"Shock" lung is a progressive damage to lung tissue in response to a number of extreme conditions accompanied by acute pulmonary failure and hemodynamic impairment. This syndrome is a nonspecific reaction of lung tissue to a primary violation of general and then pulmonary circulation after massive trauma, blood loss, severe surgery, etc.

Symptoms of shock lung:

Progressive shortness of breath.

Rapid breathing.

Lack of oxygen.

Decreased urine output.

Causes of shock lung:

Shock lung is usually a consequence of shock. Blood flow in the capillaries of the lungs, the smallest blood vessels that weave through the alveoli, decreases. Blood vessels contract, capillary walls are damaged, greatly increasing their permeability. In this case, blood plasma can penetrate into the lung tissue. When blood flow is weakened, the cells of the walls of the pulmonary alveoli are affected, producing a certain substance that does not allow the alveoli of a healthy person to collapse. As a result, foci of atelectasis appear in the lungs: the walls of the pulmonary alveoli are pressed against each other, and when inhaling, the alveoli are not filled with air. In addition, during shock, blood clotting begins in the smallest blood vessels. Small blood clots (microthrombi) appear in the capillaries of the lungs, increasing circulatory problems. As a result, lung function is impaired.

Etiology

Often the primary etiological factors of acute respiratory distress syndrome in adults are trauma and traumatic shock. Acute respiratory distress syndrome in adults complicates burns and mechanical injuries, including bone fractures, head injuries, lung contusions, and internal organ injuries. This complication often develops after surgical interventions, in patients with cancer after operations such as Gerlock and Lewis. Massive transfusion of preserved blood without microfilters can also be a source of significant pulmonary microembolism and the primary etiological factor of the disease. The possibility of developing respiratory distress syndrome in adults after the use of extracorporeal circulation (“post-perfusion lung”) has been proven.

Dissemination of intravascular blood coagulation is one of the causes of multiple organ failure and pulmonary dysfunction. Previous critical conditions (prolonged hypotension, hypovolemia, hypoxia, blood loss), transfusion of large volumes of blood and solutions are considered as possible etiological factors of acute respiratory distress syndrome in adults. Fat embolism is one of the causes of pulmonary damage. Medicines (narcotic analgesics, dextrans, salicylates, thiazides and others) can also cause this complication.

The prevalence of adult acute respiratory distress syndrome in intensive care units depends on the patient population and the diseases in which the syndrome is likely to develop.

Pathogenesis

The main pathology is damage (destruction) of the pulmonary alveolar-capillary barrier. Pathophysiological changes: swelling and edema of the alveolar-capillary membrane, the formation of intercellular gaps in it, the development of interstitial edema. Adult acute respiratory distress syndrome is not just a form of pulmonary edema caused by increased capillary permeability, but also a manifestation of a general systemic pathological reaction leading to dysfunction not only of the lungs, but also of other organs.

The pathophysiological consequences of pulmonary edema in adult respiratory distress syndrome include decreased lung volumes, significantly decreased lung compliance, and the development of large intrapulmonary shunts. The predominance of blood flow in the ventilation/blood flow ratio is due to the perfusion of non-ventilated lung segments. A decrease in residual lung volume is also reflected in the unevenness of this ratio.

The destruction of pulmonary surfactant and a decrease in its synthesis can also be the reasons for a decrease in functional lung volumes and contribute to the increase in pulmonary edema. An increase in alveolar surface tension reduces hydrostatic pressure in the interstitium and increases water content in the lungs. A decrease in the compliance of an edematous lung leads to an intensification of the respiratory system and is accompanied by fatigue of the respiratory muscles. Quantitatively, the degree of pulmonary edema corresponds to the volume of intravascular water in the lungs, the value of which gradually increases, which largely determines the clinical and radiological picture of the disorder. A nonspecific disseminated reaction contributes to the formation of intravascular thrombi in the pulmonary artery system and an increase in pressure in it. The symptom of increased pressure in the pulmonary artery system is usually reversible, is not associated with left ventricular failure and, as a rule, does not exceed 18 mm Hg. The reversibility of pulmonary hypertension in adult acute respiratory distress syndrome within 72 hours of its development is confirmed by the administration of nitroprusside. In other words, pulmonary hypertension in acute respiratory distress syndrome in adults is not as manifest as in hydrostatic (cardiogenic) pulmonary edema. Typically, pulmonary artery wedge pressure is within normal limits. Only in the terminal stage of adult acute respiratory distress syndrome is it possible to increase pulmonary artery wedge pressure, which is associated with heart failure. Patients dying from progression of pulmonary failure and the inability of the lungs to perform gas exchange function in adult acute respiratory distress syndrome typically experience a marked decrease in lung compliance (extensibility), profound hypoxemia, and increased dead space with hypercapnia. Pathomorphological studies reveal extensive interstitial and alveolar fibrosis.

