ISCHAEMIA AND INFARCTION

By,

Dr. R.Waduge

Dept. of Pathology

What is ischaemia ?

Is a state, when a tissue or organ has it’s arterial perfusion lowered relative to its metabolic needs.

Is simply defined as a condition of inadequate blood supply.

When ischemia is severe death of tissue results. ( necrosis of cells occur)

What is an infarct ?

An ‘infarct’ is an area of ischaemic necrosis within a tissue or organ, produced by occlusion of either its arterial supply or its venous drainage.

“Infarctive “

The causes of altered tissue perfusion

A) Arterial obstruction –

Thrombosis, embolism – 99%

Spasm, atheroma, occlusive pressure

B) Venous occlusion –

Extensive venous obstruction leads to an engorgement of the area drained by the vein.

These causes increase tissue pressure which eventually leads to arterial obstruction.

e.g :- Mesenteric vein thrombosis

Strangulation of a hernia

Torsion of the testis

Cavernous sinus thrombosis

Ileo femoral thrombosis

Twisted testis

Phlebothrombosis

Strangulated umbilical hernia

C) Capillary occlusion –

- Vasculitis

- Frost bite

- DIC

- Fat embolism

Types of infarcts –Many descriptive categories

1) Pale ( Anaemic ), Red ( Haemorrhagic )

2) Bland and septic

3) Arterial and venous

Pale infarcts -

In arterial occlusion and in solid organs – heart, spleen, kidney

As soon as the occlusion occurs blood seeps in to the affected area.

Venous backflow also occurs. So it’s initially – Red in colour.

Acute renal infarction

Splenic infarction

But soon the necrotic cell swell and pushes the blood out.

Also the red cells that have

leaked out will lyse and the haemoglobin diffuses out.

Also osmosis pulls H2O in and further increases cell swelling.

Red or haemorrhagic infarction - Occurs with –

1. Venous occlusion2. In loose tissue – Lung3. In tissue with a double circulation –

lung / liver or tissue rich in anastomosis – Intestine

4. In previously congested tissue – lung

5. Haemorrhage in to a pale infarct

Several infarcts of the liver

infarction produced by a medium-sized thromboembolus

to the lung

Infarcts may be classified as bland and septic ( infected ).

According to whether they are sterile or contain organisms.

In a septic infarction abscess results in.

Cerebral abscess - There is a liquefactive center with yellow pus surrounded by a

thin wall

Morphology and sequelae The shape of the infarct depends on area

supplied by the artery.

Usually infarcts of lung, liver, kidney and spleen occur due to blocking of end arteries, the shape is like a “wedge”.

The apex of the blood vessel and the base toward the surface of the organ.

Acute renal infarction

In the first 12 -24 hrs infarct is not easily visible.

Infarct becomes better defined in 24 hrs.

Firm – a zone of inflammation is seen.

The serosal surface is also inflammed – fibrinous.

In the next few days – they become pale due to breakdown of Hb and tissue products.

After about a week the phase of demolition followed by fibrosis occur.

Then the infarct become “white”.

Calcification may occur.

Secondary infection abscess.

Brain – the process is somewhat different.

1. The necrotic tissue undergoes rapid colliquative necrosis.

2. The macrophages engulf the debris and becomes a cyst surrounded by gliosis.

In the intestine – gangrene occur.

Acute cerebral infarct

Acute cerebral infarction reveals marked edema (the pale areas).

1. The nature of the vascular supply.

2. The rate of development of the occlusion.

3. The vulnerability of the tissue to hypoxia.

Factors that condition the development of an infract -

Neurons are very sensitive.

Heart cells are hard.

Fibroblasts are hardy.

Cells of proximal convoluted tubule are very susceptible.

The general effects of infarction - Constitutional effects –

– Fever Acute – Neutrophil leucocytosis phase

– Raised ESR response

In addition –– The necrotic tissue may release it’s enzymes

in to the circulation.

In myocardial infarction -

SGOT rises from a normal level of

( 5 – 17 IU ) to > 200 IU.

Creatine phosphokinase ( CPK ) Lactate dehydrogenase ( LDH )

CPK rises early and returns to normal within 3 days. ( specific )

The LDH begins to rise by 12 hrs, reaches a maximum at 48 hrs, returns to normal by the 11th day.

There are five isoenzyme bands of LDH in electrophoresis.

A fast moving LDH, is specific for heart.

LDH 5 – slow moving. Helpful in liver necrosis.

2 hrs cardiac Troponin T

The effects of ischemia on various organs - Heart – thrombosis and embolism are

the commonest causes of arterial occlusion.

Gradual occlusion – Angina– Regional infarction– Subendocardial infarction

Coagulative necrosis

Heals by a scar

Pericarditis

Mural thrombosis

Aneurysmal dilatation

Rupture ( myomalacia cardis )

Arrythmias

Transmural infarction

Fibrinous pericarditis

Rupture of myocardium 3 weeks after MI

Nervous tissue - Has a high rate of metabolism and cannot

tolerate hypoxia.

With complete ischaemia functional changes occur within seconds and cell death within a few minutes.

Causes – thrombosis of vessels and embolism from heart

Colliquative necrosis Fits

cerebral infarct from an arterial

embolus

liquefactive necrosis in a cerebral infarction

Lung -

Pulmonary infarction ( heart failure, mitral stenosis )

Embolus arising in leg veins. Conical in shape. Red in colour.

( Chronic venous congestion ) Heamorrhagic pleural effusion is

common. Can get pyaemic abscesses and

empyema.

Haemorrhagic pulmonary

infarction

Haemorrhagic infarction

Pyeamic abscess

Intestine -

Cause of intestinal ischaemia is a mechanical obstruction

Thrombosis of superior mesenteric artery.

Dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the

bottom

Extremities ( limbs ) -

Causes – peripheral vascular diseasethrombosisspasmRaynaud’s phenomenonDM

If the collateral are defective intermittent claudication occur.

Ulceration followed by infarction occur.

The infarcted area become dry, shriveled and black.

The dead tissue is colonized by bacteria and putrefaction occur – ( wet gangrene )

http://en.wikipedia.org/wiki/Image:Gangrene_early-01.jpg