Bleeding from varicose veins of the esophagus. Bleeding from varicose veins of the esophagus. Symptoms of bleeding from varicose veins of the esophagus

RCHD (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 ruptured hemorrhagic syndrome (K22.6), Portal hypertension (K76.6)

Gastroenterology, Surgery

general information

Short description

Recommended
Expert Council
RSE on PVC "Republican Center for Health Development"
Ministry of Health
and social development
dated September 30, 2015
Protocol #10

Bleeding out varicose veins esophagus is a complication of portal hypertension syndrome. Esophageal EVs are portosystemic collaterals that connect the portal venous and systemic venous circulations. They form as a sequence 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 ruptured 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;
VRV - 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 - the volume of circulating blood;
PT - prothrombin time;
PD - portal pressure;
FDP - fibrinogen degradation product;
PTI - prothrombin index;
SBP - systolic blood pressure
SPH - portal hypertension syndrome;
TV - thrombin time;
LE - level of evidence;
Ultrasound - ultrasound examination;
FA - fibrinolytic activity;
CVP - central venous pressure;
CP - cirrhosis of the liver;
NRR - respiratory rate;
HR - heart rate;
AP - alkaline phosphatase;
EG - endoscopic hemostasis
ECG - electrocardiography;
EFGDS - esophagogastroduodenoscopy;
D-dimer - fibrin breakdown product;
EVL - endoscopic ligation of veins;
Hb - hemoglobin;
Ht - hematocrit;
ISMN - nitrates;
NBSS - non-selective β-blockers;
HRS - hepato-renal syndrome;
SBP, spontaneous bacterial peritonitis;
HE - hepatic encephalopathy;
KOS - acid-base state;
ELISA - enzyme immunoassay;
ACE - alpha-ketoprotein;
TIPS - transjugular portosystemic shunt;
PON - multiple organ failure;
MAP - mean arterial pressure.

Date of development/revision of the protocol: 2015

Protocol Users: surgeon, anesthesiologist-resuscitator, emergency doctor, paramedic, functional diagnostics doctor (endoscopist), gastroenterologist, therapist, general practitioner.

Classification

Clinical classification:

Classification of VRV of the esophagus and stomach according to Paquet (1983):
1 degree- single vein ectasias;
2 degree- single well-demarcated trunks of veins, mainly in the lower part of the esophagus, which remain distinctly expressed 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;
3 degree- a distinct narrowing of the lumen of the esophagus by the trunks of the VRV, located in the s/z and n/z of the esophagus, which only partially decrease during air insufflation. The knotted shape of the veins is noted, on the tops of the veins - "red markers".
4 degree- the lumen of the esophagus is completely filled with VRV, the expansion of the veins affects the / from the esophagus. The epithelium over the veins is thinned, many "red markers" of the wall are determined.

Three-degree classification (Soehendra N., Bimoeller K., 1997):
VRV of the esophagus:
I degree- the diameter of the veins does not exceed 5 mm, elongated and located only in the lower part of the esophagus;
II degree- VRV 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 not more than 5 mm, barely visible above the gastric mucosa;
II degree- VRV 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 form of the veins (grade II - moderate risk of bleeding) and nodular (grade III - high risk of bleeding).

Classification of VRV of the stomach:
VRVZh are classified depending on localization.
Gastroesophageal veins (GOV) - VRVs that pass from the esophagus to the stomach - are divided into 2 types:
Type 1 (GOV1) - pass along the lesser curvature of the stomach (the principles of treatment correspond to the principles of the 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 esophageal vein dilatation and are divided into 2 types:
Type 1 (IGV1) - located in the fundus of the stomach, convoluted (occurs with thrombosis of the splenic vein);
2nd type (IGV2) - pass in the body of the stomach, antrum or around the pylorus. The most dangerous are the veins located in the fundus of the stomach (fundic veins). Other risk factors are the size of the nodes, the class of the CPU, the presence of a symptom of a "red spot".
The division by the degree of RVV is based on the same parameter as the division of RVV, the size of the nodes:
1st degree - the diameter of the VRV is not more than 5 mm, the veins are barely visible above the gastric mucosa;
2nd degree - the diameter of the VRV is 5-10 mm, the veins are solitary-polypoid in nature;
3rd degree - the diameter of the VRV is more than 10 mm, the veins are thin-walled, polypoid in nature, they represent an extensive conglomerate of nodes.

The classification of the American Association for the Study of Liver Diseases (AASLD) distinguishes 3 stages of VRV):
· 1st stage- small veins, minimally rising above the mucosa of the esophagus;
· 2nd stage- middle veins, tortuous, occupying less than a third of the lumen of the esophagus;
· 3rd stage- large veins.
In international classifications, it is proposed to use the most simplified division of varicose veins into 2 stages:
· small veins(up to 5 mm);
· Large veins(greater than 5 mm), since the risks associated with bleeding are the same for medium and large veins. The frequency of bleeding is 5-15% per year, it stops spontaneously in 40% of patients, recurring, in the absence of treatment, develops in about 60% of patients, on average within 1 to 2 years after the first episode.

Clinical picture

Symptoms, course

Diagnostic criteria for making a diagnosis:

Complaints and anamnesis:

Complaints:
vomiting of scarlet (fresh) blood/coffee grounds;
tarry stools / loose stools with little blood change (clinical signs of bleeding);
· weakness;
· dizziness;
cold clammy sweat
· noise in ears;
frequent heartbeat;
short-term loss of consciousness;
Thirst and dry mouth (clinical signs of blood loss).

Disease history:
intake of rough, spicy food, alcohol, drugs (NSAIDs and thrombolytics);
repeated vomiting, bloating, weight lifting;
suffers from cirrhosis of the liver, past hepatitis, suffers from chronic alcoholism;
History of episodes of bleeding
Previously transferred endoscopic ligation of the VRV of the esophagus, vein sclerotherapy.

Physical examination(Appendix 1, 2):
State patient with severe bleeding
· 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;
decrease in skin turgor;
an increase in the volume of the abdomen (ascites);
The presence of dilated veins on the lateral surface of the abdomen (jellyfish head);
Percussion borders of the liver are enlarged (may be reduced);
palpation surface of the liver is bumpy, the edges are rounded;
The presence of telangiectasias on the skin;
hepatic palms;
The presence of edema on the lower extremities, on the lateral and lower abdomen;
The nature of the pulse> 100 in 1 min., frequent, weak filling;
· GARDEN (< 100 мм.рт.ст.) тенденция к снижению в зависимости от степени кровопотери;
· NPV (20 and > in 1 min) tendency to increase;
oxygen saturation in venous blood< 90%.

Diagnostics

The list of basic and additional diagnostic measures:

Basic (mandatory) diagnostic examinations performed at the outpatient level: not performed.

