Necrosis

2 reactions following necrosis

• mineralisation

• inflammatory response of surrounding tissue

3 causes of necrosis

1. loss of blood supply

   • tissue ischemia

     • compression → intestinal torsion (long axis) or volvulus (via mesentary/blood supply) (short axis)

     • narrowing

       • arterio-sclerosis → blood vessel wall → thickening tunic media (smooth muscle)→ hypertension

       • athero-sclerosis → fatty plaques

     • blockage - thrombosis and embolism

       • aortic (saddle) thrombus

         • aorta → external bifurcation Iliac arteries (internal iliac branch later)

       • valvular (vegetative) endocarditis → acute renal infarcts

2. non-living agents

   • physical - hot burns), cold (frostbite), trauma (Burdizzo)

   • chemical

     • toxic (tannins - oak poisoining → acute tubular necrosis (foal) )

     • or corrosive/caustic

3. living agents

   • Caudal vena cava syndrome - Bacterial - abscesses

   • Hardware disease/traumatic reticulitis - Bacterial - abscesses

   • Blacks disease = fasciola hepatica + C. novyi B

Reduced oxygen definitions

Hypoxia - reduced blood SUPPLY

Hypoxaemia - reduced O2 in the blood

Ischaemia - loss of blood supply

• collateral blood supply? → liver and lungs

  • end arterial supply → kidney

• more metabolic - more susceptible

• parenchyma vs connective tissue

Infarction - necrotic tissue due to ischaemia

Caudal vena cava syndrome

• abdominal abscess (clinical or subclinical acidosis)

• ruminitis

• rumen ulceration

• spreads to liver

• spreads to caudal vena cava

• part of abscess = infective thrombus

Traumatic Reticulitis (Hardware disease)

• wires from tires

• enter reticulum

• penetrate abdominal cavity or pericardial sac

Intestinal torsion/volvulus

• Venous → thinner easier to compress → impeded first

• passive congesion (high hydrostatic pressure) - blood cannot leave

• oedema - fluid lost to interstitium

• arterial flow stops due to oedema

• ischemic necrosis of mucosal barrier

• intestinal blood barrier comprimised

• Bacterial toxin absorbed

• Friable intestine prone to rupture → death

Necrotic lesions

centre - sphere of necrosis - near causal agent

zone of degradation

inflammation - reacting to dead tissue

Gross necrosis

paler

friable, soft

loss of structure and definition

focal, diffuse or multifocal

Histological necrosis

Pyk-nosis - dark dense nucleus (dark purple)

Kary-orr-hexis - nucleus breaking up

Kary-o-lysis - nucleus dissolution - no nuclear detail

Types of necrosis [4]

1. Coagulative - firm

2. Liquefactive - liquid

3. Caseous necrosis

4. Fat necrosis (enzymatic, traumatic, diet)

Coagulative necrosis

• Caused by loss of blood supply → infarction

  • Bacterial, foci of viral replication

• Gross

  • Firmer and drier on cut surface

  • Outline preserved

• Microscopic

  • Tissue architecture preserved - ghost cells

    • cell membranes persist, but nuclei disappear (karyolysis, pyknosis, or karyorrhexis)

  • Cells may be larger and lose outline

  • Cytoplasm structureless + homogenous

Liquefactive Necrosis

• Tissue is digested into a liquid, semi-viscous mass.

  • Caused by enzymatic degradation, especially by hydrolytic enzymes from neutrophils or dying cells

    • kill incoming neutriphils

  • pus = dead, dying neutrophils + degrading cell tissue to due to autolysis

  • So in infectious liquefactive necrosis, pus is the by-product.

• Brain infarct (sterile) → Liquefactive necrosis with no pus.

  • Malacia = softening in liquefactive necrosis of CNS

    • Liquefactive cerebrocortical necrosis in ruminats → caused by thiamine (vitB12) deficienct

    • fluorescent under UV

    • grossly - holes in grey-white matter junctions

    • histo - white spaces surrounded by inflammation

    • Similar symptoms in ruminant lead poisoning + salt poisoning or water deprivation in pigs

    • enzymatic digestion of tissue into a liquid/semi-liquid mass, regardless of whether pus is present.

• Bacterial abscess (infected) → Liquefactive necrosis with pus.

Abscess structure

Central necrotic area

• homogenous and structureless → degenerating neutrophils + tissue cells

Outer pyogenic membrane

• reddish membrane on inner capsule

• composed on BV → transporting neutrophils to the lesion

Outermost fibrous capsule

• age of abscess = thickness capsule

• protects the body

Caseous Necrosis

• mixture of coagulative and liquefactive

• some dry and crumbling

• others - cottage cheese

Typically mycobacteria

Granulomatous inflammation

• macrophages and giant cells

Acid fast bacteria → Ziehl-Neelson stain (red carbol fuschin, trapped by mycolic acids)

Erosion

basement membrane intact → epithelium regenerates - stem cells present

Ulceration

Basement membrane breached

Fibrotic repair

stem cells damaged

• cells at edge of lesions can grow to cover ulcerated area → FMDV vesicles

Small foci of necrosis

Replaced by fibrous tissue

• liver milk spot → Ascaris suum

Larger foci of necrosis

Encapsulated by fibrous inflammation

E.g. sequestrum = fibrous capsule with degenerate tissue in middle of normal functional tissue

• pulmonary sequestration

Fat necrosis

• white, pale, chalky & firm

Causes

• enzymatic necrosis (lipases) → damaged pancreas → enters adjacent mesenteric fat (pancreatitis)

• subcutaneous tissue following trauma (parturition) or recumbant animals - prolonged pressure in 1 area → brisket (pectorals)

  • ischaemia leads to enzyme leakage

• diet - cats with diets lacking in antioxidants (vit E)

Gross - focal opacity (spots of white), hard consistency

Pathogenesis

• Adipocytes die

• Fat broken down into fatty acids

• Saponification → fatty acids combine with Ca2+, K+, Na+ to form soaps

• Soaps are foreign → inflammation

• Foci remain and calcify

Gangrene definition

• Wet gangrene → life threatening

  • Primary → agent kills tissue

  • Secondary → agent invades following tissue death

• Dry gangrene → non life threatening

Postnecrotic change → degradation of dead tissue

Primary wet gangrene

Gangrenous mastitis (Staph. aureus)

• Causes necrosis + putrefaction (decomposition of dead matter)

• Sloughed off

Secondary wet gangrene

• Arm trapped (compression)

• Ischaemic necrosis

• Necrotic tissue invaded by environmental bacteria → putrefaction

Dry gangrene

• Septicaemic salmonellosis in calves

• Bacteria block blood vessels supplying ear tips → ischaemic necrosis

• Ear tips slough off

• Mummification → leathery