bubble_chart Overview

Severe infections, particularly those caused by Gram-negative bacteria, often lead to septic shock. Septic shock, also known as septicemia-associated shock, refers to a sepsis syndrome accompanied by shock, induced by microorganisms and their toxins or byproducts. Microorganisms and their toxins, cell wall components, and other substances from the infection site enter the bloodstream, activating various host cells and humoral systems. This triggers the production of cytokines and endogenous mediators, which act on multiple organs and systems in the body, impairing perfusion and leading to tissue hypoxia, metabolic disturbances, functional impairment, and even multiple organ failure. This critical syndrome is known as septic shock. Thus, septic shock results from the interaction between microbial factors and the host's defense mechanisms, with the virulence and quantity of the microorganisms, as well as the host's internal environment and response, playing crucial roles in determining the progression of septic shock.

bubble_chart Etiology

(1) Pathogenic Bacteria Common pathogenic bacteria causing septic shock are Gram-negative bacteria, such as Enterobacteriaceae (e.g., Escherichia coli, Klebsiella, Enterobacter, etc.); non-fermentative bacteria (e.g., Pseudomonas, Acinetobacter, etc.); Neisseria meningitidis; Bacteroides, etc. Gram-positive bacteria, such as Staphylococcus, Streptococcus, Streptococcus pneumoniae, and Clostridium, can also induce shock. Certain viral diseases, such as epidemic hemorrhagic fever, are prone to shock during their course. Some infections, such as Gram-negative bacteremia, fulminant meningococcal meningitis, pneumonia, suppurative cholangitis, intra-abdominal infections, and bacillary dysentery (especially in children), are more likely to complicate with shock.

(2) Host Factors Underlying chronic diseases, such as cirrhosis, diabetes, malignant tumors, leukemia, burns, organ transplantation, and long-term use of immunosuppressants (e.g., corticosteroids), antimetabolites, bacterial toxins, or radiation therapy, or the use of indwelling catheters or intravenous catheters, can predispose to septic shock. Therefore, this condition is more common in nosocomial infections, particularly in elderly individuals, infants, postpartum women, and those with poor physical recovery after major surgery.

(3) Special Types of Septic Shock Toxic Shock Syndrome (TSS) TSS is a severe syndrome caused by bacterial toxins. Initially reported cases of TSS were caused by Staphylococcus aureus, but in recent years, similar syndromes have been found to be caused by Streptococcus.

Staphylococcal TSS is caused by exotoxins produced by non-invasive Staphylococcus aureus. The first case was reported in 1978. Early cases were mostly associated with tampon use in menstruating women, with a distinct geographic distribution, primarily in the United States, followed by Canada, Australia, and some European countries. With improvements in tampon design and the discontinuation of highly absorbent tampons, the incidence of staphylococcal TSS has significantly declined. However, non-menstrual TSS has increased, with infection sites mainly involving the skin and subcutaneous tissues, wound infections, followed by upper respiratory infections, etc., showing no gender, racial, or regional specificity. Almost all cases reported in China are non-menstrual TSS. Staphylococcus aureus can be isolated from the vagina or cervical lesions of patients, but blood cultures are negative. The non-invasive Staphylococcus aureus produces pyrogenic exotoxin C (PEC) and enterotoxin F (SEF), collectively referred to as toxic shock syndrome toxin-1 (TSST-1), which is believed to be associated with the pathogenesis of TSS. Injection of purified TSST-1 into animals can induce symptoms similar to human TSS. The main clinical manifestations of TSS include sudden high fever, headache, confusion, scarlatiniform rash, and skin desquamation (especially on the soles) after 1–2 weeks, along with severe hypotension or orthostatic syncope. Multiple systems are often affected, including: gastrointestinal (vomiting, diarrhea, diffuse abdominal pain); muscular (myalgia, elevated CPK); mucous membranes (conjunctival, pharyngeal, vaginal) congestion; central nervous system (headache, vertigo, disorientation, altered consciousness, etc.); liver (jaundice, elevated ALT and AST); kidneys (oliguria or anuria, proteinuria, elevated blood urea nitrogen and creatinine); heart (possible heart failure, myocarditis, pericarditis, and atrioventricular block); and hematologic (thrombocytopenia, etc.). Menstrual TSS patients often have vaginal discharge, cervical congestion, erosion, and adnexal tenderness. The recurrence rate is approximately 3%.

Streptococcal Toxic Shock Syndrome (STSS), also known as Streptococcal TSS-like Syndrome (TSLS). Since 1983, cases of toxic shock syndrome (STSS) caused by Group A streptococci have been reported in North America and Europe. The main pathogenic substance is pyrogenic exotoxin A (SPEA), which acts as a superantigen (SAg) stimulating monocytes to produce tumor necrosis factor (TNF-α) and interleukin (IL-1). It can also directly inhibit myocardial function, causing capillary leakage and leading to shock. From autumn 1990 to spring 1991, outbreaks of scarlet fever-like diseases were observed in certain areas of the Yangtze River Delta (such as Hai'an and Wuxi), which were rare in recent decades. The onset was abrupt, with symptoms including fear of cold, fever, headache, sore throat (40%), pharyngeal congestion, vomiting (60%), and diarrhea (30%). On the second day of fever, a scarlet fever-like rash appeared, followed by desquamation and peeling during the stage of convalescence. Systemic toxic symptoms were severe, with nearly half of the patients experiencing varying degrees of hypotension and even unconsciousness. A few cases showed multi-organ dysfunction. Streptococcus mitis with strong virulence was isolated from throat swabs of most patients. The same pathogen was also detected in the blood of some cases, but no beta-hemolytic streptococci were isolated. Corresponding antibodies were detected in the serum of patients during the stage of convalescence. Injecting the isolated strains into rabbits or guinea pigs caused local swelling and suppurative lesions, accompanied by elevated body temperature. With timely antibiotic treatment (using penicillin, erythromycin, or clindamycin) and anti-shock therapy, the vast majority of patients recovered.

bubble_chart Pathogenesis

The pathogenesis of septic shock is extremely complex. The microcirculatory dysfunction theory proposed in the 1960s laid the foundation for the pathogenesis of shock, and current research has advanced to the cellular and molecular levels. Microorganisms and their toxins, as well as cell wall components (such as lipopolysaccharide, LPS, etc.), activate various responsive cells in the body (including monocytes-macrophages, neutrophils, endothelial cells, etc.) and the humoral system (such as the complement, kinin, coagulation, and fibrinolytic systems), producing various endogenous mediators and cytokines, which play a crucial role in the pathogenesis. Septic shock is the result of multiple factors interacting and mutually reinforcing. (1) The Occurrence and Development of Microcirculatory Dysfunction During the progression of shock, changes in microvascular volume can undergo three stages: spasm, dilation, and paralysis. That is, the microcirculatory changes include the ischemic hypoxia phase, the stagnant hypoxia phase, and the disseminated intravascular coagulation (DIC) phase:

1. Ischemic Hypoxia Phase The characteristics of microcirculatory changes in this phase are: except for the heart and brain, the microvessels of the skin and internal organs (especially the abdominal organs) constrict, microcirculatory perfusion decreases, and the capillary network becomes ischemic and hypoxic. Hydrostatic pressure decreases, and interstitial fluid enters the microcirculation through capillaries, partially refilling the capillary network (autotransfusion). The mechanisms involved in these microcirculatory changes mainly include catecholamines released by the sympathetic-adrenal medullary system, the renin-angiotensin system, and vasoactive lipids (bioactive substances generated by cell membrane phospholipids under the action of phospholipase A₂, such as platelet-activating factor, PAF; and arachidonic acid metabolites, such as thromboxane A₂, AxA₂, and leukotrienes, LT).

2. Stagnant Hypoxia Phase The characteristics of this phase are an increase in anaerobic metabolites (lactic acid), increased release of histamine from mast cells, and elevated bradykinin formation. The micro-arterioles and precapillary sphincters dilate, while the micro-venules remain constricted. Leukocytes adhere to the vessel walls and become lodged, leading to blood stasis in the microcirculation, increased hydrostatic pressure in capillaries, increased capillary permeability, plasma extravasation, and hemoconcentration. The effective circulating blood volume decreases, venous return to the heart further declines, and blood pressure drops significantly. Hypoxia and acidosis become more pronounced. Increased generation of oxygen free radicals causes widespread cellular injury.

3. Microcirculatory Failure Phase The blood continues to concentrate, blood cells aggregate, and blood viscosity increases. Additionally, due to vascular endothelial injury and other factors, the coagulation system is activated, leading to DIC, microvascular bed obstruction, further reduction in perfusion, and bleeding. This results in multiple organ failure, making the shock irreversible.

Based on hemodynamic changes, septic shock can be classified into hyperdynamic (high-output, low-resistance) and hypodynamic (low-output, high-resistance) types. If the former is not corrected in time, it will eventually progress to the hypodynamic type. The occurrence of hyperdynamic shock may be related to the release of histamine and bradykinin; the opening of arteriovenous shunts, forming non-nutritive blood flow channels in the microcirculation, allowing blood to return to the heart via shunts, maintaining or even increasing cardiac output, while nutritive blood flow perfusion in the visceral microcirculation decreases; endotoxin activates histidine decarboxylase, accelerating histamine production, and mast cells release more histamine. Additionally, endotoxin directly injures vascular smooth muscle cell membranes, impairing their normal calcium ion transport capacity and reducing vascular tension. The occurrence of hypodynamic shock is related to α-receptor stimulation.

(II) Cellular Mechanisms of Shock While microcirculatory disturbances are indeed significant in the pathogenesis of shock, cellular injury can occur prior to hemodynamic changes. In other words, metabolic dysfunction in cells may be primary and could be directly induced by internal toxins. The earliest manifestation is dysfunction of the cell membrane. Cell membrane injury impairs the function of Na⁺-K⁺-ATPase on the membrane, leading to increased intracellular Na⁺ and decreased K⁺, resulting in cellular edema. Mitochondria are the first organelles to undergo changes during shock. When damaged, mitochondria can trigger the following alterations: ① Dysfunction of the respiratory chain, leading to metabolic disturbances; ② Impaired oxidative phosphorylation, disrupting the tricarboxylic acid (TCA) cycle, reducing ATP production, and causing lactic abdominal mass; ③ Dysfunction of ion pumps on the cell membrane, disrupting the concentration gradients of Na⁺, K⁺, Ca⁺⁺, Mg⁺⁺, and other ions across the membrane. K⁺ and Ca⁺⁺ are lost from the mitochondria, while cytoplasmic Ca⁺⁺ increases. This activates phospholipase A₂ on the cell membrane, leading to phospholipid breakdown, membrane injury, and increased permeability. Na⁺ and water enter the mitochondria, causing swelling and structural damage. Lysosomes contain various enzymes and serve as the primary intracellular digestive system. During shock, lysosomal membrane permeability increases, leading to the release of lysosomal enzymes and subsequent autolytic cell death.

In addition to activating the humoral system, internal toxins can also directly act on various reactive cells to produce cytokines and metabolites:

① Endothelial cells: causing cytotoxic reactions (NO), etc. ② Neutrophils: inducing chemotaxis, aggregation, opsonization, and phagocytosis; synthesizing PAF, T_xA₂, prostaglandins (PGE), LTB₄, etc.; releasing oxygen free radicals, lysosomal enzymes, elastase, etc. ③ Platelets: aggregation, synthesis of T_xA₂, etc. ④ Mononuclear macrophages: releasing tumor necrosis factor (TNF), interleukin-1 (IL-1), lysosomal enzymes, plasminogen activator precursor, etc. ⑤ Basophils and mast cells: releasing histamine, PAF, LT, etc. ⑥ Pituitary gland and hypothalamus: releasing ACTH, β-endorphin, and thyrotropin-releasing hormone (TRH), respectively.

The importance of TNF in shock has been widely recognized. TNF can bind to specific receptors on various cells in the body, producing multiple physiological effects: TNF has synergistic interactions with cytokines such as IL-1, IL-6, IFN-γ, and PAF, playing a significant role in vascular endothelial cell injury, while transforming growth factor (TGF-β₁) can mitigate the effects of TNF and other factors. TNF can activate neutrophils and lymphocytes, increasing the expression of adhesion proteins on the cell membrane and enhancing the adhesion between leukocytes and endothelial cells. The expression of adhesion proteins on the leukocyte membrane is also strengthened, leading to endothelial cell injury, increased permeability, and promotion of blood coagulation. Animal experiments have shown that administering a large dose of TNF can produce hemodynamic, hematologic, and pathological changes similar to septic shock, causing rapid death in animals.

