Bleeding from esophageal varices in portal hypertension syndrome. Bleeding from esophageal varices
Bleeding from these veins is usually hidden, difficult to stop, and usually occurs against the background of coagulopathy, thrombocytopenia, and sepsis.
Drugs that cause mucosal erosions, such as salicylates and other NSAIDs, can also cause bleeding. Varicose veins in other areas become a source of bleeding relatively rarely.
Bleeding from esophageal varices: diagnosis
Anamnesis and general examination may suggest that varicose veins are the cause. gastrointestinal bleeding. In 30% of patients with liver cirrhosis, another source of bleeding is identified. If a disease is suspected, it is necessary to perform fibrogastroduodenoscopy as early as possible. Along with rupture of varicose veins of the stomach and esophagus, the cause of bleeding in rare cases is hypertensive gastropathy.
Bleeding from esophageal varices: conservative therapy
Transfusion of blood, fresh frozen plasma and platelets depending on hematological parameters. Vitamin K is administered in a dose of 10 mg intravenously once to exclude its deficiency. Avoid excess transfusion.
Metoclopramide 20 mg is administered intravenously. This drug allows you to briefly increase blood pressure lower section esophagus and thereby reduce blood flow in the v. system. azy-gos.
Antibacterial therapy. A sample of blood, urine, and ascitic fluid is collected for culture and microscopy. Several studies have found an association with sepsis. Antibiotics are prescribed. Duration antibacterial therapy should be 5 days.
Terlipressin causes vasospasm in the celiac trunk, thereby stopping bleeding from the esophageal varices of the esophagus (decreasing mortality by approximately 34%). Serious side effects occur in 4% of cases and include myocardial ischemia, peripheral vasospasm, which may be accompanied by serious arterial hypertension, skin ischemia and circulatory disorders internal organs. Nitrates may reverse the peripheral effects of vasopressin but are not usually prescribed to treat the side effects of terlipressin. Octreotide is a synthetic analogue of somatostatin. It has no side effects on the heart, and therefore the administration of nitrates during its administration is not required. According to latest research from the Cochrane Database, octreotide does not affect disease mortality and has minimal effect on the need for transfusion therapy.
Endoscopic introduction of scerosing substances into the varicose veins and surrounding tissues allows to stop acute bleeding. Side effects (serious - in 7%) include the occurrence of chest pain and fever immediately after injection, the formation of ulcers on the mucous membrane, and late strictures of the esophagus. In the future, the administration of scerosing substances should be continued until the veins are completely obliterated. The greatest difficulties arise when performing injections into the gastric varices; in this case, thrombin should be used.
Ligation of varicose veins is often used.
Balloon tamponade with a Sengstaken-Blakemore or Linton probe. Usually only this is enough to stop the bleeding. The probe should not be used for more than 12 hours due to the risk of ischemia, the risk of which increases with simultaneous administration of terlipressin.
Treatment liver failure: to prevent encephalopathy, lactulose should be prescribed orally or through a tube, 10-15 ml every 8 hours, as well as thiamine and multivitamin preparations. Patients with severe encephalopathy are prescribed magnesium sulfate and phosphate enemas.
In case of acute bleeding from varicose veins of the esophagus, the correction of hemodynamic disturbances (infusion of blood and plasma products) is of utmost importance, since under conditions of hemorrhagic shock, blood flow in the liver decreases, which causes a further deterioration of its functions. Even in patients with confirmed varicose veins veins of the esophagus, it is necessary to establish the localization of bleeding using FEGDS, since in 20% of patients other sources of bleeding are identified.
Local treatment
To stop bleeding from esophageal varices, endoscopic techniques, balloon tamponade, and open dissection of the esophagus are used.
Esophageal vein ligation and sclerotherapy
These are the most commonly used initial treatments. Ligation is a more complex procedure than sclerotherapy. If there is active bleeding, endoscopic procedures may be difficult. In such cases, balloon tamponade should be performed.
Balloon tamponade
A Sengstaken-Blakemore probe with 2 tamponade balloons is used. There are modified versions of the probe (for example, Minnesota tube) that allow aspiration of the contents of the stomach and esophagus. The probe is inserted through the mouth, its penetration into the stomach is controlled by auscultation of the epigastric region during balloon inflation or x-ray. Light traction is necessary to ensure compression of the varicose veins. The first step is to fill only the gastric balloon with air (200-250 ml) - this measure is usually sufficient to stop bleeding. Filling of the gastric balloon should be stopped if the patient experiences pain, since if the balloon is incorrectly placed in the esophagus, rupture may occur during its filling. If gastric tamponade is not enough to stop bleeding and you have to resort to esophageal tamponade, the esophageal balloon should be deflated for 10 minutes every 3 hours. The pressure in the esophageal balloon is monitored using a sphygmomanometer. Special attention When placing a tube, care should be taken to prevent aspiration of gastric contents (if necessary, the patient is intubated).
Esophageal dissection
Ligation of varicose veins can be done using a stapler, although there is a risk of further development of esophageal stenosis; the operation is usually combined with splenectomy. This procedure usually used if there is no effect from all other methods of therapy listed above and it is impossible to perform transjugular intrahepatic portacaval shunting. Surgeries are associated with frequent complications and high mortality.
X-ray vascular therapy methods
IN specialized centers transvenous intrahepatic portosystemic shunting is possible. Access through the jugular or femoral vein catheterizes the hepatic veins and between them (low pressure system) and the portal venous system ( high pressure) an expandable stent is inserted. The pressure in the portal vein should decrease to 12 mm or lower.
Surgery
Urgent portacaval shunting allows to stop bleeding in more than 95% of cases, but is characterized by high (>50%) intraoperative mortality and does not affect long-term survival. This treatment method is currently used only in isolated cases.
Prognosis for varicose veins of the esophagus
Mortality rate overall is 30%. It is higher in patients with severe liver disease.
The effectiveness of therapy aimed at stopping bleeding from the esophageal varices
Injection of sclerosing drugs or vein ligation - 70-85%.
Balloon tamponade - 80%.
Terlipressin - 70%.
Octreotide - 70%.
Vasopressin and nitrates - 65%.
Bleeding from varicose veins (hereinafter referred to as varicose veins) of the esophagus. Long-term therapy
Injection of a scerosing drug in a volume of 0.5-1 ml into the tissue around the cervical vein or 1-5 ml into varicose veins every week until the veins are completely obliterated; then at intervals of 3-6 months.
Ligation is carried out in the same regimen as sclerotherapy, with obliteration of varicose veins occurring faster (39 days versus 72 days).
The administration of propranolol reduces the frequency of relapses. No reduction in mortality was noted.
Transvenous intrahepatic portosystemic shunt and other shunt procedures are considered to be more reliable in preventing rebleeding, which can only occur if the shunt is blocked. However, when they are carried out, the incidence of chronic hepatic encephalopathy increases.
Prevention of rebleeding
During endoscopic ligation, varicose veins are aspirated into the lumen of a special endoscopic instrument and tied using elastic rubber bands. The ligated vein is subsequently obliterated. The procedure is repeated every 1-2 weeks until the veins are obliterated. In the future, regular endoscopic monitoring is necessary for timely treatment recurrence of varicose veins. Endoscopic ligation is generally more effective than sclerotherapy. To prevent secondary bleeding due to ulcerations induced by ligatures, antisecretory therapy with Na + , K + -ATPase (proton pump) inhibitors is prescribed.
Sclerosing therapy
Sclerotherapy is the introduction of sclerosing agents into varicose veins. After the introduction of endoscopic ligation, this method is used relatively rarely. Sclerosation therapy is not without its drawbacks, as it may be accompanied by transient pain, fever, temporary dysphagia, and sometimes esophageal perforation. It is also possible to develop esophageal strictures.
Transjugular intrahepatic portacaval shunt
The operation consists of installing an intrahepatic stent between the portal and hepatic veins, which provides portacaval shunting and reduces pressure. The procedure is performed under x-ray control. Before surgery, it is necessary to confirm the patency of the portal vein using angiography and prescribe prophylactic antibiotic therapy. The occurrence of rebleeding is usually associated with narrowing or occlusion of the shunt (appropriate examination and treatment, such as angioplasty, is necessary). Transjugular intrahepatic portacaval shunting can provoke the development of hepatic encephalopathy; to relieve it, it is necessary to reduce the diameter of the shunt.
Portocaval shunt operations
Portocaval shunt operations help prevent recurrent bleeding. The application of non-selective portacaval shunts leads to an excessive reduction in the flow of portal blood into the liver. Taking this into account, selective bypass operations have been developed, in which the risk of developing postoperative hepatic encephalopathy is lower. However, over time, hepatic portal blood flow decreases.
P-adrenergic receptor antagonists (p-blockers)
Propranolol or nadolol reduce blood pressure. They can be used to prevent recurrent bleeding. However, for secondary preventionβ-blockers are rarely used. Treatment compliance with these drugs may be low.
Mallory-Weiss syndrome
Rupture of the mucous membrane in the area of the esophagogastric junction, which occurs as a result of strong gagging movements and is especially often observed with excessive consumption alcohol. At first, the vomit is of normal color, and then blood appears in it.
Treatment
- In most cases, bleeding stops spontaneously. Tamponade with a Sengsteken-Blakemore probe may be required.
- In some cases it is necessary to perform surgery with suturing of a bleeding vessel or selective angiography with embolization of the feeding artery.
- The Child score can effectively determine the severity of liver disease in a patient with cirrhosis. It should not be used in patients with primary biliary cirrhosis or spersosing cholangitis.
- Group A<6 баллов.
Bleeding from varicose veins of the esophagus is a severe complication of a number of diseases of the upper gastrointestinal tract and liver, associated with the onset of heavy hemorrhage into the lumen of the organs. This condition is characterized by a rapid onset and a negative response to any type of treatment other than surgery. It is very important to understand the general manifestations of this complication and the principles of its treatment, both at the first and emergency care, and in a medical hospital setting.
