Welcome to Critical Care Congress. Thank you for this opportunity. I am Markeisha Wilder, a nurse practitioner who practices at the James Cancer Hospital in the Ohio State University Wexner Medical Center in Columbus, Ohio. I am honored to be able to speak with you today. I have no disclosures, and I would also like to take this time to thank my home institution and my mentors. We will be discussing critical care related to the oncology population. Our objectives are to review aspects of tumorigenesis related to chemotherapeutic action and complications, to identify toxicities related to novel therapies, and to understand the special considerations for the oncology patients admitted to the intensive care unit. According to the International Agency for Research in Cancer, one in every five persons will develop cancer in their lifetime. A little over 5% of those patients will require ICU admission within the first two years of their diagnosis. Cancer is one of the leading causes of death worldwide, and it is of vital importance that we are well-versed in the subtle distinction of care required for cancer patients in the ICU as compared to patients without cancer. Most ICU admissions are due to treatment-related or cancer-specific complications, and a multidisciplinary approach is needed to identify and manage their complex needs. Advancements in cancer therapies have improved survival and quality of life for patients. However, these novel therapies come with a host of new toxicities, some of which are life-threatening and can lead to the need for ICU care. Now we will discuss tumerigenesis, chemotherapeutic targets, and their adverse events. First, we will discuss tyrosine kinase inhibitors, so you may ask, what is a tyrosine kinase? A tyrosine kinase is an enzyme involved in the cellular signaling cascade and are implicated in cellular growth, differentiation, metabolism, and apoptosis. Tyrosine kinases can become mutated, dysregulated, or overexpressed, resulting in constitutive activation, also described as constant activation. The constant activation of tyrosine kinases have been implicated in the process of normal cells gaining malignant properties, also referred to as tumerigenesis, and tyrosine kinase inhibitors block this process. Tyrosine kinase inhibitors are approved to treat a broad range of cancers, as shown on this slide. Some of them include leukemia, hepatocellular, pancreatic, and renal cell carcinoma, to name a few. Some of their targets include vascular endothelial growth factor, platelet-derived growth factor receptor, or genes such as BCR, ABL1. While it is great that tyrosine kinase inhibitors have shown a survival benefit for solid tumors, they also can cause unintended consequences that range from less severe to lethal. This is because tyrosine kinases are also expressed in non-cancerous cells and are also acted on by tyrosine kinase inhibitors. The severity of adverse effects are determined by the binding site on the target enzyme and complications decrease as tyrosine kinase inhibitors become more selective for their targets. Patients who develop or who are at risk for lethal toxicities may require ICU care. Patients can experience renal, neurologic, cardiac, hepatic, pulmonary, skin, and hematologic toxicities. Examples include, but are not limited to, pneumonitis, ischemic stroke, posterior reversible encephalopathy syndrome, intracranial hemorrhage, seizures, tumor lysis syndrome, interstitial nephritis, acute coronary syndrome, arrhythmias, and cerebral and or intestinal hemorrhage. Research efforts continue to improve tyrosine kinase selectivity to tumor cells with the goal of decreasing adverse effects and tumor resistance. Disease progression may occur because cancer cells have the ability to mutate or amplify growth factor genes. Now we will discuss monoclonal antibodies and their potential adverse effects. Monoclonal antibodies are produced in a laboratory and function similarly to the body's own natural antibodies. These laboratory created monoclonal antibodies target specific cell molecules required for tumor development and growth. They can be created to bind to a specific tumor antigen, recruit immune cells, block proteins that are essential in the tumor proliferation signaling process to heart cell growth, or deliver cytotoxic agents directly to tumor cells, resulting in tumor death. Although monoclonal antibodies are created to target specific cells, non-targeted immune cells and mediators may inadvertently become activated or suppressed, leading to cellular injury in normal cells. This is due to prolonged binding at both target and non-targeted immune cells and mediators. Monoclonal antibodies are used to treat a variety of cancers, including but not limited to colorectal, esophageal, and gastric. Listed here are their drug names and targets. Serious and life-threatening effects have been associated with monoclonal antibody use. Listed here are some cardiac, neuro, pulmonary, renal, and other toxicities that can occur. Examples include acute coronary syndrome, intracerebral hemorrhage, pneumonitis, pulmonary embolism, interstitial nephritis, and transfusion reaction. It is also important to be aware that tumor cells can eventually oppose all of the mechanisms of action of monoclonal antibodies and develop resistance. Immune checkpoint inhibitors are monoclonal antibodies