(3) Metabolic changes, electrolyte imbalance, and acid-base disturbances during shock

In shock stress conditions, glycogen and fat catabolism are hyperactive. Initial stage [first stage]: blood glucose, fatty acids, and triglycerides are all elevated; as shock progresses, glycogen is depleted, blood glucose decreases, insulin secretion is reduced, while glucagon secretion increases. In the initial stage [first stage] of shock, due to the direct stimulation of bacterial toxins on the respiratory center or the reflexive stimulation caused by reduced effective circulating blood volume, respiration accelerates and hyperventilation occurs, leading to respiratory alkalosis. Subsequently, due to insufficient oxygenated blood perfusion in organs, impaired biological oxidation processes, inhibition of the tricarboxylic acid cycle, reduced ATP production, and increased lactate formation, metabolic acidosis occurs, with deep and rapid breathing. In the advanced stage of shock, mixed acidosis often occurs due to damage to the central nervous system or pulmonary function, leading to changes in respiratory rhythm or amplitude. Insufficient ATP production often causes malfunction of the sodium pump on the cell membrane, resulting in abnormal ion distribution inside and outside the cell: Na⁺ influx brings water, causing cell edema, with mitochondria significantly swollen and matrix altered; K⁺ flows out of the cell. The concentration difference of Ca⁺⁺ inside and outside the cell is a thousand-fold, and this gradient is maintained by the permeability of the cytoplasmic membrane to Ca⁺⁺ and the external pump function. When the cell membrane is damaged, calcium⁺⁺ influx occurs, and Ca⁺⁺ overload in the cytoplasm can produce many harmful effects, such as activating phospholipase A₂, hydrolyzing cell membrane phospholipids to produce arachidonic acid, which is then metabolized via the cyclooxygenase and lipoxygenase pathways to produce prostaglandins (PGF_α, PGE₂, PGD₂), prostacyclin (PGI₂), T_xA₂, and LTs (LTB₄, LTC₄, LTD₄, LTE₄), among other inflammatory mediators. These products can affect vascular tone, microvascular permeability, and act on platelets and neutrophils, causing a series of pathophysiological changes that play an important role in the occurrence and progression of shock.

(IV) Functional and Structural Changes in Vital Organs During Shock

1. Kidneys The renal vasculature contains abundant A-V shunts in smooth muscle. During shock, renal cortical vessels constrict, while the medullary microcirculatory shunts open extensively, leading to a significant reduction in cortical blood flow while relatively preserving medullary perfusion. If shock persists, renal tubules may undergo necrosis due to ischemia and hypoxia, accompanied by interstitial edema, increasing the risk of acute renal failure. In cases complicated by DIC, widespread thrombosis in the glomerular capillary tufts can result in cortical necrosis.

2. Lungs During shock, pulmonary circulation changes primarily involve pulmonary microvascular constriction, increased resistance, and extensive opening of A-V shunts, leading to inadequate capillary perfusion. Blood bypasses alveolar gas exchange via stirred pulse flow, entering pulmonary veins directly, causing ventilation-perfusion mismatch and impaired oxygen diffusion. PO₂ decreases, resulting in systemic hypoxia. This condition is termed adult respiratory distress syndrome (ARDS). Neutrophils are considered a key factor in ARDS pathogenesis. Complement activation product C_5a attracts neutrophils to aggregate in pulmonary circulation and adhere to capillary endothelial surfaces, releasing various injurious mediators such as proteolytic enzymes, elastase, collagenase, arachidonic acid metabolites (prostaglandins, T_xA₂, LTs, etc.), and oxygen free radicals, damaging lung parenchymal cells, endothelial cells, and fibroblasts. This increases alveolar-capillary permeability, causing plasma extravasation and interstitial edema. TNF and IL-1 cytokine release also promotes neutrophil chemotaxis, pulmonary sequestration, and enhanced endothelial adhesion. Under hypoxic conditions, alveolar surfactant secretion decreases, reducing lung compliance and predisposing to atelectasis. Alveolar epithelial and capillary endothelial swelling further exacerbates ventilation-perfusion mismatch. Plasma fibronectin (Fn) levels often decline due to reduced synthesis, accelerated degradation, and increased consumption, impairing alveolar-capillary membrane integrity and hindering clearance of bacteria, toxins, and fibrin degradation products, facilitating ARDS development.

3. Heart The heart has high oxygen demand, and coronary perfusion significantly impacts myocardial function. When stirred pulse pressure drops markedly and diastolic pressure falls below 5.3 kPa (40 mmHg), coronary stirred pulse perfusion decreases substantially. Myocardial ischemia and hypoxia lead to subcellular structural changes, impaired sarcoplasmic reticulum calcium uptake, and reduced activity of sarcolemmal Na⁺-K⁺-ATPase and adenylate cyclase. Metabolic disturbances, acidosis, and hyperkalemia further impair cardiac function. Myocardial depressant factor and β-endorphins from the pituitary inhibit the cardiovascular system. Oxygen free radicals generated during myocardial ischemia-reperfusion also contribute to myocardial suppression and injury. Although cardiac output may remain normal during shock, ventricular dysfunction manifests as reduced ejection fraction and ventricular dilation. Myocardial fibers may show degeneration, necrosis, rupture, and interstitial edema. In DIC, microthrombi form in myocardial vessels.

4. Liver The liver receives dual blood supply. Portal system smooth muscle is highly sensitive to catecholamines, and the portal system's low pressure gradient results in relatively slow flow, making the liver prone to ischemia, stasis, and DIC during shock. As the primary site for metabolism, detoxification, and synthesis of clotting and fibrinolytic factors, prolonged hypoxia impairs liver function, leading to systemic metabolic disturbances, lactate accumulation, weakened barrier function, and DIC, often rendering shock refractory. Hepatocytes in the central lobular zone degenerate and necrose, with microthrombi forming in central veins.

5. Brain The brain tissue has a high oxygen demand and very low glycogen content, relying mainly on continuous blood supply. When blood pressure drops below 7.9 kPa (60 mmHg), cerebral perfusion becomes insufficient. During cerebral hypoxia, astrocytes first swell and compress blood vessels, while vascular endothelial cells also swell, leading to microcirculation disorders and abnormal blood flow patterns, which exacerbate cerebral hypoxia. Once ATP stores are depleted, the sodium pump function fails, causing cerebral edema. If cerebral circulation is not restored within a short period, the progression of cerebral edema becomes difficult to reverse.

6. Others The intestinal tract is richly innervated by sympathetic nerves. During shock, its blood circulation diminishes, leading to intestinal mucosal ischemia and injury, followed by edema and hemorrhage. Bacterial invasion allows internal toxins to enter the bloodstream, exacerbating the shock. Additionally, histidine decarboxylase activation releases histamine, causing congestion in the abdominal viscera and portal vascular bed, as well as plasma extravasation, which worsens the shock. Severe ischemia and hypoxia trigger the release of proteolytic enzymes from pancreatic lysosomes, resulting in serious consequences.

bubble_chart Clinical Manifestations

Except for a few cases of high cardiac output and low resistance shock (warm shock), most patients exhibit symptoms of sympathetic nervous system excitation: the patient is conscious but dysphoric, anxious, and tense, with a pale complexion and skin, grade I cyanosis of the lips and nail beds, and cold, clammy extremities. Nausea and vomiting may occur. Urine output is reduced. The heart rate increases, breathing becomes deep and rapid, blood pressure remains normal or slightly low, and pulse pressure is narrow. Fundoscopic and nail fold microcirculation examinations may reveal arteriolar spasm.

