPORT EI(AMPLE. ..,.... 7l

3

Chapter 1 Easia Patlrology Belinitions

THE IMPORTANCE O.F .IVECROPSjr

Necropsy is the animal analory to humanautopsy. At its core, it is the systematicdissection and examination of an animalcarcass to search for abnormal anatomicalchanges (lesions) in the tissues. It is generallyused to determine the cause of death, but isalso used to chronicle disease progression.Necropsy is the purest form of patholory. Itinvolves the direct visualization of diseasedorgans and tissues (grossly and/ormicroscopically) and can provide a wealth ofinformation, not only about the animal beingnecropsied, but about the cause, progression,and possible outcome of diseases in otherpatients. Necropsy results can provide feedbackon implemented therapies, and confirm or denyclinical assumptions and diagnoses.

Obviously, a knowledge of the normal anatomyis necessar5r to make a distinction betweennormal tissues and lesions. The proper,standardized necropsy procedures are designedto allow the prosector (the person doing thenecropsy) maximal exposure of organs formaximum visualization of possible lesions.

Obtaining the maximum benefit andinformation from a necropsy requires not onlyknowledge of the proper necropsy dissectionprocedure, but loeowledge of basic diseaseprocesses. In particular an understanding ofbasic pathologr processes is paramount,starting with standard basic pathologicaldelinitions.

BASIC PATHOLOGY DEFINTTIO NSPathology is the study of disease.

Disease is any variation from the normalmorpholory or physiolory of a living organism.Disease results from various causes, such asinfection, genetic defect, or environmentalstress, and is characterwed by an identifiablegroup of lesions, clinical signs, and/orsSrmptoms. Diagnosis of disease is importantfor proper treatment.

Anatomical patholory strives to diagnosedisease by concentrating on those anatomical(morphological) changes in living tissue at thegross and microscopic levels.

Clinical pathology strives to diagnose diseaseby the use of tests on various body fluids andbody 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 ormicroscopically.

Clinical signs are changes in behavior orfunction that are observable by a third partywhich indicates disease. Limping is an exampleof a clinical sign which would suggest a brokenleg (a lesion). The terms "clinical signs' and"s5rmptoms" are often used interchangeably,although technically s5rmptoms are changes inbehavior or function which cannot be observedobjectively by a third party. Symptoms can onlybe detected by the individual (such as the painof a headache), however it may cause theanimal to behave in a way that is detectible as aclinical sign (such as head pressing).

Morphologic diagnosis is a short phrase inwhich the most important aspects of tissuechanges (either gross or microscopic) aresummed up and communicated.

The most important part of the morphologicdiagnosis is the naming of the lesion, with othercomponents giving specific information aboutthe 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" renaltubularcoagrulatlon necrosls"

, Marked, chronlc, focallg esctenslae,lgmphoplasmacgtlc, cholanglohepatltlso

7

*hxpt*r 1 Basi* ?at}a*Z<tgy t3*f?r:it!$&c

An etiolory is the cause of a disease or lesion.Etiologies are numerous and diverse andinclude infectious agents such as bacteria,fungr, or parasites, and physical damage suchas blunt force trauma or thermal burns (toname a very few). An etiologic diagnosisnames the etiologr (ex. Histoplasmosis).Determining the etiolory when possible is veryimportant as it often dictates proper treatment.

Disease Names: When a condition features aunique combination of lesions, clinical signs,arrd/or s5rmptoms, that condition may be givena narne. For example, a disease of youngpuppies caused by a morbillivirus that resultsin pneumonia, encephalitis, and the formationof eosinophilic inclusion bodies in epithelialtissues has been named Canine Distemper.

BAS.IC PATHOLAGICAL ?ISSUECHANGES TTESTOJVS/Broadly speaking, the primary lesions detectiblegrossly and/or microscopically in body tissuesinclude degeneration, necrosis, infl ammation,and neoplasia.

Degeneration represents the gradualdeterioration of cells or tissue due to tl:e loss ofspecific cellular functions and manifested inspecifi c morphologic abnormalities.Degeneration is usually reversible if the cause isreversed. Examples include cloudy sutelllngand hgdroplc ch.ange of hepatocytes, resultingfrom the failure of plasma membranes sodium-potassium pump to keep out water.

Necrosis is the morphologically recognizabledeath of cells andlor tissue. Necrosis is notreversible. In general, changes in the nucleusof cells are the primary indicators of necrosis.These changes include pgknosls,karyon'hexlq and karyolysls. A pyknoticnucleus is one which has shrunken andbecome very dense and dark, with little if anyrecognizable chromatin. A karyorrhecticnucleus is one which has fragmented intoseveral pieces. A karyolytic nucleus features aslow loss of nuclear chromatin, resulting in avery faded appeararlce.

Inflammation is the vascular and cellularresponse of the body to injury. Grossly,inflammation is characterized by a swelling andreddening of the affected tissue.Microscopically, inflamed tissues feature thepresence of vascular congestion, edema, andthe presence of one or more t5rpes ofinflammatory cells. The types of inflammatorycells present usually give some indication of thecause of the inflammation.

Neoplasia (tumor, cancer) is the abnormal anduncontrolled proliferation of body cells. A11

tumors originate from some existingtissue/body cell. Neoplastic cells usually try tomimic their tissue of origin, which is animportant feature in helping to identify them.Broadly, all body cells can be classified aseither epithelial or non-epithelial.

In naming tumors, those that arise fromepithelial cells and are determined to be benignare designated with the suffix -oma appendedto their tissue/celI type (hepatoma, marnmaryadenoma). Those that arise from epithelialtissue and determined to be malignant aredesignated with the suffix <o,rcinoma(hepatocellular carcinoma, marnmarJradenocarcinoma). T\rmors of non-epithelialorigin and determined to be benign also use thesuffix -oma (fibroma, osteoma). T\rmors of non-epithelial origin and determined to be malignantuse the suffix -sarcofltq. (fibrosarcoma,osteosarcoma). There are numerous exceptionsto these rules, with lymphoma and melanomabeing two glaring examples.

8

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WHEN AND WHERE TO DO AivEcRoPsvThe best time to do a necropsy is immediatelyafter the death of an animal to minimizepostmortem autolysis. When a necropsy has tobe delayed, the carcass should be refrigerated.Refrigeration slows, but does not stop, autolysisby slowing down enz5rmatic reactions. Ifpossible, avoid freezing the carcass. For one

thing, it is impossible to necropsy afrozencarcass and thawing can take 24 hours or more

depending on the size of the carcass. More

importantly, however, ice crystals which formduring freezing damages the tissues at themicroscopic level making histopatholo$/ more

difficult. However, if the necropsy is to be

delayed for a week or more, freezing ispreferable to the prolonged but continuing slow

autolysis of refrigeration.

The necropsy location should have adequate

light, water, ventilation, drainage, and

provisions for cadaver storage and disposal. Inclinical settings, necropsies are often done on

an exarn table, however these tables do notprovide 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 linedbiohazard garbage can for excised tissue,

formalin containers, and toxicolory and

microbiolory collection materials.

Pre- and post storage ofthe cadaver and

necropsy remains requires some form of

refrigeration. This can be problematic for large

animals. In larger dedicated necropsy rooms,

large walk-in coolers are often used. In smaller

necropsy rooms, an open top refrigerator may

suffice.

Figure 1: Wet prep table.

Figure 2: Dedicated necropsy room aldnecropsy table.

Figure 3: Specialized necropsy table withdowndraft ventilation and built-in disposal.

10

Chaptsr ? Fre-I$eerop*y arad &er:eral eonsi,derations

BASrC JVECROP,SY EQWPME NTThe choice of equipment for necropsy dependsin part on the size and type animal, t-he t5rpe ofexamination requested, and the individualpreferences of the examiner. Most small animalnecropsies 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 tapemeasure

. An ink pen/marking pen and note paper

' A plastic cutting board

,, Large syringes for collecting and measuringfluids

. Some means of cutting bone; either manualhacksaw, bone shears, and/or a Strykersaw.

, Plastic or metal containers for temporaqrviscera holding

'' A scale of some type for weighing organs

. Formalin-filled container for collection oftissues for histopath

' Multiple, variably-sized Whirl-Pak orZiplock bags for fresh tissue collection

. Digital carnera (optional)

. Supplies and containers for collectingspecimens (formalin jars and whirl-pakbags)

Figure 3; lO%o neutralbuffered formalin

Figure 2: The Stryker saw is a specialmotorized saw used for cutting bone.Essentially the same as a cast cutter, it is usedprimarily for cutting the flat bones of the skull toremove the brain. The blade oscillates, so it onlycuts bone and not soft tissue.

Figure 4: Whirl-pakbag 11

Figure 1: Basic necropsy equipment

Figure 5: Digital camera

Ciapter 2 Fr*-tr.cercps-'' =::d, General €}qansiderati*&x

PROTECTIVE CLOTHING

The wearing of prc:e::-,-e ciothing is meant toprotect the exa=:::e: =f= contamination withblood, tissues a:-: 3:cl- iluids from thecadaver tha: a:e:::e::iaL carriers of infectiouspanicies. T::e :es: ::otective clothing shouldproride cc=:-?:: :c -re examiner while notcomDro-.' s=g ;:oiection against possibleco:::a-'-:ajc::. The primary clothing should bee:=e: s-::3:cr- scrubs or cotton utilitycc;e:: 's. lqeali]', a second outer coverings*c:: as a surgical gown or a plastic aprons::o-*-c 3e \\-orn to give added protection. Thesea:-:c-es must be washed clean and disinfecteda::e: each use.

Proper gloves are paramount when performinga necropsy. Although latex surgery orexarnination gloves are often used, theygenerally are not hardy enough for a fullnecropsy on animals larger than smallrodents, young kittens, or puppies. A pair ofordinary garden or kitchen latex gloves ofappropriate size are best for performing anecropsy on most dogs, cats, and largeanimals. Compared with the latex glove, thelatter are less expensive, more durable andprovide greater protection. The gloves shouldht the hands and fingers of the examiner

se*

Flgure 2: Plastic apron

Figure 3: Paper booties Figure 4: Rubber boots

without interfering with manual dexterity and causing numbness. Disposable paper booties are goodfor providing protection for your footwear from contamination, however, many formal necropsy roomsare often wet environments. If the necropsy is performed in such a wet environment, rubber bootsshould be worn.

F'igure 1: Scrubs

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t2

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THE SUBMIS.SIOIV PORMThe style and type of necropsy submission forms vary from laboratory to laboratory, depending on the mode ofdocument storage and retrieval system in use.

At a minimum, submission forms should include the following information:

Clinic ldentification - Clinic name, lD#, address, phone number, doctor's name

Case ldentification - Assigned necropsy case number, clinical case number, and the date of submission

and examination

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

' Specimen ldentification - Animal's name, species, breed, age, weight, and sex

Clinical History! - lncludes the details of clinical findings, signs and symptoms observed (especiallyperimortem 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 grosslesions alone is often not possible and mayrequire the use of other ancillary laboratorydiagnostic procedures. Specimens for thosediagnostic procedures may be collected duringthe necropsy as deemed necessary. Specimensare often collected for:

Histopathology: Specimens should beroutlnely collected from every majororgans in all necropsies

Microbiology: Specimens are onlycollected when the history, clinicaldiagnosis, or necropsy lesions suggest acausative infectious agent

Toxicology: Specimens are only collectedwhen the history, clinical diagnosis, ornecropsy lesions suggest a toxic agent(poison).

