What Factors Are Involved in a Septic Shock Diagnosis?

Severe infections, especially Gram-negative bacteria, can often cause septic shock. Septic shock, also known as septic shock, refers to sepsis syndrome with shock caused by microorganisms and their toxins and other products. Microorganisms, their toxins, and cell wall products in infected foci invade the blood circulation, activate various host cells and humoral systems, produce cytokines and endogenous mediators, affect various organs and systems of the body, affect their perfusion, and cause tissue Cell ischemia and hypoxia, metabolic disorders, dysfunction, and even multiple organ failure.

Basic Information

nickname

Septic shock

English name

septicshock

Visiting department

surgical

Common causes

Pathogens, host factors, special types of septic shock

Common symptoms

Sympathetic nerve symptoms

Causes of septic shock

Pathogenic bacteria

Common pathogenic bacteria of septic shock are Gram-negative bacteria, such as Enterobacteriaceae (Escherichia coli, Klebsiella, Enterobacteriaceae, etc.); Fermentative Bacillus (Pseudomonas, Acinetobacter, etc.); Meningococcus; bacilli. Gram-positive bacteria such as Staphylococcus, Streptococcus, Streptococcus pneumoniae, Clostridia, etc. can also cause shock. Certain viral diseases, such as epidemic hemorrhagic fever, are also prone to shock during their course. Certain infections, such as Gram-negative bacterial sepsis, fulminant meningitis, pneumonia, suppurative cholangitis, abdominal infections, and bacillary dysentery (young children) are prone to shock.

Host factor

Existing chronic underlying diseases, such as liver cirrhosis, diabetes, malignant tumors, leukemia, burns, organ transplantation, and long-term acceptance of immunosuppressive agents such as adrenal corticosteroids, antimetabolites, bacterial poisons and radiation therapy, or indwelling catheters Or intravenous catheters can induce septic shock. Therefore, this disease is more common in patients with nosocomial infections, especially the elderly, infants and young children, women who give birth, and those with poor physical recovery after major surgery.

3. Special types of septic shock

Toxic shock syndrome (TSS) is a severe syndrome caused by bacterial toxins. TSS was originally reported to be caused by S. aureus. In recent years, it has been found that similar groups can also be caused by Streptococcus.

Clinical manifestations of septic shock

Except for a few cases of high-exhaustion and low-resistance shock (warm shock), most patients have sympathetic nervous excitement. The patient is still conscious, but irritable, anxious, nervous, pale and skin, mild cyanosis of lips and nail beds, The end is damp and cold. May have nausea and vomiting. Reduced urine output. Heart rate increases, breathing is deep and fast, blood pressure is normal or low, and pulse pressure is small. Fundus and nail microcirculation examination showed arterial spasm. With the development of shock, the patient is irritable or unconscious, shallow breathing, low heart sounds, slow pulse, and disappears with a slight pressure. Superficial veins collapse, blood pressure decreases, and systolic blood pressure drops below 10.6kPa (80mmHg). For those with high blood pressure, the blood pressure is reduced by 20% to 30% compared with the basic level, and the pulse pressure is small. Skin is moist, cold, cyanotic, with less or even no urine. DIC and important organ failure may occur in the later stage of shock, often with refractory hypotension and extensive bleeding (skin, mucous membrane and / or internal organs, cavity bleeding). Multiple organ failure, the main symptoms are: acute renal failure; acute heart failure; acute pulmonary failure (ARDS); brain dysfunction; gastrointestinal dysfunction; liver failure caused coma and jaundice Wait.

Septic shock test

Blood image

Most white blood cell counts increased. Between 15 × 10 ⁹ / L and 30 × 10 ⁹ / L, neutrophils increased with nuclear left shift. Hematocrit and increased hemoglobin are signs of blood concentration. Progressive platelet decrease in patients with diffuse intravascular coagulation (DIC).

2. Etiological examination

Blood (or other body fluids, exudates) and pus cultures (including anaerobic cultures) are routinely performed before antimicrobial treatment. After the pathogenic bacteria were isolated, the drug sensitivity test was performed. The lysate test (LLT) facilitates the detection of endotoxins.

