Chemotherapy is widely recognized as an effective treatment for tumors and is widely used before and after surgery as well as in the palliative treatment of advanced tumors. The majority of chemotherapy drugs currently used exert their anti-tumor effects by inhibiting cell proliferation, which is a common feature of both normal and cancer cells, and therefore these drugs are highly toxic to humans, and some chemotherapy-associated emergency diseases may occur with normal use.
To take stock of chemotherapy-related emergency diseases and summarize their treatment and management measures, as follows.
First, chemotherapy drug extravasation
Chemotherapy drugs are highly toxic and irritating, and extravasation of the drug will often cause serious consequences, how to deal with it?
(1) Treatment of drug extravasation.
Chemotherapy drug extravasation can cause local pain, local tissue swelling and ulcer necrosis, or the formation of local hard nodes.
The general principles of treatment for extravasation of intravenous drug infusion are.
①Stop the infusion; ②Elevate the limb;
③ Retain the needle and pump back the extravasated drug;
④Inject 5-10ml of saline to dilute the exuded drug;
⑤ Topical antidote;
⑥Topical steroid hormone;
⑦2% procaine local seal;
⑧Cold compress;
⑨ topical application of traditional Chinese medicine mannitol powder or magnesium sulfate, or topical application of thin potato slices or cucumber slices.
(2) Treatment of phlebitis formation.
First, there is drug extravasation, then there is a vein hardening in the form of striated changes, local skin pigmentation, severe local limb numbness swelling pain.
Phlebitis focuses on prevention. Choosing a good intravenous infusion, or choosing a deep vein placement to infuse chemotherapy drugs, can eliminate such phenomena. In addition, the drug should be diluted to a certain concentration and the speed should be regulated when infusing.
Treatment measures: local hot compresses and topical application of Xanax cream help to reduce symptoms and recovery.
Second, allergic reactions
Allergic reactions to paclitaxel occur frequently, with an incidence of 10%-20%. The main thing is to take preventive measures and have anti-allergic drugs ready at all times. The corticosteroid dexamethasone tablets and the antihistamine benadryl are routinely given as pre-treatment before drug administration, which can reduce or prevent the occurrence of allergic reactions. There are of course other chemotherapeutic drugs to which allergy is possible.
For allergic reactions, there is no need to wait for laboratory test results, and epinephrine, oxygen therapy, nebulized inhalation β2 agonists, and antihistamines are given in the first instance.
(1) Preferred epinephrine.
Immediate intramuscular injection of 0.3-0.5 ml of 1:1000 epinephrine dilution is required for patients with laryngeal edema, bronchospasm, and urticaria. Repeat the administration every 10-15 minutes if necessary, for a total of 3 doses. Patients with critical conditions such as severe hypotension, severe bronchospasm, and severe upper respiratory edema may be treated with a one-time intravenous push of 0.5-1.0 ml of 1:10,000 epinephrine dilution (the dose can be repeated after an interval of 10-15 minutes).
After the above treatment, if there is still no significant improvement in symptoms, epinephrine can be continuously infused intravenously at a rate of 1-4 Pg/min until the patient’s symptoms are relieved. If intravenous access cannot be established within a short period of time, the drug can be administered endotracheally in an emergency at a dose twice that of the above intravenous dose.
(2) Oxygen therapy.
Patients with respiratory distress may be given mask oxygen. Tracheal intubation may be given in the presence of severe drowsiness and hypoxemia. If the patient has upper airway edema that prevents tracheal intubation, a tracheotomy is required. The target value for oxygen therapy is a blood saturation > 90% (PO2 > 60 mmHg).
(3) Bronchodilators.
For patients with persistent bronchospasm, albuterol can be used by nebulized inhalation.
(4) Antihistamines.
Adrenaline treatment may be followed by benadryl 25-50 mg every 4-6 hours intravenously/intramuscularly/orally and cimetidine 50 mg intravenously or 150 mg orally every 8 hours (or other H2 receptor antagonists) to help reduce the histamine release effect and further alleviate hypotension and mild urticaria-related symptoms.
(5) Glucocorticoids.
Patients who develop bronchospasm due to allergic reactions may be given glucocorticoid therapy. The first dose is methylprednisolone 120 mg IV once, followed by 60 mg IV every 6 hours. The above hormone therapy also helps to reduce the late symptoms of allergic reactions (which can occur 6 to 12 hours after the appearance of early manifestations).
(6) Circulatory support.
Hypotension usually responds to epinephrine therapy, but in patients whose blood pressure does not rise despite epinephrine therapy, saline supplementation may be required. In patients with intractable hypotension despite aggressive volume supplementation, vasopressors such as norepinephrine or epinephrine may be given to maintain it if necessary.