HistapathologyHistopathologr is the primary ancillary testassociated with necropsy and provides thedefinitive answers in many cases. A1l grossnecropsies should involve the collection oftissue 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 thepresence or absence ofgross lesions. Anyobvious lesions should of course be taken,however, when no lesions are present, 7 or 2random samples should be taken from eachtissue. These specimens should beimmediately fixed in 10% neutral bufferedformalin. Formalin stops all autolysis andhardens the tissue in preparation for being cutthinly for microscopic slides. The pieces oforgans and tissues should be collected as soonas possible, and should not be more than 1.5cm thick. Collected tissue should be placed in avolume of formalin that is 10 times the tissuevolume.

MicrobiologgSpecimens intended for microbiologicalexamination should be collected aseptically aspossible. One technique is to sear the surfaceof the organ or tissue with a hot spatula, thenincise and collect the required material from thedeeper portion of solid organs, abscess, orcoagulated masses. From this incision, sterile

swabs, tissue fragments, and aspirates maythen be taken. Place sterile swabs and aspiratesin a special transport media, especially if thesuspect organism is a fastidious one. Thechoice of transport media depends largely onthe microorganism suspected to be present inthe specimen. If cultures are required, sterileswabs should be used immediately before fullyexposing body cavities or openings. Holloworgans such as segments of the gastrointestinaltract are best handled by obtaining a loop ofintestine tied at both ends and placing them ina sterile petri dish.

Toxico'l.agyMaterials for toxicological examination shouldbe collected without contamination bychemicals being used during necropsy.Chemicals that may contaminate the specimeninclude fixatives, detergents and disinfectantsroutinely used during necropsy. Althoughdifferent toxicants require specific samples forchemical analyses, in general certain tissuesamples are best. These include whole bloodand sera, tissue blocks (about 100 grams) ofboth liver and kidneys, urine, and stomach andintestinal contents.

Contact the toxicolory laboratory where thesamples will be sent to ensure that the rightspecimens and amount are collected ald thatadequate precautions for handling andpreservation are observed.

It is important to note that most laboratories donot have the capabilities to do "todcologrscreening", i.e. checking a single sample for awide range of possible toxins (like they do onCSI). In general, specific tests can be run forspecific toxins, each test having it's ownassociated cost. Obviously, random testing isimpractical, so it is important to have some ideaof what toxin to test for. The problem is thatmost toxins cause death without producingsignificant (or any) gross or microscopic lesionswhich might give clues to the cause. Generally,the most important information on which toxinto check for comes from the clinical historyand/or antemortem clinical signs. Whiletoxicologr screening is not widely available,toxicolory panels, in which a group of individualtests are run together, are common. A commontoxicologr panel would include thosecompounds commonly used in maliciousand/or accidental animal poisoning such asstrychnine, arsenic, metaldehyde, and warfarin.

t4

Chapter 2 Pre-}lecr*psy and GeEreral, Considerations

COMMO N POSTMORTEM CITA.NTGES

When an abnormality is found duringnecropsy, it must be judged whether it is anantemortem leslon or a postmortemchange. Antemortem lesions occurred beforedeath and therefore may have contributed tothe death or disease of the animal;postmortem changes occur only after deathand therefore cannot have contributed to thedeath of the animal. Judging which is whichis very important so that a properinterpretation c€m be made.

Postmortem autolysis result from thedegradation of tissues associated with therelease of proteolytic lysosomal enz5rmes fromtissue cells when they die, as well as from theaction of postmortem bacterial enzJrrnes(putrefaction). Bacteria that form part of thenormal microbial flora in the intestineproliferate soon after death. Invasion oforgans and tissue occurs primarily throughthe vessels and lymphatics.

Postmortem autolysis can be slowed bydecreasing the animal's temperature viarefrigeration soon after death. Since mostlysosomal enArmes and bacterial enz5rmes aretemperature dependent, lower temperaturesslows (but does not completely stop) thedegradation of the tissues. Lower temperaturealso inhibits bacterial growth. Freezing is not,however, recommended because the icecrystals which form damage cells and canmake this histopath difficult to interpret. Still,if the necropsy must be delayed a week ormore, freezingis recommended since thecontinued degradation of tissue refrigeratedlonger than would have even more harmfulconsequences.

Figure 1: Hemoglobin imbibition of the smallintestine

There are several tissue changes which canoccur after death however the more commonpostmortem changes seen at necropsy includehemoglobin imbibition, pseudomelanosis, andlivor mortis.

Hemoglobln tnhlbttton is the pinkish toreddish coloration imparted to tissues due tothe lysis of red blood cells. It is most evident onthe outer surfaces of light-colored organs likethe intestine or brain, or on the inner surfacesoflarge arteries or in tl:e heart.

Blle tnblbitlon is the greenish-yellowcoloration imparted to tissues in contact withthe gallbladder after death. This is usually seenon the surrounding liver tissue, as well as onloops of gut.

Pseudomelcnosis is a blue-green to blackishdiscoloration imparted to tissues due to theaction of bacteria on hemoglobin, resulting inthe formation hydrogen sulfide and iron sulfide.This discoloration is often black within theanaerobic environment of the abdominal cavity,but is often more greenish in the more aerobicenvironment of the skin.

Lluor morals (hypostattc congestlon/ iscaused by the settling of blood to the down sideof the animal's body due to gravity. Thisgravitational settling of blood and body fluidsresults in a darker reddish coloration of theorg€rns and tissues on the down side of thecadaver.

Figure 2: Hemoglobin imbibition of thebrain 15

ehapter 2 Fre-Saero3:sy and &eraera? Consideraticne

Figure 3: Pseudomelanosis of the kidneys. Inthe anaerobic abdomen, pseudomelanosis hasa black to dark blue-green hue

Figure 5: Pseudomelanosis in the ventralabdominal skin. In the more aerobicenvironment of the skin, pseudomelanosis hasa lighter green hue.

Figure 6: Livor mortis in the lungs. Blood hassettled in the left lung lobes due to gravit5r,making them much darker than the right lobes

Figure 8: Though this looks like a myocardialinfarct, it is only an area of postmortemautolysis

Figure 4: Pseudomelanosis of the pancreas

Figure 7: Pale pox-marking of the liver andsmall gas bubbles due to bacterial putrefacation.

t6

Chapter 2 Fre-I$eeropsy and GeneraL Considerations

DESCRIBIIVG GROSS LESIOJVS

The general rule in recording necropsy findings is to be descriptive rather than interpretive.Interpretation of lesions should be described in the diagnosis andlor conclusion section.

When applicable tissues/lesions should be described by:

-,:Shape/margins (irregular, circular, ovoid, oblong, polypoid, botryoid, wedge-shaped, papillary,pedunculated, indistinct, well-demarcated, infiltrative, etc.)

-,.iConsistency (hard, firm, gritty, soft, rubbery, sponry, viscous, friable, etc.)

'...,,Color (black, brown, mahogony, grey-green, red, tan, white, off-white, yellow)

.,.:Size (measured in centimeters)*tDistribution and location (bilateral, unilateral, diffuse, focal, multiple, multifocal, patchy, etc.)

.lSurface appearance (bulging, ulcerated, eroded, rough, reticulated, smooth, pitted, umbilicated,verrucous, etc.)

Figure L: "Lung and liuer lobes arecharacterized bg firultifocal, coalescing darkcircular lesions in the parenchgma. These lesionsuary in size from .2 to .Scm, and haue a.firmconsistencg on palpation." (Metastaticmelanosarcoma)

Figure 3z "Both kidnegs feafiire similarpathological changes. Both kidnegs areenlarg e d uith slightlg distorted conformatio n.There are multifocal, uariablg sized, pale, firmma.sses present throughout the renalparenchgma. Mang blood uessels contain largeocclusiue thrombi and scattered areas of theparenchg ma are reddened.Gross Diaqnosi.s: Bilateral, multifocal irregularrenal masses with uascular thrombosis andhemorrhag e (fuing al infection - Phg comg co sis).

Figure 2z oThe kidneg features multifocal,roughlg tiangula4 pale areas in the cortex.Eachis bordered bg a thin zone of reddeningand are approximatelg 1 x 2 cm in size." (renalcortical infarcts)

t7

Chapter * Fra-?6ecro3:s3r a:ad &erqeral ec::siderati&ns

HIs.TORYThe lmporAance of a good history cannot be oueremphaslzed. Arriving at a proper diagnosisand/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 thedisease process, warrant greater scrutiny. The history may suggest the examination of tissues notnormally 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 doesnot affect what is seen at necropsy, it will affect the interpretation of what is seen. Consider thefollowing examples.

Figure 1: Edema fluid in tissues appears asa clear translucent, almost gelatinousmaterial. It can be seen here in thesubcutaneous tissues of a dog's forearm.This is a good example of subcutaneousedema.

Figure 2: A similar clear translucent fluidlayer is present here in the skin taken fromthe dorsal back ofa dog. Subcutaneousedema would be the most likelyinterpretation. Subcutaneous edemasuggests many possible pathogenic scenariosincluding heart failure andf orhypoproteinemia. However, the historyindicated the animal was being giventherapeutic subcutaneous fluids in this area.This fluid is, in fact, the result of that therapyand not from pathological edema. Withoutthat history, many erroneous interpretationsof this lesion could have been made.

18

Ckapter 2 Fre-Ir{e*a'*psy *rad **vzera? e*cesideratit>xs

ROUfiNE YS. COSMETIC NECROPSTA routlne necropsy is the standardized, systemic gross dissection of the carcass whose goal is toassure that all important organs and tissues are',risualized with maximal exposure to avoidoverlooking important lesions. Since the aim of the technique is thoroughness, there is considerablemutilation of the carcass.

A cosmetic necropsy is one where the dissection is not as extensive (or as mutilating) as in a routinenecropsy. It is commonly requested by owners who have a strong aversion to the mutilation of theirpet, and/or wish some post-necropsy viewing of the body. Such necropsies are not nearly completeand 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 ventralmidline incision. Visualization of organs and lesions can be difficult, and many of the cuts needed toremove 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 thethorax. Cut the diaphragm as completely as possible from its attachments.Reaching as far as possible into the cranial mediastinum, cut the esophagus, trachea, andcranial mediastinal vessels at the thoracic inletRemove the heart and lungs by pulling the esophageal-tracheal stump through the abdominalincision, tearing or cutting them free from their dorsal attachments

, Cutting the root of the mesentery will allow the liver, stomach, spleen, and small intestines tobe partially extracted through the skin incision. Cutting the colon as far caudally as possiblewill 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 theabdominal 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 thesides.Using whichever bone cutting implement you have available, cut the calvarium to exposethe brain.Sever the spinal cord and lift the brain carefully. Cut all of the nerves at the base of thebrain. Tilt the head upward and backward to simplify removal of the brain from the cranialcavity.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 specimensdeemed necessary

The carcass should be returned to as near a pristine state as possible. Clean any blood and fluidsfrom the hair coat. Sutures should be continuous and as neat as possible.

t9

ekapt*r * ?h* IX**r*pe3r Fr*ec*;:r*

OVERWEWThe goal ofthe gross dissection phase ofthenecropsy is the removal and close examinationof the major organs for lesions, and for thecollection of tissue samples for further ancillarytesting. In most animals this involves thereflection of the front and hind limbs on oneside to get greater access to the thoracic andabdominal cavities. Once the body cavities areexposed, cursory examination of the organs isperformed prior to the complete removal of theorgans, with the more detailed organexaminations performed outside of the body.

