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WS/T 624-2018: Classification of transfusion reactions
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Basic data

Standard ID WS/T 624-2018 (WS/T624-2018)
Description (Translated English) Classification of transfusion reactions
Sector / Industry Health Industry Standard (Recommended)
Classification of Chinese Standard C05
Word Count Estimation 9,955
Date of Issue 2018-09-26
Date of Implementation 2019-04-01
Regulation (derived from) National Health Newsletter (2018) No.20
Issuing agency(ies) National Health Commission

WS/T 624-2018: Classification of transfusion reactions


---This is a DRAFT version for illustration, not a final translation. Full copy of true-PDF in English version (including equations, symbols, images, flow-chart, tables, and figures etc.) will be manually/carefully translated upon your order.
Classification of transfusion reactions ICS 11.020 C 05 WS People's Republic of China Health Industry Standard Blood transfusion response classification 2018 - 09 - 26 released 2019 - 04 - 01 Implementation National Health and Wellness Committee of the People's Republic of China

Foreword

This standard was drafted in accordance with the rules given in GB/T 1.1-2009. This standard was drafted. Shanghai Sixth People's Hospital, Beijing Hospital, the First Affiliated Hospital of China Medical University, Peking Union Medical College Hospital, Xiangya Hospital of Central South University, Tongji Hospital affiliated to Tongji Medical College of Huazhong University of Science and Technology, West China Hospital of Sichuan University, Blood Center of Fujian Province, Haishi Blood Center, Beijing Tongren Hospital affiliated to Capital Medical University, Sino-Japanese Friendship Hospital of Jilin University, First Affiliated Hospital of Zhengzhou University, New People's Hospital of Xinjiang Uygur Autonomous Region, Second Affiliated Hospital of Kunming Medical University, First Hospital of Lanzhou University. The main drafters of this standard. Li Zhiqiang, Gong Jiwu, Hao Yiwen, Bai Lianjun, Li Bijuan, Wei Qing, Qin Li, Guo Yongjian, Qian Kaicheng, Li Shuping, Liu Tiemei, Lu Xianping, Wen Jun, Xu Guangfang, Yi Sihua. Blood transfusion response classification

1 Scope

This standard specifies the classification of transfusion reactions. This standard is applicable to the diagnosis and treatment of blood transfusion reactions at various levels of medical institutions across the country, as well as the management supervision and evaluation of the health administrative department. Provide the basis for the trial.

2 Terms and definitions

The following terms and definitions apply to this document. 2.1 Transfusion reactions/transfusion reactions/transfusion reactions/complications Adverse reactions with timing correlation with blood transfusion. The cause of the adverse reaction may be an adverse event, or it may be the patient and the blood transfused interaction. 2.2 Acute/immediate transfusion reactions; ATR/ITR The transfusion reaction occurs during the blood transfusion process, immediately after transfusion, and within 24 hours after transfusion. 2.3 Chronic/delayed transfusion reactions; CTR/DTR The transfusion reaction occurred 24h to 28d after the end of blood transfusion. 2.4 Transfusion-transmitted infections; TTI/transfusion-transmitted infectious reactions; TTIR The pathogen enters the recipient's body from the blood donor through a blood transfusion process and causes a corresponding infection or disease. 2.5 Transfusion-transmitted non-infectious reactions; TTNIR Adverse reactions caused by non-pathogens with time-series correlation with blood transfusion.