that promote T cell activation and anti-tumor activity by antagonizing immune system inhibitors such as cytotoxic T lymphocyte-associated antigen, the programmed cell death protein, and its ligand. This can lead to over-activation of the immune system and can cause autoimmune damage to normal cells, which mimics autoimmune disease. This is known as an immune-related adverse event and is relevant because it occurs in up to 40% of patients who receive immune checkpoint inhibitors. Immune checkpoint inhibitors are approved to treat Hodgkin's lymphoma, melanoma, non-small cell lung carcinoma, renal cell carcinoma, and urodelial cancer. As listed on the slide, you can see the drug names and their targets that fall under this category. Immune-related adverse events from immune checkpoint inhibitors can occur in any organ or system and symptom presentation is dependent on which organs display autoimmune-like activity. The onset is variable and can range from days to 26 weeks with a median of 40 days from treatment initiation. Studies show that the cytotoxic T lymphocyte antigen 4 class has a higher incidence of immune-related adverse events than the programmed death 1 and its ligand. Although it is difficult to generalize immune-related adverse event risk factors, some risk factors have been identified and are listed on this slide. These include but are not limited to age less than 60, chronic smoking, low muscle mass, chronic kidney disease, and hypertension. Patients receiving proton pump inhibitors or diuretics, those with high disease burden or high tumor mutations, and those who are concurrently receiving traditional therapy may also have higher risk. As listed on this slide, there are some biomarkers that can be used to predict who will develop immune-related adverse events. This includes a complete blood count and thyroid-stimulating hormone, which are both readily available. It is difficult to generalize immune-related adverse event risk factors and predictive biomarkers for the entire class of immune checkpoint inhibitors because studies today are either disease specific or immune checkpoint inhibitor specific. Immune-related adverse events are classified using the common terminology criteria for adverse events, which is a standardized method for reporting. There are four grades with grade 1 being the least severe and grade 4 being the most severe, which is defined as life-threatening. Common toxicities of each organ system is broken down and described in a standardized way based on the severity of the symptoms. The American Society of Clinical Oncology Journal guideline also provides treatment-specific recommendations based on this grading system. Each toxicity has well-defined definitions of how each grade is classified. For example, the definition of grade 2 colitis is an increase of four to six stools per day from baseline, and the aforementioned guideline has specific treatment recommendations for grade 2 colitis and many other common immune-related adverse events. This is important because the continued management of immune checkpoint inhibitors and symptom management is based on what grade the toxicity is classified as. Grade 1 symptoms are mild and only require supportive care, and immune checkpoint inhibitors can be continued apart from some neurologic, hematologic, and cardiotoxicities until patients develop grade 2 symptoms. Grade 2 symptoms are defined as moderate or requiring local or non-invasive interventions. Grade 2 symptoms or higher should hold their immune checkpoint inhibitors, and the initiation of corticosteroids with the initial dose of 0.5 to 1 mg per kg a day of prednisone or its equivalent should also be considered after infection has been ruled out. Patients who develop grade 1 or 2 symptoms likely will not require ICU care, however, patients who develop grade 3 or 4 symptoms may require ICU care. Grade 3 symptoms usually are not immediately life-threatening, but are medically significant. If grade 3 or 4 symptoms are present, immune checkpoint inhibitors should be stopped and high-dose corticosteroids such as prednisone 1-2 mg per kg a day or its equivalent should be started with a plan to taper over 4-6 weeks. Consideration should also be given to adding GI prophylaxis and or pneumocystis prophylaxis. For some toxicities, influximab may be given if symptoms do not improve after 48-72 hours of high-dose corticosteroids. This slide highlights the difference between grade 3 and 4 symptoms, with the main difference being that grade 4 symptoms are life-threatening or have life-threatening consequences. Immune checkpoint inhibitors should be permanently stopped for patients with grade 4 symptoms with the exception of endocrinopathies that have been controlled by hormone replacement therapy. Symptom and organ-specific management is paramount in all grades of symptoms. Immune checkpoint inhibitors can be re-challenged when symptoms and or laboratory values revert back to grade 1. The most common toxicities involve the skin, GI tract, and renal system. This slide shows the grading for the most common toxicities, specifically cutaneous lesions, colitis, hepatitis, nephritis, and renal dysfunction. By all means, this is not a full list, but I did include a few toxicities here so that you can become familiar with the concept and format of the Common Terminology Criteria for Adverse Events