As shock progresses, the patient becomes dysphoric or confused. Breathing becomes shallow and rapid. Heart sounds are muffled. The pulse is thready and rapid, disappearing with moderate pressure. Superficial veins collapse. Blood pressure drops, with systolic pressure falling below 10.6 kPa (80 mmHg); in patients with pre-existing hypertension, blood pressure decreases by 20–30% from baseline, with narrow pulse pressure. The skin becomes cold and clammy, with pronounced cyanosis and mottling. Urine output further decreases or even ceases.

In the advanced stage of shock, DIC and multiple organ failure may occur.

(1) DIC: Persistent hypotension and widespread bleeding (skin, mucous membranes, and/or internal organs, cavity bleeding) are common.

(2) Multiple organ failure: ① Acute renal failure—marked reduction or absence of urine output. Fixed urine specific gravity, elevated blood urea nitrogen, creatinine, and potassium. ② Acute cardiac insufficiency—patients often experience sudden rapid breathing and cyanosis. Heart rate increases, heart sounds become muffled, and gallop rhythm or arrhythmias may occur. If the heart rate is not rapid or is relatively moderate but the complexion turns ashen with cyanosis of the extremities, this is also a sign of cardiac insufficiency. Elevated central venous pressure indicates reduced right ventricular output, excessive blood volume, or increased pulmonary vascular resistance; elevated pulmonary capillary wedge pressure suggests left ventricular dysfunction. ECG may show myocardial damage, subendocardial ischemia, arrhythmias, and conduction block. ③ Acute respiratory failure (ARDS)—manifested as progressive dyspnea and cyanosis unrelieved by oxygen, without irregular rhythm. Fine crackles or diminished breath sounds may be heard at the lung bases. Chest X-rays show scattered patchy infiltrates that gradually expand and coalesce. Blood gas analysis reveals PO₂ < 9.33 kPa (70 mmHg), or < 6.65 kPa (50 mmHg) in severe cases. ④ Brain dysfunction leads to unconsciousness, transient spasms, limb paralysis, and changes in pupil size and breathing. ⑤ Others—liver failure causes unconsciousness, jaundice, etc. Gastrointestinal dysfunction presents as abdominal distension and gastrointestinal bleeding.

bubble_chart Auxiliary Examination

(1) Blood Picture The white blood cell count is mostly elevated, ranging between 15×10⁹ and 30×10⁹/L, with an increase in neutrophils accompanied by a left shift phenomenon. Elevated hematocrit and hemoglobin levels are markers of hemoconcentration. Platelets progressively decrease when DIC is complicated. (2) Etiological Examination Before antibiotic treatment, routine blood (or other body fluids, exudates) and pus cultures (including anaerobic culture) are performed. After isolating the pathogenic bacteria, drug sensitivity tests are conducted. The Limulus lysate test (LLT) aids in the detection of internal toxins. (3) Urinalysis and Renal Function Tests In cases of renal failure, the urine specific gravity shifts from being initially high to low and fixed (around 1010); blood urea nitrogen and creatinine levels rise; the urine-to-blood creatinine ratio is <20; urine osmolality decreases, and the urine-to-blood osmolality ratio is <1.1; urinary Na (mmol/L) excretion exceeds 40; the renal failure index is >1; and the fractional excretion of Na (%) is >1. These tests can differentiate it from prerenal renal insufficiency. (4) Blood Gas Analysis for Acid-Base Balance Carbon dioxide combining power (CO₂CP) is a commonly measured clinical parameter. However, in cases of respiratory failure and mixed acidosis, blood gas analysis must also be performed to determine blood pH, arterial pCO₂, standard HCO₃^-, actual HCO₃^-, buffer base, and base excess. Urine pH measurement is simple and practical. Blood lactate level measurement has prognostic significance. (5) Serum Electrolyte Measurement Serum sodium levels in shock patients are often low, while serum potassium levels vary depending on renal function status. (6) Serum Enzyme Measurement Serum ALT, CPK, and LDH isoenzyme levels can reflect damage to organs such as the liver and heart. (7) Hemorheology and DIC-Related Tests During shock, blood flow slows, capillaries become congested, and blood cells, fibrin, and globulins aggregate, increasing blood viscosity. Initially, the blood is hypercoagulable, followed by hyperfibrinolysis, transitioning to hypocoagulability. DIC-related tests include consumptive coagulation disorders and hyperfibrinolysis: the former includes platelet count, prothrombin time, fibrinogen, and kaolin clotting time; the latter includes thrombin time, fibrin degradation products (FDP), plasma protamine paracoagulation (3P) and ethanol gel tests, as well as euglobulin lysis time. (8) Others Electrocardiograms, X-rays, and other tests can be performed as needed.

bubble_chart Diagnosis

Patients with certain infectious diseases prone to shock should be closely monitored for changes in their condition. The following signs may indicate the onset of shock: excessively high (>40.5°C) or low (<36°C) body temperature; altered mental status in non-neurological infections, such as apathy or dysphoria; rapid breathing accompanied by hypoxia and/or increased plasma lactate levels, with no abnormalities on chest X-rays; increased heart rate disproportionate to the rise in body temperature or the occurrence of arrhythmias; reduced urine output (<0.5 ml/kg) for at least one hour; blood pressure <12 kPa (90 mmHg) or postural hypotension; decreased platelet and white blood cell (mainly neutrophil) counts; and unexplained liver or kidney dysfunction.

Shock is a severe and dynamic pathological process. In most cases, the initial response is often a manifestation of heightened sympathetic nervous activity, with hypotension possibly appearing only later. Early recognition of symptoms and signs of sympathetic nervous system excitation, close monitoring of condition changes, and the formulation of appropriate treatment plans are crucial for successful resuscitation. Therefore, familiarity with clinical, hemodynamic, and laboratory indicators reflecting microcirculation and organ function is essential.

(1) Clinical Manifestations

1. Consciousness and mental state (reflecting cerebral blood flow): After initial agitation, progression to depression, apathy, or even unconsciousness indicates a shift from excitatory to inhibitory neural cell responses, signaling worsening condition. Patients with preexisting cerebral arteriosclerosis or hypertension may show delayed responses even when blood pressure drops to around 10.64/6.65 kPa (80/50 mmHg). Conversely, individuals with good constitution may tolerate hypoxia better, but this is extremely short-lived.