(Respiratory distress syndrome in adults, post-traumatic pulmonary failure, traumatic wet lung syndrome)
In recent years, it has been discovered that following an episode of “shock” due to various reasons (trauma, major surgery, burn, bleeding, infection, drug overdose, acute vascular pathology or pathology in the abdominal cavity), progressive respiratory failure can develop. This usually occurs a few days after the start of intensive care and resuscitation, including transfusion of large volumes of blood or blood substitutes, prolonged oxygen inhalation, and administration of large doses of various medications. Therefore, “shock lung” syndrome is sometimes associated not with the nature of “shock” itself, but with its excessive therapy. An early symptom of “shock lung” is hyperventilation with hypocapnia, respiratory alkalosis and progressive hypoxia, not corrected by oxygen inhalation. Scattered moist rales are detected in combination with radiological signs of pulmonary edema and segmental atelectasis, mainly in the basal regions. Secondary pneumonia usually develops. Spontaneous ventilation is often inadequate, but sometimes even mechanical breathing is not able to provide adequate ventilation of the alveoli and oxygenation of the blood. In the most severe cases, increasing hypercapnia and hypoxia lead to respiratory and metabolic acidosis, and death occurs from arrhythmia.
Treatment
There is no specific effective therapy for various forms of non-cardiogenic pulmonary edema. Cardiac glycosides and diuretics are usually ineffective, but corticosteroids have been used successfully for acute pulmonary edema caused by inhalation of nitrogenous fumes. In severe cases, regardless of the cause, tracheal intubation or tracheostomy followed by artificial ventilation with intermittent positive pressure is necessary. To straighten collapsed alveoli and reduce intrapulmonary shunting of blood, it is recommended to use positive end-expiratory pressure during artificial ventilation. If a secondary infection develops, it is necessary to select the appropriate antibiotic. The patient may require oxygen therapy, correction of the acid-base status and transfusion therapy, however, especially in some forms of “shock lung”, they can only be carried out under conditions of careful frequent monitoring of the gas and electrolyte composition of the blood, as well as central venous pressure.

Shock lung (traumatic lung, wet lung, respiratory lung, progressive pulmonary consolidation, hemorrhagic atelectasis, post-perfusion or post-transfusion lung, hyaline membranes in adults, etc.) - adult respiratory distress syndrome (ARDS) - a syndrome of severe respiratory failure with specific changes in lungs, characteristic of shock, edema, loss of elasticity, alveolar collapse.

ARDS develops gradually, reaching a peak on average 24-48 hours after the onset of damage, and ends with massive, usually bilateral damage to the lung tissue. Regardless of the cause, RDV has a clearly defined clinical picture.

There are four stages of ARDS:

Stage I - damage (up to 8 hours after stress exposure). Clinical and radiological examination usually does not reveal changes in the lungs.

Stage II - apparent stability (6-12 hours after stress exposure). Tachypnea, tachycardia, normal or moderately reduced oxygen pressure in arterial blood (PaO 2). A dynamic study reveals the progression of arterial hypoxemia, the appearance of dry wheezing in the lungs, and hard breathing. The X-ray shows the first manifestations of changes in the lungs: an increase in the vascular component of the pulmonary pattern, turning into interstitial pulmonary edema.

Stage III - respiratory failure (12-24 hours after stress exposure). Clinical picture of severe acute respiratory failure: shortness of breath, hyperpnea, participation of auxiliary muscles in breathing, tachycardia, significant drop in PaO 2 (less than 50 mm Hg), harsh breathing, dry rales from the lungs. The appearance of moist rales indicates the accumulation of fluid in the alveolar space. The radiograph shows pronounced interstitial edema of the lobes; against the background of an enhanced vascular pattern, focal-like shadows appear, sometimes horizontal. The shadows of the vessels are blurred, especially in the lower sections. Obvious infiltrative shadows representing perivascular fluid are visible.

Stage IV - terminal. Progression of symptoms. Deep arterial hypoxemia, cyanosis. Respiratory and metabolic acidosis. Cardiovascular failure. Alveolar pulmonary edema.