Classification System. Listed here are some cardiac, neuro, pulmonary, renal, and other toxicities that can occur. Toxicities that may progress to a need for ICU care include but are not limited to meningitis, seizures, encephalitis, cerebral edema, pneumonitis, alveolar hemorrhage, pericarditis, interstitial nephritis, and thyroid dysfunction. Now we will discuss chimeric antigen receptor therapy, also referred to as CAR T. It is a type of immune effector cell therapy successfully used to send B cell leukemia and lymphoma into disease remission. Immune effector cell therapy involves removing white blood cells from a patient, separating out the T cells, and altering them in the laboratory by adding a gene for a specific chimeric antigen receptor, essentially a synthetic receptor protein. Over several weeks, the CAR T cells are grown and multiplied in the laboratory and eventually transfused back to the patient. The CAR T cells target a specific antigen, which typically is a tumor cell surface antigen. Over 30 to 40% of patients who receive CAR T therapy will require ICU level care. Because of this, we must become familiar with two of the most significant toxicities associated with CAR T therapy. Those are cytokine release syndrome and immune effector cell associated neurotoxicity syndrome. Immune cell activation and CAR T cell activation are the cause for treatment toxicity, so some amount of toxicity is expected and risk versus benefit must be weighed. The mechanism by which normal cells are damaged involves cytokine release, which is part of the CAR T cell activation process. This can result in a massive supraphysiologic release of cytokines, causing the immune system to become dysregulated and overwhelmed by the counterregulatory homeostasis mechanisms. This results in widespread life-threatening damage to both normal and abnormal cells and tissues from systemic inflammation. This describes cytokine release syndrome. Additional damage can be caused by binding of antigens expressed on non-target normal cells, also resulting in cellular injury. Cytokine release syndrome is defined by the American Society for Transplantation and Cellular Therapy as a supraphysiological response following any immune therapy that results in the activation or engagement of endogenous or infused T cells and or other immune effector cells. Symptoms can be progressive, must include fever at the onset, and may include hypotension, hypoxia, and end organ dysfunction. And there must be a correlation between these effects and the immune effector therapy received. Other possible conditions, such as infection, must also be ruled out. Featured here is the American Society for Transplantation and Cellular Therapy Toxicity Grading for cytokine release syndrome. Grading is based on the degree of fever, hypotension, and hypoxia not attributable to any other cause. There are four grades, with grade one being the least severe and grade four being the most severe. The onset is variable and peaks at two to seven days, but has been reported up to three weeks after receiving the infusion. Mild symptoms are treated with supportive care. Higher grade cytokine release syndrome, or patients with symptoms that are prolonged, may be treated with tocilizumab, a monoclonal antibody which antagonizes interleukin-6, or anakinra, and interleukin-1 receptor antagonist. Both interleukins are known to be involved in cytokine release syndrome. Sepsis can present with the same symptoms as cytokine release syndrome and must be carefully ruled out. Severe consequences of cytokine release syndrome can include cardiovascular collapse requiring vasopressors due to vasodilatory and or cardiogenic shock, respiratory failure requiring mechanical ventilation, acute kidney injury necessitating renal replacement therapy, or even death. A multicenter study demonstrated that of the patients admitted to the ICU with grade 3 or 4 toxicities from CAR T cell or other immune effector cell therapy, only 22.9% met criteria for meeting vasopressors, mechanical ventilation, or renal replacement therapy. 28 ICU mortality was low at 8.6%, suggesting that ICU management has a role in early detection and treatment of cytokine release syndrome, even if patients do not meet the standard ICU indications, such as meeting vasopressors. Another dangerous complication highly associated with CAR T cell therapy is called immune effector cell associated neurotoxicity syndrome, abbreviated as ICANS. ICANS is not the same thing as cytokine release syndrome. ICANS is described separately and can occur independently, simultaneously, or after resolution of cytokine release syndrome, or not at all. ICANS has a median onset time of four days after the infusion, typically lasting between 5 to 17 days. Symptoms can range from difficulty concentrating to cerebral edema and seizures, with expressive or global aphasia being the most distinctive feature. ICANS is defined by the American Society for Transplantation and Cellular Therapy as a disorder characterized by a pathologic process involving the central nervous system following any immune therapy that results in the activation or engagement of endogenous or infused T cells and or other immune effector cells. Symptoms or signs can be progressive and may include aphasia, altered level of consciousness, impairment of cognitive skills, motor weakness, seizures, and