2. Respiratory rate and depth (reflecting acid-base imbalance or pulmonary and central nervous system dysfunction): For details, refer to "Metabolic Changes in Shock," acid-base imbalance, and major organ dysfunction.

3. Skin color, temperature, and moisture (reflecting peripheral perfusion): Pale or cyanotic skin with patchy constriction indicates poor microcirculatory perfusion. Capillary refill in nail beds can also serve as a reference. Petechiae or ecchymoses on the chest or abdominal wall suggest possible DIC.

4. Jugular and peripheral vein distension: Collapsed veins indicate hypovolemia, while excessive distension suggests cardiac dysfunction or fluid overload.

5. Pulse: Before blood pressure drops in early shock, the pulse often becomes thready and rapid or even imperceptible. As shock improves, pulse strength typically recovers before blood pressure.

6. Urine output (reflecting visceral perfusion): When blood pressure is around 10.6 kPa (80 mmHg), average urine output is 20–30 ml/h. Output >50 ml/h indicates adequate renal perfusion.

7. Nailfold microcirculation and fundus examination: Under low magnification, observe the number, diameter, length, clarity, and pattern of nailfold capillary loops; blood color, flow velocity, uniformity, and continuity; degree of red blood cell aggregation; vasomotor status; and clarity. In shock, nailfold capillary loops decrease in number, become narrow and shortened, appear fragmented, and show poor filling. Blood color turns purple, flow slows and loses uniformity, and severe cases may show clotting. Fundus examination may reveal arteriolar spasm, venular dilation, and a shift in the normal arteriovenous ratio from 2:3 to 1:2 or 1:3. Severe cases may show retinal edema. Increased intracranial pressure may cause optic disc edema.

(2) Hemodynamic Changes

1. Stirred Pulse Pressure and Pulse Pressure: Systolic blood pressure dropping below 10.64 kPa (80 mmHg), a decrease of more than 20% in those with pre-existing hypertension, pulse pressure <4 kPa, along with manifestations of tissue hypoperfusion, can be diagnosed as shock. The degree of hypotension generally correlates with the severity of shock, but exceptions exist.

2. Central Venous Pressure (CVP) and Pulmonary Artery Wedge Pressure (PAWP) The normal range of CVP is 0.59–1.18 kPa (6–12 cmH₂O), primarily reflecting the volume of venous return and the pumping function of the right ventricle. It can also serve as a parameter for assessing vascular tone and should be interpreted in conjunction with blood pressure. In cases of impaired cardiac function, monitoring PAWP is more reliable than CVP for guiding fluid administration and preventing pulmonary edema. The normal range of PAWP is 1.06–1.6 kPa (8–12 mmHg), which effectively reflects the pumping function of the left ventricle. An elevated PAWP indicates pulmonary congestion, and fluid administration should be restricted when PAWP exceeds 2.4 kPa (18 mmHg).

(3) Laboratory Diagnosis For details, refer to the "Laboratory Tests" section.

bubble_chart Treatment Measures

In addition to actively controlling the infection, measures should be taken to address the pathophysiology of shock, including replenishing blood volume, correcting acidosis, adjusting vasomotor function, eliminating blood cell aggregation to prevent microcirculatory stasis, and maintaining the function of vital organs. The goal of treatment is to restore blood perfusion and normal metabolism in tissues and organs throughout the body. During treatment, close observation is essential to fully assess changes in the condition and implement timely prevention and control measures.

disease cause Treatment

Before the pathogenic bacteria are identified, the most likely causative bacteria can be inferred based on the primary lesion and clinical manifestations, and potent, broad-spectrum bactericidal agents should be selected for treatment. After isolating the bacteria, drugs should be chosen based on drug sensitivity test results. The dose should be relatively large, with an initial loading dose administered intravenously via drip or slow injection. To better control the infection, combination therapy is advisable, though a dual regimen is usually sufficient. Commonly used combinations include a β-lactam antibiotic plus an aminoglycoside, with caution or avoidance of the latter in patients with renal impairment. To mitigate toxemia, short-term use of adrenal corticosteroids may be considered under effective antibacterial therapy. The primary infection site and any metastatic sexually transmitted disease sites should be promptly addressed. Comprehensive supportive care is essential to enhance the body's disease resistance. The core region of lipopolysaccharide (LPS) and lipid A structure of different pathogenic bacteria are highly conserved, allowing for cross-protection through passive immunization. Human anti-large intestine bacillus J₅variant serum has been used to reduce mortality in patients with Gram-negative bacteremia and/or septic shock, but it has not been widely accepted. The efficacy of HA-IA (human anti-lipid A IgM monoclonal antibody) and E₅mouse IgM monoclonal antibody, produced using monoclonal antibody technology, remains uncertain.

Anti-shock therapy

(1) Replenishing blood volume: Insufficient effective circulating blood volume is a critical issue in septic shock. Therefore, volume expansion therapy is fundamental in anti-shock treatment. The fluids used for volume expansion should include both colloids and crystalloids. A rational combination of various fluids is necessary to maintain the body's internal environment. Colloids include low-molecular-weight dextran, plasma, albumin, and whole blood. Among crystalloids, sodium bicarbonate compound formula saline is preferable. Early shock is associated with hyperglycemia, and the body's utilization of glucose is impaired. Hyperglycemia can lead to glycosuria and osmotic diuresis, resulting in the loss of sodium and water, so glucose solutions should be used sparingly at this stage.

1. Colloids: ① Low-molecular-weight dextran (molecular weight 20,000–40,000): It coats red blood cells, platelets, and vascular endothelium, increasing mutual repulsion, thereby preventing red blood cell aggregation, inhibiting thrombus formation, and improving blood flow. Infusion increases plasma osmotic pressure, counteracts plasma extravasation, replenishes blood volume, dilutes blood, reduces blood viscosity, improves microcirculation, and prevents DIC. It also exerts osmotic diuretic effects in renal tubules. Its peak effect occurs 2–3 hours after intravenous injection and diminishes after 4 hours, so rapid infusion is recommended. The daily dose is 10% 500–1500 ml, usually 1000 ml. It is contraindicated in severe renal impairment, congestive heart failure, and bleeding tendencies. Allergic reactions may occasionally occur. ② Plasma, albumin, and whole blood: Suitable for cases such as cirrhosis or chronic nephritis with hypoalbuminemia and acute pancreatitis. Blood transfusion is unnecessary in the absence of anemia and should be used cautiously in patients with DIC. Hematocrit should be maintained at 35–40%. ③ Others: Hydroxyethyl starch (706 plasma substitute) increases colloid osmotic pressure, expands blood volume, has few side effects, and is non-antigenic, rarely causing allergic reactions.