Varicose veins are frequent companions of liver diseases and other diseases of the gastrointestinal tract.
Esophagoscopy: esophageal varices
Causes
Bleeding from the veins of the esophagus can occur as a result of a number of diseases of the digestive tract, ranging from direct damage to the esophagus and ending with liver pathology. It is liver damage as a result of viral or toxic damage that is the most common cause of esophageal varicose veins.
Local causes of the development of this complication include any processes with damage to the mucous membrane of the esophagus - reflux esophagitis, inflammatory conditions of other causation, Barrett's esophagus, tumors, most often adenocarcinoma or squamous cell carcinoma. In addition, bleeding can develop as a result of trauma to the esophagus by a foreign body, burn injuries, or ingestion of other toxic substances. Do not forget that the source of bleeding can be an esophageal diverticulum or strangulation of the hernial sac in diaphragmatic hernias. A special place among the causes is occupied by medical errors during diagnostic procedures and surgical operations.
However, the most important disease leading to bleeding is cirrhosis and other chronic liver diseases with the development of portal blood stasis and esophageal varicose veins. These conditions lead to expansion of the superficial venous plexus in the lower part of the esophagus. These venous vessels are located directly under the mucous membrane. They are very easily injured and become a source of heavy bleeding, which is very difficult to stop using traditional methods.
Main manifestations
Bleeding from the esophageal veins does not occur very often. However, in the presence of an underlying disease affecting the esophagus, stomach or liver, the risk of this terrible complication increases several times. Chronic bleeding from small defects of the mucous membrane, as a rule, does not have pronounced symptoms and is manifested by an anemic syndrome - increased fatigue of the patient, rapid physical and mental fatigue, pallor skin and mucous membranes, frequent headaches and dizziness. All these symptoms should be the reason for prescribing a clinical blood test, where an experienced doctor, based on the number of red blood cells and hemoglobin, will easily identify chronic anemia and prescribe additional examination.
Chronic anemia can be caused by prolonged bleeding from varicose veins
Acute bleeding is most often profuse and manifests itself with various symptoms, which can be single or multiple. The most characteristic manifestation is bloody vomiting “mouth full”. The blood is bright red, but there are no clots - these are characteristic signs of acute, massive bleeding caused by injury or acute ulceration in the wall of the organ. If the bleeding is small, the color of the vomit resembles coffee due to the formation of hydrochloric acid hematin - hemoglobin changed under the influence of hydrochloric acid.
Bleeding from esophageal varices (EVV) is distinguished by the dark cherry color of the blood and the frequent presence of clots. However, it is important to remember that in a real situation it is impossible to determine the source of bleeding only by the nature of the blood.
The second most common symptom is changes in stool. A characteristic manifestation of bleeding in the gastrointestinal tract is melena, or a change in the properties of feces. It becomes black, semi-liquid, and looks like tar. It is worth noting that this symptom does not appear immediately after the start of bleeding, but is characteristic of the late stage of bleeding (several hours after it starts), since the blood takes time to pass through the gastrointestinal tract to the rectum.
A characteristic symptom of acute bleeding associated with ulceration of dilated veins is pain localized in the lower part of the chest in the retrosternal region or in the upper, epigastric part of the abdomen. Rarely, URVP may be the cause of snoring during pregnancy.
Bleeding may be accompanied by pain
Basic diagnostic methods
The development of this complication can be suspected by detailed questioning of the patient or his relatives about the conditions under which bleeding occurred (lifting heavy objects, taking suspicious liquids, etc.), as well as the presence of concomitant diseases of the gastrointestinal tract (liver cirrhosis, chronic hepatitis, gastroesophageal reflux disease, peptic ulcer). stomach).
A screening method for the presence of chronic bleeding is a general and clinical blood test, which allows you to determine the hemoglobin concentration and the number of red blood cells. Chronic blood loss is characterized by a decrease in these parameters. In addition, if there are difficulties in making a diagnosis, a stool test for occult blood is used if the patient does not have characteristic melena-type stool changes.
The “gold standard” in making a diagnosis is endoscopic examination of the lumen of the esophagus. This method allows you to visually assess the presence of bleeding in the esophagus, identify its source and determine further treatment tactics depending on the volume and nature of the lesion, as well as the intensity of blood loss.
Bleeding from varicose veins is an emergency condition that requires immediate hospitalization and professional medical care.
Treatment
Bleeding from dilated veins of the esophagus requires emergency care, both at the stages of first and at the stage of professional medical care in a hospital setting.
Principles of First Aid
First aid is aimed at reducing blood loss and should be provided by any person in our country. Due to the fact that it is impossible to apply tourniquets or simply compress the vessel in this condition, the optimal solution at this stage of treatment is to provide the patient with physical rest in a lying position, as well as psychological support.
If you suspect esophageal bleeding, call an ambulance immediately
It is important to call an ambulance, or, if possible, quickly transport the patient to a medical facility for highly specialized medical care.
Treatment in hospital
The main method of emergency medical care is the use of a Blackmore tube, which is an inflatable tube inserted into the esophagus. When inflated, this probe compresses the dilated venous vessels in the wall of the organ and stops bleeding. At the same time, the patient should receive abundant infusion therapy with various solutions (Disol, Trisol, isotonic sodium chloride solution) to replenish the volume of circulating blood and prevent the development of a state of shock.
After the condition is compensated and normalized, other treatment methods are started in case of low effectiveness of the probe. The main method of treatment in this case is surgical intervention aimed at ligating or ligating the dilated veins of the esophagus, to form anastomoses between the portal vessels and other venous systems of the body. The last step allows you to unload the portal system and reduce blood flow to the esophageal veins.
Never self-medicate for such complications! Even qualified medical care does not guarantee 100% recovery.
Varicose veins of the esophagus are very often complicated by the onset of bleeding. In this regard, patients with this disease should be monitored and undergo regular medical examinations in order to determine the risk of bleeding and choose tactics for its prevention and treatment.
Pediatric surgery: lecture notes by M. V. Drozdov
LECTURE No. 6. Bleeding from dilated veins of the esophagus with portal hypertension
The most severe and common complication of portal hypertension syndrome is bleeding from esophageal varices.
The cause of bleeding is mainly an increase in pressure in the portal system, the peptic factor, as well as disorders in the blood coagulation system. Bleeding from dilated veins of the esophagus may be the first clinical manifestation of portal hypertension.
The first indirect signs of beginning bleeding are the child’s complaints of weakness, malaise, nausea, and lack of appetite.
Body temperature rises. The sudden appearance of profuse bloody vomiting explains the sharp deterioration in the child’s general condition.
Vomiting recurs after a short period of time. The child turns pale, complains of headache, dizziness, becomes lethargic and drowsy. Tarry, foul-smelling stool appears.
Blood pressure decreases to 80/40–60/30 mmHg. Art. A blood test reveals increasing anemia. The volume of circulating blood decreases sharply. After 6-12 hours, the severity of the condition is aggravated by intoxication as a result of the absorption of blood breakdown products from the gastrointestinal tract.
Differential diagnosis
The symptom of hematemesis in children can be caused not only by bleeding from varicose veins of the esophagus. To determine the cause of bleeding, anamnestic data are of primary importance.
If a child is admitted to the surgical clinic again due to bleeding due to portal hypertension syndrome or has undergone surgery for this disease, then the diagnosis should not be in doubt.
It is more difficult to carry out a differential diagnosis if bleeding was the first manifestation of portal hypertension, since similar clinical symptoms occur in children with a bleeding stomach ulcer, with a hiatal hernia, after severe nosebleeds (in children with Werlhof's disease and hypoplastic anemia).
Children with bleeding from a chronic gastric ulcer usually have a characteristic and long-lasting “ulcerative” history. Profuse bleeding occurs extremely rarely in them.
An acute ulcer in children who have been receiving hormonal therapy for a long time is also rarely complicated by bleeding (perforation is more typical), but if there is an appropriate history, the diagnosis usually does not cause difficulties.
In children with a hiatal hernia, periodic bloody vomiting is not profuse, and the presence of “black” stool is not always observed.
The child's general condition deteriorates slowly over many months.
Children are usually admitted to the clinic with mild anemia of unknown etiology. Clinical and radiological examination determines the presence of a hiatal hernia.
The cause of bloody vomiting that occurs after nosebleeds is clarified by taking a detailed history and examining the patient.
Treatment
In all cases of bleeding, treatment measures should begin with complex therapy.
Conservative therapy in some cases it leads to stopping bleeding. Once the diagnosis is established, the child is given a blood transfusion.
The amount of blood administered depends on the general condition of the child, hemoglobin levels, red blood cell count, hematocrit and blood pressure.
Sometimes 200–250 ml is required, and in case of severe unstoppable bleeding, 1.5–2 liters of blood products are transfused on the first day.
You should more often resort to direct transfusions, combining them with transfusion of conservative blood. For hemostatic purposes, concentrated plasma, Vicasol, pituitrin are administered; aminocaproic acid, adroxon, thrombin, and hemostatic sponge are prescribed orally.
The child is completely excluded from oral feeding and is prescribed parenteral administration of an appropriate amount of fluid and vitamins (C and group B).
The infusion is carried out slowly, since a sharp overload of the vascular bed can lead to re-bleeding. An ice pack should be placed on the epigastric area.
All children are prescribed broad-spectrum antibiotics and detoxification therapy. To combat hypoxia, humidified oxygen is constantly given through nasal catheters. In case of severe intractable bleeding, hormonal therapy is included (prednisolone 1–5 mg per 1 kg of child’s body weight per day).
Patients with intrarenal portal hypertension are prescribed a 1% solution of glutamic acid to prevent liver failure. If conservative treatment is successful, after 4–6 hours the general condition improves somewhat.
Pulse and blood pressure are leveled out and made stable. The child becomes more contact and active. All this gives reason to believe that the bleeding has stopped, but despite the improvement in the general condition, treatment measures should be continued.
