Treatment of shock

Treatment of shock conditions in children aims to restore oxygen delivery to tissues and optimize the balance between tissue perfusion and metabolic tissue needs. This requires improving blood oxygenation, increasing cardiac output and its distribution, reducing tissue oxygen consumption, and correcting metabolic disorders. The intensive treatment program for a patient in shock includes the following medical actions:

• replenishment of the BCC deficit and ensuring optimal pre- and post-load;
• maintaining myocardial contractile function;
• respiratory support;
• analgosedation;
• use of steroid hormones;
• antibiotic therapy;
• prevention of reperfusion injury;
• correction of hemostasis disorders (hypo- and hyperglycemia, hypocalcemia, hyperkalemia and metabolic acidosis).

Replenishment of the BCC deficit and provision of an optimal level of preload and afterload must always be carried out. Absolute or relative BCC deficit is eliminated by infusion therapy under the control of CVP and hourly diuresis, which should normally be at least 1 ml/kg h). CVP should be 10-15 mm Hg, while the preload is adequate, and hypovolemia does not cause circulatory failure. The intensity of infusion therapy and the need to use inotropic agents may be limited by the appearance of symptoms such as an increase in liver size, the appearance of a wet cough, increasing tachypnea and wet wheezing in the lungs. A decrease in preload below normal almost always leads to a decrease in cardiac output and the appearance of signs of circulatory failure. Despite the fact that the neuroendocrine reactions of a child to bleeding correspond to an adult organism, the degree of hypotension and decreased cardiac output accompanying moderate (15% of blood volume) blood loss are relatively greater in a child, so compensation of even moderate blood loss plays an important role. The volumes of infusion agents and their interrelationships largely depend on the stage of medical care and the stage of shock. Replenishment of the BCC leads to an increase in venous return with a subsequent increase in blood pressure, cardiac output, which in turn increases perfusion and oxygenation of tissues. The volume and rate of infusion depend on the expected magnitude of hypovolemia. It is recommended to begin infusion therapy with the use of bolus administration of saline. The first bolus - 20 ml / kg - is administered 5-10 minutes, with subsequent clinical assessment of its hemodynamic effect. In hypovolemic, distributive and obstructive shock, the infusion volume in the first hour can be up to 60 ml/kg, and in septic shock even up to 200 ml/kg. In cardiogenic shock and poisoning (beta-blockers and calcium channel blockers), the volume of the first bolus should be no more than 5-10 ml/kg, administered 10-20 minutes before.

After the introduction of isotonic crystalloids at a dose of 20-60 ml/kg and if fluid administration is necessary, colloidal solutions can be used, especially in children with low oncotic pressure (with dystrophy, hypoproteinemia).

In hemorrhagic shock, erythrocytes (10 ml/kg) or whole blood (20 ml/kg) are used to replace blood loss. Blood transfusion increases the concentration of hemoglobin, which leads to a decrease in tachycardia and tachypnea.

Positive dynamics from infusion therapy are indicated by a decrease in heart rate, an increase in blood pressure and a decrease in the shock index (HR/BP).

Persistent arterial hypotension increases mortality rate by two times with each hour.

If at such a rate no effect is obtained by the end of the first hour, then it is necessary to continue the infusion and simultaneously prescribe dopamine. Sometimes it is necessary to resort to jet injection of solutions, which is considered to be a rate of over 5 mlDkg x min). It should also be taken into account that simple compensation of the BCC deficit can be difficult against the background of widespread vascular spasm, due to the influence of pathological afferent impulses, including the pain factor. In this regard, it is indicated to carry out a neurovegetative blockade with a 0.25% solution of droperidol at a dose of 0.05-0.1 ml / kg. Normalization of microcirculation can also be ensured by the introduction of antiplatelet agents, such as dipyridamole (curantil) 2-3 mg / kg, pentoxifylline (trental) 2-5 mg / kg, heparin 300 U / kg.

Afterload reduction is important for improving myocardial function in children. In the stage of decentralized circulation in shock, high systemic vascular resistance, poor peripheral perfusion and reduced cardiac output can be compensated by reducing afterload. Such a combination of influence on afterload with inotropic effect can provide optimal working conditions for the damaged myocardium. Sodium nitroprusside, nitroglycerin cause vasodilation, reduce afterload, generate nitric oxide - a factor that relaxes the endothelium, reduce ventilation-perfusion disorders. The dose of sodium nitroprusside for children is 0.5-10 mcg / kg x min), nitroglycerin - 1-20 mcg / kg x min).