Additional diagnostic examinations performed at the outpatient level: not performed.

The minimum list of examinations that must be carried out when referring to planned hospitalization: not carried out

The main (mandatory) diagnostic examinations performed at the inpatient level (in case of emergency hospitalization, diagnostic examinations are performed that were not performed at the outpatient level):

physical examination (counting the pulse, counting the respiratory rate, measuring blood pressure, measuring saturation, digital examination of the rectum);
· general blood analysis;
· general urine analysis;
biochemical blood test (total protein and its fractions, bilirubin, ALT, AST, alkaline phosphatase, LDH, cholesterol, creatinine, urea, residual nitrogen, blood sugar),
· KOS;
determination of the blood group according to the ABO system;
Determination of the Rh factor of the blood;
· coagulogram (PTI, INR, TV, APTT, fibrinogen, clotting time);
· D-dimer;
· PDF;
ECG;
EFGDS to remove the previously noted level of evidence

Additional diagnostic examinations performed at the inpatient level (in case of emergency hospitalization, diagnostic examinations are performed that were not performed at the outpatient level):
determination of hepatitis markers by ELISA;
Determination of oncomarker (AFP) by ELISA;
bacteriological culture of urine;
Ultrasound of the abdominal organs;
· Ultrasound of the kidney;
CT scan of the abdomen
X-ray examination of the esophagus and stomach with contrasting (double contrasting);
splenoportography.

Diagnostic measures taken at the stage of emergency care:
collection of complaints, anamnesis of the disease and life;
physical examination (counting the pulse, heart rate, counting the respiratory rate, measuring blood pressure).

Instrumental research:
ECG- there are changes that depend on the initial state of the cardiovascular system (signs of myocardial ischemia, a decrease in the T wave, ST segment depression, tachycardia, rhythm disturbance).
EFGDS - the presence of dilated veins of the esophagus, their length, shape (tortuous or stem), localization, size, state of hemostasis, predictors of bleeding risk (red markers).
EFGDS should be done as early as possible. The timing of this study is 12-24 hours from the moment the patient arrives.(UD-class I, level A).
On EFGDS, the presence or absence of red signs on varicose veins of the esophagus and stomach should be noted (LE-class IIa, level C).

Indications for consultation of narrow specialists:
consultation with a nephrologist in case of suspected kidney pathology;
consultation with an oncologist in case of suspected oncopathology;
consultation of an infectious disease specialist in the detection of infectious diseases and the development of toxic hepatitis;
consultation with a cardiologist in case of pathology of the cardiovascular system;
consultation of a neuropathologist in case of pathology of the nervous system;
Consultation of an obstetrician-gynecologist in the presence of pregnancy to resolve issues of treatment tactics.

Laboratory diagnostics

Laboratory research:
· general blood analysis: decrease in red blood cells, 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) by 2 times or more from the norm, an increase in thymol > 4 U, a decrease in sublimate test, alkaline phosphatase, LDH-214- 225 U/l; lowering cholesterol< 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 increase by 0.5 µmol/l, urea > 6.5 mmol/l.
· coagulogram: decrease in PTI< 70%, фибриноген < 2 г/л, АЧТВ >60 sec, PT > 20%, TI > 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 a particular 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 of bleeding from varicose veins of the esophagus in portal hypertension syndrome.

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Treatment

Treatment goals:

control of the source of bleeding;
prevention and treatment of SBP, HRS. HE;
Prevention of secondary bleeding from VRV.

Treatment tactics:

Non-drug treatment:
Mode- I.II;
Diet- table number 5 (Appendix 3).

Medical treatment:

At the outpatient level, urgently:
Sodium chloride solution 0.9% 400.

On inpatient treatment:
Replenishment of the BCC.
ITT for mild blood loss:
· Blood loss of 10-15% BCC (500-700 ml): intravenous transfusion of crystalloids (dextrose, sodium acetate, sodium lactate, sodium chloride 0.9%) in the amount of 200% of the volume of blood loss (1-1.4 l).
ITT with an average degree of blood loss:
Blood loss 15-30% 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:
With 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% from the volume of blood loss (3-6 liters). Transfusion of blood components is indicated (erythrocyte mass, FFP 30% of the transfused volume, platelet concentrate at the level of platelets< 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, erythrocytes, coagulogram indicators: INR, PTI, fibrinogen.
The critical level of indicators is: hemoglobin - 70 g/l, hematocrit - 25-28%. . It is necessary to maintain the level of hemoglobin ~ 80 g/l (LE-class I, level B).
· With hemocoagulation syndrome and thrombocytopenia, the safest colloidal solution is succinylated gelatin. The rate of infusion is determined by the level of blood pressure. Until the bleeding stops, SBP should not exceed 90 mmHg. But the infusion rate should exceed the rate of blood loss - 200 ml / min in 1 or 2-3 veins.
Criteria for the adequacy of the conducted ITT:
An increase in CVP (10-12 cm of water column);
hourly diuresis (not less than 30 ml/hour);
until the CVP reaches 10-12 cm of water. and hourly urine output of 30 ml/hour ITT should be continued.
· with a rapid increase in CVP above 15 cm. it is necessary to reduce the rate of transfusion and reconsider the volume of infusion;
Clinical criteria for the restoration of BCC (elimination of hypovolemia):
increase in blood pressure;
decrease in heart rate;
increase in pulse pressure;
increase in blood saturation;
warming and discoloration of the skin (from pale to pink).
Vitamin K supplements:
Menadione sodium bisulfite 2 ml 3 times / intravenously.
proteolysis inhibitors(aprotinin/analogues: contrycal, aprotinin) reduce the need for replacement therapy and reduce blood loss. It is recommended to use 50,000 IU of contrykal, then 10,000-20,000 every 4-6 hours. The initial dose of aprotinin in hemorrhagic shock is 500 thousand CIE. The rate of administration is not more than 5 ml / min, then in / in the drip of 50 thousand CIE per hour (UD - D).
Pharmacological therapy to reduce portal pressure:
The use of vasoactive drugs help stop bleeding in 75-80%. (UD-class I, level A).
Of the vasoconstrictor drugs (to reduce PP) used in the treatment of bleeding from VRV, meropenem and its analogues, octreotide and vapreotide, have an advantage, as they have a low side effect. Their use is possible immediately, as soon as bleeding from the VRV is established and even if it is suspected (LE-class I, level A). .
Octreotide: is administered as an intravenous bolus of 50 mcg/h, followed by continuous intravenous administration through a doser of 50 mcg/h for 5 days or drip intravenously for 5 days (UD-5D). Or 0.025 mg/h (UD-A) is administered.
Terlipressin: patient weight<50 кг - 1 мг; 50-70 кг - 1,5 мг; вес >70 kg - 2 mg. Then intravenous bolus 2 mg every 4 hours for 48 hours, from day 3, 1 mg every 4 hours up to 5 days (Appendix 4). Or 1000 mcg every 4-6 hours for 3-5 days before stopping and for another 2-3 days to prevent recurrence of bleeding.
Somatostatin: IV bolus of 250 mcg over 5 minutes and may be repeated 3 times within 1 hour. Then continuous administration of 6 mg (=250 µg) for 24 hours. The dose may be increased up to 500 mcg/h. Side effects are rare and there are no contraindications. Compared to terlipressin, the effect is the same (reduces relapse and controls bleeding). In the absence of this drug, its synthetic analogues are shown - octreotide or vapreotide.