2. Crystalloids: Balanced salt solutions such as sodium bicarbonate Ringer's solution and sodium lactate Ringer's solution contain ion concentrations closer to those in proximal bleeding plasma than physiological saline, increasing functional extracellular fluid volume and partially correcting acidosis. Sodium bicarbonate Ringer's solution is preferable for patients with significant liver impairment.

5-10% glucose solution mainly provides water and calories, reducing the breakdown of proteins and fats. 25-50% glucose solution also has a short-term volume expansion and osmotic diuretic effect, but it is not suitable for use in the early stages of shock.

Volume Expansion Infusion Procedure, Rate, and Volume Generally, low-molecular-weight dextran (or balanced salt solution) is administered first. For patients with significant acidosis, 5% sodium bicarbonate may be given initially. In special cases, albumin or plasma may be infused. The drip rate should start fast and then slow down, with the dosage adjusted based on the patient’s specific condition and underlying cardiac and renal function: patients with significant dehydration, intestinal obstruction, paralytic ileus, or purulent peritonitis may require increased fluid volume, while those with heart disease should have a slower drip rate and reduced infusion volume. During infusion, close monitoring for signs of dyspnea or pulmonary rales is essential. If necessary, infusion can be guided by CVP or PAWP monitoring. Simultaneous measurement of plasma colloid osmotic pressure and the PAWP gradient provides valuable reference for preventing pulmonary edema. If the pressure difference between the two exceeds 1.07 kPa, the risk of pulmonary edema is relatively low. The goals of volume expansion therapy include: ① Adequate tissue perfusion: the patient appears calm, with pink lips, warm extremities, and no cyanosis; ② Systolic blood pressure >12 kPa (90 mmHg), pulse pressure >4.0 kPa; ③ Heart rate <100 beats/min; ④ Urine output >30 ml/h; ⑤ Hemoglobin returns to baseline levels, and hemoconcentration resolves.

(2) Correcting Acidosis The fundamental measure lies in improving tissue hypoperfusion. Buffer bases primarily address symptoms, and their efficacy is limited when blood volume is insufficient. Correcting acidosis enhances myocardial contractility, restores vascular responsiveness to vasoactive drugs, and prevents DIC. The preferred buffer base is 5% sodium bicarbonate, followed by 11.2% sodium lactate (not suitable for patients with liver impairment). Tromethamine (THAM) is suitable for patients requiring sodium restriction, as it easily penetrates cells, aiding in correcting intracellular acidosis. However, its drawbacks include local tissue necrosis if extravasation occurs and respiratory depression or even arrest if infused too rapidly. Additionally, it may cause hyperkalemia, hypoglycemia, nausea, and vomiting. The dose of buffer base can be determined based on CO₂CP measurements: 0.3 ml/kg of 5% sodium bicarbonate or 0.6 ml/kg of 3.63% THAM can increase CO₂CP by 1 VOL% (0.449 mmol/L).

(3) Use of Vasoactive Drugs The aim is to regulate vasomotor function and relieve microcirculatory stasis to facilitate shock reversal.

1. Vasodilators Must be used after adequate volume expansion. Suitable for low-output, high-resistance shock (cold shock). Commonly used agents include:

(1) α-Receptor Blockers: These relieve microvascular spasms and stasis caused by endogenous norepinephrine. They can redirect blood from the pulmonary circulation to the systemic circulation, preventing pulmonary edema. The representative drug is phentolamine (Regitine), which acts rapidly and briefly, making it easy to control. The dose is 5–10 mg per administration (0.1–0.2 mg/kg for children), diluted in 500–100 ml of glucose solution for IV infusion, starting slowly and adjusting the rate based on response. In emergencies, a small dose may be injected slowly in 10–20 ml of glucose or saline, followed by IV infusion at 0.1–0.3 mg/min. For patients with cardiac dysfunction, it should be combined with positive inotropic agents or vasopressors to prevent sudden blood pressure drops. Chlorpromazine has significant central nervous system sedative and hypothermic effects, reducing tissue oxygen consumption. It also blocks α-receptors, relieving vascular spasms and improving microcirculation. It is suitable for patients with dysphoria, convulsions, or high fever but is contraindicated in elderly patients with atherosclerosis, respiratory depression, or liver impairment. The dose is 0.5–1.0 mg/kg per administration, added to glucose solution for IV infusion or given intramuscularly, with repeat doses as needed.

(2) β-receptor agonists: The typical representative is isoproterenol, which has strong β₁ and β₂ receptor agonist effects. It enhances myocardial contraction, accelerates heart rate, improves conduction, and moderately dilates blood vessels. While strengthening myocardial contraction, it significantly increases myocardial oxygen consumption and ventricular irritability, making it prone to induce arrhythmias. It is contraindicated in patients with coronary heart disease. The dose is 0.1–0.2 mg%, with an infusion rate of 2–4 μg/min for adults and 0.05–0.2 μg/kg/min for children. The heart rate should preferably not exceed 120 beats/min (140 beats/min for children). Dopamine is a precursor for the synthesis of norepinephrine and epinephrine. Its effects vary depending on the dose, acting on α, β, and dopamine receptors: at a dose of 2–5 μg/kg per minute, it primarily stimulates dopamine receptors, dilating visceral blood vessels, especially increasing renal blood flow and urine output; at a dose of 6–15 μg/kg per minute, it mainly stimulates β receptors, enhancing myocardial contraction and increasing cardiac output, with minimal effects on heart rate and a lower likelihood of inducing arrhythmias, while its effect on β₂ receptors is weaker; at a dose >20 μg/kg per minute, it primarily acts as an α-receptor agonist and may also constrict renal blood vessels, which should be noted. The usual dose is 10–20 mg%, initially infused at 2–5 μg/kg per minute, then adjusted as needed, with a maximum infusion rate of 0.5 mg/min. Dopamine is currently a widely used anti-shock agent, particularly effective for shock patients with weakened myocardial contraction, reduced urine output, and adequately replenished blood volume.