In the absence of repeated bloody vomiting, the drip infusion device is removed after 24–36 hours. The child is given chilled kefir, milk, and cream. Gradually, the diet is expanded, on the 3-4th day puree, 10% semolina porridge, broth are prescribed, from the 8th-9th day - a common table.
Blood transfusions are carried out 2-3 times a week, and vitamin administration is continued. The course of antibiotics is completed on the 10-12th day. Hormonal drugs are canceled, gradually reducing their dosage.
After the child’s general condition improves, a detailed biochemical blood test, splenoportography and tonometry are performed to determine the shape of the portal system block in order to choose a rational method of further treatment.
Along with the indicated conservative therapy, try to mechanically stop the bleeding. This is achieved by inserting an occlusive Blackmore probe into the esophagus, the inflated cuff of which presses the esophageal varices.
Sedatives are prescribed to reduce anxiety associated with the tube being in the esophagus. If during this period the conservative measures taken have not stopped the bleeding, the question of urgent surgical intervention should be raised.
The choice of method of surgical treatment at the height of bleeding primarily depends on the general condition of the patient and on whether the child has been operated on for portal hypertension before or the bleeding occurred as one of the first manifestations of portal hypertension.
In children who have previously been operated on for portal hypertension (splenectomy, creation of organ anastomoses), the operation is reduced to direct ligation of varicose veins of the esophagus or the cardia of the stomach. In patients who have not previously been operated on for portal hypertension syndrome, surgery should be aimed at reducing the pressure in the v. portae by reducing blood flow to esophageal varices.
At the time of suturing varicose nodes, severe bleeding may occur; esophagotomy is sometimes complicated by infection of the mediastinal space, the development of purulent mediastinitis and pleurisy.
In order to reduce blood flow to varicose veins of the esophagus, a modified operation is used
Tanner - suturing the veins of the precordial region without opening the lumen of the stomach. The latter significantly shortens the time of surgical intervention (which is especially important during surgery at the height of bleeding), reduces the risk of infection of the abdominal cavity and minimizes the possibility of gastric suture failure.
In children who have not previously been examined for portal hypertension, surgical splenoportography and splenometry are performed to resolve the issue of the form of the disease and the extent of intervention. If an intrahepatic block is detected, in addition to suturing the cardiac part of the stomach, it is rational to simultaneously create organoanastomoses: suturing the omentum to the decapsulated kidney and to the left lobe of the liver after its marginal resection. In the presence of pronounced hypersplenism, the spleen is removed. The abdominal cavity is then closed tightly after antibiotics are administered.
Postoperative treatment is a continuation of the activities carried out before the operation. A child needs parenteral nutrition for 2–3 days. Then the patient begins to drink, gradually expanding the diet (kefir, 5% semolina, broth, etc.). By the 8th day, the usual postoperative table is prescribed. Hormonal therapy is canceled on the 4-5th day, the administration of antibiotics is completed on the 7-10th day after surgery. Blood and plasma transfusions are prescribed daily (alternating) until anemia is eliminated.
If the postoperative period is smooth, on the 14th–15th day the children are transferred to a pediatric clinic for further treatment.
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RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2015
Gastroesophageal rupture-hemorrhagic syndrome (K22.6), Portal hypertension (K76.6)
Gastroenterology, Surgery
general information
Short description
Recommended
Expert advice
RSE at PVC "Republican Center for Health Development"
Ministry of Health
and social development
dated September 30, 2015
Protocol No. 10
Protocol name: Bleeding from esophageal varices in portal hypertension syndrome
Bleeding from
varicose veins esophagus is a complication of portal hypertension syndrome. Esophageal varices are portosystemic collaterals that connect the portal venous and systemic venous circulations. They form as a sequence of development of portal hypertension, mainly in the submucosa of the lower esophagus. As a result of portal crises, the pressure in the vessels of the portal system increases several times, leading to ruptures of the walls of varicose veins in areas with reduced resistance due to dystrophic changes, which is a necessary condition for the development of bleeding.Protocol code:
ICD-10 code(s):
K22 Other diseases of the esophagus
K22.6 Gastroesophageal rupture-hemorrhagic syndrome
K76.6 Portal hypertension
Abbreviations used in the protocol:
BP - blood pressure;
ALT - alanine aminotransferase;
AST - aspartate aminotransferase;
APTT - activated partial thromboplastin time;
AFP - tumor marker alpha-fetoprotein;
varicose veins;
HSH - hemorrhagic shock;
DIC - disseminated intravascular coagulation;
ITT - infusion-transfusion therapy;
CT - computed tomography;
LDH - lactate dehydrogenase;
INR - international normalized ratio;
NSAIDs - non-steroidal anti-inflammatory drugs;
BCC - circulating blood volume;
PT - prothrombin time;
PP - portal pressure;
FDP is a product of fibrinogen degradation;
PTI - prothrombin index;
SBP - systolic blood pressure
PPH - portal hypertension syndrome;
TV - thrombin time;
EL - level of evidence;
Ultrasound - ultrasound examination;
FA - fibrinolytic activity;
CVP - central venous pressure;
LC - liver cirrhosis;
RR - respiratory rate;
HR - heart rate;
ALP - alkaline phosphatase;
EG - endoscopic hemostasis
ECG - electrocardiography;
EFGDS - esophagogastroduodenoscopy;
D-dimer is a fibrin breakdown product;
EVL - endoscopic vein ligation;
Hb - hemoglobin;
Ht - hematocrit;
ISMN - nitrates;
NBSS - non-selective β-blockers;
HRS - hepatorenal syndrome;
SBP - spontaneous bacterial peritonitis;
HE - hepatic encephalopathy;
AOS - acid-base state;
ELISA - enzyme-linked immunosorbent assay;
ACE - alpha-ketoprotein;
TIPS - transjugular portosystemic shunt;
MON - multiple organ failure;
MAP - mean arterial pressure.
Date of protocol development/revision: 2015
Protocol users: surgeon, anesthesiologist-resuscitator, ambulance and emergency doctor, paramedic, functional diagnostics doctor (endoscopist), gastroenterologist, therapist, general practitioner.
| Classification | Description |
| Class I | Conditions for which there is evidence and/or general agreement that the given diagnostic evaluation, procedure, or treatment is useful, helpful, and effective |
| Class II | Conditions for which there is conflicting evidence and/or divergence of opinion about the usefulness/effectiveness of a diagnostic evaluation, procedure, or treatment. |
| Class IIa | Weight of evidence/opinion in favor of usefulness/effectiveness. |
| Class IIb | Usefulness/effectiveness is less clearly established by evidence/opinion. |
| Class III | Conditions for which there is evidence and/or general agreement that the diagnostic evaluation/procedure/treatment is not helpful/effective and in some cases may be harmful. |
Level of Evidence Table
The table of recommendations is taken from this source:
Prevention and treatment of gastroesophageal varices and esophageal varices bleeding in liver cirrhosis
Guadalupe Garcia-Cao, Dr. medical sciences, 1 Arun J. Sanyal, MD, 2 Norman D. Grace, MD, FACG, 3 William D. Carey, MD, MACG, 4 American Association for the Study of Liver Diseases Practice Guidelines Committee and the American Association for the Study of Liver Diseases Practice Parameters Committee College of Gastroenterology
1 Division of Digestive Diseases, Yale University School of Medicine and VA-CT Health System, New Haven, CT; 2 Department of Gastroenterology, Virginia Commonwealth University Medical Center, Richmond, Virginia, 3 Department of Gastroenterology, Brigham and Women's Hospital in Boston, Massachusetts; 4 Cleveland Clinic, Cleveland, Ohio
Classification
Clinical classification:
Classification of varicose veins of the esophagus and stomach according to Paquet (1983):
1st degree- single venous ectasia;
2nd degree- single well-demarcated vein trunks, mainly in the lower part of the esophagus, which remain clearly visible during air insufflation. The shape of the veins is tortuous, there is no narrowing of the lumen of the esophagus, there is no thinning of the epithelium on the veins and there are no red wall markers;
3rd degree- a distinct narrowing of the lumen of the esophagus by the trunks of the esophagus, located in the s/z and n/s of the esophagus, which only partially decrease with air insufflation. The nodular shape of the veins is noted, with “red markers” at the tops of the veins.
4th degree- the lumen of the esophagus is completely filled with varicose veins, the dilation of the veins affects the intraocular esophagus. The epithelium over the veins is thinned, and many “red markers” of the wall are visible.
Three-degree classification (Soehendra N., Bimoeller K., 1997):
esophageal esophagus:
I degree- the diameter of the veins does not exceed 5 mm, they are elongated and are located only in the lower part of the esophagus;
II degree- ERV with a diameter of 5 to 10 mm, convoluted, extending to the middle third of the esophagus inclusive;
III degree- the size of the veins is more than 10 mm, the shape is nodular, tense with a thin wall, located close to each other, there are “red markers” on the surface of the veins.
VRV of the stomach:
I degree- the diameter of the veins is no more than 5 mm, barely visible above the gastric mucosa;
II degree- VVV from 5 to 10 mm, solitary-polypoid character;
III degree- veins with a diameter of more than 10 mm, represent an extensive conglomerate of nodes, thin-walled, polypoid in nature. For practical purposes, it is important to take into account the tortuous shape of the veins (grade II - moderate risk of bleeding) and nodular (grade III - high risk of bleeding).
Classification of gastric varices:
ARVZh are classified depending on location.
Gastroesophageal veins (GOV) - VVs passing from the esophagus to the stomach - are divided into 2 types:
· 1st type (GOV1) - run along the lesser curvature of the stomach (the principles of treatment correspond to the principles of treatment of varicose veins);
· Type 2 (GOV2) - located in the fundus of the stomach, more extended and tortuous.
Isolated gastric veins (IGV) develop in the absence of dilation of the esophageal veins and are divided into 2 types:
· Type 1 (IGV1) - located in the fundus of the stomach, tortuous (occurs with thrombosis of the splenic vein);
· Type 2 (IGV2) - occur in the body of the stomach, antrum or around the pylorus. The veins located in the fundus of the stomach (fundic veins) pose the greatest danger. Other risk factors are the size of the nodes, the class of CPU, and the presence of the “red spot” symptom.
