Liver transplantation

In 1955, Welch made the first liver transplantation in dogs. In 1963, a group of researchers led by Starzla carried out the first successful liver transplantation in humans.

The number of liver transplantations is steadily growing, and in 1994, 3,450 patients underwent surgery in the United States. The annual survival rate after routine liver transplantation in patients at low risk is 90%. Improving the results can be related to more careful selection of patients, improvement of surgical techniques and methods of postoperative period, as well as more frequent repetitive transplantations in case of rejection. Improvement of methods of immunosuppressive therapy also favorably affected the results of the operation.

Liver transplantation is the most complicated method of treatment, which does not begin with an operation and does not end with it. It can only be carried out by specialized centers that have all the necessary conditions for this.

The patient and his family need psychological and social support. There should be a program to provide donor agencies. Surviving patients need lifelong observation by a hepatologist and surgeon and treatment with expensive drugs (immunosuppressants and antibiotics).

Observers of these patients should contact the transplant center. They should be aware of late complications, especially infectious, chronic rejection, biliary complications, lymphoproliferative and other malignant diseases.

Not surprisingly, the cost of liver transplantation is high. Technical advances, an increase in the number of transplant teams and the creation of cheaper immunosuppressants can reduce the cost of treatment. It should be comparable to the cost of treatment in the last year of life of patients who, due to some circumstances, liver transplantation was not performed.

The irreversible progression of liver failure leads to the need for transplantation due to the occurrence of serious complications (for example, HCC, encephalopathy, coma, uremia), threatening the life of the patient. With acute hepatic failure, intensive care methods allow survival of 5-20% of patients. At the same time, the total annual survival of recipients for orthotopic liver transplantation reached 80% or more. Indicators of long-term survival are also quite high with a marked improvement in the quality of life.

[1], [2], [3], [4], [5], [6]

Pathophysiological changes in terminal hepatic insufficiency

The liver has numerous synthetic and metabolic functions, so the terminal stage of the disease is reflected in virtually all organs and body systems.

For patients in the terminal stage of hepatic insufficiency, the picture of the hyperdynamic status of the cardiovascular system with a significant increase in CB, tachycardia, and a decrease in OPSS is characteristic. In diseases that destroy the normal hepatic architecture, portal hypertension develops and in the abdominal wall, omentum, retroperitoneal space, the gastrointestinal tract, extensive varicose venous collaterals are formed. In addition to the significant danger associated with bleeding from varicose vessels, a branched network of arteriovenous anastomoses leads to low systemic vascular resistance and high CB.

In patients with cirrhosis, oxygenation, transport and delivery of oxygen of various degrees are usually detected. Intrapulmonary bypass, often observed in patients with end-stage liver disease, leads to hypoxemia and is complicated by pleural effusions and bilateral atelectasis with an increase in VBD due to pronounced splenomegaly and ascites. Intrapulmonary bypass is the result of an increase in the concentration of vasodilating substances (glucagon, vasoactive intestinal polypeptide, ferritin), which play an important role in the development of hypoxemia. Often there is a gas retention in the lower parts of the lungs and a decrease in the ventilation-perfusion ratio with subsequent hypoxemia. The increase in CB and bcc in cirrhosis may be reflected again in the pulmonary vascular bed, followed by the development of pulmonary hypertension.

The pathogenesis of fluid retention in patients with cirrhosis is rather complicated, and its mechanisms include increased secretion of ADH, as well as reduced delivery of the filtrate to the nephron outgoing segments. There are many nerve, hemodynamic and hormonal factors that are important in the pathogenesis of sodium retention in patients with cirrhosis. With a decrease in the "effective" volume, changes in the sympathetic nervous system increase, most likely due to stimulation of bulk receptors. This is accompanied by an increase in the activity of renin, which by means of the angiotensin system increases the secretion of aldosterone. An increase in the tone of the sympathetic nervous system and an increase in aldehsterone activity lead to sodium retention in the tubules. The delay is aggravated by the redistribution of the intrarenal blood flow, which is the result of both an increase in the vasoconstrictor effect of the sympathetic nervous system and activation of the renin-angiotensin system. PG and kallikrein-kinin system also participate in sodium retention, performing a compensatory or neutralizing role in the functioning and circulation of the kidneys. As soon as the further increase in the concentration of these substances ceases, decompensation begins and kidney failure of varying severity develops.