(7) Cardiac monitoring.
Patients who need to receive epinephrine treatment after an allergic reaction should be routinely given close monitoring, or even need to be placed under observation in an intensive care unit. Sometimes the condition appears repeatedly and can manifest itself only hours after the appearance of early symptoms, so monitoring needs to continue for at least 24 hours before being withdrawn.
Third, bone marrow suppression
Most chemotherapy drugs can cause bone marrow suppression to varying degrees. Regular blood tests are needed, usually followed by leukopenia and then thrombocytopenia, the former being more severe than the latter, and a few may develop severe anemia. If severe myelosuppression occurs, combined with granulocyte-deficient infection, the patient should be transferred to a laminar flow bed urgently, bedside protective measures should be taken, and primary care and, if necessary, intensive care should be given.
Specific treatment measures.
(1) Discontinue medication.
(2) Prevent and treat the infection.
(3) Oral administration of various leukocyte-lifting drugs. Ricorun tablets, leukostim, shark liver alcohol, etc.
(4) In case of severe leukopenia (grade III or higher), granulocyte colony-stimulating factor (G-CSF) 100 or 200 μg subcutaneously once or twice daily for 3 days.
(5) Component transfusion if blood transfusion is indicated.
(6) Albumin and plasma input.
(7) For short-term significant reduction of platelets, use IL-11 subcutaneously and give hemostatic drugs to prevent bleeding.
Fourth, gastrointestinal toxicity
(1) Mucosal inflammation
Chemotherapy drugs tend to cause stomatitis, tongue inflammation, esophagitis and oral ulcers, resulting in pain and reduced eating. Common drugs include 5-fluorouracil and methotrexate. Treatment is based on symptomatic treatment, should pay attention to oral hygiene, keep clean and moist, rinse with saline or rehabilitation new, etc.; severe stomatitis discontinue chemotherapy.
(2) Nausea, vomiting
The most common adverse reactions, severe vomiting can lead to dehydration, electrolyte disorders. Chemotherapy-induced vomiting can be divided into acute vomiting, delayed vomiting and anticipatory vomiting. Acute vomiting is vomiting that occurs within 24 hours after chemotherapy; delayed vomiting is vomiting that occurs from 24 hours to 7 days after chemotherapy; anticipatory vomiting is nausea and vomiting that occurs before the next chemotherapy dose after the patient has experienced unpleasant acute vomiting during the previous treatment cycle, and is a conditioned reflex.
Treatment: The commonly used antiemetic drugs are currently the most effective 5-HT3 receptor antagonists. Use: Granisetron 3mg, 0.5~-1 hour before chemotherapy intravenously; ondansetron 8mg intravenously or orally 0.5~-1 hour before chemotherapy; or use metoclopramide, diphenhydramine and dexamethasone triple antiemetic, also has good effect on light to moderate intensity vomiting.
(3) Other
Chemotherapy can also cause loss of appetite, bloating, diarrhea and constipation, which can be treated symptomatically. Diarrhea is mainly caused by chemotherapeutic drugs such as irinotecan, and it is mainly recommended to use “Emmenthal” as a backup when necessary.
Fifth, skin toxicity
Chemotherapy drugs can cause skin toxicity, including itching, hair loss, rash, dermatitis, hyperpigmentation and so on. Hair loss is a common adverse effect of many chemotherapy drugs, mainly anthracyclines, paclitaxel, CTX, VP-16, VCR, 5-FU and so on. The resulting alopecia is reversible, and hair loss usually occurs 2 to 3 weeks after the first dose of chemotherapy and grows back gradually 6 to 8 weeks after stopping chemotherapy. It has been reported that special ice caps are available for patients using Adriamycin, which have some anti-hair loss effect.
Sixth, chemotherapy cardiotoxicity
Many antitumor drugs have certain toxic effects on the heart, mainly anthracycline antibiotics, of which ADM is the most important, can cause a dose-related cardiomyopathy. If these drugs are used, cardiac monitoring must be performed and cardiac function must be tested regularly.
Among the relevant factors affecting adriamycin cardiotoxicity, the cumulative total dose is the most important risk factor. The choice of liposomal adriamycin with low cardiotoxicity is available.
Anthracycline cardiomyopathy can be clinically classified into three types.