The division into degrees of VRVZ is based on the same parameter as the division of VRVZ - on the size of the nodes:
· 1st degree - the diameter of the ventricular vein is no more than 5 mm, the veins are barely visible above the gastric mucosa;
· 2nd degree - the diameter of the varicose veins is 5-10 mm, the veins are solitary-polypoid in nature;
· 3rd degree - the diameter of the varicose vein is more than 10 mm, the veins are thin-walled, polypoid in nature, and represent an extensive conglomerate of nodes.
The American Association for the Study of Liver Diseases (AASLD) classification distinguishes 3 stages of varicose veins:
· 1st stage- small veins, minimally rising above the esophageal mucosa;
· 2nd stage- middle veins, tortuous, occupying less than a third of the lumen of the esophagus;
· 3rd stage- large veins.
International classifications propose using the most simplified division of varicose veins into 2 stages:
· Small veins(up to 5 mm);
· Large veins(more than 5 mm), since the risks associated with bleeding are the same for medium and large veins. The incidence of bleeding is 5-15% per year, it stops spontaneously in 40% of patients, and again, in the absence of treatment, develops in approximately 60% of patients, on average within 1 to 2 years after the first episode.
Clinical picture
Symptoms, course
Diagnostic criteria for diagnosis:
Complaints and anamnesis:
Complaints:
· vomiting scarlet (fresh) blood/coffee grounds;
· tarry stool/loose stool with slightly changed blood (clinical signs of bleeding);
· weakness;
· dizziness;
· cold sticky sweat;
· noise in ears;
· frequent heartbeat;
· short-term loss of consciousness;
Thirst and dry mouth (clinical signs of blood loss).
History of the disease:
· intake of rough, spicy food, alcohol, medicines(NSAIDs and thrombolytics);
· repeated vomiting, bloating, heavy lifting;
· suffers from liver cirrhosis, previous hepatitis, suffers from chronic alcoholism;
· history of bleeding episodes;
· previous endoscopic ligation of esophageal varices, sclerotherapy of veins.
Physical examination(Appendix 1, 2):
State patient with severe blood loss:
· restless behavior;
Confusion of consciousness lethargy;
· there is a picture of collapse, up to coma;
General inspection:
yellowness of the sclera/skin;
· pallor of the skin;
· skin covered with cold sweat;
· decreased skin turgor;
· increase in abdominal volume (ascites);
· presence of dilated veins on the lateral surface of the abdomen (head of the jellyfish);
· percussion borders of the liver are enlarged (may be reduced);
· palpation of the surface of the liver is lumpy, the edges are rounded;
· presence of telangiectasia on the skin;
· liver palms;
· the presence of edema in the lower extremities, in the lateral and lower abdomen;
· pulse character > 100 per minute, frequent, weak filling;
· GARDEN (< 100 мм.рт.ст.) тенденция к снижению в зависимости от степени кровопотери;
· NPV (20 and > 1 min) tends to increase;
oxygen saturation in venous blood < 90%.
Diagnostics
List of basic and additional diagnostic measures:
Basic (mandatory) diagnostic examinations performed on an outpatient basis: not performed.
Additional diagnostic examinations performed on an outpatient basis: not performed.
Minimum list of examinations that must be carried out when referring for planned hospitalization: not carried out
Basic (mandatory) diagnostic examinations carried out at the inpatient level (in case of emergency hospitalization, diagnostic examinations are carried out that were not carried out at the outpatient level):
physical examination (pulse counting, respiratory rate calculation, blood pressure measurement, saturation measurement, finger examination rectum);
· general analysis blood;
· general urine analysis;
· biochemical analysis blood (total protein and its fractions, bilirubin, ALT, AST, alkaline phosphatase, LDH, cholesterol, creatinine, urea, residual nitrogen, blood sugar),
· CBS;
· determination of blood group according to the ABO system;
Determination of the Rh factor of blood;
· coagulogram (PTI, INR, TV, APTT, fibrinogen, clotting time);
· D-dimer;
· PDF;
· ECG;
· EFGDS remove previously noted level of evidence
Additional diagnostic examinations carried out at the inpatient level (in case of emergency hospitalization, diagnostic examinations are carried out that were not carried out at the outpatient level):
· determination of hepatitis markers using ELISA;
· determination of tumor marker (AFP) by ELISA;
· bacteriological culture urine;
· Ultrasound of the abdominal organs;
Ultrasound of the kidney;
· CT scan of the abdominal cavity;
· X-ray examination of the esophagus and stomach with contrast (double contrast);
· splenoportography.
Diagnostic measures carried out at the stage of emergency care:
· collection of complaints, medical history and life history;
· physical examination (pulse count, heart rate, respiratory rate count, blood pressure measurement).
Instrumental studies:
ECG- changes are observed that depend on the initial state of cardio-vascular system(signs of myocardial ischemia, decreased T wave, ST segment depression, tachycardia, rhythm disturbance).
EFGDS - the presence of dilated veins of the esophagus, their length, shape (twisted or stem), location, size, state of hemostasis, predictors of the risk of bleeding (red markers).
EGD should be performed as early as possible. Dates this study is 12-24 hours from the moment the patient arrives(UD - class I, level A).
On EGD, the presence or absence of red signs on varicose veins of the esophagus and stomach should be noted (UD-class IIa, level C).
Indications for consultation with specialists:
· consultation with a nephrologist if kidney pathology is suspected;
· consultation with an oncologist if cancer is suspected;
· consultation with an infectious disease specialist upon detection infectious diseases and development toxic hepatitis;
· consultation with a cardiologist for pathology of the cardiovascular system;
· consultation with a neurologist when identifying pathology from nervous system;
· consultation with an obstetrician-gynecologist in the presence of pregnancy to resolve issues of treatment tactics.
Laboratory diagnostics
Laboratory research:
· general blood analysis: decreased red blood cell count, hemoglobin (Hb) and hematocrit (Ht) levels;
· blood chemistry: an increase in blood sugar above 6 µmol/l, bilirubin above 20 µmol/l, an increase in the level of transaminases (ALT, AST) 2 times or more from the norm, an increase in thymol > 4 units, a decrease in the sublimate test, alkaline phosphatase, LDH-214- 225 U/l; cholesterol reduction< 3,6 ммоль/л, снижение общего белка < 60 г/л, альбумина < 35 г/л, снижение альбумин/глобулинового коэффициента ниже 1,5, повышение креатинина >105 µmol/l or an increase of 0.5 µmol/l, urea > 6.5 mmol/l.
· coagulogram: decrease in PTI< 70%, фибриноген < 2 г/л, АЧТВ >60 sec., PT > 20%, TT > 15 sec., INR > 1.0, prolongation of FA, clotting time, fibrinogen degradation products > 1/40, dimers > 500 ng/ml; KOS - pH< 7,3, дефицит оснований ≥ 5 ммоль/л, повышение уровня лактата >1 mmol/l;
· electrolytes: decrease in K, Na, Ca;
· hepatitis markers: identified markers indicate the presence of one or another viral infection;
· blood test for tumor markers: increase in AFP tumor markers above 500 ng/ml (400 IU/ml).
Differential diagnosis
Differential diagnosis:
Table 1. Differential diagnosis bleeding from varicose veins of the esophagus with portal hypertension syndrome.
| Diseases | Features of the disease history and clinical manifestations | Endoscopic signs |
| Bleeding from acute and chronic ulcers and erosions of the stomach and duodenum | More often, stress, long-term use of medications (NSAIDs, thrombolytics), poisoning with surrogates of alcohol, poisons, severe trauma, major surgery, diabetes mellitus, heart failure, history of ulcers | The presence of an ulcerative defect within the mucous membrane of the stomach and duodenum or deep defects affecting all layers of the wall, of various diameters, single or multiple without inflammatory and with an inflammatory shaft. Signs of bleeding according to J. Forrest classification. |
| Hemorrhagic gastritis | More often after long-term use medicines, alcohol, against the background of sepsis, acute renal failure and chronic renal failure | Absence of ulcers in the stomach or duodenum, the mucous membrane is swollen, hyperemic, abundantly covered with mucus, multiple erosions |
| Mallory-Weiss syndrome | Suffering from toxicosis of pregnancy, acute pancreatitis, cholecystitis. More often after prolonged and heavy drinking of alcohol, repeated vomiting, first with food, then with blood | More often, the presence of longitudinal ruptures of the mucous membrane in the esophagus, gastric cardia of varying lengths |
| Bleeding from disintegrating cancer of the esophagus, stomach | Presence of minor symptoms: increased fatigue, increasing weakness, weight loss, taste distortion, change in pain irradiation | The presence of a large ulcerative defect of the mucous membrane, undermined edges, bleeding on contact, signs of mucosal atrophy |
| Wilson-Konovalov disease | The disease manifests itself between the ages of 8 and 18 years. Accompanied by damage to the nervous system, increased copper deposition, a Kayser-Fleischer ring is formed around the cornea, and pigmentation of the skin of the body. | Bleeding may develop in late dates diseases, with the formation of portal hypertension syndrome. The complication is rare. |
| Budd-Chiari syndrome | Thrombosis of large hepatic veins, which develops after abdominal trauma, SLE, pancreatic tumor, liver tumor, in pregnant women and women taking contraceptives. The main manifestation of the syndrome is ascites, abdominal pain, hepatosplenomegaly. | EGD is characterized by the presence of esophageal varices. Bleeding from the esophageal vein is rare in these patients. |
| Schistosomiasis | The disease is caused by Schistosoma haematobium and occurs as a result of helminthic infestation through the genitourinary area. Manifested by dysuric disorders, anemia. Liver cirrhosis and portal hypertension syndrome are rare, mainly in late stage diseases. Often found among residents of Egypt and Sudan. | EGD is characterized by the presence of esophageal varicose veins in 30% of cases. Bleeding from varicose veins is main reason death of these patients. |
Treatment
Treatment goals:
· control of the source of bleeding;
· prevention and treatment of SBP, HRS. HE;
· prevention of secondary bleeding from varicose veins.