Ascites develop as a result of venous hypertension, reduced protein synthesis and retention of sodium and liquid due to the relative excess of aldosterone and vasopressin. Treatment often involves diuretics, which in turn can cause electrolyte and acid-alkaline disorders and a decrease in intravascular volume. However, diuretic therapy is often accompanied by a number of complications, such as hypovolemia, azotemia, sometimes hyponatremia and encephalopathy. The causes of hypokalemia observed in cirrhosis may be an inadequate diet, hyperaldehistoremia and diuretic therapy. It is obvious that diuretic therapy without proper control of the volume of fluid can reduce the effective volume of plasma, followed by decompensation of kidney function and the development of hepatorenal syndrome.

Hepatorenal syndrome usually develops in patients with classical symptoms of hepatic cirrhosis, portal hypertension and especially ascites. These patients usually have normal urination, but urine, even concentrated, almost does not contain sodium, and the levels of creatinine and urea gradually increase. In fact, urine indicators in patients with hepatorenal syndrome are similar to those in patients with hypovolemia. The pathogenesis of the hepatorenal syndrome has not been fully clarified, but it can be assumed that the vasoconstriction of the kidney vessels with subsequent reduction of renal blood flow is the primary moment responsible for the development of the hepatorenal syndrome. According to some researchers, hepatorenal syndrome develops due to a decrease in the volume of plasma, as well as active diuretic therapy, HCC and paracentesis. Most patients with hepatorenal syndrome die, so careful monitoring of diuretic therapy and vollemic status is necessary to prevent this syndrome.

With jaundice with high values of circulating bilirubin, its toxic effects on the tubule of the kidneys can be the cause of the development of OKH, which is often complicated by AH and infection. Patients with cirrhosis have a significantly limited ability to mobilize blood from the visceral (including hepatic) vascular space to increase the BCC. Thus, in response to even very moderate bleeding, these patients may develop severe hypotension followed by tubular necrosis.

Other severe clinical manifestations are severe swelling, ascites, metabolic disorders, significant weight loss, skin itch caused by high hyperbilirubinemia (up to 1300 mmol / l), hypoproteinemia, hypoalbuminemia, etc. The reasons for the decrease in the albumin concentration are quite complex and are primarily associated with a violation of the protein-synthetic function, as well as a general increase in the volume of fluid in the body and some other factors.

At the terminal stage of cirrhosis, the CNS is affected, progressive toxic encephalopathy occurs, leading to edema of the brain, followed by death. In patients with hepatic encephalopathy, the usual manifestations of it are inhibition and mental disorders. In such patients, there is an increase in the concentration of nitrogen-containing compounds in the blood, while increasing the urea concentration in the blood in a number of cases determines the severity of hepatic encephalopathy. However, in some patients with hepatic encephalopathy there is no increase in blood urea, while in other patients with a high concentration of urea in the blood there are no signs of encephalopathy.

Lightning (fulminant) liver failure progresses from jaundice to encephalopathy extremely quickly, sometimes in less than one week. Such patients develop a cytotoxic edema in the brain, which is especially pronounced in the gray matter of the cortex. The etiology of cerebral edema is not fully understood. Obviously, urea and glutamine play a very important role in the pathophysiology of the process. A possible mechanism for increasing osmolarly active intracellular elements is known, which are formed faster than the ability of the brain to adapt by eliminating extraneous ions or molecules. For a prognosis of the state, a careful analysis of the EEG changes is of some value, but it has no great therapeutic value until a non-convulsive epileptic status becomes clinically apparent.