Treatment of spontaneous bacterial peritonitis (SBP):
Antibiotic therapy (within 7-8 days):
Third generation cephalosporins (cefotaxime, ceftriaxone, cefoperazone, ceftazidime):
Cefotaxime 2 g 2 times a day IV, ceftazidime 1 g 2 times a day IV;
amoxicillin/clavulanate 1 g 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 IV;
imipenem 500 mg twice or 1 g once a day IV;
doripenem 500 mg 2 times / in;
Meropenem 1 g 1 time / in;

In nosocomial SBP, piperacillin/tazobactam 2 g once daily IV is recommended as empiric 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 enter at the rate of 1 g/kg of the patient's weight on the 3rd day of treatment.
Contraindications:
The use of diuretics in the acute period;
the use of aminoglycocides.

Treatment of hepatic encephalopathy:
Reducing the daily intake of protein 20-30 g;
Reception of lactulose 30-50 ml every 1-2 hours (before defecation). 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:
With deterioration of kidney function (increased creatinine):
Discontinue diuretics;
albumin in / in 1 g / kg of weight;
Sodium chloride solution 0.9% 400 ml intravenously drip. If this does not reduce creatinine, then perform an ultrasound of the kidneys, 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 to 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 BP. The goal of treatment is to increase the MAP by 15 mm. rt. Art.

Drug treatment provided at the stage of emergency emergency care:
Sodium chloride solution 0.9% 400 ml IV drip;
Dopamine 4% or 0.5% solution 5 ml IV drip.

Other treatments:

Other types of outpatient treatment
oxygen inhalation.

Other types provided at the stationary level:
oxygen inhalation;
catheterization of 2 peripheral veins or 1 central vein;
Endotracheal intubation (indications, mode).
IVL is indicated for severe patients (with massive severe bleeding and impaired level of consciousness), should be performed in patients before EFGDS.

Indications for IVL are:
impairment of consciousness (less than 10 points on the Glasgow scale) (Appendix 2);
lack of spontaneous breathing (apnea);
Increased breathing more than 35-40 per minute, if this is not associated with hyperthermia (body temperature above 38.5 ° C) or severe uncorrected hypovolemia.

Arterial blood gases:
PaO 2< 60 мм рт ст при дыхании атмосферным воздухом или PaСО 2 >60 mm Hg in the absence of metabolic alkalosis;

Bleeding control with obturators:(UD-class I, level B).
Sengstaken-Blakemore probe:
Indications:
continued bleeding from the esophagus
Contraindications:
Stopped bleeding from the esophagus.
Monitoring the effectiveness of hemostasis is carried out by dissolving the cuff of the probe 4 hours after its installation. When the bleeding stops, the cuffs are deflated. The duration of the probe is up to 24 hours.

Linton tube
Indications:
gastric localization of VRV;
Contraindications:
Stopped bleeding from the RVV of the stomach.

Danish stent(self-healing):
Indications:
Continuing 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). (Annex 5) :
Endoscopic ligation(EVL) :
Indications:

Contraindications:
the agonal state of the patient;
anatomical defects of the esophagus (strictures).

(performed intravasally and paravasally):
Indications:
Continuing and/or stopped bleeding from the esophagus VRV.
Contraindications:
the agonal state of the patient;
anatomical defects of the esophagus (strictures).

Cleansing enema:
Indications:
The presence of blood in the intestinal lumen.

Enema with lactulose:
Indications:

300 ml of lactulose per 1 liter of water, injected every 4-6 hours.

Using the "MARS- Molecular Adsorbent Recirculating System» - albumin dialysis:
Indications:
hepatic encephalopathy.

vasoconstrictor therapy ( bridge therapy) for patients awaiting liver transplant :
Indications:
hepato-renal syndrome.

Other types of treatment provided at the stage of emergency medical care:
oxygen inhalation;
transfer to mechanical ventilation according to indications in critical condition;
catheterization of peripheral veins.

Surgical intervention:

Surgical intervention provided on an outpatient basis: not performed.

Surgical intervention provided in a hospital:
OperationTIPS
Indications:
With the ineffectiveness of pharmacological therapy and EG.
TIPS and bypass surgery are indicated in Child-Pugh class A (LE-class I, level C).
Contraindications:
The severity of the disease class B / C according to Child-Pugh (decompensated stage).
Liver transplant:
Indications:
· cirrhosis of the liver;
some forms of chronic hepatitis;
Some forms of malignant neoplasms of the liver.
Contraindications:
chronic infections;
Presence of the HIV virus in the body
mycobacterium tuberculosis,
· syphilis;
viral hepatitis.

Patsior's operation (transverse subcardial gastrotomy):
Indications:
ongoing bleeding from the VRV of the cardioesophageal junction and the stomach in the absence of conditions for endoscopic hemostasis and other methods of stopping
Contraindications:
the agonal state of the patient;
PON.

Treatment effectiveness indicators:
stop bleeding from the VRV of the esophagus and stomach;
Prevention of recurrent bleeding
prevention and relief of HRS, SBP, HE;
Decreased mortality rates.

Drugs (active substances) used in the treatment

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 discontinued;
· NSBB significantly reduces the risk of rebleeding.
For the prevention of secondary bleeding from the VRV of 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 by decreasing heart rate (bring 55-60 in 1 min);
+ VRV ligation (EVL). Apply up to 6 rings to the veins every 1-2 weeks. The first control EFGDS after 1-3 months and then every 6-12 months to control the recurrence of VRV. (UD-class I, level C).

Second line therapy:
If NSBB+ EVL was not effective, then TIPS or bypass surgery is indicated, but only in class A patients according to 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) VRV is associated with a lower rate of rebleeding and is the method of choice.
If a patient experiences rebleeding from a VRV despite a combination of pharmacological and endoscopic treatment, TIPS or bypass surgery is recommended in such cases (subject to local conditions and experience with their use. (LEV class I, level A). Candidates for liver transplantation should be referred to a transplant center (LE-class I, level C).