Occurs when:

Accidents (aspiration of water or acidic gastric contents);

Effects of drugs;

Injuries;

Inhalation of toxic gases, inhalation of high concentrations of oxygen;

Diseases (pneumonia, sepsis, pancreatitis, tuberculosis, diabetic ketoacidosis, carcinomatosis, eclampsia, shock of any etiology);

Artificial circulation;

Microembolism of the pulmonary circulation,

Extensive surgical interventions;

Suffered critical conditions (prolonged hypotension, hypovolemia, hypoxia, bleeding).

Transfusion of large volumes of blood and solutions.

DIFFERENTIAL DIAGNOSIS with:

Left ventricular failure;

Severe pneumonia (bacterial, viral, fungal, aspiration, atelectatic);

PREHOSPITAL STAGE

1. Elimination of the cause that caused ARDS.

2. Oxygen therapy.

3. Pain relief: analgin 50% 2-4 ml, possible combination with diphenhydramine 1% 1 ml IM or pipolfen 2.5% 1 ml IM.

4. If blood pressure drops: mezaton 1% 2 ml s.c. or i.v.

5. For heart failure: strophanthin 0.05% 0.5 ml i.v. per physical. solution.

6. For bronchospastic syndrome - Euphyllip 2.4% K) ml

7. Hospitalization in the intensive care unit.

HOSPITAL STAGE

1. Treatment of the underlying disease.

2. Overcoming the pulmonary barrier to O2 transport:

a) oxygen therapy;

b) application of positive pressure at the end of the outlet (PEEP);

c) gentle modes of artificial pulmonary ventilation (ALV);

d) physical therapy.

3. For the bronchospastic component - aminophylline 2.4% 10 ml IV, prednisolone 60 mg IV bolus and 60 mg N/M and further depending on the stage of the status (see "treatment of status asthmaticus").

a) analgin 50% 2-4 ml in combination with diphenhydramine 1% 1 ml IM or pipolphen 2.5% 1 ml IM;

b) sodium hydroxybutyrate (GHB) 20% 5 ml IV slowly on glucose 5%" 10 ml;

c) inhalation of a mixture of nitrous oxide and oxygen in a ratio of 1:1 or 2:1 for 10-15 minutes.

5. For hypotension:

a) mezaton 1% 0.5-1 ml IV;

b) norepinephrine 0.2% 0.5-1 ml intravenously in a 5% glucose solution or saline;

c) dopamine 0.5% - 20 ml (100 mg) diluted in 125-400 ml of isotonic sodium chloride solution or 5% glucose solution intravenously;

d) steroid hormones - prednisolone 90-150 mg or hydrocortisone 150-300 mg in isotonic sodium chloride solution intravenously.

6. Normalization of rheology and microcirculation, CBS:

a) reopolyglucin or reomacrodex;

b) heparin, streptodecase;

c) sodium bicarbonate 4% - 200 ml intravenously;

d) infusion electrolyte solutions.

The total volume of fluid for a patient weighing 70 kg (in the absence of pathological losses) should be 2.3-2.5 l/day.

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The lungs are always damaged during shock. The respiratory system responds as a standard to both direct damage to the lungs (aspiration of gastric contents, pulmonary contusion, pneumothorax, hemothorax), as well as to shock and other pathological factors. Endotoxins and liposaccharides have a direct damaging effect on pulmonary endothelial cells, increasing their permeability. Other active mediators, such as platelet activating factor, tumor necrosis factor, leukotrienes, thromboxane A2, activated neutrophils, also have pathological effects on the lungs.

Aggressive metabolites, inflammatory mediators and blood cell aggregates formed during shock enter the systemic circulation, damage the alveolar capillary membrane and lead to a pathological increase in the permeability of the pulmonary capillaries. Moreover, even in the absence of increased capillary hydrostatic or decreased oncotic pressure, not only water, but also plasma protein intensively penetrates through the wall of the pulmonary capillaries. This leads to overflow of the interstitial space with fluid, sedimentation of protein in the epithelium of the alveoli and the endothelium of the pulmonary capillaries.

