INFLAMMATION, INFECTION, PYAEMIA, TOXEMIA,.pptx

inflammation

1. INFLAMMATION, INFECTION, PYAEMIA, TOXEMIA,SEPTICEMIA, ABSCESS & PRINCIPLE OF MANAGEMENT

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

7. Types– superficial, deep, organ/ space. Source– patient, staff, surgeon, operation theatre. Risk factors Age, DM, Obesity, Smoking, Malnutrition, Immune Compromised, Prolonged stay How to prevent Shower, Shaving, Patient dress, theatre staff dress, Hand washing, antibiotic prophylaxis. Skin preparation, draping,wound dressing.

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.

15. EVALUATION— Clinical assessment, CBC, LFT,KFT, coagulation profile, ABG, culture, X-Ray chest, imaging as needed. TREATMENT— Fluid therapy, Antibiotics, I/O, vitals monitoring, blood transfusion, O2 supplementation, management of complication.

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.

17. Mode of infection– direct, haematogeneous , lymphatic, and extension from adjacent tissues. Bacteria– Staphylococcus aureus, streptocococcus pyogens , E.Coli , Klebsiella Sites external– fingers, hand, dental, tonsillar, oral, neck, breast, parotid etc internal– subphrenic, pelvic, paracolic, liver, pancreatic etc

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