(3) Anticholinergic drugs: A therapeutic approach pioneered in China. These include atropine, tangut anisodus alkaloids, and scopolamine, which relieve spasms and improve microcirculation; block M receptors to maintain the intracellular cAMP/cGMP ratio; stimulate the respiratory center, relieve bronchospasm, inhibit glandular secretion, and ensure proper ventilation; regulate the vagus nerve—higher doses can counteract vagal inhibition of the heart, accelerating heart rate; and inhibit platelet and neutrophil aggregation, among other effects. High doses of atropine may cause dysphoria, restlessness, flushed skin, burning sensations, excitation, mydriasis, tachycardia, and dry mouth. Scopolamine primarily suppresses the central nervous system, exerting a notable sedative effect, but excessive doses can lead to delirium and agitation. Tangut anisodus alkaloids offer higher selectivity in relieving spasms with relatively fewer side effects, making them clinically preferable for septic shock, often replacing atropine or scopolamine. These drugs are contraindicated in patients with glaucoma. Dosages are as follows: atropine—adults 0.3–0.5 mg/dose, children 0.03–0.05 mg/kg/dose; scopolamine—adults 0.3–0.5 mg/dose, children 0.006 mg/kg/dose; tangut anisodus alkaloids—adults 10–20 mg/dose. Administer intravenously, repeating doses as needed, gradually extending intervals as the condition improves until discontinuation. If no effect is observed after 10 doses or if significant toxicity occurs, discontinue immediately and switch to alternative medications.

2. Vasoconstrictors: These drugs only increase perfusion pressure while constricting blood vessels, reducing tissue perfusion. Adding vasoconstrictors to IV fluids limits infusion rates and volumes and may falsely elevate CVP readings. From a pathophysiological standpoint, vasoconstrictors in shock management often present more drawbacks than benefits, so their use must be strictly indicated. Consider them in the following scenarios: - Sudden hypotension when blood volume cannot be promptly restored—short-term low-dose use to raise blood pressure, enhance myocardial contraction, and ensure cardiac and cerebral perfusion. - Combined with α-receptor blockers or other vasodilators to counteract α-receptor stimulation while preserving β-receptor effects, and to offset the hypotensive action of α-blockers—particularly useful in shock cases with concurrent cardiac dysfunction. Common vasoconstrictors include norepinephrine and metaraminol. Dosages: norepinephrine 0.5–2.0 mg%, infusion rate 4–8 μg/min; metaraminol 10–20 mg%, infusion rate 20–40 drops/min. Recent reports indicate shock reversal in cases unresponsive to volume expansion and low-dose dopamine after norepinephrine administration.

(4) Protecting Vital Organ Function

1. Use of Cardiotonic Drugs: Severe shock and late-stage (stage III) cases often complicate with cardiac dysfunction due to bacterial toxins, myocardial hypoxia, acidosis, electrolyte imbalances, myocardial depressant factor, pulmonary vascular spasms, elevated pulmonary artery pressure, pulmonary edema (increasing cardiac load), and inappropriate fluid management. The elderly and young children are particularly susceptible. Prophylactic use of strophanthin-K or lanatoside C may be considered. If signs of cardiac dysfunction appear, strictly control IV fluid volume and infusion rates. In addition to rapid-acting cardiotonics, vasodilators may be given but must be combined with norepinephrine or dopamine to prevent sudden blood pressure drops. High-dose glucocorticoids can enhance cardiac output, reduce peripheral vascular resistance, and increase coronary blood flow—consider short-term early use. Concurrent measures include oxygen therapy, correction of acidosis and electrolyte imbalances, and energy cocktails to address cellular metabolic disturbances.

2. Maintain respiratory function and prevent ARDS. The lung is one of the primary target organs of shock, and refractory shock often complicates pulmonary failure. Additionally, cerebral hypoxia and cerebral edema can also lead to respiratory failure. All shock patients should receive oxygen, administered via nasal catheter (4–6 L/min) or intermittent positive-pressure mask. The inspired oxygen concentration should be around 40%. It is essential to keep the airway unobstructed. After adequate fluid resuscitation, if the patient remains unconscious, has difficulty clearing secretions, or shows signs of airway obstruction, early consideration should be given to endotracheal intubation or tracheostomy with assisted ventilation (intermittent positive pressure), along with clearing respiratory secretions and preventing secondary infections. For cases with A-V shunting where oxygen therapy fails to achieve satisfactory PO₂ levels (>9.33–10.7 kPa) and intermittent positive-pressure ventilation is ineffective, positive end-expiratory pressure (PEEP) should be initiated early. PEEP can continuously expand airways and alveoli, increase functional residual capacity, reduce intrapulmonary shunting, improve stirred pulse oxygen partial pressure, enhance lung compliance, and increase vital capacity. In addition to correcting hypoxemia, vasodilators should be administered early to reduce pulmonary vascular resistance, while fluid infusion should be carefully controlled, minimizing crystalloid use. To alleviate pulmonary interstitial edema, 25% albumin and high-dose furosemide can be given (if blood volume is not low). The clinical efficacy of high-dose corticosteroids varies and requires further validation. If necessary, early high-dose, short-term (no more than 3 days) therapy may be considered to maximize therapeutic effects while minimizing adverse effects. Pulmonary surfactant (PS) undergoes quantitative and qualitative changes in ARDS. Replacement therapy with natural or synthetic PS has proven effective in neonatal RDS; in a few prospective, randomized, controlled studies of ARDS, synthetic PS aerosol therapy has also demonstrated efficacy and improved survival rates. Pentoxifylline provides significant protection against acute lung injury. Early administration can reduce neutrophil accumulation in the lungs, inhibit pulmonary capillary leakage, prevent pulmonary edema, and block RDS progression. IL-1 and TNF are key injurious mediators in ARDS, and pentoxifylline can inhibit their activation of leukocytes, making it a promising drug for treating ARDS and multiple organ failure. It has shown protective effects in experimental animal models of RDS.

3. Maintenance of Renal Function When shock patients present with oliguria, anuria, azotemia, etc., attention should be paid to distinguishing whether it is caused by prerenal factors or acute renal insufficiency. After effective cardiac output and blood pressure are restored, if the patient still exhibits persistent oliguria, a fluid load and diuretic test can be performed: rapidly administer 100–300 ml of mannitol via intravenous drip or inject 40 mg of furosemide intravenously. If urine output does not increase significantly and cardiac function remains stable, the test can be repeated once. If there is still no urine output, it may indicate the onset of acute renal insufficiency, and appropriate measures should be taken.

4. Prevention and Treatment of Cerebral Edema During cerebral hypoxia, cerebral edema is prone to occur, manifesting as unconsciousness, transient spasms, and signs of increased intracranial pressure, and may even lead to brain herniation. Early intervention should include vasodilators, anticholinergic drugs, osmotic dehydrating agents (e.g., mannitol), furosemide, local cooling, and high-dose corticosteroids (e.g., dexamethasone 10–20 mg) administered intravenously, as well as high-energy compound solutions.