For secondary prevention of bleeding from VRV is not indicated:
· NSBB + sclerotherapy;
EVL + sclerotherapy.

Antibacterial prophylaxis of spontaneous bacterial peritonitis (SBP):
The use of quinolones within 7 days: (UD-class I, level A).
norfloxacin 400 mg 2 times a day per os for 7 days;
or ciprofloxacin 400 mg IV drip 1 time for 7 days;
Or ceftriaxone 1 g IV once a day for up to 7 days. This drug is more effective in patients with ascites, encephalopathy, and in 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 discharge from the hospital, the patient is referred to a gastroenterologist or hepatologist;
Selection and referral for liver transplantation (transplantologist).

Information

Sources and literature

1. Minutes of the meetings of the Expert Council of the RCHD MHSD RK, 2015
   1. List of used literature (valid research references to the listed sources are required in the text of the protocol): 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 of the 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 March 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 hem-orrhage in cirrhosis N. Engl J. Med., 2010, 362: 823-832 20) De Franchis R., Revising consensus in portal hypertensio n: 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 06.11.2000. Rules for the storage, transfusion of blood, its components and preparations. Appendix No. 501 dated July 26, 2012 "Rules for the storage, 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) A large reference book of medicines / under Red Ziganshina L.E. et al., M., 2011

Information

List of protocol developers with qualification data:
1) Zhantalinova Nurzhamal Asenovna - Doctor of Medical Sciences Professor of the Department of internship and residency in surgery of the RSE on REM “KazNMU named after A.I. S.D. Asfendiyarov".
2) Menshikova Irina Lvovna - Candidate of Medical Sciences, Associate Professor, Head of the Endoscopy Course of the Department of Gastroenterology and Hepatology with the Course of Endoscopy, 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 on REM "Scientific Research Institute of Cardiology and Internal Diseases".
3) Gulzhan Akhmetzhanovna Zhakupova - SME NA REM Burabay Central District Hospital. Deputy chief physician for audit, anesthesiologist - resuscitator, the highest category.
4) Mazhitov Talgat Mansurovich - doctor of medical sciences, professor of JSC "Astana Medical University", doctor of clinical pharmacology of the highest category, general practitioner of the highest category.

Indication of no conflict of interest: No

Reviewers: Turgunov Ermek Meyramovich - Doctor of Medical Sciences, Professor, Surgeon of the highest qualification category, RSE on REM "Karaganda State Medical University" of the Ministry of Health of the Republic of Kazakhstan, Head of the Department of Surgical Diseases No. 2, an independent accredited expert of the Ministry of Health of the Republic of Kazakhstan.

Indication of the conditions for revising the protocol: Revision of the protocol 3 years after its publication and from the date of its entry into force or in the presence of new methods with a level of evidence.

Attachment 1

Appendix 2

Appendix 3

Appendix 4

Annex 5

Attached files

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Stopping bleeding, restoring hemodynamics and ensuring effective oxygen transport to the tissues, as the main urgent measures successfully carried out in the first days from the onset of gastrointestinal bleeding, should be transferred to the treatment program for anemia and the disease that caused bleeding. Their treatment is carried out taking into account the etiology, pathogenesis, localization, as well as the characteristics of the clinical manifestation and course of the disease, and is aimed not only at preventing the recurrence of bleeding, but also at achieving the possibility of a complete recovery of the patient.

The source of bleeding in the esophagus can be varicose veins, gastroesophageal reflux disease (GERD), tumors, hiatal hernia (HH). Rare causes of bleeding may be manifestations of esophageal diverticula, as well as ruptures of the thoracic aorta during its aneurysm or medical manipulations (bougienage of cicatricial stenosis of the esophagus).

The most frequent and severe bleeding occurs from varicose veins of the lower third of the esophagus in portal hypertension syndrome. They are characterized by a particular severity of clinical manifestations due to massive blood loss against the background of functional decompensation of the liver.

The resulting high pressure in the portal vein system leads to a restructuring of the blood circulation, first to its expansion of the normally existing portcosal anastomoses, and then to the development of varicose veins (phlebectasia), enlargement of the spleen and the appearance of ascites. Varicose veins are exposed mainly to the branches of the coronal veins of the stomach, which directly anastomose with the veins of the esophagus. Veins, due to which anastomoses are formed, gradually expand, their walls become thinner, resulting in the formation of saccular and serpentine protrusions into the lumen of the cardial esophagus and the cardia of the stomach.

Phlebectasia is divided into 3 degrees:
I degree - veins of the cardia up to 3-4 mm in diameter,
II degree - tortuous veins of the cardia and the fornix of the stomach up to 4-6 mm in size,
Grade III - large clusters > 6 mm.

Violation of blood circulation leads to trophic changes in the walls of the veins and the mucous membrane of the esophagus, thinning and increased compliance of the esophageal wall. At the same time, its lumen does not narrow.

Acute bleeding occurs due to rupture of esophageal phlebectasia. 3 factors contribute to its occurrence: hemodynamic (hypertension in the form of a crisis in the portal system), peptic (erosion of the mucous membrane of the esophagus and cardia), and a violation of the blood coagulation system. Bleeding is preceded by emotional stress, physical overload, coughing, eating coarse food and alcohol.

The clinical manifestation of bleeding from varicose veins of the esophagus is characterized, as a rule, by an acute onset. After a short period of disturbance of general well-being (weakness, dizziness, nausea, pain and rumbling in the abdomen), uncontrollable vomiting of little-changed blood with clots occurs. Often, bloody vomiting that occurred against the background of apparent well-being was the reason for the initial visit to the doctor about cirrhosis of the liver.

A little later, a plentiful, fetid, tar-like stool (melena) appears. Bleeding from ruptures of esophageal-cardiac phlebectasia is usually profuse and quickly leads to the development of a characteristic clinical picture of hemorrhagic shock.

In patients with cirrhosis of the liver, clinical signs of decompensation of its function appear relatively quickly after the first bleeding. Initially, they manifest themselves in the form of encephalopathy (lethargy, weakness, drowsiness, disorientation in time and space, or vice versa, euphoria, motor excitation, inadequate assessment of one's own state occurs). Then there is yellowness of the sclera and skin, a characteristic sweetish "liver" smell from the mouth, diuresis decreases, and ascites increases. Then a coma develops. For the extrahepatic form of portal hypertension, hepatocellular insufficiency is less typical.

Facilitates the diagnosis of bleeding from varicose veins of the esophagus, the presence of an enlarged dense liver, splenomegaly, ascites, dilated saphenous veins on the anterior abdominal wall. During bleeding, the size of the spleen may decrease. After the bleeding stops, it usually gradually reaches its original size.