Changes in the lungs progress especially quickly during inadequate infusion-transfusion therapy. These disorders lead to non-cardiogenic pulmonary edema, loss of surfactant and collapse of the alveoli, the development of intrapulmonary shunting and perfusion of poorly ventilated and unventilated alveoli with subsequent hypoxia. The lungs become “hard” and poorly extensible. These pathological changes are not immediately and not always determined radiographically. Radiographs of the lungs may initially be relatively normal, and often radiological manifestations lag behind the actual changes in the lungs by 24 hours or more.

Such changes in the lungs were originally referred to as “shock lung” and are now referred to as “acute lung injury syndrome” and “acute respiratory distress syndrome”. These syndromes differ from each other only in the degree of severity of respiratory failure. In surgical practice, they most often develop in patients with septic, traumatic and pancreatogenic shock, as well as with fat embolism, severe pneumonia, after extensive surgery and massive blood transfusions, with aspiration of gastric contents and the use of concentrated oxygen inhalations. Acute respiratory distress syndrome is characterized by the following symptoms:

• severe respiratory failure with severe hypoxemia even with inhalation of a mixture with a high concentration of oxygen (pa02 below 50 mm Hg);
• diffuse or focal infiltrates without cardiomegaly and increased vascular pattern on chest x-ray*
• decreased lung compliance;
• extracardiac pulmonary edema.

In acute respiratory syndromes, it is necessary to identify and treat the underlying disease and provide respiratory support aimed at effective oxygenation of the blood and provision of oxygen to tissues. Diuretics and limiting the volume of fluid administered in patients with acute respiratory distress syndrome do not have any effect on pathophysiological changes in the lungs and do not provide a positive effect. Under conditions of pathological permeability of the pulmonary capillaries, the administration of colloidal solutions such as albumin also does not lead to an effective reduction of extravascular fluid in the lungs. The incidence of acute lung injury did not change with the use of anti-inflammatory drugs (ibuprofen) and anti-cytokine therapy (IL-1 receptor antagonists and monoclonal antibodies to tumor necrosis factor).

Pulmonary edema can be reduced if a minimum level of pulmonary capillary pressure is maintained, sufficient only to maintain adequate CO, and the volume of the volume is replenished with starch preparations, which reduce “capillary leakage”. At the same time, the level of hemoglobin in the blood must remain at least 100 g/l to ensure the required delivery of oxygen to the tissues.

Artificial ventilation with moderate positive end-expiratory pressure allows maintaining a pa02 level above 65 mmHg. when the oxygen concentration in the inhaled mixture is below 50%. Inhalation of higher concentrations of oxygen through an endotracheal tube can displace nitrogen from the alveoli and cause their collapse and atelectasis. It can cause oxygen toxicity to the lungs, impair oxygenation, and lead to the formation of diffuse pulmonary infiltrates. Positive expiratory pressure prevents the collapse of bronchioles and alveoli and increases alveolar ventilation.

Mortality in acute respiratory distress syndrome is extremely high and exceeds an average of 60%, and in septic shock - 90%. With a favorable outcome, both complete recovery and the formation of pulmonary fibrosis with the development of progressive chronic pulmonary failure are possible. If patients manage to survive the acute period of lung damage, secondary pulmonary infection becomes a serious threat for them. In patients with acute respiratory distress syndrome, it is difficult to diagnose associated pneumonia. Therefore, if clinical and radiological findings suggest pneumonia, active antimicrobial therapy is indicated.

Savelyev V.S.

Surgical diseases

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Morphological changes in internal organs during shock (compendium) -.

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Shock- a clinical condition associated with a decrease in effective cardiac output, impaired autoregulation of the microcirculatory system and characterized by a generalized decrease in blood supply to tissues, which leads to destructive changes in internal organs.

Based on the characteristics of etiology and pathogenesis, the following types of shock are distinguished: hypovolemic, neurogenic, septic, cardiogenic and anaphylactic.

1. Hypovolemic shock. This type of shock is based on:
-decrease in blood volume as a result of bleeding (both external and internal);
-excessive loss of fluid (dehydration), for example, with diarrhea, vomiting, burns, excessive sweating;
-peripheral vasodilation. Generalized dilatation of small vessels leads to excessive deposition of blood in peripheral vessels. As a result, there is a reduction in effective blood volume, which is accompanied by a decrease in cardiac output (peripheral circulatory failure). Peripheral vasodilation can occur under the influence of metabolic, toxic or humoral factors.

2. Neurogenic shock. Common fainting is a form of neurogenic shock; this condition resolves on its own because when a person falls to the floor in a supine position, the venous return to the heart increases and, thus, cardiac output is restored. As a variation of this type of shock, we can consider traumatic shock, the triggering moment of which is excessive afferent (mainly pain) impulses. In some cases, it can occur with inadequate anesthesia or damage to the spinal cord and peripheral nerves.