In a routine necropsy, there is no generally adetailed dissection of the musculoskeletalsystem, joints, spine or spinal cord, the eyes,sinus cavities, or the inner ears unless thehistory, clinical signs, or obvious necropsychanges warrant detailed attention.

Position the carcass on the table in left lateralrecumbency. Carefully examine the animal'sexterior. Measure the carcass length from tailbase to nose-tip. Observe the eyes, ears, andother body openings for the presence ofsecretions or excretions, prolapse, andabnormal coloring of mucus membranes.Examine the hair coat, and note for thepresence of ectoparasites, areas of alopecia,thickening of the skin, tumor masses, andpossible wounds. Palpate the continuity of bonystructures and look for evidences of fractures,enlarged joints, and abnormal masses. Openthe mouth and examine the oral cavity (if rigorpermits). Many types of abnormalities areevident from the external exarn.

Figure 2: Alopecia and hyperpigmentation(demodecosis)

Figure 4: Blood in the anterior chamber ofthe eye (hyphema)

Figure 1: Traditionally,with their left side downrecumbency)

animals are positioned(left lateral

Figure 3: Severe emaciation (crueltystarvation case) 21

Figure 5: Marked dental tartar

Figure 7: Severe fetal edema (anasarca)("water puppy")

Figure 9: A large sublingual cystic mass full ofcollected sa-liva resulting from a rupturedsalivary duct (a sublingual mucocele or ranulal

Figure 6: Severely worn teeth

Marked oral icterus

Figure 1O: Prior to the necropsy, x-rays canbe very useful in helping to localized brokenbones and finding small metal projectiles

22

Chapter S ?*le l$eeropsSr Procedure

STEP 2: LIMB AND S.IrriVREFLECTION

Grasp and lift the right forelimb upward andcut all muscles between the subscapular areaand the rib cage to free the limb. Reflect theleg dorsally. Hold the right hind limb up andcut down to the hip joint. Cut the joint capsuleand the round ligament to free the head of thefemur. Continue cutting through the softtissue and reflect the freed hind limb to thedorsum of the specimen. Inspect the hip jointfor signs of Degenerative Joint Disease orother changes.

Figure 1: Cut through the axillary region toreflect the front limb, and through theinguinal area to the coxofemoral joint toreflect the hindlimb

Figure 3: Both left limbs have been reflectedalong with the thoracic and flank skin to revealsevere subcutaneous hemorrhage. Thishemorrhage resulted from the improper use of aheating pad.

Connect the skin opening made when reflectingthe front leg to the skin opening made whenreflecting the hind leg by cutting beneath theskin along the right lateral thorax and abdomen.

Reflect the skin both dorsally and ventrally,exposing the subcutaneous tissues of the thoraxand abdomen. The subcutaneous tissuesshould be inspected for hemorrhage, edema,icterus, and other lesions.

Figure 2: Connect the exposed areas fromthe two limb reflections and reflect the skinoff of the trunk and thorax dorsally andventrally.

Figure 4: Exposed coxofemoral joint. This jointfeatures a thickened capsule and erodedfemoral head cartilage with polishing of theunderlying bone (ebernation). These are allsigns of Degenerative Joint Disease.

23

*tzaptxx 3 ?}:ln: l{*er*pe3, F*:a:*edaar*

ICTERUSA distinctive yellowing is often noted in thesubcutaneous as well as abdominal tissues onnecropsy. This yellowing is called icterus orjaundice and is caused by the deposition ofthe compound bilirubin. Bilirubin is a normalbreakdown product of heme and icterus onlyoccurs when it present in high amounts in theblood stream. Normal heme metabolism startswith the phagocytosis of old or damaged RBCsin the spleen by splenic macrophages.Hemoglobin is removed and separated into itsheme, globin, and iron components. The ironis converted to ferritin and hemosiderin forstorage and recycling. The globin is brokendown into amino acids for recycling. Theheme cannot be recycled and therefore mustbe excreted. It is first converted to Figure 1: Icterus

unconjugated bilirubin within the splenic macrophage, then transferred via the blood-stream to theliver while attached to albumin. Within the liver cell it is conjugated with glucoronic acid to becomeconJugated bilirubtn. It is then put into the bile via the bile caniculi, the small tracts between thehepatic cords. Bilirubin is not a bile salt and does not aid in the breakdown of fat; it is only in thebiliary system as a means of disposal.

The three primary mechanisms of icterus are intravascular or extravascular hemolysis, liverdisease, and bile duct obstruction.

With hemolysis, the spleen is forced to deal with an excessive amount of heme, either from increasedphagocytosis (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 forprocessing by the liver. The liver is unable to process all of this extra bilirubin which consequentlyremains 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 fromnormal heme metabolism. The excess unconjugated bilirubin remains in the bloodstream and stainsthe tissues yellow. In addition, the swelling of hepatocJrtes causes some obstruction of the bilecaniculi, 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 gainaccess to the biliary system, spills over into the bloodstream and stains the tissues yellow.

g:lururonk acld

l,*-l-*lfree g6&J6*esA

Lrilit ubin Hlir$bic

hepatosyte

I lnto{} sil.

ull.lulnin

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phagocyte

Figure 1: Normal Heme Metabolism24

Chapter 3 ?he lYeeropsy Prceedure

STEP 3: REMOVAL OF THE TONGUE,TRACHEA, AND ESOPHAGUS

Make a skin incision from the mandibularsymphysis along the mid-ventral neck, to thethoracic inlet. Reflect the skin as before toexpose the underlying structures.

The tongue must be removed to thoroughlyexamine the buccal cavity. Cut the muscularand tissue attachments of the tongue along theinner surfaces of both sides of the mandible.After cutting, the tongue can be pulled outthrough the floor of mandible. Reflect thetongue back to the pharyngeal hyoid bones,continuing to cut all muscular attachments.Cut through the hyoid bones by severing theircartilaginous articulations (the cornu).

Once the tongue is reflected back, examine the palate, pharyngeal mucosa, and tonsillar tissues.Continue dragging the tongue backward and dissect free the trachea and esophagus, cutting allattachments back to the thoracic inlet. Identify and remove the thyroid glands and parathyroidglands.

Figure 1: Make a submandibular skin incisionthen reflect the skin

Figure 3: Pull the tongue out through thebottom of the mandible

Figure 4: Cut the hyoid bones at theircartilaginous articulation (the "cornu")

Figure 2: Cut the musclesalong each side of themandible

Figure 4: Expose the retropharyngeal hyoidbones

25

Chapter 3 The l{ecropsy ?roeedure

Figure 5: Dissect the tissues covering theventral neck to expose the ventral trachea

Figure 7: Identify and remove the thyroids andthe parathyroid glands.

Figure 9: Elongated soft palate (part ofBrachycephalic Syndrome).

Figure 6: Reflect the tongue, trachea, andesophagus back to the thoracic inlet

Figure 8: Marked tracheal hypoplasia (part ofBrachycephalic Syndrome)

Figure 1O: Tracheal collapse (part ofBrachycephalic Syndrome)

*kap{ar S ?ke tr€*er*g:"*y Fr*a:*eiaar*

S?EP 4; OPE"ItrIIIG A:VD .EJCAMIHruVGTTT& ABDOMTNAT, CAWTY

The abdominal cavity is opened by removingthe abdominal (flank) wall along the ventralmidline, the curve of the last rib, and dorsallyat the level of the kidneys. Usually theabdominal viscera is initially obscured by fattyomentum which can be removed.

The viscera should be regarded in situ forobvious lesions, fluid accumulations, relativesizes, and malpositions, however, no detailedexamination is done until all organs arecompletely removed. Inflammation of theperitoneal cavity (peritonitis) is generallynoted by the presence of reddening androughening ofthe serosal surfaces ofthevisceral organs, along with the presence ofIibrinous tags.

Any abdominal fluids should be collected andquantified. Broadly, abdominal fluids can beexudates, transudates, or blood. Blood in theabdominal cavity is referred to as ahemoabdomen. When large amounts of bloodare present, it is important to try anddetermine the source of the bleed beforeremoving the abdominal viscera as thisgenerally makes it more difficult to determinethe origin. The presence of transudates andexudates in the abdominal cavity is calledascites. When transudates areuncontaminated with blood they generallyhave a clear yellowish (straw-colored)appearance. When blood is present it tints thefluid 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 aregenerally the best features to distinguish itfrom serosanguineous fluid.

The liver should be assessed in situ. Extensionwell beyond the last rib is consideredhepatomegaly.

The thoracic cavity should be assessed fornegative pressure by inspection of thediaphragm. It should be pulled taut toward thethoracic cavity, and puncturing it shouldproduce an in-rush of air and a relaxation ofthe muscle.

Figure Normal abdominal viscera

Figure 2: Enlarged liver, extending well beyondthe last rib

Figure 3: The diaphragm is checked toconfirm negative pressure in the thorax. Thediaphragm should be pulled tauted against thethoracic cavity 27

Chapter 3 ?he Fleeropsy Proeed,ure

Figure 4: Marked abdominal hemorrhage(hemoabdomen)

Figure 5: Serosanguinous ascitic fluid. Thoughit looks like blood, its low viscosity as judgedduring the necropsy suggested it was in factblood-tinged fluid.

Figure 7'. An unknown intra-abdominal massturned out to be a granuloma formed aroundgauze left from a previous surgery. This iscaused a gossiphiboma (it's scary that it occursoften enough to have a name!)

Figure 6: Straw-colored ascitic fluid

28

Ckapt*r S ??ae i***r*p*y Frr***&zzx*

FELTNA TNFECTTOUS PERTTOJVr?IS (FrP)

FIP is a serious, fatal, infectious but non-contagious viral infection of cats. It is caused by a mutationof the feline enteric coronavirus. FIP causes widespread pyogranulomatous inflammatory lesionsthroughout the abdominal visceral and/or thoracic organs, and often a thick viscous yellow ascitic orpleural fluid. The widespread infection causes weight loss, anorexia, non-responsive fever, andeventually organ failure and death.

The disease pathogenesis involves complement fixation and the release of vasoactive amines thatcauses increased vascular permeability and endothelial cell retraction. In addition, antigen-antibodycomplexes result in systemic vasculitis. These changes lead to the exudation of fluid and Plasmaproteins typical of tn6 effusive "wet" form, as well as organ damage due to imPaired blood flow. The wetiorm generally causes death within a few weeks. The "dry" form is more insidious, leading to deathover a much longer period (often years).

