Professor of Pathology Faculty of Medicine Ain Shams University Dr. Riham Abu-Zeid Professor of Pathology Faculty of Medicine Ain Shams University Inflammation 6

Toxemia Septicemia Bacterial infection of blood Bacteremia Pyemia

Effects and complications: Fever, headache, rigors ,pain 1-Toxemia: A-Acute Toxemia presence of bacterial toxins in blood. typhoid fever, diphtheria, pneumonia ,bacillary dysentery Effects and complications: Fever, headache, rigors ,pain Fatty change of parenchymatous organs. Toxic myocarditis >> acute heart failure. necrosis of the liver. Necrosis of suprarenal cortex > acute adrenal insufficiency and death. Bilateral tubular necrosis of the kidney > acute renal failure. Endotoxic (septic) shock. pain allover the body. necrosis of the liver. Necrosis of suprarenal cortex > acute adrenal insufficiency and death. Bilateral tubular necrosis of the kidney > acute renal failure. Endotoxic (septic) shock.

Endotoxic (septic) shock Acute Toxemia Myocarditis AHF Bil. TN & ARF acute adrenal insufficiency Liver Necrosis Endotoxic (septic) shock Fever Toxins produced by pathogens cause an immune response; in gram-negative bacteria these are endotoxins, which are bacterial membrane lipopolysaccharides At high levels of LPS, the syndrome of septic shock supervenes; the same cytokine and secondary mediators, (TNF )now at high levels, result in systemic 1-vasodilation (hypotension), 2-diminished myocardial contractility, widespread 3-endothelial injury and activation, causing systemic leukocyte adhesion and diffuse alveolar capillary damage in the lung 4-activation of the coagulation system, culminating in disseminated intravascular coagulation (DIC). The hypoperfusion from the combined effects of widespread vasodilation, myocardial pump failure, and DIC causes multiorgan system failure that affects the liver, kidneys, and central nervous system, among others.  Unless the underlying infection (and LPS overload) is rapidly brought under control, the patient usually dies. TN :tubular necrosis ARF:Acute renal failure

Loss of weight and prolonged low grade fever. B-Chronic toxaemia as in TB Effects and complications: Loss of weight and prolonged low grade fever. Amyloidosis. Normocytic anemia due to bone marrow depression.

2-Bacteremia presence of small number of bacteria in the blood which do not multiply significantly commonly not detected by direct microscopy. Blood culture is done for their detection e.g. infection with Salmonella typhi, Streptococcus viridians and Escherichia coli.

presence of rapidly multiplying 3-Septicemia presence of rapidly multiplying highly pathogenic bacteria in the blood. Causative organisms: Pyogenic cocci Bacilli of plague… etc. N.B It is a very serious condition with severe toxemia and shock. An Atypical Inflammatory Reaction In a typical inflammatory reaction, the local pro-inflammatory processes are balanced by systemic anti-inflammatory processes and are automatically terminated within a short time. In sepsis, however, cytokine production continues unending and the circulatory spread of the cytokines then causes increased cytokine production at distant sites Endotoxin is a lipopolysaccharide in the cell wall of Gram-negative bacteria. When it gets into the circulation, endotoxin strongly activates the coagulation and complement systems throughout the body. Endothelial Damage a normal inflammatory reaction activates local endothelial cells but it also damages those same cells. Sepsis multiplies this effect by activating and damaging endothelial cells in patches throughout the entire vascular tree. In sepsis there are many places in the body where the barrier between the bloodstream and the surrounding tissues has become leaky and crowded with immune cells The damaged endothelial surface inhibits anticoagulant properties as well as increases antifibrinolysis, which can lead to intravascular clotting, the formation of blood clots in small blood vessels, and multiple organ failure  Organ Damage Sepsis can evolve to multiple organ dysfunction syndrome (MODS), An organ with significant damage to its vascular endothelium ends up poorly perfused and ischemic. Such an organ will function poorly (organ dysfunction) or it will fail altogether. Progression to Shock Severe sepsis occurs when organ dysfunction progresses to organ failure. If arteries fail to constrict,dt excessive production of chemicals that dilate blood vessels such as nitric oxide, a deficiency of chemicals that constrict blood vessels such as vasopressin, and activation of ATP-sensitive potassium channels.septic shock occurs. https://www.atrainceu.com/course-module/1884975-107_sepsis-module-04

Pathological features(postmortum); 3-Septicemia Pathological features(postmortum); Petechial hemorrhages. Massive adrenal hges & DIC Acute bacterial endocarditis Acute splenic swelling. Petechial haemorrhages allover the body.(leaky blood vessels) Acute bacterial endocarditis if streptococci invade cusps of valves

3-Septicemia Acute splenic swelling. Normal spleen Gross enlarged, soft with semifluid cut surface that can be washed by tap water. Microscopically lymphoid follicles are atrophied, sinusoids are congested & contain acute & chronic inflammatory cells. spleen is moderately enlarged, very soft with semifluid cut surface that can be washed by tap water. Normal spleen

Characters of pyemic abscess; are multiple small abscesses bacteria Trombus 4-Pyemia Dissemination of small septic emboli in the blood resulting in pyemic abscesses at the sites where they are lodged Characters of pyemic abscess; are multiple small abscesses nearly of the same size surrounded by zone of congestion. . Inflamed (stasis +endoth inj )…>>thrombi +infection ..arteries give branches of arterioles >arrest of thrombi necrosis dt cut of supply necrosis with superdeed bacteria begin abscess as usual

Systemic Pyemia Portal To liver Into arterial side To lung eg.GIT To liver Into venous side Into arterial side eg.left side of heart lung Live\ may be involved in both portal and systemic (arterial) pyemia NB internal hemorroides drain into porta>>portal pyemia External hemooroides drain to systemic veins go to lung To lung To brain, liver, kidney, spleen

when septic emboli are carried by systemic circulation Types of pyemia Systemic pyemia Portal pyemia when septic emboli are carried by systemic circulation when septic emboli are carried by portal circulation Acute hematogenous osteomyelitis. Puerpural sepsis Suppurative otitis media Suppurative lung disease e.g. abscess (emboli arising from lung veins). Acute bacterial endocarditis Acute suppurative appendicitis. Infected internal piles Suppuration of gall bladder and large intestine.

venous side (a, b & c) >>pyemic abscesses in LUNG. Types of pyemia (cont ) Systemic pyemia Portal pyemia Emboli arising from venous side (a, b & c) >>pyemic abscesses in LUNG. -Emboli in general arterial circulation(d& e) producing pyemic abscesses in brain, liver, kidney, spleen, skin, intestine… etc., Emboli arrested in LIVER, producing multiple abscesses

Toxins in blood Bacteremia Toxemia Septicemia Not detected in blood –needs blood culture Toxins in blood Rapidly multiplying highly pathogenic bacteria Moving Infected thrombus Bacteremia Toxemia Pyemia Septicemia

Exudate Transudate Inflammatory cause alteration in normal vascular permeability. Transudate Diminished colloid osmotic pressure in the plasma. Increased hydrostatic pressure across the vessel wall No or minmal increase in vascular permeability. alteration in normal vascular permeability in the area of injury.