TU05 sepsis that is used in clinical micro.pptx

heathcare is very important

1. CLINICAL MICROBIOLOGY Sepsis Clinical case and diagnostics UNIVERSITY OF EAST SARAJEVO Faculty of Medicine in Foča

2. Sepsis Systemic inflammatory reaction in response to invasion by microorganisms.

3. Gram-bacteria (60%) Gram+ cocci (20%) Fungi (2-5%) Mycobacteria Viruses Protozoa The penetration of microorganisms into the bloodstream is not decisive for the onset of sepsis. Systemic spread of micro-organism products also causes sepsis. Etiology

4. Gram-bacteria

5. Risk factors for Gram- bacteremia : Diabetes mellitus Lymphoproliferative diseases Liver cirrhosis Burns Invasive procedures Artificial valves... Drugs that cause neutropenia Risk factors for Gram+ bacteremia : Venous catheters Burns Intravenous drug addiction Artificial valves... Etiology

6. A local infection in the urogenital tract, biliary tract, lungs, skin or digestive system can spread to the bloodstream. Pathogenesis

7. Pathogenesis A local infection in the urogenital tract, biliary tract, lungs, skin or digestive system can spread to the bloodstream.

8. Microorganisms can be introduced directly into the bloodstream. In a small number of cases, there are no visible sites of primary infection. The penetration of microorganisms into the bloodstream is not decisive for the onset of sepsis. Systemic spread of micro-organism products also causes sepsis. Pathogenesis

9. The host's immune system recognizes certain molecules of microorganisms as foreign. Lipopolysaccharide ( LPS ) is a product of Gram- bacteria and a very powerful stimulator of the immune response. Peptidoglycan and lipoteichoic acid of Gram+ bacteria, certain polysaccharides and exotoxins cause a similar effect to LPS. The immune response to these molecules is less well studied. LPS is a potent activator of macrophages. It binds to CD14 and TLR4 receptors on macrophages and dendritic cells. Systemic changes in patients with disseminated bacterial infection represent a reaction to cytokines whose production is initiated and stimulated by LPS. Pathogenesis

10. Neutrophilia . Bone marrow response to circulating cytokines, primarily G-CSF. Increased production and release of neutrophils that replace those consumed in the inflammatory reaction. Elevated temperature . LPS (exogenous pyrogen) stimulates leukocytes to produce the cytokines IL-1 and TNF- α ( endogenous pyrogens) which enhance cyclooxygenase-2 enzyme activity and increase the synthesis of prostaglandins from aradidonic acid in vascular and perivascular cells of the hypothalamus, which raises the temperature. Acute phase proteins . Plasma proteins synthesized primarily in the liver. In response to LPS, their plasma concentration increases. C -reactive protein Fibrinogen Serum amyloid A The synthesis of these molecules is regulated by IL-6 , IL-1 and TNF- α Fibrinogen - erythrocyte sedimentation A mild form of sepsis

11. Disseminated intravascular coagulation . Increased expression of pro-coagulant proteins (tissue factor) and decreased anti-coagulant activity of endothelial cells (consequence of TNF-α). Inflammation and intravascular thrombosis develop in many organs. Tissue damage . Activation of neutrophils before exiting the vascular bed damages endothelial cells and reduces blood flow. The lungs and liver are particularly sensitive. Neutrophilic damage to the lung endothelium allows fluid to escape from the blood vessels into the air space of the lungs - ARDS (Adult Respiratory Distress Syndrome). Liver damage leads to reduced gluconeogenesis and a drop in glycemia. A severe form of sepsis

12. Disseminated intravascular coagulation

13. ARDS

14. Presentation of a patient with sepsis

15. Mister White, a 35-year-old journalist, was healthy all his life. A few days after a surgical intervention in the oral cavity, he noticed frequent fatigue, sleepiness, muscle pain and loss of appetite. He did not consult a doctor. The next day, he developed a high fever, rapid breathing and a disturbance of consciousness. Sepsis is easily suspected in a patient with a local infection who suddenly develops a fever . Hyperventilation is often a useful clue to diagnosis even though its cause is not clear enough.Disorientation and other signs of encephalopathy can also be early signs of sepsis. Presentation of a patient with sepsis