3. Septic shock. In septic shock, circulating bacterial endotoxin (lipopolysaccharide) binds to CD14 receptors on macrophages, which leads to a massive release of cytokines, especially TNF (tumor necrosis factor), the main manifestations of which are changes in vascular permeability and intravascular blood coagulation. In septic shock, DIC syndrome is most pronounced because bacterial endotoxins have a direct effect on the blood coagulation system. As a result, septic shock is characterized by: necrosis of the anterior pituitary gland, necrosis and hemorrhages in the adrenal glands (Friderichsen-Waterhouse syndrome), cortical necrosis of the kidneys.

4. Anaphylactic shock. The development of anaphylactic shock is based on hypersensitivity of the reagin (1) type, caused by the fixation of IgE on blood basophils and tissue basophils. With the repeated introduction of an antigen, an antigen/antibody reaction develops on the surface of these cells, which leads to a massive release of BAS (biologically active substances - histamine, bradykinin and leukotrienes) into the tissue, which are released during degranulation of tissue basophils and blood basophils and cause expansion of precapillaries and “draining” ” blood into the microhemocirculatory system. A drop in blood pressure leads to the activation of compensatory mechanisms - catecholamines, which are designed to enhance the contractile activity of the heart (increase cardiac output) and cause spasm of arterioles, thereby ensuring the restoration of blood pressure. However, in anaphylactic shock, a “catecholamine storm” is usually ineffective because the previous histamine release causes the blockade? and?-receptors. The massive release of histamine also causes the development of spasm of the smooth muscles of the bronchi (bronchospasm) and intestines, up to the development of acute intestinal obstruction.

5. Cardiogenic shock. Cardiogenic shock occurs when there is a marked decrease in cardiac output as a result of primary heart damage and a sharp decrease in ventricular contractility, for example, in acute myocardial infarction, acute myocarditis, certain types of arrhythmias, acute valve perforation, rapid accumulation of fluid in exudative pericarditis. One type of cardiogenic shock is obstructive shock, in which there is an obstruction to blood flow in the heart or large pulmonary arterial vessels. This is observed with a massive pulmonary embolism or a large thrombus of the left atrium closing the opening of the mitral valve. Severe impairment of ventricular filling, which is observed when the heart is compressed (tamponade) by escaping blood (heart rupture) or inflammatory fluid (exudative pericarditis), leads to a significant drop in cardiac output.

Note 1: In shock, which develops due to a primary decrease in cardiac output, the pressure in the jugular vein is increased. In shock, which develops due to decreased venous return, the pressure in the jugular vein is reduced.
Note 2: A decrease in blood flow leads to its further decrease, i.e. a vicious circle occurs (eg, erythrocyte sludge, myocardial ischemia, shock lung, intestinal ischemia). This leads to irreversible shock.
Note 3: Generalized tissue hypoxia leads to progressive acidosis.

Clinical and morphological changes in shock

Any type of shock is based on a single complex multiphase development mechanism. The early period of shock is characterized by relatively specific symptoms due to the peculiarities of etiology and pathogenesis. In the late period of shock, the relative specificity of signs due to the peculiarities of its etiology and pathogenesis disappears, its clinical and morphological manifestations become stereotypical.

There are three stages of shock development:

1. Compensation stage: in response to a decrease in cardiac output, the sympathetic nervous system is activated, which leads to an increase in the heart rate (tachycardia) and causes constriction of peripheral vessels, thereby maintaining blood pressure in vital organs (brain and myocardium). The earliest clinical evidence of shock is a fast, low-amplitude (thready) pulse.
Peripheral vasoconstriction is most pronounced in the least vital tissues. The skin becomes cold and clammy sweat appears, which is another early clinical manifestation of shock. Vasoconstriction in the renal arterioles reduces pressure and glomerular filtration rate, resulting in decreased urine production. Oligouria (low urine output) is a compensatory mechanism aimed at preserving fluid in the body. The term prerenal uremia is used to refer to the state of oliguria that occurs due to various extrarenal causes; Kidney damage does not occur at this stage and the condition quickly improves with an increase in cardiac output.