Testing for the disease clinically can be problematic. Exposure to the virus with the production of anantibody titer does not mean the virus has mutated and will cause FIP. Higher titers could be moresuggestive, however some cats with fulminant FIP may have no titer. Most tests involve "statisticalprobabilities" 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 theratio is greater than 0.8 there is a 610/o statistical chance the cat does not have FIP. Another statisticalmethod is Rivalta's Test. This test is performed by taking a test tube that is filled with distilled waterand 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 negativeRivalta'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 valueof 3.5 mg/dl or higher.

At necropsy, the wet form of FIP is characterized by a viscous yellowish fluid which generally clots soonafter the abdomen is opened. The serosal surfaces of the intestine, kidneys, liver, and pancreas areoften covered to varying degrees with small white nodules. These nodules represent pyogranulomas,accumulations of macrophages and neutrophils. This reaction is more common to fungal infectionsthan to viral ones. In fact, fungal infections such as histoplamosis, cr5ptococcosis, blastomycosis, andcoccidiomycosis must be considered as part of the differential. To delinitively diagnosis FIP,immunohistochemistry staining (IHC) of affected organs is necessar5r. In IHC staining, antibodiesspecific for the feline coronavirus are attached to a stain and exposed_to the affected tissue. Ifcoronavirus is present in the lesion, the antibody will stick and so will the stain, conlirming FIPinfection.

Figure 1: The abdomen is Iilled with copiousamounts of a clear but viscous yellowish fluidwith tags of fibrin throughout

Figure 2: Soon after opening the cavity, thefluid has clotted.

29

Chapter 3 The $ecropsy Procedure

FDLItte INFDCTIOUS PEP,ITOMTIS (continued)

Figure 3: Small white nodular lesions cover theserosal surfaces of the small intestine.Microscopically these nodules featureaccumulations of macrophages and neutrophils

Figure 5: Small nodules and tags of clottedfluid cling to the surface of the spleen

Figure 4: Small nodules and tags of clottedfluid cling to the sudace of the liver

Figure 6: Small white raised nodular lesions(pyogranulomas) are evident in theparenchyma of both kidneys

30

Chapter 3 The $eeropsy Frocedure

MALPOSITIONSVolrnrlus/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 tosuffer from a buildup of carbon dioxide and, eventually, a lack of oxygen. A common consequence seenis bloating (gaseous dilationl of the stomach. The twisting also pulls the spleen from the left side of thebody 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 bloodsupply draining the telescoped portion is cut off so the cells die from lack of o:<ygen. Occasionally instrbhg trauma cases (such a hit by car) the diaphragm will rupture allowing the intestines to move upinto the chest cavity (diaphragmatic hernia). These abdominal organs interfere with the normalfunctioning of the heart and lungs.

Figure 1: Large congested spleen evident on theright side of the body caused by rotation of thestomach

Figure 3: Section of gut telescoped on itself(intussusception). The telescoping cuts offvenous dralnage from the affected area andthe effect on the tissue is identical to a torsion

Figure 2: Gas-filled and hemorrhagic stomachsubsequent to gastric torsion/volvulus

3l

Figure 4z Localized intestinal torsion

Chapter 3 The l,{eeropsy Procedure

STEP 5: OPENING AND EXAMIMNGTHE THORACIC CAWTY

The thoracic cavity or the abdominal cavit5r canbe opened next. When opening the thoraciccavity, first cut the right ribs dorsally a few inchesbelow their vertebral attachments using boneshears. Next, cut along the costo-chondraljunction. The rib cage can then be removed bycutting any remaining muscle or soft tissues.Removal of the rib cage exposes the thoracicorgans in situ.

Upon opening the thoracic cavit5r, make note ofany fluid in the chest or in the pericardial sac.Blood in the thoracic cavity is calledhemothorax. If there is fluid in the chest cavitythat is not blood, the term is hydrothorax orpleural effusion. If the fluid is not blood, but isred because it is *blood-tinged", it is described asserosanguinous.

Figure 2: Normal heart and lungs exposedafter removing the rib cage

Rih Cage

Figure 1: The ribs are cut along thecostochondral junction and near their dorsalspinal attachments

Figure 3: Blood accumulation in the thoraciccavity (hemothorax)

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

Chapter 3 The l$eeropsy Froeedure

Figure 4: Serosanguinous fluid in the thorax(hydrothorax/pleural effusion). Though the fluidis red, it is evident that it is translucent and notthick enough to be actua,l blood.

Figure 6: Here the chest cavity is filled with avery thick red exudate (often called a "tomatosoup" exudate) consistent with blood-tingedpus (pyothorax) caused by Nocardia.

Figure 5: Milky white fluid in the thoraciccavity (chylothorax). This condition is usuallyseen in association with cardiomyopathy, andrarely, (although it is a common misconception)due to thoracic duct rupture.

Figure 7: Much of the intestines havemigrated into the thoracic cavity via a hole inthe diaphragm (diaphragmatic hernia). Thenegative pressure in the thorax facilitates themovement of intestines into the thorax eventhrough very small openings.

JJ

Chapter 3 ?he Necropsy Proeedure

STEP 6: REMOWNG THE HDART AND.LUTVGS

The esophagus should be separated from thetrachea and is reflected to the point where itgoes through the diaphragm into the stomach.The aorta and vena cava are cut and thetrachea, heart, and lungs ("the pluck") areremoved en masse. The trachea should beopened and followed as far into the bronchi aspossible. Foamy fluid in the bronchi ortrachea indicates pulmonary edema.

Figure 1: The esophagus is separated from thetrachea back to the diaphragm

The external color of the lungs should beassessed and all lobes palpated for firmnessand/or nodular lesions. At necropsy, theappearance of unormal" lungs can vary from anuncongested pale light pink, to an irregularsplotchy reddened congestion. Other grosslyevident findings include hemorrhage, edema,neoplasia, and pneumonia.

Figure 2: Tlrre heart and lungs (the "pIuck")removed

Figure 4: Normal uncongested lungs(microscopic)

Figure 3: Normal, uncongested lungs

Figure 5: Normal, irregularly congested lungs

Figure 7: Foamy tracheobronchial fluidindicative of pulmonar5r edema

Figure 6: Normal congested lungs(microscopic). The vasculature is distended \Mithblood but the alveoli are clear

Figure 8: Pulmonar5r edema (microscopic).Many alveoli contain eosinophilic staining fluid.

Figure 1O: Pulmonary atelectasis (microscopic).The alveoli are devoid of air and collapsed. 35

Figure 9: Pulmonary atelectasis

Figure 11 : Pulmonar5r emphysema Figure 12 : Pulmonar5r emphysema(microscopic). The alveoli are dilated, ruptured,and coalescing.

Figure 14: Pulmonar5r hemorrhage(microscopic). The alveoli are filled with bloodwith no significant inflammation. Non-inflammatory pulmonary hemorrhage mayresult from pulmonar5r tJrromboembolism, lunglobe torsion, or coagulopathy.

Figure 13: Pulmonar5r hemorrhage

CS.aapter S ?')a* 3€**a*p*V ?r*';<,*taz::

PNEUMOMAPneumonia is inflammation of the lungs. It ischaracterized by the accumulation ofinflammatory cells and fluid within alveoli.Grossly, it can be difficult to distinguishbetween inflammation from physiological orpassive congestion of the lungs since bothfeature a reddening of the lung parenchyma.Three gross characteristics of pneumonia canhelp in distinguishing the two. First, sincepneumonia is usuaily caused by bacteria whichenter the lungs via the trachea(bronchopneumonia), the inflammation startswhere the bacteria initially settle in the lungs.

Figure 1: Gross bronchopneumonia. Note thepattern of reddening in the anterior and ventralregions of the lung lobes

Figure 3: Pneumonia (microscopic). Note thepresence of inflammatory cells filling thealveoli. Palpation of this tissue would result ina firm feel, and there is no air to allow it tofloat when placed in liquid.

This is usually the anterior and ventral regionsof the lungs, giving the reddening an "antero-ventral" distribution. Non-inflammatorycongestion is irregular and/or diffuse. Second,because of the accumulation of inflammatorycells in the alveoli, there is litfle or no air in thealveoli, resulting in a firm feel to theparenchyma (consolidation). Third, the lack ofair in the lungs in pneumonia causes the lungsto sink when placed in water or fixative,whereas congested lungs will still float.

Figure 2: Gross bronchopneumonia. Note thepattern of reddening in the anterior and ventralregions of the lung lobes

Figure 4: Close-up of pneumonia lung. Thealveoli are filled with inflammatory cells anddevoid of air.

37

Chapter 3 ?he l{ecropsy Proeed,ure

STEP 7: OPENING AND EXAMININGTHE HEART

The outer surface of the heart should beexamined before opening. Assess the sharpnessof the apex; rounding may suggest hypertrophyor dilation. If a scale is available, the heartshould be weighed. The normal heart weight (g)to body weight (kg) ratio is 7.4 + 0.2 however,care must be taken when interpreting thisnumber as certain factors can affect the formula.In a fat or obese animal, the ratio will be skewedlow, where as in a thin or emaciated animal itwill be skewed high.

One of the most widely accepted methods ofopening the heart is by following the normal pathof blood flow. Beginning in the caudal vena cavaand/or entrance to the right atrium, a V-shapedincision is made by cutting down through theright atrio-ventricular valve, following the inter-ventricular septum to the bottom of the ventricle,then back to the base of the heart and outthrough the pulmonary valve. This cut producesa V-shaped flap which can be lifted to expose theright ventricle, right atrium, and tricuspid valve.

The left side of the heart is opened in a similarway. A single incision is made through the leftatrial free wall, down ttrrough the lateral borderof mitral valve and the left ventricular free wallall the way down to the apex. A cut is thenmade through the medial leaves of the mitralvalve into and out of the aorta.

Sometimes a better in situ visualization of thevalves, as well as an opportunity to compare therelative thickness of the right and left ventricularmyocardium, can be determined by doing asingle longitudinal cut. The cut starts throughthe middle of the right ventricle and proceedsthrough the RV lumen, the interventricularseptum, the LV lumen, and finally through theLV 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 thebottom of the right ventricle.

Figure 1: Grossly normal heart. Note thesharp apex.

Figure 2: Yery rounded apex indicatingeither hypertrophy or dilation

Figure 4: Cut along the septum and exit theright ventricle through the pulmonary artery.

38

elrapter S ?he l*earergrsy Froeedure

Figure 5: The flapvisualization of thetricuspid valve.

produced allowsright atrium, ventricle, and

Figure 6: To open the left heart, cut into theleft atrium via the pulmonar5r veins andcontinue the cut through the mitral valve andalong the free wall to the bottom of the leftventricle.

Figure 8: By lining up on the middle of theright ventricle, a single cut through the rightventricle, interventricular septum, and the leftventricle will allow a better comparativevisualization of the chambers. In this normalheart, note the 3:1 ratio of left ventricularthickness to right ventricular thickness. Alsonote the relatively tubular shape of the leftventricular lumen, not a round or bowl shapeas is the popular misconception.

Figure 7: Cut through the mitral valve to exitthe left ventricle through the aorta.

