Inflammation

 

 

The inflammatory response is both normal and necessary.

A non specific local response to a recent or ongoing insult.

Inflammation literally means, "to set afire".

Suffix "itis" is used to describe an inflammatory response.

Inflammation is the first stage in the healing process.

(John Hunter, English, c 1780)

 

 

Clinical features

(Cornelius Celsus, Roman, first century AD)

Heat

Pain

Redness

Swelling

Loss of function

 

 

Causes

Mechanical trauma

Chemical agents

Thermal injuries

Immunological reactions

Infection

Radiation

Ischaemia

Necrosis

 

 

Infection

Conjunctivitis

Meningitis

Encephalitis

Gastritis

Cholecystitis

Cystitis

Pyelonephritis

Colitis

Tonsillitis

Appendicitis

Peritonitis

Poliomyelitis

Bronchitis

Pneumonia

Urethritis

Dermatitis - eczema

Wound infection

Abscess

 

 

Mechanical trauma

Cuts, abrasions, crush injuries, friction, pressure

 

 

Chemical agents

Acids, alkalis, some organic compounds, alcoholic gastritis or hepatitis, biliary peritonitis, pancreatitis.

 

 

Thermal injuries

Heat, cold

 

 

Radiation

Ultraviolet light in sunshine

 

 

Immunological reactions

Autoimmune diseases

Allergic reactions

 

 

Characteristics

Vasodilation

Increased capillary permeability

Production of protein rich inflammatory exudate

Clotting of fluid in the extracellular spaces

Walling off, blocking local tissue spaces and lymphatics

Migration of granulocytes then monocytes, lymphocytes, plasma cells

Phagocytosis, antibody production, cytokines, growth factors.

 

 

Mediators

There are numerous substances that act as inflammatory mediators; they may be derived from plasma or cells. Kinins (e.g. bradykinin), clotting factors and complement are inflammatory mediators derived from plasma.

 

 

Histamine

Tissue insult

Mast cell degranulation

Histamine (and some bradykinin)

Vasodilation

Nociceptors sensitization

Antihistamines block histamine receptors by competitive blockage of tissue bound histamine receptors.

 

 

Prostaglandins and Leukotrienes

 

Cell membrane phospholipid released into tissues

 

Phospholipase A

 

Arachidonic acid

 

Cyclo-oxygenase (COX)

 

Prostaglandins

 

 

The purpose of inflammation

Hyperaemia will increase the blood supply so increase glucose and oxygen delivery.

Increases in the supply of amino acids, vitamins and minerals.

Exudate will dilute toxins.

Pain and muscle splinting promote immobilisation.

Fibrinogen enters the tissues to compartmentalise infected areas, blocks lymphatics.

Leucocytes migrate into tissue spaces to phagocytose.

Leucocytes also release chemical mediators.

Therefore inflammation is essential for healing.

 

 

Lines of tissue defence

1. Tissue macrophages, activated by tissue damage to release cytokines which in turn attract other inflammatory cells.

2. Neutrophil diapedesis and chemotaxis (many found in inflammed tissue 90 minutes after injury, peaking at 24 48).

3. Neutrophilia within a few hours from 4 5 000 up to 20 000 as a result of inflammatory mediators entering the blood. Neutrophils are released from the bone marrow.

4. Monocyte migration followed by cell enlargement into macrophages.

5. After 3 4 days monocyte and granulocyte production in bone marrow is increased (production rates may be 20 50 times normal).

 

(Increased production of neutrophils and monocytes is stimulated by cytokines from activated monocytes in the inflamed tissues).

 

 

Pus

 

Often collects in a hollowed out area.

Abscess formation.

Dead granulocytes and macrophages.

Dead and phagocytosed tissue cells.

Dead and living bacteria.

Liquefaction necrosis.

Tissue fluid.

If not evacuated pus will autolyze and gradually be absorbed into surrounding tissue.

 

Suppurate to produce pus

Purulent contains lots of pus

Empyema pus filling a cavity

 

 

 

Possible outcomes of inflammation

 

Resolution

Scaring

Chronic inflammation / abscess formation

Spread

Death

 

 

 

Chronic inflammation

 

Inflammation which lasts for more than 2 weeks.

Causes include parasites, bacteria, viruses, ongoing trauma, cancer, autoimmunity.

Many mononuclear cells, (monocytes, lymphocytes, plasma cells) present.

 

 

 

Management principles

 

Remove cause

Treat pain

Do not mask clinical features

Establish priorities, e.g. airway swelling

Fluid balance

Nutrition

Oxygen supply

Elevate

Keep warm (usually)

Rest

Holistic care

 

 

 

Systemic effects of inflammation - acute phase response

 

Triggered by the release of inflammatory mediators and cytokines into the blood.

Collectively these can be called the acute phase reactions.

Fever, pyrogens.

Leucocytosis.

Skeletal muscle catabolism.

Decreased appetite.

Lethargy (cytokines affecting CNS).

Acute phase proteins increased production of clotting proteins, C-reactive protein and complement.

Trauma or stress increases ADH, ACTH, adrenaline and growth hormone.

Metabolic changes lead to malaise, weakness, loss of appetite.

 

 

Bacterial infections neutrophilia.

Viral infections lymphocytosis.

Allergies or parasitic infection eosinophilia.