What Is the Connection between Strep and Sepsis?

Mainly the manifestations of systemic inflammatory response and insufficient organ perfusion and insufficiency. Due to different pathogenic bacteria, the performance also varies.

Sepsis and bacteremia

Sepsis is a collective term for surgical infections that manifest systemic inflammatory responses, such as changes in body temperature, breathing, and circulation. It is the damage caused by the absorption of endotoxin and exotoxin produced by pathogenic bacteria and various inflammatory mediators to the body tissues. When sepsis is accompanied by insufficient organ perfusion, such as lactic acidosis, oliguria, and acute conscious changes, it is called pyemia syndrome. If bacteria invade the blood circulation and the blood culture is positive, it is called bacteremia. Sepsis and bacteremia are often secondary to severe post-traumatic infections and various purulent infections. The pathogenic bacteria are numerous, numerous, and virulent. Generally, the onset is rapid, the condition is severe, the change is rapid, and the organ perfusion is often insufficient. Clinically, it is necessary to provide positive comprehensive treatment, while fighting against infection, pay attention to correct electrolyte disturbances and acid-base imbalances, timely grasp the heart, lungs, liver, kidneys and other important organs involved and actively deal with them.

Symptoms and signs of sepsis and bacteremia

Mainly the manifestations of systemic inflammatory response and insufficient organ perfusion and insufficiency. Due to different pathogenic bacteria, the performance also varies.

1. Gram-positive bacterial sepsis may or may not have chills, and the fever is stagnant or relaxation fever. The patient was flushed, his limbs were warm and dry, and most of them were delirious and unconscious. There are often rashes, diarrhea, vomiting, and metastatic abscesses, such as subcutaneous abscesses, splenitis, liver and kidney abscesses, etc. Prone to myocarditis. Shock occurs later and blood pressure drops more slowly.

2. Gram-negative bacillus sepsis generally begins with a sudden chill, fever can be intermittent, and in severe cases, the temperature does not rise or is lower than normal. The patient's limbs were cold, cyanosis, oliguria, or anuria. Sometimes the increase in white blood cell count is insignificant or reversed. Shock occurs early and lasts a long time.

3. Fungal sepsis resembles Gram-negative bacillus sepsis. Sudden occurrence of chills and high fever (39.5-40 ° C), the patient's general condition deteriorated rapidly, and she appeared indifferent, lethargic, decreased blood pressure, and shock. A few patients still have gastrointestinal bleeding. Peripheral blood can often show a leukemia-like response, with late myelocytes and mesophils, and white blood cell counts up to 25 × 109 / L.

Drug treatment for sepsis and bacteremia

Sepsis should be based on the treatment of the primary infection and a comprehensive systemic treatment.

1. Treatment of primary infections Early treatment of primary infections and migration. Abscesses should be opened and drained in time; acute peritonitis, suppurative cholangitis, and strangulated intestinal obstruction should be surgically removed in time; the necrotic tissue and foreign bodies in the wound should be removed, and the dead space should be opened to fully drain; when the venous catheter is infected, remove the catheter Is the first measure.

When the primary focus is difficult to find for a while, attention should be paid to potential sources and routes of infection, such as intravenous catheterization, indwelling urinary catheters, and intestinal infections. Critically ill patients with suspected intestinal infections should promptly correct shock to restore intestinal mucosal blood perfusion as soon as possible; promote early intestinal mucosal repair through early enteral nutrition; orally take intestinal ecological preparations to maintain normal intestinal flora.

2. Application of antibacterial drugs According to the nature of the primary infection, antibacterial drugs can be selected empirically. Broad-spectrum or combined use of two antibiotics is usually selected. Then, according to the treatment effect, disease evolution, bacterial culture, and drug sensitivity determination, targeted selection of anti-infective drugs. The therapeutic dose is sufficient and administered intravenously. The drug is usually discontinued after the temperature drops, the white blood cell count is normal, the condition improves, and the local lesion is controlled. For systemic fungal infections, broad-spectrum antibiotics should be discontinued and antifungal drugs such as ketoconazole and amphotericin B should be selected.

3. Supportive therapy Patients should rest in bed and be given nutritious and digestible food. For those who cannot eat orally, glucose, amino acid and electrolyte solution can be infused intravenously. If necessary, intravenous high nutrition can be applied. For anemia and hypoproteinemia, fresh blood and plasma can be given to improve the patient's condition, and to correct the imbalance of water, electrolyte and acid-base metabolism. The original underlying diseases, such as diabetes and liver cirrhosis, should be treated accordingly.

4. Symptomatic treatment If the fever is high, medication or physical cooling is appropriate. In severe patients, artificial hibernation or adrenocortical hormone can be used to reduce the symptoms of poisoning. However, it should be noted that artificial hibernation has an impact on blood pressure, and hormones can only be used with large doses of antibiotics to prevent the spread of infection; when shock occurs, anti-shock therapy should be actively and quickly performed.