Diagnosis of a critical increase in intracranial pressure due to clinical symptoms is unreliable. In a comatose patient, the onset of development of brainstem edema ("wedging") is extremely difficult to detect. However, this important point, in fact, solves the issue of the possibility of liver transplantation to a patient whose condition may have already progressed to irreversible structural neurological disorders.

Most patients with cirrhosis have violations of the blood coagulation system of varying degrees. The coagulation potential of the blood is reduced, as the synthesis of hepatic coagulation factors (I [fibrinogen], II [prothrombin], V, VII, IX, X), as well as fibrinolytic factors is disturbed. Factors II, IX and X are vitamin-K-dependent. Changes in prothrombin time usually reflect well the degree of dysfunction. Leukocytopenia and thrombocytopenia are caused by suppression of bone marrow function, splenomegaly and ICE. Practically in all patients, pronounced coagulopathy occurs as a result of thrombocytopenia (up to 15 x 109 / ml) and a decrease in the concentration of plasma clotting factors synthesized by the liver. Clinically, this is manifested by an increase in APTT, prothrombin index, VSK. Coagulopathy necessitates the maximum precision of puncture and catheterization of the central veins and arteries, since the danger of uncontrolled bleeding and the occurrence of large hematomas on the neck, in the pleural cavity and in the mediastinum at the slightest technical error is extremely high.

Preoperative preparation and assessment of the patient's condition before liver transplantation

The status of candidates for such a procedure as liver transplantation varies from chronic fatigue with mild jaundice to coma with multiple organ failure. The chances of success of liver transplantation are quite high even in patients in extremely serious condition. With timely operation, you can count on the reverse development of hepatic encephalopathy with severe neurological disorders. Emergency liver transplantation even with fulminant liver failure can lead to success in 55-75% of cases. Without transplantation, for the majority of patients with fulminant hepatic insufficiency, the prognosis is extremely poor.

Many physiological disorders associated with the terminal stage of liver disease can not be corrected without transplantation. Therefore, the main emphasis in the preoperative assessment of the patient should be made on the most important violations of the physiological status and on the treatment of pathology, which directly threatens the safe induction of anesthesia. For example, pleural effusions can cause a sharp decrease in the pH of the blood, and despite the presence of clotting disorders, it may be necessary to perform a pleurocentesis.

Some rare diseases, cured with the help of such procedures as liver transplantation, create additional problems for anesthesiologists. For example, during transplantation in Badda-Chiari syndrome, which is usually accompanied by extensive hepatic venous thrombosis, an active anticoagulant therapy may be necessary. Children with a rare disease - Kriegler-Nayar syndrome (bilirubin-glucuronide-glucuronosyl transferase deficiency) should avoid using drugs that interfere with the binding of bilirubin to albumin (for example, barbiturates).

The disrupted vollemic status of patients with encephalopathy in the oliguric form of renal failure may require the removal of excess BCC by arteriovenous hemofiltration or hemodialysis prior to the onset of correction of coagulopathy. Plasmapheresis also has a theoretical benefit for the removal of potential encephalotoxins, as well as the proven effect of transfusion of blood components. Although plasmapheresis is used in many transplant centers when trying to improve the conditions for transplantation, the indications and timing of its use are inconclusive.

Therapy of increased intracranial pressure should be started when appropriate symptoms appear and continue throughout the preoperative period. Sometimes simple measures, such as raising the upper body by 30 °, sometimes help, but excessive reduction of cerebral perfusion pressure in patients with hypotension should be avoided. It is noted that in some patients with head lifting intracranial pressure rises, which is probably due to a violation of CSF outflow through foramen magnum as a result of caudal displacement of the brainstem. It is possible to use mannitol, but with a decrease in the excretory function of the kidneys, the use of this osmotically active drug can lead to fluid overload:

Mannitol IV / 0.25-1 g / kg, the frequency of administration is determined by clinical feasibility.