The most effective method of emergency diagnosis is fibroesophagogastroscopy. It allows not only to identify varicose veins in the esophagus, to clarify their localization, but also in 1/3 of cases to identify the direct source of bleeding in the form of erosion on the surface of the varicose vein covered by a blood clot.

In addition, with varicose veins of the esophagus, other causes of gastric bleeding can be established, more often from a peptic ulcer in the pyloroduodenal zone. Morphological changes in the liver, spleen and venous vessels are well detected by sonography in the form of enlargement and fibrosis of the liver, expansion of the portal and splenic veins, enlargement of the spleen, ascites.

X-ray diagnostics is less effective and unsafe. It is used when planning an operative intervention or using the Blakemore probe for tamponade of the source of bleeding. Of the laboratory indicators, in addition to the general clinical blood test, it is important to determine the level of bilirubin in the blood serum, the content of total protein and protein fractions, the activity of alkaline phosphatase, alanine and aspartate aminotransferases, gammaglutamine transpeptidase, blood sugar levels, and a detailed coagulogram.

The main objectives of the treatment of acute portal bleeding are:
1) Stop bleeding and prevent its recurrence;
2) Restoration of hemodynamics;
3) Prevention of universal liver failure.

Stopping bleeding begins with conservative measures. Hemostasis in most patients is achieved by local action on the source of bleeding using a three-cavity probe with inflating Blakemore-Sengstaken-type balloons (Fig. 15). Stopping bleeding is achieved by mechanical compression of phlebectasia by inflating first the cardiac and then the esophageal cuff.

At the same time, the contents of the stomach are aspirated through the internal lumen of the main probe and washed with antacid solutions. If the bleeding has stopped, then after 2-3 hours, liquid nutrient mixtures can be introduced in small portions through the probe. The probe is left in the esophagus for two or even three days. At the same time, every 12 hours the air from the cylinders is released and the patient is allowed to rest for 1-2 hours.

You can also stop bleeding by injecting sclerosing agents (thrombovar, varicocid) into the damaged esophageal vein through an endoscope. Balloon tamponade, according to various authors, gives an effect of 42 to 85%, endoscopic injection scleropathy - from 72 to 93%. In recent years, the dominant role in stopping bleeding from varicose veins of the esophagus has been occupied by endoscopic clipping and ligation of the bleeding node.

Along with this, medications are used, the action of which is aimed, on the one hand, at reducing pressure in the portal vein, and on the other hand, at increasing the blood coagulation potential. In solving the first problem, sandostatin and its analogues became widespread (described in detail in Chapter 10).

It is possible to use pituitrin, which is better to be administered intravenously at a dose of 15-20 U per 200 ml of 5% glucose solution with repeated administration of 5-10 U per 20 ml of glucose solution after 30 minutes. The use of vasopressin and its analogues, nitrates (nitroglycerin and nitroprussin) also contributes to a decrease in pressure in the portal vein.

For the same purpose, non-selective β-blockers (propranolol from 0.04 to 0.2 per day), calcium antagonists (verapamil) in combination with diuretics are used. Vikasol, calcium chloride, aminocaproic acid and other drugs listed in the section of general measures for gastrointestinal bleeding contribute to an increase in the coagulation potential and the prevention of fibrinolysis.

Persistent conservative treatment is more justified in the case of extrahepatic portal hypertension. With cirrhosis of the liver, it is necessary to achieve a final stop of bleeding in a short time, since its continuation inevitably leads to the development of universal liver failure, which completely excludes the possibility of surgical intervention under anesthesia.

Scientific achievements in the study of pathogenesis, the development of new methods of diagnosis and treatment as they accumulate, are regularly reviewed at various international forums with the revision and addition of recommendations for doctors of all levels on the tactics of managing patients with bleeding from varicose veins in the esophagus.

The latest Baveno IV consensus (Italy, 2005) adopted the following provisions (De Frenchis R, 2005):
1.1. The control of ongoing hemostatic therapy and the stabilization of BCC is based on the results of studies at the beginning and 6 hours after the onset of bleeding according to systolic pressure, hematocrit (Hst up to 27%) and hemoglobin (Hb up to 90 g / l).

1.2. The doctor should assess the possibility of recurrent bleeding within 5 days after the onset of bleeding by the release of fresh blood 2 hours after the start of basic therapy in the form of the following indicators:

1.2.1. Isolation through the installed nasogastric tube more than 100 ml of fresh blood;
1.2.2. Decrease in Hb and Hst by more than 3 and 9 units, respectively;
1.2.3. The death of the patient;
1.2.4. Changes in the integral index of the normalized blood transfusion index ABRI (Adjusted blood transfusion requirement index) above 0.75 at any time during therapy.

ABRI \u003d (Hstk - Hstn) x KEUP + 0.1,

Where Hstk is the final hematocrit,
Hst - initial hematocrit,
KEUP - the number of units of infusion solutions.

The use of blood transfusions is advisable when the following indicators are reached: Hct = 24% and Hb = 80 g/l.
1.3. The conclusion about the recurrence of bleeding is carried out on the basis of the following criteria:
1.3.1. The presence of the release of fresh blood through a nasogastric tube in the amount of 100 ml or the appearance of melena;
1.3.2. ABRI > 0.5;
1.3.3. Decreased Hb by 3 g/l without the use of blood transfusion.

Assessment of the severity of liver cirrhosis is based on simple criteria:
I degree - without varicose veins and ascites;
II degree - varicose veins without ascites;
III degree - varicose veins and ascites;
IV degree - bleeding from varicose veins and ascites.

The obligatory diagnostic confirmation that the bleeding is from varicose veins is the following data:
1) endoscopic examination of the esophagus;
2) Hepatic vein pressure gradient (HVPG) is the most important criterion for evaluating the effectiveness of measures taken in the treatment of varicose bleeding.

The overall severity of the condition of a patient with liver cirrhosis and the risk of mortality is assessed based on the study of indicators obtained using the Child rating scale, taking into account HVPG, the presence of "spontaneous bacterial peritonitis", hepatorenal syndrome and other systemic manifestations of the disease.

The Baveno IV Consensus also adopted the following decisions on the prevention and treatment of bleeding in patients with portal hypertension syndrome:
1. An indicator of esophageal varices is an HVPG gradient > 12 mm Hg. Art. Its dynamics may indicate the formation of portosystemic collaterals. At the same time, the effectiveness of monotherapy with non-selective beta-blockers correlates with a decrease in the HVPG gradient. However, this monitoring is not recommended for routine use in everyday practice.

2. There is no reliable evidence that the use of any combination of therapy, including the use of beta-blockers, can prevent varicose veins of the esophagus and stomach.

