Disturbances of Circulation

Histopathology Lab #2

(Web)

Paul Hanna Winter 2015

Slide #96

History:

• pig was fine in the morning & found dead in the afternoon

• there was ~100 mls of clear fluid in the pericardial sac

• patchy red areas evident on the epicardium & throughout the ventricular myocardium

• the lungs were red, heavy and wet

Questions from the history?

What is the term used to indicate a clear fluid (ie non-inflammatory transudate)

within the pericardial sac?

• Hydropericardium

What is indicated by the lungs being red, heavy and wet?

• Pulmonary congestion and edema

Note the ecchymotic to suffusive hemorrhages

on the epicardial surface of the heart. Also note

on the cut surface of the ventricle, the multifocal

to coalescing hemorrhage within the

myocardium.

Appearance of heart

Low power magnification is not very exciting. You might be able to

determine that this is heart and that there are hypereosinophilic areas. Slide #96

Slide #96

Slide #96 At medium magnification you can start to appreciate the congestion,

hemorrhage and slight separation of the myofibers by edema.

Slide #96

Also note

apparent

fibrin

thrombi

within

some of

the small

vessels

At medium magnification you can start to appreciate the congestion,

hemorrhage and slight separation of the myofibers by edema.

At high magnification you can clearly see the blood outside the capillaries (ie hemorrhage) and

the swelling, acidophilia, loss of striation and karyolysis of the cardialc myofibers (ie necrosis).

PAS stain – note fibrin thrombi within capillaries

Description:

• multiple areas of congestion & hemorrhage are scattered throughout the myocardium

• in some areas cardiac myofibres show karyolytic / pyknotic / karyorrhectic nuclei and

have hypereosinophilic cytoplasm (ie indicative of coagulative necrosis)

• the interstitium is mildly edematous

• fibrin thrombi are present within many capillaries (seen best with PAS stain)

Comment:

• the findings in this case are characteristic of “Mulberry Heart Disease” (note, similar

gross lesions can be seen with certain bacterial infections, esp Strep. suis infection)

• MHD is associated with a deficiency of Vit E (and sometimes selenium)

• some other diseases in swine associated with deficiencies of Vit E & Selenium, and

can occur separately or in conjunction with MHD, include:

Nutritional myopathy (white muscle disease)

Hepatosis dietetica (see massive hepatic necrosis)

Nutritional fat necrosis (aka “steatitis” or “yellow fat disease”)

This is a Mulberry!

Slide #96

Morph Dx: 1) Myocardial congestion & hemorrhage, multifocal to coalescing, severe

with microvascular thrombosis

2) Myocardial degeneration and necrosis, multifocal, acute, severe

Slide #39

History:

• a 4-year-old Standardbred horse with a history of going around the race

track twice and then losing control of its hind limbs

• hind limbs were cold to the touch & weak pulse felt in femoral artery

• at necropsy a thrombus / thromboembolus was present at the bifurcation

(“quadrifurcation”) of the abdominal aorta

Fig 21-24 (Dyce) Branches of the abdominal

aorta, horse; 1, Aorta; 10, external iliac a.; 11,

internal iliac a.;

Fig 11-52 (Evans & de Lahunta) Branches of the

abdominal aorta, ventral aspect, dog.

Aortic-iliac thrombosis is occasionally seen in horses & causes exercise intolerance & hind-leg lamness.

The underlying cause is usually not identified, but speculation about strongyle-related thromboemboli or

hypercoagulability syndromes associated with sepsis / endotoxemia have been suggested.

You can see why

they are called

saddle thrombi

Saddle thrombi are also occasional seen in dogs,

esp those with hypercoagulability states (eg loss

of antithrombin 3 with glomerular disease)

Saddle thromboemboli are most often seen in cats

which have cardiomyopathy with dilation and

turbulence in the left atrium (ie thrombi form in the

left atrium and then travel / impact at the bifrucation

of the abdominal aorta)