5. Intensive care should be strengthened to pay attention to vital signs, consciousness, urine output, arterial blood gas, etc. The presence of hypovolemia should expand blood volume, and if necessary, dopamine and dobutamine should be given to maintain tissue perfusion.

6. Therapeutic methods that inhibit the formation of inflammatory mediators or block the effects of mediators. Although mediator inhibitor therapy has proven effective in animal studies, clinical control studies have not reached a firm conclusion on its effectiveness.

Diet and health care for sepsis and bacteremia

1. What foods are good for sepsis and bacteremia:

Encourage patients to drink plenty of water and give a high-protein, high-vitamin, digestible liquid diet.

2. What foods are best not to eat for sepsis and bacteremia:

Carbohydrate snacks and fruits.

Preventive care for sepsis and bacteremia

Actively treat primary infection lesions and use antibiotics reasonably; for long-term venous catheters and urinary catheters, the local skin cleaning and disinfection should be strengthened. Patients who have been using glucocorticoids, immunosuppressants and anticancer drugs for a long time have low disease resistance. While strengthening nutrition and improving their physical fitness, protective isolation should be done.

Pathogenic causes of sepsis and bacteremia

Often secondary to large-area burn wound infections, open fractures with infection, condyles, diffuse peritonitis, biliary or urinary tract infections, and acute obstructive suppurative cholangitis. Due to the incomplete limitation of the infection focus, a large number of virulent pathogens constantly or frequently invade the blood circulation, or a large number of inflammatory mediators from local infection enter the blood, which stimulates systemic inflammatory reactions and causes sepsis.

Common predisposing factors

(1) weakening of human resistance: such as chronic diseases, old age, young children, malnutrition, anemia, hypoproteinemia, etc.

(2) The long-term use of glucocorticoids, immunosuppressive agents, anticancer drugs, etc. has led to changes in normal immune function, or the use of broad-spectrum antibiotics has changed the state of the original commensal bacteria, and non-pathogenic or conditional pathogens have multiplied in large numbers. Causes infections by pathogenic bacteria, such as systemic fungal infections.

(3) Improper management of local lesions: the abscess failed to drain in time, the debridement was incomplete, and foreign matter, dead space, and poor drainage were present in the wound.

(4) Indwelling venous catheters for a long period of time can help the pathogens to multiply and directly invade the bloodstream, and stimulate the systemic inflammatory response.

2. Common pathogenic bacteria There are many types of pathogenic bacteria that cause sepsis. The common pathogenic bacteria are:

(1) Gram-negative bacilli: Gram-negative bacilli have surpassed Gram-positive cocci in contemporary surgical infections. Commonly, they are E. coli, Bacteroides, Pseudomonas aeruginosa, and Proteus, followed by Klebsiella and intestines. Bacillus and so on. On the one hand, the results of antibiotic screening, and on the other hand, necrotic tissue caused by trauma are beneficial to the growth of such bacteria. The main toxin of Gram-negative bacilli is endotoxin, which is a kind of lipopolysaccharide (LPS), which is released from the cell wall after bacterial death, and acts on phagocytic cells to cause the release of cytokines, thereby triggering a series of chain reactions. Abdominal infections, urogenital system, and perineal infections are often difficult to avoid contamination.

Gram-negative bacillus-induced sepsis is generally more severe, with three low phenomena (low body temperature, low white blood cells, and low blood pressure), and more people with septic shock.

(2) Gram-staining cocci: The main virogen is exotoxin, such as enterotoxin, toxic shock syndrome toxin-1 (TSST-1), and so on. The more common pathogenic bacteria are:

Staphylococcus aureus: due to multiple drug-resistant strains in recent years, including resistance to -lactams and aminoglycosides, these strains also tend to spread blood and can form metastatic abscesses in the body. Local infection of some strains can also cause high fever, rash, and even shock.

Staphylococcus epidermidis: has been classified as "non-pathogenic bacteria" for many years. Because it is easy to adhere to medical plastic products such as venous catheters, bacteria are embedded in the mucus, which can evade the body's defense and the role of antibiotics. The infection rate has increased significantly in recent years.

Enterococcus: It is a resident bacteria in the human intestinal tract. It can participate in multiple infections of various parts of the body. Some enterococcal sepsis is difficult to find the primary focus.

(3) Anaerobic bacteria without spores: Anaerobic bacteria without spores cannot be detected by ordinary bacterial culture, and it is easy to be ignored. Abdominal abscesses, appendic abscesses, paraanal abscesses, empyema, brain abscesses, aspiration pneumonia, oral and maxillofacial necrotic inflammation, perineal infections, and many more contain anaerobic bacteria. About 2/3 of anaerobic infections are combined with aerobic infections. The two types of bacteria have a synergistic effect, which can increase necrotic tissue, easily form abscesses, and pus may have fecal odor. Common anaerobes are Bacteroides, Clostridium, Anaerobic Staphylococcus, and Anaerobic Streptococcus.