3. For patients who, against the background of "small varicose veins" of the esophagus, have not previously had bleeding, it is advisable to include non-selective beta-blockers in the treatment in order to prevent bleeding. The best result of such treatment was noted in patients in whom "small" varices are red in color or those patients who belong to class C on the Child-Pugh scale.

4. It is not recommended to use monotherapy with isosorbitol mononitrate or its combination with a non-selective beta-blocker, as well as the combination of a non-selective beta-blocker with spironolactone, in order to prevent primary bleeding.

5. In patients with "medium to large varices" of the veins of the esophagus, endoscopic knot ligation is recognized as a priority and is also recommended for patients who have contraindications for the use of non-selective beta-blockers. However, statistical data indicate that the mortality rate in both groups did not have a significant difference.

6. Treatment of acute bleeding in portal hypertension syndrome should include:
a) restoration of hemodynamics using plasma-substituting solutions to a stable achievement of hemodynamic parameters, Hb not lower than 80 g/l, taking into account such other indicators as the patient's age, previous blood pressure level, comorbidities:
c) there are no convincing data on the benefits of measures to prevent coagulopathy and thrombocytopenia;
c) the use of coagulation factor proenzymes VIIla (von Willebrand factor) may be promising;
d) the use of broad-spectrum antibacterial drugs is justified as prophylactic agents in the complex therapy for active bleeding;
e) interventions for the prevention of hepatic encephalopathy with the use of drugs based on lactulose / lacitol are recommended, although there is no convincing evidence of their unconditional benefit.

7. In order to predict the risk of recurrent bleeding, it is advisable to focus on the indicators presented in the Child-Pugh scale, on endoscopic signs, the HVPG gradient, the risk of infection, signs of liver failure and thrombosis of the veins of the portal system, as well as the level of ALaT. At the same time, it was noted that there is no reliable individual model for predicting the recurrence of bleeding in patients with portal hypertension syndrome.

The main method for predicting the risk of rebleeding is endoscopic assessment of the esophageal mucosa, the condition of varicose veins, their size, blood accumulation, and wall color. It is recommended that endoscopic examination of patients undergoing conservative treatment be performed at least every 12 hours.

8. Balloon tamponade is appropriate only in patients with massive bleeding and only as a temporary measure lasting no more than 24 hours until an adequate medical management is determined.

9. With regard to vasoactive drugs, somatostatin, terlipressin, octreotide, etc., it was approved that they should be prescribed even before endoscopic clarification of the source of bleeding in all cases, except for individual intolerance to the drug, and for at least 2-5 days.

10. Endoscopic methods of stopping active bleeding are more preferable than medical treatment alone. In this case, when bleeding from varicose veins of the esophagus, it is advisable to perform ligation of varicose veins. In case of bleeding from varicose veins of the upper parts of the stomach, the use of adhesive tissues based on N-butyl cyanoacrylate is more effective.

11. Patients with bleeding in portal gastropathy, who are contraindicated for non-selective beta-blockers, should use the methods of early surgical shunting or TIPS (Transjugular Intrahepatic Portosystemic Sunting) - a technique that consists in the formation of a portosystemic anastomosis by creating a message between the branches of the hepatic and portal veins using puncture of the portal vein from the hepatic branch through the liver parenchyma, followed by dilation and stenting of the formed canal.

TIPS is the treatment of choice for patients at high risk of surgery, as well as the only palliative treatment for cirrhotic patients awaiting liver transplantation with incurable ascites and a high risk of esophageal bleeding.

12. Questions remain unexplored:
a) the optimal duration of the use of vasoactive drugs;
b) the effectiveness of early TIPS;
c) prospects for conservative or endoscopic hemostasis in bleeding from gastric varices;
d) development of an individual prognostic scale of risk factors for rebleeding.

It is not always possible to achieve a stable stop of bleeding from RVV using conservative and minimally invasive methods, despite the indisputable achievements in their development and widespread implementation. Therefore, both in stopping acute bleeding and especially in preventing its recurrence, surgical operations continue to retain their importance [Onopriev V.I. et al. 2005; Abdurakhmanov D, 2009].

The volume of the operation depends on the degree of expansion and localization of varicose veins, the frequency of hypertensive portal crises, the assessment of compensation for cirrhosis of the liver [Nazirov F.T. et al. 2005]. Thus, in assessing the compensation of liver cirrhosis, respectively, and the risk of surgery in this pathology, the Child-Pugh gradation scale remains the most common. The ball assessment of the patient's condition on this scale is divided into three classes of Table. 38.

Tab. 38 Operational risk assessment for bleeding from esophageal varices in liver cirrhosis

The condition of the patient of class B (subcompensation), the sum of the scores is 7-9, allows performing bypass surgery only in the absence of active bleeding, but a high risk of recurrence, that is, it is possible to carry out pathogenetic correction of portal hypertension. In all other cases, azigoportal separation operations are performed [Eramishantsev A.K. et al., 2006; Zhantalinova N.A., 2006].

Practical activity shows that in patients with portal hypertension class A is not determined, and class B is diagnosed only in 1.53.0%. In class C - the sum of the scores is 10 and above, the decompensation of the pathological process with the maximum operational risk is stated. In addition, this class includes patients with a 3-point score of two indicators on the Child-Pugh scale with bilirubinemia over 68 µmol/l, albumin level below 28 g/l, and prothrombin index less than 50%.

The operation in this category of patients is aimed only at stopping bleeding according to vital indications in a minimal amount. However, an extremely severe degree of hepatorenal insufficiency with the development of coma is an absolute contraindication to surgical treatment and justifies further attempts at conservative hemostasis.

With indications for palliative surgery, ligation, clipping, and suturing of varicose veins are most often performed both intraorganically (through the gastrostomy opening) and extraorganically. These operations of azigoportal dissociation have recently been performed: traditional (laparotomy) from a mini-access and laparoscopically. In the latter case, extraorganic clipping of esophageal varicose veins is performed after seromyotomy and under endoscopic control. Circular stitching is recommended to be supplemented with selective proximal vagotomy with the formation of antireflux cardia.

Azigoportal dissociation is supplemented with splenectomy in case of thrombosis or occlusion of more than 80% of the splenic vein, the existence of an arteriovenous anastomosis of the spleen. Taking into account the high degree of operational risk class B or C, these operations are the method of choice for stopping bleeding of this genesis.

At low operational risk, bypass operations are widely used to create an artificial anastomosis between the portal and systemic inferior vena cava. A large number of methods of bypass surgery are conventionally divided into selective and non-selective. With non-selective shunting, a direct portocoval anastomosis is formed.