39

Figure 9: The nodular thickening noted in themitral valve of this partially fixed heart isValrmlar Endocardiosis (Degenerative MitralValve Disease). In this condition, the heartvalve (usually the mitral) is thickened by theproliferation of the valve's fibrous andm5n<omatous tissue. This proliferation distortsthe leaves of the valve, giving them a nodularappearance. This change is usually mild and isa common incidental finding at necropsy of noclinical consequence. It can get worse with age,however, and can be significant in older dogs.When severe, the valves do not close properlyand blood regurgitates into the left atrium onsystole (causing a systolic murmur). Theeventual consequence of this regurgitation ischronic heart failure. King Charles CavalierSpaniels have a very high genetic disposition todevelop this condition at an early age.

Figure 11: Severe left ventricular dilation.There is thinning of the free wall and septumand smoothing of the endocardial surface. Thelumen shape is more bowl-like as opposed to amore normal tubular shape.

Figure 10: Severe left ventricular hypertrophyis evident in this partially fixed heart. Thelumen is extremely narrowed by the markedthickening of the septum and free wall.Cardiomyopathy (with a big C) refers toprimary cardiac disease in which someinherent (and idiopathic) defect in the heartmuscle itself results in hlrpertrophy or dilationof the myocardium (Hypertrophic or DilativeCardiomyopathy). Secondar5r dilation orhypertrophy (due to valvular defects, septaldefects, h5pertension, etc.) does not constituteCardiomyopathy.

Figure 12: Heart-based tumor(chemodectoma)

40

Chapter 3 The Hecropsy Procedure

Figure 15: Small metal projectile (bb)penetrated the heart and lungs causing markedhemorrhage

Figure 14: Metastatic salivary glandcarcinoma

Figure 16: Subendocardial hemorrhage onthe papillary muscle

Figure 13: Metastatic thyroid carcinoma

4t

Ckapter S ?h.c ffe*r*psy Fr*cedare

THROMBOSIS as. POSTMORTDMCLOTTINGDuring the necropsy examination,differentiating postmortem clotting fromantemortem clotting is very important. Clotsare common in the heart and larger vessels.Thrombi are always pathological andsignificant, while postmortem clots hold nosignificance.

The normal clotting mechanism in the livinganimal leads to the formation of fibrin to plugopenings in blood vessels to prevent bleeding.When clotting occurs within the vascularsystem in response to endothelial injury, theresulting clot is called a thrombus and canblock blood flow to tissues and cause necrosis(infarction). Blood also clots after death inresponse to the release oftissue factors. Theseare called postmortem clots. Distinguishingantemortem clots (thrombi) that areimportant in causing disease from postmortemclots that are of no significance is importantduring necropsy. Even though they are botl:clots, the mechanism of their formation makesthem physically distinguishable from eachother. Postmortem clots form as a solid net offibrin within the vessel, entrapping largenumbers of red blood cells. Consequentlypostmortem clots are dark red in color, theyhave a gelatinous consistency, and are smooth,wet and shiny. They are also usually well-molded to the shape of the vessel. Thrombi areformed by the sequential deposition of plateletsand fibrin, forming a layered effect without theincorporation of significant numbers of redcells. Consequently thrombi have a friable("crumbly like a cookie") consistency, and havea paler, drier, rougher appearance. Because ofthis friabilit5r, pieces easily break off the mainthrombi and float down the bloodstream as athromboembolus, and can lodge in smallervessels, block blood flow, and cause an infarct.

TWo different t5pes of postmortem clots canoccur after death. The most common tSpe iscalled a ucurrantJellgu clot. This is the verycommon, red, shiny, and smooth gelatinousclot. If clotting is delayed for some reason afterdeath, the stagnant blood will have a chance toseparate (the red cells settle to the bottom),leaving a yellowish layer of plasma at the top.When clotting ultimately occurs, a currant jellyclot is formed at the bottom, and a plasma clot(called a "chlckenfat clotl is formed at thetop. The appearance of chicken fat clots inmost animals denotes a possible clottingdisorder since postmortem clotting was delayed.Horse red blood cells, however, normally settlerapidly due to rouleaux formation so chicken fatclots in horse are inconsequential.

Figure 1: TWo "currant jel$ postmortem clotswithin the heart chambers. Note the smoothdark red, shiny, and gelatinous appearance.

Figure 2: Microscopically, currant jellypostmortem clots consists almost exclusively ofred blood cells with a few entrapped white bloodcells. Fibrin is usually not clearly recognizable.

Figure 3: In this heart, both a currant jellyclot and a chicken fat clot are evident. Bothare postmortem clots. 42

C?aapter 3 ?he ffi*er*pcy Fr*e*cluie

THROMBOSIS as. POSTMORTEM CLOTTING (continued)

Figure 4: TWo thrombi attached to the mitralva-lve. Valvular thrombi are often caused bybacterial endocardial damage and constitutes"vegetative endocarditis".

Figure 5: A thrombus attached to the aorticvalve. Note the pale , dull and roughappearance.

Figure 6: Microscopically, thrombi often havealayered appearance (called "Lines ofZahrn").Here, a thrombus nearly occludes a bloodvessel. The dark purple blobs are bacteria (thisis a "septic" thrombus)

Figure 7: Viewed here is an opened leftpulmonar5r artery containing one leg of asaddle thrombus (arrows). The thrombusstarted at the junction of the pulmonary trunkthen extended into the lungs along eachbranch (pulmonary thromboembolism).

i,,

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fi

I43

Chapter 3 The llecropsy Procedtrre

STEP 8: REMOVAL AND DXAMINATIONOF THE LIVER

After removal of heart, lungs, and thediaphragm, the abdominal viscera can beremoved systematically, starting with the liver.Before removal of the liver, the bile ductconnection to the duodenum should bechecked for patency. Make a small slit in theproximal duodenum and identify the mqjorduodenal papilla. Squeeze the gallbladder tosee if bile can be easily expressed through theduct and out the papilla. If not, the bile ductshould be opened and traced back up to thegallbladder. The liver can then be removed bycutting the bile duct and all diaphragmaticand body wall connections.After removal of the liver, the size,conformation, and color should be assessed.

Alternating pale and dark areas can produce aareticulated" or ttnutmeg" appearance.Frominent fat infiltration can produce a veryyellowish liver. Obviously, €uf,y masses ornodules should be noted.After assessing the surface, the liver should be"bread-1oafed", cut into small l-2crl: slicesfrom end to end, to expose possible lesionsdeep within the parenchyma that are notvisible on the surface. The gallbladder shouldbe opened to assess the character ofthe bile,the presence of any stones or concretions, andthe possibility of hyperplasia or neoplasia ofthe gallbladder epithelium.

Figure 1: The bile duct is checked for patency.Rs the gallbladder is squeezed, note the streamof bile from mqjor duodenal papilla (arrow)

Figure 2: Grossly normal liver

Figure 3: Focal area ofhepatic necrosis Figure 4: Severe hepatic lipidosis

Chapter 3 The llecropsy Procedure

Figure 6: Nutmeg liver (chronic passivecongestion)

Figure 5: Hepatic nodular hyperplasia

Figure 7: Gallstone in the gallbladder Figure 8: Hepatic biliary adenocarcinoma

F'igure 9: Metastatic hemangiosarcoma Figure 1O: Hepatocellular carcinoma

*iaaptcr 3 ?*:e ,S**rca;sy 3x*e*elur*

JVECROSISNecrosis is common in the liver and othertissues and must be properly identified andcategorized when it occurs.

Necrosis is the death of cells within the bodythat occurs prior to somatic death (death of theanimal). It can be recognized both grossly andmicroscopically, and varies depending on thetype ofnecrosis. The types ofnecrosis arecoagulative, caseous, and liquefactlve.

Coagulative necrosis is defined as necrosiswhere cellular and/or tissue architecture ispreserved (the cells still look like cells).Grossly, coagulative necrosis is usuallycharaclerved by a distinct paleness of thetissue. Depending on the degree of hemorrhagepresent, the tissue may be red or might have ared border. One of the most common causes ofcoagulative necrosis is hypoxia/ischemia, whichin turn is often due to loss of blood supply. Anarea ofnecrosis due to hypoxia is called aninfarct. Microscopically, coagulative necrosis ischxacterized by dead cells, recognizable due todistinct nuclear changes. The nuclear changesthat represent undeniable cell death arepyknosis, karyorrhexis, and karyolysis.Sknotic nuclei are shrunken, dense and dark.Kar5rorrhectic nuclei are fragmented into severalpieces. Karyolytic nuclei have lost much oftheir dark staining, resulting in either a palenucleus or no

Figure 1: The pale regions of this muscle arenecrotic. Aside from the color change, thetissue architecture is still present (the affectedareas still look like muscle) so this would becoagulative necrosis

nucleus at all. Caseous necrosis is necrosiswhere the dead tissue is still present but hasdegenerated into an unrecognizable matrix.Grossly, caseous necrosis has a dry, cottagecheese-like appearance and texture.Microscopically, caseous necrosis is aeosinophilic granular material with norecognizable cells. Certain types ofbacteria areoften the cause of caseous necrosis includingMgcobacteium ar.d some Corynebacteiumspecies.

Liquefactlve necrosis is necrosis where thetissue cells have been completely liquefied,leaving only fluid, inflammatory cells, andpossibly the causative agent. Liquefactivenecrosis is the most common t5rpe of necrosis inthe brain due to the high water and lipidcontent. In other tissues, liquefactive necrosisusually only occurs due to infections by certainbacteria with very powerful enzyrnes which canliquefy tissue ("pyogenic" bacteria). Because ofthese bacteria, neutrophils are generallypresent in high numbers within the liquefiedtissue. Grossly, liquefactive necrosis ischaracterized by a cavity filled with a creamywhite, viscous, and often foul-smelling fluid(pus). When this cavity is well-defined andwalled off with connective tissue, it is referred toas an abscess. Microscopically, no tissue cellsare present, only the neutrophils and thebacteria.

Figure 2z TLre pale regions of this cow kidneyare necrotic. Since the gross tissue architectureis still present, this represents coagulativenecrosis

i

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ill

46

elaxpt*r * ?h* l{e*rcgrey Froeedure

JVECROSIS (continued)

Figure 3: Coagulative necrosis. The cortexfeatures multiple infarcts, roughly triangularpale regions bordered by a thin zone ofredhemorrhage

Figure 5: Coagulative necrosis. Clearevidence of cell death is apparent (pyknoticand karyorrhectic nuclei), but the cellulararchitecture is still intact

Figure 4: Microscopic coagulative necrosis ofthe liver. Many necrotic cells have pyknoticnuclei (white arrow) and karyolytic nuclei (greenarrow). There is also an increased cytoplasmiceosinophilia and vacuolization, however cellulararchitecture is still maintained.

Figure 6: Coagulative necrosis can alsorepresent preservation of tissue detail. In thiskidney, renal tubular cells are unrecognizablehowever the tissue/tubular shape(architecture) is preserved.

47

.IVECROSIS (continued)

fkap?-er 3 '{"hr }f **rr;px.y Frc**e9:.ar*

Figure 7: Grossly, caseous necrosis has a dry,granular, "cottage cheese-like" consistency.

Figure 9: Grossly liquefactive necrosis isoften characterized by a well-circumscribedwatled-off cavity containing a creamy palefoul-smelling viscous liquid (pus) forming anabscess.

