Toxic reactions to antineoplastic drugs, which lack selective effects to varying degrees, cannot be completely avoided. In clinical practice, the benefits and possible toxicity of antineoplastic drugs should be weighed against the losses and gains of drug use, and the appropriate management of toxic reactions of antineoplastic drugs is also equivalent to improving the efficacy. Toxic reactions of antineoplastic drugs can be broadly classified into immediate and long-term toxic reactions according to the chronological order of occurrence. Recent toxic reactions generally refer to toxic reactions occurring within four weeks after drug administration, and can be divided into two categories: local reactions and systemic reactions. The local reactions of antineoplastic drugs mainly include local leakage of antineoplastic drugs causing tissue reaction or necrosis and embolic phlebitis. The extravasation of drug can cause pain, swelling and local tissue necrosis or local sclerosis, fibrosis contracture and ulcer. Phlebitis can cause hyperpigmentation. Chemotherapy drug extravasation can be treated by the following measures: stop infusion, elevate the limb; keep the needle, pump back the extravasated drug; inject 5-10ml saline to dilute the exuded drug; use topical antidote according to different drugs; topical steroid; 2% procaine local seal; cold compress; topical magnesium sulfate. Among the commonly used chemotherapeutic drugs, those that are strong irritants include ActD, ADM, MMC, VDS, etc., and those that are obvious irritants include DTIC, VM26, Vp-16, etc. In addition, ADM, DTIC, VM26, VDS, NVB, and 5-FU are prone to cause embolic phlebitis. Prevention is better than cure in the management of phlebitis. The drug should be diluted to a certain concentration, the drip rate should be adjusted, and the appropriate vein and deep vein placement should be selected. Local hot compresses can help reduce symptoms and recovery. 2. Systemic reactions (1) Systemic allergic reactions At present, paclitaxel is an important drug that causes allergic reactions clinically and has the characteristics of type I allergic reactions. Others that are prone to cause allergic reactions include VM26, VP-16, DDP, etc. Routinely use prophylactic treatment, starting 1-3 days before dexamethasone or prednisone, paracetamol, ranitidine administration. (2) Fever Fever with WBC reduction and infection is an early manifestation of drug toxicity and can also be part of the acute systemic reaction to the drug, independent of leukopenia. The drugs that cause fever are BLM, ADM, MTX (HD), DTIC and so on. Bleomycin BLM is most likely to cause hyperthermia, often with chills, usually 2-4 hours after drug administration, and is usually self-limiting in toxicity, with occasional reports of death. Patients with lymphoma are more sensitive and should be observed for temperature and blood pressure, timely rehydration, antipyretic and hormone application. (3) Hematopoietic system reactions Antitumor drugs cause different degrees of myelosuppression, initially as leukopenia, followed by thrombocytopenia, and in severe cases, hemoglobin is also reduced, and the degree of suppression is related to individual bone marrow storage capacity. The degree of suppression is related to the individual’s bone marrow storage capacity. Those who have liver disease, hypersplenism or have undergone radiotherapy or chemotherapy before the drug administration are more likely to cause significant suppression. The speed and duration of myelosuppression and the degree of inhibition of each lineage are not the same for different drugs. Nitrosamides, cyclophosphamide, adriamycin, 5-Fu, MTX, CBP, and tylosin have severe suppression of bone marrow, with maximum suppression days ranging from 7-42 days and recovery times ranging from 14-90 days. Vincristine and MMC are severely inhibited, and DDP is mildly inhibited. In the past, myelosuppression was a dose-limiting toxicity, and the application of hematopoietic factor G-CSF/GM-CSF can now solve this problem. Platelet transfusion is available for thrombocytopenia, and platelet growth factor IL-11/TPO can also be applied for clinical use. Anemia can be treated with component transfusion and EPO. (4) Gastrointestinal reactions Gastrointestinal reactions often appear earlier than bone marrow suppression. Loss of appetite may occur 1-2 days after chemotherapy and generally requires no special treatment. Gastrointestinal reactions can also include nausea and vomiting, which are the most common toxic reactions to antineoplastic drugs. The emetogenicity of different drugs varies greatly and can be divided into five groups. The frequency of group 1 is less than 10%: such as BLM, VDS, NVB, MTX <50mg/m2; the frequency of group 2 is 10%-30%: such as Tysol, Kinsei, MMC, 5-Fu <1g/m2, VP-16, etc.; the frequency of group 3 is 30%-60%: such as CTX <750mg/m2, IFO205-1000Mmg/m2, EPI <90mg/m2, etc. EPI<90mg/m2, etc.; Group 4 occurrence frequency 60%-90%: e.g. DDP<50mg/m2, 50mg/m290%: e.g. CTX>1500mg/m2, DDP>50mg/m2. There are also nausea and vomiting unrelated to chemotherapy, such as opioid analgesics, brain metastases, vomiting caused by digestive tract obstruction, infection, radiotherapy, etc. Currently, the main antiemetic drugs are 5-HT3 receptor antagonists (granisetron, paloxetine, etc.), gastrofacial, chlorpromazine, and hormones (e.g., dexamethasone, methylprednisolone, etc.). For pre-emetic vomiting antiemetics are often ineffective, psychological relief or anxiolytics can be given. (5) Mucosal reactions Mucosal ulceration and ulcers are one of the most serious and symptomatic toxicities of chemotherapy. After the occurrence of stomatitis, oral care should be strengthened, food adjustment and support should be enhanced. Gastrointestinal ulcers and bleeding should be treated symptomatically. (6) Diarrhea Chemotherapeutic drugs causing diarrhea are most common in the 5-Fu class, and chemotherapeutic drugs should be discontinued if the number of diarrhea exceeds 5 times a day or if there is bloody diarrhea. For those with low white blood cells, infectious diarrhea can have serious consequences. Currently, diarrhea caused by CPT-11 is the most serious. (7) Constipation The main drugs that cause constipation are vincristine such as VDS and NVB, and in patients who are also using 5-HT3 receptor antagonists or morphine-based pain medications, constipation is more serious and can be treated with fruit guide and senna. (8) Skin and appendages Chemotherapy drugs can cause increased skin photosensitivity, hyperpigmentation, hyperkeratosis, rash, and hair loss. Hair loss mainly causes mental burden. The main drugs causing alopecia are CTX, ADM, VP-16, thaumaturgic, etc., which can gradually grow out 6-8 weeks after complete cessation of chemotherapy. (9) Cardiotoxicity Anthracyclines and Herceptin are most valued, among which ADM is the most important and can cause dose-related cardiomyopathy. 1/3 show hypotension, arrhythmia, myocardial strain, ventricular hypertrophy, and 2% can have heart enlargement and cardiogenic shock. The cumulative dose of ADM should generally be <550mg/m2, and the cumulative dose of E-ADM should generally be <800mg/m2. The cumulative dose of ADM should not be >450mg/m2 for such patients. ADM cardiotoxicity can be monitored by EKG, ultrasound and cardiac function, and cardiac biopsy can be performed if necessary. If necessary, cardiac biopsy can be performed. Control of cumulative dose is an effective measure to prevent cardiotoxicity, and myocardial protective drugs are beneficial for prevention. (10) Pulmonary toxicity is mainly manifested as interstitial pneumonia and pulmonary fibrosis. The main chemotherapeutic agents prone to pulmonary toxicity are BLM, ADM, CTX, MTX, VDS and small-molecule targeted drugs such as Erysal and Troche. Others are TAM, IFN, IL-2, TNF, G-CSF, and leukocyte transfusion. The total dose of BLM is positively correlated with the onset of pulmonary symptoms and changes in pulmonary function, and generally the cumulative dose should not exceed 300 mg. Pulmonary function and X-ray should be performed every 3 months during the drug administration. If there is no sure effective treatment for lung damage, it should be stopped immediately. (11) Hepatotoxicity Anti-tumor drugs can cause hepatocellular insufficiency and chemical hepatitis, veno-occlusive disease and chronic liver fibrosis. Possible drugs are MTX (long-term), IFN (HD), CTX, MMC, DTIC, etc. Chemotherapy patients with hepatic insufficiency should use or reduce the amount of chemotherapy drugs with caution, especially those with liver damage. Generally, transaminase elevation within a short period of time is mostly transient and can be recovered after stopping the drug. The treatment can be continued with the administration of liver protection drugs. Late onset of liver function damage should be taken seriously, and it is best to discontinue the drug. (12) Renal damage Most of the cytotoxic drugs that cause renal dysfunction damage the tubules rather than the glomeruli. Common drugs include IL-2, DDP, MMC, IFO, DTIC, etc., of which DDP has the most prominent nephrotoxicity. When applying DDP, renal function should be monitored, adequately hydrated, and the amount of each dose should be reduced, and should not be combined with aminoglycoside antibiotics at the same time. In addition, the newly studied protective agent clofenteine can reduce its nephrotoxicity. (13) Hemorrhagic cystitis CTX, IFO can cause aseptic chemical cystitis, the dosage should be sufficient rehydration and prevented with the protective agent methotrexate, and the drug should be stopped when cystitis occurs. (14) Neurotoxicity Chemotherapy drugs can cause peripheral and central neurotoxicity. Common drugs include vincristine, platinum oxalate, tylosin, DDP, MTX, 5-Fu, IFN (HD), etc. Most drug toxicity is dose-dependent and usually recovers after drug discontinuation. VCR is more neurotoxic and its derivatives VDS, NVB are now commonly used in clinical practice. DDP can cause high frequency deafness and tinnitus. Platinum oxalate can aggravate toxicity and have abnormal laryngeal response when exposed to cold. High doses of 5-Fu can cause cerebellar ataxia, and intrathecal MTX can cause chemical arachnoiditis and encephalopathy. Long-term toxicity Long-term toxicity includes growth retardation, infertility, liver fibrosis, neurological damage and second primary tumors. Gonadal: Caution should be exercised especially in pediatric and young patients, and a clear account of possible long-term reactions such as infertility, growth retardation, teratogenic potential, and premature aging is needed. Second primary tumor: mostly leukemia and certain solid tumors. A high peak is seen in 3-9 years.