Treatment tactics:
Non-drug treatment:
Mode- I.II;
Diet- table No. 5 (Appendix 3).
Drug treatment:
On an outpatient basis urgently:
Sodium chloride solution 0.9% 400.
During inpatient treatment:
Replenishment of blood volume.
ITT for mild blood loss:
· Blood loss 10-15% of the bcc (500-700 ml): intravenous transfusion of crystalloids (dextrose, sodium acetate, sodium lactate, sodium chloride 0.9%) in a volume of 200% of the blood loss (1-1.4 l).
ITT at medium degree blood loss:
· Blood loss 15-30% of the bcc (750-1500 ml): intravenous crystalloids (glucose solution, sodium chloride 0.9%, sodium acetate, sodium lactate) and colloids (gelatin), in a ratio of 3:1 with a total volume of 300 % of the volume of blood loss (2.5-4.5 liters);
ITT for severe blood loss:
· For blood loss of 30-40% of the bcc (1500-2000 ml): intravenous crystalloids (dextrose, sodium chloride 0.9%, sodium acetate, sodium lactate) and colloids (gelofusin) in a ratio of 2:1 with a total volume of 300% on the volume of blood loss (3-6 liters). Transfusion of blood components is indicated (packed red blood cells, FFP 30% of the transfused volume, platelet concentrate at platelet levels< 50х10 9) и препарата крови - раствор альбумина при гипопротеинемии (общий белок < 60 г/л) и гипоальбуминемии (альбумин < 35 г/л).
When determining indications for replacement therapy, they are guided only by tests taken from venous blood:Hb,
Ht, red blood cells, coagulogram indicators: INR, PTI, fibrinogen.
Critical level indicators are: hemoglobin - 70 g/l, hematocrit - 25-28%. . It is necessary to maintain the hemoglobin level ~ 80 g/l (UD-class I, level B).
· For hemocoagulation syndrome and thrombocytopenia, the safest colloidal solution, succinylated gelatin, is recommended. The rate of infusion is determined by the level of blood pressure. Before bleeding stops, SBP should not exceed 90 mmHg. But the infusion rate must exceed the rate of blood loss - 200 ml/min in 1 or 2-3 veins.
Criteria for the adequacy of the conducted ITT:
· increased central venous pressure (10-12 cm of water column);
· hourly diuresis (at least 30 ml/hour);
· until the central venous pressure reaches 10-12 cm of water column. and hourly diuresis of 30 ml/hour ITT must be continued.
· at rapid increase Central venous pressure is higher than 15 cm of water column. it is necessary to reduce the rate of transfusion and reconsider the volume of infusion;
· clinical criteria for restoration of blood volume (elimination of hypovolemia):
· increased blood pressure;
· decrease in heart rate;
· increase pulse pressure;
· increase in blood saturation;
Warming and change in skin color (from pale to pink).
Vitamin K preparations:
Menadione sodium bisulfite 2 ml 3 times intravenously.
Proteolysis inhibitors(aprotinin/analogues: contrical, aprotinin) reduce the need for replacement therapy and reduce blood loss. It is recommended to use 50,000 units of contrical, then 10,000-20,000 every 4-6 hours. The initial dose of aprotinin for hemorrhagic shock 500 thousand KIE. The rate of administration is no more than 5 ml/min, then intravenous drip of 50 thousand KIU per hour (UD - D).
Pharmacological therapy to reduce portal pressure:
The use of vasoactive drugs helps stop bleeding in 75-80%. (UD - class I, level A).
From vasoconstrictor drugs(to reduce PD) used in the treatment of bleeding from varicose veins, meropenem and its analogues: octreotide and vapreotide have the advantage, since they have a low side effect. Their use is possible as soon as bleeding from the varicose veins is established and even if suspected (UD-class I, level A). .
Octreotide: a bolus of 50 mcg/hour is administered intravenously, followed by continuous intravenous administration through a dispenser of 50 mcg/hour for 5 days or IV drip for 5 days (UD-5D). Or 0.025 mg/h (UD - A) is administered.
Terlipressin: patient's weight<50 кг - 1 мг; 50-70 кг - 1,5 мг; вес >70 kg - 2 mg. Next, an intravenous bolus of 2 mg every 4 hours for 48 hours, from 3 days, 1 mg every 4 hours to 5 days (Appendix 4). Or 1000 mcg every 4-6 hours for 3-5 days until stopping and for another 2-3 days to prevent recurrent bleeding.
Somatostatin: bolus IV 250 mcg over 5 minutes and can be repeated 3 times within 1 hour. Next, continuous administration of 6 mg (=250 mcg) for 24 hours. The dose may be increased to 500 mcg/hour. Side effects are rare and there are no contraindications. Compared to terlipressin, the effect is the same (reduces relapse and controls bleeding). With absence this drug its synthetic analogues - octreotide or vapreotide - are shown.
Treatment of spontaneous bacterial peritonitis (SBP):
Antibiotic therapy (for 7-8 days):
Cephalosporins III generation(cefotaxime, ceftriaxone, cefoperazone, ceftazidime):
· cefotaxime 2 g 2 times a day IV, ceftazidime 1 g 2 times a day IV;
Amoxicillin/clavulanate 1g IV 3 times a day;
Ampicillin/sulbactam 1 g IV 3 times a day.
Alternative antibiotic therapy in the absence of renal dysfunction and encephalopathy:
Fluoroquinolones:
Ofloxacin per os 400 mg per day;
· ciprofloxacin per os 200 mg 2 times a day.
Carbapenems:
· meropenem 500 mg 2 times or 1 g 1 time per day intravenously;
· imipenem 500 mg 2 times or 1 g 1 time per day intravenously;
Doripenem 500 mg 2 times IV;
Meropenem 1 g 1 time IV;
For nosocomial SBP, piperacillin/tazobactam 2 g once daily IV is recommended as empirical antibiotic therapy. In its absence, third generation cephalosporins (cefotaxime, ceftriaxone, cefoperazone, ceftazidime).
Albumin 1.5 g/kg of the patient’s weight during the first 6 hours, then administered at the rate of 1 g/kg of the patient’s weight on the 3rd day of treatment.
Contraindications:
· application in acute period diuretics;
· use of aminoglycocides.
Treatment of hepatic encephalopathy:
· reduction daily consumption protein 20-30 g;
· taking lactulose 30-50 ml every 1-2 hours (before the start of bowel movements). After defecation (2-3 soft stools), the dose of lactulose is 15-30 ml 2 times a day.
Alternative therapy:
neomycin per os + magnesium/sorbitol;
Rifaximin 400 mg per os;
· ornithine aspartate and benzoate.
Treatment of hepato-renal syndrome:
If kidney function deteriorates (creatinine increases):
· cancel diuretics;
Albumin IV 1 g/kg body weight;
· sodium chloride solution 0.9% 400 ml intravenous drip. If creatinine does not decrease, then perform an ultrasound of the kidneys and take a bacteriological urine culture.
Basic treatment:
Terliressin 0.5 - 1.0 mg IV every 4-6 hours. If creatinine does not decrease by more than 25% within 2 days, the dose should be increased to 2 mg every 4-6 hours. If creatinine does not decrease by 50% within 7 days, then treatment is stopped. If there is a response, then continue treatment for up to 14 days;
· octreotide 100 mg 3 times subcutaneously + midodrine 5-7.5 mg 3 times / day per os, if necessary, the dose of midodrine is increased to 12.5-15 mg;
· or octreotide 100 mg 3 times subcutaneously + terliressin 0.5-2 mg every 4-6 hours intravenously;
· albumin 50-100 g/day at the rate of 1 g/kg of the patient’s weight for 7 days. Monitor blood pressure. The goal of treatment is to increase MAP by 15 mm. rt. Art.
Drug treatment provided at the emergency stage:
· sodium chloride solution 0.9% 400 ml intravenously;
· dopamine 4% or 0.5% solution 5 ml intravenously.
Other treatments:
Other types of treatment provided on an outpatient basis
· oxygen inhalation.
Other types of services provided at the stationary level:
oxygen inhalation;
· catheterization of 2 peripheral veins or 1 central vein;
· endotracheal intubation (indications, mode).
Mechanical ventilation is indicated for severe patients (with severe massive bleeding and impaired level of consciousness) and should be performed in patients before endoscopy.
Indications for mechanical ventilation are:
· impaired consciousness (less than 10 points on the Glasgow scale) (Appendix 2);
Lack of spontaneous breathing (apnea);
· increased respiration rate of more than 35-40 per minute, unless this is associated with hyperthermia (body temperature above 38.5°C) or severe unresolved hypovolemia.
Gases arterial blood:
PaO 2< 60 мм рт ст при дыхании atmospheric air or PaCO 2 > 60 mm Hg in the absence of metabolic alkolosis;
Control bleeding with obturators:(UD - class I, level B).
Sengstaken-Blakemore probe:
Indications:
ongoing bleeding from the esophagus
Contraindications:
Stopped bleeding from the esophagus.
The effectiveness of hemostasis is monitored by unraveling the probe cuff 4 hours after its installation. When the bleeding stops, the cuffs are lowered. The duration of use of the probe is up to 24 hours.
Linton pipe
Indications:
· gastric localization of varicose veins;
Contraindications:
· Stopped bleeding from the gastric varices.
Danish stent(self-correcting):
Indications:
· ongoing bleeding from the esophagus.
The stent is installed during endoscopy for no more than 1 week (removed endoscopically).
Contraindications:
Endoscopic hemostasis(UD - class I, level A). (Appendix 5) :
Endoscopic ligation(EVL) :
Indications:
Contraindications:
· agonal state of the patient;
· anatomical defects of the esophagus (strictures).