Premedication

Components of premedication before liver transplantation are antihistamine drugs (chloropyramine, diphenhydramine), H2 blockers (ranitidine, cimetidine), betamethasone, benzodiazepines (midazolam, diazepam). When prescribing sedative drugs, one should take into account the psychoemotional state of the patient, his adequacy and the presence of signs of encephalopathy:

Diazepam v / m 10-20 mg, once for 25-30 minutes before the patient's delivery to the operating room or Midazolam IM 7.5-10 mg, once for 25-30 minutes before the patient's delivery to the operating room

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Diphenhydramine 50-100 mg, once for 25-30 minutes before delivering patients to the operating room or Chloropyramine IM 20 mg, once for 25-30 minutes before the patient was administered to the operating room

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Cimetidine in / m 200 mg, once for 25-30 minutes before the patient's delivery to the operating room

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Betamethasone IV IM 4 mg, once for 25-30 minutes before the patient's delivery to the operating room.

Basic methods of anesthesia

Induction of anesthesia:

Midazolam IV 2.5-5 mg, once

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Ketamine in / in 2 mg / kg, once

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Fentanyl IV 3.5-4 mg / kg, single dose

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Pipecuronium bromide IV 4-6 mg, single dose or Midazolam IV 5-10 mg, single dose

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Thiopental sodium IV / 3-5 mg / kg, once (or other barbiturates)

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Fentanyl IV 3.5-4 μg / kg, single dose

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Pipecuronium bromide iv 4-6 mg, once Propofol iv 2 mg / kg, once

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Fentanges IV / 3.5-4 μg / kg, single dose

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Pipecuronium bromide IV 4-6 mg, once.

During liver transplantation, there is a very high risk of surgical bleeding with large and rapid blood loss. Therefore, it is necessary to ensure the possibility of rapid recovery of large volumes of liquid. Typically, at least two peripheral venous cannulas with a large lumen are located, one of which is used to use a rapid transfusion device, and central veins are also catheterized.

The presence of a double-lumen hemodialysis catheter and a Swan-Ganz catheter in both internal jugular veins provides the opportunity for rapid and effective infusion and replenishment of virtually any blood loss. To conduct continuous monitoring of systemic BP, the radial artery is catheterized. Invasive monitoring using arterial and pulmonary catheters is standard, as significant changes in intravascular volume are common, and the period of reperfusion of the donor liver is accompanied by predictable hypotension. Sometimes, in addition to the radial, a femoral arterial catheter is placed as well. The distal arterial flow can be compromised during the imposition of aortic clamps during anastomosing the hepatic artery.

Patients in the terminal stage of hepatic insufficiency have numerous causes for delayed release of the stomach, such as ascites or active bleeding from the upper gastrointestinal tract. Therefore, prevention of aspiration is mandatory, and induction of OA should be performed either technically fast or in patients with hemodynamic instability or significant hypovolemia intubation is performed with preserved consciousness under local anesthesia.

The standard induction protocol is the use of midazolam, ketamine (or thiopental sodium), fentanyl, pipecuronium bromide.

A number of authors recommend etomidate as an injectable drug for introductory anesthesia, but it should be borne in mind that prolonged infusion and general high doses of this drug can cause suppression of adrenal function and require the appointment of GCS. In addition, etomidate can aggravate neurologic disorders, it is not recommended for use in doses greater than 0.3 mg / kg.

Maintaining anesthesia:

(general balanced anesthesia based on isoflurane)

Isoflurane 0.6-2 MAK (in the minimal-flow mode) with dinitrogen oxide and oxygen (0.3: 0.2 l / min)

Fentanyl IV bolusno 0,1-0,2 mg, the frequency of administration is determined by the clinical feasibility

Midazolam IV bolus 0.5-1 mg, the frequency of administration is determined by clinical feasibility or (TBVA)

Propofol in / in 1,2-Zmg / kg / h

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Fentanyl IV bolusno 0,1-0,2 mg, the frequency of administration is determined by clinical feasibility.

Muscle relaxation:

Atracuria bezylate 1-1.5 mg / kg / h or Cisatracurium bezylate 0.5-0.75 mg / kg / h.