3 blood transfusion response classification

3.1 transfusion-transmitted infections (TTI) There was no history of pathogen infection before transfusion, no clinical symptoms, and serum markers were negative. But after the blood transfusion, the corresponding pathogen infection Symptoms, and the isolation of the pathogen from the recipient is highly homologous to the pathogen in the donor. 3.1.1 transfusion-transmitted virus infections (TTVI) 3.1.1.1 Viral hepatitis. caused by hepatitis virus, mainly involving hepatitis B, C, D and E virus. 3.1.1.2 acquired immunodeficiency syndrome (AIDS). immunodeficiency by human Caused by human immunodeficiency virus (HIV), which can be complicated by various opportunistic infections and tumors. In severe cases, it can lead to death. Die. 3.1.1.3 cytomegalovirus infection (CMVI). by cytomegalovirus (cytomegalovirus, CMV) causes the virus to be confined to the parotid gland and some to systemic infection. CMV infection is mostly subclinical, dominant infection There are a variety of clinical manifestations, and severe cases can lead to death. 3.1.1.4 Epstein Barr virus infection (EBVI). caused by EB virus, more than 95% of adults can carry Band, and is associated with the occurrence of nasopharyngeal carcinoma, childhood lymphoma, and the like. 3.1.1.5 Human parvovirus B19 infection (HPB19I). by human parvovirus B19 (human parvovirus B19) can cause infectious erythema and acute joint disease. In some blood system diseases and immune damage Patients can cause a crisis of aplastic disorders. 3.1.1.6 adult T-cell leukemia/lymphoma (ATLL). by human T lymphocytes Caused by human T-lymphotropic virus (HTLV-1), may cause acute or chronic onset, may cause skin damage, Peripheral blood lymphocyte counts were significantly increased, liver and spleen and lymph nodes were enlarged. 3.1.1.7 West Nile virus infection (WNVI). caused by West Nile virus, 80% sense Dyeing as a recessive infection; a few people may have symptoms similar to upper respiratory tract infections; very few people may present with viral encephalitis, meningoencephalitis and brain Membrane and so on. 3.1.1.8 The virus infection not mentioned above. 3.1.2 transfusion-transmitted bacterial infections (TTBI) 3.1.2.1 Gram positive cocci infection. common in Staphylococcus aureus, epidermal grape Bacteria, Enterococcus and Streptococcus. 3.1.2.2 Gram negative bacilli infection. common in Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Proteus, Yersinia, Serratia marcescens, and the like. 3.1.2.3 Anaerobic infection. commonly found in Bacteroides, Clostridium, and Clostridium perfringens. 3.1.2.4 Bacterial infection not covered by the above. 3.1.3 transfusion-transmitted parasitic infections (TTPI) 3.1.3.1 malaria (malaria). caused by Plasmodium infection, with repeated episodes of intermittent chills, high fever, and subsequent sweating Point, can cause splenomegaly, anemia and other performance. 3.1.3.2 Babesiosis. A zoonotic infection caused by Babesia (babesia) infection through a sputum. hair At the beginning of the disease, the symptoms are very different. Acute onset is quite similar to malaria, with intermittent heat, splenomegaly, jaundice and hemolysis. Chronic patient Bacterial septicemia can last from a few months to several years. 3.1.3.3 Trypanosomiasis. caused by trypanosoma cruzi. Fever can occur in the acute phase, Systemic lymphadenopathy, enlarged heart, etc.; chronic phase may have myocarditis, enlarged heart, esophageal or colonic expansion. 3.1.3.4 Parasitic infections not covered by the above. 3.1.4 Transfusion to spread other pathogen infections 3.1.4.1 syphilis. caused by Treponema pallidum, usually in addition to invasion of the skin mucosa, It can also affect the corresponding clinical manifestations of internal organs. 3.1.4.2 Creutzfeldt-Jakob disease. caused by prion virus infection A comorbid degenerative disease of the central nervous system. A prion is a protein virus, a protein-infecting particle, and the only one that does not use DNA. RNA is a genetic material of a virus. 3.1.4.3 fungal infection. Candida albicans is the vast majority, also found in Candida tropical, Mucor. 4.1.4.4 The above does not involve other pathogen infections. 3.2 transfusion-transmitted non-infectious reactions (TTNIR) 3.2.1 Allergic reaction The interaction between allergens and existing antibodies in the body. In some cases, the input comes from blood donation with hereditary allergies. The antibody will also occur. Partially seen in patients with congenital IgA deficiency. According to clinical manifestations can be divided into local and systemic allergic reactions. 3.2.2 hemolytic transfusion reaction (HTR) 3.2.2.1 acute/immediate hemolytic transfusion reaction (acute/immediate hemolytic transfusion reaction, AHTR/IHTR) often occurs during transfusion, immediately after transfusion, or within 24 hours after transfusion. Because the input blood is not compatible with the patient's immunity Capacitance leads to accelerated red blood cell lysis or/and clearance. Often caused by IgM antibodies, mostly intravascular hemolysis, most common in ABO blood group incompatibility Blood transfusion. 3.2.2.2 chronic/delayed hemolytic transfusion (chronic/delayed hemolytic transfusion) Reaction, CHTR/DHTR) often occurs 24h to 28d after the end of blood transfusion. The patient's intention to produce red blood cell type antigen after transfusion External antibodies; when transfused again, unexpected antibodies in the body can interact with the input red blood cells, resulting in accelerated red blood cell lysis and/or clearance. often Caused by IgG antibodies, mostly extravascular hemolysis, most commonly in Rh blood group incompatible blood transfusion. 3.2.3 delayed serological transfusion reaction (DSTR) Accidental antibodies with clinically significant red blood cell types appear in patients after transfusion, often for months to years, peripheral blood red eggs The change in white value is not obvious. 3.2.4 non-hemolytic febrile transfusion reaction (NHFTR) Within 4 hours after transfusion or blood transfusion, the patient's basal body temperature increased by more than 1 °C or accompanied by chills, no primary disease, allergies, hemolysis and fine Evidence of fever caused by bacterial contamination. Mainly due to the infusion of blood components containing white blood cells and antibodies against existing antibodies in patients Should, or/and soluble cytokines released by leukocytes during blood storage. 