The pulmonary vascular bed plays a pathogenetically important role in patients with hemodynamic disturbances in shock combined with high pulmonary hypertension due to some congenital heart defects, respiratory distress syndrome, and sepsis. Careful monitoring and maintenance of circulating blood volume are necessary when using vasodilators to reduce pulmonary vascular resistance. Calcium channel blockers such as nifedipine and diltiazem may reduce pulmonary vascular resistance, but experience with their use in children is currently limited.

One of the most important problems in the treatment of shock conditions is maintaining the contractile function of the myocardium. The cardiac index should be at least 2 l / min x m ² ) in cardiogenic and from 3.3 to 6 l / min x m ² ) in septic shock. At present, various agents affecting the inotropic function of the heart are widely used for this purpose. The most rational of these drugs is dopamine, which stimulates a-, B- and dopaminergic sympathetic receptors and has a variety of effects. In small doses - 0.5-2 mcg / kg x min) - it primarily causes dilation of the kidney vessels, maintaining renal perfusion, reduces arteriovenous shunting in tissues, increasing peripheral blood flow, improving coronary and mesenteric circulation. The effects of small doses are preserved when acting on the pulmonary circulation, which helps eliminate pulmonary hypertension. In average doses - 3-5 mcg / kg x min) - its inotropic effect is manifested with an increase in stroke volume and cardiac output, myocardial contractility is enhanced. In this dose, dopamine slightly changes the heart rate, reduces venous return of blood to the heart, that is, reduces preload. Dopamine, having vasoconstrictor activity, reduces peripheral and renal perfusion, increasing the afterload on the myocardium. An increase in systolic and diastolic blood pressure predominates. The degree of manifestation of these effects is individual, so careful monitoring is necessary to assess the patient's response to dopamine. Dobutamine is also used as an inotropic vasodilator, used in a dose of 1-20 mcg / kg x min). Since dobutamine is a beta1-adrenergic antagonist with a positive inotropic and chronotropic effect. it dilates peripheral vessels in the systemic and pulmonary circulation, weakens pulmonary vasospasm in response to hypoxia. At doses greater than 10 mcg/kg x min), especially in children under 2 years of age, dobutamine can cause hypotension due to a significant decrease in afterload caused by a ₂ -mediated blockade of norepinephrine release from presynapses. Dobutamine does not have the properties of a selective renal perfusion stimulant, and is currently considered the drug that best meets the concept of a "pure inotropic drug".

Epinephrine (adrenaline) in a dose of 0.05-0.3 mcg/kg/min) stimulates alpha- and beta _1-, _B2 -adrenoreceptors, causing a generalized sympathetic reaction: this increases cardiac output, blood pressure, increases oxygen consumption, pulmonary vascular resistance increases, and renal ischemia occurs.

Epinephrine increases myocardial contractility and causes contraction of a stopped heart. However, its use for extreme cases is limited by many adverse effects, such as anaphylactic shock and cardiopulmonary resuscitation. Large doses of adrenaline can slow down blood circulation in the heart or even worsen myocardial blood supply. Parasympathomimetics (atropine) are usually useless in the treatment of shock in children, although they increase sensitivity to endogenous and exogenous catecholamines, especially when restoring cardiac activity through the slow rhythm phase. Currently, atropine is used to reduce bronchorrhea when administering ketamine. The use of active calcium preparations (calcium chloride, calcium gluconate) to stimulate cardiac activity, until recently traditionally used in resuscitation practice, currently seems questionable. Only in hypocalcemia do calcium preparations provide a distinct inotropic effect. In normocalcemia, intravenous bolus administration of calcium only causes an increase in peripheral resistance and contributes to the intensification of neurological disorders against the background of cerebral ischemia.

Cardiac glycosides such as digoxin, strophanthin, lily of the valley herb glycoside (korglikon) are able to improve blood circulation parameters in shock due to their positive effect on cardiac output and chronotropic effect. However, in the development of acute heart failure and arrhythmia in shock, cardiac glycosides should not be first-line drugs due to their ability to increase the myocardial oxygen demand, causing tissue hypoxia and acidosis, which sharply reduces their therapeutic effectiveness and increases the likelihood of intoxication. Cardiac glycosides can be prescribed only after initial shock therapy and restoration of homeostasis. In these cases, rapid digitalization is more often used, in which half the dose of the drug is administered intravenously and half intramuscularly.