Figure 8: Microscopically, caseous necrosis isgenerally a pink, amorphous matrix with norecognizable cells or cellular structure

Figure 1O: Microscopically liquefactivenecrosis features completely loss (liquefaction)of the parenchymal tissue, with onlyinflammatory cells (usually neutrophils)remaining.

48

S?aapter 3 ?trae m*erclg:sy Fr**edure

AIECROSIS (continued)The microscopic pattern of necrosis in an organcan be helpful in determining the cause. In theliver, necrosis can occur randomly throughoutthe liver, or in one of three zones of the hepaticlobule.

Random necrosis of the liver is usuallyassociated with infectious organs which gainaccess to the liver via the vascular system. Thistype of necrosis is usually associated withinflammation, though some viral infection maybe non-inflammatory.

Patterns of necrosis of the hepatic lobule arethe result of its microanatomy and function.The hepatic lobule is an irregular hexagonalstructure with a large vein at the center (thecentral vein) and portal regions at theperiphery. The portal regions consist of thehepatic artery pringing o>grgenated blood to theliver), the hepatic vein (bring unoxygenated butnutrient-rich blood from the GI tract), and a bileduct. O>rygenated blood which enters via thehepatic artery drains through the sinusoidalspaces into the central vein, where it iseventually dumped into the vena cava. Becausethe hepatocytes around the central veins arethe last to receive o><ygenated blood, they areextremely susceptible to hypoxia and anemia.

Centrllobular necrosis is most commonlyassociated with anemia of any cause, orwith passive congestion of the liver due toright sided heart failure. Centrilobularhepatocytes also contain the highestconcentrations of mixed function oxidases(MFOs). MFOs are er:vjrmes responsible forthe metabolism of chemical substances inthe blood. Metabolism of some substancesmay produce toxic metabolites which may inturn cause degeneration and necrosis of thecentrilobular hepatocytes. Substanceswhich can cause this pattern of necrosisinclude acetaminophen and aspirin.

Mid-zonal necrosis, necrosis in region ofthe hepatic lobular between thecentrilobular region and the periportalregion, is uncommon but is seen in raretodcities (like hexacholorophene in cats).

Pet'tporaal necrosis occurs in toxicitieswhere the toxin does not require metabolismby MFOs, but is already toxic when it entersthe liver through the hepatic artery or vein.Because the periportal hepatocytes are thefirst affected, they suffer more degenerationand necrosis then the mid-zonal orcentrilobular regions.

Figure 11: Centrilobular hepatic necrosis Figure 12: Periportal hepatic necrosis

49

ekapter 3 ?lae l{**r*Xasy Fr*eedure

THE INTES?IIVEThe esophagus, stomach, small intestine, largeintestine, pancreas, and spleen are removed enmasse by cutting the diaphragm and the root ofthe mesentery. The colon is typically cut as itpasses into the pelvic canal. If pathologr issuspected in the pelvic canal, it is opened bycutting the pubic and ischial bones on bothsides, allowing the removal of the floor of thepelvis.

Once the viscera is removed, the spleen is cutaway and set aside for later examination. Thepancreas is also examined, cut away from itsduodenal attachments and examined.

To facilitate opening of the gastrointestinal (GI)tract, all of the mesentery is cut away from thebowel loops, thereby allowing the entire tract tobe laid out straight. Opening starts in theesophagus, proceeds along the greatercurvature of the stomach, and extendsthroughout the length of the small and largeintestine. Stomach and intestinal contents areassessed, along with the surface mucosa. Anyforeign objects and/or parasites should beidentified and their possible impact ongastrointestinal function assessed. The entiretract should be assessed for inflammation,ulceration, thickening, and / or neoplasia.

Flgure 1: Remove the GI tract by cutting theroot of the mesentery (marked by the scissors)

Figure 3: Full GI tract. These small intestinesare thickened, h5peremic, and have a slightlypitted surface, all evidence of inflammation.

Figure 2: When necessarJr, open the pelvis bycutting the pubic (white arrow) and ischialbones (green arrow) on each side to remove thefloor of the pelvic canal.

Figure 4: The mesentery has been cut awayto facilitate opening the intestines.

50

Ckapt*r 3 ?*a* }Ic*ro;:sy Froecdarr*

Figure 5: The intestine and liver are knottedtogether in a tight ball by fibrin (fibrinousperitonitis)

Figure 7: Roundworms (?oxocara canls) inthe small intestine

Figure 9: Severely hemorrhagic intestine(Panroviral Enteritis)

Figure 6: Multifocal petechial hemorrhagingin the mucosa of the small intestine due tohookworms

Figure 8: Whipworms (?Hcarls trulpls) rnthe large intestine

Figure 1O: Hemorrhagic mucosa surface ofjejunum (Panroviral Enteritis) 51

elaapter S ?k* I€eeronrsy Froeedure

Figure 11: Markedly thickened cross-sectionof small intestine with multifocal pale yellownecrotic regions. Microscopically, there wasprominent pyogranulomatous and necrotizingenteritis with large numbers of hyphai fungalorganisms (Phycomycosis)

Figure 13: Thickened region of the jejunumwith focal perforation and leakage of intestinalcontents.

Figure 12: Neurofibrosarcoma on the colon

Figure 14: Section of intestine from Figure 13opened up. Microscopically there was aninfiltration of neoplastic lymphocytes(lymphosarcoma) which weakened the walland led to the perforation.

Figure 15: Severe esophageal inflammationand ulceration from gastric reflux (Gastro-esophageal Reflux Dlsease or GERD)

Figure 15: Multifocal gastric ulcerations andhemorrhage (injudicious NSAIDS use)

Figure 18: This stomach was filled withclearly recognizable pieces of sausage. This wasnot deemed important until considered withthe history. The owner stated that she fed theanimal a strict commercial dog food diet. Thismade the presence of sausage suspicious. Theanimal had died acutely with no clinical signs.Closer inspection of the sausage revealed smallpellets (see insert) consistent with Strychninepellets. Subsequent todcolory was positive forStrychnine. The history was pivotal in thiscase as it affected the consideration of aseemingly benign finding.

Figure 17: Gastric foreign body

53

elaagpter 3 ?ia* S**r;*gr*y Fr*e*du.re

PAJVCR.EAS

Changes involving the pancreas includeinflammation, hemorrhage, and neoplasia.When acute, pancreatitis is often hemorrhagic,however hemorrhage can be an agonal changeso interpretation grossly is tentative unlesssupported by accompanying lesions. Acutepancreatitis is characterized by loss (necrosis)of pancreatic tissue, as well as varying degreesof necrosis of the surrounding tissues. Theperi-pancreatitic fat is commonly involved andthe result is saponification, the formation ofsoap due to the action of the strongly alkalineenzJfines leaking from the parrcreas on the fat.This generally appears as white plaques withinthe fat. When pancreatitis is chronic, thegland is generally very nodular in

Figure Grossly normal pancreas

appearance due to the formation of prominentconnective tissue, as well as due to regenerativenodules.

There are numerous possible causes ofpancreatitis. Nutritional factors believed tocontribute to pancreatic acinar-cell injuryinclude obesity, high fat diets, andhyperlipoproteinemia. Drugs are also suspectedof causing some cases of pancreatitis an theseinclude sulfonamides, tetracycline, andcorticosteroids. Surgical manipulation, bluntabdominal trauma, and biliary tract diseaseshave also been implicated.

Figure 2: Marked pancreatic hemorrhage andedema (acute pancreatitis)

Figure 4: Pancreatitis with fat saponification.Note the white plaques in the adipose tissue.

Figure 3: Chronic pancreatitis

54

The spleen should be examined for its size,shape and conformation. A normal spleen canbe either contracted or congested at necropsy,although contracted is most common. Thecontracted spleen has a lightly brownish hue,often with wrinkling of the capsule. Thecongested spleen is very dark red, with a smoothtaut outer surface and a gelatinous cut surface.Sometimes the spleen features irregular areas ofcongestion which cal be confused withhyperplastic nodules or neoplasia. Hyperplasticnodules are usually well circumscribed andsessile in appearance. These masses are notneoplastic but can rupture and bleed likemalignant tumors. A common finding on theedges of spleens are fibrosiderotic (or justsiderotic) plaques. These plaques have aqghir$an appea-rance. They represent small areas of chronic degeneration with fibrous connectivetissue proliferation and dystrophic calcium deposits. The cause is unknown but they are of noclinical or pathological significance.

Figure 3: Cut surface of congested spleen

Figure 5: Cut surface of hyperplastic spleen(Histoplasmosis)

Figure 1: Grossly normal contracted spleen

Figure 2: Grossly normal congested spleen

Figure 4: Hyperplastic spleen (Histoplasmosis)55

Chapter 3 ?he *leeropsy Procedure

Figure 6: Incomplete contraction (irregularcongestion)

Figure 8: Multiple dark red hyperplasticsplenic nodules with tan llbrosideroticplaques along the splenic edges (arrow)

Figure 1O: Marked splenomegaly due tol5rmphosarcoma

Figure 7: Ruptured and hemorrhagingnodular splenic hyperplasia

Figure 9: Ruptured hemangiosarcoma withblood clot

Figure 11: Focal splenic infarction

I

elaapter 3 ?he fifeeropsy Proeedure

HEMANGIOSARCOMA

Hemangiosarcoma is a tumor of neoplastic endothelial cells which often form vascular channels filledwith blood. It occurs most commonly in the spleen and right atrium of the heart, however, a primaryhemangiosarcoma can occur anywhere due to the ubiquitous nature of endothelium. Splenichemangiosarcomas are often as5rmptomatic until they rupture, with the resulting peracute abdominalhemorrhaging causing h5povolemic shock and death. Atrial hemangiosarcomas may beasymptomatic or may cause cardiopulmonary signs. They often rupture resulting inhemopericardium, cardiac tamponade, cardiogenic shock and peracute death. Metastasis usuallyoccurs 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, andschistocytosis due to red blood cell damage as they pass through the neoplastic blood channels ofthe tumor (microangiopathy). The presence of acanthocytes (acanthocytosis) is an especiallyimportant signal of possible hemangiosarcoma.

Figure 1: The pericardial sacwith blood after rupture of anhemangiosarcoma

Figure 3: Ruptured hemangiosarcoma on theright atrial auricle.

Figure 2: Opened pericardial sac revealinghemopericardium

Figure 4: Marked hemoabdomen due to aruptured splenic hemangiosarcoma

is distendedatrial

57

*k*r:tcr 3 ?ke iSalar*ps3r Fr***ciur*HEMA NGIO SARC OMA ( c o ntinue d)

Figure 6: Metastatic foci of hemangiosarcomain the lungs

Figure 8: Microscopically, hemangiosarcomasoften form irregular and abnormal bloodvessels and vaicular passages filled with blood

The microscopic vascular appearance ofhemangiosarcomas (HSA) are very important forthe pathologist to make a definitive diagnosis.When the tumor is undifferentiated and thisvascular pattern is not evident, it may not bepossible to make a definitive diagnosis withH&E histolory alone. In such cases,immunohistochemistry staining (IHCf can bevery useful. IHC staining uses antibodiesdirected against certain proteins that areexclusive (or nearly exclusive) to a certain t5peof tissue. In the case of HSA, the antibodies aredirected against the endothelial cellproteinFactor 8-related antigen. These antibodies areconjugated with a stain so that if the antigensare present and the antibodies stick to thetissue, the tissue will stain. When this stain ispositive, it is definitive for hemangiosarcoma,regardless of the tumor's histologic appearance.