3.2.5 post transfusion purpura (PTP) More common in the 5d ~ 10d after transfusion, mainly due to the combination of platelet-specific antibodies in the patient and the corresponding antigen on the blood donor platelets Forming an antigen-antibody complex that causes destruction of the patient's platelets. There may be a significant reduction in the number of peripheral blood platelets, skin defects or/and ecchymoses, A self-limiting disease. 3.2.6 transfusion-associated graft versus host disease (TA-GVHD) Immunologically active lymphocytes are infused into patients with impaired immune function or immune function, survive and proliferate in their bodies, and Attack host tissue cells. May have fever, rash, liver damage, complete blood cell reduction; low bone marrow hyperplasia, and hematopoietic cell reduction And lymphocytosis and so on. 3.2.7 transfusion-related acute lung injury (TRALI) Acute dyspnea with progressive hypoxemia within 6 hours after transfusion or transfusion, blood oxygen partial pressure/oxygenation index (PaO2/FiO2) ≤ 300mmHg, chest X-ray showed bilateral pulmonary infiltration, and no transfusion-related circulating overload (TACO) and severe allergic reactions caused by blood transfusion Bacterial pollution response and other performance. 3.2.8 transfusion-associated dyspnea (TAD) Respiratory distress occurs within 24 hours after the end of transfusion, does not meet the transfusion-related acute lung injury (TRALI), transfusion-related cyclic overload (TACO) or allergic reactions and other diagnostic basis, and can not be explained by the patient's potential or existing disease. 3.2.9 transfusion-associated circulation overload (TACO) Acute due to excessive blood transfusion rate or (and) excessive blood transfusion or potential cardiopulmonary disease in patients cannot effectively receive blood transfusion volume Heart failure. There may be manifestations such as purpura, shortness of breath, heart palpitations, auscultation and wet rales or blisters. 3.2.10 transfusion-associated hypotension (TAH) The only decrease in blood pressure during the blood transfusion or within 1 h after the end of transfusion, and the decrease in systolic blood pressure (< 90 mmHg or lower than the baseline blood pressure) Drop ≥ 40mmHg) or decrease pulse pressure (< 20mmHg). 3.2.11 iron overload Long-term multiple blood transfusions can cause iron overload in the patient's body and accumulate in the body's parenchymal cells, leading to organs such as heart, liver and endocrine glands. Tissue damage and skin pigmentation. 3.2.12 pulmonary vascular microembolization (PVM) As the blood components are stored, the microparticles formed by white blood cells, platelets and fibrin can pass through a standard pore transfusion filter. Entering the patient's body causes pulmonary vascular embolism leading to acute pulmonary insufficiency. 3.2.13 air embolism Due to the air entering the patient's venous system through the blood vessel during the blood transfusion process. 3.2.14 massive transfusion related complication 3.2.14.1 Coagulation dysfunction. due to loss or large consumption of the patient during coagulation Platelet and clotting factors, or/and blood components, platelet and unstable clotting factor levels decrease with prolonged shelf life, or/and Anticoagulant citrate is a major component of blood preparations for large infusion, or/and anti-shock expansion when a large number of intravenous infusion of crystalloid to the patient machine Residual platelets and clotting factors are lower. 3.2.14.2 citrate toxicity. Most of the whole blood and blood components are resistant with citrate. Coagulant. When a large amount of blood transfusion or blood component replacement is performed, the concentration of citrate in the plasma of the patient can reach 1 g/L or more, which is easy to cause poison. 3.2.14.3 Hyperkalemia. The concentration of potassium ion in whole blood and red blood cell components gradually increases with the preservation time. When a large number of whole blood and red blood cell components with relatively long shelf life are infused, the blood potassium ion concentration of the patient's body may be significantly increased. 3.2.14.4 Hypocalcemia. Most of the whole blood and blood components are anticoagulants with citrate as the main component. Big When blood transfusion or blood component replacement is performed, it is easy to cause a significant decrease in blood calcium ion concentration in patients. 3.2.14.5 Hyperammonemia. Blood ammonia in whole blood and red blood cell components gradually increases with the preservation time. Massive loss Note that when the whole blood and red blood cell components are stored for a long period of time, the blood ammonia concentration of the patient's body may be significantly increased. 3.2.14.6 Acid-base imbalance. The whole blood and red blood cell components contain citrate. With The storage time prolongs the increase in lactic acid production. A large number of infusions can lead to an imbalance in the body's acid-base balance. 3.2.14.7 hypothermia. due to the rapid infusion of whole blood and blood components at a temperature below the patient's body temperature, the patient machine Body temperature ≤ 36 ° C, so that hemoglobin and oxygen affinity increase, which affects the release of oxygen in organs and tissues, eventually leading to organs and tissues Anoxic condition. 3.2.15 Other The non-infectious reaction of blood transfusion not mentioned above. references [1] Blood Donation Law of the People's Republic of China (Presidency of the People's Republic of China No. 93) [2] “Administrative Measures for Clinical Blood Use in Medical Institutions” (Order No. 85 of the Ministry of Health) [3] "Technical Specifications for Clinical Blood Transfusion" (Wei Yi Fa [2000] No. 184) [4] Department of Health, Ministry of Health of the People's Republic of China. National clinical inspection procedures [M]. Beijing. People's Medical Publishing House,.2015. [5] “Administrative Measures for Clinical Laboratories of Medical Institutions” (Wei Yi Fa [2006] No. 73) [6] American association of blood bands(AABB).Standards for Blood Banks and Transfusion Services, 31st Edition[M].Bethesda.AABB.2018.
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