Nausea and vomiting is caused by numerous factors including chemotherapy and surgery. Nausea and vomiting can lead to serious medical complications such as dehydration, electrolyte imbalances, and esophageal tears. It is easier to prevent nausea and vomiting than treating it once it has started. Although significant progress has been made in the management of nausea and vomiting, these side effects are some of the most worrisome and undesirable effects reported by patients receiving chemotherapy.
The etiology of nausea and vomiting is complex. The chemoreceptor trigger zone (CTZ), located outside the blood–brain barrier, is activated by chemotherapy and other irritants. The CTZ is triggered by various neurotransmitters including dopamine, serotonin, histamine, and neurokinin-1 (substance P) (Figure 41-1). The activation of the CTZ stimulates the vomiting center. This process occurs in chemotherapy-induced nausea and vomiting (CINV). In addition to the CTZ, the gastrointestinal (GI) tract releases serotonin in response to chemotherapy, which can also cause CINV. Current antiemetic medications block the neurotransmitter receptors with the intent to mitigate CINV.
Chemoreceptor trigger zone (CTZ) and activating neurotransmitters.
There are several risk factors that increase the possibility of experiencing CINV. The emetogenic potential of the chemotherapy agent or agents is the most important factor. Agents are classified into high, moderate, low, or minimal risk for causing CINV (Table 41-1). Dose and rate of infusion of the agent can also affect risk (the higher the dose, the higher the risk of CINV). Bolus infusions also tend to have higher risk of CINV than extended infusions. Younger patients (<50 years), women, patients with low alcohol consumption (<1oz of alcohol/day) and patients with a history of poorly controlled CINV are at increased risk of developing problems despite adequate antiemetic treatment. Patients who have a history of motion sickness or nausea with pregnancy can see an increase in the risk of CINV, but to a lesser extent than previously mentioned risks. One study suggests that smoking may also increase the risk of acute CINV.
TABLE 41-1Emetic Risk of Commonly Administered Chemotherapy Agents |Favorite Table|Download (.pdf) TABLE 41-1Emetic Risk of Commonly Administered Chemotherapy Agents
|Emetic Risk ||Incidence Without Antiemetics ||Agenta |
|High ||>90% ||Cisplatin |
|High ||>90% ||Cyclophosphamide (≥1500 mg/m2) |
|High ||>90% ||Cyclophosphamide/doxorubicin combination |
|High ||>90% ||Cyclophosphamide/epirubicin combination |
|Moderate ||30%-90% ||Carboplatin |
|Moderate ||30%-90% ||Cytarabine (>1 g/m2) |
|Moderate ||30%-90% ||Doxorubicin |
|Moderate ||30%-90% ||Ifosfamide |
|Moderate ||30%-90% ||Imatinib (po) |
|Moderate ||30%-90% ||Irinotecan |
|Moderate ||30%-90% ||Oxaliplatin |
|Low ||10%-30% ||Capecitabine (po) |
|Low ||10%-30% ||Docetaxel |
|Low ||10%-30% ||Etoposide (po and IV) |
|Low ||10%-30% ||Everolimus (po) |
|Low ||10%-30% ||Fluorouracil |
|Low ||10%-30% ||Gemcitabine |
|Low ||10%-30% ||Lenalidomide (po) |
|Low ||10%-30% ||Methotrexate |
|Low ||10%-30% ||Paclitaxel |
|Minimal ||<10% ||Bevacizumab |
|Minimal ||<10% ||Dasatinib |
|Minimal ||<10% ||Erlotinib (po) |
|Minimal ||<10% ||Methotrexate (po) |
|Minimal ||<10% ||Rituximab |
|Minimal ||<10% ||Sorafenib (po) |
|Minimal ||<10% ||Vincristine |
There are several types of CINV: acute, delayed, anticipatory, breakthrough, and refractory. Acute CINV is defined as nausea and vomiting that occurs within the first 24 hours following the administration of chemotherapy. Delayed CINV develops more than 24 hours after chemotherapy is administered and can be seen up to 7 days following chemotherapy. Chemotherapeutic agents that commonly cause delayed CINV include cisplatin, carboplatin, cyclophosphamide, ...