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    Home > Active Ingredient News > Digestive System Information > Upper gastrointestinal bleeding combined with venous thrombosis, cerebral infarction, hemostasis or anticoagulation?

    Upper gastrointestinal bleeding combined with venous thrombosis, cerebral infarction, hemostasis or anticoagulation?

    • Last Update: 2021-04-14
    • Source: Internet
    • Author: User
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    Only for medical professionals to read the reference article to solve puzzles! Upper gastrointestinal bleeding refers to the gastrointestinal tract above the ligament of flexion, including bleeding caused by lesions such as esophagus, stomach, duodenum, pancreas and gallbladder (jejunal lesions bleeding after gastrojejunostomy also belongs to this range), and its clinical The main manifestations are hematemesis and melena.
    Heavy bleeding is often accompanied by acute peripheral circulatory failure caused by hypovolemia, causing hemodynamic instability, and venous thrombosis or cerebral infarction may be complicated during the treatment.
    Please see the following two cases: Case 1 The patient, a 65-year-old male, was admitted to the hospital for "three days of black bowel movements, one day of hematemesis, vague articulation, and left limb weakness for one day".

    The patient had a history of similar upper gastrointestinal bleeding 6 years ago.

    A history of hypertension for 10 years, blood pressure control is still good.

    No history of liver disease and alcohol abuse.

    Admission examination: blood pressure 120/70mmHg, heart rate 90 beats/min.

    Clear mind, good spirits, moderately anemic appearance, vague pronunciation, no special auscultation of cardiopulmonary, no liver palms and spider moles, negative ascites signs, soft abdomen, mild tenderness under the xiphoid process.

    Muscle strength of the left limb is grade IV.

    CT showed: multiple lacunar infarction in the right basal ganglia; blood routine: hemoglobin 70g/L, strong fecal occult blood was positive.

    Diagnosis: 1.
    Upper gastrointestinal bleeding; 2.
    Multiple lacunar infarction.

    Case 2 is a 76-year-old male who was admitted to the hospital because of "black stool for 5 days and hematemesis once".

    The patient had diabetes for 7 years and lacunar infarction for 3 years.

    Usually, insulin injections can be used to control blood sugar, and aspirin (100mg/day) and clopidogrel (75mg/day) are often taken by mouth.

    Physical examination: body temperature: 37.
    2°C; pulse: 108 beats/min, breathing: 19 beats/min, blood pressure: 93/59 mmHg. Poor appetite, lethargy, no dry and wet rales in both lungs, flat and soft abdomen, no tenderness and rebound pain, not reach under the ribs of liver and spleen, no percussion pain in liver and kidney area; no mobile dullness, bowel sounds5 Times/min.

    On the 9th day after admission, he developed edema of the left lower extremity.

    Laboratory examination: (1) Blood test showed: white blood cell 13.
    69×109/L, red blood cell 2.
    63×1012/L, hemoglobin 88g/L; (2) Urine and stool test: stool occult blood was positive, and urine test showed no obvious abnormality.

    (3) Random intravenous blood glucose 7.
    7mmol/L (4) Six items of coagulation: fibrinogen amount 4.
    27g/L, fibrin degradation product 89.
    5μg/ml, D dimer 26.
    12μg/ml.

    Color Doppler ultrasound of both lower extremities showed that the arterial blood flow in both lower extremities was unobstructed, and deep vein thrombosis was formed in the left lower extremity.

    Diagnosis: 1.
    Upper gastrointestinal bleeding (causes to be investigated), moderate hemorrhagic anemia; 2.
    Hypertension level 1 (high-risk group) 3.
    Diabetes; 4.
    Deep vein thrombosis in the left lower extremity.

    One of the above two cases is upper gastrointestinal hemorrhage combined with cerebral infarction, and the other is upper gastrointestinal hemorrhage combined with venous thrombosis.

    Clinically, when encountering patients with upper gastrointestinal bleeding combined with venous thrombosis or cerebral infarction, there is a contradiction between hemostasis and anticoagulation in treatment.
    Hemostasis hinders anticoagulation, and anticoagulation affects hemostasis.
    When he is caught in hemostatic drugs, he dare not use or anticoagulation.
    If you dare not use drugs for dredging blood vessels, it will aggravate the brain damage of the patient and prone to poor prognosis.