The severity of the patient's initial condition and peculiarities of surgical intervention in liver transplantation-the possibility of a rapid change in the vollemic status, severe hemodynamic disturbances that arise during the dislocation of the liver, clogging of the main vessels, etc., necessitate the provision of maximum controllability of anesthesia. First of all, it concerns the depth of anesthesia, on which the vascular tone and efficiency of cardiac activity largely depends. Therefore, preference is given to modern combined anesthesia based on IA as the most mobile and controlled method.

In modern transplantology, OA is the choice method, the main component of which is a powerful IA (in most cases - isoflurane). Expressed violations of the blood coagulation system exclude the use of RAA methods as potentially dangerous due to possible hemorrhagic complications.

Anesthesia is supported by drugs that retain visceral blood flow (opioids, isoflurane, muscle relaxants), except for cases of fulminant hepatic insufficiency, when the possibility of intracranial hypertension serves as a contraindication to the use of powerful IA.

To use dinitrogen oxide, there are no contraindications, but this drug is usually avoided because of its ability to expand the intestine and increase the size of the gas bubbles entering the bloodstream. In some studies, the results of the use of TBAV in liver transplantation are presented. The use of infusion of propofol, remifentanil and cisatracurium bezila-ta, i.e. LS with extrahepatic metabolism, allows to avoid the pharmacological load on the transplant that has just undergone surgical stress and ischemia, and ensures safe early extubation of the recipient.

The main drugs for anesthesia are opioid fentanyl (1.2-1.5 μg / kg / h) and IA isoflurane (0.5-1.2 MAK) in combination with mechanical ventilation oxygen-to-oxide mixture (1: 1), used in mode minimal-flow (0,4-0,5 l / min). Since the beginning of the operation and until the end of the light-hearted period, muscular relaxation is provided by bolus injections of pipecuronium bromide (0.03-0.04 mg / kg / h), and after restoration of blood flow through the graft, cisatrakurium bezylate (0.07-0.08 mg / kg / h).

The result of an increase in the volume of distribution for cirrhosis of the liver may be an increase in the initial induction dose of nondepolarizing myo-relaxants and prolongation of their action. At the same time, the kinetics of fentanyl is practically unchanged. Although a well-preserved liver transplant can quickly begin to metabolize drugs, many pharmacokinetic changes (eg, decreased serum albumin levels, increased distributional volumes) counteract the detoxification function of the graft.

The essential point of the operation is the use of warm medicines for infusion, moistened gas mixture, warming blankets and mattresses, insulating covers for the head and extremities. Otherwise, hypothermia develops rapidly, which is caused by transfusion, loss of fluid during convection and evaporation from the open abdominal organs, a decrease in the energy productivity of the liver, and implantation of a cold donor organ.

Orthotopic liver transplantation consists in replacing a patient with native liver with a cadaver organ or a liver fraction from a living related donor; in most cases it is possible to implement it in anatomical position. This occurs in three stages: pre-insecure, non-hepatic and non-hepatic (post-care).

Pre-sufficiency stage includes dissection of liver gates structures and its mobilization. Instability of the cardiovascular system is normal at this stage due to hypovolemia, acute loss to the third space (ascites) and bleeding from the venous collaterals of the abdominal wall, organs and mesentery. Citrate-induced hypocalcemia, hyperkalemia with rapid blood transfusion and haemolysis, difficulty in venous return during liver traction or a sharp fall in the WBD also contribute to hemodynamic instability. During sudden volumetric shifts, the initially asymptomatic effusions into the pericardial cavity may reduce CB. Possible surgical blood loss, often occurring when crossing varicose veins and paracentesis, can be exacerbated by the inconsistency of the coagulation system and hemodilution, as well as fibrinolysis. These disorders should be controlled by traditional and special methods of studying the blood coagulation system (prothrombin time, partial thromboplastin time, bleeding time, fibrinogen, fibrin degradation products and platelet count) and thromboelastography.

