2. INFLAMMATION
• Protective response involving host cells, blood vessels and proteins
and other mediators that is intended to eliminate the initial cause of
cell injury, as well as the necrotic cells and tissues resulting from the
original insult and to initiate the process of repair.
• It accomplishes its protective mission by first diluting , or otherwise
neutralizing harmful agents(e.g- microbes , toxins)
• It then sets into motion the events that eventually heal and repair the
sites of injury.
• Without inflammation, infection would go unchecked and wounds
would never heal.
3. • Inflammation can be acute or chronic.
• Acute inflammation is rapid in onset and of short duration lasting
from a few minutes to as long as a few days, and is characterized by
fluid and plasma protein exudation and a predominantly neutroplilic
leukocyte accumulation.
• Chronic inflammation may be more insidious, is of longer duration
and is typified by influx of lymphocytes and macrophages and fibrosis.
4. • Inflammation is induced by chemical mediators that are produced by
host cells in response to injurious stimuli.
• When a microbes enters a tissue or the tissue is injured, the presence
of the infection or damage is sensed by the resident cells, mainly
macrophages, but also dendritic cells, mast cells, and other cell types.
• These cells secretes molecules(cytokines and others mediators) that
induce and regulates the subsequent inflammatory response.
• Some of the mediators promotes the efflux of plasma and the
recruitment of circulating leukocytes to the sites where the offending
agent is located.
• The recruited leukocytes are activated and they try to remove the
offending agent by phagocytosis.
5. • The cardinal signs of inflammation are—
• Calor (heat), rubor (redness), tumor (swelling), dolor (pain), functio
laesa (loss of function).
• Inflammation is normally controlled and self limited.
• The mediators and cells are activated only in response to injurious
stimulus and are short lived and they are degraded or become
inactive as the injurious agent is eliminated.
• If the injurious agent cannot be quickly eliminated, the result may be
chronic inflammation, which can have serious pathologic
consequences.
6. INFECTION
• Infection of surgical incision
• Within 30 days
• Within 1 year if FB is implanted
• Commonest hospital acquired infection
8. • Treatment of infection—
Drainage of pus.
Debridement.
Antibiotics.
Removal of FB.
9. PYAEMIA
• Presence of multiplying bacteria in blood as emboli which spread and
lodge in different organs in the body like liver , lungs , kidney, spleen
brain causing pyaemic abscess
• May lead to MODS
• May endangers life if not treated properly.
• Presented with fever with chills and rigors, jaundice, oliguria,
drowsiness, hypotension.
• Treatment – Fluids, Antibiotics.
10. TOXEMIA
• Clinical systemic state caused by a wide spread activation of host
defence mechanisms to the presence of toxins produced by bacteria
or injury to tissue.
• Toxemia does not include the diseases caused by toxic substances
produced by plants or insects or ingested organic or inorganic
poisons.
11. • Clinical signs of acute Toxemia
• The syndrome varies with the speed and severity of the toxic process
but the variation are largely of degree.
• Depression, anorexia and muscular weakness are most common.
• Diarrhoea.
• Increase HR, Pulse- weak rapid but regular.
• Fever, muscular weakness.
12. • Clinical sign of chronic toxemia
• Lethargy, separation from the group, inappetence, failure to grow or
produce and emaciation
• Treatment
• Removal of foci of infection
• Broad spectrum antibiotics
• Aggressive fluid therapy
• NSAIDS
• Steriods.
13. SEPTICEMIA
• Presence of overwhelming and multiplying bacteria in the body with
toxins causing SIRS or MODS which may later progress into MSOF.
• Sepsis actually means body response to its own organs.
• Sepsis is SIRS with infection.
• Severe sepsis is sepsis syndrome with MODS or MSOF.
14. • Septicemia can be gram positive or gram negative.
• Gram Positive– staphylococcus, streptococcus, pneumococcus etc.
common in children, old age, diabetes and after splenectomy.
• Gram Negative– common in acute abdomen conditions like
peritonitis, abscess, biliary, pancreatitis, GI or urinary tract infection.
Commonly seen in malnourished, old age, immunocompromised
people and diabetics.. Common bacteria are- E.Coli, Klebsiella,
Pseudomonas, Proteus.
16. ABSCESS
• Localised collection of pus in a cavity lined by granulation tissue,
covered by pyogenic membrane.
• Contains pus in loculi
• WBC, multiplying bacteria, toxins and necrotic material.
• Macrophages and polymorphs release lysosomal enzymes which
cause liquefaction of tissues leading into pus formation.
• Toxins and enzymes released causes tissue destruction and pus
formation.
18. PRINCIPLE OF MANAGEMENT
• INVESTIGATIONS
TLC, BLOOD SUGAR, USG OF PART, X RAY CHEST, CT, MRI
BLOOD CULTURE, LFT.
• TREATMENT
Drainage of abscess
Wound not closed
Pus sent for culture and sensitivity
Antibiotics