5. Treatment of DIC Once the diagnosis of DIC is confirmed, medium-dose heparin should be administered at 1.0 mg/kg (usually 50 mg, equivalent to 6,250 units) via intravenous injection or drip every 4–6 hours, keeping the clotting time (tube method) within twice the normal range. Heparin can be discontinued only after DIC is under control. If dipyridamole is used concurrently, the dose may be adjusted accordingly. In the late stage (third stage) of DIC, when secondary fibrinolysis becomes the main cause of bleeding, antifibrinolytic drugs may be added.

6. Corticosteroids and β-Endorphin Antagonists Corticosteroids have multiple pharmacological effects, such as reducing peripheral vascular resistance and improving microcirculation; enhancing myocardial contraction and increasing cardiac output; maintaining the integrity and stability of vascular walls, cell membranes, and lysosomal membranes; mitigating and preventing capillary leakage; stabilizing the complement system and inhibiting the activation of neutrophils; maintaining normal oxidative phosphorylation in liver mitochondria and the function of hepatic enzyme systems; inhibiting arachidonic acid metabolism; suppressing pituitary β-endorphin secretion; antagonizing endotoxins and reducing toxemia; and exerting nonspecific anti-inflammatory effects by inhibiting the secretion of inflammatory mediators and cytokines. Additionally, they can relieve bronchospasm, inhibit bronchial gland secretion, promote inflammation absorption, reduce intracranial pressure, and alleviate cerebral edema. Animal experiments and early clinical applications (using high doses: 30 mg/kg of prednisolone or 2 mg/kg of dexamethasone) showed promising results. However, recent multicenter prospective controlled studies have failed to confirm the efficacy of corticosteroids. Therefore, except in cases of suspected adrenal insufficiency, their use in septic shock is not recommended. Similarly, early use of the β-endorphin antagonist naloxone has been reported to yield satisfactory results, but detailed controlled studies have not confirmed its efficacy.

7. Other Adjuvant Therapies Septic shock is the result of complex interactions between microbial components and their toxins, the activation of the body's humoral and inflammatory cell systems. Therefore, targeting a single pathological process often fails to provide sufficient protection. Current therapeutic research focuses on three main aspects: ① bacterial components; ② inflammatory mediators and cytokines produced by the host; and ③ limiting or mitigating tissue and organ injury.

⑴ Bacterial components: Prevent microbial components from activating host cells, such as using anti-internal toxin antisera, monoclonal antibodies, etc. The activation site of LPS on host cells is the receptors on the effector cell membrane, CD₁₄ (glycosylphosphatidylinositol-anchored protein). LPS binds to serum proteins to form LBP (LPS-binding protein), which acts as a carrier protein to enhance the sensitivity of CD₁₄ to LPS. The use of anti-CD₁₄ monoclonal antibodies can inhibit the binding of LPS/LBP to cells. Certain endogenous proteins produced by neutrophils can also bind and neutralize LPS, such as BPI (bactericidal/permeability-increasing protein). The affinity of BPI for LPS is 10–1000 times stronger than that of LBP, allowing it to compete with LBP for LPS binding. Additionally, modifying the structure of lipid A, the main component of LPS, can reduce its toxicity. Various lipid A analogs or their precursors have been tested for antagonizing internal toxins.

(2) Inflammatory mediators and cytokines: Key players include TNF-α, IL-1, etc. TNF monoclonal antibodies and IL-1 receptor antagonists (IL-1 Ra) have demonstrated protective effects in animal models. Inhibiting complement (C) activation also exhibits anti-inflammatory properties. Anti-C_5a monoclonal antibodies, PAF receptor antagonists (PAF, Ra), inhibitors of arachidonic acid metabolites like TaX₂ inhibitors, leukotriene (LT) inhibitors, cyclooxygenase and lipoxygenase inhibitors, NO synthase inhibitors, phosphodiesterase inhibitors (such as pentoxifylline), etc., have undergone extensive animal testing and some clinical research.

(3) Control of tissue and organ damage: Most tissue damage in sepsis results from activated neutrophils migrating to tissues and releasing destructive enzymes and reactive molecules. Blocking neutrophil chemotaxis, activation, and endothelial adhesion can interrupt this process, for example, using C_5a monoclonal antibodies, IL-6 monoclonal antibodies, phosphodiesterase inhibitors, CD₁₈ (neutrophil β₂-integrin subunit) monoclonal antibodies, endothelial-leukocyte adhesion molecule (ELAM) monoclonal antibodies, IL-4, and transforming growth factor-β. Antioxidants and oxygen radical scavengers, such as superoxide dismutase (SOD), liposomal catalase, allopurinol, deferoxamine, dimethyl sulfoxide, vitamins C and E; as well as protease inhibitors, like aprotinin and antithrombin III, also provide protective effects against tissue injury.

bubble_chart Prognosis

It depends on the following factors: ① Treatment response: If the patient becomes conscious and calm, with warm limbs, disappearance of cyanosis, increased urine output, rising blood pressure, and widened pulse pressure after treatment, the prognosis is good; ② The prognosis is better if the primary infection site can be completely removed or controlled; ③ Those with severe acidosis and hyperlactatemia often have a poor prognosis, and those complicated by DIC or organ failure also have a high mortality rate; ④ Shock is often difficult to reverse in patients with severe underlying diseases such as leukemia, lymphoma, or other malignancies; the prognosis is also poor in those with other conditions such as diabetes, cirrhosis, or heart disease.

bubble_chart Prevention

1. Actively prevent and treat infections and various diseases that are prone to cause septic shock, such as sepsis, bacterial dysentery, pneumonia, epidemic cerebrospinal meningitis, peritonitis, etc.

2. Properly handle on-site treatment of trauma, such as timely hemostasis, analgesia, and keeping warm.

3. For patients with excessive blood loss or fluid loss (such as vomiting, diarrhea, hemoptysis, gastrointestinal bleeding, excessive sweating, etc.), fluids or blood transfusions should be promptly administered as appropriate.

bubble_chart Differentiation

Septic shock should be differentiated from hypovolemic shock, cardiogenic shock, anaphylactic shock, and neurogenic shock. Hypovolemic shock is often caused by a sudden reduction in blood volume due to massive bleeding (internal or external hemorrhage), fluid loss (such as vomiting, diarrhea, intestinal obstruction, etc.), or loss of plasma (such as extensive burns, etc.). Cardiogenic shock results from impaired cardiac pumping function and is commonly secondary to acute myocardial infarction, acute cardiac tamponade, severe arrhythmias, various myocarditis and cardiomyopathies, or acute pulmonary heart disease. Anaphylactic shock is usually triggered by an allergic reaction to certain drugs (such as penicillin) or biological products. Neurogenic shock can be caused by trauma, severe pain, spinal cord injury, or anesthesia accidents, leading to peripheral vasodilation due to neural effects and a relative reduction in effective blood volume.