(performed intravasally and paravasally):
Indications:
· ongoing and/or stopped bleeding from the esophagus.
Contraindications:
· agonal state of the patient;
· anatomical defects of the esophagus (strictures).
Cleansing enema:
Indications:
· presence of blood in the intestinal lumen.
Lactulose enema:
Indications:
300 ml of lactulose per 1 liter of water, administered every 4-6 hours.
Using the MA systemR.S.- Molecular Adsorben Recirculating System" -
albumin dialysis:
Indications:
· hepatic encephalopathy.
Vasoconstrictor therapy ( bridging therapy) for patients awaiting liver transplantation :
Indications:
· hepatorenal syndrome.
Other types of treatment provided during emergency medical care:
oxygen inhalation;
transfer to mechanical ventilation according to indications for critical condition;
· catheterization of peripheral veins.
Surgical intervention:
Surgical intervention performed in outpatient setting: not carried out.
Surgical intervention provided in an inpatient setting:
OperationTIPS
Indications:
· if pharmacological therapy and EG are ineffective.
TIPS and bypass surgery are indicated for patients with Child-Pugh class A (UD-class I, level C).
Contraindications:
· disease severity class B/C according to Child-Pugh (decompensated stage).
Liver transplantation:
Indications:
· cirrhosis of the liver;
· some forms chronic hepatitis;
· some forms malignant neoplasms liver.
Contraindications:
· chronic infections;
presence of the HIV virus in the body,
Mycobacterium tuberculosis,
· syphilis;
· viral hepatitis.
Patziora operation (transverse subcardial gastrotomy):
Indications:
· ongoing bleeding from the VV of the cardioesophageal junction and stomach in the absence of conditions for endoscopic hemostasis and other methods of stopping
Contraindications:
· agonal state of the patient;
MON.
Indicators of treatment effectiveness:
· stopping bleeding from the esophagus and stomach;
· prevention of recurrent bleeding;
· prevention and relief of HRS, SBP, HE;
· reduction in mortality rates.
Drugs ( active ingredients), used in the treatment
| Albumin human |
| Amoxicillin |
| Ampicillin |
| Aprotinin |
| Vapreotide |
| Dextrose |
| Dopamine |
| Doripenem |
| Imipenem |
| Clavulanic acid |
| Menadione sodium bisulfite |
| Meropenem |
| Midodrine |
| Sodium acetate |
| Sodium lactate |
| Sodium chloride |
| Neomycin |
| Octreotide |
| Ornithine |
| Ofloxacin |
| Rifaximin |
| Somatostatin |
| Succinylated gelatin |
| Sulbactam |
| Terlipressin |
| Cefoperazone |
| Cefotaxime |
| Ceftazidime |
| Ceftriaxone |
| Ciprofloxacin |
Hospitalization
Indications for hospitalization indicating the type of hospitalization:
Indications for emergency hospitalization:
· bleeding from the esophagus and stomach.
Indications for planned hospitalization: No.
Prevention
Preventive actions:
Prevention of secondary bleeding:(UD - class I, level A).
· NSBB should be started as soon as vasoactive drugs (terlipressin, octreotide or vapreotide) are stopped;
· NSBB significantly reduces the risk of rebleeding.
For the prevention of secondary bleeding from the esophagus and stomach, it is indicated :
First line therapy combination therapy:(UD - class I, level A).
· use of non-selective β-blockers (NSBB) to reduce portal pressure: propranolol at a dose of 20 mg 2 times a day or nadolol 20-40 mg 1-2 times a day. Dose adjustment to reduce heart rate (bring it to 55-60 per minute);
· + EVL ligation. Up to 6 rings are applied to the veins every 1-2 weeks. The first control EGDS after 1-3 months and subsequently every 6-12 months to monitor the recurrence of varicose veins. (UD - class I, level C).
Second line therapy:
· if NSBB+ EVL was not effective, then TIPS or shunt surgery is indicated, but only for patients of class A in terms of the severity of cirrhosis. Class B and C these operations are not indicated, as they lead to the development of encephalopathy.
Alternative therapy:
NSBB ( β-blockers)+ ISMN (nitrates in tablet form);
· NSBB+ISMN+EVL. This combination of pharmacological (NSBB+ISMN) and ligation (EVL) of HRV is associated with more low level recurrent bleeding and is the method of choice.
If the patient has rebleeding from varicose veins despite combinations of pharmacological and endoscopic treatment, in such cases the use of TIPS or bypass surgery is recommended (if present) local conditions and experience in their use. (UD-class I, level A). Candidates for liver transplantation should be referred to a transplant center (UD-Class I, Level C).
For secondary prevention of bleeding from varicose veins, the following is not indicated:
· NSBB+sclerotherapy;
· EVL+sclerotherapy.
Antibacterial prophylaxis of spontaneous bacterial peritonitis (SBP):
Use of quinolones for 7 days: (UD-class I, level A).
· norfloxacin 400 mg 2 times a day per os for 7 days;
· or ciprofloxacin 400 mg intravenously 1 time for 7 days;
· or ceftriaxone 1 g IV 1 time per day for up to 7 days. This drug is more effective in patients with ascites, encephalopathy, and previous quinolone therapy. Especially in centers with high resistance to quinolones (UD-class I, level B).
Further management:
· Treatment of the underlying disease. After stopping the bleeding and being discharged from the hospital, the patient is referred to a gastroenterologist or hepatologist;
· Selection and referral for liver transplantation (transplantologist).
Information
Sources and literature
- Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health of the Republic of Kazakhstan, 2015
- List of used literature (valid research references to the listed sources in the text of the protocol are required): 1) Khanevich M.D., Khrupkin V.I., Zherlov G.K. et al., Bleeding from chronic gastroduodenal ulcers in patients with intrahepatic portal hypertension. – Novosibirsk: Nauka, 2003. – 198 p. 2) Guideline Summary World Gastroenterology Organization (WGO). Esophageal varices. Milwaukee (WI): World Gastroenterology Organization (WGO); 2014. 14 p. 3) De Franchis R. Evolving Consensus in Portal Hypertension Report of the Baveno IV Consensus Workshop on methodology of diagnosis and therapy in portal hypertension. J Hepatol 2005; 43: 167 – 76. 4) Garcia-Tsao G, Sanyal AJ, Grace ND et al. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology 2007; 46: 922 – 38. 5) Garcia-Tsao G, Sanyal AJ, Grace ND et al. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Am J Gastroenterol 2007; 102: 2086 – 102. 6) Longacre AV, Imaeda A, Garcia-Tsao G, Fraenkel L. A pilot project examining the predicted preferences of patients and physicians in the primary prophylaxis of variceal hemorrhage. Hepatology. 2008;47:169–176. 7) Gluud LL, Klingenberg S, Nikolova D, Gluud C. Banding ligation versus β-blockers as primary prophylaxis in esophageal varices: systematic review of randomized trials. Am J Gastroenterol. 2007; 102:2842–2848; quiz 2841, 2849. 8) Bosch J, Abraldes JG, Berzigotti A, Garcia-Pagan JC. Portal hypertension and gastrointestinal bleeding.Semin Liver Dis. 2008; 28:3–25. 9) Abraldes JG, Tarantino I, Turnes J, Garcia-Pagan JC, Rodés J, Bosch J. Hemodynamic response to pharmacological treatment of portal hypertension and long-term prognosis of cirrhosis. Hepatology. 2003; 37:902–908. 10) Villanueva C, Aracil C, Colomo A, Hernández-Gea V, López-Balaguer JM, Alvarez-Urturi C, Torras X, Balanzó J, Guarner C. Acute hemodynamic response to β-blockers and prediction of long-term outcome in primary prophylaxis of variceal bleeding. Gastroenterology. 2009; 137:119–128. 11) Fernández J, Ruiz del Arbol L, Gómez C, Durandez R, Serradilla R, Guarner C, Planas R, Arroyo V, Navasa M. Norfloxacin vs ceftriaxone in the prophylaxis of infections in patients with advanced cirrhosis and hemorrhage. Gastroenterology. 2006; 131:1049–1056; quiz 1285. 12) Bernard B, Lebrec D, Mathurin P, Opolon P, Poynard T. B-adrenergic antagonists in the prevention of gastrointestinal rebleeding in patients with cirrhosis: a meta-analysis. Hepatology. 1997; 25:63–70. 13) Gonzalez R, Zamora J, Gomez-Camarero J, Molinero LM, Bañares R, Albillos A. Meta-analysis: Combination endoscopic and drug therapy to prevent variceal rebleeding in cirrhosis. Ann Intern Med. 2008;149:109–122. 14) Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N Engl J Med. 2010; 362:823–832. 15) Luca A, D "Amico G, La Galla R, Midiri M, Morabito A, Pagliaro L. TIPS for prevention of recurrent bleeding in patients with cirrhosis: meta-analysis of randomized clinical trials. Radiology. 1999; 212:411– 421. 16) Henderson JM, Boyer TD, Kutner MH, Galloway JR, Rikkers LF, Jeffers LJ, Abu-Elmagd K, Connor J. Distal splenorenal shunt versus transjugular intrahepatic portal systematic shunt for variceal bleeding: a randomized trial. Gastroenterology. 2006. ;130:1643–1651. 17) Khurram Bari and Guadalupe Garcia-Cao. Treatment of portal hypertension. World J Gastroenterol. 2012 Mar 21;18 (11): 1166-1175. 18) De Franchis R. Evolving consensus in portal hypertension "Report of the Baveno IV consensus workshop on methodology of diagnosis and therapy in portal hypertension. J. Hepatol., 2005, 43: 167-176. 19) Garcia-Tsao G., Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N. Engl. J. Med., 2010, 362: 823-832. 20) De Franchis R., Revising consensus in portal hypertension: report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension. J. Hepatol., 2010, 53: 762-7682010. 21) WGO Practice Guideline Esophageal Varices, 2014]. 22) Order of the Ministry of Health of the Republic of Kazakhstan No. 666 Appendix No. 3 dated November 6, 2000. "Rules for storage, transfusion of blood, its components and preparations." Appendix No. 501 dated July 26, 2012 “Rules for the storage and transfusion of blood, its components and preparations.” 23) Evidence-Based Gastroenterology and Hepatology, Third Edition John WD McDonald, Andrew K Burroughs, Brian G Feagan and M Brian Fennerty, 2010 Blackwell Publishing Ltd. 24) Large reference book of medicines / under Red Ziganshina L.E. et al., M., 2011
Information
List of protocol developers with qualification information:
1) Zhantalinova Nurzhamal Asenovna - Doctor of Medical Sciences Professor of the Department of Internship and Residency in Surgery at the Russian State University at the KazNMU named after. S.D. Asfendiyarov".