Slide #39 note thrombus obstructing most of the lumen of this large artery;

also note crescent shaped area of palor (ie area of organization)

at the bottom segment of the lumen

note thrombus composed of fibrin and

entrapped cells & basophilic debris note area of organization with

a few “recanalized” vessels

note area of organization with

a few “recanalized” vessels

Slide #39 at this magnification you can see that the area of organization is composed

of fibrous connective tissue with a few newly formed “recanalized” vessels

Slide #39 at this magnification you are starting to see the macrophages that

contain pigments from erythrocyte breakdown; the dark brown granular

pigment (ie hemosiderin which is from iron storage) and the bright

yellow pigment (ie hematoidin which is from bilirubin accumulation)

Slide #39 at this magnification you are starting to see the macrophages that

contain pigments from erythrocyte breakdown; the dark brown granular

pigment (ie hemosiderin which is from iron storage) and the bright

yellow pigment (ie hematoidin which is from bilirubin accumulation)

Slide #39

At this magnification you can clearly see the macrophages with the

hemosiderin & hematoidin embedded in abundant fibrous connective tissue

Slide #39

Comment:

• the clinical signs can be accounted for by ischemia to the rear legs resulting from

the thrombus, ie cold temperature, lack of arterial pulse & muscle weakness.

• there is not complete ischemia and infarction of the hindlimbs because of collateral

circulation and this also accounts for the loss of function only showing up during

exercise

Morphologic Diagnosis: Arterial organizing thrombus, chronic, severe

Description:

• this is a section of a large, muscular artery.

• the lumen is nearly completely occluded by a thrombus.

• at one margin there is a crescent shaped area of organization where there has been

removal of the thrombotic material (as evidenced by macrophages containing

hemosiderin and hematoidin pigment, derived from phagocytosed rbc’s that were

trapped in the thrombus) and replacement with fibrous connective tissue.

• note the “recanalized” areas within the area of organization.

Clinical History:

• a necropsy was performed on an aged cat.

• the gross pathological changes included:

widespread subcutaneous edema,

ascites,

hydrothorax,

multiple, pale, wedge-shaped lesions in kidneys

Slide #91

Well demarcated pale wedge shaped lesion in renal

cortex; with base of the wedge near the capsule and

apex near cortico-medullary junction.

Normal kidney, gross sagittal section, cat (above left) and normal histology of the kidney

Well demarcated pale

wedge shaped lesion

in renal cortex; with

base of the wedge

near the capsule and

apex near cortico-

medullary junction.

Slide #91

note – within the

affected area the

basic

architectural

arrangement of

the glomeruli and

tubules is

apparent however

the cells

resemble

eosinophilic

shadow (ghost-

like remnant) of

the original cells.

Note –

surrounding layer

of inflammatory

cell debris.

note – within

the affected

area the basic

architectural

arrangement

of the

glomeruli and

tubules is

apparent

however the

cells resemble

eosinophilic

shadows

(ghost-like

remnants) of

the original

cells

Note –

surrounding

layer of

inflammatory

cell debris

Note –

surrounding

layer of

inflammatory

cell debris.

note – within

the affected

area the basic

architectural

arrangement

of the

glomeruli and

tubules is

apparent

however the

cells resemble

eosinophilic

shadows

(ghost-like

remnants) of

the original

cells. Most

nuclei are

inapparent (ie

karyolysis)

note – within

the affected

area the basic

architectural

arrangement

of the

glomeruli and

tubules is

apparent

however the

cells resemble

eosinophilic

shadows

(ghost-like

remnants) of

the original

cells. Most

nuclei are

inapparent (ie

karyolysis)

Slide #91

Description:

• on low-power this section of kidney contains an irregular, wedge-shaped pale eosinophilic area which has a basophilic border.

• the apex of this triangular area is within the medulla, while the base is approximately 1-2 mm from the capsular surface.

• the inner material is composed of ghost-like remnants of the renal parenchyma (coagulation necrosis of tubules, glomeruli, etc) and the whole area is surrounded by a thick layer of inflammatory cell debris.

• there is an increase of fibrous connective tissue and some inflammatory cells within the interstitium of the remainder of the renal cortex (pre-existing nephritis).

Morphologic Diagnosis: Renal infarct

Slide #91

Comment:

• an interlobar artery was obstructed by a thrombus or thromboembolus resulting in ischemia to the renal parenchyma and subsequently coagulation necrosis.