(4) Fungi: Conditional pathogens, which often occur in the continuous application of broad-spectrum antibiotics. Bacteria are widely inhibited, allowing fungi to overgrow and become a double infection after general bacterial infections. The basic disease is severe, plus the application of immunosuppressants , Hormones, etc., further weaken the immune function; long-term indwelling intravenous catheters.

Common pathogenic fungi in surgical fungal infections are Candida albicans, Aspergillus, Mucor and Neococcus.

Diagnosis of sepsis and bacteremia

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Test methods for sepsis and bacteremia

Laboratory inspection:

1. The white blood cell count is obviously increased, usually it can reach more than (20 30) × 109 / L, or it decreases, the nucleus shifts to the left, the juvenile type increases, and toxic particles appear.

2. Bacterial culture (aerobic and anaerobic)

(1) Blood bacteria culture.

(2) Culture of pus bacteria.

If the two obtained bacteria are the same, the diagnosis of bacteremia is established. However, many patients have been treated with antibacterial drugs before the occurrence of bacteremia, making it difficult to obtain positive results in a single culture. Therefore, blood should be drawn several times a day for bacterial culture. It is best to choose the time for blood draw before the chill and fever are expected to increase the positive rate.

3. Bone marrow bacterial culture Blood bacterial culture is negative, and when bacteremia is highly suspected, bone marrow bacterial culture is feasible.

4. Fungal culture If you have fungal bacteremia, you can do urine and blood fungal examination and culture.

5. Blood biochemistry Patients with sepsis may develop azotemia.

6. Blood gas analysis Sepsis patients may have varying degrees of acidosis.

7. Renal function test In patients with sepsis with impaired renal function, protein, blood cells, ketone bodies, etc. may appear in the urine.

8. Immunological test is a reference index for judging the prognosis. Activated complement, leukotriene, thromboxane, TNF-1 inflammatory mediators have a large increase in duration and long duration, then the disease is serious and the prognosis is poor.

Other auxiliary checks:

Ophthalmoscope: fungal bacteremia, often small, white, shiny, round bulges on the fundus retina and choroid.

Complications of sepsis and bacteremia

1. Osteomyelitis tends to occur in children, and more Gram-positive bacteria infections are common.

2. Myocarditis When Gram-positive bacteria are infected, bacterial toxins can invade myocardial tissue and cause myocarditis.

3. Gastrointestinal bleeding Sepsis caused by fungal infections is prone to gastrointestinal bleeding.

4. Septic shock Gram-negative bacilli are prone to cause septic shock.

Prognosis of sepsis and bacteremia

The prognosis of sepsis is poor, with a mortality rate of 20% to 50%. Systemic inflammatory response syndrome, sepsis, sepsis, and septic shock reflect the different severity of the same disease. A survey found that the mortality rates were 7%, 16%, 20%, and 46%, respectively. The prognosis worsens as the disease progresses.

Pathogenesis of sepsis and bacteremia

Changes in the body during sepsis are more common than activation of inflammatory responses than local infections, and they lack a clear targeted lesion in local reactions. Germs and their products escape local defenses and enter the circulatory system. Causes activation of intravascular complement and coagulation factors. Histamine and serotonin (5-HT) released by mast cells are activated systemically, leading to vasodilation and increased permeability. When local inflammation is severe, a large number of pro-inflammatory signals such as TNF can be released, causing circulating macrophages and neutrophils to be activated, and macrophages in distant sites, such as alveolar macrophages, and Kupffre cells in the liver. Is activated, causing activation of disseminated inflammatory cells. Inflammation at the systemic level is initiated, leading to systemic vasodilation, increased blood flow (high hemodynamic state), and systemic edema. The chemokines produced by the inflammatory response promote the interaction and migration of leukocytes and endothelial cells. The systemic pro-inflammatory cytokine chain reaction stimulates neutrophils to release lysosomal enzymes, interleukin-1, interleukin-6, and interleukin-8, and generates oxygen free radicals through respiratory bursts to kill engulfed bacteria and break down necrotic tissue It has the function of defending against bacteria. However, it can also cause damage to the vascular endothelium and surrounding areas. Inflammatory damage to the microcirculation causes platelet aggregation and vasoconstriction, eventually leading to the interruption of microcirculation and tissue destruction. The formation of necrotic tissue can trigger a focal inflammatory response and spread throughout the body, thus forming a vicious cycle. Tissue-specific destruction mediated by systemic inflammatory response is a direct mechanism for the development of multiple organ dysfunction.