(1) Acute myocardial pericarditis: it usually occurs within a few days of drug administration and manifests as transient arrhythmias, pericardial effusion and myocardial insufficiency. Occasionally, this leads to transient heart failure and death;
②Subacute cardiotoxicity: The onset is insidious and symptoms may appear after the last dose, but the most frequent onset is 3 months after the last dose. The clinical manifestations may be tachycardia and fatigue, and eventually emphysema, right heart congestion signs and reduced cardiac output may appear. Application of cardiotonic drugs may stabilize the condition.
Treatment of anthracycline cardiomyopathy usually requires intravenous administration to enhance myocardial contractility and reduce cardiac afterload. Angiotensin-converting enzyme inhibitors play an important role in stabilizing heart failure and delaying the progression of cardiomyopathy. Selective beta-blockers may also be used if they are ineffective.
The manifestations of cardiotoxicity with high-dose continuous fluorouracil infusion can be: precordial pain, ST-T changes, atrial arrhythmias, myocardial infarction, cardiac insufficiency, and sudden death. the cardiac effects of DDP can be atrial fibrillation, angina pectoris, and ST-T changes.
Seventh, pulmonary toxicity
A series of antineoplastic drugs can cause pulmonary toxicity, and many other non-antineoplastic drugs can also cause damage to the lung parenchyma. Pulmonary toxicity caused by antineoplastic drugs is mainly manifested as interstitial lung inflammation and pulmonary fibrosis.
Bleomycin is the most likely drug to cause pulmonary toxicity, with 3% to 12% of cases having x-ray or physiological function changes and 1% to 2% having acute fatal lung damage.
The best way to deal with chemotherapy-related pulmonary toxicity is to prevent it. There is no sure effective treatment for the lung damage that has occurred, and once toxicity is detected, the primary measure is to discontinue the drug. The effect of corticosteroid therapy has not been confirmed by controlled studies, but it is still available.
Eighth, hepatotoxicity
Antineoplastic drugs cause hepatotoxicity in three main ways: direct damage to hepatocytes; leading to aggravation of underlying liver diseases, especially viral hepatitis; altering the metabolism of antineoplastic drugs due to underlying liver diseases, leading to prolonged metabolism in vivo and increased side effects.
Chemotherapy patients should know the medical history including drug history in advance, and those with liver insufficiency should use antitumor drugs with caution or reduce the dosage. During chemotherapy, liver function including AKP, GT and other enzymatic measurements should be checked regularly to differentiate from metastatic liver cancer or liver infiltration and viral hepatitis.
Generally speaking, liver cell damage, especially transaminase elevation within a short period of time after the drug, is mostly transient and can recover rapidly after stopping the drug. Bifenacin, glutathione, ezetimibe, diammonium glycyrrhizate, and hepatocysteine can help normalize the transaminases. If you can give liver protection drugs most of them can still continue to receive treatment.
Ninth, urinary system adverse reactions
The urinary effects of antineoplastic drugs mainly include renal damage and bloody cystitis.
(1) Renal damage
Most of the cytotoxic drugs that cause renal dysfunction damage the renal tubules rather than the glomeruli, and can occur immediately or delayed, appearing during long-term use or after discontinuation of the drug. It usually occurs in 7 to 12 days and can be recovered in about 1 month, with a few taking several months and some having irreversible renal failure.
CTX and IFO are analogues with similar chemical structures and have similar toxicity and antitumor effects, but their nephrotoxicity is significantly different. CTX has no nephrotoxicity, while IFO can cause a variety of renal abnormalities, some of which can be fatal or cause irreversible renal failure requiring long-term hemodialysis. The use of amphotericin may reduce or prevent the nephrotoxicity of DDP.
Treatment: Regular testing of renal function, adequate hydration, and reduction of single-drug doses using combination chemotherapy are preventive measures. To reduce the occurrence of nephrotoxicity, other drugs that may cause renal damage should not be used concurrently with DDP chemotherapy.
(2) Hemorrhagic cystitis
Mainly seen with CTX or IFO, CTX can cause aseptic chemical cystitis. Adequate rehydration should be given with high doses. Long-term use of the drug requires regular follow-up urine routine. IFOs cause chemical cystitis in the same way as CTX. It can be largely prevented by the use of methotrexate.
Tenth, neurological reactions
Peripheral neurotoxic reactions are common.
Paclitaxel analogs mainly cause peripheral neurotoxicity, which is dose-dependent and usually recovers gradually after discontinuation of the drug.
The incidence of DDP neurotoxicity is about 50%, and the common neurotoxicity is peripheral nerve damage, motor function is generally not affected.
L-OHP peripheral neurotoxicity is particularly pronounced and requires prophylactic use of protective gloves on the day of administration or the following day to prevent cold and keep warm.
The 5-FU class is mainly prophylactic with vitamin B6.