Correction of metabolic acidosis improves the function of the myocardium and other cells, reduces systemic and pulmonary vascular resistance, and decreases the need for respiratory compensation for metabolic acidosis. It should be remembered that metabolic acidosis is only a symptom of the disease, and therefore all efforts should be aimed at eliminating the etiologic factor, normalizing hemodynamics, improving renal blood flow, eliminating hypoproteinemia, and improving tissue oxidative processes by administering glucose, insulin, thiamine, pyridoxine, ascorbic, pantothenic, and pangamic acids. Acidosis with signs of insufficient tissue perfusion that persists during shock treatment may indicate inadequacy of therapy or ongoing blood loss (in hemorrhagic shock). Correction of acid-base balance by administration of buffer solutions should be performed only after elimination of hypovolemia and hypoglycemia in the presence of decompensated acidosis with pH less than 7.25 and in case of metabolic acidosis with a low anion gap associated with large renal and gastrointestinal losses of bicarbonates. In shock, correction of acidosis with sodium bicarbonate should be performed with caution, since conversion of acidosis to alkalosis worsens the oxygen-transport properties of blood due to shift of the oxyhemoglobin dissociation curve to the left and promotes accumulation of sodium in the body, especially with reduced renal perfusion. There is a risk of development of hyperosmolar syndrome, which can cause intracranial hemorrhage, especially in newborns and premature infants. In children of the first months of life, the sodium load is not compensated by increased natriuresis, sodium retention leads to development of edema, including cerebral edema. Sodium bicarbonate is administered slowly intravenously at a dose of 1-2 mmol/kg. In newborns, a solution at a concentration of 0.5 mmol/ml is used to avoid an acute change in blood osmolarity. Often, the patient needs 10-20 mmol/kg to correct deep acidosis. Sodium bicarbonate can be prescribed for mixed respiratory and metabolic acidosis against the background of mechanical ventilation. Tromethamine (trisamine), which is an effective buffer that eliminates extra- and intracellular acidosis, is also indicated for the correction of metabolic acidosis. It is used at a dose of 10 ml/kg h) with the addition of sodium and potassium chlorides and glucose to the solution, since trometamol increases the excretion of sodium and potassium from the body. Newborns are administered trometamol with the addition of glucose only. Tromethamine is not indicated for central respiratory disorders and anuria.

Steroid hormone therapy has been widely used in the treatment of shock for many years. The most commonly used drugs are hydrocortisone, prednisolone, and dexamethasone. The theory of GC treatment is based on a variety of effects, including the property of these drugs to increase cardiac output. They have a stabilizing effect on the activity of lysosomal enzymes, an antiaggregatory effect on platelets, and a positive effect on oxygen transport. The antihypotensive effect, together with the membrane-stabilizing and anti-edematous effects, as well as the effect on microcirculation and inhibition of the release of lysosomal enzymes, form the basis of their anti-shock action and the ability to prevent the development of multiple organ failure. When determining the indications for the use of glucocorticoids, it is necessary to assess the etiology of shock. Thus, anaphylactic shock is an absolute indication for glucocorticoid therapy after the administration of adrenaline and antihistamines. In hemorrhagic and septic shock, glucocorticoids are used against the background of specific therapy. Replacement therapy or stress doses of corticosteroids will be necessary for these types of shock. In adrenal insufficiency, physiological [12.5 mg/kg x day)] or stress doses of 150-100 mg/(kg x day)| hydrocortisone are used. Relative contraindications in shock conditions are minimal, since the indications are always of a vital nature. The success of steroid therapy obviously depends on the time of its initiation: the earlier the treatment with steroid hormones is started, the less pronounced the symptoms of multiple organ failure. However, along with the positive effects of steroid therapy, negative aspects of their action are also currently noted in septic shock. It is noted that massive steroid therapy contributes to the development of an extravascular infectious factor, since the inhibition of polymorphonuclear cells slows their migration into the extracellular space. It is also known that steroid therapy contributes to the occurrence of gastrointestinal bleeding and reduces the tolerance of the patient's body in a state of shock to the glucose load.