2. Stage of disturbance of blood flow in tissues: prolonged excessive vasoconstriction leads to disruption of metabolic processes in tissues and a decrease in their oxygenation, which entails a transition to anaerobic glycolysis with the accumulation of lactic acid in tissues and the development of acidosis, as well as the sludge phenomenon (increased aggregation of blood cells). This creates an obstacle to blood flow in the capillaries. With severe disturbances of blood flow in tissues, cell necrosis occurs, which is most often observed in the epithelium of the renal tubules.

3. Stage of decompensation: As shock progresses, decompensation occurs. Reflex peripheral vasoconstriction gives way to vasodilation, probably as a result of increasing capillary hypoxia and acidosis. Generalized vasodilation and stasis (stopping blood flow) occurs, which leads to a progressive drop in blood pressure (hypotension) until the blood supply to the brain and myocardium reaches a critical level. Hypoxia of the brain leads to acute disruption of its activity (loss of consciousness, edema, degenerative changes and death of neurons). Myocardial hypoxia leads to a further decrease in cardiac output and rapid death.

Morphological changes in internal organs during shock

At autopsy, attention is drawn to the redistribution of blood with its pronounced accumulation in the vessels of the microvasculature. The cavities of the heart and large vessels are empty, in the rest the blood is in a liquid state. There is dilatation of venules, more or less diffuse edema (edema), multiple hemorrhages, microscopically - gluing of red blood cells in capillaries, microthrombi (sludge phenomenon, disseminated intravascular coagulation syndrome). Among other injuries, it is necessary to note multiple foci of necrosis in the internal organs, where they are located selectively around sinusoidal capillaries, usually passable for blood. Certain features of the morphological picture observed during shock in the internal organs gave rise to the use of the term “shock organ”.

With shock kidney macroscopically, the cortical layer is increased in volume, pale, swollen, in contrast to the pyramids, which have a brownish-red tint as a result of the accumulation of hemoglobinogenic pigment and a sharp congestion of the juxtaglomerular zone due to blood shunting. Microscopically, anemia of the cortex, acute necrosis of the convoluted tubule epithelium with rupture of the basement membranes of the tubules and interstitial edema are revealed. In the lumen of the tubules, protein casts, hemoglobinogenic pigments, and desquamated decaying epithelial cells are visible. These damages are segmental and focal in nature, that is, only a segment of the tubule is affected, for example, the distal one, and not all nephrons, but individual groups of them. The structure of the glomeruli of the kidneys is usually preserved, except in cases where symmetrical cortical necrosis develops. Such acute tubular nephropathy is accompanied by the development of acute renal failure. But with timely and intensive therapy, a favorable outcome is possible due to the regeneration of the destroyed epithelium.

In shock lung(respiratory distress syndrome [RDS]) are determined by uneven blood filling, the phenomena of disseminated intravascular coagulation with sludge of erythrocytes and microthrombi, multiple small necrosis, alveolar and interstitial edema, focal hemorrhages, serous and hemorrhagic alveolitis, the formation of hyaline-like (fibrin) membranes; with a protracted process, resolution always occurs through focal pneumonia.

In the liver: hepatocytes lose glycogen (light, optically empty, do not perceive coloring for fat and glycogen), undergo hydropic degeneration, and anoxic necrosis occurs in the central region of the hepatic lobule (centrilobular necrosis). Macroscopically, on a section, the liver has the appearance of yellow marble chips.

Myocardial changes in shock, they are represented by dystrophic changes in cardiomyocytes with the disappearance of glycogen in their cytoplasm and the appearance of lipids, contractures of myofibrils. Small foci of necrosis may appear, mainly under the endocardium.

In the stomach and intestines Many small hemorrhages are detected in the mucous layer in combination with ulceration - they are called “stress ulcerations”. Ischemic intestinal necrosis is important because it is often aggravated by the release of bacterial endotoxins (due to microorganisms from the intestine entering the bloodstream, where they are destroyed by the immune and complement systems), which further worsen the condition.
Despite their originality, the described morphological changes in the internal organs are not absolutely specific to shock.

The prognosis for shock depends on several factors, the most important of which is the underlying cause. When the cause can be treated (for example, fluid or blood can be given for hypovolemia), most patients survive, even if they are severely ill.

In recovering patients, necrotic cells (eg, renal tubular cells and alveolar epithelial cells) usually regenerate, and these tissues regain normal function. Patients may die if the cause of shock cannot be eliminated (for example, with extensive myocardial infarction) and if treatment is started late, when irreversible tissue damage has already occurred.