16. Mister White then reports to the doctor. During the examination, the doctor confirmed a high temperature, rapid breathing and a disturbance of consciousness, but he also discovered a rapid heartbeat and a drop in blood pressure. He also noticed skin lesions. Hypotension and disseminated intravascular coagulation create ischemic necrosis of peripheral tissues . Bacterial toxins can spread hematogenously and cause diffuse skin changes . Skin lesions can sometimes point to a specific trigger. Presentation of a patient with sepsis

17. The doctor asks the patient if he has had nausea, vomiting or other gastrointestinal complaints. Gastrointestinal manifestations (nausea, vomiting, diarrhea , ileus, ulcer, cholestatic jaundice) may precede other signs of sepsis. In most cases, it is a hepatocellular disorder. Prolonged or severe hypotension can cause acute liver damage. Presentation of a patient with sepsis

18. Laboratory findings: thrombocytopenia, increased lactates, hypoglycemia , increased S-reactive protein, fibrinogen, complement components, accelerated sedimentation. Serum lactates are elevated primarily due to incomplete hepatic clearance. Impaired gluconeogenesis leads to hypoglycemia . Cytokines IL-6, IL-1 and TNF- α induce the synthesis of acute phase proteins in the liver: C-reactive protein , fibrinogen, complement components. Thrombocytopenia suggests DIK. Presentation of a patient with sepsis

19. Blood was taken for microorganism isolation and final diagnosis. A Gram-causing agent of the infection was discovered, which spread into the bloodstream. Sepsis can quickly kill the patient. Successful treatment requires prompt treatment of local infection, ensuring hemodynamics of the cardiovascular system and treatment of other sepsis symptoms. Presentation of a patient with sepsis

20. Laboratory diagnosis of sepsis Microbiological confirmation of clinically diagnosed sepsis is established by isolating microorganisms from blood. Blood for blood culture is taken by venipuncture and inoculated into a medium for isolating microorganisms next to the patient's bed. It is a critical point for possible sample contamination. The percentage of contamination ranges from 0.6% to 6%, on average 2 - 3%.

21. Taking a sample for blood culture Everything must be done with gloves. It is necessary to disinfect the place of venipuncture, usually first with alcohol and then with iodine disinfectant, wait for the optimal time required for the effective effect of the disinfectant (at least 1 minute). After disinfection, the vein should not be palpated. After venipuncture, the iodine disinfectant should be removed with a swab soaked in alcohol. The practice of "two needles" (one needle is used for venipuncture, and the other is used to puncture the vial and inoculate the substrate) was abandoned in the 1980s due to the risk of HIV infection. The use of systems specially adapted for blood collection for hemoculture , with a protected attachment for puncturing the bottle, is the best protection against contamination and the safest for healthcare workers.

22. Taking a sample for blood culture

23. During sepsis, relatively low numbers of microorganisms are often present in the blood - typically <30/mL, so it is recommended to: younger than 10 years: 1 mL of blood for each year of life older than 10 years: 20-30 mL of blood For blood culture, it is optimal to take three blood samples from the patient within 24 hours. Most often, blood is taken at intervals of half an hour to one hour. Blood should be taken at the first symptoms or signs of a rise in temperature, and you should not wait for a rise to 38.5°C. Blood is sown in a ratio of 1:9 (blood: medium). Substrates adapted to the isolation of aerobic bacteria, anaerobic bacteria, Mycobacteria, and fungi ( molds /yeasts) can be used. Usually, the sample is seeded in one set of vials each - for aerobic and anaerobic bacteria. Taking a sample for blood culture

24. Taking a sample for blood culture

25. Taking a sample for blood culture The main ingredient of all bases is nutritionally rich broth. The pads may contain "resins" that inactivate antibiotics, if the patient has already received treatment. Blood culture media can be adapted for conventional diagnostics (manual processing) or for culturing in automatic systems. Cloudiness, appearance of hemolysis , appearance of gas, appearance of colonies in blood culture are observed. Blood cultures are incubated for up to 7 days. Under special circumstances, e.g. suspicion of brucellosis, up to 21 days or even longer. The problem of interpreting the findings: what is a pathogen and what is a contaminant (presence of signs and symptoms of the disease, biochemical markers, history of the disease, isolation of microorganisms from two or more vials).