3. Urine routine and renal function tests

When renal failure occurs, the urine specific gravity changes from an initial high to a low and fixed (about 1.010); blood urea nitrogen and creatinine values increase; the urine / blood creatinine ratio is <20; the urine osmotic pressure decreases, and the urine / blood osmosis The ratio is 40mmol / L; renal failure index> 1; Na + excretion fraction> 1%.

4. Blood biochemical examination of acid-base balance

Carbon dioxide binding capacity (CO ₂ CP) is a clinically measured parameter, but in the case of respiratory failure and mixed acidosis, blood gas analysis must be performed at the same time to measure blood pH, arterial blood PaCO ₂ , standard HCO ₃ ^- and actual HCO _3- , Buffered alkali and alkali remain and so on. Determination of urine pH is simple and easy.

5. Determination of serum electrolytes

Most patients with shock disease have low blood sodium and different levels of potassium, depending on the state of renal function.

6. Determination of serum enzymes

The measurement of serum ALT, CPK, LDH isoenzymes can reflect the damage of liver, heart and other organs.

7. Hemorheology and DIC-related tests

During shock, blood flow slows down, capillaries become stagnant, blood cells, fibrin, and globulin accumulate, and blood viscosity increases. Therefore, the blood is initially hypercoagulable, and then fibrinolysis becomes hypocoagulation. Examination of DIC includes two aspects of wasting coagulopathy and hyperfibrinolysis: the former includes platelet count, thrombin time, fibrinogen, and clay clay thromboplastin time; the latter includes thrombin time, fibrin degradation products FDP), plasma protamine paracoagulation (3P), ethanol gel test, and euglobulin dissolution test.

8. Other

ECG, X-ray examination, etc. can be performed as needed.

Septic shock diagnosis

Patients with infectious diseases that are prone to concurrent shock should closely observe the changes in the condition, detect blood images, etiological examination, urine routine and renal function tests, blood biochemical examination, serum electrolyte measurement, serum enzyme measurement, and hemorheology related to DIC. Examination and so on to make a diagnosis.

Septic shock treatment

In addition to actively controlling infections, supplementation of blood volume, correction of acidosis, adjustment of vasomotor function, elimination of blood cell aggregation to prevent microcirculatory stasis, and maintenance of vital organ functions should be provided for the pathophysiology of shock. The purpose of treatment is to restore blood perfusion and normal metabolism of various organ tissues throughout the body. During the treatment process, it is necessary to observe closely, fully estimate the change of the condition, and prevent and control it in time.

Cause treatment

Before the pathogens are unclear, the most likely pathogenic bacteria can be inferred based on the primary lesions and clinical manifestations, and a powerful, broad-spectrum antiseptic fungicide should be selected for treatment. After the pathogens are isolated, drugs should be selected according to the results of the drug test. The dose should be large, the impact amount is given for the first time, by intravenous drip or slow bolus. In order to better control the infection, it is advisable to use a combination of drugs, but generally the two are sufficient. In order to reduce toxemia, short-term application of adrenocortical hormone can be considered under effective antibacterial treatment. Primary infections and migratory lesions should be addressed in a timely manner. Attach importance to systemic supportive treatment to improve the body's disease resistance.

2. Anti-shock therapy

(1) Supplementing blood volume The lack of effective circulating blood volume is a prominent contradiction in sensible shock. Therefore, expansion therapy is the basic means of anti-shock. The liquid used for volume expansion should include colloids and crystals. A reasonable combination of various liquids can maintain a constant body environment.

(2) Correction of acidosis The fundamental measure is to improve the hypoperfusion state of the tissue. The buffer alkali mainly plays a role in treating the symptoms, and when the blood volume is insufficient, the effectiveness of the buffer alkali cannot be fully exerted. Correcting acidosis can enhance myocardial contractility, restore vascular response to vasoactive drugs, and prevent the occurrence of DIC.

(3) The application of vasoactive drugs aims to adjust the vasomotor function and dredge the microcirculation stasis to facilitate the reversal of shock.

(4) Maintain the functions of important organs Application of cardiac drugs; Maintain respiratory function and prevent ARDS; Maintenance of renal function; Prevention and treatment of cerebral edema; Treatment of DIC; Adrenocortical hormone and -endorphin Antagonists; other adjuvant treatments.