Types of acute inflammation I Suppurative inflammation associated

Types of acute inflammation I. Suppurative inflammation: associated with pus formation. II. Non- suppurative inflammation: not : associated with pus formation • Types of acute suppurative inflammation. Localized: Abscess, Carbuncle, Furuncle Diffuse: cellulitis I- Suppurative inflammation • Definition: Severe acute inflammation characterized by formation of Pus. • Causes: Pyogenic microorganisms as: staphylococcus aureus , streptococcus haemolyticus and pneumococci.

Mechanism of pus formation: 1. Pyogenic microorganisms cause: tissue destruction (necrosis) by its toxins and strong chemotaxis on polymorphs. 2. Many polymorphs are killed and are called pus cells, which release proteolytic enzymes leading to liquefaction of the necrotic tissue. 3. The resulting liquefied necrotic material mixes with the other products of the inflammatory process (inflammatory fluid exudate , inflammatory cells and the causative organism) forming pus Abscess • Definition: A localized suppurative inflammation resulting in the formation of a cavity containing pus. • Cause: Often by staphylococcus aureus. Staphylococci produce coagulase enzyme which helps fibrin formation that localizes the inflammation. • Sites: Skin, subcutaneous tissue and internal organs as: lung, brain and liver.

Pathogenesis: 1 - Early: The abscess is formed of two zones: • Central necrotic zone. • Peripheral zone of acute inflammation containing large number of polymorphnuclear leucocytes. 2 - Later: Proteolytic enzymes from dead polymorphs (pus cells) cause liquefaction of the necrotic tissue. The liquefied necrotic tissue mixes with pus cells to form the pus. So, a well developed abscess is formed of three zones: • Central necrotic zone. (the core) • Middle zone of pus ( abscess cavity). • Peripheral zone of acute inflamed tissue (called pyogenic membrane). • • Fate: • Small abscess: Pus is absorbed and healing occur by fibrosis. • Large abscess: should be surgically evacuated to allow healing (as pus is absorbed very slowly).

Complications: 1. Spread of infection: a) Lymphatic spread: cause lymphangitis and lymphadenitis. b) Blood spread: may lead to toxaemia, bacteraemia, pyaemia or septicaemia. 2. Chronicity : inadequate drainage change the acute abscess into chronic abscess which has a thick fibrous wall. 3. Complications of healing: in the form of chronic ulcer, sinus discharching pus, fistula in hollow organs such as perianal fistula. Carbuncle • It is an extensive form of abscess (localized suppurative inflammation) in which pus is present in multiple communicating foci, discharged through several multiple openings (sinuses) on the skin surface. • Occurs in the back of the neck and scalp. • Diabetes mellitus is a common predisposing factor.

Furuncle (Boil) • It is a small abscess (localized suppurative inflammation) related to a hair follicle or sebaceous gland. • Occur in the axilla, face and head. 2 -Diffuse Suppurative inflammation (Cellulitis ) • Definition: Acute diffuse suppurative inflammation. • Cause: Commonly caused by streptococcus haemolyticus that produces streptokinase and hyaluronidase enzymes which dissolve fibrin helping spread of infection(diffuse). • Sites: Loose connective tissue as subcutaneous tissue, tissues of the orbit, scrotum and wall of the appendix. Complications: Spread of infection by: • Lymphatic spread causing lymphangitis and lymphadenitis. • Blood spread causing toxaemia, pyaemia or septicaemia.

II-Acute non - suppurative inflammation • Definition: Types of acute inflammation not associated with pus formation. 1 - Catarrhal inflammation Mild acute inflammation of the mucous membranes. It is characterized by excess mucous secretion from the inflamed mucous membrane, e. g. of nose (catarrhal rhinitis or common cold), Catarrhal bronchitis and appendicitis. 2 - Serous inflammation: Non-suppurative acute inflammation characterized by outpouring of watery excess serous fluid exudate. • Inflammation of the serous membrane: as pleura, pericardium andperitoneum (Pleural effusion, pericardial effusion and ascites). • Skin blisters resulting from a burn or viral infection. 3 - Fibrinous inflammation: Non-suppurative acute inflammation characterized by an exudate rich in fibrin. The fibrin appears as meshwork of threads. • Inflammation of the serous membranes: as Fibrinous pleurisy, Fibrinous pericarditis and Fibrinous peritonitis. • Lung as in lobar pneumonia: the alveoli are filled with inflammatory exudate rich in fibrin. Complications: healing by fibrosis (scarring) that obliterates the pericardial space and restricts myocardial function.

4 - Sero-Fibrinous inflammation: Non- suppurative acute inflammation characterized by formation of excess fluid exudate rich in fibrinogen. As Inflammation of the serous membranes (pleura, pericardium and peritoneum). 5 - Pseudo-Membranous inflammation Severe form of non-suppurative acute inflammation characterized by pseudo-membrane on the affected surface which is formed of necrotic tissues, acute inflammatory cells and fibrin. -Bacteria that secretes exotoxins causing patchy mucosal necrosis such as: • Mycobacterium diphtheria that affects the palatine tonsil causing diphtheria. • Clostridium difficile that affects intestinal mucosa causing Pseudomembranous colitis. • The pseudo-membrane is formed of necrotic tissues, acute inflammatory cells (Polymorphs and pus cells) and fibrin. 6 - Necrotizing (Ulcerative) inflammation: Non- suppurative acute inflammation characterized by marked tissue necrosis and sloughing (shedding) of the inflammed necrotic tissue (ulcer). • Inflammatory necrosis of the mucosa of the mouth, stomach, intestines or genitourinary tract. the best example is seen in typhoid intestinal ulcers. 7 - Allergic inflammation: Non-suppurative acute inflammation caused by hypersensitivity reaction and characterized by inflammatory exudate rich in eosinophils. as Allergic rhinitis and bronchial asthma.

Course (Fate) of acute inflammation 1 - Resolution (complete recovery): 2 - Healing by fibrosis: It occurs when there is extensive tissue destruction in tissues that don’t regenerate or when inflammation is severe. 3 - Transition to chronic inflammation: It occurs when the causing agent is not completely removed. 4 - Progression and spread: If the bacteria overcome the defense mechanism , it spreads directly by lymphatics and by blood causing fatal septicemia.