cerebral edema. Shown here is the American Society for Transplantation and Cellular Therapy grading system for ICANS. There are four grades, with grade one being the least severe and grade four being the most severe. Grading is based on level of consciousness, seizure activity, motor weakness, or paralysis, and an elevated intracranial pressure or cerebral edema, not attributable to any other cause. Grading uses the most severe event among the different domains. To complete the aforementioned toxicity grading, another scoring assessment, which tests for encephalopathy, must also be completed and is shown here. It is titled the ICE Assessment Tool and scores patient's ability to answer orientation questions correctly, name three objects, follow commands, and assesses their ability to write and maintain attention. Patients can score from 0 to 10. And again, this is used in conjunction with the ICANS toxicity grading classification shown on the prior slide. It is important to be aware of this dangerous complication because 70% to 80% of patients who receive CAR T cellular therapy will experience ICANS. Most grade one symptoms are self-limiting and resolve with supportive care. Corticosteroids are considered for grade two and highly recommended for grades three and four. If there are no improvement after 24 hours of corticosteroids, the patient should be evaluated for cerebral edema with neuroimaging and lumbar puncture with opening pressure and cerebral spinal fluid evaluation. Tocilizumab should not be administered unless cytokine release syndrome is occurring concurrently because tocilizumab cannot cross the blood-brain barrier and may worsen neurotoxicity. Patients who receive monoclonal antibodies, CAR T therapy, or immune checkpoint inhibitors may experience infusion reactions, including anaphylaxis, which is life-threatening. The onset of anaphylaxis is fast, occurs within seconds to minutes of exposure, and involves mass cell degradation and release of histamines, leukotrienes, and prostaglandins. Patients with anaphylaxis may experience hypotension leading to shock. They could also experience bronchospasm and angioedema, which can lead to an airway obstruction. The mainstays of treatment include removing the inciting cause and administering antihistamines, epinephrine, and corticosteroids. Earlier, we discussed cytokine release syndrome in connection with CAR T therapy. It is important to know that there are also some monoclonal antibodies that can also cause cytokine release syndrome. This table provides pearls on how to differentiate monoclonal antibody-induced cytokine release syndrome from a hypersensitivity reaction. The pearls are the onset of symptoms and the number of doses received. As you can see here, cytokine release syndrome, either from CAR T therapy or from monoclonal antibodies, will occur over two hours after receiving the first dose as compared to at least receiving one uneventful dose for hypersensitivity reactions. This is relevant to determine if the treatment plan should include tocilizumab in addition to corticosteroids, as tocilizumab is indicated in the management of cytokine release syndrome but not in the treatment of hypersensitivity reaction. So far, we have discussed the adverse events, dangerous complications, and infusion reactions, and anaphylaxis of tyrosine kinase inhibitors, monoclonal antibodies, immune checkpoint inhibitors, and CAR T cell therapy. Now we will discuss the unique critical care concerns of the patient who has cancer. Oncologic disease and the immunomodulary agents used to treat cancer can cause physiologic changes that lead to common reasons for ICU care, such as organ failure and sepsis. Furthermore, cancer and chemotherapies can cause critical illness that is unique to the oncologic population. First, we will discuss respiratory failure, since it is the leading cause of ICU admission and death for patients with or without cancer. Some of the things that make respiratory failure and cancer nuanced is the immunosuppression and treatment effects from the cancer treatment, such as chemotherapy, immunotherapy, radiation, surgical resection, stem cell transplants, and other targeted therapies. Bacterial pneumonia is the leading cause of respiratory failure in patients who have cancer. On this slide, you will find other causes of respiratory failure in the cancer patient, which includes, but is not limited to, aspiration, pneumonitis, which was mentioned quite a few times as potential unintended consequences of the therapies that we reviewed earlier. Acute respiratory failure syndrome and pulmonary embolism are also other causes of respiratory failure in cancer patients. Sepsis is one of the major reasons patients are admitted to the ICU. 20% of all sepsis-related ICU admissions are patients who have cancer. Given the unique attributes previously mentioned, these patients have increased risk of infection and a higher associated mortality. Something to be aware of is that up to 50% of patients with cancer who have sepsis or septic shock will not have positive microbiological culture data. Cancer patients who are suspected to have sepsis require immediate source control and broad spectrum antibiotics, just like a patient without cancer would. Local antibiograms should be taken into consideration when choosing antibiotics. The most common sources of infection