    Especially for patients with basic diseases such as hypertension, hyperlipidemia, coronary heart disease, diabetes, etc.
    , this situation may be more dangerous, with high mortality, and more difficult to treat.

    So, what should we do if we encounter such patients in clinical practice? How to correctly handle the contradiction between hemostasis and anticoagulation? This article combines the literature and talks about my superficial views for readers.

    Upper gastrointestinal hemorrhage is a common clinical disease in internal medicine.
    It is mostly caused by diseases such as peptic ulcer, acute gastric mucosal disease, liver cirrhosis, portal hypertension, or gastric cancer.

    Upper gastrointestinal hemorrhage complicated by acute cerebral infarction or venous thrombosis, or gastrointestinal hemorrhage is the reason for the first diagnosis, or after the application of hemostatic drugs.

    Although this disease is relatively rare in clinical practice, once it occurs, it often aggravates the patient’s condition and affects its prognosis.
    In severe cases, the patient will die.
    The possible pathogenesis is as follows: (1) When gastrointestinal bleeding occurs, the patient’s blood volume decreases sharply and blood pressure It drops rapidly, forming hypovolemic shock, reflexes cause increased release of catecholamines, constriction of peripheral small blood vessels, and even occlusion of cerebral vasospasm, increased cerebrovascular resistance, decreased blood flow, occlusion of deep small arteries, and hypoxia in brain tissue.

    Especially those with hypertension, hyperlipidemia, coronary heart disease, diabetes and other arteriosclerosis-related diseases are more likely to have cerebral infarction, which usually occurs 1 to 7 days after upper gastrointestinal bleeding.

    (2) Patients with gastrointestinal hemorrhage often stay in bed absolutely after admission, causing the blood flow to slow down.
    In addition, after gastrointestinal hemorrhage, blood is concentrated, normal blood flow stratification disappears, and platelets will flow into the periphery of the blood vessel and may adhere to the vascular endothelium.
    Sex is greatly increased.

    At the same time, coagulation factors are easy to accumulate locally and be activated to initiate the coagulation process.

    Slow blood flow easily damages vascular endothelial cells, and tissue damage at the bleeding site releases tissue factor, thereby activating the exogenous coagulation system, which can easily lead to thrombosis.

    (3) Some patients with gastrointestinal hemorrhage caused by liver cirrhosis have limited heart response to increased front and rear load, which leads to increased heart rate and increased myocardial oxygen consumption, thereby affecting the hemodynamics of the systemic circulation.

    In addition, the level of plasma endothelin in patients with advanced liver cirrhosis can be increased compensatoryly, which causes vascular smooth muscle contraction, resulting in cerebral artery stenosis, spasm, and cerebral infarction.

    (4) Various hemostatic drugs used in the treatment of gastrointestinal bleeding all increase the risk of thrombosis.

    Improper use of large-dose anti-fibrinolytic hemostatic drugs can easily cause platelet aggregation and induce thrombosis side effects, abnormal structure of plasminogen, reduced activity, and inhibit microthrombolysis.

    How to deal with it? The treatment of gastrointestinal hemorrhage complicated by acute cerebral infarction or venous thrombosis requires comprehensive consideration of all aspects according to the condition, weighing the risks of bleeding and ischemia, formulating individualized hemostasis and anticoagulation programs, and correctly handling the contradiction between hemostasis and anticoagulation .

    The cause of upper gastrointestinal bleeding is generally caused by mucosal damage.
    Strong acid suppression should be the main reason.
    Proton pump inhibitors, somatostatin, etc.
    should be used to avoid indiscriminate use of hemostatic agents, especially antifibrinolytic drugs (such as aminomethylbenzoic acid).
    , Tranexamic acid and other drugs).

    (1) To control gastrointestinal bleeding, the first choice for the treatment of acute upper gastrointestinal bleeding is still drug therapy.

    For patients with first onset, unknown cause, and critical illness, while volume resuscitation and life support, the "empirical combination medication" is the first choice for the emergency treatment of bleeding, that is, proton pump inhibition + intravenous somatostatin (or its analogues) Octreotide), hemostatic drugs should be used with caution.

    The "Expert Consensus on the Emergency Diagnosis and Treatment Process of Acute Upper Gastrointestinal Bleeding" (updated in 2020) recommends the following methods of drug use: ①Esomeprazole: 80 mg intravenous bolus, continuous intravenous pumping at a rate of 8 mg/h or Instillation, the administration method that lasts for 72 hours takes effect quickly and can be maintained within the pH range of acid suppression and hemostasis for a long time.