Due to the rapid progression of liver failure, non-selective shunting operations (portocoval, mesenteric-cooval, splenorenal, etc.) have given way to selective ones. Partial shunting is classified as selective, although in fact it is an intermediate option. The most positive long-term results in terms of recurrence of bleeding from varicose veins of the esophagus are obtained by side-to-side splenorenal anastomosis, which reduces portal blood flow by 20-25%.

Selective shunting is more preferable due to dosed (partial) decompression of portal hypertension with its division into the mesentericoportal and esophagogastrolienal systems.

Proposed by Warren W. (1998), distal splenorenal shunting is widely used today due to the simplicity of the operation, good immediate and long-term results, and a low risk of developing acute liver failure. This creates an anastomosis between the splenic and left hepatic veins [Pavlenko P.P. et al., 2005].

The introduction of new technologies (endostaplers, prostheses, shunts) into vascular surgery using minimally invasive approaches expands the possibilities for performing selective bypass surgery, but the surgical risk factors remain consistently high with unfavorable long-term results. Therefore, the correction of risk factors for decompensation of portal hypertension remains an unresolved issue of modern surgery [Zherlov T.K. et al., 2005; Sparrow A.V. from osavt., 2007; Yeramishantsev L.K., 2007].

Stepanov Yu.V., Zalevsky V.I., Kosinsky A.V.

Bleeding with varicose veins is the most dangerous complication that requires immediate hospitalization of the victim. The causes of the disease and the methods of helping the patient with bleeding from varicose veins in the lower extremities will be discussed in this article.

Possible causes of bleeding

Varicose veins most often affect women (in 75% of cases) older than 30 years of age. Very often, varicose veins occur in women during pregnancy and after childbirth. There are also varicose veins in men, especially those who are at risk (leading a sedentary lifestyle, experiencing excessive stress on the legs, having a genetic predisposition, etc.). It is extremely rare, but still there are varicose veins in children.

If varicose veins do not receive the necessary treatment, they continue to thin out, and sooner or later there comes a critical moment when the vessel ruptures under the influence of blood that has stagnated in it. Most often, the rupture occurs in the lower leg. Bleeding is very profuse, and the loss of blood is so great that the consequence of this can be fatal.

Provoking factors for the occurrence of bleeding can be:

• mechanical impacts (impacts, cuts, bruises, punctures);
• weight lifting;
• significant physical activity;
• coughing;
• prolonged stay on the legs;
• constant squeezing of the veins with uncomfortable clothes or shoes;
• hypertensive crisis.

At the initial stage, the disease very often proceeds secretly, however, with its exacerbation, the risk of bleeding increases sharply due to the weakness of the veins. Bleeding is localized in the lower third of the lower leg and in the ankle. Areas with pronounced venousness are especially vulnerable.

There is a classification of bleeding based on their causes and intensity:

1. Spontaneous. They arise as a result of neglected varicose veins, when the patient did not seek qualified help in time. The veins in such patients are clearly expressed, their pattern is clearly visible under the skin. Venous nodes and trophic ulcers are often noted. Usually not only veins are torn, but also nearby tissues.
2. Traumatic. Occur as a result of mechanical action on the vein. Even with minor injuries (for example, a small cut), blood flows in a powerful stream, although the victim may not feel it right away. It will not be possible to stop the loss of blood in an upright position. As a rule, the patient loses a lot of blood.
3. Subcutaneous. They can be either spontaneous or resulting from trauma. Depending on the site on which the affected vein is located, blood loss may be mild or significant. Subcutaneous bleeding is visually indicated by hematomas. The most potentially dangerous type of bleeding is from a vein in the area of ​​​​the ulcerative bottom. The cause of such an outpouring can be a purulent infectious process or autoimmune aggression, which led to tissue and venous necrosis.
4. Outdoor. Bleeding begins as a result of damage to the surface of the skin. Due to a cut or puncture of the dermis, the vascular walls are destroyed, and blood begins to leave a nearby vein.

For all types of bleeding from the dilated veins of the legs, the absence of pain in the patient is characteristic, even when it comes to traumatic injury. External blood loss is much more common than subcutaneous effusions.

Bleeding from the lower extremities is characterized by moderate or intense blood loss of dark blood from the damaged area. If a hematoma occurs, then a pain syndrome appears, entailing temporary disability.

Danger of bleeding

Since the victim most often does not experience pain at the time of bleeding, it is very likely that he will not notice the beginning of the process. As a result, patients often lose a lot of blood. In addition, when the patient becomes aware of blood loss, he may fall into a panic state, which excludes the adoption of reasonable decisions and only aggravates the situation. The consequence of panic is an increase in blood pressure, an acceleration of the heart rate and blood flow, which leads to even more intense blood loss.

It is impossible to predict the amount of blood loss in advance, but it is clear that the situation must be brought under control in order to prevent shock and death. To prevent the dangerous consequences of rupture of the veins, the patient must receive first aid.

emergency measures

If a vein in your leg bursts, you need to force yourself to remain calm. If done correctly, the bleeding can be stopped.

You need to take the following actions:

1. A hemostatic sponge is placed at the site of the ruptured vein. If a sponge is not available, you can use a clean piece of cloth folded several times.
2. A sterile gauze pad is placed on a sponge or piece of cloth. It must be folded several times.
3. An elastic bandage is applied on top.
4. When the bandage is applied, a very cold object (ice) should be applied to the affected area for 20-30 minutes.
5. Immediately after applying the bandage, you need to take a supine position with your legs raised up. If the bleeding started on the street, you don’t need to run around in search of a cold object yourself, but it’s better to ask the people around you about it.

1. The next step is to call for emergency medical assistance. If we are talking about an external rupture with varicose veins, doctors can apply finger pressure, applying a tight bandage. In cases with ruptures in ulcerated areas of the skin, a vein will need to be sutured to rule out septicopyemia and thromboembolism. If necessary and technically feasible, sclerotherapy with compression can be performed.
2. If the blood loss is large, antibiotics are given to prevent infection. In the case of internal ruptures, external ointment formulations, painkillers and non-steroidal anti-inflammatory drugs are used. Phlebotonics and phleboprotectors must be used.

Steps to take after bleeding has stopped

First of all, you need to make sure that the bleeding has stopped. This can be done as follows: we are located on a horizontal surface and lie with our leg raised for about half an hour, watching the bandage to see if the blood stain is increasing on it. If the spot does not change in size, it can be concluded that the bleeding has stopped. After that, you can lower the lower limb to the level of the body. For the rest of the day, strict bed rest should be observed. The bandage can not be removed until the morning.

During the day after the bleeding stops, you can not take drugs that thin the blood. You also need to pay special attention to the level of blood pressure.

In the morning you can not abruptly get out of bed. Too much activity can cause bleeding to resume.