2) Irina Lvovna Menshikova - candidate of medical sciences, associate professor, head of the endoscopy course of the department of gastroenterology and hepatology with an endoscopy course, chairman of the Society of Endoscopists of the Republic of Kazakhstan at the Republican Association of Nutritionists, Gastroenterologists and Endoscopists of the Republic of Kazakhstan. RSE at the Scientific and Research Institute of Cardiology and Internal Medicine.
3) Zhakupova Guldzhan Akhmetzhanovna - State Public Enterprise at the Burabay Central Regional Hospital. Deputy Chief Physician for Audit, anesthesiologist-reanimatologist, highest category.
4) Mazhitov Talgat Mansurovich - Doctor of Medical Sciences, Professor of Astana Medical University JSC, clinical pharmacologist of the highest category, general practitioner of the highest category.
Disclosure of no conflict of interest: No
Reviewers: Turgunov Ermek Meiramovich - Doctor of Medical Sciences, Professor, surgeon of the highest qualification category, RSE at the Karaganda State Medical University of the Ministry of Health of the Republic of Kazakhstan, head of the Department of Surgical Diseases No. 2, independent accredited expert of the Ministry of Health of the Republic of Kazakhstan.
Indication of the conditions for reviewing the protocol: Review of the protocol 3 years after its publication and from the date of its entry into force or if new methods with a level of evidence are available.
Annex 1
Clinical classification of GS:. Shock I degree: consciousness is preserved, the patient is communicative, slightly lethargic, systolic blood pressure exceeds 90 mmHg, pulse is rapid;
. Shock II degree: consciousness is preserved, the patient is lethargic, systolic blood pressure is 90-70 mmHg, pulse is 100-120 per minute, weak filling, shallow breathing;
. Shock III degree: the patient is adynamic, lethargic, systolic blood pressure is below 70 mm Hg, pulse is more than 120 per minute, threadlike, central venous pressure is 0 or negative, there is an absence of urine (anuria);
. IV degree shock: terminal state, systolic blood pressure is below 50 mmHg or cannot be determined, breathing is shallow or convulsive, consciousness is lost.
Determination of the degree of HS using the Algover index:
P/SBP (pulse/systolic blood pressure ratio). Normal is 0.5 (60\120).
· I degree - 0.8-0.9;
· II degree - 0.9-1.2;
· III degree - 1.3 and above.
Assessment of the severity of HS and BCC deficiency:
| Index | Decrease in BCC, % | Volume of blood loss (ml) | Clinical picture |
| 0.8 or less | 10 | 500 | No symptoms |
| 0,9-1,2 | 20 | 750-1250 | Minimal tachycardia, decreased blood pressure, cold extremities |
| 1,3-1,4 | 30 | 1250-1750 | Tachycardia up to 120 per minute, decreased pulse pressure, systolic 90-100 mmHg, anxiety, sweating, pallor, oliguria |
| 1.5 or more | 40 | 1750 or more | Tachycardia more than 120 per minute, decreased pulse pressure, systolic below 60 mmHg, stupor, severe pallor, cold extremities, anuria |
Using Moore's formula to determine the volume of blood loss: V=P*q*(Ht1-Ht2)/Ht1
V - volume of blood loss, ml;
P - patient’s weight, kg
q is an empirical number reflecting the amount of blood per kilogram of body weight - 70 ml for men, 65 ml for women
Ht1 - normal hematocrit (for men - 50, for women - 45);
Ht2 is the patient’s hematocrit 12-24 hours after the onset of bleeding;
Determination of the degree of blood loss and HO deficiency according to classification:(Gorbashko A.I., 1982):
| Indicators | Lightweight | Average | Heavy |
|
Red blood cells |
>3.5x1012/l | 3.5-2.5x1012/l | <2,5х1012/л |
| Hemoglobin | >100 g/l | 83-100 g/l | <83 г/л |
| Pulse per 1 min. | Up to 80 | 80-100 | >100 |
| Systolic blood pressure | >110 | 100-90 | <90 |
| Hematocrit number | >30 | 30-25 | <25 |
| Deficiency of civil defense from what it should be | up to 20 | from 20-30 | >30 |
Appendix 2
· Pressure in the portal system is above 10-12 mm Hg;
· Class B/C according to Child-Pugh;
· Large sizes of VRV - 5 mm or more with red spots;
· Alcoholic cirrhosis of the liver;
· Hemocoagulation syndrome.
Clinical signs of unstable hemostasis:
1. The degree of hepatic dysfunction (severity of cirrhosis), assessed using the Child-Pugh or Child-Turcotte-Pugh scale, is a predictor of bleeding from the cervical vein in patients with decompensated stage: B and C class;
Criteria for assessing the severity of liver disease according to Child-Pugh:
| Rating, point | |||
| 1 point | 2 points | 3 points | |
| Ascites | No | Transitional (soft) | Stable (tense) |
| Encephalopathy, stages | No | 1-2 | 3-4 |
| Bilirubin, µmol/l | <34 | 35-51 | >51 |
| Primary biliary cirrhosis, µmol/l | <68 | 69-171 | >171 |
| Albumin, g/l | >35 | 28-35 | <28 |
| Prothrombin index, % | 90-75 | 75-62,5 | <62,5 |
Assessment and determination of functional groups (class) according to Child-Pugh:
class A- up to 6 points (compensated stage);
class B- up to 9 points (subcompensated stage);
class C- 10-11 or more points (decompensated stage).
Criteria for assessing the severity of liver disease according to Child-Turcotte-Pugh:
| Clinical and biochemical signs | Points | ||
| 1 | 2 | 3 | |
| Encephalopathy | No | Score 1-2 (or caused by a precipitating factor) | Score 3-4 (or chronic) |
| Ascites | No | Small medium, responsive to diuretics | Severe diuretic refractory |
| Bilirubin mg/l | <2 | 2-3 | >3 |
| Albumin g/l | >3,5 | 2,8-3,5 | <2,8 |
| PT | <4 | 4-6 | >6 |
| INR (INR) | <1,7 | 1,7-2,3 | >2,3 |
Class A- 5-6 points;
ClassB- 7-9 points;
Class C- 10-15 points.
1. According to the guidelines of Western countries, classes (groups) B and C refer to the decompensated stage of the disease (jaundice, ascites, encephalopathy occur). In addition to the listed complications, the following are observed: SBP, HRS, bleeding from the varicose vein. The treatment strategy for patients depends on this.
2. The patient has a history of an episode of bleeding from varicose veins (≈70% of repeated bleedings compared to ≈30% of primary ones). The greatest risk of rebleeding is observed in the first 48 hours (≈ 50% of all rebleedings). In addition, risk factors for recurrent bleeding are:
· GSH in the patient at the time of admission;
· Severe blood loss;
· Signs of coagulopathy.
Endoscopic signs of unstable hemostasis:
Size of varices: varicose vein diameter >5 mm and node wall tension indicate a high risk of bleeding. The risk of bleeding and the size of the esophageal vein correlate independently [Borisov A.E. et al., 2006; Sarin S.K. et al.];
Availability of red markers:
· symptom of a red scar (Red wale mark) - an elongated red vein resembling a velvet scar;
· Cherry red spots - flat cherry-red redness located separately on top of the ER;
· spots from hemorrhages: flat red spots located separately on top of the varicose veins and resembling blood blisters;
Diffuse erythema: continuous redness of the cervical vein.
Appendix 3
By diet:· Patients with signs of ongoing bleeding are given parenteral nutrition.
· In case of spontaneous cessation of bleeding from the esophageal vein and stable hemostasis, enteral nutrition is prescribed.
Enteral nutrition is a priority. During the first day, the amount of nutritional mixtures (Nutricomp, Nutrilan, Nutrien, Unipid) is up to 500 ml per day. If well tolerated, you can increase the dose to 2 liters.
During decompensated cirrhosis liver with impaired ability to neutralize ammonia, as well as in a precomatous state, it is necessary to significantly limit the consumption of protein in food (up to 20-30 g per day). If the patient's condition does not improve, proteins are completely excluded from the diet. The amount of fat can be up to 90 g per day. In this case, most of the total amount of fats should be vegetable fats, the remaining half should be milk fats.
Allowed to eat: black and white bread (stale), jam, honey, sugar, soft dough cookies, fresh fruits or fruit compotes, jelly, mousses, puddings, jellies.
Prohibited: legumes, sorrel, butter cookies, strong tea, coffee, cocoa, spicy foods, spices, vegetables containing essential oils (raw onions, garlic, radishes), cold dishes and drinks. Drinking alcohol is strictly prohibited. Lamb, beef, goose and other fats should be completely excluded from the diet.
Appendix 4
How to use terlipressinContraindications to the use of terlipressin:
· Heart failure;
· Severe heart rhythm disturbances;
· Obstructive pulmonary diseases;
· Severe bronchial asthma;
· Peripheral vascular diseases (atherosclerotic lesions, diabetic angiopathy);
· Uncontrolled arterial hypertension;
· Epilepsy.
The risk of side effects is reduced with continuous administration of 2-4 mg over 24 hours.
Note: should be combined with glycerol trinitrate 20 mg transdermally for 24 hours or 0.4 mg sublingually every 30 minutes.