Figure 5: Two hemangiosarcoma masses onthe head and tail of the spleen. The largermass ruptured resulting in hemoperitoneum.

Figure 7: Metastatic foci of hemangiosarcomain the intestine and on the spleen

Figure 9: Undifferentiated spindle cell tumorfrom the spleen. A hemangiosarcoma issusoectedbut cannot be cdnfirmed because itlaclis the definitive vascular pattern. 58

Chapter 3 ?he l{*cropsy Frecedure

Before removal of the kidneys, the adrenalglands should be identified and removed. Theadrenal glands are retroperitoneal structures.

The left adrenal gland is slightly craniomedial tothe left kidney, and ventrolateral to the aortabetween origins of the cranial mesenteric andleft renal arteries. It is centrally constricted withenlarged extremities, having a "dumbbell" or"peanut" shape.

The right adrenal is craniomedial to hilus of theright kidney, dorsal or dorsolateral to thecaudal vena cava, and cranial to the right renal

artery and cranial mesenteric artery. It has aocomma', "wedge", or "boomerang" shape.

The phrenicoabdominal vein course across thebody of each gland slightly ventral to the center.Adrenocortical hyperplasia is a common findingin the adrenal glands. It may be noted as alarge nodular mass, or may appear as multiplescattered pale yellowish regions. Neoplasticmasses include adrenocortical adenoma andadrenocortical carcinoma, both of which cancause Cushing's Syndrome andpheochromoc5rtoma.

Figure 2z l,eft adrenal gland with palehyperplastic cortical foci

Figure 1: Grossly normal right adrenal gland

Figure 3: Adrenocortical nodular hyperplasia Figure 4: Adrenal pheochromoc5rtoma

Both ureters should be identified andexamined for enlargements, strictures, stones,or other abnormalities. If they are normal, enmasse removal of both kidneys, ureters, andbladder together does not have be be done.Each kidney can be cut out of the perirenal fatseparately. The size and shape of each shouldbe noted, and evidence ofnecrosis,hemorrhage, inflammation, and neoplasiashould be sought. The capsule should peeleasily off of each kidney; excessive adhesionsuggests inflammation. Inflammation of thekidney may or may not be evident grossly.Inflamed kidneys may have areas of petechialhemorrhaging and congestion.

Figure 3: Bilateral polycystic kidneys on cutsurface

Necrosis is most often in the form of an infarct.Infarcts are generally roughly trialgular inshape, and when acute, are pale with a redhemorrhagic rim. When chronic they can bevery pale and fibrotic, and cause considerabledistortion of the renal conformation. Renalcysts are usually congenital and appear asfluid-filled cavities of varying size. Degenerativechange such as hydronephrosis ischaracterized by dilation of the pelvis and lossof medullary or cortical parenchyma. Inextreme cases, the kidney can be greatlyenlarged and consist only of a fluid filled sac.Neoplasia, either primary or metastatic, isusually obvious as variably-sized massesandlor diffuse infiltration in the parenchyma.

Figure 2: Polycystic cat kidneys (the palecolor and subcapsular veins are normal incats).

Figure 1: Normal dog kidneys

Figure 4: Focal renal abscess

60

Figure 5: Bilateral chronic renal infarcts. Theaffected areas are markedly shrunken,distorting the shape of the kidney

Figure 7: Hydronephrosis with dilation of therenal pelvis

F'igure 9: Infiltrative neoplastic disease(lyrnphosarcoma)

Figure 5: Bilateral chronic renal infarcts. Theaffected areas are markedly shrunken,distorting the shape of the kidneys

Figure 8: Severe unilateral hydronephrostsand hydroureter

Figure 1O: To distinguish the left kidney fromthe right kidney after removal, it is customar5rto cut t}re right kidney at a right angle, andthe left longitudinally. 6l

ffuapter S ?&* Se*r*psy Pra:*edrxr*

AIYIYLOIDO,SIS

Amyloidosis is any disease entity characterized by the formation of amyloid. Amyloid is a proteinwhich is formed when a protein or parts of a protein becomes misfolded into an abnormal beta-pleated sheet arrangement. There have been more than 15 proteins identilied that can becomemisfolded 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 importantin domestic animals. Amyloid associated (AA amyloid) is formed from a common acute phaseprotein called serum amyloid (SAA), amyloid light chain (AL amyloid) is formed from the lightchains 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 pancreaticislets of old cats

AA amyloid is commonly associated with chronic inflammatory disease which, of course, producelots of the acute phase protein SAA. Normally, SAA should be degraded aJter it has performed itsfunction, however occasionally some component becomes (inexplicitly) folded in the b-pleated sheetformation and becomes amyloid. Because the amyloidosis is secondar5r to whatever is causing thechronic 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 tobe predisposed to amyloid formation has not been identified.

AL amyloid is commonly associated with immunologic conditions resulting in the production oflarge amounts of immunoglobulin. Occasionally (inexplicably) some of the light chains of theimmunoglobulins become folded in the b-pleated sheet formation and become amyloid. The mostcommon immunologic condition associated with AL amyloidosis is multiple myeloma or plasma cellneoplasia. Neoplastic plasma cells produce very large amounts of immunoglobulins, some of whichbecome folded and form amyloid. AL amyloidosis is known as "primar5/ amyloidosis.

Figure 1: Molecular pattern of a b-pleatedsheet. The pleating refers to the "warf folding(like drapery pleats) of the polypeptides.

62

Cfuapt*r 3 ?3re I{*er*3:s3r Frc**darr*

AlltY LOI DOSIS ( c o ntinued)In humans, a protein called amyloid precursor protein (APP) is an integral plasma membrane proteinwhich is found in highest concentrations in neurons nea.r s5mapses. Misfolding of this protein formsamyloid which commonly deposits in blood vessels of the brain and is associated with Alzheimer'sdisease. Currently, no association of amyloid and Cognitive Dysfunction Syndrome, a s5n:drome inanimals analogous to Alzheimer's, has been established.

By far, however, the most common "form" of amyloidosis is idiopathic, when the condition cannot belinked to any of the above stated conditions.

As previously stated, regardless of the parent protein that causes amyloid, microscopically it all looksthe same. The b-pleating of the proteins makes amyloid very resistant to normal degradation byproteolytic enannes. Since it can't be broken down or excreted through the kidneys, the amyloid isdeposited in numerous extravascular sites. It can be deposited anywhere, however, commonextravascular sites of deposition include the hepatic sinusoids, renal glomeruli, and splenicsinusoids. Amyloid is not toxic to the cells in these areas however its presence causes slow pressureatrophy and eventual necrosis of the surrounding tissue. Obviously, the clinical s5mdrome associatedwith amyloidosis has a lot to do with where it is deposited. In renal glomerular amyloidosis, the lossof glomerular cells leads to a loss of proper filtration, renal failure, and the presence of veryprominent proteinuria.

In the liver, severe amyloidosis can eventually cause chronic liver failure by its slow atrophy anddestruction of hepatocytes. More commonly, however, hepatic amyloidosis leads to fatal abdominalhemorrhage. In severe cases, the presence of the amyloid markedly weakens the structural integrityof the liver, making it very friable. Because of this friability, minor trauma to the liver can result infracturing/cracking of the parenchyma, severe hemorrhage, and death from exsanguination.

Figure 2: Grossly, hepatic amyloidosis hascaused this liver to have a swollen, puffyappearance, and there are several cracks andfractures on the surface which have resultedin fatal hemorrhage.

Figure 3: Microscopic hepatic amyloidosis.Notice how the hepatic cords (white arrow) arethin and atrophic, being separated ancompressed by the pale amorphous amyloid(green arrow) in the sinusoids. This separationand destruction of the hepatic cords weakensthe liver's structural integrity, predisposing itto fracturing and hemorrhage.

63

AIYIYLOI DOSIS (c o ntinue d)

Chapter S ?he l$eerogrsy Froeedure

Figure 4: Grossly, renal amyloidosis ischaracterized by a nondescript paleness,although it can cause tl:e tissue to have a wa.>ry

feel when severe.

Figure 6: Amyloid can look similar to otherdeposits (like fibrin and collagen) so Congo Redstaining is used to confirm. Under polarizedlight it fluoresces an bright apple-green color.

Figure 5: Microscopically, amyloid has a palepinkish appearance. Here in the glomeruli it isexpanding and destroying the tuft

Figure 7: Amyloid can deposit in the whitepulp or the red pulp of the spleen. When thedeposits are in the white pulp they look likegrains of sand (or sago) and it is called a "sagospleen" (the above picture). A "lardaceousspleen" has its amyloid in the red pulp, andusually indicates amyloid AL.

64

Ckx.pter 3 ?he $eer*psy Fro*ed*r*

S?EP 74: REMOVAL & EXAMINATIONOF THE BLADDER

The bladder should be opened and thecharacter of the urine should be noted (red =,hemoglobinuria; brown => myoglobinuria;cloudy => cystitis). The bladder wall should bechecked for inflammation and/or hemorrhage,and the lumen for the presence of uroliths.

A urolith is a rocklike body that can formanywhere in the urinar5r tract from naturallyoccurring mineral saits in the urine and whichcan become lodged along the tract. Uroliths mayvary in size from sand-like particles, to larger,sometimes radiographically visible "stones".

Figure I : Large, distended, and hemorrhagicbladder (blocked cat; FLUTD)

Uroliths may be smooth, jagged, or "point5/. Indogs and cats, bladder stones are more commonthan kidney stones.

A serious problem in cats, especially males, iscalled Feline Lower Urinaty Tract Disease(FLUTD). It is sometimes also called by itsprevious narne, Feline Urologic Syndrome (FUS).This is a disease of the urinary tract that isoften related to the buildup of crystals(crystalluria) and/or bladder stones, leading toinflammation of the lining of the urinary bladderand urethra.

Figure 2: Severe hemorrhagic cystitis withmarked mucosal emphysema caused by gas-forming bacteria

Figure 4z Large stone (urolith) in the lumen ofthe bladder

65

Figure 3: Hemorrhagic cystitis (FLUTD)

Chapter 3 'lhe ltecropsy Procedure

STEP 75: REMOVAL OF THE BRAINThe examination of the brain is most easilyfacilitated by removal of the head from the restof the carcass, and opening the cranial cavity.To remove the head, use your knife to sever allattachments at the atlanto-occtpttal Jotnt.After removing the head, all muscle over thecalvarium (primarily the temporalis muscle)should be removed. To open the cranial cavityand expose the brain, a hacksaw or Stryker sawmay be used to saw through the flat bones.

Figure 1: Exposure of the atlanto-occipitaljoint and foramen magnum. The spinal cord issevered at the foramen, and the cutting of thelateral and dorsal spinal ligaments at thislocation 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 isevident.