Immunotherapeutic approaches to the treatment of septic shock are constantly progressing. For the purpose of detoxification, polyclonal FFP with a high titer of antiendotoxic antibodies, immunoglobulin preparations - normal human immunoglobulin (pentaglobin, intraglobin, immunovenin, octagam) are used. Pentaglobin is administered intravenously to newborns and infants at a dose of 1.7 ml / (kg h) using a perfusor. Older children are given 0.4 ml / kg h) continuously until a dose of 15 ml / kg is reached within 72 hours.

Recombinant analogue of human interleukin-2 (rIL-2), in particular yeast recombinant analogue - domestic drug roncoleukin has proven itself as an effective means of immunotherapy in severe purulent-septic pathology. In children, roncoleukin is used intravenously by drip. The schemes for the use of roncoleicine in children and adults are the same. The drug is diluted in isotonic sodium chloride solution for injection. A single dose of the drug in children depends on age: from 0.1 mg for newborns to 0.5 mg in children over 14 years old.

This targeted immunocorrection allows achieving an optimal level of immune protection.

Shock conditions in children are accompanied by suppression of the reticuloendothelial system, therefore antibiotics should be included in the treatment complex, but it should be remembered that their administration is not as vital in the first hours of emergency measures compared to targeted immunotherapy. Treatment begins with third-generation cephalosporins [cefotaxime 100-200 mg / kg x day), ceftriaxone 50-100 mg / kg x day), cefoperazone / sulbactam 40-80 mcg / (kg x min)] in combination with aminoglycosides [amikacin 15-20 mg / kg x day)]. Of particular interest is bowel damage in shock, since the syndrome of general reactive inflammation, leading to multiple organ failure, is associated with the intestine. The method of selective decontamination of the intestine and enterosorption are used as a variant of antibacterial therapy. Selective decontamination with the use of an enteral mixture of polymyxin, tobramycin, and amphotericin selectively suppresses nosocomial infection. Enterosorption with the use of such drugs as smectite doctohedrally (smecta), colloidal silicon dioxide (polysorb), wollen, and chitosan allows for a reduction not only in the activity of nitrogenous wastes, but also in the degree of endotoxemia.

Analgesia and sedation are necessary components of the treatment program for many types of shock, in which pain factors and CNS hyperactivity play a significant role. In these cases, the use of inhalation and non-inhalation anesthetics is indicated. From the extensive arsenal of non-inhalation narcotic drugs, sodium oxybate (sodium oxybutyrate) and ketamine are used. The advantage of these drugs is associated with the antihypoxic effect and the absence of a depressing effect on blood circulation. Sodium oxybate is administered against the background of constant oxygen therapy at a dose of 75-100 mg / kg. Ketamine at a dose of 2-3 mg / kg [0.25 mg / kg h) subsequently] causes dissociated anesthesia - a condition in which some areas of the brain are suppressed, and others are excited. In the treatment of shock, it is important that the manifestation of this process is a pronounced analgesic effect in combination with superficial sleep and stimulation of blood circulation. In addition, ketamine, releasing endogenous norepinephrine, has an inotropic effect on the myocardium, and also, by blocking the production of interleukin-6, reduces the severity of the systemic inflammatory response. Combinations of fentanyl with droperidol and metamizole sodium (baralgin) are also used as first-line drugs for pain syndrome. Opioid analgesics: omnopon and trimeperidine (promedol) - as a method of pain relief in shock in children have significantly more limitations than indications due to the ability to increase intracranial pressure, suppress the respiratory center and cough reflex. It is necessary to avoid including papaverine in analgesic mixtures, which can cause cardiac arrhythmia and increased arterial hypotension.

The high efficiency of such antioxidants as vitamin E (tocopherol*), retinol, carotene, allopurinol, acetylcysteine, and glutathione in intensive therapy of shock has been clearly demonstrated.