To replace blood loss, crystalloids (solutions of electrolytes and dextrose), plasmaexpanders, NWFP, and donor EM indications are used.

Average volumes of components of infusion therapy (total volume - 11-15 ml / kg / h):

• crystalloids - 4-6 ml / kg / h;
• colloids - 1-2 ml / kg / h;
• FFP - 4-7 ml / kg / h;
• donor erythrocyte mass - 0.5-1.5 ml / kg / h;
• Washed autoerithrocytes - 0.2-0.3 ml / kg / h.

In order to reduce the infusion of donor blood components, the Cell Saver device for collecting and washing red blood cells is routinely used to collect and wash extravasal blood. It is used in cases of absence of active infection or malignancy. Many clinics use fast infusion systems designed to introduce heated fluids or blood products at a rate of up to 1.5 l / min. These devices are equipped with pressure monitors in the mains, filters, air detectors and liquid level sensors to minimize damage to blood cells and to prevent air ingress.

The initial metabolic acidosis is aggravated by the arising periods of hypotension and can be very pronounced in the absence of metabolic function of the liver. For its treatment, sodium bicarbonate is used:

Sodium bicarbonate, 4% rr, w / c 2.5-4 ml / kg, the periodicity of administration is determined by clinical expediency. However, with deep acidosis, an alternative to sodium bicarbonate may be trometamol - LS, which avoids hyperosmolar hypernatremia.

Oliguria is common at this stage, therefore, as soon as prerenal causes are excluded, it is necessary to begin active therapy with osmotic diuretics or other drugs with a diuretic effect, for example dopamine, in a "renal dose" (2.5 mg / kg / min):

Furosemide IV bolus 5-10 mg, the frequency of administration is determined by the clinical feasibility

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Dopamine iv / 2-4 μg / kg / min through the perfusor, the duration of administration is determined by clinical feasibility.

Prebesechenchenochnaya liver transplantation is characterized by the need to use relatively high doses of anesthetics: in this period, the concentration of isoflurane in the gas mixture was, as a rule, maximum - 1.2-2% (1-1.6 MAK), it is necessary to use relatively much - 3.5 ± 0.95 μg / kg / h (up to 80% of the total) of fentanyl and pipecuronium bromide in the form of bolus injections. This can be explained by the fact that, on the one hand, the body is saturated with pharmacological drugs, on the other, because this stage is the most traumatic in the surgical sense. For the pre-incubation stage, there are significant mechanical liver displacements that arise due to the need for surgical manipulation (traction, rotation, dislocation) in the allocation of the liver and preparation for hepatectomy. These moments have a very significant effect on systemic hemodynamics, causing a periodic decrease in preload under pressure on the lower vena cava, rapid fluctuations in systemic blood pressure, and relative hypovolemia.

Non-hepatic transplantation of the liver begins from the moment of removal of the native liver shortly after the cessation of its blood supply and the intersection of the hepatic artery and portal vein, as well as compression of the supra- and subhepatic divisions of the inferior vena cava. At a high risk of rupture of varicose veins of the esophagus during clamping of the inferior vena cava, a Blakemore probe can be temporarily performed. In most transplant centers, in order to avoid a sharp decrease in venous return and fall of CB, as well as venous overload in the lower half of the body, intestines and kidneys, a venovenous bypass is used. It allows you to take blood from the femoral and portal veins and extracorporeally delivers it to the axillary vein. The centrifugal pump makes it possible to provide blood transfer in the volume of 20-50% of the usual systemic blood flow. In the circuit, heparinized trunk systems can be used that eliminate the need for systemic heparinization. Venous bypass helps to maintain renal function and does not increase the overall rates of complications and mortality, but nevertheless it can cause air embolism and lead to thrombosis. In addition, the use of venovenous bypass can prolong the procedure and promote heat loss. In addition, when conducting circumvention, it may be necessary to use inotropic support to maintain the CB.

