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 drug extravasation often causes serious consequences, how to deal with the occurrence?
(1) the 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.
② Elevate the limb.
③ Retain the needle and draw back the extravasated drug.
④Inject 5-10 ml of saline to dilute the exuded drug.
⑤ topical application of antidote.
⑥topical topical steroid hormone.
⑦2% procaine local seal.
⑧ cold 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, serious 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 the laboratory test results and give epinephrine, oxygen therapy, nebulized inhaled β2 agonists and antihistamines in the first instance.
(1) Preferably 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 for a total of 3 doses if necessary. 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 twice the dose of the above intravenous drug.
(2) Oxygen therapy.
Patients with respiratory distress may be given mask oxygen. In case of severe drowsiness and hypoxemia, tracheal intubation may be given. If the patient has upper airway edema and tracheal intubation is not possible, tracheotomy is required. The target value for oxygen therapy is blood saturation > 90% (PO2 > 60 mmHg).
(3) Bronchodilators.
For patients with persistent bronchospasm, salbutamol can be used by nebulized inhalation.
(4) Antihistamines.
Epinephrine 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 120mg IV once, followed by 60mg IV every 6 hours. The above hormone therapy also helps to reduce the late symptoms of the allergic reaction (which may appear 6 to 12 hours after the appearance of the 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 require epinephrine treatment after the development of an allergic reaction should be routinely given close monitoring, or even need to be placed under observation in an intensive care unit. Sometimes the disease recurs and can manifest itself only a few hours after the appearance of early symptoms, so monitoring should be continued 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. Licoderm tablets, leucovorin, shark liver alcohol, etc.
(4) In case of severe leukopenia (grade III or higher), granulocyte colony-stimulating factor (G-CSF) 100 or 200 μg can be injected subcutaneously once or twice daily for 3 days.
(5) If blood transfusion is indicated, component transfusion.
(6) Albumin and plasma input.
(7) Short-term significant reduction of platelets, use IL-11 subcutaneous injection 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. Attention should be paid to oral hygiene, keeping clean and moist, rinsing with saline or rehabilitating new etc.; stop chemotherapy for severe stomatitis.
(2) Nausea and vomiting
The most common adverse reaction, severe vomiting can lead to dehydration and 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 of 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 uncomfortable 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, intravenous injection 0.5~-1 hour before chemotherapy; ondansetron 8mg intravenous or oral injection 0.5~-1 hour before chemotherapy; or 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, etc. It is 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 leading to transient heart failure and death.
(ii) Subacute 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. 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 of high-dose continuous infusion of fluorouracil 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, there are three main ways.
① Direct damage to hepatocytes.
② leading to aggravation of the underlying liver disease, especially viral hepatitis.
(③) Altering the metabolism of antitumor drugs due to underlying liver diseases, resulting in prolonging their metabolism in vivo and increasing 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 urological effects of antineoplastic drugs mainly include renal damage and hemorrhagic cystitis.
(1) Renal damage
Most cytotoxic drugs that cause renal dysfunction damage renal tubules rather than glomeruli, and can occur immediately or delayed, either 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, concomitant use of other drugs that may cause renal damage is contraindicated 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%, 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.