are the lungs, intra-abdominal, primary bacteremia, or even the urinary tract. Neutropenic patients with cancer have a decrease in functional white blood cells. Placing these patients at higher risk for infection and careful antibiotic selection is a priority. In cancer patients with cancer, the lower the absolute neutral fill count, the higher the infection risk. The risk for opportunistic infections also increase as the absolute neutral fill count decreases. According to the Infectious Diseases Society of America, neutropenia is defined as a condition of less than 500 cells, or a condition that is expected to decrease to less than 500 cells or ANC that is expected to decrease to less than 500 cells during the next 48 hours. Unlike the immunocompetent patient, the only sign of infection in a patient who is immunocompromised may be a fever and this is due to the weakened immune system. This slide shows common microorganisms in neutropenic patients with cancer. Some of these are Staph aureus, Enterococcus, Strep pneumoniae, E. coli, and Klebsiella and that's just to name a few. Initial therapy in patients with sepsis include an anti-pseudomonal beta-lactam agent and agents against aerobic gram-positive cocci should be considered in patients with hemodynamic instability or high concern for pneumonia, soft tissue infection, or catheter-related infections. When there is evidence or concern for antibiotic-resistant microorganisms, the antibiotic regimen should be tailored to those microorganisms. should be considered when fever is persistent or reoccurs after 4-7 days of broad-spectrum antibiotics or when neutropenia is expected to last more than 7 days. Immunocompromised patients who have cancer and especially those receiving hemopoietic stem cell transplant are at risk for reactivation of viral infections from herpes simplex virus, varicella zoster virus, cytomegalovirus, Epstein-Barr virus, and Kaposi sarcoma-associated herpes virus. Virus-specific tests such as polymerase chain reaction or immunohistochemical staining should be considered for immunocompromised patients who have cancer given their high risk for atypical presentations. Patients can experience a range of effects including viral dissemination and even death. Patients with active infections should be treated appropriately with antiviral agents. Most commonly used is acyclovir. Patients who are receiving intensive cytotoxic therapy for leukemia and those who have received an autogenic hemopoietic stem cell transplant are among the highest at risk for atypical and opportunistic infections. Prophylaxis against candida species, invasive aspergillosis, and herpes simplex viruses should be considered. Now we will talk about acute kidney injury in cancer patients. I will refer to acute kidney injury as AKI. In these patients, AKI may be caused by the cancer itself, the nephrotoxic effects of the cancer treatment, or both. AKI in patients who have cancer oftentimes leads to reduction in or cessation of anti-cancer agents. This increases mortality, lowers remission rates, and increases healthcare costs compared to those cancer patients without AKI. Cancer-related causes of AKI include direct infiltration or obstruction, multiple myeloma protein deposits, cancer-induced hypercalcemia, cancer-related thrombotic microangiography, and paraneoplastic glomerulonephropathies. Cancer-treatment-related causes include direct injury from CAR-T cell therapy infiltration, damage from cytokine release syndrome and tumor lysis syndrome, which can occur due to CAR-T cell therapy, monoclonal antibodies, or high hematologic tumor burden, or acute tubular interstitial nephritis, which is caused by immune checkpoint inhibitors. Definitions and diagnostic testing of AKI are the same as for the general population. A special consideration in cancer patients is to consider is when monoclonal gammopathy of renal significance is suspected. In this case, serum protein electrophoresis, serum and urine immunofixation, and free light chain measurements should be performed. Biochemical tests, such as uric acid, can be useful to help identify tumor lysis syndrome and thrombotic microangiography. The measurement of ADAMS-13 activity can be used to evaluate for thrombocytopenic purpura, and if all else fails, renal biopsy can be considered. Treatment of pre-renal AKI is the same for patients with or without cancer, and focuses on maintaining adequate perfusion and avoiding nephrotoxic agents. Acute medical problems should be properly treated if they arise, for example, sepsis, pneumonia, abdominal compartment syndrome, or active hemorrhage. AKIs can be caused by a wide variety of things, and we will not be able to cover them all in this talk, but I will highlight common ones that occur in cancer patients. For example, hypercalcemia. Patients who develop hypercalcemia should be treated in the usual way of providing adequate hydration and perfusion. In patients who have ureteral obstructions and or compression, nephrostomy tubes and or ureteral stents should be considered. When initiating cytotoxic chemotherapy, adequate hydration is paramount to reduce the number of free light chains, and in patients with multiple myeloma, it should be considered to make sure they are adequately hydrated. It is also important to be aware that cisplatin is highly associated with development of AKIs, and it is