Native liver removal and non-treatment implantation are usually accompanied by active surgical manipulations under the diaphragm, a decrease in respiratory compliance, the appearance of atelectasis and hypoventilation. At this stage, adding PEEP and increasing inspiratory pressure can help minimize these undesirable effects. Due to the lack of metabolic function of the liver during the non-serous period, the risk of citrate intoxication resulting from rapid blood transfusion is dramatically increased, therefore it is necessary to administer calcium so that the content of ionized calcium is above 1 mmol / l. The most commonly used calcium chloride is bolus 2-4 ml.

During the non-attendant period, progressive hyperkalemia can be treated with insulin infusion, despite the absence of the liver, but metabolic acidosis, including lactate, remains largely uncorrected.

During the non-attendant phase, the consumption of anesthetics is usually very mild. The required concentration of isoflurane can be reduced to 0.6-1.2 vol% (0.5-1 MAK), the need for fentanyl decreases to 1 ± 0.44 μg / kg / h. In most patients, the need for muscle relaxants is sharply reduced.

Non-hepatic (post-afferent, post-perfusional) stage begins with anastomosing the hepatic and portal veins and triggering blood flow through the transplant. Even before removal of the clamps from the vessels for removing air, cell disintegration products and preservative solution, the graft is washed with albumin or blood discharged from the portal vein. Despite this, the final removal of the clamps can cause the discharge of large amounts of potassium and acid metabolites of acids into the bloodstream. At this point, there may be arrhythmias, hypotension and cardiac arrest, and the anesthesiologist should be ready for immediate treatment of these complications due to metabolic causes. To treat hypotension caused by myocardial depression by vasoactive mediators, inadequacy of the right heart with its overload or venous air embolism, inotropic support is necessary. The cause of cardiovascular collapse during reperfusion may be pulmonary thromboembolism.

As a rule, after correction of sudden shifts of hemodynamics arising during reperfusion through the transplant, a period of relative hemodynamic stability is observed. However, the second wave of CCC depression occurs when blood flow is started through the hepatic artery. At this stage there are no signs of an overload of the right heart, there are no prerequisites for hypervolemia and a pronounced vascular dystonia accompanied by a decrease in CB is due to a second toxic wave, i.e. Leaching of acid metabolites from the arterial system of the liver. Stable systemic vasodilation develops quite rapidly, characterized by a marked decrease in diastolic pressure (up to 20-25 mm Hg). To correct this condition, sometimes it is required to connect the vasopressors (mezaton, norepinephrine), the infusion therapy is activated.

In addition to these moments, the period of reperfusion is accompanied by the need to correct violations of the hemocoagulation system. The initial state of hypocoagulation, caused by hepatic insufficiency and a violation of the protein-synthetic function of the liver, is exacerbated by the need for systemic administration of sodium heparin before the beginning of a hardware veinovenous bypass. After its termination, it is necessary to neutralize free heparin sodium with protamine. However, this point may be potentially dangerous, on the one hand, possible thrombosis of vascular anastomoses during the elimination of hypocoagulation, on the other - increased bleeding tissue and continued bleeding, if neutralization is not performed. An indicator that can be considered acceptable by the time of completion of vascular anastomoses is APTTV, equal to 130-140 sec. At these rates, sodium heparin is not used. At the same time, an active infusion of FFP (7-8 ml / kg / h) is carried out, protease inhibitors (aprotinin), a-aminocaproic acid are used. Constant monitoring of coagulation status is very important, because during the operation, pronounced coagulopathy can develop. Some coagulopathies that occur during liver transplantation can be associated with undesirable sequestration of sodium heparin and subsequent washing out of the graft when it is included in the systemic circulation.

The postreperfusion stage is characterized by a gradual increase in the glucose level (up to 12-20 mmol / l) and lactate (up to 8-19 mmol / l). However, as soon as the transplant begins to function, hemodynamic and metabolic stability is gradually restored. The introduction of a large volume of FFP (up to 3-4 liters) and erythrocyte mass can cause an increase in the plasma concentration of citrate, which together with the previous active therapy with sodium bicarbonate can cause the occurrence of metabolic alkalosis. The need for inotropic support usually decreases, and diuresis is increased even in patients with a previous hepatorenal syndrome, although in most cases it is necessary to stimulate it with furosemide. The operation ends with one or another form of recovery of bile outflow - direct anastomosis of the bile ducts of the recipient and the transplant or choledochoejunostomy by Roux.