So, getting out of bed should be done in several stages:

1. At first they sit on the bed, but the legs do not hang down - they are on the bed.
2. They sit on the bed for about 2-3 minutes, after which they lower their legs to the floor.
3. Again they wait a little and slowly rise to their feet.

The bandage during the time he was on the leg, firmly dries to the wound. It is categorically not recommended to tear it off by force, since in this case the bleeding will begin again. To avoid this, the bandage is moistened in a weak solution of potassium permanganate, furatsilina or plain water. The lower limb is lowered into a container with liquid for several minutes. When the bandage gets wet, it is removed, and a bactericidal patch is applied to the wound, which is worn for 2-3 days.

Rules of behavior

With a sudden rupture of a vein, it is important to adhere to several rules:

1. In the presence of varicose veins, carry with you the simplest set of medical supplies for first aid.
2. Don't panic.
3. Do everything possible to stop or stop the bleeding until the doctors arrive.
4. Do not use a tourniquet to stop bleeding. This method of stopping bleeding can only be used by experienced doctors. The fact is that stagnation in veins affected by varicose veins can cause bleeding from nearby vessels. If the blood loss is very intense, you can use finger compression of the vessels through a napkin.
5. When the bleeding is stopped, it is important to observe a calm mode of behavior during the day (or even more), avoiding physical exertion and stress.
6. In no case in the coming days, do not go to the bathhouse and do not take hot baths. As a result of a sharp expansion of blood vessels, blood loss can resume.

Prevention

Bleeding with varicose veins is a very dangerous complication of this disease. To prevent such a development of events, it is necessary to take a number of preventive measures:

1. Do not lift too heavy objects, avoid sports with jerky loads.
2. Maintain physical activity (with the help of therapeutic exercises, swimming).
3. Monitor body weight.
4. Avoid prolonged stay in an upright position.
5. Monitor blood pressure levels.
6. Avoid injury.
7. Wear comfortable, non-constricting clothing and shoes.
8. Do not delay with the treatment of varicose veins.

Thus, prevention is based on the prevention of those factors that can provoke bleeding. However, if nevertheless an unpleasant event has occurred, it is necessary to take all the measures described above to stop the bleeding and immediately call an ambulance.

Gap prediction

Within 2 years after the detection of liver cirrhosis, bleeding from varicose veins of the esophagus occurs in 35% of patients; in the first episode of bleeding, 50% of patients die.

There is a clear correlation between the size of varicose veins seen during endoscopy and the likelihood of bleeding. The pressure inside the 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. Schematic representation of the incision of the liver in the area of ​​the gate, where nodes are visible, squeezing the portal vein. The rest of the liver looks normal.

An important factor indicating a greater likelihood of bleeding are red spots that can be seen with endoscopy.

To assess the function of hepatocytes 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 assigned to 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 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 - allow the most reliable prediction of bleeding (Fig. 10-51).

Alcoholic cirrhosis has the highest risk of bleeding.

The likelihood of bleeding can be predicted using Doppler ultrasound. At the same time, the velocity 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), the likelihood of early development of bleeding is high.

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 the exclusion of spices, as well as the use of long-acting H2-blockers, do not prevent the development of coma.

Propranolol - a non-selective b-blocker that reduces pressure in the portal vein 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 at a dose that reduces the resting heart rate by 25% 12 hours after administration. The degree of pressure reduction in the portal vein is not the same in different patients. Taking even high doses in 20-50% of cases does not give the expected effect, especially with advanced cirrhosis. The pressure in the portal vein should be maintained at a level no higher than 12 mm Hg. . Monitoring of hepatic vein wedge pressure and endoscopically determined portal pressure is desirable.

Table 10-4. Classification of hepatocellular function in cirrhosis according to Child

Rice. 10-51. The significance of the increase in the size of varicose veins [small (M), medium size (C) and large (K)] in combination with the appearance of red spots (KP) on their surface (absent, single, many) and Child's group (A, B, C) to determine the likelihood of bleeding during 1 year.

Propranolol should not be prescribed for obstructive pulmonary disease. This can make resuscitation difficult if bleeding occurs. In addition, it contributes to the development of encephalopathy. Propranolol has a significantly pronounced “first pass” effect, therefore, with advanced cirrhosis, in which the excretion of the drug by the liver is slowed down, unpredictable reactions are possible. In particular, propranolol somewhat suppresses mental activity.

A meta-analysis of 6 studies suggests a significant reduction in bleeding but not mortality (Fig. 10-52). A subsequent meta-analysis of 9 randomized trials found a significant reduction in 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 sizes of 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 vein dilatation. Similar results were obtained with the appointment overwhelmed. 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 therefore not be used in advanced cirrhosis with ascites.

Meta-analysis of studies on preventive sclerotherapy found generally unsatisfactory results. There are no data on the effectiveness of sclerotherapy in preventing the first episode of bleeding or improving survival. Preventive sclerotherapy is not recommended.

Diagnosis of bleeding

AT clinical picture of bleeding from varicose veins of the esophagus, in addition to the symptoms observed with other sources of gastrointestinal bleeding, there are symptoms of portal hypertension.

Bleeding may be mild and manifest as chalky rather than hematemesis. The bowel may fill with blood before bleeding that has lasted for several days is recognized.

Bleeding from varicose veins in cirrhosis adversely affects hepatocytes. The reason for this may be a decrease in oxygen delivery due to anemia or an increase in metabolic requirements 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.

Often there is also bleeding that is not associated with varicose veins: from duodenal ulcers, gastric erosions, or in Mallory-Weiss syndrome.

In all cases, endoscopic examination should be performed to identify the source of bleeding (Fig. 10-53). Ultrasound is also required to determine the lumen of the portal and hepatic veins and to exclude mass formation, such as HCC.

Rice. 10-52. Meta-analysis of 6 studies on the prophylactic use of propranolol (a beta-blocker). Mortality data are unreliable due to the incomparability of the studied groups. Nevertheless, a non-significant (ND) decrease in the frequency of bleeding was found.

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, mortality from bleeding from varicose veins is about 40% with each 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 hepatocellular insufficiency. The triad of unfavorable signs - jaundice, ascites and encephalopathy - is accompanied by 80% mortality. The one-year survival rate for low risk (Child groups A and B) is about 70%, and for high risk (Child group C) is about 30% (Table 10-5). The definition of survival is based on the presence of encephalopathy, prothrombin time, and the number of blood units 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 passed under its control. Then the gastroscope is removed and a ligating device is fixed to its end. After that, the gastroscope is reintroduced into the distal esophagus, the varicose vein is identified, and it is aspirated into the lumen of the ligating device. Then, by 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. Each of them impose from 1 to 3 rings.

Table 10-7. Sclerotherapy of varicose veins

The method is simple and gives fewer complications than sclerotherapy, although more sessions are required for ligation of varicose veins)