also known that methotrexate is nephrotoxic. AKIs that are caused by immune checkpoint inhibitors may be treated with corticosteroids. However, one must be aware that corticosteroids may decrease the efficacy of immune checkpoint inhibitors, making this a very complex problem to treat. Supportive care and treatment of cytokine release syndrome and tumor lysis syndrome are the mainstays of therapy when AKI is caused by CAR T therapy. And ultimately, indications for renal replacement therapy remain the same as in the non-cancer population and renal replacement therapy should be offered when it is indicated. Tumor lysis syndrome can occur spontaneously or after initiation of chemotherapy and is considered an oncologic emergency. Tumor lysis syndrome is most commonly associated with a large hematologic tumor burden and is caused by rapid release of intracellular components into the systemic circulation from lysed tumor cells in amounts that exceed the kidney's ability to excrete them. Laboratory values will show hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. This is important because in addition to AKI, the metabolic derangements place patients at risk for seizures, cardiac arrhythmias, and even death. Signs and symptoms are related to the aforementioned metabolic derangements. Tumor lysis syndrome is commonly associated with non-Hodgkin lymphoma, particularly Burkitt lymphoma, acute myeloid leukemia, and acute lymphoblastic leukemia. Tumor lysis syndrome is less associated with solid tumors. This table is the Cairo-Bishop classification for diagnosis of tumor lysis syndrome. It involves both laboratory and clinical criteria for diagnosis and also risk stratification criteria. Depending on how at risk a patient is, a patient may consider allopurinol or rasburicase prophylactically. Hydration and electrolyte correction are mainstays in the treatment and, if severe enough, renal replacement therapy may be indicated. Superior vena cava syndrome occurs when blood flow through the SBC is obstructed and cancer is the leading cause of SBC syndrome. Other causes are intravascular devices with associated thrombus, such as a pacemaker or defibrillator leads or central venous catheters. Compression can be intraluminal from a thrombus or it can also be caused by direct tumor invasion or can result from extraluminal compression from surrounding pathological structures. Decreased blood flow through the SBC will lead to backup of blood from the head, neck, and upper extremities. Signs and symptoms may include edema and fullness of the face and neck, upper extremity edema, distended neck and chest veins, headache, hoarseness, shortness of breath, or cough. SBC syndrome is mostly associated with small cell lung cancer and non-Hodgkin lymphoma. Imaging is needed to evaluate the extent of the obstruction, determine the underlying cause, and guide further treatment. A histologic diagnosis is required to determine malignancy status. Treating the underlying cause is of the utmost importance. The first-line treatment for severe disease entails endovascular techniques such as angioplasty stents or catheter-related thrombus removal and open surgical treatment and bypass can also be considered. Now we will shift to post-operative management of patients who have cancer. Patients with cancer have unique needs during the post-operative setting. Some patients who have cancer can have planned surgery, whereas others will undergo emergency surgery due to either disease progression or a complication of the cancer treatment. It is common practice and the standard of care for some patients to receive neoadjuvant systemic chemotherapy and or radiation prior to surgery. Given the immunocompromised state of cancer patients, careful monitoring and high suspicion for post-operative infection are necessary. And as previously mentioned, fever may be the only sign. Some patients with cancer are malnourished prior to surgery, which will decrease wound healing. Post-operatively, patients have an increased risk for development of thromboembolic disease and DVTs. It is paramount that cancer patients have DVT prophylaxis started as soon as possible. Because it is common for chemotherapy and other cancer treatments to be stopped after emergency surgery, surgeons must work closely with medical oncology to evaluate when cancer treatments can be resumed. In summary, patients with cancer have unique pathophysiologic characteristics related to their cancer and cancer treatments that must be taken into consideration and guide their care. Some patients who have cancer require care that differs from that provided to non-cancer patients and it is important to identify how the patient who has cancer differs. Today, we have reviewed aspects of tumerigenesis related to chemotherapeutic action and complications. We identified toxicities related to novel therapies, specifically tyrosine kinase inhibitors, monoclonal antibodies, immune checkpoint inhibitors, and immune effector cells. We also described special considerations for the oncology patients admitted to the intensive care unit. Thank you for your time. I am honored to be able to present this information to you today. Thank you.

Markeisha Wilder

nurse practitioner

James Cancer Hospital

critical care

oncology patients

tumorigenesis

chemotherapeutic action

tyrosine kinase inhibitors

monoclonal antibodies