[7], [8], [9], [10], [11]

Liver transplantation in children

Approximately 20% of orthotopic transplants worldwide are performed in children and a significant proportion of these recipients are younger than 5 years of age. The most common cause of liver failure in children is congenital atresia of the biliary tract, followed by congenital metabolic disorders, which include diseases such as alpha1-antitrypsin deficiency, glycogenoses, Wilson-Konovalov's disease and tyrosinemia. The last three states primarily include biochemical defects of hepatocytes and therefore can only be cured by a procedure such as liver transplantation.

Some aspects of orthotopic liver transplantation in children are unique. For example, sick children with biliary atresia already quite often undergo decompression in the first days or weeks of life through the operation Kasai (choledochoejunostomy). Previous operation on the intestine can complicate laparotomy in the course of pre-care stage of liver transplantation, as well as recovery of bile excretion. Many authors note that a venovenous bypass is often not feasible in patients up to 20 kg, because venous overload of the lower half of the body, accompanying clamping of the portal and inferior vena cava, can lead to oliguria and intestinal complications in young children of this group. A transplant too large is able to sequester a significant part of the blood volume, increasing the risk of excessive release of potassium after reperfusion and leading to severe hypothermia.

However, our own experience has shown the possibility of successful transplantation using a veno-venous bypass in children weighing 10-12 kg. We can note that a problem specific to young children is the temperature imbalance. Moreover, the displacement of body temperature can occur both in the direction of hypothermia, exacerbated during extracorporeal detour, and in the direction of increasing the temperature to 39 ° C. The most effective method of combating hypo- and hyperthermia, in our view, is the use of water thermo-mattresses and thermal suits giving the ability to remove excess heat production or warm the patient, depending on the circumstances.

According to world statistics, the total annual survival of children after orthotopic liver transplantation is 70-75%, but the results for younger (less than 3 years) and small (less than 12 kg) sick children are not so rosy (annual survival is 45-50%). The main reason for the lower survival is the high incidence of hepatic artery thrombosis in young children, which in turn is related to the size of the artery and the use of a split liver of a reduced size.

Correction of violations

In a well-functioning graft, metabolic acids, including lactate, continue to be metabolized and systemic alkalosis arising at the final stage of the operation may require correction. Careful post-operative care for the lungs is necessary, since complications such as damage to the diaphragm, nosocomial pneumonia, RDS with massive blood transfusion are possible. The primary lack of graft function is now a fairly rare complication of liver transplantation, possibly because of the widespread use of modern preservatives and the improvement of surgical techniques and anesthesia techniques.

The precise stage of the operation determines the tactics of the anesthesiologist's actions in accordance with the surgical situation and the patient's condition. The use of modern drugs - isoflurane, midazolam, laxant miros with extrahepatic metabolization (cisatracuria bezilata) makes it possible to increase the manageability of anesthesia and to ensure early extubation of patients.

[12], [13], [14], [15]

Liver transplantation: assessment of the patient's condition after surgery

The use of modern anesthesia techniques based on modern anesthetics of isoflurane and sevoflurane made it possible to drastically reduce the time of postoperative artificial and auxiliary ventilation of the lungs to 2-4 hours. Early extubation significantly reduces the number of possible complications from the respiratory system, but leaves the actual problem of adequate and reliable anesthesia in the postoperative period. For this purpose, opioids are traditionally used - morphine, trimeperidine, tramadol, and also ketorolac and other drugs. Doses are selected strictly individually. The appointment of immunosuppressants (prednisolone, cyclosporine) causes the presence of almost constant hypertension in these patients. In some patients, during early adaptation, headaches, convulsive alertness are noted.