Appendix 5
Endoscopic ligation (EL)It allows you to achieve the desired result faster, is safer and is easier to tolerate for patients.
However, ligation does not lead to pronounced fibrosis of the submucosal layer of the esophagus, which is achieved with sclerotherapy.
There are methods of local (point) and spiral (intensive) ligation. This technique uses elastic rings (ligature loops).
The best effect is achieved by combining these two methods.
EL (EVL) must be carried out in the presence of conditions, during the diagnosis of the source of bleeding. Necessary conditions for EL (EVL): a specialist who knows the methodology, availability of consumables, and provision of anesthesiological support.
Up to 6 rings are applied at a time, depending on the size and degree of damage to the esophagus by varicose veins, and the presence of signs of a threat of recurrent bleeding.
Repeated ligation is indicated only in cases of recurrent bleeding or uncontrolled bleeding during the first unsuccessful attempt to apply rings. The method itself is safer, more effective, and has better control over bleeding.
Endoscopic sclerotherapy
Sclerosis begins mainly with intravasal administration of the drug. The sclerosant is injected into each varicose node, starting at the gastroesophageal junction, then proximally to the middle third of the esophagus. During each injection, 1 to 3 ml of ethoxysclerol solution (polidocanol) is used. After intravasal administration, paravasal administration is carried out. The total volume of the drug should not exceed 30 ml.
From the third session, the sclerosant is introduced only paravasally to create a dense fibrous lining. Treatment continues until the eradication effect is achieved or until the risk factor disappears. This requires 5-6 sessions of sclerotherapy, the first 2-3 sessions are carried out with an interval of 5-8 days, the subsequent ones - 2-4 weeks.
With the paravasal method of administration sclerosant into the submucosal layer, primary hemostasis is achieved due to edema, leading to mechanical compression of the vein wall and then local aseptic inflammation develops with the formation of a connective tissue framework in the submucosal layer. Veins thrombose within 7-10 days.
An important point is the creation of unfavorable conditions for the development of collateral circulation and the opening of pre-existing collaterals in cirrhosis.
Paravasal component of sclerotherapy blocks the development of collateral circulation in the esophagus and thereby prevents the formation of new varicose veins.
From the third session, the sclerosant is introduced only paravasally to create a dense fibrous lining. Treatment continues until the eradication effect is achieved or until the risk factor disappears. This requires 5-6 sessions of sclerotherapy, the first 2-3 sessions are carried out with an interval of 5-8 days, the subsequent ones - 2-4 weeks.
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Predicting the gap
Within 2 years after the diagnosis of liver cirrhosis, bleeding from varicose veins of the esophagus occurs in 35% of patients; the first episode of bleeding kills 50% of patients.
There is a clear correlation between the size of varicose veins visible during endoscopy and the likelihood of bleeding. The pressure inside varicose veins is not so important, although it is known that for the formation of varicose veins and subsequent bleeding, the pressure in the portal vein must be above 12 mm Hg. .
Rice. 10-50. Partial nodular transformation of the liver. A section of the liver in the portal area is schematically shown, where nodes compressing the portal vein are visible. The rest of the liver appears normal.
An important factor that indicates a greater likelihood of bleeding is the red spots that can be seen during endoscopy.
To assess hepatocyte function in cirrhosis, use Child's criteria system, which includes 3 groups - A, B, C (Table 10-4). Depending on the degree of dysfunction of hepatocytes, patients are classified into one of the groups. The Child group is the most important indicator for assessing the likelihood of bleeding. In addition, this group correlates with the size of the varicose veins, the presence of red spots on endoscopy, and the effectiveness of treatment.
Three indicators - the size of varicose veins, the presence of red spots and hepatocellular function - make it possible to most reliably predict bleeding (Fig. 10-51).
In alcoholic cirrhosis, the risk of bleeding is highest.
The likelihood of bleeding can be predicted using Doppler ultrasound. At the same time, the speed of blood flow through the portal vein, its diameter, the size of the spleen and the presence of collaterals are assessed. At high values stagnation index(the ratio of the area of the portal vein to the amount of blood flow in it) there is a high probability of early development of bleeding.
Prevention of bleeding
It is necessary to strive to improve liver function, for example by abstaining from alcohol. Aspirin and NSAIDs should be avoided. Dietary restrictions, such as avoiding spices, or taking long-acting H2 blockers do not prevent the development of coma.
Propranolol - a non-selective b-blocker that reduces portal pressure by constricting the vessels of the internal organs and, to a lesser extent, reducing cardiac output. It also reduces blood flow through the hepatic artery. The drug is prescribed in a dose that reduces resting heart rate by 25% 12 hours after administration. The degree of decrease in pressure in the portal vein varies in different patients. Taking even high doses in 20-50% of cases does not give the expected effect, especially with advanced cirrhosis. The portal vein pressure should be maintained at a level not exceeding 12 mmHg. . Monitoring of hepatic vein wedge pressure and portal pressure determined endoscopically is desirable.
Table 10-4. Classification of hepatic cell function in cirrhosis according to Child
|
Index |
Child group |
||
|
Serum bilirubin level, µmol/l |
|||
|
Serum albumin level, g% |
|||
|
Easy to treat |
Difficult to treat |
||
|
Neurological disorders |
Minimum |
Precoma, coma |
|
|
Decreased |
Exhaustion |
||
|
Hospital mortality, % |
|||
|
One-year survival rate, % |
|||
Rice. 10-51. The significance of the increase in the size of varicose veins [small (M), medium-sized (S) and large (K)] in combination with the appearance of red spots (RS) on their surface (absent, single, many) and Child’s group (A, B, C) to determine the likelihood of bleeding over 1 year.
Propranolol should not be prescribed for obstructive pulmonary diseases. This may make resuscitation efforts difficult if bleeding occurs. In addition, it contributes to the development of encephalopathy. Propranolol has a significantly pronounced “first pass” effect, so in cases of advanced cirrhosis, in which the elimination of the drug by the liver is slow, unpredictable reactions are possible. In particular, propranolol somewhat suppresses mental activity.
A meta-analysis of 6 studies suggests a significant reduction in the incidence of bleeding, but not mortality (Fig. 10-52). A subsequent meta-analysis of 9 randomized trials found a significant reduction in the incidence of bleeding with propranolol treatment. It is not easy to select patients for whom this treatment is indicated, since 70% of patients with esophageal varices do not bleed. Propranolol is recommended for significant varicose veins and when red spots are detected during endoscopy. With a venous pressure gradient of more than 12 mm Hg, patients should be treated regardless of the degree of venous dilatation. Similar results were obtained when prescribing overdone. Similar rates of survival and prevention of the first episode of bleeding were obtained with treatment isosorbide-5-mononitrate [I]. This drug may impair liver function and should not be used in advanced cirrhosis with ascites.
Meta-analysis of studies on preventive sclerotherapy revealed generally unsatisfactory results. There is no evidence that sclerotherapy is effective in preventing the first episode of bleeding or improving survival. Prophylactic sclerotherapy is not recommended.
Diagnosis of bleeding
IN clinical picture of bleeding from varicose veins of the esophagus, in addition to the symptoms observed with other sources of gastrointestinal bleeding, symptoms of portal hypertension are noted.
Bleeding may not be severe and may appear as melena rather than bloody vomiting. The intestines may fill with blood before bleeding is recognized, lasting several days.
Bleeding from varicose veins in cirrhosis adversely affects hepatocytes. This may be due to decreased oxygen delivery due to anemia or increased metabolic demands due to protein breakdown after bleeding. A decrease in blood pressure reduces blood flow in the hepatic artery, which supplies blood to the regeneration nodes, as a result of which their necrosis is possible. Increased absorption of nitrogen from the intestine often leads to the development of hepatic coma (see Chapter 7). Deterioration of hepatocyte function can provoke jaundice or ascites.
Bleeding not associated with varicose veins is also often observed: from duodenal ulcers, gastric erosions or Mallory-Weiss syndrome.
In all cases, endoscopic examination should be performed to identify the source of bleeding (Fig. 10-53). An ultrasound is also required to determine the lumen of the portal and hepatic veins and to exclude a space-occupying lesion, such as HCC.
Rice. 10-52. Meta-analysis of 6 studies of prophylactic propranolol (beta blocker). Mortality data are unreliable due to the incomparability of the groups studied. However, a non-significant (ND) reduction in the incidence of bleeding was detected.
Rice. 10-53. Treatment of bleeding from varicose veins of the esophagus.
Based on a biochemical blood test, it is impossible to differentiate bleeding from varicose veins from ulcerative bleeding.
Forecast
In cirrhosis, the mortality rate from variceal bleeding is about 40% per episode. In 60% of patients, bleeding recurs before discharge from the hospital; Mortality within 2 years is 60%.
The prognosis is determined by the severity of hepatic cellular failure. The triad of unfavorable signs - jaundice, ascites and encephalopathy - is accompanied by 80% mortality. One-year survival rate at low risk (Child's groups A and B) is about 70%, and at high risk (Child's group C) - about 30% (Table 10-5). Determination of survival is based on the presence of encephalopathy, prothrombin time, and the number of units of blood transfused during the previous 72 hours. A conventional end-view gastroscope is inserted into the lower part of the esophagus and an additional probe is inserted under its control. Then the gastroscope is removed and a ligating device is fixed to its end. After this, the gastroscope is reinserted into the distal esophagus, the varicose vein is identified and aspirated into the lumen of the ligating device. Then, pressing on the wire lever attached to it, an elastic ring is put on the vein. The process is repeated until all varicose veins are ligated. From 1 to 3 rings are placed on each of them.
Table 10-7. Sclerotherapy for varicose veins
|
Preventative |
Emergency |
Planned |
|
Efficacy not proven |
Experience required Stops bleeding Impact on survival (?) |
Reduces mortality from bleeding Numerous complications Patient adherence to treatment is important Survival rate remains unchanged |
The method is simple and has fewer complications than sclerotherapy, although ligation of varicose veins requires more sessions)