One of the main goals in shock therapy is to ensure optimal oxygen delivery. Mixed venous (pulmonary artery) saturation is recognized as the ideal method for assessing oxygen consumption. Superior vena cava venous saturation greater than 70% is equivalent to 62% mixed venous saturation. Superior vena cava blood saturation can be used as a surrogate marker of oxygen delivery. Its value greater than 70% with hemoglobin greater than 100 g/L, normal arterial pressure, and capillary refill time less than 2 s may indicate adequate oxygen delivery and consumption. In children with shock, hypoxia develops not only as a result of impaired tissue perfusion, but also due to hypoventilation and hypoxemia caused by decreased respiratory muscle function, as well as intrapulmonary shunting due to respiratory distress syndrome. There is an increase in blood filling in the lungs, hypertension occurs in the pulmonary vascular system. Increased hydrostatic pressure against the background of increased vascular permeability promotes the transition of plasma into the interstitial space and into the alveoli. As a result, there is a decrease in lung compliance, a decrease in surfactant production, a violation of the rheological properties of bronchial secretions, and microatelectasis. The essence of the diagnosis of acute respiratory failure (ARF) in shock of any etiology consists in the consistent solution of three diagnostic problems:

• assessment of the degree of acute respiratory failure, as this dictates the tactics and urgency of treatment measures;
• determination of the type of respiratory failure, necessary when choosing the nature of the measures to be taken;
• assessment of the response to primary measures to make a prognosis of a threatening condition.

The general treatment regimen consists of restoring airway patency by improving the rheological properties of sputum and tracheobronchial lavage; ensuring gas exchange function of the lungs by oxygenation in combination with constant positive expiratory pressure. If other methods of treating respiratory failure are ineffective, artificial ventilation is indicated. Artificial ventilation is the main component of replacement therapy used in case of complete decompensation of the external respiratory function. If the victim fails to eliminate arterial hypotension within the first hour, this is also an indication for transferring him to artificial ventilation with FiO2 ₌ 0.6. In this case, high concentrations of oxygen in the gas mixture should be avoided. It is important to note that inadequate respiratory therapy also poses a potential threat of developing severe neurological disorders. For example, prolonged ventilation using high oxygen concentrations without monitoring pO2 _and pCO2 _can lead to hyperoxia, hypocapnia, respiratory alkalosis, against which severe spasm of cerebral vessels develops with subsequent cerebral ischemia. The situation is significantly worsened by a combination of hypocapnia and metabolic alkalosis, the development of which is facilitated by unreasonably frequent use of furosemide (lasix).

Analgosedation and mechanical ventilation also reduce oxygen consumption.

It is necessary to note the features of treatment of such types of shock as obstructive, anaphylactic and neurogenic. Recognition and elimination of the causes of obstructive shock is the main task of therapy, along with infusion. Restoration of stroke volume and tissue perfusion occurs after pericardiocentesis and drainage of the pericardial cavity in cardiac tamponade, puncture and drainage of the pleural cavity in tension pneumothorax, thrombolytic therapy (urokinase, streptokinase or alteplase) in pulmonary embolism. Immediate continuous round-the-clock infusion of prostaglandin E1 or E2 in newborns with ductus-dependent heart defects prevents closure of the arterial duct, which saves their lives in such defects. In case of a functioning ductus arteriosus and suspected ductus-dependent defect, prostin administration is started with low doses of 0.005-0.015 mcg/(kg x min). If there are signs of closure of the ductus arteriosus or if the ductus arteriosus is reliably closed, the infusion is started with the maximum dose of 0.05-0.1 mcg/(kg x min). Subsequently, after the ductus arteriosus opens, the dose is reduced to 0.005-0.015 mcg/(kg x min). In case of anaphylactic shock, adrenaline at a dose of 10 mcg/kg, antihistamines (a combination of H2- and H3-histamine receptor blockers is more effective) and glucocorticoid hormones are administered intramuscularly first. To relieve bronchospasm, salbutamol is inhaled through a nebulizer. To eliminate hypotension, infusion therapy and the use of inotropic agents are necessary. When treating neurogenic shock, several specific points are highlighted:

• the need to place the patient in the Trendelenburg position;
• use of vasopressors in shock refractory to infusion therapy;
• warming or cooling as needed.

Treatment goals

The principles and methods of intensive therapy of shock in children developed and implemented in clinical practice contribute to the optimization and improvement of treatment results. The immediate goal in shock therapy is to achieve normalization of arterial pressure, frequency and quality of peripheral pulse, warming of the skin of the distal parts of the extremities, normalization of the capillary filling time, mental status, venous blood saturation of more than 70%, the appearance of diuresis of more than 1 ml / (kg h), reduction of serum lactate and metabolic acidosis.