    ②Somatostatin: the first dose of 250μg is given by rapid intravenous drip (or slow bolus), followed by 250μg/h intravenous pump (or drip), and the course of treatment is 5 days.

    The drug takes effect within 1 minute after intravenous injection, and reaches the peak concentration within 15 minutes.
    The half-life is about 3 minutes, which is beneficial to the early and rapid control of acute upper gastrointestinal bleeding, but the half-life of somatostatin is extremely short.
    Can not be interrupted, if the interruption exceeds 3 minutes, the injection should be re-injected.

    ③When varicose bleeding is highly suspected, use vasopressin (or its analog terlipressin) on the basis of the above treatment for up to 5 days, and use antibiotics prophylactically to reduce bacterial infections.
    Reduce bacterial infection mortality, all-cause mortality and rebleeding events.

    (2) The treatment of cerebral infarction can be treated with neutral treatment and adequate fluid replacement before the bleeding of the gastrointestinal tract stops.

    After patients have symptoms related to cerebral infarction, reduce or stop related hemostatic drugs in time, and add or switch to drugs that improve cerebral circulation, protect brain cells, and prevent cerebral edema.
    For example, you can use free radical scavengers and ida Lavone, mannitol and other drugs are used for brain protection therapy.

    Because ischemia and hypoxia cause brain cell edema, which in turn may cause stress ulcers and aggravate gastrointestinal bleeding, it is important to actively control brain edema.

    During the treatment period, we must pay attention to changes in blood pressure.
    Once abnormal changes occur, rescue as soon as possible.

    (3) The patient's limb venous thrombosis, the thrombus may fall off at any time, thromboembolism can cause pulmonary infarction, cerebral infarction, myocardial infarction, etc.
    , which may lead to sudden death, so for patients with gastrointestinal bleeding and acute venous thromboembolism (VTE) The first treatment is to prevent the progression of thrombosis, reduce the occurrence of pulmonary embolism and prevent the recurrence of thrombosis.

    At present, the main treatments for deep vein thrombosis include thrombolysis, anticoagulation, circulatory pressure bands and proper getting out of bed, but for patients with gastrointestinal bleeding, thrombolysis is absolutely contraindicated.

    The correct treatment measures should be given low-dose low-molecular-weight heparin (4000 IU subcutaneous injection qd) anticoagulation treatment about 20 days after no active bleeding, observe for 3 days without bleeding, and gradually increase the dose (4000 IU subcutaneous injection q12h).
    Until lower extremity edema subsides, blood pressure is stable, and avoid oral anticoagulant drugs.

    Of course, the best treatment is prevention.
    It is the key for patients with gastrointestinal bleeding to replenish sufficient energy, water and electrolytes.
    Maintain normal blood circulation as much as possible and help prevent venous blood from clotting and forming thrombus.
    Once the gastrointestinal bleeding alarm is lifted, it can be Proper activities and gradually return to normal activities, from fasting to a liquid diet, and gradually transitioning to a normal diet, that is, return to normal living habits as soon as possible, which can avoid venous thrombosis.
    In addition, wearing elastic stockings or using air compression pumps and other anti-thrombotic devices are also available Preventive effect.

    Reference materials: [1].
    Yongheli.
    Clinical analysis of 22 cases of upper gastrointestinal hemorrhage complicated with cerebral infarction[J].
    Western Medicine, 2009, 21(8): 1367-1368.
    [2].
    Li Baoli.
    Upper gastrointestinal hemorrhage Analysis of the clinical characteristics of 20 cases with acute cerebral infarction.
    China Medical Herald, 2009, 6 (19): 215-216.
    [3] Huang Zhilong, Hu Qiong, Yao Hongmei, et al.
    A case report of gastrointestinal hemorrhage combined with venous thromboembolism and literature review[J].
    Guizhou Medicine, 2017,41(6):596-597.
    [4] Emergency Physician Branch of Chinese Medical Doctor Association, Emergency Medicine Branch of Chinese Medical Association, All Military Emergency Medicine Professional Committee, Chinese Emergency Specialist Medical Consortium, Beijing Association of Emergency Medicine.
    Expert consensus on the emergency diagnosis and treatment process of upper gastrointestinal bleeding in emergency department[J].
    Chinese Emergency Medicine,2021,1(1):1-10.
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