After exposure, invert the head and cut allattaching cranial nerves to remove the brain.After removal, the brain should be cuttransversely at about lcm intervals to check forhemorrhages, malacia, and masses in the innerparenchyma. The brain's soft consistency c€mmake sectioning difficult while it is fresh, so itis best to place the entire brain in formalin toharden for 24 hours before cutting and takingsamples for histopathologr.

Figure 2z F,Jlter the head is removed, it shouldbe skinned dorsally and the temporalismuscles cut away.

Figure 4: Starting just above the occipitalcondyle, cut cranial to just behind the orbit,then dorsally to the top of the skull. Repeat onthe other side. When the cuts are connected,the calvarium can be removed. 66

Figure 5: Removal of the ca-lvarium exposesthe brain.

Figure 7: Grossly normal dog brain removedfrom cranial cavity

Figure 9: Multifocal leptomeningeajhemorrhaging.

Figure 5: Inverting the head and cutting thecranial nerves will allow the brain to beremoved.

Figure 8: Subdural hematoma

1O: Focal cerebral malacia

67

elaapter i3 Yhe ffeer*grs3r Fre*edur*

Figure 13: Extensive intra-cerebralhemorrhage

Figure 12: Multifocal metastatichemangiosarcoma

Figure 14: Hydrocephalus with enlargementof the lateral ventricles and loss of the septumpellucidum

68

Figure 11: Benign choroid plexus papilloma

Chaptcr 4 T'h.e ffieeropsy K,eport

STEP 76: WRITING THD NECROPST REPORTThe 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. Ifancillary tests are pending (especially histopath), a preliminary gross report may be written, howeverits conclusions may be contradicted later by the microscopic findings. The final report should be acompilation of all the gross and microscopic findings, as well as any ancillary tests, with commentsand 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 ofsubmission and examination

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

..Specimen Identification - Animal's name, species, breed, age, weight, and sex

.-,Clinical History - Includes the details of clinical findings, signs and s5rmptoms observed(especially peri-mortem signs), and the clinical diagnosis.

..,Gross necropsy findings, often arranged by organs/system. This may or may not includepictures of the significant lesions and/or mqjor organs. For each organ, there should be a fulldescription followed by a morphologic diagnosis.

;The microscopic findings (if this is the final report)

..:Necropsy Conclusions and Comments - The examiners final interpretation and diagnoses basedon the clinical history, the gross lesions, and the ancillary test findings, as well as any pertinentand useful comments on the case.

STEP 77: WRITING THE NECROPST CO.IICLUSIOffThe necropsy report conclusion is arguably the most important part of the report. It is where all ofthe lindings and information (the clinical history, gross findings, and the ancillary test findings) areinterpreted together and conclusions are drawn about the cause of death and/or the clinicals5rndrome. The conclusion should be written in narrative form and contain the following:

..iA direct statement of the morphologic cause of death or the clinical s5rndrome (if it has beendetermined), including a statement about the etiolory if determined

'. e.g. "This animat diedfrom exsanguination (bleeding out) into the chest cauitg subseqrtent to

traumatic injuies to the heart and lungs inflicted bg a high powered projectile"

' e.g. "The cause of death in this case u)as humane euthanasia"

.;A brief patJrogenesis for the cause of death or clinical sSmdrome, as well as any other significantfindings (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 thefindings inter-relate to each other

.,:If a specific condition or neoplasia is found to be the cause of death (ex. lgmphosarcomal, write abrtef, general description about the condition

,.,If the specific cause of death could not be determined, speculations based on gross and/ormicroscopic 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.

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

.-),r-E^aD-JJJU J EV'tDIAGNOSTICS

NECROPSY REPORT

NA2005-55Some Great Veterinary Hospital5555 Main Street., Los Angeles, CADr. JonesJohn SmithGizmoMale5-6 monthsCanine-15lbs05/05/05

HISTORYGizmo was at a local groomer for a grooming on 05-04-05. During the final brush out hecollapsed and died (no other details provided). He was delivered DOA to the veterinaryhospital. He has had a history of a distended abdomen.

GROSS EXAMINATIONThe animal submitted for necropsy is Gizmo, a male Shih Tsu canine (Figures 1 - 2). Hemeasures 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 grosslesions are observed in the skin, subcutaneous, or musculoskeletal tissues.

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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). Alarge fluid-hiled

"ac, laier determined to be the left kidney, is displacilO the intestines

.r"iirlly, and there is very marked peri-renal accumulation of yellow fluid (urine) (Figures 4 -

S). The small intestinal bowel loops are pale and there is no evidence of inflammation,

rupture, or necrosis. The stomach contains only fluid and mucus, and no significant gross

lesions are observed. The left testicle is present in the abdominal cavity at the entrance to the

inguinal canal (Figure 6). The pancreas is pale with no inflammation, necrosis or masses

noted.Gross Dia-qnosis.'1) Illlarked uro-abdomen2) Prominent gastric and intestinal pallor3) Grossly normal pancreas4) Left testicular cryptorchidism

Figure 4

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Liver:The liver features relatively sharp edges and afaint reticulated surface appearance. Theparenchyma has a reddish appearance withseveral linear pale regions (postmortem ribimpressions), and the capsular surface issmooth and glistening (Figure 7). There is nosignificant oozing of blood on cut surface. Nomasses, nodules, or evidence of inflammationor necrosis is noted. The gallbladder is intactwith no stones or evidence of inflammationGross Dta-onosis: Grossly normal liver andgallbladder

Spleen:The spleen is normally contracted, measures approximately 9cm in length, and features noelevated 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 (Figure8). There is prominent foamy and bloody fluid in the trachea primarily at the tracheobronchialbifurcation (Figure 9). There is approximately 2ml of clear, slightly red-tinged fluid in thepericardial sac. The heart measures approximately 4.5 cm from its base to the apex (Figure10). The left and right ventricular walls are of normal size and conformation, and the tricuspidand mitral valves appear normal (Figure 11).

Gross Dia-onosls.'1) Prominent pulmonary congestion, edema, and hemorrhage2) Grossly normal heart

Figure 7

Figure 8 Figure 9

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Urogenital System:There is very marked enlargement of the left kidney, with normal size and conformation of theright (Figure 12). There is complete atrophy of the left renal parenchyma, leaving only afluid-filled, dilated pelvis, fibrous calyxes, and capsule (Figures 13 - 14). No overt rupturecould 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 thetrigone of the bladder, and the other is patent, markedly dilated, and ends blindly in the regionof the prostate (Figure 15). There is mild to moderate vascular congestion of the cortex andmedulla 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 doubleureters, and hydroureter2) Moderate vascular congestion of the right kidney3) Grossly normal bladder

Figure 10 Figure 11

Figure 14

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DIAGNOST!CS

Adrenal glands and thyroid glands:No significant gross lesions are noted in the adrenals or thyroid glands. Both sets of glands

appear to be of normal size and conformation with no nodules or masses noted.

Gross Dragnosrs: Grossly normal adrenals and thyroid glands

Brain:The brain is characterized by moderatecongestion of the cerebral vessels (Figure 16).It was serially sliced transversely at Smmintervals and no hemorrhage, malacia, orneoplasia was observed.Gross Dra-qnosr1s.' Moderatece reb rov asc u I ar co n gesti o n

Figure 15

Figure 16

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HISTOPATHOLOGYSTOMACH: Examined sections of gastric glandular mucosa features areas ofpostmortem change but mostly an intact, columnar epithelial mucosal border withoutevidence of erosion or ulceration. There are no significant inflammatory infiltratesnoted 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 noevidence of blunting, ulceration, necrosis, or inflammation. There is no evidence ofrupture of the bowel wall and no evidence of peritonitis, but there is mild edema. Thecolon appears similarly normal histologically.Microscopic Diasnosis: Mildly edematous small intestine with normal colon

PANCREAS.' Ihe pancreas featured normally arranged acini, and normal numbers ofwell-spaced pancreatic islets. The interstitium is mildly expanded by edema fluid andvascular 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 ismost notable in the central veins and periacinar regions. The hepatic cords around thecentral veins are attenuated and slightly pale, imparting a distinct reticulatedappearance 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 areextensive areas throughout the lung fissue characterized by prominent intra-alveolarhemorrhage. No evidence of inflammation or necrosis are noted in association withthis hemorrhage. Pulmonary edema rs also prominent, and scattered atelectic regionsare present.Microscopic Diagnosis: Marked, focally ertensive intra-alveolar pulmonaryhe 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 separationcharacteristic of interstitial edema. Overall there were no significant histologic lesionsbeyond mild vascular congestion. Myocardial fibers are intact, organized, and featureno hyalinization, degeneration, or inflammatory changes.Microscopic Diasnosis: Mild myocardial edema

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SPLEEN: Examination of the splenic secfions reveals contraction of the parenchymawith prominence of the fibroleiomatous sepfae. Both the vascular red pulp and thewhite pulp follicles are adequate with no evidence of inflammation, necrosis, orneoplasia.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'scapsules are not thickened. There is moderate vascular congestion involving thecorticomedultary junction and the medulla. No crystaluria or proteinuria is noted in therenal tubules. Atmost no recognizable renal parenchyma was present in the leftkidney. The tissue featured only a connective fissue capsule with scant evidence ofatrophied tubules. No inflammation was noted.Micioscopic Diagnosis: Moderate right renal congestion with severe left renalhydronephrosis a nd atrophy

BLADDER.' Sectrons of btadder are characterized by mild to moderate mucosal andsubmucosal congestion. There is no evidence of significant inflammation, necrosis, orneoplasia.Microscopic Diagnosis: Mild to moderate bladder congestion

LEFT AND RTGHT ADRENAL GLANDS; Examined sectrons from the left and rightadrenal glands features a normal cortical and medullary architecture. No hyperplasticor 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 featurednormal follicular developing with no hyperplastic or neoplastic growth obserued.There is no evidence of inflammation or necrosis. The obserued parathyrotd fissue tsnormal.Microscopic Diasnosis: Histologically normal thyroid and parathyroid glands

BRAIN: Examined are multiple sections of brain featuring no significant histologiclesions 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

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COMMENTS AND CONCLUSIONS:The gross and microscopic examinations rule out trauma and physical abuse as the cause ofdeath of this animal. Also eliminated are neoplasia, infection/inflammation, and ischemictissue necrosis (infarction). No foreign material was evident in the stomach or intestine tosuggest poisoning. While most of the findings noted were postmortem and/or nonspecific innature, several lesions do suggest a pathogenesis for the cause of death. Though the deathwas 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 theleft 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 theureter 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 orillness was reported previously by the owners. lt appears, however, that there was somesudden loss of integrity of the dilated, urine-filled kidney that resulted in significant urineleakage into the surrounding tissues and the abdomen. This uroperitoneum led to peracuteazotemia, toxicity, and possibly hypovolemic shock. Finally, it appears there was severepulmonary 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 mayempty 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 coursedto the level of the proximal prostate, at which point it could no longer be identified. Ectopicureters are most commonly diagnosed in animals younger than one year of age, and morecommonly (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 goldenretrievers, Labrador retrievers, Newfoundland retrievers, West Highland White Terriers, WireFox Terrier and the Poodle. Urinary tract infections are a common complication though thiswas not present in this case.

Pathologist:R.E. Moreland BS, DVMAntech Necropsy Coordinator

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Small Animal Necropsy

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